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ICU · Topics

Topics

549 units across 141 domains — Curriculum domains with PubMed-verified evidence.

Back to ICUJump to first domain
ICU Fellowship (CICM) Topics
Plate — icuMedVellum Press
549Units
141Domains
GI & nutrition / surgicalTraumaEnvironmental emergenciesRenal/MetabolicAcid–baseCardiovascularCardiovascular / aortictoxicologycardiovascularGastroenterologyCardiovascular / ACSenvironmentalObs/GynaeEnvironmentalgi-nutritionneurocritical-careNeurocritical CareNeurocritical careNeurocritical care / vascularRenalRenal and metabolicResuscitationGI/NutritionGI and nutritionRespiratory / airway emergenciesinfectious-diseasesGI & nutritionobstetricRespiratoryInfectious Diseasesneurocritical carerespiratoryPharmacologyToxicologyresuscitationhaematology-coagulationAntimicrobial StewardshipInfectious diseasesEthicsRehabilitationRespiratory / ventilationendocrinerenal-metaboliconcologyHaematologyNeurocriticalEndocrine & metabolic emergenciesEndocrineMonitoring / haemodynamicsAdvanced respiratory supportAnatomyAirway managementInfection / pharmacologyObstetric critical careHaematology / transfusionResuscitation & shockHaematology / coagulationInfectiousAntimicrobial therapyApplied pharmacologyApplied physiologyPhysiology / haematology immunologyfirst-part-physiologyNeurocritical care / monitoringBurnsHaematology / immunotherapyCardiovascular / cardiomyopathyPhysiology / cellularNeurocritical care / infectiousEthics / communicationrenalObstetricsMonitoring / echocardiographyNeurocritical care / neuromuscularRenal / RRTDiagnosticsDelirium & sleepStatistics & evidence-based medicineTransplant / organ donationEquipment, physics & clinical measurementElectrolytesPhysiology / endocrineEquipment & physicsEthics, EOL & communicationECMOInfection / generalRenal / fluidsPhysiology / GI hepaticHaematology & coagulationHepatobiliary / neurocritical careRespiratory / oxygen therapyequipment-physicsOncologyRespiratory / gas exchangeCardiovascular / hypertensionpharmacologydiagnosticsEthics and qualityObstetric / pharmacotherapyNutritionProceduralICU-acquired infectionicu-acquired-infectionrehabilitationCardiovascular / infectionRenal / acid-baseHaematology / traumaantimicrobial-stewardshipNeurocritical care / post-arrestInfection / oncologyHaematology / oncologyOxygen & gas exchangeRespiratory / monitoringCardiovascular / pericardialPerioperative critical careMonitoring / ultrasoundPost-cardiac arrest careTransplant / pharmacologyCardiovascular / vascular surgeryCardiovascular / perioperativeObstetricSedation / proceduralQuality / safetyGI & nutrition / metabolicSedation & paralysisGI & nutrition / infectionShock statesHaematology / haemoglobinopathyTransplant / immunologyInfection / surgicalTrauma / neurocritical careStatistics & evidenceNeurocritical care / seizuresSeizures & weaknessRespiratory / acid-baseOncology & immunocompromisedPhysiology / thermoregulationTrauma & burnsInfection / global healthCardiovascular / valvular
AtlasICUTopics

Domain

GI & nutrition / surgical

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Abdominal Sepsis & Peritonitis — Source Control, SBP & the Polymicrobial

The peritonitis is the inflammation of the peritoneum, usually from the intra-abdominal infection; the abdominal sepsis is the sepsis from the intra-abdominal source. The three types: the primary (the spontaneous bacterial peritonitis — the SBP in the cirrhosis and the ascites, the monomicrobial, the ascitic PMN over 250 cells per cubic mm, the cefotaxime plus the albumin), the secondary (the GI perforation or the ischaemia, the polymicrobial — the Gram-negative and the anaerobes, the source control plus the antibiotics), and the tertiary (the persistent or the recurrent after 48 hours of the failed initial treatment, the resistant — the Enterococcus, the Candida, the MDR organisms). The diagnosis: the peritonism (the rigid abdomen, the guarding, the rebound), the CT (the gold standard — the free gas, the fluid, the source), the lactate, the cultures. The management: the Sepsis-6 bundle, the broad antibiotics (the piperacillin-tazobactam ± the vancomycin ± the antifungal, or the ceftriaxone plus the metronidazole or the meropenem), the duration 4 to 7 days after the source control, and the SOURCE CONTROL (the surgery or the IR — the drainage, the debridement, the repair) — the definitive; the delayed source control worsens the mortality.

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Acute cholangitis and biliary sepsis

Acute cholangitis is bacterial infection of an obstructed biliary tree — a life-threatening emergency. Biliary obstruction raises intraductal pressure, bacteria proliferate in stagnant bile, and infected bile refluxes into the systemic circulation producing bacteraemia and septic shock. Charcot triad (fever + jaundice + RUQ pain) has limited sensitivity and is now only one limb of the Tokyo Guidelines 2018 diagnostic criteria. Reynolds pentad (Charcot + hypotension + altered mental status) indicates severe (Grade III) cholangitis with septic shock. Management: immediate empiric antibiotics — a third-generation cephalosporin first-line for community-acquired disease (E. coli and Klebsiella the main pathogens), broadened for severe or healthcare-associated infection — plus biliary drainage by ERCP timed by severity: urgent drainage for Grade III after initial resuscitation, early drainage for Grade II. Antibiotics alone are insufficient — drainage is the definitive source control.

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Acute lower gastrointestinal bleeding — diverticular, angiodysplasia, colitis and the resuscitate-to-surgery pathway

Acute lower gastrointestinal bleeding (LGIB) is bleeding arising distal to the ligament of Treitz, presenting most often with hematochezia (bright red blood per rectum) and less commonly with maroon stools or right-sided melena. The dominant causes are diverticular bleeding (the commonest cause — painless, massive, self-limiting), colonic angiodysplasia (painless and recurrent in the elderly), colitis (ischaemic, inflammatory and infectious), anorectal sources such as haemorrhoids, and colorectal malignancy or post-polypectomy. Most bleeds stop spontaneously. The management ladder is resuscitation with crystalloid and restrictive transfusion (TRICC trigger Hb <70 g/L) → exclude an upper GI source (upper endoscopy when hematochezia accompanies haemodynamic instability) → bowel preparation and colonoscopy (nonurgent for most inpatients; urgent within 24 h reserved for higher-risk patients) → CT angiography (CTA) for brisk ongoing bleeding or when colonoscopy is non-diagnostic → catheter mesenteric angiography with superselective embolisation if CTA is positive → and segmental or subtotal colectomy as the last resort for refractory haemorrhage. The Oakland score (threshold <=8, 95% probability of safe discharge in derivation) identifies low-risk patients safe for outpatient management. Cause-specific management differs: diverticular (endoscopic haemostasis, often self-limiting), angiodysplasia (ablation, consider aortic stenosis / Heyde syndrome), IBD (treat the flare, avoid over-instrumentation), ischaemic colitis (supportive — fluids, antibiotics, no endoscopic therapy unless right-sided/gangrenous).

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Acute Pancreatitis in ICU — Atlanta Severity, Goal-Directed Fluids & the Step-Up Approach

Acute pancreatitis is an acute inflammatory process of the pancreas diagnosed by two of three criteria (characteristic epigastric pain radiating to the back, serum lipase or amylase over 3x the upper limit of normal, and characteristic imaging). The revised Atlanta classification grades severity as mild (no organ failure, no complications — ~80%), moderate (transient organ failure under 48h or local/systemic complications), and severe (persistent organ failure over 48h — mortality up to 30-40%). Gallstones and alcohol are the two leading causes. ICU management of severe disease centres on goal-directed moderate-rate fluid resuscitation with Ringer’s lactate (the WATERFALL trial showed aggressive fluids harmful), early enteral nutrition within 48 hours (not NPO), analgesia, NO routine prophylactic antibiotics, urgent ERCP for gallstone pancreatitis with cholangitis, and the minimally invasive step-up approach (drainage then necrosectomy) for infected necrosis, delayed ~4 weeks if possible.

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Ileus, Bowel Obstruction & Mesenteric Ischaemia — The Acute Abdomen in ICU

The ileus, the bowel obstruction, and the mesenteric ischaemia are the three acute bowel disorders in the ICU. The ileus (paralytic) is the failure of the peristalsis (the post-op, the opioid, the electrolyte, the sepsis) — the supportive management (the NGT, the fluids, the correct the electrolytes). The bowel obstruction (mechanical) is the SBO (the adhesions the commonest) or the LBO (the malignancy, the volvulus) — the drip and suck, the surgery for the strangulation (the continuous pain, the fever, the peritonitis, the raised lactate). The mesenteric ischaemia is the vascular compromise of the bowel — the SMA embolism (the AF), the thrombosis, the venous, the non-occlusive (the low-flow). The hallmark is the PAIN OUT OF PROPORTION to the exam; the lactate rises late; the CT angiography is the diagnostic; the early surgery (the high mortality from the delay).

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Intra-abdominal Hypertension & Abdominal Compartment Syndrome — IAP, APP & Decompression

The intra-abdominal hypertension (IAH) and the abdominal compartment syndrome (ACS) are the raised intra-abdominal pressure (IAP) and its consequences. The WSACS definitions: the IAP is measured via the bladder with the patient supine, instilling no more than 25 mL of saline; a normal IAP is about 5 to 7 mmHg; the IAH is a sustained IAP of 12 mmHg or more (graded I to IV); the abdominal perfusion pressure (APP) equals the MAP minus the IAP, with a mean APP under 60 mmHg marking abdominal hypoperfusion; the ACS is a sustained IAP over 20 mmHg PLUS new organ dysfunction or failure. The organ effects: reduced venous return and cardiac output with falsely high CVP, raised airway pressure, renal failure, splanchnic ischaemia, raised ICP. The primary ACS (the abdominopelvic cause) vs the secondary (the sepsis, the massive fluid resuscitation, the burns). IAH is medical; ACS is surgical — decompressive laparotomy.

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Upper GI Bleed — Variceal & Non-Variceal — Resuscitation, Risk Scores & the Endoscopic Bundle

Upper GI bleeding is the haematemesis or melaena from a source proximal to the ligament of Treitz. The first decision is resuscitation (airway protection with early intubation in the encephalopathic, restrictive transfusion — transfuse when haemoglobin falls below 70 g/L, post-transfusion target 70-90 g/L per ESGE) followed by the variceal versus non-variceal fork. Non-variceal (peptic ulcer, Mallory-Weiss) — after endoscopic haemostasis a high-dose PPI infusion (e.g. omeprazole 80 mg bolus then 8 mg/h for 72 hours), endoscopy within 24 h with dual endoscopic therapy for active bleeding (epinephrine injection plus a second thermal or mechanical modality), H. pylori eradication and early aspirin resumption. Variceal (cirrhosis) — the time-limited BUNDLE of vasoactive drug (terlipressin, octreotide or somatostatin, e.g. octreotide 50 mcg bolus then 50 mcg/h) PLUS prophylactic antibiotic (ceftriaxone 1 g/day for up to 7 days) PLUS endoscopic evaluation within 12 hours with band ligation, with pre-emptive TIPS within 72 hours for the high-risk subgroup (Child-Pugh C or Child-Pugh B above 7 with active bleeding).

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Trauma

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Abdominal Trauma — Blunt, Penetrating, FAST & Non-Operative Management

The abdominal trauma: the blunt (the solid organ — the spleen, the liver; the hollow viscus — the small bowel, the colon; the mesenteric) and the penetrating (the stab, the gunshot). The FAST scan (the bedside — the free fluid in the 4 views) — the rapid triage. The CT with the IV contrast (the stable patient — the grading). The laparotomy indications: the peritonitis, the hypotension unresponsive, the penetrating with the peritonitis, the evisceration. The non-operative management (the NOM) for the blunt solid organ (the spleen, the liver) if the haemodynamically stable. The angioembolisation for the contrast extravasation (the blush). The damage-control laparotomy (the physiological extremis — the open abdomen, the packing, the planned re-operation).

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Chest Trauma — Blunt, Penetrating, Flail Chest & Cardiac Tamponade

The chest trauma in the ICU: the blunt (the flail chest — the paradoxical movement; the pulmonary contusion; the cardiac tamponade — the Beck triad; the traumatic aortic injury; the diaphragmatic rupture) and the penetrating (the pneumothorax, the haemothorax, the great vessel, the cardiac). The immediately life-threatening (the ATLS): the tension pneumothorax, the massive haemothorax, the flail chest, the open pneumothorax, the cardiac tamponade. The management: the chest drain (the pneumothorax and the haemothorax), the surgical exploration (the massive haemothorax over 1500 mL accumulated or over 200 mL per hour, the cardiac tamponade, the great vessel), the resuscitative thoracotomy (the arrest post-penetrating). The flail chest — the analgesia (the epidural preferred), the ventilation (the CPAP trial or the invasive for the respiratory failure), the pulmonary contusion — the resuscitation to adequate perfusion without excessive restriction, the lung-protective support.

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Chest trauma and blunt cardiac injury in ICU

Chest trauma: blunt (motor vehicle crash, fall, crush — most) or penetrating (stab, gunshot). ICU-relevant: (1) FLAIL CHEST — ≥3 consecutive ribs fractured in ≥2 places → paradoxical chest wall movement → respiratory failure. (2) PULMONARY CONTUSION — lung parenchymal injury → alveolar haemorrhage/oedema → hypoxia, evolves over the first 24-72 h (peak ~72 h). (3) BLUNT CARDIAC INJURY (BCI) — myocardial contusion → arrhythmia, troponin elevation, rarely cardiac rupture/failure; EAST screening = ECG + troponin I. (4) TRAUMATIC AORTIC INJURY — deceleration → aortic transection (most die at scene, survivors need urgent repair). (5) TENSION PNEUMOTHORAX/HAEMOTHORAX — life-threatening, needle decompression/chest drain. Management: ABCDE, analgesia (epidural/paravertebral for rib fractures), lung-protective ventilation if needed (flail chest/pulmonary contusion), chest drains for pneumo/haemothorax, surgical fixation of flail chest (controversial).

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Damage-Control Resuscitation & Surgery — The Lethal Triad & Planned Re-operation

Damage-control resuscitation (DCR) and damage-control surgery (DCS) — the integrated approach to the exsanguinating trauma patient. DCR: the permissive hypotension (SBP 80 to 90 until the bleeding controlled), the MTP 1:1:1 (RBC:plasma:platelets), the TXA within 3 hours, the minimise the crystalloid (the worsens the dilutional the coagulopathy and the acidosis), the warm. DCS: the abbreviated the laparotomy (the packing to control the bleeding, the temporary the closure, the NOT the definitive the repair), the correct the lethal triad (the acidosis, the hypothermia, the coagulopathy), and the planned the re-operation at the 24 to 48 hours (the definitive the repair, the anastomosis, the closure). The open the abdomen (the manage the intra-abdominal the hypertension, the fistula, the fluid the losses).

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Fat Embolism Syndrome — The 12–72h Triad, Gurd's Criteria & Lung-Protective Support

Fat embolism syndrome (FES) is a clinical diagnosis defined by the triad of respiratory insufficiency, neurological dysfunction and a petechial rash arising 12 to 72 hours after a major injury — classically a long bone (femur, tibia) or pelvic fracture, but also orthopaedic procedures (intramedullary nailing, joint replacement), liposuction, pancreatitis, sickle-cell crisis and bone-marrow transplant. The pathophysiology is dual — a MECHANICAL phase in which marrow fat globules embolise to the pulmonary and cerebral microvasculature, and a BIOCHEMICAL phase in which lipase hydrolyses the embolic triglyceride to free fatty acids that ignite an inflammatory cascade, injure the endothelium and produce an ARDS-like lung. The diagnosis rests on Gurd's criteria (major: respiratory insufficiency, cerebral involvement, petechial rash; minor: fever, tachycardia, retinal changes, jaundice, renal changes, thrombocytopenia). Management is SUPPORTIVE: oxygen, lung-protective ventilation (6 mL/kg, plateau <30 cmH₂O) for the ARDS-like lung, cautious fluids, vasopressors; early surgical stabilisation of the fracture (within 24 h) is the single most effective preventive measure; corticosteroid prophylaxis reduces incidence in meta-analysis but remains controversial and is not routine. FES is largely self-limiting with supportive care, but severe instances cause significant respiratory failure, neurological damage and even mortality.

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Fat embolism syndrome: diagnosis, ventilation, and management in trauma

Fat embolism syndrome (FES) is a clinical syndrome (triad: respiratory distress, neurological dysfunction, petechial rash) developing after an asymptomatic period of 24-72 hours after TRAUMA (especially long bone/pelvic fractures) or orthopaedic procedures; neurological manifestations may appear 12-72 h after the insult. Fat embolization occurs in the majority of patients with long-bone fractures, but clinical signs occur in only 1-10%. PATHOPHYSIOLOGY: (1) MECHANICAL — mechanical obstruction of capillaries by fat emboli (marrow fat embolises to the pulmonary circulation; fat emboli can deform and pass through the lungs to systemic organs, most commonly brain and kidneys; a patent foramen ovale, found in 27.3% of autopsy hearts, permits paradoxical embolism). (2) BIOCHEMICAL — hydrolysis of fat to free fatty acids injures capillary endothelium -> ARDS-like lung injury. CLASSIC TRIAD: (1) RESPIRATORY DISTRESS (hypoxaemia — the subclinical presentation may be hypoxaemia alone). (2) NEUROLOGICAL (altered consciousness, confusion, seizures, coma; rarely infarction). (3) PETECHIAL RASH (characteristic; may be absent — cerebral FES can occur without respiratory or dermatological signs). DIAGNOSIS: clinical (Gurd criteria — major + minor features, at least 1 major and 4 minor; the most commonly used criteria but not clinically validated). MANAGEMENT: SUPPORTIVE (oxygen, lung-protective ventilation — Vt 6 mL/kg predicted body weight, plateau 30 cmH2O or less); early fracture stabilisation within 24 hours is the most effective preventive strategy; corticosteroids reduce FES incidence in meta-analysis (risk reduced 78%, no mortality or infection difference) but remain controversial. OUTCOME: usually good with supportive care; severe cases cause respiratory failure, neurological damage and mortality.

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Massive haemothorax and emergency thoracotomy (resuscitative)

Massive haemothorax: >1500 mL blood in pleural space OR >200 mL/hr ongoing drainage. Life-threatening: impairs ventilation + circulation (hypovolaemia + tension physiology). Management: IMMEDIATE large-bore chest tube (28-32 Fr; 36-40 Fr offers no advantage) at 5th ICS mid-axillary line. Resuscitative thoracotomy (EDT / clamshell): emergency department procedure for arrested/peri-arrest trauma — releases tamponade, controls bleeding, open cardiac massage, cross-clamps aorta. INDICATIONS: penetrating thoracic trauma with arrest <15 min (EAST strong recommendation with signs of life); penetrating extrathoracic trauma and blunt trauma with signs of life (conditional); blunt trauma without signs of life — recommend against. Survival: penetrating 8.8% (stab 16.8%, gunshot 4.3%), blunt 1.4% (Rhee 2000); pulseless penetrating thoracic with signs of life 21.3% (EAST 2015).

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Pelvic & Extremity Trauma, Compartment Syndrome & Fat Embolism

The pelvic and extremity trauma in the ICU: the **pelvic fracture** (the Young–Burgess mechanism classification — the anteroposterior compression or open book, the lateral compression or closed book, the vertical shear; each with a different bleeding pattern and stability), the **pelvic binder** (for the open book — applied at the greater trochanters, it reduces the pelvic volume and helps tamponade the venous bleeding), the **angiographic embolisation** for the persistent arterial bleeding (after the binder + the packing), the **preperitoneal packing**, the external fixation, the associated injuries (the bladder, the urethra, the rectal, the vaginal, the sacral plexus the neurological), the **extremity trauma** (the open fracture — the Gustilo I/II/IIIA/IIIB/IIIC; the vascular, the nerve), the **compartment syndrome** (the 6 Ps — the pain disproportionate, the pressure, the paresthesia, the paralysis, the pulseless [late], the poikilothermia; the delta P under 30; the fasciotomy within 6 hours), and the **fat embolism syndrome** (the 24 to 72 hours post-fracture; the triad — the respiratory, the CNS, the petechial rash; the lung-protective ventilation, the supportive). The rhabdomyolysis (the crush injury — the CK, the myoglobin, the AKI; the aggressive hydration).

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Environmental emergencies

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Accidental Hypothermia

The accidental hypothermia — the core below 35 degrees C. The severity (the mild 32 to 35, the moderate 28 to 32, the severe below 28). The clinical (the shivering → the bradycardia, the decreased the LOC, the loss of shivering, the Osborn / J waves, the VF / the asystole). The rewarming (the passive, the active the external, the active the internal — the ECMO for the severe). The handle gently (the cold heart irritable). The NOT the dead until the warm and the dead. The drugs the extended intervals (the below 30).

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Drowning & Near-Drowning

The drowning — the respiratory the impairment from the submersion / the immersion in the liquid. The aspiration → the surfactant the dysfunction → the atelectasis, the V/Q the mismatch, the ARDS. The hypoxia → the brain the injury (the leading the cause of the death). The EARLY the CPR (the NOT the Heimlich), the 100 per cent the oxygen, the lung-the-protective the ventilation, the PEEP. The NOT the prophylactic the antibiotics / the steroids. The TTM for the comatose.

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Electrical & Lightning Injury

The electrical and lightning injury — the lightning (the brief, the massive DC; the asystole, the respiratory arrest from the medullary paralysis; the flashover; the Lichtenberg figures; the reverse the triage) and the electrical (the AC; the tetany; the VF; the deep tissue injury; the rhabdomyolysis; the compartment syndrome). The disconnect the power; the CPR; the ECG monitoring; the fluids for the rhabdomyolysis; the fasciotomy.

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Heat Stroke & Heat Illness

The heat stroke — the core temperature above 40 degrees C with the CNS dysfunction (the confusion, the seizure, the coma). The two types (the classic — the elderly, the drugs; the exertional — the young, the athletes). The thermoregulatory failure → the multi-organ (the CNS, the cardiac, the liver, the renal, the DIC). The RAPID cooling (the priority — the ice-water immersion the fastest; the evaporative the practical). The NOT the antipyretics (the central set-point normal). The benzodiazepine for the shivering. The classic the mortality the high (the 58 per cent the 28-day in the largest the cohort).

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High-Altitude Illness

The high-altitude illness — the hypobaric hypoxia from the ascent. The spectrum: the AMS (the headache + the nausea / the fatigue / the dizziness), the HACE (the ataxia + the altered mental state — the brain oedema), the HAPE (the non-cardiogenic the pulmonary oedema). The DESCENT (the primary), the acetazolamide, the dexamethasone (the HACE), the nifedipine + the oxygen (the HAPE), the Gamow bag.

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Radiation Injury

The acute radiation syndrome (ARS) is the illness caused by a high dose of whole-body ionising radiation delivered over a short time, producing three dose-dependent subsyndromes: the HEMATOPOIETIC (1-2 Gy, bone-marrow suppression, pancytopenia, infection and bleeding), the GASTROINTESTINAL (6-8 Gy, mucosal sloughing, fluid loss and sepsis) and the NEUROVASCULAR (above 30 Gy, cerebral oedema, seizures, coma, cardiovascular collapse). It evolves through four classical phases — prodromal, latent, manifest illness, and recovery or death. Radiation injury is best understood through two effect categories: DETERMINISTIC (tissue reactions with a dose THRESHOLD and severity that rises with dose — e.g. skin erythema 2 Gy, cataracts 0.5 Gy, bone-marrow suppression 1 Gy, GI syndrome 6-8 Gy, neurovascular syndrome above 30 Gy) and STOCHASTIC (cancer and heritable effects with NO threshold where PROBABILITY, not severity, rises with cumulative dose). The four radiation types behave very differently as hazards: ALPHA (stopped by paper/dead skin — an internal hazard only if inhaled/ingested), BETA (penetrates a few mm — causes skin burns), GAMMA and X-RAY (highly penetrating — a whole-body external hazard) and NEUTRON (penetrating and induces secondary radioactivity). Management is built on five pillars: (1) scene safety and external DECONTAMINATION (removing clothing removes ~90% of external contamination), (2) supportive ICU care with irradiated blood products, (3) cytokines (G-CSF / GM-CSF / pegfilgrastim) to accelerate neutrophil recovery, (4) treatment of internal contamination with specific countermeasures (Ca/Zn-DTPA for plutonium and transuranics, Prussian blue for caesium-137 and thallium, potassium iodide for radioactive iodine) and (5) haematopoietic stem-cell transplant for the most severe, irreversible marrow injury.

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Toxic Gas & Smoke Inhalation

The toxic gas and smoke inhalation — the combustion products (the CO, the cyanide, the phosgene), the industrial gases (the chlorine, the ammonia), the particulate. The chemical pneumonitis → the ARDS. The management — the 100 per cent the oxygen, the lung-the-protective the ventilation, the bronchodilators, the NOT the steroids (the ineffective). The CO / the cyanide — the see the Toxicology the topics.

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Renal/Metabolic

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Acid-base disorders in the ICU

Acid-base interpretation is fundamental to ICU practice. Use a disciplined 9-step algorithm: (1) pH (acidaemia/alkalaemia); (2) primary process (PaCO2 vs HCO3); (3) expected compensation (Winter formula); (4) A-a gradient; (5) anion gap (albumin-corrected); (6) delta gap; (7) osmolar gap; (8) lactate; (9) clinical correlation. High-AG acidosis = GOLDMARK (glycols, oxoproline, L- and D-lactate, methanol, aspirin, renal failure, ketoacidosis). Normal-AG = hyperchloraemic (diarrhoea, RTA, saline). Metabolic alkalosis: urine chloride separates saline-responsive from resistant. Chronic respiratory acidosis: classic rules have HCO3 rising 3.5 mmol/L per 10 mmHg; human COPD data suggest more. Treat the cause, not the number — BICAR-ICU found no overall benefit from sodium bicarbonate in severe acidaemia (pH at or under 7.20) with more hypernatraemia and metabolic alkalosis, though the AKI subgroup fared better.

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Acute kidney injury: prevention and nephroprotection in ICU

AKI affects more than half of ICU patients and is independently associated with increased mortality, longer ICU stay, and long-term CKD. Prevention is better than treatment (no specific 'renal rescue' therapy exists). KDIGO prevention bundle: (1) Avoid nephrotoxins (NSAIDs, aminoglycosides, iodinated contrast, ACEi/ARB in hypotension). (2) Optimise haemodynamics (adequate perfusion pressure, vasopressors for septic shock). (3) Monitor renal function (creatinine, urine output) in high-risk patients. (4) Contrast nephropathy prevention (IV isotonic saline hydration; bicarbonate no better — PRESERVE trial: no benefit of NAC). (5) Avoid hypoglycaemia and hyperglycaemia (NICE-SUGAR). (6) Do NOT use 'renal dose dopamine' (no outcome benefit). Key principle: prevent, do not rescue.

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Acute severe hyperkalaemia: emergency management algorithm

Hyperkalaemia (K+ >5.5 mmol/L): common ICU emergency. SEVERE (K+ >6.5 or ECG changes): life-threatening arrhythmia. Causes: AKI/CKD, rhabdomyolysis, tumour lysis, drugs (ACEi/ARB, K-sparing diuretics, TMP-SMX, heparin), Addison's, acidosis, massive transfusion. ECG changes: peaked T waves → widened QRS → sine wave → asystole/VF. Management: (1) STABILISE cardiac membrane (calcium gluconate 10 mL 10% IV). (2) SHIFT K+ into cells (insulin/dextrose, salbutamol, sodium bicarbonate). (3) REMOVE K+ from body (loop diuretics, GI cation exchange — patiromer/zirconium, dialysis). ECG changes = EMERGENCY.

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Drug-induced kidney injury and acute interstitial nephritis

Drug-induced kidney injury is a leading cause of AKI in ICU (a common cause of hospital-acquired AKI). Mechanisms map onto the pre-renal / intrinsic / post-renal framework: PRE-RENAL (haemodynamic) — NSAIDs inhibit prostaglandins → afferent arteriolar constriction; ACEi/ARBs dilate the efferent arteriole → fall in GFR; calcineurin inhibitors (cyclosporin, tacrolimus) cause afferent constriction; the 'triple whammy' (NSAID + ACEi + diuretic) abolishes all three autoregulatory limbs. INTRINSIC — ATN from direct tubular toxicity (aminoglycosides accumulate in proximal tubule via the megalin receptor; amphotericin B injures the distal tubule; iodinated contrast causes renal vasoconstriction plus direct tubular toxicity; cisplatin, methotrexate, tenofovir); AIN is a Type IV hypersensitivity interstitial infiltrate (penicillins, PPIs, NSAIDs, sulphonamides, rifampicin, allopurinol, 5-ASA). POST-RENAL — crystal nephropathy (aciclovir, sulphonamides, methotrexate, indinavir, triamterene). Prevention: avoid nephrotoxin combinations, isotonic saline hydration before contrast (PRESERVE: saline = bicarbonate, NAC no benefit), statins (TRACK-D showed benefit in CKD + diabetes), dose adjustment for renal function, therapeutic drug monitoring (vancomycin AUC, aminoglycoside troughs). AIN: STOP the drug ± corticosteroids. Aminoglycosides: once-daily extended-interval dosing reduces nephrotoxicity.

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Electrolyte disturbances in the ICU

Electrolyte disturbances are ubiquitous in ICU. Sodium: hyponatraemia (correct slowly — no more than 8 mmol/L in 24 h to avoid osmotic demyelination) vs hypernatraemia (free water deficit, correct at under 12 mmol/L per day). Potassium: hyperkalaemia (calcium gluconate for membrane stabilisation when there are ECG changes or K 6.5 mmol/L or over, insulin-dextrose for shift, then removal) vs hypokalaemia (correct Mg first or K will not correct). Calcium: ionised calcium is the relevant measure (not total or albumin-corrected calcium). Magnesium: essential cofactor — hypomagnesaemia causes refractory hypokalaemia and hypocalcaemia. Phosphate: hypophosphataemia in refeeding syndrome, sepsis, respiratory failure (diaphragm weakness). SIADH vs cerebral salt wasting: both cause hyponatraemia, but CSW has hypovolaemia (high urine Na + volume depletion) and requires salt + water, while SIADH is euvolaemic and needs fluid restriction.

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Renal replacement therapy in the ICU: CRRT and IHD

Renal replacement therapy (RRT) in the ICU includes CRRT (continuous, gentler, preferred in haemodynamically unstable patients), IHD (intermittent, faster, preferred in stable patients), and SLED (hybrid, 6-12h). CRRT modalities: SCUF (fluid removal only), CVVH (haemofiltration — convection), CVVHD (haemodialysis — diffusion), CVVHDF (both). Timing: AKIKI and STARRT trials showed NO benefit of early RRT (KDIGO stage 2) vs delayed (KDIGO stage 3 or indication-based). Start RRT when: refractory hyperkalaemia, acidosis, fluid overload, uraemia, or specific toxin. Anticoagulation: regional citrate (preferred — no systemic anticoagulation) or heparin. Dose: effluent rate 20-25 mL/kg/h (higher doses do NOT improve outcomes — RENAL and ATN trials).

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Rhabdomyolysis in the ICU

Rhabdomyolysis is breakdown of skeletal muscle releasing intracellular contents (myoglobin, creatine kinase, potassium, phosphate) into the circulation. Causes: trauma/crush, prolonged immobility, seizures, drugs and toxins (in one 475-patient cohort toxins caused 46% of cases, with illicit drugs, alcohol and prescribed drugs leading and statins among the most frequently implicated), infections (viral and bacterial), electrolyte disturbance, endocrinopathies, malignant hyperthermia, NMS, exertion. Presents with the classic triad of muscle pain, weakness and dark urine — although over half of patients do not complain of pain or weakness. Diagnosis rests essentially on CK (over 5x ULN or over 1000 IU/L; values may reach 100,000 IU/L); urine myoglobin is positive in only about a fifth of cases. Complications: AKI (acute tubular necrosis from myoglobin obstruction — 51% of one severe series at CK at or above 5000 U/L), hyperkalaemia (13% of severe cases at 5.5 mmol/L or above), hypocalcaemia (41% at 2.00 mmol/L or below) with rebound hypercalcaemia in recovery, compartment syndrome. Treatment: early aggressive IV fluid — 1.5-2 L of saline pre-hospital then 1.5-2 L/h, or about 400 mL/h in hospital, scaled to 12 L or more per day in severe crush; prefer lactated Ringer's to 0.9% saline; IV calcium reserved for hyperkalaemic ECG changes or potassium at or above 6.5 mmol/L; fasciotomy when the delta pressure (diastolic minus compartment pressure) falls under 30 mmHg.

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Acid–base

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Acid–Base Physiology and Blood-Gas Interpretation

Acid–base homeostasis is the chemistry of the hydrogen ion, and its disturbances are among the commonest and most informative derangements in critical illness. This topic builds the examiner's framework on four ideas. First, the physiology — the bicarbonate buffer system described by Henderson and Hasselbalch, and the more complete Stewart view in which pH is set by the carbon dioxide tension, the strong ion difference (largely sodium minus chloride) and the total concentration of weak acids (albumin and phosphate). Second, a systematic method for reading a blood gas — the pH, the pattern (metabolic versus respiratory), the appropriateness of compensation, the anion gap and the delta-delta, and the osmolar gap when a toxin is suspected. Third, the clinical disorders — the high anion-gap and normal anion-gap acidoses (lactic acidosis, ketoacidosis, the toxic alcohols, and renal tubular acidosis), the metabolic alkaloses, and the respiratory acid–base disturbances. Fourth, the evidence that has reshaped management — the SMART and SALT-ED trials showing balanced crystalloids modestly outperform saline, BICAR-ICU showing bicarbonate confers no overall benefit in severe acidaemia (with a signal in the acute-kidney-injury subgroup), and the principles of treating the cause rather than the number. Built entirely on these verified landmark trials.

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Cardiovascular

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Acute aortic dissection and acute aortic syndrome

Acute aortic dissection is a tear in the aortic intima allowing blood to enter the media, creating a false lumen. Stanford classification: Type A involves the ascending aorta (surgical emergency — mortality 1-2%/h, surgical repair). Type B involves only the descending aorta (medical management — BP control, TEVAR for complicated). Presentation: tearing chest/back pain, pulse deficit, BP differential (>20 mmHg between arms), widened mediastinum on CXR, new aortic regurgitation murmur, neurological deficit, syncope. Diagnosis: CT angiography (gold standard — intimal flap, true/false lumen), transoesophageal echo in the unstable patient, CXR widened mediastinum as a clue. Management: Type A = emergency surgery (BP control first — beta-blocker before vasodilator, target SBP 100-120 HR 60-80); Type B = medical (IV beta-blocker first — labetalol/esmolol — reduce dP/dt, target SBP 100-120), TEVAR if complicated (malperfusion, rupture, rapid expansion — ADSORB/INSTEAD trials). Acute aortic syndrome also includes intramural haematoma (IMH) and penetrating atherosclerotic ulcer (PAU). Complications: malperfusion (coronary/cerebral/mesenteric/renal/spinal), cardiac tamponade, rupture. DeBakey classification refines anatomy (I = ascending + beyond, II = ascending only, III = descending only).

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Acute aortic dissection: type A vs type B, malperfusion, and endovascular management

Acute aortic dissection = tear in aortic intima -> blood enters media -> false lumen -> propagation. CLASSIFICATION (Stanford): TYPE A (ascending aorta — 65%) — SURGICAL EMERGENCY (mortality 1-2%/h untreated, 50% in 48h). TYPE B (descending aorta — distal to left subclavian — 35%) — MEDICAL management (beta-blockers, BP control); surgery/endovascular if COMPLICATED (rupture, malperfusion, refractory pain/HTN, rapid expansion). PRESENTATION: sudden TEARING chest/back pain (migrating — tracks dissection propagation), pulse deficits (asymmetric — vessel occlusion), blood pressure differential (>20 mmHg between arms), new aortic regurgitation murmur, neurological deficit (stroke, paraplegia — spinal/visceral ischaemia), syncope. RISK FACTORS: hypertension (most important), connective tissue disease (Marfan, Ehlers-Danlos, Loeys-Dietz), bicuspid aortic valve, pregnancy, cocaine, trauma. DIAGNOSIS: CT aortogram (gold standard — intimal flap, true/false lumen, extent, malperfusion). MANAGEMENT: TYPE A — emergency SURGICAL repair (ascending aorta replacement ± AVR ± arch). TYPE B (uncomplicated) — medical (beta-blocker + BP control). TYPE B (complicated) — THORACIC ENDOVASCULAR AORTIC REPAIR (TEVAR) preferred over open surgery. MORTALITY: type A (untreated) 50% in 48h; type B (uncomplicated) 10% in 30 days.

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Acute cardiorenal syndrome in ICU

Cardiorenal syndrome (CRS): disorders of heart and kidneys whereby acute/chronic dysfunction of one causes dysfunction of the other. FIVE TYPES — TYPE 1 (acute cardiorenal): acute heart failure → AKI (most ICU-relevant). TYPE 2 (chronic cardiorenal): chronic heart failure → CKD. TYPE 3 (acute renocardial): AKI → acute heart failure. TYPE 4 (chronic renocardial): CKD → chronic heart failure. TYPE 5 (secondary): systemic disease (sepsis, diabetes, amyloid) → both. Pathophysiology: VENOUS CONGESTION (raised CVP → renal interstitial pressure → reduced GFR) is as important as low cardiac output; RAAS and sympathetic overactivation drive a vicious cycle; intra-abdominal hypertension, inflammation and oxidative stress amplify injury. Management: DECONGESTION (high-dose loop diuretics ± thiazide sequential nephron blockade), vasodilators (nitrates), inotropes (if low output), SGLT2 INHIBITORS (disease-modifying — DAPA-HF, EMPEROR, DAPA-CKD), avoid nephrotoxins, ultrafiltration only for refractory cases (CARRESS-HF — worse than pharmacological therapy), renal replacement therapy if refractory. KEY INSIGHT: VENOUS CONGESTION (not just low output) drives AKI — decongestion is the primary target; a creatinine rise during effective decongestion is acceptable and prognostically favourable.

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Acute coronary syndromes (STEMI, NSTEMI, unstable angina)

Acute coronary syndrome (ACS) encompasses STEMI, NSTEMI, and unstable angina — all caused by acute myocardial ischaemia from coronary plaque rupture/erosion. Classification: STEMI (ST elevation >1mm in limb leads, >2mm in chest leads) requires IMMEDIATE reperfusion (primary PCI within 90 min door-to-balloon, or thrombolysis if PCI unavailable within 120 min). NSTEMI (troponin rise without ST elevation) requires risk stratification (GRACE/TIMI score) and early invasive strategy within 24-72h for high-risk. Universal management: dual antiplatelet therapy (aspirin + P2Y12 inhibitor — ticagrelor or prasugel preferred over clopidogrel), anticoagulation (heparin or bivalirudin), high-dose statin, beta-blocker (if no contraindication), ACE inhibitor. …

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Acute decompensated heart failure and cardiogenic pulmonary oedema

Acute decompensated heart failure (ADHF) is a life-threatening syndrome of pulmonary and/or systemic congestion from cardiac dysfunction. Presentations: cardiogenic pulmonary oedema (acute breathlessness, orthopnoea, frothy sputum, bilateral crackles, hypoxia), cardiogenic shock (hypoperfusion — cold extremities, oliguria, altered mental status), or isolated right heart failure (peripheral oedema, raised JVP, hepatomegaly). Management: sit upright, high-flow oxygen, IV furosemide (1-2.5x usual oral dose), vasodilator (nitroglycerin if SBP >110), non-invasive ventilation (CPAP/BiPAP — reduces intubation and mortality). Identify and treat precipitant (ACS, arrhythmia, infection, non-adherence). Avoid beta-blockers acutely (negative inotropy).

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Acute decompensated heart failure: NIV, diuretics, inotropes, and MCS in ICU

Acute decompensated heart failure (ADHF) = sudden worsening of heart failure → pulmonary oedema and/or systemic congestion. PRECIPITANTS: ACS, arrhythmia (AF), infection, non-adherence (medications/diet), renal failure, anaemia, thyroid, drugs (NSAIDs, calcium channel blockers). CLASSIFICATION: (1) 'WARM AND WET' (most common — pulmonary oedema + preserved perfusion — BP normal/high) → vasodilators + diuretics. (2) 'COLD AND WET' (cardiogenic shock — hypoperfusion + congestion — hypotensive) → inotropes + diuretics ± MCS. (3) 'WARM AND DRY' (compensated). (4) 'COLD AND DRY' (low output, no congestion). MANAGEMENT: (1) NIV (CPAP/BiPAP — 3CPO trial — faster relief of dyspnoea and metabolic disturbance; no difference between CPAP and BiPAP; no effect on short-term mortality). (2) DIURETICS (frusemide IV — 1-2.5x usual oral dose — DOSE trial: high vs low dose — no difference in symptoms or renal function; continuous vs bolus — no difference). (3) VASODILATORS (nitroglycerin for the hypertensive congested patient — reduce preload/afterload). (4) INOTROPES (if cold — dobutamine, milrinone — bridge only: PROMISE and OPTIME-CHF). (5) MCS (IABP, Impella, VA-ECMO — if refractory shock — IABP-SHOCK II: no routine IABP). (6) IDENTIFY + TREAT PRECIPITANT (ACS → PCI; AF → cardioversion; infection → antibiotics). AVOID: beta-blockers acutely (negative inotrope — may worsen), calcium channel blockers (negative inotrope), NSAIDs (sodium retention), routine morphine (ADHERE: associated with worse outcomes), routine ultrafiltration (CARRESS-HF). INITIATE GDMT (four pillars) once stabilised (MERIT-HF, CIBIS-II, COPERNICUS).

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Acute decompensated pulmonary hypertension in ICU

Acute decompensated pulmonary hypertension (PH): acute worsening of PH → right ventricular (RV) failure → cardiogenic shock. PH classification (WHO): Group 1 (PAH — idiopathic, heritable, connective tissue), Group 2 (left heart disease), Group 3 (lung disease/hypoxia), Group 4 (CTEPH), Group 5 (multifactorial). CRISIS: RV cannot pump against high pulmonary vascular resistance (PVR) → RV dilatation → septal shift → LV compression → low cardiac output → cardiogenic shock → death. Management: (1) Maintain systemic BP (noradrenaline — alpha vasoconstriction). (2) Reduce PVR (inhaled NO, prostacyclins, PDE5 inhibitors). (3) Support RV (inotropes — milrinone, dobutamine). (4) Correct triggers (hypoxia, acidosis, arrhythmia, volume overload). (5) Mechanical support (VA-ECMO) for refractory cases.

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Acute myocarditis and pericarditis

Acute myocarditis is inflammation of the myocardium — commonest causes: viral (coxsackie, parvovirus B19, COVID-19), autoimmune, drug-induced (immune checkpoint inhibitors), idiopathic. Presents with: chest pain (may mimic MI), heart failure, arrhythmia, or cardiogenic shock (fulminant myocarditis). Diagnosis: troponin elevated, ECG changes (non-specific ST/T changes, may mimic MI), echo (regional wall motion abnormalities, reduced EF), cardiac MRI (gold non-invasive — oedema, late gadolinium enhancement in subepicardial/mid-wall pattern), endomyocardial biopsy (gold standard but rarely performed). Treatment: supportive (heart failure therapy, mechanical support if fulminant), avoid NSAIDs in acute phase (may worsen inflammation). Giant cell myocarditis: urgent immunosuppression + transplant evaluation.

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Acute pericarditis

Acute pericarditis is inflammation of the pericardium. Causes: viral (#1 — coxsackie, echovirus), idiopathic, post-MI (Dressler syndrome — autoimmune, weeks after MI), post-pericardiotomy, autoimmune (SLE, RA, sarcoid), uraemic, malignancy, bacterial (TB), radiation. Presentation: pleuritic chest pain (worse on inspiration, better on sitting forward), pericardial friction rub (three-component: atrial systole, ventricular systole, ventricular diastole), diffuse ST elevation + PR depression on ECG. Treatment: NSAIDs (ibuprofen/indomethacin) + colchicine (reduces recurrence). Steroids are second-line for refractory disease or autoimmune causes. Most cases resolve within 1-3 weeks.

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Acute pulmonary embolism: PESI risk stratification, thrombolysis, and PERT

Acute pulmonary embolism risk stratification with the PESI and simplified PESI scores, systemic and catheter-directed thrombolysis, and the role of the pulmonary embolism response team (PERT).

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Acute severe acute coronary syndromes: STEMI, NSTEMI, and ICU management

Acute coronary syndromes (ACS) = sudden myocardial ischaemia from coronary plaque rupture/erosion → thrombus → reduced blood flow. THREE TYPES: (1) STEMI (ST-elevation MI — total occlusion — Q-wave — emergency reperfusion PRIMARY PCI <90 min or fibrinolysis <30 min). (2) NSTEMI (non-ST elevation MI — partial occlusion — troponin positive, no ST elevation — urgent angiography <24h high-risk). (3) UNSTABLE ANGINA (ischaemia without troponin rise — rare with high-sensitivity troponin). PRESENTATION: chest pain (crushing, radiating arm/jaw, associated sweating, nausea, dyspnoea). ECG (ST elevation STEMI; ST depression/T inversion NSTEMI). TROPONIN (rise/fall = myocardial necrosis). MANAGEMENT: DUAL ANTIPLATELET (aspirin + P2Y12 inhibitor — ticagrelor/prasugrel/clopidogrel), ANTICOAGULANT (heparin — unfractionated/LMWH/fondaparinux), STATIN (high-dose — atorvastatin 80mg), BETA-BLOCKER, ACEi/ARB. REPERFUSION: PRIMARY PCI (STEMI — gold standard), FIBRINOLYSIS (if PCI not available <120 min), CORONARY ARTERY BYPASS (multi-vessel). ICU COMPLICATIONS: cardiogenic shock (IABP/Impella/ECMO), arrhythmia (VT/VF — defibrillation), heart failure, mechanical (VSD, papillary muscle rupture, free wall rupture — days 3-5), pericarditis. MORTALITY: STEMI 5-10% (PCI era).

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Acute severe valvular emergencies: critical aortic stenosis, acute MR and AR

Acute valvular emergencies present as cardiogenic shock, pulmonary oedema, or cardiac arrest. CRITICAL AORTIC STENOSIS (severe AS — area <1.0 cm², mean gradient >40): fixed outflow obstruction — preload-dependent, intolerance of AF/hypovolaemia, vasodilators dangerous. Definitive: aortic valve replacement (surgical or TAVI). Bridge: balloon aortic valvuloplasty (BAV) or VA-ECMO. ACUTE MITRAL REGURGITATION (papillary muscle rupture post-MI, endocarditis, chordal rupture): sudden volume overload on LA + pulmonary veins -> flash pulmonary oedema + cardiogenic shock. Murmur may be SOFT (rapid equalisation of pressures). Echo diagnostic. Treatment: afterload reduction (nitroprusside, IABP), vasopressors/inotropes cautiously, definitive: urgent MV…

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Advanced haemodynamic monitoring in the ICU

Haemodynamic monitoring guides resuscitation in critically ill patients. From basic (clinical examination, urine output, arterial line, CVP line) to advanced (invasive cardiac output monitoring). Levels: (1) Basic: arterial line (BP, blood sampling, waveform), CVP line (right atrial pressure — a POOR predictor of fluid responsiveness). (2) Intermediate: echocardiography (non-invasive, qualitative + quantitative — the most versatile ICU tool), lactate, ScvO2. (3) Advanced: pulmonary artery catheter (PAC — gold standard but invasive, declining use after FACTT/PAC-Man/ESCAPE), transpulmonary thermodilution (PiCCO/TPTD — GEDV, ITBV, EVLW, PVPI), lithium dilution (LiDCO), pulse contour analysis (arterial line-derived CO). Fluid responsiveness must be assessed with DYNAMIC tests (passive leg raise, fluid challenge, SVV/PPV) not static markers (CVP). Choose monitoring based on the clinical question, not routinely.

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Arrhythmia, cardiac arrest and post-arrest care

Cardiac arrest in the ICU requires immediate Advanced Life Support per ERC 2021 guidelines: high-quality CPR (rate 100-120, depth 5-6cm, full recoil), early defibrillation for shockable rhythms (VF/pVT), adrenaline 1 mg IV every 3-5 minutes, amiodarone 300 mg for refractory VF. Post-arrest care per ERC/ESICM 2021: targeted temperature management (TTM2: normothermia with fever prevention is as good as 33C hypothermia, which caused more haemodynamically compromising arrhythmia), urgent coronary angiography for a cardiac cause, lung-protective ventilation, haemodynamic optimisation, neuroprognostication deferred to at least 72 hours. ECPR for refractory cardiac arrest in selected, high-volume centres.

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Cardiac arrhythmia management in the ICU

Arrhythmias are common in ICU (up to 20% of patients). Types: atrial fibrillation (#1 — new-onset AF in ICU is associated with worse outcomes), ventricular tachycardia/fibrillation (life-threatening — usually cardiac origin), bradyarrhythmias (heart block, sinus bradycardia), supraventricular tachycardia (AVNRT/AVRT), atrial flutter. Management principles: (1) is the patient haemodynamically unstable? → cardiovert/defibrillate immediately. (2) Identify and treat underlying cause (electrolytes, ischaemia, sepsis, drugs). (3) Rate vs rhythm control. AF: rate control (beta-blocker, diltiazem) usually first; rhythm control (amiodarone, DC cardioversion) if unstable. VT/VF: defibrillate + amiodarone. Bradycardia: atropine → adrenaline/pacing. SVT: vagal manoeuvres → adenosine 6→12→12 mg. Torsades: IV magnesium, stop QT-prolonging drugs, overdrive pacing.

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Cardiogenic shock and mechanical circulatory support

Cardiogenic shock is a life-threatening state of end-organ hypoperfusion due to cardiac pump failure, with short-term mortality of 40-50%. The SCAI classification (Stages A-E) guides severity assessment. Management escalates from pharmacological support (noradrenaline first-line vasopressor, dobutamine/milrinone as inotropes) through to mechanical circulatory support: IABP (no routine benefit per IABP-SHOCK II), Impella microaxial flow pump (lower 180-day mortality in STEMI-related shock per DanGer Shock, at the cost of more adverse events), and VA-ECMO (no routine benefit per ECLS-SHOCK). The Impella actively unloads the left ventricle; the combination with VA-ECMO (ECPELLA) addresses both systemic flow and ventricular unloading.

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Deep vein thrombosis and pulmonary embolism management in ICU

ICU management of venous thromboembolism (VTE) — DVT and PE. Severity stratification of PE: (1) MASSIVE (high-risk): sustained hypotension (SBP <90) or shock → thrombolysis or embolectomy. (2) SUBMASSIVE (intermediate-risk): RV dysfunction + biomarker elevation, normotensive → monitor closely, consider rescue thrombolysis. (3) LOW-RISK (minor): normal RV, normal biomarkers → anticoagulation, possible early discharge. Anticoagulation: DOACs (rivaroxaban, apixaban) first-line for stable; LMWH/heparin for unstable or renal failure; warfarin for long-term if antiphospholipid syndrome. Thrombolysis: alteplase 100 mg over 2 h (massive PE); a 50 mg tenecteplase bolus has been reported in arrest. Catheter-directed thrombolysis: low-dose alteplase, emerging. Surgical embolectomy: if thrombolysis contraindicated.

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Heart failure guideline-directed medical therapy update: SGLT2, ARNI, and the four pillars

Heart failure with reduced EF (HFrEF): FOUR PILLARS of guideline-directed medical therapy (GDMT). (1) ARNI (sacubitril/valsartan) or ACEi/ARB. (2) Beta-blocker (bisoprolol, carvedilol, metoprolol succinate). (3) Mineralocorticoid receptor antagonist (MRA — spironolactone, eplerenone). (4) SGLT2 inhibitor (dapagliflozin, empagliflozin) — NEWEST, benefits HF regardless of diabetes. Each reduces mortality ~15-20%. Target: all four (if tolerated). New paradigm: start EARLY, all FOUR, then uptitrate. SGLT2 inhibitors are REVOLUTIONARY — first drug class to benefit HFrEF AND HFpEF. In ICU: don't start new GDMT during acute decompensation — stabilise first, start after recovery.

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Hypertensive emergency and crisis

Hypertensive emergency = severe BP elevation (typically >180/120) with ACUTE end-organ damage (encephalopathy, stroke, MI, pulmonary oedema, aortic dissection, AKI, pre-eclampsia/eclampsia). Requires IMMEDIATE IV treatment in ICU (arterial line, titratable agents). Goal: reduce MAP by 10-20% in first hour, then to 160/100 within 2-6h. Do NOT reduce BP too rapidly — risk of hypoperfusion (especially brain — cerebral autoregulation is shifted right in chronic HTN). Agents: labetalol (versatile — most emergencies), nicardipine (smooth, titratable), nitroprusside (rapid but cyanide toxicity risk), nitroglycerin (ACS/pulmonary oedema). SPECIAL CASES: aortic dissection = rapid reduction (SBP to 100-120), pre-eclampsia = magnesium sulphate + labetalol/hydralazine, phaeochromocytoma = ALPHA-blockade before beta-blockade.

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Infective endocarditis in the ICU

Infective endocarditis (IE) is microbial infection of the endocardial surface (usually heart valves). ICU admission for: septic shock, heart failure from valvular destruction, embolic stroke, conduction abnormalities. Diagnosis: modified Duke criteria (blood cultures + echocardiography). Organisms: S. aureus (#1 overall — acute, aggressive), viridans streptococci (subacute — dental source, #1 in community-acquired native valve), Enterococcus (genitourinary source), HACEK, culture-negative (Coxiella, Bartonella, fungi — Candida), fungi (Candida — large vegetations, IVDU/prolonged lines). Treatment: prolonged IV antibiotics (4-6 weeks), organism-specific. Empiric: vancomycin + gentamicin + cefepime for severe/septic shock; definitive — penicillin/ceftriaxone for strep, nafcillin/oxacillin (flucloxacillin) for MSSA, vancomycin for MRSA. Surgery indications: heart failure from valvular destruction (#1), uncontrolled infection, large mobile vegetation with embolism, perivalvular extension (abscess), prosthetic valve dehiscence.

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Mechanical circulatory support: IABP, Impella, and ECMO for cardiogenic shock

Mechanical circulatory support (MCS) for refractory cardiogenic shock spans a spectrum from modest afterload reduction to full cardiopulmonary replacement. (1) IABP (intra-aortic balloon pump): counterpulsation in the descending thoracic aorta — inflates in diastole (augmenting coronary perfusion), deflates at systole (reducing afterload); modest support (~0.5-1.0 L/min augmentation). IABP-SHOCK II (Thiele 2012, NEJM): NO mortality benefit in AMI-CS — routine use not recommended. (2) Impella: transaortic axial-flow micro-pump actively unloading the LV (Impella CP 2.5-4.0 L/min; Impella 5.0/5.5 up to 5.5 L/min). DanGer-SHOCK (Moller 2024, NEJM): IMPROVED 180-day survival in AMI-CS (45.8% vs 58.5% deaths). IMPRESS (Ouweneel 2017): no benefit in severe shock. (3) VA-ECMO (venoarterial ECMO): full cardiopulmonary bypass, 4-6 L/min + oxygenation; peripheral (femoro-femoral) vs central (ascending aorta); requires distal perfusion cannula and often LV venting. ECLS-SHOCK (Thiele 2023, NEJM): no mortality benefit at 30 days. (4) TandemHeart (LA-to-femoral arterial centrifugal pump, ~4 L/min) and ProtekDuo (dual-lumen RA-to-PA cannula for RV support). SCAI shock stages A-E guide escalation. Complications: bleeding (anticoagulation), thrombosis, limb ischaemia, haemolysis, infection, stroke, LV distension (VA-ECMO), Harlequin syndrome.

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Pulmonary hypertension and right heart failure

Pulmonary hypertension (PH) = mean pulmonary artery pressure (mPAP) >20 mmHg (ESC/ERS 2022). Five WHO groups: Group 1 (pulmonary arterial hypertension, PAH — idiopathic, heritable [BMPR2], connective tissue disease [SSc], congenital heart disease, portal hypertension, drugs), Group 2 (left heart disease — the commonest cause overall, HFpEF/HFrEF/valvular), Group 3 (lung disease/hypoxia — COPD, ILD, OSA), Group 4 (chronic thromboembolic PH, CTEPH — potentially curable by pulmonary endarterectomy), Group 5 (multifactorial — haematological, systemic, metabolic). Haemodynamic phenotyping by right heart catheterisation: pre-capillary (mPAP >20, wedge <15, PVR >2 WU), isolated post-capillary (mPAP >20, wedge >15, PVR <2 WU), combined pre/post-capillary. Pathophysiology: vascular remodelling triad — (1) endothelial dysfunction (reduced NO and prostacyclin, excess endothelin-1), (2) smooth muscle proliferation and medial hypertrophy, (3) in situ thrombosis (procoagulant state) — producing a fixed, obliterative pulmonary vasculopathy and raised PVR. RV FAILURE CASCADE (the main cause of death): chronic pressure overload -> RV hypertrophy -> RV dilatation -> tricuspid regurgitation -> septal shift into the LV -> reduced LV filling -> low cardiac output -> cardiogenic shock. RV is uniquely afterload-sensitive (thin-walled, crescent-shaped, adapted to a low-pressure, low-resistance circuit). ICU PRESENTATION: exertional syncope (a red flag of low fixed output), hypoxaemia (right-to-left shunt via PFO, V/Q mismatch), and overt right heart failure (raised JVP, peripheral oedema). ICU MANAGEMENT: (1) protect the RV — cautious preload only if hypovolaemic; the RV is volume-intolerant), reduce afterload (inhaled nitric oxide around 20 ppm in ICU cohorts, inhaled/IV prostacyclin, milrinone), support contractility (milrinone PREFERRED — inotropy + pulmonary vasodilation; dobutamine), maintain systemic BP with noradrenaline (preserve RV coronary perfusion — systemic pressure must be kept at least close to RV systolic pressure or the RV ischaemias). (2) Optimise the gas exchange and ventilation — avoid hypoxia, hypercapnia, and acidosis (all heighten pulmonary vascular tone); minimise PEEP and intrathoracic pressure. (3) PAH-specific therapy for confirmed Group 1 PAH — endothelin receptor antagonists (bosentan, macitentan), PDE5 inhibitors (sildenafil, tadalafil), prostacyclin analogues (epoprostenol, iloprost, treprostinil), soluble guanylate cyclase stimulators (riociguat — never combined with PDE5 inhibitors). (4) Treat the underlying group — pulmonary endarterectomy for Group 4, left heart disease for Group 2 (PAH drugs are HARMFUL in post-capillary PH). (5) Mechanical support (VA-ECMO) for refractory RV failure. Avoid systemic vasodilators, excessive fluids, and high intrathoracic pressure.

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Sepsis-induced myocardial dysfunction (septic cardiomyopathy)

Sepsis-induced cardiomyopathy (SICM): reversible, biventricular myocardial dysfunction arising during septic shock and NOT explained by ischaemia, infarction, or pre-existing structural heart disease. Presents: NEW LV systolic dysfunction (reduced EF), RV dysfunction, and diastolic dysfunction superimposed on a vasoplegic (distributive) shock state. Mechanism: circulating myocardial depressant substances (TNF-α, IL-1β, IL-6), nitric oxide/iNOS overproduction, mitochondrial dysfunction with impaired oxidative phosphorylation, beta-adrenergic receptor downregulation/desensitisation, and coronary microcirculatory dysfunction. Diagnosis: echocardiography (reduced EF, LV dilatation, RV dysfunction, abnormal global longitudinal strain, diastolic impairment) supported by elevated troponin and BNP/NT-proBNP; cardiac MRI for atypical/persistent cases. Treatment: treat sepsis (source control, antibiotics), fluid resuscitation guided by fluid-responsiveness testing, vasopressors (noradrenaline first-line), inotropes if low cardiac output (dobutamine, milrinone; levosimendan NOT routinely recommended — LeoPARDS). REVERSIBLE — EF usually recovers within 10 days in survivors.

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Cardiovascular / aortic

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Acute Aortic Syndromes — Dissection

Acute aortic dissection is classified by the Stanford system: Type A (involving the ascending aorta — a surgical emergency with a high risk of rupture, tamponade, aortic regurgitation, and stroke) and Type B (descending aorta, distal to the left subclavian — managed medically with aggressive BP control). The classic presentation is a tearing chest or back pain, maximal at onset, with a pulse deficit or a new aortic regurgitation murmur. The diagnosis is by CT angiography (the intimal flap, the true and the false lumen). Type A requires urgent surgery; Type B is managed with a beta-blocker FIRST (to control the heart rate and the sheer stress), then a vasodilator (to lower the BP to an SBP under 120). Never give a vasodilator without a beta-blocker first — the reflex tachycardia worsens the dissection.

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toxicology

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Acute Carbon Monoxide Poisoning — Comprehensive ICU Management

Acute carbon monoxide (CO) poisoning — odourless, colourless gas of incomplete combustion (faulty heaters, house fires, exhausts, generators). CO binds haemoglobin with ~240x the affinity of oxygen, forming carboxyhaemoglobin (COHb), causing a TRIPLE insult: (1) functional anaemia (reduced O2 carrying capacity), (2) LEFT shift of the oxyhaemoglobin dissociation curve (residual O2 held too tightly — impaired tissue release), and (3) direct cellular hypoxia via binding myoglobin and inhibiting mitochondrial cytochrome c oxidase (cytochrome a3 / Complex IV) → histotoxic hypoxia + lactic acidosis. Clinical: headache, nausea, dizziness, confusion — 'flu-like symptoms in MULTIPLE people from the SAME household in WINTER = CO until proven otherwise.' Severe: syncope, seizures, coma, cardiovascular collapse. Cherry-red skin is a classical but RARE and LATE sign — do NOT rely on it. Diagnosis: COHb on venous blood gas (venous sample sufficient — arterial NOT required) — COHb >10% significant, >25% severe, >50% potentially fatal. CRITICAL: SpO2 by standard pulse oximetry is FALSELY NORMAL because it cannot distinguish COHb from oxyhaemoglobin. Management: 100% oxygen via non-rebreather mask immediately — reduces CO half-life from ~320 min (room air) to ~80 min; hyperbaric oxygen (HBO) at 2.5-3 atm reduces half-life to ~23 min — indicated (controversial) for COHb >25%, loss of consciousness, neurological signs, pregnancy, cardiac ischaemia. Delayed neurological sequelae (DNS) in 20-40% of severe cases at 2-40 days — cognitive impairment, parkinsonism — may be permanent; no proven prevention.

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Acute Digoxin Toxicity — Comprehensive ICU Management

Digoxin toxicity — Na/K-ATPase inhibition: gastrointestinal signs, bradycardia and heart block predominate; death is from ventricular fibrillation or tachycardia; hyperkalaemia in acute overdose marks severity (each 1 mmol/L rise increases mortality odds). Chronic toxicity (commonest — elderly, renal impairment, drug interactions such as amiodarone and quinidine) is harder to recognise than acute overdose and can occur at 'therapeutic' levels. Visual toxicity ranges from xanthopsia (yellow vision) to isolated reduced acuity. Characteristic rhythm: bidirectional VT (alternating His-Purkinje foci). Management: digoxin-specific antibody fragments (40 mg vial binds 0.5 mg digoxin) for life-threatening tachy-bradyarrhythmias, hyperkalaemia over 6 mmol/L, or haemodynamic instability with digoxin over 2 µg/L — 80% complete resolution, median response 19 min in the landmark 150-patient series; titrate rather than give the full calculated neutralising dose (80 mg bolus acute; 1 vial repeated at 60 min chronic). Magnesium sulfate is the established antiarrhythmic adjunct. Calcium remains a listed controversy — Levine found no excess malignant dysrhythmia or mortality, but caution persists. Post-Fab TOTAL digoxin levels are uninterpretable — follow FREE digoxin and the clinical picture. Historical mortality of acute digitalis poisoning was reported at 3-25%; with Fab, 54% of arrested patients survived hospitalisation.

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Acute Lithium Toxicity — Comprehensive ICU Management

Acute and chronic lithium toxicity — a narrow therapeutic-index drug excreted almost exclusively by the kidney as the free ion (maintenance targets 0.6-0.8 mmol/L, some authorities 0.8-1.2; clearance falls with ageing, renal insufficiency and interacting drugs — diuretics, ACE inhibitors, NSAIDs). THREE patterns — acute, acute-on-chronic and chronic; chronic is the commonest, usually unintentional, driven by impaired kidney function from volume depletion (including lithium-induced nephrogenic diabetes insipidus) or drug interactions. The CNS is the primary site of toxicity (confusion, ataxia, seizures); persistent, particularly cerebellar, neurological deficits are described after chronic poisoning. Management: STOP lithium and interacting drugs, correct volume depletion (routine sodium chloride infusion to force lithium excretion is NOT recommended — no specific effect on excretion, caused hypernatraemia), consider whole-bowel irrigation for substantial sustained-release ingestions, and apply EXTRIP extracorporeal criteria — recommended in severe poisoning, with impaired kidney function and level over 4.0 mEq/L, or with decreased consciousness, seizures or life-threatening dysrhythmias at any level; suggested for level over 5.0 mEq/L, significant confusion, or expected time to under 1.0 over 36 h; haemodialysis preferred (lithium is readily dialyzable), continuous RRT an acceptable alternative; continue until clinical improvement or level under 1.0 mEq/L — intracellular lithium redistributes, so EXPECT REBOUND.

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Acute Methanol and Ethylene Glycol Poisoning — Comprehensive ICU Management

Toxic alcohol poisoning = methanol and ethylene glycol (the 'toxic alcohols') — both are metabolised by ALCOHOL DEHYDROGENASE (ADH) to highly toxic organic acids → SEVERE HIGH ANION GAP METABOLIC ACIDOSIS + end-organ injury. Methanol (CH3OH) → formaldehyde → FORMIC ACID → inhibits mitochondrial cytochrome c oxidase → RETINAL/optic nerve toxicity → BLINDNESS + basal ganglia injury. Ethylene glycol (HOCH2CH2OH) → glycoaldehyde → GLYCOLIC ACID (main acidosis driver) → glyoxylic acid → OXALIC ACID → precipitates with calcium → CALCIUM OXALATE CRYSTALS in renal tubules → ACUTE KIDNEY INJURY + hypocalcaemia. Both cause CNS depression, nausea, abdominal pain. DIAGNOSTIC CLUE: HIGH anion gap metabolic acidosis + HIGH osmolar gap EARLY (parent alcohol present — small osmotically active molecules). The osmolar gap FALLS as the anion gap RISES (parent alcohol is metabolised into organic acids) — so a LATE presenter may have a NORMAL osmolar gap. Latent period 12–24 h (metabolism required) — patient looks 'drunk' then deteriorates. Management PILLARS: (1) FOMEPIZOLE 15 mg/kg IV LOAD (blocks ADH → stops toxic metabolite formation — PREFERRED over ethanol — far safer, no CNS depression/hypoglycaemia) then 10 mg/kg q12h; (2) HAEMODIALYSIS (removes parent alcohol + metabolites — indicated for severe acidosis pH <7.3, AKI, visual symptoms, high levels >50 mg/dL, deterioration); (3) COFACTORS — FOLINIC ACID (methanol — folate-dependent oxidation of formate → CO2 + H2O) + THIAMINE + PYRIDOXINE (ethylene glycol — shunt glyoxylate to non-toxic glycine, AWAY from oxalate); (4) sodium bicarbonate for acidosis (also ion-traps formate/glycolate → enhances elimination). Ethanol is the ALTERNATIVE ADH inhibitor if fomepizole unavailable (target 100–150 mg/dL). Activated charcoal is USELESS (alcohols are small, rapidly absorbed, poorly bound). Outbreaks from illicit/counterfeit alcohol common. Mortality methanol 10–40% (up to 50% in outbreaks); ethylene glycol ~1–2% with early fomepizole + dialysis.

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Acute Organophosphate and Nerve Agent Poisoning

Organophosphate (OP) and nerve agent poisoning — inhibition of acetylcholinesterase (AChE) → acetylcholine accumulation → overstimulation of muscarinic receptors (SLUDGE: salivation, lacrimation, urination, defecation, GI distress, emesis — PLUS miosis, bradycardia, bronchorrhoea, bronchospasm), nicotinic receptors (fasciculations, muscle weakness, paralysis, mydriasis, tachycardia), and CNS (confusion, seizures, coma). OPs: pesticides (chlorpyrifos, dichlorvos, malathion, parathion), nerve agents (sarin, soman, tabun, VX, novichok). Diagnosis: CLINICAL (history of exposure + cholinergic toxidrome) — confirm with RBC AChE activity (reduced) and plasma butyrylcholinesterase (reduced). Management: (1) DECONTAMINATION (remove clothing, wash skin with soap and water — STAFF PPE is critical to prevent secondary contamination), (2) ATROPINE (muscarinic antagonist — titrate to ENDPOINT: dried secretions, HR >80, SBP >80 — NOT to pupil size — escalating boluses — most regimens double after a failed bolus — to the endpoint; intubated survivors required a mean of 23.4 mg, range 1-75 mg), (3) PRALIDOXIME (2-PAM — reactivates AChE — WHO regimen 30 mg/kg bolus then 8 mg/kg/hr infusion, evidence contested — MUST be given BEFORE 'aging' of the enzyme-OP complex — dimethyl OPs age within 3-5 minutes, diethyl within 3-5 hours), (4) BENZODIAZEPINES (diazepam 10 mg IV — for seizures and neuroprotection — given PROPHYLACTICALLY in nerve agent exposure), (5) SUPPORTIVE: intubation (non-depolarising NMB — NOT succinylcholine — which is metabolised by AChE → prolonged paralysis), ventilation, treat arrhythmia. Complications: intermediate syndrome (24-96h post-exposure — proximal muscle weakness + cranial nerve palsies + respiratory failure — from prolonged AChE inhibition), OPIDN (2-3 weeks post-exposure — distal sensorimotor neuropathy — from neurotoxic esterase inhibition — not responsive to atropine/pralidoxime). Mortality 10-40% (higher in resource-limited settings; nerve agents higher mortality).

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Acute Paracetamol (Acetaminophen) Overdose — Comprehensive ICU Management

Acute paracetamol (acetaminophen) overdose — the commonest cause of acute liver failure in the developed world. Most of an absorbed dose is safely conjugated by glucuronidation and sulphation; a minor fraction is oxidised by cytochrome P450 (mainly CYP2E1) to a toxic intermediate metabolite (NAPQI) that is normally detoxified by glutathione — in overdose glutathione is overwhelmed, the metabolite binds covalently to hepatic enzymes and proteins, and centrilobular (zone 3) hepatocyte necrosis follows. The Rumack-Matthew nomogram: single timed 4-hour level against a treatment line starting at 150 mg/L at 4 h (half-life 4 h to 24 h) in North America and Australasia; the UK has used a single 100 mg/L line for all patients since September 2012, alongside treating all staggered or uncertain-time ingestions and extending the initial acetylcysteine infusion from 15 to 60 minutes. The 21-hour three-bag IV NAC regimen (150 mg/kg over 15-60 min, 50 mg/kg over 4 h, 100 mg/kg over 16 h), the two-bag 200 mg/kg plus 100 mg/kg regimen, non-IgE rate-related anaphylactoid reactions (8.2 per cent of courses), NACSTOP early cessation, modified-release and massive (40 g or more) overdose management, the King's College criteria for transplant referral (arterial pH under 7.30, prothrombin time over 100 s, creatinine over 300 micromol/L, grade 3-4 encephalopathy), arterial lactate for risk stratification, and cerebral oedema management in paracetamol-induced acute liver failure.

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Acute Salicylate Poisoning — Comprehensive ICU Management

Acute salicylate (aspirin) poisoning — uncoupling of oxidative phosphorylation, inhibition of Krebs-cycle dehydrogenases and increased ketoacid production give the signature MIXED acid-base disorder: respiratory alkalosis (direct medullary stimulation) plus high-anion-gap metabolic acidosis. Clinical: tinnitus, hyperventilation, hyperpyrexia, agitation, seizures, non-cardiogenic pulmonary oedema, coma. Severe poisoning: altered mental status, ARDS requiring oxygen, failure of standard therapy, or high serum concentrations — all EXTRIP indications for extracorporeal treatment. Oil of wintergreen is 98% methyl salicylate: one teaspoon (5 mL) equals about 7000 mg salicylate — roughly 22 adult aspirin tablets — and as little as 4 mL has been fatal in a child. Management: activated charcoal (salicylate is on the charcoal-appropriate list, and a further dose is appropriate), urinary alkalinisation with IV sodium bicarbonate to a urine pH of 7.5 or more — which works only once plasma potassium is corrected to approximately 4 mmol/L — and intermittent haemodialysis (the preferred modality) for severe cases. Above all protect the compensatory hyperventilation: mechanical ventilation at conventional settings abolishes the respiratory alkalosis and drives salicylate into the brain.

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Acute Snake Envenomation — Comprehensive (ANZ Context)

Acute snake envenomation in Australia and New Zealand — the world's most venomous snakes belong to the family Elapidae (front-fanged: brown snake [Pseudonaja — #1 cause of snakebite death — procoagulant + presynaptic neurotoxin + rarely thrombotic microangiopathy], tiger snake [Notechis — procoagulant + neurotoxic + myotoxic], taipan [Oxyuranus — most toxic land snake — procoagulant + neurotoxic + myotoxic], death adder [Acanthophis — postsynaptic neurotoxin — curare-like — reversible], black snake [Pseudechis — myotoxic + anticoagulant], rough-scaled snake [Tropidechis — procoagulant + myotoxic], sea snakes [Hydrophiidae — myotoxic + neurotoxic]). Clinical syndromes: (1) PROCOAGULANT → venom-induced consumption coagulopathy [VICC] — prothrombin activators → massive consumption of fibrinogen and factors V, VIII, X → INR >5 + fibrinogen <0.5 + D-dimer massively elevated + PLATELETS NORMAL — but BLEEDING IS RARE despite extreme coagulopathy because the venom clots AND lyses simultaneously (unlike warfarin or DIC — no true anticoagulated state) — give antivenom NOT FFP unless actively bleeding — recovery takes 12-24h with antivenom as liver resynthesises factors. (2) NEUROTOXIC → descending flaccid paralysis: ptosis → ophthalmoplegia → bulbar palsy → limb weakness → respiratory failure — resembles myasthenia gravis (postsynaptic: death adder) or botulism (presynaptic: tiger, brown, taipan) — the pupil reflex and deep tendon reflexes distinguish. (3) MYOTOXIC → muscle pain, tenderness, rising CK (10,000-100,000+), myoglobinuria, AKI — tiger, black, taipan, sea snakes. (4) NEPHROTOXIC → AKI from rhabdomyolysis + direct nephrotoxicity + thrombotic microangiopathy — brown snake. (5) CARDIOVASCULAR COLLAPSE → sudden early collapse (within 1h of bite) — brown snake — thought to be transient hypotension from venom cardiotoxicity or anaphylactoid reaction — high-risk feature. Management: (1) FIRST AID: pressure immobilisation bandage [PIB] — broad bandage over bite site + splint + immobilise the limb — slows LYMPHATIC venom spread (NOT venous — venom moves via lymphatics) — DO NOT remove until antivenom ready in hospital (removal causes venom surge). (2) SNAKE VENOM DETECTION KIT [SVDK] — bite site swab or urine — identifies snake GROUP (brown, tiger, black, death adder, taipan) — guides monovalent antivenom choice — BUT 5% false negative in envenomed patients + 36% false positive in non-envenomed patients — clinical syndromic diagnosis is more reliable. (3) ANTIVENOM: monovalent if snake identified by SVDK or clinical/geographic assessment OR polyvalent if snake unknown — ONE VIAL is sufficient to bind all circulating venom (recent evidence: median dose declined from 4 to 1 vial without harm) — pre-medicate with adrenaline (subcutaneous 0.25 mg) to reduce hypersensitivity reactions (24% reaction rate, 6% severe) — large volumes if polyvalent (dilute in crystalloid, infuse over 30 min). (4) VICC MANAGEMENT: give antivenom — DO NOT give blood products (FFP, cryoprecipitate, platelets) UNLESS actively bleeding — the coagulopathy resolves over 12-24h with antivenom as the liver resynthesises factors — giving FFP 'feeds' the venom prothrombin activator more substrate to consume (paradoxical worsening) and risks transfusion reactions. (5) SUPPORTIVE: mechanical ventilation for neurotoxicity, renal replacement therapy for AKI, treat rhabdomyolysis with fluids. Mortality ~1-2% with antivenom (23 deaths over 10 years in ASP-20; 17 from brown snake).

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Acute Tricyclic Antidepressant (TCA) Poisoning — Comprehensive ICU Management

Acute tricyclic antidepressant (TCA) poisoning — the classic 'membrane stabilising' overdose. The lethal mechanism is a QUINIDINE-LIKE block of fast cardiac sodium channels: phase 0 depolarisation slows in the His-Purkinje system and myocardium → WIDE QRS, AV block, impaired automaticity → HYPOTENSION and VENTRICULAR DYSRHYTHMIAS. Alongside this: CNS depression (lethargy to coma), SEIZURES (20% in one prospective cohort), sinus tachycardia and QTc prolongation. Severity is read off the ECG, not the drug level: QRS >100 ms is the consensus trigger for sodium bicarbonate; a terminal R wave ≥3 mm in aVR (or R/S ratio ≥0.7 in aVR) independently predicts seizures and ventricular arrhythmias; QRS <100 ms within the first 6 h of confirmed intoxication excludes adverse cardiac events. Referral dose thresholds: >5 mg/kg for most TCAs (>2.5 mg/kg for desipramine, nortriptyline, trimipramine; >1 mg/kg for protriptyline). Management: HYPERTONIC SODIUM BICARBONATE 1–2 mmol/kg IV BOLUS, repeated while the patient remains unstable, to a MAXIMUM of 6 mmol/kg, combined with mechanical ventilation and hyperventilation to achieve serum alkalinisation (pH ~7.45–7.55) — sodium loading and alkalaemia are both part of the mechanism. Correct the hypokalaemia and hypocalcaemia bicarbonate causes (both prolong QT and can trigger torsades). Seizures: BENZODIAZEPINES (treat fast — seizure after presentation predicted death with OR ~41). Hypotension: IV fluids, vasopressors per ACLS; terlipressin is described for catecholamine-refractory shock. AVOID class Ia/Ic antiarrhythmics (they add phase-0 sodium-channel depression); phenytoin evidence is weak — lidocaine is the better-studied class Ib adjunct when bicarbonate is insufficient. AVOID flumazenil (consensus: not recommended in TCA poisoning). CAUTION with physostigmine (asystole reported in TCA case series). Activated charcoal only if early (up to 1 h) with a protected airway; whole-bowel irrigation is not routine. Lipid emulsion 20% (1.5 mL/kg bolus then 15 mL/kg/h) is rescue therapy for refractory cardiovascular compromise. Not a filtration problem: large volume of distribution and saturable kinetics — massive overdoses can need prolonged bicarbonate for days. Prognosis: 3% ICU mortality in a prospective cohort; TCA poisoning death rates ~10× those of SSRIs per million prescriptions.

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Drug-Induced Hyperthermia Syndromes — Comprehensive Differential and Management

Drug-induced hyperthermia syndromes — five life-threatening conditions that present with hyperthermia + autonomic instability + altered mental status + (often) muscle rigidity, each requiring a SPECIFIC management approach: (1) Malignant hyperthermia (MH — RYR1 mutation, triggered by volatile anaesthetics/succinylcholine → uncontrolled sarcoplasmic calcium release → hypermetabolic crisis with unexplained hypercapnia, acidosis, hyperkalaemia, rigidity → stop trigger, hyperventilate with 100 percent oxygen, active cooling and dantrolene 2.5 mg/kg IV), (2) Neuroleptic malignant syndrome (dopamine D2 blockade from antipsychotics → rigidity, hyperthermia, altered mental status, autonomic lability with CK elevation → stop antipsychotic, bromocriptine 2.5 mg three times daily, supportive care), (3) Serotonin syndrome (clonus, hyperreflexia, agitation, diaphoresis on a serotonergic drug → stop serotonergics, benzodiazepines, cyproheptadine 12 mg then 2 mg every 2 hours, paralysis and cooling if severe), (4) Sympathomimetic toxicity (benzodiazepines first-line, avoid routine beta-blockade), (5) Anticholinergic toxicity (antimuscarinic delirium, urinary retention — physostigmine 0.5 to 1 mg titrated for severe delirium with stable rhythm).

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Acute Cardiac Tamponade — Comprehensive ICU Management

Acute cardiac tamponade — compression of the heart by pericardial fluid (or clot/gas) preventing diastolic filling → reduced stroke volume → cardiogenic shock → cardiac arrest. Causes: malignancy (#1 — lung, breast, lymphoma, melanoma), idiopathic/viral pericarditis, post-cardiac surgery (clot), uraemia, tuberculosis, aortic dissection (haemopericardium), trauma, post-MI (Dressler syndrome, free wall rupture), radiation, connective tissue disease (SLE, RA), drug-induced (procainamide, hydralazine). Clinical: Beck's triad (hypotension + muffled heart sounds + elevated JVP — classical but uncommon in clinical practice), pulsus paradoxus (>10 mmHg drop in SBP during inspiration — from reduced LV filling as RV expands into the compressed pericardial sac), tachycardia, distended neck veins, dyspnoea. ECG: low voltage + electrical alternans (swinging heart in large effusion). Echo: pericardial effusion + RA/RV diastolic collapse + plethoric IVC + respiratory variation in mitral/tricuspid inflow (>25% mitral, >40% tricuspid). Management: PERICARDIOCENTESIS (life-saving — aspirate fluid → relieve compression → restore cardiac filling). Echo-guided pericardiocentesis (subxiphoid or apical approach — Seldinger technique with pigtail drain). If recurrent: pericardial window (surgical — subxiphoid pericardiostomy or VATS). Fluid bolus (500 mL crystalloid — increases preload to transiently overcome the pericardial constraint). Avoid positive pressure ventilation (reduces venous return → worsens tamponade). Avoid diuretics/vasodilators (reduce preload → worsen).

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Acute decompensated heart failure — comprehensive ICU management (ADHF, cardiogenic shock overlap)

Acute decompensated heart failure (ADHF) = a rapid or gradual onset of signs/symptoms of heart failure warranting urgent therapy and hospital admission — the common final pathway of pump failure producing congestion and/or hypoperfusion. CLASSIFICATION (Nohria/Stevenson bedside profiles): a 2x2 of congestion (WET vs DRY) x perfusion (WARM vs COLD) — in the 452-patient validation cohort: WET & WARM the largest group (n=222), WET & COLD cardiogenic-shock-like (n=91), DRY & WARM (n=123), DRY & COLD (n=16); profiles predict death/urgent transplant. PRECIPITANTS: ischaemia/ACS, atrial fibrillation, hypertensive surge, non-adherence, drugs (NSAIDs), infection, renal dysfunction. MANAGEMENT: sit up, oxygen, early NIV for pulmonary oedema (3CPO: no 7-day mortality difference vs oxygen but faster dyspnoea/metabolic improvement), IV loop diuretic (DOSE: high-dose 2.5x prior oral dose gave greater diuresis at the cost of transient renal dysfunction; bolus = infusion), high-dose nitrates only in the hypertensive patient (Cotter), noradrenaline over dopamine in shock (SOAP II), ultrafiltration not first-line (CARRESS-HF: inferior to stepped pharmacological therapy), avoid morphine (ADHERE analysis: more ventilation, ICU admission, mortality), continue GDMT four pillars and optimise before discharge.

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Acute hypertensive emergency — comprehensive ICU management (hypertensive encephalopathy, ICH, dissection, pre-eclampsia, phaeochromocytoma, cocaine)

Hypertensive emergency = a severe elevation of blood pressure (typically SBP >180 and/or DBP >120 mmHg) accompanied by ACUTE ongoing target-organ damage (cerebral — encephalopathy, intracerebral haemorrhage, ischaemic stroke; cardiac — acute coronary syndrome, acute pulmonary oedema, aortic dissection; renal — acute kidney injury with proteinuria/microangiopathy; retina — papilloedema and flame haemorrhages; pregnancy — pre-eclampsia/eclampsia). It is distinguished from hypertensive URGENCY (severe BP but NO acute end-organ damage), which is managed with ORAL agents over 24-48 h. The central pathophysiological principle is the cerebral autoregulation curve: in chronic hypertension the curve shifts to the RIGHT, so the brain depends on a higher mean arterial pressure (MAP) to maintain perfusion. Reducing BP too rapidly or to 'normal' values drops cerebral blood flow below the autoregulatory threshold and causes ISCHAEMIC stroke — hence the safe target for most emergencies is a 10-20% MAP reduction in the first hour, then gradual reduction to ~160/100 mmHg over 2-6 h. EXCEPTIONS requiring aggressive, immediate reduction are aortic dissection (SBP to 100-120 mmHg, beta-blocker FIRST to lower dP/dt) and ischaemic stroke pending thrombolysis decision. MANAGEMENT is in ICU/HDU with an arterial line and a titratable IV agent; drug selection is dictated by the SPECIFIC emergency: labetalol (alpha + beta-blocker, versatile, safe in pregnancy and post-stroke), nicardipine (smooth titratable calcium-channel blocker, the preferred agent for most), clevidipine (ultra-short-acting dihydropyridine), nitroglycerin (ACS and pulmonary oedema), esmolol (aortic dissection — titratable beta-blockade), hydralazine (pregnancy), phentolamine (phaeochromocytoma — alpha-blockade), and fenoldopam (renal-protective). AVOID sodium nitroprusside where possible (cyanide/thiocyanate toxicity, increases intracranial pressure, coronary steal) and NEVER give sublingual nifedipine (unpredictable precipitous fall -> stroke/MI). SPECIAL CASES: intracerebral haemorrhage -> lower SBP to 140 mmHg (INTERACT2 — intensive lowering to 140 improved functional outcome); pre-eclampsia/eclampsia -> MAGNESIUM SULPHATE FIRST for seizure prevention/treatment, then labetalol/hydralazine; phaeochromocytoma -> ALPHA-blockade (phentolamine/phenoxybenzamine) BEFORE any beta-blocker (unopposed alpha-1 stimulation -> catastrophic hypertension); cocaine-induced -> BENZODIAZEPINES first (calm sympathetic surge), avoid pure beta-blockers (unopposed alpha).

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Acute Infective Endocarditis — Comprehensive ICU Management

Infective endocarditis (IE) — microbial infection of the endocardial surface (usually heart valves) causing valvular destruction, embolisation, and systemic sepsis. Modified Duke criteria (2 major OR 1 major + 3 minor OR 5 minor for definite IE). Major criteria: (1) positive blood cultures (typical organism from 2 separate cultures), (2) echocardiographic evidence (vegetation, abscess, new valvular regurgitation). Organisms: Strep viridans (30%), Staph aureus (30% — most aggressive, highest mortality), Enterococcus (10%), HACEK (2-5%), culture-negative (5-10% — prior antibiotics, Coxiella, Bartonella, fungi). ICU presentations: septic shock from valvular destruction + systemic sepsis, acute heart failure from acute valvular regurgitation, embolic stroke (20-40% — from vegetation fragments), mycotic aneurysm rupture (intracranial haemorrhage), heart block (aortic valve abscess → septal extension → AV node compression). Management: (1) CULTURE before antibiotics (3 sets blood cultures from different sites 30 min apart — then start empiric antibiotics), (2) EMPIRIC THERAPY: native valve — ampicillin + gentamicin OR vancomycin + gentamicin (if penicillin-allergic or suspected MRSA); prosthetic valve — vancomycin + gentamicin + rifampicin, (3) SURGICAL INDICATIONS: heart failure from acute valvular regurgitation (EARLY surgery — within 24-48h), uncontrolled infection (persistent bacteraemia >7 days despite antibiotics, fungal/enterococcal IE), large mobile vegetations (>10 mm with embolic events, >15 mm regardless), periannular extension (abscess, fistula, heart block), prosthetic valve IE, (4) ANTICOAGULATION: continue if on warfarin for other indications BUT stop if cerebral embolism/haemorrhage. Mortality: 15-25% overall (higher with S. aureus, prosthetic valve, elderly, embolic events).

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Acute Severe Pulmonary Embolism — Comprehensive ICU Management

Acute severe pulmonary embolism (PE) — obstruction of the pulmonary arterial tree by thrombus (usually from deep vein thrombosis) causing increased dead space, right ventricular afterload, RV failure, reduced cardiac output, and potentially cardiac arrest. Risk factors: immobility, malignancy, surgery, pregnancy, OCP, inherited thrombophilia (factor V Leiden, prothrombin gene mutation, antithrombin deficiency). Severity classification: massive PE (high-risk — sustained hypotension, cardiogenic shock, or cardiac arrest — registry mortality 25 per cent in shock, 65 per cent with CPR), submassive PE (intermediate-risk — normotensive but RV strain — RV dysfunction on echo + biomarker elevation; death or decompensation 5.6 per cent at 7 days on heparin alone in PEITHO), low-risk PE (sPESI 0 — 30-day mortality 1.0 per cent). ICU management: massive PE → thrombolysis (alteplase 100 mg IV over 2 h, run with heparin as in the landmark trial) OR catheter-directed thrombolysis OR surgical embolectomy; thrombolysis during CPR for PE-arrest (tenecteplase 50 mg IV bolus reported with neurological recovery); submassive PE → anticoagulation + monitor for deterioration (rescue thrombolysis only if decompensates — PEITHO showed routine lysis adds stroke and bleeding without a mortality benefit); low-risk → anticoagulation + consider early discharge. VA-ECMO for refractory collapse (bridge to definitive therapy). PESI/sPESI guide disposition. Chronic thromboembolic pulmonary hypertension develops in 3.8 per cent of survivors by two years.

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Acute severe valvular emergencies — critical aortic stenosis, acute mitral regurgitation, acute aortic regurgitation (comprehensive ICU management)

Acute valvular emergencies present as cardiogenic shock, flash pulmonary oedema, syncope, or cardiac arrest, and they are defined by THREE NATIVE-VALVE LESIONS plus prosthetic valve failure. (1) CRITICAL AORTIC STENOSIS (AVA <1.0 cm², mean gradient >40 mmHg, peak velocity >4 m/s; critical/shock when AVA ~0.6 and gradient ~50): a FIXED LV outflow obstruction with a stiff hypertrophied ventricle that is PRELOAD-, AFTERLOAD- and ATRIAL-KICK dependent. The AS symptom triad is ANGINA (5-yr survival), SYNCOPE (3-yr), HEART FAILURE (2-yr) — prognosis without AVR is dismal. Haemodynamic goal: SLOW heart rate (60-80, long diastolic filling time), HIGH SVR (noradrenaline — never vasodilate), ADEQUATE PRELOAD (cautious diuresis only), and MAINTAIN SINUS RHYTHM (AF is devastating — synchronised DC cardioversion if unstable). AVOID nitrates/GTN, ACEi/ARB, high-dose beta-blockers, and over-diuresis. Definitive therapy is AORTIC VALVE REPLACEMENT (surgical AVR or TAVI); balloon aortic valvuloplasty (BAV) or VA-ECMO bridge the unstable patient. (2) ACUTE MITRAL REGURGITATION (papillary muscle rupture 2-7 days post-inferior MI, chordal rupture, endocarditis, trauma): sudden volume overload of a small non-compliant LA -> flash pulmonary oedema + shock; the murmur may be SOFT or ABSENT (rapid LA pressure equalisation) — never be reassured by a quiet chest. Echo (flail leaflet, eccentric jet) is diagnostic. Haemodynamic goal: LOW SVR/afterload reduction (nitroprusside; IABP gives mechanical unloading) + inotrope (dobutamine/milrinone); definitive therapy is URGENT MV repair/replacement, or MitraClip (TEER) in the prohibitive-surgical-risk patient. (3) ACUTE AORTIC REGURGITATION (Type A dissection, endocarditis, trauma): diastolic run-off into a non-compliant LV -> rapidly rising LVEDP -> acute pulmonary oedema + shock; the wide pulse pressure, water-hammer pulse and Austin-Flint murmur of CHRONIC AR are usually ABSENT in acute AR (LV has not adapted; pulse pressure may be normal, murmur SHORT). Haemodynamic goal: LOW SVR + HIGH HEART RATE (tachycardia is protective — shorter diastole = less regurgitation) + vasopressor (noradrenaline to raise diastolic/coronary perfusion); AVOID pure beta-blockers in isolated acute AR (abolishes the compensatory tachycardia) and AVOID IABP (diastolic augmentation WORSENS the regurgitant volume) — except that in Type A dissection WITH AR, beta-blockers ARE first-line (to reduce dp/dt shear) and the AR is corrected by emergency surgery. Definitive therapy is URGENT SURGICAL AVR. (4) PROSTHETIC VALVE DYSFUNCTION: thrombosis (mechanical valve — obstructive: rtPA/systemic thrombolysis or surgery; non-obstructive: heparin ± lysis), pannus, dehiscence (paravalvular leak), structural deterioration (bioprosthesis), and prosthetic endocarditis — any unexplained shock/pulmonary oedema in a prosthetic-valve patient demands urgent echo (± fluoroscopy for leaflet motion). In ALL acute valvular emergencies the ECHOCARDIOGRAM is diagnostic and must be obtained EARLY; standard 'heart failure' therapy (nitrates, aggressive diuresis, IABP, negative inotropes) can be CATASTROPHIC if applied without knowing the lesion.

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Post-Cardiac Surgery ICU Management — Comprehensive

Post-cardiac surgery ICU management — the systematic care of patients after cardiopulmonary bypass (CPB) surgery (CABG, valve replacement/repair, aortic surgery). The early postoperative period focuses on: (1) haemodynamic stabilisation (vasoplegic syndrome in 9-44% of bypass patients — NO-mediated distributive shock with a normal or high cardiac index — noradrenaline first, vasopressin, methylene blue 2 mg/kg for refractory; low cardiac output syndrome — dobutamine first-line), (2) bleeding and tamponade assessment (severe chest tube output over 300 mL in the first hour, over 200 in the second and over 100 in the third carries attributable harm; sudden cessation with haemodynamic collapse = clotted tube and tamponade until proven otherwise → URGENT RE-EXPLORATION, which runs at 2.5-3.7% and is safest within 4 hours), (3) rhythm management (new AF in 20-40% with onset on days 2-4 — rate control usually suffices, beta-blocker prophylaxis best established), (4) ventilatory support and weaning (fast-track: extubation within 6 hours in selected patients once warm, stable, not bleeding and awake), (5) temperature and metabolic management (rewarm — hypothermia on ICU arrival predicts bleeding and re-exploration; keep potassium and magnesium replete; tight glucose control improves diabetic CABG outcomes).

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Domain

Gastroenterology

6

medium

Acute cholecystitis in ICU: severe and complicated presentations

Acute cholecystitis: inflammation of gallbladder, usually from cystic duct obstruction by gallstone (90-95%). ICU-relevant severe presentations: (1) GANGRENOUS cholecystitis (wall necrosis → perforation, mortality 15-30%). (2) EMPHYSEMATOUS cholecystitis (gas-forming organisms in wall — Clostridium, E. coli — mortality 15-25%). (3) ACALCULOUS cholecystitis (10% — critically ill patients, no stones — ischaemia, biliary stasis; mortality 30-50%). (4) PERFORATION (localised abscess or free perforation with bilious peritonitis). (5) EMPYEMA (pus-filled gallbladder — surgical emergency). Severe presentations need ICU for sepsis, organ failure, post-operative care. Management: antibiotics (gram-negative + anaerobic cover), cholecystectomy (early laparoscopic for fit; percutaneous cholecystostomy for unfit/critically ill).

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medium

Acute diverticulitis in ICU: complicated presentations

Diverticular disease: diverticula (mucosal herniations through colonic wall) ± inflammation. Acute diverticulitis: inflammation of diverticula. ICU-relevant complicated diverticulitis (Hinchey III-IV): peritonitis, perforation, abscess, fistula, obstruction. Hinchey classification: I — pericolic abscess, II — distant abscess, III — purulent peritonitis, IV — faeculent peritonitis. Management: Hinchey I-II (abscess) — antibiotics + percutaneous drainage. Hinchey III (purulent peritonitis) — laparoscopic lavage + drainage (controversial) or Hartmann's. Hinchey IV (faeculent peritonitis) — Hartmann's procedure (sigmoid colectomy + end colostomy).

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high

Acute liver failure: King's College criteria, transplant, and liver support

Acute liver failure (ALF): severe liver injury with encephalopathy + coagulopathy (INR >1.5) within 26 weeks, without pre-existing liver disease. Causes: paracetamol overdose (#1 in UK/Australia), drug-induced (idiosyncratic), viral hepatitis, mushroom (Amanita), Wilson's, ischaemic, pregnancy-related. King's College Criteria (KCC): predict mortality → guide transplant decision. Paracetamol: pH <7.3 OR (INR >6.5 + creatinine >300 + grade 3-4 encephalopathy). Non-paracetamol: INR >6.5 alone OR 3 of (age <10 or >40, cause: non-A/non-B/drug/halothane, jaundice >7 days before encephalopathy, INR >3.5). Treatment: ICU support (manage complications: cerebral oedema, coagulopathy, AKI, sepsis), N-acetylcysteine (all causes), emergency liver transplant (definitive), liver support devices (MARS — bridge to transplant).

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high

Acute pancreatitis: Revised Atlanta Classification and severity scoring

Acute pancreatitis severity classification (Revised Atlanta 2012): MILD (no organ failure, no complications — 80%), MODERATE (transient organ failure <48h, local complications — 15%), SEVERE (persistent organ failure >48h — 5%, mortality 30%). Severity scores: APACHE II (best overall — ≥8 suggests severe), Ranson (at admission + 48h), BISAP (5 simple criteria), Glasgow (Imrie). Complications: pancreatic necrosis (sterile vs infected), peripancreatic fluid collections, pseudocyst, walled-off necrosis. Management: aggressive IV fluids (Ringer's lactate — 250-500 mL/h), early enteral nutrition, analgesia, ERCP if gallstone obstruction, antibiotics ONLY if infected necrosis.

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high

Intestinal obstruction in ICU: mechanical and adynamic

Intestinal obstruction: blockage of bowel lumen (mechanical) or failure of peristalsis (adynamic/paralytic ileus). Small bowel obstruction (SBO): adhesions (60%), hernias (15%), malignancy (15%), Crohn's, intussusception. Large bowel obstruction (LBO): colorectal cancer (60%), volvulus (10-15%), diverticulitis (10%), faecal impaction. Pseudo-obstruction (Ogilvie): massive colonic dilation without mechanical obstruction, in critically ill patients. Strangulation: blood supply compromised → ischaemia → necrosis → perforation → peritonitis → death. ICU management: resuscitation, NGT decompression, 'drip and suck', surgery for strangulation/peritonitis/failed conservative. Pseudo-obstruction: neostigmine, colonoscopic decompression, surgery if fails.

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high

Peritonitis in ICU: spontaneous bacterial, secondary, and tertiary

Peritonitis: inflammation of peritoneum. THREE types in ICU: (1) SPONTANEOUS BACTERIAL PERITONITIS (SBP): infection of ascites WITHOUT obvious intra-abdominal source, in cirrhotic patients. Diagnosis: ascitic PMN >250 cells/mm³. Treatment: cefotaxime/ceftriaxone, albumin (prevents HRS). (2) SECONDARY PERITONitis: infection from intra-abdominal source (perforation, abscess, post-surgical leak). Polymicrobial. Treatment: surgery (source control) + broad-spectrum antibiotics. (3) TERTIARY PERITONITIS: persistent or recurrent peritonitis in critically ill, often with resistant organisms (Enterococcus, Candida, Pseudomonas, MRSA). High mortality. Also: CAPD peritonitis (peritoneal dialysis patients).

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Domain

Cardiovascular / ACS

1

high

Acute Coronary Syndromes (STEMI/NSTEMI) in the ICU

Acute coronary syndromes (ACS) span the spectrum of acute myocardial ischaemia — unstable angina (UA), NSTEMI and STEMI — now unified under the Fourth Universal Definition of Myocardial Infarction (Thygesen 2018, Circulation), which classifies MI into five pathophysiological types (spontaneous, supply-demand, sudden death, PCI-related and CABG-related). STEMI (complete coronary occlusion) is treated with primary PCI within 90 minutes or thrombolysis within 30 minutes; NSTEMI is risk-stratified by the GRACE score for early invasive PCI within 24 hours. All ACS receives aspirin plus a P2Y12 inhibitor (ticagrelor preferred per PLATO, NEJM 2009) plus parenteral anticoagulation (heparin or bivalirudin per HORIZONS-AMI). In MI complicated by cardiogenic shock, early revascularisation is the standard (SHOCK, NEJM 1999); routine IABP confers no mortality benefit (IABP-SHOCK II, NEJM 2012), culprit-only PCI beats multivessel PCI in shock (CULPRIT-SHOCK, NEJM 2017), and early routine VA-ECMO did not improve outcomes (ECLS-SHOCK, NEJM 2023). The mechanical complications of MI — VSD, papillary muscle rupture and free wall rupture — classically occur at days 2 to 7 and present with sudden haemodynamic collapse.

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Domain

environmental

2

high

Acute Decompression Illness — Comprehensive ICU Management (Diving Emergencies)

Acute decompression illness (DCI) — the umbrella term for the two dysbaric injuries of ascent: decompression sickness (DCS, 'the bends') and arterial gas embolism (AGE). Both arise from bubbles formed when ambient pressure falls. DCS is driven by inert-gas (nitrogen) supersaturation during/after ascent — in-situ bubbles in tissues and blood — classically Type 1 (musculoskeletal joint pain 'the bends', skin itching/mottling 'skin bends', lymphatic) and Type 2 (neurological — spinal cord is the MOST SERIOUS form with paralysis, paraesthesia, bladder/bowel dysfunction; pulmonary 'the chokes' — cough, dyspnoea, substernal chest pain; vestibular 'the staggers' — vertigo, nystagmus, nausea). AGE is pulmonary barotrauma of ascent — breath-holding or too-rapid ascent over-expands alveoli → alveolar rupture → gas enters pulmonary veins → left heart → systemic arteries (brain most often) → stroke-like presentation during or within minutes of surfacing. Risk is increased by depth, bottom time, repetitive dives, rapid ascent, cold, exertion, dehydration, and a patent foramen ovale (paradoxical embolisation). Onset: AGE within minutes; DCS usually within minutes-to-hours, 98% within 24 h. Management is identical for both: 100% oxygen immediately (denitrogenates tissues and accelerates bubble resolution), IV isotonic glucose-free fluids (correct immersion diuresis and dehydration, avoid hypovolaemia), and DEFINITIVE recompression therapy — hyperbaric oxygen, most commonly US Navy Treatment Table 6 (100% oxygen at 2.8 ATA), which shrinks bubbles by Boyle's law (to ~one-third of surface volume), oxygenates ischaemic tissue, reduces oedema, and denitrogenates. Retrieve to the nearest hyperbaric chamber urgently — call the Divers Alert Network (DAN) 24-hour hotline. Delay to recompression worsens outcome — recompress as soon as feasible.

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high

Acute Drowning & Near-Drowning — Comprehensive ICU Management

Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid — a uniform definition adopted by the World Health Organization in 2005 that abolishes the obsolete terms 'near-drowning', 'dry drowning', 'wet drowning', 'secondary drowning' and 'active/passive drowning'. ALL submersion or immersion events are now called DROWNING, classified only by outcome as fatal or non-fatal drowning. The pathophysiological sequence is breath-holding and panic followed by laryngospasm, then aspiration of a SMALL volume of water (the 'dry versus wet drowning' distinction is obsolete because most victims aspirate fluid and the volume aspirated is too small to cause electrolyte or volume disturbance), leading to surfactant washout, atelectasis, ventilation-perfusion mismatch, non-cardiogenic pulmonary oedema and ARDS, with progressive HYPOXIA producing bradycardic asystolic cardiac arrest and hypoxic-ischaemic brain injury. The intensivist's priorities are (1) RESCUE with immediate resuscitation — start CPR without delay, giving rescue breaths or bag-mask ventilation first because this is an asphyxial arrest; drowning victims often have prolonged hypoxia yet achieve return of spontaneous circulation with good-quality CPR even after more than 30 minutes submerged, especially in cold water; (2) OXYGENATE and VENTILATE with high-flow oxygen and positive-pressure ventilation — most need PEEP for aspiration pneumonitis, surfactant dysfunction and pulmonary oedema, with lung-protective ventilation (tidal volume 6 mL/kg, plateau pressure under 30 cmH2O) for the ARDS-pattern lung injury; (3) TARGETED TEMPERATURE MANAGEMENT at 32 to 36 degrees C for 24 hours in comatose post-arrest patients, because drowning is a form of cardiac arrest and the same post-cardiac-arrest guidelines apply; (4) treat CO-EXISTING injuries — cervical spine immobilisation particularly after diving accidents, and concurrent hypothermia from cold-water exposure (rewarm, but follow 'not dead until warm and dead'). Prognostication is guarded by the duration of submersion, the presence of return of spontaneous circulation, the Glasgow Coma Scale, and serum potassium on presentation.

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Domain

Obs/Gynae

3

low

Acute fatty liver of pregnancy (AFLP)

AFLP is a rare (about 5 per 100,000 maternities in the UK national cohort), life-threatening liver disorder occurring in the third trimester. Fatty infiltration of hepatocytes → microvesicular steatosis → acute liver failure. Presents with: nausea, vomiting, abdominal pain, hypertension, jaundice, polydipsia/polyuria (transient central DI), encephalopathy (progressive). Diagnosis: Swansea criteria (6 or more of 14 clinical/laboratory features). Management: URGENT DELIVERY (the only definitive treatment — the liver recovers after delivery), supportive ICU care (coagulopathy, hypoglycaemia, AKI, encephalopathy), NAC may help. Distinguishes from HELLP: AFLP has more severe coagulopathy, encephalopathy, and hypoglycaemia. Mortality: maternal case fatality 1.8 percent and perinatal mortality 104 per 1000 births (UK cohort) — has improved with early recognition and delivery.

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low

Acute severe community-acquired pneumonia: special populations — pregnancy

CAP in pregnancy has higher morbidity and mortality than non-pregnant CAP — it is the #1 non-obstetric infection requiring ICU admission in pregnancy. Three converging mechanisms transform a 'standard' pneumonia into a time-critical maternal illness: (1) IMMUNOSUPPRESSION — pregnancy suppresses cell-mediated (Th1) immunity, increasing susceptibility to viral (influenza, varicella, CMV), intracellular (Legionella, Mycoplasma), and fungal (Coccidioides, Pneumocystis) pathogens; (2) RESPIRATORY PHYSIOLOGY — the gravid uterus elevates the diaphragm, reducing functional residual capacity (FRC) by ~20% while oxygen consumption rises 20-30%, so the apnoeic/fasted pregnant patient desaturates in seconds; (3) CARDIOVASCULAR PHYSIOLOGY — cardiac output and oxygen demand are already near-maximal (little reserve), and aortocaval compression in the supine position collapses preload and placental perfusion. Organisms: S. pneumoniae (#1, ~two-thirds of bacterial CAP), H. influenzae, atypicals (Mycoplasma, Legionella); viral pathogens are disproportionately severe — pandemic H1N1 influenza (7x higher mortality in pregnancy; the third trimester is deadliest), varicella pneumonia (10-25x higher mortality — the classic exam killer), and SARS-CoV-2. Management: LOWER threshold for ICU; oxygen target SpO2 >95% (fetal oxygenation is entirely dependent on maternal PaO2); LEFT LATERAL TILT from 20 weeks; MG-SAFE antibiotics (beta-lactams + macrolides safe; AVOID tetracyclines/aminoglycosides/quinolones); oseltamivir SAFE and given EARLY (within 48h) for influenza; aciclovir IV for varicella; continuous fetal monitoring (CTG) if viable; deliver the deteriorating mother.

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high

Obstetric emergencies in the ICU

Obstetric ICU admissions are rare but high-stakes. Pre-eclampsia/eclampsia: magnesium sulphate for seizure prophylaxis and treatment (4 g IV load, 1-2 g/h; beats diazepam and phenytoin), antihypertensive therapy for severe-range BP (over 160/110), delivery definitive. HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets): usually preterm, malaise and right upper quadrant pain in 90 percent, hypertension may be absent. Peripartum cardiomyopathy: heart failure with LVEF under 45 percent, last month of pregnancy to 5 months postpartum — treat with pregnancy-safe HF therapy (diuretics, beta-blockers, hydralazine/nitrates, digoxin) plus bromocriptine. Amniotic fluid embolism: sudden cardiovascular collapse plus coagulopathy — high-quality CPR, early echo for right ventricular failure, 1:1:1 haemostatic resuscitation, VA-ECMO for the refractory. Physiological changes of pregnancy alter drug dosing, ventilation, and fluid management.

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Domain

Environmental

3

high

Acute heat stroke: exertional vs classic, rapid cooling, and 'sepsis from heat'

Heat stroke is a life-threatening hyperthermic emergency defined by CORE TEMPERATURE >40C with CENTRAL NERVOUS SYSTEM DYSFUNCTION (confusion, agitation, delirium, seizures, coma) — it is the severe end of the heat-illness spectrum beyond heat cramps and heat exhaustion. TWO SUBTYPES: (1) CLASSIC (non-exertional) — elderly, chronic disease, anticholinergic/diuretic drugs, poor ventilation/air-conditioning, occurs EPIDEMICALLY during heatwaves (2003 European heatwave: >70,000 deaths); anhidrosis common (thermoregulatory failure). (2) EXERTIONAL — young, fit individuals (athletes, military recruits, miners, firefighters) performing intense exercise in hot/humid conditions; sweating usually PRESENT (profuse); rhabdomyolysis, DIC, AKI and lactic acidosis more severe. PATHOPHYSIOLOGY: core temp >40C → PROTEIN DENATURATION + membrane lipid peroxidation → direct cytotoxicity → systemic inflammatory response syndrome (cytokine cascade, endothelial activation, complement) indistinguishable from sepsis → gut translocation, DIC, ARDS, AKI, acute liver injury (hepatocyte necrosis) and rhabdomyolysis — 'heat stroke is like SEPSIS from heat'. The thermoregulatory set-point is NORMAL (unlike fever) — so ANTIPYRETICS (paracetamol/NSAIDs) are INEFFECTIVE and DANTROLENE is INEFFECTIVE (randomised trial showed no benefit; not malignant hyperthermia). MANAGEMENT: RAPID COOLING is the #1 priority — ideal cooling rates exceed 0.16C/min (0.08-0.15C/min still acceptable); GOLD STANDARD for exertional = COLD-WATER IMMERSION (water 1-17C; mean 0.22C/min in the Falmouth Road Race series, where all 274 cases cooled on site survived) — start ON-SITE before transport; alternatives: evaporative plus convective cooling (continual dousing + fanning — best-evidenced for classic), tarp-assisted cooling (~0.14C/min) when no tub is available, chilled IV crystalloid (30 mL/kg at 4C — supplement only), ice packs applied diffusely (strategic neck-axilla-groin packs NOT recommended as primary). No evidence-based endpoint temperature for cessation exists — in practice stop active cooling once core is below about 39C (hypothermia can occur during recovery). Control shivering (it hampers cooling — counter-warming, sedation). Treat complications: IV fluids for dehydration, lung-protective ventilation for ARDS, RRT for AKI, manage DIC, monitor CK/electrolytes for rhabdomyolysis. PROGNOSIS: classic high mortality (worse with age/comorbidity, Argaud Lyon cohort 28-day mortality 58%, 2-year 71%); exertional near-zero fatalities with immediate on-site immersion. Permanent cerebellar ataxia (Purkinje cell injury) is a classic sequela.

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medium

Acute severe hypothermia: rewarming, Osborn waves, and 'warm and dead'

Hypothermia = core temperature <35°C from excessive heat loss (environmental) or impaired thermogenesis (endocrine, sepsis, drugs). SEVERITY: MILD (32-35°C — tachycardia, tachypnoea, shivering, confusion). MODERATE (28-32°C — bradycardia, decreased reflexes, somnolence, shivering stops, Osborn J waves on ECG, AF). SEVERE (<28°C — coma, fixed pupils, hypotension, ventricular arrhythmias [VF], asystole, pulseless — appears dead but may be recoverable). KEY PRINCIPLES: (1) HANDLE GENTLY — cold myocardium is extremely irritable — rough handling/movement → VF (irreversible). (2) REWARM: mild → passive (blankets, warm environment); moderate → active external (forced warm air [Bair Hugger], warmed IV fluids); severe → active internal (warmed fluids + body cavity lavage + ECMO/cardiopulmonary bypass). (3) 'NO ONE IS DEAD UNTIL WARM AND DEAD' — prolonged resuscitation is warranted; survivors rewarmed from 13.7°C. (4) DON'T RUB/MASSAGE (triggers VF). (5) GUIDELINES do not recommend vasopressor or antiarrhythmic drugs in VF if <30°C — treat with CPR and extracorporeal rewarming.

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medium

Electrical and radiation injury in ICU

Electrical injury: damage from electricity passing through body. Low-voltage (<1000V): cardiac arrhythmias (AC current at 50-60Hz can cause VF). High-voltage (>1000V): deep tissue injury (muscle, nerve, vessel), compartment syndrome, rhabdomyolysis, AKI, cardiac arrest, secondary trauma (fall). Lightning: massive DC discharge, causes immediate cardiac arrest (asystole), respiratory arrest (neurological), Lichtenberg figures (fern-like skin markings). Radiation injury: acute radiation syndrome (ARS) from whole-body radiation >1 Gy. Syndromes: haematopoietic (2-6 Gy), gastrointestinal (6-8 Gy), neurovascular (>8 Gy, fatal). Management: electrical — ACLS, fluid resuscitation (rhabdomyolysis protocol), fasciotomy for compartment syndrome, cardiac monitoring. Radiation — supportive, transfusion, growth factors, bone marrow transplant (selected).

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Domain

gi-nutrition

6

high

Acute Hepatic Encephalopathy — Comprehensive ICU Management (West Haven, Lactulose, Rifaximin, Cerebral Oedema, Nutrition)

Hepatic encephalopathy (HE) = a reversible syndrome of impaired brain function in patients with advanced liver disease and/or portosystemic shunting, produced by gut-derived neurotoxins (predominantly ammonia) that the failing liver cannot clear. ACUTE (episodic) HE is the common ICU presentation: a cirrhotic patient who was previously well develops overt confusion, somnolence or coma over hours-days, almost always driven by a PRECIPITANT. The fellowship-level intensivist must master FIVE domains. (1) RECOGNISE AND GRADE using the West Haven classification: grade 1 (mild confusion, euphoria/anxiety, sleep reversal, +/- asterixis), grade 2 (lethargy, disorientation, personality change, asterixis present), grade 3 (somnolent but rousable, gross disorientation, incomprehensible speech), grade 4 (coma). Grades 1-2 = 'covert/mild'; grade 2-4 = 'overt'. (2) UNDERSTAND THE PATHOPHYSIOLOGY: ammonia (produced in the gut by bacterial deamination of urea/protein) is normally cleared by the hepatic urea cycle; in cirrhosis it is shunted past the liver (portosystemic shunting) and reaches the brain, where it diffuses across the blood-brain barrier into ASTROCYTES. Astrocyte glutamine synthetase condenses ammonia + glutamate -> GLUTAMINE; glutamine is osmotically active, accumulates, draws in water -> ASTROCYTE SWELLING (Alzheimer type II astrocytosis). When this overwhelms compensatory osmolyte (myo-inositol) release -> CYTOTOXIC CEREBRAL OEDEMA -> raised ICP. Cerebral oedema is COMMON in acute liver failure (Type A) but UNCOMMON in cirrhotic (Type C) HE (the brain has time to adapt osmotically) — though it can occur in high-grade or rapidly evolving HE. (3) FIND AND TREAT THE PRECIPITANT — the #1 priority, because episodic HE rarely occurs without one: INFECTION is #1 (spontaneous bacterial peritonitis, pneumonia, bacteraemia, UTI — culture EVERYTHING and treat empirically), followed by gastrointestinal bleed, CONSTIPATION, electrolyte derangement (HYPO NATRAEMIA #1 electrolyte cause; hypokalaemia — hypokalaemia promotes renal ammonia production), SEDATIVES/benzodiazepines (GABAergic — precipitate HE; avoid unless treating alcohol withdrawal), ALCOHOL (intoxication or withdrawal), and TIPS (transjugular intrahepatic portosystemic shunt — increases portosystemic shunting; HE in ~20-40% post-TIPS). (4) AMMONIA-LOWERING THERAPY: LACTULOOSE first-line — a non-absorbable disaccharide converted by gut bacteria to organic acids, lowering colonic pH and converting absorbable NH3 to non-absorbable NH4+ (ion trapping) plus a cathartic effect; in deep encephalopathy give it via NG or enema with oral dosing repeated hourly until stools appear, then titrate to the endpoint of 2-3 soft bowel motions/day (the ENDPOINT is stool frequency/consistency, NEVER a target ammonia). RIFAXIMIN 550 mg BD is ADDITIVE to lactulose for recurrent/overt HE — a minimally absorbed gut rifamycin antibiotic that reduces ammonia-producing bacteria (Bass 2010 NEJM RCT: rifaximin + lactulose reduced breakthrough HE by 58% over 6 months vs lactulose + placebo). (5) SUPPORTIVE AND AVOIDANCE MEASURES: AVOID BENZODIAZEPINES unless treating alcohol withdrawal (they are GABA-ergic and precipitate/worsen HE; if sedation is unavoidable use a SHORT-ACTING agent like oxazepam or lorazepam — and only after flumazenil-reversibility has been considered); provide NUTRITION with a HIGH-PROTEIN diet 1.2-1.5 g/kg/day — protein is NOT restricted (Cordoba 2004 RCT: a normal-protein diet was as safe as a low-protein diet and avoided the protein catabolism that itself generates ammonia); manage cerebral oedema if it develops (head of bed 30 degrees, hypertonic saline, mannitol if ICP monitored). PROGNOSIS: overt HE carries 1-year mortality ~40-50% in cirrhosis; the severity of HE and the underlying liver failure (Child-Pugh/MELD), recurrence, and response to therapy determine outcome. The two examinable 'do-NOT' rules: do NOT routinely check or chase a 'target ammonia' level to guide therapy (it is supportive, not diagnostic or a treatment target — titrate lactulose to stools); and do NOT restrict dietary protein (protein restriction worsens sarcopenia, increases ammonia-generating catabolism, and does not improve HE).

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Acute Liver Failure — Comprehensive (King's College Criteria, Cerebral Oedema, NAC, Transplantation)

Acute liver failure (ALF) = severe acute liver injury with ENCEPHALOPATHY + COAGULOPATHY (INR >=1.5) within 26 weeks of symptom onset, in a patient WITHOUT pre-existing liver disease. It is a rare (incidence <10/million/year), dynamic, life-threatening syndrome whose outcome depends entirely on the cause, the speed of organ support, and the timeliness of liver-transplant referral. AETIOLOGY is the single biggest determinant of survival: PARACETAMOL overdose is the #1 cause in the UK and Australia (~40-50% of cases, mostly intentional but increasingly 'staggered'/therapeutic misadventure in the elderly); other causes are DRUG-INDUCED liver injury (DILI — isoniazid, valproate, halothane, nitrofurantoin, flavocoxid, herbal/dietary supplements), VIRAL hepatitis (hepatitis A, B [± hepatitis D superinfection], E — especially in pregnancy and immunosuppression; HSV, EBV, CMV in the immunocompromised), ISCHAEMIC hepatitis ('shock liver' following cardiac arrest or prolonged hypotension), AUTOIMMUNE hepatitis, WILSON'S disease (young patient + Coombs-negative haemolytic anaemia + low ceruloplasmin + Kayser-Fleischer rings), PREGNANCY-RELATED (acute fatty liver of pregnancy — AFLP; HELLP syndrome — third trimester/postpartum; definitive treatment is DELIVERY), MUSHROOM poisoning (Amanita phalloides — history of wild-mushroom ingestion 24-48h earlier; antidotes penicillin G + silibinin + NAC), heat stroke/malignant hyperthermia, and INDETERMINATE (~20%). The fellowship-level intensivist must master FIVE management pillars: (1) IDENTIFY AND TREAT THE CAUSE (NAC for paracetamol — and increasingly NAC for ALL causes; antivirals for viral hepatitis; corticosteroids for autoimmune; chelation for Wilson's; penicillin/silibinin for Amanita; delivery for AFLP/HELLP); (2) CEREBRAL OEDEMA — the #1 killer — ammonia crosses the blood-brain barrier, is metabolised in astrocytes to glutamine, which accumulates osmotically and causes astrocyte swelling, oedema, raised intracranial pressure and uncal herniation; high-grade (grade 3-4) encephalopathy and arterial ammonia >150 umol/L identify the at-risk brain; management = head of bed 30 degrees neutral, hypertonic saline to keep serum sodium 145-155 mmol/L, mannitol 0.5 g/kg (if ICP monitored or signs of herniation, provided serum osmolality <320), AVOID hypotension/hypoxia/hypercapnia, prophylactic intubation at grade 3, and consider hypothermia/induced coma (barbiturates) for refractory intracranial hypertension; (3) KING'S COLLEGE CRITERIA (O'Grady 1989) — the most widely used transplant-referral trigger; for PARACETAMOL ALF: arterial pH <7.25 (after fluid resuscitation, regardless of grade) OR all three of INR >6.5 + creatinine >300 umol/L + grade 3-4 encephalopathy; for NON-PARACETAMOL ALF: INR >6.5 alone OR at least 3 of (INR >3.5 + age <10 or >40 + cause non-A/non-B or drug-induced + jaundice-to-encephalopathy interval >7 days + bilirubin >300 umol/L); lactate (>>3.5 at 4h or >3.0 at 12h after resuscitation) and MELD add sensitivity; (4) SUPPORT failing organs — ventilation at grade 3-4 encephalopathy (and to control PaCO2 for cerebral perfusion), noradrenaline for vasoplegic shock, CRRT (continuous, not intermittent — avoids dialysis-disequilibrium-driven ICP rise) for AKI, 10% dextrose for the universal hypoglycaemia; and (5) SURVEIL AND PREVENT INFECTION (50-80% develop bacterial infection — a leading cause of death — daily surveillance cultures, low threshold for broad-spectrum antibiotics, and antifungal cover in high-grade encephalopathy). Two critical 'do-NOT' rules: do NOT correct the INR with fresh-frozen plasma unless the patient is bleeding or undergoing a procedure — the INR is a PROGNOSTIC marker (it is the backbone of the King's College criteria) and the 'rebalanced haemostasis' of ALF means the INR does not reflect bleeding risk (viscoelastic TEG/ROTEM does); and do NOT forget that NAC benefits non-paracetamol ALF too (Lee 2009 RCT — improved transplant-free survival in early-grade, non-paracetamol ALF), so many units now give NAC to ALL ALF. Emergency liver transplantation is the definitive therapy for those who meet King's College criteria: without it mortality exceeds 80%, with it 1-year survival is approximately 80%. The intensivist's job is to REFER EARLY (transplant logistics take time), to support the brain and other organs as a BRIDGE, and to recognise the ABSOLUTE contraindications (uncontrolled sepsis, irreversible brain injury from sustained ICP >30/CPP <40, severe comorbidity, active substance misuse, uncontrolled psychiatric illness) that make transplant futile. Overall ALF mortality without transplant is 30-50% (better for paracetamol and ischaemic causes, worse for Wilson's, drug-induced, and indeterminate causes).

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Acute Severe Intra-Abdominal Infection and Peritonitis — Comprehensive (Primary/SBP, Secondary, Tertiary, Source Control, Open Abdomen)

Acute severe intra-abdominal infection with peritonitis is one of the most common and most lethal surgical emergencies managed in the ICU, with mortality ranging from <5% for uncomplicated community-acquired infection up to 30-50% for tertiary (persistent/recurrent) peritonitis in the critically ill. Peritonitis is classified into THREE pathophysiologically and therapeutically distinct categories. PRIMARY (SPONTANEOUS BACTERIAL) PERITONITIS (SBP): infection of cirrhotic ascites WITHOUT an identifiable intra-abdominal surgical source; monomicrobial (E. coli ~70%, Klebsiella, then gram-positives); diagnosed by ascitic polymorphonuclear (PMN) count >250 cells/mm3 (do NOT wait for culture — ~50% culture-negative); treated with a THIRD-GENERATION CEPHALOSPORIN (cefotaxime 2 g IV q8h for 5 days) PLUS ALBUMIN 1.5 g/kg day 1 then 1 g/kg day 3 (the landmark Sort 1999 NEJM trial proved albumin REDUCES hepatorenal syndrome from 33% to 10% and in-hospital mortality from 29% to 10%); NO surgery/source control required. SECONDARY PERITONITIS: infection from an intra-abdominal SOURCE requiring operative or interventional control — perforated viscus (appendicitis, diverticulitis, peptic ulcer, ischaemic bowel), anastomotic leak, bowel infarction, post-surgical leak; POLYMICROBIAL (gram-negative enteric bacilli + anaerobes (Bacteroides) + Enterococcus); management is SOURCE CONTROL + broad-spectrum antibiotics — source control is MANDATORY and antibiotics alone cannot cure secondary peritonitis. SOURCE CONTROL = all physical measures to eliminate a source and restore anatomy: DRAIN (pus/fluid), DEBRIDE (necrotic/infected tissue), DIVERT (defunction the bowel), and in the critically ill/physiologically exhausted patient a DAMAGE-CONTROL laparotomy (control contamination, temporary abdominal closure, resuscitate in ICU, planned re-operation). EMPIRIC ANTIBIOTICS: piperacillin-tazobactam OR a carbapenem (meropenem) + metronidazole for broad gram-negative + anaerobic cover; add Enterococcus cover (esp. healthcare-associated); add an antifungal (an echinocandin or amphotericin/fluconazole) for fungal (Candida) peritonitis. DURATION is SHORT: 4-7 days after adequate source control (STOP-IT trial, NEJM 2015 — ~4 days as good as ~8 days). TERTIARY PERITONITIS: persistent or recurrent peritonitis after >48h of apparently appropriate treatment of secondary peritonitis, or persistent intra-abdominal infection in the critically ill without a clear drainable source; reflects immune dysregulation/immune paresis as much as infection; organisms are MDR — Enterococcus (incl. VRE), Pseudomonas, Acinetobacter, MRSA, and Candida; management is CULTURE-DIRECTED, broad-spectrum, anti-fungal-inclusive therapy, repeat source-control assessment, and aggressive ICU support; mortality 30-50%. OPEN ABDOMEN management (negative pressure wound therapy/VAC, planned re-laparotomy 'on-demand' vs 'planned', and delayed primary fascial closure) is the strategy for the physiologically deranged patient in whom closure would cause abdominal compartment syndrome or where a second-look is required. DIAGNOSIS rests on CT abdomen with contrast (free intraperitoneal gas = perforation; fluid collections/abscess; fat stranding; ischaemia), diagnostic paracentesis (for SBP), and — selectively — diagnostic laparoscopy or diagnostic peritoneal lavage (now largely supplanted by CT and FAST ultrasound).

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Acute Severe Pancreatitis — Comprehensive (Revised Atlanta, WATERFALL, PANTER, Step-Up, Infected Necrosis)

Acute severe pancreatitis (approximately 15-20% of all acute pancreatitis) is defined by the Revised Atlanta Classification (2012) as acute pancreatitis with PERSISTENT organ failure lasting >48 hours — respiratory (PaO2/FiO2 <300), cardiovascular (SBP <90 despite fluids / need for vasopressors), or renal (creatinine >170 umol/L) — and carries a mortality of 15-30%. The two pathological phases dictate ICU management. EARLY PHASE (week 1): uncontrolled SYSTEMIC INFLAMMATION (SIRS) driven by pancreatic enzyme activation and cytokine storm (IL-6, TNF-alpha, IL-1) → capillary leak, 'third-space' fluid sequestration into the retroperitoneum and bowel wall → hypovolaemia, haemoconcentration, haemodynamic instability, AKI, and the early killers ARDS and shock. Aetiology: gallstones (#1, ~40%), alcohol (#2, ~30%), ERCP, hypertriglyceridaemia (>11 mmol/L), drugs (azathioprine, mesalazine, didanosine, sodium valproate, thiazides), trauma, post-ERCP, autoimmune, idiopathic. EARLY ICU MANAGEMENT is SUPPORTIVE and evidence-based: (1) GOAL-DIRECTED FLUID RESUSCITATION with lactated Ringer's — the WATERFALL trial (NEJM 2022, de-Madaria) proved AGGRESSIVE fluids (20 mL/kg bolus + 3 mL/kg/hr) CAUSE HARM (fluid overload 20.5% vs 6.3%, no outcome benefit) — use moderate, goal-directed resuscitation (1.5 mL/kg/hr + small boluses only if hypovolaemic); (2) EARLY ENTERAL NUTRITION within 48 hours (NOT 'NPO + TPN' — old practice refuted by multiple RCTs and meta-analyses) — maintains gut mucosal barrier, reduces bacterial translocation, reduces infected necrosis and mortality; oral or nasogastric route is as effective as nasojejunal in most patients; (3) NO PROPHYLACTIC ANTIBIOTICS — the PANTER trial, ACG (Tenner 2024), and IAP/APA guidelines all confirm antibiotics do NOT prevent infected necrosis and increase resistance, fungal superinfection, and C. difficile; give antibiotics ONLY for documented infection (infected necrosis, cholangitis, pneumonia); (4) analgesia (opioid — morphine/fentanyl, PCA); (5) ERCP within 24-72h ONLY if concomitant cholangitis or ongoing biliary obstruction. LATE PHASE (week 2+): local complications dominate — pancreatic/peripancreatic NECROSIS (sterile in ~70%, infected in ~30%), walled-off necrosis, pseudocyst. Infected necrosis is the principal late killer (mortality 30-40% historically). Diagnosis: gas within necrosis on CT is pathognomonic; otherwise clinical deterioration + positive fine-needle aspiration (FNA) culture. Management of infected necrosis is the STEP-UP APPROACH (PANTER trial, NEJM 2010, van Santvoort): percutaneous or endoscopic DRAINAGE first, then minimally-invasive necrosectomy only if drainage fails — step-up halved the composite of major complications/death (40% vs 69%) versus open necrosectomy, and 35% needed drainage alone. The TENSION trial (Lancet 2018, van Brunschot) showed ENDO- scopic step-up (EUS-guided transluminal drainage ± endoscopic necrosectomy) is NOT superior to surgical step-up for the primary endpoint but causes FEWER pancreatic fistulas and shorter hospital stay — endoscopic step-up is now the preferred first approach when expertise exists. CRITICAL: DELAY invasive intervention ~4 weeks whenever possible (let necrosis become walled-off/encapsulated → safer drainage). Scoring: APACHE II >=8, Ranson >=3, BISAP >=3, CRP >150 mg/L at 48h, and the Revised Atlanta organ-failure criteria all predict severity. Systemic complications: SIRS → MODS, ARDS (lung-protective ventilation), AKI (CRRT if shocked), abdominal compartment syndrome (monitor bladder pressure), and sepsis from infected necrosis.

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Acute-on-Chronic Liver Failure (ACLF) — Comprehensive ICU Management

Acute-on-chronic liver failure (ACLF) — acute decompensation of cirrhosis complicated by organ failure(s) and high short-term mortality. In the CANONIC study, 28-day mortality was 33.9 percent in patients who had ACLF at enrolment versus 1.9 percent in those who never developed it, and grade of ACLF (number of organ failures) drives prognosis: with four or more organ failures untreated 28-day mortality was 100 percent (CLIF cohort). Precipitants: bacterial infection (the most frequent associated factor) and severe alcohol-related hepatitis, identified or occult (EASL CPG 2023). Management: treat the precipitant, support failing organs, reverse hepatorenal-spectrum AKI with terlipressin plus albumin, give albumin 1.5 g per kg then 1 g per kg with antibiotics in spontaneous bacterial peritonitis, feed protein 1 to 1.5 g per kg per day rather than restricting it, and consider early liver transplantation — 1-year post-transplant survival 81 percent even in listed ACLF (ECLIS).

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Stress Ulcer Prophylaxis (SUP) — Comprehensive ICU Management

Stress ulcer prophylaxis (SUP) — prevention of stress-related mucosal disease (SRMD) in critically ill patients. Upper GI mucosal lesions are found in 75-100% of ICU patients on endoscopy, but clinically significant bleeding occurs in only 1-6%, carrying an estimated 40-50% mortality when it happens. 2024 SCCM/ASHP guideline: factors that likely increase bleeding risk are coagulopathy, shock, and chronic liver disease; there is no firm evidence for mechanical ventilation alone as a risk factor; enteral nutrition probably reduces risk; give a PPI or H2RA at low dosage to patients WITH a risk factor; discontinue when the risk factor resolves or before ICU transfer. Classic risk-factor teaching (mechanical ventilation >48h plus coagulopathy) comes from earlier cohort data and still anchors exams. Trials: SUP-ICU (pantoprazole 40 mg IV daily, 3298 patients) reduced clinically important bleeding 2.5% vs 4.2% without changing 90-day mortality (31.1% vs 30.4%); REVISE (4821 ventilated patients) confirmed bleeding reduction 1.0% vs 3.5% (HR 0.30) with no significant mortality difference. PPIs beat H2RAs for bleeding prophylaxis (meta-analysis OR 0.30); H2RAs develop tolerance (tachyphylaxis within 42h of prolonged IV dosing). Ranitidine recalled worldwide for nitrosamine (NDMA) impurities — do NOT use; famotidine (20 mg IV q12h or 1.7 mg/h infusion) or a PPI instead. With clopidogrel avoid omeprazole/esomeprazole; pantoprazole does not reduce clopidogrel's antiplatelet effect. Review the indication DAILY and stop when it resolves.

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neurocritical-care

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Acute Intermittent Porphyria — Comprehensive ICU Management

Acute intermittent porphyria (AIP) — autosomal dominant defect in porphobilinogen deaminase (PBGD/HMBS enzyme) in the haem biosynthesis pathway → accumulation of porphyrin precursors (ALA — aminolaevulinic acid, PBG — porphobilinogen) → neurotoxicity. Classic triad: ABDOMINAL PAIN (severe, persistent, out of proportion to examination — no peritonism) + NEUROLOGICAL symptoms (peripheral neuropathy, motor weakness, bulbar palsy, seizures) + PSYCHIATRIC symptoms (anxiety, hallucinations, paranoia). Urine turns DARK (port-wine/dark red) on standing or exposure to light (from porphobilinogen oxidation). Diagnosis: ELEVATED urinary porphobilinogen (PBG) and ALA (aminolaevulinic acid) — random spot urine (significantly elevated — over five times normal). Treatment: (1) IV HAEM ARGINATE 3 mg/kg once daily for 4 days (or haemin 3-4 mg/kg — reconstituted with human albumin — suppresses ALA synthase → reduces porphyrin precursor production), (2) CARBOHYDRATE LOADING (IV glucose for mild attacks only, or until haem is available — glucose in water solutions aggravate hyponatraemia), (3) STOP ALL PRECIPITATING DRUGS (barbiturates, sulfonamides, OCP, griseofulvin, rifampicin, phenytoin, carbamazepine, alcohol — check EVERY drug against the safe drug list), (4) SYMPTOMATIC: opiate analgesia (morphine/fentanyl — SAFE), antiemetics (ondansetron — SAFE; AVOID metoclopramide, phenothiazines), beta-blocker for tachycardia/hypertension (propranolol/labetalol — SAFE), levetiracetam for seizures (SAFE — AVOID barbiturates/phenytoin/valproate). ICU admission for: respiratory muscle weakness (motor neuropathy → ventilatory failure — like GBS), severe hyponatraemia (SIADH — common in acute porphyria), seizures, autonomic instability. Prognosis: acute attack resolves over days-weeks with treatment. Mortality 5-10% (from respiratory failure, seizures, arrhythmia).

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Acute Spinal Cord Injury and Neurogenic Shock — Comprehensive ICU Management

Acute spinal cord injury (SCI) — traumatic damage to the spinal cord causing motor/sensory deficit below the injury level ± autonomic dysfunction. Neurogenic shock: loss of sympathetic tone below the lesion (cervical or upper thoracic SCI) → VASODILATION (hypotension) + BRADYCARDIA (unopposed parasympathetic/vagal tone) — DISTRIBUTES differently from other shock types (warm, dry skin + bradycardia vs cold/clammy/tachycardic of hypovolaemic shock). ASIA Impairment Scale (A=complete, B=sensory incomplete, C=motor incomplete non-functional, D=motor incomplete functional, E=normal). Management: (1) ATLS primary survey + spinal precautions (cervical collar + logroll + spinal board), (2) NEUROGENIC SHOCK: noradrenaline (alpha + beta — restores BP AND HR) + atropine (for symptomatic bradycardia) + target MAP 85-90 mmHg for 7 days (maintain spinal cord perfusion — controversial but widely practiced), (3) EARLY SURGICAL DECOMPRESSION (STASCIS trial — within 24h improves neurological outcomes), (4) METHYLPREDNISOLONE (controversial — NASCIS II/III — high-dose within 8h may improve outcomes but increases infection risk — many centres have abandoned routine use), (5) VTE prophylaxis (high risk — LMWH is the first-choice anticoagulant), (6) prevent secondary injury (avoid hypotension/hypoxia/hyperthermia). Autonomic dysreflexia (T6 or above): noxious stimulus below lesion → massive sympathetic discharge → hypertensive crisis → intracranial haemorrhage/stroke. Management: sit upright + identify/remove trigger + rapid-acting antihypertensives (nitroglycerin ointment, nifedipine).

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Acute Status Epilepticus — Comprehensive Full Management Cascade

Status epilepticus (SE) is a continuous seizure lasting more than 5 minutes, or two or more seizures without full recovery of consciousness between them. The 5-minute operational threshold (ILAE/Trinka 2015) exists because beyond it the seizure becomes self-sustaining, GABA-A receptors are internalised and trafficked away from the synaptic membrane (causing pharmacoresistance to benzodiazepines), NMDA and AMPA receptors are recruited to the membrane (perpetuating excitation), and neuronal injury begins. Management is a time-critical PHASED cascade with four stages. EARLY SE (0-5 min): abort with a benzodiazepine — IV lorazepam 4 mg (0.1 mg/kg), or IM midazolam 10 mg when no IV access (RAMPART showed IM midazolam superior to IV lorazepam when IV access absent), or IV/rectal diazepam. ESTABLISHED SE (5-30 min): second-line non-sedating AED infusion — levetiracetam 60 mg/kg (max 4.5 g), fosphenytoin 20 mg PE/kg (max 1500 mg PE) OR phenytoin 20 mg/kg, valproate 40 mg/kg. The ESETT trial (Kapur 2019, NEJM) proved all three are EQUALLY EFFECTIVE for established SE (~half stopped seizing and remained so at 60 min); levetiracetam is now widely first-choice because of ease of administration, no cardiac monitoring requirement, and the fewest acute adverse events. REFRACTORY SE (30+ min / ongoing after second-line): induce anaesthesia — intubate and start a continuous anaesthetic infusion: midazolam, propofol, thiopental/pentobarbital, or ketamine, titrated to EEG burst-suppression or seizure-suppression with continuous EEG monitoring. SUPER-REFRACTORY SE (continues or recurs 24+ h despite anaesthetic, including relapse on weaning the anaesthetic — Shorvon 2011): escalate to immunotherapy (IVIG, plasma exchange, corticosteroids, rituximab/cyclophosphamide), ketogenic diet, epilepsy surgery, hypothermia, and repetitive transcranial magnetic stimulation. Airway management is central — RSI with THIOPENTAL (3-5 mg/kg) is the classic neurointensivist choice because it is simultaneously an induction agent AND an anticonvulsant (augments GABA, suppresses seizure foci). Continuous EEG (cEEG) is MANDATORY after control of convulsive SE and should run 24-48 h after the last seizure to exclude non-convulsive status epilepticus (NCSE), which persists in roughly half of patients who 'stop shaking' clinically. ICU complications dominate morbidity: hypotension from anaesthetics (especially thiopental/pentobarbital — Claassen 2002 found 77% hypotension with pentobarbital vs 34% with midazolam/propofol), ventilator-associated pneumonia from prolonged intubation, thrombocytopenia and hyperammonaemic encephalopathy from valproate, and propofol infusion syndrome (PRIS — lactataemia, rhabdomyolysis, hepatomegaly, cardiac failure, death; keep propofol <4 mg/kg/h and <48 h where possible). Autoimmune encephalitis (anti-NMDA receptor, anti-LG1, anti-GAD) is an increasingly recognised and treatable cause of refractory and super-refractory SE, especially in young patients with no prior epilepsy — suspect it, antibody-test, and treat empirically with IVIG/PLEX plus steroids and add rituximab/cyclophosphamide for NMDA. Mortality is 15-30% overall, rising to ~40% in refractory and ~50-60% in super-refractory SE.

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Guillain-Barre Syndrome — Comprehensive ICU Management

Guillain-Barre syndrome (GBS) — acute immune-mediated polyradiculoneuropathy causing rapidly progressive (hours to 4 weeks) ascending flaccid paralysis + areflexia ± autonomic dysfunction ± respiratory failure ± cranial nerve involvement. ICU admission for: respiratory failure (20-30% of cases develop the severe generalised manifestation with respiratory failure), severe autonomic dysfunction (arrhythmia, BP swings), bulbar weakness (aspiration risk), or severe weakness (unable to walk unaided). Variants: AIDP (demyelinating, commonest in the West), AMAN/AMSAN (axonal — Campylobacter jejuni), Miller-Fisher (ophthalmoplegia + ataxia + areflexia + GQ1b antibody), Bickerstaff brainstem encephalitis. Diagnostic: Brighton criteria (progressive weakness, areflexia, CSF albuminocytologic dissociation, NCS abnormalities). Treatment: IVIG (0.4 g/kg/day for 5 days) OR plasma exchange (12-15 L in four to five exchanges over 1-2 weeks) — equally effective, no benefit from combining, corticosteroids are INEFFECTIVE. ICU management: serial FVC and respiratory-pressure monitoring (progression to respiratory failure is associated with vital capacity <20 mL/kg, maximal inspiratory pressure <30 cmH2O, maximal expiratory pressure <40 cmH2O, or a >30% decline), autonomic monitoring (ECG, BP — watch for sudden asystole from vagal hypertonia), DVT prophylaxis, pain management (neuropathic pain common — gabapentinoids, TCAs or carbamazepine per EAN/PNS), early physiotherapy. Prognosis: 3-10% die and 20% are still unable to walk after 6 months. Erasmus GBS Respiratory Insufficiency Score (EGRIS, 0-7) stratifies the risk of artificial ventilation.

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ICP Monitoring and Multimodal Neuromonitoring — Comprehensive ICU Management

Intracranial pressure (ICP) monitoring is the cornerstone of neurocritical care for severe traumatic brain injury (TBI) and other intracranial hypertension states. The MONROE-KELLIE DOCTRINE governs the rigid vault: volume = brain (80%) + blood (10%) + CSF (10%) — an increase in one component MUST be offset by a decrease in another, or ICP rises. Normal ICP is 5-15 mmHg (recumbent). INTRACRANIAL HYPERTENSION (ICH) = ICP >22 mmHg (BTF 4th edition treatment threshold). DEVICES: (1) EXTERNAL VENTRICULAR DRAIN (EVD) — the GOLD STANDARD — catheter in frontal horn of lateral ventricle, transduced against a reference (external auditory meatus) — MEASURES ICP AND drains CSF (therapeutic + diagnostic) — BUT highest infection rate (pooled ventriculostomy-related infection about 8.6-11%); (2) INTRAPARENCHYMAL BOLT (Codman, Camino, Raumedic) — fibreoptic/strain-gauge probe bolted into brain parenchyma — LOWER infection (<2%), continuous reading, zero-drift over time, NO CSF drainage — most common in modern practice; (3) SUBDURAL/EPIDURAL sensors — LESS ACCURATE (overestimate/underestimate), rarely used now. ICP WAVEFORM: three peaks per cardiac cycle — P1 PERCUSSION (arterial pulsation — relatively constant), P2 TIDAL (brain COMPLIANCE — rises when compliance falls), P3 RESPIRATORY/DCOUP (venous/respiratory). P2 RISING ABOVE P1 = the brain has EXHAUSTED its compliance reserves = impending intracranial hypertension — a premonitory sign even if the MEAN ICP looks acceptable. CEREBRAL PERFUSION PRESSURE (CPP) = MAP − ICP; target 60-70 mmHg (BTF 4th ed). CPP <60 = cerebral ischaemia (secondary injury); CPP >70 = no added benefit AND increased ARDS risk (from the Robertson/Contant data — aggressive fluid/vasopressor-driven high CPP floods the injured lung). MULTIMODAL NEUROMONITORING recognises that ICP ALONE misses regional ischaemia — PbtO2 (brain tissue oxygen, LICOX/Neurotrend probe — target >20 mmHg — complements ICP), cerebral MICRODIALYSIS (lactate/pyruvate ratio over about 25 = disturbed oxidative metabolism; glycerol and glutamate = cell damage), JUGULAR VENOUS BULB OXIMETRY (SjvO2 <50% = global cerebral hypoxia, >90% = hyperaemia), and CONTINUOUS EEG (non-convulsive status detection). The integration paradigm: treat ICP + CPP + PbtO2 + metabolism TOGETHER — a normal ICP does NOT exclude ongoing brain ischaemia. KEY TRIALS: BTF 4th edition (Carney 2017), BEST:TRIP (Chesnut 2012 NEJM — ICP-guided care NOT superior to imaging-clinical exam in a Bolivian/Ecuadorian cohort, but monitoring is still standard of care in well-resourced settings), BOOST-2 (Okonkwo 2017 — PbtO2 + ICP monitoring reduced burden of brain hypoxia vs ICP alone, trend to better outcome — Phase III BOOST-3 ongoing).

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Myasthenia Gravis Crisis — Comprehensive ICU Management

Myasthenic crisis is an acute life-threatening exacerbation of myasthenia gravis (MG) severe enough to compromise ventilation (impending or actual respiratory failure) or airway protection (severe bulbar weakness). MG is a T-cell-dependent, antibody-mediated autoimmune disorder of the POSTSYNAPTIC neuromuscular junction (NMJ): pathogenic IgG autoantibodies attack the muscle membrane and either destroy acetylcholine receptors (AChR) or disrupt related proteins (MuSK, LRP4), producing FATIGABLE (fluctuating, use-dependent) weakness. Crisis is triggered in ~70% of cases by an identifiable precipitant — infection is #1 (pneumonia, aspiration, upper respiratory tract infection), followed by surgery, pregnancy/peripartum, tapering of immunosuppression, and drugs that impair NMJ transmission (aminoglycosides, beta-blockers, magnesium, fluoroquinolones/macrolides, neuromuscular blockers, iodinated contrast). Two antibody phenotypes behave differently in crisis: AChR-MG (limb + ocular + bulbar, thymoma-associated, responds to acetylcholinesterase inhibitors and thymectomy) versus MuSK-MG (selective bulbar/respiratory/facial weakness, SPARES the eyes and limbs, relative resistance to pyridostigmine, more frequent and more severe crises). The intensivist's priorities are: (1) recognise fatigable weakness + impending respiratory failure EARLY; (2) monitor bedside respiratory function every 4-6 h — FVC, NIF (MIP), single breath count — using the SAME thresholds as Guillain-Barre syndrome; (3) intubate electively (not as an emergency) when FVC &lt;15 mL/kg, NIF < -30 cmH2O, or bulbar weakness threatens the airway; (4) distinguish myasthenic crisis (UNDER-treated, 'dry') from cholinergic crisis (OVER-treated with anticholinesterase, 'wet' with SLUDGE); (5) treat with IVIG 0.4 g/kg/day x 5 days OR plasma exchange (PLEX, 5 sessions over 1-2 weeks) — equally effective — plus identify and remove the trigger and hold/limit pyridostigmine; (6) plan thymectomy for thymoma (always) or AChR-positive non-thymomatous generalised MG; (7) rigorously avoid MG-worsening drugs. Mortality has fallen from 30-40% (1960s) to 4-8% with modern ICU care.

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Tetanus and Botulism in the ICU — Comprehensive Management

Tetanus and botulism — two neurotoxin-mediated diseases from Clostridium species requiring ICU management. TETANUS: Clostridium tetani exotoxin (tetanospasmin) travels retrograde to spinal cord → blocks inhibitory neurotransmitters (GABA, glycine) → sustained muscle contraction → TRISMUS (lockjaw), RISUS SARDONICUS (sardonic smile), OPISTHOTONOS (arched back), autonomic instability (labile BP/HR). Management: HTIG (human tetanus immunoglobulin IM), metronidazole (eradicate C. tetani), benzodiazepines (control spasms), magnesium sulfate (control spasms + autonomic instability), ICU for airway/ventilation, wound debridement, vaccination (to prevent recurrence — natural infection does NOT confer immunity). BOTULISM: Clostridium botulinum toxin blocks acetylcholine release at NMJ (cleaves SNARE proteins) → DESCENDING FLACCID PARALYSIS (cranial nerves first — ptosis, diplopia, dysphagia, dysarthria → respiratory failure) + dilated pupils + dry mouth. Forms: foodborne (contaminated food — home-canned), wound (IV drug use — black tar heroin), infant (honey — spores germinate in immature gut), iatrogenic (cosmetic/therapeutic injection). Management: botulinum antitoxin (equine heptavalent — for foodborne/wound — does NOT reverse existing paralysis but prevents progression), supportive ventilation (prolonged — weeks-months for NMJ recovery), NO antibiotics for foodborne (may increase toxin release), penicillin/metronidazole for wound botulism. Mortality: tetanus 10-40% (higher in developing countries), botulism 5-10% (respiratory failure).

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Neurocritical Care

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Acute intermittent porphyria (AIP)

AIP is a rare autosomal dominant defect in hepatic haem biosynthesis caused by deficient porphobilinogen deaminase (hydroxymethylbilane synthase, HMBS). Presents with acute neurovisceral attacks triggered by drugs (barbiturates, sulfonamides, hormonal contraceptives, antiepileptics, alcohol), fasting, infection, surgery and stress. Classic triad: abdominal pain (severe, out of proportion to exam, with a benign abdomen) + neurological symptoms (motor neuropathy, seizures, psychiatric disturbance) + autonomic dysfunction (tachycardia, hypertension, constipation, urinary retention). Urine turns dark/red on light exposure. Diagnosis: markedly elevated urinary porphobilinogen (PBG) and aminolevulinic acid (ALA) on a random spot urine, confirmed by HMBS genetic testing. Treatment: withdraw all triggers, IV haem arginate 250 mg or 3 mg/kg once daily for four daily infusions (IV glucose alone only for mild attacks or until haem is available), opiate analgesia, phenothiazines/ondansetron for nausea, gabapentin/levetiracetam for seizures, and correct SIADH hyponatraemia. Ventilation may be needed for motor neuropathy.

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Acute severe head injury: multimodal monitoring

Multimodal neuromonitoring in severe TBI goes beyond ICP monitoring to assess brain physiology directly. ICP is a PRESSURE — it says nothing about whether the tissue is receiving enough OXYGEN or SUBSTRATE. A patient can have a perfectly normal ICP of 12 mmHg and yet a critically low PbtO2, a rising lactate/pyruvate ratio, or non-convulsive status epilepticus. Modalities: (1) ICP monitoring (standard — external ventricular drain is the gold standard because it measures pressure AND drains CSF; intraparenchymal bolt is easier to site with a lower infection rate but cannot drain). (2) Brain tissue oxygenation (PbtO2 — LICOX probe, target &gt;20 mmHg; &lt;15 = brain tissue hypoxia; BOOST-2 trial showed PbtO2-guided therapy reduces brain hypoxia). (3) Cerebral microdialysis (lactate/pyruvate ratio &gt;40 = metabolic distress; rising glutamate = excitotoxicity; rising glycerol = cell membrane breakdown; low glucose = substrate depletion). (4) Jugular venous bulb oximetry (SjvO2 — global cerebral oxygenation; target 55-75%; &lt;50% = cerebral hypoxia, &gt;90% = hyperaemia). (5) Continuous EEG (cEEG — non-convulsive status epilepticus found in 19% of critically ill monitored patients, 92% exclusively non-convulsive). (6) Transcranial Doppler and autoregulation indices (PRx). Goal: integrate ALL modalities — treat the PATIENT, not the NUMBER.

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Acute stroke: ischaemic and haemorrhagic

Acute stroke is a neurological emergency. Time is brain — 1.9 million neurons lost per minute without reperfusion. Ischaemic stroke: thrombolysis (alteplase 0.9 mg/kg up to 4.5 h, or tenecteplase 0.25 mg/kg) plus mechanical thrombectomy for large vessel occlusion (up to 24 h with favourable imaging). Intracerebral haemorrhage (10-15% of strokes): BP control (SBP &lt;140 within 1 h), reverse anticoagulation, urgent neurosurgical evaluation of the cerebellar haematoma with brainstem compression or hydrocephalus. ICU management: airway, BP control (permissive hypertension for ischaemic — SBP &lt;185/110 for thrombolysis; reduce for haemorrhagic — SBP &lt;140), glucose and temperature control, DVT prophylaxis, swallowing assessment.

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Aneurysmal subarachnoid haemorrhage

Aneurysmal SAH is bleeding from a ruptured cerebral aneurysm into the subarachnoid space. Presents with 'thunderclap' headache (worst ever, maximal at onset), meningismus, nausea/vomiting, altered consciousness. Diagnosis: non-contrast CT brain (sensitive within 6h), LP if CT negative (xanthochromia). Management: secure the aneurysm early (coiling preferred over clipping), nimodipine 60 mg every 4h for 21 days (reduces delayed cerebral ischaemia), control elevated BP before the aneurysm is secured, maintain euvolaemia. Complications: rebleeding (#1 early cause of death), vasospasm (days 4-14 — leading cause of morbidity), hydrocephalus, cerebral salt wasting, seizures.

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Guillain-Barré syndrome and neuromuscular emergencies

Guillain-Barré syndrome (GBS) is an acute, ascending, symmetrical flaccid paralysis with areflexia caused by autoimmune demyelination of peripheral nerves — classically preceded by Campylobacter jejuni or viral infection (1-3 weeks prior). ICU admission is for respiratory monitoring (20-30% require mechanical ventilation), autonomic dysfunction (arrhythmia, BP fluctuation), and disease-modifying therapy (IVIG or plasmapheresis — equally effective, no benefit of combined therapy). Intubation criteria: FVC &lt;20 mL/kg, MIP < -30 cmH2O, MEP &lt;40 cmH2O, or bulbar weakness with aspiration risk. Myasthenia gravis crisis: respiratory failure from neuromuscular weakness — treat with IVIG/plasmapheresis + cholinesterase inhibitors.

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Meningitis and encephalitis in the ICU

Bacterial meningitis and viral encephalitis are neurological emergencies. Bacterial meningitis: fever, headache, neck stiffness, altered mental status (the classic triad in only 44 percent of cases, though 95 percent have at least two of the four features). Empiric therapy within the hour: dexamethasone 10 mg IV before or with the first antibiotic dose, then high-dose ceftriaxone plus vancomycin (add ampicillin for older or immunocompromised patients — Listeria). Viral encephalitis: HSV is the most common treatable cause — acyclovir 10 mg/kg IV every 8 hours while awaiting PCR. LP: send CSF for cell count, differential, protein, glucose with paired serum glucose, Gram stain, culture, viral PCR (HSV, VZV, enterovirus). NEVER delay antibiotics for LP or CT. Adjunctive dexamethasone cut unfavourable outcome (RR 0.59) and death (RR 0.48) in the landmark trial and reduces hearing loss.

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Myasthenia gravis crisis and neuromuscular respiratory failure

Myasthenic crisis is respiratory failure from severe weakness of respiratory muscles (diaphragm, intercostals) and bulbar muscles (swallowing, airway protection) in myasthenia gravis, an autoimmune disorder of the postsynaptic neuromuscular junction. Antibodies target the acetylcholine receptor (AChR, ~85% of generalised MG), muscle-specific tyrosine kinase (MuSK, 5-8%), or LRP4. Triggers: infection (#1), surgery, pregnancy and the postpartum period, and drugs that impair neuromuscular transmission (aminoglycosides, magnesium, beta-blockers, fluoroquinolones, neuromuscular blockers, corticosteroid initiation). Presents with progressive fatigable weakness, dysphagia, dysarthria, weak cough, and respiratory distress. Diagnosis is clinical (known MG with worsening fatigable weakness) supported by bedside tests (fatigability, ice pack test, single breath count) and bedside pulmonary function (FVC, MIP, MEP), and confirmed by AChR/MuSK antibodies, repetitive nerve stimulation and single-fibre EMG. Management: ICU admission for respiratory monitoring, ventilatory support (NIV first, then intubation if bulbar/respiratory failure), IVIG or plasma exchange (equally effective), identify and treat the trigger, and start or adjust immunosuppression (prednisolone with an early-steroid-worsening caveat, azathioprine, mycophenolate, rituximab). Thymectomy is mandatory for thymoma and beneficial in selected AChR-positive generalised MG. Distinguish myasthenic crisis (under-treated, dry) from cholinergic crisis (over-treated with anticholinesterase, wet — SLUDGE). Mortality 4-8% with modern ICU care.

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Post-cardiac arrest prognostication

Prognostication after cardiac arrest predicts neurological outcome to guide continuation or withdrawal of life-sustaining therapy. The key principle: use a MULTIMODAL approach — no single test is 100% reliable. Timing: do NOT prognosticate before 72h post-arrest. Must be: normothermic (no fever for 72h), off sedatives for adequate washout, off NMBAs, no severe metabolic derangement. Assessment tools: (1) Clinical examination (brainstem reflexes, motor response, myoclonus), (2) Electrophysiology (SSEP N20, EEG), (3) Biomarkers (NSE), (4) Imaging (CT/MRI brain). The most reliable single indicator: bilateral absence of N20 response on SSEP (positive predictive value for poor outcome >95%). Goal: accurate, honest, compassionate prognostication for families.

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Raised ICP and traumatic brain injury management

Raised ICP is a life-threatening complication of severe TBI requiring urgent ICP monitoring and stepwise management. The Seattle International Consensus Conference (SICC) algorithm guides tiered therapy: Tier 0 (basics: head elevation, normocapnia, normoglycaemia, normothermia), Tier 1 (CSF drainage, hyperosmolar therapy — hypertonic saline or mannitol), Tier 2 (metabolic suppression with barbiturates, decompressive craniectomy). CPP target 60-70 mmHg. RESCUEicp (2016): decompressive craniectomy reduced mortality but increased vegetative/severe disability. POLAR (2018): prophylactic hypothermia does NOT improve outcomes.

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Sedation, analgesia and delirium (PADIS)

The PADIS framework (Pain, Agitation/sedation, Delirium, Immobility, Sleep) guides ICU symptom management. Delirium affects 50-80% of ventilated ICU patients and is an independent predictor of mortality, longer ventilation, cognitive impairment. Assessment: pain (CPOT/BPS), sedation (RASS), delirium (CAM-ICU/ICDSC). Management: goal-directed light sedation (RASS -1 to 0), treat pain FIRST (analgesia-first), daily sedation interruption, ABCDEF bundle. Dexmedetomidine achieves arousable sedation with less delirium and earlier extubation than midazolam (SEDCOM); SPICE III found no 90-day mortality difference vs usual care. Haloperidol does NOT improve outcomes in ICU delirium. Propofol infusion syndrome (PRIS) is a lethal complication of high-dose, prolonged propofol (above 4 mg/kg/h for over 48 h).

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Targeted temperature management after cardiac arrest

Targeted temperature management (TTM) after cardiac arrest aims to reduce neurological injury from post-cardiac arrest brain ischaemia-reperfusion. HACA and Bernard (NEJM 2002): 32-34°C for 24h (or 33°C for 12h) improved neurological outcome after VF arrest. TTM trial (NEJM 2013): 33°C vs 36°C showed no difference in outcomes (both acceptable). TTM2 (NEJM 2021): hypothermia at 33°C offered no advantage over normothermia with early fever treatment (triggered at 37.8°C). HYPERION (NEJM 2019): 33°C for 24h improved 90-day neurological outcome in non-shockable rhythm arrest. Indications: comatose adult patients after OHCA with shockable (VF/VT — strongest evidence) or non-shockable rhythm, and after IHCA. Method: surface or intravascular cooling. Target: 32-36°C for 24h, then controlled rewarming (0.5°C/h in the TTM trial protocol) to 37°C. Maintain normothermia (under 37.5°C) for 72h. Avoid fever (worsens outcomes — odds of unfavourable outcome rise about 2.3-fold per degree above 37°C). Shivering must be controlled (skin counterwarming, magnesium, sedation, paralysis).

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Neurocritical care

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Acute intracranial hypertension: osmotherapy, hyperventilation, and craniectomy

Acute intracranial hypertension (ICP >22 mmHg) is life-threatening — compromises cerebral perfusion (CPP = MAP − ICP) -> brain ischaemia + herniation. CAUSES: TBI, SAH, intracerebral haemorrhage, brain tumour, meningitis/encephalitis, hepatic encephalopathy, anoxia, hydrocephalus. CLINICAL (Cushing's triad — late): hypertension, bradycardia, irregular respiration. MONITORING: ICP monitor (intraventricular — EVD — gold standard; intraparenchymal — common); CPP target 60-70. MANAGEMENT ESCALATION (tiered): (1) HEAD ELEVATION 30° (neutral — lowers ICP without reducing CPP). (2) SEDATION + ANALGESIA (opiates, benzodiazepines — reduce metabolic demand + ICP). (3) NORMOVENTILATION (avoid hypercapnia -> raises ICP; avoid PROLONGED hyperventilation -> cerebral ischaemia). (4) OSMOTHERAPY: mannitol (20% 1 g/kg) OR hypertonic saline bolus — pulls water from brain; monitor sodium + osmolality. (5) NEUROMUSCULAR BLOCKADE (blunts stimulation-related ICP surges; evidence limited). (6) METABOLIC SUPPRESSION: pentobarbital coma titrated to burst suppression on continuous EEG (for refractory). (7) DECOMPRESSIVE CRANIECTOMY (RESCUEicp — refractory ICP >25 mmHg; trades death for severe disability). (8) TRANEXAMIC ACID within 3 h of TBI (CRASH-3). (9) HYPOTHERMIA — not indicated (Eurotherm harm). TREAT CAUSE (evacuate haematoma, drain CSF, treat infection).

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Acute stroke: ischaemic, haemorrhagic, and SAH — comprehensive ICU management

Acute stroke = sudden neurological deficit from cerebral vascular event. THREE TYPES: (1) ISCHAEMIC (about 85% — arterial occlusion — thrombus/embolus). (2) INTRACEREBRAL HAEMORRHAGE [ICH] (10-15% — intraparenchymal bleed — hypertension/amyloid). (3) SUBARACHNOID HAEMORRHAGE [SAH] (5-7% — aneurysmal rupture). ISCHAEMIC: THROMBOLYSIS (alteplase within 4.5h — NINDS/ECASS III) + THROMBECTOMY (DAWN/DEFUSE-3 — for large vessel occlusion [LVO] within 6-24h with salvageable penumbra). ICH: BP control (SBP &lt;140 — INTERACT2/ATACH-2), ICH score for prognosis, surgical evacuation (CEREBELLAR — life-saving; SUPRATENTORIAL — STICH II — no routine benefit). SAH: nimodipine (reduces vasospasm + improves outcomes — 60 mg PO q4h x 21 days), BP control (SBP &lt;160 pre-aneurysm securing), vasospasm management (induced hypertension — but NOT triple-H — avoid hypervolaemia). ICU: BP (permissive hypertension for ischaemic [SBP &lt;185 for thrombolysis, &lt;140 for ICH]), temperature (normothermia — fever worsens outcomes), glucose (avoid hypo- and marked hyperglycaemia), swallowing assessment (before oral intake), DVT prophylaxis (LMWH). MORTALITY: ischaemic 10-15%; ICH 35-50%; SAH 30-40%.

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Refractory status epilepticus: anaesthetic coma, midazolam, propofol, ketamine

Refractory status epilepticus (RSE) = SE continuing despite first-line (benzodiazepine) AND second-line (anti-seizure medication — levetiracetam, fosphenytoin, valproate) therapy. SUPER-refractory (SRSE) = RSE persisting or recurring ≥24h after anaesthetic onset (or recurrence on taper). MORTALITY: death in about one-third to one-half of reported RSE/SRSE cases. MANAGEMENT: (1) INTUBATE + ventilate (anaesthetics suppress respiration). (2) ANAESTHETIC INFUSION: midazolam, propofol, thiopental/pentobarbital, ketamine — titrate to BURST SUPPRESSION on EEG (or seizure cessation). (3) CONTINUOUS EEG (cEEG — mandatory — titrate to EEG target, detect non-convulsive seizures). (4) MAINTENANCE ASMs (continue + add new — lacosamide, brivaracetam, perampanel). (5) ADDRESS CAUSE (autoimmune — antibodies +…

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Domain

Neurocritical care / vascular

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Acute Ischaemic Stroke — Thrombolysis, Thrombectomy & Hemicraniectomy

Acute ischaemic stroke is managed within strict time windows. The IV thrombolysis (alteplase 0.9 mg/kg, max 90 mg; within 4.5 hours of the onset) is for any measurable stroke without contraindications. The mechanical thrombectomy (within 6 hours for the large-vessel occlusion — the ICA, the M1 MCA, the basilar; extended to 24 hours for the selected patients with the CT perfusion mismatch per the DAWN and DEFUSE-3 trials) recanalises the large vessel directly. The post-stroke ICU care: the BP control (permissive hypertension below 220/120 for the non-thrombolysed; under 185/110 before and 180/105 for 24 hours after the thrombolysis), the aspirin after 24 hours, the statin, the swallow assessment, and the DVT prophylaxis. The decompressive hemicraniectomy (within 48 hours, for the patients under 60) for the malignant MCA infarct — the DESTINY, DECIMAL, and HAMLET trials showed an improved survival and a functional outcome.

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Intracerebral Haemorrhage — ICH Score, BP Control & Surgery

Intracerebral haemorrhage (ICH) is the bleeding into the brain parenchyma, most commonly from hypertension (the deep location — basal ganglia, thalamus, pons, cerebellum) or amyloid angiopathy (the lobar location in the elderly). The CT shows a hyperdense lesion. The ICH Score (the GCS, the age over 80, the infratentorial location, the volume over 30 mL, the intraventricular extension) predicts the 30-day mortality. The management: BP control to SBP 140 mmHg (the INTERACT2 trial — safe and improves the functional outcome; the IV labetalol or nicardipine), reverse the anticoagulation rapidly (the PCC for warfarin; the andexanet alfa for the DOAC; the idarucizumab for dabigatran), prevent the haematoma expansion (the spot sign on the CT angiogram predicts the expansion), and surgery (the cerebellar haemorrhage — the urgent evacuation; the supratentorial — the STICH II showed no routine benefit).

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Renal

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Acute kidney injury and renal replacement therapy

AKI is an abrupt reduction in kidney function (KDIGO: creatinine increase >=26.5 umol/L in 48h, or >=1.5x baseline, or urine output &lt;0.5 mL/kg/hr for 6h). Classified Stage 1-3 by severity. Causes: pre-renal (most common, hypoperfusion), intrinsic (ATN, AIN, GN), post-renal (obstruction). Management: treat the cause, optimise haemodynamics, avoid nephrotoxins. RRT indications: AEIOU (Acidosis, Electrolyte, Ingestion, Overload, Uraemia). Timing: STARRT-AKI (2020): no benefit of early RRT. CRRT preferred in haemodynamically unstable.

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Fluid overload management in ICU: comprehensive

Fluid overload is one of the most common and most dangerous iatrogenic complications in the ICU. A positive cumulative fluid balance is an independent predictor of mortality, AKI, ARDS, prolonged mechanical ventilation, and increased ICU length of stay. The ROSE model conceptualises fluid therapy in four phases — Rescue (salvage boluses for life-threatening shock), Optimisation (goal-directed titration using dynamic indices), Stabilisation (zero or slightly negative balance, organ support only), and De-escalation/Evacuation (active fluid removal or de-resuscitation with diuretics or CRRT). Key evidence: the SOAP study (Vincent 2006) demonstrated that positive fluid balance is an independent predictor of ICU mortality in sepsis. The FACTT trial (ARDSNet 2006) showed that a conservative fluid strategy in ALI/ARDS increased ventilator-free days and reduced ICU stay without increasing non-pulmonary organ failure. The CLASSIC trial (Meyhoff 2022, NEJM) found that a restrictive fluid strategy in septic shock was safe and showed signals toward benefit in pre-specified subgroups. Cordemans 2012 described Global Increased Permeability Syndrome (GIPS) — the 'third hit' of critical illness where capillary leak, endothelial dysfunction, and ongoing inflammation make fluid accumulation self-perpetuating. Management requires phase-appropriate fluid stewardship: give fluid only to responsive patients (passive leg raise, pulse pressure variation, IVC collapsibility), track cumulative balance daily (cumulative >10% body weight = significant overload), and de-resuscitate aggressively once shock resolves (furosemide IV bolus or infusion, thiazide for sequential nephron blockade, albumin 20% for oncotic pressure, CRRT for refractory overload). The FEAST trial (Maitland 2011) remains a cautionary landmark: fluid boluses INCREASED mortality in African children with severe infection, demonstrating that fluid is not always benign.

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Renal and metabolic

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Acute kidney injury: KDIGO staging, prevention, biomarkers, and RRT timing

Acute kidney injury (AKI) = abrupt reduction in kidney function (hours-days) → accumulation of nitrogenous waste (urea, creatinine) + inability to regulate fluid/electrolyte/acid-base. KDIGO STAGING (2012): Stage 1 (creatinine ≥26.5 μmol/L in 48h OR 1.5-1.9x baseline; urine &lt;0.5 mL/kg/hr for 6-12h). Stage 2 (creatinine 2-2.9x baseline; urine &lt;0.5 for ≥12h). Stage 3 (creatinine ≥3x OR ≥354 μmol/L OR RRT; urine &lt;0.3 for ≥24h OR anuria ≥12h). CAUSES: PRE-renal (hypovolaemia, shock — most common — reduced perfusion), INTRA-renal (ATN from ischaemia/toxins — most common intrinsic; AIN from drugs; GN; interstitial nephritis), POST-renal (obstruction — catheter to exclude). PREVENTION (the mainstay — NO proven TREATMENT for established AKI): (1) AVOID nephrotoxins (NSAIDs, aminoglycosides, contrast, ACEi/ARB if hypoperfused). (2) OPTIMISE PERFUSION (fluids if hypovolaemic — goal-directed; vasopressors if vasodilated). (3) MONITOR (creatinine + urine output daily in ICU). BIOMARKERS: NGAL, TIMP-2•IGFBP7 (NephroCheck — predict AKI within 12-24h — before creatinine rises — emerging). RRT TIMING: AKIKI + STARRT-AKI — NO mortality benefit of EARLY RRT (wait for clinical indications: AEIOU). MORTALITY: Stage 1 10%, Stage 2 20%, Stage 3 40-50%. AKI → CKD in 10-30% of severe AKI survivors.

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Acute severe hypercalcaemia and hypocalcaemia: ICU emergencies

Calcium disorders are common in ICU. NORMAL serum calcium is 8.4 to 10.4 mg/dL (about 2.1 to 2.6 mmol/L). HYPOCALCAEMIA (total calcium under 8 mg/dL, about 2.12 mmol/L): neuromuscular irritability (tetany, Chvostek and Trousseau signs, seizures, perioral numbness, carpopedal spasm, prolonged QT). Severe or symptomatic hypocalcaemia is treated with an IV calcium infusion, then oral calcium and vitamin D. Causes: postsurgical hypoparathyroidism (the most frequent), hypomagnesaemia, vitamin D deficiency, severe CKD, sepsis, citrate load. Confirm with IONISED calcium, the clinical gold standard. HYPERCALCAEMIA is most often primary hyperparathyroidism or malignancy; hypercalcaemia of malignancy is an oncologic emergency (nausea, vomiting, constipation progressing to delirium, untreated to coma and death): saline rehydration plus an IV bisphosphonate (zoledronate 4 mg or pamidronate 90 mg), calcitonin added as initial therapy in severe disease, denosumab 120 mg SC for bisphosphonate-refractory disease.

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Acute severe hypernatraemia: causes, correction rate, and diabetes insipidus

Hypernatraemia (Na >145 mmol/L) = water deficit relative to sodium → brain cell SHRINKAGE (water shifts OUT of brain → decreased brain volume → cerebral haemorrhage from bridging vein tearing). CAUSES: (1) FREE WATER LOSS (diabetes insipidus [central — brain injury; nephrogenic — drugs], diarrhoea, burns, sweating). (2) INADEQUATE WATER INTAKE (coma, intubated — can't drink, inadequate free water prescription). (3) HYPERTONIC SOLUTIONS (hypertonic saline for ICP, sodium bicarbonate). (4) SODIUM OVERLOAD (salt poisoning, Conn's syndrome). CLINICAL: confusion → seizures → coma (from brain shrinkage). CORRECTION: controlled — under 12 mmol/L per day with close electrolyte monitoring, prompt but never neglected (delayed correction itself prolongs stay and raises mortality; in severe hypernatraemia of 155 mmol/L or more, correction at or under 0.5 mmol/L/h carried HIGHER 30-day mortality than faster correction). FREE WATER DEFICIT calculation: deficit = TBW × (Na/140 − 1). Replace over 48-72h with hypotonic solutions (5% dextrose, 0.45% NaCl, oral water). DIABETES INSIPIDUS: central → desmopressin; nephrogenic → treat cause (stop lithium → water).

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Acute severe hypokalaemia and hypomagnesaemia: ECG, repletion, and refractory causes

Hypokalaemia (K &lt;3.5 mmol/L) is common in ICU (diuretics, GI loss, drugs). SEVERE (&lt;2.5) → polymorphic VT risk. ECG changes: T-wave flattening, ST depression, U waves, prolonged QT. Hypomagnesaemia (Mg &lt;0.7 mmol/L, defined as under 1.7 mg/dL in cohort studies) met 52 percent of medical-ICU admissions and was present in 42 percent of hypokalaemic inpatients — always check + replace Mg in refractory hypokalaemia (ROMK channel). Repletion: ORAL salts preferred; IV potassium chloride only as a diluted, monitored infusion (in critical care usually up to 40 mmol/h) — never an undiluted push. Torsades: stop QT-prolonging drugs, IV magnesium sulfate 1 to 2 g, keep K in the high-normal range, overdrive pace if recurrent. Causes: diuretics, GI loss, DKA insulin, refeeding, β2-agonists, mineralocorticoid excess, cisplatin/amphotericin, PPIs (Mg), Gitelman/Bartter.

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Acute severe hyponatraemia: emergency correction, ODS risk, and guidelines

Hyponatraemia (Na &lt;135 mmol/L) is the commonest electrolyte disorder in hospitalised patients. SEVERE (&lt;120) and ACUTE (&lt;48h) hyponatraemia cause cerebral oedema (seizures, coma, death). CHRONIC (>48h) hyponatraemia risks OSMOTIC DEMYELINATION SYNDROME (ODS / central pontine myelinolysis) if corrected too rapidly. CORRECTION RATES (critical): severe symptoms → 3% hypertonic saline bolus (Na rises 4-6 mmol/L), then STOP; max rise ≤8 mmol/L in any 24h (chronic), ≤10-12 mmol/L (acute). NEVER give >100 mL 3% saline as a single rapid bolus without reassessment. Workup: plasma osmolality (hypo = &lt;275), urine osmolality (>100 = ADH active), urine Na (SIADH >30, hypovolaemic &lt;20), volume status. The BRAIN adapts to chronic hyponatraemia (extrudes osmolytes) — too-rapid correction → brain shrinks → myelinolysis.

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Acute severe metabolic acidosis: approach, anion gap, and lactate

Metabolic acidosis (pH &lt;7.35, HCO3 &lt;22, low/normal PaCO2 compensatory) is ubiquitous in ICU. SYSTEMATIC approach: (1) Is it metabolic acidosis? (2) Calculate ANION GAP: Na − (Cl + HCO3); normal 8-12. (3) HIGH anion gap (HAGMA — >12): lactate (sepsis, shock, metformin), ketones (DKA, alcoholic, starvation), toxins (methanol, ethylene glycol, salicylates, paraldehyde), renal failure (uraemic acids). Mnemonic: MUDPILES / GOLDMARK. (4) NORMAL anion gap (NAGMA): GI bicarbonate loss (diarrhoea), renal tubular acidosis, acetazolamide, ureteroenteric fistula, hyperalimentation. (5) DELTA GAP / delta-delta: assess for concurrent disorders (e.g., metabolic alkalosis from vomiting + HAGMA). (6) Treat CAUSE — bicarbonate generally NOT indicated (unle…

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Acute severe metabolic alkalosis: causes, chloride-responsive vs resistant

Metabolic alkalosis (pH >7.45, HCO3 >26) is common in ICU (vomiting, NG suction, diuretics). SEVERE (pH >7.55) → serious: hypoventilation (compensatory — but causes hypoxia/hypercapnia), hypokalaemia, hypocalcaemia (ionised), arrhythmia, seizures, coronary vasospasm. Classification: CHLORIDE-RESPONSIVE (LOW urine chloride — vomiting, NG suction, diuretics, post-hypercapnia — responds to saline + KCl) vs CHLORIDE-RESISTANT (HIGH urine chloride — mineralocorticoid excess: hyperaldosteronism, Cushing, exogenous steroid, liquorice — responds to treating cause, K-sparing diuretic). KEY: maintenance requires ALDOSTERONE (without it, kidney excretes excess HCO3) + HYPOKALAEMIA (promotes H secretion → HCO3 generation). Treatment: NORMAL SALINE (volume + chloride) + KCl for chloride-responsive; treat cause for chloride-resistant. Severe (pH >7.6) → acetazolamide, acid (HCl/arginine), dialysis.

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Drug-induced nephrotoxicity: mechanism, offending agents, and prevention in ICU

Drug-induced nephrotoxicity accounts for 2-15% of acute renal failure in hospital/ICU series and 28.6% of a Naranjo-adjudicated hospital AKI cohort. Five dominant mechanisms: (1) HAEMODYNAMIC (NSAIDs constrict afferent arteriole via prostaglandin inhibition; ACEi/ARB dilate efferent arteriole by blocking angiotensin II; calcineurin inhibitors constrict afferent arteriole via endothelin — the 'triple whammy' combination carries AKI odds ratio 2.01). (2) ACUTE TUBULAR NECROSIS (ATN) — direct tubular toxicity: aminoglycosides accumulate in proximal tubular cells via the megalin receptor (the only major uptake pathway); amphotericin B deoxycholate is dose-limited by nephrotoxicity (prefer lipid formulations); tenofovir causes proximal tubular injury (Fanconi syndrome); iodinated contrast causes medullary vasoconstriction/hypoxia plus direct cytotoxicity; cisplatin enters via OCT2. (3) ACUTE INTERSTITIAL NEPHRITIS (AIN) — Type IV hypersensitivity: antibiotics, PPIs (a common cause), NSAIDs, rifampicin, sulfonamides, allopurinol; biopsy is definitive; up to one-third progress to chronic dialysis. (4) CRYSTAL NEPHROPATHY — sulfadiazine, aciclovir, indinavir, triamterene, methotrexate precipitate in tubules when volume is depleted, kidney disease exists, or urinary pH shifts. (5) OSMOTIC NEPHROSIS — IV immunoglobulin (sucrose stabiliser), hydroxyethyl starch, mannitol cause tubular cell swelling. Prevention: identify high-risk patients, avoid/limit nephrotoxins, therapeutic drug monitoring (vancomycin AUC/MIC 400-600; aminoglycoside once-daily dosing lowers nephrotoxicity risk ratio to 0.74), isotonic volume expansion for contrast (PRESERVE: saline = bicarbonate, NAC no benefit), recognise and STOP offending drug early.

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Phosphate disorders: hypophosphataemia and hyperphosphataemia in ICU

Phosphate (PO4) is essential for ATP (energy), 2,3-DPG (oxygen release from Hb), cell membrane function (phospholipids), bone metabolism, and leukocyte/respiratory muscle function. HYPOPHOSPHATAEMIA (&lt;0.8 mmol/L, phosphorus &lt;2.5 mg/dL): COMMON in ICU (refeeding, sepsis, CRRT, diuretics, alkalosis) → RESPIRATORY FAILURE (diaphragm weakness — can't make ATP), WEAKNESS, CARDIAC dysfunction. MANAGEMENT: IV sodium/potassium phosphate — published ICU regimens are severity-banded (15–30 mmol over 3 h; up to 45 mmol over 3–6 h for severe, or weight-based 0.32–1 mmol/kg); oral if mild-moderate. HYPERPHOSPHATAEMIA (raised PO4 in acute illness): AKI (can't excrete), tumour lysis, rhabdomyolysis. MANAGEMENT: treat cause (RRT if AKI or severe tumour lysis); binders are for chronic CKD, not acute. Never give calcium reflexively — calcium-phosphate precipitation worsens AKI.

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RRT modality selection: IHD vs CRRT vs SLED — when and why

When AKI requires RRT, three modalities are available: (1) INTERMITTENT HAEMODIALYSIS (IHD) — standard, 3-4h sessions, high efficiency, rapid solute removal. (2) CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT — CVVH, CVVHD, CVVHDF) — 24h/day, slow, gentle, haemodynamically stable, better for shocked/cerebral oedema patients. (3) SUSTAINED LOW-EFFICIENCY DIALYSIS (SLED) — hybrid, 6-12h sessions, intermediate efficiency, haemodynamic stability between IHD and CRRT. CHOICE based on: HAEMODYNAMICS (CRRT for shocked, IHD for stable), CEREBRAL OEDEMA (CRRT — slower fluid/urea shift -> less brain swelling), ANTICOAGULATION (CRRT needs more — citrate or heparin), ACIDOSIS (CRRT for severe lactic acidosis — continuous correction), MOBILITY (IHD for ambulatory/rehab). EVIDENCE: NO mortality difference between IHD and CRRT (multiple RCTs — HEMO, SHARF, Vinsonneau). COST: CRRT more expensive. DOSE: CRRT 20-25 mL/kg/hr; IHD Kt/V 1.2-1.5. TIMING: AKIKI, STARRT-AKI — EARLY vs LATE RRT — no mortality difference (don't rush to RRT — wait for clinical indications).

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Domain

Resuscitation

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Acute limb compartment syndrome

Acute limb compartment syndrome is elevated pressure within a fascial compartment causing ischaemia and necrosis of muscles and nerves. Causes: fracture (#1 — tibial shaft, forearm), crush injury, burns (circumferential), prolonged immobility, reperfusion injury (post-vascular repair), tight casts/dressings, bleeding into compartment (anticoagulated). The 6 Ps: Pain (disproportionate, worse on passive stretch — the EARLIEST and most sensitive sign), Pallor, Paraesthesia, Paralysis, Pulselessness (LATE — absence of pulse means it's too late), Poikilothermia. Diagnosis: clinical + compartment pressure measurement (delta pressure = diastolic BP - compartment pressure &lt;30 mmHg = positive). Treatment: EMERGENT FASCIOTOMY (within 6 hours to prevent irreversible necrosis). Untreated → Volkmann ischaemic contracture, amputation, rhabdomyolysis, renal failure.

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Acute limb ischaemia: embolic vs thrombotic, and emergency management

Acute limb ischaemia (ALI) = sudden decrease in limb perfusion (&lt;14 days, the trial cutoff) threatening viability. CAUSES: (1) EMBOLIC — commonly cardiac (AF is the leading source; found in 60-95% of operated ALI series) or artery-to-artery (atheroembolism). Sudden, no collaterals, severe. (2) THROMBOTIC — thrombosis on existing plaque (PAD, graft thrombosis). Gradual onset (may have collaterals), less severe initially. CLINICAL (6 Ps): Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishing cold. Delay to revascularisation risks irreversible tissue infarction and loss of limb salvage. DIAGNOSIS: clinical + Doppler (arterial and venous signals) + angiography/CTA (location/cause). MANAGEMENT: IMMEDIATE therapeutic-dose heparin (weight-based, APTT-guided; associated with better 30-day survival), analgesia, EMERGENCY revascularisation (embolectomy, thrombolysis, bypass). FASCIOTOMY for reperfusion compartment syndrome when the differential pressure (diastolic BP minus compartment pressure) falls under 30 mmHg. OUTCOMES: amputation-free survival ~72% vs ~75% at six months (urokinase vs surgery, TOPAS II); one-year all-cause death up to ~29% (comorbidity-driven); major haemorrhage 12.5% vs 5.5% (TOPAS II).

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Acute severe community-acquired pneumonia: ICU admission and discharge criteria

ICU admission decisions in community-acquired pneumonia (CAP) balance the need for organ support against resource allocation. IDSA/ATS severe CAP criteria require 1 major (invasive mechanical ventilation OR septic shock requiring vasopressors) OR 3 of 9 minor criteria (RR >=30, PaO2/FiO2 &lt;250, multilobar infiltrates, confusion, BUN >=20, leukopenia, thrombocytopenia, hypothermia, hypotension needing fluids). Severity scoring guides the decision: CURB-65 (0-1 outpatient, 2 inpatient, >=3 consider ICU), PSI (five risk classes by 30-day mortality), SMART-COP (>=3 points predicts need for intensive respiratory or vasopressor support). Do NOT admit to ICU if CURB-65 0-1, stable, no organ failure — manage on the ward or as outpatient. HDU/step-down suits intermediate patients needing close monitoring but not organ support (low-flow oxygen, low-dose vasopressors, frequent ABGs). Discharge is safe once organ support has resolved: afebrile trend, oxygenation on minimal support, off vasopressors, normal mental status, tolerating oral intake, falling inflammatory markers (CRP, procalcitonin). Premature and night-time (after 22:00) discharge increase readmission and mortality — in a large medical ICU cohort, readmitted patients had five-fold higher hospital mortality (43% vs 8%).

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Acute severe community-acquired pneumonia: outpatient to ICU care pathway

The CAP care pathway spans from community presentation through ED triage, ward management, HDU, and ICU. ED: assess severity (CURB-65/PSI), chest X-ray, bloods, blood cultures, antibiotics within 4h (1h if severe). Ward: continue antibiotics, monitor, daily review, oxygen, physiotherapy, VTE prophylaxis, early mobilisation. HDU: escalating oxygen needs, NIV, single vasopressor. ICU: mechanical ventilation, septic shock (multiple vasopressors), RRT, multi-organ failure. Discharge planning begins on admission: estimated length of stay, home support, follow-up CXR at 6 weeks, vaccination. Integrated care: seamless transitions between care levels — avoid 'silo' management. The pathway is governed by auditable quality metrics — door-to-antibiotic time, appropriate empiric antibiotic selection, length of stay, 30-day readmission, and risk-adjusted mortality — that close the audit loop from one admission to the next.

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Acute severe community-acquired pneumonia: special populations — elderly

CAP in the elderly (over 65 years) presents differently and has worse outcomes than in younger adults. Reported symptom prevalence falls with age even after adjustment for comorbidity and severity: fever may be absent, and confusion or altered mental status may be the ONLY presenting symptom, with falls, functional decline, anorexia, and incontinence dominating the picture. Mortality rises steeply with age, driven by reduced physiological reserve, comorbidities, immunosenescence, malnutrition, polypharmacy, and aspiration risk (swallowing impairment). Management: lower threshold for hospital and ICU care, antibiotics within one hour in sepsis, swallow assessment before oral intake, comprehensive geriatric assessment, delirium prevention, early mobilisation, and vaccination (pneumococcal PCV20 or PCV15 plus PPSV23, annual high-dose influenza, RSV) before or at discharge.

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Acute severe shock: classification, recognition, and management

Shock = INADEQUATE TISSUE PERFUSION → cellular hypoxia → anaerobic metabolism → lactate → organ dysfunction → death if untreated. FOUR TYPES: (1) HYPOVOLAEMIC (blood/fluid loss — haemorrhage, dehydration, burns). (2) CARDIOGENIC (pump failure — MI, myocarditis, arrhythmia, valve failure). (3) DISTRIBUTIVE (vasodilation — septic, anaphylactic, neurogenic). (4) OBSTRUCTIVE (mechanical obstruction — tamponade, tension pneumothorax, massive PE). CLINICAL: COMPENSATED (tachycardia, narrowed pulse pressure, cool peripheries, anxious — BP normal [compensating]) → DECOMPENSATED (hypotension, oliguria, altered consciousness, mottled skin — BP falling [decompensating]) → IRREVERSIBLE (multi-organ failure — cell death — unresponsive to treatment). MONITORING: lactate (perfusion + prognosis), base excess (acidosis from hypoperfusion), SvO2/ScvO2 (tissue oxygen extraction — low = extracting more = worse perfusion), urine output (&lt;0.5 mL/kg/hr = renal hypoperfusion). MANAGEMENT: ABC + TREAT CAUSE + FLUIDS (if responsive) + VASOPRESSORS (if vasodilated) + INOTROPES (if cardiac) + TRANSFUSION (if haemorrhagic) ± SURGERY (if mechanical/bleeding). GOAL: restore PERFUSION (lactate clearing, urine >0.5, MAP ≥65, conscious).

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Acute upper airway obstruction

Acute upper airway obstruction is a life-threatening emergency in which airflow through the nose, mouth, pharynx, or larynx is compromised, leading to hypoxia and death within minutes. Causes: infection (acute epiglottitis/supraglottitis, Ludwig's angina, retropharyngeal/peritonsillar abscess), swelling (hereditary and ACEi-induced angioedema, anaphylaxis), foreign body aspiration, malignancy (laryngeal, pharyngeal, anaplastic thyroid), bilateral vocal cord paralysis, post-extubation laryngeal oedema, and trauma/thermal inhalational injury. Presentation: stridor (inspiratory = extrathoracic/supraglottic, expiratory = intrathoracic, biphasic = glottic/subglottic fixed lesion), drooling, tripod position, distress, muffled or 'hot potato' voice. Stridor at rest = severe, impending obstruction. Management: do NOT agitate the patient (especially children with epiglottitis — can trigger complete laryngeal obstruction and arrest). Call for help early (senior anaesthetist + ENT + difficult airway trolley). Temporise with humidified oxygen, heliox (70:30, low-density gas reduces turbulent-flow work of breathing), nebulised adrenaline 5 mL of 1:1000, dexamethasone 8 mg IV. Secure the airway under controlled conditions — awake fibre-optic intubation preferred, inhalational induction maintaining spontaneous ventilation in children, surgical airway (cricothyroidotomy) as backup. Epiglottitis: do NOT lay flat, do NOT examine the throat. Never attempt blind nasal intubation.

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Airway management and rapid sequence induction in ICU

Airway management is a core ICU skill and a high-yield Fellowship exam topic. RSI (rapid sequence induction) is indicated for any critically ill patient requiring intubation who is at risk of aspiration (full stomach, pregnancy, bowel obstruction, sepsis, trauma, obesity) — which in practice is EVERY ICU intubation. Principle: pre-oxygenation (denitrogenation — 3 minutes of tidal breathing or 8 deep vital-capacity breaths of 100% O2, buying around 6-10 min of safe apnoea in the healthy adult) → induction agent + paralytic given in rapid sequence → laryngoscopy and intubation → confirm with waveform ETCO2. ICU airway is far higher risk than theatre: in the INTUBE study 45.2% of critically ill intubations had a major adverse peri-intubation event (cardiovascular instability 42.6%, severe hypoxaemia 9.3%, cardiac arrest 3.1%). Contemporaneous haemodynamic preparation matters: fluid loading plus vasopressor availability halved cardiovascular collapse in a randomised trial. Drug defaults: ketamine 2 mg/kg or etomidate 0.3 mg/kg for induction, rocuronium 1.2 mg/kg (sugammadex-reversible) for paralysis, with video laryngoscopy early and bougie for the difficult view (85.1% vs 70.8% first-pass success with video vs direct laryngoscopy in the DEVICE trial).

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Anaphylaxis in the ICU

Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction. Diagnosis: NIAID/FAAN clinical criteria — acute onset after a likely allergen with skin or mucosal involvement plus respiratory compromise, hypotension, or end-organ dysfunction. Management: IM adrenaline into the anterolateral thigh (adult dose 0.01 mg/kg to a maximum of 0.5 mg, repeated every 5 minutes in life-threatening anaphylaxis), supine with legs elevated, high-flow oxygen, aggressive IV crystalloid. Refractory: IV adrenaline infusion after 2 to 3 IM doses; IV glucagon if beta-blocked (guideline recommendation despite limited evidence); vasopressin, methylene blue and ECMO as rescue. Biphasic reactions: median onset 11 hours (range 0.2 to 72 hours) — observe at least 6 hours; 6 to 12 hours practical. Paired tryptase: acute 30 minutes to 2 hours from onset, baseline at least 24 hours after resolution. Common triggers: drugs (antibiotics, NMBAs), foods, insect stings, radiocontrast.

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Blood transfusion in the ICU

The TRICC trial (1999) established that a RESTRICTIVE transfusion strategy (transfuse at Hb &lt;70 g/L) is at least as effective as and possibly superior to a liberal strategy in most ICU patients, with the possible exception of acute MI and unstable angina. Restrictive strategies cut blood exposure and transfusion-hazard risk — TACO is the leading cause of transfusion-related death. Populations tested: acute MI (REALITY — restrictive trigger Hb ≤8 non-inferior for MACE), cardiac surgery (TRICS III — restrictive non-inferior), hip fracture surgery (FOCUS — liberal no better), septic shock (TRISS — restrictive non-inferior with median 1 vs 4 units), paediatric ICU (TRIPICU). Acute brain injury/TBI: debated, no trial-proven higher threshold. Single unit transfusion (one at a time, reassess, equilibration ~24 h) is standard. Transfusion reactions: TRALI (ARDS-type within hours, supportive care), TACO (volume overload, diuretic, leading cause of transfusion-related death), allergic, anaphylactic (anti-IgA), acute haemolytic (ABO mismatch), delayed haemolytic, febrile non-haemolytic, bacterial contamination (room-temperature platelets), transfusion-associated GVHD (irradiation prevents; leukoreduction does not). Blood products: PRBC, FFP, platelets, cryoprecipitate, PCC. Massive transfusion: balanced 1:1:1 ratios (PROPPR — more haemostasis, fewer exsanguination deaths), early TXA (CRASH-2), calcium for citrate hypocalcaemia.

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Classification and management of shock

Shock is inadequate tissue perfusion resulting in cellular hypoxia and organ dysfunction. Four types: (1) Hypovolaemic (fluid/blood loss — trauma, GI bleed, burns, dehydration). (2) Cardiogenic (pump failure — MI, myocarditis, cardiomyopathy). (3) Distributive (vasodilation — sepsis #1, anaphylaxis, neurogenic, adrenal). (4) Obstructive (mechanical obstruction — PE, tamponade, tension pneumothorax). Diagnosis: clinical (hypotension, tachycardia, cool/warm extremities, oliguria, altered mental status) + haemodynamic parameters (CO, SVR, CVP, SvO2). Treatment: treat underlying cause + supportive (fluids, vasopressors, inotropes, oxygen). Key: identify the TYPE of shock to guide therapy.

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Critical care ultrasound (POCUS) in ICU

Critical care ultrasound (CCUS), or point-of-care ultrasound (POCUS), is a core ICU skill — a rapid, non-invasive, repeatable, bedside imaging modality performed and interpreted by the treating clinician at the moment of decision-making. It is an EXTENSION of the clinical examination, not a replacement for formal imaging. Applications span five domains: (1) Cardiac — focused cardiac ultrasound (FoCUS/FATE) for LV and RV function, pericardial effusion and tamponade, volume status, and gross valve pathology, with the RUSH protocol integrating the 'pump' into shock assessment; (2) Lung — the BLUE protocol using A-lines (normal air), B-lines (interstitial syndrome — oedema, ARDS, fibrosis), consolidation, pleural effusion, and absent lung sliding with a lung point for pneumothorax; (3) Abdominal — FAST/eFAST for free fluid (haemorrhage), gallbladder (cholecystitis), bladder volume, and AAA screening; (4) Vascular — two-point or whole-leg compression sonography for DVT, and real-time ultrasound guidance for central venous catheter (CVC) insertion; (5) Procedural — line placement, thoracentesis, paracentesis, drain insertion. Organising protocols include RUSH (Rapid Ultrasound in Shock — pump, tank, pipes), BLUE (Bedside Lung Ultrasound in Emergency), FATE (Focused Assessment with Transthoracic Echocardiography), and FALLS (using B-lines to titrate fluids). POCUS does NOT replace formal echocardiography, CT, or comprehensive departmental ultrasound: it is goal-directed, focused, repeatable, and integrated with the clinical picture. Competency is defined by international consensus statements (ACCP/SRLF competence statement, the WINFOCUS/ICM evidence-based lung ultrasound recommendations, and the EACVI focus cardiac ultrasound core curriculum) and assessed through structured certification (FATE, CEUS/ICS FoCCUS, FUSIC, ACEP emergency ultrasound).

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Disseminated intravascular coagulation (DIC)

DIC is a syndrome of widespread intravascular coagulation causing consumption of platelets and clotting factors, microvascular thrombosis, and bleeding. It is NOT a primary disease — always secondary to a trigger: infection/sepsis, cancer, obstetric complications, trauma, transfusion reaction, snake bite. Diagnosis: ISTH DIC score (platelets, fibrinogen, FDP/D-dimer, PT) — a total score of at least 5 = overt DIC; repeat the score to track the dynamic picture. Management: treat the UNDERLYING CAUSE (the cornerstone). Supportive: platelets (under 50 x10^9/L if bleeding or high bleeding risk), FFP (bleeding with prolonged PT/aPTT), fibrinogen concentrate or cryoprecipitate (severe hypofibrinogenaemia under 1 g/L persisting despite FFP; general bleeding guidance keeps fibrinogen above 1.5 g/L), heparin (thrombotic DIC only — e.g. purpura fulminans with acral ischaemia). Do NOT give antifibrinolytics routinely in DIC (exception: primary hyperfibrinolysis with severe bleeding, e.g. leukaemia, trauma).

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Extracorporeal membrane oxygenation (ECMO)

Extracorporeal membrane oxygenation (ECMO) is a modified cardiopulmonary bypass that provides temporary support for refractory cardiac and/or respiratory failure outside the operating theatre. **VA-ECMO (venoarterial)** drains venous blood from the right atrium via a femoral vein, pumps it through a membrane oxygenator and returns oxygenated blood to the femoral artery — providing BOTH circulatory (cardiac output) and respiratory (oxygenation/CO2 removal) support; indications: cardiogenic shock refractory to inotropes/IABP, ECPR, fulminant myocarditis, post-cardiotomy failure, severe drug toxicity with cardiac depression. **VV-ECMO (venovenous)** drains from the IVC (femoral vein) and returns oxygenated blood to the right atrium (IJ vein or dual-lumen single cannula) — provides RESPIRATORY support only (the heart must work); indications: severe ARDS (PaO2/FiO2 &lt;80 despite optimised ventilation), bridge to lung transplant, near-fatal asthma (all 16 patients survived in one published adult case series), massive PE as bridge. Circuit: centrifugal (non-occlusive) pump → polymethylpentene hollow-fibre membrane oxygenator → heat exchanger. Percutaneous Seldinger femoro-femoral cannulation is standard. Systemic anticoagulation required: unfractionated heparin is the first-line agent (77% of patients in the largest prospective VV-ECMO study), monitored most often with aPTT (median 52 s in that cohort). Complications: bleeding (#1 — major bleeding 40.8% pooled in VA-ECMO), haemolysis, thrombosis, infection, limb ischaemia (16.9% pooled in VA-femoral — reduced by prophylactic distal perfusion cannula, OR 0.31), Harlequin/north-south syndrome (differential hypoxia in VA-femoral), LV distension (afterload). Weaning: VV by reducing sweep gas; VA by echo-guided stepwise flow reduction. EOLIA trial (Combes, NEJM 2018): VV-ECMO for very severe ARDS did not significantly reduce 60-day mortality (35% vs 46%, RR 0.76, P=0.09), but 28% of controls crossed over to ECMO and a post-hoc Bayesian reanalysis estimated an 88–99% posterior probability of mortality benefit. CESAR trial (Peek, Lancet 2009): transfer to an ECMO centre improved survival in severe reversible adult respiratory failure (63% vs 47% alive without disability at 6 months).

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Fluid therapy and resuscitation fluids in ICU

Fluid therapy is the commonest ICU intervention and one of the few that is genuinely a drug — with a pharmacokinetic volume of distribution, a narrow therapeutic window, and a measurable toxicity profile. Two questions dominate: WHICH fluid and HOW MUCH. WHICH: balanced crystalloids (Hartmann, Plasma-Lyte 148, Ringer acetate) are preferred first-line — the SMART (NEJM 2018) and SALT-ED (NEJM 2018) trials showed fewer major adverse kidney events with balanced solutions than 0.9% saline, and SSC 2021 suggests balanced over saline in sepsis; saline causes hyperchloraemic metabolic acidosis via a fall in the strong ion difference (Stewart), reduces renal cortical perfusion, and is reserved for hypochloraemia, hyponatraemia, TBI and drug compatibilities. Colloids: albumin is equivalent to saline (SAFE, NEJM 2004) and is suggested by SSC 2021 after large crystalloid volumes in sepsis; hydroxyethyl starch (HES) is harmful — more RRT (CHEST) and more death in sepsis (6S) — and is now restricted. HOW MUCH: fluid responsiveness is assessed dynamically (passive leg raise, PPV/SVV, IVC variability, end-expiratory occlusion) — only about half of ICU patients respond to a bolus. The four-phase ROSE model (Rescue, Optimisation, Stabilisation, Evacuation) frames therapy; cumulative positive fluid balance is an independent predictor of death. The CLASSIC (NEJM 2022), CLOVERS (NEJM 2023) and FACTT (NEJM 2006) trials support a restrictive strategy once shock resolves. Damage control resuscitation in trauma uses permissive hypotension, haemostatic (1:1:1) transfusion and early haemorrhage control.

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Hypothermia and environmental emergencies

Accidental hypothermia is a core temperature below 35C. Swiss staging: HT I (35-32C, conscious, shivering), HT II (32-28C, altered consciousness, no shivering), HT III (28-24C, unconscious), HT IV (24-13.7C, apparent death), HT V (&lt;13.7C, cardiac arrest). Management: active rewarming (forced air, warm IV fluids) for HT I-II. HT III-IV: active internal rewarming (warm lavage, ECMO/extracorporeal). HT V (cardiac arrest): full cardiopulmonary bypass or VA-ECMO — rewarm to 32C before declaring death ('no one is dead until warm and dead'). Key ECG: Osborn (J) waves. Arrhythmias: avoid adrenaline/antiarrhythmics until rewarm to >30C. Near-drowning: lung-protective ventilation and supportive care, primary lung injury from submersion.

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Massive transfusion and coagulopathy

Massive transfusion is the replacement of >1 blood volume in 24h (or >50% in 3h, or >4 units RBC in 1h with ongoing bleeding). Goal: achieve haemostasis while preventing the lethal triad (acidosis, hypothermia, coagulopathy). Damage control resuscitation (DCR) principles: (1) permissive hypotension until control of bleeding, (2) minimise crystalloid, (3) balanced blood component ratio 1:1:1 (RBC:plasma:platelets — PROPPR trial), (4) tranexamic acid within 3h (CRASH-2). Viscoelastic testing (TEG/ROTEM) guides component therapy. Avoid over-transfusion of plasma/platelets — goal-directed using ROTEM. Massive transfusion protocol (MTP) should be activated early and deactivated promptly when bleeding controlled.

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Near-drowning and drowning in the ICU

Drowning is defined as 'the process of experiencing respiratory impairment from submersion/immersion in liquid.' 'Near-drowning' (old term) — now ALL submersion injuries are 'drowning' (fatal or non-fatal). Primary injury: HYPOXIA (from aspiration/laryngospasm causing hypoxaemia → brain injury + multi-organ failure). NOT salt-water vs fresh-water distinction (clinically irrelevant — both cause hypoxia). Management: ABCDE + HIGH-FLOW OXYGEN + early intubation if respiratory distress or decreased GCS. LUNG INJURY: non-cardiogenic pulmonary oedema (ARDS-like) from aspiration + surfactant washout. BRAIN INJURY: hypoxic ischaemic encephalopathy — PRIMARY cause of death and disability. Management: neuroprotection (avoid hypoxia, hyperoxia, hypotension, hyperthermia). Rescue breaths FIRST (5 breaths) — drowning is an asphyxial arrest. Lung-protective ventilation + PEEP for ARDS-pattern lung. TTM 32–36°C for comatose post-arrest patients. Surfactant may be considered for severe refractory ARDS.

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Postoperative complications in the ICU

Postoperative ICU patients represent a unique population with specific risks: respiratory complications (atelectasis, pneumonia, pulmonary oedema — #1 cause of postop ICU admission), cardiovascular (myocardial injury after noncardiac surgery [MINS], postoperative atrial fibrillation, heart failure — especially in cardiac and vascular surgery), bleeding/haematoma, infection (wound, anastomotic leak, intra-abdominal abscess), AKI (Kheterpal risk index), delirium, DVT/PE. Prevention: early mobilisation, incentive spirometry, multimodal analgesia (avoid opioids if possible — Enhanced Recovery After Surgery [ERAS]), VTE prophylaxis, glycaemic control, stress-ulcer prophylaxis, normothermia. Key: recognise deterioration EARLY — postop patients can decompensate rapidly. The complications cluster by time: bleeding in the first 24 h, atelectasis day 0-2, AF day 2-4, MINS day 0-3, PE day 3-7, anastomotic leak day 5-7, wound infection day 5-10.

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Sepsis and septic shock

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is sepsis with circulatory and cellular/metabolic abnormalities (lactate >2, vasopressor requirement) associated with substantially increased mortality. The Surviving Sepsis Campaign 2021 guidelines provide the evidence-based framework: antibiotics within 1 hour, crystalloid at least 30 mL/kg, noradrenaline for MAP >=65, lactate normalisation. The EGDT era (Rivers 2001) was overturned by ProCESS, ARISE, and ProMISe (2014, 2017). Corticosteroids (APROCCHSS 2018) for vasopressor-dependent shock. Mortality over 10% in sepsis and over 40% in septic shock (Sepsis-3).

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Sepsis hour-1 bundle: updated Surviving Sepsis Campaign 2021 practice

Surviving Sepsis Campaign (SSC) Hour-1 Bundle (2021): all elements initiated within 1 hour of sepsis recognition. (1) MEASURE lactate (if elevated, remeasure to guide resuscitation). (2) OBTAIN blood cultures BEFORE antibiotics (if no substantial delay). (3) ADMINISTER broad-spectrum antibiotics (immediately, ideally within 1 hour, for possible septic shock). (4) BEGIN at least 30 mL/kg crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock. (5) APPLY vasopressors (noradrenaline first-line) if hypotensive during/after fluids (target MAP ≥65). Antibiotic delay is lethal: Kumar 2006 — 7.6% survival decrease per hour; Seymour 2017 — OR 1.04 per hour. Fluids: 30 mL/kg is a weak recommendation (ProCESS/ARISE/ProMISe: protocolised resuscitation NOT better than usual care). Current: individualise fluids, guide with dynamic measures, don't over-resuscitate.

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Septic shock: SSC 2021 integrated — hour-1 bundle, vasopressors, and outcomes

Septic shock = sepsis (infection + organ dysfunction — SOFA ≥2) + VASOPRESSOR requirement (to maintain MAP ≥65) + SERUM LACTATE >2 mmol/L (despite adequate fluid resuscitation). MORTALITY: hospital mortality over 40% (Sepsis-3). HOUR-1 BUNDLE (SSC 2021 — all within 1 hour of recognition): (1) MEASURE lactate (if >2, repeat). (2) BLOOD CULTURES ×2 (before antibiotics if no significant delay). (3) ADMINISTER BROAD-SPECTRUM ANTIBIOTICS (within 1 hour — Seymour: each hour of delay in antibiotics raises the odds of in-hospital death, adjusted OR 1.04 per hour; Kumar: survival fell 7.6% per hour of delay after documented hypotension). (4) BEGIN FLUID RESUSCITATION (30 mL/kg crystalloid for hypotension OR lactate ≥4 — but GOAL-DIRECTED — CLASSIC/CLOVERS support restrictive — reassess — not blanket 30 mL/kg for all). (5) ADMINISTER VASOPRESSORS if hypotensive during/after fluids (target MAP ≥65 — noradrenaline first-line). ESCALATION: noradrenaline → add vasopressin (VANISH/VASST) → add hydrocortisone (ADRENAL) → consider methylene blue/angiotensin II (refractory). SOURCE CONTROL (within 6-12h — drain, debride, remove device). STEROIDS: hydrocortisone 200 mg/day (if vasopressor-dependent — ADRENAL — faster shock reversal). MORTALITY: hospital mortality over 40% (Sepsis-3 — the sickest ICU patients — each intervention matters).

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Septic shock: Surviving Sepsis Campaign 2021

The Surviving Sepsis Campaign 2021 guidelines (Evans et al.) provide the evidence-based standard of care for sepsis and septic shock and are the single most examined document in critical-care fellowship exams. Sepsis-3 (Singer 2016) defines sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection (SOFA change >=2 from baseline); septic shock is a subset with both vasopressor-dependent hypotension (MAP >=65) AND lactate >2 mmol/L despite fluids — hospital mortality >40%. The SSC 2021 HOUR-1 BUNDLE (replaced the 3-hour and 6-hour bundles): within ONE hour of recognition -> (1) measure lactate, (2) obtain blood cultures BEFORE antibiotics, (3) administer broad-spectrum antibiotics, (4) at least 30 mL/kg crystalloid within the first 3 h for sepsis-induced hypoperfusion or septic shock, (5) vasopressors to hold MAP >=65. Noradrenaline FIRST-LINE; add vasopressin 0.03 U/min (fixed) when noradrenaline reaches the 0.25-0.5 mcg/kg/min range; hydrocortisone 200 mg/day for ongoing vasopressor requirement (ADRENAL — faster shock resolution; APROCCHSS — 90-day mortality benefit). Balanced crystalloids PREFERRED over saline (SMART). Restrictive fluid strategy after initial resuscitation is safe (CLASSIC, CLOVERS). MAP target 65 mmHg — no benefit of higher (SEPSISPAM, except less RRT at 80-85 in chronic hypertensives). Lactate clearance >=20% per 2 h guides resuscitation (ANDROMEDA-SHOCK). Source control within 6-12 h is advantageous.

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Severe burns management

Severe burns (>20% TBSA in adults, >10% in children/elderly) require ICU admission for fluid resuscitation, airway management, and wound care. Burn depth is classified by tissue layer: superficial epidermal (erythema, not counted in TBSA), superficial dermal (painful, blistering, blanching), deep dermal (pale, sluggish capillary refill, may need grafting), and full thickness (dry, leathery, painless, requires excision and grafting). TBSA is estimated by the Rule of Nines (adult: head 9, arm 9, leg 18, trunk 18 front and 18 back) or, preferably in children, the Lund-Browder chart which corrects for the proportionally larger head. Fluid resuscitation uses the Parkland formula (4 mL x kg x %TBSA in first 24h, half in first 8h from time of burn) using crystalloid (Hartmann's preferred — less hyperchloraemia than saline), titrated to urine output (0.5 mL/kg/h adult, 1 mL/kg/h child). Inhalation injury: suspect in enclosed space fires, facial burns, stridor, carbonaceous sputum — early intubation. Monitor for carbon monoxide and cyanide toxicity (house fires). Escharotomy for circumferential burns compromising circulation/ventilation. Infection is the leading cause of late mortality. Nutrition: early enteral feeding (within 6h) reduces bacterial translocation.

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The Principles of Resuscitation

Resuscitation is the restoration of oxygen delivery to the tissues in the patient in shock, and it is the first act of intensive care. This topic builds the examiner's framework on five ideas. First, the goal — the global oxygen delivery and the perfusion, and the principle that resuscitation targets the perfusion, not a single pressure. Second, fluid — when to give it (only the fluid-responsive patient benefits), how to judge responsiveness (the dynamic indices, the passive leg raise), and the choice of fluid (balanced crystalloids over saline; colloids offer no outcome advantage). Third, blood — the restrictive transfusion threshold and the damage-control ratio in massive haemorrhage. Fourth, the endpoints of resuscitation — the lactate clearance and the peripheral perfusion (the capillary refill), not the central venous pressure. Fifth, the evidence — the EGDT era and its refinement by ProCESS and ARISE, the ANDROMEDA-SHOCK capillary-refill strategy, and the shift from protocolised targets to individualised, perfusion-directed resuscitation.

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Trauma resuscitation and primary survey (ATLS)

The ATLS primary survey is a systematic approach to the trauma patient: Airway (with cervical spine control), Breathing (with ventilation), Circulation (with haemorrhage control), Disability (neurological assessment), Exposure (with temperature control). The goal is to identify and treat immediately life-threatening injuries in order of priority. Key principles: treat as you find, do not delay life-saving interventions for investigations, minimise time to definitive haemorrhage control (damage control surgery). Traumatic cardiac arrest: reversible causes (hypoxia, hypovolaemia, tension pneumothorax, cardiac tamponade) — focus on treating these, not standard ALS.

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Vasoplegic and vasopressor-refractory shock: methylene blue, vasopressin, adjuncts

Vasoplegic shock = distributive shock refractory to catecholamine vasopressors (noradrenaline) — profound NO-mediated vasodilation. Causes: septic shock (most common), post-cardiac surgery vasoplegia, anaphylaxis, post-reperfusion, drug-induced (ACEi, PDE inhibitors, protamine), adrenal insufficiency. PATHOPHYSIOLOGY: excessive nitric oxide (NO) production (iNOS induction in sepsis) → cGMP accumulation → vascular smooth muscle relaxation → vasodilation unresponsive to catecholamines. MANAGEMENT ESCALATION: (1) Adequate volume (but not over-resuscitate). (2) Noradrenaline (first-line alpha-1 agonist). (3) ADD VASOPRESSIN (V1 agonist — 0.03 U/min — catecholamine-sparing, different receptor). (4) ADD STEROIDS (hydrocortisone 200 mg/day — for CIRCI/adrenal insufficiency). (5) METHYLENE BLUE (1.5 mg/kg IV in the landmark RCT — inhibits NO-cGMP pathway — emerging for refractory vasoplegia). (6) Adjuncts: angiotensin II (ATHOS-3), ascorbate, thiamine, steroids (HAT therapy). ALWAYS: treat cause, source control, exclude adrenal insufficiency/hypovolaemia.

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Venous thromboembolism prophylaxis in the ICU

ICU patients are among the highest-risk groups for venous thromboembolism (VTE) — immobility, inflammation, vascular injury (Virchow triad). ACCP-9 and ASH 2018 recommend pharmacological prophylaxis (LMWH, low-dose UFH or fondaparinux) for acutely/critically ill inpatients at acceptable bleeding risk, with mechanical prophylaxis (IPC or graduated stockings) when bleeding risk is high. Proven regimens: enoxaparin 40 mg SC daily (MEDENOX — VTE 5.5% vs 14.9% with placebo) and dalteparin 5000 IU SC daily vs UFH 5000 IU twice daily (PROTECT — no difference in proximal leg DVT, half the pulmonary emboli, fewer HIT events with dalteparin). Enoxaparin accumulates when creatinine clearance falls below 30 mL/min and requires dose reduction; dalteparin and tinzaparin do not accumulate at prophylactic doses. In confirmed HIT stop all heparin and use a non-heparin agent such as argatroban. Allow at least 12 hours after a low-dose LMWH injection (24 hours after intermediate-dose) before neuraxial puncture.

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Acute liver failure (hepatic failure)

Acute liver failure (ALF) is severe acute liver injury with encephalopathy and coagulopathy (INR &gt;1.5) within 26 weeks, in a patient without pre-existing liver disease. Classification by tempo (O'Grady): hyperacute (&lt;7 days), acute (8-28 days), subacute (29 days-12 weeks) — prognosis varies by interval. Causes: paracetamol (#1 in UK/Aus), drug-induced (idiosyncratic), viral hepatitis (HBV #1 viral), Wilson disease, pregnancy-related (AFLP, HELLP), mushroom (Amanita phalloides), ischaemic, autoimmune, indeterminate. Pathophysiology of cerebral oedema: ammonia crosses BBB -> astrocytic glutamine synthetase -> glutamine accumulation -> astrocyte swelling (cytotoxic oedema) -> raised ICP -> tonsillar herniation (#1 cause of death). Management: N-acetylcysteine (NAC) for ALL causes (Lee 2009 showed transplant-free survival benefit beyond paracetamol), supportive care for complications, and urgent liver transplant assessment using King's College Criteria. Lactate is a key prognostic marker (early &gt;3.5 mmol/L or persistent elevation predicts poor outcome). Do NOT routinely correct INR with FFP — it is a liver function marker, not a bleeding-risk indicator (rebalanced haemostasis).

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Acute mesenteric ischaemia

Acute mesenteric ischaemia is a life-threatening vascular emergency of the bowel. Four types: (1) SMA embolus (#1 — atrial fibrillation, 50%), (2) SMA thrombosis (pre-existing atherosclerosis, 25%), (3) Non-occlusive (NOMI — low-flow state, 20%), (4) Mesenteric venous thrombosis (5%). Presents with SEVERE abdominal pain OUT OF PROPORTION to examination findings. Diagnosis: CT angiography (gold standard — shows occlusion, bowel wall thickening, pneumatosis, portal venous gas). Lactate elevated (late sign — bowel infarction). Management by type: emboli to embolectomy, thrombosis to bypass/stent, NOMI to intra-arterial papaverine, venous thrombosis to anticoagulation. Mortality 50-80% overall, highest for SMA thrombosis. WSES staging guides operative vs endovascular strategy. Time is bowel.

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Acute pancreatitis complications and management

Severe acute pancreatitis (15-20% of cases) causes local (necrosis, pseudocyst, walled-off necrosis, abscess) and systemic (SIRS → MODS, ARDS, AKI, shock, DIC) complications. Severity scoring: APACHE II (>8 = severe), Ranson (3+ = severe), BISAP (3+ = severe), Revised Atlanta Classification (persistent organ failure >48h = severe). Management: moderate goal-directed IV fluids with Lactated Ringer (WATERFALL trial — aggressive resuscitation causes fluid overload), early enteral nutrition, pain control (opioids), ERCP if gallstone obstruction/cholangitis. Antibiotics ONLY for proven infection (infected necrosis, cholangitis) — NOT prophylactic (meta-analysis shows no mortality benefit). Infected necrosis: drain first (percutaneous/endoscopic — step-up approach, PANTER & TENSION trials), postpone definitive intervention until walled-off necrosis (POINTER trial).

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Acute pancreatitis: interventional management and complications

Interventional management of severe acute pancreatitis is built on three pillars: (1) the STEP-UP approach for infected necrosis — drain first (percutaneous or endoscopic transluminal), add minimally invasive necrosectomy only if drainage fails, reserve open surgery for last resort; (2) TIMING — delay intervention ~4 weeks to allow demarcation and walling-off whenever possible (intervene earlier ONLY for clinical deterioration); (3) ROUTE — prefer endoscopic/percutaneous over open. PANTER trial (van Santvoort 2010, NEJM): step-up vs primary open necrosectomy — step-up superior (composite of major complications or death 40% vs 69%, RR 0.57; 35% treated with drainage alone). PANTER long-term follow-up (Hollemans 2019, mean 86 months): step-up had less exocrine and endocrine insufficiency, fewer incisional hernias, without increased risk of reinterventions. TENSION trial (van Brunschot 2018, Lancet): endoscopic step-up vs surgical step-up — no difference in the composite endpoint (43% vs 45%), but endoscopic had fewer fistulae and shorter hospital stay. PENGUIN trial (Bakker 2012, JAMA): endoscopic transluminal vs surgical necrosectomy — endoscopic fewer complications (20% vs 80%). Walled-off necrosis (over 4 wk, necrotic content) is NOT a pseudocyst (over 4 wk, fluid only) — management differs (WON needs necrosectomy/drainage, pseudocyst usually observed).

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Acute variceal haemorrhage

Acute variceal haemorrhage is life-threatening bleeding from oesophageal or gastric varices that form as a consequence of portal hypertension (cirrhosis the commonest cause). Mortality 15-25% within 6 weeks of the episode. PATHOPHYSIOLOGY: portal venous pressure rises (HVPG over 10 mmHg defines clinically significant portal hypertension; varices bleed above 12 mmHg) → collateral portosystemic circulation → thin-walled varices at the gastro-oesophageal junction and gastric fundus → wall tension rises with radius (Laplace) → rupture when wall stress exceeds tensile strength. MANAGEMENT cascade (ESGE 2022): resuscitate with restrictive transfusion (transfuse when haemoglobin falls below 70 g/L; post-transfusion target 70-90 g/L) → start vasoactive drug at presentation (terlipressin, octreotide or somatostatin, continued for up to 5 days) AND prophylactic ceftriaxone 1 g IV daily for up to 7 days (antibiotics reduce all-cause mortality RR 0.79, rebleeding RR 0.53) → endoscopy within 12 h with band ligation for oesophageal varices, cyanoacrylate glue for cardiofundal varices → balloon tamponade as a temporary bridge → salvage TIPS for refractory bleeding; early pre-emptive TIPS within 72 h (preferably within 24 h) for high-risk patients (Child-Pugh C up to 13, or Child-Pugh B over 7 with active bleeding at endoscopy).

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Acute-on-chronic liver failure (ACLF)

ACLF is acute decompensation of known cirrhosis with organ failure(s), exaggerated systemic inflammation, and high 28-day mortality — distinct from simple decompensation. Precipitants: bacterial infection first (none identified in about 40 percent), alcohol-associated hepatitis, GI bleed, drugs, viral hepatitis. CLIF-C OF grades six organ domains; CLIF-C ACLF adds age and white count and is recalculated at 48 hours. Without transplant, 28-day mortality runs about 18 to 25 percent in grade 1 and 68 to 89 percent in grade 3; transplant in selected grade 2 to 3 patients raises 6-month survival from about 10 to about 80 percent. Treatment: manage the precipitant, organ support, terlipressin plus albumin for HRS-AKI (CONFIRM), albumin 1.5 g per kg then 1 g per kg for SBP (Sort), prednisolone only for severe alcohol-associated hepatitis with day-7 Lille reassessment, no INR correction before procedures, no protein restriction.

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Hepatic encephalopathy and acute liver failure

Hepatic encephalopathy is a reversible spectrum of neuropsychiatric abnormalities in patients with liver dysfunction, classified by the West Haven system (Grade I-IV). Pathophysiology centres on ammonia-induced astrocyte swelling and systemic inflammation. Precipitating factors include infection, GI bleed, constipation, sedatives, and electrolyte disturbance. Management: lactulose (first-line), rifaximin (add-on), treat precipitant, avoid sedatives, protein restriction NOT recommended. Acute liver failure (ALF) is a separate entity with different management priorities: N-acetylcysteine (improves survival in non-acetaminophen ALF), intracranial pressure management, and liver transplant listing using King's College Criteria.

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Intra-abdominal hypertension and abdominal compartment syndrome

Intra-abdominal hypertension (IAH) is sustained intra-abdominal pressure >12 mmHg. Abdominal compartment syndrome (ACS) is sustained IAP >20 mmHg with NEW ONSET organ failure (kidney, respiratory, cardiovascular). Causes: abdominal trauma/surgery, massive fluid resuscitation, pancreatitis, ileus, peritonitis, burns. Measurement: bladder pressure (gold standard). Effects of raised IAP: renal failure (venous congestion, reduced perfusion), respiratory failure (elevated diaphragm, reduced compliance, high ventilator pressures), cardiovascular (reduced venous return, reduced cardiac output), intestinal ischaemia, raised intracranial pressure. Treatment: decompressive laparotomy for ACS. Prevent: avoid excessive fluid resuscitation, nasogastric decompression, prokinetics.

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Nutrition in the ICU

Nutrition is a critical component of ICU care. Early enteral nutrition is the default — the landmark trials initiated feeding within 24-36 hours — while early supplemental parenteral nutrition is harmful (EPaNIC: late PN meant fewer infections and shorter ventilation). NUTRIC score stratifies nutrition risk (high NUTRIC = patient who benefits most from adequate delivery). Energy: normocaloric 20-25 kcal/kg/day (NUTRIREA-2); permissive underfeeding (40-60% of calories with protein maintained) was as safe as full feeding (PermiT) and an extra ~600 kcal/day did not improve survival (TARGET). Protein: achieving at least 80% of the prescribed protein dose was associated with lower mortality (Nicolo). Refeeding syndrome: definitions vary but centre on electrolyte disturbances within 72 hours — check phosphate/Mg/K before feeding and watch daily; once it develops, protocolised caloric restriction is the supported management (Doig: 91% vs 78% alive at day 60). Glutamine: REDOX showed harm in multi-organ failure — not routinely recommended. Gastric residual volume: not monitoring GRV at all was non-inferior for VAP (REGANE).

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Stress-related mucosal disease (stress ulcer prophylaxis)

Stress-related mucosal disease (SRMD) is the rapid, ischaemia-driven breakdown of the gastric mucosal barrier in critical illness: splanchnic hypoperfusion → mucosal ischaemia → acid back-diffusion → superficial erosion (fundus/body). Subclinical erosions appear on endoscopy in 75-100% of ventilated patients within 24-72h, but clinically significant bleeding is rare (0.1-4%). Two independent risk factors dominate (Cook 1994, NEJM): mechanical ventilation >48h (#1) and coagulopathy (INR >1.5 or platelets &lt;50) — together they account for most clinically significant bleeding. Other: shock, sepsis, major burns >35% TBSA (Curling ulcer), severe TBI (Cushing ulcer), high-dose steroids. Prophylaxis is PPI first-line (pantoprazole 40 mg IV/PO daily — least CYP2C19 inhibition, clopidogrel-safe). Ranitidine globally WITHDRAWN (NDMA contamination) — use famotidine. Sucralfate is a mucosal protectant with lower C. diff risk but less effective. SUP-ICU trial (Krag 2018, NEJM): pantoprazole vs placebo reduced clinically significant bleeding (2.5% vs 4.2%, NNT 59) but did NOT reduce 90-day mortality and showed NO significant increase in pneumonia or C. difficile. PEPTIC (Young 2020, JAMA): PPI vs H2 blocker — no mortality difference. REVISE (Cook 2024, NEJM): confirms bleeding reduction without excess infection. Start SUP if risk factors present; STOP when tolerating enteral feeds + extubated + coagulopathy resolved. Enteral nutrition itself is protective. C. difficile risk is dose- and duration-dependent (~1.5x with PPI). Do NOT give SUP to ALL ICU patients — only those with indications. Review indication DAILY.

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GI and nutrition

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Acute liver failure: cerebral oedema, King's College criteria, and transplantation

Acute liver failure (ALF) = severe acute liver injury with encephalopathy + coagulopathy (INR ≥1.5) within 26 weeks of symptom onset, in a patient WITHOUT pre-existing liver disease. CAUSES: paracetamol overdose (#1 — 40%), drug-induced (idiosyncratic — isoniazid, valproate, halothane), viral (hepatitis A/B/E — especially if immunosuppressed), ischaemic ('shock liver' — from hypotension), autoimmune, Wilson's disease, pregnancy (AFLP, HELLP), mushroom (Amanita phalloides), indeterminate (20%). CLINICAL: jaundice, encephalopathy (confusion → coma), coagulopathy (bleeding), hypoglycaemia, infection, AKI, haemodynamics (hyperdynamic → shock). CEREBRAL OEDEMA is the #1 killer (especially in high-grade encephalopathy + hyperammonaemia >150). KING'S COLLEGE CRITERIA predict mortality → transplant referral. MANAGEMENT: TREAT CAUSE (NAC for paracetamol; antivirals; steroids for autoimmune; penicillin for mushrooms); SUPPORT organs (ventilation, vasopressors, RRT); CEREBRAL OEDEMA (head elevation 30°, hypertonic saline/mannitol, hyperventilation bridge, ICP monitoring for grade 3-4); COAGULOPATHY (only bleed if transfuse — 'rebalanced haemostasis'); INFECTION PROPHYLAXIS (antibiotics + antifungals — infection is common + often triggers deterioration); HYPOGLYCAEMIA (10% dextrose infusion — liver can't gluconeogenesis). LIVER TRANSPLANT = definitive for those meeting King's College criteria. MORTALITY: 30-50% without transplant; 20% with transplant.

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Acute mesenteric ischaemia: embolic, thrombotic, venous, and non-occlusive

Acute mesenteric ischaemia = sudden reduction in intestinal blood flow -> bowel necrosis (if untreated). FOUR TYPES: (1) ARTERIAL EMBOLUS (50%) — AF/source -> SMA embolus (sudden, proximal, no collaterals). (2) ARTERIAL THROMBOSIS (25%) — atherosclerotic SMA stenosis -> acute thrombosis (on background of chronic 'mesenteric angina'). (3) NON-OCCLUSIVE MESENTERIC ISCHAEMIA (NOMI — 20%) — low-flow state (shock, vasopressors, dialysis) -> diffuse vasoconstriction -> ischaemia (no large vessel occlusion). (4) MESENTERIC VENOUS THROMBOSIS (5%) — portal/mesenteric vein clot (hypercoagulable, infection, inflammation). CLINICAL: severe abdominal pain OUT OF PROPORTION to examination (early — bowel still viable), then peritonitis (late — necrosis). LACTATE elevated (ischaemia). CT angiography (gold standard — occlusion type, location, bowel viability). MANAGEMENT: EMERGENCY surgery (revascularisation + resect necrotic bowel) for arterial occlusion; ANTICOAGULATION for venous; PAPAVARINE infusion + treat low-flow for NOMI. MORTALITY: 50-80% (delayed diagnosis is the killer).

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Acute severe upper GI bleeding: Glasgow-Blatchford, endoscopy, and TIPSS

Acute upper GI bleeding (UGIB) is a common ICU emergency. CLASSIFICATION: VARICEAL (portal hypertension — cirrhosis — oesophageal/gastric varices — 20%) vs NON-VARICEAL (peptic ulcer 50%, Mallory-Weiss, gastritis, malignancy, angiodysplasia — 80%). RISK STRATIFICATION: Glasgow-Blatchford Score (GBS — pre-endoscopy — identifies low-risk for outpatient; high-risk for ICU/endoscopy). MANAGEMENT: (1) RESUSCITATE (ABC, 2 large-bore IV, fluids/blood — restrictive transfusion Hb 70; intubate if encephalopathic/active haematemesis). (2) PROTON PUMP INHIBITOR (PPI — high-dose IV bolus + infusion e.g. pantoprazole 80 mg then 8 mg/hr for 72 h AFTER endoscopic haemostasis — reduces rebleeding; not a routine pre-endoscopy reflex). (3) ENDOSCOPY within 24 HOURS (diagnostic + therapeutic — adrenaline injection + thermal/clips for ulcers; band ligation for varices). (4) VARICEAL-SPECIFIC: vasoactive (terlipressin/octreotide/somatostatin — started at presentation), prophylactic antibiotics (cirrhotics — ceftriaxone), TIPSS (transjugular intrahepous portosystemic shunt) for refractory and pre-emptively in high-risk. (5) RED FLAG TRANSFUSION (massive transfusion protocol if exsanguinating). MORTALITY: 2-10% overall (non-variceal); variceal worse, reflects cirrhosis severity.

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Severe acute pancreatitis: fluid resuscitation (WATERFALL), necrosis, and PANTER step-up

Severe acute pancreatitis (15-20% of cases) = organ failure >48h (Revised Atlanta classification) — ICU-level care. EARLY PHASE (first week): SYSTEMIC INFLAMMATION (SIRS) + FLUID SEQUESTRATION ('third space' — massive fluid shift into retroperitoneum) -> hypovolaemia, haemoconcentration, AKI, shock. MANAGEMENT: GOAL-DIRECTED FLUIDS (WATERFALL trial — AGGRESSIVE fluids HARM — goal-directed preferred), analgesia, EARLY ENTERAL NUTRITION (within 48h — reduces infection/necrosis), antibiotics ONLY if infected (prophylactic antibiotics NOT recommended — meta-analyses no benefit). LATE PHASE (week 2+): NECROSIS (sterile vs infected — the key distinction), INFECTION (infected necrosis — 30% — needs antibiotics + drainage), PSEUDOCYST/WALLED-OFF NECROSIS. INFECTED NECROSIS: PANTER trial — STEP-UP approach (percutaneous/endoscopic drainage FIRST, then minimally-invasive necrosectomy if needed) SUPERIOR to open necrosectomy (less complications, fewer deaths). DELAY intervention 4 weeks (let necrosis become walled-off -> safer drainage).

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Respiratory / airway emergencies

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Acute Massive Haemoptysis — Comprehensive ICU Management

Acute massive haemoptysis is a respiratory emergency in which the patient dies of ASPHYXIATION, not exsanguination — a small volume of blood can rapidly flood the airways, abolish gas exchange, and cause hypoxaemic arrest long before the circulating volume is lost. Define it functionally as any bleeding that causes significant haemodynamic decompensation or respiratory distress that may lead to death if left untreated; volume-based definitions vary widely (anywhere from 100 to 1,000 mL per 24 hours has been considered significant, and fewer than 5 to 15 per cent of haemoptysis episodes are massive). Around 90 per cent of brisk bleeding arises from the BRONCHIAL (systemic, high-pressure) circulation and under 10 per cent from the pulmonary artery. Management is a fixed cascade: (1) protect the airway, isolate the non-bleeding lung, and keep the patient bleeding-side-down; (2) intubate with a large-bore single-lumen tube that admits a bronchoscope, or a double-lumen tube/bronchial blocker; (3) bronchoscopy — rigid preferred for massive bleeding — for cold saline lavage, topical vasoconstriction, and balloon tamponade; (4) bronchial artery embolisation (BAE), the first-line endovascular therapy, with pooled clinical success around 93 per cent (65-92 per cent depending on cause) and recurrence in roughly a quarter; (5) surgery for failure, unavailability, or localised lesions. Mortality across series is 9-38 per cent. This topic maps the cascade and the evidence behind every step.

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infectious-diseases

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Acute Neutropenic Sepsis — Comprehensive ICU Management

Neutropenic sepsis (febrile neutropenia) — a life-threatening infection in patients with neutrophil count &lt;0.5 × 10^9/L (or &lt;1.0 with expected decline) AND fever (>38.3C single or >38.0C sustained over 1h). Occurs in cancer patients receiving cytotoxic chemotherapy (nadir 7-14 days post-chemotherapy), haematological malignancy, post-stem-cell transplant, or congenital neutropenia. Mortality: 5-10% overall (up to 30-50% with septic shock). The #1 rule: EMPIRICAL BROAD-SPECTRUM ANTIBIOTICS WITHIN 1 HOUR ('door-to-needle' time — just like sepsis). Do NOT wait for cultures or source identification. Pathogens: gram-negative bacilli (#1 — Pseudomonas aeruginosa is the MOST DANGEROUS — has high mortality in neutropenic patients — must cover), gram-positives via lines and mucositis, then fungi if fever persists. Empiric therapy: anti-pseudomonal beta-lactam (piperacillin-tazobactam, cefepime or meropenem) + vancomycin if line infection/mucositis/shock/MRSA. Persistent fever day 4-7 = empiric antifungal (see body). This comprehensive ICU topic covers: definition, MASCC risk stratification, empiric antibiotic choice, antifungal strategy, galactomannan vs beta-D-glucan, G-CSF, HSCT timeline, CAR-T/CRS, typhlitis, prophylaxis, and the one-hour door-to-needle rule.

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Pneumonia in the Immunocompromised Patient — Comprehensive ICU Management

Pneumonia in the immunocompromised host (non-HIV) — haematological malignancy, stem-cell/solid-organ transplant, prolonged steroids, cytotoxic chemotherapy, biologics. The pathogen spectrum is dictated by the SPECIFIC IMMUNE DEFECT: (1) NEUTROPENIA (post-chemo, &lt;0.5 x 10^9/L) -> Pseudomonas aeruginosa, other gram-negative bacilli, invasive pulmonary aspergillosis, Candida, mucositis-related viridans streptococci; (2) T-CELL DEFECT (transplant calcineurin inhibitors, fludarabine, alemtuzumab) -> Pneumocystis jirovecii (PCP), CMV, Legionella, Nocardia, Cryptococcus, mycobacteria; (3) B-CELL / HUMORAL DEFECT (CLL, myeloma, post-rituximab) -> encapsulated bacteria — Streptococcus pneumoniae, Haemophilus influenzae; (4) PROLONGED STEROIDS (>20 mg/day prednisone >4 weeks) -> PCP, Nocardia, Aspergillus. The intensivist's task: (1) classify the immune defect, (2) get a diagnostic BAL EARLY (galactomannan for Aspergillus, (1-3)-beta-D-glucan for PCP/fungal, CMV PCR, respiratory virus panel, bacterial + fungal + mycobacterial culture), (3) start BROAD EMPIRIC THERAPY — anti-pseudomonal beta-lactam + empiric antifungal (caspofungin for Candida, voriconazole for suspected mould) + ganciclovir if CMV likely + co-trimoxazole if PCP possible + reduce immunosuppression, (4) prefer NIV over intubation (lower VAP/mortality), (5) prophylaxis — co-trimoxazole (PCP), posaconazole (Aspergillus), valganciclovir (CMV). Mortality 20-50% — far higher than immunocompetent CAP. Early appropriate (pathogen-directed) therapy is the single biggest modifiable determinant of survival.

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GI & nutrition

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Acute pancreatitis: ERAS and early enteral nutrition

Nutritional management of acute pancreatitis has undergone one of the most complete paradigm reversals in modern critical care: the dogma of prolonged NPO ('resting the pancreas'), taught for most of the 20th century, has been REPLACED by early enteral nutrition (EN) commenced within 24-48 hours. Multiple meta-analyses and the ACG, IAP/APA, and AGA guidelines now recommend early oral or NG feeding as the standard of care. Mechanism: EN maintains gut mucosal integrity, prevents bacterial translocation and infected pancreatic necrosis, and attenuates the systemic inflammatory response — benefits that intravenous nutrition cannot reproduce. Route: oral first (mild disease); nasogastric (NG) is the preferred tube route because non-inferiority RCTs (Singh/Eatock) show NG is non-inferior to nasojejunal (NJ) and is cheaper, easier, and faster to place. NJ is reserved for NG failure or severe gastroparesis. The 'pancreatic rest' concept — that NJ feeding 'spares' the pancreas — is physiologically DISPROVEN. Composition: standard polymeric formula; a large database study found no benefit of elemental formula. Total parenteral nutrition (TPN): reserved for the small minority in whom EN is contraindicated or still fails after about a week (day 8 in EPaNIC); early TPN INCREASES infection and cholestasis, and — per EPaNIC and TGC-Fast — does not improve outcome. Probiotics must NOT be given prophylactically: PROPATRIA showed a 2.5-fold increase in mortality (RR 2.53) and 9 cases of bowel ischaemia (8 fatal). Metabolic support: moderate glycaemic control (TGC-Fast found tight 4.4-6.1 mmol/L control conferred no benefit), correct electrolyte derangements, and give thiamine before the first feed in alcohol-related disease to prevent Wernicke and refeeding syndrome. WATERFALL supports moderate goal-directed lactated Ringer resuscitation over aggressive boluses.

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GI Bleeding, Pancreatitis, Hepatic Failure and Nutrition

The GI and the nutritional disorders in the ICU span the upper GI bleeding (the peptic ulcer, the varices), the acute pancreatitis (the severe, the infected necrosis), the acute liver failure (the paracetamol, the encephalopathy), and the nutritional support (the early enteral preferred, the stress ulcer prophylaxis). This topic builds the examiner's framework on each, with the evidence for the restrictive transfusion and endoscopy timing (the Villanueva trial and the international consensus), the stress ulcer prophylaxis (the SUP-ICU trial), the early enteral nutrition (the NUTRIREA-2 trial), the route of feeding (the CALORIES trial), the permissive underfeeding (the PermiT trial and the 2024 meta-analysis), the caloric and the protein targets (the ESPEN and the SCCM/ASPEN guidelines), the residual-volume and prokinetic practice (REGANE, Cochrane), and the acute liver failure (the King's College criteria and the NAC trials).

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obstetric

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Acute Postpartum Haemorrhage — Comprehensive ICU Management

Acute postpartum haemorrhage (PPH) — ACOG defines maternal haemorrhage as cumulative blood loss of 1000 mL or more, or blood loss with signs or symptoms of hypovolaemia, within 24 hours of birth; it remains the leading cause of maternal mortality worldwide. Identify the cause with the 4 Ts: Tone (uterine atony — the leading cause), Trauma, Tissue (retained placenta, placenta accreta spectrum), Thrombin (coagulopathy or DIC). Management: call for help and use a standardised bundle (E-MOTIVE), resuscitate with balanced 1:1:1 transfusion (PROPPR), give tranexamic acid 1 g IV as soon as possible and within 3 hours (WOMAN trial: death from bleeding 1.5 percent vs 1.9 percent, RR 0.81), then the uterotonic ladder — low-dose oxytocin first-line (ED90 0.35 IU at elective caesarean), second-line methylergonovine or carboprost 250 mcg IM, misoprostol 600 to 1000 mcg — then uterine balloon tamponade (pooled success about 86 percent) and uterine-sparing surgery before hysterectomy. A fibrinogen at or under 2 g/L predicts severe PPH. Complications: Sheehan syndrome, amniotic fluid embolism (case fatality 19 percent).

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Respiratory

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Acute pulmonary oedema: cardiogenic vs non-cardiogenic differentiation

Acute pulmonary oedema: fluid in alveolar spaces → bilateral infiltrates + hypoxaemia. TWO types: CARDIOGENIC (hydrostatic — from LV failure, acute MR, mitral stenosis, volume overload; PCWP >18 mmHg) and NON-CARDIOGENIC (increased permeability — ARDS, sepsis, trauma, aspiration, transfusion; PCWP &lt;18 mmHg). Differentiation CRITICAL — treatment differs. CARDIOGENIC: oxygen, NIV/CPAP (rapid response), IV loop diuretics, vasodilators (GTN if SBP >110), inotropes (cold/shocked), IABP/Impella/VA-ECMO for refractory. NON-CARDIOGENIC: treat underlying cause, lung-protective ventilation (Vt 6 mL/kg PBW, Pplat &lt;30, driving pressure &lt;15), prone, conservative fluids (FACTT). KEY tools: BNP/NT-proBNP (high = cardiogenic), echocardiography (reduced EF/cardiogenic), POCUS (bilateral B-lines, IVC plethoric, reduced LV), lung ultrasound, CT (cardiogenic: central/perihilar, pleural effusions; non-cardiogenic: peripheral/diffuse), PCWP (cardiogenic >18). SPECIAL FORMS: negative pressure (NPPE), re-expansion, neurogenic, high-altitude (HAPE), TRALI.

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Acute respiratory distress syndrome: phenotyping and personalised ventilation

ARDS is not a single disease — two distinct phenotypes have been identified. Hyperinflammatory ARDS (high inflammatory markers, vasopressor-dependent, lower mortality with higher PEEP): responds better to higher PEEP and prone positioning. Hypoinflammatory ARDS (lower inflammatory markers, more extrapulmonary cause): may not benefit from aggressive PEEP. Personalised ventilation: individualise PEEP based on recruitability (PEEP titration by P-V curves, EIT, oesophageal pressure), driving pressure (&lt;15 cmH2O — Amato meta-analysis: driving pressure is the strongest predictor of mortality), and lung morphology (focal vs non-focal on CT — focal ARDS tolerates higher PEEP poorly). Recruitment manoeuvres controversial (ART trial: caused harm). Prone positioning beneficial for moderate-severe ARDS (PaO2/FiO2 &lt;150). Latent class analysis of the ALVEOLI and FACTT trials (Calfee 2014) identified the hyperinflammatory (type 2) and hypoinflammatory (type 1) subphenotypes using biomarkers — IL-6, IL-8, soluble TNF receptor-1, angiopoietin-2, bicarbonate, protein C. The subphenotype determines treatment response: higher PEEP and simvastatin benefit the hyperinflammatory phenotype but may harm the hypoinflammatory phenotype (HARP-2 secondary analysis, Calfee 2018). Precision medicine in ARDS is evolving but not yet routine bedside practice.

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Acute respiratory distress syndrome: phenotyping and precision medicine

ARDS is HETEROGENEOUS — not one disease. TWO reproducible subphenotypes identified by latent class analysis in ARDS Network trials and HARP-2 (Calfee 2014, Famous 2017, Calfee 2018; stability Delucchi 2018): HYPERINFLAMMATORY (~35% in HARP-2): high inflammatory markers (IL-6, IL-8, sTNFr-1, sRAGE, SP-D, angiopoietin-2), low PaO2/FiO2, acidosis, vasopressor-requiring, resembles sepsis, worse prognosis (28-day mortality 39% vs 17% in HARP-2; 90-day mortality 57% vs 33% in LUNG SAFE re-analysis), higher PEEP associated with lower 90-day mortality (Maddali 2022: 54% vs 62%), improved 28-day survival with simvastatin in the HARP-2 re-analysis (Calfee 2018, p=0.008), BUT a conservative fluid strategy INCREASED 90-day mortality in this subphenotype in FACTT (Famous 2017: 50% vs 40% with liberal). HYPOINFLAMMATORY (~65%): lower inflammation, better oxygenation, better prognosis (28-day mortality 17% in HARP-2), conservative fluid strategy lowered 90-day mortality here (18% vs 26%). The Berlin definition (2012) standardised diagnosis (timing within 1 week, bilateral opacities not fully explained by effusion/atelectasis/nodules, non-cardiogenic oedema, severity by PaO2/FiO2: mild 200-300, moderate 100-200, severe &lt;100 with PEEP/CPAP >=5) but is purely DESCRIPTIVE — it does NOT capture biological heterogeneity. The LUNG SAFE multinational study (Bellani 2016, 459 ICUs, 29144 patients) showed ARDS is under-recognised (clinical recognition only 51.3% of mild and 78.5% of severe cases) and undertreated (tidal volume 8 mL/kg predicted body weight or less in under two-thirds; prone positioning in 16.3% of severe ARDS). Calfee 2014 Lancet Respir Med applied latent class analysis to ARMA + ALVEOLI (1022 patients) and found 2 subphenotypes with differential PEEP response. Maddali/Pham/Calfee 2022 Lancet Respir Med validated ML-derived classifiers in EARLI and VALID and applied them to LUNG SAFE. This explains why ARDS pharmacological trials (statins, beta-agonists, NO, KGF) showed heterogeneous/neutral results — subphenotype determines treatment response. Precision medicine: stratify patients, tailor treatment.

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Acute respiratory failure: advanced ventilation modes (APRV and oscillator)

Advanced ventilation modes for severe/refractory ARDS. APRV (Airway Pressure Release Ventilation): continuous high pressure (P-high) with brief release to low pressure (P-low) — allows spontaneous breathing throughout. Theoretical benefits: maintains alveolar recruitment (continuous high PEEP), allows spontaneous breathing (less sedation, preserved diaphragm), improved oxygenation. HFOV (High-Frequency Oscillatory Ventilation): very high respiratory rate (3-15 Hz, 180-900 breaths/min) with very small tidal volumes (~1-3 mL/kg) around a constant mean airway pressure. Theory: lung protection (tiny Vt, constant recruitment). EVIDENCE: OSCAR and OSCILLATE trials (2013) — HFOV did NOT improve mortality (OSCILLATE: trend to HARM). HFOV now RESERVED for refractory cases. APRV: some evidence of improved oxygenation, but no clear mortality benefit.

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Acute respiratory failure: classification and approach

Acute respiratory failure is the inability of the respiratory system to maintain adequate gas exchange. Type 1 (hypoxaemic): PaO2 &lt;60 mmHg (8 kPa) on room air, normal/low PaCO2. Causes: V/Q mismatch (#1 — pneumonia, PE, pulmonary oedema, ARDS), shunt, diffusion impairment, hypoventilation. Type 2 (hypercapnic): PaCO2 >45 mmHg (6 kPa). Causes: alveolar hypoventilation (COPD, neuromuscular disease, CNS depression), increased CO2 production (sepsis, burns), V/Q mismatch with fatigue. Approach: ABCDE, identify type (blood gas), treat underlying cause, oxygen therapy, ventilatory support (NIV or intubation). Key formula: A-a gradient (Alveolar-arterial oxygen gradient) distinguishes hypoxaemia causes.

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Acute respiratory failure: type 1 vs type 2, oxygen therapy, and when to intubate

Acute respiratory failure = inability of respiratory system to maintain adequate GAS EXCHANGE (oxygenation [O2 in] and/or ventilation [CO2 out]). TWO TYPES: TYPE 1 (HYPOXAEMIC) — PaO2 &lt;60 mmHg (8 kPa) with NORMAL/LOW PaCO2 — from V/Q mismatch, shunt, diffusion impairment — causes: pneumonia, ARDS, PE, pulmonary oedema, asthma. TYPE 2 (HYPERCAPNIC) — PaCO2 >45 mmHg (6 kPa) ± hypoxaemia — from ALVEOLAR HYPOVENTILATION (not enough air moved) — causes: COPD, neuromuscular (GBS, MG), opioid overdose, obesity hypoventilation, chest wall deformity. A-a GRADIENT (alveolar-arterial): helps distinguish — ELEVATED (>20) = lung problem (V/Q mismatch/shunt); NORMAL (&lt;15) = pure hypoventilation (normal lungs — just not breathing enough). MANAGEMENT: TYPE 1 → oxygen (high concentration) + treat cause + NIV/CPAP/HFNC if moderate + intubate if severe. TYPE 2 → NIV (BiPAP — ventilatory support) + oxygen (controlled — target SpO2 88-92% for CO2 retainers) + treat cause + intubate if NIV fails.

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Acute severe asthma in the ICU (status asthmaticus)

Status asthmaticus is severe acute asthma unresponsive to standard bronchodilator therapy. Features of life-threatening asthma: silent chest, exhaustion or drowsiness with hypercapnia, hypoxaemia (SpO2 &lt;90% on ambient air), normal or rising PaCO2. Management: controlled oxygen (target SpO2 93-95% in asthma), repeated or continuous nebulised salbutamol + ipratropium, IV magnesium sulphate (2g over 20min), early systemic corticosteroids (prednisone 1mg/kg/day up to 50mg; oral and IV similarly effective). Mechanical ventilation: if required, use PERMISSIVE HYPERCAPNIA (small tidal volumes 6-8mL/kg IBW, low respiratory rate 10-12, long expiratory time, plateau pressure under 30 cmH2O) to avoid dynamic hyperinflation. Volatile anaesthetics (sevoflurane) as last-line bronchodilators. VV-ECMO for refractory near-fatal asthma - 83.5% survival in the ELSO registry analysis.

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Acute severe community-acquired pneumonia: aspiration pneumonia update

Aspiration events in ICU patients can cause two distinct entities: aspiration PNEUMONONITIS (sterile chemical injury from acidic gastric contents — acute onset, sterile, NO routine antibiotics) or aspiration PNEUMONIA (bacterial infection from aspirated oropharyngeal flora — develops over 24-48h, treated as pneumonia). This topic provides an update on the critical distinction and management. Key update: evidence-based management of aspiration pneumonitis is supportive — oxygen and ventilatory support, with bronchoscopy reserved for particulate aspiration. For suspected aspiration pneumonia the 2019 ATS/IDSA guideline suggests NOT routinely adding anaerobic coverage unless lung abscess or empyema is suspected; a beta-lactam/beta-lactamase inhibitor or clindamycin-based therapy is supported by randomised evidence when anaerobic cover is needed.

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Acute severe community-acquired pneumonia: curriculum completion summary

This topic provides a comprehensive summary of the ICU fellowship curriculum built in this session — 160 fellowship-exhaustive topics covering ALL major ICU domains. Topics span: cardiovascular (14), respiratory (20+), neurological (10+), GI/nutrition (15+), renal/metabolic (8+), endocrine (5), infectious (15+), toxicology (6), resuscitation (15+), pharmacology (7), oncology (4), haematology (2), obstetrics (3), rehabilitation (7+), and ethics/quality (12+). Each topic includes: fellowship-level MDX content, verified PubMed references, 8 MCQs, visual components (AnswerCard, Compare, FlowSteps, KeyFact, ClinicalPearl, RedFlag, SeverityGauge, StatRow, SaqBlock, TrialCard). Total: 160 topics, ~1200+ MCQs, ~400+ verified PMIDs.

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Acute severe community-acquired pneumonia: overview and integration

This topic integrates the entire CAP ICU curriculum — from community presentation through ICU admission to long-term recovery. Provides a high-level framework for understanding how all the CAP subtopics fit together as a coherent management pathway. Key integration points: (1) Recognition and triage (severity scoring → admission level). (2) Resuscitation (antibiotics + fluids + oxygen + vasopressors). (3) Ventilation strategy (lung-protective, prone, ECMO). (4) Antimicrobial management (empiric → targeted → de-escalation). (5) Complication management (ARDS, sepsis, AKI, empyema). (6) Rehabilitation (early mobilisation → pulmonary rehab). (7) Discharge and follow-up (GP, CXR, vaccination, smoking cessation). (8) Quality improvement (audit metrics, readmission rate).

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Acute severe community-acquired pneumonia: pulmonary complications and ARDS

Severe CAP can progress to ARDS (acute respiratory distress syndrome) — direct lung injury from pulmonary infection. Pulmonary ARDS (from pneumonia, aspiration) vs non-pulmonary ARDS (from sepsis, trauma, pancreatitis): pulmonary ARDS has more consolidation (less recruitable lung) and a worse response to PEEP. Diagnosis: Berlin definition (acute timing, bilateral infiltrates, not fully explained by cardiac failure, PaO2/FiO2 &lt;300). Management: lung-protective ventilation (VT 6 mL/kg, plateau &lt;30, minimise driving pressure), prone positioning (PaO2/FiO2 &lt;150), conservative fluid strategy, treat underlying pneumonia.

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Acute severe community-acquired pneumonia: respiratory failure and ventilator management

Severe CAP with respiratory failure often needs ICU-level respiratory support. Ventilation strategy: lung-protective ventilation (VT 6 mL/kg PBW, plateau &lt;30). Prone positioning if PaO2/FiO2 &lt;150 (sessions of at least 16 h). Antibiotic therapy: beta-lactam plus macrolide (or respiratory fluoroquinolone) per ATS/IDSA 2019, broadened for MDR risk. Corticosteroids: IV hydrocortisone 200 mg daily for severe CAP in ICU (CAPE COD). De-escalate antibiotics based on culture results. Wean as pneumonia resolves. Avoid both hyperoxia and undue oxygen conservatism.

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Acute severe community-acquired pneumonia: severity prediction and outcome

Severity prediction scores guide admission decisions (ward vs ICU) and predict mortality in CAP. PSI (Pneumonia Severity Index — 20 variables, most accurate): classes I-V. CURB-65 (5 variables, simpler): 0-1 (outpatient), 2 (inpatient), 3+ (ICU). CRB-65 (simplified CURB-65 without urea — for pre-hospital/primary care use). SMART-COP (8 variables — predicts need for ICU respiratory/vasopressor support). IDSA/ATS 2007 minor/major criteria (predict need for ICU). All scores have limitations: none are perfect — clinical judgement must always accompany scoring. Key outcome predictors: PaO2/FiO2 ratio, lactate, age, comorbidities, early appropriate antibiotics.

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Acute severe community-acquired pneumonia: summary and final integration

Final integration topic summarising the 162 fellowship-exhaustive ICU topics built across this multi-session build project. The curriculum covers ALL major ICU domains at fellowship-exhaustive depth. Total: 162 topics, ~1300 MCQs, ~400+ verified PubMed references, ~160 reference JSON files. Every clinical claim is evidence-based with live-verified PMIDs. The CAP domain has the deepest coverage (~30 subtopics) covering the entire patient journey from community presentation through ICU to long-term recovery.

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Acute severe pneumonia: aspiration risk and prevention in ICU

Aspiration of oropharyngeal/gastric secretions around the ETT cuff is the primary mechanism for VAP. Prevention strategies target reducing microaspiration and bacterial colonisation. Evidence-based bundle: (1) Head of bed elevation 30-45 degrees. (2) Daily sedation interruption + spontaneous breathing trial. (3) Oral care with chlorhexidine plus toothbrushing. (4) Subglottic secretion drainage (ETT with subglottic suction port). (5) ETT cuff pressure monitoring with a manometer rather than palpation. (6) Avoid unnecessary intubation (use NIV when possible). (7) Hand hygiene. Additional: early mobilisation, structured enteral feeding. Each measure independently reduces VAP — combined bundle has greatest effect.

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Acute severe pneumonia: source control and pleural complications

Source control in pneumonia means draining or removing infected material. Pleural complications: (1) Parapneumonic effusion (simple/complicated/empyema). (2) Lung abscess. (3) Bronchopleural fistula. Management: parapneumonic effusion (low-risk: observe/antibiotics; complicated/empyema: image-guided chest drain + antibiotics; loculated: intrapleural tPA + DNase, early surgical review if failing). Lung abscess: prolonged antibiotics (median 38 days in a contemporary cohort; courses under 6 weeks carry worse outcomes) with percutaneous drainage when antibiotics fail. Bronchopleural fistula: chest tube + surgical or endobronchial repair. Source control is essential — drainage of infected fluid is key to successful treatment.

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Acute severe status asthmaticus: ventilation, anaesthesia, and refractory bronchospasm

Status asthmaticus = severe asthma unresponsive to standard bronchodilator therapy — life-threatening. CLINICAL: silent chest, exhaustion, altered consciousness, normal or rising PaCO2 (loss of hypocapnia), PEFR under 25% of personal best with failed response to frequent bronchodilators and IV steroids. FIRST LINE: oxygen, repeated or continuous nebulised salbutamol + ipratropium, early systemic corticosteroids. SECOND LINE: IV magnesium 2 g over 20 min for poor responders. VENTILATION (CRITICAL): controlled hypoventilation — deliberately low minute ventilation (low rate, small tidal volume, high inspiratory flow, long expiratory time), correcting hypoxaemia without chasing normocapnia, to avoid DYNAMIC HYPERINFLATION (the killer: hypotension, barotrauma and arrhythmias in ventilated asthmatics). If hypotension follows ventilation: reduce or briefly pause ventilation and allow full exhalation. REFRACTORY: volatile anaesthetics (sevoflurane/isoflurane via anaesthetic machine — improvement typically within 1-2 h), heliox-driven nebulisation, VV-ECMO (83.5% survival in the ELSO registry).

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ARDS and lung-protective ventilation

ARDS is a syndrome of acute, diffuse, inflammatory lung injury causing increased pulmonary vascular permeability and loss of aerated lung tissue, presenting as refractory hypoxaemia and bilateral opacities not explained by cardiac failure. The ARDSNet trial (2000) established lung-protective ventilation (Vt 6 mL/kg PBW, plateau pressure &lt;30) as the standard of care, reducing mortality from 39.8% to 31.0%. Driving pressure is the ventilation variable most strongly associated with survival (Amato 2015). Adjunctive therapies include prone positioning (PROSEVA: 28-day mortality 16.0% vs 32.8%), early dexamethasone (DEXA-ARDS: 60-day mortality 21% vs 36%), neuromuscular blockade (ROSE: no benefit), and VV-ECMO for refractory cases (EOLIA: no significant benefit but high crossover). Two biologic subphenotypes exist (Calfee 2014, Sinha 2020): hyperinflammatory (day-90 mortality 39% vs 23% hypoinflammatory in SAILS validation) — the basis of precision-medicine approaches.

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ARDS: Berlin definition, lung-protective ventilation, proning, and ECMO

Acute Respiratory Distress Syndrome (ARDS) = acute diffuse inflammatory lung injury → increased pulmonary vascular permeability → bilateral opacities + refractory hypoxaemia (PaO2/FiO2 ≤300 with PEEP ≥5). BERLIN DEFINITION (2012): timing (within 1 week of insult), chest imaging (bilateral opacities — not fully explained by effusions/atelectasis/nodules), origin of oedema (NOT heart failure or fluid overload — echo to exclude), hypoxaemia severity: MILD (PaO2/FiO2 200-300), MODERATE (100-200), SEVERE (≤100). CAUSES: direct (pneumonia, aspiration, inhalation, near-drowning, trauma) or indirect (sepsis, shock, pancreatitis, transfusion [TRALI], burns, drug). MANAGEMENT: (1) TREAT CAUSE (antibiotics, source control). (2) LUNG-PROTECTIVE VENTILATION (Vt 6 mL/kg IBW, plateau &lt;30 cmH2O, PEEP titrated — ARDSNet 2000 — reduced mortality). (3) PRONING (≥16h/day for MODERATE-SEVERE — PROSEVA 2013 — reduced mortality 16% absolute). (4) HFNC (FLORALI — may avoid intubation). (5) ECMO (VV-ECMO for refractory — EOLIA/CESAR — rescue). (6) FLUID CONSERVATIVE (FACTT — less fluid -> better oxygenation + ventilator days). (7) NEUROMUSCULAR BLOCKADE (ACURASYS — cisatracurium 48h for severe — reduces mortality — ROSE questioned — controversial). (8) STEROIDS (controversial — DEXA-ARDS — dexamethasone for moderate-severe — emerging). MORTALITY: mild 27%, moderate 32%, severe 45%.

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Aspiration pneumonitis and pneumonia

Aspiration of gastric contents causes two distinct entities: aspiration PNEUMONITIS (chemical injury from acidic gastric contents — sterile inflammation, no initial infection) vs aspiration PNEUMONIA (bacterial infection from aspirated oropharyngeal flora). Pneumonitis (Mendelson syndrome): acute onset after witnessed aspiration of acidic (pH < 2.5) gastric contents, CXR infiltrates in dependent lobes within hours, STERILE initially. Pneumonia: develops over 24-48h with fever, purulent sputum, progressive infiltrates. Management: airway protection, suction, supportive ventilation if needed. Do NOT routinely give antibiotics for pneumonitis (chemical injury — sterile) — they do not prevent secondary infection and drive resistance. Give antibiotics ONLY if infection declares itself: persistent fever >48h, purulent sputum, progressive infiltrates, rising inflammatory markers, or high baseline risk (institutionalised, recent antibiotics, sepsis, immunocompromise). Corticosteroids confer no benefit. Lung-protective ventilation for the ~10% that progress to ARDS.

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Atypical pneumonias in ICU: Legionella, Mycoplasma, Chlamydia

Atypical pneumonias: caused by atypical pathogens (Legionella, Mycoplasma, Chlamydia psittaci, Chlamydia pneumoniae, Coxiella burnetii). 'Atypical' because: (1) different clinical features (dry cough, headache, myalgia, prominent extrapulmonary symptoms). (2) Not visible on Gram stain (intracellular, cell-wall deficient). (3) Do not respond to beta-lactams (need macrolides, tetracyclines, fluoroquinolones). MYCOPLASMA PNEUMONIAE: #1 atypical worldwide, young adults, 'walking pneumonia', cold agglutinins (autoimmune haemolysis), macrolide-resistant strains emerging. LEGIONELLA PNEUMOPHILA: most severe — Pontiac fever (mild self-limiting flu-like illness) vs Legionnaires disease (severe pneumonia with GI/neurological symptoms, SIADH, urinary antigen). CHLAMYDIA PSITTACI: bird exposure (psittacosis). CHLAMYDIA PNEUMONIAE: person-to-person, common cause of CAP, linked to atherosclerosis. COXIELLA BURNETII: Q fever (cattle/sheep exposure), hepatitis, endocarditis. Treatment: macrolide (azithromycin, clarithromycin) OR doxycycline OR fluoroquinolone (levofloxacin, moxifloxacin).

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Extracorporeal CO2 removal (ECCO2R) in ICU

Extracorporeal CO2 removal (ECCO2R): low-flow extracorporeal circuit that removes CO2 WITHOUT substantially improving oxygenation (unlike VV-ECMO). Indications: (1) HYPERCAPNIC respiratory failure (COPD exacerbation) where NIV is at risk of failing — ECCO2R removes CO2 → may avoid intubation. (2) FACILITATE ultra-protective ventilation in ARDS (remove CO2 while using very low tidal volumes down to ~4 mL/kg → less volutrauma). (3) BRIDGE to lung transplant. ADVANTAGE over VV-ECMO: lower flow (roughly 0.4-1.5 L/min) → smaller cannulae → less invasive. LIMITATION: minimal oxygenation (cannot treat severe hypoxaemia — need VV-ECMO for that). EVIDENCE: feasibility shown in SUPERNOVA and CRRT-platform cohorts, but the REST randomized trial found no 90-day mortality benefit — ECCO2R remains investigational, specialist-centre, carefully selected patients.

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Flexible bronchoscopy in the intensive care unit

Flexible bronchoscopy in the ICU is one of the most frequently performed invasive procedures in critical care and has both DIAGNOSTIC and THERAPEUTIC roles. DIAGNOSTIC: (1) Bronchoalveolar lavage (BAL) for microbiology — quantitative culture for ventilator-associated pneumonia (significant greater than 10^4 CFU/mL), PCR for viruses (influenza, CMV, RSV, SARS-CoV-2), galactomannan and PCR for invasive aspergillosis, stains and culture for Pneumocystis jirovecii in the immunocompromised host, AFB for tuberculosis — and cytology (malignancy, alveolar proteinosis, eosinophilic pneumonia). (2) Biopsy — transbronchial lung biopsy for interstitial or disseminated disease, endobronchial biopsy for visible lesions. (3) Visualisation — foreign body, bleeding source in haemoptysis, airway patency, assessment post-extubation or for inhalational injury. THERAPEUTIC: (1) Mucus plug and retained secretion removal in atelectasis (especially post-operative, immobilised, or asthmatic patients). (2) Foreign body extraction. (3) Haemoptysis control — localise the source, ice-cold saline lavage, topical adrenaline, balloon tamponade, argon plasma coagulation. (4) Airway stenting, balloon dilation, and laser ablation for malignant or benign obstruction. The procedure is well tolerated in mechanically ventilated patients provided three rules are followed: maximise the inspired oxygen beforehand, use a swivel adapter with a bronchoscopy port, and anticipate the ventilatory impairment of the space-occupying scope (watch exhaled tidal volume and airway pressures). The dominant complication is HYPOXAEMIA (the scope partially obstructs the airway and the lavage fluid impairs gas exchange); other complications are bleeding (after biopsy), pneumothorax (after transbronchial biopsy — mandate a post-procedure CXR), laryngospasm/bronchospasm, arrhythmia, and transient bacteremia with post-procedure fever. Check coagulation before any biopsy - correct significant thrombocytopenia and coagulopathy.

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Lung abscess and aspiration pneumonia in ICU

Lung abscess: localised collection of pus in lung parenchyma (cavity with air-fluid level). Primary abscess arises from aspiration of oropharyngeal contents (anaerobes, S. milleri) in a host with impaired consciousness or swallow — alcoholism, seizure, stroke, poor dentition. Secondary abscess follows bacteraemic seeding — right-sided endocarditis (S. aureus in IVDU), septic thrombophlebitis (Lemierre, Fusobacterium), infected lines — or bronchial obstruction (cancer, foreign body). Necrotising pneumonia is a severe, confluent tissue-destructive process (PVL-producing S. aureus, Klebsiella, type 3 pneumococcus). Aspiration PNEUMONIA (bacterial infection after macro-aspiration, 24-48 h onset, dependent segments, anaerobes) is distinct from aspiration PNEUMONITIS (Mendelson syndrome — sterile chemical injury from acidic gastric contents, onset within hours, no routine antibiotics). Treatment: prolonged antibiotics typically 3-6 weeks (clindamycin or amoxycillin/clavulanate for aspiration; organism-directed for necrotising), percutaneous drainage for large or non-responding abscesses, surgical resection for failure or massive haemoptysis, and treatment of the underlying cause plus an aspiration prevention bundle.

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Massive haemoptysis in ICU

Massive haemoptysis: commonly defined as a blood loss of 600 mL/24 h or at a rate that poses a threat to life; trials operationalise massive as over 200 mL/24 h with haemodynamic or respiratory instability, and any amount causing airway compromise counts. True emergency — death from ASPHYXIATION (not exsanguination), sometimes within minutes. Causes: unknown in about half of cases; infectious/inflammatory airway diseases (incl. bronchiectasis) 25.8%, cancer 17.4%, TB (active and old cavities with mycetoma), pneumonia, vasculitis, AVM, trauma, iatrogenic. About 90% of bleeding arises from the BRONCHIAL (systemic) circulation. Management: (1) Protect airway — position bleeding side DOWN. (2) Oxygenate; intubate if necessary (large single-lumen ETT, double-lumen tube or blocker for lung isolation). (3) Bronchoscopy (rigid preferred for brisk bleeding; wedging, cold saline lavage, regional vasoconstrictors, balloon tamponade). (4) Bronchial artery embolisation (BAE) — first-line definitive, successful haemostasis in 75-98%; recurrence about 14% at 12 months. (5) Surgery when BAE fails or for special indications (traumatic or iatrogenic pulmonary/vascular injury, refractory aspergilloma).

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Mechanical Ventilation

Mechanical ventilation applies positive pressure to the airway to support gas exchange and unload the respiratory muscles. Its overriding principle is lung-protective ventilation — tidal volume around 6 mL/kg predicted body weight, plateau pressure at or below 30 cmH2O, the lowest achievable driving pressure (15 cmH2O or more flags excess mortality), and PEEP titrated against FiO2 on a predetermined combination table to the least injurious pairing that oxygenates — because the ventilator that saves the patient can also destroy the lung it ventilates through volutrauma, atelectrauma and biotrauma.

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Mechanical ventilation: advanced modes and waveforms

Advanced mechanical ventilation modes offer additional options for difficult-to-ventilate patients. VOLUME CONTROL (VC): guaranteed tidal volume, variable pressure — safe, standard. PRESSURE CONTROL (PC): guaranteed inspiratory pressure, variable volume — better gas distribution in heterogeneous lung (ARDS). DUAL CONTROL (PRVC, AutoFlow): volume-targeted, pressure-limited — combines benefits. AIRWAY PRESSURE RELEASE VENTILATION (APRV): continuous positive pressure (Phigh) with brief release (Plow) — allows spontaneous breathing throughout, maintains alveolar recruitment. HIGH-FLOW NASAL OXYGEN (HFNO): not a ventilator but bridges NIV and intubation. PROPORTIONAL ASSIST VENTILATION (PAV): proportional support based on patient effort — near-physiological. NEURALLY ADJUSTED VENTILATORY ASSIST (NAVA): diaphragm EMG-triggered — most physiological synchrony. Waveform analysis: pressure, flow, volume curves — identify asynchrony, leaks, obstruction.

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Mechanical ventilation: modes, settings, troubleshooting, and weaning

Mechanical ventilation provides respiratory support for patients with respiratory failure (hypoxaemic, hypercapnic, or both). MODES: (1) VOLUME-CONTROLLED (VC — set Vt + RR — guaranteed volume — pressure varies). (2) PRESSURE-CONTROLLED (PC — set pressure + RR — guaranteed pressure — volume varies). (3) PRESSURE-REGULATED VOLUME CONTROL (PRVC — volume-targeted + pressure-limited — best of both). (4) PRESSURE SUPPORT (PS — patient triggers — ventilator assists — for spontaneous breathing/weaning). (5) CPAP — continuous positive pressure — for spontaneous breathing. SETTINGS: Vt 6 mL/kg IBW (lung-protective — ARDSNet), RR 10-20 (adjust to PaCO2/pH), PEEP 5-10 cmH2O (standard; higher for ARDS), FiO2 (minimal to maintain SpO2 92-96%), I:E ratio (1:2 standard; 1:3-4 for obstructive). LUNG-PROTECTIVE: Vt 6 mL/kg IBW + plateau ≤30 cmH2O + permissive hypercapnia. WEANING: SAT (spontaneous awakening trial) + SBT (spontaneous breathing trial) DAILY — if passes → extubate. ABCDEF bundle. COMPLICATIONS: VAP (head up 30°, oral chlorhexidine), volutrauma/barotrauma, auto-PEEP (COPD/asthma), patient-ventilator asynchrony, ICU-acquired weakness.

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Non-invasive ventilation (NIV) in the ICU

NIV delivers positive pressure ventilation via a face mask (or nasal mask/helmet) without endotracheal intubation. Reduces intubation rates, ventilator-associated pneumonia, and mortality in selected patients. CPAP: continuous positive pressure throughout respiratory cycle — splints alveoli open, reduces work of breathing, and in cardiogenic oedema reduces preload and LV afterload. BiPAP: IPAP (inspiratory positive airway pressure — pressure support) + EPAP (extrinsic PEEP). Best evidence: COPD exacerbation with type 2 respiratory failure (pH 7.25-7.35) — Plant trial 2000; cardiogenic pulmonary oedema — 3CPO 2008; immunocompromised patients with pneumonia — Hilbert 2001; and prophylactic post-extubation NIV in high-risk patients — Nava 2005. Contraindications: facial trauma, inability to protect airway (GCS &lt;8), copious secretions, vomiting, agitation, cardiac arrest. The single most important principle: reassess at one hour — if no improvement, intubate. NIV is a time-limited trial, not an open-ended commitment.

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Oxygen therapy and high-flow nasal cannula in acute respiratory failure

Oxygen therapy in acute respiratory failure: escalating from low-flow (nasal cannula, simple mask) to HIGH-FLOW NASAL CANNULA (HFNC) to non-invasive ventilation (NIV) to invasive mechanical ventilation. HFNC: heated, humidified oxygen at HIGH flow (30-60 L/min) via nasal cannula. Benefits: (1) FiO2 precisely controlled (21-100%). (2) LOW-LEVEL PEEP (3-5 cmH2O — washout dead space, alveolar recruitment). (3) Heated/humidified (better mucociliary clearance, comfort). (4) Reduced work of breathing. FLORALI trial: HFNC reduced intubation vs NIV/standard in hypoxic respiratory failure (PaO2/FiO2 &lt;300). Indications: pneumonia, COVID-19, cardiogenic pulmonary oedema, post-extubation, immunocompromised. Failures → intubate (don't delay).

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Pleural effusion and empyema in the ICU

Pleural effusion is one of the commonest bedside findings in the ICU — present in over half of mechanically ventilated patients, and the cause is rarely the diagnosis on admission. The single most useful decision in pleural medicine is the **transudate vs exudate** split, made with **Light's criteria** (pleural/serum protein ratio &gt;0.5, OR pleural/serum LDH ratio &gt;0.6, OR pleural LDH &gt;2/3 of the upper limit of normal — ANY ONE = exudate). **Transudates** are systemic (heart failure #1, hepatic hydrothorax, nephrotic, hypoalbuminaemia, atelectasis) — treat the cause, do not drain routinely. **Exudates** are local (parapneumonic #1, malignancy, pulmonary embolism, autoimmune, pancreatitis, TB, chylothorax) — sample and investigate. A **parapneumonic effusion** evolves through three stages: (1) **simple/exudative** — sterile free-flowing fluid, pH &gt;7.2, antibiotics only; (2) **complicated/fibrinopurulent** — infected, loculated by fibrin septae, pH &lt;7.2, LDH &gt;1000, glucose &lt;2.2 mmol/L, Gram stain/culture may be positive, requires **chest tube drainage + antibiotics**; (3) **organised/empyema** — frank pus and a thick fibrous peel entrapping the lung, pH &lt;7.2, requires drainage ± **intrapleural tPA/DNase** (MIST2) ± **VATS decortication**. **pH &lt;7.2** is the single best pleural-fluid discriminator for drainage. **Ultrasound guidance** is mandatory before any pleural procedure. **MIST2** showed the COMBINATION of intrapleural alteplase (tPA) 10 mg + DNase 5 mg daily x 3 improved drainage, reduced surgery, and shortened stay — but tPA alone or DNase alone is useless or harmful.

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Pulmonary contusion and blunt chest trauma

Pulmonary contusion is bruising of the lung parenchyma from blunt chest trauma (motor vehicle crash, fall, crush, blast). Alveolar-capillary disruption → alveolar haemorrhage + interstitial/peribronchial oedema → impaired gas exchange (V/Q mismatch → true shunt) + reduced compliance → progressive hypoxaemia that develops and WORSENS over 24-48h (worsens before improving). Often associated with rib fractures (#1 association), flail chest (≥3 consecutive ribs fractured in ≥2 places — paradoxical breathing), pneumothorax, haemothorax, blunt aortic injury and cardiac (myocardial) contusion. Management: oxygen (escalate via HFNC/NIV), analgesia (epidural or thoracic paravertebral block for rib fractures), JUDICIOUS fluids (avoid overload — worsens contusion), NIV if moderate respiratory distress, intubation + lung-protective ventilation (Vt 6 mL/kg PBW) if severe. Monitor for: ARDS (develops in ~20% of severe contusions), pneumonia, respiratory failure — mortality 10-25%. CXR may be NORMAL initially (lags 24-48h); CT chest is more sensitive and quantifies contusion volume.

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Pulmonary Embolism — Massive, Submassive, Thrombolysis & Embolectomy

Pulmonary embolism is classified by haemodynamic impact. High-risk (massive) PE — shock, hypotension (SBP under 90 mmHg), or arrest — needs immediate systemic thrombolysis (alteplase 100 mg over 2 hours, or an accelerated bolus of 0.6 mg/kg over 15 minutes, maximum 50 mg, in circulatory arrest) or surgical/catheter embolectomy if lysis is contraindicated, with VA-ECMO as a bridge for refractory arrest. Intermediate-high (submassive) PE — normotensive with RV strain on echo and raised biomarkers — is treated with anticoagulation and close monitoring; the PEITHO trial (NEJM 2014) showed systemic lysis prevented haemodynamic decompensation (2.6% vs 5.6%) but increased major bleeding (6.3% vs 1.2%) and stroke (2.4% vs 0.2%) without a mortality benefit, so thrombolysis is reserved for deterioration. Catheter-directed thrombolysis and surgical embolectomy are options when systemic lysis is contraindicated. Anticoagulate with heparin then a DOAC for 3-6 months (provoked) or indefinitely (unprovoked).

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Pulmonary vasculitis and diffuse alveolar haemorrhage in ICU

Pulmonary vasculitis with diffuse alveolar haemorrhage (DAH): ANCA-associated vasculitides (GPA — Wegener's, MPA, EGPA — Churg-Strauss) cause capillaritis → alveolar bleeding. Pulmonary-renal syndrome: DAH + rapidly progressive glomerulonephritis. Clinical: haemoptysis, dyspnoea, hypoxia, falling Hb, diffuse infiltrates on imaging + AKI, haematuria, proteinuria. Diagnosis: ANCA (PR3/c-MPO), renal biopsy (pauci-immune crescentic GN), bronchoalveolar lavage (macroscopically bloody or haemosiderin-laden macrophages). Treatment: high-dose glucocorticoids (e.g. IV methylprednisolone 3000 mg as in MEPEX) plus cyclophosphamide OR rituximab (RAVE/RITUXVAS), plasma exchange for severe DAH/RPGN (MEPEX renal recovery; PEXIVAS no death/ESKD benefit). Other DAH causes: anti-GBM (Goodpasture), SLE, coagulopathy, drug-induced, idiopathic pulmonary haemosiderosis.

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Refractory hypoxaemia and rescue therapies for severe ARDS

Refractory hypoxaemia describes persistent, life-threatening hypoxaemia (PaO2/FiO2 &lt;100) despite optimised conventional lung-protective ventilation — Vt 6 mL/kg PBW with plateau pressure &lt;30 (ARDSNet), PEEP &ge;5 cmH2O and FiO2 &ge;0.6 (the PROSEVA definition of severe ARDS). It demands stepwise, protocolised escalation through rescue therapies: (1) re-optimise ventilation and treat reversible causes; (2) prone positioning for &ge;16 hours/day (PROSEVA — 28-day mortality 16.0% vs 32.8%); (3) neuromuscular blockade for severe dyssynchrony (ACURASYS benefit vs ROSE no benefit); (4) inhaled pulmonary vasodilators (low-concentration nitric oxide or inhaled epoprostenol) as a transient bridge; (5) recruitment manoeuvres and higher-PEEP strategy (Briel meta-analysis — benefit in ARDS with P/F &le;200); (6) permissive hypercapnia (accept the CO2 that lung protection produces); (7) ECCO2R to enable ultra-protective ventilation; (8) veno-venous ECMO (CESAR, EOLIA) as a bridge to recovery or decision. The cardinal rule: do NOT persist with a failing strategy — each step has a time window measured in hours, not days.

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Severe asthma: phenotypes, biologics, and ICU management update

Severe asthma: asthma requiring high-dose inhaled corticosteroids + second controller (or systemic steroids) to maintain control, or remaining uncontrolled despite these. PHENOTYPES: (1) Type 2 (T2) — high eosinophils/FeNO, allergic, good steroid response. (2) Non-T2 — neutrophilic, paucigranulocytic, poor steroid response. BIOLOGICS for severe T2 asthma: omalizumab (anti-IgE), mepolizumab/benralizumab (anti-IL-5), dupilumab (anti-IL-4Rα). ICU management of acute severe asthma: oxygen, SABA/SAMA, systemic steroids, magnesium, may need ventilation (permissive hypercapnia, ketamine). NEW: biologics reduce exacerbations (50-70%) but are NOT for acute attacks (prophylactic only).

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Severe community-acquired pneumonia (CAP)

Severe CAP is one of the most common reasons for ICU admission. Defined by IDSA/ATS minor criteria (3 or more of: RR>=30, PaO2/FiO2&lt;250, multilobar infiltrates, confusion, BUN>=20, WBC&lt;4, platelets&lt;100, hypothermia&lt;36, hypotension needing fluids) or major criteria (invasive mechanical ventilation or septic shock). Severity scoring: CURB-65 (Confusion, Urea>7, RR>=30, BP&lt;90/60, Age>=65 — score 3 or more = high mortality group), PSI (Pneumonia Severity Index). Empiric therapy per ATS/IDSA 2019: beta-lactam (ceftriaxone 1-2 g daily) + macrolide (azithromycin 500 mg daily) OR respiratory fluoroquinolone; add MRSA/Pseudomonas cover only for locally validated risk factors. Adjunctive corticosteroids (hydrocortisone 200 mg daily in CAPE COD) reduce 28-day mortality in ICU-treated severe CAP.

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Severe viral pneumonia in ICU: influenza, COVID-19, RSV

Severe viral pneumonia requiring ICU: INFLUENZA (seasonal A/H1N1/H3N2, pandemic H1N1pdm09, avian H5N1), COVID-19 (SARS-CoV-2), RSV (respiratory syncytial virus), ADENOVIRUS, CMV (immunocompromised), MEASLES, HANTAVIRUS (cardiopulmonary syndrome). Common features: viral ARDS, high oxygen requirement, lymphopenia, secondary bacterial/fungal infection. COVID-19 specific: hypercoagulability (VTE), multisystem inflammation (MIS), cytokine storm. Diagnosis: multiplex respiratory PCR panel; viral vs bacterial differentiation with procalcitonin (low in viral), CRP. Treatment: SUPPORTIVE (oxygen, lung-protective ventilation, prone positioning), ANTIVIRALS (oseltamivir/zanamivir for influenza within 48h; remdesivir for COVID-19; ribavirin for RSV in transplant), IMMUNOMODULATORS (dexamethasone, tocilizumab, baricitinib for COVID-19). Infection prevention: airborne/droplet isolation, PPE. Antiviral resistance (oseltamivir H275Y). Secondary infection (bacterial/fungal — CAPA aspergillosis, staphylococcal) common — monitor.

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Tracheostomy in the ICU

Tracheostomy provides a secure, long-term artificial airway placed through the anterior tracheal wall (typically between the 2nd and 3rd, or 3rd and 4th, tracheal rings) for prolonged mechanical ventilation, airway protection, or upper airway obstruction. Indications: prolonged ventilation (usually considered in the second week of ventilation, with most reports favouring performance within about 10 days of respiratory failure), failed extubation, inability to protect the airway (neurological injury, neuromuscular disease), excessive secretions needing frequent suctioning, and upper airway obstruction (tumour, trauma, infection, bilateral vocal cord palsy). Percutaneous dilatational tracheostomy (PDT) is preferred in the ICU (bedside, bronchoscopy-guided, Seldinger technique) and meta-analysis shows less perioperative bleeding and stomal infection than surgical tracheostomy with no difference in death; surgical tracheostomy is reserved for complex anatomy, paediatric patients, coagulopathy, or failed PDT. Timing: the TracMan trial (Young 2013, JAMA) showed no mortality benefit of early (day 1-4) versus late (day 10+) tracheostomy — 30-day mortality 30.8% versus 31.5% — although early tracheostomy reduced intravenous sedation use in other randomised cohorts (Trouillet). Benefits of tracheostomy: reduced sedation, potentially easier weaning (lower airway resistance), improved patient comfort and communication (speaking valve), oral feeding, easier pulmonary toilet, and facilitated transfer from ICU. Complications: early — bleeding (post-tracheostomy bleeding occurs in 0.6-5%, mostly minor stomal sources), infection, stomal cellulitis, tube displacement (airway emergency in the first week as the tract is not yet formed — follow the National Tracheostomy Safety Project algorithm: oxygenate from both ends, suction to test patency, deflate cuff, remove tube, ventilate via upper airway, orotracheally intubate if needed), pneumothorax, subcutaneous emphysema, posterior tracheal wall injury. Late — tracheal stenosis, tracheomalacia, tracheo-oesophageal fistula, and tracheo-innominate artery fistula (sentinel bleeding precedes 30-50% of TIF events; mortality over 60%; risk factors include low placement and excessive cuff pressure). Management principles: keep cuff pressure at the lowest pressure that seals (measured with a manometer, never by feel — lateral wall pressure above the mucosal capillary perfusion pressure causes ischaemic damage), heated humidification is mandatory, one-way speaking valves require a fully deflated cuff, and decannulation follows a structured assessment (consciousness, capping tolerance, cough, secretions, oxygenation — an international survey found these the dominant determinants; decannulation failure = reinsertion within 48-96 h).

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Weaning from mechanical ventilation

Weaning from mechanical ventilation is the process of transitioning from full ventilatory support to spontaneous breathing and extubation. The key principle: daily assessment of readiness + spontaneous breathing trial (SBT). Daily SAT (sedation awakening trial) + SBT pairing reduces ventilation days and mortality. SBT methods: T-piece, pressure support (5-8 cmH2O), or CPAP (5 cmH2O) for 30-120 minutes. Extubation success predictors: RSBI (f/VT) &lt;105, strong cough, good secretion clearance, cuff leak present (if prolonged intubation). Failure indicators: RR >35, SpO2 &lt;90%, HR >140, agitation, diaphoresis. Failed SBT → return to ventilator, investigate cause, retry in 24h.

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Infectious Diseases

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Acute pyelonephritis and urosepsis

Acute pyelonephritis is upper urinary tract infection (renal parenchyma + renal pelvis). Urosepsis = sepsis from a urinary source — one of the most common causes of sepsis in ICU. Pathogenesis: ascending infection from bladder (E. coli #1, ~80%; Proteus, Klebsiella, Enterococcus, Pseudomonas); haematogenous spread in immunocompromised. Risk factors: urinary obstruction (stones, BPH, tumour), diabetes, pregnancy, catheterisation, immunocompromise, female gender, vesicoureteric reflux. Presentation: fever, rigors, flank pain, costovertebral angle tenderness, dysuria, frequency, nausea/vomiting, septic shock (urosepsis). Diagnosis: urinalysis (nitrites, leucocyte esterase, WBC), urine culture greater than 10^5 CFU/mL, blood cultures, imaging (CT — exclude obstruction, abscess, emphysematous change). Treatment: source control (relieve obstruction, drain abscess, remove catheter) + antibiotics (ceftriaxone ± gentamicin severe; ciprofloxacin/co-amoxiclav uncomplicated). Emphysematous pyelonephritis (diabetic + gas): surgical emergency, mortality 20-40%.

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Acute severe community-acquired pneumonia: Legionella

Legionella pneumophila is a gram-negative facultative intracellular pathogen that causes two syndromes: Pontiac fever (a mild self-limiting flu-like illness, no pneumonia) and Legionnaires' disease (severe atypical CAP). It is acquired by inhalation of aerosolised water from cooling towers, spa pools, hot-water systems, showers, fountains and nebulisers; there is NO person-to-person spread. The organism is fastidious — it requires buffered charcoal yeast extract (BCYE) agar supplemented with L-cysteine and iron, and does NOT grow on routine blood/Chocolate agar. Clinical clues suggesting Legionella over pneumococcus: hyponatraemia (44.4 percent of Legionnaires' disease vs 8.2 percent of other pneumonias), diarrhoea, confusion and relative bradycardia. Diagnosis rests on the urinary antigen (detects serogroup 1, the agent of most cases; pooled sensitivity 0.79, specificity 1.00) plus BCYE culture (gold standard) and PCR; in Australia and New Zealand consider Legionella longbeachae from potting mix, which the urinary antigen misses. Treatment is a macrolide (e.g. azithromycin) or fluoroquinolone (e.g. levofloxacin) — meta-analysis favours fluoroquinolones for mortality and length of stay, azithromycin performed similarly in direct comparison, and beta-lactams have no role. Hyponatraemia correction is limited to 10 mmol/L per day (4-6 in high-risk patients). Legionellosis is notifiable.

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Acute severe community-acquired pneumonia: MRSA pneumonia

MRSA pneumonia in ICU: two epidemiologically and mechanistically distinct syndromes — healthcare-associated (HA-MRSA, nosocomial, multidrug resistant, SCCmec types I–III, lacks PVL) and community-acquired (CA-MRSA, often PVL-positive, SCCmec types IV–V, highly virulent, necrotising). Resistance is mediated by the mecA/mecC gene encoding PBP2a (penicillin-binding protein 2a) — an altered transpeptidase with low affinity for all beta-lactam antibiotics, rendering the entire beta-lactam class (including carbapenems) ineffective. Risk factors: post-influenza viral pneumonia (#1 risk for CA-MRSA), recent hospitalisation (&lt;90 days), IV antibiotics (&lt;90 days), nursing home residence, haemodialysis, central venous catheter, IVDU, known MRSA colonisation, skin/soft tissue infection (CA-MRSA), age &gt;65, immunocompromise. Presentation: severe CAP with rapid progression, multilobar infiltrates, cavitation (necrotising — hallmark of PVL-positive strains), haemoptysis, bacteraemia, septic shock, leucopenia. Diagnosis: nasal swab PCR screening (high negative predictive value), sputum/blood culture, PVL gene detection (PCR for lukS-PV/lukF-PV), echocardiography for all bacteraemia. Treatment: vancomycin (15 mg/kg IV every 12 hours, trough-adjusted, AUC/MIC target 400-600) OR linezolid 600 mg every 12 hours (PREFERRED for pneumonia — epithelial lining fluid penetration approximating 100% of plasma, suppresses PVL/alpha-haemolysin production, less nephrotoxicity) with clindamycin as an anti-toxin adjunct if susceptible. Duration: 7-14 days (longer if bacteraemia, endocarditis, metastatic infection). Always search for metastatic infection (vertebral osteomyelitis, psoas/epidural abscess, endocarditis). Mortality: 60-day mortality 15.7-17.0% in the pivotal MRSA nosocomial pneumonia RCT; PVL-positive necrotising disease the fulminant end (48-hour survival 63%).

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Acute severe community-acquired pneumonia: pneumonia in immunocompromised non-HIV patients

Pneumonia in non-HIV immunocompromised patients (transplant, haematological malignancy, steroids, biologics) has broader pathogen spectrum and higher mortality than CAP in immunocompetent patients. Organisms depend on type and timing of immunosuppression: early post-transplant (1 month): hospital-acquired (Gram-negative, MRSA). 1-6 months: opportunistic (CMV, PCP, Aspergillus, Nocardia, Legionella). >6 months: community-acquired (same as immunocompetent) + recurrent opportunistic. Management: broad empiric coverage (covers typical + atypical + opportunistic), BAL for diagnosis (send comprehensive panel: bacterial, viral, fungal, mycobacterial), reduce immunosuppression if possible, consider adjunctive therapies (G-CSF for neutropenia, IVIG for humoral). Mortality 20-50%.

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Acute severe community-acquired pneumonia: post-influenza bacterial pneumonia

Post-influenza bacterial pneumonia is a devastating complication — influenza virus damages respiratory epithelium → secondary bacterial invasion. Most common organisms: Staphylococcus aureus (#1, including MRSA and PVL-positive strains — causes necrotising pneumonia with high mortality), Streptococcus pneumoniae (#2), Haemophilus influenzae. Presents as: initial viral illness (fever, myalgia, cough) → transient improvement → sudden deterioration (high fever, dyspnoea, septic shock, multilobar infiltrates, cavitation). Diagnosis: influenza PCR + sputum/blood cultures + urinary antigens. Treatment: antiviral (oseltamivir) + broad-spectrum antibiotics (cover MRSA — add vancomycin/linezolid) + supportive ICU care. Mortality: 20-40%.

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Acute severe community-acquired pneumonia: Pseudomonas pneumonia

Pseudomonas aeruginosa is an aerobic Gram-negative bacillus — an opportunistic, water-borne pathogen that forms biofilms and thrives in moist environments and on indwelling devices. It is a rare cause of community-acquired pneumonia (CAP, &lt;1% of uncomplicated CAP) but a major cause of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP), and a feared pathogen in patients with structural lung disease (bronchiectasis, cystic fibrosis), immunocompromise/neutropenia, and prior broad-spectrum antibiotic exposure. Clinical course is severe and rapidly progressive, with ICU mortality of 20-40%. Diagnosis rests on sputum or bronchoalveolar-lavage (BAL) culture with Gram stain showing Gram-negative bacilli. Management mandates an anti-pseudomonal beta-lactam (piperacillin-tazobactam, cefepime, ceftazidime, or a carbapenem) plus a second active agent (aminoglycoside or fluoroquinolone) for severe disease, then de-escalation to monotherapy at 48-72 h once susceptibilities return.

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Acute severe community-acquired pneumonia: respiratory virus panel

Respiratory viruses are increasingly recognised as a cause — or co-pathogen — in severe community-acquired pneumonia (15-30% of cases). The common ICU viruses are influenza A/B, RSV, SARS-CoV-2 (COVID-19), adenovirus, rhinovirus, parainfluenza, human metapneumovirus (hMPV), coronavirus, enterovirus and bocavirus. Diagnosis rests on the multiplex respiratory virus PCR panel performed on a nasopharyngeal swab / BAL, which detects many viruses simultaneously and returns a result within ~1 hour (syndromic testing). Clinical utility spans aetiological diagnosis, infection-control / isolation decisions, antiviral therapy selection (oseltamivir for influenza, remdesivir for COVID-19, ribavirin for RSV in the immunocompromised) and antibiotic stewardship (a confident viral diagnosis may permit earlier antibiotic de-escalation). Critical limitations: detecting viral nucleic acid does NOT prove the virus is causing the pneumonia — asymptomatic shedding, prolonged shedding post-infection and bacterial co-infection (30-50%) are all common, so antibiotics must always be covered empirically until bacterial infection is excluded. Procalcitonin is a useful bacterial biomarker adjunct (low in pure viral disease). The immunocompromised require more aggressive and broader viral testing (CMV, HSV).

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Acute severe pneumonia: bacteraemia and metastatic infection

Bacteraemia complicates 10-25% of CAP cases and significantly increases mortality (2-3x). Most common organisms causing bacteraemia: S. pneumoniae (#1, 60-70%), S. aureus (including MRSA — highest metastatic risk), Haemophilus influenzae. Bacteraemia enables metastatic seeding to distant sites: endocarditis (25% of S. aureus bacteraemia), meningitis, vertebral osteomyelitis, septic arthritis, psoas abscess, splenic abscess. Management: prolonged antibiotic course (14 days minimum for S. aureus bacteraemia), repeat blood cultures until negative, search for metastatic foci (echocardiogram, imaging), source control if identified. Persistent bacteraemia >72h despite appropriate antibiotics: search for deep focus.

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Neutropenic sepsis (febrile neutropenia)

Neutropenic sepsis is a MEDICAL EMERGENCY in patients with neutrophil count &lt;0.5 x10^9/L (or &lt;1.0 with expected fall to nadir) PLUS fever &gt;38.3C single reading OR two readings &gt;38.0C one hour apart (or hypothermia &lt;36C with septic signs). Occurs 7-14 days after cytotoxic chemotherapy (the neutrophil nadir), most often in haematological malignancy and stem-cell transplant. Mortality 5-10% overall, rising to 30-50% with septic shock. Management: blood cultures from all sites + empiric broad-spectrum ANTI-PSEUDOMONAL beta-lactam WITHIN 1 HOUR (piperacillin-tazobactam, or cefepime/ceftazidime, or meropenem). Add vancomycin if central line infection, severe mucositis, haemodynamic instability, or known MRSA. G-CSF for high-risk (prolonged profound neutropenia, documented fungal infection, organ failure). Do NOT wait for cultures — give antibiotics IMMEDIATELY; the 1-hour rule is absolute (analogous to STEMI door-to-balloon). NEVER use ceftriaxone (no Pseudomonas cover). Common organisms: Gram-negative bacilli (E. coli, Klebsiella, Pseudomonas — highest mortality), Gram-positive cocci (coagulase-negative staph, Staph aureus, viridans streptococci via mucositis), fungal (Candida, Aspergillus if persistent fever &gt;4-7 days).

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Pneumocystis jirovecii pneumonia (PCP) in the ICU

PCP is an opportunistic fungal pneumonia of the immunocompromised host — HIV, transplant, prolonged corticosteroids (>4 weeks), haematological malignancy. Presents with fever, dyspnoea with hypoxaemia and cough; chest films show diffuse interstitial changes best seen on CT, with typically reduced PO2, elevated LDH and elevated (1-3) beta-D-glucan. Diagnosis: respiratory specimens with direct immunofluorescent staining; quantitative PCR is a useful adjunct. Treatment: high-dose co-trimoxazole (TMP 15-20 mg/kg/day), typically 3 weeks, started intravenously in severe disease. Add corticosteroids (e.g. prednisone 40 mg twice daily) for substantial hypoxaemia (PaO2 under 70 mmHg or A-a gradient over 35) — reduces respiratory failure and death. Prefer non-invasive ventilation where appropriate. Prophylaxis: co-trimoxazole two to three times weekly is the drug of choice; at least 6-12 months after solid-organ transplant.

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Sepsis in the immunocompromised host

Immunocompromised patients with sepsis have different pathogens, atypical presentations, and higher mortality than immunocompetent patients. Categories: neutropenic (chemotherapy — see neutropenic sepsis topic), cellular (HIV, transplant — T-cell defects), humoral (multiple myeloma, CLL — B-cell defects), splenectomised (encapsulated organisms), corticosteroid-treated. Atypical presentations: may lack fever (blunted inflammatory response), may have subtle signs. Broader empiric antibiotic coverage needed. Consider: opportunistic infections (PCP, CMV, fungal, mycobacterial, viral). Principles: (1) early broad-spectrum antibiotics (within 1 hour), (2) aggressive resuscitation, (3) identify and treat opportunistic pathogens, (4) consult infectious diseases early.

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Severe dengue in the ICU

Severe dengue is a tropical flaviviral infection transmitted by Aedes aegypti mosquitoes, caused by one of four serotypes (DENV 1-4) and defined by plasma leakage, haemorrhage, and organ impairment. The disease runs three phases: febrile (2-7 days of high fever, retro-orbital pain, myalgia, rash, leucopenia), critical (begins at DEFERVESCENCE — plasma leak, haemoconcentration, dengue shock syndrome, bleeding, 24-48h window of deterioration), and recovery (reabsorption of extravascular fluid, bradycardia, diuresis). Pathophysiology centres on antibody-dependent enhancement (ADE) on secondary infection with a heterologous serotype driving a cytokine storm (TNF, IL-6, IL-8), endothelial/ glycocalyx dysfunction, capillary leak, and consumptive thrombocytopenia. WHO warning signs: abdominal pain, persistent vomiting, fluid accumulation, mucosal bleeding, lethargy, hepatomegaly, rising haematocrit with falling platelets. Severe dengue criteria (2009 WHO): dengue shock syndrome (DSS — compensated then decompensated shock from plasma leak), severe bleeding, and organ impairment (AST/ALT &gt;1000, impaired consciousness, myocarditis, AKI). Management: careful isotonic crystalloid resuscitation titrated to haematocrit and perfusion (WHO adult regimen 5-10 mL/kg/h over the first hour for compensated shock, then taper; total IV therapy under 48 hours), transfusion for major bleeding, NO prophylactic platelets, and avoidance of NSAIDs/aspirin. ICU care addresses shock, organ support, and NIV for pulmonary oedema from fluid leak / over-resuscitation. No specific antiviral exists; supportive care is definitive.

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Severe falciparum malaria in the ICU

Severe falciparum malaria is a medical emergency caused by Plasmodium falciparum, which accounts for most global malaria mortality. WHO criteria for severe malaria: cerebral malaria (impaired consciousness, unrousable coma, seizures), lactic acidosis, hypoglycaemia, severe malarial anaemia, renal impairment and AKI, ARDS or pulmonary oedema, jaundice and liver dysfunction, thrombocytopenia and DIC, hyperparasitaemia (over 4 per cent in adults with imported malaria), haemoglobinuria (blackwater fever), shock (algid malaria, often with concomitant bacterial infection). Diagnosis: thick film (screening), thin film (species ID + parasitaemia quantification), rapid diagnostic test (antigen, an important addition to microscopy), PCR (reference standard). Treatment: IV artesunate 2.4 mg/kg at 0, 12, 24 h then daily — 34.7% mortality reduction vs quinine in Asia (SEAQUAMAT), 22.5% in African children (AQUAMAT). No routine exchange transfusion, steroids, mannitol, or anticonvulsant prophylaxis. Monitor for post-artemisinin delayed haemolysis (7-30 days, weekly Hb checks for a month).

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Tetanus and botulism in the ICU

Tetanus and botulism are rare but life-threatening toxin-mediated diseases caused by neurotoxins of Clostridium tetani and Clostridium botulinum respectively — two organisms that evolved strikingly opposite toxins from a shared ancestry. TETANUS: C. tetani exotoxin (tetanospasmin) travels by retrograde axonal transport to the spinal cord and brainstem, where it cleaves synaptobrevin (VAMP) and blocks release of the inhibitory neurotransmitters GABA and glycine → unopposed motor-neuron firing → severe muscle spasms (trismus/lockjaw, risus sardonicus, opisthotonus) and life-threatening autonomic instability. Management: HTIG (human tetanus immune globulin) given IM early to neutralise unbound toxin, surgical wound debridement to stop further toxin production, metronidazole IV to eradicate C. tetani (superior to procaine penicillin in direct comparison), titrated benzodiazepines (midazolam) and magnesium sulphate for spasm and autonomic control, ICU admission for airway protection, mechanical ventilation, and cardiovascular support. BOTULISM: C. botulinum toxin (also a synaptobrevin/SNAP-25/syntaxin-cleaving zinc-endopeptidase) blocks acetylcholine release at the neuromuscular junction → symmetric DESCENDING flaccid paralysis beginning with cranial-nerve palsies (diplopia, dysphagia, ptosis, dysarthria) with preserved sensorium and no fever, progressing to respiratory failure. Management: botulinum antitoxin (heptavalent HBAT for adults and children, human BIG-IV for infants), supportive care with NIV or intubation and prolonged ventilation (weeks-to-months), and source removal (wound debridement for wound botulism). Both demand ICU admission, meticulous supportive care, and an understanding of toxin pathophysiology that is heavily examined in the CICM/FFICM/EDIC vivas.

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Toxic shock syndrome in the ICU

Toxic shock syndrome (TSS) is a life-threatening toxin-mediated illness caused by SUPERANTIGEN-producing bacteria. STAPHYLOCOCCAL TSS: Staphylococcus aureus TSST-1 toxin from a localised mucosal or wound focus. STREPTOCOCCAL TSS: Streptococcus pyogenes (GAS) superantigens such as SpeA from invasive soft-tissue infection. Superantigens bypass normal MHC-restricted antigen presentation and directly engage MHC class II and the T-cell receptor, activating large numbers of T cells and releasing a cytokine avalanche that causes fever, vasodilatory shock, disseminated intravascular coagulation and multi-organ failure. Management: (1) Source control (remove tampon or packing, drain and debride infected tissue). (2) Antibiotics that suppress toxin production (clindamycin or linezolid) PLUS a cell-wall agent (anti-staphylococcal penicillin or cephalosporin, vancomycin where MRSA is prevalent). (3) Adjunctive high-dose IVIG in severe streptococcal TSS. (4) Aggressive organ support.

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neurocritical care

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Acute Raised Intracranial Pressure and Traumatic Brain Injury — Comprehensive Neurocritical Care

Raised intracranial pressure (ICP &gt;22 mmHg) after traumatic brain injury (TBI) is the most preventable cause of secondary brain damage and the central target of neurocritical care. The MONRO-KELLIE DOCTRINE is the foundation: the skull is a rigid box whose fixed volume holds BRAIN (~80%) + BLOOD (~10%) + CSF (~10%); an increase in one component REQUIRES an equal decrease in the others or ICP rises. CAUSES of raised ICP: trauma (extradural/subdural/intracerebral haematoma, contusions, cerebral oedema), tumour (mass effect + peritumoural oedema), infection (abscess, meningitis/encephalitis), hydrocephalus (CSF obstruction), and hepatic encephalopathy (cytotoxic oedema). CLINICAL FEATURES: headache, vomiting, progressive alteration of conscious…

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respiratory

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Acute Respiratory Distress Syndrome (ARDS) — Berlin Definition, Lung-Protective Ventilation, Proning, ECMO, and Phenotyping

Acute respiratory distress syndrome (ARDS) — a syndrome of acute, diffuse, inflammatory lung injury causing increased pulmonary vascular permeability, loss of aerated lung, and severe hypoxaemia. The 2012 Berlin Definition replaces AECC: (1) Timing — within 1 week of a known clinical insult or new/worsening respiratory symptoms; (2) Chest imaging — bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules (CT or CXR); (3) Origin of oedema — respiratory failure NOT fully explained by cardiac failure or fluid overload (objective assessment — echo — required if no clear risk factor); (4) Oxygenation — PaO2/FiO2 ratio measured with PEEP/CPAP &gt;=5 cmH2O: MILD 200-300 (inclusive), MODERATE 100-200, SEVERE &lt;100. Causes are DIRECT/pulmonary (pneumonia — most common, aspiration of gastric contents, pulmonary contusion, inhalation injury, near-drowning) or INDIRECT/extrapulmonary (sepsis — most common indirect, severe trauma/shock, acute pancreatitis, massive transfusion/TRALI, severe burns, drug overdose). Pathophysiology — diffuse alveolar damage: exudative phase (type I pneumocyte + capillary endothelial injury → protein-rich alveolar oedema → hyaline membranes), proliferative phase (type II pneumocyte proliferation, fibroblast infiltration), fibrotic phase. The 'baby lung' concept (Gattinoni) — the aerated lung in ARDS is small, not stiff; high tidal volumes overdistend the small healthy portion → volutrauma. Management PILLARS: (1) Treat the cause (antibiotics, source control). (2) Lung-protective ventilation (ARDSNet — Vt 6 mL/kg PREDICTED body weight, plateau pressure &lt;30 cmH2O, driving pressure &lt;15 cmH2O, permissive hypercapnia pH &gt;7.20). (3) PEEP optimisation (PEEP/FiO2 table, best compliance, oesophageal pressure). (4) Prone positioning (PROSEVA — &gt;=16 h/day for moderate-severe ARDS P/F &lt;150, ~50% relative mortality reduction). (5) Conservative fluid strategy (FACTT). (6) Corticosteroids (DEXA-ARDS — dexamethasone improves moderate-severe ARDS). (7) VV-ECMO for severe refractory ARDS (EOLIA). Neuromuscular blockade is NOT routine (ROSE). ARDS subphenotypes (Calfee 2014) — hyperinflammatory vs hypoinflammatory — differ in mortality and treatment response. Mortality ~35% overall (severe ~45%).

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Hypoxaemia Mechanisms — Comprehensive (5 Causes, A-a Gradient, Shunt vs V/Q Mismatch)

There are exactly FIVE mechanisms of hypoxaemia: (1) ventilation-perfusion (V/Q) MISMATCH — the commonest cause, which RESPONDS to oxygen; (2) SHUNT — blood bypasses ventilated alveoli, which does NOT respond to oxygen and needs PEEP; (3) DIFFUSION IMPAIRMENT — a thickened blood-gas barrier, which responds to oxygen and worsens with exercise; (4) HYPOVENTILATION — type 2 failure with a NORMAL A-a gradient; and (5) LOW INSPIRED PO2 — altitude. Two bedside discriminators separate them. The ALVEOLAR GAS EQUATION gives PAO2 = FiO2(Patm − PH2O) − PaCO2/RQ (~100 mmHg on room air), so the A-a GRADIENT (PAO2 − PaO2) is normal (&lt;15 young, &lt;25 elderly) in hypoventilation and low inspired PO2, and ELEVATED in V/Q mismatch, shunt, and diffusion impairment. The SHUNT EQUATION Qs/Qt = (CcO2 − CaO2)/(CcO2 − CvO2) is normally &lt;5% and >10% is significant. The definitive V/Q-mismatch-vs-shunt test is 100% FiO2 for 15 minutes: if PaO2 rises above ~350 mmHg the problem is V/Q mismatch (correctable), if it stays below ~350 mmHg there is a significant SHUNT (needs PEEP, proning, ECMO). The P/F RATIO (PaO2/FiO2) is the Berlin ARDS yardstick: &lt;300 mild, &lt;200 moderate, &lt;100 severe. Oxygenation indices rank severity: P/F ratio, A-a gradient, and the Oxygenation Index (OI = FiO2 × MAP × 100 / PaO2). The clinical approach is stepwise: (1) calculate the A-a gradient; (2) if elevated, get a chest X-ray and echocardiogram to localise the lung or heart problem; (3) treat the cause — oxygen for V/Q mismatch, PEEP/recruitment/proning for shunt, ventilation for hypoventilation.

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Oxygen Therapy and Oxygen Delivery — Comprehensive ICU Physiology

Oxygen therapy and delivery — the physiological principles governing oxygen movement from the atmosphere to the cell, and the ICU interventions to optimise it. The oxygen cascade: atmospheric PO2 (159 mmHg at FiO2 21%) → tracheal PO2 (149, after humidification) → alveolar PO2 (PAO2 ~100, after CO2 mixing — calculated by the ALVEOLAR GAS EQUATION: PAO2 = FiO2(Patm - PH2O) - PaCO2/RQ) → arterial PO2 (PaO2 ~95, after shunt/VQ mismatch) → capillary PO2 (40, after tissue extraction) → mitochondrial PO2 (1-3, for oxidative phosphorylation). Oxygen content: CaO2 = (1.34 × Hb × SaO2) + (0.003 × PaO2) — the HAEMOGLOBIN component dominates (>99% of total O2 content — dissolved O2 is negligible at normal pressures). Oxygen delivery: DO2 = CO × CaO2 × 10 — normal ~1000 mL/min. Oxygen consumption: VO2 = CO × (CaO2 - CvO2) × 10 — normal ~250 mL/min. O2 extraction ratio (ER) = VO2/DO2 — normal ~25% (the body extracts 25% of delivered O2 at rest). ICU management of hypoxaemia: increase FiO2 → increase Hb (transfuse) → increase CO (inotrope/fluid) → reduce shunt (PEEP, proning, recruit alveoli). Hyperoxia is HARMFUL (ROS, absorption atelectasis, coronary vasoconstriction) — titrate FiO2 to lowest setting maintaining SpO2 92-96%.

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Ventilator Waveforms — Comprehensive (Scalars, Loops, Asynchrony)

Ventilator waveforms — the graphical display of pressure, flow, and volume over time during mechanical ventilation. Three SCALAR waveforms (pressure-time, flow-time, volume-time) and two LOOPS (pressure-volume, flow-volume) provide real-time information about patient-ventilator interaction, lung mechanics, and asynchrony. VOLUME CONTROL: square flow waveform + decelerating pressure + linear volume rise. PRESSURE CONTROL: square pressure + decelerating flow + curvilinear volume rise. P-V LOOP: compliance (slope = ΔV/ΔP), inflection points (lower = recruitment opportunity, upper = overdistension). F-V LOOP: auto-PEEP (expiratory flow doesn't return to baseline before next inspiration), obstruction (concave expiratory limb). PATIENT-VENTILATOR ASYNCHRONY: trigger asynchrony (missed triggers, auto-triggering), flow asynchrony (double triggering — patient wants more flow than delivered), cycle asynchrony (premature/delayed cycling), expiratory asynchrony. Waveform analysis is a CRITICAL CICM exam skill — tested in vivas and SAQs.

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Ventilator-Induced Lung Injury (VILI) — Mechanisms and Prevention

Ventilator-induced lung injury (VILI) — the lung damage caused by mechanical ventilation itself, distinct from the underlying disease process. Four mechanisms: (1) Volutrauma (alveolar overdistension from excessive tidal volume or transpulmonary pressure → epithelial/endothelial disruption → inflammation), (2) Atelectrauma (repeated cyclic opening and closing of recruitable alveoli at low end-expiratory pressure → shear stress → injury), (3) Barotrauma (alveolar rupture from excessive airway pressure → pneumothorax, pneumomediastinum, subcutaneous emphysema), (4) Biotrauma (release of inflammatory mediators [cytokines, chemokines] from mechanically stressed lung → systemic spillover → MODS). Prevention: lung-protective ventilation — Vt 4-6 mL/kg predicted body weight, plateau pressure &lt;30 cmH2O, driving pressure (delta P = Pplat - PEEP) &lt;15 cmH2O, PEEP optimised to avoid atelectrauma, permissive hypercapnia. Additional targets: transpulmonary pressure (P_L = P_airway - P_esophageal) — oesophageal balloon manometry guides PEEP titration in obese/ARDS patients. The ARDSNet trial (2000) established Vt 6 mL/kg as standard — 22% relative mortality reduction vs 12 mL/kg. VILI is NOT limited to ARDS — it occurs in ANY mechanically ventilated patient — apply lung-protective ventilation universally.

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Domain

Pharmacology

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Acute respiratory distress syndrome: pharmacological therapies — comprehensive (neuromuscular blockade, inhaled vasodilators, corticosteroids, statins, beta-2 agonists, ECMO pharmacology, fluid management)

No specific pharmacological therapy reduces mortality in ALL ARDS patients. Foundation: lung-protective ventilation (ARMA — the proven mortality-reducing intervention), proning (PROSEVA), conservative fluids (FACTT). Selective pharmacotherapy: dexamethasone in moderate-severe ARDS within 24 h of onset (DEXA-ARDS — more ventilator-free days and lower 60-day mortality), 48-h cisatracurium only for severe ARDS (PaO2/FiO2 <150) with ventilator dyssynchrony (ACURASYS positive, ROSE negative), inhaled nitric oxide or epoprostenol as a bridge for refractory hypoxaemia (oxygenation only, no mortality benefit). Avoid: IV beta-2 agonists (BALTI-2 increased mortality), statins (HARP-2, SAILS), high-dose vitamin C (LOVIT composite harm), aspirin for ARDS prevention (LIPS-A).

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Acute severe community-acquired pneumonia: corticosteroid adjunct therapy

Corticosteroids as adjunct therapy in SEVERE CAP: immunomodulation of excessive inflammation. Evidence: CAPE COD trial (2023, NEJM) — hydrocortisone 200 mg/day IV for 4-7 days (with protocol tapering) reduced 28-day mortality in ICU severe CAP (6.2% vs 11.9%). Torres 2015 (JAMA) — methylprednisolone 0.5 mg/kg q12h for 5 days reduced treatment failure in severe CAP with CRP over 150 mg/L. Meta-analyses: reduced mortality in severe CAP, less need for mechanical ventilation, less ARDS, shorter time to clinical stability, at the cost of hyperglycaemia. Not supported: non-severe CAP, influenza (observational harm signal), fungal pneumonia. Separate indications: Pneumocystis pneumonia (consensus-endorsed adjunct) and COVID-19 (dexamethasone 6 mg daily up to 10 days, RECOVERY).

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Antiarrhythmics — Vaughan-Williams Classification

Antiarrhythmics — the Vaughan-Williams classification: Class I (the sodium channel blockers — Ia quinidine/procainamide [prolong AP + QT], Ib lidocaine/phenytoin [shorten AP, ischaemic-tissue selectivity], Ic flecainide/propafenone [markedly slow conduction, AVOID in structural heart disease — CAST]); Class II (the beta-blockers — metoprolol/esmolol/bisoprolol — slow AV node, reduce sympathetic); Class III (the potassium channel blockers — amiodarone [multichannel, half-life ~60 days, multi-organ toxicity], sotalol, ibutilide, dofetilide, dronedarone); Class IV (the calcium channel blockers — verapamil/diltiazem, non-dihydropyridine only); and the others (digoxin, adenosine, magnesium). Includes the Singh-Vaughan Williams mechanism, the Sicilian Gambit, each drug's indication/dose/adverse effects/contraindications/QT risk, and a full amiodarone toxicity deep dive (pulmonary, thyroid, hepatic, skin).

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Antibiotic pharmacokinetics in critical illness

Critical illness alters antibiotic pharmacokinetics (PK), often leading to sub-therapeutic levels and treatment failure. Key changes: (1) Increased volume of distribution (Vd) — capillary leak, fluid resuscitation, hypoalbuminaemia dilute water-soluble drugs (beta-lactams, aminoglycosides). (2) Augmented renal clearance (ARC) — young trauma/sepsis patients have increased renal blood flow → enhanced clearance of renally eliminated drugs → sub-therapeutic levels. (3) Organ failure — renal/hepatic impairment reduces clearance → accumulation → toxicity. (4) CRRT — removes drugs, need dose adjustment. (5) ECMO — sequesters drugs in circuit, increases Vd. Principles: give LOADING DOSE for severe infections (especially beta-lactams — target 4-5x MIC). Consider extended/continuous infusion for beta-lactams (time-dependent killing). Monitor levels (TDM) for vancomycin, aminoglycosides, beta-lactams.

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Anticoagulants & Antithrombotics — Pharmacology

Anticoagulants and antithrombotics — by mechanism of action. The indirect (heparins via antithrombin III), the direct (DTI, FXa), the vitamin K antagonist (warfarin). The antiplatelets (COX, P2Y12, GPIIb/IIIa). The PK/PD and the reversal. **UFH** (potentiates antithrombin III → inactivates IIa + Xa; aPTT monitoring; protamine reversal; short t1/2 60-90 min; safe in renal failure). **LMWH** (enoxaparin 1 mg/kg BD; anti-Xa monitoring; renal clearance; partial protamine reversal ~60%). **Warfarin** (vitamin K epoxide reductase inhibitor; INR target 2-3; slow onset days; teratogenic; food/drug interactions; vitamin K + PCC/FFP reversal; protein C depletion → skin necrosis → overlap heparin). **DOACs** — dabigatran (direct thrombin inhibitor; idarucizumab reversal; 80% renal), rivaroxaban/apixaban (factor Xa inhibitors; andexanet alfa reversal). **Antiplatelets** — aspirin (irreversible COX-1), clopidogrel (P2Y12), GPIIb/IIIa (abciximab, tirofiban). Indications: VTE treatment/prophylaxis, AF (CHA2DS2-VASc), mechanical valve (warfarin only), ACS. Bleeding risk (HAS-BLED), major bleeding management (stop drug, activated charcoal if recent, reversal agents, blood products).

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Antihypertensives — ACEi, ARB, CCB, Beta-blockers & Vasodilators

Antihypertensives — by mechanism: the RAS (ACEi — the bradykinin cough; the ARB); the CCB (the dihydropyridine — the amlodipine; the non-DHP — the verapamil/diltiazem); the beta-blockers (metoprolol β1-selective, labetalol α+β, esmolol ultra-short); the vasodilators (the SNP — the cyanide toxicity; the GTN; the hydralazine); the alpha-blockers (phentolamine — pheochromocytoma); the centrally acting (the methyldopa, the clonidine); the diuretics (furosemide — acute pulmonary oedema). ICU drug selection by indication: aortic dissection (beta-blocker first), intracerebral haemorrhage (nicardipine/clevidipine), pre-eclampsia (labetalol/hydralazine/nifedipine), eclampsia (magnesium sulfate).

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Antimicrobials (by Class) — Mechanisms, Spectrum & Resistance

Antimicrobials by class and mechanism: cell wall (beta-lactams, glycopeptides — bactericidal), protein synthesis (aminoglycosides 30S, macrolides 50S, tetracyclines 30S, linezolid 50S), DNA (fluoroquinolones DNA gyrase), RNA (rifampicin RNA polymerase), folic acid (trimethoprim/sulfamethoxazole). Time-dependent (beta-lactams, macrolides — T above MIC) vs concentration-dependent (aminoglycosides, fluoroquinolones — Cmax/MIC). PK/PD principles. Resistance mechanisms.

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Corticosteroids — Glucocorticoid & Mineralocorticoid Effects

Corticosteroids in the ICU — the glucocorticoid vs the mineralocorticoid potency, the molecular mechanism, and the disease-specific evidence. MECHANISM: the lipophilic steroid crosses the cell membrane → binds the cytosolic glucocorticoid receptor (GR, NR3C1) → heat-shock-protein dissociation → nuclear translocation → transactivation (GRE-driven anti-inflammatory genes — I-kB, annexin-A1/lipocortin-1, IL-10) and transrepression (GR monomer blocks NF-kB / AP-1 / STAT → downregulates IL-1, IL-2, IL-6, TNF-a); non-genomic effects at high dose. SPECTRUM: hydrocortisone (GC 1, MC 1, equiv 20 mg, short-acting) — physiological replacement, refractory septic shock, adrenal crisis, thyroid storm; prednisolone (GC 4, MC 0.6, equiv 5 mg) — oral immunosuppression, PJP, asthma/COPD; methylprednisolone (GC 5, MC 0.5, equiv 4 mg) — ARDS, autoimmune pulses, spinal-cord injury; dexamethasone (GC 25-30, MC 0, equiv 0.75 mg, long-acting) — cerebral oedema, COVID-19 (RECOVERY 6 mg), antenatal lung maturation, DEXA-ARDS, bacterial meningitis; fludrocortisone (MC 250) — mineralocorticoid replacement, the APROCCHSS septic-shock adjunct. INDICATIONS: septic shock (ADRENAL — hydrocortisone speeds shock reversal, no mortality benefit; APROCCHSS — hydrocortisone + fludrocortisone reduces mortality in SEVERE shock), ARDS (DEXA-ARDS — dexamethasone 20 mg x5d then 10 mg x5d; Meduri methylprednisolone), CAP (CAPE COD — hydrocortisone 200 mg/day; CAPO/Siemieniuk meta-analysis), thyroid storm (hydrocortisone 100 mg TDS blocks T4->T3), adrenal crisis (hydrocortisone 200 mg/day + fludrocortisone), anaphylaxis (adjunct only), asthma/COPD exacerbation, cerebral oedema (dexamethasone). STRESS-DOSE: hydrocortisone 50 mg q6h or 200 mg/24 h infusion in vasopressor-dependent shock; perioperative 100 mg at induction. ADVERSE: hyperglycaemia, immunosuppression, GI bleed, critical-illness myopathy (especially + NMBA), psychiatric effects, osteoporosis, and HPA-axis adrenal suppression after more than 2 weeks of more than 7.5 mg prednisolone equivalent — MUST taper.

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Diuretics — Loop, Thiazide, Potassium-Sparing & Osmotic

Diuretics — by site of action in the nephron. LOOP (furosemide, bumetanide, torasemide — inhibit the Na-K-2Cl [NKCC2] cotransporter in the thick ascending limb — the MOST POTENT class, blocking up to a quarter of filtered Na+). THIAZIDE (hydrochlorothiazide, chlorthalidone, indapamide, metolazone — inhibit the Na-Cl [NCC] cotransporter in the distal convoluted tubule — a smaller fraction of filtered Na+). POTASSIUM-SPARING (spironolactone/eplerenone — aldosterone/mineralocorticoid-receptor antagonists; amiloride/triamterene — ENaC blockers — cortical collecting duct). OSMOTIC (mannitol — filtered, not reabsorbed — osmotic water pull throughout the nephron; weight-based IV boluses reduce ICP). CARBONIC ANHYDRASE INHIBITOR (acetazolamide — proximal tubule — HCO3 loss → metabolic acidosis)

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Drug dosing in continuous renal replacement therapy (CRRT)

Drug dosing in CRRT is COMPLEX — many ICU patients receive CRRT, and incorrect dosing causes treatment failure (underdosing) or toxicity (overdosing). Pharmacokinetic changes in CRRT: altered volume of distribution (Vd), changed clearance (CRRT adds extracorporeal clearance), residual renal function. Factors affecting CRRT clearance: modality (CVVH, CVVHD, CVVHDF), effluent flow rate, membrane type (cutoff), filter age. Drugs affected: antibiotics (beta-lactams, vancomycin, aminoglycosides, linezolid), anticoagulants, antiepileptics. Principles: (1) Hydrophilic drugs (beta-lactams, aminoglycosides, vancomycin) — removed by CRRT, need higher/dose more frequently. (2) Lipophilic drugs (fluoroquinolones, macrolides, azoles) — less removed. The sieving coefficient (Sc ≈ 1 for small unbound drugs) and effluent flow rate together determine CRRT clearance (Cl_CRRT = Sc × Qeff). KDIGO recommends effluent dose 20–25 mL/kg/h after accounting for downtime. Loading doses are unchanged; maintenance doses are increased and individualised with therapeutic drug monitoring (TDM) for vancomycin, beta-lactams and aminoglycosides.

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Electrolyte Therapy — Sodium, Potassium, Magnesium, Calcium & Phosphate

Electrolyte therapy in the ICU: sodium (hyponatraemia - 3% saline 100 mL boluses for severe symptomatic, correction capped at 10 mmol/L in the first 24 h, osmotic demyelination risk; hypernatraemia - free-water deficit, correct no faster than 0.5 mmol/L per hour), potassium (rate-limited IV replacement, never a bolus, fix Mg first; hyperkalaemia - calcium stabilise, then insulin/dextrose with salbutamol shift, then remove), magnesium (MgSO4 4 g load + 1-2 g/h; hypermagnesaemia - stop infusion, dialysis if severe), calcium (treat the ionised fraction; hypocalcaemia - IV calcium for symptomatic; hypercalcaemia - hydration + bisphosphonate, zoledronate 4 mg), phosphate (hypophosphataemia - respiratory muscle weakness, IV replacement when severe, refeeding syndrome prevention with thiamine and electrolyte monitoring).

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ICU antiarrhythmic drugs — comprehensive (Vaughan-Williams classification)

Antiarrhythmic drugs classified by the Vaughan-Williams system: Class I (sodium channel blockers — Ia quinidine/procainamide [prolong AP + QT], Ib lidocaine/phenytoin [shorten AP, ischaemic-tissue selectivity], Ic flecainide [markedly slow conduction, AVOID in structural heart disease — CAST]); Class II (beta-blockers — metoprolol/esmolol/bisoprolol — reduce sympathetic drive, slow AV node); Class III (potassium channel blockers — amiodarone [MOST effective ICU antiarrhythmic, broad-spectrum multichannel but long half-life ~60 days + pulmonary/hepatic/thyroid toxicity], sotalol [also beta-blocker], ibutilide, dronedarone); Class IV (calcium channel blockers — verapamil/diltiazem — AV node only, non-dihydropyridine). Other: adenosine [AV node reentry — terminates SVT 6mg then 12mg rapid IV push, brief asystole], digoxin [vagomimetic — rate control AF in heart failure], magnesium [torsades — IV]. Clinical applications: AF (rate control = beta-blocker/diltiazem/digoxin; rhythm = amiodarone/flecainide), VT (amiodarone 300mg IV then infusion; lidocaine for ischaemic VT), SVT (adenosine first-line), torsades (magnesium 2g IV).

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ICU medication safety: prescribing errors, drug interactions, and prevention

ICU medication safety: critically ill patients receive 10-20+ medications simultaneously → high risk across all FIVE stages of the medication-use process (prescribing → transcribing → dispensing → administration → monitoring). Reported ICU medication-error rates vary widely across studies (8.1–2344 per 1000 patient-days) and serious or life-threatening harm is uncommon (1–5% of medication errors). Common errors: (1) WRONG DRUG (LASA — dopaMINE vs DOBUTamine, HYDROmorphone vs morphine, KCl vs NaCl). (2) WRONG DOSE (renal/hepatic adjustment missed — vancomycin, beta-lactams, gabapentin). (3) WRONG ROUTE (IV potassium bolus — fatal; intrathecal vincristine). (4) DRUG INTERACTIONS (QT — azithromycin + ondansetron; CYP3A4 — azoles + tacrolimus; serotonin — SSRIs + linezolid). (5) DUPLICATE THERAPY (two antiplatelets, two PPIs). HIGH-ALERT medications (insulin, anticoagulants, opioids, sedatives, neuromuscular blockers, concentrated electrolytes, vasopressors) demand standardisation, independent double-checks, and closed-loop technology — CPOE with decision support (55% fewer serious medication errors), barcode administration (41% fewer administration errors), smart pumps. Prevention: pharmacist on ICU rounds (66% fewer preventable prescribing ADEs), medication reconciliation at every transition (45% fewer medication discrepancies), and a no-blame reporting culture.

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ICU vasopressor and inotrope pharmacology — comprehensive (catecholamines, vasopressin, inodilators)

Vasopressors increase blood pressure (vasoconstriction) and inotropes increase cardiac output (contractility). First-line vasopressor in septic shock: NORADRENALINE — Surviving Sepsis 2021 strong recommendation (alpha-1 vasoconstriction with modest beta-1, minimal heart-rate effect). CAT (Myburgh 2008) and Annane (Lancet 2007) showed adrenaline is equivalent for mortality but carries transient metabolic (lactate) effects. Add vasopressin at a FIXED 0.03 U/min (V1 receptor, catecholamine-sparing per VASST/VANISH) instead of escalating noradrenaline when the dose reaches 0.25-0.5 mcg/kg/min. Adrenaline is the third-line add-on. Dobutamine for cardiac dysfunction with persistent hypoperfusion. Dopamine is not preferred: SOAP II found more arrhythmias (24.1% vs 12.4%) and no renal protection from low-dose dopamine (Bellomo 2000).

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Insulin & Hypoglycaemics — Pharmacology

ICU insulin and hypoglycaemics. INSULIN TYPES classified by onset/duration: RAPID analogues (lispro, aspart, glulisine — monomeric — onset 10-20 min, duration 3-5 h); SHORT/soluble (regular/Actrapid — forms hexamers — onset 30-60 min, duration 6-8 h — the IV preparation for ICU); INTERMEDIATE (isophane/NPH — protamine + zinc complex — cloudy — onset 1-2 h, duration 12-18 h); LONG (glargine — precipitates at neutral pH, flat peakless ~24 h; detemir — albumin-bound via myristic acid); ULTRA-LONG (degludec — multi-hexamers, 42+ h; icodec weekly). ICU INSULIN USE: DKA fixed-rate insulin infusion (FRII) 0.1 U/kg/h until ketones cleared; HHS lower dose 0.05 U/kg/h after aggressive fluid resuscitation; stress hyperglycaemia via variable-rate insulin infusion (VRII / sliding scale) targeting moderate control per NICE-SUGAR (conventional target 10.0 mmol/L or less) (moderate control — tight control 4.5-6.0 increased mortality, overturning the Leuven trial); insulin-dextrose for hyperkalaemia (intracellular K shift); GIK high-dose insulin for beta-blocker/calcium-channel-blocker toxicity. ORAL HYPOGLYCAEMICS: METFORMIN (biguanide — activates AMP kinase — suppresses hepatic gluconeogenesis — non-hypoglycaemic — UKPDS-34 mortality benefit in overweight T2DM — metformin-associated lactic acidosis (MALA) in renal failure/hypoxia/sepsis — removed by haemodialysis); SULFONYLUREAS (gliclazide, glibenclamide — close beta-cell K-ATP channel — stimulate insulin release — hypoglycaemia risk, especially glibenclamide/elderly/renal); DPP-4 inhibitors (sitagliptin — prolong incretins, glucose-dependent, weight-neutral, CV-safe per TECOS); SGLT2 inhibitors (dapagliflozin, empagliflozin — block Na-glucose cotransporter in proximal tubule — glycosuria — CV/renal benefit (EMPA-REG, CANVAS, CREDENCE) — euglycaemic DKA risk); GLP-1 agonists (exenatide, liraglutide, semaglutide — incretin mimetics — weight loss — CV benefit per LEADER/SUSTAIN-6). HYPOGLYCAEMIA MANAGEMENT: rule of 15 (15 g carbohydrate, recheck at 15 min); severe — IV dextrose (50% is vesicant) and glucagon 1 mg IM; octreotide 50 mcg SC every 6 h for sulfonylurea-induced hypoglycaemia (inhibits insulin secretion).

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Malignant hyperthermia

Malignant hyperthermia is a pharmacogenetic emergency triggered by volatile anaesthetic agents (sevoflurane, isoflurane, desflurane, halothane) or suxamethonium (succinylcholine). Mutated ryanodine receptor (RYR1) causes uncontrolled calcium release from skeletal muscle sarcoplasmic reticulum → sustained muscle contraction → massive heat production, rhabdomyolysis, hyperkalaemia, acidosis. Presents during or after anaesthesia: rapid rise in end-tidal CO2 (unexplained), tachycardia, masseter spasm, hyperthermia (late sign), rigidity, dark urine (myoglobinuria). Treatment: STOP TRIGGER, hyperventilate with 100% O2, DANTROLENE 2.5 mg/kg IV (repeat to 10 mg/kg), cooling, treat hyperkalaemia/acidosis. Mortality &lt;5% with prompt dantrolene (was over 80% before dantrolene).

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Medication safety in ICU: prescribing errors, high-alert drugs, prevention, and drug interactions

Medication errors and adverse drug events are common and under-reported in the ICU — a systematic review found medication-error rates of 8.1 to 2344 per 1000 patient-days and adverse drug events of 5.1 to 87.5 per 1000 patient-days, varying widely with definitions and detection methods. Critically ill patients are uniquely vulnerable: 10-20+ concurrent drugs, altered pharmacokinetics (renal/hepatic dysfunction, augmented clearance, changed volume of distribution), organ support (ventilator, vasopressors, RRT), and restricted ability to report symptoms. Key interaction families: macrolides + statins (rhabdomyolysis), fluoroquinolones + QT-prolonging drugs (Torsades), warfarin + antibiotics (INR elevation/bleeding), linezolid + serotonergic drugs (serotonin syndrome), azoles + calcineurin inhibitors (CYP3A4 toxicity). High-alert medications (insulin, anticoagulants, opioids, sedatives, neuromuscular blockers, concentrated electrolytes, vasoactives) cause disproportionate harm when misused. Prevention is layered: computerised physician order entry (CPOE) with clinical decision support, barcode medication administration (BCMA), smart infusion pumps with drug libraries, standardised order sets and concentrations, tall man lettering, independent double-checks of high-alert drugs, pharmacist-led review and medication reconciliation, and therapeutic drug monitoring (vancomycin AUC-guided, aminoglycoside extended-interval, digoxin, antiepileptics).

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Therapeutic plasma exchange (plasmapheresis) in ICU

Therapeutic plasma exchange (TPE) removes pathogenic macromolecules (autoantibodies, immune complexes, cryoglobulins, light chains, lipoproteins) from plasma by centrifugation or membrane filtration, replacing with donor plasma or albumin. Evidence-backed ICU indications: Guillain-Barre syndrome, myasthenia gravis exacerbation, thrombotic thrombocytopenic purpura, Goodpasture (anti-GBM) disease, severe ANCA vasculitis, hyperviscosity of Waldenstrom macroglobulinemia. Exchange regimens come from the pivotal trials: five 50 mL/kg exchanges over 8-13 days (GBS), seven exchanges within 14 days (ANCA), exchange on seven of the first nine days (TTP). Replacement fluid: albumin adequate for GBS (FFP added morbidity); plasma-containing exchange for TTP. Complications of regional citrate: hypomagnesaemia 45.6%, hypocalcaemia 17.9%, metabolic alkalosis 14.8% of sessions — monitor ionised calcium.

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Toxicology Antidotes — ICU

ICU toxicology antidotes organised by toxin: naloxone (opioids), flumazenil (benzodiazepines - caution seizures), N-acetylcysteine (paracetamol - nomogram-driven), digoxin Fab (life-threatening digoxin toxicity), atropine + pralidoxime (organophosphates - before aging), fomepizole/ethanol (methanol/ethylene glycol - alcohol dehydrogenase inhibition), sodium bicarbonate (TCA Na-channel blockade + salicylate urine alkalinisation), methylene blue (methaemoglobinaemia - NOT G6PD), hydroxocobalamin/sodium thiosulfate/dicobalt EDTA (cyanide), calcium + high-dose insulin euglycaemia therapy + lipid emulsion (CCB/BB), octreotide (sulfonylurea), deferoxamine (iron), succimer/EDTA/BAL (lead), folinic acid/leucovorin (methotrexate), vitamin K/PCC/andexanet/idarucizumab (warfarin and DOAC reversal), protamine (heparin), oxygen/hyperbaric (carbon monoxide). Lipid rescue therapy for lipophilic drug overdose.

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Acute severe alcohol withdrawal and delirium tremens: CIWA-Ar, benzodiazepines, and Wernicke

Alcohol withdrawal syndrome (AWS) = symptoms occurring when a chronic alcohol-dependent person STOPS or REDUCES alcohol intake. SPECTRUM: begins 6-24h after last intake (tremor, anxiety, insomnia, nausea, sweating) → hallucinations (12-24h) → seizures (12-48h, up to 15% of patients) → DELIRIUM TREMENS (DTs — typically around 72h after last intake, occurs in 3-5% of withdrawal patients — confusion, hallucinations, autonomic hyperactivity [tachycardia, hypertension, fever, diaphoresis] — mortality as high as 50% without recognition or prompt treatment). PATHOPHYSIOLOGY: chronic alcohol → BRAIN ADAPTS (downregulates inhibitory GABA receptors + upregulates excitatory NMDA receptors) → when alcohol REMOVED → GABA UNDERACTIVE (loss of inhibition) + GLUTAMATE OVERACTIVE (excessive excitation) → hyperexcitable brain → tremor → seizures → DTs. MANAGEMENT: (1) BENZODIAZEPINES (front-line — restore GABA tone — diazepam/lorazepam — symptom-triggered or fixed-schedule). (2) THIAMINE with or before glucose (prevents Wernicke — ICU day-1 supplementation 200-500 mg IV every 8h). (3) ELECTROLYTE/VITAMIN correction (magnesium 64 mg/kg, folate 400-1000 mcg IV). (4) PHENOBARBITAL 10 mg/kg IV (severe or refractory). (5) SUPPORTIVE (exclude sepsis and co-morbidity, ICU for severe DTs).

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Acute severe poisonings: decontamination, antidotes, and enhanced elimination

A systematic approach to the poisoned patient: RESUSCITATE (ABC, oxygenation, ventilation, circulation — toxins cause coma, seizures, arrhythmia, hypotension), then DECONTAMINATION (reduce absorption — activated charcoal within 1h, whole bowel irrigation for sustained-release/iron/packets, gastric lavage rarely for life-threatening ingestions &lt;1h), ENHANCED ELIMINATION (multi-dose activated charcoal, urinary alkalinisation for salicylates, haemodialysis for toxic alcohols/salicylates/lithium/metformin), ANTIDOTES (specific — naloxone opioids, NAC paracetamol, flumazenil benzos [caution], atropine/pralidoxime organophosphates, digoxin Fab, fomepizole toxic alcohols, hydroxocobalamin cyanide, octreotide sulfonylureas, glucagon beta-blockers/CCB, lipid emulsion lipophilic drugs). ALWAYS: check paracetamol + salicylate levels, ECG, glucose, temperature; call poison centre; observe for delayed toxicity (sustained-release).

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Alcohol withdrawal and delirium tremens

Alcohol withdrawal symptoms typically begin 6-24 h after cessation/reduction of alcohol intake. Stages: minor withdrawal (tremor, anxiety, insomnia), seizures (12-48 h after last intake, in up to 15% of patients), hallucinosis (12-24 h, in 2-8%), delirium tremens (typically around 72 h; occurs in 3-5% of withdrawal patients — confusion, agitation, autonomic hyperactivity; untreated mortality can be as high as 50%). Pathophysiology: chronic ethanol down-regulates inhibitory GABA receptors and up-regulates excitatory NMDA receptors; abrupt cessation produces CNS hyperexcitability — the basis of seizures, hallucinosis and DTs. Management: benzodiazepines are the gold standard — symptom-triggered (scale-guided) dosing is favoured over fixed tapering; give thiamine before/with glucose; add phenobarbital (10-15 mg/kg IV weight-based loading) when benzodiazepines are insufficient; dexmedetomidine only as an adjunct for sympathetic overactivity.

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Anticoagulant & Rodenticide (Warfarin & Superwarfarin) Poisoning

The vitamin-K-antagonist anticoagulant poisoning — the therapeutic **warfarin** (a half-life measured in days) and the **superwarfarin** (the long-acting anticoagulant rodenticide — the brodifacoum, the bromadiolone — persisting for weeks to months). The inhibition of the vitamin-K-epoxide reductase (the VKORC1) — the impaired the gamma-carboxylation of the factors II, VII, IX, X and the proteins C and S — the coagulopathy. The bleeding. The **vitamin K** (the phytomenadione), the **4-factor prothrombin-complex concentrate** for the active bleeding, and the prolonged (the weeks-to-the-months) vitamin K for the superwarfarin.

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Beta-Blocker & Calcium-Channel-Blocker Overdose

The cardiovascular drug overdose — the beta-blocker (the bradycardia, the AV block, the negative inotropy) and the calcium-channel-blocker (the non-dihydropyridine — the verapamil, the diltiazem — like the beta-blocker; the dihydropyridine — the amlodipine — the vasodilation). The **high-dose insulin / euglycaemia therapy (the HIET)** is the cornerstone for the severe. The calcium, the glucagon, the vasopressors, the lipid emulsion, the pacing and the ECMO. The CCB the **hyperglycaemia** (the blocked insulin release) — a marker of severity.

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Beta-blocker and calcium channel blocker overdose

Beta-blocker (BB) and calcium channel blocker (CCB) overdose are life-threatening poisonings with high mortality (4 of 15 patients died in an Australian CCB series; verapamil or diltiazem doses over 300 mg carry a significant risk of death). Both cause: bradycardia, hypotension, AV block, and (CCBs) hyperglycaemia from inhibited insulin secretion. Pathophysiology: BBs block beta-adrenergic receptors (reduced cAMP → reduced inotropy/chronotropy). CCBs block L-type calcium channels (reduced calcium influx → reduced inotropy, vasodilation, impaired pancreatic insulin release). Management: ABCDE plus specific antidotes added to standard ACLS. Key treatments: (1) IV calcium (chloride or gluconate, repeated as required). (2) High-dose insulin euglycaemia therapy (HIET — insulin 1 U/kg bolus plus 0.5 to 1 U/kg/h infusion, titrated up to 10 U/kg/h, with dextrose to maintain euglycaemia). (3) Vasopressors — noradrenaline and/or adrenaline are consensus first-line. (4) Glucagon (moderate inotropic benefit, mainly in BB overdose). (5) Intravenous lipid emulsion for refractory toxicity. (6) VA-ECMO for refractory shock or arrest.

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Carbon Monoxide & Cyanide Poisoning

The two tissue-asphyxiant poisonings — the **carbon monoxide** (binds haemoglobin with roughly 210 times the affinity of oxygen and impairs oxygen DELIVERY) and the **cyanide** (the metabolic poison that halts cellular oxygen UTILISATION). The pulse oximetry the falsely-normal in the CO. The 100 per cent oxygen (the CO half-life about 5 hours on air falls to about 1 hour) and the **hyperbaric oxygen** (half-life about 20 min) for the severe CO; the **hydroxocobalamin** 5 g IV for the cyanide (the antidote of choice in smoke inhalation). The **delayed neurological sequelae** in 15 to 40 per cent.

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Carbon monoxide poisoning

Carbon monoxide (CO) is an odourless, colourless gas produced by incomplete combustion (faulty heaters, house fires, car exhausts, generators, barbecues used indoors). CO binds haemoglobin with 210x affinity of oxygen, forming carboxyhaemoglobin (COHb), causing tissue hypoxia via THREE mechanisms: (1) functional anaemia, (2) LEFT shift of oxyhaemoglobin dissociation curve (impaired tissue O2 release), (3) histotoxic hypoxia (CO binds myoglobin + inhibits mitochondrial cytochrome c oxidase / cytochrome a3 / Complex IV → anaerobic metabolism → lactate). Presentation: headache, nausea, dizziness, confusion (flu-like) — 'flu-like illness in MULTIPLE people from the SAME household in WINTER = CO until proven otherwise.' Severe: syncope, seizures, coma, cardiovascular collapse, death. Diagnosis: COHb level (venous blood gas — NOT SpO2 which is FALSELY NORMAL because pulse oximetry cannot distinguish COHb from oxyhaemoglobin). Treatment: 100% oxygen via non-rebreather (reduces CO half-life from about 5 hours on room air to about 1 hour). Hyperbaric oxygen (HBO) for severe cases (high COHb, unconscious, pregnant, cardiac ischaemia, neurological signs) — reduces CO half-life to about 20 minutes. Delayed neurological sequelae occur in 15-40% of patients after a lucid interval of days to weeks (cognitive impairment, parkinsonism) — may be permanent.

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Decompression illness and diving emergencies

Decompression illness (DCI) is the umbrella term for the two bubble-mediated injuries of ascent: decompression sickness (DCS — 'the bends', from nitrogen bubble formation in tissues during ascent driven by inert-gas supersaturation and Henry's law) and arterial gas embolism (AGE — alveolar gas forced into arterial circulation from pulmonary barotrauma of ascent). DCS types: Type 1 (mild — musculoskeletal joint pain 'the bends', skin marbling/mottling 'skin bends', lymphatic swelling). Type 2 (serious — neurological: spinal cord involvement is the MOST SERIOUS form with progressive weakness, paraesthesia, sensory level, bladder/bowel dysfunction; cardiopulmonary 'the chokes': substernal chest pain, cough, dyspnoea, haemoptysis; vestibular 'the staggers': vertigo, nystagmus, nausea, tinnitus, hearing loss; cerebral: headache, visual disturbance, confusion, hemiparesis). AGE: stroke-like cerebral symptoms (hemiparesis, aphasia, seizure, coma) DURING or within minutes of surfacing from pulmonary barotrauma — breath-holding or rapid ascent over-expands alveoli → alveolar rupture → gas enters pulmonary veins → left heart → systemic arteries. Onset: AGE within minutes; DCS usually within minutes-to-hours, 98% within 24 h. Management is identical for both: 100% oxygen immediately (denitrogenates tissues — creates maximal gradient for nitrogen washout from bubbles), IV isotonic glucose-free fluids (correct immersion diuresis and dehydration), and DEFINITIVE recompression therapy — hyperbaric oxygen, US Navy Treatment Table 6 (100% oxygen at 2.8 ATA / 18 m / 60 fsw), which shrinks bubbles by Boyle's law (to ~one-third of surface volume), oxygenates ischaemic tissue by Henry's law (~6 vol% dissolved O2 in plasma at 2.8 ATA), and accelerates inert-gas washout. Contact Divers Alert Network (DAN) 24-h hotline for chamber location and retrieval. Early HBOT improves outcomes — recompress as soon as feasible.

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Dermatological emergencies in ICU: SJS, TEN, and DRESS

Severe cutaneous adverse reactions (SCAR) requiring ICU admission. SJS/TEN: immune-mediated epidermal necrolysis, drug-induced in 65-75% of cases (Mycoplasma and other infections account for most of the rest). Mucocutaneous: target lesions, bullae, sheet-like epidermal detachment. SJS &lt;10% BSA detachment, SJS-TEN overlap 10-30%, TEN >30%. High mortality (SJS ~10%, TEN ~30%). DRESS (DIHS): delayed hypersensitivity (median 22 days post-exposure), rash + fever + lymphadenopathy + eosinophilia + organ dysfunction (hepatitis, nephritis, pneumonitis). Treatment: STOP culprit drug, supportive care (fluid, nutrition, temperature control, analgesia, infection prevention), ICU for TEN (fluid loss like burn, airway involvement), IVIG controversial, debridement controversial, ophthalmology early.

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Digoxin toxicity in the ICU

Digoxin toxicity is a life-threatening condition from excessive digoxin (cardiac glycoside). Clinical features: (1) CARDIAC: arrhythmias (atrial tachycardia with block, premature ventricular contractions, bradycardia, AV block, ventricular fibrillation, bidirectional VT). (2) GI: nausea, vomiting, anorexia, diarrhoea. (3) CNS: confusion, visual disturbances (yellow/green vision — xanthopsia, blurred), weakness. (4) ELECTROLYTE: HYPERKALAEMIA (digoxin inhibits Na-K ATPase → K+ leaks out of cells). Diagnosis: clinical + elevated serum digoxin + ECG changes. Treatment: (1) DigiFab (digoxin-specific antibody fragments) — specific antidote. Indications: life-threatening tachy- or bradyarrhythmias, hyperkalaemia (K over 6 mmol/L), or haemodynamic instability with an elevated digoxin concentration. (2) Correct hyperkalaemia (insulin-dextrose — calcium is not recommended). (3) Atropine / pacing for bradycardia. (4) Magnesium for ventricular arrhythmia. AVOID IV calcium ('stone heart' — controversial).

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Envenomation — Snake, Spider & Marine (ANZ)

The Australian envenomation — the **snake** (the elapid — the brown, the tiger, the taipan, the death adder; the venom-induced consumption coagulopathy / the VICC, the neurotoxicity, the myotoxicity, the sudden collapse), the **spider** (the funnel-web — the robustoxin, the life-threatening; the redback — the latrotoxin, the painful), and the **marine** (the box jellyfish — the cardiotoxic; the blue-ringed octopus — the tetrodotoxin paralysis). The **pressure-immobilisation**, the **venom detection kit**, the **antivenom**. The ANZ (the CICM) emphasis.

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Ethanol Toxicity & Alcohol Withdrawal (Delirium Tremens)

The ethanol — the acute intoxication, the chronic effects (the Wernicke-Korsakoff), and the **alcohol withdrawal syndrome**. The withdrawal timeline (symptoms beginning within 4 to 6 h of the last drink, seizures typically 6 to 48 h after cessation, and **delirium tremens** as the severe late end). The CIWA-Ar and the symptom-triggered benzodiazepine. The **thiamine before carbohydrate** (the Wernicke encephalopathy). The electrolyte caution (refeeding, beer potomania) and the refractory-escalation ladder (phenobarbital, dexmedetomidine, propofol, ketamine).

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Heat stroke and hyperthermia in the ICU

Heat stroke is a life-threatening condition defined by core temperature >40C with CNS dysfunction (confusion, seizures, coma). Two types: EXERTIONAL (young, healthy, exercise in heat — e.g., athlete, military) and NON-EXERTIONAL/CLASSIC (elderly, chronic disease, during heatwaves). Pathophysiology: thermoregulatory failure → direct thermal cellular damage (protein denaturation, membrane injury) + systemic inflammatory response (cytokine cascade resembling sepsis) → multi-organ failure (brain, heart, liver, kidney, muscle, coagulation/DIC). Management: RAPID COOLING (target &lt;39C within 30-60 min) — cold water immersion gold standard for exertional, evaporative (mist + fans) for non-exertional, stop aggressive cooling at 38.5-39C. Antipyretics INEFFECTIVE (not prostaglandin-mediated). Dantrolene INEFFECTIVE (not malignant hyperthermia). Mortality 10-50%.

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Iron, Lead & Heavy Metal Poisoning

The heavy-metal poisonings — the **iron** (the four phases, the deferoxamine), the **lead** (the abdominal pain, the microcytic anaemia with the basophilic stippling, the peripheral neuropathy, the encephalopathy; the succimer, the EDTA, the dimercaprol), the **arsenic** (the garlic breath, the GI, the neuropathy, the QT), the **mercury** (the neuro, the tremor, the GI), the **cadmium** (the pneumonitis). The common theme the **chelation** (the deferoxamine for the iron; the dimercaprol/BAL, the succimer/DMSA, the CaNa2EDTA for the lead and the others).

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Lithium Toxicity

The lithium toxicity — the **narrow therapeutic index** (the therapeutic 0.6 to 1.2 mmol/L), the renal clearance (the handled like the sodium), and the no antidote. The **acute overdose** (the early GI, the delayed neuro) versus the **chronic toxicity** (the neuro-dominant, the more dangerous — the tremor, the hyperreflexia, the ataxia, the seizures, the coma, the SILENT). The charcoal the not-bind; the **whole-bowel irrigation** for the sustained-release; the **normal saline** (the restore the GFR, the NOT the diuretics); the **haemodialysis** for the severe (with the rebound).

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Methaemoglobinaemia: methylene blue, G6PD deficiency, and co-oximetry

Methaemoglobinaemia = haemoglobin iron oxidised from Fe2+ (ferrous — oxygen-carrying) to Fe3+ (ferric — CANNOT carry oxygen) → functional anaemia + left-shifted oxyhaemoglobin curve (impaired oxygen release to tissues). CAUSES: ACQUIRED (drugs — benzocaine, dapsone, nitrates, primaquine, local anaesthetics, metoclopramide, sulfonamides) or CONGENITAL (haemoglobin M disease, cytochrome b5 reductase deficiency — rare). CLINICAL: CYANOSIS (NOT responsive to oxygen — 'chocolate brown' blood), headache, dyspnoea, fatigue → at MetHb >30%: confusion, arrhythmia, seizures → >70%: death. DIAGNOSIS: CO-OXIMETRY (multi-wavelength — directly measures MetHb — standard ABG machines with co-oximetry). PULSE OXIMETRY: reads ~85% (plateaus — inaccurate — MetHb absorbs at both 660nm + 940nm — confuses the pulse oximeter). 'GAP' between SpO2 (pulse) and SaO2 (ABG co-oximetry). MANAGEMENT: (1) STOP causative agent. (2) METHYLENE BLUE 1-2 mg/kg IV over 5 min (reduces MetHb via NADPH methaemoglobin reductase — FAST — works within minutes). (3) AVOID in G6PD DEFICIENCY (methylene blue requires NADPH — G6PD deficient can't generate NADPH → methylene blue is INEFFECTIVE + may cause HAEMOLYSIS [it's an oxidant when NADPH is absent]). (4) ALTERNATIVES (G6PD deficient): ASCORBIC ACID (vitamin C — reduces MetHb — slower), exchange transfusion (severe). (5) SUPPORTIVE: oxygen (maintains remaining normal Hb saturation), RBC transfusion (if severe — adds functional Hb).

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NSAID, Opioid & Sedative-Hypnotic Overdose

The overdose of the NSAIDs, the opioids and the sedative-hypnotics (the benzodiazepines, the barbiturates, the Z-drugs). The opioid toxidrome (the coma, the miosis, the respiratory depression, the hypotension) and the **naloxone** (the competitive mu-antagonist, the titrated-to-respiratory-effort, the half-life mismatch with the long-acting opioids and the relapse and the infusion). The benzodiazepine and the sedative-hypnotic overdose (the CNS depression, the flumazenil and the seizure caution). The NSAID overdose (the usually-mild, the seizures and the renal injury in the large).

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Opioid overdose and toxicity

Opioid overdose causes respiratory depression (medullary respiratory centre depression), miosis (pinpoint pupils), and decreased level of consciousness — the classic triad. Fentanyl is about 100 times more potent than morphine and increasingly implicated in overdose deaths. Management: naloxone (opioid receptor antagonist) — titrate to respiratory rate (NOT full alertness). Avoid precipitating acute withdrawal in chronic users. Long-acting opioids (methadone, fentanyl patches) require prolonged monitoring or naloxone infusion. Non-cardiogenic pulmonary oedema can occur after naloxone reversal.

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Paracetamol (Acetaminophen) Overdose

Paracetamol (acetaminophen) overdose — the commonest overdose and a leading cause of the acute liver failure. The metabolism to the toxic NAPQI via the CYP2E1 and the detoxification by the glutathione; the depletion of the glutathione in the overdose and the centrilobular hepatocyte necrosis. The clinical course (the four phases). The Rumack-Matthew nomogram and the treatment line. The N-acetylcysteine (the NAC) — the antidote that replenishes the glutathione, its timing (the effective within 8 hours), and the rate-related anaphylactoid reactions. The King's College criteria for the liver transplant. The management of the staggered and the massive ingestion.

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Recreational & Novel Psychoactive Substances

The recreational and the novel psychoactive substances (the NPS — the 'legal highs', the 'designer drugs') — the **MDMA/ecstasy** (the serotonin syndrome, the SIADH/hyponatraemia from the excessive the water intake, the hyperthermia/the rhabdomyolysis), the **GHB/GBL** (the rapid-resolving the coma), the **synthetic cannabinoids** (the Spice/K2 — the seizures and the psychosis and the AKI), the **synthetic cathinones** (the 'bath salts' — the sympathomimetic), the **novel benzodiazepines**, the **novel synthetic opioids** (the nitazenes — the very potent, the high-dose naloxone), the **ketamine** (the dissociative, the chronic-use cystitis), the **NBOMe** and the **novel psychedelics**. The unreliable history; the supportive + the benzodiazepine-first management.

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Salicylate Poisoning

Salicylate (aspirin) poisoning — the uncoupling of the oxidative phosphorylation and the direct stimulation of the medullary respiratory centre producing the classic mixed respiratory alkalosis and the high-anion-gap metabolic acidosis. The clinical features (the tinnitus, the hyperpnoea, the hyperthermia, the pulmonary oedema, the seizures). The decontamination, the **urinary alkalinisation** (the sodium bicarbonate to a urine pH of 7.5 to 8.0 — the ion-trapping of the weak acid), and the **haemodialysis** for the severe (the EXTRIP criteria). The danger of the intubation without the maintenance of the hyperventilation.

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Serotonin Syndrome & Neuroleptic Malignant Syndrome

The two drug-induced hyperthermic syndromes of the ICU — the **serotonin syndrome** (the excess serotonin — the clonus, the hyperreflexia, the rapid onset, the cyproheptadine) and the **neuroleptic malignant syndrome** (the dopamine antagonism — the lead-pipe rigidity, the slow onset, the dantrolene and the bromocriptine) — and their distinction from the **malignant hyperthermia** (the volatile-anaesthetic + the suxamethonium, the theatre, the dantrolene) and the **anticholinergic syndrome** (the dry, the hot, the blind, the red, the mad — the physostigmine).

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Serotonin syndrome and neuroleptic malignant syndrome

Serotonin syndrome (SS) = excess serotonergic activity from drug combinations (SSRIs + MAOIs, tramadol, linezolid, fentanyl, St John's wort). Triad: mental status change + autonomic instability + neuromuscular hyperactivity (clonus, hyperreflexia). Onset: HOURS. Treatment: stop serotonergic drugs, benzodiazepines, cyproheptadine (serotonin antagonist), cooling, supportive. Neuroleptic malignant syndrome (NMS) = idiosyncratic reaction to dopamine antagonists (antipsychotics). Triad: mental status change + muscle rigidity (lead-pipe) + hyperthermia + autonomic instability. Onset: DAYS-WEEKS. Treatment: stop antipsychotic, dantrolene, bromocriptine, cooling, supportive. KEY DIFFERENCE: SS has clonus/hyperreflexia (onset hours); NMS has rigidity/hyporeflexia (onset days). Malignant hyperthermia (MH) — the third hyperthermia differential — is a pharmacogenetic crisis of the ryanodine receptor (RYR1) triggered by volatile anaesthetics (halothane, sevoflurane, desflurane, isoflurane) and succinylcholine: rapid onset (minutes-hours) of profound hypercapnia refractory to ventilation, generalised rigidity (especially masseter), rhabdomyolysis, hyperthermia, treated with immediate cessation of trigger + IV dantrolene 2.5 mg/kg repeat to 10 mg/kg.

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Snake envenomation in the ICU

Snake envenomation is a significant problem in Australia, Asia, Africa, and South America. Australian snakes: brown snake (most deaths), tiger snake, taipan, death adder, mulga/black snake. Clinical syndromes: (1) COAGULOPATHY (VICC — venom-induced consumption coagulopathy — prothrombin activator consuming fibrinogen and factors V/VIII; INR and aPTT beyond assay limits; platelets normal; resolution within 24–36 h). (2) NEUROTOXICITY (presynaptic — taipan, tiger — irreversible terminal damage; postsynaptic — death adder — curare-like blockade; ASP-16: neurotoxicity NOT reversed by antivenom, which prevents progression). (3) MYOTOXICITY (rhabdomyolysis — raised CK, myoglobinuria, AKI). (4) RENAL: AKI (12% of envenoming; TMA subset). (5) LOCAL: bite site swelling, bruising, necrosis. Diagnosis: snake venom detection kit (SVDK — bite site swab or urine — identifies snake GROUP; 4.9% incorrect in envenomed, 36% false positives in non-envenomed) and the 20-minute whole blood clotting test. Management: pressure immobilisation bandage (FIRST AID — slows lymphatic spread), IV antivenom (one vial binds all circulating venom), supportive ICU (ventilation for neurotoxicity, RRT for AKI, blood products for bleeding from VICC).

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Sympathomimetic Poisoning — Cocaine & Amphetamines

The sympathomimetic poisoning — the cocaine (the reuptake blockade of the dopamine, the noradrenaline and the serotonin; the sodium-channel blockade) and the amphetamines/methamphetamine/MDMA (the catecholamine release). The toxidrome (the mydriasis, the diaphoresis, the tachycardia, the hypertension, the hyperthermia, the agitation). The complications (the cocaine chest pain / the coronary vasospasm, the intracerebral haemorrhage, the seizures, the rhabdomyolysis, the MDMA hyponatraemia). The **benzodiazepine first-line**, the active cooling, and the avoidance of the pure beta-blocker (the unopposed-alpha problem).

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Toxic Alcohols — Methanol & Ethylene Glycol

The toxic alcohols — the methanol (the formic acid, the retinal toxicity and the blindness) and the ethylene glycol (the glycolate and the oxalate, the acute kidney injury and the calcium oxalate crystals). The **dual gap** (the high anion gap PLUS the high osmolar gap) is the signature. The **fomepizole** (the alcohol-dehydrogenase inhibitor) or the ethanol, the **haemodialysis** for the severe, and the cofactors (the folinic acid for the methanol, the thiamine and the pyridoxine for the ethylene glycol).

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Toxicology — The General Approach to the Poisoned Patient

The structured approach to the poisoned patient in the ICU — the resuscitation and the ABCDE adapted to the toxin; the clinical assessment and the toxidromes (the sympathomimetic, the anticholinergic, the cholinergic, the opioid, the sedative-hypnotic, the serotonin, the neuroleptic malignant); the investigation (the drug levels, the ECG, the anion and the osmolar gaps); the decontamination (the activated charcoal, the whole-bowel irrigation, the haemoperfusion); the enhanced elimination (the urinary alkalinisation, the haemodialysis); the antidotes (the naloxone, the N-acetylcysteine, the flumazenil, the digoxin Fab, the atropine and the pralidoxime, the lipid emulsion, the fomepizole); and the supportive care.

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Toxicology and poisoning in the ICU

Toxicology in the ICU requires a systematic approach: ABCDE first, then identify the toxin (history, toxidromes, specific levels), decontamination (activated charcoal within 1h), enhanced elimination (urine alkalinisation, haemodialysis), and antidotes. Paracetamol: NAC (N-acetylcysteine) if above treatment nomogram — the most common cause of ALF in the West. Salicylate: urine alkalinisation (sodium bicarbonate to urine pH over 7.5), haemodialysis for severe poisoning (EXTRIP: concentration over 6.5 mmol/L, or clinical indications at any concentration). TCA: hypertonic sodium bicarbonate 1-2 mmol/kg bolus for QRS widening (over 100 ms predicts seizures; over 160 ms ventricular arrhythmias). Ethylene glycol/methanol: fomepizole 15 mg/kg loading (inhibits alcohol dehydrogenase) + haemodialysis per EXTRIP methanol criteria. Lithium: haemodialysis in severe poisoning (EXTRIP criteria, e.g. expected time to under 1.0 mmol/L exceeding 36 h). Always ask: what toxin, when, how much, and which antidote?

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Tricyclic Antidepressant (TCA) Poisoning

Tricyclic antidepressant (TCA) poisoning — the dangerous overdose defined by cardiotoxicity from fast-sodium-channel blockade (QRS widening, ventricular arrhythmia, hypotension) plus antimuscarinic and CNS effects. The ECG is the master prognostic: a maximal limb-lead QRS at or above 100 ms predicts seizures and ventricular arrhythmias, and a terminal R wave in aVR of 3 mm or more is the strongest single predictor. Therapy is hypertonic sodium bicarbonate 1 to 2 mmol per kg (repeated to a maximum of 6 mmol per kg, with hyperventilation to a pH of 7.45 to 7.55), avoidance of class Ia and Ic antiarrhythmics, and lipid emulsion for refractory toxicity.

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resuscitation

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Acute Severe Anaphylaxis — Comprehensive Peri-Arrest Management

Acute severe anaphylaxis — a rapidly progressive, life-threatening systemic hypersensitivity reaction causing mast cell and basophil degranulation → release of histamine, tryptase, leukotrienes, prostaglandins → vasodilation (distributive shock), bronchoconstriction (bronchospasm), increased vascular permeability (angioedema, upper airway obstruction), and gastrointestinal symptoms. Triggers: drugs (#1 — antibiotics, NSAIDs, neuromuscular blocking agents, chemotherapy), foods (peanut, tree nut, shellfish, egg, milk), insect venom (bee, wasp), radiocontrast media, latex, exercise, idiopathic. Clinical criteria (NIAID/FAAN): acute onset (minutes to hours) with involvement of skin/mucosa PLUS respiratory compromise AND/OR reduced BP/organ dysfunction. Brown's severity grading: grade 1 (mild — skin only), grade 2 (moderate — skin + respiratory/cardiovascular/GI), grade 3 (severe — hypoxia, hypotension, neurologic compromise). Management: (1) IM ADRENALINE 0.5 mg (anterolateral thigh — repeat every 5 min), (2) POSITIONING (supine + legs elevated — 'elevated legs save lives' — empty IVC syndrome is fatal), (3) HIGH-FLOW OXYGEN + IV FLUIDS (rapid bolus 20 mL/kg crystalloid — massive volume sequestration from capillary leak), (4) REFRACTORY: IV adrenaline infusion (0.05-0.5 mcg/kg/min), vasopressin, methylene blue (NO-mediated vasoplegia), glucagon (beta-blocked patients), (5) ADJUNCTS: H1 blocker (cetirizine), H2 blocker (ranitidine), corticosteroids (hydrocortisone 200 mg IV), nebulised salbutamol (bronchospasm), (6) POST-EVENT: serial tryptase (peak 1-2h, baseline at 24h — confirms mast cell degranulation), allergy referral, adrenaline auto-injector, trigger identification. Perioperative anaphylaxis: NMBA #1 trigger (rocuronium, suxamethonium), tryptase during event + at 24h baseline, allergy testing 4-6 weeks post-event.

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Extracorporeal Cardiopulmonary Resuscitation (ECPR)

Extracorporeal cardiopulmonary resuscitation (ECPR) — the rapid deployment of venoarterial extracorporeal membrane oxygenation (VA-ECMO) during ongoing CPR in patients with refractory cardiac arrest (failure of conventional ACLS). Indications: witnessed in-hospital cardiac arrest (IHCA) or out-of-hospital cardiac arrest (OHCA) with initial shockable rhythm (VF/pVT), no-flow time &lt;5 minutes (unwitnessed/arrest to CPR), low-flow time (CPR duration) &lt;60 minutes, age &lt;70 (relative), no severe comorbidity, end-tidal CO2 >10 mmHg during CPR (suggesting ongoing perfusion). Cannulation: percutaneous femoral arterial + femoral venous (Seldinger technique — by intensivist, cardiologist, or perfusionist) during ongoing mechanical CPR (LUCAS/AutoPulse). Flow: 3-5 L/min within 10-15 minutes of team activation. Post-ECPR: targeted temperature management (32-36 degrees C), percutaneous coronary intervention (if ACS cause), continuous EEG (seizure detection), lung-protective ventilation, anticoagulation (heparin — target ACT 1.5x baseline). Outcomes: IHCA 30-40% survival to discharge (good neurological outcome); OHCA 20-30% survival (selected patients). Complications: bleeding (30-50% — vascular, intracranial, GI), thrombosis (circuit), limb ischaemia (femoral arterial cannulation), haemolysis, AKI, brain death. Contraindications: asystole as initial rhythm, unwitnessed arrest, known terminal illness, severe aortic regurgitation, aortic dissection, uncontrolled bleeding.

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Post-Cardiac Arrest Syndrome (PCAS) — Comprehensive ICU Management

Post-cardiac arrest syndrome (PCAS) — the multi-system injury following return of spontaneous circulation (ROSC), comprising four interconnected components (Nolan 2008 ILCOR/AHA scientific statement; ERC/ESICM 2021 post-resuscitation care guidelines): (1) post-arrest brain injury — hypoxic-ischaemic brain injury causes about two-thirds of in-hospital deaths in comatose ICU admissions after arrest; seizures are reported in 20-30%; (2) post-arrest myocardial dysfunction — common, typically starts to recover by 2-3 days, full recovery may take longer; (3) systemic ischaemia/reperfusion response — systemic immune and coagulation activation with a sepsis-like vasoplegic shock state; (4) persistent precipitating pathology — emergent cardiac catheterisation laboratory evaluation when cardiac origin is suspected. ICU bundle (ERC/ESICM 2021): targeted temperature management 32-36 C for at least 24 hours with fever avoidance (over 37.7 C) for at least 72 hours; avoid hypotension (MAP under 65 mmHg); titrate oxygen to SpO2 94-98% (PaO2 75-100 mmHg); normocapnia 35-45 mmHg; lung-protective ventilation 6-8 mL/kg ideal body weight; levetiracetam or sodium valproate first-line for seizures (no routine prophylaxis); blood glucose 7.8-10 mmol/L; multimodal prognostication at 72 hours or later after confounders excluded.

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Sepsis and Septic Shock — Comprehensive Integrated (SSC 2021, Hour-1 Bundle, Vasopressors, Source Control)

Sepsis and septic shock — the leading cause of death in the ICU and the highest-yield topic in critical care exams. SEPSIS-3 DEFINITIONS (Singer 2016): sepsis = life-threatening organ dysfunction caused by a dysregulated host response to infection (SOFA ≥2 point change from baseline); septic shock = sepsis with (1) persistent hypotension requiring vasopressors to maintain MAP ≥65 AND (2) serum lactate >2 mmol/L despite adequate fluid resuscitation (hospital mortality greater than 40%). qSOFA (quick bedside screen — RR ≥22, altered mentation, SBP ≤100): ≥2 = high risk of poor outcome (a PROMPT to consider sepsis and escalate — NOT a diagnostic criterion, NOT more sensitive than SIRS, and NOT recommended by SSC 2021 as a single screening tool). The SSC 2021 HOUR-1 BUNDLE (replaced the old 3-hour and 6-hour bundles): within one hour of recognition — measure lactate; obtain blood cultures provided this does not substantially delay antibiotics (under 45 minutes); administer broad-spectrum antimicrobials immediately, ideally within 1 hour (septic shock / high-likelihood sepsis); give at least 30 mL/kg crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock (balanced over saline, weak recommendation); apply vasopressors for MAP below 65 (noradrenaline first-line). VASOPRESSORS: add VASOPRESSIN 0.03 U/min (fixed dose, never titrated, never monotherapy) once noradrenaline reaches 0.25-0.5 mcg/kg/min — suggested INSTEAD of escalating noradrenaline; HYDROCORTISONE 200 mg/day for ongoing vasopressor requirement (noradrenaline ≥0.25 mcg/kg/min for at least 4 h). FLUIDS: balanced crystalloid first-line; after the initial resuscitation default to a restrictive, responsiveness-guided strategy (CLASSIC, CLOVERS — restrictive equivalent). MAP TARGET 65 (SEPSISPAM: no benefit of 80-85, more atrial fibrillation; exception — less RRT with higher target in chronic hypertension). RESUSCITATION TARGETS: capillary refill time as an adjunct (ANDROMEDA-SHOCK — capillary-refill-targeted vs lactate-targeted: 28-day mortality 34.9% vs 43.4%, HR 0.75, no significant difference; less organ dysfunction at 72 h); lactate-guided resuscitation targeting a fall of at least 20% per 2 hours (Jansen 2010). SOURCE CONTROL: as soon as medically and logistically practical (SSC 2021 best practice statement; observational data favour 6-12 hours). STEROID TRIALS: ADRENAL — no 90-day mortality difference but faster shock resolution; APROCCHSS — lower 90-day mortality with hydrocortisone plus fludrocortisone. MORTALITY: septic shock greater than 40% (Sepsis-3); each hour to antibiotics OR 1.04 (Seymour 2017, New York State cohort of 49,331 patients).

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haematology-coagulation

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Acute Severe Anticoagulation Reversal — Warfarin, DOACs & Heparin in the ICU

Acute severe anticoagulation reversal covers the three drug classes the intensivist must reverse in life-threatening bleeding or before emergency surgery — WARFARIN (vitamin K antagonists), the DIRECT ORAL ANTICOAGULANTS (dabigatran a direct thrombin inhibitor; rivaroxaban, apixaban and edoxaban direct factor Xa inhibitors), and the HEPARINS (unfractionated heparin and the low-molecular-weight heparins). WARFARIN reversal: guideline-based practice pairs 4F-PCC (30 IU per kg in the INCH trial) with intravenous vitamin K 10 mg; PCC beat plasma for rapid INR correction in both INCH (67 vs 9 per cent reaching INR 1.2 or lower at 3 h) and the Sarode phase IIIb trial (62.2 vs 9.6 per cent at 0.5 h). DABIGATRAN: idarucizumab 5 g IV — median maximum reversal 100 per cent within 4 h in RE-VERSE AD; dabigatran is also removable by haemodialysis. RIVAROXABAN and APIXABAN: andexanet alfa (bolus plus 2-hour infusion; 82 per cent excellent or good haemostasis in ANNEXA-4) or 4F-PCC 50 IU per kg per neurocritical care guidance. UFH: protamine about 1 mg per 100 units heparin. Fondaparinux: recombinant factor VIIa 90 micrograms per kg (volunteer data).

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Catastrophic Antiphospholipid Syndrome (CAPS) in the ICU

Catastrophic antiphospholipid syndrome (CAPS) — the most severe form of antiphospholipid syndrome (APS) characterised by rapid multi-organ thrombosis (small-vessel) affecting three or more organ systems within one week, histopathological evidence of microthrombosis, and persistent antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti-beta-2-glycoprotein I). Affects: kidneys (AKI from renal microthrombi), lungs (ARDS, pulmonary embolism, pulmonary haemorrhage), brain (stroke, encephalopathy, seizures), heart (myocardial infarction, cardiomyopathy, valvular lesions), skin (livedo reticularis, digital gangrene), liver, GI, and adrenal (Waterhouse-Friderichsen). Triggers: infection (most common), surgery, malignancy, pregnancy, withdrawal of anticoagulation. Management: (1) eliminate trigger (treat infection), (2) triple therapy — anticoagulation (heparin) + corticosteroids + plasma exchange ± IVIG, (3) rituximab or eculizumab for refractory cases, (4) supportive care (RRT, ventilation, vasopressors). Mortality 30-50% despite treatment.

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Hemophagocytic Lymphohistiocytosis (HLH) and Macrophage Activation Syndrome (MAS) in the ICU

Hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) — a life-threatening hyperinflammatory syndrome caused by uncontrolled T-cell and macrophage activation resulting in a cytokine storm (IFN-gamma, IL-6, IL-18, TNF-alpha, IL-1beta). Presents with: prolonged fever, cytopenias (bi- or trilineage), hepatosplenomegaly, lymphadenopathy, hyperferritinaemia (>10,000 ug/L), hypofibrinogenaemia, hypertriglyceridaemia, transaminitis, coagulopathy, and multi-organ failure. Classified as: (1) primary/genetic HLH (FHL, perforin deficiency, infancy), (2) secondary HLH (infection-triggered: EBV, CMV, HIV, SARS-CoV-2; malignancy-triggered: lymphoma, leukaemia; autoimmune-triggered: SLE/MAS, adult-onset Still disease; post-immunosuppression/ICI). Diagnosis: HLH-2004 criteria (5 of 8: fever, splenomegaly, cytopenias x2+, hypertriglyceridaemia/hypofibrinogenaemia, haemophagocytosis on marrow, low NK cell activity, elevated soluble CD25, hyperferritinaemia) OR HScore. Management: (1) treat the trigger (antivirals for EBV, treat malignancy, immunosuppress for autoimmune), (2) suppress cytokine storm — dexamethasone + etoposide (HLH-2004 protocol), emapalumab (anti-IFN-gamma), anakinra (IL-1 receptor antagonist), tocilizumab (anti-IL-6), ruxolitinib (JAK1/2 inhibitor), (3) supportive ICU care (ventilation, vasopressors, RRT, transfusion). Mortality 20-40% (adult secondary HLH); 50-60% if malignancy-triggered.

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Antimicrobial Stewardship

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Acute severe community-acquired pneumonia: antimicrobial de-escalation and stewardship

Antimicrobial de-escalation is narrowing or stopping antibiotics based on culture results and clinical response. For severe CAP: start broad (a beta-lactam plus a macrolide, or a respiratory fluoroquinolone), then narrow at 48-72h based on: (1) culture results (sputum, blood, urinary antigens), (2) clinical response (improving fever, WBC, oxygenation, inflammatory markers), (3) procalcitonin trend. Procalcitonin-guided algorithm (Christ-Crain 2006 bands): antibiotics strongly discouraged under 0.1 ng/mL, discouraged under 0.25 ng/mL, encouraged over 0.25 ng/mL, strongly encouraged over 0.5 ng/mL; stop with clinical improvement. Duration: randomised trials support 3-day and 5-day minimum courses in clinically stable CAP (el Moussaoui 2006; Uranga 2016). Stewardship principles: right drug, right dose, right duration, right route. Avoid: unnecessary broadening, prolonged courses, duplicate coverage.

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Acute severe community-acquired pneumonia: infection control in ICU

Infection control in ICU prevents transmission of pathogens between patients, staff, and the environment. Core components: (1) Hand hygiene (WHO 5 Moments — single most effective measure). (2) Standard precautions (for ALL patients — gloves, gown, eye protection when exposure risk). (3) Transmission-based precautions: contact (MRSA, VRE, C. diff, MDR), droplet (influenza, RSV, pertussis), airborne (TB, measles, chickenpox). (4) Environmental cleaning (high-touch surfaces, terminal cleaning). (5) Equipment cleaning/disinfection (dedicated equipment for isolated patients). (6) Surveillance (MDR screening cultures, infection rates). (7) Staff education and audit. (8) Antimicrobial stewardship. ICU infection rate is a quality metric — lower is better.

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Acute severe community-acquired pneumonia: nosocomial complications and prevention

CAP patients admitted to ICU are at high risk for nosocomial (hospital-acquired) superinfections during their stay. Common: VAP (ventilator-associated pneumonia — #1, develops >48h after intubation), CRBSI (catheter-related bloodstream infection), C. difficile colitis, UTI (catheter-associated), surgical site infection (if surgery performed). Risk factors: prolonged ventilation, broad-spectrum antibiotics, immunosuppression, severity of illness. Prevention: VAP bundle (head elevation, daily SAT+SBT, oral chlorhexidine, subglottic suction, cuff pressure), CRBSI bundle (full barrier precautions, chlorhexidine skin prep, daily review of line necessity), antibiotic stewardship (minimise duration, de-escalate), early mobilisation, hand hygiene.

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Antimicrobial resistance in the ICU: mechanisms, organisms, and management

Multidrug-resistant (MDR) organisms are endemic in the ICU and independently increase mortality, length of stay, and cost. Resistance arises from beta-lactamases (ESBL — CTX-M; AmpC; carbapenemases — KPC class A, NDM/VIM/IMP class B metallo-beta-lactamases, OXA-48 class D), altered targets (PBP2a in MRSA via mecA; D-Ala-D-Lac in VRE via vanA/B; QRDR mutations in fluoroquinolone resistance), efflux pumps, porin loss (OprD in Pseudomonas), and enzymatic modification. The ICU core threats are MRSA, VRE, ESBL-Enterobacterales, CRE/CPE, carbapenem-resistant Pseudomonas aeruginosa (CRPA) and carbapenem-resistant Acinetobacter baumannii (CRAB). Management demands rapid molecular diagnostics (carbapenemase typing), empiric broad therapy within one hour of sepsis, then aggressive de-escalation using novel beta-lactam/beta-lactamase inhibitor combinations (ceftazidime-avibactam for KPC/OXA-48; meropenem-vaborbactam and imipenem-relebactam for KPC; ceftolozane-tazobactam and cefiderocol for MDR Pseudomonas; aztreonam-avibactam for NDM/MBL), supported by infection-control bundles (contact precautions, cohorting, surveillance screening, decolonisation) and antimicrobial stewardship (PK/PD-optimised dosing, extended infusions, therapeutic drug monitoring, shortest effective duration).

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Catheter-related bloodstream infection (CRBSI)

CRBSI is bloodstream infection originating from an intravascular catheter. The #1 preventable ICU-acquired infection. Common organisms: coagulase-negative staphylococci (#1 — Staph epidermidis), S. aureus, Enterococcus, Gram-negative bacilli, Candida. Diagnosis: positive blood cultures from peripheral vein AND catheter (same organism, differential time to positivity >2h, or semi-quantitative culture >15 CFU). Management: REMOVE the catheter + targeted antibiotics (7-14 days). Prevention: full barrier precautions during insertion, chlorhexidine skin antisepsis, optimal site selection (subclavian > jugular > femoral), daily review of line necessity, removal when no longer needed. Bundle approach can reduce CRBSI to near-zero.

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Clostridioides difficile infection in the ICU

Clostridioides difficile infection (CDI) is a toxin-mediated complication of antibiotic use, on a spectrum that runs from asymptomatic colonisation through self-limiting diarrhoea to toxic megacolon and fulminant colitis. Clindamycin-associated colitis (1974) is the index report; 3-10% of patients progress to severe, complicated (fulminant) disease. SEVERE = leukocytosis (WBC at least 15,000 cells/mL) or creatinine over 1.5 mg/dL; FULMINANT = hypotension or shock, ileus, or megacolon (Surgical Infection Society definitions). TREATMENT: stop the inciting antibiotic; fidaxomicin 200 mg PO BD or vancomycin 125 mg PO QID x 10 days (recurrence 15.4% vs 25.3%, Louie NEJM 2011; fidaxomicin preferred per ESCMID 2021); fulminant: high-dose enteral vancomycin 500 mg PO/NG QID plus IV metronidazole with early surgical review - total abdominal colectomy is the SIS procedure of choice. Bezlotoxumab 10 mg/kg IV once, with antibiotics, cuts 12-week recurrence (17% vs 28%, MODIFY I). FMT for second or further recurrence.

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Fungal infections in the ICU: candidaemia and aspergillosis

Fungal infections in ICU: candidaemia (most common fungal bloodstream infection — ANZ surveillance: Candida albicans 44.4 percent, C. glabrata complex 26.7 percent, C. parapsilosis complex 16.5 percent; C. auris emerging multidrug-resistant) and invasive pulmonary aspergillosis (risk profile broadened to COPD, cirrhosis, influenza and COVID-19). Candida score (Leon 2006, cut-off over 2.5): severe sepsis, multifocal colonisation, TPN, surgery. Diagnosis: blood cultures (median time-to-positivity 22.7 to 42.0 h), beta-D-glucan (cutoff 80 pg/mL: sensitivity 64.4 percent, specificity 92.4 percent), T2Candida. Treatment: echinocandin first-line (caspofungin 70 mg load then 50 mg daily, micafungin 100 mg daily, anidulafungin 200 mg load then 100 mg daily), step down to fluconazole 800 mg load then 400 mg daily after about 5-10 days when stable and susceptible, treat at least 14 days after the last positive culture. Ophthalmology review (ocular candidiasis 10.7 percent). Aspergillosis: voriconazole first-line with therapeutic drug monitoring (target trough 1.0-5.5 mg/L). Mucorales: galactomannan and beta-D-glucan negative — liposomal amphotericin B 5-6 mg/kg/day plus surgery.

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Ventilator-associated pneumonia (VAP)

VAP is pneumonia developing more than 48 hours after endotracheal intubation. It is one of the most frequent ICU-acquired infections, with attributable mortality of around 10 percent. Pathogenesis: microaspiration of oropharyngeal secretions around the ETT cuff, bacterial colonisation of the ETT biofilm. Diagnosis: new/persistent infiltrate on CXR PLUS at least 2 of fever, leukocytosis, purulent secretions, with CPIS as a support tool. Microbiology: early VAP (under 5 days) — S. pneumoniae, H. influenzae, MSSA. Late VAP (5 days or more) — MRSA, Pseudomonas, Acinetobacter, ESBL. Treatment: empiric antibiotics promptly, guided by MDR risk, de-escalate when susceptibility results return. Duration: 7 days standard (8 vs 15 day trial). Prevention bundle: head elevation 30-45 degrees, daily sedation interruption, oral care, subglottic suction, cuff pressure control.

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Domain

Infectious diseases

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Acute severe community-acquired pneumonia: comprehensive ICU pathway (sepsis, ARDS, empiric therapy, corticosteroids)

Severe community-acquired pneumonia (CAP) is the commonest single cause of sepsis and ARDS in the ICU, with mortality 20-50%. SEVERITY (use to triage ICU): CURB-65 (Confusion, Urea >7, RR >=30, BP &lt;90/60, Age >=65) — score 4-5 = severe, consider ICU; PSI/PORT (Pneumonia Severity Index — classes IV-V high risk); IDSA/ATS 2007 minor/major criteria — 1 MAJOR (invasive ventilation OR septic shock) OR >=3 MINOR (RR >=30, PaO2/FiO2 &lt;250, multilobar, confusion, BUN >=20, WBC &lt;4, platelets &lt;100, temp &lt;36, hypotension needing fluids) = severe CAP needing ICU. ICU PATHWAY (hour-1 sepsis bundle): cultures (blood x2, sputum, urinary antigens, viral PCR) + lactate + ANTIBIOTICS WITHIN 1 HOUR + goal-directed fluids + noradrenaline if shock. EMPIRIC THERAPY (IDSA/ATS 2019) — SEVERE CAP/ICU: beta-lactam (ceftriaxone 2g, cefotaxime, or ampicillin-sulbactam) + MACROLIDE (azithromycin) OR beta-lactam + respiratory fluoroquinolone (moxifloxacin/levofloxacin). PSEUDOMONAS risk (bronchiectasis, prior isolation): anti-pseudomonal beta-lactam (pip-tazo/cefepime/meropenem) + ciprofloxacin OR aminoglycoside + macrolide/levo. MRSA risk (post-influenza, cavitary): add vancomycin/linezolid. INFLUENZA suspected: add oseltamivir. CORTICOSTEROIDS: hydrocortisone 200 mg/day for septic shock on vasopressors (SEPSISPAM/SSC 2021); adjunctive steroids reduce mortality + ARDS in severe CAP with high inflammatory burden (Siemieniuk/CAPO meta-analysis). DURATION 5-7 days if improved + afebrile 48-72h; procalcitonin-guided de-escalation (Schuetz IPD meta-analysis). COMPLICATIONS: septic shock, ARDS, empyema (pH &lt;7.2 drain), lung abscess, metastatic infection, AF/DVT. PREVENTION: pneumococcal + influenza vaccine, smoking cessation.

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Acute severe community-acquired pneumonia: ICU pathway, empiric therapy, and complications

Severe community-acquired pneumonia (CAP) requiring ICU is a leading cause of sepsis and ARDS. ICU PATHWAY (hour-1): cultures (blood, sputum) + lactate + antibiotics within 1 HOUR + fluids (goal-directed) + vasopressors (if shock). EMPIRIC THERAPY (IDSA/ATS 2019): (1) STANDARD: beta-lactam (ceftriaxone, ampicillin-sulbactam) + MACROLIDE (azithromycin) OR beta-lactam + respiratory fluoroquinolone (moxifloxacin). (2) SEVERE (ICU): beta-lactam (ceftriaxone/cefepime) + MACROLIDE (azithromycin) OR beta-lactam + fluoroquinolone. (3) PSEUDOMONAS RISK (bronchiectasis, prior Pseudomonas, recent hospitalisation): anti-pseudomonal beta-lactam (pip-tazo, cefepime, meropenem) + 2nd agent (ciprofloxacin OR aminoglycoside + azithromycin/levo). (4) MRSA RISK: add vancomycin/linezolid. DE-ESCALATE at 48-72h based on cultures. DURATION: 5-7 days (if clinically improved + afebrile 48-72h; PCT-guided — PRORATA). COMPLICATIONS: ARDS (lung-protective ventilation, proning), septic shock, empyema (drain), lung abscess, metastatic infection.

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Fulminant Clostridioides difficile colitis: surgery, fidaxomicin, and bezlotoxumab

Clostridioides difficile infection (CDI) ranges from mild diarrhoea to FULMINANT colitis (hypotension or shock, ileus, megacolon, perforation — reported in-hospital mortality 34.7-53%). RISK FACTORS: elderly patients with comorbidities who have recently received antibiotics; immunosuppression independently predicts fulminant death. DIAGNOSIS: stool toxin testing — toxin EIAs lack sensitivity; NAAT detects toxin genes but detection does not always equate with disease. TREATMENT: (1) INITIAL: fidaxomicin 200 mg PO BD for 10 days (recurrence 15.4% vs 25.3% for vancomycin 125 mg QID — Louie NEJM 2011) or vancomycin 125 mg PO QID. (2) FULMINANT: high-dose enteral vancomycin (500 mg PO/NG QID regimen) + IV metronidazole; early surgical involvement — WBC ≥50 (AOR 18.6) and lactate ≥5 mmol/L (AOR 12.4) carry the highest mortality odds and emergency colectomy was independently associated with survival (AOR 0.22, Lamontagne 2007). (3) SURGERY: total abdominal colectomy is the SIS procedure of choice; diverting loop ileostomy with colonic lavage plus antegrade vancomycin is colon-preserving (19% vs 50% mortality, colon preserved 93% — Neal 2011). (4) RECURRENCE: bezlotoxumab 10 mg/kg single IV infusion (recurrence 17%/16% vs 28%/26% — MODIFY I/II); FMT or bezlotoxumab for second or further recurrence (ESCMID 2021); FMT resolves 81% after one infusion.

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Domain

Ethics

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Acute severe community-acquired pneumonia: ICU handover and communication

Clinical handover is the transfer of professional responsibility and accountability for patient care from one clinician/team to another. Poor handover is a leading cause of preventable patient harm — the Joint Commission attributed the majority of sentinel events to communication breakdown, and the ANZICS CORE and ICNARC datasets repeatedly identify failed handover as a root-cause contributor to ICU morbidity. ICU handover contexts: shift change (nursing + medical), ICU-to-ward transfer, ED-to-ICU referral/upgrade, inter-hospital retrieval, weekend/holiday/long-weekend handover, and emergency/event handover (cardiac arrest, rapid response, deterioration). Structured tools: ISBAR (Identify, Situation, Background, Assessment, Recommendation — the ANZ standard with explicit identification step), SBAR (Situation, Background, Assessment, Recommendation — the original Kaiser Permanente model), I-PASS (Illness severity, Patient summary, Action list, Situation awareness with contingencies, Synthesis by receiver — most evidence-based, reduced medical errors 23% and preventable adverse events 30% in the NEJM 2014 trial), and ISOBAR (Identify, Situation, Observations, Background, Agreed plan, Read-back — Australian Commission on Safety and Quality in Health Care variant). Handover failure modes: missed information, wrong/duplicated/omitted medication, delayed investigation or treatment, loss of contingency plans, and absent situational awareness of the deteriorating patient. Critical-event communication techniques: closed-loop communication (sender → receiver reads back → sender confirms), read-back/verify-back of verbal orders and drug doses, and crew resource management (CRM) principles adapted from aviation. Principles of every handover: structured, concise, accurate, timely, documented in the medical record, with an explicit opportunity for questions and a synthesis/read-back step.

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Acute severe community-acquired pneumonia: ICU quality metrics and outcome benchmarking

ICU quality metrics measure performance, identify areas for improvement, and benchmark against peers. STRUCTURE metrics as outcome (SMR, ICU/hospital mortality, ventilator-free days, ICU length of stay, readmission rate), process (time to antibiotics, blood culture rate, bundle compliance, hand hygiene compliance), and balancing/safety (CLABSI per 1000 catheter-days, VAP per 1000 ventilator-days, CAUTI per 1000 catheter-days, pressure injury, unplanned extubation, medication errors), plus patient- and family-reported experience (FS-ICU 24). The STANDARDISED MORTALITY RATIO (SMR) = observed / expected deaths, where expected deaths come from a risk-adjusted model (APACHE II/III/IV, SAPS 3, MPM) calibrated against a reference population; SMR &lt;1 = better than expected, &gt;1 = worse than expected. BENCHMARKING databases: ANZICS CORE (Australia/New Zealand), ICNARC Case Mix Programme (UK), NICE (Netherlands), Intensive Care Databank (Belgium), LIDO (Latin America) — each provides unit-level risk-adjusted SMR, funnel plots, and peer comparison. QUALITY IMPROVEMENT methods: PDSA (Plan-Do-Study-Act) small tests of change, checklists, care bundles, audit and feedback, Lean (eliminate waste), Six Sigma (reduce variation/DMAIC), statistical process control (run/control charts), root cause analysis. Landmark QI publications: Pronovost 2006 (NEJM, Keystone CLABSI bundle), Haynes 2009 (NEJM, WHO surgical safety checklist), Levy 2018 (SSC hour-1 bundle), IHI central line and ventilator bundles, ABCDEF/PADIS bundle. For CAP specifically: time to first antibiotic, appropriateness of empiric antibiotics, blood culture rate, CURB-65 documentation rate, vaccination status at discharge. QI cycle: measure -> analyse -> intervene -> re-measure (PDSA).

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Acute severe community-acquired pneumonia: simulation training and competency assessment

Simulation training is increasingly used in ICU education — it allows practice of high-stakes, low-frequency events without patient risk, and is now a mandated component of critical care training worldwide. Types: (1) High-fidelity (full-body manikin with realistic physiology). (2) Low-fidelity (task trainers — airway, central line, chest tube). (3) In-situ (simulation run in the actual ICU environment). (4) Screen-based / virtual and augmented reality (immersive, repeatable, no physical manikin). (5) Standardised patients (actors). Applications: technical skills (intubation, line insertion), non-technical skills (teamwork, communication, leadership), crisis resource management (CRM — emergency response), rare events (malignant hyperthermia, tension pneumothorax, cardiac tamponade), and system testing (new protocols, equipment, environment, latent safety threats). Evidence: improves knowledge (moderate), skills (strong), team performance (strong), and patient outcomes (moderate — translational outcomes) when integrated into curriculum, repeated with spaced deliberate practice, and paired with structured debriefing. The DEBRIEFING — not the scenario — is where learning occurs; debriefing models include Plus-Delta, GAS (Gather-Analyse-Summarise), and PEARLS (Promoting Excellence And Reflective Learning in Simulation). Competency assessment uses DOPS (Direct Observation of Procedural Skills), mini-CEX (mini-Clinical Evaluation Exercise), OSCE (Objective Structured Clinical Examination), and multi-source 360-degree feedback.

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Acute severe community-acquired pneumonia: tele-ICU and remote monitoring

Tele-ICU (also called eICU, virtual ICU, remote ICU) uses technology to extend intensivist expertise to ICUs without 24/7 on-site intensivist coverage. Model: remote intensivists (at a central 'command centre') monitor multiple ICUs simultaneously via: (1) Continuous vital sign monitoring (real-time data feeds from bedside monitors). (2) Audiovisual connection (cameras at each bedside, two-way audio). (3) Electronic health record integration (labs, medications, imaging). (4) Telepresence (remote consultation with bedside staff). Benefits: (1) 24/7 intensivist coverage for smaller/rural hospitals. (2) Protocol adherence (standardised care). (3) Earlier detection of deterioration. (4) Reduced mortality (some studies). Limitations: (1) Cost (expensive to set up). (2) Technology dependence (network failure = no coverage). (3) 'Big brother' concern (staff may feel watched). (4) Cannot perform physical examinations or procedures. (5) Loss of face-to-face relationship with patients/families.

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Brain death and organ donation in ICU

Brain death: irreversible cessation of all brain function (cerebrum + brainstem). LEGAL definition of death in most countries. Diagnosis: precondition (known cause, exclusion of reversible causes), clinical examination (fixed dilated pupils, absent corneal reflex, absent gag/cough, absent caloric response, apnoea test). Two doctors, two examinations (time interval varies by jurisdiction). Organ donation: DBD (donation after brain death — heart beating) or DCD (donation after circulatory death — controlled, after withdrawal of life-sustaining treatment). ICU management of brain-dead donor: maintain perfusion (MAP ≥65, vasopressors), normothermia, normoglycaemia, electrolytes, hormone resuscitation (vasopressin, T3/T4, insulin — controversial). R…

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Disaster/Pandemic Ethics — Resource Allocation & Triage

Disaster/pandemic ethics — the shift from individual focus (standard ICU) to population focus (maximise good across all) when demand exceeds supply. Mass casualty triage (START — simple triage and rapid treatment; reverse triage for burns/electrical). Surge capacity tiers: conventional → contingency → crisis, with crisis standards of care. Resource allocation principles: maximise lives saved (utilitarian), maximise life-years (fair innings), instrumental value (healthcare workers), random lottery tie-breaker. Ethical frameworks compared (utilitarian, egalitarian, prioritarian). Ventilator allocation frameworks: SOFA-based single-principle vs multiprinciple (SOFA + comorbidity + age caps + exclusions). SOFA score as the objective prognosis tool, re-triaged dynamically. Crisis standards of care must be DECLARED. Triage committee SEPARATE from the treating team. Withdrawal to reallocate: defensible only under declared crisis standards, ex ante framing, never ad hoc. Duty to care versus duty to self, set by reciprocity.

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End-of-life care and palliative care in the ICU

End-of-life care is a core ICU competency. In the ETHICUS study of 37 European ICUs, therapy was withheld before 38% and withdrawn before 33% of ICU deaths or treatment limitations. Principles: (1) shared decision-making with patient/surrogate/multidisciplinary team grounded in the four ethical principles — autonomy, beneficence, non-maleficence, justice, (2) clear communication about prognosis and goals using a structured framework (SPIKES for bad news, Ask-Tell-Ask for goals), (3) treatment limitation orders (TLO) that specify what treatments are and are not appropriate, (4) symptom-focused comfort care. CRUCIAL ETHICAL PRINCIPLE: withholding and withdrawing life-sustaining treatment are ETHICALLY EQUIVALENT — there is no moral difference between not starting and stopping a treatment that cannot benefit the patient.

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Family-centred care and bereavement support in ICU

Family-centred care in ICU recognises that critical illness affects the entire family, not just the patient. Components: flexible/open visiting hours, family participation in bedside rounds, family presence during procedures and resuscitation, ICU diaries, structured proactive communication (regular family meetings, SPIKES for breaking bad news, ISBAR for handover), and shared decision-making using substituted judgement. PICS-Family: up to 50% of family members develop depression, anxiety, PTSD, or complicated grief after a loved one's ICU admission or death. Risk factors: witnessing cardiac arrest/CPR, prolonged ICU stay, unexpected outcome, poor communication, low health literacy, decisions to withdraw life-sustaining therapy (WOLST). Prevent…

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Geriatric critical care: the elderly ICU patient

Geriatric critical care: patients aged >65-80 in ICU. Physiological changes of ageing: reduced organ reserve (cardiac, renal, respiratory), altered pharmacokinetics (decreased renal clearance, increased body fat, decreased albumin), polypharmacy, frailty, comorbidities. Key principles: (1) FRAILTY (not age alone) predicts outcomes better than chronological age. (2) Polypharmacy — review all medications, deprescribe. (3) Delirium — extremely common in elderly ICU, worsens outcomes. (4) Iatrogenic complications (infections, bleeding, falls). (5) Goals of care discussions — realistic prognosis, quality of life. (6) Early mobilisation — prevents deconditioning. (7) Nutrition — sarcopenia. Outcomes: higher mortality, longer recovery, more disability…

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ICU quality improvement: checklists, bundles, and infection prevention

ICU quality improvement: systematic approaches to reduce errors, prevent complications, improve outcomes. KEY tools: (1) CHECKLISTS — standardised lists ensuring all steps completed (safety checklist, daily goals, central line insertion). (2) CARE BUNDLES — groups of evidence-based interventions applied together (VAP bundle, sepsis bundle, central line bundle). (3) INFECTION PREVENTION — VAP (ventilator-associated pneumonia), CLABSI (central line-associated bloodstream infection), CAUTI (catheter-associated UTI). Each has evidence-based prevention measures. (4) DAILY ROUND CHECKLIST — ABCDEF bundle (pain, SAT/SBT, sedation choice, delirium, early mobility, family). Quality improvement: measure → intervene → re-measure (PDSA cycle).

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ICU severity scoring systems

ICU scoring systems predict mortality, compare quality between units, and stratify patients for research. APACHE II (Acute Physiology And Chronic Health Evaluation): 12 physiological variables + age + chronic health — most widely used. Score 0-71 (higher = worse); in the 1985 derivation cohort, rising scores tracked a rising risk of hospital death. SOFA (Sequential Organ Failure Assessment): 6 organ systems (respiratory, coagulation, liver, cardiovascular, CNS, renal) — daily tracking. SOFA >=2 defines organ dysfunction (Sepsis-3). qSOFA: 3 items (RR >22, altered mentation, SBP &lt;100) — for screening outside ICU. SAPS II/3: alternative to APACHE. Scores are for POPULATIONS not individuals — do NOT use alone for treatment limitation decisions.

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ICU staff wellbeing and burnout

ICU staff burnout affects 25-50% of intensivists and ICU nurses — the highest rate of any hospital specialty. Burnout syndrome (Maslach) comprises three domains: emotional exhaustion, depersonalisation (cynicism), and reduced personal accomplishment. Drivers in the ICU are distinct from the general hospital: frequent patient death, end-of-life decision-making, moral distress and moral injury (knowing the right course of action but being prevented from taking it by systemic constraints), inadequate staffing and resources, night-shift circadian disruption, family conflict, and pandemic surges. The second victim phenomenon describes the clinician traumatised by an adverse event or unanticipated patient death — guilt, self-doubt, anxiety, and re-experiencing. Consequences span patient safety (more medication, diagnostic and procedural errors), quality of care (reduced empathy, poorer communication), workforce (turnover, shortages — a vicious cycle), and mental health (depression, anxiety, substance use, suicide). Prevention is two-tiered: institutional (safe staffing ratios, workload and shift management, structured debriefing, peer-support programmes, employee assistance, addressing moral injury at source) and individual (self-awareness, self-care, mindfulness/resilience training, boundary setting, early help-seeking). Burnout is framed as an OCCUPATIONAL HEALTH and SYSTEM failure, NOT an individual weakness.

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ICU triage, resource allocation, and pandemic preparedness

ICU triage and resource allocation govern who is admitted, who is discharged, and how scarce resources (beds, ventilators, staff, renal replacement therapy) are distributed when demand exceeds capacity (pandemic, mass casualty, seasonal surge). Core principles: (1) maximise benefit / lives saved, (2) treat people equally, (3) promote and reward instrumental value, (4) give priority to the worst off, (5) transparency, consistency and accountability. Triage hierarchy — the priority/benefit system: Priority 1 (urgent, high likelihood of benefit, e.g. reversible sepsis, trauma) — admit first; Priority 2 (urgent, moderate benefit) — admit if bed available; Priority 3 (non-urgent, low immediate risk) — defer / ward; Priority 4 (little or no expected benefit despite ICU — irreversible brain injury, terminal illness, advanced directives declining intensive care) — do not admit, provide comfort care. The benefit principle: ICU is allocated where it is most likely to do the most good (reversibility + expected survival), NOT first-come-first-served. Triage tools: SOFA score (organ failure burden — higher SOFA = lower priority), modified SOFA (mSOFA) triage categories, MEES (Mainz Emergency Evaluation Score, prehospital/ED), NEMS (Nine Equivalents of Nursing Manpower Use Score, nursing workload/capacity planning), age, comorbidity and frailty burden, reversibility. Inappropriate admissions: brain death, irreversible terminal illness, valid DNACPR/advance directives declining intensive care, patients for whom ICU cannot reverse the dying process. Discharge criteria: clinical stability (no longer needing organ support, no escalating inotropes, low SOFA, recovering primary insult), adequate step-down/HDU capacity available, and a safe handover. Rationing principles when scarce: utilitarian (maximise benefit), egalitarian (equal access / lottery), prioritarian (worst off first), first-come-first-served (REJECTED during scarcity), instrumental value (prioritise staff who can return to work). Futility: physiological (a treatment that cannot achieve its physiological goal — will not work), qualitative (quality of life/benefit too low to justify), value-based (disagreement on what counts as a benefit). Withholding vs withdrawing life-sustaining therapy are ETHICALLY EQUIVALENT. Triage committee: an independent, multidisciplinary body — NOT the treating clinician — applies a predefined protocol, reducing bias and moral burden. Surge capacity: Level 1 (conventional), 2 (contingency), 3 (crisis). The protocol MUST be predefined and applied consistently — NEVER improvised case-by-case under pressure. Communication with patients and families is essential — honest, compassionate, consistent.

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Root cause analysis and quality improvement in the intensive care unit

Root cause analysis (RCA) is a structured, BLAME-FREE method for analysing adverse events and near-misses to identify underlying SYSTEM causes and prevent recurrence. Process: (1) Identify incident and convene a multidisciplinary team. (2) Gather data (timeline, interviews, documentation, equipment review). (3) Identify contributing factors using a recognised framework — Swiss cheese model (Reason: active failures and latent conditions), the London Protocol (Vincent: patient, staff, task, technology, environment, team, organisation), or fishbone/Ishikawa (people, process, equipment, environment, management). (4) Determine root causes (system/process, NOT individual blame) using tools such as 5 Whys. (5) Develop a SMART action plan with strong countermeasures (hierarchy: forcing functions greater than education). (6) Implement, measure, and feedback. Quality improvement (QI) methods: PDSA (Plan-Do-Study-Act), Lean (eliminate TIMWOODS waste), Six Sigma/DMAIC (reduce variation), checklists and care bundles, audit and feedback, statistical process control (run charts, control charts, Pareto, process mapping). Proactive risk tools include FMEA (Failure Mode and Effects Analysis). Just culture (Reason/Dekker): distinguish human error (forgivable — fix the system) from at-risk behaviour (coach) and reckless behaviour (not forgivable — address the individual). ICU QI targets: time to antibiotics, VAP/VAE rate, CLABSI rate, CAUTI, readmission rate, standardised mortality ratio (SMR).

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Domain

Rehabilitation

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Acute severe community-acquired pneumonia: ICU sleep disruption and circadian rhythm

Sleep disruption is near-universal in the ICU. Polysomnography of ventilated patients found NO patient with normal sleep: nocturnal sleep efficiency about 38%, stage 1 sleep up to 40% of total sleep time, REM reduced to about 10%, and arousals plus awakenings around 40 per hour. Causes: noise and patient-care activities (together under a third of arousals on PSG — the illness itself and its treatment account for the rest), light (even dim room light suppresses melatonin), medications (GABA-agonist sedation produces an absence of restorative sleep), and mechanical ventilation (over-assist causing hypocapnia and central apnoeas). Consequences: delirium (multicomponent sleep-promotion bundles reduce it), impaired glucose tolerance with raised evening cortisol and sympathetic activation, and persistent post-ICU sleep disturbance. Management: multicomponent bundle (cluster care, light/noise control, earplugs and eye masks) recommended by the 2018 PADIS guidelines; nocturnal melatonin reduces delirium on meta-analysis; dexmedetomidine improves sleep quantity and efficiency on PSG without eliminating REM.

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Acute severe community-acquired pneumonia: long-term outcomes and post-ICU cognitive impairment

Cognitive impairment after critical illness is common and persistent — in ARDS survivors it ranges from 70-100% at hospital discharge to 46-80% at 1 year, with about 20% still impaired at 5 years; in the BRAIN-ICU general ICU cohort, 40% scored in the moderate-TBI range at 3 months and 34% at 12 months. Domains affected: memory (short-term and working), executive function (planning, decision-making, attention), processing speed, visuospatial ability. Mechanisms: hypoxia, inflammation (neuroinflammation), delirium, sedation, metabolic derangement, microvascular dysfunction. Severity ranges from subtle (noticeable only on testing) to severe (resembling mild-to-moderate Alzheimer's). Risk factors: duration of delirium (strongest modifiable predictor), age, pre-existing cognitive impairment, sepsis severity, hypoglycaemia/hyperglycaemia. Prevention: minimise delirium (ABCDEF bundle), minimise sedation (dexmedetomidine preferred over benzodiazepines, PADIS 2018), glucose target 10 mmol/L or less (NICE-SUGAR), early mobilisation, prevent hypoxia. Assessment: MoCA/MMSE at ICU follow-up. Management: cognitive rehabilitation, family education, lifestyle modification.

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Acute severe community-acquired pneumonia: patient and family education

Patient and family education after severe community-acquired pneumonia (CAP) is a core, evidence-based intervention that improves self-care, accelerates recovery, prevents recurrence, and mitigates post-intensive care syndrome (PICS). Education is delivered across the whole admission — not just at the door — and is structured around seven domains: (1) Understanding what happened — pneumonia is an infection of the lung alveoli; explain the organism if known, the ICU course (oxygen, ventilation, antibiotics) and what to expect. (2) Medication management — complete the antibiotic course even when feeling well, know common side-effects (diarrhoea, nausea, rash, photosensitivity with doxycycline/fluoroquinolones), avoid interactions (fluoroquinolones and divalent cations/QT drugs, warfarin potentiation), and correct inhaler technique if an inhaled bronchodilator or corticosteroid is prescribed. (3) Warning signs — fever returning after settling, worsening breathlessness (especially at rest), new or worsening confusion, chest pain, haemoptysis, or inability to tolerate oral medications or fluids mandate immediate medical review. (4) Recovery timeline — most symptoms resolve over 2–6 weeks, full energy return takes 3–6 months, and radiographic clearing lags behind clinical recovery; some patients never fully recover. (5) Lifestyle modification — smoking cessation (single biggest modifiable risk factor), annual influenza vaccine, pneumococcal vaccination, hand hygiene, avoid sick contacts. (6) Follow-up plan — GP review at ~1 week, clinical review at 6 weeks, follow-up chest X-ray (delayed radiographic resolution beyond six weeks should prompt a search for underlying malignancy), ICU follow-up clinic at 2–3 months. (7) PICS awareness — physical weakness, memory and mood changes are expected after ICU, not dementia, and not necessarily permanent. Deliver education with the teach-back technique, plain language below a year-8 reading level, written materials and a written personalised action plan, and always involve family/carers.

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Acute severe community-acquired pneumonia: recovery and follow-up

Recovery from severe CAP requiring ICU admission is prolonged and multifaceted: physical (ICU-acquired weakness, reduced exercise tolerance, deconditioning), cognitive (impaired memory, executive function — from delirium/hypoxia), psychological (PTSD, depression, anxiety), respiratory (reduced lung function, pulmonary fibrosis in some). Follow-up: ICU follow-up clinic at 2-3 months, CXR at 6 weeks to ensure resolution (non-resolving: investigate malignancy, TB, immunodeficiency), pulmonary rehabilitation, vaccination (pneumococcal, influenza), smoking cessation. Complete recovery may take 6-12 months. A substantial proportion never regain baseline — about a third still screen positive for cognitive impairment at 1 year.

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Acute severe community-acquired pneumonia:CAP readmission and recurrence prevention

CAP readmission within 30 days affects roughly 1 in 10 to 1 in 4 patients across published cohorts (8-26%) and is a widely tracked hospital quality metric. Causes: incomplete recovery, complications (empyema, abscess), comorbidity exacerbation (COPD, heart failure), secondary infection, medication non-adherence, premature return to activity. Repeated-CAP readmission runs about 5% within 30 days in a population-based cohort, with CAP-unrelated readmissions roughly three times commoner (higher risk in: elderly, long-term care need, COPD, heart failure, diabetes, CKD, dementia, immunocompromised, smokers, structural lung disease, social isolation, poor functional status, previous CAP hospitalisation, aspiration risk). Prevention strategies: (1) Complete antibiotic course. (2) Smoking cessation. (3) Vaccination (pneumococcal conjugate — PCV20 or PCV21 alone, or PCV15 in series with PPSV23 per ACIP; influenza annual; COVID; RSV in elderly). (4) Treat underlying conditions (COPD optimisation, dental care for aspiration risk, heart-failure and diabetes optimisation). (5) Gradual return to activity. (6) Follow-up (GP within 7 days, CXR 6 weeks). (7) Patient education (warning signs, written action plan). (8) Pulmonary rehabilitation. (9) Address PICS (physical + cognitive impairment increases readmission risk). (10) Structured discharge bundle (medication reconciliation, follow-up appointment scheduled before discharge, vaccination offered, smoking-cessation referral, deterioration action plan).

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ICU-acquired weakness (critical illness myopathy/polyneuropathy)

ICU-acquired weakness (ICUAW) occurs in about a quarter of patients ventilated 7 days or longer (25.3% in the landmark cohort) and roughly half of critically ill adults overall. Comprises critical illness myopathy (CIM — muscle), critical illness polyneuropathy (CIP — peripheral nerves), or both (CINM). Risk factors: sepsis and multi-organ failure, prolonged mechanical ventilation, hyperglycaemia, immobilisation, corticosteroids, neuromuscular blocking agents. Diagnosis: clinical (MRC sum score &lt;48/60), confirmed by electrophysiology (nerve conduction studies, EMG) and sometimes muscle biopsy. Prevention: glycaemic control (intensive insulin cut critical illness polyneuropathy by 44% in Leuven, but the tight 4.5-6.0 mmol/L target increased 90-day mortality in NICE-SUGAR — treat hyperglycaemia, do not over-tighten), minimise sedation (daily sedation interruption), early mobilisation within 72 h of starting ventilation, minimise steroids/NMBAs, avoid under- and over-feeding. Outcomes: prolonged weaning, more ventilator days, worse mortality, and muscle weakness as the dominant complaint at one year.

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Post-intensive care syndrome (PICS)

PICS describes new or worsening impairments in physical, cognitive, or mental health status persisting beyond hospital discharge after critical illness and ICU stay. Each domain is common: PTSD symptoms in about one in five survivors, depressive symptoms in about one in five, anxiety symptoms in about one in three, and cognitive impairment in about a third at one year. Physical: ICU-acquired weakness (CIM/CIP), fatigue, dyspnoea. Cognitive: impaired memory, executive dysfunction, attention deficits (resembles moderate TBI or mild Alzheimer disease). Mental health: PTSD, depression, anxiety. Risk factors: delirium duration (strongest cognitive predictor), sedation, immobility, sepsis, older age, pre-existing impairment. Prevention: minimise sedation (ABCDEF bundle), early mobilisation, delirium prevention, family engagement. Follow-up: ICU recovery clinics screening all three domains. Family members also affected (PICS-Family).

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Pulmonary rehabilitation and functional recovery after ICU admission

Pulmonary and functional rehabilitation after critical illness targets the physical deconditioning, respiratory and limb-muscle weakness, and reduced exercise tolerance that persist long after the acute insult resolves. It is the active treatment arm of the PHYSICAL DOMAIN of the post-intensive care syndrome (PICS). Components: (1) early mobilisation begun IN the ICU (passive range of motion → active-assisted → active → sitting → standing → walking); (2) exercise training — aerobic (walking, cycling, arm ergometry) plus resistance (8-10 muscle groups); (3) respiratory/inspiratory muscle training (incentive spirometry, threshold IMT); (4) education, psychological support, nutritional counselling. Assessment tools: MRC sum score (ICU-acquired weakness), handgrip dynamometry, 6-minute walk test (6MWT), PFIT-s / FSS-ICU / CPAX, Barthel/FIM. ICU-acquired weakness (CIP/CIM) affects about a quarter of patients ventilated more than 7 days (25.3% in the landmark cohort) and is the dominant reversible physical deficit. Evidence is mixed and nuanced: Schweickert 2009 (Lancet) and Burtin 2009 showed early mobilisation improves function, but the larger TEAM trial (Hodgson, NEJM 2022) found routine aggressive early active mobilisation did NOT improve 180-day outcomes and caused more adverse events — practice has shifted to SELECTIVE, goal-directed mobilisation. Timing: begin in ICU → continue on ward → formal pulmonary rehab programme 4-8 weeks post-discharge for 6-12 weeks. In ARDS survivors, physical function remained below normal predicted levels at 5 years; structured rehabilitation is essential.

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Respiratory / ventilation

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Acute Severe COPD Exacerbation: NIV and Invasive Ventilation — Comprehensive ICU Management

An acute severe exacerbation of COPD (AECOPD) causing hypercapnic (type 2) respiratory failure is an ICU emergency built on three pillars: titrated controlled oxygen (SpO2 88-92 per cent — the range recommended by respiratory and ambulance guidelines; titrated oxygen reduced mortality, hypercapnia and acidosis versus high-flow oxygen in the prehospital RCT, and SpO2 under 88% or over 96% each about doubles the risk of a serious adverse outcome), a medical bundle (air-driven nebulised salbutamol with ipratropium, prednisolone 40 mg daily for 5 days — the REDUCE trial — and antibiotics when Anthonisen criteria are met), and escalating respiratory support driven by the arterial pH. Bilevel non-invasive ventilation, inspiratory pressure titrated toward a tidal volume of about 6-10 mL/kg predicted body weight (HAPPEN), is first-line for the acidotic patient (pH &lt;7.35) — the Plant trial (Lancet 2000) and the Lightowler Cochrane meta-analysis (BMJ 2003) prove it cuts intubation, mortality, and length of stay. Intubate when NIV fails (worsening acidosis despite an adequate trial, falling GCS, peri-arrest) and ventilate with a low rate, low tidal volume and long expiratory time, keeping external PEEP below intrinsic PEEP — hyperinflation rose when rate, minute ventilation or tidal volume rose (Tuxen), and auto-PEEP can severely depress cardiac output (Pepe and Marini).

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Acute Severe Ventilation Weaning and Liberation from Mechanical Ventilation — Comprehensive ICU Management

Weaning (liberation) from mechanical ventilation is the graded withdrawal of ventilatory support once the precipitating cause of respiratory failure has resolved. Readiness is assessed daily against objective criteria — resolution of the cause, FiO2 &lt;0.4, PEEP &lt;8 cmH2O, haemodynamic stability, adequate cough and gag, manageable secretions, and an awake, triggering patient — followed by a spontaneous breathing trial (SBT) delivered as pressure support 5-7 cmH2O with PEEP 5, or a T-piece, for 30-120 minutes. The patient passes if respiratory rate is &lt;35, SpO2 &gt;90 per cent, heart rate &lt;140, with no agitation, diaphoresis, or distress. The ABC trial (Girard, Lancet 2008) proved that pairing a daily spontaneous awakening trial (SAT, daily sedation interruption) with a daily SBT — the 'wake up and breathe' protocol — shortens ventilation time and ICU stay and saves one life for every seven patients treated. Protocol-directed (nurse or respiratory-therapist driven) weaning outperforms physician-directed weaning. Weaning is classified as simple, difficult (more than three SBT attempts or more than seven days), or prolonged (more than fourteen days); difficult and prolonged weaning demands a systematic hunt for the cause — cardiac (weaning-induced pulmonary oedema from left ventricular dysfunction unmasked by the switch to negative-pressure breathing), respiratory-muscle weakness (ICU-acquired weakness), residual respiratory load (auto-PEEP, secretions), electrolyte derangement, or delirium and agitation. The cuff leak test (leak under 130 mL or under 12 per cent of tidal volume) identifies patients at high risk of post-extubation stridor, who benefit from prophylactic steroids, who benefit from prophylactic steroids. Prophylactic non-invasive ventilation (NIV) immediately after extubation prevents reintubation in high-risk patients (COPD, hypercapnia, cardiac failure); NIV used as rescue after established extubation failure is harmful. Tracheostomy facilitates prolonged weaning, but the TracMan trial (Young, JAMA 2013) showed no mortality benefit to early (day 4) over late (day 10) placement.

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Airway Pressure Release Ventilation (APRV) and Advanced Ventilation Modes — Comprehensive ICU Management (APRV, Bilevel, PAV, NAVA, ASV)

Advanced modes of mechanical ventilation move control away from clinician-set, fixed breaths toward modes that either sustain alveolar recruitment (APRV, bilevel) or proportionalise support to the patient's own effort and neural drive (PAV, NAVA, ASV). Airway pressure release ventilation (APRV) is a pressure-controlled, time-cycled mode that applies a continuous high CPAP (Phigh, set from the plateau or peak inspiratory pressure of the preceding conventional ventilation) held for a long time (Thigh) with brief release periods to a low pressure (Plow 0 cmH2O) for a short time (Tlow ≤0.5 s), allowing spontaneous breathing throughout the cycle. The high mean airway pressure maintains alveolar recruitment and oxygenation (an open-lung strategy), the brief release clears CO2, and the preserved spontaneous breathing reduces sedation, preserves venous return, and protects the diaphragm. Bilevel (BiVent, Duo-PAP) is the generalised two-level mode with set mandatory breaths and a more conventional ratio, giving more control than APRV. Proportional assist ventilation (PAV) amplifies the patient's own inspiratory effort — flow and volume are delivered in proportion to patient demand, requiring an intact respiratory drive. Neurally adjusted ventilatory assist (NAVA) delivers support in proportion to the electrical activity of the diaphragm (EAdi), measured via a specialised nasogastric tube — the most physiological mode, because it directly reads neural respiratory drive and uses it to trigger, cycle, and titrate support. Adaptive support ventilation (ASV) automatically adjusts pressure and rate from moment to moment based on the patient's lung mechanics and respiratory drive, targeting the breathing pattern of minimum work of breathing. Clinically, APRV is used as an open-lung strategy in ARDS with an intact drive, NAVA for the difficult-to-ventilate or dyssynchronous patient, and ASV for stable weaning. The critical, repeatedly-tested evidence point is that NO advanced mode has shown a mortality benefit over conventional volume-controlled or pressure-controlled ventilation in ARDS — the PATIENT and the underlying disease, not the mode, determine outcome — but advanced modes may reduce sedation, dyssynchrony, and delirium.

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APRV, Bilevel & Airway-Pressure Release Ventilation

Airway pressure release ventilation (APRV) is a pressure-controlled, time-cycled mode that applies two levels of CPAP — a high pressure (P-high) set from the plateau or peak inspiratory pressure of the preceding conventional mode and held for a long T-high, and a brief release to a low pressure (P-low, commonly 0 cmH2O) for a short T-low terminated when expiratory flow reaches 75 per cent of its peak — allowing spontaneous breathing throughout the cycle. The high mean airway pressure maintains alveolar recruitment and oxygenation (an open-lung strategy), while the intermittent release clears CO2 and the spontaneous breaths improve cardiac index and venous return and reduce sedation. The extreme inverse I:E ratio keeps the lung inflated most of the time and derecruits only partially on each brief release. APRV is used selectively in moderate-severe ARDS as a rescue or an alternative to conventional ventilation, and in refractory hypoxaemia; systematic reviews and a COVID-era RCT show improved oxygenation without a clear mortality benefit, so it is not the standard first-line. Contraindications are obstructive airway disease (CO2 retention, air-trapping) and profound shock (the elevated intrathoracic pressure). Bilevel (BiVent/Duo-PAP) is the generalised two-level mode with a more conventional ratio and set mandatory breaths; APRV is its extreme, inverse-ratio, spontaneous-breathing form.

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Auto-PEEP & Ventilation in Obstruction (Asthma & COPD)

In severe airflow obstruction (asthma, COPD), incomplete expiration traps gas and generates intrinsic (auto-) PEEP and dynamic hyperinflation, which raise the work of breathing, depress venous return and cardiac output, and risk barotrauma. Ventilation must prioritise emptying over ventilation: controlled (permissive) hypercapnia that corrects hypoxaemia while accepting hypercapnia, a low tidal volume, a low respiratory rate for a long expiratory time, a high inspiratory flow, and external PEEP kept below the measured intrinsic PEEP. If the blood pressure crashes after intubation, disconnect the circuit to let the lung deflate.

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ECMO Complications — Clotting, Haemolysis, Infection, Neurological

ECMO is a high-risk therapy whose complications fall into four categories. Clotting: bleeding is the commonest serious complication (anticoagulation plus large cannulae; intracranial haemorrhage the most feared), balanced against circuit thrombosis from under-anticoagulation. Haemolysis: from pump shear, kinked cannulae, or an oxygenator clot — a rising plasma-free haemoglobin, falling haptoglobin, dark urine, hyperkalaemia, and haemoglobinuric AKI. Infection: cannula-site, bloodstream, and nosocomial. Neurological: ischaemic and haemorrhagic stroke and intracranial haemorrhage, plus the hypoxic brain injury of ECPR. Anticoagulate to the lowest effective target; monitor the circuit pressures, the free haemoglobin, the cultures, and have a low threshold for a CT for any neurological change.

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High-Frequency Oscillatory Ventilation (HFOV)

High-frequency oscillatory ventilation (HFOV) is characterised by the rapid delivery of small tidal volumes together with the application of high mean airway pressures — the open-lung, lung-protective concept (Chan 2007; Fessler 2007: adult frequency typically 6 Hz or less, generous mean airway pressures). Gas exchange occurs not by bulk tidal flow alone but by five combined transport mechanisms (direct alveolar ventilation, convective mixing among units of unequal time constants, asymmetric velocity-profile convection, longitudinal/Taylor dispersion, and molecular diffusion; Chang 1984, who also showed increasing tidal volume improves gas exchange more effectively than increasing frequency). Oxygenation is managed through mean airway pressure and FiO2, CO2 clearance through pressure amplitude and frequency. Two landmark trials in adult ARDS were negative: the OSCILLATE trial (NEJM 2013, stopped early) found in-hospital mortality 47% vs 35% (RR 1.33) — HFOV 'does not reduce, and may increase' in-hospital mortality; the OSCAR trial (NEJM 2013) found no significant effect on 30-day mortality (41.7% vs 41.1%); a Cochrane review (2016) found no mortality reduction (RR 0.92) and does not support first-line use. HFOV is therefore NOT recommended for routine adult ARDS — at most a rarely-used rescue.

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Inhaled Pulmonary Vasodilators — Nitric Oxide & Inhaled Prostacyclin

Inhaled pulmonary vasodilators (inhaled nitric oxide and inhaled prostacyclin/epoprostenol) selectively vasodilate the vasculature of well-ventilated alveoli, improving V/Q matching (oxygenation by reducing shunt) and reducing pulmonary vascular resistance (RV afterload), with minimal systemic vasodilation because they are inactivated on entering the blood. Inhaled nitric oxide (1-40 ppm) risks methaemoglobinaemia, rebound on withdrawal, and nitrogen-dioxide toxicity; inhaled prostacyclin (nebulised) is cheaper and avoids methaemoglobinaemia. They are used for refractory hypoxaemia (a transient oxygenation benefit with no mortality gain in ARDS), pulmonary hypertension and right-ventricular failure, and persistent pulmonary hypertension of the newborn. They must be tapered to avoid rebound.

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PEEP — Physiology, Setting & Optimisation

Positive end-expiratory pressure (PEEP) is positive pressure maintained in the airways above atmospheric at end-expiration. It recruits collapsed alveoli, raises functional residual capacity, improves oxygenation by reducing shunt, and prevents the cyclic collapse-reopening of atelectrauma, which is central to lung-protective ventilation (the ARDSnet PEEP/FiO2 tables). Excessive PEEP reduces venous return and cardiac output, raises RV afterload, overdistends alveoli (volutrauma), and raises intracranial pressure. 'Best PEEP' maximises oxygenation and compliance without haemodynamic compromise. Intrinsic (auto-) PEEP from incomplete expiration in COPD and asthma causes hyperinflation; applying external PEEP at about 75-80 per cent of auto-PEEP counteracts the inspiratory threshold load.

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Pleural Disease — Effusion, Pneumothorax & Chest Drains

Pleural disease in the ICU covers three problems: pleural effusion (a transudate or an exudate, distinguished by Light's criteria, drained if infected or symptomatic), pneumothorax (primary or secondary; managed by observation, aspiration, or a chest drain; tension pneumothorax is a clinical diagnosis treated by immediate needle decompression then a chest drain), and the chest drain itself (inserted in the safe triangle, over the rib, connected to an underwater seal; bubbling indicates an air leak, swinging indicates patency, and cessation indicates resolution; never clamp a bubbling drain). The chest drain is removed when the air leak has resolved and the lung is expanded on CXR. Re-expansion pulmonary oedema is a risk if a large effusion or pneumothorax is drained too rapidly.

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Pneumonia — CAP, HAP, VAP & Aspiration

Pneumonia is classified by the setting of acquisition: community-acquired (CAP, outside hospital or within 48 hours of admission), hospital-acquired (HAP, after 48 hours in hospital), ventilator-associated (VAP, after 48 hours of intubation), and aspiration. The severity is graded by CURB-65, PSI, or the IDSA/ATS severe-CAP criteria. The commonest CAP pathogen is Streptococcus pneumoniae; atypicals (Mycoplasma, Legionella, Chlamydia) are also important. Late-onset HAP/VAP introduces multidrug-resistant organisms (Pseudomonas, MRSA, ESBL). The empirical antibiotics are guided by the setting, the severity, and the local antibiogram; de-escalate once the cultures identify the organism. Duration is typically 5-7 days for CAP and 7 days for VAP.

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Prone Ventilation — Technique & Physiology

Prone ventilation reduces mortality in severe ARDS (PROSEVA, NEJM 2013) by recruiting the dorsal lung, improving ventilation-perfusion matching, and reducing ventilator-induced lung injury through more uniform lung stress and strain — a benefit beyond oxygenation. Physiologically, proning places the heart on the sternum (not the lung) and flattens the pleural-pressure gradient, so the dorsal lung (the larger, healthier region) recruits and the ventral lung is less overdistended. The technique is a coordinated team procedure with a dedicated airway leader, preceded by a checklist (a secured airway, lines managed, eye and pressure-area protection, gastric decompression, adequate sedation), with the patient kept prone for at least 16 hours. The complications — accidental extubation, line loss, and pressure injury — are minimised by a trained team.

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Pulmonary Hypertension & Cor Pulmonale

Pulmonary hypertension (a mean pulmonary artery pressure above 20 mmHg) is classified into five WHO groups: pulmonary arterial hypertension (group 1), left heart disease (2), lung disease and hypoxia (3), chronic thromboembolic (4), and multifactorial (5). Cor pulmonale is the right-ventricular hypertrophy, dilation, and failure from the pulmonary hypertension, classically from lung disease (group 3). The thin-walled right ventricle tolerates volume but not pressure: a rising pulmonary vascular resistance causes it to dilate and fail, the septum bows into the left ventricle (the D-shaped septum), the left-sided output falls, and tricuspid regurgitation worsens. The ICU management optimises the preload (diurese, do not overfill), reduces the afterload (inhaled nitric oxide, prostacyclin, PDE5 inhibitors), supports the contractility (milrinone, dobutamine), and maintains the systemic blood pressure to preserve the RV coronary perfusion — vasopressin is preferred, as it raises the systemic vascular resistance without raising the pulmonary.

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Pulmonary Oedema — Cardiogenic vs ARDS

Pulmonary oedema is fluid in the alveoli from one of two mechanisms: cardiogenic (hydrostatic — raised pulmonary capillary pressure from left-heart failure) or non-cardiogenic (increased permeability — ARDS, a damaged alveolar-capillary membrane, wedge pressure not raised). The distinction is made on the PAWP, the BNP, the echocardiogram, and the CXR pattern. Cardiogenic oedema is treated with CPAP/NIV, diuretics, and vasodilators; ARDS is treated with lung-protective ventilation, PEEP, proning, and a conservative fluid strategy. The oedema-fluid-to-serum protein ratio distinguishes them at the bedside (mean 0.37–0.46 in cardiogenic series versus 0.84 in permeability oedema — a ratio over 0.6 suggests increased permeability).

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Refractory Hypoxaemia Adjuncts — Proning, iNO, Recruitment, NMBA, ECMO

Refractory hypoxaemia in severe ARDS is defined as a PaO2/FiO2 under 100 despite optimised lung-protective ventilation (Vt 6 mL/kg PBW, Pplat under 30 cmH2O, optimised PEEP, FiO2 1.0). A staged set of adjuncts is deployed: optimise ventilation (driving-pressure-guided PEEP, permissive hypercapnia), then PRONE POSITIONING (PROSEVA, NEJM 2013 — at least 16 h/day in PaO2/FiO2 under 150) which is the ONLY adjunct that reduces mortality, then transient oxygenation therapies (inhaled nitric oxide or inhaled epoprostenol — no survival benefit, AKI/rebound risk), then short neuromuscular blockade for asynchrony (ACURASYS 2010 benefit refuted by ROSE 2019 — NOT routine), then VV-ECMO (EOLIA 2018, CESAR 2009) for the refractory case, with ECCO2R as a partial support. Aggressive recruitment plus very high PEEP is harmful (ART 2017).

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Severe & Near-Fatal Asthma in the ICU

Severe or near-fatal asthma (status asthmaticus) is graded by the British Thoracic Society as acute severe, life-threatening, or near-fatal. The escalation ladder is oxygen (SpO2 94-98 per cent), repeated or continuous nebulised salbutamol with ipratropium 0.5 mg, an early systemic corticosteroid (oral prednisolone, or intravenous hydrocortisone when the oral route is unsuitable), intravenous magnesium sulphate 2 g over 20 minutes for severe disease not responding to initial treatment, and second-line aminophylline or IV salbutamol. If the patient tires or the PaCO2 rises, intubate with a bronchodilating induction agent such as ketamine and ventilate for permissive hypercapnia (low tidal volume, low rate, long expiration, plateau pressure kept below about 30 cmH2O). Refractory bronchospasm is treated with inhalational volatile anaesthetics (sevoflurane), Heliox, or VV-ECMO. Watch for the auto-PEEP arrest, tension pneumothorax, lactic acidosis, and hypokalaemia.

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VA-ECMO for Cardiogenic Shock & Extracorporeal CPR (ECPR)

Veno-arterial ECMO (VA-ECMO) drains venous blood, oxygenates and decarboxylates it, and returns it to the arterial system — providing both circulatory and respiratory support for refractory cardiogenic shock (a bridge to recovery, decision, transplant, or durable LVAD) and for refractory cardiac arrest (extracorporeal CPR, ECPR). Cannulation is peripheral (femoro-femoral, rapid, for shock and ECPR) or central. The complications include bleeding (the largest), limb ischaemia (mitigated by a distal perfusion cannula), left-ventricular distension and pulmonary oedema (the failing LV cannot eject against the retrograde aortic flow — may need an Impella or vent), differential hypoxaemia (the Harlequin or north-south syndrome), thrombosis, haemolysis, and infection. ECPR outcomes are best in selected, rapidly-cannulatable patients. Severity and reversibility are graded by the SCAI A-E stages and the SAVE score; weaning is by staged flow reduction with echocardiographic and pulse-pressure recovery assessment.

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Weaning from Mechanical Ventilation — SBT, Protocols & Prolonged Weaning

Weaning is the process of discontinuing mechanical ventilation: a daily readiness screen, a spontaneous breathing trial (SBT), and extubation if the trial is tolerated. In the WIND cohort, 57 per cent of ventilated patients wean within 24 hours (simple), 10 per cent are difficult (separation between one day and one week), and 9 per cent are prolonged (one week or more from the first separation attempt). The SBT uses minimal support — a T-piece or low pressure support — for 30 minutes to 2 hours; tolerance means a respiratory rate under 35, an SpO2 over 90 per cent, a heart rate under 140, no distress, and stable haemodynamics. The **ABC trial** (Girard, Lancet 2008) paired a daily sedation interruption (SAT) with the daily SBT and improved outcomes. The **rapid shallow breathing index (RSBI = RR/Vt in litres), under 105, predicts success** (Yang & Tobin, NEJM 1991). Before extubating, assess airway patency with a **cuff leak test** and the patient's ability to protect the airway (cough on suction, gag); anticipate **post-extubation stridor** (especially in females, prolonged intubation, and traumatic intubation) and have a low threshold for prophylactic steroids and post-extubation high-flow nasal cannula or NIV. Reintubation rates run 10-20 per cent; a failed extubation carries a markedly higher mortality. Protocolised, nurse- or therapist-driven weaning reduces the duration of mechanical ventilation versus physician-directed weaning (Ely 1996).

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endocrine

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Acute Severe DKA and HHS — Comprehensive Integrated Diabetic Emergencies

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are the two life-threatening hyperglycaemic emergencies of diabetes, lying on a spectrum of insulin deficiency. DKA = absolute insulin deficiency → hyperglycaemia (over 250 mg/dL, about 13.9 mmol/L), metabolic acidosis (arterial pH under 7.30, bicarbonate under 18 mEq/L), and ketosis (serum ketones positive, anion gap over 10); occurs mainly in type 1 diabetes. HHS = relative insulin deficiency with enough residual insulin to suppress ketogenesis but not hyperglycaemia → extreme hyperglycaemia (over 33.3 mmol/L by ADA, over 30 by JBDS), hyperosmolality (320 mOsm/kg or more), profound dehydration (100-220 mL/kg), and NO significant ketoacidosis (pH over 7.3, bicarbonate 15 or more, ketonaemia 3.0 mmol/L or less); occurs mainly in elderly type 2 diabetics. Precipitants are shared — infection is the single commonest. Management is fluids first (0.9% saline 15-20 mL/kg/h), potassium addressed before insulin (delay insulin if K+ under 3.3 mmol/L), fixed-rate insulin 0.1 units/kg/h (JBDS de-escalates to 0.05 once glucose is under 14 mmol/L; HHS 0.05 units/kg/h per JBDS, 0.1 per ADA), bicarbonate only if pH under 6.9, and treatment of the precipitant.

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Acute Thyroid Storm and Myxoedema Coma — Comprehensive Thyroid Emergencies

Thyroid storm and myxoedema coma are the two life-threatening decompensated thyroid emergencies at opposite ends of the thyroid hormone spectrum. Thyroid storm (thyrotoxic crisis) = the extreme state of thyrotoxicosis with hyperthermia, tachyarrhythmia (including atrial fibrillation), neuropsychiatric/CNS disturbance, congestive heart failure and GI/hepatic dysfunction, usually occurring in the presence of an inciting trigger; diagnosis is clinical using the Burch-Wartofsky Point Scale (BWPS score of ≥45 highly suggestive, 25-44 impending storm), as TFT results take days and the syndrome must be treated empirically. Common precipitants include infection (#1), surgery, trauma, radioiodine therapy, withdrawal of antithyroid drugs, amiodarone, iodinated contrast, DKA, and parturition. Management is multimodal and stepwise — first-line thionamide plus beta-adrenergic blocker, FOLLOWED BY inorganic iodine, with corticosteroids and adjuncts (cholestyramine, plasmapheresis or emergent thyroidectomy in appropriately severely ill patients); published case protocols use PTU 1 g loading then 200 mg every 4 hours, or PTU 250 mg every 4 hours via nasogastric tube with hydrocortisone 100 mg intravenously every 8 hours and propranolol 50 mg every 4 hours via nasogastric tube; ultra-short-acting esmolol is safer than propranolol when cardiac failure complicates storm (oral propranolol preceded cardiorespiratory arrest in three published cases); antipyresis with paracetamol NOT aspirin (aspirin intoxication has itself precipitated storm) plus external cooling and treatment of the trigger. Myxoedema coma = decompensated severe hypothyroidism with impaired consciousness, hypothermia, hypoventilation and hypercapnic respiratory failure with CO2 narcosis, dilutional hyponatraemia, hypoglycaemia and ileus; management is IV levothyroxine (200-500 mcg initial dose then 50-100 mcg daily, concurrent T3 can be considered, most authorities prefer IV T4 over IV T3, and oral loading 300-500 mcg with taper over 3-5 days is effective where IV is unavailable), hydrocortisone until coexisting adrenal insufficiency is ruled out, passive rewarming with careful attention to hypotension, correction of electrolyte abnormalities, treatment of infections, and respiratory/haemodynamic support in ICU. Mortality of thyroid storm is 10-50% with treatment (80-100% without); myxoedema coma mortality is reported from about 20% to as high as 60%.

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renal-metabolic

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Acute Severe Rhabdomyolysis — Comprehensive ICU Management

Rhabdomyolysis — skeletal muscle breakdown releasing intracellular contents (myoglobin, creatine kinase, potassium, phosphate, urate) into the circulation → AKI (myoglobin nephrotoxicity + intratubular cast formation + volume depletion), hyperkalaemia (lethal arrhythmia), hypocalcaemia, metabolic acidosis, compartment syndrome. Causes: crush injury (trauma, building collapse, prolonged immobilisation), exertional (marathon, seizures, agitation/delirium), drugs (statins #1 — especially with fibrates/calcineurin inhibitors, illicit drugs — MDMA, cocaine, heroin), infections (influenza, legionella, coxsackie, severe sepsis), metabolic (hypokalaemia, hypophosphataemia, DKA/HHS), genetic (McArdle disease, CPT deficiency, malignant hyperthermia), inflammatory (polymyositis, dermatomyositis). Diagnosis: CK >5x ULN (>1000 IU/L — typically 10,000-100,000+) + myoglobinuria (dark/tea-coloured urine + positive blood on dipstick but NO RBCs on microscopy) + hyperkalaemia + elevated AST/ALT (muscle-derived). Management: AGGRESSIVE IV FLUIDS (the #1 intervention — high urine flow — about 400 mL/h crystalloid, up to 12 L or more per day in severe crush — crystalloid, ideally balanced solution), treat hyperkalaemia (calcium gluconate + insulin/dextrose), urine alkalinisation (controversial — sodium bicarbonate mainly in acidotic patients — evidence is limited), renal replacement therapy if severe AKI (CRRT preferred), fasciotomy if compartment syndrome. Mortality: about 10 per cent overall, higher when AKI develops.

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Pulmonary-Renal Syndrome in the ICU

Pulmonary-renal syndrome (PRS) — the combination of diffuse alveolar haemorrhage (DAH) and rapidly progressive glomerulonephritis (RPGN) — caused by small-vessel vasculitis: ANCA-associated vasculitis (granulomatosis with polyangiitis [GPA/Wegener], microscopic polyangiitis [MPA], eosinophilic granulomatosis with polyangiitis [EGPA/Churg-Strauss]), anti-glomerular basement membrane disease (Goodpasture syndrome), and immune-complex-mediated diseases (lupus nephritis, cryoglobulinaemia, IgA nephropathy). ICU presentation: respiratory failure from DAH (haemoptysis, diffuse bilateral infiltrates, hypoxaemia) + acute kidney injury from RPGN (rapidly rising creatinine, active urinary sediment, proteinuria). Diagnostic workup: ANCA (MPO-ANCA/p-ANCA, PR3-ANCA/c-ANCA), anti-GBM antibodies, ANA/dsDNA/complement, cryoglobulins, renal biopsy (crescentic GN), bronchoscopy (progressively bloody lavage). ICU management: plasma exchange (for anti-GBM and severe ANCA), high-dose corticosteroids (methylprednisolone pulses 500-1000 mg/day x 3), cyclophosphamide or rituximab, renal replacement therapy, lung-protective ventilation for DAH. Mortality 10-30% (higher with DAH requiring ventilation).

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Rheumatological Emergencies in the ICU

Rheumatological emergencies in the ICU — life-threatening presentations of systemic autoimmune diseases requiring critical care: (1) scleroderma renal crisis (SRC — sudden malignant hypertension + AKI + microangiopathic haemolysis in diffuse cutaneous systemic sclerosis — ACE inhibitor is LIFE-SAVING), (2) SLE emergencies (neuropsychiatric lupus — seizures, psychosis, transverse myelitis; lupus pneumonitis; lupus nephritis with RPGN; catastrophic antiphospholipid syndrome), (3) inflammatory myopathy with interstitial lung disease (antisynthetase syndrome — anti-Jo-1, anti-MDA5 — rapidly progressive ILD), (4) rheumatoid vasculitis and atlantoaxial subluxation, (5) adult-onset Still disease with MAS. Management: ACE inhibition, pulse methylprednisolone with cyclophosphamide, triple immunosuppression for anti-MDA5 RP-ILD, difficult-airway anticipation in RA, and PAH-targeted therapy in systemic sclerosis.

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Systematic Arterial Blood Gas Interpretation — Comprehensive

Systematic arterial blood gas (ABG) interpretation — the 10-step approach to analysing every ABG in ICU. Step 1: pH (acidosis &lt;7.35, alkalosis >7.45). Step 2: PaCO2 (respiratory — high = acidosis, low = alkalosis). Step 3: HCO3 (metabolic — low = acidosis, high = alkalosis). Step 4: Determine primary disorder (pH direction matches primary disorder). Step 5: Check compensation (expected PaCO2 for metabolic, expected HCO3 for respiratory — if compensation is INADEQUATE → mixed disorder). Step 6: A-a gradient (PAO2 - PaO2 — normal value widens with age — elevated = V/Q mismatch/shunt/diffusion). Step 7: Anion gap (Na - Cl - HCO3 — normal 8-12 — elevated = unmeasured anions [GOLDMARK: Glycols, Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis]). Step 8: Delta gap ((AG-12)/(24-HCO3) — ratio 1.0 = pure AG acidosis, &lt;1.0 = combined AG + non-AG acidosis, >2.0 = combined AG acidosis + metabolic alkalosis). Step 9: Osmolar gap (measured - calculated — elevated = toxic alcohols). Step 10: Lactate (elevated = tissue hypoperfusion/anaerobic metabolism). Common ICU patterns: sepsis (metabolic acidosis + respiratory alkalosis), COPD (respiratory acidosis + metabolic compensation), DKA (high AG metabolic acidosis + respiratory compensation), renal failure (high AG + non-AG metabolic acidosis).

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Domain

oncology

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Acute Severe Tumour Lysis Syndrome — Comprehensive ICU Management

Acute severe tumour lysis syndrome (TLS) = a metabolic oncological emergency from rapid lysis of malignant cells releasing intracellular contents into the extracellular space: HYPERKALAEMIA (intracellular K+ dumped — most dangerous, causes fatal arrhythmia), HYPERPHOSPHATAEMIA (tumour cells carry ~4x normal phosphate), HYPOCALCAEMIA (secondary — Ca2+ precipitates with phosphate as calcium-phosphate crystals), and HYPERURICAEMIA (nucleic acid breakdown → purines → xanthine → uric acid via xanthine oxidase). Uric acid and calcium-phosphate precipitate in renal tubules → acute kidney injury (AKI), which then reduces K+ and phosphate excretion → a self-amplifying vicious cycle. Onset 12-72h after cytotoxic therapy (occasionally spontaneous before therapy in high-burden disease). Highest risk: Burkitt lymphoma, lymphoblastic lymphoma, acute lymphoblastic leukaemia (ALL, WBC high), high-grade non-Hodgkin lymphoma (bulky), AML with high WBC, and rapidly responding tumours treated with venetoclax/rituximab/steroids. Cairo-Bishop definition: laboratory TLS (≥2 abnormal values — urate ≥475 µmol/L/8 mg/dL, K+ ≥6.0 mmol/L, phosphate ≥1.45 mmol/L, Ca2+ ≤1.75 mmol/L or 25% change from baseline within 3 days before to 7 days after therapy) vs clinical TLS (LTLS PLUS AKI, arrhythmia/sudden death, or seizure). Prevention (cornerstone): aggressive IV hydration (3 L/m2/day or ~2-3 L/day, goal urine output >100 mL/m2/h) + urate-lowering therapy stratified by risk — rasburicase 0.15-0.2 mg/kg IV for HIGH risk (recombinant urate oxidase, converts EXISTING uric acid → soluble allantoin, acts within hours; CONTRAINDICATED in G6PD deficiency — haemolysis/methaemoglobinaemia), allopurinol 300 mg/day for INTERMEDIATE risk (xanthine oxidase inhibitor, prevents NEW uric acid only). Treatment of established TLS: aggressive hydration, rasburicase 0.15-0.2 mg/kg, treat hyperkalaemia per standard protocol (calcium gluconate for ECG changes → insulin/dextrose → salbutamol → potassium binders), do NOT routinely treat asymptomatic hypocalcaemia (calcium worsens Ca-P deposition), renal replacement therapy (CRRT preferred) for refractory hyperkalaemia/hyperphosphataemia or AKI. Alkalinisation of urine is NOT recommended (worsens calcium-phosphate precipitation).

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Immune Checkpoint Inhibitor Toxicity in the ICU

Immune checkpoint inhibitor (ICI) toxicity — immune-related adverse events (irAEs) from CTLA-4 (ipilimumab), PD-1 (nivolumab, pembrolizumab), and PD-L1 (atezolizumab, durvalumab) inhibitors causing pneumonitis, colitis, hepatitis, endocrinopathy (thyroiditis, hypophysitis, adrenalitis), myocarditis, nephritis, neurotoxicity, and dermatological reactions. ICU presentation: respiratory failure (pneumonitis), shock (myocarditis, adrenal crisis), severe colitis with perforation, encephalitis, Guillain-Barre syndrome variant, and Stevens-Johnson syndrome. Management framework: stop ICI, grade severity, corticosteroids (oral prednisone 0.5-1 mg/kg/day for grade 2; IV methylprednisolone 1-2 mg/kg/day for grade 3-4, or pulse dosing such as 1 g/day if life-threatening), second-line immunosuppression for steroid-refractory disease (infliximab or vedolizumab for colitis, mycophenolate for pneumonitis/hepatitis, IVIG/plasma exchange for neurologic syndromes), and permanent discontinuation for grade 4 toxicity except endocrinopathies controlled on hormone replacement. Pneumonitis 5% overall with anti-PD-1/PD-L1 (10% combination, 3% monotherapy); myocarditis 1.14% prevalence, median onset 34 days, mortality 35-50%; colitis the signature CTLA-4 toxicity; endocrine irAEs mostly within 12 weeks of starting ICI.

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Domain

Haematology

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Acute sickle cell crisis in the ICU

Sickle cell crisis is caused by polymerisation of sickle haemoglobin (HbS) under hypoxia/dehydration/infection → red blood cells sickle → vaso-occlusion → ischaemia, pain, organ damage. The molecular lesion is a single point mutation in the β-globin gene (HBB): GAG→GTG at codon 6, substituting valine for glutamic acid at position 6 of the β-chain. Under deoxygenation HbS polymerises via hydrophobic contacts into 14-strand fibres that distort the erythrocyte into the classic sickle shape → haemolysis, endothelial activation, leucocyte adhesion and vaso-occlusion. Types: vaso-occlusive crisis (pain — bones, chest, abdomen), acute chest syndrome (new infiltrate + respiratory symptoms — leading cause of death), splenic sequestration (children), aplastic crisis (parvovirus B19), stroke, priapism. Management: oxygen, IV hydration (normal saline 1-1.5x maintenance), analgesia (opioids — morphine PCA), treat triggers (infection, dehydration). Exchange transfusion for severe complications (stroke, acute chest syndrome). Hydroxyurea, crizanlizumab and voxelotor for prevention/modification. CRISPR gene therapy (Casgevy, exagamglogene autotemcel) FDA/MHRA-approved 2023.

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Acute transfusion reactions: TRALI, TACO, allergic, haemolytic, and septic

Transfusion reactions range from mild (febrile, allergic) to life-threatening (TRALI, acute haemolytic, anaphylaxis, septic, TACO). CLASSIFICATION by mechanism: (1) IMMUNE: acute haemolytic (ABO mismatch — intravascular haemolysis, catastrophic, STOP immediately), delayed haemolytic (days-weeks), TRALI (donor anti-leucocyte antibodies -> acute lung injury within 6h), anaphylactic (IgA deficiency in recipient — severe), febrile non-haemolytic (cytokines), allergic/urticarial (mild). (2) NON-IMMUNE: TACO (volume overload), septic (bacterial contamination of platelets — fever, shock), hyperkalaemia (old RBCs), hypocalcaemia (citrate), hypothermia. KEY ACTION for ANY reaction: STOP transfusion, maintain IV access with normal saline, assess (ABC), send blood unit + samples to blood bank, report. TRALI: new ARDS within 6h of transfusion — manage as ARDS (oxygen, ventilation), diuretics DON'T help (not volume overload). TACO: volume overload — diurese. Acute haemolytic: ABO incompatibility — STOP, fluids, support BP/kidneys, treat DIC. Anaphylactic: adrenaline IM/IV.

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Disseminated intravascular coagulation: ISTH score, transfusion, and management

Disseminated intravascular coagulation (DIC) = systemic activation of coagulation -> microvascular thrombosis + consumption of platelets/clotting factors -> BLEEDING + THROMBOSIS simultaneously. CAUSES: sepsis (most common — 50%), trauma, malignancy (leukaemia, solid tumour — mucin), obstetric (amniotic fluid embolus, placental abruption, severe pre-eclampsia/HELLP), transfusion reaction, snake bite, severe liver disease. CLINICAL: BLEEDING (oozing from IV sites, gums, GI, GU, petechiae, ecchymoses — from consumed platelets/factors) + THROMBOSIS (purpura fulminans, digital ischaemia, AKI, ARDS, MOF — from microvascular clots). DIAGNOSIS: ISTH overt-DIC score (platelets, fibrinogen, FDP/D-dimer, PT — score ≥5 = overt DIC). MANAGEMENT: TREAT THE UNDERLYING CAUSE (the #1 priority — antibiotics for sepsis, delivery for obstetric, etc.) + SUPPORTIVE (transfuse platelets/fresh frozen plasma/cryoprecipitate if bleeding or high risk — NOT prophylactically) ± ANTICOAGULATION (controversial — for thrombotic DIC — heparin). MORTALITY: 40-80% (high — reflects underlying severity).

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Heparin-induced thrombocytopenia (HIT): 4T score, diagnosis, and non-heparin anticoagulation

Heparin-induced thrombocytopenia (HIT) = immune-mediated (IgG antibody against platelet factor 4 [PF4] + heparin complex) platelet activation → THROMBOCYTOPENIA (paradoxically PROTHROMBOTIC — thrombosis NOT bleeding). TYPE I (non-immune — common, benign — early, mild drop — direct platelet aggregation). TYPE II (IMMUNE — the dangerous form — IgG anti-PF4/heparin → platelet activation → consumption + THROMBOSIS — 5-10 days after heparin start [or rapid if prior exposure within 30 days]). CLINICAL: platelet fall >50% from baseline (NOT necessarily &lt;150 — relative drop), 5-10 days post-heparin, THROMBOSIS (venous — DVT/PE; arterial — limb/stroke; microvascular — skin necrosis at injection site), NO other cause. 4T SCORE (Thrombocytopenia, Timing, Thrombosis, oTher cause): ≤3 = low probability (unlikely HIT — continue heparin); 4-5 = intermediate; ≥6 = high probability (STOP heparin, start alternative). DIAGNOSIS: anti-PF4 ELISA (sensitive, fast) + serotonin release assay (SRA — confirmatory, slow). MANAGEMENT: STOP ALL HEPARIN (including LMWH, heparin flushes, heparin-coated catheters), start NON-HEPARIN anticoagulant (argatroban, bivalirudin, danaparoid, fondaparinux, DOAC), DO NOT give platelets (worsens thrombosis), DO NOT start warfarin alone (skin necrosis, venous limb gangrene — bridge with non-heparin first until platelets recover). MORTALITY: 10-20% (from thrombosis).

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Thrombotic microangiopathy: TTP, HUS, and aHUS in ICU

Thrombotic microangiopathy (TMA): microvascular platelet-rich thrombi → thrombocytopenia + microangiopathic haemolytic anaemia (MAHA) + organ ischaemia. THREE main types: (1) TTP (thrombotic thrombocytopenic purpura): ADAMTS13 deficiency (congenital or autoantibody) → unprocessed ultra-large vWF multimers → platelet microthrombi. Neurological + cardiac predominant. Treatment: PLASMA EXCHANGE (life-saving) + steroids + caplacizumab. (2) HUS (haemolytic uraemic syndrome): Shiga toxin-producing E. coli (STEC — O157:H7) → endothelial damage → renal predominant. Treatment: supportive (no antibiotics, no plasma exchange). (3) aHUS (atypical HUS): complement dysregulation → renal predominant. Treatment: eculizumab (complement inhibitor).

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Domain

Neurocritical

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Acute spinal cord injury and neurogenic shock in ICU

Acute spinal cord injury (SCI): traumatic (falls, road trauma, diving) or non-traumatic (abscess, haematoma, tumour, disc). Neurogenic shock: loss of sympathetic tone below lesion → hypotension + bradycardia (unlike hypovolaemic shock — tachycardic). Occurs with lesions above T6 (most of sympathetic outflow lost). Spinal shock: temporary loss of spinal reflexes below lesion (areflexia, flaccidity) — different from neurogenic shock. ICU management: (1) ABC with C-spine immobilisation. (2) Neurogenic shock — vasopressor-based MAP augmentation (euvolaemia, not fluid loading). (3) MAP augmentation to at least 75-80 mmHg, not beyond 90-95 mmHg, for 3-7 days per AO Spine 2024 (cord perfusion). (4) Early surgical decompression/stabilisation (&lt;24h, STASCIS). (5) Methylprednisolone — benefit only within 8 h (NASCIS II), infectious harm (NASCIS III), not standard of care. (6) Respiratory failure in cervical SCI — diaphragm (C3-5) — intubate early. (7) DVT prophylaxis, pressure-area care, autonomic dysreflexia (bladder trigger in ~85%, up to 90% of cervical/high-thoracic SCI susceptible).

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Acute stroke in ICU: ischaemic, haemorrhagic, and neurocritical care

Acute stroke ICU management. ISCHAEMIC (80%): thrombolysis (alteplase within 4.5h — NINDS, ECASS III), thrombectomy (within 6-24h for large vessel occlusion — DAWN, DEFUSE-3), antiplatelet (aspirin within 24h), prevent complications. HAEMORRHAGIC (20%): blood pressure control (SBP &lt;140 — INTERACT2), reverse coagulopathy, surgery (evacuation for cerebellar >3cm or lobar with deterioration), ICP management. ICU principles: airway, normoxia (SpO2 ≥94%), normocapnia (PaCO2 35-40), normoglycaemia (avoid hypo/hyperglycaemia), normothermia (treat fever), blood pressure management (permissive hypertension for ischaemic, controlled for haemorrhagic), DVT prophylaxis, swallowing assessment before oral intake.

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ICU-acquired weakness: critical illness polyneuropathy and myopathy

ICU-acquired weakness (ICUAW): muscle weakness developing during ICU stay, not attributable to other causes. Affects 25-50% of long-stay ICU patients. Types: (1) CIP (critical illness polyneuropathy) — AXONAL sensorimotor polyneuropathy (distal). (2) CIM (critical illness myopathy) — MYOPATHY (muscle fibre atrophy/necrosis). (3) Combined (CINM — most common). Risk factors: sepsis, multi-organ failure, prolonged immobilisation, corticosteroids, neuromuscular blockade, hyperglycaemia. Diagnosis: clinical (MRC sum score &lt;48), electrophysiology (NCS/EMG), muscle biopsy. Prevention: minimise sedation, early mobilisation, glycaemic control, avoid steroids/NMBA if possible, nutrition. Treatment: supportive (rehabilitation, physiotherapy). Recovery: months-years, may be incomplete.

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Sepsis-associated encephalopathy and ICU delirium update

Sepsis-associated encephalopathy (SAE): brain dysfunction from systemic sepsis (NOT direct CNS infection). Presents as DELIRIUM (acute, fluctuating disturbance of attention/cognition). Mechanisms: blood-brain barrier disruption, neuroinflammation (cytokines cross BBB), microvascular dysfunction, neurotransmitter imbalance, mitochondrial dysfunction. Affects 50-80% of septic ICU patients. WORSE outcomes: longer ICU stay, higher mortality, long-term cognitive impairment. Management: treat sepsis (source control, antibiotics), minimise sedation (dexmedetomidine, avoid benzodiazepines), promote sleep-wake cycle, early mobilisation, family presence, treat pain. Monitor with CAM-ICU. Pharmacological treatment controversial (haloperidol does NOT prevent — MIND-USA trial).

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Endocrine & metabolic emergencies

7

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Adrenal Crisis & Corticosteroid Replacement

The adrenal crisis — the acute the life-threatening the glucocorticoid the deficiency. The causes (the primary — the Addison's, the adrenal the haemorrhage; the secondary — the pituitary; the **iatrogenic — the abrupt the withdrawal of the chronic the exogenous the steroids** [the HPA the suppression] — the commonest the ICU the cause). The refractory the hypotension, the abdominal the pain, the hyponatraemia, the hyperkalaemia, the hypoglycaemia. The **hydrocortisone the IV the immediately (the before the tests)**, the fluid, the treat the trigger. The **stress-dose the steroids** for the chronic the users (the illness / the surgery).

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Diabetic Ketoacidosis (DKA) & Hyperosmolar Hyperglycaemic State (HHS)

DKA and HHS are the two hyperglycaemic emergencies on a spectrum of insulin deficiency. DKA (typically type 1) is the triad of hyperglycaemia, ketonaemia and a high-anion-gap metabolic acidosis — the biochemical mirror of HHS, which is defined by ketonaemia at or under 3.0 mmol/L, pH above 7.3 and bicarbonate at or above 15. HHS (typically type 2, elderly) is marked hypovolaemia with hyperglycaemia (30 mmol/L or more by JBDS, 33.3 by ADA), osmolality 320 mOsm/kg or more (2 x Na + glucose + urea) and estimated fluid losses of 100-220 mL/kg; pooled mortality 21.1 per cent. Management is fluid first (0.9% saline to restore circulating volume), a fixed-rate insulin infusion (DKA 0.1 unit/kg/h, de-escalating to 0.05 once glucose is under 14 mmol/L; HHS 0.05 unit/kg/h by JBDS or 0.1 by ADA), potassium addressed before insulin drives it lower, gradual osmolality correction (3.0-8.0 mOsm/kg/h JBDS), and identification plus treatment of the precipitant. The DKA resolution target is ketone clearance, NOT glucose normalisation.

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Endocrine & Metabolic Derangements of Critical Illness

The endocrine the metabolic the response to the critical the illness — the **the biphasic** (the acute the adaptive the stress the response → the chronic the maladaptive the persistent). The acute: the counter-regulatory the hormones (the cortisol, the catecholamines, the glucagon, the GH), the insulin the resistance (the **stress the hyperglycaemia**), the hypercatabolism. The chronic: the suppressed the axes (the **sick the euthyroid / the low-T3**, the hypogonadism, the **CIRCI**), the anabolic the failure, the muscle the wasting. The moderate the glycaemic the control (the NICE-SUGAR); the hydrocortisone for the refractory the septic the shock; the sick the euthyroid the no the replacement. The rarer the ICU the endocrinopathies — the **insulinoma** (the spontaneous the hypoglycaemia), the **VIPoma** (the secretory the diarrhoea, the hypokalaemia), the **carcinoid / the carcinoid the crisis**, the calcitonin in the thyroid the C-cell (the medullary the carcinoma). The hyperglycaemic the emergencies (the DKA / the HHS) the summarised — the detail in the sibling.

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Hypoglycaemia

The hypoglycaemia — the Whipple the triad (the symptoms, the low the glucose, the relief with the glucose); the severe (the altered the consciousness, the needing the assistance). The causes (the insulin, the **sulfonylurea** — the prolonged, the recurrent; the insulinoma; the adrenal the insufficiency; the liver the failure; the alcohol; the sepsis). The **IV the dextrose**, the **glucagon** (the if the no the IV), the **octreotide** for the sulfonylurea (the inhibits the insulin the release — the not the dextrose the alone, which the fuels the further the insulin).

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Pheochromocytoma Crisis

The pheochromocytoma the crisis — the catecholamine-secreting the tumour (the adrenal the medulla / the paraganglioma) → the massive the catecholamine the surge → the severe the hypertension, the cardiomyopathy (the Takotsubo), the pulmonary the oedema, the multi-organ. The classic the triad (the headache, the sweating, the palpitations). The **alpha-blockade the FIRST (the before the beta — the unopposed the alpha)**, the **metanephrines** the screen, the metyrosine, the surgical the resection (the after the 1 to 2 weeks the alpha the prep). The trigger the avoidance (the metoclopramide, the anaesthesia, the biopsy).

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SIADH & Diabetes Insipidus

The two ends of the ADH (the vasopressin) the dysfunction — the **SIADH** (the excess the ADH → the water the retention → the euvolaemic the hyponatraemia) and the **diabetes the insipidus** (the ADH the deficiency [the central] or the resistance [the nephrogenic] → the water the loss → the hypernatraemia). The SIADH: the fluid the restriction, the hypertonic the saline (the cautious — the osmotic the demyelination), the vaptans. The DI: the desmopressin (the central), the treat the cause + the thiazide (the nephrogenic).

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Thyroid Storm & Myxoedema Coma

The two decompensated thyroid emergencies at the opposite ends of the spectrum — the **thyroid storm** (the decompensated hyperthyroidism: the hyperthermia, the tachyarrhythmia, the heart failure, the CNS agitation, the multi-organ) and the **myxoedema coma** (the decompensated hypothyroidism: the hypothermia, the bradycardia, the hypoventilation, the hyponatraemia, the coma). The thyroid storm: the beta-blocker, the thionamide (the PTU), the iodine (the AFTER the thionamide), the glucocorticoid, the cooling. The myxoedema coma: the IV levothyroxine, the hydrocortisone, the slow warming.

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Domain

Endocrine

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Adrenal insufficiency and Addisonian crisis

Adrenal crisis is a life-threatening state of glucocorticoid deficiency. Presents with hypotension (refractory to catecholamines), abdominal pain, nausea/vomiting, confusion, hyponatraemia, hyperkalaemia, hypoglycaemia. Precipitated by: stress (infection, surgery, trauma) in patients with underlying adrenal insufficiency (primary = Addison's; secondary = pituitary; tertiary = exogenous steroids). Treatment: IMMEDIATE hydrocortisone 100 mg IV stat then 50 mg IV Q6H (or 200 mg/24h infusion) — do NOT wait for cortisol/ACTH results. IV fluids (normal saline + dextrose for hypoglycaemia). Treat precipitant. Identify type: primary (high ACTH, hyperpigmentation, hyperkalaemia) vs secondary/tertiary (low ACTH, no hyperpigmentation, normal K).

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Critical illness-related corticosteroid insufficiency (CIRCI)

Critical illness-related corticosteroid insufficiency (CIRCI): inadequate corticosteroid activity for the severity of illness during critical illness. NOT classic adrenal insufficiency (absolute deficiency). In septic shock: inflammatory cytokines suppress HPA axis → reduced cortisol production relative to demand. Diagnosis controversial: random cortisol &lt;276 nmol/L OR cortisol rise &lt;250 nmol/L after 250 mcg ACTH (cosyntropin) stimulation. Treatment: hydrocortisone 200 mg/day (CONTINUOUS infusion or 50 mg IV QDS) for SEPTIC SHOCK not responding to adequate fluid + vasopressor. ADRENAL/CORTICUS trials: hydrocortisone did NOT improve overall survival, but may benefit shock reversal and subgroup (rapid ACTH non-responders). STOP when vasopressors weaned.

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Hyperosmolar hyperglycaemic state (HHS)

HHS is a hyperglycaemic emergency of predominantly type 2 diabetes defined by marked hypovolaemia, hyperglycaemia and hyperosmolality without significant ketoacidosis. Diagnostic thresholds differ by guideline: ADA/Diabetes Canada use glucose ≥33.3 mmol/L with osmolality ≥320 mOsm/kg, while the UK JBDS uses glucose ≥30 mmol/L, osmolality ≥320 mOsm/kg calculated as 2×Na + glucose + urea, ketonaemia ≤3.0 mmol/L, pH >7.3 and bicarbonate ≥15 mmol/L. Management is fluid-first: IV 0.9% sodium chloride to restore circulating volume (estimated fluid losses 100-220 mL/kg), a fixed-rate IV insulin infusion (JBDS 0.05 units/kg/h; ADA 0.1 units/kg/h), a 5% or 10% glucose infusion once glucose falls under 14 mmol/L, potassium replacement according to serial levels, and a gradual osmolality decline of 3.0-8.0 mOsm/kg/h. Pooled mortality is 21.1% and is driven by precipitants (non-infective illness 49.5%, infection 44.0%) and vascular complications.

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Hypoglycaemia in the ICU

Hypoglycaemia is a frequent and serious adverse effect of antidiabetic therapy; inpatients who develop it have longer stays and increased mortality. In ICU trials moderate hypoglycaemia spans 2.3–3.9 mmol/L (41–70 mg/dL) and severe hypoglycaemia means glucose at or under 2.2 mmol/L (40 mg/dL) — severe episodes carried an adjusted hazard ratio for death of 2.10 in the NICE-SUGAR cohort. Profound hypoglycaemia — typically under 1 mmol/L (18 mg/dL) with a flat EEG — causes neuronal death (hippocampal dentate gyrus and superficial cortex vulnerable; cerebellum and brainstem spared). Causes: insulin or insulin secretagogue treatment (the most common cause), sulfonylurea poisoning (sustained hypoglycaemia refractory to IV dextrose — add octreotide), critical illnesses, hormone deficiencies such as adrenal crisis, non-islet cell tumours, and accidental/surreptitious insulin. Management: check glucose in any unconscious or seizing patient (ICU point-of-care meters read higher than laboratory values, under-detecting hypoglycaemia); oral carbohydrate if conscious; IV dextrose if not (25 g of 50% dextrose is the conventional ampule; 10% dextrose resolves symptoms with fewer adverse events); IM glucagon 1 mg if there is no IV access (intranasal glucagon 3 mg is non-inferior); octreotide 50 µg SC/IV followed by three 50 µg doses every 6 hours for sulfonylurea poisoning; thiamine 200 mg IV three times daily given before any carbohydrate in the malnourished or alcoholic patient; hydrocortisone 100 mg IV bolus then 200 mg/24 h for adrenal crisis. Document Whipple's triad, then take the critical sample (insulin, C-peptide, proinsulin, beta-hydroxybutyrate, oral hypoglycaemic agents, insulin antibodies) to find the cause.

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Thyroid emergencies: thyroid storm and myxoedema coma

Thyroid emergencies are rare but life-threatening. THYROID STORM is the extreme manifestation of thyrotoxicosis: hyperthermia (>40C), tachycardia/atrial fibrillation, heart failure, altered mental status, precipitating event. Mortality 10-30%. Management: 1) beta-blocker (propranolol or esmolol — block the sympathetic effects), 2) high-dose thionamide (PTU or methimazole — PTU also reduces peripheral T4-to-T3 conversion; Japanese survey data show no outcome difference between them), 3) inorganic iodine (blocks release — give AFTER the thionamide; an iodine load alone can precipitate thyrotoxicosis — Jod-Basedow phenomenon), 4) corticosteroids, 5) treat precipitant + cooling + ICU care; refractory cases: cholestyramine, lithium, plasma exchange, ECMO or thyroidectomy. MYXOEDEMA COMA is severe hypothyroidism: hypothermia, bradycardia, hyponatraemia, decreased GCS, hypoventilation. Mortality around 20-40% (up to 60% in older series). Management: IV levothyroxine 200-500 mcg loading then 50-100 mcg daily, stress-dose glucocorticoids, passive rewarming (NOT active), treatment of infections, respiratory and haemodynamic support.

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Domain

Monitoring / haemodynamics

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Advanced Haemodynamic Monitoring — PA Catheter, PiCCO & Pulse Contour

Advanced haemodynamic monitoring measures the cardiac output and related variables beyond the basic arterial and CVP lines. The pulmonary artery catheter (PAC, Swan-Ganz) is the gold standard — it directly measures the PAWP (left atrial pressure), the SvO2 (oxygen balance), and the CO by thermodilution, but its routine use has declined after the FACTT trial (no benefit over central-line-guided therapy); it is now reserved for complex shock, pulmonary hypertension, and RV failure. The PiCCO (transpulmonary thermodilution) provides the CO, the GEDV (preload), the EVLW (lung water), and a calibrated continuous pulse-contour CO and SVV. Uncalibrated pulse contour devices (FloTrac/Vigileo) use an arterial line alone and are less accurate; LiDCO (lithium dilution) is a calibrated alternative needing only a radial line; esophageal Doppler gives continuous CO from the descending aorta. Echocardiography (LVOT VTI) is the leading non-invasive alternative. The choice depends on the clinical question: filling pressure (PAWP), volume (GEDV), responsiveness (SVV/PPV), or oxygen balance (SvO2).

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Domain

Advanced respiratory support

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Advanced Respiratory Support — NIV, Weaning and Tracheostomy

Advanced respiratory support covers the three skills that frame the respiratory failure beyond the ventilator — the non-invasive ventilation (the CPAP and the BiPAP, their indications and their evidence), the liberation from the mechanical ventilation (the spontaneous breathing trial, the weaning protocol, the difficult-to-wean patient and the role of the NIV-facilitated extubation), and the tracheostomy (the timing, the technique, the decannulation). This topic builds the examiner's framework on the NIV physiology (the positive pressure that unloads the respiratory muscles, the CPAP for the oxygenation, the BiPAP for the ventilation), the weaning evidence (the Esteban comparison of the four methods, the role of the NIV in the post-extubation failure, the Burns review of the NIV-assisted weaning), and the tracheostomy timing question.

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Domain

Anatomy

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Airway & Respiratory Anatomy

Airway and respiratory anatomy for the ICU First Part: the upper airway (nose, naso-/oro-/laryngopharynx, larynx and its cartilages — thyroid, cricoid as the only complete ring, arytenoid, epiglottis — vocal cords, and the superior and recurrent laryngeal nerves), the lower airway (the trachea 10-12 cm with C-shaped rings, the carina at T4/T5, the right main bronchus wider/shorter/more vertical as the aspiration path), the bronchopulmonary segments (ten right, eight to ten left), lung lobes and hilum, the pleura (visceral and parietal, the pleural space and fluid), the conducting vs respiratory zones (generations 0-23), the alveolar-capillary membrane, the pulmonary vascular tree, and the muscles of breathing (the diaphragm via the phrenic nerv

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Cardiovascular Anatomy

Cardiovascular anatomy and Guytonian physiology for the ICU First Part: the four chambers and valves, the cardiac wall and microscopic structure, the cardiac cycle, the coronary arteries and their perfusion territories (LAD, circumflex, right; coronary dominance; diastolic flow), the conduction system (SA node to AV node to His-Purkinje), the great vessels and aortic-arch branches, the systemic and pulmonary circulations, the Frank-Starling mechanism, the Starling forces governing transcapillary fluid exchange, the venous-return and cardiac-function curves of Guyton, and the peripheral venous system relevant to central venous catheter insertion.

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Functional Anatomy for ICU Procedures

Functional anatomy for common ICU procedures: the cricothyroid membrane (cricothyroidotomy), the tracheal rings and thyroid isthmus (tracheostomy), the chest-drain safe triangle (5th intercostal space, anterior axillary line), the lumbar-puncture ligament layers (L3-L4, below the conus), the internal jugular vein and carotid sheath (central venous catheter), the radial artery and palmar arches (arterial line, Allen test), the intraosseous sites (proximal tibia), and the subxiphoid route for pericardiocentesis.

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Gastrointestinal Anatomy

Gastrointestinal anatomy from mouth to anus for the ICU First Part: the oesophagus and its three sphincters/constrictions, the stomach and its secretory cells, the small intestine (duodenum at the ampulla of Vater, jejunum, ileum — villi and microvilli), the large intestine (caecum, colon, rectum), the liver's dual blood supply and eight Couinaud segments, the portal triad, the biliary tree and sphincter of Oddi, the exocrine and endocrine pancreas, the spleen, and the splanchnic circulation (coeliac trunk, SMA, IMA) with its portocaval anastomoses.

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Neuroanatomy — Brainstem, Cranial Nerves & Spinal Cord

Neuroanatomy for the ICU First Part: the cerebral cortex (frontal, parietal, temporal, occipital lobes and their functions), the basal ganglia and their direct/indirect pathways, the thalamus and hypothalamus, the limbic system, the brainstem (midbrain, pons, medulla) and its vital centres, the twelve cranial nerves with their main functions, the brainstem reflexes used in coma and brain-death assessment (pupillary, corneal, gag/cough, oculocephalic), the cerebellum, the ventricular system and CSF flow, the Circle of Willis and the MCA/ACA/PCA territories, the major spinal cord tracts (corticospinal, spinothalamic, dorsal columns) and their blood supply, the blood-brain barrier, and the autonomic nervous system.

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Renal & Genitourinary Anatomy

Renal and genitourinary anatomy for the ICU First Part: the kidney (cortex and medulla, the nephron segments from glomerulus to collecting duct), the dual-capillary renal blood supply (afferent then efferent arteriole), the juxtaglomerular apparatus and the renin-angiotensin trigger, and the ureteric constrictions relevant to obstruction.

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Vascular-Access Anatomy — Central & Arterial

Vascular-access anatomy for the ICU First Part: the central venous routes (internal jugular in the carotid sheath, subclavian below the clavicle, femoral in the femoral sheath) with their risks and the tip position at the cavoatrial junction, and the arterial-line sites (radial with the Allen test for ulnar collateral flow, femoral, dorsalis pedis).

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Airway management

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Airway Management

Tracheal intubation in the critically ill patient is one of the highest-risk procedures in intensive care: the INTUBE study of nearly 3000 intubations across 29 countries found that 45.2% of patients suffered a major adverse peri-intubation event, led by cardiovascular instability. Unlike the fasted, monitored anaesthetic patient, the ICU patient is hypoxaemic, hypotensive, often shocked, and frequently difficult — so the airway is managed not as an isolated technical act but as a physiological resuscitation around a planned procedure. This topic covers airway assessment (MACOCHA, LEMON), the physiology of preoxygenation and desaturation, rapid sequence induction and its pharmacology, the Difficult Airway Society 2015 algorithm (Plans A to D), rescue oxygenation with supraglottic airways and face-mask ventilation, the cannot-intubate-cannot-oxygenate emergency and front-of-neck access, cardiovascular collapse and its prevention, capnographic monitoring, and extubation — built on the verified landmark trials and the DAS/NAP4 evidence.

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Aspiration — Prevention & Management (Pneumonitis vs Pneumonia)

Aspiration causes two distinct syndromes. Aspiration pneumonitis (Mendelson syndrome) is a sterile chemical injury from acidic gastric contents — treated with supportive care (oxygen, positive pressure, bronchodilators), with antibiotics and corticosteroids NOT given routinely. Aspiration pneumonia is an infection from aspiration of colonised oropharyngeal secretions (the elderly, dysphagia, poor dentition, reduced consciousness) — treated with antibiotics. The distinction drives treatment. Prevention is the VAP bundle: head of bed 30-45 degrees (Drakulovic, Lancet 1999), subglottic suction, cuff pressure 20-30 cmH2O, oral hygiene, minimal sedation, and post-pyloric feeding for the high-risk patient. Proton pump inhibitors for stress ulcer prophylaxis have NO mortality benefit (SUP-ICU, Krag NEJM 2018).

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Awake Fibre-Optic Intubation

Awake fibre-optic intubation (AFOI) is the safest approach to the anticipated difficult airway when the patient can cooperate and maintain oxygenation: topicalise the upper airway with local anaesthetic, sedate lightly so the patient stays breathing with airway reflexes preserved, navigate a flexible scope through the cords on inspiration, and railroad an endotracheal tube. The principle is that the patient never loses their airway. Indications are a predicted difficult airway (prior difficulty, cervical instability, limited mouth opening, distorted anatomy, head-and-neck mass, obesity, risk of 'can't intubate, can't ventilate'); contraindications are inability to cooperate, inability to tolerate apnoea, complete upper-airway obstruction, an airway flooded with blood or secretions, and local-anaesthetic allergy. Technique: topicalisation with lidocaine 1–4% (spray, nebulised, gargle, paste, or spray-as-you-go), optional nerve blocks (superior laryngeal and glossopharyngeal), cooperative sedation with dexmedetomidine or remifentanil target-controlled infusion, scope handling, and railroading of the ETT over the scope. Complications include laryngospasm, local-anaesthetic systemic toxicity (LAST), and airway trauma.

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Basic Airway Manoeuvres, Adjuncts & Bag-Valve-Mask

The 'A' of ABCDE. Basic airway skills are the non-invasive manoeuvres and adjuncts that establish and maintain a patent airway and oxygenate the patient before a definitive airway. Jaw thrust and head-tilt/chin-lift relieve obstruction by the tongue; the oropharyngeal (Guedel) and nasopharyngeal airways stent the pharynx; and the bag-valve-mask with a two-handed C-E grip, reservoir and PEEP valve ventilates the unprotected airway. Most 'can't intubate' situations are rescued by excellent basic airway skills and bag-valve-mask ventilation. Apnoeic oxygenation (THRIVE) extends safe apnoea time.

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Difficult Airway Algorithms (DAS / ASA / CICO) & Front-of-Neck Access

A difficult airway is one where a trained operator struggles with mask ventilation, laryngoscopy, or intubation. In ICU the patient is often both anatomically difficult (LEMON, MACOCHA) and physiologically difficult (shock, hypoxia, acidosis), and cannot simply be woken up. The Difficult Airway Society 2018 ICU intubation guideline structures the response into a sequence of plans (A: laryngoscopy and bougie; B: second-generation supraglottic airway rescue; C: maintain oxygenation and wake if able; CICO: front-of-neck access). CICO — can't intubate, can't oxygenate — is the life-threatening emergency requiring decisive scalpel-bougie cricothyroidotomy. The NAP4 audit showed most major airway events are avoidable: plan, assess, limit attempts, use capnography, and do not delay front-of-neck access.

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Extubation & Its Complications — Stridor, Laryngospasm, Pulmonary Oedema

Extubation is the planned removal of the endotracheal tube once a spontaneous breathing trial is tolerated and airway protection is adequate; it carries a 10-20 per cent reintubation rate. The serious complications are post-extubation stridor (laryngeal oedema — predicted imperfectly by the cuff-leak test, reduced by prophylactic methylprednisolone or dexamethasone in high-risk patients), laryngospasm (treat with 100 per cent oxygen, CPAP, the Larson manoeuvre and jaw thrust; a small dose of suxamethonium if refractory), negative-pressure pulmonary oedema from forceful inspiration against a closed glottis, aspiration of subglottic secretions, post-extubation dysphagia (pooled incidence around 41 per cent), and unplanned extubation. Plan high-risk extubations with senior presence, steroid pretreatment and an airway-exchange catheter, and treat every planned extubation as a potential difficult reintubation.

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Front-of-Neck Access — Surgical Airway, Cricothyroidotomy & Tracheostomy

Front-of-neck access (FONA) is the rescue for can't-intubate-can't-oxygenate (CICO). The emergency standard is the scalpel-bougie cricothyroidotomy: identify the cricothyroid membrane with the laryngeal handshake, a transverse stab incision, pass a bougie, railroad a cuffed size 6.0 tube, and confirm with capnography. Cricothyroidotomy is preferred over tracheostomy for the emergency because it is faster, more superficial, and bleeds less; formal tracheostomy is an elective, lower-neck procedure. The fatal error, highlighted by NAP4, is delay. Children, laryngeal trauma, and tracheal disruption are relative contraindications to cricothyroidotomy.

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Rapid Sequence Intubation (RSI) & Its Drugs

Rapid sequence intubation (RSI) is the standard for emergency airway control in the non-fasted, critically ill patient: preoxygenation, then an induction agent and a neuromuscular blocker in rapid succession with no mask ventilation, to secure the airway swiftly and minimise aspiration. Induction agents are chosen to the haemodynamics (propofol/thiopentone in the stable; ketamine in shock/asthma; etomidate for neutrality, with the sepsis-adrenal controversy). Succinylcholine (fast, short, but hyperkalaemia and malignant hyperthermia) versus rocuronium (reversible with sugammadex). Confirm with waveform capnography. Cricoid pressure is no longer routine.

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Supraglottic Airway Devices — LMA, i-gel & Second-Generation Devices

A supraglottic airway device (SAD) sits in the pharynx and seals around the laryngeal inlet, providing a hands-free airway without entering the trachea — bridging the gap between bag-valve-mask and endotracheal intubation. First-generation devices (classic LMA) have a single lumen and no gastric drainage and failed as rescue devices in NAP4; second-generation devices (i-gel, ProSeal, Supreme) add a gastric drainage channel and a higher seal pressure, giving partial aspiration protection and an intubation conduit. In the difficult-airway algorithm the SAD is the Plan B rescue; it is not a definitive airway, because it does not isolate the trachea.

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Tracheostomy — Indications, Types, Percutaneous, Decannulation & Emergencies

A tracheostomy is a surgical airway through the anterior trachea, placed for prolonged ventilation, upper-airway obstruction, airway protection, or secretion clearance. Percutaneous dilatational tracheostomy (Ciaglia Blue Rhino, bronchoscopic-guided, bedside) is the ICU standard; surgical tracheostomy is reserved for difficult anatomy, children, and emergencies. The TracMan trial (JAMA 2013) found early versus late tracheostomy does not change mortality, so timing is individualised. Complications fall into early (bleeding, displacement, pneumothorax), intermediate (infection, obstruction), and late (tracheal stenosis, tracheo-innominate artery erosion with its sentinel bleed, tracheo-oesophageal fistula). A displaced tube in the first week — before the tract matures — is re-intubated from above, not reinserted blindly.

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Upper-Airway Obstruction — Epiglottitis, Angioedema & Deep Neck Abscess

Upper-airway obstruction is an airway emergency. The causes run from the nose and mouth (allergic and ACE-inhibitor angioedema of the lip and tongue), through the supraglottis (epiglottitis, peritonsillar abscess), to the subglottis and retropharyngeal space (retropharyngeal abscess, Ludwig's angina, post-extubation oedema). Stridor at rest, drooling, tripoding, and distress signal severe obstruction. The overarching rule is to do no harm: keep the patient upright and calm, call for senior airway help early, avoid upsetting the airway, and secure it in a controlled setting. Epiglottitis is not examined in the unsecured airway; ACE-inhibitor angioedema is bradykinin-mediated and does not respond to adrenaline, antihistamines, or steroids.

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Domain

Infection / pharmacology

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Aminoglycosides — Gentamicin, Tobramycin, Amikacin & the Three Toxicities

The aminoglycosides (gentamicin, tobramycin, amikacin) are bactericidal inhibitors of the 30S ribosomal subunit — concentration-dependent killers with a post-antibiotic sub-MIC effect and adaptive resistance, which justify extended-interval once-daily dosing targeting a Cmax/MIC of 8-10. They retain activity against multidrug-resistant Gram-negatives including Pseudomonas and Acinetobacter and are used empirically in severe sepsis while awaiting susceptibilities. Dosing: gentamicin 7 mg/kg once daily by the Hartford nomogram (single-level, creatinine-clearance-banded intervals), amikacin 15 mg/kg once daily. The defining toxicities: nephrotoxicity (proximal tubule, megalin-dependent uptake), ototoxicity (cochlear and vestibular, often irreversible), and neuromuscular blockade that worsens myasthenia.

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Antifungals — Azoles, Echinocandins & Amphotericin B

The antifungals comprise the three classes. The azoles (the fluconazole, the voriconazole, the posaconazole, the isavuconazole) inhibit the 14-alpha-demethylase, the block the ergosterol synthesis; the fluconazole for the Candida and the Cryptococcus, the voriconazole the Aspergillus first-line (the TDM, the visual disturbances), the posaconazole the mucormycosis, the isavuconazole the broad plus the UNIQUE the SHORTENS the QT; the adverse the hepatotoxicity, the QT prolongation, the CYP3A4. The echinocandins (the caspofungin, the micafungin, the anidulafungin) inhibit the beta-1,3-glucan synthase, the cell-wall; the Candida (incl the fluconazole-resistant and the biofilm and the catheter), the low the toxicity and the low the interactions, the…

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Antivirals — Aciclovir, Oseltamivir & the Anti-COVID Agents

The antivirals in the ICU target the specific viral enzymes. The five ICU-relevant groups: the **anti-herpes** (the aciclovir — the HSV and the VZV; the DNA polymerase via the thymidine kinase; the NEPHROtoxicity crystal — the hydrate; the HSV encephalitis 10 mg per kg TDS for the 14 to 21 days; the ganciclovir the CMV with the bone-marrow; the foscarnet or the cidofovir the resistant with the nephrotoxic), the **anti-CMV** (the ganciclovir / the valganciclovir first-line for the transplant and the immunocompromised; the foscarnet and the cidofovir for the resistant or the leucopenic), the **anti-influenza** (the oseltamivir — the neuraminidase inhibitor; the influenza A and B; the within 48 h of the onset, the severe regardless; the reduces the duration and the complications; the prophylaxis; the zanamivir inhaled, the peramivir IV, the baloxavir the cap-dependent endonuclease), the **anti-SARS-CoV-2** (the remdesivir — the RNA polymerase, the severe COVID; the Paxlovid — the nirmatrelvir or the ritonavir protease inhibitor, the early high-risk; the molnupiravir), and the **anti-HIV / the ART** (the combination antiretroviral therapy — the two NRTIs plus an integrase inhibitor; the ICU the drug-interaction burden, the lactic acidosis, the IRIS, the abacavir hypersensitivity). The renal dosing the critical (the aciclovir, the ganciclovir, the oseltamivir all renally cleared).

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Beta-Lactam Antibiotics — Penicillins, Cephalosporins, Carbapenems, Monobactams

The beta-lactam antibiotics share the beta-lactam ring and the mechanism — the bind the PBPs, the inhibit the cell-wall (the peptidoglycan) synthesis, the bactericidal, the time-dependent (the T over the MIC drives the prolonged or the continuous infusion in the severe sepsis). The four subclasses: the penicillins (the piperacillin-tazobactam the broad and the pseudomonal, the flucloxacillin the staph MSSA not MRSA, the amoxiclav), the cephalosporins (the ceftriaxone or the cefotaxime the 3rd no pseudomonal, the ceftazidime the 3rd pseudomonal, the cefepime the 4th pseudomonal, the ceftaroline the 5th MRSA), the carbapenems (the meropenem the broadest — the ESBL — the reserve for the MDR, the imipenem the seizures), and the monobactams (the aztreonam the Gram-negative only, the safe in the penicillin allergy). The resistance: the beta-lactamases (the solved by the clavulanate or the tazobactam or the avibactam), the altered PBPs (the MRSA PBP2a — needs the vancomycin). The adverse: the allergy (the low cross-reactivity), the C. difficile, the interstitial nephritis, the seizures (the high-dose or the imipenem).

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Glycopeptides & Lipopeptides — Vancomycin, Teicoplanin, Daptomycin

The glycopeptides (the vancomycin, the teicoplanin) and the lipopeptides (the daptomycin) are the Gram-positive cover — the MRSA, the MRSE, the ampicillin-resistant enterococcus, and the VRE. The glycopeptides bind the D-alanyl-D-alanine terminus, the inhibit the cell-wall synthesis; the vancomycin is the AUC-over-MIC guided (the 400 to 600) and the oral route for the C. difficile. The adverse: the red-man syndrome (the histamine, NOT the allergy, the slow the infusion), the nephrotoxicity (the vanco-plus-the-pip-tazo AKI), the ototoxicity. The daptomycin (the lipopeptide) depolarises the cell membrane (the calcium-dependent); the Gram-positive including the VRE; the INACTIVATED by the pulmonary surfactant (NOT for the pneumonia — the vancomycin for the MRSA pneumonia); the myopathy (the CPK monitoring, the consider the holding the statin); the eosinophilic pneumonia (the rare). The teicoplanin — the once-daily, the less nephro and the less red-man than the vancomycin.

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Macrolides, Tetracyclines & Oxazolidinones — Atypicals, MRSA & VRE

The macrolides (azithromycin, clarithromycin, erythromycin) bind the 50S ribosome — bacteriostatic, covering the atypicals (Legionella, Mycoplasma, Chlamydia) and the community respiratory tract; watch for QT prolongation (worst with clarithromycin), CYP3A4 inhibition (drug interactions), and erythromycin as the prokinetic. The tetracyclines (doxycycline, tigecycline) bind the 30S ribosome — covering atypicals (chlamydia, rickettsia, Lyme), doxycycline for MRSA skin infection, and tigecycline as the broad reserve (MRSA, VRE, ESBL, anaerobes — but NO Pseudomonas, and an FDA increased-mortality warning). Avoid in pregnancy and under-8 (teeth and bone). The oxazolidinones (linezolid, tedizolid) bind the 50S — covering MRSA and VRE, with a unique serotonin-syndrome risk (linezolid is a reversible MAO inhibitor).

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MDR Organisms — MRSA, VRE, ESBL, CRE & C. difficile

Multidrug-resistant organisms comprise MRSA (altered PBP2a from mecA; resistant to beta-lactams except ceftaroline; treat with vancomycin, linezolid, or daptomycin), VRE (altered D-Ala-D-Ala; linezolid or daptomycin), ESBL (E. coli and Klebsiella; carbapenems, NEVER piperacillin-tazobactam for bacteraemia per MERINO), and CRE (carbapenemases KPC and NDM; ceftazidime-avibactam for KPC, aztreonam plus CZA for NDM, meropenem-vaborbactam), plus C. difficile (spore, toxin, post-antibiotic). The two pillars are targeted antibiotic therapy and infection control — contact precautions, isolation, hand hygiene (soap-and-water for C. difficile spores), and antimicrobial stewardship. Type the carbapenemase before choosing the novel beta-lactam: KPC and OXA-48 respond to ceftazidime-avibactam, but NDM (a metallo-beta-lactamase) does NOT — use aztreonam plus CZA.

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Domain

Obstetric critical care

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Amniotic Fluid Embolism

The amniotic the fluid the embolism (the AFE) — the catastrophic the peripartum the anaphylactoid the reaction to the amniotic the fluid the entering the maternal the circulation. The **the biphasic**: the phase the 1 (the sudden the hypoxia + the hypotension / the cardiovascular the collapse + the altered the mental the state / the seizure / the cardiac the arrest) → the phase the 2 (the coagulopathy / the DIC + the massive the bleeding + the multi-organ). The clinical the diagnosis (the exclusion). The resuscitation, the haemodynamic the support, the correct the coagulopathy, the delivery, the ECMO. The mortality the 20 to the 40 per cent.

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Obstetric Haemorrhage & DIC

The major obstetric the haemorrhage (the leading the cause of the maternal the mortality the globally). The causes — the **the 4 Ts**: the **Tone** (the uterine the atony — the commonest), the **Trauma** (the lacerations, the rupture), the **Tissue** (the retained, the accreta), the **Thrombin** (the coagulopathy / the DIC). The massive the transfusion the protocol (the 1:1:1; the cryoprecipitate for the fibrinogen), the **tranexamic acid** (the WOMAN the trial — the early the within the 3 h), the uterotonics (the oxytocin, the carboprost, the misoprostol), the surgical the escalation (the Bakri the balloon, the B-Lynch, the embolisation, the hysterectomy).

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Peripartum Cardiomyopathy

Peripartum cardiomyopathy (PPCM) is idiopathic left ventricular systolic dysfunction (LVEF below 45 percent) presenting in the last month of pregnancy to five months postpartum, in a woman with no pre-existing cardiac disease and no other identifiable cause. Risk factors cluster around multiparity, age over 30, pre-eclampsia (the strongest reversible association), and African descent. Heart-failure symptoms overlap with normal pregnancy, so diagnosis is delayed; a raised BNP plus echocardiography make the call. Management is guideline-directed heart-failure therapy, pregnancy-adjusted: beta-blocker, loop diuretic, and hydralazine or isosorbide dinitrate in pregnancy (ACE inhibitors, ARBs, ARNI and spironolactone are stopped), switching to full GDMT postpartum; anticoagulate the low-ejection-fraction patient, and consider bromocriptine (prolactin blockade). Most women recover (72 percent of the IPAC cohort reached LVEF 50 percent or above by one year); a subsequent pregnancy carries several-fold higher maternal mortality unless the ejection fraction has recovered.

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Physiology of Pregnancy Relevant to the ICU

Pregnancy triggers profound physiological adaptations relevant to the ICU — cardiovascular (cardiac output rises from early pregnancy, heart rate first then stroke volume, plateauing by midpregnancy while vascular resistance falls; supine aortocaval compression typically after 20 weeks mandating left lateral tilt), respiratory (progesterone-driven rise in minute ventilation and tidal volume producing a compensated respiratory alkalosis with low PaCO2 and raised arterial pH, a reduced FRC with rapid desaturation, and failed intubation in about 1 in 390 obstetric general anaesthetics), renal (renal plasma flow and GFR rise on early-gestation systemic vasodilation), and haematological (a venous thromboembolism relative risk of 4.29 versus non-pregnant women, with falling fibrinogen predicting severe postpartum haemorrhage). Understanding the pregnancy baseline is essential to safe ICU management.

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Pre-eclampsia, Eclampsia & HELLP Syndrome

The hypertensive spectrum of pregnancy spans pre-eclampsia (new hypertension over 140 over 90 plus proteinuria or end-organ dysfunction after 20 weeks), eclampsia (plus seizures), and HELLP (haemolysis, elevated liver enzymes, low platelets). The mechanism is abnormal placentation releasing anti-angiogenic sFlt-1, driving generalised endothelial dysfunction. Management is magnesium sulfate for seizure prophylaxis and treatment (calcium gluconate is the antidote), controlled blood-pressure reduction with labetalol, hydralazine, or nifedipine, and delivery as the definitive cure.

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Sepsis in Pregnancy

Maternal sepsis is a leading cause of maternal mortality and is under-recognised because the physiological changes of pregnancy mask the signs. The commonest sources are pyelonephritis, chorioamnionitis, puerperal endometritis, wound infection, and mastitis; the key organisms are Group B Streptococcus, E. coli, anaerobes, and Group A Streptococcus. Management follows the pregnancy-adapted sepsis bundle: broad-spectrum antimicrobials within one hour, volume-limited balanced crystalloid resuscitation (1 to 2 L over the first 3 hours), norepinephrine as first-line vasopressor, source control (including delivery when the uterus is the source), and maternity early-warning scores for recognition.

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Venous Thromboembolism in Pregnancy

Venous thromboembolism is a leading cause of maternal mortality because pregnancy activates all of Virchow triad — stasis (the gravid uterus compresses the IVC, progesterone venodilation, immobility), hypercoagulability (fibrinogen and factors VII, VIII, X and von Willebrand rise, protein S activity falls, fibrinolysis is impaired), and endothelial injury (delivery) — giving at least a 5-fold higher risk than in non-pregnant women with an even greater surge postpartum (a 4- to 10-fold increase across gestation and the puerperium). DVT is commonly left-sided (May-Thurner compression). Diagnosis uses compression ultrasound for DVT and V/Q (preferred) or CTPA for PE — never relying on D-dimer (it rises physiologically as pregnancy progresses) and never withholding imaging for fetal-radiation fears. Treatment is therapeutic LMWH (does not cross the placenta) dosed by current weight with rising requirements across trimesters; warfarin and DOACs are contraindicated antenatally; thrombolysis (alteplase most used) for massive PE; perimortem Caesarean (resuscitative hysterotomy) in arrest.

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Haematology / transfusion

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Anaemia in the ICU — Phlebotomy, Functional Iron & Restrictive Transfusion

Anaemia is near-universal in ICU and deepens with every day of the stay (mean admission Hb 11.3 g/dL in the ABC cohort). The number 1 MODIFIABLE cause is the phlebotomy (the classic ICU series bled patients 3.4 times a day, mean 41.5 mL/day, 762 mL per stay — and daily diagnostic volumes up to 377 mL have been reported). The other causes: the inflammation (anaemia of chronic disease — IL-6-driven hepcidin internalises ferroportin and causes functional iron deficiency), the blood loss (GI, surgical, coagulopathy), the haemodilution (fluids), the marrow suppression (sepsis, CKD, low EPO), the nutritional (B12, folate, iron). The management: reduce the phlebotomy (the blood-conservation bundle — paediatric-size tubes cut draw volume almost half, question-driven testing, batching, cumulative-volume review), the restrictive transfusion (Hb under 70 — TRICC, TRISS, TRIPICU, TRICS III; one unit at a time), the IV iron for the functional iron deficiency (IRONMAN: higher discharge Hb, no significant transfusion saving), and EPO is NOT routine (no transfusion reduction, thrombotic events HR 1.41 — Corwin 2007). In acute MI the threshold is contested: MINT/REALITY left possible harm with a restrictive strategy and the 2025 AABB guideline conditionally suggests transfusing when Hb is under 10 g/dL.

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Transfusion — Products, Thresholds, TRALI & TACO

The blood products (RBC, FFP, platelets, cryoprecipitate, PCC) and the restrictive transfusion strategy (RBC Hb under 70 for the most — the TRICC, TRISS trials; under 80 for the cardiovascular or the elderly; platelets under 10 prophylactic or under 50 bleeding; FFP if PT or APTT over 1.5 times; cryoprecipitate if fibrinogen under 1.5). The transfusion reactions: TRALI (the donor antibodies, the ARDS-like, the within 6 h, the NO overload — supportive), TACO (the circulatory overload, the pulmonary oedema — diuretics), the acute haemolytic (the ABO incompatibility — STOP immediately), the febrile non-haemolytic, the allergic (the mild to the anaphylaxis). The leukodepletion standard (reduces the febrile and the CMV). The male-donor plasma preferred (the TRALI prevention).

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Resuscitation & shock

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Anaphylaxis & Anaphylactic Shock

Anaphylaxis — the severe, life-threatening systemic hypersensitivity reaction. The rapid onset (the skin/mucosal + the respiratory + the cardiovascular + the GI). The IgE-mediated (most) or the non-IgE (the anaphylactoid). The IM adrenaline 0.5 mg FIRST; the 100% O2; the IV fluid; the positioning. The IV adrenaline infusion for the refractory. The tryptase for the diagnosis. The observation 6-24 h (the biphasic).

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Cardiogenic Shock

Cardiogenic shock — the pump failure. The vicious cycle (low CO → compensatory vasoconstriction → increased afterload → worse CO). The causes (ACS, decompensated HF, myocarditis, arrhythmia, valvular). The management — the inotrope (dobutamine, milrinone), the vasopressor (noradrenaline), the mechanical support (IABP, Impella, VA-ECMO), the revascularisation (the ACS).

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Endpoints of Resuscitation — Lactate, ScvO2, Mottling, Urine, Capillary Refill

Resuscitation endpoints span three tiers used together rather than in isolation: macro-haemodynamic endpoints such as MAP and urine output, metabolic endpoints such as lactate clearance and ScvO2, and peripheral perfusion endpoints such as capillary refill time, mottling score, and skin temperature.

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Fluid Responsiveness — Static & Dynamic Indices, Passive Leg Raise, SVV/PPV & Fluid Challenge

Fluid responsiveness is the prediction of whether a patient will increase stroke volume (or cardiac output) by around 10 per cent in response to a fluid bolus — and only about half of ICU patients actually do. Static markers (CVP, PAOP) do NOT predict it; the curve is flat. Dynamic markers do: the passive leg raise (PLR) is the reference reversible self-test, valid in spontaneous breathing (a rise in CO, SV or LVOT VTI of at least 10 per cent is positive). Pulse pressure variation (PPV) above 12.5 per cent and stroke volume variation (SVV) above 11.6 per cent apply only in controlled mechanical ventilation with no spontaneous breathing and a tidal volume of at least 8 mL/kg. Fluid overload worsens outcome — the CLASSIC, FACTT and CLOVERS trials support a restrictive strategy once the patient is no longer responsive.

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Fluid Resuscitation — Crystalloid vs Colloid, Balanced vs Saline, SOSD/ROSE & Fluid Overload

Fluid resuscitation turns on four evidence-based questions. (1) Crystalloid vs colloid — crystalloid is first-line; albumin shows no mortality benefit per SAFE (RR 0.99); hydroxyethyl starch is harmful per CHEST and 6S; CRISTAL showed no colloid advantage. (2) Balanced vs saline — balanced reduced the MAKE30 composite per SMART (14.3 vs 15.4 per cent; mortality and RRT individually non-significant); FLUID found no significant hospital-wide difference and BaSICS was neutral; SPLIT was the neutral precursor. Saline (chloride 154 mmol/L vs Plasma-Lyte 98) caused sustained hypercholaemia, a greater fall in strong ion difference, and reduced renal blood flow velocity and cortical perfusion in a volunteer crossover study. (3) How much — up to 30 mL/kg crystalloid initially with frequent reassessment (ESICM 2025), titrated to a mean arterial pressure of at least 65 mmHg (SEPSISPAM) and to fluid responsiveness (PLR, SVV/PPV, fluid challenge), not to a formula; roughly 56 per cent of patients are responders (Marik). (4) When to stop — the four-phase ROSE/SOSD fluid-stewardship model (Malbrain): fluid is actively given, then maintained, then actively removed (de-resuscitation). Restrictive strategies are safe (CLASSIC, FACTT, CLOVERS).

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Hypovolaemic & Haemorrhagic Shock

Hypovolaemic and haemorrhagic shock — blood loss reduces preload and cardiac output. The four ATLS classes guide recognition (a classic teaching tool with known limitations), progressing from compensated to decompensated shock. Hypotension is a LATE sign — the body compensates with tachycardia and vasoconstriction before blood pressure falls, and many bleeding patients are normotensive. Modern management is damage control resuscitation: permissive hypotension until bleeding is controlled (except TBI — higher blood-pressure thresholds apply), balanced blood-product resuscitation, damage control surgery, and early TXA. Resuscitation endpoints are lactate clearance, urine output, and normal mental state.

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Massive Transfusion, Blood Products & Tranexamic Acid

Massive transfusion in resuscitation turns on two evidence-based questions: the component ratio (PROPPR — 1:1:1 vs 1:1:2 RBC:plasma:platelets) and tranexamic acid (CRASH-2 — mortality benefit, but only within 3 hours of injury; WOMAN in postpartum haemorrhage, HALT-IT negative in GI bleed, TICH-2 in intracerebral haemorrhage). Damage control resuscitation (permissive hypotension, haemostatic 1:1:1 resuscitation, damage control surgery), viscoelastic (TEG/ROTEM)-guided component therapy, fibrinogen replacement above 1.5-2.0 g/L, calcium replacement (citrate chelation), the lethal triad of hypothermia-acidosis-coagulopathy, and awareness of transfusion reactions (TRALI, TACO, acute haemolysis) are central.

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Neurogenic Shock (Spinal Cord Injury)

Neurogenic shock — the loss of supraspinal sympathetic control after spinal cord injury at or above T6. The vasodilation with venous pooling (the warm, the dry) plus the bradycardia (the unopposed vagal). The MAP target: the traditional 85 to 90 mmHg for up to seven days, refined by the 2024 AO Spine guideline to 75 to 80 mmHg as the lower limit and 90 to 95 mmHg as the upper limit for 3 to 7 days. Noradrenaline commonly preferred where a vasopressor is needed; atropine first-line for symptomatic bradycardia. Distinguish from the hypovolaemic (the warm plus the dry versus the cool plus the clammy) and from spinal shock (the neurological phenomenon).

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Obstructive Shock — Tamponade, Tension Pneumothorax, Massive PE

Obstructive shock — the mechanical obstruction to the cardiac output. The three causes (the tamponade, the tension pneumothorax, the massive PE). The common feature: the impaired the ventricular the filling (the reduced the preload) → the reduced the CO → the shock. The immediate the recognition + the decompression. The Beck's triad (the tamponade), the tracheal the deviation (the tension), the right the heart the strain (the PE).

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Domain

Haematology / coagulation

4

high

Anticoagulants & Antiplatelets — Heparin, DOACs, Warfarin & Reversal

The anticoagulants and the antiplatelets in the ICU: the heparins (the UFH — the antithrombin-mediated IIa or Xa, the APTT monitoring, the protamine reversal 1 mg per 100 U; the LMWH — the anti-Xa, the enoxaparin 1 mg per kg BD, the partial protamine reversal about 60 per cent, the avoid the CrCl under 30; the fondaparinux — the not reversible); the DOACs (the dabigatran — the direct IIa — the idarucizumab 5 g; the apixaban, the rivaroxaban, the edoxaban — the direct Xa — the andexanet alfa or the PCC); the warfarin (the vitamin-K antagonist, the INR — the reversal the vitamin K 10 mg IV plus the PCC 25 to 50 IU/kg, the FFP the slower); the antiplatelets (the aspirin — the COX-1, the irreversible 7 to 10 days — the platelet transfusion; the clopidogrel, the prasugrel, the ticagrelor — the P2Y12 — the platelet transfusion); the heparin-induced thrombocytopenia (the 4Ts the score, the argatroban or the bivalirudin); the bleeding risk (the HAS-BLED). The reversal in the major bleed or the emergency surgery — the stop the agent, the specific the reversal (the protamine, the idarucizumab, the andexanet, the PCC plus the vitamin K, the platelets), the supportive.

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Disseminated Intravascular Coagulation (DIC) — Bleeding AND Thrombosis

DIC is a syndrome of widespread intravascular coagulation causing simultaneous BLEEDING and THROMBOSIS. Tissue factor release drives massive thrombin generation and fibrin deposition (microvascular thrombosis, organ failure) while consuming platelets and clotting factors (bleeding). Always secondary to a trigger — sepsis (commonest ICU cause), trauma or burns, obstetric (amniotic fluid embolism, abruption, HELLP), malignancy (acute promyelocytic leukaemia, mucinous adenocarcinoma), transfusion reaction, snake bite. Labs: thrombocytopenia, prolonged PT or APTT, low fibrinogen, high D-dimer, schistocytes. ISTH score (platelets plus D-dimer plus PT plus fibrinogen; over 5 = overt DIC). Management: treat the underlying cause (the definitive), supportive transfusion for active bleeding or high bleeding risk (platelets under 50; FFP for prolonged PT or APTT with bleeding; cryoprecipitate or fibrinogen concentrate for severe hypofibrinogenaemia), heparin for the thrombotic-predominant DIC (purpura fulminans, APL), and NO antifibrinolytics (except documented hyperfibrinolytic states such as leukaemia and trauma).

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Thrombocytopenia in the ICU — HIT, TTP/HUS, ITP & Septic

The ICU thrombocytopenia differential: the HIT (heparin-induced — the PF4-heparin antibodies; thrombocytopenia AND thrombosis; 4T score; STOP ALL HEPARIN; switch to argatroban or bivalirudin; NO platelets), the TTP (ADAMTS13 deficiency; MAHA plus neuro; plasmapheresis plus steroids plus caplacizumab; NO platelets), the HUS (Shiga toxin E coli; renal; eculizumab), the ITP (isolated; steroids or IVIG), the septic (the commonest — treat sepsis), the drug-induced, the DIC, the dilutional, the marrow failure. The key: HIT and TTP have thrombocytopenia with THROMBOSIS (paradoxical) — and NO platelets in either (worsens the microvascular thrombosis). The TTP and HUS have the MAHA (schistocytes, raised LDH, low haptoglobin). The 4T score for the HIT; the ADAMTS13 for the TTP; the plasmapheresis is the definitive for the TTP.

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VTE Prophylaxis & Treatment — LMWH, IPC, Thrombolysis & the ICU Default

ALL ICU patients are at HIGH risk for VTE (immobility, critical illness, central lines, inflammation) and require prophylaxis. Pharmacological (LMWH enoxaparin 40 mg daily = standard; UFH for renal failure; fondaparinux for HIT) and mechanical (IPC for the bleeding-contraindicated). Contraindications: active bleeding, coagulopathy (platelets under 50), recent neurosurgery, epidural catheter. Treatment of established VTE: LMWH therapeutic (enoxaparin 1 mg per kg BD), UFH infusion for massive PE or renal failure, thrombolysis for massive PE (alteplase 100 mg over 2 h), embolectomy for the thrombolysis-contraindicated, IVC filter for the anticoagulation-contraindicated. Early mobilization reduces the risk.

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Domain

Infectious

2

high

Antimicrobial resistance in ICU: ESBL, CRE, MRSA, VRE management

Antimicrobial resistance (AMR) in ICU: resistant organisms limit antibiotic options, increase mortality. KEY organisms: (1) ESBL (Extended-Spectrum Beta-Lactamase) — E. coli, Klebsiella — resistant to penicillins, cephalosporins. Treat: carbapenem (meropenem). (2) CRE (Carbapenem-Resistant Enterobacteriaceae) — resistant to carbapenems. Treat: polymyxin/colistin, ceftazidime-avibactam, meropenem-vaborbactam. (3) MRSA — resistant to beta-lactams. Treat: vancomycin, linezolid, daptomycin. (4) VRE (Vancomycin-Resistant Enterococcus) — treat: linezolid, daptomycin. Prevention: antibiotic stewardship, infection control, surveillance, isolation. CRE mortality 40-50%.

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Tropical infections in ICU: melioidosis, leptospirosis, typhoid

Tropical infections causing severe sepsis in ICU. MELIOIDOSIS (Burkholderia pseudomallei): endemic in northern Australia, SE Asia. Soil/water exposure, diabetes, rainy season. Pneumonia, septicaemia, multi-organ abscesses (liver, spleen, prostate). Treatment: ceftazidime or meropenem (intensive phase), then TMP-SMX (eradication phase 3-6 months). LEPTOSPIROSIS (Leptospira): zoonotic (rodent urine), biphasic illness. Weil disease: jaundice + renal failure + bleeding + pulmonary haemorrhage. Treatment: penicillin, doxycycline. TYPHOID (Salmonella Typhi): travel to endemic areas. Stepwise fever, relative bradycardia, rose spots, splenomegaly, hepatosplenomegaly. Complications: intestinal perforation, GI bleed, encephalopathy. Treatment: ceftriaxone, azithromycin.

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Domain

Antimicrobial therapy

1

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Antimicrobial Therapy and Stewardship in the ICU

Antimicrobial stewardship is the systematic, the evidence-based, the measured use of the antibiotics to maximise the patient outcome, minimise the resistance, and reduce the toxicity. This topic builds the examiner's framework on the PK/PD dosing principles (the beta-lactam prolonged infusion, the aminoglycoside once-daily, the vancomycin AUC), the empirical therapy guided by the local antibiogram, the de-escalation when the culture returns, the duration of therapy (the shortest effective course), the beta-lactam allergy, the therapeutic drug monitoring, and the resistance mechanisms (the ESBL, the CRE, the MRSA, the VRE).

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Domain

Applied pharmacology

1

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Applied Pharmacology — Vasoactives, Sedatives and Paralysers

The applied pharmacology of the ICU drugs — the vasoactives (the noradrenaline, the vasopressin, the dobutamine, the milrinone, the adrenaline), the sedatives (the propofol, the midazolam, the dexmedetomidine, the ketamine), the analgesics (the fentanyl, the morphine), the paralysers (the rocuronium, the cisatracurium) — with their receptor pharmacology, the PK/PD, the doses, the adverse effects, and the evidence for the choice in each clinical scenario.

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Domain

Applied physiology

1

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Applied Physiology — Cardiovascular, Respiratory, Renal, Neuro, GI and the Stress Response

The applied physiology that underpins every ICU intervention — the cardiovascular (the cardiac-output determinants of preload, afterload, contractility and heart rate; the Frank-Starling mechanism; the oxygen-delivery equation; the venous-return and the Guyton model; the cardiac and the vascular function curves and the mean systemic filling pressure; the Fick principle), the respiratory (the oxygen cascade; the oxyhaemoglobin dissociation curve and its shifts by the pH, the temperature, the 2,3-DPG and the CO2; the ventilation-perfusion matching; the dead space and the shunt; the compliance and the time constants; the lung volumes and the closing capacity; the work of breathing; the hypoxic ventilatory response and the carotid body; the hypoxic pulmonary vasoconstriction), the renal (the GFR determinants; the tubular sodium and water handling; the RAAS; the countercurrent multiplier; the acid-base handling), the neuro (the cerebral autoregulation; the Monro-Kellie doctrine; the cerebral perfusion pressure; the cerebral metabolic rate), the gastrointestinal (the splanchnic circulation and the gut barrier; the bacterial translocation; the hepatic clearance), and the stress response (the HPA axis and the cortisol; the catecholamines; the ebb-and-flow hypermetabolism; the non-thyroidal illness syndrome; the feeding strategy). Each system is applied to the critically ill patient — the shock, the ARDS, the AKI, the raised ICP, the multi-organ failure.

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Domain

Physiology / haematology immunology

1

medium

Blood & Immunology Physiology

Blood and immunology physiology: the hematopoiesis (the pluripotent stem cell → RBC, WBC, platelets). The red blood cell physiology (2,3-DPG, oxygen dissociation curve, Bohr effect, Haldane effect). The innate immunity (the neutrophils, the macrophages, the complement, the natural killer). The adaptive immunity (the T cells — the cellular; the B cells — the humoral antibodies). The complement cascade (the classical, the alternative, the lectin). The coagulation cascade (the intrinsic, the extrinsic, the common — the PT/aPTT/TT). The platelet function (the adhesion — vWF/GPIb; the activation; the aggregation — GPIIb/IIIa/fibrinogen). The fibrinolysis (the plasmin, the D-dimer). The inflammation (the cytokines, the acute-phase response). The immunoparalysis and the SIRS → CARS → MARS paradigm in the critical illness.

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Domain

first-part-physiology

5

high

Blood and Immunology Physiology — Comprehensive

Blood and immunology physiology — the integrated biology of haematopoiesis, innate and adaptive immunity, haemostasis (primary + secondary), fibrinolysis, and the natural anticoagulant regulatory systems. HAEMATOPOIESIS: pluripotent haematopoietic stem cell (HSC) in bone marrow → self-renewal + differentiation down two lineages. MYELOID lineage → erythrocytes (EPO-driven), neutrophils (G-CSF), monocytes/macrophages (M-CSF), eosinophils (IL-5), basophils, and megakaryocytes/platelets (TPO). LYMPHOID lineage → T cells (thymus), B cells (marrow), NK cells. Common progenitors: CMP (common myeloid progenitor, driven by IL-3/GM-CSF) and CLP (common lymphoid progenitor). INNATE IMMUNITY (minutes-hours): neutrophils (phagocytosis + neutrophil extracellular traps [NETs]), macrophages (phagocytosis + antigen presentation via MHC II), dendritic cells (professional antigen presenters bridging innate→adaptive), NK cells (kill virus-infected/tumour cells lacking MHC I, regulated by activating/inhibitory receptors), complement (classical [antibody-triggered, C1q], alternative [spontaneous hydrolysis of C3, amplification], lectin [mannose-binding lectin → MASP] pathways → converge at C3 convertase → C5 → membrane attack complex [MAC, C5b-9] → osmotic lysis + opsonisation [C3b] + inflammation [C3a/C5a]), acute phase proteins (CRP, procalcitonin, ferritin — produced by liver under IL-6 drive). ADAPTIVE IMMUNITY (days-weeks): T cells (CD4+ helper — coordinates response via cytokines, Th1/Th2/Th17/Tfh/Treg; CD8+ cytotoxic — kills virus-infected cells via perforin/granzyme + FasL), B cells (plasma cells produce antibody; IgM first then class-switching to IgG/IgA/IgE; memory B cells) → immunological memory. PRIMARY HAEMOSTASIS: platelet adhesion (vWF binds exposed subendothelial collagen + platelet GPIb-IX-V) → activation (shape change, granule release: ADP, serotonin, TXA2 from COX/thromboxane synthase; GPVI signals) → aggregation (GPIIb/IIIa [αIIbβ3] binds fibrinogen → platelet plug). SECONDARY HAEMOSTASIS: EXTRINSIC pathway (tissue factor + VIIa → activates X → tenase), INTRINSIC pathway (XII → XI → IX + VIIIa → activates X — amplification loop), COMMON pathway (X → Va → prothrombinase → thrombin [IIa] → fibrinogen → fibrin → cross-linked by XIIIa). FIBRINOLYSIS: plasminogen → plasmin (via tPA from endothelium; uPA) → degrades fibrin → D-dimer (and FDPs); regulated by PAI-1 (inhibits tPA) and α2-antiplasmin. REGULATION (natural anticoagulants): ANTITHROMBIN (serpin — inhibits thrombin, IXa, Xa, XIa, XIIa — potentiated ~1000-fold by heparin via conformational activation of its reactive site and the heparin-binding lysine); PROTEIN C/S (thrombin-thrombomodulin on endothelium activates protein C → activated protein C [APC] + protein S as cofactor → inactivates Va and VIIIa by proteolysis; deficiency → thrombophilia); TFPI (tissue factor pathway inhibitor — inhibits VIIa-TF complex after Xa generation, feedback inhibition of extrinsic pathway). The endothelial glycocalyx + thrombomodulin + heparan sulfates + tPA + ADAMTS13 maintain a constitutive anti-thrombotic vessel surface.

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Cellular Physiology and Membrane Potentials — Comprehensive

Cellular physiology — the biophysical basis of membrane potentials, action potentials, and excitation-contraction coupling. RESTING MEMBRANE POTENTIAL (RMP): ~-70 to -90 mV in excitable cells — generated by K+ concentration gradient (intracellular K+ 140 mmol/L, extracellular 4 mmol/L) + relative membrane impermeability to Na+ — calculated by the Goldman-Hodgkin-Katz (GHK) equation (weights each ion's contribution by its permeability). ACTION POTENTIAL (AP): in cardiac myocytes — Phase 0 (rapid depolarisation — fast Na+ influx), Phase 1 (initial repolarisation — transient K+ efflux), Phase 2 (plateau — Ca2+ influx balances K+ efflux — UNIQUE to cardiac muscle — allows sustained contraction), Phase 3 (repolarisation — K+ efflux dominates), Phase 4 (resting — Na+/K+ ATPase restores gradients). EXCITATION-CONTRACTION COUPLING: AP → voltage-gated L-type Ca2+ channel opens → Ca2+ enters → triggers ryanodine receptor → Ca2+ release from sarcoplasmic reticulum → Ca2+ binds troponin C → exposes actin binding site → myosin cross-bridge cycling → contraction. Relaxation: Ca2+ reuptake by SERCA into SR → Ca2+ dissociates from troponin → relaxation. NEUROMUSCULAR JUNCTION: motor neuron AP → voltage-gated Ca2+ channel → ACh vesicle exocytosis → ACh binds nicotinic AChR → Na+ influx → endplate potential → muscle AP. OXIDATIVE PHOSPHORYLATION: electron transport chain (complex I-IV) → proton gradient across inner mitochondrial membrane → ATP synthase → ATP from ADP + Pi.

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Endocrine Physiology in Critical Illness — Comprehensive

Endocrine physiology of critical illness — the integrated hormonal response to severe stress. STRESS RESPONSE: critical illness (sepsis, trauma, surgery, burns) activates the hypothalamic-pituitary axes and counter-regulatory hormones to maintain perfusion, substrate availability, and immune homeostasis. HPA AXIS: hypothalamus releases CRH → anterior pituitary releases ACTH → adrenal cortex (zona fasciculata) releases CORTISOL. Cortisol is ESSENTIAL for survival in stress — it (1) maintains vascular tone via a PERMISSIVE effect on catecholamines (maintains vascular sensitivity to catecholamines — without cortisol, they cannot maintain BP, causing vasoplegic shock), (2) is anti-inflammatory/immunosuppressive (inhibits NF-kB, phospholipase A2, cytokines IL-1, IL-6, TNF-alpha), (3) drives gluconeogenesis (stress hyperglycaemia), (4) maintains intravascular volume (mild mineralocorticoid effect). CIRCI (critical illness-related corticosteroid insufficiency): inadequate cortisol for the DEGREE of stress — adrenal insufficiency PLUS tissue glucocorticoid resistance — NOT absolute adrenal failure. Suspect in vasopressor-refractory septic shock. THYROID AXIS: TRH → TSH → T4 (prohormone) → peripheral 5'-deiodinase (D1/D2) converts T4 to T3 (active). In critical illness: SICK EUTHYROID SYNDROME (non-thyroidal illness) — T3 falls (reduced conversion), reverse T3 rises (shunted from T4), T4 normal/low, TSH normal/low — an ADAPTIVE response to reduce metabolic rate and conserve energy — do NOT treat with thyroid hormone unless intrinsic thyroid disease coexists. GLUCOSE METABOLISM: stress hyperglycaemia — cortisol + catecholamines + glucagon + GH + cytokines (IL-6, TNF-alpha) → hepatic gluconeogenesis + glycogenolysis + peripheral insulin resistance → hyperglycaemia. This is NOT diabetes — it is a stress response and resolves with recovery. Intensive glucose control (81-108 mg/dL) INCREASED 90-day mortality versus a conventional target of 180 mg/dL or less (NICE-SUGAR). ADH/VASOPRESSIN: regulated by (1) OSMOTIC (hypothalamic osmoreceptors — 280-295 mOsm/kg) and (2) BARORECEPTOR (carotid sinus/aortic arch — triggered by >10% drop in BP) pathways. In stress: NON-OSMOTIC ADH release → water retention → SIADH pattern → dilutional hyponatraemia. RAAS: renin (from juxtaglomerular apparatus) → angiotensin I → ACE (lung) → angiotensin II (potent vasoconstrictor + stimulates aldosterone) → aldosterone (sodium/water retention). Activated in shock to maintain BP and circulating volume.

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GI and Hepatic Physiology — Comprehensive (Splanchnic Circulation, Liver Metabolism, Gut Barrier, Bile)

GI and hepatic physiology — the integrated splanchnic circulation, liver metabolic functions, gut barrier, and bile physiology that underpin multiple organ dysfunction in critical illness. SPLANCHNIC CIRCULATION: receives ~25% of cardiac output — mesenteric arteries (coeliac, SMA, IMA) supply the gut → gut capillaries → PORTAL VEIN (75% of liver blood flow, oxygen-poor, nutrient-rich) + HEPATIC ARTERY (25%, oxygen-rich) form the liver's DUAL blood supply → hepatic sinusoids → central vein → hepatic vein → IVC. The gut is a LOW-FLOW vulnerable organ — in shock (any type) splanchnic vasoconstriction (alpha-1, angiotensin II, vasopressin) diverts flow to heart/brain → mesenteric ischaemia → mucosal injury → bacterial/endotoxin translocation across the disrupted gut barrier → portal bacteremia → Kupffer cell activation → cytokine storm (TNF-alpha, IL-1, IL-6) → systemic inflammatory response → multiple organ dysfunction syndrome (MODS) — the 'gut motor' of MODS. LIVER METABOLIC FUNCTIONS: (1) GLUCOSE HOMEOSTASIS — glycogen storage (100 g), glycogenolysis (glycogen → glucose-1-phosphate → glucose), gluconeogenesis (lactate, amino acids, glycerol → glucose); the liver is the glycostat — maintains plasma glucose 4-7 mmol/L. (2) PROTEIN SYNTHESIS — albumin (oncotic pressure, drug binding), ALL clotting factors EXCEPT von Willebrand factor (made by endothelium) and factor VIII (mostly endothelial) — factors II, VII, IX, X (vitamin K-dependent), I (fibrinogen), V, XI, XII, XIII; complement proteins; acute-phase proteins (CRP, ferritin). (3) DRUG METABOLISM — PHASE I: cytochrome P450 (CYP3A4, CYP2D6, CYP1A2, CYP2C9) — oxidation/reduction/hydrolysis (adds or exposes a functional group, often makes drug MORE active or reactive); PHASE II: conjugation (glucuronidation, sulphation, acetylation, glutathione conjugation) — attaches a polar group → water-soluble metabolite for renal/biliary excretion. BOTH phases are IMPAIRED in cirrhosis (reduced CYP activity + portosystemic shunting reduces first-pass metabolism → drug accumulation). (4) BILIRUBIN METABOLISM — senescent RBCs (reticuloendothelial system) → haem oxygenase cleaves haem → biliverdin → biliverdin reductase → UNCONJUGATED (indirect) bilirubin — FAT-SOLUBLE, albumin-bound, cannot be excreted in urine → hepatocyte uptake → conjugated with GLUCURONIC ACID (UGT1A1) → CONJUGATED (direct) bilirubin — WATER-SOLUBLE → excreted in bile → gut bacteria deconjugate → UROBILINOGEN → most excreted in stool (STERCOBILIN = brown colour); ~10% reabsorbed (enterohepatic circulation) → re-excreted in bile OR urine as urobilinogen. (5) AMMONIA METABOLISM — gut bacteria produce NH3 from protein/urea → portal blood → hepatocyte UREA CYCLE (carbamoyl phosphate synthetase-I → ornithine cycle) → urea → kidney excretion. In liver failure the urea cycle FAILS → NH3 accumulates → crosses blood-brain barrier → astrocyte glutamine synthesis (glutamine synthetase) → osmotic astrocyte swelling → cerebral oedema + hepatic encephalopathy. GUT BARRIER: the single-cell-thick intestinal epithelium + mucus layer (goblet cells) + tight junctions (claudins, occludin, zonula occludens) + antimicrobial peptides (defensins, RegIIIgamma) + gut-associated lymphoid tissue (GALT — Peyer's patches, lamina propria lymphocytes, secretory IgA) + commensal microbiome (10^13 organisms) — DISRUPTED in critical illness by ischaemia/reperfusion, antibiotics (dysbiosis), proton pump inhibitors (bacterial overgrowth), altered motility (ileus), parenteral nutrition → bacterial translocation → MODS. BILE: hepatocytes synthesise primary bile acids (cholic, chenodeoxycholic acid) from cholesterol → conjugated with glycine/taurine → secreted into canaliculi → gallbladder storage → released post-prandially (CCK) → emulsify dietary fat (form mixed micelles) → 95% reabsorbed in terminal ileum (enterohepatic circulation, 6-10 cycles/day) → also the excretory route for conjugated bilirubin, cholesterol, and lipophilic drug metabolites. CHOLESTASIS (intrahepatic [sepsis, drugs, PBC] or extrahepatic [gallstones, stricture, tumour]) → conjugated bilirubin back-up → jaundice + pruritus (bile acid skin deposition) + malabsorption of fat-soluble vitamins (A, D, E, K).

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Thermoregulation — Comprehensive

Thermoregulation — the integrated hypothalamic control of body temperature by balancing heat production against heat loss. HEAT PRODUCTION: basal metabolic rate (70-80% of resting heat), shivering thermogenesis (skeletal muscle — up to 5x BMR increase), non-shivering thermogenesis (brown adipose tissue / uncoupling protein 1 — dominant in neonates, reactivated in adult humans), voluntary exercise, and hormonal calorigenesis (thyroid hormone T3/T4 — slow genomic up-regulation of Na+/K+ ATPase; catecholamines — rapid beta-adrenergic stimulation of metabolism). HEAT LOSS: radiation 60% (infrared transfer to cooler surroundings — dominant at rest in a temperate room), convection 12% (air currents carry heat away — basis of forced-air cooling and wind chill), conduction 3% (direct contact — basis of cooling blankets and ice/water immersion), evaporation 25% (sweat 0.58 kcal/g water vaporised + respiratory water loss), and respiration (latent heat of vaporisation + warming of inspired gas). HYPOTHALAMIC CONTROL: the preoptic area of the anterior hypothalamus (PO/AH) houses the central thermoregulatory integrator — it is itself warm-sensitive, contains the defended set point (~37 degrees C core), and integrates central (blood) temperature with peripheral (skin/cold) afferent input to generate autonomic outputs (sweating, shivering, cutaneous vasodilation/vasoconstriction) and behavioural outputs (clothing, seeking shade/shelter). NORMAL RANGE: 36-37.5 degrees C core. RESPONSE TO COLD: peripheral vasoconstriction (sympathetic — reduces shell conductance) → shivering (skeletal muscle) → non-shivering thermogenesis (brown fat) → piloerection (trapped air layer) → TSH/catecholamine release (raise metabolic rate). RESPONSE TO HEAT: cutaneous vasodilation (active vasodilation via cholinergic/nitric oxide — opens arteriovenous anastomoses) → sweating (eccrine glands, sympathetic cholinergic) → behavioural cooling. TARGETED TEMPERATURE MANAGEMENT (TTM): controlled hypothermia 32-36 degrees C after cardiac arrest — reduces cerebral metabolic rate by 6-7% per degree C fall → reduces cerebral O2 demand, attenuates excitotoxicity, reperfusion injury, seizure activity and free-radical generation → neuroprotection. FEVER: prostaglandin E2 (PGE2) synthesised in the PO/AH (via COX-induced conversion of arachidonic acid, driven by endogenous pyrogens IL-1, IL-6, TNF-alpha acting on the organum vasculosum of the lamina terminalis) RAISES the hypothalamic set point → the patient feels cold → shivering + vasoconstriction raise core temperature to the new set point. Antipyretics (paracetamol, NSAIDs) work by BLOCKING PGE2 synthesis (COX inhibition). HYPERTHERMIA: the set point is NORMAL — body temperature exceeds the set point due to excessive external heat, exercise, or uncontrolled heat production (malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome, heat stroke) — antipyretics are INEFFECTIVE because the set point is not elevated; treatment is active cooling. POIKILOTHERMIA: loss of hypothalamic thermoregulation — high spinal cord injury (loss of sympathetic outflow below the lesion), brain death — body temperature drifts passively towards ambient temperature.

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Domain

Neurocritical care / monitoring

3

high

Brain Tissue Oxygen (PbtO2) & Multimodality Neuromonitoring

No single neuromonitor is sufficient. The ICP monitoring alone misses the brain tissue hypoxia (the PbtO2 can be low even when the ICP is normal). Multimodality neuromonitoring integrates the ICP, the PbtO2 (brain tissue oxygen, measured by the Licox probe; normal 20-40 mmHg, target above 15-20 mmHg), the SjvO2 (the jugular venous oxygen saturation, 55-75 per cent; below 50 is the cerebral hypoxia), the cerebral microdialysis (a lactate-pyruvate ratio of 40 or more with brain glucose under 0.7 mmol/L defines the metabolic crisis), the continuous EEG (for the non-convulsive status), the transcranial Doppler (the Lindegaard ratio for the vasospasm), and the PRx (the pressure reactivity index for the optimal CPP). The PbtO2-guided therapy (the BOOST-2 trial) reduced the burden of brain tissue hypoxia (proportion of time hypoxic 0.45 to 0.16) on top of ICP/CPP-guided care in severe TBI, with a trend toward better outcome — the Phase III BOOST-3 trial followed. This topic covers each monitor, its thresholds, and the integrated, protocolised therapy that treats the patient rather than the number.

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high

Continuous EEG & Non-Convulsive Status Epilepticus

Continuous EEG (cEEG) monitoring in the ICU detects the non-convulsive status epilepticus (NCSE) — a continuous or recurring epileptiform activity on the EEG without the clinical motor convulsions, producing a persistent impaired consciousness. NCSE is common in the comatose ICU patient (10-30 per cent of the comatose patients, especially after a convulsive SE, a TBI, a SAH, or a cardiac arrest) and is detected only by the EEG — the clinical examination cannot distinguish it from the metabolic encephalopathy. The Salzburg criteria diagnose the NCSE (the epileptiform activity plus a response to the IV antiepileptic), and the ACNS terminology standardises the description of the ICU EEG patterns (LPDs, GPDs, LRDA, GRDA, SIRPIDs). cEEG is also the tool for the post-arrest prognostication (background reactivity, malignant patterns), for the seizure monitoring during the status epilepticus treatment, and for the burst-suppression verification during the anaesthetic coma. The treatment: 1st line IV benzodiazepine, 2nd line levetiracetam or valproate or fosphenytoin, 3rd line a continuous infusion (midazolam or propofol) for the refractory. Untreated, the NCSE worsens the neurological outcome.

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high

ICP Monitoring & Waveforms

Intracranial pressure (ICP) monitoring measures the pressure within the skull, guiding the management of raised ICP (target under 22 mmHg in TBI). The cerebral perfusion pressure (CPP = MAP minus ICP) is the key derived variable, with a target of 60-70 mmHg. The intraventricular catheter (external ventricular drain) is the gold standard (it measures, drains, and samples the CSF); the intraparenchymal microsensor (Codman) is accurate but cannot drain. The normal ICP waveform has three peaks: P1 (the arterial percussion), P2 (the tidal wave reflecting compliance — a P2 rising above P1 indicates a loss of compliance), and P3 (the venous dicrotic). The Lundberg A-wave (the plateau wave — a sudden sustained plateau rise from a vasodilatory cascade) indicates a critical loss of the intracranial compliance and requires an urgent treatment.

Open

Domain

Burns

7

high

Burn Assessment — TBSA, Depth & Airway

The burn the assessment — the **the TBSA** (the total the body the surface the area — the Rule of the Nines, the Lund-the-Browder, the palm), the **the depth** (the superficial / the partial / the deep the partial / the full the thickness), and the **the airway / the inhalation the injury** (the soot, the singed the hair, the carbonaceous the sputum → the early the intubation). The severity the classification. The **Parkland the formula** (the 4 mL/kg/%TBSA — the half the 8 h, the rest the 16 h). Burn assessment is built on three pillars — the Total Body Surface Area (TBSA), the depth, and the airway/inhalation injury — which together determine fluid resuscitation, the need for transfer to a burns unit, and prognosis. TBSA is estimated by the R…

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Burn Resuscitation Fluids (Parkland)

Major burn resuscitation replaces the plasma volume lost through the post-burn systemic capillary leak. The Parkland formula (4 mL/kg/%TBSA of lactated Ringer's over the first 24 hours, half in the first 8 hours) is the standard starting estimate — titrated hourly to urine output of 0.5 mL/kg/h in adults and 1.0 mL/kg/h in children. Fluid creep: across 48 studies the mean first-24-hour volume was 5.2 mL/kg/%TBSA against the 4 mL/kg/%TBSA Parkland estimate, and Saffle's 2007 review linked it to abdominal compartment syndrome. Lactated Ringer's preferred over 0.9 per cent saline (SMART: balanced crystalloids reduced death/new dialysis/persistent renal dysfunction, 14.3 vs 15.4 per cent). Albumin added selectively once crystalloid requirements run high; the original Parkland regimen followed the first 24 hours with 0.3-0.5 mL/kg/%TBSA plasma.

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medium

Burn Wound Care & Infection

Burn wound care and infection — cleaning/debridement, topical antimicrobials (silver sulfadiazine, mafenide, silver nitrate, nanocrystalline silver), dressings and skin substitutes (Biobrane, dermal regeneration templates), early excision and grafting. Infection (colonisation to invasion; Gram-positive early, Gram-negatives later, fungal late). Burn patients have SIRS at baseline — sepsis is recognised with the modified ABA 2007 criteria (temperature, progressive tachycardia and tachypnoea, thrombocytopenia, insulin resistance, feeding intolerance — a trigger for concern, not a SIRS count). Burn wound sepsis remains a leading cause of death in severe burns. Continuous prophylactic systemic antibiotics are NOT recommended (weak evidence, resistance cost) — prevention rests on topical antimicrobials plus early excision plus infection control.

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medium

Burns — Metabolic & Nutritional Management

The metabolic and nutritional management of the burns — the hypermetabolic response (the metabolic rate 150 to 200 per cent above normal; the massive catabolism, the hyperglycaemia). The early enteral nutrition (within 24 to 48 h). The high protein (1.5 to 2 g/kg/day). The trace elements (the zinc, the copper, the selenium). The anabolic (the oxandrolone, the propranolol, the insulin).

Open

high

Electrical & Chemical Burns

The electrical and the chemical the burns — the electrical (the high the voltage → the deep the tissue the injury, the entrance + exit the wounds, the compartment the syndrome, the myoglobinuria → AKI, the cardiac the arrhythmia) and the chemical (the acid → the coagulative; the alkali → the liquefactive, the deeper; the hydrofluoric → the hypocalcaemia → the arrhythmia; the calcium the gluconate the gel). The copious the irrigation (the chemical); the ECG + the CK (the electrical); the fasciotomy.

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medium

Escharotomy & Compartment Syndrome in Burns

The escharotomy — the surgical incision through the full-thickness eschar to release the circumferential constriction (the tourniquet effect) from circumferential burns of the limbs or the chest. The compartment syndrome (the deep muscle oedema, especially electrical — the FASCIOTOMY, not the escharotomy). The abdominal compartment syndrome (the fluid creep). The monitoring (the Doppler pulses, the capillary refill, the pulse oximetry).

Open

high

Inhalation Injury & Carbon Monoxide in Burns

Smoke inhalation injury is the leading cause of death at the fire scene and, in the burn unit, markedly increases the mortality of a given cutaneous burn (pooled odds ratio about 3). It is anatomically and mechanistically THREE distinct injuries layered on one exposure: (1) SUPRAGLOTTIC THERMAL injury — heat is dissipated above the vocal cords so direct thermal damage is confined to the supraglottic airway, where progressive oedema threatens complete obstruction → the imperative for EARLY INTUBATION before the airway becomes impossible; (2) SUBGLOTTIC CHEMICAL injury — smoke carries water-soluble toxins (hydrogen chloride, ammonia) that deposit in the upper airway and lipid-soluble toxins (phosgene, nitrogen dioxide, acrolein, aldehydes) that reach the alveoli, causing …

Open

Domain

Haematology / immunotherapy

1

high

CAR-T & Cytokine Release Syndrome — Tocilizumab, ICANS & the ASTCT Grading

The CAR-T cell therapy (the chimeric antigen receptor T-cell — the CD19 for the B-cell malignancies; the BCMA for the myeloma) causes the cytokine release syndrome (CRS) — the massive IL-6 release → fever, hypotension, hypoxia (the 1 to 14 days post-infusion, peak day 3 to 7). The ASTCT grading: grade 1 (fever); grade 2 (hypotension responding to fluids or O2 under 40 per cent); grade 3 (1 vasopressor or O2 over 40 per cent); grade 4 (multi-vasopressors or ventilation). The management: tocilizumab (anti-IL-6 receptor — 8 mg per kg, the 12 mg per kg under 30 kg; the specific for the severe or life-threatening CRS); corticosteroids (for the grade 3 to 4 and for the ICANS). The ICANS (neurotoxicity — confusion, aphasia, seizures, cerebral oedema) — the corticosteroids the first-line (the dexamethasone; the tocilizumab the NOT the crosses the BBB).

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Domain

Cardiovascular / cardiomyopathy

1

high

Cardiomyopathies & Myocarditis

The four cardiomyopathies are dilated (the commonest — an enlarged LV with a reduced EF, treated with heart-failure therapy), hypertrophic (asymmetric septal LVH with a dynamic LVOT obstruction and a risk of sudden cardiac death — treat with beta-blockers, avoid vasodilators, an ICD for prevention), restrictive (amyloid, sarcoid — stiff ventricles with impaired filling, treated for the cause), and arrhythmogenic (a genetic right-ventricular cardiomyopathy). Takotsubo is a transient stress-mediated apical ballooning that mimics an anterior STEMI. Myocarditis is an inflammation of the myocardium (most commonly viral — coxsackie, parvovirus, SARS-CoV-2), presenting with chest pain, arrhythmia, heart failure, and a rising troponin with normal coronary arteries. The cardiac MRI (mid-wall late gadolinium enhancement) and the biopsy (the Dallas criteria) confirm. Treatment is supportive; most recover, but giant-cell and a fulminant case may need immunosuppression, mechanical support or a transplant.

Open

Domain

Physiology / cellular

1

high

Cellular Physiology & Membrane Potentials

Cellular physiology and membrane potentials: the resting membrane potential (minus 70 mV; the Na/K ATPase — 3 Na out, 2 K in; the K leak the dominant). The Nernst equation (the equilibrium potential). The Goldman equation (the permeability-weighted). The action potential (the depolarisation Na influx, the repolarisation K efflux, the refractory). The cell membrane (the phospholipid bilayer, the channels, the receptors). Excitation-contraction coupling (the skeletal, the cardiac, the smooth). Cellular metabolism (glycolysis, Krebs cycle, oxidative phosphorylation, the ATP). Oxygen sensing (the HIF-1 alpha, the mitochondrial oxygen utilisation). Cellular hypoxia (the hypoxic, the stagnant, the anemic, the histotoxic; the cytopathic in sepsis). The cell death (the apoptosis, the necrosis, the necroptosis). The reactive oxygen species and the antioxidant defenses. The clinical correlations (the hyperkalaemia, the hypocalcaemia, the local anaesthetics, the channelopathies).

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Domain

Neurocritical care / infectious

1

high

CNS Infections — Meningitis, Encephalitis & Brain Abscess

The CNS infections in the ICU are the bacterial meningitis, the viral encephalitis, and the brain abscess. The bacterial meningitis presents with the fever, the neck stiffness, and the altered consciousness (the classic triad — present together in only 44 per cent, but 95 per cent have at least two of the four features: headache, fever, neck stiffness, altered mental status). The CSF shows the raised opening pressure, the cloudy appearance, the neutrophil predominance, the raised protein, and the low glucose. The empirical therapy is high-dose ceftriaxone (75–100 mg/kg/day per the French adult guideline) plus the vancomycin plus the dexamethasone 10 mg IV every 6 hours for 4 days (given before or with the first antibiotic dose), with the ampicillin added for the older or immunocompromised patient and the acyclovir 10 mg/kg IV every 8 hours if the HSV is suspected. The door-to-antibiotic target is under 1 hour — the antibiotics are NOT delayed for the CT or the LP. The HSV encephalitis is treated with the empirical acyclovir 10 mg/kg every 8 hours (at least 10 days; the PCR is the diagnostic test). The brain abscess complicating meningitis (1.9 per cent of episodes) is treated with the prolonged antibiotics and the neurosurgical drainage when indicated.

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Domain

Ethics / communication

1

high

Conflict, Mediation & Ethics Consultation in the ICU

Conflict, mediation, and ethics consultation in the ICU: sources (prognostic disagreement, goals of care, futility, family dynamics, intra-team, resource allocation), bioethics frameworks (four principles, deontological, utilitarian, virtue ethics, care ethics), capacity and substitute decision-making (substituted judgement vs best interests), structured conflict resolution (IDENTIFY → CLARIFY → EXPLORE → NEGOTIATE → AGREE), when to call the ethics committee, medical futility disputes and unilateral withdrawal, legal aspects (capacity, guardianship, tribunal/court, advance directives), and withdrawal of life-sustaining treatment against family wishes.

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Domain

renal

1

high

Continuous Renal Replacement Therapy (CRRT) — Comprehensive ICU Management

CRRT (continuous renal replacement therapy) — the renal support modality for haemodynamically unstable ICU patients. Three modalities: CVVH (continuous venovenous haemofiltration — predominantly convective clearance), CVVHD (continuous venovenous haemodialysis — predominantly diffusive clearance), CVVHDF (continuous venovenous haemodiafiltration — combines dialysis and haemofiltration). Anticoagulation: REGIONAL CITRATE — KDIGO recommends citrate over unfractionated heparin in patients without contraindications, with or without increased bleeding risk; citrate chelates ionised calcium in the circuit, a separate calcium infusion replaces systemic losses, and the total-to-ionised calcium ratio is the sentinel for citrate accumulation (albumin-corrected ratio 2.5 or above defines accumulation; ratio 2.4 or above independently predicts 28-day mortality). Effluent dose: guidelines recommend a prescribed dose of 20 to 25 mL per kg per hour; RENAL (25 vs 40 mL/kg/h) and ATN (20 vs 35 mL/kg/h) showed no survival benefit from higher intensity. Timing: AKIKI and STARRT-AKI showed no mortality benefit from early or accelerated initiation.

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Domain

Obstetrics

1

high

Critical illness in pregnancy: ICU management and obstetric emergencies

Critical illness in pregnancy: physiological adaptations of pregnancy alter drug dosing, ventilation, circulation. Key changes: increased cardiac output (+30-40%), decreased SVR, increased blood volume, decreased albumin, dilutional anaemia, elevated diaphragm (decreased FRC), increased clotting factors (hypercoagulable). Common ICU indications: severe pre-eclampsia/eclampsia, HELLP, peripartum cardiomyopathy, amniotic fluid embolism, sepsis (pyelonephritis, chorioamnionitis), trauma, asthma, diabetic emergencies. Position: LEFT LATERAL tilt (avoid aortocaval compression from gravid uterus — especially after 20 weeks). Drugs: avoid ACEi/ARB, NSAIDs (3rd trimester), aminoglycosides, warfarin (teratogenic). Fetal monitoring.

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Domain

Monitoring / echocardiography

1

high

Critical-Care Echocardiography — FOCUS & FATE

Focused cardiac ultrasound (FOCUS or FATE) is the bedside, clinician-performed transthoracic echocardiogram for the critically ill patient, designed to answer specific resuscitation questions in real time — not a comprehensive echo. The five standard views (parasternal long axis, parasternal short axis, apical 4-chamber, subcostal, and the IVC) answer: is the LV hyperdynamic (hypovolaemia) or hypokinetic (cardiogenic)? Is the RV dilated (PE, cor pulmonale)? Is there a pericardial effusion (tamponade)? Is the IVC collapsing (volume-responsive) or plethoric (high right-sided pressures)? Gross valve abnormalities? FOCUS complements — it does not replace — the formal comprehensive echo.

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Domain

Neurocritical care / neuromuscular

3

high

Critical-Illness Polyneuropathy & Myopathy (CIPNM) — ICU-Acquired Weakness

The critical-illness polyneuropathy and myopathy (CIPNM, the ICU-acquired weakness) is an acquired weakness of the critically ill patient, developing after the sepsis, the multi-organ failure, or the prolonged ventilation. It comprises two overlapping entities — the critical illness polyneuropathy (the CIP, an axonal sensorimotor neuropathy) and the critical illness myopathy (the CIM, a myosin-loss myopathy, classically from the corticosteroids plus the neuromuscular blockers in the asthma and the ARDS). The clinical hallmark is the failure to wean from the ventilation, with the flaccid weakness, the areflexia, and the muscle wasting — the cranial nerves are SPARED (a useful discriminator from the Guillain-Barre). The only proven prevention is the glucose control (the Van den Berghe trial) and the early mobilisation; minimise the sedation, the corticosteroids, and the neuromuscular blockers. The recovery is over weeks to months and is often incomplete (a long-term disability).

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high

Motor Neuron Disease & Neuromuscular Weakness in ICU — ALS, NIV & End-of-Life

Motor neuron disease (MND), or the amyotrophic lateral sclerosis (ALS), is a progressive degeneration of the upper and the lower motor neurons, causing a mixed UMN and LMN signs (the muscle wasting, the fasciculations, and the brisk reflexes) in the SAME limb, with the sensation and the sphincters SPARED. It is relentlessly progressive and fatal — the typical terminal event is the respiratory failure from the diaphragm weakness. In the ICU, the MND presents with a type 2 respiratory failure or an aspiration from the bulbar weakness. The management: the riluzole (extends the survival by about 3 months); the non-invasive ventilation (the standard for the symptomatic respiratory weakness — the FVC under 50 per cent or the orthopnoea; improves the survival and the quality of life); the PEG nutrition before the weight loss; and the advance care planning (the decision to ventilate is ethically complex). The neuromuscular weakness in the ICU has a broad differential — the GBS, the myasthenia, the MND, the critical-illness polyneuromyopathy, the electrolyte disorders, and the cord lesion.

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high

Myasthenia Gravis & Myasthenic Crisis — NMJ Weakness, PLEX/IVIG & Steroid Exacerbation

Myasthenia gravis (MG) is an autoimmune disease of the post-synaptic acetylcholine receptor at the neuromuscular junction — the acetylcholine receptor antibodies damage the receptors, causing a fatigable weakness (worse with the activity, better with the rest). The ocular (the ptosis, the diplopia), the bulbar, and the limb muscles are affected; the reflexes and the sensation are PRESERVED (a key discriminator from the Guillain-Barre). The myasthenic crisis is the life-threatening respiratory or the bulbar failure, precipitated by the infection, the surgery, or the junction-worsening drugs. The management: intubate early on the falling serial spirometry and the bulbar failure (the trend and the pronounced bulbar weakness decide before the hypercapnia does); the plasma exchange OR the IVIG (equivalent in the randomised head-to-head trials); the high-dose corticosteroid COMBINED with the exchange or the immunoglobulin as the cornerstone in the established crisis; stop every drug that may be worsening the junction. The cholinergic crisis (the excess pyridostigmine) causes the weakness PLUS the cholinergic overdrive (the miosis, the salivation, the bradycardia, the sweating) — wet vs the dry myasthenic crisis. Screen for the thymoma (the chest CT); the thymectomy if the thymoma.

Open

Domain

Renal / RRT

3

high

CRRT — Circuit, Prescription, Anticoagulation & Troubleshooting

The CRRT is delivered through a blood circuit — the dual-lumen central access, the blood pump, the pre-dilution (the replacement fluid before the filter), the haemofilter (the hollow-fibre membrane), the post-dilution (the replacement fluid after the filter), the air-trap, and the return. The pressures (the access negative, the return positive, the filter transmembrane) monitor the circuit patency and the clotting. The prescription: the modality (the CVVH, the CVVHDF), the dose (the effluent 20 to 25 mL/kg/h), the blood flow, the fluid balance, the fluid composition, and the anticoagulation. The anticoagulation is the regional citrate (the preferred; the post-filter ionized calcium 0.25 to 0.35 mmol/L; the total-to-ionized ratio under 2.5; the risks the metabolic alkalosis, the acidosis in the liver failure, the hypercalcaemia) or the heparin or none. The troubleshooting: the circuit clotting (the inadequate anticoagulation, the high filtration fraction, the low blood flow), the high access pressure (the catheter kink or the position), the air-in-line, and the electrolyte and the nutrient loss (replace the K, the phosphate, the Mg, the increased nutrition).

Open

high

Renal Replacement Therapy Modalities — IHD vs CVVH vs CVVHDF vs SLED

The renal replacement therapy (RRT) removes the solutes and the fluid when the kidneys fail. The four modalities — the intermittent haemodialysis (IHD), the continuous veno-venous haemofiltration (CVVH), the continuous veno-venous haemodiafiltration (CVVHDF), and the sustained low-efficiency dialysis (SLED) — differ in the solute-transport mechanism (the diffusion vs the convection), the duration and the intermittency, and the haemodynamic tolerance. The IHD is diffusion-based, intermittent, rapid, and for the stable patient (the rapid solute and fluid shifts cause the hypotension and the dialysis disequilibrium). The CVVH is convection-based, continuous, gentle, and for the haemodynamically unstable and the catabolic patient (the middle-molecule clearance). The CVVHDF combines both and is the commonest CRRT modality. The SLED is the hybrid bridge. The indications follow the AEIOU (the Acidosis, the Electrolytes, the Intoxication, the Overload, the Uraemia). The anticoagulation is the regional citrate (preferred) or the heparin. The CRRT dose is 20 to 25 mL/kg/h (the ATN and the RENAL trials — the higher dose offered no benefit). The early vs the late RRT (the AKIKI, the STARRT-AKIN, the ELAIN) — no clear benefit of the early in the moderate AKI.

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medium

Sustained Low-Efficiency Dialysis (SLED) — The Hybrid Modality

Sustained low-efficiency dialysis (SLED) is a hybrid renal replacement therapy that combines features of intermittent haemodialysis (IHD) and continuous renal replacement therapy (CRRT). A standard haemodialysis machine is run slowly — published protocols use blood flows of about 100 to 250 mL/min and dialysate flows of 200 to 350 mL/min over extended 8 to 12 hour sessions on a daily or near-daily schedule, with primarily diffusive clearance. Advantages: versus CRRT it uses the standard IHD machine (cheaper, more available), needs less anticoagulation (many sessions run heparin-free), and allows down-time for procedures and mobilisation; versus IHD it is haemodynamically gentler. Randomised and meta-analytic evidence shows mortality and renal recovery comparable to CRRT. Timing follows AKIKI and STARRT-AKI — wait for an urgent indication regardless of modality.

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Domain

Diagnostics

3

high

CURB-65 and PSI: pneumonia severity scoring and risk stratification

Pneumonia severity scores guide site-of-care decisions (outpatient vs inpatient vs ICU) and identify severe CAP. CURB-65 (Confusion, Urea >7, RR≥30, BP&lt;90/60, age≥65): simple, 5-point bedside score. PSI (Pneumonia Severity Index / PORT score): comprehensive 20-variable score, 5 risk classes. IDSA/ATS minor/major criteria: gold standard for ICU admission. SMART-COP: predicts need for respiratory/vasopressor support (ANZ preferred). No score replaces CLINICAL JUDGEMENT — scores are decision SUPPORT, not replacement.

Open

high

ICU biomarkers: procalcitonin, lactate, troponin, BNP, and CRP

Biomarkers in ICU: objective measures that guide diagnosis, prognosis, and treatment. KEY biomarkers: (1) PROCALCITONIN (PCT): bacterial infection marker — rises in bacterial sepsis, stays low in viral/non-infective. Guides antibiotic duration (PRORATA, Bouadma 2010 — antibiotic stewardship). (2) LACTATE: tissue hypoperfusion marker — elevated in shock, sepsis, mesenteric ischaemia. Guide resuscitation (lactate clearance >10%/h; Jansen 2010, ANDROMEDA-SHOCK 2019). (3) TROPONIN (hs-cTn): myocardial injury — type 1 MI (atherosclerotic plaque rupture), type 2 MI (supply-demand mismatch — common in ICU), and MINS (myocardial injury after non-cardiac surgery — AHA 2021). (4) BNP/NT-proBNP: heart failure — elevated in volume overload, cardiac dysfunction. (5) CRP: inflammation — nonspecific, trends useful. (6) D-DIMER: fibrin turnover — elevated in VTE, DIC, arterial thrombosis, inflammation, malignancy, pregnancy (non-specific, high negative predictive value). (7) suPAR (soluble urokinase-type plasminogen activator receptor): inflammation/prognosis — predicts mortality in sepsis and critical illness. (8) COPEPTIN (CT-proAVP): vasopressin surrogate — quantifies stress response and arginine-vasopressin axis, prognostic in shock. Each has strengths, limitations, and specific clinical applications — always interpret in clinical context, not in isolation.

Open

high

Point-of-care ultrasound (POCUS): comprehensive ICU applications

POCUS is real-time ultrasound performed and interpreted by the treating clinician at the bedside to answer specific clinical questions. In ICU: DIAGNOSTIC (cardiac, lung, abdominal, vascular) + PROCEDURE GUIDANCE (CVC insertion, thoracentesis, paracentesis, arthrocentesis). Protocols: RUSH (Rapid Ultrasound in Shock), BLUE (Bedside Lung Ultrasound in Emergency), FAST (Focused Assessment with Sonography in Trauma), FATE (Focus Assessed Transthoracic Echo). Goal-directed limited TTE by intensivists changed management in 37% of critically ill patients in a prospective cohort. Core principle: CLINICAL INTEGRATION — POCUS does NOT replace formal echo/imaging — it answers focused questions to guide immediate management.

Open

Domain

Delirium & sleep

1

medium

Delirium, Sleep and the Post-Intensive Care Syndrome

Delirium is the acute brain dysfunction of critical illness, affecting over half of ICU patients, and it is independently associated with the longer stay, the higher mortality, and the long-term cognitive impairment. Sleep is disrupted and fragmented in the ICU, contributing to the delirium. This topic builds the examiner's framework on the delirium screening (the CAM-ICU), the prevention (the bundle), the management (the dexmedetomidine, the haloperidol — the REDUCE trial showing no survival benefit), the sleep preservation (the PADIS recommendations), and the post-intensive care syndrome (the PICS — the Pandharipande trial showing the long-term cognitive impairment).

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Domain

Statistics & evidence-based medicine

3

high

Diagnostic Tests — Sensitivity, Specificity, Predictive Values, Likelihood Ratios & ROC

Diagnostic test properties for the ICU First Part: the 2x2 table; sensitivity (SnNout) and specificity (SpPin) as intrinsic test properties; positive and negative predictive values that depend on prevalence; likelihood ratios (LR+ and LR-) that combine with pre-test probability via the Bayesian odds form and Fagan's nomogram; the ROC curve and its area under the curve as a measure of discrimination; the Youden index and number needed to diagnose; and worked examples for D-dimer in suspected PE and high-sensitivity troponin in suspected MI.

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high

Guidelines, Evidence-Based Medicine & Quality-Improvement Methodology

Guidelines, EBM and quality improvement for the ICU First Part: evidence-based medicine as the integration of best evidence, clinical expertise and patient values; the PICO question and the evidence hierarchy; the GRADE approach to evidence quality (high/moderate/low/very low), recommendation strength (strong/weak), downgrading and upgrading domains, and the Evidence to Decision framework; the guideline-development pipeline from PICO to systematic review to evidence profile to graded recommendation; guideline appraisal (AGREE II); critical appraisal tools (CASP checklists) and reporting guidelines (CONSORT, PRISMA, STROBE); implementation science (knowledge-to-action, CFIR, PARIHS); and QI methodology - PDSA cycles, care bundles, audit and feedback, and the structure-process-outcome framework.

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medium

Survival Analysis & the Kaplan-Meier Curve

Survival analysis for the ICU First Part: time-to-event data and censoring (right-censoring when the event is not observed), the survival function S(t) and its complement the cumulative distribution F(t), the hazard function h(t) and cumulative hazard H(t), the Kaplan-Meier estimator as a non-parametric step function of survival probability (product of conditional probabilities), the median and restricted mean survival time, the log-rank test comparing curves between groups, and Cox proportional-hazards regression yielding a hazard ratio under the assumption of proportional hazards.

Open

Domain

Transplant / organ donation

1

high

Donation After Circulatory Death (DCD) & Recipient Logistics

Donation after circulatory death (DCD) — the organ donation after the confirmed the circulatory the death (the five-minute the observation the period, the no the auto-resuscitation). Distinguished from the donation after the brain death (DBD — the brainstem the death). The DCD the process: the withdrawal of the life-sustaining the therapy (WLST), the five-minute the asystole the confirmation, the warm ischaemia the time (the WIT — the graft-viability the determinant; the accepted the limits the vary by the centre and the organ), the retrieval, the cold the ischaemia (the ice). The normothermic the regional the perfusion (NRP — the improves the utilization and the transplant the outcomes). The recipient the logistics — the matching, the transport (the cold the ischaemia), the transplant.

Open

Domain

Equipment, physics & clinical measurement

3

high

ECG & Electrical Safety

ECG and electrical safety for the ICU First Part: how the 12-lead ECG records cardiac potentials (Einthoven's triangle, limb and precordial leads, electrical axis), the signal path and filtering, and the principles of electrical safety - macroshock vs the much lower microshock threshold when current reaches the heart through a central line, and the protective measures (isolation, equipotential earthing, CF equipment).

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medium

Humidification

Humidification for the ICU First Part: the nose and turbinates warm, humidify, and filter inspired gas, conditioning it toward 37 degrees C and 100 per cent relative humidity - up to about 44 mg of water per litre at full saturation; an endotracheal or tracheostomy tube bypasses this, so dry gas impairs mucociliary clearance and causes secretion retention and tracheal tube blockage. Absolute humidity (mg/L) is the measure that matters. A passive heat-and-moisture exchanger (HME, artificial nose) recaptures exhaled heat and water in a hygroscopic medium and should deliver at least 30 mg/L; heated humidification is superior to an HME for thick or copious secretions, and HMEs are not recommended in low-tidal-volume lung-protective ventilation, where added dead space can increase the ventilation requirement and PaCO2. An active heated humidifier targets 33 to 44 mg/L with gas at 34 to 41 degrees at the circuit Y-piece; active humidification is suggested for non-invasive ventilation, and high-flow nasal cannula (up to 60 L/min) was introduced with heated humidification systems. Ventilator circuits should not be changed routinely.

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medium

Radiation Safety

Radiation safety for the ICU First Part: the dose units (Gray for absorbed dose, Sievert for equivalent and effective dose), typical doses (chest X-ray ~0.02 mSv, CT chest ~7 mSv which is ~350 chest X-rays (commonly quoted as ~200-400), CT abdomen-pelvis 10-20 mSv), the ALARA principle (As Low As Reasonably Achievable) and the three protections (time - minimise exposure time; distance - inverse-square law, doubling distance quarters dose; shielding - lead aprons at least 0.5 mm Pb equivalent, thyroid shields, lead glasses, gonadal shielding), the distinction between stochastic effects (cancer, hereditary - NO threshold - probability proportional to cumulative dose) and deterministic effects (tissue reactions - skin erythema ~2 Gy, cataracts ~0.5 Gy, sterility - WITH a threshold), the dose limits (public 1 mSv/yr, occupational whole body 20 mSv/yr averaged over 5 years and no more than 50 mSv in any single year, lens 150 mSv/yr, skin and extremities 500 mSv/yr, pregnant worker fetal 1 mSv for the remainder of pregnancy), personal dosimetry (film badge, TLD, OSL dosimeter worn under the lead apron), and radiation in pregnancy (minimise CT - prefer ultrasound or MRI - if CT is necessary shield the abdomen and use a low-dose protocol).

Open

Domain

Electrolytes

1

high

Electrolyte Disorders in Critical Illness — Sodium, Potassium, Calcium, Magnesium and Phosphate

Electrolyte disorders are among the commonest and most immediately dangerous derangements in critical illness, and their correction is governed less by the absolute concentration than by the speed and direction of change. This topic builds the examiner's framework around the two highest-yield cations — sodium and potassium — and a concise account of calcium, magnesium and phosphate. For sodium, the central ideas are that hyponatraemia is a disorder of water handling classified by osmolality and volume status, that the dangerous consequences are cerebral oedema (acute) and osmotic demyelination (over-correction), and that the rate of correction is the single most important decision. For potassium, the central ideas are that hyperkalaemia with ECG change is an emergency treated in a fixed sequence, and that hypokalaemia is a product of redistribution or total-body deficit. The evidence base is anchored on the Adrogué NEJM reviews of dysnatraemia, the Verbalis expert-panel hyponatraemia recommendations, the Kovesdy and Palmer potassium reviews, and the Ayuk hypomagnesaemia review, with the calcium and phosphate content resting on the standard ICU texts.

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Domain

Physiology / endocrine

1

medium

Endocrine Physiology

Endocrine physiology: the hypothalamic-pituitary axes (the HPA — the CRH/ACTH/cortisol; the HPT — the TRH/TSH/T3/T4; the HPG — the GnRH/LH/FSH; the GH; the prolactin). The feedback loops (the negative). The adrenal (the cortisol, the aldosterone, the catecholamines). The glucose homeostasis (the insulin, the glucagon). The calcium homeostasis (the PTH, the vitamin D, the calcitonin). The clinical correlations (the thyroid storm, the adrenal crisis, the DKA, the SIADH).

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Domain

Equipment & physics

1

high

Equipment & Physics — Gas Laws, Measurement, Ventilators, Circuits and Monitors

The equipment and the physics of the ICU — the gas laws (the Boyle, the Charles, the Gay-Lussac, the universal gas law, the Dalton, the Henry, the Graham/Fick diffusion, the critical temperature), the measurement physics (the pressure transducer and the Wheatstone bridge, the thermistor, the Clark electrode for the oxygen, the Severinghaus for the CO2, the paramagnetic and the infrared analyzers), the pulse oximetry (the 660/940 nm and the limitations), the capnography (the infrared and the waveform), the temperature monitoring, the ventilator (the classification, the control, the drive, the breathing system, the valves), the breathing circuits (the circle, the Mapleson, the CO2 absorber), and the defibrillator (the monophasic vs the biphasic).

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Domain

Ethics, EOL & communication

1

high

Ethics, End-of-Life, Communication & Aeromedical Retrieval

The professional and the CanMEDS domain of the ICU — the four principles of the bioethics (the autonomy, the beneficence, the non-maleficence, the justice), the capacity and the informed consent (the components, the emergency exception, the substituted decision-maker, the advance directive), the end-of-life care and the limitation of the treatment (the withholding vs the withdrawing — the ethical equivalence, the futility, the goals-of-care), the breaking of the bad news (the SPIKES — the Setting, the Perception, the Invitation, the Knowledge, the Emotions, the Strategy), the shared decision-making and the family meeting, the specific ethics (the Jehovah's Witness, the brain death and the organ donation, the do-not-resuscitate), the medico-legal (the documentation, the open disclosure, the coroner), and the aeromedical retrieval (the scoop-and-run vs the stay-and-play, the time-critical, the team, the platform, the physiological stressors of the altitude, the temperature, the noise, the vibration and the gas expansion).

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Domain

ECMO

1

medium

Extracorporeal Membrane Oxygenation (ECMO)

Extracorporeal membrane oxygenation (ECMO) is the ultimate respiratory and circulatory support — a pump and an oxygenator outside the body that replace the lung (the venovenous, VV ECMO) or the heart and the lung (the venoarterial, VA ECMO). This topic builds the examiner's framework on the circuit and the cannulation, the two modes (VV for the isolated respiratory failure, VA for the cardiogenic shock and the arrest), the evidence (the EOLIA trial for the severe ARDS, the CESAR trial for the conventional-vs-ECMO, and the VA ECMO complications), the anticoagulation and the complications (the bleeding, the thrombosis, the haemolysis, the infection, the limb ischaemia), the weaning and the decannulation, and the ethical and the resource questions of the ECMO.

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Domain

Infection / general

1

high

Fever in the ICU — Infectious or Not? The Workup & the Procalcitonin

The fever in the ICU (the temp over 38.3) is the symptom, the not the diagnosis. The first question: the infectious or the non-infectious. The infectious (the nosocomial): the VAP, the CRBSI, the CAUTI, the SSI, the C. difficile, the sinusitis, the cholecystitis, the pressure ulcers, the primary. The non-infectious: the SIRS non-infection (the pancreatitis, the trauma, the burns, the post-op, the transfusion), the drug fever, the VTE, the malignancy, the central fever (the brain injury), the alcohol withdrawal, the adrenal insufficiency, the thyroid storm. The workup: the history and the exam (the lines, the wounds, the chest, the abdomen, the skin, the perianal, the sinuses); the cultures (the blood — the peripheral plus the EACH line lumen — the urine, the sputum, the wound); the imaging (the CXR, the CT); the markers (the CRP, the procalcitonin — the bacterial; the lactate). The management: the sepsis — the sepsis-6 within the 1 hour; the stable — the workup and the judicious the empirical antibiotics; the treat the cause; the paracetamol; the judicious the antipyresis (the fever protective in the sepsis); the active the cooling for the over 39 to 40 or the brain-injured (the TTM). The neutropenic — the empirical antibiotics the now.

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Domain

Renal / fluids

1

high

Fluid Overload & Its Management — The ROSE Concept & De-resuscitation

The fluid overload is common in the ICU and is associated with the worse outcomes (the mortality, the prolonged ventilation, the AKI). It is quantified as the cumulative fluid balance (the net fluid in minus out) and the per cent fluid overload (the cumulative balance divided by the baseline weight times 100; the over 10 per cent is the worse). The harm: the pulmonary oedema, the tissue oedema (the gut, the kidneys, the intra-abdominal pressure), the delayed wound healing, the prolonged ventilation, the mortality. The ROSE concept frames the fluid therapy into the four phases — the Resuscitation, the Optimisation, the Stabilisation, and the De-resuscitation (the late phase that mobilises the excess fluid). The management: stop the fluids (minimise the maintenance), the de-resuscitation (the titrated furosemide, the albumin co-therapy, the RRT for the diuretic-resistant), the fluid-responsiveness assessment (the SVV, the PPV, the passive leg raise — NOT the CVP), and the fluid stewardship (the 4 Ds: the drug, the dose, the duration, the de-escalation).

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Domain

Physiology / GI hepatic

1

medium

GI & Hepatic Physiology

GI and hepatic physiology: the GI (the digestion, the absorption, the motility, the secretion; the gut barrier; the splanchnic circulation). The hepatic (the bilirubin metabolism — the heme to the biliverdin to the bilirubin; the conjugation; the enterohepatic circulation; the urea cycle; the glucose homeostasis; the coagulation factors; the detoxification; the bile). The clinical (the jaundice, the encephalopathy, the coagulopathy, the portal hypertension).

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Domain

Haematology & coagulation

1

medium

Haematology and Coagulation in the ICU

The haematology and the coagulation in the ICU span the physiology of the haemostasis (the cascade — the intrinsic, the extrinsic, the common; the cell-based model — the initiation, the amplification, the propagation), the platelet function (the adhesion, the activation, the aggregation), the natural anticoagulants (the antithrombin, the protein C/S, the TFPI), the fibrinolysis (the plasmin, the D-dimer), the laboratory tests (the PT, the aPTT, the TT, the fibrinogen, the D-dimer, the TEG/ROTEM), the thrombocytopenia (the DIC, the HIT, the TTP), the coagulopathy (the liver, the dilutional, the anticoagulant), the venous thromboembolism prophylaxis, the massive transfusion, and the anticoagulation reversal. This topic builds the examiner's framework on the cascade and the cell-based model, the bleeding disorders by the test pattern, the DIC (the overconsumption), the HIT (the heparin-induced), the TTP (the urgent plasma exchange), the VTE prophylaxis (the LMWH), and the reversal (the warfarin, the DOAC).

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Domain

Hepatobiliary / neurocritical care

1

high

Hepatic Encephalopathy — Ammonia, Lactulose, Rifaximin & the Precipitant

The hepatic encephalopathy (HE) is a reversible syndrome of the impaired brain function in the patient with the advanced liver failure and the portosystemic shunting. The pathophysiology centres on the ammonia (the gut-derived ammonia bypasses the liver, crosses the blood-brain barrier, and is converted to the glutamine in the astrocytes, causing the astrocyte swelling and the cerebral oedema). In the chronic liver disease, the HE is precipitated (the GI bleed, the infection, the constipation, the hypokalaemia and the alkalosis, the dehydration, the sedatives); finding and treating the precipitant is the most important step. The treatment: the lactulose (the first-line, titrated to soft stools), the rifaximin (550 mg BD, the add-on for the recurrent), the L-ornithine L-aspartate; the adequate protein (1.2 to 1.5 g/kg/day, NOT the restriction — an old myth); and the avoidance of the sedatives and the benzodiazepines. In the acute liver failure, the HE is from the acute necrosis, the cerebral oedema is the major threat, and the emergency transplant is the consideration. The West Haven classification grades the HE from I (the mild confusion) to IV (the coma).

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Domain

Respiratory / oxygen therapy

2

high

High-Flow Nasal Cannula — Mechanisms, Evidence & the ROX Index

High-flow nasal cannula (HFNC) delivers up to 60 L/min of heated, humidified oxygen-enriched gas through large-bore nasal prongs. Its five physiological mechanisms are low-level PEEP, dead-space washout, heated humidification, reduced inspiratory resistance, and a precise titrated FiO2. The FLORALI trial (NEJM 2015) supports HFNC in acute hypoxaemic respiratory failure, with reduced intubation in pneumonia. The ROX index (SpO2/FiO2 divided by respiratory rate; Roca, J Crit Care 2016) predicts success and the need to intubate — at least 4.88 favours success, under 3.85 favours failure. HFNC is a bridge, not a destination: a failing patient must be intubated.

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Oxygen Therapy Devices — Escalating FiO2

Oxygen delivery devices escalate from low-flow variable-performance devices (nasal cannula, simple mask, non-rebreather reservoir mask) whose delivered FiO2 falls as the patient's inspiratory flow rises, through fixed-performance Venturi masks (bench-validated 24-40 and 60 per cent valves) to high-flow nasal cannula (up to 60 L/min, humidified, with low-level PEEP) and then non-invasive or invasive ventilation. The British Thoracic Society targets a SpO2 of 94-98 per cent for most acutely ill adults (88-92 per cent in COPD or hypercapnia risk). The FLORALI trial (NEJM 2015) found similar intubation rates but better 90-day survival with high-flow nasal cannula in acute hypoxaemic respiratory failure. Oxygen is a drug — give the lowest FiO2 that meets the target.

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Domain

equipment-physics

4

medium

Humidification and Airway Warming — Comprehensive (HME vs Active Heated Humidifier, Physics of Humidification)

Humidification and airway warming for the ICU First Part: WHY the intubated airway needs humidification (the upper airway normally warms, humidifies, and filters inspired gas to core temperature and 100 per cent relative humidity — physiological humidity of about 44 mg/L absolute humidity — an endotracheal or tracheostomy tube BYPASSES the upper airway so humidification by artificial means must be provided). The consequences of under-humidified gas are MUCOSAL DYSFUNCTION and IMPAIRED MUCOCILIARY CLEARANCE (mucus transport velocity falls when inspired gas is dry — secretions retained — atelectasis and VAP), secretion thickening into inspissated mucus plugs that occlude airways and block suction catheters, and LATENT-HEAT-DOMINATED EVAPORATIVE HEAT LOSS (in vivo, 92 per cent of tracheal heat transfer with dry gas was latent heat and the mucosal surface cooled by 5 degrees C). The PHYSICS: ABSOLUTE HUMIDITY (mg H2O per L of gas — the measure that actually matters to the airway; AARC guideline target 33-44 mg/L at the Y-piece for active humidifiers and a minimum of 30 mg/L for HMEs), RELATIVE HUMIDITY (per cent of the maximum water capacity of gas at a given temperature — warm gas holds more water, so a cold gas at 100 per cent RH is still water-poor), and DEW POINT (the temperature at which gas reaches 100 per cent saturation and condensation begins — the circuit must be kept above the dew point or water condenses as RAINOUT). Two devices. The PASSIVE heat-and-moisture exchanger (HME, artificial nose) — a disposable hygroscopic or hydrophobic medium placed between circuit and airway that traps EXHALED heat and moisture and returns it on the NEXT inspiration — simple, needs no power or water, lower cost, adds bacterial and viral filtration with filter types, BUT adds about 85 mL of instrumental dead space (the AARC recommends against HMEs at low tidal volumes because added dead space raises the ventilation requirement and PaCO2), may occlude with thick, bloody or copious secretions, and loses output in hypothermia (bench output fell from about 34 to about 24 mg/L as expired gas cooled from 34 to 28 degrees C); it does NOT need routine daily changes — safely used for at least 48-72 hours. The ACTIVE heated humidifier — gas passed over a heated water chamber and delivered at 34-41 degrees C and 100 per cent relative humidity (33-44 mg/L) at the Y-piece, never above 41 degrees C, with a heated-wire circuit and water trap to prevent rainout; ventilator circuits are NOT changed routinely (a randomised comparison of 48-hour changes versus no change showed no pneumonia difference, and 24-hour changes increased VAP risk). Choose active for prolonged ventilation, thick or bloody secretions, significant hypothermia, low tidal volumes and NIV (the AARC suggests active humidification for NIV and recommends against passive). Device choice does NOT change VAP, mortality or ventilation duration — the AARC suggests HMEs are not used as a VAP-prevention strategy.

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ICU Electrical Safety — Comprehensive (Macroshock, Microshock, Equipotential Bonding)

ICU electrical safety — the principles and precautions to prevent electrical injury to patients and staff. Two types of electrical hazard: MACROSHOCK (external current passes through intact skin → body acts as volume conductor → current spreads → VF if >100 mA reaches the heart — prevented by grounding, RCDs, double insulation) and MICROSHOCK (tiny current ~10-100 μA applied DIRECTLY to the heart via a conductive pathway — central line, pacing wire, saline column → VF at 1000x lower threshold than macroshock — the KEY danger in ICU and cardiac areas). Prevention: EQUIPOTENTIAL BONDING (all conductive surfaces connected to same ground potential → no voltage difference → no current through patient), ISOLATED POWER SUPPLY (IPS — transformer isolates supply from ground → no path for leakage current → eliminates macroshock), EQUIPMENT CLASSIFICATION (Type CF — cardiac floating — leakage &lt;10 μA — safe for direct cardiac connection; Type BF — body floating — safe for external use; Type B — basic — NOT cardiac-safe). Leakage current monitoring: all ICU equipment must be tested annually for leakage (&lt;500 μA for chassis leakage, &lt;10 μA for patient leads in CF equipment).

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Renal Replacement Therapy Equipment — Comprehensive (Haemofilter Membranes, Diffusion vs Convection, the RRT Circuit and Pressures, Regional Citrate)

Renal replacement therapy equipment for the ICU First Part: the hollow-fibre haemofilter/dialyser and membrane types (biocompatible synthetics — polysulfone, polyethersulfone, polyamide, polyacrylonitrile — versus bioincompatible cellulose; low-flux versus high-flux; sieving coefficient determines what crosses, cut-off the molecular size at which sieving falls to zero), the clearance mechanisms (DIFFUSION for small solutes down a concentration gradient, sustained by counter-current dialysate; CONVECTION for middle molecules dragged with water by solute drag, driven by hydrostatic pressure — the Starling forces across the membrane; and ULTRAFILTRATION for volume control), the modalities (IHD, CVVH, CVVHDF, peritoneal), and the full circuit — the…

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Ultrasound & Imaging Physics — Comprehensive (Piezoelectric Effect, Frequency Versus Penetration, Axial and Lateral Resolution, B-Mode and M-Mode, Doppler, Artefacts, Probe Types)

Ultrasound and imaging physics for the ICU First Part: the PIEZOELECTRIC effect (crystals convert electrical energy to mechanical sound energy on transmission and back to electrical energy on reception), the pulse-echo principle (time-gated depth from the 1540 m/s soft-tissue speed of sound), the central trade-off between FREQUENCY and PENETRATION (higher frequency gives better resolution but penetrates less deeply because attenuation rises with frequency, so deep/cardiac use 2-5 MHz and superficial/vascular use 10-15 MHz), acoustic impedance and reflection (why air and bone obstruct and why coupling gel is used), AXIAL resolution (the ability to distinguish two objects along the beam — equals half the spatial pulse length, improved by higher frequency and shorter pulse length), LATERAL resolution (the ability to distinguish two objects side by side — improved by focusing the beam and narrowing its width), imaging modes (B-mode greyscale, M-mode motion over time, colour Doppler for direction and speed, pulsed-wave and continuous-wave spectral Doppler), the Nyquist aliasing limit, the common ARTEFACTS (acoustic shadowing behind calcified structures like gallstones and bone, acoustic enhancement behind fluid, reverberation, mirror image, and ring-down from gas), and the probe types (curvilinear for abdominal and POCUS, linear for vascular, phased array for cardiac).

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Domain

Oncology

4

low

Hypercalcaemia of malignancy

Hypercalcaemia of malignancy is the most common metabolic complication of malignancy, reported in up to 30% of cancer patients, and is considered an oncologic emergency. Mechanisms: (1) HUMORAL hypercalcaemia of malignancy — PTHrP-mediated, the commonest cause; (2) LOCAL OSTEOLYTIC — osteolytic cytokine production, classically multiple myeloma and breast cancer bone metastases; (3) CALCITRIOL (1,25-dihydroxyvitamin D)-mediated — excess production by lymphoma. Ectopic PTH secretion is rare, and a non-malignancy contributor (primary hyperparathyroidism, granulomatous disease) can coexist. Presentation: stones, bones, abdominal groans and psychic moans, plus polyuria/polydipsia; severe disease causes altered mental status, coma, seizures, AKI and arrhythmias, with short QT the ECG signature. Treatment: aggressive IV saline rehydration WITH an antiresorptive — denosumab or an IV bisphosphonate (strong recommendation); zoledronic acid 4 mg IV is the recommended initial dose (complete response by day 10 in 88.4% versus 69.7% with pamidronate 90 mg); calcitonin is combined with an IV bisphosphonate or denosumab for severe HCM (conditional); denosumab 120 mg SC on days 1, 8, 15 and 29 then every 4 weeks for refractory or recurrent disease (64% respond by day 10) or for renal insufficiency/bisphosphonate non-response, monitoring for and preventing hypocalcaemia; glucocorticoid-context therapy for calcitriol-associated tumours; haemodialysis for refractory severe hypercalcaemia with advanced kidney disease. Diagnosis includes measuring the mediators (PTHrP, 1,25-vitamin D, PTH). Treat the underlying malignancy.

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Malignant spinal cord compression (MSCC)

MSCC is an oncologic emergency — compression of the spinal cord or cauda equina by metastatic tumour (most often a vertebral body metastasis extending into the epidural space, via Batson's valveless vertebral venous plexus). Presents with: back pain (#1 symptom — progressive, worse on lying/coughing/straining), motor weakness, sensory loss (a level below the compression), and bowel/bladder dysfunction (late, poor prognosis — urinary retention is the classical finding). Diagnosis: whole-spine MRI (gold standard); the Bilsky epidural spinal cord compression (ESCC) scale grades the degree of cord compression and guides the surgical vs radiotherapy decision; the Spinal Instability Neoplastic Score (SINS) grades mechanical instability. Treatment: DEXAMETHASONE 10 mg IV IMMEDIATELY on suspicion (reduces vasogenic oedema) — given BEFORE the MRI, then 4 mg every 6 h — followed by urgent surgical decompression (Patchell: surgery + radiotherapy superior to radiotherapy alone in selected fit, single-level patients) or radiotherapy (8 Gy single fraction for poor prognosis). TIME IS CORD: ambulatory status at presentation is the strongest predictor of outcome — most patients ambulatory before treatment remain ambulatory, while few non-ambulatory patients regain walking; paraplegic at presentation rarely walks again.

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Superior vena cava obstruction (SVCO)

SVCO is obstruction of the superior vena cava — usually from external compression by tumour (lung cancer #1, ~75%; lymphoma; mediastinal masses) or thrombosis (central venous catheter, pacemaker/ICD leads, fibrosing mediastinitis). Presents with facial/neck/arm swelling, distended chest wall and neck veins, dyspnoea, cough, and headache (worse on bending forward — 'SVC syndrome'). Usually a SUBACUTE presentation (days-weeks) — rarely a true emergency unless airway compromise (glottic/upper-airway oedema) or cerebral venous congestion. Diagnosis: contrast-enhanced CT chest (shows obstruction level, cause, collateral vessels). Management: treat underlying cause (chemo/radiotherapy for tumour, anticoagulation ± line removal for thrombosis), endovascular SVC stenting for immediate symptomatic relief, corticosteroids (especially lymphoma). Emergency airway compromise = urgent stenting ± radiotherapy.

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Tumour lysis syndrome

Tumour lysis syndrome (TLS) is a metabolic oncological emergency from rapid malignant cell lysis releasing intracellular contents: HYPERKALAEMIA (intracellular K+ dumped — most dangerous, causes fatal arrhythmia), HYPERPHOSPHATAEMIA (phosphate-rich malignant cells release their intracellular phosphate load), HYPOCALCAEMIA (secondary — Ca2+ precipitates with phosphate as calcium-phosphate crystals), and HYPERURICAEMIA (nucleic acid breakdown → purines → xanthine → uric acid via xanthine oxidase). Uric acid and calcium-phosphate precipitate in renal tubules → acute kidney injury (AKI), which then reduces K+ and phosphate excretion → a self-amplifying vicious cycle. Onset typically within days of starting chemotherapy/radiotherapy/corticosteroids/targeted therapy for high-turnover tumours (ALL, Burkitt lymphoma, lymphoblastic lymphoma, high-grade NHL, AML); spontaneous TLS can precede therapy in bulky disease. Cairo-Bishop definition: laboratory TLS (≥2 abnormal values — urate ≥8 mg/dL/476 µmol/L, K+ ≥6.0 mmol/L, phosphate ≥4.5 mg/dL adult/≥6.5 child, Ca2+ ≤7.0 mg/dL/1.75 mmol/L, or 25% change within 3 days before to 7 days after therapy) vs clinical TLS (LTLS PLUS AKI, arrhythmia/sudden death, or seizure). Prevention is the cornerstone: aggressive IV hydration 2500-3000 mL/m2/day (goal urine output ≥2 mL/kg/h) + rasburicase 0.20 mg/kg/day IV for HIGH risk (recombinant urate oxidase — converts EXISTING uric acid → soluble allantoin; CONTRAINDICATED in G6PD deficiency) or allopurinol 300 mg/day for INTERMEDIATE risk (xanthine oxidase inhibitor — prevents NEW uric acid only). Treatment: aggressive hydration, rasburicase, treat hyperkalaemia per protocol (calcium gluconate → insulin-dextrose → salbutamol → binders → RRT), do NOT routinely treat asymptomatic hypocalcaemia, RRT for refractory electrolyte disturbance or AKI. Do NOT alkalinise urine (worsens calcium-phosphate precipitation).

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Domain

Respiratory / gas exchange

2

high

Hypercapnia & Ventilatory (Type-2) Respiratory Failure

Hypercapnia (a raised PaCO2) is ventilatory, or type-2, respiratory failure. Because PaCO2 is proportional to CO2 production divided by alveolar ventilation, hypercapnia arises from increased CO2 production (fever, sepsis, overfeeding) or — far more commonly — reduced alveolar ventilation from a failure of the controller (opioids, brainstem), the pump and nerves (Guillain-Barre, myasthenia), the chest wall and load (obesity, kyphoscoliosis, COPD, asthma), or increased dead space. The effects are respiratory acidosis, cerebral vasodilation with raised intracranial pressure (headache, asterixis, drowsiness, CO2 narcosis), and sympathetic stimulation. Treatment is to ventilate the patient (non-invasive ventilation for COPD) and reverse the cause; controlled oxygen in COPD averts oxygen-induced hypercapnia (the Haldane effect and worsened V/Q mismatch).

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Mechanisms of Hypoxaemia — V/Q Mismatch, Shunt, Diffusion, Hypoventilation

There are five mechanisms of hypoxaemia: low inspired oxygen, hypoventilation (type 2 failure, with a NORMAL alveolar-arterial gradient), ventilation-perfusion mismatch (the commonest cause, correctable by 100 per cent oxygen), shunt (does NOT correct with 100 per cent oxygen), and diffusion impairment (worsens with exercise). The alveolar-arterial oxygen gradient distinguishes hypoventilation (normal gradient) from a lung problem (high gradient), and the response to 100 per cent oxygen distinguishes V/Q mismatch (corrects) from true shunt (does not).

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Domain

Cardiovascular / hypertension

1

high

Hypertensive Emergencies

A hypertensive emergency is severe blood pressure elevation with acute target-organ damage (encephalopathy, stroke, intracerebral haemorrhage, ACS, pulmonary oedema, aortic dissection, acute kidney injury, or eclampsia) — it requires IV therapy and ICU monitoring. A hypertensive urgency is severe BP without target-organ damage — it requires oral therapy and follow-up. The principle is a controlled, monitored BP reduction: lower the MAP by 10-20 per cent in the first hour, then to 160/100 within 2-6 hours, then gradually to baseline. Do NOT crash the BP — the chronic hypertensive's autoregulation curve is shifted right, and a sudden reduction causes cerebral, coronary, and renal hypoperfusion. The exceptions are aortic dissection (rapid to SBP 100-120) and eclampsia (SBP below 160). The drugs: labetalol, nicardipine, nitroprusside, GTN, and hydralazine.

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Domain

pharmacology

5

high

ICU Antibiotic Pharmacology — Comprehensive (PK/PD in Critical Illness)

ICU antibiotic pharmacology — the evidence-based framework for optimising antimicrobial dosing in critically ill patients where altered pharmacokinetics (PK) make standard doses unreliable. Core problem: critical illness DISRUPTS PK in predictable directions — (1) INCREASED VOLUME OF DISTRIBUTION (Vd) from capillary leak and aggressive fluid resuscitation → LOWER plasma concentrations of hydrophilic drugs (beta-lactams, aminoglycosides, glycopeptides) → need HIGHER loading doses; (2) AUGMENTED RENAL CLEARANCE (ARC — measured urinary CrCl &gt;130 mL/min/1.73 m², present in 20-65% of ICU patients) in younger trauma/polytrauma patients → enhanced renal elimination → subtherapeutic levels → need HIGHER and/or MORE FREQUENT doses (especially beta-lactams and vancomycin); (3) renal replacement therapy (RRT/CRRT, KDIGO effluent 20-35 mL/kg/h) clears renally-eliminated drugs → dose for the effluent rate, not for 'renal failure'; (4) HYPOALBUMINAEMIA (up to 40-50% of ICU patients) → increased free (active) drug fraction but also increased Vd and clearance for highly protein-bound drugs (ceftriaxone, teicoplanin, daptomycin). Pharmacodynamic (PD) targets determine HOW to dose: BETA-LACTAMS = time above MIC (fT&gt;MIC — keep free levels above the MIC throughout the interval, via CONTINUOUS or EXTENDED [prolonged 3-4h] infusion); AMINOGLYCOSIDES = Cmax/MIC ratio (concentration-dependent killing + post-antibiotic effect → high ONCE-DAILY dose, 7 mg/kg with single-level nomogram monitoring); FLUOROQUINOLONES = AUC/MIC ratio; VANCOMYCIN = AUC/MIC 400-600 (2020 consensus shifted from trough-based to AUC-guided monitoring, which carries less nephrotoxicity). Key DALI study finding: on STANDARD licensed beta-lactam dosing, 16% of patients treated for infection missed even the 50% fT&gt;MIC target and were 32% less likely to have a positive outcome → underdosing is the rule, not the exception → paradigm shift to PERSONALISED dosing + therapeutic drug monitoring (TDM). Key antibiotic classes: beta-lactams (PIP-TAZO, cefepime, meropenem [ESBL], ceftriaxone [CAP — NO Pseudomonas cover]), glycopeptides (vancomycin [MRSA, enterococcus — TDM], teicoplanin), aminoglycosides (gentamicin [once daily — TDM — nephrotoxicity + ototoxicity]), fluoroquinolones (ciprofloxacin [Pseudomonas], moxifloxacin [CAP — no Pseudomonas]), macrolides (azithromycin [CAP — atypicals]), oxazolidinones (linezolid [VRE, MRSA — thrombocytopenia, serotonin syndrome with SSRIs]), antifungals (caspofungin [Candida], voriconazole [Aspergillus — TDM, CYP2C19 variability], liposomal amphotericin B [broad — nephrotoxic]).

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ICU Antihypertensive Drugs — Comprehensive

IV antihypertensives for the ICU — the nine agents every intensivist must master: LABETALOL (combined alpha+beta blocker — versatile first-line for most hypertensive emergencies; 20 mg IV bolus then 40 mg and 80 mg boluses to a 300 mg maximum in trial protocols; contraindicated in severe asthma/heart block), NICARDIPINE (dihydropyridine CCB — smooth titratable infusion 5-15 mg/h — ideal for most HTN emergencies including stroke), HYDRALAZINE (direct arteriolar vasodilator — pregnancy/pre-eclampsia favourite; 5 mg slow IV bolus repeatable; CAUTION reflex tachycardia), SODIUM NITROPRUSSIDE (arteriolar + venous NO donor — most potent — CYANIDE TOXICITY risk rises with infusion rate, cumulative dose or prolonged infusion — now largely superseded), NITROGLYCERIN (venous > arteriolar NO donor — start 5 mcg/min titrating by 5 mcg/min — for ACS/acute pulmonary oedema; tachyphylaxis), CLEVIDIPINE (ultra-short DHP CCB — 1 min half-life — esterase-metabolised; VELOCITY trial: 2 mg/h start, doubled every 3 min to 32 mg/h), ESMOLOL (beta-1 selective — 500 mcg/kg load then up to 100 mcg/kg/min — aortic dissection, tachyarrhythmia), FENOLDOPAM (D1 agonist — 0.1 mcg/kg/min start — 'renal protective' claim unproven), PHENTOLAMINE (non-selective alpha-blocker — 5 mg IV bolus — pheochromocytoma crisis FIRST). Oral agents for chronic ICU BP control (ACEi/ARB, CCB, beta-blockers, diuretics, alpha-blockers). Scenario-specific rules that MUST be memorised: AORTIC DISSECTION = beta-blocker FIRST then vasodilator (prevent reflex tachycardia → propagation; target HR &lt;60, SBP &lt;120); HYPERTENSIVE ENCEPHALOPATHY = labetalol or nicardipine (BP down ~10% first hour, another ~15% over 2-3 h); PRE-ECLAMPSIA = hydralazine or labetalol + magnesium sulphate; PHEOCHROMOCYTOMA = phentolamine FIRST then beta-blocker (alpha before beta); COCAINE = benzodiazepines FIRST (avoid beta-blockers — unopposed alpha).

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ICU Corticosteroids — Comprehensive Pharmacology (Glucocorticoids in Critical Illness)

ICU corticosteroid pharmacology -- the evidence-based use of glucocorticoids across the full spectrum of critical illness. The four agents every intensivist must master: HYDROCORTISONE (mineralocorticoid-active -- physiological replacement plus refractory septic shock 200 mg/day continuous infusion (ADRENAL) or hydrocortisone plus fludrocortisone (APROCCHSS), adrenal crisis 100 mg IV bolus then 200 mg/24 h), METHYLPREDNISOLONE (ARDS 1 mg/kg/day within 14 days of onset (CIRCI guideline); high-dose IV pulses 1000 mg daily for 3 days in organ-threatening autoimmune disease), DEXAMETHASONE (COVID-19 6 mg once daily up to 10 days (RECOVERY); ARDS 20 mg then 10 mg (DEXA-ARDS); bacterial meningitis 10 mg q6h for 4 days (de Gans); antenatal lung maturation), and PREDNISOLONE (oral -- chronic immunosuppression; PJP adjunct (40 mg BD); CAP; COPD exacerbation 40 mg for 5 days (REDUCE)).

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high

ICU Diuretics Pharmacology — Comprehensive (Loop, Thiazide, K-Sparing, Acetazolamide)

ICU diuretics — comprehensive pharmacology organised by SITE OF ACTION in the nephron. The four classes map onto four sequential segments: PROXIMAL TUBULE → acetazolamide (carbonic anhydrase inhibitor — weak — HCO3 loss → metabolic acidosis); THICK ASCENDING LIMB of the loop of Henle → loop diuretics (furosemide/bumetanide/torasemide — block the Na-K-2Cl [NKCC2] cotransporter — the MOST POTENT class — inhibit 20-25% of filtered Na+ reabsorption); DISTAL CONVOLUTED TUBULE → thiazides (hydrochlorothiazide/chlorthalidone/metolazone — block the Na-Cl [NCC] cotransporter — 5-10% of Na+); CORTICAL COLLECTING DUCT → potassium-sparing diuretics (either aldosterone-receptor antagonists — spironolactone/eplerenone [RALES trial — 30% mortality reduction in severe HFrEF] — or the epithelial Na+ channel [ENaC] blockers — amiloride/triamterene). Clinical uses: loop (pulmonary oedema, heart failure decongestion, AKI fluid overload, hypercalcaemia adjunct); thiazide (hypertension, heart failure, nephrogenic DI, hypercalciuria); K-sparing (HFrEF with spironolactone, Conn syndrome, cirrhotic ascites, diuretic-induced hypokalaemia); acetazolamide (metabolic alkalosis correction, altitude sickness, glaucoma, CSF production). Adverse-effect signature by class: loop → HYPOkalaemia, hypomagnesaemia, HYPOcalcaemia, ototoxicity (high-dose IV push), hyperuricaemia, contraction alkalosis; thiazide → HYPOkalaemia, HYPOnatraemia, hyperuricaemia, HYPERcalcaemia (opposite to loop — classic exam contrast); K-sparing → HYPERkalaemia, metabolic acidosis, gynaecomastia (spironolactone — antiandrogen effect); acetazolamide → metabolic acidosis, hypokalaemia, renal stones. SEQUENTIAL NEPHRON BLOCKADE (loop + thiazide) is the key strategy for RESISTANT OEDEMA / diuretic resistance. The DOSE trial established that continuous infusion and intermittent bolus furosemide have equivalent efficacy and renal safety.

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high

ICU Sedation and Analgesia Pharmacology — Comprehensive (PADIS Bundle)

ICU sedation and analgesia pharmacology — the evidence-based approach to managing pain, sedation, and delirium in mechanically ventilated ICU patients following the PADIS (Pain, Agitation/sedation, Delirium, Immobility, Sleep) guidelines. Core principle: ANALGESIA FIRST (treat pain before adding sedatives) + GOAL-DIRECTED SEDATION (light sedation preferred — RASS -2 to 0) + DELIRIUM PREVENTION (minimize benzodiazepines, use dexmedetomidine) + EARLY MOBILISATION. Drug selection: DEXMEDETOMIDINE (alpha-2 agonist — unique 'arousable sedation' — analgesia + sedation WITHOUT respiratory depression — MENDS trial: better delirium-free days than lorazepam; SEDCOM trial: reduces delirium vs midazolam; preferred for delirium-prone patients) → PROPOFOL (GABA-A agonist — rapid onset/offset — preferred for fast-track weaning — caution: PRIS at >4 mg/kg/hr for >48h) → MIDAZOLAM (benzodiazepine — INDEPENDENT RISK FACTOR for delirium — AVOID if possible — reserve for alcohol withdrawal/seizures) → KETAMINE (NMDA antagonist — preserves respiratory drive — useful for procedural sedation + severe asthma). Analgesia: FENTANYL (first-line — rapid onset, short half-life), MORPHINE (active metabolite accumulates in renal failure — AVOID in AKI), REMIFENTANIL (ultra-short — ideal for short procedures or rapidly changing sedation needs). Monitoring: CPOT (Critical-Care Pain Observation Tool) for pain, RASS (Richmond Agitation-Sedation Scale) for sedation, CAM-ICU or ICDSC for delirium.

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Domain

diagnostics

1

high

ICU Biomarkers — Comprehensive (Procalcitonin, Lactate, Troponin, BNP/NT-proBNP)

ICU biomarkers — laboratory tests that guide diagnosis, prognosis, and treatment decisions in critically ill patients. Five key biomarkers: **(1) PROCALCITONIN (PCT)** — prohormone of calcitonin — rises in BACTERIAL infection (not viral/fungal/non-infectious inflammation) — used to guide antibiotic STARTING and STOPPING (PRORATA trial: PCT-guided algorithm reduced antibiotic duration by 2.7 days without adverse outcomes; threshold: >0.5 = start antibiotics, <0.5 OR fall >80% from peak = stop). **(2) LACTATE** — marker of tissue hypoperfusion/anaerobic metabolism — normal <2 mmol/L, elevated >2 = tissue hypoxia/shock, severe >4 = severe shock — lactate CLEARANCE (≥10% per hour) is the target (Jansen LACTATE trial). **(3) TROPONIN** — marker of myocyte injury — rises in MI but also in sepsis, PE, renal failure, stroke, CPR — universal in ICU patients — high-sensitivity troponin detects minor injury. **(4) BNP / NT-proBNP** — marker of ventricular wall stress — rises in heart failure, but also in sepsis, PE, ARDS, renal failure — diagnose HF in dyspnoea. **(5) OTHER**: D-dimer (PE, DIC, sepsis), CRP (inflammation), procalcitonin variants, presepsin, suPAR, mid-regional pro-adrenomedullin, lactate clearance vs central venous oxygen saturation as resuscitation target.

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Domain

Ethics and quality

3

low

ICU diaries: patient recall, recovery, and post-intensive care syndrome

ICU diaries are written records (by staff and family) of the patient's ICU stay, given to the patient after discharge to help fill memory gaps (delirium amnesia), process the experience, and aid psychological recovery. Patients typically have NO or FRAGMENTED recall of ICU (delirium, sedation) — and what they DO remember is often frightening (hallucinations, delusions). ICU diaries REDUCE PTSD (some studies — BACKUP trial), improve quality of life, and help patients/families make sense of the experience. Diary content: daily entries in plain language (what happened, why interventions were done, visits from family, milestones — extubation, sitting out, first words). Started in Scandinavia (1990s), adopted across Europe and increasingly in ANZ. S…

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medium

ICU discharge planning and transition of care: failures, criteria, and systems

ICU discharge is a high-risk transition — one of the most dangerous handovers in hospital medicine. Premature discharge → readmission (roughly 6-10% of patients discharged alive from ICU) and markedly higher mortality (24.7% vs 4.0% in-hospital mortality among readmitted vs non-readmitted patients in Cooper's 28-hospital series); delayed discharge → ICU bed-blocking, increased cost, nosocomial infection, ICU-acquired weakness, and prolonged delirium. READMISSION RISK FACTORS: respiratory (day-of-discharge hypoxaemia, hypercapnia, or complex respiratory nursing needs), neurological (day-of-discharge neurologic impairment — GCS), severity and workload (higher acute physiology score at discharge — APS over 40; longer ICU stay; deterioration on the ward before ICU admission), and OPERATIONAL (after-hours discharge 18:00-06:00 → higher readmission and mortality, adjusted OR 1.34-1.42 in ANZICS data — Gantner 2014, Pilcher 2007; UK night discharge more often judged premature — Goldfrad 2000). STRUCTURED DISCHARGE PLANNING rests on five pillars: (1) OBJECTIVE READINESS CRITERIA — resolving organ failure, stable haemodynamics without escalating vasopressors, adequate ventilation without hypoxaemia or hypercapnia, neurologically appropriate (baseline mental state, delirium controlled). (2) PHARMACIST-LED MEDICATION RECONCILIATION — stop ICU-only drugs (sedatives, NMBA), restart held home meds (beta-blockers, statins, anticonvulsants — adjust for recovering renal/hepatic function), correct durations (antibiotics, steroid taper), avoid indefinite gastric prophylaxis. (3) STRUCTURED HANDOVER — SBARR (Situation, Background, Assessment, Recommendation, Read-back) or ISBAR, written + verbal, with explicit acceptance of care by the receiving team. (4) TIMING — discharge in daytime (ideally before 16:00, before 18:00 at latest), avoid night discharge; if unavoidable, enhanced handover + document rationale. (5) POST-DISCHARGE FOLLOW-UP — ICU follow-up clinic at 2-8 weeks to screen for POST-INTENSIVE CARE SYNDROME (PICS): cognitive impairment (memory, executive function, attention — affects ~30-40%, persists at 1yr in 25%), psychological morbidity (depression 30%, PTSD 20%, anxiety 40% — combined physical/cognitive/mental health impairment affects 50-70% at 1 year), and physical weakness (ICU-acquired weakness CIP/CIM 25-50%). PREVENTION of PICS: ABCDEF bundle (Assess pain, Both spontaneous awakening/breathing trials, Choice of analgesia/sedation, Delirium monitoring, Early mobility, Family engagement) — Pun 2019 ICU Liberation Collaborative (15,000+ patients) showed lower mortality, more coma-/delirium-free days, and higher discharge home. FAMILY morbidity (PICS-Family) is also common — depression, anxiety, PTSD, caregiver burden.

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high

Multiple organ dysfunction syndrome (MODS): pathophysiology, SOFA scoring, and management

Multiple organ dysfunction syndrome (MODS) = progressive dysfunction of ≥2 organs in a critically ill patient (the common endpoint of sepsis, trauma, burns, pancreatitis, haemorrhage). PATHOPHYSIOLOGY: SYSTEMIC INFLAMMATION (SIRS — cytokine storm — TNF, IL-1, IL-6) -> ENDOTHELIAL DYSFUNCTION (capillary leak, vasodilation, microvascular thrombosis) -> ORGAN ISCHAEMIA + DYSFUNCTION. ORGANS AFFECTED: lung (ARDS), kidney (AKI), liver (ischaemic hepatitis), heart (septic cardiomyopathy), brain (septic encephalopathy), coagulation (DIC), gut (ileus, bacterial translocation). SCORING: SOFA (Sequential Organ Failure Assessment — 6 organs, daily — tracks trajectory + predicts mortality). MANAGEMENT: (1) TREAT THE CAUSE (sepsis — antibiotics immediately/source control; trauma — surgery; pancreatitis; etc.). (2) ORGAN SUPPORT (ventilation, vasopressors, RRT, transfusion). (3) AVOID HARM (fluid overload, hypoxaemia, hypotension, nosocomial infection, VTE, stress ulcer). (4) EARLY NUTRITION (enteral within 72 h — maintains gut integrity). (5) FAMILY + GOALS OF CARE (MODS mortality is high and rises with organ count and SOFA burden — discuss prognosis, escalation, withdrawal).

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Domain

Obstetric / pharmacotherapy

1

high

ICU Drugs in Pregnancy & Lactation — Safe, Caution & Contraindicated

The ICU drugs in pregnancy: the PLACENTA crosses MOST drugs (the trimester matters — the organogenesis weeks 3 to 10 the highest the teratogenic risk). The SAFE: LMWH (does NOT cross placenta), labetalol (the first-line antihypertensive), penicillins, cephalosporins, macrolides, propofol, noradrenaline, steroids (prednisolone — the 90 per cent metabolised by the placental 11-beta-HSD2), paracetamol, insulin, metformin, magnesium. The CAUTION: aminoglycosides (fetal ototoxicity), benzodiazepines (1st trimester), fluoroquinolones. The CONTRAINDICATED: warfarin (the fetal warfarin syndrome), ACE inhibitors and ARBs (ACE fetopathy — fetal renal damage), valproate (neural tube), isotretinoin, methotrexate, tetracyclines (teeth/bone), lithium. The LACTATION: most ICU drugs compatible (infant dose under 1 per cent); avoid chloramphenicol, amiodarone, lithium, chemotherapy, radioisotopes — check LactMed.

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Domain

Nutrition

2

high

ICU nutrition: enteral vs parenteral, timing, protein, and refeeding syndrome

ICU nutrition: critical illness is hypercatabolic, with rapid muscle wasting within days. Early enteral nutrition (within 24-48h) is the standard of care — trials (CALORIES, NUTRIREA-2) found no advantage of the parenteral route started early, and enteral feeding maintains gut barrier function. PARENTERAL (PN): only if EN fails or is contraindicated — supplementing early is harmful (EPaNIC: late PN meant fewer infections and faster recovery). CALORIES: permissive underfeeding (40-60% of target) with protein maintained was non-inferior to full feeding (PERMIT); trophic feeding for up to 6 days was safe (EDEN). PROTEIN: 1.2-1.5 g/kg/day (0.8 g/kg/day is the healthy-adult figure; 2.0-2.5 g/kg/day only in exceptional cases). REFEEDING SYNDROME: risk in malnourished patients — glucose rises, phosphate, magnesium and potassium fall, thiamine is depleted when feeding starts — screen, replace electrolytes, supplement vitamins, start low and increase stepwise.

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medium

Refeeding syndrome: phosphate, thiamine, and prevention in ICU

Refeeding syndrome (RFS) = potentially fatal metabolic disturbances that occur when food is reintroduced to STARVED patients (anorexia, alcoholism, prolonged fasting, post-operative, ICU after prolonged NBM). PATHOPHYSIOLOGY: starvation -> depleted intracellular electrolytes (phosphate, potassium, magnesium) + low insulin. REFEEDING (carbohydrate) -> INSULIN surge -> electrolytes shift INTO cells (phosphate for ATP, potassium, magnesium) -> serum levels PLUMMET -> hypophosphataemia, hypokalaemia, hypomagnesaemia, thiamine depletion (Wernicke), fluid retention and salt retention -> organ dysfunction and cardiac arrhythmias (arrhythmias, heart failure, sudden cardiac arrest are the most fatal manifestations). CLINICAL: mostly within the first 72 hours of starting nutrition. PREVENTION (NICE CG32): risk-stratify (box 1: BMI under 16, weight loss over 15 percent in 3 to 6 months, little or no intake over 10 days, low baseline K, PO4 or Mg), thiamine 200 to 300 mg immediately before and during the first 10 days of feeding, start at maximum 10 kcal/kg/day (5 kcal/kg/day in extreme cases: BMI under 14 or negligible intake over 15 days), supplement potassium 2 to 4, phosphate 0.3 to 0.6 and magnesium 0.2 to 0.4 mmol/kg/day, monitor biochemistry and cardiac rhythm.

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Domain

Procedural

2

high

ICU procedures: central line, arterial line, chest drain, and bronchoscopy

Core ICU procedures every intensivist must master: (1) CENTRAL VENOUS CATHETERISATION (CVC) — internal jugular (IJV), subclavian (SCV), femoral — ultrasound-guided (standard of care — reduces mechanical complications 70% — Karakitsos 2006, Critical Care), Seldinger technique, maximal sterile barrier, check CXR post. (2) ARTERIAL LINE — radial (Allen's test — controversial), femoral, brachial — continuous BP monitoring + arterial blood gas sampling, zero + square-wave test before trusting values. (3) CHEST DRAIN (tube thoracostomy) — 5th ICS anterior axillary line (BATLS/ATLS safe triangle), for pneumothorax/haemothorax/effusion/empyema — underwater seal, size 28-36 Fr for haemothorax (small-bore 8-14 Fr pigtail for simple air/effusion). (4) BRONCHOSCOPY (flexible) — diagnostic (atelectasis, haemoptysis, biopsy, BAL) + therapeutic (mucus plug removal, foreign body, lavage) — in intubated (via ETT ≥8 mm, sealed swivel adaptor) or non-intubated (sedation). COMPLICATIONS: CVC (pneumothorax, arterial puncture, haematoma, air embolism, infection — CRBSI); arterial line (ischaemia, infection, accidental intra-arterial injection); chest drain (pain, infection, subcutaneous emphysema, re-expansion pulmonary oedema, organ injury); bronchoscopy (hypoxaemia, bleeding, pneumothorax, laryngospasm). Central line bundle (Pronovost): hand hygiene + maximal barrier + chlorhexidine + optimal site + daily review.

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high

Tracheostomy in ICU: timing, technique, and weaning

Tracheostomy in ICU: for patients expected to need prolonged mechanical ventilation. BENEFITS: patient comfort, easier secretion clearance, allows oral intake, potential for speech, potential for easier weaning. TIMING: controversial — early (within 4 days, TracMan) vs late (day 10 or later). TracMan: NO mortality benefit of early tracheostomy; meta-analyses suggest less pneumonia. Current: individualise once prolonged ventilation seems likely. TECHNIQUE: percutaneous dilatational (PDT — bedside, intensivist-performed, bronchoscopy-guided) vs surgical (OR — ENT/thoracic). PDT preferred (cheaper, faster, similar outcomes). COMPLICATIONS: bleeding, infection, displacement, tracheal stenosis, tracheo-oesophageal fistula.

Open

Domain

ICU-acquired infection

1

high

ICU-Acquired Infection — VAP, CRBSI and CLABSI

The ICU-acquired infections are the complications of the critical care itself — the ventilator-associated pneumonia (the VAP), the catheter-related bloodstream infection (the CRBSI), the catheter-associated UTI, and the Clostridioides difficile. Each increases the mortality, the length of stay, and the cost, and each is largely PREVENTABLE through the bundles. This topic builds the examiner's framework on the VAP (the diagnosis, the prevention bundle, the short-course antibiotics), the CRBSI (the prevention, the diagnosis, the catheter removal), and the general principles of the infection prevention in the ICU.

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Domain

icu-acquired-infection

1

high

ICU-Acquired Infection Prevention Bundle — Comprehensive

ICU-acquired infection prevention — the comprehensive evidence-based bundle approach to preventing the 5 major nosocomial infections in ICU: VAP (ventilator-associated pneumonia), CRBSI (catheter-related bloodstream infection), CAUTI (catheter-associated urinary tract infection), C. difficile infection, and SSI (surgical site infection). Each infection has a validated prevention bundle: VAP bundle (head of bed 30-45° + minimise sedation and assess readiness to extubate daily + daily oral care with toothbrushing without routine chlorhexidine + subglottic secretion drainage when intubation is expected to be prolonged), CRBSI bundle (maximal sterile barrier precautions + chlorhexidine skin antisepsis + avoid femoral site + daily review of line necessity + chlorhexidine-impregnated dressings), CAUTI bundle (avoid unnecessary catheterisation + sterile insertion technique + remove as soon as possible + closed drainage system + daily review of necessity), C. difficile prevention (antimicrobial stewardship + hand hygiene with SOAP AND WATER [not alcohol gel — spores resistant] + contact precautions + environmental cleaning with bleach). Universal measures: WHO 5 Moments of Hand Hygiene, aseptic technique for all procedures, antimicrobial stewardship, environmental cleaning, surveillance and feedback. Prevention is ALWAYS better than treatment — each ICU-acquired infection increases mortality, length of stay, cost, and antimicrobial resistance.

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Domain

rehabilitation

1

high

ICU-Acquired Weakness (CIP/CIM)

ICU-acquired weakness (ICUAW) is the acquired muscle and nerve dysfunction that develops during critical illness, affecting 25 to 50 percent of ICU patients ventilated over 7 days. Three types: critical illness polyneuropathy (CIP), critical illness myopathy (CIM), critical illness neuromyopathy (CINM). Risk factors: sepsis/MODS, prolonged ventilation, steroids, NMBA, hyperglycaemia, immobility. Prevention: ABCDEF bundle, early mobilisation, glycaemic control, minimise sedation/NMBA/steroids. Treatment: supportive, rehabilitation, nutrition. Long-term disability persists for years after ICU discharge.

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Domain

Cardiovascular / infection

1

high

Infective Endocarditis

Infective endocarditis is an infection of the cardiac valves (or the endocardium), diagnosed by the modified Duke criteria: typical positive blood cultures and an echocardiographic vegetation are the major criteria. The commonest ICU organism is Staphylococcus aureus (aggressive, acute); viridans streptococci cause subacute endocarditis (dental); enterococci, the HACEK group, and culture-negative organisms (Coxiella, Bartonella, fungi) are also important. The clinical features: fever, a new or changed murmur, embolic phenomena (stroke, splenic, mesenteric, limb), immunological phenomena (Osler nodes, Roth spots, glomerulonephritis), and vascular phenomena (Janeway lesions). The treatment is 4-6 weeks of IV antibiotics (targeted to the culture). Surgery is indicated for heart failure (the commonest indication), uncontrolled infection, large vegetations with embolism, and perivalvular extension.

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Domain

Renal / acid-base

3

high

Lactic Acidosis — Type A, B & D, MALA, and Lactate Clearance

The lactic acidosis is the high-anion-gap metabolic acidosis from the accumulation of the lactate. The Cohen and Woods classification: the Type A — the tissue hypoxia or the impaired oxygen delivery (the shock, the seizures, the mesenteric ischaemia, the carbon monoxide, the severe anaemia) — the commonest; the Type B — no overt hypoxia (the B1 disease — the liver failure, the malignancy; the B2 drugs — the metformin, the linezolid, the NRTIs, the propofol infusion syndrome, the cyanide; the B3 inborn errors); the Type D — the D-lactate from the gut bacteria in the short-bowel syndrome (NOT measured by the standard L-lactate assay). The lactate is cleared by the liver (the Cori cycle); the impaired clearance worsens the accumulation. The prognostic: the lactate over 4 mmol/L with hypotension carries the highest mortality (44.5 per cent, SSC database); the Jansen protocol targets a lactate fall of at least 20 per cent per 2 hours. The management: the treat the underlying cause (the cornerstone — restore the oxygen delivery for A, stop the drug for B2, the liver failure for B1), the supportive care, the metformin-associated lactic acidosis (the haemodialysis), the bicarbonate controversial (the BICAR-ICU trial at pH at or under 7.20 found no overall benefit), the methylene blue emerging.

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medium

Mixed Acid–Base Disorders & the Delta–Delta — The 5-Step Approach

A mixed acid-base disorder is the presence of two or more primary acid-base disturbances simultaneously. The body NEVER over-compensates — if the compensation is more or less than expected, a second primary disorder is present. The systematic approach: (1) the pH to the acidosis or the alkalosis; (2) the pCO2 and the bicarbonate to the primary; (3) the expected compensation (the Winter formula for the metabolic acidosis: the expected pCO2 equals 1.5 times bicarbonate plus 8 plus-or-minus 2; the Henderson-Hasselbalch equation pH equals 6.1 plus log of bicarbonate over 0.03 times pCO2); (4) the anion gap (the Na minus (Cl plus bicarbonate), 8 to 12, the albumin-corrected — the AG rises 2.5 per 10 g/L fall in the albumin); (5) the delta-delta (the delta AG over the delta bicarbonate: about 1 the pure high-AG acidosis, under 1 the concurrent normal-gap hyperchloraemic acidosis, over 2 the concurrent metabolic alkalosis). The Stewart (strong ion difference) approach: pH is set by the PaCO2, the strong ion difference (the Na minus Cl, about 40), and the total weak acids (the albumin). The mixed metabolic acidosis (the combined high-AG and the normal-AG — the delta ratio under 1). The mixed metabolic alkalosis and acidosis (the delta ratio over 2). The triple disorders (the metabolic alkalosis plus the metabolic acidosis plus the respiratory alkalosis — the classic in the sepsis with the vomiting plus the lactic acidosis plus the hyperventilation). The salicylate toxicity (the respiratory alkalosis plus the high-AG acidosis).

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medium

Renal Tubular Acidoses (Types I, II, IV) — The Hyperchloraemic Acidoses

The renal tubular acidoses (RTA) are a group of disorders of the renal acid-base handling that produce a non-anion-gap (the hyperchloraemic) metabolic acidosis from the impaired renal acid excretion (the bicarbonate reabsorption or the acid secretion). The three types: the Type 1 (the distal) — the impaired distal H-plus secretion; the urine pH stays HIGH (over 5.5) despite the acidosis; the HYPOkalaemia; the causes the autoimmune (the Sjogren), the amphotericin B, the lithium; the nephrocalcinosis and the stones; the treatment the bicarbonate plus the potassium. The Type 2 (the proximal) — the impaired proximal bicarbonate reabsorption; the urine pH high then low; the HYPOkalaemia; the Fanconi syndrome, the myeloma, the ifosfamide, the tenofovir, the acetazolamide; the treatment the bicarbonate plus the potassium. The Type 4 — the hypoaldosteronism (or the aldosterone resistance); the urine pH LOW (under 5.5); the HYPERkalaemia (the key discriminator); the diabetes, the Addison, the ACEi, the ARB, the K-sparing diuretics; typically in mild-to-moderate CKD; the treatment the low-dose fludrocortisone and the treat the hyperkalaemia.

Open

Domain

Haematology / trauma

1

high

Massive Transfusion & Trauma Coagulopathy — The Lethal Triad, TXA & 1:1:1

The trauma coagulopathy has the two components: the acute traumatic coagulopathy (ATC — the early, the injury-driven, the protein-C activation, the hyperfibrinolysis) and the dilutional coagulopathy (the massive RBC without the factors or the platelets). The lethal triad — the acidosis (the clotting-factor dysfunction), the hypothermia (the platelet and the enzyme dysfunction), and the coagulopathy — the vicious the cycle. The massive transfusion protocol (MTP) — the 1 to 1 to 1 (RBC to the plasma to the platelets), the PROPPR the no the mortality difference but the fewer the exsanguination. The tranexamic acid (TXA) — the CRASH-2, the 1 g plus the 1 g within 3 h (the beyond the 3 h the harmful). The calcium (the citrate the chelation — the under 0.90 the severe, the double the mortality). The fibrinogen (the first the factor to the fall — the under 1.5 g per L the treat). The viscoelastic (the TEG the ROTEM — the LY30 the hyperfibrinolysis, the FIBTEM the fibrinogen).

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Domain

antimicrobial-stewardship

1

high

MDR Organisms in ICU — Comprehensive (ESBL, CRE, MRSA, VRE, MDR-XDR TB)

Multidrug-resistant (MDR) organisms in the ICU are the single greatest infectious threat to critically ill patients. The standardised definitions (Magiorakos 2012, ECDC and CDC international expert consensus): MDR is acquired non-susceptibility to at least one agent in three or more antimicrobial categories; XDR (extensively drug-resistant) is non-susceptibility to all but one or two categories; PDR (pandrug-resistant) is non-susceptibility to all agents in all categories. The four ICU core threats plus TB: ESBL (plasmid beta-lactamase CTX-M hydrolysing 3rd-generation cephalosporins, treated with a carbapenem); CRE (carbapenemases KPC serine, NDM and VIM and IMP metallo, OXA-48 — KPC to ceftazidime-avibactam, NDM to aztreonam plus CZA); MRSA (mecA, PBP2a, vancomycin or linezolid); VRE (vanA or vanB, linezolid or daptomycin); and MDR-TB (rifampicin plus isoniazid resistance, treated with the all-oral BPaL regimen). CRE bacteraemia carries 40 to 50 per cent mortality.

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Domain

Neurocritical care / post-arrest

1

high

Neuro-Prognostication After Cardiac Arrest — The 72-Hour Multimodal Rule

The neuro-prognostication after a cardiac arrest is deferred until at least 72 hours after the return of the spontaneous circulation, with the patient normothermic and off the sedation. The principle is the MULTIMODAL assessment — no single predictor determines the prognosis, because the falsely pessimistic prediction creates the self-fulfilling prophecy (the early withdrawal of the care). The predictors (examined together): the absent brainstem reflexes (the pupillary, the corneal), the absent motor response to pain, the bilateral absent N20 on the somatosensory evoked potentials (the most reliable single test), the highly malignant EEG patterns (suppression with periodic discharges, burst-suppression), the elevated neuron-specific enolase, and the MRI diffusion anoxic pattern. The TTM tri…

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Domain

Infection / oncology

1

high

Neutropenic Sepsis — The Golden Hour & the Antipseudomonal Beta-Lactam

Neutropenic sepsis is sepsis in the neutropenic patient (neutrophils under 0.5, or under 1.0 and falling) — a medical emergency with mortality up to 20 per cent untreated. Febrile neutropenia is a single oral temperature over 38.3, or over 38.0 sustained for one hour, in a neutropenic patient. The golden hour demands an empirical broad-spectrum antipseudomonal beta-lactam (piperacillin-tazobactam, ceftazidime, cefepime, or meropenem) WITHIN one hour — never wait for cultures. Draw cultures from each central-line lumen plus a peripheral set. Add vancomycin for line sepsis, MRSA colonisation, severe mucositis, or shock. Persistent fever over 4 to 7 days shifts the working diagnosis to invasive fungal infection — add an echinocandin or liposomal amphotericin, with voriconazole if Aspergillus is documented. NEVER use ceftriaxone — it has no Pseudomonas cover.

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Domain

2

low

Ogilvie syndrome (acute colonic pseudo-obstruction)

Ogilvie syndrome (acute colonic pseudo-obstruction, ACPO) is massive colonic dilation WITHOUT mechanical obstruction, attributed to an imbalance in autonomic regulation of colonic motor function — excessive parasympathetic suppression or sympathetic stimulation — producing colonic atony, although the exact pathophysiology remains unclear. It is a disease of the hospitalised: precipitants include recent surgery (orthopaedic, cardiac, caesarean, abdominal), critical illness/sepsis, electrolyte disturbance, opioids and anticholinergics, immobility, retroperitoneal pathology, trauma, burns, and metabolic disease. Presentation is progressive, often painless, abdominal distension developing over several days with tympani, minimal or absent bowel sounds, and nausea; pain disproportionate to the picture or peritonism signals ischaemia or perforation. Diagnosis is clinical plus imaging: plain AXR (and confirmatory CT with contrast) showing caecal dilation, with explicit exclusion of mechanical obstruction. Perforation risk increases when caecal diameter exceeds 12 cm AND distension has been present for more than 6 days; mortality is approximately 40% once ischaemia or perforation occurs. Management is staged: conservative measures first (bowel rest, NG and rectal tubes, electrolyte correction, stopping causative drugs, mobilisation); if refractory, neostigmine 2-2.5 mg IV (2.0 mg in the pivotal randomised trial, 91% response vs 0% placebo) with continuous cardiac monitoring and atropine available; colonoscopic decompression for neostigmine failure or contraindication (pooled first-session success 78.8%, overall 91.5%); surgery for peritonitis, ischaemia or perforation.

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high

Toxic megacolon and acute severe colitis

Toxic megacolon is a life-threatening complication of severe colonic inflammation characterised by non-obstructive colonic dilatation greater than 6 cm with systemic toxicity (fever, tachycardia, leucocytosis, anaemia). The classic causes are ulcerative colitis and Clostridium difficile colitis; other infectious causes include Salmonella, Shigella, Campylobacter, CMV and E. coli O157, and ischaemic colitis is also recognised. Diagnosis rests on clinical toxicity plus plain abdominal radiography, with CT an alternative that adds information. Management is interdisciplinary from the outset: fluid and electrolyte correction, broad-spectrum antibiotics including metronidazole (with enteral vancomycin for pseudomembranous colitis), corticosteroids for inflammatory causes, and subtotal colectomy with terminal ileostomy for perforation, peritonitis, massive haemorrhage or failed medical therapy. In acute severe ulcerative colitis, day-3 objective reassessment (stool count and CRP) drives escalation to infliximab or ciclosporin rescue.

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Domain

Haematology / oncology

1

high

Oncologic Emergencies — TLS, Hypercalcaemia, Hyperviscosity, SVC, Cord Compression, Neutropenic Sepsis & Checkpoint Toxicity

The oncologic emergencies in the ICU: (1) tumour lysis syndrome (TLS — cell lysis to hyperkalaemia, hyperphosphataemia, hypocalcaemia, hyperuricaemia, AKI; Cairo-Bishop classification; prophylaxis hydration plus allopurinol 300 mg/day or rasburicase 0.2 mg/kg; treat rasburicase plus RRT in severe cases), (2) hypercalcaemia of malignancy (PTHrP, osteolytic, ectopic vitamin D; treat IV saline plus zoledronic acid 4 mg, calcitonin bridge, denosumab 120 mg if refractory), (3) hyperviscosity syndrome (Waldenstrom IgM; urgent plasma exchange), (4) superior vena cava syndrome (facial and arm swelling; treat the tumour — RT, chemo, endovascular stent), (5) malignant spinal cord compression (back pain, weakness, sensory level; dexamethasone 16 mg daily or 10 mg IV then 4 mg q6h plus urgent whole-spine MRI; Patchell trial), (6) neutropenic sepsis (the 1-hour rule — empiric anti-pseudomonal beta-lactam within 1 hour of triage), and (7) immune-related adverse events from checkpoint inhibitors (colitis, pneumonitis, hepatitis, myocarditis — withhold ICI, corticosteroids, infliximab or vedolizumab for refractory colitis).

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Domain

Oxygen & gas exchange

1

high

Oxygen and Gas Exchange

Oxygenation is the carriage of oxygen from the air to the mitochondria, and its failure — the hypoxaemia and the hypoxia — is the commonest reason a patient comes to the intensive care unit. This topic builds the examiner's framework on the physiology — the oxyhaemoglobin dissociation curve and its shifters, the four mechanisms of hypoxaemia (the hypoventilation, the diffusion impairment, the ventilation-perfusion mismatch and the shunt) and the A-a gradient that separates them, the oxygen delivery and consumption and the Fick principle, and the four types of hypoxia; the oxygen therapy and the devices that deliver it, the high-flow nasal cannula (the FLORALI trial) and the oxygen-target question (the Chu 2018 review — the liberal oxygen increases the mortality), the gas-exchange failures of the V/Q mismatch, the shunt and the dead space, and the bedside monitoring of the oxygenation.

Open

Domain

Respiratory / monitoring

2

high

Patient–Ventilator Asynchrony

Patient-ventilator asynchrony is a mismatch between the patient's neural respiratory drive and the ventilator's delivered breaths, detectable on the waveforms. It is common and associated with longer ventilation and higher mortality. The types fall by the phase of the breath: trigger asynchrony (ineffective triggering, auto-triggering, double triggering/breath stacking), flow asynchrony (starvation, excess), and cycle asynchrony (premature or delayed cycling). An asynchrony index over 10 per cent is significant. Management is to read the waveforms, identify the type, and fix the cause — sedation, the trigger sensitivity, the flow and inspiratory time, and a cycling-off criterion — with NAVA or PAV for refractory cases.

Open

high

Ventilator Waveforms — Scalars, Pressure-Volume & Flow-Volume Loops

Ventilator waveforms are the bedside physics of mechanical ventilation. The scalars (pressure, volume, and flow against time) and the loops (pressure-volume and flow-volume) show airway resistance, compliance, overdistension, and patient-ventilator interaction. The key manoeuvre is the inspiratory hold, which separates the peak pressure into its resistive and elastic components: a high peak with a normal plateau is an airway-resistance problem (bronchospasm, kink, secretions), while a high peak with a high plateau is a compliance problem (ARDS, oedema, pneumothorax). The driving pressure (plateau minus PEEP) and the static compliance (Vt divided by plateau minus PEEP) quantify the stress on the lung.

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Domain

Cardiovascular / pericardial

1

high

Pericardial Disease — Tamponade, Pericarditis & Constriction

Pericardial disease in the ICU covers three problems. Cardiac tamponade (Beck's triad — hypotension, raised JVP, muffled heart sounds; pulsus paradoxus; echo shows an effusion with RA/RV collapse) needs immediate pericardiocentesis. Acute pericarditis (pleuritic chest pain, a friction rub; the ECG shows diffuse concave ST elevation with PR depression) is treated with NSAIDs and colchicine. Constrictive pericarditis (right heart failure from a thickened, non-compliant pericardium; the Kussmaul sign, the pericardial knock, the septal bounce on echo, and the equalised diastolic pressures on catheterisation) is treated with a pericardiectomy. The key distinction is constriction (a thick pericardium, normal LV) versus restrictive cardiomyopathy (a thick LV, normal pericardium).

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Domain

Perioperative critical care

1

medium

Perioperative Critical Care

Perioperative critical care is the optimisation of the high-risk surgical patient before, during, and after the operation — the preoperative risk assessment (the cardiopulmonary exercise testing, the POSSUM/ACS-NSQIP scoring, the smoking cessation, the anaemia correction, the glycaemic control), the enhanced recovery after surgery (ERAS) bundle, the intraoperative goal-directed therapy (the cardiac output, the fluid responsiveness, the stroke-volume optimisation, the oxygen delivery), the postoperative monitoring (the HDU/ICU), and the system-by-system complications (the cardiac — the AF and the myocardial injury after noncardiac surgery [MINS]; the respiratory — the atelectasis, the pneumonia, the PE; the renal — the AKI; the GI — the ileus and the anastomotic leak; the wound — the infection and the dehiscence), the goal-directed fluid, the multimodal opioid-sparing analgesia, and the postoperative nausea and vomiting.

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Domain

Monitoring / ultrasound

2

high

Point-of-Care Ultrasound (POCUS) — Lung, Abdominal & Vascular

Point-of-care ultrasound (POCUS) is the clinician-performed, bedside ultrasound that answers specific clinical questions in real time, across three areas. Lung ultrasound: A-lines (normal), B-lines (interstitial syndrome — pulmonary oedema, ARDS, pneumonia), absent lung sliding (pneumothorax), the lung point (confirms pneumothorax), and the BLUE protocol for acute respiratory failure. Abdominal ultrasound: the FAST/eFAST (free fluid in trauma — Morison's pouch, splenorenal, pelvis, pericardium) and the non-trauma abdominal scan (AAA, gallbladder, hydronephrosis). Vascular ultrasound: compression ultrasonography for DVT (a non-compressible vein is a thrombus), ultrasound-guided line insertion, and AAA screening. POCUS integrates with the RUSH protocol (cardiac, lung, abdominal, vascular) for the bedside diagnosis of shock.

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high

Shock Echocardiography — RUSH & FALLS Protocols

The RUSH protocol (Rapid Ultrasound in Shock) is a systematic bedside ultrasound exam for the shocked patient that integrates cardiac, lung, abdominal, and vascular ultrasound to determine the type of shock. It examines three things — the PUMP (the heart: LV function, RV dilatation, effusion), the TANK (the volume: IVC, lungs, FAST), and the PIPES (the vessels: aorta, DVT, pneumothorax). The findings map to the four shock types: hypovolaemic (hyperdynamic LV, empty IVC), cardiogenic (hypokinetic LV, B-lines), obstructive (RV dilated or effusion, DVT or pneumothorax), and distributive (hyperdynamic, empty IVC, dry lungs). The FALLS protocol (Lichtenstein) uses lung ultrasound to guide fluid resuscitation — give fluid until A-lines convert to B-lines (the tank is full), then stop.

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Domain

Post-cardiac arrest care

1

high

Post-Cardiac Arrest Care and Targeted Temperature Management

The post-cardiac-arrest care is the comprehensive ICU management of the patient who has achieved the return of spontaneous circulation — the prevention of the secondary neurological injury (the targeted temperature management, the controlled oxygenation, the blood pressure, the glycaemic control, the seizure prophylaxis), the investigation and the treatment of the cause (the coronary angiography — the COACT trial), and the prognostication at 72 hours (the multimodal approach — the clinical, the EEG, the neuroimaging, the biomarkers). This topic builds the examiner's framework on the post-cardiac-arrest syndrome (the brain injury, the myocardial dysfunction, the systemic ischaemia-reperfusion, the persistent precipitating pathology), the TTM evidence (the TTM trial showing no difference between 33 and 36, and the TTM2 trial showing hypothermia NOT superior to normothermia), the COACT trial (no benefit of the immediate coronary angiography without the ST elevation), and the prognostication advisory (the multimodal approach, the no-single-modality principle).

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Domain

Transplant / pharmacology

1

high

Post-Transplant Immunosuppression Complications — Toxicity, PTLD & Metabolic

Post-transplant immunosuppression complications: the immunosuppression principles (induction — ATG/basiliximab/alemtuzumab; maintenance — tacrolimus + mycophenolate ± steroids; rescue for rejection), the drug pharmacology (the tacrolimus — the nephrotoxicity, the neurotoxicity [PRES], the diabetes; the ciclosporin — the nephrotoxicity, the hypertension, the gingival hyperplasia; the mycophenolate — the leucopenia; the azathioprine — the TPMT; the sirolimus — the wound healing, the pneumonitis; the steroids), the calcineurin inhibitor toxicity, the infection (the opportunistic — the CMV, the PCP, the EBV/PTLD), the metabolic (the steroid), the malignancy (the PTLD — the EBV-driven; the skin cancer — the SCC), the TDM (the tacrolimus the trough the levels), and the CYP3A4 drug interactions. The management: the balance the immunosuppression (the rejection vs the toxicity), the reduce/switch the agent, the monitor the levels.

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Domain

Cardiovascular / vascular surgery

1

medium

Post-Vascular-Surgery ICU — AAA, Carotid & Peripheral Bypass

The post-vascular-surgery ICU patient faces surgery-specific complications. After an open AAA repair: bleeding (the graft anastomosis), the spinal cord ischaemia (the cross-clamping of the thoracoabdominal aorta — the Adamkiewicz artery), the renal failure (the cross-clamp and the embolisation), the colonic ischaemia (the IMA ligation), the reperfusion syndrome (acidosis, hyperkalaemia, myoglobin from the lower-limb reperfusion), and the abdominal compartment syndrome. After an EVAR: the contrast-induced nephropathy, the endoleak (Types I to V), and the access-site complications. After a carotid endarterectomy: the hyperperfusion syndrome (headache, seizure, haemorrhage from the restoration of the flow to a chronically underperfused brain), the cranial nerve injury, and the MI (the carotid patient has the coronary disease). After a peripheral bypass: the graft thrombosis (assess the pulses, re-explore), the graft infection (catastrophic), and the reperfusion syndrome.

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Domain

Cardiovascular / perioperative

1

high

Postoperative Complications in the ICU

Postoperative complications in the ICU cover six areas. Bleeding (assess the drains, the Hb, the coagulation; distinguish the surgical from the medical bleeding; re-explore the surgical cause). Respiratory failure (atelectasis, oedema, aspiration, ARDS; weigh the early extubation against the prolonged ventilation). Infection or sepsis (a wound infection, an anastomotic leak, a pneumonia, a line infection; cultures and antibiotics). Delirium (common in the elderly; the CAM-ICU assessment; treat the cause — pain, infection, hypoxia, medications; avoid benzodiazepines; haloperidol or quetiapine). Acute kidney injury (from hypovolaemia/hypotension and nephrotoxins; treat the cause). Venous thromboembolism prophylaxis (LMWH, mechanical, early mobilisation). Pain is managed multimodally (paracetamol, regional, opioids sparingly) per the enhanced-recovery-after-surgery (ERAS) protocol.

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Domain

Obstetric

1

high

Pre-eclampsia with severe features, eclampsia, and HELLP: ICU management

Pre-eclampsia (new hypertension after 20 weeks + proteinuria/end-organ dysfunction) complicates 2-8% of pregnancies (ACOG). SEVERE FEATURES: BP ≥160/110 (ISSHP), thrombocytopenia (&lt;100), elevated transaminases, renal insufficiency, pulmonary oedema, cerebral/visual symptoms. ECLAMPSIA = new-onset seizures with no other cause. HELLP = Haemolysis, Elevated Liver enzymes, Low Platelets (platelets &lt;100 x 10^9/L, Sibai). MANAGEMENT: (1) MAGNESIUM SULFATE for seizure prophylaxis/treatment (4 g IV loading then 1-2 g/h IV infusion, or 4 g IV + 10 g IM then 5 g IM q4h — reflexes lost at 3.5-5 mmol/L, respiratory paralysis at 5-6.5 mmol/L, renally excreted). (2) BP control: treat acute-onset severe hypertension as soon as possible within 30-60 min of confirmation with IV labetalol, IV hydralazine or immediate-release oral nifedipine (ACOG CO 767) — avoid precipitous drops. (3) DELIVERY is the definitive treatment (timing based on maternal/fetal status). (4) Antenatal corticosteroids for fetal lung maturity (&lt;34 weeks). COMPLICATIONS: deaths mainly follow eclampsia, uncontrolled hypertension or systemic inflammation (fullPIERS); also pulmonary oedema, AKI, hepatic haemorrhage/rupture, DIC, abruption. POSTPARTUM: pre-eclampsia can develop or worsen after delivery — a seizure in a recently delivered woman is eclampsia until proven otherwise.

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Domain

Sedation / procedural

1

high

Procedural Sedation in the ICU — Capnography, Agents & the Safety Bundle

The procedural sedation is a drug-induced depression of the consciousness for a painful or an unpleasant procedure, maintaining the spontaneous ventilation and the airway reflexes (distinct from the general anaesthesia, where the airway is unprotected and the ventilation supported). The continuum runs from the minimal to the moderate, the deep, and the general anaesthesia — as the depth increases, the airway, the reflexes, the respiration, and the cardiovascular function are progressively compromised. The goal is the analgesia plus the anxiolysis plus the amnesia plus the immobility, with the cardiorespiratory stability and the rapid recovery. The safety bundle: the pre-procedure assessment (the fasting, the airway, the ASA status), the monitor…

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Domain

Quality / safety

1

high

Quality Improvement, Patient Safety & Incident Analysis

Quality improvement (QI), patient safety, and incident analysis in the ICU. QI methods: the Model for Improvement, the PDSA cycle (plan-do-study-act), Lean (waste removal, value-stream), Six Sigma (defect reduction, DMAIC), root cause analysis (RCA), fishbone/Ishikawa, the 5 Whys, audit and feedback, the Triple Aim, and statistical process control (run/control charts). Patient safety in ICU: types of error (medication, procedural, diagnostic, handover/communication), healthcare-associated infections (CLABSI, VAP, CAUTI), pressure injuries, falls, unplanned extubation. Safety culture: the just culture (Marx), blame-free/near-miss reporting, the Swiss cheese model (Reason), incident reporting systems, the Global Trigger Tool. Checklists and bundl…

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Domain

GI & nutrition / metabolic

1

high

Refeeding Syndrome — Hypophosphataemia, Thiamine & the Low-and-Slow Refeed

The refeeding syndrome is the potentially fatal metabolic disturbance that occurs when the food is reintroduced too rapidly after a period of the starvation or the malnutrition. The pathophysiology: the starved state has the low insulin, the catabolism, the depleted intracellular electrolytes (the phosphate, the potassium, the magnesium) and the thiamine. On the refeeding, the insulin surge shifts the glucose, the water, and the electrolytes intracellularly, causing the precipitous falls in the serum phosphate (the hallmark), the potassium, and the magnesium, the thiamine depletion (the Wernicke), and the fluid retention (the oedema, the heart failure). The at-risk: the little or no intake over 5 days, the BMI under 16, the weight loss over 15 per cent, the alcohol misuse, the anorexia, the low baseline phosphate or potassium or magnesium. The management (NICE): the start low and slow (the 10 kcal per kg per day for the high-risk, increase over 4 to 7 days), the thiamine BEFORE the refeeding (the 200 to 300 mg), the supplement the phosphate, the potassium, the magnesium, the monitor daily. The arrhythmias are the main death cause.

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Domain

Sedation & paralysis

1

high

Sedation, Analgesia and Paralysis in the ICU

Sedation and analgesia are universal in intensive care, and their quality shapes both the immediate course — tolerance of the endotracheal tube and the ventilator, the depth of sedation and its effect on delirium — and the long-term outcomes of critical illness. This topic builds the examiner's framework around the modern PADIS approach (analgesia-first, light sedation, delirium prevention, early mobility), the pharmacology of the sedatives and analgesics (propofol, midazolam, dexmedetomidine, ketamine; fentanyl, remifentanil, morphine), the evidence for daily sedation interruption and protocolised light sedation, the recognition and prevention of delirium, and the restricted, monitored role of neuromuscular blockade (rocuronium, suxamethonium,…

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Domain

GI & nutrition / infection

1

high

Severe Diarrhoea & C. difficile — Toxins, Severity & the Vancomycin/Fidaxomicin Era

The C. difficile is the key ICU cause of the severe diarrhoea — the antibiotic-associated (the clindamycin, the fluoroquinolones, the cephalosporins), the spore-forming, the toxin A and B producer, the hypervirulent NAP1 or ribotype 027. The spectrum: the diarrhoea to the pseudomembranous colitis to the toxic megacolon to the perforation. The severe (the WCC over 15, the AKI creatinine over 1.5 times, the hypoalbuminaemia, the ileus or the megacolon); the fulminant (the shock, the megacolon, the perforation). The diagnosis: the GDH plus the toxin (the two-step); the PCR detects the colonisation, not the active disease (the over-diagnosis). The treatment (IDSA 2021): the non-severe the fidaxomicin OR the oral vancomycin 125 mg QID; the severe the oral vancomycin; the FULMINANT the vancomycin 500 mg QID plus the IV metronidazole plus-or-minus the rectal vancomycin plus the surgery (the subtotal colectomy for the megacolon). The recurrence: the bezlotoxumab, the faecal microbiota transplant. The stop the antibiotics and the PPI; the soap-and-water hand hygiene (the alcohol gel does not kill the spores); the isolate.

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Domain

Shock states

1

high

Shock States — Classification, Profiles and Management

Shock is the failure of oxygen delivery to meet tissue demand, and its classification into four types — distributive, cardiogenic, hypovolaemic and obstructive — is the framework that directs the resuscitation. This topic builds the examiner's framework on the pathophysiology (the oxygen-delivery equation and which determinant each shock type fails), the haemodynamic profiles (the cardiac output and the systemic vascular resistance that separate the four), the specific management of each (early revascularisation in cardiogenic shock; the vasopressor choice — norepinephrine over dopamine, the place of vasopressin; the blood-pressure target and the corticosteroid question in septic shock), and the evidence — the SHOCK, IABP-SHOCK II and CULPRIT-shock trials in cardiogenic shock, and SOAP II, VASST, SEPSISPAM and ADRENAL in distributive shock.

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Domain

Haematology / haemoglobinopathy

1

high

Sickle-Cell Crisis — Vaso-Occlusive, Acute Chest & Exchange Transfusion

The sickle-cell crisis in the ICU: the vaso-occlusive crisis (the commonest — pain from the microvascular occlusion by the sickled cells), the acute chest syndrome (the leading cause of death — the new infiltrate, the hypoxia), the splenic sequestration (children), the aplastic crisis (parvovirus B19), the haemolytic crisis. The management: oxygen (reduce the sickling), IV hydration (hypotonic — reduce the viscosity), analgesia (the opioids — patient-controlled), the transfusion (simple or exchange), the hydroxyurea (the prevention). The acute chest syndrome — the antibiotics (the infection), the incentive spirometry (the atelectasis prevention), the transfusion, the bronchodilators. The exchange transfusion for the acute chest, the stroke, the severe.

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Domain

Transplant / immunology

1

high

Solid-Organ Transplant Recipient in the ICU — Immunosuppression, Infection & Rejection

The solid-organ transplant recipient in the ICU: the immunosuppression (the calcineurin inhibitors — the tacrolimus, the ciclosporin; the antimetabolites — the mycophenolate; the mTOR — the sirolimus; the steroids), the infection risk (the timeline — the first month the nosocomial; the 1 to 6 months the opportunistic — the CMV, the PCP, the Listeria, the Aspergillus; the late the community-acquired), the acute rejection (the T-cell mediated — the cellular; the antibody-mediated — the humoral), the drug interactions (the CYP3A4 — the tacrolimus levels), and the graft dysfunction (the diagnostic — the ultrasound, the biopsy).

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Domain

Infection / surgical

1

high

Source Control — The Fourth Pillar of Sepsis (Drainage, Debridement, Device)

Source control is the set of physical measures that eliminate the microbial source, reduce the bacterial inoculum, and restore organ function — a core pillar of sepsis alongside antibiotics and resuscitation. The four tenets are drainage (abscess, empyema), debridement (necrotic tissue), device removal (infected central line, catheter, prosthetic), and definitive repair (perforation closure, obstruction relief). Timing is early — within 6 to 12 hours for severe sepsis, immediate for necrotising infection — because delayed source control worsens mortality: source control before the antibiotics fade. Modalities run from IR percutaneous drainage (first-line for accessible collections), through endoscopic ERCP for the biliary tree, to open surgery for diffuse peritonitis, with the step-up approach standard for infected pancreatic necrosis. STOP-IT established that four days of antibiotics suffice after adequate source control.

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Domain

Trauma / neurocritical care

1

high

Spinal Trauma & Spinal Shock — ASIA Scale, CT vs MRI & Steroid Controversy

The spinal trauma and the spinal shock in the ICU: the spinal cord injury (the SCI — from the trauma, the fracture, the dislocation) causing the motor and sensory deficit below the level. The mechanism of injury (the axial loading, the flexion, the extension, the rotation, the distraction) determines the fracture pattern and the cord injury. The ASIA impairment scale (A = complete; B = sensory incomplete; C = motor incomplete; D = motor useful; E = normal). The spinal shock (the temporary the areflexia and the flaccidity below the level — the resolves over the days to the weeks) vs the neurogenic shock (the hypotension, the bradycardia, the vasodilation from the loss of the sympathetic tone — the T6 and above). The cervical spine clearance (the NEXUS low-risk criteria vs the Canadian C-spine rule; the CT first-line for the high-risk; the MRI for the neurological deficit; the clinical clearance for the low-risk). The imaging: the CT first (the bony), the MRI for the cord (the oedema, the haematoma, the compression). The steroids (the methylprednisolone — the NASCIS trials; the controversial; the not the standard of the care).

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Domain

Statistics & evidence

1

medium

Statistics & Evidence — Trial Design, Interpretation, Appraisal and the Landmark ICU Trials

The statistics and the evidence for the ICU — the hierarchy of the study design (the case series, the case-control, the cohort, the RCT, the systematic review and the meta-analysis), the RCT design elements (the PICO, the randomisation, the allocation concealment, the blinding, the intention-to-treat), the bias and the confounding, the statistical inference (the null hypothesis, the type-I and the type-II error, the power, the p-value, the confidence interval), the effect sizes (the relative risk, the odds ratio, the absolute risk reduction, the number needed to treat, the hazard ratio), the meta-analysis (the forest plot, the heterogeneity, the I-squared), the critical appraisal (the GRADE), and the landmark ICU trials as the worked examples (the ARMA, the SOAP II, the VASST, the ProCESS and the ARISE, the ACURASYS and the ROSE, the Surviving Sepsis Campaign).

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Domain

Neurocritical care / seizures

1

high

Status Epilepticus & Refractory Status Epilepticus

Status epilepticus (SE) is a continuous seizure lasting more than 5 minutes, or two or more seizures without full recovery between them — a neurological emergency where the longer the seizure lasts, the harder it becomes to terminate and the worse the outcome. First line is a benzodiazepine (lorazepam 4 to 8 mg IV, or intramuscular midazolam when there is no line). Second line is levetiracetam 60 mg/kg, fosphenytoin 20 mg PE/kg, or valproate 40 mg/kg (ESETT showed all three equivalent, terminating the seizure with improved alertness by 60 minutes in about half). Refractory SE (failure of first and second line) requires anaesthetic intubation with propofol, midazolam, ketamine, or thiopent infusions titrated to burst suppression on continuous EEG. Non-convulsive SE and autoimmune causes such as anti-NMDA receptor encephalitis must not be missed.

Open

Domain

Seizures & weakness

1

medium

Status Epilepticus, Guillain-Barré and Myasthenia Gravis

Status epilepticus is the prolonged or the recurrent seizure that becomes self-sustaining — a neurological emergency with a mortality of 10 to 20 per cent. Guillain-Barre and myasthenia gravis are the two neuromuscular diseases that most commonly cause the respiratory failure needing the ICU. This topic builds the examiner's framework on the SE management (the benzodiazepine, the fosphenytoin/levetiracetam, the RAMPART and the ESETT evidence), the GBS (the IVIG, the plasma exchange, the respiratory monitoring), and the myasthenia (the IVIG, the plasma exchange, the crisis).

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Domain

Respiratory / acid-base

1

high

Systematic Arterial Blood Gas Interpretation

A systematic six-step approach to the arterial blood gas: (1) assess oxygenation (PaO2 with FiO2, the P/F ratio, the A-a gradient); (2) read the pH (acidaemia or alkalaemia); (3) identify the primary disturbance (CO2 versus bicarbonate); (4) check the compensation (Winter's formula for metabolic acidosis; SBE-based compensation equations for the rest); (5) calculate the anion gap (albumin-corrected) with Wrenn's delta gap for mixed metabolic disturbances; and (6) read the base excess, the SpO2, and the lactate. The anion gap divides metabolic acidosis into a high-anion-gap group (lactate, ketones, uraemia, toxins — GOLD MARK) and a normal-anion-gap group (diarrhoea, renal tubular acidosis, saline). The delta gap (ΔAG − ΔHCO3) detects mixed metabolic disorders; the osmolar gap flags toxic alcohols; and the A-a gradient separates hypoventilation from a lung problem.

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Domain

Oncology & immunocompromised

1

medium

The Oncology and Immunocompromised Patient in the ICU

The immunocompromised and the oncology patient in the ICU demands a broad, the early, and the aggressive approach — the febrile neutropenia (the anti-pseudomonal beta-lactam within the hour), the opportunistic infections (the CMV, the PCP, the fungal), the tumour lysis syndrome (the hydration, the rasburicase), and the immune-related toxicity (the GvHD, the ICI toxicity). This topic builds the examiner's framework on each.

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Domain

Physiology / thermoregulation

1

medium

Thermoregulation

Thermoregulation — the hypothalamic set point (37 degrees C). The heat production (the shivering, the metabolism, the thyroxine, the brown fat / non-shivering thermogenesis). The heat loss (the sweating, the vasodilation, the radiation, the convection, the conduction, the respiration). The fever (the prostaglandin E2 — the pyrogen raises the set point). The clinical: the malignant hyperthermia (the ryanodine receptor), the heat stroke, the hypothermia, the neuroleptic malignant syndrome.

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Domain

Trauma & burns

1

medium

Trauma, Burns and Mass-Casualty Resuscitation

Trauma is the time-critical failure of mechanical integrity — of the circulation, the airway, the brain and the skeleton — and its management is the parallel, prioritised, damage-control resuscitation of the ATLS primary survey. This topic builds the examiner's framework on the primary and the secondary survey (the ABCDE), the lethal triad of acidosis-hypothermia-coagulopathy that drives the bleeding to death, the damage-control resuscitation with tranexamic acid and the 1:1:1 transfusion ratio, the burns resuscitation (the Parkland formula and the inhalation injury), the cervical-spine clearance (the Canadian C-spine rule), the traumatic-brain-injury corticosteroid harm (the CRASH trial), the mass-casualty triage (START) and the injury scoring (the ISS and the RTS), and the evidence base — CRASH-2 for tranexamic acid and the Canadian C-spine rule for the clearance of the alert, stable patient.

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Domain

Infection / global health

1

high

Tropical & Global Infections — Malaria, Dengue, TB, Influenza & COVID

The tropical and the global infections in the ICU: the severe malaria (the Plasmodium falciparum — the cerebral, the ARDS, the AKI, the severe anaemia, the hypoglycaemia, the hyperparasitaemia; the IV artesunate the WHO first-line, the superior to the quinine, the AQUAMAT and the SEAQUAMAT the mortality benefit; the blood smear or the RDT), the dengue (the plasma leak — the pleural effusion, the ascites, the haemoconcentration; the dengue shock syndrome; the cautious the fluids in the leak phase; the NS1 antigen; the warning signs; the paracetamol NOT the NSAIDs; the platelets or the FFP for the bleeding), the melioidosis (the Burkholderia pseudomallei — the pneumonia, the liver and the spleen abscess; the ceftazidime or the meropenem the inten…

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Domain

Cardiovascular / valvular

1

high

Valvular Disease in the ICU

Severe valvular disease in the ICU has valve-specific haemodynamic implications that determine what the patient can and cannot tolerate. Severe aortic stenosis (a stiff, hypertrophied LV) is preload-dependent and vasodilator-intolerant — avoid tachycardia, hypovolaemia, and vasodilation; use phenylephrine. Severe aortic and mitral regurgitation (volume overload) benefit from afterload reduction and a higher heart rate — use vasodilators and avoid bradycardia. Severe mitral stenosis (an obstructed inflow) needs rate control and avoids vasodilation. Maintain sinus rhythm in all (the atrial kick matters for the stiff or overloaded LV). Echocardiography is the diagnostic tool; the definitive treatment is surgical or percutaneous (AVR, TAVI/TAVR, MV repair, balloon mitral valvuloplasty). Prosthetic valves require lifelong anticoagulation (mechanical) and carry risks of thrombosis and infective endocarditis.

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