Acute Pancreatitis

Meet the patient

A 52-year-old woman arrives at 2am with severe, constant epigastric pain that bores straight through to her back. She has vomited three times, cannot get comfortable lying flat, and is leaning forward in the chair. Her lipase is over three times the upper limit of normal. The ultrasound already ordered shows gallstones.[9]

Three questions decide her next 48 hours, and they are the three that decide every pancreatitis case: is this really pancreatitis?, how severe will it get?, and am I about to make it worse with the fluids? Hold those three and the whole topic falls into place.[1]

Two of three — the diagnosis that needs no scan

You do not need a CT to make this diagnosis. The 2012 Revised Atlanta classification lays down the two-of-three rule — acute pancreatitis is present when any two of these three are met:[1]

1. Characteristic pain — acute onset of severe, constant epigastric pain, frequently radiating straight through to the back, often eased by sitting forward.
2. Lipase or amylase over three times the upper limit of normal — and lipase is the preferred enzyme, because it is more specific and persists longer than amylase.
3. Characteristic imaging on contrast-enhanced CT, MRI, or ultrasound.[1]

When the clinical picture and the enzymes agree, imaging is not required to confirm the diagnosis — ordering a scan delays fluids and adds nothing. The corollary is the trap that costs marks: a normal amylase does not exclude pancreatitis. It falls in hypertriglyceridaemic pancreatitis (lipaemic serum fouls the assay) and in late presentations after the enzyme has already cleared. Reach for lipase first.[9]

The number rule: 2-of-3. Two of three makes the diagnosis; one of three forces you to image. Say it once in the viva and the criteria marks are banked.[1]

Etymology for viva gold: pancreas is Greek pan-kreas, "all flesh" — the ancients noted a gland that was almost entirely digestive tissue with no obvious mechanical job. Trypsin is from Greek tryein, "to wear away" — which is precisely what it does to the gland when it fires early.[1]

I GET SMASHED — and the two that own three-quarters

Gallstones and alcohol together cause 70 to 80 percent of pancreatitis. Name them first, every time, then recite the rest. The mnemonic every final-prof candidate is expected to reproduce is I GET SMASHED.[3]

• Gallstones — 40 to 50 percent. Small stones (under 5 mm) and microlithiasis are the dangerous ones, because they are just small enough to migrate through and transiently obstruct the ampulla of Vater.
• Alcohol — 25 to 35 percent. Typically chronic heavy intake (over 50 to 80 g/day for 5 or more years); the acute flare may be the first sign of underlying chronic disease.[1]

The remaining causes live in the mnemonic, and each carries an exam hook:[3]

[1]

Drug-induced pancreatitis is a diagnosis of exclusion. The drug must be temporally related, other causes excluded, and the pancreatitis resolves on withdrawal (and recurs on rechallenge in classical cases). The highest-risk drugs are azathioprine and 6-mercaptopurine, didanosine, thiazides, sodium valproate, mesalazine, oestrogens, tetracyclines, and — increasingly flagged — the GLP-1 receptor agonists.[3]

Two metabolic causes are high-yield exam triggers, and both have a catch. In hypertriglyceridaemic pancreatitis (triglycerides over 11.3 mmol/L / 1000 mg/dL), look for lipaemic milky plasma and eruptive xanthomata — and remember the amylase may be falsely normal. In hypercalcaemia (usually primary hyperparathyroidism), always check the corrected calcium — but remember the serum calcium falls in severe pancreatitis as free fatty acids saponify peripancreatic fat. A normal calcium on day two does not exclude a hypercalcaemic cause.[1]

Trypsin switched on inside the cell — the mechanism in one chain

The single sentence that earns the mechanism marks: acute pancreatitis begins when trypsinogen is activated to trypsin inside the pancreatic acinar cell — before it ever reaches the duodenal lumen where activation is meant to happen — and the gland digests itself.[9]

Normally several brakes keep trypsin silent inside the pancreas, and pancreatitis is what happens when they fail:[1]

• Trypsinogen is meant to be activated in the duodenal lumen by enterokinase on the brush border — never inside the gland.
• Inside the acinar cell it is held inactive by the trypsinogen-activation peptide, SPINK1, and chymotrypsin C-mediated degradation.
• Abnormal sustained calcium signals — from bile acids, alcohol metabolites, or hypercalcaemia — switch trypsinogen on inside the cell and divert secretion to the basolateral membrane into the interstitium.
• Failure of SPINK1 (genetic) or of lysosomal degradation lets trypsin persist and fire the rest of the zymogen cascade.[1]

Once trypsin lights the zymogen cascade, autodigestion follows along a chain you can recite — and each enzyme explains a complication:[9]

• Elastase digests the elastic lamina of vessels — the basis of haemorrhagic, necrotising pancreatitis.
• Phospholipase A2 digests cell-membrane phospholipids — acinar necrosis, and in the lungs surfactant destruction driving ARDS.
• Lipase digests peripancreatic fat; free fatty acids bind calcium into soaps — the hypocalcaemia of severe disease.
• Kallikrein and bradykinin drive vasodilation and capillary leak — the third-space loss behind shock.[1]

The systemic cascade is the bridge to organ failure. Injured acinar cells release DAMPs and cytokines — IL-6, IL-8, TNF-alpha, IL-1 beta — producing SIRS, which drives capillary leak (the intravascular hypovolaemia behind shock, and the fluid overload that follows over-resuscitation), ARDS, AKI, and DIC.[9]

Why gallstones do it: most people share a common channel at the ampulla where the bile duct and pancreatic duct join. A migrating stone transiently obstructs the pancreatic duct, raising pressure and sometimes refluxing bile into it — either way, premature trypsinogen activation. Persistent obstruction, in contrast, causes obstructive jaundice and ascending cholangitis — the indications for urgent ERCP.[9]

Why alcohol does it: direct acinar toxicity (fatty acid ethyl esters), protein-plug precipitation that blocks small ductules, and sphincter of Oddi spasm. Chronic exposure builds chronic pancreatitis; an acute flare rides on top.[9]

[1]

The severity fork — mild, in the middle, or killing them

The morphological split and the severity split are two different axes — do not blur them. Morphology is what the CT shows; severity is what the bedside and the scores show. The Revised Atlanta classification defines three severity grades, and reproducing them verbatim is a viva staple:[1]

• Mild — around 80 percent — no organ failure, no local or systemic complications. Resolves within a week; discharge with cause-specific prevention.
• Moderately severe — transient organ failure resolving under 48 hours, OR local or systemic complications without persistent organ failure. Manage on a monitored ward or HDU.
• Severe — persistent organ failure over 48 hours, defined by a Marshall score of 2 or more in any one of respiratory (PaO2 over FiO2 under 300), renal (creatinine over 170 micromol/L), or cardiovascular (systolic BP under 90 mmHg unresponsive to fluids). Mortality 10 to 30 percent. Requires ICU.[1]

By morphology the split is between interstitial oedematous pancreatitis (the commoner pattern — diffuse gland enlargement, no necrosis, usually mild) and necrotising pancreatitis (non-enhancing tissue on contrast CT, around 20 percent, higher complication and mortality rate, risk of infection). The face-off is the one examiners reach for:[1]

[1]

The discriminator line: necrosis equals lack of enhancement on contrast CT — not "a big pancreas". An oedematous gland enhances normally; a necrotic one does not.[1]

Read the pain, then read the severity — the bedside

The classic pain is unmistakable and it teaches the anatomy. Acute onset of severe, constant, deep-seated epigastric pain radiating straight through to the back, eased by sitting forward (the autonomic plexus sits posteriorly) and worsened by lying flat, eating, coughing, and deep inspiration. It reaches maximum intensity within minutes to hours — distinguishing it from the waxing colic of biliary or renal origin. Nausea and vomiting are invariable.[9]

The examination findings track the severity, so grade as you examine.[1]

• Mild disease — looks unwell but systemically well: low-grade fever under 38.5 degrees, mild tachycardia, mild epigastric tenderness, bowel sounds normal or slightly reduced.
• Moderate to severe — signs of SIRS: fever over 38 degrees or hypothermia under 36, heart rate over 90, respiratory rate over 20, WBC over 12 or under 4. Hypotension, oliguria, hypoxia, confusion signal developing organ failure.
• Established severe or haemorrhagic — distended abdomen from ileus and third-space ascites, tender and guarded epigastrium, absent bowel sounds; a palpable epigastric mass later means pseudocyst.[1]

The two eponymous bruising signs are rare but a viva favourite — and specific for severe necrotising or haemorrhagic disease.[9]

• Grey-Turner's sign — bluish-green or yellowish-brown flank bruising, blood tracking from the retroperitoneum along fascial planes.
• Cullen's sign — periumbilical bruising, blood tracking via the falciform ligament.
• Less commonly examined: Fox's sign — bruising in the upper thigh along the inguinal ligament.[1]

Atypical presentations are the ones that bite, because they are missed:[9]

• The elderly present with confusion, falls, hypothermia, or non-specific decline rather than classic pain — lower threshold to image and to admit.
• Pregnancy (usually third trimester) is mostly gallstone pancreatitis, sometimes hypertriglyceridaemic; it is missed because epigastric pain is blamed on hyperemesis, reflux, or pre-eclampsia.
• Diabetic ketoacidosis may precipitate pancreatitis and be its consequence — check ketones and a gas in any diabetic with pancreatitis.
• Hypertriglyceridaemic pancreatitis shows lipaemic milky plasma and eruptive xanthomata; the amylase may be falsely normal.
• Post-ERCP pancreatitis declares itself as pain, nausea, and a rising amylase within 4 to 24 hours of the procedure.[1]

The mimics that also raise amylase — exclude the AAA

Several lethal abdomens can raise the amylase and masquerade as pancreatitis. The differential of severe epigastric pain radiating to the back is the differential of an acute abdomen, and the recurring preventable miss is the leaking abdominal aortic aneurysm.[9]

• Perforated peptic ulcer — sudden knife-like epigastric pain becoming generalised, peritonism with a rigid board-like abdomen, free intraperitoneal gas under the diaphragm on an erect chest X-ray or CT. Amylase can be mildly raised. Upper-GI surgical emergency.
• Mesenteric ischaemia or infarction — pain out of proportion to examination in an elderly vasculopath with atrial fibrillation, lactic acidosis, rectal bleeding; pneumatosis or bowel-wall thickening on CT angiography. A raised amylase is common and misleading.
• Leaking or ruptured abdominal aortic aneurysm — tearing epigastric and back pain, syncope, hypotension, a pulsatile epigastric mass in an elderly male smoker. A raised amylase is well described. A fatal miss.
• Inferior myocardial infarction — epigastric pain, nausea, diaphoresis, inferior ST elevation, raised troponin. An ECG is mandatory in any adult with acute epigastric pain.
• Diabetic ketoacidosis — abdominal pain and vomiting with ketotic breath, high-anion-gap acidosis, hyperglycaemia.
• Acute cholecystitis or biliary colic — right-upper-quadrant pain with a positive Murphy sign, normal or mildly raised lipase; cholangitis adds Charcot's triad of fever, jaundice, and rigors.[1]

The scores that decide the bed — BISAP at the door, Ranson and Glasgow at 48 hours

Severity grading is not a tick-box exercise — it decides ICU versus ward, and it predicts infected necrosis. Begin with ABCDE, run a focused abdominal exam, then deploy the score that fits the clock.[1]

ABCDE — look for the organ failure that defines severe disease:[1]

• Airway — patent; protect if vomiting with a reduced GCS.
• Breathing — respiratory rate, SpO2 on air. Hypoxia (SpO2 under 92 percent or PaO2 under 8 kPa) signals respiratory organ failure.
• Circulation — heart rate, blood pressure, capillary refill, JVP. Systolic under 90 mmHg signals cardiovascular organ failure.
• Disability — GCS or AVPU; confusion is a marker of severe disease and a Glasgow or BISAP criterion.
• Exposure — fully expose the abdomen.[1]

Bedside observations that define severity: catheterise for hourly urine output (target over 0.5 mL/kg/h — the most sensitive perfusion marker) in moderate-severe disease, continuous SpO2 and ECG, hourly respiratory rate and blood pressure, four-hourly temperature.[1]

SIRS at the bedside — two or more of temperature over 38 or under 36 degrees, heart rate over 90, respiratory rate over 20, WBC over 12 or under 4. SIRS at admission and at 48 hours predicts severe disease and infected necrosis.[9]

Ranson criteria — 11 variables, two timepoints

At admission (5): age over 55, WBC over 16 x 10^9/L, glucose over 10 mmol/L (200 mg/dL), AST over 250 IU/L, LDH over 350 IU/L.[1]

During the first 48 hours (6): haematocrit fall over 10 percentage points, calcium under 2 mmol/L (8 mg/dL), PaO2 under 8 kPa (60 mmHg), base deficit over 4 mEq/L, fluid sequestration over 6 L, urea rise over 1 mmol/L (3.6 mg/dL).[1]

Score interpretation: 0 to 2 mild (mortality under 1 percent), 3 to 4 around 15 percent, 5 to 6 around 40 percent, over 6 near 100 percent. A score of 3 or more equals severe.[1]

Glasgow (modified Glasgow or Imrie) — eight criteria, international

Assessed within 48 hours of admission, with no race-specific admission variables:[1]

• Age over 55, WBC over 15 x 10^9/L, Glucose over 10 mmol/L, LDH over 600 IU/L, AST over 200 IU/L, Urea over 16 mmol/L, Calcium under 2 mmol/L, PaO2 under 8 kPa (60 mmHg).
• Score of 3 or more equals severe. Albumin under 32 g/L is included in some versions, making it nine criteria.[1]

BISAP — the one to use at the door

A simple 5-point score computed within the first 24 hours, derived by Wu et al. 2008 from a large US population-based dataset. This is the bedside score that is actually usable at admission:[4]

• Blood urea nitrogen over 8.6 mmol/L (25 mg/dL)
• Impaired mental status (GCS under 15)
• SIRS (two or more of temperature, heart rate, respiratory rate, WBC)
• Age over 60 years
• Pleural effusion on imaging
• Score 0 to 5; a score of 3 or more marks high mortality (over 5 to 20 times that of low scores).[1]

APACHE-II and CRP

APACHE-II is a dynamic physiological ICU score; 8 or more defines severe pancreatitis — more accurate but complex and time-consuming, used in research and ICU. And at 48 hours, CRP over 150 mg/L independently predicts pancreatic necrosis.[1]

Cross-sectional imaging — when and why

Contrast-enhanced CT is not needed at admission in obvious cases. It is indicated when the diagnosis is uncertain, when severity must be assessed at 48 to 72 hours to detect necrosis (the timing matters — necrosis may not be visible on day one), or when a complication is suspected. The lack of parenchymal enhancement defines necrosis. MRI or MRCP is equivalent for diagnosis and preferred in pregnancy and to characterise the biliary tree non-invasively; EUS hunts occult microlithiasis, sludge, and small tumours in unexplained recurrent disease.[1]

Diagnosing infected necrosis: gas within necrosis on CT is highly suggestive; a positive Gram stain or culture on image-guided fine-needle aspiration is confirmatory. Reserve FNA for the clinically deteriorating patient in whom infection is suspected but unproven.[5]

[1]

Three dogmas overturned — the modern management

Admit everyone; severe disease goes to ICU or HDU. Run ABCDE — high-flow oxygen to target SpO2 94 to 98 percent (88 to 92 percent in a chronic CO2 retainer), two large-bore cannulae, a urinary catheter for hourly output, reliable IV access.[3]

The single most important early intervention is goal-directed fluid resuscitation — and the single most important lesson is that aggressive fluids harm.[2]

[2]

Analgesia is a quality indicator — adequate, not rationed. Titrate an IV opioid: morphine 0.05 to 0.1 mg/kg every 4 to 6 hours (or patient-controlled analgesia), fentanyl 25 to 50 micrograms every 1 to 2 hours, or tramadol 50 to 100 mg every 6 to 8 hours. The old worry that morphine spasm the sphincter of Oddi and worsens pancreatitis is not supported by clinical evidence — morphine remains reasonable first-line. Avoid IM injections (they interfere with CK and absorb variably).[3]

Escalate to ICU or HDU the moment organ failure develops or persists — persistent hypoxia, hypotension unresponsive to fluids, oliguria not responding to a fluid challenge, confusion. That persistence is the definition of severe pancreatitis.[1]

Feed the gut, withhold the antibiotic, time the ERCP

Early enteral feeding within 24 to 48 hours is the standard of care — and it overturned the old nil-by-mouth dogma.[3]

• In mild pancreatitis, start a low-fat solid or liquid diet orally within 24 to 48 hours and advance as tolerated.
• In severe disease or gastric intolerance, nasogastric feeding is as effective as nasojejunal in most trials — reserve NJ for those who fail NG.
• Total parenteral nutrition is reserved for prolonged ileus, fistula, or enteral failure — it does not improve outcome and increases infection.[1]

Antibiotics are the most important "less is more" lesson in the topic. Routine prophylactic antibiotics do not reduce infected necrosis or mortality — and they cause harm: resistant organisms, fungal overgrowth, and Clostridioides difficile. Do not give them. This is a meta-analysis-level conclusion.[7]

Give antibiotics only when:[7]

1. Infected necrosis — proven by gas in necrosis on CT or positive FNA, OR strongly suspected by clinical deterioration with raised inflammatory markers.
2. Acute cholangitis (fever, jaundice, rigors, abdominal pain — Charcot's triad) with biliary obstruction.
3. An extrapancreatic infection — pneumonia, UTI, bacteraemia.[7]

Choice for infected necrosis: a carbapenem — imipenem-cilastatin 500 mg IV every 6 hours or meropenem 1 g IV every 8 hours — OR ciprofloxacin 400 mg IV every 12 hours plus metronidazole 500 mg IV every 8 hours. These penetrate necrosis well. Continue until clinical and biochemical improvement and resolution of the collection — typically 4 to 7 days of effective source control.[1]

ERCP is early, but only for specific indications — and routine ERCP without obstruction is the recurring trainee error:[8]

• Within 24 hours for acute cholangitis and persistent biliary obstruction (jaundice, dilated CBD with a stone, or worsening LFTs).
• NOT routinely in gallstone pancreatitis without obstruction — the Cochrane review (Tse and Yuan 2012) showed no benefit and a trend to harm in this group.[8]

[1]

Cholecystectomy, hypertriglyceridaemia, and the step-up for necrosis

Same-admission cholecystectomy in mild gallstone pancreatitis is non-negotiable — recurrence without it is 20 to 30 percent within 12 weeks.[3]

• Mild gallstone pancreatitis — same-admission laparoscopic cholecystectomy after symptoms settle, cutting recurrence from around 20 to 30 percent to under 5 percent.
• Severe pancreatitis (necrosis, organ failure) — delay cholecystectomy until complete resolution, sometimes staged after recovery from necrosectomy.
• Unfit for surgery — ERCP plus sphincterotomy before discharge defunctions the sphincter and reduces recurrence as a second-line approach.[1]

Hypertriglyceridaemic pancreatitis needs cause-specific therapy. An insulin infusion (with dextrose to hold euglycaemia) activates lipoprotein lipase and clears triglycerides; plasmapheresis removes triglycerides rapidly in very high TG (over 1000 mg/dL) with severe disease; long-term a fibrate (fenofibrate 145 to 200 mg daily) is first-line, with omega-3 fatty acids, a statin, dietary fat restriction, and tight diabetic control.[3]

Autoimmune pancreatitis responds dramatically to steroids — prednisolone 30 to 40 mg daily for 4 to 6 weeks then taper — with a radiological and biochemical response in type 1 (IgG4-related) so striking it doubles as a diagnostic trial.[3]

The step-up approach for infected necrosis is the modern standard — open necrosectomy is now the last resort. The PANTER and TENSION trials established it:[5]

• Delay intervention around 4 weeks if possible — it lets the collection wall off and become drainable, reducing bleeding and organ failure.
• Step 1: percutaneous or endoscopic (EUS-guided) catheter drainage — controls sepsis in most.
• Step 2: if drainage fails, endoscopic or minimally invasive necrosectomy — PANTER and TENSION showed the endoscopic step-up is superior to open necrosectomy: less organ failure, fewer fistulas, lower long-term diabetes and incisional hernia.[6]

The complications clock — by content and by timing

Local complications are classified by content (fluid versus necrosis) and by timing (under or over 4 weeks) — reproduce the four-box table.[1]

[1]

A pseudocyst is a fluid collection encapsulated by a non-epithelial fibrous wall, without necrosis, persisting over 4 weeks — drain (endoscopic or surgical) only if symptomatic, infected, over 6 cm, or persisting over 6 weeks.[1]

Other local complications, each with a one-line teaching point:[1]

• Infected necrosis — the leading cause of late death; diagnose by gas in necrosis on CT or positive FNA; treat with carbapenem plus step-up drainage.
• Haemorrhage — erosion into splenic, gastroduodenal, or pancreaticoduodenal arteries; diagnose by CT angiography, treat by interventional radiology embolisation.
• Splenic and portal vein thrombosis — splenic vein thrombosis may cause gastric varices with a bleed risk.
• Gastric outlet or duodenal obstruction — compression by a phlegmon or walled-off necrosis.[5]

Systemic complications track the cytokine cascade: SIRS and sepsis, organ failure (ARDS from phospholipase A2 destroying surfactant, AKI, shock, DIC), metabolic derangement (hypocalcaemia from saponification, hyperglycaemia or diabetes from endocrine loss, hypomagnesaemia), and stress ulceration with DVT or PE risk — prophylactic LMWH once bleeding risk is controlled.[9]

Long-term, watch for the insufficiencies: exocrine failure (steatorrhoea, weight loss — pancreatic enzyme replacement) and endocrine failure (type 3c diabetes), recurrent pancreatitis, and progression to chronic pancreatitis.[1]

How pancreatitis patients come to harm — the preventable list

• A leaking AAA labelled pancreatitis because the amylase was mildly raised — the preventable death.[9]
• Aggressive fluids chasing a falling haematocrit into pulmonary oedema and abdominal compartment syndrome (WATERFALL).[2]
• Prolonged nil by mouth starving the gut into bacterial translocation and infected necrosis.[3]
• Routine prophylactic antibiotics breeding resistance, fungi, and C. difficile with no benefit.[7]
• Early open necrosectomy on day three, before the collection walls off — high mortality.[5]
• Routine ERCP without obstruction, causing more ERCP-related pancreatitis and cholangitis.[8]
• Forgetting same-admission cholecystectomy in mild gallstone pancreatitis — a 20 to 30 percent recurrence.[1]
• Over-relying on amylase, missing the hypertriglyceridaemic or late-presenting case where it is normal.[9]

The trials that overturned the dogma

[2] [5] [6] [4]

The antibiotic question is settled at the meta-analysis level. Poropat and colleagues' 2022 systematic review with trial sequential analysis confirmed that prophylactic antibiotics do not reduce infected necrosis or mortality — the modern guideline position.[7]

Special populations — what changes

Pregnancy. The commonest cause is gallstones, with risk rising in the third trimester (progesterone-driven gallbladder hypomotility) and with hyperemesis-related biliary stasis; hypertriglyceridaemia also rises. Presentation is as the non-pregnant but may be missed — blamed on hyperemesis, reflux, or pre-eclampsia. Safe imaging is ultrasound and MRI or MRCP; avoid CT. Manage as the non-pregnant — moderate goal-directed LR, early enteral feeding, ERCP for cholangitis with foetal shielding and obstetric involvement, same-admission or early postpartum cholecystectomy. Maternal mortality is low; foetal loss rises in severe disease.[3]

The elderly. Atypical and blunted — confusion, falls, hypothermia — with higher comorbidity and higher mortality. Lower threshold for ICU and for cross-sectional imaging. Use NSAID analgesia cautiously (renal and GI bleeding); give DVT prophylaxis.[3]

The alcoholic patient. Thiamine before glucose (prevent Wernicke) — thiamine 100 mg IV or IM daily for 3 to 5 days; correct magnesium, potassium, phosphate; CIWA-based withdrawal prophylaxis with benzodiazepines; refer to alcohol liaison for relapse prevention. Recurrent pancreatitis is the path to chronic pancreatitis.[3]

The immunocompromised. Broaden the differential to opportunistic infection (CMV, Mycobacterium avium, invasive fungal) and drug toxicity (didanosine, antiretrovirals). Lower threshold for imaging and microbiological work-up.[3]

Children. Rare — consider trauma (handlebar injury, non-accidental injury), structural disease (pancreas divisum, choledochal cyst, annular pancreas), systemic disease (cystic fibrosis, hypercalcaemia), drugs (valproate, corticosteroids), and infection (mumps). Manage in a specialist paediatric centre.[3]

The mantra, and the mnemonic

The mantra: two of three for the diagnosis, BISAP at the door, moderate Ringer's not a torrent, feed the gut, keep the antibiotic in the drawer — and wait four weeks before you drain.[1][2]

Ward-round test — three stems, thirty seconds each

Stem 1 — the woman from the top of the topic (answer)

The 52-year-old with epigastric pain boring to the back, vomiting, lipase over three times the upper limit of normal, and gallstones on ultrasound. What are your first three moves? Model: This is acute pancreatitis by two of three (pain plus enzymes) — no CT needed yet. (1) Admit, ABCDE, two large-bore cannulae, urinary catheter for hourly output. (2) Start goal-directed moderate lactated Ringer's at 10 to 15 mL/kg/h, reassessing against a falling haematocrit, normalising urea, and urine output over 0.5 mL/kg/h — not an aggressive bolus. (3) Score BISAP at the door, give adequate IV opioid analgesia, and plan early enteral feeding within 24 to 48 hours. The ALT is already pointing to a gallstone cause, so plan same-admission cholecystectomy once she settles.[1][2]

Stem 2 — the older man with a mildly raised amylase (answer)

A 74-year-old male smoker presents with severe epigastric and back pain, syncope, hypotension, and amylase mildly raised. What must you exclude before you accept the pancreatitis label? Model: Exclude a leaking abdominal aortic aneurysm. A pulsatile epigastric mass in an elderly vasculopath with tearing back pain and syncope, plus a mildly raised amylase, is an AAA until proven otherwise — and anticoagulating or fluid-loading the wrong diagnosis is a preventable death. Palpate the aorta, get a CT angiography. Mesenteric ischaemia is the other mimic that raises amylase — look for pain out of proportion and lactic acidosis. The amylase does not make it pancreatitis.[9]

Stem 3 — the necrosis that turns septic at week three (answer)

A patient with severe necrotising pancreatitis develops fever, raised inflammatory markers, and gas within the necrosis on CT at day 22. What is the diagnosis, the drug, and the timing of intervention? Model: This is infected necrosis — the leading cause of late death. Start a carbapenem (imipenem-cilastatin 500 mg IV every 6 hours or meropenem 1 g IV every 8 hours) now. But delay drainage around four weeks if the patient can be stabilised, so the collection walls off into walled-off necrosis and drains with less bleeding. Then pursue the step-up approach — percutaneous or endoscopic catheter drainage first, minimally invasive necrosectomy only if drainage fails. Open necrosectomy is the last resort. Routine prophylactic antibiotics were never indicated; these are therapeutic, for proven infection.[5][6]

References

1. [1]Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus Gut, 2013.PMID 23100216
2. [2]de-Madaria E, Buxbaum JL, Maisonneuve P, et al. Aggressive or Moderate Fluid Resuscitation in Acute Pancreatitis N Engl J Med, 2022.PMID 36103415
3. [3]Tenner S, Vege SS, Sheth SG, et al. American College of Gastroenterology Guidelines: Management of Acute Pancreatitis Am J Gastroenterol, 2024.PMID 38857482
4. [4]Wu BU, Johannes RS, Sun X, et al. The early prediction of mortality in acute pancreatitis: a large population-based study Gut, 2008.PMID 18519429
5. [5]van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis N Engl J Med, 2010.PMID 20410514
6. [6]Onnekink AM, Boxhoorn L, Timmerhuis HC, et al. Endoscopic Versus Surgical Step-Up Approach for Infected Necrotizing Pancreatitis (ExTENSION): Long-term Follow-up of a Randomized Trial Gastroenterology, 2022.PMID 35580661
7. [7]Poropat G, Goričanec K, Lacković A, et al. Systematic Review with Trial Sequential Analysis of Prophylactic Antibiotics for Acute Pancreatitis Antibiotics (Basel), 2022.PMID 36139970
8. [8]Tse F, Yuan Y. Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis Cochrane Database Syst Rev, 2012.PMID 22592743
9. [9]Boxhoorn L, Voermans RP, Bouwense SA, et al. Acute pancreatitis Lancet, 2020.PMID 32891214