Psychiatric Emergencies & Acute Agitation

Overview & Definition

A psychiatric emergency is any acute disturbance of thought, mood, perception or behaviour that requires immediate intervention to prevent serious harm to the patient or to others. The clinician at the bedside must hold three streams of thought simultaneously: (i) safety (the patient, the staff, other patients, the public); (ii) diagnosis (is this a primary psychiatric presentation, an organic/medical mimic, or a drug effect?); and (iii) law (does the patient have capacity? If not, under what authority can treatment proceed?). The single most dangerous cognitive error in this arena is treating a disturbed patient as "just psychiatric" without considering an organic cause — hypoglycaemia, hypoxia, intracranial bleed, encephalitis, sepsis and drug withdrawal all present with acute behavioural disturbance and kill silently while sedation is being delivered.[1]

The clinically distinct entities that constitute a psychiatric emergency, each with its own time-critical bundle, are:[5]

• Acute agitation and aggression — the most common; can complicate any psychiatric disorder, intoxication or delirium.
• Acute psychosis with risk (command hallucinations, persecutory delusions driving harm).
• Suicide attempt and suicidal crisis — every presentation of self-harm requires psychosocial assessment before discharge.
• Delirium — the most common cause of acute disturbance in medical, surgical and elderly inpatients.
• Drug-induced / substance-related agitation — stimulants, alcohol intoxication and withdrawal, novel psychoactive substances.
• Neuroleptic malignant syndrome (NMS) — antipsychotic-induced hyperthermic rigidity.
• Serotonin syndrome / serotonin toxicity — excess 5-HT from serotonergic polypharmacy.
• Lithium toxicity — narrow therapeutic index, common in overdose.
• Acute dystonia, akathisia — early antipsychotic movement emergencies.
• Catatonia and malignant catatonia — under-recognised, treatable, lethal if missed.
• Postpartum (puerperal) psychosis — onset within two weeks of delivery; dual risk of maternal suicide and infanticide.
• Excited delirium (acute behaviour disturbance in custody) — high sudden-death risk. [1]

The cardinal clinical principles — taught by NICE NG10 (2015), the BAP/NAPICU 2018 consensus and the American Project BETA consensus — are:[5]

1. Safety first: enough trained staff, a safe environment, weapons removed, panic alarms, police if firearms are involved.
2. De-escalation before medication: verbal techniques, environmental modification, offer oral medication, treat unmet needs (pain, hunger, fear).
3. Medication only if necessary, oral before IM: pharmacological calm, not chemical restraint.
4. Always exclude a medical cause: blood glucose, oxygenation, vital signs, neurological examination in every disturbed patient.
5. Capacity assessment and the lawful basis for any intervention: consent, Mental Capacity Act, Mental Health Act, or emergency common law. [1]

Classification

The emergencies fall into three pathophysiological families — useful because the family determines the drug class.[1][5]

[1] [5] [7] [11] [14] [16] [18] [22]

[4] [16] [11] [10]

Epidemiology & Risk Factors

Agitation occurs in a variety of medical and psychiatric conditions and, when severe, can result in behavioural dyscontrol — rapid tranquillisation exists precisely to calm such patients quickly, decrease dangerous behaviour and permit treatment of the underlying cause. The demographics and risk factors differ by syndrome:[1][5]

• Acute agitation/aggression: prior violence, intoxication (especially alcohol and stimulants), active psychosis with persecutory delusions or command hallucinations, non-adherence with treatment, antisocial/borderline personality traits, younger age, male sex, social isolation and recent loss.
• Acute psychosis with risk: schizophrenia, bipolar mania, psychotic depression; risk heightened by comorbid substance use, recent relapse, recent discharge, command hallucinations to harm.
• Suicide attempt: previous attempt (the single strongest risk factor for completed suicide); active depressive or bipolar illness; hopelessness; intoxication; recent loss or crisis; access to lethal means (firearms in USA, pesticides/organophosphates in rural Asia, hanging globally). Completed suicide is the leading cause of psychiatric-emergency death.
• Neuroleptic malignant syndrome: reported with virtually all neuroleptics, including newer atypicals, and with other drugs affecting central dopaminergic neurotransmission (including withdrawal of dopamine agonists). Uncommon, but requires prompt recognition to prevent significant morbidity and death; predictors of mortality are failure to stop the antipsychotic, respiratory problems, severity of hyperthermia and older age.[4][6][8]
• Serotonin syndrome/serotonin toxicity: a wide range of drugs has been implicated — the classical interaction is between serotonergic agents and monoamine oxidase inhibitors; toxicity represents a spectrum from mild to life-threatening, and the true incidence is unknown because there is no consensus diagnostic threshold.[23][26]
• Lithium toxicity: narrow therapeutic index; toxicity burden drives non-adherence; renal, thyroid and parathyroid effects necessitate periodic blood monitoring; risk rises with dehydration, renal impairment and interacting drugs.[13]
• Acute dystonia: about 2.5 percent of patients develop acute dystonia within 48 hours of commencing neuroleptic therapy; symptoms remit on drug withdrawal or with anticholinergic therapy.[14]
• Postpartum psychosis: a psychiatric emergency that generally warrants acute inpatient care; marked by sudden onset of affective and psychotic symptoms with rapid deterioration, on the bipolar-disorder spectrum.[2]
• Catatonia: under-recognised and treatable — in the landmark prospective series 16 of 21 patients (76 percent) resolved on a systematic lorazepam trial, and ECT rescued those who failed; a positive parenteral challenge predicts lorazepam response.[16]
• Delirium: an important organic mimic in every disturbed patient; antipsychotic use in dementia carries increased mortality (conventional agents at least as hazardous as atypicals), so drug treatment is a carefully weighed, low-dose, short-duration decision.[25]

Pathophysiology

The molecular and circuit-level mechanism unifies the whole topic: [1]

Acute agitation and psychosis. At the circuit level, the disturbance is a hyperactive amygdala-driven threat-detection system with loss of top-down inhibitory control from the prefrontal cortex. Three neurotransmitters dominate. Dopaminergic mesolimbic hyperactivity drives the positive symptoms of psychosis (delusions, hallucinations, paranoia) and contributes to aggression — this is why D2 receptor blockade with antipsychotics is effective. GABAergic underactivity in the limbic system removes inhibitory tone, allowing arousal, fear and motor activation to run unchecked; this is why benzodiazepines (positive allosteric modulators of GABA-A) are effective across nearly every psychiatric emergency. Noradrenergic excess produces the autonomic hyperarousal — tachycardia, hypertension, mydriasis, diaphoresis — seen in agitation, NMS, serotonin syndrome and excited delirium.[1]

Neuroleptic malignant syndrome. NMS is an acute, profound reduction in central dopaminergic tone, most often from sudden D2 receptor blockade (high-potency antipsychotics, depot, or rapid dose escalation) but also from rapid withdrawal of dopamine agonists in Parkinson disease. The consequence is hypothalamic thermoregulatory failure (hyperthermia), basal ganglia rigidity (lead-pipe), autonomic instability (tachycardia, labile blood pressure, diaphoresis, incontinence) and conscious-state depression. The downstream cascade — sustained muscle contraction generating heat, rhabdomyolysis, acute kidney injury, hyperkalaemia, disseminated intravascular coagulation — is what kills. The mechanism parallels malignant hyperthermia clinically but is central (D2 blockade) rather than peripheral (ryanodine receptor), which is why dantrolene works symptomatically in both but bromocriptine is specific to NMS.[4]

Serotonin syndrome (serotonin toxicity). Excessive 5-hydroxytryptamine (5-HT, serotonin) activity in the central and peripheral nervous systems, mediated principally through 5-HT2A and 5-HT1A receptors. The neuromuscular findings (clonus, hyperreflexia, rigidity) reflect 5-HT excess in the spinal cord and brainstem; the autonomic findings (hyperthermia, tachycardia, mydriasis, diaphoresis, diarrhoea) reflect peripheral 5-HT receptor activation. Onset is within hours of a serotonergic agent — classically an SSRI added to an MAOI, or a combination of tramadol/linezolid/triptan with an SSRI/SNRI. The molecular distinction from NMS is fundamental: serotonin toxicity is 5-HT excess with hyperreflexia and clonus; NMS is dopamine deficit with rigidity and bradyreflexia.[3]

Acute dystonia. D2 receptor blockade in the nigrostriatal pathway produces relative cholinergic (muscarinic) overactivity, which drives sustained involuntary muscle spasm. The classic presentations are torticollis, oculogyric crisis, oromandibular dystonia, opisthotonos and — most dangerously — laryngospasm with stridor. Treatment is an anticholinergic (procyclidine, benztropine, diphenhydramine), which restores the dopamine/acetylcholine balance.[1]

Akathisia. D2 blockade produces a subjective, intensely unpleasant inner restlessness with objective movement (pacing, leg crossing). Network meta-analysis of double-blind trials shows mirtazapine, biperiden and vitamin B6 have the greatest efficacy, with propranolol (20 mg/day in trials) an effective alternative — akathisia occurs in 14 to 35 percent of patients on antipsychotics and is associated with increased suicidality and decreased adherence.[15]

Catatonia. A syndrome of GABA-A hypofunction and glutamate excess in the frontal cortex and basal ganglia, manifesting as motor dysregulation (stupor, posturing, waxy flexibility, negativism, catalepsy) and — in malignant catatonia — autonomic instability and hyperthermia indistinguishable from NMS. The reason benzodiazepines and ECT work is exactly this GABA-A deficiency; lorazepam restores inhibitory tone, ECT produces a profound GABAergic reset.[16]

Excited delirium (acute behaviour disturbance in custody). Characterised by delirium, agitation, acidosis and hyperadrenergic autonomic dysfunction, typically in the setting of acute-on-chronic drug abuse, serious mental illness, or both; a proportion die suddenly from cardiac arrest despite optimal therapy. The treatment emphasis is chemical sedation over physical restraint, with aggressive management of hyperthermia and acidosis — sudden cardiovascular collapse can occur with little warning.[21][22]

Lithium toxicity. Lithium has a narrow therapeutic index. Toxicity is through CNS accumulation — tremor, gastrointestinal upset, ataxia, dysarthria, confusion and, at high levels, reduced consciousness and seizures. Lithium is dialyzable (level of evidence A), so extracorporeal removal — haemodialysis preferred — is the definitive treatment in severe poisoning.[11][12][13]

Clinical Presentation

The presentations divide by syndrome. Each has classic, often highly characteristic, features and a set of atypical presentations in special populations.[1][3][4]

Acute agitation/aggression. Pacing, shouting, threatening, posturing, clenched fists, throwing objects, weapon access. The patient may be too aroused to give a history; collateral is essential. Risk is imminent when threats name a target or when command hallucinations are present. [1]

Acute psychosis with risk. Persecutory delusions ("the police are coming"), passivity phenomena ("my thoughts are being controlled"), thought broadcasting, and — most importantly for risk — command hallucinations directing harm to self or others. Insight is impaired; the risk is when content drives action. [1]

Suicide attempt. Presentation is by method: overdose (drowsy/agitated, post-paracetamol asymptomatic early — danger of late presentation), hanging (hypoxic brain injury, laryngeal fracture), wrist cutting, organophosphate ingestion (cholinergic toxidrome — miosis, salivation, lacrimation, fasciculations, bronchorrhoea, seizures), jumping (multiple trauma). Always reassess suicide risk once medically stable. [1]

Neuroleptic malignant syndrome — the NMS tetrad. Rigidity, hyperthermia (consensus critical value: over 38.0 °C on at least 2 occasions), altered mental status and autonomic dysfunction (sympathetic nervous system lability, tachycardia plus tachypnea), on a background of recent dopamine-antagonist exposure or dopamine-agonist withdrawal, with a negative work-up for other causes. Laboratory hallmarks: creatine kinase elevation to at least 4 times the upper limit of normal, leukocytosis and transaminitis (LDH, AST), typically with a low serum iron — a profile that distinguishes NMS from serotonin syndrome.[4][6][7]

Serotonin syndrome — the triad. (i) Neuromuscular: clonus (spontaneous, inducible or ocular), hyperreflexia, tremor; (ii) autonomic: hyperthermia, diaphoresis; (iii) mental state: agitation, altered mental status — the Hunter criteria found these five features alone predicted clinical toxicologist-diagnosed serotonin toxicity, with hypertonicity and maximum temperature over 38 °C universal in life-threatening cases. Onset follows exposure to serotonergic agents; the classical trigger is a serotonergic drug combined with a monoamine oxidase inhibitor.[10][23][26][3]

Lithium toxicity. Tremor, gastrointestinal upset (nausea, diarrhoea), ataxia, dysarthria, confusion, progressing at high levels to reduced consciousness, seizures and dysrhythmias. Extracorporeal treatment is recommended when kidney function is impaired and the level is over 4.0 mEq/L, or with decreased level of consciousness, seizures or life-threatening dysrhythmias irrespective of the level; it is suggested above 5.0 mEq/L, with significant confusion, or when the expected time to bring the level under 1.0 mEq/L exceeds 36 hours.[11][13]

Acute dystonia. Sudden-onset (typically within 48 hours of the first dose) sustained muscle spasm: torticollis, oculogyric crisis (eyes forced upward and sideways), oromandibular dystonia (tongue protrusion, jaw clenching), opisthotonos (severe arching), or laryngospasm (life-threatening stridor). About 2.5 percent of patients started on a neuroleptic are affected; the syndrome remitting on drug withdrawal or with anticholinergic therapy is the diagnostic response.[14]

Akathisia. Subjective inner restlessness with objective movement — pacing, leg crossing, inability to sit still — typically within days of starting or increasing an antipsychotic. It is dose-dependent and carries a high association with suicidality if unrecognised. [1]

Catatonia (DSM-5: 12 features, ≥3 required). Stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerisms, stereotypy, agitation (not influenced by external stimuli), grimacing, echolalia, echopraxia. Malignant catatonia adds fever and autonomic instability; it overlaps phenotypically with NMS (and may be the same entity). [1]

Postpartum psychosis. The cardinal prodrome is insomnia for two or more nights despite exhaustion. This is followed by rapid onset of delusional beliefs about the infant ("the baby is not mine", capgras-type), perceptual abnormalities (auditory hallucinations with threat content), and a labile or expansive mood (mixed affective–psychotic picture). The dual risks are maternal suicide and infanticide, which classically occur in the context of the delusional beliefs.[2]

Alcohol withdrawal and delirium tremens. Coarse tremor, autonomic hyperarousal, visual hallucinations (classically animals — Lilliputian), withdrawal seizures (typically 6 to 48 hours after last drink), and — at 48 to 96 hours — delirium tremens (full delirium, marked autonomic instability, mortality 5 percent untreated). Wernicke encephalopathy presents with the triad of ataxia, ophthalmoplegia (nystagmus or sixth-nerve palsy) and confusion — but only about 10 percent of cases present with the complete triad. [1]

Atypical presentations. The elderly commonly present with quiet delirium, falls, new incontinence or wandering rather than agitation. The pregnant and postpartum patient may conceal intent through shame. The intellectually disabled or autistic patient may show behavioural change rather than verbalised distress. The diabetic with hypoglycaemia may present combative and appear intoxicated; the post-ictal patient may be aggressive. The implication is universal: check the glucose, check the oxygen saturation, examine neurologically and exclude an organic cause before sedation.[5]

Differential Diagnosis

The most important diagnostic step in any psychiatric emergency is to exclude an organic (medical) cause. The standard frame is the functional vs organic distinction, refined for each syndrome.[1][3][4]

[1] [7] [10] [23]

A few specific distinctions worth memorising:[3][4]

• Acute dystonia vs tetanus vs strychnine vs hypocalcaemic tetany: dystonia is focal, sustained and drug-induced; tetanus has trismus, risus sardonicus and opisthotonos with a wound; strychnine causes symmetrical tetany with intact sensorium; tetany has carpopedal spasm and Trousseau/Chvostek signs.
• Postpartum psychosis vs baby blues vs postnatal depression vs postpartum thyroiditis vs postpartum eclampsia: blues are transient (days 3–5), resolve spontaneously, with preserved bonding; PND is over 2 weeks, with pervasive low mood/anhedonia, no psychosis; thyroiditis has lab abnormalities; eclampsia has seizures, hypertension and proteinuria.
• Agitation vs akathisia vs restless legs vs intoxication: akathisia is drug-induced, recent-onset, with subjective restlessness; intoxication has toxidrome features. [1]

Clinical & Bedside Assessment

The structured assessment in a psychiatric emergency proceeds in a fixed sequence, regardless of the underlying cause.[1][5]

1. Scene safety. Before approaching, ensure: enough trained staff (at least four or five for a restraint team), no weapons visible (ask the patient to relinquish any), a single exit and a clear escape route for staff, panic alarm within reach, removal of objects that could be thrown, and police attendance if a firearm or knife is involved. Never turn your back on an agitated patient; never examine in a confined space alone. [1]

2. ABCDE primary survey — every disturbed patient. Airway patent; Breathing (rate, SpO2, signs of respiratory distress); Circulation (heart rate, blood pressure, capillary refill, signs of injury or bleeding); Disability — Glasgow Coma Scale, blood glucose (BM) and pupils — and Exposure (temperature, signs of trauma, needle marks, hydration). A finger-prick blood glucose is mandatory in every disturbed or unconscious patient because hypoglycaemia mimics anything and is instantly reversible. [1]

3. De-escalation (Project BETA consensus, 2012). The ten core techniques: respect personal space; do not be provocative (no crossed arms, no direct confrontation); establish verbal contact with a single trained staff member; use concise, simple language; identify wants and feelings ("help me understand what you need"); listen closely to what the patient says; agree or agree to disagree ("I understand you are frightened"); set limits clearly; debrief afterwards; offer choices, including oral medication. The aim is to defuse arousal without triggering further escalation. [1]

4. Risk assessment. Structured enquiry: (a) Self-harm/suicide — ideation, intent, plan, access to means, preparatory acts (giving away possessions, writing a note), recent attempt, protective factors; (b) harm to others — threats, weapon access, identifiable victim, command hallucinations to harm, history of violence; (c) self-neglect — refusal to eat/drink, inability to care for self; (d) vulnerability — child safeguarding, elder abuse, domestic abuse, exploitation. Use the Columbia Suicide Severity Rating Scale (C-SSRS) for a structured suicidal-risk assessment. [1]

5. Mental state examination (MSE). Appearance and behaviour (posture, eye contact, motor activity), speech (rate, volume, fluency), mood (subjective and objective — and ask directly about suicidal and homicidal ideation), thought (form — flight of ideas, thought block; content — delusions, obsessions, overvalued ideas), perception (hallucinations — modality, content, third-person vs second-person vs command), cognition (attention — months of the year backwards; orientation — time, place, person — to exclude delirium), and insight. [1]

6. Collateral history. Carers, family, GP, prior psychiatric records, current medications (specifically: recent antipsychotic initiation, lithium therapy, serotonergic combinations), substance use, recent physical illness or surgery, and recent life events. [1]

7. Capacity assessment. Two-stage test under the Mental Capacity Act 2005 (England & Wales): Stage 1 (diagnostic) — is there an impairment of, or disturbance in the functioning of, the mind or brain? (mental disorder, intoxication, delirium, dementia, head injury); Stage 2 (functional) — does the impairment mean the person is unable to make the decision? They are unable if they cannot do any one of: understand the information, retain it (long enough to decide), weigh or use it in the balance, or communicate the decision (by any means). Capacity is decision-specific and time-specific, and is presumed until shown otherwise. [1]

8. Specific bedside manoeuvres for the drug-induced emergencies: [1]

• Inducible clonus at the ankle: with the knee flexed, rapidly dorsiflex the foot — sustained rhythmic contractions indicate 5-HT excess (serotonin syndrome).
• Tone at wrists and elbows: lead-pipe rigidity (sustained, uniform resistance through the range) indicates NMS.
• Reflex testing: hyperreflexia, especially lower-limb and asymmetric (lower greater than upper) in serotonin syndrome; bradyreflexia or normal reflexes in NMS.
• Pupil size and reactivity: mydriasis in serotonin syndrome and anticholinergic toxicity; miosis in opioid or organophosphate toxicity.
• Skin: dry and hot in NMS, anticholinergic toxicity, heat stroke; diaphoretic in serotonin syndrome and alcohol withdrawal. [1]

9. Recognise excited delirium. Agitation with hyperthermia, metabolic acidosis and struggling against restraint — high sudden-death risk. Treat with benzodiazepines, cooling and intravenous fluids; do not allow prolonged prone restraint (positional asphyxia). Continuous SpO2 and cardiac monitoring.[5]

Investigations

Investigations serve two purposes: excluding organic causes and confirming the specific syndrome (NMS, serotonin syndrome, lithium toxicity). The clinician must be careful: many psychiatric-emergency tests are not diagnostic but confirmatory.[4][7][23]

Bedside. Blood glucose (every disturbed patient); ECG (prolonged QRS in TCA overdose, QTc prolongation with antipsychotics, T-wave changes with lithium); urine drug screen; pregnancy test (β-hCG) in any woman of reproductive age; temperature; alcohol breathalyser or salivary assay. [1]

Bloods. Full blood count (leukocytosis in NMS, sepsis); urea and electrolytes (renal function — drives lithium clearance and the extracorporeal-treatment decision); liver function tests (LDH, AST elevation in NMS); creatine kinase (consensus NMS critical value: at least 4 times the upper limit of normal; rhabdomyolysis); serum iron (low in NMS — a discriminator from serotonin syndrome); glucose; calcium; magnesium; phosphate; thyroid-stimulating hormone; C-reactive protein; troponin; lactate; lithium level (extracorporeal-treatment thresholds apply to measured concentration with renal function); paracetamol and salicylate levels in overdose.[4][7][11]

Septic and infection screen. Blood cultures; mid-stream urine; chest X-ray; lumbar puncture if meningitic signs or HSV encephalitis suspected (fever, seizure, new confusion) — cerebrospinal fluid for cells, protein, glucose, MCV PCR (HSV), bacterial culture. [1]

Neuroimaging. CT brain if first psychiatric presentation, focal neurology, head injury, anticoagulation, or any atypical feature — to exclude subdural, intracerebral bleed, mass lesion or hydrocephalus. [1]

EEG if non-convulsive status epilepticus suspected (subtle fluctuating conscious state, post-ictal confusion) or to objectively confirm delirium (generalised slowing). [1]

Named diagnostic criteria (reproduce verbatim)

[16] [1]

Important caveat on suicide-risk scales. No blood test, biomarker, rating scale or algorithm has sufficient positive predictive value to predict individual suicide. Scales (C-SSRS, SAD PERSONS, Beck Hopelessness Scale) structure and document assessment but cannot substitute for clinical judgement — an international consensus concluded that available assessment instruments need further validation of utility, reliability and validity. [1][5]

Management — Resuscitation

Resuscitation in psychiatric emergencies is time-critical, syndrome-specific and never "give a sedative".[1][3][4][5]

The disturbed/agitated patient — universal resuscitation bundle

1. Scene safety — staff (at least four to five for restraint), weapons removed, environment secured, police if firearm.
2. ABCDE — oxygen if hypoxic; IV access if needed; blood glucose early.
3. De-escalation — Project BETA techniques; offer oral medication; treat unmet needs (pain, hunger, fear).
4. Rapid tranquillisation if oral refused and risk is imminent (see Definitive management).
5. Post-IM monitoring — blood pressure, pulse, respiratory rate, SpO2, temperature and consciousness every 15 minutes for 1 hour after IM administration; ECG if high-dose or cardiac history. [1]

NMS resuscitation

• STOP the antipsychotic immediately (and any other dopamine antagonist) — failure to stop it is an independent predictor of death.
• Supportive measures: active cooling, IV fluids, and intensive monitoring of rigidity, temperature, renal function and respiratory status.
• Dantrolene — the most effective evidence-based drug treatment for NMS (per the SS-vs-NMS contrast review), used in more severe cases alongside supportive care.
• Benzodiazepines and other pharmacological interventions (e.g. dopamine agonists such as bromocriptine) are described for more severe cases; supportive care remains the backbone.
• Do not reintroduce the antipsychotic during the acute episode — a 2-week neuroleptic washout minimises the chance of recurrence.
• ICU for severe cases; early recognition and treatment keep mortality low. [6][7][8]

Serotonin syndrome resuscitation

• STOP all serotonergic agents immediately — discontinuation of the causative agent plus supportive care is the primary treatment.
• Supportive care first: benzodiazepines for agitation and neuromuscular excitation, active cooling and IV fluids — there are no evidence-based drug treatments for serotonin syndrome beyond supportive care.
• Cyproheptadine — a 5-HT receptor antagonist adjunct described in a five-patient case series, dosed 4 to 8 mg orally with resolution of signs (three complete resolutions); oral/NG only.
• Antipyretics are ineffective — the hyperthermia is muscle-generated, not prostaglandin-mediated.
• Severe (life-threatening) toxicity: hypertonicity and temperature over 38 °C were universal in life-threatening cases — intubation, neuromuscular paralysis and aggressive cooling in ICU.
• Most mild-to-moderate cases resolve with supportive care once the agent is stopped.[9][10][23][26][3]

Lithium toxicity resuscitation

• STOP lithium and correct volume depletion — management is based on the renal handling of lithium.
• IV normal saline — volume expansion to enhance renal lithium clearance.
• Extracorporeal treatment (haemodialysis preferred; continuous RRT acceptable): recommended in severe poisoning; if kidney function is impaired and the level is over 4.0 mEq/L; or with decreased consciousness, seizures or life-threatening dysrhythmias irrespective of the level. Suggested if the level is over 5.0 mEq/L, significant confusion, or expected time to bring the level under 1.0 mEq/L exceeds 36 hours. Continue until clinical improvement or a level under 1.0 mEq/L; a minimum of 6 hours if the level is not readily measurable — rebound after dialysis reflects redistribution, so repeat sessions and re-check levels.[11][12][13]

Acute dystonia

• Anticholinergic therapy (e.g. procyclidine or diphenhydramine) — acute dystonia remits with anticholinergic treatment (or drug withdrawal), typically rapidly; the response is itself diagnostic.
• Review the antipsychotic: reduce the dose, switch agent, or add prophylactic cover for subsequent exposures.[14]

Akathisia

• Reduce or switch the antipsychotic where possible.
• Drug options with placebo-beaten efficacy in double-blind trials: mirtazapine (15 mg/day), biperiden (6 mg/day), vitamin B6 (600–1200 mg/day) — the greatest efficacy, with vitamin B6 the best tolerated; trazodone (50 mg/day), mianserin (15 mg/day) and propranolol (20 mg/day) are effective alternatives.
• Cyproheptadine, clonazepam, zolmitriptan and valproate did not beat placebo in the network meta-analysis.[15]

Catatonia

• Parenteral lorazepam challenge: an initial intravenous challenge with a positive response predicts final lorazepam response.
• Definitive: systematic parenteral and/or oral lorazepam for up to 5 days — 16 of 21 patients (76 percent) completing a lorazepam trial had full resolution of catatonic signs.
• ECT: the four patients failing lorazepam in the landmark series responded promptly to ECT — the treatment of malignant or refractory catatonia.[16]

Wernicke encephalopathy

• Parenteral B-vitamin (thiamine) treatment BEFORE any glucose — Royal College of Physicians guidance: patients with chronic alcohol misuse and suspected poor diet showing (or at risk of) Wernicke encephalopathy should receive B vitamins intravenously or intramuscularly at the outset, especially when clinical signs are masked by intoxication; give glucose only after thiamine to avoid precipitating Wernicke–Korsakoff syndrome.[24]

Excited delirium

• Chemical sedation over physical restraint — patients may benefit from chemical rather than physical restraint; sudden cardiovascular collapse can occur with little warning and laboured breathing may precede death, so prompt airway and haemodynamic control is key.
• Benzodiazepines titrated to arousal are first-line.
• Ketamine 5 mg/kg IM was superior to haloperidol 10 mg IM for time to sedation in a prospective prehospital study (median 5 vs 17 minutes) — but with complications in 49 percent (hypersalivation, emergence reactions, vomiting, laryngospasm) and a 39 percent intubation rate: an emerging option requiring airway monitoring.
• Aggressively manage hyperthermia and acidosis (cooling, IV fluids).
• ICU for severe cases. [20][21][22]

Restraint (if absolutely necessary)

Last resort only, under NICE NG10 (2015): minimum force, trained team, supine or lateral — never prolonged prone, time-limited (review every 15 minutes), documented, with a clear legal basis (Mental Health Act or common-law emergency), and a formal debrief for patient and staff afterwards. [1]

Management — Definitive & Stepwise

Rapid tranquillisation ladder (BAP/NAPICU 2018; NICE NG10; Maudsley Guidelines)

The ladder proceeds in five steps; the cardinal rule is oral before IM, and never combine IM olanzapine with parenteral lorazepam.[1][5][18]

[1] [5] [17] [18] [19]

Post-IM monitoring (mandatory)

After IM rapid tranquillisation, monitor regularly with blood pressure, pulse, respiratory rate, SpO2, temperature and consciousness level; add an ECG when high-dose, cardiac history, electrolyte abnormality or QTc-prolonging combinations (haloperidol + promethazine). The main complications to detect are respiratory depression (especially after benzodiazepine combinations), postural hypotension and QTc prolongation with Torsades de Pointes — in the TREC trials each regimen produced a serious adverse event (one grand-mal seizure on haloperidol-promethazine, one transient respiratory depression on midazolam).[1][5][18][19]

Syndrome-specific definitive management

Acute psychosis with risk. Rapid tranquillisation agents per the ladder above (IM haloperidol 5–10 mg ± promethazine up to 50 mg, or IM/parenteral alternatives) control the immediate disturbance while treating the underlying disorder. Urgent psychiatric admission under the Mental Health Act if the patient lacks capacity, refuses treatment and risk is significant. Treat the underlying disorder (see the schizophrenia, bipolar and depression topics). Address substance use if relevant.[1][5][18]

Suicide attempt and self-harm. Medical stabilisation first (treat the overdose or injury). Then, before discharge, a psychosocial assessment by a trained clinician (NICE NG225, 2022): understand the patient's history, current circumstances, mental state, suicidal intent and risk, protective factors, and social context; explore the function of the self-harm. Treat the underlying disorder (depression, bipolar, borderline personality disorder). Build a safety plan (Stanley & Brown). Counsel on means restriction. Arrange follow-up within 7 days (the highest-risk window for repeat attempt is the first 1 to 2 weeks). Do not use no-suicide contracts — they have no protective value and may falsely reassure.[5]

Postpartum psychosis. Emergency admission — postpartum psychosis is a psychiatric emergency that generally warrants acute inpatient care, ideally a mother-and-baby unit so mother and infant remain together under supervised care. Exclude an organic cause. Pharmacological therapy is the mainstay of the acute phase: the best evidence supports a combination of antipsychotics and lithium; ECT can offer a rapid response where required. Once the acute episode settles, lithium has the best evidence for relapse prevention and prophylaxis; psychoeducation is essential and bipolar-style psychosocial interventions may help.[2]

Acute dystonia. Anticholinergic therapy (procyclidine or diphenhydramine) — the dystonia remits on withdrawal of the drug or with anticholinergic treatment; review antipsychotic choice and dose.[14]

NMS. See resuscitation. A 2-week neuroleptic washout minimises the chance of recurrence; when restarting, use the lowest effective dose with careful monitoring and informed consent. Document the previous reaction prominently in the chart.[7]

Serotonin syndrome. See resuscitation. After recovery, review the serotonergic medication regimen carefully — supportive care and stopping the agent resolve the acute episode, but the underlying polypharmacy must be addressed to prevent recurrence; case-series experience with cyproheptadine supports its adjunctive role.[9][23]

Lithium toxicity. See resuscitation. After recovery, review the indication, dose, renal and thyroid function, parathyroid status, concurrent medications and adherence — lithium's side-effect and toxicity burden is a key driver of non-adherence.[13]

Catatonia. A parenteral lorazepam challenge (a positive response predicts treatment response), then systematic lorazepam for up to 5 days; ECT for patients who fail lorazepam (prompt response in the landmark series) or for malignant catatonia. Treat the underlying cause (psychiatric, organic, drug-induced).[16]

Delirium. Treat the cause (infection, metabolic, hypoxia, drug, withdrawal, impaction, urinary retention, pain). Non-pharmacological measures first: orientation cues, sensory aids, mobilisation, sleep hygiene, family at bedside. If drug therapy is needed for severe distress, use the lowest dose for the shortest time — cohort data show increased all-cause mortality with both conventional and atypical antipsychotics in dementia (conventional agents at least as hazardous), and special caution applies in Parkinson disease and dementia with Lewy bodies. Avoid benzodiazepines except in alcohol or benzodiazepine withdrawal.[25]

Alcohol withdrawal and delirium tremens. Symptom-triggered benzodiazepine therapy using a validated withdrawal scale, titrated to symptom control; severe withdrawal or delirium tremens needs parenteral benzodiazepines with intensive monitoring. Parenteral B vitamins (thiamine) at the outset, before glucose, per Royal College of Physicians guidance, to prevent Wernicke–Korsakoff syndrome.[24]

Escalation triggers for ICU

• Sustained hyperthermia (greater than 40 °C) not responding to cooling
• Rigidity unresponsive to benzodiazepines
• Rising creatine kinase or acute kidney injury
• Cardiac instability (arrhythmia, ischaemia, hypotension)
• Hypercapnia or respiratory depression (post-sedation or from rigidity)
• Status epilepticus [1]

Disposition and discharge criteria

• ED short-stay / medical admission if medically unstable (overdose, head injury, sepsis).
• Psychiatric inpatient if active suicidal/homicidal risk, severe psychosis, inability to care for self.
• Crisis Resolution Home Treatment Team (CRHT) for moderate risk in the community, with daily contact.
• Outpatient follow-up within 7 days for low-risk discharges; ALL patients receive a safety plan, crisis contacts, means restriction, and carer involvement (with consent / capacity).
• Document the risk formulation, the capacity assessment, and the lawful basis for any non-consensual intervention. [1]

Specific Subtypes & Scenarios

Each major psychiatric emergency has its own time-critical pathway; this section collates them.[1][2][3][4]

Acute agitation/aggression (general adult psychiatry setting). De-escalation first, oral medication offered before parenteral; IM only if refused or risk imminent. The objective is calm, not deep sedation. [1][5]

Acute psychosis with command hallucinations or persecutory delusions. Risk is identified when the content drives harm — a hallucination directing the patient to harm a named person, or a delusion that a family member is a persecutor. Antipsychotic via the rapid-tranquillisation ladder plus urgent admission under the Mental Health Act if capacity/refusal is an issue. [1][18]

Suicidal crisis / post-attempt. Every patient who has attempted suicide or self-harmed receives a psychosocial assessment before discharge. Treat the underlying disorder. Means restriction. Safety planning. Early follow-up. [1][5]

Drug-induced / substance-related agitation. Stimulants (cocaine, methamphetamine) — excited delirium pathway: chemical sedation with benzodiazepines, aggressive cooling and management of acidosis, prompt airway and haemodynamic control. Cannabis and hallucinogens — usually supportive, benzodiazepine if severely agitated. Novel psychoactive substances — unpredictable, supportive. Always rule out delirium and medical complications. [21][22]

Delirium. Find and treat the cause; non-pharmacological measures first; drug therapy only for severe distress, lowest dose, shortest time — antipsychotics increase mortality in dementia. [25]

Neuroleptic malignant syndrome. Stop the antipsychotic, supportive care, dantrolene (best-evidenced drug) with other pharmacological options in severe cases; 2-week washout before considering rechallenge. [6][7]

Serotonin syndrome. Stop serotonergic agents, supportive care, benzodiazepines, cyproheptadine (case series) if needed. [9][23][26]

Wernicke encephalopathy presenting as acute confusion. Give parenteral B vitamins before any glucose-containing fluid; this is a clinical diagnosis, not a radiological one. [24]

Lithium toxicity. Stop lithium, isotonic saline, extracorporeal treatment per EXTRIP criteria (haemodialysis preferred). [11][12]

Acute dystonia. Anticholinergic (procyclidine or diphenhydramine) — remits with treatment or drug withdrawal. [14]

Akathisia. Mirtazapine, biperiden or vitamin B6 have the greatest trial efficacy; propranolol among effective alternatives. [15]

Catatonia / malignant catatonia. Lorazepam (parenteral challenge, then systematic trial) ± ECT. [16]

Postpartum psychosis. Emergency admission (mother-and-baby unit where available); antipsychotic + lithium best evidence; ECT for rapid response; lithium for prophylaxis. [2]

Excited delirium. Chemical sedation (benzodiazepines; ketamine 5 mg/kg IM an emerging but complication-prone option), cooling, fluids, ICU; manage acidosis and hyperthermia aggressively. [20][21]

Emergency in children and adolescents (CAMHS). Use lower, specialist-protocol dosing; involve parents/guardians; consider Gillick competence and parental responsibility; minimise restraint; rule out abuse as a driver. [5]

Emergency in pregnancy and postpartum. Postpartum psychosis: antipsychotics and lithium are the best-evidenced acute treatment, ECT can offer rapid response, and lithium has the best prophylactic evidence — plan pregnancy care with specialist input to balance teratogenic and relapse risks. [2]

Emergency in intellectual disability and autism. Behaviour may be communication of pain or distress; sensory-adjusted environment (low stimulation, single room); involve familiar carers; use specialist learning-disability psychiatry; recognise behavioural equivalents of psychiatric symptoms. [1]

Complications & Pitfalls

Mortality remains the central concern: completed suicide; NMS — failure to stop the antipsychotic, respiratory problems, severity of hyperthermia and older age predict death; life-threatening serotonin toxicity — hypertonicity with temperature over 38 °C; lithium poisoning — decreased consciousness, seizures and dysrhythmias drive the extracorporeal-treatment decision; excited delirium — sudden cardiac death despite optimal therapy; untreated postpartum psychosis — maternal suicide and infanticide risk.[2][6][8][10][11][22]

Morbidity: rhabdomyolysis and acute kidney injury (NMS, serotonin syndrome, excited delirium, prolonged restraint); hypoxic brain injury after hanging or post-overdose cardiac arrest; contractures and pressure injury from prolonged restraint; trauma to staff and patient; psychological trauma for the patient. [1]

Complications of rapid tranquillisation: over-sedation; respiratory depression (especially with lorazepam + olanzapine combinations, which is why they must never be combined parenterally); postural hypotension (haloperidol, olanzapine); QTc prolongation with Torsades de Pointes (haloperidol, droperidol, especially IV and in elderly/electrolyte-abnormal patients); acute dystonia (early); akathisia (days); NMS (days to weeks); falls and aspiration. [1]

Complications of restraint: positional asphyxia (especially prone), rhabdomyolysis, mechanical injury, psychological trauma, staff injury, and medico-legal consequences. [1]

Legal and medico-legal pitfalls: unlawful restraint; failure to assess capacity; failure to use the Mental Health Act correctly; missed medical cause; wrong-patient or wrong-drug medication error; discharge of a high-risk patient without a safety plan or follow-up; breach of confidentiality to family without consent (except where risk to others mandates disclosure); failure to involve an Independent Mental Capacity Advocate (IMCA) for an unbefriended patient lacking capacity. [1]

[1]

Prognosis & Disposition

Prognosis depends on the syndrome and, above all, on how quickly the causative drug is stopped or the underlying cause treated. The key prognostic features by syndrome:[6][8]

• NMS: stopping the antipsychotic reduces mortality; independent predictors of death are failure to discontinue, respiratory problems, severity of hyperthermia and older age. Early recognition and treatment keep mortality low; a 2-week washout minimises recurrence.[6][7][8]
• Serotonin syndrome: discontinuation of the agent plus supportive measures is primary treatment; toxicity is a spectrum from mild to life-threatening, with hypertonicity and temperature over 38 °C universal in life-threatening cases.[10][26]
• Postpartum psychosis: early detection and prompt treatment with antipsychotics and lithium, followed by lithium maintenance, is associated with a favourable prognosis; lithium has the best evidence for relapse prevention.[2]
• Suicidal crisis: structured follow-up and safety planning matter more than risk scores — assessment instruments need further validation of predictive utility.[5]
• Catatonia: 16 of 21 patients (76 percent) completing a lorazepam trial resolved; the four lorazepam failures responded promptly to ECT; longer duration of symptoms before treatment predicts poorer lorazepam response.[16]
• Acute dystonia: remits on drug withdrawal or anticholinergic therapy.[14]
• Lithium toxicity: haemodialysis is the cornerstone for severe poisoning; extracorporeal treatment continues until clinical improvement or a level under 1.0 mEq/L.[11][12]

Disposition options (matched to risk): [1]

• Emergency department short-stay / medical admission — medical stabilisation (overdose, head injury, sepsis, delirium).
• Psychiatric inpatient — active suicidal or homicidal risk, severe psychosis, inability to care for self, postpartum psychosis (to a MBU).
• Crisis Resolution Home Treatment Team (CRHT) — moderate risk in the community, with daily contact and rapid access back to ward.
• Outpatient follow-up within 7 days — low-risk discharge; ALL patients receive a safety plan, crisis contacts, means restriction, and carer involvement (with consent / capacity). [1]

Document the risk formulation, the capacity assessment, the lawful basis for any non-consensual intervention, and the follow-up plan in the record. [1]

Special Populations

Pregnancy and postpartum. Postpartum psychosis is a psychiatric emergency requiring admission, ideally to a mother-and-baby unit. Evidence supports antipsychotics plus lithium acutely, ECT where a rapid response is required, and lithium for relapse prevention and prophylaxis; plan pregnancy and postpartum prescribing with specialist input to balance fetal and maternal risks.[2]

Children and adolescents. CAMHS pathway with specialist, lower, protocol-based dosing. Involve parents/guardians; consider Gillick competence (under 16) and parental responsibility; minimise restraint; rule out abuse as a driver of presentation.[5]

Elderly. Delirium is the dominant cause of acute disturbance; antipsychotic use in dementia increases all-cause mortality — a cohort of nursing-home residents showed increased death with conventional agents (haloperidol highest) versus atypicals, on top of the meta-analysed excess with atypicals — so use the lowest dose, shortest duration, only for severe distress, and avoid benzodiazepines. Always treat pain, sensory impairment, infection, constipation, urinary retention and hypoxia first.[25]

Intellectual disability and autism. Behaviour may be communication of pain or distress. Sensory-adjusted environment (low stimulation, single room). Involve familiar carers. Use specialist learning-disability psychiatry. Recognise behavioural equivalents of psychiatric symptoms. Use adapted assessment tools. [1]

Medical inpatients. Delirium from sepsis, post-operative state, ICU, opioids. Liaison psychiatry involvement. Non-pharmacological first. [1]

Anticoagulated or dual-antiplatelet patients. High risk of intracranial bleed from restraint-related head injury. CT brain if any head trauma. Reverse anticoagulation if major bleed (idarucizumab for dabigatran, andexanet or PCC for factor Xa inhibitors, PCC/vitamin K for warfarin). [1]

Substance-intoxicated. Stimulants (cocaine, methamphetamine) — excited delirium pathway: chemical sedation first, aggressive cooling and acidosis management. Opioids — naloxone titrated per protocol, beware re-narcotisation with long-acting opioids. Alcohol — parenteral B vitamins before glucose, benzodiazepine withdrawal regimen. Cannabis — usually supportive. Novel psychoactive substances — unpredictable; supportive. [21][24]

Cultural and linguistic. Use a professional interpreter; culturally informed assessment; recognise cultural expressions of distress; avoid misdiagnosis. Involve cultural consultants where appropriate. [1]

Evidence, Guidelines & Regional Differences

Controversies. [1]

• Ketamine 5 mg/kg IM for severe prehospital agitation sedates faster than haloperidol 10 mg IM (5 vs 17 minutes) but with 49% complications and 39% intubation — emerging, airway-intensive, not established for routine use.[20]
• "Excited delirium" nomenclature remains contested even though an ACEP task force concluded it is a real syndrome with uncertain, likely multiple, aetiologies; early recognition and chemical sedation are the priorities.[21][22]
• ECT for catatonia remains under-utilised despite prospective evidence of prompt response after lorazepam failure; access is variable.[16]
• Suicide-risk scales: an international consensus concluded available instruments need further validation of utility, reliability and validity — structured assessment yes, prediction no.[5]
• Serotonin-toxicity diagnostic criteria themselves have shortfalls — of 55 published fatal "serotonin toxicity" cases, 22% were unlikely to be serotonin toxicity at all; diagnosis requires a plausible serotonergic exposure, not symptom checklists alone.[23]

Regional deltas. [1]

• United Kingdom: NICE NG10 (aggression), NICE NG225 (self-harm), BAP/NAPICU 2018 (rapid tranquillisation), Mental Capacity Act 2005, Mental Health Act 1983 (amended 2007), Royal College of Psychiatrists standards.
• United States: Project BETA consensus; state-by-state involuntary commitment laws (e.g. Florida Baker Act, California 5150 hold — 72-hour evaluation); EMTALA requires medical screening examination of every emergency patient; CMS and Joint Commission standards on restraint and seclusion.
• India: Mental Healthcare Act 2017 — decriminalisation of suicide (Section 115), presumption of mental illness, rights-based, advance directives, ban on chained restraint, ECT only under anaesthesia and muscle relaxation (banned for minors).
• Australia: state-specific Mental Health Acts (e.g. NSW Mental Health Act 2007); Australia LifeSpan suicide-prevention framework.
• WHO: mhGAP Intervention Guide for non-specialist settings in low- and middle-income countries. [1]

Exam Pearls

[1]

Exam application bank (NEET-PG / INICET)

One-line answer

Psychiatric emergencies are acute situations requiring immediate intervention to prevent harm to the patient or others. The core scenarios are: acute agitation/aggression (de-escalation first, then oral medication, then rapid tranquillisation — IM lorazepam, IM olanzapine or IM aripiprazole; IM haloperidol 5–10 mg + promethazine up to 50 mg as the TREC second-line regimen; never combine IM olanzapine with parenteral lorazepam), acute psychosis (risk assessment, antipsychotic, admission if risk), suicide attempt / self-harm (medical stabilisation, psychosocial assessment before discharge), delirium (identify and treat cause; antipsychotics increase mortality in dementia), neuroleptic malignant syndrome (stop antipsychotic — this reduces mortality; supportive care; dantrolene best-evidenced; 2-week washout), serotonin syndrome (stop serotonergic agents, supportive care, cyproheptadine 4–8 mg orally per case series), lithium poisoning (saline; haemodialysis preferred when renal impairment with level over 4.0 mEq/L or reduced consciousness/seizures/dysrhythmias at any level), acute dystonia (anticholinergic — procyclidine or diphenhydramine), akathisia (mirtazapine/biperiden/vitamin B6 greatest efficacy; propranolol effective), catatonia (parenteral lorazepam challenge — 76% respond; ECT for failures), excited delirium (chemical sedation over physical restraint; ketamine 5 mg/kg IM emerging but complication-prone), and postpartum psychosis (emergency admission; antipsychotic + lithium; ECT for rapid response; lithium prophylaxis).[1][2][4][5][14][15][16][18]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Psychiatric Emergencies & Acute Agitation.

References

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2. [2]Jairaj C, Seneviratne G, Bergink V. Postpartum psychosis: A proposed treatment algorithm J Psychopharmacol, 2023.PMID 37515460
3. [3]Boyer EW, Shannon M. The serotonin syndrome N Engl J Med, 2005.PMID 15784664
4. [4]Gurrera RJ, Caroff SN, Cohen A, et al. An international consensus study of neuroleptic malignant syndrome diagnostic criteria using the Delphi method J Clin Psychiatry, 2011.PMID 21733489
5. [5]Patel MX, Sethi FN, Barnes TR, et al. Joint BAP NAPICU evidence-based consensus guidelines for the clinical management of acute disturbance: De-escalation and rapid tranquillisation J Psychopharmacol, 2018.PMID 29882463
6. [6]Berman BD. Neuroleptic malignant syndrome: a review for neurohospitalists Neurohospitalist, 2011.PMID 23983836
7. [7]Perry PJ, Wilborn CA. Serotonin syndrome vs neuroleptic malignant syndrome: a contrast of causes, diagnoses, and management Ann Clin Psychiatry, 2012.PMID 22563571
8. [8]Guinart D, Cuffe N, Kishore T, et al. A systematic review and pooled, patient-level analysis of predictors of mortality in neuroleptic malignant syndrome Acta Psychiatr Scand, 2021.PMID 34358327
9. [9]Graudins A, Stearman A, Chan B. Treatment of the serotonin syndrome with cyproheptadine J Emerg Med, 1998.PMID 9696181
10. [10]Dunkley EJ, Isbister GK, Sibbritt D, et al. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity QJM, 2003.PMID 12925718
11. [11]Decker BS, Goldfarb DS, Dargan PI, et al.; EXTRIP Workgroup. Extracorporeal Treatment for Lithium Poisoning: Systematic Review and Recommendations from the EXTRIP Workgroup Clin J Am Soc Nephrol, 2015.PMID 25583292
12. [12]Okusa MD, Crystal LJ. Clinical manifestations and management of acute lithium intoxication Am J Med, 1994.PMID 7942943
13. [13]Gitlin M. Lithium side effects and toxicity: prevalence and management strategies Int J Bipolar Disord, 2016.PMID 27900734
14. [14]Rupniak NM, Jenner P, Marsden CD. Acute dystonia induced by neuroleptic drugs Psychopharmacology (Berl), 1986.PMID 2871578
15. [15]Gerolymos C, Solmi M, Stauber G, et al. Drug Efficacy in the Treatment of Antipsychotic-Induced Akathisia: A Systematic Review and Network Meta-Analysis JAMA Netw Open, 2024.PMID 38451521
16. [16]Bush G, Fink M, Petrides G, et al. Catatonia. II. Treatment with lorazepam and electroconvulsive therapy Acta Psychiatr Scand, 1996.PMID 8686484
17. [17]Richmond JS, Berlin JS, Fishkind AB, et al. Verbal De-escalation of the Agitated Patient: Consensus Statement of the American Association for Emergency Psychiatry Project BETA De-escalation Workgroup West J Emerg Med, 2012.PMID 22461917
18. [18]Huf G, Coutinho ES, Adams CE; TREC Collaborative Group. Rapid tranquillisation in psychiatric emergency settings in Brazil: pragmatic randomised controlled trial of intramuscular haloperidol versus intramuscular haloperidol plus promethazine BMJ, 2007.PMID 17954515
19. [19]TREC Collaborative Group. Rapid tranquillisation for agitated patients in emergency psychiatric rooms: a randomised trial of midazolam versus haloperidol plus promethazine BMJ, 2003.PMID 14512476
20. [20]Cole JB, Moore JC, Nystrom PC, et al. A prospective study of ketamine versus haloperidol for severe prehospital agitation Clin Toxicol (Phila), 2016.PMID 27102743
21. [21][No authors listed] Towards evidence-based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 1: excited delirium syndrome and sudden death Emerg Med J, 2013.PMID 24142942
22. [22]Vilke GM, DeBard ML, Chan TC, et al. Excited Delirium Syndrome (ExDS): defining based on a review of the literature J Emerg Med, 2012.PMID 21440403
23. [23]Chiew AL, Buckley NA. The serotonin toxidrome: shortfalls of current diagnostic criteria for related syndromes Clin Toxicol (Phila), 2022.PMID 34806513
24. [24]Thomson AD, Cook CC, Touquet R, et al. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department Alcohol Alcohol, 2002.PMID 12414541
25. [25]Liperoti R, Onder G, Landi F, et al. All-cause mortality associated with atypical and conventional antipsychotics among nursing home residents with dementia: a retrospective cohort study J Clin Psychiatry, 2009.PMID 19906339
26. [26]Sternbach H. The serotonin syndrome Am J Psychiatry, 1991.PMID 2035713
27. [27]Levenson JL. Neuroleptic malignant syndrome Am J Psychiatry, 1985.PMID 2863986