Neuroleptic malignant syndrome diagnosis and management (MEQ)

(i) Diagnosis and discriminators. Working diagnosis: neuroleptic malignant syndrome after dopamine antagonist exposure (olanzapine escalation plus IM haloperidol). Map to Gurrera IEC elements: recent antagonist exposure; hyperthermia >38.0 C on at least two occasions; rigidity; mental-status alteration (mute); CK well above 4× ULN (1,860 vs ULN 200); sympathetic lability with large BP swings; tachycardia and tachypnoea well above baseline thresholds (HR ≥25% and RR ≥50% above baseline). Negative infection/metabolic work-up must still be pursued. Versus serotonin toxicity: no serotonergic drugs, bradyreflexia without clonus/hyperreflexia, tempo over days after antipsychotics. Versus malignant catatonia: marked neuroleptic exposure makes NMS primary, but catatonic features (mutism, rigidity) overlap — keep both in mind if course becomes refractory and consider BAP catatonia pathways including benzodiazepines/ECT.[1][2][5]

(ii) Immediate management. Stop all antipsychotics and other dopamine antagonists (including PRN). Medical emergency: ABCDE, external cooling, IV fluids, airway protection, continuous monitoring, serial CK/U&E, investigate infection and other mimics. Benzodiazepines for agitation/catatonic features; do not give more antipsychotic. Escalate HDU/ICU early given autonomic instability and rigidity.[6][1]

(iii) Specific therapies. No large RCTs. Supportive care is universal first-line. Kuhlwilm 2020 case-series synthesis: overall no clear mortality/duration superiority of dantrolene, bromocriptine, or ECT versus supportive care alone, but severe cases showed lower mortality with specific pharmacotherapy or ECT (ECT lowest in that severe subgroup). Practical approach: bromocriptine (e.g. start about 2.5 mg PO/NG two–three times daily, titrate under specialist advice) and/or IV dantrolene (case regimens often ~1–2.5 mg/kg IV) for severe non-resolving NMS; ECT for refractory disease or malignant catatonia overlap.[3][6][5]

(iv) Rechallenge. Only after full resolution (afebrile, rigidity gone, CK normalising). Delay — often at least about two weeks after recovery is cited; longer if depot. Prefer a different agent, start low, titrate slowly, preferably inpatient with temperature/tone/CK monitoring. Rosebush: most can eventually tolerate rechallenge; success tracks time since recovery. Document adverse reaction and contingency plan.[4][6]