Antipsychotic overdose
Acute antipsychotic overdose produces central nervous system depression, anticholinergic signs, alpha-1 blockade hypotension, and agent-specific cardiac conduction abnormalities, and is usually survivable with airway protection, cardiac monitoring, and isotonic crystalloid; sodium bicarbonate treats QRS widening, magnesium treats torsades, and norepinephrine treats refractory hypotension.
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What this article covers
- Overview
A mixed sedative, anticholinergic, and cardiotoxic overdose syndrome: central nervous system depression, anticholinergic features, alpha-1 blockade hypotension with reflex tachycardia, and, for…
- Epidemiology
Predominantly an intentional self-poisoning in adolescents or adults with an established psychiatric diagnosis, using their own prescription or a household member's.
- Risk factors
Active suicidal ideation or a prior attempt: the strongest predictor of a deliberate large ingestion.
- Pathophysiology
Dopamine D2 antagonism is the therapeutic target, not the acute overdose threat: the cardiovascular and central nervous system effects come from the drugs' other receptor and channel activity.
- Clinical features
Time course: most immediate-release ingestions produce symptoms within 1 to 4 hours; sustained-release formulations and quetiapine have a delayed, prolonged onset.
- Differential diagnosis
Neuroleptic malignant syndrome: fever, lead-pipe rigidity, and autonomic instability evolve over 1 to 3 days after starting or increasing an antipsychotic, with markedly elevated creatine kinase, not within hours of a single ingestion.
- Diagnosis
The diagnosis is established clinically: antipsychotic exposure with sedation, an anticholinergic examination, alpha-1 blockade hypotension with reflex tachycardia, and an electrocardiogram showing a…
- Management
First, airway, breathing, and circulation: intubate for coma, seizure, or inability to protect the airway; continuous cardiac monitoring; intravenous access.
- Complications
Torsades de pointes and cardiac arrest: from unresolved QTc prolongation, particularly with thioridazine, ziprasidone, haloperidol, or iloperidone.
- Prognosis
Most patients survive with supportive care alone, without an antiarrhythmic intervention.
- Prevention
Assess suicidal ideation before prescribing or refilling any antipsychotic, particularly a first-generation or QTc-prolonging agent.
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Related articles
- Neuroleptic malignant syndrome
Neuroleptic malignant syndrome is a rare, life-threatening idiosyncratic reaction to dopamine-blocking agents, presenting days to weeks after starting or raising the dose, with fever, lead-pipe rigidity, autonomic instability, altered mental status, and a markedly elevated creatine kinase. Diagnosis is clinical. First-line management is stopping the offending drug, aggressive cooling, and IV fluid resuscitation, escalating to lorazepam, dantrolene, and bromocriptine.
- Extrapyramidal symptoms
Extrapyramidal symptoms are a time-ordered family of movement disorders caused by dopamine D2 receptor blockade from antipsychotics or antiemetics: acute dystonia within hours to days, akathisia within days to weeks, drug-induced parkinsonism within days to months, and tardive dyskinesia after months to years. Diagnosis is clinical; treatment is syndrome-specific, from intramuscular benztropine for dystonia to a vesicular monoamine transporter 2 (VMAT2) inhibitor such as valbenazine for tardive dyskinesia.
- Antipsychotics
Antipsychotics block the dopamine D2 receptor, with second-generation agents adding serotonin receptor blockade, and are first-line treatment for schizophrenia and other psychotic and manic states; a second-generation agent such as risperidone 2 to 8 mg/day or olanzapine 10 to 20 mg/day is chosen first, clozapine is reserved for treatment-resistant disease after two adequate trials fail, and treatment requires baseline and ongoing metabolic, cardiac, and, for clozapine, hematologic monitoring.
- Torsades de pointes
Torsades de pointes is a polymorphic ventricular tachycardia occurring on a background of QT prolongation, with a characteristic twisting of QRS complexes around the baseline. Management is intravenous magnesium, correction of the underlying QT-prolonging cause, and rate acceleration by pacing or isoproterenol; unstable episodes are defibrillated.
- Rhabdomyolysis
Rhabdomyolysis is necrosis of skeletal muscle with release of myoglobin, creatine kinase, and intracellular electrolytes into the circulation, diagnosed by a serum creatine kinase at least five times the upper limit of normal (typically over 1500 U/L) with a urine dipstick positive for blood but no red cells on microscopy; treatment is aggressive isotonic intravenous fluid to a urine output of 200 to 300 mL/h and correction of hyperkalemia, with acute kidney injury from pigment nephropathy the dominant complication.