Chloroquine poisoning
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The library has limited dedicated content on chloroquine poisoning as a standalone topic. Let me read the most relevant sections found.
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Based on what the library contains, combined with established clinical knowledge, here is a comprehensive overview of chloroquine poisoning:
Chloroquine Poisoning
Overview
Chloroquine (and its analogue hydroxychloroquine) is an aminoquinoline antimalarial that has a narrow therapeutic index. Acute poisoning is a life-threatening emergency with a reported mortality of up to 25–30% in severe cases. Children are particularly vulnerable to accidental overdose — a dose as small as 20–30 mg/kg can be fatal.
Mechanism of Toxicity
Chloroquine is a cationic amphiphilic drug with multiple toxic mechanisms:
| System | Mechanism |
|---|---|
| Cardiac | Blocks myocardial voltage-gated sodium channels (like quinidine), slowing depolarization → QRS widening, QTc prolongation, ventricular arrhythmias |
| Cardiac | Blocks potassium channels → QT prolongation, risk of torsades de pointes |
| Electrolyte | Inhibits K⁺ channels (like barium), preventing K⁺ efflux → severe hypokalemia via intracellular shift |
| CNS | Seizures, coma — often preceding cardiovascular collapse |
| Retinal | Lysosomal accumulation → retinal pigment epithelium toxicity (chronic use) |
| Neuromuscular | Vacuole formation, lysosomal storage → toxic myopathy (chronic high doses >500 mg/day) |
— Goldman-Cecil Medicine, Cardiopulmonary Effects; Henry's Clinical Diagnosis, Hypokalemia section
Clinical Features
Rapid onset — symptoms typically within 1–3 hours of ingestion.
Cardiovascular (most dangerous)
- Hypotension — direct myocardial depression + vasodilation
- QRS widening — sodium channel blockade (like tricyclic antidepressants)
- QTc prolongation — potassium channel blockade → torsades de pointes
- Ventricular tachycardia / ventricular fibrillation
- Complete heart block, asystole
- Depressed myocardial contractility (visible on bedside echo)
Neurological
- Agitation, confusion → rapid progression to seizures and coma
- Visual disturbances (acute)
Electrolyte
- Profound hypokalemia — via K⁺ channel inhibition causing intracellular K⁺ shift (same mechanism as barium poisoning)
- Severity of hypokalemia correlates with toxicity severity
Respiratory
- Respiratory depression, ARDS possible
Severity Assessment
| Feature | Severe Poisoning |
|---|---|
| Ingested dose | >5 g in adult; >20 mg/kg in child |
| QRS duration | >120 ms |
| Hypotension | Systolic <80 mmHg |
| Hypokalemia | K⁺ <2.5 mmol/L |
| Coma | GCS <8 |
Management
Immediate Resuscitation
- Airway protection — intubate early given rapid CNS deterioration
- IV access, continuous cardiac monitoring, 12-lead ECG
- Bedside echocardiography to assess contractility
Antidotal/Specific Treatment
- Epinephrine (adrenaline) — first-line vasopressor; high doses often required (0.1–1 mcg/kg/min). Has been shown to reduce mortality in severe cases
- Diazepam (high dose, e.g. 1–2 mg/kg IV over 30 min) — dual role: anticonvulsant + direct cardioprotective effect (counteracts chloroquine-induced cardiac toxicity); reduces mortality in clinical studies
- Sodium bicarbonate — for QRS widening (>120 ms), to overcome sodium channel blockade (same approach as TCA overdose; target pH 7.45–7.55)
- Potassium replacement — aggressive IV potassium for hypokalemia; paradoxically, K⁺ normalises as the patient recovers — do NOT over-correct
- Activated charcoal — if airway protected and <1 hour post-ingestion
Do NOT Use
- Antiarrhythmic drugs (quinidine, procainamide, amiodarone) — worsen sodium/potassium channel blockade
- Fluid loading as first-line for hypotension — use vasopressors preferentially
Refractory Shock
- Intra-aortic balloon pump or ECMO (extracorporeal membrane oxygenation) — considered in refractory cardiovascular collapse
- Lipid emulsion therapy has been reported but evidence is limited
ECG Changes
| ECG Feature | Mechanism |
|---|---|
| Prolonged PR interval | AV conduction slowing |
| Widened QRS | Na⁺ channel blockade |
| Prolonged QTc | K⁺ channel blockade |
| ST/T wave changes | Myocardial toxicity |
| Ventricular arrhythmias | Combined channel effects |
Chronic Toxicity (Therapeutic Doses — Distinct from Poisoning)
- Retinopathy — most feared; occurs with cumulative dose; risk very low in first 10 years at recommended doses. Screen ophthalmologically every 6–12 months. Chloroquine may be more retinotoxic than hydroxychloroquine — Fitzpatrick's Dermatology
- Myopathy — amphiphilic cation myopathy with lysosomal vacuolation; occurs at doses >500 mg/day; elevated CK — Adams & Victor's Neurology
- Cardiac arrhythmias — including toxic psychosis, grand mal seizures — Fitzpatrick's Dermatology
- Bone marrow suppression — rare with recommended doses
- G6PD hemolysis — rarely
Key Points to Remember
- Chloroquine poisoning is a toxicological emergency — deterioration can be precipitous
- The classic triad: cardiovascular collapse + seizures + hypokalemia
- Hypokalemia is a marker of severity, not a cause — aggressive correction risks rebound hyperkalemia as the drug is cleared
- Diazepam + epinephrine is the established management cornerstone (Riou protocol)
- Activated charcoal only if airway is secured and patient presents early
Sources: Goldman-Cecil Medicine (Cardiopulmonary Toxicology, Poisoning Management); Henry's Clinical Diagnosis and Management by Laboratory Methods (Hypokalemia); Fitzpatrick's Dermatology (Antimalarials); Adams & Victor's Principles of Neurology (Toxic Myopathies)
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