Introduction
This topic covers acute poisoning with quinine, a cinchona alkaloid that was long used as an antimalarial and, in many countries, for nocturnal leg cramps. It explains how an overdose or a toxic reaction injures the heart, nervous system, eyes and metabolism, and how the poisoning is recognised and managed in the emergency setting. Quinidine, its stereoisomer, produces essentially the same toxicity and is discussed in the same terms.
Mechanism and sources of toxicity
Quinine is a narrow therapeutic index drug. Its main toxic effects come from several actions:
- Sodium channel blockade in cardiac myocytes slows conduction, widening the QRS complex, similar to class I antiarrhythmics.
- Potassium channel blockade (including the hERG-mediated rapid delayed rectifier current) prolongs repolarisation, lengthens the QT interval and predisposes to torsades de pointes.
- Peripheral vasodilatation and direct negative inotropic effects lower blood pressure.
- Stimulation of pancreatic beta cells releases insulin, causing hypoglycaemia.
- Retinal and optic nerve injury follows vasospasm and ischaemia of the retinal circulation.
Poisoning usually results from intentional overdose, from repeated self-medication for cramps or malaria, or from accidental ingestion by children. Some patients develop toxic reactions at ordinary doses because of individual hypersensitivity or reduced drug clearance.