Quinine is an optical isomer of quinidine, a class Ia sodium channel blocking antidysrhythmic drug, with which it shares similar pharmacologic effects. Quinine is the primary alkaloid found in the bark of the cinchona tree and was once widely used for the treatment of malaria and is still occasionally used for chloroquine-resistant cases. A 2006 FDA advisory warned against the use of quinine in the treatment of nocturnal muscle cramps. Quinine is found in tonic water and has been used to cut street heroin. It has also been used as an abortifacient.

1. The mechanism of quinine toxicity is believed to be similar to that of quinidine; however, quinine is a much less potent cardiotoxin.
2. Quinine also has toxic effects on the retina that can result in blindness. Recent evidence indicates a direct toxic effect on photoreceptor and ganglion cells.
3. Inhibition of potassium channels may result in impaired hearing, tinnitus and vertigo and hypoglycemia.
4. Quinine has direct irritant effects on the gastrointestinal tract and stimulates CNS centers responsible for nausea and vomiting.
5. Hypersensitivity reactions include urticaria, photosensitivity dermatitis, cutaneous vasculitis, angioedema, and thrombocytopenia (“cocktail purpura”).
6. Pharmacokinetics. Well absorbed with peak levels 1-3 hours after ingestion. Volume of distribution 1.2-1.7 L/kg. Protein binding 80%. Elimination half-life 8-14 hours.

Quinine sulfate is available in capsules and tablets containing 130-325 mg. The minimum toxic dose is approximately 3-4 g in adults; 1 g has been fatal in a child.

Toxic effects involve the cardiovascular and central nervous systems, the eyes, and other organ systems.

1. Mild intoxication produces nausea, vomiting, and cinchonism (tinnitus, deafness, vertigo, headache, and visual disturbances).
2. Severe intoxication may cause ataxia, confusion, obtundation, convulsions, coma, and respiratory arrest. With massive intoxication, quinidine-like cardiotoxicity (hypotension, QRS- and QT-interval prolongation, atrioventricular [AV] block, and ventricular arrhythmias) may be fatal.
3. Retinal toxicity occurs 9-10 hours after ingestion and includes blurred vision, impaired color perception, constriction of visual fields, and blindness. The pupils are often fixed and dilated. Funduscopy may reveal retinal artery spasm, disc pallor, and macular edema. Although gradual recovery occurs, many patients are left with permanent visual impairment.
4. Other toxic effects of quinine include hypokalemia, hypoglycemia, hemolysis (in patients with glucose-6-phosphate dehydrogenase [G6PD] deficiency), and congenital malformations when used in pregnancy.

Is based on a history of ingestion and the presence of cinchonism and visual disturbances. Quinidine-like cardiotoxic effects may or may not be present.

1. Specific levels. Serum quinine levels can be measured by the same assay as for quinidine, as long as quinidine is not present. However, most hospital-based clinical laboratories no longer offer these assays. Plasma quinine levels above 10 mg/L have been associated with visual impairment; 87% of patients with levels above 20 mg/L reported blindness. Levels above 16 mg/L have been associated with cardiac toxicity.
2. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, creatinine, arterial blood gases or oximetry, cardiac troponin, and ECG monitoring.

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary.
   2. Treat coma, seizures, hypotension, and arrhythmias if they occur.
   3. Avoid types Ia and Ic antiarrhythmic drugs; they may worsen cardiotoxicity.
   4. Continuously monitor vital signs and the ECG for at least 6 hours after ingestion, and admit symptomatic patients to an intensive care unit.
2. Specific drugs and antidotes
   1. Treat cardiotoxicity with sodium bicarbonate, 1-2 mEq/kg by rapid IV bolus.
   2. Stellate ganglion block is no longer recommended for quinine-induced blindness, due to lack of evidence of efficacy and potential for serious complications.
   3. Treat hypoglycemia with dextrose and, if needed, octreotide.
3. Decontamination. Administer activated charcoal orally if conditions are appropriate (see Table I-37). Gastric lavage is not necessary after small-to-moderate ingestions if activated charcoal can be given promptly.
4. Enhanced elimination. An expert consensus panel concluded that hemodialysis is not effective for quinine. Acidification of the urine may slightly increase renal excretion but does not significantly alter the overall elimination rate and may aggravate cardiotoxicity.