Side effects of quinine

Quinine is a substance with highly irritating properties (also for the gastric mucosa: nausea is not uncommon). Capsules are therefore best taken after a meal. Quinine may also increase the secretion of insulin from the pancreas, with the risk of hypoglycaemia. Quinine allergy is not common. What is common is a range of side effects such as tinnitus, temporary deafness for high frequencies, headache, nausea and palpitations. These toxic phenomena are known as cinchonism. This reduces the patient’s compliance. Quinine increases irritability of the pregnant uterus. In case of need one must not hesitate to use quinine in a pregnant woman with malaria (malaria itself can lead to abortion, preterm labour or death in utero). To prevent an impending premature labour, a tocolytic agent can be given, such as the 2-mimetic ritodrine (Pre-par®), fenoterol or salbutamol. Quinine and primaquine may be used therapeutically in persons with porphyria (Fansidar® is contraindicated in these patients). Prolongation of the PR, QRS and QT intervals may occur during the use of quinine (as with quinidine). If the patient has atrial fibrillation, conversion to sinus rhythm may occur, with possibly arterial embolic complications. Atrial fibrillation which has already been present for more than 48 hours is a contra-indication for quinine. Congenital long QT syndrome and Brugada syndrome are equally formal contra-indications for using quinine. Both syndromes are caused by molecular abnormalities in the cardiac Na⁺ -ion channels. In congenital long QT syndrome the activity of the channels is increased, while they function less well in Brugada. The latter, an autosomal dominant inherited syndrome, results in episodes of sudden syncope, with a right bundle branch block and ST-elevations in the right precordial leads (V1-3) on the ECG. Isolated episodes of ventricular fibrillation occur without other signs of organic heart disease. The syndrome may be suppressed on the ECG by beta-blockers, and made more prominent by ajmaline, flecainide and procainamide. It is responsible for many cases of sudden death. Quinine is a common cause of drug-associated TTP-HUS (thrombotic thrombocytopenic purpura - haemolytic uraemic syndrome)., e.g. in patients who take quinine against nocturnal leg cramps.

Overdosage of quinine may lead to very severe situations such as deafness, delirium, bradycardia, hypotension, respiratory arrest or death (lethal dose approximately 8 gram). Overdosage may also lead to blindness via a direct toxic effect on the retina and possibly also due to spasms of the retinal blood vessels and subsequent retinal ischaemia. The half-life of quinine in the blood is short (12 hours). Most of the quinine in blood is bound to proteins. The bound fraction increases from 80% to 90% in acute malaria (increase in acute phase proteins). Overdosage is thus less dangerous in active malaria. The total quinine blood level is of much less importance than the blood level of free quinine, which is much more difficult to measure. 95% of the quinine is converted in the liver and then eliminated via the kidneys.

Category: Medicine Notes