Salicylic acid-containing drug poisoning

Salicylic acid is a white crystalline powder with sweetish acrid taste. If prepared from natural methyl salicylate, it may have a faint mint like odour. It is available in forms of ointments, cream, transdermal patches, liquids and plaster.

With salicylic acid, concomitant use of other drugs which may contribute to elevated serum salicylate levels should be avoided where the potential for toxicity is present. In children under twelve years of age and those patients with renal or hepatic impairment, the area to be treated should be limited and the patient monitored closely for signs of salicylate toxicity: nausea, vomiting, dizziness, lethargy, hyperpnea, diarrhea, psychic disturbances.

In the event of salicylic acid toxicity, the use of Salicylic acid gel should be discontinued. Fluids should be administered to promote urinary excretion. Treatment with sodium bicarbonate (oral or intravenous) should be instituted as appropriate. Prolonged use over large areas, especially in children pregnant or nursing mothers,and those patients with significant renal or hepatic impairment, could result in salicylism. Management of acute salicylic acid poisoning includes prevention of absorption, correction of acid-base, fluid and electrolyte imbalance and enhancing of the drug elimination.

Salicylate ingestion can cause nausea, vomiting, and abdominal pain. Salicylate stimulation of medullary chemoreceptors and local irritation of the GI tract produce emesis. Upper GI ulceration and bleeding can occur. Gastrointestinal effects are much more prominent in acute ingestion.

Acid-base disturbances, electrolyte abnormalities, and central nervous system sometimes effects characterize salicylate poisoning. The wide range of toxic effects varies depending on the age of the patient and whether the ingestion is chronic/ acute.

In salicylate toxicity, as salicylate levels increase, the acid-base disturbance progresses from respiratory alkalosis to mixed respiratory alkalosis and then to metabolic acidosis. In children, the progression to metabolic acidosis sometimes occurs more rapidly. Salicylates directly stimulate respiratory centers in the medulla, causing hyperventilation and, then respiratory alkalosis.

Salicylates also cause the uncoupling of oxidative phosphorylation, which leads to decreased adenosine triphosphate production, increased oxygen consumption, increased carbon dioxide production, and increased heat production. Derangement in the Krebs cycle and in carbohydrate metabolism leads to an accumulation of organic acids, including pyruvate, lactate, and acetoacetate, causing metabolic acidosis.

Toxic levels of salicylates also displace large amounts of plasma bicarbonate, worsening the metabolic acidosis.

Dose-dependent hepatotoxicity can also occur with salicylate poisoning. A small percentage of patients might develop hepatitis, but most generally develop an asymptomatic elevation of transaminases. Sources of salicylate poisoning include aspirin overdose and excessive topical application or ingestion of ointments that contain methyl salicylate (oil of wintergreen).

Of late, despite the reduction of poisonings due to repackaging, salicylate toxicity remains a significant cause of morbidity and mortality.