Methyl Salicylate Case Study

1647 Words7 Pages

Cerebral palsy following Methyl salicylate poisoning in a young child
The first reported case

Introduction
Methyl salicylate is used as a local application for musculoskeletal pain. It is the main compound in oil of wintergreen. “One teaspoon of oil of wintergreen (5 mL) is equivalent to approximately 7000 mg of salicylate, or 21.7 adult aspirin tablets”.1 This concentrated liquid is readily absorbed via gut. Therefore, swallowing is lethal specially for children and there are numerous reports published [3].
There have been several deaths due to accidental ingestion of oil of wintergreen among children younger than 6 years in Sri Lanka6, however no case reports have been published related to this deadly compound. Here we report a case of …show more content…

It is a rare method of deliberate self-harm. Oil of wintergreen is an essential ingredient in most of over the counter local application remedies used in musculoskeletal pain. Some of the state hospital is still issuing pure oil of wintergreen (98%) to their patients in orthopedic and rheumatology clinics. Toxic potential of this deadly preparation is not fully understand by the general public as well as the physicians. One teaspoon of pure oil is equivalent to 7000 mg of salicylate, that is approximately 22 adult aspirin tablets (325 mg). Less than one teaspoon, as 4ml in a young child can be mortal. The exact amount taken by our child is not obvious, but apparently he has taken 1-2 teaspoons from the half diluted solution …show more content…

CNS effects include an initial direct stimulation of the medullary respiratory center producing an increase in rate and depth of respiration and a corresponding primary respiratory alkalosis, tinnitus, deafness and confusion10. In severe poisoning, where systemic acidaemia enhances cerebral penetration of unionized salicylate, coma, convulsions and cerebral oedema occur. Metabolic effects include direct uncoupling of oxidative phosphorylation and inhibition of Krebs cycle enzymes leading to systemic acidaemia, hyperglycaemia, hyperthermia, derangement of carbohydrate, amino acid and lipid metabolism. Increased oxygen consumption and carbon dioxide production are also apparent. Dehydration results from increased insensible respiratory and cutaneous fluid losses, as well as from nausea and vomiting from gastro – intestinal (GI) irritation. Inhibition of platelet aggregation as well as Vitamin-K sensitive clotting factor function may produce a mild coagulopathy. Haemorrhage rarely occurs in humans following severe salicylate poisoning. Salicylate-induced non-cardiogenic pulmonary oedema is also reported in association with severe poisoning11. Classical phases of salicylate poisoning may not usually be evident in young children and they normally present with initial metabolic acidosis rather than respiratory alkalosis10.

Open Document