Salicylate (Aspirin) Toxicity

Salicylate poisoning is not simply excess aspirin causing sedation. Salicylates directly stimulate the medullary respiratory centre, increasing ventilation and lowering carbon dioxide. This produces a primary respiratory alkalosis, often early in the illness. At the same time, salicylates uncouple oxidative phosphorylation. Cells become less efficient at producing energy, generate excess heat and organic acids, and develop a high anion-gap metabolic acidosis. The respiratory alkalosis may initially keep the pH normal or high, masking the severity of the metabolic process. As the poisoning progresses, metabolic acidosis can predominate. That mixed disturbance explains a classic bedside mismatch: the patient is breathing rapidly and deeply, yet the blood gas may look alkalemic rather than acidemic. A high pH does not make the patient safe. The respiratory effort may be the patient’s compensation. Tinnitus is an early clue produced by salicylate effects on the auditory system. Hyperthermia reflects impaired cellular energy handling. Severe toxicity can cause altered mental status, seizures, cerebral edema, and non-cardiogenic pulmonary edema. Urinary alkalinisation improves renal elimination. Raising urine pH keeps salicylate in a more ionised form, so the kidneys...