Case #036

The blood gas is the whole case. A pH of 7.44 looks reassuring until the numbers underneath are read together: the pCO₂ is far too low and so is the bicarbonate, and neither explains the other. Salicylate stimulates the respiratory centre directly, producing a primary respiratory alkalosis, and at the same time uncouples oxidative phosphorylation, producing a high anion gap metabolic acidosis. The two push the pH in opposite directions and hold it near normal, which is why a mixed picture in a hyperventilating patient is close to diagnostic. A pure metabolic acidosis would never drive the pCO₂ to 2.6, and a pure respiratory alkalosis would not consume bicarbonate. Uncoupling also explains the fever and the drenching sweat, both of which invite a mistaken diagnosis of sepsis. Tinnitus and muffled hearing are early and characteristic. The rest of the screen closes the other causes of a raised anion gap: normal glucose and ketones exclude the ketoacidoses, a normal osmolar gap excludes ethylene glycol and methanol, and the paracetamol level matters because co-ingestion is common and silent. Finally, levels still climbing at eight hours show absorption is continuing, often from a mass of tablets in the stomach, so one reassuring early level never excludes toxicity. Treatment then follows from the chemistry. Salicylate is a weak acid, so raising the urine pH traps it as an ion in the tubule and stops it being reabsorbed: her urine pH of 5.4 is the number to move, with intravenous sodium bicarbonate. Potassium goes in alongside, since a depleted kidney exchanges potassium for hydrogen and quietly undoes the alkalinisation. Hemodialysis is held for a level above roughly 700 mg/L, renal failure, refractory acidosis, seizures or altered consciousness. The one thing not to do is intubate her for that respiratory rate of 34: the hyperventilation is all that holds her pH at 7.44, and a ventilator failing to match it lets the pH fall off a cliff.