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Severity of salicylate poisoning has been classified in terms of blood concentrations. However, in decisions on treatment, other factors must be taken into account.
A woman of 86 was brought to the emergency department having been found unresponsive in her chair by a relative. Her medical history included polymyalgia rheumatica, transient ischaemic attacks and depression. Her regular daily medication was aspirin 75 mg, prednisolone 5 mg and nitrazepam 10 mg. On examination she was apyrexial but tachypnoeic with oxygen saturation 92% on air. She opened her eyes and moved all her limbs to command. Routine blood examination showed a raised white cell count with neutrophilia and deranged renal function (urea 23.8 mmol/L, creatinine 288 μmol/L). Arterial blood analysis revealed a pH of 7.50, pCO2 2.23 KPa, pO2 12.2 KPa, bicarbonate 19 mmol/L (base deficit 4.5 mmol/L) and lactate 2.7 mmol/L. CT of the head was normal. Because of the respiratory alkalosis salicylate was measured and proved to be 850 mg/L.
A regional toxicology service advised that, in a patient with salicylate 4700 mg/L, haemofiltration would normally be indicated. The patient was given activated charcoal to minimize gastrointestinal salicylate absorption and transferred to the intensive care unit where a bicarbonate infusion (1.4% sodium bicarbonate at 300 mL/h) was set up to combat the metabolic acidosis and alkalinize the urine. Urinary pH was maintained at 47.5. Within 4 h of the infusion being started, the patient's level of consciousness had improved greatly, blood gases were returning to normal and the salicylate concentration was lower. She later told us that she had taken an intentional overdose of aspirin (tablets of 300 mg, not the 75 mg tablets she received on prescription).
Salicylates when taken in excess cause respiratory alkalosis by direct stimulation of the respiratory centre in the medulla, followed by a metabolic acidosis due to uncoupling of oxidative phosphorylation and blocking of the Krebs cycle. Once absorbed, they remain in the ionized form and hence do not diffuse easily into tissues unless a metabolic acidosis supervenes; they are then converted into the non-ionized form which readily diffuses into the brain. Similarly, the non-ionized form is readily reabsorbed from the renal tubules, slowing elimination. The effects vary from nausea, vomiting, tinnitus, deafness and confusion to coma.1,2
The severity of salicylate toxicity has been classified by blood concentration—mild 300–500 mg/L, moderate 500–700 mg/L, severe 4700 mg/L. However, there is a view that concentration is not the only or even the major criterion. Additional criteria relating to severity include age over 70 or under 10 years, central nervous system features, hyperpyrexia, metabolic acidosis, pulmonary oedema and late presentation.3 Standard treatment includes the use of activated charcoal or gastric lavage, prompt rehydration and correction of any electrolyte abnormalities. A bicarbonate infusion should be started to combat acidosis, which aids in conversion of the non-ionized form of the drug to the ionized form, minimizing tissue toxicity and increasing renal elimination. Although haemofiltration has been recommended for patients with a salicylate exceeding 700 mg/L, our patient's age and frailty led us to try urinary alkalinization first and she showed rapid clinical improvement. A previous paper5 has compared the use of bicarbonate infusion with haemofiltration in a single patient following two episodes of severe salicylate poisoning. The initial rate of decline in the salicylate concentration was faster with alkalinization of urine.