Salicylate poisoning is difficult to treat, and consideration should be given to consultation with a medical toxicologist. The goals in the management of the salicylate-poisoned patient are fluid resuscitation, correction of metabolic disturbances, decreasing further absorption of drug and enhancement of elimination. These goals are highly time-sensitive. Because there is no antidote, the only effective treatment is to reduce the ingress of salicylate into the central nervous system.
For moderately to severely poisoned patients, intravascular volume must be restored by boluses of normal saline at doses of 10 to 20 mL/kg until adequate perfusion is assured. Intravenous bicarbonate should be administered by bolus to any patient who is acidemic using intermittent boluses of 0.5 to 1 mEq/kg every 10 minutes. Correcting acidemia decreases the entry of salicylic acid into the brain and other tissues. Dextrose, typically 2 mL/kg of D25W in young children and 1 mL/kg of D50W in adolescents, should also be administered intravenously to any patient with altered mental status or seizures unless the serum glucose exceeds 140 mg/dL.
Patients with severe toxicity may need to be intubated and mechanically ventilated. These patients will require very high minute ventilation, arterial Pco2 values below 20 mm Hg to prevent further falls in blood pH and catastrophic shift of drug into the brain.4 It is essential, for the same reason, to avoid simply sedating and restraining a patient with seizures or agitation when the cause is severe salicylate poisoning.
Severely poisoned patients need emergency hemodialysis to be arranged, usually before confirmatory concentrations are reported by the laboratory. Hemodialysis removes salicylate three to five times faster than systemic alkalinization. Indications for hemodialysis include pulmonary edema, coma, seizure, severe metabolic acidosis, and renal failure. The salicylate concentration per se is not useful as a sole criterion for dialysis due to differences between serum and tissue (brain) concentrations, delays in measurement, and the need to anticipate the need for dialysis before patients become moribund. Continuous renal replacement therapy is insufficient to remove salicylate rapidly.
All symptomatic patients and those likely to have ingested >150 mg/kg should receive gastrointestinal decontamination. While experts may disagree on the best modality,5 activated charcoal is advisable, even if many hours have passed since ingestion. Large ingestions of enteric-coated preparations may benefit from whole bowel irrigation.6 Salicylate elimination is enhanced by urinary alkalinization,7 which is indicated in any symptomatic patient (any patient with at least mild toxicity and acid–base disturbances). Serum alkalemia by itself is not a contraindication to administration of sodium bicarbonate to alkalinize the urine and to compensate for ongoing renal losses. Increasing the urine pH decreases passive reabsorption of salicylic acid in the distal tubule. The goal of alkalinization is to increase the urine pH to 7 and ensure a urine output of 1 to 2 mL/kg/h. This is accomplished by infusing sodium bicarbonate after intravascular volume resuscitation. The first step is to place a urinary catheter and measure the volume and urine pH every hour. For the infusion, 132 to 150 meq sodium bicarbonate is typically added to each liter of a D5W solution and started at a rate of twice maintenance. If hypernatremia is present, a more hypotonic solution is recommended. Potassium should also be present in the infusion at 40 mM initially.
Hypokalemia is common in salicylism, and total body potassium depletion is always present in symptomatic patients. Potassium deficits will impair attempts to alkalinize the urine since potassium is exchanged for hydrogen in the tubular fluid when serum potassium is low resulting in a paradoxical aciduria. Inadequate fluid resuscitation will also render urine alkalinization impossible. Adjustments in infusion rate, potassium supplementation, and additional boluses of sodium bicarbonate are then made based on serial (every 2–4 hours) blood gas, electrolyte and salicylate concentrations, as well as the hourly urine output and pH. Safely alkalinizing a patient requires careful attention to detail, and frequent reassessments, to avoid the complications of volume overload, excessive alkalemia (pH >7.55), hypokalemia and hypernatremia and yet optimizing elimination of salicylate commensurate with the severity of the poisoning. Pulmonary edema, cerebral edema, and oliguric renal failure all render urinary alkalinization difficult and signal the need for hemodialysis, but theoretical fears of precipitating pulmonary edema should not preclude appropriate fluid therapy.