Toxicology

in the liver to the active component, salicylic acid. In overdoses, the liver cannot metabolize the excess

drug, and most is then excreted unchanged by the kidneys (Postgrad Med 2009;121:162-8).

The most common clinical symptoms associated with a salicylate overdose are hyperventilation

(causing respiratory alkalosis), tinnitus, and GI irritation. Symptoms may vary depending on the serum

salicylate concentration; however, these may be low to normal early in the presentation (Postgrad Med

2009;121:162-8):

Serum concentration less than 30 mg/dL: Asymptomatic

Serum concentration 15–30 mg/dL: Therapeutic concentrations

Serum concentration 30–50 mg/dL: Hyperventilation, nausea, vomiting, tinnitus, dizziness

Serum concentration greater than 70 mg/dL: Coma, seizures, hallucinations, stupor, cerebral

edema, dysrhythmias, hypotension, oliguria, renal failure

Acute salicylate toxicity is typically associated more with GI symptoms; chronic toxicity is more

associated with CNS-type symptoms.

Absorption may be delayed up to 36 hours because of gastric pylorospasm, bezoar formation (precipitate

concretions because of poor solubility), or enteric-coated formulations; therefore, these ranges should be

There is no antidote for salicylate poisoning; the goals of therapy are to limit the additional absorption

of salicylates and to provide supportive care.

respiratory acidosis; however, do not mechanically ventilate patients unless clinically necessary as this

will interfere with the patient’s ability to appropriately compensate and maintain pH.

Gastric decontamination with a single dose of activated charcoal is recommended within 60 minutes of

acute ingestions and if the patient is alert with the absence of vomiting. However, there may be a role for

administration after this time frame, as well as multidose administration based on the characteristics

of the ingestion.

Administer intravenous crystalloid fluids at a rate of 10-20 mL/kg/hr for the first 2 hours to maintain a

normal BP and a urine output of 1–1.5 mL/kg/hr.

Administer intravenous glucose for hypoglycemia or significant neurologic symptoms.

Urine alkalinization is recommended to enhance renal elimination and increase the glomerular filtration

rate.

The following administration strategies have been described in the literature:

Administer 250 mL of sodium bicarbonate 8.4% over 1 hour; then administer additional 50-

mL boluses as needed to maintain a goal urine pH range of 7.5–8.5.

ii.

Administer a continuous infusion of 150 mL of sodium bicarbonate 8.4% in 1 L of 5% dextrose

in water at 2–3 mL/kg/hour to maintain a urine output of 1–2 mL/kg/hour. Do not allow the

serum pH to fall below 7.4.

Oral bicarbonate is not recommended because it may enhance salicylate absorption by accelerating

tablet dissolution.

Discontinue bicarbonate once the serum salicylate concentrations are less than 30 mg/dL or there

is a resolution of clinical symptoms.

Alkaline diuresis will increase potassium secretion, and hypokalemia will make it more challenging to

raise the urine pH. Adequate potassium concentrations should be aggressively maintained.