Salicylate
Pathophysiology
Interference with cellular metabolism (Uncouple oxidative phosphorylation) produces lactic acidosis and generates heat causing anion gap metabolic acidosis, hyperpyrexia, and hypoglycemia
Stimulate respiratory centers to cause hyperventilation causing respiratory alkalosis and increased insensible fluid losses
Salicylate exists more in the uncharged form at an acidic pH and is able to cross the blood-brain barrier causing CNS toxicity
Stimulation of chemoreceptors in the medulla causes nausea and vomiting
Toxic doses:
Aspirin PO: 150 mg/kg or 6.5 grams
Any PO oil of wintergreen exposure
Significant dermal exposures & signs of toxicity
Examples of salicylates : Aspirin, Pepto-Bismol, Ben-gay, and wintergreen oil
Presentation
Early: tinnitus, vertigo, tachypnea (respiratory alkalosis*), GI symptoms,
*Children almost never manifest a respiratory alkalosis and, when significantly poisoned, almost always progress right to acidemia secondary to metabolic acidosis.
Late: metabolic acidosis, hypovolemia, hypokalemia, hypoglycemia
Severe intoxication: fever, AMS, seizures, pulmonary edema
Diagnosis
Consult Poison Control: 1-800-222-1222
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Although there is no absolute correlation between plasma salicylate concentration and symptoms, most patients show signs of intoxication when the plasma concentration exceeds 30 mg/dL.
Repeat every 2 hours until the level is declining. Life-threatening complications of salicylate intoxication may occur when plasma concentrations are decreasing or near-therapeutic. A decreasing plasma concentration in a patient with progressive clinical manifestations may indicate increased tissue and/or CNS distribution.
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Monitor for hypoglycemia. Salicylate-poisoned patients’ mental status can improve significantly with just glucose administration. This is something that should be acted upon very early. These patients can often have hypoglycorrhachia even with relatively normal serum glucose measurements.
Repeat every 2 hours until acid-base status is stable or improving
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Monitor for hypernatremia 2/2 dehydration, hypokalemia, hypoglycemia, AKI
Monitor for leukocytosis, impaired clotting
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Urine pH is used to monitor the success of alkalization
Assess for other co-ingestions
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Monitor for arrhythmias especially if hypokalemic
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To evaluate for pulmonary edema in presence of hypoxemia or crackles
Management
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A: Avoid intubation! Patients require their own high-minute ventilation to create a respiratory alkalosis to "trap" salicylate anions in the blood preventing them from crossing into the CNS. If intubation is absolutely necessary, give a bolus dose of sodium bicarbonate IV (2 mEq/kg IV) just prior to intubation to alkalinize blood and urine.
B: Provide supplemental oxygen as needed. Consider CPAP if persistently hypoxic secondary to pulmonary edema.
C: Start D5W+ NaHCO3 + 20-40KCl @ 1.5 - 2 xmIVF. Avoid if pulmonary or cerebral edema is present. Hypokalemia must be treated aggressively as it promotes the excretion of H+ in exchange for K in the kidneys, thus interfering with urinary alkalization.
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Activated charcoal
(1 g/kg; max 50 g) every 4 hours until symptoms resolve or plasma salicylate concentration is <40 mg/dL.
Aspirins can form gastric concretions which may delay absorption as long as 60 hours after large ingestions, so AC should be given for any clinical signs of salicylate poisoning, even several hours after ingestion.
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Maintenance therapy: 100 to 150 mEq sodium bicarbonate in 1 L of D5W, run at 250 mL/hour in adults OR run at 1.5 to 2 times maintenance in children.
The goal is to achieve a urine pH >7.5 while maintaining a serum pH no greater than 7.55. Alkalemia (arterial pH up to 7.55) is NOT a contraindication to sodium bicarbonate therapy. The sodium bicarbonate infusion should continue until clinical findings of toxicity have resolved and the plasma salicylate concentration is less than 30 mg/dL (300 mg/L).
Correct hypokalemia, hypocalcemia and other electrolyte abnormalities. IV sodium bicarbonate is NOT compatible with calcium salts.
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Dialysis is recommended if ANY of the following are met (Regardless of the plasma salicylate levels, if severe clinical manifestations are present, do not delay hemodialysis as fatal poisonings have been seen despite low salicylate levels):
- [salicylate] > 7.2 mmol/L (100 mg/dL)
- [salicylate] > 6.5 mmol/L (90 mg/dL) in the presence of impaired kidney function
- presence of altered mental status
- presence of new hypoxemia requiring supplemental oxygen
If standard therapy (supportive measures, bicarbonate, etc.) fails, dialysis is suggested if any of the following are met:
- [salicylate] > 6.5 mmol/L (90 mg/dL)
- [salicylate] > 5.8 mmol/L (80 mg/dL) in the presence of impaired kidney function
- Systemic pH is ≤ 7.20
References
Juurlink DN, Gosselin S, Kielstein JT, Ghannoum M, Lavergne V, Nolin TD, Hoffman RS; EXTRIP Workgroup. (2015) "Extracorporeal Treatment for Salicylate Poisoning: Systematic Review and Recommendations From the EXTRIP Workgroup." Ann Emerg Med. 266(2):165-81. https://www.extrip-workgroup.org/salicylates
