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General Reference

Ann IM 1976;85:745

Pathophys and Cause

Cause:ASA ingestion of >10 gm (120 mg/kg), >500 mg/kg usually fatal, acutely or chronically build level up

Pathophys:Respiratory stimulation via respiration centers and chemoreceptors; oxidative metabolism uncoupling. Direct CNS stimulation; gastric irritant

Epidemiology

Common in children, adult suicides, and the elderly treating various medical illnesses with ASA (insidious, high morbidity, and mortality)

Signs and Symptoms

Sx:Dizziness; can be precipitated by steroid withdrawal; nausea, tinnitus, emesis

Si:Fever and hypermetabolism; respiratory alkalosis then metabolic acidosis; confusion evolving into convulsions

Complications

CNS damage with seizures, from anoxia; coma; shock

Pulmonary edema even as ASA level decreasing due to increased capillary permeability, especially in smokers (Ann IM 1981;95:405)

Lab and Xray

Lab:

Chem:Salicylate level initially and 6 h postingestion; >70 mg % (indicates 10-30 gm ingested); therapeutic levels in RA lteq.gif30 mg %; lytes show respiratory alkalosis evolving into metabolic acidosis or a combination of both

Hem:Protime increased

Urine:10% FeCl3 to 1 mL of urine shows a purple color

Xray:KUB may show size of pill bolus in gi tract

Treatment

Rx:

Respiratory alkalosis alone usually requires no rx

Glucose iv to avoid ASA-induced hypoglycemia (Nejm 1973;288:1110) of metabolic acidosis: supportive care and respirator; correct lyte imbalances, eg, acidosis; dialyze soon; NaHCO3 1 mM/kg w 20 mEq KCL diluted in 500 D51/2S at 2-3 mL/kg/h iv to alkalinize urine or as iv push without increasing fluids probably best (BMJ 1982;285:1383)

Vit K for protime prolongation

Hemodialysis if initial salicylate level >120 mg % or 6-h level >100 mg %, or renal failure, or hypoxia, CHF, pulmonary edema, or persistent CNS changes (seizures, coma, confusion)