At the Bedside

  • Think of it in any patient with tinnitus, tachypnea, diaphoresis, vomiting, fever, confusion, or unexplained acid-base abnormalities.
  • Initial assessment
  • Vitals, mental status, temperature, work of breathing.
  • Look for tachypnea with respiratory alkalosis early; later a high anion gap metabolic acidosis develops.
  • Evaluate for co-ingestants and intentional overdose.
  • Key diagnostics
  • ABG/VBG and BMP with anion gap.
  • Serum salicylate level: obtain on arrival and repeat q2 hours until clearly downtrending and clinical improvement is evident.
  • Glucose: serum glucose may be normal while CNS glucose is low; check bedside glucose.
  • CMP, creatinine, LFTs, lactate, CBC, coagulation studies.
  • EKG: nonspecific; evaluate for co-toxicity.
  • CXR if pulmonary edema or respiratory symptoms.
  • Classic acid-base pattern
  • Early: respiratory alkalosis from medullary stimulation.
  • Later: respiratory alkalosis + anion gap metabolic acidosis.
  • Severe disease may show acidemia, rising salicylate level, altered mental status, hypoxemia.
  • Decontamination
  • Activated charcoal if early presentation and airway protected; can be considered later in large ingestions or enteric-coated tablets if ileus not present.
  • Alkalinization
  • IV sodium bicarbonate is first-line for significant toxicity.
  • Goal: serum pH ~7.50–7.55 and urine pH 7.5–8.0.
  • Replete potassium aggressively; hypokalemia prevents urine alkalinization.
  • Typical approach: isotonic bicarbonate infusion (institution-specific), with boluses if acidemic.
  • Disposition / dialysis
  • Hemodialysis for severe poisoning: altered mental status, seizures, pulmonary edema, refractory acidosis, renal failure, rising levels despite therapy, or significant clinical deterioration.
  • Dialysis is also favored when serum salicylate is very high or symptoms are severe; thresholds vary with chronicity and clinical status, so use a toxicology reference.
  • ICU for most significant cases.
  • Important pitfall
  • Do not intubate casually: apnea or inadequate post-intubation minute ventilation can rapidly worsen acidemia and CNS salicylate penetration. If intubation is unavoidable, match or exceed the patient’s pre-intubation minute ventilation and involve toxicology/dialysis early.
A Classic Presentation
A 24-year-old with tinnitus, vomiting, and rapid breathing after ingesting “a bunch of aspirin” 6 hours ago is tachycardic, diaphoretic, and mildly confused. VBG shows respiratory alkalosis with low bicarbonate and elevated anion gap; salicylate level is elevated and rising on repeat. He is started on bicarbonate infusion with potassium repletion and admitted to the ICU; nephrology is notified early for possible dialysis.

Study Directive

  • Draw the salicylate acid-base timeline from memory: early respiratory alkalosis → mixed disorder → severe metabolic acidosis.
  • Memorize the urine pH goal (7.5–8.0) and the reason potassium must be corrected.
  • Practice a 1-minute toxicology oral script: “salicylate patient, what is your resuscitation, what labs do you repeat, when do you dialyze?”
  • Review your institution’s bicarbonate infusion recipe and dialysis escalation pathway.
  • Read 3 practice questions focused on intubation pitfalls in salicylate toxicity.

Recent Literature