Salicylate poisoning is a serious complication of aspirin overdose and is characterized by mixed respiratory alkalosis and increased anion gap metabolic acidosis.
Pathophysiology
- Early mixed respiratory alkalosis → ↑ anion gap metabolic acidosis
- Salicylates directly stimulate the respiratory center of the brain → hyperventilation → CO2 washout → primary respiratory alkalosis
- Disruption of mitochondrial oxidative phosphorylation → inhibition of TCA cycle and ATP production → accumulation of lactic acid and ketones → ↑ anion gap metabolic acidosis
- Fatigue impairs the ability to compensate for acidosis (via hyperventilation) → hemodynamic instability and end-organ damage
- ↑ Pulmonary capillary permeability → ARDS with pulmonary edema.
Clinical features
- Early symptoms: tinnitus, nausea, vomiting, tachypnea, hyperpnea
- Late symptoms: hyperthermia, agitation, delirium, seizures, noncardiogenic pulmonary edema
Diagnostics
Differential diagnostics
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Feature Salicylate (ASA) Poisoning Acetaminophen (APAP) Poisoning Reye Syndrome Classic Hx Overdose (intentional/accidental) Intentional OD; chronic EtOH use Child after viral illness + ASA use Pathophysiology Uncouples ox-phos;
Resp center stim;
Direct ototoxicityGlutathione depletion → toxic metabolite (NAPQI) → liver necrosis Mitochondrial dysfunction → fatty liver & encephalopathy Presentation Tinnitus, fever, hyperventilation, AMS Asymptomatic initially → RUQ pain → fulminant liver failure Profuse vomiting, delirium/coma, NO jaundice Key Lab Finding Mixed resp. alkalosis + metabolic acidosis Massive AST/ALT elevation (>1000s) Hyperammonemia, elevated LFTs, hypoglycemia Antidote / Tx IV Sodium Bicarbonate, Hemodialysis N-acetylcysteine (NAC) Supportive care (manage ICP, hypoglycemia) Buzzword ”Mixed acid-base disorder" "Rumack-Matthew nomogram" "Child + virus + aspirin”
Treatment
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