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
    1. Salicylates directly stimulate the respiratory center of the brain → hyperventilation → CO2 washout → primary respiratory alkalosis
    2. Disruption of mitochondrial oxidative phosphorylation → inhibition of TCA cycle and ATP production → accumulation of lactic acid and ketones → ↑ anion gap metabolic acidosis
    3. 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


FeatureSalicylate (ASA) PoisoningAcetaminophen (APAP) PoisoningReye Syndrome
Classic HxOverdose (intentional/accidental)Intentional OD; chronic EtOH useChild after viral illness + ASA use
PathophysiologyUncouples ox-phos;
Resp center stim;
Direct ototoxicity
Glutathione depletion toxic metabolite (NAPQI) liver necrosisMitochondrial dysfunction fatty liver & encephalopathy
PresentationTinnitus, fever, hyperventilation, AMSAsymptomatic initially RUQ pain fulminant liver failureProfuse vomiting, delirium/coma, NO jaundice
Key Lab FindingMixed resp. alkalosis + metabolic acidosisMassive AST/ALT elevation (>1000s)Hyperammonemia, elevated LFTs, hypoglycemia
Antidote / TxIV Sodium Bicarbonate, HemodialysisN-acetylcysteine (NAC)Supportive care (manage ICP, hypoglycemia)
Buzzword”Mixed acid-base disorder""Rumack-Matthew nomogram""Child + virus + aspirin”
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Treatment


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