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Key Features

Essentials of Diagnosis

  • Tachypnea, altered mental status

  • Metabolic acidosis

  • Typical arterial blood gases reveal respiratory alkalosis and metabolic acidosis

  • Elevated salicylate level diagnostic

General Considerations

  • Salicylates (eg, aspirin, methyl salicylate, bismuth subsalicylate) are found in a variety of over-the-counter and prescription medications

  • Salicylates uncouple cellular oxidative phosphorylation, resulting in anaerobic metabolism and excessive production of lactic acid and heat, and interfere with several Krebs cycle enzymes

  • A single ingestion of more than 200 mg/kg of salicylate can cause intoxication

  • Poisoning may also occur as a result of excessive dosing over several days

  • Although the half-life of salicylate is 2–3 h after small doses, it may increase to 20 h or more in patients with intoxication

Clinical Findings

Symptoms and Signs

  • Acute ingestion

    • Nausea and vomiting, occasionally with gastritis

  • Moderate intoxication

    • Hyperpnea (deep and rapid breathing), tachycardia, and tinnitus

  • Serious intoxication

    • Agitation, confusion, seizures

    • Cardiovascular collapse, pulmonary edema, hyperthermia

    • Death

Differential Diagnosis

  • Other causes of anion gap acidosis

    • Alcoholic ketoacidosis

    • Metformin toxicity

    • Isoniazid poisoning

    • Iron poisoning

    • Methanol or ethylene glycol toxicity

    • Carbon monoxide poisoning

  • Acetaminophen poisoning (common coingestion)

Diagnosis

Laboratory Tests

  • Diagnosis is suspected in any patient with an anion gap metabolic acidosis and is confirmed by measuring the stat serum salicylate level

  • Patients with serum salicylate levels > 100 mg/dL (1000 mg/L or 7.2 mcmol/L) after an acute overdose are more likely to have severe poisoning

  • Patients with subacute or chronic intoxication may suffer severe symptoms with serum salicylate levels of only 60–70 mg/dL (4.3–5 mcmol/L)

  • Arterial blood gases typically reveal a respiratory alkalosis with an underlying metabolic acidosis

  • Prothrombin time is often elevated owing to salicylate-induced hypoprothrombinemia

  • Central nervous system intracellular glucose depletion can occur despite normal measured serum glucose levels

Treatment

Medications

Emergency and supportive measures

  • Activated charcoal

    • Administer 60–100 g orally or via gastric tube, mixed in aqueous slurry

    • Do not use for comatose or convulsing patients unless it can be given by gastric tube and the airway is protected by a cuffed endotracheal tube

    • Extra doses of activated charcoal may be needed in patients who ingest more than 10 g of aspirin (desired ratio of charcoal to aspirin: ~10:1 by weight)

    • Although extra doses cannot always be given as a single dose, they may be administered over the first 24 h in divided doses every 2–4 h along with whole bowel irrigation

  • Give glucose-containing fluids to reduce the risk of cerebral hypoglycemia

  • Treat metabolic acidosis with intravenous sodium bicarbonate

    • This is critical because acidosis (acidemia, pH < 7.40) promotes greater entry of salicylate into cells, worsening toxicity

Specific treatment

  • Alkalinization of the urine enhances renal salicylate excretion by trapping the salicylate anion in the urine

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