Internal Medicine · Year 3 · from Internal Medicine

Case 2: Salicylate Toxicity with Mixed Acid-Base Disorder

Patient Demographics

  • Age: 67 years
  • Sex: Male
  • Occupation: Retired engineer

Chief Complaint

"I'm confused and hearing ringing in my ears."

History of Present Illness

The patient's wife brought him to the emergency department after finding him confused at home. She reports he has been complaining of severe headaches for the past 3 days and has been taking "extra aspirin" for pain relief. The patient has a history of chronic pain from osteoarthritis and has been using over-the-counter aspirin regularly. His wife found multiple empty aspirin bottles in the bathroom. The patient appears agitated and keeps complaining of a loud ringing in his ears. He has also been breathing rapidly and seems short of breath despite having clear lungs.

Vital Signs

  • Temperature: 100.4 degrees F (38.0 degrees C)
  • Blood pressure: 146/88 mmHg
  • Heart rate: 108 bpm
  • Respiratory rate: 32/min (tachypneic)
  • Oxygen saturation: 98% on room air

Physical Examination

General: Agitated, diaphoretic, confused HEENT: Pupils reactive, tinnitus reported, mucous membranes dry Cardiovascular: Tachycardic, regular rhythm Pulmonary: Tachypneic with clear lung fields, no wheezes or crackles Abdomen: Mild epigastric tenderness, no guarding Neurologic: Disoriented to time and place, tremulous, hyperreflexic

Laboratory Findings

Arterial Blood Gas:

  • pH: 7.48 (high - alkalemia)
  • PaCO2: 22 mmHg (low)
  • PaO2: 92 mmHg
  • HCO3: 16 mEq/L (low)

Basic Metabolic Panel:

  • Sodium: 140 mEq/L
  • Potassium: 3.4 mEq/L
  • Chloride: 106 mEq/L
  • Bicarbonate: 16 mEq/L
  • BUN: 24 mg/dL
  • Creatinine: 1.1 mg/dL
  • Glucose: 78 mg/dL

Additional Studies:

  • Anion gap: 140 - (106 + 16) = 18 mEq/L (elevated)
  • Salicylate level: 68 mg/dL (therapeutic 10-30, toxic > 40)
  • Serum lactate: 2.8 mmol/L (mildly elevated)

Systematic ABG Interpretation

Step 1 - pH Assessment: pH 7.48 indicates alkalemia

Step 2 - Primary Disorder: High pH with low PaCO2 = primary respiratory alkalosis BUT: HCO3 is also low, which is unexpected if this were pure respiratory alkalosis with compensation

Step 3 - Analyzing the Pattern: This is the classic mixed acid-base disorder of salicylate toxicity:

  • Respiratory alkalosis: Salicylates directly stimulate the medullary respiratory center, causing hyperventilation (low PaCO2)
  • Metabolic acidosis: Salicylates uncouple oxidative phosphorylation, causing accumulation of organic acids (elevated anion gap with low HCO3)

Step 4 - Expected Values:

  • For acute respiratory alkalosis: HCO3 should decrease by 2 mEq/L for every 10 mmHg decrease in PaCO2
  • Expected HCO3 = 24 - 2 x (40-22)/10 = 24 - 3.6 = 20.4 mEq/L
  • Actual HCO3 = 16 mEq/L (lower than expected)
  • The HCO3 is lower than respiratory compensation alone would predict, confirming concurrent metabolic acidosis

Diagnosis

Salicylate toxicity with mixed respiratory alkalosis and anion gap metabolic acidosis

  • Salicylate level 68 mg/dL (severely elevated)
  • Characteristic mixed acid-base disorder
  • Tinnitus, altered mental status, hyperpnea, hyperthermia

Management

Immediate stabilization:

  1. Activated charcoal 50g PO/NG if within 2 hours of ingestion
  2. IV access and continuous cardiac monitoring
  3. Serial salicylate levels every 2 hours until declining

Urinary alkalinization:

  1. Sodium bicarbonate drip: 150 mEq NaHCO3 in 1L D5W at 200 mL/hour
  2. Goal urine pH 7.5-8.0 (ion trapping enhances renal salicylate excretion)
  3. Monitor serum potassium closely (alkalinization causes hypokalemia)
  4. Replace potassium to maintain K > 4.0 mEq/L (required for effective urinary alkalinization)

Hemodialysis indications (present in this case):

  1. Nephrology consultation for urgent hemodialysis
  • Salicylate level > 60 mg/dL with symptoms
  • Altered mental status
  • Renal failure (relative indication)
  • Pulmonary edema
  • Failure to respond to urinary alkalinization

Supportive care:

  1. Avoid intubation if possible (loss of respiratory compensation can be fatal)
  2. IV fluids for volume depletion
  3. Dextrose supplementation (salicylates deplete CNS glucose)
  4. Temperature monitoring and cooling measures

Clinical Pearl

Salicylate toxicity produces a nearly pathognomonic mixed acid-base disorder: respiratory alkalosis from direct stimulation of the respiratory center combined with anion gap metabolic acidosis from uncoupled oxidative phosphorylation. The pH may be elevated, normal, or low depending on which process predominates - early toxicity favors respiratory alkalosis while late or severe toxicity favors metabolic acidosis. A critical management principle is to avoid intubation if at all possible: the patient's hyperventilation is a life-saving compensatory mechanism, and controlled mechanical ventilation cannot match the minute ventilation these patients generate spontaneously. Loss of respiratory compensation upon intubation can cause precipitous acidosis and cardiovascular collapse.

Clinical Image

Image Description: Diagram illustrating the metabolic derangements in acid-base disorders, highlighting how salicylate toxicity produces the characteristic mixed respiratory alkalosis and metabolic acidosis pattern.

Attribution: Image from Wikimedia Commons. Licensed under CC BY-SA 3.0. Source: https://commons.wikimedia.org/wiki/File:Metabolic_acidosis.svg

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