A 12-year-old girl is brought to the emergency department 4 hours after ingesting an unknown amount of aspirin (acetylsalicylic acid) during a suicide attempt. She complains of tinnitus, nausea, vomiting, and feels “hot”. On examination: alert but anxious, respiratory rate 32/min (deep, rapid breathing), heart rate 120 bpm, blood pressure 110/70 mm Hg, temperature 38.2°C. No focal neurologic deficits.
🎯 Task (examiner observed): Interpret the ABG, identify the acid-base disorder(s), explain the pathophysiology of salicylate toxicity, and outline immediate management including airway, IV fluids, bicarbonate administration, and indications for hemodialysis.
Step 1: pH = 7.50 → ALKALEMIA (primary disorder must be alkalosis). Step 2: PCO2 = 20 mm Hg (↓) → low PCO2 causes alkalemia → primary respiratory alkalosis. Step 3: HCO3 = 15 mEq/L (↓) – this is NOT causing alkalemia (low HCO3 causes acidosis). So we have two opposing primary disorders: respiratory alkalosis (low PCO2) AND metabolic acidosis (low HCO3). Step 4: Is compensation appropriate? For acute respiratory alkalosis, expected HCO3 drops by 2 for every 10 mm Hg drop in PCO2. PCO2 drop = 20 → expected HCO3 = 24 - (2×2) = 20. But actual HCO3 is 15, which is lower than expected → indicates a concurrent primary metabolic acidosis. Conclusion:MIXED DISORDER: Primary respiratory alkalosis + primary metabolic acidosis (high anion gap metabolic acidosis) from salicylate toxicity.
⚠️ SALICYLATE TOXICITY – Classic ABG Pattern (Nelson Ch 73.7):
Salicylates directly stimulate the respiratory center → primary respiratory alkalosis (hyperventilation, low PCO2). Simultaneously, salicylates cause high anion gap metabolic acidosis due to accumulation of organic acids (salicylic acid, lactic acid, ketoacids). The net pH depends on which process dominates. Children often present with mixed picture as seen here (alkalemic but with metabolic acidosis). As toxicity worsens, metabolic acidosis predominates → pH becomes acidemic.
🩺 Tinnitus (classic)
🌬️ Tachypnea 32/min
🤢 Nausea/vomiting
🌡️ Fever 38.2°C
📈 Anion gap 22
💊 Salicylate level 45 mg/dL
💡 Examiner instruction: Candidate must: (1) correctly interpret mixed acid-base disorder, (2) recognize that this child has both respiratory alkalosis and metabolic acidosis, (3) explain salicylate pathophysiology, (4) outline treatment: activated charcoal (if early), IV fluids, potassium repletion, sodium bicarbonate for urinary alkalinization, (5) discuss indications for hemodialysis (level >90-100 mg/dL, severe acidosis, altered mental status, renal failure).
❓ Q1 (Examiner): “Interpret this ABG: pH 7.50, PCO2 20, HCO3 15. What are the primary acid-base disorders?”
✅ Mixed disorder: Primary respiratory alkalosis + primary high anion gap metabolic acidosis.
Respiratory alkalosis from salicylate-induced central hyperventilation. Metabolic acidosis from accumulation of salicylic acid, lactic acid (due to uncoupled oxidative phosphorylation), and ketoacids. The pH is alkalemic because respiratory alkalosis is dominant at this stage.
❓ Q2 (Examiner): “What is the pathophysiology of salicylate-induced acid-base disturbances?”
✅ Salicylates directly stimulate the respiratory center in the medulla → increased rate and depth of breathing → respiratory alkalosis. Simultaneously, salicylates cause uncoupling of oxidative phosphorylation → increased metabolic rate, oxygen consumption, and lactate production → lactic acidosis. Also, accumulation of salicylic acid (weak acid) and increased ketoacid production (due to altered fat metabolism) → high anion gap metabolic acidosis. Infants and young children present more often with acidosis; older children may have mixed picture as seen here.
❓ Q3 (Examiner): “What is the expected appropriate respiratory compensation for a primary metabolic acidosis? Why is this not appropriate compensation?”
✅ For primary metabolic acidosis, Winter's formula: PCO2 = 1.5 × [HCO3] + 8 ± 2. Here: 1.5×15 + 8 = 30.5 ± 2 = 28.5-32.5 mm Hg. But actual PCO2 is 20, which is much lower than expected for compensation. Therefore, the low PCO2 is NOT just compensation – it represents a primary respiratory alkalosis.
❓ Q4 (Examiner): “What is the expected metabolic compensation for acute respiratory alkalosis and how does it compare to this patient?”
✅ For acute respiratory alkalosis, HCO3 decreases by 2 mEq/L for every 10 mm Hg drop in PCO2. Drop of 20 mm Hg → expected HCO3 = 24 - 4 = 20 mEq/L. Actual HCO3 is 15 (<20), which is lower than expected → indicates a concurrent primary metabolic acidosis.
❓ Q5 (Examiner): “What is the anion gap in this patient? Why is it elevated?”
✅ Anion gap = Na – (Cl + HCO3). Assuming normal electrolytes, AG ~22 (normal 8-12). Elevated due to unmeasured anions from salicylic acid, lactate, acetoacetate, and beta-hydroxybutyrate. This confirms a high anion gap metabolic acidosis component.
❓ Q6 (Examiner): “What is the first-line treatment for salicylate poisoning? Discuss urinary alkalinization.”
✅ Urinary alkalinization with IV sodium bicarbonate is cornerstone. Goal: achieve urine pH 7.5-8.0. Mechanism: alkalinization traps salicylate in ionized form in renal tubule, preventing reabsorption and enhancing excretion. Protocol: 1-2 mEq/kg IV sodium bicarbonate bolus, then infusion (e.g., D5 0.45% NS + 3 ampules NaHCO3/L) at 1.5-2× maintenance. Monitor urine pH, serum potassium (critical – hypokalemia prevents alkalinization), and serum salicylate levels.
❓ Q7 (Examiner): “Why is potassium repletion critical during urinary alkalinization?”
✅ Hypokalemia impairs the kidney's ability to acidify urine and excrete bicarbonate. Without adequate potassium, urine cannot be alkalinized. Always check K+ and replete before or simultaneously with bicarbonate infusion. Target K+ >4.0 mEq/L.
❓ Q8 (Examiner): “What are the indications for hemodialysis in salicylate poisoning?”
✅ Indications for hemodialysis (EXTRIP guidelines):
- Serum salicylate level >90 mg/dL (acute ingestion) or >100 mg/dL (chronic)
- Severe metabolic acidosis (pH <7.20) refractory to bicarbonate
- Altered mental status (seizures, coma)
- Acute kidney injury or pulmonary edema
- Failure of conservative management (rising levels despite alkalinization)
- End-organ damage (hepatitis, coagulopathy)
Hemodialysis rapidly removes salicylate and corrects acid-base abnormalities.
❓ Q9 (Examiner): “What is the role of activated charcoal in salicylate overdose?”
✅ Activated charcoal (1 g/kg, max 50 g) is effective if given <1-2 hours post-ingestion. Multiple-dose charcoal (q4h for 2-3 doses) may enhance elimination via “gastrointestinal dialysis” because salicylates undergo enterohepatic recirculation. Contraindications: unprotected airway (risk of aspiration), ileus, bowel obstruction.
❓ Q10 (Examiner): “What other supportive measures are important in salicylate poisoning?”
✅ Supportive care: IV fluids (correct dehydration from vomiting and insensible losses), dextrose to prevent hypoglycemia (especially children), electrolyte monitoring (K+, Ca2+), temperature control (fever increases metabolic demand), seizure management (benzodiazepines), and respiratory support if needed (intubation risks: may worsen acidosis if hyperventilation is compensatory).
❓ Q11 (Examiner): “Why is intubation dangerous in severe salicylate poisoning?”
✅ Intubation and mechanical ventilation may abruptly lower the respiratory rate, removing the compensatory hyperventilation that partially corrects the metabolic acidosis. This can cause rapid worsening of acidemia and cardiovascular collapse. If intubation is required (e.g., for airway protection), hyperventilate aggressively to maintain PCO2 at 25-30 mm Hg and give sodium bicarbonate pre-emptively.
❓ Q12 (Examiner): “What is the classic clinical triad of salicylism?”
✅ Tinnitus, hyperventilation (tachypnea), and vomiting. Also: fever, diaphoresis, altered mental status (confusion, delirium, seizures, coma), noncardiogenic pulmonary edema, hypoglycemia (especially children), and acute kidney injury.
📢 Examiner probe: “What if the patient had a pH of 7.25 instead of 7.50?” → That would indicate predominant metabolic acidosis, which is more severe and has worse prognosis. Hemodialysis is more urgent.
💊 Management of Salicylate Overdose (Nelson Chapter 73.7)
2. DECONTAMINATION (if early and patient is stable):
- Activated charcoal 1 g/kg (max 50 g) if within 1-2 hours; multiple-dose charcoal (q4h x 3 doses) for severe ingestion due to delayed gastric emptying and enterohepatic circulation
- Gastric lavage rarely beneficial if >1 hour unless massive ingestion
3. URINARY ALKALINIZATION (core treatment):
- Goal: urine pH 7.5-8.0, serum pH 7.45-7.55 (avoid over-alkalemia)
- Sodium bicarbonate: bolus 1-2 mEq/kg IV, then infusion: D5 0.45% NS + 3 ampules NaHCO3 (150 mEq) per liter, run at 1.5-2× maintenance
- ⚠️ MUST replete potassium (K+ >4.0) to allow urinary alkalinization
- Monitor urine pH q1h, serum pH q2-4h, salicylate level q4h
4. SUPPORTIVE CARE:
- IV fluids (maintain euvolemia)
- Dextrose infusion to prevent hypoglycemia
- Correct hypokalemia aggressively (KCl 20-40 mEq/L in fluids or IV push if severe)
- Antipyretics (physical cooling; avoid NSAIDs/acetaminophen if possible)
🚨 CONTRAINDICATIONS to urinary alkalinization: Pulmonary edema, acute kidney injury (oliguric), severe hypokalemia refractory to repletion, uncontrolled seizures. In these cases, proceed directly to hemodialysis.
📊 MONITORING FREQUENCY:
- Salicylate level: every 2-4 hours until level falls and patient improves
- ABG/VBG: every 2-4 hours during active alkalinization
- Urine pH: hourly during bicarbonate infusion
- Electrolytes (especially K+): every 2-4 hours
- Glucose: hourly if altered mental status
🩸 Hemodialysis & Prognosis · Disposition Criteria
🩸 Hemodialysis indications (EXTRIP) Level >90 mg/dL (acute) or >100 mg/dL (chronic); severe acidosis (pH <7.20) refractory to bicarbonate; altered mental status; pulmonary edema; renal failure; rising levels despite alkalinization.
⚡ Why hemodialysis works Rapid removal of salicylate (clearance 100-150 mL/min vs 50-80 for kidneys), corrects acidosis, removes other organic acids, and removes salicylate in severe overdose where alkalinization insufficient.
📉 Prognosis Mortality <1% with prompt treatment. Poor prognostic factors: delayed presentation, very high level (>100), severe acidosis (pH <7.1), seizures, coma, multi-organ failure, age <2 years or >70 years.
🏥 Disposition criteria PICU admission for all symptomatic patients. Discharge when: salicylate level <30 mg/dL, normal mental status, no acidosis, able to maintain oral hydration, resolved symptoms.
👩⚕️ Family Counseling / Psychiatric Evaluation:
This was a suicide attempt in an adolescent. After medical stabilization:
- Psychiatric consult for safety assessment
- Suicide risk evaluation
- Safe disposal of medications at home
- Follow-up with mental health services
- Family support and education about medication storage
📖 Nelson Chapter 73.7 – Key quote: “Salicylate intoxication is now much less common because aspirin is no longer recommended for fever control in children. Acute salicylate intoxication occurs after a large overdose. In children, the metabolic acidosis is usually the more significant finding. Other symptoms of salicylate intoxication are fever, seizures, lethargy, and coma. Hyperventilation may be particularly marked. Tinnitus, vertigo, and hearing impairment are more likely with chronic salicylate intoxication.”
⭐ TAKE-HOME POINTS FOR TOACS:
- Salicylates cause a mixed respiratory alkalosis + high anion gap metabolic acidosis.
- pH may be alkalemic, normal, or acidemic depending on which component dominates.
- Treatment: activated charcoal (early), urinary alkalinization with sodium bicarbonate (goal urine pH 7.5-8.0), potassium repletion.
- Hemodialysis for severe toxicity (level >90, pH <7.2, altered mental status).
- Do NOT intubate without hyperventilating – may worsen acidosis.