Treatment of High Anion Gap Metabolic Acidosis
The treatment of high anion gap metabolic acidosis (HAGMA) requires prompt identification and management of the underlying cause while providing supportive care to correct the acidosis. 1
Initial Assessment
- HAGMA is confirmed by an anion gap ≥17 with low serum bicarbonate (CO2 <20 mEq/L) 1
- Laboratory evaluation should include plasma glucose, BUN/creatinine, serum ketones, electrolytes, osmolality, urinalysis, arterial blood gases, and CBC 1
- Identify the underlying cause (diabetic ketoacidosis, lactic acidosis, toxin ingestion, renal failure) as treatment varies by etiology 1, 2
General Management Principles
Fluid Resuscitation
- Begin with isotonic saline (0.9% NaCl) at 15-20 ml/kg/h during the first hour to expand intravascular volume and restore renal perfusion 1
- For patients with risk of hyperchloremia, consider balanced crystalloid solutions like Ringer's Lactate 2
Electrolyte Management
- Once renal function is assured, include 20-30 mEq/L potassium (2/3 KCl and 1/3 KPO4) in the infusion fluid 1
- Monitor serum electrolytes every 2-4 hours until stabilized 1
- Consider phosphate replacement (20-30 mEq/L potassium phosphate) for patients with serum phosphate <1.0 mg/dL 1
Specific Treatment Based on Etiology
Diabetic Ketoacidosis (DKA)
- Administer regular insulin as continuous IV infusion at 0.1 units/kg/h after an initial bolus of 0.1 units/kg 1
- For mild DKA, a "priming" dose of regular insulin (0.4-0.6 units/kg) can be given, half as IV bolus and half as subcutaneous/intramuscular injection 3
- Continue insulin until ketoacidosis resolves (pH >7.3, bicarbonate ≥18 mEq/L, and normalized anion gap) 1
- Monitor resolution when glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, and venous pH >7.3 3
Lactic Acidosis
- Focus on treating the underlying cause (shock, tissue hypoxia, medications) 4
- Effective therapy of lactic acidosis due to shock is to reverse the cause 4
Toxin-Induced Acidosis
- For toxins like methanol, ethylene glycol, or salicylates, consider specific antidotes and extracorporeal treatment if criteria are met 2
- For severe toxin ingestion with pH ≤7.20, consider hemodialysis 2
Renal Failure
- If metabolic acidosis persists despite medical management, consider renal replacement therapy 2
- For patients with impaired kidney function (creatinine >2 mg/dL), hemodialysis may be necessary 2
Bicarbonate Therapy
Bicarbonate therapy is generally not recommended for pH >7.0, as it has not been shown to reduce morbidity or mortality and may worsen intracellular acidosis. 1, 4
- For severe acidosis with pH <7.0, consider sodium bicarbonate administration 1, 5
- For pH 6.9-7.0, administer 50 mmol sodium bicarbonate diluted in 200 ml sterile water at 200 ml/h 3
- For pH <6.9, administer 100 mmol sodium bicarbonate in 400 ml sterile water at 200 ml/h 3
- In cardiac arrest with severe acidosis, 44.6-100 mEq may be given initially and continued at 44.6-50 mEq every 5-10 minutes if necessary 5
- Be cautious with rapid infusion as bicarbonate solutions are hypertonic and may produce undesirable rise in plasma sodium 5
Monitoring and Follow-up
- Monitor blood gases, pH, electrolytes, BUN, creatinine, and glucose every 2-4 hours until stabilized 1
- Direct measurement of ketones may be necessary to monitor resolution of ketoacidosis 3
- Venous pH (usually 0.03 units lower than arterial pH) and anion gap can be followed to monitor resolution of acidosis 3
- Watch for cerebral edema, especially in pediatric patients 1
- Monitor for hypoxemia and pulmonary edema 1
Pitfalls to Avoid
- Avoid excessive normal saline administration, which can worsen hyperchloremic acidosis 2
- Avoid overzealous bicarbonate therapy, which can cause fluid overload and paradoxical CNS acidosis 2
- Don't rely on nitroprusside method for ketone measurement as it only measures acetoacetic acid and acetone, not β-hydroxybutyrate (the strongest and most prevalent acid in DKA) 3
- Don't delay treatment while waiting for complete diagnostic workup in severe acidosis 3
- Avoid continued use of non-invasive ventilation when the patient is deteriorating rather than escalating to invasive mechanical ventilation in respiratory acidosis 3