Management of Ethanol Poisoning Induced Severe Metabolic Acidosis
For severe metabolic acidosis from ethanol poisoning (pH <7.2), immediately administer intravenous sodium bicarbonate while providing aggressive supportive care including fluid resuscitation, correction of hypoglycemia, and treatment of any coexisting conditions. 1
Initial Assessment and Stabilization
Immediate Laboratory Evaluation
- Obtain arterial blood gas to quantify pH, PaCO2, and severity of acidosis 2, 3
- Measure serum bicarbonate, anion gap (Na+ + K - Cl - HCO3-), and lactate levels 2, 4
- Check blood glucose immediately, as hypoglycemia commonly coexists with severe alcohol intoxication 4
- Assess renal function and electrolytes, particularly potassium, as correction of acidosis can precipitate hypokalemia 2, 3
Critical Clinical Features to Identify
- Level of consciousness using Glasgow Coma Scale 5
- Signs of shock: tachycardia, hypotension, prolonged capillary refill time (≥2 seconds), cold peripheries 5
- Respiratory status: work of breathing, oxygen saturation, respiratory rate 5
- Volume status and urine output (<1 ml/kg/hour suggests hypovolemia) 5
Bicarbonate Therapy Protocol
Indications for Sodium Bicarbonate
- Strongly indicated when pH <7.2 or serum bicarbonate <18 mmol/L 2, 1
- In cardiac arrest from severe acidosis, give rapid IV bolus of 44.6-100 mEq (one to two 50 mL vials) initially, then 44.6-50 mEq every 5-10 minutes as guided by arterial pH 1
Dosing for Non-Arrest Situations
- Administer 2-5 mEq/kg body weight over 4-8 hours for initial correction 1
- Target initial bicarbonate level of approximately 20 mEq/L within the first 24 hours, not full correction to normal 1
- Attempting complete normalization in the first day risks overshooting to alkalosis due to delayed ventilatory readjustment 1
Monitoring During Bicarbonate Administration
- Repeat arterial blood gases frequently to assess response 2, 1
- Monitor for complications: fluid overload, paradoxical CSF acidosis, hypocalcemia, and hypernatremia 3, 1
- In patients with respiratory compromise, use bicarbonate cautiously as it generates CO2 which may worsen respiratory acidosis if ventilation is impaired 3
Fluid Resuscitation
Fluid Selection and Administration
- Use balanced crystalloid solutions rather than 0.9% normal saline, as normal saline worsens hyperchloremic acidosis 2
- In absence of coma (GCS >8), administer 20-40 ml/kg of balanced crystalloid or 0.9% saline to correct hypovolemia and shock 5
- In patients with coma (GCS ≤8) and shock, use more cautious volume expansion; consider 4.5% albumin solution which showed lower mortality (5%) versus saline (46%) in this subgroup 5
Volume Resuscitation Endpoints
- Stop fluid boluses once signs of circulatory failure reverse 5
- Target urine output >1 ml/kg/hour as indicator of adequate renal perfusion 5
- After 40 ml/kg without improvement, consider elective intubation and central venous pressure monitoring 5
Supportive Care Measures
Airway and Breathing Management
- Maintain airway patency; consider elective intubation if GCS ≤8 or persistent shock despite fluids 5
- When initiating mechanical ventilation in severe acidosis, avoid rapid rise in PaCO2 even to normal levels before acidosis is partly corrected, as patients may be compensating with very low PaCO2 5
- Provide supplemental oxygen to maintain saturation >95% 5
Metabolic Corrections
- Immediately correct hypoglycemia (blood glucose <3 mmol/L) with IV dextrose 5, 4
- Monitor and correct electrolyte abnormalities, particularly potassium, magnesium, and phosphate 3, 4
- Address hypothermia if present, as this commonly accompanies severe alcohol intoxication 4
Role of Hemodialysis
When to Consider Hemodialysis
While the provided evidence focuses primarily on ethylene glycol and methanol poisoning rather than ethanol, hemodialysis for ethanol-induced severe metabolic acidosis should be considered when 6, 7:
- Severe refractory metabolic acidosis (pH ≤6.90) despite aggressive bicarbonate therapy
- Profound lactic acidosis (lactate >16 mmol/L) with hemodynamic instability 4
- Acute kidney injury (KDIGO stage 2 or 3) complicating management 5
Hemodialysis Prescription
- Use high-flux dialyzer with large surface area (≥1.5 m²) 6, 7
- Blood flow rate 250-350 ml/min, dialysate flow 500 ml/min 6, 7
- Session duration 4-6 hours 6, 7
- Use bicarbonate-based dialysate enriched with phosphorus and potassium to prevent HD-induced electrolyte depletion 6
Treatment Targets and Endpoints
Acid-Base Goals
- Initial target: bicarbonate ≥20 mEq/L and pH >7.2 within first 24 hours 1
- Subsequent target: bicarbonate ≥22 mmol/L for ongoing management 2, 3
- Anion gap <18 mmol/L indicates adequate correction 5
Clinical Endpoints
- Resolution of altered mental status (excluding other causes) 5
- Hemodynamic stability with adequate urine output 5
- Normalization of lactate levels 4
Common Pitfalls to Avoid
- Do not overcorrect acidosis to normal or alkaline pH in first 24 hours - this causes rebound alkalosis due to delayed ventilatory compensation 1
- Do not use normal saline as primary resuscitation fluid - it exacerbates hyperchloremic acidosis 2
- Do not withhold bicarbonate in severe acidosis (pH <7.2) despite theoretical concerns about CO2 generation 2, 1
- Do not assume adequate volume resuscitation based on blood pressure alone - use urine output, capillary refill, and lactate clearance 5
- Do not forget to screen for toxic coingestions - 44% of intentional poisonings involve multiple substances 5
Special Considerations
Alcohol-Related Lactic Acidosis
Ethanol can cause profound lactic acidosis (Type B) through multiple mechanisms including impaired hepatic lactate clearance, thiamine deficiency, and mitochondrial dysfunction 4. This requires the same aggressive approach as outlined above with particular attention to thiamine supplementation.