Treatment of Metabolic Acidosis
Treatment of metabolic acidosis must be directed at the underlying cause rather than routine bicarbonate administration, as sodium bicarbonate has not demonstrated mortality benefit in most acute organic acidoses and may worsen intracellular acidosis. 1, 2, 3
Etiology-Based Treatment Approach
Acute Organic Acidoses (Lactic Acidosis, Diabetic Ketoacidosis)
Focus on treating the underlying cause rather than administering bicarbonate, as the only effective treatment for organic acidosis is cessation of acid production via improvement of tissue oxygenation 4, 5
For diabetic ketoacidosis: Prioritize insulin therapy, fluid resuscitation, and electrolyte replacement as the standard of care 2, 3
For sepsis-related metabolic acidosis from tissue hypoperfusion: DO NOT use sodium bicarbonate, as it may worsen intracellular acidosis, reduce ionized calcium, and produce hyperosmolality 1, 3
For severe malaria in children: Metabolic acidosis resolves with correction of hypovolemia and treatment of anemia by adequate blood transfusion; no evidence supports sodium bicarbonate use 1
Chronic Kidney Disease-Associated Acidosis
Treat when serum bicarbonate is consistently < 18 mmol/L to prevent bone and muscle metabolism abnormalities 2, 3
Oral sodium bicarbonate 2-4 g/day (25-50 mEq/day) can effectively increase serum bicarbonate concentrations 2
Target serum bicarbonate ≥ 22 mmol/L in maintenance dialysis patients 2
Benefits of correction include increased serum albumin, decreased protein degradation rates, and increased plasma concentrations of branched chain amino acids 2
Avoid citrate alkali salts in CKD patients exposed to aluminum salts, as they may increase aluminum absorption 2
Hyperchloremic (Normal Anion Gap) Acidosis
Address gastrointestinal bicarbonate losses or renal tubular acidosis as appropriate 4, 6
In children with renal tubular acidosis, normalization of serum bicarbonate is important for normal growth parameters 2
When Sodium Bicarbonate IS Indicated
Sodium bicarbonate may be appropriate in specific acute situations where rapid increase in plasma CO2 content is crucial 7:
Cardiac arrest: Initial rapid IV dose of 44.6-100 mEq (one to two 50 mL vials), continued at 44.6-50 mEq every 5-10 minutes as indicated by arterial pH and blood gas monitoring 7
- Note: In cardiac arrest, the risks from acidosis exceed those of hypernatremia 7
Severe shock with circulatory insufficiency 7
Severe dehydration 7
Drug intoxications (barbiturates, salicylates, methyl alcohol) where alkalinization is beneficial 7
Hemolytic reactions requiring alkalinization of urine 7
Dosing for Non-Emergency Situations
For older children and adults: 2-5 mEq/kg body weight over 4-8 hours, depending on severity of acidosis 7
Initial infusion: 2-5 mEq/kg over 4-8 hours produces measurable improvement 7
Target total CO2 of approximately 20 mEq/L at end of first day rather than full correction, as complete normalization within 24 hours may cause unrecognized alkalosis due to delayed ventilatory readjustment 7
Critical Monitoring Requirements
Monitor electrolytes, particularly potassium levels, as acidosis causes hyperkalemia due to transcellular potassium shift 2, 3
- Hyperkalemia may complicate severe metabolic acidosis at admission and should be treated per Advanced Paediatric Life Support guidelines 1
In shock-associated acidosis: Monitor blood gases, plasma osmolarity, arterial blood lactate, hemodynamics, and cardiac rhythm 7
Monthly serum bicarbonate monitoring in maintenance dialysis patients 2
Common Pitfalls to Avoid
DO NOT use furosemide unless hypervolemia, hyperkalemia, and/or renal acidosis are present 1
DO NOT use dopamine in an attempt to improve renal function 1
DO NOT use hypotonic fluids (e.g., glucose solutions) for fluid resuscitation 1
Avoid attempting full correction of low total CO2 content during the first 24 hours, as this may be accompanied by unrecognized alkalosis 7
Recognize that bicarbonate solutions are hypertonic and may produce undesirable rise in plasma sodium concentration 7