What are the treatment guidelines for metabolic acidosis?

Metabolic Acidosis: Approach and Treatment Guidelines

Diagnostic Approach

The initial evaluation of metabolic acidosis requires calculating the anion gap to categorize the disorder as either high anion gap (organic acids) or normal anion gap (hyperchloremic), which fundamentally determines treatment strategy. 1

Key Diagnostic Steps

• Calculate the anion gap using the formula: [Na+] - ([HCO3-] + [Cl-]), with normal values typically 8-12 mEq/L 1
• Measure arterial blood gases to determine pH, PaCO2, and confirm metabolic acidosis (pH <7.35, bicarbonate <22 mmol/L) 2
• Assess for appropriate respiratory compensation: expect PaCO2 to decrease by approximately 1 mmHg for every 1 mmol/L fall in serum bicarbonate 1
• Identify the underlying etiology based on anion gap classification:
  • High anion gap: lactic acidosis, ketoacidosis, renal failure, toxic ingestions (methanol, ethylene glycol, salicylates) 3
  • Normal anion gap: gastrointestinal bicarbonate loss, renal tubular acidosis, early renal failure, drug-induced hyperkalemia 3

Treatment Guidelines by Clinical Context

Acute Organic Acidosis (Lactic Acidosis, Diabetic Ketoacidosis)

The primary treatment for acute organic acidosis is addressing the underlying cause rather than administering bicarbonate, as sodium bicarbonate has not demonstrated mortality benefit and may worsen intracellular acidosis. 4

Diabetic Ketoacidosis Management

• Administer continuous intravenous insulin as the standard of care for critically ill patients, which is the definitive treatment that resolves ketoacidosis 4
• Restore circulatory volume with aggressive fluid resuscitation (2-3 L/m² per day in pediatrics) 5, 4
• Bicarbonate therapy is NOT indicated unless pH falls below 6.9-7.0 2, 4
• When bicarbonate is required (pH <6.9), administer 1-2 mEq/kg IV slowly in children, or 44.6-100 mEq initially in adults 4, 6
• Monitor arterial or venous blood gases to assess treatment response 2

Lactic Acidosis and Septic Shock

• Focus on restoring tissue perfusion with fluid resuscitation and vasopressors rather than administering bicarbonate 4
• Sodium bicarbonate should NOT be used to treat metabolic acidosis from tissue hypoperfusion in sepsis, as it may worsen intracellular acidosis 4
• The only effective treatment is cessation of acid production via improvement of tissue oxygenation 3

Chronic Kidney Disease-Associated Metabolic Acidosis

Oral sodium bicarbonate supplementation is the first-line treatment when serum bicarbonate falls below 22 mmol/L, with pharmacological intervention strongly recommended when bicarbonate drops below 18 mmol/L. 2, 4

Treatment Algorithm by Bicarbonate Level

• Bicarbonate ≥22 mmol/L: Monitor monthly without pharmacological intervention 2
• Bicarbonate 18-22 mmol/L: Consider oral alkali supplementation (0.5-1.0 mEq/kg/day divided into 2-3 doses) with or without dietary intervention 2
• Bicarbonate <18 mmol/L: Initiate pharmacological treatment with oral sodium bicarbonate (2-4 g/day or 25-50 mEq/day) 2, 4

Monitoring Requirements

• Measure serum bicarbonate monthly initially, then at least every 3-4 months once stable 2, 4
• Monitor blood pressure, serum potassium, and fluid status regularly after initiating treatment 2
• Target bicarbonate ≥22 mmol/L to prevent protein catabolism, bone disease, and CKD progression 2, 4

Important Caveats

• Avoid citrate-containing alkali in CKD patients exposed to aluminum salts, as citrate increases aluminum absorption 2, 4
• Exercise caution in patients with advanced heart failure, severe hypertension, or significant edema 2
• In pediatric CKD patients, treat more aggressively (even with bicarbonate >18 mmol/L) to optimize growth and bone health 2

Severe Metabolic Acidosis with Acute Kidney Injury

Hemodialysis is the definitive treatment for severe acidosis (pH <7.20) with acute kidney injury, as it simultaneously corrects acidemia, removes uremic toxins, and manages volume status. 4

• Do not delay dialysis while attempting medical management, as acidosis is refractory to conservative measures with severe renal impairment 4
• Admit to ICU with urgent nephrology consultation for dialysis initiation 4
• Once stabilized, maintain serum bicarbonate ≥22 mmol/L through dialysate bicarbonate concentration adjustment 4

Intravenous Sodium Bicarbonate Administration

When IV bicarbonate is indicated, administer cautiously as bicarbonate solutions are hypertonic and may produce undesirable rises in plasma sodium concentration. 6

Dosing Guidelines

• Cardiac arrest: Initial rapid 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 6
• Less urgent metabolic acidosis: 2-5 mEq/kg body weight over 4-8 hours, depending on severity 6
• Target initial correction to total CO2 of approximately 20 mEq/L, not full normalization 6

Critical Monitoring During IV Bicarbonate

• Measure blood gases, plasma osmolarity, arterial lactate, and hemodynamics in shock-associated acidosis 6
• Avoid full correction in the first 24 hours, as this may cause unrecognized alkalosis due to delayed ventilatory readjustment 6
• Monitor for complications: hypernatremia, hyperosmolality, decreased ionized calcium, worsening intracellular acidosis 4, 6

Pediatric-Specific Considerations

In preterm infants, severe metabolic acidosis (pH <7.2, base deficit >10 mmol/L, bicarbonate <12 mmol/L) during parenteral nutrition may be induced by excessive chloride intake. 5

• Use "chloride-free" sodium and potassium solutions in preterm infants on parenteral nutrition to reduce risk of hyperchloremic acidosis 5
• High-risk infants include those with large PDA, weight loss >15%, or extremely low birth weight 5
• Limit cumulative chloride intake to <3.3 mmol/kg/day during first 3 days and <4.5 mmol/kg/day during first 10 days 5

Common Pitfalls to Avoid

• Do not routinely administer bicarbonate for acute organic acidosis (lactic acidosis, DKA with pH >6.9), as it does not improve outcomes and may cause harm 4, 3
• Do not attempt rapid full correction of chronic metabolic acidosis in the first 24 hours, as this risks rebound alkalosis 6
• Do not use alkalinization in tumor lysis syndrome, as it increases risk of calcium phosphate crystal precipitation 5
• Do not reduce protein intake in hospitalized CKD patients with acidosis, as the catabolic state requires increased protein 2
• Monitor potassium closely when treating acidosis, as correction shifts potassium intracellularly and may unmask or worsen hypokalemia 4, 7