What is the treatment for metabolic acidosis?

Treatment of Metabolic Acidosis

The treatment of metabolic acidosis depends fundamentally on the underlying etiology: for diabetic ketoacidosis (DKA), prioritize insulin therapy, fluid resuscitation, and electrolyte replacement rather than bicarbonate administration; for chronic kidney disease-associated acidosis, use oral sodium bicarbonate when serum bicarbonate is consistently <18 mmol/L; and reserve intravenous bicarbonate only for severe acute metabolic acidosis with pH <7.0. 1, 2, 3

Diabetic Ketoacidosis (DKA)

Initial Management

• Begin with aggressive fluid resuscitation using isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (1-1.5 liters in average adult) during the first hour to restore intravascular volume and renal perfusion. 2
• After initial resuscitation, continue with 0.45% NaCl at 4-14 mL/kg/hour if corrected serum sodium is normal or elevated; use 0.9% NaCl if corrected serum sodium is low. 2

Insulin Therapy

• Administer continuous intravenous insulin as the standard of care for critically ill patients with DKA, which is the cornerstone of treatment. 1, 2
• For mild DKA, subcutaneous or intramuscular regular insulin every hour (0.1 unit/kg) after a priming dose of 0.4-0.6 units/kg (half IV, half SC/IM) is equally effective. 4
• When glucose falls to 200-250 mg/dL, add dextrose to IV fluids while continuing insulin infusion to ensure complete resolution of ketoacidosis and prevent hypoglycemia. 2

Electrolyte Management

• Monitor potassium closely and begin replacement when serum potassium falls below 5.5 mEq/L (once renal function is confirmed), using 20-30 mEq/L potassium (2/3 KCl and 1/3 KPO₄) in the infusion. 2
• Total body potassium is depleted despite potentially normal or elevated initial levels due to transcellular shifts from acidosis. 2

Bicarbonate Therapy in DKA

• Bicarbonate administration is NOT recommended for DKA, as multiple studies show it does not improve resolution of acidosis, time to discharge, or clinical outcomes. 1, 2
• The American Diabetes Association notes that bicarbonate may be considered only when pH <6.9, but is not necessary if pH ≥7.0. 4
• Bicarbonate can worsen intracellular acidosis, reduce ionized calcium, and produce hyperosmolality. 1

Monitoring and Resolution

• Monitor blood glucose every 1-2 hours and draw blood every 2-4 hours for electrolytes, glucose, BUN, creatinine, osmolality, and venous pH. 4, 2
• DKA is resolved when glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L. 4, 2
• Use direct measurement of β-hydroxybutyrate rather than nitroprusside methods, as the latter only measures acetoacetic acid and can be misleading during treatment. 4, 5

Transition to Subcutaneous Insulin

• Administer basal insulin 2-4 hours before stopping IV insulin to prevent recurrence of ketoacidosis and rebound hyperglycemia. 5, 2
• Continue IV insulin for 1-2 hours after starting subcutaneous regimen to ensure adequate plasma insulin levels. 4

Chronic Kidney Disease-Associated Acidosis

Treatment Indications

• Treat when serum bicarbonate is consistently <18 mmol/L to prevent bone and muscle metabolism abnormalities. 1
• The goal is to maintain serum bicarbonate at or above 22 mmol/L in maintenance dialysis patients. 1

Oral Bicarbonate Therapy

• Administer oral sodium bicarbonate 2-4 g/day (25-50 mEq/day) to effectively increase serum bicarbonate concentrations. 1
• Correction of acidemia improves serum albumin, decreases protein degradation rates, and increases plasma concentrations of branched chain amino acids. 1
• In children with renal tubular acidosis, normalization of serum bicarbonate is critical for normal growth parameters. 1

Important Caveat

• Avoid citrate alkali salts in CKD patients exposed to aluminum salts, as they increase aluminum absorption. 1

Severe Acute Metabolic Acidosis (Non-DKA)

Intravenous Bicarbonate Indications

• IV sodium bicarbonate is indicated for severe metabolic acidosis where rapid increase in plasma CO₂ content is crucial: cardiac arrest, circulatory insufficiency due to shock or severe dehydration, severe primary lactic acidosis, drug intoxications (barbiturates, salicylates, methyl alcohol), and hemolytic reactions. 3
• The FDA label specifies that vigorous bicarbonate therapy is required when pH is critically low and rapid correction is necessary. 3

Dosing for Severe Acidosis

• In cardiac arrest, give 1-2 vials (44.6-100 mEq) rapidly IV initially, then continue at 50 mL (44.6-50 mEq) every 5-10 minutes as indicated by arterial pH and blood gas monitoring. 3
• For less urgent metabolic acidosis, infuse 2-5 mEq/kg body weight over 4-8 hours initially, with subsequent doses based on clinical response. 3
• It is unwise to attempt full correction of low total CO₂ content during the first 24 hours, as this may cause unrecognized alkalosis due to delayed ventilatory readjustment. 3
• Target total CO₂ content of approximately 20 mEq/L at the end of the first day; complete normalization usually occurs with normal kidney function once the underlying cause is controlled. 3

Monitoring During IV Bicarbonate

• Monitor blood gases, plasma osmolarity, arterial lactate, hemodynamics, and cardiac rhythm in shock-associated metabolic acidosis. 3
• Be cautious of hypertonic bicarbonate solutions producing undesirable rises in plasma sodium concentration, though in cardiac arrest the risks from acidosis exceed those of hypernatremia. 3

General Principles

Etiology-Based Approach

• Always identify and treat the underlying cause of metabolic acidosis (e.g., insulin in diabetes, blood volume restoration in shock, treating infection). 3, 6
• Bicarbonate therapy should be superimposed on measures designed to control the basic cause, as ancillary effects may take time to manifest. 3

Electrolyte Monitoring

• Monitor potassium levels closely, as acidosis causes transcellular shift of potassium leading to hyperkalemia, which reverses with treatment. 1
• This is particularly critical in ESRD patients who are prone to dangerous hyperkalemia. 5