Acidosis, lactic (Acidosis)

Introduction
Lactic acidosis is a serious metabolic acidosis characterized by an accumulation of lactate in the blood (typically > 4 mmol/L) with decreased blood pH (< 7.35). It results from impaired tissue oxygen delivery, mitochondrial dysfunction, or excessive lactate production. Lactic acidosis is associated with high morbidity and mortality, often occurring in critically ill patients, and requires rapid recognition and targeted therapy.

1. Immediate Stabilization

• Oxygen therapy: Supplemental oxygen to optimize tissue oxygenation.

• Hemodynamic support: IV fluids for volume resuscitation; vasopressors (e.g., norepinephrine) if hypotension persists.

• Mechanical ventilation: For severe hypoxemia or respiratory fatigue.

2. Treat Underlying Causes

• Sepsis: Broad-spectrum intravenous antibiotics within the first hour, fluid resuscitation, and source control (e.g., abscess drainage).

• Shock states: Management of cardiogenic, hypovolemic, or distributive shock with tailored therapies.

• Tissue hypoxia/ischemia: Revascularization in acute limb ischemia or correction of hypoxemia in respiratory failure.

• Medications/toxins: Discontinue offending drugs (e.g., metformin, nucleoside reverse transcriptase inhibitors, linezolid). Consider antidotes or dialysis when indicated.

• Mitochondrial dysfunction: Supportive management; investigational therapies (e.g., dichloroacetate) have limited clinical use.

3. Metabolic Correction

• IV Sodium bicarbonate: Considered if arterial pH < 7.1, but used cautiously as it may increase CO₂ generation and worsen intracellular acidosis.

• Renal replacement therapy (hemodialysis or continuous renal replacement therapy): For severe, refractory lactic acidosis, particularly in the presence of renal failure or toxin ingestion.

4. Adjunctive Therapies

• Thiamine supplementation: 100–300 mg IV daily, especially in malnourished or alcoholic patients, to improve pyruvate metabolism and reduce lactate production.

• Insulin therapy: For lactic acidosis related to diabetic ketoacidosis overlap.

• Dichloroacetate (DCA): Experimental; stimulates pyruvate dehydrogenase but not routinely recommended.

5. Supportive and Preventive Measures

• Frequent monitoring of arterial blood gases, lactate levels, electrolytes, and renal function.

• Optimizing tissue perfusion and oxygen delivery in high-risk patients.

• Careful selection and monitoring of medications that may predispose to lactic acidosis.

6. Multidisciplinary Management

• Critical care specialists for hemodynamic and respiratory support.

• Infectious disease consultants in sepsis-related lactic acidosis.

• Nephrologists for renal replacement therapy decisions.