Type A and Type B Lactic Acidosis: Classification and Key Differences
Type A lactic acidosis results from tissue hypoxia and inadequate tissue perfusion, while Type B lactic acidosis occurs without tissue hypoxia due to metabolic disturbances, drug toxicity, or malignancy. 1
Type A Lactic Acidosis: Hypoxia-Driven
Type A lactic acidosis develops when tissues cannot receive adequate oxygen, forcing cells into anaerobic metabolism with excessive lactate production. 1
Primary causes include:
- Circulatory shock states (cardiogenic, septic, hypovolemic) with inadequate tissue perfusion 1
- Severe infections, particularly in patients with underlying conditions like diabetes mellitus 1
- Trauma and severe hypoxemia 2
- Cardiac failure leading to decreased oxygen delivery 1
The pathophysiology centers on inadequate oxygen delivery to tissues, triggering anaerobic glycolysis and lactate accumulation as cells struggle to meet energy demands without sufficient oxygen. 1
Type B Lactic Acidosis: Metabolic Dysfunction Without Hypoxia
Type B lactic acidosis occurs in the absence of tissue hypoperfusion or shock, arising from metabolic disturbances rather than oxygen deprivation. 1, 2
Major causes include:
Medication-Induced
- Metformin (incidence 2-9/100,000 patients/year), especially with renal impairment (eGFR <30 mL/min/1.73m²) 1
- Nucleoside reverse transcriptase inhibitors (NRTIs) in HIV treatment, particularly stavudine and didanosine, causing mitochondrial toxicity (incidence 1.3 cases/1,000 person-years of NRTI exposure) 1
- Linezolid and lorazepam 3
Metabolic and Organ Dysfunction
- Liver disease, which impairs lactate clearance since the liver is the major site of lactate removal through gluconeogenesis 1
- Renal impairment, reducing lactate clearance (reported in 30-65% of adults with chronic kidney disease) 1
- Hematologic malignancies (lymphomas, leukemias) through the Warburg effect—cancer cells preferentially use anaerobic glycolysis even with adequate oxygen 4, 5
Other Causes
- D-lactic acidosis in patients with short bowel syndrome and preserved colon 1
- Grand mal seizures 2
- Thiamine deficiency 2, 3
- Congenital enzyme deficiencies including methylmalonic acidemia, propionic acidemia, and maple syrup urine disease 1
Critical Diagnostic Distinctions
Laboratory findings for both types include:
- Arterial pH <7.35 (or <7.3 in severe cases) 1
- Lactate >2 mmol/L (elevated), >5 mmol/L (abnormal), >10 mmol/L (serious/life-threatening) 1
- Increased anion gap (Na - [Cl+CO2] >16) 1
The key differentiator is clinical context: Type A presents with evidence of shock, hypotension, or tissue hypoperfusion, while Type B presents with stable hemodynamics but persistently elevated lactate. 4
Clinical Pitfall: Mixed Presentations
Both types can co-occur in the same patient, making management particularly challenging. 6 For example, a patient with lymphoma may develop Type B lactic acidosis from the malignancy itself, then superimpose Type A lactic acidosis if septic shock develops. 6, 4 In such cases, treating the shock may improve lactate initially, but persistent elevation despite hemodynamic stability should prompt investigation for Type B causes. 6
Management Implications
Type A requires aggressive restoration of tissue perfusion:
- Fluid resuscitation (15-20 mL/kg/h isotonic saline initially) 1
- Hemodynamic support with vasopressors if needed 1
- Treatment of underlying shock state (sepsis, cardiac failure, hemorrhage) 1
Type B requires identification and treatment of the specific metabolic cause:
- Immediate discontinuation of offending medications (metformin, NRTIs) 1
- Chemotherapy for malignancy-associated lactic acidosis 6, 5
- Hemodialysis for metformin-associated lactic acidosis (definitive treatment) 1
- For D-lactic acidosis: restrict mono/oligosaccharides, provide thiamine supplements, administer broad-spectrum antibiotics 1
Sodium bicarbonate is NOT recommended for pH ≥7.15, as it does not improve hemodynamics, may increase lactate production, and has never been shown to improve survival. 1, 3