Can Sepsis Cause Lactic Acidosis?
Yes, sepsis absolutely causes lactic acidosis and is one of the most common causes of elevated lactate in critically ill patients. Lactic acidosis is a defining feature of septic shock and serves as a key marker of disease severity and prognosis 1.
Mechanism and Pathophysiology
Sepsis-induced lactic acidosis occurs through multiple mechanisms, not solely from tissue hypoxia as traditionally believed:
Increased pyruvate production is the primary driver of lactate accumulation in sepsis, rather than inadequate oxygen delivery alone 2. Studies using dichloroacetate demonstrate that septic patients have substantially elevated rates of pyruvate production and can increase oxygen consumption further when stimulated, proving that tissue oxygenation is not the limiting factor 2.
Cellular metabolic dysfunction occurs due to the dysregulated host response to infection, with profound circulatory and cellular-metabolic abnormalities that characterize septic shock 1.
Type A lactic acidosis (tissue hypoxia-related) can coexist with Type B mechanisms (non-hypoxic), including increased glycolysis by inflammatory cells, impaired hepatic lactate clearance, and mitochondrial dysfunction 3.
Clinical Definitions and Significance
Severe sepsis is defined as sepsis with organ dysfunction, hypotension, or hypoperfusion abnormalities that may include lactatemia, oliguria, or altered mental status 1.
Septic shock is operationally defined as requiring vasopressor therapy to maintain mean arterial pressure >65 mmHg and an increased plasma lactate level >2 mmol/L 1. This dual requirement emphasizes that lactic acidosis is not merely a marker but a defining component of septic shock.
Perfusion abnormalities in septic shock specifically include lactic acidosis, oliguria, or acute alteration in mental status, and these may persist despite vasopressor therapy 1.
Prognostic Implications
Lactate clearance is a more reliable prognostic indicator than initial lactate value alone 4. A decrease in lactate of at least 10% within the first 6,24, and 48 hours of treatment is associated with improved survival 4.
Persistent lactic acidosis despite adequate fluid resuscitation and vasopressor support indicates profound cellular-metabolic abnormalities and substantially increases mortality 1.
The 7-day mortality rate in severe sepsis patients with lactic acidosis can exceed 70%, particularly when lactate clearance is inadequate 4.
Important Clinical Caveats
Not all lactic acidosis in septic patients is from sepsis itself. Consider alternative diagnoses when:
- Blood cultures remain negative despite appropriate sampling 5
- Lactate continues to rise despite adequate resuscitation and source control 5
- Clinical features don't align with typical sepsis presentation 5, 6
Alternative causes include malignancy-induced lactic acidosis (lymphoma, leukemia), medication effects, and other metabolic derangements 5, 6. These Type B causes can present with severe lactic acidosis even without hemodynamic instability 6.
Treatment Considerations
Sodium bicarbonate is NOT recommended for sepsis-induced lactic acidosis when pH ≥7.15 1, 7, 8. The Surviving Sepsis Campaign explicitly recommends against bicarbonate therapy for hypoperfusion-induced lactic acidemia at this threshold, as it does not improve hemodynamics or reduce vasopressor requirements 7, 8.
The definitive treatment is addressing the underlying infection with appropriate antimicrobials and restoring adequate circulation through fluid resuscitation and vasopressor support 1, 7.