Why do burn injuries result in metabolic acidosis?

Why Burns Cause Metabolic Acidosis

Burns cause metabolic acidosis primarily through tissue hypoperfusion and anaerobic metabolism, which generates lactate as cells shift to glycolysis in the absence of adequate oxygen delivery during the shock phase. 1

Primary Mechanisms of Acidosis in Burns

Tissue Hypoperfusion and Lactate Production

• Hypovolemic shock from massive fluid shifts leads to cellular hypoxia, forcing tissues to rely on anaerobic glycolysis, which produces lactate as the primary acid accumulation. 1
• Blood lactate serves as a sensitive marker of the extent of bleeding and tissue hypoperfusion in burn patients, reflecting the severity of shock. 1
• The amount of lactate produced is directly proportional to anaerobic glycolysis activity, making it an indirect but reliable marker of cellular hypoxia. 1
• Altered liver perfusion during burn shock further prolongs lactate clearance, compounding the acidotic state. 1

Futile Metabolic Cycling

• Burns trigger accelerated gluconeogenesis and considerable futile cycling of carbohydrate intermediates, including anaerobic lactate metabolism and Cori cycle activity arising from wound metabolism. 2
• This futile cycling perpetuates lactate production even after initial resuscitation, as the hypermetabolic state drives continued substrate cycling. 2

Secondary Contributors to Acidosis

Hypermetabolic State

• The profound hypermetabolic response following thermal injury increases oxygen consumption and metabolic rate, which can reach up to 180% of basal rate in the first week. 1
• This extreme hypermetabolism is fueled partly by evaporative heat loss from wounds and likely by direct central effects of inflammation on the hypothalamus. 2
• The hypermetabolic state persists for months to years post-injury in severe cases, maintaining metabolic stress. 1

Protein Catabolism and Amino Acid Oxidation

• Burn patients exhibit increased amino acid oxidation, urea synthesis, and protein breakdown, which contributes to metabolic derangement. 2
• Protein catabolism occurs at rates 50% higher than baseline, with patients oxidizing amino acids at accelerated rates. 1

Renal Impairment

• Acute kidney injury is a common complication in severe burns, which can impair acid excretion and bicarbonate regeneration, worsening metabolic acidosis. 3

Iatrogenic Causes to Avoid

Fluid Resuscitation Errors

• Normal saline (0.9% NaCl) should never be used as the primary resuscitation fluid because it causes hyperchloremic metabolic acidosis and increases the risk of acute kidney injury. 3
• Balanced crystalloid solutions like Ringer's Lactate have electrolyte concentrations closer to plasma and do not increase acidosis risk. 3, 4

Topical Agent Absorption

• Povidone-iodine absorption through burn wounds can cause severe metabolic acidosis that requires large amounts of sodium bicarbonate to correct, with serum iodine levels reaching toxic concentrations. 5
• Chemical burns from formic acid can result in profound metabolic acidosis with extremely elevated serum formate levels. 6

Clinical Monitoring Approach

• Serial lactate measurements provide early and objective evaluation of patient response to resuscitation therapy and predict survival in shock. 1
• Base deficit from arterial blood gas analysis provides an indirect estimation of global tissue acidosis due to impaired perfusion and is a potent independent predictor of mortality. 1
• While blood lactate and base deficit correlate with shock, they do not strictly correlate with each other—lactate levels more specifically reflect the degree of tissue hypoperfusion. 1

Key Pitfall

• The reliability of lactate determination may be lower when traumatic burn injury is associated with alcohol consumption, requiring interpretation in clinical context. 1