What is the management of Lactic Acidosis?

From the Guidelines

Lactic acidosis management should focus on treating the underlying cause and supporting organ function, with sodium bicarbonate therapy generally not recommended for patients with pH ≥ 7.15, as evidenced by the 2016 Surviving Sepsis Campaign guidelines 1. The initial steps in managing lactic acidosis include ensuring adequate oxygenation, ventilation, and circulation through supplemental oxygen, mechanical ventilation if needed, and fluid resuscitation with crystalloids like normal saline.

• Key interventions include:
  • Ensuring adequate oxygenation and ventilation
  • Fluid resuscitation with crystalloids
  • Vasopressor support with agents like norepinephrine for persistent hypotension
  • Identifying and addressing the specific cause of lactic acidosis, such as sepsis, diabetic ketoacidosis, or medication-induced causes
• The use of sodium bicarbonate is controversial and, according to the guidelines, should be avoided in patients with hypoperfusion-induced lactic acidemia with pH ≥ 7.15 1, due to the lack of evidence supporting its effectiveness in improving hemodynamics or reducing vasopressor requirements.
• Regular monitoring of arterial blood gases, lactate levels, and electrolytes is crucial to guide therapy and assess the response to treatment.
• In severe cases or when conventional treatment is ineffective, considerations may include continuous renal replacement therapy, especially for patients with kidney failure.
• The fundamental approach to managing lactic acidosis involves addressing tissue perfusion and oxygen delivery, as the condition arises from tissue hypoxia leading to anaerobic metabolism and excess lactic acid production.

From the Research

Lactic Acidosis Management

• The management of lactic acidosis is a complex process, and the use of sodium bicarbonate is a controversial topic 2, 3, 4.
• The 2008 Surviving Sepsis guidelines recommend against the use of bicarbonate in patients with pH at least 7.15, while deferring judgment in more severe acidemia 2.
• Some studies suggest that bicarbonate therapy may not improve cardiovascular function or reduce mortality in patients with lactic acidosis 3, 4.
• The use of bicarbonate can lead to a decrease in serum calcium concentration and generation of excess carbon dioxide, which can worsen intracellular acidification 3, 4.
• Alternative treatments, such as THAM or Carbicarb, or dialysis, may provide base with fewer untoward effects 3, 5.
• The cellular injury associated with lactic acidosis is partly due to activation of NHE1, a cell-membrane Na(+)/H(+) exchanger, and selective NHE1 inhibitors may improve cardiovascular function and reduce mortality 3.
• Targeting the mechanisms that contribute to lactic acid accumulation, such as tissue hypoxia and epinephrine-induced stimulation of aerobic glycolysis, could allow for more specific therapy 3.
• Effective therapy of lactic acidosis due to shock is to reverse the cause 2, 6.

Treatment Approaches

• Sodium bicarbonate may be considered in patients with severe acidemia (pH < 7.2) and acute kidney injury, but its use should be cautious and with careful monitoring 4.
• Carbicarb administration may improve hemodynamics compared with sodium bicarbonate or sodium chloride administration in hypoxic lactic acidosis 5.
• The use of continuous renal replacement therapy with bicarbonate-based replacement fluid may be recommended over citrate-based fluid in severe acidosis 2.

Key Considerations

• Treating the underlying causes of the acid-base disturbances is the only warranted intervention in lactic acidosis 6.
• Lactic acidosis is still associated with high mortality, and effective management requires a comprehensive approach 6.
• The use of sodium bicarbonate should be individualized and based on the patient's specific condition and response to treatment 2, 3, 4.