From the Guidelines
The management of lactic acidosis associated with liver (hepatic) failure should prioritize the use of bicarbonate as a buffer in continuous renal replacement therapy (CRRT) to correct metabolic acidosis, as lactate can worsen acidosis in these patients.
Key Considerations
- Initial treatment involves fluid resuscitation with crystalloids to improve tissue perfusion and oxygen delivery.
- Vasopressors like norepinephrine may be needed if hypotension persists despite adequate volume replacement.
- Mechanical ventilation should be considered for patients with respiratory distress to optimize oxygenation.
- CRRT can help clear lactate and correct acidosis in severe cases, particularly when conventional measures fail, with bicarbonate preferred over lactate as the buffer due to the risk of worsening acidosis with lactate in liver failure, as noted in studies 1.
- Thiamine supplementation (100 mg IV daily for 3-5 days) is recommended as deficiency can contribute to lactic acidosis.
- Sodium bicarbonate administration remains controversial but may be considered for severe acidosis (pH < 7.1) at 1-2 mEq/kg IV over 1-2 hours.
- Avoid medications that impair lactate clearance, including metformin, which should be discontinued in patients at risk for lactic acidosis, such as those with liver failure, as highlighted in recent guidelines 1.
Treatment Approach
The definitive treatment for lactic acidosis due to liver failure is addressing the underlying liver dysfunction, which may ultimately require liver transplantation evaluation in appropriate candidates. This approach targets the pathophysiological mechanisms of lactic acidosis in liver failure: impaired lactate clearance by the liver, tissue hypoperfusion, and increased lactate production due to anaerobic metabolism.
Buffer Selection in CRRT
The choice of buffer in CRRT is critical, with bicarbonate being the preferred choice over lactate in patients with lactic acidosis or liver failure, as it does not contribute to the accumulation of lactate and can more effectively correct metabolic acidosis, as suggested by studies on CRRT management 1.
From the FDA Drug Label
In cardiac arrest, a rapid intravenous dose of one to two 50 mL vials (44.6 to 100 mEq) may be given initially and continued at a rate of 50 mL (44. 6 to 50 mEq) every 5 to 10 minutes if necessary (as indicated by arterial pH and blood gas monitoring) to reverse the acidosis. In metabolic acidosis associated with shock, therapy should be monitored by measuring blood gases, plasma osmolarity, arterial blood lactate, hemodynamics and cardiac rhythm. Bicarbonate therapy should always be planned in a stepwise fashion since the degree of response from a given dose is not precisely predictable Initially an infusion of 2 to 5 mEq/kg body weight over a period of 4 to 8 hours will produce a measurable improvement in the abnormal acid-base status of the blood.
The management of lactic acidosis associated with liver (hepatic) failure is not directly addressed in the provided drug labels. Key points to consider in the management of metabolic acidosis include:
- Monitoring of blood gases, plasma osmolarity, arterial blood lactate, hemodynamics, and cardiac rhythm
- Stepwise planning of bicarbonate therapy
- Initial infusion of 2 to 5 mEq/kg body weight over 4 to 8 hours 2 2
From the Research
Management of Lactic Acidosis
The management of lactic acidosis associated with liver (hepatic) failure involves several key considerations:
- Treating the underlying cause of the lactic acidosis is crucial, as it is the most effective way to manage the condition 3, 4
- Eliminating the triggering conditions, such as tissue hypoxia or sepsis, is essential in reducing mortality rates 5
- Sodium bicarbonate administration is not recommended, as it can reduce serum calcium concentration and generate excess carbon dioxide, leading to intracellular acidification 5, 3
- Other treatment options, such as dichloroacetate, Carbicarb, or hemofiltration, have shown promise in animal studies or anecdotal experiences, but more research is needed to confirm their effectiveness in humans 5, 3, 6
Treatment Approaches
Different treatment approaches have been explored, including:
- Targeting the mechanisms that contribute to lactic acid accumulation, such as tissue hypoxia and epinephrine-induced stimulation of aerobic glycolysis 5
- Using selective NHE1 inhibitors, which have shown promise in animal studies by improving cardiovascular function and reducing mortality 5
- Examining the use of other buffers, such as THAM or Carbicarb, which may provide base with fewer untoward effects 5
Clinical Implications
Lactic acidosis in end-stage liver disease (ESLD) patients is a complex clinical problem that requires careful management: