What is the management of hyperlactatemia (elevated lactic acid level)?

From the Guidelines

Management of high lactic acid levels should focus on treating the underlying cause and supporting the body's metabolic needs, with the primary approach involving fluid resuscitation with crystalloids and vasopressors as needed, as well as guiding resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion 1. The goal of treatment is to normalize lactate levels below 2 mmol/L, and this can be achieved through various interventions, including:

• Fluid resuscitation with crystalloids (typically 30 ml/kg bolus initially) to address tissue hypoxia and ensure adequate oxygen delivery 1
• Vasopressors like norepinephrine (starting at 0.05-0.1 mcg/kg/min) to maintain perfusion if needed
• Mechanical ventilation to optimize oxygenation
• Specific treatments depending on the cause, such as:

• Antibiotics for sepsis (broad-spectrum initially, then targeted based on cultures)
• Discontinuation of offending medications
• Dialysis for severe acidosis (pH < 7.1)
• Insulin for diabetic ketoacidosis (0.1 units/kg/hr)
• Thiamine supplementation (100-500 mg IV daily for 3-5 days) for alcoholics or malnourished patients It is also important to note that bicarbonate therapy is generally not recommended except in severe acidosis (pH < 7.1) as it may paradoxically worsen intracellular acidosis 1. Continuous monitoring of lactate levels every 2-6 hours helps assess response to treatment, and the effectiveness of treatment depends on promptly identifying whether lactic acidosis stems from tissue hypoxia (type A) or metabolic dysfunction (type B), as management strategies differ significantly between these causes.

From the FDA Drug Label

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.

Management of high lactic acid levels involves administering sodium bicarbonate intravenously.

• The dose is 2 to 5 mEq/kg body weight over a period of 4 to 8 hours.
• Therapy should be monitored by measuring blood gases, plasma osmolarity, arterial blood lactate, hemodynamics, and cardiac rhythm.
• Bicarbonate therapy should be planned in a stepwise fashion due to the unpredictable response to a given dose 2.

From the Research

High Lactic Acid Level Management

• Lactate levels are commonly evaluated in acutely ill patients, and elevated levels can be caused by various factors, including tissue hypoperfusion, shock, sepsis, cardiac arrest, trauma, seizure, ischemia, diabetic ketoacidosis, thiamine deficiency, malignancy, liver disease, toxins, overdose, and medication 3.
• The management of patients with elevated lactate levels requires awareness of the underlying cause of elevation, as the clinical and prognostic importance of an elevated lactate level varies widely by disease state 3.
• Therapy for lactic acidosis is designed to maximize oxygen delivery to reduce tissue hypoxia, and buffering agents such as sodium bicarbonate have not been shown to materially affect outcome from lactic acidosis caused by shock 4.
• The use of sodium bicarbonate for the treatment of lactic acidosis is controversial, and its benefits have not been proven, with some studies suggesting that it may even have negative side effects 5, 6.
• Current recommendations suggest that sodium bicarbonate should not be used for patients with pH at least 7.15, and that effective therapy for lactic acidosis due to shock is to reverse the cause 6.
• Future directions for the treatment of lactic acidosis may include the use of other buffers, such as THAM or Carbicarb, or dialysis, as well as selective NHE1 inhibitors, which have shown promise in animal studies 7.
• Targeting the mechanisms that contribute to lactic acid accumulation, such as tissue hypoxia and epinephrine-induced stimulation of aerobic glycolysis, could also allow for more specific therapy 7.