Lactic Acidosis Treatment & Management

Treatment is directed towards correcting the underlying cause of lactic acidosis and optimizing tissue oxygen delivery by cardiopulmonary support. Evidence so far indicates that alkali therapy is not beneficial; it may, in fact, cause harm by worsening intracellular acidosis. Furthermore, bicarbonate therapy may lead to electrolyte disturbances, such as hypokalemia and hypocalcemia, primarily a decrease in ionized calcium.

Although patients may be tachypneic initially, ventilatory muscle fatigue may ensue rapidly and may require mechanical assistance.

Cardiovascular collapse should be treated with fluid replacement, preferably with isotonic sodium chloride preparations, avoiding solutions containing lactate.

Every effort should be made to avoid using vasoconstrictor drugs because of their potential to exacerbate ischemia in critical tissue beds.

The therapy also should be directed at administration of appropriate antibiotics, surgical drainage and debridement of a septic focus, chemotherapy of malignant disorders, discontinuation of causative drugs, and dietary modification in certain types of congenital lactate acidosis.

Go to Emergent Management of Lactic Acidosis for complete information on this topic.

Controversy continues to surround the use of alkali in treating lactic acidosis. As sodium bicarbonate (NaHCO₃) breaks down into carbon dioxide and water in the tissues, patients must have effective ventilation to eliminate carbon dioxide and should be able to handle additional sodium and volume load.

The animal models of lactic acidosis have shown that intravenous administration of NaHCO₃ may increase lactate production (particularly by the splanchnic bed), decrease portal vein flow, lower intracellular pH in muscle and liver, lower arterial pH, and worsen the cardiac output.

In a double-blind, placebo-controlled trial of intravenous NaHCO₃ administration, no improvement in cardiac hemodynamics occurred, although significant improvement in PaCO₂ was observed.

The current evidence is strongly against the routine use of intravenous NaHCO₃ in the treatment of acquired forms of lactic acidosis, regardless of the arterial pH or serum bicarbonate level. Although several anecdotal reports have suggested the use of bicarbonate dialysate as therapy for lactic acidosis, this approach has not been evaluated vigorously.

The improvement noted in hemodynamic status when bicarbonate is administrated during acidosis may be caused by mechanisms other than correction of acidosis (eg, increased preload, effect of tonicity). The arterial pH could always be corrected by lowering the PaCO₂ by increasing the rate of ventilation. This may correct the extracellular and intracellular acidosis. The use of bicarbonate in patients with severe metabolic acidosis and arterial pH less than 7.15 should be reserved to maintain the pH above 7.15 until the underlying process is corrected.

The amount of NaHCO₃ can be calculated by the following formula: NaHCO₃ required = (bicarbonate desired - bicarbonate observed) x 0.4 x body weight (kg)

The benefit of alkali administration in hypoxia-induced lactic acidosis remains controversial. The judicious use of bicarbonate in patients with severe metabolic acidosis and hemodynamic instability is recommended.

Dichloroacetate is the most potent stimulus of pyruvate dehydrogenase, the rate-limiting enzyme for the aerobic oxidation of glucose, pyruvate, and lactate. Dichloroacetate may inhibit glycolysis and, thereby, lactate production. Dichloroacetate also exerts a positive inotropic effect that has been attributed to improvement in myocardial glucose use and high-energy phosphate production.

The data from animal studies and 1 placebo-controlled, double-blind clinical trial showed dichloroacetate to be superior to placebo in improving the acid-base status of the patients; however, the magnitude of change was small and did not alter hemodynamics or survival.

Carbicarb is a new buffering agent with potential use in metabolic acidosis. It is an equimolecular mixture of sodium bicarbonate and sodium carbonate. Carbicarb has a buffering capacity similar to sodium bicarbonate but does not generate carbon dioxide.

In animal models of hypoxic lactic acidosis, Carbicarb reduced circulating lactate and improved tissue and blood acid-base status compared with sodium bicarbonate.

Controlled studies with Carbicarb in patients with metabolic studies are lacking.

Dialysis may be a useful mode of therapy when severe lactic acidosis exists in conjunction with renal failure or congestive heart failure. Dialysis would allow bicarbonate infusion without precipitating or worsening fluid overload. Therefore, dialysis would correct acidosis by restoring the buffer pool.^[20]

Hemodialysis or continuous hemofiltration used in conjunction with alkali infusion may be tolerated in a patient with cardiovascular instability. However, the overall benefit of such therapy to a patient's outcome is not known. Metformin-induced lactic acidosis has been reported to improve after prolonged hemodialysis.^[21]

A number of other therapies have been advocated at one time or another for lactate acidosis, including methylene blue, glucose and insulin, tris-[hydroxymethyl]-aminomethane (THAM, tromethamine, or tris buffer), thiamine, and nitroprusside. The oxidizing agent methylene blue was proposed as a means of pharmacologically altering intracellular redox potential but has proved to be ineffective. THAM has been advocated for its alkalizing properties and more rapid cellular permeability, but the effect on patient outcome is uncertain.

Theoretical reasons and some clinical evidence exist for thiamine treatment to improve lactic acidosis associated with thiamine deficiency. Thiamine is indicated in patients with beriberi and generally is indicated in patients hospitalized for alcoholism because of their increased tendency for developing thiamine deficiency. Similarly, thiamine can be administered safely to patients with lactic acidosis, particularly in the absence of an obvious alternate etiology. Thiamine is administered intravenously as 50-100 mg followed by 50 mg/d orally for 1-2 weeks.

The treatment for D-lactic acidosis is NaHCO₃ to correct acidemia and antibiotics to decrease the number of organisms producing D-lactate.

Lactic acidosis is observed frequently in patients who are critically ill. Despite a large number of potential etiologies, tissue hyperfusion is by far the most common etiology.

Aggressive cardiorespiratory resuscitation designed to restore tissue perfusion is the fundamental approach to these patients.

Titrating therapies to traditional endpoints may not ensure that the microvascular bed is reperfused. Monitoring blood lactate concentration not only allows for prognostication but also serves as an indicator of when supportive therapies are restoring tissue perfusion.

Go to Emergent Management of Lactic Acidosis for complete information on this topic.

Consultation with a critical care medicine specialist for further diagnostic procedures and supportive therapy is a must for patients who are critically ill.

Patients with chronic, mild hyperlactemia should be referred to an endocrinologist for elucidation of the underlying pathology and appropriate management.