What is included in emergency treatment of lactic acidosis?

Updated: Dec 09, 2020
  • Author: Bret A Nicks, MD, MHA; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Lactic acidosis, the combination of elevated blood lactate and concurrent acidosis, has been traditionally viewed as a marker of tissue hypoxia resulting from inadequate oxygen delivery, and as a predictory of adverse outcomes. However, while it is most commonly associated with tissue hypoperfusion related to acute circulatory failure, this view of lactic acidosis is too simplified and does not take into account the myriad causes related to increased lactate accumulation that can occur in addition to (type A) or in the absence of (type B) tissue hypoxia. [15]

Treatment of lactic acidosis requires prompt identification of the underlying illness, directed resuscitative and therapeutic interventions, and serial reassessment. Restoration of tissue oxygen delivery, thereby causing cessation of acid production and enhancing lactate clearance, remains the primary therapeutic focus when tissue hypoperfusion is the cause of the lactic acidemia. Resuscitative efforts should be complemented by measures targeting the cause or causes of lactic acidosis. Such strategies can include the treatment of sepsis (recognizing common goal-directed therapies), restoration of circulating fluid volume, improvement of cardiac function, source identification and control, early antimicrobial intervention, and resection of any potential ischemic regions. [7, 16]  Reassessment for ongoing lactate clearance assists ongoing medical management, but treatment success or failure cannot be determined by lactate alone. [17, 15]  Also recognize that an increase in blood lactate following pressor use in septic shock (eg, epinephrine) may occur secondary to increased glycolysis concurrent with improved oxygen delivery. [18, 15]

When findings of systemic hypoperfusion are not present, consider possible toxin-induced or bowel-associated impairment of cellular metabolism as the cause of lactic acidosis, as can occur with biguanide therapy (metformin-associated lactic acidosis), malignancy (lymphoma, leukemia, solid malignancies), alcoholism, human immunodeficiency virus (HIV) medications (reverse transcriptase inhibitors), or short gut (malabsorptive) syndromes.

In addition, when considering ongoing laboratory assessments, recognize that anion gap screening does not predict lactate levels. A normal anion gap does not exclude the possibility of lactic acidosis, which can present with a normal anion gap up to 50% of the time. Even in the setting of lactic acidosis, additional causes of an elevated anion gap should be explored. [19]

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