Lactic acidosis medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Overview

The main treatment for lactic acidosis is to correct the medical problem that causes the condition. Treatment depends on the underlying mechanism of excess lactate, however it mostly involves optimizing oxygenation in tissues by providing fluids, packed red blood cells, vasopressors or inotropic agents, or both.[1] Fluids should be given until the patient is no longer preload-dependent, however, the ability to respond to fluid and when to hold them is a controversial topic[2]. In many cases, fluid resuscitation by itself may be enough to restore hemodynamic stability, improve tissue perfusion, and reduce elevated lactate concentrations[3][4].

A more positive fluid balance early in the course of septic shock, and over 4 days has been associated with a higher mortality. Furthermore, giving fluids to patients with shock due to impaired left ventricular function (cardiogenic shock) may cause or worsen existing pulmonary edema. There has been no significant difference found between crystalloids and colloids in fluid resuscitation in terms of lactate clearance.

Type B lactic acidosis is mainly treated by therapy aimed at the underlying condition.[1]

References

  1. 1.0 1.1 Reddy AJ, Lam SW, Bauer SR, Guzman JA (2015). "Lactic acidosis: Clinical implications and management strategies". Cleve Clin J Med. 82 (9): 615–24. doi:10.3949/ccjm.82a.14098. PMID 26366959.
  2. Durairaj L, Schmidt GA (2008). "Fluid therapy in resuscitated sepsis: less is more". Chest. 133 (1): 252–63. doi:10.1378/chest.07-1496. PMID 18187750.
  3. Vincent JL, Dufaye P, Berré J, Leeman M, Degaute JP, Kahn RJ (1983). "Serial lactate determinations during circulatory shock". Crit Care Med. 11 (6): 449–51. doi:10.1097/00003246-198306000-00012. PMID 6406145.
  4. Boyd JH, Forbes J, Nakada TA, Walley KR, Russell JA (2011). "Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality". Crit Care Med. 39 (2): 259–65. doi:10.1097/CCM.0b013e3181feeb15. PMID 20975548.


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