الفهرس 
Biochemical aspects of Lactatic acidosisOnly 14 pages are availabe for public view
 |  | from | 102 |  |  |
| | | from | 102 | | |
Abstract
This work aims to highlight the mechanisms underlying lactate elevations, note the risks associated with lactic acidosis, and outline a recent approach for its treatment in intensive care unit.
Lactate, or lactic acid, is produced from pyruvate as an end product of glycolysis under anaerobic conditions. It is produced in most tissues in the body, but primarily in skeletal muscle, brain, intestine, and red blood cells. During times of stress, lactate is also produced in the lungs, white blood cells, and splanchnic organs. Most lactate in the blood is cleared by the liver, where it is the substrate for gluconeogenesis, and a small amount is cleared by the kidneys.
Lactic acidosis results from the accumulation of lactate and protons in the body fluids and is often associated with poor clinical outcomes. The effect of lactic acidosis is governed by its severity and the clinical context. Mortality is increased by a factor of nearly three when lactic acidosis accompanies low-flow states or sepsis, and the higher the lactate level, the worse the outcome.
An elevated lactate level can be the result of increased production, decreased clearance, or both (as in liver dysfunction).
Patients exhibiting a disorder of lactate metabolism are typically significantly ill and are at risk for developing multiple organ failure. Patients suffer a hospital mortality rate that increases nearly linearly with the concentration of serum lactate. Several studies have shown that vigilant correction of hyperlactemia is associated with decreased morbidity and mortality.
An elevated lactate level should prompt an evaluation for causes of decreased oxygen delivery, due either to a systemic low-flow state (as a result of decreased cardiac output) or severe anemia, or to regionally decreased perfusion. If tissue hypoxia is ruled out after an exhaustive workup, consideration should be given to causes of hyperlactatemia without concomitant tissue hypoxia (type B acidosis). Treatment differs depending on the underlying mechanism of the lactate elevation; nevertheless, treatment is mostly related to optimizing oxygen delivery by giving fluids, packed red blood cells, and vasopressors or inotropic agents, or both.