Interpreting lactate measurement in critically ill horses: diagnosis, treatment, and prognosis.

In hospitalized horses, hypovolemia and the resulting decrease in tissue perfusion is the most common cause of hyperlactatemia. Therefore, measurement of blood lactate concentration can be a useful tool for guiding fluid therapy. Similarly, measuring blood lactate concentration can be used to assess the need for and adequacy of transfusions in horses receiving whole blood. Inflammatory leukocytes within closed body cavities consume glucose and produce lactate. Simultaneous measurement of blood lactate concentration and lactate concentration of peritoneal, pleural, or synovial fluid has been used to help differentiate septic from nonseptic effusions. A fluid lactate concentration higher than the blood lactate concentration provides evidence for a bacterial cause of the effusion. In horses evaluated for colic, a peritoneal lactate concentration higher than the simultaneously measured blood lactate concentration is indicative of intestinal strangulation and ischemia. Veterinary studies have suggested that serial blood lactate measurements might be a more useful prognostic indicator than a single lactate measurement. In hospitalized adult horses and foals, blood lactate concentration is higher at all time points in nonsurvivors compared with survivors, although the differences tend to be subtle. Measuring the rate at which lactate concentrations return to normal might also prove useful in equine medicine, but this requires further investigation.

Lactate production and measurement in critically ill horses.

Blood lactate concentration can be easily measured by practitioners using inexpensive point-of-care meters. Anaerobic tissue metabolism resulting from inadequate oxygen delivery (DO2) is the most important cause of an increase in blood lactate concentration in equine patients. However,hyperlactatemia also occurs under conditions of apparently adequate DO2, usually in association with sepsis and an intense inflammatory reaction. Numerous mechanisms have been proposed for aerobic hyperlactatemia, including increased Na+/K+-ATPase activity in response to inflammatory mediators; inhibition of pyruvate dehydrogenase, a key enzyme in glucose metabolism; and increased lactate production by activated inflammatory cells. The liver is responsible for most lactate metabolism, and liver disease might contribute to an increase in blood lactate concentration in some patients. Skeletal muscle is usually considered the most important source of lactate during sepsis. The roles of the lungs and the gastrointestinal tract in lactate production have been investigated but remain uncertain.