Lactate in Veterinary Critical Care: Pathophysiology and Management

Introduction

Hyperlactatemia and lactic acidosis occur commonly in veterinary critically ill patients having clinical disorders such as shock, low cardiac output states, acute liver failure, severe sepsis, neoplasia, seizure, poisoning, and drug therapy.^1–5 With the advent of hand-held lactate analyzers that are inexpensive and readily available, lactate is rapidly becoming a valuable test in the armamentarium of clinicians in the assessment of lactate kinetics and response to therapy. In addition to reflecting the systemic repercussions of various disease states, increased attention is being focused on the use of lactate as a diagnostic tool and prognostic indicator in cavitary effusions.^2,6–22 The purposes of this article are to summarize the physiology and pathophysiology of lactate production and lactic acidosis, to describe current indications for measurement, to highlight novel applications in the evaluation of cavitary effusions, and to present a guide to therapy of lactic acidosis.

Definitions

The following definitions are based on human definitions. Hyperlactatemia is usually a mild to moderate (2 to 5 mmol/L⁻¹) increase in lactate concentration without concurrent metabolic acidosis. Lactic acidosis is a persistently elevated (often >5 mmol/L⁻¹) lactate concentration in association with metabolic acidosis (pH<7.35).

Studies in dogs and cats have investigated normal lactate levels and identified the presence of hyperlactatemia, although a precise definition of lactic acidosis in dogs and cats has not yet been determined. The following section summarizes studies of normal lactate levels in dogs and cats published to date.

Normal Plasma Lactate Levels

It is important to realize that lactate is produced under normal conditions of aerobic metabolism in low concentrations. This equates to lactate production of approximately 0.8 mmol/L⁻¹ per kg⁻¹ per hour⁻¹ in people, resulting in a resting value of <1 mmol/L.^23–25 Similarly, several studies have investigated resting lactate values in dogs and cats, the findings of which are summarized below. These provide guidelines as to the normal range of values for plasma lactate.

An earlier study aiming to establish baseline values for plasma lactate in healthy beagles, ranging in age from 5 to 9 months, reported a mean (range) of plasma lactate concentrations of 1.11 (0.42 to 3.58) mmol/L.²⁶ Samples were analyzed using an enzymatic technique, and samples were collected from a jugular vein.

A study by McMichael et al., aimed to generate a reference range for plasma lactate values in young (4- to 80-day old) and adult, healthy, mixed-breed dogs. Thirty to 52 dogs were sampled at each age level.²⁷ Adult dogs were found to have a mean (± standard deviation [SD]) plasma lactate concentration of 1.80±0.84 mmol/L.²⁷ Dogs aged 70 or 80 days at the time of sampling did not have a statistically significant difference in lactate levels when compared with adult dogs. In contrast, resting lactate levels were higher in dogs <70 days of age, with the highest values found in the youngest sampling group (4-day-old dogs; 3.83±1.38 mmol/L). Lactate levels decreased from age 4 days to 70 days, reaching adult values at 70 days of age. Samples were analyzed using enzymatic amperometry (see below), and all samples were taken from a jugular vein.

A study investigating the effect of sampling site on plasma lactate measurements reported that samples from the jugular vein of 60 healthy, adult dogs revealed a mean ± SD of 1.25±0.49 mmol/L.²⁸ Furthermore, although there was a significant difference between samples obtained from different sites, this difference was small, and it was suggested that normal plasma lactate values in dogs are <2.5 mmol/L regardless of sampling site.²⁸

From the above studies, it can be concluded that in healthy, adult dogs at rest, lactate concentrations are <2.0 mmol/L, although the normal range may extend up to approximately 3.5 mmol/L.

In cats, two studies have reported plasma lactate concentrations that were sampled from the jugular vein in healthy, adult animals. One study investigating differences between 12 healthy and diseased cats reported lactate levels of 1.6±1.0 mmol/L in the healthy population.²⁹

A second study, with the aim of recording the effect of a standardized stressor (bathing) on various biochemical values, including lactate, reported mean (range) resting lactate levels of 0.77 (0.30 to 1.69) mmol/L.³⁰ This study also demonstrated a 10-fold increase in lactate levels in response to the stress of bathing. This increase was transient.

In summary, plasma lactate concentrations in healthy, adult cats at rest are <2 mmol/L. However, this concentration is derived from the small number of animals studied, and acute stress/struggling may have a marked impact on lactate concentration.³⁰

Ideally, reference ranges should be developed by individual hospitals for their patient population, and they should be specific to the lactate analyzer in use. Most blood-gas analyzers (bench-top and hand-held) use enzymatic amperometry specific to the measurement of L-lactate. Hand-held point-of-care analyzers are now easily available, inexpensive, and they compare favorably to bench-top analyzers.^31,32

Enzymatic amperometry involves the indirect measurement of a substance of interest (in this case, lactate) by the enzyme-driven generation of an electroactive analyte. A commonly employed technique uses the enzyme lactate oxidase. Lactate oxidase, immobilized in the lactate biosensor, selectively converts lactate to pyruvate and hydrogen peroxide (H₂O₂). The liberated hydrogen peroxide (the electroactive analyte) is oxidized at a platinum electrode to produce a current that is proportional to the sample lactate concentration. Another electroactive analyte in common use is potassium ferrocyanide—this time generated by the enzymatic activity of lactate oxidase upon lactate and potassium ferricyanide.

Blood chemistry analyzers often use a spectrophotometric method, whereby the oxidation of L-lactate by oxidized nicotinamide adenine dinucleotide (NAD+) is catalyzed by lactate dehydrogenase, producing reduced nicotinamide adenine dinucleotide (NADH). The NADH is then detected using spectrophotometry at a wavelength of 340 nanometer. The levels of NADH are in linear proportion to the level of L-lactate in the sample.

Sampling Techniques

Clinicians should be aware of several potential pitfalls regarding sampling techniques. The sampling site can have a minor effect on the measurement of lactate levels, particularly as peripheral venous samples will tend to reflect regional lactate kinetics. A study of 60 healthy dogs identified the following variations in lactate levels: cephalic vein (1.57±0.47 mmol/L), femoral artery (1.43±0.52 mmol/L), and jugular vein (1.25±0.49 mmol/L).²⁸ Although it is clear that sampling sites do affect lactate measurement, these differences do not appear to be clinically significant. Theoretically, arterial samples would better reflect systemic lactate concentrations, as they are less influenced by regional differences in lactate kinetics.^28,33 It is also possible to have a mild increase in lactate levels with prolonged occlusion of a vein when drawing the blood sample for lactate analysis.³⁴ When venous samples are taken, blood stasis should be avoided by collecting the sample using a free-flow technique. Stress and struggling (induced by bathing) was demonstrated to result in a tenfold increase in plasma lactate concentrations in cats.³⁰ This should be taken into account when interpreting lactate levels in light of clinical history.

As red blood cells do not contain mitochondria, they are lactate producers. Lactate production by red blood cells continues following blood sampling.²⁹ Lactate concentrations may increase by as much as 20% during each hour of storage at 25°C in serum clot tubes.²⁹ This may be clinically significant given the relatively narrow normal range for lactate. Therefore, it is essential that blood samples are analyzed rapidly (<5 minutes) following sampling. Alternatively, samples may be temporarily stored on ice, although this does not arrest lactate production.

Blood samples submitted for laboratory analysis should be collected in tubes containing sodium fluoride (NaF). Sodium fluoride inhibits several glycolytic enzymes, limiting significant increases in lactate levels (and cellular consumption of glucose).²⁹ The reported means for NaF and serum clot samples in this study were 1.6±1.0 mmol/L and 2.0±1.1 mmol/L, respectively. Again, it is debatable if such a difference would affect clinical decision making.

A human study demonstrated that intravenous fluid solutions containing lactate, which are inadequately cleared from intravenous catheters, can falsely increase the lactate concentrations measured in blood samples collected from that catheter.³⁵ The reverse is also true, in that solutions that do not contain lactate, which are inadequately cleared from intravenous catheters, can falsely decrease blood lactate concentrations through a dilutional effect.³⁵ This emphasizes the importance of proper blood collection technique if samples are to be drawn through indwelling intravenous catheters. In addition, solutions containing 5% dextrose, in either normal saline or Ringer’s lactate, have been shown to result in significant increases in blood lactate concentration over time.³⁶

Lactate Physiology and Pathophysiology

Several in-depth reviews of lactate physiology and pathophysiology exist, and what follows is an overview of lactate metabolism.^33,34,37

It should be noted that lactate exists as a pair of stereoisomers (more specifically, enantiomers). The following discussion pertains to the L (+) stereoisomer of lactate, as this is the stereoisomer produced by mammalian cells and has greater clinical significance. Accumulation of the D (−) stereoisomer and subsequent lactic acidosis have been reported in people and ruminants.^38,39 D-lactate is produced following metabolism of glucose and carbohydrates by bacteria in the gastrointestinal tract. In man, this has been associated with short-bowel syndrome following significant small intestinal resection. In ruminants, D-lactic acidosis has been associated with grain overload, as well as diarrhea in calves.^39,40

Lactate may be produced by all body tissues as a byproduct of glycolysis. However, skeletal muscle, brain, erythrocytes, and renal medulla are responsible for the majority of normal production.²⁵

Under normal conditions, all lactate is derived from pyruvate, which is generated as a normal step in glycolysis [see Figure].⁴¹ This reaction is catalyzed by lactate dehydrogenase. Under aerobic conditions, the majority of pyruvate enters mitochondria and undergoes oxidative decarboxylation, resulting in the production of carbon dioxide and water and the generation of 30 to 36 moles of adenosine triphosphate (ATP) per molecule of glucose metabolized.⁴² Under anaerobic conditions, including states of hypoperfusion, pyruvate can no longer undergo oxidative decarboxylation, and energy production becomes predominantly dependent on the process of glycolysis. The generation of ATP in anaerobic states is greatly reduced (2 moles of ATP for every mole of glucose metabolized to lactate) compared with aerobic metabolism.⁴² Despite being an inefficient means of energy production, anaerobic metabolism does allow for the continued production of energy. The metabolism of pyruvate results in the production of lactate and water [see Figure]; thus, lactate formation is a necessary and critical step in the process of anaerobic metabolism and continued ATP production.

The relatively small quantity of lactate produced under normal conditions is consumed primarily by the liver and kidneys.^34,37 Within these organs, lactate is converted back to pyruvate, the reaction catalyzed by lactate dehydrogenase. The majority of the produced pyruvate then enters into oxidative metabolism (Kreb’s cycle) or gluconeogenesis (Cori cycle [see Figure]).

The liver accounts for the majority (60% to 70%) of lactate consumption, and experimental hepatectomy in dogs resulted in significant increases in plasma lactate levels. ^34,37,43 Lactate is also metabolized (20% to 30%) by the kidneys, where it is freely filtered by the glomerulus (before near complete reabsorption in the proximal convoluted tubule), resulting in <2% excretion in urine.^34,37,45 Provided there is adequate oxygen delivery, both hepatic and renal consumption of lactate may substantially increase during hyperlactatemia to accommodate the increased lactate load.⁴⁵ It should be noted, however, that lactate consumption by these organs is a saturable process and that hyperlactatemia rapidly ensues when lactate production exceeds consumption.³⁷ In addition, skeletal muscle may act as an important site of lactate consumption (via oxidation) during hyperlactatemia.³⁷

The key role of the liver in lactate homeostasis is reflected by the severe abnormalities that result from liver dysfunction. In shock states, the role of the liver as a consumer of lactate may switch to being that of a lactate producer.^28,34 In cases of experimental hepatic insufficiency in dogs, metabolism of lactate continued until total hepatic blood flow fell to 70% of control levels, or until hepatic venous partial pressure of oxygen (PO₂) was <24 mm Hg, at which point plasma lactate concentrations rapidly increased.⁴⁶ The role of the liver as the primary consumer of lactate, accounting for 60% to 70% of lactate consumption, highlights the importance of reinstating adequate hepatic perfusion and oxygen delivery during therapy for states of hypoperfusion, such as shock (see following section on Therapy). Similarly, severe renal hypoperfusion (i.e., a 90% decrease in renal blood flow) results in a switch from renal consumption of lactate to production.⁴⁷

Hyperlactatemia may exist without a concurrent state of acidosis or academia. The hydrogen ions necessary for lactic acid formation are not produced as a direct result of lactate production. Instead, hydrogen ions are generated from the hydrolysis of ATP to adenosine diphosphate (ADP) and inorganic phosphate in the cytosol. Ordinarily, the hydrogen ions produced may be titrated by bicarbonate and nonbicarbonate buffers or consumed by oxidative phosphorylation, provided the oxygen supply is adequate. Lactic acid formation is favored when these processes are impaired, resulting in lactic acidosis. Therefore, hyperlactatemia may be present without concurrent acidosis or acidemia when buffering systems are able to titrate a decrease in pH and organ perfusion is adequate.⁴⁸

During recovery from a state of lactic acidosis or hyperlactatemia, the availability of oxygen results in conversion of lactate back into pyruvate (catalyzed by lactate dehydrogenase) and subsequent entry into the Kreb’s cycle as aerobic metabolism continues, or gluconeogenesis by entry of pyruvate into the Cori cycle [see Figure].

In summary, hyperlactatemia and lactic acidosis result when lactate production exceeds consumption and/or pathways for lactate consumption are defective. Hyperlactatemia may occur without lactic acidosis, provided tissue perfusion, oxygenation, and buffering systems are intact. In such cases, continued overproduction or decreased uptake and clearance of lactate will eventually lead to lactic acidosis as homeostatic mechanisms are exceeded.

Classification of Lactic Acidosis

Following initial work by Huckabee in recognizing the presence of lactic acidosis, with and without adequate oxygen delivery, Cohen and Woods developed a classification of lactic acidosis.^23,24,34 The broad divisions of the original classification have remained, with some refinement and new examples added over time. Originally, type A lactic acidosis encompassed all causes of hypotension with resultant hypoperfusion and arterial oxygen desaturation. Type B lactic acidosis originally described any cases that did not fall into the type A classification; that is, lactic acidosis cases without clinical/measurable evidence of poor tissue perfusion or oxygenation. Subsequently, the original classification has been repeatedly adapted in human and veterinary medicine.

Currently, type A lactic acidosis may be subclassified as that resulting from inadequate oxygen delivery or increased oxygen demand—both of which cause tissue hypoperfusion [Table 1].²⁵ Shock is a classic example of decreased oxygen delivery, and seizures are an example of increased oxygen demand with a rapid increase in metabolic rate outstripping lactate consumption and glucose metabolism exceeding the oxidative capacity of mitochondria.^49,50

In contrast, type B lactic acidosis occurs in the presence of normal blood oxygen content and systemic arterial blood pressure, the causes of which may be subclassified into inadequate utilization of oxygen, congenital errors of metabolism, drugs/toxins, and other causes [Table 2].

Type A lactic acidosis is more frequently encountered in clinical practice, although critically ill patients frequently have features of both types A and B lactic acidosis.^4,51 Sepsis is an example that often has features involving types A and B presentations, including tissue hypoperfusion, reduced lactate clearance and entry of pyruvate into Kreb’s cycle, and abnormal mitochondrial function.⁵²

Note: Many of the examples in Tables 1 through 3 have been associated with hyperlactatemia in veterinary patients. However, it is not always clear whether a definitive diagnosis of lactic acidosis has been achieved, as blood-gas analysis has not been routinely performed or reported.^1,4,7,46

Prognostic Value of Lactate

In people, numerous studies in different critically ill patient populations have demonstrated the prognostic value of lactate levels.^62–66 In some cases, a single measurement of lactate levels was associated with a prognosis of survival.^54,62,66 However, other studies have found no significant differences in lactate levels between survivors and nonsurvivors at initial presentation, and decreased lactate levels (hours to days after presentation) in response to therapy provided a better prediction of outcome.^{56,63–65,67} The patient populations studied included critically ill surgical patients and those with septic shock. Furthermore, hemodynamic parameters should not be disregarded, as the use of lactate levels in conjunction with assessment of systemic arterial blood pressure and/or evaluation of acid-base status have been shown in some studies to more accurately predict outcome than lactate levels alone.^56,63,65,66

From the available evidence, it appears that human patients with hypotension and elevated lactate levels (>5 mmol/L) have a high mortality rate (>80%), as do patients who fail to clear lactate within 24 to 48 hours.²⁵ At present, it is unclear if these or similar conclusions apply to veterinary patients. Furthermore, it is important to note that lactate levels reflect the global, systemic situation. Individual organs or regions may be hypoxic and produce increased levels of lactate without a detectable effect systemically.

A few studies have investigated the relationship between hyperlactatemia and outcome in dogs. An early study evaluated lactate levels in dogs that were presented to an intensive care unit (ICU) with various underlying disease conditions; this study showed that dogs with the highest blood lactate levels at admission were more likely to die.⁴ In a study investigating 102 dogs with gastric dilatation and volvulus (GDV), those with plasma lactate levels >6 mmol/L had a 58% survival rate, whereas those with values <6 mmol/L had a survival rate of 99%.¹ This study also found that preoperative measurement of plasma lactate levels might be useful in determining the risk of gastric necrosis in dogs with GDV.¹ In a more recent study evaluating lactate measurements in dogs with GDV, only one of nine dogs with a lactate level >6 mmol/L died.⁶⁸ Although drawing definite conclusions from the small study population (n=28) is difficult, the increased survival rate in this study emphasizes the concern of determining prognosis based on a single lactate measurement. In addition, the magnitude of a single lactate value may be misleading if taken out of context of the disease.^56,63,65 An early study in human patients presenting with various types of shock demonstrated that the prognosis of lactic acidosis tends to vary with the underlying cause of hypoperfusion.⁵⁵ It was demonstrated in this study that patients with hemorrhagic shock tolerate higher lactate levels than patients with cardiogenic shock. In animals, prognosis also appears to vary with the underlying disease, and some animals with very high lactate values (>10 mmol/L) may still respond to resuscitative efforts and survive.⁴ Studies in people have also demonstrated that serial lactate measurements and the change in lactate levels in response to therapy are more reliable at determining outcome than a single-admission lactate measurement (see above). These findings are further supported in a study of dogs suffering from severe or complicated canine babesiosis.⁵⁸ In this study, although the presence of hyperlactatemia prior to therapy was suggestive of a poor prognosis, serial lactate measurements and response to therapy were much stronger predictors of survival. Dogs with lactate levels >4.4 mmol/L after 24 hours, despite therapeutic efforts, had a very poor prognosis. To the authors’ knowledge, no studies have examined the prognostic significance of blood lactate levels in cats, although clinical experience would suggest a similar relationship exists.

Lactate Measurement in Cavitary Effusions

The value of measuring lactate concentration in body fluids other than blood has been investigated. Body fluid lactate concentrations may increase from diverse processes, including reduced blood flow, hypoxia, and the increased production of lactate by granulocytic or bacterial metabolism when these cells are present in the body fluids.²²

Therapy

Type A lactic acidosis unto itself is not a disease, but rather a consequence of decreased DO₂ to the tissues or increased VO₂ [Table 1], which may reflect an underlying disease process or transient imbalance in homeostasis. Therefore, the therapy for type A lactic acidosis must be directed toward identifying and treating the underlying cause while simultaneously improving DO₂ to the tissues. Appropriate resuscitative efforts include restoration of the effective circulating volume, improving or increasing cardiac function, resection of ischemic or necrotic tissue, and correction of septic conditions.^61,71 In the absence of cardiac disease, which may preclude fluid therapy, this will usually involve aggressive fluid resuscitation using crystalloids, colloids, blood products, or a combination thereof.⁶¹ As hemoglobin content is an important component in determining DO₂, animals with concurrent acute anemia may benefit from a blood transfusion to maintain the hematocrit >18% to 21%.⁷² Acute hemodilution to a hematocrit <10% is associated with hyperlactatemia.⁷² In people, it has been suggested that persistent hyperlactatemia in the face of appropriate resuscitative efforts warrants a poor prognosis, and a search for an undiagnosed underlying cause (such as an unidentified focus of infection) should be undertaken.⁷³ Although not investigated, one can infer that similar results will be found in dogs and cats. If a septic focus is identified, the source should be removed as soon as the animal is stabilized. This may require surgical intervention. When assessing lactate in regard to the patient’s response to therapy, it is important to remember that lactate dynamics vary with the cause of hyperlactatemia, and, therefore, the expected decline following resuscitative efforts will also vary. For example, the half-life of lactate (i.e., the time for plasma lactate concentrations to decrease by 50%) during seizures in people is approximately 60 minutes with little, if any, impairment of lactate metabolism.⁷⁴ In contrast, the half-life of lactate in human patients with shock may be as long as 18 hours.⁷³ This difference in lactate half-life may be the result of a decrease in clearance of lactate, a persistent increase in its production, or a combination of the two in hypovolemic or septic patients.^75,76 To the authors’ knowledge, the half-life of lactate in healthy dogs and cats and in patients with various underlying states of hypoperfusion has not been investigated. In people with circulatory shock, it has been suggested that if after 1 hour of aggressive therapy a decrease in lactate of >10% is not achieved, a change in therapy should be considered.⁷⁴ In the authors’ experience, the decrease in lactate concentration following successful aggressive therapy for circulatory shock is often significantly >10% within 1 hour, although it does tend to vary with the underlying cause of shock.

A common concern that is frequently encountered in treating patients with lactated Ringer’s solution (LRS) is whether the lactate contained within this fluid will influence blood lactate values. Lactated Ringer’s solution contains 28 mmol/L of sodium lactate in the form of a racemic mixture (containing both D- and L-isomers of lactate in varying concentrations, depending on the product used).⁷⁷ Interestingly, it has been demonstrated in human and canine studies that LRS administered as a 15 to 20 mL/kg bolus does not result in a significant change in plasma L-lactate concentrations in normal subjects and those with hemorrhagic shock.^36,78,79 This is likely explained by analyzers measuring only the Lisomer and not the D-isomer of lactate contained in LRS.³³ The dilution and metabolism of L-lactate following its administration may also minimize any increases in lactate that might otherwise have occurred.³⁶ In contrast, when measured using specific enzyme analyzers, D-lactate levels in swine have been shown to increase up to 20-fold following large boluses of LRS.⁸⁰ The clinical significance of an increase in D-lactate following the administration of LRS remains to be determined. However, as most analyzers do not detect it, any increase in the D-isomer concentration should not affect interpretation of lactate measurements. To the authors’ knowledge, no studies in dogs or cats have evaluated the effect of large boluses (60 to 90 mL/kg) of LRS on plasma lactate concentrations. The administration of LRS at a rate of 4.125 mL/kg per hour for 6 hours to dogs with lymphoma resulted in a transient increase in the L-isomer concentration.³ It was concluded that dogs with lymphoma have a transient inability to handle an increased lactate load and that lactate-containing fluids should be used cautiously in dogs with lymphoma.³ It is possible that patients with impaired liver and/or renal function may also have increased levels of lactate following administration of lactate-containing solutions, which could make the interpretation of hyperlactatemia difficult in these patients.

The administration of sodium bicarbonate to patients with lactic acidosis has received a lot of attention, and the current general consensus is that sodium bicarbonate is not of benefit in the therapy of most cases of lactic acidosis. ^25,45,71,81 Following successful resuscitative efforts with improved DO₂ to the tissues, pH will often improve as the metabolism of lactate is accompanied by a concurrent increase in bicarbonate production by the liver.⁷³ This may result in an overshoot alkalosis in cases that previously received sodium bicarbonate. Further detrimental effects associated with the administration of sodium bicarbonate include a transient fall in mean arterial pressure and an increase in intracranial pressure following rapid intravenous administration, decreased ionized calcium concentration (which may affect left ventricular contractility), decreased DO₂ through decreased unloading of oxygen from hemoglobin at the tissue level (Bohr effect), and paradoxical central nervous system acidosis (especially in patients that are hypercarbic due to hypoventilation).^81–84

Although hypoperfusion is the most common cause of lactic acidosis, it is important to consider other causes (type B) and look for supporting evidence of impaired DO₂ in patients presenting with hyperlactatemia. Supporting evidence of impaired DO₂ may include tachycardia, pale mucous membranes, weak pulses, prolonged capillary refill time, decreased mentation, and hypotension. For example, it would be inappropriate to institute shock therapy for treatment of hyperlactatemia in the lymphoma patient that is hemodynamically stable with normal tissue perfusion. As type B lactic acidosis, by definition, is not associated with tissue hypoxia, its therapy does not usually require the same emergency interventions associated with type A lactic acidosis. ⁷¹ In addition, very little information is available regarding nonacidotic hyperlactatemia or type B lactic acidosis in dogs and cats, and further studies are required before recommendations regarding outcomes or therapy can be made in these patients. However, the presence of hyperlactatemia in symptomatic and asymptomatic cancer patients, or in those receiving medications such as activated charcoal, may confound the assessment of lactate levels in animals presented with life-threatening conditions. As is the case for type A lactic acidosis, type B lactic acidosis is the result of an underlying disease process, and therapy is generally directed at identifying and correcting the underlying disease.

Conclusion

Lactate measurement is a very useful diagnostic test, which may be performed at the bedside. It aids in the detection of hypoperfusion (the most common cause of lactic acidosis in veterinary species), and it has prognostic implications for type A lactic acidosis and its treatment. Lactate measurement may also prove useful in helping to detect or rule out the presence of a septic effusion in various cavitary effusions, and it may have prognostic implications when measured in fluids such as CSF following trauma. Published studies in veterinary medicine are few at this time, and future studies will likely further define the role of lactate in the diagnosis and management of dogs and cats presenting to the ICU.