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Compendium January 2012 (Vol 34, No 1)

Interpreting Lactate Measurement in Critically Ill Horses: Diagnosis, Treatment, and Prognosis

by Brett S. Tennent-Brown, BVSc, MS, DACVIM, DACVECC

    CETEST This course is approved for 3.0 CE credits

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    Abstract

    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.

    Click here to read the companion article: “Lactate Production and Measurement in Critically Ill Horses.”

    Blood lactate concentration has long been recognized as a useful indicator of disease severity in humans1 and has received attention as a prognostic indicator in horses with colic2–4 and in critically ill equine neonates.5–7 Although numerous studies in human and veterinary medicine have identified associations between hyperlactatemia and both morbidity and mortality, blood lactate concentration at hospital admission is not always strongly correlated with outcome.8 Furthermore, there is often considerable overlap in blood lactate concentrations among survivors and nonsurvivors.9–12 Although disappointing, the inability of a single laboratory value to discriminate between survivors and nonsurvivors should not be surprising when clinicians consider the multitude of factors involved in the pathophysiology of disease in critically ill patients.1 This article reviews the interpretation of lactate concentration measurements in blood and other body fluids.

    Using Lactate Concentration in Diagnosis and Treatment

    Lactate as a Resuscitation End Point

    The most common and important cause of an increase in blood lactate concentration in hospitalized horses is decreased tissue perfusion and oxygen delivery with subsequent anaerobic metabolism.13 In adult horses, decreased tissue perfusion is most often due to hypovolemia, but inappropriate vascular tone during severe sepsis may also contribute to hyperlactatemia. In septic equine neonates, hypovolemia, inappropriate vascular tone, and decreased cardiac output have all been implicated as causes of hyperlactatemia.5,7 The half-life of lactate is approximately 20 minutes in humans14 and is probably similar in veterinary species.15 Consequently, lactate has been suggested to be an ideal resuscitation end point to guide fluid and vasopressor or inotrope therapy.16 As evidence of this, people with reduction in lactate concentration of >5% in the first hour or 10% in the first 6 hours after initiation of resuscitation had improved survival rates compared with patients in whom lactate concentration did not decrease over the same time period.17 However, in many human studies, particularly those examining septic patients, in whom causes of hyperlactatemia may be numerous, blood lactate concentration lacks precision as an acute resuscitation end point and concentrations may remain increased despite restoration of tissue oxygenation.18 In contrast, in a large group of adult horses admitted to a university emergency service, mean blood lactate concentration decreased to within normal range within 12 hours after presentation in most patients, suggesting that blood lactate concentration may be a useful end point for acute resuscitation in such patients.13 Because blood lactate concentration in healthy neonatal foals is increased for the first 48 to 72 hours of life, defining an appropriate resuscitation “target” value for these animals is more difficult; nevertheless, there should be a consistent decrease in blood lactate concentration in foals that are adequately volume resuscitated.5–7

    Lactate as a Transfusion Trigger

    Some have suggested that an increase in blood lactate concentration could serve as a “trigger” for initiating blood transfusions and that blood lactate concentration should be monitored to determine when adequate oxygen delivery is restored.19 Lactate concentrations are uncommonly described as transfusion triggers for human patients, in whom hemoglobin concentrations form the basis for most recommendations.20,21 In horses, blood lactate concentration appears to be a sensitive indicator of blood loss, although changes may be relatively subtle after mild to moderate hemorrhage.22 In one study, mean blood lactate concentrations increased significantly from a baseline of 0.7 ± 0.2 mmol/L to 2.2 ± 1.0 mmol/L after approximately 16 mL/kg of blood (15% to 26% of blood volume) was removed from healthy mares, although there was some overlap in the ranges of blood lactate concentrations measured before and after hemorrhage (0.4 to 1.1 mmol/L versus 0.5 to 6.7 mmol/L).22 In 17 horses requiring whole blood transfusion, mean blood lactate concentration was increased (consistent with inadequate oxygen delivery) before transfusion, although the increase in some horses was mild.23 Mean blood lactate concentrations returned to normal after autologous transfusion22 or after blood transfusion in horses with hemorrhagic anemia.23 Thus, blood lactate concentration appears to be useful for assessing the adequacy of transfusion. However, blood lactate concentrations remained increased after transfusions in horses with hemolytic anemia or anemia attributable to erythropoietic failure, suggesting that other mechanisms may be responsible for hyperlactatemia in these patients.23

    Lactate in Septic Effusions

    The presence of bacterial (or fungal) infections in a closed body cavity has been associated with an increase in lactate concentration and, usually, a decrease in glucose concentration in effusions from the affected cavity.24 Lactate concentration within these effusions increases independently of the blood lactate concentration in these cases.24 The concentrations of lactate and glucose in these effusions may be determined in an attempt to rapidly characterize the nature of the fluid, particularly when other findings are equivocal or delayed. The cause of the increased lactate concentration in the effusion is unclear, but it may be due to tissue anoxia subsequent to impaired blood flow (secondary to tissue swelling) or increased glucose metabolism with subsequent lactate production by inflammatory leukocytes.24

    Peritoneal Lactate Concentration

    Human studies have suggested that peritoneal lactate concentrations may be used to establish a diagnosis of septic peritonitis and differentiate it from other conditions that may cause an exudative effusion.24 Studies in small animals have shown that peritoneal lactate concentrations are increased in dogs with septic peritoneal effusions compared with dogs with nonseptic effusions.25,26 However, Nester et al27 reported that peritoneal fluid lactate concentrations were also increased in dogs with neoplastic effusions compared with dogs with nonneoplastic (and nonseptic) effusions. Calculation of the difference between abdominal fluid and peripheral blood lactate concentrations may improve the ability to discriminate between septic and nonseptic effusions.25,26 Although these findings are interesting and consistent with human reports, they should be interpreted with caution, as they have involved a small number of animals and the inclusion criteria (presence of bacteria on cytology and/or positive culture results) of the studies comparing septic and nonseptic effusions may have resulted in misclassification of some patients. Furthermore, in studies examining differences between septic and nonseptic effusions, neoplastic conditions were included in both patient groups and could have limited the ability to differentiate between septic and nonseptic effusions. Despite these shortcomings, increased lactate concentrations (>2.5 mmol/L) in peritoneal fluid should prompt consideration of a septic or neoplastic process.28 In horses, peritoneal fluid lactate concentration has been more commonly used to identify ischemic bowel lesions (see below) and, to my knowledge, has not been formally evaluated for diagnosing septic peritonitis.

    Pleural Lactate Concentration

    Increased lactate concentrations have been documented in human patients with malignancy and infections of the pleural cavity.24 In horses with nonseptic pleural effusion, there was no significant difference in mean lactate (and glucose) concentration between venous blood and pleural fluid. In contrast, horses with septic pleural effusions (defined as the presence of bacteria on cytology and/or positive culture results) had a significantly higher lactate (and lower glucose) concentration in their pleural fluid than in their venous blood.29 Because four horses with pleural effusions secondary to lymphosarcoma were included in the nonseptic group, concentrations of lactate and glucose in pleural fluid may help rule out neoplastic processes in this species. It is important to note that this would be in stark contrast to the situation in human and small animal studies, and additional studies with greater numbers of horses are needed.24

    Synovial Lactate Concentration

    Based on the results of studies in human patients in the late 1970s and early 1980s, it was suggested that measurement of synovial fluid lactate concentration could be a useful tool to rapidly differentiate septic from nonseptic arthritis.24 In those studies, lactate concentration in the synovial fluid appeared to be a more sensitive diagnostic indicator of sepsis than the results of Gram staining, particularly if antimicrobials had been administered before collection of synovial fluid.30 In addition, lactate concentration could be determined even when the synovial fluid was too thick for a cell count to be performed.30 It was often possible for a clinician to obtain the synovial fluid lactate concentration before synovial fluid cell counts and differentials were available.30 However, more recently, it was concluded that there is insufficient evidence to support the use of lactate measurements for diagnosing septic arthritis in humans.31 In six horses with septic arthritis induced by intraarticular injection of Staphylococcus aureus, synovial fluid lactate concentrations had increased from a baseline value of 2.02 ± 0.76 mmol/L to >6.9 mmol/L at 24 hours; mean synovial fluid lactate concentrations in control joints (injected with saline) never exceeded 4.0 mmol/L.32 Between 24 hours and 8 days after bacterial inoculation, synovial fluid lactate concentration in septic joints varied considerably (i.e., 2.3 to 22.9 mmol/L).32 Thus, synovial fluid lactate concentration may be useful for diagnosing septic arthritis, particularly in the acute phase, but results may be more difficult to interpret in chronic conditions.32

    Pericardial Lactate Concentration

    Lactate concentration in pericardial fluid was assessed in 41 dogs in an attempt to identify parameters that distinguish between neoplastic and nonneoplastic effusions.33 Pericardial fluid lactate concentration was significantly higher than blood lactate concentration in all dogs with pericardial effusion. Most dogs with neoplastic pericardial effusions had masses associated with the heart. Lactate concentrations were significantly greater in pericardial fluid from dogs with neoplasia (n = 28) than in fluid samples from dogs without neoplasia (n = 13); however, the considerable overlap between the two groups precluded clinical usefulness.33 Because of a low glucose concentration in neoplastic effusions, the difference between glucose concentrations in peripheral blood and pericardial fluid was significantly greater in dogs with neoplasia; however, this difference was not present for lactate concentrations, perhaps because 61% of all dogs with pericardial effusion were hyperlactatemic.33 To my knowledge, lactate concentrations in pericardial effusions have not been evaluated in horses.

    Cerebrospinal Fluid Lactate Concentration

    Measurement of lactate concentrations in the cerebrospinal fluid (CSF) of human patients allows accurate differentiation of bacterial (septic) and nonseptic (commonly viral) meningitis.24 Increases in CSF lactate concentration reportedly occur with bacterial infections, but not with nonseptic meningitis. Unfortunately, increases in CSF lactate concentration may also occur with any condition that results in reduced brain oxygenation and/or increased intracranial pressure. Normal CSF lactate concentrations in horses vary slightly depending on the site of collection, with values reported for samples collected from the atlanto-occipital space being slightly lower (0.21 ± 0.01 mmol/L) than those for samples collected from the lumbosacral space (0.26 ± 0.01 mmol/L).34 Increased lactate concentrations in CSF have been reported for horses with brain abscesses, Eastern equine encephalomyelitis, and head trauma.34 Increased lactate concentration may be the only CSF abnormality in horses with brain abscesses, although lactate concentration appears to be less useful for distinguishing bacterial from viral brain infections in horses than in other species.34

    Lactate as a Diagnostic Indicator of Intestinal Ischemia

    The reliability of several point-of-care monitors has been demonstrated for measuring peritoneal lactate concentration in horses.35,36 This has allowed rapid and simultaneous measurement of venous blood and peritoneal fluid lactate concentrations.35,37 In healthy horses, the peritoneal fluid lactate concentration is approximately 0.7 mmol/L and is always lower than the plasma lactate concentration38; however, peritoneal fluid lactate concentration increases rapidly with intestinal ischemia.37 In one study, horses with strangulating intestinal obstructions had higher mean peritoneal fluid lactate concentrations (8.45 ±5.52 mmol/L) than horses with nonstrangulating obstructions (2.09 ±2.09 mmol/L).37 Furthermore, because lactate concentrations in peritoneal fluid appear to increase more rapidly than concentrations in plasma, measuring lactate in paired peritoneal fluid and plasma samples may provide more prognostic insight than either measurement alone.37 In horses with strangulating lesions, peritoneal lactate concentrations are consistently higher than plasma lactate concentrations, although this difference diminishes with onset of systemic shock as plasma lactate concentration increases.35,37

    Using Lactate Concentration for Prognosis

    Numerous studies have demonstrated an association between blood lactate concentration at hospital admission and patient outcome (usually survival or hospital discharge) in both human and veterinary medicine.1–7,9–12 However, blood lactate concentration at hospital admission does not always correlate well with prognosis, and there is often considerable overlap between values obtained from survivors and nonsurvivors.2–7,9–12 The relationship between blood lactate concentration at admission and prognosis is almost certainly influenced by the underlying disease condition. Additionally, lactate metabolism is a dynamic process, and the time point at which lactate concentration is measured in the course of disease is likely an important confounder in interpreting this parameter. For example, in human studies, lactate concentration may be measured at admission to an intensive care unit after brief resuscitation in the emergency room and may not, therefore, accurately reflect disease severity. Additionally, blood lactate concentration and acid-base status are not always strongly correlated, which may reflect either the underlying disease process or the patient’s ability to compensate for an acid-base disturbance.5,11

    More recently, blood lactate has been measured serially to determine the rate at which lactate concentration returns to normal.9–12,17,39,40 In human critical care medicine, this approach appears to provide data that more accurately predict outcome or identify the need for more aggressive therapy than a single measurement. Persistent hyperlactatemia despite treatment has been associated with lower survival rates and a higher incidence of multiple organ failure in human patients.17,39,40 Therefore, serial lactate measurement may be valuable for guiding therapy and indicating prognosis in veterinary medicine.

    Hospital Admission Lactate Concentration in Foals

    The results of three recent studies indicate that hospital admission lactate concentration is significantly higher in nonsurviving equine neonates than in survivors.5–7 Although there was considerable overlap in the ranges of lactate concentrations in these three studies,5–7 by using an admission lactate concentration of 6.9 mmol/L as a cutoff, Henderson and colleagues6 determined that the outcome could be predicted in more than 85% of cases. Two of these studies also detected significant differences in admission lactate concentration when the foals were divided into different diagnostic groups; septic or bacteremic foals and foals with hypoxic-ischemic (neonatal) encephalopathy had higher admission lactate concentrations than foals with enteritis/colitis or a localized bacterial infection (e.g., septic arthritis, an infected umbilical remnant).5,6 In one of these studies, there was a moderate inverse correlation between lactate (and creatinine) concentration and mean arterial blood pressure, suggesting that the hyperlactatemia was at least partially due to tissue hypoperfusion (although there was no association between lactate concentration and either heart rate or packed cell volume).5 In that same study, a correlation was also found between lactate concentration and evidence of systemic inflammatory response syndrome.5 This latter finding and the modest associations between lactate concentration and blood pressure support the contention that an inflammatory reaction is important in the pathogenesis of hyperlactatemia in some sick foals.

    Hospital Admission Lactate Concentration in Adult Horses

    Several studies examining horses with colic have shown a solid association between hospital admission blood lactate concentration and outcome.2,3 The authors of a recent study measured lactate concentration in 250 horses that presented for emergency evaluation (including 152 horses with colic) and showed that the odds ratio for a poor outcome (death or euthanasia) increased by 29% for every 1 mmol/L that admission plasma lactate concentration increased.13 However, as in earlier studies, there was considerable overlap between the admission lactate concentrations of nonsurvivors and survivors.13 Furthermore, although the prognosis probably worsens considerably once blood lactate concentration exceeds 8 to 10 mmol/L, there is no concentration beyond which death is certain.

    Serial Measurement of Lactate Concentration in Foals

    In equine neonates in which blood lactate concentrations were serially measured, mean concentrations were consistently higher in nonsurvivors than survivors at all time points.5–7 In a large retrospective study examining blood lactate concentration in foals, Wotman et al7 reported that the odds ratio for survival decreased for every day that lactate concentration remained increased. Despite these results, two of three studies have been unable to detect a significant relationship between the rate at which blood lactate concentration decreases and patient outcome.5,6 However, when changes in lactate concentration over time were used to approximate lactate clearance, the rate of decline in blood lactate concentration was lower in nonsurvivors.7 Although the mechanism for the delay in achieving normolactatemia in these foals is unknown, these findings suggest that serial measurement of lactate concentration in foals may be a useful predictor of outcome.7

    Serial Measurement of Lactate Concentration in Adult Horses

    In a retrospective study of adult horses with large colon volvulus, postoperative mean blood lactate concentrations were lower than preoperative values in survivors and nonsurvivors; however, although lactate concentrations returned to normal in survivors, nonsurvivors remained hyperlactatemic.4 Mean blood lactate concentration was significantly higher in nonsurvivors than survivors preoperatively (10.64 ± 3.28 versus 3.55 ± 2.62 mmol/L, respectively) and at 24 hours after surgery (3.24 ± 2.08 versus 0.96 ± 0.06 mmol/L, respectively).4 Measurement of blood lactate concentrations at 6, 12, 24, 48, and 72 hours after hospital admission also appears to be of value in predicting outcome in adult horses presented for emergency evaluation and treatment.13 In this report, lactate concentration was significantly higher in nonsurvivors at all time points, and the odds ratio for nonsurvival increased the longer that lactate concentration remained increased. In contrast to results reported for equine neonates, there were temporal changes in the rate of lactate clearance (also estimated from changes in lactate concentration between sampling points). Initially, the change in lactate concentration tended to be positive and higher in nonsurvivors than survivors (i.e., lactate concentration tended to decrease more rapidly in nonsurvivors, suggesting that lactate clearance mechanisms were intact), although this difference did not reach statistical significance. However, between 24 and 48 hours after admission, the change in lactate concentration in nonsurvivors became negative (i.e., lactate concentration increased) and was significantly different from that in survivors.13

    Additional studies are required to determine whether this decrease in lactate clearance represents impaired metabolism or increased production. Further, although serial measurement of lactate concentration appears to be a promising tool in large animal critical care, optimal sampling times and duration as well as the appropriate patient populations to be monitored need to be defined.13 Another point to recognize is that changes in lactate concentration in nonsurvivors are relatively subtle. For example, when all cases were considered at 72 hours after admission, mean blood lactate concentration was 0.83 ± 0.21 mmol/L in survivors and 1.59 ± 0.68 mmol/L in nonsurvivors.13

    Conclusion

    Blood lactate concentration is a useful indicator of disease severity in veterinary medicine and appears to be a useful guide for fluid resuscitation, particularly in adult horses. Blood lactate concentration may also be used as an indicator for the need for blood transfusion and to determine the adequacy of erythrocyte replacement in horses with blood loss anemia. Only limited information is available to determine the value of measuring lactate concentrations in effusions in horses; however, an increased lactate (and decreased glucose) concentration should prompt consideration of a septic or neoplastic process. Further, increases in peritoneal lactate concentration (compared with peripheral blood concentration) in horses with colic support a diagnosis of intestinal ischemia and the need for surgery. Increased blood lactate concentrations are associated with mortality, but measurement at a single time point often does not distinguish survivors from nonsurvivors. Lactate concentrations measured serially over the first several days of hospitalization appear to provide better prognostic information in human critical care medicine and may have use in equine patients. Determining lactate clearance rates may also be of value, although more studies are required to determine whether decreases in fractional clearance represent impaired metabolism or increased production of lactate.

    Downloadable PDF

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    2. Moore JN, Owen RR, Lumsden JH. Clinical evaluation of blood lactate levels in equine colic. Equine Vet J 1976;8(2):49-54.

    3. Furr MO, Lessard P, White NA. Development of a colic severity score. Vet Surg 1995;24(2):97-101.

    4. Johnston K, Holcombe SJ, Hauptman JG. Plasma lactate as a predictor of colonic viability and survival after 360° volvulus of the ascending colon in horses. Vet Surg 2007;36(6):563-567.

    5. Corley KTT, Donaldson LL, Furr MO. Arterial lactate concentration, hospital survival, sepsis and SIRS in critically ill neonatal foals. Equine Vet J 2005;37(1):53-59.

    6. Henderson ISF, Franklin RP, Boston RC, et al. Association of hyperlactatemia with age, diagnosis and survival in equine neonates. J Vet Emerg Crit Care 2008;18(5):496-502.

    7. Wotman K, Wilkins PA, Palmer JE, et al. Association of blood lactate concentration and outcome in foals. J Vet Intern Med 2009;23(3):598-605.

    8. Bakker J. Lactate: may I have your votes please? Intensive Care Med 2001;27(1):6-11.

    9. Cerovic O, Golubovic V, Spec-Marn A, et al. Relationship between injury severity and lactate levels in severely injured patients. Intensive Care Med 2003;29(8):1300-1305.

    10. Husain FA, Martin MJ, Mullenix PS, et al. Serum lactate and base deficit as predictors of mortality and morbidity. Am J Surg 2003;185(5):485-491.

    11. Hatherill M, McIntyre AG, Wattie M, et al. Early hyperlactataemia in critically ill children. Intensive Care Med 2000;26(3):314-318.

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    13. Tennent-Brown BS, Boston RC, Wilkins PA. Admission and sequentially measured plasma lactate concentrations as prognostic indicators in adult equine emergencies. American College Veterinary Internal Medicine Scientific Forum. J Vet Intern Med 2008;22(3):754.

    14. Levraut J, Ciebiera J-P, Chave S, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than over production. Am J Respir Crit Care Med 1998;157(4 pt 1):1021-1026.

    15. Lagutchik MS, Ogilvie GK, Wingfield WE, et al. Lactate kinetics in veterinary critical care: a review. J Vet Emerg Crit Care 1996;6(2):81-95.

    16. Prittie J. Optimal end-points of resuscitation and early goal-directed therapy. J Vet Emerg Crit Care 2006;16(4):329-339.

    17. Nguyen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 2004;32(8):1637-1642.

    18. Dellinger RP, Levy MM, Carlet JM, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med 2008;34(1):17-60.

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    20. Revell M, Greaves I, Porter K. Endpoints for fluid resuscitation in hemorrhagic shock. J Trauma 2003;54(5):S63-S67.

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    22. Magdesian KG, Fielding CL, Rhodes DM, et al. Changes in central venous pressure and blood lactate concentration in response to acute blood loss in horses. J Am Vet Med Assoc 2006;229(9):1458-1462.

    23. Hurcombe SD, Mudge MC, Hinchcliff KW. Clinical and clinicopathologic variables in adult horses receiving blood transfusions: 31 cases (1999–2005). J Am Vet Med Assoc 2007;231(9):267-274.

    24. Brook I. The importance of lactic acid levels in body fluids in the detection of bacterial infections. Rev Infect Dis 1981;3(3):470-478.

    25. Levine GM, Bonczynski JJ, Ludwig LL, et al. Lactate as a diagnostic test for septic peritoneal effusions in dogs and cats. J Am Anim Hosp Assoc 2004;40(5):364-371.

    26. Bonczynski JJ, Ludwig LL, Barton LJ, et al. Comparison of peritoneal fluid and peripheral blood pH, bicarbonate, glucose, and lactate concentration as a diagnostic tool for septic peritonitis in dogs and cats. Vet Surg 2003;32(2):161-166.

    27. Nester DD, McCullough SM, Schaeffer DJ. Biochemical analysis of neoplastic versus nonneoplastic abdominal effusions in dogs. J Am Anim Hosp Assoc 2004;40(5):372-375.

    28. Pang DS, Boysen S. Lactate in veterinary critical care: pathophysiology and management. J Am Anim Hosp Assoc 2007;43(5):270-279.

    29. Brambaugh GW, Benson PA. Partial pressures of oxygen and carbon dioxide, pH, and concentrations of bicarbonate, lactate, and glucose in pleural fluid from horses. Am J Vet Res 1990;51(7):1032-1037.

    30. Rioordam T, Doyle D, Tabaqchali S. Synovial fluid lactate acid measurement in the diagnosis and management of septic arthritis. J Clin Pathol 1982;35(4):390-394.

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    32. Tulamo RM, Bramlage LR, Gabel AA. Sequential clinical and synovial fluid changes associated with acute infectious arthritis in the horse. Equine Vet J 1989;21(5):325-331.

    33. de Laforcade AM, Freeman LM, Rozanski EA, et al. Biochemical analysis of pericardial fluid and whole blood in dogs with pericardial effusion. J Vet Intern Med 2005;19(6):833-836.

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    35. Saulez MN, Cebra CK, Dailey M. Comparative biochemical analyses of venous blood and peritoneal fluid from horses with colic using a portable analyzer and an in-house analyzer. Vet Rec 2005;157(8):217-223.

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    37. Latson KM, Nieto JE, Beldomenico PM, et al. Evaluation of peritoneal fluid lactate as a marker of intestinal ischemia in equine colic. Equine Vet J 2005;37(4):342-346.

    38. Moore JN, Traver DS, Turner MF, et al. Lactic acid concentration in peritoneal fluid of normal and diseased horses. Res Vet Sci 1977;23(1):117-118.

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    References »

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