Maximizing use of haematology and serum chemistries in equine practice (Proceedings)
The potential value of haematology in equine practice is well documented by numerous case series reports and experimental studies. The maximal use of haematology is to help with diagnosis and/or prognosis of the ill horse. In cases where the diagnosis can be arrived at from the history, signalment, and clinical exam, and the prognosis can be accurately predicted, haematology may not be the best use of the client's financial resources. The information on hematology in this handout refers almost exclusively to adult horses. Responses in foals may differ and will be mentioned in the presentation.
Abnormally high values (spurious polycythemia) are most commonly seen in horses with abdominal pain and/or colitis or rhabdomyolysis. The high values are caused by intravascular volume depletion and splenic contraction. A retrospective study on equine abdominal pain found horses with HCT > 50% are at increased risk of death (Orsini 1988). Monitoring of HCT% and plasma protein after abdominal surgery is routine and will provide prognostic information (Proudman et al, 2005). These values should be used along with clinical findings such as mucus membrane color, heart rate, and response to treatment and peritoneal fluid analysis in predicting prognosis.
On rare occasion, horses have absolute polycythemia, most commonly associated with neuroendocrine neoplasia or hepatic disease.
A moderately low HCT (21-26%) is most commonly a result of a chronic inflammatory disease. In many cases, plasma protein will be elevated indicating increased globulin production from chronic antigenic stimulation and/or elevated acute phase proteins. If the inflammatory disease involves the bowel (parasites or inflammatory bowel disease), the total protein is often abnormally low.
Lower hematocrits (<20%) may occur from hemolytic or hemorrhagic disorders. For hemolytic diseases, the HCT%, along with heart rate, clinical signs, PVO2, blood lactate, and persistence of the hemolytic process can be used to determine need of transfusion. There is no single HCT number that serves as a "transfusion trigger" with a range from 10-20%. Low HCT will not be seen with acute hemorrhage; in fact, animals may die from acute hypoxia/hypotension caused by acute hemorrhage but normal HCT (Divers 2000).
Severe non-regenerative anemias are rarely seen, but may result from adverse reaction to erythropoietin injections (red cell aplasia), fell pony syndrome, and rarely from cytotoxic drug reactions or neoplasia. MCV would be expected to be low in these cases.
When blood is spun in a micro hematocrit tube, the plasma should always be examined for icterus, hemolysis and lipemia.
Platelet counts can help determine the severity of an illness and as a laboratory clue for neoplasia. Horses with severe systemic inflammation/coagulopathy may have thrombocytopenia (usually in the 40-70,000 range), increased D-dimers and low anti-thrombin III levels; fibrinogen is often normal or high. Horses with marked thrombocytopenia (< 20,000) usually have drug-induced or neoplasia related (immune) thrombocytopenia. In the horse, another cause of "reportedly" low platelet count is pseudothrombocytopenia (Hinchcliff 1993).
The neutrophil count and morphology are one of the most valuable laboratory tests in equine medicine. High neutrophil counts (neutrophilia) can be used, along with acute phase protein measurements, e.g., serum amyloid, and serum iron and globulin concentration to help determine if an inflammatory disease is present and, to some extent, the duration of the inflammatory response. Other common causes of a mature neutrophilia include excitement and either physiologic stress or corticosteroid administration. If band neutrophils and/or toxic changes are present, this is highly suggestive of a bacterial infection. One mechanism for this is the causative relationship between sepsis, increased TNF, and early release of neutrophils into circulation. In creased adhesion activity associated with sepsis results in margination of neutrophils and neutropenia. Although there is no evidence-based publication to confirm such, this author believes that most horses that develop laminitis due to systemic inflammatory illness undergo either a "left shift", and/or have toxic changes in neutrophils 12-36 hours prior to the clinical signs.
Neutropenia with a left shift and/or toxic changes is frequently observed in acute bacterial infections and/or endotoxemia. In horses with acute colitis and/or severe systemic inflammation, a change from neutropenia to neutrophilia is commonly observed during the first 3-4 days of the illness. Although this is generally thought to be a favorable response (less margination of neutrophils and less systemic inflammatory mediators), I am not aware of published data to support this. Persistent neutropenia may be seen in some horses in association with drug administration, e.g., TMP-S, NSAID. Acute viral infections may cause severe neutropenia with variable lymphocyte counts, but left shift and toxic changes are usually absent. Lymphocyte, monocyte, and eosinophil counts are of less value to the equine practitioner and, due to a word limit for this abstract, will not be discussed.
An important analyte often reported with the equine hemogram is plasma fibrinogen. Plasma fibrinogen is an acute phase protein and a component of the coagulation pathway. Increases in fibrinogen may occur with either local or systemic inflammatory responses with elevations occurring as quickly as 24-36 hours. Although this measurement is of clinical value, other measurements, such as abnormal neutrophil numbers, low serum iron, and increased serum amyloid occur more quickly following inflammation and should be used along with plasma fibrinogen in determining presence or absence of inflammation and response to therapy.
Total plasma protein is an important measurement in clinical practice. Horses with inflammation, either acute or chronic, often have elevations in plasma protein with the most elevated amount occurring in horses with chronic infection (abscessation). Abnormally low total protein concentration is most commonly associated with enteric loss or hemorrhage. Protein-losing nephropathy and "third spacing" of protein, i.e., peritonitis, is rare in the horse. Additionally, liver disease in the horse rarely causes low total protein; albumin may be decreased, but this is often offset by increased globulins.
Serum or plasma routine chemistries are used to detect electrolyte abnormalities, organ system disease, inflammatory markers, and some metabolic diseases. Hyponatremia is common with diarrheal and some urinary system diseases. The finding of hyponatremia, hypochloremia and neutropenia in a colicy horse or foal is suggestive of colitis/enteritis, even if there is no diarrhea present. The degree of hyponatremia in foals is important to establish as to rapid correction may result in neurologic signs/disease. Hyponatremia and hypochloremia are also present with acute or chronic renal failure, ruptured bladder and severe myopathy/myositis. These finding may also be present with severe edema, peritonitis and or body cavity effusion. Another cause of marked hyponatremia and hypochloremia in foals < 10 days of age is hydroureter; an interesting and as yet unpublished syndrome. With ruptured bladder (in foals) and severe muscle disease, the potassium is often elevated and in foals with ruptured bladder, the hyperkalemia may be a serious management problem. With acute or chronic renal failure the potassium is variable, generally either normal or high. Of course, another cause of hyperkalemia in Quarter horses is HYPP. The "dash board" effect on chemistries is not as dramatic in horses as some other species with glucose (decreasing) being the only consistently dramatic finding when samples are carried in the truck all day before submission. Low potassium is most common in foal diarrhea, often reaching a life threatening level! Although anorexic horses may maintain normal serum potassium, their total body potassium is always low. Only 1.5% of body potassium is in plasma.
Bicarbonate measurement is very useful in determining the metabolic acid/base status of the horse or foal and the need for either enhanced fluid therapy (perfusion) or less commonly bicarbonate administration. A low bicarbonate is a metabolic acidosis (if the ph is also low then there is a metabolic acidosis with academia). The most common cause of a metabolic acidosis is titration of HCO3 by lactic acid or other strong anions that are not routinely measured. Lactic acid can be indirectly measured by measuring lactate. Other strong anions accumulations such as sulfates are most commonly elevated by renal dysfunction and can cause a metabolic acidosis. The anion gap [(sodium + potassium)- (chloride + bicarbonate)] is usually elevated (normal, 15 meq/l) if there is an increase in lactate or sulfates and this magnitude often gives us a clue as to the severity of the disease. The anion gap may not be increased in spite of increased in unmeasured anions if albumin values are low such as commonly occurs in horses with colitis. Hypoalbuminemia can cause a mixed metabolic acidosis (increased lactic acid/lactate) and mild metabolic alkalosis (increased bicarbonate) with a normal calculated anion gap. The important clinical message is fluids are still needed to combat both the lactic acidosis (poor perfusion most likely) and the hypoalbuminemia (colloids) in those horses. Extremely severe and sometimes persistent metabolic acidosis is most common in foals with diarrhea. Many of these cases require bicarbonate therapy in order to correct the acidosis suggesting excessive loss of bicarbonate rather than titration with acid or relative excess administration of chloride. When administering bicarbonate to foals serum potassium must be monitored very carefully!! A common cause of hyperchloremic metabolic acidosis with a normal anion gap is large volume of NACL treatment. Hypochloremic metabolic alkalosis with elevated anion gap is common with excessive sweating, e.g., myopathy, exhaustion, diarrhea and renal failure; severe cases may develop metabolic acidosis. Bicarbonate should rarely if ever be administered to these horses.
Blood glucose, if measured within 1 hour or on separated plasma samples should be routine in sick foals as hypoglycemia is common. Although sick horses rarely have hypoglycemia, they may have a nutritional need for glucose supplementation, especially pregnant mares. High blood glucose is common in "colicy" horses and horses with hyperammonemia. High blood glucose is also present in many horses with Cushing syndrome, but is rare with equine metabolic syndrome. Horses with metabolic syndrome often have triglycerides > 57mg/dl and equines with hyperlipidemia syndrome and triglycerides > 1500mg/dl have a poor prognosis.
Muscle disease is best detected by elevations in CK and/or AST (if it has been 2-7 days since the possible muscle "episode"). Horses with CIR should be jogged for 10-15 minutes and a CK sample taken 3 hours later to help confirm myopathy. QHs with PSSM generally have very high CK and AST when clinically-affected, while draft/warmbloods may have only modest elevations in some cases.
Renal function tests include BUN and creatinine. Differentiating prerenal azotemia from primary renal dysfunction is best done by combining history, clinical exam, CBC and other chemistries, urinalysis and speed of return to normal values following fluid therapy. Thoroughbreds generally have lower creatinines than QHs or WBs, and this should be considered when evaluating renal function, particularly if the horse is being treated with nephrotoxic drugs; in other words a TB whose creatinine is 1.8mg/dl (still within published normal range for the horse) while on aminoglycosides could be highly significant.
Point of care instruments can provide rapid results for most electrolytes including ionized calcium, blood gases, glucose and cardiac troponin I and are now used more in our hospital than is the bench testing in the clinical pathology laboratory.
1. Orsini, J.A., Elser, A.H., Galligan, D.T., Donawick, W.J., and Kronfeld, D.S. Prognostic index for acute abdominal crisis (colic) in horses. Am J Vet Res 1988;49(11):1969-1971.
2. Proudman, C.J., Edwards, G.B., Barnes, J., and French, N.P. Factors affecting long-term survival of horses recovering from surgery of the small intestine. Equine Vet J 2005;37(4):360-365.
3. Divers, T.J. Blood transfusion therapy in horses. In: Proceeding 7th Internation Vet Emer Crit Care Symposium 2000; pgs. 658-661.
4. Hinchcliff, K.W., Kociba, G.J., and Mitten, L.A. Diagnosis of EDTA-dependent pseudothrombocytopenia in a horse. J Am Vet Med Assoc 1993;203(12):1715-1716.