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Proceedings of the 16th


Italian Association of Equine Veterinarians
Congress

Carrara, Italy
January 29-31, 2010

Next SIVE Meeting:

Feb. 4-6, 2011 – Montesilvano, Pescara, Italy

Reprinted in the IVIS website with the permission of the


Italian Association of Equine Veterinarians – SIVE

http://www.ivis.org
Published in IVIS with the permission of SIVE Close window to return to IVIS

Practical use of the clinical laboratory


and stall side testing in equine practice

Thomas Divers
DVM, DACVIM, DACVECC
Cornell University, Ithaca NY, USA

INTRODUCTION LOW HCT

The potential value of haematology in equine A moderately low HCT (21-26%) is most com-
practice is well documented by numerous case monly a result of a chronic inflammatory dis-
series reports and experimental studies. The ease. In many cases, plasma protein will be ele-
maximal use of haematology is to help with vated indicating increased globulin production
diagnosis and/or prognosis of the ill horse. In from chronic antigenic stimulation and/or ele-
cases where the diagnosis can be arrived at vated acute phase proteins. If the inflammatory
from the history, signalment, and clinical ex- disease involves the bowel (parasites or inflam-
am, and the prognosis can be accurately pre- matory bowel disease), the total protein is often
dicted, haematology may not be the best use abnormally low. Lower hematocrits (<20%)
of the client’s financial resources. The infor- may occur from hemolytic or hemorrhagic dis-
mation on hematology in this handout refers orders. For hemolytic diseases, the HCT%,
almost exclusively to adult horses. Responses along with heart rate, clinical signs, PVO2, blood
in foals may differ and will be mentioned in lactate, and persistence of the hemolytic process
the presentation. 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%.
HEMATOCRIT Low HCT will not be seen with acute hemor-
rhage; in fact, animals may die from acute hy-
Abnormally high values (spurious poly- poxia/hypotension caused by acute hemorrhage
cythemia) are most commonly seen in horses but normal HCT. Severe non-regenerative ane-
with abdominal pain and/or colitis or rhab- mias are rarely seen, but may result from adverse
domyolysis. The high values are caused by in- reaction to erythropoietin injections (red cell
travascular volume depletion and splenic con- aplasia), fell pony syndrome, and rarely from cy-
traction. A retrospective study on equine ab- totoxic drug reactions or neoplasia. MCV would
dominal pain found horses with HCT > 50% be expected to be low in these cases.
are at increased risk of death. Monitoring of When blood is spun in a micro hematocrit tube,
HCT% and plasma protein after abdominal the plasma should always be examined for
surgery is routine and will provide prognostic icterus, hemolysis and lipemia!!! Lipemia is
information. These values should be used common in sick ponies and miniature horses
along with clinical findings such as mucus and can be fatal due to hepatic lipidosis.
membrane color, heart rate, and response to
treatment and peritoneal fluid analysis in pre-
dicting prognosis. PLATELET COUNT
On rare occasion, horses have absolute poly-
cythemia, most commonly associated with Platelet counts can help determine the severi-
neuroendocrine neoplasia or hepatic disease. ty of an illness and as a laboratory clue for
60
Proceedings of the Annual Meeting of the Italian Association of Equine Veterinarians, Carrara, Italy 2010
Published in IVIS with the permission of SIVE Close window to return to IVIS

neoplasia. Horses with severe systemic in- tropenia may be seen in some horses in associ-
flammation/coagulopathy may have thrombo- ation with drug administration, e.g., TMP-S,
cytopenia (usually in the 40-70,000 range), in- NSAID. Acute viral infections may cause se-
creased D-dimers and low anti-thrombin III vere neutropenia with variable lymphocyte
levels; fibrinogen is often normal or high. counts, but left shift and toxic changes are
Horses with marked thrombocytopenia (< usually absent. Lymphocyte, monocyte, and
20,000) usually have drug-induced or neopla- eosinophil counts are of less value to the
sia related (immune) thrombocytopenia. In the equine practitioner and, due to a word limit for
horse, another cause of “reportedly” low this abstract, will not be discussed.
platelet count is pseudothrombocytopenia. An important analyte often reported with the
equine hemogram is plasma fibrinogen. Plas-
ma fibrinogen is an acute phase protein and a
LEUKOGRAMS component of the coagulation pathway. In-
creases in fibrinogen may occur with either lo-
The neutrophil count and morphology are one cal or systemic inflammatory responses with
of the most valuable laboratory tests in equine elevations occurring as quickly as 24-36
medicine. High neutrophil counts (neutrophil- hours. Although this measurement is of clini-
ia) can be used, along with acute phase protein cal value, other measurements, such as abnor-
measurements, e.g., serum amyloid, and mal neutrophil numbers, low serum iron, and
serum iron and globulin concentration to help increased serum amyloid occur more quickly
determine if an inflammatory disease is pres- following inflammation and should be used
ent and, to some extent, the duration of the in- along with plasma fibrinogen in determining
flammatory response. Other common causes presence or absence of inflammation and re-
of a mature neutrophilia include excitement sponse to therapy.
and either physiologic stress or corticosteroid Total plasma protein is an important measure-
administration. If band neutrophils and/or tox- ment in clinical practice. Horses with inflam-
ic changes are present, this is highly sugges- mation, either acute or chronic, often have el-
tive of a bacterial infection. One mechanism evations in plasma protein with the most ele-
for this is the causative relationship between vated amount occurring in horses with chron-
sepsis, increased TNF, and early release of ic infection (abscessation). Abnormally low
neutrophils into circulation. Increased adhe- total protein concentration is most commonly
sion activity associated with sepsis results in associated with enteric loss or hemorrhage.
margination of neutrophils and neutropenia. Protein-losing nephropathy and “third spac-
Although there is no evidence-based publica- ing” of protein, i.e., peritonitis, is rare in the
tion to confirm such, this author believes that horse. Additionally, liver disease in the horse
most horses that develop laminitis due to sys- rarely causes low total protein; albumin may
temic inflammatory illness undergo either a be decreased, but this is often offset by in-
“left shift”, and/or have toxic changes in neu- creased globulins.
trophils 12-36 hours prior to the clinical signs. Serum or plasma routine chemistries are used to
Neutropenia with a left shift and/or toxic detect electrolyte abnormalities, organ system
changes is frequently observed in acute bacte- disease, inflammatory markers, and some meta-
rial infections and/or endotoxemia. In horses bolic diseases. Hyponatremia is common with
with acute colitis and/or severe systemic in- diarrheal and some urinary system diseases. The
flammation, a change from neutropenia to neu- finding of hyponatremia, hypochloremia and
trophilia is commonly observed during the first neutropenia in a colicy horse or foal is sugges-
3-4 days of the illness. Although this is gener- tive of colitis/enteritis, even if there is no diar-
ally thought to be a favorable response (less rhea present. The degree of hyponatremia in
margination of neutrophils and less systemic foals is important to establish as to rapid correc-
inflammatory mediators), I am not aware of tion may result in neurologic signs/disease. Hy-
published data to support this. Persistent neu- ponatremia and hypochloremia are also pres-
61
Proceedings of the Annual Meeting of the Italian Association of Equine Veterinarians, Carrara, Italy 2010
Published in IVIS with the permission of SIVE Close window to return to IVIS

ent with acute or chronic renal failure, rup- gap [(sodium + potassium)- (chloride + bicar-
tured bladder and severe myopathy/myositis. bonate)] is usually elevated (normal, 15
These finding may also be present with severe meq/l) if there is an increase in lactate or sul-
edema, peritonitis and or body cavity effusion. fates and this magnitude often gives us a clue
Another cause of marked hyponatremia and as to the severity of the disease. The anion gap
hypochloremia in foals < 10 days of age is hy- may not be increased in spite of increased in
droureter; an interesting and as yet unpub- unmeasured anions if albumin values are low
lished syndrome. With ruptured bladder (in such as commonly occurs in horses with colitis.
foals) and severe muscle disease, the potassi- Hypoalbuminemia can cause a mixed metabol-
um is often elevated and in foals with ruptured ic acidosis (increased lactic acid/lactate) and
bladder, the hyperkalemia may be a serious mild metabolic alkalosis (increased bicarbon-
management problem. With acute or chronic ate) with a normal calculated anion gap. The
renal failure the potassium is variable, gener- important clinical message is fluids are still
ally either normal or high. Of course, another needed to combat both the lactic acidosis
cause of hyperkalemia in Quarter horses is (poor perfusion most likely) and the hypoal-
HYPP. The “dash board” effect on chemistries buminemia (colloids) in those horses. Ex-
is not as dramatic in horses as some other tremely severe and sometimes persistent
species with glucose (decreasing) being the metabolic acidosis is most common in foals
only consistently dramatic finding when sam- with diarrhea. Many of these cases require bi-
ples are carried in the truck all day before sub- carbonate therapy in order to correct the aci-
mission. Low potassium is most common in dosis suggesting excessive loss of bicarbonate
foal diarrhea, often reaching a life threatening rather than titration with acid or relative ex-
level! Although anorexic horses may maintain cess administration of chloride. When admin-
normal serum potassium, their total body istering bicarbonate to foals serum potassium
potassium is always low. Only 1.5% of body must be monitored very carefully!! A common
potassium is in plasma. cause of hyperchloremic metabolic acidosis
Bicarbonate measurement is very useful in de- with a normal anion gap is large volume of
termining the metabolic acid/base status of the NACL treatment. Hypochloremic metabolic
horse or foal and the need for either enhanced alkalosis with elevated anion gap is common
fluid therapy (perfusion) or less commonly bi- with excessive sweating, e.g., myopathy, ex-
carbonate administration. A low bicarbonate is haustion, diarrhea and renal failure; severe
a metabolic acidosis (if the pH is also low then cases may develop metabolic acidosis. Bicar-
there is a metabolic acidosis with acidemia). bonate should rarely if ever be administered to
The most common cause of a metabolic aci- these horses.
dosis is titration of HCO3 by lactic acid or oth- Blood glucose, if measured within 1 hour or
er strong anions that are not routinely meas- on separated plasma samples should be rou-
ured. Lactic acid can be indirectly measured tine in sick foals as hypoglycemia is common.
by measuring lactate. The point of care meas- Although sick horses rarely have hypo-
urement of lactate is of great value in the im- glycemia, they may have a nutritional need for
mediate evaluation of critical care horses and glucose supplementation, especially pregnant
foals. The magnitude of the elevation in lac- mares. High blood glucose is common in “col-
tate is not as important prognostically as the icy” horses and horses with hyperammone-
lactate measurement following aggressive mia. High blood glucose is also present in
treatment, ie. if it does not go down the prog- many horses with Cushing syndrome, but is
nosis is guarded or worse. A lactate above 6.0 rare with equine metabolic syndrome. Horses
meq/l has been associated with prognosis in with hyperlipidemia syndrome and triglyc-
horses with large colon volvulus. Other strong erides > 1500 mg/dl may have a poor progno-
anions accumulations such as sulfates are sis although this is quite variable. In some cas-
most commonly elevated by renal dysfunction es the triglycerides decease remarkably fast
and can cause a metabolic acidosis. The anion and the hose/pony quickly recovers!
62
Proceedings of the Annual Meeting of the Italian Association of Equine Veterinarians, Carrara, Italy 2010
Published in IVIS with the permission of SIVE Close window to return to IVIS

Muscle disease is best detected by elevations bilirubin concentration, indirect bilirubin (not
in CK and/or AST (if it has been 2-7 days specific for liver as hemolysis and fasting also
since the possible muscle “episode”. Horses cause elevations), prothrombin and partial
with CIR should be jogged for 10-15 minutes prothrombin times, ammonia and total bile
and a CK sample taken 3 hours later to help acids. Bile acids are increased prior to the oth-
confirm myopathy. QHs with PSSM generally er test in the progression of most equine he-
have very high CK and AST when clinically- patic diseases. Bile acids are increased some
affected, while draft/warmbloods may have due to anorexia and foals < 6 weeks of age of-
only modest elevations in some cases. ten have higher concentrations than the nor-
Renal function tests include BUN and creati- mal adult range.
nine. Differentiating prerenal azotemia from Point of care instruments can provide rapid re-
primary renal dysfunction is best done by sults for most electrolytes including ionized
combining history, clinical exam, CBC and calcium, blood gases, glucose, lactate and car-
other chemistries, urinalysis and speed of re- diac troponin I and are now used more in our
turn to normal values following fluid therapy. hospital than is the bench testing in the clini-
Thoroughbreds generally have lower crea- cal pathology laboratory.
tinines than QHs or WBs, and this should be
considered when evaluating renal function,
particularly if the horse is being treated with REFERENCES
nephrotoxic drugs; in other words a TB whose
creatinine is 1.8 mg/dl (still within published Orsini, J.A., Elser, A.H., Galligan, D.T., Donawick, W.J.,
normal range for the horse) while on amino- and Kronfeld, D.S. Prognostic index for acute ab-
dominal crisis (colic) in horses. Am J Vet Res
glycosides could be highly significant.
1988;49(11):1969-1971.
Liver disease is detected by measuring liver Proudman, C.J., Edwards, G.B., Barnes, J., and French,
enzymes in the serum. These enzymes may be N.P. Factors affecting long-term survival of horses
from hepatocellular origin or biliary in origin recovering from surgery of the small intestine.
and are helpful in determining the etiopathol- Equine Vet J 2005;37(4):360-365.
Divers, T.J. Blood transfusion therapy in horses. In: Pro-
ogy of the liver disease. Consideration of half
ceeding 7th Internation Vet Emer Crit Care Sympo-
life and liver specificity of the enzymes should sium 2000; pgs. 658-661.
also be duly noted in the evaluation. GGT is Hinchcliff, K.W., Kociba, G.J., and Mitten, L.A. Diagno-
the most sensitive enzyme for detecting seri- sis of EDTA-dependent pseudothrombocytopenia
ous liver disease in horses but it test disease in a horse. J Am Vet Med Assoc 1993;203(12):
1715-1716.
and not function. Its decline often lags behind
Johnston K, Holcombe SJ, Hauptman JG,. Plasma lactate
the other enzymes during recovery from he- as a predictor of colonic viability and survival after
patic injury and greatest elevations occur with 360 degrees volvulus of the ascending colon in
biliary diseases. Function test include direct horses. Vet Surg. 2007 Aug;36(6):563-7.

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Proceedings of the Annual Meeting of the Italian Association of Equine Veterinarians, Carrara, Italy 2010

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