Weight Loss
Investigating weight loss
Clinical examination will often give important clues to the cause of
weight loss (e.g. quidding, diarrhoea, dyspnoea etc..) and examination
will be directed accordingly. However, some cases shown no concerns
other than weight loss and may be more challenging. Assuming the
horse is eating an adequate ration, table 1 lists important conditions
to consider in such vague cases.
Several laboratory tests are useful to provide an initial insight into
differential diagnosis and should all be considered as a first
clinicopathological step in all unexplained “examination negative”
weight loss cases.
- HAEMATOLOGY
Anaemia is commonly seen in weight loss cases. If it is marked or
chronic a bone marrow aspirate and biopsy should be considered to
investigate the type and therefore potential cause of the anaemia (see
later section on bone marrow). Mild non-regenerative anaemia is a
very common, non-specific finding in chronic weight loss cases and is
often unhelpful in the determining the diagnosis. A regenerative
anaemia is more helpful diagnostically and is suggestive of a chronic
source of blood loss or immune-mediated haemolysis (see separate
section on Anaemia).
First check adequate nutrition and ingestion of ration
Protein losing enteropathies are common (with or without
diarrhoea)
o Important to rule out parasites and NSAID toxicity
Other main causes include hepatopathy, chronic
inflammatory/neoplastic disease, PPID, renal failure and
diabetes mellitus
Neutrophilia can be a feature of septic and non-septic conditions such
as infectious diseases (viral, bacterial or parasitic), IBD, neoplasia,
immune-mediated diseases and PPID. A band neutrophilia (left shift)
is often more suggestive of septic than non-septic conditions.
Neutropaenia is common in acute sepsis (especially when loss into
effusions occurs – e.g. peritonitis) but uncommon in chronic
inflammatory diseases.
Eosinophilia is a general indicator of inflammation in addition to being
an indicator of allergic or infiltrative eosinophilic diseases. Parasitism
and multisystemic eosinophilic epitheliotropic disease (MEED) are
potential causes of weight loss which may be associated with
peripheral eosinophilia.
DIFFERENTIAL DIAGNOSES FOR WEIGHT LOSS IN THE ABSENCE OF APPARENT CAUSE
ABNORMAL NUTRIENT HANDLING – DIGESTION/METABOLISM/LOSSES:
Protein losing enteropathy
o Parasitism
o NSAID toxicity
o Inflammatory bowel disease (IBD)
o Neoplasia (lymphoma)
o Lawsonia intracellularis infection
o Sand enteropathy
Hepatic disease
PPID
Chronic renal failure
Diabetes mellitus
Renal tubular acidosis
INCREASED DEMAND FOR NUTRIENTS:
Increased physical activity, pregnancy, lactation
Neoplasia
Infection/Sepsis
Chronic pain
NEUROMUSCULAR WASTING DISORDERS
Equine motor neuron disease
Immune-mediated myositis
Polysaccharide storage myopathy
- INITIAL SCREENING BIOCHEMISTRY
Serum Proteins (albumin and globulin)
Serum amyloid A, serum iron
AST, GGT, AP, GLDH, CK, bilirubin, creatinine, urea
Serum Proteins have a circadian rhythm and may vary by as much as
10-15 g/L over the day (high evening, low noon) associated with
hydration status.
Serum albumin is the first thing to check in weight loss cases given
how common protein losing enteropathy is. Marked
hypoalbuminaemia (<20g/L) strongly indicates protein losing
enteropathy although occasionally marked protein losses associated
with renal failure will be seen. Mild to moderate hypoalbuminaemia
(20-29g/L) may result from hepatopathy, malnutrition, chronic blood
loss, chronic inflammation or protein-losing nephropathy.
Increased globulin concentration is common in weight loss cases and
may indicate a general state of chronic inflammation associated with
parasitism, infections, neoplasia or immune mediated disease.
Remember that hepatic insufficiency commonly causes high globulin
concentration so always check liver enzymes. High, normal or low
globulins may occur in protein losing enteropathy cases.
Acute Phase Proteins comprise serum amyloid A (SAA), and serum
iron. They are sensitive indicators of inflammation or infection.
Highest levels may suggest bacterial infectious processes with milder
increases associated with viral disease and non-septic tissue
inflammation (e.g. neoplasia) although this is not always the case.
AST arises from many tissue sources but elevated plasma levels are
usually of hepatic and/or muscular origin (cross-check with CK, GGT,
and GLDH). It has a long half-life and can remain elevated for 1-2
weeks after resolution of the inciting cause.
GGT is the most sensitive liver enzyme and it is unusual to have
significant liver disease in the absence of increased GGT. However,
increased GGT concentrations are sometimes misleading and
associated with mild liver disease or even non-hepatic disease (e.g.
gastrointestinal disease). The pancreas contains high concentrations
of GGT but pancreatic disease is rare in horses. Damaged renal tubules
may also release GGT but this appears in urine rather than blood.
Anecdotally, enteropathies and colics may often have raised GGT in
the absence of liver disease – perhaps due to the close anatomic and
vascular association between the gut and the liver. Colon
displacements, particularly right dorsal displacements frequently have
high circulating GGT concentrations. GGT may remain elevated for a
long time after hepatic insult is resolving (possibly due to biliary
hyperplasia).
AP arises from many sources but high levels in adult horses are usually
from hepatopathy or enteropathy. AP is also released from monocytes
and may non-specifically reflect inflammation. Young, growing horses
normally have high levels derived from bone sources. The placenta
may also be a source in pregnant mares
GLDH generally indicates hepatic insult although very high levels are
sometimes seen following relatively minor hepatic disease. I t is very
sensitive and primary intestinal insults sometimes cause increases in
GLDH also (possibly from increased endotoxin reaching the liver?)
Bilirubin is usually increased in hepatic failure and also in other
conditions such as haemolysis and anorexia. Very high levels (>300
μmol) often indicate biliary obstruction or haemolysis whereas
increases of lesser magnitude could indicate hepatocellular disease
(30-150) or anorexia (typically up to 100-150). In these equivocal cases
direct bilirubin is more useful for indicating hepatopathy. Direct
bilirubin should be no more than 10-20% (usually <5%) of total
bilirubin, however if hepatobiliary disease and cholestasis are present
then direct bilirubin may account for a greater percentage of total
bilirubin. Occasionally horses are encountered with mysterious
persistently high bilirubin levels and these may well have genetic
bilirubin processing problems.
CK is useful to check for the site of tissue damage if AST is increased
(i.e. determining muscle vs liver). Modest increases in CK are also seen
in cases of polysaccharide storage myopathy or equine motor neuron
disease, the latter may present as little more than w eight loss. Muscle
catabolism itself can also lead to mild increases in CK (e.g. 500-
800iu/L) as can increased recumbency or IM injections.
Creatinine and urea will be increased If renal disease is severe enough
to be causing weight loss. Creatinine is the preferred marker for renal
failure and will typically be > 250μmol/L in such cases. Mild increases
in creatinine and urea may be due to dehydration (worth checking
urine specific gravity). Urea may be low in hepatic failure.
- FAECAL ANALYSIS
Parasite eggs/Larvae are often hard to find even in weight loss cases
caused by parasitism as owners will almost invariably have dewormed
a thin horse. Larval cyathostominosis is a common cause of acute (and
sometimes chronic) weight loss usually, but not necessarily always,
with diarrhoea. Overreliance on fenbendazole could lead to a
significant parasite problem in horses which are reportedly ‘well
wormed’ as it often has a poor effect on adult or larval cyathostomes
even when repeated for 5 days. Very short egg reappearance periods
(< 1 month) are now sometimes seen following moxidectin also.
Sand ingestion may cause chronic weight loss from an abrasive
enteropathy due to voluntary or involuntary sand consumption. Sand
can easily be detected by sedimentation in a suspended faecal sample,
but the quantity that is regarded as normal in a horse grazing sandy
pasture is debatable. Colonic sand accumulation may be best
identified and quantified radiographically.
Faecal Occult blood generally indicates colonic bleeding rather than
gastric or small intestinal – bleeding e.g. colitis, NSAID toxicity,
neoplasia or merely prior rectal examination. High numbers of
leucocytes in stained smears may be significant. There is a hand-held
test available for faecal occult blood that it is claimed can identify the
presence of gastric and colonic ulcers, although its diagnostic value is
debatable.
Faecal bacterial culture is rarely helpful in chronic weight loss cases.
Clostridial toxin immunoassay (C.difficile Tox A/B, C.perfringens
betatoxin) is useful to look for toxins typically in colitis cases. However,
In the absence of diarrhoea, faecal samples positive for clostridial
toxins have been associated with necrotic intestinal lesions including
neoplasia.
Lawsonia intracellularis PCR is worth checking especially in post-
weaning foals of 3 to 13 months of age, although the disease has been
seen rarely in older horses. PCR can be used to identify Lawsonia DNA
in faeces but might occasionally be found in the absence of disease.
Excretion of Lawsonia may also be short-lived after initiation of
antimicrobial therapy and PCR may not be reliable once treatment has
commenced.
- FURTHER SIMPLE BLOOD TESTS DEPENDING ON INITIAL FINDINGS
Bile acids are a useful test of hepatic function. After excretion in bile,
BAs are reabsorbed into the circulation via the ileum and should then
be removed from the portal circulation by the liver for recycling. High
BAs are suggestive of liver failure but can sometimes be increased to
around 20μmol/L with anorexia of gastrointestinal problems without
liver disease. Normal levels are slightly higher in foals.
Glucose is often not run in equine samples meaning that Diabetes
mellitus (defined as a persistent hyperglycaemia) is easily missed in
horses. Weight loss and polydipsia/polyuria may be the only signs and
the latter are easily missed especially in turned out horses. Most, but
not all cases are a result of PPID (see later).
Plasma ACTH concentration is worth checking especially in older
horses. PPID is an uncommon cause of marked weight loss in isolation
but may be a contributing factor. (See section on the diagnosis of
PPID).
Vitamin E concentration is a useful check in possible equine motor
neurone disease cases where vitamin E will be almost invariably found
to be low.
Acid-base balance and electrolytes are worth checking in vague
weight loss cases with no specific findings.
Hypercalcaemia may arise in some cases of neoplasia or chronic renal
failure. Hypophosphataemia may occur in the latter cases too. An
increased serum chloride along with metabolic acidosis is suggestive
of renal tubular acidosis which may present as weight loss and
lethargy without marked azotaemia.
Lawsonia intracellularis serology may be a useful indicator of possible
disease but merely indicates exposure rather than active infection.
Seroconversion can occur within days of clinical signs developing and
may persist for up to 6 months.
Serum protein electrophoresis is an exceedingly overinterpreted test
that rarely, if ever, provides reliable evidence of cause of disease. Its
only established value is in the detection of monoclonal globulin
spikes caused by plasma cell myelomas which are obviously very rare.
Its use in other conditions such as infection, parasitism neoplasia, liver
disease lacks any evidence basis in horses.
- OTHER WORTHWHILE TESTS/TECHNIQUES
ORAL GLUCOSE ABSORPTION TEST (OGAT)
The OGAT is a valuable test for the detection of small intestinal
malabsorption syndromes and is generally performed if a protein
losing enteropathy is suspected. This test has no relevance to large
intestinal disease (see section on Intestinal Disease).
PERITONEAL FLUID ANALYSIS
Peritoneal fluid analysis may be useful in the investigation of intra-
abdominal disease, particularly septic peritonitis or neoplasia.
ULTRASONOGRAPHIC EXAMINATION
Ultrasonography may provide evidence of peritoneal effusion,
intestinal thickening (small and/or large bowel), pathology of other
abdominal organs or the presence of neoplasms or abscesses. Small
intestinal wall thickening (normal measurement 2-3mm) would be
typical of problems such as Lawsonia infection, IBD and lymphoma.
Large intestinal thickening is more typical of parasitism.
GASTROSCOPIC EXAMINATION
Gastroscopy may provide evidence of gastric ulcers or (rarely) gastric
neoplasia. It also provides a means of examining and biopsying the
duodenum. Gastric ulcers are an unlikely cause of marked weight loss.
URINALYSIS
Urinalysis is worthwhile in cases of polydipsia/polyuria, or in horses
with an abnormal pattern of urination
(dysuria/stranguria/pollakiuria), unexplained hypoproteinaemia or
cases with significant increases in serum urea and/or creatinine (see
separate section on urinalysis).
TISSUE BIOPSIES
Rectal or intestinal biopsies are generally required to provide a
definitive diagnosis if disease has been localised to the intestinal tract
(see intestinal biopsy section).