Page 904 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Liver disease 879

VetBooks.ir as well as reduced platelet numbers and function. risk, associated with further investigation of subclin-
ical liver disease as discussed further below.
An increase in procoagulant proteins synthesised
at non-hepatic sites is also often seen including fac-
tor VIII, von Willebrand factor and monocyte tis- Diagnostic tests
sue factor. Despite the complexities of effects on Clinicopathological assessment of the liver
individual proteins, the net effect of hepatic failure Following a general clinical examination of a horse
on haemostasis is invariably impairment of coagu- with suspected liver disease, analysis of blood
lation as determined by increased activated partial samples is the most likely subsequent investigative
thromboplastin time (APTT) and prothrombin approach. There are many measurable substances
time (PT). Vitamin K-dependent factors (prothrom- in the blood that may reflect liver disease and they
bin, factors VII, IX and X and proteins C and S) are are broadly divisible into intracellular enzymes that
generally affected first, although many further fac- are released into the circulation following damage
tors and platelets will eventually become affected by to liver cells, and other biochemical substances that
hepatic insufficiency. Although laboratory measures reflect the effectiveness of various hepatic functions
of coagulation are commonly abnormal in cases of (Table 5.1). Further functional assessment protocols
hepatic failure, clinical evidence of bleeding such are possible, including monitoring excretion of exog-
as petechiation (Fig. 5.5), ecchymoses, epistaxis or enously administered agents and also radionuclide
prolonged bleeding after venepuncture are far less imaging, although these are not widely practiced.
commonly seen. The usefulness of biochemical markers of liver
There is a real danger that when horses are iden- disease can be considered diagnostically in terms of
tified with liver disease (usually via blood tests) in sensitivity and specificity for liver disease, and also
the absence of moderate to severe clinical signs, the prognostically in terms of association with survival
case is taken less seriously, and further investigation or non-survival. Intuitively, increased concentrations
often delayed in favour of simple monitoring of the of liver-derived enzymes will relate to the severity
clinical and serum biochemical picture. This danger and extent of damaged liver cells, but not directly to
is specifically that a proportion of these subclini- those functional and undamaged liver cells remain-
cal or mild clinical cases will continue to progress ing. In contrast, functional indicators will directly
towards more severe hepatic insufficiency, which
may then become more refractory to treatment and
associated with a poorer prognosis. One study indi-
cated survival of 94% when horses were identified Table 5.1 Biochemical substances measurable in
with liver disease at a subclinical or mildly clinical serum and plasma that may reflect
stage, in contrast to only 49% surviving when clini- hepatic injury and function
cal signs of hepatic insufficiency were present. This
represented a greater than 10-fold reduction in sur- BIOCHEMICAL MARKERS
vival times when comparing horses with liver dis- LIVER-DERIVED ENZYMES OF HEPATIC FUNCTION
ease that were treated at a clinical versus subclinical Alkaline phosphatase (ALP) Acute phase proteins (serum
amyloid A, fibrinogen)
stage. Therefore, delaying the investigation of liver Aspartate aminotransferase Albumin
(AST)
disease based on an absence of concerning clinical Gamma-glutamyltransferase Amino acids
signs seems inadvisable. Clearly the corollary of this (GGT) Ammonia
is that further investigation might be performed Glutamate dehydrogenase Bile acids
(GLDH)
on some horses with mild and subclinical disease Iditol dehydrogenase (IDH) Bilirubin (total, unconjugated,
conjugated)
that would otherwise have recovered uneventfully, Lactate dehydrogenase Clotting tests (APTT, PT)
without the need for further possibly invasive tests. (LDH) Creatinine
This dilemma can only be resolved by informed Sorbitol dehydrogenase Globulins
discussion with the horse’s owner and should be (SDH) Glucose
Urea
considered alongside the expense, but extremely low