Page 1038 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

H aemolymphatic system 1013

VetBooks.ir deficiency is inherited in an autosomal recessive 9.14
manner and haemophilia A is sex-linked (males only)
and recessive. Individual clotting factor deficiencies,
if sufficient to cause clinical signs, result in bleed-
ing into muscle, joints or body cavities. However,
affected animals frequently do not haemorrhage
spontaneously and the abnormality may only be
noted after trauma, surgery or venipuncture.

Clinical presentation
Horses with prekallikrein deficiency may exhibit
prolonged bleeding after castration, but frequently
they are able to clot normally. Haemophilia A
patients do not usually exhibit spontaneous bleeding
unless factor VIII activity is <5%.

Differential diagnosis Fig. 9.14 Flowers of sweet clover. (Photo courtesy
Other diseases that may need to be considered Kristian Peters ©)
include DIC, anticoagulant poisoning, mouldy sweet
clover intoxication and liver disease.
also rarely result in a similar condition that occurs
Diagnosis by the same mechanism (Fig. 9.14).
Since many of these factors are part of the contact
activation (or intrinsic) pathway, the APTT may be Aetiology/pathophysiology
prolonged. A definitive diagnosis of which protein is Coumarin, other coumarin-derivative products
affected is then made by demonstrating deficiency or found in mouldy sweet clover and anticoagulant
absence of specific factor activity. rodenticides interfere with activation of the vitamin
K-dependent coagulation proteins. Sweet clover may
Management be found in hay and pasture over a wide geographic
The only potential treatment for these deficiencies, if range. Grazing of sweet clover has not been associ-
anaemia from the blood loss is severe, is replacement ated with coagulopathy.
with blood products. This is not usually practical. Mouldy sweet clover and anticoagulant rodenti-
cides cause haemorrhage because they antagonise
Prognosis the effects of vitamin K. Vitamin K is required
Successful treatment is not possible, but clinical for activation of procoagulant factors II, VII, IX
signs are usually absent or minor. In some cases of and X and anticoagulant protein factors C and S.
haemophilia A, where there is complete absence Without proper activation, inactive factors accumu-
of factor activity, the animal may repeatedly bleed late that cannot participate in forming a fibrin clot.
spontaneously, warranting a poorer prognosis. Subsequently, affected animals cannot form clots
well and therefore bleed. Rarely, if the diet is defi-
ANTICOAGULANT TOXICITY cient in vitamin K, the effect may be exacerbated.
Additionally, the presence of protein-bound drugs
Definition/overview (e.g. phenylbutazone) or hypoalbuminaemia can
Horses being treated with warfarin are at risk of increase the proportion of free (active) toxin.
haemorrhage, especially if the diet contains less vita-
min K or there is concurrent administration of highly Clinical presentation
protein-bound drugs. Ingestion of mouldy sweet clo- Clinical signs are typically observed within 3–8 weeks
ver (Melitotus spp.) or anticoagulant rodenticide may of ingestion of mouldy sweet clover and 3–5 days of