Page 1039 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1014 CHAPTER 9

VetBooks.ir 9.15 also be present. Hypoxic damage to the liver may result
in elevations in hepatocellular enzyme activity.

Management
Therapeutic measures include removing the animal
from the source of toxin, volume replacement and
vitamin K administration. Restoration of circulating
volume may be accomplished with i/v fluids or blood
products if the anaemia and hypoproteinaemia are
severe. Administration of fresh plasma also provides
active clotting factors and may be useful if ongoing
haemorrhage is present or suspected. Vitamin K1
(1.0–1.5 mg/kg s/c or i/m q4–12 h for 3 days until PT
has returned to reference interval) should be admin-
istered. The PT and APTT can be used to monitor
for successful therapy. Improvement in PT is often
observed within 24 hours of treatment. As there is a
Fig. 9.15 Horse with mild nasal haemorrhage.
(Photo courtesy J Scott Weese) risk of significant haemorrhage, nothing should be
administered via a nasogastric tube. Severely anaemic
animals may benefit from intranasal oxygen therapy.
ingestion of anticoagulant rodenticides. Affected ani- Alfalfa is rich in vitamin K and may be fed if there
1
mals are usually presented with multiple-site bleeding, are no concurrent reasons to avoid this type of feed.
often from the nose (Fig. 9.15), gastrointestinal (GI) Vitamin K should not be administered because of its
3
tract and urinary tract. Bleeding into body cavities lower efficacy and risk for nephrotoxicity. If mouldy
and joint spaces may occur. Subcutaneous haematomas sweet clover toxicosis is suspected, all hay should be
may occur with relatively mild trauma. Clinical signs examined prior to feeding or be discarded.
of hypovolaemia and shock may ensue if haemorrhage
is severe. Prognosis
Horses often recover fully if the problem is recog-
Differential diagnosis nised early, proper therapy is instituted and haemor-
Other causes of multiple-site haemorrhage, includ- rhage is not life-threatening.
ing DIC and, rarely, severe trauma or an inherited
haemostatic defect, should be considered. NEONATAL ISOERYTHROLYSIS

Diagnosis See Chapter 14, p. 1335.
The combination of clinical signs and history of expo-
sure to the toxin is often highly suggestive. The diet IMMUNE-MEDIATED
should be evaluated for the presence of mouldy sweet HAEMOLYTIC ANAEMIA
clover, and owners should be queried about the use of
rodenticides in the vicinity. Lack of a history of roden- Definition/overview
ticide use does not exclude rodenticide toxicosis as a IMHA is caused by destruction of erythrocytes by
cause, because malicious poisoning may have occurred. the immune system. This can be a truly autoimmune
PT and APTT are frequently prolonged. Factor VII phenomenon (primary IMHA) when the process is
has the shortest half-life, so the PT may initially be directed against a self-antigen, or it can be induced
the only abnormal test. Response to vitamin K ther- secondarily to infectious, inflammatory, neoplastic
apy may also support the diagnosis. If haemorrhage is or drug-related stimuli (secondary IMHA). The lat-
severe enough, anaemia and hypoproteinaemia may ter is more common in horses.