Page 844 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Gastrointestinal system: 4.2 The lower gastrointestinal tr act 819

VetBooks.ir Differential diagnosis Prognosis
Lactase production should be restored in a few days
Clostridial enteritis, salmonellosis, rotaviral enteri-
tis, idiopathic colitis and other causes of diar-
mary insult. The prognosis is excellent if adequate
rhoea, maldigestion and malabsorption should be to a few weeks, depending on the severity of the pri-
considered. supportive care is provided.

Diagnosis ASCARID INFECTION
Other causes of diarrhoea (Salmonella, C. difficile,
C. perfringens, rotavirus) should be ruled out or Definition/overview
treated. Lactose intolerance can occur concurrently Ascarid infestation is common in horses, par-
with infectious enteritis. Response to supplementa- ticularly those housed on crowded pastures with
tion with oral lactase is suggestive but not diagnos- frequent mixing of horses and inadequate parasite-
tic. The oral lactose tolerance test is most widely control programmes. Ascarid impaction is an
used to diagnose lactose intolerance (Table 4.8). uncommon but life-threatening problem that typi-
cally occurs after deworming weanlings with large
Management parasite burdens.
The standard approach to management of affected
foals is supplementation with oral lactase (1,000– Aetiology/pathophysiology
3,000 IU p/o q4–12 h). Weaning should be consid- Infection occurs following ingestion of infec-
ered in older foals, particularly if oral administration tive Parascaris equorum larvae that develop within
of lactase is problematic. Supportive treatment or 10 days on pasture from faeces of infected horses.
treatment of the primary cause should be provided Following ingestion, the larvae migrate through
if necessary. the wall of the small intestine, pass through the
liver via the portal vein and eventually reach the
pulmonary circulation. Larvae moult in the lung,
Table 4.8 Protocol for lactose tolerance testing in ascend the trachea and are swallowed, with final
foals moulting and maturation occurring in the small
intestine.
1 Fast the foal for approximately 4 hours
2 Obtain a baseline blood glucose level. Stall-side testing
with a glucometer can be performed. Red blood cells Clinical presentation
will consume glucose in vitro. If samples must be Ascarids can be present in the small intestine with-
stored or shipped for >1 hour before testing, plasma or out any obvious clinical signs. Clinical ascarid infes-
serum should be separated or tubes containing tation is usually non-specific and characterised by
sodium fluoride should be used a pot-bellied appearance and varying degrees of
3 Administer 1 g/kg lactose, as a 20% solution in water, decreased growth rate, poor haircoat and lethargy.
via bottle or NG tube
Concurrent low-grade respiratory disease is not
4 Determine blood glucose levels every 30 minutes for uncommon. Ascarid impaction is a serious condition
3 hours
characterised by acute, often severe, colic. Ascarid
5 An increase in blood glucose of <2 mmol/l indicates
maldigestion or malabsorption. The peak value is impaction should be considered in all cases of colic
usually obtained at 60–90 minutes that develop in foals shortly after deworming.
6 A glucose absorption test should be performed on all Intestinal rupture may occur, with the associated
foals with an abnormal lactose tolerance test to development of peritonitis.
differentiate maldigestion from malabsorption
7 A glucose absorption test is performed as described Differential diagnosis
for the lactose tolerance test, substituting lactose with A variety of other causes of ill-thrift such as malnu-
1 g/kg glucose. An increase in blood glucose of at least trition, poor management, other intestinal parasites
75% should occur
and chronic infection should be considered. Many