The three most common gastrointestinal problems that are seen in the foal include colic, gastric ulcer disease and diarrhea. Though these are also common in the adult the foal has different specific etiologies and treatments.
The three most common gastrointestinal problems that are seen in the foal include colic, gastric ulcer disease and diarrhea. Though these are also common in the adult the foal has different specific etiologies and treatments.
Colic
Incidence of colic in the foal < than 6 months of age is about 18 times less than in the adult but there are some specific etiologies of colic in the foal that should be examined. Some of them include congenital problems, meconium impaction, uroperitoneum, intussusception, gastric ulcers, enteritis, and hernias. The age of the foal may narrow your differential diagnosis: Congenital (lethal white, atresia) – 12-24 hours of age, Meconium impaction – 12 – 48 hours of age, Uroperitoneum – 48-96 hours of age, Fecalith in a miniature horse – 3-4 weeks of age, Intussusceptions – 3-5 weeks of age, and Strangulating lesions such as volvulus, incarcerated hernia no specific age.
Clinical signs are variable and intensity is not necessarily indicative of etiology. Some of these signs include reduced frequency of nursing, prolonged recumbency with frequent adjustment of position – stretching necking roll on back, general restlessness, tail swishing and a “camped under" stance. It may be difficult to distinguish between surgical and medical problems because foals tend to have a low tolerance for abdominal pain and may act with extreme agitation for a simple medical colic.
Diagnostic options in the foal include a digital palpation for presence meconium in the very young foal, abdominocentesis, and imaging. The abdominocentesis can be done with an 18 gauge needle at the most dependent area of the abdomen. A teat canula can also be used to obtain fluid but a belly wrap must be applied because omentum will often protrude from the site.
Diagnostic imaging is very helpful in the colicky foal. Radiologic studies of the abdomen can demonstrate obstruction with gas distension of the intestine. Meconium impactions can also be visualized and can be further evaluated with a contrast enema. Ultrasound is helpful in meconium impactions as well as intussceptions. In the case of bladder ruptures an increased amount of fluid in the abdomen can be seen by ultrasound as well as a collapsed bladder.
Meconium impactions
Meconium is the “caramelized” first feces of the newborn foal. It is composed of swallowed amniotic fluid and cellular debris. The total weight of meconium is about 1% of the foal's weight and foals start to evacuate it after ingesting colostrum which has a laxative effect. Most should be evacuated by 12 hours of age.
Treatment of meconium impactions usually involves the use of gentle enemas. Fleet mineral or phosphate enemas are routinely used by clients. A warm soapy water enema administered through an enema bag is often the next step. Finally if impaction remains, one could try a retention enema. For the retention enema a 30 French Foley catheter is inserted in the rectum and the balloon is inflated. A mixture of 8 gms of acetylcysteine, 20 g of baking soda and 200 mls of water is introduced into the rectum and the Foley catheter is clamped for 20 minutes. Acetylcysteine is a mucolytic and is helpful is softening the meconium. If the foal is greater than 24 hours of age, mineral oil can be given via a nasogastric tube to act as a laxative.
Analgesics that are helpful in the foal include judicious use of torbugesic, ketophen, butorphanol. Most meconium impactions resolve in 24 hours but on the rare occasion surgical intervention is necessary.
Lethal White Syndrome
Ileocolonic aganglionosis or Lethal White Syndrome is a fatal autosomal recessive disorder seen principally in overo Paint horses. It is caused by a point mutation in the endothelin receptor B amino acid. This receptor is responsible for migration of neural crest cells to become melanoctyes and neurons to the intestinal tract. The lack of nerves to the colon results in a contraction of the large intestine. This is not atresia coli. Affected foals are mostly completely white – there may be a small pigmented area around the face. They present like a foal with meconium impaction but they have not passed any feces except perhaps a small amount of diarrhea. Over the course of the day their abdomens become progressively distended.
The diagnosis of LWS is presumptively made on signalment, parentage, lack of response to treatment and sometime surgical exploration. The definite diagnosis can be made by DNA testing but it takes several weeks and the foal will not survive. Not all white foals from Paint mares are lethal whites but it is more common. Genetic testing of breeding animal will help to eliminate this problem.
Gastric Ulceration
Gastric ulceration can occur in foals as young as 24 hours of age. The incidence has been cited as high as 50% of normal asymptomatic foals. Foals stressed by concurrent disease, especially orthopedic pain have a higher incidence. Healthy foals have an acid gastric baseline pH on average of 3.2 – 3.7. Prolonged recumbency and decreased suckling will cause the pH to drop below 2.5. Not all sick foals have an acid secretory profile. Though most ulcers occur at the margo plicatus, 40 percent of sick foals in one study had ulceration in the glandular portion of the stomach.
Taharguchi et al found the following clinical signs in a group of foals with gastric ulceration.
· Depression and intermittent nursing – 82.5%
· Diarrhea – 65%
· Colic – 37.5%
· Bruxism – 10%
· Ptyalism – 7.5%
Gastroscopy is the most sensitive and specific method of diagnosing gastric or esophageal ulceration. Lesions can vary in severity form a mild gastritis to a perforation of the stomach wall. Lesions must be distinguished from normal desquamation of gastric epithelia. Thin sheets of epithelia will be shed in foals up to 35 days of age. Occasionally the ulcers will rupture causing a septic peritonitis. Radiographs of the abdomen may be helpful in determining if there is pneumoperitoneum which is indicative of bowel rupture.
Several treatments are available for this problem. They include the following:
Sulcralfate (10-20 mg/kg q 8 hours), ranitidine (6.6 mg/kg q 8 hours)), and Omeprazole (4mg/kg q once daily). If the foal appears to a gastric emptying problem then Metaclopramide (0.02-0.04 mg/kg/hr at a constant rate infusion) can be given. Metaclopramide can cause behavioral changes so it is important to be aware of the side effects and decrease dose as needed.
Diarrhea
Diarrhea in the foal can have many causes. A history of the foal and the farm may help to lead you to the correct etiology. Premature foals, foals that have peripartum asphyxia and foals with sepsis are at higher risk for developing diarrhea. Foals from high producing mares may be at risk for Clostridial diarrhea. “Foal heat” diarrhea is the result of intestinal maturation. It occurs between 7-10 days and is self limiting. If there are many foals affected on a farm then the clinician should think about highly infectious causes such as Rotoviral diarrhea or possibly salmonellosis.
Diagnostics for determining the etiology of the diarrhea include PCR, ELISA, culture, and fecal smears for parasites such as Giardia or Cryptosporidia. Several laboratories have foal diarrhea panels that will do all the diagnostics for a single package.
Treatment involves the judicious use of intravenous fluids to keep the foal hydrated. Some foals also have electrolyte abnormalities from active secretion and loss. These should be monitored and corrected. Rotovirus causes lactose intolerance in foals and an osmotic diarrhea. These foals may need to have lactase added as a medication in order to help digest the mare's milk.
The prognosis for foals with diarrhea is fairly good if their hydration is maintained.