Horse colic
[9] This is caused by an impaction of food material (water, grass, hay, grain) at a part of the large bowel known as the pelvic flexure of the left colon where the intestine takes a 180 degree turn and narrows.
Impaction generally responds well to medical treatment, usually requiring a few days of fluids and laxatives such as mineral oil,[12] but more severe cases may not recover without surgery.
[15] Hypertrophy gradually decreases the size of the lumen, resulting in intermittent colic, and in approximately 45% of cases includes weight loss of 1–6 month duration and anorexia.
[17] Medical management usually resolves the colic, but if improvement doesn't occur within a few hours then surgery must be performed to flush the colon of any sand, which procedure that has a 60–65% survival rate.
Many displacements (~96% of LDD, 64% of RDD)[27] resolve with medical management that includes fluids (oral or intravenous) to rehydrate the horse and soften any impaction that may be present.
[11][15] Abdominal distention is common due to strangulation and rapid engorgement of the intestine with gas, which then can lead to dyspnea as the growing bowel pushes against the diaphragm and prevents normal ventilation.
Colic signs are referable to those seen with a strangulating lesion, such as moderate to severe abdominal pain, endotoxemia, decrease gut sounds, distended small intestine on rectal, and nasogastric reflux.
It is potentially caused by infectious organisms, such as Salmonella and Clostridial species, but other possible contributing factors include Fusarium infection or high concentrate diets.
[19] DPI usually is managed medically with nasogastric intubation every 1–2 hours to relieve gastric pressure secondary to reflux,[19][28] and aggressive fluid support to maintain hydration and correct electrolyte imbalances.
Acute cases are medical emergencies as the horse rapidly loses fluid, protein, and electrolytes into the gut, leading to severe dehydration which can result in hypovolemic shock and death.
[15] Cecal impactions can be fatal, so care must be taken to monitor the horse for large intestinal ileus after orthopedic surgery, primarily by watching for decreased manure production.
[34] Large strongyle worms, most commonly Strongylus vulgaris, are implicated in colic secondary to non-strangulating infarction of the cranial mesenteric artery supplying the intestines, most likely due to vasospasm.
[15] Treatment includes typical management of colic signs and endotoxemia, and the administration of aspirin to reduce the risk of thrombosis, but surgery is usually not helpful since lesions are often patchy and may be located in areas not easily resected.
[35] Foals will stop suckling, strain to defecate (presents as an arched back and lifted tail), and may start showing overt signs of colic such as rolling and getting up and down.
Although meconium impactions rarely cause perforation, and are usually not life-threatening, foals are at risk of dehydration and may not get adequate levels of IgG due to decreased suckling and not enough ingestion of colostrum.
Lethal white syndrome, or ileocolonic aganglionosis, will result in meconium impaction since the foal does not have adequate nerve innervation to the large intestine, in essence, a nonfunctioning colon.
When laboratory tests are not available, hydration can be crudely assessed by tenting the skin of the neck or eyelid, looking for sunken eyes, depression, high heart rate, and feeling for tackiness of the gums.
[43] Buscopan is sometimes used to facilitate rectal examination and reduce the risk of tears, because it decreases the smooth muscle tone of the gastrointestinal tract, but can be contraindicated and will produce a very rapid heart rate.
Horses with proximal enteritis usually have an intestinal diameter that is narrower, but wall thickness is often greater than 6mm,[19] containing a hyperechoic or anechoic fluid, with normal, increased, or decreased peristalsis.
Abdominal distention may indicate the need for surgical intervention, especially if present with severe signs of colic, high heart rate, congested mucous membranes, or absent gut sounds.
[11] High heart rates (>60 bpm), prolonged capillary refill time (CRT), and congested mucous membranes suggest cardiovascular compromise and the need for more intense management.
Soon after this apparent improvement, the horse will display signs of shock, including an elevated heart rate, increased capillary refill time, rapid shallow breathing, and a change in mucous membrane color.
[11] Strangulating obstructions are usually extremely painful, and the horse may have abdominal distention, congested mucous membranes, altered capillary refill time, and other signs of endotoxemia.
Nasogastric intubation, a mainstay of colic management, is often repeated multiple times until resolution of clinical signs, both as a method of gastric reflux removal and as a way to directly administer fluids and medication into the stomach.
[41] This process of secretion into the intestinal lumen leads to dehydration, and these horse require large amounts of IV fluids to prevent hypotension and subsequent cardiovascular collapse.
[15] Adhesions occur most commonly in horses with small intestinal disease (22% of all surgical colics), foals (17%), those requiring enterotomy or a resection and anastomosis, or those that develop septic peritonitis.
[8] Incisional infection doubles the time required for postoperative care, and dehiscence may lead to intestinal herniation, which reduces the likelihood of return to athletic function.
[4] After the incision has healed adequately, the horse is turned out in a small area for another 2–3 months, and light exercise is added to improve the tone and strength of the abdominal musculature.
Weight loss of 75–100 pounds is common after colic surgery, secondary to the decreased function of the gastrointestinal tract and from muscle atrophy that occurs while the horse is rested.
Draft horses tend to have more difficulty post-surgery because they are often under anesthesia for a longer period of time, since they have a greater amount of gastrointestinal tract to evaluate, and their increased size places more pressure on their musculature, which can lead to muscle damage.
