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Horse colic


Colic in horses is defined as abdominal pain, but it is a clinical sign rather than a diagnosis. The term colic can encompass all forms of gastrointestinal conditions which cause pain as well as other causes of abdominal pain not involving the gastrointestinal tract. The most common forms of colic are gastrointestinal in nature and are most often related to colonic disturbance. There are a variety of different causes of colic, some of which can prove fatal without surgical intervention. Colic surgery is usually an expensive procedure as it is major abdominal surgery, often with intensive aftercare. Among domesticated horses, colic is the leading cause of premature death. The incidence of colic in the general horse population has been estimated between 4 and 10 percent over the course of their lifetime. Clinical signs of colic generally require treatment by a veterinarian.

Colic can be divided broadly into several categories:

These categories can be further differentiated based on location of the lesion and underlying cause (See Types of colic).

This is characterised by a physical obstruction of the intestine, which can be due to impacted food material, stricture formation, or foreign bodies. The primary pathophysiological abnormality caused by this obstruction is related to the trapping of fluid within the intestine oral to the obstruction. This is due to the large amount of fluid produced in the upper gastrointestinal tract, and the fact that this is primarily re-absorbed in parts of the intestine downstream from the obstruction. The first problem with this degree of fluid loss from circulation is one of decreased plasma volume, leading to a reduced cardiac output, and acid-base disturbances.

The intestine becomes distended due to the trapped fluid and gas production from bacteria. It is this distension, and subsequent activation of stretch receptors within the intestinal wall, that leads to the associated pain. With progressive distension of the intestinal wall, there is occlusion of blood vessels, firstly the less rigid veins, then arteries. This impairment of blood supply leads to hyperemia and congestion, and ultimately to ischaemic necrosis and cellular death. The poor blood supply also has effects on the vascular endothelium, leading to an increased permeability which first leaks plasma and eventually blood into the intestinal lumen. In the opposite fashion, gram-negative bacteria and endotoxins can enter the bloodstream, leading to further systemic effects.


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