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Colic Pathophysiology in Horses (view source)
Revision as of 17:53, 24 May 2010
, 17:53, 24 May 2010no edit summary
Strangulating infarctions have all the same pathological features as a simple obstruction, but the bloody supply is immediately affected and so they often present as an acute abdominal crisis. The patholphysiological changes are more acute and severe and the mortality rate of cases that go to surgery, is high. Common causes of strangulating obstruction are incarcerations, intussusceptions and intestinal volvulus.
Strangulating infarctions have all the same pathological features as a simple obstruction, but the bloody supply is immediately affected and so they often present as an acute abdominal crisis. The patholphysiological changes are more acute and severe and the mortality rate of cases that go to surgery, is high. Common causes of strangulating obstruction are incarcerations, intussusceptions and intestinal volvulus.
Both arteries and veins may be effected immediately, or progressively as in simple obstruction.
Both arteries and veins may be effected immediately, or progressively as in simple obstruction. Venous occlusion makes the affected segment of bowel a deep red color. If there is arterial occlusion as well, the intestine becomes cyanotic. Vascular stasis quickly purses and the bowel becomes red/black. Immediately, the vascular epithelium starts to degenerate and becomes more permeable. Plasma is lost into the tissue. Within a few hours, the damage is so severe that that blood is lost out of the vessel into the tissue and then the lumen (venous infacrction stage).
The subsequent hypoxia causes degeneration of the mucosal villi and within hours, the mucosal epithelium is completely necrotic. As time passes, the degeneration continues through the different layers of the intestinal wall and the barrier is compromised. Gram-negative bacteria and endotoxins enter the circulation and cause damage to the endothelium and platelets. The platelets release potent vasoconstricor substances (thromboxane and serotonin). The vascular epithelium releases prostacyclins in response to the damage. The prostacyclins cause a massive release of neutrophils systemically but predominantly in the lungs and affected portion of bowel. These mediators are responsible for the horse going into endotoxic shock that is apparrent clinically. It is dose-related and more severe with larger portions of gut involved.
The clinical signs are acute in onset and of severe unrelenting pain that shows no or little reponse to analgesia. The rate of deterioration is rapid and untreated cases of small intestinal strangulation will die in 24-36 hours of the onset of clinical signs. Surgical correction must be carried out within a few hours of the strangulation occurring if it is to be successful. Strangulation of the large intestine has a similar pathophysiology to that of the small intestine.
===Non-strangulating Infarction===
===Non-strangulating Infarction===
In a non-strangulating infarction, blood supply to a section of intestine is occluded, without any obstruction to ingesta present within the intestinal lumen. The most common cause is infection with ''Strongylus vulgaris'' larvae, which develop within the (primarily cranial) [[mesenteric artery]].
In a non-strangulating infarction, blood supply to a section of intestine is occluded, without any obstruction to ingesta present within the intestinal lumen. The most common cause is infection with ''Strongylus vulgaris'' larvae, which develop within the (primarily cranial) [[mesenteric artery]].