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| 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 imbalance|acid-base disturbances]]. | | 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 imbalance|acid-base disturbances]]. |
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− | There also occur serious effects on the intestine itself, which becomes distended due to the trapped fluid, and by gas production from bacteria. It is this distension, and subsequent activation of [[Stretch receptor|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 veins, then arteries. The difference in time to onset of occlusion is due to the relatively more rigid walls of arteries compared with veins. This impairment of blood supply leads firstly to [[hyperaemia]] 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. This results initially in leakage of [[plasma]], and eventually blood into the intestinal lumen. In the opposite fashion, [[gram-negative]] bacteria and [[endotoxin]]s can enter the bloodstream, leading to further systemic effects. | + | There are also serious effects on the intestine itself. The continued secretion of trapped fluids and the gas production from bacteria cause an increase in the intraluminal hydrostatic pressure and distends the intestine. It is this distension, and subsequent activation of [[Stretch receptor|stretch receptors]] within the intestinal wall, that leads to the associated pain. [[Peristalsis]] is reduced and subsequently stops all together. With progressive distension of the intestinal wall, there is occlusion of blood vessels, firstly veins, then arteries. The difference in time to onset of occlusion is due to the relatively more rigid walls of arteries compared with veins. This impairment of blood supply leads firstly to [[hyperaemia]] 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. This results initially in leakage of [[plasma]], and eventually blood into the intestinal lumen. In the opposite fashion, [[gram-negative]] bacteria and [[endotoxin]]s can enter the bloodstream, leading to further systemic effects. |
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| ===Strangulating Infarction=== | | ===Strangulating Infarction=== |
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| ===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]]. |
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| + | ==References== |
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| + | * Edwards B. (2006, Diagnosis and Pathophysiology of Intestinal Obstruction, in Equine Gastroenterology courtesy of the University of Liverpool, pp 3-18 |
| + | * Meuller E, Moore J. N, (2008) Classification and Pathophysiology of Colic, Gastrointestinal Emergencies and Other Causes of Colic, in Equine Emergencies- Treatments and Procedures, 3rd Edition, Eds Orsini J. A, Divers T.J, Saunders Elsevier, pp 107 |