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Colic Pathophysiology in Horses (view source)
Revision as of 13:40, 13 May 2010
, 13:40, 13 May 2010Created page with '==Pathophysiology== This can be divided broadly into simple obstructions, strangulating obstructions, and non-strangulating infarctions. ===Simple Obstruction=== This is cha…'
==Pathophysiology==
This can be divided broadly into simple obstructions, strangulating obstructions, and non-strangulating [[infarctions]].
===Simple Obstruction===
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 gastro-intestinal tract (around 125L daily), 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 imbalance|acid-base disturbances]].
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.
===Strangulating Infarction===
Strangulating infarctions have all the same pathological features as a simple obstruction, but the bloody supply is immediately affected. Both arteries and veins may be effected immediately, or progressively as in simple obstruction. Common causes of strangulating obstruction are pedunculated lipomas, and displacement of intestine through a hole, such as a [[hernia]], a mesenteric rent, or the [[epiploic foramen]].
===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]].
This can be divided broadly into simple obstructions, strangulating obstructions, and non-strangulating [[infarctions]].
===Simple Obstruction===
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 gastro-intestinal tract (around 125L daily), 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 imbalance|acid-base disturbances]].
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.
===Strangulating Infarction===
Strangulating infarctions have all the same pathological features as a simple obstruction, but the bloody supply is immediately affected. Both arteries and veins may be effected immediately, or progressively as in simple obstruction. Common causes of strangulating obstruction are pedunculated lipomas, and displacement of intestine through a hole, such as a [[hernia]], a mesenteric rent, or the [[epiploic foramen]].
===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]].