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Colic Pathophysiology in Horses (view source)
Revision as of 13:50, 24 May 2010
, 13:50, 24 May 2010no edit summary
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 as the affected bowel continues to fill with fluid and results in reflux into the stomach. 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. The damage may also allow for the absorption of [[gram-negative]] bacteria and [[endotoxin]]s into the circulation, causing the release of [[prostaglandins]] and [[leucotrienes]], which lead to further cardiovascular and systemic effects. [[Hypovolaemia]] and [[acid-base imbalance|acid-base disturbances]] are the major causes of cardiovascular collapse. Endotoxaemia plays a limited role in the death of cases with a simple obstruction.
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 as the affected bowel continues to fill with fluid and results in reflux into the stomach. 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. The damage may also allow for the absorption of [[gram-negative]] bacteria and [[endotoxin]]s into the circulation, causing the release of [[prostaglandins]] and [[leucotrienes]], which lead to further cardiovascular and systemic effects. [[Hypovolaemia]] and [[acid-base imbalance|acid-base disturbances]] are the major causes of cardiovascular collapse. Endotoxaemia plays a limited role in the death of cases with a simple obstruction.
The location and degree of the obstruction (partial or complete) determines the severity of the clinical signs. Proximal obstructions of the small intestine produce greater pain and have an acute onset of clinical signs. They have a more rapidly fatal course than distal obstructions. A large quantity of gastric fluid is produced and sequestrated in cases of proximal obstructions. This fluid contains a large quantity of chloride. The acidic gastric fluid can be lost by a nasogastric tube and will result in an initial metabolic alkalosis for the patient. As the disease progresses and the horse becomes hypoperfused, the acid-base abnormality is further complicated by acidosis. Distal obstructions of the small intestine produce less painful clinical signs with a slower onset. The fluid lost by nasogastric intubation is high in bicarbonate and has an alkaline pH. Distal small intestinal obstructions can be identified by a metabolic acidosis and low serum concentrations of bicarbonate.
Simple obstructions of the large intestine produce milder clinical signs compared to the small intestine and have a slower rate of deterioration. Partial obstructions allow for the passage of some ingesta and gas and hence the clinical signs and level of dehydration are milder as some ingesta and water can pass into the caecum. If the obstruction becomes complete, the gas and ingesta cannot pass and cause intestinal distention. This exerts a pressure on the diaphragm which impairs pulmonary function and inhibits the venous return to the heart by compressing of the vena cava. If these cases are untreated, the distention can become so marked that there is a fatal risk of rupture of the devitalised portions of colon or caecum.
===Strangulating Infarction===
===Strangulating Infarction===