Changes

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]].

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.

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.  

===Strangulating Infarction===

===Strangulating Infarction===