The physiology of intestinal oxygenation and the pathophysiology of intestinal ileus.

Intestinal Ileus is Gut Shock caused by Bowel Hypoxia. The morbidity and mortality of Intestinal Ileus has puzzled more than two generations of investigators because they have overlooked the fact that the gas which collects in obstructed small intestine is mostly (90+%) Nitrogen. For some strange reason a gut full of nitrogen has not been looked on as comparable to a lung full of nitrogen, even though the lung and gut have a common embryological origin. My proposal is that intestinal epithelium lining a nitrogen filled lumen becomes as oxygen starved as alveolar lining in a similar circumstance. Bowel hypoxia may be brought about either by failure of the intestine to "breathe out", having breathed in due to mechanical block, or gut paralysis, from any cause, of which one may be failure of blood borne oxygen transport to the bowel, Individually, or together, these may reduce or stop the flow of air and/or aerated intestinal contents along the lumen. Local (bowel) or general underperfusion +/- hypovolaemia +/- anaemia may be a particular cause of paresis or paralysis (aperistalsis) of intestinal muscle. The non-contracting gut then fails to transport the luminal current of fluid and air (oxygen), and adds lumenal to blood-borne oxygen deficiency. The intestinal mucosa utilises oxygen from the current of air churned along the bowel by normal peristalsis to mix with and dissolve in the luminal contents. Should this current be obstructed or the propulsive churning activity cease, oxygen will be "used up", the residual gas become almost entirely nitrogen, and the mucosa must necessarily become oxygen starved and suffocated. Hypoxic mucosa lives in a dangerous environment, at risk of autodigestion by self-produced proteolytic or other enzymes secreted into the lumen by exocrine glands, and it may rapidly become necrotic and gangrenous. Different presentations of Ileus are different degrees of the same Gut Shock due to different levels and durations of tissue hypoxia brought about by different mechanisms with that final common path, complicated by different degrees of autodigestive mucosal destruction, bowel wall oedema, and fluid exudation into the lumen comparable to that through BURNED skin. This idea is new only in so far as it has been put together in this way. Parts have been anticipated by other writers. No new ways of managing ileus are proposed, but it is suggested that existing empirical methods be rationalised and applied more widely and logically.