The occurrence of mesenteric vascular insufficiency in the absence of embolus or thrombosis has been recognized for several years. In the past, the absence of organic vascular occlusion at the time of postmortem examination has been explained on a mechanical basis, such as the dislodging of the obstructing embolus of thrombus at the time of the prosection. Though the definite clinical entity of mesenteric vascular ischemia without occlusion has recently been recognized, its causes are still obscure and have been explained on such phenomena as vasospasm, anaphylaxis, impaired capillary permeability, and arteriolar instability.
The incidence of mesenteric vascular insufficiency in the absence of organic vascular occlusion has been recently reported to be as high as 21% in a series of 110 cases by Berger and Byrne.1 Johnson and Baggenstoss,2 in a review of 60 cases at the Mayo Clinic from 1911-1945, found 10% of the cases had an