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Nonocclusive mesenteric ischemia (NOMI) is a condition that can encompass ischemia, inflammation, and infarction of the intestinal wall. In contrast to most patients with acute mesenteric ischemia, NOMI is distinguished by patent arteries and veins. The clinical presentation of NOMI is often insidious and nonspecific, resulting in a delayed diagnosis. Patients most at risk are those with severe acute and critical disease, including major surgery and trauma. Nonocclusive mesenteric ischemia is part of a spectrum, from mild, asymptomatic, and an unexpected finding on CT scanning, through to those exhibiting abdominal distension and peritonitis. Severe NOMI is associated with a significant mortality rate. This review of NOMI pathophysiology was conducted to document current concepts and evidence, to examine the implications for diagnosis and treatment, and to identify gaps in knowledge that might direct future research. The key pathologic mechanisms involved in the genesis of NOMI represent an exaggerated normal physiological response to maintain perfusion of vital organs at the expense of mesenteric perfusion. A supply-demand mismatch develops in the intestine due to the development of persistent mesenteric vasoconstriction resulting in reduced blood flow and oxygen delivery to the intestine, particularly to the vulnerable superficial mucosa. This mismatch can be exacerbated by raised intra-abdominal pressure, enteral nutrition, and the use of certain vasoactive drugs, ultimately resulting in the development of intestinal ischemia. Strategies for prevention, early detection, and treatment are urgently needed.

Aims/hypothesis: The role of peri-islet CD45-positive leucocytes, as one component of insulitis, in beta cell death during human type 1 diabetes remains unclear. We undertook a case study, comparing and quantifying leucocytes in the peri- and intra-islet areas in insulin-positive and -negative islets, to assess whether peri-islet leucocytes are pathogenic to beta cells during type 1 diabetes., Methods: Pancreatic sections from 12 diabetic patients (0.25-12 years of disease) and 13 non-diabetic individuals with and without autoantibodies were triple-immunostained for islet leucocytes, insulin and glucagon cells. Islets were graded for insulitis, enumerated and mapped for the spatial distribution of leucocytes in peri- and intra-islet areas in relation to insulin- and glucagon-immunopositive cells., Results: In the non-diabetic autoantibody-negative group, the percentage of islets with insulitis was either absent or <1% in five out of eight cases and ranged from 1.3% to 19.4% in three cases. In the five non-diabetic autoantibody-positive cases, it varied from 1.5% to 16.9%. In the diabetic group, it was <1% in one case and 1.1-26.9% in 11 cases, with insulitis being absent in 68% of insulin-positive islets. Peri-islet leucocytes were more numerous than intra-islet leucocytes in islets with insulin positivity. Increasing numbers of exocrine leucocytes in non-diabetic autoantibody-positive and diabetic donors were also present., Conclusions/interpretation: The prominence of peri-islet leucocytes in insulin-positive islets in most long-standing diabetic individuals suggests that they may be pathogenic to residual beta cells. Increasing numbers of leucocytes in the exocrine region may also participate in the pathogenesis of type 1 diabetes.