The Pathogenesis of Nonocclusive Mesenteric Ischemia: Implications for Research and Clinical Practice

Author:

Al-Diery Hussam1,Phillips Anthony12,Evennett Nicholas3,Pandanaboyana Sanjay13,Gilham Michael4,Windsor John A.1235

Affiliation:

1. Faculty of Medical and Health Sciences, Department of Surgery, School of Medicine, University of Auckland, Auckland, New Zealand

2. Applied Surgery and Metabolism Laboratory, School of Biological Sciences, University of Auckland, Auckland, New Zealand

3. HBP/Upper GI Unit, Department of General Surgery, Auckland City Hospital, Auckland, New Zealand

4. Cardiovascular Intensive Care Unit, Auckland City Hospital, Auckland, New Zealand

5. Surgical Centre for Outcomes Research and Evaluation, Department of Surgery, University of Auckland, Auckland, New Zealand

Abstract

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.

Publisher

SAGE Publications

Subject

Critical Care and Intensive Care Medicine

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