The performance of the currently available serological markers is suboptimal for routine clinical use, but novel markers of intestinal ischemia such as D-lactate, GST, and i-FABP may offer improved diagnostic accuracy. The early diagnosis of intestinal ischemia remains a challenge, and further research is required to identify improved serological markers and to demonstrate their clinical utility in the individual patient.

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.

collected hourly for five hours. Abdominal pain was quantified using visual analogue pain scores. Reference ranges were 23 to 300 U/l for serum lipase and 30 to 110 U/l for serum amylase. The 24 patients subsequently underwent TDS/TAS and the Nardi test was repeated 12 months postoperatively. The gastrointestinal quality of life index (GIQLI) 6 was measured preoperatively and 12 months postoperatively. The two studies were approved by the ethics committees of the University of Nottingham Medical School and Nottingham University Hospitals. Informed written consent was obtained.The median (range) age of the 14 male and six female volunteers was 21 (18 to 23) years. Serum lipase and amylase concentrations increased more than fourfold over baseline in 15 (75%) and 13 (65%) healthy subjects, respectively, after morphine-prostigmine provocation. The median (interquartile range) baseline and maximum post-provocation concentrations of serum lipase were 120 (74 to 138) and 2930 (344 to 7824) U/l, respectively; corresponding values for serum amylase were 61 (44 to 81) and 220 (91 to 545) U/l (p,0.001, Wilcoxon signed ranks test). Figure 1 shows the maximum increase in enzymes over baseline for each subject, none of whom experienced pain during the study.The median (range) age of the three male and 21 female patients was 42 (25 to 64) years. The post-provocation enzymatic increases were significantly greater preoperatively than post-

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Prospectively registered at Australia and New Zealand Clinical Trials Register (ACTRN 12611000751976) and retrospectively registered at Clinical Trials (NCT1486680).