She participated very actively in the process of developing these guidelines, in particular the important chapters on chronic arterial and venous mesenteric ischaemia. Six days after the second meeting of the task force she died unexpectedly, to our great despair and loss. We honour her dedication and scientific integrity by completing these guidelines. Among many other commitments she was a very productive reviewer and an associate editor of this journal. You can read more about Paola's important contributions to science and to the vascular community in the April 2016 issue of the European Journal of Vascular and Endovascular Surgery. 1

Chronic mesenteric ischaemia is a severe and incapacitating disease, causing complaints of post-prandial pain, fear of eating and weight loss. Even though chronic mesenteric ischaemia may progress to acute mesenteric ischaemia, chronic mesenteric ischaemia remains an underappreciated and undertreated disease entity. Probable explanations are the lack of knowledge and awareness among physicians and the lack of a gold standard diagnostic test. The underappreciation of this disease results in diagnostic delays, underdiagnosis and undertreating of patients with chronic mesenteric ischaemia, potentially resulting in fatal acute mesenteric ischaemia. This guideline provides a comprehensive overview and repository of the current evidence and multidisciplinary expert agreement on pertinent issues regarding diagnosis and treatment, and provides guidance in the multidisciplinary field of chronic mesenteric ischaemia.

Gastrointestinal mucosal pH (pHi), calculated from tono-similar to changes in gastrically determined tonometric variables. This may also apply to sepsis and shock, even if metrically measured P CO2 in the gastrointestinal lumen and the oxygen demands by the bowel wall increase, 101 and to blood bicarbonate content using the Henderson-Hasselbalch cardiopulmonary bypass surgery, during which bowel wall equation, has been suggested to constitute an index of the oxygen demands may decrease following hypothermia and adequacy of splanchnic mucosal perfusion. This may relate increase during rewarming. 3 11 29 53 106 110 111 129 Moreover, to the prognosis of critically ill patients, as bowel wall shock may result in early selective splanchnic vasoconstrichypoperfusion may result in tissue injury, increased pertion so that gastric tonometry may reveal an early indicator meability, endotoxin-bacterial translocation and a harmful of general hypoperfusion. 33 36 46 55 101 134 The gastric tonoinflammatory (cytokine) response. 11 12 26 30 37 54 61 68 71 73 98 metric P CO2 gradient proved an early, sensitive indicator of 106 114 122 130 131 The theory is that hypoperfusion below hypovolaemia during haemorrhage in healthy volunteers. 55 a critical level causes tissue (mucosal) carbon dioxide An increase in the gastric P CO2 gradient and decrease in accumulation and acidosis. As carbon dioxide diffuses pHi during general hypoperfusion in humans may relate to easily across membranes, the P CO2 in the gut lumen also angiotensin II-induced selective splanchnic vasoconincreases, leading to widening of the tonometer-blood P CO2 striction. 67 109 gradient. In fact, pHi has been used successfully to guide Experimental studies using vascular occlusion and repertreatment and to improve the outcome of critically ill fusion, induction of shock or pharmacological splanchnic patients. 36 46 49 61 68 Nevertheless, tonometry has not yet vasoconstriction have revealed that changes in blood flow become a routine intensive care monitoring technique. to the gut wall, as measured by microspheres, laser Doppler, This may relate to uncertainties regarding its physiological electromagnetic or ultrasonic flow probes, or reflectance background, methodology and clinical usefulness. 46 This spectrophotometry, were paralleled by concordant changes review will therefore update current thoughts on these in tonometric variables. 2 57 70 73 82 84 101 108 115 117-119 125 131 aspects. 36 46 134 A decrease in blood flow to less than 50% of baseline during incremental hypoperfusion leads to an increased Physiological background tonometric P CO2 relative to supplying (and draining) blood values. This results in a decrease in pHi, in parallel with Gastrointestinal hypoperfusion the decreasing blood flow and decrease in tissue P O2 and Several conditions may lead to altered gut perfusion (Table oxygen consumption. 1 2 13 36 46 50 55 57 73 82 84 101 103 108 115 1). Haemorrhagic hypotension, cardiac tamponade, cardiac 117-119 125 134 This may result in tissue damage and...

Heavy physical exercise may cause gastrointestinal signs and symptoms, and, although splanchnic blood flow may decrease through redistribution by more than 50%, it is unclear whether these signs and symptoms relate to gastrointestinal ischemia. In 10 healthy volunteers, we studied the effect of exercise on gastric mucosal perfusion adequacy using air tonometry. Two relatively short (10 min) exercise stages were conducted on a cycle ergometer, aiming for 80 and 100% of maximum heart rate, respectively. The intragastric-arterial PCO(2) gradient (Delta PCO(2)) was elevated by 1.1 +/- 1.0 kPa over baseline values (-0.1 +/- 0.3 kPa) only after maximal exercise (P < 0.001). Delta PCO(2) positively correlated with the arterial lactate level taken as an index of exercise intensity (Spearman's rank test: r = 0.76, P < 0.0001). By bilinear regression analysis, a lactate level of 12 mmol/l, above which a sharp rise in the Delta PCO(2) occurred, was calculated. We conclude that, in healthy volunteers with normal splanchnic vasculature, gastric ischemia may develop during maximal exercise as judged from intragastric PCO(2) tonometry.

The results of this study suggest that the celiac axis compression syndrome exists and that the actual ischemia can be detected by gastric exercise tonometry and treated safely, with success.

The prevalence of GI complaints during and after running was low compared with that reported in other studies, which is partly due to the definition of "symptomatic" used in our study. The risk factors associated with becoming symptomatic were identical to those in other studies. The relationship between complaints during the run and the type of complaints afterwards suggests a role of GI ischaemia in the pathophysiology of running-induced GI symptoms.

Summary Background The prevalence of exercise‐induced gastrointestinal (GI) symptoms has been reported up to 70%. The pathophysiology largely remains unknown. Aim To review the physiological and pathophysiological changes of the GI‐tract during physical exercise and the management of the most common gastrointestinal symptoms. Methods Search of the literature published in the English and Dutch languages using the Pubmed database to review the literature that focused on the relation between splanchnic blood flow (SBF), development of ischaemia, postischaemic endotoxinemia and motility. Results During physical exercise, the increased activity of the sympathetic nervous system (SNS) redistributes blood flow from the splanchnic organs to the working muscles. With prolonged duration and/or intensity, the SBF may be decreased by 80% or more. Most studies point in the direction of increased SNS‐activity as central driving force for reduction in SBF. A severely reduced SBF may frequently cause GI ischaemia. GI‐ischaemia combined with reduced vagal activity probably triggers changes in GI‐motility and GI absorption derangements. GI‐symptoms during physical exercise may be prevented by lowering the exercise intensity, preventing dehydration and avoiding the ingestion of hypertonic fluids. Conclusions Literature on the pathophysiology of exercise‐induced GI‐symptoms is scarce. Increased sympathetic nervous system activity and decreased splanchnic blood flow during physical exercise seems to be the key factor in the pathogenesis of exercise‐induced GI‐symptoms, and this should be the target for symptom reduction.

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