Nonocclusive mesenteric ischemia (NOMI), a subtype of acute mesenteric ischemia (AMI), is primarily caused by mesenteric arterial vasoconstriction and decreased vascular resistance, leading to impaired intestinal perfusion.Commonly observed after cardiac surgery, NOMI affects older patients with cardiovascular or systemic diseases, accounting for 20-30% of AMI cases with a mortality rate of ∼50%. This review explores NOMI's pathophysiology, clinical implications in aortic dissection, and the unmet needs in diagnosis and management, emphasizing its prognostic significance.

A comprehensive literature review was conducted using multiple electronic databases to extract relevant data and information.

NOMI is a life-threatening condition characterized by mesenteric vasoconstriction and reduced splanchnic blood flow, often triggered by cardiac surgery, hemodialysis, or hypotensive episodes. Epidemiological studies highlight its prevalence in intensive care unit settings, with a high mortality rate linked to delayed diagnosis and systemic hypoperfusion. Risk factors include advanced age, vasopressor use, and inflammatory markers. Biomarkers such as intestinal fatty acid binding protein, citrulline, and D-lactate show potential for early detection but lack robust clinical validation. Management includes fluid resuscitation, vasodilators, and surgical intervention for bowel necrosis. Emerging endovascular approaches show promise but are limited to select cases without bowel infarction. This review underscores the critical need for timely diagnosis, risk factor identification, and tailored interventions to improve outcomes.

NOMI remains poorly understood despite advances in surgical and perioperative care. Its pathophysiology, linked to cardiopulmonary bypass and intraoperative factors, requires heightened clinical vigilance. Limited evidence underscores the need for a multidisciplinary approach involving surgeons, radiologists, and anesthetists to improve diagnosis, management, and outcomes in aortic surgery patients.

This study aimed to predict cases of acute superior mesenteric artery (SMA) occlusion requiring bowel resection using occlusion site and time from symptom onset to diagnosis at five Japanese institutions. Advances in imaging, endovascular treatment, and perioperative management have improved the clinical outcomes of patients with acute SMA occlusion; however, in clinical practice it remains difficult to effectively determine patients requiring bowel resection.

We retrospectively analyzed the data of 48 patients (mean age: 82.5 y; male: 37.5%) diagnosed with acute SMA occlusion between June 2009 and August 2018. Background data of patients who required and did not require bowel resection were compared. A multivariable predictive model was developed using the time from symptom onset to diagnosis and whether SMA occlusion was proximal, including the origin of the middle colic artery.

Fifteen patients (31.3%) died during the hospital stay. Atrial fibrillation (83.3%) was the most common comorbidity. The median time from symptom onset to diagnosis was 13.0 (interquartile range, 4.75-24.0) h. Laparotomy, bowel resection, and thrombus embolectomy were performed in 41 (85.4%), 26 (54.2%), and 21 (43.8%) patients, respectively. A logistic regression model achieved 78.6% sensitivity in predicting cases not requiring bowel resection. Proximal occlusion was significantly associated with the requirement for bowel resection (P = .039).

The time from symptom onset to diagnosis and occlusion site contributed to high sensitivity in determining the need for bowel resection in patients with acute SMA occlusion. Further prospective studies are warranted to investigate the clinical impact of this model.

Mortality related to acute mesenteric arterial occlusion remains very high. Patient survival is dependent on prompt recognition and revascularization before ischemia progresses to intestinal gangrene. Biphasic computed tomography angiography has surpassed angiography as the diagnostic test of choice due to its ability to define the arterial anatomy and to evaluate secondary signs of mesenteric ischemia. Unlike chronic mesenteric ischemia, the treatment of acute arterial mesenteric ischemia, either embolic or thrombotic, remains largely surgical. This is due to the emergent need for revascularization combined with a careful evaluation of the intestines. Endovascular techniques remain useful, however, and can save precious time in the treatment of these challenging patients if integrated into a treatment pathway combined with definitive surgical treatment. A new hybrid endovascular-surgical treatment for the treatment of acute mesenteric thrombosis is described.

The normal pattern of carbon dioxide (CO2) levels in the human stomach and small bowel after meals is unknown. The intraluminal carbon dioxide level is a sensitive and early marker for organ mucosal ischemia. CO2 levels in both the stomach and small bowel are influenced by multiple factors other than adequacy of perfusion. Gastric acid production, salivary bicarbonate and CO2 produced or absorbed by meals are the disturbing variables. Prolonged gastric (and jejunal) tonometry after meals can be of additional value in the work-up of patients suspected of (chronic) gastrointestinal ischemia. The purpose of this study was to challenge these problems using in vitro tested meals and a rigid acid-suppression regimen in a group of healthy subjects.

Standard meals were tested in vitro on the ability to produce and buffer CO2. Meals with the least CO2 variations were subsequently used in healthy subjects. Tonometry of the stomach and jejunum was performed for 24 h, with optimal and controlled acid suppression.

Ten subjects were enrolled in the study. Acid production was sufficiently suppressed. The gastric PCO2 baseline (fasting) was 6.5 (1.0), and significantly lower than the jejunum PCO2 baseline of 7.6 (0.9) kPa. The gastric baseline during the day was 6.9 (1.6), and significantly lower than the gastric baseline during the night of 8.0 (1.8), suggesting a diurnal variation of PCO2. Increases in PCO2 levels were seen in all subjects, after meals and between meals.

Prolonged gastric and jejunal tonometry is feasible in humans. PCO2 levels were seen to peak after, but also in-between, most meals. The diurnal variation in PCO2 might reflect reversible gastric mucosal ischemia.

The aim of this study was to investigate mesenteric ischaemia by determining intragastric PCO(2) (iPCO(2)) with gastric tonometry during rest and exercise stress testing in patients with chronic heart failure (CHF). In CHF inflammatory immune activation is hypothesized to result from a chronic endotoxin challenge due to bacterial translocation of hypoperfused intestinal mucosa.

In 10 patients with CHF and ten healthy controls a tonometry catheter was inserted into the stomach. IPCO(2) was measured at rest and during bicycle exercise every 5 min. At rest arterial pCO(2) (aPCO(2)), intragastric pCO(2) (iPCO(2)) and the intragastric/arterial gap did not differ between patients and controls. During low level exercise (25 W), patients showed an increase in iPCO(2) compared to resting iPCO(2), whereas controls did not show an increase in iPCO(2) (change in iPCO(2): 12+/-2% vs. 1+/-0.4%, P<0.001). In CHF, iPCO(2) during peak exercise was 25+/-3% higher than at rest, compared to controls (increase 2+/-1, P<0.0001).

Patients with CHF already at low level exercise develop an increase in iPCO(2). This is likely to reflect hypoperfusion of the intestinal mucosa, which may contribute to the development of bacterial translocation.

We sought to estimate the incidence of hospitalization for upper and lower gastrointestinal bleeding among older persons and to identify independent risk factors.

Prospective cohort study.

The Cardiovascular Health Study (CHS).

5,888 noninstitutionalized men and women age 65 years or older in four U.S. communities enrolled in the CHS.

Gastrointestinal bleeding events during the period 1989 through 1998 were identified using hospital discharge diagnosis codes and confirmed by medical records review. Risk-factor information was collected in a standardized fashion at study baseline and annually during follow-up.

Among CHS participants (mean baseline age 73.3 years, 42% male), the incidence of hospitalized gastrointestinal bleeding was 6.8/1,000 person-years. In multivariate analyses, advanced age, male sex, unmarried status, cardiovascular disease, difficulty with daily activities, use of multiple medications, and use of oral anticoagulants were independent risk factors. Compared with nonsmokers, subjects who smoked more than half a pack per day had a multivariate-adjusted hazard ratio (HR) of 2.14 (95% confidence interval [CI] = 1.22-3.75) for upper gastrointestinal bleeding and a multivariate-adjusted HR of 0.21 (95% CI = 0.03-1.54) for lower gastrointestinal bleeding. Aspirin users did not have an elevated risk of upper gastrointestinal bleeding (HR = 0.76, 95% CI = 0.52-1.11), and users of other nonsteroidal anti-inflammatory drugs had a HR of 1.54 (95 % CI = 0.99-2.36). Low ankle-arm systolic blood pressure index was associated with higher risk of gastrointestinal bleeding among subjects with clinical cardiovascular disease but not among those without clinical cardiovascular disease.

This study identifies risk factors for gastrointestinal bleeding, such as disability, that may be amenable to modification. The findings will help clinicians to identify older persons who are at high risk for gastrointestinal bleeding.

The subsets of acute mesenteric ischaemia include mesenteric arterial occlusion (by embolus or thrombosis), mesenteric venous thrombosis and non-occlusive mesenteric ischaemia. Despite advances in pathophysiology, laboratory diagnosis and imaging techniques, acute mesenteric ischaemia is still associated with mortality rates of more than 60% and continues to be a challenging diagnostic problem. The key to a better outcome (and the main problem in clinical practice) is early diagnosis. Clinical presentation may be unspecific, but is often characterized by an initial discrepancy between severe subjective pain and relatively unspectacular findings on physical examination. Up to now, there are no simple and non-invasive diagnostic tests of sufficient sensitivity and specificity; thus, angiography remains the cornerstone of diagnosis and should be performed early in all patients in which mesenteric ischaemia is a realistic differential diagnosis. Treatment for obstructive mesenteric arterial syndromes and most patients with mesenteric venous thrombosis is surgical, whereas non-occlusive mesenteric ischaemia may be managed by pharmacological vasodilation.

The tonometric detection of a high intragastric regional P(CO2) (PrCO2) reflecting an elevated intramucosal P(CO2) can be helpful to diagnose mucosal ischemia, if acid secretion is suppressed to avoid intragastric CO2 production through buffering of acid by bicarbonate in the stomach. It is recommended to perform tonometry in the fasting state, but this may hamper feeding of the critically ill. On the other hand, postfeeding tonometry could serve as a diagnostic stress test because feeding increases mucosal blood flow demand, provided that the meal itself does not hamper diffusion of CO2 from mucosa to tonometer balloon and does not generate intragastric CO2, independently from intramucosal P(CO2). We therefore studied the effect of a standard meal on intragastric PrCO2 tonometry in healthy volunteers with suppression of meal-stimulated gastric acid secretion and, presumably, with an adequate mucosal blood flow reserve.

The gastric juice pH and tonometric PrCO2 were measured in 14 human volunteers, after gastric acid secretion suppression by either ranitidine (100-mg bolus, followed by 25 mg/h i.v., n = 7) or by ranitidine plus pirenzepine (10-mg bolus, followed by 3 mg/h i.v., n=7) to suppress any residual meal-stimulated gastric acid secretion, before and at 30-minute intervals until 120 minutes after oral ingestion of a standard liquid test meal (Pulmocare [Abbott, the Netherlands]; 500 mL, 750 kcal, P(CO2) 5 mm Hg, pH 7.50).

The gastric juice pH, which was >4.0 in all individuals throughout the study, and the PrCO2 did not depend on the regimen for gastric acid secretion suppression, and therefore the data were pooled. The PrCO2 (median [range]) after feeding was 69% (56% to 170%) of baseline (42 [37-51] mm Hg) from 0 to 30 minutes (P < .001), 85% (72% to 167%) of baseline from 30 to 60 (P < .05), 97% (57% to 193%) from 60 to 90 minutes, and 112% (97% to 189%) of baseline from 90 to 120 minutes with a rise above baseline in 10 of 14 patients. In vitro, the liquid test meal generated CO2 after adding bicarbonate but not after hydrochloric acid.

We recommend intragastric tonometry to be performed in the fasting state and discourage tonometry after feeding as a stress test, because a single test meal changes tonometric PrCO2 in a time-dependent manner until 2 hours after gastric feeding of healthy volunteers. The fall in PrCO2 directly after feeding can be attributed to dilution, whereas a rise above baseline in some patients may have been caused, as supported by CO2 production after adding bicarbonate to the test meal in vitro, by CO2 production through buffering of meal-derived acid by gastric bicarbonate, in the absence of stimulated gastric acid secretion by feeding.