In cases of suspected acute mesenteric ischemia, current guidelines recommend computed tomography angiography as the initial diagnostic modality, with direct laparoscopy advised in uncertain cases. However, the occurrence of nontherapeutic laparoscopies remains a clinical concern. Notably, endoscopy is not yet incorporated into standard diagnostic algorithms.

Intestinal pseudo-obstruction is characterized by the dilation of bowel in the absence of an anatomical obstruction. Patients present with the signs and symptoms of bowel obstruction, including nausea, vomiting, abdominal distension, and obstipation with bowel dilation on x-ray or CT imaging. Pseudo-obstruction can be acute or chronic. Acute colonic pseudo-obstruction (ACPO), also known as Ogilvie syndrome, most commonly affects the large intestine from the cecum to the splenic flexure. The exact pathophysiology is unknown, but it has been linked to dysregulation of the autonomic nervous system. Most cases are found in patients who have undergone surgery or are critically ill. After a mechanical obstruction is ruled out, initial management includes bowel rest, nasogastric decompression, intravenous fluid resuscitation, and treatment of the underlying cause. Further treatment options include administration of Neostigmine as well as endoscopic, percutaneous, or surgical decompression. Chronic intestinal pseudo-obstruction (CIPO) is a more rare form of pseudo-obstruction, usually causing early satiety, nausea, bloating, and distension.  Causes are usually infectious, metabolic, neurologic, autoimmune, or idiopathic.

Chronic cerebral hypoperfusion (CCH) contributes to vascular dementia (VaD) through intestinal dysfunction, reduced hippocampal short-chain fatty acids (SCFAs), neuroinflammation, mitochondrial dysfunction, and neuronal apoptosis. This study investigated whether fructooligosaccharides (FOS) alleviate CCH-induced cognitive and intestinal dysfunction and explored the potential involvement of SCFA-associated gut-brain signaling. CCH was induced in male Sprague-Dawley rats by bilateral common carotid artery occlusion (BCCAO). Rats were assigned to Sham, BCCAO, Sham + FOS, and BCCAO + FOS groups, and FOS were administered orally at 14 g/kg/day for four weeks. Cognitive function, intestinal barrier integrity, hippocampal SCFAs, neuroinflammation, apoptosis, and mitophagy were assessed. Primary neurons exposed to hypoxia were treated with SCFAs to evaluate apoptosis and mitophagy. FOS improved locomotor activity, anxiety-like behavior, spatial learning, and memory in BCCAO rats. FOS restored colonic goblet cells (P < 0.001) and ZO-1 expression (P < 0.01) and reduced intestinal TNF-α, IL-6, IL-17, and IL-33 levels (P < 0.05). In the hippocampus, FOS increased acetate and valerate levels (P < 0.05), decreased TNF-α and IL-33 expression, reduced cleaved caspase-3 (P < 0.01), preserved NeuN-positive neurons (P < 0.05), and alleviated mitochondrial injury. BCCAO-induced increases in P62, LC3B, Beclin-1, BNIP3, and NIX (P < 0.05) were attenuated by FOS, whereas PINK1/Parkin signaling remained unchanged. In primary neurons, SCFAs reduced CoCl2-induced apoptosis and BNIP3/NIX activation and preserved MAP2/Tau-positive neuronal morphology. FOS alleviated intestinal barrier dysfunction, neuroinflammation, neuronal apoptosis, and cognitive impairment after CCH. These effects were accompanied by increased hippocampal SCFAs and changes in BNIP3/NIX-related mitophagy, supporting a potential role for SCFA-associated gut-brain signaling in FOS-mediated neuroprotection.

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is a multisystemic disorder that can present with diverse clinical features, including cardiomyopathy and chronic intestinal pseudo-obstruction. However, diagnosing MELAS can be challenging when its manifestations overlap with other genetic syndromes, leading to diagnostic anchoring and potential mismanagement.

The case series involves 4 patients aged 60-71 years with unusual cecal pathology: mobile cecum, cecal volvulus, and cecal bascule. The clinical manifestations were diverse, showing chronic and intermittent abdominal pain on 1 side, and acute intestinal obstruction on the other, indicating the diagnosis challenge of the conditions. The diagnosis in all cases relied on computed tomography, but there was 1 presentation that was first thought to be gastric distention, underlining the importance of meticulous radiologic evaluation. One patient experienced postoperative volvulus, and another incidental appendiceal neoplasm. Three patients needed surgical management which consisted of open hemicolectomy and robotic-assisted ileocolic resection whereas 1 was treated conservatively. The importance of having high index of suspicion of cecal pathology in patients who have unexplained symptoms and are either elderly or postoperative is emphasized in this series. Detection during CT early and timely management to avoid ischemia, perforation, and negative outcomes is crucial.

Background/Objectives: Acute mesenteric ischemia (AMI) resembles non-vascular intestinal ischemia (NSII) and non-specific abdominal pain (NSAP) at presentation yet carries 50-80% mortality. We tested how well admission data separate these conditions and predict in-hospital mortality, the primary endpoint. Methods: We studied 197 consecutive adults (2015-2021): AMI (n = 61), NSII (n = 62), and NSAP controls (n = 74). Admission demographics, comorbidities, laboratory markers, the Mannheim Peritonitis Index (MPI), and APACHE-II were compared by ROC/DeLong analysis and multivariable logistic regression (STROBE). Results: AMI had more atrial fibrillation, thromboembolism, chronic kidney disease (CKD), and dyslipidemia (p ≤ 0.028) and higher in-hospital mortality than NSII (47.5% vs. 16.1%; p < 0.001). Inflammatory ratios, lactate, and albumin separated AMI from NSAP well (AUC up to 0.93) but from NSII modestly (lactate, 0.672). APACHE-II (AUC 0.861) and MPI (0.810) predicted in-hospital death and improved combined (0.897; DeLong p = 0.014). Independent predictors were MPI (adjusted odds ratio 1.14, 95% CI 1.06-1.23), CKD (3.72, 1.25-12.10), and arterial lactate (1.20, 1.03-1.45). Conclusions: A composite admission panel was internally consistent but hypothesis-generating, not a triage tool ready for clinical use. CT angiography remains essential, since these markers cannot separate vascular from non-vascular ischemia; prospective external validation is required.

Mesenteric artery thrombosis (MAT) is a condition involving occlusion of the arterial vascular supply of the intestinal system. It is a severe and potentially fatal illness typically of the superior mesenteric artery (SMA),  which provides the primary arterial supply to the small intestine and ascending colon.[1] The occlusion may occur due to in-situ thrombosis of the vessel, most commonly due to underlying atherosclerotic disease, or embolic occlusion from a distant source, as may occur in patients with atrial fibrillation. The condition possesses a high mortality rate, and prompt recognition and treatment are of utmost importance.  This articles will focus on acute arterial occlusion of the superior mesenteric artery. Other mesenteric vascular entities including chronic intestinal ischemia, mesenteric veno-occlusive disease, SMA syndrome, etc., are reviewed separately. 

Vascular cognitive impairment (VCI) is a major form of dementia with a complex pathogenesis. Emerging evidence indicates a strong interaction between intestinal mucosal barrier integrity and neuroinflammation, which has been proposed as a candidate contributor in VCI progression. This review comprehensively reviews the initiation and amplification of neuroinflammation in chronic cerebral ischemia. It highlights how impairment of the intestinal mucosal barrier, gut microbiota dysbiosis, and translocation of microbial metabolites contribute to central neuroinflammation via circulatory and neural pathways, suggesting a potential self-sustaining pathological cycle within the gut-brain axis. Furthermore, we analyze the underlying molecular mechanisms, critique current limitations, and suggest promising directions for future research.

Intestinal malrotation is a congenital anomaly of midgut rotation and fixation that typically manifests in infancy, with most cases diagnosed within the first year of life. Although rare, accounting for ~0.2%-0.5% of all malrotation cases, intestinal malrotation can present in adults, with nonspecific symptoms that may delay diagnosis. We report the case of a 48-year-old male with a four-year history of recurrent colicky abdominal pain and non-bilious vomiting that progressively worsened over the preceding three months, with vomiting increasing to nearly ten episodes daily. A contrast-enhanced abdominal computed tomography demonstrated marked dilatation of the proximal duodenum with a transition point at the mid-duodenum suggestive of a partial obstruction. Upper gastrointestinal fluoroscopy confirmed midgut malrotation with an incomplete volvulus. The patient subsequently underwent a Ladd procedure. Adult midgut malrotation should be considered in patients with chronic, unexplained abdominal pain and vomiting. Early diagnosis is essential to prevent life-threatening complications such as a volvulus and bowel ischemia.

We report a case of acute-on-chronic mesenteric ischemia (AOCMI) in an 85-year-old woman presenting with progressive postprandial abdominal pain, signs of panperitonitis, and free intraperitoneal air. Emergency laparotomy revealed diffuse small bowel ischemia without clear demarcation, reflecting acute ischemia superimposed on chronic hypoperfusion. Intraoperative indocyanine green (ICG) fluorescence angiography enabled selective resection of nonviable bowel, preserving potentially salvageable intestine. Delayed recognition of a nine-month history of chronic mesenteric ischemia (CMI) prompted staged endovascular revascularization of the superior mesenteric artery (SMA). Despite transient short bowel syndrome (SBS) requiring parenteral nutrition, bowel continuity was ultimately restored. This case highlights the diagnostic challenge of AOCMI and demonstrates that selective bowel salvage combined with staged multidisciplinary intervention can preserve bowel function and quality of life even in elderly high-risk patients.

The case of an 88-year-old male patient with progressive, unintentional weight loss is reported. The condition was subjectively asymptomatic and subsequently completely reversible. Following a comprehensive internal medicine examination, chronic mesenteric ischemia due to arteriosclerosis was identified as the cause and treated interventionally. Over time, the patient experienced significant weight gain, a comparatively rare phenomenon in very old geriatric patients. Broad and targeted investigation of the cause and interventional therapies are safe and feasible even in old age.

Sympathetic overactivity and gut microbiota dysbiosis drive chronic heart failure (CHF) progression. This study explored the associations of mesenteric denervation (MDN) with cardioprotection and potential involvement of the nerve-microbiota-heart axis in MI-induced CHF mice. C57BL/6 mice were randomized into control, CHF, and CHF_MDN groups. CHF was induced by LAD ligation, and MDN was performed via phenol ablation of the superior mesenteric artery. MDN was associated with suppressed mesenteric sympathetic activity, improved left ventricular ejection fraction, and reduced myocardial fibrosis and serum BNP. MDN correlated with restoration of colonic tight junction protein expression, reduced myocardial NLRP3 inflammasome activation, and decreased systemic inflammation (LPS, TNF-α, IL-6). 16S rRNA sequencing showed MDN reshaped gut microbiota (decreased F/B ratio, increased facultative anaerobes). Untargeted metabolomics identified 30 differential metabolites in CHF_MDN mice; MDN reduced pro-inflammatory metabolites (hippuric acid, deoxycholic acid) and increased metabolites linked to energy metabolic reprogramming (2-hydroxybutyric acid, ketoleucine, acetylglycine). Integrated analysis revealed that Campylobacterota and Halobacterota (altered by MDN) correlated with sarcosine and linoleic acid. MDN improves cardiac function in MI-induced CHF, alongside inhibition of mesenteric sympathetic activity, restoration of intestinal barrier function, reduction of inflammation, and modulation of gut microbiota and metabolic profiles. These findings suggest the nerve-microbiota-heart axis as a potential therapeutic target.