Bupropion is an atypical antidepressant that inhibits norepinephrine and dopamine reuptake. Poison control data demonstrate toxic effects at doses as low as 600 mg. Common adverse effects of overdose include tachycardia, seizures, and cardiac arrhythmias. Gastrointestinal complications are rarely described. Our case shows an 18-year-old male presented to the emergency department after witnessed seizure-like activity. Family reported ingestion of approximately thirty 300-mg sustained-release bupropion tablets 4-5 hours prior to presentation. On arrival, he required endotracheal intubation for airway protection. Sedation was initiated with propofol and fentanyl; fentanyl was rapidly discontinued. Given delayed presentation and sustained-release ingestion, whole bowel irrigation was initiated with nasogastric administration of 50 g activated charcoal followed by 6 L polyethylene glycol-electrolyte solution. Subcutaneous methylnaltrexone (12 mg) was administered to reverse potential opioid-related ileus without effect. Worsening abdominal distension prompted contrast-enhanced computed tomography of the abdomen and pelvis, which demonstrated diffuse fluid-filled colonic distension with distal small bowel dilation and no evidence of mechanical obstruction or pill bezoar. Gastroenterology performed colonoscopic decompression with rectal tube placement. This resulted in successful decompression. The patient was extubated the following day with return of bowel function on post-decompression day two. In supratherapeutic states, bupropion exhibits anticholinergic properties through poorly understood mechanisms, which may impair intestinal motility. Colonic complications remain rare, with only isolated reports describing colonic ischemia or pseudo-obstruction associated with bupropion toxicity. Clinicians should consider severe gastrointestinal dysmotility when managing sustained-release bupropion toxicity.

Ischemic stroke is a devastating neurological disorder. Despite advances in acute reperfusion therapy, patients still face high risks of poor functional recovery and stroke recurrence, highlighting the urgent need to explore new pathological mechanisms and therapeutic targets. In recent years, the Gut-Brain Axis-a bidirectional communication network connecting the brain, gut, and gut microbiota-has provided a novel framework for understanding stroke pathophysiology. This review systematically summarizes how gut microbiota correlates with the progression of major stroke risk factors including hypertension and atherosclerosis, and explicitly distinguishes that most human observational data only support correlative associations, while causal evidence is largely limited to preclinical animal models. We further clarify the two-way communication pathway after stroke: cerebral ischemia impairs intestinal barrier function and causes microbial imbalance through autonomic and inflammatory responses; in turn, disturbed gut microbiota and metabolites correlate with aggravated brain damage and hindered repair via immune, metabolic, and neural signaling, mainly by regulating neuroinflammation and controlling key metabolites such as short-chain fatty acids and trimethylamine N-oxide. Based on these mechanisms, we comprehensively assess preclinical and clinical evidence of microbiota-targeted interventions, including dietary modification, probiotics, and fecal microbiota transplantation. We emphasize that existing clinical evidence is mostly derived from small-sample, single-center trials with inconsistent outcomes, and large-scale multicenter sham-controlled randomized controlled trials are mandatory before any routine clinical application can be recommended. We also discuss key challenges such as distinguishing causal relationships from correlative observations, bridging preclinical translational gaps, and addressing inter-individual heterogeneity across patient populations, and propose future translational research directions. Targeting the Gut-Brain Axis represents a promising preclinical systemic strategy for stroke prevention, acute care, and long-term rehabilitation, yet robust human validation is still lacking. This approach marks a fundamental paradigm shift in the field of stroke research, though overoptimistic clinical translation expectations should be avoided given the substantial unresolved translational limitations.

Acute mesenteric ischemia (AMI) is a life-threatening vascular emergency associated with high morbidity and mortality, largely because diagnosis is frequently delayed by non-specific clinical manifestations. Although computed tomography angiography (CTA) remains the diagnostic gold standard, considerable research has focused on identifying laboratory biomarkers that may facilitate earlier recognition and improve clinical decision-making. This narrative review summarizes the current evidence regarding routinely available and emerging laboratory biomarkers for the diagnosis of AMI. A comprehensive literature search was performed using PubMed/Medical Literature Analysis and Retrieval System Online (MEDLINE), Scopus, Web of Science, and the Cochrane Library, supplemented by manual review of reference lists. Routine laboratory markers, including leukocyte count, C-reactive protein (CRP), serum lactate, metabolic acidosis, D-dimer, amylase, phosphate, and procalcitonin (PCT), were evaluated alongside investigational biomarkers, such as intestinal fatty acid-binding protein (I-FABP), D-lactate, citrulline, ischemia-modified albumin (IMA), alpha-glutathione S-transferase (α-GST), interleukin-6 (IL-6), and cell-count-derived inflammatory indices. Current evidence demonstrates that no single laboratory biomarker possesses sufficient sensitivity and specificity to independently confirm or exclude AMI. Serum lactate and metabolic acidosis primarily reflect advanced intestinal injury and systemic hypoperfusion, rather than early ischemia, whereas D-dimer offers relatively high sensitivity but poor specificity. Enterocyte-specific biomarkers, particularly I-FABP, remain biologically attractive because they may detect early mucosal injury; however, inconsistent diagnostic performance, limited assay availability, and methodological heterogeneity have prevented routine clinical implementation. Emerging multimarker strategies integrating indicators of enterocyte injury, coagulation activation, inflammation, and tissue hypoperfusion may improve diagnostic accuracy but require prospective validation. At present, laboratory investigations should be regarded as complementary tools that increase clinical suspicion, assist with risk stratification, and reinforce the need for urgent CTA. They should never delay definitive imaging or revascularization when AMI is suspected. Further high-quality prospective studies are required to establish standardized biomarker panels capable of facilitating earlier diagnosis and improving patient outcomes.

Midgut volvulus is a life-threatening surgical emergency that most commonly presents during infancy, whereas delayed presentation in older children is uncommon and can be diagnostically challenging. An 11-year-old boy presented with acute abdominal pain, bilious vomiting, abdominal distension, and obstipation of two days' duration after four prior episodes of subacute intestinal obstruction over three years that had been managed conservatively. Contrast-enhanced computed tomography of the abdomen demonstrated the classical whirlpool sign, suggestive of midgut volvulus secondary to intestinal malrotation. Emergency exploratory laparotomy confirmed incomplete intestinal malrotation with a 180-degree clockwise midgut volvulus around a narrow mesenteric base. The bowel was congested but fully viable, without ischemia or necrosis. The patient underwent Ladd's procedure with counterclockwise derotation, division of Ladd's bands, widening of the mesenteric base, and bowel repositioning. Caecopexy and sigmoidopexy were also performed because of marked intraoperative mobility of the caecum and redundant sigmoid colon. Recovery was uneventful, and the patient was discharged on postoperative day 7. This case highlights the need to consider malrotation with volvulus beyond infancy in children with recurrent bilious vomiting or episodic intestinal obstruction, because early imaging and timely surgery can preserve bowel viability.

Colonoscopy is the gold standard for colorectal cancer screening, yet it carries the risk of iatrogenic perforation. A rare, hazardous subtype involves colonoscope incarceration and perforation within an inguinal hernia sac, mechanically driven by a "hinge effect" during withdrawal. The confined anatomical space often masks typical peritoneal signs, challenging diagnosis. A case is presented of a 71-year-old male (Body Mass Index: 24.2 kg/m[2]) undergoing a routine screening colonoscopy. Significant resistance occurred at the sigmoid colon during withdrawal, revealing a 1.0 cm full-thickness defect. First, an immediate endoscopic "damage control" strategy was employed using a through-the-scope purse-string suture technique combining a nylon endoloop with titanium clips to seal the defect acutely within 15 min. Crucially, an emergency contrast-enhanced Computed Tomography (CT) scan performed at Hour 1:00 post-event identified the perforated segment entrapped within a 4 cm left inguinal hernia sac, suggesting surgical exploration over exclusive conservative observation due to visceral ischemia risks. Consequently, the patient underwent laparoscopic partial sigmoidectomy of a 10 cm segment and high ligation of the hernia sac with internal ring closure under a stable 12 mmHg pneumoperitoneum (operative duration: 165 min; blood loss: 15 mL). The patient recovered uneventfully and was discharged on the seventh postoperative day. Quantified follow-up at 1 and 3 months confirmed complete functional recovery and zero recurrence. This case highlights the need for pre-procedural hernia assessment and suggests that a hybrid approach, pairing immediate endoscopic containment with planned surgical repair, may present a feasible alternative pathway for managing this rare emergency.

Background Early recognition of bowel strangulation in acute mechanical intestinal obstruction (AMIO) is critical but remains difficult when computed tomography (CT) is unavailable, delayed, or not immediately actionable. This study aimed to develop and internally validate a CT-independent bedside prediction score for estimating the risk of bowel strangulation in adults with AMIO in Taiz, Yemen. Materials and methods This 12-month prospective observational cohort study, with diagnostic and prediction-model components, enrolled consecutive adults with suspected AMIO at Al-Thawra Hospital and Al-Jumhuri General Teaching Hospital in Taiz, Yemen. Clinical, laboratory, imaging, operative, and outcome data were recorded prospectively. Final strangulation was defined by operative evidence of bowel ischemia, gangrene, necrosis, nonviability, or resection for compromised bowel; successful conservative resolution without later evidence of bowel compromise was classified as non-strangulated. A CT-independent Strangulated Intestinal Obstruction (SIO) score was derived from a five-predictor logistic model and internally validated with 1,000 bootstrap resamples. Results Of 230 adults, 212/230 (92.2%) underwent surgery, and 109/212 (51.4%) had intraoperative strangulation. The complete-case prediction cohort included 226 patients. The final score retained pain changing to persistent, abdominal distension, tenderness grade, neutrophilia greater than 75%, and systemic inflammatory response syndrome (SIRS) status. The apparent area under the receiver operating characteristic curve (AUC) was 0.953, and the optimism-corrected area under the curve was 0.947. At a score of 7 or higher, sensitivity was 100/109 (91.7%), specificity was 92/117 (78.6%), positive predictive value was 100/125 (80.0%), negative predictive value was 92/101 (91.1%), and accuracy was 192/226 (85.0%). Observed strangulation risk was 1/76 (1.3%) in the low-risk category, 25/63 (39.7%) in the intermediate-risk category, and 83/87 (95.4%) in the high-risk category. Conclusion The score showed promising internal performance as an early triage and escalation aid in this resource-limited pathway. It should support, rather than replace, senior surgical judgment and requires external validation before routine use.

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 gut has a profound influence on the liver through their anatomical connection via the portal vein. During acute inflammation, gut tissue injury leads to increased barrier permeability, allowing the translocation of external contents that can affect hepatic function. Gut-liver crosstalk contributes to the pathophysiology of acute inflammatory disorders, such as sepsis, intestinal ischaemia-reperfusion, hepatitis and drug-induced liver injury. This organ-to-organ crosstalk is mediated by the microbiome, pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs) and various proinflammatory mediators. Different types of gut and liver resident cells as well as circulating cells also facilitate inflammatory gut-liver crosstalk. These cell types include intestinal epithelial and myeloid cells, Kupffer cells, sinusoidal endothelial cells, hepatic stellate cells, hepatocytes, lymphocytes and neutrophils. PAMPs and DAMPs activate pattern recognition receptors, such as Toll-like receptors, on various cells, leading to proinflammatory signal transduction, including NFκB activation, cytokine and chemokine production, and NETosis. Collectively, these soluble and cellular factors exacerbate acute inflammation and tissue injury via the gut-liver axis, leading to poor outcomes in critically ill patients. Potential therapeutic interventions for this deadly clinical condition include modulation of the microbiome and pharmacological inhibition of proinflammatory mediators and cellular interactions. In this article we review the pathophysiology of inflammatory gut-liver crosstalk and potential therapeutic interventions.

Meckel's diverticulum (MD) is one of the most common congenital anomalies of the gastrointestinal tract in children, although it may occasionally be detected in adults. It is typically located within 100 cm of the ileocecal valve in the distal ileum. The diverticulum varies in size and morphology; many patients remain asymptomatic throughout life. In children, the most common clinical presentation is painless gastrointestinal bleeding, followed by intestinal obstruction. Intussusception may also occur. Once complications develop, patients often present with acute abdomen. Failure to establish a timely diagnosis and initiate appropriate management may result in intestinal ischemia or even necrosis. Furthermore, acute intestinal obstruction may obscure the underlying pathology, increasing the risk of misdiagnosis or missed diagnosis on radiologic evaluation. We report a rare case of Meckel's diverticulum complicated by band adhesion resulting in internal hernia and small bowel obstruction, further associated with peritonitis and massive ascites. The diverticulum was located approximately 40 cm proximal to the ileocecal valve. A fibrous diverticular band adhered to adjacent bowel loops, forming a hernia orifice that caused obstruction of the neighboring small intestine and mesentery. The patient underwent surgical resection of the Meckel's diverticulum, partial ileal resection, and end-to-end ileo-ileal anastomosis. The procedure was uneventful, and postoperative recovery was satisfactory. Internal hernia caused by Meckel's diverticulum band adhesion with associated peritonitis and massive ascites is rare. This case broadens the differential diagnosis of pediatric intestinal obstruction without prior abdominal surgery.

We analyzed the effects of melatonin (MT) administered via rectal suppositories on the composition of the mucosa-associated and luminal microbiota of the distal colon and neurological status of Wistar rats under conditions of experimental acute ischemic stroke (EAIS). The animals received original 100-mg rectal suppositories containing 2.5 mg of MT every 24 h for 3 days. Neurological status was assessed using the Garcia scale and the limb placing test, while microbiota composition in the distal colon was determined using real-time PCR. In rats with EAIS, neurological deficit was observed, characterized by a significant decrease in the Garcia and limb placing scores. In parallel, changes in the colon microbiota were observed: appearance of Clostridioides difficile, Fusobacterium nucleatum, Enterobacter spp., and the disappearance of Enterococcus spp. The administration of original MT-containing rectal suppositories led to partial recovery of neurological deficit, as manifested by in an increase in the Garcia score and limb placing test performance, which was accompanied by the appearance of Bacteroides thetaiotaomicron and the disappearance of Cl. difficile in the colon microbiota. Correlation analysis demonstrated that the amelioration of the neurological deficit was accompanied by changes in the gut microbiota. The effect of MT in rectal suppositories on neurological status and the gut microbiota is attributed to its neuroprotective and bacteriostatic properties.