Tuberculous aortitis with jejunal artery mycotic pseudoaneurysm managed by endovascular coil embolisation.

Mycotic aneurysm in a visceral artery due to tuberculosis (TB) is a rare occurrence. Imaging plays a critical role in its diagnosis. Over the last few years, minimally invasive interventional radiological treatment has replaced more invasive surgical procedures. Here, we report a case presenting with abdominal pain, diagnosed with jejunal artery mycotic pseudoaneurysm (PSA) secondary to TB, managed by endovascular coiling. Coil embolisation of the superior mesenteric artery branch was done using three coils, closing both the front door, back door and sac of the mycotic aneurysm. Visceral PSA following TB infection is rare and can be fatal if left untreated. Coil embolisation is a minimally invasive procedure with a high success rate and comparatively fewer complications.

Jejunal ischaemia following inferior mesenteric artery angioembolisation for type 2 endoleak.

We present a rare case of short-segment jejunal infarction following inferior mesenteric artery embolisation for type 2 endoleak in a patient who previously underwent endovascular repair of abdominal aortic aneurysm. Potential causes for the event might include thromboembolism or traumatic thrombosis of a jejunal branch of the superior mesenteric artery (SMA) caused by a buddy guide wire used to maintain the position of the long vascular sheath in the SMA hiatus. The condition was recognised on CT and treated with resection of the infarcted segment of the small bowel followed by primary anastomosis.

Mesenteric sparing approach for advanced nodal extent in small intestinal neuroendocrine tumors. Is there a limit to the vascular resection in order to avoid creating a short small bowel syndrome? An anatomic research study.

PURPOSE: By selectively perfusing the first three jejunal arteries (JA), we aim to assess the individual perfusion length of small bowel (SB) and its impact on nodal resection in stage III-up small-intestinal neuroendocrine tumors (SI-NET). METHODS: Our anatomical research protocol implies a midline laparotomy and three measures of the SB length. We then perform a classical anterior approach of the superior mesenteric vessels. We carry on with the complete dissection and checking of the superior mesenteric artery (SMA) in order to identify the first three JA. Then we selectively perfuse each artery with colored latex solutions and measure the length of small bowel perfused respectively. RESULTS: We conducted our protocol on six cadaveric subjects. Mean(SD) SB length was 413(5.7), 535(13.2), 485(15), 353(25.1), 730(17.3) and 525(16° cm respectively from subject one to six. Most JA originated from the left side of the SMA. The first JA originated from its posterior wall in two subjects. Mean(SD) distance of origin of the first three JA was 4.6(1.3)cm, 6(1.1)cm and 7.1(0.9)cm respectively. Mean(SD) diameter of SMA was 10.8(3.3)mm. Mean diameter of the three first JA was 4(1.4)mm, 4(1.5)mm and 5(1.2)mm respectively. Mean(SD) SB length perfused by first and second JA was 224(14.9)cm, 175(8.6)cm, 238.3(7.6)cm, 84.3(5.1)cm, 233.3(5.8)cm and 218.3(10.4)cm respectively from subject one to six. CONCLUSION: We observed a trend suggesting that the first and second JA may sustain a SB length beyond the viable 1.5 m limit, implying the feasibility of stage III-up SI-NET resection with just two JA.

Outcomes of endoscopic sclerotherapy for jejunal varices at the site of choledochojejunostomy (with video): Three case reports.

BACKGROUND: Hemorrhage associated with varices at the site of choledochojejunostomy is an unusual, difficult to treat, and often fatal manifestation of portal hypertension. So far, no treatment guidelines have been established. CASE SUMMARY: We reported three patients with jejunal varices at the site of choledochojejunostomy managed by endoscopic sclerotherapy with lauromacrogol/α-butyl cyanoacrylate injection at our institution between June 2021 and August 2023. We reviewed all patient records, clinical presentation, endoscopic findings and treatment, outcomes and follow-up. Three patients who underwent pancreaticoduodenectomy with a Whipple anastomosis were examined using conventional upper gastrointestinal endoscopy for suspected hemorrhage from the afferent jejunal loop. Varices with stigmata of recent hemorrhage or active hemorrhage were observed around the choledochojejunostomy site in all three patients. Endoscopic injection of lauromacrogol/α-butyl cyanoacrylate was carried out at jejunal varices for all three patients. The bleeding ceased and patency was observed for 26 and 2 months in two patients. In one patient with multiorgan failure and internal environment disturbance, rebleeding occurred 1 month after endoscopic sclerotherapy, and despite a second endoscopic sclerotherapy, repeated episodes of bleeding and multiorgan failure resulted in eventual death. CONCLUSION: We conclude that endoscopic sclerotherapy with lauromacrogol/α-butyl cyanoacrylate injection can be an easy, effective, safe and low-cost treatment option for jejunal varicose bleeding at the site of choledochojejunostomy.

The Ischemic Tolerance up to Four Hours of Free Jejunum Flap: A Retrospective Cohort Study.

BACKGROUND: While free jejunum transfer (FJT) following total pharyngo-laryngo-esophagectomy (TPLE) is a reliable reconstruction technique, the jejunum flap is viewed as more susceptible to ischemia than a standard free flap. Animal studies have indicated that the jejunum can tolerate ischemia for as little as 2 to 3 hours. Clinical studies also reported increased complications after the FJT with more than 3 hours of ischemia. Traditionally, our institution has carried out FJT with an initial intestinal anastomosis, followed by a vascular anastomosis, which often results in extended jejunal ischemia time. In this study, we retrospectively examined the actual tolerance of the jejunum to ischemia, considering perioperative complications and postoperative dysphagia. METHODS: We retrospectively studied 402 consecutive cases involving TPLE + FJT. Patients were divided into five groups based on jejunum ischemia time (∼119 minutes, 120∼149 minutes, 150∼179 minutes, 180∼209 minutes, 210 minutes∼), with each variable and result item compared between the groups. Univariate and multivariate analyses were conducted to identify independent factors influencing the four results: three perioperative complications (pedicle thrombosis, anastomotic leak, surgical site infection) and dysphagia at 6 months postoperatively. RESULTS: The mean jejunal ischemia time was 164.6 ± 28.4 (90-259) minutes. When comparing groups divided by jejunal ischemia time, we found no significant differences in overall outcomes or complications. Our multivariate analyses indicated that jejunal ischemia time did not impact the three perioperative complications and postoperative dysphagia. CONCLUSION: In TPLE + FJT, a jejunal ischemia time of up to 4 hours had no effect on perioperative complications or postoperative dysphagia. The TPLE + FJT technique, involving a jejunal anastomosis first followed by vascular anastomosis, benefits from an easier jejunal anastomosis but suffers from a longer jejunal ischemia time. However, we found that ischemia time does not pose significant problems, although we have not evaluated the effects of jejunal ischemia extending beyond 4 hours.

Jejunal Dieulafoy lesion with intraintestinal calcification on computerized tomography: A case report.

RATIONALE: A Dieulafoy lesion is a rare cause of gastrointestinal (GI) bleeding, especially in the jejunum, and the presence of calcifications on CT might be suspicious of the diagnosis. PATIENT CONCERNS: We describe a 72-year-old woman with anemia and melena. Hemoglobin was 6.0 g/dL, and the stools were positive for occult blood (4+). Blood pressure was 116/54 mm Hg. Physical examination showed pale face and pitting edema in both lower limbs. Abdominal computerized tomography showed calcification in the small intestine of the left lower abdomen. Capsule endoscopy showed a blood clot. DIAGNOSES: Dieulafoy lesion. INTERVENTIONS: Single balloon endoscopy was performed via the oral approach and showed a blood clot on the suspected submucosal tumor of jejunum. A hemostatic clip was placed at the base of the lesion to allow the surgeon to locate it during the operation. Laparoscopy was performed, and the lesion was resected. OUTCOMES: The postoperative pathology showed a Dieulafoy lesion. The lower extremity edema subsided. GI bleeding did not recur over 1 year of follow-up, and hemoglobin was 12.2 g/dL. A Dieulafoy lesion is a rare cause of GI bleeding, and it is even rarer in the jejunum. LESSONS: A Dieulafoy lesion does not have special imaging features, but the presence of calcifications in the small intestine on computerized tomography might be suspicious of the diagnosis. When endoscopic treatment is difficult, surgical treatment could be considered.

Ischaemic postconditioning reduces apoptosis in experimental jejunal ischaemia in horses.

BACKGROUND: Ischaemic postconditioning (IPoC) refers to brief periods of reocclusion of blood supply following an ischaemic event. This has been shown to ameliorate ischaemia reperfusion injury in different tissues, and it may represent a feasible therapeutic strategy for ischaemia reperfusion injury following strangulating small intestinal lesions in horses. The objective of this study was to assess the degree cell death, inflammation, oxidative stress, and heat shock response in an equine experimental jejunal ischaemia model with and without IPoC. METHODS: In this randomized, controlled, experimental in vivo study, 14 horses were evenly assigned to a control group and a group subjected to IPoC. Under general anaesthesia, segmental ischaemia with arterial and venous occlusion was induced in 1.5 m jejunum. Following ischaemia, the mesenteric vessels were repeatedly re-occluded in group IPoC only. Full thickness intestinal samples and blood samples were taken at the end of the pre-ischaemia period, after ischaemia, and after 120 min of reperfusion. Immunohistochemical staining or enzymatic assays were performed to determine the selected variables. RESULTS: The mucosal cleaved-caspase-3 and TUNEL cell counts were significantly increased after reperfusion in the control group only. The cleaved-caspase-3 cell count was significantly lower in group IPoC after reperfusion compared to the control group. After reperfusion, the tissue myeloperoxidase activity and the calprotectin positive cell counts in the mucosa were increased in both groups, and only group IPoC showed a significant increase in the serosa. Tissue malondialdehyde and superoxide dismutase as well as blood lactate levels showed significant progression during ischaemia or reperfusion. The nuclear immunoreactivity of Heat shock protein-70 increased significantly during reperfusion. None of these variables differed between the groups. The neuronal cell counts in the myenteric plexus ganglia were not affected by the ischaemia model. CONCLUSIONS: A reduced apoptotic cell count was found in the group subjected to IPoC. None of the other tested variables were significantly affected by IPoC. Therefore, the clinical relevance and possible protective mechanism of IPoC in equine intestinal ischaemia remains unclear. Further research on the mechanism of action and its effect in clinical cases of strangulating colic is needed.

Larazotide acetate induces recovery of ischemia-injured porcine jejunum via repair of tight junctions.

Intestinal ischemia results in mucosal injury, including paracellular barrier loss due to disruption of tight junctions. Larazotide acetate (LA), a small peptide studied in Phase III clinical trials for treatment of celiac disease, regulates tight junctions (TJs). We hypothesized that LA would dose-dependently hasten recovery of intestinal ischemic injury via modulation of TJs. Ischemia-injured tissue from 6-8-week-old pigs was recovered in Ussing chambers for 240-minutes in the presence of LA. LA (1 µM but not 0.1 µM or 10 µM) significantly enhanced transepithelial electrical resistance (TER) above ischemic injured controls and significantly reduced serosal-to-mucosal flux LPS (P<0.05). LA (1 µM) enhanced localization of the sealing tight junction protein claudin-4 in repairing epithelium. To assess for the possibility of fragmentation of LA, an in vitro enzyme degradation assay using the brush border enzyme aminopeptidase M, revealed generation of peptide fragments. Western blot analysis of total protein isolated from uninjured and ischemia-injured porcine intestine showed aminopeptidase M enzyme presence in both tissue types, and mass spectrometry analysis of samples collected during ex vivo analysis confirmed formation of LA fragments. Treatment of tissues with LA fragments had no effect alone, but treatment with a fragment missing both amino-terminus glycines inhibited barrier recovery stimulated by 1 µM LA. To reduce potential LA inhibition by fragments, a D-amino acid analog of larazotide Analog #6, resulted in a significant recovery response at a 10-fold lower dose (0.1 µM) similar in magnitude to that of 1 µM LA. We conclude that LA stimulates repair of ischemic-injured epithelium at the level of the tight junctions, at an optimal dose of 1 µM LA. Higher doses were less effective because of inhibition by LA fragments, which could be subverted by chirally-modifying the molecule, or microdosing LA.

Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death.

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson's trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

Technical details of a left-side approach to the superior mesenteric artery during pancreaticoduodenectomy.

BACKGROUND AND PURPOSE: To describe the procedure for a left-side approach to the superior mesenteric artery (SMA) during pancreaticoduodenectomy (PD) in a cadaveric study. OPERATIVE PROCEDURE: After dividing the upper jejunum, the jejunal artery (JA) is followed to its origin. At the cranial side of the JA, the mesojejunum to be dissected is detached from the ventral to the dorsal side and from the peripheral to the origin side of the SMA. The inferior pancreatoduodenal artery (IPDA), which is usually the common trunk of the IPDA and the first JA, is able to be visualized at the cranio-dorsal side of the origin of the JA. After cutting the IPDA, the mesojejunum can be detached from the SMA from the dorsal aspect to the right side. Subsequently, the pancreas head is dissected easily from the right aspect of the SMA. CONCLUSION: This left-side approach to the SMA may become a standard procedure.

Arteriovenous malformation as a cause for acute confusion and gastrointestinal bleeding in a primigravida pregnancy.

Acute confusion in pregnancy is generally uncommon, given the relatively young and healthy population obstetricians care for. We present an unusual and rare case of acute confusion in a term pregnancy with antecedent history of gastrointestinal (GI) bleeding. A primigravida with no medical history of note, was found to have a haemoglobin of 67 g/L at booking and was commenced on oral iron supplementation. In the third trimester, she presented with haematochezia and had several admissions, requiring 18 units of red blood cells during her pregnancy. At term, she was admitted with acute confusion and GI bleeding, and was subsequently delivered by caesarean section to facilitate ongoing investigation and management of her symptoms. She was diagnosed postnatally with an arteriovenous malformation in the jejunum which required interventional radiology and surgical management for symptom resolution. Her confusion was attributed to hyperammonaemic levels secondary to her high protein load.

Hypothermia induces opposite response in vascular and non-vascular smooth muscles.

BACKGROUND AND AIM: The mechanism of cooling-induced response of smooth muscles remains little understood despite the increasing importance given to it in recent years. The aim of this study was to examine the possibility of releasing a relaxant or a contractile substance during cooling from vascular and non-vascular smooth muscles. METHODS: Assessing the effect of cooling for two different smooth muscles together, vascular (aorta or carotid) which induced relaxation, and non-vascular (jejunum or bladder) which induced contraction. Hanging a pair of smooth muscle strips from different body organs in the same organ bath filled with Krebs solution, each strip was connected to its own transducer and recorder and stepwise cooling was applied. Recordings of isometric tension using organ-bath techniques. RESULTS: Step-wise cooling (37 °C-4 °C) of aorta and carotid smooth muscle preparations induced reproducible graded relaxation while jejunum and bladder preparations induced reproducible graded tonic contractions, inversely proportional to temperature. The responses of all the smooth muscle preparations were the same magnitude either alone or as a pair in the organ bath. Cooling abolished rhythmic smooth muscle activity of jejunum and bladder. Cooling-induced contraction was reduced by incubation in Ca2+-free solution. The effect of cooling either relaxation or contraction was not enhanced or attenuated by the presence of the two different smooth muscles with opposite response in the same organ bath, proving the absence of a relaxant or a contractile substance released during cooling. CONCLUSIONS: Cooling of aorta and carotid artery induced relaxation while jejunum and bladder induced contraction. The response to cooling is inversely proportional to the temperature. There was neither a relaxant nor a contractile substance released from vascular or non-vascular smooth muscles during cooling. Our study suggested that the effect of cooling is through a thermal receptor with two subtype one in the vascular smooth muscle (deep blood vessels) which induces relaxation, and the second in non-vascular smooth muscles (non-vascular organs) that induces contraction and the responses depend on extracellular calcium.

Elevated postischemic tissue injury and leukocyte-endothelial adhesive interactions in mice with global deficiency in caveolin-2: role of PAI-1.

Ischemia/reperfusion (I/R)-induced rapid inflammation involving activation of leukocyte-endothelial adhesive interactions and leukocyte infiltration into tissues is a major contributor to postischemic tissue injury. However, the molecular mediators involved in this pathological process are not fully known. We have previously reported that caveolin-2 (Cav-2), a protein component of plasma membrane caveolae, regulated leukocyte infiltration in mouse lung carcinoma tumors. The goal of the current study was to examine if Cav-2 plays a role in I/R injury and associated acute leukocyte-mediated inflammation. Using a mouse small intestinal I/R model, we demonstrated that I/R downregulates Cav-2 protein levels in the small bowel. Further study using Cav-2-deficient mice revealed aggravated postischemic tissue injury determined by scoring of villi length in H&E-stained tissue sections, which correlated with increased numbers of MPO-positive tissue-infiltrating leukocytes determined by IHC staining. Intravital microscopic analysis of upstream events relative to leukocyte transmigration and tissue infiltration revealed that leukocyte-endothelial cell adhesive interactions in postcapillary venules, namely leukocyte rolling and adhesion were also enhanced in Cav-2-deficient mice. Mechanistically, Cav-2 deficiency increased plasminogen activator inhibitor-1 (PAI-1) protein levels in the intestinal tissue and a pharmacological inhibition of PAI-1 had overall greater inhibitory effect on both aggravated I/R tissue injury and enhanced leukocyte-endothelial interactions in postcapillary venules in Cav-2-deficient mice. In conclusion, our data suggest that Cav-2 protein alleviates tissue injury in response to I/R by dampening PAI-1 protein levels and thereby reducing leukocyte-endothelial adhesive interactions.NEW & NOTEWORTHY The role of caveolin-2 in regulating ischemia/reperfusion (I/R) tissue injury and the mechanisms underlying its effects are unknown. This study uses caveolin-2-deficient mouse and small intestinal I/R injury models to examine the role of caveolin-2 in the leukocyte-dependent reperfusion injury. We demonstrate for the first time that caveolin-2 plays a protective role from the I/R-induced leukocyte-dependent reperfusion injury by reducing PAI-1 protein levels in intestinal tissue and leukocyte-endothelial adhesive interactions in postcapillary venules.

Recurrent gastrointestinal bleeding due to jejunal artery vasculitis as debut presentation of granulomatosis with polyangiitis.

Granulomatosis with polyangiitis (GPA) is characterised by systemic necrotising vasculitis of small arteries and veins with multitude of organ involvement, with the most common being the upper and lower respiratory tract and renal system. Gastrointestinal involvement is a rare late manifestation with a high mortality rate and usually results in intestinal perforation. Our patient presented with gastrointestinal bleeding secondary to jejunal artery vasculitis. Gastrointestinal bleeding as initial presentation of GPA is very rarely documented. CT mesenteric angiogram is helpful for the localisation of bleed in these cases. In case of refractory bleeding, surgical excision is required.

Ischemic jejunal stricture in patients with extrahepatic portal vein obstruction.

Ischemic jejunal stricture due to mesenteric vein thrombosis (MVT) rarely occurs in patients with extrahepatic portal vein obstruction (EHPVO). This is because the thrombus often occludes only a short segment of superior mesenteric vein adjacent to splenoportal confluence, facilitating development of collateral veins that protect bowel from ischemia. However, ischemic strictures can develop when the thrombus involves jejunal veins, venous arcades or vasa recta. We report three patients with EHPVO, who developed jejunal strictures due to MVT. They presented with symptoms of proximal bowel obstruction. Two of these patients had evidence of recurrent deep vein thrombosis (DVT), suggesting possibility of an underlying prothrombotic state. One of them had completely occluded bilateral iliac veins and inferior vena cava following DVT, 10 years ago. At the same time, he was identified as having a portal cavernoma. Contrast-enhanced computed tomography showed portal cavernoma together with MVT in all the patients. The thrombus was identified in the jejunal veins in two patients and in the entire superior mesenteric vein up to splenic vein in one patient. All three patients were found to have a tight concentric stricture involving a long length of proximal jejunum. Two patients required urgent surgical intervention and one died.

The distribution of the jejunal arteries in the cat.

The arterial supply of the cat jejunum was studied by gross dissection and polyurethane corrosion cast. The results showed that the jejunal arteries, which originate from the cranial mesenteric artery, varied from 5 to 15 in number. Their number was independent of the length of the cranial mesenteric artery as well as of the length of the jejunum. These arteries divided into branches giving rise to a series of orders of division from a minimum of 1 to a maximum of 7. The last orders of division terminated in a series of anastomosing arcades which resulted in a marginal artery coursing only a few millimeters from the mesenteric margin of the jejunum. This artery gave rise to straight arteries (vasa recta), whose mean number was 450 ± 60. According to their length, the vasa recta can be differentiated into short (vasa brevia) and long (vasa longa) branches. The vasa brevia ended branching into the mesenteric side of the jejunum whereas the vasa longa coursed beneath the serosa on the lateral jejunal surfaces, and reached the antimesenteric border. During their course, the vasa recta ramified and anastomosed with each other. Numerous antimesenteric anastomoses between opposing vasa longa were also observed. Based on the literature consulted, due to the large number of vasa recta (approximately one vessel per 2.9 mm of jejunal length) and the rich anastomotic network, the cat jejunum might have a better intramural distribution of blood flow and would seem less predisposed to ischemic phenomena than that of other mammals.

Effects of Norepinephrine on the Intestinal Vascular System in Rabbits With Endotoxic Shock.

ABSTRACT: We hypothesized that jejunal mucosal tissue blood flow would decrease following norepinephrine (NE) administration in endotoxic shock. We aimed of this study to evaluate changes in superior mesenteric venous (SMV) blood flow and jejunal mucosal tissue blood flow of the intestinal vascular system over time by administration of NE in rabbits with endotoxic shock. We created four groups (n = 8 each): control group, lipopolysaccharide (LPS; 1 mg/kg) group, NE (2 µg/kg/min) group, and LPS+NE group. As indicators of circulation, we measured mean arterial blood pressure (MAP), cardiac output, SMV blood flow, and jejunal mucosal tissue blood flow every 30 min from 0 to 240 min. The drop in MAP observed in the LPS group was suppressed by NE administration. SMV blood flow dropped temporarily with LPS administration, but then rose thereafter. Administration of NE to the LPS group suppressed the transient decline in SMV blood flow, which did not drop below that of the control group. In the LPS group, jejunal mucosal tissue blood flow transiently dropped and then rose, reflecting the pattern in SMV blood flow. In the LPS+NE group, however, although there was no drop in SMV blood flow, jejunal mucosal tissue blood flow remained low. An interaction between NE and LPS was observed regarding jejunal mucosal tissue blood flow from 90 to 180 min (P = 0.033). We showed that NE maintained MAP and SMV blood flow but decreased jejunal mucosal tissue blood flow. In a rabbit model of endotoxic shock, NE had a negative effect on jejunal mucosal tissue blood flow.