Treatment controversies in a rare case of a simultaneous branch retinal artery and vein occlusion secondary to hyperhomocysteinemia and hypertension

Dear Editor,Combined vascular occlusions involving retinal arteries and veins have been reported in the past. Combined occlusion of the central retinal vein （CRVO） and artery （CRAO）is well described;. Cilioretinal artery occlusion along with CRVO is frequently reported and is well characterized;.

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 choledochojejun-ostomy 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 pancre-aticoduodenectomy with a Whipple anastomosis were examined using conven-tional upper gastrointestinal endoscopy for suspected hemorrhage from the afferent jejunal loop.Varices with stigmata of recent hemorrhage or active he-morrhage 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 sclero-therapy,repeated episodes of bleeding and multiorgan failure resulted in eventual death.CONCLUSION We conclude that endoscopic sclerotherapy with lauromacrogol/α-butyl cyanoac-rylate injection can be an easy,effective,safe and low-cost treatment option for jejunal varicose bleeding at the site of choledochojejunostomy.

Anticoagulation therapy prevents portal-splenic vein thrombosis after splenectomy with gastroesophageal devascularization

AIM:To compare the incidence of early portal or splenic vein thrombosis(PSVT) in patients treated with irregular and regular anticoagulantion after splenectomy with gastroesophageal devascularization.METHODS:We retrospectively analyzed 301 patients who underwent splenectomy with gastroesophageal devascularization for portal hypertension due to cirrhosis between April 2004 and July 2010.Patients were categorized into group A with irregular anticoagulation and group B with regular anticoagulation,respectively.Group A(153 patients) received anticoagulant monotherapy for an undesignated time period or with aspirin or warfarin without low-molecular-weight heparin(LMWH) irregularly.Group B(148 patients) received subcutaneous injection of LMWH routinely within the first 5 d after surgery,followed by oral warfarin and aspirin for one month regularly.The target prothrombin time/international normalized ratio(PT/INR) was 1.25-1.50.Platelet and PT/INR were monitored.Color Doppler imaging was performed to monitor PSVT as well as the effectiveness of thrombolytic therapy.RESULTS:The patients' data were collected and analyzed retrospectively.Among the patients,94 developed early postoperative mural PSVT,including 63 patients in group A(63/153,41.17%) and 31 patients in group B(31/148,20.94%).There were 50(32.67%) patients in group A and 27(18.24%) in group B with mural PSVT in the main trunk of portal vein.After the administration of thrombolytic,anticoagulant and antiaggregation therapy,complete or partial thrombus dissolution achieved in 50(79.37%) in group A and 26(83.87%) in group B.CONCLUSION:Regular anticoagulation therapy can reduce the incidence of PSVT in patients who undergo splenectomy with gastroesophageal devascularization,and regular anticoagulant therapy is safer and more effective than irregular anticoagulant therapy.Early and timely thrombolytic therapy is imperative and feasible for the prevention of PSVT.

Ultrasound Diameter of the Portal Vein to Healthy Adult in Parakou (Benin)

Introduction: The portal vein (PVD) diameter is one of the predictive variables of portal hypertension. This diameter can differ according to the population. The objective of this study was to determine the PVD in a healthy adult population in Parakou using ultrasonography. Methods: A cross-sectional descriptive study was conducted in the medical imaging department of the Borgou and Alibori University-affiliated Hospitals in Parakou from July 1st to October 1st, 2019. The study population consisted of 201 healthy adults. The ultrasound diameter of the portal vein was measured at the level of the hepatic hilum on a cross-sectional epigastric view and on an oblique intercostal view. An association was sought between the PVD and sociodemographic and anthropometric factors. Results: The mean age was 28.97 ± 10.56 years and the sex ratio (M/F) was 0.79. The mean PVD in regular breathing (FB) was 9.83 ± 0.95 mm with a 95% confidence interval of [9.70;9.97], a 95th percentile of 11.49 mm with extremes of 7.50 mm and 12.23 mm. PVD was correlated with age, sex, weight, height and abdominal girth. After multiple linear regressions (r = 0.19), there was correlation between the PVD in normal breathing with age (p = 0.0090), weight (p = 0.0026), body mass index (p = 0.0171) and body surface (p = 0.004). Conclusion: A PVD greater in normal adults is less than 12 mm and seems to be correlated to the subject age, weight, body mass index and body surface. A more than 13 mm PVD should lead to the suspicion of portal vein hypertension in adults in our populations.

Correlations of portal hypertensive gastropathy of hepatitis B cirrhosis with other factors

Objective: To study the clinical relations of portal hy- pertensive gastropathy (PHG) of hepatitis B cirrho- sis to other factors. Methods: Three groups of subjects were studied pro- spectively at our hospital from March 2000 to March 2001: 159 hepatitis B cirrhotic patients with portal hypertension, 114 hepatitis B cirrhotic patients with- out portal hypertension, and 97 control subjects. Free portal vein pressure (FPP) was measured dur- ing surgery. Liver function was assessed by Pugh's modification of Child's criteria. The area of liver collagen fibrin was studied using color image analysis system. Esophageal varices were identified by Dagra- di grading. Gastric varices were identified according to Northern Italian Endoscopic Council (NIEC) grading. Hypersplenism was assessed with the reduc- tion of WBC, HGB and PLT. Hepatitis B virus in the gastric mucosa was detected by immunizing histo- chemistry. Helicobacter pylori (H. pylori) organisms were identified by rapid urease testing and/or exami- nation of the stained biopsy specimens (haematoxylin and eosin). To analyze the correlation between these endoscopic signs at the gastric level and other fac- tors. Results: The differences of FPP among the three groups (patients with grade Ⅰ, Ⅱ, and Ⅲ gastropa- thy) were not significant. There was no correlation between Child-Pugh classification grading and the se- verity of gastropathy (P=0. 153). The differences of the area of liver collagen fibrin among the three grade gastropathy were not statistically significant (P =0. 801). There was a significant difference in the prevalence of severe PHG among grade Ⅰ, Ⅱ, Ⅲ, Ⅳ and Ⅴ esophageal varices (P<0. 001). PHG was present in a similar percentage of patients with gas- tric varices compared with those without gastric vari- ces (P=0. 209). There was a significant difference in the severity between PHG and hypersplenism (P= 0. 003). Seven patients with PHG had no microscopic evidence of hepatitis B virus infection in the gastric wall. There was no correlation between Child-Pugh classification grading and infection of H. pylori (P= 0. 7491). Conclusions: The most important element causing PHG is the increased portal pressure as a prerequi- site. In addition, other factors may contribute to the development of PHG. PHG often occurs in patients with the presence of esophageal varices. There is a marked correlation between the severity of PHG and hypersplenism. Hepatitis B virus and H. pylori infec- tion are unlikely to be involved in the pathogenesis of PHG. The development of PHG is less influenced ei- ther by the severity of liver disease (Child-Pugh grade) and cirrhosis or by the presence or non pre- sence of gastric varices.

Nutcracker syndrome

The nutcracker phenomenon [left renal vein(LRV) entrapment syndrome] refers to compression of the LRV most commonly between abdominal aorta and superior mesenteric artery.Term of nutcracker syndrome(NCS) is used for patients with clinical symptoms associated with nutcracker anatomy.LRV entrapment divided into 2 types:anterior and posterior.Posterior and right-sided NCSs are rare conditions.The symptoms vary from asymptomatic hematuria to severe pelvic congestion.Symptoms include hematuria,orthostatic proteinuria,flank pain,abdominal pain,varicocele,dyspareunia,dysmenorrhea,fatigue and orthostatic intolerance.Existence of the clinical features constitutes a basis for the diagnosis.Several imaging methods such as Doppler ultrasonography,computed tomography angiography,magnetic resonance angiography and retrograde venography are used to diagnose NCS.The management of NCS depends upon the clinical presentation and the severity of the LRV hypertension.The treatment options are ranged from surveillance to nephrectomy.Treatment decision should be based on the severity of symptoms and their expected reversibility with regard to patient's age and the stage of the syndrome.

APPLICABILITY OF PROSTAGLANDIN E_1 INDIRECT PORTAL VEIN ANGIOGRAPHY IN PATIENTS WITH PORTAL HYPERTENSION

The imaging quality of the portal vein was obviously improved with prostaglandin E1 (PGE1) indirect portal vein digital subtraction angiography (DSA) in 23 cases. The time-density curve showed that the occurrence rate of opposite hepatic blood flow of splenic vein (SV) was the highest (17.4%). The total visualization rate of the left gastric vein (LGV) was 78.3%, and the visualization rate of the short gastric vein (SGV) was 36.4%. 38.9% of the LGV and all the SGV were visualized with indirect portal vein DSA through SA. Indirect portal vein angiography through superior mesenteric artery and that through splenic artery were of equal importance. In portal hypertension patients with hemorrhage of the digestive tract, when LGV and SGV could not be visualized in PGE1 indirect portal vein DSA, the possibility of non-varices vein bleeding should be considered. When opposite hepatic blood flow with obvious dilation appeared in LGV and SGV, devascularization of the pericardial blood vessels would be justifiable.

Pathological morphology alteration of the splanchnic vascular wall in portal hypertensive patients

To investigate the pathological morphology alteration of the splanchnic vascular wall in portal hypertensive patients Methods Splenic arteries, veins and gastric coronary veins from portal hypertensive pati ents (n=50) were removed during esophagogastric devascularization with splenecto my and were observed under optic and electron microscopes The expression of iN OS in the splenic artery wall was analysed with immunohistochemistry Results The internal elastic membrane and medial elastic fibers of the splenic artery wa ll were broken and degenerated Atrophy, apoptosis and phenotypic changes were seen in smooth muscle cells of splenic arteries Positive staining for iNOS was seen in the cytoplasm of smooth muscle cells and iNOS activity was elevated com pared with the non cirrhotic patients ( P 【0 01) In the splenic and gastri c coronary veins of cirrhotic patients, we found proliferative intima, extensive thrombi adhering to the venous wall, mimicked arteriosclerosis plaques accompan ied with hypertrophy of smooth muscle cells, and thickened muscle fibers of vein s with increase in extracelluar matrix Conclusion Portal hypertension may be complicated by splanchnic arterial and venous vasculo pathy There may be an interactive relationship among portal hypertension, spla nchnic hyperdynamic disturbances and splanchnic vasculopathy in the pathogenesis of portal hypertension