A case of colonic varices complicated by alcoholic cirrhosis treated using balloon-occluded retrograde transvenous obliteration

A 44-year-old man with cirrhosis arising from alcohol abuse manifested melena caused by the rupture of esophageal varices. He received endoscopic variceal ligation for the initial hemostasis, followed by endoscopic injection sclerotherapy as an additional consolidation therapy. A CT examination performed at the time of admission revealed collateral veins developing around the ascending colon, in which the feeding and draining vessels were identified as the superior mesenteric vein and the right testicular vein, respectively. Moreover, large nodular varices were observed in the ascending colon during a colonoscopy. To prevent the rupture of the colonic varices, balloon-occluded retrograde transvenous obliteration (B-RTO) was performed through the right testicular vein using a microballoon catheter. A CT examination performed 4 days after the B-RTO procedure revealed the disappearance of blood flow with thrombosis formation in both the colonic varices and the feeding vein. The varices in the ascending colon had completely disappeared when examined during a colonoscopy performed 4 months after the B-RTO procedure. B-RTO is a useful and minimally invasive procedure for the treatment of colonic varices to prevent bleeding.     

A case of liver cirrhosis due to hepatits C virus infection complicating giant anorectal varices treated with balloon-occluded retrograde transvenous obliteration

A 73-year-old man with liver cirrhosis due to hepatitis C virus infection was admitted to our hospital because of massive bleeding from external varices. Colonoscopic examination revealed that giant anorectal varices had developed between the anus and rectal ampulla, and had ruptured at the perianal site. On three-dimensional computed tomography imaging, the feeding and drainage vessels of the varices were identified as the inferior mesenteric vein and right inferior hemorrhoidal vein, respectively. Endoscopic therapies were not employed for the bleeding varices, because the blood flow volume of the feeding vessel was extremely large. Balloon-occluded retrograde transvenous obliteration (B-RTO) was therefore carried out through the drainage vessels. The variceal blood flow disappeared after B-RTO therapy, and the varices decreased in size with thrombus formation verified by colonoscopy. Bleeding from the external varices also ceased. B-RTO therapy may be an effective approach for giant anorectal varices presenting as a complication in liver cirrhosis patients in whom the main drainage vessels can be determined.     

A case of liver cirrhosis with bleeding from stomal varices successfully treated using balloon-occluded retrograde transvenous obliteration

A 66-year-old male patient with liver cirrhosis because of alcohol intake underwent a Hartmann’s procedure for rectal cancer. Four months later, bleeding from the sigmoid stoma occurred and persisted for 2 months. A colonoscopic examination revealed bleeding from stomal varices. Three-dimensional computed tomography (CT) imaging demonstrated the inferior mesenteric vein and left superficial epigastric vein as the feeding and drainage vessels, respectively. Balloon-occluded retrograde transvenous obliteration (B-RTO) through the left epigastric vein was performed using a microballoon catheter inserted from the right femoral vein according to the Seldinger method. A CT examination performed 2 days after the B-RTO procedure revealed that the blood flow had disappeared, with thrombosis formation in both the stomal varices and the feeding vein. No recurrent bleeding from the stoma occurred. B-RTO using a microballoon catheter is useful as a therapeutic procedure for stomal varices to prevent bleeding, since the procedure can be performed with minimal invasion using the Seldinger method.     

Formation, hemodynamics and new management options for gastric varices

Abstract   Gastric varices develop in patients with portal hypertension, including liver cirrhosis, idiopathic portal hypertension as well as left sided-local portal hypertension such as splenic vein thrombosis or splenic AV malformation. The inflow vein is the left gastric vein, posterior vein, or short gastric vein, while the outflow vein is the gastro-renal shunt in most of the patients with gastric varices. The form of the gastric varices is classified into three types of venous dilatation; tortuous type, notched type and tumor type according to the shape and size of the varices. The location is classified into five sites; the posterior site, anterior site, greater curvature site and lesser curvature site of the cardiac area, and the fundic area. The risk of the rupture depends on the mucosal factor of the varices as well as the location and the form. The hemostasis rate has been improved to 94–97% with the usage of the endoscopic occlusive agent such as Histoacryl. It is absolutely necessary to eradicate the gastric varices within a few weeks after rupture of the gastric varices. There are new management options such as laparoscopic Hassab's operation or balloon-occluded retrograde transvenous obliteration of the varices (B-RTO). The 5-year cumulative rate of the non-variceal bleeding is more than 90% after the B-RTO as well as after surgery. Further prospective clinical trials are to be investigated for an evidence-based medicine.     

A case of gastric varices with gastropericardiac shunt successfully treated by balloon-occluded retrograde transvenous obliteration via the pericardiophrenic vein using a microballoon catheter

Gastric fundal varices developed in a 72-year-old female patient with liver cirrhosis due to hepatitis C virus infection after endoscopic injection sclerotherapy for esophageal varices. Three-dimensional computed tomography (CT) imaging demonstrated that gastrorenal shunts were absent as the drainage vessels of the varices, and the blood flows drained mainly into the pericardiophrenic vein. Balloon-occluded retrograde transvenous obliteration (B-RTO) was performed using a microballoon catheter to prevent bleeding from the gastric varices. The left inferior phrenic vein detectable as the second drainage vessel by venography was embolized with metallic coils and ethanolamine oleate solution was injected into the varices following occlusion of blood flow with a microballoon located in the pericardiophrenic vein. CT examination performed 7 days following B-RTO therapy revealed that the blood flow had disappeared with thrombus formation in the varices. B-RTO therapy with a microballoon catheter may be a useful therapy for gastric fundal varices even in cases without gastrorenal shunts, if the main drainage vessels are determined.     

Abdominal bleeding due to spontaneous mesenteric vein rupture

Hepatic cirrhosis is the leading cause of portal hypertension and is usually associated with the development ofsplacnic varices. Variceal intraabdominal rupture is a rare cause of hemoperitoneum. A case of spontaneous mesenteric vein rupture is reported. CLINICAL CASE: 43-year-old man with hepatic cirrhosis (Child-Pugh C stage) and previous bleeding of esophageal varices, admitted to hospital because of orthostatic hypotension episodes (positive tilt test) and abdominal distention. Laboratory: anemia, low platelet count and abnormal coagulation tests. CT scan showed abdominal fluid. Exploratory laparotomy was performed and 3 liters of blood were found into the abdominal cavity. The mesenteric vein had a ruptured variceal dilatation with intermitent jet bleeding. No organ abnormalities were found. Repair of the dilated vein was performed. The patient evolved well and was dismissed from hospital ten days after admittance. OBJECTIVE: To present a case in which a rare cause of intraabdominal bleeding, usually associated with high mortality rate, is follawed by a good clinical evolution.     

Spontaneous splenic rupture during induction chemotherapy for acute promyelocytic leukemia successfully treated with splenectomy

We report a case of acute promyelocytic leukemia who suffered spontaneous splenic rupture with massive hemoperitoneum while receiving intensive induction chemotherapy. Emergency computed tomography of the abdomen helped in the diagnosis of intra-abdominal bleeding. The patient was successfully treated with immediate splenectomy and made an uneventful postoperative recovery. Ten days after surgery chemotherapy could be resumed and complete remission was achieved. Although spontaneous splenic rupture is a rare complication of hematologic malignancies, this diagnosis should be considered in all patients with leukemia who develop acute abdominal pain with hypotension, even in the absence of splenomegaly.     

HEMOPERITONEUM DUE TO SPONTANEOUS RUPTURK OF THE UMBILICAL VEIN

Portal hypertension often leads to collateralization of blood flow via variceal vessels that shunt blood from the portal to the systemic circulation. Rupture of an intra-ahdominal varix is an unusual complication of portal hypertension that can lead to lire-threatening hemoperitoneum. We describe a patient with portal hypertension secondary to liver cirrhosis who presented with acute intra-abdominal hemorrhage. At laparotomy, she was found to have a rupture of the umbilical vein. The vessel was ligaled, and the patient recovered uneventfully. The causes of hemoperitoneum in cirrhosis arc discussed, and the previously reported eases of intra-abdominal variceal bleeding arc reviewed.     

Hemoperitoneum secondary to spontaneous rupture of the umbilical vein

Patients with ascites can develop spontaneous hemoperitoneum after injury or as a complication of diagnostic or therapeutic techniques. Spontaneous rupture of intra-abdominal varices is a rare complication of portal hypertension and an infrequent cause of hemoperitoneum that causes high mortality (75%). We present a new case of spontaneous hemoperitoneum secondary to umbilical vein rupture in a male patient with liver cirrhosis and review the cases previously described in the literature.     

Fatal spontaneous gallbladder variceal bleeding in a patient with alcoholic cirrhosis

Gallbladder varices are unusual ectopic varices that may develop in patients with portal hypertension, particularly in those with portal vein occlusion. In rare instances, these varices may cause hemobilia, life-threatening bleeding, or even rupture of the gallbladder. We report the first case of a 41-year-old man with alcoholic cirrhosis and patent portal vein who developed massive hemoperitoneum from spontaneous rupture of varices in the gallbladder fossa. The diagnosis of gallbladder varices eluded conventional imaging and was made only at autopsy. Gallbladder variceal hemorrhage is a rare, but potentially catastrophic complication of cirrhosis.     

Combined approach for spontaneous rupture of hepatocellular carcinoma

Ruptured hepatocellular carcinoma is a rare, emergency occurrence in western countries with high mortality risk. A number of hypotheses have been formulated in order to explain the precise mechanism that leads to hepatocellular carcinoma (HCC) rupture: sub-capsular location, dimensions, portal hypertension, tumour necrosis, local increase of venous pressure due to the outflow reduction caused by neoplastic invasion, and the presence of a previous vascular injury which might predispose to HCC rupture. There is still a debate in the literature concerning the best approach in cases of HCC rupture. Surgery is the first option for treatment of acute abdominal bleeding. However the advent of endovascular treatments widens the range of possible therapies for acute bleeding control and subsequent ablation purposes. We report a case of hemoperitoneum from spontaneous rupture of undiagnosed HCC, that was treated successfully by emergency surgical resection followed by transarterial chemo-embolization for local recurrence.     

Treatment of gastric fundal varices by balloon-occluded retrograde transvenous obliteration

Although less common than oesophageal varices in portal hypertension, gastric fundal varices carry a higher mortality rate when they rupture. They are less amenable to sclerotherapy. We have developed a minimally invasive balloon-occluded retrograde transverse obliteration (B-RTO) procedure to treat gastric fundal varices. B-RTO involves inserting a balloon catheter into an outflow shunt (gastric-renal or gastric-vena caval inferior) via the femoral or internal jugular vein. Blood flow is then blocked by inflating the balloon, and 5% ethanolamine oleate iopamidol is injected in a retrograde manner. The embolized gastric varix subsequentlyl disappears. B-RTO was performed in 32 patients with gastric varices. Follow-up endoscopies were performed at intervals of 2–4 months for an average observation period of 14 months. Eradication of the varices has been confirmed in 31 of 32 patients. No recurrence occurred in any patients in the follow-up period. There were no significant changes in liver function after the procedure. We conclude that B-RTO is a safe and effective procedure for the treatment of gastric fundal varices.     

Emergency balloon-occluded retrograde transvenous obliteration for gastric varices

Background We evaluated the efficacy of emergency balloon-occluded retrograde transvenous obliteration (B-RTO) performed within 24 h after initial hemostasis for the prevention of rebleeding from ruptured gastric varices. Methods From December 1995 to March 2003, 11 patients who had undergone B-RTO within 24 h after the control of gastric variceal bleeding at Maebashi Red Cross Hospital were investigated. They were followed up for complete eradication, recurrence of varices, and rebleeding. Efficacy was determined by endoscopic examination and computed tomography. Results The 4 patients with acute bleeding from ruptured gastric varices were treated with endoscopic therapy—endoscopic variceal ligation (EVL) in 2 patients, and clipping treatment in 2. Initial hemostasis was achieved in all 4; the other 7 patients had already stopped bleeding at endoscopy. After hemostasis was achieved, emergency B-RTO was immediately performed within 24 h and was successful in all 11 patients. Ten (90.9%) of the 11 gastric varices were obliterated and the other 1 (9.1%) was diminished in size. During the mean follow-up period of 1136 days, no rebleeding or recurrence as found. Four patients died during the follow-up period, but none died from variceal bleeding. Survival rates were 90.9% and 70.7%, respectively, at 1 year and 3 years. In 6 patients, development of esophageal varices appeared during the follow-up period, all of which were controlled by usual endoscopic therapy. No severe side effects were found after the B-RTO treatment. Conclusions Emergency B-RTO is an effective treatment for the prevention of rebleeding from ruptured gastric varices.     

Prophylactic balloon-occluded retrograde transvenous obliteration for gastric varices in compensated cirrhosis.

BACKGROUND & AIMS: Because gastric variceal bleeding is associated with a high mortality rate, its prophylaxis is expected to improve survival. We investigated the effectiveness of balloon-occluded retrograde transvenous obliteration (B-RTO) for the treatment of gastric fundal varices. METHODS: A prospective nonrandomized study was conducted. Prophylactic B-RTO was performed in 17 patients (B-RTO group), whereas the remaining 17 patients received no specific treatment (control). The nonbleeding rate, cumulative survival rate, and prognostic values of the patients were assessed. RESULTS: The respective nonbleeding rates at 1, 3, and 5 years were 100%, 100%, and 83% in the B-RTO group and 81%, 59%, and 39% in the control. The respective cumulative survival rates at 1, 3, and 5 years were 94%, 85%, and 39% in the B-RTO group and 71%, 41%, and 22% in the control. Both the nonbleeding rate and the cumulative survival rate of the B-RTO group were significantly higher than those of the control (P = .01 and .04, respectively). B-RTO was determined by multivariate analysis to be a significant factor for low bleeding rate (relative risk, 0.06; 95% confidence interval [CI], 0.004-0.79), whereas B-RTO (0.11; 95% CI, 0.03-0.44) and Child-Pugh class A (0.10; 95% CI, 0.03-0.39) were the significant factors for a low mortality rate, and the presence of hepatocellular carcinoma (5.68; 95% CI, 1.49-21.7) was the significant factor for a high mortality rate. CONCLUSIONS: Prophylactic B-RTO is effective in preventing gastric variceal rupture and consequently improves patient survival.     

Therapeutic effect of balloon-occluded retrograde transvenous obliteration on portal-systemic encephalopathy in patients with liver cirrhosis

OBJECTIVE: Balloon-occluded retrograde transvenous obliteration (B-RTO) has recently been introduced as a new interventional modality to prevent fatal bleeding from solitary gastric varices. A large portal-systemic shunt including gastric varices also causes severe encephalopathy in some cirrhotic patients. In this study, we evaluated the effect of B-RTO as a candidate therapeutic method to treat chronic recurrent hepatic encephalopathy due mainly to a portal-systemic shunt. PATIENTS AND METHODS: Since July 1995, we experienced 43 cirrhotic patients with chronic reccurent hepatic encephalopathy. Among them, six patients had anigographically proven large (>1 cm in diameter) portal-systemic shunt, and received B-RTO. B-RTO was carried out only once using 5% ethanolamine oleate with iopamidole to obliterate the portal-systemic shunt for 30 minutes. The median observation period after B-RTO was 29 months (range 23-46 months). RESULTS: In all 6 patients, encephalopathy had disappeared after B-RTO, and the patients were free of encephalopathy during the following 6 months. B-RTO significantly reduced blood ammonia levels at one month, 3 months, and 6 months later, without affecting serum aspartate aminotransferase activity, total bilirubin and albumin concentrations, and plasma prothrombin time. Encephalopathy relapsed in 4 patients between 6 and 30 months. Additional B-RTO was required and effective in 2 of them. CONCLUSION: B-RTO is an effective treatment for chronic recurrent hepatic encephalopathy with an angiographically proven portal-systemic shunt.     

Patent paraumbilical vein: hemodynamic importance in Mansoni's hepatosplenic portal hypertension (Study with ultrasonography Doppler

BACKGROUND: The hemodynamical effect of the collateral portosystemic circulation upon the portal system has not yet been fully understood. The US-Doppler made possible the non-invasive study of the portal system by evaluating the parameters: flow direction, diameter and flow velocity in it's vessels. AIMS: To study the paraumbilical vein as a collateral portosystemic pathway and identify patterns for appraising its hemodynamic importance to the portal system. METHOD: US-Doppler study of the portal system of 24 patients with Mansoni's hepatosplenic schistosomic portal hypertension, previous esophagic variceal bleeding and patent paraumbilical vein with hepatofugal flow. The diameter and the mean flow velocity were measured in the paraumbilical vein and so were the mean flow velocity in the portal vein, right and left portal branches. The Pearson test (linear correlation) was applied to the portal vein's mean flow velocity and the paraumbilical vein's diameter and mean flow velocity. The patients were divided in four groups: D1-paraumbilical vein with diameter < 0.68 cm (n = 14), D2-paraumbilical vein with diameter > or = 0.68 cm (n = 10), V1-paraumbilical vein with mean flow velocity < 18.41 cm/seg (n = 13) and V2-paraumbilical vein with mean flow velocity > or = 18.41 cm/seg (n = 11). The mean flow velocity in the portal vein, right and left portal branches of the four groups were compared. RESULTS: The paraumbilical vein diameter was 0.68 +/- 0.33 cm (range: 0.15-1.30 cm) and the mean flow velocity was 18.41 +/- 11.51 cm/seg (range: 5.73-38.20 cm/seg). The linear correlation between the portal vein's mean flow velocity/paraumbilical vein diameter and the paraumbilical vein's mean flow velocity showed r = 0.504 and r = 0.735, respectively. In the group D2 there was an increase in the mean flow velocity in the portal vein (17.80 +/- 3.42/22.30 +/- 7.67 cm/seg) and in the left portal branch (16.00 +/- 4.73/22.40 +/- 7.90 cm/seg). In the group V2 there was an increase in the mean flow velocity in the portal vein (16.31 +/- 3.49/21.96 +/- 5.89 cm/seg) and in the left portal branch (14.22 +/- 4.41/21.94 +/- 7.20 cm/seg). There was no change in the right portal branch (13.67 +/- 5.74/15.43 +/- 3.43 cm/seg). CONCLUSIONS: In portal hypertension due to hepatosplenic schistosomiasis, the patent paraumbilical vein, with hepatofugal flow, diameter > or = 0.68 cm and mean flow velocity > or = 18.41 cm/seg causes an increase of the mean flow velocity in the portal vein and left portal branch. The best US-Doppler parameter to appraise the paraumbilical vein influence upon the portal system is the mean flow velocity. The correlation between the increase in portal vein's mean flow velocity is stronger with the paraumbilical vein's mean flow velocity than with its diameter. The increase in the portal vein's and left portal branch's mean flow velocity may be understood as the paraumbilical vein's hemodynamic influence upon the portal system. An active portosystemic collateral pathway increases the mean flow velocity in the vein's segment proximal to its point of origin.     

Percutaneous paraumbilical embolization as an unconventional and successful treatment for bleeding jejunal varices

A 48-year-old Indian male with alcoholic liver cirrhosis was admitted after being found unresponsive. He was hypotensive and had hematochezia. Esophagogastroduodenoscopy （EGD） showed small esophageal varices and a clean-based duodenal ulcer. He continued to have hematochezia and anemia despite blood transfusions. Colonoscopy was normal. Repeat EGD did not reveal any source of recent bleed. Twelve days after admission, his hematochezia ceased. He refused further investigation and was discharged two days later. He presented one week after discharge with hematochezia. EGD showed non-bleeding Grade 1 esophageal varices and a clean-based duodenal ulcer. Colonoscopy was normal. Abdominal computed tomography （CT） showed liver cirrhosis with mild ascites, paraumbilical varices, and splenomegaly. He had multiple episodes of hematochezia, requiring repeated blood transfusions. Capsule endoscopy identified the bleeding site in the jejunum. Concurrently, CT angiography showed paraumbilical varices inseparable from a loop of small bowel, which had herniated through an umbilical hernia. The lumen of this loop of small bowel opacified in the delayed phase, which suggested variceal bleeding into thesmall bowel. Portal vein thrombosis was present. As he had severe coagulopathy and extensive paraumbilical varices, surgery was of high risk. He was not suitable for transjugular intrahepatic porto-systemic shunt as he had portal vein thrombosis. Percutaneous paraumbilical embolization via caput medusa was performed on day 9 of hospitalization. Following the embolization, the hematochezia stopped. However, he defaulted subsequent follow-up.     

An Adult Case of Congenital Extrahepatic Portosystemic Shunt Successfully Treated with Balloon-occluded Retrograde Transvenous Obliteration

A 42-year-old woman visited our hospital due to syncope. Contrast-enhanced CT revealed portosystemic shunt, portal vein hypoplasia, and multiple liver nodules. The histological examination of a liver biopsy specimen exhibited portal vein hypoplasia and revealed that the liver tumor was positive for glutamine synthetase. The patient was therefore diagnosed with congenital extrahepatic portosystemic shunt type II, and with focal nodular hyperplasia (FNH)-like nodules. She had the complication of severe portopulmonary hypertension and underwent complete shunt closure by balloon-occluded retrograde transvenous obliteration (B-RTO). The intrahepatic portal vein was well developed at 1 year after B-RTO, and multiple liver nodules completely regressed. Her pulmonary hypertension also improved.     

Percutaneous paraumbilical embolization as an unconventional and successful treatment for bleeding jejunal varices

A 48-year-old Indian male with alcoholic liver cirrhosis was admitted after being found unresponsive. He was hypotensive and had hematochezia. Esophagogastroduodenoscopy (EGD) showed small esophageal varices and a clean-based duodenal ulcer. He continued to have hematochezia and anemia despite blood transfusions. Colonoscopy was normal. Repeat EGD did not reveal any source of recent bleed. Twelve days after admission, his hematochezia ceased. He refused further investigation and was discharged two days later. He presented one week after discharge with hematochezia. EGD showed non-bleeding Grade 1 esophageal varices and a clean-based duodenal ulcer. Colonoscopy was normal. Abdominal computed tomography (CT) showed liver cirrhosis with mild ascites, paraumbilical varices, and splenomegaly. He had multiple episodes of hematochezia, requiring repeated blood transfusions. Capsule endoscopy ident i f ied the bleeding s i te in the jejunum. Concurrently, CT angiography showed paraumbilical varices inseparable from a loop of small bowel, which had herniated through an umbilical hernia. The lumen of this loop of small bowel opacified in the delayed phase, which suggested variceal bleeding into the small bowel. Portal vein thrombosis was present. As he had severe coagulopathy and extensive paraumbilical varices, surgery was of high risk. He was not suitable for transjugular intrahepatic porto-systemic shunt as he had portal vein thrombosis. Percutaneous paraumbilical embolization via caput medusa was performed on day 9 of hospitalization. Following the embolization, the hematochezia stopped. However, he defaulted subsequent follow-up.     

Periarteritis nodosa complicated by intrapancreatic vascular rupture

Clinical pancreatic manifestations are unusual in polyarteritis nodosa. A case of intrapancreatic hemorrhage due to vascular rupture occurring during the course of histologically proven polyarteritis nodosa is described. The patient presented with massive hemoperitoneum requiring emergency laparotomy. Splenopancreatectomy was performed to control bleeding. Steroid therapy was continued during the postoperative course, with favorable outcome. The mechanism of vascular rupture is not clear, but is probably related to focal arteritis with consequent infarction. No ruptured microaneurysm was found in this case.