The value of emergency upper gastrointestinal fibre-endoscopy, followed where required by the use of a modified Sengstaken tube, was studied during 84 episodes of acute bleeding in 75 patients who had evidence of portal hypertension with varices. The portal hypertension was due to alcoholic cirrhosis in 80% and to cryptogenic cirrhosis in 9% of the patients. By definition, varices were present in all patients, but in only 66% of episodes were the varices the cause of the bleed. The correct diagnosis of the source of bleeding was made at endoscopy in 89%. A Boyce modification of the Sengstaken-Blakemore tube was passed in 73% of the episodes of variceal bleeding. It effectively stopped the bleeding primarily in 85% of patients but was successful as a final definitive measure only in 46%. Furthermore, only 40% of the patients in whom the tube was passed, survived. Mortality rate could be related to the severity of the bleed and to hepatocellular dysfunction. Survival increased from 23% in those patients with jaundice, ascites, and encephalopathy on admission to 92% in those without these manifestations. The in-hospital survival rate was 52% in patients bleeding from varices and 64% in those bleeding from other causes, with an overall survival rate of 56%, indicating the poor prognosis in cirrhotic patients with gastrointestinal bleeding, irrespective of the cause.
Isolated ectopic varices located in the small bowel are uncommon. Portal hypertension caused by liver cirrhosis is the most common predisposing risk factor.
PRESENTATION OF CASE
We present an unusual case of massive gastrointestinal bleeding from idiopathic jejunal varices in a 73-year-old Caucasian male without portal hypertension. Exploratory laparotomy disclosed ectopic varices located in the small intestine. Segmental resection of the jejunum with end to end anastomosis resulted in a complete resolution of the haemorrhage. During a 5 year follow up, the patient is stable with no bleeding recurrence.
Information on aetiology, diagnosis and management of jejunal varices is reviewed.
Diagnosis and management of isolated jejunal varices is challenging. Surgeons as well as acute care physicians have to consider idiopatic form of jejunal varices as a potential cause of gastrointestinal bleeding when gastroduodenoscopy and colonoscopy are negative.
Jejunal varices; Gastrointestinal haemorrhage; Diagnosis; Management
anti-inflammatory drugs (NSAIDs) can have severe gastrointestinal
effects and cause peptic ulcers to bleed. Acute bleeding from
oesophageal varices is a major complication of cirrhosis of the liver.
investigate the role, using a case-control study, of NSAIDs in first
bleeding episodes associated with oesophageal or cardial varices in
structured interview was conducted of 125cirrhotic patients with
bleeding mainly related to oesophageal varices and 75 cirrhotic
controls with oesophageal varices who had never bled.
patients who were admitted for bleeding related to portal hypertension
were more likely to have used NSAIDs during the week before the index
day (31 of 125 (25%)) than the cirrhotic controls (eight of 75 (11%);
odds ratio = 2.8, p = 0.016). Use of aspirin alone or combined with
other NSAIDs was also more prevalent in the cases (21 of 125 (17%))
than in the controls (three of 75 (4%); odds ratio = 4.9, p = 0.007).
Logistic regression analysis showed that NSAID use (p = 0.022, odds
ratio = 2.9, 95% confidence interval = 1.8 to 4.7) and variceal size
(p<0.001, odds ratio = 4.0, 95% confidence interval = 1.4 to 11.5)
were the only variables independently associated with the risk of bleeding.
used alone or combined with other NSAIDs, was associated with a first
variceal bleeding episode in patients with cirrhosis. Given the life
threatening nature of this complication, the possible benefit of this
treatment should be weighed against the risk shown here. No firm
conclusions could be drawn on non-aspirin NSAIDs used alone.
portal hypertension; non-steroidal anti-inflammatory
drugs; variceal bleeding; aspirin; cirrhosis
A patient is described presenting with an acute lower gastrointestinal haemorrhage as a result of extensive colonic varices. Further investigation revealed that there were no oesophageal varices or splenomegaly. Liver biopsy showed grade II fatty change only, with no other specific or significant pathological features. Transhepatic portography showed a raised portal pressure (20 mm/Hg) but the portal system was patent throughout. There was an abnormal leash of vessels in the caecum thought to represent a variceal plexus. This patient was diagnosed as having idiopathic colonic varices. This case is discussed together with nine other reports of idiopathic colonic varices from the published literature. Four of these reports describe idiopathic colonic varices in more than one member of the same family. Possible modes of inheritance, aetiology of variceal change, natural history, and prognosis are discussed.
Duodenal varices are a rare complication of portal hypertension secondary to liver cirrhosis. Compared to oesophageal varices, they bleed less often but are also more difficult to diagnose and treat. There is no established treatment for bleeding duodenal varices and different treatment strategies have been employed with variable results. The authors present a case of 52-year-old male who was admitted with melaena. Upper gastrointestinal endoscopy was performed which identified bleeding varices in the second part of duodenum. The varices were injected with cyanoacrylate and the outcome was favourable. Subsequent endoscopies showed complete resolution of the varices. The authors conclude that cyanoacrylate injection is an effective first-line treatment for bleeding duodenal varices.
Varices of the colon are a rare cause of lower gastrointestinal bleeding, usually associated with portal hypertension due to liver cirrhosis or other causes of portal venous obstruction. Idiopathic colonic varices are extremely rare. Recognition of this condition is important as idiopathic colonic varices may be a cause of recurrent lower gastrointestinal bleeding.
We report the case of a 21-year-old Asian man from north India who presented with recurrent episodes of lower gastrointestinal bleeding. Colonoscopy revealed varices involving the terminal ileum and colon to the sigmoid. Thorough evaluation was undertaken to rule out any underlying portal hypertension. Our patient underwent subtotal colectomy including resection of involved terminal ileum and an ileorectal anastomosis.
Colonic varices are an uncommon cause of lower gastrointestinal bleeding. Idiopathic colonic varices are diagnosed after excluding underlying liver disease and portal hypertension. Recognition of this condition is important as prognosis is good in the absence of liver disease and is curable by resection of the involved bowel.
Patients with haemorrhage from oesophageal varices associated with portal hypertension are poor risks for anaesthesia and surgery. One method of controlling such haemorrhage is injection of the oesophageal varices (sclero-therapy) via an oesophagoscope. Careful preoperative preparation and use of the Sengstaken-Blakemore tube in combination with the anaesthetic technique of intermittent Althesin and suxamethonium with artificial ventilation with nitrous oxide and oxygen enables sclerotherapy to be carried out successfully.
Oesophageal varices and gastrointestinal bleeding are common complications of liver cirrhosis. More rarely, oesophageal varices occur in patients with non-cirrhotic portal hypertension that results from thromboses of portal or splanchnic veins.
We describe 2 young men who initially presented with varices as a result of portal vein thromboses. In the clinical follow-up, both were tested positive for a JAK2 mutation and consequently diagnosed with myeloproliferative neoplasms (MPNs). In an attempt to characterise the frequency of gastrointestinal complications in patients with JAK2-positive MPNs, we retrospectively analysed all known affected patients from our clinic for the diagnosis of portal vein thromboses and oesophageal varices. Strikingly, 48% of those who had received an oesophagogastroduodenoscopy had detectable oesophageal or gastric varices, and 82% of those suffered from portal or splanchnic vein thromboses.
While the association between JAK2, myeloproliferative disease and thrombotic events is well established, patients with idiopathic oesophageal varices are not regularly tested for JAK2 mutations. However, the occurrence of oesophageal varices may be the first presenting symptom of a MPN with a JAK2 mutation, and affected patients may profit from a close haematological monitoring to assure the early detection of developing MPN.
Oesophageal varices; Variceal bleeding; Splanchnic vein thrombosis; Portal vein thrombosis; JAK2; Myeloproliferative neoplasms
Portal hypertension occurs as a complication of liver cirrhosis and complications such as variceal bleeding lead to significant demands on resources. Endoscopy is the gold standard method for screening cirrhotic patients however universal endoscopic screening may mean a lot of unnecessary procedures as the presence of oesophageal varices is variable hence a large time and cost burden on endoscopy units to carry out both screening and subsequent follow up of variceal bleeds. A less invasive method to identify those at high risk of bleeding would allow earlier prophylactic measures to be applied. Hepatic venous pressure gradient (HVPG) is an acceptable indirect measurement of portal hypertension and predictor of the complications of portal hypertension in adult cirrhotics. Varices develop at a HVPG of 10-12 mmHg with the appearance of other complications with HPVG > 12 mmHg. Variceal bleeding does not occur in pressures under 12 mmHg. HPVG > 20 mmHg measured early after admission is a significant prognostic indicator of failure to control bleeding varices, indeed early transjugular intrahepatic portosystemic shunt (TIPS) in such circumstances reduces mortality significantly. HVPG can be used to identify responders to medical therapy. Patients who do not achieve the suggested reduction targets in HVPG have a high risk of rebleeding despite endoscopic ligation and may not derive significant overall mortality benefit from endoscopic intervention alone, ultimately requiring TIPS or liver transplantation. Early HVPG measurements following a variceal bleed can help to identify those at risk of treatment failure who may benefit from early intervention with TIPS. Therefore, we suggest using HVPG measurement as the investigation of choice in those with confirmed cirrhosis in place of endoscopy for intitial variceal screening and, where indicated, a trial of B-blockade, either intravenously during the initial pressure study with assessment of response or oral therapy with repeat HVPG six weeks later. In those with elevated pressures, primary medical prophylaxis could be commenced with subsequent close monitoring of HVPG thus negating the need for endoscopy at this point. All patients presenting with variceal haemorrhage should undergo HVPG measurement and those with a gradient greater than 20 mmHg should be considered for early TIPS. By introducing portal pressure studies into a management algorithm for variceal bleeding, the number of endoscopies required for further intervention and follow up can be reduced leading to significant savings in terms of cost and demand on resources.
Variceal haemorrhage; Portal hypertension; Portal pressure; Varices; Hepatic venous pressure gradient
Long-term results of surgical treatment were analysed in 42 patients with extrahepatic portal hypertension treated in the Department of Surgery, Institute of Haematology in Warsaw in the period 1971-1987. In all, 71 operations were carried out, and 20 patients were treated by endoscopic sclerotherapy of oesophageal varices. Recurrence of haemorrhage was found in 6 out of 11 patients 54% after venous shunting, in 13 out of 17 patients (76%) after treatment by ligation of oesophageal varices and in 32 out of 35 patients (91%) after splenectomy. Following repeated sclerotherapy of oesophageal varices, recurrence of haemorrhage occurred in 3 out of 20 patients (15%). During 17 years four deaths occurred (10%) none of which was due to haemorrhage from oesophageal varices. The authors conclude that the method of repeated sclerotherapy is presently the most effective way of preventing haemorrhage from oesophageal varices and consider this form of management as the treatment of choice in patients with extrahepatic portal hypertension.
OBJECTIVE--To study whether somatostatin or its derivative octreotide is more effective than placebo for treating bleeding oesophageal varices. METHODS--Randomised, double blind trial and meta-analysis with blinded analysis of data and writing of manuscripts. SETTING--Departments of medical and surgical gastroenterology in Copenhagen. SUBJECTS--Patients suspected of bleeding from oesophageal varices and of having cirrhosis of the liver. MAIN OUTCOME MEASURES--Survival, number of blood transfusions, and use of Sengstaken-Blakemore tube. RESULTS--86 patients were randomised; in each group 16 died within six weeks (95% confidence interval for difference in mortality--19% to 22%). There were no differences between those treated with somatostatin or placebo in median number of blood transfusions (8 v 5, P = 0.07, 0 to 4 transfusions) or in numbers of patients who needed balloon tamponade (16 v 13, P = 0.54, -11% to 28%). In a meta-analysis of three trials involving 290 patients somatostatin had no effect on survival compared with placebo (P = 0.59, odds ratio 1.16; 0.67 to 2.01). For blood transfusions and use of balloon tamponade there was heterogeneity between the trials with no convincing evidence in favour of somatostatin. No placebo controlled trials have been performed with octreotide. CONCLUSION--Within the limited power of this study and meta-analysis we were unable to show a clinical benefit of somatostatin in the emergency treatment of bleeding oesophageal varices.
Bleeding from oesophageal varices, oesophageal ulcers or oesophagitis is occasionally massive and difficult to control. Octreotide, a synthetic analogue of somatostin lowers portal pressure and collateral blood flow including that through varices, increases lower oesophageal sphincter pressure, and inhibits the gastric secretion of acid as well as pepsin. Our current experience suggests it is effective in controlling acute variceal haemorrhage. Therefore we have examined the efficacy of octreotide in the control of postsclerotherapy bleeding from oesophageal varices, oesophageal ulcers and oesophagitis. During the study period 77 patients experienced a significant gastrointestinal bleed (blood pressure < 100 mm Hg, pulse >
100 beats per min or the need to transfuse 2 or more units of blood to restore the haemoglobin level) following injection sclerotherapy of oesophageal varices. The source of bleeding was varices in 42 patients, oesophageal ulcers in 31 and oesophagitis in 4. All patients received a continuous intravenous infusion of octreotide (50 μg/h) for between 40–140h. If bleeding was not controlled in the first 12h after commencing octreotide hourly bolus doses (50 μg) for 24h were superimposed on the continuous infusion. Haemorrhage was successfully controlled by an infusion of octreotide in 38 of the 42 patients with bleeding from varices, in 30 of 31 patients with oesophageal ulceration, and all patients with oesophagitis. In the 1 patient with persistent bleeding from oesophageal ulceration and in 2 of the 4 with continued haemorrhage from varices, haemostasis was achieved by hourly boluses of 50 μg octreotide for 24h in addition to the continuous infusion. No major complications were associated with octreotide administration. The results of this study clearly indicate that octreotide is a safe and effective treatment for the control of severe haemorrhage after technically successful injection sclerotherapy.
The effect of prophylactic treatment of oesophageal varices by endoscopic injection sclerotherapy before the first episode of variceal haemorrhage was studied in patients with cirrhosis in a prospective, randomised and controlled multicentre trial. From February 1984 to March 1987 patients with liver cirrhosis and large varices (stage III-IV according to Paquet) were treated and followed up. The sample comprised 87 patients: 45 in the prophylactic treatment and 42 in the control group. After excluding drop outs, 41 patients were treated in each group. Twenty nine per cent of patients in the sclerotherapy group and 34% in the control group had a variceal haemorrhage during the period of observation. There was no significant difference in the distributions of the bleeding free intervals between the sclerotherapy and the control groups. During the follow up period 24% of patients in the sclerotherapy group and 46% in the control group died. The distribution of survival times indicates a tendency towards longer survival of patients with prophylactic sclerotherapy, particularly in those with alcoholic cirrhosis.
The clinical data of 180 episodes of upper gastrointestinal bleeding in 168 patients with cirrhosis of the liver are examined. The source of bleeding had been determined by early endoscopy in all cases. In men under the age of 50 years, and without symptoms of liver failure, bleeding was due to ruptured gastro-oesophageal varices in 84% of cases. Severe liver failure was associated with acute lesions of gastric mucosa in many cases. No presumptive diagnosis of the source of haemorrhage could be based on the examination of other clinical data (presence of ascites, mode of presentation and pattern of bleeding, history of ulcer disease, alcoholism, and previous medication.
Duodenal varices are a rare complication in patients with portal hypertension. Bleeding from duodenal varices often results in a severe prognosis. Diagnosis of the disease is usually based on findings obtained by endoscopy or angiography. However, it occasionally fails to detect the lesion and demonstrate its porto-systemic shunt vessels which are necessary information to decide an appropriate treatment. Recent advances in CT may make it possible for us to reveal duodenal varices with complicated porto-systemic shunt vessels. We report the case of a 58-year-old man with liver cirrhosis with repeated bleeding from duodenal varices. Esophagogastroduodenoscopy (EGD) revealed multinodular varices in the third portion of the duodenum. Then we conducted a capsule endoscopy (CE) and found fresh blood in the duodenum, suggesting duodenal variceal hemorrhage. Angiography depicted the varices with one afferent and two efferent vessels. Abdominal CT examination was conducted using a four-channel multi-detector row CT scanner. The multiplanar reconstructed images revealed not only the varices, but also three afferent and two efferent vessels. The patient was treated by surgical ligation and sclerotherapy, because of its complicated porto-systemic shunt and reserved liver function. No gastrointestinal bleeding has been seen after the surgery. Our case suggests the usefulness of multi-detector CT with multiplanar reconstruction (MPR) for the diagnosis and therapeutic decision of duodenal varices.
Varices; Computed tomography; Duodenum; Surgical hemostasis
While esophagogastric varices are common manifestations of portal hypertension, variceal bleeding from the jejunum is a rare complication of liver cirrhosis. In addition, ectopic variceal bleeding occurs in the duodenum and at sites of previous bowel surgery in most cases, including of stomas. We report a case of obscure overt gastrointestinal bleeding from jejunal varices in a 55-year-old woman who had not previously undergone abdominal surgery, who had liver cirrhosis induced by the hepatitis C virus. Emergency endoscopy revealed the presence of esophageal varices without stigmata of recent bleeding, and no bleeding focus was found at colonoscopy. She continued to produce recurrent melena with hematochezia and received up to 21 units of packed red blood cells. CT angiography revealed the presence of jejunal varices, but no active bleeding was found. Capsule endoscopy revealed fresh blood in the jejunum. The patient submitted to embolization of the jejunal varices via the portal vein, after which she had a stable hemoglobin level and no recurrence of the melena. This is a case of variceal bleeding from the jejunum in a liver cirrhosis patient without a prior history of abdominal surgery.
Jejunal varices; Liver cirrhosis; Portal hypertension
Sixty-three patients with acute variceal haemorrhage were treated with the Sengstaken-Blakemore tube (SBT). Bleeding was initially controlled with the gastric balloon in 37 patients (60%) and with both gastric and oesophageal balloons in another 17 (27%), giving overall primary success in 54 patients (87%). Sixteen (26%) patients re-bled within 24 hours of deflation of the tube. Repeat balloon tamponade helped in controlling bleeding in 9 of these. Thus, a total of 47 (75%) patients stopped bleeding with SBT. There was no mortality. The only major complication was pulmonary infection (15%), which improved with antibiotics. Use of the SBT was found to be simple, quick, low cost and attended with few complications. Its use is recommended in patients with acute variceal bleeding, especially in developing countries with limited resources.
Varices that occur at sites other than the esophagogastric area are termed ectopic varices. An ileal varix is a very rare cause of lower gastrointestinal bleeding. Although ileal varices are generally associated with prior intra-abdominal surgery and adhesions, an arteriovenous malformation (AVM) in the ileocecal area can cause ileal varices and bleeding in patients with portal hypertension who have not received previous intra-abdominal surgery, which is due to an intestinal or colonic AVM dilating the collateral veins and further aggravating portal hypertension. Surgical treatment should be considered in patients with massive ectopic variceal bleeding. We report a case of massive ileocecal variceal bleeding associated with an AVM that occurred in a patient with alcoholic liver cirrhosis.
Ileocecal varix; Arteriovenous malformation; Portal hypertension
Variceal bleeding is one of the dreaded complications of portal hypertension. Although its prognosis has improved over the last several decades, it still carries substantial mortality. Although most portal hypertensive bleeds result from the ruptured distal esophageal varices, bleeding from other sources such gastric varices, portal hypertensive gastropathy, and ectopic varices can lead to clinically significant bleeding.
Variceal bleeding typically presents as massive gastrointestinal (GI) bleeding with hematemesis, melena or hematochezia. In general, the terapeutic aims of management are to initially correct hypovolemia, to control bleeding, to prevent complications of bleeding, such as infection and renal failure and to prevent early rebleeding.
The treatment of bleeding esophageal varices differs substantially foom the treatment of other lesions of the upper gastrointestinal tract. Moreover, patients with esophageal varices typically have severe liver disease and thus are likely from poor nutrition, blood clotting disorders, and encephalopathy, all of which can adversaly affect morbidity and mortality.
stabilization of the patient’s hemodynamic status; severe liver disease; encephalopathy; rebleeding; mortality
A 68-year-old man with hemophilia A and liver cirrhosis caused by hepatitis C virus was referred to our hospital to receive prophylactic endoscopic treatment for gastroesophageal varices (GOV). He had large, tense, and winding esophageal varices (EV) with cherry red spots extending down to lesser curve, predicting the likelihood of bleeding. Esophageal endoscopic injection sclerotherapy (EIS) was performed with a total 15 mL of 5% ethanolamine oleate with iopamidol (EOI). Radiographic imaging during EIS demonstrated that 5% EOI reached the afferent vein of the varices. He was administered sufficient factor VIII concentrate before and after EIS to prevent massive bleeding from the varices. Seven days after EIS, upper gastrointestinal endoscopy (UGIE) showed that the varices were eradicated almost completely. Eighteen months after EIS, the varices continued to diminish. We report a successful case of safe and effective EIS for GOV in a high-risk cirrhotic patient with hemophilia A.
Patients with systemic sclerosis may develop mild abnormalities of liver function tests. More serious hepatic involvement has been well documented but is rare. Idiopathic portal hypertension had been reported only in a few female patients with systemic sclerosis.
An 82-year-old man with known systemic sclerosis presented with melaena. Urgent gastroscopy revealed oesophageal varices, which re-started bleeding during the procedure and were treated ensocopically, with Sengstaken tube and glypressin. Liver function tests and coagulation were normal. Non-invasive liver screen (including hepatitis viral serology and autoantibodies) was negative. Ultrasound scan of the abdomen revealed a small liver with coarse texture and no focal lesion. Hepato-portal flow was demonstrated in the portal vein. The spleen was enlarged. A moderate amount of free peritoneal fluid was present. A CT scan confirmed the absence of portal vein thrombosis. One month following discharge the patient had a liver biopsy. Histological examination showed essentially normal liver tissue; there was no evidence of any excess inflammation and no features to suggest cirrhosis or drug-induced liver disease. Taking into account the above evaluation we concluded that the patient had idiopathic portal hypertension.
Both male and female patients with systemic sclerosis may – rarely – develop idiopathic portal hypertension.
A simple and safe procedure providing sensitive and reproducible direct measurement of intravascular oesophageal variceal pressure (IOVP) during routine oesophagoscopy is described. The method requires only commercially available equipment. First results were obtained in 16 patients with oesophageal varices caused by liver cirrhosis (Child's A) can be summarised as follows: intravascular oesophageal variceal pressure was nearly identical in different varices of the single patient. Varices grade III exhibited a significantly higher intravascular oesophageal variceal pressure than varices grade II (22.7 +/- 2.5 vs 15.7 +/- 0.6 mmHg, p less than 0.05). After Valsalva's manoeuvre there was a remarkable increase in intravascular oesophageal variceal pressure by 13.6 +/- 1.0 mmHg irrespective of the variceal size. The high intravascular oesophageal variceal pressure values observed in grade III varices during the rise of the intraabdominal pressure may indicate an important risk factor for variceal haemorrhage. Glyceryltrinitrate (1.2 mg sprayed onto the tongues of 14 patients) very effectively lowered the intravascular oesophageal variceal pressure from 22.8 +/- 2.0 to 12.0 +/- 0.4 mmHg in grade III varices, and from 16.3 +/- 0.4 to 10.0 +/- 0.4 mmHg in grade II varices (p less than 0.005 in both groups). We conclude that this method provides a suitable tool to study the effect of drugs with presumed influence on the oesophageal variceal pressure and that the impressive effect of glyceryltrinitrate in lowering intravascular oesophageal variceal pressure warrants further study on the effect of longer acting nitrates on intravascular oesophageal variceal pressure, and the rebleeding rate after oesophageal variceal haemorrhage.
Fatal oesophageal rupture is described as a complication of the management of bleeding oesophageal varices with repeated sclerotherapy and tamponade using the Sengstaken-Blakemore tube. The importance of chest radiographs is stressed in the early detection and prevention of malposition of the Sengstaken-Blakemore tube, as inflation of the gastric balloon in the oesophagus can result in oesophageal rupture.
We report a case of a 64-year-old female patient who underwent a right lobectomy of the liver (including total resection of the caudate lobe), dissection of the group 2 lymph nodes, left hepaticojejunostomy (Roux-en-Y fashion), and reconstruction of the portal vein (end-to-end anastomosis between the main portal vein and the left portal branch) for treatment of hepatic hilar bile duct cancer in 1996. In 2001, the anastomotic site of the hepaticojejunostomy was dissected and re-anastomosed due to gastrointestinal bleeding caused by variceal rupture in the jejunal loop. In 2006, splenectomy was performed for recurrence of gastrointestinal bleeding due to another variceal rupture in the jejunal loop. Portal venography performed perioperatively showed a decrease in portal blood flow into the liver via the jejunal varices and an increase in portal blood flow into the liver via the left gastric vein. She had two jejunal variceal ruptures at five-year intervals after extrahepatic portal obstruction and underwent successful treatments.
The results of a modified Sugiura devascularisation
procedure were assessed in 14 patients with thrombosis
of the portal and splenic vein requiring surgery
for variceal hemorrhage, with no vein suitable
for orthodox shunt surgery. The venous anatomy
was determined by ultrasonography with Doppler
studies and portovenography. Liver biochemistry as
well as liver architecture on histopathology was
normal in all. The surgery was elective in 9 cases for
documented bleed from diffuse fundal gastric
varices (FGV) and emergency in 5 cases, 3 having
bleeding FGV and 2 for failure of emergency
esophageal variceal sclerotherapy. All were subjected
to a transabdominal extensive devascularisation
of the upper two third of the stomach and lower
7–10cm of the esophagus. Stapled esophageal
transection (n=11) or esophageal variceal under-running
(n=1) was performed in all with esophageal
varices. FGV were underrun. Follow up endoscopies
were done six monthly. There were 9 males and 5
females with a mean age of 17.2 years (SD 12.8).
There was no operative mortality. Acute variceal
bleeding was controlled in all patients. Over a mean
follow up of 38 months, all but one remain free of
recurrent bleeding. We conclude that a modified
Sugiura devascularisation procedure is effective in
the immediate and medium term control of variceal
bleeding in patients with “unshuntable” portal