Effects of vasopressin on left gastric venous flow in cirrhotic patients with esophageal varices

To assess vasopressin control of esophageal variceal bleeding, we investigated the effect of vasopressin on the left gastric venous flow, portal venous flow, superior mesenteric venous flow, and splenic venous flow in seven cirrhotic patients with esophageal varices, using a duplex system consisting of a real-time ultrasonograph and an echo-Doppler flowmeter. Infusion of vasopressin (0.3 U/min) significantly decreased the blood flow in the left gastric vein (-56%), portal trunk (-54%), superior mesenteric vein (-54%), and splenic vein (-56%) as a result of decrease of blood velocity in these vessels. Thus, vasopressin seems to control esophageal variceal bleeding, in part, by reducing blood velocity and blood flow in the left gastric vein following reduction of blood velocity and blood flow in the superior mesenteric vein and splenic vein.     

Splenic and portal venous obstruction in chronic pancreatitis

The aim of this study was a prospective search for splenoportal venous obstruction (SPVO) in a medical-surgical series of 266 patients with chronic pancreatitis who were followed up a mean time of 8.2 years. SPVO was systematically searched for using ultrasonography and then confirmed by angiography or computed tomography. SPVO was found in 35 patients (13.2%) but was symptomatic in only two. Initial obstruction involved the splenic vein in 22 patients, the portal vein in 10, and the superior mesenteric vein in three. Since venous obstruction extended from the splenic to the portal vein in five patients, the prevalence of portal obstruction was 5.6% (15/266). Acute pancreatitis and pseudocysts were the probable cause of SPVO in 91.4% of our cases. Half the cases of splenic venous obstruction were related to pseudocysts of the caudal pancreas. Esophageal varices were found in two patients and gastric varices in four at the time of diagnosis and during follow-up. At the end of follow-up, 12 patients had undergone splenopancreatectomy (N = 11) or splenectomy (N = 1). Only one patient was operated on for massive esophageal variceal bleeding, and another patient died due to intractable colic variceal bleeding. In four of six patients operated on with portal vein obstruction, surgery was difficult due to venous collaterals. Ten patients were not operated on and 13 patients operated on were not treated for SPVO. The mean follow-up after diagnosis of SPVO for these final 23 patients was 28.9 months. None of these patients bled.(ABSTRACT TRUNCATED AT 250 WORDS)     

Total gastrectomy after shunt failure as therapy for recurrent gastric variceal bleeding due to portal and mesenteric vein thrombosis

A 37-yr-old man with portal hypertension due to portal vein thrombosis was referred because of recurrent episodes of variceal hemorrhage. He had previously undergone two portal-systemic shunt procedures. Both of the shunts, as well as the superior mesenteric vein, ultimately thrombosed. Endoscopic variceal sclerotherapy was able to control the bleeding from his esophageal varices, but he repeatedly bled from large gastric varices. The patient underwent a total gastrectomy and has had no further gastrointestinal hemorrhage during a follow-up of 36 months.     

Clinical and endoscopic features of gastric varices secondary to splenic vein occlusion

Aim: This study provides a retrospective evaluation of cases with gastric varices secondary to splenic vein occlusion. Methods: Our study group consisted of 14 patients. The clinical manifestations, diagnostic methods and therapeutic modalities were analyzed retrospectively. Results: Eleven patients had co‐existing pancreatic diseases: seven with chronic pancreatitis, three with cancer of the pancreatic body or tail and one with severe acute pancreatitis. Among the three remaining patients, one had advanced left renal cancer, one had myeloproliferative disease and the third had splenic vein occlusion due to an obscure cause. A diagnosis of gastric varices was made following endoscope gastroduodenoscopy or endoscopic color Doppler ultrasonography (ECDUS), and splenic vein occlusions were diagnosed from enhanced computed tomography in all cases. Specific findings of gastric varices secondary to splenic vein occlusion were based on ECDUS color flow images of gastric variceal flow that clearly depicted round cardiac and fundal regions at the center, with varices expanding to the curvatura ventriculi major of the gastric body. For three cases with gastric variceal bleeding, endoscopic injection sclerotherapy using a mixture of histoacryl and lipiodol (70% histoacryl solution) was performed, after which no further bleeding from gastric varices was detected. Due to a high risk of gastric variceal rupture, splenectomy was performed in two cases and splenic arterial embolization in another two cases. Conclusion: ECDUS color flow images of gastric variceal flow depicted specific findings of gastric varices secondary to splenic vein occlusion. Treatment should take into account the diseases underlying these conditions.     

The natural history of splenic vein thrombosis due to chronic pancreatitis: indications for surgery

Eleven patients with angiographically demonstrated splenic vein thrombosis associated with chronic pancreatitis were followed for an average of 6.5 yr to determine the natural history of this condition. Repeat angiography was performed in five patients. Significant gastric or gastroesophageal varices were noted in six cases. In another patient, peri-colonic varices and spleno-portal collaterals were demonstrated. Two patients bled massively during follow-up; one from gastric varices and one from colonic varices. Another patient, with known gastric varices, intermittent hematochezia and iron deficiency anemia, underwent surgery. All three patients responded well to splenectomy. Since three of the seven patients with splenic vein thrombosis and significant varices eventually required surgical correction, it may be that the long-term risk of gastrointestinal bleeding exceeds the risks of elective splenectomy in these patients.     

Splenic artery embolization for variceal hemorrhage following blocked distal splenorenal shunt

A blocked distal splenorenal shunt presents with torrential bleeding from gastric varices. Reoperation in the presence of portal hypertension in an unstable patient is difficult. Two patients with a blocked distal splenorenal shunt were subjected to splenic artery embolization. This stopped variceal bleeding from gastric varices resulting from the congested spleen due to thrombosis of the splenic vein. The procedure was successful in stopping the acute bleed in both patients. There were no serious complications or recurrent variceal bleeding and the varices were collapsed at one year on follow-up endoscopy. Splenic artery embolization is a safe and effective minimally invasive treatment for patients with bleeding from a blocked distal splenorenal shunt.     

Prevalence of spontaneous hepatofugal portal flow in liver cirrhosis. Clinical and endoscopic correlation in 228 patients

The prevalence of spontaneous reversal of flow in the portal venous system was non invasively evaluated by Doppler ultrasound in 228 patients with liver cirrhosis and portal hypertension. Reversed flow was detected in the portal vein in 7 patients (3.1%), in the splenic vein in 7 patients (3.1%), and in the superior mesenteric vein in 5 patients (2.1%), with an overall prevalence of 8.3% (19/228). This prevalence did not differ in relation to the etiology of liver cirrhosis, whereas hepatofugal flow was found in more patients classified as Child's C (15.4%) and B (12.5%) than those classified as Child's A (2.7%) (P less than 0.02) and was associated with a higher frequency of hepatic encephalopathy (21% vs. 7.2%; P less than 0.05). Endoscopic evaluation of esophageal varices did not reveal any correlation between the presence and size of varices and hepatofugal flow, whereas red signs were detected more frequently in patients with this hemodynamic pattern (42.1% vs. 24.4%; NS). The rate of previous variceal bleeding was not significantly different in patients with and without hepatofugal flow (30.8% vs. 24.4%; NS). Conversely, the prospective evaluation of 15 patients with hepatofugal flow and 29 matched patients with hepatopetal flow, derived from the group of 228 patients, followed up for a period of 12-18 months, showed that variceal bleeding occurred in 9 of 29 patients with hepatopetal flow and in none of the 15 patients with hepatofugal flow (P less than 0.02). However, no statistical difference was found in the survival rates. This study indicates that the actual prevalence of reversed flow in the portal, splenic, and superior mesenteric veins in a nonselected cirrhotic population is 8.3%. From a clinical point of view, the data suggest that this finding might be considered an important prognostic factor because, while occurring in cirrhotic patients with more severe functional impairment, it might play a protective role against the risk of bleeding.     

Extensive portal and splenic vein thrombosis: differences in hemodynamics and management

BACKGROUND/AIMS: To assess the incidence of extensive portal and splenic vein thrombosis in patients with extrahepatic portal vein obstruction and determine the differences in presentation, portal hemodynamics and management as compared to patients with portal vein thrombosis alone. METHODOLOGY: 118 patients of extrahepatic portal vein obstruction presenting with variceal hemorrhage, having received no definitive treatment prior to presentation were divided into two groups--with portal and splenic vein thrombosis and with portal vein thrombosis, based on ultrasonography and splenoportography. Collateralization patterns on splenoportography were studied. Results of endoscopic variceal sclerotherapy were compared. RESULTS: Portal and splenic vein thrombosis was seen in 39 patients. Collateralization in case of portal and splenic vein thrombosis, in contrast to portal vein thrombosis, was predominantly left sided (74% vs. 9%, p < 0.0001). Fundal gastric varices were seen more often in patients with portal and splenic vein thrombosis (28% vs. 11%, p = 0.02), developing even after variceal obliteration, though obliteration was achieved in fewer sessions. Surgery for control of variceal bleed was performed more in the portal and splenic vein thrombosis group (33% vs. 15%, p = 0.02), especially for gastric varices (28% vs. 9%, p = 0.006). CONCLUSIONS: Portal and splenic vein thrombosis is present in 33% of patients with extrahepatic portal vein obstruction. Hemodynamic patterns differ, accounting for the preponderance of gastric varices on presentation in patients with portal and splenic vein thrombosis and an increased need for surgery.     

Hepatofugal flow on computed tomography of arterial portography: its correlation with esophageal varices bleeding

BACKGROUND/AIMS: To study the portal flow patterns from CTAP (computed tomography of arterial portography), then to predict the existence of esophageal varices bleeding clinically. METHODOLOGY: 192 patients who underwent CTAP from superior mesenteric artery infusion were recruited in this study. The obtained images were classified according to our proposed criteria. Stage 0: hepatopetal flow, when all the contrast medium from the superior mesenteric vein entered the portal vein. Stage 1: when the contrast medium opacified the splenic vein or the other collateral vessels. Stage II: when the contrast medium opacified the paraesophageal vessels without entering the inner wall of the esophagus. Stage III: when the contrast medium opacified the collaterals up to the inner wall of the esophagus. RESULTS: The incidence of bleeding esophageal varices was correlated to the different stages of collateral flows pattern obtained. The esophageal varices bleeding rates were 0/137, 1/16, 1/14, 16/25 for stage 0, I, II and III, respectively. The incidence of bleeding esophageal varices was significantly higher in stage III group than in the other groups (P < 0.001). The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of stage III patients in regard to the occurrence of bleeding esophageal varices were estimated as 80.0%, 98.8%, 88.9%, 94.8%, and 94.3%, respectively. CONCLUSIONS: Our results show that CTAP demonstrates the portal flow patterns and collateral veins clearly, which can serve as an excellent imaging modality to predict the risk of esophageal varices bleeding.     

Clinical and Portal Hemodynamic Features in Cirrhotic Patients Having a Large Spontaneous Splenorenal and/or Gastrorenal Shunt

Clinical and portal hemodynamic features in 28 cirrhotic subjects with a large spontaneous spleno- and/or gastrorenal shunt were studied in comparison with 30 control cirrhotic cases without such collaterals. Forty-six percent of the former had chronic hepatic encephalopathy, but none of the latter was encephalopathic. These patients with large renal shunts were divided into those with and those without encephalopathy. Large esophageal varices were significantly less common in patients with a large shunt and encephalopathy compared with those who had a large shunt but no encephalopathy, and the control. But there was no significant difference of past variceal bleeding among these three groups. In all those with encephalopathy, part of superior mesenteric venous blood was shunting through these collaterals into the left renal vein or inferior vena cava, but the same was not demonstrable in patients with a large shunt and no encephalopathy and control cirrhotics. In the chronic encephalopathic, portal venous flow was estimated to be less than one-half of that in control cirrhotics, and the portion of superior mesenteric venous blood that was flowing hepatofugally through a large shunt into the left renal vein seemed about the same or greater than the portal venous flow. Thus, a large spontaneous spleno- and/or gastrorenal shunt might prevent development of large esophageal varices but not variceal hemorrhage and it increased a risk of chronic hepatic encephalopathy.     

Sinistral portal hypertension. A case report

Sinistral portal hypertension is a clinical syndrome of gastric variceal hemorrhage in the setting of splenic vein thrombosis due to a primary pancreatic pathology. The distinguishing features from other forms of portal hypertension are preserved liver function and a patent extrahepatic portal vein. The important causes include acute and chronic pancreatitis, pancreatic pseudocysts and pancreatic carcinomas. Benign pancreatic neoplasms only rarely cause sinistral portal hypertension. Splenic vein thrombosis complicates 7-20% of patients having pancreatitis or a pancreatic pseudocyst; however, bleeding occurs in only approximately 5% of patients. The diagnosis of sinistral portal hypertension is achieved by a combination of gastroscopy, liver function tests, ultrasound examination (with Doppler) and/or contrast-enhanced CT scan of the abdomen. A mere demonstration of sinistral portal hypertension does not warrant intervention. An expectant management is justifiable in asymptomatic patients with pancreatitis. However, concomitant splenectomy may be considered in patients undergoing operative treatment of symptomatic chronic pancreatitis if sinistral portal hypertension and gastroesophageal varices are present. In patients presenting with gastric variceal hemorrhage, splenectomy (with treatment for the primary pancreatic pathology, e.g. distal pancreatectomy) is curative with excellent long term results.     

Splenogastrorenal shunt in portal hypertension: a little known entity. Study of 6 cases and review of the literature

The authors report 6 cases of portal hypertension with gastrorenal shunt. This shunt did not arise from the left gastric vein, but from the splenic vein. Portal hypertension was related to alcoholic cirrhosis in 3 cases, to extensive portal thrombosis in 2 cases, and to nodular regenerative hyperplasia of the liver in one case. A gastrointestinal hemorrhage revealed portal hypertension and the liver disease in the 3 cases of alcoholic cirrhosis and complicated the course of the disease in the other cases. Hemorrhage was either massive and life-threatening or often recurred. It was related to a rupture of fundic varices in all cases. The fundic varices were not associated with esophageal varices in the 3 cases of cirrhosis. The degree of portal hypertension was above 20 mm Hg, as assessed by the portohepatic gradient (one case), or the pressure gradient between a tributary portal system vein and the inferior vena cava during laparotomy (5 cases). Definitive control of hemorrhage could not be achieved by endoscopic variceal sclerotherapy (2 cases) or percutaneous transhepatic embolization (one case). Portacaval shunt or splenectomy was performed in 5 cases. These findings suggest that spontaneous splenogastrorenal shunt is a clinical and hemodynamic entity which requires specific treatment when associated with gastric variceal bleeding.     

Treatment of bleeding stomal varices by balloon-occluded retrograde transvenous obliteration

Although stomal varices are a rare complication, bleeding stomal varices often need to be treated owing to symptoms of hypovolemic shock, recurrence of stomal bleeding, or deterioration in the quality of life. Various treatment strategies for the management of bleeding stomal varices have thus far been reported. We report the case of a 60-year-old woman with refractory recurrent bleeding from varices in a sigmoid stoma, along with nonalcoholic steatohepatitis and marked splenomegaly. A physical examination revealed that the skin was discolored and bluish around the circumference of the sigmoid stoma. The venous phase of a celiac arteriogram revealed an afferent vein from the splenic vein and another from the inferior mesenteric vein, and veins draining into the left superficial epigastric vein. A balloon-occluded retrograde transvenous obliteration (BRTO) procedure was performed. The skin around the stoma, initially discolored bluish, improved markedly. After 10 months of follow-up, the patient has remained well without further episodes of stomal bleeding. To our knowledge, this is the first case of recurrent hemorrhage from stomal varices that was successfully treated by BRTO in a patient with portal hypertension.     

Portal and mesenteric venous thrombosis as a complication of endoscopic sclerotherapy

We report on the occurrence of portal and mesenteric venous thrombosis in two patients who underwent endoscopic injection sclerotherapy (EIS) for bleeding esophageal varices. One patient was diagnosed at autopsy, and portal and mesenteric venous thrombosis was not suspected during life. The second patient was suspected on ultrasound examination and was diagnosed by angiography. In the second case, therapy was effective and symptoms disappeared. He was treated by a distal splenorenal shunt after he had stabilized for 1 month. During the operation, no evidence of mesenteric infarction was found. The venous phase of the superior mesenteric arteriogram 1 month after surgery revealed an organized thrombosis in the right intrahepatic portal branches. No other thrombi were seen. This patient is the first reported who has survived portal and mesenteric venous thrombosis after sclerotherapy.     

Acute gastric hemorrhage secondary to wandering spleen

Summary A patient presenting with acute life-threatening upper gastrointestinal hemorrhage caused by a wandering spleen is reported. Emergency laparotomy revealed profuse gastric bleeding, large engorged varicose veins in the gastric wall, and a normal liver parenchyma. Gastroscopy after arrest of the hemorrhage showed varicose veins in the fundus without esophageal varices. Angiography revealed an ectopic spleen, occlusion of the splenic vein, and large venous collaterals in the gastric fundus. Elective splenectomy was performed. Wandering spleen as a cause of left-sided portal hypertension, also referred to as segmental splenic hypertension, is discussed.     

Myelofibrosis, splenomegaly, and portal hypertension

A patient with chronic myelofibrosis and massive splenomegaly developed portal hypertension with haematemesis occurring from radiologically proven oesophageal varices. Transjugular liver biopsy showed only myeloid metaplasia, and radiological evaluation of the portal vascular system was undertaken to establish a diagnosis of hyperkinetic portal hypertension as a basis for therapeutic splenectomy. The alternative and rare situation of splenic and portal vein occlusion was demonstrated and therefore removal of the spleen was not an appropriate procedure for relief of portal hypertension. The variceal bleeding was successfully controlled with injection sclerotherapy.     

Treatment of gastric varices with partial splenic embolization in a patient with portal vein thrombosis and a myeloproliferative disorder

Therapeutic options for gastric variceal bleeding in the presence of extensive portal vein thrombosis associated with a myeloproliferative disorder are limited. We report a case of a young woman who presented with gastric variceal bleeding secondary to extensive splanchnic venous thrombosis due to a Janus kinase 2 mutation associated myeloproliferative disorder that was managed effectively with partial splenic embolization.     

Membranous obstruction of the portal vein. A case report

Membranous obstruction of the portal vein has not been previously reported. This 56-yr-old Indonesian man with a history of a tropical fever 5 yr earlier presented with variceal bleeding. Transhepatic obliteration of the varices was attempted, but the catheter placed in the right portal branch would not pass beyond the porta hepatis. Another catheter was inserted into the portal trunk under ultrasound guidance. Simultaneous opacification through the two catheters demonstrated a complete membranous obstruction of the portal vein at the porta hepatis and a portal-superior mesenteric-venous axis that had lost communication with incoming veins and the left portal branch, most likely because of multiple thrombosis. Other angiographic procedures also revealed marked hepatopetal collaterals (cavernous transformation) entering the liver through the hilum. Liver biopsy showed acute posttransfusion hepatitis superimposed upon portal fibrosis. The possible mechanism for membrane formation in relation to thrombosis is discussed.     

Ileal Varices Revealed by Recurrent Hematuria in a Patient with Portal Hypertension and Mekong Schistosomiasis

This present report describes a unique case of a patient with ileal varices revealed by recurrent bleeding from vesical varicosities. Ileal varices were associated with portal hypertension secondary to portal thrombosis. An unusual ileovesical shunt was demonstrated by the venous phase of the superior mesenteric arteriogram. This shunt was favored by adhesions between an abnormal ileal loop, which was infiltrated with ova of schistosome mekongi, and the superior vesical wall. The patient was treated successively by lysis of adhesions and ileal resection. No portacaval shunt was performed.     

Portal hemodynamics in patients with gastric varices. A study in 230 patients with esophageal and/or gastric varices using portal vein catheterization

The hemodynamic features of gastric varices are not well documented. The purpose of this study was to investigate the nature of hepatofugal collateral veins, their origins, the direction of blood flow in the major veins and collateral veins, and portal venous pressure. To this end, 230 patients, mostly cirrhotic, who had esophageal or gastric varices, or both, demonstrated by endoscopy were investigated by portal vein catheterization. The findings were correlated with endoscopically assessed degrees of varices. Gastric varices were seen in 57% of the patients with varices due to portal hypertension. In most of the patients with advanced gastric varices, esophageal varices were minimal or absent. When patients with gastric varices were compared with those having predominantly esophageal varices, it was found that advanced gastric varices were more frequently supplied by the short and posterior gastric veins, they were almost always associated with large gastrorenal shunts, and portal venous pressure in patients with large gastric varices was lower. Chronic portal systemic encephalopathy was more common in patients with large gastric varices due to hepatofugal flow of superior mesenteric venous blood in the splenic vein than in patients with predominantly esophageal varices. Thus, the hemodynamics in patients with large gastric varices are distinctly different from those in patients with mainly esophageal varices, and such differences seem to account for the differing incidence of chronic encephalopathy and variceal bleeding.