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Surgical management of extrahepatic portal vein obstruction at university hospital
Abstract and Figures
Introduction
Extrahepatic portal vein obstruction (EHPVO) is a second most common cause of portal hypertension which causes upper gastrointestinal (GI) bleeding. Primary management of upper GI bleeding is endoscopic therapy. However, surgery is performed as a secondary management of upper GI bleeding and if patients fails to respond endoscopic management or complications of EHPVO develops. The aim of the study was to determine the perioperative outcome of surgery done for EHPVO.
Methods
This is retrospective observational study of all the patients of EHPVO, who were undergone surgical management at Tribhuvan University Teaching Hospital in between April 2015 to March 2017. Data were collected from case sheets of the patients. The demographic and clinical characteristics of the patients, and perioperative and short term outcome of the surgical management of EHPVO patients were analysed.
Results
Total 34 patients were included in the study including 20 males (58.8%) and 14 (41.2%) females with median age of 17 years (4 to 45 years). Most common presentation of EHPVO were fullness in upper abdomen (34/34) upper GI bleeding (29/34). Most of the patients had anemia (33/34), splenomegaly (34/34) and hypersplenism (28/34). Shunt surgery was performed in 20 patients and modified Hassab’s procedure in 14 patients. There was no post-operative severe complication except one mortality in Hassab’s procedure. The median duration of surgery was higher in shunt surgery group compared to devascularisation group (240 minutes versus 180 minutes). There were no significant differences in intraoperative blood loss, total hospital stays and recurrent upper GI bleeding in both surgery groups.
Conclusions
Surgical management for EHPVO have good perioperative and short term outcome.
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Non-cirrhotic portal hypertension refers to causes of portal hypertension (PHT) other than cirrhosis which are pre-sinusoidal in nature. The major causes are extra-hepatic portal vein obstruction (EHPVO) and congenital hepatic fibrosis (CHF). Non-cirrhotic portal fibrosis also constitutes a small proportion of paediatric PHT. EHPVO is characterized by obstruction of the extra-hepatic portal vein with or with-out involvement of the intra-hepatic portal veins or splenic or superior mesenteric veins. What causes EHPVO is unknown however; various theories like infection, umbilical sepsis and hypercoagulable states have been postulated. Endoscopic management is highly successful in controlling acute variceal bleeding and eradication of esophageal varices. At present the focus in EHPVO has gradually shifted to the management of long-term problems of bleeding from gastric and ectopic varices, growth retardation, portal biliopathy, massive splenomegaly with poor quality of life, hypersplenism and minimal hepatic encephalopathy. Improved outcomes of surgical management of EHPVO along with newer surgical procedures have changed the outlook towards surgery. Congenital hepatic fibro-sis has a good long-term outcome in the absence of renal cysts and recurrent cholangitis due to bil-iary cystic disease. Non-cirrhotic portal fibrosis is seen in adolescents and has a good outcome with endoscopic and surgical management.
Pediatric portal hypertension management is a team approach between the patient, the patient's family, the primary caregiver, and specialty providers. Evidence-based practice guidelines have not been established in pediatrics. This article serves as a review for the primary care NP in the management of pediatric portal hypertension, discussing the etiology, pathophysiology, and clinical presentation of pediatric portal hypertension, diagnostic tests, and treatment and management options.
Objective
To evaluate the clinical presentation, possible etiological factors, management and outcome of patients in our hospital with extrahepatic portal vein obstruction (EHPVO).
Materials and Methods
This study included patients with EHPVO followed up in our department during last 10 years. Patients of cirrhosis with EHPVO were excluded. Patients’ clinical presentation, etiology of EHPVO, management and outcome results were analyzed.
Results
Of 30 patients, 19 (67.9%) were males. Median age was 12 years. Of 14 patients who underwent liver biopsy 9 had histological activity index stage of 1/6. History of omphalitis and pulmonary tuberculosis was present in one case each. Of 22 patients with the available thrombophilia profile, nine patients had a deficiency of protein C, five patients had a deficiency of protein S, one each had reduced level S of anti-thrombin III and factor V mutation. The predominant presenting symptom was hematemesis (15 patients, 53.6%). Seven patients (25%) had splenomegaly. Three patients (10.7%) had no esophageal varices on endoscopy. Three patients underwent splenectomy due to severe pancytopenia. Endoscopic retrograde cholangipancreatography was performed in four patients (14.3%) due to portal biliopathy. Common bile duct stenting was performed in all four patients. Of them, one patient underwent splenorenal shunt operation for indication of hemobilia. One patient died at the age of 40 years, due to cholangitis and sepsis.
Conclusions
Results from this study show that the anticoagulant deficiency is a common cause of EHPVO in our setup. Hematemesis is a common presenting symptom. Some of these patients have symptomatic portal biliopathy.
A proportion (10%-15%) of patients with variceal bleeding do not respond to medical management and require surgical intervention.
Retrospective analysis of 82 consecutive patients (median age 31 years, range 3-71; 60 male) who underwent salvage surgery for variceal bleeding between 1989 and 2005.
Immediate control of variceal bleeding was achieved in 78 (95%) patients. Four patients (cirrhosis 3, portal vein block 1) continued to bleed in the postoperative period following gastro-esophageal devascularization (3) or portacaval shunt (1). Twelve (15%) patients died in hospital; the commonest cause of death (n=7) was liver failure and sepsis leading to multi-system organ failure. The mortality rate was higher among patients who had undergone emergency surgery for active bleeding than among those who had been adequately resuscitated and evaluated prior to surgery (12/45 vs. 0/37; p< 0.001). Mortality rate tended to be higher in patients with cirrhosis (overall 10/45 [22%]; Child A 1/9 [11%], Child B 4/20 [20%], Child C 5/16 [31%]) than in those with non-cirrhotic portal hypertension (3/37 [8%]; p=ns).
Our data suggest that salvage surgery is justified in patients with variceal bleed in whom non-surgical measures fail.
Portal vein thrombosis (PVT) is a relatively common complication in patients with liver cirrhosis, but might also occur in absence of an overt liver disease. Several causes, either local or systemic, might play an important role in PVT pathogenesis. Frequently, more than one risk factor could be identified; however, occasionally no single factor is discernable. Clinical examination, laboratory investigations, and imaging are helpful to provide a quick diagnosis, as prompt treatment might greatly affect a patient's outcome. In this review, we analyze the physiopathological mechanisms of PVT development, together with the hemodynamic and functional alterations related to this condition. Moreover, we describe the principal factors most frequently involved in PVT development and the recent knowledge concerning diagnostic and therapeutic procedures. Finally, we analyze the implications of PVT in the setting of liver transplantation and its possible influence on patients' future prognoses.
Background:
Proximal splenorenal shunt (PSRS) is a well-accepted surgical procedure for non-cirrhotic portal hypertension (NCPH). Though a patent shunt is important for good long term outcome, there are very few studies on patency of these shunts. We analysed shunt patency using dynamic computed tomographic (CT) portography and compared it with other modalities.
Methods:
From 2004 to 2014, 50 patients with PSRS were evaluated prospectively for shunt patency using dynamic CT portography, clinical parameters and ultrasound Doppler.
Results:
The causes of NCPH were extrahepatic portal vein obstruction (EHPVO) in 38 patients and non-cirrhotic portal fibrosis (NCPF) in 12 patients. The shunt patency rate using clinical parameters, ultrasound Doppler and dynamic CT portography were 70%, 40% and 60% respectively. Clinical parameters overestimated while ultrasound Doppler underestimated the shunt patency rate. Dynamic portography had 100% correlation with conventional angiography in the five patients when this was done. The site of shunt could be demonstrated convincingly by dynamic CT portography. The shunt patency rate decreased over time. It was 64%, 60% and 43% in <1 year, 1-5 years and >5 years respectively. Our NCPF patients had a greater shunt patency rate compared to EHPVO patients (9/12 vs. 21/38) though the difference was not significant. Only size of the splenic vein had a significant impact on the shunt patency rate on statistical analysis.
Conclusions:
Dynamic CT portography is useful for evaluation of shunt patency. Proximal splenorenal shunts have a high blockage rate which has hitherto not been reported.
Non-cirrhotic portal hypertension (NCPH) encompasses a wide range of disorders, primarily vascular in origin, presenting with portal hypertension (PHT), but with preserved liver synthetic functions and near normal hepatic venous pressure gradient (HVPG). Non-cirrhotic portal fibrosis/Idiopathic PHT (NCPF/IPH) and extrahepatic portal venous obstruction (EHPVO) are two prototype disorders in the category. Etiopathogenesis in both of them centers on infections and prothrombotic states. Presentation and management strategies focus on repeated well tolerated episodes of variceal bleed and moderate to massive splenomegaly and other features of PHT. While the long-term prognosis is generally good in NCPF, portal biliopathy and parenchymal extinction after prolonged PHT makes outcome somewhat less favorable in EHPVO. While hepatic schistosomiasis, congenital hepatic fibrosis and nodular regenerative hyperplasia have their distinctive features, they often present with NCPH.
A total of 152 consecutive children with oesophageal varices have been endoscopically reviewed since 1979. In all, 108 of these children presented with variceal bleeding which was managed by injection sclerotherapy. Variceal obliteration was achieved in 33 (92 per cent) children with extrahepatic portal hypertension and 54 (75 per cent) with intrahepatic portal hypertension. Prophylactic injection sclerotherapy was used to obliterate large varices in 11 children with no history of haemorrhage. Bleeding episodes occurred in 38 (39 per cent) children before variceal obliteration was complete. However, the mortality rate from variceal bleeding was only 1 per cent. Complications were oesophageal ulceration (29 per cent) and stricture (16 per cent) which both resolved with conservative management. During a mean follow-up period of 2.9 years after sclerotherapy, recurrent oesophageal or gastric varices developed in 12 (12 per cent) cases, with rebleeding in 9 (9 per cent), but all responded successfully to a second course of treatment. These results are superior to contemporary surgical management and injection sclerotherapy should therefore currently be the primary treatment of choice for bleeding oesophageal varices in children.
Choledocholithiasis is a common clinical problem. In more than 95% of cases, ductal stones occur after gallbladder stones have migrated via the cystic duct or rarely a fistulous tract. 1 Certain conditions can cause a predisposition to ductal stones in the absence of gallbladder stones. These include traumatic or inflammatory biliary strictures, papillary stenosis, 2 juxtapapillary duodenal diverticula, biliary parasitism, 3 and extrinsic pressure on the bile duct by the adjacent structures. Portal biliopathy is a term used to describe abnormalities of the intrahepatic and extrahepatic bile ducts (with or without gallbladder involvement) in patients with portal hypertension. 4 Biliary stasis is produced by pressure effects from engorged paracholedochal and epicholedochal collaterals on the bile ducts. Such collaterals are present in all patients with extrahepatic portal v ein obstruction (EHPVO), and the frequency and severity of portal b iliopathy is greater in these patients than in patients with liver disease. This report describes four patients with EHPVO who had choledocholithiasis and were managed with endoscopic sphincterotomy.