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Refractory Ascites (refractory + ascites)
Selected AbstractsManagement of refractory ascites and hepatorenal syndromeJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2002Anuchit Chutaputti Abstract, Refractory ascites and hepatorenal syndrome (HRS) are the late complications of the terminal stages of cirrhosis. The definitions of refractory ascites and HRS proposed by the International Ascites Club in 1996 are now widely accepted, and are useful in diagnosis, treatment and research in this field. In both conditions, the only treatment of proven value for improved survival is liver transplantation. However, because of better understanding about the pathophysiology of HRS, including the roles of portal hypertension, ascites formation and hemodynamic derangements, treatments such as transjugular intrahepatic portasystemic shunt (TIPS) and new pharmacological agents may be considered to alleviate the problem prior to transplantation. Symptomatic treatment of refractory ascites includes TIPS and repeated large volume paracentesis. Transjugular intrahepatic portasystemic shunt can improve survival while waiting for liver transplantation. Practical management guidelines for TIPS and large volume paracentesis, including the prevention and management of further complications, are considered in this review. © 2002 Blackwell Publishing Asia Pty Ltd [source] Refractory ascites: can it be defined only by the response to furosemide and spironolactone?LIVER INTERNATIONAL, Issue 9 2010George Kalambokis No abstract is available for this article. [source] Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome,HEPATOLOGY, Issue 6 2007Aleksander Krag Patients with advanced cirrhosis and ascites are characterized by circulatory dysfunction with splanchnic vasodilatation and renal vasoconstriction, which often lead to ascites. The vasoconstrictor terlipressin improves renal function in hepatorenal syndrome (HRS). The aim of this study was to evaluate if terlipressin also improves renal function in patients with ascites without HRS. Twenty-three patients with cirrhosis participated; 15 with nonrefractory ascites were randomized to either terlipressin (N group, n = 11) or a placebo (P group, n = 4), and 8 had refractory ascites and received terlipressin (R group). The glomerular filtration rate (GFR), sodium clearance (CNa), lithium clearance (CLi), osmolal clearance (COsm), and urine sodium concentration (UNa) were assessed before and after the injection of 2 mg of terlipressin or the placebo. GFR increased in the N group (69 ± 19 versus 92 ± 25 mL/min, P < 0.005) and in the R group (31 ± 19 versus 41 ± 31 mL/min, P < 0.05) after terlipressin. In the N group, terlipressin induced an increase in CNa (0.89 ± 0.21 versus 1.52 ± 1.45 mL/min, P < 0.05), CLi (17.3 ± 8.9 versus 21.5 ± 11.6 mL/min, P < 0.05), and COsm (2.10 ± 0.81 versus 3.06 ± 2.0 mL/min, P < 0.05). In the R group, terlipressin induced an increase in CNa (0.11 ± 0.18 versus 0.35 ± 0.40 mL/min, P < 0.05) and CLi (5.5 ± 4.2 versus 9.5 ± 8.55 mL/min, P < 0.05). UNa increased in both groups after terlipressin (P < 0.005). Plasma norepinephrine (P < 0.05) and renin (P < 0.05) decreased after terlipressin. All parameters remained unchanged after the placebo. Conclusion: The vasopressin 1 receptor agonist terlipressin improves renal function and induces natriuresis in patients with cirrhosis and ascites without HRS. Vasoconstrictors may represent a novel future treatment modality for these patients. (HEPATOLOGY 2007.) [source] The effect of single oral low-dose losartan on posture-related sodium handling in post-TIPS ascites-free cirrhosis,HEPATOLOGY, Issue 3 2006George Therapondos Post-TIPS ascites-free patients with cirrhosis and previous refractory ascites demonstrate subtle sodium retention when challenged with a high sodium load. This is also observed in pre-ascitic patients with cirrhosis. This phenomenon is dependent on an intrarenal angiotensin II (ANG II) mechanism related to the assumption of erect posture. We investigated whether similar mechanisms were involved in post-TIPS ascites-free patients, by studying 10 patients with functioning TIPS and no ascites. We measured the effect of changing from supine to erect posture on sodium excretion at baseline and after single oral low dose losartan (7.5 mg) which has been shown to blunt proximal and distal tubular sodium reabsorption in pre-ascites. At baseline, the assumption of erect posture produced a reduction in sodium excretion (from 0.30 ± 0.06 to 0.13 ± 0.02 mmol/min, P = .05), which was mainly due to an increase in proximal tubular reabsorption of sodium (PTRNa) (69.7 ± 3.1% to 81.1 ± 1.8%, P = .003). The administration of losartan resulted in a blunting of PTRNa (supine 69.7 ± 3.1% to 63.9 ± 3.9%, P = .01 and erect 81.1 ± 1.8% to 73.8 ± 2.4%, P = .01), accompanied by an increased distal tubular reabsorption of sodium in both postures, with no overall improvement in sodium excretion on standing. In conclusion, post-TIPS ascites-free patients with cirrhosis exhibit erect posture-induced sodium retention. We speculate that (1) this effect is partly mediated by the effect of ANG II on PTRNa and (2) that the inability of low dose losartan to block the erect posture-induced sodium retention may be related to the erect posture-induced rise in aldosterone which is unmodified by losartan. (HEPATOLOGY 2006;44:640,649.) [source] Serum sodium predicts mortality in patients listed for liver transplantation,HEPATOLOGY, Issue 1 2005Scott W. Biggins With the implementation of the model for end-stage liver disease (MELD), refractory ascites, a known predictor of mortality in cirrhosis, was removed as a criterion for liver allocation. Because ascites is associated with low serum sodium, we evaluated serum sodium as an independent predictor of mortality in patients with cirrhosis who were listed for liver transplantation and whether the addition of serum sodium to MELD was superior to MELD alone. This is a single-center retrospective cohort of all adult patients with cirrhosis listed for transplantation from February 27, 2002, to December 26, 2003. Listing laboratories were those nearest the listing date ±2 months. Of the 513 patients meeting inclusion criteria, 341 were still listed, while 172 were removed from the list (105 for transplantation, 56 for death, 11 for other reasons). The median serum sodium and MELD scores were 137 mEq/L (range, 110-155) and 15 (range, 6-51), respectively, at listing. Median follow-up was 201 (range, 1-662) days. The risk of death with serum sodium < 126 mEq/L at listing or while listed was increased, with hazard ratios of 7.8 (P < .001) and 6.3 (P < .001), respectively, and the association was independent of MELD. The c-statistics of receiver operating characteristic curves for predicting mortality at 3 months based upon listing MELD with and without listing serum sodium were 0.883 and 0.897, respectively, and at 6 months were 0.871 and 0.905, respectively. In conclusion, serum sodium < 126 mEq/L at listing or while listed for transplantation is a strong independent predictor of mortality. Addition of serum sodium to MELD increases the ability to predict 3- and 6-month mortality in patients with cirrhosis. (HEPATOLOGY 2005;41:32,39.) [source] Liver transplantation for the sequelae of intra-operative bile duct injuryHPB, Issue 3 2002E De Santibañes Background Intra-operative bile duct injuries (IBDI) are potentially severe complications of the treatment of benign conditions, with unpredictable long-term results. Multiple procedures are frequently needed to correct these complications. In spite of the application of these procedures, patients with severe injuries can develop irreversible liver disease. Liver transplantation (LT) is currently the only treatment available for such patients, but little information has been published concerning the results of LT. Methods Eight patients with LT for end-stage liver disease for IBDI were studied retrospectively. They had failure of multiple previous treatments and experienced recurrent episodes of cholangitis, oesophageal variceal bleeding, severe pruritus, refractory ascites and spontaneous peritonitis. Results Mean recipient hepatectomy time was of 243 minutes (range 140,295 min), the complete procedure averages 545 minutes (260,720) and intraoperative red-blood-cells consumption was 6.5 units (1,7). One patient required reoperation due to perforation of a Roux-en-Y loop, and three developed minor complications (2 wound infections, 1 inguinal lymphocele). One patient died due to nosocomial pneumonia (mortality rate 12.5%). One patient required retransplantation due to delayed hepatic artery thrombosis. At follow-up 75% of patients are alive with normal graft function and an excellent quality of life. Conclusions LT represents a safe curative treatment for end-stage liver disease after IBDI, albeit a major undertaking in the context of a surgical complication in the treatment of benign disease. The complications of the surgical procedure and the long-standing immunosupression impart a high cost for resolutions of these sequelae but LT represents the only long-term effective treatment for these selected patients. [source] Evaluation of hernia repair operation in Child,Turcotte,Pugh class C cirrhosis and refractory ascitesJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2007Joo Kyung Park Abstract Background and Aim:, Abdominal wall hernia is a common feature of decompensated liver cirrhosis and frequently causes life-threatening complications or severe pain. However, there have been no data reported on postoperative mortality, hepatic functional deterioration and recurrence rate according to Child,Turcotte,Pugh (CTP) class and to the presence of refractory ascites. Methods:, The study population comprised 53 liver cirrhosis patients who underwent hernia repair operation. Comparisons were made of 30-day mortality among the different CTP classes, and between those with or without refractory ascites. Liver function was also analyzed just before the operation, in the immediate postoperative period, and in the remote postoperative period. Results:, Seventeen patients were in CTP class A, 27 patients in class B, and 9 patients in class C. The median follow-up duration was 24 months. There was single 30-day postoperative mortality in class C, and no CTP class deterioration after 30 days of operation. There was no mortality or recurrences in 17 patients with medically refractory ascites. The difference in 30-day mortality according to CTP class and the presence of refractory ascites did not show statistical significance (P = 0.17 and 0.97, respectively). Conclusion:, Hernia operation could be done safely in CTP class A and B with low rate of recurrences, and there was no definitive increase in the operative risk in class C. In addition, refractory ascites did not increase operative risk and recurrence rate. Therefore, surgical repair might be recommended even in patients with refractory ascites and poor hepatic function to prevent life-threatening complications or severe pain. [source] Management of refractory ascites and hepatorenal syndromeJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2002Anuchit Chutaputti Abstract, Refractory ascites and hepatorenal syndrome (HRS) are the late complications of the terminal stages of cirrhosis. The definitions of refractory ascites and HRS proposed by the International Ascites Club in 1996 are now widely accepted, and are useful in diagnosis, treatment and research in this field. In both conditions, the only treatment of proven value for improved survival is liver transplantation. However, because of better understanding about the pathophysiology of HRS, including the roles of portal hypertension, ascites formation and hemodynamic derangements, treatments such as transjugular intrahepatic portasystemic shunt (TIPS) and new pharmacological agents may be considered to alleviate the problem prior to transplantation. Symptomatic treatment of refractory ascites includes TIPS and repeated large volume paracentesis. Transjugular intrahepatic portasystemic shunt can improve survival while waiting for liver transplantation. Practical management guidelines for TIPS and large volume paracentesis, including the prevention and management of further complications, are considered in this review. © 2002 Blackwell Publishing Asia Pty Ltd [source] Managing hyponatremia in cirrhosis,JOURNAL OF HOSPITAL MEDICINE, Issue S3 2010Elizabeth Ross MD Abstract The development of hyponatremia represents an ominous event in the progression of cirrhosis to end-stage liver disease. It usually develops in those with refractory ascites and is a manifestation of the non-osmotic release of arginine vasopressin (AVP). In the hospitalized cirrhotic patient, hyponatremia is associated with increased disease severity and mortality. In this article, we review the pathophysiology of hyponatremia, its clinical implications, evaluation, and treatment. Journal of Hospital Medicine 2010;5:S8,S17. © 2010 Society of Hospital Medicine. [source] Clinical Trial: High-dose furosemide plus small-volume hypertonic saline solutions vs. repeated paracentesis as treatment of refractory ascitesALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2009G. LICATA Summary Background, In patients with cirrhosis, ascites is defined as refractory when it cannot be mobilized or recurs early in standard diuretic therapy. Aim, To compare the safety and efficacy of intravenous high-dose furosemide + hypertonic saline solutions (HSS) with repeated paracentesis in patients with cirrhosis and refractory ascites. Patients and methods, Eighty-four subjects (59/25 M/F) with cirrhosis, mostly of viral aetiology, admitted for refractory ascites, were randomly assigned to receive furosemide (250,1000 mg/bid i.v.) plus HSS (150 mL H2O with NaCl 1.4,4.6% or 239,187 mEq/L) (60 patients, Group A) or to repeated paracentesis and a standard diuretic schedule (24 patients, Group B). Results, During hospitalization, Group A patients had more diuresis (1605 ± 131 mL vs. 532 ± 124 mL than Group B patients; P < 0.001) and a greater loss of weight at discharge (,8.8 ± 4.8 kg vs. ,4.5 ± 3.8 kg, P < 0.00). Control of ascites, pleural effusions and/or leg oedema was deemed significantly better in Group A. Conclusions, This randomized pilot study suggests that HHS plus high-dose furosemide is a safe and effective alternative to repeated paracentesis when treating hospitalized patients with cirrhosis and refractory ascites. Larger studies will be needed to evaluate long-term outcomes such as readmission and mortality. [source] Urotensin II: a novel vasoactive mediator linked to chronic liver disease and portal hypertensionLIVER INTERNATIONAL, Issue 9 2007William Kemp Abstract Background/Aims: Urotensin II (UII) is recognised as the most potent human vasoconstrictor; however, its role in chronic liver disease (CLD) is unknown. Aim: We sought to determine serum UII levels in CLD and explore its relationship with clinical features and outcomes of patients with CLD and portal hypertension. Methods: UII was analysed by radio-immunoassay on cirrhotic patients undergoing hepatic venous pressure gradient (HVPG) determination and age- and sex-matched controls. Follow-up data were prospectively recorded. Results: From 1997 to 2004, 80 patients (male/female: 74/6) underwent a total of 94 HVPG assessments. UII was higher in cirrhotic patients compared with controls (2.05±0.06 and 1.55±0.09 pmol/L, P<0.001) and was correlated with HVPG (r=+0.35, P=0.001) and severity of CLD (r=+0.6, P<0.001). UII was higher in patients who developed refractory ascites (2.45±0.13 vs. 1.7±0.12 pmol/L, P<0.001) and in those who died during the follow-up period (2.27±0.15 pmol/L vs. 1.95±0.08 pmol/L, P<0.05). Conclusion: Serum UII is elevated in patients with CLD, and is associated with the severity of the underlying liver disease and the degree of portal hypertension. Baseline levels can predict future complications such as refractory ascites and patient survival. [source] Clinical characteristics and outcome of patients with cirrhosis and refractory ascitesLIVER INTERNATIONAL, Issue 5 2004Richard Moreau Abstract: Background: In patients with cirrhosis, refractory ascites is associated with a poor prognosis and is an indication for liver transplantation. However, factors that determine prognosis remain unclear. Aims: To investigate the predictive factors of prognosis in patients with refractory ascites. Methods: Seventy-five patients with refractory ascites were followed-up for 18±13 months (mean±SD) and survival was analyzed. Results: The 1-year probability of survival was 52%. Univariate analyses showed that older patients, hepatocellular carcinoma and diabetes, all assessed at entry, were associated with significantly increased risk ratios of death. The risk ratio of death was significantly lower in abstinent alcoholics than in patients with nonalcoholic cirrhosis. The risk ratio of death did not significantly differ between patients with nonalcoholic cirrhosis and nonabstinent alcoholics. Child,Pugh score at entry had no prognostic value. Multivariate analysis showed that older age, hepatocellular carcinoma, diabetes and abstinence were independent prognostic factors. Conclusions: In patients with cirrhosis and refractory ascites, older age, hepatocellular carcinoma and diabetes, but not Child,Pugh score at entry, were independent predictive factors of poor survival while abstinence was an independent predictive factor of good survival. These findings should be taken into account when deciding on liver transplantation in patients with refractory ascites. [source] Recurrent familial hypobetalipoproteinemia,induced nonalcoholic fatty liver disease after living donor liver transplantationLIVER TRANSPLANTATION, Issue 7 2009Noboru Harada Familial hypobetalipoproteinemia (FHBL) is one of the causes of nonalcoholic steatohepatitis (NASH) and a codominant disorder. Patients heterozygous for FHBL may be asymptomatic, although they demonstrate low plasma levels of low-density lipoprotein (LDL) cholesterol and apolipoprotein B. Here we report a nonobese 54-year-old man with decompensated liver cirrhosis who underwent living donor liver transplantation with his son as the donor. Low albuminemia and refractory ascites persisted after transplantation. A biopsy specimen obtained 11 months after liver transplantation revealed severe steatosis and fibrosis, and recurrent NASH was diagnosed on the basis of pathological findings. Both the patient's and donor's laboratory tests demonstrated low LDL cholesterol and apolipoprotein levels. Because mutations in messenger RNAs of microsomal triglyceride transfer protein and apolipoprotein B genes were excluded neither in the recipient nor in the donor, both were clinically diagnosed as being heterozygous for FHBL. We successfully treated the recipient with heterozygous FHBL,induced recurrent NASH after liver transplantation using our diet and exercise programs. Liver Transpl 15:806,809, 2009. © 2009 AASLD. [source] Sclerosing peritonitis and mortality after liver transplantationLIVER TRANSPLANTATION, Issue 4 2009Kristin Mekeel Sclerosing peritonitis describes the development of a peel or rind of fibrosis that spreads over the peritoneal surface and can lead to recalcitrant ascites, bowel obstruction, and sepsis. It is well described as a complication of peritoneal dialysis, especially with episodes of bacterial peritonitis. It is also a complication of end-stage liver disease with ascites and liver transplantation. This article describes 3 cases of sclerosing peritonitis present at the time of liver transplantation or soon after. All 3 patients had massive refractory ascites with episodes of spontaneous bacterial peritonitis prior to transplantation. Two patients had evidence of a fibrous peel at the time of transplantation. Postoperatively, all 3 patients continued to have refractory ascites and episodes of peritonitis, along with partial small bowel obstructions, abdominal pain, and malnutrition. Two patients also had constriction of the graft, including biliary obstruction and inferior vena cava and outflow obstruction, which has not been previously described. All 3 patients eventually died from complications related to the sclerosing peritonitis. Liver Transpl 15:435,439, 2009. © 2008 AASLD. [source] Use of splenic artery embolization to relieve tense ascites following liver transplantation in a patient with paroxysmal nocturnal hemoglobinuriaLIVER TRANSPLANTATION, Issue 11 2007Charissa Y. Chang Recurrent venous thrombosis following liver transplantation for Budd-Chiari syndrome is common, particularly in the setting of an underlying myeloproliferative disorder. We describe a patient who developed refractory ascites due to portal vein thrombosis following liver transplantation for Budd-Chiari syndrome in the setting of paroxysmal nocturnal hemoglobinuria. Extensive portal vein thrombosis, dense abdominal adhesions, and portosystemic collaterals precluded the use of a transjugular intrahepatic portosystemic shunt or surgical portosystemic shunt to manage the patient's ascites. Splenic artery embolization to decrease portal hypertension was performed, and this resulted in complete resolution of ascites. This case demonstrates the successful use of splenic artery embolization to manage ascites due to portal vein thrombosis following liver transplantation. Splenic artery embolization may be considered as an alternative option for the management of refractory ascites due to portal hypertension in patients who are unable to undergo safe transjugular intrahepatic portosystemic shunt or surgical shunt placement. Liver Transpl 13:1532,1537, 2007. © 2007 AASLD. [source] Vitamin A toxicity: When one a day doesn't keep the doctor awayLIVER TRANSPLANTATION, Issue 12 2006Rekha Cheruvattath Vitamin A toxicity has been reported to cause severe liver disease and, occasionally, liver failure. Herein we present the case of a 60-year-old male with symptoms of muscle soreness, alopecia, nail dystrophy, and ascites. He continued to deteriorate with the development of refractory ascites, renal insufficiency, encephalopathy, and failure to thrive. A liver biopsy demonstrated presence of Ito cells and vacuolated Kupffer cells without the presence of cirrhosis. His clinical history revealed ingestion of large doses of vitamin A. His worsening clinical situation ruled out the possibility of a transjugular intrahepatic portosystemic shunt. The patient underwent orthotopic liver transplantation with resolution of symptoms. Vitamin A toxicity should be considered in the differential diagnosis of noncirrhotic portal hypertension. In conclusion, liver transplantation is a valid option if no improvement occurs in spite of cessation of the medication. Liver Transpl 12:1888,1891, 2006. © 2006 AASLD. [source] Ascites after liver transplantation,A mysteryLIVER TRANSPLANTATION, Issue 5 2004Charmaine A. Stewart Ascites after liver transplantation, although uncommon, presents a serious clinical dilemma. The hemodynamic changes that support the development of ascites before liver transplantation are resolved after transplant; therefore, persistent ascites (PA) after liver transplantation is unexpected and poorly characterized. The aim of this study was to define the clinical factors associated with PA after liver transplantation. This was a retrospective case,control analysis of patients who underwent liver transplantation at the University of Pennsylvania. PA occurring for more than 3 months after liver transplantation was confirmed by imaging studies. PA was correlated with multiple recipient and donor variables, including etiology of liver disease, preoperative ascites, prior portosystemic shunt (PS), donor age, and cold ischemic (CI) time. There were 2 groups: group 1, cases with PA transplanted from November 1990 to July 2001, and group 2, consecutive, control subjects who underwent liver transplantation between September 1999 and December 2001. Both groups were followed to censoring, May 2002, or death. Twenty-five from group 1 had ascites after liver transplantation after a median follow-up of 2.6 years. In group 1 vs group 2 (n = 106), there was a male predominance 80% vs 61% (P = .10) with similar age 52 years; chronic hepatitis C virus (HCV) was diagnosed in 88% vs 44% (P < .0001); preoperative ascites and ascites refractory to treatment were more prevalent in group 1 (P = .0004 and P =.02, respectively), and CI was higher in group 1, (8.5 hours vs 6.3 hours, P = .002). Eight of the 25 (group 1) had portal hypertension with median portosystemic gradient 16.5 mm Hg (range, 16,24). PS was performed in 7 of 25 cases, which resulted in partial resolution of ascites. The development of PA after liver transplantation is multifactorial; HCV, refractory ascites before liver transplantation, and prolonged CI contribute to PA after liver transplantation. (Liver Transpl 2004;10:654,660.) [source] Transjugular intrahepatic portosystemic shunts: an updateLIVER TRANSPLANTATION, Issue 3 2003Barbara Rosado Transjugular intrahepatic portosystemic shunts (TIPS) have been used in the treatment of complications of portal hypertension. TIPS is used for the control of acute variceal bleeding and for the prevention of vericeal rebleeding when pharmacologic therapy and endoscopic therapy have failed. Patients with refractory ascites with adequate hepatic reserve and renal function who fail to respond to large volume paracentesis may be reasonable candidates for TIPS. Promising indications for TIPS are Budd-Chiari syndrome uncontrolled by medical therapy, severe portal hypertensive gastropathy, refractory hepatic hydrothorax, and hepatorenal syndrome. TIPS cannot be recommended for preoperative portal decompression solely to facilitate liver transplantation. Special care should be taken to insure proper placement of the stent to avoid increasing the technical difficulty of the transplantation procedure. The major limiting factors for TIPS success are shunt dysfunction and hepatic encephalopathy. Because shunt stenosis is the most important cause of recurrent complications of portal hypertension, a surveillance program to monitor shunt patency is mandatory. The MELD score may be useful in predicting post-TIPS survival, and also in counseling patients and their families. [source] Sclerosing encapsulating peritonitis (abdominal cocoon) associated with liver cirrhosis and diffuse large B-cell lymphoma: Autopsy casePATHOLOGY INTERNATIONAL, Issue 9 2009Sohsuke Yamada A case of sclerosing encapsulating peritonitis (SEP) associated with liver cirrhosis (LC) and complicated by diffuse large B-cell lymphoma (DLBCL) is reported herein. A 49-year-old Japanese man had undergone peritoneo-venous shunt against refractory ascites due to hepatitis C virus-positive uncompensated LC for 2 years. After he received a diagnosis of DLBCL of the left neck lymph node 3 months before his death, palliative care was given because of his poor general condition. He developed severe abdominal distention and pain over 1 week and was found to have marked ascites and whole bowel lumped together on abdominal CT. At autopsy, the peritoneum was covered with a thick white membrane and the bowel could not be distinguished, which was macroscopically characterized by a cocoon-like appearance. Histology indicated a proliferation of diffusely thickened or hyalinized fibrocollagenous tissue in the entire peritoneum with a slight chronic inflammatory infiltrate and without remarkable change of mucosa. A diagnosis of SEP, also known as abdominal cocoon, was established based on these features. Additionally, in the abdominal cavity, a large amount of serous ascites and multiple peritoneal nodules or masses involved by DLBCL were recognized. To the authors' knowledge this is the first case report of SEP associated with LC and complicated by the invasion of DLBCL in the abdominal cavity. [source] Transjugular intrahepatic portosystemic shunt: an analysis of outcomesANZ JOURNAL OF SURGERY, Issue 10 2009Timothy P. Kurmis Abstract Background:, Transjugular intrahepatic portosystemic shunts (TIPS) are utilized for the management of complications of portal hypertension, particularly diuretic-resistant ascites and recurrent variceal bleeding. It has also been applied in Budd,Chiari syndrome and hepatorenal syndrome. We report the results in a small series, over 9 years, from a single centre, and compare these to those published in the literature. Methods:, A retrospective case note review of 20 consecutive TIPS procedures performed at Flinders Medical Centre from January 1997 to December 2005 was completed. All indications were included in the analysis. Underlying liver disease, peri-procedure complications, relief of symptoms and patient survival were recorded. Data on type of TIPS, shunt patency and method of follow-up were recorded. Results:, Thirty-six TIPS were performed in 20 subjects. All initial TIPS attempts were successful. Indications were: refractory ascites (18), acute variceal bleeding (12) and hepatorenal syndrome (2). There were no peri-procedure deaths, however. Ninety-day mortality was 20%. Outcomes in model of end-stage liver disease score and biochemical characteristics post-TIPS were comparable to those reported. Overall, TIPS dysfunction rate was 35% at 1 year. TIPS follow-up and patency surveillance was an ad hoc combination of Doppler ultrasound and venography. Conclusion:, TIPS procedure outcomes in our centre are similar to those reported in the literature from large centres. TIPS patency rates may be improved with regular monitoring and early intervention when stenosis occurs. [source] |