warfarin and Ascites

Budd-Chiari syndrome is a rare disorder characterised by hepatic venous outflow obstruction. It affects 1.4 per million people, and presentation depends upon the extent and rapidity of hepatic vein occlusion. An underlying myeloproliferative neoplasm is present in 50% of cases with other causes including infection and malignancy. Common symptoms are abdominal pain, hepatomegaly and ascites; however, up to 20% of cases are asymptomatic, indicating a chronic onset of hepatic venous obstruction and the formation of large hepatic vein collaterals. Doppler ultrasonography usually confirms diagnosis with cross-sectional imaging used for complex cases and to allow temporal comparison. Myeloproliferative neoplasms should be tested for even if a clear causative factor has been identified. Management focuses on anticoagulation with low-molecular-weight heparin and warfarin, with the new oral anticoagulants offering an exciting prospect for the future, but their current effectiveness in Budd-Chiari syndrome is unknown. A third of patients require further intervention in addition to anticoagulation, commonly due to deteriorating liver function or patients identified as having a poorer prognosis. Prognostic scoring systems help guide treatment, but management is complex and patients should be referred to a specialist liver centre. Recent studies have shown comparable procedure-related complications and long-term survival in patients who undergo transjugular intrahepatic portosystemic shunting and liver transplantation in Budd-Chiari syndrome compared with other liver disease aetiologies. Also, the optimal timing of these interventions and which patients benefit from liver transplantation instead of portosystemic shunting remains to be answered.

Topics: Abdominal Pain; Adult; Anticoagulants; Ascites; Budd-Chiari Syndrome; Heparin, Low-Molecular-Weight; Hepatomegaly; Humans; Liver Transplantation; Middle Aged; Portasystemic Shunt, Transjugular Intrahepatic; Prognosis; Ultrasonography, Doppler, Color; Warfarin

Peritoneal tuberculosis is an important problem in regions of the world where tuberculosis is still prevalent (Chest 1991; 99:1134). Atypical presentations such as portal vein thrombosis can delay diagnosis or result in misdiagnosis (Gut 1990; 31:1130, Acta ClinBelg 2012; 67(2):137-9, J Cytol Histol 2014; 5:278, Digestive Diseases and Sciences 1991; 36(1):112-115). A high index of suspicion is required for the diagnosis of peritoneal tuberculosis, as the analysis of peritoneal fluid for tuberculous bacillus is often ineffective, and may increase mortality due to delayed diagnosis. (Clin Effect Dis 2002;35: 409-13) In light of new evidence, peritoneal biopsy through laparoscopy or laparotomy has emerged as the gold standard for diagnosis (Clin Effect Dis 2002; 35: 409-13).. We report a case of a 35 year old Sri Lankan female employed in a Middle - Eastern country who presented with progressive abdominal distention and constitutional symptoms for four months duration. She had been investigated abroad and diagnosed with ascites with chronic portal vein thrombosis following which warfarin therapy had been commenced suspecting an underlying thrombophilia. Despite treatment her symptoms had worsened. Therefore she had decided to return to Sri Lanka for further evaluation. After ruling out inherited thrombophilic states and the antiphospholipid syndrome, further investigations revealed a transudative ascites and high inflammatory markers. The tuberculosis work up on peritoneal fluid was negative. Therefore, we proceeded with laparoscopy which showed multiple nodular deposits on abdominal wall, bowel and omentum and peritoneal biopsy revealed granulomatous inflammation with caseous type necrosis compatible with mycobacterium tuberculosis infection. This was confirmed by tuberculosis genome identification on the biopsy sample confirming a diagnosis of peritoneal tuberculosis with secondary portal vein thrombosis and cavernous formation due to local inflammation. The patient was started on anti-tuberculosis treatment and warfarin was discontinued, following which she made a remarkable recovery.. Peritoneal tuberculosis can present with unusual manifestations such as portal vein thrombosis and transudative ascites causing a diagnostic dilemma. Ascitic fluid analysis is generally not diagnostic. Under such circumstances peritoneal biopsy should be performed as it has a good diagnostic yield and accuracy.

Topics: Adult; Anticoagulants; Antitubercular Agents; Ascites; Ascitic Fluid; Diagnosis, Differential; Female; Humans; Laparoscopy; Mycobacterium tuberculosis; Peritonitis, Tuberculous; Portal Vein; Sri Lanka; Venous Thrombosis; Warfarin

The Budd-Chiari syndrome (BCS) is characterized by hepatic venous outflow obstruction involving the hepatic veins, inferior vena cava, or both. BCS has occasionally been reported in the literature as a very rare complication of ulcerative colitis. However, association of Crohn's disease (CD) and BCS is extremely rare with only a single case reported in the world literature to date. We report a case of a young woman with chronically active, therapy-resistant CD who developed massive ascites, elevation of liver enzymes, and coagulopathy in the course of her disease. She was subsequently diagnosed with BCS for which a successful liver transplantation was performed. Chronically active therapy resistant CD and methylenetetrahydrofolate reductase gene mutation have been identified as possible risk factors for development of BCS in this patient.

Topics: Adrenal Cortex Hormones; Ascites; Budd-Chiari Syndrome; Crohn Disease; Female; Hepatic Veins; Humans; Immunosuppressive Agents; Liver; Liver Transplantation; Methylenetetrahydrofolate Reductase (NADPH2); Mutation; Phlebography; Risk Factors; Tacrolimus; Tomography, X-Ray Computed; Vena Cava, Inferior; Warfarin; Young Adult

The natural history of chronic portomesenteric (PM) and portosplenomesenteric (PSM) venous thrombosis is defined poorly. Therapeutic options are limited, and are directed at the prevention of variceal bleeding and the control of abdominal pain related to gastrointestinal hyperemia.. Patients with extensive PM and PSM thrombosis were reviewed retrospectively to evaluate the efficacy of medical therapy and to determine which clinical variables had prognostic significance regarding long-term survival.. Sixty patients, with a median age at diagnosis of 44 years (range, 18-68 y), were assessed. The median follow-up period was 3.5 years (range, 0.2-32.0 y). The overall survival rate was 73.3%, with 1- and 5-year survival rates of 81.6%, and 78.3%, respectively. One- and 5-year survival rates, excluding patients who died from malignancy-related causes, were 85.7% and 82.1%, respectively. Factors associated with improved survival included treatment with beta-blockers (P = .02; odds ratio [OR], .09; 95% confidence interval [CI], 0.01-0.70) and anticoagulation (P = .005; OR, 0.01; 95% CI, <0.01 to 0.26). Eighteen patients in total were anticoagulated, including 8 patients who had variceal bleeding, all of whom underwent endoscopic band ligation of esophageal varices before anticoagulation. By using Cox regression analysis, variables associated with reduced survival were the presence of ascites (P = .001; OR, 42.6; 95% CI, 5.03-360), and hyperbilirubinemia (P = .01; OR, 13.8; 95% CI, 1.9-100) at presentation. Six patients died of variceal hemorrhage.. Patients with chronic PM and PSM venous thrombosis without underlying malignancy have an acceptable long-term survival. Treatment with beta-blockers and anticoagulation appears to improve outcome.

Topics: Adolescent; Adrenergic beta-Antagonists; Adult; Aged; Anticoagulants; Ascites; Chronic Disease; Esophageal and Gastric Varices; Female; Follow-Up Studies; Gastrointestinal Hemorrhage; Humans; Hyperbilirubinemia; Ligation; London; Male; Mesenteric Vascular Occlusion; Mesenteric Veins; Middle Aged; Multivariate Analysis; Serum Albumin; Survival Rate; Venous Thrombosis; Warfarin

Topics: Adult; Ascites; Budd-Chiari Syndrome; Factor V; Hemoglobinuria; Hemoglobinuria, Paroxysmal; Heterozygote; Humans; International Normalized Ratio; Male; Methylenetetrahydrofolate Dehydrogenase (NAD+); Mutation; Prothrombin; Spleen; Thrombophilia; Time Factors; Tomography, X-Ray Computed; Warfarin

Hypothetical clinical cases were used to investigate transfusion-related decision-making. Three red cell, three fresh frozen plasma (FFP) and three albumin transfusion decision cases were administered by questionnaire to 228 medical staff. The transfusion decision triggers were identified and comparisons made between resident and specialist groups and between Melbourne and Sydney participants. Factors important in red cell transfusion decisions included haemoglobin, symptoms of anaemia, presence of co-morbidities or surgery, gender, period of hospitalisation and the degree of documented blood loss. FFP administration was influenced by an abnormal coagulation test, the presence of co-morbidities and by the number of red cell units transfused. The administration of albumin, concentrated or 5% SPPS, was influenced by the period of hospitalisation and clinical circumstances such as a falling urine output postoperatively, and by the presence of hypotensive complications. Different transfusion responses were noted: resident staff transfused red cells and FFP earlier than specialists; Sydney specialists were more conservative of red cell transfusion; Melbourne specialists more conservative of FFP administration and surgeons were four times more likely to transfuse patients than physicians or anesthetists at certain haemoglobin values.

Topics: Abruptio Placentae; Adult; Aged; Ascites; Blood Component Transfusion; Blood Loss, Surgical; Blood Transfusion; Cesarean Section; Colonic Neoplasms; Decision Making; Disseminated Intravascular Coagulation; Epistaxis; Female; Humans; Hypoproteinemia; Male; Medical Staff, Hospital; Middle Aged; Peptic Ulcer Hemorrhage; Plasma; Pregnancy; Serum Albumin; Sex Factors; Warfarin; Wounds and Injuries

The i.p. inoculation of C3H mice with 5 times 10-6 cells of a transplantable ovarian carcinoma invariably evokes accumulation of large amounts of ascitic fluid. Histological and pharmacotherapeutic studies indicate that obstruction to peritoneal lymphatic drainage is a key factor in the formation of carcinomatous ascites in this model. In the early stages of ascites formation, an intense inflammatory reaction appears to occlude the condusts that connect the peritoneal cavity to the subdiaphragmatic lymphatic plexus. This inflammatory reaction, elicited by the presence of tumor cells within the peritoneal cavity, can be inhibited with high-dose systemic corticosteroid therapy. Ascitic fluid accumulation in animals so treated is markedly retarded. Tumor cells do not gain access to lymphatic capillaries draining the peritoneal cavity until ascitic fluid accumulation is massive. Systemic anticoagulation with heparin or sodium warfarin does not prevent lodgment of tumor cells within these lymphatic capillaries, nor does it alter the pattern of ascitic fluid accumulation. Various considerations suggest that excess production of ascitic fluid is not a likely pathogenetic factor in murine carcinomatous ascites.

Topics: Animals; Ascites; Female; Heparin; Hydrocortisone; Inflammation; Injections, Intraperitoneal; Lymph Nodes; Male; Mice; Mice, Inbred C3H; Neoplasms, Experimental; Ovarian Neoplasms; Peritoneum; Warfarin