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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Budd-Chiari syndrome (BCS) is a venous outflow obstruction of the liver that has a dismal outcome if left untreated. Most cases of BCS in the Western world are caused by thrombosis of the hepatic veins, sometimes in combination with thrombosis of the inferior vena cava. Typical presentation consists of abdominal pain, hepatomegaly and ascites, although symptoms may vary significantly. Currently, a prothrombotic risk factor, either inherited or acquired, can be identified in the majority of patients. Moreover, in many patients with BCS a combination of risk factors is present. Myeloproliferative disorders are the most frequent underlying cause, occurring in approximately half of the patients. Recent discovery of the Janus Kinase 2 (JAK2) mutation has significantly contributed to the diagnosis of myeloproliferative disorders. Anticoagulation is indicated for all patients with BCS and additional therapy depends on the severity of symptoms and the extent of venous obstruction. A stepwise therapeutic approach is recommended, with increasing invasiveness and guided by the response to previous treatment. A transjugular intrahepatic portosystemic shunt (TIPS) is proving to be a good therapeutic option in patients with BCS, diminishing the need for surgical shunts. When all other therapy is unsuccessful or in patients with fulminant hepatic failure, a liver transplantation should be considered. Advances in diagnosis and treatment have dramatically improved the prognosis of patients with BCS. Still, many aspects of this complicated disorder remain to be clarified.
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PMID:Vascular liver disorders (I): diagnosis, treatment and prognosis of Budd-Chiari syndrome. 1915 47

Budd-Chiari syndrome is a rather unusual clinical situation caused by occlusion of the hepatic vein of inferior vena cava, the classical triad of which are abdominal pain, ascites and hepatomegaly. A 29-year-old gravida 3 para 1 woman delivered an immature male baby weighing 2172 g with an Apgar score of 9 points at 35 weeks and 3 days of gestation. She was transferred to the National Hospital Organization Osaka National Hospital 112 days after delivery due to the sudden development of massive ascites. Magnetic resonance angiography and enhanced computed tomography detected the occlusion by thrombosis of both the middle and left hepatic veins, so she was diagnosed with Budd-Chiari syndrome. Her protein C antigen and activity were 37% and 50%, respectively, corresponding to type 1 protein C deficiency. Conservative treatment by continuous oral treatment of spironolactone (25 mg/day), furosemide (20 mg/day) and prophylactic warfarin (2 mg/day) much improved the ascites.
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PMID:Case of Budd-Chiari syndrome 3 months after vaginal delivery. 1884 Jan 63

Budd-Chiari syndrome is a clinical disorder caused by hepatic venous obstruction with manifestations of abdominal pain, hepatomegaly, and ascites. Secondary Budd-Chiari syndrome is defined as an obstruction that results from material not originating from the venous system. We describe a rare case of fulminant Budd-Chiari syndrome secondary to renal cell carcinoma with tumor thrombus of the inferior vena cava and hepatic veins. The 59-year-old man was admitted to our hospital because of progressive appetite loss and markedly elevated serum transaminase. Abdominal ultrasonography revealed thrombosis in the hepatic veins and the inferior vena cava. Renal cell carcinoma with hepatic vein invasion was suggested by abdominal computed tomography and confirmed after a biopsy was taken from the hepatic venous thrombus. The patient died of fulminant liver failure within 10 days after admission. The clinical scenario and rationale for the selected management are further discussed.
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PMID:Fulminant Budd-Chiari syndrome caused by renal cell carcinoma with hepatic vein invasion: report of a case. 1921 12

Alveolar echinococcosis of the liver is a rare larval cestode disease which is due to the intrahepatic growth of the tapeworm Echinococcus multilocularis. This cestode naturally evolves as a larval stage within cysts in the body of carnivores. Humans are accidental intermediate hosts and become infected, either by eating food contaminated with carnivore-originated eggs or by touching foxes. It behaves as malignant liver tumour and rarely causes Budd-Chiari syndrome and variceal bleeding. Budd-Chiari syndrome is a hepatic venous outflow tract obstruction and may be present abdominal pain, hepatomegaly and ascites. Parasitic cysts may cause compression and thrombosis of the hepatic venous outflow tract. It may present as portal hypertension and variceal upper gastrointestinal bleeding. We here in report a 47-year-old woman without a prior history of liver disease presented with Budd-Chiari syndrome and variceal bleeding due to Alveolar echinococcosis. The course of this rare disease is demonstrated by means of the most important laboratory, serologic and radiologic parameters.
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PMID:[Case report: Budd-Chiari syndrome and esophageal variceal bleeding due to alveolar echinococcosis]. 2095 22

Ascites in systemic lupus erythematosus (SLE) had once been thought to only occur as a consequence of nephrotic syndrome, protein-losing enteropathy, constrictive pericarditis or Budd-Chiari syndrome. In more recent years, both acute and chronic lupus peritonitis have been documented as another major cause of lupus ascites. Acute lupus peritonitis with ascites tends to develop rapidly, is accompanied by significant abdominal pain and is often associated with other symptoms of lupus flares such as fevers, arthritis, and rashes. On the other hand, chronic lupus peritonitis with ascites develops over several months, is recurrent, and tends to be recalcitrant to treatment with systemic steroids. We present the case of an 18-year-old African-American female whose initial presentation of SLE was gradual onset of massive painless ascites accompanied by anorexia, nausea, vomiting, and diarrhea. The ascites responded well to steroids and immunosuppressive therapy and has not recurred.
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PMID:Insidious onset of massive painless ascites as initial manifestation of systemic lupus erythematosus. 2133 98

We report two cases of Budd-Chiari syndrome. Case 1: A 57-year-old man presented with leg edema and esophageal varices. Cavography showed obstruction of the inferior vena cava with antiphospholipid syndrome. Further, the patient showed positive serology for hepatitis C virus and consumed large quantities of alcohol. Percutaneous transluminal angioplasty was performed on this patient and anticoagulants administered; leg edema and esophageal varices were ameliorated although liver biopsy showed cirrhosis without evident congestion. More than 9 months since the diagnosis, restenosis of the inferior vena cava has not occurred. Case 2: A 73-year-old woman presented abdominal pain but no edema or varices. Cavography showed membranous obstruction of the inferior vena cava which required no therapy. Manifestation of portal hypertension was not present and liver function was maintained although liver biopsy showed obvious congestion. These cases showed untypical features against histopathology, and careful observation will be required for emergence of hepatocellular carcinoma.
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PMID:Budd-Chiari syndrome: two cases with different courses. 2149 Aug 97

Acute hepatic vascular complications are rare. Acute portal vein thrombosis (PVT) and the Budd-Chiari syndrome (BSC) are the leading causes. Coagulopathy and local factors are present in up to 80% of cases. Diagnosis is established by colour-coded Doppler sonography, contrast-enhanced computed tomography or magnetic resonance imaging. Patients with acute PVT present with abdominal pain and disturbed intestinal motility. In the absence of cirrhosis anticoagulation with heparin is established followed by oral anticoagulation. In severe cases, surgical thrombectomy or transjugular thrombolysis with stent shunt may be necessary. Acute or fulminant BCS may require emergency liver transplantation or a transjugular intrahepatic portosystemic stent shunt, if patients present with acute liver failure. Milder cases receive anticoagulation for thrombolysis of occluded hepatic veins. Sinusoidal obstruction syndrome (SOS) is diagnosed after total body irradiation or chemotherapy, the term SOS replacing the former veno-occlusive disease. The treatment of congenital vascular malformations, complications in the setting of OLTX as well as patients with hepatic involvement of hereditary hemorrhagic telangiectasia requires significant expertise in a multidisciplinary approach.
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PMID:[Acute hepatic vascular complications]. 2166

We report a case of 27 year old female patient who was admitted to the hospital with an acute flare up of ulcerative colitis. The patient presented with complaints of persistent abdominal pain and bloody diarrhea despite aggressive therapy for her ulcerative colitis. A CT scan of the abdomen on admission revealed hepatic vein thrombosis, suggesting a diagnosis of Budd-Chiari syndrome. Significantly, an associated thrombosis of the inferior mesenteric vein was also detected. Based on imaging data and clinical assessment, the patient was started on anticoagulation therapy and an extensive work-up for hypercoagulability was initiated. Up to the time of publication, no significant findings suggesting this patient has an underlying coagulation disorder have been found. Based on our search of PUBMED, this report is one of only five reported adult cases of Budd-Chiari Syndrome associated with ulcerative colitis in the English literature in living patients without evidence of a co-existing coagulation disorder. This case highlights the potential for thrombosis at unusual sites in ulcerative colitis patients even in the absence of classical coagulation abnormalities. In addition to the case presented, we provide a brief review of previously reported cases of Budd-Chiari Syndrome occurring in patients with inflammatory bowel disease.
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PMID:Budd-Chiari syndrome in a patient with ulcerative colitis and no inherited coagulopathy. 2186 Jun 76

Inferior vena cava (IVC) thrombosis at its hepatic portion (also known as obliterative hepatocavopathy [OH]), in the absence of systemic or local diseases such as vasculitis, coagulopathy, infection and malignancy, is a rare event. We report the case of a 25-year-old woman with progressive abdominal pain and leg edema after exercise. Imaging showed congestive liver and IVC occlusion at the intrahepatic portion. A liver biopsy demonstrated portal congestion without evidence of fibrosis; after unsuccessful percutaneous attempts for recanalization, consideration was given to liver transplantation with IVC reconstruction versus IVC bypass. Due to the presence of preserved liver function, an externally supported 16-mm ringed polytetrafluoroethylene graft was used to bypass from the suprarenal IVC to the suprahepatic IVC. At five years, she remains symptom-free, with normal liver function and a patent graft on systemic anticoagulation. This report highlights the successful surgical management of a patient with OH with a thick membrane. It supports other published proposals that this entity differs significantly from classic Budd-Chiari syndrome with thrombosis that affects only the hepatic veins and, thus, OH should be approached and managed differently.
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PMID:Inferior vena cava bypass for the treatment of obliterative hepatocavopathy with five-year follow-up. 2191 43

Focal nodular hyperplasia (FNH) is a relatively common benign liver tumor with rare indications to surgery. Early after pregnancy, a 35-year-old woman developed right upper quadrant abdominal pain with fever. A large abdominal mass was palpable. Abdominal CT scan showed a 18-cm FNH substituting all liver segments but S6 and S7, compressing middle and left hepatic vein near their origin, displacing and compressing right hepatic vein, with ascites. Surgery consisted of a left hepatectomy extended to S5-S8 and S1. Main technical challenge was the preservation of the right hepatic vein. Intermittent pedicle clamping was performed, associated with hepatic vascular exclusion with preservation of caval flow; total duration of ischemia was 210 min. The postoperative course was uneventful, except for a transient fall in prothrombin time, and the formation of a sub-diaphragmatic serous collection, which was percutaneously drained. The patient is well 25 months after the operation. To our knowledge, this is the second reported case requiring surgery for a FNH causing a Budd-Chiari syndrome. In these peculiar cases a cumbersome operation may be required, maximizing all precautions to perform a risk-free procedure.
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PMID:Giant focal nodular hyperplasia determining Budd-Chiari syndrome: an operative challenge requiring 210 min of liver ischemia. 2192 17


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