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

Portal vein thrombosis, except in hepatocellular carcinoma and severe cirrhosis, is due to one or several prothrombotic disorders with or without a local precipitating factor. We report a case of a portal and splenic vein thrombosis, without cavernoma and varices which occurred in a 72-year-old man with abdominal pain and weakness. Three prothrombotic states including latent myeloproliferative disorder, antiphospholipid syndrome, and factor II G202101 mutation, were observed. Anticoagulant treatment resulted in complete repermeation of the portal and splenic veins without a hemorrhagic event. This illustrates that several prothrombotic states may occur in a single patient with portal vein thrombosis. Early anticoagulant therapy, in recent portal vein thrombosis, can result in repermeation.
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PMID:[Portal vein thrombosis associated with a myeloproliferative disorder, prothrombin G20210A mutation, antiphospholipid syndrome, with repermeation during anticoagulant therapy]. 1152 Nov 10

Portal cavernoma is a network of veins whose caliber, initially millimetric or microscopic, is increased and which contain hepatopedal portal blood. It results from occlusion, thrombotic and always chronic, of the extra-hepatic portal system. Diagnosis is mainly done by imaging. Clinical signs of portal cavernoma are usually related to extra-hepatic portal hypertension (hematemesis due to rupture of oeso-gastric varices, splenomegaly, rectal bleeding from ano-rectal varices, growth retardation in children) and sometimes to the cause of portal hypertension (abdominal pain, venous bowel infarction). Occurrence of portal thrombosis is often the conjunction of a local cause and a prothrombotic disorder which must be systematically detected. Biliary consequences of cavernoma are related to compression of common bile duct and are usually asymptomatic. In case of jaundice or cholangitis, portal decompression by portosystemic shunt can be performed to treat both biliary symptoms and portal hypertension.
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PMID:[Portal cavenorma: diagnosis, aetiologies and consequences]. 1253 94

Portal vein thrombosis usually appears in the course of acute abdominal septic complications or after splenectomy, though in 50% of cases no aetiological factors can be identified. In our department we recently treated two patients affected by portal vein thrombosis, the first after splenectomy for haematological disease, and the second after sigmoid diverticulitis. When portal vein thrombosis occurs after splenectomy for haematological reasons, the increased viscosity of the blood due to thrombocytosis is the main factor regarded as being the cause. In the first case, acute abdominal pain appeared 15 days after splenectomy and the diagnosis was suspected and confirmed by Doppler ultrasonography. The clinical course in the second case was less typical, because, although the sigmoid diverticular disease was known, the symptomatology presented with high fever but no clear subjective or objective abdominal picture. The diagnosis was achieved by computed tomography. The clinical picture may vary greatly but usually abdominal pain, fever and intestinal ischaemia are present. Nowadays the diagnosis has improved as a result of the extensive use of Doppler ultrasonography and computed tomography. Fibrinolytic therapy and acetylsalicylic acid are the treatment of choice and in our experience the clinical picture tends to clear up rapidly. When the patient presents a number of risk factors, prophylaxis of portal vein thrombosis should be planned.
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PMID:Portal vein thrombosis. A multifactorial clinical entity. 1287 81

DIAGNOSTIC CIRCUMSTANCES: Portal vein thrombosis is the second cause of portal hypertension after cirrhosis in Western countries. Diagnosis can be either made at the acute stage in the context of abdominal pain or after appearance of a porto-portal collateral venous circulation leading to the formation of a portal cavernoma, the diagnosis being made in the circumstance of rupture of oesophageal varicose veins or manifestations of hypersplenism. AETIOLOGICAL SURVEY: In the absence of hepatocellular carcinoma, causes that need to be investigated are cirrhosis, local factors (intra-abdominal sepsis, abdominal surgery, splenectomy or pancreatitis), and one or several prothrombotic affections (acquired or inherited prothrombotic states are present in 70% of cases, with myeloproliferative disease ranking first). REGARDING TREATMENT: Anticoagulant therapy generally allows recanalisation of the thombosed veins in recently constituted thrombosis. Some patients at the portal cavernoma stage can also benefit from anticoagulant therapy: patients with a prothrombotic state without large oesophageal-gastric varicose veins. In the case of large oesophageal-gastric varicose veins that have never bled, treatment to prevent haemorrhages due to portal hypertension according to the same modalities as in cirrhosis must be associated with the prescription of an anticoagulant. In the absence of prothrombotic affection or in patients having already suffered from haemorrhages due to portal hypertension, the benefit of anticoagulant therapy is less clearly established.
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PMID:[Portal vein thrombosis]. 1453 80

Portal vein thrombosis (PVT) following splenectomy is a potentially life-threatening complication, and the true incidence of PVT in splenectomized patients is unknown. The objective of this study was to determine the incidence of symptomatic PVT after splenectomy. The hospital database was searched to identify cases of PVT associated with splenectomy from January 1990 to May 2002. Six hundred eighty-eight patients underwent splenectomy during this period, 321 of them for hematologic diseases. Eleven of the 688 patients had PVT associated with splenectomy, and the charts of these patients were reviewed. Six patients developed PVT after splenectomy. Five had hematologic diseases. Symptoms were abdominal pain (6), ileus (5), fever (3), or diarrhea (2). Diagnosis was confirmed by computed tomography (CT) (4), duplex ultrasonography (1), and magnetic resonance imaging (1). The indications for splenectomy included hemolytic anemia (3), thalassemia (1), and myelofibrosis (1). One patient had an incidental splenectomy during gastrectomy. There were four laparoscopic and two open splenectomies. The median interval between splenectomy and diagnosis of PVT was 40 days (range, 13-741). One patient died of pulmonary embolism. Five of six patients with postsplenectomy PVT had splenomegaly and hemolysis. We conclude that the risk of PVT is higher in patients with hematologic conditions associated with splenomegaly and hemolysis.
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PMID:Portal vein thrombosis following splenectomy: identification of risk factors. 1462 54

Portal vein thrombosis (PVT) has rarely been documented in patients after splenectomy for gastric malignancy. We report a case of PVT that occurred after splenectomy as part of an en-bloc node dissection performed to treat gastric malignant lymphoma. A 38-year-old man underwent total gastrectomy and splenectomy with en-bloc D2 lymph node dissection. The spleen weighed 480 g. On postoperative day (POD) 31, the patient complained of abdominal pain in the right upper quadrant accompanied by fever. Moderate elevations of C-reactive protein (CRP), aspartate transaminase (AST), and alanine transaminase (ALT) were noted. Contrast-enhanced computed tomography (CT) and ultrasonography disclosed thrombus in the portal vein and the splenic vein. There were no abnormalities in the levels of lupus anticoagulant, protein C antigen, protein S antigen, or antithrombin III (AT III). A diagnosis of PVT was made, and prompt treatment, including intravenous heparin combined with tissue plasminogen activator (tPA) was initiated, followed by longterm warfarin. This treatment resulted in clinical improvement, but failed to achieve thrombolysis in the portal vein. At follow-up after 6 months, the patient complained of postprandial abdominal pain with persistent peripheral edema and ascites. This case indicates that splenectomy for en-bloc node dissection in gastric malignancy is a possible cause of PVT. Because both the symptoms and the laboratory data in PVT are nonspecific, a high level of clinical suspicion and a low threshold for obtaining imaging examinations are important in the early diagnosis of PVT. Surgeons should remember PVT among several other complications whenever patients treated with radical gastrectomies are symptomatic and imaging studies are considered necessary.
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PMID:Portal vein thrombosis after splenectomy for gastric malignant lymphoma. 1471 20

We herein report a 34-year-old man who was investigated for severe abdominal pain. Portal vein thrombosis (PVT) and mesenteric vein thrombosis (MVT) were diagnosed. An association with two predisposing factors for thrombosis was noted: (1) heterozygous factor II 20210G/A mutation and (2) homozygous methylenetetrahydrofolate reductase (MTHFR) 677C/T mutation with hyperhomocysteinemia. Our case is of particular interest because the patient reported herein, is homozygote for the MTHFR 677C/T mutation, while the only two other cases reported in the literature with similar gene mutations, were heterozygotes for the mutation.
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PMID:Heterozygous prothrombin 20210G/A mutation, associated with hyperhomocysteinemia, and homozygous methylenetetrahydrofolate reductase 677C/T mutation, in a patient with portal and mesenteric venous thrombosis. 1557 Mar 1

Portal vein thrombosis may complicate splenectomy in patients with hemolytic anemia and myeloproliferative disease, whereas the frequency of portal vein thrombosis in case of trauma is not defined. A case of right portal vein thrombosis after splenectomy for trauma is reported in this paper. Hematologic workup did not reveal an underlying platelet or coagulation disorder. The patient was promptly anti-coagulated with complete recanalization of the portal vein. We conclude that mild symptoms, like abdominal pain and fever, after splenectomy should be investigated with a color Doppler ultrasonography to confirm or rule out a diagnosis of portal thrombosis and to anti-coagulate the patient with thrombosis, thus preventing bowel infarction and secondary portal hypertension. Routine postoperative color Doppler might also be justified in all postsplenectomy patients (without hematologic diseases) for early detection of a portal vein thrombosis.
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PMID:Right portal vein thrombosis after splenectomy for trauma. 1586 58

Portal vein thrombosis (PVT) seems rare among HIV infected patients. Even though, the report of such cases is of great interest because it may help to determine the factors of occurrence. We describe cases of PVT in 4 HIV-infected men, aged 32 - 64. Two of them were co-infected with hepatitis C virus (HCV). The four patients had a history of disseminated mycobacterial infection (one case of tuberculosis, 3 cases of mycobacterium avium complex infection) with abdominal lymphadenitis. Despite HAART, their immunodeficiency was profound (CD4: 65 to 216/mm(3)). At the time of diagnosis, two patients were treated with protease-inhibitor containing regimen: indinavir (one case), ritonavir-saquinavir (one case). PVT was revealed by haematemesis (one case), abdominal pain (ome case), anasarca (2 cases). In three patients, the diagnosis of PVT was confirmed by imagery (echo-doppler or angio- RMI), and for the last patient, PVT was found during the transjugular intrahepatic portosystemic shunt setup. A low level of C protein was diagnosed in one case. Cirrhosis was not found in HIV-HCV co-infected patients. Two patients died early after diagnosis, one patient died 3 years after the onset of symptoms. Various factors may cause the development of a PVT in HIV infected patient. Serious immunodeficiency, opportunistic infections such as tuberculosis and mycobacterium avium complex related infection with abdominal lymphadenitis can further the development of PVT. Protease-inhibitor might have facilitated the process. Due to the severe prognosis of advanced cases, early evocation of diagnosis is needed.
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PMID:[Portal vein thrombosis in HIV-infected patients: report of four cases]. 1592 31

Portal vein thrombosis (PVT) consists of two different entities: acute PVT and chronic PVT. Acute PVT usually presents as abdominal pain. When the thrombus extends to the mesenteric venous arches, intestinal infarction can occur. Chronic PVT is usually recognized after a fortuitous diagnosis of hypersplenism or portal hypertension, or when there are biliary symptoms related to portal cholangiopathy. Local risk factors for PVT, such as an abdominal inflammatory focus, can be identified in 30% of patients with acute PVT; 70% of patients with acute and chronic PVT have a general risk factor for PVT, most commonly myeloproliferative disease. Early initiation of anticoagulation therapy for acute PVT is associated with complete and partial success in 50% and 40% of patients, respectively. A minimum of 6 months' anticoagulation therapy is recommended for the treatment of acute PVT. For patients with either form of PVT, permanent anticoagulation therapy should be considered if they have a permanent risk factor. In patients with large varices, beta-adrenergic blockade or endoscopic therapy seems to prevent bleeding as a result of portal hypertension, even in patients on anticoagulation therapy. In patients with jaundice or recurrent biliary symptoms caused by cholangiopathy, insertion of a biliary endoprosthesis is the first treatment option. Overall, the long-term outcome for patients with PVT is good, but is jeopardized by cholangiopathy and transformation of underlying myeloproliferative disease into myelofibrosis or acute leukemia.
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PMID:Nonmalignant portal vein thrombosis in adults. 1695 67


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