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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splenectomy for massive splenomegaly and hypersplenism carries a significant morbidity and mortality. We have used partial splenic embolization (PSE) as an effective alternative to splenectomy. Ten PSE procedures were performed on nine patients without mortality and with minimal morbidity. The age of the patients ranged from 8 months to 32 years (mean 14 years). The causes of splenomegaly and hypersplenism included cystic fibrosis with cirrhosis (2), tyrosinemia and cirrhosis (1); thalassemia (1), hemophilia with Human Immune Deficiency Virus infection (2), chronic hepatitis with portal hypertension (1), malignant histiocytosis (1), and Wiskott-Aldrich Syndrome (1). All procedures were performed under local anesthesia with sedation. A percutaneous femoral artery approach to the splenic artery was used to deliver Ivalon sponge particles (280-800 microns) into the spleen. Splenic infarction was assessed by postembolization angiograms. All of the patients except one demonstrated improvement of hematologic parameters. In one patient, however, cytopenia improved only after a second embolization. In the total series, there was an early mean rise of 8,600/mm3 in the leukocyte count (range 2,900-14,900) and 212,000/mm3 in the platelet count (range 30,000-718,000). Follow-up ranged from 4 months to 7 years. Improvement of the blood picture has been persistent in seven of the eight patients who showed initial improvement. Transient procedural complications included fever (5), pleural effusion (2), pneumonia (1), and splenic abscess (1). One patient had paralytic ileus lasting for 10 days and one patient developed a streptococcal peritonitis 3 weeks after embolization. No patient developed pancreatitis or vascular compromise of other abdominal viscera.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Partial splenic embolization. An effective alternative to splenectomy for hypersplenism. 226 5

Portal vein thrombosis (PVT) is usually a complication of pre-existing cirrhosis, abdominal malignancy (e.g., pancreatic or hepatocellular carcinoma), or abdominal inflammation (e.g., appendicitis, diverticulitis, pancreatitis). Less frequently, PVT can be associated with myeloproliferative or connective tissue disorders or inflammatory bowel disease [1]. PVT can cause or exacerbate portal hypertension; variceal bleeding or hypersplenism may then develop acutely or several years later. PVT also complicates portosystemic shunt surgery or hepatic transplantation. Unfortunately, the signs and symptoms of PVT can be subtle or nonspecific and can be overshadowed by the underlying illness. The radiologist may be the only physician to suggest the preoperative or premortem diagnosis of PVT. Familiarity with the imaging findings of PVT, therefore, is imperative.
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PMID:Portal vein thrombosis: imaging findings. 827 95

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

Splenic arterial interventions are increasingly performed to treat various clinical conditions, including abdominal trauma, hypersplenism, splenic arterial aneurysm, portal hypertension, and splenic neoplasm. When clinically appropriate, these procedures may provide an alternative to open surgery. They may help to salvage splenic function in patients with posttraumatic injuries or hypersplenism and to improve hematologic parameters in those who otherwise would be unable to undergo high-dose chemotherapy or immunosuppressive therapy. Splenic arterial interventions also may be performed to exclude splenic artery aneurysms from the parent vessel lumen and prevent aneurysm rupture; to reduce portal pressure and prevent sequelae in patients with portal hypertension; to treat splenic artery steal syndrome and improve liver perfusion in liver transplant recipients; and to administer targeted treatment to areas of neoplastic disease in the splenic parenchyma. As the use of splenic arterial interventions increases in interventional radiology practice, clinicians must be familiar with the splenic vascular anatomy, the indications and contraindications for performing interventional procedures, the technical considerations involved, and the potential use of other interventional procedures, such as radiofrequency ablation, in combination with splenic arterial interventions. Familiarity with the complications that can result from these interventional procedures, including abscess formation and pancreatitis, also is important.
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PMID:Splenic arterial interventions: anatomy, indications, technical considerations, and potential complications. 1622 91

Pancreatitis induced ruptured pseudoaneurysm (PSA) of the peri-pancreatic and splenic arteries may become a source of life-threatening hemorrhage. Its management is challenging and requires an individualized and multidisciplinary approach. The index case is a 32-year-old chronic alcoholic male presented with multiple episodes of hematemesis and melena. Pathological and imaging findings were consistent with anemia and acute pancreatitis with ruptured PSA of branch of splenic artery, portal cavernoma formation, and splenomegaly. Thrombosis of PSA sac, embolization of offending branch of splenic artery, and splenic infarction were successfully contemplated in a single session by direct percutaneous embolization with gelfoam and glue as embolic agents under guidance of duplex ultrasound imaging. We describe a modified sandwich embolization technique, its long-term success and complications of simultaneous management of ruptured PSA of branch of splenic artery and hypersplenism syndrome in limited resource scenario.
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PMID:An innovative modification of sandwich embolization technique for simultaneous management of ruptured pseudoaneurysm of branch of splenic artery and hypersplenism syndrome. 2590 May 42

BACKGROUND This study aimed to assess the prevalence, clinical characteristics, and risk factors for sinistral portal hypertension in patients with moderate or severe acute pancreatitis. MATERIAL AND METHODS A retrospective study included 825 patients with moderate or severe acute pancreatitis. Clinical and demographic data, the Acute Physiology and Chronic Health Evaluation (APACHE II) and the Ranson scores for severity of acute pancreatitis, and the computed tomography (CT) severity index (CTSI) were evaluated. The formation of collateral vessels, bleeding, splenomegaly, hypersplenism during hospitalization or follow-up, and early anticoagulation and the occurrence of sinistral portal hypertension were evaluated. RESULTS Of the 825 patients with moderate or severe acute pancreatitis, 103 patients (12.5%) developed sinistral portal hypertension. The median time to diagnosis was 8 months, and the median patient age was 39 years. The most common causes of pancreatitis were biliary (46.3%), hypertriglyceridemia (31.5%), alcohol (14.9%), and others (7.3%). Independent risk factors for sinistral portal hypertension were male gender (OR, 4.666; 95% CI, 2.54-8.572; P<0.001), recurrent acute pancreatitis (OR, 9.556; 95% CI, 5.218-17.5; P<0.001), hypertriglyceridemia (OR, 2.056; 95% CI, 1.184-3.57; P=0.001), glucose >10 mmol/L (OR, 6.965; 95% CI, 4.027-12.045; P<0.001), smoking (OR, 6.32; 95% CI, 3.544-11.269; P<0.001), and infection of walled-off necrosis (OR=1.637; 95% CI, 1.061-2.524; P=0.015). Anticoagulation during hospitalization was not significantly associated with sinistral portal hypertension. CONCLUSIONS Hypertriglyceridemia, hyperglycemia, infection of walled-off necrosis, recurrent acute pancreatitis, and smoking were risk factors for sinistral portal hypertension, and early anticoagulation did not prevent the occurrence.
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PMID:Clinical Characteristics and Risk Factors for Sinistral Portal Hypertension Associated with Moderate and Severe Acute Pancreatitis: A Seven-Year Single-Center Retrospective Study. 3140 Feb 75