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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Visceral artery aneurysms (VAA) can be treated by revascularization, ligation, or, most often, endovascular techniques depending on clinical presentation, hemodynamic status, and location. From 1975 to 2002 a total of 42 VAA in 34 patients were treated. The lesion involved the splenic artery (SA; 19), pancreaticoduodenal artery (PDA; 6), celiac trunk (CT; 5), superior mesenteric artery (SNA; 4), common hepatic artery (CHA; 3), gastroduodenal artery (GDA; 2), left hepatic artery (LHA; 1), a branch of the inferior mesenteric artery (BIMA; 1), and a branch of the SMA (BSMA; 1). Twenty-seven VAA in 21 patients (64%) were uncomplicated (group I) and 15 VAA in 13 patients (36%) had ruptured (group II) (PDA; 6; CT, 3; SA, 1; CHA, 1; LHA, 1; BSMA, 1; BIMA, 1). In group I VAA were treated by embolization (n = 11), splenectomy (n = 6), bypass (n = 7), ligation (n = 2), and aneurysmorraphy (n = 1). No deaths were observed. The morbidity rate associated with surgical treatment was 12% including hepatic bypass thrombosis without ischemic complications in two cases. The morbidity rate associated with endovascular treatment was 18% including cholecystitis in one case and bile duct stenosis in one case. The VAA recanalization rate following embolization was 9%. In group II, 12 VAA (80%) were treated by ligation in association with splenectomy in two cases and left hepatectomy in one case. Only one bypass procedure was performed and embolization was used to treat two VAA (1 SMA and 1 PDA). The mortality rate was 20% (3/15). The morbidity rate associated with surgical treatment was 46% (6/13) including bile duct stenosis in one case, ischemic cholecystitis in one case, duodenal fistula in one case, pancreatic fistula in one case, bile tract fistula in one case, and colonic ischemia in one case. No patient died after endovascular treatment and the morbidity rate was 50% (1/2) with duodenal stenosis occurring in one case. In sum, VAA can rupture. Emergency cases can be treated by ligation in most cases or by embolization if the hemodynamic status of the patient allows. Regardless of treatment technique, the morbidity and mortality rate remains high after rupture, especially in cases involving PDA. Embolization can be proposed as a first-line treatment for most VAA. Because of the risk of rupture, endovascular or open repair is warranted for VAA and has a favorable prognosis.
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PMID:Treatment of visceral artery aneurysms: description of a retrospective series of 42 aneurysms in 34 patients. 1559 27

The pathophysiology of pain in chronic pancreatitis (CP) is incompletely understood. Several hypotheses have been advanced, including pancreatic and extrapancreatic causes. The existence of different hypotheses to explain the genesis of pain in CP also reflects the different therapeutic approaches to pain in these patients. Increased intraductal pressure as a result of single or multiple strictures and/or calculi is believed to be a common cause of pain in CP patients with a dilated main pancreatic duct. Other suggested causes include pancreatic fibrosis, interstitial hypertension and pancreatic ischemia. Additionally, extrapancreatic causes like duodenal and common bile duct stenosis with scarring due to pancreatic inflammation are suggested as factors causing pain in CP. The 'neurogenic inflammation' hypothesis is a fascinating theory which is supported by different studies. Immunohistological reports have shown that the amount of neurotransmitters, such as substance P and its receptor, calcitonin gene-related peptide and other neurotransmitters, are increased in afferent pancreatic nerves and a correlation between pain and immune cell infiltration of the nerves has been reported in CP. In this review we will discuss the different pain hypotheses and will present the perspective that neuroimmune interaction is an important factor for pain generation in CP.
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PMID:Pathogenesis of pain in chronic pancreatitis. 1575 9

Pain is a major clinical manifestation of chronic pancreatitis (CP) and a common indication for surgery in these patients. Pathogenesis of pain in CP is multifactorial and the mechanisms of pain may differ from patient to patient. This can explain why one therapeutic method of treatment of pain does not work in all patients and in different stages of the disease. Two main complimentary pathogenetic theories have been proposed to explain the mechanisms of pain in CP, the neurogenic theory and the theory of increased intraductal/intraparenchymal pressures. According to the neurogenic theory, in CP there are alterations of pancreatic/peripancreatic nerves, exposing them to noxious substances and/or activated immune cells, thereby generating pain ("neuroimmune interaction"). The other theory of intraductal/intraparenchymal hypertension suggests that pain in CP is generated as a result of increased pressures within the pancreatic ductal system and/or pancreatic parenchyma, like the pain in the classic compartment syndrome. The theory of intraductal/intraparenchymal hypertension is strongly supported by the good results of drainage procedures in the surgical management of CP. Pancreatic ischemia, oxygen-free radicals, centrally sensitized pain state, acute exacerbations of CP, development of complications from the pancreas (most commonly, pseudocysts) or adjacent organs (usually, duodenal and/or common bile duct stenosis), etc. are other possible contributing factors. Different patterns of pain have been described in idiopathic (early vs. late onset) and in alcoholic CP. Interestingly, pain is automatically relieved during the natural course of the disease in some patients (the "burn-out" phenomenon), after a relatively long time (from a few years to up to 3 decades). However, this is an unpredictable evolution for the individual patient. Therefore, surgery should be offered when pain is intense and after failure of conservative treatment. Surgical management should be individualized, depending on the particular findings of each patient. The knowledge of the pathophysiologic basis and of natural course of pain in CP is of paramount importance for the surgeon to select appropriate therapy for the individual patient with CP.
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PMID:Mechanisms and natural history of pain in chronic pancreatitis: a surgical perspective. 1766 54