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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients undergoing pylorus-preserving pancreatoduodenenectomy (PPPD) have a risk of up to 50% for developing delayed gastric emptying (DGE) in the early postoperative course. From 1994 to August 2002, a total of 204 patients underwent PPPD for pancreatic or periampullary cancer (50%), chronic pancreatitis (42%), and other indications (8%). Retrocolic end-to-side duodenojejunostomy was performed below the mesocolon. DGE was defined by the inability to tolerate a regular diet after day 10 (DGE10) or day 14 (DGE14) postoperatively, as well as the need for a nasogastric tube at or beyond day 10 (DGE10GT). Postoperative morbidity was 38%, 30-day mortality was 2.9%, and median postoperative length of stay was 15 days. DGE occurred in 14.7% (DGE10), 5.9% (DGE14), and 6.4% (DGE10GT), respectively. After further exclusion of 21 patients (10.3%) with major complications and no possible oral intake (because of death, reoperation, or mechanical ventilation), the frequencies of DGE10, DGE14, and DGE10GT in the remaining group of 183 patients were 9%, 2%, and 2%, respectively. Multivariate analysis revealed postoperative complications (P<0.001), the presence of portalvenous hypertension (P<0.01), and tumors as indications for surgery (P<0.01) as independent risk factors for DGE10. The overall incidence of DGE was low after PPPD. In those patients experiencing DGE, however, other postoperative complications were the most important factor associated with its occurrence.
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PMID:Delayed gastric emptying after pylorus-preserving pancreatoduodenectomy is strongly related to other postoperative complications. 1312 53

The etiology of pain in chronic pancreatitis may be ductal hypertension, increased parenchymal pressure, or neural damage. It is difficult to assess the severity of pain in this patient population, a problem made more challenging by the frequency of narcotic dependency. Therapeutic interventions developed to relieve the pain of chronic pancreatitis include denervation of the pancreas, decompression of the main duct of the pancreas, resection of part or all of the diseased pancreas, and reduction of pancreatic secretion. Operative intervention for patients with chronic pain is indicated when severe pain, complications of pain, or potential malignancy are present. The operations that consistently provide long-lasting pain relief all have in common resection of all or a portion of the head of the pancreas. Adverse effects on exocrine and endocrine function, nutrition, and quality of life are related to the amount of pancreas resected. The ideal procedure should be easy to perform, have a low morbidity and mortality rate, provide long-lasting pain relief, and not augment endocrine and exocrine insufficiency. No single operation fulfills this ideal. The local resection of the head of the pancreas combined with longitudinal pancreaticojejunostomy (LR-LPJ) proposed by Frey and the duodenum-preserving resection of the head of the pancreas (DPHR) proposed by Beger are discussed. The conceptualization, development, and technique of LR-LPJ are discussed, and comparisons of patient outcomes are made with the outcomes of other procedures for chronic pancreatitis.
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PMID:Comparison of local resection of the head of the pancreas combined with longitudinal pancreaticojejunostomy (frey procedure) and duodenum-preserving resection of the pancreatic head (beger procedure). 1453 21

The pathogenesis of pain in chronic pancreatitis remains an enigma. The cause of pain is almost certainly multifactorial and may vary at different stages of the disease process. These factors may include the release of excessive oxygen-derived free radicals, tissue hypoxia and acidosis, inflammatory infiltration with influx of pain transmittent substances into damaged nerve ends, and the development of pancreatic ductal and tissue fluid hypertension due to morphological changes of the pancreas. Investigations into the causes of pain have been limited by changes in the dynamics with the progression of the disease process, limitations in studying functional and morphological changes of the pancreas in the clinical setting, and the psychosomatic profile of patients. Many of these patients are addicted to alcohol, and suffer from personality disorders. The difficulty in quantifying pain, which is at best subjective, further compounds the issue, especially when assessing the efficacy of treatment.
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PMID:Pathogenesis of pain in chronic pancreatitis: ongoing enigma. 1457 90

Samples of the stomach, duodenum and pancreas removed from 76 patients obtained during organ-preserving operations for ulcer and chronic pancreatitis were examined morphologically. It is found that the most frequent type of changes in the intraorgan arteries is their wall hypertrophy in combination with hyperelastosis and elastotic fibrosis. This characterizes chronic local arterial hypertension. An additional morphological symptom complex caused by a vegetative vascular crisis is formed in the arteries of the damaged organ in exacerbation of the disease. The complex includes prominent dystonic and alterative changes of small arteries leading to stasis and thrombogenesis in the microvessels. Unknown so far phenomenon of arterial invagination in 18 patients was observed. It leads to a complete block of circulation, acute ischemia followed by tissue necrosis which was most typical for ulcer exacerbation and chronic pancreatitis.
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PMID:[Morphofunctional characteristics of arterial bed in exacerbation of gastroduodenal ulcer disease and chronic pancreatitis]. 1496 64

The results of endoscopic thoracic sympathectomy performed for 787 patients during a 30-year period are presented. Six hundred seventy three patients were operated on for upper limb arterial occlusion of distal and diffuse type, Raynaud's disease or syndrome, 7 patients - for causalgic pain in upper limbs and Sudeck's syndrome, 85 - for hyperhidrosis. Twelve patients underwent lower thoracic sympathectomy for painful chronic pancreatitis, 4 - total destruction of thoracic sympathetic trunk due to pernicious hypertension of unknown origin, and 6 - endoscopic thoracic sympathectomy for acute thrombosis of upper limb arteries with distal circulation impairment. Immediate positive effect of interventions was detected in all cases except for acute arterial thrombosis. One patient died postoperatively due to arrhythmia-related cardiac arrest. Postoperative complications - lung border damage and intercostal vascular hemorrhage - were detected in 0.2% of cases. Increased air effusion from pleural cavity and intercostal neuralgia were observed postoperatively in some cases but did not require any special management. Long-term outcomes were followed up for period of 5-10 years, 72.7% of monitored patients had stable positive outcomes. Our experience has demonstrated that endoscopic thoracic sympathectomy is a safe, minimally invasive and effective intervention for upper limb chronic arterial insufficiency of distal and diffuse type or for hyperhidrosis.
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PMID:Multiyear experience in endoscopic thoracic sympathectomy. 1516 77

First cause of secondary hypertension is renovascular hypertension which presents abdominal bruit in 16 to 20% of cases. This clinical sign is also associated with other vascular disease of the abdomen such as celiac trunk stenosis and/or aneurysms located on the pancreaticoduodenal or gastroduodenal arcs level, with little representation among aneurysm. They usually appear on a context of digestive complications like neoplasias, chronic pancreatitis or gastric obstructions possibly with obstructive icterus, hemorrhage and acute abdomen episodes. Its presentation in other contexts is rare and constitutes a diagnostic challenge. Diagnosis is made by abdominal arteriography which is the best method because you can locate the problem as well as intervene therapeutically with embolization of the aneurysme. We would like to emphasize the importance of a quick diagnosis due to the risk of rupture and the high morbi-mortality associated.
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PMID:[Abdominal bruit associated with hypertension]. 1521 82

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

Based on the rheographic studies of the postprandial transformation of the splanchnic blood flow and morphological study of the resected parts of the pancreas in patients with chronic fibrosing pancreatitis, the authors revealed functional and morphological attributes of local arterial hypertension and, at the stage of exacerbation of disease--manifestations of a vascular crisis. Local arterial hypertension with vascular crises originating on its basis is an important pathogenetic factor of the progression of chronic pancreatitis. It is assumed that local arterial hypertension develops against the background of depression of cholinergic effects and domination of sympathetic effects.
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PMID:[Local arterial hypertension in the pathogenesis of chronic pancreatitis]. 1593 55

Acute pancreatitis develops immediately after the causative impulse, while chronic pancreatitis develops after the long-term action of the noxious agent. A typical representative of acute pancreatitis is biliary pancreatitis, chronic pancreatitis develops in alcoholism and has a long latency. As alcoholic pancreatitis is manifested at first as a rule by a potent attack, it is classified in this stage as acute pancreatitis. The most frequent etiological factors in our civilization are thus cholelithiasis and alcoholism (both account for 20-50% in different studies). The assumed pathogenetic principles in acute biliary pancreatitis are the common canal of both efferent ducts above the obturated papilla, duodenopancreatic reflux and intrapancreatic hypertension. A detailed interpretation is however lacking. The pathogenesis of alcoholic pancreatitis is more complicated. Among others some part is played by changes in the calcium concentration and fusion of cellular membranes. Idiopathic pancreatitis occurs in up to 10%, part of the are due to undiagnosed alcoholism and cholelithiasis. Other etiologies are exceptional. Similarly as in cholelithiasis pancreatitis develops also during other pathological processes in the area of the papilla of Vater such as dysfunction of the sphincter of Oddi, ampulloma and juxtapapillary diverticulum, it is however usually mild. The incidence of postoperative pancreatitis is declining. Its lethality is 30% and the diagnosis is difficult. In the pathogenesis changes of the ion concentration are involved, hypoxia and mechanical disorders of the integrity of the gland. Pancreatitis develops in association with other infections--frequently in mumps, rarely in hepatitis, tuberculosis, typhoid and mycoses. Viral pancreatitis is usually mild. In parasitoses pancreatitis develops due to a block of the papilla Vateri. In hyperparathyroidism chronic pancreatitis is more likely to develop, recent data are lacking. As to dyslipoproteinaemias, pancreatitis develops in the Ist, IVth and Vth type of Frederikson's classification, in rare recessive disorders and other conditions such as hypothyroidism, renal insufficiency, oestrogen substitution and others. In pancreas divisum chronic pancreatitis is more likely to develop. In exotic countries tropical pancreatitis is most frequent. It is however similarly as alcoholic pancreatitis primarily chronic. A very serious course is usual in traumatic pancreatitis. Risk factors of pancreatitis after ERCP are in particular undilated biliary pathways, dysfunction of the sphincter of Oddi and the use of a needle knife (bistoury). Medicamentous prevention is not substantiated. Drug induced pancreatic damage is much rarer than hepatotoxicity. Pancreatitis is caused most frequently by immunosuppressives, methyldopa, corticoids and oestrogens. The question remains to what extent the course of pancreatitis is influenced by its etiology. Biliary, alcoholic, traumatic and postoperative pancreatitis is usually severe, pancreatitis associated with viroses and induced by drugs is usually mild.
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PMID:[Etiological factors of acute pancreatitis]. 1673 20

This study was designed to examine whether continuous pancreatic ductal hypertension (PDH) plays an important role in the onset and development of chronic pancreatitis (CP). Pancreatic, biliary, and duodenal cannulas were implanted in male Wistar rats. PDH was induced by vertically raising the free end of the pancreatic duct cannula to exert a hydrostatic pressure and maintained for 2 wk. PDH was gradually increased, but when the pancreatic juice (PJ) flow was interrupted, PDH was decreased to restore PJ flow. The induction of PDH resulted in a marked reduction of amylase activity in PJ and an increase in serum amylase activity. At 2 wk after persistent PDH, pancreatic exocrine function was markedly decreased in response to a bolus injection of secretin (100 pmol/kg) compared with the control group. Histological examination revealed interlobular as well as intralobular fibrosis in the form of nodular pancreatitis at 2 wk after the induction of PDH. Immunohistochemistry revealed the expression of fibronectin and collagen types I and III. Quantitative real-time RT-PCR showed an increase in transforming growth factor-beta(1) mRNA expression in the pancreas during PDH. The present results suggest that PDH plays an important role in the onset and development of CP. Furthermore, our animal model seems useful for investigating the mechanisms of CP in rats.
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PMID:A new model of chronic pancreatitis in rats. 1695 55


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