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

The pancreas, like the kidney, is highly vulnerable to ischemic necrosis. This form of pancreatic injury may express itself as prolonged hyperamylasemia with only minimal signs or symptoms of inflammation, or may produce severe pancreatitis followed by abscesses and death. Autopsy examination of patients dying after oligemic shock showed a 9% incidence of major pancreatic injury if there was not concomitant acute renal tubular necrosis (ATN), but a 50% incidence in those with ATN. Similarly, among patients dying after non-oligemic shock, 12% of those without ATN had major pancreatic injury but 35% with ATN also had pancreatic ischemic injury. Among 13 selected patients examined prospectively after being in shock, pancreatic injury was indicated by hyperamylasemia, hyperlipasemia, elevated amylase/creatinine clearance ratio, and elevated circulating isoamylases specifically of pancreatic origin. Four of the 13 had clinical manifestations of pancreatitis. Not only must shock be added to this list of causes of pancreatitis, but pancreatic ischemia due to hypoperfusion may also be the critical factor which causes the progression from edema to necrosis in other forms of pancreatitis, including those associated with alcohol and biliary disease.
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PMID:Susceptibility of the pancreas to ischemic injury in shock. 68 87

In a group of 260 non-selected cases of acute or subacute pancreatitis, severe complications occurred in 60 (23.1%). Long lasting shock and/or massive internal bleeding (5.4%), severe renal problems (anuria, tubular necrosis, nephrosis) (5.4%) and frank hepatic failure due to extensive liver necrosis or other severe destruction (5.0%), invariably lead to death. The clinical group of findings pointing to a fatal course usually manifested themselves during the first three days. Severe renal and hepatic lesions were in many cases secondary to shock in fulminant rapidly deteriorating cases. Preventing and efficient management of shock are thus essential prerequisites for saving the patient. Other important complications included severe intra-abdominal suppuration and abscesses, peritonitis and sepsis (3.9%), pseudocysts of the pancreas (5.4%) and biliary statis (18.4%). Severe obstruction to bile flow with associated jaundice occurred in only 4.6% of cases; unselected operative biliary decompression does not therefore appear indicated. If an early laparotomy is performed, efficient debridement and drainage are of utmost importance. Fatal panreatitis was associated with extensive necrosis of the pancreas in about 80% of cases; possibly subtotal pancreatic resection at an early laparotomy would have given better results in these most severe cases, as recently reported in the literature.
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PMID:Complications in acute pancreatitis. 103 80

In a group of 260 non-selected cases of acute or subacute pancreatitis, severe complications occurred in 60 (23.1%). Long lasting shock and/or massive internal bleeding (5.4%), severe renal problems (anuria, tubular necrosis, nephrosis) (5.4%) and frank hepatic failure due to extensive liver necrosis or other severe destruction (5.0%), invariably lead to death. The clinical group of findings pointing to a fatal course usually manifested themselves during the first three days. Severe renal and hepatic lesions were in many cases secondary to shock in fulminant rapidly deteriorating cases. Prevention and efficient management of shock are thus essential prerequisites for saving the patient. Other important complications included severe intra-abdominal suppuration and abscesses, peritonitis and sepsis (3.9%), pseudocysts of the pancreas (5.4%) and biliary stasis (18.4%). Severe obstruction to bile flow with associated jaundice occurred in only 4.6% of cases; unselected operative biliary decompression does not therefore appear indicated. If an early laparotomy is performed, efficient debridement and drainage are of utmost importance. Fatal pancreatitis was associated with extensive necrosis of the pancreas in about 80% of cases; possibly subtotal pancreatic resection at an early laparotomy would have given better results in these most severe cases, as recently reported in the literature.
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PMID:Complications in acute pancreatitis. 108 10

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

Hepatitis E virus (HEV) is a significant public health problem that affects almost 20 million individuals annually and cause acute liver injury in 3,5 million. Hepatitis E virus can cause acute, fulminant and chronic hepatitis and has been associated with a range of extrahepatic manifestation. The spectrum of these manifestation is still emerging. Acute pancreatitis and neurological, renal, hematologic, and muscoloskeletal manifestations have been described. Renal injury include membranoproliferative glomerulonephritis with or without cryoglobulinemia, membranous glomerulonephritis and tubular necrosis. The etiopathogenesis of extrahepatic manifestation is only supposed. It could be caused by a direct tossic effect of HEV or by an autoimmune process. We report a case of a 46 years old man who presented with acute hepatitis E. He was diagnosed to have acute severe renal failure and severe pancreatitis due to hepatitis E. Few cases have been reported in the literature concerning patients suffering from hepatitis E and severe extraepatic manifestations with a benign course and complete recovery.
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PMID:[Extra-hepatic manifestations associated with Hepatitis and virus infection]. 2958 66

On March 2, 2005 ~70 rough-toothed dolphins (Steno bredanensis) mass stranded along mud flats and associated canals on the Atlantic Ocean side of Marathon Key, Florida. Forty-six were necropsied and placed into two groups for analysis: Group-1 animals (N = 34; 65%) that died prior to medical intervention and rehabilitative efforts and Group-2 animals (N = 12; 35%) that died in rehabilitation. Thirty-four animals were females (18 adults, 5 juvenile/subadult, 7 calves, and 4 of undetermined age) and 12 were males (6 adults, 4 juvenile/subadults, 1 calf, and 1 of undetermined age). Body condition overall was fair to good in Group-1 and fair to poor in Group-2. Lesions were observed in multiple body systems. Greater than 90% of animals in both groups had respiratory lesions. Verminous sinusitis and bronchopneumonia were 2-3 times more prevalent in Group-2. Capture/exertional rhabdomyolysis was observed in Group-2 (42%). Vacuolar hepatopathies were observed in both groups including hepatic lipidosis (Group-1) and mixed etiologies (Group-2). Pancreatic and gastrointestinal tract pathologies were prevalent in Group-2 animals 56 and 75%, respectively, and included gastritis, gastric ulceration, enterocolitis, pancreatic atrophy, and pancreatitis related to physiologic stress. Group-2 more frequently had evidence of hemorrhagic diathesis present which included increased extramedullary hematopoiesis in various organs, increased hemosiderosis, and hemorrhage and hemorrhagic drainage in various organs. Central nervous system disease, primarily edema, and mild inflammation were equally prevalent. Renal proteinuria, tubular necrosis, and pigmentary deposition were observed in Group-2. Dental attrition was observed in ~40% of the groups. Gammaherpesviral-associated pharyngeal plaques were observed in 46 and 54% of Group-1 and 2 animals, respectively. Other lesions observed were mild and incidental with a frequency rate <20%. The findings from this Steno stranding provide a unique window into baseline individual and population clinical conditions and additional perspective into potential clinical sequelae of rehabilitation efforts.
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PMID:Macroscopic and Histopathologic Findings From a Mass Stranding of Rough-Toothed Dolphins (Steno bredanensis) in 2005 on Marathon Key, Florida, USA. 3298 13