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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extensive fat necrosis may be sometimes seen in patients suffering from acute pancreatitis even if pancreas itself is not seriously damaged. Infection of the necrotic areas of fat may produce serious intoxication and even death of the patient. If the infection occurs, evacuation of the necrosis should be carried out, even several times if necessary. In some cases fat necroses colliquate. The liquid may be reabsorbed or pseudocyst formation follows. In the cases of colliquation without infection a close observation of the patient is necessary to choose the time for surgery.
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PMID:[Voluminous fatty necrosis in acute pancreatitis]. 85 49

Acute pancreatitis was studied by electron microscopy after retrograde infusion of either trypsin, and/or beta-glucuronidase into the canine pancreatic duct. Marked changes were induced by the mixture of trypsin and beta-glucuronidase. (1) The acinar cells were initially excavated from the acinar lumen and formed cystic bodies in themselves. The cystic bodies were then disrupted at their marginal membranes, and the acinar cells were filled with a large amount of fibrillar materials which originated from the contents of the cystic bodies. At this time, the luminal margin of the acinar cells completely disappeared. (2) The cellular organellas and the intracellular fibrillar materials in the acinar cells were discharged into the interstitial space through the disrupted basal lamina. Infection in the pancreatic ductal system was considered to play an important role in the pathogenesis of acute hemorrhagic pancreatitis.
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PMID:Ultrastructural studies of experimental acute pancreatitis. 97 83

The authors observed 53 cases of diabetic ketoacidosis treated with low doses of insulin. Mean age of the patients was 41 +/- 17 years, duration of diabetes mellitus 7.5 +/- 6.4 years. Ketoacidosis was due to: infections in 36%, other diseases in 7%, and cessation of insulin therapy in 25% of cases. Ketoacidosis was a first sign of diabetes mellitus in 19% of cases while causative factor was not detected in 13% of cases. At the admission to hospital mean blood pH was 7.02 +/- 0.15, mean bicarbonate concentration 6.17 +/- 3.45 mM/l, and glycaemia 40.6 +/- 16.8 mM/l. Therapy of ketoacidosis was complicated by hypopotassemia in 1 patient and transient hypoglycaemia in another patient. Five patients (9.6%) died. Infections, myocardial infarction, acute pancreatitis, pulmonary edema, and disseminated intravascular coagulation were the causes of deaths.
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PMID:[Analysis of the cause of death in diabetic ketoacidosis based on 5 years of personal observation]. 251 62

The case histories of the 49 patients who died in a series of 165 patients admitted to the Medical Unit between 1958 and 1984 with polyarteritis nodosa (PAN) were reviewed. The causes of death of the 29 men and 20 women, mean age 51.44 +/- 7.4 years, were classified into 6 groups. Infection accounted for 26.5% (13/49) of deaths, the initial site of infection being pulmonary, complicated by septicaemia in 6 cases. Cardiovascular events were responsible for death in 24.4% (11/49): terminal cardiac failure (4 cases), myocardial infarction (1 case), ventricular tachycardia (1 case), stroke (1 case), pulmonary embolism (2 cases), fulminant hemoptysis (1 case). Gastrointestinal complications were the cause of death in 16.3% (8/49): ischemic necrosis (5 cases), acute pancreatitis (2 cases), oesophageal ulceration (1 case). Renal failure was observed in 10.2% (5/49), all occurring before 1972: acute renal failure (3 cases), chronic renal failure (2 cases). Cancer was the cause of death in 10.2% (5/49): primary bronchial carcinoma (2 cases), laryngeal carcinoma (1 case), carcinoma of the vulva (1 case), bone metastases (1 case). Finally, 14.2% (7/49) could not be classified in the preceding groups. Sudden death occurred in 3 patients, shock in 1 patient, multivisceral PAN in 2 patients and anaphylactic shock in 1 patient. Three of the 12 patients who had post-mortem studies had signs of progressive vasculitis. The results are compared with other reports in the literature and the pathogenic mechanisms are discussed. The infections and cardiovascular deaths occurred early or late and were not related to the state of the activity of the vasculitis. Immunosuppressive treatment seems to play an important role in their pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Causes of death in systemic vasculitis of polyarteritis nodosa. Analysis of a series of 165 patients]. 290 28

Infection, hemorrhage and adult respiratory distress syndrome (ARDS) are pulmonary complications occurring after remission induction therapy for acute leukemia. The aim of this study was to analyze the incidence of these causes by serial roentgenogram, clinical, microbiological and laboratory tests in 21 patients (pts) with relapsed acute leukemia (18 X myeloid, 3 X lymphoblastic), an AML-pt (acute myeloid leukemia) suffering from secondary leukemia, and three pts with primary refractory leukemia following treatment with intermediate (IM) and high-dose cytosine arabinoside (HD-Ara C), in combination with amsacrine (AMSA)(n = 19), etoposide (VP 16) (n = 5) or Mitoxantrone (n = 1). Eleven out of 25 pts developed pulmonary complications, one of them with massive hemoptysis and roentgenographic signs of pulmonary bleeding, one suffering from protracted shock after a tumor lysis syndrome, two pts showing symptoms of a cardiogenic pulmonary edema complicating severe Candida pneumonia in one case and legionnaires' disease in the other. Seven of the eleven pts had a non-cardiogenic pulmonary edema with respiratory failure 1-14 days after cessation of induction or consolidation therapy. In six of the seven, there were no signs of cardiogenic, infectious or metabolic reasons, including fluid overload, for the pulmonary edema, one had as a contributing factor a Candida infection of the lung. Three of the seven patients recovered, four died (two following IM and two after HD-Ara C). Other adverse side effects, clearly attributable to HD-Ara C, included delirious state (n = 3), generalized erythema (n = 3), acute pancreatitis (n = 2), acute abdomen (n = 1) and conjunctivitis in almost all patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-cardiogenic pulmonary edema complicating intermediate and high-dose Ara C treatment for relapsed acute leukemia. 336 72

Since 1981 the authors have performed 14 orthotopic heart transplantations and one heart-lung transplantation, using cyclosporine and prednisone as immunosuppressants. Eight of the recipients had terminal congestive cardiomyopathy and six had ischemic cardiac dysfunction. The combined heart-lung transplantation was performed on a patient with a congenital ventricular septal defect with Eisenmenger's syndrome. Twelve of the patients were alive and well at follow-up 9 to 34 months (mean 17.4 months) after transplantation. One patient died of acute rejection and one of acute pancreatitis and secondary peritonitis. The third death, due to acute right ventricular failure, occurred immediately after transplantation. Rejection was diagnosed histologically on seven other occasions in four patients and was treated successfully. Infection was not a major problem. Cyclosporine -induced reversible nephrotoxicity was evident in 12 patients, 2 of whom required dialysis. Other side effects of cyclosporine seen in these patients included hypertension, gastrointestinal upset, headaches and hirsutism. This experience suggests that cyclosporine is a potent immunosuppressive agent that has greatly reduced the hazards of rejection and infection. However, the frequency of nephrotoxicity is high; careful monitoring of cyclosporine blood levels and renal function is essential.
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PMID:Cyclosporine in cardiac transplantation. 623 93

Thirty-two patients died of pancreatitis and its complications over a 10-year period. Infection (bacteremia, fungemia, or pancreatic abscess) was the major cause of death in 80%. In the remaining 20%, refractory hypotension or respiratory failure were the lethal mechanisms. In only 78% of patients was the correct diagnosis made before death. Ninety-four percent of those who died did so during their first clinical episode of pancreatitis. Prophylactic antibiotics did not prevent the development of pancreatic abscesses and organisms resistant to the antibiotics used often became the primary pathogens. Certain prognostic factors reliably separated those who died from those who lived. Peritoneal lavage and dialysis may be helpful in both the early diagnosis and therapy of severe acute pancreatitis.
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PMID:Lethal pancreatitis. 665 Apr 70

In the absence of causative therapy of acute pancreatitis the management of the disease focus on treatment and prevention of complications and symptoms. In mild acute pancreatitis intravenous fluid administration, analgetics and avoidance of oral fluid or food intake is sufficient in most cases. The treatment of severe pancreatitis involves identification of pancreatic and peripancreatic necroses, best demonstrated and evaluated by contrast-enhanced computerized tomography (CT). Infection of such necroses is the most common cause of death from acute pancreatitis. Recent data suggest that antibiotic prophylaxis is worthwhile and it should therefore always be instituted in the severe form of the disease. Careful monitoring of vital functions is mandatory and early treatment with assisted ventilation and renal dialysis is advised. Adequate volume replacement and nutritional support is important. The role of the gut in the development of infected necroses is becoming increasingly obvious. Also, the absence of food in the intestine may increase the intestinal barrier damage. Therefore, enteral nutrition is discussed as a logical step in pancreatitis treatment. However, the food should be delivered below the ligament of Treitz (below the area of the cholecystokinin (CCK) cells) as CCK stimulation probably worsen the course of the disease.
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PMID:Conservative treatment in acute pancreatitis. 766 93

The use of antibiotics in patients with severe acute pancreatitis (stage II and III) is indicated since bacterial complications are the most common cause of death in these patients. In the present study the penetration of ceftazidime into pancreatic juice, into healthy and chronically inflamed pancreatic tissue as well as into necrotic regions in cases of severe acute pancreatitis was investigated. A peak concentration of 12.9 +/- 5.9 mg/l was found 60 min after intravenous administration of 35 mg/kg of the drug, which is 32% of the corresponding serum levels. Pancreatic tissue concentrations varied between 9 and 79% of the corresponding serum levels, depending on the stage of inflammation. After five days of antibiotic treatment with doses of 2 g t.i.d., concentrations between 1.8 and 6.9 mg/kg were detected even in pancreatic necroses. This suggests that sufficient antibacterial levels of ceftazidime were present in all pancreatic compartments analyzed following administration of common therapeutic dosages. Therefore, from a pharmacokinetic point of view, ceftazidime could be a potentially effective drug for the treatment of pancreatitis.
Infection
PMID:Penetration of ceftazidime into human pancreas. 822 26

Infections from enteric bacteria are a major cause of morbidity and mortality during acute pancreatitis (AP), but the pathways by which these organisms reach distant organs remains speculative. Experiments were conducted to determine if bacterial translocation could be a mechanism for infection during this disease. AP was induced in Lewis rats by i.v. infusion of caerulein (experiment I) or ligation of the head of the pancreas (experiment II). In a third experiment, rats were gavaged with 1 x 10(8) 14C-radiolabeled Escherichia coli and pancreatitis was induced with caerulein. Results in all three experiments showed that AP increased the number of viable bacteria recovered in peritoneal fluid, mesenteric lymph nodes (MLN), liver, lungs, and pancreas. Radionuclide counting indicated that AP enhanced the gut permeability to 14C E. coli. To estimate the impact of AP on the magnitude of translocation and on the ability of the host to clear bacteria, the nuclide and colony-forming units (CFU) ratios were calculated between animals with and without AP. Blood, peritoneal fluid, and MLN had the highest nuclide ratio. During AP, these tissues may be the principal routes for bacterial spreading from the gut lumen. Peritoneal fluid, pancreas, and lung were the tissues with the highest CFU ratio. Bacterial killing ability of these tissues is likely impaired during AP.
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PMID:Bacterial translocation: a potential source for infection in acute pancreatitis. 830 91


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