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

Pulmonary edema, cardiac enlargement, and respiratory insufficiency may occur in patients with acute pancreatitis. The mechanisms are complex and incompletely understood, but probable etiologic factors include fluid overload, left ventricular failure, impaired respiratory excursion and microatelectasis, and a nonspecific response of the lung to various types of pulmonary injury including hypotension, intravenous crystalloids, and the effects of circulating pancreatic enzymes. Recognition of the association of pulmonary edema and respiratory insufficiency with pancreatitis is importance because early treatment with positive pressure breathing, careful fluid management and diuretics, and corticosteroids may prevent the development of irreversible respiratory failure.
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PMID:Pulmonary edema and respiratory insufficiency in acute pancreatitis. 12 91

Hemodynamic data were obtained within 15 hours of admission in 11 previously healthy patients (20 to 51 years of age, 7 men and 4 women) who had developed transient, reversible pulmonary edema without cardiac dilation in association with near-death from freshwater drowning (2 cases), pentobarbital overdose, heroin overdose (2 cases), smoke inhalation, chest trauma, sepsis (2 cases), pancreatitis, or prolonged abdominal surgery with suspected sepsis. Using a balloon-tipped flow-directed catheter, the pulmonary artery systolic/diastolic pressures (in mm Hg) were 25/12, 22/9, 31/11, 26/15, 20/10, 35/15, 40/15, 32/18, 20/10, 24/10, and 20/7; the corresponding pulmonary capillary wedge pressures (in mm Hg) were 8, 9, 6, 14, 6, 6, 15, 15, 10, 10, and 5, respectively. Plasma colloidal osmotic pressures measured in the latter 5 cases were 26, 18, 18, 18, and 15 mm Hg, respectively. In addition, the protein content of the alveolar fluid was 5.1, 3.4, 4.0, and 7.1 g per 100 ml in 4 patients. The concentration and distribution of the protein in plasma and alveolar fluid were very similar. These findings provide strong efidence that altered capillary permeability is responsible for the pulmonary edema.
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PMID:Hemodynamic and alveolar protein studies in noncardiac pulmonary edema. 98 76

Acute pulmonary edema appeared 3 or more days after the onset of acute pancreatitis in 7 patients, an approximate incidence of 8%. The severity of pancreatitis in these patients was characterized by massive requirements for intravenous colloid and by marked hypocalcemia. In addition, at least 5 of the 7 patients had very high serum levels of triglycerides at the time of hospital admission. Hemodynamic studies during pulmonary edema showed normal central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and pulmonary vascular resistance. Cardiac index was appropriately elevated. Respiratory treatment, consisting of endotracheal intubation and controlled ventilation with PEEP, was successful in allowing reversal of the pulmonary injury and recovery of respiratory function within 1-2 weeks in all cases. Two patients died later from pancreatic abscesses. The findings indicate that a distinct form of pulmonary injury may occur in acute pancreatitis, characterized by loss of integrity of the alveolar-capilllary membrane, leading to pulmonary edema. The mechanism of injury is not known but may be caused by circulating free fatty acids, phospholipase A, or vasoactive substances. The pulmonary membrane lesion appears to heal during the period of intensive respiratory support.
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PMID:The pathogenesis of pulmonary edema in acute pancreatitis. 110 36

A 25-year-old Japanese woman experienced pulmonary edema, shock, encephalopathy and silent pancreatitis after hysterosalpingography using lipiodol ultra fluid, because the contrast media flowed directly into the blood stream from endometrium injured by several curettages for termination of pregnancy. Total iodine concentrations in plasma and urine decreased exponentially and their half-life was 16.12 and 13.04 days, respectively. Clear correlations were observed between the iodine concentration in plasma and the amelioration of both electroencephalogram and neuropsychic abnormalities. Adverse reactions of oil-soluble contrast media are also discussed.
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PMID:Adverse reactions to lipiodol ultra fluid: report of an accidental case. 165 63

This experimental study was undertaken to clarify the role of pancreatic enzymes and endotoxin in the pathogenesis of pulmonary edema in acute pancreatitis, paying special attention to the effects of two different intravenous infusions: lactated Ringer's solution (LR) and Dextran 40 (D40). After acute pancreatitis was induced in dogs by injecting autologous gallbladder bile into the main pancreatic duct, plasma endotoxin levels increased markedly in both the LR and D40 groups, and PaO2 decreased more significantly in the D40 group. Extravascular lung water (EVLW) increased more significantly in the D40 group than in the LR group, in spite of the fact that colloid-hydrostatic pressure gradient (CHPG) had been maintained more efficiently in the D40 group. Significant correlation between EVLW and plasma endotoxin level was delineated in both groups, but the slope of the regression line in the D40 group was much greater than that of the LR group. Infusion of trypsin and elastase into the pulmonary artery in normal dogs caused moderate elevation of EVLW in the D40 group, but there was no significant alteration in the LR group. The changes of PaO2, EVLW, and CHPG after infusion of endotoxin were similar to those in the animals with experimental acute pancreatitis. In conclusion, endotoxin appears to play an important role in the pathogenesis of pancreatitis-induced pulmonary edema by causing an increase in pulmonary vascular permeability, and under these circumstances the infusion of large amount of colloid solution promotes the development of pulmonary edema.
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PMID:[An experimental study on the pathogenesis of pulmonary edema in acute pancreatitis, with special interest to the effects of colloid infusion and the role of endotoxin]. 172 52

In this experimental study, we investigated pathophysiology of respiratory failure with acute pancreatitis. Pancreatitis was induced by injection of 15% Na-taurocholate 1 ml/kg into the main pancreatic duct of the dogs. Experimental dogs were divided into two groups based on the value of Respiratory Index (R-Index). Group A included 9 dogs in whom respiratory failure was not recognized (R-Index less than 0.5) and Group B included 9 dogs with respiratory failure (R-Index less than 0.5). All the dogs were sacrificed 12 hours after induction of pancreatitis, and histological findings were examined. Quantity of water in the lung (Qwl) was also measured by gravimetric method. Group B showed severe hypoxia with hypocapnia, and increase of A-aDO2, R-Index, and decrease of a/A PO2. Qwl in Group B increased significantly comparing with Group A. In biochemical study, increase of serum lipase, triglyceride, free fatty acid, and angiotensin converting enzyme were observed in Group B. These results indicate that respiratory failure with acute pancreatitis is due to lung edema following injury of the capillary of the lung. The role of free fatty acid liberated by lipolysis was suggested in the mechanism of pulmonary damage with acute pancreatitis.
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PMID:[Experimental study of respiratory failure with acute pancreatitis in dogs]. 241

The effect of blood exchange transfusion on experimental acute pancreatitis was investigated. Acute hemorrhagic pancreatitis was induced in rats by the injection of sodium taurocholate into the pancreatic duct. One hour after the induction of pancreatitis, blood exchange transfusion was carried out in these rats. The survival rates by 24 hr significantly increased in the exchange transfusion group as compared to those in the non-treated control group. Blood exchange transfusion, though had not significant effect on the macroscopic findings at autopsy, reduced pulmonary edema. These results suggested that blood purification by exchange transfusion may be beneficial for patients with acute pancreatitis, especially at an early stage.
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PMID:Effect of blood exchange transfusion as an initial treatment of acute hemorrhagic pancreatitis. 246 34

In this study, we examined the effects of hypertonic saline-dextran resuscitation (2,400 mOsm of sodium chloride, 6 percent dextran 70) on cardiopulmonary function and extravascular lung water in acute canine pancreatitis. Acute pancreatitis was induced in 21 dogs by injecting 0.5 ml/kg of autologous bile into the pancreatic duct. In 10 dogs, resuscitation was begun with a 4 ml/kg bolus of hypertonic saline-dextran solution; 11 dogs received no bolus. Lactated Ringer's solution was infused in all dogs to maintain mean arterial pressure and cardiac output at baseline values. Pulmonary hypertension accompanied by a significant increase in pulmonary vascular resistance and a decrease in lung blood flow occurred in those dogs resuscitated with lactated Ringer's solution alone. By contrast, dogs in the hypertonic saline-dextran group maintained pulmonary artery pressure and pulmonary vascular resistance at baseline values while nutritive blood flow to the lung decreased progressively. Our data suggest that hypertonic saline-dextran resuscitation effectively restores cardiac function while it significantly reduces fluid requirements, as well as the pulmonary hypertension and pulmonary edema that frequently accompany lactated Ringer's resuscitation of acute pancreatitis.
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PMID:Hypertonic saline-dextran resuscitation of acute canine bile-induced pancreatitis. 247 51

The purpose of this study was to investigate the relation between serum lipase (LP), serum immunoreactive trypsin (IRT), and its inhibitors in patients with adult respiratory distress syndrome (ARDS) of diverse origin and to compare their time course with other acute conditions. The IRT and LP levels were determined at regular intervals in 41 patients hospitalized in the intensive respiratory unit with ARDS (n = 9), acute pancreatitis (n = 5), shock (n = 9), bronchopneumonia (n = 10), or acute cardiogenic pulmonary edema (n = 8). Several trypsin inhibitors were measured simultaneously: serum trypsin inhibitory capacity (TIC), alpha 1-antitrypsin, alpha 2-macroglobulin, and antithrombin III. Concomitantly, angiotensin-converting enzyme (ACE) activity was determined as a potential marker of the endothelial injury. A respective 19- and 13-fold increase in IRT and LP values were observed in patients with ARDS after a mean evolution of 6 days; similar increases were seen in patients with pancreatitis. These values were significantly higher than those observed in the other conditions studied. In patients with ARDS and acute pancreatitis, the evolution of IRT and LP values were associated with a sixfold rise in TIC. A low TIC/IRT ratio in patients with ARDS appeared to be an index of poor prognosis. Conversely, ACE activity evolution was characterized by an early decrease in all the conditions studied. These observations indicate that there is an acute delayed pancreas injury in ARDS. Thus, the release of pancreatic enzymes are not reliable markers of the early evolution of the disease but they may represent secondary mediators for enhancement of the increased endothelial permeability.
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PMID:Evidence for pancreas injury in adult respiratory distress syndrome. 298 86

Of 224 consecutive renal transplant patients in a prospective, randomized immunosuppressive trial, candida esophagitis developed in 5 despite nystatin prophylaxis. No differences were noted between cyclosporine and antilymphocyte globulin-azathioprine immunosuppressive treatment. All patients were diabetic, and four were recipients of cadaver kidneys. Candida esophagitis occurred within 6 months after transplantation, and only one patient had recurrence. All patients responded to treatment consisting of 2 to 6 days of intravenous amphotericin B (0.2 to 2 mg/kg total dose). The prevalence of candida esophagitis was not related to rejection episodes. Three of five patients eventually died, one 2 weeks after resolution of candida esophagitis from a hypoglycemic episode, one from acute exacerbation of pulmonary failure and relapsing pancreatitis in association with candida esophagitis and therapy-resistant candidemia, and one 17 months after candida esophagitis from pulmonary edema. Our findings show that candida esophagitis by itself is an easily managed complication, but is also a sign of potentially increased morbidity in these patients.
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PMID:Incidence and treatment of candida esophagitis in patients undergoing renal transplantation. Data from the Minnesota prospective randomized trial of cyclosporine versus antilymphocyte globulin-azathioprine. 327 75


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