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Query: UMLS:C0034063 (pulmonary edema)
 10,665 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

Acute pancreatitis and cardiac disease were diagnosed in a dog with pulmonary edema. The early clinical course and initial thoracic radiographs suggested that the pulmonary edema was noncardiogenic. The late clinical course was complicated by heart failure. The dog died, and a necropsy was performed. Histologically, an acute, severe capillary-alveolar membrane lesion was found in the lungs. Review of the human medical literature indicated that respiratory complications, including pulmonary edema, are commonly recognized in people with acute pancreatitis. Furthermore, in acute pancreatitis of human beings, the existence of specific mechanisms of pulmonary injury is suspected. Retrospective consideration of this case suggested that the initial pulmonary edema was induced by acute pancreatitis.
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PMID:Pulmonary edema in a dog with acute pancreatitis and cardiac disease. 64 Sep 32

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

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

Lung injury is a common and severe complication in acute pancreatitis. The pathogenesis of which has not been completely understood. To explore the mechanism of lung injury, ST and FFA and PLA in bronchoalveolar perfusate, FFA and PLA in blood were measured; clinical symptoms and chest film were analysed; blood gas analysis was performed. The results indicated that lung injury mostly occurs in ABNP and less in AEP. Pulmonary edema and atelectasis are essential changes of lung injury. It is believed that FFA is an important factor responsible for pulmonary edema. PLA, which plays the most important role in lung injury, not only results in atelectasis by degradating the SA in alveolar, but also induces pulmonary edema. The main reason for the increase of ST is the degradation of SA in alveolar. The levels of FFA and PLA in the blood may indicate the severity of acute pancreatitis. However, it remains unknown whether the synthesis of SA in patient with acute pancreatitis is inhibited.
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PMID:[Clinical study of lung injury in acute pancreatitis]. 209 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 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 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


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