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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The echocardiographic and radionuclide angiographic abnormalities in children after scorpion envenomation with L. quinquestriatus, were evaluated. Five children were severely hypertensive, one of them in respiratory failure and another had pulmonary edema. The results revealed poor global contractility 12-15 hr after the sting in three patients. The radionuclide angiograms also revealed poor contractility with low ejection fraction. There was enzymatic evidence of myocardial damage. The changes observed in the echocardiograms and radionuclide angiograms were attributed to catecholamine induced myocardial ischemia. The abnormalities observed suggest that systolic dysfunction plays a role in the pathogenesis of heart failure in scorpion envenomation, in addition to a decrease of left ventricular compliance and increased impedance to left ventricular emptying. The beneficial effects of nifedipine in hypertension and other cardiovascular manifestations justify the routine use of afterload reduction in children with cardiovascular manifestations after scorpion envenomation.
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PMID:Echocardiographic and radionuclide angiographic observations following scorpion envenomation by Leiurus quinquestriatus. 226 99

Adoptive immunotherapy with tumor-infiltrating lymphocytes (TIL) and interleukin-2 (IL-2) is currently being investigated in the treatment of chemoresistant cancers. In protocols using high dosages of IL-2 and adoptive transfers of lymphokine-activated killer (LAK) cells, severe pulmonary toxicities, including pulmonary edema and respiratory failure, are regularly observed. Serial measurements of pulmonary function in patients receiving TIL and continuous infusions of moderate dosages of IL-2 showed the development of mild obstructive and restrictive defects. Partial reversibility of the FEV1 with bronchodilators was observed, suggesting the development of hyperreactive airways. Decreases in lung volumes, DLCO, and gas exchange occurred and may reflect pulmonary infiltration by inflammatory cells, increased lung water, or diminished chest wall function. We conclude that adoptive immunotherapy with TIL and IL-2 produces changes in systemic immune response that may contribute to abnormal pulmonary physiology.
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PMID:Alterations in pulmonary function in cancer patients receiving adoptive immunotherapy with tumor-infiltrating lymphocytes and interleukin-2. 229 77

One hundred three relapsed leukemia patients were treated with high-dose cytosine arabinoside (Ara-C); 3 g/m2 intravenously over 2 hours every 6 to 12 hours for a total of nine to 12 doses or 3 g/m2 intravenously over 2 hours for two doses 12 hours apart followed by a continuous infusion of 1.5 g/m2 over 24 hours daily for 3 to 4 days. Thirteen of them developed adult respiratory distress syndrome (ARDS) without having any recognized reason for the development of pulmonary edema. This problem showed no correlation with age or prior chemotherapy. Four of the patients recovered, but in nine this complication was fatal. The authors have reviewed the clinical course of these 13 patients and the postmortem findings of the seven patients who had an autopsy performed. The pulmonary tissue from six patients showed massive edema and one had diffuse alveolar damage. Histologic examination revealed a highly proteinaceous intraalveolar infiltrate without any inflammatory reaction in all cases. Intestinal tissue from all patients revealed changes compatible with cytotoxic damage, and pleura and/or pericardium from six of the seven patients showed an extensive fibrinous exudate suggestive of capillary leakage. The time sequence of the clinical events and the histologic findings indicate that high-dose Ara-C treatment in leukemia may cause a capillary leakage syndrome with ARDS that may progress to fatal respiratory failure.
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PMID:Fatal pulmonary failure complicating high-dose cytosine arabinoside therapy in acute leukemia. 230 59

This is an autopsy report of multiple primary cancers observed in a patient who had clinically been diagnosed as chronic arsenic poisoning. An 88-year-old man, non-smoker, had worked in an arsenic mine for 6 years from the age of 47. He had undergone operations for Bowen's disease and gastric cancer at ages 80 and 86, respectively. At autopsy, squamous cell carcinoma of the lung and a polypoid lesion in the piriform recess were found. Furthermore, microscopic examination revealed latent prostatic adenocarcinoma and oncocytoma in the kidney. The polypoid lesion of the piriform recess appeared to originate from the duct of the minor salivary gland in the pharynx, showing an adenoid cystic carcinoma-like pattern with squamous cell carcinoma in part. The cause of death was thought to be respiratory failure due to bronchopneumonia and pulmonary edema as well as hydrothorax, and chronic heart failure following ischemic heart disease. Bowen's disease was followed by four internal malignant tumors, even though the etiological relation between these cancers and arsenic is not clear.
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PMID:Multiple primary cancers in a case of chronic arsenic poisoning--an autopsy report. 233 47

In order to prevent septicaemia with streptococci, 20 consecutive selectively decontaminated patients on intermediate high-dose Ara-C treatment for malignant haematological diseases were given penicillin G. The incidence of infection with streptococci decreased from 0.76 per episode (14 patients, 17 episodes) for controls who did not receive penicillin G to 0.11 per episode in the prophylaxis group (20 patients, 26 episodes). Simultaneously, a decrease in the incidence of respiratory failure was observed, i.e. 0.52 per episode for controls and 0.19 per episode for patients on penicillin G. The results suggest that septicaemia with streptococci triggers the development of noncardiogenic pulmonary oedema in patients with pre-existing damage of the lung due to aggressive cytotoxic treatment. This suggestion is supported by the sequence of events, regarding the occurrence of infection and respiratory failure and the results of measurements of antileukoprotease serum concentrations, a parameter for pulmonary capillary leakage. Taking into account the data in the literature and the results of the present study, the conclusion is drawn that in patients treated with (intermediate) high dose Ara-C, prevention of streptococcal septicaemia is associated with a decrease in the incidence of respiratory failure.
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PMID:Respiratory failure elicited by streptococcal septicaemia in patients treated with cytosine arabinoside, and its prevention by penicillin. 236 64

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 harmful effect of iron excess was studied in an experiment using fifteen adult sheep. The animals were divided into three groups of 5 each. The sheep of the group I were kept as controls, those of the group II and III were supplemented with iron in doses of 80 and 40 mg/kg body weight (BW)/24 h respectively. The animals of group II died after a period of 3-7 weeks showing anorexia, loss of weight, diarrhoea, depression and symptoms of circulatory and respiratory failure. From the animals of group III one died after 13 weeks, with symptoms of pulmonary oedema, while the other 4 survived for 22 weeks, together with the animals of the control group. The iron-supplemented animals presented increased values of Serum Iron (SI), Total Iron Binding Capacity (TIBC), percent Transferring Saturation (% SAT), Alanino aminotransferase (ALT), serum Alkalin Phosphatase (SAP), Serum Urea Nitrogen (SUN) Creatinine, Phosphorus and decreased values of serum Copper concentration. These parameters were greater in group II. The iron concentration in the liver, spleen, myocardium and kidneys was also much higher than in the controls. The histological examination revealed degeneration of the liver, spleen, myocardium and kidneys in both groups, while cells overloaded with hemosiderin were seen in the third group only. In conclusion, it was shown that chronic intoxication may occur in sheep overdosed with iron. The toxic dose of iron ranged between 40 and 80 (mg/Kg body weight) per day and was close to 40 mg, when iron was administered in the soluble from FeCl3.6H2O.
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PMID:Iron toxicity in sheep. 253 32

Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B4 and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. We conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and, third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.
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PMID:Reperfusion pulmonary edema. 221 74

An important goal in managing patients with respiratory failure using mechanical ventilatory support and positive end-expiratory pressure (PEEP) is to optimize tissue oxygen delivery relative to oxygen consumption. To this end, systemic hypothermia has been reported to reduce oxygen consumption. Cooling, however, may antagonize hypoxic pulmonary vasoconstriction and depress cardiac output. To determine whether these potentially adverse effects of cooling on tissue oxygen delivery would outweigh any potential benefits, we studied the effects of systemic hypothermia and end-expiratory pressure on venous admixture, intrapulmonary blood distribution, and oxygenation variables in 40 dogs with oleic acid-induced pulmonary edema of the right lung. The dogs were randomly assigned to four treatment groups of 10 dogs each: normothermia and zero end-expiratory pressure (ZEEP); normothermia and 10 cm H2O PEEP; hypothermia and ZEEP; hypothermia and PEEP. Hypothermia to 31.9 +/- 0.1 degree C (mean +/- SEM) caused no adverse effects on intrapulmonary blood flow distribution (measured by radioactive microspheres) or on venous admixture. Tissue oxygen delivery and arterial oxygenation did not improve with hypothermia, the latter being 109 +/- 13 mm Hg and 70 +/- 8 mm Hg with PEEP and ZEEP, respectively. However, hypothermia significantly reduced oxygen consumption, so that the coefficient of oxygen delivery (i.e., the ratio of oxygen supply to consumption) increased from 2.5 +/- 0.1 to 3.2 +/- 0.2 (p less than 0.01) with ZEEP and from 2.0 +/- 0.1 to 2.6 +/- 0.3 with PEEP (p = 0.016). Thus, although systemic hypothermia failed to improve arterial oxygenation and tissue oxygen delivery, it decreased systemic oxygen demands, thereby improving the oxygen supply-demand balance.
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PMID:Hypothermia with and without end-expiratory pressure in canine oleic acid pulmonary edema. 266 83

This review covers the physiological and clinical implications of lung function during anesthesia and respiratory insufficiency in the postoperative period. We have divided it into 3 main sections: 1) lung function changes induced by anesthesia and surgery, in which the impact on pulmonary mechanics, ventilation/perfusion changes and gas exchange are examined; 2) physiological implications of postoperative respiratory function secondary to decreased alveolar ventilation, development of atelectasis, and interstitial lung edema; and 3) clinical implications of postoperative respiratory failure. In this last section we analyze the current therapeutic modalities available to reduce the incidence of postoperative respiratory failure, as well as related morbidity and mortality.
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PMID:Lung function during anesthesia and respiratory insufficiency in the postoperative period: physiological and clinical implications. 268 40


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