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

The respiratory manifestations of leptospirosis are usually benign. A case is reported of leptospirosis with serious pulmonary affection. Pulmonary involvement in leptospirosis is infrequently predominant and usually without bearing on prognosis. Clinical and roentgenological features are reviewed. Severe forms with massive hemoptysis or acute respiratory failure occur occasionally. The clinical symptoms, the radiological manifestations and haemodynamic investigation were suggestive of an acute respiratory distress by non haemodynamic pulmonary oedema. In accordance with other authors, one could be justified in including this acute respiratory failure as part of the adult respiratory distress syndrome. Since leptospirosis has extremely diverse clinical features, physicians should have this diagnosis in mind in many circumstances and should request the appropriate examinations at the right moment. Carefully performed microbiological techniques may reduce the problems encountered in isolating leptospires. Serological tests requested after the 12th day of the disease and repeated several times should improve the diagnosis confirmation. The potential severity of certain forms justifies curative antibiotic therapy.
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PMID:[Acute adult respiratory distress syndrome in leptospirosis]. 193 30

Outpatient arthroscopic knee surgery carries with it certain risk factors similar to those accompanying other major knee procedures. These risks may be related to the complexity of the procedure, exposure to anesthesia, or risk factors from previous medical history. Two cases of acute pulmonary edema following arthroscopic knee surgery in otherwise healthy teenage athletes are presented. Both patients developed acute respiratory distress in the recovery room after uneventful arthroscopic knee surgery. The patients in both cases recovered and were able to return to sporting activity with no sequelae. The similarities in both cases prompted a retrospective investigation of the events from the induction of general anesthesia to the admission of the patients to the intensive care unit. Several possible causes of acute post-operative pulmonary edema include fluid overload, cardiac arrhythmia, respiratory depression, systemic drug reaction and sickle cell trait or disease. Outpatient arthroscopy still remains the procedure of choice for meniscal pathology of the knee, but the surgeon and the anesthesia personnel must be aware of and prepared for pulmonary complications that may arise in the immediate post-operative period.
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PMID:Post-arthroscopic pulmonary edema in two healthy teenage athletes. 202 15

Acute gestational pyelonephritis infrequently leads to nonhydrostatic permeability pulmonary edema known clinically as acute respiratory distress syndrome (ARDS). In this form of ARDS, sepsis is considered the primary cause of pulmonary dysfunction. Decreases in colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation are associated with a worsening prognosis in septic conditions. We sought to investigate the changes in these parameters with acute gestational pyelonephritis to gain insight into the factors that may place the patient at risk for sepsis-related morbidity. Colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation via pulse oximetry were prospectively measured during the inpatient treatment of 17 pregnant patients with acute gestational pyelonephritis. All three parameters achieved their nadir within 24 hours of hospitalization and the initiation of therapy. Although no patient developed significant pulmonary dysfunction, we believe that patient susceptibility for pulmonary edema and general morbidity could be maximal in the first 24 hours after therapy. Future studies using a larger number of patients may identify one or more of these laboratory parameters as helpful in identifying gravid patients who are at risk of developing gestational ARDS.
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PMID:Acute gestational pyelonephritis: the impact on colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation. 202 86

Four patients developed an acute respiratory distress syndrome characterised by clinical and radiological signs of pulmonary oedema, a protein-rich oedema, severe hypoxemia refractory to oxygen therapy, contrasting with normal left ventricular filling pressures and indicating increased permeability of the alveolo-capillary membrane, 24 to 72 hours after the onset of acute myocardial infarction. After having excluded the usual causes of the acute respiratory distress syndrome, the authors suggest that acute myocardial infarction, especially when extensive, may cause a lesion of the alveolo-capillary membrane by an unknown mechanism. Treatment consisted in mechanical ventilation with positive expiratory pressures in 3 cases and with continuous positive pressure during spontaneous respiration in the third patient and in relay with controlled ventilation in the other two. These techniques of ventilation improved the hypoxemia and led to complete cure in all cases without evolution to pulmonary fibrosis. In addition to mechanical ventilation, all patients were given systematic antibiotic therapy because of the possibility of an infectious etiology while waiting for the results of microbiological and serological testing and because of the high risk of superinfection which plays an essential part in the outcome of the condition. The immediate response to treatment was favourable in all cases. One patient died suddenly of cardiogenic shock two weeks after this episode. The other patients are still alive 39, 38 and 20 months after infarction. The importance of the diagnosis of the acute respiratory distress syndrome in the acute phase of myocardial infarction resides in its therapeutic implications which are quite different to those of cardiogenic shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute respiratory distress syndrome in the initial phase of myocardial infarction in adults]. 212 17

Leukoagglutinins are implicated in transfusion-related acute lung injury (TRALI). In the present study, severe lung vascular leakage was reproduced by application of a leukoagglutinating antibody of anti-5b specificity in an ex vivo lung model. The antibody originated from a multiparous donor-plasma, observed to cause noncardiogenic edema during transfusion therapy. Heated full plasma (anti-5b-titer 1/128) or purified immunoglobulin G fraction was used for the studies. Ex vivo isolated rabbit lungs were perfused with albumin buffer, and human granulocytes (PMN) were admixed to the recirculating perfusate. In presence of anti-5b antibody plus 5b-positive PMN plus rabbit plasma as complement-source, severe lung edema occurred after a latent period of 3 to 6 hours. Pulmonary artery pressure was only transiently and moderately increased, and the leakage reaction could be traced back to a several-fold increase in lung vascular permeability. In contrast, no vascular leakage was noted in lungs perfused in the absence of anti-5b antibody, PMN, or rabbit plasma. Moreover, no permeability increase occurred on use of 5b-negative PMN. This reproduction of TRALI in an ex vivo lung model corroborates the role of leukoagglutinating antibodies in initiating PMN-dependent respiratory distress and suggests a contribution of concomitant complement activation.
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PMID:Reproduction of transfusion-related acute lung injury in an ex vivo lung model. 206 73

The etiology of edema associated with pulmonary resection was investigated in five patients during the immediate postoperative period. Three patients received pneumonectomy while two patients had one lobe resected. All patients suffered from severe respiratory distress and had x-ray evidence of diffuse interstitial pulmonary edema within 12 hours of surgery. Hemodynamic data were obtained with radial and pulmonary artery catheters. Edema fluid was obtained along with blood samples for simultaneous determination of protein and albumin content. All patients studied had normal or high cardiac output, normal cardiac filling pressures, and edema fluid protein to serum protein ratio of 0.6 or greater suggestive of permeability changes contributing to edema fluid accumulation. Calculated shunt fraction exceeded 25 percent in all patients. Pulmonary edema has been noted in patients following pulmonary resection in the early postoperative period. In patients reviewed here, two factors appeared to be significant. First is an increase in pulmonary capillary pressure associated with passage of a normal to high cardiac output in a reduced volume pulmonary vascular bed. The second factor, as demonstrated by protein content in the edema fluid, is injury to the alveolar capillary membrane.
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PMID:Permeability pulmonary edema following lung resection. 222 69

To specify differential and diagnostic criteria of hemodynamic and non-hemodynamic pulmonary edema, canine experimental simulation (15 trials) of different types of abnormal hemodynamic and lung capillary permeability parameters was carried out. The X-ray pictures of 71 patients with and acute diffuse lesion of the pulmonary vascular channel (including 51 with adult respiratory distress and 20 with hemodynamic pulmonary edema) was analysed. The findings substantiated the possibility of making a differential diagnosis of pulmonary edema of various genesis. Symptom complexes, typical of predominantly higher permeability of the lung capillaries and hemodynamic disturbance, were formulated.
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PMID:[Roentgenological diagnosis of acute lesions of the lungs with disorders of blood circulation and vascular permeability]. 223 46

The paper is devoted to the potentialities of aposterior image processing in adult patients with the respiratory distress-syndrome (RDS). Thirty one cases of optical processing of radiograms were analyzed. Pulmonary changes were absent in 10 persons of the control group. The authors described spatial and frequency characteristics of the structural elements of an x-ray picture of RDS (change of interstitial tissue, the state of pulmonary markings, micro-atelectases, edematous and small hemorrhagic parts). The localization of disease is mostly peripheral. The authors paid attention to probable criteria of differential diagnosis between RDS and other conditions, manifesting themselves in clinically acute parenchymatous respiratory insufficiency (lung edema, acute pneumonia, thromboembolism of the pulmonary artery).
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PMID:[Optical image processing in the analysis of the structural elements of the x-ray picture of the adult respiratory distress syndrome]. 227 Jun 63

The causes of respiratory distress in O2 toxicity are not well understood. The purpose of this study was to better define the airway abnormalities caused by breathing 100% O2. Sheep were instrumented for measurements of dynamic compliance (Cdyn), functional residual capacity by body plethysmography (FRC), hemodynamics, and lung lymph flow. Each day Cdyn and FRC were measured before, during, and after the application of 45 min continuous positive airway pressure (CPAP) at 15 cmH2O. The amount of aerosol histamine necessary to reduce Cdyn 35% from baseline (ED35) was measured each day as was the response to aerosol metaproterenol. Cdyn decreased progressively from 0.083 +/- 0.005 (SE) 1/cmH2O at baseline to 0.032 +/- 0.004 l/cm H2O at 96 h of O2. Surprisingly, FRC did not decrease (1,397 +/- 153 ml at baseline vs. 1,523 +/- 139 ml at 96 h). The ED35 to histamine did not vary among days or from air controls. Metaproterenol produced a variable inconsistent increase in Cdyn. We also measured changes in Cdyn during changes in respiratory rate and static pressure-volume relationships in five other sheep. We found a small but significant frequency dependence of compliance and an increase in lung stiffness with O2 toxicity. We conclude that in adult sheep O2 toxicity reduces Cdyn but does not increase airway reactivity. The large reduction in Cdyn in O2 toxicity results from processes other than increased airway reactivity or reduced lung volume, and Cdyn decreases before the development of lung edema.
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PMID:Lung mechanics and airway reactivity in sheep during development of oxygen toxicity. 227 71

A 22 year-old man was brought to our hospital about twenty-three minutes following a high-speed motorbicycle accident in which he had blunt chest trauma. He was in severe respiratory distress with marked dyspnea and restless with extensive subcutaneous emphysema involving anterior chest wall, cervical and bilateral inguinal regions. A chest X-ray revealed bilateral pneumothorax involving mediastinal emphysema and also fracture of right submandibular and clavicula. In spite of orotracheal intubation and insertion of bilateral chest tube, continuous air leak and pneumothorax did not improve. Bronchoscopy revealed the disruption of mucosa of the right main bronchus at the bifurcation. Emergency right thoracotomy was performed and there was the complete disruption of the right main bronchus. Anastomosis of the right main bronchus with circumferential resection was undertaken on May 30, 1987 about two hours after trauma. About three months after reconstruction, bronchoscopic examination revealed stomal stenosis with deformation of tracheobronchial cartilage and granulation. The stenosis showed severe irregularity by deformed cartilage and thickened scar, so widening by Nd-YAG laser vaporization was inadequate in effect. Seven months after first reconstruction, we performed re-reconstructive operation, right upper sleeve lobectomy with partial resection of carcina and right wall of trachea for scar with severe deformation of cartilage. Following the operation, the patient suffered from sepsis with pneumonitis accompanied by lung edema. This complication was treated successfully. We considered that acute pneumonitis was caused by reventilation with increase of perfusion after tracheobronchial reconstruction. Consequently, we thought it important to treat such patients with long term IPPB postoperatively with adequate medication for respiratory system.
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PMID:[Successful re-reconstruction for complete disruption of the right main bronchus by blunt chest trauma]. 232 99


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