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

We have discussed several diseases that diffusely affect the pulmonary parenchyma. The diagnostic problem is to separate cardiac pulmonary edema from noncardiac pulmonary edema, diffuse interstitial fibrosis, and lymphangitic spread of carcinoma. Frequently, this may not be possible by radiographic means alone, and additional historic and physiologic information must be obtained. It is also important to know that cardiac pulmonary edema may present in a focal or regional distribution in patients with chronic obstructive pulmonary disease. Several additional radiographic tests may be used to evaluate abnormal pulmonary parenchymal densities seen on the portable chest radiograph, when the differential diagnosis includes increased extravascular water, pneumonia, and pulmonary fibrosis. The easiest of these tests to perform is the gravitational shift test.
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PMID:The ICU chest film: cardiac versus pulmonary disease. 654 46

Eleven Friesian steers were given 3, methyl indole (3MI) orally at dose rates ranging from 0.1 to 0.3 g/kg. Three of these (group B) received a single oral dose of 0.2 g/kg and subsequently developed respiratory distress. Their plasma 3MI concentrations six hours after dosing were between 2.25 and 7.23 micrograms/ml. The steer with the highest six-hour plasma value died at this stage and the dominant pathological feature was severe pulmonary oedema. The other two steers survived until they were slaughtered 96 hours after dosing; the major pathological findings in them were interstitial emphysema, hyaline membranes and alveolar epithelial hyperplasia. The other eight steers (group C) each received weekly oral doses of 0.1 g 3MI/kg for 10 weeks. One animal died after developing severe respiratory distress following its third dose. Thereafter, the others developed two separate patterns of response. Three steers (subgroup C1) became progressively more tolerant to oral 3MI, even in the face of dose rates increased to 0.2 and 0.3 g/kg during the 11th to 14th weeks of the study and also in the presence of relatively high plasma 3MI concentrations after dosing. One animal was slaughtered after its 10th dose and two after their 14th dose of 3MI; post mortem examinations revealed that their lungs were macro- and microscopically normal. The other steers (subgroup C2) all continued to react after each weekly oral dose of 3MI and their post-dosing plasma 3MI concentrations consistently remained relatively low. Latterly, each of the three steers which survived to the 14th week also exhibited persistent tachypnoea and marked hyperpnoea between dosings. On post mortem examination, in addition to the signs generally associated with acute 3MI toxicity (see above), each of the subgroup C2 steers were found to have diffuse pulmonary fibrosis and an alveolitis. While certain cattle appear to become tolerant to the effects of repeated doses of 3MI, the results of this study clearly demonstrated that, in others, such treatment eventually gives rise to diffuse pulmonary fibrosis and alveolitis.
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PMID:Experimental production of diffuse pulmonary fibrosis and alveolitis in cattle: the effects of repeated dosage with 3, methyl indole. 683 86

Non-cardiac pulmonary edema in a woman with long-lasting diabetes resulted in a distressing pulmonary fibrosis. It is suggested that pulmonary edema of non-cardiac origin might be more common in diabetes because of increased capillary permeability in this disease. Early recognition is important, and steroid treatment should be instituted to prevent development of pulmonary fibrosis.
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PMID:Adult respiratory distress syndrome and diabetes. 708 Aug 68

A 47-year-old man with a history of industrial exposure and interstitial lung disease was admitted for acute pulmonary decompensation. Clinical course was characterized by severe dyspnea at rest, fever, hypoxemia, and elevated pulmonary arterial pressures. At autopsy, pulmonary problems were explained by a selective veno-occlusive process. Associated with pulmonary phlebitis was cerebral vasculitis and lymph node enlargement with erythrophagocytosis suggesting underlying viral infection. Pulmonary veno-occlusive disease should be considered in cases of pulmonary fibrosis, pulmonary hypertension with cor pulmonale, and pulmonary edema and congestion with normal left atrial pressures.
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PMID:Pulmonary veno-occlusive disease. Morphological changes suggesting a viral cause. 725 18

Plastics can induce three main groups of respiratory accidents.--Acute and subacute intoxications related to the inhalation of volatil substances from decomposing plastics (mostly during burning and pyrolysis) or on the contrary during synthesis. They are accidental chemical broncho-pneumopathies (acute tracheo-bronchitis and pulmonary edema).--Chronic broncho-pneumopathies following repeated inhalation of dusts or suspension of plastics: pneumoconioses and thesaurismoses leading to pulmonary fibrosis.--Broncho-pneumopathies related to the irritant and sensitizing action of some components of plastics: professional asthma and sensitization pneumopathies. Diagnosis of such diseases therefore imposes a careful study of working conditions. Proof rests on two arguments:--curing by risk eviction;--analysis of the products in order to reveal their toxicity.
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PMID:["Plastic lung". Broncho-pulmonary pathology related to plastics (author's transl)]. 746 86

To examine intensive care unit (ICU) admission rates and diagnoses of patients with HIV infection, and to determine the outcomes of different critical illnesses, we analyzed data derived from the 63 patients who were admitted to an ICU from among the 1,130 adults with HIV infection who did not have AIDS at the time of enrollment in a multicenter prospective study. Patients were admitted and treated according to the judgment of their physicians. During 4,298 patient-years of follow-up for the entire cohort, there were 1,320 hospital admissions, of which 68 (5%) included admission to an ICU. Twenty-five (40%) of the patients admitted to the ICU died during that admission. Twenty-four patients (38%) were admitted with a principal diagnosis of lung disease; 11 had Pneumocystis carinii pneumonia (PCP), one of whom was coinfected with Aspergillus fumigatus and Legionella pneumophilia, and six of them (55%) died. Four had bacterial pneumonia, two had pulmonary edema caused by renal failure, and one each had pulmonary tuberculosis, pulmonary Kaposi's sarcoma, pneumothorax, adult respiratory distress syndrome, severe pulmonary fibrosis, cytomegalovirus pneumonitis, and metastatic adenocarcinoma to the lungs. Eleven of these 14 patients (79%) died. Thirty-nine patients had 44 admissions for nonpulmonary diagnoses, including gastrointestinal disorders (14 admissions), cardiovascular disorders (nine), sepsis syndrome (six), neurologic disorders (four), monitoring and ICU nursing care during or after a procedure (four), metabolic disorders (three), trauma (two), drug overdose (one), and unknown reasons (one). Nine (23%) of these patients died. Twenty-eight patients underwent mechanical ventilation, and 16 (57%) died. Seven (25%) had PCP (five died), seven had other primary pulmonary diseases (six died), and 14 were placed on mechanical ventilation for nonpulmonary disorders (five died). Survival did not correlate with CD4 count determined within 6 mo of admission to the ICU. In conclusion, the range of indications for critical care in patients with HIV infection is diverse. PCP accounted for only 16% of the ICU admissions, and mechanical ventilation for PCP and other pulmonary disorders was associated with a high mortality rate. In contrast, mechanical ventilation for nonpulmonary disorders, and admission to the ICU for nonpulmonary diagnoses was associated with a more favorable outcome.
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PMID:Intensive care of patients with HIV infection: utilization, critical illnesses, and outcomes. Pulmonary Complications of HIV Infection Study Group. 900 Dec 91

Keratinocyte growth factor (KGF), a potent growth factor for type II pneumocytes and Clara cells, has been shown to prevent the end-stage pulmonary fibrosis and mortality in a rat model of bleomycin-induced lung injury. In this study, protective effects of KGF were explored during the earlier course of bleomycin-induced lung injury by studying protein exudation in alveolar edema fluids, pulmonary expression of transforming growth factor-beta (TGF beta) and platelet-derived growth factor-BB (PDGF-BB), and changes in type II pneumocytes and Clara cells after i.t. (intratracheal) bleomycin injection following KGF- or saline-pretreatment in rats. Total protein in bronchoalveolar lavage (BAL) fluids after bleomycin injury from KGF-pretreated rats was significantly lower than the levels in saline-pretreated rats. TGF beta protein in BAL fluids which peaked at day 3 after i.t. bleomycin in saline-pretreated lungs was not significantly increased at any time points in KGF-pretreated rats. PDGF-BB protein in whole lung tissues of KGF-pretreated rats also remained near normal throughout the course after i.t. bleomycin, in contrast to the significant increase in saline-pretreated rats. Numbers of type II pneumocytes and Clara cells in KGF-pretreated lungs after a high dose of bleomycin were close to the normal in intact lungs. At the same dose of bleomycin injury, type II pneumocytes in saline-pretreated lungs were markedly decreased, while the number of Clara cells in these rats was relatively preserved as the pre-injury level. In conclusion, KGF prevents bleomycin-induced end-stage pulmonary injury and mortality probably at least partly by decreasing protein-rich pulmonary edema, protein expression of fibrogenic cytokines TGF beta and PDGF-BB, and type II cell loss during the course of lung injury.
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PMID:Keratinocyte growth factor decreases pulmonary edema, transforming growth factor-beta and platelet-derived growth factor-BB expression, and alveolar type II cell loss in bleomycin-induced lung injury. 960 18

The development of pulmonary disease as a result of cancer therapy is an increasingly recognized clinical problem. Chemotherapeutic drugs can induce an acute pneumonitis, pulmonary edema, and pulmonary fibrosis, as well as a variety of other pulmonary diseases in cancer patients.
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PMID:Pulmonary complications of cancer therapy. 1039 Jun 56

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92

This study examined the effect of the prone position on mechanically ventilated patients with hydrostatic pulmonary edema (HPE). Eight patients with acute HPE and mechanically ventilated in the prone position (Group 1) were studied. Six patients with acute HPE and mechanically ventilated in the supine position (Group 2), 20 patients with ARDS (Group 3), and 5 patients with pulmonary fibrosis (PF) (Group 4) served as control patients. Patients with HPE, who after being mechanically ventilated for at least 6 h needed an FI(O(2)) >/= 0.6 to achieve an Sa(O(2)) of approximately 90%, and did not respond to recruitment maneuvers, were turned to the prone position. Parameters of oxygenation, lung mechanics, and hemodynamics were determined in both the supine and prone positions. All patients with HPE exhibited improvement of oxygenation when they were placed in the prone position. The Pa(O(2))/FI(O(2)) ratio increased from 72 +/- 16 in the supine position to 208 +/- 61 after 6 h in the prone position (p < 0.001); the rise in Pa(O(2)) was persistent, without detrimental effect on hemodynamics. Fifteen of 20 patients with ARDS (75%) improved oxygenation when in the prone position. The Pa(O(2))/FI(O(2)) ratio increased from 83 +/- 14 in the supine position to 189 +/- 34 after 6 h in the prone position (p < 0.001). In contrast, 5 of 20 patients with ARDS (25%) and none of the patients with PF responded favorably to prone positioning. Patients with HPE and early ARDS responded better to prone positioning than did patients with late ARDS and PF. Patients with HPE and ventilated in the supine position had a lower Pa(O(2))/FI(O(2)) ratio and the duration of mechanical ventilation was longer compared with that of patients in the prone position. Our results show that the prone position may be a useful maneuver in treating patients with severe hypoxemia due to pulmonary edema. The presence of pulmonary edema, as in early ARDS and HPE predicts a beneficial effect of the prone position on gas exchange. In contrast, the presence of fibrosis, as in late ARDS and pulmonary fibrosis, predisposes to nonresponsiveness to prone positioning.
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PMID:Effect of the prone position on patients with hydrostatic pulmonary edema compared with patients with acute respiratory distress syndrome and pulmonary fibrosis. 1067 72


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