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

We present the pulmonary findings in 36 autopsies of children affected by the acquired immunodeficiency syndrome (AIDS). Twenty-three patients were male and 13 were female, ranging in age between 3 days and 13 years. Twenty children had human immunodeficiency virus (HIV)-positive parents or parents who were at high risk of exposure (intravenous drug abusers and prostitutes), five had a history of transfusion, and one had a history of renal transplantation and blood transfusion. Clinically, the patients presented with recurrent infections, failure to thrive, hepatosplenomegaly, fever, cough, and/or hemoptysis. Histologically, specific infectious processes were the most common finding (75% of cases), with Pneumocystis carinii pneumonia being the most prevalent type of infection, followed by bacterial pneumonia. Neoplastic conditions and lymphoid interstitial pneumonia were less frequent (approximately 10% of cases). In addition, in approximately 10% of the cases the pulmonary findings were non-specific (ie, pulmonary edema and atelectasis) and probably unrelated to HIV infection. Our findings suggest that specific infectious conditions constitute the most common type of pulmonary pathology in children with AIDS. However, because there is a small percentage of children with nonspecific findings, a transbronchial biopsy is important for proper evaluation before institution of therapy.
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PMID:The spectrum of pathological changes in the lung in children with the acquired immunodeficiency syndrome: an autopsy study of 36 cases. 808 62

The term adult respiratory distress syndrome (ARDS) was first introduced by Ashbaugh and Petty more than two decades ago. Since then, our understanding of this clinicopathologic entity has increased significantly. However, little therapeutic progress has been achieved, and the mortality remains high. ARDS is characterized by diffuse pulmonary microvascular injury resulting in increased permeability and, thus, noncardiogenic pulmonary edema. Ventilation-perfusion lung studies have demonstrated that the predominant pathogenesis of hypoxemia in ARDS is related to intrapulmonary shunts. Common symptoms include dyspnea, tachypnea, dry cough, retrosternal discomfort, and moderate to severe respiratory distress. In most cases the diagnosis of ARDS is that of exclusion. The mainstay of therapy for this syndrome is the management of the underlying disorder causing it. To date, there are no specific pharmacologic interventions of proven value for the treatment of ARDS. Once the potentially treatable sources have been found and their therapy started, the main treatment for ARDS is supportive.
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PMID:Adult respiratory distress syndrome (ARDS): the basics. 816 9

Drug-induced disease of any system or organ can be associated with high morbidity and mortality, and it is tremendously costly to the health care of our country. More than 100 medications are known to affect the lungs adversely, including the airways in the form of cough and asthma, the interstitium with interstitial pneumonitis and noncardiac pulmonary edema, and the pleura with pleural effusions. Patients commonly do not even know what medications they are taking, do not bring them to the physician's office for identification, and usually do not relate over-the-counter medications with any problems they have. They assume that all nonprescription drugs are safe. Patients also believe that if they are taking prescription medications at their discretion, meaning on an as-needed basis, then these medications are also not important. This situation stresses just how imperative it is for the physician to take an accurate drug history in all patients seen with unexplained medical situations. Cardiovascular drugs that most commonly produce a pulmonary abnormality are amiodarone, the angiotensin-converting enzyme inhibitors, and beta-blockers. Pulmonary complications will develop in 6% of patients taking amiodarone and 15% taking angiotensin-converting enzyme inhibitors, with the former associated with interstitial pneumonitis that can be fatal and the latter associated with an irritating cough that is not associated with any pathologic or physiologic sequelae of consequence. The beta-blockers can aggravate obstructive lung disease in any patient taking them. Of the antiinflammatory agents, acetylsalicyclic acid can produce several different airway and parenchymal complications, including aggrevation of asthma in up to 5% of patients with asthma, a noncardiac pulmonary edema when levels exceed 40 mg/dl, and a pseudosepsis syndrome. More than 200 products contain aspirin. Low-dose methotrexate is proving to be a problem because granulomatous interstitial pneumonitis develops in 5% of those patients receiving it. This condition occurs most often in patients receiving the drug for rheumatoid arthritis, but it has been reported in a few patients receiving it for refractory asthma. Chemotherapeutic drug-induced lung disease is almost always associated with fever, thus mimicking opportunistic infection, which is the most common cause of pulmonary complications in the immunocompromised host. However, in 10% to 15% of patients, the pulmonary infiltrate is due to an adverse effect from a chemotherapeutic agent. This complication is frequently fatal even when recognized early.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Drug-induced pulmonary disease. 817 59

A 45-year-old, healthy, well-trained man climbed within 12 hours from 300 m above sea level to a shelter at 2500 m in the Tyrolean Alps. During the following 3 days he undertook ski tours to the surrounding mountains up to 3356 m. On the 4th day he suddenly suffered from headache, coughing and very severe dyspnoea even at rest, accompanied by loss of appetite and the feeling of suffocation. The following day he was rescued by a helicopter and taken to hospital. At the time of admission the patient was severely hypoxaemic (capillary PO2 = 25.7 mmHg), and the chest X-ray revealed signs of bilateral alveolar pulmonary edema localised predominantly in the right lung. High-altitude pulmonary edema (HAPE) was diagnosed because of the typical clinical course. Pulmonary gas exchange normalised within hours, and complete restitution was achieved within 2 days. The chest X-ray was normal on the 4th day after admission. HAPE is a non-cardiogenic pulmonary edema which develops in healthy individuals usually above 3000 m. Among the predisposing factors are rapid ascent, severe physical effort, diminished hypoxic ventilatory response and abnormal fluid balance. The treatment of choice is descent to a lower altitude, administration of oxygen and of nifedipine and expiratory positive airway pressure.
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PMID:[High altitude pulmonary edema at a medium height. A case report]. 817 68

We report on eight cases of amiodarone pulmonary toxicity. Main clinical symptoms are acute/subacute dyspnea or progression in some cases. Amiodarone responsibility is difficult to ascertain. Several arguments can be presented: clinical symptoms with dyspnea and/or fever and/or cough, interstitial or in diffusing capacity for carbon monoxide, abnormal broncho-alveolar lavage cytopreparation smear with increased percentage of lymphocytes and polymorphonuclear leucocytes in typical cases; trans-bronchoscopic lung biopsy failed to provided information on amiodarone toxicity in the two patients where biopsy were performed. Differential diagnosis is an essential step to eliminate other possible causes ie pulmonary micro-organism infections, cancer or pulmonary oedema secondary to heart failure. In one case acute pulmonary toxicity occurred early, after introduction of amiodarone, with a proposed immuno-allergic mechanism. In other cases, chronic amiodarone deposition in the lungs can explain clinico-radiologic features. In six cases improvement was observed after discontinuation of therapy within a 6-months period.
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PMID:[Pneumopathy caused by amiodarone in internal medicine: 8 cases]. 819 Oct 72

We retrospectively evaluated the computed tomography (CT) findings in 20 patients with pulmonary drug toxicity that followed high-dose chemotherapy and autologous bone marrow transplantation (ABMT). Eighty-five patients with Stage II or III breast cancer that involved > or = 10 axillary lymph nodes were enrolled in a treatment protocol that included four cycles of standard-dose therapy (CAF) followed by one cycle of high-dose treatment (CPA/cDDP/BCNU). After chemotherapy, ABMT was performed. Twenty-six patients (31%) developed pulmonary drug toxicity. Serial thoracic CT studies were available in 20 of these 26 patients. All 20 patients exhibited clinical symptoms (i.e., dyspnea, nonproductive cough, and fever) and abnormal pulmonary function following transplantation. Thirteen patients had pathologically proven drug toxicity, and seven patients had clinical features and treatment responses highly suggestive of this diagnosis. Multiple sputum and blood cultures were negative in all patients. CT scans of 13 patients (65%) demonstrated scattered, predominantly peripheral ground-glass or consolidated opacities that occasionally looked nodular or masslike. Two patients (10%) had CT scans suggestive of pulmonary edema and in five patients (25%), the CT examinations revealed no significant abnormalities. Pleural effusions and adenopathy were uncommon. Pulmonary drug toxicity after high-dose chemotherapy and ABMT should be suspected in the appropriate clinical and radiographic setting, and therapy may be initiated on the basis of these observations.
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PMID:Pulmonary drug toxicity following high-dose chemotherapy with autologous bone marrow transplantation: CT findings in 20 cases. 820 80

A 18-year-old woman presented to our hospital complaining of an acute onset of progressive dyspnea with nonproductive cough and high fever. The patient was in her usual good health until the previous day, when she started to develop symptoms 8 hours after taking aspirin for a headache. The chest roentgenogram revealed Kerley's lines (A and B), perivascular cuffing and hilar haze with bilateral pleural effusions. Body temperature was 38 degrees C and PaO2 was 48 torr. Infectious diseases and extrinsic allergic alveolitis were excluded. The lymphocyte stimulating test was negative for aspirin. Acute eosinophilic pneumonia was strongly suggested by bronchoalveolar lavage showing a marked increase in eosinophils without peripheral eosinophilia. By the seventh hospital day all clinical and radiographic signs were improved without steroid therapy. Most cases of acute eosinophilic pneumonia reported previously showed diffuse infiltrative shadows on the chest roentgenogram. The present case had interesting radiographic findings which suggested interstitial pulmonary edema.
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PMID:[A case of acute eosinophilic pneumonia with Kerley's lines (A and B) on chest X-ray]. 823 Aug 83

Two cases of acute eosinophilic pneumonia (AEP) are described and the radiographic findings discussed. Two patients presented acute fever and cough, which led to acute respiratory insufficiency in 3 days. There was no past history of asthma, hypersensitivity or allergy. They became well within 5 to 12 days, with corticosteroid in one and spontaneously in another. Bronchoalveolar lavage showed more than 80% eosinophils. Plain chest roentgenogram showed air space consolidation with peripheral predominance in case 1 and ground-glass shadow with reticular pattern in case 2. On CT, dense and faint air-space opacities were noted in both entire lung fields in case 1 and faint opacities with thickened interlobular septa in case 2. Bilateral pleural effusion and mild mediastinal lymphadenopathy were noted in both. The increased lung densities showed non-segmental distribution. However, these findings are non-specific and such opacities are seen in other diffuse lung diseases such as hypersensitive pneumonitis, BOOP and pulmonary edema. Pleural effusion (44% of reported cases including ours) and mediastinal lymphadenopathy were frequently seen, and pleural effusion with or without mediastinal lymphadenopathy could represent specific findings for this disease. The authors stress that in young patients with acute respiratory insufficiency with pleural effusion and/or mediastinal lymphadenopathy on the plain chest radiograph or on CT, the possibility of AEP should be considered in the differential diagnosis.
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PMID:[Acute eosinophilic pneumonia: a report of two cases]. 837 40

Six men were accidentally exposed to NO2 when they were changing a propeller using a gas burner in the poorly ventilated hold of a ship. All of them were admitted to hospital with shortness of breath and cough. Chest X-ray on admission revealed diffuse, patchy and infiltrative shadows, leading to the diagnosis of pulmonary edema in all five patients. Steroid therapy was effective and followed by a quick recovery in all patients. None developed third phase manifestations characterized pathologically by bronchiolitis obliterans.
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PMID:[Five cases of acute pulmonary failure associated with nitrogen dioxide inhalation]. 851 27

High-altitude pulmonary edema (HAPE) occurs in unacclimatized individuals who are rapidly exposed to altitudes in excess of 2450 m. It is commonly seen in climbers and skiers who ascend to high altitude without previous acclimatization. Initial symptoms of dyspnea, cough, weakness, and chest tightness appear, usually within 1-3 days after arrival. Common physical signs are tachypnea, tachycardia, rales, and cyanosis. Descent to a lower altitude, nifedipine, and oxygen administration result in rapid clinical improvement. Physiologic studies during the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pulmonary artery pressure, severe arterial unsaturation, and usually a low cardiac output. Pulmonary arteriolar (precapillary) resistance is elevated. A working hypothesis of the etiology of HAPE suggests that hypoxic pulmonary vasoconstriction is extensive but not uniform. The result is overperfusion of the remaining patent vessels with transmission of the high pulmonary artery pressure to capillaries. Dilatation of the capillaries and high flow results in capillary injury, with leakage of protein and red cells into the alveoli and airways. HAPE represents one of the few varieties of pulmonary edema where left ventricular filling pressure is normal.
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PMID:High-altitude pulmonary edema: current concepts. 871 81


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