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

This report describes a 28-yr-old patient with pulmonary veno-occlusive disease (PVOD). She presented with pulmonary hypertension, hypoxemia, and interstitial pneumonitis. We report the discordance between the response of her hypoxemia and interstitial pneumonitis, which resolved with corticosteroid therapy, and her progressive pulmonary hypertension, which caused fatal right heart failure. This report emphasizes that the radiographic interstitial shadowing of PVOD may be caused by either (1) an inflammatory interstitial pneumonitis (which may be responsive to anti-inflammatory therapy) or (2) interstitial pulmonary edema, or both.
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PMID:Pulmonary veno-occlusive disease. Fatal progression of pulmonary hypertension despite steroid-induced remission of interstitial pneumonitis. 202 25

A patient presenting with the rare association of congenital unilateral pulmonary venous atresia in one lung and pulmonary veno-occlusive disease in the other is described. The patient first presented at the age of 3 1/2 years with anemia, hemoptysis, and pulmonary hypertension. After cardiac catheterization and angiocardiography, a diagnosis of atresia of the left pulmonary veins was made for which left pneumonectomy was done. Four years later the patient presented with right-sided congestive failure and radiologic evidence of right-sided pulmonary edema from which death resulted. At autopsy, the right lung showed changes of pulmonary veno-occlusive disease, while the major veins were not involved.
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PMID:Congenital unilateral pulmonary venous atresia with pulmonary veno-occlusive disease in contralateral lung: an unusual association. 382 68

Continuous-infusion prostacyclin improves symptom scores and decreases mortality in patients with primary pulmonary hypertension, but use of prostacyclin in patients with pulmonary veno-occlusive disease may precipitate pulmonary edema. A patient with pulmonary veno-occlusive disease received a graduated intravenous infusion of prostacyclin and pulmonary capillary pressures were calculated during prostacyclin dose ranging. Calculated capillary pressure increased with low-dose prostacyclin (< or = 6 ng/kg/min) but decreased with higher doses. These data suggest that the post-capillary pulmonary venules in our patient had reversible vasomotor tone, but required a higher dose of prostacyclin to vasodilate than did the precapillary arterioles.
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PMID:Effect of prostacyclin on microvascular pressures in a patient with pulmonary veno-occlusive disease. 749 99

Respiratory failure is the main cause of death in patients undergoing bone marrow transplantation (BMT). In this paper, clinical and research aspects as well as diagnostic, prophylactic and therapeutic strategies concerning the various forms of pulmonary and bronchial complications, which may evolve after BMT, are discussed. Both cytomegalovirus (CMV)-induced interstitial pneumonia (PM) and the idiopathic pneumonia syndrome rarely occur in the cytopenic phase post-BMT. Haematological reconstitution with donor type cells seems to be a prerequisite to the development of these complications, suggesting a key role of immunological reactions. While CMV pneumonia can be effectively treated or prevented by ganciclovir, the idiopathic syndrome is usually fatal. Due to improved prophylaxis and therapy, lethal interstitial PM due to Pneumocystis carinii, herpes simplex, varizella zoster or Toxoplasma gondii as well as lethal PM caused by bacteria or Candida species are comparatively rare events. Aspergillus species, on the other hand, have emerged as frequent causative pathogens in lethal PM during the past years. Prolonged granulocytopenia and prolonged medication with corticosteroids are major risk factors of pulmonary aspergillosis, which is usually fatal; effective prophylaxis may be achieved by sterile air supply during the hospital stay and by inhalation of amphotericin B thereafter. Pulmonary haemorrhage, as diagnosed by bronchoalveolar lavage (BAL), may develop due to the toxicity of the conditioning regimen, or may be secondary to infectious PM of various kind. Congestive heart failure or the application of cytokines might give rise to the development of pulmonary oedema. Patients with hepatic veno-occlusive disease have a high risk of subsequent pulmonary complications, possibly on the basis of toxic lung injury. Venous thromboembolism or air embolism may occur; they are usually venous catheter-associated. Pleural effusions may develop secondary to infection, congestive heart failure, veno-occlusive disease, pulmonary embolism or malignancy. Patients with bronchiolitis obliterans, which leads to progressive respiratory failure, present with an obstructive pattern in lung function tests and hyperinflated lungs on chest radiographs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The lung as a critical organ in marrow transplantation. 772 20

There are frequently respiratory complications with cancer particularly in primary lung carcinoma. Among these are bronchopulmonary infections with or without endobronchial obstruction, carcinomatous lymphangitis, thromboembolic disease and haemorrhagic disease as well. Radiotherapy and chemotherapy may induce various respiratory complications which diagnosis can be of varying shades of difficulty. The classical post radiation pneumonitis occurring exclusively in the field of radiation hardly poses any problem unless it could be masking a recurrence. Certain clinical manifestations address very difficult problems of differential diagnosis by their lack of specificity and by their often unforeseeable character (except for bleomycin fibrosis which is perfectly dose dependent). Moreover patients often have multiple treatments and the identification of the single responsible agent becomes very difficult. We will not discuss here the infectious or secondary haemorrhagic complications of radiotherapy or chemotherapy but rather the anaphylactic manifestations, diffuse interstitial pneumonia with lymphocytic alveolitis or fibrosis, eosinophilic pneumonia, non-cardiogenic pulmonary oedema, bronchiolitis obliterans with organising pneumonia and the rare pulmonary vascular disorders such as pulmonary veno-occlusive disease.
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PMID:[Radiation- and chemically-induced respiratory manifestations]. 948 Apr 78

Continuous intravenous epoprostenol (prostacyclin) produces hemodynamic and symptomatic responses and improves survival in patients with severe primary pulmonary hypertension refractory to conventional medical therapy. However, it has been recently shown that short-term infusion of epoprostenol can produce pulmonary edema in pulmonary veno-occlusive disease, presumably because of increased pulmonary perfusion in the presence of downstream vascular obstruction. We describe two additional cases of pulmonary edema complicating continuous intravenous epoprostenol in patients displaying severe pulmonary hypertension and pulmonary capillary hemangiomatosis, a rare condition characterized by the proliferation of thin-walled microvessels in the alveolar walls. This report indicates that epoprostenol therapy should not be used in patients with severe pulmonary hypertension secondary to pulmonary capillary hemangiomatosis.
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PMID:Pulmonary edema complicating continuous intravenous prostacyclin in pulmonary capillary hemangiomatosis. 960 54

Pulmonary edema may be classified as increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema. Pulmonary edema has variable manifestations. Postobstructive pulmonary edema typically manifests radiologically as septal lines, peribronchial cuffing, and, in more severe cases, central alveolar edema. Pulmonary edema with chronic pulmonary embolism manifests as sharply demarcated areas of increased ground-glass attenuation. Pulmonary edema with veno-occlusive disease manifests as large pulmonary arteries, diffuse interstitial edema with numerous Kerley lines, peribronchial cuffing, and a dilated right ventricle. Stage 1 near drowning pulmonary edema manifests as Kerley lines, peribronchial cuffing, and patchy, perihilar alveolar areas of airspace consolidation; stage 2 and 3 lesions are radiologically nonspecific. Pulmonary edema following administration of cytokines demonstrates bilateral, symmetric interstitial edema with thickened septal lines. High-altitude pulmonary edema usually manifests as central interstitial edema associated with peribronchial cuffing, ill-defined vessels, and patchy airspace consolidation. Neurogenic pulmonary edema manifests as bilateral, rather homogeneous airspace consolidations that predominate at the apices in about 50% of cases. Reperfusion pulmonary edema usually demonstrates heterogeneous airspace consolidations that predominate in the areas distal to the recanalized vessels. Postreduction pulmonary edema manifests as mild airspace consolidation involving the ipsilateral lung, whereas pulmonary edema due to air embolism initially demonstrates interstitial edema followed by bilateral, peripheral alveolar areas of increased opacity that predominate at the lung bases. Familiarity with the spectrum of radiologic findings in pulmonary edema from various causes will often help narrow the differential diagnosis.
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PMID:Clinical and radiologic features of pulmonary edema. 1055 72

Bone marrow transplantation (BMT) is a successful and recognised treatment option for patients with a number of haematological and non-haematological malignant and non-malignant conditions. Pulmonary complications both infectious and non-infectious are common after BMT. Multiple factors are thought to contribute to pulmonary complications, including the type and duration of immunological defects produced by the underlying disease and treatment, the development of graft-versus-host disease (GVHD), and the conditioning regimens employed. These complications are classified as early or late, depending on whether they occur before or after 100 days from transplantation. Early non-infectious pulmonary complications typically include pulmonary oedema, upper airway complications, diffuse alveolar haemorrhage, cytolytic thrombi, and pleural effusion. Bronchiolitis obliterans, veno-occlusive disease, and secondary malignancies occur late after BMT. Idiopathic pneumonia syndrome, GVHD, and radiation induced lung injury can occur in early or late period after BMT.
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PMID:Non-infectious pulmonary complications after bone marrow transplantation. 1215 65

Pulmonary capillary hemangiomatosis (PCH) is a rare cause of primary pulmonary hypertension characterized by thin-walled microvessels infiltrating the peribronchial and perivascular interstitium, the lung parenchyma, and the pleura. These proliferating microvessels are prone to bleeding, resulting in accumulation of hemosiderin-laden macrophages in alveolar spaces. Here we report 2 cases of PCH with pulmonary hypertension, 1 of them associated with mechanical intravascular hemolysis, a feature previously reported in other hemangiomatous diseases, but not in PCH. Case 2 was diagnosed by pulmonary biopsy; to our knowledge the patient is the second adult to be treated with interferon alpha-2a. Review of the literature identified 35 patients with PCH and pulmonary hypertension. The prognosis is poor and median survival was 3 years from the first clinical manifestation. Dyspnea and right heart failure are the most common findings of the disease. Hemoptysis, pleural effusion, acropachy, and signs of pulmonary capillary hypertension are less common. Chest X-ray or computed tomography scan usually shows evidence of interstitial infiltrates, pulmonary nodules, or pleural effusion. Hemodynamic features include normal wedge pressures. Radiologic and hemodynamic findings are undifferentiated from those of pulmonary veno-occlusive disease but differ from other causes of primary pulmonary hypertension. Epoprostenol therapy, considered the treatment of choice in patients with primary pulmonary hypertension, may produce pulmonary edema and is contraindicated in patients with PCH. Regression of lesions was reported in 1 patient treated with interferon therapy and 2 other patients stabilized, including our second patient. PCH was treated successfully by lung transplantation in 5 cases. Early recognition of PCH in patients with suspected primary pulmonary hypertension is possible based on clinical and radiologic characteristics. Diagnosis by pulmonary biopsy is essential for allowing appropriate treatment.
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PMID:Pulmonary capillary hemangiomatosis associated with primary pulmonary hypertension: report of 2 new cases and review of 35 cases from the literature. 1244 98

The case of a patient with pulmonary veno-occlusive disease associated with systemic sclerosis is reported. The patient presented with progressive dyspnoea. Echocardiography and cardiac catheterization study demonstrated right-sided heart failure. The CXR suggested pulmonary hypertension and interstitial pulmonary oedema. We suspected pulmonary veno-occlusive disease based on radiological and haemodynamic findings. Treatment with prednisolone resulted in a reduction in pulmonary arterial pressure and CXR findings improved 2 months later, but no further effect was observed. The patient died 7 months later and at autopsy the lungs showed prominent thickening of the interlobular septa and small branches of pulmonary veins showed intimal thickening.
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PMID:A case of pulmonary veno-occlusive disease associated with systemic sclerosis. 1452 85


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