Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 23-year-old male with complete collapse of the right lung due to spontaneous pneumothorax was admitted 11 days after its onset. Paying close attention to the re-expansion pulmonary edema (REPE), water seal drainage was performed. Following couple episodes of persistent severe cough, four hours later, he developed dyspnea and began to expectorate frothy massive sputum. Chest X-ray revealed pulmonary edema of the entire right lung field. Measurement of total proteins and neutrophil elastase in airway exudates showed 5.5 g/dl (ratio to plasma, 0.89) and 7000 micrograms/l, respectively. Because of marked difference of compliance between bilateral lungs, management with right and left-separated mechanical ventilation and PEEP applied only to the right lung was performed. Although transient mediastinal deviation to the left was observed, successful management was achieved by the maneuver. High concentrations of total proteins and neutrophil elastase in edema fluid suggest that increased vascular permeability due to endothelial cell injury via activated neutrophils is mainly responsible for REPE. In the present case, rapid expansion of the collapsed lung accelerated by severe cough seems to be a predisposing factor of REPE. In patient with prolonged pneumothorax, suppression of cough is thought to be important for the prevention of REPE even with water seal drainage.
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PMID:[A case of re-expansion pulmonary edema following water seal drainage for spontaneous pneumothorax--management with right and left-separated mechanical ventilation]. 163 63

The clinical hallmarks of asthma are wheezing and reversibility. Any disease that impairs air flow through obstructed airways may cause wheezing. Patients with true asthma may give a history of allergy and past attacks of dyspnea and wheezing occurring when exposed to allergens, inhaled irritants, upper respiratory infection, cold and humid air, exercise, and emotional stress. When encountering a wheezing dyspneic patient who does not report such a history, it behooves the physician to entertain the possibility that the patient may have a disease other than asthma. Chronic bronchitis, pulmonary emphysema, cardiogenic pulmonary edema pulmonary emboli, aspiration of gastric contents, and upper airway obstruction are the common causes of nonasthmatic wheezing. In almost every instance a wide spectrum of easily obtainable data, particularly historical, are available to alert the physician that the patient's dyspnea and wheezing are not due to asthma. Laboratory data are also readily available to buttress the correct diagnosis.
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PMID:The differential diagnosis of asthma. 176 18

A 35 year old woman with multiple pulmonary arterial stenoses and occlusions was admitted with increasingly severe breathlessness. Balloon angioplasty of a life threatening stenosis in a remaining pulmonary artery branch was attempted on two occasions but without success. When a self-expanding stainless steel stent was inserted at the site of stenosis after a further angioplasty acute localised pulmonary oedema developed as blood flow distal to the lesion increased considerably. This was followed by a slow and dramatic improvement in the patient's condition. She no longer required an urgent transplant and resumed an active life.
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PMID:Successful stenting of a life threatening pulmonary arterial stenosis. 177 15

Forty-two healthy dogs were randomly divided equally into a control group (CG) and a treated group (TG). All were inflicted with severe smoke inhalation injury and pulmonary was demonstrated. The dogs in TG were treated with injection of shenmai zhusheye, ketoprofen, anisodamine, sodium aesculin, hydrocortisone succinate, vitamin C and E, penicillin, amikacin, oxygen inhalation and airway suctioning after injury. The results showed that the increase in extravascular lung water volume, lung edema shadow in x-ray films, elevation of lung vascular resistance, carbonemia, hypoxemia, respiratory alkalosis, metabolic acidosis, dyspnea, dry and moist rales of the lungs, reduction of tidal volume, etc, were markedly improved in TG as compared with that of CG. It indicated that the pulmonary edema and lung dysfunction was markedly ameliorated in TG. The mortality was 19.1% in TG, which was significant lower than that of CG which was 47.6%.
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PMID:[Experimental study on combined treatment in smoke inhalation injury]. 181 46

Three cases are reported of unilateral pulmonary edema, two following rapid reexpansion after prolonged tension pneumothorax, with total collapse of the right lung and one after reexpanded atelectasis following left intrabronchial obstruction. In all cases decrease of blood pressure and tachycardia not responding to intravenous fluid substitution were already present within the first 15 min after chest drainage or after removal of the intrabronchial obstruction. The preexistent dyspnea failed to improve. A cloudy opacity of the reexpanded lung was found immediately after drainage in 2 cases. After immediate application of a continuous positive airway pressure mask no more extensive therapy was necessary in one patient. The two others in whom treatment was begun with more than 1 hour delay required artificial ventilation and adrenergics for 2 and 4 days, respectively.
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PMID:The importance of early detection and therapy of reexpansion pulmonary edema. 188 81

Intravenous fluorescein angiography is a commonly performed and extraordinarily valuable diagnostic procedure. The frequency of adverse reactions after angiography has varied considerably in previous reports. In a prospective study of 2789 angiographic procedures in 2025 patients, the authors found that the percentage of adverse reactions depended strongly on the patient's angiographic history. Overall, adverse reactions followed 4.8% of the angiographic procedures. These reactions included nausea (2.9%), vomiting (1.2%), flushing/itching/hives (0.5%), and other reactions (dyspnea, syncope, excessive sneezing) (0.2%). No cases of anaphylaxis, myocardial infarction, pulmonary edema, or seizures occurred. The percentage of reactions was 1.8% for patients who had had previous angiography without ever having had an adverse reaction. In contrast, the percentage of reactions was 48.6% for patients who had had an adverse reaction to angiography previously.
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PMID:Frequency of adverse systemic reactions after fluorescein angiography. Results of a prospective study. 189 Dec 25

Clinically, lung injury is characterized by one or more of the following: altered gas exchange, dyspnea, decreased static compliance, and nonhydrostatic pulmonary edema. Although many antioxidants have been investigated in in vitro systems and in animal models, only some are at the developmental stage, or safe for clinical trials. Considerable evidence has recently accumulated supporting the hypothesis that leukocyte activation involves release of large quantities of highly reactive oxygen radicals, and hydrogen peroxide is partially responsible for diffuse microvascular and tissue injury in septic patients. Granulocyte depletion in animal models reduces the degree of fall in dynamic lung compliance and the increase in airflow resistance, lymph flow, and hypoxemia secondary to endotoxin administration. We hypothesized that the partial benefit derived from granulocyte depletion was due to the effective removal of a major source of oxygen radicals. Among the list of free radical scavengers, N-acetylcysteine stands out, because of its established usefulness in at least one human disease thought to be secondary to free radical organ damage (acetaminophen or paracetamol overdose). It is an extremely safe agent with a wide toxic-therapeutic window. An increasing number of animal studies indicate efficacy for this agent in the prevention and therapy of lung injury involving toxic oxygen species. We developed a randomized, double-blind protocol for the study of intravenous N-acetylcysteine in patients with established adult respiratory distress syndrome (ADRS). Results of this trial are preliminary. Nevertheless, they indicate that plasma and red cell glutathione levels are decreased in ADRS patients, and that N-acetylcysteine increases plasma cysteine as well as plasma and red cell glutathione. There are also indications that cardiopulmonary physiology is favorably affected by such therapy including improvements in chest radiograph edema scores, pulmonary vascular resistance, static compliance, oxygen delivery, and oxygen consumption.
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PMID:N-acetylcysteine in experimental and clinical acute lung injury. 192 12

In patients with mitral stenosis the need for therapeutic intervention can be assessed by clinical and non-invasive data. Mitral valve replacement is indicated when marked dyspnoea on mild exertion, dyspnoea at rest or pulmonary oedema, haemoptysis, atrial fibrillation, recurrent systemic emboli or right ventricular failure occur in a patient with a mitral valve area of less than 1.5 cm2, as measured by Doppler echocardiography. This treatment will entail life-long anticoagulation in the majority of patients. Closed commissurotomy is no longer considered a valid therapeutic alternative due to its limited success rate but open commissurotomy and balloon valvotomy may be performed in patients with no significant calcification of valve cusps and no major concomitant mitral regurgitation. Preservation of the subvalvular apparatus and left ventricular geometry can be considered the most important advantages of these techniques. More severe chronic symptoms are generally required as indication for mitral valve replacement because of the additional long-term imponderabilities imposed by an implanted artificial device. Therefore, in patients with mitral stenosis different symptoms and clinical findings will eventually lead to different interventions.
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PMID:Treatment of mitral stenosis. 193 35

Ten patients with severe hematologic malignancies (four with acute leukemia, three with multiple myeloma, one with prolymphocytic leukemia, one with malignant lymphoma and one with blastic crisis of chronic myelogenous leukemia) developed respiratory failure during the period between April 1986 and May 1990. Clinically, the patients manifested high-fever, dyspnea refractory to oxygen therapy, diffuse pulmonary rales and severe hypoxemia without evidence of cardiogenic pulmonary edema. Chest roentgenograms displayed diffuse alveolar infiltrates. Respiratory failure occurred as early as 48 hours and as late as 66 days after the administration of intensive anti-neoplastic chemotherapy. At that time leukocyte count was between 100/microliters and 54,900/microliters. Marked leukocytosis was observed in two patients with AML and PLL. Respiratory failure was preceded by sepsis in one patient with AML and by pneumonia in nine patients. DIC was diagnosed in four patients. All patients treated with high dose methyl prednisolone (mPSL) within 12 hours after the onset of respiratory failure. Only one patient required assisted ventilation. High dose mPSL had significant effect on seven of ten patients. But three patients died from progressive respiratory failure, sepsis, pneumonia and multi-organ failure.
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PMID:[Clinical investigation on acute respiratory failure in patients with severe hematologic malignancy]. 194 22

This is the report of a welder who performed argon-shielded electric arc welding in an atmosphere containing trichloroethylene. He developed immediate respiratory symptoms, pulmonary edema 12 hours after exposure, and recurring dyspnea ten days after exposure. These pulmonary reactions might be explained by inhalation of decomposition products of trichloroethylene such as dichloroacetyl chloride and phosgene.
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PMID:Pulmonary reactions caused by welding-induced decomposed trichloroethylene. 198 76


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