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 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

Platelet-activating factor (PAF) has been reported to play a role in the inflammatory reaction, but the mechanism of PAF in humans is still unclear. We examined the presence of PAF in pleural fluids from 23 patients with pleural effusion and in all cases detected PAF associated with eosinophil and/or neutrophil infiltrations. The amounts of PAF in pleural fluids were, respectively, 340, 50 to 170, and 1,250 to 2,130 fmol/ml for a patient with eosinophilic pneumonia, those with pneumothorax (n = 9), and empyema (n = 3). In contrast, patients with tuberculous pleuritis (n = 2), lung edema (n = 3), or malignant disease (n = 5) had no detectable amounts of pleural fluid PAF (less than or equal to 10 fmol/ml). The amount of PAF showed a close correlation with the numbers of eosinophils and neutrophils in the pleural fluids. Furthermore, PAF was mostly detected in the cellular fractions, and the molecular species of PAF from the patients with empyema were almost consistent with those of PAF generated by human blood neutrophils. These results indicate that neutrophils and, presumably, eosinophils were the cellular source of PAF in the pleural fluids in the pathologic state of inflammation.
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PMID:The presence of platelet-activating factor associated with eosinophil and/or neutrophil accumulations in the pleural fluids. 235 88

The pathophysiological mechanism of pulmonary oedema following rapid re-expansion of a collapsed lung is poorly understood. It has been suggested that the period of collapse or subsequent reinflation produces an increase in pulmonary microvascular permeability. To investigate this, the pulmonary accumulation of the plasma protein transferrin was measured by radiolabelling it in vivo with indium-113m. Plasma protein accumulation was calculated after correcting the accumulation of transferrin for changes in intrathoracic blood distribution by simultaneously monitoring technetium-99m labelled red blood cells. Functional images of plasma protein accumulation were constructed for the lung fields on a pixel by pixel basis. Investigations were performed on 14 subjects after drainage of a pleural effusion (n = 9) or evacuation of a pneumothorax (n = 5), and on 11 control subjects. Plasma protein accumulation was greater over the regions of lung re-expansion (-0.1-9.6, mean 2.9 x 10(-3)/min) than over the corresponding region of the contralateral lung (-1.2-0.8, mean 0.01 x 10(-3)/min; p less than 0.001). Patients who had undergone re-expansion procedures also had significantly greater plasma protein accumulation than normal controls. Nine of the 14 patients in the re-expansion group had clearly identifiable areas of increased plasma protein accumulation that corresponded to the part of the lung that had been re-expanded; no regional abnormalities were recorded in the control group. These results suggest that the reinflated lung displays abnormal microvascular permeability.
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PMID:Changes in pulmonary microvascular permeability accompanying re-expansion oedema: evidence from dual isotope scintigraphy. 239 90

Diabetes mellitus produces serious complications in several major organ systems. The pulmonary complications, although uncommon and not well recognized, may be life-threatening. We describe a 20-year-old patient with diabetic ketoacidosis in whom pulmonary zygomycosis developed. This condition was complicated by stenosis of the left upper lobe bronchus despite successful treatment of the zygomycosis. Bronchial obstruction has become a well-recognized complication of pulmonary zygomycosis. In addition to infections caused by Zygomycetes, mycobacteria, viruses, and bacteria, the pulmonary complications described in patients with diabetes include pulmonary edema, disordered breathing during sleep, and reductions in elastic recoil of the lungs, diffusing capacity of the lungs for carbon monoxide, and bronchomotor tone. Other reported complications are respiratory alkalosis, cardiorespiratory arrest, pneumothorax, pneumomediastinum, plugging of the airways with mucus, and aspiration pneumonia attributable to diabetic gastroparesis.
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PMID:Pulmonary complications in diabetes mellitus. 250 1

A 27-year old man was admitted with a right-sided pneumothorax of 2-3 weeks duration. A chest tube was inserted and connected to an underwater seal drainage system without the application of external suction. Three hours later, the patient developed unilateral re-expansion pulmonary oedema and severe hypotension. Active management consisted of ventilating the patient with the addition of PEEP, and the administration of liberal amounts of fluids, including plasma and gelatin solution. The mechanism of re-expansion pulmonary oedema is different from that of cardiogenic pulmonary oedema, and the treatment consequently different. The cause of the hypotension may be due to hypovolaemia, from rapid pooling of fluid within the thorax, pre-existing volume depletion and myocardial depression. One must specially be aware of this possible complication when the pneumothorax is large and of more than 3 days, and it is to be stressed that suction should never initially be used in the treatment of a pneumothorax.
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PMID:Life threatening re-expansion hypotension and pulmonary oedema following treatment of a pneumothorax. 261 7

Clinical studies in an acute medical unit were aimed at the analysis of the onset and clinical appearance of masked acute pneumonia. Such acute pneumonia masks as pulmonary edema, paroxysmal tachycardia, infective toxic shock, acute surgical conditions, hepatitis, pneumothorax considerably complicate the diagnosis of the underlying disease. However, some manifestations typical for acute pneumonia are recognizable. These, in combination with the above misleading symptoms, can be managed properly only provided close comprehensive examination of the patients is carried out.
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PMID:[Masks of acute pneumonia at an emergency care unit]. 262 13

Exercise and physical fitness are becoming increasingly popular in our society. As a result there are more individuals who are at risk for the development of acute respiratory emergencies associated with sports and athletics. EIB is a common feature of asthma and is characterized by a postexercise fall in FEV1 of more than 10 per cent. Although a variety of medications have been used for the prevention of EIB, cromolyn sodium and inhaled adrenergic agonists have been shown to be the most effective. EIA and cholinergic urticaria are two physical allergies in which hypotension can be brought on by exercise. In some individuals, EIA develops only in association with the ingestion of a particular food. Associated with sports and recreational activities in alpine areas is the risk of developing acute high-altitude medical problems. One of the most dramatic and potentially life threatening is high-altitude pulmonary edema. The management of this condition can be problematic, particularly if rapid descent to lower elevations is not possible. Although rare, spontaneous pneumothorax and pulmonary emboli do develop in the otherwise well-conditioned athlete. These entities must be considered when the physician evaluates any athlete in whom acute cough and dyspnea develop.
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PMID:Acute respiratory emergencies in emergency treatment of the injured athlete. 266 79

Unilateral pulmonary edema is uncommon and is usually associated with prolonged surgical procedures or rapid evacuation of a hydro- or pneumothorax. Unilateral pulmonary edema due to left heart failure in the absence of known lung disease is rare. It is therefore not readily recognized and is often confused with other unilateral alveolar or interstitial infiltrates. We describe 2 patients, a 69-year-old man and a 78-year-old woman, who had repeated episodes of unilateral pulmonary edema due to left heart failure. In both cases several other diagnoses were considered, but the cardiac origin of the infiltrates was supported by the rapid clearing of the lung after diuretic therapy. Awareness of this unusual clinical condition is important for the early institution of proper therapy.
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PMID:[Recurrent unilateral pulmonary edema due to left heart failure]. 271 94

The chest radiographs of 71 patients who had chest pain or shortness of breath following the smoking of highly potent "crack" cocaine were retrospectively evaluated. Nine patients had abnormal findings on radiographs as follows: atelectasis or localized parenchymal opacification in four, pneumomediastinum in two, pneumothorax in one, hemopneumothorax in one, and pulmonary edema in one. Radiographic detection of these abnormalities was important in the clinical management of these patients. This spectrum of findings is presented with a discussion of the pathophysiologic mechanisms responsible.
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PMID:Chest pain and dyspnea related to "crack" cocaine smoking: value of chest radiography. 274 26

Cocaine smoking can cause a number of medical complications. Pneumomediastinum and pneumothorax due to barotrauma have been the most common radiographic abnormalities reported in the medical literature. The hospital records of five patients with pulmonary edema who smoked cocaine just before admission were reviewed. Except for cocaine abuse no other possible cause for the pulmonary edema was found. Although chest radiographic abnormalities in these patients are uncommon, these cases are reported to inform the radiologist of this possible complication of cocaine smoking. The presence of pulmonary edema in a young, otherwise healthy patient without predisposing risk factors should alert the radiologist to the possible diagnosis of cocaine abuse.
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PMID:Pulmonary edema in cocaine smokers. 274 27


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