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

A 32-year-old man with a long history of grand mal seizures but otherwise good health had recurrent episodes of postictal pulmonary edema when he failed to take anticonvulsant medication regularly. This case illustrates most of the features observed in other reported cases of postictal pulmonary edema. Symptoms include dyspnea and cough with production of various quantities of mucoid fluid that may be copious and frankly hemorrhagic. Blood pressure is normal, and temperature may be normal also but is frequently elevated to 100 or 101 F. No cardiac irregularities are heard on auscultation, and the ECG is often normal, but a wide range of abnormalities may be seen. Considerable arterial hypoxemia may occur, and leukocytosis (11,000 to 14,000 cells per cubic millimeter) is common. Rales and rhonchi are audible, and chest films often show bilateral upper and middle lobe infiltrates. The patient is usually clinically improved within 24 hours and the pulmonary edema completely cleared in three to five days.
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PMID:Case report: Recurrent postictal pulmonary edema. 41 95

Two patients with chemical pneumonitis secondary to inhalation of an epoxy curing material used in the coating of pipes had similar patterns of cough, hemoptysis, and dyspnea associated with diffuse bilateral alveolar infiltrates shortly following the exposure. Pulmonary function studies showed a volume-restrictive defect with severe hypoxemia, but an elevated diffusing capacity. All lung function studies returned toward normal within 1 month of exposure. One patient underwent an open lung biopsy which showed changes consistent with a nonspecific injury to the alveolar wall. This epoxy curing material, trimellitic anhydride, represents another cause of diffuse lung injury that can result in pulmonary edema.
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PMID:Chemical pneumonitis secondary to inhalation of epoxy pipe coating. 88 55

A rebreathing technique was utilized to assess changes in diffusing capacity (DCO), pulmonary capillary blood volume (Vc), pulmonary parenchymal tissue volume (Vt), and cardiac output (Qc), after infusion of 2 liters of 0.9% saline intravenously in 13-25 min in five healthy subjects. Blood hemoglobin concentration decreased an average of 17%. Vc increased strikingly in all five subjects. No significant changes in Vt, or in Vt per unit lung volume were observed. Radiographic evidence of interstitial pulmonary edema was present in four of the five subjects. Radiographic total lung capacity was reduced significantly in four of the five subjects. Significant reductions in forced vital capacity (FVC), forced expiratory volume in 1.0 and 3.0 s, and mean forced expiratory flow during the middle half of the FVC occurred in three of the five subjects. No dyspnea, cough, or physical examination abnormalities of lungs or heart occurred. This noninvasive, ventilation-limited, rebreathing technique appears capable of detecting early changes in pulmonary congestion, at a time when definitive radiographic changes and changes in the physical examination are absent. It appears capable of detecting the increase in Vc associated with hypervolemia in man.
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PMID:Rebreathing pulmonary capillary and tissue volume in normals after saline infusion. 89 78

The experience of a group of nine men employed in a manufacturing plant, who developed attacks of illness during the course of working with polytetrafluoroethylene (PTFE), is reported. The cause was presumed to be the inhalation of fumes from PTFE-contaminated cigarettes. Eight of the nine employees reported chest pain, shortness of breath, and cough. One had documented pulmonary edema. In view of the potential seriousness of the respiratory complications reported by use and by others we raise the question whether "polymerfume fever" is an adequate or appropriate term to apply to the human inhalation reaction to pyrolysis products of PTFE. Under some conditions of PTFE use, special precautions need to be taken, in addition to those usually recommended, to prevent exposure of to this substance.
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PMID:Pulmonary problems associated with the use of polytetrafluoroethylene. 90 44

The effects of oxides of nitrogen inhalation are reported in a 21-year-old gardener exposed to silage gas. Initial nausea, cough and fever remitted, but respiratory failure developed 3 weeks later. Roentgenograms and lung function studies revealed pulmonary edema, volume restriction, and severely impaired gas exchange. Needle biopsy showed a nonspecific interstitial pneumonia. With steroid therapy all functional parameters except diffusing capacity returned to normal. Failure to inquire about non-occupational activities led to delayed diagnosis. A brief review of toxic effects of nitrogen oxides is presented.
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PMID:Silo-Filler's disease. 111 73

This is the ninth recorded case of the rare complication of unilateral pulmonary oedema following drainage of a pneumothorax. The complication should be anticipated if the pneumothorax has been present for longer than 3 days, or if coughing and shock develop after insertion of the drain. Radiological confirmation and prompt treatment are necessary. The literature is reviewed.
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PMID:Unilateral pulmonary oedema after drainage of a spontaneous pneumothorax. Case report and review of the literature. 117 35

A girl with Thalassemia major reacted to a transfusion of packed red blood cells with increasing respiratory distress until death 12 1/2 hours later. Chills and fever were followed by dry cough, dyspnea, and pulmonary edema. The recipient had lymphocytotoxic antibodies specific for donor leukocyte antigens HL-A11 and possibly W14. At autopsy, the lungs showed pulmonary edema with extensive nonspecific acute alveolar injury. Similar cases in the literature are reviewed.
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PMID:Fatal pulmonary hypersensitivity reaction to HL-A incompatible blood transfusion:report of a case and review of the literature. 125 14

Five patients with neurogenic pulmonary edema (NPE) were reported. The edemas were caused by head injuries in four patients and by a craniotomy in the fifth. The onset of NPE was either acute (3 hours after injury) or was slow to develop (4 days later). Clinical symptoms included the sudden onset of coughing, tachypnea, tachycardia, and pink bubbly sputum. Moreover, the patients also suffered cyanosis, confusion, or respiratory failure. The distribution of the resulting pulmonary edema was diffuse in 4 cases and localized within a single lobe of the lung in 1 case. Treatment of the NPE included reducing intracranial pressure (glycerol), diuresis (furosemide and mannitol), narcotics (morphine, phenobarbital), and blocking the peripheral effect of sympathetic reflex activity (hydralazine, sodium nitroprusside). Mechanical ventilation support (CPU-1) in combination with controlled hyperventilation may also be necessary. The inability to correct hypoxemia without toxic levels of oxygen necessitates the use of PEEP (positive end-expiratory pressure, +5-10 cmH2O). Resolution of symptoms was noted 24 to 48 hours after treatment in 4 patients. Early diagnosis and intensive care of the pulmonary edema may have a significant bearing on the recovery of lung functions. Unfortunately, 4 of the patients failed to survive because of central nervous system failure. We therefore want to emphasize that NPE can cause secondary deterioration of neurological functions. In conclusion, when dealing with respiratory distress patients with CNS injuries, the possibility of additional damage from a NPE must be taken into consideration.
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PMID:[Neurogenic pulmonary edema: five cases report]. 129 67

Of 113 methyl isocyanate (MIC)-exposed subjects studied initially at Bhopal, India, 79, 56, 68, and 87 were followed with clinical, lung function, radiographic, and immunologic tests at 3, 6, 12, 18, and 24 months. Though our cohort consisted of subjects at all ages showing a varied severity of initial illness, fewer females and young subjects were seen. Initially all had eye problems, but dominant symptoms were exertional dyspnea, cough, chest pain, sputum, and muscle weakness. A large number showed persistent depression mixed with anxiety, with disturbances of personality parameters. The early radiographic changes were lung edema, overinflation, enlarged heart, pleural scars, and consolidation. The persistent changes seen were interstitial deposits. Lung functions showed mainly restrictive changes with small airway obstruction; there was impairment of oxygen exchange. Oxygen exchange improved at 3-6 months, and spirometry improved at 12 months, only to decline later. The expiratory flow rates pertaining to large and medium airway function improved, but those for small airways remained low. There were changes of alveolitis in bronchoalveolar lavage fluid on fiber optic bronchoscopy, and in 11 cases positive MIC-specific antibodies to IgM, IgG, and IgE were demonstrated. On follow up, only 48% of the subjects were clinically stable, while 50% showed fluctuations. Thirty-two percent of the subjects had lung function fluctuations. Detailed sequential behavior over 2-4 years was predicted for dyspnea, forced vital capacity, maximum expiratory flow rate (0.25-0.75), peak expiratory flow rate, VO2, and depression score. A model for clinical behavior explained a total variance of 52.4% by using the factors of cough, PCO2 and X-ray zones in addition to above five parameters. The behavior of the railway colony group (1640 patients) revealed a similar pattern of illness. When this observed pattern of changes was transferred to the affected Bhopal city sections (with an equitable age-sex distribution), our model results were again validated. Thus the picture of MIC-induced disease seems similar despite the differences for age-sex and initial severity of illness in our cohort and in the population of Bhopal city as predicted by our model.
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PMID:Sequential respiratory, psychologic, and immunologic studies in relation to methyl isocyanate exposure over two years with model development. 139 63

Eighty-two patients were hospitalized following an accidental exposure to chlorine. All patients presented with dyspnoea and cough. The other symptoms included irritation of throat (53.6%), irritation of eyes (42.3%), headache (29.2%), abdominal pain (26.8%), vomiting (24.3%) and giddiness (9.7%). All of them had bronchospasm and 5 (6%) had cyanosis at the onset. An x-ray of the chest revealed patchy infiltrates in 3 (3.85%) and hilar congestion in 2 (2.44%). Pulmonary function tests showed an obstructive pattern in 27.4%, restrictive in 3.25% and mixed in 53.2%. Pulmonary functions were normal in 16.1% of the patients. Bronchoscopy revealed tracheobronchial mucosal congestion in all cases, hemorrhagic spots in 35.7%, erosions and ulcers in 12.5%. All patients were treated with oxygen, aminophylline, hydrocortisone and antibiotics. Haematemesis (n = 1) and pulmonary oedema (n = 2) developed 12 hours after the admission. Two other patients developed pneumonia 48 hours later. All patients recovered satisfactorily. On follow-up 16 patients had no sequelae after one year. Pulmonary functions were normal in 5 patients after 3 years of follow-up.
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PMID:Acute accidental exposure to chlorine fumes--a study of 82 cases. 145 67


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