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)

Five patients are reported who developed evidence of acute lung damage after proved ingestion of paraquat. In two the lung changes resolved; in one an aspiration pneumonia occurred, which was successfully treated, while two developed fatal pulmonary oedema. These pulmonary complications after paraquat intoxication appear more common than the progressive pulmonary fibrosis previously described. It is suggested that acute pulmonary oedema is a response to large doses, usually of Gramoxone, that subclinical lung changes result from small doses, usually of Weedol, and that pulmonary fibrosis occurs after intermediate doses. Preliminary data on plasma paraquat concentrations suggest that these are of value in prognosis.
Thorax 1979 Apr
PMID:Further clinical observations on the pulmonary effects of paraquat ingestion. 48 82

A case of haemorrhagic pulmonary oedema after successful pulmonary embolectomy is presented. The relevant literature is reviewed. Thirteen cases are analysed as well as the four survivors. The aetiology appears to be ischaemic damage of the capillary bed. This had previously been called incomplete infarction by Castleman. The incidence is low after acute pulmonary embolectomies but appears to be much higher after chronic endarterectomies, especially with severe pulmonary hypertension. Therapy is outlined.
Thorax 1976 Oct
PMID:Haemorrhagic pulmonary oedema: post-pulmonary embolectomy. 99 24

Clinical details are given of two patients who developed ipsilateral pulmonary oedema following re-expansion of their spontaneous pneumothoraces by intercostal drainage of air. The possible mechanisms underlying the oedema are discussed, and prior literature is analysed. Reference is made particularly to its predictability and to precautions recommended to minimize the frequency of this potentially fatal complication in the management of spontaneous pneumothorax.
Thorax 1975 Feb
PMID:Re-expansion pulmonary oedema. 112 29

The case is reported of a 61-year-old man with primary diffuse alveolar septal pulmonary amyloidosis. Amyloid infiltration of the heart and other organs was also observed. The clinical findings and laboratory investigations reveal features characteristic of defective gas transfer with pulmonary oedema due to left ventricular failure from myocardial involvement.
Thorax 1975 Apr
PMID:Primary diffuse alveolar septal amyloidosis. 117 16

Accumulation of radioisotope labelled transferrin in the lungs of guinea pigs was determined with an external detection system. The method is based on the intravascular and extravascular distribution of indium-113m labelled transferrin compared with the intravascular distribution of technetium-99m labelled red blood cells. Guinea pigs were given iloprost, a prostacyclin analogue and potent pulmonary vasodilator, and noradrenaline, a pulmonary vasoconstrictor, in an attempt to increase and decrease respectively the blood volume in the lungs. Neither agent altered transferrin accumulation in the lung by comparison with a saline infusion. Iloprost infused before and after oleic acid infusion reduced macro-molecular leakage when compared with oleic acid alone. These data suggest that the double isotope method can distinguish between hydrostatic and injury induced pulmonary oedema.
Thorax 1990 Sep
PMID:External detection of pulmonary accumulation of indium-113m labelled transferrin in the guinea pig. 169 94

Many possible pulmonary complications of renal disease have been described, but little is known of their physiological importance or the effects on them of different forms of renal replacement therapy. Four groups were recruited, each containing 20 patients. The groups consisted of patients with chronic renal failure before dialysis (group 1); patients receiving continuous ambulatory peritoneal dialysis, never having received a transplant (group 2); patients receiving haemodialysis, never having received a transplant (group 3); and patients after their first successful cadaveric renal transplant (group 4). All were attending the same regional dialysis and transplant unit. None was known to have clinically important lung or chest wall disease. Flow-volume loops were recorded before and after 400 micrograms of salbutamol, and plethysmographic lung volumes and airway conductance and single breath carbon monoxide transfer factor were measured. Only nine of 80 patients had normal lung function. The reductions in spirometric values were minor. Whole lung carbon monoxide transfer factor was reduced in all groups (mean % predicted with 95% confidence intervals: group 1 81.7% (74-89%); group 2 69.7% (62-77%); group 3 87.5% (80-96%); group 4 82.5% (78-87%]. The values were significantly lower in those having continuous ambulatory peritoneal dialysis (group 2). Residual volume was reduced significantly in the group who had undergone renal transplantation (85.7%, 77-94%). There was no correlation between these changes and smoking habit, age, duration or severity of renal failure, duration of treatment, or biochemical derangement. It is concluded that abnormal lung function is common in renal disease. The main change is a reduction in carbon monoxide transfer that persists after transplantation. The likeliest explanation is that subclinical pulmonary oedema progresses to fibrosis before transplantation. The fibrosis may worsen further to cause the reduced residual volume in the recipients of grafts.
Thorax 1991 Jun
PMID:Pulmonary function in chronic renal failure: effects of dialysis and transplantation. 166 77

A 63 year old woman developed progressive shortness of breath, pulmonary hypertension, and respiratory failure and died from pulmonary fibrosis 45 years after thoracic fistulography with Thorotrast. Bouts of acute respiratory failure occurred with features of noncardiogenic pulmonary oedema. Lung tissue obtained by biopsy and at necropsy showed abundant radioactive particles of thorium dioxide in the lungs. The particles were congregated in the walls of blood vessels and in perivascular fibrous zones, consistent with a causal role of Thorotrast in the development of lung fibrosis. It is suggested that the fibrosis was due to the combined effects of alpha radiation on the interstitial perivascular zones and of recurrent pulmonary oedema due to endothelial damage.
Thorax 1990 Nov
PMID:Lung fibrosis induced by Thorotrast. 225 23

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.
Thorax 1990 Jun
PMID:Changes in pulmonary microvascular permeability accompanying re-expansion oedema: evidence from dual isotope scintigraphy. 239 90

A patient with hypertrophic cardiomyopathy developed unilateral right sided pulmonary oedema. Pulmonary angiography showed a proximal severe narrowing of the left pulmonary artery.
Thorax 1990 Aug
PMID:Unilateral pulmonary oedema in a patient with hypertrophic cardiomyopathy and severe narrowing of the left pulmonary artery. 240 32

The occurrence of re-expansion pulmonary oedema immediately after excision of a pleural histiocytoma is described.
Thorax 1989 Aug
PMID:Unilateral pulmonary oedema following the removal of a giant pleural tumour. 255 1


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