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)

Methotrexate, an antifolate cytotoxic drug, is used in anticancer chemotherapy as well as an immuno suppressive in rheumatoid arthritis. It is responsible for numerous secondary effects, amongst which is a characteristic acute pneumonia known since 1969. This pneumonitis has been described in detail, up to the present time in 78 cases gathered in this review. The prevalence of this complication is estimated at around 7%. This pneumonia may occur whatever the age, indication for which methotrexate is prescribed, the route of administration of the product (including the intra-thecal route) and the dose. It includes dyspnoea, fever, (sometimes quite marked) and frequently an acute reversible respiratory failure. Radiologically the opacities are usually diffuse interstitial and symmetrical with a basal predominance with sometimes some confluence and occasionally a pleural reaction. In a small number of cases a transient mediastinal adenopathy has been described. Respiratory function tests show a rapidly developing restrictive syndrome accompanied by hypoxia and hypocapnia. Broncho-alveolar lavage is characterised by hypercellularity with a frank and apparently transitory lymphocytosis. Histologically the most frequent lesion sighted is an extensive acute granulomatous reaction with or without oedema. Most often the outcome is favourable (75% of cases). However 6 deaths due to respiratory failure have been reported. Even though there has not been any formal test, steroid therapy in high dosage seems to accelerate recovery. Progress to an irreversible pulmonary fibrosis is possible but rare. The mechanism of this drug related acute pneumonia is not known but would seem to resemble that of other granulomatosis. Besides this rapidly progressive pneumonitis, methotrexate is responsible for a very small number of cases of severe pulmonary oedema and of acute painful pleurisies.
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PMID:[Pneumopathy caused by methotrexate]. 225 35

Simple cardiopulmonary functions were studied serially in 26 mountaineers between sea level and an altitude of 25,200 ft. Up to 12,000 ft there was no altitude sickness, though there were complaints of leech bite (26.9%) and blisters (3.8%). One member died of exhaustion, two developed pulmonary oedema, one "flu" (at 15,600 ft) and one pleural rub (at 21,000 ft). Up to 16,000 ft altitude, 4 to 7.7% developed diarrhoea or epistaxis only, but at higher levels 25 to 50% subjects developed several symptoms, besides excessive dyspnea. These included diarrhoea (35-60%), vomiting (30%) abdominal pain (35-60%), rectal bleeding (15%), chest pain (10-40%), dry cough (40-60%), giddiness (30%) and poor memory (7.7%). A small rise in blood pressure was seen (for systolic at lower and diastolic at greater altitudes). After 18,200 ft the steady increase seen in VE slowed and the rise in heart rate and respiratory rate (f) became steeper. After a small rise at 7,800 ft, FVC and FEV1 showed a gradual decline at higher altitudes. After a large initial increase in PEFR up to 12,000 ft, a gradual decline was seen. The mean weight loss during the expedition was 8 +/- 2.7 kg. These changes seem to be due to an incomplete acclimatisation, which future mountaineering teams should take into consideration to avoid health problems and improve performance.
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PMID:Cardiopulmonary functional changes in acute acclimatisation to high altitude in mountaineers. 225 31

Twenty patients (ten with mitral and/or aortic valve disease and ten with ischemic heart disease, all in the New York Heart Association class IV, aged between 18 and 74 yr, with cardiogenic pulmonary edema unresponsive to drug treatment) were treated with polysulphone membrane ultrafiltration (UF) in a veno-venous circuit. All patients had dyspnea, pulmonary rales, hypoxemia, tachycardia, hypotension, overhydration, radiologic evidence of engorged pulmonary vasculature, and Kerley-B lines. Systemic and pulmonary arterial pressures, cardiac output (by thermodilution), and intrapulmonary shunt fraction (Qsp/Qt) were determined and chest x-ray was obtained at the beginning and the end of UF. Average duration of the treatment was 150 +/- 28 min; UF volume averaged 3000 +/- 170 ml. UF reduced the Qsp/Qt by 58% from control condition, and did not significantly affect hemodynamic variables. Chest x-rays documented clearing of alveolar edema and venous congestion. These changes were associated with unequivocal clinical improvement and no mechanical ventilation was necessary to improve gas exchange. Short-term fluid subtraction did not result in undesired circulatory alternations. Because the ultrafiltrate composition is similar to plasmatic fluid, no modification in the plasma osmolarity was detected. In conclusion, UF may be considered an effective tool for the treatment of acute pulmonary edema refractory to drug therapy, as an alternative to mechanical ventilation, and as a remedy for excessive extravascular lung water.
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PMID:Isolated ultrafiltration in cardiogenic pulmonary edema. 229 64

Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.
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PMID:Unilateral pulmonary edema following acute subglottic edema. 231 May 80

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

The beneficial effects of physiologic dual-chamber (DDD) pacing in the treatment of end-stage idiopathic dilated cardiomyopathy were evaluated in 16 patients in whom conventional drug therapy had failed. Candidates for cardiac transplantation as well as patients not accepted for transplantation participated. During DDD pacing at an atrioventricular delay of 100 ms, left ventricular ejection fraction increased from 16.0 +/- 8.4 to 25.6 +/- 8.6% (p less than 0.001) accompanied by a striking improvement in clinical symptoms, such as severe dyspnea at rest and pulmonary edema. The New York Heart Association class decreased from 3.6 +/- 0.4 to 2.1 +/- 0.5 (p less than 0.001). The decrease in cardiothoracic ratio from 0.60 +/- 0.06 to 0.56 +/- 0.05 (p less than 0.001) coincided with a decrease in left atrial and right ventricular echocardiographic dimensions, indicating a decrease in preload. Systolic blood pressure increased from 108 +/- 29 to 126 +/- 21 mm Hg (p less than 0.01) and diastolic blood pressure from 67 +/- 15 to 80 +/- 11 mm Hg (p less than 0.01). Normalization of heart rate was achieved. No major complications developed as a consequence of DDD pacing. All patients could be discharged from the hospital within 3 weeks after pacemaker implantation and return to a relatively normal life. Within 1 year after onset of DDD pacing only 4 of the patients died (from either sudden death or stroke). DDD pacing could represent an alternative approach to the management of chronic heart failure due to dilated cardiomyopathy, especially for heart transplant candidates and patients who are not accepted for cardiac transplantation, but no longer respond to drug therapy.
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PMID:Usefulness of physiologic dual-chamber pacing in drug-resistant idiopathic dilated cardiomyopathy. 237 55

Out of 160 prospectively followed patients with aortic regurgitation, the clinical courses of 53 patients with pure, severe, and chronic aortic regurgitation and without coronary artery disease who were selected for surgery on the basis of predefined criteria is discussed. Surgical criteria were either unequivocal symptoms or documentation of impaired left ventricular dysfunction (defined as angiographic ejection fraction of less than 50% plus and end-systolic volume index greater than 60 ml/m2). According to preoperative status, patients were divided as follows: 11 asymptomatic patients (group A), 30 patients with moderate (classes II to III) symptoms (group B), and 12 patients with dyspnea at rest and pulmonary edema when first seen (group C). Surgical mortality was one patient (from group C). Late death occurred in four patients (one from group B, three from group C). At the end of follow-up (minimum 1 year, mean 3.6 years) 41 patients were in functional class I, four patients in class II, and one patient in class III. All patients except one in functional classes II and III belonged to group C. Before surgery, patients from groups A and B had similar ventricular dimensions and ejection fractions, whereas patients from group C had larger end-systolic diameters and volumes and lower ejection fractions. End-diastolic and end-systolic diameters decreased significantly at 1 and 2 years after surgery. Patients from group C continued to have dilated hearts as did those patients from groups A and B who had preoperative end-systolic diameters greater than 55 mm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical evaluation of a prospective protocol for the timing of surgery in chronic aortic regurgitation. 238

Three cases of high altitude pulmonary edema (Hurtado's disease) are described. The onset of the symptoms occurred within 72 hours after arrival from the sea level. Their main clinical features were dry cough, shortness of breath, tachycardia, progressive dyspnea and weakness. Rales and obstructive bronchial signs were detected on chest auscultation. Treatment included oxygen administration, diuretics and bed rest, with satisfactory clinical evolution within four days. Hurtado's disease is a form of noncardiogenic pulmonary edema, increased pulmonary vascular pressure and permeability are, probably, the main factors in its development. It has been suggested that both factors could a be consequence of hypobaric hypoxia.
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PMID:[Pulmonary edema in high altitude]. 248 89

A 38-year-old female was admitted to our hospital because of dyspnea. The diagnosis of total lipodystrophy was made by following findings: (1) gaunt appearance; (2) insulin-resistant diabetes mellitus; (3) hyperlipidemia; (4) fatty liver. Chest X-ray demonstrated cardiomegaly, pulmonary edema and pleural effusion. Echocardiogram was characterized by left ventricular hypertrophy with asymmetrical septal hypertrophy and left ventricular dysfunction. Renal biopsy revealed focal glomerulosclerosis. We reported a patient with total lipodystrophy combined with heart failure and renal failure, which have been rarely associated with the disease.
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PMID:Total lipodystrophy with heart failure and renal failure: report of a case. 253 Mar 77

We present the case of a patient who attempted suicide by ingestion of the rodenticide zinc phosphide. Zinc phosphide manifests its immediate toxicity through production of phosphine gas. Signs and symptoms of toxicity include nausea, vomiting, dyspnea, and changes in mental status; immediate death results from pulmonary edema. Delayed effects are secondary to the absorption of phosphide, affecting primarily the liver, heart and kidneys. Delayed deaths are related to a direct cardiotoxicity. Treatment is mainly symptomatic and supportive; aggressive airway management and circulatory support are critical to a successful outcome.
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PMID:Zinc phosphide ingestion: a case report and review. 257 17


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