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)

Thirty-two consecutive preterm infants with birth weights under 1,500 grams and with respiratory distress syndrome (RDS) complicated by a patent ductus arteriosus (PDA) underwent ligation of PDA. The indications for operation were massive left-to-right shunting associated with heart failure (cardiomegaly and pulmonary edema) unresponsive to medical treatment. The clinical manifestations of heart failure were related to the severity of RDS. Infants with mild-to-moderate RDS (21) often recovered and later developed typical findings of PDA (bounding pulses, hyperactive precordium, and murmur). They are now operated upon as soon as respiratory support is required. Infants with severe RDS (11) develop cardiomegaly earlier, and retrograde aortography may show massive left-to-right shunting before the presence of a murmur. Ligation is indicated when blood-gas values deteriorate despite medical treatment. Nineteen (59 per cent) of these extremely preterm infants survived to be discharged and 16 (50 per cent) are developing normally. Three have neurologic impariment. None of the survivors has clinical respiratory disease, and their radiologic findings of bronchopulmonary dysplasia are improving.
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PMID:Improving the results of ligation of patent ductus arteriosus in small preterm infants. 124 41

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

The drug of choice for the treatment of iron poisoning is desferrioxamine, though the best route of administration, dose, and duration of treatment are unclear. We report fatal lung injury in four patients who were treated with continuous intravenous infusions. The patients, aged 19-26 years, had received desferrioxamine infusions of 15 mg/kg per h for 65-92 h. Respiratory distress developed after 32-72 h. The patients met clinical, physiological, and necropsy criteria for the diagnosis of adult respiratory distress syndrome (ARDS); none had any of the known risk factors for the development of this disorder. We reviewed the records of forty-three iron-poisoned patients treated with desferrioxamine infusions. No patient treated for less than 24 h had pulmonary complications; however, of the fourteen treated for longer than 24 h, four were the patients with ARDS and four others had pulmonary oedema of other causes. We suggest that the pulmonary complications are caused by continuous infusion of desferrioxamine and that the ARDS in these patient was a consequence of free-radical generation. We recommend that desferrioxamine infusion should not be administered for longer than 24 h.
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PMID:Pulmonary toxic effects of continuous desferrioxamine administration in acute iron poisoning. 135 68

Fumonisin B1 (FB1), a recently identified mycotoxin produced by Fusarium moniliforme in corn, has been shown to cause death in swine due to pulmonary edema, an apparently species specific effect, and to interfere with sphingolipid metabolism in vitro. Here we characterize the toxicity of fumonisins, using female cross-bred swine weighing 6 to 13 kg, and present a hypothesis regarding the mechanism of fumonisin-induced pulmonary edema in swine. FB1 was given daily intravenously (IV) to pig 1 for 9 days for a total of 72 mg (7.9 mg/kg) and to pig 2 for 4 days for a total of 67 mg (4.6 mg/kg). Pig 3 (control) was given saline IV for 9 days. Corn screenings naturally contaminated with FB1 (166 ppm) and FB2 (48 ppm) were fed to pigs 4, 5, and 6, and ground corn was fed to pigs 7 and 8 (controls). Pigs 4 and 7 were killed on day 5; pig 5 was found dead on day 6; and pigs 6 and 8 were killed on day 15. Pigs 4 and 5 had ingested 187 and 176 mg total fumonisins, respectively, while pig 6 had ingested 645 mg. Feed consumption had decreased in pigs fed corn screenings, with an additional sharp decrease prior to onset of clinical signs. Increases in serum liver enzymes, total bilirubin, and cholesterol were present, but electrocardiograms, heart rate, and body temperature were unaffected. Pigs dosed IV with FB1, developed mild intermittent respiratory abnormalities, while those fed screenings developed respiratory distress within 5 days. Mild interstitial pulmonary edema was observed in pig 1. Severe interstitial pulmonary edema, pleural effusion, and increased lung wet/dry weight ratio were observed in pigs 4 and 5. All pigs given fumonisin (either IV or orally) had hepatic changes characterized by hepatocyte disorganization and necrosis; pancreatic acinar cell degeneration was also observed. Ultrastructural changes in orally dosed swine included loss of sinusoidal hepatocyte microvilli; membranous material in hepatic sinusoids; and multilamellar bodies in hepatocytes, Kupffer cells, pancreatic acinar cells and pulmonary macrophages. Pulmonary intravascular macrophages (PIMs) contained large amounts of membranous material. Thus, the target organs of fumonisin in the pig are the lung, liver, and pancreas. At lower doses, slowly progressive hepatic disease is the most prominent feature, while at higher doses, acute pulmonary edema is superimposed on hepatic injury and may cause death. We hypothesize that altered sphingolipid metabolism causes hepatocellular damage resulting in release of membranous material into the circulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Characterization of fumonisin toxicity in orally and intravenously dosed swine. 138 61

Interleukin-2 is a glycoprotein physiologically produced by human lymphocytes which is capable of mediating some still unknown immunologic reactions. In vitro, interleukin-2 was seen to induce a lytic reaction against tumor cells through the activation of a cytolytic system of natural killer cells. If administered to man in heavy doses, it causes a clinical response in the treatment of metastases from melanoma and renal cell carcinoma in 20-40% of cases. However, the clinical use of the drug, in therapeutic doses, is prevented by the occurrence of several side-effects, the major one being increased permeability of alveolar vessels with capillary leak and interstitial pulmonary edema (Vascular Leak Syndrome in the English literature). Thus, this work was aimed at evaluating chest radiographs during interleukin-2 treatment to detect, in the pulmonary district, the early stages of the vascular leak syndrome--i.e., pulmonary edema, pleural and pericardial effusions. Forty-three patients had been treated for metastases from renal cell carcinoma and melanoma November 1989 through September 1991: standard chest radiographs demonstrated 26 cases (60%) of pulmonary edema, 14 cases (32%) of bilateral pleural effusions and 12 cases (27%) of pericardial effusions. Daily chest films of the patients undergoing interleukin-2 therapy allowed the early stage of the vascular leak syndrome to be depicted, thus enabling the physician to use the highest tolerated doses and eventually to stop infusion before marked respiratory distress develops.
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PMID:[Radiologic characteristics of the thorax during therapy with interleukin-2]. 145 17

Combustion toxicology is complex so, although victims exposed to combustion products are mainly treated symptomatically, it is important to identify those situations when specific therapeutic measures might be of importance. Victims presenting respiratory symptoms including severe cough, bronchoconstriction, hypoxia and respiratory distress should be given oxygen and ventilatory assistance or support. Furthermore, bronchoconstriction should be treated with bronchodilators (beta-2-adrenoreceptor agonists, theophylline). Corticosteroids should be considered both for inhalation and systemically due to the risk of developing toxic pulmonary oedema that may appear after a symptom-free interval that might last up to 48-72 h. Victims with impaired consciousness should be regarded as being exposed to carbon monoxide and cyanides. Apart from oxygen and optimal symptomatic treatment hyperbaric oxygen therapy should be considered in carbon monoxide poisoning. Certain cyanide antidotes, namely those with low intrinsic toxicity (as sodium thiosulphate, hydroxocobalamin) should be given liberally in these situations. Other specific therapeutic measures that might be considered when appropriate are administration of organophosphate antidotes (atropine, oximes), heavy metal chelators (e.g. dimercaptopropane sulfonate, dimercaptosuccinic acid) and methemoglobinemia antidotes (methylthionine, toluidine blue). Inhalation of hot fumes may cause upper respiratory tract oedema (e.g. laryngeal oedema) necessitating orotracheal intubation and ventilatory support.
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PMID:Hospital treatment of victims exposed to combustion products. 147 Nov 83

A case with diagnosis of non-Hodgkin's lymphoma and superior vena cava obstruction on chemotherapy, presented with respiratory distress and massive pleural effusion of right hemithorax. On removal of 3.5 litres of fluid, he developed pulmonary edema of the same side and hypotension.
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PMID:Re-expansion pulmonary edema and hypotension. 152 78

To define better the clinical presentation and perioperative outcome in children undergoing adenotonsillectomy (T&A) for relief of upper airway obstruction (UAO), we reviewed the hospital records of 60 consecutive, otherwise normal children aged 12 years or younger. Seven patients with trisomy 21, neurologic impairments, or preoperative cor-pulmonale were excluded. Intraoperative and postoperative complications were experienced by 15 (34%) and 13 (25%), respectively, of the 53 children with preoperative UAO. The most severe complications comprised pulmonary edema and prolonged postoperative oxyhemoglobin desaturation. Multivariate logistic regression analysis found a history of prematurity and/or low birth weight to be the most significant risk factors related to the occurrence of complications. Twenty-eight % of the study population had a history of prematurity and they had approximately 85% of the perioperative complications seen in children with UAO undergoing T&A. Other significant risk factors included adenoidal facies and evidence of respiratory distress at the time of surgery. It appears that T&A poses significant risk for children with UAO who were born prematurely and have evidence of abnormal facial development or respiratory distress preoperatively.
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PMID:Adenotonsillectomy for upper airway obstruction carries increased risk in children with a history of prematurity. 152 32

Activation of complement and serum changes in anaphylatoxin (C3a and C5a) were studied in 8 patients who underwent open-heart surgery using a membrane oxygenator. C1 esterase inhibitor (C1-EI), C3, C5, CH50, C3a and C5a were measured serially at 7 points. C1-EI, C3, and C5 were measured by single radial immunodiffusion, CH50 by Mayer's method, and C3a and C5a by radioimmunoassay. Levels of C1-EI, C3 and C5 decreased significantly from 10 min after initiation to 120 min after the end of CPB compared with base line values. Degree of activation of complement increased in proportion to duration of CPB. Significant decreases of C3 and C5 continued until first postoperative day. Level of C3a increased significantly 10 min after initiation of CPB, and gradually increased till immediately after the end of CPB, when the level was maximum (4625 +/- 560 ng.ml-1) among 7 points. Level of C3a decreased gradually till 120 min after end of CPB. C5a was not detected during whole course. No patient showed respiratory distress of pulmonary edema. In conclusion, membrane oxygenator activated classical pathway of complement at 10 min after initiation of CPB. C3a increased significantly from 10 min after initiation of CPB to 120 min after end of CPB, but C5a was not detected at all during the whole course. The significant activation of complement continued till first postoperative day.
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PMID:[Activation of complement and serial changes of anaphylatoxin (C3a, C5a) in patients for open-heart surgery using a membrane oxygenator]. 155 59


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