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 9-year-old boy underwent biopsy of the tumor at the external auditory meatus under general anesthesia with a laryngeal mask airway(LMA). During emergence from anesthesia, laryngospasm with marked inspiratory effort and cyanosis occurred. The LMA was removed and the patient was orotracheally intubated following vecuronium administration. In spite of controlled ventilation with 100% oxygen, oxygen saturation remained at low 90s and pink frothy sputum appeared in the tracheal tube. We suspected negative pressure pulmonary edema and treated him with mechanical ventilation with positive end-expiratory pressure. Seventeen hours later the pink frothy sputum decreased and he was extubated. Laryngospasm during emergence from anesthesia with an LMA can induce negative pressure pulmonary edema, especially in pediatric patients.
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PMID:[Pulmonary edema in a child following laryngospasm triggered by a laryngeal mask airway during emergence from anesthesia]. 1129 48

We describe the case of a male newborn infant, whose mother developed varicella 20 days before delivery. At 2 hours of life the infant's general state suddenly deteriorated and he presented cyanosis, respiratory distress and emission of pink foam in his mouth. The infant was diagnosed with bilateral bronchopneumonia, of probable varicellosus etiology, with a component of hemorrhagic pulmonary edema. He required mechanical ventilation and inotropic support for 48 hours. Response to endovenous acyclovir was favorable. At 10 days of life varicella-zoster virus (VZV) in cerebrospinal fluid was detected by polymerase chain reaction and seroconversion of IgG anti-VZV was positive.
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PMID:[Neonatal varicella: report of a case of bronchopneumonia and hemorrhagic pulmonary edema]. 1246 59

Transfusion-related acute lung injury (TRALI) is a second most serious complication of the blood transfusion. It is a group of symptoms and signs such as dyspnoea, hypotension, cyanosis, cough, elevated temperature, fever and lung oedema that usually develops within an hour or two after transfusion. The full stage clinical presentation is developed between 4th and 6th hours after transfusion. The syndrome is caused by leucoagglutinins or by other lymphocytotoxic antibodies specific for some antigens present on the donor's leukocytes. Alveoles of the lung are the main place of the pathological changes such as intra-alveolar oedema, haemorrhage, hyaline membrane formation, alveolar cell hypertrophy and scant interstitial inflammation. Chest X-ray showed bilateral pulmonary infiltrates but without vascular congestion and with normal cardiac silhouette comparing to the status before transfusion. The syndrome has to be distinquished from pulmonary oedema caused by acute cardial insufficiency, overhydration, trauma and sepsis.
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PMID:[Acute lung injury related to blood transfusion]. 1143 32

Three cases of pulmonary aspiration of gastric acid as a complication of obstetrical anesthesia are described. The clinical picture consists of dyspnea, cyanosis, tachycardia and shock appearing several hours after the aspiration has occurred. On examination, the chest may be quite clear, but the chest radiograph shows a picture indistinguishable from that of pulmonary edema. The most important therapeutic measure is the intravenous administration of corticosteroids in large doses for several days. Bronchoscopy is contraindicated. With routine use of epidural anesthesia, this obstetrical complication can be avoided.
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PMID:PULMONARY ASPIRATION OF GASTRIC ACID--MENDELSON'S SYNDROME. 1428 37

A 33 years old woman was admitted to the hospital after four days with cough, dyspnea, orthopnea and hemoptysis. Blood pressure was 170/90 mmHg, pulse was 112 and temperature was normal. She had cyanosis and a left ventricular gallop, without heart murmurs. A chest radiograph revealed pulmonary edema and echocardiogram showed a global left ventricular systolic disfunction. Oxygen and furosemide were started, but cardiopulmonary collapse ensued. The patient was supported with mechanical ventilation and treated with inotropic drugs. A right sided cardiac catheterization showed pulmonary wedge pressure of 18 mmHg and a cardiac index of 3 l/min/m2. The levels of creatinine and urea nitrogen were elevated and a urine protein was 97 mg/dl. Coagulation tests were normal except by a positive lupic anticoagulant. Markers of connective tissue diseases or vasculitis were negatives. The clinical evolution suggested that a catastrophic antiphospholipid syndrome was ongoing. Intravenous corticoids, gammaglobulin and cyclophosphamide were administered with transient improvement. On her fourth day of treatment, the patient presented sudden pulmonary bleeding and embolism. A plasmapheresis was performed with improvement of renal, cardiac and pulmonary function. After this episode, the patient has been treated with prednisone and oral anticoagulants treatment for the last two years, without further clinical events.
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PMID:[Catastrophic antiphospholipid syndrome and acute heart failure. Report of a case]. 1463 91

A 22-yr-old, 86-kg, morbidly obese female orangutan (Pongo pygmaeus abelii) was immobilized and transported to the Denver Zoological Gardens hospital for a routine physical examination. Immediately after arriving at the hospital, cyanosis and apparent inadequate ventilatory efforts were noted. Clinically significant hypoxia occurred despite attempts to ventilate the orangutan through face mask, and attempts to place an endotracheal tube began. A large volume of pink-tinged frothy fluid flowed from the trachea when the laryngoscope was inserted into the oropharynx. Severe pulmonary edema due to negative-pressure pulmonary edema, precipitating life-threatening hypoxia was suspected. The orangutan was maintained on a mechanical ventilator using the neuromuscular blocking agent cisatracurium besylate and sedation with periodic doses of isoflurane and midazolam for 48 hr. Positive end-expiratory pressure was used while the orangutan was ventilated mechanically to improve respiratory function. The edema and hypoxia improved, but respiratory arrest ensued 30 min after extubation, when the orangutan was removed from mechanical ventilation. Necropsy and histopathology demonstrated that serious lung injury had led to acute respiratory distress syndrome.
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PMID:Negative-pressure pulmonary edema complicated by acute respiratory distress syndrome in an orangutan (Pongo pygmaeus abelii). 1507 17

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

A 3-week-old Thoroughbred colt was presented for weakness and cyanosis. A pansystolic regurgitant murmur and other physical findings suggested that the foal developed pulmonary oedema as a consequence of congenital heart disease. A large atrial septal defect, a high ventricular septal defect and dysplasia of the atrioventricular valves were visualised echocardiographically. A persistent common atrioventricular canal was observed at necropsy.
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PMID:Common atrioventricular canal in a foal. 1603 29

Infants with hypoplastic left heart syndrome (HLHS) and restrictive or intact atrial septum (rAS) present with cyanosis, pulmonary edema, and are critically ill. A previous report from our institution on emergent Norwood for HLHS with rAS showed 10% survival. We hypothesized that transcatheter left atrial (LA) decompression in HLHS with rAS would safely and effectively relieve LA hypertension, improve oxygenation, and improve Norwood survival. Between 1996 and 2004, 30 patients with HLHS and rAS underwent cardiac catheterization for pre-Norwood intervention. Twenty-eight atrial septostomies were performed: 23 static balloon dilations, 4 Rashkind septostomies, and 1 intra-atrial stent. Two procedures were aborted due to perforation (n = 1) or inability to enter the LA (n = 1). Eight total patients required surgical septectomy, for a failure rate of 27%. There were no catheter-related mortalities, although two patients died within 36 hr of the procedure after surgical septectomy. Major complications occurred in three patients (10%)--atrial perforations requiring intervention. Mean atrial septal defect gradient fell from 16.7 +/- 4.9 to 6.3 +/- 3.4 mm Hg (P < 0.001; n = 18). Mean LA pressure dropped from 21.8 +/- 5.5 to 13.1 +/- 6.5 mm Hg (P < 0.001; n = 16). Mean PaO(2) rose from 29.5 +/- 9.1 to 36.5 +/- 5.1 torr (P < 0.001; n = 23). Seventeen of 30 patients (57%) survived to discharge from Norwood. Thirteen have undergone hemi-Fontan and nine Fontan. Sixteen of 22 successful decompressions (73%) survived to discharge. Transcatheter decompression of the LA for patients with HLHS and rAS can be performed safely, reduces the transatrial gradient, and improves oxygenation. Catheter intervention improves survival compared to historical controls undergoing emergent Norwood.
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PMID:Catheter-based decompression of the left atrium in patients with hypoplastic left heart syndrome and restrictive atrial septum is safe and effective. 1654 29

Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.
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PMID:Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus. 1669 44


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