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

Pulmonary edema (PE) which is similar to the neurogenic type was induced by adrenaline (AD) administration (0.1 mg/kg) in rats. Acute progressive respiratory distress, cyanosis and dyspnea occurred. All the experimental animals in the PE group died within 20 min after AD injection, with a pulmonary index (PI) of 1.70 +/- 0.47 (mean +/- S) which was much higher than that in the normal group. The mortality rate was 100%. It was found that in rats with PE, a protein-rich fluid filled the alveolar and interstitial spaces, and ecchymosis occurred. The capillary permeability as estimated by Evans blue injection showed that Evans blue from extraction fluid and bronchoalveolar lavage (BAL) in the PE rats was at a much higher level than that in the normal control (NC) rats. In anisodamine (ADM, 654-2) and tetramethylpyrazine (TMP) treated rats, almost all the damage was diminished or absent, and the mortality rates were decreased from 100% to 4.4% and 20%, respectively. 654-2 and TMP could significantly inhibit the increase of pulmonary permeability.
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PMID:Hemodynamic and nonhemodynamic mechanisms of experimental pulmonary edema in rats and the effect of anisodamine and tetramethylpyrazine. Part 1: Survival rate, pulmonary index, pathological change and pulmonary vascular permeability. 829 2

Streptokinase is the mainstream therapy for acute myocardial infarction. A fifty-seven-year-old man with acute MI was admitted to the intensive cardiac care unit and received streptokinase and heparin. At the time of admission, he was not receiving any drugs and denied any previous exposure to a hepatotoxic agent. Five hours later he developed a dramatic hypersensitivity reaction including high fever, pulmonary edema, cyanosis, and convulsions. Within twelve hours, his clinical state was stabilized. After forty-eight hours, he developed jaundice and transaminasemia, which subsided by the eighth day. Only a few reports of overt jaundice are associated with streptokinase.
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PMID:Jaundice induced by streptokinase. 863 72

High-altitude pulmonary edema (HAPE) occurs in unacclimatized individuals who are rapidly exposed to altitudes in excess of 2450 m. It is commonly seen in climbers and skiers who ascend to high altitude without previous acclimatization. Initial symptoms of dyspnea, cough, weakness, and chest tightness appear, usually within 1-3 days after arrival. Common physical signs are tachypnea, tachycardia, rales, and cyanosis. Descent to a lower altitude, nifedipine, and oxygen administration result in rapid clinical improvement. Physiologic studies during the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pulmonary artery pressure, severe arterial unsaturation, and usually a low cardiac output. Pulmonary arteriolar (precapillary) resistance is elevated. A working hypothesis of the etiology of HAPE suggests that hypoxic pulmonary vasoconstriction is extensive but not uniform. The result is overperfusion of the remaining patent vessels with transmission of the high pulmonary artery pressure to capillaries. Dilatation of the capillaries and high flow results in capillary injury, with leakage of protein and red cells into the alveoli and airways. HAPE represents one of the few varieties of pulmonary edema where left ventricular filling pressure is normal.
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PMID:High-altitude pulmonary edema: current concepts. 871 81

A 10-year-old male cat was presented with sudden onset of respiratory difficulties. Clinical examination revealed an acute dyspnoea with cyanosis associated with a left systolic heart murmur. Standard thoracic radiographs excluded pulmonary oedema and showed very few pulmonary changes given the intensity of the respiratory compromise. Echocardiographic examination revealed hypertrophic cardiomyopathy and a thrombus in the right pulmonary artery. Pulmonary scintigraphy confirmed a pulmonary thromboembolism with hypovascularisation of the left cranial lobe and of the ventral segment of the right lobe. Conservative treatment was instituted using an antibiotic (doxycycline), anticoagulants (heparin, coumadine) and a calcium inhibitor (diltiazem). The cat was given absolute rest. The general condition of the animal improved.
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PMID:Diagnosis of pulmonary thromboembolism in a cat using echocardiography and pulmonary scintigraphy. 923 34

A severely restrictive atrial septal defect (ASD) in neonates with hypoplastic left heart syndrome (HLHS) results in pulmonary venous hypertension, pulmonary edema, and intractable hypoxia. Between January 1983 and June 1998, 21 of 355 neonates presenting with HLHS (5.9%) underwent cardiac catheterization at median age 1 day (range 0 to 25), for creation or enlargement of a restrictive or absent interatrial communication. One patient died during preliminary angiography. Three underwent blade septostomy with 2 procedure-related deaths, and 1 had balloon atrial septostomy (BAS); all 4 died before surgical intervention. Fifteen underwent Brockenbrough atrial septoplasty with transatrial needle puncture and serial balloon dilations of the new ASD, 5 after unsuccessful BAS. The most recent patient had a stent placed across the atrial septum after transatrial needle puncture. In the 16 patients treated with septoplasty or stent, oxygen saturation increased from 50 +/- 4% to 83 +/- 2% (p <0.0001) and transatrial pressure gradient decreased from 16 +/- 1 to 6 +/- 1 mm Hg (p <0.0001). One patient died awaiting transplantation, supportive care only was requested in 1, and 14 underwent stage 1 palliation. Eight of 14 (57%) survived to hospital discharge. Six of 7 (86%) survived bidirectional Glenn and the 3 who have undergone fenestrated Fontan are alive. In neonates with HLHS, a restrictive ASD resulting in profound cyanosis demands urgent intervention. BAS is frequently unsuccessful and blade septostomy has high mortality. Pulmonary venous hypertension can be adequately relieved by Brockenbrough atrial septoplasty or stenting, allowing stabilization before reconstructive surgery or while awaiting transplant.
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PMID:Preoperative management of pulmonary venous hypertension in hypoplastic left heart syndrome with restrictive atrial septal defect. 1021 89

A 30-year-old man underwent tonsillectomy and laryngomicrosurgery under nitrous oxide oxygen-isoflurane anesthesia. Preoperative physical examinations and interview revealed no cardiopulmonary abnormalities. Two minutes after extubation, he showed dyspnea with marked inspiratory efforts and cyanosis due to laryngeal spasm. The SpO2 decreased from 100% to 80%. He was reintubated after administration of suxamethonium 100 mg and ventilated with 100% oxygen. At that time pink frothy sputum came out from his airway. He was diagnosed as pulmonary edema from analysis of arterial blood gases and chest X-ray. He received mechanical ventilation with positive end-expiratory pressure in the ICU. Twenty hours later the pulmonary edema was improved and he was extubated uneventfully. He was discharged from the hospital on the 8th post-operative day. We reported a case of pulmonary edema after laryngeal spasm. It was suggested that a patient after acute upper airway obstruction should be carefully treated considering secondary pulmonary edema.
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PMID:[A case of pulmonary edema following upper airway obstruction after general anesthesia]. 1048 27

Congenital aortic stenosis accounts for about 5% of cardiac malformations recognized in childhood. It belongs to the category of acyanotic congenital heart disease. These lesions produce a load on the heart because of left ventricular outflow tract obstruction. Severe aortic stenosis in the newborn period (critical aortic stenosis) presents with signs of left sided heart failure (pulmonary edema, poor perfusion), right sided heart failure (hepatomegaly, peripheral edema) and may progress rapidly to total circulatory collapse. We present a case of an infant with critical aortic stenosis presenting with cyanosis, who was entirely dependent on ductal patency for systemic output. When oxygen was given, the ductus started to close, with a worsening of the left sided output and subsequent acidosis. With the right to left shunt across the ductus, the baby was cyanotic and dependent on prostaglandin to keep the ductus open. There was minimal flow across the aortic valve because of the stenosis and extremely poor left ventricular function prior to surgery. After relief of the aortic valvular obstruction, there was finally good antegrade flow across the aortic valve, terminating cyanosis.
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PMID:One day old infant with acyanotic congenital heart disease: critical aortic stenosis. 1056 81

An unusual case diagnosed as connective tissue-type mast cell leukemia with marked mastocyte infiltration into visceral organs in a seven-year-old female Curly-Coated retriever is presented. Acute circulatory collapse, emesis, diarrhea, abdominal enlargement, icterus, cyanosis, dyspnea, pulmonary edema, hepatomegary, ascites, and right ventricular enlargement were observed. Hematologic and biochemical examinations revealed mast cell leukemia, mature neutrophilia, monocytosis, thrombocytopenia, hemolytic hyperbilirubinemia, hyperhistaminemia, renal and hepatic injuries. Mast cells were distributed systemically, but predominantly in the diaphragm and liver with a large mass among the serosa of ileum, cecum and colon. Mast cells were stained intensely by both safranin and berberine sulfate.
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PMID:Connective tissue-type mast cell leukemia in a dog. 1072 Jan 89

Acute respiratory distress syndrome (ARDS) is the result of severe injuries of different etiologies of the capillary system in patients with previously healthy lungs, resulting in noncardiogenic pulmonary edema. The authors studied 42 infants in whom the histopathologic aspects were suggestive for ARDS. The etiologic factors of this syndrome were: severe gastroenteritis with hypovolemic or endotoxic shock (13 cases), sepsis (9 cases), fulminans purpura (2 cases), severe neurological disorders (13 cases), pulmonary infections (5 cases). In such conditions, if the infant presents hyperpnea followed by generalised cyanosis, refractory to oxygen therapy, and if there are clinical and radiologic signs of acute pulmonary edema, the diagnosis of ARDS must be considered and a complete intensive care therapy is compulsory in order to alleviate the severe prognosis of this syndrome.
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PMID:Etiological, clinical and pathomorphological aspects of acute respiratory distress syndrome in children. 1075 53

Anaesthesia was required in an 18-month-old Dorper ewe scheduled for surgical repair of an abdominal hernia. Anaesthesia was induced with diazepam (0.15 mg/kg) and ketamine (6 mg/kg), and maintained with halothane in oxygen on a circle anaesthetic machine. Hypotension, hypoxaemia, cyanosis and pulmonary oedema were observed from the start of surgery, but the symptoms improved towards the completion of the procedure. The aetiology of this condition could not be established. It is suggested that propylene glycol, the organic solvent in the diazepam formulation, may have stimulated the release of vasoactive substances that resulted in pulmonary oedema.
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PMID:Hypoxaemia and suspected pulmonary oedema in a Dorper ewe after diazepam-ketamine induction of anaesthesia. 1094 21


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