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 37-year-old woman had undergone aortic valve replacement with Smeloff-Cutter prosthetic valve in 1967. She visited our hospital because of dyspnea and chest pain about 22 years after the operation. Severe aortic regurgitant murmur was audible and a chest X-ray demonstrated lung edema. A diagnosis was made of acute left heart failure due to prosthetic valve dysfunction, and emergency operation was performed. The Silastic ball was severely deformed and shrunken. Therefore, the ball was easily put off outside the cage. A St. Jude medical prosthetic valve was implanted. The postoperative course was uneventful.
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PMID:[A case report of ball variance of Smeloff-Cutter prosthetic valve]. 224 49

A registry of suspected cases of cancer-associated hemolytic-uremic syndrome (C-HUS) was established in May 1984. Records of 85 patients from the registry, all with history of cancer, hematocrit less than or equal to 25%, platelet count less than 100,000, and serum creatinine greater than or equal to 1.6 mg/dL were subjected to in-depth analysis. Eighty-nine percent of patients had adenocarcinoma, including 26% with gastric cancer. Microangiopathic hemolysis was reported in 83 patients; coagulation studies were normal with rare exception. Bone marrow examination ruled out chemotherapy-induced myelosuppression in 68 of 85. Thirty-five percent of patients were without evident cancer at time of syndrome development. Mitomycin (MMC) was part of the treatment regimen in 84 patients; all but nine received a cumulative dose greater than 60 mg. Pulmonary edema, generally noncardiogenic, developed in 65% of patients, often after blood product transfusions. C-HUS has a high mortality: over 50% of patients died of or with syndrome, most within 8 weeks of syndrome development. Conventional treatment was ineffective, although ten of 21 treated with staphylococcal protein A (SPA) immunopheresis showed significant responses. Statistical analysis found only absence of obvious tumor and treatment with SPA to suggest favorable prognosis. C-HUS is distinguishable from related syndromes such as childhood HUS, thrombotic thrombocytopenic purpura (TTP), consumption coagulopathy, and microangiopathic hemolysis associated with advanced carcinoma. MMC is likely involved in the development of C-HUS; the risk of developing C-HUS after treatment with MMC is between 4% and 15%. However, possible bias in patients referred to the registry and reports of non-MMC C-HUS cases must be remembered. Recommendations include careful monitoring of renal and hematologic function in patients treated with MMC, aggressive nontransfusion in patients with suspected C-HUS, and consideration of treatment with SPA immunopheresis in patients with definite syndrome.
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PMID:Cancer-associated hemolytic-uremic syndrome: analysis of 85 cases from a national registry. 251 Dec 78

The combined transplantation of heart and lungs, first done successfully by the Stanford Team (USA) in 1982, at present seems to be superseding lung transplantation alone, and has broadened the indications of heart transplantation to include terminal heart failure with fixed pulmonary arterial hypertension. After reviewing the causes for failure in lung transplants, the authors stress the superiority of heart-lung transplants compared to isolated lung transplantations: healing of the tracheal anastomosis, ease of detection of rejects by endomyocardial biopsy and the lack of inhomogeneity of the ventilation/perfusion ratios. This operation still poses problems of surgical technique as the mediastinal nerves need to be preserved and the risk of haemorrhage linked to the mediastinal dissection or to the eventual pulmonary separation under cardiopulmonary bypass is important. Donor subjects for cardiopulmonary transplantation are rare as they ought to have a thoracic cage of matching size to the recipient and to be free of pulmonary infection and trauma. The post-operative complications are essentially those of immediate haemorrhage, graft rejection, pulmonary oedema and infection. The late complications are coronary atherosclerosis and bronchiolitis obliterans. The indications of such a transplant are currently reserved for primary or secondary pulmonary hypertension and to respiratory failure with a normal thoracic cage and ventilatory mechanics.
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PMID:[Heart-lung transplantation]. 310 71

Several drugs including antineoplastic drugs and immunosuppressant can induce hemolytic uremic syndrome. Mitomycin C are well known to cause cancer associated HUS, and its frequency are reported to be 4-15%. Noncardiogenic pulmonary edema frequently ( > 50%) develops, especially after blood transfusion, among MMC induced HUS. Cancer associated HUS has a high mortality and no effective therapy has been established. Combination of vinblastin and bleomycin also induces HUS. Cisplatin, one of the most frequently used antineoplastic drugs, also induces HUS. Cyclosporin causes HUS, probably due to endothelial damage and/or an inhibition of prostacyclin synthesis. A case of FK506 induced HUS has been recently reported. Quinine and Cocaine also can induce HUS. Prognosis of cancer associated HUS is quite poor, whereas Quinine and Cocaine induced HUS may resolve.
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PMID:[Drug induced hemolytic uremic syndrome]. 767 50

Pleuropulmonary amebiasis is the common and pericardial amebiasis the rare form of thoracic amebiasis. Low socioeconomic conditions, malnutrition, chronic alcoholism, and ASD with left to right shunt are contributing factors to the development of pulmonary amebiasis. Although no age is exempt, it commonly occurs in patients aged 20 to 40 years, with an adult male to female ratio of 10:1. Children rarely develop thoracic amebiasis: when it does occur there is an equal sex distribution. The infection usually spreads to the lungs by extension of an amebic liver abscess. Infection may pass to the thorax directly from the primary intestinal lesion through hematogenous spread, however. Lymphatic spread is one possible route. Inhalation of dust containing cysts and aspiration of cysts or trophozoites of E histolytica in the lungs are some other hypothetical routes. The lung is the second most common extraintestinal site of amebic involvement after the liver. Usually the lower lobe, and sometimes the middle lobe of the right lung, are affected, but it may affect any lobe of the lungs. The patient develops fever and right upper quadrant pain that is referred to the tip of the right shoulder or in between the scapula. Hemophtysis is common. The diagnosis of thoracic amebiasis is suggested by the combination of an elevated hemidiaphragm (usually right), hepatomegaly, pleural effusion, and involvement of the right lung base in the form of haziness and obliteration of costophrenic and costodiaphragmatic angles. Infection is usually extended to the thorax by perforation of a hepatic abscess through the diaphragm and across an obliterated pleural space, producing pulmonary consolidation, abscesses, or broncho-hepatic fistula. Empyema develops when a liver abscess ruptures into the pleural space. Rarely, a posterior amebic liver abscess can burst into the inferior vena cava and develop an embolism of the inferior vena cava and thromboembolic disease of the lungs with congestive cardiac failure or corpulmonale. Diagnosis by finding E histolytica in stool specimens is of limited value. In a limited number of cases amebae might be found in aspirated pus or expectorated sputum. "Anchovy sauce-like" pus or sputum may be found. Presence of bile in sputum indicates that the pus is of liver origin. Serological tests are of immense value in diagnosis. Liver enzymes are usually normal and neutrophilic leucocytosis may or may not be found. ESR is invariably elevated. Anti-amebic antibodies can be detected by ELISA, IFAT, and IHA. Amebic antigen can be detected from serum and pus by ELISA. Detection of Entamoeba DNA in pus or sputum may be a sensitive and specific method. Pleuropulmonary amebiasis is easily confused with other illnesses and is treated as pulmonary TB, bacterial lung abscesses, and carcinoma of the lung. A single drug regimen with metronidazole with supportive therapy usually cures patients without residual anomalies. Aspiration of pus from empyema thoracis may be needed for confirmation and therapeutic purposes. The pericardium is usually involved by direct extension from the amebic abscess of the left lobe of the liver, sometimes from the right lobe of the liver, and rarely from the lungs or pleura. An initial accumulation of serous fluid due to reactive pericarditis followed by intrapericardial rupture may develop either (1) acute onset of severe symptoms with chest pain, dyspnea, and cardiac tamponade, shock, and death, or (2) progressive effusion with thoracic cage pain, progressive dyspnea, and fever. Chest radiograph, ultrasound examination, and CT scan usually confirm the presence of a liver abscess in continuity with the pericardium and fluid within the pericardial sac with or without the fistulous tract. Echocardiography may demonstrate fluid in the pericardial cavity. Patients should be cared for in the ICU and ambecides should be started without delay. Pericardiocentesis usually confirms the diagnosis and improves the general condition of the patient. Aspiration of the accumulated fluid should be performed urgently in cardiac tamponade; repeated aspiration may be needed. Surgical drainage should be done if needed. Acanthamoeba, a free-living ameba, may also infect the lungs in the form of pulmonary nodular infiltration and pulmonary edema in association with amebic meningoencephalitis in immunocompromised patients. It usually spreads to the meninges of the brain by way of the blood from its primary lesion in the lung or skin. Early diagnosis and institution of treatment may be life saving for these patients. A literature review shows that HIV/AIDS patients are not prone to infection with E histolytica. It is now clear that there are an increasing number of HIV-seropositive patients among amebic liver abscess patients, however, which suggests that although the incidence of intestinal infection is not high among HIV-seropositive or AIDS patients they are more susceptible to an invasive form of the disease.
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PMID:Thoracic amebiasis. 1209 41

Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal meningoencephalitis complicated with neurogenic pulmonary oedema. Its pathogenesis, especially the CNS involvement, is not clearly understood. The aim of this study was to set up a mouse EV71 infection model with CNS involvement. EV71 virus was administrated orally to neonatal mice. The EV71-infected mice manifested a skin rash at an early stage and hind limb paralysis or death at a later stage. Immunohistochemical staining and virus isolation demonstrated that EV71 replicated in the small intestine, induced viraemia and spread to various organs. Kinetic studies showed that EV71 antigen was first detected in the intestine at 6 h, in the thoracic spinal cord at 24 h, in the cervical spinal cord at 50 h and in the brain stem at 78 h post-infection. Leukocyte infiltration was evident in the spinal cord and brain stem. Furthermore, EV71 virus could be transmitted to littermates within the same cage.
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PMID:A murine oral enterovirus 71 infection model with central nervous system involvement. 1471 21

A free-ranging, adult male Florida panther (Puma concolor coryi) was immobilized and evaluated for hematuria following routine capture. Prior to anesthetic recovery, the panther was fitted with a telemetry collar. After an initially quiet recovery, the panther began thrashing in the transport cage, and was again immobilized. Pink foam was evident from the nostrils, and crackles were ausculted over the chest, indicating pulmonary edema. Postobstructive pulmonary edema was diagnosed based on history, clinical signs, radiographic evaluation, and blood gas analysis. The animal was treated intensively for several hours with diuretics, oxygen, and manual ventilation. The panther responded rapidly to therapy and was released back into the wild 48 hr after presentation. Postobstructive pulmonary edema, also called negative-pressure pulmonary edema, may be underrecognized in veterinary medicine. In this case, the telemetry collar, in conjunction with anesthetic recovery in a small transport crate, may have contributed to tracheal obstruction. Wildlife veterinarians and biologists should be aware of the risk of airway obstruction when placing tracking collars, and animals should be continuously monitored during anesthetic recovery to ensure the presence of a patent airway.
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PMID:Diagnosis and treatment of presumptive postobstructive pulmonary edema in a Florida panther (Puma concolor coryi). 1767 17

Two groups of chickens (Gallus domesticus; White Leghorn; age, 4 d and 2 wk) housed in a university research vivarium were found dead or moribund without prior signs of illness. The overall mortality rates were 92.3% (60 of 65 birds) for the 4-d-old birds and 80% (8 of 10) for the 2-wk-old birds. All chicks were housed in brooders with heat lamps in a temperature- and humidity-controlled room. Primary gross findings were mild to moderate dehydration and hepatic lipidosis. The most consistent histologic findings were pulmonary hemorrhage and edema in all 7 of the 4-d-old birds evaluated and in all 4 of the 2-wk-old birds assessed. In addition, 1 of the 4-d-old birds had multifocal centrilobular hepatic necrosis. These findings suggested an inhaled toxicant and hypoxia, respectively. Inspection of the animal room revealed that approximately 50% of the heat lamp bulbs in the brooder cage were coated with polytetrafluoroethylene (PTFE). Two published case reports detail similar experiences in birds exposed to PTFE-coated heat-lamp bulbs. Birds are highly sensitive to inhaled toxicants owing to the high efficiency of their respiratory systems, and PTFE toxicosis is known to cause pulmonary edema and hemorrhage in pet birds after exposure to overheated nonstick cookware. In the present case, the bulbs were replaced, and no similar problems subsequently have been noted. This case illustrates the sensitivity of avian species to respiratory toxicants and serves as a reminder that toxicosis can be encountered even in the controlled environment of a laboratory vivarium.
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PMID:Polytetrafluoroethylene toxicosis in recently hatched chickens (Gallus domesticus). 2233 Jun 51

Starr-Edwards ball-in-cage prosthetic heart valves, although durable, are associated with a particularly high rate of thromboembolic complications. This valve is seldom used in North America, and is certainly not the valve of choice in a woman of childbearing age. Few reports exist from the 1970s of thrombotic complications in pregnant women with Starr-Edwards prostheses, and the optimal management strategy for such valves is unclear. Here, the case is reported of a 31-year-old woman with a Starr-Edwards prosthesis in the mitral position who was transferred to the authors' center at six weeks' gestation with pulmonary edema. Transthoracic echocardiography demonstrated thrombosis of the prosthetic valve, with a mean gradient of 23 mmHg. When treated initially with intravenous heparin and furosemide the patient improved significantly; however, the optimal management going forward was unclear. Here, the options for anticoagulation during pregnancy and for management in the event of valve thrombosis are reviewed. In the absence of any clear guidelines, a thorough discussion of the various risks and benefits with the patient is necessary, but ultimately any consideration of the risk to the mother is paramount.
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PMID:A case of Starr-Edwards valve thrombosis in pregnancy. 2340 62

CASE DESCRIPTION Three 21-week-old sexually intact female sibling domestic shorthair cats were brought to an emergency clinic because of signs of sudden respiratory distress that were noted by the owner after the cats had been confined for approximately 10 hours in a room with an operating ozone-generating air purifier. No other potential toxicant exposures were reported. CLINICAL FINDINGS On initial examination, the 3 cats were severely dyspneic and tachypneic. Pulmonary crackles were audible on thoracic auscultation. Thoracic radiography revealed a marked peribronchial, unstructured interstitial pulmonary pattern that coalesced to a patchy alveolar pattern, consistent with noncardiogenic pulmonary edema. TREATMENT AND OUTCOME A diuretic (furosemide, 2 mg/kg [0.9 mg/lb], IV) and bronchodilator (terbutaline sulfate, 0.01 mg/kg [0.005 mg/lb], IM) were administered, and supplemental oxygen was provided by placing the cats in an oxygen cage at 80% oxygen saturation. By 24 hours after placement in the oxygen cage, all cats had unremarkable respiratory rates and thoracic auscultation findings. Complete resolution of the respiratory signs and radiographic pulmonary lesions was achieved within 48 to 72 hours after initial evaluation. At a recheck examination performed 3 months after initial evaluation, the cats remained free of respiratory signs, and no radiographic pulmonary lesions were detected. CLINICAL RELEVANCE To the authors' knowledge, this was the first reported case of pulmonary toxicosis believed to have been caused by ozone exposure in cats. Associated respiratory signs were successfully and rapidly reversed following oxygen supplementation and medical treatment.
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PMID:Noncardiogenic pulmonary edema associated with ozone exposure in three kittens. 3039 24


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