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

We analyzed data on renal allograft recipients over a 27-year period in order to investigate the frequency, etiology, and outcome of pericarditis developing during the first two months following renal transplantation. Of the 1497 patients receiving renal transplants between 1963 and 1990, 34 patients developed 36 episodes of pericarditis and/or pericardial effusions, for an overall incidence of 2.4%. Pericarditis was attributed to uremia in 14 episodes, cytomegalovirus infection in three, both uremia and CMV infection in four, nonspecific bacterial infection in three, and tuberculosis and minoxidil therapy in one episode each. No etiologic diagnosis could be established in 10 episodes. No statistically significant differences were found between pericarditis and case-matched control patients considering demographic features, the number of immediately functioning grafts, the duration of posttransplant acute renal failure, the number of supportive dialysis days, pre- and postoperative CMV status of the patients, and pretransplant BUN and serum creatinine levels. There were more uremic-related complications (pulmonary edema, gastrointestinal bleeding, central nervous system symptoms) in the pericarditis group. Five allografts in the pericarditis group never functioned, versus only one in the control group. Three patients with pericarditis developed pericardial tamponade. Early diagnosis, close follow-up, and in the case of cardiac tamponade early invasive treatment, should improve the prognosis of this potentially life-threatening complication.
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PMID:Pericarditis following renal transplantation. 164 5

Catheter ablation of ventricular tachycardia (VT) was attempted in 24 patients (mean age 49 +/- 15.1 years) with a history of recurrent sustained VT resistant to previous antiarrhythmic drug therapy. 14 patients (58.3%) had also failed to respond to long-term administration of amiodarone alone and in combination with class I antiarrhythmic drugs. Endocardial catheter mapping during induced or spontaneous VT and/or pacemapping were performed to identify the site of origin of VT. Direct-current high-energy anodal shocks were delivered from a conventional cardioverter with stored energies of 100, 200 or 400 J via the distal electrode of conventional catheters. A total of 139 shocks was delivered during the ablation procedure. One patient died from wall perforation. Within 1 week of ablation, nine patients developed spontaneous recurrences of monomorphic sustained VT, identical to the clinical VT, and one patient developed a VT with a new morphology. In addition, four patients had a recurrence of their clinical VT after several weeks. In seven of 14 patients with spontaneous recurrences after the first ablation procedure and in three patients in whom VT was again inducible at the end of the first week, a second ablation procedure was performed. One patient with inducible VT after the first and second ablation sessions was given a third ablation procedure, and was discharged from hospital on anti-arrhythmic drugs which were successful despite being previously ineffective. After a mean follow-up period of 14.1 +/- 9.1 months, there were no spontaneous recurrences of sustained VT in 17 patients (71%) (nine without antiarrhythmic drugs and eight on antiarrhythmic drugs). In the remaining patients, incessant non-sustained VT (n = 2) or recurrent sustained VT (n = 2) occurred, and two patients died suddenly (at 2 and 21 months). There was no correlation between catheter mapping data or the results of pre-discharge electrophysiological study and clinical outcome during long-term follow-up. Complications related to catheter ablation included pulmonary oedema, cardiac tamponade, femoral artery occlusion, multiple episodes of ventricular tachycardia/fibrillation and thrombus formation, each in one patient (major complications; n = 7,29.1%), as well as transient third degree AV block, transient right or left bundle branch block, transient marked ST elevation or transient atrial tachycardia (minor complications; n = 8, 33.3%). The results suggest that catheter ablation might become an effective procedure for the non-pharmacological treatment of sustained VT.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Catheter ablation of ventricular tachycardia using defibrillator pulses: electrophysiological findings and long-term results. 276 72

A case is reported of a 73 year old female patient who died during surgery for enlarged nephrectomy as a result of a massive non-cardiogenic pulmonary oedema. She had been given 2 red cell concentrates (450 g) and 3 fresh frozen plasma units (900 g). A postmortem examination did not reveal any pulmonary embolus, acute myocardial infarct, haemorrhage or cardiac tamponade. Further tests on the sera of the 5 plasma donors revealed a neutrophil-specific anti-NA2 antibody. Alveolar leukostasis was confirmed on the postmortem lung slices. This type of transfusion accident occurs for about 1 in 5,000 units transfused, fortunately not all as serious. This case confirms once more that fresh frozen plasma is not the ideal treatment for acute hypovolaemia, 4% human albumin being safer.
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PMID:[Fatal pulmonary leukoagglutination after administration of fresh frozen plasma]. 281 45

A case is reported of acute airway obstruction and pulmonary oedema of mixed origin (cardiogenic and non cardiogenic), occurring in a patient after surgical treatment for pericardial tamponade due to a mediastinal tumour. This 45 year old female patient had a non-Hodgkin lymphoma, mostly located within the anterior and middle mediastinum. When she developed cardiac tamponade, emergency cardiac decompression was carried out. The surgical procedure went well, despite an episode of severe hypotension. Immediately after extubation, she developed paradoxical breathing with retraction and cyanosis. She was reintubated and ventilated. The chest X-ray showed bilateral alveolar infiltrates, mostly around the hilar. Two hours later, she was again extubated and developed again the same respiratory failure. This time, she was intubated and ventilated for 48 h. She was then extubated with no problem. It seemed most probable that transmission to the interstitial space of a negative intrapleural pressure due to the inspiratory efforts made against an occluded airway was the principal mechanism responsible for the accumulation of fluid to this space.
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PMID:[Acute pulmonary edema following airway obstruction and cardiac tamponade related to mediastinal tumor]. 322 41

We studied the role of O2 supply and demand factors for producing diaphragmatic failure in a canine model of cardiogenic shock with pulmonary edema. We produced pulmonary edema with oleic acid and then hypotension with cardiac tamponade and followed the animals until respiratory failure began, which was defined by a 50% fall in frequency of breathing and diaphragmatic pressure-time index (PTI; cmH2O.s-1.min-1) with no decrease in the diaphragmatic electromyogram. Regional blood flows were measured with radiolabeled microspheres. Diaphragmatic O2 consumption (VO2 di) (ml.min-1.100 g-1) was determined from the diaphragmatic blood flow (Qdi) and the arterial and phrenic venous O2 contents. With oleic acid-induced pulmonary edema, PTI Qdi, and VO2 di increased from control of 101.7 +/- 31.7, 17 +/- 1.8, and 0.81 +/- 0.11, respectively, to 187.2 +/- 27.6, 42.2 +/- 7.2, and 3.32 +/- 0.35 (P less than 0.05). With tamponade, PTI did not change (186.7 +/- 60.0), whereas VO2 di increased further to 3.98 +/- 0.98 (P less than 0.05) due to increased O2 extraction and no significant change in Qdi (32.8 +/- 4.0). As fatigue developed, VO2 di decreased to 2.30 +/- 0.23 due to the combined effects of small declines in Qdi and the arterial O2 content but remained higher than control even though the energy demands returned to control values. In conclusion, when cardiogenic shock is added to pulmonary edema VO2 di and energy output do not increase further and eventually fall.
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PMID:Diaphragmatic energetics and blood flow during pulmonary edema and hypotension. 339 91

We describe the complications of pericardiocentesis and their management in an 18 year-old man. This patient was admitted because of dyspnea and was found on echocardiogram to have cardiac tamponade with coexisting left ventricular dysfunction. He developed acute left ventricular failure with severe pulmonary edema immediately after pericardiocentesis. This complication may have been caused by an abrupt increase in venous return to the failing left ventricle following the release of the pericardial compression. Therefore, pericardial fluid must be drained with caution in pericardiocentesis, especially in cardiac tamponade patients with left ventricular dysfunction, and hemodynamics should be monitored both during and after this procedure.
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PMID:Acute left ventricular failure with pulmonary edema following pericardiocentesis for cardiac tamponade--a case report. 775 46

From 1972 to 1992, 170 patients with acute renal failure (87 M, 83 F; mean age 32.51 +/- SE 0.945) underwent hemodialysis at the renal unit of the Korle Bu Teaching Hospital, Accra. Vascular access was established initially by arteriovenous shunt (133 cases), femoral venous cannulation (10 cases), and subclavian vein cannulation (27 cases). The overall mortality for acute renal failure (ARF) was 31.8% (54/170). The mortality for obstetric cases was 43.7% (14/32); for surgical cases, 33.3% (6/18); medical cases, 28.3% (13/32); and gynecologic (posthysterectomy) cases, 28.3% (2/7). The most important causes of death in ARF were pulmonary edema (42%), sepsis (20%), and cardiac tamponade (10.4%). Hemodialysis is now established as a form of treatment for ARF and a overall survival rate of 68.2% justifies the development of our program. With improvement of economies of developing countries and health insurance schemes, this form of treatment should be available in all developing countries.
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PMID:Hemodialysis in the treatment of acute renal failure in tropical Africa: a 20-year review at the Korle Bu Teaching Hospital, Accra. 882 98

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

Acute heart failure is always an indication for referral to an intensive care unit. In the widest sense, the term acute heart failure includes the manifestation forms of pulmonary edema, cardiogenic shock or rapid-onset decompensated cardiac insufficiency unaccompanied by shock or pulmonary edema (low-output syndrome). Acute heart failure may occur in the absence of previously known heart disease. Existing prior specific diseases that may end in acute cardiac insufficiency include acute myocardial infarction, decompensated cardiomyopathy, myocarditis, cardiac tamponade, endocarditis or arrhythmogenic heart failure.
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PMID:[Acute heart failure]. 1537 19

The immediate postoperative complications of 1011 consecutive patients undergoing surgical repair of atrial septal defects between 1980 and 1998 at Marie Lannelongue Hospital were analysedwith the ultimate objective of comparing their incidence with that of percutaneous closure. Five patients died (0.49%) of low cardiac output (N=3), pulmonary oedema (N=1) or pulmonary hypertension (N=1). A total of 356 patients (35.2%) had 448 postoperative complications. There were 77% minor and 23% major complications. The minor complications included arrhythmias and conduction defects (N=130), respiratory complications (N=90) and pericardial effusions (N=64). The main major complications were cardiac failure (N=27), cardiac tamponade (N=13), neurological complications (N=8) and reoperation (N=28). Of the survivors, 95.6% of patients were discharged from hospital with no residual problem and 41 (4.4%) had sequellae: arrhythmias (N=29, including one pacemaker implantation), neurological complications (N=4), acquired mitral regurgitation (N=2), phrenic nerve paralysis (N=1) and minimal residual shunt (N=10). Factors correlated with surgical morbidity were age, the severity of pulmonary hypertension, the type of atrial septal defect (less morbidity with ostium secundum defects), the presence of associated malformations, the surgical approach (less morbidity with the right postero-lateral thoracic approach). This study demonstrated the incompressible risk of open heart cardiac surgery. It will form a basis for a comparative study of the two modern methods of treating atrial septal defect: surgical and percutaneous closure.
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PMID:[Surgical repair of atrial septal defect in 1011 consecutive patients]. 1596 97


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