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Query: UMLS:C0034065 (pulmonary embolism)
14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here the occurrence of focal pulmonary edema within 4 h after massive acute pulmonary embolism. The edema appeared to develop only in areas with intact pulmonary arterial blood flow and occurred in the apparent absence of left ventricular dysfunction. This pattern of pulmonary edema after precapillary obstruction is similar to that seen in animal models of permeability pulmonary edema induced by acute nonuniform pulmonary arterial obstruction.
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PMID:Focal pulmonary edema after massive pulmonary embolism. 723 63

The causes of lethality were studied in 49 patients with acute myocardial infarction of an average age 71.24 +/- 12.12. that died within the first 6 hours after their admission to hospital in the period 972-1979. They represent 15.46 per cent of all patients with infarction that died during that period. The anterior localization of the infarction (extent of necrosis), the repeated myocardial infarction and existing cardiac insufficiency are of significance for the lethality out of the factors studied. The acute rhythm and conductivity disturbances are the cause for the lethality in 38.78 per cent of the patients, acute cardiovascular failure (shock and/or pulmonary edema)--52.02 per cent, whereas rupture of the ventricular wall and pulmonary embolism are rare--8.16 per cent and 2.04 per cent respectively. During the first hour of hospital admission--30.64 per cent of the patients died, whereas during the rest of the hours up to the sixth hour the lethality was respectively--18.38%, 12.24%, 20.4%, 8.16% and 10.20% of the patients. Some of the other factors of significance for the early lethality were also analyzed and some measures for their prophylaxis or reduction of intensity of their effect were recommended.
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PMID:[Causes of early mortality in myocardial infarct]. 733 10

Respiratory failure is the main cause of death in patients undergoing bone marrow transplantation (BMT). In this paper, clinical and research aspects as well as diagnostic, prophylactic and therapeutic strategies concerning the various forms of pulmonary and bronchial complications, which may evolve after BMT, are discussed. Both cytomegalovirus (CMV)-induced interstitial pneumonia (PM) and the idiopathic pneumonia syndrome rarely occur in the cytopenic phase post-BMT. Haematological reconstitution with donor type cells seems to be a prerequisite to the development of these complications, suggesting a key role of immunological reactions. While CMV pneumonia can be effectively treated or prevented by ganciclovir, the idiopathic syndrome is usually fatal. Due to improved prophylaxis and therapy, lethal interstitial PM due to Pneumocystis carinii, herpes simplex, varizella zoster or Toxoplasma gondii as well as lethal PM caused by bacteria or Candida species are comparatively rare events. Aspergillus species, on the other hand, have emerged as frequent causative pathogens in lethal PM during the past years. Prolonged granulocytopenia and prolonged medication with corticosteroids are major risk factors of pulmonary aspergillosis, which is usually fatal; effective prophylaxis may be achieved by sterile air supply during the hospital stay and by inhalation of amphotericin B thereafter. Pulmonary haemorrhage, as diagnosed by bronchoalveolar lavage (BAL), may develop due to the toxicity of the conditioning regimen, or may be secondary to infectious PM of various kind. Congestive heart failure or the application of cytokines might give rise to the development of pulmonary oedema. Patients with hepatic veno-occlusive disease have a high risk of subsequent pulmonary complications, possibly on the basis of toxic lung injury. Venous thromboembolism or air embolism may occur; they are usually venous catheter-associated. Pleural effusions may develop secondary to infection, congestive heart failure, veno-occlusive disease, pulmonary embolism or malignancy. Patients with bronchiolitis obliterans, which leads to progressive respiratory failure, present with an obstructive pattern in lung function tests and hyperinflated lungs on chest radiographs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The lung as a critical organ in marrow transplantation. 772 20

Respiratory insufficiency is one of the most common and most serious complications of the postoperative period. Preexisting risk factors include cardiopulmonary disease, significant smoking history, obesity and advanced age. The risk of postoperative respiratory insufficiency is increased in emergency surgical procedures (particularly those related to trauma), procedures involving the chest or upper abdomen and procedures requiring prolonged anesthesia. Postoperatively, prolonged sedation or neuromuscular blockade, cardiovascular instability, respiratory problems and immobilization are important risk factors. Common clinical causes of respiratory insufficiency are atelectasis, aspiration, pulmonary edema and pulmonary embolism. Management strategies are directed at treatment of the cause of the insufficiency and restoration of pulmonary function. All surgical patients should be carefully assessed before surgery, monitored closely during and after the procedure, and aggressively treated to prevent or correct respiratory insufficiency.
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PMID:Postoperative respiratory insufficiency. 773 49

Twenty-four patients with ventricular fibrillation or sustained ventricular tachycardia underwent implantation of a new transvenous defibrillator. All patients had a device implanted without thoracotomy. High placement of a shock lead in the anonymous vein and inversion of the shock-wave polarity allowed avoidance of placement of subcutaneous patches. Implantation time decreased from 138 minutes for the first 12 patients to 82 minutes for the last 12 patients, with 4 and 11 subpectoral pockets, respectively. Three patients required a minor reintervention. No bleeding or infection occurred. One episode of pulmonary edema and one pulmonary embolism were seen in the postoperative course. No postoperative deaths were observed. During a mean follow-up period of 4.12 months, 58% of the 24 patients had symptomatic arrhythmic episodes, with shocks in 50% of the 24. Inappropriate shocks were delivered in three cases (atrial fibrillation and T-wave sensing). One episode was not terminated even with four internal shocks. One patient had ventricular fibrillation because of a sensing problem. By reprogramming of sensitivity, back-up pacing, and adjustment of drug therapy these arrhythmic complications could be prevented. Pectoral implantation of a cardioverter-defibrillator is easy and can be performed by cardiologists experienced in pacemaker implantation. Careful postoperative observation, reprogramming after the first spontaneous event, and prehospital discharge induction of ventricular fibrillation will prevent arrhythmic complications.
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PMID:A new transvenous internal cardioverter-defibrillator: implantation technique, complications, and short-term follow-up. 783 96

"At first glance the lungs may seem uncomplicated, but many wise men have gone astray in their labyrinths." These words were written by Dr. A.A. Liebow, a famous pathologist, in a foreword to the first edition of Pathology of the Lung by H. Spencer. This same thought can also be applied to the field of medicolegal autopsies. 1. The gross appearance of the lungs in medicolegal autopsies Plucks consisting of the lungs, neck organs, the esophagus and the aorta were removed from human cadavers and after taking photos of the frontal and rear view, the lungs were carefully examined to reveal whether the lung shows characteristic morphological changes depending on causes of death. Based on their appearance, the lungs were classified into the 3 following types: a collapsed, a non-collapsed and an inflated type, each of these types reflecting the probable cause of death. The collapsed type of lung was seen in cases of death from exanguination, and the lung falling into shrinkage due to traumatic pneumo- and/or hemo-thorax was also classified into the collapsed type. The non-collapsed type of lung was seen in cases whose lungs were thermo-coagulated and in a case of death from a pulmonary embolism. Also, the deflating lungs of drowning victims before falling into collapse, were classified into a non-collapsed type. The inflated type of lung consisted of lungs that showed ballooning soon after death by drowning, and lungs that had inflated due to emphysema or edema from various causes. This lung study has reconfirmed that the lungs show hypostatic changes more clearly than any other organs of the body, and in the absence of skin color changes reflecting hypostasis, the settling of the blood in the lung could be detected in most cases. 2. Early histopathological lung changes induced by shock One hundred and thirty medicolegal cases were reviewed to detect early histopathological changes of the lung induced by shock. In many cases of death from various causes, pulmonary edema and hemorrhage were noted, but the incidence of such changes did not reveal any significant differences among the causes of death. When death had resulted from a hemorrhage or occurred during a state of shock, megakaryocytes in the pulmonary vessels tended to increase. However, if death from such causes had occurred shortly after the event, no increase in megakaryocytes was noted.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Some findings of the lung in medicolegal autopsy cases]. 786 36

Cardiogenic shock is a syndrome of different etiologies resulting in the inability of the heart to provide adequate O2 delivery to peripheral organs and tissues with or without signs of severe pulmonary congestion or pulmonary edema. Clarification of the underlying etiologies is essential for prognosis and therapy. Depending on the various etiologies, the therapeutic procedure may be totally different. Furthermore, it is decisive to differentiate between an acute shock (e.g., acute myocardial infarction) and the development of a cardiogenic shock state on the basis of preexisting chronic congestive heart failure (e.g., congestive cardiomyopathy). Whenever possible the underlying disease should be treated causally (e.g., PTCA or thrombolytic therapy in AM, lysis in acute pulmonary embolism) in addition to symptomatic pharmacologic treatment with vasodilators and/or inodilators. In myogenic cardiogenic shock, the treatment with inotropic drugs (with and without vasodilatory potency) and, if necessary, in combination with additional vasodilators may be life-saving. At present, there is no alternative to catecholamines in the acute state with apparent hemodynamic instability. Catecholamines still represent the initial first line treatment. A Swan-Ganz catheter is mandatory in such situations. In view of the rapid beta 1-receptor down-regulation induced by endogenous catecholamines, long-term administration of exogenous catecholamines (adrenalin, dopamine, dobutamine), seems essentially problematic, since these compounds intensify and accelerate this process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of cardiogenic shock]. 786 6

Cocaine inhalation is associated with multiple pulmonary complications including pulmonary infiltrates, pulmonary edema, barotrauma, tracheal injury, and alveolar hemorrhage. Little has been reported about ventilation/perfusion (V/Q) lung scanning in patients who smoke cocaine. The authors report a case of inhalation cocaine abuse mimicking pulmonary embolism by V/Q scan criteria. This case report documenting perfusion abnormalities within hours of cocaine smoking which resolved within days provides the first in vivo evidence for pulmonary vasoconstriction.
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PMID:Crack cocaine mimicking pulmonary embolism on pulmonary ventilation/perfusion lung scan. A case report. 789 42

We present the case of a patient with acute onset of dyspnoea after a long-distance flight. Pulmonary embolism was suspected, but could be excluded by perfusion scintigraphy. The electrocardiogram and chest X-ray were compatible with acute myocardial infarction and pulmonary oedema, but the slightness of the elevation of pulmonary capillary wedge pressure allowed cardiogenic pulmonary oedema to be excluded. The clinical picture was then interpreted as pneumonia with sepsis and hypotension. The rapid and full clinical recovery within 48 h, together with the close temporal relationship of ingestion of hydrochlorothiazide and the onset of symptoms, allowed the diagnosis of drug-induced pulmonary oedema and anaphylactoid hypotension.
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PMID:Pulmonary oedema and hypotension induced by hydrochlorothiazide. 800 Apr 16

Despite the development of several lung transplantation procedures, the most advantageous for pulmonary hypertension remains controversial. Between 1986 and February 1992, 30 patients with end-stage primary pulmonary hypertension (n = 24), chronic pulmonary embolism (n = 4), and hystiocytosis X (n = 2) underwent heart-lung (n = 21), double lung (n = 8), or single lung (n = 1) transplantation. Indications for double lung transplantation were similar to those for heart-lung transplantation, and the preoperative clinical and hemodynamic parameters were not significantly different between the two groups. There were no intraoperative deaths, but two reoperations were needed for pleural hematoma. Five early deaths were related to graft failure (two heart-lung transplantations), mediastinitis (one heart-lung transplantation), multiorgan failure (one double lung transplantation), and aspergillosis (one double lung transplantation). There was a similar improvement in early (days 0 and 2) and late (6 months postoperatively) right-sided hemodynamic function in patients undergoing heart-lung and double lung transplantation. Three double lung transplant recipients had early and reversible left ventricular-failure. The early postoperative course of the one patient who had single lung transplantation was characterized by severe pulmonary edema, left ventricular failure, and persistent desaturation and later on by moderate pulmonary hypertension and an important ventilation/perfusion mismatch. The pulmonary function results were also similar in the heart-lung and double lung transplantation groups. The overall projected 2- and 4-year survivals were 49% and 41%, respectively, and were not significantly different between the heart-lung and double lung recipients. Results demonstrate that heart-lung and double lung transplantation are equally effective in obtaining early and durable right-sided hemodynamic and respiratory improvement and similar respiratory function. In patients with pulmonary hypertension, double lung transplantation should be preferred to single lung transplantation because of the critical postoperative course and the uncertain long-term results of single lung transplantation.
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PMID:Comparative outcome of heart-lung and lung transplantation for pulmonary hypertension. 834 Oct 71


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