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

Severe congestive heart failure and cardiogenic shock don't resemble a homogeneous clinical picture, but a syndrome that is based on very different etiologies. What all the etiologies have in common is the inadequate peripheral O2-supply to essential organs with or without signs of severe pulmonary congestion up to pulmonary edema. For prognosis and therapy is a fast diagnostical clarification of the causes crucial. The therapeutical procedure for the various etiologies may be diametrically opposed. For the therapy is it also dicisive to distinguish between acute myocardial failure, e.g. acute myocardial infarction, and the development of myocardial failure from a longer existing consistent congestive heart failure (cardiomyopathy). Whenever possible, next to symptomatically therapy of cardiogenic shock the basic conditions of the disease should be cured (e.g., PTCA, lysis with acute myocardial infarction, lysis in acute pulmonary embolism). In myogenic cardiogenic shock the use of positive-inotropic substances with and without simultaneous vasodilatory effects, if necessary in combination with other vasodilators, may be life-saving. Up until now there still doesn't exist an alternative to the catecholamines in the acute phase, initially they should be used as a first-line-therapy to stabilize the hemodynamics. The insertion of a Swan-Ganz-catheter for invasive therapy-monitoring, especially for the regulation of the therapy is a "condition sine qua non" for every patient with unstable hemodynamics. Because of the prompt beta-receptor-down-regulation during shock, caused by endogenous catecholamines, successful therapy with exogenous catecholamines is limited (adrenaline, dopamine, dobutamine), on account of the acceleration and intensification of the beta-receptor-down-regulation process. Possible beta-receptor independent alternatives are beta 2-agonists (dopexamine), PDE-III-inhibitors (amrinone, milrinone, enoximone) as well as H2-receptor agonists (impromidine, arpromidine) and finally the calcium-sensitisers (pimobendane). First results give rise to optimism to effectively reduce the mortality of congestive heart failure. The combination of these new pharmacological possibilities with interventional transcutaneous applicable assist-systems (aortic counterpulsationpump IABP, hemopump, transcutaneous heart-lung-machine) as well as the transitory application of an artificial heart (Novacor) can possibly increase the success of these therapeutic strategies. So far there are no convincing results shown in the world literature.
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PMID:[Pharmacotherapy of severe heart failure with inodilators--new approaches]. 902 10

Over 30 years ago hemodynamic studies on patients with high altitude pulmonary edema (HAPE) excluded the prior contention that the basic cause was left ventricular failure and correctly implicated the pulmonary circulation as the culprit. Physiological 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 (pre-capillary) resistance was 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. While hypoxic vasoconstriction appears to be the major cause of patchy vascular obstruction the occurrence of thrombi in the pulmonary vessels may also play a role in more severe and advanced cases. The above concept of the mechanism of HAPE has been further supported by animal studies showing pulmonary edema occurring when increased pressure and flow is produced in a portion of the pulmonary vascular bed. Clinical studies which have supported this concept include the susceptibility to HAPE of patients with an absent pulmonary artery, pulmonary edema occurring in pulmonary embolism, following removal of pulmonary arterial thrombi and following balloon dilatation of stenoses of branches of the pulmonary artery. In addition to those hemodynamic factors an increase in capillary permeability due to cell derived products resulting from capillary wall injury is an important aspect of edema formation.
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PMID:High altitude pulmonary edema: hemodynamic aspects. 905

Hysteroscopy is used as a diagnostic tool for intrauterine pathology. Gas embolism with air or carbon dioxide is a rare but sometimes fatal complication of laparoscopy or hysteroscopy. We present a patient who developed pulmonary air embolism during hysteroscopy that caused a noncardiogenic pulmonary edema in the recovery room. This case report emphasizes that early intervention can prevent life-threatening events associated with pulmonary embolism during hysteroscopy. Pathophysiology of pulmonary gas embolism, as well as that of noncardiogenic pulmonary edema, is discussed. A protocol for the prevention, early detection, and management of this emergency is provided.
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PMID:Successful early intervention in air embolism during hysteroscopy. 917 36

In this review, three aspects of pleural disease are discussed. Although it was thought for many years that the origin of pleural fluid was the capillaries in the parietal or visceral pleura, recent evidence suggests that in many cases the origin of pleural fluid is the interstitial space of the lung. The interstitial space of the lung appears to be the source of the pleural fluid in patients who have congestive heart failure, parapneumonic effusions, pulmonary embolism, and lung transplants. The Hantavirus pulmonary syndrome is characterized by rapidly progressive, noncardiogenic pulmonary edema in relatively young, previously healthy individuals. The mortality rate with this syndrome is approximately 60%, and at autopsy most patients have large pleural effusions. Patients after lung transplantation frequently have profuse drainage from their chest tubes because most of the fluid that enters the lung must exit through the pleural space. The incidence of pleural effusion is very high in patients who have a complication of their lung transplantation, but the pleural fluid findings in patients after lung transplantation have not been well studied. Similarly, virtually all patients who undergo liver transplantation have a right-sided pleural effusion. The effusion usually reaches its maximum size around the third postoperative day. If the effusion increases in size after this time, serious complications should be suspected. The approach to pleural diseases has been altered with the advent of videothoracoscopy. Videothoracoscopy should be considered in patients who have undiagnosed pleural effusions and are not improving; in patients who have had recurrent pneumothorax, or a spontaneous pneumothorax with a persistent airleak or unexpanded lung; or in patients who have a traumatic hemothorax with clotted blood.
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PMID:Diseases of the pleura. 936 70

In patients with chronic pulmonary embolism, pulmonary thromboendarterectomy may result in a unique form of noncardiogenic pulmonary edema termed reperfusion edema. This report reviews the authors' experience after pulmonary thromboendarterectomy with particular emphasis on the radiographic manifestations of reperfusion edema. The clinical and radiographic record of 25 patients who underwent pulmonary thromboendarterectomy at the University of Pennsylvania from 1985 through 1995 were reviewed. The zonal distribution of radiographic opacity, time to maximal opacity, and the time to clearance of reperfusion edema were determined. The relationship of these radiographic manifestations to clinical severity of disease and clinical outcome was examined. Reperfusion edema, characterized by patchy bilateral perihilar alveolar opacities, occurred in all but one patient. There is a lower lung zone predominance of opacities, but in individual cases, striking unilateral or haphazard arrangements of opacities may be seen. In this small sample of patients, no association between preoperative pulmonary arterial pressures and radiographic appearance or clinical outcome was found. However, severity of radiographic opacities, as measured by the extent of involved lung, correlated with disease severity, as measured by time to extubation and time to discharge. Pneumonia, defined as a radiographic opacity that evolves discordantly with the reperfusion edema opacities, occurred in 20% of cases. Reperfusion edema is a common consequence of pulmonary thromboendarterectomy. The severity of radiographic manifestations and clinical severity of disease are related. This characteristically appears as perihilar alveolar opacities.
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PMID:Reperfusion edema after thromboendarterectomy: radiographic patterns of disease. 967 19

Negative pressure is a rarely occurring cause of pulmonary edema. It has previously been reported only in the presence of a closed glottis or obstructed airway. A 64-year-old man with 74% body surface burn without any inhalation injury experienced acute pulmonary edema on hospital day 11 associated with high-minute volume and negative inspiratory pressures at the ventilator. The edema cleared after sedation and paralysis. Workup disclosed pulmonary emboli and normal cardiac-filling pressures. A mechanical model, simulating his breathing, measured intrathoracic pressure of -37 +/- 12 mm Hg, which is sufficiently negative to cause pulmonary edema despite a patent airway. Pulmonary emboli increased his respiratory drive to amounts greater than what the ventilator could deliver, thus leading to the large negative intrathoracic pressure and pulmonary edema.
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PMID:Negative-pressure pulmonary edema with a patent airway. 971 Jul 29

This report concerns an apparently healthy woman who presented simultaneously with acute massive bilateral pulmonary embolism and mitral regurgitation, subsequently, a month later, resulting in pulmonary edema secondary to chordae rupture of the mitral valve. The authors believe that massive pulmonary embolism predisposed to chordal rupture in this case. It is suggested that increased awareness of ruptured chordae tendineae as a cause of mitral regurgitation and the prompt use of transesophageal echocardiography will facilitate the early recognition of this potentially fatal, but treatable, cause of mitral regurgitation in patients with pulmonary embolism.
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PMID:Massive bilateral pulmonary embolism in a patient with subsequent occurrence of severe mitral regurgitation due to ruptured chordae tendineae--a case report. 978 52

Pulmonary edema may be classified as increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema. Pulmonary edema has variable manifestations. Postobstructive pulmonary edema typically manifests radiologically as septal lines, peribronchial cuffing, and, in more severe cases, central alveolar edema. Pulmonary edema with chronic pulmonary embolism manifests as sharply demarcated areas of increased ground-glass attenuation. Pulmonary edema with veno-occlusive disease manifests as large pulmonary arteries, diffuse interstitial edema with numerous Kerley lines, peribronchial cuffing, and a dilated right ventricle. Stage 1 near drowning pulmonary edema manifests as Kerley lines, peribronchial cuffing, and patchy, perihilar alveolar areas of airspace consolidation; stage 2 and 3 lesions are radiologically nonspecific. Pulmonary edema following administration of cytokines demonstrates bilateral, symmetric interstitial edema with thickened septal lines. High-altitude pulmonary edema usually manifests as central interstitial edema associated with peribronchial cuffing, ill-defined vessels, and patchy airspace consolidation. Neurogenic pulmonary edema manifests as bilateral, rather homogeneous airspace consolidations that predominate at the apices in about 50% of cases. Reperfusion pulmonary edema usually demonstrates heterogeneous airspace consolidations that predominate in the areas distal to the recanalized vessels. Postreduction pulmonary edema manifests as mild airspace consolidation involving the ipsilateral lung, whereas pulmonary edema due to air embolism initially demonstrates interstitial edema followed by bilateral, peripheral alveolar areas of increased opacity that predominate at the lung bases. Familiarity with the spectrum of radiologic findings in pulmonary edema from various causes will often help narrow the differential diagnosis.
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PMID:Clinical and radiologic features of pulmonary edema. 1055 72

OBJECTIVE - To assess the incidence of fatal pulmonary embolism (FPE), the accuracy of clinical diagnosis, and the profile of patients who suffered an FPE in a tertiary University Hospital. METHODS - Analysis of the records of 3,890 autopsies performed at the Department of General Pathology from January 1980 to December 1990. RESULTS - Among the 3,980 autopsies, 109 were cases of clinically suspected FPE; of these, 28 cases of FPE were confirmed. FPE accounted for 114 deaths, with clinical suspicion in 28 cases. The incidence of FPE was 2.86%. No difference in sex distribution was noted. Patients in the 6th decade of life were most affected. The following conditions were more commonly related to FPE: neoplasias (20%) and heart failure (18.5%). The conditions most commonly misdiagnosed as FPE were pulmonary edema (16%), pneumonia (15%) and myocardial infarction (10%). The clinical diagnosis of FPE showed a sensitivity of 25.6%, a specificity of 97.9%, and an accuracy of 95.6%. CONCLUSION - The diagnosis of pulmonary embolism made on clinical grounds still has considerable limitations.
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PMID:Fatal pulmonary embolism in hospitalized patients. Clinical diagnosis versus pathological confirmation. 1075 80

Recent qualms about the safety of aesthetic lipoplasty may be attributable more to support system flaws than to technical process deficiencies. The authors here focus on perfunctory patient monitoring when sedative or analgesic drugs are given, cavalier infiltration of mega-dose lidocaine, cursory intraoperative patient observation by team members with conflicting responsibilities, anesthesia providers unfamiliar with the unique surgical physiology of liposuction, hurried-discharge policies that virtually ignore the residual depressant effects of sedatives and analgesics, and compressive dressings that impair postoperative chest-wall expansion and venous return. Whereas pulmonary embolism remains the leading process cause of morbidity from liposuction, complications from austere resource allocation to dedicated patient monitoring should be largely preventable. Not all lipoplasties require an anesthesia provider but-when heavy sedation, mega-dose lidocaine, or both, are projected-a trained team member dedicated exclusively to patient safety and comfort should be a minimum patient care standard. The potential role of lidocaine cardiotoxicity in tumescent anesthesia is widely underappreciated and that of hypothermia goes mostly unrecognized. These, plus largely preventable or potentially correctable perioperative events such as pulmonary edema, fluid imbalance, or improperly administered sedative and analgesic drugs, demand upgrading and expansion of monitoring, resuscitative, and recuperative facilities in physician offices. In fact, ASPS guidelines urge that anesthesia services be engaged for dedicated patient care whenever "major" liposuction or conscious sedation is projected, because liposuction is neither as benign nor as simple a procedure as heretofore reputed. To assess objectively the operative and anesthetic risk of obesity, document body mass index for the preoperative record; morbid obesity (body mass index >/= 35.0), for instance, is a known risk multiplier for sedatives and analgesics. Other system issues such as the dynamic profile of high-dose lidocaine pharmacokinetics, the deportation of fat globules in the bloodstream, and the incidence of intraoperative hypothermia remain as unresolved topics for interdisciplinary, multi-institutional clinical research.
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PMID:Perioperative management of cosmetic liposuction. 1125 1


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