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At least 145 records · Page 8Linked to original sources
PubMed2004

Inhaled nitric oxide as an adjunct to suction thrombectomy for pulmonary embolism.

Pulmonary suction thrombectomy can be a successful interventional tool in the treatment of pulmonary thromboembolism. Removal of clot burden typically results in prompt recovery of hemodynamic stability and improved oxygenation. However, in rare cases, clot removal does not sufficiently improve the clinical situation. Herein, two patients with massive pulmonary thromboembolism are presented whose condition improved only after they received nitric oxide as an adjunct to pulmonary suction thrombectomy. The treatment with this inhalable vasodilator was based on the hypothesis that prolonged ischemia had induced microcirculatory vasospasm, persistent after removal of the central clot.

Administration, Inhalation↗
PubMed1992

Surgery for massive pulmonary embolism.

Pulmonary embolectomies were performed in 30 patients from January 1973 until December 1991 in the University Hospital of Leuven. There was an 80% hospital survival. The late follow-up showed no recurrent pulmonary emboli. The preoperative haemodynamic status was the most important predictor for survival. Patients, under cardiopulmonary resuscitation or in profound cardiogenic shock before surgery, had a survival of only 50% while all other patients survived. Angiography, performed in only 23% of the cases, remained the most important diagnostic tool until the advent of transthoracic and transoesophageal echocardiography. Thrombolysis is an acceptable alternative in the stable patient, but pulmonary embolectomy is life-saving in the haemodynamically unstable patient and when thrombolysis is contraindicated.

Adult↗
PubMed1989

Pulmonary embolism.

Pulmonary thromboembolism is perhaps one of the most challenging diseases to recognize, diagnose, and treat appropriately in medicine today. Although the clinician is offered a variety of diagnostic modalities, a highly sensitive and specific diagnostic modality without significant risk does not yet exist. The newer noninvasive tests may offer valuable alternatives to the more invasive venogram and pulmonary angiogram. Figure 1 offers an algorithm for the diagnosis and management of thromboembolic disease. Failure to diagnose this entity can result in significant patient morbidity and mortality. Physicians must maintain a high index of suspicion as well as have an organized approach to diagnosis and management to improve survival of patients with thromboembolic disease.

Combined Modality Therapy↗
PubMed1986

Preventive and therapeutic approach to venous thromboembolic disease and pulmonary embolism--can death from pulmonary embolism be prevented?

Venous thromboembolism produces chronic sequelae in the legs and occasional immediate mortality due to pulmonary embolism. Because it occurs in certain high risk situations (for example, after surgery) its prevention is a practical proposition. This has been attempted using many different approaches. Administration of low dose heparin with or without dihydroergotamine to enhance venous return has been one of the most widely tested regimens. There is little doubt that this can prevent, in many patient groups, postoperative deep venous thrombosis and fatal pulmonary embolism, with a low incidence of adverse reactions. Some particularly high risk postoperative patient groups (for example, those undergoing hip surgery) warrant more aggressive measures to prevent thrombosis. Surveys have shown that increasing use is being made of this approach, and it is hoped that all surgeons will adopt a policy that will reduce postoperative venous thrombosis and pulmonary embolism. A reduction in the incidence of venous thromboembolism in large acute myocardial infarction is achieved by low dose heparin, although early mobilization is important. In addition, many of the patients at risk merit full dose anticoagulation to prevent intracardiac thromboembolism. Established venous thrombosis is treated effectively by intravenous heparin, followed by warfarin to keep the prothrombin time at 1.2 to 1.5 times control, as assessed using rabbit thromboplastin; most patients need three months of treatment. Anticoagulation is warranted for pulmonary embolism, with fibrinolytic therapy reserved for patients with massive embolism and hemodynamic compromise. Embolectomy is a heroic measure, which may occasionally be lifesaving.

Dihydroergotamine↗
PubMed1996

Color Doppler Transesophageal Echocardiography in Detection of Massive Pulmonary Embolism: Is Pulmonary Angiography Always the Gold Standard?

In this article, the potential value of color Doppler in improving diagnostic accuracy of transesophageal echocardiography (TEE) in patients with incomplete obstruction of large pulmonary vessels is illustrated. We present an unusual case of massive pulmonary embolism that was unequivocally detected by color Doppler TEE both before and after pulmonary angiography, which failed to demonstrate filling defects in the pulmonary artery. (ECHOCARDIOGRAPHY, Volume 13, November 1996)

Journal Article↗
PubMedDate not supplied

Pulmonary angiography and the diagnosis of pulmonary embolism.

Pulmonary angiography is the definitive study for the identification of embolism. The development of accurate noninvasive methods for the detection of deep venous thrombosis has altered the indications for angiography. Many angiographic techniques have been developed, providing the opportunity to tailor the angiogram to the clinical situation of individual patients. Strict criteria must be used for interpretation of angiographic studies, and using state of the art equipment will diminish technically unsatisfactory examinations. CT and MR angiography will assume a significantly larger role in the identification of PE in the very near future. MR may become the method of choice, because it is the one noninvasive technique that shows promise for the study of both the deep venous system of the legs and pelvis and the pulmonary circulation.

Angiography↗
PubMed2003

Syncope in patients with pulmonary embolism: comparison between patients with syncope as the presenting symptom of pulmonary embolism and patients with pulmonary embolism without syncope.

Syncope as an initial presentation of pulmonary embolism occurs in 10% of patients. We compared clinical and instrumental parameters in patients with syncope as the presenting symptom of pulmonary embolism and in patients with documented pulmonary embolism without syncope. Seventy patients with the diagnosis of pulmonary embolism and apparently stable clinical conditions were evaluated. They were divided in two groups: 10 patients with syncope as the presenting symptom of pulmonary embolism (group 1) and 60 patients without syncope (group 2). Patients with syncope showed a more pronounced tendency to present with main pulmonary artery embolus than patients without syncope (contingency coefficient = 0.301, p < 0.04; one-tailed). However, despite the evidence that patients with syncope have significant reductions in systolic and/or diastolic blood pressure, shock was not observed in any patient. In no case was thrombolytic treatment given and all patients received standard anticoagulation with unfractioned heparin and oral anticoagulant. We suggest that syncope in the setting of non-massive pulmonary embolism may be due to vaso-vagal mechanism that can lead to a reduction of arterial blood pressure when central artery thrombosis is involved.

Aged↗
PubMed1982

Circulating negative inotropic agent(s) following pulmonary embolism.

Pulmonary emboli may impair myocardial performance, causing declines in cardiac index (CI) and right and left ventricular stroke work (LVSW) because of mechanical events. We postulate that embolism also leads to the generation of a humoral factor(s) that may reduce cardiac contractility. Eleven mongrel dogs were infused with 0.5 gm/kg clot. Decreases in CI and LVSW were observed 1 hour after embolization. The stable metabolites of prostacyclin and thromboxane (Tx) A2--6-keto-PGF1 alpha and TxB2, respectively--increased within 30 minutes (P less than 0.005, P les than 0.001) and then decreased. These changes did not correlate with the declines in CI or LVSW. Plasma from embolized animals used to bathe an isolated rat papillary muscle reduced developed tension (Tpd) (P less than 0.001) and decreased calcium ATPase (Ca++-ATPase) activity of a myofibril preparation (P less than 0.001) obtained from rat cardiac muscle. The correlation between the reduction of TPd and myofibril Ca++-ATPase activity was 0.72 (P less than 0.001). The decline in Ca++-ATPase was also related to the decreases in CI (r = 0.59, P less than 0.001) and LVSW (r = 0.57, P less than 0.001). Five animals pretreated with indomethacin prior to embolization had no decrease in LVSW as compared with controls (P less than 0.001). Postembolism plasma did not depress papillary muscle Tpd and did not lower Ca++-ATPase activity of myofibrils. Anesthesia itself did not alter cardiopulmonary function. These results suggest that pulmonary emboli cause the release of a negative inotropic agent(s) into plasma that affects energy availability in the heart and reduces contractility. The production of this agent(s) is inhibited by indomethacin pretreatment.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

[The hemodynamics of the lung circulation of minipigs after experimentally-caused Sedlarik's pulmonary embolism. I. Sedlarik's pulmonary embolism model in comparison to existing embolism models].

The necessity of a clinical relevant pulmonary embolism model is described because of the international importance and the consequence for certain special branches. The multifarious pathophysiologic mechanism in the human requires an approximation of the model. The pulmonary embolism model according to Sedlarik approaches these demands and it became the basis of this study.

Animals↗