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PubMed1993

[Prospective study of determining the value of D-dimer in diagnosing pulmonary embolism].

Pulmonary embolism (PE) is still misdiagnosed in a high proportion of cases. 107 patients admitted for suspected pulmonary embolism were studied prospectively to shed light on the value of ELISA-D-dimer and Latex-D-dimer. Pulmonary embolism was ruled out by negative perfusion scans in 66 patients (61.7%) and by angiography in 24 patients. 58% of the scans suggesting a high probability of PE were confirmed by angiography, but only 18% of the scans suggesting a low or intermediate probability of PE. Sensitivity and specificity were 88% and 79%, respectively for the D-dimer ELISA, versus 94% and 90% for the Latex agglutination test. The Latex test increased the positive predictive value of lung scanning suggesting low to intermediate probability of PE (group B) from 18% to 75% and that of lung scanning suggesting high probability of PE (group C) from 58% to 93%. The positive predictive value was improved by ELISA-D-dimer in both groups to 75%. In order to augment the diagnostic efficacy in clinical practice the determination of Latex-D-dimer simultaneously with lung scanning is recommended.

Adult↗

PubMed1984

Assessment of pulmonary ventilation scans using xenon-127 in the diagnosis of pulmonary embolism.

Pulmonary ventilation scans using 127Xe were compared with scans using 133Xe in the diagnosis of pulmonary embolism. A perfusion scan using 99mTc -microspheres and ventilation scans with each of the xenon isotopes were performed on 44 patients referred for lung scanning to confirm or exclude a suspected clinical diagnosis of pulmonary embolism. No significant difference was found in the frequency of diagnosis of pulmonary embolism when comparing each of the ventilation scans with the corresponding perfusion scan. For reasons discussed, 127Xe may be more useful than 133Xe for pulmonary ventilation scanning.

Humans↗

PubMed1983

Adult respiratory distress syndrome following thrombolytic therapy for pulmonary embolism.

Pulmonary edema is rare in patients with pulmonary embolism and to our knowledge has not been described in association with thrombolytic therapy. We describe a patient with massive pulmonary embolism in whom the adult respiratory distress syndrome (ARDS) developed shortly after a course of streptokinase therapy. The possible association between streptokinase therapy or pulmonary embolism and ARDS should be recognized as streptokinase gains wider clinical use.

Female↗

PubMed1997

Clinical aspects of pulmonary embolism.

Pulmonary embolism is a common disease in the United States, affecting as many as 500,000 persons annually. Unfortunately, this disorder is commonly undiagnosed, resulting in significant excess morbidity and mortality. The clinical symptoms and signs caused by pulmonary embolism are nonspecific and may be confused with a variety of other cardiopulmonary disorders having similar presentations. However, accurate diagnostic tests are available for diagnosing pulmonary embolism, even in the face of coexistent cardiopulmonary disorders. This article describes the clinical characteristics of pulmonary venous thromboembolism, reviewing its typical symptoms and signs, its routine laboratory tests, and chest radiographic abnormalities.

Acute Disease↗

PubMed1989

Indications for thrombolytic therapy in acute pulmonary embolism.

Pulmonary thromboembolism is commonly misdiagnosed and is associated with significant morbidity and mortality both in the early and late stages. A major cause of late morbidity is chronic pulmonary hypertension. Although the incidence of chronic thromboembolic pulmonary hypertension is unknown, there is anatomic and physiologic evidence that it is responsible for a significant degree of the late morbidity and mortality following acute pulmonary embolism. In the absence of underlying cardiopulmonary disease, pulmonary artery pressure is a useful indicator of the severity of acute pulmonary embolism and of the patient's prognosis. Thrombolytic agents accelerate the lysis of the thromboemboli, offer an excellent alternative to emergency embolectomy, and are likely to decrease the incidence of chronic pulmonary hypertension. All currently available agents have been shown to be effective and have similar bleeding-complication profiles. In this review, we discuss the natural history and pathophysiology of pulmonary thromboembolic disease, as well as applications of thrombolytic therapy in the treatment of acute pulmonary embolism.

Journal Article↗

PubMed1985

Pleural effusion associated with pulmonary embolization.

Pulmonary embolization should be considered as a possible cause of any pleural effusion of unknown etiology. This disorder may be the one that is most commonly overlooked in the work-up of patients with pleural effusions. Although para-embolic effusions have classically been considered to be bloody exudates with a predominance of polymorphonuclear leukocytes, many such effusions have none of these characteristics. Up to 25 per cent may be transudates and the RBC count exceeds 100,000 per mm3 in fewer than 20 per cent of such effusions. The WBC may range from less than 100 to more than 50,000 cells per mm3. Characteristics of these effusions are so variable that no diagnostic patterns can be said to occur. Paraembolic effusions usually begin to resolve within a few days after institution of anticoagulant therapy, although those that are associated with parenchymal infiltrates may resolve more slowly. Unless complications occur (which are rare), pulmonary embolism with associated pleural effusion is treated no differently than is pulmonary embolism without effusion.

Anticoagulants↗

PubMed1998

[Chest pain and electrocardiogram abnormalities: consider pulmonary embolism].

Pulmonary embolism is a serious and potentially life-threatening disease that requires early recognition and treatment. In three patients, two men aged 60 and 61 and a woman aged 76, prominent severe chest pain and electrocardiographic changes suggesting ischaemic heart disease, lack of response to treatment, marked dyspnoea and haemodynamic instability eventually led to the clinical suspicion and subsequent diagnosis of pulmonary embolism. Electrocardiographic changes are indicative of right-sided overload and sometimes of arterial hypoxaemia. Although ECG changes are very frequent in cases of pulmonary embolism, the abnormalities observed are mostly nonspecific ST-T segment changes.

Chest Pain↗

PubMed1985

Interruption of the inferior vena cava for the prevention of recurrent pulmonary embolism.

Pulmonary embolism in high-risk patients may be minimized by inferior vena caval interruption by ligation, plication, intraluminal filters, or intraluminal balloons. Vena caval filter implantation is the least traumatic of all surgical methods of preventing pulmonary embolism. These nonocclusive methods are preferred to minimize the possible sequelae of venous insufficiency. The prevention of septic emboli requires complete ligation of the inferior vena cava. The transvenous approach to caval interruption by intraluminal filters is particularly useful in severely ill patients. When major surgical procedures are performed for the purpose of caval interruption, the intra-abdominal approach has greater associated mortality and morbidity than does the retroperitoneal approach. The Mobin-Uddin and Kim-Ray Greenfield filters are at present the most frequently used modalities for prevention of fatal pulmonary embolism when intervention is required. In large series of patients where intraluminal caval filters have been utilized, there has been an operative mortality of under 1 per cent, with an incidence of recurrent emboli of under 2 per cent, and an incidence of venous stasis sequelae of approximately 20 per cent. Some clinicians prefer the Greenfield filter over the Mobin-Uddin umbrella because of greater ease and flexibility of placement. In general, however, both transvenous intraluminal filters have been used effectively with acceptable mortality and morbidity, and the device used might properly be determined by the experience of the surgeon.

Anticoagulants↗

PubMed1999

[Physiopathology of pulmonary arterial hypertension and gas exchange in acute pulmonary embolism].

Pulmonary embolism alters the distribution of ventilation/perfusion relationships, and increases pulmonary vascular resistance. These changes lead to hypoxemia and hypocapnia, and eventually, to right heart failure. The thin-walled and compliant right ventricle adapts to any increase in afterload by dilatation and decreased stroke volume, but this is largely prevented or delayed by the pulmonary circulation being a low resistance, recruitable and distensible circuit. Pulmonary embolism cannot be associated with a mean pulmonary artery pressure higher than 40 mmHg. More severe pulmonary hypertension indicates the presence of a hypertrophied right ventricle in the context of preexistent cardiac or pulmonary disease. Gas exchange is initially affected because of increased ventilation/perfusion ratios in embolized lung areas, and decreased ventilation/perfusion ratios in remaining non embolized lung areas. Both physiologic shunt and physiologic dead space increase accordingly, resulting in hypoxemia and hypocapnia. However, these changes are rapidly affected by an increase in ventilation, and by a "pneumoconstriction" which decreases physiologic dead space in embolized areas. In addition, a series of secondary alterations contribute to increase perfusion to lung units with low ventilation/perfusion ratios, thereby aggravating hypoxemia, while hypocapnia persists.

Acute Disease↗

PubMed2001

Pulmonary Takayasu's arteritis masquerading as acute pulmonary embolism.

Pulmonary involvement may sometimes be the initial presentation of Takayasu's arteritis (TA). Since the signs and symptoms of pulmonary TA may be subtle and may not be easily distinguishable from other pulmonary diseases, one has to maintain a high index of suspicion. Cases of pulmonary TA mimicking chronic thromboembolism have been reported. We describe a patient with TA whose initial presentation mimicked acute pulmonary embolism. The patient presented with a 3-day history of cough and shortness of breath and had multiple bilateral perfusion defects on ventilation-perfusion scan, typical of acute pulmonary embolism. However, the constellation of clinical features, elevated erythrocyte sedimentation rate and the angiographic appearance helped us establish the correct diagnosis of pulmonary Takayasu's arteritis. At a 6-year follow-up, the patient had no worsening of pulmonary symptoms but presented with postural dizziness with angiographic evidence of carotid and innominate artery stenosis; she underwent arterial bypass grafting. In young women presenting with a clinical picture of acute pulmonary embolism without the previous history (or risk factors) of thromboembolism, pulmonary TA must be considered in the differential diagnosis.

Journal Article↗

PubMed1999

[Importance of multiplane transesophageal echocardiography in the diagnosis of pulmonary embolism].

Pulmonary thromboembolism (PTE) is a clinical entity difficult to diagnose, its setting is often confused with other pathological entities. The inexistence of isotopic techniques in most centres and the difficulty and delay in performing a pulmonary angiography leads transesophageal echocardiography (TEE) to be, a method of increasing importance for its diagnosis. From January 1996 to November 1997, echocardiographic evaluation was requested for 33 patients due to clinical suspicion of pulmonary thromboembolism. A transthoracic assessment was made previously in 21 patients (average ages 58.3 years, 52% males) which had signs of right overload (dilatation of the right cavities, anomalous movement of the intraventricular septum and pulmonary hypertension) a TEE was performed. The TEE was negative in 10 patients (TEEn) without evidence of thrombi in the trunk and main branches of the pulmonary artery (PA); there was one death on this group for repeated pulmonary microembolisms confirmed by necropsy. The TEE was positive in 11 patients (TEEp) with evidence of thrombi in the PA trunk in 3 patients, bilaterally in both branches in 3 patients and in the right branch in 5 patients. There were dilatations of the right cavities in all patients, paradoxal movement of the interventricular septum and bulging of the intra-auricular septum to the left atria. Foramen ovale was detected in 2 patients. The best visualisation of the PA was achieved in the intermediate planes between 30-70 degrees and between 90-130 degrees (plane for transverse slice of the right branch of the pulmonary artery). In 7 patients with TEEp, PTE was confirmed by CT-scan (visualisation of the thrombi in the trunk and main branches of the PA) and/or ventilation-perfusion scintigraphy and/or pulmonary angiography. In three cases of massive pulmonary embolism in young patients, with severe pulmonary hypertension, thrombolysis was performed with rTPA, under TEE control before and after rTPA in one of the cases. In conclusion, transesophageal echocardiography is an easy technique to be performed in the case of clinical suspicion of PTE. The existence of a negative examination does not invalidate the existence of PTE since only the trunk and the main branches of the PA are accessible by this technique. The detection of thrombi at this level in patients with clinical suspicion of massive pulmonary embolism confirms the diagnosis and supports the indication of thrombolysis.

Adult↗

PubMed1994

[Role of low molecular weight heparins for treating non-massive pulmonary embolism].

Pulmonary revascularization after submassive pulmonary embolism can be achieved within 14 days in 50% of the patients treated with intravenous heparin then oral anticoagulants. Recurrence is estimated at 5% and risk of severe haemorrhage at 5 to 6%. For deep vein thrombosis, low-molecular weight heparins are at least as effective as unfractionated heparin and have a comparable or lower rate of complications. For submassive pulmonary embolism, two low-molecular weight heparins (calcium nadroparin and sodium dalteparin) have been compared with unfractionated heparin. Pulmonary revascularization on day 8 was about 68% for all treatment regimens. No cases of recurrent embolism were recorded and no severe haemorrhage occurred in patients given low-molecular weight heparin but did occur in 6% of those given unfractionated heparin. These early results, together with easy subcutaneous administration and the absence of daily dose adaptation requirement, suggest that low-molecular weight heparins could play a major role in treating submassive pulmonary embolism and thromboembolism in general.

Biological Availability↗

PubMedDate not supplied

Syncope as an emergency department presentation of pulmonary embolism.

Pulmonary embolism presenting as an isolated syncopal spell can be a difficult clinical correlation to make. We present three cases of pulmonary embolism-induced syncope and review the pathophysiology and diagnostic considerations in this setting. Pulmonary embolism should be considered in the differential diagnosis of every syncopal event that presents to the emergency department, even in the face of cardiac dysrhythmias and normal pulse oximetry values.

Adult↗

PubMed1996

[Spiral CT in acute pulmonary embolism].

Pulmonary embolism is a frequent and potentially life-threatening event with uncharacteristic clinical manifestations. Diagnosis is commonly established by ventilation/perfusion scintigraphy and pulmonary angiography. Both methods, however, carry substantial drawbacks. Therefore, clinicians claim that there is a need for an accurate and non-invasive diagnostic modality. Spiral CT of the pulmonary arteries is a recent modality, that allows reliable visualization of emboli in pulmonary arteries up to fourth-order branches. This paper reviews the technical aspects, typical findings and diagnostic pitfalls of this recent technique. The potential role of spiral CT in the screening of patients with suspected pulmonary embolism is discussed and selected cases are presented.

Algorithms↗

PubMed1992

[Acute pulmonary embolism and pulmonary infarction].

32 cases of pulmonary embolism were reported, 18 cases had been autopsied (massive pulmonary embolism 9 cases. moderate pulmonary embolism 23 cases). The incidence risk factors pathogenesis, clinical manifestations of pulmonary embolism were presented. The relation between pulmonary embolism and pulmonary infarction and treatment of massive pulmonary infarction were discussed.

Acute Disease↗

PubMed2002

Pharmacotherapy of pulmonary embolism.

Pulmonary embolism (PE) and deep vein thrombosis are common causes of illness and death. The pharmacological approach to pulmonary embolism includes the use of anticoagulants, unfractionated heparin for the acute phase, and oral anticoagulants for prophylaxis. In massive PE, the use of thrombolytic agents is suggested to reduce systemic hypotension and right ventricular failure and increase cardiac output. Thrombolytic agents act on pulmonary vascular obstruction. In clinical practice, thrombolytic therapy is recommended in case of massive embolism with haemodynamic failure. Recent studies suggest the use of thrombolytic drugs in patients with normal systemic blood pressure who show right ventricular dysfunction at echocardiographic examination. A large randomised trial on lytic agents in submassive PE is therefore needed. Anticoagulants were primarily indicated for prevention of recurrences. Due to the development of low molecular weight heparin, the role of anticoagulants needs to be re-evaluated.

Anticoagulants↗

PubMedDate not supplied

Digital angiography in pulmonary embolism.

Pulmonary digital subtraction angiography was diagnostic in 98.3 per cent of patients with possible acute pulmonary embolism. The procedure was well tolerated even in severely ill patients. A large image intensifier made simultaneous imaging of both lungs possible, reducing the number of contrast injections necessary. Small volumes of low iso-osmolar concentration of modern contrast media were used. There was no need for catheterization of the pulmonary artery. Theoretical considerations and our limited experience indicate that this will reduce the number of complications compared with conventional pulmonary angiography. The procedure is rapidly performed and the diagnostic accuracy high. This makes digital subtraction angiography cost effective. Digital pulmonary angiography can be recommended as the primary diagnostic method in most patients with possible pulmonary embolism.

Adult↗

PubMed1990

Modern treatment of pulmonary embolism.

Pulmonary embolism is diagnosed over 100,000 times yearly in the United States and is the recognized primary cause of death in at least 10,000 cases. Thrombolytic therapy has been successful in reducing clot burden substantially; however, clinical data are lacking to indicate that thrombolytic therapy improves mortality rates in patients with pulmonary emboli or that the pharmacologic removal of clot will improve future quality of life. The use of thrombolytic agents has been limited by the potential for producing hemorrhagic complications. This paper discusses the pharmacology of numerous thrombolytic agents and their clinical use in research studies intended to determine the safest and most efficacious regimens. Recombinant t-PA infusions appear quite safe and produce very rapid lyses of pulmonary emboli. Innovative administration regimens of urokinase also appear promising. The availability of extremely safe and efficacious treatment regimens should allow for large epidemiologic studies to be conducted to determine whether thrombolytic therapy will improve the morbidity and mortality of pulmonary embolism.

Fibrinolytic Agents↗