Modern Treatment of Pulmonary Embolism
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Copyright #ERS Journals Ltd 2002 Eur Respir J 2002; 19: Suppl. 35, 22s–27s European Respiratory Journal DOI: 10.1183/09031936.02.00271102 ISSN 0904-1850 Printed in UK – all rights reserved ISBN 1-904097-21-9 Modern treatment of pulmonary embolism S.Z. Goldhaber Modern treatment of pulmonary embolism. S.Z. Goldhaber. #ERS Journals Ltd 2002. Correspondence: S.Z. Goldhaber ABSTRACT: Modern treatment of acute pulmonary embolism requires rapid and Cardiovascular Division accurate diagnosis followed by risk stratification to devise an optimal management Brigham and Women9s Hospital strategy. Patients at low risk have good outcomes simply with intensive anticoagulation Harvard Medical School Boston treatment. Higher-risk patients may require more aggressive intervention with MA 02115 thrombolysis or embolectomy. USA Clinical risk factors for an adverse outcome include increasing age, cancer, con- Fax: 1 617 2645144 gestive heart failure, systemic arterial hypotension, chronic obstructive pulmonary Email: [email protected] disease and right ventricular dysfunction. A promising approach is the Geneva Prognostic Score, which is based upon a rapid clinical assessment. Keywords: Deep vein thrombosis On physical examination, signs of right ventricular failure, including distended embolectomy pulmonary embolism jugular veins and a right-sided S3 gallop, should be looked for. The electrocardiogram may show evidence of right ventricular strain with a new right bundle branch block or T thrombolysis wave inversion in leads V1–V4. The troponin level may be elevated as a marker of Received: August 10 2001 cardiac injury and right ventricular microinfarction, even in the absence of coronary Accepted August 10 2001 artery disease. The most useful imaging marker of high risk is the presence of moderate or severe right ventricular dilatation and hypokinesis on the echocardiogram, especially with progressively worsening right ventricular function despite intensive anticoagulation treatment. Patients at high risk should be considered for thrombolytic therapy or embolectomy rather than management with anticoagulation therapy alone. Special care must be taken to avoid thrombolytic therapy among patients who might be susceptible to intracranial haemorrhage. Intracranial haemorrhage reached a surprisingly high rate of 3.0% in the International Cooperative Pulmonary Embolism Registry of 2,454 prospectively evaluated acute pulmonary embolism patients at 52 hospitals in seven countries. An alternative approach to patients at high risk is a catheter-based or open surgical embolectomy. It is crucial to refer these patients as quickly as possible, rather than delaying intervention until cardiogenic shock has ensued. Fortunately the current tools for risk stratification provide an "early window" for prognostication and can help the coordination of a definitive treatment plan with optimal results. Eur Respir J 2002; 19: Suppl. 35, 22s–27s. Modern treatment of pulmonary embolism (PE) countries. The aims were to establish a 3-month all- relies upon rapid identification, risk stratification cause mortality rate and identify factors associated and anticoagulation treatment as the foundations of with death [1]. therapy. Patients identified as at high risk of adverse The 3-month follow-up was completed in 98% of outcomes often benefit from early intervention with patients. The all-cause mortality rate was 11.4% thrombolytic therapy or embolectomy. Depending during the first 2 weeks after diagnosis and 17.4% at upon the severity and specific problems related to the 3 months. After exclusion of patients in whom PE was acute PE, special expertise might be required from first discovered at autopsy, the mortality rate was radiologists, vascular medicine specialists, cardio- 15.3%. Importantly, most patients who died had logists, pulmonologists, critical care intensivists, inter- succumbed to PE, and not to other comorbidities ventional angiographers or cardiac surgeons. Optimal such as cancer. Specifically, regarding the most management requires a coordinated interdisciplinary common causes of death, 45% of deaths were ascribed approach that follows algorithms established by to PE, 18% were due to cancer, 12% were sudden consensus at individual hospitals. cardiac deaths (which undoubtedly included some undiagnosed PEs) and 12% were considered due to respiratory failure, which may also have included Clinical outcome some deaths due to PE. Nonfatal recurrent PE occurred in 4% of patients. The International Cooperative Pulmonary Embo- Age w70 yrs increased the likelihood of death by lism Registry (ICOPER) enrolled 2,454 consecutive 60%. Six other risk factors independently increased PE patients from 52 participating hospitals in seven the likelihood of mortality two- to three-fold (table 1): MODERN TREATMENT OF PE 23s Table 1. – Risk factors for mortality after pulmonary Table 2. – The Bounameaux pulmonary embolism point embolism in the International Cooperative Pulmonary score Embolism Registry: a multivariate analysis Variable Point score Variable Hazard ratio (95% CI) Cancer z2 Heart failure z1 Age w70 yrs 1.6 (1.1–2.3) Prior DVT z1 Cancer 2.3 (1.5–3.5) Hypotension z2 Clinical congestive heart failure 2.4 (1.5–3.7) Hypoxaemia z1 Chronic obstructive pulmonary disease 1.8 (1.2–2.7) DVT on ultrasound z1 Systolic blood pressure v90 mmHg 2.9 (1.7–5.0) Respiratory frequency v20 breathe?min-1 2.0 (1.2–3.2) DVT: deep vein thrombosis. (From [3].) Right ventricular hypokinesis 2.0 (1.3–2.9) The final model included 815 patients. CI: confidence view; 2) a right ventricular end-diastolic diameter of interval. (From [1].) w30 mm; and 3) paradoxical right ventricular septal systolic motion. Among 209 consecutive PE patients, 65 (31%) pre- cancer, clinical congestive heart failure, chronic sented with the combination of normal systemic obstructive pulmonary disease, systemic arterial hypo- arterial pressure and echocardiographic evidence of tension with a systolic blood pressure of v90 mmHg, tachypnoea (defined as w20 breaths?min-1) and right right ventricular dysfunction. Of this group, six (10%) ventricular hypokinesis on the echocardiogram, an developed cardiogenic shock within 24 h of diagnosis especially useful sign for identifying high-risk patients and three (5%) died during the initial hospitalization. who might be suitable for aggressive interventions Conversely, none of the 97 normotensive patients with such as thrombolytic therapy or embolectomy. normal right ventricular function on echocardiogra- In Japan, a recently completed PE registry showed phy suffered PE-related mortality [4]. remarkable similarities to the ICOPER [2]. The in- When Doppler echocardiography gives an estimated hospital mortality rate was 14% among the 533 PE pulmonary artery systolic pressure of w50 mmHg at patients enrolled in the registry. Predictors of morta- the time of PE diagnosis, chronic pulmonary hyper- lity included male sex, cardiogenic shock, cancer and tension is likely to ensue. Such patients are less likely prolonged immobilization. to survive during the ensuing 5 yrs than those whose pulmonary arterial pressure and right ventricular function normalize during the first 5–6 weeks after the acute PE [4]. Risk stratification Right ventricular microinfarction can result from the right ventricular pressure overload caused by In patients with massive PE, right ventricular dys- acute PE and can be diagnosed by means of elevated function can be identified at the bedside. Findings troponin levels. Such patients may have no underlying include a left parasternal heave, distended jugular veins, and a systolic murmur of tricuspid regurgitation atherosclerosis of the right coronary artery. Troponin that increases with inspiration and is best heard at the level elevation in acute PE is associated with right left lower sternal border. The electrocardiogram may ventricular dysfunction [5]. Furthermore, troponin demonstrate a new right bundle branch block or other level elevations help identify PE patients with an evidence of right ventricular strain, such as inverted T otherwise poor prognosis in whom aggressive inter- waves in leads V1–V4. vention may be warranted. In a prospective study of The Geneva Risk Score was developed using data 56 PE patients, those with elevated troponin levels from 296 PE patients [3]. It predicts the risk of major were more likely to die, suffer cardiogenic shock, adverse outcomes, defined as death, recurrent PE and require inotropic agents and need mechanical ventila- major bleeding. Six prognostic variables are consi- tion [6]. The mortality rate from PE was 44% in dered. Patients receive a point for each variable and troponin-positive patients (i.e. those with elevated an estimate of the likelihood of an adverse outcome (tables 2 and 3). Cancer and hypotension receive the Table 3. – The Bounameaux adverse outcome score greatest weight, followed by congestive heart failure, prior venous thromboembolism, hypoxaemia and Points Patients evidence of acute deep vein thrombosis (DVT) on ultrasound examination. n cumulative % adverse outcome % (n) Right ventricular dysfunction has been reliably established as a predictor of increased likelihood of 0 52 19.4 0 (0) death from PE. Identification of moderate or severe 1 79 48.9 2.5 (2) right ventricular dysfunction is usually carried out 2 49 67.2 4.1 (2) qualitatively and is ordinarily readily apparent to 3 56 88.1 17.8 (10) observers with only modest experience. The most 4 22 96.3 27.3 (6) 5 7 98.9 57.1 (4) commonly employed quantitative