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Fifty per cent of patients with pulmonary embolism can be treated as outpatients

2010; Elsevier BV; Volume: 8; Issue: 11 Linguagem: Inglês

10.1111/j.1538-7836.2010.04055.x

1538-7933

Trevor Baglin,

Acute Ischemic Stroke Management

See also Kovacs MJ, Hawel JD, Rekman JF, Lazo‐Langner A. Ambulatory management of pulmonary embolism: a pragmatic evaluation. This issue, pp 2406–11; Erkens PMG, Gandara E, Wells P, Shen AY‐H, Bose G, Le Gal G, Rodger M, Prins MH, Carrier M. Safety of outpatient treatment in acute pulmonary embolism. This issue, pp 2412–7. See also Kovacs MJ, Hawel JD, Rekman JF, Lazo‐Langner A. Ambulatory management of pulmonary embolism: a pragmatic evaluation. This issue, pp 2406–11; Erkens PMG, Gandara E, Wells P, Shen AY‐H, Bose G, Le Gal G, Rodger M, Prins MH, Carrier M. Safety of outpatient treatment in acute pulmonary embolism. This issue, pp 2412–7. If at least 50% of patients presenting with symptomatic pulmonary embolism (PE) can be treated as outpatients, the question is which 50%? In this issue of the journal, two studies further validate the practice of treating selected patients with PE as outpatients [1Kovacs M.J. Hawel J.D. Rekman J.F. Lazo‐Langner A. Ambulatory management of pulmonary embolism: a pragmatic evaluation.J Thromb Haemost. 2010; 8: 2406-11Abstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar, 2Erkens P.M.G. Gandara E. Wells P. Shen A.Y.H. Bose G. Le Gal G. Rodger M. Prins M.H. Carrier M. Safety of outpatient treatment in acute pulmonary embolism.J Thromb Haemost. 2010; 8: 2412-7Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar]. In the RIETE registry, fatal PE occurred in 12% of patients presenting with massive PE and in 3% of patients with non‐massive PE [3Laporte S. Mismetti P. Decousus H. Uresandi F. Otero R. Lobo J.L. Monreal M. Clinical predictors for fatal pulmonary embolism in 15,520 patients with venous thromboembolism: findings from the Registro Informatizado de la Enfermedad TromboEmbolica venosa (RIETE) Registry.Circulation. 2008; 117: 1711-16Crossref PubMed Scopus (561) Google Scholar]. However, as the majority of patients with acute PE are normotensive at presentation, the deaths among patients with non‐massive PE represent 90% of all embolic deaths. Therefore, the dilemma for clinicians who treat patients with deep vein thrombosis at home [4Schraibman I.G. Milne A.A. Royle E.M. Home versus in‐patient treatment for deep vein thrombosis.Cochrane Database Syst Rev. 2001; Crossref PubMed Google Scholar] is whether it is also safe to treat patients with submassive PE at home, and if so which patients. A solution is to stratify patients by using risk models for early embolic death and treat accordingly, with escalation of therapy for high‐risk patients and identification of low‐risk patients who might be safely treated as outpatients [5Aujesky D. Hughes R. Jimenez D. Short‐term prognosis of pulmonary embolism.J Thromb Haemost. 2009; 7: 318-21Crossref PubMed Scopus (23) Google Scholar]. Death attributable to acute PE results from an acute fall in cardiac output. This is caused by a combination of physical obstruction of the pulmonary vascular bed by thrombus and the release of vasoconstrictive mediators, which also produce vascular shunting. In patients without pre‐existing heart or lung disease, the hemodynamic disturbance correlates with the extent of obstruction of the pulmonary circulation [6McIntyre K.M. Sasahara A.A. Determinants of right ventricular function and hemodynamics after pulmonary embolism.Chest. 1974; 65: 534-43Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar]. With only 5–15% obstruction, hypoxemia occurs. When obstruction reaches 25%, pulmonary hypertension (pulmonary artery pressure greater than 20 mmHg) occurs, and right ventricular dysfunction becomes evident. When 40% obstruction occurs, pulmonary hypertension is critical, and with more than 50% obstruction, the pulmonary artery pressure begins to fall. At this point, small increases in pulmonary arterial occlusion lead to acute systemic hypotension and shock, owing to inadequate filling of the left ventricle. It is apparent that hemodynamic status at presentation is the most important prognostic factor. Approximately 40% of patients have right ventricular dysfunction at presentation and are at higher risk of a fatal embolic event than patients without dysfunction [7Sanchez O. Trinquart L. Colombet I. Durieux P. Huisman M.V. Chatellier G. Meyer G. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: a systematic review.Eur Heart J. 2008; 29: 1569-77Crossref PubMed Scopus (430) Google Scholar]. Elevated levels of cardiac biomarkers, such as troponins and brain natriuretic peptides, also identify patients with ventricular strain and a worse prognosis [8Becattini C. Vedovati M.C. Agnelli G. Prognostic value of troponins in acute pulmonary embolism: a meta‐analysis.Circulation. 2007; 116: 427-33Crossref PubMed Scopus (607) Google Scholar, 9Klok F.A. Mos I.C. Huisman M.V. Brain‐type natriuretic peptide levels in the prediction of adverse outcome in patients with pulmonary embolism: a systematic review and meta‐analysis.Am J Respir Crit Care Med. 2008; 178: 425-30Crossref PubMed Scopus (288) Google Scholar]. Despite studies that have examined the prognostic accuracy of echocardiography combined with cardiac biomarkers, the safety of outpatient treatment of low‐risk PE patients based on these methods remains uncertain [5Aujesky D. Hughes R. Jimenez D. Short‐term prognosis of pulmonary embolism.J Thromb Haemost. 2009; 7: 318-21Crossref PubMed Scopus (23) Google Scholar]. Furthermore, the availability of echocardiography and the availability and timeliness of reporting of biomarkers in practice is variable. Consequently, a natural step is to develop simple clinical prediction models that can be used at the bedside [10Wicki J. Perrier A. Perneger T.V. Bounameaux H. Junod A.F. Predicting adverse outcome in patients with acute pulmonary embolism: a risk score.Thromb Haemost. 2000; 84: 548-52Crossref PubMed Scopus (311) Google Scholar]. The most extensively validated model is the Pulmonary Embolism Severity Index (PESI), which stratifies patients into five risk categories of all‐cause mortality on the basis of 11 clinical parameters, without the need for echocardiography but including blood gas analysis [11Aujesky D. Roy P.M. Le Manach C.P. Verschuren F. Meyer G. Obrosky D.S. Stone R.A. Cornuz J. Fine M.J. Validation of a model to predict adverse outcomes in patients with pulmonary embolism.Eur Heart J. 2006; 27: 476-81Crossref PubMed Scopus (229) Google Scholar, 12Chan C.M. Woods C. Shorr A.F. The validation and reproducibility of the pulmonary embolism severity index.J Thromb Haemost. 2010; 8: 1509-14Crossref PubMed Scopus (102) Google Scholar]. Fatal embolism is rare in patients in the low‐risk classes. With or without the use of a validated prediction model, it has become common practice in many hospitals to treat patients with non‐massive PE as outpatients at the discretion of the treating physician. This was the current practice at each of the institutes from which fatality rates are reported in this issue of the journal. Essentially, patients who were hemodynamically stable and did not require oxygen therapy were treated as outpatients. In each study, approximately 50% of patients presenting with PE qualified for this treatment, giving a total of nearly 600 patients. None of the patients died of fatal emboli within 3 months. Thirteen patients suffered from recurrent thromboembolic events, but a low non‐fatal clinical recurrence rate is expected in patients treated with anticoagulant therapy. The incidence of events was not different from that observed in patients treated as inpatients. These two reports are important, because they reflect current clinical practice in many parts of the world and indicate that outpatient treatment is relatively safe, and hence reasonable, in patients with PE who have a normal pulse and blood pressure and do not require oxygen therapy. Is this too simple to be true? These were retrospective analyses of outcome in patients who were considered to be low risk by the treating physicians. The influence of the clinical acumen of the treating physicians cannot be determined from these studies, and so a degree of caution is necessary. Until a simple prognostic prediction model based on hemodynamic status and oxygen requirement alone is shown to be safe, independently of clinical acumen, then the decision to treat patients with PE as outpatients should be made by experienced clinicians. It is probably prudent to define the criteria, such as pulse < 100 min–1 and systolic blood pressure > 100 mmHg, and to provide clear instructions to patients to return to hospital if they develop new symptoms, for example chest pain, difficulty in breathing, light‐headedness (or syncope) or palpitations. Additionally, patients with comorbid conditions identified as poor prognostic factors in the PESI score (cancer, heart failure or chronic lung disease) who do not require hospitalization for treatment of the co‐morbid condition itself may be at relatively higher risk of a severe embolic event and might be best treated initially in hospital. This may have happened in practice in the institutes from which the results are reported. The interpretation of these studies might reasonably be summarized as follows: at least 50% of patients presenting acutely with symptomatic PE can be treated as outpatients, and these patients are those without serious comorbid conditions who have a normal pulse and blood pressure and do not require oxygen therapy. Some clinicians may be uncomfortable with such a simple risk stratification, and until a direct comparison of this approach with a more sophisticated estimate of risk, such as PESI, is conducted, clinicians will probably be divided by what they consider to be appropriate and acceptable. That aside, it is certain that outpatient treatment of PE will continue, and is only likely to increase with the introduction of new oral anticoagulant drugs that obviate the need for injections of low molecular weight heparin and monitoring of vitamin K antagonists. At the very least, these studies provide some assurance that appropriate clinical assessment and early discharge of selected patients with PE is safe, and that up to 50% of patients may be treated at home. Very occasionally, a low‐risk patient will die as a result of further embolism. In one study, mortality following cardiac arrest resulting from PE was more than 90%, regardless of whether the arrest occurred in or out of hospital and regardless of whether thrombolysis was given [13Kurkciyan I. Meron G. Sterz F. Janata K. Domanovits H. Holzer M. Berzlanovich A. Bankl H.C. Laggner A.N. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome.Arch Intern Med. 2000; 160: 1529-35Crossref PubMed Scopus (267) Google Scholar]. The authors state that he has no conflict of interest.