Intended for healthcare professionals

Practice Easily Missed?

Pulmonary embolism

BMJ 2010; 340 doi: https://doi.org/10.1136/bmj.c1421 (Published 13 April 2010) Cite this as: BMJ 2010;340:c1421
  1. Guy Meyer, MD123,
  2. Pierre-Marie Roy, MD PhD4,
  3. Serge Gilberg, MD1,
  4. Arnaud Perrier, MD5
  1. 1Université Paris Descartes, Paris, France
  2. 2Assistance Publique Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Service de Pneumologie et Soins Intensifs, Paris, France
  3. 3INSERM Unité 765, Paris, France
  4. 4Université d’Angers, IFR 132 et Centre Hospitalier Universitaire, Service d’accueil et traitement des urgences, Angers, France
  5. 5Division of General Internal Medicine, Geneva University Hospital, Switzerland
  1. Correspondence to: Dr G Meyer, Service de Pneumologie, Hopital Europeen Georges Pompidou, 20 rue Leblanc, 75015 Paris, France, guy.meyer{at}egp.aphp.fr
  • Accepted 21 February 2010

Complete occlusion of a peripheral pulmonary artery usually results in a pulmonary infarction with pleuritic chest pain and haemoptysis. When the blood clot is lodged in more proximal pulmonary arteries and is not occlusive, pulmonary infarction does not occur and pulmonary embolism might present as isolated dyspnoea. Massive pulmonary embolism is caused by large bilateral proximal clots resulting in haemodynamic collapse.1

Case scenario

A non-smoking, previously well woman in her 70s complained of recent onset of dyspnoea. She had no cardiovascular or thromboembolic risk factors and clinical examination was normal apart from a heart rate of 96 beats per minute. With no clear explanation for the symptoms, her general practitioner applied a decision rule (table) to evaluate the clinical probability of pulmonary embolism. The result was intermediate, prompting him to request a D-dimer level, which was raised. He referred the patient to hospital, where pulmonary embolism was confirmed on computed tomography.

View this table:

How common is it?

  • The incidence of diagnosed pulmonary embolism increases with age

  • The annual rate is about 1 in 10 000 in individuals below 40 years of age and can reach 1 in 100 in patients over 80 years2 3

  • According to autopsy studies, the disease is clinically suspected in less than half of fatal cases, so the real incidence is probably underestimated4

  • However, most episodes of pulmonary embolism carry a low mortality risk (about 1%) when properly diagnosed and treated

  • Massive pulmonary embolism represents only 5% of all cases of pulmonary embolism and is fatal in about 40% of patients1

Why is it missed?

The classic triad of pleuritic chest pain, dyspnoea, and haemoptysis occurs in less than 10% of patients, but the most common symptoms (dyspnoea, chest pain) are non-specific. In 40% of cases, major thromboembolic risk factors are absent. Clinical signs of deep vein thrombosis are observed in only 15% of patients and haemoptysis in only 4.5-11% of cases.1 5 Pulmonary infarction with fever may mimic pneumonia. Chest pain reproducible on palpation also does not rule out pulmonary embolism.6 In addition, abnormalities in chest radiographs or electrocardiograms are non-specific; sinus tachycardia is the most common electrocardiogram abnormality whereas right heart strain is observed only in severe cases. Arterial partial pressure of oxygen and the alveolar-arterial oxygen gradient are normal in 20% of patients; hypoxaemia with hypocapnia is the most common abnormality in blood gas pressures, but is non-specific.1 Symptoms and initial test findings can also be ascribed to underlying disease such as heart failure or chronic lung disease.7

Why does it matter?

Without adequate treatment, pulmonary embolism recurs in 30-50% of cases, with a case fatality rate of between 10-45%.8 Non-diagnosed cases therefore have a high risk of recurrence and death.

How is it diagnosed?

Consider a diagnosis of pulmonary embolism in patients with:

  • Dyspnoea, pleuritic chest pain, and haemoptysis

  • Any chest symptoms and clinical features suggesting deep vein thrombosis

  • Dyspnoea or chest pain, and a major risk factor for pulmonary embolism (table)

  • Unexplained dyspnoea, chest pain, or mild haemoptysis, whether or not they have minor risk factors for pulmonary embolism.

Once the diagnosis is suspected, conduct a clinical or pre-test probability assessment based on risk factors and clinical features, as post-test probability depends on test characteristics and pre-test probability. The assessment can be done either by implicit clinical judgment or by using a validated prediction rule such as the Geneva or Wells scores (table). These rules have a fair accuracy in large prospective series of patients with suspected pulmonary embolism: prevalence of pulmonary embolism is about 10% in patients with a low clinical probability, 30% in those with a moderate clinical probability, and 65% in those with a high clinical probability.9 10

Investigations

  • Plasma D-dimer measurement is the next step for most outpatients. D-dimer levels are raised in many situations and a positive test result is non-specific. However, based on a negative likelihood ratio of 0.08, a negative result for a quantitative, enzyme linked immunosorbent assay (ELISA) D-dimer test excludes pulmonary embolism and the need for further testing in about 30% of patients, provided that the clinical probability is low or moderate.11 Quantitative latex based and whole blood qualitative D-dimer assays have a negative likelihood ratio of 0.20 to 0.30 and allow exclusion of pulmonary embolism only in patients with a low clinical probability.11 In patients with a high clinical probability, no D-dimer test is sensitive enough to rule out pulmonary embolism.

  • Refer patients with a positive D-dimer test for multidetector spiral computed tomography. This procedure confirms pulmonary embolism when an intraluminal defect is seen in several subsegmental arteries or in a more proximal pulmonary artery (figure).12 A ventilation and perfusion lung scan may be selected when multidetector spiral computed tomography is contraindicated (renal failure, allergy to contrast medium) but yields a high rate of inconclusive results. Finally, compression ultrasonography of the leg veins showing a proximal deep vein thrombosis in a patient with thoracic symptoms allows confirmation of pulmonary embolism without further testing, but has a low diagnostic yield, except in patients with clinical symptoms of deep vein thrombosis.9 11

  • Excluding pulmonary embolism on inappropriate criteria, for example, low D-dimer reading in a patient with a high clinical probability or a low probability lung scan in a patient with a high clinical probability, exposes patients to an increase risk of it recurring and death.7

Figure1

Fig Multidetector spiral computed tomogram showing bilateral filling defects [arrowed] in the pulmonary artery

How is it managed?

In patients with a high clinical probability, start anticoagulant treatment before objective confirmation of the disease. Low molecular weight heparin and fondaparinux are the first line options but are contraindicated in patients with severe renal insufficiency. In these patients, unfractionated heparin is still used for initial treatment.13 Start vitamin K antagonists on the first day and give for at least three months.13

Key points

  • Suspect pulmonary embolism in cases of unexplained dyspnoea or chest pain, or both, even in the absence of obvious risk or triggering factors

  • Clinical probability assessment is the cornerstone of all validated diagnostic strategies

  • Always conduct objective tests to confirm or exclude suspected pulmonary embolism. Most patients diagnosed and treated according to guidelines have an uneventful outcome. On the other hand, unrecognised and untreated pulmonary embolism carries a 50% risk of recurrence and a 25% risk of death

Notes

Cite this as: BMJ 2010;340:c1421

Footnotes

  • This is a series of occasional articles highlighting conditions that may be more common than many doctors realise or may be missed at first presentation. The series advisers are Anthony Harnden, university lecturer in general practice, Department of Primary Health Care, University of Oxford, and Richard Lehman, general practitioner, Banbury. If you would like to suggest a topic for this series please email us (easilymissed.bmj{at}bmjgroup.com).

  • Contributors: All authors contributed equally to the design and drafting and approved the final version of the submitted article. All authors are guarantors.

  • Competing interests: None declared.

  • Provenance and peer review: Not commissioned; externally peer reviewed.

  • Patient consent not required (patient anonymised, dead, or hypothetical).

References

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