3 Diagnosis

The diagnosis of pulmonary embolism (PE), suspected on the basis of shortness of breath and chest pain, with or without an abnormal X-ray, can be confirmed by a medical test called a "ventilation-perfusion scan" (or V/Q scan), which shows that some areas of the lung are being ventilated but not perfused with blood (due to obstruction by a clot).

In low/moderate suspicion of PE, a normal ( D-dimer) blood test is enough to exclude the possibility of PE (Bounameaux et al 1994).

Instead of the V/Q scan spiral computed tomography (spiral CT) is increasingly being used, especially when other lung disorders are part of the differential diagnosis.

In massive PE, dysfunction of the right side of the heart can be seen on echocardiography.

Lower limb ultrasound can be used as a surrogate. The presence of deep venous thrombosis is in itself enough to warrant anticoagulation, without requiring the expensive V/Q or spiral CT scans.

4 Further analysis

When a PE is being suspected, a number of blood tests are also done, in order to exclude important secondary causes of PE. This includes a full blood count, clotting status (PT, APTT, TT), and some screening tests ( Erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes). If one of these is abnormal, further investigations might be warranted.

5 Treatment

Anticoagulation is the mainstay of treatment. ( Heparin or low molecular weight heparin, and later warfarin or coumadins are given, generally for 6 months.

Massive PE, as confirmed by spiral CT or echocardiography, is treated with thrombolysis.

Acutely, supportive treatments, such as oxygen or analgesia, are often required.

6 Prognosis

Prognosis depends on the amount of lung that is affected and on the co-existence of other debilitating conditions. Chronic embolisation to the lung can lead to pulmonary hypertension.

After a first PE, the search for secondary causes is usually brief. Only when a second PE occurs, and especially when this happens while still under anticoagulant therapy, a further search for underlying conditions is undertaken. This will include testing (see above for full list) for Factor V Leiden mutation, antiphospholipid antibodies, protein C and S and antithrombin levels, and later prothrombin mutation, MTHFR mutation, Factor VIII concentration and rarer inherited coagulation abnormalities.

7 History

After a trial in 1960 (Baritt & Jordan), anticoagulation became the most important therapeutic intervention in pulmonary embolism. This study revealed that without treatment, mortality of pulmonary embolism was 26%. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957. This study rapidly set the pace, considering that no other study of anticoagulation in PE ever had a placebo group (as this would have been unethical).

8 References

• Barritt DW, Jorden SC. Anticoagulant drugs in the treatment of pulmonary embolism: a controlled trial. Lancet 1960;1:1309-1312. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids= } Medline abstract] (PMID }).
• Bounameaux H, de Moerloose P, Perrier A, Reber G. Plasma measurement of D-dimer as diagnostic aid in suspected venous thromboembolism: an overview. Thromb Haemost. 1994 Jan;71(1):1-6. (Medline abstract)

Health science - Medicine - Hematology

Hematological malignancy and White blood cells

Lymphoma ( Hodgkin's disease, NHL) - Leukemia ( ALL, AML, CLL, CML) - Multiple myeloma - MDS - Myelofibrosis - Myeloproliferative disease ( Thrombocytosis, Polycythemia) - Neutropenia

Red blood cells

Anemia - Hemochromatosis - Sickle-cell anemia - Thalassemia - other hemoglobinopathies

Coagulation and Platelets

Thrombosis - Deep venous thrombosis - Pulmonary embolism - Hemophilia - ITP - TTP

Hematology Pulmonology

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