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Pulmonary embolism



Pulmonary embolism
Classification & external resources
ICD-10 I26.
ICD-9 415.1
DiseasesDB 10956
MedlinePlus 000132
eMedicine med/1958  emerg/490 radio/582

Pulmonary embolism (PE) is a blockage of the pulmonary artery (or one of its branches), usually when a venous thrombus (blood clot from a vein), becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs. This process is termed thromboembolism.

Symptoms may include difficulty breathing, pain in the chest during breathing, and in more severe cases collapse, circulatory instability and sudden death. Treatment, usually, is with anticoagulant medication, such as heparin and warfarin, and rarely (in severe cases) with thrombolysis or surgery. In other, rarer forms of pulmonary embolism, material other than a blood clot is responsible; this may include fat or bone (usually in association with significant trauma), air (often when diving), clumped tumor cells, and amniotic fluid (affecting mothers during childbirth).

Additional recommended knowledge

Contents

Signs, symptoms and risk factors

Clinical presentation

Signs of PE are sudden-onset dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of "pleuritic" nature (worsened by breathing), cough, hemoptysis (coughing up blood), and may aid in the diagnosis. More severe cases may be associated with cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability. About 15% of all cases of sudden death are attributable to PE.

Risk factors

The most common sources of embolism are proximal leg deep venous thrombosis (DVTs) or pelvic vein thromboses. Any risk factor for DVT also increases the risk that the venous clot will dislodge and migrate to the lung circulation, which happens in up to 15% of all DVTs. The conditions are generally regarded as a continuum termed venous thromboembolism (VTE).

The development of thrombosis is classically due to a group of causes named Virchow's triad (alterations in blood flow, factors in the vessel wall and factors affecting the properties of the blood). Often, more than one risk factor is present.

Diagnosis

The diagnosis of PE is based primarily on validated clinical criteria combined with selective testing because the typical clinical presentation (shortness of breath, chest pain) cannot be definitively differentiated from other causes of chest pain and shortness of breath.

Risk prediction

The decision to do medical imaging is usually based on clinical grounds, i.e. the medical history, symptoms and findings on physical examination.

Development of the Wells score

The most commonly used method to predict clinical probability, the Wells score, is clinical prediction rule, whose use is complicated by multiple versions being available. In 1995, Wells et al initially developed a prediction rule (based on a literature search) to predict the likelihood of PE, based on clinical criteria.[1] The prediction rule was revised in 1998[2] This prediction rule was further revised when simplified during a validation by Wells et al in 2000.[3] In the 2000 publication, Wells proposed two different scoring systems using cutoffs of 2 or 4 with the same prediction rule.[3] In 2001, Wells published results using the more conservative cutoff of 2 to create three categories.[4] An additional version, the "modified extended version", using the more recent cutoff of 2 but including findings from Wells's initial studies[1][2] were proposed.[5] Most recently, a further study reverted to Wells's earlier use of a cutoff of 4 points[3] to create only two categories.[6]

There are additional prediction rules for PE, such as the Geneva rule. More importantly, the use of any rule is associated with reduction in recurrent thromboembolism.[7]

Wells score

The Wells score:[8]

  • clinically suspected DVT - 3.0 points
  • alternative diagnosis is less likely than PE - 3.0 points
  • tachycardia - 1.5 points
  • immobilization/surgery in previous four weeks - 1.5 points
  • history of DVT or PE - 1.5 points
  • hemoptysis - 1.0 points
  • malignancy (treatment for within 6 months, palliative) - 1.0 points
Interpretation of the Wells score

Traditional interpretation[3][4][9]

  • Score >6.0 - High (probability 59% based on pooled data[10])
  • Score 2.0 to 6.0 - Moderate (probability 29% based on pooled data[10])
  • Score <2.0 - Low (probability 15% based on pooled data[10])

Alternate interpretation[3][6]

  • Score > 4 - PE likely. Consider diagnostic imaging.
  • Score 4 or less - PE unlikely. Consider D-dimer to rule out PE.

Blood tests

In low/moderate suspicion of PE, a normal D-dimer level (shown in a blood test) is enough to exclude the possibility of thrombotic PE.[11]

When a PE is being suspected, a number of blood tests are 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.

Medical imaging

The gold standard for diagnosing pulmonary embolism (PE) is pulmonary angiography. Pulmonary angiography is used less often due to wider acceptance of CT scans, which are non-invasive.

Non-invasive imaging

CT pulmonary angiography (CTPA) is a pulmonary angiogram obtained using computed tomography (CT) with radiocontrast rather than right heart catheterization. Its advantages are clinical equivalence, its non-invasive nature, its greater availability to patients, and the possibility of identifying other lung disorders from the differential diagnosis in case there is no pulmonary embolism. Assessing the accuracy of CT pulmonary angiography is hindered by the rapid changes in the number of rows of detectors available in multidetector CT (MDCT) machines.[12] A study with a mixture of 4 slice and 16 slice scanners reported a sensitivity of 83% and a specificity of 96%. This study noted that additional testing is necessary when the clinical probability is inconsistent with the imaging results.[13] CTPA is non-inferior to VQ scanning, and identifies more emboli (without necessarily improving the outcome) compared to VQ scanning.[14]

Ventilation/perfusion scan (or V/Q scan or lung scintigraphy), which shows that some areas of the lung are being ventilated but not perfused with blood (due to obstruction by a clot). This type of examination is used less often because of the more widespread availability of CT technology, however, it may be useful in patients who have an allergy to iodinated contrast or in pregnancy due to lower radiation exposure than CT.[15]

Low probability diagnostic tests/non-diagnostic tests

Tests that are frequently done that are not sensitive for PE, but can be diagnostic.

  • Chest X-rays are often done on patients with shortness of breath to help rule-out other causes, such as congestive heart failure and rib fracture. Chest X-rays in PE are rarely normal,[16] but usually lack signs that suggest the diagnosis of PE (e.g. Westermark sign, Hampton's hump).
  • Ultrasonography of the legs, also known as leg doppler, in search of deep venous thrombosis (DVT). The presence of DVT, as shown on ultrasonography of the legs, is in itself enough to warrant anticoagulation, without requiring the V/Q or spiral CT scans (because of the strong association between DVT and PE). This may be valid approach in pregnancy, in which the other modalities would increase the risk of birth defects in the unborn child. However, a negative scan does not rule out PE, and low-radiation dose scanning may be required if the mother is deemed at high risk of having pulmonary embolism.

Electrocardiogram findings

An electrocardiogram (ECG) is routinely done on patients with chest pain to quickly diagnose myocardial infarctions (heart attacks). An ECG may show signs of right heart strain or acute cor pulmonale in cases of large PEs - the classic signs are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III ("S1Q3T3").[17] This is occasionally (up to 20%) present, but may also occur in other acute lung conditions and has therefore limited diagnostic value; the most commonly seen sign in the ECG is sinus tachycardia.

Echocardiography findings

In massive and submassive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure. Some studies (see below) suggest that this finding may be an indication for thrombolysis. Not every patient with a (suspected) pulmonary embolism requires an echocardiogram, but elevations in cardiac troponins or brain natriuretic peptide may indicate heart strain and warrant an echocardiogram.[18]

The specific appearance of the right ventricle on echocardiography is referred to as the McConnell sign. This is the finding of akinesia of the mid-free wall but normal motion of the apex. This phenomenon has a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism.[19]

Combining tests into algorithms

Recent recommendations for a diagnostic algorithm have been published by the PIOPED investigators; however, these recommendations do not reflect research using 64 slice MDCT.[10] These investigators recommended:

  • Low clinical probability. If negative D-dimer, PE is excluded. If positive D-dimer, obtain MDCT and based treatment on results.
  • Moderate clinical probability. If negative D-dimer, PE is excluded. However, the authors were not concerned that a negative MDCT with negative D-dimer in this setting has an 5% probability of being false. Presumably, the 5% error rate will fall as 64 slice MDCT is more commonly used. If positive D-dimer, obtain MDCT and based treatment on results.
  • High clinical probability. Proceed to MDCT. If positive, treat, if negative, addition tests are needed to exclude PE.

Treatment

In most cases, anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such as oxygen or analgesia, are often required.

Massive PE causing hemodynamic instability (marked decreased oxygen saturation, tachycardia and/or hypotension) is an indication for thrombolysis, the enzymatic destruction of the clot with medication. Some advocate its use also if right ventricular dysfunction can be demonstrated on echocardiography.[20]

Anticoagulation

Main article: anticoagulant

In most cases, anticoagulant therapy is the mainstay of treatment. Heparin, low molecular weight heparins (such as enoxaparin and dalteparin), or fondaparinux is administered initially, while warfarin therapy is commenced (this may take several days, usually while the patient is in hospital). Warfarin therapy often requires frequent dose adjustment and monitoring of the INR. In PE, INRs between 2.0 and 3.0 are generally considered ideal. If another episode of PE occurs under warfarin treatment, the INR window may be increased to e.g. 2.5-3.5 (unless there are contraindications) or anticoagulation may be changed to a different anticoagulant e.g. low molecular weight heparin. In patients with an underlying malignancy, therapy with a course of low molecular weight heparin may be favored over warfarin based on the results of the CLOT trial.[21] Similarly, pregnant women are often maintained on low molecular weight heparin to avoid the known teratogenic effects of warfarin.

Warfarin therapy is usually continued for 3-6 months, or "lifelong" if there have been previous DVTs or PEs, or none of the usual risk factors is present. An abnormal D-dimer level at the end of treatment might signal the need for continued treatment among patients with a first unprovoked pulmonary embolus.[22]

 

Inferior vena cava filter

Main article: inferior vena cava filter

If anticoagulant therapy is contraindicated and/or ineffective an inferior vena cava filter may be implanted.[23]

Thrombolysis

Main article: Thrombolysis

Thrombolysis can be given for severe PEs when surgery is not immediately available or possible (e.g. periarrest or during cardiac arrest). The only trial that addressed this issue had 8 patients; the four receiving thrombolysis survived, while the four who received only heparin died.[24] The use of thrombolysis in moderate PEs is still debatable. The aim of the therapy is to dissolve the clot, but there is an attendant risk of bleeding or stroke.[25]

Surgical management of PE

Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently, it has gone through a resurgence with the revision of the surgical technique and is thought to benefit selected patients.[26]

Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.

Prognosis

Mortality from untreated PE is said to be 26%. This figure comes from a trial published in 1960 by Barrit and Jordan,[27] which compared anticoagulation against placebo for the management of PE. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957. This study is the only placebo controlled trial ever to examine the place of anticoagulants in the treatment of PE, the results of which were so convincing that the trial has never been repeated as to do so would be considered unethical. That said, the reported mortality rate of 26% in the placebo group is probably an overstatement, given that the technology of the day may have detected only severe PEs.

Prognosis depends on the amount of lung that is affected and on the co-existence of other medical conditions; chronic embolisation to the lung can lead to pulmonary hypertension. There is controversy over whether or not small subsegmental PEs need to be treated at all[28] and some evidence exists that patients with subsegmental PEs may do well without treatment.[29][13]

Predicting mortality

The PESI and Geneva prediction rules can estimate mortality and so may guide selection of patients who can be considered for outpatient therapy.[30]

Evaluation for underlying causes for recurrence

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 ("thrombophilia screen") 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.

References

  1. ^ a b Wells PS, Hirsh J, Anderson DR, Lensing AW, Foster G, Kearon C, Weitz J, D'Ovidio R, Cogo A, Prandoni P (1995). "Accuracy of clinical assessment of deep-vein thrombosis". Lancet 345 (8961): 1326-30. doi:doi:10.1016/S0140-6736(95)92535-X. PMID 7752753.
  2. ^ a b Wells PS, Ginsberg JS, Anderson DR, Kearon C, Gent M, Turpie AG, Bormanis J, Weitz J, Chamberlain M, Bowie D, Barnes D, Hirsh J (1998). "Use of a clinical model for safe management of patients with suspected pulmonary embolism". Ann Intern Med 129 (12): 997-1005. PMID 9867786.
  3. ^ a b c d e Wells P, Anderson D, Rodger M, Ginsberg J, Kearon C, Gent M, Turpie A, Bormanis J, Weitz J, Chamberlain M, Bowie D, Barnes D, Hirsh J (2000). "Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer.". Thromb Haemost 83 (3): 416-20. PMID 10744147.
  4. ^ a b Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer JF, Barnes D, Forgie M, Kovacs G, Ward J, Kovacs MJ (2001). "Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer". Ann Intern Med 135 (2): 98-107. PMID 11453709.
  5. ^ Sanson BJ, Lijmer JG, Mac Gillavry MR, Turkstra F, Prins MH, Büller HR (2000). "Comparison of a clinical probability estimate and two clinical models in patients with suspected pulmonary embolism. ANTELOPE-Study Group". Thromb. Haemost. 83 (2): 199-203. PMID 10739372.
  6. ^ a b van Belle A, Büller H, Huisman M, Huisman P, Kaasjager K, Kamphuisen P, Kramer M, Kruip M, Kwakkel-van Erp J, Leebeek F, Nijkeuter M, Prins M, Sohne M, Tick L (2006). "Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography". JAMA 295 (2): 172-9. doi:10.1001/jama.295.2.172. PMID 16403929.
  7. ^ Roy PM, Meyer G, Vielle B, Le Gall C, Verschuren F, Carpentier F, Leveau P, Furber A (2006). "Appropriateness of diagnostic management and outcomes of suspected pulmonary embolism". Ann. Intern. Med. 144 (3): 157-64. PMID 16461959.
  8. ^ Neff MJ (2003). "ACEP releases clinical policy on evaluation and management of pulmonary embolism". American family physician 68 (4): 759-60. PMID 12952389.
  9. ^ Yap KS, Kalff V, Turlakow A, Kelly MJ (2007). "A prospective reassessment of the utility of the Wells score in identifying pulmonary embolism". Med. J. Aust. 187 (6): 333–6. PMID 17874979.
  10. ^ a b c d Stein PD, Woodard PK, Weg JG, Wakefield TW, Tapson VF, Sostman HD, Sos TA, Quinn DA, Leeper KV, Hull RD, Hales CA, Gottschalk A, Goodman LR, Fowler SE, Buckley JD (2007). "Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II Investigators". Radiology 242 (1): 15-21. doi:10.1148/radiol.2421060971. PMID 17185658.
  11. ^ Bounameaux H, de Moerloose P, Perrier A, Reber G (1994). "Plasma measurement of D-dimer as diagnostic aid in suspected venous thromboembolism: an overview". Thromb. Haemost. 71 (1): 1-6. PMID 8165626.
  12. ^ Schaefer-Prokop C, Prokop M (2005). "MDCT for the diagnosis of acute pulmonary embolism". European radiology 15 Suppl 4: D37-41. PMID 16479644.
  13. ^ a b Stein PD, Fowler SE, Goodman LR, et al (2006). "Multidetector computed tomography for acute pulmonary embolism". N. Engl. J. Med. 354 (22): 2317-27. doi:10.1056/NEJMoa052367. PMID 16738268.
  14. ^ Anderson DR, Kahn SR, Rodger MA et al (2007). "Computed tomographic pulmonary angiography vs ventilation-perfusion lung scanning in patients with suspected pulmonary embolism". JAMA 298 (23): 2743-53.
  15. ^ Scarsbrook AF, Gleeson FV (2007). "Investigating suspected pulmonary embolism in pregnancy". BMJ 334 (7590): 418–9. doi:10.1136/bmj.39071.617257.80. PMID 17322258.
  16. ^ Worsley D, Alavi A, Aronchick J, Chen J, Greenspan R, Ravin C (1993). "Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study.". Radiology 189 (1): 133-6. PMID 8372182.
  17. ^ McGinn S, White PD. Acute cor pulmonale resulting from pulmonary embolism. J Am Med Assoc 1935;104:1473–1480.
  18. ^ Kucher N, Goldhaber SZ (2003). "Cardiac biomarkers for risk stratification of patients with acute pulmonary embolism". Circulation 108 (18): 2191-4. doi:10.1161/01.CIR.0000100687.99687.CE. PMID 14597581.
  19. ^ McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT (1996). "Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism". Am. J. Cardiol. 78 (4): 469-73. PMID 8752195.
  20. ^ Goldhaber SZ. Pulmonary embolism. Lancet 2004;363:1295-305. PMID 15094276.
  21. ^ Lee AY, Levine MN, Baker RI, Bowden C, Kakkar AK, Prins M, Rickles FR, Julian JA, Haley S, Kovacs MJ, Gent M (2003). "Low-molecular-weight heparin versus a coumarin for the prevention of recurrent venous thromboembolism in patients with cancer.". N Engl J Med 349 (2): 146-53. PMID 12853587.
  22. ^ Palareti G, Cosmi B, Legnani C, et al (2006). "D-dimer testing to determine the duration of anticoagulation therapy". N. Engl. J. Med. 355 (17): 1780-9. doi:10.1056/NEJMoa054444. PMID 17065639.
  23. ^ Decousus H, Leizorovicz A, Parent F, Page Y, Tardy B, Girard P, Laporte S, Faivre R, Charbonnier B, Barral F, Huet Y, Simonneau G (1998). "A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. Prévention du Risque d'Embolie Pulmonaire par Interruption Cave Study Group". N Engl J Med 338 (7): 409-15. PMID 9459643.
  24. ^ Jerjes-Sanchez C, Ramirez-Rivera A, de Lourdes Garcia M, Arriaga-Nava R, Valencia S, Rosado-Buzzo A, Pierzo JA, Rosas E. Streptokinase and Heparin versus Heparin Alone in Massive Pulmonary Embolism: A Randomized Controlled Trial. J Thromb Thrombolysis 1995;2:227-229. PMID 10608028.
  25. ^ Dong B, Jirong Y, Liu G, Wang Q, Wu T. Thrombolytic therapy for pulmonary embolism. Cochrane Database Syst Rev 2006;(2):CD004437. PMID 16625603.
  26. ^ Augustinos P, Ouriel K (2004). "Invasive approaches to treatment of venous thromboembolism". Circulation 110 (9 Suppl 1): I27-34. PMID 15339878.
  27. ^ Barritt DW, Jordan SC (1960). "Anticoagulant drugs in the treatment of pulmonary embolism: a controlled trial.". Lancet 1: 1309–1312. PMID 13797091.
  28. ^ Le Gal G, Righini M, Parent F, van Strijen M, Couturaud F (2006). "Diagnosis and management of subsegmental pulmonary embolism". J Thromb Haemost 4 (4): 724-31. PMID 16634736.
  29. ^ Perrier A, Bounameaux H (2006). "Accuracy or outcome in suspected pulmonary embolism". N Engl J Med 354 (22): 2383-5. PMID 16738276.
  30. ^ Jiménez D, Yusen RD, Otero R, et al (2007). "Prognostic models for selecting patients with acute pulmonary embolism for initial outpatient therapy". Chest 132 (1): 24-30. doi:10.1378/chest.06-2921. PMID 17625081.
 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Pulmonary_embolism". A list of authors is available in Wikipedia.
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