|
Pulmonary embolism (PE) is the third most common acute cardiovascular disease after ischemic heart disease and stroke. It is a potentially fatal disorder that is often difficult to recognize and diagnose.
Risk Factors
The strongest risk factor for PE is prior thromboembolic disease including past PE and deep-venous thrombosis (DVT). PE is detected on perfusion imaging in a majority of patients with documented DVT even in the absence of clinical findings.
The classic triad of stasis, hypercoaguability, and endothelial injury forms the basis
for the many other causes (see Table 3H.1).
Diagnosis
- Clinical presentation: depends on the size of the clot and the degree of subsequent hemodynamic compromise. Signs and symptoms can be extremely subtle and nonspecific (even non-existent) and a high degree of suspicion is often necessary to make the diagnosis.
- The classic presentation is acute onset of sharp, pleuritic chest pain with associated dyspnea. Other symptoms include cough, non-pleuritic chest pain, reproducible chest pain, anxiety, syncope, and hemoptysis.
- Physical findings may include cyanosis, tachypnea, tachycardia, hypotension, diaphoresis, fever, S3 or S4, or clinical signs of a lower extremity DVT.
Risk factors for pulmonary embolism
| Causative Factor |
Comment |
| Stasis |
Immobility (bed rest, casting, air/car travel), paralysis, obesity,
heart failure, varicose veins, myocardial infarction |
| Hypercoagulability |
Prior thromboembolic disease, malignancy, inflammatory
disease, nephrotic syndrome, sepsis |
| Hematologic Disorder |
Protein C & S deficiencies, antiphospholipid antibodies,
antithrombin III deficiency, polycythemia |
| Increased Estrogen |
Pregnancy and < 3 mo postpartum, oral contraceptive use |
| Endothelial Injury |
Trauma, intravenous drug use, surgery, central venous catheters |
- Evaluation
- CXR is normal in only 30% of patients with PE. While the diagnosis is rarely made by CXR alone, this study can help exclude other diseases with a similar presentation such as PTX, pneumonia, or pulmonary emergencies, pulmonary edema. A wedge-shaped, pleural-based density that points to the hilum (Hampton’s hump) and a prominent central pulmonary artery with decreased distal pulmonary vessels (Westermark’s sign) are fairly specific radiographic findings for PE but are not commonly seen. Other nonspecific findings include an elevated hemidiaphragm, pleural effusion, or atelectasis.
- EKG should be performed on all patients with suspected PE. The most common abnormalities are sinus tachycardia and nonspecific ST-segment and T-wave changes.
Evidence of right heart strain, such as right bundle branch block, right axis deviation, or a right ventricular strain pattern are seen in a minority of patients with PE. The most specific, although insensitive, EKG finding is a prominent S-wave in lead I, with an inverted T-wave and prominent Q-wave in lead III (S1Q3T3 pattern).
- ABG can lend support to the diagnosis. Specific findings include hypoxia, hypocapnia or an elevated alveolar-arterial (A-a) gradient. In the PIOPED study, 85% of the patients had a PO2 <90 mm Hg, while 80% had an A-a gradient >20. This test cannot be used to exclude the diagnosis since 5-15% of patients with PE have a
normal ABG.
- D-dimer assays have been suggested to have diagnostic utility. Unfortunately, these assays lack specificity, and there is a large range of sensitivity depending on the assay used (69-100%). The most sensitive is the ELISA assay. A normal D-dimer by ELISA assay decreases the likelihood that a patient has a PE, but by itself cannot
exclude the diagnosis.
- V/Q scan has classically been the diagnostic study of choice although helical CT is now being used in many centers. The results of V/Q scanning are reported as normal, low probability, intermediate probability, and high probability. Clinical interpretation of results depends on the degree of clinical suspicion for PE. A
normal or scan in combination with a low clinical suspicion makes the diagnosis of PE unlikely. A high probability scan in combination with a high clinical suspicion makes the diagnosis of PE very likely although not definite. All other combinations of V/Q scan results and clinical suspicion are not definite enough to
either rule in or out PE and additional diagnostic testing is indicated.
- Helical CT scan can also be used to identify a PE. This scan may be useful in patients with significantly abnormal CXR when there is a high likelihood that the V/Q scan will be nondiagnostic. Although in most studies this test is very sensitive for diagnosing PE in the larger pulmonary vessels, it has been shown to lack sensi
Fibrinolytic dosing for pulmonary embolism
| Urokinase |
4400 IU/kg over 10 min then 4400 IU/kg/h
for 12 h |
| Streptokinase |
250,000 IU over 30 min then 100,000 IU/h
for 24 h |
| Tissue Plasminogen Activator |
100 mg over 2 h |
tivity for emboli in the smaller, subsegmental branches. Therefore a negative CT scan does not rule out the diagnosis.
- Lower extremity venous studies may aid in the diagnosis for patients with intermediate probability V/Q scans. A lower extremity DVT is present 50-70% of all patients with a proven PE. Evaluation for DVT can be done by impedance plethysmography, doppler ultrasound, or venogram. The gold standard for diagnosis of a
DVT is the venogram; however this is an invasive procedure and is technically difficult. The duplex ultrasound is the most commonly used tool for the diagnosis of a DVT. It has 93% sensitivity and 98% specificity for diagnosis of proximal DVT. The sensitivity is much lower for calf DVTs (60%). Note that a negative venous study does not rule out PE—the tests are only helpful if positive.
- The gold standard for diagnosis of PE is the pulmonary angiogram although even angiography can miss small, distal emboli. It is an invasive procedure with a low risk of mortality. However, in most institutions this study is not available 24 h a day. It is generally used only to confirm the diagnosis in patients with nondiagnostic V/Q
scans or when results of V/Q scanning does not correlate with clinical suspicion.
- Echocardiography is useful when evaluating a hemodynamically unstable patient with suspected PE. This modality can help diagnose other potential etiologies and can identify changes consistent with PE such as right ventricular enlargement, pulmonary artery dilatation, and tricuspid regurgitation.
Treatment
- Support of airway, breathing, and circulation is the initial goal of therapy.
- Treatment of the stable patient consists of anticoagulation. This should be started prior to final diagnosis when there is a high degree of clinical suspicion for PE.
There are two options for anticoagulation. Low molecular weight heparin (LMWH) has been shown to effective in patients with PE. The most commonly used agent is enoxaparin 1 mg/kg SQ every 12 h. The alternative is standard heparin administered as an initial bolus of 80 units/kg followed by an intravenous drip of 18 units/ kg/h. Relative contraindications to anticoagulation include recent stroke or major surgery, advanced liver or kidney failure, or bleeding diathesis.
- Fibrinolytics should be considered in hemodynamically unstable patients. The dosing differs from the protocols used for myocardial infarction (see Table 3H.2).
- Surgical embolectomy is the final option for hemodynamically unstable patients who have failed medical therapy or who have a contraindication to fibrinolytics.
Disposition
All patients with suspected PE should be admitted to a telemetry bed for monitoring and anticoagulation. Intensive care unit admission is necessary for patients with hemodynamic compromise.
Suggested Reading
- Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263:2753-9.
- Curtin JJ, Mewissen MW, Crain MR, Lipchik RJ. Postcontrast CT in the diagnosis and assessment of response to thrombolysis in massive pulmonary embolism. J Comput Assist Tomogr 1994; 18:133-5.
- Fisman DN, Malcolm ID, Ward ME. Echocardiographic detection of pulmonary embolism in transit: Implications for institution of thrombolytic therapy. Can J Cardiol 1997; 13:685-7.
- Goldhaber SZ. Treatment of pulmonary thromboembolism. Intern Med 1999; 38:620-5.
- Kline JA, Johns KL, Colucciello SA, Israel EG. New diagnostic tests for pulmonary embolism. Ann Emerg Med 2000; 35:168-80.
- Perrier A, Desmarais S, Miron MJ et al. Non-invasive diagnosis of venous thromboembolism in outpatients. Lancet 1999; 353:190-5.
- Rathbun SW, Raskob GE, Whitsett TL. Sensitivity and specificity of helical computed tomography in the diagnosis of pulmonary embolism: A systematic review. Ann Intern Med 2000; 132:227-32.
|
