Pulmonary Embolism

by Mohammed Moinuddin, M.D., F.A.C.P.

Pulmonary Embolism (PE), often discussed as a disease entity, is really a complication of the disease--venous thrombosis. Reali- zation of this concept is important to understand the implication of therapy, which is basically prophylactic. This disorder is common enough to cross all subspecialties to present a challenge to internists, generalists, urologists, pulmonologists, ortho- pedists, general surgeons, gynecologists, etc. The following article briefly presents an overview or summary of opinions of experts in this field.

Incidence:
It is estimated that some five million Americans suffer from venous thrombosis every year; approximately 600,000 develop PE and 200,000 die. This makes PE the third common cause of death in the United States. This substantial toll can be easily reduced if we can identify the risk factors and offer preventive measures to the patients.

Pathogenesis:
In approximately 90% of patients, PE is consequence of deep vein thrombosis (DVT) in lower extremities. In the deep veins, a platelet nidus is formed near the valve, this subsequently leads to red fibrin thrombus. Accretion of more platelets and fibrin enlarges the thrombus which may get detached, often in fragments but rarely completely from its primary site, to be trapped in pulmonary circulation resulting in PE. In the remaining 10% of patients, PE arises from renal veins, inferior vena cava, pelvic veins, dilated or infarcted right ventricle, rarely from upper extremities.

Most often PE (65-70%) is bilateral. Lower lobe vessels are more commonly involved than upper lobes. Large central emboli in main pulmonary trunk or its main branches are uncommon. Pulmonary infarction occurs in a small number of patients with PE because of dual blood supply of lungs from pulmonary and bronchial arteries, and also because of oxygen delivery from the inspired air. When infarction occurs, it is usually in small distal segmental vessels.

Clinical Manifestation:
The clinical features of PE can be diverse and confusing, ranging from no symptoms to sudden death. The symptoms, when present, will depend upon the extent of pulmonary arterial occlusion. The most common symptoms are dyspnea and chest pain. Sudden apprehension of impending doom with tachypnoea and elevation of right heart pressures with or without syncope usually indicate massive PE (more than 40-45% of pulmonary circulation is involved).

Hemoptysis is less commonly seen in PE. The recognition of risk factors, such as venous stasis and coagulopathy, is extremely important. Although the history and physical findings may suggest PE, the clinical diagnosis alone is often unreliable. The diagnosis of DVT is also similarly very difficult clinically, and false positive and false negative diagnoses are quite common. The following tests are often done to narrow down the differential diagnosis.

Arterial blood gases:
Hypoxia is common in PE but normal pO2 is seen in significant minority of patients. Alternatively, hypoxia is also observed in other differential diagnosis such as pneumonitis, COPD, CHF, etc. Severe hypoxia in a patient with PE and no other lung or heart disease signify severity.

Electrocardiogram:
The main importance of EKG is to rule out MI, which is often in the differential diagnosis. Non-specific abnormalities may be present on EKG, such as T wave inversion, right heart strain and rarely S, Q3 T3 pattern.

Chest X-Ray:
This is usually normal, but when abnormal, it is rarely specific. The chest radiograph may show infiltrate, effusion, elevated diaphragm, atelectasis, focal oligemia. Chest x-ray is more important in excluding other diagnosis such as pneumonitis, CHF, pneumothorax, cancer, etc.

Diagnosis:
The diagnosis of PE rests on imaging the pulmonary circulation. Lung scan is an initial screening test, which provides safe and sensitive means of assessing pulmonary blood flow. Lung scintigraphy is sensitive but non-specific. Therefore, to improve its specificity, ventilation scanning is added and the procedure is referred to as V/Q scan.

On the basis of literature survey, the following guidelines are outlined.

1. Normal lung scan rules out PE. Patients suspected of PE whose lung scans are normal should be investigated for other diseases.

2. High probability lung scan for PE carries more than 85% chance of PE.

3. Intermediate probability lung scan carries 0-50% chance of PE.

4. Low probability lung scan carries less than 10% chance of PE according to some studies, and 10-40% according to others.

5. It provides road map to the angiographer prior to angiography.

Because of the uncertainty in the diagnosis of PE on lung scans alone, the PIOPED study has recommended using clinical criteria as well. Therefore, according to the PIOPED study, high probability lung scan, with high clinical index, indicates 96% probability of PE. Conversely, low probability lung scan, with low clinical index, has 98% chance of not having PE.

Pulmonary Angiography:
This is the gold standard for the diagnosis of PE and carries high accuracy. However, it is not required for confirmation in all cases. Pulmonary angiography should be performed when uncertainty in diagnosis exists even after scan and clinical examination and when confidence level is not high enough to commit anticoagulant therapy. Advances in technique have made this procedure safe in patients without severe pulmonary hypertension or cardiopulmonary disease.

Evaluation Of Source Of PE:
Since clinical examination of lower extremities for DVT is unreliable, objective means of diagnosing DVT are essential for instituting anticoagulant therapy. Contrast venography is the gold standard for DVT. Because of the discomfort associated with this test and the use of contrast agent, non-invasive methods recently have been developed. These include Impedance Plethysmography and Doppler ultrasonography.

The accuracy of these two tests is comparable. Doppler ultrasonography is approximately 90% sensitive for DVT in thigh, but its sensitivity drops considerably for calf veins. In the past, it was felt that thrombi in calf veins are of little or no significance. However, recently it has been shown that they can also cause clinically significant PE. At the BMH, Doppler is commonly used for the detection of thrombo embolic disease.

There are many algorithms that are proposed for work up of PE. On the basis of local experience at the BMH, and literature review, the following algorithm is recommended.

Pulmonary Angiography is also indicated:

1. when there is disparity between V/Q scans and clinical suspicion,

2. when thrombolytic therapy is anticipated,

3. when anticoagulants are contra indicated.

Future Directions:

1. Angioscopy: Central large thrombi/emboli can be visualized in pulmonary circulation. It is useful in embolectomy in patients with chronic pulmonary hypertension.

2. Transesophageal Echocardiography: Can visualize large central emboli.

3. Radiolabelled platelets, CT and MRI are under investigation.

References

1. Moser KM. State of the Art: Venous thrombo embolism. AM REV RESP DIS 1990; 141:235-249.

2. Dalen, JE. Alpert JS. Natural History of Pulmonary Embolism. PROG CARDIOVASC DIS 1975; 17:259-270.

3. Kelley, MA, Carson, JL, Palevsky, HI, Schwartz, JS. Diagnosing Pulmonary Embolism: New Facts And Strategies. ANN INT MED 1991; 114:300-306.

4. PIOPED Investigators. Value of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). JAMA 1990, 263:2753-2759.

5. Goldhaber, SZ, Morpurgo, M., for the WHO/ISFC Task Force on Pulmonary Embolism. JAMA 1992, 268:1727-1733.

6. Senior RM, Pulmonary Embolism. In Text Book of Internal Medicine.