symptoms. When VTE is seriously considered in the differential diagnosis, it should be confirmed or excluded by appropriate testing.

In the fourth quarter 2008 issue of The Doctor’s Advocate, I reviewed the risk factors for VTE, the prevention of VTE, and the diagnosis of DVT. The discussion in this issue will focus on the diagnosis and treatment of acute pulmonary embolism.

Diagnosis of Acute PE
Without treatment, pulmonary embolism has a mortality rate of 30 percent, result¬ing largely from recurrent embolism. Most emboli are multiple, primarily involve the lower lobes, and cause pulmonary hemor¬rhage. Only 10 percent of emboli cause pulmonary infarction. The symptoms and signs of PE are relatively nonspecific and include dyspnea, pleuritic pain, cough, hemoptysis, tachypnea, and tachycardia. Fewer than one-third of patients have symptoms or signs of DVT.

Lab tests often show leukocytosis and elevation of lactate dehydrogenese (LDH) and aspartate aminotransferase (AST) with normal bilirubin. Troponin 1 and troponin T are elevated in 30 to 50 percent of patients with moderate to large PE, due to right ventricular strain. Arterial blood gases (ABGs) may show hypoxemia, hypocapnia, and respiratory alkalosis; however, these changes are often absent, so ABGs have limited diagnostic value. ECG and chest x-ray abnormalities are usually nonspecific and are seldom helpful diagnostically. Echocardiograms show abnormalities suggestive of PE in 30 to 40 percent of patients (increased right ventricular size, decreased RV function, and tricuspid regurgitation). Clinical assessment and these studies alone are usually not sufficient to reliably confirm or exclude the diagnosis of PE— and further testing is required.

• Ventilation/perfusion lung scan (V/Q scan) is the best validated non¬invasive approach to evaluating patients with suspected PE. However, a high percentage of scans are nondiagnostic, and scans are most useful when they are either negative or indicate a high probability of PE.
  • Patients with both a high clinical and high V/Q scan probability have a 95 percent likelihood of PE.
  • Patients with both a low clinical and low V/Q scan probability have a 5 percent likelihood of PE.
  • A normal V/Q scan virtually excludes PE.
• Pulmonary angiography is the defini¬tive diagnostic test. When negative, the diagnosis of clinically significant PE is excluded.
• Spiral (helical) CT scanning with intravenous contrast (CT pulmonary angiography, CT-PA) is an increas¬ingly available noninvasive approach, although results vary depending on the experience of the person interpreting the images:
  • 83 percent of patients with PE have a positive CT-PA (sensitivity).
  • 96 percent of patients without PE have a negative CT-PA (specificity).
• CT-PA in conjunction with the modified Wells score.
  • If the CT-PA is positive, the likelihood of PE in patients with high, intermediate, or low clinical probability is 96, 92, and 58 percent, respectively.
  • If the CT-PA is negative, the likeli¬hood that PE is absent in patients with low, intermediate, or high clini¬cal probability is 96, 89, and 60 percent, respectively.

1. CT experienced institutions:
   • If PE is suspected, apply the modified Wells criteria (clinical criteria used to estimate the probability of PE).
   • If a patient is classified as PE unlikely, proceed to the D-dimer test. A negative test (<500 ng/ml) excludes PE.
   • Patients classified as PE likely or who are PE unlikely with elevated D-dimer levels (>500 ng/ml) should undergo CT-PA. A positive CT-PA confirms the diagnosis of PE; if negative, PE is excluded.
2. CT inexperienced institutions:
   • If PE is suspected, apply the modified Wells criteria and obtain a V/Q scan.
   • A normal V/Q scan regardless ofclinical probability excludes PE.
   • A low probability V/Q scan plus a low clinical probability excludes PE.
   • A high probability V/Q scan plus a high clinical probability confirms PE.
   • For all other combinations, obtain either pulmonary angiogram or
     serial lower extremity venous ultra¬sound examinations.

Treatment of VTE
Most deaths from PE occur within the first few hours due to recurrent PE. Therefore, if there is high clinical suspicion or a diagnosis of PE, anticoagulant therapy is promptly initiated—usually with subcuta¬neous low molecular weight (LMW) hepa¬rin or intravenous unfractionated heparin with the goal of achieving a therapeutic level within the first 24 hours. Heparin should be continued for at least five days. For most patients, oral anticoagulation can be started simultaneously with the heparin and overlapped with heparin for at least four to five days. Heparin can be discontinued on day five or six if the internationalized normalized ratio (INR) has been therapeutic for two consecutive days. Persistent hypotension due to PE is an accepted indication for thrombolytic therapy. However, due to the risk of major hemorrhage, anticoagulation must be temporarily discontinued during infusion.

Hospital medical staff protocols for the treatment of VTE should be followed.