**6. Clinical prediction rules**

PE is suspected in many patients presenting with acute worsening of dyspnea or chest pain. When evaluating patients for the possibility of PE, the use of a validated tool to predict pretest

Figure 1. Acute pathophysiologic responses of the right ventricle to pulmonary thromboembolism (Adapted

extensively validated rules were the three-level Wells, two-level Wells, Geneva score, revised Geneva score, and the Charlotte rule (Ceriani 2010). The available CPRs incorporate patient's symptoms and the likelihood of alternative etiologies to determine the probability of PE as the cause of symptoms. These tools serve as valuable guides to assess the likelihood of PE as the cause of symptoms and often are used to determine the extent of testing performed during

Pulmonary Embolism Score Interpretation

Score > 6:High probability Score > 2 and < 6:Moderate probability Score < 2:Low Probability

Acute Thromboembolic Pulmonary Hypertension

http://dx.doi.org/10.5772/56719

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evaluation of suspected pulmonary thromboembolism. (Table 2)

Symptoms of DVT 3 points No alternative diagnosis better explains the illness 3 points Tachycardia with pulse >100 1.5 points Immobilization (≥3 days) or surgery in the previous four weeks 1.5 points Prior history of DVT or pulmonary embolism 1.5 points Presence of hemoptysis 1 point Presence of malignancy 1 point

**Table 2.** Wells Score to predict pulmonary embolism (adapted from Wells 2000)

The D-dimer antigen is a marker of fibrin degradation. It is formed by the sequential action of thrombin, Factor XIIIa and plasmin. D-dimer antigen can exist on fibrin degradation products derived from soluble fibrin before its incorporation into a fibrin gel or after the fibrin clot has been degraded by plasmin (Adam 2009). D-dimer has been found to be useful in evaluating outpatients for the presence of venous thromboembolism (VTE) (Wells 2001). D-dimer levels >500 ng/mL are considered elevated (Stein 2004). 95% of patients with proven PE will have an elevated D-dimer by ELISA assay (Stein 2004). Unfortunately, only 40-68% of patients without VTE have a negative D-dimer (Stein 2004). D-dimer elevation occurs in multiple other conditions besides PE including renal failure, surgery, cancer, sepsis, and pregnancy (Rathbun 2004). Thus, the use of d-dimer to evaluate VTE in hospitalized or otherwise chronically ill patients is limited. D-dimer is best used to exclude VTE in outpatients with low or moderate clinical suspicion for a thromboembolic event (Rathbun 2004, Wells 2000, Wells 2001, Stein

**Pulmonary Embolism Wells Score**

Total Criteria Point Count:

**7. D-dimer**

2006, Stein 2007).

**Figure 1.** Acute pathophysiologic responses of the right ventricle to pulmonary thromboembolism (Adapted from Piazza and Goldhaber 2005)

probability of this diagnosis may be utilized. Several clinical prediction rules (CPRs) are available for the assessment of the clinical pretest probability for PE including but not limited to the Wells (Wells 1998), modified Wells (Bahia 2011), Geneva, and modified Geneva scores. In a meta-analysis performed by Ceriani et al (Ceriani 2010) in 2010, nine different clinical prediction tools for PE were reviewed. This meta-analysis suggests that all rules have compa‐ rable accuracy; however, there were differences in the extent of validation testing. The most extensively validated rules were the three-level Wells, two-level Wells, Geneva score, revised Geneva score, and the Charlotte rule (Ceriani 2010). The available CPRs incorporate patient's symptoms and the likelihood of alternative etiologies to determine the probability of PE as the cause of symptoms. These tools serve as valuable guides to assess the likelihood of PE as the cause of symptoms and often are used to determine the extent of testing performed during evaluation of suspected pulmonary thromboembolism. (Table 2)


**Table 2.** Wells Score to predict pulmonary embolism (adapted from Wells 2000)
