Wells Score Calculator

The Wells score for pulmonary embolism (PE) is a clinical prediction rule that estimates the pre-test probability of PE. It uses seven criteria weighted by their diagnostic value: clinical signs of DVT (+3), PE as most likely diagnosis (+3), heart rate > 100 (+1.5), immobilization/surgery within 4 weeks (+1.5), previous DVT/PE (+1.5), hemoptysis (+1), and active cancer (+1).

Wells score interpretation: < 2 points = low probability (PE risk ~1.3%). 2–6 points = moderate probability (PE risk ~16.2%). > 6 points = high probability (PE risk ~40.6%). In low probability patients, a negative D-dimer effectively rules out PE. High probability patients proceed directly to CTPA imaging.

The Wells criteria for DVT uses different variables: active cancer (+1), paralysis/paresis (+1), bed rest > 3 days (+1), localized calf tenderness (+1), entire leg swelling (+1), calf swelling > 3 cm (+1), pitting edema (+1), collateral superficial veins (+1), and alternative diagnosis (−2). Score ranges from −2 to 9 for DVT assessment.

The Revised Geneva score is an alternative clinical prediction rule for PE that uses only objective criteria: age > 65 (+1), previous DVT/PE (+2), surgery/fracture within 1 month (+2), active cancer (+2), unilateral leg pain (+3), hemoptysis (+2), clinical DVT signs (+4), and heart rate (75–94 = +1, ≥ 95 = +2). It does not rely on subjective assessment.

The PERC (Pulmonary Embolism Rule-out Criteria) rule identifies low-risk patients who can safely forego D-dimer testing. PERC criteria: age > 50, heart rate > 100, SaO2 < 95%, prior DVT/PE, hemoptysis, surgery/immobilization, estrogen use, unilateral leg swelling. If all are negative, PE risk is < 2% and no further testing is needed.

Start with the Wells score to determine pre-test probability. If Wells indicates low probability (< 2), then apply PERC. If PERC criteria are all negative, PE is ruled out without D-dimer. If any PERC criterion is positive, order a D-dimer. For moderate or high Wells probability, proceed with D-dimer or imaging directly.

The Wells score has been extensively validated. In low probability patients (score < 2), the prevalence of PE is approximately 1.3%. In moderate probability (2–6), approximately 16.2%. In high probability (> 6), approximately 40.6%. The discriminatory power varies by clinical setting and patient population.

Normal D-dimer is typically < 500 ng/mL (0.5 µg/mL FEU). However, D-dimer specificity decreases with age. Age-adjusted D-dimer (age × 0.1 mg/L for patients > 50 years) improves specificity in elderly patients. A negative D-dimer in low or moderate probability patients effectively rules out VTE.

D-dimer is a fibrin degradation product elevated in acute thrombosis. It has high sensitivity (> 95%) but low specificity (∼50%) for VTE. It is used as a rule-out test in low and moderate probability patients. In high probability patients, D-dimer should be skipped in favor of direct imaging due to the high pre-test probability.

CTPA (CT Pulmonary Angiography) is the first-line imaging modality for diagnosing PE. It uses intravenous contrast to visualize pulmonary arteries. It has > 95% sensitivity for detecting PE. Contraindications include contrast allergy, renal insufficiency (eGFR < 30), and pregnancy (though with appropriate shielding, it can be used).

Ventilation-Perfusion (V/Q) scanning is an alternative to CTPA for PE diagnosis. It measures airflow (ventilation) and blood flow (perfusion) match/mismatch in the lungs. It is preferred in patients with contrast allergy, renal impairment, or when radiation exposure is a concern (e.g., pregnancy). A normal V/Q scan effectively rules out PE.

Common PE symptoms include acute onset dyspnea (shortness of breath), pleuritic chest pain (sharp, worse with inspiration), cough, hemoptysis (coughing up blood), and in severe cases, syncope or cardiac arrest. Signs include tachypnea, tachycardia, hypoxia, and signs of DVT (unilateral leg swelling).

Deep vein thrombosis (DVT) is a blood clot in a deep vein, usually in the legs. PE occurs when part of the clot breaks off and travels to the pulmonary arteries. DVT and PE are manifestations of the same disease process called venous thromboembolism (VTE). Approximately 50% of patients with proximal DVT have silent PE.

VTE encompasses both DVT and PE as part of the same disease spectrum. It is the third most common cardiovascular disease after myocardial infarction and stroke, with an incidence of 1–2 per 1000 persons per year. Risk factors include surgery, cancer, immobility, pregnancy, and thrombophilia.

VTE is primarily treated with anticoagulation: initial therapy with heparin (UFH, LMWH, or fondaparinux) followed by oral anticoagulation (warfarin, rivaroxaban, apixaban, edoxaban, or dabigatran). Treatment duration is typically 3–6 months, but may be extended for unprovoked VTE or ongoing risk factors.

NOACs (Non-Vitamin K Oral Anticoagulants) include rivaroxaban, apixaban, edoxaban, and dabigatran. Compared to warfarin, NOACs have faster onset, fixed dosing, fewer drug/food interactions, and no routine lab monitoring. Meta-analyses show NOACs have similar or better efficacy with lower risk of major bleeding, especially intracranial hemorrhage.

For provoked VTE (caused by surgery or transient risk factor), 3 months of anticoagulation is standard. For unprovoked VTE, at least 3–6 months, then consider extended therapy based on bleeding risk. For cancer-associated VTE, LMWH or DOACs for 3–6 months minimum. Recurrent VTE or antiphospholipid syndrome requires indefinite anticoagulation.

Major bleeding risk on anticoagulation is approximately 1–3% per year. Risk factors include age > 75, renal impairment, liver disease, prior bleeding, and concurrent antiplatelet therapy. The HAS-BLED score can estimate bleeding risk. Anticoagulation benefit (preventing fatal PE) generally outweighs bleeding risk in most patients.

Untreated PE has a mortality rate of approximately 30%. With appropriate anticoagulation, mortality drops to 2–8%. Massive PE with hemodynamic instability has a mortality of up to 50% even with treatment. Prompt diagnosis and treatment are critical for reducing PE-related deaths.

Massive (high-risk) PE is defined by sustained hypotension (SBP < 90 mmHg for > 15 min) or cardiac arrest. These patients require urgent reperfusion therapy (systemic thrombolysis or embolectomy) rather than anticoagulation alone. Mortality in massive PE is 25–50% even with treatment.

Absolute contraindications: prior intracranial hemorrhage, known structural cerebrovascular lesion, active bleeding, recent major trauma/surgery (< 3 weeks), recent head trauma. Relative contraindications: uncontrolled hypertension (> 180/110), recent GI bleed, pregnancy, advanced age > 75, low body weight.

Subsegmental PE refers to clots in the smallest branches of the pulmonary arteries. With modern CT scanners, these are increasingly detected. The clinical significance is debated. In patients without proximal DVT and good cardiopulmonary reserve, some experts recommend observation without anticoagulation, but guidelines vary.

Cancer increases VTE risk 4–7 fold through multiple mechanisms: tumor-derived procoagulants, compression of veins, chemotherapy-induced endothelial damage, and central venous catheters. Pancreatic, gastric, ovarian, and lung cancers carry the highest VTE risk. Cancer-associated thrombosis requires LMWH or DOAC therapy.

HIT is a life-threatening immune reaction to heparin therapy causing thrombocytopenia and paradoxical thrombosis (both arterial and venous). It occurs in 1–5% of patients exposed to unfractionated heparin. Treatment involves stopping all heparin and starting a non-heparin anticoagulant (argatroban, bivalirudin, fondaparinux).

Compression ultrasound (CUS) is the first-line imaging test for DVT. It visualizes the deep veins of the leg and assesses compressibility. Lack of full compression indicates DVT. Proximal CUS (femoral and popliteal veins) has > 95% sensitivity. Serial CUS (day 5–7) is used for suspected distal DVT.

Proximal DVT involves the popliteal, femoral, or iliac veins and carries a 50% risk of PE if untreated. Distal (calf) DVT involves the below-knee veins and has a lower embolization risk (∼5%). Treatment for distal DVT may be observation or short-term anticoagulation depending on symptoms and risk factors.

Pregnancy increases VTE risk 5–10 fold. D-dimer is normally elevated in pregnancy, reducing specificity. Compression ultrasound is safe. For suspected PE, CTPA (low radiation to fetus) or V/Q scan (higher fetal radiation but less maternal radiation) are used after weighing risks and benefits. LMWH is the preferred anticoagulant in pregnancy.

Inherited thrombophilia increases VTE risk and includes: Factor V Leiden (most common, 5% of Caucasians, 3–7 fold increased VTE risk), Prothrombin G20210A mutation, Antithrombin deficiency, Protein C deficiency, and Protein S deficiency. Testing is controversial and typically reserved for young patients, recurrent VTE, or strong family history.

APS is an acquired thrombophilia characterized by arterial/venous thrombosis and/or pregnancy loss with positive antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, β2-glycoprotein I). Treatment requires indefinite anticoagulation with warfarin (target INR 2–3 or 3–4 for recurrent thrombosis). DOACs are less effective in APS.

Diagnosing recurrent VTE is challenging after an initial event. For suspected recurrent DVT, compare ultrasound with prior studies. A new non-compressible segment or a 4+ mm increase in thrombus diameter suggests recurrence. For suspected recurrent PE, new perfusion defects on V/Q scan or new filling defects on CTPA are diagnostic.