DVT/PE

DEEP VENOUS THROMBOSIS & PULMONARY EMBOLISM

Outline:

– Definition

– Pathophysiology

– Risk factors

– Clinical features

– Wells Criteria for DVT/PE probability

– Investigation

– Management

Deep Venous Thrombosis:

– Formation of thrombus in deep veins usually occurring in the lower limbs but may affect deep veins of other sites:

  – Upper limb veins

  – Intracranial veins

  – Splanchnic veins

Pathophysiology:

– Based on Virchow’s triad:

Virchow’s triad provides a framework for understanding the pathogenesis of DVT by highlighting three main factors that contribute to clot formation: venous stasis, hypercoagulability and endothelial dysfunction.

Stasis:This refers to venous stasis which is the slowing or stagnation of blood flow within the veins. This can occur due to various factors such as immobility, prolonged sitting or bed rest, obesity, or conditions that impede venous return to the heart. When blood flow slows down, it becomes more prone to clotting. Additionally, decreased blood flow may lead to pooling of blood in the veins, causing further stasis and increasing the risk of clot formation.

  – Hypercoagulable State:This refers to an increased tendency of the blood to clot. It can be caused by inherited or acquired factors that disrupt the normal balance of coagulation and anticoagulation mechanisms in the blood. For example, certain genetic mutations, such as Factor V Leiden mutation or prothrombin gene mutation, can predispose individuals to excessive clotting. Additionally, certain medical conditions like cancer, inflammatory disorders, or hormonal factors (e.g., oral contraceptives) can contribute to a prothrombotic state. In hypercoagulable conditions, the blood contains elevated levels of clotting factors, making it more prone to clot formation.

  – Endothelial Dysfunction:Damage to the inner lining of the veins can occur as a result of physical or chemical injury. This damage can be caused by factors such as fractures, trauma, surgical procedures, or the presence of intravenous (IV) lines. When the vessel wall is injured, it becomes rough and irregular, leading to the activation of clotting factors and platelets. The damaged inner lining also becomes sticky, promoting the adherence and accumulation of clotting components, ultimately resulting in the formation of a blood clot.

Risk factors:

– Prolonged immobility

– Major surgery (orthopedic, abdominal)

– Obesity

– Estrogen therapy

– Pregnancy

– Clotting disorder

– Smoking

– Malignancy

Wells’ Score for DVT:

Clinical features:

– Acute vs. Chronic DVT

– Symptoms:

  – Calf pain

  – Swelling

– Signs:

  – Edema

  – Tenderness

  – Differential warmth

  – Redness and engorged superficial veins

  – Positive Homan sign* (calf pain on dorsiflexion of foot)

Differential diagnosis:

– Cellulitis

– Achilles tendinitis

– Ruptured baker’s cyst

– Calf hematoma

– Fracture

– Peripheral vascular disease

– Lymphedema

Investigation:

– D-Dimer test

– Doppler USG (Ultrasound)

– Venography

– FBC (Full Blood Count)

– Clotting profile

Complications:

– Pulmonary embolism

– Paradoxical emboli

– Recurrent DVT

– Post-thrombotic syndrome

Management:

– Main aim is to prevent PE.

– Anticoagulation with heparin and warfarin.

– Bed rest until fully anticoagulated.

– Drug therapy continued up to 6 months in patients with temporary or unknown risk factors.

– Recurrent DVT and permanent risk factors may require long-term anticoagulation.

-Heparin- Inhibits activated factor X

– Initiate management with:

  – Heparin (unfractionated): 80 units/kg IV bolus, then continuous infusion of 18 units/kg/hr. Monitor aPTT (activated partial thromboplastin time) until 2 successive therapeutic levels.

  – LMWH (Low Molecular Weight Heparin):

    – SC Enoxaparin (Clexane): 1.5 mg/kg daily (or 2x daily).

    – SC Dalteparin (Fragmin): 200 units/kg, max. 18,000 units.

Rivaroxaban (Xarelto, Xa inhibitor): 15 mg twice daily for 21 days, then 15 mg daily.

Initiate Heparin therapy with oral Warfarin (Vitamin K inhibitor).

– Continue both Heparin and oral Warfarin for about 3 to 5 days until Warfarin therapy reaches its efficacy.

– Switch to oral Warfarin only: 5 to 10 mg daily and titrate dose based on INR (International Normalized Ratio).

– Aim at INR of 2 to 3 (therapeutic).

LMWH as DVT prophylaxis for at-risk patients.

– SC Enoxaparin: 40 to 80 mg daily.

– SC Dalteparin: 5000 IU daily.

TED stockings.

Lifestyle modifications: smoking cessation, exercise.

PULMONARY EMBOLISM

This refers to migration of thrombus from deep veins through circulation into pulmonary vasculature resulting in a hemodyanamic compromise. It is the main complication of a DVT.

Clinical features

  • Most patients are initially asymptomatic
  • Symptomatic patients classically present with:
  • Abrupt onset of pleuritic chest pain
  • Shortness of breath
  • Also, seizures, syncope, fever, productive cough, hemoptysis, abdominal pain

Clinical features- Signs

  • Tachypnoea
  • Tachycardia
  • Rales
  • Lower extremity edema
  • Diaphoresis
  • Cyanosis

Wells score for PE

Investigation

•Pulmonary angiography (CTPA)

  • D-Dimer assay
  • Arterial blood gases/ ABGs
  • FBC
  • Cardiac Enzymes and Troponins
  • Chest X Ray- the Hampton hump in pulmonary infarction: triangular opacity with base to pleura and apex to hilus.
  • ECG- Sinus tachycardia, S1Q3T3

Complications

  • Sudden death
  • Shock
  • Pulseless electrical activity
  • Arrhythmias
  • Lung infarction
  • Pleural effusion
  • Cor pulmonale

Management

  • Thrombolysis with recombinant tissue plasminogen activator, e.g. reteplase, alteplase.
  • Anticoagulation for at least 3 months.
  • Embolectomy.
  • Vena cava filters.
  • Use of TED Stockings

A quick reference to the clotting factors, Cascade…