Deep Vein Thrombosis & Pulmonary Embolism

Deep vein thrombosis (DVT) is primarily influenced by Virchow's triad of risk factors: venous stasis, hypercoagulability, and endothelial injury. Venous stasis can be precipitated by conditions such as hospitalization, long flights, or heart failure. Hypercoagulability is often associated with conditions like cancer, pregnancy, oral contraceptive pills (OCPs), and genetic mutations like factor V Leiden and prothrombin gene mutations. Endothelial injury can be induced by factors like surgery, smoking, or atherosclerotic plaque.

Clinical presentation of DVT is variable and depends on the site of the thrombus. While DVTs in small distal veins of the leg may cause minor pain and swelling, more significant DVTs in large proximal veins such as the popliteal, femoral, or iliac veins are more likely to embolize and present with acute symptoms like warmth, pain, and edema.

To evaluate the risk and presentation of DVT, the Wells score may be employed, incorporating both risk factors from Virchow's triad and physical exam findings like swelling, edema, and pain. Diagnosis typically involves venous ultrasound of the leg veins and is supported by an increased D-dimer level, though D-dimer is not specific for DVT.

Treatment strategies primarily focus on anticoagulation, often through the use of medications like heparin or warfarin. In cases where anticoagulation is contraindicated, an inferior vena cava (IVC) filter may be placed as an alternative.

Complications of DVT can be chronic, leading to conditions like post-thrombotic syndrome, which can cause venous hypertension and valvular incompetence, resulting in chronic venous insufficiency. Symptoms of chronic venous insufficiency can range from edema to skin pigmentation and venous stasis dermatitis. In severe cases, it can lead to lipodermatosclerosis, which is fibrosis of subcutaneous tissue starting at the medial ankle.

Pulmonary embolism (PE) occurs when a thromboembolism travels from the venous system, through the right heart, to lodge in the pulmonary vasculature. Often a consequence of more proximal DVTs, PE manifests with various physiological alterations. These include increased V-Q ratios due to decreased perfusion but normal ventilation in the occluded areas, leading to hypoxemia and an increased A-a gradient, as blood that would normally perfuse the occluded vascular territory gets redistributed to other lung areas.

Clinically, PE triggers hyperventilation due to activation of chemoreceptors and pulmonary irritant sensors. This leads to respiratory alkalosis as CO2 is ‘blown off,’ resulting in decreased PaCO2 and increased arterial pH. PE affecting the lung periphery can cause infarction, leading to a wedge-shaped area of necrosis, which in turn may present with pleuritic chest pain, hemoptysis, and specific radiologic signs like Hampton's hump & Westermark sign on chest X-ray (CXR).

Diagnosis involves spiral CT angiography, complemented by clinical signs such as tachypnea, dyspnea, and respiratory alkalosis. Severe forms of PE can elevate pulmonary vascular resistance due to arterial occlusion, causing acute pulmonary hypertension. This may lead to life-threatening situations, often triggered by a saddle embolus, which straddles the bifurcation of the pulmonary artery and can cause hemodynamic collapse, right heart failure, tachycardia, and even cardiogenic shock.

Treatment primarily mirrors that of DVT, utilizing anticoagulants like heparin and warfarin. In severe or life-threatening cases, thrombolytic agents like tissue plasminogen activator (tPA) can be administered to dissolve the thrombus. Chronic complications may include chronic thromboembolic pulmonary hypertension, which significantly elevates the risk of developing right heart failure.