Deep Vein Thrombosis & Pulmonary Embolism

Deep Vein Thrombosis Etiology: According to Virchow’s triad Changes in the vessel wall (endothelial damage) Changes in the blood flow (stasis) Changes in blood composition (hypercoagulation)

Clinical Presentation: Asymptomatic Pain, redness, swelling with difficulty in walking Features of pulmonary embolism may be the presenting feature in 30% of the patients

On examination: Pitting oedema of the ankle, Dilated surface veins, A stiff calf Tenderness. Homans’ sign A low-grade pyrexia may be present Signs of pulmonary embolism or pulmonary hypertension

Investigations: D-dimer measurement Duplex ultrasound Ascending and descending venography

Prophylaxis: Low risk: young, with minor illnesses, who are to undergo operations lasting 30 min or less. Moderate risk: over 40 or with a debilitating illness or are to undergo major surgery. High risk: over 40 who have serious medical conditions, or undergoing major surgery with an additional risk factor.

Methods of prophylaxis: Mechanical methods: graduated elastic compression stockings external pneumatic compression passive foot movement (foot paddling machine) simple limb elevation Pharmaceutical methods: low molecular weight heparin unfractionated heparin warfarin

Graduated elastic compressive stocking

External pneumatic compression

Foot Paddling Machine

Treatment: Medical conservative treatment: Surgical treatment Bed rest Elevation Bandage anticoagulation Thrombolytic therapy (phlegmasia cerulea dolens ) Surgical treatment Venous thrombectomy IVC filter

Pulmonary embolism ½ times as common as MI 3 times more common than CVA 3rd most common cause of death Majority are silent Acute major PE  15-20% die within 48 hours

Pathophysiology: Hemodynamic effect depends on the size of the embolus, the degree of PA obstruction the pre-embolus pulmonary function The degree of PA obstruction depends on Mechanical obstruction Hormonal obstruction 50-60% of PA obstructed  symptoms PA obstruction  RV failure   Cardiac output

Clinical presentation: Minor Pulmonary Embolism: Tachycardia, rales, low-grade fever, pleural rub. Heart sounds and systemic blood pressure are often normal. ABG are normal. Pulmonary angiograms: less than 30% occlusion of the pulmonary arterial vasculature

Major (submassive) Pulmonary Embolism: Dyspnea, tachypnea, dull chest pain, ± syncope Tachycardia, mild to moderate hypotension, and elevation of central venous pressure. Adequate cardiac output. ABG: moderate hypoxia, and mild hypocarbia. Echocardiograms may show right ventricular dilatation. Pulmonary angiograms indicate that 30–50% of the pulmonary vasculature is blocked

Massive pulmonary embolism: Dyspnea, tachypnea, sweating ± loss of consciousness Urine output falls, and peripheral pulses are poor Tachycardia, hypotension, CVP with distended neck veins Low cardiac output and cardiac arrest may occur ABG: severe hypoxia, hypocarbia, and acidosis Echo.; Dilated RV and RV failure Pulmonary angiography: more than 50% occlusion of pulmonary vasculature

Investigations: ECG: tachycardia and nonspecific changes. CXR oligemia or linear or triangular consolidation, Ventilation–perfusion (V/Q) areas of normal ventillation with poor perfusion. Pulmonary angiograms: filling defects or obstruction of pulmonary arterial branches. Echocardiography

Medical treatment: Supplementary O2 Mechanical ventilation Invasive cardiac monitoring Pharmaceutical myocardial support, mechanical myocardial support Immediate anticoagulation with i.v. heparin Consider thrombolysis in patients with major-to-massive pulmonary embolism.

Surgical treatment: Emergency pulmonary embolectomy is indicated in Critical hemodynamic instability or severe respiratory distress thrombolytic or anticoagulation therapy is contraindicated, The presence of a large clot trapped within the right atrium or ventricle

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