Pulmonary embolism 1-

Pulmonary embolism 1-

• 1.
  Pulmonary embolism (PE) Definition: Pulmonaryembolism represents a mechanical obstruction of one or more branches of the pulmonary vasculature, usually due to a blood clot (thromboembolism) from deep vein thrombosis (DVT). Etiology: Virchow's triad (i.e., venous stasis, vessel wall damage, and hypercoagulability) 1-Venous stasis: increased venous stasis is associated with: • age >40 years • immobility • general anaesthesia • paralysis, spinal cord injury • myocardial infarction • prior stroke • varicose veins • advanced congestive heart failure, and advanced COPD. 2-Vessel wall damage: endothelial cell damage promotes thrombus formation, usually at the venous valves. Damage to the vessel wall can occur after a number of insults including: • trauma • previous DVT • surgery • venous harvest • central venous catheterization. 3-Hypercoagulability: a number of other conditions (both inherited and acquired) increase the risk of PE: • cancer • high-oestrogen states • inflammatory bowel disease • nephrotic syndrome • sepsis • blood transfusion • inherited thrombophilia Pathogenesis: • factors contributing to development of venous thromboembolism include o endothelial injury o hypercoagulability o circulatory stasis
• 2.
  • lower extremity orpelvic deep vein thromboses most common source of pulmonary emboli • degree of clot burden and resulting pulmonary vasculature occlusion determines consequences o 25% occlusion may cause increased pulmonary arterial pressure and decrease in arterial oxygen tension o 35%-40% may cause increased right atrial pressure • occlusion may result in hypoxemia and pulmonary vasoconstriction which increase pulmonary vascular resistance • increase in pulmonary vascular resistance and subsequent increase in pulmonary artery pressure causes decrease in right ventricular stroke volume • initial compensatory tachycardia followed by continued increase in right ventricular afterload may lead to: o increased wall stress and oxygen demand of ventricular tissue o ischemia, infarction, and right ventricular dilation o circulatory failure due to decrease in left ventricular preload, resulting from  pulmonary outflow obstruction  reduced left ventricular compliance from interventricular septum shifting into left ventricular cavity • resulting circulatory failure may lead to death presentation: History: • symptoms are nonspecific and include: o dyspnea o tachypnea o pleuritic chest pain o cough o fever o symptoms of shock in patients with massive (high-risk) pulmonary embolism • less common presentation may include: o hemoptysis o leg pain or swelling o syncope o symptoms of encephalopathy o seizure • patients may be asymptomatic with diagnosis made incidentally General physical: • heart rate o sinus tachycardia may be present o in patients with massive (high-risk) pulmonary embolism, persistent profound bradycardia (heart rate < 40 beats per minute), and/or pulselessness may be present sustained hypotension may occur in patients with massive (high-risk) pulmonary embolism • fever may be present • use of accessory muscles suggests severe respiratory distress Extremities: • signs of deep vein thrombosis (DVT) may be present o unilateral pitting edema o unilateral extremity swelling
• 3.
  • o tenderness, especiallyupon deep venous palpation o prominent superficial veins complications : • acute cor pulmonale which may lead to shock and death • recurrent pulmonary embolism • atrial flutter • atrial fibrillation • chronic thromboembolic pulmonary hypertension • heparin-induced thrombocytopenia diagnosis : Investigations: CTPA (CT pulmonary angiography) • CTPA is the preferred investigation for definitive confirmation of PE. Echocardiography: • The presence of any signs of right ventricular (RV) dysfunction is sufficiently suggestive of PE D-dime: • the most sensitive test for thromboembolic disease. V/Q scan: • can be performed in patients with an elevated D-dimer and a contraindication to CTPA (such as pregnancy, renal impairment, or contrast allergy). CXR: • Not diagnostic of PE but may be useful to support the diagnosis and is important to rule out other causes. lower limb compression venous ultrasound: to investigate patients suspected of having a concurrent deep vein thrombosis (DVT). Coagulation studies: • INR, PT, aPTT Prognosis:
• 4.
  • Management: 1-Give oxygen andstart heparin immediately before the diagnosis is confirmed and while the diagnostic workup is being completed. Once the diagnosis is confirmed • Heparin—LMWH or unfractionated for 5–7 days (or until INR is therapeutic) • Warfarin—should be started with heparin and continued for 6 months for both pulmonary emboli and DVT. 2-In patients that develop recurrent thrombosis while on anticoagulants, consider HIT or cancer-related thrombosis (very resistant). Consider placing an inferior vena cava (IVC) filter or using some of the newer anticoagulant classes (e.g., hirudin derivatives). IVC filters are associated with clot formation around the filter site and may cause pulmonary thromboembolism.
• 5.
  Done by/ Maged HemaidMohamed Salem