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Pulmonary Embolism

Pulmonary Embolism. M.A.ZOHAL PULMUNOLOGIST. Venous thromboembolism (VTE), which encompasses deep venous thrombosis (DVT) and pulmonary embolism (PE), is one of the three major cardiovascular causes of death, along with myocardial infarction and stroke.

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Pulmonary Embolism

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  1. Pulmonary Embolism M.A.ZOHAL PULMUNOLOGIST

  2. Venous thromboembolism (VTE), which encompasses deep venous thrombosis (DVT) and pulmonary embolism (PE), is one of the three major cardiovascular causes of death, along with myocardial infarction and stroke.

  3. VTE can cause death from PE or, among survivors, chronic thromboembolic pulmonary hypertension and postphlebitic syndrome

  4. PE is the most common preventable cause of death among hospitalized patients • Approximately three of four symptomatic VTE events occur in the community, and the remainder are hospital acquired

  5. Approximately 14 million (M) hospitalized patients are at moderate to high risk for VTE in the United States annually: 6 M major surgery patients and 8 M medical patients with comorbidities such as heart failure, cancer, and stroke.

  6. The long-term effects of nonfatal VTE lower the quality of life. Chronic thromboembolic pulmonary hypertension is often disabling and causes breathlessness. A late effect of DVT is postphlebitic syndrome, which eventually occurs in more than one-half of DVT patients

  7. PE • Epidemiology • Pathophysiology • Prevention/Risk factors • Screening • Diagnosis • Treatment

  8. PE • Epidemiology • Five million cases of venous thrombosis each year • 10% of these will have a PE • 10% will die • Correct diagnosis is made in only 10-30% of cases • Up to 60% of autopsies will show some evidence of past PE

  9. PE • Epidemiology • 90-95% of pulmonary emboli originate in the deep venous system of the lower extremities • Other rare locations include • Uterine and prostatic veins • Upper extremities • Renal veins • Right side of the heart

  10. Virchow’s Triad • Rudolf Virchow postulated more than a century ago that a triad of factors predisposed to venous thrombosis • Local trauma to the vessel wall • Hypercoagulability • Stasis of blood flow • It is now felt that pts who suffer a PE have an underlying predisposition that remains silent until a acquired stressor occurs

  11. CHF Malignancy Obesity Estrogen/OCP Pregnancy (esp post partum) Lower ext injury Coagulopathy Venous Stasis Prior DVT Age > 70 Prolonged Bed Rest Surgery requiring > 30 minutes general anesthesia Orthopedic Surgery Risk Factors

  12. Risk Factors cancer, obesity, cigarette smoking, systemic arterial hypertension, chronic obstructive pulmonary disease, chronic kidney disease, blood transfusion, . long-haul air travel, air pollution, oral contraceptives, pregnancy, postmenopausal hormone replacement, surgery, and trauma

  13. Risk Factors • immobilization • surgery • malignancy • previous thrombophlebitis • lower extremity trauma • estrogen use • Stroke • 3 months post-partum.

  14. Hypercoagulability state • Factor V Leiden mutation • Protein C deficiency • Protein S deficiency • Antithrombin deficiency • Prothrombin gene mutation A20210 • Anticardiolipin antibodies • Lupus anticoagulant • Hyperhomocystinemia

  15. common predisposing factors • cancer, • systemic arterial hypertension, • chronic obstructive pulmonary disease, • long-haul air travel, • air pollution, obesity, • cigarette smoking, • eating large amounts of red meat, • oral contraceptives, pregnancy, • postmenopausal hormone replacement, • surgery, and trauma

  16. Factor V Leiden • Most frequent inherited predisposition to hypercoagulability • Resistance to activated Protein C • Single point mutation (Factor V Leiden) • Single nucleotide substitution of glutamine for arginine • Frequency is about 3% in healthy American male physicians participating in the Physicians’ Health Study

  17. PE • When venous emboli become dislodged from their site of origin, they embolize to the pulmonary arterial circulation or, paradoxically to the arterial circulation through a patent foramen ovale • About 50% of pts with pelvic or proximal leg deep venous thrombosis have PE • Isolated calf or upper extremity venous thrombosis pose a lower risk for PE

  18. Pathophysiology • Increased pulmonary vascular resistance • Impaired gas exchange • Alveolar hyperventilation • Increased airway resistance • Decreased pulmonary compliance

  19. Increased pulmonary vascular resistance • vascular obstruction • platelet secretion of vasoconstricting neurohumoral agent such as serotonin

  20. Impaired gas exchange increased alveolar dead space from • vascular obstruction, • hypoxemia : • alveolar hypoventilation relative to perfusion in the nonobstructed lung, • right-to-leftshunting, • impaired carbon monoxide transfer due to loss of gas exchange surface.

  21. Alveolar hyperventilation • reflex stimulation of irritant receptors.

  22. Increased airway resistance constriction of airways distal to the bronchi

  23. Decreased pulmonary compliance • lung edema, • lung hemorrhage, • loss of surfactant

  24. Right Ventricular Dysfunction • Progressive right heart failure is the usual immediate cause of death from PE • As pulmonary vascular resistance increases, right ventricular wall tension rises and perpetuates further right ventricle dilation and dysfunction • Interventricular septum bulges into and compresses the normal left ventricle

  25. Clinical Syndromes • Pts with massive PE present with systemic arterial hypotension and evidence of peripheral thrombosis • Pts with moderate PE will have right ventricular hypokinesis on echocardiogram but normal systemic arterial pressure • Pts with small to moderate PE have both normal right heart function and normal systemic arterial pressure

  26. Diagnosis • Clinical Syndromes • Pulmonary Infarction usually indicates a small PE, but is very painful, because it lodges near the innervation of the pleural nerves

  27. Physical Signs & Symptoms • Dyspnea 73% • Pleuritc Pain 66% • Cough 43% • Leg Swelling 33% • Leg Pain 30% • Hemoptysis 15% • Palpitations 12% • Wheezing 10% • Angina-Like pain 5%

  28. Common symptoms

  29. Common physical signs

  30. Diagnosis • H&P • Always ask about prior DVT, or PE • Family History of thromboembolism • Dyspnea is the most frequent symptom of PE • Tachypnea is the most frequent physical finding • Dyspnea, syncope, hypotension, or cyanosis suggest a massive PE • Pleuritic CP, cough, or hemoptysis

  31. Differential Diagnosis • PE is known as “the great masquerader” • pericarditis, acute coronary syndrome , MI • Pneumonia, bronchitis, copd • CHF • Asthma • Costochondritis, Rib Fx, • Pneumothorax • PE can coexist with other illnesses!!

  32. A Summary so Far… • History alone is unreliable • Physical exam is close to useless • However, studies have shown that our clinical suspicion of PE is useful in interpreting diagnostic tests

  33. WELLS CRITERIA • Suspected DVT3 • An alternative diagnosis is less likely than PE 3 • Heart rate > 100 beats / min 1.5 • Immobilization>3 days or surgery within four weeks 1.5 • Pervious DVT / PE1.5 • Hemoptysis 1 • Malignancy(on treatment or treated in past 6 1 months )

  34. Imaging tests to diagnose PTE

  35. Diagnosis • Serum Studies • D-dimer • Elevated in more than 90% of pts with PE • Reflects breakdown of plasmin and endogenous thrombolysis • Not specific: Can also be elevated in MI, sepsis, or almost any systemic illness • Negative predictive value • ABG-contrary to classic teaching, arterial blood gases lack diagnostic utility for PE

  36. Diagnosis • CXR • A normal or nearly normal chest x-ray often • occurs in PE • Classic abnormalities include: • Westermark’s Sign - focal oligemia • Hampton’s Hump - wedge shaped density above the diaphragm • Enlarged Right Descending Pulmonary Artery (Palla’s sign)

  37. HamptonsHump PE

  38. Westermark’s Sign PE

  39. PE which appears like a mass.

  40. PE with hemorrhage or pulmonary edema

  41. PE with effusion and elevated diaphragm

  42. Spiral CT Scan • Identifies proximal PE (which are the ones usually hemodynamically important) • Not as accurate with peripheral PE

  43. CT revealing pulmonary infarct

  44. DIAGNOSIS OF VENOUS THROMBOEMBOLISM Spiral chest CT scan

  45. DIAGNOSIS OF VENOUS THROMBOEMBOLISM Spiral chest CT scan

  46. Venous Ultrasonography • Relies on loss of vein compressibility as the primary criterion • About 1/3 of pts will have no imaging evidence of DVT • Clot may have already embolized • Clot present in the pelvic veins (U/S usually inadequate) • Workup for PE should continue even if dopplers (-) in a pt in which you have a high clinical suspicion

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