1. M.A.ZOHAL PULMUNOLOGIST
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
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

13. 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

14. Risk Factors 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

15. 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

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

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

18. 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

19. 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

20. 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

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

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

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

24. Alveolar hyperventilation
reflex stimulation of irritant receptors.

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

26. Decreased pulmonary compliance
lung edema,
lung hemorrhage,
loss of surfactant

27. 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

28. 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

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

30. 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%

31. Common symptoms

32. Common physical signs

33. 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

34. 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!!

35. 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

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

38. Imaging tests to diagnose PTE

39. 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

40. 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)

41. Hamptons Hump PE

42. Westermark’s Sign PE

43. PE which
appears like
a mass.

44. PE with hemorrhage or pulmonary edema

45. PE with effusion
and elevated diaphragm

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

47. CT revealing pulmonary infarct

48. DIAGNOSIS OF VENOUS THROMBOEMBOLISM
Spiral chest CT scan

49. DIAGNOSIS OF VENOUS THROMBOEMBOLISM
Spiral chest CT scan

50. 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

51. V/Q Scan
Historically, the principal imaging test for the diagnosis of PE
A perfusion defect indicates absent or decreased blood flow
Ventilation scan obtained with radiolabeled gases
A high probability scan is defined as two or more segmental perfusion defects in presence of nl ventilation scan

53. V/Q Scan
Useful if the results are normal or near normal, or if there is a high probability for PE
As many as 40% of pts with high clinical suspicion for PE and low probability scans have a PE on angiogram

54. High Probability V/Q Scan

55. Pulmonary Angiogram Most specific test available for diagnosis of PE
Can detect emboli as small as 1-2 mm
Most useful when the clinical likelihood of PE differs substantially from the lung scan result or when the lung scan is intermediate probability

57. Echocardiogram Useful for rapid triage of pts
Assess right and left ventricular function
Diagnostic of PE if hemodynamics by echo are consitent with clinical hx

58. high risk of an adverse clinical outcome
Hemodynamic instability,
RV dysfunction on echocardiography,
RV enlargement on chest CT,
Elevation of the troponin level due to RV microinfarction outcome

59. Primary therapy Fibrinolysis
Pharmacomechanical catheter-directed therapy
surgical embolectomy
pulmonary thromboendarterectomy

60. Fibrinolysis
(1) dissolving much of the anatomically obstructing pulmonary arterial thrombus, (2) preventing the continued release of serotonin and other neurohumoral factors that exacerbate pulmonary hypertension, (3) lysing much of the source of the thrombus in the pelvic or deep leg veins, thereby decreasing the likelihood of recurrent PE.

61. fibrinolysis massive PE
For patients with submassive PE, who have preserved systolic blood pressure but moderate or severe RV dysfunction, use of fibrinolysis remains controversial

62. Secondary prevention Anticoagulant Ivc filter
graduated compression stocking
Intermittent pneumatic compression devices

63. Treatment
(1) the conventional strategy of parenteral therapy “bridged” to warfarin,
(2) parenteral therapy “bridged” to a novel oral anticoagulant such as dabigatran (a direct thrombin inhibitor) or edoxaban (an anti-Xa agent)
(3) oral anticoagulation with rivaroxaban or apixaban (both are anti-Xa agents)

64. parenteral therapy three heparin-based parenteral anticoagulants are:
(1) unfractionated heparin (UFH),
(2) low-molecular-weight heparin (LMWH),
(3) fondaparinux.
For patients with suspected or proven heparin-induced thrombocytopenia, there are two parenteral direct thrombin inhibitors: argatroban and bivalirudin

65. Treatment
Begin treatment with either unfractionated heparin or LMWH, then switch to warfarin (Prevents additional thrombus formation and permits endogenous fibrinolytic mechanisms to lyse clot that has already been formed, Does NOT directly dissolve thrombus that already exists)
Warfarin for atleast 3 months, INR 2-3

66. IVC filter indication
(1) active bleeding that precludes anticoagulation
(2) recurrent venous thrombosis despite intensive anticoagulation.
Softer indication:
Prevention of recurrent PE in patients with right heart failure who are not candidates for fibrinolysis
prophylaxis of extremely high-risk patients

67. IVC filter

68. graduated compression stocking

69. Intermittent pneumatic compression devices

70. Conclusion PE is often a misdiagnosed clinical disorder.
Rapid identification and appropriate treatment may often prevent unnecessary morbidity and mortality.