1. Pulmonary Embolism

2. Pulmonary Embolism Thrombotic Nonthrombotic Fat Embolism
Amniotic Fluid Embolism
IVDA (Talc, cotton, etc)

3. 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.

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. In the United States, the Surgeon General
estimates there are 100,000 to 180,000 deaths annually from PE

6. 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.

7. 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

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
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. predisposing factors cancer obesity cigarette smoking, hypertension
COPD
Surgery and trauma
chronic kidney disease
blood transfusion,
long-haul air travel ,
air pollution,
oral contraceptives, pregnancy ,
postmenopausal hormone replacement,

15. Factor V Leiden mutation
Prothrombin gene mutation A20210
Protein C deficiency
Protein S deficiency
Antithrombin deficiency
Anticardiolipin antibodies
Lupus anticoagulant

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
increased alveolar dead space from vascular obstruction,
hypoxemia from alveolar hypoventilation relative to perfusion in the nonobstructed lung, right-to-left shunting, or impaired carbon monoxide transfer due to loss of gas exchange surface.
Alveolar hyperventilation
Increased airway resistance
Decreased pulmonary compliance

19. Clinical Syndromes
Pts with massive PE present with systemic arterial hypotension and evidence of dyspnea, syncope, hypotension, and cyanosis
Pts with moderate PE will have right ventricular hypokinesis on echocardiogram but normal systemic arterial pressure
Pts with low risk PE have both normal right heart function and normal systemic arterial pressure

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

21. 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

22. Symptom list 73% Dyspnea 66% Pleuritc Pain 43% Cough 33% Leg Swelling
30% Leg Pain
15% Hemoptysis
12% Palpitations
10% Wheezing
5% Angina-Like pain

23. Common symptoms

24. Common physical signs

25. 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%

26. Differential Diagnosis
PE is known as “the great masquerader”
Unstable angina , MI
Pneumonia, bronchitis
CHF
Asthma
Costochondritis , Rib Fx,
Pneumothorax
PE can coexist with other illnesses!!

27. 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

28. WELLS CRITERIA Suspected DVT 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats / min
Immobilization or surgery in pervious 4 week 1.5
Pervious DVT / PE
Hemoptysis
Malignancy(on treatment or treated in past months )

29. Low clinical Likelihood of DVT if Point Score Is Zero or Less;
Moderate Likelihood if Score Is 1 to 2;
High Likelihood if Score Is 3 or Greater

30. Estimation of Pretest Clinical Probability of Pulmonary Embolism Pretest Clinical Probability Clinical Findings
Low-probability (unlikely)1. Symptoms incompatible with pulmonary embolism or compatible symptoms (see below; high-probability section) that can be explained by an alternative process, such as pneumonia, pneumothorax, or pulmonary edema 2. No radiographic or electrocardiographic abnormalities compatible with pulmonary embolism, or findings that can be explained by an alternative diagnosis 3. Absence of risk factors for venous thromboembolism
Intermediate-probability (possible/probable)1. Symptoms compatible with pulmonary embolism, but no associated radiographic or electrocardiographic findings 2. Constellation of findings not consistent with low or high clinical probability
High-probability (very likely)1. Symptoms compatible with pulmonary embolism (sudden-onset dyspnea, pleuritic chest pain, tachypnea, or syncope), not explained otherwise 2. Radiographic or electrocardiographic findings compatible with pulmonary embolism, or widened alveolar-arterial oxygen gradient, not explained otherwise 3. Presence of risk factors for venous thromboembolism

31. 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

32. A-a Gradient Alveolar arterial oxygen gradient 148-1.2(PaCO2) - PaO2
Gradient > is considered abnormal.
Done at Room air.

33. Diagnosis CXR Usually reveals a non specific abnormality. 14% normal
Classic abnormalities include:
Westermark’s Sign - focal oligemia
Hampton’s Hump - wedge shaped density
Enlarged Right Descending Pulmonary Artery (Palla’s sign)

34. Hamptons Hump PE

35. Westermark’s Sign PE

36. PE which
appears like
a mass.

37. PE with hemorrhage or pulmonary edema

38. PE with effusion
and elevated diaphragm

39. 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

40. 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

42. 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

43. High Probability V/Q Scan

44. 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

46. 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

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

48. CT revealing pulmonary infarct

49. DIAGNOSIS OF VENOUS THROMBOEMBOLISM
Spiral chest CT scan

50. DIAGNOSIS OF VENOUS THROMBOEMBOLISM
Spiral chest CT scan

51. 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

52. Treatment Pain Relief Supplemental Oxygen
Dobutamine for pts with right heart failure and cardiogenic shock
Volume loading is not advised because increased right ventricular dilation can lead to further reductions in left ventricular outflow

53. Treatment Thrombolysis
1. Hemodynamically compromised by PE – definitie indication
2. Pulmonary hypertension or right ventricular dysfunction detected by echocardiography, pulmonary arterial catheterization, or new electrocardiographic evidence of right heart stain. (controversial)
Embolectomy
Reserved for pts at high risk for death and those at risk for recurrent PE despite adequate anticoagulation, contraindication for thrombolytics

54. Adjunctive Therapy Duration of Anticoagulation
Dependent upon the clinical situation
Cancer, and Obesity most likely will need indefinite treatment
For other pts with isolated calf vein thrombosis (3 mos), proximal leg DVT (6 mos) and PE (1 year)
Inferior Vena Caval Filter
When anticoagulation cannot be undertaken
Recurrent thrombosis despite anticoagulation

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

56. The two principal indications for insertion of an IVC filter are
(1) active bleeding that precludes anticoagulation
(2) recurrent
venous thrombosis despite intensive anticoagulation