1. BY
Dr- MOUSA ELSHAMLY

3. PE refers to obstruction of the pulmonary artery
or one of its branches by material (eg, thrombus,
tumor, air, or fat ) that originated elsewhere in
the body
DEFINITIONS

4. PE
 Epidemiology
 Pathophysiology
 Prevention/Risk factors
 Screening
 Diagnosis
 Treatment

5. 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

6. 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

7. 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

8. 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

9. Venous Stasis
 Accumlation of activated procoagulants.
 Immobilization
 Inadequate cardiac pump.
 Promotes thrombus formation.

10. Vessel Wall Injury
 Acute or chronic injury to vessel endothelium.
 Leads to activation of platelets and clotting cascade.
 Promotes thrombus formation.

11. Vessel Injury

12. Platelet Adhesion

13. Aggregation

15. Alternations in Coagulation
 Increase in procoagulant factors.
 By trauma to vascular wall or extravascular tissues.
 Releases tissue thromboplastin and phospholipid.
 Leads to formation of prothrombin activator.
 Prothrombin  Thrombin

16. Alterations in Coagulation
 Decrease in anticoagulant factors.
 Thrombomodulin
 Antithrombin III
 Heparin
 Alpha2-Marcoglobulin
 Plasmin
 Leads to hypercoagulable state by formation of
thrombin.

17. Thrombosis Formation
 Platelet nidus at site of injury.
 Growth by aggregation of platelets and fibrin.
 Activation of clotting cascade.
 Larger growth to a red fibrin thrombus.
 Thrombus fractures and embolizes to other areas of
the body.

18. Predisposing Factors or Diseases for
Development of PTE
 Hypercoagulable state
 Nephrotic syndrome
 Immobilization
 Amyloidosis
 Early DIC
 Hyperadrenocorticism
 Capillary fragility
 Activation of clotting cascade.

19. Predisposing Factors or Diseases for
Development of PTE
 Hypercoagulable state
 Capillary fragility
 Diabetes Mellitus
 Immune–mediated hemolyitc anemia
 Sepsis
 Hyperadrenocorticism
 Activation of clotting cascade.

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

21. Predisposing Factors or Diseases for
Development of PTE
 Hypercoagulable state
 Capillary fragility
 Activation of clotting cascade.
 Sepsis
 Pneumonia/pyothorax
 Heartworm disease
 Surgery
 Bacterial endocarditis
 Neoplasia

22. 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 .

23. 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

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

25. Consequences of PTE
 Respiratory.
 Increased alveolar dead space.
 Hyperventilation.
 Hypoxemia.
 Ventilation/perfusion inequality.
 Intrapulmonary shunts.

26. Normal Alveolus

27. Increased Alveolar Dead Space

28. Hypoxemia
Results from ventilation-perfusion
inequality, physiologic shunting and
increased dead space.

29. Intrapulmonary Shunts
 Blood that has not been to areas of ventilated lung and
enters systemic circulation without gas exchange
taking place.
 Poorly oxygenated blood enters the arterial system
lowering the PaO2.
 Not responsive to oxygen therapy.

30. Ventilation/Perfusion Inequality
 V/Q inequality occurs when distribution of blood is
altered to the alveoli.
 O2 increase in the alveoli and CO2 decreases.

31. Hemodynamic Changes
 Increase in pulmonary vascular resistance.
 Increased afterload to the right heart.
 Can lead to circulatory collapse and shock.

32. 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

33. 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

34. Well’s Criteria
Clinical Signs and Symptoms of DVT?
(Calf tenderness, swelling >3cm, errythema, pitting
edema affected leg only)
+3
PE Is #1 Diagnosis, or Equally Likely +3
Heart Rate > 100 +1.5
Immobilization at least 3 days, or Surgery in the
Previous 4 weeks
+1.5
Previous, objectively diagnosed PE or DVT? +1.5
Hemoptysis +1
Malignancy w/ Rx within 6 mo, or palliative? +1
>6: High Risk
2 to 6: Moderate Risk
2 or less: Low
Adapted with permission from Wells PS, Anderson DR, Rodger M, Ginsberg JS, Kearon C, Gent M, et al. Derivation of a simple
clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED d-dimer.
Thromb Haemost 2000;83:416-20.

35. 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

36. Signs of P.E.
 Tachypnea
 Rales
 Tachycardia
 Hypoxia
 S4
 Accentuated pulmonic component of S2
 Fever: T <102 F

37. Signs in Massive P.E.
 “Massive PE”: hemodynamic instability with SBP <90
or a drop in baseline SBP by >/=40mmHg for more
then 30 min
 Signs as before PLUS:
 Acute right heart failure
 Elevated J.V.P.
 Right-sided S3
 Parasternal lift

38. P.E. & Leg Symptoms
 Most patients with P.E. do not have leg symptoms at
time of diagnosis
 Patients with leg symptoms may have asymptomatic
P.E.

39. Differential Diagnosis
 USA, MI
 Pneumonia
 CHF
 Asthma
 Costochondritis, Rib Fx,
 Pneumothorax
 PE can coexist with other illnesses!!

40. 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%

41. 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

42. 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)

43. Chest X-ray Eponyms of PE
 Westermark's sign
 A dilation of the pulmonary vessels proximal to the
embolism along with collapse of distal vessels,
sometimes with a sharp cutoff.
 Hampton’s Hump
 A triangular or rounded pleural-based infiltrate with the
apex toward the hilum, usually located adjacent to the
hilum.
43

44. PE
Hamptons
Hump

45. PE
Westermark’s Sign

46. Radiographic Eponyms
- Hampton’s Hump, Westermark’s Sign
46
Westermark’s
Sign
Hampton’s Hump

47. PE which
appears like
a mass.

48. PE with effusion
and elevated diaphragm

49. How About This???
Westermark's Sign: an abrupt tapering of a vessel caused by
pulmonary thromboembolic obstruction.
This CXR shows enlargement of the left hilum accompanied by left
lung hyperlucency, indicating oligemia (Westermark's sign).

50. What’s This???
Hampton’s Hump

51. Lab & Radiologic Findings in P.E.
 ABG
 BNP
 Cardiac Enzymes: Troponin
 D-dimer
 EKG
 CXR
 Ultrasound
 V/Q Scan
 Angiography

52. Lab Findings in P.E.
(ABG)
 ABG:
 Hypoxemia
 Hypocapnia (low CO2)
 Respiratory Alkalosis
 Massive PE: hypercapnia, mix resp and metabolic
acidosis (inc lactic acid)
 Patients with RA pulse ox readings <95% are at
increased risk of in-hospital complications, resp failure,
cardiogenic shock, death

53. Lab Findings in P.E. (BNP)
 BNP (beta natruretic peptide)
 Insensitive test
 Patient’s with PE have higher levels than pts without,
but not ALL patients with PE have high BNP
 Good prognostic value measure: if BNP >90
associated with adverse clinical outcomes (death, CPR,
mechanical vent, pressure support, thrombolysis,
embolectomy)

54. Lab Findings in P.E. (Troponin)
 Troponin
 High in 30-50% of pts with mod to large PE
 Prognostic value if combined pro-NT BNP
 Trop I >0.07 + NT-proBNP >600 = high 40 day mortality

55. Lab Findings in P.E.
(D-dimer)
 D-dimer:
 Degredation product of fibrin
 >500 is abnormal
 Sensitivity: High, 95% of PE pts will be positive
 Specificity: Low
 Negative Predictive Value: Excellent

56. Lab Findings in P.E. (cont’d)
 EKG
 2 Most Common finding on EKG:
 Nonspecific ST-segment and T-wave changes
 Sinus Tachycardia
 Historical abnormality suggestive of PE
 S1Q3T3
 Right ventricular strain
 New incomplete RBBB

58. S1Q3T3!!!

59. RAD
Right Atrial Enlargement

60. 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

61. 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

62. 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

63. High Probability V/Q Scan

64. 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

65. Pulmonary Angiogram

66. PE on pulmonary angiogram

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

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

69. CT revealing pulmonary infarct

70. CT revealing emboli in pulmonary artery.

71. Diagnosis
Spiral CT/ Multislice
Ascending Aorta
Lt Pulmonary
Artery
Main Pulmonary
Artery
Rt Pulmonary
Artery
Descending
Aorta
Thrombus

72. Bilateral PE

73. SPIRAL CT SCAN
Criteria for PE extension:
 obstruction index according to the scoring system
of Qanadli
∑ (n · d)
n = number of segmental
branches
d = obstruction degree
(1 if partial 2 if complete)

74. 2-slice CT
1992
2 x 2.7 mm
25 sec
4-slice CT
1998
4 x 1 mm
25 sec
64-slice
2004
64 x 0.625 mm
4 sec
16-slice CT
2002
16 x 0.75 mm
10 sec
PE at MDCT

76. Diagnosis
MRI MR Angiogram
 Very good to visualize the blood flow.
 Almost similar to invasive angiogram

77. Clinical probability assessment
Low or intermediate High (≈ 30%)
Diagnosis of PE in stable patients
D-dimer
Normal Elevated
PE excluded (≈30%)
Multi-detector CT
Positive for PE No PE
Treat

78. Echocardiography
RVD present No RVD
Diagnosis of PE in un-stable patients
Treat & stabilize
Multidetector CT
Search for alternative
diagnosis

79. 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

80. 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

81. Anticoagulation
 Start during resuscitation phase itself
 If suspicion high, start emperic anticoagulation
 Evaluate patient for absolute contraindication
(i.e.: active bleeding)

82. Anticoagulation (cont’d)
 HEPARIN:
 Lovenox: if hemodynamically stable, no renal function
 1mg/kg BID OR 1.5mg/kg QDay
 Heparin gtt: if hypotension, renal failure
 80units/kg bolus then 18units/kg infusion
 Goal PTT1.5 to 2.5 times the upper limit of normal
 COUMADIN:
 Start once acute anticoagulation achieved
 Start with 5mg PO qday OR 10mg PO q day
 If start with 10mg then achieve therapeutic INR 1.4 days sooner
 Complications and morbidity no different in 5mg or 10mg start
 Goal INR 2 to 3

85. Duration of Anticoagulation for DVT or
PE*
Event Duration Strength of
Recommendation
First Time event of
Reversible cause
(surgery/trauma)
At least 3 mos A
First episode of
idiopathic VTE
At least 6 mos A
Recurrent idiopathic
VTE or continuing risk
factor (e.g.,
thrombophilia, cancer)
At least 12 mos B
Symptomatic isolated
calf-vein thrombosis
6 to 12 weeks A
*From American College of Chest Physicians

86. Thrombolysis
 Considered once P.E. diagnosed
 If chosen, hold anticoagulation during
thrombolysis infusion, then resumed
 Associated with higher incidence of major
hemorrhage
 Indications: persistent hypotension, severe
hypoxemia, large perfusion defecs, right
ventricular dysfunction, free floating right
ventricular thrombus, paten foramen ovale
 Activase or streptokinase

87. IVC Filter
 Indication:
 Absolute contraindication to anticoagulation (i.e.
active bleeding)
 Recurrent PE during adequate anticoagulation
 Complication of anticoagulation (severe bleeding)
 Also:
 Pts with poor cardiopulmonary reserve
 Recurrent P.E. will be fatal
 Patient’s who have had embolectomy
 Prophylaxis against P.E. in select patients
(malignancy)

88. Embolectomy
 Surgical or catheter
 Indication:
 Those who present severe enough to warrant
thrombolysis
 In those where thrombolysis is contraindicated or fails

89. Recommendations Heparin therapy should be continued for at least five
days.
 Oral anticoagulation should be overlapped with
heparin therapy for four to five days.
 Heparin and warfarin therapy can be initiated
simultaneously, with heparin therapy discontinued
on day five or six if the INR has been therapeutic for
two consecutive days.
 Longer periods of initial heparin therapy may be
considered in the case of massive pulmonary
embolism or iliofemoral thrombosis.

90. Recommendations
 Therapy of acute deep vein thrombosis or
pulmonary embolism should be initiated with IV
heparin …

91. Recommendations Heparin therapy should be continued for at least five
days.
 Oral anticoagulation should be overlapped with
heparin therapy for four to five days.
 Heparin and warfarin therapy can be initiated
simultaneously, with heparin therapy discontinued
on day five or six if the INR has been therapeutic for
two consecutive days.
 Longer periods of initial heparin therapy may be
considered in the case of massive pulmonary
embolism or iliofemoral thrombosis.

92. Recommendations
 LMW heparin may be used in place of
unfractionated heparin.
 Dosing requirements are individualized for each
product.

93. Recommendations
Duration of therapy
 First thromboembolic event in the context of a
reversible risk factor
-- treated for three to six months
 Idiopathic first thromboembolic event
-- AT LEAST full six months of treatment
-- further therapy at discretion of clinician
 Recurrent venous thrombosis or a continuing risk
factor -- treated indefinitely.

94. Recommendations IVC filter placement is recommended when
-- anticoagulation is contraindicated
-- recurrent thromboembolism despite adequate
anticoagulation
-- chronic recurrent embolism with pulmonary
hypertension
-- high-risk of recurrent embolization
-- conjunction with the performance of pulmonary
embolectomy or endarterectomy

95. Treatment
IVC filter With filter 5% risk of
recurrent pulmonary
embolus, especially after 6
mos.
 complication of leg swelling
can occur.
 anticoagulation is continued
if possible.

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