This document contains a series of questions and answers about the management of pulmonary embolism from Gamal Agmy, a professor of chest diseases. It discusses issues such as when to use thrombolysis for intermediate risk PE, the risks of thrombolysis for patients with recent surgery or stroke, and alternatives to thrombolysis if it is deemed too unsafe. It also addresses questions about managing PE in pregnant patients, PE with right atrial thrombus, and the appropriate use of IVC filters.

2. Gamal Rabie Agmy, MD, FCCP
Professor of Chest Diseases, Assiut University
Head of Chest Department, Assiut University

3. Thrombotic Pulmonary Embolism
Gamal Agmy

4. Pulmonary embolism. A 1.2 – 1.5 mm triangular subpleural
lung consolidation. B. Vascular sign at the margin, not central
Gamal Agmy

5. • On color Doppler sonography,
PE-based peripheral lesions do
not show flow signals inside,
a phenomenon defined as
“consolidation with little
perfusion”
Gamal Agmy

6. Schematic representation of the parenchymal, pleural and vascular
features associated with pulmonary embolism.(Angelika Reissig, Claus
Kroegel. Respiration 2003;70:441-452)
Gamal Agmy

7. PULMONARY EMBOLISM
Gamal Agmy

8. PE DIAGNOSTIC CRITERIA
PE confirmed
Two or more typical lesions
Sensi.: 44.4%
Speci.: 98.7%
PPV: 97.4%
NPV: 62.1%
PE probable
One typical lesion and low grade
pleural effusion
Sensi.: 71.0%
Speci.: 94.9%
PPV: 93.8%
NPV: 75.1%
Mathis G et al. Thoracic Ultrasound for Diagnosing Pulmonary Embolism: A Prospective Multicenter Study of
352 Patients. Chest 2005;128:1531-1538
Gamal Agmy

9. PE DIAGNOSTIC ACCURACY
LUS for diagnosis of PE
Metaanalysis:
- Sens.: 80% (75-83%)
- Spec.: 93% (89-96%)
Niemann T et al. Transthoracic sonography for the detection of pulmonary embolism–a meta-analysis.
Ultraschall Med 2009 30:150–156
Gamal Agmy

10. Gamal Agmy

11. Gamal Agmy

12. Gamal Agmy

13. Gamal Agmy

14. Gamal Agmy

15. Gamal Agmy

16. Gamal Agmy

17. Gamal Agmy

18. Gamal Agmy

19. Gamal Agmy

20. Gamal Agmy

21. Gamal Agmy

22. Gamal Agmy

23. Gamal Agmy

24. Gamal Agmy

25. Gamal Agmy

26. Gamal Agmy

27. Gamal Agmy

28. Gamal Agmy

29. Gamal Agmy

30. Gamal Agmy

31. Gamal Agmy

32. Gamal Agmy

33. Gamal Agmy

34. Nonthrombotic Pulmonary Embolism
Gamal Agmy

35. Nonthrombotic Pulmonary Embolism
Gamal Agmy

36. Nonthrombotic Pulmonary Embolism
Gamal Agmy

37. Nonthrombotic Pulmonary Embolism
Gamal Agmy

38. Nonthrombotic Pulmonary Embolism
Gamal Agmy

39. Developmental Anomalies
Gamal Agmy

40. Developmental Anomalies
Gamal Agmy

41. Developmental Anomalies
Gamal Agmy

42. Developmental Anomalies
Gamal Agmy

43. Pulmonary A-V Malformations
Gamal Agmy

44. Pulmonary Artery Aneurysms
Gamal Agmy

45. Pulmonary Artery Aneurysms
Gamal Agmy

46. Pulmonary –Systemic Communications
Gamal Agmy

47. Pulmonary –Systemic Communications
Gamal Agmy

48. Pulmonary –Systemic ommunications
Gamal Agmy

49. Abnormal Systemic Arteries
Gamal Agmy

50. Pulmonary Hypertension
Gamal Agmy

51. CTEPH =
Chronic thrombembolic
pulmonary hypertension
Gamal Agmy

52. Mosiac pattern
Gamal Agmy

53. Where is the pathology ???????
in the areas with increased density
meaning there is ground glass
in the areas with decreased density
meaning there is air trapping
Gamal Agmy

54. Pathology in black areas
Airtrapping: Airway
Disease
Bronchiolitis obliterans (constrictive bronchiolitis)
idiopathic, connective tissue diseases, drug reaction,
after transplantation, after infection
Hypersensitivity pneumonitis
granulomatous inflammation of bronchiolar wall
Sarcoidosis
granulomatous inflammation of bronchiolar wall
Asthma / Bronchiectasis / Airway diseases
Gamal Agmy

55. Airway Disease
what you see……
In inspiration
sharply demarcated areas of seemingly increased
density (normal) and decreased density
demarcation by interlobular septa
In expiration
‘black’ areas remain in volume and density
‘white’ areas decrease in volume and increase in
density
INCREASE IN CONTRAST
DIFFERENCES
AIRTRAPPING Gamal Agmy

56. Bronchiolitis
obliterans
Gamal Agmy

57. Pathology in white Areas
Alveolitis / Pneumonitis
Ground glass
desquamative intertitial pneumoinia (DIP)
nonspecific interstitial pneumonia (NSIP)
organizing pneumonia
In expiration
both areas (white and black) decrease in
volume and increase in density
DECREASE IN CONTRAST
DIFFERENCES
Gamal Agmy

58. DI
P Gamal Agmy

59. Cellular
NSIP
Gamal Agmy

60. Mosaic Perfusion
Chronic pulmonary embolism
LOOK FOR
Pulmonary hypertension
idiopathic, cardiac disease, pulmonary
disease
Gamal Agmy

61. Pulmonary Hemorrhage
Gamal Agmy

62. INTERSTITIAL SYNDROME
Gamal Agmy

63. INTERSTITIAL SYNDROME
Gamal Agmy

64. Gamal Agmy

65. Gamal Agmy

66. Gamal Agmy

67. Gamal Agmy

68. Gamal Agmy

69. Aortic Aneurysms
• Location
– Ascending / Anterior mediastinum
– Arch / Middle mediastinum
– Descending / Posterior mediastinum
• Characteristics
– Mediastinal "mass" density
– Extrapleural
– Calcification of wall
• Dissecting
– Inward displacement of calcified intima
– Wavy margin
– Inlet to outlet shadow
– Left pleural effusion
Gamal Agmy

70. Gamal Agmy

71. Gamal Agmy

72. Gamal Agmy

73. Dissecting Aneurysm
Mediastinal widening
Inlet to outlet shadow
on left side
Retrocardiac: Intact
silhouette of left heart
margin
Pulmonary artery
overlay sign: Density
behind left lower lobe
Wavy margin
Gamal Agmy

74. Management Dilemmas in
Acute Pulmonary Embolism
Prof. Gamal Agmy, MD, FCCP
Prof. of Chest Diseases, Assiut University

75. Fourteen clinical dilemmas were identified
by Respiratory and Hematology physicians
with specific interests in acute and chronic
PE. Current evidence and guidelines were
reviewed and a practical approach
suggested.

76. Which patients with Intermediate
Risk PE should I thrombolyse?

77. In Intermediate risk PE we would not
routinely administer thrombolysis. PESI
score and the presence or absence of
single or multiple poor prognostic factors
should be balanced against factors
associated with increased risk of bleeding
(including age) in identifying suitable
candidates for thrombolysis.

79. What is the risk of thrombolysis
in a patient with recent surgery,
previous stroke or intracranial
space-occupying lesion?

80. In patients with a massive PE within 1 week of
surgery we would favor mechanical treatment if
available. Within 1–2 weeks following surgery,
thrombolysis may be an acceptable risk depending
on the nature of the surgery. In our opinion
previous ischemic stroke is not an absolute
contraindication to thrombolysis but there are no
data to guide an acceptable timescale since the
stroke. Selected intracranial space occupying
lesions, for example meningiomas, would not
influence our decision to thrombolyse.

81. A patient with an acute cerebral
infarct is found to have an
acute PE: what should I do
regards anticoagulation?

82. The risk–benefit ratio for individual
patients should be assessed; however, our
general approach is to anticoagulate all
patients with a cerebral infarct and PE. In
patients with PE with a primary
hemorrhagic stroke or recent significant
hemorrhagic transformation we would
consider inferior vena cava (IVC) filter
insertion and delayed anticoagulation.

83. What is the optimal type and
dose of thrombolytic agent
and what should I do if a
patient is already on low
molecular weight heparin?

84. If thrombolysis is indicated for PE we would
administer a 10 mg bolus of alteplase
followed by a further 90 mg over 2 h (up to
a maximum of 1.5 mg/kg). If thrombolysis is
indicated but there is a high risk of
haemorrhage we would consider using a
half-dose regimen

85. Which patients in an arrest or
peri-arrest situation should I
consider thrombolysing in the
absence of definitiv radiological
evidence of PE?

86. Thrombolysis should be administered in
the peri-arrest or arrest situation when PE
is either known or suspected.

87. I feel it is too unsafe to
perform thrombolysis: what
are the surgical and non-
surgical alternatives?

88. No comparative data exist to guide
primary management of massive PE in the
presence of a strong contraindication to
systemic thrombolysis. Management is
dependent on local availability of
cardiothoracic surgery and catheter-based
therapy.

89. A patient with a recent acute
PE fails to respond to initial
therapy: what should I do?

90. Thrombolysis should be considered
when a patient initially treated with
anticoagulation alone develops worsening
cardiovascular instability or respiratory
failure. Failure to improve following
thrombolysis should trigger reassessment
for residual clot or complication of PE.
Surgical embolectomy is preferable to re-
thrombolysis for persistent obstructing acute
PE.

91. How should I manage a pregnant
patient with significant PE?

92. Therapeutic LMWH is the anticoagulant of
choice in pregnancy. Systemic thrombolysis
should be administered for massive PE in
pregnancy; however if bleeding risk is high
(eg, in the peripartum period) then surgical
or mechanical methods are suggested,
depending on local availability

93. An echo demonstrate thrombus
in the right atrium: what is the
optimal management?

94. Right atrial thrombus occurs in 4–8% of patients with acute
PE.86–90 Two main types of thrombus have been described:
type A has high early mortality and consists of long, thin, worm-
like mobile thrombi associated with clinically severe PE. Low
cardiac output, higher pulmonary arterial pressure and more
severe tricuspid regurgitation may slow transit of clot from
peripheral veins to the pulmonary vasculature.
Type B consists of immobile, non-specific thrombi with absence
of associated PE in 60% of cases and low early mortality. A small
proportion of thrombi are intermediate in character
(type C), being mobile but not worm-like in shape, and have the
potential to obstruct right atrial or ventricular outflow. CTPA is
highly effective at identifying type A thrombi with a sensitivity of
100%, although false positives may be observed in patients with
non-dilated right ventricles due to incomplete contrast filling.

95. Thrombolysis is suggested for type A thrombus
while type B thrombus may be treated with
anticoagulation alone. Surgical embolectomy is
suggested for thrombus straddling a PFO; if this
is not available then anticoagulation alone is a
reasonable approach unless thrombolysis is
indicated due to the severity of the underlying PE.
Surgical embolectomy is suggested for type C
thrombus if the thrombus is extremely large and
associated with risk of right atrial or ventricular
outflow tract obstruction should it dislodge.

96. Which patients with acute PE
may benefit from an IVC
filter?

97. We generally limit IVC filter use in acute
PTE to the small number of patients in
whom anticoagulation is contraindicated.
Routine placement of IVC filters in
submassive PE and proximal DVT is not
supported by current evidence. If
possible we use retrievable filters, which
should ideally be removed within the
recommended time scale.

98. In which patients should I
consider early discharge?

99. Patients with a very low or low PESI score
may be offered early discharge and
outpatient anticoagulation but a robust
system of support and follow-up is
mandatory.

100. What is the role of the newer
oral agents in the management
of acute PE?

101. New oral agents can be considered an
option for the acute management of
haemodynamically stable patients with PE

102. What should I do about an
incidental or isolated
subsegmental PE?

103. Incidental and isolated subsegmental PE
should generally be managed in the same
manner as symptomatic and non-
subsegmental PE.

104. Management of pulmonary
embolism in patients with
cancer

105. When selecting the mode of
anticoagulation in patients with cancer
and acute PE, LMWH administered in the
acute phase (except for high-risk PE) and
continued over the first 3–6 months
should be considered as first-line therapy.