This document discusses pulmonary embolism (PE), including its definition, epidemiology, risk factors, pathophysiology, clinical features, diagnosis, and management. Some key points: - PE is an obstruction of the pulmonary artery or its branches by a thrombus originating in the venous system or right heart. It is a common cause of preventable death in hospitalized patients. - The annual incidence of PE ranges from 23-69 cases per 100,000 people in India. Worldwide, the incidence of venous thromboembolism (which includes PE and DVT) is 117 cases per 100,000 person-years. - Risk factors for PE include hereditary clotting disorders, immobil

1. PULMONARY
EMBOLISM
PRESENTED BY
Dr. Marwan Abdel Rahman Sneymeh

2. DEFINITION
 It is an obstruction of the pulmonary artery or one
of its branches by a thrombus that
originates somewhere in the venous system or in
the right side of heart.
It is most common preventable cause of death
among hospitalized patient

3. EPIDEMOLOGY (INDIAN SCENARIO)
Overall, the annual incidence of PE
ranges between 23 and 69 cases per
100,000 population
Responsible for up to 15% of all inhospital
deaths

4. EPIDEMOLOGY (GLOBAL SCENARIO)
The incidence of venous thromboembolism(VTE), which
includes PE and deep venous thrombosis (DVT), has
remained relatively constant, with age- and sexadjusted
rates of 117 cases per 100 000 person-years.
VTE incidence rises sharply after age 60 in both men and
women, with PE accounting for the majority of the increase.
The mortality rate associated with PE is
underappreciated; it exceeds15% in the first 3 months
after diagnosis.
In nearly 25% of patients with PE, the initial clinical
manifestation is sudden death.

5. VIRCHOW’S
TRIAD

6. PREDISPOSING
FACTORS

7. PATHOPHYSIOLOGY
Virchow’s triad of
inflammation
Recruitment of
activated platelets
releasing micro
particle
Microparticle
containing
proinflammatory
mediator binds
neutrophils
Neutrophil releases
nuclear material
forming web like
extra cellular
network
Aggregation of
platelet and
platelet dependent
thrombin
generation

8. PATHOPHYSIOLOGY

9. HEREDITARY FACTORS
 Antithrombin III deficiency
 Protein C deficiency
 Protein S deficiency
 Factor V Leiden
 Plasminogen abnormality
 Fibrinogen abnormality

10. CLINICAL FEATURES

11. 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

12. DIAGNOSIS

13.  Dr. Wells demonstrated the utility of his scoring
system for determining the pre-test probability for PEs,
known now as the Wells Criteria. This study evaluated
946 patients, and based on the criteria, divided them
into low, moderate and high probability of having a
PE. These criteria included: clinical signs and
symptoms of DVT (3 points), PE as the most likely
diagnosis (3 points), tachycardia (1.5 points),
immobilization for at least 3 days or surgery within the
previous 4 weeks (1.5 points), previous objectively
diagnosed PE or DVT (1.5 points), hemoptysis (1
point), and malignancy (1point). Risk score
interpretation (probability of PE) was the following: >6
points: high risk (78.4%); 2 to 6 points: moderate risk
(27.8%);
Annals Intern Med 2001;135:98-107

15. ORIGINAL GENEVA CRITERIA

16. REVISED GENEVA CRITERIA

17. PERC RULE
 In 2004, Kline conducted a prospective study looking at eight
variables to rule out pulmonary embolism.
 The rule-out test (with poor specificity of 27% in low-risk
patients and 15% in very-low-risk patients)
 Pulmonary Embolism Rule out Criteria
(PERC) are as follows:
1. Age greater than or equal to 50 years
2. Heart rate greater than or equal to 100 beats per minute
3. Arterial oxygen saturation (SaO 2) on room air less than 95%
4. Venous thromboembolism
5. Recent (<28 days) trauma or surgery
6. Unilateral leg swelling
7. Hemoptysis
8. Oral hormone use

18.  Pulmonary embolism workup can be ruled out if
1. None of the above eight variables is positive.
2. A PERC evaluation is considered positive if any
one of the eight criteria are met.

19.  In 2015, pulmonary embolism guidelines were released by
the American College of Physicians and are summarizedas
follows .
1. Use either the Wells or Geneva rules to choose tests based on a patient's risk for
pulmonary embolism.
If the patient is at low risk, clinicians should use the eight PERC; if a patientdoes
not meet all eight criteria, the risks of testing are greater than the risk for
embolism, and no testing is needed.
For patients at intermediate risk, or for those at low risk who do not meet all of
the rule-out criteria, use a high-sensitivity plasma D-dimer test as the initial test.
In patients older than 50 years, use an age-adjusted threshold (age × 10 ng/mL,
rather than a blanket 500 ng/mL), because normal D-dimer levels increase with
age.
Patients with a D-dimer level below the age-adjusted cutoff should not receive
any imaging studies.
Patients with elevated D-dimer levels should then receive imaging.
Patients at high risk should skip the D-dimer test and proceed to CT pulmonary
angiography, because a negative D-dimer test will not eliminate the need for
imaging in these patients.
Clinicians should only obtain ventilation-perfusion scans in patients with a
contraindication to CT pulmonary angiography or if CT pulmonary angiographyis
unavailable.
2.
3.
4.
5.
6.
7.
8.
Skwarecki B. Pulmonary embolism guidelines
released by ACP. Medscape Medical News. WebMD
Inc. Sept 28, 2015.

22. CHEST X-RAY
Fleishner sign
Hampton hump
Westermark sign

23. FLEISHNER SIGN

29. ECG

30. D - DIMER
 D-dimer ELISA is an excellent screening test
for suspected PE
 A negative D-Dimer assay in low clinical
probability case rules out PE
 D-dimer ELISA was often elevated in the
absence of PE like sepsis ,cancer,acute medical
illness
 Low specificity and poor positive predictive
value
 Sensitivity >80% for DVT and >95% for PE

31. ECHO
 Right ventricular enlargement or
hypokinesis, especially free wall
hypokinesis, with sparing of the apex (the
McConnell sign)
 Interventricular septal flattening and
paradoxical motion toward the left
ventricle, resulting in a D-shaped left
ventricle in cross section
 Tricuspid regurgitation
 Direct visualization of
thrombus (more likely
with transesophageal
echocardiography

32. CT PULMONARY
ANGIOGRAPHY
 It is investigation of
choice

33. CT PULMONARY ANGIOGRAPHY

34. 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

38. LUNG SCAN
 As many as 40% of pts with high clinical suspicion
for PE and low probability scans have a PE on
angiogram
 It has become second line diagnostic test for
patients who cannot tolerate intravenous
contrast
 Small particulate aggregates of albumin labelled
with gamma emitting radio nucleid is injected
 Ventilation can be obtained by radio labelled
inhaled gas such as xenon, krypton
 A high probability scan is defined as two or
more segmental perfusion defects in
presence of normal ventilation scan
 The diagnosis of PE is very unlikely in pt with
normal or near normal scan.

41. 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
Definitive diagnosis is visualization of
an intraluminal filling defect .
Secondary sign is abrupt occlusion of
vessel, segmental oligemia,prolonged arterial
phase with slow filling .

44. MANAGEMENT

46. HEPARIN
 Choices include either intravenous
unfractionated heparin (UFH)
or subcutaneous low-molecular-weight
heparin (LMWH) preparations
 Initial intravenous bolus of 80 units of
heparin per kilogram followed by a
continuous infusion initiated at 18 units per
kilogram per hour.
 The heparin drip is adjusted based on
monitoring of the activated partial
thromboplastin time (aPPT), drawn 6hours
after initial bolus dose, then 6 hours after
each dose adjustment , with a target
aPPT ratio of 2.0 to 3.5
 More recently, an approach using a fixed
dose of subcutaneous unfractionated
heparin , administered as an initial dose of
333 U/kg followed by a dose of 250 U/kg
every 12 hours, has been demonstrated to
be as safe and effective as LMWH.

47.  Situations in which the use of UFH is
appropriate
1. Renal insufficiency.
2. Extremes of body weight.
3. Hypertensive crisis,
o Rapid adjustment of anticoagulation is
needed, such as…
A. Women in the late pregnancy who may need
caesarian sections,
B. Patients with recent surgery or
C. Recent history of bleeding

48. LMWH
 Advantages of LMWH compared with UFH include:
1. Longer half-life and ease of use
2. Ability to consistently achieve early therapeutic anticoagulation
3. No need to monitor anticoagulant effects
4. Reduced incidence of major bleeding complications
 In general, therapeutic monitoring is not needed with LMWH, but
there are situations where the therapeutic effetcts may be less
predictable and monitoring with ant-Xa levels is indicated
 Typical examples include:
1. Patients with antiphospholipid antibodies or other circulating
anticoagulants who have elevated baseline a PPT
2. Extremes of body weight(<40kgs and >50kgs)
3. Significant renal disease(creatinine clearance <30 ml/min)
4. Pregnancy
5. Unexplained bleeding or recurrent thrombosis during therapy

49. FONDAPARINUX
 A synthetic pentasaccharide, selective for
factor Xa
 By binding rapidly and strongly to antithrombin,
fondaparinux catalyzes specifically the inhibition
of factor Xa, which results in inhibition of
thrombin generation
 Half-life of approx 17 hours, and is exctreted
almost completely by the kidneys
 It does not cause heparin induced
thrombocytopenia

50. THROMBOLYTIC THERAPY
1. Streptokinase
2. Urokinase
3. rt PA
 these agents convert circulating plasminogen to plasmin.
 The preferred fibronolytic regimen is 100mg rt PAover 2
hour.
Contraindication :
 Intracranial disease
 Recent surgery
 Trauma

51.  The exact role of thrombolytic agents in acute
pulmonary embolim remains controversial. While
thrombolytic therapy does appear to accelerate the
rate of thrombolysis, there is no convincing evidence
to suggest that
 It decreaes mortality,
 Increases the ultimate extent of embolic resolution when
measured at 7 days,
 Reduces thromboembolic recurrence rates,
 improves symptomatic outcomes,
 Decreases the incidence of thromboembolic
pulmonary hypertension
 Catheter- directed techniques have been successfully
employed in the setting of acute ileo- femoral DVT
using doses of urokinase ranging from 1.4 to 16
million units delivered over an
average of 30 hours.

52. INTERVENTIONA
L
RADIOLOGIC TE
CHNIQUES
 Interventional thrombus
fragmentation.
 The devices use either
pressured saline or
a rotating impeller to
fragment central
thrombi.
 The fragments are either
aspirated through a separate
port on the catheter or
allowed to migrate distally.
 There limitations, including
a risk of
paradoxical embolism from
the clot fragments

53. PULMONARY EMBOLECTOMY
 It is reasonable to consider surgical embolectomy in
patients with
1. Persistent hypotension.
2. Shock.
3. Cardiac arrest.
4. Failed thrombolysis.
5. Contraindications to
thrombolytics.

54. ORAL
ANTICOAGULANTS
 Warfarin inhibits gamma carboxylation
activation of coagulation factors II, VII,
IX, and X as well as proteins C and S
 Use of Warfarin without heparin
is strongly discouraged
 It generally takes 3 to 5 days
of warfarin to achieve full
therapeutic eficacy.
 In patients with protein C deficiency,
skin necrosis or paradoxical
thrombosis may occur.

55. WARFARIN
 INR range between 2 and 3 is
recommended for most patients
 Another rare complication of warfarin
use is cholesterol microembolism
(“purple toes” syndrome), which
is thought to be due to cholesterol
crystal release from ulcerated
intravascular plaques
 an initial daily dose of 5 or 10 mg with
use of an standardized nomogram to
dose adjust based on INR values
obtained on days 3 and 5
 patients should receive atleast 5 days of
combined heparin and warfaein therapy,
including atleast 2 days in which the INR
is in a therapeutic range prior to
stopping heparin
 Because of the teratogenic potential of
warfarin, UFH or LMWH should be used
in pregnant women who developed VTE
in the first trimesters

56. DURATION
OF
THERAPY
 The risk of recurrent disease after 3 months
of anticoagulation is still in the region of
10%; therefore, the patients should
be treated with warfarin for 3 to 6 months
 Patients with idiopathic thromboembolism
have higher rate of recurrence therefore
treated for atleast 6 to 12 months
 Patients with antiphospholipid antibody
syndrome have considerable risk of
recurrence, therefore treated for
minimum 12 months with consideration of
life-long therapy
 In patients with >2 episodes of recurrence
life-long anticoagulation given

57. DEEP VEIN THROMBOSIS
 Thrombolysis
 Anticoagulation
 Vena cava filter

58. VENA CAVAFILTER
 Used in patients with contraindication to
anticoagulation or patients
with recurrent embolism while on adequate
anticoagulation
 Long term IVC filter increases risk of
thromboembolism
 This observation lead to recent development of
retrievable filters
 Four types of retrievable filters:
1. Gunther tulip filter
2. ALN filter
3. Recovery filter
4. OptEase filter

59. VENA CAVAFILTER

60. PROPHYLAXIS

61. INTERMITTENT PNEUMATIC COMPRESSION
 The sleeves are inflated for
a few seconds, one leg at a
time, to compress the veins
in the legs every minute or
so.
 By causing contraction of
the leg muscles, the
sleeves mimic the
process of walking in
immobilized patients. This
ensures blood is pushed
around the system, rather
than pooling in the legs

62. GRADUATED COMPRESSION STOCKING
 Compression stockings
are made of a special
elastic fabric. They are very
tight at the ankle and are
less tight as the stocking
moves up the leg. This
graduated tightness helps
the leg muscles squeeze
fluid up the leg, which
improves blood flow from the
leg back to the heart and
decreases leg swelling and
pain.

64. TYPE OF
EMBOLISM
Fat embolism
Venous air embolism
Amniotic fluid embolism
Septic embolism
Tumour embolism
Sickle cell disease

65. FAT EMBOLISM
 Due to entry of neutral at in vascular system
 Leads to dyspnea, hypoxemia, petechiae, mental confusion
 Lag time of 24 to 72 hours in the onset of syndrome following
the inciting event
 Most common inciting event, fracture of long bones
 Pathophysiology :
 Actual vascular obstruction by neutral particle of fat
 Injurious effect of free fatty acids released by the action of lipases
on the neutral fat
 Supportive treatment advised
 Other suggested treatment intravenous ethanol, albumin, dextran,
heparin

66. VENOUS AIR EMBOLISM
 Due to indwelling central venous catheter, positive pressure
ventilation, trauma to thorax
 Physiological consequence due to abrupt rise in pulmonary
artery pressure
 Treatment is prevention and early detection
 Patient positioning (Trendelenburg position with left side
down)
 Removal of air through central venous catheter
 Direct needle aspiration
 Closed chest cardiac massage
 Increase absorption with use of 100% oxygen

67. AMNIOTIC FLUID EMBOLISM
 Third leading cause of maternal mortality
 Amniotic fluid contains particulate material that can
cause pulmonary vascular obstruction
 Amniotic fluid has thromboplastic activity that leads
to extensive fibrin deposition in lung vasculature
that leads to consumptive coagulopathy leading to
hypofibrinogenemia and thrombocytopenia
 Presence of squamous cell in pulmonary arterial
blood once considered pathognomonic.

68. SEPTIC EMBOLISM
 Microscopically septic phlebitis consist of
purulent material mixed with fibrin thrombus
 Chest X-ray display pulmonary infiltrates
 Treatment consists of anti microbial agents

69. TUMOUR EMBOLISM
 Most common site of origin breast, lungs,
prostate, stomach and liver
 Clinical feature is typically subacute and involves
progressive dyspnea, tachypnea, tachycardia
 Pulmonary angiographic findings reveal
delayed vascular filling, pruning and
tortuosity