1. Pulmonary embolism is an obstruction of the pulmonary artery or its branches by a thrombus originating in the venous system or right side of the heart. 2. The annual incidence of PE ranges from 23-69 cases per 100,000 population in India. Globally, the incidence of venous thromboembolism remains relatively constant at 117 cases per 100,000 person-years. 3. Diagnosis involves using criteria like Wells criteria and PERC rule to determine pre-test probability, D-dimer testing, and imaging like CT pulmonary angiography or lung scan if needed based on risk level and test results. Management involves anticoagulation with heparin or low molecular weight he

1. PULMONARY
EMBOLISM
PRESENTED BY
Dr. RAHUL GUPTA

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 exceeds
15% 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 (1 point).
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 summarized as
follows .
1. Use either the Wells or Geneva rules to choose tests based on a patient's risk for
pulmonary embolism.
2. If the patient is at low risk, clinicians should use the eight PERC; if a patient does
not meet all eight criteria, the risks of testing are greater than the risk for
embolism, and no testing is needed.
3. 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.
4. 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.
5. Patients with a D-dimer level below the age-adjusted cutoff should not receive
any imaging studies.
6. Patients with elevated D-dimer levels should then receive imaging.
7. 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.
8. Clinicians should only obtain ventilation-perfusion scans in patients with a
contraindication to CT pulmonary angiography or if CT pulmonary angiography is
unavailable.
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

26. ECG

27. 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

28. 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

29. CT PULMONARY ANGIOGRAPHY
 It is investigation of choice

30. CT PULMONARY ANGIOGRAPHY

31. 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

33. 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.

36. 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 .

39. MANAGEMENT

41. 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 6 hours after initial bolus
dose, thn 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.

42.  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

43. 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

44. FONDAPARINUX
 A synthetic pentasaccharide, selective for factoe
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

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

46.  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
1.
2. It decreaes mortality,
3. Increases the ultimate extent of embolic resolution when measured
at 7 days,
4. Reduces thromboembolic recurrence rates,
5. improves symptomatic outcomes,
6. 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.

47. INTERVENTIONAL RADIOLOGIC
TECHNIQUES
 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

48. 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.

49. 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
1. It generally takes 3 to 5 days of warfarin to
achieve full therapeutic eficacy.
2. In patients with protein C deficiency, skin necrosis
or paradoxical thrombosis may occur.

50. 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

51. 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

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

53. VENA CAVA FILTER
 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

54. VENA CAVA FILTER

55. PROPHYLAXIS

56. 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

57. 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.

59. TYPE OF EMBOLISM
1. Fat embolism
2. Venous air embolism
3. Amniotic fluid embolism
4. Septic embolism
5. Tumour embolism
6. Sickle cell disease

60. FAT EMBOLISM
 Due to entry of neutral at in vascular system
 Leads to dysnea, 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 :
1. Actual vascular obstruction by neutral particle of fat
2. 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

61. 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

62. 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.

63. 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

64. TUMOUR EMBOLISM
 Most common site of origin breast, lungs, prostate, stomach and liver
 Clinical feature is typically subacute and involves progressive dysnea
, techypnea, techycardia
 Pulmonary angiographic findings reveal delapyed vascular filling,
pruning and tortuosity