PULMONAR

Y
EMBOLISM

Dr. NOUH BOTAN

It is most common preventable cause of death
among hospitalized patient

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
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.
VIRCHOW’S
TRIAD
PREDISPOSING FACTORS
PATHOPHYSIOLOGY

Virchow’s triad of Aggregation of

inflammation platelet and
platelet dependent
thrombin
generation

Recruitment of
activated platelets
releasing micro Neutrophil releases
particle nuclear material
forming web like
extra cellular
network
Microparticle
containing
proinflammatory
mediator binds
neutrophils
PATHOPHYSIOLOGY
HEREDITARY FACTORS
 Antithrombin III deficiency
 Protein C deficiency

 Protein S deficiency

 Factor V Leiden

 Plasminogen abnormality

 Fibrinogen abnormality
CLINICAL FEATURES
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
DIAGNOSIS
 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

ORIGINAL GENEVA CRITERIA
REVISED GENEVA CRITERIA
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
 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.
 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
4.
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
5.
increase with age.
Patients with a D-dimer level below the age-adjusted cutoff should not receive
6.
any imaging studies.
7.
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
8.
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 angiography
is unavailable.

Skwarecki B. Pulmonary embolism guidelines

released by ACP. Medscape Medical News. WebMD
Inc. Sept 28, 2015.
CHEST X-RAY
 Fleishner sign
 Hampton hump

 Westermark sign
ECG
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

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
CT PULMONARY ANGIOGRAPHY
 It is investigation of choice
CT PULMONARY ANGIOGRAPHY
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
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.
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 .
MANAGEMENT
HEPARI
N
 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.
 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
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
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
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
 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.
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
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.
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.
WARFARI
N
 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
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
DEEP VEIN THROMBOSIS
 Thrombolysis

 Anticoagulation

 Vena cava filter

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