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Pulmonary EmbolismPulmonary Embolism
Dr. Muhammad Bayazid
M.D Final part student, Cardiology, DMCH
DVT : Blood clot formation with inDVT : Blood clot formation with in
the large veins usually in the legsthe large veins usually in the legs
PE results from DVTs that havePE results from DVTs that have
broken off and travelled tobroken off and travelled to
pulmonary arterial circulationpulmonary arterial circulation
The majority of pulmonary emboliThe majority of pulmonary emboli
( 80%) arise from the propagation of( 80%) arise from the propagation of
lower limb DVTlower limb DVT
Other causes : Air, AmnioticOther causes : Air, Amniotic
Fluid, Fat EmbolismFluid, Fat Embolism
Venous thromboembolism
 DVT
 Pulmonary
Embolism
DEFINITIONDEFINITION
Pulmonary embolismPulmonary embolism ( (PEPE) is) is
a blockage of an artery in the lungs  by aa blockage of an artery in the lungs  by a
substance that has traveled from elsewhere in thesubstance that has traveled from elsewhere in the
Why it is important?Why it is important?
PE is the most common preventable cause ofPE is the most common preventable cause of
death in hospitalized patientsdeath in hospitalized patients
Majority of patient die because of failure ofMajority of patient die because of failure of
diagnosis rather than inadequate therapy.diagnosis rather than inadequate therapy.
80% of pulmonary emboli occur without prior80% of pulmonary emboli occur without prior
warning signs or symptomswarning signs or symptoms
Mortality rate without treatment is 30%,Mortality rate without treatment is 30%,
whereas with adequate treatment is only 2-8%whereas with adequate treatment is only 2-8%
Early treatment is highly effectiveEarly treatment is highly effective
TypesTypes
Non thrombtic pulmonaryNon thrombtic pulmonary
embolismembolism
 Fat embolism.Fat embolism.
 Air embolism.Air embolism.
 Amniotic fluid embolism.Amniotic fluid embolism.
 Tumor embolism (Tumor embolism (HCCHCC && RCCRCC).).
Thrombotic pulmonaryThrombotic pulmonary
embolismembolism
Hypercoagulability
Hereditary Deficiencies:
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden
Prothrombin gene
mutation
Dysfibrinogenemia
Acquired:
Cancer
Pregnancy & postpartum
period
Oral contraceptives
Hormone replacement
therapy
Polycythemia rubravera
Smoking
Anti phospholipid syndrome
Chemotherapy
Stasis
Immobility/cast/travel
Advanced age
Acute medical illness
Major surgery
Spinal cord injury
Obesity
Endothelial Damage
Major surgery
Trauma
Central venous
catheterization
Risk for thromboembolism approximately doubles for each decade beyond
age 60 years
Risk factors
Major Risk (RR 5-20)Major Risk (RR 5-20)
•Major and abdominal surgeryMajor and abdominal surgery
•Lower Limb OrthopedicLower Limb Orthopedic SurgerySurgery
•Obstetric – Late preganancy,Obstetric – Late preganancy,
LSCS, Pre eclampsiaLSCS, Pre eclampsia
•Maliganancy- Pelvic ,Maliganancy- Pelvic ,
abdominal or metastaticabdominal or metastatic
•Lower Leg # , varicose veinsLower Leg # , varicose veins
•History of proven VTEHistory of proven VTE
Minor Risk Factors ( RR
CVS : HF, HTN, Congenital
Heart Disease, Central lines
Estrogen : OCP, HRT
Others : Occult malignancy,
COPD
Neurological disability, obesity,
thrombotic mayeloproliferative
disease, nephrotic syndrome
Inflammatory bowel disease
Risk factors
PathophysiologyPathophysiology
ClinicalClinical
PresentationPresentation Massive PEMassive PE::
Symptom:Symptom:
Severe central chest pain, Severe dyspnoea,Severe central chest pain, Severe dyspnoea,
Syncope, Pallor, Sweating,Syncope, Pallor, Sweating,
Sign:Sign:
Major circulatory collapse, tachycardia, hypotension,Major circulatory collapse, tachycardia, hypotension,
Shock,Shock,
Central cyanosis, Elevated JVP, Loud P2, S2 split,Central cyanosis, Elevated JVP, Loud P2, S2 split,
gallop rhythm.gallop rhythm.
 Small or Medium PESmall or Medium PE : SOB, Pleuritic chest pain,: SOB, Pleuritic chest pain,
Haemoptysis, Tachycardia, Tachypnea, Pleural rub.Haemoptysis, Tachycardia, Tachypnea, Pleural rub.
Crackles, pleural effusionCrackles, pleural effusion
 Chronic PEChronic PE: Exertional dyspnoea, symptoms of: Exertional dyspnoea, symptoms of
pulmonary HTN or right heart failure,pulmonary HTN or right heart failure,
17/08/1717/08/17 1313
Proportion with PE
65%
30
10%
1717
DiagnosisDiagnosis
 CXRCXR
 ABG:ABG:
 ECGECG
 V/QV/Q
 Spiral CTSpiral CT
 EchoEcho
 AngioAngio
 Fibrin Split Products/D-dimerFibrin Split Products/D-dimer
Contd…Contd…
ECGECG
 Sinus tachycardia –Sinus tachycardia –  m/c abnormality m/c abnormality
 Complete or incomplete RBBB –Complete or incomplete RBBB –  a/w ↑ mortality a/w ↑ mortality
 RV strain pattern –RV strain pattern –  T wave ↓ in the right precordial leads T wave ↓ in the right precordial leads
(V1-4) ± the inferior leads(V1-4) ± the inferior leads
 Right axis deviationRight axis deviation
 S1, Q3, T3 patternS1, Q3, T3 pattern
 Right atrial enlargement (P pulmonale) –Right atrial enlargement (P pulmonale) – peaked Ppeaked P
wave in lead II > 2.5 mm in heightwave in lead II > 2.5 mm in height
 Atrial Tachyarrhythmias –Atrial Tachyarrhythmias –  AF, Flutter AF, Flutter
 Non specific ST-segment & T wave changesNon specific ST-segment & T wave changes
1919
S1 Q3 T3 Pattern
2020
T-wave inversion
2121
Rt. Bundle Branch Block
2222
Rt. Bundle Branch Block
Chest X-rayChest X-ray
 Chest X ray – most common finding with aChest X ray – most common finding with a
PE is a normal x-rayPE is a normal x-ray
 But they are useful as X-rays help to ruleBut they are useful as X-rays help to rule
out pneumonia and pneumothorax asout pneumonia and pneumothorax as
causes of dyspnoea etccauses of dyspnoea etc
 A normal CXR in the presence ofA normal CXR in the presence of
significant dyspnoea and hypoxemia insignificant dyspnoea and hypoxemia in
absence of bronchospasm and anatomicabsence of bronchospasm and anatomic
cardiac shunt is highly suggestive of PEcardiac shunt is highly suggestive of PE
Chest XrayChest Xray
 Chest radiograph findings in patient withChest radiograph findings in patient with
pulmonary embolismpulmonary embolism
ResultResult PercentPercent
CardiomegalyCardiomegaly 27%27%
Normal studyNormal study 24%24%
AtelectasisAtelectasis 23%23%
Elevated HemidiaphragmElevated Hemidiaphragm 20%20%
Pulmonary Artery EnlargementPulmonary Artery Enlargement 19%19%
Pleural EffusionPleural Effusion 18%18%
Parenchymal Pulmonary InfiltrateParenchymal Pulmonary Infiltrate 17%17%
Am Heart J
1997;134:479-87
Radiographic signs of acute pulmonaryRadiographic signs of acute pulmonary
embolismembolism
 Signs with relative high specificity but lowSigns with relative high specificity but low
sensitivity for acute pulmonary embolism:sensitivity for acute pulmonary embolism:
 Decreased vascularity in the peripheral lungDecreased vascularity in the peripheral lung (Westermark sign).(Westermark sign).
 Enlargement of the central pulmonary arteryEnlargement of the central pulmonary artery (Fleischner sign).(Fleischner sign).
 Enlarged right descending pulmonary arteryEnlarged right descending pulmonary artery (Palla's sign)(Palla's sign)
 Pleural based areas of increased opacity (Pleural based areas of increased opacity (Hampton humpHampton hump).).
 Hemidiaphragm elevation.Hemidiaphragm elevation.
(Hampton hump)(Hampton hump)
•The classic radiographic findings of
pulmonary infarction
• a wedge-shaped, pleura-based
triangular opacity with an apex
pointing toward the hilus
The Westermark sign : focal oligemia distal
to a PE
Atelectic band
D-dimerD-dimer
 By-product of fibrinBy-product of fibrin
degradationdegradation
 As clot degraded byAs clot degraded by
enzymes, Fibrinenzymes, Fibrin
Degradation ProductsDegradation Products
(FDP) are released, one(FDP) are released, one
of these is the D-dimerof these is the D-dimer
 Little clots in body releaseLittle clots in body release
D-dimers, therefore if testD-dimers, therefore if test
+ve - do not know if it is+ve - do not know if it is
from a PE,from a PE,
 But test is so sensitiveBut test is so sensitive
that if no D-dimer ( –ve)that if no D-dimer ( –ve)
you can rule out PEyou can rule out PE
CTPACTPA
 Contrast injected into body,Contrast injected into body,
 CT Scan obtained as this isCT Scan obtained as this is
occurringoccurring
 Vessels viewed on end andVessels viewed on end and
seen if they light up withseen if they light up with
contrast.contrast.
 If only partially light up withIf only partially light up with
contrast there may be a bloodcontrast there may be a blood
clot present stopping flowclot present stopping flow
 Do not use if in renal failureDo not use if in renal failure
((Creatanine) (could useCreatanine) (could use
HCOHCO33 cover to stopcover to stop
nephrotoxic effect of contrast)nephrotoxic effect of contrast)
 Unlike VQ Scan if patient hasUnlike VQ Scan if patient has
a pneumonia it will not affecta pneumonia it will not affect
resultsresults
CT findings of acute pulmonary embolismCT findings of acute pulmonary embolism
Vascular abnormalities:Vascular abnormalities:
 Intraluminal filling defects that forms an acute angle withIntraluminal filling defects that forms an acute angle with
the vessel wall & may be surrounded by contrast materialthe vessel wall & may be surrounded by contrast material
(polo mint sign or railway sign).(polo mint sign or railway sign).
 Total cutoff of vascular enhancement.Total cutoff of vascular enhancement.
 Enlargement of the occluded vessel.Enlargement of the occluded vessel.
Ancillary findings:Ancillary findings:
 Pleural based wedge shaped areas of increased attenuationPleural based wedge shaped areas of increased attenuation
with no contrast enhancement.with no contrast enhancement.
 Linear atelectasis.Linear atelectasis.
Partial eccentric filling defect with acutePartial eccentric filling defect with acute
angle with the vessel wallangle with the vessel wall
Intraluminal filling defectIntraluminal filling defect
(polo mint sign)(polo mint sign)
Intraluminal filling defectIntraluminal filling defect
(railway track sign)(railway track sign)
 V /Q lung scanning remains an option andV /Q lung scanning remains an option and
cancan be used when CTA is not available or isbe used when CTA is not available or is
contraindicated.contraindicated.
V /Q Scan
Advantages
relatively low radiation dose
no requirement for contrast
dye
Limitations
Unreliable in pts with COPD and
other conditions in which there is
structural Lung disease
When holding breath is difficult.
Normal
Ventilation
Left UL PE
Perfusion scanVentillation scan
Probability of PEProbability of PE
 Normal - Full ventilationNormal - Full ventilation
and perfusion seenand perfusion seen
 Low Pobability for PE –Low Pobability for PE –
(<20%)(<20%)
 Intermediate probabilityIntermediate probability
for PE-for PE- V andV and P inP in
same areasame area
(Matched deficit) (20-(Matched deficit) (20-
80%)80%)
 High Probability for PE –High Probability for PE –
Normal V andNormal V and P (Un-P (Un-
Matched deficit) (>80%)Matched deficit) (>80%)
Normal
Ventilation
Left UL PE
Perfusion scanVentillation scan
EchocardiographyEchocardiography
 This modality generally hasThis modality generally has
limited accuracy in thelimited accuracy in the
diagnosis.diagnosis.
 The overall sensitivity andThe overall sensitivity and
specificity for diagnosis ofspecificity for diagnosis of
central and peripheralcentral and peripheral
pulmonary embolism bypulmonary embolism by
ECHO is 59% and 77%.ECHO is 59% and 77%.
 It may allow diagnosis ofIt may allow diagnosis of
other conditions that may beother conditions that may be
confused with pulmonaryconfused with pulmonary
embolism.embolism.
ECHO signs of PEECHO signs of PE
 RV enlargementRV enlargement
 Hypokinesis especially free wall hypokinesis, withHypokinesis especially free wall hypokinesis, with
sparing of the apexsparing of the apex (the McConnell’s sign)(the McConnell’s sign)
 Interventricular septal flattening and paradoxicalInterventricular septal flattening and paradoxical
motion toward the LV resulting in a “D-shaped” LV inmotion toward the LV resulting in a “D-shaped” LV in
cross section.cross section.
 Tricuspid regurgitationTricuspid regurgitation
 Lack of inspiratory collapse of IVCLack of inspiratory collapse of IVC
 Direct visualization of thrombusDirect visualization of thrombus
 60/60 Sign-60/60 Sign- Acceleration time of RV ejection <60ms inAcceleration time of RV ejection <60ms in
the presence of TR pressure gradient </= 60mmHg.the presence of TR pressure gradient </= 60mmHg.
Echocardiograms before and after Thrombolysis
Echocardiography-RV Dilation
ECHOECHO
 The severity of this PulmonaryThe severity of this Pulmonary
Artery Pressure (PAP) and theArtery Pressure (PAP) and the
severity of the clot, is found byseverity of the clot, is found by
looking at the tricuspid valvelooking at the tricuspid valve
and noting how much regurgeand noting how much regurge
occurs (Tricuspid jet)occurs (Tricuspid jet)
 If tricuspid jet is high then PAPIf tricuspid jet is high then PAP
differential between RA anddifferential between RA and
RV is great and the clot burdenRV is great and the clot burden
is largeis large
 All these tests may help in theAll these tests may help in the
possible diagnosis of a PE, butpossible diagnosis of a PE, but
are not definitive testsare not definitive tests
UltrasoundUltrasound
 Non-invasiveNon-invasive
 Looks at lower limbsLooks at lower limbs
 Doppler USS looks atDoppler USS looks at
vein for flow andvein for flow and
compressibilty to seecompressibilty to see
if clot presentif clot present
Magnetic resonance angiographyMagnetic resonance angiography
(MRA)(MRA)
MRA appears promising & avoids ionising radiation but has poor
sensitivity for subsegmental clot.
MRA findingsMRA findings
 Visualization of the intravascular fillingVisualization of the intravascular filling
defect.defect.
 Provide physiologic information includingProvide physiologic information including
the regional distribution of ventilation &the regional distribution of ventilation &
perfusion.perfusion.
4848
Pulmonary angiogramPulmonary angiogram
Pulmonary angiographicPulmonary angiographic
findingsfindings
Primary signs:Primary signs:
The only primary sign of acute pulmonaryThe only primary sign of acute pulmonary
embolism is filling defect.embolism is filling defect.
Secondary signs:Secondary signs:
Abrupt occlusion of pulmonary artery.Abrupt occlusion of pulmonary artery.
Areas of oligemia with pruning of theAreas of oligemia with pruning of the
branching vessels.branching vessels.
cardiac troponinscardiac troponins
•Recently, cardiac troponins I and T have been
shown to be associated with early mortality and
a complicated hospital course in patients with
PE.
The assessment of cardiac plasma troponin
levels revealed ventricular injury, especially in
patients with massive PE who had hypotension
or shock.
B Natriuretic PeptideB Natriuretic Peptide
(BNP)(BNP)
•BNP is a neurohormone secreted from the
cardiac ventricles in response to dilatation or
an increase of pressure.
• BNP levels may increase with right ventricle
dysfunction when the patients is in bed and
decrease with treatment.
•Serum brain natriuretic peptide levels of > 90 pg/mL
have a sensitivity of 85% and a specificity of 75% for
predicting adverse clinical outcomes
5252
Autopsy findings of
PULMONARY EMBOLISM
Treatment optionsTreatment options
 Symptomatic treatment:Symptomatic treatment:
– ABCD approachABCD approach
– OxygenOxygen
– AnalgesiaAnalgesia
 Anticoagulation:Anticoagulation:
– IV HeparinIV Heparin
– S/C LMWH eg Enoxaparine, DalteparineS/C LMWH eg Enoxaparine, Dalteparine
– Oral WarfarinOral Warfarin
 IVC filter:IVC filter: If there is contra-indications for anti-coagulationIf there is contra-indications for anti-coagulation
 Thrombolysis:Thrombolysis: tPA eg Alteplase, TenectaplasetPA eg Alteplase, Tenectaplase
 Surgical procedures:Surgical procedures: Pulmonary embolectomyPulmonary embolectomy
General MeasureGeneral Measure
 Oxygen inhalationOxygen inhalation
 Opiates to relieve painOpiates to relieve pain
 Circulatory shock should be treated with I/V fluidCirculatory shock should be treated with I/V fluid
and plasma expenderand plasma expender
 Inotropic agents have limited value as hypoxicInotropic agents have limited value as hypoxic
dilated right ventricle maximally stimulated bydilated right ventricle maximally stimulated by
endogenous catecolaminesendogenous catecolamines
 Diuretics and vasodilator should be avoidedDiuretics and vasodilator should be avoided
because they reduce the cardiac output.because they reduce the cardiac output.
 Precordial thump , which may dislodge thePrecordial thump , which may dislodge the
thrombusthrombus
AnticoagulationAnticoagulation
 Ideally start Fast acting and slow acting anticoagulants,Ideally start Fast acting and slow acting anticoagulants,
when slow acting anticoagulants at desired level, stopwhen slow acting anticoagulants at desired level, stop
fast actingfast acting
 Fast acting -Heparin productsFast acting -Heparin products
Heparin (IV) orHeparin (IV) or
Low Molecular Weight Heparin (S/C)Low Molecular Weight Heparin (S/C)
 Slow acting – Vitamin K AntagonistsSlow acting – Vitamin K Antagonists
WarfarinWarfarin
HeparinHeparin
•The initial treatment of PE is LMWH or UHF for
at least 5 days, followed by warfarin.
•Dose of UFH: 80 U/kg bolus followed by18
U/kg/hour
. Monitoring by APTT(1.5-2.5 )times normal.
•It binds to endogenous antithrombin, This
heparin - antithrombin complex catalyzes the
inactivation of factor Xa and IIa (thrombin).
LMWHLMWH
.
•It should be used whenever possible for the
initial inpatient treatment of DVT & PE.
•Outpatient ttt of DVT, and possibly PE,is safe
and cost-effective for carefully selected
patients.
Adverse effect of heparinAdverse effect of heparin
•Adverse drug reactions include bleeding,
heparin-induced thrombocytopenia, and
osteoporosis .with prolonged use .
Oral anticoagulantOral anticoagulant
•We can give warfarin
•Target international normalised ratio
[INR], 2.0–3.0) for at least 3–6 months.
New oral anti coagulantNew oral anti coagulant
 Oral direct thrombin inhibitor: DabigatranOral direct thrombin inhibitor: Dabigatran
 It is as effective as warfarin for theIt is as effective as warfarin for the
treatment of acute VTE with similar safetytreatment of acute VTE with similar safety
profileprofile
 Dabigatran was also not inferior to S/CDabigatran was also not inferior to S/C
enoxaparin in the prevention of VTEenoxaparin in the prevention of VTE
 Oral direct factor X a inhibitor,Oral direct factor X a inhibitor,
RivaroxabanRivaroxaban
 It has relatively short half life 5-9 hoursIt has relatively short half life 5-9 hours
and rapid onset of action 2.5 to 4 hoursand rapid onset of action 2.5 to 4 hours
 It is not inferior to S/C enoxaparinIt is not inferior to S/C enoxaparin
followed by warfarin in the treatment offollowed by warfarin in the treatment of
acute symptomatic DVTacute symptomatic DVT
Duration of anticoagulationDuration of anticoagulation
•A patient with a first thromboembolic event occurring in the
setting of reversible risk factors, should receive warfarin therapy
for at least 3 months.
•Patients without a clearly defined predisposition to initial thrombo
embolism should be treated for 6 months or more.
•Patient who have active cancer or recurrent DVT require long
term ( indefinite period)
 Recurrent DVT & PE: Vena cava filterRecurrent DVT & PE: Vena cava filter
17/08/1717/08/17 6464
Indication of venacava filterIndication of venacava filter
 Contra indication to anti coagulationContra indication to anti coagulation
 Recurrent embolism while on adequateRecurrent embolism while on adequate
therapytherapy
 Significant bleeding complication duringSignificant bleeding complication during
anti coagulationanti coagulation
Thrombolytic TherapyThrombolytic Therapy
•The ACCP guidelines recommend that thrombolytic therapy
should be used in
•patients with acute PE associated with hypotension (systolic BP<
90 mm HG) who do not have a high bleeding risk .
•select patients with acute PE not associated with hypotension
and with a low bleeding risk whose initial clinical presentation or
clinical course after starting anticoagulation suggests a high risk of
developing hypotension
•Tissue plasminogen activator (tPA) has a short
infusion time and has been recommended as the best
agent for this reason.
EmbolectomyEmbolectomy
In case of massive life threateningIn case of massive life threatening
pulmonary embolismpulmonary embolism
 Catheter EmbolectomyCatheter Embolectomy
 Surgical EmbolectomySurgical Embolectomy
17/08/1717/08/17 6969
Catheter Embolectomy & FragmentationCatheter Embolectomy & Fragmentation
An alternative in high-risk PE patients when thrombolysis
is absolutely contraindicated or has failed
Kucher N Chest 2007;132:657-663
EmbolectomyEmbolectomy
PREVENTIONPREVENTION
Blood Pressure
Category
Systolic
mm Hg
 
Diastolic
mm Hg
Normal less than 120 and less than 80
Prehypertension 120 – 139 or 80 – 89
Stage 1 HTN 140 – 159 or 90 – 99
Stage 2 HTN 160 or higher or 100 or higher
Intermittent pneumatic compression (IPC) devices
are used to help prevent blood clots in the deep
veins of the legs. The devices use cuffs around
the legs that fill with air and squeeze your legs.
This increases blood flow through the veins of
your legs and helps prevent blood clots.
Intermittent pneumaticIntermittent pneumatic
compressioncompression
Graduated compressionGraduated compression
stockingsstockings
 Graduated compression stockings exertGraduated compression stockings exert
the greatest degree of compression at thethe greatest degree of compression at the
ankle, and the level of compressionankle, and the level of compression
gradually decreases up the garmentgradually decreases up the garment
 They are often used to treat chronicThey are often used to treat chronic
venous disease and edemavenous disease and edema
ComplicationsComplications
 Instant DeathInstant Death
 Chronic pulmonary hypertensionChronic pulmonary hypertension
 Respiratory failureRespiratory failure
 Congestive heart failureCongestive heart failure
 RecurrenceRecurrence
17/08/1717/08/17 7777
Home messageHome message
 Prevention is better than curePrevention is better than cure
 Early diagnosis and treatment is lifeEarly diagnosis and treatment is life
savingsaving
 Risk of pulmonary embolism significantlyRisk of pulmonary embolism significantly
increases with a flight distance more thanincreases with a flight distance more than
5000 km or duration more than 8 hours .5000 km or duration more than 8 hours .
Pulmonary embolism dr.bayazid

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Pulmonary embolism dr.bayazid

  • 1. Pulmonary EmbolismPulmonary Embolism Dr. Muhammad Bayazid M.D Final part student, Cardiology, DMCH
  • 2. DVT : Blood clot formation with inDVT : Blood clot formation with in the large veins usually in the legsthe large veins usually in the legs PE results from DVTs that havePE results from DVTs that have broken off and travelled tobroken off and travelled to pulmonary arterial circulationpulmonary arterial circulation The majority of pulmonary emboliThe majority of pulmonary emboli ( 80%) arise from the propagation of( 80%) arise from the propagation of lower limb DVTlower limb DVT Other causes : Air, AmnioticOther causes : Air, Amniotic Fluid, Fat EmbolismFluid, Fat Embolism Venous thromboembolism  DVT  Pulmonary Embolism
  • 3. DEFINITIONDEFINITION Pulmonary embolismPulmonary embolism ( (PEPE) is) is a blockage of an artery in the lungs  by aa blockage of an artery in the lungs  by a substance that has traveled from elsewhere in thesubstance that has traveled from elsewhere in the
  • 4. Why it is important?Why it is important? PE is the most common preventable cause ofPE is the most common preventable cause of death in hospitalized patientsdeath in hospitalized patients Majority of patient die because of failure ofMajority of patient die because of failure of diagnosis rather than inadequate therapy.diagnosis rather than inadequate therapy. 80% of pulmonary emboli occur without prior80% of pulmonary emboli occur without prior warning signs or symptomswarning signs or symptoms Mortality rate without treatment is 30%,Mortality rate without treatment is 30%, whereas with adequate treatment is only 2-8%whereas with adequate treatment is only 2-8% Early treatment is highly effectiveEarly treatment is highly effective
  • 6. Non thrombtic pulmonaryNon thrombtic pulmonary embolismembolism  Fat embolism.Fat embolism.  Air embolism.Air embolism.  Amniotic fluid embolism.Amniotic fluid embolism.  Tumor embolism (Tumor embolism (HCCHCC && RCCRCC).).
  • 8.
  • 9. Hypercoagulability Hereditary Deficiencies: Antithrombin deficiency Protein C deficiency Protein S deficiency Factor V Leiden Prothrombin gene mutation Dysfibrinogenemia Acquired: Cancer Pregnancy & postpartum period Oral contraceptives Hormone replacement therapy Polycythemia rubravera Smoking Anti phospholipid syndrome Chemotherapy Stasis Immobility/cast/travel Advanced age Acute medical illness Major surgery Spinal cord injury Obesity Endothelial Damage Major surgery Trauma Central venous catheterization Risk for thromboembolism approximately doubles for each decade beyond age 60 years Risk factors
  • 10. Major Risk (RR 5-20)Major Risk (RR 5-20) •Major and abdominal surgeryMajor and abdominal surgery •Lower Limb OrthopedicLower Limb Orthopedic SurgerySurgery •Obstetric – Late preganancy,Obstetric – Late preganancy, LSCS, Pre eclampsiaLSCS, Pre eclampsia •Maliganancy- Pelvic ,Maliganancy- Pelvic , abdominal or metastaticabdominal or metastatic •Lower Leg # , varicose veinsLower Leg # , varicose veins •History of proven VTEHistory of proven VTE Minor Risk Factors ( RR CVS : HF, HTN, Congenital Heart Disease, Central lines Estrogen : OCP, HRT Others : Occult malignancy, COPD Neurological disability, obesity, thrombotic mayeloproliferative disease, nephrotic syndrome Inflammatory bowel disease Risk factors
  • 12.
  • 13. ClinicalClinical PresentationPresentation Massive PEMassive PE:: Symptom:Symptom: Severe central chest pain, Severe dyspnoea,Severe central chest pain, Severe dyspnoea, Syncope, Pallor, Sweating,Syncope, Pallor, Sweating, Sign:Sign: Major circulatory collapse, tachycardia, hypotension,Major circulatory collapse, tachycardia, hypotension, Shock,Shock, Central cyanosis, Elevated JVP, Loud P2, S2 split,Central cyanosis, Elevated JVP, Loud P2, S2 split, gallop rhythm.gallop rhythm.  Small or Medium PESmall or Medium PE : SOB, Pleuritic chest pain,: SOB, Pleuritic chest pain, Haemoptysis, Tachycardia, Tachypnea, Pleural rub.Haemoptysis, Tachycardia, Tachypnea, Pleural rub. Crackles, pleural effusionCrackles, pleural effusion  Chronic PEChronic PE: Exertional dyspnoea, symptoms of: Exertional dyspnoea, symptoms of pulmonary HTN or right heart failure,pulmonary HTN or right heart failure, 17/08/1717/08/17 1313
  • 15.
  • 16.
  • 17. 1717 DiagnosisDiagnosis  CXRCXR  ABG:ABG:  ECGECG  V/QV/Q  Spiral CTSpiral CT  EchoEcho  AngioAngio  Fibrin Split Products/D-dimerFibrin Split Products/D-dimer
  • 18. Contd…Contd… ECGECG  Sinus tachycardia –Sinus tachycardia –  m/c abnormality m/c abnormality  Complete or incomplete RBBB –Complete or incomplete RBBB –  a/w ↑ mortality a/w ↑ mortality  RV strain pattern –RV strain pattern –  T wave ↓ in the right precordial leads T wave ↓ in the right precordial leads (V1-4) ± the inferior leads(V1-4) ± the inferior leads  Right axis deviationRight axis deviation  S1, Q3, T3 patternS1, Q3, T3 pattern  Right atrial enlargement (P pulmonale) –Right atrial enlargement (P pulmonale) – peaked Ppeaked P wave in lead II > 2.5 mm in heightwave in lead II > 2.5 mm in height  Atrial Tachyarrhythmias –Atrial Tachyarrhythmias –  AF, Flutter AF, Flutter  Non specific ST-segment & T wave changesNon specific ST-segment & T wave changes
  • 19. 1919 S1 Q3 T3 Pattern
  • 23. Chest X-rayChest X-ray  Chest X ray – most common finding with aChest X ray – most common finding with a PE is a normal x-rayPE is a normal x-ray  But they are useful as X-rays help to ruleBut they are useful as X-rays help to rule out pneumonia and pneumothorax asout pneumonia and pneumothorax as causes of dyspnoea etccauses of dyspnoea etc  A normal CXR in the presence ofA normal CXR in the presence of significant dyspnoea and hypoxemia insignificant dyspnoea and hypoxemia in absence of bronchospasm and anatomicabsence of bronchospasm and anatomic cardiac shunt is highly suggestive of PEcardiac shunt is highly suggestive of PE
  • 24. Chest XrayChest Xray  Chest radiograph findings in patient withChest radiograph findings in patient with pulmonary embolismpulmonary embolism ResultResult PercentPercent CardiomegalyCardiomegaly 27%27% Normal studyNormal study 24%24% AtelectasisAtelectasis 23%23% Elevated HemidiaphragmElevated Hemidiaphragm 20%20% Pulmonary Artery EnlargementPulmonary Artery Enlargement 19%19% Pleural EffusionPleural Effusion 18%18% Parenchymal Pulmonary InfiltrateParenchymal Pulmonary Infiltrate 17%17% Am Heart J 1997;134:479-87
  • 25. Radiographic signs of acute pulmonaryRadiographic signs of acute pulmonary embolismembolism  Signs with relative high specificity but lowSigns with relative high specificity but low sensitivity for acute pulmonary embolism:sensitivity for acute pulmonary embolism:  Decreased vascularity in the peripheral lungDecreased vascularity in the peripheral lung (Westermark sign).(Westermark sign).  Enlargement of the central pulmonary arteryEnlargement of the central pulmonary artery (Fleischner sign).(Fleischner sign).  Enlarged right descending pulmonary arteryEnlarged right descending pulmonary artery (Palla's sign)(Palla's sign)  Pleural based areas of increased opacity (Pleural based areas of increased opacity (Hampton humpHampton hump).).  Hemidiaphragm elevation.Hemidiaphragm elevation.
  • 26. (Hampton hump)(Hampton hump) •The classic radiographic findings of pulmonary infarction • a wedge-shaped, pleura-based triangular opacity with an apex pointing toward the hilus
  • 27. The Westermark sign : focal oligemia distal to a PE
  • 28.
  • 30. D-dimerD-dimer  By-product of fibrinBy-product of fibrin degradationdegradation  As clot degraded byAs clot degraded by enzymes, Fibrinenzymes, Fibrin Degradation ProductsDegradation Products (FDP) are released, one(FDP) are released, one of these is the D-dimerof these is the D-dimer  Little clots in body releaseLittle clots in body release D-dimers, therefore if testD-dimers, therefore if test +ve - do not know if it is+ve - do not know if it is from a PE,from a PE,  But test is so sensitiveBut test is so sensitive that if no D-dimer ( –ve)that if no D-dimer ( –ve) you can rule out PEyou can rule out PE
  • 31. CTPACTPA  Contrast injected into body,Contrast injected into body,  CT Scan obtained as this isCT Scan obtained as this is occurringoccurring  Vessels viewed on end andVessels viewed on end and seen if they light up withseen if they light up with contrast.contrast.  If only partially light up withIf only partially light up with contrast there may be a bloodcontrast there may be a blood clot present stopping flowclot present stopping flow  Do not use if in renal failureDo not use if in renal failure ((Creatanine) (could useCreatanine) (could use HCOHCO33 cover to stopcover to stop nephrotoxic effect of contrast)nephrotoxic effect of contrast)  Unlike VQ Scan if patient hasUnlike VQ Scan if patient has a pneumonia it will not affecta pneumonia it will not affect resultsresults
  • 32. CT findings of acute pulmonary embolismCT findings of acute pulmonary embolism Vascular abnormalities:Vascular abnormalities:  Intraluminal filling defects that forms an acute angle withIntraluminal filling defects that forms an acute angle with the vessel wall & may be surrounded by contrast materialthe vessel wall & may be surrounded by contrast material (polo mint sign or railway sign).(polo mint sign or railway sign).  Total cutoff of vascular enhancement.Total cutoff of vascular enhancement.  Enlargement of the occluded vessel.Enlargement of the occluded vessel. Ancillary findings:Ancillary findings:  Pleural based wedge shaped areas of increased attenuationPleural based wedge shaped areas of increased attenuation with no contrast enhancement.with no contrast enhancement.  Linear atelectasis.Linear atelectasis.
  • 33. Partial eccentric filling defect with acutePartial eccentric filling defect with acute angle with the vessel wallangle with the vessel wall
  • 34. Intraluminal filling defectIntraluminal filling defect (polo mint sign)(polo mint sign)
  • 35. Intraluminal filling defectIntraluminal filling defect (railway track sign)(railway track sign)
  • 36.  V /Q lung scanning remains an option andV /Q lung scanning remains an option and cancan be used when CTA is not available or isbe used when CTA is not available or is contraindicated.contraindicated. V /Q Scan Advantages relatively low radiation dose no requirement for contrast dye Limitations Unreliable in pts with COPD and other conditions in which there is structural Lung disease When holding breath is difficult.
  • 38. Probability of PEProbability of PE  Normal - Full ventilationNormal - Full ventilation and perfusion seenand perfusion seen  Low Pobability for PE –Low Pobability for PE – (<20%)(<20%)  Intermediate probabilityIntermediate probability for PE-for PE- V andV and P inP in same areasame area (Matched deficit) (20-(Matched deficit) (20- 80%)80%)  High Probability for PE –High Probability for PE – Normal V andNormal V and P (Un-P (Un- Matched deficit) (>80%)Matched deficit) (>80%)
  • 40. EchocardiographyEchocardiography  This modality generally hasThis modality generally has limited accuracy in thelimited accuracy in the diagnosis.diagnosis.  The overall sensitivity andThe overall sensitivity and specificity for diagnosis ofspecificity for diagnosis of central and peripheralcentral and peripheral pulmonary embolism bypulmonary embolism by ECHO is 59% and 77%.ECHO is 59% and 77%.  It may allow diagnosis ofIt may allow diagnosis of other conditions that may beother conditions that may be confused with pulmonaryconfused with pulmonary embolism.embolism.
  • 41. ECHO signs of PEECHO signs of PE  RV enlargementRV enlargement  Hypokinesis especially free wall hypokinesis, withHypokinesis especially free wall hypokinesis, with sparing of the apexsparing of the apex (the McConnell’s sign)(the McConnell’s sign)  Interventricular septal flattening and paradoxicalInterventricular septal flattening and paradoxical motion toward the LV resulting in a “D-shaped” LV inmotion toward the LV resulting in a “D-shaped” LV in cross section.cross section.  Tricuspid regurgitationTricuspid regurgitation  Lack of inspiratory collapse of IVCLack of inspiratory collapse of IVC  Direct visualization of thrombusDirect visualization of thrombus  60/60 Sign-60/60 Sign- Acceleration time of RV ejection <60ms inAcceleration time of RV ejection <60ms in the presence of TR pressure gradient </= 60mmHg.the presence of TR pressure gradient </= 60mmHg.
  • 42. Echocardiograms before and after Thrombolysis Echocardiography-RV Dilation
  • 43. ECHOECHO  The severity of this PulmonaryThe severity of this Pulmonary Artery Pressure (PAP) and theArtery Pressure (PAP) and the severity of the clot, is found byseverity of the clot, is found by looking at the tricuspid valvelooking at the tricuspid valve and noting how much regurgeand noting how much regurge occurs (Tricuspid jet)occurs (Tricuspid jet)  If tricuspid jet is high then PAPIf tricuspid jet is high then PAP differential between RA anddifferential between RA and RV is great and the clot burdenRV is great and the clot burden is largeis large  All these tests may help in theAll these tests may help in the possible diagnosis of a PE, butpossible diagnosis of a PE, but are not definitive testsare not definitive tests
  • 44.
  • 45. UltrasoundUltrasound  Non-invasiveNon-invasive  Looks at lower limbsLooks at lower limbs  Doppler USS looks atDoppler USS looks at vein for flow andvein for flow and compressibilty to seecompressibilty to see if clot presentif clot present
  • 46. Magnetic resonance angiographyMagnetic resonance angiography (MRA)(MRA) MRA appears promising & avoids ionising radiation but has poor sensitivity for subsegmental clot.
  • 47. MRA findingsMRA findings  Visualization of the intravascular fillingVisualization of the intravascular filling defect.defect.  Provide physiologic information includingProvide physiologic information including the regional distribution of ventilation &the regional distribution of ventilation & perfusion.perfusion.
  • 49. Pulmonary angiographicPulmonary angiographic findingsfindings Primary signs:Primary signs: The only primary sign of acute pulmonaryThe only primary sign of acute pulmonary embolism is filling defect.embolism is filling defect. Secondary signs:Secondary signs: Abrupt occlusion of pulmonary artery.Abrupt occlusion of pulmonary artery. Areas of oligemia with pruning of theAreas of oligemia with pruning of the branching vessels.branching vessels.
  • 50. cardiac troponinscardiac troponins •Recently, cardiac troponins I and T have been shown to be associated with early mortality and a complicated hospital course in patients with PE. The assessment of cardiac plasma troponin levels revealed ventricular injury, especially in patients with massive PE who had hypotension or shock.
  • 51. B Natriuretic PeptideB Natriuretic Peptide (BNP)(BNP) •BNP is a neurohormone secreted from the cardiac ventricles in response to dilatation or an increase of pressure. • BNP levels may increase with right ventricle dysfunction when the patients is in bed and decrease with treatment. •Serum brain natriuretic peptide levels of > 90 pg/mL have a sensitivity of 85% and a specificity of 75% for predicting adverse clinical outcomes
  • 53.
  • 54. Treatment optionsTreatment options  Symptomatic treatment:Symptomatic treatment: – ABCD approachABCD approach – OxygenOxygen – AnalgesiaAnalgesia  Anticoagulation:Anticoagulation: – IV HeparinIV Heparin – S/C LMWH eg Enoxaparine, DalteparineS/C LMWH eg Enoxaparine, Dalteparine – Oral WarfarinOral Warfarin  IVC filter:IVC filter: If there is contra-indications for anti-coagulationIf there is contra-indications for anti-coagulation  Thrombolysis:Thrombolysis: tPA eg Alteplase, TenectaplasetPA eg Alteplase, Tenectaplase  Surgical procedures:Surgical procedures: Pulmonary embolectomyPulmonary embolectomy
  • 55. General MeasureGeneral Measure  Oxygen inhalationOxygen inhalation  Opiates to relieve painOpiates to relieve pain  Circulatory shock should be treated with I/V fluidCirculatory shock should be treated with I/V fluid and plasma expenderand plasma expender  Inotropic agents have limited value as hypoxicInotropic agents have limited value as hypoxic dilated right ventricle maximally stimulated bydilated right ventricle maximally stimulated by endogenous catecolaminesendogenous catecolamines  Diuretics and vasodilator should be avoidedDiuretics and vasodilator should be avoided because they reduce the cardiac output.because they reduce the cardiac output.  Precordial thump , which may dislodge thePrecordial thump , which may dislodge the thrombusthrombus
  • 56. AnticoagulationAnticoagulation  Ideally start Fast acting and slow acting anticoagulants,Ideally start Fast acting and slow acting anticoagulants, when slow acting anticoagulants at desired level, stopwhen slow acting anticoagulants at desired level, stop fast actingfast acting  Fast acting -Heparin productsFast acting -Heparin products Heparin (IV) orHeparin (IV) or Low Molecular Weight Heparin (S/C)Low Molecular Weight Heparin (S/C)  Slow acting – Vitamin K AntagonistsSlow acting – Vitamin K Antagonists WarfarinWarfarin
  • 57. HeparinHeparin •The initial treatment of PE is LMWH or UHF for at least 5 days, followed by warfarin. •Dose of UFH: 80 U/kg bolus followed by18 U/kg/hour . Monitoring by APTT(1.5-2.5 )times normal. •It binds to endogenous antithrombin, This heparin - antithrombin complex catalyzes the inactivation of factor Xa and IIa (thrombin).
  • 58. LMWHLMWH . •It should be used whenever possible for the initial inpatient treatment of DVT & PE. •Outpatient ttt of DVT, and possibly PE,is safe and cost-effective for carefully selected patients.
  • 59. Adverse effect of heparinAdverse effect of heparin •Adverse drug reactions include bleeding, heparin-induced thrombocytopenia, and osteoporosis .with prolonged use .
  • 60. Oral anticoagulantOral anticoagulant •We can give warfarin •Target international normalised ratio [INR], 2.0–3.0) for at least 3–6 months.
  • 61. New oral anti coagulantNew oral anti coagulant  Oral direct thrombin inhibitor: DabigatranOral direct thrombin inhibitor: Dabigatran  It is as effective as warfarin for theIt is as effective as warfarin for the treatment of acute VTE with similar safetytreatment of acute VTE with similar safety profileprofile  Dabigatran was also not inferior to S/CDabigatran was also not inferior to S/C enoxaparin in the prevention of VTEenoxaparin in the prevention of VTE
  • 62.  Oral direct factor X a inhibitor,Oral direct factor X a inhibitor, RivaroxabanRivaroxaban  It has relatively short half life 5-9 hoursIt has relatively short half life 5-9 hours and rapid onset of action 2.5 to 4 hoursand rapid onset of action 2.5 to 4 hours  It is not inferior to S/C enoxaparinIt is not inferior to S/C enoxaparin followed by warfarin in the treatment offollowed by warfarin in the treatment of acute symptomatic DVTacute symptomatic DVT
  • 63. Duration of anticoagulationDuration of anticoagulation •A patient with a first thromboembolic event occurring in the setting of reversible risk factors, should receive warfarin therapy for at least 3 months. •Patients without a clearly defined predisposition to initial thrombo embolism should be treated for 6 months or more. •Patient who have active cancer or recurrent DVT require long term ( indefinite period)
  • 64.  Recurrent DVT & PE: Vena cava filterRecurrent DVT & PE: Vena cava filter 17/08/1717/08/17 6464
  • 65.
  • 66. Indication of venacava filterIndication of venacava filter  Contra indication to anti coagulationContra indication to anti coagulation  Recurrent embolism while on adequateRecurrent embolism while on adequate therapytherapy  Significant bleeding complication duringSignificant bleeding complication during anti coagulationanti coagulation
  • 67. Thrombolytic TherapyThrombolytic Therapy •The ACCP guidelines recommend that thrombolytic therapy should be used in •patients with acute PE associated with hypotension (systolic BP< 90 mm HG) who do not have a high bleeding risk . •select patients with acute PE not associated with hypotension and with a low bleeding risk whose initial clinical presentation or clinical course after starting anticoagulation suggests a high risk of developing hypotension •Tissue plasminogen activator (tPA) has a short infusion time and has been recommended as the best agent for this reason.
  • 68.
  • 69. EmbolectomyEmbolectomy In case of massive life threateningIn case of massive life threatening pulmonary embolismpulmonary embolism  Catheter EmbolectomyCatheter Embolectomy  Surgical EmbolectomySurgical Embolectomy 17/08/1717/08/17 6969
  • 70. Catheter Embolectomy & FragmentationCatheter Embolectomy & Fragmentation An alternative in high-risk PE patients when thrombolysis is absolutely contraindicated or has failed Kucher N Chest 2007;132:657-663
  • 72. PREVENTIONPREVENTION Blood Pressure Category Systolic mm Hg   Diastolic mm Hg Normal less than 120 and less than 80 Prehypertension 120 – 139 or 80 – 89 Stage 1 HTN 140 – 159 or 90 – 99 Stage 2 HTN 160 or higher or 100 or higher
  • 73. Intermittent pneumatic compression (IPC) devices are used to help prevent blood clots in the deep veins of the legs. The devices use cuffs around the legs that fill with air and squeeze your legs. This increases blood flow through the veins of your legs and helps prevent blood clots.
  • 75. Graduated compressionGraduated compression stockingsstockings  Graduated compression stockings exertGraduated compression stockings exert the greatest degree of compression at thethe greatest degree of compression at the ankle, and the level of compressionankle, and the level of compression gradually decreases up the garmentgradually decreases up the garment  They are often used to treat chronicThey are often used to treat chronic venous disease and edemavenous disease and edema
  • 76.
  • 77. ComplicationsComplications  Instant DeathInstant Death  Chronic pulmonary hypertensionChronic pulmonary hypertension  Respiratory failureRespiratory failure  Congestive heart failureCongestive heart failure  RecurrenceRecurrence 17/08/1717/08/17 7777
  • 78. Home messageHome message  Prevention is better than curePrevention is better than cure  Early diagnosis and treatment is lifeEarly diagnosis and treatment is life savingsaving  Risk of pulmonary embolism significantlyRisk of pulmonary embolism significantly increases with a flight distance more thanincreases with a flight distance more than 5000 km or duration more than 8 hours .5000 km or duration more than 8 hours .

Editor's Notes

  1. Massive PE: obstructing more than 50% of pulmonary vasculature
  2. Cardiomegaly was the most frequent finding in those with PE of In-patients Out-patients, it seemed to be atelectasis in the above study.
  3. Echocardiograms before and after Thrombolysis. A 29-year-old woman presented with progressive shortness of breath. A computed tomographic scan of the chest showed a central &amp;quot;saddle&amp;quot; pulmonary embolism. An echocardiogram (Panel A) showed an enlarged right ventricle and hypokinetic motion of the right ventricular free wall. After treatment with alteplase, the right ventricular size and wall motion returned to normal (Panel B). Echocardiograms courtesy of Scott D. Solomon, M.D., and Jose M. Rivero. (Videos of these images are available with the full text of this article at http://www.nejm.org.)‏
  4. Figure 21-11. Pulmonary angiogram showing pulmonary embolism. Pulmonary angiography remains the diagnostic gold standard for pulmonary embolism. Access to the pulmonary artery is obtained via transvenous catheter placement. The diagnosis is confirmed by persistent filling defect or abrupt cut-off of flow. Abrupt cut-off of flow to the right and left upper lobe vessels is seen in this patient.
  5. If anticoagulant or thrombolytic therapy is CI or fails to prevent thrombo-embolism, Patients with massive PE who survive (in whom a second PE may be fatal) Greenfield filter inserted above the level of renal veins