Pulmonary thromboembolism and management

1. Clinical aspects of Pulmonary
Embolism
Hod : Dr B J Subhash chandra
Chairpersons: Dr Prasanna Kumar H R
Dr Rajendra prasad S
Presenters : Dr Poojitha G
Dr Karthik G

2. Introduction
• Pulmonary embolism and DVT together
constitute one of the “big three” cardiovascular
diseases , the other two being MI and Stroke .
• Global incidence range from 1.2-2.7 per 1000
per year.

3. Molecular pathophysiology
• The Virchows triad of stasis ,hypercoagulabilty ,
and endothelial injury often activates the patho
physiologic cascade leading to VTE .

4. As thrombi start to organize , neutrophils infiltrate NETs ,
NETs provide scaffold that binds RBCs and promote further
aggregation .
Histone stimulate platelet aggregation and platelet dependent
thrombin generation.
Activated platelets binds to neutrophils which release nuclear material
called NETs
[NETs constitute DNA ,Histones , Neutrophil granule constituents ]
Infection / Inflammation leads to recruitment of platelets
Platelets release polyphosphates, procoagulant microparticles ,
proinflammatory mediators

5. PULMONARY EMBOLISM
INCREASED PAAND RV
AFTERLOAD
DECREASED RV OUTPUT AND
INTERVENTRICULAR SEPTAL
SHIFT TO LV
RV DILATITION
/DYSFUNCTION
DECREASED LV
PRELOAD
DECREASED LV OUTPUT
DECREASED SYSTEMIC
PERFUSION
INCREASED RV
WALL TENSION
INCREASED
RV O2
DEMAND
DECREASED
RV O2 SUPPLY
DECREASED
CORONARY
PERFUSION
HYPOTENSION

6. CLASSIFICATION OF PTE
CATEGORY PRESENTATION THERAPY
MASSIVE PTE
(5-10%)
Systolic BP less than 90 mmhg
/poor tissue perfusion or
multisystem organ failure , such
as saddle PE /Right or left main
pulmonary artery thrombus
Anticoagulation (high dose UFH
) Plus systemic thrombolysis ,
catheter directed therapy ,
surgical embolectomy , IVC
filters
SUBMASSIVE
PTE
(HIGH RISK-
15%)
Haemodynamically stable but
moderate or severe RV
dysfunction or enlargement , with
biomarkers elevation indicative
of RV microinfarction /RV
pressure overload
Anticoagulation ,
Systemic thrombolysis is
contraversial
SUBMASSIVE
PTE (LOW RISK
-5-10%)
Haemodynamically stable with
RV dysfunction or Biomarker
elevation , but not both
Anticoagulation followed by
watch and wait
Small or Normal haemodynamics and Anticoagulation only

7. Major risk factors of VTE
• Advanced age
• Arterial disease
• Family history of thrombo embolism
• Recent surgery, Trauma immobilty , Stroke
• CHF
• COPD
• Acute Infection
• Blood transfusion
• IBD/CKD/ICD
• Pregnancy / OC pills /Hormone replacement therapy
• Anti thrombin /Protein C /Protein S deficiencies

8. Signs and symptoms of Pulmonary
embolism
Symptoms
• Unexplained
dyspnea(most
common )
• Chest pain
• Anxiety
• Cough
Signs
• Tachypnea(most common)
• Tachycardia
• Low grade fever
• Left parasternal lift
• Jugular venous distension
• Tricuspid MR
• Accentuated P2
• Right sided S3 gallop
• Hemoptysis
• Leg edema /erythema
/tenderness

9. CLINICAL PRESENTATION
• Symptoms like Dyspnea , chest pain , syncope
, cyanosis
• Hypotension
• Acute cor pulmonale (acute RV failure)
• Elevated JVP /S3 Gallop
• EKG : S1 Q3 T3 / New RBBB / RV ischemia /
T inversions from V1 –V4

10. DIAGNOSIS
• Most useful approach is clinical assessment of
likelihood of PTE using WELL CRITERIA .
• D DIMER
• ECG/ECHO/ X RAY
• CT Pulmonary angiogram

11. CLASSIC WELLS CRITERIA FOR
CLINICAL ASSESSMENT OF PTE
CRITERION SCORING
DVT signs and symptoms 3
Any alternative diagnosis is less likely than
PTE
3
HR > 100 /MIN 1.5
IMMOBILIZATION OR SURGERY WITHIN
4 WEEKS
1.5
HAEMOPTYSIS 1
CANCER TREATED WITHIN 6 MONTHS
OR METASTATIC
1

12. PLASMA D DIMER ASSAY
• Screening test
• Fibrin degradation product
• Sensitive but not specific
• Remains elevated for at least 1 week in post
operative conditions
• Abnormally high in MI , Sepsis , Cancer , Systemic
illness
• Hence it is usually used for screening outpatients and
in ED
• Not useful in acutely Ill patients

13. ECG in PTE
• Most famous sign S1 Q3 T3 , Most common sign T
inversion in v1 to v4.
• RV strain pattern can also be seen in COPD ,
Asthma, Idiopathic pulmonary hypertension.

14. Imaging in PTE
• CHEST XRAY : Near normal xray in setting
of severe respiratory compromise is highly
suggestive of PTE.
• X ray Signs in PTE
1. Westermark’s sign
2. Hampton`s hump sign
3. Palla’s sign

15. Chest radiograph
A lateral wedge-
shaped opacity
(white arrow) in the
right lower zone
(Hampton’s hump),
A focal area of
oligemia (space
between white
arrow heads) in the
right lower zone
(Westermark’s sign)
A prominent right
descending
pulmonary artery
(black arrow)
(Palla’s sign).

16. Imaging in PTE
• LUNG SCANNING : VQ mismatch
• ECHOCARDIOGRAPHY
• MRI
• PULMONARY
ANGIOGRAM:Polo mint
sign

17. Management of PTE
• Haemodynamic and respiratory support with
pressors and mechanical ventilation.
• Anticoagulation
• Systemic thrombolysis
• Pharmacomechanical cather assisted therapy
• Surgical embolectomy .

18. Parentral anticoagulation
• Anticoagulation is the corner stone of treatment
in acute PTE
• UFH acts by binding anti thrombin which in turn
inhibits thrombin (factor IIa) , Xa, IXa, XIa,XIIa.
• Dosage : IV bolus 80 units /kg followed by 18
units /kg/hr.
• aPTT should be targeted between 1.5-2.5.

19. Low molecular weight heparin in PTE
• Lmwx has greater bioavailability as it exhibit
less binding to plasma proteins and endothelial
cells.
• Predictable dose response.
• Longer half life than UFH.
• No laboratory tests required
• Dose adjustment required in renal failure

20. Warfarin in PTE
• Vitamin K antagonist
• Prevents gamma carboxylation activation of factors
II , VII, IX, X .
• Full anticoagulation effect evident after 5-7 days
• INR target : 2-3
• Warfarin overlap with heparin : Done for at least 5
days as warfarin monotherapy decreases
endogenous protein C and S.

21. NOAC IN PTE
• Dabigatran :Oral thrombin inhibitor
• Rivaroxaban/apixaban/edoxaban : Factor Xa
inhibitor.
• Rapid onset of action (within hours of ingestion).
• Fixed dosed without laboratory monitoring
• Minimal drug interactions
• Shorter half life
• Do not require bridging when stopped for invasive
procedures
• Not inferior to warfarin in VTE treatmenr , Superior
to warfarin in safety.

22. 2016 American College of Chest
Physician Guidelines
“Recommends NOACs rather than warfarin to
treat VTE(without cancer)”.
Antidotes for NOACs
• Idarucizumab is an antidote to reverse Dabigatran
• Andexanet to reverse Rivaroxaban,Apixaban and
Edoxaban .

23. Advanced therapy in Pulmonary
embolism
• Systemic thrombolysis : FDA has approved
Alteplase for massive PTE, in a dose of 100 mg
through peripheral vein as continuous infusion over
2 hours without concomittent heparin.
• Meta analysis
Thrombolytic therapy versus anticoagulation alone ,
thrombolytic therapy resulted in a 47% reduction in
all cause mortality, 60% decrease in recurrent PE ,
A 2.7 fold increase in major bleeding and 4.6 fold
increase in intracaranial haemorrhage

24. Advanced therapy in Pulmonary
embolism
• Pharmaco mechanical catheter directed therapy
Good efficacy
Lower rates of bleeding owing to low dose of
tissue plasminogen activator(24 mg compared
to 100 mg for systemic administration).
• Surgical Embolectomy
• Inferior Vena Cava filters

25. PREVENTION OF PTE : IN HOSPITAL
PROPHYLAXIS
• Common regimen used
Medical illness : UFH 5000 units S/C BD/TID
Enoxaparin 40 mg SC qd
Graduated compression
stocking
Dalteparin /Fondaparinux
• General surgery :UFH 5000 units S/C BD/TID
Enoxaparin 40 mg SC qd
•

26. PREVENTION OF PTE : IN HOSPITAL
PROPHYLAXIS
• Major orthopedic surgery : Warfarin (Target INR
2-3),
• Enoxaparin 30 mg SC bid or 40 mg qd
• Aspirin 81 mg qd
• Dabigatran 220 mg qd
• Dalteparin / Fondaparinux/ apixiban / rivaroxaban

27. Risk assessment for VTE in
Hospitalized patients

28. Differential Diagnosis of PTE
• Anxiety ,Pleurisy, Costocondritis
• Pneumonia, Bronchitis
• Acute Coronary Syndrome
• Pericarditis
• Congestive Heart Failure
• Aortic Dissection
• Idiopathic Pulmonary Hypertension

29. Thank you.