2. stasis
Coagulation
activation
Virchow’s
triad
Vascular
injury
•>90% of PE- thrombi arise from deep veins of leg
• clinically important PE- thrombi arise from popliteal or
more proximal deep veins of leg
•Clinical manifestation of PE
size, site and number of thrombi + cardiorespiratory reserve of patient
•Recurrence of VTE is more with ileofemoral vein thrombosis
than popliteal vein thrombosis
4. CXR
• plate like atelectasis
•Elevation of hemidiaphram
•Pleural effusion
EKG- signs of RV strain , RBBB
•Non specific
•Helpful in exclusion of other causes
•Usually found in massive PE
•Can be caused by other causes
ABG- ↓PaO2, ↑A-aO2
Normal in upto 20% patients
5. D- dimer
degradation product of cross linked fibrin
Elevated in presence of acute clot formation
simultaneous activation of coagulation and fibrinolysis
But fibrin is also produced in
inflammation, necrosis, malignancy, dissection of aorta, aging
high negative predictive value, low positive predictive value
6. DVT
Detection of DVT in proven PE
venography – 70%
compression USG – 50%
Compression USG
•Sensitivity-90%, specificity-95% for proximal DVT
•Not sensitive for isolated calf vein thrombosis
•Negative result-Should be repeated after 1 week
COMPRESSION USG **
•back up procedure to avoid false positive results with SDCT
•Patients with contraindication to dye or irradiation
**GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008
7. Objectively documented DVT
50% suffer PE, many are asymptomatic
Angiographically documented PE
50-70% have detectable DVT
clinically suspected PE
>50%-diagnosis not confirmed by investigation
Objective test for diagnosis of PE
•V/Q scan
•Pulmonary angiography
•Spiral CT- chest
•MR angiography
•costly
•Invasive
•Radiation
•Mobilization of patient
•≥40% of vascular bed obtstruction
to produce detectable features of RV overload
•2 D echocardiography
•TEE more valuable than TTE
•Coexistent cardiorespiratory disease
•Not useful in hemodaynamically stable patients
8. •Clinical signs, symptoms and routine investigation do not help in
confirmation or exclusion of PE
•Help in increasing the index of suspicion
9. Suspected PE
which patient should be mobilized for costly, invasive/ radiation exposure investigation
Clinical probability of PE
Low- 9% prevalence of PE
Intermediate-30% prevalence of PE
High-68% prevalence of PE
Clinical prediction rule
Based on history, sign and symptoms
10. CLINICAL PREDICTION RULE
WELLS score
predisposing factors:
nPrevious
nRecent
documented DVT or PE
1.5
immobilization ≥ 3 days or major surgery in last 4 weeks
nActive
cancer- receiving treatment or treated in last 6 months or
palliative care
1.5
1
Clinical sign/ symptoms:
nClinical
nHR
signs and symptoms of DVT
3
>100
1.5
nhemoptysis
1
nAlternate
3
clinical diagnosis less likely than VTE
CLINICAL PROBABILITY
2 level
> 4- -------- likely PE
0-4-------- unlikely PE
3 level
0-1--------------- low
2-6---- intermediate
≥7--------------- high
11. WELLS SCORE
clinical prediction rule
More than10,000 patients studied
•
•
•
Clinical probability- PE unlikely
D-dimer- negative
No treatment with anticoagulants
<1% develop VTE
within 90 days of evaluation
•Clinical probability- PE likely
•Clinical probability- PE unlikely
but D- dimer- positive
Prevalence of PE- 20%
12. Risk stratification according to expected PE related early mortality risk
GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008
RISK MARKERS
MORTALITY
RISK
HIGH
> 15%
NONHIGH
INTER
MEDIA
TE
3-15%
LOW
<1%
Shock
or
hypotension
RV dysfunction
Myocardial
injury
+
+a
+a
-
+
+
-
-
-
Thrombolysis
or
Embolectomy
+
-
POTENTIAL
TREATMENT
IMPLICATIONS
+
-
-
-
Hospital
admission
Early discharge
or
Home treatment
a in the presence of shock or hypotension it is not necessary to confirm presence of
RV dysfunction/ myocardial injury to classify as high risk PE related mortality risk.
13. Principle markers use for risk stratification
Clinical markers
Shock or hypotensiona
Markers of
RV dysfunction
ECHO- RV dialatation, hypokinesia or pressure overload
SPIRAL CT- RV dialatation
PA catheter- increased pressures
Biochemical- elevated BNP, pro BNP
Markers of
myocardial injury
Elevated Trop T, Trop I
a SBP<90 or drop of ≥ 40 from baseline for >15 min, if not caused by new onset arrhythmia,
hypovolemia or sepsis
GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008
14. Diagnostic algorithm for suspected HIGH RISK PE
CT
Immediately available
NO or
patient unstable to be transported
ECHO
RV overload
NO
YES
CT available or
Patient stabilizes
YES
MD-CTPA
POSITIVE
NEGATIVE
No other test available
or patient unstable
Search for other causes
Consider thrombolysis or
embolectomy
Search for other causes
Surgical embolectomy- where thrombolysis is contraindicated or failed
Percutaneous catheter embolectomy or fragmentation- alternate to surgical embolectomy
GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008
15. Diagnostic algorithm for suspected non-HIGH RISK PE
ASSESS CLINICAL PROBABILITY
Clinical prediction rule score
Low/ intermediate probability
or PE unlikely
High probability
or PE likely
D-dimer
MD-CTPA
Negative
positive
negative
positive
Search for other causes
MD-CTPA
No treatment
or investigate further
Treatment
antithrombosis
Positive
negative
Compression
Treatment
antithrombosis
No treatment
USG
GUIDELINES ON THE DIAGNOSIS AND MANAGEMENT OF ACUTE PULMONARY EMBOLISM- EHJ 2008
16. anticoagulation
Start without delay, awaiting definitive diagnostic confirmation
Drugs
Unfractionated heparin, LMWH, anti Xa- fondaparinux, vit K antagonist
High risk PE- unfractionated heparin
LMWH was not included in study for safety
Non high risk PE- LMWH, fondaparinux
except when
renal failure- CLcr<30 or high risk of bleeding- unfractionated heparin
Vit K antagonist- warfarin
start simultaneouly with heparin,
stop heparin only after INR is 2-3 for 2 consecutive days
17. HEPARIN
UNFRACTIONATED
•Efficacy depends on achieving therapeutic level within first 24 hours
•Failure associated with 23.3% recurrent VTE
•Dose- 80 U/kg iv stat, then 18 U/kg/hr
•Dose titrated according to normogram
•aPTT Q4h- modify dose accordingly- achieve target within 24 hour
•Once target achieved – aPTT Q24h
18. Heparin Normogram
aPTT ( sec)
Dose modification
<35 ( < 1.2 times control)
80 U/kg bolus, ↑ infusion rate by 4 U/kg/hr
35-45 ( 1.2-1.5 times control)
40 U/kg bolus, ↑ infusion rate by 2 U/kg/hr
46-70 ( 1.5-2.3 times control)
No change
71-90 ( 2.3- 3.0 times control)
↓ infusion rate by 2 U/kg/hr
>90 ( > 3 times control)
Stop infusion for 1 hr, then ↓ infusion rate by 3 U/kg/hr
19. Vit K antagonist
WARFARIN
Inhibits vit K dependent gamma corboxylation of factors
Clotting facors- II, VII, IX, X
Anticoagulant factors- protein C, protein S
Decreased levels of protein C, protein S – procoagulant activity
Combined with heparin for first 5 days
Factor VII has shortest T1/2- 6 hours
Anticoagulant activity starts in 6 hours, but full effect takes 36-72 hours
Target INR- 2-3
Start simultaneously with heparin
5 mg PO OD – titrate according to INR
Stop Heparin once INR is 2-3 for 2 consecutive days
20. Vit K antagonist
WARFARIN
vit K bioavailabity
• Diet
• Drugs
1. Antimicrobials- gut flora producing vit K
2. Interaction with warfarin
Protein binding
Metabolism
3. Increase potency for causing bleeding- antiplatelets
21. WARFARIN OVERANTICOAGULATION
Antagonist- vit K
•INR 3-5 -------- hold dose of that day
•INR ≥5 – 7.5-- hold dose of that day + vit K 1 mg ivi stat
•INR ≥7.5-10----hold dose of that day + vit K 2 mg ivi stat
•INR ≥10 --------hold dose of that day + vit K 3 mg ivi stat
•If active bleeding – fresh frozen plasma- 10-15ml/kg bw
demonstrable reduction in INR- 6-8 hours
correction on INR-----------------12-24 hours
Half life of vit K < warfarin– repeat dose may be required
22. Hemodynamic support
Volume challenge
•modest and cautious
Ionotropes and vasodialators
•Iv- isoprenaline- added advantage of pulmonary vasodialatation
•Iv- Dobutamine, noradrenaline, adrenaline
•Iv- Levosimenden- ionodialator
•Oral/ iv- Sildenafil
•Inhaled- NO, PGI2
