2. Why care?
PE is the most common
preventable cause of death in
hospitalized patients
~600,000 deaths/year
80% of pulmonary emboli occur
without prior warning signs or
symptoms
2/3 of deaths due to pulmonary
emboli occur within 30 minutes of
embolization
Death due to massive PE is often
immediate
Diagnosis can be difficult
Early treatment is highly effective
6. Natural History of VTE
40-50% of patients with DVT develop PE, often
“silent”
PE presents 3-7 days after DVT
Fatal within 1 hour after onset of respiratory
symptoms in 10%
Shock/persistent hypotension in 5-10% (up to 50% of
patients with RV dysfunction)
Most fatalities occur in untreated patients
Perfusion defects completely resolve in 75% of
all patients (who survive)
7. Diagnosis: Clinical Presentation
Dyspnea, tachypnea, or pleuritic chest pain most
common
Pleuritic pain = distal emboli pulmonary infarction
and pleural irritation
Isolated dyspnea of rapid onset= central PE with
hemodynamic sequlea
Retrosternal angina like symptoms = RV ischemia
Syncope=rare presentation, but indicates
severely reduced hemodynamic reserve
symptoms can develop over weeks
In patients with pre-existing CHF or COPD,
worsening dyspnea may indicate PE
12. Clinical Diagnosis of PE
In summary, clinical signs, symptoms and
routine tests do not allow for the exclusion
or confirmation of acute PE but may
increase the index of its suspicion
Consider PE in cases of unexplained
tachycardia or syncope
13. Diagnosis-Probability Assessment
Implicit clinical judgement is fairly
accurate: “Do you think this patient has a
PE?”
Validated prediction rules standardize
clinical judgement
Wells
Geneva
17. Spiral CT
• Direct visualization of emboli.
• Both parenchymal and mediastinal
structures can be evaluated.
• Offers differential diagnosis in 2/3 of cases
with a negative scan.
BUT…
•Dye load and large radiation dose
•Optimally used when incorporated into a
validated diagnostic decision tree
20. 3 month
VTE rate 0.5% (all non fatal) 1.3%
This algorithm allowed for a management decision in 98% of
patients presenting with symptoms suggestive of PE
21. Diagnosis- Summary
History and physical examination
Then 1,2,3 approach:
1. Clinical decision score
2. D-Dimer test
3. Chest CT
3’. (V/Q scan remains a valid option for patients
with contraindication to CT)
22. Clinical Presentation
After disembarking from a 10 hour airline
flight, a 69 year old man w/o past medical
hx presents to the ER with acute dyspnea.
BP is 120/80 (baseline) and pulse is 120
BPM. Wells score = 5 (intermediate), D-
Dimer is positive.
Spiral CT shows bilateral pulmonary emboli
in >50% of arterial tree.
23. Poor Prognostic Signs
Hypotension (not caused by arrhythmia,
sepsis, or hypovolemia)
SBP <90 mm Hg = 53% 90-day all cause
mortality
SBP drop of 40 mm Hg for at least 15 minutes
= 15% in–hospital mortality
Syncope= bad
Shock= really bad
26. Treatment
Pulseless patient with suspected PE: Start ACLS and consider
administration of thrombolytics
Stabilize the patient and provide supportive care
Oxygen supplementation in patients with SpO2 < 90%
For patients with respiratory failure: airway management and/or
mechanical ventilation
(IV fluids, gentle bolus normal saline ≤ 500 mL). Avoid volume
overload, which may be harmful in cases of right ventricular strain
Analgesics: for patients with pain, Morphine. Avoid NSAIDs if patient
receiving anticoagulation or thrombolytics
Assess bleeding risk
27. Initiate therapy based on risk stratification
and bleeding risk.
Massive PE: thrombolytic therapy or
thrombectomy.
Submassive and nonmassive PE:
anticoagulation or IVC filter
28. Thrombolytic therapy
Fibrinolytic therapy, Thrombolysis
The pharmacologic breakdown of blood
clots formed in vessels. Indications include
STEMI, stroke, massive pulmonary
embolism, severe deep vein thrombosis,
and acute limb ischemia. Agents used
include streptokinase and alteplase.
29. Alteplase
Tissue plasminogen activator
Abbreviation: tPA, PLAT, rtPA
A serine protease found on endothelial
cells of the blood vessels. Catalyzes the
conversion of plasminogen to plasmin,
which is the main enzyme responsible for
clot breakdown.
30. Approved thrombolytic regimens for
pulmonary embolism
Streptokinase 250 000 IU as a loading dose
over 30 min, followed by 100 000 IU/h over 12–
24 h
Accelerated regimen: 1.5 million IU over 2 h
Urokinase 4400 IU/kg as a loading dose over 10
min, followed by 4400 IU/kg/h over 12–24 h
Accelerated regimen: 3 million IU over 2 h
rtPA (Alteplase)100 mg over 2 h or 0.6 mg/kg
over 15 min (maximum dose 50 mg)
31. Catheter Embolectomy & Fragmentation
An alternative in high-risk PE patients when thrombolysis
is absolutely contraindicated or has failed
Kucher N Chest 2007;132:657-663
32. Bottom line
The decision to use thrombolytic therapy
in the intermediate risk PE group should
be made on a case-by-case basis after
carefully weighing the strength of the
indication, the potential benefits, the
contraindications, and potential adverse
effects.
33. IVC Filters
•May provide lifelong protection against PE
•Unclear effect on overall survival
• Complications:
•DVT (20%)
•Post thrombotic syndrome (40%)
•IVC thrombosis (30%)
•Risk/benefit ratio difficult to determine since no
randomized control evidence
•Use when there are absolute contraindications to
anticoagulation and a high risk of Venous
thromboembolism recurrence
•Consider in pregnant women with extensive
thrombosis
•Optimal duration of retrievable filters is unclear
34. The key is prevention
DVT prophylaxis in at-risk patients is quite
effective