2. Pulmonary Embolism
• Thrombosis that originates in the venous
system and embolizes to the pulmonary
arterial circulation
– DVT in veins of leg above the knee (>90%)
– DVT elsewhere (pelvic, arm, calf veins, etc.)
– Cardiac thrombi
3. How Common?
• 650,000 cases in the US each year
• 150,000 – 200,000 US deaths each year
• Most common preventable cause of
hospital death
• 3rd most common acute cardiovascular
emergency (MI and stroke)
4. Risk Factors (for DVT)
• Venous injury
– Alterations in blood flow (stasis): best rest,
inactivity/immobilization, CHF, paralysis
– Injury to endothelium: trauma, surgery
– Thrombophilia: Factor V Leiden, Protein C or S deficiency, etc.
• Age >50
• History of varicose veins
• History of MI
• History of malignancy
• History of atrial fibrillation
• History of ischemic stroke
• History of diabetes mellitus
• Previous VTE, obesity, pregnancy
6. 6
Risk Factors
Hypercoagulability
Malignancy
Nonmalignant thrombophilia
Pregnancy
Postpartum status (<4wk)
Estrogen/ OCP’s
Genetic mutations (Factor V Leiden, Protein C & S deficiency, Factor
VIII, Prothrombin mutations, anti-thrombin III
deficiency)
Venous Statis
Bedrest > 24 hr
Recent cast or external fixator
Long-distance travel or prolong automobile travel
Venous Injury
Recent surgery requiring endotracheal intubation
Recent trauma (especially the lower extremities and pelvis)
7. 7
Clinical Presentation
• The Classic Triad: (Hemoptysis, Dyspnea, Pleuritic
Pain)
• Not very common!
• Occurs in less than 20% of patients with documented
PE
• Three Clinical Presentations
– Pulmonary Infarction
– Submassive Embolism
– Massive Embolism
10. Nonspecific Workup
• Chest X-ray: abnormal in 88% of acute PE
– Atelectasis (60-70%): most common finding in PE without infarction
– “Classic” findings:
• Westermark sign (increased lucency in area of embolus)
• Hampton Hump (wedge-shaped pleural-based infiltrate)
• Abrupt cutoff of vessel
– Pleural effusion
• EKG
– Most common: sinus tachycardia +/- nonspecific ST-segment and T-
wave changes
– “Classic S1-Q3-T3 pattern”
– Other signs of right heart strain (ie, new RBBB and ST changes in V1,2
• ABG
– Normal does NOT rule out PE
– “Classic” findings:
• Hypoxia, hypocapnia, respiratory alkalosis, increased A-a gradient
11. 11
Chest X-ray Eponyms of PE
• Westermark's sign
– A dilation of the pulmonary vessels proximal to the
embolism along with collapse of distal vessels,
sometimes with a sharp cutoff.
• Hampton’s Hump
– A triangular or rounded pleural-based infiltrate with
the apex toward the hilum, usually located adjacent to
the hilum.
13. 13
Diagnostic Testing
– EKG’s
• EKG
– Most Common Findings:
• Tachycardia or nonspecific ST/T-wave changes
– Acute cor pulmonale or right strain patterns
• Tall peaked T-waves in lead II (P pulmonale)
• Right axis deviation
• RBBB
• S1-Q3-T3 (occurs in only 20% of PE patients)
15. Evaluation and Diagnosis
• Evaluation and imaging
is dependent upon
estimated pretest
probability (Modified
Wells’ Criteria)
• Pretest probability:
– Low (<2 points)
– Intermediate (2-6 points)
– High (>6 points)
VARIABLE POINTS
S/S of DVT 3.0
HR >100 1.5
Immobilization
(bed rest >/= 3d)
OR surgery within
4 weeks
1.5
Prior DVT or PE 1.5
Hemoptysis 1.0
Malignancy
(treated within the
past 6 months or
palliative
1.0
Other diagnoses
less likely than PE
3.0
16. Preliminary Lab. Testing & Pretest Probability -2
• EKG:unexplained tachycardia:common in
APE but nonspecific
• acute cor pulmonale: S1, Q3, T3 pattern,
RBBB , P-wave pulmonale, or RAD : more
common with massive embolism ---
nonspecific
• CXR: generally nondiagnostic
• arterial oxygen tension may be normal
• A–a oxygen difference may be normal
17. Preliminary Lab. Testing & Pretest Probability -3
• D-dimer test (+): VTE are possible
diagnoses
• this test is nonspecific
• infection,other inflammatory states, cancer,
& trauma
• D-dimer testing is best considered
together with clinical probability
18. Preliminary Lab. Testing & Pretest Probability -4
• D-dimer test (-):with a low or moderate
pretest probability, likelihood of VTE is low
• precludes the need for specific imaging
studies
• high pretest probability: imaging should be
performed instead of D-dimer testing
• Other biomarkers: cardiac troponin levels,
plasma levels of brain natriuretic peptide
19. D-dimer in evaluation of PE
• High sensitivity but poor specificity
• Negative ELISA has >95% negative predictive value and can be
used to r/o PE in low risk patients (less than 2 points)
Low (<2) Intermediate
(2-6)
High (>6)
Overall 3% 20% 60%
(-) D-dimer 2% 6% 20%
(+) D-dimer 7% 36% 75%
20. Helical CT
• Sensitivity 85% (more sensitive for
proximal emboli)
• Specificity 95%
• Values vary widely in literature
22. V/Q Scan
• Identifies mismatches between areas that are ventilated
but not perfused
• Best initial test in patients with clear CXR
• Scan can be interpreted as High, Intermediate, or Low
probability of PE, or normal
– Normal rules out PE
– High-probability scan is diagnostic of PE if the clinical suspicion
is also high
– Low-probability scan rules out PE only in a pt with low pretest
clinical probability (because PE is found in roughly 15% of pts
with low-probability scans)
– Intermediate-probability scan requires further evaluation (16-
66% chance of PE depending on pretest probability)
24. Duplex US with compression of the
lower extremities
• Non-invasive test that accurately detects
proximal DVT in LE (70-80% of pts with
PE have concomitant proximal DVT)
• Often used in workup of PE before going
to more invasive procedures
25. Pulmonary Angiography
• “Gold Standard”
• Invasive study
• 5% morbidity
• < 0.5% mortality
• Indicated if the diagnosis remains
uncertain after noninvasive testing
27. Treatment of PE
• Acute anticoagulation to therapeutic levels
– IV UFH: 80 U/kg bolus, then 18 U/kg/hr to goal PTT of
46-70 seconds OR
– LMWH: ie) lovenox 1 mg/kg SUBQ BID then start
warfarin (when PTT is therapeutic on UFH or on day 1
of LMWH), overlap x 5 days, titrate to INR 2.0 to 3.0
– Thrombolysis: for massive PE causing
hemodynamic compromise
– IVC Filter: if anticoagulation is contraindicated (ie,
active GI bleed, intracranial neoplasm, know bleeding
diathesis), if thrombus formed despite adequate
anticoagulation, or with a large burden of thrombosis
in the LE that could be fatal if embolized
28. Treatment of PE
• Long-term anticoagulation
– 1st event with reversible RF: 3-6 mo warfarin
– Idiopathic PE/DVT: > or = 6 mo warfarin
– 2nd event, cancer, non-modifiable RF: 12 mo
to lifelong warfarin
• LMWH has been shown to be superior to warfarin
in long term treatment in pts with cancer
