Pulmonary embolism is a blockage in the pulmonary arteries caused by blood clots that travel from deep veins. It has several risk factors and causes around 650,000 cases and 150,000-200,000 deaths annually in the US. Diagnosis involves assessing probability based on symptoms and risk factors, then tests like CT, VQ scan, ultrasound, or angiogram depending on probability. Treatment consists of blood thinners like heparin or warfarin to prevent further clots and long term anticoagulation to prevent recurrence based on the cause of clotting.

1. Pulmonary Embolism
Diagnosis, Treatment, and Prevention
By: (Afework A.)

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

5. 5
Pathophysiology
Rudolph Virchow, 1858
Triad:
• Hypercoagulability
• Stasis to flow
• Vessel injury

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

8. Clinical Presentation
• Asymptomatic
• Sudden onset of unexplained dyspnea
• Pleuritic chest pain
• Tachypnea
• Tachycardia
• Anxiety/agitation, cough, hemoptysis, syncope,
fever, cyanosis, isolated crackles, pleural friction
rub, loud P2, right-sided S3, pulmonary
insufficiency murmur, elevated JVP, right
ventricular heave, acute worsening of heart
failure or lung disease

9. Broad Differential
• Pneumothorax
• Myocardial ischemia
• Pericarditis
• Asthma
• Pneumonia
• MI with cardiogenic shock
• Cardiac tamponade
• Aortic dissection
• etc, etc, etc

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.

12. 12
Radiographic Eponyms
- Hampton’s Hump, Westermark’s Sign
Westermark’s
Sign
Hampton’s Hump

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)

14. EKG Findings

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

21. Bilateral PE

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)

23. V/Q Scan

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

26. PE on pulmonary angiogram

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