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Pulmonary Embolism

Diagnosis, Treatment, and Prevention

Philip Keith

March 26, 2008

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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

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How Common?

650,000 cases in the US each year

150,000 200,000 US deaths each year

Most common preventable cause ofhospital death

3rd most common acute cardiovascular

emergency (MI and stroke)

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Risk Factors (for DVT)

Virchows Triad 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

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Clinical presentation

The Classic Triad: (Hemoptysis, Dyspnea, PleuriticPain)

Not very common!

Occurs in less than 20% of patients with documented PE

Three Clinical Presentations

Pulmonary Infarction Submassive Embolism

Massive Embolism

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Clinical Presentation

Asymptomatic

Sudden onset of unexplained dyspnea

Pleuritic chest pain

Tachypnea Tachycardia

Anxiety/agitation, cough, hemoptysis, syncope,fever, cyanosis, isolated crackles, pleural frictionrub, loud P2, right-sided S3, pulmonaryinsufficiency murmur, elevated JVP, rightventricular heave, acute worsening of heartfailure or lung disease

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Broad Differential

Pneumothorax

Myocardial ischemia

Pericarditis

Asthma Pneumonia

MI with cardiogenic shock

Cardiac tamponade Aortic dissection

etc, etc, etc

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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

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Westermark Sign

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Hampton Hump

Occurs 12 to 36 hours after symptoms begin;

usually indicates pulmonary infarction

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EKG Findings

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Evaluation and Diagnosis

Evaluation andimaging is dependentupon estimatedpretest probability(Modified WellsCriteria)

Pretest probability: Low (6 points)

VARIABLE POINTSS/S of DVT 3.0

HR >100 1.5

Immobilization

(bed rest >/= 3d)

OR surgery within4 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

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REFER TO ALGORITHM

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D-dimer in evaluation of PE

High sensitivity but poor specificity

Negative ELISA has >95% negative predictive value and can beused to r/o PE in low risk patients (less than 2 points)

Low (6)

Overall 3% 20% 60%

(-) D-dimer

2% 6% 20%(+) D-dimer 7% 36% 75%

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Helical CT

Sensitivity 85% (more sensitive for

proximal emboli)

Specificity 95%

Values vary widely in literature

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Bilateral PE

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V/Q Scan

Identifies mismatches between areas that are ventilatedbut 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 suspicionis 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 ptswith low-probability scans)

Intermediate-probability scan requires further evaluation (16-66% chance of PE depending on pretest probability)

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V/Q Scan

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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

SEE ALGORITHM

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Pulmonary Angiography

Gold Standard

Invasive study

5% morbidity < 0.5% mortality

Indicated if the diagnosis remains

uncertain after noninvasive testing

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PE on pulmonary angiogram

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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 day1 of LMWH), overlap x 5 days, titrate to INR 2.0 to 3.0

Thrombolysis: for massive PE causinghemodynamic compromise

IVC Filter: if anticoagulation is contraindicated (ie,

active GI bleed, intracranial neoplasm, know bleedingdiathesis), if thrombus formed despite adequateanticoagulation, or with a large burden of thrombosisin the LE that could be fatal if embolized

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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

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DVT/PE Prophylaxis

Moderate to High Risk Patients (>2 RF) Lovenox 30 mg SUBQ q 12 hours OR

Lovenox 40 mg SUBQ daily

SCD at all times except when ambulating

Low to Moderate Risk Patients ( 1 RF) Lovenox 40 mg SUBQ daily OR

SCD at all times except when ambulating

No Risk Factors Ambulate in hallways or room QID

TED hose or SCD