Pulmonary Embolism: Diagnosis, Treatment, and Prevention Philip Keith March 26, 2008

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Pulmonary Embolism

Diagnosis, Treatment, and Prevention Philip Keith March 26, 2008

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

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)

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

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

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

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

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 Twave 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

Westermark Sign

Hampton Hump

Occurs 12 to 36 hours after symptoms begin; usually indicates pulmonary infarction

EKG Findings

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
S/S of DVT HR >100 Immobilization (bed rest >/= 3d) OR surgery within 4 weeks Prior DVT or PE Hemoptysis Malignancy (treated within the past 6 months or palliative Other diagnoses less likely than PE

POINTS
3.0 1.5 1.5

1.5 1.0 1.0

3.0

REFER TO ALGORITHM

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) Overall (-) D-dimer (+) D-dimer

Intermediate (2-6)

High (>6)

3%
2% 7%

20%
6% 36%

60%
20% 75%

Helical CT
Sensitivity 85% (more sensitive for proximal emboli) Specificity 95% Values vary widely in literature

Bilateral PE

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 (1666% chance of PE depending on pretest probability)

V/Q Scan

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

Pulmonary Angiography
Gold Standard Invasive study 5% morbidity < 0.5% mortality Indicated if the diagnosis remains uncertain after noninvasive testing

PE on pulmonary angiogram

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

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

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

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