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

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Presentation on theme: "Pulmonary Embolism Diagnosis, Treatment, and Prevention Philip Keith March 26, 2008."— Presentation transcript:

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

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 3 rd most common acute cardiovascular emergency (MI and stroke)

4 Risk Factors (for DVT) Virchow’s 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

5 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

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

7 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

8 Westermark Sign

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

10 EKG Findings

11 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) VARIABLEPOINTS S/S of DVT3.0 HR > Immobilization (bed rest >/= 3d) OR surgery within 4 weeks 1.5 Prior DVT or PE1.5 Hemoptysis1.0 Malignancy (treated within the past 6 months or palliative 1.0 Other diagnoses less likely than PE 3.0

12 REFER TO ALGORITHM

13 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%

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

15 Bilateral PE

16 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)

17 V/Q Scan

18 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

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

20 PE on pulmonary angiogram

21 Treatment of PE Acute anticoagulation to therapeutic levels –IV UFH: 80 U/kg bolus, then 18 U/kg/hr to goal PTT of 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

22 Treatment of PE Long-term anticoagulation – 1 st event with reversible RF: 3-6 mo warfarin – Idiopathic PE/DVT: > or = 6 mo warfarin –2 nd 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

23 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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