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Deep Venous Thrombosis and Pulmonary Embolism : Diagnostic Approach and Current Guidelines in Therapy. Diagnostic Vascular Ultrasonography

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Acute pulmonary embolism: Overview, Diagnosis, Treatment

Acute pulmonary embolism: Overview, Diagnosis, Treatment
DVT/PE in pregnancy
Prevalence of PE in COPD exacerbations
Diagnostic vascular ultrasonography

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Deep Venous Thrombosis and Pulmonary Embolism : Diagnostic Approach and Current Guidelines in Therapy. Diagnostic Vascular Ultrasonography Deep Venous Thrombosis and Pulmonary Embolism : Diagnostic Approach and Current Guidelines in Therapy. Diagnostic Vascular Ultrasonography Presentation Transcript

  • Deep Venous Thrombosis and Pulmonary Embolism : Diagnostic Approach and Current Guidelines in Therapy Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow University of Illinois Medical Center at Chicago
  • DISCLOSURE AND ACKNOWLEDGMENT
    • No relationships to disclose
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Objective
    • Acute pulmonary embolism
      • Overview
      • Diagnosis
      • Treatment
    • DVT/PE in pregnancy
    • Prevalence of PE in COPD exacerbations
    • Diagnostic vascular ultrasonography
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism : Overview
    • Obstruction of the pulmonary artery or one of its branches by
      • Thrombus
      • Tumor
      • Air
      • Fat
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism : Overview
    • PE:
      • Acute
        • Symptoms and signs immediately after obstruction of pulmonary vessels
      • Chronic
        • Slowly progressive dyspnea over a period of years due to pulm HTN
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism : Overview
    • Massive PE
      • Hypotension (SBP < 90 mmHg or a drop of ≥ 40 mmHg from baseline for a period >15 minutes)
      • Massive PE > increased (PVR) > decreased RV outflow > reducing LV preload > diminished CO > Hypotension
      • Accompanied by an elevated CVP
    • Submassive PE
      • All acute PE not meeting the definition of massive PE
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism : Overview
    • Saddle PE
      • Lodges at the bifurcation of the main pulmonary artery
    • Most saddle PE are submassive
        • Retrospective study
        • 546 patients with PE
        • 14 (2.6 %) had a saddle PE
        • Only two of the patients with saddle PE had hypotension
    Ryu et al. Saddle pulmonary embolism diagnosed by CT angiography: frequency, clinical features and outcome. Respir Med 2007; 101:1537.
  • Acute Pulmonary Embolism : Overview
    • EPIDEMIOLOGY
    • Pulmonary embolism mortality in the United States
      • Over a 20-year duration
      • More than 42 million deaths
      • 600,000 pts (1.5%) were diagnosed with PE
    Horlander et al. Pulmonary embolism mortality in the United States, 1979-1998: an analysis using multiple-cause mortality data. Arch Intern Med 2003; 163:1711.
  • Acute Pulmonary Embolism : Overview
    • PROGNOSIS
    • Mortality rate of acute PE
      • 30 % without treatment (primarily due to recurrent PE within the first few hours )
      • 2-8% with anticoagulant therapy
    Carson et al. The clinical course of pulmonary embolism: One year follow-up of PIOPED patients. N Engl J Med 1992; 326:1240 .
  • Acute Pulmonary Embolism : Overview
    • POOR PROGNOSTIC FACTORS
    • INCREASED PE RELATED MORTALITY
    • RV dysfunction
    • RV thrombus
    • Elevated BNP
    • Elevated troponin
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism : Overview
      • POOR PROGNOSTIC FACTORS
      • RV DYSFUCTION
    • Meta-analysis of seven studies
    • (3395 normotensive or hypotensive pts with PE)
    • RV dysfunction was associated with a two-fold increase in PE-related mortality
    • RV dysfunction correlates poorly with PE-related mortality , in normotensive pts
    Wolde et al. Prognostic value of echocardiographically assessed right ventricular dysfunction in patients with pulmonary embolism. Arch Intern Med 2004; 164:1685.
  • Acute Pulmonary Embolism : Overview
      • POOR PROGNOSTIC FACTORS
      • RV DYSFUCTION
    • Predict recurrent PE or DVT
      • Prospective cohort study
      • 301 patients who had experienced their first PE were categorized:
        • No RV dysfunction
        • RV dysfunction with regression (present at admission but not at discharge)
        • Persistent RV dysfunction (more likely to have a recurrent DVT/PE, or PE-related death) – 3 YRS follow up
    Grifoni et al. Association of persistent right ventricular dysfunction at hospital discharge after acute pulmonary embolism with recurrent thromboembolic events. Arch Intern Med 2006; 166:2151 .
  • Acute Pulmonary Embolism : Overview
      • POOR PROGNOSTIC FACTORS
      • RV THROMBUS
    • Pts with PE and (RV) thrombus have a higher mortality than patients without an RV thrombus
      • 14-day mortality (21 vs. 11 %)
      • Three-month mortality (29 vs. 16 %)
    Torbicki et al. Right heart thrombi in pulmonary embolism: results from the International Cooperative Pulmonary Embolism Registry. J Am Coll Cardiol 2003; 41:2245.
  • Acute Pulmonary Embolism : Overview
    • POOR PROGNOSTIC FACTORS
    • ELEVATED BNP
    • Predicts RV dysfunction and mortality
    • The mortality rate correlates with BNP level
    • Meta-analysis of 16 studies
      • BNP >100 pg/mL
        • Increased short-term mortality X 6
      • BNP >600 pg/mL
        • Increased short-term mortality X 16
    Cavallazzi et al. Natriuretic peptides in acute pulmonary embolism: a systematic review. Intensive Care Med 2008
  • Acute Pulmonary Embolism : Overview
    • POOR PROGNOSTIC FACTORS
    • ELEVATED BNP
    • Observational study of 73 pts with acute PE
      • BNP <50 pg/mL
        • Benign clinical course
      • BNP >90 pg/mL
        • a/w cardiopulmonary resuscitation, mechanical ventilation, vasopressor therapy, thrombolysis, and embolectomy, as well as death
    Kucher et al. Prognostic role of brain natriuretic peptide in acute pulmonary embolism. Circulation 2003; 107:2545.
  • Acute Pulmonary Embolism : Overview
    • POOR PROGNOSTIC FACTORS
    • ELEVATED TROPONIN
    • Meta-analysis of 20 observational studies (1985 pts)
      • Elevated troponin I or troponin T level was a/w an increased risk death due to PE (OR 9.44, 95% CI 4.14-21.49)
    Becattini et al. Prognostic value of troponins in acute pulmonary embolism: a meta-analysis. Circulation 2007; 116:427.
  • Acute Pulmonary Embolism : Overview
    • PATHOPHYSIOLOGY
    • Proximal vein thrombi (iliac, femoral, and popliteal vein) are the source of most clinically recognized PE
    • Most distal vein thrombi (calf vein) resolve spontaneously and only 20 -30 % extend into the proximal veins if untreated
    Weinmann et al. Deep-vein thrombosis. N Engl J Med 1994; 331:1630. Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism : Overview
    • Pulm HTN in PE
    • Nonhematogenous obstruction (tumor, air, fat)
      • solely due to mechanical obstruction
        • 60-70% of the pulmonary artery must be obstructed to increase PAP
    • PE
      • Due to a combination of mechanical obstruction and vasoconstriction
        • only 25%–30% of the pulmonary artery must be obstructed to increase PAP
        • PE stimulate neutrophils/endothelium/platelets to produce serotonin/histamine..that cause vasoconstriction
    Stratmann et al. Neurogenic and humoral vasoconstriction in acute pulmonary thromboembolism. Anesth Analg. 2003 Aug;97(2):341-54
  •  
  • Acute Pulmonary Embolism : Overview
    • RISK FACTORS
    • Immobilization
    • Surgery within the last three months
    • Stroke, paresis, paralysis
    • History of venous thromboembolism
    • Malignancy
    • Central venous instrumentation within the last three months
    • Chronic heart disease
    Heit, et al. Relative impact of risk factors for deep vein thrombosis and pulmonary embolism: a population-based study Arch Intern Med 2002; 162:1245.
  • Acute Pulmonary Embolism : Overview
    • RISK FACTORS
    • Additional risk factors identified in women
      • Obesity (BMI ≥29 kg/m2)
      • Heavy cigarette smoking (>25 cigarettes per day)
      • Hypertension
    Goldhaber et al. A prospective study of risk factors for pulmonary embolism in women. JAMA 1997; 277:642. Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism : Overview
  • Acute Pulmonary Embolism : Overview
    • SYMPTOMS / SIGNS 
    • Clinical presentation is variable and nonspecific
    • 47 % of pts had symptoms or signs of LE (DVT)
      • edema, erythema, tenderness, or a palpable cord in the calf or thigh
    Stein et al. Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med 2007; 120:871.
  • Acute Pulmonary Embolism: Diagnosis Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism: Diagnosis
    • LABORATORY
    • Leukocytosis
    • Increased ESR
    • Elevated serum LDH
    • ABGs: hypoxemia, hypocapnia, and respiratory alkalosis
      • Massive PE with hypotension can cause hypercapnia and a combined respiratory and metabolic acidosis (due to lactic acidosis)
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • 18 % may have normal PaO2 (85-105 mmHg)
    • 6 % may have a normal alveolar-arterial gradient for oxygen
    Stein et al. Clinical, laboratory, roentgenographic and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. Chest 1991; 100:598 .
  • Acute Pulmonary Embolism: Diagnosis
    • LABORATORY
    • Elevated BNP
        • Insensitive, nonspecific
        • Case-control study of 2213 hemodynamically stable pts with suspected acute PE
        • BNP had 60% sensitivity and 62% specificity
        • BNP may have a prognostic role in PE
    Sohne et al. Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism. J Thromb Haemost 2006; 4:552.
  • Acute Pulmonary Embolism: Diagnosis
    • LABORATORY
    • Elevated Troponin
      • 30-50 % of pts who have a moderate to large PE
      • Due to acute right heart overload
      • Resolve within 40 hrs (more prolonged elevation after acute MI)
    Muller-Bardorff et al. Release kinetics of cardiac troponin T in survivors of confirmed severe pulmonary embolism. Clin Chem 2002; 48:673.
  • Acute Pulmonary Embolism: Diagnosis
    • ELECTROCARDIOGRAPHY
    • 70 % of pts with acute PE had ECG abnormalities
    • Most commonly
      • Sinus tachycardia
      • nonspecific ST-segment and T-wave changes
    • &quot;S 1 Q 3 T 3 &quot; pattern of acute cor pulmonale (acute right heart strain) is classic
      • infrequent during acute PE
      • Common among patients with massive acute PE and cor pulmonale
    Panos et al. The electrocardiographic manifestations of pulmonary embolism. J Emerg Med 1988; 6:301. Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • S1 Q3 T3
  • Acute Pulmonary Embolism: Diagnosis
    • ELECTROCARDIOGRAPHY
    • The following ECG abnormalities are associated with a poor prognosis
      • Atrial arrhythmias
      • Right bundle branch block
      • Inferior Q-waves
      • Precordial T-wave inversion and ST-segment changes
    Geibel et al. Prognostic value of the ECG on admission in patients with acute major pulmonary embolism. Eur Respir J 2005; 25:843.
  • Acute Pulmonary Embolism: Diagnosis
    • CHEST RADIOGRAPHY
    • Usually CXR is normal
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Stein et al. Clinical, laboratory, roentgenographic and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. Chest 1991; 100:598 .
    • CXR shows RLL collapse
    • Ventilation perfusion scan showing perfusion defect in right side + corresponding ventilation defect
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • ‘ classical’ appearance of a pulmonary infarction – a wedge-shaped lesion peripherally set against the pleura
  • Acute Pulmonary Embolism: Diagnosis
    • VENTILATION-PERFUSION (V/Q) SCAN
    • The PIOPED study
    • Accuracy is greatest when the V/Q scan is combined with clinical probability
    • All patients enrolled in the study were to have a V/Q scan and a pulmonary arteriogram
    Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263:2753.
  •  
  • Acute Pulmonary Embolism: Diagnosis
    • VENTILATION-PERFUSION (V/Q) SCAN
    • Interpretation of V/Q scan for PE as used in PIOPED:
      • Segmental defect (vascular):
        • perfusion abnormality
        • triangular or rectangular shaped
        • periphery based
        • located within one or several vascular segments.
      • Nonsegmental defect (nonvascular) :
        • unlikely to represent PE. (e.g., cardiomegaly, enlarged aorta, enlarged hila, elevated diaphragm)
    Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263:2753.
  • Acute Pulmonary Embolism: Diagnosis
    • VENTILATION-PERFUSION (V/Q) SCAN
    • Interpretation of V/Q scan for PE as used in PIOPED:
      • Small defect (small subsegmental): < 25% of a segment
      • Moderate defect (moderate subsegmental): 25%-75% of a segment
      • Large defect (segmental): > 75% of a segment
    Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263:2753.
  • Acute Pulmonary Embolism: Diagnosis
    • VENTILATION-PERFUSION (V/Q) SCAN
    • High Probability (80-100% likelihood for PE)
      • 2 or more large perfusion defects
    • Intermediate Probability (20-80% likelihood for PE)
      • One moderate to 2 large perfusion defects
    • Low Probability (0-19% likelihood for PE)
      • Any number of small perfusion defects with a normal chest radiograph
      • Multiple matched V/Q abnormalities
      • Nonsegmental (nonvascular) perfusion defects (e.g., cardiomegaly, enlarged aorta, enlarged hila, elevated diaphragm).
    Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263:2753.
    • No areas of defects in ventilation or perfusion scans; low probability of PE
    Perfusion
    • Defect in right lung in lateral segment of right middle lobe w/ no match to ventilation study; intermediate probability for PE
    • A normal V/Q scan virtually excluded PE
    • High-probability V/Q + high clinical probability
      • 95 % likelihood of having PE
    • Low-probability V/Q scan + low clinical probability
      • 4 % likelihood of having PE
    Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263:2753.
  • Acute Pulmonary Embolism: Diagnosis
    • ULTRASOUND
    • Only 29 % of pts with PE had venous thrombosis detected by compression ultrasound
    Turkstra, et al. Diagnostic utility of ultrasonography of leg veins in patients suspected of having pulmonary embolism. Ann Intern Med 1997; 126:775.
  • Acute Pulmonary Embolism: Diagnosis
    • D-DIMER 
    • It can be detected in serum using a variety of different assays
      • Enzyme-linked immunosorbent assay (ELISA) (results in >8 hrs)
      • Quantitative rapid ELISA (results in 30 min)
      • Semi-quantitative rapid ELISA (results in 10 min)
      • Qualitative rapid ELISA (results in 10 min)
      • Quantitative latex agglutination assay (results in 10 to 15 min)
      • Semi-quantitative latex agglutination assay (results in 5 min)
      • Erythrocyte agglutination assay (SimpliRED) (results in 2 min)
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism: Diagnosis
    • D-DIMER 
    • >500 ng/mL is usually considered abnormal
    • Abnormal D-dimer levels being common among hospitalized patients, especially those with malignancy or recent surgery
    • D-dimer levels are abnormal in approximately 90-95 % of all pts with PE
    • D-dimer levels are normal in only 40-68 % of pts without PE
    • Good sensitivity and NPV
    • Poor specificity and PPV
    • D-dimer level <500 ng/mL is sufficient to exclude PE in patients with a low or moderate pretest probability of PE
    Stein et al. D-dimer for the exclusion of acute venous thrombosis and pulmonary embolism: a systematic review. Ann Intern Med 2004; 140:589.
  •  
  • Acute Pulmonary Embolism: Diagnosis
    • ANGIOGRAPHY
    • &quot;gold standard&quot; in the diagnosis of acute PE
    • A negative pulmonary angiogram excludes clinically relevant PE
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  •  
    • Pulmonary angiogram in a patient with PE. The clot appears as a filling defect (arrow).
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism: Diagnosis
    • CT PULMONARY ANGIOGRAPHY
    • PIOPED II (824 patients)
    • 83 % of pts with PE had a positive CT-PA (sensitivity)
    • 96 % of pts without PE had a negative CT-PA (specificity)
    Stein, PD et al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med 2006; 354:2317.
    • CT-PA requires concomitant pretest clinical probability assessment to be an effective diagnostic tool
    Stein, PD et al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med 2006; 354:2317.
  • What if CTA is Negative?
    • Substantial number of pts with PE may be missed by CT-PA
    • Prospective cohort study of 1041 pts with suspected PE and negative CTA
      • The incidence of PE
        • < 2% Low or intermediate clinical probability
        • 5% High clinical probability
    • CT-PA results should be interpreted with caution if the clinical probability of PE and CT-PA are discordant
    Musset, et al. Diagnostic strategy for patients with suspected pulmonary embolism: a prospective multicentre outcome study. Lancet 2002; 360:1914.
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  • CTA is Not Inferior to V/Q Scanning for Ruling Out PE
    • Randomized, controlled trial
    • 1417 pts with suspected PE
    • Underwent CT-PA or V/Q scanning
    • Similar prevalence of PE in both groups
    • Among patients in whom PE was excluded, the CT-PA and V/Q scans had a similar incidence of PE during the three month follow-up period
    Anderson et al. Computed tomographic pulmonary angiography vs ventilation-perfusion lung scanning in patients with suspected pulmonary embolism: a randomized controlled trial. JAMA 2007; 298:2743.
  • Acute Pulmonary Embolism: Diagnosis
    • MRA
    • Limited by respiratory and cardiac motion artifact
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism: Diagnosis
    • ALVEOLAR DEAD SPACE 
    • Acute PE the areas of lung with vascular occlusion are ventilated but not perfused
    • Alveolar dead space fraction (ADF) increases
    • 98% pts with PE have an abnormal ADF (defined as >20 %) or a positive D-dimer
    • Common false positive results
    • Difficulty obtaining accurate ADF measurements
    Rodger et al. Steady-state end-tidal alveolar dead space fraction and D-dimer: bedside tests to exclude pulmonary embolism. Chest 2001; 120:115.
  • Acute Pulmonary Embolism: Diagnosis
    • ECHOCARDIOGRAPHY 
    • Useful if a rapid diagnosis is required to justify the use of thrombolytic therapy
    • PE related mortality increases with
      • RV dysfunction
      • RV thrombus
        • 35% of pts with RV thrombus have PE
        • only 4 % of pts with PE have an RV thrombus
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism: Diagnosis
    • ECHOCARDIOGRAPHY 
    • Echocardiographic findings in PE
      • RV dilation and dysfunction
      • RV thrombus
      • RA dilation
      • TR
      • Pulm HTN
      • Paradoxical septal movement
        • Increases in RV pressure will displace the septum towards the LV during systole and/or diastole
      • Dilated and invariable IVC
      • McConnell Sign
        • Regional wall motion abnormalities that spare the right ventricular apex
        • 77% sensitivity, 94% specificity
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Apical 4 chamber view
    • RV triangular shape, less than 60% LV
    • RV size
      • < 60% LV: normal
      • 60-100% LV: moderately dilated
      • RV > LV: severely dilated
    • Normal heart: apex formed by the LV
    • Acute cor pulmonale: apex formed by RV
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • RV pressure overload with septal flattening causes D sign
      • EchoJournal: Echocardiography Videos and Discussions - RV pressure overload causes D sign
        • McConnell’s Sign: Regional wall motion abnormalities that spare the right ventricular apex
          • http://www.echojournal.org/video/132/McConnells-Sign-RV-dysfunction-in-pulmonary-embolus
        • RV dilation (RV > LV), apex formed by RV, Tricuspid regurgitation (RV failure in acute pulmonary embolus )
          • http://www.echojournal.org/video/133/Huge-Tricuspid-Regurg-Jet
          • http://www.echojournal.org/video/79/Classic-appearance-of-RV-failure-in-acute-pulmonary-embolus-1-of-2
          • http://www.echojournal.org/video/80/Classic-appearance-of-RV-failure-in-acute-pulmonary-embolus-2-of-2
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
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  • RECOMMENDED DIAGNOSTIC APPROACH CT Experienced Institutions: Christopher study  
  • RECOMMENDED DIAGNOSTIC APPROACH CT inexperienced institutions: PIOPED Study
  • PERC FOR LOW RISK OUTPATIENT POPULATIONS
    • This approach has been best studied in the emergency department
    • Acute PE can probably be excluded without further diagnostic testing if the patient meets all PERC criteria
      • Age < 50 years
      • HR < 100 bpm
      • O2 SAT ≥ 95 %
      • No hemoptysis
      • No estrogen use
      • No prior DVT or PE
      • No unilateral leg swelling
      • No surgery or trauma requiring hospitalization within the past 4 weeks
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • PERC FOR LOW RISK OUTPATIENT POPULATIONS
    • Multicenter, prospective cohort study
    • 8138 ED pts with suspected PE
    • Chest pain or dyspnea was the chief complaint
    • 1666/8138 pts fulfilled all of the PERC + low clinical suspicion for PE
    • only 15/1666 (< 1 %) developed a DVT or PE within 45 days
    Kline et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost 2008; 6:772.
  • Acute Pulmonary Embolism: Treatment Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • Mortality rate of acute PE
      • 30 % without treatment (primarily due to recurrent PE within the first few hours )
      • 2-8% with anticoagulant therapy
    Acute Pulmonary Embolism: Treatment Carson et al. The clinical course of pulmonary embolism: One year follow-up of PIOPED patients. N Engl J Med 1992; 326:1240 .
  • ACUTE PULMONARY EMBOLISM: TREATMENT ANTICOAGULATION
    • The goal of anticoagulation
      • Decrease mortality (from 30% to 2-8%) by preventing recurrent PE
    • Its efficacy depends upon achieving a therapeutic level of treatment within the first 24 hours of treatment
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • WHEN SHOULD I INITIATE ANTICOAGULANT THERAPY?
    • Indications
      • High clinical suspicion of PE
      • PE has been confirmed
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • WHICH ANTICOAGULANT SHOULD I INITIATE? IV UFH vs. SC LWMH
    • IV UFH
      • Persistent hypotension (massive PE)
        • The clinical trials that evaluated LMWH in acute PE excluded this patient subgroup
      • Increased risk of bleeding
        • shortest-acting anticoagulant and its activity can be reversed (protamine sulfate) if major bleeding occurs
      • Concern about subcutaneous absorption (morbid obesity, severe anasarca)
      • Thrombolysis is being considered
      • Creatinine clearance is ≤30 mL/min
    • SC LMWH
      • Hemodynamically stable patients with PE
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • WHICH ANTICOAGULANT SHOULD I INITIATE? IV UFH vs. SC LWMH
    • Severe renal insufficiency (CrCl <30 mL/minute)
      • UFH should be used instead of LMWH
      • If LMWH is used, there should be an approximately 50 % daily dose reduction (also monitor the anti-Xa activity)
    Hirsh et al. Parenteral anticoagulants: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133:141S
  • THE ADVANTAGES OF USING SC LMWH
    • Meta-analysis of randomized trials
      • In 18 trials (8054 patients), SC LMWH decreased mortality (odds ratio 0.76, 95% CI 0.62-0.92).
      • In 22 trials (8867 patients), SC LMWH decreased recurrent thrombosis (odds ratio 0.68, 95% CI 0.55-0.84).
      • In 12 trials, thrombus size reduction was more common with LMWH (odds ratio 0.69, 95% CI 0.59-0.81).
    • Less major bleeding
    • Fixed dosing that does not require adjustment
    • Decreased likelihood of thrombocytopenia
    van Dongen et al. Fixed dose subcutaneous low molecular weight heparins versus adjusted dose unfractionated heparin for venous thromboembolism. Cochrane Database Syst Rev 2004; :CD001100.
  • WHAT ABOUT THE USE OF FONDAPARINUX?
    • No studies directly compared SC LMWH and fondaparinux
    • Fondaparinux and IV UFH appear to be equivalent
      • Open-label randomized trial
      • 2213 pts with symptomatic PE
      • Similar rates of recurrent PE, bleeding, thrombocytopenia, and death
    • Dose
      • 5 mg for patients <50 kg
      • 7.5 mg for patients 50 to 100 kg
      • 10 mg for patients >100 kg
    • Contraindicated in patients with severe renal insufficiency (CrCl <30 mL/minute)
    Buller et al. Subcutaneous fondaparinux versus intravenous unfractionated heparin in the initial treatment of pulmonary embolism. N Engl J Med 2003; 349:1695.
  • LONG-TERM ORAL ANTICOAGULANT: WARFARIN
    • Suppress production of the vitamin K-dependent clotting factors (II, VII, IX, and X)
    • Long-term vs. short term (1-4 mon) treatment with warfarin
      • Decreased likelihood of recurrent PE or DVT with long-term warfarin (odds ratio 0.18, 95% CI 0.13-0.26)
    • It should NOT be initiated prior to heparin
      • Warfarin alone 3 X higher incidence of recurrent PE or DVT
    Hutten et al. Duration of treatment with vitamin K antagonists in symptomatic venous thromboembolism. Cochrane Database Syst Rev 2006; :CD001367.
  • FOR HOW LONG SHOULD WE OVERLAP WORFARIN WITH HEPARIN
    • Minimum of five days and until the (INR) is therapeutic (2.0 to 3.0) for at least 24 hours
      • During the first few days of warfarin therapy, the prolonged PT reflects only the loss of factor VII (which has a half-life of 5-7 hrs) and does not represent adequate anticoagulation because the intrinsic clotting pathway remains intact
    • Pts with known protein C deficiency have an increased risk of warfarin-induced skin necrosis
    Kearon et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133:454S.
  •  
  • HOW SHOULD I MONITOR LMWH?
    • LMWH (anti-Xa levels )
      • Not necessary for most pts
      • Warranted
        • Morbid obesity (BMI >40)
        • Low body weight (<45 kg women, <57 kg men)
        • Severe renal insufficiency (CrCl <30 mL/minute)
        • Pregnancy
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • HOW SHOULD I MONITOR UFH?
    • UFH (aPTT)
      • Measures the antithrombotic activity of heparin
      • The therapeutic aPTT is 1.5 to 2.5 times the control aPTT
    • The efficacy depends on achieving a therapeutic level of treatment within the first 24 hours
      • Failure was associated with
        • Higher rate of recurrent DVT or PE (23 vs. 3 %)
        • For at least 3 months, despite ongoing therapeutic anticoagulation
    Hull et al. Relation between the time to achieve the lower limit of the APTT therapeutic range and recurrent venous thromboembolism during heparin treatment for deep vein thrombosis. Arch Intern Med 1997; 157:2562. Hull et al. The importance of initial heparin treatment on long-term clinical outcomes of antithrombotic therapy. The emerging theme of delayed recurrence. Arch Intern Med 1997; 157:2317.
  • HOW SHOULD I MONITOR COUMADIN?
    • Target an INR of 2.5 (range 2.0 to 3.0)
      • INR <2.0 is associated with an increased likelihood of recurrent PE or DVT
      • INR > 3.0 is associated with bleeding
    Kearon et al. Comparison of Low-Intensity Warfarin Therapy with Conventional-Intensity Warfarin Therapy for Long-Term Prevention of Recurrent Venous Thromboembolism. N Engl J Med 2003; 349:631 .
  • WHAT ARE THE COMMON COMPLICATIONS?
    • Major bleeding
      • Intracranial hemorrhage
      • Retroperitoneal hemorrhage
      • Bleeding that led directly to death, hospitalization, or transfusion
    • The frequency of major bleeding
      • IV UFH <3%
      • Fondaparinux < 3%
      • Warfarin < 3%
      • SC LMWH (significantly lower rate )
    • Management 
      •   Protamine sulfate
      • Vitamin K and fresh frozen plasma
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • WHAT ARE THE COMMON COMPLICATIONS?
    • Heparin-induced thrombocytopenia (HIT)
      • Risk factors for developing HIT
        • Previous episode of HIT
      • Less common after the use of LMWH compared to UFH
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • FOR HOW LONG SHOULD I TREAT?
    • First episode of PE / DVT
      • Reversible risk factor  (immobilization, surgery, and trauma): warfarin for at least three months
        • 6 months therapy : no additional benefit
        • < 3 months therapy: more recurrent PE or DVT (11 VS. 4 %)
      • Unprovoked (idiopathic): conflicting data
        • 2 Randomized trials enrolled patients with DVT or PE :
          • 3 months therapy vs. long term ( 2 years) therapy: fewer recurrent PE or DVT
        • Another randomized trial enrolled patients with PE only :
          • 3 months therapy vs. > 3 months: no difference in the rate of recurrent DVT or PE, or mortality
    Kearon et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133:454S.
  • FOR HOW LONG SHOULD I TREAT?
    • Recurrent PE / DVT (two or more episodes)
      • Indefinite warfarin therapy
        • Randomized trial of 227 pts with recurrent PE or DVT
        • Therapy for 6 months vs. indefinitely
        • 4 years follow up
        • Fewer recurrent PE or DVT (3 vs. 21 %)
        • Higher major bleeding (9 vs. 3 %)
    Kearon et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133:454S.
  • Acute Pulmonary Embolism: Treatment
    • A 58-year-old man is evaluated in the emergency department because of dyspnea and hypotension of 3 hours’ duration. Three weeks ago, he fractured his right tibia in a motor vehicle accident, requiring open reduction and fixation. A cast was placed that included ankle and knee joints. On physical examination, his pulse rate is 120/min and blood pressure is 95/55 mm Hg (preoperative blood pressure was 135/85 mm Hg). Chest radiography shows no infiltrates. The SaO 2 when the patient is breathing room air is 89%. Ventilation-perfusion scanning shows two unmatched lobar defects and two segmental defects. A Doppler study shows a deep venous thrombosis in the femoral vein of the right leg.
    • Which of the following therapies is most likely to restore hemodynamic stability within the first 24 hours?
    • ( A ) Unfractionated heparin ( B ) Low-molecular-weight heparin ( C ) Tissue plasminogen activator (t-PA) followed by heparin ( D ) Unfractionated heparin plus an inferior vena cava filter ( E ) Warfarin
  • SHOULD I ADMINISTER THROMBOLYTIC THERAPY?
    • Only pts in whom the diagnosis of (PE) has been confirmed
    • Accelerates clot lysis and is a/w
      • short-term physiologic benefits (RV function and pulmonary perfusion)
      • No mortality benefit
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • Large saddle PE
    • 24 hours after IV TPA therapy
      • resolution of the saddle embolus
    Fam, NP, Verma, A. Thrombolysis of a massive pulmonary embolism. N Engl J Med, 2002; 347:1161. Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Thrombolytic Therapy Does Not Improve Mortality
    • Meta-analysis of 9 randomized trials (461 pts)
    • Thrombolytic therapy followed by heparin vs. heparin alone
      • No statistically significant effect on mortality
        • (relative risk 0.63, 95% CI 0.32-1.23)
      • No statistically significant effect on recurrence of PE
        • (relative risk 0.59, 95% CI 0.30-1.18)
      • Increase risk of major hemorrhage
        • (relative risk 1.76, 95% CI 1.04-2.98)
    Thabut et al. Thrombolytic therapy of pulmonary embolism: a meta-analysis. J Am Coll Cardiol 2002; 40:1660. Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Thrombolytic Therapy Improves Important Physiologic Parameters
    • LONG TERM IMPROVEMENT
    • Randomized study of 40 pts with acute PE
    • Anticoagulation plus thrombolysis vs. anticoagulation alone
    • After 2 wks
      • More complete resolution of emboli
    • Longer-term follow-up (7 yrs)
      • Lower pulmonary artery pressure and pulmonary vascular resistance
    • Sharma et al. Effect of thrombolytic therapy on pulmonary-capillary blood volume in patients with pulmonary embolism.
    • N Engl J Med 1980; 303:842.
    • SHORT TERM IMPROVEMWNT
    • Prospective study of 40 pts with acute PE
    • Thrombolytic therapy plus anticoagulation vs. anticoagulation alone
    • 12 hours
      • Improved right ventricular function
    • One week later
      • No difference in RV function
    • Konstantinides et al. Comparison of alteplase versus heparin for resolution of major pulmonary embolism.
    • Am J Cardiol 1998; 82:966.
  • Kearon, et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133 Suppl 6:454.
  • Thrombolytic Therapy in Patients Undergoing CPR due to PE-induced Cardiac Arrest
    • Case reports
    • Insufficient data
    • Successful in PE-induced Cardiac Arrest?!?
    • No outcome improvement when the cardiac arrest manifests as PEA
    Bailen et al. Thrombolysis during cardiopulmonary resuscitation in fulminant pulmonary embolism: A review. Crit Care Med 2001; 29:2211. Abu-Laban et al. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med 2002; 346:1522.
  • Adverse Effect Associated with Thrombolysis
    • Bleeding
      • Intracranial hemorrhage occurs in up to 3 % of pts who receive thrombolytic therapy for PE
    • SK: allergic reactions and hypotension (anaphylaxis <0.5 %)
      • Particularly with repeat administration
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Thrombolytic Therapy in DVT
    • Not recommended
    • Catheter-directed thrombolysis, rather than systemic thrombolysis (Grade 2B)
      • Massive iliofemoral or proximal femoral DVT with a high risk of limb gangrene
      • Within 2 wks of the onset of symptoms
      • Alternative therapies
        • catheter extraction
        • catheter fragmentation
        • surgical thrombectomy
    • WEAK RECOMMENDATION, JUST A SUGGESTION
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Systemic vs. Catheter-directed Thrombolysis: Which One is Better?
    • Randomized trial on 32 pts with iliofemoral DVT
    • Catheter-directed vs. systemic thrombolysis followed by anticoagulation
      • Lower doses of thrombolytics, resulting in fewer bleeding complications
      • Normal valve function preserved in more patients!!!
    Laiho et al. Preservation of venous valve function after catheter-directed and systemic thrombolysis for deep venous thrombosis. Eur J Vasc Endovasc Surg 2004; 28:391
  • Kearon, et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; 133 Suppl 6:454.
  • The ATTRACT Trial
    • A large, randomized, multicenter trial
    • In progress
    • Pharmacomechanical catheter-directed thrombolysis
    • This approach combines thrombolytic therapy with a catheter-mounted clot removal device
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Acute Pulmonary Embolism: Treatment
    • A 35-year-old woman is evaluated for treatment of a pulmonary thromboembolism. Four days ago she was involved in an automobile accident resulting in fractures of the left lower ribs and required an emergency splenectomy. Two hours ago she developed pleuritic chest pain and dyspnea. Noninvasive ultrasound and Doppler studies of the leg veins show a deep venous thrombosis in the right leg extending beyond the femoral vein into the iliac system. Ventilation-perfusion lung scanning shows two segmental unmatched perfusion defects in the right lung and a similar defect in the left lung. On physical examination, her heart rate is 120/min, respiration rate is 24/min, and blood pressure is 95/60 mm Hg. Arterial blood gases when the patient is breathing room air are PaO 2 , 58 mm Hg; PaCO 2 , 28 mm Hg; and pH, 7.44.
    • Which of the following is the most appropriate next step?
    • ( A ) Tissue plasminogen activator ( B ) Pulmonary angiography ( C ) Unfractionated heparin ( D ) Inferior vena cava filter ( E ) Warfarin
  • SHOULD AN IVC FILTER BE PLACED?
    • Indications:
      • Absolute contraindication to anticoagulation
        • active bleeding
        • Major surgery
      • Recurrent PE despite adequate anticoagulant therapy
      • Complication of anticoagulation
        • severe bleeding
      • Hemodynamic or respiratory compromise (another PE may be lethal )
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • IVC FILTERS: OUTCOME
    • Randomized trial
    • 400 pts with proximal DVT
    • Anticoagulation alone vs anticoagulation plus an IVC filter
      • Decrease recurrent PE
      • Increase recurrent DVT
      • No reduction in mortality
    Decousus et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. N Engl J Med 1998; 338:409 .
  • IVC FILTERS: COMPLICATIONS
    • Complications related to the insertion process (bleeding, venous thrombosis at the insertion site)
    • Filter misplacement
    • Filter migration
    • Filter erosion and perforation of the IVC wall
    • IVC obstruction due to filter thrombosis
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • LONG-TERM vs. RETRIEVABLE IVC FILTERS
    • Permanent IVC filter placement is discouraged
    • Investigation of their effectiveness and adverse effects is still in its early stages
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • EMBOLECTOMY
    • Persistent hypotension due to PE
    • Thrombolytic therapy fails or is contraindicated
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Catheter Embolectomy
    • Rheolytic embolectomy (AngioJet embolectomy )
      • Injecting pressurized saline through the catheter
      • The saline and fragments of clot are then sucked back into the catheter
    • Rotational embolectomy 
      • Rotating device to fragment the thrombus, while continuously aspirating the fragments.
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Normal inferior pulmonary artery and peripheral reperfusion immediately and one month after thrombectomy Huge thrombus in the right inferior pulmonary artery Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Surgical Embolectomy 
    • Experienced surgeon
    • Cardiopulmonary bypass
    • Small observational cohort study on pts failed the initial thrombolysis
      • Surgical embolectomy vs repeat thrombolysis
      • Fewer recurrent PE
      • Fewer deaths and fewer major bleeding
      • But not statistically significant
    Meneveau et al. Management of unsuccessful thrombolysis in acute massive pulmonary embolism. Chest 2006; 129:1043.
  • Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Deep Vein Thrombosis and Pulmonary Embolism in Pregnancy Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Deep Vein Thrombosis and Pulmonary Embolism in Pregnancy
    • The incidence is higher during in pregnancy ( x 4-50)
    • Incidence rate of 1 / 500 - 2000
    • Maternal Mortality
      • PE 20 %
      • Maternal hemorrhage 17 %
      • Pregnancy-associated hypertension 16 %
    Chang et al. Pregnancy-related mortality surveillance--United States, 1991--1999. MMWR Surveill Summ 2003; 52:1.
  • Deep Vein Thrombosis and Pulmonary Embolism in Pregnancy
    • More common in the postpartum period
      • DVT is 2 X higher after cesarean delivery than vaginal birth
    • Antepartum DVT/PE is equally distributed across trimesters
    Simpson et al. Venous thromboembolism in pregnancy and the puerperium: incidence and additional risk factors from a London perinatal database. BJOG 2001; 108:56.
    • DVT is more common in the left than the right leg
      • 60 pregnant women with a first episode DVT
      • 58 left lower extremity DVTs
      • 2 bilateral DVTs
      • No isolated right lower extremity DVTs
    • Increased venous stasis in the left leg
        • Compression of the left iliac vein by the right iliac artery
        • Compression of the IVC by the uterus
    Deep Vein Thrombosis and Pulmonary Embolism in Pregnancy Ginsberg et al. Venous thrombosis during pregnancy: Leg and trimester of presentation. Thromb Haemost 1992; 67:519.
    • PATHOGENESIS AND RISK FACTORS
    • Virchow's triad
      • Venous stasis
      • Endothelial injury
      • Hypercoagulable state
    Deep Vein Thrombosis and Pulmonary Embolism in Pregnancy Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • PATHOGENESIS AND RISK FACTORS
      • VENOUS STASIS
      • Progesterone induced dilation of veins
        • Venous pooling
        • Valvular incompetence
      • Compression of large veins by the gravid uterus
    Deep Vein Thrombosis and Pulmonary Embolism in Pregnancy Goodrich et al. Peripheral venous distensibility and velocity of venous blood flow during pregnancy or during oral contraceptive therapy. Am J Obstet Gynecol 1964; 90:740.
    • PATHOGENESIS AND RISK FACTORS
      • ENDOTHELIAL INJURY
    • At the uteroplacental surface
    • Probably accounts for the frequency of DVT/PE in the immediate postpartum period
    • Forceps, vacuum extraction, or surgical delivery can exaggerate vascular intimal injury and amplify this phenomenon
    Deep Vein Thrombosis and Pulmonary Embolism in Pregnancy Marik et al. Venous thromboembolic disease and pregnancy. N Engl J Med 2008; 359:2025. Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • PATHOGENESIS AND RISK FACTORS
      • HYPERCOAGULABLE STATE
    • Increase coagulation factors, such as factors I, II, VII, VIII, IX, and X
    • Decrease in protein S
    • Increase in resistance to activated protein C
    • Inherited thrombophilias
    • Antiphospholipid antibodies
    Deep Vein Thrombosis and Pulmonary Embolism in Pregnancy Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Marik et al. Venous thromboembolic disease and pregnancy. N Engl J Med 2008; 359:2025
  • Diagnosis of DVT/PE During Pregnancy can be a Challenge
    • Lower extremity swelling and discomfort are common in advanced pregnancy
    • Dyspnea (the most frequent symptom of PE) occurs at some point in up to 70 % of normal pregnancies
    • Respiratory alkalosis is a very common feature of both pregnancy and PE
    • Wells Score, have not been validated in pregnancy
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Diagnosis of DVT/PE During Pregnancy can be a Challenge
    • D-Dimer is elevated in uncomplicated pregnancy
      • Increases with gestational age and peaks at the time of delivery and in the early postpartum period
    Kline et al. D-dimer concentrations in normal pregnancy: new diagnostic thresholds are needed. Clin Chem 2005; 51:825.
    • The recommended initial test in the workup of DVT
      • Doppler ultrasound
      • Should be done with the pt in the left lateral decubitus position
    • If U/S results are equivocal then
      • contrast venography with abdominal-pelvic shielding
        • The delivered radiation to the fetus is small (<500 mcGy) with shielding
        • shielding renders the test relatively insensitive to isolated iliofemoral thrombosis
    • In cases of contraindications of contrast, or strong clinical suspicion of pelvic thrombosis
      • MRI
    Diagnosis of DVT During Pregnancy Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • The recommended initial test in the workup of PE
      • LE’s Doppler ultrasound
    • The diagnostic test of choice in the workup of PE in pregnancy
      • CT angiography
        • Mean radiation dose to the fetus is 3 to 131 mcGy
    • In case of contraindication to radiocontrast:
      • (V/Q) scan
      • Pulmonary angiography
    Diagnosis of PE During Pregnancy Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
    • There are no systematic differences in the diagnostic strategies for DVT and PE in the pregnant and the non-pregnant pt
    • Avoiding radiation-requiring studies in pregnant pts may result with greater harm to the pt and the fetus from the failure to detect VTE
      • Fetal radiation exposure from the combination of a chest radiograph, V/Q scanning, and pulmonary arteriography is less than 5000 mcGy
    Guidelines on diagnosis and management of acute pulmonary embolism. Task Force on Pulmonary Embolism, European Society of Cardiology. Eur Heart J 2000; 21:1301.
  • Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD
    • 30% of all exacerbations of COPD do not have a clear etiology
    • COPD pts are at a high risk for PE
      • Limited mobility
      • Inflammation
      • Comorbidities
    Rizkallah et al. Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD: A Systematic Review and Meta-analysis CHEST March 2009 vol. 135 no. 3 786-793
  • Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD
    • Systematic review and metaanalysis
    • 5 cross-sectional or prospective studies
    • Used CT scanning or pulmonary angiography for PE diagnosis
    • Sample size 550 patients
    Rizkallah et al. Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD: A Systematic Review and Meta-analysis CHEST March 2009 vol. 135 no. 3 786-793
    • One of four COPD patients who require hospitalization for an acute exacerbation may have PE
    Rizkallah et al. Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD: A Systematic Review and Meta-analysis CHEST March 2009 vol. 135 no. 3 786-793
  • Diagnostic Vascular Ultrasonography Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Should we Perform our Own Compression Studies?
    • Bedside procedure
    • Progressively practiced by Intensivists
    • Easy to learn
    • Available 24/7
    • Fast and safe
    • Can be repeated
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Lower Extremity Deep Venous Anatomy
    • Great Saphenous Vein (GSV)
    • Superficial vein
    • GSC thrombosis is not cause for anticoagulation
    • With the exception of the most proximal portion of the vein
    Proximal Distal Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Why Do we Ignore Calf DVT?
    • Most distal vein thrombi (calf vein) resolve spontaneously
    • 20-30 % of calf DVTs extend proximally if untreated
    • If left untreated
      • 80% become symptomatic
      • 50% then become PE
    • So, from 100 calf DVTs, there will be 8 PE’s
    • From 100 proximal DVTs, there will be 50 PE’s
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Why Do we Ignore Calf DVT?
    • Most distal vein thrombi (calf vein) resolve spontaneously
    • 20-30 % of calf DVTs extend proximally if untreated
    • If left untreated
      • 80% become symptomatic
      • 50% then become PE
    • So, from 100 calf DVTs, there will be 8 PE’s
    • From 100 proximal DVTs, there will be 50 PE’s
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Incidence of DVT in ICU
    • High incidence of DVT in the ICU (8%-18% first wk)
    • Cook , Crit Care Med, 2005
      • 261 MICU/SICU pts (expected stay > 72hrs)
      • Ultrasound done within 48hrs and 2x/week
      • All on ppx
      • 2.7% prevalence of proximal DVT
      • 9.6% incidence of proximal DVT
    • Ibrahim, Crit Care Med 2002
      • MICU pts on vent > 7 days
      • Duplex done every 7 days
      • All on ppx
      • 18% with proximal LE DVT, 5 % with UE DVT
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Do we Need to Utilize Doppler and Color Modalities?
    • Lensing, Ann Int Med, 1997
      • Added color Doppler to simple compression study, found to result in no added sensitivity or specificity
    • Blaivas, Acad Emerg Med, 2000
      • 17% DVT had normal augmentation
      • 12% normal studies had poor augmentation
      • Color doppler decreased “indeterminate” diagnoses
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Do we Need to Scan Every 2 cm from CFV to PV?
    • Poppitti 1995
      • 2 site compression vs. complete doppler exam
      • No additional proximal DVT with complete study
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Can We Accurately Perform Compression Studies
    • Magazzini, Acad Emerg Med, 2006
      • ED physicians took 30 hr ultrasound course, performed LE ultrasound on ED pts, discharge pt if results normal
      • Radiologist did “formal” study within 24-48hrs
      • 399 pts scanned, mean time for study was 13 min
      • PPV 96%, NPV 100%, only 2% “uncertain”
      • No pts died or developed DVT within 1 month
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Can We Accurately Perform Compression Studies
    • Jang T, Acad Emerg Med, 2004
      • 8 ED residents , PGY 1-3
      • Training:
        • One week general introductory course
        • One hour PowerPoint lecture on DVT U/S with images, performed tow practice studies on normal volunteers
      • 72 pts, full compression study performed
      • Results compared to venography, vasc lab U/S, or CTV
      • 100% SENSETIVITY, 92% SPECIFICITY
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Can We Accurately Perform Compression Studies
    • Blaivas 2000 – ED physician study
      • ED physicians experienced in ultrasound (but not for DVT)
      • Training
        • 2 hrs didactics
        • 3 hrs hands-on training
    • 103 high risk ED pts with signs and symptoms
    • 2 site compression + color augmentation
    • Then duplex done by vascular laboratory
    • 30% of pts found with DVT
    • 1 false positive ED finding
    • 1 true positive ED (negative by vasc lab, + on venography)
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Can We Accurately Perform Compression Studies
    • Trottier, CHEST 1996
      • Investigator with no prior experience
      • Training
        • 35 practice studies
      • 100 med-surg hospitalized pts
      • Compression study done with 1-2 cm intervals, compared to vas lab duplex
      • 94% sensitivity, 99% specificity
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Can We Accurately Perform Compression Studies in Acutely Ill Medical Patients?
    • Tomkowski WZ, Haematoligica, 1999
      • Moderate risk hospitalized pts (CHF, COPD exac, PNA/UTI)
      • Screening compression U/S on day 6-16 of hospital
      • Venography performed same day
      • 3.2% proximal DVT
      • Sensitivity 60%, specificity 99%
      • PPV 75%, NPV 98%
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Can We Accurately Perform Compression Studies in High Risk Patients?
    • Lensing, Arch Int Med, 1997
      • 204 post-op knee/hip ortho surgery pts
      • Screened for asymptomatic DVT
      • Compression with color compared to contrast venography
      • 60% sensitivity , 71% specificity
      • Color added no additional DVT accuracy
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Summary Slide
    • Simple compression study is sufficient
      • No need for doppler color/ augmentation maneuver
    • Compression studies can be accurately performed by clinicians with minimal training
      • Has only been shown in ED and medical ward patients
      • Not sensitive in high risk or acutely ill medical pts
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Performance of Compression Study
    • Vascular “linear” transducer (7.5 MHz)
    • Pt in supine position with slight external rotation
    • Position transducer just distal to inguinal ligament, marker at 9 o’clock
    Blaivas M. Ultrasound in the detection of venous thromboembolism. Crit Care Med 2007 Vol. 35 No. 5
  • Compression Technique
    • Apply pressure until vein collapses
    • If artery starts to deform and vein is not collapsing, this suggests possibility of a thrombus in lumen
    • If a DVT is found, mark most proximal location
      • This allows eval of progression or treatment failure
    Blaivas M. Ultrasound in the detection of venous thromboembolism. Crit Care Med 2007 Vol. 35 No. 5 Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Compression Points
    • Femoral Compressions
      • Start on CFV just distal to inguinal ligament
      • Then q 1 cm until the medial entry of the GSV (the bean sign)
      • Then q 1 cm until CFV splits into DFV and SFV
      • Then continue 1-2 cm
      • Then may go straight to PV
    Blaivas M. Ultrasound in the detection of venous thromboembolism. Crit Care Med 2007 Vol. 35 No. 5 1 2 3 4 5 Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  •  
  •  
  •  
  •  
  •  
  • BEAN SIGN CFV GSV
  • Compression Points
    • Popliteal Compressions
      • Locate PA and PV behind knee
      • Compress last 2 cm of PV and just distal to it’s trifurcation
    Blaivas M. Ultrasound in the detection of venous thromboembolism. Crit Care Med 2007 Vol. 35 No. 5 1 2
  • PA PV PA
  • PA PA PV PV
  • How to Distinguish Acute from Chronic Thrombus
    • Consider MRI to distinguish acute from chronic DVT
    • Acute DVT
      • Anechoic (black) but may be echogenic
        • Confirm with compression
    • Chronic DVT (organized thrombus)
      • Organization occur between 5-10 days
      • More echogenic (brighter)
      • More irregular
      • Recannulize centrally
      • Blood flow can be seen through or around the thrombus
      • Thickened venous walls
      • Collateral may be present
    Blaivas M. Ultrasound in the detection of venous thromboembolism. Crit Care Med 2007 Vol. 35 No. 5 Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
  • Important Hints
    • Do not compress a free-floating thrombus
      • Risk for embolization
    • Echogenic lumen not specific for clot. An acute thrombus can be anechoic
      • Confirm patency by complete apposition of the anterior and posterior walls of the vessel
    • Differentiate a lymph node or Baker's cyst from DVT
      • The transducer can be moved proximally and distally to identify the edges of the lymph node or cyst
      • LN usually oval and encapsulated
    • If the vein seems to be only partially filled, a long axis view is warranted
    Blaivas M. Ultrasound in the detection of venous thromboembolism. Crit Care Med 2007 Vol. 35 No. 5 Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow
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    • Integrating bedside ultrasound for thromboembolic disease into an ICU-based protocol for DVT prophylaxis, screening, and diagnosis holds promise for decreasing deadly sequelae such as PE
    Bassel Ericsoussi, MD Pulmonary and Critical Care Fellow