8/16/2012. Pulmonary Embolism

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1 Pulmonary Embolism Rita M. Williams, NP-C, PA PeaceHealth Medical Group, Pulmonary & Critical Care Pulmonary Embolism Acute pulmonary embolism (PE) is a common and frequently fatal disease Clinical presentation is variable and nonspecific, making accurate diagnosis difficult with more than half likely undiagnosed Introduction of computed tomographic pulmonary angiography (CTA) into routine clinical practice has affected the estimated incidence of PE Increasing from 62.1 cases per 100,000 to cases per 100,000 1

2 Definition PE is defined as an obstruction of the pulmonary artery or one of its branches by material (thrombus, tumor, air, or fat) that originated elsewhere in the body (B. Taylor Thompson, M.D., Charles A. Hales, M.D., Overview of acute pulmonary embolism ) Classifications Acute Develop s/sx immediately after obstruction of pulmonary vessels Chronic Develop s/sx slowly with progressive dyspnea over a period of years Due to pulmonary hypertension Acute further classified as massive or submassive Massive Causes hypotension SBP <90 or drop in SBP >40 mmhg from baseline for >15 minutes Suspect anytime hypotension with elevated CVP or neck vein distension not explained by AMI, tension pneumo, pericardial tamponade, or new arrhythmia Frequently results in acute right ventricular failure and death! Death often within 1-2 hours of the event Continued increased risk of death for hours All PE s not meeting criteria for massive PE are considered submassive PE Classification is a clinical presentation, not a radiologic interpretation 2

3 Saddle PE Thrombus lodges at bifurcation of the main pulmonary artery into the right and left pulmonary arteries Usually submassive Response to treatment same as other types of PE Mortality rate of 5.4% Untreated PE associated with a mortality rate of about 30% Recurrent PE is the most common cause of death Prognosis-risk factors for increased mortality Right ventricular dysfunction due to PE Associated with a twofold increase in PE related mortality May also predict recurrent PE or DVT BNP may predict other adverse outcomes BNP>90 four hours after presentation has been associated with CPR mechanical ventilation vasopressor therapy Thrombolysis Embolectomy Death 95% of patients with a BNP <50 had a benign clinical course 3

4 Deep vein thrombosis (DVT) Frequently coexists with PE Associated with increased risk for mortality Diagnosed with Doppler ultra-sound of the bilateral lower extremities May be source of PE Be suspicious of asymmetrical lower extremity edema, especially if acute/new onset RV thrombus Association with PE has a higher 14-day mortality (21% vs. 11%) and 3-month mortality (29% vs. 16%) than patients without RV thrombus Troponins Elevated serum troponin is associated with increased mortality in patients with PE More precise prognostic indicator when combined with BNP level 4

5 Hyponatremia at time of presentation has been associated with increased mortality and hospital readmission Prognostic models Pulmonary embolism severity index (PESI) Acute PE Difficult to apply in busy clinical setting due to so many variables to consider Simplified PESI developed with accuracy similar to original PESI Point assigned to each variable Age >80 years History of cancer Chronic cardiopulmonary disease HR >110 bpm SBP <100 SpO2 <90% Total point score 0 = low risk mortality Total point score >1 = high risk of mortality Pathophysiology Most come from DVT of the lower extremities 50-80% of iliac, femoral, and popliteal vein thrombi (proximal vein thrombi) start below the popliteal vein (calf vein thrombi) Remainder from proximal veins Most calf vein thrombi resolve spontaneously 20-30% extend to the proximal veins if untreated Most develop at sites of decreased flow Valve cusps bifurcations Other sites of origin are Right heart Pelvic veins Renal veins Upper extremity veins 5

6 Pathophysiology Large emboli lodge at the bifurcation of the main pulmonary artery or the lobar branches resulting in hemodynamic compromise Smaller emboli continue on distally and more likely the cause of pleuritic chest pain Initiate an inflammatory response adjacent to the parietal pleura Only 10% of emboli cause pulmonary infarction Usually in patients with pre-existing cardiopulmonary disease Most emboli are multiple Most involve the lower lobes Pathophysiology Impaired gas exchange is related to the release of inflammatory mediators rather than simply mechanical obstruction of the vascular bed with altered ventilation perfusion ratio Results in surfactant dysfunction, atelectasis, and functional intrapulmonary shunting Pathophysiology Hypotension Due to decreased cardiac output from increased pulmonary vascular resistance (PVR) Due to physical vascular bed obstruction by thrombus and vasoconstriction Vasoconstriction is due to effects of inflammatory mediators and hypoxia Impedes right ventricular outflow which reduces left ventricular preload 6

7 Pathophysiology Coexisting cardiopulmonary disease results in more substantial decrease in cardiac output than in those without coexisting disease Right ventricular failure is more common after PE in patients with CAD Risk factors Common complication of DVT >50% of cases of DVT associated with acute PE Immobilization Surgery within the last 3 months Stroke Paresis Paralysis History of VTE Malignancy Central venous access within the last 3 months Chronic heart disease Risk factors Additional risks specific to women include Obesity (BMI > 29 kg/m2) Heavy cigarette smoking (>25 cigarettes /day) Hypertension 7

8 Signs and symptoms Symptoms of PE without preexisting cardiopulmonary disease Dyspnea at rest or on exertion (73%) Onset usually within seconds (46%) or minutes (26%) Pleuritic chest pain (44%) Cough (34%) >2-pillow orthopnea (28%) Calf or thigh pain (44%) Calf or thigh swelling (41%) Wheezing (21%) Signs of PE without preexisting cardiopulmonary disease Tachypnea (54%) Tachycardia (24%) Rales (18%) Decreased breath sounds (17%) Accentuated pulmonic component of 2 nd heart sound (15%) JVD (14%) Signs and symptoms of PE without preexisting cardiopulmonary disease Circulatory collapse is uncommon Massive PE may be associated with acute right ventricular failure JVD Right sided S3 Parasternal lift Signs and symptoms of PE without preexisting cardiopulmonary disease Signs or symptoms of DVT are common (47%) Edema Erythema Tenderness Palpable cord in calf or thigh 8

9 PE is frequently asymptomatic! And when they do present, they are highly variable, nonspecific, and common among patients with and without PE. Diagnosis-the work-up Routine lab results are nonspecific Leukocytosis Increased erythrocyte sedimentation rate (ESR or sed rate) Elevated serum LDH or AST (SGOT) with a normal serum bilirubin Diagnosis-the work-up continued ABG s and pulse oximetry have limited roles ABG Hypoxemia Hypocapnia Respiratory alkalosis SpO2 on room air SpO2 <95% at time of diagnosis are at increased risk of in-hospital complications Respiratory failure Cardiogenic shock death 9

10 Diagnosis-the work-up continued BNP usually higher in patients with PE Unfortunately many patients don t have elevations Many other causes of BNP elevation Diagnosis-the work-up continued Troponin I and T elevated in 30-50% of patients with moderate to large PE Likely related to right heart overload Elevations usually resolve within 40 hours after the PE MI associated elevation is longer Not useful for diagnosis, but may be useful in prognosis as they are associated with adverse outcomes Diagnosis-the work-up continued EKG May or may not see changes Changes not specific to PE Massive acute PE or cor pulmonale may see evidence of right ventricular strain or new incomplete RBBB Changes associated with poor prognosis Atrial arrhythmias RBBB Inferior Q-waves Precordial T-wave inversion and ST-segment changes 10

11 Diagnosis-the work-up continued Chest X-ray Abnormalities are common but not helpful diagnostically V/Q scan (ventilation-perfusion scan) Most reliable when there is a high clinical suspicion of PE Normal V/Q scan excludes PE V/Q scan mis-match Diagnosis-the work-up continued Ultrasound Lower extremity Management of positive DVT is similar to confirmed PE Risk of false positive results Missed diagnosis of PE due to true negative DVT One study found only 29% of patients with PE had DVT on Doppler US Quality of the ultrasound exam is operatordependent 11

12 Diagnosis-the work-up continued D-dimer Good sensitivity with negative predictive value Poor specificity and positive predictive value Wells criteria and modified Wells criteria: clinical assessment for pulmonary embolism Clinical symptoms of DVT (leg swelling, pain with palpation) 3.0 Other diagnosis less likely than pulmonary embolism 3.0 Heart rate > Immobilization ( 3 days) or surgery in the previous four weeks 1.5 Previous DVT/PE 1.5 Hemoptysis 1.0 Malignancy 1.0 Probability Score Traditional clinical probability assessment (Wells criteria) High >6.0 Moderate 2.0 to 6.0 Low <2.0 Simplified clinical probability assessment (Modified Wells criteria)* PE likely >4.0 PE unlikely 4.0 Data from van Belle, A, et al. JAMA 2006; 295:

13 Pulmonary angiographydefinitive diagnostic technique or gold standard in diagnosing PE Contrast injected into pulmonary artery branch via a percutaneous catheter A filling defect or abrupt cutoff of a small vessel indicates an embolus Pulmonary Angiogram Negative pulmonary angiogram excludes clinically relevant PE 13

14 CT pulmonary angiography (CT-PA or CTA) Increasing use Ability to identify alternate pulmonary abnormalities to explain symptoms Generally less radiation exposure than pulmonary angiogram Spiral / Multislice CT Results Main Pulmonary Artery Ascending Aorta Thrombus Rt Pulmonary Artery Descending Aorta Lt Pulmonary Artery 14

15 Accuracy of CT-PA similar to pulmonary angiography MR angiography currently not reliable diagnostic for PE Future technologic advances seem promising Echocardiogram % of patients with PE are abnormal Right ventricular hypertrophy Decreased RV function Tricuspid regurgitation Identification of RV thrombus 35% of patients with thrombus have a PE Regional wall motion abnormalities spare RV apex More likely in presentation of a massive PE May be useful in justifying use of thrombolytic RV dysfunction due to PE predicts increased PE-related mortality 2-fold increase in PErelated mortality 15

16 Alveolar dead space Ventilation-perfusion mismatch Due to areas of lung with vascular occlusion ventilated but not perfused PE rule-out criteria (PERC) Age <50 years HR <100 bpm SpO2 >95% No hemoptysis No estrogen use No prior DVT or PE No unilateral leg swelling No surgery or trauma resulting in hospitalization within the previous 4 weeks PE probably excluded without further diagnostic testing if... All PERC criteria AND a low clinical suspicion for PE according to either the Wells criteria or low gestalt probability determined by the clinician prior to testing for PE Only used in setting with low prevalence of PE 16

17 Fibrinolytic (thrombolytic) therapy Thrombolytic agents activate plasminogen to plasmin which results in an accelerated lysis of the thrombus Thrombolytic agents have been used in a variety of thrombotic disorders MI PE DVT Efficacy of thrombolytics Comparison to anticoagulation alone is well studied Evidence suggests thrombolytic therapy accelerates clot lysis and is associated wit short-term physiologic benefits None have shown to improve mortality Despite lack of mortality benefit in patients with massive PE, most providers accept massive PE as an indication for thrombolytic therapy, as it can be lifesaving 17

18 Potential hemodynamic benefits May improve PA pressure RV function Pulmonary perfusion Indications Considered ONLY after PE confirmed Adverse effects of treatment can be severe Consider treatment if one of the following present Persistent hypotension SBP <90 Drop in SBP >40 mmhg from baseline Severe hypoxemia Large perfusion defect on V/Q scan Extensive embolic burden on CT RV dysfunction Free-floating RA or RV thrombus Patent foramen ovale 18

19 Only persistent hypotension due to PE is widely accepted as an indication for thrombolytic therapy Based on evidence thrombolysis accelerates clot lysis and clinical trials have shown a trend toward better outcomes in patients with hemodynamic compromise Value of thrombolysis to treat PE in other settings is uncertain and should be determined on a case-by-case basis Contraindications to thrombolytic therapy Risk vs. benefit should always be considered on a case-by-case basis All thrombolytic agents associated with risk of hemorrhage Others have drug specific risks Hemorrhage is the most common adverse effect Menstruating women may experience moderate bleeding but hemorrhage is rare and menstruation is not a contraindication 19

20 Thrombolytic agents Streptokinase (SK) Polypeptide derived from beta-hemolytic streptococcous cultures Binds to plasminogen forming an active enzyme which activates plasmin Least expensive More commonly associated with adverse effects Especially allergic reactions and hypotension Anti-SK antibodies are elevated for up to 7.5 yearswith potential for suboptimalresponseor allergic reaction to SK given several years later tpa (alteplase) Recombinant tissue type plasminogen activator Naturally occurring enzyme produced in a several tissues including endothelial cells Binds to fibrin, increasing its affinity for plasminogen, enhancing plasminogen activator Responsible for initiating intravascular fibrinolysis More expensive than SK Favored due to short infusion time (2 hr) and no allergic reaction or hypotension Urokinase Also plasminogen activator, normally in urine Major activator of fibrinolysis in extravascular compartment Regimens SK Initial 30 minutes 250,000 units IV Then 100,000 units/hr for 24 hours Monitor closely for Hypotension Anaphylaxis Asthma Allergic reactions Mild adverse reactions may respond to decreased infusion rate tpa 100 mg IV over 2 hours 20

21 Urokinase 4400 units/kg IV over initial 10 minutes Then 4400 units/kg/hr for 12 hours Unnecessary invasive procedures should be minimized or avoided while considering thrombolytic therapy Thrombolytic agent is administered via peripheral IV site Anticoagulation is stopped during the thrombolytic infusion Monitoring Activated partial thromboplastin time (aptt) measured when infusion is complete Heparin resumed without loading dose when aptt <2x upper limit of normal If aptt >2x normal, repeat aptt every 4 hours until <2x upper limit of normal and then start heparin 21

22 Monitoring for adverse reactions Bleeding Usually from sites of previous invasive procedures If significant or refractory bleeding transfuse 10 units cryoprecipitate 2 units fresh frozen plasma Reassess Protamine sulfate considered to reverse effect of any heparin Most devastating complication is intracranial hemorrhage Occurs in up to 3% of patients Monitor closely for neurologic changes Summary Clinical presentation is variable and nonspecific Diagnostic testing is needed to confirm or exclude diagnosis of PE 22

23 Summary-continued Diagnostics tests most frequently used CTA V/Q scan D-dimer Ultrasound Venous Doppler US of lower extremities Pulmonary angiography Clinical probability assessment Summary-continued Thrombolytic therapy accelerates clot lysis and has short-term physiologic benefit Thrombolysis considered only after PE is confirmed Adverse effects of thrombolytic therapy can be severe Thrombolytic therapy NOT recommended in patients with PE without hemodynamic or respiratory compromise Thrombolytic therapy IS recommended in patient who is persistently hypotensive due to PE and without risk of bleeding Summary-continued Thrombolytic therapy is always decided on a case-by-case basis Thrombolytics are infused via peripheral IV Thrombolytics with short infusion times preferred over long infusions Contraindications for thrombolytics or treatment failure, consider catheter or surgical embolectomy 23

24 Questions? 24