Acute Pulmonary Embolism

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     1  Acute Pulmonary Embolism ??? ?? 2008-Apr.-11
     2  Outline__________________________________________ Introduction Epidemiology & Pathophysiology Risk Factors Diagnostic Approaches Treatment Pregnancy & APE Conclusions
     3  Introduction-1 most commonly originating from deep venous thrombosis ( DVT ) of the legs Asymptomatic incidentally discovered emboli massive embolism causing immediate death
     4  Introduction-2 Chronic sequelae of venous thromboembolism(VTE) (DVT & PE) post-thrombotic syndrome chronic thromboembolic pulmonary H/T
     5  Introduction-3 Acute pulmonary embolism ( APE ) may occur rapidly & unpredictably may be difficult to diagnose
     6  Introduction-4 Treatment can reduce the risk of death appropriate primary prophylaxis : effective rate of death in the next year: 1.5% vs. 0.4% Patients treated for APE appear to die of recurrent thromboembolism (1.5% ) patients treated for DVT (0.4% )
     7  Epidemiology & Pathophysiology
     8  Epidemiology & Pathophysiology-1 Thrombi commonly form in deep veins in the calf propagate into the proximal veins, including & above the popliteal veins from which they are more likely to embolize
     9  Epidemiology & Pathophysiology-2 About 79% of patients with PE have evidence of DVT in their legs PE occurs in up to 50% of patients with proximal DVT Dual pulmonary circulation ( pulmonary & bronchial arteries ), pulmonary infarction : not usually present
     11  Epidemiology & Pathophysiology-3 APE, anatomical obstruction is the most important cause of compromised physiology release of vasoactive & bronchoactive agents (serotonin from platelets )---- deleterious ventilation–perfusion matching
     12  Epidemiology & Pathophysiology-4 As RV afterload increases, tension in RV wall rises dilatation, dysfunction, & ischemia of RV Death results from RV failure.
     13  Epidemiology & Pathophysiology-5 VTE is a worldwide problem, esp. in people with known risk factors Less common in certain regions, eg. Asia Average annual incidence in US : 1 episode per 1000 registered patients US :300,000 people/year die from APE Dx is often not made until autopsy Hospitalized pts are at particularly high risk
     14  Risk Factors
     15  Acquired Risk Factors Certain risk factors increase the likelihood Overall, acute medical illness may be the most common setting Prolonged air or ground travel increases the risk eThrombosis:extended periods of sitting at a computer terminal Advancing age is another clear risk factor, with the risk increasing after age 40
     17  Genetic Disorders & Thromboembolic Risk
     18  Risk Factors for VTE
     19  Virchow's classic triad of risk Hypercoagulability Stasis Venous injury
     20  Diagnostic Approaches
     21  Clinical Manifestations -1 Recognition of the symptoms & signs of VTE may reduce diagnostic delays Symptoms of cough, palpitations, & dizziness & signs of fever, wheezing, & crackles : PE or concomitant illnesses Tachypnea & tachycardia : common but nonspecific findings
     22  Clinical Manifestations -2 Signs of pulm. HTN : elevated neck veins, loud P2, right-sided gallop, & RV lift Signs & symps. of VTE : highly suggestive but neither sensitive nor specific extent of symptoms depends on the thromboembolic burden massive PE:sudden onset of near syncope or syncope,hypotension,severe hypoxemia, EM dissociation, or cardiac arrest.
     23  Clinical Manifestations -3 Leg pain, warmth, or swelling:DVT dyspnea or chest pain, either sudden onset or evolving over a period of days to weeks:APE Pleuritic chest pain , a pleural rub (more peripheral emboli ) & hemoptysis: pulmonary infarction
     24  Preliminary Lab. Testing & Pretest Probability -1 Hx., PE, & known risk factors EKG, CXR, & ABG analysis
     25  Preliminary Lab. Testing & Pretest Probability -2 EKG:unexplained tachycardia:common in APE but nonspecific acute cor pulmonale: S1, Q3, T3 pattern, RBBB , P-wave pulmonale, or RAD : more common with massive embolism ---nonspecific CXR: generally nondiagnostic arterial oxygen tension may be normal A–a oxygen difference may be normal
     26  Preliminary Lab. Testing & Pretest Probability -3 D-dimer test (+): VTE are possible diagnoses this test is nonspecific infection,other inflammatory states, cancer, & trauma D-dimer testing is best considered together with clinical probability
     27  Clinical Prediction Scores for Suspected APE-1
     28  Clinical Prediction Scores for Suspected APE-2
     29  Clinical Prediction Scores for Suspected APE-3
     30  Preliminary Lab. Testing & Pretest Probability -4 D-dimer test (-):with a low or moderate pretest probability, likelihood of VTE is low precludes the need for specific imaging studies high pretest probability: imaging should be performed instead of D-dimer testing Other biomarkers: cardiac troponin levels, plasma levels of brain natriuretic peptide
     31  Imaging Studies -1 Contrast-enhanced CT arteriography the greatest sensitivity & specificity for detecting emboli in the main, lobar, or segmental pulmonary arteries false (+) CT arteriography : unusual sensitivity of spiral CT arteriography alone = 83%, combination of this & CT venography ,up to 90%
     32  Imaging Studies -2 Ventilation–perfusion scan : diagnostic in the absence of cardiopulmonary disease A normal perfusion lung scan effectively rules out APE high probability scan:APE should be considered diagnostic , unless clinical suspicion is low or Hx. of PE with an identical previous scan
     33  Imaging Studies -3 if the clinical story strongly suggests PE,with a nondiagnostic V–P scan, Dx. should be rigorously pursued nondiagnostic V–P scan : with low probability or with moderate probability but negative D-dimer test , no additional testing or therapy is indicated
     34  Imaging Studies -4 a recent study of 221 patients with susp. APE, MRI of the lung followed by MR venography ---successfully search for both DVT & PE Echocardiography may reveal findings that strongly support hemodynamically significant PE, offering the potential to guide treatment
     36  Treatment
     37  Anticoagulation-1 Bed rest is not recommended for DVT unless substantial pain & swelling PE diagnosed, inpatient therapy with initial bed rest for 24 to 48 hrs : often recommended
     38  Anticoagulation-2 APE (+):IV anticoagulation with LMW heparin , or standard, UF heparin should be initiated unless contraindicated Not thrombolytic, but decreasing the thromboembolic burden If the suspicion of PE is high, parenteral anticoagulation should be considered even before imaging
     39  Anticoagulation-3 Warfarin can be initiated on day 1 of therapy SC LMWH or weight-based UFH IV should be administered for at least 5 days until INR=2.0 to 3.0 for 2 consecutive days With standard heparin,aPTT checked Q6h until it is =1.5 to 2.5 X control Achieving a therapeutic aPTT within 24 hours ,reduce the risk of recurrence
     40  Anticoagulation-4 LMWHs have advantages over UFH : greater bioavailability, more predictable dosing, SC delivery, & a lower risk of heparin-induced thrombocytopenia ( HIT ) Monitoring LMWH by anti–factor Xa : morbidly obese (weighing >150 kg) or very small (<40 kg), pregnant, & very severe renal insufficiency or rapidly changing renal function
     41  Anticoagulation-5 VTE require long-term anticoagulation to prevent extension & recurrence Documented VTE with transient risk factors should treat 3 to 6 months, but more extended treatment is appropriate when significant risk factors persist, idiopathic or previous episodes of VTE D-dimer levels may help guide decisions about the duration of therapy
     42  Anticoagulation-6 Tx. with a direct thrombin inhibitor (e.g., argatroban or lepirudin) for HIT with thrombosis Tx. with warfarin should not be initiated until disease process has been controlled & platelet count has returned to the normal range---potential for worsening thrombotic complications :venous limb gangrene & warfarin-induced skin necrosis
     43  Placement of a Vena Caval Filter contraindications to anticoagulation major bleeding during anticoagulation recurrent embolism under adequate therapy filters are effective in reducing the incidence of PE, they increase the subsequent incidence of DVT,but do not increase overall survival
     44  Treatment of Massive PE PE causing hemodynamic instability resulting RV failure---compromised LV preload If saline is infused for hypotension, it should be done with caution Vasopressor therapy (e.g., dopamine) should be considered if BP is not rapidly restored
     45  Complications of Thrombolytic Therapy-1 most widely accepted indication for thrombolytic therapy :proven PE with cardiogenic shock frequently considered : systemic hypotension without shock may be considered : severely compromised oxygenation or a massive embolic burden identified by image
     46  Complications of Thrombolytic Therapy-2 The most devastating complication :ICH retroperitoneal & GI bleeding & bleeding from surgical wounds or sites of recent invasive procedures Contraindications : intracranial, spinal, or ocular surgery or disease, recent major surgery or other invasive procedures, active or recent major bleeding, pregnancy, & clinically obvious risks of bleeding
     48  Prognosis The 3-month overall mortality :15 - 18% Shock at presentation : increase in mortality by a factor of 3 to 7 post-thrombotic syndrome (chronic leg pain & swelling) & chronic thromboembolic pulmonary hypertension :possible long-term sequelae of APE
     49  Prevention-1 Without prophylaxis, risk of VTE among acutely ill, hospitalized medical patients : as high as 15% Unfortunately, prophylaxis is grossly underused ( U.S. & international studies ) Anticoagulant prophylaxis is more effective than lower-limb mechanical prophylaxis
     50  Prevention-2 After total hip or knee replacement, the risk of venous thrombosis : 50% or higher without prophylaxis Trauma & spinal cord injury :also very-high-risk scenarios Every hospitalized patient should be assessed for the need for prophylaxis
     51  Pregnancy & Acute Pulmonary Embolism
     52  Pregnancy & APE-1 increased risk for VTE : pregnancy , postpartum period ,& hormone therapy Risk of a first episode of VTE= 5-fold as high in the postpartum period as during pregnancy Risk of PE = 15-fold as high during the postpartum period as d