Pulmonary embolism. Paweł Balsam MD, PhD

Transcription

1 Pulmonary embolism Paweł Balsam MD, PhD

2 Venous thromboembolism (VTE) Pulmonary embolism (PE) and deep vein thrombosis (DVT) are two clinical presentations of veonus thromboembolism

3 Pulmonary embolism A pulmonary embolism is a blockage in one of the blood vessels in your lungs. It can be fatal if the obstruction is very large and blocks the main blood supply to the lungs.

4 Pulmonary embolism

5 CLOT

6 Pulmonary embolism Virchow's Triad - Causes of Thrombosis Changes in the blood vessel wall Changes in the blood flow Changes in the blood composition

7 Changes in the blood flow The first category, alterations in normal blood flow, refers to several situations. These includeturbulence, stasis, mitral stenosis, and varicose veins. The equivalence of Virchow's version and the modern version has been disputed.

8 Changes in the blood vessel wall The second category, injuries and/or trauma to endothelium includes damage to the veins arising from shear stress or hypertension.

9 Changes in the blood composition The last category, alterations in the constitution of blood, has numerous possible risk factors such as hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severetrauma or burn, disseminated cancer, late pregnancy and delivery, race, age, whether the patient is a smoker, and obesity. All of these risk factors cause the situation called hypercoagulability.

10 Pulmonary embolism

11 Pulmonary embolism Pulmonary embolism (PE) is cardiovascular emergency. Occlusion of pulmonary artery may lead to life threatning but potientially reversible right ventricle failure.

12 Epidemology The prevalence of PE among hospitalized patients is 0.4% It gives about patients cases/year in USA

13 Mortality 2-8% treated (diagnosed) 30% non-treated (non-diagnosed)

14 Predisposing factors Strong predisposing factors: -fracture (hip or leg) -hip or knee replacement -major general surgery -major trauma -spinal cord injury

15 Predisposing factors Moderate predisposing factors: -arthroscopic knee surgery -central venous lines -chemotherapy -chronic heart or respiratory failure -hormone replacement therapy -malignancy -oral contraceptive therapy -paralytic stroke -pregnancy -previous VTE -thrombofilia

16 Predisposing factors Weak predisposing factors: - Bed rest > 3 days - Immobilitydueto sitting (prolonged trip) - Increasing age - Laparoscopic surgery - Obesity - Varicose veins

17 Primary risk factors AT III deficiency factor V Leiden (APC-R) mutation of protromine gene 20210A dysfibrynogenemia hiperhomocysteinemia anticardiolipin a-bodies protein C deficiency plasminogen deficiency protein S deficiency

18 PE Risk factors - secondary CHF immobilization older age neoplasm stroke obesity surgery central iv lines smoking pregnancy/peripartum oral contraceptives long distance travels

19 Pathophysiology Key consequences of pulmonary embolism are hemodynamic. Large and mutiple emobli may increase pulmonary vascular resistance to a level of afterload which cannot be matched by a right ventricle (RV)

20 Pathophysiology Sudden death occurs mainly in the mechanism of electromechanical dissociation.

21 Severity of PE Markers of severity: 1. Clinical markers: Shock and Hypotension 2. Markers of RV dysfunction: dilation, hypokinesis or pressure overload on echocardiography RV dilation on spiral computed tomography BNP or NT-proBNP elevation Elevated right heart pressure on RHC 3. Markers of myocardial injury: cardiac troponin T or I

22 Risk stratification PE related EARLY MORTALITY RISK CLINICAL RISK MARKERS RV dysfuntion Myocardia l injury Treatment implications HIGH (15%) + (+)* (+)* Thrombolysis or embolectomy NON HIGH Intermed iate (3-15%) - Low <1% Hospital admission Early discharge or home treatment

23 Prognostic assesment Shock and hypotension are principal markers of high risk of early death in acute PE

24 Prognostic assesment RV dysfunction is related to intermediate risk of short-term mortality Its prognostic value is limited by the lack of universally accepted criteria

25 Prognostic assesment Myocardial injury isrelated to intermediaterisk of short-term mortality Its prognostic value is limited by the lack of universally accepted criteria.

26 Diagnosis Clinical presentation D-dimer Compression ultrasonography and computed tomographic venography Ventilation-perfusion scintigraphy Computed tomography Pulmonary angiography Echocardiography

27 Clinical presentation Symptoms: -dyspnoea 80% -chest pain 52% -cough 20% -hemoptysis -cyanosis -collapse

28 Clinical presentation Signs: Tachypnea (respiratory rate >16/min): 96% Rales: 58% Accentuated second heart sound: 53% Tachycardia (heart rate >100/min): 44% Fever (temperature >37.8 C): 43% Diaphoresis: 36% S 3 or S 4 gallop: 34% Clinical signs and symptoms suggesting thrombophlebitis: 32% Lower extremity edema: 24% Cardiac murmur: 23% Cyanosis: 19%

29 Assesment of clnical probability of Variable PE Wells score Predisposing factors: Previous DVT or PE Recent surgery or immobilization Cancer Points Symptoms Hemoptysis +1 Clinical signs Heart rate >100 beats/min Clinical signs of DVT Clinical judgement Alternative diagnosis less likely than PE +3

30 Assesment of clnical probability of PE Wells score Clinical probability Low Intermediate High Total

31 Differential diagnosis of PE: Pneumonia or bronchitis Asthma Exacerbation of chronic obstructive disease MI Pulmonary edema Anxiety

32 Differential diagnosis of PE: Dissection of the aorta Pericardial tamponade Lung cancer Primary pulmonary hipertension Rib fracture Pneumothorax

33 D-dimer The product of a cross-linked fibrin. Very high negative predictive value. Very low positive predictive value increased level: cancer, inflamation, necrosis, dissection of the aorta Negative D-dimer result in a higly sensitive assay safely excludes the PE in a patientns with low ormoderate clinical risk

34 Compression ultrasonography (CUS) 90% of PE is due to DVT in lower limb. CUS has 90% sensitivity and 95% specificity for diagnosing proximal DVT Thus finding a proximal DVT in patients with suspected PE is sufficient to start anticoagualnt treatment

35 Ventilation-perfusion scintigraphy Combination of perfusion and ventilation scans. In case of PE the perfusion scan is abnormal but the ventilation scan is normal Thereisperfusion-ventilation mismatch

36 Ventilation-perfusion scintigraphy Normal perfusion scan is very safe to exclude PE Combination of non-diagnostic V/Q in a patient with low clinical probability of PE i acceptable for excluding PE. High probability ventilation-perfusion scans establish the diagnosis of PE with a high degree of probability, but further tests are required

37 Computed tomography SDCT single detector computed tomography SENSITIVITY 70%; SPECIFICITY 90% Negative SDCT test is not safe for ruling out PE In association with absence of proximal DVT is a good method for ruling out the PE

38 Computed tomography MDCT multi detector computed tomography has high spatial and temporal resolution. SENSITIVITY 83%; SPECIFICITY 96% MDCT showing a thrombus up to the segmental level can be adequate evidence of PE. In a patient with non-high clinical probability of PE, negative MDCT may be used as a stand alone test to exclude PE

39 Pulmonary angiography Is an invasive method associated with some risk. Currently it is useful when the results of noninvasive methods are equivocal.

40 Echocardiography In the presence of shock and hypotension the lack of echocardiographic signs of RV overload or dysfunction excludes PE as the cause of hemodynamic compromise. It also helps to find the reason of such a condition: tamponade, acute valvular dysfunction, acutemyocardial infarction.

41 Diagnostic strategies Suspected high-risk PE Suspected non-high risk PE

42 Diagnostic strategies Suspected high-risk PE CT immediately available no yes Echo RV overload no yes CT available CT stable patient positive negative Search for No other test available other causes orpatient unstable PE-specific Search for other causes treatment justified

43 Diagnostic strategies Suspected non-high-risk PE Asses clinical probability of PE Low/intermediate clinical probability of PE D dimer High clinical probability of PE negative positive Multidetector CT (no treatment) Multidetector CT No PE PE No PE PE No treatment TREATMENT!!! No treatment TREATMENT!! Investigate further

44 Treatment The scheme of treatment depends on severity of PE.

45 Treatment In high risk patients the respiratory and hemodynamicsupport isnecessary. Hemodynamic support: dopamine, dobutamine, epinephrine, norepinephrine

46 Treatment High risk patients Thrombolytic therapy is the first line treatment in high-risk patients presenting with cardiogenic shock and/or persistent arterial hypotension with a very few absolute cantraindications.

47 Treatment High risk patients Routine use of thrombolysis in non-high risk patients is not recomended. It may be considered in intermediate risk patients after thorough consideration of conditions increasing the risk of bleeding.

48 Thrombolysis contraindications Absolute: -Haemorrhagic stroke or stroke of unkown origin at any time -Ishemic stroke in preceding 6 months -Central nervous system damage or neoplasms -Recent major trauma/surgery/head injury (within preceding 3 weeks) -Gastrointestinal bleeding within thelastmonth -Known bleeding

49 Thrombolytic regimens for PE treatment Streptokinase: IU as a loading dose over 30 minutes -followed by IU/h over 12-24h Urokinase: -4400IU/kg as a loading dose over 10min -followed by 4400IU/kg/h over 12-24h

50 Thrombolytic regimens for PE treatment rtpa 100mg over 2h or 0.6 mg/kg over 15 min (maxium dose 50mg)

51 Surgical pulmonary embolectomy With current surgical techniques, pulmonary emobolectomy is a valuable therapeutic option in patients with high-risk PE in whom thrombolysis is absolutely contraindicated or has failed.

52 Percutaneous catheter embolectomy and fragmentation Catheter embolectomy or fragmentation of proximal pulmonary clots may be considered as an alternative to surgical treatment in patients with high-risk PE in whom thrombolysis is absolutely contraindicated or has failed.

53 Anticoagulant therapy Anticoagulant therapy with unfractioned heparin, LMWH or fondaparinux should be initiated without delay in patients with confirmed PE and those with high or intermediate risk clinical probability of PE while diagnostic workup is still ongoing.

54 Anticoagulant therapy Except for patients at high risk of bleeding and those with severe renal dysfunction, subcutaneous LMWH or fondaparinux rather than intravenous unfractioned heparin should be considered for initial treatment

55 Anticoagulant therapy Unfractioned heparin: -bolus of 80U/kg, followed by infusion at the rate of 18U/kg/h. -subsequent doses should be adjusted using the activated partial thromboplastin time(aptt). -reach and maintain the prolongation of aptt between 1.5 and 2.5 -aptt should be measured 3-4 hours after bolus and 3 hours after each dose adjustment

56 Anticoagulant therapy - UFH aptt Change of dosage <35 s (<1.2 times control) 80 U/kg bolus; increase infusion rate by 4U/kg/h 35-45s ( times control) 46-70s ( times control) 71-90s ( times control) 40 U/kg bolus; increase infusion rate by 2U/kg/h No change Reduce the infusion rate by 2 U/kg >90s (>3.0 times) Stop infusion for 1 hour then reduce infusion rate by 3 U/kg/h

57 Anticoagulant therapy In patients at high risk of bleeding (non-high risk PE) and in those with severe renal dysfunction, unfractioned heparin with an aptt target range of times normal is a recommended form of initial treatment.

58 Anticoagulant therapy LMWH enoxaparin -dose: 1.0 mg/kg every 12h -contraindicated in severe renal failure (creatinine clearance <30 ml/min) Fondaparinux selective factor Xa inhibitor -dose: 5mg body weight <50g 7.5mg body weight kg 10mg body weight > 100kg

59 Anticoagulant therapy Rivaroxaban 2 x 15 mg Dabigatran 2 x 150 mg

60 Anticoagulant therapy Parenteral anticoagulation should be continued for at least 5 days VKA a should be initiated as soon as possible and preferably on the same day as initial anticoagulant. Parenteral anticoagulant should be stopped when the INR lies between 2.0 and 3.0 for at least 2 consecutive days

61 Class o recomedation

62 Level of evidence

63

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65 Oral anticoagulant therapy

66 Thank You