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PULMONARY EMBOLISM. PROF. DR. YESARİ KARTER. Pulmonary Embolism: Impaction of material into branches of the pulmonary arterial bed. Mortality- 50 000 death/year (decreasing) Hospitalisation: 300-600 000/year
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PULMONARY EMBOLISM PROF. DR. YESARİ KARTER
Pulmonary Embolism: Impaction of material into branches of the pulmonary arterial bed
Mortality- 50 000 death/year (decreasing) Hospitalisation: 300-600 000/year Male>Female American Africans old > young
RISK FACTORS - inherited - acquired
Inherited Risk Factors Family History (+) Acquired risk factor (-) Prior deep venous thrombosis
Inherited Risk Factors (2) -Antithrombin III deficiency -Protein C deficiency -Protein S deficiency -Protein C resistance (Factor V Leiden) -Hyperhomocystinemi -Abnormal fibrinogen -Abnormal fibrinolytic system
Acquired Risk Factors -surgery or trauma of pelvis/lower extremities -immobilization -surgery with >30 min general anesthesia -local tissue trauma and vessel destruction -pregnancy especialy in the puerperism and after cesarian section -estrogen therpy
Acquired Risk Factors (II) -Age > 40 -Malignity -Obesity -Heart Failure -Myocard infarction
Acquired Risk factors (III) -Prior DVT -Nephrotic Syndrome -Antiphospholipid Syndrome -PNH -Waldenström
Thromboembolic risk of the patient -Risk of the patient (acquired / inherited) -Risk of the clinical condition
Diagnose -Young patient -Family history (+) -Acquired risk factors (-) ___ inherited
Symptoms -Chest pain -Pleuritic pain -Dyspnea -Cough -Hemoptysis -Syncope
Laboratory Standart test ECG Chest rontgenography Arterial blood gases Echocardiography Imaging venous thrombus Imaging pulmoner emboli
Standart tests -Leucocytosis (infarctuse) -ESR increases -D-Dimer increases low---- Exclusion of PE
ECG Nonspesific changes -Massive emboli-----RV load Differential diagnosis -Myocardial infarctuse -Accelere atrial rythm Typical findings -RV strain -T (-) and or ST elevation (V1-3) -P pulmonale (right axis) -S1Q3T3
Chest Radiography Usually nonspesific Not sensitive or specific Proximal, large segmental artery Multiple small segmental artery
Chest Radiography (II) -Atelectasis -Elevation of the hemidiaphragm -Pleural efusion -Dilatation of the main branches of PA -Paranchymal densities (in the lower lung fields, pleural based) -Zones of oligemia
Arterial Blood Gases Acute PaCO2 decreases Massive PaO2 decreases Submassive Normal / Nearnormal
Echocardiography -Shows emboli in main pulmonary arteries, but not in lober and segmentary arteries -Dilated hypokinetic RV -Distorsion of the interventricular septum in diastole -Tricuspid regurgitation associated with increase in systolic pressure in pulmonary artery
Deep Vein Thrombosis -90% of PE originates from DVT (poplitea or proximal leg veins) -leg pain or swelling -Homan’s sign -signs of infection in subcutan veins
Deep Vein Thrombosis -Phlebography -Doppler
Imaging pulmonary emboli -Chest radiography -Ventilation-Perfusion Lung Scan -Pulmonary angiography -hCT -MR angiography
Ventilation-Perfusion Lung Scan Perfusion (-) and Ventilation (+) ---PE Perfusion (N) and Clinical sym and signs (N) ----PE excluded Low probability PVLS and low probability of clinical sym and signs ----PE excluded High probability PVLS and high probability of clinical symp and signs ---- Anticoagulation
Clinical Probability of acute PE -High Probability (80-100%) Risk factors (+) Dyspnea Tachypnea Chest pain Radiology (+) PaO2 decreases P (A-a)O2 increases -Intermediate Probability (20-79%) -Low Probability (1-19%) Risk Factors (-) Clinical and laboratory findings can be explained
Dichotomous clinical probability assesment: • PE likely > 4 • Pe unlikely < 4 or = 4
PE likely--------h CT • ------normal----exclude • ------findings (+)----PE • ------indeterminate----LE US • PA • PE unlikely-----D-dimer(+) • -------h (CT) • D-dimer(-) • -------exclude PE
Pulmonary Angiography Gold standart İmages PE in subsegmental and peripheral arteries
hCT -two dimensional angiographic image -specifity 90% -dimension of the emboli -mediastinal and parenchymal patologies
MR Angiography Sensitivity-70 – 90 % Specifity- 77 – 100 % (Central arteries) Also asseses RV function
Treatment -to prevent death -to reduce morbidity -to prevent pulmoner hypertension progresing due to thromboemboli
Treatment (II) Supportive -Oxygen -IV liquid -Vasopressors
Anticoagulation -unfractioned heparin -LMWH -Thrombolysis -Embolectomy
Unfractioned Heparin IV 5000 U bolus + 30-35 000 U/kg aPTT- twice the control value -Thrombocytopeni early: thrombocyte agregation slight, reveresible, no need to stop late: antibodies against trombocytes arterial and venous thromboemboli -Osteopeni
LMWH -long acting -less binding to plasma protein -greater bioavailibity -no need monitorisation
Prognosis -Mortality rate – 30% -Depends on associated pathology -Resolution – 5 days 36% 2 weeks 52% 3 months 73% Pulmonary hypertension recurrent microemboli (rare)
Secondary prevention UFH + oral anticoagulan (6 months) LMWH SC + oral anticoagulan (6 months ) LMWH (pregnancy) Recurrance / unknown origin / permanantly increased risk (throughout life)
Thrombolysis Massive pulmoner emboli with hemodynamic instability -streptokinase -urokinase -t-PA **serious bleeding
REFERENCES: • Agnelli G. Anticoagulation in thepreventionandtreatment of pulmonaryembolism.Chest 1995. 107;39-44. • BellWR,Simon TL; DeMets DL. Theclinicalfeatures of massiveandsubmassivepulmonaryembolism. Am J Med 1977; 62: 355-360. • Braunwald E. Pulmonaryembolism. Braunwald’sheartdisease. Braunwald (ed)Philedalphia. WB Saunders 1992 .562-1568. • Herold CJ, Bankier AA, Burghaiber OC, Minar E, Watzke HH. PulmonaryEmbolism. ComprehensivePulmonaryMedicine. Albert R, Spiro S, Jett J (eds). HarcaurtBraceandCompanyLimitedLondon 1999. 50.1-50.12 • Hyers TH . Diagnosis of pulmonaryembolism. Thorax 1995; 50: 930-932. • Lane D, Manucci PM, Bauer KA, et al. Inheritedthrombophilia: Part I.ThrombHaemost 1996;76: 651-662. • Remy -Jerden M, Remy J,Deschildre F. Diagnosis of pulmonaryembolismwith spiral CT: comparisonwithpulmonaryangiographyandscintigraphy. Radiology 1996; 200(3):699-706.