PULMONARY EMBOLISM PROF DR YESAR KARTER Pulmonary Embolism

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PULMONARY EMBOLISM PROF. DR. YESARİ KARTER

PULMONARY EMBOLISM PROF. DR. YESARİ KARTER

Pulmonary Embolism: Impaction of material into branches of the pulmonary arterial bed

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 >

Mortality- 50 000 death/year (decreasing) Hospitalisation: 300 -600 000/year Male>Female American Africans old > young

RISK FACTORS - inherited - acquired

RISK FACTORS - inherited - acquired

Inherited Risk Factors Family History (+) Acquired risk factor (-) Prior deep venous thrombosis

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

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

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 (II) -Age > 40 -Malignity -Obesity -Heart Failure -Myocard infarction

Acquired Risk factors (III) -Prior DVT -Nephrotic Syndrome -Antiphospholipid Syndrome -PNH -Waldenström

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

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

Diagnose -Young patient -Family history (+) -Acquired risk factors (-) ___ inherited

Symptoms -Chest pain -Pleuritic pain -Dyspnea -Cough -Hemoptysis -Syncope

Symptoms -Chest pain -Pleuritic pain -Dyspnea -Cough -Hemoptysis -Syncope

Laboratory Standart test ECG Chest rontgenography Arterial blood gases Echocardiography Imaging venous thrombus Imaging

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

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

ECG Nonspesific changes -Massive emboli-----RV load Differential diagnosis -Myocardial infarctuse -Accelere atrial rythm Typical findings -RV strain -T (-) and or ST elevation (V 1 -3) -P pulmonale (right axis) -S 1 Q 3 T 3

Chest Radiography Usually nonspesific Not sensitive or specific Proximal, large segmental artery Multiple small

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

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 Pa. CO 2 decreases Massive Pa. O 2 decreases Submassive

Arterial Blood Gases Acute Pa. CO 2 decreases Massive Pa. O 2 decreases Submassive Normal / Nearnormal

Echocardiography -Shows emboli in main pulmonary arteries, but not in lober and segmentary arteries

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)

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

Deep Vein Thrombosis -Phlebography -Doppler

Imaging pulmonary emboli -Chest radiography -Ventilation-Perfusion Lung Scan -Pulmonary angiography -h. CT -MR angiography

Imaging pulmonary emboli -Chest radiography -Ventilation-Perfusion Lung Scan -Pulmonary angiography -h. CT -MR angiography

Ventilation-Perfusion Lung Scan Perfusion (-) and Ventilation (+) ---PE Perfusion (N) and Clinical sym

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

Clinical Probability of acute PE -High Probability (80 -100%) Risk factors (+) Dyspnea Tachypnea Chest pain Radiology (+) Pa. O 2 decreases P (A-a)O 2 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 <

• Dichotomous clinical probability assesment: • PE likely >4 • Pe unlikely < 4 or = 4

 • PE likely----h CT • ------normal----exclude • ------findings (+)----PE • ------indeterminate----LE US •

• 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

Pulmonary Angiography Gold standart İmages PE in subsegmental and peripheral arteries

h. CT -two dimensional angiographic image -specifity 90% -dimension of the emboli -mediastinal and

h. CT -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

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

Treatment -to prevent death -to reduce morbidity -to prevent pulmoner hypertension progresing due to thromboemboli

Treatment (II) Supportive -Oxygen -IV liquid -Vasopressors

Treatment (II) Supportive -Oxygen -IV liquid -Vasopressors

Anticoagulation -unfractioned heparin -LMWH -Thrombolysis -Embolectomy

Anticoagulation -unfractioned heparin -LMWH -Thrombolysis -Embolectomy

Unfractioned Heparin IV 5000 U bolus + 30 -35 000 U/kg a. PTT- twice

Unfractioned Heparin IV 5000 U bolus + 30 -35 000 U/kg a. PTT- 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

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%

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

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

Thrombolysis Massive pulmoner emboli with hemodynamic instability -streptokinase -urokinase -t-PA **serious bleeding

REFERENCES: • Agnelli G. Anticoagulation in the prevention and treatment of pulmonary • •

REFERENCES: • Agnelli G. Anticoagulation in the prevention and treatment of pulmonary • • • embolism. Chest 1995. 107; 39 -44. Bell. WR, Simon TL; De. Mets DL. The clinical features of massive and submassive pulmonary embolism. Am J Med 1977; 62: 355 -360. Braunwald E. Pulmonary embolism. Braunwald’s heart disease. Braunwald (ed)Philedalphia. WB Saunders 1992. 562 -1568. Herold CJ, Bankier AA, Burghaiber OC, Minar E, Watzke HH. Pulmonary Embolism. Comprehensive Pulmonary Medicine. Albert R, Spiro S, Jett J (eds). Harcaurt Brace and Company Limited London 1999. 50. 1 -50. 12 Hyers TH. Diagnosis of pulmonary embolism. Thorax 1995; 50: 930 -932. Lane D, Manucci PM, Bauer KA, et al. Inherited thrombophilia: Part I. Thromb Haemost 1996; 76: 651 -662. Remy -Jerden M, Remy J, Deschildre F. Diagnosis of pulmonary embolism with spiral CT: comparison with pulmonary angiography and scintigraphy. Radiology 1996; 200(3): 699 -706.