pulmonary embolism prof. dr. yesarİ karter karter
TRANSCRIPT
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PULMONARY EMBOLISMPULMONARY EMBOLISM
PROF. DR. YESARİ PROF. DR. YESARİ
KARTER KARTER
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Pulmonary Embolism: Impaction of material into branches of the pulmonary arterial bed
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Mortality- 50 000 death/year
(decreasing)
Hospitalisation: 300-600 000/year
Male>Female
American Africans
old > young
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RISK FACTORS - inherited
- acquired
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Inherited Risk FactorsFamily History (+)
Acquired risk factor (-)
Prior deep venous thrombosis
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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
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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
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Acquired Risk Factors (II) -Age > 40
-Malignity
-Obesity
-Heart Failure
-Myocard infarction
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Acquired Risk factors (III)
-Prior DVT -Nephrotic Syndrome -Antiphospholipid Syndrome -PNH -Waldenström
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Thromboembolic risk of the patient
-Risk of the patient (acquired / inherited)
-Risk of the clinical condition
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Diagnose-Young patient
-Family history (+)
-Acquired risk factors (-)
___ inherited
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Symptoms
-Chest pain -Pleuritic pain
-Dyspnea -Cough
-Hemoptysis -Syncope
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Laboratory
Standart test
ECG
Chest rontgenography
Arterial blood gases
Echocardiography
Imaging venous thrombus
Imaging pulmoner emboli
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Standart tests
-Leucocytosis (infarctuse)
-ESR increases
-D-Dimer increases
low---- Exclusion of PE
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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
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Chest Radiography
Usually nonspesific
Not sensitive or specific
Proximal, large segmental artery
Multiple small segmental artery
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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
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Arterial Blood Gases
Acute PaCO2 decreases
Massive PaO2 decreases
Submassive Normal / Nearnormal
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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
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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
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Deep Vein Thrombosis
-Phlebography
-Doppler
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Imaging pulmonary emboli
-Chest radiography
-Ventilation-Perfusion Lung Scan
-Pulmonary angiography
-hCT
-MR angiography
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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
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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
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• DDichotomous clinical probability assesment:ichotomous clinical probability assesment:
• PE likely > 4PE likely > 4
• Pe unlikely < 4 or = 4Pe unlikely < 4 or = 4
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• PE likely--------h CTPE likely--------h CT• ------normal----exclude------normal----exclude• ------findings (+)----PE------findings (+)----PE• ------indeterminate----LE US ------indeterminate----LE US • PAPA• PE unlikely-----D-dimer(+)PE unlikely-----D-dimer(+)• -------h (CT)-------h (CT)• D-dimer(-)D-dimer(-)• -------exclude PE-------exclude PE•
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Pulmonary Angiography
Gold standart
İmages PE in subsegmental and peripheral arteries
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hCT-two dimensional angiographic image
-specifity 90%
-dimension of the emboli
-mediastinal and parenchymal patologies
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MR Angiography
Sensitivity-70 – 90 %
Specifity- 77 – 100 %
(Central arteries)
Also asseses RV function
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Treatment
-to prevent death
-to reduce morbidity
-to prevent pulmoner hypertension
progresing due to thromboemboli
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Treatment (II)
Supportive
-Oxygen
-IV liquid
-Vasopressors
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Anticoagulation
-unfractioned heparin
-LMWH
-Thrombolysis
-Embolectomy
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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
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LMWH
-long acting
-less binding to plasma protein
-greater bioavailibity
-no need monitorisation
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Prognosis
-Mortality rate – 30%
-Depends on associated pathology
-Resolution – 5 days 36%
2 weeks 52%
3 months 73%
Pulmonary hypertension
recurrent microemboli (rare)
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Secondary prevention
UFH + oral anticoagulan (6 months)
LMWH SC + oral anticoagulan (6 months )
LMWH (pregnancy)
Recurrance / unknown origin / permanantly increased risk (throughout life)
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Thrombolysis
Massive pulmoner emboli with
hemodynamic instability
-streptokinase
-urokinase
-t-PA
**serious bleeding
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REFERENCES:REFERENCES:
• Agnelli G. Anticoagulation in the prevention and treatment of Agnelli G. Anticoagulation in the prevention and treatment of pulmonary embolism.Chest 1995. 107;39-44.pulmonary embolism.Chest 1995. 107;39-44.
• BellWR,Simon TL; DeMets DL. The clinical features of massive and BellWR,Simon TL; DeMets DL. The clinical features of massive and submassive pulmonary embolism. Am J Med 1977; 62: 355-360.submassive pulmonary embolism. Am J Med 1977; 62: 355-360.
• Braunwald E. Pulmonary embolism. Braunwald’s heart disease. Braunwald E. Pulmonary embolism. Braunwald’s heart disease. Braunwald (ed)Philedalphia. WB Saunders 1992 .562-1568.Braunwald (ed)Philedalphia. WB Saunders 1992 .562-1568.
• Herold CJ, Bankier AA, Burghaiber OC, Minar E, Watzke HH. Pulmonary Herold CJ, Bankier AA, Burghaiber OC, Minar E, Watzke HH. Pulmonary Embolism. Comprehensive Pulmonary Medicine. Albert R, Spiro S, Jett J Embolism. Comprehensive Pulmonary Medicine. Albert R, Spiro S, Jett J (eds). Harcaurt Brace and Company Limited London 1999. 50.1-50.12(eds). Harcaurt Brace and Company Limited London 1999. 50.1-50.12
• Hyers TH . Diagnosis of pulmonary embolism. Thorax 1995; 50: 930-Hyers TH . Diagnosis of pulmonary embolism. Thorax 1995; 50: 930-932.932.
• Lane D, Manucci PM, Bauer KA, et al. Inherited thrombophilia: Part Lane D, Manucci PM, Bauer KA, et al. Inherited thrombophilia: Part I.Thromb Haemost 1996;76: 651-662.I.Thromb Haemost 1996;76: 651-662.
• Remy -Jerden M, Remy J,Deschildre F. Diagnosis of pulmonary Remy -Jerden M, Remy J,Deschildre F. Diagnosis of pulmonary embolism with spiral CT: comparison with pulmonary angiography and embolism with spiral CT: comparison with pulmonary angiography and scintigraphy. Radiology 1996; 200(3):699-706.scintigraphy. Radiology 1996; 200(3):699-706.