PULMONARY EMBOLISM PROF DR YESAR KARTER Pulmonary Embolism

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 (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 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 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 -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 -h. CT -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 (+) 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 < 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

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 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 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

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

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