PULMONARY EMBOLISM PROF. DR. YESARİ KARTER

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
2 weeks
36%
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 the prevention and treatment of pulmonary
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