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    Pulmonary Embolism: Dr. Nurfitriani, SP.P

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    Afifulichwan
    The document provides information on pulmonary embolism (PE), including its definition, pathogenesis, risk factors, signs and symptoms, diagnosis, differential diagnosis, and management. PE is caused by blockage of the pulmonary arteries by blood clots (thrombi) that travel from deep veins, most often in the legs. It can be life-threatening and cause respiratory failure or heart failure. Diagnosis involves assessment of clinical probability (e.g. using Wells or Geneva scores) and testing such as CT pulmonary angiogram or ventilation-perfusion scan. Treatment focuses on thrombolysis to break up clots, anticoagulation to prevent new clots, and supportive care.

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    Pulmonary Embolism: Dr. Nurfitriani, SP.P

    Uploaded by

    Afifulichwan
    52 views44 pages
    The document provides information on pulmonary embolism (PE), including its definition, pathogenesis, risk factors, signs and symptoms, diagnosis, differential diagnosis, and management. PE is caused by blockage of the pulmonary arteries by blood clots (thrombi) that travel from deep veins, most often in the legs. It can be life-threatening and cause respiratory failure or heart failure. Diagnosis involves assessment of clinical probability (e.g. using Wells or Geneva scores) and testing such as CT pulmonary angiogram or ventilation-perfusion scan. Treatment focuses on thrombolysis to break up clots, anticoagulation to prevent new clots, and supportive care.

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    Blok respirasi Mahmud Hary Pranggono

    Original Title

    emboli paru

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    The document provides information on pulmonary embolism (PE), including its definition, pathogenesis, risk factors, signs and symptoms, diagnosis, differential diagnosis, and management. PE is caused by blockage of the pulmonary arteries by blood clots (thrombi) that travel from deep veins, most often in the legs. It can be life-threatening and cause respiratory failure or heart failure. Diagnosis involves assessment of clinical probability (e.g. using Wells or Geneva scores) and testing such as CT pulmonary angiogram or ventilation-perfusion scan. Treatment focuses on thrombolysis to break up clots, anticoagulation to prevent new clots, and supportive care.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    52 views44 pages

    Pulmonary Embolism: Dr. Nurfitriani, SP.P

    Uploaded by

    Afifulichwan
    The document provides information on pulmonary embolism (PE), including its definition, pathogenesis, risk factors, signs and symptoms, diagnosis, differential diagnosis, and management. PE is caused by blockage of the pulmonary arteries by blood clots (thrombi) that travel from deep veins, most often in the legs. It can be life-threatening and cause respiratory failure or heart failure. Diagnosis involves assessment of clinical probability (e.g. using Wells or Geneva scores) and testing such as CT pulmonary angiogram or ventilation-perfusion scan. Treatment focuses on thrombolysis to break up clots, anticoagulation to prevent new clots, and supportive care.

    Copyright:

    © All Rights Reserved
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    of 44

    PULMONARY EMBOLISM

    DR. NURFITRIANI, SP.P


    STANDAR KOMPETENSI DOKTER INDONESIA
    • TINGKAT KEMAMPUAN = 1 (MENGENALI DAN MENJELASKAN)
    1. LULUSAN DOKTER MAMPU MENGENALI DAN MENJELASKAN
    GAMBARAN KLINIK PENYAKIT DAN MENGETAHUI CARA YANG
    PALING TEPAT UNTUK MENDAPATKAN INFORMASI LEBIH LANUT
    TENTANG PENYAKIT INI
    2. MAMPU MENENTUKAN RUJUKAN YANG PALING TEPAT BAGI
    PASIEN
    3. MAMPU MENINDAKLANJUTI SETELAH KEMBALI DARI RUJUKAN
    DEFINITION
    EMBOLISM INFARCTION

    Impaction of a The pathological


    thrombus or foreign changes in the lung
    matter in the as a result of
    pulmonary vascular pulmonary
    bed embolism
    EMBOLUS

    NON THROMBOTIC

    THROMBOTIC
    Fat, air, tumour,
    amniotic fluid, IV
    drug abuser
    PULMONARY THROMBOEMBOLISM

    THROMBOSIS OF PERIPHERAL
    PRIMARY THROMBOSIS IN
    VEINS , EMBOLIZATION OF
    PULMONARY ARTERIES AND
    PULMONARY ARTERIES AND
    VEINS
    PULMONARY INFARCTION.
    EPIDEMIOLOGY
    1 2 3

    Described Rarely
    Often a
    by Rudolf diagnosed
    terminal
    Virchow before
    event
    (1856) death
    Mortality Rate

    60.000 – 100.000 2300 deaths


    Deaths Per (0,4% from all
    Annum In US deaths) in 2012
    (CDC) (UK)

    340 deaths (0,2%


    from all deaths) in
    2015
    (Australia)
    PATHOGENESIS
    VIRCHOW'S TRIAD.

    Paul A. Kyrle, and Sabine Eichinger Blood 2009;114:1138-1139


    VIRCHOW'S
    TRIAD
    • EMBOLI  INCREASE RESISTANCE AND PRESSURE IN THE PULMONARY ARTERIES  RELEASE
    VASOCONSTRICTOR COMPOUNDS, PLATELET AGGREGATION & MAST CELLS
    • PULMONARY ARTERY VASOCONSTRICTION & HYPOXEMIA  PULMONARY ARTERIAL
    HYPERTENSION  RIGHT VENTRICULAR PRESSURE INCREASES
    • RIGHT VENTRICULAR DILATATION AND DYSFUNCTION  INTRAVENTRICULAR SEPTAL
    SUPPRESSION TO THE LEFT SIDE AND TRICUSPID VALVE REGURGITATION  INTERFERE WITH
    THE VENTRICULAR FILLING PROCESS
    • REDUCED LEFT VENTRICULAR FILLING  SYSTEMIC CARDIAC OUTPUT DECREASE AND REDUCE
    CORONARY PERFUSION
    • A DECREASE IN CORONARY FLOW  MYOCARDIAL INFARCTION  CARDIOGENIC SHOCK 
    CIRCULATION FAILURE AND DEATH.
    • RESPIRATORY INSUFFICIENCY IN PULMONARY EMBOLISM  CAUSED BY LOW
    CARDIAC OUTPUT  DESATURATION OF VENOUS BLOOD ENTERING
    PULMONARY BLOOD CIRCULATION
    • VENTILATION-PERFUSION IMBALANCE  SHORTNESS OF BREATH AND
    HYPOXEMIA
    • HEMOPTYSIS, PLEURISY & MILD PLEURAL EFFUSION CAN BE FOUND DUE TO
    RUPTURE OF BLOOD VESSELS AROUND THE ALVEOLAR
    SIGNS AND SYMPTOMS
    Asymptomatic
     life
    threatening
    CLINICAL SYMPTOMS
    1. ACUTE ONSET OF DYSPNEA
    Consideration of PE as
    2. PLEURITIC PAIN possible diagnosis
    3. COUGH
    4. HEMOPTYSIS Concurent symptoms of
    5. SWELLING IN THE LOWER LIMBS deep venous thrombosis
    (DVT)
    6. WHEEZE
    CLINICAL SIGNS
    1. TACHYPN0EA (≽ 20 BPM)
    2. TACHYCARDI (≽ 100 BPM)
    3. HYPOXIA
    4. RONCHI
    5. CYANOSIS
    6. S3 AND S4 (GALLOP)
    7. FEVER (≽ 38,5 OC)
    RISK FACTORS
    HOW TO MAKE A
    DIAGNOSIS?
    PHYSICAL
    ANAMNESIS
    EXAMINATION

    DIAGNOSIS

    LABORATORIUM
    FINDINGS IMAGING
    WELLS SCORE
    WELLS SCORE
    • SCORE 0-1  LOW PROBABILITY
    • SCORE 2-6  MODERATE PROBABILITY
    • SCORE > 6  HIGH PROBABILITY
    GENEVA SCORE
    Variables Points
    Age > 65 yrs old 1
    Previous DVT or PE 3
    Surgery or fracture within 1 month 2
    Active malignancy 2
    Unilateral lower limb pain 3
    Hemoptysis 2
    Pain on deep vein palpation of lower limb and unilateral edema 4
    Heart rate 75 to 94 bpm 3
    Heart rate greater than 94 bpm 5
    GENEVA SCORE
    • SCORE 0-3  LOW PROBABILITY, < 8%
    • SCORE 4-10  MODERATE PROBABILITY, ± 28%
    • SCORE > 10  HIGH PROBABILITY, ± 74%
    PULMONARY RULE OUT CRITERIA (PERC)
    PULMONARY RULE OUT CRITERIA (PERC)

    • PERC SCORE IS >0  AN ENZYME-LINKED IMMUNOSORBENT


    ASSAY (ELISA)-TYPE D-DIMER IS RECOMMENDED
    • PERC SCORE NEGATIVE (0)  PULMONARY EMBOLISM IS RULED
    OUT AND NO FURTHER INVESTIGATION IS REQUIRED;
    LABORATORIUM FINDINGS
    1. INCREASE OF WBC 4. INCREASE OF D DIMER LEVELS
     ( ⩾20.000/MM3)  ENDOGENOUS FIBROLYSIS
    2. HYPOXAEMIA PROCESS RELEASED IN THE
     SHUNTING & DECREASE OF CIRCULATION WHEN A CLOT IS
    VENTILATION FOUND
    3. DECREASE OF PACO2  HIGH SENSITIVITY ( ⩾ 94%) BUT
     < 35 MMHG ET CAUSA LOW SPECIFICITY ( < 45%)
    HYPERVENTILATION
    IMAGING
    1. CHEST X- RAY
    • NORMAL
    • EFUSI PLEURA ATAU ATELEKTASIS

    2. COMPUTED TOMOGRAPHY PULMONARY ANGIOGRAM (CTPA)


    • GOLD STANDARD
    • INVASIVE AND HIGH RISK
    • SENSITIVITY 70%, SPESIFICITY 90%
    • FILLING DEFECT AND ABRUPT CUT OFF OF THE BLOOD VESSELS
    IMAGING
    3. VENTILATION PERFUSION SCINTIGRAPHY (V/Q SCAN)
    • NORMAL VENTILATION IN AREAS THAT DO NOT EXPERIENCE OCCLUSION
    DUE TO EMBOLISM
    4. ECHOCARDIOGRAPHY TRANSTHORACAL
    • NON-INVASIVE DIAGNOSTIC TOOL
    • TO ASSESS PRESSURE OVERLOAD OF THE RIGHT VENTRICLE CAUSED BY
    MASSIVE PULMONARY EMBOLISM
    IMAGING
    5. ELEKTROCARDIOGRAPHY
    • LESS SPECIFIC IF DONE IN PATIENTS WITH MILD TO MODERATE PULMONARY EMBOLISM  CAN
    PROVIDE A NORMAL ECG.
    • IN SEVERE PE :
    a. NARROW Q WAVE FOLLOWED BY AN INVERSION OF THE T WAVE ON LEAD III IS
    ACCOMPANIED BY AN S WAVE IN LEAD I  INDICATES A CHANGE IN THE POSITION OF THE
    HEART DUE TO DILATION OF THE RIGHT ATRIUM AND VENTRICLE. AXIS DEVIATION CAN ALSO
    BE FOUND TO THE RIGHT
    b. P PULMONAL
    c. NEW RIGHT BUNDLE BRANCH BLOCK
    d. RIGHT VENTRICULAR STRAIN WITH INVERSION T WAVE IN LEADS V1 TO V4
    e. SUPRAVENTRICULAR ARRHYTHMIAS OR SINUS TACHYCARDIA
    OTHER INVESTIGATIONS

     CARDIAC BIOMARKERS
    • ESTIMATE THE PROGNOSIS IN PATIENTS WITH PULMONARY EMBOLISM
    • KONSTANTINIDES : AN INCREASE IN THE LEVELS OF TROPONIN T AND I 
    A WORSE PROGNOSIS
    • THE RISK OF MORTALITY INCREASED 3.5 TIMES
    • HEART-TYPE BINDING PROTEIN FATTY ACID (H-FABP) IS THE BEST MARKER
    FOR DETECTING PULMONARY EMBOLISM
    APPROACH TO
    INVESTIGATION
    OF
    PULMONARY
    EMBOLISM

    Doherty S. Pulmonary Embolism: An Update. Australian Family


    Physician. 46(11), 2017. 816-20.
    DIAGNOSTIC
    APPROACH OF
    PULMONARY
    EMBOLISM
    DIAGNOSTIC
    APPROACH OF
    PULMONARY
    EMBOLISM
    DIFFERENTIAL DIAGNOSIS
    1. PNEUMONIA 9. PERICARDIAL TAMPONADE
    2. BRONCHITIS 10. LUNG CANCER
    3. BRONCHIAL ASTHMA 11. PRIMARY PULMONARY HYPERTENSION
    4. ACUTE EXACERBATION OF COPD 12. FRACTURE OF COSTAE
    5. MYOCARDIAL INFARCTION 13. PNEUMOTHORAX,
    6. LUNG EDEMA 14. COSTOCHONDRITIS,
    7. ANXIETAS 15. MUSCULOSCELETAL PAIN
    8. AORTA DISSECTION
    MANAGEMENT OF
    PULMONARY EMBOLISM
    • SUPPORTIVE TREATMENT  RIGHT HEART FAILURE
    • OXYGENATION WITH NASAL CANULE  HYPOXEMIA
    • THROMBOLITIC TREATMENT  OPEN BLOCKAGE OF THROMBOEMBOLIC
    • EMBOLEKTOMY
    • ANTICOAGULANT TREATMENT  PREVENT MORTALITY AND RECURRENCY
    • POSITIVE PRESSURE MECHANICAL VENTILATION  MUST BE AVOIDANCE
    THROMBOLITIC AGENTS
    1. STREPTOKINASE: 250.000 UNIT WITHIN 30 MINUTES, FOLLOWED BY 100.000
    UNIT/HOURS WITHIN 12-24 HOURS.
    2. UROKINASE: 4.400 UNIT WITHIN 10 MINUTES, DIIKUTI DENGAN 4.400
    UNIT/KG/HOURS WITHIN 12-24 HOURS.
    3. RECOMBINANT TISSUE PLASMINOGEN ACTIVATOR (RTPA): 100 MG WITHIN 2
    HOURS ATAU 0.6 MG/KG WITHIN 15 MINUTES. MAXIMAL DOSE FOR RTPA 
    50 MG.
    ANTICOAGULANT AGENTS
    • UNFRACTIONED HEPARIN  DOSE 80 UNITS/KG BOLUS FOLLOWED BY MAINTANCE
    DOSE 18 UNIT/KG/HOURS
    • APTT TEST SHOULD BE DONE EVERY 4-6 HOURS AFTER BOLUS INJECTION
    • UNFRACTIONED HEPARIN DOSE SHOULD BE ADJUSTED BASED ON THE RESULTS OF
    THE APTT
    • LOW-MOLECULAR-WEIGHT HEPARIN (LMWH) OR SUBCUTANEAL FONDAPARINUX
    • MORE RECOMMENDED THAN UNFRACTIONED HEPARIN IN PATIENTS ARE NOT AT
    HIGH RISK FOR BLEEDING AND HAVE GOOD KIDNEY FUNCTION
    ANTICOAGULANT AGENTS
    • ORAL VITAMIN K ANTAGONIST ADMINISTER AFTER HEPARIN
    • LONG-TERM MANAGEMENT AND PROPHYLAXIS FOR PATIENTS WITH
    PULMONARY EMBOLISM  VITAMIN K ANTAGONISTS FOR AT LEAST 3
    MONTHS
    DOMO ARIGATO GOZAIMASU

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