Emboli ParuEmboli Paru

Dr. Abdul Rohman, SpP

K-1K-1

Gejala tidak banyak dan tidak spesifik Sarana diagnostik terbatas sekali

SULIT

PENDAHULUAN

DIAGNOSTIK TATA LAKSANA

Penyebab : - semula tidak diketahui

- autopsi trombus pembuluh darah

Virchow : hub. trombosis - vena perifer - emboli paru

• Trendelenburg : tind. embolektomi tungkai bawah

1939 : Antikoagulan pengobatan & pencegahan

PEMBULUH DARAH

PATOFISIOLOGI

ALIRANDINDING

BRONKOKONSTRUKSI

OBSTRUKSI

PEMBEKUAN DARAH

PARU

VASOKONSTRUKSI

arterivev

a

patofisiologi• Emboli paru terjadi dari lepasnya trombus

yang berasal dari pembuluh vena kaki

• Trombus terbentuk dari beberapa elemen sel dan fibrin yg berisi protein plasma (plasminogen)

• Trombus arteri terjadi karena rusaknya dinding pembuluh arteri (lapisan intima)

• Trombus vena terjadi karena perlambatan aliran darah dalam vena tanpa adanya kerusakan dinding pembuluh darah

patofisiologi• abad 16 – Virchow - oleh karena :

1. Melambatnya sistem aliran darah vena

2. Adanya kelainan dinding pembuluh arteri

3. Adanya perubahan sistem pembekuan darah

• Faktor berpengaruh dalam pembentukan trombus,

yaitu: hiperkoagubilitas & hiperagregasi trombosit.

• Pada emboli paru ada 2 keadaan sebagai akibat obstruksi pembuluh darah, yaitu:

1. Terjadinya vasokonstriksi

2. Terjadinya bronkokonstriksi

Infark paru

DIAGNOSA1. Emboli paru sering berasal :

a.Trombus vena ekstremitas inferior

(terbanyak)

b.Trombus ruang atrium kanan

c. Fokus septik : endokarditis

trikuspidalis

d.Tumor tanpa adanya trombosis

intra-vena

e.Ateroemboli aneurisma aorta

abdominalis

f. Cairan amnion

g.Lain : lemak, udara, sumsum

tulang, jar. trofoblast dan desidua,

parasit, dll.

Jumlah emboli udara sebesar 100- 150 cc sudah dapat menimbulkan kematian

2. Faktor-faktor predisposisi

a.Imobilisasi

b.Umur

c.Peny. jantung

d.Trauma

e.Obesitas

DIAGNOSA

f. Kehamilan & nifas

g. Obat-obatan

h. Peny. Hematologi

i. Peny. Metabolik

j. Neoplasma

3. Keluhan dan Gejala

sesak napas – nyeri dada –hemoptisis

a. Arteri utama/lebih 1 arteri besar: masif dg ggguan hemodinamik berat : renjatan, hipotensi, takikardia, takipnea, hipertensi pulmonal akut & strain ventrikel kanan pada elektrokardiogram

b. Arteri sedang hampir = masif tapi tidak ada hipertensi pulmonal & strain ventrikel kanan pda elektrokardiogram

c. Arteri kecil amat ringan & bervariasi..

Keluhan % Gejala %

Dispnea 77 Takikardia 59Sakit dada 63

Demam 43Hemoptisis 26 Ronki paru 42Perub. Mental 23 Takipnea 38Dispnea + Sakit 14

Edema kaki + nyeri 23dada + haemoptisis Kenaikan tek. Vena 18

Renjatan 11

Bising P2 meningkat 11

Sianosis 9

Efusi pleura 9

CLINICAL FEATURES OF MASSIVE PE

Sudden-onset severe chest pain and dyspnea

Often – during defecation Classically - ≥ a week after operationSign of shock :

- tachycardia- low blood pressure- right ventricular heave- gallop rhythm

- a prominent a-wave in jugular venous pulse

Sudden death

4. Pemeriksaan penunjang

a. Pemeriksaan Laboratorium

AGD (not diagnostic) : acute resp. alkalosis, hipoksemia, (A-aDo2) melebar

Darah tepi : leukositosis &LED meninggi

Kimia darah : LDH, SGOT dan CPK meningkat

D-dimer : normal rules out DVT

4.Pemeriksaan penunjang

b. Pemeriksaan elektrokardiografi

Adanya strain ventrikel kanan

Perputaran searah jarum jam

Terdapat S1, Q3 dan QR pd aVF dan III

serta elevasi ST yang menyerupai infark

jantung akut

Terdapat RBBB komplet/ inkomplet

P Pulmonal pada II, III dan aVF

Lain-lain berupa aritmia, takikardia, dan

atrial flutter.

PENDEKATAN DIAGNOSIS

• KLINIS : sesak napas tiba-tiba, nyeri dada/pleuritis atau hemoptisis

+EKG + Foto dada + AGD

+Trombus vena perifer

(non pitting edema tungkai, nyeri tekan pada betis & poplitea saat dorsofleksi)

Dx definitif : angiografi paru

SKEMA PENDEKATAN Dx / PENATALAKSANAAN EMBOLI PARU

RIWAYAT PENYAKIT + PEMERIKSAAN FISIS TERSANGKA EMBOLI PARU

BERIKAN HEPARIN

INFUS CAIRAN ANALISA GAS DARAH

EKG LABORATORIUMFOTO DADA

LESI BESAR

PEFUSION LUNG SCAN

LESI MEDIUM, KECIL VENTILATION SCAN

NORMAL LUNG SCAN EMBOLI PARU

VENOGRAMANGIOGRAF PARU

HEPARIN ATAU OBAT TROMBOLITIK

DROPLER ISOTOP VENOGRAF IPG

+ +

PENGOBATAN

1. Tindakan pertama fungsi vital:

• Oksigen cegah hipoksia• Cairan stabilitas output

ventrikel kanan dan aliran darah pulmoner.

2.Pengobatan lain ~ indikasi spesifik - vasopresor - inotropic agent

-anti aritmia - digitalis - dan lain-lain

d. Embolektomi pulmoner

Dikerjakan jika terdapat kontra- indikasi pemakaian anti koagulan atau terhadap penderita emboli paru kronik

Jarang dikerjakan

c. Obat-obat trombotik

Bekerja sebagai fibrinolisis endogen Streptokinase 250.000 U/hari I.V.

selama 30 menit seterusnya 100.000 U/hari

Urokinase 4.400 U/kg BB selama 10 menit dan selanjutnya 4.400 U/kg BB tiap jam selama 12 - 24 jam

Monitor pemeriksaan masa trombin

Perbaikan nampak: - 12 jam untuk Urokinase

- 24 jam untuk Streptokinase

Pengobatan trombolitik diikuti dengan heparin dan warfarin

DIAGNOSIS BANDING

Infark miokard akut PneumoniaCongestive heart failure Pleuritis Pneumothorax Percardial tamponade

PROGNOSIS Kurang baik masif : lebih buruk kematian 75 % dalam 2 jam Kronik dan berulang buruk

Resolusi terjadi terapi fibronolisis progresif Terapi trombolitik resolusi dalam 30 jam

Resolusi komplit 7 – 19 hari tergantung :

mulai, adequat tidaknya terapi dan berat ringan

.

S

THANK YOU FOR YOUR THANK YOU FOR YOUR ATTENTION ATTENTION

ABOUT ABOUT “Pulmonary “Pulmonary Embolism”Embolism”

Pulmonary embolismKEY FEATURESESSENTIAL OF DIAGNOSIS • Predisposition to venous thrombosis,

usually of the lower extremities.• Usually either dyspnea, chest pain,

hemoptysis, or syncope.• Tachypnea and a widened alveolar-

arterial PO2 difference.• Characteristic defects on ventilation-

perfusion lung scan, spiral CT scan of the chest, pulmonary angiogram.

GENERAL CONSIDERATIONS.• Cause of an estimated 50.000 deaths

annually in the US and the most common cause of death in hospitalized patients.

• Most cases are not recognized antemortem : <10 % with fatal emboli receive specific treatment.

• Pulmonary embolism (PE) and deep venous thrombosis (DVT) are manifestations of the same disease, with the same risk factors.

- Immobility (bed rest, stroke, obesity).- Hyper viscosity ( polycythemia).- Increased CVP (low cardiac output, pregnancy)-Vessel damage (prior DVT, orthopedic surgery, trauma)-Hyper coagulable states, either acquired or inheritedPulmonary thromboemboli most often originate in deep veins of the major calf muscles50-60% of patient with proximal lower extremity DVT develop PE; 50% of these events are asymptomaticHypoxemia results from vascular obstruction leading to dead space ventilation, right-to-left shunting, and decreased cardiac outputType of pulmonary emboli:- Fat embolism- Air embolism- Amniotic fluid embolism- Septic embolism (eg, endocarditis)- Tumor embolism (eg, renal cell

carcinoma)- Foreign body embolism (eg. talc in IV drug

use)- Parasite egg embolism (schistosomiasis)

- indeterminate scans are common and do not further refine clinical pretest probabilities

• Helical CT arteriography is supplanting V/Q scanning as the initial diagnostis study

- It requires administration of intravenous radio-contrast dye but is otherwise noninvasive

- It is very sensitive for the detection of thrombus in the proximal pulmonary arteries but less so in the segmental and subsegmental arteries

• Venous thrombosis studies- Venous ultrasonography is the test of choice in

most centers- Diagnosing DVT establishes the need for

treatment and may preclude invasive testing in patients in whom there is a high suspicion for PE

• In the setting of a nondiagnostic V/Q scan, negative serial DVT studies over 2 weeks predict a low risk (< 2%) of subsequent DVT over the next 6 weeks

• Pulmonary angiography is the reference standard for the diagnosis of PE

- Invasive, but safe – minor complications in < 5%- Role in the diagnosis of PE controversial, but

generally used when there is a high clinical probability and negative noninvasive studies

• MRI is a primary research tool for the diagnosis of PE• Integrated approach (Figure 2)

TREATMENTMEDICATIONS

• Anticoagulation regimen use unfractionated heparin (UFH) followed by warfarin to maintain the INR 2.0 – 3.0

• Compared with UFH, low-molecular-weight heparins (LMWH) are

- Easier to dose and require no monitoring- Have similar hemorrhage rates- Are at least as effective• LMWH enables home-based therapy in

selected patients• Wafarin is contraindicated in pregnancy;

LMWH can be used instead• Guidelines for the duration of full

anticoagulation- 6 months for an initial episode with

reversible risk factor- 12 months after an initial, idiopathic episode

CLINICAL FINDINGSSYMPTOMPS AND SIGNS

• Clinical findings depend on the size of the embolus and the patient’s preexisting cardiopulmonary status

• Dyspnea occurs in 75-85% and pain in 65-75% of patients

• Tachypnea is the only sign reliably found in more than 50% of patients

• 97% of patients in the PIOPED study had at least one of the following

- Dyspnea

- Tachypnea

- Chest pain with breathing

DIFFERENTIAL DIAGNOSIS

• Myocardial infraction (heart attack)

• Pneumonia

• Pericarditis

• Congestive heart failure

• Pleuritis (phleurisy)

• Pneumothorax

• Pericardial tamponade

DIAGNOSISLABORATORY TESTS

• ECG is abnormal in 70% of patients

- Sinus tachycardia and nonspecific ST-T changes are the most common findings

• Acute respiratory alkalosis, hypoxemia, and widened arterial-alveolar O2 gradient (A-a Do2), but these findings are not diagnostic (table 30)

• A normal D-dimer level by the ELISA assay virtually rules out DVT (sensitivity is 97%%); however, many hospitals use a less-sensitive latex-agglutination assay.

IMAGING STUDIES

• Chest x-ray – most common findings

- Atelectasis

- Infiltrates

- Pleural effusions

- Westermark’s sign is focal oligemia with a prominent central pulmonary artery

- Hampton’s hump is pleural-based area of increased intensity from intraparenchymal hemorrhage

• Lung scanning (V/Q sca

- A normal scan can exclude PE

- A high-probability scan is sufficient to make the diagnosis in most cases

TREATMENT PLAN PRIMARY CARE VISIT

Patient presents w/ signs & symptoms 1 of pulmonary embolism (PE)

DIAGNOSISImaging modalities2

confirm PE ?

No

No

Yes

Yes

ALTERNATIVE DIAGNOSIS

CHOICE OF THERAPY

Does patient present w/ massive life threatening PE3 or w/ risk factors4 ?

1 SIGNS & SYMPTOMS•Hemoptysis•Dyspnea•Chest pain•Abdominal pain•Syncope•Wheezing

TREATMENT-MASSIVE PE & PATIENTS W/ RISK FACTORS

Hemodynamic & Resp SupportInitial supportive treatment may prevent deaths•Hemoxemia/ hypocapnia- Monitored O2 therapy•Patients w/ low cardiac index & normal BP may benefit from:-IV fluids challenge-Dopamine & Dubutamine (IV): May increase cardiac output (CO) & decrease pulmonary vascular resistance

Thrombolytic Therapy•Appropriate in the absence of contraindicatons-Recombinant tissue plasminogen activator (rt-PA)-Other thrombolytic agents

TREATMENT – NON-MASSIVE PEAnticoagulant therapy•Heparins-Unfractionated heparin (UFH) IV -Low molecular weight heparins (LWMH) SC for 5 – 10 days•Oral Anticoagulants-Starts on day 1 oh heparin & overlap therapy for 4 – 5 days-Discontinue heparin once INR: > 2 for 2 consecutive days (target INR: 2 – 3)

Duration of Treatment of Oral Anticoagulant•1st episode of PE or time limited risk factors (surgery, trauma, estrogen use): 3 – 6 month•1st episode of PE w/ idiopathic VTE: ≥ 6 month•1st episode of PE w/ unresolved cancer, anticardiopilin antibody, antithrombin deficiency. Recurrent event, idiophatic or w/ thrombophilia: 12 month – lifetime

2 Imaging modalities: Angiography, VQ scan, SCT3 Massive PE: PE w/ shock, hypotension (systolic BP < 90 mmHg / BP drop > 40 mmHg for 5 min not caused by new onset of arrhythmias, hypovolemia or sepsis4 Possible risk factor for adverse outcomes: Increasing age, cancer, CHF, systemic arterial hypotension, COPD, RV dysfunction. Treatment using thrombolytic therapy.