Emboli paru

Emboli Paru
K-1

Dr. Abdul Rohman, SpP

PENDAHULUAN
DIAGNOSTIK SULIT TATA LAKSANA

Gejala tidak banyak dan tidak spesifik Sarana diagnostik terbatas sekali

 Penyebab : - semula tidak diketahui

pembuluh darah

autopsi

trombus

 Virchow : hub. trombosis

- vena

perifer - emboli paru
• Trendelenburg :

tind. embolektomi

tungkai bawah

PATOFISIOLOGI
arteri

veva

PEMBULUH DARAH

DINDING

ALIRAN

PEMBEKUAN DARAH

PARU OBSTRUKSI

BRONKOKONSTRUKSI

VASOKONSTRUKSI

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

DIAGNOSA
1. 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

DIAGNOSA
2.

Faktor-faktor predisposisi

a. Imobilisasi b. Umur

f. Kehamilan & nifas

g. Obat-obatan c. Peny. jantung
d. Trauma

e. Obesitas

h. Peny. Hematologi i. Peny. Metabolik

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 59 Sakit dada 63 Demam 43 Hemoptisis 26 Ronki paru 42 Perub. Mental 23 Takipnea 38 Dispnea + Sakit 14 Edema kaki + nyeri 23 dada + haemoptisis Kenaikan tek. Vena 18 Renjatan 11

CLINICAL FEATURES OF MASSIVE PE

 Sudden-onset severe chest pain and dyspnea  Often – during defecation  Classically - ≥ a week after operation  Sign 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.

4.Pemeriksaan penunjang
c. Pemeriksaan foto dada
Pemeriksaan ini tidak spesifik Banyak emboli paru  foto dada normal.

d. Pemeriksaan khusus
• Scanning Paru
1. 2.

Perfusion pulmonary scanning Ventilation pulmonary scanning

• Arteriografi Paru
- tepat & spesifik utk deteksi - invasif, tenaga ahli, mahal dan lama

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

INFUS CAIRAN

ANALISA GAS DARAH

BERIKAN HEPARIN
FOTO DADA

EKG LABORATORIUM

PEFUSION LUNG SCAN

LESI BESAR

LESI MEDIUM, KECIL VENTILATION SCAN

NORMAL LUNG SCAN EMBOLI PARU

ANGIOGRAF PARU +

VENOGRAM +

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 -anti aritmia - dan lain-lain

- inotropic agent - digitalis

3.Pengobatan utama lain: a. Heparin - Emboli paru tidak masif Heparin sebagai antikoagulan Dosis 25 U/kg BB = 5.000 U I.V drip glukosa 5 % /NaCl 0,9 % setiap 4 jam selama 7 – 10 hari, sesudah 48 jam diberikan antikoagulan oral - Pada emboli masif dosis heparin ditingkatkan menjadi 10.000 U - Kontrol dgn PPT  target 1,5 – 2 kali normal

b.Warfarin
- Menghambat aktivitas vitamin K - Diberikan setelah heparin o.k awal kerja lambat -Dosis 10 – 15 mg/kg BB selama 12 minggu

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  Pneumonia  Congestive 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 ATTENTION ABOUT “Pulmonary Embolism”

Pulmonary embolism
KEY FEATURES
ESSENTIAL OF DIAGNOSIS • Predisposition to venous thrombosis, usually of the lower extremities. • Usually either dyspnea, chest pain, hemoptysis, or syncope. • Tachypnea and a widened alveolararterial PO2 difference. • Characteristic defects on ventilationperfusion 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 inherited  Pulmonary thromboemboli most often originate in deep veins of the major calf muscles  50-60% of patient with proximal lower extremity DVT develop PE; 50% of these events are asymptomatic  Hypoxemia results from vascular obstruction leading to dead space ventilation, right-to-left shunting, and decreased cardiac output  Type 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

CLINICAL FINDINGS
SYMPTOMPS AND SIGNS
• Clinical findings depend on the size of the

embolus and the patient’s preexisting cardiopulmonary status patients

- 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-

• Dyspnea occurs in 75-85% and pain in 65-75% of • Tachypnea is the only sign reliably found in more

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

than 50% of patients one of the following
- Dyspnea - Tachypnea

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

- Chest pain with breathing

DIFFERENTIAL DIAGNOSIS
• Myocardial infraction (heart attack) • Pneumonia • Pericarditis • Congestive heart failure • Pleuritis (phleurisy) • Pneumothorax • Pericardial tamponade

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

DIAGNOSIS
LABORATORY TESTS
• ECG is abnormal in 70% of patients

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)

TREATMENT
MEDICATIONS
• Anticoagulation regimen use unfractionated

- 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) virtually rules out DVT (sensitivity is 97%%); however, many hospitals use a less-sensitive latex-agglutination assay.

heparin (UFH) followed by warfarin to maintain the INR 2.0 – 3.0
• Compared with UFH, low-molecular-weight

• A normal D-dimer level by the ELISA assay

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

IMAGING STUDIES
• Chest x-ray – most common findings - Atelectasis - Infiltrates - Pleural effusions - Westermark’s sign is focal oligemia with a

selected patients
• Wafarin is contraindicated in pregnancy;

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

prominent central pulmonary artery

- Hampton’s hump is pleural-based area of

anticoagulation
- 6 months for an initial episode with

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

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

use) - Parasite egg embolism (schistosomiasis)

diagnosis in most cases

TREATMENT PLAN
PRIMARY CARE VISIT
Patient presents w/ signs & symptoms 1 of pulmonary embolism (PE) SIGNS & SYMPTOMS Hemoptysis Dyspnea Chest pain Abdominal pain Syncope Wheezing
1

ALTERNATIVE DIAGNOSIS

No

DIAGNOSIS
Imaging modalities2 confirm PE ? Yes

• • • • • •

No

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

Yes

TREATMENT – NON-MASSIVE PE Anticoagulant 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

TREATMENT-MASSIVE PE & PATIENTS W/ RISK FACTORS Hemodynamic & Resp Support Initial 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

2 3

Imaging modalities: Angiography, VQ scan, SCT 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 sepsis 4 Possible risk factor for adverse outcomes: Increasing age, cancer, CHF, systemic arterial hypotension, COPD, RV dysfunction. Treatment using thrombolytic therapy.