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

- autopsi trombus
pembuluh darah

 Virchow : hub. trombosis - vena

perifer - emboli paru

• Trendelenburg : tind. embolektomi

tungkai bawah

 1939 : Antikoagulan  pengobatan &

 PATOFISIOLOGI
veva
arteri

PEMBULUH DARAH
ALIRAN

DINDING

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
f. Kehamilan &
b.Umur nifas

c.Peny. jantugn. gObat-

obatan

d. Trauma h. Peny.
Hematologi
e. Obesit
as i. Peny.
Metaboli
k
 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 MASSIVEPE

 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. Perfusion pulmonary scanning

2. 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 VENOGRAM
PARU

+ +

PARIN 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
3. Pengobatan utama lain:
a.HHeparin
- 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 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 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
use)
- Parasite egg embolism (schistosomiasis) SYMPTOMPS 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
DIAGNOSIS
LABORATORY 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
 with reversible risk factor
- indeterminate scans are common and do
- 12 months after an initial, idiopathic
not
episode
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)

TREATMENT
MEDICATIONS
• 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
 TREATMENT PLAN
PRIMARY CARE VISIT
Patient presents w/ signs & symptoms 1

of pulmonary embolism (PE)

1 SIGNS& SYMPTOMS
ALTERNATIVE No DIAGNOSIS Hemoptysis
Imaging modalities2 confirm PE ? Dyspnea
DIAGNOSIS
Chest pain
Abdominal pain
Yes Syncope
Wheezing

CHOICE OF THERAPY
Does patient present w/ massive life threatening PE3 or w/ risk factors4 ?
No Yes

TREATMENT-MASSIVE PE & PATIENTS W/ RISK FACTORS

Hemodynamic & Resp Support
Initial supportive treatment may prevent
deaths
or 5 – 10 days Hemoxemia/ hypocapnia
Monitored O2 therapy
y for 4 – 5 days Patients w/ low cardiac index & normal BP
ecutive days (target INR: 2 – 3) may benefit from:
t IV fluids challenge
surgery, trauma, estrogen use): 3 – 6 month Dopamine & Dubutamine (IV): May increase cardiac output (CO) & decrease pulm
h Thrombolytic Therapy
ardiopilin antibody, antithrombin deficiency. Appropriate
Recurrent event,
in theidiophatic
absence of
or w/ thrombophilia: 12 month – lifetime
contraindicatons
Recombinant tissue plasminogen activator (rt-PA)
Other thrombolytic agents

2 Imaging modalities: Angiography, VQ scan, SCT

3 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.