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
Virchow : hub. trombosis
trombus
- vena
perifer - emboli paru • Trendelenburg :
tungkai bawah
tind. embolektomi
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 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.
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
ANGIOGRAF PARU +
HEPARIN ATAU OBAT TROMBOLITIK
NORMAL LUNG SCAN EMBOLI PARU
VENOGRAM +
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
use) - Parasite egg embolism (schistosomiasis)
CLINICAL FINDINGS 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
- 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
• Pleuritis (phleurisy)
- Invasive, but safe – minor complications in < 5%
• Pneumothorax
- Role in the diagnosis of PE controversial, but
• Pericardial tamponade
generally used when there is a high clinical probability and negative noninvasive studies
DIAGNOSIS
• MRI is a primary research tool for the diagnosis of PE
LABORATORY TESTS
• Integrated approach (Figure 2)
• ECG is abnormal in 70% of patients
TREATMENT
- 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.
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
IMAGING STUDIES
- Have similar hemorrhage rates
• Chest x-ray – most common findings
- Are at least as effective
- 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
• 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
TREATMENT PLAN PRIMARY CARE VISIT Patient presents w/ signs & symptoms 1 of pulmonary embolism (PE) 1
No
ALTERNATIVE DIAGNOSIS
DIAGNOSIS Imaging modalities2 confirm PE ? Yes
No
CHOICE OF THERAPY Does patient present w/ massive life threatening PE3 or w/ risk factors4 ?
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
2
• • • • • •
SIGNS & SYMPTOMS Hemoptysis Dyspnea Chest pain Abdominal pain Syncope Wheezing
Yes
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
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. 3
