PENYAKIT ARTERI PERIFER

OKLUSIF

Dr. Dion Faisal

DEFINISI
Penyakit Arteri Perifer Oklusif (PAPO)/
Peripheral Occlusive Arterial Disease
(POAD)/ Peripheral Arterial Disease (PAD):

Sindroma klinis yang disebabkan oleh adanya

stenosis atau oklusi lumen aorta atau arteri-
arteri ekstremitas bawah.

Harrisons Principles of Internal Medicine, 18th Ed.

2
ETIOLOGI
Arteriosklerosis (WHO): kelainan pada tunika
intima arteri yang kompleks, terdiri dari
penyumbatan setempat oleh berbagai bahan
lipida, karbohidrat, darah & komponen darah,
jaringan ikat & deposit kalsium diikuti kelainan
tunika media.
Arteritis: proses keradangan (inflamasi) dinding
arteria yang menyebabkan penebalan dinding
dan memberi sumbatan arteria yang kronis
Thromboemboli: bagian kecil dari blood clot
yang terlepas menyebabkan sumbatan pembuluh
Puruhito. Buku Ajar Primer Ilmu Bedah Toraks, Kardiak, &
darah.
Vaskular. edisi 1. 2013
3
 PATOFISIOLOGI PAPO

Lesi segmental (plak atherosklerotik dgn

deposit Ca, penipisan tunika media,
destruksi otot & serat elastik, fragmentasi
internal elastic lamina, dan thrombus yang
terdiri dari platelet & fibrin) arteri
diameter sedang hingga besar
penyempitan lumen vaskularisasi
distal lesi (iskemia) adenosin nyeri
iskemik
Lesi: percabangan arteri, turbulensi, shear
stress, & intimal injury.
Usia tua & DM >>>
Lokasi:
Femoral & popliteal 80-90%
Tibial & peroneal 40-50%
Iliaca & abdominal aorta 30%
4
 TANDA & GEJALA PAPO
GEJALA (<50% simptomatik)
Intermittent claudication rasa nyeri/kram/kebas pada
ekstremitas saat aktivitas & berkurang dengan istirahat
Iskemia ekstremitas bawah nyeri (+) saat tidak
beraktivitas (rest pain), nyeri (+) saat pada posisi horizontal
(misalnya saat tidur/ night pain), ujung kaki kebas
Lower > upper extremities

PEMERIKSAAN FISIK
Pulsasi nadi di bagian distal oklusi berkurang/ (-)
Bruits/ bising di area oklusi
Atrofi otot
Iskemia kerontokan rambut di distal oklusi, kuku
menebal, kulit tipis dan mengkilat, sianosis, akral dingin,
ulserasi (painful ulcer), kebas, hiporefleksia
5
DIAGNOSIS PAPO
ANAMNESIS
Riwayat gejala : klaudikasio, gangguan mobilitas, ulkus sulit sembuh
Komorbid : penyakit jantung/ vaskular, HT, hiperkolesterol, DM, riwayat
bedah vaskular

PEMERIKSAAN FISIK
Tanda-tanda oklusi & iskemia
Tekanan arteri ankle-brachial index (ABI)

PEMERIKSAAN PENUNJANG
Duplex ultrasonography (DUS) Sensitivitas 70% dan spesifitas 90%
Transcutaneous oxymetry
Stress testing (treadmill) analisis objektif keterbatasan fungsional
ekstremitas yang mengalami oklusi arteri
Digital Subtraction Angiogrphy (DSA) gold standard
CTA Sensitivitas dan spesifitas 9599%
MRA Sensitivitas dan spesifitas 8090%

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ANKLE-BRACHIAL
INDEX (ABI)

7
 DUS
Keuntungan:
Non invasif
Lebih murah
Mudah dikerjakan (rawat jalan
atau kamar operasi)
Terhindar dari resiko potensial
nefrotoksik agen kontras
Sensitivitas 70% dan spesifitas
90%

Kerugian:
Operator dependen

Gale L Tang1, Jason Chin2 and Melina R Kibbe2.

Advances in diagnostic imaging for peripheral arterial
disease Expert Rev. Cardiovasc. Ther. 8(10), 1447
1455 (2010)
Arterial color flow duplex. (A) Normal peroneal artery
with triphasic spectral waveform. (B) Heavily calcified
posterior tibial artery with a monophasic spectral
waveform. The calcification interrupts the color flow
imaging of the vessel lumen. 8
 DSA
Keuntungan:
Secara primer evaluasi
lumen arteri

Kerugian:
Invasif
Mahal
Resiko alergi kontras
dan paparan radiasi
Discomfort

Gale L Tang1, Jason Chin2 and

Melina R Kibbe2. Advances in
diagnostic imaging for peripheral
arterial disease Expert Rev.
Cardiovasc. Ther. 8(10), 14471455
(2010)

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 CTA
Keuntungan:
Evaluasi arterial wall dan jaringan
sekitarnya, deteksi aneurisme perifer,
karakteristik plaque, kalsifikasi,
ulserasi, thrombus atau soft plaque,
intimal hyperplasia, in-stent restenosis
dan fraktur stent.
Sensitivitas dan spesifitas 9599%

Kerugian:
Resiko alergi atau nefrotoksik
kontras
Radiasi

3D reconstruction of the aortoiliac arteries using LightSpeed

Gale L Tang1, Jason Chin2 and Melina R Kibbe2. Advances
Volume CT image acquisition. Calcified plaques in the aorta
in diagnostic imaging for peripheral arterial disease Expert
and iliacs are visualized with high resolution, as are the
Rev. Cardiovasc. Ther. 8(10), 14471455 (2010)
relationship of the arteries to bony landmarks
1
MRA
Keuntungan:
No ionizing radiation exposure
Gadolinium-based contrast agent >>
less nephrotoxic
Sensitivitas dan spesifitas 8090%

Kerugian:
Modalitas non invasif paling mahal
Waktu pemeriksaan dan toleransi
pasien
KI: pacemakers, automated
implantable cardioverterdefibrillators,
stent grafts and brain aneurysm clips
Bui BT, Miller S, Mildenberger P, Sam A 2nd, Sheng R. Comparison of contrast-enhanced MR
angiography to intraarterial digital subtraction angiography for evaluation of peripheral arterial
occlusive disease: results of a Phase III multicenter trial. J. Magn. Reson. Imaging 31(6), 1402
1410 (2010). 1
Thromboangiitis Obliterans (TAO)/
Winiwarter-Burger Disease
Alexander von Winiwarter (1879): first
case of 57 y.o. male with foot pain leading
to gangrene
Pathologic specimen showed intimal
proliferation, thrombosis, and fibrosis
Suggested that vessel changes distinct
from atherosclerosis
Leo Buerger (1908): detailed description of
11 amputated limbs at Mt. Sinai with
endarteritis & endophlebitis
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1
Etiologi
UNKNOWN!
Distinct from other vasculitis
1. thrombus is highly cellular with less intense
cellular reaction in vessel wall
2. normal immunologic markers
Strong association with smoking
No gene association found yet
Conflicting studies regarding hypercoagulable states
Increased urokinase plasminogen activator
Impaired endothelium-dependent vasorelaxation
Immunologic mechanisms may be contributory
Increased cellular sensitivity to Types I and III
collagen
1
Gejala Klinis
Classification Systems
Major Criteria
Onset of distal extremity ischemic symptoms prior to aqe 45
Tobacco abuse
Undiseased arteries proximal to brachial & popliteal
Objective documentation of distal occlusive disease by
plethysmography
Exclusion of proximal embolic source, trauma, autoimmune
disease, hypercoagulable state, atherosclerosis
Minor Criteria
Migratory superficial phlebitis
Raynauds syndrome
Upper extremity involvement
Instep claudication
No typical lab abnormalities

1
 Arteriografi
Small and medium-
sized vessels
Digital arteries of
fingers and toes
Palmar, plantar,
tibial, peroneal,
radial, and ulnar
Segmental
occlusive lesions
More severe disease
distally
Corkscrew
collaterals
Normal proximal
arteries
Yuichi Fujii et al. Circulation. 2007;116:e539-e540
A, DSA: Corkscrew collaterals around the area of occlusions. DUS:
corkscrew collaterals as color Doppler flows of a snake sign (A [arrow
1
B] and B) and a dot sign (A [arrow C] and C). Copyright American Heart Association, Inc. All rights reserved.
Terapi
STOP ALL SMOKING!
The only way to stop progression of disease &
prevent future amputation
All other therapies are palliative
Prostaglandin or prostacyclin analogue (iloprost,
beraprost)
Calcium channel blockers for vasospasm
Pentoxiphylline
Thrombolytic therapy
Sympathectomy
Surgical revascularization (limited due to skip
lesions & distal disease, <10% bypass
candidates)
1
Takayashus Arteritis (TA)/
Aortic Arch Synd./Pulseless
Disease
Inflammatory & stenotic disease of medium
and large sized arteries characterised by a
strong prediliction for the aorta & its branches.
Dr. Mikito Takayasu (1905) the retinal
changes of the disease (the Annual
Ophthalmology Society meeting, Japan).
Incidence: uncommon disease, annual
incidence rate 1.2-2.6 cases/million
Prevalent in adolescent and young women
(80%)
No racial/geographical distribution.

1
Patologi
Panarteritis, inflammmatory mononuclear
infiltrates, occasionally giant cells
Marked intimal proliferation, fibrosis,
scarring and vascularisation of media
Disruption, degeneration of elastic lamina
Narrowing of lumen +/- thrombus
Immunopathological mechanism??
uncertain
Gejala Klinis

Constitutional:
Headache (50%-70%)
Malaise (35%-65%)
Arthralgias (28%-75%)
Fever (9%-35%)
Weight loss (10%-18%)

2
Kardiak & vaskular
Bruit, most common location: carotid artery
(80%)
BP difference of extremities (45%-69%)
Claudication (38%-81%)
Carotodynia or vessel tenderness (13%-
32%)
Hypertension (28%-53%; 58% with renal
artery stenosis in one series)
Aortic regurgitation (20%-24%)
Raynauds syndrome (15%)
Pericarditis (< 8%)
Congestive heart failure (< 7%)
Neurologi

Headache (50%-70%)
Visual disturbance (16%-35%) -
Strong association with common
carotid and vertebral artery disease
Stroke (5%-9%)
Transient ischemic attacks (3%-7%)
Seizures (0%-20%)
Dermatologi

Erythema nodosum (6%-19%)

Ulcerated subacute nodular lesions
(< 2.5%)
Pyoderma gangrenosum (< 1%)
Pemeriksaan Fisik
Peripheral pulses, BP of 4 extremities, ophthalmologic
examination.
SBP difference (>10 mm Hg) between arms.
Hypertension renal artery involvement (50%).
Absent or diminished pulses are the clinical hallmark
of Takayasu arteritis, but pulses are normal in many
patients & upper limbs > lower limbs.
Ophthalmologic exam: retinal hemorrhages, cotton-
wool exudates, venous dilatation & beading,
microaneurysms of peripheral retina, optic atrophy,
vitreous hemorrhage, and classic wreathlike
peripapillary arteriovenous anastomoses (extremely
rare).
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 Artery percent Clinical manifestations

1. Subclavian 93 ARM CLAUIDACTION,

RAYNAUDS PHENOMENON
2. Common 58 VISUAL CHANGES, TIA,
carotid STROKE, SYNCOPE
3. Abdominal 47 ABDOMINAL PAIN, NAUSEA,
aorta VOMITING
4. Renal 38 HTN, RENAL FAILURE

5. Aortic 35 AORTIC INCOMPETENCE,

arch/root CCF
 ARTERY % CLINICAL
MANIFESTATIONS
1. VERTEBRAL 35 Visual changes,
Dizziness
2. COELIAC AXIS 18 Abdominal pain
Nausea, vomiting
3. SUPERIOR 18 Abdominal pain,
MESENTRIC nausea, vomiting
4. ILIAC 17 Leg claudication
5. PULMONARY 10-40 Atypical chestpain,
dyspnea
6. CORONARY <10 Chest pain, MI
 Kriteria Diagnosis

Arend, W. P., et al. (1990). "The American College of Rheumatology 1990 criteria for
the classification of Takayasu arteritis." Arthritis Rheum 33(8): 1129-1134.
Pemeriksaan Penunjang

Arteriogram/ angiogram
Complete blood count(CBC)
C-reactive protein(CRP)
Electrocardiogram(ECG)
Erythrocyte sedimentation rate(ESR)
Magnetic resonance
angiography(MRA)
Ultrasound
X-ray of the chest
2
Klasifikasi (angiogram)
Type I - Branches of the aortic arch
Type IIa - Ascending aorta, aortic arch, and
its branches
Type IIb - Type IIa region plus thoracic
descending aorta
Type III - Thoracic descending aorta,
abdominal aorta, renal arteries, or a
combination
Type IV - Abdominal aorta, renal arteries, or
both
Type V - Entire aorta and its branches
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 MEDICAL CARE

Challenging: clinical, biologic, and radiologic

information do not always correlate.
Kerr et al (NIH), assess disease activity in patients
with Takayasu arteritis. New onset or worsening of
2 following features indicates active disease:
1. Systemic features: fever & arthralgias (no
identified cause)
2. ESR
3. Vascular ischemia or inflammation: claudication,
diminished or absent pulse, bruit, carotodynia, or
asymmetric blood pressure in either upper or lower
limbs (or both)
4. Typical angiographic features
 Treatment

Difficult.
Early detection is important.
Steroids & immunosuppressive drugs:
corticosteroid therapy with or without
cytotoxic agents.
Strict management of dyslipidemia, HT, &
lifestyle
Low-dose aspirin
Surgery: bypass, angioplasty,stent.
 Pub MED.gov, 2001
Corticosteroids: oral prednison or prednisolon, started at 1
mg/kg daily or divided twice daily and tapered over week-
months. Long-term low-dose may be required. Osteoporosis
prevention.
Cytotoxic agents: steroid-resistant or relapsing. Continued for
at least one year after remission and are then tapered to
discontinuation.
Methotrexate (Rheumatrex) - 7.5-25 mg/wk oral
Azathioprine (Imuran)- 1-2 mg/kg/d oral
Cyclophosphamide (Cytoxan)- 2 mg/kg/d oral (most severe &
refractory disease states)
Anti TNF Agent: relapsing after steroids & immunosuppressive
tx.
Etanercept 25 mg twice weekly, and infliximab 3 mg/kg initially
and at 2 weeks, 6 weeks, and every 8 weeks thereafter
3
 SURGICAL CARE
Critical stenotic lesions should be treated by
angioplasty or surgical revascularization during periods
of remission.
Surgical repair or angioplasty indication:
1. Renovascular stenosis causing hypertension
2. Coronary artery stenosis leading to myocardial
ischemia
3. Extremity claudication induced by routine activity
4. Cerebral ischemia and/or critical stenosis 3 cerebral
vessels
5. Aortic regurgitation
6. Thoracic or abdominal aneurysms >5 cm in diameter
7. Severe coarctation of the aorta
8. Percutaneous transluminal coronary angioplasty
Raynauds Disease, Syndrome,
Phenomenon
Chronic episodic attacks of digital ischemia
provoked by exposure to cold or emotional stress.
Characterized by sequential colour changes: white
(pallor) blue (cyanosis) red (rubor).
10% of population, female:Male 5:1, age between
15 - 40 y.o.
First described by Maurice Raynaud (1862)
Hand > feet, the tip of ears, nose, nipples, and lips

3
Patofisiologi
Become pale or
Small arteries at
Expose to cold / white then blue, less
fingers and toes
triggering factor blood flow and low
vasospasm
O2 supply

Warm up (arteries Blood flow increase,

dilate) high O2 supply

Affected area is
Bolster MB, Maricq HR, Leff
warm and turn red,
RL. Office evaluation and
Color change to throbing pain, tingle,
bright red burn, or feel numb treatment of Raynaud's
(episodes last about phenomenon.Cleve Clin J
15 minutes) Med.1995;62:51-61.
Patofisologi
Not fully understood but centered on a
functional unit composed of vascular
endothelium, smooth muscle cells and nerve
endings.
Skin of digits supplied by both
thermoregulatory and nutritional blood flow.
Thermoregulatory system is controlled by
sympathetic nervous system while nutritive
flow is supplied by capillary network.
Secondary raynauds can lead to hypoxia
and ischaemia.
 Vascular defects both structural &
functional (primary Raynaud).
Calcitonin gene related peptide (CGRP)
which is a potent vasodialator.
Intravascular defects includes
following:-
Platelets activation thrombaxane &
serotonin .
Defective fibrinolysis fibrin
obstruction of vasculature
 Aberrant expression of endogenous
vasodilatory substances (nitric oxide,
prostacyclin, prostaglandin & leukotrienes)
and vasoconstrictors (endothelin,
angiotensin II and thromboxane A2).
WBC activation
RBC deformability impairment of blood
flow.
Oxidative stress
Genetic locus 3p21.1-p21.3.
Klasifikasi (Allen and Brown)
Primary Raynauds disease: the causes is not known
(idiopathic), symmetrical and involves several digits,
milder, reversible spasm of the smallest arteries and
arterioles, no abnormalities of the endothel.
Secondary Raynaud's syndrome: only one or a few
digits are affected and asymmetry is not unusual,
more severe, vasospasm, endothelial cell changes,
vessel obstruction, and hemorheologic deformations.
CREST syndrome:calcinosis,Raynaud's
phenomenon,esophageal dysmotility,sclerodactyly,
andtelangiectasia limited cutaneousform
ofsystemic sclerosis
 Trauma or vibration:-
Reflex sympathetic dystrophy
Vibration exposure
Arteriovenous fistula
Hypothenar hammer syndrome
(ulnar artery thrombosis)
Intra-arterial drug administration
Connective tissue disease
and vasculitis
Systemic sclerosis
SLE
Rheumatoid arthritis
Sjgrens syndrome
Mixed connective tissue disease
Dermatomyositis
Temporal arteritis
Hepatitis B antigen vasculitis
Obstructive arterial
disease
Atherosclerosis
Thromboangiitis obliterans
(TAO)(Buergers disease)
Hypothenar hammer
syndrome (ulnar artery
thrombosis)
Neurological disease
Thoracic outlet syndrome
(cervical rib)
Carpal tunnel syndrome
Hypothenar hammer
syndrome
Reflex sympathetic
dystrophy
 Haematological disease
Cryoglobulinaemia
Cold agglutinins
Cyclosporin
Paroxysmal haemoglobinuria Oral contraceptives
Waldenstrms Vinyl chloride
macroglobulinaemia Nitroglycerin withdrawal
Drugs and toxins Heavy metals
Ergot Interferon alfa
-Blockers Miscellaneous
Methysergide Paraneoplastic syndrome
Bleomycin Chronic renal failure
Amphetamines Primary pulmonary
Imipramine
Bromocriptine
hypertension
Hypothyroidism
Clonidine
Anorexia nervosa
Diagnosis
Criteria for diagnosis of primary Raynauds phenomenon:-
1. Intermittent attacks of discoloration of extremities
2. Absence of evidence of organic peripheral arterial occlusion
3. Symmetrical or bilateral distribution
4. Exclusion of any disease, occupation, trauma or drug
ingestion that could give rise to vasospastic abnormalities
5. Absence of immunological abnormalities eg. Negative ANA
6. Female sex, age under 25 years
7. History of cold intolerance since childhood
8. Normal nail fold capillaries
9. Normal ESR
10.History of symptoms for at least 2 years.
Pemeriksaan Penunjang
Cold Stimulation Test
Nailfold Capillaroscopy
Antinuclear antibody (ANA)
Erythrocyte sedimentation rate (ESR)
C-reactive protein (CRP)
Terapi

Medical treatment: calcium channel

blockers, alpha blockers, vasodilators
Surgical treatment: sympathectomy
(refracter and unresponsive to other
tx), chemical injection, amputation.
Health education: stop smooking,
excercise, stress control, avoid
caffeine, dress warmly outdoors
Protokol Terapi
Drug therapy

Bradley W. Shinn. US
PAPO EKSTREMITAS
BAWAH Penyakit Arteri Perifer Obstruktif
EKSTREMITAS BAWAH

Iskemia
Iskemia Akut
Kronis
(ALI)
(CLI)

Oklusi
Trombosis Embolisasi
aterosklerotik

4
 KLASIFIKASI PAPO
EKSTREMITAS BAWAH
KLASIFIKASI FONTAINE KLASIFIKASI RUTHERFORD
Stage Temuan Klinis Grad Kateg Temuan Klinis
e ori
I Asimptomatik 0 0 Asimptomatik
IIA Klaudikasio ringan I 1 Klaudikasio ringan
IIB Klaudikasio sedang-berat I 2 Klaudikasio sedang
III Nyeri iskemik saat I 3 Klaudikasio berat
beristirahat
IV Ulkus & gangren II 4 Nyeri iskemik saat
istirahat
III 5 Kerusakan jaringan
minor
III 6 Kerusakan jaringan
luas/mayor

5
 KLASIFIKASI PAPO
EKSTREMITAS BAWAH
Lesi Tipe A :
1. Stenosis tunggal dengan panjang 10
cm
2. Oklusi tunggal dengan panjang 5 cm
Lesi Tipe B :
1. Lesi multiple (oklusi/stenosis), @
5cm
2. Stenosis/oklusi tunggal 15 cm yg
tdk melibatkan A. Poplitea
infragenikulatum
3. Lesi tunggal/multiple tanpa bantuan
bypass distal dari Aa. tibiales
4. Lesi
Lesi oklusif
Tipe C : terkalsifikasi sepanjang
5cm multiple dengan total > 15cm,
1. Lesi
5. dengan/tanpa
Stenosis popliteal tunggal
kalsifikasi
2. Stenosis/oklusi rekuren yang tetap
memerlukan penanganan setelah 2x
intervensi
Lesi Tipe D endovaskuler
:
1. Oklusi total kronis, >20cm s/d A.poplitea
2. Oklusi total kronis s/d A. Poplitea &
trifurcation 5
ACUTE LIMB ISCHEMIA (ALI)

Definisi:penurunan perfusi ekstremitas inferior

secara mendadak atau dalam 2 minggu pasca
kejadian inisasi
Kejadian inisasi yang menjadi predisposisi:
Embolisasi AF/VF, thrombosis intramural,
kardioversi, gangguan katup jantung/PJR
Trombosis lesi aterosklerotik lokal,
hiperkoagulasi
Prosedur revaskularisasi
Trauma himpitan/entrapment pembuluh
darah dalam kompartemen
Komplikasi aneurisma vasa perifer
5
MANIFESTASI KLINIS ALI
6P (bandingkan dengan ekstremitas
kontralateral): pain nyeri iskemik pada
otot paha/betis, pallor, paresthesia, paralysis,
pulselessness,
Parameter
poikilothermia
Kategori
Viable Threatened Irreversible
Deskripsi Not Salvageable Kerusakan
immediately dgn tindakan jaringan luas
threatened segera indikasi amputasi
Capillary Baik (+), (-) tanda :
return melambat marbling
Kelemahan (-) Parsial/ringan Paralisis & rigor
otot
Gangguan (-) Ringan Parestesia/anesth
sensoris esia (+)
Temuan pada Audible Audible/inaudi Inaudible
Doppler ble 5
ALGORITM
A

5
 MANAJEMEN ALI

TROMBOLISIS
Agent of choice : rTPA Streptokinase atau Urokinase (IV)
Kelas I-IIA serta pasien dengan oklusi vasa kecil melarutkan
trombus kecil di area percabangan & mengurangi jejas endotelial
pasca administrasi
Menurunkan kejadian reperfusion injury karena mengurangi besar
trombus secara gradual
KI: riwayat stroke, tumor intrakranial, DM nefropati, insufisiensi
ginjal, gangguan koagulasi

ANTIKOAGULASI
Disarankan untuk segera diberikan mencegah propagasi thrombus
ke dinding vasa sekitarnya
KI:
GI & CNS Bleeding
DM nefropati
Alcoholic liver disease
Alergi obat
Agent of choice : Heparin (IV), Warfarin (IM, IV)
5
 Smooking cessation
Lifestyle modification
Exercise
BP: B blocker, ACEI
Cholesterol : LDL <100mg/dl, statin
Aspirin or CPG
Cilostazole: claudication distance 40-60%
Pentoxyphylline: blood viscosity, RBC
flexybility, blood flow & tissue oxygenation
Supportif: care feet

5
THROMBECTOMY

Eksisi trombus dari dinding

vasa (dilakukan sebagai
tambahan pada pasien
yang telah menjalani
trombolisis)
mempercepat rekanalisasi
dan revaskularisasi ke
jaringan yang mengalami
iskemia

5
EMBOLECTOMY

Mengeluarkan emboli dari dalam

lumen vasa dengan cara
membuat insisi pada dinding
vasa, diikuti insersi kateter untuk
mengeluarkan emboli

5
 BYPASS GRAFT THROMBECTOMY

Mengeluarkan trombus dari dalam lumen vasa dengan cara membuat

insisi, dilakukan bersamaan dengan pemasangan PTFE graft melewati
daerah yang teroklusi

5
KOMPLIKASI ALI
Reperfusion injury : perfusi kembali setelah periode iskemia
permeabilitas kapiler laju difusi ke jaringan >> produksi
ROS oleh sel endotel >> imbalance produksi ROS & NO di
jaringan inflammatory damage & hiperkalemia
Sindrom kompartemen : iskemia lama reperfusi kebocoran
isi kapiler ke area interstitial tekanan intrakompartemen
(>tekanan perfusi kapiler) iskemia
Gejala : nyeri iskemik (+) saat dilakukan passive stretching pada
kompartemen, pulsasi (+), kebas antara jari kaki 1 & 2 (kompresi
N. Peroneus profundus)
Diagnosis : ukur tekanan intrakompartemen (intraarterial line)
Manajemen : fasciotomy (jika tekanan intrakompartemen >20
mmHg) + alkalinisasi urin + diuresis paksa mencegah
rhabdomyolisis & deposisi myoglobin di tubulus ginjal
Re-thrombosis
Re-embolisasi
6
CHRONIC LIMB ISCHEMIA
Chronic Limb Ischemia
(CLI) adalah suatu
kondisi dimana gejala
iskemi ekstremitas bawah
GEJALA CLI
menetap selama >2
minggu, umumnya
disertai perburukan
gejala (rest pain &
Non Limb Limb ulserasi/gangren)
Threatening Threatening Lokasi tersering: A.
Femoralis superficial
(saat melewati canalis
Klaudikasio Nyeri hebat
adductorius)
Ulserasi &
intermiten pada saat tidak
gangren
betis (calf pain) beraktivitas

6
Managemen CLI

Bedah vaskular arteri perifer tungkai:

atherektomi, endarterektomi,
amputasi
Pintas vaskular (bypass grafting):
Bedah endovaskular: angioplasti
perkutan/ percutaneous transluminal
angioplasty (PTA)
Bedah paliatif: simpatektomi lumbo-
dorsalis dan thorakalis
6
PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY

Pemasangan kateter
melewati area plak
mengembangkan
balon untuk ekspansi
posisi stent fiksasi
stent menarik
kateter & balon
keluar dari lumen
vasa

6
 ATHEREKTOMI

Kateter dengan ujung

tajam dimasukkan ke
dalam arteri
mengikis plak atherom
dengan blade pada
kateter

6
ENDARTEREKTOMI

Memisahkan plak
atherom dari
dinding vasa

6
 Bypass

Surgical bypass for aorto-iliac disease. A:Aorto-bifemoralbypass.B:Ilio-femoral

bypass.C:Femoral-femoral bypass.D:Axillo-femoral bypass combined with femoral-
femoral bypass.
(Adapted from Neville RF, Deaton, DH. Lower extremity revascularization.Endovascular
AMPUTASI

Membuang bagian ekstremitas yang

tidak viable
Indikasi amputasi :
Kerusakan jaringan mayor
ireversibel (e.g. Posttrauma)
Kerusakan neurovaskular ireversibel
(e.g. Ulkus & gangrene)
Keganasan
Amputasi Minor :
1. Digital amputation pada jari
tertentu
2. Partial foot amputation
3. Disartikulasi ankle
Amputasi Mayor :
4. Below-knee amputation (BKA)
5. Disartikulasi lutut
6. Above-knee amputation (AKA)
7. Disartikulasi panggul
8. Hemipelvectomy

6
Lower Extremity

6
Upper Extremity

6
Sympathectomy

7
Sympathectomy

Dorsal T2 sympathectomy approach with Dorsal sympathectomy and

removal of T2 transverse process and removal of the T2 ganglion
proximal T3 rib.

7
 Endoscopic Thoracic
Sympathectomy (ETS)

T3 ganglion upper and

lower connections severed,
leading to retraction of the
cut edges

Alternative method: T3
GanglionResection. All
connections severed. Cut
edges of rami
Relatively frequent location of the T3
communicantes visible in
ganglion below the 3rd interstitial space,
the center of the image.
overlying the lower half of the 4th rib, its
grey communicating branch crossing the
4th rib back upwards
7
PROGNOSIS
Coexisting CAD & CVD
CAD on PAD: 1/3-1/2 based on clinical presentation
& ECG, >1/2 by coronary angiography.
1530% 5-year mortality rate and 2-6x increased
risk of death from coronary heart disease.
7580% of nondiabetic patients with mild-
moderate claudication remain symptomatically
stable. 12% developing critical limb ischemia.
2530% of patients with critical limb ischemia
survive & undergo amputation within 1 year.
Worse continue to smoke cigarettes or have DM

7
Referensi
Puruhito. Buku Ajar Primer Ilmu Bedah Toraks, Kardiak,
& Vaskular. edisi 1. 2013
Golomb BA et al: Peripheral arterial disease: Morbidity
and mortality implications. Circulation 114:688, 2006
Hankey GJ et al: Medical treatment of peripheral
arterial disease. JAMA 295:547, 2006
Hirsch AT et al: ACC/AHA 2005 guidelines for the
management of patients with peripheral arterial
disease (lower extremity, renal, mesenteric, and
abdominal aortic). J Am Coll Cardiol 47:1239, 2006
Harrisons Principles of Internal Medicine, 18th Ed.
Chap 234 Vascular disease of the extremities.