PENYAKIT ARTERI & VENA

PERIFER
BY
WINANGUN
 PENDAHULUAN
 PENYAKIT ARTERI &VENA PERIFER
PENYAKIT NON KARDIAK,  LIBATKAN
SELURUH SIRKULASI.
 SYNDROMA FATOFISIOLOGY ARTERI, VENA
DAN SYSTEM LIMPATIK.
 KELAINAN VASKULER UMUM,
 PERIPHERAL ARTERIAL DESEASE ( PAOD )
 MASALAH KESEHATAN GERIATRI
 PREVALELENSI 4,3% USIA 40TH ,14,5 % USIA >>
70TH RATA2  1,6- 12 %
 Veins
 are thin-walled vessels that transport
deoxygenated blood
from the capillaries back to the right side
of the heart

3 Layers – intima, media, adventitia

 there is little smooth muscle &

connective tissue  makes
the veins more distensible 
they accumulate large volumes of blood
 Major veins, particularly in the lower
extremities, have one-way valves
---allow blood flow against gravity
 Valves allow blood to be pumped back
to the heart but prevent it from
draining back into the periphery
OKLUSI PEMB DARAH
 PENGERTIAN
 SEMUA PENYAKIT / KELAINAN ARETRI YANG
KELUAR DARI JANTUNG DAN AORTA ILLIAKA
 TIDAK TERMASUK SYNDROMA KORONER AKUT
 PERUBAHAN STRUKTUR DAN FUNGSI PD
ARTERI
 GANGGUAN ALIRAN DARAH ARTERI DAN
ORGAN VISERAL DAN ANGGOTA TUBUH
 TERMASUK ARTERI KAROTIS, ARTERI RENALIS,
MESENTERIKA, AORTA ABDOMINALIS,
 SEMUA CABANG AORTA ILLIAKA, DAN
KEEMPAT EKTREMITAS.
 Vein Disorders
Venous Thrombosis (Superficial
and Deep Vein Thrombosis),
Thrombophlebitis,
Phlebothrombosis

Chronic Venous Insufficiency

Varicose Veins
SOURCES OF BRAIN ISCHEMIC / INFARCTION
 PATHOGENESIS
 PROSES PENYAKIT SYSTEMIK
 PENGARUH SIRKULASI MULTIPLE,
 PROSES PATOGENSEIS SYSTEMIK >>
ATHEROSKLEROSIS
 KELAINAN DEGENERATIF KRONIK,
DYSPLASIA
 INFLAMASI VASKULER/ ARTERITIS
 TROMBUS IN SITU  TROMBOEMBOLI
 VASKULITIS ARTERI BESAR, SEDANG ,
KECIL
 INCIDEN >> USIA LEBIH 40TH
 KEJADIAN TERTINGGI DEKADE 6-7
 PAP MENGENAI ARTERI BESAR
SEDANG,KECIL
 TROMBOANGITIS OBLITERANS,
FIBROMUSCULER DYSPLASIA,
 PREVALENSI ↑↑ PADA MANULA, HT, DM
DYSLEPEDEMIA,
HYPERHOMOSYSTEINEMIA
 PEROKOK DAN GGK.
 PX
 ATHEROSKLEROSIS  TUMPUKAN LAPISAN
LEMAK & KOLESTEROL ATEROMA
FIBROFROLIFERATIF & SEL BUSA
 PERUBAHAN UKURAN INTIMA DAN LUMEN
ARTERI
 STENOSIS DAN OKLUSI AKUT ARTERI
 SYNDROMA ISKEMIK KRONIK  GANGGREN
 LAMA DAN PARAHNYA DM ≈≈> PAP ↑↑.
 OKUSI ARTERI TIBIALIS MIKRO ANGIOPATI 
GG PENYEMBUHAN LUKA  GANGGREN
 Pathophysiology
 the great and small
saphenous veins are most
often involved
weakening of the vein wall
does not withstand normal
pressure

veins dilate , pooling of

blood


valves become stretched
and incompetent

more accumulation of blood

in the veins
 Kerusakan endotel

Jaringan subendotel terpapar

Adhesi tombosit

Rangsangan untuk reaksi faktor pembekuan

dan fibrinolisis
Hemostasis
 Thrombophlebitis
 inflammation of the veins caused by thrombus or
blood clot
Factors assoc. with the devt. of Thrombophlebitis
 venous stasis
 damage to the vessel wall
 hypercoagulability of the blood – oral contraceptive
use
 common to hospitalized pts. , undergone major
surgery (pelvic or hip surgery), MI
Pathophysiology
 develops in both the deep and superficial veins of
the lower extremity
 deep veins – femoral, popliteal, small calf veins
 superficial veins – saphenous vein
 Thrombus – form in the veins from accumulation of
platelets, fibrin, WBC and RBC
 Deep Vein Thrombosis (DVT)
 tends to occur at bifurcations of the deep veins, which are sites
of turbulent blood flow
 a major risk during the acute phase of thrombophlebitis is
dislodgment of the thrombus  embolus
 pulmonary embolus – is a serious complication arising from
DVT of the lower extremities
Clinical Manifestations:
 pain and edema of extremity – obstruction of venous flow
  circumference of the thigh or calf
 (+) Homan’s sign – dorsiflexion of the foot produces calf pain
 Do not check for the Homan’s sign if DVT is already known to
be present   risk of embolus formation
 * if superficial veins are affected - signs of inflammation may be
noted – redness, warmth, tenderness along the course of the
vein, the veins feel hard and thready & sensitive to pressure
Deep Vein Thrombosis (DVT)
 Varicose Veins
 are abnormally dilated veins with incompetent valves,
occurring most often in the lower extremities
 usually affected are woman 30-50 years old.
Causes:
– congenital absence of a valve
– incompetent valves due to external pressure on the
veins from pregnancy, ascites or abdominal
tumors
– sustained  in venous pressure due to CHF,
cirrhosis
Prevention
– wear elastic stockings during activities that require
long standing or when pregnant
– moderate exercise, elevation of legs
 PENYEBAB
 TERUTAMA ATHEROSKLEROSIS
 PENYAKIT DEGENERATIF,
 PENYAKIT KOLAGEN
 PENYAKIT FIBROMUSKULER DYSPLASIA
 OKLUSI KARENA MAKRO & MIKRO EMBOLI
 RUFTUR PLAK KOLESTEROL & TROMBUS
 PENYAKIT REYNAUD DAN TAKAYASU
 ATRIAL FIBRILASI / AF.
Atherosclerosis Timeline
Foam Fatty Intermediate Fibrous Complicated
Cells Streak Lesion Atheroma Plaque Lesion/Rupture

Endothelial Dysfunction
From first decade From third decade From fourth decade
Smooth muscle Thrombosis,
Growth mainly by lipid accumulation and collagen hematoma

Adapted from Stary HC et al. Circulation 1995;92:1355-1374.

 GEJALA
 GEJALA BILA OKLUSI/PENYEMPITAN >> 50%
 SAKIT KAKI / NYERI TUNGKAI SAAT JALAN 
ISTIRAHAT BERKURANG/ HILANG
 KLAUDIKASIO INTERMITEN
 G/ ≈≈ LOKASI OKLUSI/ SUMBATAN
 NYERI BETIS, TUNGKAI PAHA,
 NYERI TUNGKAI TIBA-TIBA KULIT PUCAT
 NYERI MENINGKKAT BILA UDARA DINGIN
 BERCAK SIANOSIS, PARASTESIA,
 NEKROSIS JARINGAN  GANGREN.
 STADIUM KEPARAHAN
 STADIUM I : TANPA KELUHAN,
 STADIUM II: NYERI SAAT JALAN/ KERJA

 STADIUN IIa: NYERI STELAH JALAN > 200 M

 STADIUM IIb: NYERI STELAH JALAN < 200M

 STADIUM III : NYERI WAKTU ISTIRAHAT

MALAM
 STADIUM IV: NEKROSIS JARINGAN /
GANGREN
 Clinical Manifestations
Primary varicosities – gradual onset and
affect superficial veins, appearance of dark
tortuous veins
S/sx – dull aches, muscle cramps, pressure,
heaviness or fatigue arising from reduced
blood flow to the tissues
Secondary Varicosities – affect the deep
veins
 occur due to chronic venous insufficiency or
venous thrombosis
S/sx – edema, pain, changes in skin color,
ulcerations may occur from venous stasis
 Symptoms
 Achy or heavy feeling,
burning, throbbing,
muscle cramping and
swelling.
 Prolonged sitting or
standing tends to
intensify symptoms.
 Pruritis
 Painful skin ulcers
 Varicose veins
 Varicose veins are a common
condition in the United States,
affecting up to 15 percent of
men and up to 25 percent of
women.
 For many people, varicose
veins and spider veins a
common, mild and medically
insignificant variation of
varicose veins — are simply a
cosmetic concern.
 For other people, varicose
veins can cause aching pain
and discomfort.
 Sometimes the condition leads
to more serious problems.
 Varicose veins may also signal
a higher risk of other disorders
of the circulatory system.
Callam, MJ. Epidemiology of varicose veins. Br J Surg 1994;81:167.
 Complications
 Extremely painful ulcers
may form on the skin
near varicose veins,
particularly near the
ankles.
 Brownish pigmentation
usually precedes the
development of an ulcer.
 Occasionally, veins deep
become enlarged.
 Bleeding
 Superficial
thrombophlebitis
Varicose veins
 PEMBAGIAN
 I PENYAKIT PEMBULUH ARTERI PERIFER
 1. Angioorganopati: oklusi akut, kronis, takayasu,
 aneurisma dan vistel a-v.
 2. Angioneuropati: peny Reynaud primer dan skunder,
 3. Angiolopati: arteriosklerosis, angiopati DM,
 angiopati peradangan ,gangguan bukan vaskuler.
 II.TUMOR PEMBULUH DARAH PERIFER.
 III. PENYAKIT PEMBULUH VENA: varicosis,
tromboflebitis, insufisiensi vena.
 IV. PENYAKIT PEMBULUH LIMPATIK PERIFIR:
limpangitis akut, limpangiopati kronis.
 FAKTOR RISIKO
 USIA  MAKIN TUA ↑ RISIKO
 GENETIK, KETURUNAN , FAKTOR KELUARGA
 RAS DAN SUKU
 HYPERTENSI
 DIABETES MELITUS
 HYPERLIPEDEMIA
 MEROKOK, INFLAMASI
 HYPERKOAGULASI DAN TROMBOFILIA
 GAGAL GINJAL KRONIK.
 DIAGNOSIS
 ANAMNESIS TELITI KELUHAN KLINIS ≈ OKLUSI
( KLAUDIKASIO INTERMITEN)
 PEM.FISIK:
 INSPEKSI: KULIT PUCAT DAN
SIANOSIS,INFLAMASI
 PALPASI: KULIT DINGIN, PULSASI ARTERI DAN
NADI PERIFER ↓↓ SAMPAI HILANG
 SUHU KULIT MENURUN
 AUSKULTASI: BISING ALIRAN PEMBULUH
DARAH MENGERAS KRN TURBULENSI OKLUSI.
 Diagnostic Evaluation
Noninvasive Techniques:
Doppler Ultrasonography
Duplex Venous Imaging
Impedance Plethysmography
Invasive Techniques
I-labeled Fibrinogen Scanning
Contrast Phlebography
 Perforating veins
 Penetrate the deep
fascia, tributaries of the
saphenous veins, valves
are located just distal to
penetration of the deep
fascia.
 Veins cross the deep
fascia obliquely
 Muscle contraction
causes the valves to
close prior to venous
compression so blood is
forced proximally
(musculo-venous pump).
 Overlap of Vascular Disease in
Patients With Atherothrombosis
Ischemic stroke Unstable angina MI PAD

Platelet
Plaque Thrombus
adhesion,
rupture formation
activation, and
aggregation

Vascular events (MI, stroke, or CV death)

Ness J, Aronow WS. J Am Geriatr Soc. 1999;47:1255-1256. Schafer

AI. Am J Med. 1996;101:199-209.
 Atherosclerotic Plaque
Stable Unstable

Lumen

Endothelium
Thrombus
Platelets

Lipid Rich Core

Thick Thin
Fibrous Cap Fibrous Cap

Falk E et al. Circulation. 1995;92:657–671.

 Formation of the Platelet Plug
1 Adhesion 3 Aggregation
Activated Gpllb/llla
Fibrinog
en

Platelets von Williebrand

Factor/Gplb bind

Collagen
Gpla/lla bind
Lipid
core

2 Activation 4 Platelet Plug

Thrombin
ADP

5 HT

TXA2

Kumar A et al. Exp Opin Invest Drugs. 1997;6:1257–1267.

 Atherosclerosis and Thrombus
Formation
 Thrombosis
Formation I –
Platelet
Activation
 Picture
 Lateral carotid angiogram in a patient who
had recent TIAs
OKLUSI PD OTAK
 PEM. PENUNJANG
 ANKLE BRACHIAL INDEX.
 RASIO TD SYSTOLIK BRACHIAL DG
TUNGKAI
 MENURUT ADA/ACC : AMERICAN DIABETIC
ASSOCIATION
 0,91 - 1,3 : NORMAL
 0,90 - 0,8 : ringan
 0,79 - 0,5 : sedang
 << 0,5 : berat.
 penunjang
 SEGNEMNTAL LIMB PRESURE & PULSE
VOLUME RECORDING
 DIUKUR DG PLAETHYSMOGRAPHIC CUFFS
 INTERPRESTASI ≈≈ ABI.
 ANALISA PERUBAHAN KONTOUR NADI
DAN AMPLITUDO
 GELOMBANG LANDAI PUNCAK DAN
PULSASI LEBAR
 AKURASI DIAGNOSTIK 97 %.
 PENUNJANG
 EXERCISE STRESS TEST
 KOMBINASI PRE DAN POST AKTIVITAS TES
 MENILAI PAP DAN PSEUDO
KLAUDICASION
 KOMBINASI TES DG ABI.
 DUPLEX ULTRA SONOGRAFI
 USG DOPLER DG KECEPATAN ALIRAN 
OPERASI
 MAGNETIC RESONANCE ANGIOGRAPHY
  KHUSUS DIAGNOSE RADIOLOGY PAP.
 PENUNJANG
 OSILOGRAFY: perbedaan tekanan dan volume
pulsasi ektremitas
 PLETISMOGRAFY : pengukuran kantitatif volume
aliran pembuluh darah arteri.
 EKO DOPPLER: dg doppler membandingkan
tekanan brachial dan tungkai bawah . Perbedaan >
20 mmHg  gg aliran
 SKINTIGRAFI RADIO ISOTOF: dg zat radioaktif
xenon 133.
 ARTERIO GRAFI KONTRAS: dimasukkan kontras
 rontgen
 Picture
 Longitudinal sonogram
OKLUSI ARTERI RENALIS
 TATA LAKSANA
 ATASI KEGAWATAN DAN SESUAI KAUSA.
 KASUS AKUT 7-10 HARI  TROMBOLISIS
 GUNA MENCAIRKAN BEKUAN DARAH (
CLOT)
 TROMBOLITIK : STREPTOKINASE,
UROKINASE, Rtpa, MAUPUN EMINASE.
 KONSERVATIF: tungkai saskit lebih rendah,
bungkus kapas/verban, dan analgetik.
 MEDIKA MENTOSA GAGAL  OPERATIF.
 MODALITAS TERAPI
 SUPORTIF, PENUNJANG, TNDAKAN UMUM

 ANTI KOAGULAN CEGAH EMBOLI DAN DVT (DEPP VEIN TROBS)

 HEPARIN 5000 U/ 12 JAM, FRAXIFARIN, WARFARIN.

 ANTI PLATELET: SINTROM ATAU ASPIRIN 160 MG / HARI.

 TINDAKAN KHUSUS: TROMBOLITIK MELISIS TROMBUS

 STREPTOKINASE 1,5 JT UNIT, HEPARIN 5000 UNIT, ATAU R TPA.

 TINDAKAN LAIN:
 REHABILITASI MEDIS PENDERITA.
 Obat - Obat Antiplatelet

 Thromboxane A2 inhibitor
– Acetylsalicylic acid (ASA)
 Phosphodiesterase inhibitor
– Dipyridamole
 Glycoprotein (GP) IIb/IIIa blockers
– Parenteral: abciximab, eptifibatide, tirofiban
 ADP-receptor antagonists
– Clopidogrel ( Plavix )
– Ticlopidine ( Ticlid , Agulan , Ticuring )
 Medical Management
Superficial thrombophlebitis
 bed rest with legs elevated
 apply moist heat
 NSAID’s ( Non – steroidal anti-inflammatory drugs) - aspirin
Deep vein thrombosis
 requires hospitalization
 bed rest w/ legs elevated to 15-20 degrees above heart level
( knees slightly flexed, trunk horizontal (head may be raised) to
promote venous return and help prevent further emboli and
prevent edema
 application of warm moist heat to reduce pain, promotes
venous return
 elastic stocking or bandage
 anticoagulants, initially with IV heparin then coumadin
 fibrinolytic to resolve the thrombus
 vasodilator if needed to control vessel spasm and improve
circulation
 Surgical Intervention
indicated or done for prevention or relief of
edema, for recurrent leg ulcers or pain or for
cosmetic purposes
Vein ligation and stripping
 the great sapheneous vein is ligated (tied)
close to the femoral junction
 the veins are stripped out through small
incisions at the groin, above & below the
knee and at the ankles.
 sterile dressing are placed over the incisions
and an elastic bandage extending from the
foot to the groin is firmly applied
Vein ligation and stripping
 Recommended Initial Antiplatelet Therapy for Patients With
Transient Ischemic Attack or Ischemic Stroke and Subsequent Therapy
for Recurrent Ischemic Events & pad

Transient Ischemic Attact (TIA)

or Ischemic Stroke

Yes Coronary Artery No

Disease (CAD)
Present?

Aspirin Plus
Aspirin Clopidogrel† Aspirin Clopidogrel† Extended-Release
Dipyridamole‡

Recurrent Recurrent
Recurrent Recurrent Recurrent
TIA/Stroke TIA/Stroke ACS ACS ACS
TIA/Stroke TIA/Stroke TIA/Stroke
or ACS or ACS

Clopidogrel Clopidogrel
Aspirin and Aspirin and Aspirin and Aspirin and Aspirin and Clopidogrel
or or
Clopidogrel Clopidogrel Clopidogrel Clopidogrel Clopidogrel or
Aspirin and Aspirin and or Aspirin and
Clopidogrel Clopidogrel Aspirin and Clopidogrel
or Axtended-
Aspirin and Release
Axtended- Dipyridamole‡
Release
Dipyridamole‡
Abbreviations: ACS indicates acute coronary syndrome; TIA, transient ischemic attack.
*Per the Antithrombotic Trialists’ Collaboration.2
†Per the CAPRIE Steering Committee.21
‡Per Diener et al24 and De Schryver et al.28
JAMA, October 20, 2004—Vol 292, No. 15
TROMBOANGIITIS OBLITERAN/(BUERGER
DESEASE)

 OKLUSI ARTERI SEDANG & KECIL. 

TROMBOFLEBITIS SUPERFISIALIS
REKUREN
 >> LAKI 20-40 TH, PEROKOK,
 EKTREMITAS ATAS, BILATERAL
 TIDAK ADA TANDA2 ATEROSKLEROSIS
 BISA OKLUSI TOTAL DAN KOLATERAL
BURUK
 HILANG & TIMBUL BILA MEROKOK
 PENYAKIT TAKAYASHU
 PAN ARTERITIS TAK SPESIFIK
 OKLUSI AORTA TORAKALIS, ABDOMINALIS,
SEGMENTAL CABANG BRACHIOCEFALIKA
 PENYEBAB PASTI???
 KASUS >> WANITA 20-40TH
 KAICHIRO MENYEBUT OTAP ( OKLUSIF
TROMBOAORTOPATHY)
 STADIUM I: OTAP TANPA KOMPLIKASI
 STADIUM II: OTAP DG MONO KOMPLIKASI
 STADIUM III: OTAP DG MULTI KOMPLIKASI
  sembuh spontan pada stadium I
 Angioneuropati( RAYNUD)
 GANGGUAN PEREDARAN DARAH FUNGSIONAL
 KONSTRIKSI UJUNG PEMBULUH DARAH
 GEJALA KULIT>>: AKRAL DINGIN, KUTIS
MARGINATA, HYPERHYDROSIS

 ETIOLOGY: GG PERSARAFAN DAN HORMONAL

 ISKEMIA AKIBAT RANGSANGAN DINGIN.
 SIFAT SIMETRIS,
 STENOSIS ATAU OKLUSI PEMBULUH DARAH
AKRAL
 DAPAT HILANG SETELAH BEBERAPA TAHUN.
 Who gets Sclerotherapy
 Who else
– Good control with Trendelenburg
– Recurrent veins
– Frail with resistant/healed ulcers

O'Donnell, TF Jr. The present status of surgery of the superficial venous system in the
management of venous ulcer and the evidence for the role of perforator interruption. J Vasc
Surg 2008; 48:1044.

Galland, RB, Magee, TR, Lewis, MH. A survey of current attitudes of British and Irish vascular
surgeons to venous sclerotherapy. Eur J Vasc Endovasc Surg 1998; 16:43.
 Microsclerotherapy

 30 g butterfly needle
 0.2% STS
 Several courses required
benefit compression
Endovenous Laser
 Surface laser therapy
 Telangiectasias,
reticular veins and
small varicose veins
<5mm
 Not used for larger
varicose veins
Subfascial endoscopic perforator
vein ligation (SEPS)
 Contraindications
 Systemic illness
 Tortuous vein
 Hypercoagulable state
 Pregnancy
 Obstructed Deep veins