ARIF ZUHAN, SANTYO W

Surgery Dept, Faculty of Medicine

Mataram University
2010
1. Arterial Disease

2. Venous Disease

1. Arterial Disease

I. Arterial wall Anatomy
Three Layer

BASIC CONSEPTS
The intima : - Collages
- Elastic fibers


The Media
Smooth muscle
Collagens
Elastic Fibers
The Adventitia
Collagens
Elastic Fibers
II. ARTERIAL DISEASE
TWO TYPES OF ARTERIAL DISEASE
A. OCCLUSIVE DISEASE
B. ANEURYSMAL DISEASE
ETIOLOG Y OF ARTERIAL DISEASE :
The etiologi of most arterial disease today is
ATHEROSCLEROSIS
Atherosclerosis is a combination of changes in
the intima and media (WHO).
The changes include focal accumulation of
lipids, hemorrhage, fibrous tissue and calcium
deposite.
PATHOGENESIS OF ATHEROSCLEROSIS
RISK FACTOR THE ATHEROSCLEROSIS
Major :
1. Tobacco (cigarette)
2. Diabetes mellitus
3. Hyperlipidemia
4. Fibrinogenemia
5. Age
6. Hypertensi.
Minor :
1. Male gender
2. High fat diet
3. Hypercoagulable states
4. Excessive alcohol
5. Non white race
The development of atherosclerotic
There is three major stages :
1. Early lesions : usually appear as fatty streaks in childhood or
young adult life.Their content is primarily lipid , they also contain
macrophage infiltration and some smooth muscle.
2. Fibrous plaques : appear in later life . The fibrous plaques have
a lipid core surrounded by a capsule of elastic and collagennous
tissue.
3. Complicated lesions : development of fibrous plaques.
Necrosis of the plaque may lead to surface ulceration.Thrombi tend
to occure at these ulcerated sites.Intramural hemorrhage also may
accor , with or without ulceration.The elasticity of the arterial wall is
lost as local calcifications accumulate. The atherosclerotic prosess
may narrow the vessel lumen or the wall may degenerated and
dilate , forming an aneurysm.

OCCLUSIVE DISEASE
Symptoms become by gradual occlusion of blood flow.
Symptoms occur when a critical arterial stenosis is reached.
Blood flow and pressure are not significanly diminished until at least
75 % of the cross-sectional area of the vessel is obliterated or
equally with a 50% reduction in lumen vessel diameter.
Factors other who influence critical arteial stenosis :
- Length stenosis
- Blood viscosity.
- Peripheral resistance.

OCCLUSION >50%
Pressure and blood flow drop because there is
the turbulence occurs in post stenosis
Pain/Angina
Diminished or absent pulses
Intermilten claudication
(Exercise Pain)
(Not total occlution)
(More than 50%)
Rest Pain
(Total Occlution)
III. EVALUATION
A. Initial patient evaluation

Preliminary diagnosis
- Simple interviewing
- Simple examination

Urgency for treatment
Need live saving or limb saving
B. GENERAL EXAMINATION
a. Checking of heart rate and rhythm
b. Checking of bilateral arm blood pressure
c. Neck auscultation for carotid bruits
d. Cardiac auscultation for arrhythmia gallops, and mur
mur
e. Abdominal palpation for an aortic aneurysm
f. Abdominal auscultation for bruits
g. Palpation of peripheral pulses
h. Auscultation of the femoral region for bruits
i. Inspection of the leg and feet for ulcers, gangrene and
microembolic phenomena

C. Non Invasive Vascular Testing
1. Vascular laboratory
2. Intrumentation
- Doppler ultrasound
- Plethysmography
- Duplex Scanning
- Transcutaneus Oximetry
- Treatmil
D. INVASIVE VASCULAR TESTING
- arteriografi
B. ANEURYSMAL DISEASE
Aneurysm are the Result of degeneration and weakening
of the network of protein fiber in the arterial wall
Pathophysiologie :

- Aging and natural degeneration of elastin
- Increased proteolytic enzyme activity
- Atherosclerotic damage to elastin and collagens
- Genetic abnormality in collagens
Rupture aneurism is emergency case and finally pasien
dead. Rupture occurs if the the intraluminal pressure
exceeds the tensile strength of the wall.
The etiology of the this wall degeneration and the
mechanisms of it dilation and rupture are not fully
understood.
The risk of aneurysm rupture increases with increased aneurysm
size.The stress in the vessel wall increases as the vessel diameter(d)
enlarge,and wall thickness (t) decrease. Wall stress is also proposional
to intraluminal pressure (P). Stress = P x d/t

Clinical examination
- Asymthomatic
- Pulsatile mass

Supporting examination
- MRA (Magnetic Resonance Angiografi)
- Arteriografi

Management
-Operatif
Penderita sering merasakan denyutan di perutnya.
Aneurisma bisa menimbulkan nyeri, terutama
berupa nyeri yang menusuk dalam di punggung.
Nyeri bisa menjadi berat dan biasanya menetap,
tetapi perubahan posisi badan bisa mengurangi
rasa nyeri ini.
Pertanda awal dari pecahnya aneurisma biasanya
adalah nyeri yang luar biasa di perut bagian
bawah dan punggung dan nyeri tumpul di atas
aneurisma.
Pada perdarahan dalam yang berat, penderita
bisa jatuh ke dalam keadaan syok.
Pecahnya aneurisma abdominalis sering berakibat
fatal.



KASUS
SEORANG Lk, 57
thn, riwyt 3 thn y.l
tungkai bawahnya
terkena clurit, luka
berdarah, Lalu dijahit.
Luka sembuh. 1 thn
kemudian timbul
benjolan berdenyut
dan makin
membesar.
Durante Op
Terdapat robekan pada
arteri tibialis.

Tindakan ; Repair arteri.

Hasil : Baik
VENOUS DISEASE
Basic concept
Anatomy
a. Valves : - Bicuspid
- Opening blood flow toward the heart
- Closing to prevent reflux
- More number in lower leg, single valve is
found in external iliac or common femoral
vein. Inferior vena cava is valve less
b. Layer : They have three wall layers but the composition
and function different w/ artery

These differences include
1. Relatively thin wall
2. Less elastic tissue
3. A media that is predominantly smooth muscle
4. Adventitia composed of collagens and elastic
vascularisation by diffusion from the blood
stream
The vein can be divided into a superficial and deep
system.
Superficial system or surface system has relatively
thick-walled and muscular vein.
Deep vein system are thinner and occompany arteries.
Communicating veins perforate the muscle fascia to
connect the deep and superficial system.
c. Musculovenous pump mechanism
Leg muscles contract blood is propelled toward the heart
The major reservoir are the soleus and gastrocnemius
sinusoida
ETIOLOGY OF THE VENOUS DISEASE.
A. Varicose veins.
B. Venous thrombosis.
C. Pulmonary embolism.
D. Postphlebitic syndrome.
A. Varicose veins
Accur when the valve cups of the saphenous system fail
to close and structure integrety of the vein weakness.
Many patiens have familial predisposition.
In other cases , the valvular incompetence is acquired
after venous thrombosis has damage the valve.
Arteriovenous shunts may be can result of varicose
veins.

B. Venous thrombosis
Etiology :
1. Venous stasis , in an immobile extremity has been
assosiated with deep vein thrombosis , the mechanism of
clot formation has been unclear.
2. Endothelial injury .
3. Hypercoagulability , shortened platelet survival or
increased platelet adhesiveness has been demonstrated in
patiens with recurrent venous thrombosis.
C. Pulmonary embolism.
The etiology of pulmonary thrombi most commonly is
embolism from lower extremity clots.


D. Postphlebitic syndrome.
The leg edema, stasis dermatitis, and ulceration appear to be
related to chronic venous hypertension in the superficial veins. Its
direct result of incompetent deep venous valve the poplitea
segment and incompetent communicating veins.
Pathophysiology of venous disease
Two factors : - Valve insufficiency
- Vein obstruction
a. Normal situation
The Musculocutaneus pump push blood from the
superficial system trough the communicating veins and
propels it via the deep system toward the heart. And
baseline pressure in foot vein, drop approximately 70%.
b. Varicose vein
Pressure drop only 30-40% , so 30-40% refluxed into the
saphenous veins and back down.
Varicose veins
c. Venous trombosis

The basic problem in venous thrombosis is obstruction of
venous out flow.

In the supine position, venous pressure in acute thrombosis about
twice normal at the foot level. If the patient is standing , the venous
pressure is only mildly elevated,but it changes minimaly with
exercise
Examination of the venous system
Venous disease usually is localized to one anatomic area.
The lower extremities most commonly are
involved,althoegh significant venous problems can
impair function of the uppe extremities.

!. Upper extremities : Acute or chronic obstruction of the
axillary or subclavian veins constitutes the main
serious venous disorder of the arms.
a. Inspection.
b. Palpation.
c. Auscultation


B.. Lower extremities.
A. Inspection.
B. Palpation
C. Auscultation.
Inspection

a. Varicosities : - Dilated greather saphenous vein
- Competent / incompetent perforating vein

Trendelenburgs test

- A soft rubber tourniquet is applied to the
leg just below the knee and patient stands
If the lower leg varicosities fill slowly with
torniquet in place but than dilated suddenly
when torniquet is released, the greater
saphenous valve are incompetent.

b. Acute deep venous trombosis
- Extremity swelling

c. Post plebitis syndrome
Irregular thickened areas of brownish skin
pigmentation appear around the ankle.


Palpation
a. Vericosities
b. Deep vein thrombosis
c. Post phlebitis syndrome
VASCULAR TRAUMA
Mechanism of injury
a. Penetration wounds
b. Blunt trauma
to couse vascular injury by severel mechanism :
1. Fracture fragments
2. Fracture dislocation

RECOGNITION
The early diagnosis and repair of vascular injury is esential to
preventing serious hemorrhage and to preserving limb or organ
function.

The following sympthoms and signs should raise suspicion of
arterial or venous demage :

1. External hemorrhage
2. A Pale, cool and pulseless extremity
3. Penetrating wound adjacent to a major versel
4. A major nerve injury
5. Fractur & dislocation
6. Large hematoma
7. A bruit or machinary mur mur at or near an injury side
Initial care
Time from vascular injury to repair is a critical in gredient in
succesfull out come (within 6-8 hours)
1. Hypotension ABC
Resuscitation
II. Fracture Splinted
Dislocation Reduced
III. Tetanus prophylaxis and intra venous antibiolic
IV. Radiographs should be order
V. When a localized penetrating injury is associated with
hemorhage, expanding hematoma or absence of distal
pulses no spesific diagnostic test are necessary.
Patient needs operating room.
VI. Arteriography as soon as possible
Buergers disease
(Tromboangitis obliterans)
Etiology : unkown.
TAO is inflamatory process involving the medium and
small artery.
The age onset is usually between 35 to 50 years old.
Risk Factor : heavy smoker.
Usualy a male.

Signs and Symptoms
Intermittent claudication.70 %.
Rest pain...91%
Ischemic ulcers:
Upper Extremity24%
Lower Extremity39%
Upper & Lower Extrimity.22%.
. Thrombophlebitis...43%
. Raynaud s phenomenon..49%
. Sensory findings77%
.Abnormal Allen s test.71%
Laboratory & Imaging
Studies.
Complet blood count, blood urea nitrogen,glucose
tolerant test & lipid profil.
Imaging studies:
-Duplex Ultrasonography.
-M.R.A
-Arteriographic.
Diagnostic Criteria
Major criteria : Onset of distal extremity
ischemic symptoms before 45-50 years old,tobaco
abuse, undisease arteries proximal,objective
documentation of distal occlusive disease by
arteriographic.
Minor criteria :
-Superficial plebitis.
-Raynauds syndrome
-Instep claudication.


Treatment.
Have the patient stop smoking.
Advis the patient to avoid passive smoking.
Treat local ischemic ulcerations and pain.
-Food care:-lubricate skin with lanolin
base cream.
-Lambs wool between toes.
-Avoid trauma.
-Trial of calcium channel blockers, antiplatelet
agent,and pentoxyfylin.
-Analgesics.
-antibiotics and non steroid anti-inflammatory for phlebitis.
. Surgery : sympathectomy , by pass , or amputate.

Acute Limb Ischemia.
Incidence : 1.7 cases per 10.000 per
years.
Etiologic : thrombosis , embolism ,
arterial trauma and dissection.

Essentials of diagnosis.
Pain, pallor , paresthesias , paralysis
,pulselessnes , poikilothermias (6 Ps).
Severe of signs and symtomes depend on
the adequasy of the preexisting collateral
circulation and durationof the ischemic
insult .
Decreased sensation on the dorsum of the
foot and loss of greattoe or ankle
dorsoflextion in advanced ischemia.

Imaging studies.
Duplex sonografi.
Arteriography.
Magnetic resonance angiography (
MRA)
Echocardiography.
Treatment.
Should be treat before or at 6 hours.
Patients with acute limb ischemia may
be categoriezed into 3 groups : 1. with
minimal ischemia , 2. with moderate
ischemia , and 3. with advanced
ischemia.
Minimal ischemia : heparinization.
Moderate ischemia : heparinization and
urgent embolectomy.
Advanced ischemia : amputation
Prognosis
Duration of symthoms was less than 6-12
hours : mortality rate is 19 % and limb
salvage rates is 93%.
Duration of symthoms was greater than 12 to
48 hours : mortality rate increase to over
31%, and limb salvage rates is 78%.
Delay treatment is significant prognostic
factor for both limb salvage and mortality.
VARICOSE VEINS
Insidence : 15% of the adult populations.
Risk Factor : family history,age (50 years or
over),female,multiparity,oral
contraceptive,standing vocation (over 6
hours/day),and obesity.
Two types : primary varicosities
secondary varicosities.
. Primary varicosities : congenital ( loss elasticity in
vein wall and absent of venous valve).
. Secundary varicosities : venous valve have been
damaged by trauma,deep vein thrombosis, or
inflammation.

Pathophysiology
There are several theories :
1.Arteriovenous Communications.
2.Valvular incompetence.
3.Incompetence of perforating Veins.
4.Defect in Structure of vein wall.
5.Secondary varicose veins
6.Congenital valcular malformations
Essentials of Diagnosis
Dilated , tortuous superficial veins in lower
extremities.
May be asymptomatic or may be
associated with bleeding,localize
pain,nocturnal cramps, or aching
discomfort and heaviness with prolonged
standing.
Pigmentation,ulceration , and oedema.
Telangiectasias ( small spider- like clusters
of venulae.
Treatment
A . Medical treatment.
The patient should be instructed to avoid:
-prolonged standing,prolonged sitting
obesity,and constricting garment.
The patient is intructed :
-Shower in the evening.
-Below-the-knee support stockings
-Elevated the feed 10-15 minutes,3-4 time
daily.
-Walk to improve the musculocutaneus pump
-Avoid trauma to varicose veins.
Sclerotheraphy
Surgical therapy
Surgical treatment
Indications : Severe aching
varicosities,varices vein
hemorrhagi,superficial tromboplebitis.
Option for surgical therapy:
-Ankle to groin saphenous vein
stripping.
-Segmental saphenous vein stripping.
-Saphenous vein ligation.
-Phlebectomy.

PEMANJANGAN
PELEBARAN
BERKELOK-KELOK
SISTEM VENA DAN
TERDAPAT GANGGUAN
SIRKULASI DARAH
DIDALAMNYA
DUA FAKTOR UTAMA VARICES
TEKANAN HIDROSTATIS
HAMBATAN ALIRAN DARAH DIPROKSIMAL
JENIS VARICES :
1. VARICES TRUNKAL
2. VARICES RETIKULARIS
3. VARICES KAPILARIS
EMPAT STADIUM VARICES
1. PEGEL LINU
2. VENEKTASI
3. VARICES MASIF
4. ULKUS VARIKOSUM
PENANGANAN
1. PENGOBATAN
2. OPERASI
Deep Vein Thrombosis
Thrombophlebitis
Thrombus with inflammation
Deep vein thrombosis
risk for pulmonary embolism
Stasis of blood flow, endothelial injury &/or
hypercoagulability
Risk factors
Surgery, pregnancy, ulcerative colitis, heart failure
Immobility

Assessment

Asymptomatic
Calf or groin tenderness & pain
Sudden onset of unilateral swelling
Pain upon dorsiflexion (Homans sign)
not recommended
Warmth & edema at site
Diagnostics
Doppler flow study
Venogram
MRI
Interventions
Non-surgical
Rest
Anticoagulants
Heparin
Lovenox
Coumadin
Thrombolytic therapy
T-PA
Platelet Inhibitors
Reo-pro
Surgical
Prevent Pulmonary
Embolis
Inferior Vena Caval
Interruption
Umbrella
Greenfield filter
Ligation or External Clips
Abdominal Laparotomy