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/AnginaDiminished 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 rhythmb. Checking of bilateral arm blood pressurec. Neck auscultation for carotid bruitsd. Cardiac auscultation for arrhythmia gallops, and mur

mure. Abdominal palpation for an aortic aneurysmf. Abdominal auscultation for bruitsg. Palpation of peripheral pulsesh. Auscultation of the femoral region for bruitsi. 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 Trendelenburg’s test

- A soft rubber tourniquet is applied to the

leg just below the knee and patient stand’s

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 syndromeIrregular thickened area’s 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 hemorrhage2. A Pale, cool and pulseless extremity3. Penetrating wound adjacent to a major versel4. A major nerve injury5. Fractur & dislocation6. Large hematoma7. 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

Buerger”s 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 Extremity……………24% Lower Extremity……………39% Upper & Lower Extrimity….22%.. Thrombophlebitis…………………...43%. Raynaud s phenomenon…………..49%. Sensory findings……………………77%.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 embolismStasis of blood flow, endothelial injury &/or

hypercoagulabilityRisk factors

○ Surgery, pregnancy, ulcerative colitis, heart failure○ Immobility

Assessment Asymptomatic Calf or groin tenderness & pain Sudden onset of unilateral swelling Pain upon dorsiflexion (Homan’s sign)

not recommended Warmth & edema at site Diagnostics

Doppler flow studyVenogramMRI

Interventions

Non-surgicalRestAnticoagulants

○ Heparin○ Lovenox○ Coumadin

Thrombolytic therapy○ T-PA

Platelet Inhibitors○ Reo-pro

SurgicalPrevent Pulmonary

EmbolisInferior Vena Caval

Interruption○ “Umbrella”○ Greenfield filter

Ligation or External Clips○ Abdominal Laparotomy