Arterial occlusive disease
Classification; Vollmar-Ratschow  1.Angioneuropathies ; vasomotor disturbancies Raynaud disease  2.Arterial oclusive diseases

1. Predominantly degenerative (aorto-iliac

disease periferic arteriopathies )  Predominantly inflamatory – trombangeitis obliterans- Buerger disease.

3. Angiolopathies – cell changes in terminal vessels acrocyanosis , erithromelalgia .

Atherosclerotic plaque

Arterial occlusive disease

Caracterisation 1. First stenosis second oclusion 2. “Multilevel disease” 3. Colateral circulation developpement

Collateral Circulation
Collateral vessels develop from the

distributing branches of large and medium sized arteries. Anatomically, as well as functionally, it is convenient to divide the collateral bed into stem arteries ,midzone collaterals and re-entry arteries These vessels are generally preexisting pathways that enlarge when a stenosis or an occlusion develops in a main artery supply and do not represent neovascularization

Arterial occlusive disease Complications due to the plaque

Trombosis –

acute (acute ischemia ) chronical (circulatory

Ulceration – emboli –acute

compensated )

ischemia Hemorage in the plaque – obstruction acute ischemia

Fontaine Classification
Stage I : well compensated –

asymptomatic Stage II: Insufficiency during exercise (intermittent claudication)
II-A – IC more than 250 m II B – less than 250 m

Stage III : rest pain Stage IV : Anoxic tissue damage

(necrosis , ulcer).

Intermittent claudication
It consists of three essential features:
the pain is always experienced in a functional

muscle unit; it is reproducibly precipitated by a consistent amount of exercise  it is promptly relieved by merely stopping the exercise

Intermittent claudication

1. High type – pain in buttocks 2. Medium type – pain in ankle 3. Distal type – pain in foot

Chronic limb ischemia and associated physical findingsRutherford classification
 Category .

Clinical description . Objective criteria.  0 .Asymptomatic with no hemodynamically significant occlusive disease. Normal treadmill or reactive hyperemia test  1. Mild claudication Completes treadmill exercise. AP after exercise >50 mmHg but at least 20 mmHg lower than resting value  2 .Moderate claudication .Between categories 1 and 3  3. Severe claudication Cannot complete standard treadmill exercise and AP after exercise is <50 mmHg

Chronic limb ischemia and associated physical findingsRutherford classification
4 Ischemic rest pain Resting AP <40 mm

Hg, flat or barely pulsatile ankle or metatarsal pulse volume recording (PVR); Toe pressure (TP) <30 mm Hg 5 .Minor tissue loss-nonhealing ulcer, focal gangrene with diffuse pedal ischemia Resting AP <60 mm Hg, ankle or metatarsal PVR flat or barely pulsatile; Toe pressure (TP) <40 mm Hg 6 Major tissue loss-extending above transmetatarsal level, functional foot no longer salvageable Resting AP <60 mm Hg, ankle or metatarsal PVR flat or barely pulsatile; Toe pressure (TP) <40 mm Hg

Stage IV:

Critical limb ischemia (CLI):
–pacient experience pain for 2 weeks - Superficial lesions of gangrene

Sistolic Index < 50 mm Hg la nondiabetic Sistolic Index< 30 mm Hg diabetic people

ankle-brachial index (ABI)
 The ankle-brachial index (ABI) is commonly used

to gauge the severity of disease in patients with chronic arterial insufficiency.  A standard blood pressure cuff is applied to the calf and inflated above systemic pressure. It is then slowly deflated while monitoring continuous-wave Doppler signals in the foot. The pressure at which a signal first appears is the systolic pressure within the interrogated artery.  The measured pressure is then normalized by dividing by the systolic blood pressure in the arm, yielding the ABI.  Measurement of the ABI is useful in grading patients with lower limb ischemia Patients with claudication have an index that usually ranging from 0.5- 0.8 while patients with rest pain tend to have ABIs of 0.3-0.5. Indices less than this are frequently seen with ischemic ulceration or gangrene.

Physical Examination and Adjunctive Testing
Routine evaluation of patients with

vascular disease should include
a thorough physical examination with

noninvasive vascular testing. A search for cervical bruits, precordial murmurs, and pulsatile masses or bruits in the abdomen is mandatory

Physical Examination and Adjunctive Testing
 The examination of the lower extremity includes

inspection, palpation, and auscultation.  1. Inspection of the legs and feet may reveal
 loss of hair on the distal aspect of the leg,  muscle atrophy,  color changes in the leg relative to position,  and ulcers or gangrene.

 Patients with severe disease may exhibit

Buerger’s Sign (also known as dependent rubor), wherein dependency of the foot causes it to appear red and engorged .  Although speculative, it is thought that the finding is generated by pooling of oxygenated blood in the maximally dilated arteriolar beds distal to an arterial occlusion.

Physical Examination and Adjunctive Testing
2.Palpation of peripheral pulses is an

integral part of the physical examination of the vascular patient. Reliable sites include the carotid, radial, femoral, dorsalis pedis, and posterior tibialis positions. 3. Auscultation : femoral artery , carotis artery!!!!!! : the presence of a bruit stenosis more than 50% of the artery.

Samuel test

Arterial Ulcer

Noninvasive –
Doppler ultrasound Treadmilll test MRI CT scan


Doppler ultrasound
Patients without palpable pulses should be

examined with continuous wave, usually via a hand-held instrument.  The Doppler probe emits 2-10 MHz ultrasonic waves which are reflected by flowing red blood cells and detected by a receiving crystal.  The audible frequency shift between the transmitting and receiving crystals is proportional to the velocity of the moving particles and provides a qualitative assessment of the degree of stenosis.

Echo Doppler bidirectional

Doppler bidirectional –masurare IBG

Treadmill test

Spectral signal

Anatomy of the wall

Duplex: 1. Doppler 2.Echography

Spectral signal

Anatomy of the wall

right comon iliac stenosis

Right comon iliac stenosis
arteriography duplex

Angioplasty and control
angioplasty control

Angioplasty and control

The functioning of a by pa

Calcificare de intima

Mediocalcinoza la diabetici

1. Invasive method 2.Give Precise Informations 3. Seldinger technique

CO2 angiograhpy

MRI Image

Tridimensional reconstruction CT -scan

Claudication is a relative benign sindrom

At 5 years

Factors influencing the developing of (critical leg ischemia=CLI)

Stage I si II -A
 medical treatment

Stage II -B, III si IV
Medical and

invasive/surgical treatment

 Exercise therapy - along with risk factor

modification, especially smoking cessation, should be the initial management of all patients with nondisabling intermittent claudication Antithrombotic therapy –Aspirin, 75 to 325 mg daily Lipid lowering

1 every exercise -30 min  2. 3 times a week

3. Walking stilll pain apear  4. At least 6 months Gardner AW et al. JAMA 1995;274:975980

Pharmacological drugs –vasodilators and antiagregants

buflomedil (Loftyl) naftidrofuryl

(Praxilene) pentoxifylline (Torental)

Antiplatelets drugs
Dipiridamol<ASA<Ticlopidine <Clopidogrel


PLAVIX - 1 tb /zi -

Percutaneous Intervention
 Percutaneous transluminal angioplasty

(PTA) with or without stent placement is a useful modality for the treatment of selected isolated iliac, femoral and popliteal stenoses.  The goal of treatment is to achieve clinical success as measured in improved walking distance, resolution of rest pain, or healing of ulcers or partial foot amputations for limb salvage.  The benefits of PTA compared to surgical intervention include less invasion, less cost, and, possibly, a lower incidence of procedural complications.

Percutaneous Intervention
 Percutaneous intervention has become the

treatment-of-choice for isolated iliac stenosis .  Its long-term success depends on indication, lesion severity, runoff, and lesion location, and overall five-year patency rates range from 53-77%.  Angioplasty of the superficial femoral and more distal arteries is less durable.  The initial success rate of 75% falls to approximately 50% at two years, depending on patient selection and indication.  Angioplasty of the infrapopliteal and tibial vessels should probably be reserved for poor risk patients as only 40-50% remain patent after one year.

The choice of surgical procedure depends on the level of arterial disease.
Aortoiliac disease

Trombendarterectomy  (2) Aortofemoral bypass is preferred by most
 (1)

surgeons to endarterectomy, but the results of endarterectomy in skilled hands are equivalent to bypass ; aortofemoral and infrainguinal bypass) are satisfactory when this procedure is performed in selected patients

 (3)

Multilevel bypass (simultaneous


(axillofemoral, femorofemoral) are satisfactory alternatives to aortofemoral bypass in patients with increased operative risk or other contraindications to aortic surgery.

4)Extra-anatomic bypass procedures

The choice of surgical procedure depends on the level of arterial disease.
Infrainguinal bypass

(1) Intact greater saphenous vein is the conduit of choice for infrainguinal bypass.  (2) Dacron or PTFE Syntetic grafts  (2) HUV Human umbilical vein) has higher long-term patency but a higher incidence of graft-related complications (aneurysm) than does PTFE  (3) the overall superiority of one prosthetic over another (PTFE versus HUV versus Dacron) for infrainguinal bypass has not been established.  infrainguinal graft patency, limb salvage,

and long-term relief of symptoms are maximized by frequent objective follow-up of operated patients with aggressive graft surveillance and repeat operation for detected lesions that threaten graft patency.


Trombendarterectomy material


Angioplasty with venous patch

Aortobifemural graft

Alternative de reconstructie aortofemurala

1. By pass-axilofemural 2. Crossover femuro-femural 3. Grefon toracofemural

By pass –syntetic material


By pass femuropopliteu


in situ


Gruentzig Baloon

Dilatatie iliaca externa

Stent in iliac artery

Ballon expander

Autoexpandabil-cu memori

Stenting art. iliaca

Stenting aorta

Tehnica PIER (recanalizare percutana) art. Femurala superficiala-endoproteza -


Iliofemoral endoprosthesis

Wat als PIER faalt?? Hemobahn Endoprotheza

 Buerger Disease Carotis interna pathology Infrarenal Aneurysms

Burger disease
In 1908, Buerger reported that the disease

was an inflammation of the artery resulting in a cellular type of thrombosis .

Although Buerger's disease affects all

races, it is more prevalent in the Middle and Far East than in Europe and the United States

Burger disease
While the cause of Buerger's disease is not

yet known, smoking is yery closely related with exacerbations and remissions of the disease. Age under 40years Hevy smoker

Pathologic Findings
 Buerger's disease is an inflammatory occlusive

disease primarily involving the medium-sized muscular and smaller arteries of the extremity.

Early Stage. Macroscopically, the

occluded artery appears to be tense or swollen and the periarterial tissue edematous .
 The lumen is obstructed with fresh thrombus in

which a focal inflammation, consisting of multinucleated giant cells, epithelioid cells, and leukocytes, in the form of microabscesses, is frequently observed

Pathologic Findings
Late Stage. Macroscopically, the occluded

artery appears to be contracted and indurated.
The artery and veins may be bound into a

rather firm cord so that they can be separated only with difficulty. The advanced lesion is characterized by some recanalization of the thrombus, a fibrous thickening of the intima, and increased fibrous tissue in the media and adventitia.

The most characteristic pathophysiologic change in Buerger's disease is stagnation of the peripheral or distal circulation in the extremity due to arterial occlusion, an atonic microvascular system, and venous occlusion Ischemic symptoms are manifested mainly in the distal parts of the extremity, and trophic lesions occur exclusively in the fingers and toes.

Clinical Presentation
Based on the observation that obstructive

lesions have been demonstrated angiographically in the arteries of the finger, hand, toe, or foot in asymptomatic patients with Buerger's disease, the disease seems to commence peripherally and extend proximally. Characteristically, the fingers or toes are cold and damp to the touch. The patient often complains of paresthesia of the finger or the foot after manual labor or walking

male-25 yers Heavy smoker Foot claudication Gangrene and ulceration may occur spontaneously (particularly spontaneous gangrene Recurrent superficial thrombophlebitis develops on the arm, the lower leg, or the foot.

Buerger disease

Multiple segmental occlusions of distal

extremity arteries are characteristic of Buerger's disease, with each occlusion being either tapered or abrupt A corrugated or accordion-like appearance is sometimes seen, mostly in the femoral or crural arteries

Buerger disease

Evolution and prognosis
Skip evolution or continuous 10% of cases -amputations at 10 years

after the diagnosis.

Medical Treatment
The only way to arrest the disease is

abstinence.from smoking. Any therapeutic procedure not accompanied by a cessation of smoking will be unsuccessful in treating the arterial insufficiency.  Although antithrombotic therapy, consisting of a fibrolytic agent and heparin, may restrain fulminant thrombotic progression of arterial lesions, the effectiveness of long-term anticoagulant therapy remains unproven

Ilomedin I.V. availability in stable form of prostacyclin (PGI2), a powerful inhibitor of platelet aggregation as well as a vasodilator

Lumbar or Thoracic

sympathectomy Debridement and Local Treatment Amputation


Important !!!

1/3 of patients with TIA

Present a major CVA in following 5 years

Carotis surgery

Chirurgia carotidiana

Carotis surgery

Carotis surgery

Carotis surgery

Carotis surgery

Carotis surgery

Cerebroprotection devices Balloon type Filter type

Theoretical advantage • Local anesthesia • patient is awake •esthetic •cranial nerves Carotid artery stenting •reduced ischemia time


An aneurysm is a permanent localized (i.e. focal) dilatation of an artery having at least a 50% increase in diameter compared to the expected normal diameter of the artery in question.

Infrarenal aorta M: 1.4 - 2.05 cm. + 0.34 F: 1.2 - 1.87 cm. + 0.37

Descending aorta M: 2.4 - 2.98 cm. + 0.31 F: 2.1 - 2.64 cm. + 0.31

Popliteal artery 0.9 cm. + 0.2 1991: Ad hoc Committee on reporting standards

Abdominal aneurysms


•Infrarenal •Juxtarenal •Pararenal


Aortography CT

AAA: Simptoms - Complicatins



Invasive aneurysm

The rupture and diameter


AAA: Tratament endovascular

EXCLUDER Endoprosthesis

Boala Raynaud
FAZA II-A –Staza in capilare .Pulsul periferic

este nemodificat. FAZA III-A- Nu este obligatorie –revenira s poate face direct sau prin aparitia unei coloratii rosiisub forma de pete care apoi conflueaza

Boala Raynaud
Tabloul linic descris de Raynaud 1862 : 3 faze: FAZA I - paloare –prin constrictie arteriolo

capilara a plexului subpapilar-dbut l virful degetelor ; sensibilitatea tactila pierduta Durata 10-15 minute. FAZA II –Cianoza-Pielea se coloreaza in albastru violaceu

Boala Raynaud
Sediul tipic –
la membrele superioare Simetric

Provocarea acceselor se face prin imersie

in apa rece la 15grade.

Boala Raynaud
Definitie -6 semne 2. Episoade provocate de frig si emotii 3. Apar bilateral 4. Absenta gangrenei(sau limitata la cea uscata) 5. Puls arterial normal 6. Absenta unei leziuni etiologice 7. Durata de cel putin 2 ani

Sindromul Raynaud
1. 2. 3. 4. 5.

Debut dupa 50 de ani Unilateral GANGRENA PROGRESIVA SI EXTENSIVA Absenta puls in periferie Sindrom inflamator: VSH, febra, leucocitoza

Sindromul Raynaud
 2. 3. 4. 5. 6. 7. 8.

Cauze Arteriopatii obliterante Afectiuni sistemice ;sclerodermia,artrita reumatoida ,lupus Traumatisme Leziuni neurologice ;TOS Intoxicatii Droguri ETC…….

Boala Raynaud
Tratament medical
Inlaturarea starilor de stres Interzicerea fumatului Tratament cu blocanti de calciu,nitroglicerina ,

antalgice in criza.

Boala Raynaud Tratament chirurgical Simpatectomia toracica

Boala Raynaud Tratament chirurgical Simpatectomia toracica

Chirurgia carotidiana
Chirurgia carotidiana a luat nastere in anii

1950 prin 3 progrese succesive : Demonstrarea relatiei certe intre infarctele cerebrale si leziunile ateromatoase ale carotidei interne . Punerea la punct a arteriografiei cerebrale. Progresele tehnice ale chirurgiei vasculare periferice .

Chirurgia carotidiana
Istoria naturala :
Infarctul cerebral Atacul ischemic tranzitoriu Leziunile asimptomatice

1.Stenoze –tulburari hemodinamice 2. Leziuni ulcerative –cu potential emboligen

Chirurgia carotidiana
 Manifestari clinice.

1.AIT lateralizat - prin embolie. - prin stenoza sau ocluzie. 2.AIT nonlateralizat -manifestat prin. vertije,ataxie,sincopa . 3.Atac vascular ischemic. a. insotit de infarct cerebral. b. In evolutie. 4.Deteriorarea functiei intelectuale.

Chirurgia carotidiana
 Leziuni carotidiene asimptomatice

a.stenozele peste 70% din diametru b.stenozele ulcerate ( cu o suprafata
peste 40 mm patrati)

Chirurgia carotidiana
 Leziuni carotidiene simptomatice (chiar.

si sub 70% stenoza ). AIT (regresie sub 24 de ore ). Accidentul vascular ischemic reversibil. (pina la 3 saptamini). AVC minore – nu altereaza autonomia pacientului. Deficit neurologic acut instabil (crescendo)

Chirurgia carotidiana
Contraindicatii. Alte afectiuni de ordin general(neoplasme). Accident vascular cerebral major. Accidentele vasculare ischemice in


Chirugia carotidiana
Trombendarterectomia Cu sau fara sunt

In functie de valoarea presiunii retrograde dupa clampare Angioplastie cu petec venos sau sutura pe transa Noi folosim suntul Yavid

Anevrisme aterosclerotice multiple -Etiopatogenie Procentajul de

mic la anevrismele ectaziante iar peretele se dezintegreaza si fractureaza sub presiunea din vase.  Patogenia anevrismului aterosclerotic stenozant este neclara.  Benjamin teoretizeaza ca ocluzia vaselor nutritive ale peretelui arterial cauzeaza modificari degenerative care pot duce la formarea anevrismului.

colagen si elastina din peretele mediei este mai

 Localizarea anevrismelor aterosclerotice


 La nivelul bifurcatiilor  Intre punctele de fixatie ale arterei  Se formeaza pe curburile de flexie ale arterei ( anterior pe

portiunea aorto-iliaca si femurala si posterior pe artera poplitee)

INFECTIE Vroeg = virulent laat = “low grade”

Aortoenterische fistel = catastrofe!!! Elke hoge GIT bloeding na AF greffe = aortoenterische fistel tot het tegendeel is bewezen



Infectie = catastrofe!!! Exerese vreemd materiaal 1. Extra-anatomische bypass 2. In situ vervanging homogreffen autoloog materiaal vena saphena vena femoralis prothese met AB??

Angiography at six months

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