LECTURE no II

Dr. POPA RADU

Arterial occlusive disease Classification; Vollmar-Ratschow 1.Angioneuropathies ; vasomotor

disturbancies Raynaud disease 2.Arterial oclusive diseases

1. Predominantly degenerative (aorto-iliac disease

periferic arteriopathies )1. Predominantly inflamatory – trombangeitis

obliterans- Buerger disease. 3. Angiolopathies – cell changes in

terminal vessels acrocyanosis , erithromelalgia .

Atherosclerotic plaque

Arterial occlusive diseaseArterial 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 diseaseComplications due to the plaque

Trombosis – acute (acute ischemia ) chronical (circulatory compensated )

Ulceration – emboli –acute 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 claudicationIt 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 findings-Rutherford 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 findings-Rutherford classification4 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 nondiabeticSistolic 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.

DiagnosisPhysical 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 TestingThe 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

Investigations Noninvasive –

Doppler ultrasound Treadmilll test MRI CT scan

Invasive Arteriography

Doppler ultrasoundPatients 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

Duplex:Spectral signal Anatomy of the wall

Duplex:

1. Doppler 2.Echography

Spectral signal Anatomy of the wall

Right comon iliac stenosis

arteriography duplex

Angioplasty and control

angioplasty control

Calcificare de intimaMediocalcinoza la diabetici

Arteriography

1. Invasive method

2.Give Precise Informations

3. Seldinger technique

MRI Image

Tridimensional reconstruction CT -scan

Claudication is a relative benign sindrom

At 5 years

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

Treatment

Stage I si II -A medical treatment

Stage II -B, III si IV Medical and invasive/surgical treatment

Medical 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

Exercise

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

3. Walking stilll pain apear 4. At least 6 monthsGardner AW et al. JAMA 1995;274:975-

980

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 InterventionPercutaneous 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

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

surgeons to endarterectomy, but the results of endarterectomy in skilled hands are equivalent to bypass ;

(3) Multilevel bypass (simultaneous aortofemoral and infrainguinal bypass) are satisfactory when this procedure is performed in selected patients

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

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

Trombendarterectomy material

Profundoplasty.

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

Reversed in situ

PTA AFS

Gruentzig Baloon

Dilatatie iliaca externa

Stent in iliac artery

STENT

Ballon expander Autoexpandabil-cu memorie

Stenting art. iliaca

Stenting aorta

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

AFS-AFS-PoplPopl

Wat als PIER faalt??Endoprotheza Hemobahn

Buerger DiseaseCarotis interna pathologyInfrarenal Aneurysms

Burger diseaseIn 1908, Buerger reported that the

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

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

EtiologyWhile the cause of Buerger's disease is

not yet known, smoking is yery closely related with exacerbations and remissions of the disease.

Age under 40yearsHevy 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 FindingsLate 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.

PathophysiologyThe 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

Pacientmale-25 yersHeavy smokerFoot claudicationGangrene and ulceration may occur

spontaneously (particularly spontaneous gangrene

Recurrent superficial thrombophlebitis develops on the arm, the lower leg, or the foot.

Buerger disease

Arteriography.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 prognosisSkip evolution or continuous10% 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

Prostaglandin Therapy.

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

Surgical

Lumbar or Thoracic sympathectomy

Debridement and Local Treatment

Amputation

CAROTIS SURGERY

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

• Local anesthesia

• patient is awake

•esthetic

•cranial nerves

•reduced ischemia timeCarotid artery stenting

Theoretical advantages

ATHEROSCLEROTIC ANEVRYSMS

THE DEFINITION

An aneurysm is a permanent localized (i.e. focal) dilatation of anartery having at least a 50% increase in diameter compared to

the expected normal diameter of the artery in question.

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

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

Popliteal artery 0.9 cm. + 0.2

1991: Ad hoc Committee on reporting standards

•Infrarenal•Juxtarenal•Pararenal

Abdominal aneurysms (AAA)

Aortography

Aortography CT

AAA: Simptoms - Complicatins

TRASH FOOT THROMBOSE

AAA IAAA

Invasive aneurysm

The rupture and

diameter

Surgery

AAA: Tratament endovascular

EXCLUDEREndoprosthesis

Boala RaynaudFAZA 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 RaynaudTabloul 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 RaynaudSediul tipic –

la membrele superioareSimetric

Provocarea acceselor se face prin imersie in apa rece la 15grade.

Boala RaynaudDefinitie -6 semne1. Episoade provocate de frig si emotii2. Apar bilateral3. Absenta gangrenei(sau limitata la cea

uscata)4. Puls arterial normal5. Absenta unei leziuni etiologice6. Durata de cel putin 2 ani

Sindromul Raynaud1. Debut dupa 50 de ani2. Unilateral3. GANGRENA PROGRESIVA SI

EXTENSIVA 4. Absenta puls in periferie5. Sindrom inflamator: VSH, febra,

leucocitoza

Sindromul Raynaud Cauze1. Arteriopatii obliterante2. Afectiuni sistemice ;sclerodermia,artrita

reumatoida ,lupus3. Traumatisme4. Leziuni neurologice ;TOS5. Intoxicatii6. Droguri7. ETC…….

Boala RaynaudTratament medical

Inlaturarea starilor de stresInterzicerea fumatuluiTratament cu blocanti de calciu,nitroglicerina

, antalgice in criza.

Boala Raynaud Tratament chirurgical Simpatectomia

toracica

Boala Raynaud Tratament chirurgical Simpatectomia toracica

Chirurgia carotidianaChirurgia 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 IndicatiiLeziuni carotidiene asimptomatice a.stenozele peste 70% din diametru

b.stenozele ulcerate ( cu o suprafata

peste 40 mm patrati)

Chirurgia carotidiana Indicatii.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

urgenta.

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 colagen si elastina din peretele mediei este mai

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.

Localizarea anevrismelor aterosclerotice este: 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

FISTEL EROSIE

Infectie = catastrofe!!!

Exerese vreemd materiaal

1. Extra-anatomische bypass

2. In situ vervanginghomogreffenautoloog materiaal

vena saphenavena femoralis

prothese met AB??