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 )
 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
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 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 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 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.
Diagnosis
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
Investigations
Noninvasive –
Doppler ultrasound
Treadmilll test
MRI
CT scan

Invasive
Arteriography
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

Anatomy of the wall

Spectral signal
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
 Arteriography
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)
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 months
Gardner 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 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

 (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 memori
Stenting art. iliaca
Stenting aorta
 Tehnica PIER (recanalizare percutana)
art. Femurala superficiala-endoproteza -
AFS-
Popl
 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 .
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
Etiology
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.
Pathophysiology
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
Pacient
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
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 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
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
 Theoretical advantage

• Local anesthesia

• patient is awake

•esthetic

•cranial nerves
Carotid artery stenting
•reduced ischemia time
ATHEROSCLEROTIC
ANEVRYSMS
 THE DEFINITION

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 Descending aorta

M: 1.4 - 2.05 cm. + 0.34 M: 2.4 - 2.98 cm. + 0.31
F: 1.2 - 1.87 cm. + 0.37 F: 2.1 - 2.64 cm. + 0.31

Popliteal artery
0.9 cm. + 0.2

1991: Ad hoc Committee on reporting standards

 Abdominal aneurysms (AAA)

•Infrarenal
•Juxtarenal
•Pararenal
Aortography
Aortography
CT
 AAA: Simptoms - Complicatins

TRASH FOOT THROMBOSE

AAA IAAA
Invasive aneurysm
The rupture and
diameter
Surgery
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. Debut dupa 50 de ani
2. Unilateral
3. GANGRENA PROGRESIVA SI EXTENSIVA
4. Absenta puls in periferie
5. Sindrom inflamator: VSH, febra,
leucocitoza
Sindromul Raynaud
 Cauze
2. Arteriopatii obliterante
3. Afectiuni sistemice ;sclerodermia,artrita
reumatoida ,lupus
4. Traumatisme
5. Leziuni neurologice ;TOS
6. Intoxicatii
7. Droguri
8. 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
Indicatii
 Leziuni 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 vervanging
homogreffen
autoloog materiaal
vena saphena
vena femoralis
prothese met AB??
Angiography at six months