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Ulcers
Defnition: Discontinuity o the skin or mucous membranes which occursdue to microsocpic death o tissues
Lower Limb UlcersPathological classifcation
• Traumatico Most common cause o leg ulcero Trauma can be physical/chemical/burns/radiatoin
• Venouso Varicose vein ulcerso Post thrombotic ulcers ! ollowing DVT"
• #rterialo #therosclerotic vascular disease$ #neurysmso %uerger&s disease/Thrombo angiitis obliteranso Vasospastic disorders e'g' (aynaud&so )ypertensive ulcers !Martorell&s *lcers"o Vasculitic ulcers e'g' (#o %lood dyscrasias e'g' +,D$ Thalassemias$ -eukaemias
• .eurogenico -eprosyo Diabeteso Paraplegiao Post' tibial nerve in ury
• Diabetic oot ulcer• Malignant ulcers 0 e'g' +1,,$ Mar olins$ %,,$ Malignant melanoma
Clinical Classifcation,linical eatures depending on type o vascular disease:
• #rterialo #therosclerosis o large arteries
2ntermittent claudication,hronic severe ischaemia/ ,hronic ischeamic rest pain#cute critical ischeamia
#cute on chronic ischaemiao 3mbolic disease
4rom heart• #cute severe ischaemia
4rom carotids• Transient 2schaemic #ttacks
o #neurysms• Diabetes
o Diabetic oot• Venous
o DVTPain 5 +welling o cal and ankle
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o ,hronic venous insu6ciency,hronic brawny oedema
Peripheral Arterial Disease
General • (esults in lower limb ischaemia• ,auses:
Acuteo #cute Thrombosis
Local Thrombosis o a popliteal aneurysm#cute thrombotic occlusion o a previous bypass gra t orangioplasty site
Widespread thrombosis o normal arteries%lood disorders
• Polycythaemia vera• Thrombocythaemia• -eukaemia• .ephrotic syndrome• )yperosmolar )yperglycaemia
-ocations2t can result in severe ischaemia in certain critical sites:
• Popliteal artery 0 has ew use ul collaterals• 37ternal iliac/,ommon emoral arterial trunk• Pro unda emorus !i superfcial emoral artery is
already occluded"o #cute on ,hronic occlusion
,an be acute on chronic occlusion: 2 an artery narrowedby atherosclerosis becomes obstructed by secondarythrombosis or pla1ue rupture)owever symptoms less severe ! " presence ocollaterals
o #cute 3mbolism+ince in acute setting$ there is no collateral supply inarteries distal to the occlusion$ there is more severeischaemiaMost originate rom:Heart
• #4• M+• M2 Mural thrombus
Aneurysms• #ortic• Popliteal
Most commonly impacts at the branching points wherethe lumen narrows abruptly e'g' #ortic bi urcation
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!saddle embolus"$ common emoral bi urcation$ poplitealtri urcation
o Trauma to vesselso #neurysm
Chronico #therosclerosiso #rteriopathies
Thromboangiiitis 8bliterans !T#8" or %uerger&s disease(aynaud&s disease
Takayasu&s diseaseo ,ollagen Vascular disorderso Diabeteso +cleroderma
• ,ollateral circulation: ,hronic ischaemia allows su6cient time orcollateral to develop so necrosis or gangrene is minimised' %ut inacute ischaemia there is not enough time or collateral to developresults in gangrene o limb i untreated
Risk Factors• +moking• Male• 8ther:
o )ypercholesterolemiao )ypertriglyceridemiao )ypercoagulable stateo )yperhomocysteinaemia
• 9nown Diabetes• 3lderly: ;
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2s almost always in cal whatever the level o arterialobstruction 0 as the superfcial emoral artery is mostcommonly a>ected frst with atherosclerosis',ommon iliac or #ortoiliac obstruction: %ilateralclaudication o gluteal regions$ thighs$ calves B absenceo emoral 5 distal pulses
• C-eriche&s +yndrome 0 bilateral claudication ogluteal regions B impotence !4" reduced per usiono internal iliac arteries ! erectile dys unction"
2lio emoral: Thigh muscles4emoropoplitieal: ,al musclesPopliteal: 4oot muscles !esp' instep"
Tibial and plantar vessels: 4oot muscleso .'%: There are di>erent types o claudication:
Pseudoclaudication !.eurogenic claudication"• ,ompression o the cauda e1uine in the spine by a
central disc protrusion or canal stenosis'• pain develops in standing or walking and
disappears immediately a ter stopping walkEnormal eeling pulses without ischaemic changesare present
Venous• 2t is observed in chronic pelvic venous obstruction
as a mechanical high venous pressure' 2t is usuallydue to iliac vein thrombosis' Peripheral pulses are
normal' T#%-3: To doo %oyd&s classifcation o grades o intermittent claudication
Frade 2 0 Patient complains o pain a ter walking acertain distance !claudication distance"' 2 patientcontinues walking pain subsides as increased blood Gow5 opening o collaterals wash away the metabolites'Frade 22 0 Pain persists on continuing walkingE butpatient can still walk with e>ortFrade 222 0 Patient has to take rest to relieve pain
o
ManagementMild Moderate claudication: ,onservative managementsu6cient' +ymptoms improve over HI months$ esp ipatient stops smoking/ e7ercises regularly/ loses e7cessweight'2 disabling claudication esp i pro7imal obstruction! emoral pulses are absent": (evascularisation
• ,hronic 2schaemic (est Paino (est pain: ,ontinuous severe burning pain in cal / eet 5 toes
which occurs due to ischaemia o the somatic nervessupplying the skin
o +evere chronic arterial obstruction ischaemic pain occurringwhen patient in bed or sitting !rest pain"'
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o H;@ o claudicants progress to rest pain 0 so most casesmani est without claudication
o Patients tend to be less physically active 5 oldero (est pain:
4elt in skin o ootVery severe%urning character8ccurs at night !due to reduced e>ect o gravityassisting arterial supply B reduced ,8"
• -ater occurs even during the day and maybecome continuous
(elieved by hanging leg out o bed or walking aroundEnot ully relieved by analgesics can lead to patientsleeping on a chair#ssociated signs:
• )yperesthesia• -ower limb oedema !due to sleeping on a chair
and not elevating leg"• Trophic changes to skin: #trophy shiny red skin$
ischaemic ulcers between toes/ oot pressureareas/leg
• Patchy necrosis o toes/skin o oot• BVe %uerger&s test• 4ailure o trivial in uries to heal• 37treme vulnerability o eet to pressure sores
o Prognosis !w/o treatment":Very small proportion improveMost continue to have intolerable painProgression to necrosis !microscopic cell death"
o ,omplication.ecrosis o deep tissues o oot local de encesbecome overwhelmed and in ection spreads widely invulnerable ischaemic tissue wet gangrene sepsisdeath
• ,ritical 2schaemia !chronic"o Defnition:
Persistent recurrent rest pain re1uiring regular analgesiaor A J weeks or ulceration or gangrene a>ecting theoot
P-*+#nkle +ystolic %P K ?; mm)g
o +kin changes or tissue loss on top o above pain !Pregangrene$ Fangrene 5 *lceration" 0 due to such severevascular insu6ciency that threatens viability o oot/leg'
.'%: 2n diabetic patients with neuropathy 0 there may be
severe ischemia without painL
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Pre gangrene: rest pain B colour changes B oedema BhyperesthesiaFangrene: Macroscopic death o tissue with/withoutputre action
• Dry gangrene: dry$ dessicated gangrenous tissuecaused by gradual reduction in arterial blood Gow'
There is a line o demarcation'• =et gangrene ! " to both arterial 5 venous block
with added in ection 5 putre action' +preadsaster and pro7imally' .on line o demarcation'
o This implies that unless there is revascularisation there will beloss o part o the limb
• .onhealing *lcero Precipitated by minor trauma 5 most commonly occurs in the
most distal part o the body e'g' tips o toeso 2schaemic arterial ulcers are deep 5 very pain ul
Acute Limb !schaemia• +udden onset Pain !similar to rest pain" 0 severe but variable
intensity'o *sually present in most distal parto )owever$ i Gow is severely reduced paraesthesia ! " never
ischaemia' +o severe pain is actually present pro7imally wherethe tissue is less ischaemic'
•
8ther symptoms:o Pallor
2schaemic area initially white but later becomes mottled!marbling" 0 due to stagnation o deo7ygenated blood'2 mottling can be blanched: -imb is still viable'2 cannot be blanched: -imb is non viable
o Pulselessness o oot pulseso Perishing coldness !mainly at oot"o Paraeasthesia/#naesthesia !i severe ischaemia"o Paralysis o cal muscles !i e7treme ischaemia" 0 patient
unable to Ge7 or e7tend toes/ankle'o -ater with continued ischaemia:+kin becomes mottled$ dusky blue and discoloured
• 2 blanches: -imb can be saved still• 2 f7ed 5 skin blisters: 2rreversible ischaemic
changes !necrosis" and limb loss inevitable always a>ects the oot and e7tends pro7imally 0well demarcated rom pro7 viable tissue
• ,omplications:o .ecrosis 0 the window o opportunity be ore necrosis is shortL
*rgent management re1uiredL
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o (eper usion in ury 5/or ,ompartment +yndrome 0 musclenecrosis 5 permanenet nerve in ury i intervention is late
Signs
Chronic Limb !schaemia• (educed/#bsent pulses distal to obstruction 0 esp' dorsal pedis$
posterior tibial$ popliteal pulses• %ruit over the site o obstruction• Trophic !nutritional" skin changes rarely present
o Thinning o skino Diminished hairo -oss o subcutaneous at
• %rittle nails• Muscle wasting• *lceration in digits• +ensation absent over gangrenous region$ but hyperesthesia along
line o demarcation• Delayed cap refll• %uerger&s test• 8ther systemic signs o atherosclerosis
Natural History
Chronic Limb !schaemia To the -eg
o -argely benign:
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o Measure resting ankle systolic pressureso .ormal #%P2 N ;'O H'Jo .'%: Values can be misleading$ so don&t base management
decision on ust H single #%P23'g' Diabetics may have spuriously elevated #%P2 !4"calcifcation o vessels which prevents proper cu>compression
o 2 patients with a good history but normal resting #%P2 dopre 5 post e7ercise #%P2
# drop in ankle pressure a ter e7ercise N indicatesdegree o arterial disease severity(ecovery rate in ankle pressure N indication o collateralcirculation
o 2 K ;'O N 2schemia' 2 K;' N ,ritical ischaemia• 4%,
o To e7clude polycythaemia 5 thrombocythaemia• Doppler */+ 0 to fnd site o block by listening or absence o
pulsations• Duple7 */+
o Provides a roadmap o atherosclerosis in the arterial tree othe legs
o ,ombines Freyscale */+ 2maging !estimates pla1uenarrowing" 5 ,olour Doppler %lood 4low 3stimation !estimatesGow velocities"
• #rteriography !#ngiography"o +hould be reserved or patients thought to re1uire angioplasty
or reconstructive surgeryo 2t maps the arterial system 0 shows sites and severity o
stenosis and occlusions$ 1uality o inGow !arteries eedingarea o concern" and runo> !arteries beyond main occlusion"
o 2t D83+ .8T measure blood Gow to tissues +o not good orassessing chronic arterial insu6ciency' 2nstead it should beused only to assess mechanics o revascularisation
o .ow direct arterial arteriography is being replaced with M( or,T angiography
Trans emoral angiography should only be done iemorals can be elt
2 emoral pulsation is not elt then angiogram is doneeither transbrachially !le t brachial artery"$ or transaortic
$reatmentConser"ati"e # Is now recognised to be as good as intervention forsimple claudication.
• -i estyle measureso +top smoking leads to resolution o symptoms by collateral
development+moking cessation programmes.icotine (eplacement therapy e'g' %upropion$Varenicline
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o Diet modifcation: reduced at$ more ruit 5 veg$ weightreduction
o +ystematic e7ercise or at least monthso =alk slowly and use a walking stick 0 can greatly e7tend
claudication distance• Medical to reduce systemic atherosclerosis B encourage
collateral vessel developmento %P ,ontrolo #nti platelet therapy 0 #spirino +tatin 0 even i cholesterol levels are normalo !,ilosta ol 0 phosphodiesterase inhibitor 0 can increase
walking distance a bit$ but has signifcant side e>ects"$%pectant
Percutaneous $ransluminal Angioplastyo Provides symptom improvement or a ew years but disease
may ultimately progresso Techni1ue:
,annulation o artery !common emoral" guidewireintroduced into remote artery advancing it to lieacross stenosis balloon catheter is passed over thewire into position balloon inGated to a high pressure
this crushes the atheroma into arterial wall andrelieves obstruction
o Most e>ective in isolated short stenoses in 2liac arterieso -onger stenosis$ occlusions in smaller vessels and distal
vessels are more di6cultReconstructi"e – now reserved for severely ischaemic limbs or whenangioplasty is unsuitable
Arterial reconstructi#e surgeryo Thromboendarterectomy 0 removal o atheromatous pla1ues
and thrombus orm the aorta and iliac arteries' .ow replacedby bypass gra ting !e7cept or carotid endarterectomy"'
o #rterial bypass gra ting4or aorto iliac obstruction: *sing knitted polyester!Dacron" Q gra t or these large arteries4or small arteries: #utogenous long saphenous veingra ts is the best option as long it is A mm in diameterand not damaged by thrombosis' 3'g' emoro poplitealdisease
Veins are also resistant to in ectionLo ,omplications o arterial surgery: To doL
&ther therapies• !V % !ntra&arterial drug therapies
o .o signifcant e>ect in relieving claudication/severe ischaemiao .ewer drugs that stimulate local angiogenesis is being looked
into
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• Sympathectomy ' can be surgical e7cision o part o lumbar symp',hain or via translumbar in ection o @ a1ueous phenol
o ,an be use ul to treat early rest pain !but .8T claudication" 0as rest pain occurs due to insu6cient blood Gow to the skin$and blood Gow to skin ! but not the muscleL" is controlled by+y.+
o 8nly H?@ o patients receive su6cient relie to avoidreconstructive operation/amputation B no way o selectingthose likely o beneft
Acute Limb !schaemia
Management•
%olus o ?;;;* o 2V )eparin 0 to prevent propagation o thrombus• # patient with sensory loss a>ecting more than ust the toes$
especially with evidence o muscle weakness$ re1uires immediatetreatment with embolectomy/thrombectomy/bypass gra t
• Distinguish b/w thrombosis or embolismo )7:
#rrhythmia$ (ecent M2 3mbolism)7 o claudication or prothrombotic blood disorderthrombosis
o 37amination
2 other limb is well per used with good pulses 5 normalankle pressure 3mbolism more likely2 arterial disease present in other limb in situthrombosis more likelyPalpate popliteal ossa 0 to e7clude a thrombosedpopliteal aneurysm+evere ischemia o both limbs e7tending into pro7 legand thigh N -arge saddle embolus at aortic bi urcation
• 2 clinical signs strongly avour embolism 2mmediate surgicalembolectomy with on table arteriography i necessary
• 2 clinical signs are indeterminate urgent duple7 scanning or ,Tangiography out o hours
• 2nterventiono 3mbolectomy$ Thrombectomy or %ypass gra to 4asciotomies 0 in pro oundly ischaemic limbs$ to prevent
compartment syndromeo Thrombolysis 0 only in patients with a thrombosed bypass
gra t whose oot is predicted to be viably or at least HJ hours•
Diabetic (ootAmputation
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Aneurysm
Defnition: -ocalised area o pathological e7cessive dilation o an artery' The e7act si e depends on artery a>ected:
• #bdominal aorta aneurysm: #P diameter AN cm
3pidemiology
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• (elatively uncommon• MAA4
o Males typically get it Aecting lower limb
o # thrombosed popliteal aneurysm carries a ?;@ risk o limbloss
• (upture symptoms
!ndications or operation )ultimately depends on the ris* o rupture+
• -eaking or ruptured aneurysmso 2s a surgical emergencyo K?;@ o these patients reach hospital alive$ and K?;@ o
these undergoing surgery survive so true mortality NI?@LL
o ,ause o death: +hock or M2 or #cute (enal 4ailure a teroperation
• +ymptomatic aneurysm !can assume or there to be imminentrupture"
o Pain B esp' tenderness ! " aneurysmo *reteric colic pain
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• 37panding aneurysm ! or ###"o #neurysms that enlarge at a rate o A ;'?cm/year
• +i e ! or ###"o ### or T## o ? ?cm 0 most vascular surgeons will operate on
thiscm is a critical point 0 as S;@ o aneurysms can be
e7pected to rupture over the ne7t yearso #ny vascular aneurysm
.'%: Mortality a ter elective operation o aneurysm is K?@
2nvestigations or aneurysms
.on ruptured ###• Periodic monitoring o small asymptomatic aneurysms using */+
o *ntil si e reaches A? or ?'?cm or A;'?cm e7pansion/yearre er to surgeons
• Pre elective surgeryo ,T scan:
to show relationship o aneurysm to renal arteries• 2n most cases the ### is in rarenal• 2n ?@ o cases ### e7tends above renal arteries
re1uires a thoraco abdominal operativeapproach greater risk
can identi y other aneurysm e'g' iliac
can show whether aneurysm is inGammatory i'e' thicklayer o inGammatory tissue on anterior sur aceto check whether there is also a thoracic ##
o #rteriography2 aneurysm patient has evidence o lower limbischaemia 0 in case combined reconstruction re1d'
-eaking/ruptured ### Treat as a surgical emergencyL• +hould be treated by a specialist team o surgeons and
anaesthetistso 8ver aggressive %P resuscitation o this hypotensive patientcan convert a leak into a ruptureLo +o many clinicians support permissive hypotension to
acilitate trans er• ,T +can !as long as the patient with a leaking ### is not
demonstrating signs o ,V instability"o #gain or same reasons as above B assessment or
emergency 3V#(
#neurysm +urgery: *nderlying principle is surgical correction o aneurysmby a gra t
• 8pen ### +urgery
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o -ong midline or transverse abdominal incisiono Patient is anticoagulated peri operatively to prevent distal
thrombosiso The iliac arteires$ in rarenal aorta and in erior mesenteric
artery are clamped again or same reasono #neurysm incised longitudinally and the clot is removedo Dacron prosthetic gra t is sutured ust above the upper limit o
the aneurysm within the aneurysmal sac !pro7imal end frst"and the to native aorta at the bi urcation within the sacdistally
!2 there is aorto iliac aneurysm disease use abi urcated trouser gra t"
o 2nlay gra ting• 3V#(
o # minimally invasive techni1ueo # stent gra t is used:
+el e7panding metal ramework with a non porous clothcovering2t is supplied in a constrained state and measuresaround Imm in diameter
o +hort transverse incisions to access common emoral arteriesin the groin
o The main device is passed into one emoral artery and guidedpro7imally using radio logical guidance to its position belowthe renal arteries
o
The constraining mechanisms is then removed and the stentopens and e7pands against the vessel wallo # ter completion$ the device looks like a complete pair o
trousers and e7tends rom renal arteries to common iliacs• 3V#( vs 8pen +urgery
8pen +urgery 3V#(Mortality ?@ H'ected byprevious abdosurgery
4ollow up/-ong termprognosis
Discharge at months(escan a ter ? < yrs
(einterventionunlikely
-ong term prognosisuncertainPotential
complications e'g'endovascular leaks
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-i elong ,T 5 */+monitoring)igh reinterventionrates o
*pper -imb 2schaemia• (are 0 bcos atherosclerosis is rare here B rich collateral blood
supply via scapular anastomoses that can bypass subclavianocclusive disease
• *sually occurs when:o +ubclavian is compressed 0 at thoracic outleto 3mboli obstruct brachial or distal arteries 0 same
cases/presentation/treatment as lower limb embolismo (aynauds disease 0 vasospastic disease causes digital
ischaemia
Thoracic 8utlet compression• Thoracic outlet N space b/w frst rib and clavicle through which
subclavian artery$ vein 5 brachial ple7us passes to enter upperlimbs
• 2 thoracic outlet gets compression neurological !most common"or arterial symptoms
o .eurological: Defcits in TH distribution N =asting andweakness o small muscles o hands$ paraesthesia o inner
orearm and hando #rterial:
*pper limb claudication in those who work with armsabove their hands !as arteries become even morenarrowed in this position"$Post stenotic aneurysm !in long standing casesE canthen collect thrombus embolism to brachial arteryacute ischaemia"-ower %P in a>ected arm which varies with posture
• ,auses:o ,ongenital e'g' cervical rib$ fbrous bandso )ealed clavicular ractureo 37cess muscle development
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• Diagnosiso Duple7 */+ or arteriography
• Managemento ,ervical rib 0 e7cisiono Division o fbrous bandso Post stenotic subclavian aneurysm 0 resect and replace with
gra t
+ubclavian +teal syndrome• +tenosis or occlusion o subclavian artery pro7imal to vertebral
artery origin retrograde Gow vertebral artery via carotids 5 circleo =illis eeds subclavian
• (emains asymptomatic until there is e7cessive demand by upperlimb blood becomes diverted rom cerebral circulationtransient cerebral ischaemia
• Treatment: #ngioplasty or +tenting o subclavian disease or %ypasswith a gra t
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,-tracranial Cerebral Arterial !nsu"ciency• 37tracranial atherosclerosis is responsible or o strokes• ,ommon sites o atherosclerosis:
o ,ommon carotid bi urcationo ,arotid siphon Distal internal carotido Vertebral arterieso 8rifces o the great vessels 0 when they branch rom aortic
arch• 8 ten frst mani ests as a T2# risk o recurrent stroke in recently
symptomatic patients with severe carotid stenosis is as high as JI@over the course o ne7t J years
• ,arotid #rtery 2nsu6ciencyo ,auses stenosis impaired cerebral blood Gow occurs when
luminal narrowing e7ceeds
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to prevent a single strokeL #lso good medicaltherapy may reduce risk even urther'
• (isks o surgeryo +troke 0 J@o M2 0 H J@
• Techni1ue: *nder F# or -#' +hunt used tomaintain cerebral per usion which bypassescarotid operating site' ,arotid artery stenoticpla1ue is dissected out and carotid closed bydirect suture i large or using vein/syntheticmaterial'
Minimally invasive stenting !,arotid angioplasty"• #dv: lower rates o haematoma$ lack o neck
incision$ less risk o cranial nerve damage$ shorterhospital stay
• Disadv: risk o embolism during procedure$ higherrate o late restenosis
• 2ncreased risk o strokes in the short and longterm compared to endarterectomyE withendarterectomy increased risk o cranial nervein ury and higher cardiac event rate
o Management in the acute setting+ymptoms re erable to potential carotid artery diseasee'g' even minor T2#$ should be investigated urgentlyL,arotid endarterectomy is most e>ective i pre ormed
within J weeks o the herald symptoms
Mesenteric 2schaemia• ,ompromised blood supply to bowels occur in S main ways:
o +trangulationMechanical problem presenting as bowel obstruction 0! " hernia$ volvulus$ adhesions
o #cute thrombotic or embolic obstruction*sually superior mesenteric artery occlusionPresentation: acute abdomen
o Transient ischaemia i'e' 2schaemic colitis2nGammation o bowel characterised by abdominal pain5 rectal bleeding
o ,hronic mesenteric artery insu6ciency N Fut claudication(are
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8ccurs when visceral blood supply is restricted to apoint where it becomes inade1uate during activedigestion but ade1uate at rest8ccurs ! " gross atherosclerotic narrowing o all mainmesenteric vesselsPresentation: +evere epigastric pain on eating whichcauses ear o ood gross weight loss
• +ometime can hear epigastric bruit onauscultation
Diagnosis: #rteriography or ,T angiography Treatment: +tenting or surgical reconstruction o mesenteric arteries origin