Ulcers

Definition: Discontinuity of the skin or mucous membranes which occurs

due to microsocpic death of tissues
Lower Limb Ulcers
Pathological classification
Traumatic
o Most common cause of leg ulcer
o Trauma can be physical/chemical/burns/radiatoin
Venous
o Varicose vein ulcers
o Post-thrombotic ulcers (following DVT)
Arterial
o Atherosclerotic vascular disease, Aneurysms
o Buergers disease/Thrombo-angiitis obliterans
o Vasospastic disorders e.g. Raynauds
o Hypertensive ulcers (Martorells Ulcers)
o Vasculitic ulcers e.g. RA
o Blood dyscrasias e.g. SCD, Thalassemias, Leukaemias
Neurogenic
o Leprosy
o Diabetes
o Paraplegia
o Post. tibial nerve injury
Diabetic foot ulcer
Malignant ulcers e.g. SqCC, Marjolins, BCC, Malignant melanoma
Clinical Classification
Clinical features depending on type of vascular disease:
Arterial
o Atherosclerosis of large arteries
Intermittent claudication
Chronic severe ischaemia/ Chronic ischeamic rest pain
Acute critical ischeamia
Acute on chronic ischaemia
o Embolic disease
From heart
Acute severe ischaemia
From carotids
Transient Ischaemic Attacks
o Aneurysms
Diabetes
o Diabetic foot
Venous
o DVT
Pain & Swelling of calf and ankle

o Chronic venous insufficiency

Chronic brawny oedema
Peripheral Arterial Disease
General
Results in lower limb ischaemia
Causes:
Acute
o Acute Thrombosis
Local
Thrombosis of a popliteal aneurysm
Acute thrombotic occlusion of a previous bypass graft or
angioplasty site
Widespread thrombosis of normal arteries
Blood disorders
Polycythaemia vera
Thrombocythaemia
Leukaemia
Nephrotic syndrome
Hyperosmolar Hyperglycaemia
Locations
It can result in severe ischaemia in certain critical sites:
Popliteal artery has few useful collaterals
External iliac/Common femoral arterial trunk
Profunda femorus (if superficial femoral artery is
already occluded)
o Acute on Chronic occlusion
Can be acute-on-chronic occlusion: If an artery narrowed
by atherosclerosis becomes obstructed by secondary
thrombosis or plaque rupture
However symptoms less severe (f) presence of
collaterals
o Acute Embolism
Since in acute setting, there is no collateral supply in
arteries distal to the occlusion, there is more severe
ischaemia
Most originate from:
Heart
AF
MS
MI Mural thrombus
Aneurysms
Aortic
Popliteal
Most commonly impacts at the branching points where
the lumen narrows abruptly e.g. Aortic bifurcation

(saddle embolus), common femoral bifurcation, popliteal

trifurcation
o Trauma to vessels
o Aneurysm
Chronic
o Atherosclerosis
o Arteriopathies
Thromboangiiitis Obliterans (TAO) or Buergers disease
Raynauds disease
Takayasus disease
o Collagen Vascular disorders
o Diabetes
o Scleroderma
Collateral circulation: Chronic ischaemia allows sufficient time for
collateral to develop so necrosis or gangrene is minimised. But in
acute ischaemia there is not enough time for collateral to develop
results in gangrene of limb if untreated

Risk

Factors
Smoking
Male
Other:
o Hypercholesterolemia
o Hypertriglyceridemia
o Hypercoagulable state
o Hyperhomocysteinaemia
Known Diabetes
Elderly: 60-70 yrs
Raised BP

Symptoms (in order of frequency)

Chronic Limb Ischaemia
Intermittent Claudication (Pain) - the main symptom of PAD.
o Definition: Ischaemia of the muscles brought on mainly by
exertion results in accumulation of Substance P & other
metabolites, which causes severe cramp-like pain
Pain begins at a reproducible distance (Walking
Distance), is worse walking uphill and increases if
walking continues. Usually predominates in one leg. The
pain subsides within a min or two of stopping walking.
It is termed disabling claudication if: severe exercise
restriction in young patients, markedly worsening
symptoms
o Affects 5% of males > 65
o Site of claudication depends on level of arterial occlusion:

Is almost always in calf whatever the level of arterial

obstruction as the superficial femoral artery is most
commonly affected first with atherosclerosis.
Common iliac or Aortoiliac obstruction: Bilateral
claudication of gluteal regions, thighs, calves + absence
of femoral & distal pulses
Leriches Syndrome bilateral claudication of
gluteal regions + impotence (F) reduced perfusion
of internal iliac arteries ( erectile dysfunction)
Iliofemoral: Thigh muscles
Femoropoplitieal: Calf muscles
Popliteal: Foot muscles (esp. instep)
Tibial and plantar vessels: Foot muscles
o N.B: There are different types of claudication:
Pseudoclaudication (Neurogenic claudication)
Compression of the cauda equine in the spine by a
central disc protrusion or canal stenosis.
pain develops in standing or walking and
disappears immediately after stopping walk;
normal feeling pulses without ischaemic changes
are present
Venous
It is observed in chronic pelvic venous obstruction
as a mechanical high venous pressure. It is usually
due to iliac vein thrombosis. Peripheral pulses are
normal.
TABLE: To do
o Boyds classification of grades of intermittent claudication
Grade I Patient complains of pain after walking a
certain distance (claudication distance). If patient
continues walking pain subsides as increased blood flow
& opening of collaterals wash away the metabolites.
Grade II Pain persists on continuing walking; but
patient can still walk with effort
Grade III Patient has to take rest to relieve pain
o Management
Mild-Moderate claudication: Conservative management
sufficient. Symptoms improve over 6-18 months, esp if
patient stops smoking/ exercises regularly/ loses excess
weight.
If disabling claudication esp if proximal obstruction
(femoral pulses are absent): Revascularisation
Chronic Ischaemic Rest Pain
o Rest pain: Continuous severe burning pain in calf/feet & toes
which occurs due to ischaemia of the somatic nerves
supplying the skin
o Severe chronic arterial obstruction ischaemic pain occurring
when patient in bed or sitting (rest pain).

o 10% of claudicants progress to rest pain so most cases

manifest without claudication
o Patients tend to be less physically active & older
o Rest pain:
Felt in skin of foot
Very severe
Burning character
Occurs at night (due to reduced effect of gravity
assisting arterial supply + reduced CO)
Later occurs even during the day and may
become continuous
Relieved by hanging leg out of bed or walking around;
not fully relieved by analgesics can lead to patient
sleeping on a chair
Associated signs:
Hyperesthesia
Lower limb oedema (due to sleeping on a chair
and not elevating leg)
Trophic changes to skin: Atrophy shiny red skin,
ischaemic ulcers between toes/foot pressure
areas/leg
Patchy necrosis of toes/skin of foot
+Ve Buergers test
Failure of trivial injuries to heal
Extreme vulnerability of feet to pressure sores
o Prognosis (w/o treatment):
Very small proportion improve
Most continue to have intolerable pain
Progression to necrosis (microscopic cell death)
o Complication
Necrosis of deep tissues of foot local defences
become overwhelmed and infection spreads widely in
vulnerable ischaemic tissue wet-gangrene sepsis
death
Critical Ischaemia (chronic)
o Definition:
Persistent recurrent rest pain requiring regular analgesia
for > 2 weeks or ulceration or gangrene affecting the
foot
PLUS
Ankle Systolic BP < 50 mmHg
o Skin changes or tissue loss on top of above pain (Pregangrene, Gangrene & Ulceration) due to such severe
vascular insufficiency that threatens viability of foot/leg.
N.B: In diabetic patients with neuropathy there may be
severe ischemia without pain!

Pre-gangrene: rest pain + colour changes + oedema +

hyperesthesia
Gangrene: Macroscopic death of tissue with/without
putrefaction
Dry gangrene: dry, dessicated gangrenous tissue
caused by gradual reduction in arterial blood flow.
There is a line of demarcation.
Wet gangrene (f) to both arterial & venous block
with added infection & putrefaction. Spreads
faster and proximally. Non line of demarcation.
o This implies that unless there is revascularisation there will be
loss of part of the limb
Nonhealing Ulcer
o Precipitated by minor trauma & most commonly occurs in the
most distal part of the body e.g. tips of toes
o Ischaemic arterial ulcers are deep & very painful

Acute Limb Ischaemia

Sudden onset Pain (similar to rest pain) severe but variable
intensity.
o Usually present in most distal part
o However, if flow is severely reduced paraesthesia (f) never
ischaemia. So severe pain is actually present proximally where
the tissue is less ischaemic.
Other symptoms:
o Pallor
Ischaemic area initially white but later becomes mottled
(marbling) due to stagnation of deoxygenated blood.
If mottling can be blanched: Limb is still viable.
If cannot be blanched: Limb is non-viable
o Pulselessness of foot pulses
o Perishing coldness (mainly at foot)
o Paraeasthesia/Anaesthesia (if severe ischaemia)
o Paralysis of calf muscles (if extreme ischaemia) patient
unable to flex or extend toes/ankle.
o Later with continued ischaemia:
Skin becomes mottled, dusky blue and discoloured
If blanches: Limb can be saved still
If fixed & skin blisters: Irreversible ischaemic
changes (necrosis) and limb loss inevitable always affects the foot and extends proximally
well demarcated from prox viable tissue
Complications:
o Necrosis the window of opportunity before necrosis is short!
Urgent management required!

o Reperfusion injury &/or Compartment Syndrome muscle

necrosis & permanenet nerve injury if intervention is late
Signs
Chronic Limb Ischaemia
Reduced/Absent pulses distal to obstruction esp. dorsal pedis,
posterior tibial, popliteal pulses
Bruit over the site of obstruction
Trophic (nutritional) skin changes rarely present
o Thinning of skin
o Diminished hair
o Loss of subcutaneous fat
Brittle nails
Muscle wasting
Ulceration in digits
Sensation absent over gangrenous region, but hyperesthesia along
line of demarcation
Delayed cap refill
Buergers test
Other systemic signs of atherosclerosis
Natural History
Chronic Limb Ischaemia
To the Leg
o Largely benign: 75% of patients stay the same or improve
walking distance
o Only 5-10% will require surgical intervention by 5 years & Only
2% will require major amputation
Smoking & Diabetes is a major risk factor for these
To the patient
o 10% have non-fatal CV event (MI/Stroke) within 5 years & 5
year mortality rate is 30% - 75% are (f) CVD
Increased risk if smoking
Severity of PAD via ABPI correlates with risk
Severe Ischaemia
Critical Ischaemia
Management of Lower Limb Ischaemia
Chronic Lower Limb Arterial Insufficiency
Investigations
ABPI

o Measure resting ankle systolic pressures

o Normal ABPI = 0.9-1.2
o N.B: Values can be misleading, so dont base management
decision on just 1 single ABPI
E.g. Diabetics may have spuriously elevated ABPI (F)
calcification of vessels which prevents proper cuff
compression
o If patients with a good history but normal resting ABPI do
pre & post-exercise ABPI
A drop in ankle pressure after exercise = indicates
degree of arterial disease severity
Recovery rate in ankle pressure = indication of collateral
circulation
o If < 0.9 = Ischemia. If <0.3 = Critical ischaemia
FBC
o To exclude polycythaemia & thrombocythaemia
Doppler U/S to find site of block by listening for absence of
pulsations
Duplex U/S
o Provides a roadmap of atherosclerosis in the arterial tree of
the legs
o Combines Greyscale U/S Imaging (estimates plaque
narrowing) & Colour Doppler Blood Flow Estimation (estimates
flow velocities)
Arteriography (Angiography)
o Should be reserved for patients thought to require angioplasty
or reconstructive surgery
o It maps the arterial system shows sites and severity of
stenosis and occlusions, quality of inflow (arteries feeding
area of concern) and runoff (arteries beyond main occlusion)
o It DOES NOT measure blood flow to tissues So not good for
assessing chronic arterial insufficiency. Instead it should be
used only to assess mechanics of revascularisation
o Now direct arterial arteriography is being replaced with MR or
CT angiography
Transfemoral angiography should only be done if
femorals can be felt
If femoral pulsation is not felt then angiogram is done
either transbrachially (left brachial artery), or transaortic
Treatment
Conservative Is now recognised to be as good as intervention for
simple claudication.
Lifestyle measures
o Stop smoking leads to resolution of symptoms by collateral
development
Smoking cessation programmes
Nicotine Replacement therapy e.g. Bupropion,
Varenicline

o Diet modification: reduced fat, more fruit & veg, weight

reduction
o Systematic exercise for at least 3 months
o Walk slowly and use a walking stick can greatly extend
claudication distance
Medical to reduce systemic atherosclerosis + encourage
collateral vessel development
o BP Control
o Anti-platelet therapy Aspirin
o Statin even if cholesterol levels are normal
o (Cilostazol phosphodiesterase inhibitor can increase
walking distance a bit, but has significant side effects)
Expectant
Percutaneous Transluminal Angioplasty
o Provides symptom improvement for a few years but disease
may ultimately progress
o Technique:
Cannulation of artery (common femoral) guidewire
introduced into remote artery advancing it to lie
across stenosis balloon catheter is passed over the
wire into position balloon inflated to a high pressure
this crushes the atheroma into arterial wall and
relieves obstruction
o Most effective in isolated short stenoses in Iliac arteries
o Longer stenosis, occlusions in smaller vessels and distal
vessels are more difficult
Reconstructive now reserved for severely ischaemic limbs or when
angioplasty is unsuitable
Arterial reconstructive surgery
o Thromboendarterectomy removal of atheromatous plaques
and thrombus form the aorta and iliac arteries. Now replaced
by bypass grafting (except for carotid endarterectomy).
o Arterial bypass grafting
For aorto-iliac obstruction: Using knitted polyester
(Dacron) Y graft for these large arteries
For small arteries: Autogenous long saphenous vein
grafts is the best option as long it is >3mm in diameter
and not damaged by thrombosis. E.g. femoro-popliteal
disease
Veins are also resistant to infection!
o Complications of arterial surgery: To do!
Other therapies
IV & Intra-arterial drug therapies
o No significant effect in relieving claudication/severe ischaemia
o Newer drugs that stimulate local angiogenesis is being looked
into

Sympathectomy can be surgical excision of part of lumbar symp.

Chain or via translumbar injection of 6% aqueous phenol
o Can be useful to treat early rest pain (but NOT claudication)
as rest pain occurs due to insufficient blood flow to the skin,
and blood flow to skin ( but not the muscle!) is controlled by
SyNS
o Only 15% of patients receive sufficient relief to avoid
reconstructive operation/amputation + no way of selecting
those likely o benefit

Acute Limb Ischaemia

Management
Bolus of 5000U of IV Heparin to prevent propagation of thrombus
A patient with sensory loss affecting more than just the toes,
especially with evidence of muscle weakness, requires immediate
treatment with embolectomy/thrombectomy/bypass graft
Distinguish b/w thrombosis or embolism
o Hx:
Arrhythmia, Recent MI Embolism
Hx of claudication or prothrombotic blood disorder
thrombosis
o Examination
If other limb is well perfused with good pulses & normal
ankle pressure Embolism more likely
If arterial disease present in other limb in situ
thrombosis more likely
Palpate popliteal fossa to exclude a thrombosed
popliteal aneurysm
Severe ischemia of both limbs extending into prox leg
and thigh = Large saddle embolus at aortic bifurcation
If clinical signs strongly favour embolism Immediate surgical
embolectomy with on table arteriography if necessary
If clinical signs are indeterminate urgent duplex scanning or CT
angiography out of hours
Intervention
o Embolectomy, Thrombectomy or Bypass graft
o Fasciotomies in profoundly ischaemic limbs, to prevent
compartment syndrome
o Thrombolysis only in patients with a thrombosed bypass
graft whose foot is predicted to be viably for at least 12 hours

Diabetic Foot
Amputation

Aneurysm
Definition: Localised area of pathological excessive dilation of an artery.
The exact size depends on artery affected:
Abdominal aorta aneurysm: AP diameter >= 3cm
Epidemiology

Relatively uncommon
M>>F
o Males typically get it >70 yrs, Females present at >80yrs

Presentation
Aorto-iliac
Unsymptomatic but pulsatile mass discovered on abdo exam
Incidental on radiological investigation
o Calcification on X-ray
o Aneurysm on CT
o U/S when looking for urinary symptoms or via routine AAA
screening in men when they reach 65yrs
Pulsatile abdominal mass noticed by patient
Symptoms of retroperitoneal leakage or rupture
o Pain can be:
acute abdomen
abdo/back pain lasting for up to one weeks duration
with tender aneurysm
mimicking ureteral/renal colic
o Cardiovascular collapse (fainting, hypotension)
o Sudden death (if rupture) often misdiagnosed as MI
Femoral aneurysms
Pulsatile mass
Rupture pain & massive swelling in the groin
Popliteal aneurysms
Acute Ischaemic Leg
o Due to thrombosis and/or embolization sudden distal
ischaemia affecting lower limb
o A thrombosed popliteal aneurysm carries a 50% risk of limb
loss
Rupture symptoms
Indications for operation (ultimately depends on the risk of
rupture)
Leaking or ruptured aneurysms
o Is a surgical emergency
o <50% of these patients reach hospital alive, and <50% of
these undergoing surgery survive so true mortality =
85%!!
o Cause of death: Shock or MI or Acute Renal Failure after
operation
Symptomatic aneurysm (can assume for there to be imminent
rupture)
o Pain + esp. tenderness (f) aneurysm
o Ureteric colic pain

Expanding aneurysm (for AAA)

o Aneurysms that enlarge at a rate of > 0.5cm/year
Size (for AAA)
o AAA or TAA of 5-5cm most vascular surgeons will operate on
this
6cm is a critical point as 40% of aneurysms can be
expected to rupture over the next years
o Any vascular aneurysm

N.B: Mortality after elective operation of aneurysm is <5%

Investigations for aneurysms
Non-ruptured AAA
Periodic monitoring of small asymptomatic aneurysms using U/S
o Until size reaches >5 or 5.5cm or >0.5cm expansion/year
refer to surgeons
Pre-elective surgery
o CT scan:
to show relationship of aneurysm to renal arteries
In most cases the AAA is infrarenal
In 5% of cases AAA extends above renal arteries
requires a thoraco-abdominal operative
approach greater risk
can identify other aneurysm e.g. iliac
can show whether aneurysm is inflammatory i.e. thick
layer of inflammatory tissue on anterior surface
to check whether there is also a thoracic AA
o Arteriography
If aneurysm patient has evidence of lower limb
ischaemia in case combined reconstruction reqd.
Leaking/ruptured AAA Treat as a surgical emergency!
Should be treated by a specialist team of surgeons and
anaesthetists
o Over-aggressive BP resuscitation of this hypotensive patient
can convert a leak into a rupture!
o So many clinicians support permissive hypotension to
facilitate transfer
CT Scan (as long as the patient with a leaking AAA is not
demonstrating signs of CV instability)
o Again for same reasons as above + assessment for
emergency EVAR
Aneurysm Surgery: Underlying principle is surgical correction of aneurysm
by a graft
Open AAA Surgery

o Long midline or transverse abdominal incision

o Patient is anticoagulated peri-operatively to prevent distal
thrombosis
o The iliac arteires, infrarenal aorta and inferior mesenteric
artery are clamped again for same reason
o Aneurysm incised longitudinally and the clot is removed
o Dacron prosthetic graft is sutured just above the upper limit of
the aneurysm within the aneurysmal sac (proximal end first)
and the to native aorta at the bifurcation within the sac
distally
(If there is aorto-iliac aneurysm disease use a
bifurcated trouser graft)
o Inlay grafting????
EVAR
o A minimally invasive technique
o A stent-graft is used:
Self-expanding metal framework with a non-porous cloth
covering
It is supplied in a constrained state and measures
around 8mm in diameter
o Short transverse incisions to access common femoral arteries
in the groin
o The main device is passed into one femoral artery and guided
proximally using radio-logical guidance to its position below
the renal arteries
o The constraining mechanisms is then removed and the stent
opens and expands against the vessel wall
o After completion, the device looks like a complete pair of
trousers and extends from renal arteries to common iliacs
EVAR vs Open Surgery
EVAR
1.7%
2-4d
Unlikely
8000
Needs
15mm
of
relatively
normal
aorta below renal
arteries
More difficult with Unaffected
by
previous
surgery/ previous
abdo
peritonitis
surgery
term Discharge
at
3 Long term prognosis
months
uncertain
Rescan after 5-7 yrs
Potential
Reintervention
complications
e.g.
unlikely
endovascular leaks

Mortality
Length of Hosp stay
ITU/HDU care
Overall cost
Anatomical
constraints
PMHx
Follow-up/Long
prognosis

Open Surgery
5%
7-10d
Likely needed
6500
AAA to Renal arteries
distance
can
be
<15mm

Lifelong CT & U/S

monitoring
High
reintervention
rates o

Upper Limb Ischaemia

Rare bcos atherosclerosis is rare here + rich collateral blood
supply via scapular anastomoses that can bypass subclavian
occlusive disease
Usually occurs when:
o Subclavian is compressed at thoracic outlet
o Emboli obstruct brachial or distal arteries same
cases/presentation/treatment as lower limb embolism
o Raynauds disease vasospastic disease causes digital
ischaemia
Thoracic Outlet compression
Thoracic outlet = space b/w first rib and clavicle through which
subclavian artery, vein & brachial plexus passes to enter upper
limbs
If thoracic outlet gets compression neurological (most common)
or arterial symptoms
o Neurological: Deficits in T1 distribution = Wasting and
weakness of small muscles of hands, paraesthesia of inner
forearm and hand
o Arterial:
Upper limb claudication in those who work with arms
above their hands (as arteries become even more
narrowed in this position),
Post-stenotic aneurysm (in long standing cases; can
then collect thrombus embolism to brachial artery
acute ischaemia)
Lower BP in affected arm which varies with posture
Causes:
o Congenital e.g. cervical rib, fibrous bands
o Healed clavicular fracture
o Excess muscle development

Diagnosis
o Duplex U/S or arteriography
Management
o Cervical rib excision
o Division of fibrous bands
o Post-stenotic subclavian aneurysm resect and replace with
graft

Subclavian Steal syndrome

Stenosis or occlusion of subclavian artery proximal to vertebral
artery origin retrograde flow vertebral artery via carotids & circle
of Willis feeds subclavian
Remains asymptomatic until there is excessive demand by upper
limb blood becomes diverted from cerebral circulation
transient cerebral ischaemia
Treatment: Angioplasty or Stenting of subclavian disease or Bypass
with a graft

Extracranial Cerebral Arterial Insufficiency

Extracranial atherosclerosis is responsible for of strokes
Common sites of atherosclerosis:
o Common carotid bifurcation
o Carotid siphon - Distal internal carotid
o Vertebral arteries
o Orifices of the great vessels when they branch from aortic
arch
Often first manifests as a TIA risk of recurrent stroke in recently
symptomatic patients with severe carotid stenosis is as high as 28%
over the course of next 2 years
Carotid Artery Insufficiency
o Causes stenosis impaired cerebral blood flow occurs when
luminal narrowing exceeds 70% (cerebral autoregulation
compensates until this)
o Can result in platelet emboli
Small emboli TIAs e.g. amaurosis fugax
Large emboli major strokes
o Diagnosis
Carotid bruits in minority; does not indicate extent of
narrowing; if significantly large it may even be silent!
Duplex doppler scanning simultaneous imaging of
carotid arteries & measurement of blood flow velocity
(which can estimate degree of stenosis)
o Management:
Medical
Aspirin 75-150mg
Clopidogrel 75mg
Strict BP control
Statins
Surgical Carotid endarterectomy
Surgery reduces stroke rate better than medical
therapy only in patients with stenosis greater than
70% - from 6% to 1.5%
Surgery does not reduce long-term mortality from
carotid artery disease even in severe stenosis!
Trials also showed a substantial risk of stroke or
death from surgery of 6-8%
Surgery in asymptomatic disease is controversial
15 asymptomatic stenoses need to be treated

to prevent a single stroke! Also good medical

therapy may reduce risk even further.
Risks of surgery
o Stroke 2%
o MI 1-2%
Technique: Under GA or LA. Shunt used to
maintain cerebral perfusion which bypasses
carotid operating site. Carotid artery stenotic
plaque is dissected out and carotid closed by
direct suture if large or using vein/synthetic
material.
Minimally invasive stenting (Carotid angioplasty)
Adv: lower rates of haematoma, lack of neck
incision, less risk of cranial nerve damage, shorter
hospital stay
Disadv: risk of embolism during procedure, higher
rate of late restenosis
Increased risk of strokes in the short and long
term
compared
to
endarterectomy;
with
endarterectomy increased risk of cranial nerve
injury and higher cardiac event rate
o Management in the acute setting
Symptoms referable to potential carotid artery disease
e.g. even minor TIA, should be investigated urgently!
Carotid endarterectomy is most effective if preformed
within 2 weeks of the herald symptoms

Mesenteric Ischaemia
Compromised blood supply to bowels occur in 4 main ways:
o Strangulation
Mechanical problem presenting as bowel obstruction
(f) hernia, volvulus, adhesions
o Acute thrombotic or embolic obstruction
Usually superior mesenteric artery occlusion
Presentation: acute abdomen
o Transient ischaemia i.e. Ischaemic colitis
Inflammation of bowel characterised by abdominal pain
& rectal bleeding
o Chronic mesenteric artery insufficiency = Gut claudication
Rare

Occurs when visceral blood supply is restricted to a

point where it becomes inadequate during active
digestion but adequate at rest
Occurs (f) gross atherosclerotic narrowing of all 3 main
mesenteric vessels
Presentation: Severe epigastric pain on eating which
causes fear of food gross weight loss
Sometime
can
hear
epigastric
bruit
on
auscultation
Diagnosis: Arteriography or CT angiography
Treatment: Stenting or surgical reconstruction of
mesenteric arteries origin