Approach in Vascular Patient
กิตติพนั ธุ์ ฤกษ์เกษม PhD, FACA
Topic
• Artery - Limb Ischaemia
- Aneurysm
• Venous - Varicose vein
• Leg ulcer
Limb Ischaemia
• Aetiology: most often atherosclerosis >
trauma
• Most management decisions are based upon
1.Differentiation acute vs chronic
2. Mechanism of occlusion
3.Location of the occlusion
4.Status of limb
5.Fitness of patients
1.Differentiation
acute vs chronic
What is acute ischaemia?
Acute ischaemia
• Period of onset in minutes or hours
• Sudden catastrophic
• Less effect in upper extremity and leg
affected by chronic ischaemia
Acute ischaemia
• Symptom 5P
pain
pulselessness
paresthesia
pallor
paralysis
Marble white
right foot in
acute limb
ischaemia
What is chronic ischaemia?
Chronic ischaemia
• Symptom of limited circulation over months
or years
• Slow deterioration of function
• Gradually symptom
• Life style changes-stop smoking or
exercise: remission collateral vv
Chronic ischaemia
• Symptom and sign
Claudication
rest pain
ulceration/gangrene
Why should the effectes of
acute arterial ischaemia
occlusion be less in someone
affected already by symptom
of chronic ischaemia or in
upper limb?
Collateral vessels!!
2. Mechanism of occlusion
Acute iscahemia caused by
•Trauma
• Non trauma
- embolus
- thrombosis
Trauma-fracture tibia
Embolus
• Mobile solid mass
• Free floating in blood
• Capable of occluding a vein or artery
distal to its site of origin
Composition of embolus
• Atheromatous debris or thrombus(clot)
(common)
Common source of atheromatous
or thrombus emboli
•
•
•
•
Left ventricle wall after MI
Left atrium in atrial fibrillation
Diseased mitral valve or aortic valve
Atheromatous plaques in aorta or iliac
vessels
This embolus lodge at the area where arterial
tree is smaller than the embolus e.g.
bifurcation or pre-existing stenosis
Atheromatous debris-blue toe syndrome
Thrombosis
• Rupture of an atheromatous plaque esp
moderate and severe stenosis
• Virchow’s triad: abnormality of flow,
blood, vessel wall
Is it possible to differentiate between
thrombosis and embolus as a cause
of acute ischaemia??
• Sometimes!!!
• Previously asymptomatic, preexisting cause
with sudden onset of severe ischaemia
(normal contralateral pulse) = embolus
• Previous claudication and sudden onset of
acute ischaemia = thrombosis
Chronic ischaemia
• Progressive narrowing
• Cause : Atheromatous disease is the common cause
Other uncommon cause: Aneurysm:
» popliteal aneurysm: special nature
» Diabetes
Some rare disease
» Buerger’s disease
» Hyperhomocysteineaemia
» Takayasu’s disease
3. Location
• Acute occlusion: more proximal, the
more extensive ischaemia
• Diagnostic location determines the best
treatment
3. Location-aorto-iliac disease
• Chronic: claudication at
buttock, thigh calf, loss
of femoral pulse
in men: Leriche
syndrome (French
surgeon who described
distal aortic occlusion
and erectile impotence)
• Acute: catastrophic for
ipsilateral limb, buttock,
perineum
Distal aorta
occlusion
Location Common femoral disease
• Chronic: thigh and calf
claudication, palpable
the femoral pulse just
below inguinal ligament
• Acute: femoral
bifurcation is the
common site of
embolus-typical
ischaemic limb
Location-superficial femoral disease
• Chronic :a very common
place for stenosis or
occlusion where it passes
posteriorly through adductor
hiatus (Hunter’s canal)
It can produce calf
claudication, but rarely
severe in presence of
profunda femoris artery
• Acute: rare
Bilateral occlusion of superficial femoral artery
with collateral circulation via profunda
Location-popliteal atery dsease
• Chronic: calf
claudication
• Acute: sudden
occlusion from
thrombus or embolus
causes severe
ischaemia due to
occlusion geniculate
arteries
Location: crural arterial disease
• Occlusion only one
out of three vessel
can asymptom
unless either chronic
or acute disease
involve all three
vessels
4. Status of the limb-acute iscahemia
Determine chance of saving limb vs amputation
• Pain: severe pain not response to opiate with
tenderness in muscle:often irreversible ischaemia
• Paresthesia: range from percentible alternation to
numbness. Numbness indicate acute critical ischaemia
• Pallor: pale
->
unfixed mottling ->
fixed mottling (do not blanch on pressure) frequently
beyond salvage
4. Status of the limb-acute ischaemia
• Pulselessness
• Paralysis: stiff of the limb, when patient cannot
move ankle joint indicated severe ischaemia
4. Status of the limb –chronic ischaemia
Early calf claudication like angina
i.e.tight, stiff or crushing pain
What factors influence
claudication distance?
Anything increases
work of walking
•
•
•
•
Excess weight
Walking uphill
Walking against wind
Carry shopping
More severe form
• Very short distance- a few steps
• Rest pain first felt in the distal parts such as toes and
dorsum of the foot – awake patient need rise from
bed and walking around to relieve
• Unable to lie flat without pain patient sleep with
hanging leg out of beds cause edema and worsen
microvascular perfusion
Hanging foot
Last stage of chronic
• Gangrene, clinical depend on the degree of
decomposition
• Range from ulcer (skin necrosis) to gangrene of toe
and foot
• Gangrene:
wet gangrene: black, soggy, discoloured green
and malodorous requires urgent amputation
Dry gangrene: black hard, brittle, wrinkle rarely
odour : may autoamputation or surgery in proper
time
5. Fitness of patient
• Determine investigation and treatment
“ surgeon need to consider the ability of the patient to
withstand our effort. Our job should be relieve the
symptom of which the patient complain”
• Common causes of unfitness
- pre-event unfitness: cardiac e.g. MI, Lung-renal-metabolic
disease
- per-event unfitness: dehydration, acidosis, uncontrolled DM
- postevent unfitness: myoglobinaemia, severe acidosis, MI
Investigation of occlusive
disease
• Clinical examination: full history
» Presence or absence of pulse
» Status of the limb
» Other test
BUN, CR, electrolyte
CBC, plasma viscosity
Coagulation
EKG, CXR
Fixed wave Doppler examination
• Ankle brachial pressure index (ABPI)
0.5-0.9 claudication
< 0.5 critial limb ischaemia
< 0.3 gangrene
Treadmill testing
• Walking incline 10%
at speed 3 km/hr
• Test of function to
allow monitoring
disease and the
result of therapeutic
effort
Ultrasound-duplex scan
• Composed of
1. B-mode ultrasound reveal the anatomy:aneurysm,
2.
occlusive lesion
Doppler signal: flow indicate stenosis
Duplex scan of SFA stenosis
Contrast arteriography
• Injection contrast agent
make lumen visible
• Conventional
angiogram: direct
intraarterial route
• Now we have digital
subtraction
angiogram(DSA)
• CT angiogram: need of
arterial puncture
• From the picture, what
is the diagnosis?
Computerised tomographic
(CT) angiograhy
• Helical CT scan with
intra-arterial contrast
injection
• Look the relation
between artery and
other structure well
Carotid body tumor
Magnetic resonance
arteriography(MRA)
• without contrast or
IV gadolinium
• Suitable in patient
should not given
iodine containing
contrast due to renal
disease or allergy
Aneurysm
• Pulsatile expansile mass
Clinical feature:
• invade surrounding tissue cause- pain
• rupture
• embolisation - ischaemia e.g.
claudication, trash foot
Ruptured AAA
Trash foot-multiple small
atheromatous debris
Investigation
• Ultrasound
• CT scan
• ??? angiogram
CT scan
“Infrarenal
AAA”
Angiogram of popliteal aneurysm
Venous disease
Functional anatomy
• Superficial venous system devided
into 3 parts
Long saphenous vein (LSV)
Short saphenous vein (SSV)
Perforating or communicating vein (PV)
Superficial venous system
• LSV: medial
malleolus to groin
• SSV: outer border of
foot behind lateral
malleolus ascend to
middle of the calf 60%
to pop V., 20% to LSV
and 20% wherelse
Superficial venous system
• PV connnect superficial and
deep vein
• > 50 PV in one leg
• PV in thigh connect
directly between
superficial and deep
system, in leg connect
indirectly via venous
plexus
Deep venous system
• 3 artery below knee,
there are 2 vein beside
of artery from foot up to
knee joint
• Then pop V beside
artery then in thigh
->superficial femoral
vein join with profunda
femoris vein -> common
femoral vein
Physiology of venous
drainage
• Normal: superficial to
deep and from
distal(foot) to
proximal(thigh and
heart )
• ?? At standing position,
blood at ankle has to
return against gravity to
heart over a distance of
> 1 metre “how”
How
4 factors support this system
• Functioning vein valves: resist > 300 mmHg
• Functioning foot and calf muscle pumps: weight
compress venous plexus in foot and calf muscle
compress sinusoidal and deep vein in leg
• Residual arterial pressure
• Negative intrathoracic pressure
“ however absent valve or damaged valve, the
muscle pump cannot work efficiently”
Pathophysiology of varicose vein
• Abnormal dilated and tortuous superficial vein of the leg
• Response to a pathological increase in the vein’s
intraluminal pressure
• This increases due to higher intraluminal pressure of deep
vein (necessary to allow movement of blood out of leg)
from deep to superficial system
Aetiology
• Primary e.g. saphenofemorla valve incompetence
Aetiology
• Secondary mostly due to previous DVT
– Simple obstruction
– Destroying the valves within deep vein
These lead to blood move to superficial system
(compensatory mechanism)
** a must to know this, otherwise we may worsen
patient with VV surgery**
Primary VV or secondary VV
Clinical feature of varicose vein
•
•
•
•
•
Cosmetic presentation
Discomfort and pain
Cramps
Swelling
Complication
- thrombophebitis
- haemorrhage
- CVI
Patients assessment in VV(1)
• History: past Hx of DVT
• Examination:
standing position
Area of VV
Brodie Tredelenberg test
Perthes’ test
Continous wave Doppler
VV
Brodie Tredelenberg test
Patients assessment in VV(2)
• Radiological evaluation when suspected of
previous DVT
Duplex scan
Ascending venography (inject radioopaque in foot and
watching it rise in the deep vein)
Varicose
eczema
Chronic leg ulcer
Neuropathic ulcer
Venous ulcer
Arterial ulcer
Acute non-traumatic leg pain
Localised to skin
soft tissue, vein
-cellulitis
-lymphagitis
-thrombophlebitis
Pain radiate from back
Exacebate by bending
-lumbosacral N root
compression
Deep pain in whole legThigh, calf
5P
Pain, uniform swelling
No paresis or sensory loss
Emboli source, no IC,N contralat pulse*heparin
+ac emboli
- ac thrombosis
DVT,
rupture of baker’s cyst
Chronic non-traumatic leg pain
Pain radiate from back
Exacebate by bending
-lumbosacral N root
compression
Pain in calf, foot
Not radiate to back
claudication
Critical limb ischaemia
Rest pain, gangrene, ulcer
Varicose vein
History of swelling, DVT
Confirm with duplex scan
Primary VV
Intervention
Sx, sclerotherapy
Secondary VV
Supportive treatment
edge
base
Ulcer
Punch out
Black, dry
Deep to tendon
position Digit, heel
Ischaemic ulcer
Flat, sloping edge, soft
Shallow, edema, erythrema
Infection, granulation tissue
Digit, pressure
Point, heel,
metartarsal head
Sensory ulcer
Above media
malleolus
Asso DVI
Venous ulcer