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Approach in Vascular

Patient
dr Putra Hendra SpPD
Uniba

Topic
Artery

- Limb Ischaemia
- Aneurysm

Venous
Leg ulcer

- Varicose vein

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
Periode of onset in minutes or hours
Sudden catastrophic
Less effect in upper extremity

Acute ischaemia
Symptom

5P

pain
pulselessness
paresthesia
pallor
paralysis

Marble white
right foot in
acute limb isch
aemia

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


Virchows 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

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
Progressive narrowing
Cause : Atheromatous disease is the common cause
Other uncommon cause: Aneurysm:
popliteal aneurysm: special nature
Diabetes
Some rare disease
Buergers disease
Hyperhomocysteineaemia
Takayasus disease

Chronic ischaemia
Symptom

and sign

Claudication
rest pain
ulceration/gangrene

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

Bilateral occlusion of superficial femoral artery


with collateral circulation via profunda

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

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?

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

Venous disease

Functional anatomy
1.

Superficial venous system:


devided into 3 parts

Long saphenous vein (LSV)


Short saphenous vein (SSV)
Perforating or communicating vein (PV)
2. Deep venous system

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 veins


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 bakers 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