Approach in Vascular Patient

กิ�ตต�พั�นธุ์� ฤกิษ์เกิษ์ม PhD, FACA

Topic

• Artery - Limb Ischaemia

- Aneurysm

• Venous - Varicose vein

• Leg ulcer

Limb Ischaemia

• Aetiology: most often atherosclerosis > trauma

• Most management decisions are based upon1.Differentiation acute vs chronic2. Mechanism of occlusion 3.Location of the occlusion4.Status of limb5.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 ischaem

ia

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 aort a 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,

occlusive lesion

2. 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 A

AA”

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 veinThese 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 scanAscending 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 backExacebate by bending-lumbosacral N root compression

Deep pain in whole legThigh, calf

Pain, uniform swellingNo paresis or sensory loss

DVT, rupture of baker’s cyst

5P

Emboli source, no IC,N contralat pulse*heparin

+ac emboli - ac thrombosis

Chronic non-traumatic leg pain

Pain radiate from backExacebate by bending-lumbosacral N root compression

Pain in calf, footNot radiate to back

Critical limb ischaemiaRest pain, gangrene, ulcer

claudication

Varicose vein

Primary VV Secondary VV

History of swelling, DVTConfirm with duplex scan

InterventionSx, sclerotherapy

Supportive treatment

Ulcer

edge

base

position

Punch out

Black, dryDeep to tendon

Digit, heel

Ischaemic ulcer

Flat, sloping edge, soft

Shallow, edema, erythremaInfection, granulation tissue

Digit, pressurePoint, heel, metartarsal head

Sensory ulcer

Above medial malleolusAsso DVI

Venous ulcer