Peripheral vascular disease

 

PVD refers to any disease of the peripheral arterial blood supply; PAD is probably a more accurate description

 

Leg arterial system

Abdominal aorta - iliac - femoral - posterior and anterior tibial - dorsalis pedis - planter arch - metatarsal arteries

 

Arterial supply is maintained by systemic blood pressure

generated in the left ventricle

 

Fluids will move from areas of high pressure to areas of low pressure

 

Aetiology of PVD

Mostly as for atherosclerosis Diabetes

Obesity Lack of exercise

 

Pathophysiology

Atherosclerosis leads to increasing distal ischaemia

 

Clinical features

Claudication Diminished peripheral pulses

Pain at night Loss of peripheral hair

Shiny thin skin Discolouration of periphery

Cold feet Peripheral neuropathy

Arterial leg ulceration Ischaemic gangrene

 

Treatments

Stop smoking Exercise

Diet Pain relief

Treat hypertension Treat hyperlipdaemia

Aspirin Avoid caffeine

Keep warm Keep low

Never use compression Sympathectomy

Angioplasty Bypass surgery

Amputation

 

All patients with PVD should have their risk factors for coronary heart disease assessed and when appropriate modified according to current guidelines

 

Leg ulcers

 

A symptom

A loss of skin below the knee which takes more than six weeks to heal

Recognised in history, were fully documented in 1446

Classified according to aetiology; arterial, venous, mixed venous and arterial, diabetic, tropical

Most common reason for DN visits in the UK

Costs to NHS are approximately 400 million per year

Many can be healed in 12 weeks with proper management

Venous anatomy and physiology

 

Superficial veins

Have valves A low pressure system

Short saphenous and great saphenous

 

Deep veins

Lie deep usually adjacent to arteries A high pressure system

 

Perforating veins

Pierce the deep fascia, also called communicator veins

Connect the superficial and deep venous systems

Valves allow flow from the superficial to the deep venous system and prevent flow from deep to superficial system

 

Venous ulcers

 

Incidence

1-2% of population at some time in their lives

Increases with age but may occur under 30 years

Arterial - 20% Mixed - 21% Venous - 59%

Women > men

 

Aetiology of venous ulcers

Most common cause of all UK leg ulcers

Poor venous return from the leg

Abnormal venous circulation usually begins with damaged or incompetent valves in the perforator veins

This allows back-flow of blood at relatively high pressure from the deep veins into the superficial veins

This increases hydrostatic pressure in the venous end of the capillaries

This reduces the reabsorption of tissue fluid

This results in relative haemo and lymphatic stasis

This causes oedema and staining of the superficial tissues

It also causes an increase in the diffusional distance between capillaries and tissue cells

Tissue cells are therefore embarrassed in terms of oxygen and nutrient supplies

They are also embarrassed in terms of waste accumulation

The combination of these factors causes reduced cell health may lead to cell death

Cell death causes area of localised tissue necrosis

Areas of tissue necrosis are essentially what an ulcer is

 

Fibrin cuff hypothesis

Normal capillary walls are thin to allow exchange of materials between capillary and tissue fluid

In venous hypertension the capillary wall is stretched due to chronically increased hydrostatic pressure

This increased the gaps between capillary wall cells allowing increased permeability

Increased permeability allow large molecules to leak out from the capillaries

Fibrinogen, a plasma protein exudes from the capillary and is converted to fibrin which accumulates around the outside of the capillary

This accumulated fibrin starts to form a sleeve or cuff around the capillary

The fibrin cuff acts as a barrier to the diffusion of oxygen and nutrients - the skin normally served by the capillaries is therefore embarrassed and eventually dies

Therefore an ulcer is formed

This has clear implications for healing and reoccurrence

 

Clinical features of venous ulcers

Skin staining Often gaiter area

Exuding wound Shallow with diffuse edge

Generalised limb oedema Some pain, (usually less than arterial)

Doppler > 0.8`Evidence of varicosities

 

Aetiology of chronic venous hypertension

 

Systemic

Often bilateral Obesity Pregnancy Right ventricular failure

 

Localised

May only effect one limb Congenital factors Varicose veins

Valve incompetence Immobility Calf pump failure

DVT Degenerative changes Occupation

 

 

Arterial ulcers

 

Aetiology

Arterial disease causing poor blood supply

 

Embolism in smaller arteries may cause severe ischaemia or even infarction leading to tissue breakdown

 

Atherosclerosis and arteriolosclerosis may lead to ischaemia

 

Arterial narrowing due to disease may also lead to tissue breakdown and ulceration but the process is more gradual than in blockage caused by an embolism

 

May extend down to the deep fascia, muscles and tendons

 

Poor blood supply ------- hypoxic cells, nutritionally deficient, accumulation of waste metabolites ------- cell embarrassment and death ------- small areas of necrosis ------- ulcer formation

 

May improve with the development of collateral circulation

 

Aetiology of arterial ulceration

As for atherosclerosis

Also emboli may occlude peripheral circulation

 

Features of leg arterial disease

Pain helped by hanging leg over the edge of the bed Pain may be worse with exercise

Doppler < 0.5` Skin in area cold

Skin in area shiny Loss of hair on leg and foot

Skin feels cold Dystrophic and ridged toe nails

Poor capillary refill Possible Claudication

RPI , 0.8` represents significant arterial impairment, refer < 0.5 to vascular surgeon

Commonly below ankle but may be any part of the leg

Usually dry wounds "Cliff" edges

May be deep, extending down to muscles and tendons

Localised oedema no skin staining Pain often worse at night

 

 

Other causes of limb swelling

Hypoproteinameia

Malnutrition

Nephrotic syndrome

 

Compression

Increases the pressure in the superficial veins so increases blood flow from superficial to deep veins, via perforator veins.

 

Once in the deep veins venous return occurs via the usual mechanisms.

 

 

Acute limb ischaemia

 

Features

Pain - may be pain on squeezing the calf, occasionally absent in complete ischaemia

Pallor - white colour then mottled

Pulseless

Paralysis - inability to wiggle toes

Paraesthesia - leading to anaesthesia - loss of touch sensation on dorsum of foot

Perishing cold - assumes ambient temperature

 

Aetiology

60% thrombosis from pre-existing lesion

30% embolism, (80% of which from Left Atria, usually from AF)

Trauma - fractures, (eg tibial), dislocations, blunt trauma

IA drugs - intense spasm and microvascular thrombosis

Aortic dissection

 

Management

Only a few hours to save the limb

Possible angiography

IV heparin to prevent extension

Surgical revascularization, embolectomy, thrombectomy

 

Reperfusion effects

 

Local

Limb swelling due to increased capillary permeability ----compartment syndrome

 

Systemic

Acidosis and hyperkalaemia from damaged cells ---- cardiac arrhythmias

Myoglobin breakdown --- myoglobinaemia --- tubular necrosis

Acute respiratory distress

Increased GI vascular permeability --- toxic shock