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
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
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