Superficial veins
Short saphenous
Great saphenous
Deep veins
Eg. popliteal,
femoral, iliac vein
Perforating veins
Pierce the fascia at three levels in
the lower leg
Capillary physiology
Leg ulcers
A loss of skin below the knee which takes more than six
weeks to heal
Incidence
1-2% of population
Arterial - 20%
Mixed -
21%
Venous - 59%
Aim of treatment
Correct underlying condition
Treat the wound
Minimise risk of recurrence
Venous ulcers
Mechanisms of tissue embarrassment in
CVH
Reduced
blood flow
Increased
diffusional distance
Fibrin
cuff hypothesis
White
cell trapping theory
Aetiology of CVH
Venous
valve incompetence
Deep vein thrombosis
Congenital disorders
Degenerative ageing changes
Calf pump
failure
Additional
aetiological factors
Pregnancy
Immobility
Genetic predisposition
Right ventricular failure
Any condition causing chronic venous hypertension (CVH)
Features of CVH
Oedema
Staining of skin
Ankle flare
Atrophy of the skin
Eczema
Varicose veins
Lipodermosclerosis
Identification of venous ulcers
Skin staining
Often gaiter area
Exuding wound
Shallow with diffuse edge
Generalised limb oedema
Some pain
ABPI > 0.8
Evidence of varicosities
Features of
leg arterial disease
Pain (partly dependent)
Pain may be worse with exercise
ABPI < 0.9
Skin - cold
Skin - shiny
Loss of hair on leg and foot
Dystrophic and ridged toe nails
Poor capillary refill
Possible Claudication
ABPI - 0.8 represents significant arterial impairment,
refer < 0.5 to vascular surgeon
Identification
Commonly below ankle
May be any part of the leg
Usually dry wounds
"Cliff" edges
May be deep
Localised oedema
No skin staining
Pain often worse at night
Differential diagnosis
Site
Floor
Edge
Discharge
Oedema
Staining
Varicosities
Pulses
Pain
ABPI
Mixed
ulcers
Identification
Mixed venous and arterial aetiology from venous and
arterial insufficiency
Doppler 0.5 - 0.8`
May be additional aetiological factors as well as
vascular
Assessment
Identify the principle aetiology as this will effect
management.
There is usually a primary aetiology
Differential
diagnosis
Additional possible aetiological influences
* Diabetes
* Rheumatoid
arthritis (vasculitis)
* Crohns (vasculitis)
* Squamous
or basal cell carcinoma
* Colitis
* Hyperthyroidism
* Sickle
cell disease
* Trauma
* IV drug
abuse
Ulcer type is usually a nursing diagnosis and vitally
alters the management
About 70% of healed vascular ulcers recur - pay
attention to continued compression, exercise, skin care, vigilance, holism
Diabetic
ulcers
Diabetes probably affects up to 3% of the
Complications affecting the feet and legs account for
47% of hospital admissions in diabetics
In the
In diabetes complications are positively correlated with
poor glycaemic control
Diabetics should take regular exercise and have a
healthy diet
Smoking must be prohibited
Diffuse glycosalation of
tissues occurs
Complications
of diabetes
Remember to take into consideration the other long term
complications of diabetes, eg. diabetic nephropathy,
ischaemic heart disease, stroke, diabetic retinopathy, other vascular disease
and excess mortality
Infections due to poor glycaemic control
;- skin, urinary, lung
Chemotaxis and phagocytosis is impaired at high
glucose concentrations
Up to 25% extra insulin may be required during
infections
Aetiology
Three main factors leading to distal necrosis are
neuropathy, ischaemia and immunosuppression.
Neuropathy
Secondary to microvascular complications and a direct
effect of chronic hyperglycaemia on the nerve fibres
BPI may be normal or near normal
Sensory
Most common neuropathy
Damage to sensory nerves
Features of sensory neuropathy
Patient fails to feel noxious stimuli (always inspect
the feet)
Test with a 10g filament
Warm and well perfused
Tingling and subjective coldness
Dilated veins
Often full pulses
Dry
Callus formation on soles due to pressure
Yellowish colour
Ulcers form below callus
Very rapid spread possible ---- severe infections
Management of sensory neuropathy
Sharp debridement
Relief of pressure to ulcer area, usually soles of feet
Wound management
Systemic corrections
Motor neuropathy
Weakness and wasting of small muscles in the feet and
can lead to deformities
Less common
Clawed toe deformity leads to exposing metatarsal heads
to pressure and trauma
Aetiological
factors in the neuropathic foot:-
Neglected/unnoticed thermal, chemical, mechanical injury
Tight or poorly fitting shoes
Neglected callosity at areas of friction or pressure is
the most common cause
Tissue necrosis occurs below the callous plaque and
serious fluid accumulates and eventually breaks through the surface with
resulting ulcer formation
After this infection may complicate the ulcer -
diabetics are more prone to infection due to abnormal glycaemic control
Usual infective organisms are skin flora, eg, staphylococcus and streptococcus
Cellulitis can develop with abscess formation
May be tracking of pus to tendons and bones
Lesions are often not very painful and may often be
debrided without anaesthetic
Ischaemia
Macrovascular
complications in diabetes
A significant excess compared to their background
population
Stroke -
twice as likely
Myocardial infarction -
three to five times as likely
Amputation of the foot -
fifty times as likely
Consider;- - duration of
diabetes
-
age
-
systolic BP
-
obesity
-
dys or hyperlipidaemia
-
proteinuria and microalbuminuria
Microvascular
complications
This pathology is specific to diabetes, unlike the
macrovascular complications
Small blood vessels throughout the body are affected but
particularly affect the retina, renal glomerulus and the nerve sheath
Atherosclerosis occurs extensively in diabetics leading
to pathology at an earlier age than in non-diabetics
In
ischaemia
Claudication and ischaemic leg changes may result
Poorly nourished tissues are therefore predisposed to
gangrene
Poor blood flow - cold, absent or diminished pulses
Ulceration often results from localised pressure
necrosis, but may be spontaneous
Often painful, even at rest
Infection may complicate the condition
Prognosis is fairly poor, surgery is common
Management
principles
Many foot problems may be delayed or avoided
;- Shoes, patient education, smoking, chiropodist
Prevent necrosis, preserve viable tissue
Infection
Takes hold rapidly - early antibiotics
Drain collections of pus
Monitor for osteomyelitis, x rays and excision if no response
to antibiotics
* debridement
* Clean
with saline
* Dry
very thoroughly, eg between toes
* Antibiotics
for usual indications
* Non
weight bearing during healing
* Dressings
Identification
Primary aetiology may not be diabetic, eg in growing toe nail or osteoarthritis
Doppler may show normal RPI
Ischaemia, neuropathy and infection may coexist, but
decide what is the primary aetiology
Feature Ischaemia Neuropathy
Symptoms
Temperature
Moisture
Pulses
Ulceration
Area effected
Tropical
ulcers
A well recognised syndrome with no
known aetiology and non-specific treatment
Various tropical infections may also cause ulceration in
the tropics
Very common in the tropics
90 % occur below the knee
Arterial and venous circulation are
normal
Aetiology
Not known
Factors may include;-
* local injury
* insect bite
* Vincent`s organisms (a fusiform
bacteria and beta-haemolytic streptococci) often isolated in culture
Evolution
Painful papule or blister which breaks down to form an
ulcer
Continued pain
Spreads over the next few weeks to form the ulcer
Mature size is typically 1-10 cm in diameter
Edges; swollen, slightly raised, red, tender
Floor penetrates to the superficial fascia
Floor covered in granulation tissue and pus
Some heal spontaneously, others persist for years
Once the ulcers become fibrosed
they often persist for life
Complications
* Deep
infection eg. bone or joint
* Septicaemia
* Epithelioma
* Secondary
infection
* Tetanus
Diagnosis
Is it a tropical ulcer or is there a specific aetiology
in the particular case
No specific diagnosis
Exclusion of other causes
Satisfactory response to non-specific treatment
Treatment
Stage 1 - Removal
of pus, slough and surface pathogens
Use 1% hydrogen peroxide or EUSOL
Apply wet antiseptic dressing
Keep wet with polythene
Change daily for 3 - 7 days until the ulcer looks clean
Stage 2 - Elimination of bacteria from tissues
Follow a protocol of large doses of injected penicillin
for 3 - 7 days
Causal organisms will respond to penicillins
Pain disappears usually in three days
Stage 3 - Non
- adherent dressings
These will permit healing
Leave on for as long as possible, eg. 10 - 14 days
Delicate dressing changes so as not to disturb delicate
new skin at the edges
If found to be re-infected in this stage clean as in
stage 1 then return to stage 3
Preserve any skin islands
This procedure will heal up all tropical ulcers of
recent onset in a few weeks
End result of healing is a thin papery scar so protect
if over a bony area
Scar breakdown may occur 35 years after original healing
If the ulcer does not respond to non-specific treatment
in 6 weeks investigate further as it may not be a tropical ulcer
Treatment
of chronic, raised fibrosed tropical ulcers
These often fail to respond to conservative treatment
Excise fibrous tissue and graft
Precede grafting with stages 1 and 2