LEG ULCERS

Contents of this document:

Etiology, differentiation of ulcer, examinations of different type of ulcers.
Management of DFU, venous ulcer, arterial ulcer, pressure ulcers.

Causes/Etiology of Ulcer

Vascular CRT>2s
cause Pulse not palpable
Loss of skin hair
Venous ulcer: at gaiter area, medial 1/3 of leg above medial malleolus
Arterial ulcer: at pressure point blood diverted from pressure point lack
of blood supply ischaemic. Highest pressure which is in contact with
shoes:
o 1st and last digit
o Tip of digit
o Calcaneus
Neuropathic Look at typical side: MTP, highest pressure at 1st and 5th metatarsal area
ulcer and tip of digit
Associated with diabetes mellitus
Claw deformity
Loss of hair
Muscle wasting
Infection Rotting appearance
Around nail and webspace
History: accidentally cut nail fold and become infected, rub webspace with
slipper ulcer infected
Inguinal lymph node enlarged sign of infection
Trauma Usually wound will heal
If not heal chronic ulcer
Malignancy Inverted margin, central raised and indurated, smells worse, borders are
spread and raised. Surrounded by lipodermatosclerosis and skin
pigmentation
Ulcer failed to heal
Check inguinal node if enlarged
Eg Marjolins ulcer, lymphoma, BCC, SCC, malignant melanoma
Ix: biopsy of the peripheral area of the ulcer in order to obtain histological
confirmation (central area is likely to contain necrotic tissue which is hard to
visualize for histological diagnosis)
Mx: wide excision and split skin grafting
Inflammatory Pyoderma gangrenosum (complication of systemic inflammatory diseases eg
Crohns disease, UC, RA) or haematological malignancies
Mx: good nursing care (bandages to prevent infection and promote healing)
and treatment of underlying disease. IV corticosteroids for UC and ulcer will
heal as UC settles.
Differentiating venous, arterial, diabetic leg ulcers

History Venous ulcers Arterial (atherosclerotic Neuropathic ulcers

ulcers)
Is the Caused by venous stasis Caused by ischaemia to the Caused by loss of
ulcer in the leg, so less painful leg, more painful when sensation (which
painful? when elevated and elevated and drained of predisposes to constant
drained of blood. blood. trauma)
30% is painful. Painful that it wakes them Due to ischaemis to
up at night delicate tissue from
Relief by lowering leg over repeated trauma and
the side of the bed pressure + reduced
ability to heal skin break
and fight infection.
Not painful
How long Less painful so present Present early due to pain Associated with loss of
has the late Often occur secondary to sensation so present late
ulcer been Long and recurring trivial trauma
there? history
Associated Chronic venous Manifest systemically, thus Sensory loss
symptoms insufficiency leads to asks about symptoms of Contractions of feet
varicose veins, pruritic PAD, coronary artery or Charcot joints
stasis eczema, and cerebrovascular dx Unsteady gait
discolouration of skin Claudication, night pain, rest Often secondary
(haemosiderin pain (increased with limb infection, if by
deposition, stasis elevation), cold extremities, anaerobes patient may
dermatitis, angina, SOB on exertion, hx comment on foul smell.
lipodermatosclerosis) of stroke or TIA
Ankle oedema (impaired How far can you walk
venous return) without calf pain?
Swollen ankles and
sensation of heavy feet
Risk Varicose veins, esp if Artherosclerosis (smoking, Mostly in patient with
factors immobile (reduced DM, HTN, hyperlipidaemia, DM or alcohol overuse
venous drainage), strong family hx of Poor foot care
and/or malnourished atherosclerotic disease)
(reduced healing) Evidence of other
DVT atherosclerotic dx: CAD
Pelvic mass (angina, MI)
(compressing iliac veins) CVD (TIA, stroke)
AV malformations PAD (claudication,
(increase venous impotence, AAA)
pressure)
Major joint replacement
assoc with DVT
Any
history of
trauma?
Clinical Examinations

Descriptions of the ulcer

Pulse status:
o Dorsalis pedis artery
o Posterior tibial artery
o Popliteal artery
o Femoral artery
Sensory
Gait: particularly ankle mobility

Clinical Venous ulcers Arterial Neuropathic Pressure ulcers

examinations (atherosclerotic ulcers
ulcers)
Site of ulcer Occur where venous Occur where Occur at site of Caused by
pressures are arterial blood repetitive constant
highest, ie gaiter supply is worst, ie trauma in a foot pressure
area: 1/3 of medial distal areas of that has lost Usually on bony
leg, above the foot (eg between sensation prominences eg
medial malleolus toes) So occur in heel or overlying
Most commonly Those that are pressure areas malleoli in
affected is above frequently of foot immobile,
medial malleolus compressed (ie Where foot rubs bedridden
because this is the ball of foot, lateral on poorly fitting patient eg
site of medial calf malleolus, bony footwear (ie sacrum
perforators prominences) beneath Usually in
Anywhere below metatarsal debilitated,
mid calf heads) elderly or
Can be at the unconscious
sole beneath patients:
metatarsal discolouration
heads or at bony necrotic
prominences: ulceration
toes, ball of
great toe and
malleoli
Characteristics Shallow Deep Thick, keratinized
of ulcer Wet Punched out Raised edges surrounding them
Irregular borders Dry (thicken skin referred as callus)
that look white and Often elliptical Raised callus edges
fragile
Sloping edges
Associated Due to increase Due to limb Due to loss of Due to immobility
signs hydrostatic (venous) ischaemia sensation and constant
pressure: oedema, Cold Loss of vibration pressure.
extravasation Pale limbs with and Leg, sacrum,
Death of poor capillary proprioception buttocks
erythrocytes (skin refill Glove and
pigmentation from Venous guttering stocking
distribution of
 haemosiderin Absent/weak peripheral
staining) pulses sensory
Scarring of skin: Atrophic skin neuropathy
atrophie blanche changes (dry, Foot deformities
Underlying tissue: shiny, hairless) due to motor
lipodermatosclerosis Buergers test: neuropathy or
(indurated, blanching of foot repetitive joint
hyperpigmented, on elevation to trauma
dry skin at gaiter o
45 and reactive secondary to
area) hyperaemia on sensory
Superficial varicose lowering leg neuropathy
vein (suggesting (Charcot joints)
Ankle flare: arterial Contractures of
Collection of small, insufficiency) foot
dark, engorged Absence/presence
superficial veins of LL pulse
Severe ABPI
lipodermatosclerosis Popliteal
may lead to inverted aneurysm/AAA
champagne bottle
appearance to the
leg

Note:
Critical limb ischaemia: rest pain + tissue loss (gangrene, ulcer), and ABPI <0.5
The Diabetic Foot (foot ulceration in diabetics represents a failure of medical mx)

Pathophysiology
Neuropathy Microangiopathy (small vessel disease) affect motor, sensory and
autonomic nerves
Motor nerves: supply small muscles of foot affected motor
nerves cause consequent unmodified traction of calf muscles
distort the morphology and weight-bearing characteristics of
the foot causing flexion deformity at interphalangeal joint
due to paralysis of small muscle of foot, long flexor and
extensor pull it to claw formation and cause reduce range of
movement clawed foota and distorted sole of foot

Sensory neuropathy: lessens pain sensation reduce

awareness of potential injury from ill-fitting footwear and
foreign bodies in shoes
Damaged autonomic nerves: disrupt vascular control loss
of hair skin, dry, pigmentation, no sweat, brittle nail
Arteriovenous Beneath the skin, diverting nutrient flow away from it
communication damaged tissues heal poorly, vulnerable to infection
Ischaemic diabetic foot can be warm and pink
Arterioles Narrowed and restrict capillary perfusion
Impaired Favour bacterial growth spreading infection
intermediary
tissue
metabolism and
glucose-rich
tissue
environment
Obliterative Increased predisposition to arterial insufficiency
atherosclerosis Atherosclerotic disease in diabetic patients follows usual
disease of arterial pattern (but more distal)
vessels Tends to develop at younger age
associated with
walls thickening
due to deposit of
cholesterol and
lipids
Identifying Primarily neuropathic or primarily atherosclerotic or BOTH
causes of o Neuropathic: painless, red, warm, strong pulse
diabetic foot o Atherosclerotic: pale, painful, cold, pulseless
problems o If BOTH: limb seriously ischaemic yet painless, warm and pink (diabetic trap)
o Only arteriography or duplex scanning will demonstrate arterial insufficiency
Patients at risk of neuropathic foot complications: elderly, poorly controlled, type 2
DM, younger patient with long standing type 1 DM, patients with diabetic renal or
retinal complications can prevent with education, regular inspection and
chiropody (podiatry)
If mixed disease arterial insufficiency needs to be treated first
4 foot
complications of Painless, deeply Usually in pressure areas caused by distortion of foot
diabetic penetrating ulcers: morphology ie 1st or 5th metatarsal head
neuropathy Organism: staphylococcus aureus
Infection and necrosis spread through plantar spaces and
along tendon sheaths
Infection and local venous thrombosis is the predominant
factors causing tissue destruction
Chronic ulceration Skin perfusion otherwise adequate
of pressure points
and sites of minor
injury
Extensive Originating in ulcer
spreading skin Caused by superficial/deep infection
necrosis Very rapid and spreads proximally
Painless necrosis of Turn blue black mummified shed spontaneously
individual toes Usually in mixed neuropathy and atherosclerosis

Management of
foot Control of infection Major complication in DFU is infection
complications o TRO osteomyelitis
o Plain film of the foot show any bony deformity,
gas in the soft tissues, signs of osteomyelitis (eg
osteolysis = reduced opacity, periosteal reaction =
formation of new bone from cortex outwards)
o If plain film inconclusive, use MRI
After excluding ischaemia
Minor foot lesions treated early with oral antibiotics
(including cover for anaerobes) + frequent local cleansing
and dressing
If there is any sign of spreading infection or systemic
involvement ie pyrexia, tachycardia or loss of diabetic
control admit hospital give parenteral a/b, elevation,
excision of necrotic tissue and blood glucose control
Immediate drainage of pus: emergency
Specialist management of blood sugar: MDT
Removal of Simple desloughing of ulcer to major amputation
necrotic tissues complete and rapid healing
Good foot care
 Before debridement, arterial inflow must be assessed
foot revascularised if necessary to maximize chances of
wound healing
Tx:
o Long term antibiotics (parenteral) or surgical
excision
o Prolonged antibiotics can increase risk of C.difficile
and emergence of multi drug resistant organisms
Prevention of Screen patient for peripheral neuropathy
diabetic foot Give detailed advice on self-care and high quality
chiropody or podiatry.
Foot care:
o Attention to footwear to correct abnormal pressure
patterns use special insoles or special shoes
o No tight-fitting shoes until ulcer is healed
o Soft, comfortable shoes
o Examine feet daily
o Follow up and regular monitoring by diabetic
specialist nurse or clinic
o Manage diabetes: optimize diabetic control
Operations on Types of local amputation:
diabetic foot o Excision of necrotic tissues
o Digit amputation
o Filleting of digit and metatarsal (cake-slice
procedure)
o Transmetatarsal amputation
Lower limb 2 principles guide:
amputation o Amputation made through healthy tissues to
prevent risk of wound breakdown and chronic
ulceration. If amputation for uncorrected
peripheral ischaemia amputate above knee to
ensure healing
o Choice of amputation level takes into account
fitting of prosthetic limb. Less energy needed for
moving prosthesis if knee joint is conserved.
Wound is left to heal by secondary intention

Above 22-25cm below greater trochanter

knee Use equal anterior and posterior skin
amputation flaps
Below knee 10-12cm below tibial tuberosity
amputation Use of long posterior muscle flap
Symes Malleoli cut level with inferior surface
(heel flap) of tibia
Mid tarsal
amputation

Rehab and limb fitting:

o At 1 week: bear weight on the other limb
o At 10 days: pneumatic walking aids
o 3 weeks: prosthesis
MANAGEMENT OF VENOUS ULCERS

Investigations
Blood FBC anaemia exacerbate ischaemia, contribute to delayed healing. Raised WCC in
infection.
Fasting lipids hyperlipidaemia contribute to atherosclerosis
ESR increase in inflammation
CRP increase in inflammation
Rheumatoid serology joint disease may cause ulcer
Capillary glucose undetected DM poor healing ulcer
TFT
Urinalysis Look for glucose: DM affects healing
Venous Gold standard
duplex Assess competence of saphenofemoral and saphenopopliteal junctions
ultrasound Assess state of perforators and deep venous system
Ankle- To exclude arterial disease as the cause
brachial Find ratio of ankle to brachial pressure
pressure Brachial pressure: measure as normally
index (ABPI) Ankle pressure: sphygmomanometer and portable Doppler probe
Significance:

ABPI < 0.8 Must not have pressure bandage applied

This suggests that ulcer is mixed arterial/venous
ulcer
Compression will make arterial ischaemia worse
ABPI < 0.5 Critical limb ischaemia, refer to vascular surgeon
Swabbing In case of spreading cellulitis
Biopsy If suspect Marjolins ulcer

Managements
Adequate Vital for healing process
nutrition Especially relevant for venous ulcers as they tend to occur in elderly patients who
may be malnourished or deficient in vitamins and minerals eg vit C, zinc
Lifestyle Encourage patients to mobilise (encourage venous blood flow in the legs)
modification Obese patient encouraged to lose weight in longer time
Leg elevation To reduce venous stasis in lower limb
Compression Applied and frequently changes
bandages To reduce pooling of venous blood in LL
Can be done safely if ABPI < 0.8
Graduated Helpful once venous ulcer has healed to prevent recurrence
class I or II
elastic
stockings
Varicose vein If there is venous duplex evidence of incompetence superficial venous system and no
surgery deep vein incompetence, it can be helpful to prevent recurrence
Split skin If other measures fail
grafting To speed up healing = only if underlying venous abnormality has been corrected.
MANAGEMENT OF ARTERIAL ULCERS

Investigations
Arterial duplex To assess patency of the arteries and potential for revascularization or bypass
ultrasonography surgery
of his lower Alternatively, do percutaneous angiography to allow assessment and treatment
limbs (or MR (angioplasty) to be done all in one.
angiography if If patient takes metformin for DM, withheld metformin 24 hours after contrast
vessels are insertion to avoid lactic acidosis if nothing happened, can resume metformin
highly calcified) back
ECG Risk of heart changes in view of atherosclerosis
Fasting serum To see if lipid and glucose control are adequate
lipids, fasting
glucose, and
HbA1c levels
FBC Anaemia can exacerbate ischaemia
Interim management
Dressing of To prevent infection
ulcers Make sure bandage is not too tight, can worsen the ischaemia
Dont prescribed compression stockings this one to prevent DVT
Analgesia PCM 1g 6 hourly
Antibiotics If there are sign of infection
Surgical intervention
Angioplasty +/- If artery is stenotic or there is a short occlusion and patent artery downstream of
stenting the occlusion
Bypass surgery Using venous graft or artificial conduit if angioplasty is not possible (requires distal
run off)
Amputation If there is no suitable target for angioplasty, and insufficient distal run-off onto
which the vascular surgeons can anastomose a bypass graft, patient with intractable
pain and ulceration will be offered an amputation
MANAGEMENT OF PRESSURE ULCERS

Record the Grade the ulcer using European Pressure Ulcer Advisory Panel classification from 1
ulcers to 4 in severity
o Measure dimensions
o Document locations
o Take photographs of the ulcer

Grade 1 Non-blanching erythema of intact skin

Grade 2 Partial thickness skin loss or blistering
Grade 3 Full thickness skin lost/ SC fat visible but not underlying tendon, bone,
muscle, etc
Grade 4 Full thickness tissue loss with involvement of bone/muscle/tendon.
Covered with thick slough or eschar.

To assess improvement or deterioration in the ulcers

Ulcer form very rapidly, and can heal or deteriorate more slowly and can be hard
to notice any change over time
Relieve the Dress the ulcer using soft, moist, padded, modern ulcer dressing (eg hydrocolloid,
ulcer hydrogel, foam)
Use pressure relieving mattress
Ensure patient is moved regularly if cannot do so themselves
Limit amount of time sitting on chair < 2 hours at a time
Physiotherapy and occupational therapy to maximize mobility
Reduce further Optimize patients nutrition
ulcers Educate carers and family members
Reassess ulcers Done regularly
Using objective parameters as described earlier
Involve the Specialist nurses who are experts at wound care and can advise on specific
tissue viability dressings and further management eg when to refer to surgical debridement
team