LEG ULCERS

Dr. Richard E. Nnabuko

Plastic and Reconstructive Surgeon
National Orthopaedic Hospital,
Enugu

EPIDEMIOLOGY
Definition: recurrent ulcers or first time
ulcers lasting longer than 6 weeks.
Prevalence of leg ulceration in the adult
population, either active or healed is
1- 2%. Oluwasanmi et al:
M:F = 2:1; Age: 2 - 80 years, peak 11 - 40.
Diabetic ulcers account for 45% -70%
of lower extremity amputations in the US.
The most common cause of leg ulcers is
venous disease.

AETIOLOGY OF ULCERS

ULCERS
BENIGN

MALIGNANT

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BENIGN ULCERS

Vascular: arterial; venous; lymphatic

Neuropathic:
Haematologic: red cell dyscrasias
Traumatic:RTA, burns
Metabolic: DM, Gout
Infective: bacterial;fungal; protozoal

BURULI ULCER

SICKLE CELL ULCER

MALIGNANT ULCERS

PRIMARY ULCERS
SECONDARY ULCERS
Metastataic ulcers
Basal Cell Ca
Squamous Cell Ca
Malignant Melanoma
Kaposi Sarcoma

DIAGNOSIS
HISTORY
Onset

and course
Symptoms:
Medical History
Family History
Drug History
Personal Habits

PHYSICAL EXAM.
General
The

Five S
Peripheral
neuropathy
Peripheral pulses
Regional LNs

COMPARISON OF FINDINGS
FINDINGS VENOUS

ARTERIAL

LOCATION MALLEOLAR

PRESSURE PRESSURE
SITES
SITES
PUNCHED OUT, THICK
NECROTIC
CALLUS
BASE

REGIONS

MORPHOL IRREGULAR
BORDERS
OGY
SURROUN
DING SKIN

HAEMOSIDERIN
PIGMENTATION

PHYSICAL VARICOSITIES;
OEDEMA;
EXAM.

SHINY,
ATROPHIC SKIN

NEUROPATHIC

VENOUS ULCER

irregular, shaggy
border.
commonly are located
in the gaiter area.
Venous ulcers are
usually superficial, with
granulation tissue
may be associated
findings such as lower
leg edema, varicose
veins, hemosiderin
pigmentation,

VENOUS ULCERS

PATHOPHYSIOLOGY OF VENOUS ULCERS

Venous system: superficial,communicating, deep.
The Calf muscle pump consists of
(i) the calf muscles
(ii) deep venous compartment or pump chamber
(iii) superficial compartment connecting the superficial
veins to the deep via perforators.
During systole(muscle contraction) flow is cephalward,
during diastole blood fills pump chamber via perforators.
Calf pump dysfunction may arise from
(i) deep vein insufficiency,
(ii) deep vein obstruction,
(iii) superficial vein insufficiency,
(iv) perforator insufficiency
(v) a-v fistulae,
(vi)neuromuscular dysfunction or a combination of the

MICROCIRCULATORY ABNORMALITIES

i) Tissue anoxia theory of Homans - 1917

(ii) A - V shunting theory of Pratt
(iii) Fibrin cuff theory of Browse and
Burnand
(iv) White cell rheology theory of Falanga
and Eaglestein
(v) Growth factor trap theory.
(vi) Focal microvascular ischaemia theory
of Bollinger

FIBRIN CUFF THEORY

Browse

and Burnand put forth the fibrin cuff

theory.
They suggest that pericapillary fibrin cuffs,
typically but not exclusively found in patients
with chronic venous insufficiency, act as an
oxygen diffusion barrier.
Persistence and continued deposition of fibrin
and certain fibrinogen fragments may inhibit the
capacity of fibroblasts to produce collagen and
thus retard repair
Alternatively, fibrin and fibrinogen receptor
breakdown products are chemotactic for
fibroblasts

WHITE CELL RHEOLOGY THEORY

With

the reduction of capillary blood flow in

venous hypertension, trains of white blood
cells cause temporary plugging of capillaries.
Glycoproteins cause leukocytes to become
attached to capillary endothelium.
These white cells become activated, releasing
free radicals, proteolytic enzymes, and
cytokines.
this chronic inflammatory state, if severe
enough, leads to tissue damage and
ulceration

GROWTH FACTOR TRAP THEORY

Fibrinogen

and other
macromolecules, which leak into the
dermis as a result of venous
hypertension and endothelial injury,
"trap" growth factors and matrix
proteins and render them unavailable
for the maintenance of tissue integrity
and repair processes.

FOCAL MICROVASCULAR
ISCHEMIA THEORY
The

main factor in venous

ulceration is focal
microvascular ischemia
secondary to the reduction of
nutritive skin capillaries seen
in chronic venous insufficiency.

ARTERIAL ULCER
suggested

by,
diminished or
absent peripheral
pulses, abnormal
capillary refilling ,
PAIN; I/C
wound bed often
shows a gray or
black base .
ABI is less than or
equal to 0.7

ARTERIAL
ULCERS

ANKLEBRACHIAL
INDEX

Doppler

examination can
determine accurately the
quality of peripheral
arterial blood flow, using
a measurement referred
to as the ankle-brachial
index (ABI). The ABI is
the ratio of systolic
pressure between the
ankle and the arm in the
supine position. In
healthy patients, it
should measure
between 0.8 and 1.1.

NEUROPATHIC ULCER

patient has a history of

diabetes,
complains of
paresthesia or
anesthesia
has a deep ulcer
located over the heel or
metatarsal heads,
surrounded by a thick
white rim of callus
Loss of sensation, light
touch, vibration, or joint
sense

INVESTIGATIONS

LABORATORY

RADIOLOGICAL

Baseline investigations
include complete blood
count, fasting blood
glucose, and serum
albumin to assess
nutritional status.
More extensive studies,
such as erythrocyte
sedimentation rate .
Wound cultures

Rule out osteomyelitis

Vascular studies are
recommended to
assess the presence of
venous outflow
obstruction
Ultrasound scanning
provides anatomic and
functional information
about both arterial and
venous systems
Wound biopsy

TREATMENT GENERAL
MEASURES
Maintain

normal weight and avoid

smoking.
Correct nutritional deficiencies and
any anaemia where present.
Encourage moderate exercise.
Treat any associated medical
disease.

TREATMENT - CONSERVATIVE
Leg

elevation above the

level of the heart
Compression should be
applied immediately after
elevation. to avoid necrosis
or gangrene of the foot, the
ankle-brachial pressure
index should always be
measured before
compression bandages are
applied.

COMPRESSION
Compression systems commonly
used in the management of venous
leg ulcers include
graduated compression stockings,
elastic and nonelastic bandages,
orthotic compression devices, and
intermittent pneumatic compression
pumps.

SURGICAL - DEBRIDEMENT
Debridement

of devitalized material and

necrotic and fibrinous debris promotes
formation of good granulation tissue and
adequate epithelization.
Debridement can be performed with a
curette, forceps, scalpel, or scissors;
moisture-retentive wound dressings
(autolytic), enzymatic preparations
(chemical), or moist saline dressings.
Debridement in neuropathic ulcers
consists of the removal of callus and
devitalized tissue

 Skin

SKIN GRAFTS

grafts often are helpful in promoting healing

of leg ulcers, because even if they do not take,
grafts seem to stimulate wound epithelialization.
For large wounds, split-thickness skin grafting
can be performed using local, spinal, or general
anesthesia.
Meshed grafts are useful for large ulcers,
. For smaller wounds, pinch grafting is a useful
option.
Multiple small pinches (or, alternatively,
superficial punch biopsies) are taken from a
donor site and placed dermal side down on the
ulcer bed.

SPECIFIC WOUND MANAGEMENT

Treat

varicose veins: surgery,

sclerotherapy or both.Removal of
superficial veins contraindicated in
deep vein disease.
Subfascial endoscopic ligation of
incompetent medial perforators.
Deep vein reconstruction.
Sclerotherapy of periulcer varices.

NEWER MANAGEMENT
TECHNIQUES
Topical recombinant human
platelet-derived growth factor
(Regranex) . Formulated into a gel
and used along with initial surgical
debridement, pressure relief and
infection control.
-Human skin equivalent (Apligraf)
and other bioengineered skin grafts.