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Leprosy: Trophic Skin Ulcers

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 January/February 2017 Volume 15 Issue 1

Core curriculum
Virendra N. Sehgal, MD, FNASc, FAMS, Section Editor

Leprosy: Trophic Skin Ulcers

Najeeba Riyaz, MD, FRCP (Glasgow); Virendra N. Sehgal, MD, FNASc, FAMS

Leprosy is a chronic infectious disease caused by Mycobacterium leprae. Approximately 30% of patients with leprosy develop nerve damage.
Trophic, or neuropathic, ulcer is a common complication of an anesthetic foot. The term plantar, trophic, or perforating ulcer was introduced
in 1959. It was dened as a chronic ulceration of the anesthetic foot, situated in well-dened areas overlying bony prominences, resistant to
local and/or systemic therapy, and characterized by a marked tendency to recur. It is responsible for much of the morbidity associated with
leprosy. (SKINmed. 2017;15:4551)

T
he proportion of new cases presenting with World
Health Organization (WHO)1 grade 2 disability ranges
from 6% to 21%. Among major endemic countries,
plantar ulceration is the most common disability. It occurs in
about 10% to 20% of patients with leprosy,2 with the front part
of the foot accounting for 71% to 90% of plantar ulcers. Its me-
dial part is more vulnerable than the lateral part. The proximal
phalanx of the large toe is the most common site for trophic
ulcers.3
Pathogenesis
Anesthesia of the foot is the central factor in the pathogenesis of
plantar ulcers. An anesthetic foot is ulcer-liable, and ulceration
of the foot makes it ulcer-prone, producing a cycle of scar-
ulcer-scar. Plantar anesthesia, unprotected walking, poor quality
of scar formation resulting from previous ulceration, excessive
load on the scar, and persisting foci of infection are some of the
main factors for the recurrence of plantar ulcers.3
The pathogenesis of plantar trophic ulcers has been extensively
investigated. Five mechanisms that produce damage to insen-
sitive tissues include: (1) continuous pressure, causing necrosis
due to lack of blood supply; (2) concentrated high pressure,
causing cutting/crushing by mechanical violence; (3) heat/cold,
causing burning or frost bite; (4) repetitive mechanical stress of
moderate degree, causing inflammation and autolysis; and (5)
pressure on the infected tissue, resulting in spread of infection.4,5
Ten percent of the ulcers arise from perceived or unperceived
neglected injuries resulting in infection and tissue damage, and
5% arise from neglect of deep cracks in the dry, anhidrotic, and
hyperkeratotic skin of the sole or from infection underneath
callosities or corns through fine cracks. The majority of plantar
ulcers6, however, arise from breakdown of plantar subcutaneous
tissue due to the stress and strain of normal walking.
All plantar intrinsic muscles exert their effect in the region of the
metatarsophalangeal joints. When these muscles are paralyzed,
the compression and shearing forces are increased, even during
normal walking. The plantar intrinsic muscles are maximally ac-
tive during the push-off stage of walking, when the forepart
of the foot pushes the ground backward in order to propel the
body forward. Their contraction creates a thrust that counters
the compressive, shearing, and distracting forces at the meta-
tarsophalangeal joint region that are normally generated at this
stage of walking. When the plantar intrinsic muscles are para-
lyzed, this protective effect is lost, and the toes get clawed during
the push-off stage of walking, causing momentary increases in
stress and strain in the region of the metatarsophalangeal joint at
each step. Even small increases in stresses can lead to breakdown
of tissue if repeated long enough, causing ulceration.6

From the Department of Dermatology Government Medical College Calicut Kerala, Dermato-Venereology (Skin/VD Centre),
Sehgal Nursing Home, Delhi, India
Address for Correspondence: Virendra N. Sehgal, MD, FNASc, FAMS, Dermato-Venerology (Skin/VD) Center, Sehgal Nursing
Home, A/6 Panchwati, Delhi-110 033, India E-mail: drsehgal@ndf.vsnl.net.in

SKINmed. 2017;15:4551 45 2017 Pulse Marketing & Communications, LLC

 January/February 2017 core curriculum

The pathogenesis of plantar ulcers is unique and includes three

stages:

Stage of threatened ulcer: This is called the preulcerative

stage of aseptic inflammation. Increased stress exerted over
a period gives rise to a traumatic (aseptic) inflammation
in the subcutaneous layer of the sole, which is most vul-
nerable to mechanical stress. This usually occurs under a
joint or a bony prominence just distal to the head of a
metatarsal. The affected site is edematous. This is seen as a
mild or obvious splaying of a toe, which stands apart from
other toes. The affected site is often tender to deep digital
pressure.

Stage of concealed ulcer: This is the stage of the ne- Figure 1. Leprosy, trophic skin ulcers: an initial stage
crotic blister. The inflamed site undergoes necrosis due depicting erythema, edema, scaling, and pigmentation
to the stress of continued walking, with the subcuta- on the sole of the right foot.
neous tissue undergoing necrosis. The liquefied tissue
mixed with blood is forced to the surface by continued
walking to present as a blister. This usually overlies the
area of necrosis, but sometimes the overlying tissue is
too tough that it may track along a path of least resis-
tance and emerge to the surface at a distance, at the side
of the toe or in the interdigital web. This stage may go
unnoticed. With the formation of the necrotic blister,
the destruction of the subcutaneous tissue is complete,
except that the ulcer is not seen or obvious because it is
still covered with skin.

Stage of overt or open ulcer: This is the stage when the

skin overlying the blister breaks open and the necrotic area
becomes exteriorized.6

Clinical Connotation

Every ulcer passes through a set of events before becoming indo-

lent. The first stage is acute ulceration, accompanied by pain and
inguinal lymphadenopathy. With rest and antibiotics, the ulcer
may improve. Due to the underlying tissue damage, however,
the ulcer heals with scaring, which may frequently break down
and result in chronic ulceration. An ulcer becomes complicated
due to spread of infection into the deeper structures with associ-
ated paralysis of the foot muscles and fixed deformities resulting
from bone and joint infection. Old healed or latent ulcers break
down and fresh ones appear (Figures 14). These ulcers resist
routine treatment, and the foot becomes the site of recurrent
plantar ulceration.7
A trophic ulcer, which is often painless, does not typically
bother the patient. It may enlarge without healing for weeks
or months. When acutely infected, the area including the
Figure 2. Leprosy, trophic skin ulcers: an initial stage
displaying erythema, edema, and pigmentation affecting
the soles.
edges of the ulcer become swollen, the edema being more
over the dorsum even when the infected site is in the sole.
There is copious discharge of pus/serosanguineous fluid. The
floor of the ulcer is often covered with necrotic tissue. There
may be associated inguinal adenitis, lymphangitis, and fever.
Polymorphonuclear leukocytosis is common. The ulcer pre-
senting with acute inflammation is often referred to as an
acute ulcer. Initially, the infection and inflammation are

SKINmed. 2017;15:4551 46 Leprosy: Trophic Skin Ulcers

 January/February 2017
Figure 3. Leprosy, trophic skin ulcers: break in the skin
apparent as an ulcer with well-defined margins.
Figure 4. Leprosy, trophic skin ulcers: an explicit ulcer on
the sole.
confined to the subcutaneous tissue without extending to
deeper tissue or structures such as bones, joints, or tendon
sheaths. This is called a simple or uncomplicated ulcer.
SKINmed. 2017;15:4551
core curriculum
Usually this stage of acute inflammation subsides with treat-
ment, and the ulcer may heal. After initial improvement, the
ulcer may sometimes recur and persist as a small raw area, a
chronic ulcer.6 Chronic ulcers have scanty discharge, hyper-
keratotic edges, and a hard fibrosed base and floor covered
with pale unhealthy granulation tissue.
Differential Diagnosis
The differential diagnosis of trophic ulcers8 includes other neu-
rogenic ulcers, arterial ulcers, venous ulcers, and ulcers due to
systemic causes. Other neurogenic ulcers are due to diabetic
neuropathy, syringomyelia, spina bifida, and pressure sores. Vas-
cular causes include peripheral arterial disease, microangiopathy,
atherosclerosis, and stasis ulcers. Systemic causes of ulceration
are vitamin B12 deficiency, severe avitaminosis, and gouty ul-
ceration.
There is a high incidence of plantar ulceration in patients with
diabetes.9 Risk factors include deformed insensitive feet, high
foot pressure when standing and walking, reduced blood flow in
feet and calves, and uncontrolled hyperglycemia. Excessive plan-
tar pressure from diabetic peripheral neuropathy is one of the
primary risk factors for foot ulceration.10 Even in the absence of
peripheral vascular disease, patients with peripheral neuropathy
have a seven-fold increase in foot ulceration11 probably caused
by persistent poor microcirculation and high plantar pressure.12
One study found that 40% of ulcerations were located at the
first metatarsal, 40% at the second to fifth metatarsals, and 20%
at the great toe.13 The incidence of heel ulceration14 was found
to be 13% in a population of 314 individuals. In another study,
11% of patients with diabetes had heel ulcers, hypothesizing
that the plantar surface rarely experiences pressure ulceration in
individuals with diabetes.15 Heel ulcerations, however, are direct-
ly correlated with peripheral neuropathy and impaired vascular
status.
Treatment
Trophic ulcers can remain for several years even after the initial
infection is resolved. The most important causal factor for neu-
ropathic foot ulcers is the presence of dynamic or static deformi-
ties leading to local areas of peak pressure on insensitive skin,
well-illustrated by pressure studies.13 This repetitive overload on
specific areas of the sole could partially explain why plantar ul-
cers are deeper and smaller than leg and ankle ulcers.
Treatment should aim at wound management, correction of de-
formity, restoration of sensation, reconstitution of normal skin,
elimination of abnormal pressures, and eradication of deep-seat-
ed infections.7
47 Leprosy: Trophic Skin Ulcers
 January/February 2017
Wound management
Wound management begins with debridement. Surgical de-
bridement should be aggressive to remove surrounding hard
callus, hyperkeratotic skin, and necrotic tissue, resulting in
soft, nonkeratotic wound edges with a well-vascularized tis-
sue bed. After debridement, wound bed preparation is per-
formed for complete healing. Deep tissue culture should be
performed during debridement. Systemic antibiotics, oral and/
or parenteral, are required in the acute infective phase, in the
presence of cellulitis or failure of a properly treated wound to
heal. Topical antimicrobials help to eliminate bacteria in the
ulcer. Osteomyelitis is ruled out by probing the ulcer. If bone
can be reached during probing, the patient most likely has de-
veloped osteomyelitis. Bone probing has a positive predictive
value of 89%. Radiography should be performed in all cases.
Magnetic resonance imaging and bone biopsy are the best tools
for confirming osteomyelitis when probing findings are nega-
tive. A moist wound environment facilitates rapid migration
of keratinocytes into the wound bed; hence, wounds should
be kept as moist as possible, while avoiding maceration of the
surrounding tissues, by constant irrigation or by using an in-
termittent spray.
The recent advent of phenytoin sodium fine powder zinc paste16
has added an innovative dimension in the management of lep-
rosy trophic skin ulcers, purported to recommend the formation
of granulation tissue and/or re-epithelialization as a vital param-
eter in wound healing.
Advanced moist wound therapy
Advanced moist wound therapy8 can be given with hydrogels
and alginates. The silver barrier dressings destroy bacteria in the
wound. The antimicrobial barrier is effective for up to 3 days.
Exudative wounds are dressed with hydrocolloid dressings,
which can absorb the exudate. Dressing selection should be reas-
sessed at regular intervals.
Off-loading pressure
Off-loading pressure is the key to successful management of a
trophic ulcer. It can be achieved by strict bed rest and use of
crutches, wheel chairs, or walkers. Pressure-reducing measures
such as air cushions, waterbeds, plaster boots, total contact cast-
ing, removable contact casting, half shoes, or specialized foot-
wear are also useful. Off-loading devices are not that useful if
they are not used consistently or if compliance is poor. Uncom-
plicated plantar ulcers can heal in approximately 6 to 8 weeks
with strict off-loading. The best off-loading device is a total con-
tact cast (TCC)/plaster boot. TCCs should be applied only after
SKINmed. 2017;15:4551
core curriculum
debridement and removal of all dead tissue. Its greatest advan-
tage is that it is a nonremovable device and thus eliminates the
problem of unreliability. The drawbacks of TCCs are that they
are technically demanding and, if wrongly applied, can lead to
more ulcers. They do not allow for daily inspection and cannot
be used in ischemic ulcers. The problem of a removable plaster
cast is that patients tend to remove it more often, and the off-
loading becomes unreliable.
A new technique for the management of plantar ulcers has been
described.17 In this technique, plaster casing with a window and
a walking iron for weight bearing is used. The advantage is that
dressing can be accomplished through the window, and the pa-
tient can be ambulatory with the walking iron. This helps in
early mobilization and prevents secondary complications such as
foul-smelling discharge, decalcification of bone, and other com-
plications.
Bioengineered tissue and growth factors have been used to
enhance healing. Examples include artificial skin made from
fibroblasts cultured from newborn foreskin and woven poliga-
lacticacid mesh.18,19 Growth factors are proteins secreted by a
variety of cell types during the different phases of wound heal-
ing such as basic fibroblast growth factor,20 epidermal growth
factor,21 and platelet-derived growth factor.22 Becaplermin is
the first recombinant formulation containing platelet-derived
growth factor.
Surgical options8 for reconstruction should be considered for
complicated ulcers with exposed bone or tendons and for non-
healing ulcers even after conservative management for 2 months.
They can range from skin grafts to local regional or free flaps
depending on the available donor tissue and the requirements
of the defects. For smaller defects, however, the best method
of resurfacing plantar ulcers is by using local tissue. While for
medium-sized defects, plantar artery skin fascia flap by Eiffel,
a medial plantar flap with a lateral plantar pedicle by Martin,
and reverse medial plantar artery flap by Gravem,2 are useful ad-
juncts. Advancement flaps, including both approximation and
V-Y advancement flap, rotation flap, or a first toe web flap can
be used for revision of scar in the forefoot. Island and rotation
flaps are helpful in heel scar revision. Availability of a large non-
weight-bearing area facilitates rising of transposition and island
flaps for scar revision in the midfoot.3
Low-level laser therapy (LLLT)23 has been used to accelerate
wound healing since the late 1960s, but its results are controver-
sial. One study24 evaluated the use of LLLT in the treatment of
leprosy ulcers with 66% cure; however, a systematic A Cochrane
review25 did not find evidence of improvement in wound heal-
48 Leprosy: Trophic Skin Ulcers
 January/February 2017
ing related to LLLT. In one study,26 LLLT did not demonstrate
any additional benefit to ulcer healing when compared with the
control group.
Prevention of trophic ulceration
Delayed diagnosis, lack of appropriate treatment, and failure in
control of leprosy reactions contribute to the occurrence of nerve
damage and neuropathic ulcers in patients with leprosy.
The prevention of trophic ulceration in anesthetic feet largely
depends on the even distribution of pressure over the sole of the
foot. The purpose of molding the sole of the shoe to the curva-
ture of the foot is to distribute pressure over more of the plantar
surface of the foot. Accurate molding to all contours of the foot
is not advisable, because the foot moves inside the shoe. An arch
support provides a simple and generally applicable approach to
molding. A metatarsal bar provides another practical approach
to better pressure distribution. A shoe with a rigid sole pivoting
on a rocker near the center of the foot most effectively reduces
pressures under the forefoot of shortened, deformed feet. The
use of insoles made of microcellular rubber is recommended.
It is important to fit each shoe to the patient with a pressure-
indicating footprint for guidance.27
Protective footwear including sports shoes have a definite role
in the protection of feet with sensation loss.28 A total of 506 pa-
tients received footwear in a prevention of disability project, of
which 122 patients with plantar ulcers achieved healing within
1 year of the project and 75% had reduction within the 3-year
period.
Self-care in the presence or absence of medical supervision is
important for prevention of trophic ulcers. Self-care can be de-
fined as the range of behavior undertaken by the individuals to
promote or restore health, or the process of enabling people
to increase control over, and to improve, their health. In self-
care, the affected persons take control of the management of
their condition. They are supported by a team of health and so-
cial care facilitators who empower individuals to solve problems
themselves.
Self-care in the prevention of disability in leprosy is one of the
prime components in the WHO Global Strategy29 for reduc-
ing the leprosy burden and sustaining quality leprosy services.
Self-care measures should include care of dry, denervated skin
of the palms and soles in order to prevent wounds, ulcers, and
skin cracks. Prevention of occupational30 injuries, such as burns
caused by handling hot objects, should be an important aspect
of the counseling of individuals with sensory loss in the limbs.
SKINmed. 2017;15:4551 49
core curriculum
Patients should also be advised regarding safe limits of walking
and the distance in which the patient can walk without damag-
ing the foot. After walking for some known distance, the patient
should rest for about 20 minutes and examine the feet for signs
of internal damage, persistent warmth, swelling or blistering,
burning sensation, or tenderness. The presence of some or all of
these signs indicates that the foot has been damaged and that the
distance walked has exceeded the safe limit for that foot. Patients
should be advised not to walk beyond a safe limit.31
Daily foot checks should be part of the patients routine from a
preventive aspect. Fungal and bacterial infections of the toenails
should be looked for and treated accordingly. Routine grooming
of the nails and feet should be performed in all cases of neuro-
pathic feet. This includes regular trimming of nails, treatment of
ingrown toenails, and application of skin creams to keep the skin
and nails soft. Regular chiropodist care is effective in preventing
ulcers in high-risk individuals.8
Cigarette smoking reduces the rate of oxygen intake and delivery
to the wound site and retards wound repair. Nicotine, carbon
monoxide, and hydrogen cyanide in the smoke also have a toxic
effect on platelets and inhibit normal cellular metabolism, which
may affect healing. Smoking may cause vasoconstriction and ac-
celerate the development of atherosclerosis.8
Record keeping is an essential part of management as it keeps the
treating surgeon and the patient aware of the progress. It should
be performed by photographic record of the ulcers and docu-
menting the length, breadth, and depth of the ulcer at weekly
intervals. If the patient is on a home care regimen, the caregivers
at home can record measurements. It helps to objectively analyze
healing and motivates patients towards self-care.8
Patient education empowers the patient and their caregivers to-
ward preventive measures. All high-risk individuals should have
the benefit of disease-specific education by the primary physi-
cian, books, pamphlets, videos, and/or disease support groups.
Hence, it is worthwhile to summarize the instructions to prevent
trophic ulcer:
Explanation in simple terms about their specific pathology
Lifestyle changes to prevent progression of disease and its
consequences
Cessation of smoking
Regular podiatric care
Strict glycemic control in patients with diabetes
Leprosy: Trophic Skin Ulcers
 January/February 2017
Compression treatment for varicosities
Daily end-of-day check of hands and feet for signs of break-
down
Self-monitoring of sole/fingertip temperature
Specialized footwear for off-loading pressure
Regular follow-up even if there are no ulcers
Anesthetic feet are at risk for developing ulcers, and once ulceration
has occurred, recurrence is likely. This cycle of events may ultimate-
ly result in mutilation of the foot but can be arrested at any stage
provided that prompt and adequate treatment is given and suitable
measures are taken to prevent recurrence of ulcers. In such patients,
even the denervated foot can serve the patient for a long time.32
Malignant transformation33 is a late complication of plantar ul-
cers in leprosy. In a retrospective study conducted at the Na-
tional Center of Leprosy in Casablanca, malignancy was found
in 10 patients, with an average duration of chronic trophic ulcers
of 34.4 years. Clinical appearance at diagnosis was ulcerative and
vegetative tumors. Six patients had metastatic spread. They were
treated by radical amputation. Prevention of such complications
should be part of the national fight against leprosy.
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core curriculum
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51 Leprosy: Trophic Skin Ulcers