Principles and Practice of Wound Care

• History
• What is Radiotherapy?
• Methods of Delivery
• Radiation Injury

– Biological Effects

– Radiation Exposure or Accidents

– Radiation Injury During Radiotherapy
• Pathophysiology of the Response to Radiation Injury

– Malignant Transformation—Effect of Chronic Low Dose


Radiation

– Infections and Radiation
• Treatment of Radiation-Induced Wounds

– Cleansers and Moisturizers

– Dressings

– Antibiotics

– Treatment for Xerosis

– Protection
• Radiation Ulcers

– Principles of Management of Radiation Ulcers

– Methods of Wound Closure
• Osteoradionecrosis

– Prophylactive Reconstruction: Pre-emptive Pre-radiation


Flap Surgery

– Pre-emptive Postirradiation Flap Surgery
• Reconstructive Breast Surgery
• Current Treatment Strategies
• Future Treatment Modalities

– Prevention of Radiation Damage to Normal Tissue

– Promotion of Wound Healing Following Radiation


Damage
INTRODUCTION
Radiotherapy has been in use for a century to treat various
cancers. As the survival from cancers improved so did the
more prolonged and profound side effects emerged. The side
effects with prolonged suffering attributed to nonhealing
ulcers, immobility due to fi brosis and other symptoms due
to radiation changes in various body tissues came to light as
the survival from cancer increased. Advances in delivery of
radiotherapy have been not only to improve the cure from
cancers but also to minimize the deleterious side effects.

It is estimated that over 50 percent of all cancer patients
receive some form of radiotherapy as adjuvant, neoadjuvant
or therapeutic mode of treatment. This translates into greater
number of patients who would exhibit secondary changes of
radiation. Also, such patients surviving with their postradiation
incapacities need treatment. Earlier the wounds attributed to
radiation were considered a price paid for survival. Attempts to
address them were limited by lack of focus and understanding.
With improvement in methods to address the pathophysiology
of radiation wounds and availability of reconstructive means
and interest, the scene is changing very rapidly. Much is
being done to prevent such complications by prophylactive
use of vascularized fl aps and early attempts at reconstruction.
The basis of this approach has been inclusion of plastic and
reconstructive surgeon in the team of oncologists treating
cancer patients.

The scope of this chapter is limited to wounds caused by
therapeutic radiation and does not profess to deal with matters
pertaining to accidental whole body exposures in much detail.
HISTORY
X-rays as we know today were discovered by William K
Rontgen in the year 1895 as a tool for diagnosis to photograph
the bones. It was not long after this, that the therapeutic
Management of
Radiation Wounds
Sandeep Mehta
22
Chapter

Types of Wounds and their Management
236
role of these rays was understood. Butlin in 1909 reported
two cases of oral cancer that showed marked regression by
the application of radium, a natural source of gamma rays
(X-rays). But unfortunately less than a decade later Frieben
reported skin cancer from chronic exposure to X-rays of
the hand of a radiology technician. During the next three
decades with frequent use of radiation for treating cancers, the
biologic effects and consequences of radiation treatment came
to be known. Paterson and Parker established the time–dose
treatment regimen and Baclesse concluded that the central
portion of tumor was more resistant to radiation. Hence
the complimentary effects of surgery and radiation came to
be established: because surgery failed at the periphery and
radiation at the center. This had been applied initially to head
and neck cancers but subsequently became a rule in treating
breast, colorectal and gynecologic cancers.1

Radiotherapy is a valuable weapon when treating cancer.
It is used to cure certain cancers, such as cancer of the retina,
central nervous system, skin, oropharynx, larynx, esophagus,
cervix, vagina, prostate and lymphomas. Radiotherapy is also
used as an adjuvant treatment, in addition to surgical resection
(and chemotherapy, when appropriate) for cancers of the
lung, breast, uterus, bladder, rectum, testis (seminoma) and
soft tissues (sarcoma). In some patients, radiotherapy has a
palliative role for pain relief and preservation of the skeleton
following bone metastases, reduction of headaches and
vomiting caused by raised intracranial pressure due to CNS
metastases and for relief of obstruction due to compression of
the bronchus, esophagus, ureter or lymphatics.1

Although radiation therapy is used to kill cancerous cells,
it also damages healthy cells, leading to many acute and long
term side effects. One of the serious complications is problems
with wound healing. The long-term effects of radiotherapy
include skin atrophy, soft tissue fi brosis and microvascular
damage. Advances in the delivery of radiotherapy have aimed
to minimize these damages by reducing the radiation effect
on healthy tissue while maximizing the effect on cancerous
tissue. However, it is inevitable that some normal tissue
will be affected, and the long-term effects of such radiation
damage may persist for decades after radiotherapy.
WHAT IS RADIOTHERAPY?
Radiotherapy is the use of high energy ionizing electromag-
netic or particulate radiation to treat cancer. Electromagnetic
ionizing radiation includes artifi cially produced X-rays and
naturally produced γ-rays, emitted as a result of disintegra-
tion of unstable atoms. Particulate radiation, photons, com-
prises subatomic particles such as α-particles (helium nuclei),
β-particles (electrons) and neutrons. As radiation penetrates
tissue, it physically interacts with electrons, either ejecting
them from atoms (ionization) or exciting them to higher en-
ergy levels.2 These electrons may ionize or excite other atoms,
resulting in a cascade of ionization events.
Figures 1A and B: DNA damage due to ratiotherapy. Radiation induces singles and double-stranded DNA breaks
and DNA strand cross-linking. The cell may repair the damaged DNA or die by apoptosis

Management of Radiation Wounds
237

The most common unit to measure therapeutic radiation is
rad; it is not the energy that leaves the source machine but the
energy that is absorbed by the tissue. One rad is equal to 100
ergs of energy absorbed per gram of tissue irradiated. A more
recent measurement is a gray (Gy), which is equal to 100 rads.
The earlier measurement of 1 rad is currently referred to as 1
cGy (centigray). Radiation exposure is however measured in
sieverts.

The most important effect of ionization and excitation
is damage to DNA, which may be lethal to the cell when it
tries to divide and cause apoptotic cell death3 (Figures 1A
and B). Damage to DNA is repaired by enzymes, with either
correction of the damage or fi xation of the damage resulting
in mutations which can lead to cell dysfunction, inability to
proliferate or later carcinogenesis. It has been postulated that
differing patient susceptibility to radiation damage may be
partly due to differences in their DNA repair mechanisms.
Ionizing radiation also leads to the generation of short-lived
free radicals and cytotoxic peroxides which damage DNA,
proteins and membranes.2
METHODS OF DELIVERY
There have been major developments in radiotherapy since
the discovery of X-rays by Roentgen in 1895 and radium (a
source of γ-rays) by the Curies in 1898. Early radiotherapy
involved huge radiation doses and was accompanied by severe
radiation sickness, radiodermatitis and other side effects. This
prompted the need to develop different modes of radiotherapy.
Fractionated radiotherapy was found to result in better tumor
control with fewer side effects, allowing healthy tissue to
recover between doses of radiation.

Teletherapy is the term applied to treatment with radioactive
material that is placed at a distance from the tissue target. For
external beam radiotherapy, megavoltage photon irradiation is
delivered by cobalt-60 sources (gamma rays) or high-energy
linear accelerators (X-rays). This is the most common method
of radiation therapy. External radiotherapy is now usually
delivered by linear accelerators, which generate radiation with
a greater depth of penetration and reduced superfi cial skin
damage. Advances in tumor imaging and computer technology
for the planning and delivery of radiotherapy have lead to
the development of stereotactic systems for the targeting of
fi ne radiation beams, with 3D conformal radiotherapy4 and
intensity modulated radiation therapy.5 These systems enable
optimal delivery of radiation to cancerous tissue, while
minimizing damage to healthy tissue.

Brachytherapy is the term used to describe treatment
with a very short distance from the radioactive source to the
tissue target; the radioactive sources may be applied directly
into the tissues by temporary needles or permanent seeds
(Iridium-192 radioactive implants) to deliver radiotherapy
directly to prostate tumors, soft tissue sarcomas (Figures 2A
and B), breast tumors and cervical tumors.6,7 Recent advances
in tumor imaging have enabled the targeted implantation of
seeds of radiotherapeutic material for internal radiotherapy.8
More recently iodine-125 seeds with half life of only 60 days
have been embedded in woven suture material, which is then
Figures 2A and B: Brachytherapy examples: (A) Soft tissue sarcoma gluteal region. Wide local excision of tumor followed by reversed latissimus
dorsi myocutaneous fl ap cover with simultaneous placement of nylon catheter which will be loaded with Iridium-192 on fi fth postoperative day
to start the brachytherapy; (B) Recurrent MFH involving the back being treated with brachytherapy. Note the previous surgical excision site with
fl ap cover on left scapular region and the right back showing earlier excision and skin grafting. The recurrence on right back has been widely
excised and covered with LD myocutaneous fl ap after laying the catheters for radiation source
A
B

Types of Wounds and their Management
238
sutured around the tumor in various parts of the body, such as
the oral cavity or neck. The isotopes used most commonly in
brachytherapy include cesium-137, iridium-192, iodine-125,
and gold-198.
RADIATION INJURY—BIOLOGICAL
EFFECTS
The term radiation injury refers to the morphological and
functional changes that occur in noncancerous tissue as a
direct result of ionizing radiation. Adverse effects of radiation
were noted from the fi rst days of radiotherapy and depend
on the radiosensitivity of the body sites being treated, the
volume of normal tissue irradiated, the total dose and the rate
of dose accumulation.9 Side effects are most evident in rapidly
proliferating tissues, such as the skin, mucosa and bone
marrow, but may arise in almost any organ system. In other
tissues such as nerves, in which the cells do not normally
reproduce, the effects might not be observed clinically or
microscopically. These tissues are said to be radioresistant.

The ability of tissues to heal after radiation depends on the
population of the surviving cells. The effi cacy of radiation to
treat (destroy) tumors depends on the lesser number of tumor
cells and slower turnover rate compared with surrounding
normal tissue. This is the reason for radiation to be least
effective in the center of the tumor where tumor cells have
greater turnover and replication. The surrounding normal cells
thus repopulate the area and healing ensues, even though some
of their population has been destroyed in the same fashion
as tumor cells. If repopulation did not occur, all therapeutic
radiation of tumors would result in open wounds as the
tumors disappeared. In general the cells are most sensitive
to radiation-kill in the G2-M stage of cell cycle, while they
are most resistant in S-phase. To catch the tumor cells in the
act of division it is necessary to fractionate the total dose of
radiation over a few days, repetitively. This fractionation also
allows the normal tissues to repair themselves.
Low-dose vs High-dose
With low-dose radiation exposure, such as with single doses
of up to 100 milligray, single-strand DNA breaks may be
produced in a cell. However, this damage may be repaired at a
relatively rapid rate because the remaining intact DNA strand
can serve as a guide to repair. With higher doses of radiation,
such as doses between 0.5 and 5 Gy, cellular death usually
occurs after one or more reproductive divisions. Such injury
is usually the result of irreparable double-strand DNA breaks.
After extremely high doses of radiation (above 5 Gy), direct
cell death occurs, known as interphase death, and is a result
of direct interaction of free radicals with essential cellular
enzymes and mechanisms.1

The technique of fractionation of doses is used to minimize
the risk of injury to normal tissue during radiation treatments.
In fractionation, the total radiation dose is delivered over
a period of time, allowing for repair of sub-lethal injury in
normal tissue and proliferation of healthy surviving cells.
Likewise, a given dose of radiation administered at a low-dose
rate produces less skin injury than the same total dose given at
a higher dose rate. Larger doses of radiation may be tolerated,
however, if they focus on small, highly specifi c areas of the
body rather than distributed over larger areas.

The absolute effects of radiation on normal tissues at
molecular level are thus random and represent an all or none
phenomenon. The damage to the cell thus depends upon the
importance of such molecule to the function of that cell. In
a dose range used for clinical treatment of tumors (1000 to
10,000 rads), the biologically signifi cant damage is to DNA,
but most of this damage can be repaired and cell function
would continue. However, genetic information is lost and the
cell loses its ability to divide and produce a clone. On the other
hand at doses hundred to thousand times the usual therapeutic
dose, as it happens in accidents or war, rapid dissolution of
cells occur and there are rapid alteration in tissues resulting in
cell-tissue-organ death. It is postulated that a cell exposed to
therapeutic radiation would retain its capacity to divide albeit
1000 times after which it too would die, thus explaining the
late complications following radiotherapy treatment. This
presents as spontaneous breakdown, radiation ulcer.

All things are poison and nothing is without poison,
only the dose permits something not to be poisonous
(Paracelsus).
Radiation Exposure or Accidents
Accidental exposure to radiation may occur affecting the whole
body, such as by atomic bombs or that which occurred with
Chernobyl nuclear reactor leak. Individuals exposed to such
massive radiation develop radiation sickness. The radiation
sickness has three phases: prodromal, latent and main. The
prodromal phase is due to loss of cells of gastrointestinal tract
causing nausea, vomiting and diarrhea. The latent phase is
due to irreparable damage to cells by 700 to 1100 cGy over a
period of hours to months. The main phase is manifested as
the effects of cell depletion begin to have clinical signifi cance
on functioning of specifi c organ or the body as a whole. Severe
radiation amounting to 20,000 cGy to brain or heart would
result in death within minutes to hours, whereas 2000 cGy to
whole body would result in fatal enteritis within two weeks.
Radiation Injury During Radiotherapy
Localized exposure to radiation with 5000 to 10,000 cGy in a
short time produces changes to the skin and soft tissues that

Management of Radiation Wounds
239
resemble thermal burn injury which evolves more slowly. The
skin becomes dry, erythematous, edematous, tender and itchy.
The early scaling and fl aking of dry desquamation stage gives
way to sloughing and ulceration of wet desquamation over
a period of one to two weeks. Further progression leads to
bacterial infection, necrosis and eschar formation. The effects
seen in local tissues are similar to those that occur during
radiotherapy to a given area (Figures 3 and 4).

There are both acute (10–14 days after starting treatment)
(Figures 3A to D) and long-term (more than 3 months after
the end of treatment) effects of radiotherapy which may be
permanent or progressive.

Wound healing problems are a long-term effect of
radiotherapy, characterized by decreased wound strength,
decreased collagen deposition and decreased angiogenesis.
These problems may lead to delayed or non-healing ulceration
(radiation ulcers), superimposed infection, carcinogenesis and
acosmesis. These complications are because of a combination
Figures 3A to D: Acute radiation changes (A and B) Radiation dermatitis developing dry desquamation on tenth day progressing to stage of
moist desquamation as seen; (C) Slough covered area of moist desquamation has the same appearance as that of a second degree deep
dermal burn; (D) The radiation reactions have settled with healing taking place by way of re-epithelialization of moist desquamation as seen
after a week
Figure 4: Severe acute radiation effects necessitating discontinuation
of radiotherapy. Onset of massive edema of fl oor of mouth during
radiotherapy treatment of base of tongue tumor which required
tracheostomy to offset respiratory distress
A
C
B
D

Types of Wounds and their Management
240
of radiation-induced DNA mutations, microvascular damage
and fi brosis.
PATHOPHYSIOLOGY OF THE RESPONSE
TO RADIATION INJURY
Traumatic cell injury results in a complex cascade which
involves infl ammation (day 0–4), proliferation of granulation
tissue (day 3–3 weeks), restitution and remodelling (week
3–2 years). Repetitive radiation injury interrupts many of
the stages in this ordered sequence of events.9-11 Although
normal tissue is irradiated at fi rst, subsequent radiation doses
are applied to damaged, preirradiated tissue, resulting in an
increasingly amplifi ed infl ammatory response and ongoing
cellular regeneration. Damage is progressive and may
continue for many years after the course of radiotherapy.
Early Morphological Changes
The skin is particularly affected by radiation damage, as it is in
the path of all external radiotherapy (Table 1). Acute reactions
occur in almost all patients, and very severe reactions may
necessitate halting the radiotherapy (Figure 4). In patients
undergoing radiotherapy, usually after one to three days, the
skin appears red, dry, and braised, becomes tender to touch,
and feels fi rm due to edema. The extent of damage depends
up on the source and intensity of radiation and duration of the
exposure. The subsequent sequential fractionated radiation
would cause varying degree of skin ulceration and necrosis,
but usually within a few days or weeks it will appear to have
healed and recovered.
Dry Versus Moist Desquamation
If the total radiation dose to the skin does not exceed
approximately 30 gray, the erythema phase is followed
during the fourth or fi fth week by a dry desquamation
phase, characterized by pruritus, scaling, and an increase in
melanin pigmentation in the basal layer. Within two months,
infl ammatory exudates and edema have subsided, leaving
an area of brown pigmentation. If the total radiation dose to
the skin is 40 Gy or greater, the erythema phase is followed
by a moist desquamation phase. This stage usually begins in
the fourth week and is often accompanied by considerable
discomfort. Bullous formation occurs suprabasally and
sometimes subepidermally. Eventually, the roofs of the bullae
are shed and the entire epidermis may be lost in portions of
the irradiated area. Edema and fi brinous exudate persist. In
the absence of infection, re-epithelization of the denuded skin
usually begins within ten days. Ulcers may appear at any
time from approximately two weeks after radiation exposure.
Ulcers formed in the early stage are a result of direct necrosis
of the epidermis; these ulcers usually heal but tend to recur
(Figures 3 and 4).

Similar changes are seen in various organs and tissues
(Figures 5A to H) affecting changes dependent upon their
functional role in the body as is summarized in Table 1.
Early Effects: Molecular Changes
Radiation injury leads to apoptotic cell death due to damaged
DNA, proteins and membranes.4 Free-radical inactivation
of anticoagulatory factors leads to rapid activation of the
Table 1: Organ response to radiotherapy
Acute complications
General
Anorexia, nausea, malaise and pain
Skin
Erythema, dry desquamation, pigmentation and hair loss
Mucosa
Edema, ulceration-mucositis, esophagitis and diarrhea
Bone
Myelosuppression
Late complications
Skin
Ischemia, ulcerations, telangiectasia, pigmentation
Bone
Necrosis and fractures-osteoradionecrosis
Cardiovascular
Atherosclerosis, pericardial fi brosis and cardiomyopathy
Respiratory
Radiation pneumonitis and pulmonary fi brosis
Gastrointestinal
Xerostomia, sialitis, recurrent mouth ulcers, bowel stenosis, fi stula, radiation enteritis with diarrhea
Genitourinary
Cystitis, hematuria, nephropathy, sexual dysfunction, dyspareunia, vaginal stenosis, menopause, infertility
Nervous system
Myelopathy, brainstem encephalopathy, sensorineural hearing loss, otitis media

Management of Radiation Wounds
241
coagulation cascade following radiation injury. Endothelial
cell apoptosis and slow regenerative proliferation results in
increased vascular permeability. These vessels denuded of
endothelium are prone to thrombosis, intimal proliferation
and
eventually
obliteration.
Infl ammation
does
not
resolve adequately following radiation injury because
of overproduction of proinfl ammatory cytokines such as
transforming growth factor-β (TGF-β); interleukin IL-4, IL-
10 and IL-13, etc. leading to perturbed cell-to-cell and cell-
to-matrix interactions, uncontrolled matrix accumulation and
fi brosis.12 Nitric oxide (NO) is synthesized in wounds by
macrophages and fi broblasts and promotes wound healing by
inducing collagen deposition.13 Whereas nitric oxide promotes
collagen deposition, tumor necrosis factor-α (TNF-α) and
interferon-γ (IFN-γ), synthesized by lymphocytes, prevent
collagen deposition. These factors are increased in irradiated
wounds.14,15 Therefore, in the early irradiated wound, the
balance of secreted factors leads to poor collagen deposition,
at a time when collagen is needed for wound strength. The
formation of granulation tissue is delayed and does not form
as effectively following radiation injury. In irradiated wounds,
expression of matrix metalloproteases 1 (MMP1) is decreased,
which shows the healing process by reducing cell migration,
angiogenesis and tissue remodelling.16
Late Effects-Molecular Basis
Long-term
effects
of
radiotherapy
include
necrosis,
atrophy, fi brosis, vascular damage and carcinogenesis. The
extracellular matrix composition is disturbed because of
complex interactions between microvascular injury, damaged
fi broblasts and altered TGF-β levels and mast cell activity.
Collagen is the main extracellular matrix component in
the skin and is secreted by fi broblasts. Extracellular matrix
components are degraded by tissue MMPs which are inhibited
by specifi c ‘tissue inhibitors of metalloproteases’ (TIMPs). In
long-standing irradiated wounds, there is an accumulation of
cross-linked type I collagen because of increased collagen
synthesis by fi broblasts and decreased degradation by
MMPs.17,18 Microvascular injury in irradiated tissue may
result in reduced blood fl ow to the tissue, ischemic damage,
fi brosis, necrosis or atrophy.19 Phenotypic changes in the
endothelial cells lead to increased expression of TNF-α and
platelet-derived growth factor (PDGF) and down-regulation
of NO synthase and thrombomodulin, all of which can
stimulate events leading to fi brosis.

Radiation-induced vessel damage, as studied by scanning
electron microscopy,20 is thought to lead to ischemia and has
Figures 5A to H: Histology of radiological burn: Representative HES (Hematoxylin-Eosin-Saffron coloration) picture of skin lesion. (A to D:
Epidermolysis, infl ammation, microvasculature network destruction, loss of dermis-epidermis adhesiveness)20 and muscle lesion; (E to H:
rhabdomyolysis, infl ammation, microvasculature network destruction)60
Figure 6: Histopathology of chronic radiation dermatitis (hematoxylin
and eosin) atypical fi broblasts (1) and telangiectasia, (2) following
radiation therapy. The remaining tissue is dermal fi brosis

Types of Wounds and their Management
242
been blamed for the long term effects of radiation injury.
However, a recent study showed that irradiated tissues
are not hypoxic,21 suggesting that other factors may be
involved in long term damage, such as permanent changes
in fi broblasts.

Radiation-induced fi broblast dysfunction results in poor
wound healing and fi brosis. Fibroblasts are stimulated to
lay down extracellular matrix, including collagen by growth
factors such as PDGF, epidermal growth factor (EGF),
fi broblast growth factor (FGF) and TGF-β. Poor wound
healing is due to defective collagen deposition by irradiated
fi broblasts. However, fi brosis may result from excessive
collagen deposition by over-recruitment and stimulation of
local fi broblast progenitors.
Late Effects–Morphology and
Clinical Presentation
Late changes in the skin are quite remarkable. The epithelium
may be thinned out to a layer only a few cells thick. The hair
follicles and sebaceous glands are usually absent but the sweat
glands being most resistant to radiation may remain. The
smooth muscle of erector-pili and of media of small arteries
is still present because of their greater radio resistance.
Elastic fi bers in the dermis are destroyed and considerable
hyalinization of the dermal collagen occurs. Beneath the
dermis there is a dense, poorly oriented fi brosis with much
collagen. Fibroblasts in dermis and subcutaneous tissues are
large and vacuolated, the lymphatics and small capillaries
are absent or are so much incarcerated in the fi brous tissues
as to be blocked (Figure 6). Muscle cells are vacuolated and
replaced by scar containing very few blood vessels. Bone
becomes devitalized and appears like marble with marked
obliteration of periosteal and endosteal vessels. Cartilage may
also show necrotic changes. Nerve tissue by itself sustains
relatively little damage but is secondarily incarcerated in
surrounding scar-fi brosis of extracellular matrix.

The most profound change and that of greatest concern
to the surgeon is the alteration in vascularity. The initial
vasodilatation is followed by fi brinoid necrosis of vessel
walls with subsequent thrombosis. The result is an obliterative
endarteritis with chronic ischemia, which predisposes to acute
tissue necrosis or subsequent infection which culminates in
necrosis and ulceration. From this point a cycle is established
that can go in one of two directions. First, the ischemia
complicated by infection can lead directly to ulceration,
progressing relentlessly to affect large amount of tissue
loss, or second there would be early tissue necrosis with
subsequent healing by scar tissue. However, with progressive
obliterative endarteritis, the chronic ischemic nature of the
tissue leads to an unstable scar, which over a period of time
breaks down and becomes infected. This leads to the same
problem, an ulcer which is a result of ischemia, is infected,
and is extremely painful and diffi cult to manage (Figures 7
and 8). Pain is one of the most prominent features of these
ulcers and often leads to narcotic addiction. Pain is believed
to be due to intense vasculitis present in these wounds.22 In
the face of the increasing amount of radiotherapy performed,
physicians are confronted with an increasing amount of
radiogenic complications in the head and neck area. Impaired
Figure 7: Late effects of radiation as evident in a case treated with
70 Gy IMRT after breast conservative surgery for carcinoma breast
involving lower inner quadrant. The atrophy of the surrounding skin
with depigmentation and frequent breakdown of epithelium herald the
formation of radiation ulcer
Figure 8: Late stage radiation ulcer. Breast conservative surgery
followed by radiotherapy leading to formation of ulcer due to breakdown
of suture line 13 months later

Management of Radiation Wounds
243
Figures 9A and B: Radical neck dissection done after the neck had received radiotherapy up to 66 Gy as treatment for base of tongue
squamous cell carcinoma. The neck fl aps underwent necrosis exposing the vital structures. Note the pale slough covering the base and rolled
skin at the edges due to radiation fi brosis
Figure 10: Late dehiscence of a primarily closed wound after wide
local excision of sarcoma in medial thigh treated with brachytherapy.
The severe cicatrization and fi brotic base of the ulcer denotes the
extent of fi brosis, pigmentary changes and atrophy due to ischemia
healing from irradiation is a source of prolonged patient
morbidity, resulting in fi stula formation, fi brosis, carotid
artery exposure or rupture, and even death (Figures 9A and B).
Postoperative complications after radiation exposure have
been reported to occur in as many as 67 percent of patients.
Similar complications commonly occur when treating soft
tissue tumors with brachytherapy (Figure 10).

Wound healing problems are partly due to defective type
of collagen deposition, due to lack of collagen synthesis
and deposition of defective collagen. Following irradiation,
fi broblasts are disorganized and have reduced proliferative
ability.23 Irradiated fi broblasts are functionally abnormal, and
injection of normal, syngeneic fi broblasts into an irradiated
wound results in normal wound healing.24 This has become
the basis of stem cell injections to promote healing.
Malignant Transformation—Effect of
Chronic Low Dose Radiation
Soon after the discovery of radium as a source of radiation, its
improper use and handling led to the development of malignant
neoplasms as was seen in radium watch dial painters. These
dial painters swallowed the radium in fl uorescent paints
when they dabbed the brush tip on their tongues. The radium
was absorbed into the gastrointestinal tract and deposited
into bones. The radium in the bones emitted alpha particles
which repeatedly bombarded the mucosa of paranasal sinuses
eventually leading to squamous cell carcinomas many years
later. A similar mechanism of chronic low dose radiation was
found to be the cause of bronchogenic carcinomas in uranium
miners of Colorado and the pitchblende miners of Europe.
Dentists and fl uoroscopists exposed to low dose radiation
suffer from radiation dermatitis which in some case progresses
to form epidermoid carcinomas.25 Short-term heavy exposure
as that occurred after Hiroshima and Nagasaki bombing
are testimonials not only to the acute effects but also to the
slowly developing cancers in later years. Extensive studies
undertaken during 25 years through the joint efforts of the
Atomic Bomb Casualty Commission of the United States
and the Japanese National Institute of Health have led to the
conclusion that there is a greater incidence of leukemia and
thyroid carcinoma among the bomb survivors. Salivary gland
tumors have also been reported from such cohorts.
A
B

Types of Wounds and their Management
244

Although radiotherapy is very successful in treating cancer,
it can also cause second cancers, often decades after the initial
course of radiation.25 For example, patients may develop
breast cancer after radiotherapy treatment for Hodgkin’s
disease (Figure 11)26 or lung cancer following radiotherapy
for breast cancer.27,28 Because the skin and soft tissues are
in the path of all external radiotherapy, they are susceptible
to the development of skin cancers or sarcomas following
radiotherapy.29,30

Chronic wounds following radiotherapy should be
investigated for malignant change by biopsy for histopathology.
Due to radiation induced changes in tissue architecture, it
may be diffi cult to detect second cancers within previously
irradiated skin or to determine whether a lesion is a recurrence
of the primary or a novel second tumor.

The potential for malignant transformation of the soft
tissue or bone within the fi eld of therapeutic radiation is
of particular concern. Cahan et al defi ned the four criteria
that have to be met before radiation can be considered to
have been responsible for malignant transformation. They
are: histologic evidence of absence of malignancy before
radiation, reasonable latent period (>10 years), occurrence
of malignancy within the fi eld of radiation and malignancy
confi rmed by histology.31 The most common cancer seen to
develop after prior radiation are the sarcomas of mandible and
pelvic bones, which are indirectly exposed to low doses of
radiation, away from the targeted focus of treatment. These
cancers have poorer prognosis and are subject to similar
treatment protocols as those occurring without radiation.
Infections and Radiation
It has been considered as fact that surgery within irradiated
fi elds leads to higher incidence of wound infection. Ketchum
reported a 60 percent incidence of infection among patients
who received a single dose of 1000 percent rads before their
surgical procedures as compared to only ten percent incidence
among control patients who had not received any radiation.32
Ariyan et al demonstrated that irradiated tissues could not
tolerate bacterial contamination as well as normal tissues
(Figures 12 and 13). The incidence of infection increased with
the increasing dose of radiation as well as with the increasing
interval from radiation to wounding.33 The factors responsible
towards this are both local as well as systemic effects of
radiation. Studies undertaken by Cruz et al to demonstrate
the inability of antibiotics to control such infections
revealed that till fi ve weeks after radiation the blood levels
of antibiotic and those in the irradiated tissue were same.34
But at ten weeks and thereafter at 15 weeks the concentration
of antibiotics in irradiated tissue was only 70 and 40 percent
respectively. This study confi rmed the decreasing perfusion of
Figures 12A and B: Radiation ulcer: Breast conservative surgery
followed by radiotherapy. Seen here is the spontaneous development
of this ulcer 3 years later. Note the fi brosis and poor healing of the
ulcer in the background of otherwise settled breast
Figure 11: Malignancy develops secondary to radiotherapy. Sarcoma
of the breast seen in a patient who had received therapeutic
radiotherapy for Hodgkin’s lymphoma 12 years back
A
B

Management of Radiation Wounds
245
circulating antibiotics in the irradiated tissue coincident with
the increasing fi brosis of the tissue following intervals after
radiation. It appears that although there may be adequate levels
of circulating antibiotics, the fi brosis and thickening of walls of
these vessels might not permit ready diffusion out of the vessels
and into the cicatrised tissues of an infected ulcer in an irradiated
fi eld. The systemic effect of radiation through its bone marrow
depression leads to altered neutrophil function after a dose of
10 to 30 Gy. This include diminished phagocytosis, superoxide
function and Mac-I expression, all resulting into poor healing
and increased susceptibility to infection.35
TREATMENT OF RADIATION-
INDUCED WOUNDS
Cleansers and Moisturizers
Erythema may appear in the irradiated area of the skin
approximately three weeks into radiation treatment. The skin
should be gently cleansed with water, normal saline, or a soap
solution and rinsed thoroughly to avoid excessive irritation.
Friction applied to the treated area should be minimized.

Numerous skin care products are available that can be used
to reduce discomfort. For example, hydrophilic preparations
that absorb water and act as mild lubricants are appropriate.
Protective ointments or gels are effective for protecting dry
lesions. All products that contain alcohol or menthol should be
avoided because they remove natural lipids and may worsen
the skin’s reaction. Dry desquamation may appear during
this same period, with the patient’s skin in the treated area
appearing red or tanned, dry, itchy, and peeling. The products
used to treat an erythematous reaction can also be applied in
this situation. Hydrophilic preparations protect and lubricate
scaly or fl aking skin resulting from the loss of sweat and
sebaceous gland function. To decrease itching, products such
as colloidal oatmeal bath, cornstarch, and mild steroids such
as hydrocortisone cream one percent can be used. Because
it may have a drying effect, daily bathing with soap is not
recommended unless a low pH, moisturizing cleanser is used.
Cornstarch should not be used on moist skin or in areas that
remain moist, such as the axilla, breast, or groin creases,
because it may promote fungal infection. Corticosteroids
should be used with caution to reduce itching because they
also delay healing by inhibiting infl ammation and reducing
blood fl ow to the skin. In addition, steroids can cause atrophy
of dermal collagen, which can thin the skin and increase
susceptibility to infection. By the fourth week of treatment,
moist desquamation may occur, especially in patients with
radiation treatment to the chest wall, supraclavicular region,
axilla, groin, or under an intact breast. Astringent soaks,
cleansers, antibiotics, and other irrigations can be used.
Hydrogen peroxide has an antibacterial effect and is effective
in cleansing wounds with purulent debris. However, full-
strength hydrogen peroxide is harmful to granulation tissue
and must be avoided.
Dressings
Wound dressings are benefi cial because they preserve a moist
environment that enhances re-epithelialization, allow enzymes
Figures 13A and B: Radiation ulcer in its worst characteristic form. A case of recurrent liposarcoma treated with wide excision and rectus
abdominis myocutaneous fl ap cover received external beam radiotherapy postoperatively. The area overlying the hip developed this ulcer
immediately after radiation probably due to sequestered seroma which got infected and lead to cellulitis and necrosis. It highlights the poor
tolerance of irradiated tissue to infection and progressive necrosis due to ensuing ischemia
A
B

Types of Wounds and their Management
246
in the wound fl uid to lyse necrotic tissue, and permit infl amma-
tory cells to phagocytose necrotic debris and bacteria. In addi-
tion to promoting wound healing, dressings cover the wound
and protect the area from external contamination and infection;
prevent soiling of clothing; and prevent further irritation, fric-
tion, or shearing. Moistened saline dressings or soaks with an
astringent precipitate protein, seal exudative surfaces, prevent
evaporative heat loss and decrease infl ammation and tissue
desiccation. Dressings should be changed from one to three
times daily, depending on the amount of drainage. Hydrocol-
loids may be left in place for fi ve to seven days.
Antibiotics
If an infection is proved by wound culture, topical antibiotics
(Neosporin should be used. A systemic antibiotic may be
needed if the area does not heal. More commonly use of
silver sulfadiazine one percent cream is recommended as an
effective preparation against gram-positive and gram-negative
organisms and against Candida albicans.
Treatment for Xerosis
Over the long-term, irradiated skin often develops chronic,
localized xerosis. For this condition, mild soaps and bath oils
may be used during bathing. Neutral soap preparations are
made with synthetic detergents and have a pH of less than 7.5,
contains a higher amount of fat that leaves a fi lm of protective
oil on the skin. Lubricants such as petroleum and mineral
and baby oils are generally more effective, but tend to be less
esthetically pleasing to patients.

Dry skin lotions, creams, or thicker preparations may be
used to lubricate the skin, prevent fi ssures, and keep the skin
pliable. Lotions are suspensions of powder in water that provide
a protective drying and cooling effect while leaving a fi lm of
powder on the skin. Creams are emulsions of oil in water that
are water washable and completely absorbed into the skin.
Protection
In some patients, irradiated skin may appear normal after
completion of radiation therapy. However, changes may
eventually become evident and adversely affect a patient’s
quality of life. The higher the dose of radiation received, the
more likely that changes, such as fi brosis of tissues and small
blood vessels, will be delayed. Patients should be taught to
protect irradiated skin from excessive sun exposure and other
trauma because the skin’s ability to respond to trauma is
reduced and the skin heals more slowly if injured. The patient
should use a sunscreen with an SPF of 15 or higher if he or
she expects to be in direct sunlight for more than 15 minutes.
In rare cases, radiation wounds may be so severe that skin
grafting may be necessary.
RADIATION ULCERS
Nonhealing ulcers may develop at any time following radio-
therapy, and up to decades afterwards (Figures 12A and B).36
Figures 14A and B: (A) Long standing ulcerations that developed in a case of medullary carcinoma of left breast 2 years after undergoing
lumpectomy and radiotherapy. The extent and nature of the ulceration demonstrates its overwhelming morbidity leading to pain, infection,
chronicity and failure to heal; (B) Note the extent of excision required to remove almost all of the tissues that had received radiotherapy and the
resultant defect reconstructed using latissimus dorsi myocutaneous fl ap. At other similar occasions it is worthwhile to do a formal mastectomy
and reconstruction with appropriate autologous fl ap
A
B

Management of Radiation Wounds
247
Radiation ulcers cause serious morbidity, including pain,
infection, acosmesis, psychological distress, reduced quality
of life and mortality due to overwhelming infection (Figures 8,
12 and 14). Conservative treatments include wound dressings,
antibiotics, gentian violet and hyperbaric oxygen.37 However,
surgical attempts at wound closure are often necessary.
Although skin grafts and local fl aps have not been successful
for the treatment of radiation ulcers, good results may be
achieved by importing vascularized myocutaneous (Figures
15A to D) or omental fl aps.38,39 High complication rates arise
because of viable fl aps not taking to the irradiated ulcer bed,
partial or total fl ap loss, or thrombosis. Recent studies of
free tissue transfer fl aps reported a 40 percent complication
rate, mainly due to problems with pedicle thrombosis when
recipient vessels were within irradiated tissue.40-42
Principles of Management of
Radiation Ulcers
The local wound care with standard wet or wet-to-dry
dressings is rarely successful in promoting satisfactory
debridement, cleansing of the wound, and subsequent growth
Figures 15A to D: Spontaneously occurring late radiation ulcer which failed to respond to conservative means and wound care including use of
hyperbaric oxygen therapy. (A) Breakdown of the previous operative scar 5 years after radiotherapy received as adjuvant treatment after breast
conservative surgery; (B) Excision of the ulcer resulted in release of tissues in the axilla and shows the extent of cicatrization caused by radiation
fi brosis; (C) Two weeks postoperative view after LD fl ap was used to cover the defect; (D) Six weeks later the fl ap and the breast have settled
as the fi brotic scar had been replaced with healthy vascular tissue. Note the persistent lymphoedema in the arm
A
C
B
D

Types of Wounds and their Management
248
Figures 16A to D: Local fl ap in dehiscence after irradiation. (A) Breakdown with ulceration at the edge of previously transferred rectus abdominis
fl ap used to cover the defect caused by excision of sarcoma in gluteal region; (B) Outline of the fl ap planned for local interposition based on
intercostals perforators. Note the scars of brachytherapy cannulae over the buttock; (C) The fl ap elevated and ready for transposition; (D) Flap
inset and donor site primarily closed. The local fl ap was available for use because of its intact vascularity and absence of widespread effects of
radiation on account of brachytherapy
of granulation tissues because the ischemic and underlying
fi brosis of the ulcer bed is not able to support granulation tissue.
Unlike other ulcerations that tend to get better with adequate
local care, dressings and debridement, radiation ulcers
frequently progress and become much worse as time goes by
(Figures 8 and 12). The underlying ischemia sets in motion
a cycle of infection and necrosis leading to development of
additional ulcerations in the surrounding vicinity and fi nally
they coalesce to frank gangrene. Infection is the key factor in
triggering this vicious cycle. For this matter early management
of the ulcer is of critical importance. This should include an
initial debridement of all nonvital tissue and then control
of local infection by use of appropriate topical antibacterial
agents, including silver sulphadiazine or mafenide. Systemic
antibiotic therapy is usually not helpful because the ulcer is
isolated from the bloodstream by its ischemia. After initial
control of infection, defi nitive debridement of the ulcer and as
much of the surrounding irradiated tissue as is feasible should
be carried out, followed immediately by wound closure.
Methods of Wound Closure
The usual methodology of application of reconstructive ladder
may be used in the management of these ulcers. These include
direct approximation of wound edges following debridement,
split thickness skin grafts, and locoregional, distant or free
fl ap coverage.

Excision followed by simple closure of the wound edge
can occasionally be accomplished without tension when the
radiation defect is small, sharply demarcated, and located
A
C
B
D

Management of Radiation Wounds
249
in soft, mobile areas (Figures 16A to D). However because
of the ischemia of the surrounding tissue due to scatter of
the radiation, wound healing may not be satisfactory and
dehiscence with infection and recurrent ulceration may ensue
(Figures 17 and 18). It is hereby affi rmed that whenever
possible two edges of skin fl aps which have received radiation
upwards of 5000 rads should not be sutured for the healing
would always be dubious. An intervening edge or base of
vascular tissue should be considered in such circumstances.

Skin grafts are the next simplest method of closure but
must have a good vascular bed to be successful. Radiation
ulcers after debridement, very rarely sprout granulations that
may be capable of supporting a skin graft uptake (Figures 8
to 10 and 12). Such circumstances do occur following acute
radiation ulcers due to radiation exposure accidents wherein
the exposure time is short and the damage is limited to skin
necrosis without altering the biology of underlying tissues.
Certainly skin grafts are not adequate or desirable coverage
for vital structures such as large vessels, nerves, bone, or
tendon.

The indications for fl ap coverage in the treatment of
radiation ulcers is no different from those for fl ap coverage
of any wound except for a more ‘hostile’ and less pliable a
tissue environment.39 Robinson had laid out indications for
fl ap coverage in 1975 when many newer better vascularized
muscle and musculocutaneous or fasciocutaneous fl aps
were not available with less prevalent use of microvascular
techniques for tissue transfers.43 The use of local tissues as
fl aps to close radiation defects is always fraught with dangers
of failure because of local ischemic effects as discussed earlier
Figures 17A and B: Failure of attempted primary closure after vulvectomy was done after radiotherapy. (A) Dehiscence of the wound in
irradiated fi eld; (B) Salvage of the wound done with bilateral gracilis myocutaneous fl aps
Figures 18A and B: Recurrent fi brosarcoma in medial thigh which recurred after radiotherapy was excised and closed primarily again.
(A) Dehiscence along the suture line exposing the extent of necrosis underneath due to progressive ischemia; (B) 5th day postoperative after
thorough debridement and cover with rectus abdominis myocutaneous fl ap
A
B
A
B

Types of Wounds and their Management
250
Figures 19A to D: (A) Soft tissue sarcoma excised from the posterior thigh underwent post operative radiotherapy. The scar in the popliteal
region gave way 2 years later. Note the fl exion contracture and contour abnormality due to radiation fi brosis and atrophy; (B) The ulcer was
widely excised and contracture released. Medial head of Gastrocnemius muscle has been elevated and ready for transfer into the defect;
(C) The transferred muscle has been skin grafted; (D) Three weeks postoperatively the graft and muscle fl ap has settled well. Note the ‘fi ll’ in the
contour and release of contracture with return of range of motion
(Figures 17 and 18). But there may be situations where such a
local fl ap is available with its vascular supply having remained
away from the harm’s way of radiation (Figures 16 and 23).
In these circumstances the single most important indication
for fl ap cover is to bring in a new blood supply (Figures 20,
21 and 33). The other indications of fl ap coverage in treating
radiation ulcers would thereby include the need to cover
exposed or potentially exposed vital structures such as large
vessels, nerves, tendons, bones, cartilage, peritoneum, pleura
or dura (Figures 10 and 34); to provide a moving or gliding
surface for tendons or joints; to provide a cover through which
future reconstructive procedures could be accomplished; to
fi ll out contours or fi ll in cavities (Figures 25, 38 and 39); to
allow more motion in kinetic areas by providing skin cover
so as to offset the cicatrization caused by radiation fi brosis
(Figures 15 and 19).

It is now possible to accomplish closure or provide
adequate cover to these extensive defects in a single stage and
at the same time to provide neovascularity for the wound by
bringing in well vascularized tissue, either as pedicled muscle
A
C
B
D

Management of Radiation Wounds
251
or musculocutaneous fl aps or by direct free tissue transfer using
microvascular techniques (Figures 20 and 21). The choice
of fl aps will be dependent of course, upon the anatomical
location of the irradiated area, the extent of the ulcer or defect
envisaged after debridement, and the availability of well
vascularized tissue in the nearby vicinity (Figures 16A to D).
Surgery and Radiotherapy—Why are
Surgeons Concerned?
Radiation is being used to treat various diseases over the
years and the recognition of injuries caused by it has led
to greater concern of protection for patients and treatment
providers. Despite this there remain several circumstances
when a reconstructive surgeon may be called upon to assuage
the ill effects of radiation.39 Most commonly such situations
would be in patients: (a) accidentally exposed to high-
doses of radiation, either from industrial accident or war,
(b) who require surgery following either planned preoperative
therapeutic radiation or radiation therapy failure, (c) who
develop radiation ulcers either shortly after or many years
after therapeutic radiation, and (d) who undergo malignant
transformation of previously irradiated tissues.

The concern of a surgeon performing surgery after
irradiation is attributed to the fear of poor healing. The
altered response to healing is attributed to permanent damage
because of radiation. Any radiation upwards from 2000 rads
would lead to damage to fi broblast, affecting their ability to
multiply, produce collagen which fails to mature, thereby
leading to atrophic and fi brotic tissues. Reduced vascularity
and tissue hypoxia due to vascular endarteritis obliterans
impair the normal response to wounding and predispose the
wound to bacterial invasion. Some investigators estimate the
complication rate at 30 percent in as simple a procedure as
breast biopsies in a previous radiation fi eld.44 The manifestation
of poor healing could be as dehiscence, at the site of incision
or suturing (Figures 17 and 18), necrosis of fl aps raised during
surgery such as neck dissection (Figure 9), early wound
infection and disruptions with sloughing seen in fascial planes,
perforations or anastomosis failures in bowel repairs, etc.
Arnold et al demonstrated that muscle or musculocutaneous
fl aps elevated from normal tissue are superior to those elevated
from irradiated tissues even if the radiation was given years
previously. There was a 32 percent complication rate for the
transposition of an irradiated muscle as fl ap as compared to
only 5 to 11 percent when radiation was not an issue.45
Timing of Irradiation Delivered Following Surgery
The initial 48 hours after wounding are most critical with
respect to successful healing. Therapeutic irradiation
administered at three to four weeks after wound production is
less likely to lead to complications because the proliferative
stage is complete. Dobbs demonstrated that whereas radiation
given one to three weeks before surgery led to a decrease in
tensile strength of wounds in rats, radiation given just 24 hours
after wounding caused no such decrease in wound strength.46
Fusi and Ariyan demonstrated that the contraction of an open
wound progresses normally to healing if the radiation to
such wounds is delayed beyond eight days after wounding.47
Hence, it is a safe practice to delay radiotherapy by at least
three weeks after surgical wounds have been closed.
Figures 20A and B: Previous biopsy site for sacral chondrosarcoma dehisced after radiotherapy. (A) The ulcer seen after regular debridement
with no evidence of healing potential but complicated by CSF leak; (B) Wider excision of radiation damaged tissue into the depth and immediate
cover with reversed latissimus dorsi myocutaneous fl ap
A
B

Types of Wounds and their Management
252
Recommendations to Avoid Wound Complica-
tions when doing Surgery in Irradiated Fields
At the time of surgery it is extremely important to handle
irradiated tissues with care. Whenever possible, the fascia
and underlying muscle should be left attached to the skin
and subcutaneous tissue as they are refl ected from the tumor.
During closure all potential dead spaces should be fi lled
with vascular tissues like muscle, etc. All wounds should be
drained and closed without tension. Seromas and hematomas
are likely to increase the incidence of late wound breakdown
and subsequent infection (Figures 12A and B). It is suggested
that sutures should remain in place for a relatively long period
of time, perhaps one month. In lower extremity tumors,
the patient should stay in bed for an extra few days, with
physiotherapy and rehabilitative activities beginning slowly.
If a complication develops within the fi rst two weeks after
surgery, it is often better to return the patient early to the
operating room to correct the problem which may involve
bringing in a vascularized muscle or musculocutaneous fl ap,
rather than waiting and hoping the wound will heal on its own
(Figures 22 and 34). If no complication arises within the fi rst
three to four weeks, healing is considered to be progressing
in reasonably normal manner. There are some reports of
use of hyperbaric oxygen therapy in such settings or in an
event when minor wound healing problems develop later
than four weeks. This is usually given in a protocol setting
and involves 90 minutes sessions at 2.4 atmospheres. The
radiation oncologist’s awareness of above complications
should prompt him to minimize the irradiation to uninvolved
tissues. Strips of skin and subcutaneous tissue, particularly
in the extremities, should be spared from irradiation to allow
for lymphatic drainage. Radiation fi elds should be planned to
avoid possible donor areas of cutaneous and myocutaneous
fl aps. Surgery should not be performed sooner than three to
four weeks after full dose radiation and that postoperative
radiation should be delivered no sooner than three to four
weeks following surgery. Although commonly recognized in
clinical practice, these suggestions are not founded on specifi c
or randomized data.
Figures 21A to C: Failure of wound to heal after brachytherapy in sarcoma of thigh. (A) The necrotic ulcer in a fi brotic bed close to the sites
of brachytherapy cannulae overlying femoral triangle; (B) The excisional debridement of the ulcer lead to exposure of vital neurovascular
structures. An ipsilateral rectus abdominis myocutaneous fl ap has been raised from the abdomen; (C) The defect covered with the fl ap
Figures 22A to C: Early salvage of brachytherapy damage. (A) Primary closure of wound in groin after wide local excision of soft tissue tumor
subjected to brachytherapy. The suture line showed necrosis and impending dehiscence on 10th postoperative day; (B) Debridement of the
devitalized tissues done on 12th day after completion of brachytherapy; (C) Immediate cover with rectus abdominis myocutaneous fl ap done.
Note the brachytherapy cannulae site showing evidence of radiation “burns” as evident by desquamation
A
B
C
A
B
C

Management of Radiation Wounds
253
Limb Salvage Surgery: Radiation and Surgery
Limb salvage protocols for soft tissue sarcomas have led us
to understand the effects of surgical creation of wounds on
irradiated structures in more ways than one. It is foremost
in demonstrating the deleterious effects of preoperative
radiotherapy and simultaneously realising the benefi ts of
pre-emptive reconstructive approach rather than creating
a situation where complications of healing raises the doubt
on salvage of the limb itself. This is because approximately
60 percent of sarcomas occur in extremities, and roughly 40
percent of all sarcomas receive adjuvant radiation therapy.
The usual dose is 55 to 65 Gy over a fi ve week period.
Most protocols that include preoperative radiation have
reported wound complications (Figures 10, 17 and 18) of
20 to 50 percent in surgery done after dosage of 35 to 62
Gy.48 Limb salvage protocols for soft tissue sarcomas have
led to some of the largest experience with radiation effects
on wounds. Closure of wounds in irradiated tissues has been
a long standing problem for reconstructive surgeons. Since
Robinson49 reported the use of local skin rotation fl aps for
radiation ulcers (Figures 23A to D), other authors have noted
the superiority of vascularized tissues for such closures.
It has been further understood that immediate coverage of
irradiated wounds after extirpation of head and neck (Figures
24A and B) and solid tumors decreased postoperative wound
complications.50,51

Barwick and others conclude that vascularized tissue
(fl aps) for primary wound closure in irradiated tissue leads
to improved wound healing, and should be considered the
procedure of choice for heavily irradiated soft tissue sarcoma
defects.52

The suggested protocol for the management of radiated
wounds after sarcoma removal is as follows: Patients
are evaluated before surgery by both the oncologic and
reconstructive surgeons. Decisions are made as to how
much skin will be removed and whether the resection will
be simply a wide local excision (subcutaneous lesions) or a
full compartmental resection (muscle based or lesions deep
to fascia). In case of bone tumors with soft tissue component,
additional planning with respect to use of vascularized bone
graft or metal bone prosthesis to replace the bone is very
important. This would entail preparations for composite tissue
transfers as osseomyocutaneous free fl aps of fi bula, iliac
crest or scapula. Plans are made for positioning the patient
on the operating table so that a fl ap can be obtained without
repositioning. The tumor resection is done by the oncologic
Figures 23A to D: Surgery after irradiation-use of loco regional vascular fl aps for complications in wound healing. (A) Base of tongue tumor
treated with curative radiation up to 70 Gy had to undergo radical neck dissection for secondaries in neck. This resulted in necrosis of neck
fl ap exposing the vital structures; (B) Debridement of the neck wound done and deltopectoral fasciocutaneous fl ap had been raised; (C) The
transposition of deltopectoral fl ap into the defect made possible by de-epithelialization of its path and primary closure of donor site laterally.
(D) Five weeks postoperative view shows a well settled fl ap in the lower neck and stable donor site closure
A
C
B
D

Types of Wounds and their Management
254
Figures 24A and B: Radical neck dissection done after irradiation. (A) The neck fl aps underwent necrosis and wound dehiscence lead to
exposure of carotid vessels seen in the picture as marble plaque covered slough in lower corner of the wound; (B) Immediate cover with
pectoralis major myocutaneous fl ap to salvage any further complications was done
Figures 25A to D: Recurrent sacral chordoma. A combined anterior and posterior approach is necessary for complete removal. (A) Patient is
made prone after anterior dissection is completed to free the rectum from the sacrum; (B) The specimen removed in its entirety; (C) The defect
as seen after sacrum excision. Note the preserved nerve roots; (D) A reversed latissimus dorsi muscle only fl ap is brought into the defect to fi ll-up
the defect and provide vascular tissue for healing as postoperative radiotherapy would be imperative
A
B
A
C
B
D

Management of Radiation Wounds
255
surgeon without regard to the size of the resulting defect.
Vascular reconstruction and bone graft replacement is done
immediately after extirpation as a joint effort by the ortho-
onco-reconstructive surgeons. The procedure is then turned
over to the reconstructive team. The wound is evaluated by
the reconstructive team for closure. Primary closure is still
done on occasion, but only when certain stringent criteria are
met. The wound must come together entirely free of tension.
In addition, the base of the wound can only be tissue (such as
muscle) that can tolerate exposure should the wound become
open (Figures 25A to D). If bone, metal prosthesis, tendon,
nerve, or major blood vessel is present in the wound, or if
brachytherapy is contemplated, a fl ap is always done. If the
base of the wound is muscle, but there is tension on the skin,
a primary split-thickness skin graft is performed. Once a
determination is made that a fl ap is required, a search is made
for any local pedicle muscle fl aps that are outside the area
of radiation but can be rotated to fi ll the defect (Figures 35
and 36). The most frequently used fl ap in this category is the
rectus abdominis muscle to cover proximal thigh or groin
defects (Figures 10 and 20). If no local fl ap is available, a
free tissue transfer is done. The most useful fl ap has been the
lattissimus dorsi muscle with a generous area of skin (Figures
26A to D). It is preferred to leave a skin paddle attached to
the muscle, instead of using a skin graft, because it heals
better to the surrounding irradiated skin. In areas where
bulk would be a problem, such as the hand, foot or ankle, a
radial forearm or anterolateral thigh fl ap as septocutaneous or
musculocutaneous fl ap is chosen (Figures 27A to G). Most
commonly in cases where bone, soft tissue and skin have to
be provided, a vascularized fi bular osseo-myo-cutaneous fl ap
serves the purpose beautifully in all ways.

It is thus established that conventional closure by
skin approximation of radiated wounds results in high
Figures 26A to D: Soft tissue sarcoma of shoulder. (A) Recurrence of STS in shoulder. Note the previous scar; (B) Extent of excision marked
out; (C) Defect created after excision including the acromioclavicular joint; (D) Reconstruction using a free latissimus dorsi myocutaneous fl ap
A
C
B
D

Types of Wounds and their Management
256
complication rates. Subsequent delayed healing leads to
secondary procedures, prolonged hospitalization, a longer
recuperative phase and decreased limb salvage success rates.
On the contrary vascularized tissue transfer for primary wound
closure leads to decreased complications, fewer secondary
procedures to achieve wound healing, shorter hospitalization
and an improved rate of limb salvage. Thus vascularized
tissue transfer should be considered the procedure of choice
for closure of soft tissue sarcoma defects that involve heavily
irradiated tissues. The author feels that all institutes work on
set protocols and a team approach with onco-ortho-plastic
surgeon cooperation achieves best results.
Figures 27A to G: Free fl ap commonly in use for radiation damaged tissues. (A) Osseocutaneous vascularized free fi bular fl ap with bone and
soft tissue and skin for mandibular and other bone reconstruction; (B) Osseocutaneous fi bular free fl ap used for mandibular reconstruction to
treat extensive ORN mandible which compounded inside the oral cavity; (C) Bony reconstruct of the ORN seen on radiograph; (D) Vascularized
bone graft from fi bula based on peroneal vessels; (E) Free fi bular bone graft vascularized by microvascular anastomosis for reconstruction in
limb salvage surgery for sarcomas; (F) Radial artery fasciocutaneous forearm fl ap for use as lining and cover where needed; (G) Facial vessels
as recipient vessels for radial artery forearm fl ap reconstruction in oral cavity
A
D
F
E
G
B
C

Management of Radiation Wounds
257
Figures 28A and B: Radiation osteitis. (A) Note the thinned out skin overlying the mandibular body in the region where bone has undergone
radiation damage leading to necrosis. The chronology of developing an ulcer and exposing the bone is just a matter of time; (B) Similar condition
with features of osteomyelitis of mandible
OSTEORADIONECROSIS
Osteoradionecrosis (ORN) has been defi ned as exposed bone
within a radiated fi eld that has not healed with conservative
therapy after a three month period. It is important here to
differentiate between radiation osteitis and osteoradionecrosis.
Radiation osteitis is the consequence of radiation damage to
osteoblasts causing demineralization and is seen on radiographs
as the overlying skin and soft tissues are intact (Figures 28A
and B). Osteoradionecrosis on the other hand is manifested with
tissue damage leading to break in cover of a bone exhibiting
features of osteomyelitis with history of radiation (Figures 29A
to E). Clinically they both may be sequential progress of same
pathology. Doses of radiation above 50 Gy usually are required
to cause ORN, and the mandible is the most commonly
involved bone. Other bones also affected include the frontal
bone, cervical spine, maxilla, temporal bones, clavicle
and nasal bones. Despite improvements in radiotherapy
techniques, the risk of osteoradionecrosis is not totally
eliminated. The avascular and possibly dead bone eventually
presents an excellent medium for bacterial contamination,
suprainfection, and then chronic infection and osteomyelitis.
Osteoradionecrosis with osteomyelitis will often present with
a draining fi stulous tract, chronic deep bone pain, erythema,
fl uctuating abscesses and deformity or instability. It can also
present with the more serious complications of pathological
fracture and over several years progress to possible malignant
transformation of sarcoma and carcinoma.

ORN occurs most commonly in the mandible with an
incidence of 2 to 22 percent. Although ORN can occur at
any time after radiation therapy, majority of cases develop
within the fi rst three years. There appears to be a consensus
in the literature that the treatment of advanced ORN requires
segmental resection of the affected bone with free fl ap
reconstruction. However, despite aggressive treatment and
resection of all necrotic and nonviable bone, a subset of
patients will nonetheless develop symptoms of recurrent ORN.

While the pathophysiology of the process is not well
defi ned, it appears to be a complex interplay of hypoxic
and hypovascular local tissue environments and chronic
infectious factors. Marx showed that ORN is a problem of
wound healing that is due to a complex metabolic and tissue
homeostatic defi ciency, and advocated the use of hyperbaric
oxygen (HBO) for treatment of irradiation complications.53
However, inconsistent treatment results with HBO, raised
questions whether the hypoxic-hypocellular-hypovascular
theory fully explains ORN.

Radiation-induced fi brosis is a more recent theory for the
pathophysiology of ORN.54 This theory suggests that the
progression of ORN is due to the activation and dysregulation
of fi broblastic activity that leads to atrophic tissue within a
previously irradiated fi eld. A cascade of cytokines and free
radicals leads to destruction of endothelial cells and vascular
thrombosis, which leads to necrosis of microvessels, local
ischemia, and tissue loss. The combination of osteoblasts death
in the mandible after irradiation, failure of the osteoblasts to
repopulate, and the excessive proliferation of myofi broblasts
and osteoclasts results in the bony matrix being replaced by
fi brous tissues. On the basis of this theory, some early promising
results are being reported with vascular and antioxidant therapy
using pentoxifylline and tocopherol.

Some evidence suggests that Actinomyces infection and
increa sed osteoclast activity could be factors in the develop-
ment of nonhealing tissues and bony destruction seen in ad-
vanced ORN.55
A
B

Types of Wounds and their Management
258

A distinct condition caused by the use of bisphosphanate drugs
has also been described, which postulates the osteoclastogenic
effect of these agents leading to demineralization and causing
pathological bone fractures as precursor to ORN.

The most important risk factor for the development of ORN
is radiation therapy. Patients with total doses in excess of 50
Gy are at signifi cantly higher risk of development of ORN
than those treated with lower dose. Primary tumor location
plays a role by determining the amount and location of jaw
exposure to radiation. The posterior mandible is denser, with
a higher mineral content. The resultant decreased vascularity
places this region at increased risk. Therefore, radiotherapy
to the base of tongue and tonsillar fossa lesions has a higher
potential risk. The second most important factor is the local
environment of the oral cavity. Poor oral hygiene, odontogenic
infections, chronic infl ammation, and local trauma (either
iatrogenic or incidental) also play a signifi cant role in the
progression and severity of ORN.56-58

The management of ORN has rested primarily on efforts
aimed at prevention and curtailing disease progression.
The traditional dictum is any marginal teeth in the fi eld of
radiation therapy should be removed prior to the onset of
treatment. While this practice is uniformly advised, recent
data suggest it may not be suffi cient or effective in preventing
late complications. Hyperbaric oxygen protocols have also
been supported by small series as potentially benefi cial in
the prevention of ORN. Unfortunately, a larger clinical trial
including a large double-blinded placebo-controlled series
found no clinical benefi t.59

Early and limited ORN may respond to conservative
management, which usually includes some combination of
local wound irrigation, oral hygiene improvement, curettage,
debridement,
sequestrectomy,
bone
fi lling,
long-term
antibiotic use, and/or hyperbaric oxygen (HBO) therapy.

The unfortunate reality is that despite appropriate manage-
ment and diligent clinical care, many patients will progress to
advanced disease with potential serious complications including
pathologic fractures, orocutaneous fi stulae and recurrent
soft tissue cellulitis (Figures 30A to E). In essence, once an
extensive segment of the mandible is necrotic and colonized
Figures 29A to E: Osteoradionecrosis of mandible. (A) Irradiated mandible exposed in the area where overlying skin has given way. The
exposed mandible shows as sequestrum with atrophic skin at the periphery tethered to bone suggestive of infl ammation and infection in
the past. There is however little attempt to form granulations or epithelialization. Note the radiation changes in rest of the skin of the neck;
(B) Orthopentogram panorouex view of mandible showing radio necrosis; (C) Similar case but having been treated by hyperbaric oxygen therapy
for the last 3 weeks; (D) There is defi nite growth of granulations at the edges and the bone after saucerization shows punctuate bleeding,
prompting to salvage the same by using some local fl ap for cover; (E) Exposure of titanium plate in a case of osteocutaneous free fi bular
reconstruction of mandible after 2 years of having received radiotherapy
A
C
B
E
C

Management of Radiation Wounds
259
Figures 30A to E: Osteoradionecrosis of clavicle. (A) Surgical extirpation and composite reconstruction of mandible and cheek with
osteocutaneous bipaddled free vascularized fi bular graft subjected to postoperative radiotherapy developed a sinus over the medial end
of clavicle; (B) CT scan showing the necrosis in the medial third of clavicle; (C) Outline of excision of sinus and approach to the clavicle;
(D) Intraoperative view after exposing the clavicle shows the extent of bony destruction due to radio necrosis; (E) Contralateral pectoralis major
muscle fl ap was used to cover the area of ORN after thorough debridement till healthy bleeding bone ends were achieved
with multimicrobial fl ora, there is no conservative approach
to restore the viability of this bone. Management then turns to
debridement when the problem is localized and ultimately to
resection and reconstruction with vascular tissue with or without
bone, as the extent of disease progresses (Figures 31A to C).
The increasing number of patients seen in this terminal state of
ORN has led to the use of surgical resection and microvascular
reconstruction as a viable treatment option. The effi cacy of
hyperbaric oxygen, which is the foundation of these treatment
paradigms, has come into question based on the result of
prospective blinded clinical trials. The vast majority of patients
usually undergo preoperative HBO without any signifi cant
benefi t and with continued progression of disease. Advocates of
HBO would argue that it was only when HBO was initiated later
in the progression of ORN that it fails to prevent irreversible
necrosis. The reality is that there are a large number of patients
who progress to late stage disease with complications despite
HBO treatment (Figures 32A to D). These end-stage ORN
cases are now treated as operative candidates with surgical
resection and vascularized bone fl ap reconstruction used as a
method for achieving disease resolution. In general, the patients
with early presentations (less than 2 years after RT) had a much
higher rate of requiring surgical debridement of the jaw bone
with vascularized bone graft replacement and reconstruction.
Late stage ORN reconstructions are uniquely challenging
surgical procedures. The irradiated local tissue usually fails to
provide any recipient vessels for microvascular anastomosis. In
more than 50 percent cases the vascular anastomosis needs to
be done in contralateral neck or to vessels outside the radiation
fi eld using vein grafts or long pedicles, e.g. transverse cervical
vessels in lower neck, etc. Fibula osteocutaneous free fl ap
is the workhorse fl ap for such reconstructions (Figure 27).
The relative geometry of the intermuscular septum with its
cutaneous perforators to the plating surface of the fi bula bone
is reversed when the contralateral neck is used for recipient
vessels. It should be highlighted here that even with successful
surgical reconstruction, long-term surveillance of these patients
is critical as continued necrosis can occur away from the initial
site of presentation. There remains 55 percent incidence of
wound infection and 25 percent incidence of recurrence of
ORN in these cases with exposure of hardware as the most
common presentation (Figure 13). While every attempt is made
A
D
B
E
C

Types of Wounds and their Management
260
Figures 32A to D: Recurrent osteoradionecrosis of maxilla. (A) ORN involving maxilla I a case of carcinoma buccal mucosa who received
postoperative radiotherapy; (B) Sequestrectomy of devitalized segment of right maxilla done and a vascular cover with a superfi cial temporal
artery fasciocutaneous fl ap done. The healing was satisfactory; (C) Recurrence of ORN seen after 2 years as seen antrocutaneous fi stula;
(D) The repair was possible with in turning of surrounding skin and advancement of local fl ap to provide a double fl ap cover
Figures 31A to C: Osteoradionecrosis of mandible.
(A) The exposed mandible shows sequestrum
and unhealthy skin in surrounding region; (B)
Defect created after it was found that the entire
hemimandible was devitalized and no proper
vascular support was available for free fl ap transfer;
(C) A pectoralis major myocutaneous fl ap was
done as a bipaddled fl ap for both lining and cover
to reconstruct the defect. Bony reconstruction was
deferred because of extent and nature of pathology
for the time being. Note the axillary contracture
because of recent burns
A
C
B
D
A
C
B

Management of Radiation Wounds
261
Figures 33A to D: Post-laminectomy dehiscence. (A) Considering high incidence of exposure of hardware used for fi xation after removal of
spinal tumor subjected to radiotherapy a pre-emptive muscle fl ap cover planned; (B) A reversed latissimus dorsi muscle fl ap elevated; (C) The
muscle fl ap brought over the laminectomy site to cover the hardware; (D) Three weeks postoperative view of well healed scars ready to receive
radiotherapy
at the time of surgery to resect the necrotic bone to healthy
bleeding margins, in some cases the remaining bone is not
or will not remain completely viable. The surgery itself may
have caused this bone to progress from a marginal status into
nonviability. All said and done emphasis has to be put on the
fact that osteoradionecrosis is a progressive disease and despite
successful surgery, new sites of ORN may arise in the same
bone. With greater use of radiotherapy and longer survival from
disease, more and more of such cases will come to light.60
Prophlactive Reconstruction: Pre-emptive
Pre-radiation Flap Surgery
There are situations in surgical management of certain
cancers when an adjuvant treatment with radiation is
planned postoperatively, therein where otherwise no special
reconstruction would be thought of, but because radiation is
to be given after surgery, and knowing the tissue changes that
will ensue, leading to catastrophic crisis when they do occur,
pre-emptive fl ap-reconstructions are done. The examples for
these are numerous and follow a protocol in certain cancer
institutions, e.g. laminectomy for tumors of spine with or without
implant fi xation requiring postoperative radiotherapy: a reversed
latissimus dorsi muscle fl ap (Figures 33A to D) or a trapezius turn
over muscle fl ap (Figures 34A to D) is used to cover the hardware
and laminectomy exposure. This prevents failures with wound
dehiscence and devastating consequences after radiotherapy.
Similar conditions would apply in limb salvage surgeries for
treating sarcomas and bone tumors (Figures 39A to F). Groin
dissection is another area where wound healing problems per se
get compounded after radiation with dangers of femoral vessel
exposure and blow-out, hence preventive use of anterolateral
thigh fl ap or rectus abdominis musculocutaneous fl ap is routine
in some centers. Use of sternal head of sternocleidomastoid
muscle as a protective cover after laryngectomy and head and
neck surgeries is based on the same principle.
A
C
B
D

Types of Wounds and their Management
262
Figures 34A to D: Laminectomy dehiscence after radiation. (A) The scar gave way 2 weeks following radiotherapy with 45 Gy; (B) A trapezius
muscle fl ap elevated; (C) The muscle fl ap was used to cover the spine in the depth of the wound; (D) The skin closed primarily over the trapezius
muscle fl ap
Pre-emptive Postirradiation Flap Surgery
These are elective fl ap reconstructions being undertaken when
surgery is done postirradiation, although no prior wounding
or ulcers due to radiation exist. The logic towards such an
approach is that when an irradiated fi eld is subjected to
surgical insult, the healing within that fi eld is compromised
because of radiation changes and complications are common
with fearsome consequences. For example, during neck
dissection for secondaries in cases of base of tongue tumors,
where primary has been effectively treated with radiation
(usual 55-65Gy), any necrosis of neck fl ap or fi stulous leak
would inevitably lead to exposure and blow-out of carotid
vessels, hence a vascular muscle in the form of pectoralis
major muscle is always used to cover the vital structures before
wound closure. Similarly in treating tumors of lung after
radiation with lobectomy or pneumonectomy, the bronchial
stump and great vessels in vicinity are covered with either a
pericardial fl ap, intercostal muscle fl ap or most effectively
with a diaphragmatic muscle fl ap or lattismus dorsi, to prevent
the occurrence of bronchopleural fi stula (Figures 37A to D).
Abdominoperenial resection done after radiotherapy is usually
morbid in postoperative period owing to poor and delayed
healing in the perineum, hence a myocutaneous fl ap not
only gives a better contour and fi ll but also promotes healing
(Figures 38A to H). Approach to ethmoidal tumors and skull
A
C
B
D

Management of Radiation Wounds
263
Figures 35A to F: Synovial sarcoma of ilium in a nine years child. (A) CT scan showing the lesion involving the ilium; (B) Defect as seen after
excision with exposed hip joint; (C) A tensor fasciae latae musculocutaneous fl ap elevated. Its skin deepithelialized to be used as turn over fl ap;
(D) The fl ap tunnelled into the defect and the dermal component used to reconstruct the capsule of hip anteriolaterally; (E) Flap spread into fi ll
the defect; (F) Brachytherapy cannulae in place and loaded with source to start delivery of radiation on 3rd day. The reconstruction of joint was
stable and the child was allowed to walk with partial weight bearing on 22nd day onwards
A
C
E
B
D
F

Types of Wounds and their Management
264
base surgeries also require the use of fl aps, the temporalis
muscle, free rectus abdominis or free anterolateral thigh fl aps,
to act as fi llers and covers of vascular tissues, vital structures
and separation of cranial and oral cavities.
Reconstructive Breast Surgery
Patients undergoing mastectomy and radiotherapy for breast
cancer, either as a primary treatment or for secondary salvage
following
unsuccessful
lumpectomy
and
radiotherapy,
frequently request reconstructive surgery. Radiation damage
to the skin may adversely affect the outcome of reconstructive
surgery. Although immediate breast reconstruction following
skin-sparing mastectomy has superior results to delayed
reconstruction,61 it appears that there are fewer complications
and better cosmetic results if reconstruction is delayed
when radiotherapy is necessary.62-64 Reconstruction of the
previously irradiated breast after salvage mastectomy is
generally unsuccessful using implant-based techniques, due
to skin fl ap ischemia, poor skin expansion, implant extrusion,
increased capsular contracture and thereby leading to poor
cosmesis (Figures 40A and B).65-67 However, autologous breast
reconstruction using musculocutaneous fl aps may be successful,
albeit with a higher complication rate and lower cosmesis scores.
CURRENT TREATMENT STRATEGIES
Irradiated tissue is still considered as a problem tissue, and
treatment strategies are currently suboptimal. Conservative
treatments such as long-term dressing,68 topical negative
pressure dressings,69,70 hyperbaric oxygen and antibiotic
treatment are fi rst in line for consideration. The main strategy
currently used to prevent wound healing problems following
radiotherapy is to limit the dose of radiotherapy to noncancerous
cells by shielding healthy areas and carefully controlling the
delivery of the radiation. Precise targeting of radiotherapy is
especially important for the treatment of soft tissue sarcomas.
More specifi c targeting of the radiotherapy reduces damage
Figures 36A to D: Soft tissue sarcoma of forearm involving tendons and muscles. (A) The excised specimen together with the defect created;
(B) Extensor tendons reconstructed with a fascia lata graft; (C) Brachytherapy cannulae inserted across the tumor bed; (D) Distally based radial
artery forearm fasciocutaneous fl ap elevated from the same forearm and used to cover the defect
A
C
B
D

Management of Radiation Wounds
265
to surrounding tissues and loss of function. Advances in the
conformal planning of external beam radiotherapy have
allowed for careful modelling of the radiation specifi cally to
the sarcoma, avoiding surrounding structures.8 More specifi c
brachytherapy techniques also enable high-doses of radiation
to be delivered specifi cally to the tumor, modelled to avoid
surrounding critical structures.71 Although irradiated tissue is
more diffi cult to repair surgically, surgery is not contraindicated.
FUTURE TREATMENT MODALITIES
Prevention of Radiation Damage to
Normal Tissue
There is ongoing research into potential methods for
specifi cally targeting radiotherapy to the tumor. Cancerous
cells may be sensitized to radiation damage by platinum
agents, taxanes,72 cyclo-oxygenase 2 inhibitors73 or antibodies
to vascular endothelial growth factor (VEGF).74 Hypothermia
has also been found to sensitize tumors to radiotherapy
in animal models.75,76 Conversely, healthy tissue may be
protected from radiation damage by radio-protectant agents
such as amifostine,77-79 the antioxidant mitochondrial enzyme
Mn-SOD (mitochondrial superoxide dismutase)80 and the
erythropoietin analog epoetin-α.

Radio immunotherapy is an exciting new fi eld in which
monoclonal antibodies are used to directly target radio
emitters to the cancerous tissues.81 Encouraging results
have been obtained in mouse models by conjugating beta-
radiation-emitting radio nucleotides to antibodies specifi c for
prostate carcinoma, β-cell non-Hodgkin’s lymphoma, ovarian
carcinoma and colorectal carcinoma.82 Microspheres have
Figures 37A to D: Diaphragmatic muscle fl ap as pre-emptive cover for bronchial stump to prevent bronchopleural fi stula when doing
pneumonectomy after radiotherapy to lung tumor. (A) Pneumonectomy completed and hilum exposed. The bronchial stump being closed with
the stapler; (B) The pleural cavity with hilum and stump of bronchus in vulnerable condition; (C) A diaphragmatic muscle fl ap based centrally is
raised as a ‘wing’. The donor defect in ipsilateral dome of diaphragm is closed primarily; (D) The muscle fl ap is laid over the entire hilum and
anchored across to cover the bronchus and vessels. This vascular buttress pre-empts formation of any fi stula
A
C
B
D

Types of Wounds and their Management
266
Figures 38A to F
A
C
E
B
D
F

Management of Radiation Wounds
267
also been used to deliver β-radiation-emitting radio nuclides to
nonresectable tumors such as brain tumors and nonresectable
liver cancer.83
Promotion of Wound Healing Following
Radiation Damage
Exciting progress is being made in identifying factors involved
in radiation-induced damage. This research is leading to
opportunities for limiting radiation damage, promoting wound
healing after irradiation or preventing radiation-induced
fi brotic reactions.

Pentoxifylline is a methylxanthine derivative that leads to
increased tissue oxygen levels. Oral pentoxifylline has been
given to patients with long-term radiotherapy complications
and has been found to reduce fi brosis by up to 67 percent.
Pentoxifylline appears to increase healing of soft tissue necrosis
and to reverse fi brosis. Further studies of pentoxifylline in
combination with tocopherol (vitamin E) have found a similar
reversal of chronic radiotherapy damage84 as well as promotion
of healing of osseoradionecrosis.85 A randomized, placebo-
controlled trial has confi rmed these results, with signifi cant
reduction in superfi cial radiation-induced fi brosis following
six months of treatment with pentoxifylline and tocopherol.86

Many growth factors are involved in the normal healing
process. Preliminary studies in animal models of radiation-
induced injury have found that application of some of these
factors, such as vascular endothelial growth factor87 and nerve
growth factor promote free-fl ap survival and wound healing
after radiation damage. These endogenous growth factors were
found to be down regulated following irradiation. Application
of exogenous growth factor to the irradiated tissue could be
a powerful tool to promote survival and healing. There have
been exciting reports of the successful use of topical platelet
derived growth factor (PDGF) in animals and humans to cure
longstanding radiation-induced ulcers.88 A large-scale trial
of all the growth factor involved in wound healing is clearly
indicated.

Transforming growth factor-beta (TGFβ) has a major
role in promoting fi brosis following irradiation. Reduction
of TGFβ activity in irradiated gastrointestinal tissue, either
by application of soluble TGFβ type II receptor (TGFβRII)
protein or the somatostatin analog octreotide, has been shown
to reduce collagen deposition and fi brosis.89 TGFβRII is
upregulated following irradiation, and interruption of TGFβ
signalling pathways has also been found to improve radiation-
induced wound healing, by inhibiting fi brosis.90 Inhibition
of the effects of TGFβ by blocking its receptor TGFβRII
with halofuginone has been found to reduce radiation
fi brosis dramatically without any toxic effects.91 The studies
on interruption of TGFβ signalling have so far only been
performed in animal models; however, this is an exciting
Figures 38A to H: Anorectal carcinoma after adjuvant radiotherapy of 60 Gy. (A) Preoperative view showing the growth prolapsing beyond anal
verge; (B) Excised specimen en bloc; (C) Defect in perenium after abdominoperineal resection; (D) Gracilis myocutaneous fl ap elevated from
right thigh; (E) Gracilis fl ap transferred into defect to provide vascular interface in perineal wound together with bulk to fi ll the defeciency. This
pre-emptive use of fl ap in APR prevents the complication of nonhealing or delayed healing seen too often when a primary closure without
vascular fl ap is undertaken; (F to H) Similar defect is treated with rectus abdominis myocutaneous fl ap which is brought out through the
abdoperineal route and hence works better in supporting the pelvic fl oor also
G
H

Types of Wounds and their Management
268
Figures 39A to F: Chest wall tumor-chondrosarcoma. (A) Chest wall tumor involving 2nd and 3rd rib and part of sternum across the midline;
(B) CT scan of the patient showing the umblication over the lung and pericardium; (C) En bloc excision of tumor in progress; (D) Specimen
removed en bloc with the ribs, sternum and overlying soft tissue including the skin; (E) The bony cage has been reconstructed with ribs harvested
from contralateral side, split into two along their lengths and laid across the cut edges of the resected ribs on left. A vertical support is added for
the sternum. The entire reconstruct is draped from within outwards with prolene mesh so that a bilaminar layer of mesh encloses the rib graft
hardware to form a shell; (F) Latissimus dorsi myocutaneous fl ap is now brought over the composite reconstruct shell to cover with muscle and
skin in respective layers. The use of composite tissues for reconstruction is mandatory both for integrity of chest wall and its endurance to stand
the onslaught of radiotherapy in postoperative period
A
C
E
B
D
F

Management of Radiation Wounds
269
Figures 40A and B: Breast implant failure after radiotherapy. (A) Implant extrusion seen in primary breast reconstruction after it was subjected
to radiotherapy; (B) Successful reconstruction of breast done with latissimus dorsi myocutaneous fl ap assisted with silicone breast implant after
radiotherapy
avenue for future therapeutic intervention. As yet, most of
these applications have only been attempted in animal models.

In humans with problem wounds, skin substitutes are
being tested to aid healing. Encouraging results were
obtained using the integra bilaminate skin substitute to
completely heal problematic irradiated scalp wounds.92 Other
interesting opportunities for wound healing modifi cation
include application of ascorbic acid93 and injection of cells
such as fi broblasts or marrow stromal cells (stem cells)
intradermally to assist with wound healing.24 The concept
that stem cell injections can promote healing has evolved
from its postulations to actual treatment for radiologically
damaged skin. Autologous human grade mesenchymal stem
cells (MSC) derived from bone marrow and enriched in cell
cultures act as multipotent progenitor cells that differentiate
into osteocytes, chondrocytes, adipocytes, and stromal cells
thereby laying the foundation of cell lines require in healing
at that point of time in the given tissues where such cells have
undergone apoptotic damage.94
SUMMARY
It is evidently clear that although irradiated tissue is more
diffi cult to repair surgically, surgery is not contraindicated.
Irradiated tissue is still considered to be problem tissue
and all strategies to limit this damage should be aimed at
limiting the dose of radiation to noncancer cells by carefully
controlling the delivery of radiation by precise targeting. With
a better understanding of radiobiology and pathophysiology
of the effects of radiation, appropriate surgical principles
and approaches can be planned. The effects of radiation are
long-term, consequences are severe, and the effects on wound
healing are discouraging. Making best use of its therapeutic
properties and at the same time limiting its side effect is the
way future treatment modalities would develop in the form
of direct intraoperative application of radioactive isotopes,
controlling the penetration of radiation to selected tissue depths
and optimizing the effects of combination of chemotherapy,
radiation and surgery. Alongside comes the hope from use
of various stem cells which would be capable to replace
or replenish the loss of genetic information destroyed by
radiation. Till that day it would be the reconstructive surgeon
who would continue to play the role of Man Friday, looking
after the early and late changes of radiation and at the same
time enabling the oncosurgeon to fearlessly wield his scalpel.
Postscript
As I conclude writing this chapter, Japan has been hit by one
of the most devastating tsunami and earthquake in recent times
leading to colossal disaster and damaging the nuclear power
facility at Fukushima which may pose even greater danger to
mankind in near future, one which would put a question mark
towards the harnessing of nuclear energy and its potential to
affect human beings with radiation for times to come. The
ghost of 1945 has come, calling again in 2011 reminding once
again that we are only but vulnerable (Figures 41A to D).
A
B

Types of Wounds and their Management
270
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50-8.

• Pathogenesis and Risk Factors

– Risk Factors Predisposing to Development of Trophic


Ulcer

– Blood Supply

– Intrinsic Muscle Paralysis

– Anhidrosis
• Clinical features
• Clinical Evaluation
• Management

– Self-care Kit as an Aid to Empowerment of Leprosy


Patients
• Surgical Management

– Debridement, Desloughing and Dressing

– Vacuum-assisted Closure Device and Hydrodebrider

– Skin Cover

– Amputation and Other Foot Procedures

– Important Ancillary Management
Introduction
The term “trophic” ulcer denotes the ulcer occurring due to
imperfect nutrition of the part.1 It is also synonymous with
ulcer in the part devoid of cutaneous sensory supply.

Sometimes, it is also called perforating ulcer. By and large
it is caused by external trauma to anesthetic feet. However, in
leprosy, it is known to occur on the weight bearing areas of
feet where long standing and shearing forces produce internal
blister and breakdown of the skin causing wound which is
termed by Price as “plantar ulcer”.2

The other etiology of trophic ulcer can be considered as
diabetes mellitus, tertiary syphilis, syringomyelia, congenital
hereditary sensory-motor neuropathy, meningomyelocele,
spina bifida and pernicious anemia.

Trophic ulcer is a type of chronic ulcer in the anesthetic sole
of the foot, situated at bony prominences, resistant to local or
systemic therapy for healing and characterized by a marked
tendency to recurrence if causative factors are not taken care of.

In majority of trophic ulcer cases, close examination of the
extremity will reveal the signs of deficiency in nutrition of
skin, starting with dryness, loss of hairs, scaling, ichthyosis,
cracks and fissures. As such in lower limb, ankle region is
known to have less blood supply, the effect of which is greater
when there is discontinuity of the skin. Author considers
trophic ulcer cure is related to overall nutrition of the skin and
hence, all types of management include skin revitalization by
creams and ointments.
Pathogenesis and Risk Factors
The most common etiology of trophic ulcer in western
countries is sensory neuropathy associated with diabetes
mellitus. In developing countries like India besides diabetes,
it is also the leprosy. Whatever may be the cause, the common
pathway of ulcerogenesis is sensory neuropathy.

Neuropathic features or a combination of neuropathic and
ischemic factors are responsible for the development of trophic
skin lesions and plantar ulceration in diabetes. In leprosy,
inflammatory and immunologic destruction of nerve fibers
results in sensory motor loss. Repeated trauma to an insensitive
part of the foot results in a callosity which suppurates underneath
and burrows to muscle tendon and bone.3
Management of Trophic
Ulcer on Feet
Atul Shah
23
Chapter

Chapter 23
Management of Trophic Ulcer on Feet 
275
Risk Factors Predisposing to Development
of Trophic Ulcer4
Posture
During standing, the body weight is periodically shifted
between the feet in a reflex mechanism at the subconscious
level, so as to maintain the vascularity of the feet. The reflex
is maintained by sensory input from the soles of the feet. The
loss of weight shift reflex in sensory neuropathy is the main
cause of ischemia and repetitive pressure at the same site
predisposing to development of the trophic ulcer.
Blood Supply
Loss of sympathetic regulation of blood circulation in the
feet as a result of autonomic neuropathy leads to local anoxic
tissue damage. Persistence of this condition does not allow
healing and epithelization necessary for protection of the skin.
Deficient epithelization on fibrotic bed is seen commonly in
many of the superficial ulcers. Improvement in blood supply
with micronutrients and tissue perfusion improvement drugs
provides the impetus to healing.
Intrinsic Muscle Paralysis
The foot with intrinsic muscle paralysis is ulcer prone. In the
normal feet, the muscle belly provides the required padding to
the sole and also protects the metatarsal heads. In cases with
intrinsic muscle palsy, clawing of toes occurs. It is associated
with loss of padding on the metatarsal heads and abnormal
pressure on the tip of the toes making them ulcer prone.
Anhidrosis
Due to sympathetic paralysis, there is loss of sweating leading
to warm and dry foot. As a consequence, the skin becomes
hard, brittle and has tendency to crack and fissure formation
(Figure 1). These cracks or fissures get infected, may deepen
and give rise to trophic ulcers. In all instances of trophic
ulcers, it is necessary to note skin condition from below knee
to the tip of the toes.
Clinical features
The clinical features of a trophic ulcer (Figure 2) consists of
punched out edges, indurated base, slough in the floor, no pus
discharge but mild serosanguinous discharge, occasionally
dorsal edema or edema in ankle region and generally no pain.

However, if the ischemic part is predominant over the
neuropathic part then there is likelihood of shooting pain. The
surrounding skin of the trophic ulcer is generally thickened
and callus. The dryness is predominant in the sole of the foot
extending up to the knee.

The common sites of ulcer in leprosy have been described
by Burke as tip of the toes, metatarsal heads, heel and lateral
aspect of the sole of the foot.5

Majority of the patients present with chronic ulceration of
few months duration with history of probable external trauma
and often they say they are not aware how wound progressed
to become a trophic ulcer. Sometimes, patient is able to
identify the cause as loss of sensation or their habit of cross
leg sitting in case of ulcer on medial malleolus.

Occasionally, there may be a foot drop leading to abnormal
gait and pressure responsible for development of plantar ulcer
on the forefoot and lateral border of sole of the foot. Pain
in the foot points to the cause as ischemia and is confirmed
by palpation which may show decreased volume of pulse.
Table 1 shows comparison of findings in neuropathic and
ischemic ulcers.

In case of diabetic feet, Meggitt and Wagner6,7 classified the
ulcerations and its progress to gangrene in various grading as
shown in Table 2. However, it is important to note or find out
Figure 1:  Planter aspect of foot showing
dry cracked skin
Figure 2:  A typical trophic ulcer

Section 3
  Types of Wounds and their Management
276
the depth of the ulcer on physical clinical examination. If the
ulcer is superficial it would be Grade I, if it is deeper up to joint
it would be Grade II. If it is associated with infection, abscess
or osteomyelitis it would be Grade III. Gangrene of forefoot or
whole foot will be Grade IV and Grade V respectively.
Clinical Evaluation
Author prefers to evaluate all trophic ulcers in respect of its size,
depth, surrounding skin, tendon or joint infection, presence of
smell, infection, type of discharge and peripheral vascularity.

The first step is to put methylene blue on the surrounding
margin and taken the impression on a plain paper which
when compared after few months will enable you to record
the healing. The next examination consists of looking for
any discharge in surrounding region (Figure 3) or during
movement which will signify the joint involvement. A culture
swab is taken and sent for culture sensitivity, the peripheral
vascular component is palpated and recorded.

The sensory evaluation of the foot is undertaken by
testing with pin prick in the surrounding region and at the
predetermined points. The Semmes – Weinstein monofilament
if available, can be used preferably with 10 gm specification.
The tuning fork test may be used to assess the vibratory
sensation. If available, vibration perception threshold meter
is used (Bioesthesiometer). The value greater than 25V is
considered as significant loss of protective sensation.

One of the common methods for recording the pressure site
on foot in leprosy has been by using the ink impression taken
with Harris-Mat.

If the vascular evaluation is necessary, a color Doppler
flow study and angiography would be necessary. In case of
involvement of deeper tissue, the X-ray of the foot would
provide adequate information for surgical management
and rarely a MRI would need to be performed. All imaging
techniques vary in their sensitivity and its specificity is limited
if cellulitis, ischemia or neuroarthropathy is present.
Management
The primary treatment of trophic ulcer would be to counsel
the patient about the cause, extent of the damage, feasibility of
recovery and steps to be taken to prevent recurrence. A “self-
care kit” (Figure 4) containing the stock of the appropriate
dressing materials is offered along with explanation of the
technique of its use. In author’s experience, 40 percent of the
patients with leprotic trophic ulcers heal in 4 months time
with domiciliary SCK supply for regular use.8
Self-care Kit as an Aid to Empowerment of
Leprosy Patients8
The author has described the “self-care kit” as a very
effective method for healing of trophic ulcers in leprosy by
empowering patients to carry out dressings at home with the
given kit.
Table 1: Essential difference between a neuropathic ulcer
and an ischemic ulcer3
Neuropathic ulcer
Ischemic ulcer
Painless
Painful
Normal arterial pulses
Reduced or absent pulses
Loss of sensation
Variable sensory findings
Warm foot
May be cold foot
Plantar ulceration
Toe ulceration
No intermittent claudication
Intermittent claudication
Treated by local measures
Requires reconstructive surgery
Table 2: Grading of ulcers
Grade 0
Intact skin
Grade 1
Superficial ulcer
Grade 2
Deep ulcer to tendon, bone or joint
Grade 3
Deep ulcer with abscess or osteomyelitis
Grade 4
Forefoot gangrene
Grade 5
Whole-foot gangrene
Figure 3: A deep discharging ulcer

Chapter 23
Management of Trophic Ulcer on Feet 
277

A self-care kit consists of an antiseptic and cleansing
solution like savlon, foot scraper, antiseptic/antibiotic ointment
(betadine/neosporin), petroleum jelly (vaseline), gauze pieces,
bandages, adhesive tape and scissors. In order to keep the skin
soft, the patient is asked to soak his feet in water in which
the antiseptic solution is added. The patient should soak his
feet for 10 minutes everyday. Any calluses or thickened ulcer
margins should be scraped with the foot scraper and petroleum
jelly applied from below knee to the tip of the toes. The ulcer is
dressed with supplied ointment and covered with sterile gauze
and bandaged. Only four turns of bandage is necessary to hold
the sterile dressing in place. The introduction to self-care kit
is carried out using a camp approach, i.e. many patients are
taught together. The self-care kit gives patients the tools to care
for disabilities and motivates them to care for and cure their
disabilities on a daily basis. The improvement ensures their
confidence in self-care. Figures 5 and 6 show improved skin
of lower limb with emolients and Figures 7 to 10 show healing
with self-care kit practice at home.

In the event, if surgical treatment is considered inevitable,
a preoperative evaluation would be carried out and appropriate
medical treatment is instituted, for example, control of blood
sugar in diabetes and improvement in neuropathy by drugs like
gabapentin and methylcobalamine. In case of leprosy, patient
may be classified for treatment purpose as Pauic Bacillary
or Multi Bacillary type and is appropriate MDT is started.
Besides this, routine investigations like hemoglobin, blood
count, urine, X-ray chest, ECG and X-ray of the local part
should be performed. Trophic ulcers arising in other diseases
like meningomyelocele, spina bifida or congenital hereditary
sensory motor neuropathy, present with longer duration of
chronicity, recurrence and infection. A culture swab is taken
to initiate appropriate antibiotic following culture sensitivity
test and frequent local dressings are imperative for clearing the
infection and improving the ulcer bed for progression to healing.
Surgical Management
The goal of surgery in plantar ulcer is to heal the plantar ulcer
with appropriate resurfacing in such a way that there are
chances of minimal recurrence at the site of ulceration.

The following surgical procedures are generally available
for resurfacing sole of the foot having trophic ulcer.

1. Debridement, desloughing and dressing

2. Skin cover:

– Advancement of surrounding skin and direct closure

– Split skin graft or latest “plantar graft”

– Flap cover

3. Amputation
Figure 4: Self-care kit
Figures 5 and 6: Improvement in trophic condition of skin by emolient creams
Figure 5
Figure 6

Section 3
  Types of Wounds and their Management
278
Debridement, Desloughing and Dressing
Despite the fact that number of studies have proved the
effectiveness of soap and water cleaning of the wound/ulcer, it
has still not gone into psyche of the people to be used by them.9,10

Debridement refers to the excision of neurotic dead tissue,
foreign material until the healthy viable tissue is reached. It is to
be carried out in operation theatre. Desloughing refers to surgical
removal of slough or its removal by other dressing techniques.
The other dressing techniques in diabetes include moist gauze
dressing. The moist gauze is allowed to dry on the wound and
is ripped off although it effectively removes dead tissue but also
removes viable tissue and is very painful in the sensate patient.
Aim of these procedures is to enhance the healing process.

In traumatic wounds and leprosy, the desloughing is
carried out with “eusol” dressing, the eusol loosens the slough
and makes it suitable for excision with surgical instruments.
The other materials used for desloughing includes collagen
granules and calendula ointment. Generally, the dressing is
carried out with few layers of dry gauze pieces and few layers
of bandage to secure the dressing in place.

There are certain alternative dressing options which are
less often described but have shown effective results. The
use of Youki is one such example.11 The Youki spray has
following ingredients: aqua, cellular extracts, amino acids,
natural proteins, quarts, repair complex, antimicrobial,
nipastat. Youki—wound spray offers an alternative approach
to wound management, without the need for a dressing.
Youki is suitable for use on superficial, wounds including
cuts and grazes. Individuals suffering from ulcers have
also benefited by using Youki. It supports the skin’s natural
repair mechanism by providing the optimum conditions for
healing.
Figures 7 to 10: Examples of healing of ulcers after use of self-care kit in two patients
Figure 7
Figure 9
Figure 8
Figure 10

Chapter 23
Management of Trophic Ulcer on Feet 
279
Vacuum-assisted Closure Device (VAC)
and Hydrodebrider12
This is required for larger wounds rather than trophic ulcers.
However, its effectiveness and shortening of duration for
obtaining clean granulations makes it mention necessary.

Once the wound is clean and adequately vascularized,
then it can be covered with a VAC dressing. The VAC applies
sub atmospheric pressure to a wound via a closed suction
mechanism. This speeds up the formation of granulation,
sterilizes the wound, and reduces tissue edema. Newly
available is a hydrosurgical debrider and dresser in OT (Versa
Jet©, Smith and Nephew, Hull, United Kingdom) that use a
high power water jet (up to 15,000 psi) to debride tissue.15
The venturi effect caused by this high pressure water jet
stream sucks the underlying tissue into the stream of water
and separates it from the underlying tissue. The debrider
works rapidly to take thin slice after thin slice of tissue with
minimal surrounding tissue trauma.
Skin Cover
In general, any wound which for some or the other reason
does not heal with primary or secondary intention exhibits
either deficient mechanism of wound healing or its inability
to compensate for process of natural wound closure. If ulcer
does not heal in reasonable time of 10 to 12 weeks surgical
management is considered necessary. The site, size, extent and
mobility of the surrounding skin along with healthy granulation
tissue determine the method of the surgical management.

The first and foremost procedure among then is mobilization
of surrounding skin, advancing in both directions (either side
to side or proximal and distal) and suturing of the freshly
debrided margins which is often called as advancement flaps
and suturing. However, the sole of the foot with its fascial
strands which are deeply attached to deeper fascia and bone
precludes more movement to enable complete closure.
In smaller ulcers, triangular advancement of skin is often
sufficient for skin closure.

If advancement of edges is ruled out then alternative
would be to obtain a bed of healthy granulation tissue and
cover it with a split skin graft. However, recently in cases of
leprosy where thousands of patients with plantar ulceration
are awaiting surgical management, the author has revived and
popularized the technique of plantar graft. The plantar graft13
per se is carried out in patients who have impaired sensation
in the sole of the foot and generally does not need even local
anesthesia. The graft is taken from the instep area of the sole
and laid over the ulcer. It is fixed in position by few absorbable
stitches and immobilization is carried out by few layers of
POP over the normal dressing.

The procedure being simple can be carried out in any
community health center by any general surgeon. The donor
area of the instep is covered with antiseptic solution over the
vaseline gauze and allowed to heal secondarily. Since, it is
done as an OPD procedure and the graft has a thicker dermal
layer, the take of the graft, takes slightly longer duration. Even
if the graft looks whitish at the first or second dressing, it
should not be thought as slough and removed. By 4 to 6 weeks
following the take of the graft, weight bearing is allowed with
a pressure-relieving sponge dressing over the grafted area.
The results of this procedure has been extremely encouraging.
Figures 11 to 14 show the results in two of the cases.

Although plantar graft is simpler and better than split skin
graft, it still does not provide the same quality of skin as that
of the sole. The graft on the bony points readily breaks down
on walking or weight bearing and the recurrence is common.
Therefore, as a rule while resurfacing the sole at the weight-
bearing areas, the general rule is to consider a flap cover from
the surrounding tissue to enable it to withstand day to day
trauma of walking. Author prefers distally based transposition
flap for the 1st metatarsal head ulcers or the neurovascular
subcutaneous pedicle island flap14 from the great toe as
described by him to provide the much needed sensation in the
flap. Figures 15 and 16 show the flap cover.

The advanced flap cover like flexor digitorum brevis
myocutaneous flap15 for heel ulcer was initially considered to
offer advantages like better vascularity, greater extent of the
availability of the skin to cover large ulcers and less recurrence.
However, in practice, fasciocutaneous transposition flap from
the local region works equally well and is simple to perform.
For the large ulcers on the posterior aspect of the heel or
Tendo-Achilles area, it was considered necessary to do a cross
leg flap, however, the sural artery flap both as an island or with
a small skin pedicle now provides adequate skin cover and
can also extend up to half of the heel pad from the posterior
aspect.

The other versatile but advanced and technically difficult
flap includes medial plantar artery island flap for resurfacing
the heel area or making it distally based to resurface the
forefoot area. The lateral calcaneal artery flap can cover the
posterior aspect of calcaneal and distal achilles defects. Free
flaps are rarely required for coverage of trophic ulcers.
Amputation and Other Foot Procedures
Amputation of the foot may be indicated when neuropathy,
vascular disease, and ulcerative deformity have led to soft
tissue necrosis, osteomyelitis, uncontrollable infection, or
intractable pain.16,17 In general, a procedure is chosen as
indicated amongst the following metatarsal osteotomy, ray
amputation, arthrodesis or a below knee amputation.

Section 3
  Types of Wounds and their Management
280
Figure 11
Figure 12
Figures 11 to 14: Plantar graft results in two cases
Figures 15 and 16: Neurovascular subcutaneous island pedicle flap described by author
Figure 13
Figure 15
Figure 16
Figure 14

Chapter 23
Management of Trophic Ulcer on Feet 
281
Important Ancillary Management
The major question is whether rest is essential for wound
healing/healing of trophic ulcers. While majority of the
people and centers particularly looking after rehabilitation in
Hansen’s disease advocate and explain the importance of rest
and often ask patient to stay home with an elevated foot. This
concept does not go well with patients who need to earn and
maintain family and therefore have to walk.

Fritschi18 advocated “healing while walking” by providing
a walking plaster cast or splint in which patient continued
to walk for work and also exhibited the healing propensity
of superficial trophic ulcer. Many other organizations have
provided total contact cast17 or mini POP boot which offer
rest to the ulcerative area, but this technique is still dependent
on the skilled professionals to apply and remove the cast.

The author in his study of “self-care kit” and MCR
footwear (Figure 17) given to all patients along with kit found
that nearly 40 percent of the patients with ulcers healed and
therefore believes that ‘rest is not absolutely essential for
healing’. Taking pressure off the ulcerative area or offloading
the foot with appropriate footwear like MCR (micro-cellular
rubber) generally takes care of chronic factors and allows
healing to occur. Thus, author’s self-care kit empowerment
program always has MCR footwear distributed to patients. In
cases which do not heal but improve to the level that surgical
management may become possible will also need the MCR
footwear postoperatively.

Another method to determine the exact area of body
weight transmitted to the ground in standing position is by
mapping of high pressure areas using the “Harris Mat”.19 This
mapping enables to carve out a cavity in the footwear, so that
Figure 17: MCR footwear
the weight is taken by the surrounding tissues. It also helps
to determine whether metatarsal arch needs support with a
metatarsal bar. In high-risk foot or where feet have resorption
and gross shortening and loss of digits, rigid rocker footwear
will maximize the foot contact area and prevent recurrence.
Majority of old leprosy cases in the colony therefore, fall in
this category of “custom made footwear” requirement.

It is not important to only heal the ulcer but to follow-up
the case to prevent the recurrence of the ulcer. The incidence
of recurrence in neuropathic ulcer is high as the primary
etiology sustains. However, its effect can be minimized with
proper education, free supply of materials and regular check
up through community health worker. Recently, integration of
leprosy into general health service and gradual involvement
of “ASHA” in leprosy disability prevention and medical
rehabilitation is likely to impact favorably in reducing the
trophic ulcers.
Summary
The term trophic ulcer is derived from the fact that ulcer
has occurred on a part which has deficient nutrition. The
affection of peripheral nerve in leprosy, diabetes or sensory
motor neuropathy results in anesthesia making the feet prone
to external and internal trauma. The punched out edges,
unhealthy granulation tissue, thickened margin, minimal
discharge and dryness continues unabated for months and
years together without apparent signs of healing. The basic
and primary management advocated by the author since over
a decade following his research in empowering the patients
in self-healing of wounds with group therapy and aided by
providing self-care kit. Not only the chronic ulcers show signs
of improvement but also in nearly 40 percent of patients, the
trophic ulcer healed completely and the surrounding skin
showed signs of renewed vitality. Author further describes
simplified techniques of reconstructive surgery for healing
those indolent ulcers which refuse to heal. These include
plantar graft and local transposition flaps. Amputation is
carried out as a last resort. Ancillary management like splints,
crutches and MCR footwear are necessary for enhancing the
wound healing and to prevent the recurrence.
References
1. Wikipedia accessed on 20/4/10.
2. Price EW. Plantar Ulcers Chapter 10, Surgical Rehabilitation
in Leprosy, In: Frank McDowell, Carl D Enna (eds); 1974. pp.
373-82.
3. Veves A, Guirini JM, LoGerto FW. The Diabetic Foot; 2nd edn;
2006. pp. 216-21.
4. Fritschi EP. Reconstructive Surgery in Leprosy; 1971. pp. 156-
60.

Section 3
  Types of Wounds and their Management
282
5. Birke JA, et al. Methods of treating plantar ulcers. Phys Ther.
1991;71(2):116-22.
6. Bowker JH, Pfiefer MA. Levin and O’Neal’s. The Diabetic
Foot, 7th edn;2008. pp. 221-26.
7. Widatalla AH, Mahadi SI, Shawer MA, Elsayem HA, Ahmed
ME. Implementation of diabetic foot ulcer classification system
for research purposes to predict lower extremity amputation.
Int J Diab Dev Ctries. 2009;29:1-5.
8. Shah Atul, Shah Neela. “Self-care Kit”—An Aid for
Empowerment for self-care of feet in leprosy. Published by
CLCP and MAA, Jan 2001, Revised Edition: Jan 2004.
9. Carol Dealey. The care of wounds : a guide for nurses, wound
management products, p. 97.
10. Fernandez R, Griffiths R. Water for wound cleansing. Cochrane
Database of Systematic Reviews 2008, Issue 1.
11. Youki.com as accessed on 20.4.10
12. Veves A, Guirini JM, LoGerto FW. The Diabetic Foot, 2nd
edn;2006. pp. 338-356,391-425
13. Shah Atul, Sagar Gundewar. “Plantar skin graft” – a simple
technique for healing the ulcers on the sole of the foot. Annual
Report, Novartis Comprehensive Leprosy Care Association;
2008. p. 29.
14. Shah Atul, Saluja Kumkum. Rehabilitation in Hansen’s Disease,
Chapter 4 in Ergonomics in Rehabilitation, Edit: Mittal and
Karwowaski, Publisher: Taylor and Francis; 1988. pp. 55-74.
15. Shah Atul, Pandit S. Reconstruction of the heel with chronic
ulceration with flexor digitorum brevis myocutaneous flap.
Lepr Rev. 1985;56:41-8.
16. Rooney J, Hutabarat SR, Grujic L, Hansen ST. Surgical recons­
truction of the neuropathic foot. The Foot. 2002;12:213-23.
17. Jasan H Calhoun. Overgaard, kristi A, et al. Diabetic foot
ulcers and infections: Current Concepts. Advances in Skin and
Wound Care. 2002;15:31-4.
18. Fritschi EP. Video from Karigiri, “Healing while walking”.
19. Srinivasan H. Prevention of Disabilities in Patients with
Leprosy, - A Practical Guide, World Health Organization, 1993.

• History
• Etiopathogenesis

– Clinical Features
• Prevention
• Laboratory Studies
• Treatment

– Conservative Wound Management

– Surgical Intervention for Pressure Sores

– Choices in Reconstruction

– Complications of Pressure Sores
INTRODUCTION
The terms pressure sores, pressure ulcers, decubitus ulcers and
bedsores all are commonly used interchangeably. Decubitus,
from the Latin word ‘decumbere’, means ‘to lie down’ and
therefore, signifi es ulcers that form over bony structures
which are prominent when lying in recumbent position.
These may form in other positions as well, like prolonged
sitting, a “chair sore”. The common denominator of all such
conditions is pressure and hence, the term ‘pressure sore’ is
the most accurate and all encompassing. (Figures 1 and 2) The
National Pressure Ulcer Advisory Panel (NPUAP, 2007) in
the United States has defi ned a pressure ulcer as “a pressure
ulcer is localized injury to the skin and/or underlying tissue
usually over a bony prominence, as a result of pressure, or
pressure in combination with shear and/or friction. A number
of contributing or confounding factors are also associated with
pressure ulcers; the signifi cance of these factors is yet to be
elucidated.” The bony prominences are, e.g. sacrum, ischium,
trochanter, etc. while the pressure is caused by a supporting
structure, e.g. a bed or a wheelchair. These patients are seen
by almost all the medical and surgical specialists although
neurologists, neurosurgeons, orthopaedic surgeons and plastic
surgeons are more likely to see most of these patients. Other
clinicians especially those looking after geriatric age group
and the general practitioners, may be required, at one time or
the other, to provide immediate advice and/or prescribe long-
term management and preventive measures. The patients as
well as his/her relatives may not be immediately aware of these
developing wounds because they often occur in bed ridden,
paralyzed and elderly. The pressure sores have been blamed to
be the second most common cause (the fi rst being adverse drug
reactions) of iatrogenic death in developed countries.

The management of this malady is one of the few domains
of plastic surgery where other surgical specialists do not
Figure 1: Multiple pressure sores in a recently operated young spinal
cord injury patient. Note the large amount of slough and undermining
Pressure Sores
Arun Goel
24
Chapter