Principles and Practice of Wound Care

Pressure Sores
285
although the exact bone differs. Also, muscle is more
susceptible to pressure-induced ischemia than skin and
starts degenerating after four hours of ischemia (due
to its greater metabolic requirements) in contrast to 12
hours for skin. Hence, the “inverted cone appearance”
of damage seen with base of cone nearer the bone. In
other words, pressure sores may be quite big by the time
they are noticed on the skin and may be representing
‘tip of an iceberg’. The unconscious, paraplegic or
debilitated patients lack the “protective sensation” that
alerts a normal individual to discomfort produced by
prolonged immobility. Absence of discomfort leads
to no urge for change in position resulting in pressure
sores. Patients undergoing prolonged surgery are also at
risk of developing pressure sores.

2. Shearing force: Shear or tangential pressure is considered
as the second most important factor in the causation of a
pressure sore. Shearing is the force created by sliding of
adjacent structures which causes a relative displacement
of tissues leading to occlusion of vessels and capillaries.
For example, when a patient seated on a chair slides down
towards the fl oor or a patient recumbent on the bed with
head-end elevated slides towards the foot end, the skin
remains stationary in relation to the chair/bed surface while
the subcutaneous tissues and muscles along with their
vessels get stretched and distorted leading to large areas
being deprived of their vascular supply. These forces may
be even more signifi cant than pressure itself in the dermis
and near the bone because the vessels run perpendicular to
both of them. Shear’s greatest effect is that lesser pressure
is required to compromise the circulation. Additionally,
the shearing forces have been shown to be increased up to
three times in elderly and paraplegic patients.
3. Friction: The third external force which acts directly
on the skin is that of friction. It contributes to skin
ulcerations through non-ischemic mechanism. Friction
between skin and bed clothes may cause loss of stratum
corneum causing in turn intraepidermal blisters and
superfi cial erosions. Lack of this integrity may cause
infection and further damage. This makes it important
not to drag a spinal cord injury victim across the bed;
rather they should be lifted, moved and then placed.

Shear forces and friction aggravate the effect of
pressure and together form the triad for the development
of a pressure sore. The microcirculation is occluded with
resultant ischemia, tissue hypoxia, cell death, necrosis
and ulceration in that order. The following factors are
contributory to the development of a pressure sore.
4. Spasticity of muscles and contractures
5. Moisture: Excessive moisture may lead to skin
maceration making the epidermis susceptible to
abrasion and breakdown. Cellulitis, rashes and skin
infections can occur. The moisture may be due to
excessive perspiration, wound drainage, urinary or fecal
incontinence with the last being most harmful because
of the presence of bacteria and enzymes that are caustic
to skin. Moisture increases the risk of developing a
pressure sore fi vefold.

6. Infection: Skin serves as the most important barrier to
infection by microbes, a number of whom are in constant
symbiotic relationship with the skin and prevents its
invasion by pathogenic organisms. Bacterial invasion
of the ischemic tissues and abraded, infl amed skin
not only leads to an increase in the size and depth of
a pressure sore, but can also spread superfi cially along
surrounding tissue planes. This invasion occurs not only
with the bacteria present locally in the skin, but also by
the distant endogenous source via blood stream. The
areas prone to pressure sore development may also be
edematous due to compression of soft tissue occluding
the venous and lymphatic outfl ow, denervation of the
blood vessels or because of the original disease of the
patient (e.g., malnutrition, renal or hepatic disease)
increasing the risk of infection. A number of gram-
positive, gram-negative and anaerobic bacteria have
been isolated from the pressure sores.

7. Nutritional status

8. Age: While pressure sores can occur at any age, changes
in skin due to aging like decreased epidermal turnover,
fl attening of the dermo-epidermal junction, loss of elastic
fi bers with decreased collagen formation, decreased
vascularity and increased skin permeability are all said
to predispose an elderly person to risk of pressure sore.

Several theories have been put forward to explain the
pathophysiology behind formation of a pressure sore.
However, the main causative factors appear to be, local
tissue hypoxia, bacterial colonization of the wound,
repetitive ischemia reperfusion injury, an altered
cellular and systemic stress response of the patient.
The fundamental mechanisms that lead to ischemia-
reperfusion injury are same in all organ systems in
the body, especially at molecular level, where reactive
oxygen species and infl ammation are the key mediators
in causing the injury. In pressure sores, this ischemia-
reperfusion is especially repetitive in an effort by the
patient and clinician to prevent the development of the
sore and the injury gets potentiated.
Clinical Features
All the pressure sore patients should be examined to identify the
original systemic disease which has led to their development.

Types of Wounds and their Management
286
In most of the patients this is already known, e.g. spinal cord
injury victims. Any co-morbidity (ies), mental (level of alertness
and cooperation) and nutritional (anemia, hypoproteinemia,
metabolic diseases) status should be evaluated.

Like all fi res, pressure sores are “small” to begin with and give
enough warning signs to contain them before becoming major
and unmanageable (Figures 3 to 5) Several staging systems have
been given for classifying them. Edberg et al (1973) described
the following stages of pressure sore development:
Stage 1
Hyperemia: Acute onset (<30 minutes) of cutaneous redness,
which disappears within one hour of pressure removal.
Stage 2
Ischemia: Develops with pressure persisting over two to six
hours. Redness requires at least 36 hours to dissipate after
relief of pressure.
Stage 3
Necrosis: Unrelieved pressure for more than six hours may
result in frank necrosis with induration and blue discoloration
of the skin. Irreversible.
Stage 4
Ulceration: A necrotic area may ulcerate within two weeks,
particularly if infected. Underlying bony exposure and
involvement may occur.

The National Pressure Ulcer Advisory Panel (NPUAP,
2007) in the United States has redefi ned the stages of pressure
ulcers, including the original four stages and adding two
stages on deep tissue injury and unstageable pressure ulcers
as follows. This was the culmination of over fi ve years of
work beginning with the identifi cation of deep tissue injury in
2001. The goal was to reduce the number of incorrectly staged
pressure sores. It is to be noted that this classifi cation system
does not mean that all pressure sores pass through the various
stages from lesser to higher, but rather describe the damage
seen at the specifi c time of examination.

1. Suspected deep tissue injury: This stage is added
only recently and is described as a purple or maroon
localized area of discolored intact skin or blood-
fi lled blister due to damage of underlying soft
tissue from pressure and/or shear. The area may be
preceded by tissue that is painful, fi rm, mushy, boggy,
warmer or cooler as compared to adjacent tissue.
Deep tissue injury may be diffi cult to detect in
individuals with dark skin tones. Evolution may include
a thin blister over a dark wound bed. The wound may
further evolve and become covered by thin eschar.
Evolution may be rapid exposing additional layers of
tissue even with optimal treatment.

2. Stage 1: Intact skin with non-blanchable redness
of a localized area usually over a bony prominence.
Darkly pigmented skin may not have visible blanching;
its color may differ from the surrounding area.
The area may be painful, fi rm, soft, warmer or cooler as
compared to adjacent tissue. Stage I may be diffi cult to
detect in individuals with dark skin tones. May indicate
“at risk” persons (a heralding sign of risk).
Figure 3: Pressure sore over trochanter showing healthy dermis
Figure 4: Multiple pressure sores over sacrum and trochanter

Pressure Sores
287
3. Stage 2: Partial thickness, loss of dermis presenting
as a shallow open ulcer with a red pink wound bed,
without slough. May also present as an intact or open/
ruptured serum-fi lled blister. Presents as a shiny or
dry shallow ulcer without slough or bruising. This
stage should not be used to describe skin tears, tape
burns, perineal dermatitis, maceration or excoriation.
Bruising indicates suspected deep tissue injury.
4. Stage 3: Full thickness tissue loss. Subcutaneous fat may
be visible but bone, tendon or muscles are not exposed.
Slough may be present but does not obscure the depth
of tissue loss. May include undermining and tunneling.
The depth of a stage III pressure ulcer varies by
anatomical location. The bridge of the nose, ear, occiput
and malleolus do not have subcutaneous tissue and stage
III ulcers can be shallow. In contrast, areas of signifi cant
adiposity can develop extremely deep stage III pressure
ulcers. Bone/tendon is not visible or directly palpable.
5. Stage 4: Full thickness tissue loss with exposed bone,
tendon or muscle. Slough or eschar may be present on
some parts of the wound bed. Often include undermining
and tunneling. The depth of a stage IV pressure ulcer
varies by anatomical location. The bridge of the nose,
ear, occiput and malleolus do not have subcutaneous
tissue and these ulcers can be shallow. Stage IV ulcers
can extend into muscle and/or supporting structures (e.g.
fascia, tendon or joint capsule) making osteomyelitis
possible. Exposed bone/tendon is visible or directly
palpable.
6. Unstageable: Full thickness tissue loss in which the
base of the ulcer is covered by slough (yellow, tan, gray,
green or brown) and/or eschar (tan, brown or black) in
the wound bed. Until enough slough and/or eschar is
removed to expose the base of the wound, the true depth,
and therefore, stage, cannot be determined. Stable (dry,
adherent, intact without erythema or fl uctuance) eschar
on the heels serves as “the body’s natural (biological)
cover” and should not be removed.

The site(s) and number of pressure sore(s) should also
be noted. Other related local fi ndings may be tenderness,
erythema and warmth of the surrounding skin with
exudates and foul odor emanating from the sore. Along
with fever, they signify severe infection. There may
be osteomyelitis and sinus tracts. The patient may be
anemic, hypoproteinemic, spastic and dehydrated.

Individuals with normal sensation, mobility and mental
faculties are unlikely to develop a pressure sore because
of the constant change in position dictated by conscious
or unconscious feedback from the area under pressure.
There are two major categories of pressure sore patients,
namely, those with or without normal skin sensation.

a. Those with normal skin sensation:

• Acute critical illness, e.g. head injury, burns, pelvic
and lower limb fractures, coma due to any cause,
etc. leading to immobility of the patient. These
patients are likely to improve or recover completely
from their basic disease and hence the prevention
and management of pressure sores is required
for a limited period of time. Patients undergoing
prolonged surgery (more than 4 hours) are also at risk
because of immobility, lowering of blood pressure
by the anesthetist, skin maceration due to pooled up
fl uids on the mattress of OT table and use of tight
positioning straps to hold the patient on to table.

• Chronic debilitating illness causing immobility of
patient, e.g. old age especially with urinary/fecal
incontinence, Parkinsonism, Alzheimer’s disease,
severe arthritis, hemiplegia, etc. Unfortunately, these
conditions are extremely diffi cult to “cure” and along
with patients with ‘absent skin sensation’ account for
most of the pressure sore patients.

b. Those with impaired/absent skin sensation: Impaired or
absent skin sensation is a primary factor contributing to
pressure sore development. These patients are immobile
and may never recover from their basic disease process
and hence the prevention and management of pressure
sores is required for rest of the life. Even some mobility
may decrease the development and severity of pressure
sore.

• Following spinal cord injury, paraplegics and
quadriplegics

• Patients of meningomyelocoeles (Neuropathic ulcers)

• Transverse myelitis and other neurologic defi cits
Figure 5: Pressure sore over trochanter with slough and undermining

Types of Wounds and their Management
288
PREVENTION
Prevention of pressure sores is clearly the best treatment. “An
ounce of prevention is better than a pound of cure.” Pressure
sores not only increase the morbidity but may also lead to
death and increase the expenditure on treatment manifold.
Initially, the preventive measures are taken by the hospital
personnel (doctors, nurses, physiotherapists, etc.). Eventually,
the patient’s family members and the patient himself have
to take over the responsibility under the guidance of the
treating clinician. It is to be noted that factors that lead to
pressure sore formation are multifactorial and very diffi cult,
if not impossible, to alter. Pressure sores occur across the full
spectrum of health care settings. Thus, they are found not only
in patients who get almost no expert medical care, but, also
in patients who are being treated in the best of medical care
facilities in the world! Whether they are really preventable
is controversial. Florence Nightingale felt that the prevention
of pressure sores lay within the hands of her professionals
and said. “If a patient develops bed sore, it is the fault of the
nurse and not the fault of the disease.” Unfortunately, even
when aggressive measures for their prevention are applied,
the incidence comes to a certain low level beyond which it
does not decrease. Thus, the development of a pressure sore
cannot always be considered synonymous with poor quality
care. Terminally in ill patients and in those orthopedic patients
where immobilization and frequent turning to relieve pressure
compete with each other, preventing a sore may be really
challenging. Conversely, religious application of various
measures for their prevention is highly advised and can
certainly bring down the incidence, prevalence and severity
of pressure sores in the society as a whole with reduced cost to
the patient and his/her family ( including quality of life, pain
and suffering), society and government exchequer.

To be able to prevent pressure sores, it is of utmost
importance to know which patients or individuals are at
risk of their development. A number of risk factors have
been identifi ed to predict the patients at risk and several risk
scales devised, so, that nursing staff and other caregivers can
maximize their efforts to apply preventive measures. The
best known are the Norton scale, the Braden scale and the
Waterlow scale. The important risk factors are age, alterations
in sensation or response to discomfort, mobility, mental and
nutritional status, bladder and bowel continence, general
physical condition, weight, etc. One should daily examine the
trochanteric, sacral, ischial, heel and other areas and institute
the following preventive measures.

i. Skin care: Skin inspection is the basis of prevention
of pressure sores. A regular and rigid schedule of
inspection must be followed as part of the patient’s
daily routine. Any sign of redness, irritation or abrasion
is the indication of an impending ulcer formation and
all pressure must be taken off the area immediately.
Special attention should be given to bony prominences.
This inspection of the skin should be performed by the
patients themselves as well, especially the paraplegics
and others who are mentally alert and normal, using
mirrors.

Skin care aims at elimination of all the factors that
may contribute to friction and excoriation of the skin.
The skin must be kept clean and dry at all the times.
Areas that sweat heavily or where body fl uids collect
(e.g. perianal) must be washed several times daily with
mild soap and water and patted dry. A fi ne talcum powder
may be dusted over the dry skin surface with special
attention to areas where moisture tends to develop. If
powder is applied to wet areas, it will form small granules
and abrade the skin during muscle spasms and position
changes. Thus, particulate matter must be removed
from the bedding. The combination of moisture, heat,
friction and pressure must be avoided. Care of bladder
(by urinary catheter, condom drainage or suprapubic
cystostomy, etc.) and care of bowel movements must
be meticulous. By maintaining proper hygiene, the
opportunity for pathogenic microorganisms to cause
infection is reduced greatly. It must be remembered
that the compressed skin has less resistance to bacterial
invasion.
ii. Relief of spasticity and contractures: The develop-
ment of a pressure sore is also contributed by the
spasticity of muscles which prolong immobility and
impede any surgical intervention. Spasticity may be due
to spinal trauma, cerebral stroke, cerebral palsy, multiple
sclerosis, etc. There may be a spasm of the bladder as
well leading to decreased capacity and spontaneous
voiding. Relief of muscle spasms is required to prevent
as well as treat an already developed sore. This can
be done either medically or surgically depending on
the severity. Physical therapy measures like full range
of motion exercises of all the joints must be done in
every case irrespective of spasticity. Pharmacological
control is done with drugs like diazepam (depresses
all levels of central nervous activity including the
limbic and reticular formation probably by increasing
GABA activity; 10–40 mg/day), baclofen (induces
hyperpolarization of afferent terminals and inhibit both
mono– and polysynaptic refl exes at spinal level;15–100
mg/day), dantrolene sodium (causes muscle relaxation
by modulating skeletal muscle contractions at a site
beyond myoneural junction and directly on the muscle
itself; 50-800 mg/day) and mephenecine carbonate (3-
15/mg/day), etc. The disadvantages of these and other
agents is that they cause drowsiness and loss of residual

Pressure Sores
289
urinary and sexual function. Intrathecal baclofen therapy
has been used in children with cerebral palsy resulting
in improvement in upper as well as lower extremity
spasms.

Surgical control can be done using neurosurgical
cordotomy, selective anterior rhizotomy or selective
posterior
rhizotomy.
Obturator
neurectomy
(for
adductor spasms), femoral nerve crush (for extensor
spasms), sciatic nerve crush (for fl exor spasms) may
be required. Intrathecal alcohol/phenol/procaine blocks
may be given. These options should be used only after
the maximal recovery from the spinal injury (around 2
years).

Contractures of varying degrees of severity are
present in many patients with long standing denervation.
Early in the course of disease, physiotherapy and
splintage may be required to prevent and correct them.
Flexion contractures of the hip and knee joints due to
their strong fl exor tendons tend to limit the positioning
options for the patient.
iii. Relief of pressure: Understanding the role of prolonged
pressure in the causation and continuation of a pressure
sore by the patient and his attendants, including medical
personnel, remains the single most important factor
in prevention of pressure sores. It is also the most
important factor for prevention of recurrent ulcers and
in facilitating spontaneous healing. In fact, it is the
key to pressure sore problem at all levels. The dictum
“where there is no pressure, there is no sore” must be
kept in the mind of all medical personnel while treating
any patient who is immobilized for prolonged periods.

Relief of pressure is done with a frequent change of
posture either mechanically by attendants or by using
various automatic turning devices. Patients who are
capable of shifting their weights themselves should be
encouraged to do so as often as possible while caregivers
should do so every two hours or less. With the putting
forward of theories that pressure sores are caused
by unrelieved pressure due to immobility came the
development of various methods and devices to take care
of pressure. Thus, Paget introduced a water bed in 1873.


A number of appliances have been devised and
promoted over the last fi ve decades with the objective of
removing pressure. They can be divided into:

i. Devices that turn or move the patient as a whole
regularly: These devices turn the patient from
supine to prone alternately at regular intervals either
automatically or mechanically by hand and thus change
the pressure points allowing perfusion of all areas. This
therapy, also known as kinetic therapy, is available
only for hospitalized patients. These beds suffer the
drawback of being large, cumbersome and expensive.
The various devices available are Foster and Stryker
frames, CircOlectric bed and Keane RotoRest bed.
ii. Devices that support the whole body in such a way that
either the pressure is minimized or equalized: Different
types of mattresses and beds have been designed. The
mattresses may be air fi lled or water fi lled and added
onto the regular mattress of the bed of the patient. The
alternating air mattress has a thick polyvinyl outer
covering and rows of air cells which are designed to
infl ate or defl ate alternately with the help of an electric
pump and thus, changing the pressure points at regular
intervals. The water mattress on the other hand is fi lled
with water and hence, very heavy and bulky with risk
of leaking water spoiling the bed. The patients must
be positioned properly on these mattresses and regular
checks done as to their functioning. Additionally, the
impervious material of these mattresses retains heat
and promotes sweating, skin maceration and infection
all of which are contributory factors for pressure sore
formation. To take care of the above problems of air
and water mattresses, air fl uidized beds were designed.
These beds (Clinitron®) suspend the patient on an air-
permeable mattress containing millions of silicone-
coated beads of uniform size. (Figures 6 and 7) Although
they effectively bring down the pressure exerted at any
point to less than 10 mm Hg and eliminate the risk of
pressure sore, they are highly costly and bulky and
unavailable for home use.
iii. Devices that support and minimize pressure over
specifi c small areas, especially bony prominences, e.g.
sacrum, malleoli, etc. Thus, gel pads made of silicone
or polyvinyl chloride are available in different size and
shapes (with a consistency of normal body fat) to act
as padding under a bony prominence or between two
prominences.

These pressure relief appliances have been shown
to reduce the incidence and severity of pressure sore
development in various degrees of effectiveness
and also help in their healing, whether treated
conservatively or surgically. Unfortunately, many of
these devices are either expensive or heavy and space
occupying or impede nursing care or diffi cult to clean or
at least unappealing to the patient or his/her attendants.
Moreover, they are adjuncts and not a panacea for the
prevention or care of pressure sores and their use is
likely to lead to complacency on the part of the patient,
his/her relatives and caregivers.

Pressure sores are most common over bony
prominences, i.e. where there is little cushioning effect
of the subcutaneous tissues. While no part is immune,

Types of Wounds and their Management
290
Table 1: Position of patient vs Site at risk
POSITION →
Supine
Side-lying
Semi-fowler
Sitting
Prone
Occiput
Side of hand
Sacrum
Scapula
Forehead
Rim of ear
Shoulder, pinna
Lateral malleoli
Sacrum
Chest
Scapula
Iliac crest
Heals
Coccyx
Iliac crests
Elbow
Trochanter
Ischium
Foot edge
Sacrum
Medial area of knees
Posterior knees
Toes
Heels
Perineum, malleoli
Figures 6 and 7: Air-fl uidized bed: Please note the silicone beads
lying on the fl oor as the bed has just been refurbished with fresh stock
of silicone beads
almost 90 percent of pressure sores occur in the lower half
of the body with the most common sites being ischium,
sacrum, trochanter and heel. Susceptible areas for pressure
sores are dependent on positioning of the patient (Table
1). The patients should be positioned to avoid pressure
over existing sores and over bony prominences. Pillows
or foam wedges can be used to raise a pressure sore off,
its support surface and prevent direct contact between
two bony prominences, e.g. knees or ankles. Wheel chair
bound patients may select a pressure-relieving cushion
based on specifi c need. However, donut–type devices are
forbidden for they impede circulation of the area in the
center and worsen the situation.
iv. Nutrition: The poor nutritional status in itself does
not lead to the formation of pressure sores, as healthy
persons getting injured and suddenly immobilized can
develop them and all malnourished patients do not get
them. However, the increase in size, exacerbation and
continuance of a pressure sore is certainly affected by
the poor nutritional state of the patient. Additionally, an
emaciated patient has little padding over his/her bony
prominences and hence, at increased risk of pressure
injury. Thus, every attempt should be made to maintain
adequate nutritional status. This is best performed
by oral route, if available. Duodenal tube feeding or
parenteral supplementation may be required to prevent
catabolism. The aim is to achieve normal wound healing.
Diabetes and other metabolic conditions must be looked
for and appropriately and vigorously treated. The
requirements for proteins, calories, vitamins (especially
ascorbic acid), trace elements (magnesium, manganese,
selenium and zinc etc.) and iron, etc. all are increased
in these patients and they should be supplemented.
Serum albumin levels have been shown to predict risk
of pressure sore development and should be monitored.
Hypoproteinemia should be corrected by infusion of
amino acid solutions, albumin, etc. Hemoglobin level
should be maintained above 11 gm percent by blood
transfusion(s), if required. Ascorbic acid, required for
the synthesis and maintenance of collagen during wound
↓
Figure 6
Figure 7

Pressure Sores
291
healing, levels have been found to be reduced in geriatric
age group and in spinal injury patients as well. Its
supplementation does lead to an improved healing. Zinc
is an essential trace element of many metalloenzymes
especially those involved in carbohydrate, lipid, protein
and nucleic acid synthesis and degradation. Its levels
have been found to be lower in pressure sore patients
and intake has been shown to improve wound healing.
Decreased fl uid intake in malnourished patients can also
affect tissue perfusion resulting in reduced pliability.

Those patients who are able to take their food orally can
be managed rather simply by appropriate diet advised by
the dietician. However, if oral feeding is not possible or is
inadequate, nasogastric feeding may be required. In patient’s
where gut is not available for enteral alimentation, parenteral
hyper-alimentation has to be instituted. Parenteral supplements
may also be needed in patients on enteral alimentation.
Weight loss and tissue wasting also causes the bony areas to
become more prominent and thus increasing the applied force
per unit area. Even obese patients are also at risk because of
decreased mobility. If a sore develops, poor nutritional status
interferes with wound healing as well whether the pressure
sore is being managed conservatively or surgically. Metabolic
disturbances like diabetes mellitus should also be taken care
of meticulously to prevent the fl air up of infection and allow
the wound to heal well, either conservatively or surgically.
LABORATORY STUDIES
Complete blood count is done. An elevated leucocytic count,
C-reactive protein and ESR may be indicative of infl ammation
and infection. Low hemoglobin needs correction. Nutritional
parameters like serum protein, albumin and prealbumin and
transferrin levels should be assessed. Urine analysis and culture
sensitivity is checked for urinary infection. Blood and wound
cultures are done when indicated to start appropriate antibiotics.
However, it must be noted that positive surface swab cultures
do not always mean wound infection (invasion into the tissues)
as bacterial colonization( harmless presence of microbes in the
wound) is the rule in most chronic wounds. A wound biopsy
may be required in chronic pressure sores if there is suspicion
of malignant change. Plain X-rays, sinograms and CT scans, to
look for bony involvement, are done when indicated. Magnetic
resonance Imaging (MRI) is highly accurate in diagnosing
osteomyelitis and also defi nes the deeper limits of the pressure
sore guiding the surgeon in his excision.
TREATMENT
Whereas total prevention is the ideal goal, early detection and
treatment halting the progression of the pressure sore with
consequent decrease in morbidity, mortality and cost is also
desirable. Early diagnosis is also desirable because a ‘Stage 4
sore’ is far more diffi cult to treat successfully than at earlier
stages. Once a pressure sore has developed, all the measures
for its prevention viz. care of the skin, relief of pressure, spasm
control and maintaining good nutritional status are either
instituted, if not being already followed or continued with
greater vigor. The basic disease process itself should also be
treated and the various risk factors identifi ed and eliminated
if possible. In addition, local wound care (conservative
treatment) with or without operative intervention(s) is
required. Effective management of these wounds can take
place only when the patient, including the pressure sore, is
treated as a whole.
Conservative Wound Management
The goals of conservative wound management are manifold viz.

1. To make the wound healthier with no dead and necrotic
tissue and minimal bacterial counts, minimizing the
wound discharge and odor in return,

2. To heal the wound completely in some cases,

3. To prepare the wound for operative closure,

4. Last but not the least, conservative management is also
a necessity where the patient is unfi t to undergo any
surgical intervention because of his/her basic disease
and/or associated co-morbid conditions.

Those patients who are likely to become ambulatory within
a reasonable period should undergo surgical intervention only
after ambulation as the postoperative care becomes minimal
and the risk of development of new or worsening of other
existing pressure sores decreases considerably. Conversely,
those patients who are not likely to ever become ambulatory
should undergo surgical intervention only after the number
and size of pressure sore(s) is decreasing and have remained
stabilized over a reasonably long period, proving thereby,
that preventive measures are being taken care of properly and
adequately by the patient, his/her attendants and the medical
personnel. Otherwise, recurrence (locally or at another place),
is very likely. Thus, to begin with every pressure sore requires
conservative management.

In the early grades of pressure sores, when the involvement
is of the skin only, the wound and the surrounding area is
cleansed with a mild antiseptic solution (e.g. Savlon), every
time a dressing is changed. Debridement of microscopic
necrotic tissues and bacterial control requires frequent
dressings and topical chemotherapy. It is, then, smeared with
one of the various topical therapeutic antimicrobial agents
available and dressed using non-stick paraffi n gauze next to
the sore followed by absorbent gauze and cotton pads. The
topical agents (creams, ointments and solutions) in common

Types of Wounds and their Management
292
use are povidone-iodine (Betadine®), triple antibiotic
(Neosporin®) ointment, framycetin (Soframycin®) cream,
nadifl oxacin (Nadoxin®) gel, nanocrystalline silver forms like
Hydroheal®, Megaheal®, etc. Hypoallergenic tapes should be
used to keep the dressings in position. These wounds may heal
with conservative treatment alone.

Unfortunately, when fi rst seen, most of the pressure sores
have already involved the deeper tissues (fat, muscle and
bone) and an eschar is present. The removal of this necrotic
tissue is essential in treating any sore. Dead tissues are ideal
for the growth of microorganisms and reduce wound healing.
Sharp debridement with a scalpel/scissors done at the bedside
without causing bleeding (i.e. leaving some dead tissue behind)
is done on a daily basis for stage 2 to 4 sores. (Figures 8A
and B) A more thorough debridement should always be done
in the operation theatre as it may lead to bleeding requiring
bipolar electro-cautery and volume replacement. After the
gross eschar is removed, mechanical debridement of the
wound may be done by irrigation with hydrogen peroxide
solution to dislodge and remove remaining necrotic debris.
The daily dressing of the wound is done with wet to dry
dressings using woven gauze with large pore size and coarse
weave till the wound becomes healthy and granulating. Twice
or thrice dressings daily may be required in patients with large
amounts of foul smelling discharge. The gauze is soaked in
Eusol (sodium hypochlorite), povidone-iodine or one percent
acetic acid solution. In these cases, wound swabs must be sent
for microbial culture-sensitivity test. Similar to a burn wound,
almost everything under the Sun has been applied to a pressure
sore in an attempt to heal it. The list includes not only various
“home remedies” but also scientifi cally developed products in
an attempt to hasten healing. An eschar gets separated from the
live, healthy wound bed by autolysis done by the enzymes in
wound. To enhance this process, various exogenous enzymes
from the plant and animal sources have been added to the
wounds. The various enzymatic debriding agents used are, e.g.
collagenase (Salutyl®), papain, urea, streptokinase, bromlein,
etc. Systemic antibiotics are not useful in the presence of gross
necrotic tissues. However, appropriate systemic antibiotics may
initially be given for a period of six to seven days to ‘sterilize’ the
surrounding infl amed and infected tissues (cellulitis) and also,
if the patient develops fever and signs of systemic infection.
Long-term systemic antibiotics are of no value. This is because
they do not penetrate the heavily scarred chronic ulcers with
thrombosed vessels and lead to development of bacterial
resistance as well. These wounds contract over a period of
time. Small ulcers may heal with conservative treatment alone,
especially if the patient has normal skin sensation and has
recovered from his acute illness and has become ambulatory.
The larger ones invariably need some surgical intervention for
their closure (Figures 9 to 11).

A moist wound environment is said to be more conducive
to faster healing of the wounds and hence, a number of
specialized occlusive wound dressings have been developed.
These are hydrocolloids (Duoderm®), hydrogels (Intra site
gel®), polymer fi lms, polymer foams, alginates, etc. Each
has its own advantages and disadvantages apart from being
costly. A number of topical agents that promote healing
(growth factors) have also been developed and used. The
various growth factors are transforming growth factors α and
Figures 8A and B: (A) Large sacral pressure sore with extensive slough and undermining with surrounding infl ammation; (B) 6 weeks after
debridement and conservative management. Please note the minimal slough and healthier wound bed
A
B

Pressure Sores
293
β, epidermal growth factor, platelet derived growth factor
interleukin-1 and interleukin-2, etc.

A number of adjunctive therapies have also been utilized
in an effort to expedite the healing of the sore. The use of
low voltage direct current and high voltage pulsed galvanic
stimulation has been shown to hasten the rate of healing and
are especially useful for Stage 3 and 4 sores not responding
to routine treatment. Hyperbaric oxygen therapy chamber has
also been used and claimed to be effective. With the availability
of VAC therapy (negative pressure wound therapy), the
armamentarium of conservative management has increased
and good results are being shown (Figures 12A to D).
Surgical Intervention for Pressure Sores
The goal of surgical intervention for any open wound is to
achieve closure to control infection and protein loss, avoid
or treat progression and bone/ joint involvement, reduce the
risk of developing amylodosis and malignant change, improve
patient’s hygiene, appearance and acceptance in society. While
every patient may not be fi t for surgical intervention, each and
every pressure sore also does not require the surgeon’s knife.
In fact, a very small percentage of patients with pressure sores
are candidates for surgical intervention. A very thorough
planning, taking into account various factors (including the
availability of prolonged post-operative care) should be done
before resorting to surgical closure if a successful outcome is
to be achieved. After all, it is no good if the ulcer recurs in the
fl ap or at some other site. Unfortunately, there is a very high
recurrence rate after surgical intervention. No clear criteria for
selecting a patient for surgery exist. The patient’s ability to
tolerate the risks of surgical procedure and anesthesia must be
evaluated. Elective reconstructive surgical intervention should
be done only after the general condition of the patient is stable
and the sore has shown signs of improvement in the form of
minimal necrotic tissue, appearance of healthy granulations
and a decrease in the size of the wound.

In general, stage 1 and 2 pressure sores can be managed non-
surgically. Stage 3 and 4 sores require surgical intervention
or else the treatment becomes unduly prolonged and may
end up in a non healing wound or early recurrence. Absolute
indications for surgical intervention include the following:

i. An ulcer too large to heal with conservative treatment
alone in a reasonable period of time.
ii. The presence of underlying osteomyelitic bone, septic
joint or abnormal calcifi ed bursa, etc.

Contraindications to surgical intervention include a
critically ill patient, patient (and relatives) who fail to
cooperate for the demands of surgical pre and postoperative
management, patients unsuitable for rehabilitation beyond a
vegetative state, etc.
Figure 9
Figure 10
Figures 9 to 11: Pressure sores being managed conservatively
showing healthy granulating bed devoid of slough and undermining.
These can be split skin grafted
Figure 11

Types of Wounds and their Management
294

The basic principles for surgical closure of pressure sores
have become well established for the last more than 50 years
and include:

1. Complete excision of the ulcer including adjacent scar
tissue and underlying bursa, sinus tract, osteomyelitic
bone, heterotopic ossifi cation and soft tissue calcifi cation.
2. Closure of the wound using well vascularized local
fl aps that may include any combination of skin,
subcutaneous tissue, and/ or muscle with padding of the
bony prominence and fi lling of the cavity with healthy
muscle. It is preferable to place suture lines away from
the pressure points using large-sized fl aps and also not
to jeopardize any other fl ap territory which may be
required later in case of recurrence.
3. Avoidance of tension and protection of the transferred
tissue from re-injury until healing has occurred followed
by mobilization.
Choices in Reconstruction

i. Direct closure: Only a very small percentage of pressure
sores allow for simple excision and direct closure. This is
possible for very small sized ulcers only where the lack
of tissue is minimal. However, it represents a surgical
compromise at its best because the scar is located over
the most prominent and vulnerable point over the bone
and there is persistent tension on the wound edges.
ii. Split skin grafting: Many surgeons have a mistaken idea
that split skin grafts are of no use for closure of pressure
ulcers. However, this is not so (Figure 13). All patients,
where the sensation of surrounding skin is normal and
the ulcer bed is shallow and fi t for split skin graft (SSG)
“take”, can be considered for split skin grafting of
the wound (either permanently or temporarily). Many
patients of paraplegia have such extensive ulcerations
Figures 12A to D: Sacral and bilateral trochanteric sores healed after application of VAC therapy
A
B
C
D

Pressure Sores
295
that no fl aps exist to close them. In these cases, an SSG
can certainly decrease the wound size, if not close it
completely and also reduce the infection and improve
nutritional status. Split skin grafts may also be required
to close donor sites of some fl aps.
iii. Local fl aps: Since the fi rst surgical intervention using
fl aps by John Staige Davis (1938), a number of local
random and axial pattern skin fl aps, fasciocutaneous
fl aps and myocutaneous fl aps have been described
and used for closure of the pressure sores at various
anatomical sites by the plastic surgeons. The presence
of osteomyelitis, sinuses and infected joints must be
diagnosed beforehand as they are responsible for wound
infection, breakdown and recurrence in stage 3 and 4
ulcers, if not taken care of.
iv. The sacral pressure sores occur in a patient lying in the
supine position and are treated by unilateral or bilateral
large random pattern rotation skin fl aps, transversely/
superiorly based lumbosacral fl ap based on lumber
perforating vessels and gluteus maximus myocutaneous
fl ap (Figures 14 and 15).

v. The ischial pressure sores occur due to the sitting
position of the patient. They have a very high recurrence
rate. They are treated by medially based posterior thigh
transposition fl ap, tensor fascia lata fl ap, gluteus muscle
fl ap, etc. (Figures 16A to F).
vi. The trochanteric pressure sores occur in patients lying
in lateral position and are commonly treated by tensor
fascia lata myocutaneous fl ap or anteriorly based fl ap
from the thigh. The donor site is split skin grafted.
vii. High thigh amputations may be required in patients
where everything else fails. The indications include
large trochanteric pressure sores with underlying
osteomyelitis of femur and pyarthroses, multiple, large
and recurrent sores with inadequate local tissues for fl ap
coverage, multiple sores with severe contractures of hip
and knee joints and osteomyelitis of pelvis. Although,
this may improve the balance and reduce the total weight
of the patient, these procedures remain controversial.
Complications of Pressure Sores
The most common complication related to pressure sores is
the increased mortality although it is not clear how it happens.
They may not cause death directly but it may be due to their
occurrence in frail elderly patients. Development of pressure
sores has been associated with several fold higher mortality
in both acute care as well as chronic care settings. A number
of other complications including osteomyelitis, pyarthroses,
amyloidosis and urethral fi stula can occur. Osteomyelitis is
very common in infected deep pressure sores. However,
Figure 13: Sacral pressure sore healed with split skin graft
A
Figures 14A and B: (A) Defect after excision of sore; (B) Transposed
lumbosacral fl ap for coverage of defect
B

Types of Wounds and their Management
296
A
B
C
Figures 15A to C: (A) Bilateral ischial sores; (B) Gluteus maximus
musculocutaneous fl ap mobilized into the defect; (C) Inset fl ap covered
defect on left side and right side closed primarily after excision of ulcer
A
B
C
Figures 16A to C
contiguous osteomyelitis is diffi cult to diagnose even with
radionuclide scans, CAT scans and needle biopsy. Bacteremia
and septicemia can also occur due to pressure sores. Patients
may need amputations. Once healed, there are great chances of
recurrence because the patient and his attendants may become

Pressure Sores
297
Figure 17: Recurrent pressure sore over sacrum after bilateral gluteal
rotation fl aps. Note the chronically scarred margins and the bed
lax (Figure 17). The relatives may simply get ‘fed up’ because
of the prolonged and permanent nature of spinal injury or other
disabling condition with no end in sight and telling heavily
upon the earning of the family. All chronic wounds exposed to
continuous trauma over several years to several decades have
the potential to turn into malignant (Marjolin’s ulcer) and a
pressure sore is no exception. (Figure 18) Any suspicion of
malignant transformation should be subjected to biopsy.
BIBLIOGRAPHY
1. Allman RM Pressure Ulcers among the Elderly. N Engl J Med
1989;320:850-3.
D
E
Figures 16A to F: (A) Ischial sore; (B) Excised wall of the ulcer;
(C) Gracilis muscle being harvested; (D and E) Gracilis muscle being
pulled into the defect to fi ll the cavity; (F) Healed ulcer
F
Figure 18: Development of malignancy in a sacral pressure sore
Figures 16D to F

Types of Wounds and their Management
298
2. Allman RM Pressure ulcer prevalence, incidence, risk factors
and impact Clin Geriatr Med 1997;13:421-36.
3. Bass MJ, Phillips LG Pressure sores Curr Prob Surg 2007;
44:94-143.
4. Brem H, Lyder C. Protocol for the successful treatment of
pressure ulcers. Am J Surg. 2004;188(suppl 1A):9S-17S.
5. Bouten C, Oomens C, Baaijens F, Bader D. The etiology of
pressure ulcers: skin deep or muscle bound Arch Phys Med
Rehabil. 2003;84:616-9.
6. Colen SR. Pressure Sores In: McCarthy JG. (Ed). Plastic Surgery
(Vol. 6). WB Saunders, Philadelphia; 1990. pp. 3797-838.
7. Constantian, MB (Ed). Pressure Ulcers: Principles and
Techniques of Management. Boston. Little, Brown and Co; 1980.
8. Conway H, Griffi th BH. Plastic Surgery for Closure of
Decubitus Ulcers in Patients with Paraplegia: Based on
Experience with 1000 Cases. Am J Surg. 1956;91:946-75.
9. Disa JJ, Carlton JM, Goldberg NH. Effi cacy of operative cure
in pressure sore patients. Plast Reconstr Surg. 1992;89:272-8.
10. Grey JE, Harding JE, Enoch S. Pressure ulcers. BMJ 2006;332:
472-5.
11. Harrop JS, Rodriguez DJ, Benzel EC. Nutritional care of the
spinal cord injured patient. In: Benzel EC (Ed). Spine Surgery:
Techniques, Complication Avoidance and Management,
Elsevier, Philadelphia; 2005. pp. 1873-86.
12. Henwood AM, Naderi S, Benzel EC. Skin and wound care.
In: Benzel EC (Ed). Spine Surgery: Techniques, Complication
Avoidance and Management, Elsevier, Philadelphia; 2005. pp.
1887-99.
13. Janis JE, Kenkel JM. Pressure sores. Selected Readings in
Plastic Surgery. 2003;9(39):1-42.
14. Johnston E. Optimising nutrition to prevent pressure ulcer
development. Clinical Review Wounds. 2007;3(1):53-7.
15. Jones G, Nahai F. Pressure ulcers. In: Habal HB, et al. (Ed).
Advances in Plastic and Reconstructive Surgery, 1991;7:209-29.
16. Klitzman B, Kalinowski C, Glasofer SL, Rugani L. Pressure ul-
cers and pressure relief surfaces. Clin Plast Surg. 1998;25:443-
50.
17. Knox KR, Datiashvili RO, Granick MS. Surgical wound bed
preparation of chronic and acute wounds. Clin Plast Surg.
2007;34:633-41.
18. Levi B, Rees R. Diagnosis and management of pressure ulcers
Clin Plast Surg. 2007;34:735-48.
19. Marschall MA, Cohen M. Pressure Sores. Mastery of Plastic
and Reconstructive Surgery. Little Brown and Co. Boston;
1994. pp. 1371-86.
20. Medina A, Scott PG, Ghahary A, et al. Pathophysiology of chron-
ic non healing wounds. J Burn Care Rehabil. 2005;26:306-19.
21. Mustoe TA, O’Shaughnessy KO, Koeters O Chronic wound
pathogenesis and current treatment strategies: a unifying
hypothesis. Plast Reconstr Surg. 2006;117:35S-40S.
22. Nizegoda JA, Mendez Eastman S. The effective management of
pressure ulcers. Adv Skin Wound Care. 2006;19 (Suppl1):3-15.
23. Parish LC, Witkowski JA, Crissey JT. The Decubitus ulcers in
Clinical Practice. Bristol, Springer-Verlag, 1997.
24. Philips LG, Robson MC. Pressure Ulcerations. In: Jurkiewicz
MJ, Krizek TJ, Mathes SJ, Ariyan S (Ed). Plastic Surgery:
Principles and Practice. St. Louis CV Mosby. 1990;2:1223-51.
25. Reuler JB, Cooney TG. The Pressure Sore: pathophysiology and
principles of management. Ann. Intern Med. 1981;94:661-6.
26. Romanelli M (Ed). Science and Practice of Pressure Ulcer
Management. London: Springer, 2006.
27. Sorensen JK, Jorgensen B, Gottrup F Surgical treatment of
pressure ulcers. Am J Surg. 2004;188(suppl 1A):42S-51S.
28. Vasconez LO, Schneider WJ, Jurkiewiez MJ. Pressure Sores.
Curr Prob Surg. 1977;14(4):1-62.

• Microbiology of Implant Infection
• Pathophysiology of Implant Infections
• Presentation
• Prevention and Management

– Investigations

– Treatment
Introduction
Louis Pasteur has rightly stated, “Germ is nothing. It is
the terrain or environment in which it grows which is
everything”. The advances in invasive surgery during the
20th century have witnessed many ambitious projects
like metallic orthopedic implants and joint replacement
prostheses. The past few decades have seen rapid advances
in antisepsis (especially modern day theaters and the
development of newer antibiotics) that in turn has permitted
an accelerated development of invasive procedures. Modern
day instrumentation and tribology have revolutionized the
orthopedic sciences at a swift pace. Like any other implanted
material, the orthopedic implants share a propensity to
infection, which may be influenced by the nature, position
and duration of the implant.

Orthopedic device infection is perhaps one of the most
devastating complications (Figures 1 and 2) and is associated
with high morbidity and substantial cost.1–4 Two million
fracture-fixation devices and 600,000 joint prostheses are
implanted every year in the US. The infection rate at first two
years post primary total hip or knee replacement is estimated
to be around one to two percent. The risk of infection after
revision surgery is considered to be 40 percent higher than
primary procedure. The incidence of infection after internal
fixation of closed fractures is generally low (2%), whereas it
may exceed to 30 percent after fixation of open fractures.
Microbiology of Implant
Infection
Bacteria as well as the normal human cells have an affinity for
molecules on the surface of the implant. Both compete for the
occupancy of this surface; the tissue cells by adaptation and
integration, and the bacteria by adhesion and colonization.
Infection can result from seeding of the microorganisms at the
time of implant insertion or from a later bacteremia. Unless
heavy contamination or a particular pathogenic organism is
involved, some time period may be required for the small
number of bacteria, introduced into an area where a brisk
inflammatory response is occurring, to multiply sufficiently
for infection to become clinically apparent.5

A variety of bacteria and few fungi have been reported to
cause orthopedic device related infections, but most of these
infections are due to few major organisms. Staphylococcus
aureus (coagulase +ve) and Staphylococcus epidermidis
(coagulase –ve) are the most commonly involved organisms.
While Staphylococcus epidermidis are ubiquitous commensals
of the skin and upper respiratory tract, Staphylococcus aureus
are present in the normal flora of approximately 20 percent
population usually in the anterior nares, axilla and perineum.
In sharp contrast, Staphylococcus aureus are intrinsically
more virulent and generally susceptible to antibiotics (except
methicillin-resistant Staphylococcus aureus). An implant
infection with Staphylococcus aureus may also result in a
Orthopedic Device
Related Infections
Sumit Batra, Sumit Arora
25
Chapter

Types of Wounds and their Management
Section 3
300
systemic disease. Staphylococcus aureus and coagulase-
negative Staphylococci isolated from biomaterial-associated
infections commonly express fibronectin-binding surface
proteins. The ability to interact with collagen as well as the
ability of coagulase-negative Staphylococci to produce surface
slime or capsular material results in infection persistence.

Coliforms (E. coli, Klebsiella, and Proteus), Pseudomonas,
Streptococcous, anaerobic bacteria (Bacteroids, Fusobacterium),
Mycobacterium tuberculosis, Candida, and even mixed infection
may frequently be encountered in such situations.
Pathophysiology of
Implant Infections
High energy trauma has been linked with a greater incidence of
infection than low energy trauma owing to associated soft tissue
injury; similarly open fractures are more commonly associated
with infection than closed fractures. The comorbid conditions
in patients like diabetes mellitus, immunodeficiency states
and obesity also predispose to infections. The use of titanium
implant may decrease the chances of infection over stainless
steel implants. Optimum theater conditions, use of universal
precautions, timely antibiotic prophylaxis, soft tissue handling
are imperative in infection prevention. Exogenous source
of infection from contaminated instruments and implant,
operating team, airborne bacteria, and exposed equipments,
while endogenous focus from distant infection and commensal
skin inhabitants may add to infection incidence.

Internal fixation devices provide a site for bacterial
adherence, decrease vascularity, and suppress the functioning
of local immunocompetent cells. Bacteria as well as human
tissue cells have an affinity for molecules on the surface of the
implant.6,7 Both compete for occupancy of the same surface:
the tissue cells by adaptation and integration, whereas the
bacteria by adhesion and colonization. This contest has been
aptly described as a Race for the surface (Gristina,1988).6
Microorganisms in nature and disease are dependent on
substratum attachment for optimal growth and development.
Similarly, implanted biomaterials tend to potentiate bacteria
on their surfaces so that the normally friendly or opportunistic
organisms become virulent pathogens. Virulence is also
enhanced because both bacteria and biomaterials interfere
with host defence mechanisms. If tissue cells win: implant
is incorporated as an inert biomaterial. If bacteria win: it
forms a layer called ‘Biofilm’. For an implant infection to
become established there must be an initial adhesion of
the microorganism to the surface of the implant and this is
probably governed by electrostatic interactions. Synthetic
polymers used for manufacturing implants show differing
affinity for bacteria, which may differ between various species
of bacteria. For example E. coli show markedly low affinity
for almost all implant materials and this may explain the rarity
of infection caused by it despite being a relatively frequent
cause of bacteriemia. Bacteria colonizing implant material
in vitro often multiply slowly within a complex biofilm. The
biofilm is an extracellular matrix produced by the organisms
that protects them from host defenses, retards the access of
antibiotics and contributes to antimicrobial resistance. In
vivo, host proteins are deposited on implants rapidly after
their interposition in the tissues; and before a bacterial bio-
film can develop, this protein deposit makes changes in
implant material surface physico-chemistry and consequent
Figure 1: Draining sinus with infected implant in situ
Figure 2: An infected exposed implant

Orthopedic Device Related Infections 
Chapter 25
301
affinity for microorganisms. The chemical nature of implants
influences the type of surrounding tissue response, but it is not
clear whether this influences later infections or not.5,7,8

Microorganisms infecting an implant are in a uniquely
privileged position. By colonizing a material that lacks a
blood supply or any other innate means of attacking them,
the microorganism are immune from the usual means of
elimination– a position akin to bacteria in necrotic tissue or in
an osteomyelitis sequestrum. Furthermore, there is evidence
that metallic materials exert a local immunosuppressive
effect and phagocytic cells drawn to the sites of implant
show exhaustion. The privileged position is of course
completely localized and organisms outgrowing this limited
area of protection are removed by the normal host defense
mechanisms. The chronic tissue reaction both to infection and
to a long-term implant immures the organism. Thus it shields
them as well as limits their multiplication and thus their
susceptibility to antimicrobials. In this sequence of events, a
chronic low-grade infective process is likely to ensue, with
the subsequent risk of bacteremia. Infections centered on
biomaterials are most difficult to eliminate and usually require
removal of the device.1,2,5,6,7,9
Presentation
On the basis of the time of onset and the clinical course of
deep infection, three stages have been identified with specific
reference to total hip arthroplasty (Coventry, 1975; Fitzgerald,
1977).1,2 The basic concept may be extended to all orthopedic
device related infection for the purpose of management. Stage
I (acute fulminating) infection usually becomes evident within
two to four weeks following surgery and presents as pain,
fever, redness, and swelling at the operative site and is usually
caused by Staphylococcus spp. Stage II (delayed) sepsis
develops as a creeping, indolent infection and usually presents
between one month and two years after surgery. It may cause
persistent pain following surgery. Low grade Staphylococcus,
Propionibacterium, and anaerobes are commonly associated
with this type of infection. Stage III (possible hematogenous)
infection develops in previously asymptomatic patients;
typically presents after two years of surgery and may exhibit
acute signs of infection. Streptococcus, Staphylococcus
aureus and other gram negative bacilli are frequent causative
organisms.
Prevention and Management
One must learn to pay attention towards the sterility of the
bone, as prevention is always better than the cure. Prevention
may include the use of suitable atmosphere and design of
operation theater, limiting the number of theater personnel,
taking universal precautions for infection prevention and
proper use of prophylactic antibiotics.
Investigations
High index of suspicion is necessary to make early diagnosis
of the orthopedic device related infection. It should be
well supported by appropriate laboratory investigations.
Total leukocyte count may be raised. Acute phase reactants
(erythrocyte sedimentation rate, C-reactive protein) have
high sensitivity in the detection of infection. Sedimentation
rate of more than 40 mm in the first hour and C-reactive
protein level more than 12 mg/L should raise the suspicion of
infection. Preoperative needle aspiration of fluid surrounding
the implant/infected joint under all aseptic precautions should
be considered whenever possible. However, intraoperative
specimens taken for culture are considered to be the best in
establishing the diagnosis of infection. Evidence of more
than five neutrophils per high power field in five or more
fields is highly suggestive of infection on histopathological
examination. The role of plain radiographs in detecting early
infection remains questionable, however, periosteal reaction
and erosions may be seen with advanced involvement. The
usefulness of computed tomography and magnetic resonance
imaging may be limited by the presence of metal. The
radionuclide imaging is not altered by the presence of metallic
hardware, thus suggesting its usefulness for evaluating the
painful and infected implants and prosthesis. The normal
results rule out any abnormality but diffusely increased
peri-prosthetic uptake is highly suggestive of infection in a
symptomatic patient. Orthopedic device related infection
may be defined as the presence of one the following features:
growth of same organism from two or more cultures (either
preoperative aspirate or intraoperative tissue specimen),
purulence of these specimens, and acute inflammation on
histopathology.
Treatment
Choice of antibiotics and duration of therapy must be
customized according to every individual case. If the pathogen
is not known, all the antimicrobials must be omitted at least
three days preoperatively. Broad spectrum antibiotics are started
by intravenous route immediately after collecting the sample
for culture and histopathology. Further choice of therapy may
depend upon organism and sensitivity pattern. Total duration of
at least six weeks of antibiotics is generally recommended.10-12
Beta-lactum antibiotics (as penicillin and cephalosporins) are
not able to penetrate biofilms, so they may not be useful for
established infections (Arizono et al. 1992).13 Glycopeptides
(such as vancomycin and teicoplanin) are formed by chains and

Types of Wounds and their Management
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302
adhere to the exopolysaccharides of the glycocalyx, remaining
trapped in the web of the biofilm. This mechanical entrapment
lowers their concentration and antimicrobial activity, so their
usefulness for chronic infections is not dependable (Isiklar et al.
1996).14 Many antibiotics are not effective against intracellular
bacteria due to various reasons. Beta lactams are unable to
penetrate phagocytes, so they are not useful for intracellular
bacteria in chronic infections. Aminoglycosides (gentamicin,
tobramycin) penetrate cells by pinocytosis (a typical active
membrane transport). Since the membrane transport is
defective (because of low metabolism), intracellular levels are
very low after antibiotic treatment (Maurin and Raoult 1994).15
Doxycyclin, amikacin and pefloxacin are inactivated by the acid
media of phagolysosomes. The antibiotics blocking bacterial
metabolism (tetracycline, amikacin, pefloxacin) are hardly
useful because bacterial metabolism is very low. Rifampicin
presents an excellent intracellular activity because of elevated
transport and activity in acid media. Its usefulness has been
demonstrated in vitro (Zimmerli et al. 1998)16 as well as in
clinical situations (Barberán et al. 2006).17 Fluoroquinolones
(ciprofloxacin, ofloxacin, levofloxacin) accumulate inside the
cytoplasm and lysosomes, thus, they present a very good activity
inside the cells. Their clinical efficiency in orthopedic infections
has also been proven (Barberán et al. 2006).17 Cotrimoxazol
(trimethoprim-sulfamethoxazole) presents a good intracellular
transportation and a great activity inside phagocytes. Their
clinical efficiency was demonstrated in a series of infected total
hip and knee arthroplasties with a 67 percent of healing after six
months of oral treatment followed by an exchange in one-stage
(Stein et al. 1998).18 Clindamycin also presents an increased
intracellular activity and has been used efficiently against MRSA
(Cordero-Ampuero et al. 2007).19 The macrolide antibiotics
(azithromycin, clarithromycin) also accumulate inside the
cytoplasm and lysosomes. These antimicrobials present great
activity inside the phagocytes but their spectrum of activity
is usually not useful for orthopedic infections. Linezolid
presents a strong activity, but side effects must be controlled
(Soriano et al. 2007).20 All these antibiotics are effective for
oral administration as they get a good oral bioavailability. At
least some of them (rifampin and quinolones) must be used in
combination to avoid development of resistances.

Adequate debridement of the soft tissues and bone must be
considered as the unchallenged cornerstone of the successful
outcome.10-12 Debridement with retention of prosthesis and
long-term antimicrobials, Girdlestone arthroplasty (for hip
prosthesis), one or two stage revisions usually with the use
of antimicrobial cement, suppressive long-term antimicrobial
therapy (for debilitated patients), and rarely arthrodesis or even
amputation are the available modalities under such conditions.
The following criteria may be taken under consideration in
favor for the retention of implant: acute infection with signs
of infection <14 to 28 weeks, stable implant without features
of loosening, clearly established diagnosis by isolating single
microorganism from multiple specimens, pathogen susceptible
to an oral bactericidal antimicrobial agent, patient able and
willing to undergo long-term antimicrobial therapy.

Maintaining stable fixation is imperative for the control
of infection as there is only one thing worse than stable
infected fracture and that is an unstable infected fracture. A
stable skeletal fixation device maintains the alignment and
reduces the soft tissue damage. All the loose infected implants
must be removed and replaced preferably with an external
fixator. Wound coverage in these situations may at times be
challenging. The collaboration of a plastic surgeon is of vital
importance for a successful outcome. Secondary suturing
usually suffices if skin cover is sufficient. Split skin grafting
may be considered if skin cover is deficient. Many a time,
various flaps like fasciocutaneous flaps or muscle flaps may
be required for bone and/or implant coverage. Restoration
of bone defects by bone grafting or by the principles
of distraction osteogenesis may be required as a staged
procedure. With the introduction of more physiologic methods
of lengthening pioneered by Ilizarov and based on the biology
of bone and soft-tissue regeneration under the conditions of
tension stress, the bone healing problems have now become
far less common and relatively easy to manage. The concept
of burning an infection in the fire of regenerate without the
need of bone resection21 has now been modified to the current
trend that persistent osteomyelitis is a surgical condition and
debridement must be the unchallenged cornerstone of the
successful therapy. Such modification to the Ilizarov method,
that adequate bone resection may be required to remove
infected and necrotic bone and to achieve a satisfactory
docking configuration, has been suggested in the literature
(Cattaneo et al. 1992; Green et al. 1992).10-12 The adequacy of
bone resection may be assessed by the appearance of cortical
bleeding, described as the so-called ‘the paprika sign’.

Future prospects are being directed towards the coating
of the implant surfaces with antimicrobial agents to reduce
the risk of infection. A peptide array technology has been
modified to permit the screening of short peptides for
antimicrobial activity while tethered to a surface. Cellulose-
amino-hydroxypropyl ether (CAPE) linker chemistry is
being used to synthesize, on a cellulose support, peptides
that remained covalently bound during biological assays.22
Summary
Orthopedic implant related infection can be a very challenging
problem. If adequate precautions are not taken during their
insertion and timely action not taken at the onset of infection
the end result will invariably be the removal of the implant.

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Therefore optimal theater conditions and aseptic operative
techniques can prevent infection at implant site. Early
diagnosis, aggressive treatment with early debridement
and antibiotics, stable fixation, early wound coverage and
restoration of bone defects are the stepping stones of successful
therapy for infected implants.
References
1. Coventry MB. Treatment of infections occurring in total hip
surgery. Orthop Clin North Am. 1975;6:991-1003.
2. Fitzgerald RH, Nolan DR, Ilstrup DM, Van Scoy RE,
Washington JA, Coventry MB. Deep wound sepsis following
total hip arthroplasty. J Bone Joint Surg Am 1977;59:847-55.
3. Barrett SP. The implant-invaded host. In: William JD, Taylor
EW (Eds). Infection in surgical practice. London. Arnold
Publisher 2003;103-15.
4. McNeur JC. The management of open skeletal trauma with
particular reference to internal fixation. J Bone Joint Surg Br.
1970;52:54-60.
5. Schmidt AH, Swiontkowski MF. Pathophysiology of infections
after internal fixation of fractures. J Am Acad Orthop Surg.
2000;8(5):285-91.
6. Gristina AG, Naylor P, Myrvik Q. Infections from biomaterials
and implants: a race for the surface. Med Prog Technol.
1988;14(3-4):205-24.
7. Gristina AG, Naylor PT, Webb LX. Molecular mechanisms in
musculoskeletal sepsis: the race for the surface. Instr Course
Lect. 1990;39:471-82.
8. Merritt K, Dowd JD. Role of internal fixation in infection of
open fractures: studies with Staphylococcus aureus and Proteus
mirabilis. J Orthop Res. 1987;5:23-8.
9. Chang CC, Merritt K. Microbial adherence on polymethyl
methacrylate (PMMA) surfaces. J Biomed Mater Res.
1992;26:197-207.
10. Cattaneo R, Catagni M, Johnson EE. The treatment of infected
non-unions and segmental defects of tibia by the method of
Ilizarov. Clin Orthop 1992;280:143-52.
11. Green SA, Jackson JM, Wall DM, Marinow H, Ishkanian J.
Management of segmental defects by the Ilizarov intercalary
bone transport method. Clin Orthop 1992;280:136-42.
12. Cierny G III, Mader JT, Penninck JJ. A clinical staging system
for adult osteomyelitis. Clin Orthop. 2003;414:7-24.
13. Arizono T, Oga M, Sugioka Y. Increased resistance of bacteria
after adherence to polymethyl-metacrilate: an in vitro study.
Acta Orthop Scand. 1992;63:661-4.
14. Isiklar ZU, Darouiche RO, Landon GC, et al. Efficacy of
antibiotics alone for orthopaedic device related infections. Clin
Orthop. 1996;332:184-9.
15. Maurin M, Raoult D. Phagolysosomal alkalinisation and
intracellular killing of Staphylococcus aureus by amikacin. J
Infect Dis. 1994;169:330-6.
16. Zimmerli W, Widmer AF, Blatter M, et al. Role of rifampin
for treatment of orthopaedic implant-related Staphylococcal
infections: a randomized controlled trial. Foreign-Body
Infection (FBI) study group. J Am Med Assoc. 1998;279:1537-
41.
17. Barberan J, Aguilar L, Carroquino G, Gimenez MJ, Sanchez B,
Martinez D, Prieto J. Conservative treatment of Staphylococcal
prosthetic joint infections in elderly patients. Am J Med.
2006;119:e7-10.
18. Stein A, Bataille JF, Drancourt M, et al. Ambulatory treatment
of multidrug-resistant Staphylococcus-infected orthopaedic
implants with high-dose oral cotrimoxazole (trimethoprim-
sulfamethoxazole). Antimicrob Agents Chemother. 1998;42:
3086-91.
19. Cordero-Ampuero J, Esteban J, Garcia-Cimbrelo E, Munuera
L, Escobar R. Low relapse with oral antibiotics plus two-stage
exchange for late arthroplasty infections in 40 patients after 2
to 9 years. Acta Orthop. 2007;78:511-9.
20. Soriano A, Gomez J, Gomez L, Azanza JR, Perez R, Romero
F, et al. Efficacy and tolerability of prolonged linezolid therapy
in the treatment of orthopaedic implant infections. Eur J Clin
Microbiol. 2007;26:353-6.
21. Ilizarov GA. The tension-stress effect on the genesis and
growth of tissues: Part I. The influence of stability of fixation
and soft-tissue preservation. Clin Orthop. 1989;238:249-81.
22. Hilpert K, Elliott M, Jenssen H, Kindrachuk J, Fjell CD,
Körner J, et al. Screening and characterization of surface-
tethered cationic peptide for antimicrobial activity. Chemistry
and Biology. 2009;16(1):58-69.

• Classification
• Microbiology
• Pathology
• Clinical features
• Diagnosis
• Management

– Surgical

– Medical
• Supportive Treatment

– Newer and Emerging Modalities
• Prognosis
• Fournier’s Gangrene
• Clostridial Cellulitis and Myonecrosis
• Non-clostridial Anaerobic Cellulitis
Introduction
Necrotizing fasciitis (NF) is a life-threatening soft tissue
infection that was first described by Hippocrates around fifth
century BC. It is commonly known as “flesh eating” disease or
flesh eating bacterial syndrome.1 Necrotizing skin infections
were also described by Jones in 1871, although at that time
the term hospital gangrene was used.2 The term necrotizing
fasciitis was coined by Wilson in the 1950s to describe necrosis
of the fascia and subcutaneous tissue with relative sparing
of the underlying muscle.3 It is an atypical wound, which is
associated with a progressive, rapidly spreading inflammatory
infection located in the deep fascia. There is secondary
necrosis of the subcutaneous tissue and the fascia that leads
to the involvement of skin due to resultant hypoxia. These
atypical wounds are “wounds that tend to occur on account
of multiple factors and etiologies compounded by factors that
delay or impair the healing process leading to an unpredictable
outcome”.4 The management involves interdisciplinary teams
with “surgeon in the role of a leader.”4 At onset, NF can be
difficult to differentiate from cellulitis and other superficial
infections of the skin. In fact, studies have shown that only 15
to 34 percent of patients with NF have an accurate admitting
diagnosis.5,6 Only early diagnosis and aggressive surgical
treatment can reduce mortality and morbidity.7

The US Centers for Disease Control (CDC) and prevention
has estimated that more than 500 to 1,000 cases of NF are
diagnosed each year in the United States.8 However, the
accuracy of this estimate is difficult to ascertain because of the
many synonyms for these entities. The annual rate of NF has
been reported to be 0.40 cases per 100,000 population,9 with a
recent exponential increase in this rate because of an increase
in immunocompromised patients including those with diabetes
mellitus, cancer, alcoholism, vascular insufficiencies, organ
transplants, HIV, etc.10-13 Risk factors for NF in the pediatric
population include malnutrition and skin infections such as
varicella.15,16 Table 1 summarizes the potential risk factors for
NF. The NF infections are usually preceded by a precipitating
Table 1: Risk factors for necrotizing fasciitis14
Diabetes
Chronic disease
Immunosuppressive drugs (e.g. Steroids)
Malnutrition
Age > 60 years
Intravenous drug abuse
Peripheral vascular disease
Renal failure
Underlying malignancy
Obesity
Necrotizing Fasciitis: An Overview
Chintamani, Rohan Khandelwal, Megha Tandon
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event, which could be traumatic or non-traumatic. Table 2
summarizes the events, following which NF can develop.
Classification
Different terms and classifications have traditionally been used
to describe necrotizing infections of the skin and subcutaneous
tissue. These include necrotizing fasciitis, synergistic necrotizing
cellulitis, streptococcal myonecrosis, and gas gangrene. Many
classifications and terminologies have been coined based on
affected anatomy, microbial cause, and depth of infection.
Terms like necrotizing fasciitis, myonecrosis, and necrotizing
adipositis refer to classification by depth of infection. Type 1
and type 2 infections refer to classification based on microbial
cause. Historically, necrotizing infections were classified
according to anatomical sites. Fournier gangrene (involving the
perineum) and Ludwig’s angina (involving submandibular and
sublingual spaces) are examples. These infections were named
after the physicians who first described them.17,18 Although
these descriptive terms are useful, they also cause a lot of
confusion. One recently proposed recommendation suggested
that the term necrotizing soft tissue infections should be used
to describe them all, as treatment is the same: early surgery and
broad spectrum antibiotics.19
Microbiology
Microbiologically, NF has been classified as either type 1
(polymicrobial) or type 2 (monomicrobial). Polymicrobial
infections are more common, with cultures yielding a mixture of
aerobic and anaerobic organisms.20 These infections typically
occur in the perineum and trunk. The isolates reflect normal
skin commensalism found adjacent to the site of infection.
For example, in NF of the perineum, anaerobic bacteria
are isolated. The etiologic isolates consist of gram-positive
organisms, such as Staphylococcus aureus, S. pyogenes, and
enterococci; gram-negative aerobes, such as Escherichia coli
and Pseudomonas species; and anaerobic organisms, such as
Bacteroides or Clostridium species.21,22 Type 1 NF usually
occurs in immunocompromised individuals, such as patients
with diabetes mellitus or chronic renal failure. In the head and
neck region bacterial penetration into the fascial compartments
can result in a syndrome known as Ludwig’s angina.

Monomicrobial infections are less common than the poly-
microbial variety. These typically occur in the limbs and afflict
healthy patients with no comorbidities. Predisposing factors
include a history of blunt trauma, nonsteroidal anti-inflammatory
agents or intravenous drug abuse. As S. pyogenes and S. aureus
are the usual pathogens, type 2 NF might be associated with
toxic shock syndrome.19 The patho-physiology of group A
Streptococcus in NF has been associated with streptococcal
M proteins types 1 and 3, exotoxins A and B, or mitogenic
factors that stimulate the immune system to cause cytokine
storm, leading to shock, organ failure, and myocardial and
immune suppression. Proteases and other enzymes generated
from Streptococcus may also contribute to tissue destruction.
Community-acquired methicillin–resistant S. aureus (MRSA)
has increasingly been described in NF. A recent retrospective
review of cases from 2000 to 2006 in Los Angeles, California,
showed that MRSA was isolated in one-third of cases.22
Pathology
Most cases commence with trauma to the skin surface,
with seeding of bacteria (Figure 1). Infection starts in the
deep tissue planes, and the epidermis might not be initially
affected. The clinical disease is expressed when infective
organisms spread through the tissue along the deep fascia.
Bacteria rapidly multiply within viable tissue, although
fibrous attachments between subcutaneous tissues and fasciae
limit spread to areas like the hands, feet, and scalp. Lack of
fibrous attachments in the trunk and limbs, however, can
Table 2: Precipitating events causing necrotizing fasciitis
Traumatic
Non-traumatic
Surgery
Burns
Minor invasive procedure (e.g. Joint
aspirations, acupuncture)
Childbirth
Intravenous drug abuse
Soft tissue infection
Penetrating injury (e.g. Animal bites)
Intramuscular injections (e.g. NSAIDs)
Figure 1: The presence of a necrotic patch may be misleading a
clinician about the extent of damage.The damage is beyond the visible
patch and can be assessed based on the induration and erythema

Types of Wounds and their Management
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lead to widespread infection and tissue destruction. Infection
also spreads to venous and lymphatic channels, leading to
edema. The spread of bacteria results in thrombosis of blood
vessels in dermal papilla, resulting in ischemia and gangrene
of subcutaneous fat and dermis23 (Figures 2A to C). If the
fascia is breached, infection of the muscle leading to myositis
occurs. Gas producing organisms such as Clostridium species
can give rise to subcutaneous gas, from which stems the
descriptive term gas gangrene. In addition, infections with
toxin-producing bacteria (S. aureus and S. pyogenes) can lead
to a toxic shock-like syndrome. Therefore, seemingly limited
infection can result in septic shock and multiorgan failure.
Clinical features
Patients with NF can have varied presentations, which make
early diagnosis difficult. Patients with NF can present with
constitutional symptoms of sepsis (e.g. fever, tachycardia,
altered mental state, and diabetic ketoacidosis) alone or with
evidence of skin inflammation, which makes diagnosis a little
more straightforward.

Limbs are among the most common sites of infection. A
retrospective review of patients treated for NF in 3 tertiary
hospitals in Canada, common sites of infection included the
lower extremities (28%), upper extremities (27%), perineum
(21%), trunk (18%), and the head and neck (5%).24

As NF first starts in the deep tissue planes, at initial
presentation there might be minimal epidermal involvement.
This can make it difficult to differentiate from non-necrotizing
skin infections and cellulitis (Figures 3A and B).

Patients with NF are usually systemically toxic, initially
presenting with fever, tachycardia, diaphoresis, and possibly
even an altered mental state. The physical examination
should include all parts of the body to search for skin
inflammation. This is especially necessary for patients who
present with sepsis of which the source is not obvious.
Patients with NF have pain out of proportion to the degree of
skin inflammation. This sign can help differentiate NF from
less serious conditions like erysipelas and cellulitis. The pain
patients experience with cellulitis usually responds to a similar
Figure 2A: The damage could be more than what is grossly visible.
Fascitis leads to thrombosis of the perforators to the skin leading
to extensive skin necrosis. Most of these patients are immuno-
compromised and need extra care. In this patient the limb could
not be salvaged and the patient had to be managed by hind quarter
amputation. The intention and effort, however should be to preserve
the organ and function
Figure 2B: The necrotic muscles of thigh and abdomen can be seen.
The hind quarter amputation in progress
Figure 2C: Associated fecal fistula can complicate the scenario
further. Fecal and urinary diversion had to be done to salvage the
wound

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analgesic, along with careful positioning of the affected area.
The pain experienced with NF, on the other hand, is often
severe, and patients can be exceedingly apprehensive and
fearful when examined. However, certain patients, notably
those with diabetic neuropathy with loss of sensation, can
experience minimal pain, resulting in a missed diagnosis.
This is especially likely in concealed sites of infection, such
as the perineum or oral cavity. Erysipelas, being an infection
of the superficial dermis, has well-defined borders and might
blister profoundly. With cellulitis, one can expect erythema
with lymphangitis and minimal blistering. Necrotizing
fasciitis typically presents with patchy discoloration of the
skin with pain and swelling, but without a defined margin or
lymphangitis23,25,26 (Figures 4 and 5).

Progression of NF is marked with the development of tense
edema, a grayish-brown discharge, vesicles, bullae, necrosis,
and crepitus.27 Hemorrhagic bullae and crepitus are sinister
signs, with the likelihood of underlying fascia and muscle
being compromised.28 Crepitus is a later sign, however, and
is found in only about 18 percent of cases of NF. Although
crepitus and blistering are the most specific signs of necrotizing
soft tissue infection, they are not sensitive. In a retrospective
case series, Elliot et al29 reported an absence of crepitus in
62 percent of cases and an absence of blistering in 76 to 95
percent of cases upon initial presentation. Lymphangitis and
lymphadenopathy are usually absent in necrotizing infections,
but are frequently seen in cellulitis.23,30
Disease Progression
Necrotizing fasciitis can follow a hyperacute or a subacute
course of progression. The patient with a hyperacute course
presents with sepsis and rapidly progresses to multiorgan
failure. Diagnosis of sepsis is obvious, and these patients need
to be hospitalized.

Several authors have described a subacute variation of
NF.31-33 Wong et al describe this entity of subacute NF as having
a slow indolent course with an absence of systemic disturbance,
gradual tissue necrosis with progressive cutaneous changes over
the affected site, followed by a sudden deterioration with rapid
progression of NF. There is progression of disease despite the
use of antimicrobials. At the time of surgery, histologic features
are consistent with NF.32 Aggressive surgical debridement
is the cornerstone of treatment in these cases. Progression of
disease is invariable in this group, and a delay in diagnosis can
lead to greater soft tissue loss and mortality.31-33 Subacute NF
Figure 3B: The limb can be salvaged by early and aggressive
debrima and fasciotomies
Figure 3A: Impending NF of the foot with extension on to the leg in a
known diabetic
Figure 4: Using topical ointments may not be very useful. The visible
skin changes are harbingers of impending gangrene

Types of Wounds and their Management
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can present a diagnostic dilemma and treating physician should
be aware of this.
Criteria for Hospitalization
The latest Infectious Diseases Society of America skin and
soft tissue infection guidelines indicate that hospitalization
should be considered in patients with “hypotension and/or
an elevated creatinine level, low serum bicarbonate level,
elevated creatine phosphokinase level (2-3 times the upper
limit of normal), marked left shift, or a C-reactive protein
level more than 13 mg/L”.34 Table 3 summarizes the other
criteria for admission.
Diagnosis
Early diagnosis of NF patients is essential in reducing the
morbidity and mortality.7 At onset, NF can be difficult to
differentiate from cellulitis and other superficial infections of
the skin. Studies have shown that only 15 to 34 percent of
patients with NF have an accurate admitting diagnosis.5,6

Investigations in these patients are performed with an aim
to determine:

• Precise diagnosis in equivocal case

• Presence of gas in the tissue

• Presence of systemic toxicity

• The precise etiology of the infectious process

• Evidence of deep tissue necrosis.

The finger test and frozen section are useful bedside
diagnostic modalities in patients with an equivocal diagnosis.
The finger test is a bedside procedure in which, under local
anesthesia, a 2 cm incision is made down to the deep fascia
and gentle probing of the index finger is performed at the level
of the deep fascia. Lack of bleeding, presence of characteristic
“dishwater pus”, and lack of tissue resistance to blunt finger
dissection are features of a positive finger test and indicate
NF.19

Another reasonable approach is a bedside incisional biopsy
down to the fascial level and an immediate frozen section,
culture and Gram stain. Punch biopsy with frozen section is
particularly useful in distinguishing between toxic epidermal
necrolysis and staphylococcal scalded skin syndrome.35
Negative results, however, cannot exclude NF.

To help decide which patients require surgical exploration,
particularly in those with equivocal clinical signs, laboratory
and radiologic tests might sometimes be useful. Leukocytosis
with neutrophilia, acidosis, altered coagulation profile,
impaired renal function, raised creatinine kinase levels, and
raised inflammatory markers, such as C-reactive protein
levels, are all helpful adjuncts to clinical examination.

Clinical scores like the laboratory risk indicator for NF
(LRINEC) score are available to help diagnose NF and
differentiate it from other skin and soft tissue infections. This
score includes an elevated CRP >150 mg/L (4 points), WBC
>25,000/mm3, blood hemoglobin <11 g/dl, Na <135 mmol/L,
serum creatinine >141 μmol/L (2 points each), and blood
glucose >10 mmol/L (1 point). The total possible score is 13
and a score of 6 and above (intermediate or high-risk) suggests
NF with a positive predictive value of 92 percent and a negative
predictive value of 96 percent.16 However, the LRINEC score
is based on retrospective studies of patients with diagnosed
or highly suspected NF. It has not been validated in patients
for whom the diagnosis of NF is not apparent in the initial
assessment.35 Further, certain tests, such as the C-reactive
protein test, are not readily available in the primary care setting,
where patients present with infection in the early stages and
where laboratory support is limited; therefore, this score is not
easily ascertained. It is notable that WBC and CRP may not be
useful in patients with liver cirrhosis because of impairment of
protein-productive function of liver for inflammatory response.

Blood cultures are usually part of the workup and yield
up to 27.3 percent positive cultures in necrotizing infections,
compared with the mere 2 percent positive blood cultures in
patients with cellulitis.36

Plain X-ray films can demonstrate subcutaneous gas, but
this is not a sensitive finding (positive in fewer than 25 percent
of cases) and absence of gas does not exclude NF. Computed
tomography and magnetic resonance imaging (MRI) might
be useful in cases where signs are equivocal or diagnosis
is in doubt. Asymmetrical fascial thickening, fat stranding,
and gas tracking along fascial planes are important imaging
findings. Computed tomography scans are estimated to have
a sensitivity of 80 percent for detecting necrotizing soft tissue
infections.37 In cases of cellulitis, MRI will demonstrate
subcutaneous thickening with fluid collection. However,
when there is deep fascial involvement with fluid collection,
thickening, and enhancement after contrast administration,
necrotizing infections must be considered.36 According to
Schmid et al,38 the sensitivity of MRI is 100 percent with a
specificity of 86 percent. This has been disputed, and other
Table 3: Criteria for hospitalization in patients with
soft tissue infections
Signs of systemic toxicity (fever, hypothermia, tachycardia,
hypotension)
Altered mental state
Immunocompromised patients
Failure of outpatient therapy
Severe infection (requiring operative procedure)
Poor social support

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authors have argued that in early cases of NF, MRI might not
show fascial involvement.39 Routine MRI for all patients at
the first suspicion of NF is not cost-effective.

In summary, if clinical suspicion is high, surgeons can
opt to explore and perform tissue biopsies rather than delay
treatment for laboratory and imaging studies. It must be
emphasized that diagnosis of NF is clinical, and the clinician
should draw information from both the patient’s condition and
the aggregate of tests. Physicians should have a high index of
suspicion and low threshold for surgical referral.
Management
Surgical
Surgical debridement is the mainstay in the management of
NF and results in significantly improved mortality compared
to cases in which surgery is delayed for even a few hours.40

The aims of surgical intervention should be:

• To inspect the deeper tissues to determine the extent and
severity of deep infections

• To surgically remove the necrotic skin, fascia and
muscle

• To obtain samples for Gram stain and culture.

Debridement is also important as tissue hypoxia limits the
efficacy of intravenous antibiotics and tissue hypoxia persists
till the time dead and necrotic tissues are present (Figure 5).

When NF is suspected, patients should be taken to the
operating room as soon as possible for aggressive and
extensive debridement. Patients need to be educated about the
gravity of the situation and the need for extensive debridement.
Involved tissues should be resected thoroughly until there is
no further evidence of infection. Initial surgery is the most
important determinant for survival and the wound must be
inspected closely after the initial debridement. Removal
of the tissues with adequate margins is recommended. The
characteristic feature of NF is the easy separation of the
fascia from other tissues by blunt dissection, due to necrosis
of the fascia and liquefaction of subcutaneous tissue. Muscle
is usually spared by the disease process, but myonecrosis
may develop secondary to the accompanying compartment
syndrome. Muscle involvement and necrosis are indicative of
an advanced stage.

A “second-look” surgery should be typically done 12 to
24 hours after the initial debridement. Patients with NF may
require anywhere from 5 to 40 sessions of surgery, and one
study found an average of 33 debridements and grafting
procedures.41 Careful follow-up of the surgical wound is also
important to detect the development of surgical site infection.
Medical
Antimicrobial therapy must be directed at the pathogens and
used in appropriate doses until repeated operative procedures
are no longer needed, the patient has demonstrated obvious
clinical improvement, and fever has been absent for 48 to 72
hours. Treatment of polymicrobial necrotizing fasciitis must
include agents effective against both aerobes and anaerobes
Table 4. In general, ampicillin is useful for coverage of
susceptible enteric aerobic organisms, such as E. coli, as well
as for gram-positive organisms, such as Peptostreptococcus
species, group B, C, or G streptococci, and some anaerobes.

Clindamycin is useful for coverage of anaerobes and aerobic
gram-positive cocci, including most S. aureus serogroups.
Metronidazole has the greatest anaerobic spectrum against
the enteric gram-negative anaerobes, but it is less effective
against the gram-positive anaerobic cocci.

Gentamicin or a fluorinated quinolone, ticarcillin-
clavulanate, or piperacillin-sulbactam is useful for coverage
against resistant gram-negative rods. Thus, the best choice
of antibiotics for community-acquired mixed infections is a
combination of ampicillin-sulbactam plus clindamycin plus
ciprofloxacin. Necrotizing fasciitis and/or streptococcal toxic
shock syndrome caused by group A streptococci should be
treated with clindamycin and penicillin. The rationale for
clindamycin is based on in vitro studies demonstrating both
toxin suppression and modulation of cytokine (i.e. TNF)
production, on animal studies demonstrating superior efficacy
versus that of penicillin, and on 2 observational studies
demonstrating greater efficacy for clindamycin than for
b-lactam antibiotics.42,43 Penicillin should be added because of
the increasing resistance of group A streptococci to macrolides,
Figure 5: The evolving necrotizing fascitis of the lower limb following
a trivial trauma in an immunocompromised patient. Aggressive
debridement is mandatory to salvage the limb

Types of Wounds and their Management
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310
although in the United States, only 0.5 percent of macrolide-
resistant group A streptococci are also clindamycin resistant.
Supportive treatment
Patients with necrotizing fasciitis, along with antibiotics
and surgical debridements, require hemodynamic support,
wound care and nutritional support. Hemodynamic instability
is often present, and stabilizing these conditions in an
intensive care unit is important to ensure that the patient
endures the disease and surgery. Hypotension in these
patients is usually not corrected by fluid alone and many of
them require vasopressors. The dose of vasopressors should
be carefully titrated as an excessive dose can lead to further
vasoconstriction and tissue necrosis. Once the infection
is controlled, daily dressing is needed at the bedside under
sedation, followed by secondary suturing of the wounds with
or without split skin grafts to cover the exposed underlying
tissues. Dressing changes with hydrogel may assist tissue
granulation.46 Although costly, a vacuum-assisted wound
closing (VAC) device has been found to be effective for non-
healing limb wounds, with reduced morbidity compared to the
conventional technique.47 Nutritional support is required from
the first day of admission, for compensation for lost protein
and fluid from the large wounds. Metabolic demands are
similar to those of other major trauma or burns. In general,
patients with severe tissue defects should receive twice their
basal caloric requirements.48 A nasogastric tube for feeding
is sometimes required to maintain adequate enteral nutrition.
Newer and Emerging Modalities
Hyperbaric oxygen has also been used as an adjunct to surgery
and antibiotics. Therapy is given at a pressure of 2.0 to 2.5
bar for 1 hour 30 minutes twice daily initially and then daily;
up to 30 sessions may be required. Necrotic fascia and skin
should be excised prior to HBO therapy.49 Tissues that have
a compromised blood supply are preserved by HBO and the
killing activity of leukocytes is enhanced. When infections are
due to anaerobes, HBO has a toxic effect on the organisms.50
Its role in necrotizing fasciitis is still ill-defined. Some
authors have reported a reduction in mortality, morbidity,
and need for repeated debridement in up to two-thirds of
cases.51-53 Well-controlled randomized controlled trials are
still lacking. Moreover, a retrospective review by Golger et
al showed that morbidity associated with NF was higher in
patients who underwent hyperbaric oxygen therapy.24 There is
ample evidence for the use of HBO in clostridial myonecrosis
and studies have shown a reduction in mortality rates.
However, no survival benefit has been well demonstrated
by a prospective, randomized, controlled trial for HBO used
for nonclostridial necrotizing soft tissue infections.54,55 In a
retrospective, uncontrolled, study carried out by Eliot et al no
survival benefit from the use of HBO was demonstrated when
compared with historical controls. However, they reported
that HBO hastened wound closure.

In type 2 NF caused by streptococci resulting in streptococcal
toxic shock syndrome, intravenous immunoglobulins might
play a therapeutic role. Although, there is ample evidence for
the role of extracellular streptococcal toxins in shock, organ
failure, and tissue destruction, different batches of IVIG
contain variable quantities of neutralizing antibodies to some
of these toxins, and definitive clinical data are lacking.56
Recently, a multicenter, randomized, double-blind, placebo-
controlled trial evaluated the safety and efficacy of intravenous
immunoglobulins in streptococcal toxic shock syndrome. The
trial was prematurely stopped because of poor recruitment,
but it showed 3.6-fold higher mortality in the placebo group
compared with the treatment group.57 One observational study
demonstrated better outcomes in patients receiving IVIG, but
these patients were more likely to have had surgery and to have
received clindamycin than were historical control subjects.58
Table 4: Antibiotics in necrotizing fasciitis44, 45
Mixed infection
Ampicillin- sulbactum
or
Piperacilin – tazobactam
Plus
Clindamycin
Plus
Ciprofloxacin
Imipenem/ cilastin
Meropenem
Cefotaxime
Plus
Metronidazole
Or
Clindamycin
Streptococcal infection
Penicillin
Plus
Clindamycin
S. aureus infection
Cefazolin
Vancomycin (for resistant strains)
Clindamycin
Clostridium infection
Clindamycin
Penicillin

Necrotizing Fasciitis: An Overview 
Chapter 26
311
Prognosis
Mortality due to NF is considerable. Without surgical
intervention, mortality approaches 100 percent. When
necrotizing infections were first described by Jones, mortality
was reported as 46 percent.2 More recent data indicate a
mortality of 16.4 percent for community-acquired necrotizing
soft tissue infections59 and 36.3 percent for postprocedural
necrotizing infections.60 All of these patients were managed
in hospital with intravenous antibiotics and surgical
interventions; considering medical progress in the last 135
years, mortality is still substantial. Mortality is higher in
patients with streptococcal toxic shock syndrome. Diabetic
patients, especially those presenting with diabetic ketoacidosis
or hyperosmolar hyperglycemic non ketotic acidosis have
higher rates of death and longer lengths of hospital stay.61 A
delay in surgery of more than 24 hours was an independent risk
factor for mortality. There is also considerable postoperative
morbidity, sometimes from extensive debridement resulting
in muscle loss. Patients might have to undergo a period of
rehabilitation to regain function of the affected areas. Scarring
and disfigurement can also be substantial.
Fournier’s Gangrene62
Fournier’s gangrene is an uncommon, rapidly progressive
infection of the male genital, perineal and perianal regions
with occasional extension to the abdominal wall. A similar
infection involving the anterior abdominal wall is known
as Meleney’s gangrene. It is characterized by a synergistic,
necrotizing fasciitis leading to the thrombotic occlusion of
small subcutaneous vessels and the development of gangrene,
which contributes to the rapid spread of infection.63 It typically
involves the scrotal and the perianal skin and the ‘testis lie
shamefully exposed’ (Figure 6). The disease process does not
involve the testis and the urethra because of their good blood
supply and tough fascial covering.

Majority of patients with Fournier’s gangrene are immuno-
compromised.65 Diabetes mellitus, obesity, peripheral vascular
disease, local trauma, urethral stricture and perianal disease
have been cited as the main predisposing factors.64-66 A minor
trauma (urinary catheterization, drainage of perianal abscess)
usually precedes the development of the symptoms (Figure 7).
It is usually a poly-microbial infection with several species
of aerobic and anaerobic organisms present in the wound.
Fournier’s gangrene is a life-threatening illness requiring
emergency surgery, despite which the patient may still not
survive. Mortality rates as high as 20 to 30 percent have been
described in some studies.64 Malignancy developing in scar
following healed Fournier’s gangrene is also a rare occurence
(Figure 8).

Certain factors influencing the survival of these patients,
primarily relating to the patient’s metabolic status and the extent
of the disease, were evaluated by Laor et al from which the
Fournier’s gangrene severity index (FGSI) was formulated.67 In
FGSI, nine parameters are measured and the degree of deviation
from normal is graded from 0 to 4. The individual values are
Figure 6: Necrotizing fascitis of the perineum is called after Alfered
Fournier as the Fournier’s gangrene.The testes lie “shamelessly”
exposed as they escape necrosis on account of dual blood supply and
a thick tunica.The necrotizing fascitis may extend on to the anterior
abdominal wall as seen in this case. Involvement of urethra is also
rare. Aggressive management in the form of extensive debridement
is necessary to reduce the mortality and morbidity in this otherwise
fatal condition
Figure 7: A scrotal abscess could be the initial presentation while the
NF (Fournier’s gangrene) may be inevitable.This patient was managed
by drainage and debridement

Types of Wounds and their Management
Section 3
312
summed to obtain the FGSI score (FGSIS). These parameters
are: temperature, heart rate, respiratory rate, levels of serum
sodium, potassium, creatinine and bicarbonate, hematocrit and
leukocyte count. In a study by Yeniyol et al the accuracy of this
index was tested and they found that the duration of symptoms
before presentation was statistically important.65 Out of the nine
parameters, temperature, heart rate and respiratory rate were
considered to be the most important by these authors. In patients
who died, however, all the parameters were abnormal. The
authors also found that lower serum albumin and total protein
levels indicated the degree of debilitation and a poor prognosis.
Lin E, Yang S et al suggested that a FGSI cut-off of nine was
an excellent predictor of outcome of cases.67 However, early
diagnosis and treatment and the arrest of the gangrene at an
early stage markedly improve outcome. A study carried out by
Tuncel et al on twenty Fournier’s gangrene patients concluded
that FGSI did not predict the disease severity and the patient
survival.

The treatment like any other necrotizing infection consists
of broad spectrum (to cover aerobes and anaerobes) antibiotics,
supportive treatment and urgent surgical debridement.
Clostridial Cellulitis and
Myonecrosis
It is usually preceded by local trauma or recent surgery.
Clostridium perfringens is the most common organism
associated with this entity. Gas is invariably found beneath
the skin; the fascia and deep muscles are spared in clostridial
cellulits but involved in myonecrosis. Clostridium perfringens
produces alpha-toxin, which liquefies muscle on contact, is
profoundly hemolytic, and necroses renal tubules. The result is
profound and often fatal septic shock. The classical treatment
is aggressive antibiotic therapy combined with radical
debridement. Even so, mortality can be high and usually more
than 15 percent.49 Hyperbaric oxygen is toxic to clostridia and
acts to shut down the production of alpha-toxin. The addition
of HBO therapy to the combination of surgery and antibiotics
can reduce mortality to around 6 percent.50 MRI or CT scan
along with serum creatine phosphokinase assay may be useful
to determine if muscle is involved or not.
Non-clostridial Anaerobic
Cellulitis
Non-clostridial anaerobic cellulitis is associated with mixed
anaerobic and aerobic organisms that produce gas in tissues.
Unlike clostridial cellulitis, this type of infection is usually
associated with diabetes mellitus, and often produces a foul
odor. This entity must be distinguished from necrotizing
cellulitis, myonecrosis, and necrotizing fasciitis by surgical
exploration.
References
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2. Jones J. Investigation upon the nature, causes and treatment of
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memoirs of the War of the Rebellion. New York, NY: Hurd and
Houghton; 1871. pp. 142-580.
3. Wilson B. Necrotising fasciitis. Am Surg. 1952;18(4):416-31.
4. Shukla VK, Mani R, Teot L, Pradhan S. (2007): Management
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7. Voros D, Pissiotis C, Georgantas D, Katsaragakis S, Antoniou
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Figure 8: Malignancy can develop in the scar of Fournier’s gangrene.
This 45-year-old gentleman who had been treated for Fournier`s
gangrene in the form of debridement and skin grafting (the wound
had healed but recurred) developed squamous cell cancer on the scar
(Chintamani et al. BMC Cancer. 2004;4:16)

Necrotizing Fasciitis: An Overview 
Chapter 26
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9. File TM Jr, Tan JS, Di Persio JR. Group A streptococcal
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23. Seal DV. Necrotizing fasciitis. Curr Opin Infect Dis.
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25. Hill MK, Sanders CV. Necrotizing and gangrenous soft tissue
infections. In: Sanders CV, Nesbitt LT Jr, eds. The skin and
infection: a color atlas and text. Baltimore, MD: Lipincott,
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26. Green RJ, Dafoe DC, Raffin TA. Necrotizing fasciitis. Chest.
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27. Headley AJ. Necrotizing soft tissue infections: a primary care
review. Am Fam Physician. 2003;68(2):323-8.
28. Hsiao CT, Lin LJ, Shiao CJ, Hsiao KY, Chen IC. Hemorrhagic
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29. Elliot DC, Kufera JA, Myers RA. Necrotizing soft tissue
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30. Dufel S, Martino M. Simple cellulitis or a more serious
infection? J Fam Pract. 2006;55(5):396-400.
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33. Jarrett P, Rademaker M, Duffill M. The clinical spectrum of
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34. Stevens DL, Bisno AL, Chambers HF, Everett ED, Dellinger
P, Goldstein EJ, et al. Practice guidelines for the diagnosis and
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35. Majeski J, Majeski E. Improved survival with early recognition
by tissue biopsy and aggressive surgical treatment. South Med
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36. Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC
(laboratory risk indicator for necrotizing fasciitis) score: a tool
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infections. Crit Care Med. 2004;32(7):1535-41.
37. Perl B, Gottehrer NP, Raveh D, Schlesinger Y, Rudensky B,
Yinnon AM. Cost effectiveness of blood cultures for adult
patients with cellulitis. Clin Infect Dis. 1999;29(6):1483-8.
38. Wyoski MG, Santora TA, Shah RM, Friedman AC. Necrotizing
fasciitis: CT characteristics. Radiology. 1997;203(3):859-63.
39. Schmid MR, Kossmann T, Duewell S. Differentiation of
necrotizing fasciitis and cellulitis using MR imaging. AJR Am
J Roentgenol. 1998;170(3):615-20.
40. McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA.
Determinants of mortality for necrotizing soft-tissue infections.
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41. File TM Jr, Tan JS, Di Persio JR. Group A streptococcal
necrotizing fasciitis. Diagnosing and treating the “flesh-eating
bacteria syndrome”. Cleve Clin J Med. 1998;65:241-9.
42. Zimbelman J, Palmer A, Todd J. Improved outcome of
clindamycin compared with beta-lactam antibiotic treatment
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43. Mulla ZD, Leaverton PE, Wiersma ST. Invasive group A
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44. Shimizu T, Tokuda Y. Necrotising fasciitis. Inter Med. 2010;
41: 1051-7.
45. Stevens LD, Bisno LA, Chambers HF, Everett D, Dellinger P,
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skin and soft- tissue infections. Clin Infec Dis. 2005; 41: 1373-
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46. Childers BJ, Potyondy LD, Nachreiner R, et al. Necrotizing
fasciitis: a fourteen-year retrospective study of 163 consecutive
patients. Am Surg. 2002;68:109-16.
47. Huang W, Hsieh S, Hsieh C, Schoung J, Huang T. Use of
vacuum-assisted wound closure to manage limb wounds in
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48. Simonart T, Simonart JM, Derdelinckx I, et al. Value of
standard laboratory tests for the early recognition of group A
β-Hemolytic streptococcal necrotizing fasciitis. Clin Infect
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49. Bennett P, Elliott D. The physiology and medicine of diving.
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S, Follin P, et al. Intravenous immunoglobulin G therapy in
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61. Oncul O, Erenoglu C, Top C, Küçükardali Y, Karabudak O,
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• Epidemiology
• Pathophysiology
• Clinical Manifestations
• Management
• Complications
• Human Bites

– Clenched Fist Injuries

– Occlusive Bites

– Clinical Assessment

– Treatment
Introduction
Humans are exposed to bites from both domestic and wild
animals depending upon their residence and occupation.
Apart from that, bites from pets are also common. Finally,
possibility of human bite will always remain, which may be
accidental and as a part of assault.
EPIDEMIOLOGY
It is difficult to ascertain exact incidence as most of the cases
remain unreported especially those occurring in the remote
areas. In US, the estimated dog bite incidence is five million
per year. Annual rabies incidence is about two per one lakh
population.1 In India, the exact incidence is unknown. Various
studies implicate dogs as the major culprits. Around 92 to 95
percent of all bite cases in our country are due to dog bites.2,3
Cats and monkeys are next to dogs as far as frequency of
animal bites in India is concerned. Others include bear, fox,
cows, buffaloes, horses, etc. Around 64.7 percent of these
bites are unprovoked bites by stray animals.4 Bear bites are
very often seen in our country in the hilly areas where the
villages are in close vicinity of the forests. This is in contrast to
data from the US where provoked bites from pets outnumber
unprovoked bites. Males and children are the most frequent
victims. Children constitute 47.5 percent of the total victims.
Females on the other hand are more commonly bitten by cats.
As far as serious mortality and morbidity is concerned, it is
most common in children with bites in the head and neck
region but overall, extremities are most commonly involved
in animal bites. Sixty three percent of bites are of category III.
Pathophysiology
The effects of the animal bite depend on various factors viz. the
animal involved, the resident flora of the oral cavity of the animal
and the anatomical region where the bite has been caused.

Dogs exert around 450 psi pressure leading to tissue
devitalization and laceration. The reason being that the
jaws of dogs are strong and broad and can exert such huge
amounts of force. In such wounds, there is always a risk of
injury to deeper tissue like muscles, nerves, tendons, vessels,
joints and bones. Similarly, bites from large herbivores also
have greater crushing effect. Even, bites and mauling by wild
animals like bears, tigers, crocodiles cause severe crushing
and lacerating injuries as well as amputations (Figure 1).
Bites from smaller animals like cats and rats are however
different. They generally have sharper and smaller teeth that
result in puncture wounds (Figure 2). This leads to deposition
of bacteria deeper inside the tissue and therefore greater
chance of wound infection.5
Bite Wounds
Deepak Nanda, Thakur Thussu
27
Chapter

Section 3
  Types of Wounds and their Management
316

The site of the bite also has definite implications. Bites
over regions with reduced blood supply are susceptible to
infections. Bites in the head and neck region, particularly
in children cause maximum mortality and morbidity due to
injuries to major vessels, trachea and cervical spine.

Infections caused by various animals depend upon the
resident oral microbial flora. Usually, it is a polymicrobial
picture. Time between bite and onset of infection is 12 hours
in cat bites and 24 hours in dog bites. Common infections
after a dog bite are caused by staphylococci, streptococci,
Escherichia, Proteus, Pasteurella, Haemophilus, Klebsiella,
Enterobacter, Moraxella, Corynebacterium, Bacteroides,
Neisseria,
Fusobacterium
and
Prevotella.
Whereas,
common infections after a cat bite are caused by Pasteurella,
Propionibacterium, fusobacter, actinomycosis, clostridia,
Peptostreptococci, staphylococci and streptococci.

Pasteurella is prevalent in the oral cavities of both cats
(90%) and dogs (40%). In cats , the predominant species
is P. multocida and in dogs, the predominant species is
P. dagmatis.
CLINICAL MANIFESTATIONS
Major resuscitation is rarely required. Small children mauled
by large aggressive breed of dogs especially in the head and
neck area may require resuscitation and repair (Figures 3A
to C). Proper evaluation of puncture or crush injuries needs to
be done with proper investigative tools as and when required.
Infection is the most common presenting sign which occurs in
approximately 20 percent of all cases. While in contrast it occurs
in 30 to 40 percent of hand bites. This is because the hand has
small and closed compartments, fascial planes, small nerves,
several bones and joints adjacent to the surface of the skin.
Depending on the organism which is predominant in causing
infection there can be systemic bacteremia or other sequelae.
MANAGEMENT
History regarding timing of the bite, location of bite, whether
provoked or unprovoked, type of animal, site of bite, first aid
status and patients medical history regarding allergies to dogs,
immune status, diabetes is noted. Detailed clinical examination
of the wound is done regarding distal neurovascular status,
injury to tendons, bones, joints. If the evaluation requires
investigative tools like X-rays, CT or MRI, they are done.
They rule out foreign bodies like teeth and their fragments.

Initial treatment involves decision regarding antirabies
vaccination. WHO’s recommendation for antirabies prophylaxis
is as per in Table 1.

The treatment modality then is decided on three basic
steps namely: (1) treatment of immediate superficial injury;
(2) treatment of immediate deep injury; (3) treatment of risk
of infection.

Treatment of immediate superficial injury: For this copious
irrigation with normal saline is done (100–200 ml/sq inch) for
both superficial and deep wounds to dislodge any bacteria and
foreign matter. This can be done ideally with a 19 G blunt needle
and 35 cc syringes. This is followed by debridement of devitalized
tissue. Primary closure of the wound can be undertaken in face
related wounds but not puncture wounds as due to rich vascular
supply the infection rate is low and cosmesis is an important
factor (Figures 4 and 5). Whenever primary suturing is planned,
Figure 1: Severe bear mauling presenting late
Figure 2: 2-month-old child with rate bite on nose with total loss of nose

Chapter 27
Bite Wounds 
317
Table 1: Recommended postexposure prophylaxis for rabies infection
Category of exposure to suspect rabid animal
Postexposure measures
Category I – Touching or feeding animals, licks on intact skin (i.e. no exposure)
None
Category II – Nibbling of uncovered skin, minor scratches or abrasions without
bleeding
Immediate vaccination and local treatment of the
wound
Category III – Single or multiple transdermal bites or scratches, licks on broken
skin; contamination of mucous membrane with saliva from licks, exposures to
bats
Immediate vaccination and administration of rabies
immunoglobulin; local treatment of the wound
Figures 3A to C: (A) Small child presented with dog bite on cheek;
(B) Sutured primarily with loose approximating sutures; (C) After
stitch removal
B
A
C

Section 3
  Types of Wounds and their Management
318
half the dose of ARS should be instilled locally. Other wounds
are best treated by delayed primary closure or secondary
reconstruction (Figure 6).

Treatment of deep injury also includes copious irrigation
and debridement as in previous case. In addition, there is
evaluation of deeper tissue injury and if found is referred to
specialist surgeon for necessary action. A small culture from
the deeper wounds is preferable but not mandatory if the
wound is not infected. Infected wounds of both categories
require wound culture and sensitivity. Bite wounds of hands
require bulky dressings, splint age and hand elevation.

Tetanus and rabies prophylaxis is considered for all wounds
unless it is a pet which is properly vaccinated but was provoked
into biting and can be kept under observation for a long-time.

Oehler et al6 established management strategies to prevent
severe complication:

• Gram-stains, aerobic and anaerobic culture if abscess,
cellulitis or sepsis is present.

• Wound irrigation with normal saline copiously using a
high pressure jet from a syringe.

• Removal of any foreign body and debridement of dead
tissue.

• Investigations as required (X-rays, CT, MRI).

• Wound closure not done except in face

• Antibiotic therapy is usually prophylactic and based on the
type of animal. The first line drugs include trimethoprim
Figures 4A and B: Photograph (A) Showing a man from Uttarakhand with injuries on face as a result of bear mauling; (B)
Appearance of the same person after primary repair
Figures 5A and B: Photograph (A) Showing a patient of bear
mauling; (B) Same patient postoperatively
A
B
A
B

Chapter 27
Bite Wounds 
319
sulphamethoxazole, doxycycline, minocycline and
Clindamycin.

• If there is fever, sepsis, spreading cellulitis, edema, crush
injury in immunocompromised patients then hospital
admission is required.

• Immunization includes tetanus—only booster if
original three doses have been given but not in last year.
Primary dose is given along with immunoglobulin if
patient has never been vaccinated. Rabies vaccine and
immunoglobulins need is assessed and given if required.

In the authors unit after thorough irrigation and debridement
loose sutures are only applied to reposition the avulsed soft
tissues along with local infiltration of antirabies vaccine.
COMPLICATIONS

1. Wound infection

2. Sepsis

3. Cosmetic deformity

4. Loss of limb

5. Loss of function.

Treatment of wound infection is outlined below. Treatment
of the sepsis syndrome: The most common pathogen causing
sepsis are C. cun, P. multocida, Staphylococcus including
MRSA. Organisms like Bacteroides, Fusobacterium, Neisseria
and Prevotella produce sepsis in immunocompromised
patients and patients on long-term steroid use. Meningitis,
peritonitis and endocarditis have been reported. In all these
cases hospitalization is required with intravenous antibiotics
according to culture given in combinations. Therapy should
be started as soon as possible. In a study from Stockholm
relating to cat bites, it was found that symptoms started in
50 percent cases within three hours. Most common pathogen
was Pasteurella which grew in 80 percent of cultures. When
symptoms appear after 24 hours then Staphylococcus aureus
and Streptococcus may be suspected.
Human Bites
Human bites are a separate entity. These are notoriously
deceptive and can lead to severe consequences. Causes include
aggressive behavior, often in combination with alcohol, sexual
assault, domestic violence, child abuse, occupational injuries
(dentists), seizure related tongue lacerations and self inflicted
wounds. The teeth of humans are less sharp so there is more
of crush injury element with laceration. As a rule, the infection
in these cases is polymicrobial with more than five isolates per
wound. The infection rate in these bites ranges from 10 to 50
percent depending on location (hand –50% and rest 0–20%).
Infection varies from simple cellulitis to osteomyelitis. Five
percent need amputation from vascular injury.

Human bites are classified into two main groups:

1. Clenched fist injuries

2. Occlusive bites.
Clenched Fist Injuries
These injuries are most common and of greater clinical
consequences. These occur as the closed fist strikes the teeth of
another individual with sufficient force to create a small wound.
This injury usually occurs over dorsal surface of middle finger
metacarpophalangeal joint of the dominant hand. Potential
injuries include joint penetration, metacarpal fracture, extensor
tendon laceration, etc. and as the fingers extend the bacterial
inoculum may be carried proximally with the tendon. This
makes irrigation of the wound difficult. These are the most
serious human bite wounds and require aggressive management.
Occlusive Bites
These occur when the teeth bite a part of the body with
sufficient force to violate the integrity of the skin. Many a
times the body part like ear and lip, etc. is bitten off the body
completely (Figure 7). Commonly isolated infective agents
include aerobes like Eikenella corrodens, Staphylococci,
Streptococci and Corynebacterium. Staphylococcus infection
is associated with some of the most severe infections leading
to severe consequences in these cases. E. corrodens, on
the other hand is a slow growing gram negative bacillus
frequently associated with chronic infection and abscess
formation. Commonly isolated anaerobes include Bacteroides
and peptostreptococci.

In addition to the risk of local infections, potentially life-
threatening infections have also been associated with human
Figure 6: Post of picture of lady suffering from facial defect following
bear bite. Reconstruction done with free radial forearm flap

Section 3
  Types of Wounds and their Management
320
bites. Hepatitis B is one such infection as 75 percent of patients
with hepatitis B infection harbor the virus in their saliva. The
transmission of HIV is less likely although several cases suggest
this mode as a possible mode of transmission. Other diseases in
this group include tuberculosis, actinomycosis and tetanus.
Clinical Assessment
When a patient with human bite reaches the emergency room,
certain guidelines are generally followed. In case of human
bites many a times the patient comes with a tissue defect as
part of ear or lip or nose or cheek has been bitten off by his
attacker in a fit of rage. Reimplantation or reconstruction of
these defects was not been done primarily in the earlier times
but now the protocol has changed with the advent of good
antibiotics.

Initially a subjective and objective assessment is done.
The former includes the history leading to the circumstance
of the injury, time of the injury, tetanus immunization status,
drug history and disease history. The objective assessment
includes vital signs like temperature, blood pressure, heart
rate. Dimensions of wound, depth and severity, signs of
inflammation, assessment of vascular or neurological
injury or muscle/tendon injury with possible photographic
documentation.

Supportive lab investigations: Any other diagnostic
procedure like blood culture, WBC count, HIV, HCV, HBV
status, cultures for both anaerobic and aerobic bacteria.
Radiographic evaluation for any bony or joint injury.

Once the exact grievousness of the injury is found, the
patient has to be educated regarding the (1) Exact diagnosis;
(2) Risk associated with wounds; (3) Goals of treatment.

It is essential to assess whether it is a (a) Clenched fist bite
where clenched fist hits the teeth during a fight or (b) occlusal
or simple bites which occur due to actual biting (Figures 8
and 9).
Figure 8: Case of human bite resulting in almost total loss of ear
except the lobule
Figure 9: Another case of human bite with near total avulsion of ear
Figure 7: Case of human bite on ear with no loss of tissue

Chapter 27
Bite Wounds 
321
Treatment
Nonpharmacological treatment starts with hemostasis usually
with pressure. Then the skin preparation is done which
includes: (1) Disinfection; (2) Debridement of devitalized
tissue with high pressure syringing or surgically. Then the
wound can be repaired if they show no signs of inflammation.
Superficial wounds can be approximated with steri-strips or
loose sutures.

Pharmacological treatment includes:

• Systemic antibiotics which should be given prophylac­
tically. Amoxyclav, Clindamycin or doxycycline are usual
choices.

• Analgesics usually ibuprofen or acetaminophen.

• Topical antibiotic ointments like bacitracin.

• Tetanus prophylaxis as required.

• Hepatitis B prophylaxis—Hepatitis B immunoglobulin,
hepatitis B vaccine

• HIV prophylaxis—Zidovudine 300 mg bd and
Lamivudine 150 mg bd and Tenofovir 300 mg od.

Finally, the referral and surgery for complicated wounds which
need exploration, debridement and repair of complex structures
which may be done under magnification and anesthesia. The
general indications for surgical interventions include:

1. Joint penetration

2. Underlying fracture

3. Tendon injury

4. Osteomyelitis

5. Tenosynovitis

6. Septic arthritis

7. Neurovascular compromise

8. Foreign bodies

9. Abscess
10. Severe cellulitis.

Follow-up—for course of hepatitis B vaccine and retest for
HIV is very important and should not be ignored.
REFERENCES
1. Sudarshan, et al. Assessing the burden of human rabies in
India: results of a national multicentre epidemiological survey
S Int J Infect Dis. 2007;(1):29-35.
2. Chhabra M, et al. Animal bites: current management guidelines.
Indian Journal of Pediatrics. 2003;70(Suppl 1):S1-11.
3. Ichhpujani, et al. Epidemiology of animal bites and rabies in
India: a multicentre study. J Commun Dis. 2008;40(1):27-36.
4. Sudarshan, et al. An epidemiological study of animal bites in
India: result of a WHO sponsored national multicentre study. J
Commun Dis. 2006;38(1):32-9.
5. Katarina Westling, et al. Cat bite wound infections: a prospective
clinical and microbiological study at three emergency wards in
Stolkholm, Sweeden. Journal of Infection. 2006;53:403-7.
6. Richard L Oehler. Bite related and septic syndromes caused by
cats and dogs. Lancet Infect Dis. 2009;(9):439-47.

• Incidence
• Impact on Quality of Life
• Etiopathogenesis
• Wound Malodors
• Symptoms
• Diagnosis of Malignant Wounds
• Management of Malignant Wounds

– Aims

– Assessment

– Risk Assessment

– Patient Assessment

– Wound Assessment

– Pain Assessment

– Wound Cleaning

– Management of Malodor

– Exudate Management

– Dressings

– Bleeding

– Pain Control

– Pruritis

– Excoriation

– Impact of Malignant Wounds
Introduction
These wounds have been defined as a break in epidermal
integrity by infiltration of malignant cells (Cooper 1993).
British Columbia Cancer Agency defines an ulcerating
malignant skin lesion as “a cancerous lesion involving the
skin, which is open and may be draining. The lesion may be a
result of a primary cancer, a metastasis to the skin from a local
tumor or from a tumor in a distant site. It may take form of a
cavity, an open area on the surface of the skin, skin nodules, or a
nodular growth extending from the surface of the skin.”1 These
lesions are also called cutaneous fungating wounds. Mortimer
describes a fungating wound as, “a condition of proliferation
and ulceration which arises when malignant tumor cells
infiltrate and erode through the skin.”2 Although only a small
number of patients with cancer develop the traumatic and
devastating complication of a malignant cutaneous wound, it
can be a very distressing occurrence.3 The understanding of
the behavior and the management is based on an exploratory,
experiential and experimental approach, rather than a readily
accessible body of research knowledge. The literature is silent
on most issues concerning these wounds.4
Incidence
Cutaneous metastases occur in five to ten percent of cancer
patients. Lookingbill, et al. reported that approximately ten
percent of patients with metastatic disease have cutaneous
metastasis.1 More recently, Maida, et al (2008) reported that
malignant wounds occur in 14.5 percent of patients with
advanced cancer.2
Impact on quality of life
The wounds are often disfiguring or malodorous and heavily
exudating and hence can have a significant impact on the
patients psychological status, body image and social, physical
and sexual relationships.5 Many people with this type of
wound do not seek help and advice from health professionals
and manage the wound on their own.6 The failure to seek help
may arise from a fear of diagnosis of cancer or embarrassment
due to the location of the wound.

Malignant cutaneous wounds can result from primary
skin cancer such as squamous cell or basal cell carcinoma
and malignant melanoma, if left untreated.10 They could
Malignant Wounds
Chintamani, Megha Tandon, Rohan Khandelwal
28
Chapter

Malignant Wounds 
Chapter 28
323
also result from a primary tumor invading and eroding
the skin, a presentation often seen in locally advanced
untreated, metastatic or recurrent cancer. It is estimated that
five to ten percent of patients with metastatic cancer will
develop such a wound.8 Chronic wounds such as leg ulcers
can develop malignant changes and produce a malignant
cutaneous wound. The most common tumor sites associated
with malignant cutaneous wounds include breast (62%),
head and neck (24%), groin and genitals (3%), back (3%)
and other areas (8%).9 Wood has categorized the location
of malignant ulceration by anatomic site, namely, head and
neck, thorax, perineum, abdomen and extremities.11 Head and
neck lesions are frequently of squamous cell origin and are
especially difficult to treat. The major lesion in the thorax is
female breast cancer and less often large sarcomas that may
encompass the abdominal region as well. Perineal ulcerating
wounds are frequently seen as a result of a primary or
recurrent gynecological cancer. Abdominal cancer can grow
out of stomas and drain sites.
Etiopathogenesis
Malignant cutaneous wounds develop following virtually any
malignancy and most commonly from the following cancers:
breast, head and neck, skin, vulva, penis, bladder, lung, colon,
anal canal, cervix, vagina, bone tumors, etc. (Table 1). The skin
changes seen with these wounds are caused by infiltration of
the skin and the supporting lymphovascular system by local
malignancy or by metastatic spread from a primary elsewhere.
The malignant cells penetrate the surrounding lymph and blood
circulation and this may result in capillary enlargement and
possible rupture. The wound is considered fungating once the
tumor penetrates the skin through the process of proliferation
and ulceration.2 These tumors can grow rapidly and may take
on a cauliflower like appearance. They may also be invasive,
may ulcerate and form shallow craters that can be complicated
by the presence of an associated sinus or fistula.12 The spread
tends to be through tissues that offer the least resistance, i.e.
between tissue planes, along blood and lymph vessels and in
perinerual spaces. Without treatment, the fungation has the
potential to extend and cause massive damage to the wound
site through a combination of proliferative growth, loss of
vascularity and ulceration.4,12-14 Unbridled tissue growth in the
fungating tumors leads to areas of tissue hypoxia, development
of nonviable tissue and necrosis and subsequent infection
resulting in the characteristic malodor, exudation and discharge
from the wound. Deficiencies may also arise in the lymphatic
system and thereby affect interstitial tissue drainage. When left
unchecked, onset of primary or secondary lymphedema can
result and become a chronic problem for the patient.
Mechanism of Development
of Malignant Wounds
• A primary tumor invading up into and through the skin,
e.g. fungating breast cancers and oral cancers (Figures 1 to
3).
• Tumor has invaded blood or lymph vessels–small skin
capillaries trap malignant cells.
• During surgery–seeding of malignant cells in the dermis
occurs.
Figure 1A: Most malignant wounds tend to be maladorous and
nonhealing. It is unrealistic to expect them to heal on their own or with
any kinds of dressings. Fungation, bleeding and secondary infections
(with anaerobes and fungi) destroy the quality of life of the patient. The
management involves an R0 resection (microscopic freedom from the
disease) with reconstruction using skin cover in the form of a graft
or flaps. A case of recurrent soft tissue sarcoma (the old scar and
skin graft may be seen) of the head and neck region with secondary
infection (and maggots) in a 50-year-old male that required extensive
wide local excision with reconstruction
Table 1: Etiology of malignant wounds
Common sites involved:
• Breast/chest
• Head and neck
• Extremities
• Back, trunk and abdomen
• Perineum/genitals
Tumor origins of malignant wounds:
• Breast (most common)-47.1% of the wounds were associated
with this diagnosis
• Head and neck cancers
• Ano-rectal carcinoma
• Esophagus

Types of Wounds and their Management
Section 3
324
• Conversion: Malignant wound develops in another chronic
ulcer/scar tissue (Figures 4 and 5).
Wound Malodors
Wound malodor is caused mainly by bacteria, both aerobic
and anaerobic, which colonize moist areas of necrotic tissue.
These organisms flourish in the accessible necrotic tissues
of fungating tumors. Brusis and Luckhaupt16 detected
distinct populations of anaerobes in patients with extensive
Figure 1C: The tumor has been resected with a clear margin along
with right sided modified radical neck dissection. The right internal
jugular vein, and brachial plexus (BP) may be seen
Figure 1D: The resection would leave behind a large wound defect
that would need to be provided skin and soft tissue cover
Figure 1E: The intercostal, deltopectoral flaps along with skin grafts
has been used to provide the cover
Figure 1B: Maggots may be seen. Most patients in the developing
countries would be presenting as locally advanced cancers
tumors of the head and neck associated with putrid odor. The
most frequently demonstrated organism was Bacteroides
melaninogenicus and investigators attributed the foul odor
to this Bacteroides species. If the presence of anaerobic
organisms is inappropriately treated, the production of by-
products such as lactic, propionic and succinic acid will
result and these by-products will mix with body fluid exuding
from the wound. The malodorous volatile fatty acids that are
released as a metabolic end-product are responsible for the
offensive smell.17 The production of exudates is attributed to

Malignant Wounds 
Chapter 28
325
Figure 2: A 32-year-old lady with a nonhealing ulcer in the nasolabial
fold that turned out to be due basal cell cancer. This cancer usually
occurs in the region of face above the line joining the angle of the
mouth with the ear lobule and can be severely disfiguring as it is locally
infiltrative. The tumor has been resected along with reconstruction
using naso-labial flap with a satisfactory outcome
Figure 3A: These are sights are unfortunately not very rare in the
developing countries.These orla cancers are common in tobacco
chewers with a tendency to put the quid in the gingivo-buccal sulcus.It
is intriguing to know the delays even in such obvious malignancies. No
dressings and any amount of patience can help these wounds heal.
They need aggressive approach in the form of R0 composite resection
(with soft tissue and mandible) and reconstruction for providing inner
lining and outer cover. (Case by Dr Chintamani, Rakesh Kain)
Figure 3B: The composite resection completed along with radical
neck dissection on the right side.The common carotid artery may be
seen
Figure 3C: Fore head flap based on superficial temporal artery
being raised for reconstruction while the support is being provided
by mandibular plate

Types of Wounds and their Management
Section 3
326
Figure 3E: Reconstruction completed
Figure 4A: A 25-year-old gentleman (known tobacco chewer) with
squamous cell cancer of the left buccal mucosa, managed by wide
local excision and left sided neck dissection
Figure 4B: Reconstruction being done using radial artery
forearm flap
Figure 3D: The reconstruction in progress
the activity and role of bacterial enzymes (proteases) in tissue
breakdown. If this fluid (exudates) is not controlled effectively
such as by absorbent wound dressing materials, maceration
and stripping of the tissue surrounding the original lesion will
quickly occur.15
Causes of Malodor
• Anaerobic bacteria infecting or colonizing necrotic tissue-
putrescent, cadaverine-Klebsiella, Pseudomonas and Proteus

Malignant Wounds 
Chapter 28
327
• Necrotic tissue odor
• Stale exudates.
Bleeding as a Feature of Malignant Wound
Bleeding from the wound can result from trauma during
wound care or invasion into the vascular system by the tumor
itself. Significant spontaneous bleeding can occur because of
the erosion of the capillaries of the tumor.18,19
Symptoms
Every malignant cutaneous wound is unique in appearance and
presenting symptoms. The wound may have the appearance of
a raised fungating nodule or an ulcerated crater with a distinct
margin. Some patients have multiple symptoms and others
have very few.20 The most common symptoms are malodor,
discharge, pain, bleeding and pruritis. High exudates level
can cause anxiety, embarrassment, and discomfort and may
result in the breakdown of the skin. Leakage through the
dressing may be distressing as it may soil clothing, and be
malodorous.21 Infected wounds and those with large surface
area can produce high levels of exudates. Necrotic tissue
that is attached to the wound bed and is being debrided will
also produce increased exudates. Malodor associated with
fungating wounds cause great distress as the individual
feels unclean and may isolate himself or herself for fear of
offending others. It may also cause nausea and problems with
appetite.22 High absorbency dressings, such as cellulose fiber
or some foam dressings, can become saturated and pull away
from the wound resulting in poor management of exudates or
malodor.14 Other problems include the presence of necrotic
tissue that predisposes the wound to infection. Heavy exudates
from a fungating wound can also damage the surrounding
Figure 5: Cancer of a male breast may also produce a fungating and
nonhealing wound that would need surgical intervention in the form of
mastectomy and skin cover and no amount of dressings would help
Figure 6A: Primary squamous cell cancer of thyroid in a 35-year-
old male. [Chintamani, et al. Int Semin Surg Oncol. 2007 Mar
27;4:8]
Figure 6B: Aggressive cancers sometimes may make it into a life
threatening wound with infiltration into the airway as in this case
of “Primary squamous cell cancer” of thyroid gland, an extremely
aggressive and rare cancer. This 45-year-old lady was managed
by total thyroidectomy along with laryngectomy and bilateral neck
dissection [Chintamani, et al. Int Semin Surg Oncol. 2007 Mar 27;4:8]
skin.10,20 Fitting and retention of dressings which depends on
location, size and shape of the wound can cause difficulties
related to the frequency of dressing change which could also
be associated with considerable pain.10,23

Complications of large, fungating head and neck tumors
include airway obstruction (Figures 6A to C) and invasion
of major blood vessels with the possibility of erosion and

Types of Wounds and their Management
Section 3
328
fatal hemorrhage. Tracheostomy may be needed to secure a
patent airway. Lesions over the carotid artery may erode into
the artery resulting in fatal hemorrhage. Sinuses and fistulae
can also develop in patients with malignant cutaneous wound.
Patients with abdominal or perineal malignant cutaneous
wounds are particularly prone to develop sinuses and fistulas12
(Figure 7). Fistula formation such as recto-perineal and vesico-
perineal fistulae could be associated with the fungating wound
of a gynecological cancer. Constant bloody ooze is another
complication of perineal ulceration. Subcutaneous and fascial
infections can occur adjacent to large fungating lesions.7
Characteristics of Malignant Wounds
• Malignant wounds may be ulcerating or fungating. The
term “fungating” implies that the tumor is showing both
ulceration and proliferation. Most solid tumors can produce
cutaneous lesions through direct extension of the tumor
through the skin.
• Malignant wounds may occur on any part of the body. The
most common sites in order of prevalence are: (i) chest and
abdomen, (ii) head and neck, and (iii) extremities.
• Malignant wounds generally are difficult to treat for a
number of reasons, including irregular size and shape,
presence of copious drainage, infection, odor, bleeding,
pain, pruritis (itching), and disease progression.
• Malignant wounds may affect the individual’s ability
to function and have a profound psychological effect on
individuals and families because the wound is a visible
sign of cancer and indicates a poor prognosis for recovery.
Diagnosis of Malignant Wounds
Diagnosis is based on:
• High index of suspicion based on history and examination.
• Tissue diagnosis is made by obtaining imprint smears or by
incisional or excisional biopsies.
• Ruling out benign conditions such as varicose ulcers,
traumatic wound, tubercular ulcers and diabetic ulcers.
Investigations
Investigations would aid both in the diagnosis of the condition
and associated medical conditions that would have a bearing
on the management plan.
• Hemoglobin level, total leukocyte count, platelet count,
bleeding time and clotting time.
• Fasting blood sugar and postprandial blood sugar levels.
• Blood urea and serum creatinine levels.
• Liver function tests.
• Radiological examinations such as roentgenogram of the
chest, X-ray of the region if near a bone, ultra sonogram of
the abdomen, color Doppler study of the wound, CT/MRI
scan as indicated.
• Cytological and histopathological investigations from
the wound and from the primary site if the wound has
developed at a metastatic site.
• Bacteriological culture and sensitivity of exudates from the
wound.
• Examination of the wound fluid for electrolytes, glucose
content, cells.
Management of Malignant Wounds
Aims of Management
• Pain control
• Control of exudates
• Control of odor
• Control of bleeding
Figure 6C: Reconstruction done using bilateral deltopectoral flaps
[Chintamani, et al. Int Semin Surg Oncol. 2007 Mar 27;4:8]
Types of malignant wounds
Symptoms of malignant
wounds
Four principal classes
• Pain
• Nodules and indurations
• Mass effect
• Malignant ulcers
• Esthetic distress
• Other (Zoster form and mixed)
• Exudation
• Odor
• Pruritis
• Bleeding
• Crusting

Malignant Wounds 
Chapter 28
329
• Prevention of infection
• Fewer dressing changes
• Trauma free dressing removal
• Cosmesis
• Improved quality of life
• Optimization of the patient’s healing potential
• Optimization of the local healing environment
• Reduction of the effects of any complications associated
with the lesion.
Assessment
Risk Assessment
Individuals with malignant wounds require a comprehensive
assessment, including cancer history and prior treatment,
medical and medication history, and assessment of social
support. All persons with cancer—and particularly those
with breast cancer, head and neck cancer, and primary skin
cancers—are at risk for developing cutaneous malignant
wounds. A thorough assessment of skin integrity should be
undertaken during the initial assessment and repeated on a
regular basis. Malignant wounds are often not preventable
but early detection of a subcutaneous tumor site may allow
treatment (e.g. radiation or chemotherapy) to prevent the
tumor from breaking through the skin (Figure 8).
Assessment for Management
The prerequisite to the development of a wound management
plan is individualized patient assessment. Lack of a
classification system for malignant cutaneous wound hinders
the performance of a proper assessment.24 No universal
guidelines exist to assist in objectively describing the wound
or the size or to record objectively the progress of the
wound.3 Photography and ultrasound can be used to assess a
wound. However, photography is only two dimensional and
Ultrasonography uses a probe that comes in contact with the
wound. Hence, descriptions are the only way to continually
assess and describe a wound. The descriptions need to be
documented in a concise and systematic manner to increase
the reliability of the continuing assessment.3,13 A detailed
framework for the assessment and management of fungating
wounds which is also presented as an easy reference wall
chart has been developed by Moody and Grocott.4 According
to them the criteria for assessing patients with malignant
cutaneous wounds is divided into two levels:

Level 1–involves the collection of baseline data about the
wound.

Level 2–requires the application of critical thinking skills
for the data collection.
Assessment under level 1 would include:
• Patient assessment
• Wound assessment
• Pain assessment.
Patient Assessment
The suffering of patients with fungating wounds that is
associated with altered body image, loss of dignity and
independence and psychological distress can be immense.25
Patient assessment needs to take into consideration the
Figure 7: A discharging wound 25 years following radiotherapy
for cancer penis. The detrimental effects of radiotherapy on wound
healing are well known. The healing may be significantly delayed and
rarely complications line spontaneous enterocutaneous fistula may
result. [Chintamani, et al. World J Surg Oncol. 2003 Nov 3;1(1):23]
Figure 8: Rarely Fournier`s gangrene may be the result or cause of
a cancer like in this case of squamous cell cancer developing in the
scar of Fournier`s gangrene. [Chintamani, et al. BMC Cancer. 2004
Apr 27;4:16]

Types of Wounds and their Management
Section 3
330
effects of the wound on the patient’s quality of life and on
their family. The patient’s primary concern may not be the
treatment but something else, such as in the patient reported
by Dowset25 whose priority was not her treatment but to see
her grandchild born. The patient’s needs change frequently
as their condition progresses or if there is benefit from
the definitive treatment such as surgery, radiotherapy or
chemotherapy. Hence, assessment needs to be ongoing. The
factors to assess include:
• General health status
• Wound history and cause of wound
• Ongoing treatment (e.g. Radiotherapy)
• Previous treatment
• Past medical history and other current health problems
• Activities of living
• Nutritional status
• Patients’ environment and career
• Patient/attendants or carer’s knowledge and acceptance of
diagnosis and prognosis
• Patient/attendants or carer’s aims and expectations
• Patient/attendants or carer’s perception of impact of wound
on daily life
• Professional/lay support being provided.
Wound Assessment
The underlying cause of the wound needs to be identified. Any
current treatment such as radiotherapy that may have an effect
on the type of dressing and frequency of change of dressing
needs to be taken into consideration.
• Wound size, shape and type
• Hidden extensions if any
• Amount and nature of exudates
• Odor
• Fistula and type of fistula fluid
• Location of wound
• Size, depth and shape
• Presence and level of malodor
• Type of tissue present
• Signs and symptoms of infection
• Nature and type of pain
• Condition of periwound skin
• Condition of the wound bed: bleeding, exudates, infection,
necrotic tissue, maceration, depth, color, surrounding tissue.

The location of the wound is important in terms of the
patient’s body image and application of dressing. Location
can also assist in the identification of the etiology of the
lesion. Patients with a visible wound such as on the face,
head and neck may become withdrawn and isolated. Patients
with a wound on the breast or genitalia may have problems
expressing sexuality or feel less “whole” as a person. The
irregular size and shape of the wounds and presence in areas
that are awkward to dress sometimes make them difficult to
dress.25

Assessment of odor should be from the patient’s
perspective, as nurses often become desensitized to odor when
caring for patients with chronic wounds.26,27 The condition of
the surrounding skin is important in terms of protection from
maceration with excess exudates and in the choice of wound
dressing. Adhesive dressings will not be appropriate where
the surrounding skin is macerated, as this will cause further
skin trauma.25

There are a number of methods available for assessing
wounds visually, including computer mapping, polaroid
photography incorporating a scale and tracing wounds using a
clean transparent film or sheet. However, it is not advisable to
trace fungating wound as contact between the tracing material
and friable tissues can induce local bleeding from the surface
of the wound.15 The condition of the skin surrounding the
wound might indicate the presence of wound infection or
might highlight the problem of tissue maceration.
Pain Assessment
These wounds are commonly associated with pain. Distinction
needs to be made with regard to pain in relation to the underlying
condition and specifically in relation to pain at wound site and
at the time of change of dressing. Nociceptive pain (caused
by stimulation of nerve endings) has to be differentiated from
neuropathic pain (caused by nerve dysfunction).

Assessment of pain should include the following:
• Location
• Nature
• Duration
• Onset and frequency
• Severity
• Influence on activities of living
• Aggravating and alleviating factors
• Analgesic use
• Effect of treatment.28

The most frequently used tools for the assessment of pain
are the pain scales such as the visual analogue scale and
descriptive scales which are included in wound assessment
charts.29 Pain could also be present at the time of dressing
changes and the pain scales can also be used at such a time. It
is also required to record the time and frequency of analgesia.
At night, patients might complaint of more pain because the
number of distracters is usually reduced and they have time to
focus on their bodies.

Assessment under level 2 would include the following:
• Are the treatment options, i.e. surgery, radiotherapy,
chemotherapy, hormone therapy, etc. exhausted?

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• Can the patient’s prognosis be estimated in days, weeks or
months and does this influence the wound management?
• What are the patient’s and attendants/carer’s priorities
and what are the resources available to them to meet these
priorities? Are the priorities realistic and do they differ
from the view of the multidisciplinary team?
• What multidisciplinary team support is available and
what level and aspect of multidisciplinary team support is
appropriate for the patient and attendant/carer?

The assessment at this level would provide, (1) a statement of
symptom control needs in relation to the wound, (2) an insight
into patient, carer and multidisciplinary team priorities for wound
care, (3) reconciliation of any differences in the priorities.4

Following assessment, a wound management plan is
formulated keeping the patient, care provider and professional
priorities in order of significance.

The criteria by which these priorities are ordered reflects,
(1) the patient’s perception of priorities (2) that symptom
control at the wound site is a priority for palliative management
to alleviate physical distress and the emotional, spiritual and
social elements of human suffering (3) that healing may not be
a priority (Figure 9). Even when healing is not an achievable
goal, wound management principles based on moist wound
healing may have the potential to meet the needs of patients
with malignant wounds.4,30-34

The challenges involved in prioritizing the care of fungating
malignant wounds have been summarized by Moody and
Grocott4 as follows:
• Wounds are dynamic.
• Application of dressing may be difficult because of size,
shape and site of wound.
• Signs and symptoms are complex and interrelated.
• The tumor may be close to a major blood vessel with
potential for hemorrhage.
• Patient may have a localized disease that is destructive and
disfiguring and a long life expectancy.
• The patient may have disseminated disease with a short life
expectancy.
• Iatrogenic effects of treatment may increase morbidity
including wound deterioration.
• The impact of the wound on the patient and the family may
be significant.
• Management is time consuming and may result in the
neglect of the patient’s and family’s psychological needs
and a disproportionate amount of professional time being
spent with one patient.
• The cost implications for the use of time and materials in a
resource limited setting may have ethical considerations.

Symptoms associated with these wounds present a
challenge to the person managing them. An integrated
management approach is needed to minimize symptoms,
provide comfort, and improve the quality of life.35 A holistic
and multidisciplinary team approach is of paramount
importance if opportunities for treatment and symptom
control are not to be missed, or complications arising from the
underlying pathology overlooked4 (Figures 10 and 11).

Practitioners who have “supplemented knowledge and
skill with those other important qualities of being honest,
open, questioning and challenging are best able to service
the interests of these people who, often when they are at
their most dependent and vulnerable, have no option but to
place themselves in the care of people who are professionally
qualified to respond to their needs.”36

The management will need to focus on control of tumor
growth, arrest bleeding, control exudates and infection and
restore skin integrity where possible. Several management
options are available that aim to improve the quality
of life. Attempts at tumor control can mitigate further
problem associated with growth of invasive tumor. Surgery,
chemotherapy, radiotherapy, laser therapy or hormone
therapy when used to treat the underlying disease may help in
controlling a fungating wound. In the absence of treatment or
in the presence of ineffective treatment, unchecked disease can
result in worsening of the wound and the symptoms. Such a
situation will warrant the institution of palliative management
that involves such measures as general wound care, odor
control and control of exudates.14 Palliative radiotherapy can
reduce wound exudates and bleeding. Chemotherapy can
reduce the size of the tumor, pain, bleeding and irritation.
Hormone therapy can reduce the symptoms associated with
hormone responsive tumor such as breast cancer. Surgery can
be useful to excise the tumor, minimize the risk of fungation
Figure 9: A fungating wound due to anal cancer are common sites
and these nonhealing wounds cause severe distress to the patient
and are often managed suboptimally [Case by Dr Chintamani
FRCS]

Types of Wounds and their Management
Section 3
332
and reduce size of the tumor.37 Such measures will improve
the quality of life of the patient. Healing in cancer patients
is affected by age, smoking habits, alcohol consumption
and nutrition, treatment with steroids, stress and anxiety.
Good local care is of importance in managing these patients.
Keeping the area of the fungating mass dry and clean will
prevent superimposed infections. Rectoperineal fistulae are
best treated by permanently diverting the fecal stream such as
with an end colostomy. However, vesicoperineal fistulae are
difficult to manage. Large fungating lesions of the extremities
may require palliative amputation.
Wound Cleaning
Improper cleaning can cause trauma to the wound resulting in
pain and bleeding. It is recommended that malignant wounds
be cleaned by gentle irrigation with warmed 0.9 percent
sodium chloride or water. Care is taken to avoid cotton wool
because of the risk of fiber shedding. Cold irrigation fluid or
high pressure irrigation can be helpful or unpleasant for the
patient and are avoided.10 Wood11 suggests cleansing with
an inexpensive solution consisting of equal parts hydrogen
peroxide and normal saline. Following twice daily lavage,
small gauze packing soaked in 0.25 percent Dakin’s solution
(sodium hypochlorite) overnight helps to improve the smell.
Management of Malodor
Initial treatment may involve debridement. However,
mechanical debridement is avoided because of propensity
of malignant wounds to bleed at the slightest trauma.38
Hydrogel dressing soften the necrotic tissue, facilitate
separation from the tumor bed, and the use of this dressing is
the most gentle method of debridement. Occlusive dressing
may greatly help overcome this problem. Activated charcoal
dressings can be useful for the containment of malodor.
These dressings act as filters to absorb malodorous chemicals
from the wound before they pass into the air. They vary in
composition and structure and perform best when fitted as
a sealed unit.39,40 Metronidazole, which is effective against
both anaerobic and aerobic organisms, is commonly used
for the management of wound malodor both systemically
and as a topical dressing. A successful treatment option is
metronidazole 200 mg orally tds. Nausea associated with
this reduces compliance. It may be more useful to apply
Metronidazole topically in the form of gel. When used
on the surface of a fungating wound, it should be applied
liberally after cleansing and be covered with an appropriate
secondary dressing. No undesirable side effects have been
reported when used in this way.15 However, disadvantage of
the use of gel form is the cost and the fact that this form of
application may be less useful when there is large amount of
exudates. Clindamycin (300 mg qid) may be more effective
than metronidazole.13,41 Silver impregnated dressings and
hydropolymer dressings have been useful because of their
antibacterial actions.42 Sugar paste dressings and honey have
antibacterial properties and are useful for the management
of malodor in these wounds.43-45 Providing air conditioning
unit or using air fresheners or aromatherapy may be helpful
for patients with fungating wounds.
Figure 10: Maladorous and nonhealing wounds that are a challenge
to any surgeon are a common scenario for a surgeon in the developing
world and effort should be made to palliate the patient with tailored
dressings and supportive care. [Case by Dr Chintamani FRCS]
Figure 11: Such grossly advanced cancers produce wounds that are
only amenable to surgical knife.One can see a direct communication
due to the malignancy destroying the soft tissue and the bone. [Case
by Dr Chintamani FRCS]

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333
Exudate Management
Conventional treatments to aid wound healing are less useful
in the management of malignant cutaneous wound and
the priorities for patients with such wounds are controlling
exudate and malodor if any. This is difficult to achieve as many
wounds require frequent daily dressing changes to control
symptoms. Further, these wounds are complicated by their
rapidly changing nature. Hence, daily dressing plans will need
to be flexible.22 Protection of the skin surrounding the wound
is essential and barrier creams and liquid barrier films are
used. Where the skin is already sore or broken, liquid barrier
film is used along with the use of absorptive dressings to
manage excess exudates and prevent maceration. Comfortable
dressing materials that can fit to the wound and to the
body’s natural curves can help in exudates management.14,16
Improved fluid handling designs of wound dressing materials,
such as vertical or lateral wicking, maximize the amount of
absorbent surface area.47 Dressings with a high moisture
vapor transfer rate vent excess fluid instead of allowing it
to accumulate.46 Naylor28 used a hydropolymer dressing to
provide a high-level of comfort. Thomas48 observed that a
hydrocolloid dressing those result in an airtight seal over the
surface of the wound can reduce exudate production by 50
percent. It is suggested that the dressing forms a chamber over
the wound surface which becomes filled with exudates that is
under pressure. This exerts back pressure on the capillaries
and inhibits production of further fluid.20
Useful dressings are:
• Hydrophilic foam (e.g. Lyofoam, Allevyn). Available as
sheets or cavity dressings.
• Alginates (e.g. Sorbsan, Kaltostat)
• Semipermeable film dressing (e.g. Bioclusive, Opsite).
These help contain the exudate and odor.

Large amount of padding with absorbent materials are
sometimes helpful. Wound drainage or colostomy bag, if the
wound can be contained and the bags will adhere, can also be
useful. Medical adhesive that can be removed with a suitable
solvent are useful. Moulded latex can be used to make an
occlusive barrier through which the exudate can be drained
with the use of a wound drain22
Dressings
Grocott49 identified the principles that should be considered
when choosing a dressing material for patients with fungating
wounds:
• Control of pain by maintenance of optimum humidity at
the site by using dressings that do not adhere to the tumor.
• Facilitation of wound debridement with removal of excess
exudates and toxic materials.
• Control of odor using topical antibiotics/antibacterial, as
appropriate.
• Dressing removal without trauma.
• Restoration of body symmetry through the use of cavity
dressings.
• Achievement of cosmetic acceptability, without the need
for bulky secondary dressings.
• Control of bleeding when it occurs by using hemostatic
dressings.

Thomas9 has recommended the following type of dressing
in the management of fungating wounds:
1. Bleeding wounds: Alginate sheet dressings (Kaltostat or
Sorbsan)
2. Lightly
exuding
wound:
Hydrocolloid
sheets,
semipermeable films, Lyofoam, Sorbsan SA or Kaltoclude.
Alternatively, Silicone NA or Tegapore used with a
secondary dressing.
3. Heavily exuding wound: Hydrofibers, Sorbsan, Kaltostat
Fortex covered with an absorbent pad or Sorbsan plus or
Allevyn sheet may be applied.
4. Cavity wounds: Alginate rope or packing, Allevyn cavity
wound dressing or Silastic foam.
5. Malodorous wounds: Dressings containing activated
charcoal, e.g. Actissorb Plus, Kaltocarb, Lyofoam C,
topical Metronidazole, Intrasite (Scherisorb) gel containing
Metronidazole or sugar paste.
6. Infected wounds: Topical Metronidazole or Intrasite
gel with Metronidazole, sugar paste, Sorbsan, products
containing iodine or povidone.
7. Necrotic/sloughy wounds: Intrasite gel, Sorbsan, sugar
paste, Debrisan paste, Iodosorb.
Bleeding
These wounds are fragile and are prone to bleeding which
is usually slow capillary ooze. Bleeding can occur when the
dressing is changed. Gentle wound irrigation and the use of
nonadherent dressings reduces the risk of bleeding.10

Measures to reduce the risk of bleeding include:
• Oral tranexamic acid 1g tds for about 190 days.
• Topical applications of sucralfate paste (crush a 1g tablet
and mix with KY jelly to appropriate consistency).
• Topical adrenaline 1:1000 on a dressing pad can be
applied to areas that are bleeding heavily to induce local
vasoconstriction.
• Hemostatic surgical dressings are needed for heavier
bleeding.
• Referral to a surgeon for cauterization or ligation may
be needed for serious hemorrhage that may occur from
malignant ulcer following erosion from a major blood
vessel.