Principles and Practice of Wound Care

Skin Avulsion Injuries
135
Figures 11A to I: (A to D) Avulsed and necrosed fl aps on the thigh, knee and leg; (E and F) Conservative debridement and dressings over
a period of time resulting in healthy granulating wound ready for split skin grafting; (G to I) Postoperative result after split skin grafting. Needs
massage and pressure garment therapy to improve the appearance and maturation of graft
Figures 11H and I
which are the mainstay of provision of wound cover. Areas
which heal with adherent scars with repeated breakdowns or
where grafts do not take and granulations also do not form or
which do require a fl ap cover for later reconstructive surgery
are covered with fl aps electively rather than in emergency.

In some situations like an avulsion on the dorsum of hand
with exposed and bare tendons, an immediate fl ap cover with,
say, a pedicled distally based radial forearm fl ap or a groin fl ap
is highly desirable to save the bare tendons and must be done
in emergency. Similarly, a localized avulsion of heel pad may
be treated by immediate coverage with instep island fl ap or a
distally based superfi cial sural artery neurocutaneous fl ap.
AVULSION INJURY OF SPECIALIZED
STRUCTURES
The avulsion injury may involve some specialized areas like
scalp, pinna and face, penoscrotal region, hand and sole of
the foot.

Avulsions injuries of scalp, pinna and face: As early as 3000
BC, the Egyptians noted the seriousness of the avulsion injury
of the integument over the calvarium and the necessity to
provide cover for the exposed bone.42 The advent of industrial
revolution saw a number of women workers, with their long
hair getting caught in unprotected belts and gears of power
driven machines, becoming victims of scalp avulsion injuries.
John Staige Davis in 1911 reported 81 cases of industrial
scalping while McWilliams reviewed 173 cases reported in
literature up to 1924 with no success in the 40 cases where the
scalp was replaced.42 The state of Punjab in Northern India
has a large population of Sikhs whose religion forbids them
to trim scalp hair for either of the sexes. Moreover, a very
high percentage of population is involved in agriculture for
their living with both men as well as women working on the
farms the whole day. This exposes them to the risk of their
long and loose hanging hair getting caught in the farm rotating
machinery (e.g. thrasher) especially during harvesting season.
It is thus not surprising to fi nd a very large series of 46 cases
in 10 years getting published from that region.43

The scalp usually avulses in the loose areolar plane taking
the skin, subcutaneous tissue and galea aponeurotica along
with it while leaving the periosteum. Unfortunately, in several
patients the periosteum (or the pericranium) is also avulsed at
many places leaving a large part of skull bare. The scalp fi rst
tents up from the skull and then tears up following the points
where the skin is thinner. Thus, the line of tear is usually through
the upper eyelids, the eyebrows, the zygoma, the superior helix
of the ear and the nape of the neck. A part of cheeks and face
also sometimes gets avulsed along with. Muscles of the scalp
(namely, frontalis, temporalis and occipitalis) do not offer much
resistance as compared to galea aponeurotica and oblique
tears may occur in these regions.44 The scalp is supplied by

Types of Wounds and their Management
136
Figures 12A to E: (A) Extensive, almost circumferential, avulsion injury of left thigh in a young adult male. Please note the friction injury marks
on the abdomen. However, patient had no intra-abdominal injury; (B) After conservative debridement and dressings, the wound became fi t for
split skin grafting; (C to E) Late result. Please note the contour deformities. However, patient is ambulatory without any support
Figures 13A and B

Skin Avulsion Injuries
137
5 pairs of arteries with a rich network of anastomosis amongst
them so that the whole scalp can survive on a single vascular
pedicle. These vessels are present in the subcutaneous layer
immediately superfi cial to galea with minimal contributions
to pericranium. The latter is supplied by middle meningeal
vessels and intracranial circulation so that an avulsion of the
scalp does not lead to necrosis of calvarium. However, if a soft
tissue cover is not timely provided, the periosteum dries up and
the outer table of calvarium sequestrates.

Victims of extensive scalp avulsion injury usually
present with hemorrhagic shock because the scalp vessels
do not retract. They need management of shock before
any reconstructive surgery is contemplated. Till then, the
scalp is dressed with moist dressings after control of any
Figures 13A to F: (A and B) Circumferential avulsion injury of right thigh and popliteal region in a 20-year adult male with uncontrolled diabetes.
Please note the road side grit and gravel in the wound; (C and D) Conservative management produced a wound fi t for skin grafting; (E and F)
Postoperative result after 10 months
Figures 13C to F

Types of Wounds and their Management
138
Figures 14A to E: (A and B) Extensive avulsion injury of lower back and perineum necessitating a diverting colostomy for wound management;
(C) Healthy granulating wound being split skin grafted; (D and E) Late result after grafting. Please note the closed colostomy wound

Skin Avulsion Injuries
139
Figures 15A to D: (A) Extensive avulsion injury of right thigh and perineum requiring a diverting colostomy; (B) Healthy granulating wound;
(C) Healed wound after application of split skin graft. Please note that the patient had a fracture of the left femur as well which was operated on
the day of injury itself; (D) Closed colostomy wound
Figures 16A to C

Types of Wounds and their Management
140
Figures 16 A to E: (A and B) Avulsion injury of gluteal region; (C) Being split skin grafted after conservative management. Perineum itself was
intact and colostomy was avoided; (D and E) Postoperative appearance. Please note symmetrical inferior gluteal folds
Figures 17A to C: (A) Extensive injury resulting in loss of lower extremity and a large raw area over lower back and buttock;
(B and C) The raw area was split skin grafted
Figures 16D and E

Skin Avulsion Injuries
141
Figures 18A to F

Types of Wounds and their Management
142
bleeding vessels. Transfusion of intravenous fl uids including
plasma expanders and blood may be required along with
hemodynamic monitoring. If the scalp has been brought along
with and is healthy enough to be replantable and the facilities
for microsurgery are available, this is the treatment of choice.
However, if the scalp has not been brought along with and
is not retrievable or is damaged enough so as to be unfi t for
microsurgical replantation or the facility for microsurgery is
not available within a reasonable distance (still common in our
Figures 19A to C: (A and B) Avulsion of whole of scalp with complete loss of tissues into the thrasher machine. Healthy granulating wound
after conservative treatment; (C) Early result after graft application
Figures 18A to G: (A and B) Patient presented with necrosed avulsed
fl aps on upper limb; (C) After conservative debridement; (D and E)
Healthy granulating wound; (F and G) Healed wound
Figure 18G
country), the scalp reconstruction is done with sheets of split
skin grafts harvested from thighs (Figures 19 and 20). The
attempts by various workers to convert the avulsed scalp into a
full or partial thickness skin graft to cover the periosteum have
invariably been unsuccessful. Very commonly the victim’s
skull may have a lot of foreign material requiring thorough
debridement and cleansing. If the periosteum is intact all over,
split skin grafting may be done. In cases where the periosteum
is missing, the outer table is immediately chiseled down to
bleeding bone and split skin sheet grafts applied. This saves
most of the outer table intact and decreases the morbidity. In our
country, it is very common to see several patients presenting
to a plastic surgeon several weeks or months after sustaining
the injury with severe anemia and dried up calvarium. They
require build up of nutritional status, chiseling of outer
table, keeping the diploe moist and split skin grafting after
the granulations develop (usually 5–7 days). The practice of
burring holes into the outer table for granulations to develop
is to be highly condemned. The granulations are extremely
slow to develop and then become confl uent for grafting to be
successful and the sequestrated bone chips go on coming out
of graft at one place or the other over several months to years,
with the area being always unstable.

Lu (1969)45 reported a successful replant of partially avulsed
scalp in a child with subsequent hair growth. However, the
fi rst successful microvascular replantation was done by Miller,
Anster and Snell (1976).46 Buncke et al. (1978)47 reported
another two cases. Since then, this has become the standard
treatment wherever possible and technical considerations in
avulsed scalp replantation have been described by several
authors.48-52 This is the best form of reconstruction, if feasible

Skin Avulsion Injuries
143
Figures 20A to D: Late result after extensive avulsion injury of scalp was treated with split skin graft.
Please note partial loss of left eyebrow and left pinna
and successful, following an avulsion injury to the scalp. Apart
from preventing the psychological trauma, it not only restores
the scalp but also other structures like forehead, eyebrows,
eyelids, pinna, etc. which are so commonly avulsed along
with hair-bearing scalp. There is greatly reduced requirement
of hospitalization with decreased number of days ‘off work’.
The need for multiple reconstructive procedures is almost nil.
Cheng et al. (1996)50 published the largest series of 20 cases
treated by microvascular surgery and highlighted the need for
multiple teams working together to decrease the operative
time. However, scalp replantations constitute a very small
work load of a microvascular team. Thus, Sabapathy et al.
(2006)51 from Southern India performed six scalp replants
as compared to around 300 extremity replants in a very
busy trauma center during an eight-year period from 1996 to
2004. They have excellently described some of the technical
refi nements in their article, especially the technique of shaving
of the avulsed scalp and control of hemorrhage from the scalp
after the circulation is restored.

In patients where scalp avulsion was partial and the raw
area had been treated by split skin grafts, suffi cient scalp
may be available for tissue expansion to restore the whole of
hair bearing scalp as a secondary reconstructive procedure.
Still smaller defects may be treatable by a rotation fl ap.
However, in present scenario, it is inadvisable to use the
earlier techniques of trying to cover the scalp by multiple
local fl aps. If unfortunately, no worthwhile hair bearing scalp
is available, the patient is left with the only option of wearing
a wig. In patients where scalp wounds have healed with split
skin grafts applied to raw areas over periosteum or after

Types of Wounds and their Management
144
chiseling the outer table of skull, there may be problems of
unstable areas with repeated break downs. These may need
regrafting, overgrafting or even distant free fl aps to make the
area stable. McLean and Buncke (1972)53 and Ikuta (1975)54
reported autotransplant of omentum with skin grafting to
cover denuded skull. Maxwell, Stuber and Hoopes(1978)55
transferred fi rst free latissimus dorsi musculocutaneous fl ap
with microvascular anastomosis to treat the instability. For
partial defects skin fl aps like groin fl ap, etc. have been used.
If left untreated, they run the risk of malignant degeneration
(Marjolin’s ulcer) after several years.

Due to its exposed position on the side of the head,
the pinna is especially vulnerable to avulsion injuries.56
Human and animal bites, motor vehicular accidents and
falls from heights are common causes of external ear
avulsion. A partially avulsed pinna, even if it is attached by
a comparatively very small pedicle, is able to survive and
needs only local wound toilet followed by simple suturing of
the part and contour dressing. Musgrave and Garrett (1967)56
reviewed the conventional methods of treatment of amputated
ears. Microvascular surgical reimplantation is required for
complete detachment or when the pedicle is very small and
insuffi cient. The fi rst successful microsurgical replantation
of external ear was reported by Pennington, Lai and Pelly57
in 1980 and several cases have since been reported.58 A
successful replantation of the pinna results in an immediate
restoration of normal appearance unsurpassed by any other
reconstructive procedure(s). In case of complete or partial
losses, late reconstructions by different techniques are
required after the local areas have healed and scars are soft
and supple. Eyelids can also get avulsed very rarely by one
of the same mechanisms as for pinna. They may need simple
resuturing, replantation or else need reconstruction.59

Avulsions injuries of hand: The economic and esthetic
importance of hand injuries is all too obvious. It not only
drastically reduces the chances of employment and earning
capacity but also affects the psyche of the victim greatly
as the hands, like face, are uncovered parts of the body.
Extensive avulsion injuries of the hand and upper limb as a
whole, whether by road side vehicular trauma or by roller
and wringer injuries in machines at home or industry often
pose great problems in restoration of form and function,
requiring several operative procedures and lengthy physio-
occupational therapy. In patients where the avulsion injury is
limited to loss of skin only, the musculoskeletal unit is intact
and hence the movements of the hand including digits are
preserved. However, during the period of restoration of skin
cover, scarring and stiffness results requiring limb elevation,
pressure garments, active and passive movements, static and
dynamic splints, massage with bland creams and ultrasonic
therapy to soften the scars, etc. by a trained person to restore
normal function.60 End result may still leave a lot to be desired
by the patient and the surgeon alike.

Entin (1955)61 wrote an exhaustive essay on roller and
wringer injuries. He carried out extensive experimental work
on healthy male rats in laboratory and correlated with his
clinical experience to determine the pathogenesis, various
factors involved in the mechanism of production of injury and
the specifi c injury that results, apart from practical clinical
classifi cation and its application to patient care. Roller and
wringer injuries are due to crushing of the limb between
rollers or cylinders. The injury results due to the forces of
compression (because of narrow gap between the rollers),
rotation (produces friction and torque, generating heat as
well) and stripping (due to moving roller sliding the soft
tissue over rigid bony structures; in addition, there is dragging
force due to attempt to withdraw the limb from the machine).
Thus the extent of damage depends upon the gap between the
rollers, force of compression, length of time in rollers, age of
individual (whether skin loose or not), one or both rollers are
geared to motor, force of attempt to withdraw the limb and
any chemicals/foreign bodies entering the wound.61

Avulsion injuries of hand can involve mainly palmar
aspect or dorsal aspect or both (Palmo-dorsal; ‘degloving’)
surfaces of hand.61 While wringer has only one roller geared
to the motor, the roller machines have both rollers geared.
The associated injuries may be tearing of muscles, fracture
of bones, dislocation or ligament tears of joints, injuries to
neurovascular pedicle, grinding of foreign bodies, grease and
dirt into the wound, etc. (Figure 21). The avulsion injuries of
the hand are considered as amongst the most diffi cult injuries
to manage because the tendons and neurovascular pedicles are
injured far away from the site of injury and the damage may be
irreversible. Injuries involving loss of dorsal skin are generally
distally based and paratenon is preserved. It is better that the
avulsed skin is excised and the area split skin grafted taking
care that the graft is applied with fi ngers in fl exion to achieve
full range of motion. Palmar skin avulsions are also treated
by excision and skin grafting. Palmar avulsions are usually
associated with injury to thenar and hypothenar musculature
and may leave residual defi cits. Injuries superfi cial to palmar
aponeurosis accept skin grafts very well. However, if the
tendons or underlying bone are exposed or some tendon grafting
will be required later on, an appropriate fl ap cover in the form
of groin fl ap or distally based radial artery forearm fl ap, etc. is
required. Palmo-dorsal avulsions are more mutilating and very
often accompanied by amputations of digits. They may need
burying the hand into an abdominal pocket and release and
resurfacing in several stages.

Although there is no system for classifying avulsion injuries
of hand, Edstrom (2005)62and some other worker have tried
to apply the most widely used classifi cation system given by

Skin Avulsion Injuries
145
Urbaniak in 1981 for ring avulsion injuries to the whole hand.
In class I injuries, the circulation is adequate while Class II
retain some tissue attachment but with inadequate circulation
and need vessel repair. Class III injuries are those with
complete degloving or amputation and need revascularization
although the outcome may be severely compromised. An
extended Urbaniak classifi cation system compiled by Edstrom
(2005)62 is as follows:

Class I: Circulation adequate.

Class IIa: Circulation inadequate; only digital arteries
damaged.

Class IIb: Circulation inadequate; other structures damaged
as well.
Class IIIa: Complete amputation or complete degloving;
skin avulsion at the level of proximal phalanx and
amputation of the distal interphalangeal joint with intact
fl exor digitorum superfi cialis.
Class IIIb: Complete amputation or complete degloving;
skin avulsion and complete amputation at the level of the
proximal phalanx with severance of both fl exor tendons.

In Class I injuries where the vascularity is intact, simple
suturing may be all what is required apart from standard
wound toilet, etc. In cases where the skin is lost but the
hand as a whole or the avulsed fi nger(s) are viable with their
intact tendon system and joints, provision of skin cover with
a split skin graft or else an appropriate fl ap from the vast
armamentarium of the plastic surgeon is required. Adani
et al. (1995)63 attempted revascularization in the few cases
where the degloved skin was available and the vessels were
not damaged irreversibly by trauma. However, reestablishing
the sensitivity is very diffi cult to achieve despite repair of the
nerves. In class III injuries it is futile to replace the avulsed
skin or sometimes even the amputated digit(s) and a detailed
knowledge of managing a mutilated hand is required to deal
with such injuries. (This is beyond the scope of this chapter
and the reader is advised to refer to Weinzweig and Weinzweig,
200564 and other such works). Ring avulsion injury is a special
type of injury where the metallic ring, a person is wearing,
gets caught in some another metallic projection or hook and
takes away the entire skin and tendons and neurovascular
bundles of the digit. There may be amputation at one or the
other level (Figures 22 A and B).

Avulsions injuries of penoscrotum: Avulsion injuries of the
penoscrotum are devastating to the patient not only physically
but also psychologically. This injury was fi rst described by
Gibbs in 1855 (Finical, 1999).65 It is the laxity of the male
external genital skin having a protective role66 otherwise,
which becomes a liability and leads to degloving injury of the
penoscrotum. The skin of the shaft of the penis is loose from
its root at the pubis to an area just behind the coronal sulcus
where it is continuous with the skin over the glans penis which
is fi rmly fi xed to underlying tissues with no mobility at all.
There is a natural plane of cleavage between the deeper Buck’s
fascia and the overlying loose areolar tissue that surrounds
it. The dartos fascia is in continuity with Colles’ fascia in
the perineum and continues over the abdomen as Scarpas’
fascia. The avascular plane deep to these fascial structures
anatomically determines the pattern of avulsions. Thus, the
degloved skin includes the dartos fascia, the subcutaneous
veins and the loose areolar tissue. The preservation of Buck’s
fascia ensures that both the corpus cavernosum and the corpus
spongiosum including urethra and deep dorsal artery, vein
and nerve are all saved from this injury. These injuries usually
occur on the farm or industry where the loose trousers or
any loose garment tied around the waist of the victim (loin
cloth or “dhoti”) get entangled in a rotating machinery and
Figure 21: Avulsion of palmer skin
Figures 22A and B: Ring avulsion injury

Types of Wounds and their Management
146
twisted off up to the genital region67. The rapidly revolving
gears of the “power take off” machinery forcibly rip off the
clothing taking the loose penoscrotal skin along with it from
behind forwards. Hence, Brown and Fryer (1957)68 called
this as “power take off injury”. The testes, spermatic cords
and the penis gets denuded partially or totally, (Figures 23A
and B) Use of suction devices (Vacuum cleaner) for sexual
arousal has also produced this type of injury. Gonzalez Ulloa
(1963)69 reported a rare case of avulsion during professional
bull fi ghting. Blood loss is minimal because the degloving
occurs in surgical planes superfi cial to Buck’s fascia and deep
to dartos in the scrotum.

The penile skin is best reconstructed by covering with
intermediate thickness split skin grafts from the thigh or
other suitable site after removing the distally based avulsed
skin fl ap.67,70,71,72 This should be done immediately within a
few hours before infection settles. The avulsion injury tears
off the penile shaft skin at its root near the pubis which is
then turned down like a sleeve up to the corona. Sometimes
in uncircumcized patients a large amount of inner layer of
prepuce may remain which has been utilized by some workers
to cover the denuded shaft.67 However, this distally based
skin develops edema which may be prolonged because of
the disruption of lymphatic drainage. Use of avulsed skin of
the penile shaft to cover the denuded area is not advisable
as it invariably becomes necrotic and is always destined to
die. Its removal, control of infection and subsequent split
skin grafting prolongs the morbidity. Only a rim of about
5 mm of skin around the corona is saved for stitching the
graft margin while the rest of the skin is discarded. A single
sheet of 10X20 cm size split skin graft of intermediate to thick
type is usually suffi cient to cover the whole of shaft.73 The
patients are usually operated under spinal anesthesia. The
area is thoroughly cleansed with mild detergent and saline to
remove hair and dirt from the wound.74 The graft is generally
immobilized by ‘tie-over dressing’ with sutures being placed
at the base of penis and the corona. It is preferable to place
the longitudinal junction line of the graft along the dorsum of
penis longitudinally with interdigitations to avoid any straight
line contracture leading to “chordee”. An indwelling foley
catheter of appropriate size is inserted and penis elongated
to its full length before ‘tie-over’ sutures are tied. The penis
has also been covered by burial of the shaft into the abdomen
or into the scrotum or by application of various local fl aps.
Obviously, these techniques are multistage and give bulky
unesthetic organ.

The scrotal skin is extremely elastic and tolerates tension
well. The posterior part of the scrotal skin usually escapes
injury and may be available for either primary closure of the
scrotum (after stretching) over the denuded testes or else may
need augmentation with a small split skin graft in the anterior
region. In either case the results are very good functionally
as well as esthetically. However, if the loss is extensive and
the testes are hanging outside, different techniques have
been utilized to provide cover. The testes may be banked on
either side into the thigh or the groin and later a scrotum is
reconstructed. The implantation into the thigh should be
at different levels for the ease of walking till the scrotum is
reconstructed.75 The burial should be under thin skin fl ap as
otherwise higher temperature may damage the testes. Bilateral
Figures 23A and B: (A) Completely denuded penis and testes; (B) Penile and scrotal avulsion with loss of one testis

Skin Avulsion Injuries
147
fl aps from the thigh have been used to construct scrotum.
The pocket of scrotum may also be reconstructed by tissue
expansion techniques. These are multi-staged techniques.
Testes may also be covered with split skin graft resulting in
a single staged operation with good functional and esthetic
results. The testes are stitched together with a few absorbable
sutures to avoid bifi d appearance and ease of application
of split skin graft. The graft application is a little diffi cult
because of the irregular surface. Traumatic severance of
the testis along with penoscrotal skin avulsion is extremely
rare. Because of the great psychological signifi cance and the
younger age group of the individuals, with the availability
of microvascular techniques, attempts have been made to
reimplant the severed testicle(s) with satisfactory results.76,77

Avulsions injuries of heel and sole of foot: Owing to
the specialized anatomical nature of the plantar skin and
consequently the problems of reconstruction (restoring like
with like tissues) the avulsion injuries of the sole and heel pad
should be recognized as an entity in themselves.78 The skin on
the dorsum of foot is thin, mobile, nonspecialized with very
thin layer of subcutaneous fat. On the other hand, the heel
and sole of the foot are areas which are weight-bearing and
Figures 24A to D: (A) Distally based avulsion of sole; (B and C) Conservative management has produced healthy granulations; (D) Whole of
weight-bearing sole has survived while the raw area on nonweight bearing area of foot has been split skin grafted

Types of Wounds and their Management
148
Figures 25A to C: (A) Proximally based avulsion of sole. Please compare the plane of avulsion and hence the thickness of avulsed fl ap as
compared to Figures 24A and B; (B) After debridement and development of granulations; (C) Result after application of skin graft
Figures 26A and B

Skin Avulsion Injuries
149
subject to trauma by footwear. The skin of the sole in general
and heel pad in particular consists of very thick epidermis
due to thick keratin layer. Just deep to the dermis, there are
superfi cial and deep subcutaneous layers separated by a thick
horizontal septum composed of bundles of fi bers. The deeper
layer contains the thick septa, the plantar aponeurosis and is
attached to calcaneum. Furthermore, a complex of fi brous
elastic septae running perpendicular to the surface connects
the plantar skin to the underlying plantar aponeurosis.
Presence of semisolid loculi of fat interspersed between the
septae helps in dispersing the weight of the individual during
walking. This limits the effect of shearing forces to which the
sole is subjected in walking. In addition, presence of an intact
sensation through sensory and proprioceptive nerve fi bers
is highly important for maintaining a stable weight bearing
surface.78,79

When avulsion occurs in this region, a conservative
approach may save more of this specialized skin which may
ultimately cover a weight-bearing area with surrounding non
weight bearing raw areas being covered with skin grafts or fl aps
of nonspecialized skin (Figures 24A to D and 25A to C). More
extensive defects in the region of weight-bearing heel pad and
sole require fl ap cover. Because of anatomical differences of
the imported skin fl aps, this type of repair is not without its
problems. Jeng and Wei (1997)78 gave a classifi cation scheme
for foot avulsion injuries based on anatomical considerations
and proposed treatment options for each group.

Group I Suprafacial avulsion: skin grafting. The avulsed
fl ap, if available, may be converted into a free full thickness
graft. Or else, split skin graft from thigh or other suitable
area.

Group II Subfacial avulsion with proximally based fl ap:
Primary tension free repair. The avulsed fl ap is redraped
into its original position without any tension.

Group IIIa Subfacial avulsion with distally based fl ap:
Primary microvascular vascularization is to be attempted.
If it fails and necroses, secondary reconstruction is required
as for Group IIIb.

Group IIIb Subfacial avulsion with distally based fl ap, not
suitable for revascularization and failures of Group IIIa:
Secondary reconstruction.

A number of options are available at present to treat the
avulsion injuries of the sole.25,79-81 These can vary from split
skin grafts to local (instep island fl ap, fi llet fl ap, etc.), regional
(distally based superfi cial sural artery fl ap) or distant (cross
leg fl ap) pedicled fl aps to distant free fl aps (Latissimus dorsi
muscle fl ap, anterolateral thigh fl ap or a perforator fl ap). These
may be done immediately after thorough debridement or after
initial conservative debridement and multiple dressings over a
period of time. Additionally, fl ap covers are sometimes required
in chronic cases where the initial management was less than
satisfactory and the patient develops unstable scars and ulcers,
especially over weight-bearing areas, after the patient becomes
ambulatory (Figures 26A to D). Sommerlad and McGrouther
(1978)80 found that no form of sole replacement appeared
satisfactory and that most patients avoided weight bearing
on the area. Unfortunately, despite several new techniques
being developed since their study, this is true to a large extent
Figures 26A to D: Old case of avulsion of heel pad being treated by instep island fl ap
Figures 26C and D

Types of Wounds and their Management
150
even today. This is not surprising because the sole skin is
irreplaceable. Hence, the approach should be conservative. It
should be preserved wherever possible until necrosis declares
itself as even a centimeter of it may make the life comfortable
by covering the weight bearing area.
SOME OTHER AVULSIONS
Although this chapter concerns only with the avulsion injuries
of skin, for the sake of completion, it will be appropriate
here to just mention some other conditions where the word
“avulsion” is used. Apart from skin and subcutaneous tissues,
a number of other structures like the nails, major nerves and
nerve trunks, teeth and bones may also get avulsed. Surgeons
also use the mechanism of traumatic avulsion in some
operations. Thus, saphenous veins are avulsed in patients of
varicose veins. An ingrowing toe-nail is avulsed in patients
with chronic paronychia. Nail plate can be torn from the nail
bed by an injury. The nail bed forms a germinal layer which
hardens as the cells acquire keratin and a new nail forms. Till
then, the exposed nail bed which is highly sensitive should
be covered with non-adherent dressings. Brachial plexus may
be avulsed from the spinal cord during delivery or in motor
vehicular accidents. A nerve may also be avulsed to treat its
hyperactivity. A tooth (or teeth) may be avulsed from the
socket.

An avulsion fracture is an injury to the bone at the site
of attachment of a ligament or tendon. When forcible pull
is applied to a ligament or tendon, a small fragment of the
bone tears away from the main mass leading to an avulsion
fracture. A ligament may be pulled due to the application of
an external force while a muscular contraction stronger than
the force holding the bone together may lead to a piece of
bone coming out attached to the tendon. Highly trained
athletes can produce a far greater force capable of breaking
and avulsing the bone. Avulsion fractures can occur anywhere
in the body but are common in some areas, e.g. pelvis. The
avulsion fractures of the pelvis generally affect the anterior
superior iliac spine, anterior inferior iliac spine and the ischial
tuberosity. The Sartorius, rectus femoris and the hamstrings
originate from these areas respectively. Since these fractures
commonly affect the young athletes, they are also known as
‘sprinter injuries’.
OUTCOME OF AVULSION INJURIES:
EARLY AND LATE
The major degloving or the avulsion injuries require prolonged
hospitalization for primary treatment and result into a lot of
delayed problems/chronic disability for the patient:
1. Morbidity: The massive avulsion injuries are a cause of
great morbidity and sometimes mortality to the victim.
They not only require multiple operations for complete
wound closure but also suffer from the pain, discomfort
and immobilization of repeated dressings over a period
of several months. In addition, there are severe esthetic
defects as discussed later. Prolonged measures for
several months to a year or so are required before the
grafts mature and the scars become soft and pliable and
mobile over the bed.

2. Contour defects: The avulsion injuries are treated by
skin grafts to close the wounds and are generally applied
onto the muscles directly. This leads to a sudden change
in the circumference of the limb at the junction of
proximal /distal uninvolved areas and the avulsed skin
grafted area. Thus, contour defects are least obvious in
thin and more obvious in fatty individuals. In addition,
the muscle bellies and their unesthetic contractions are
visible under the skin graft (Waikakul, 1997).21

3. Scars: There may be unesthetic scars which may be
atrophic or hypertrophic. In hairy individuals the healthy
skin appears contrasting with the shiny, hyperpigmented
and hairless skin of grafted areas. The junctional areas of
two grafts and the areas which heal by epithelialization
from the graft margins, frequently hypertrophy requiring
prolonged pressure therapy. Meshed skin grafts also give
a cobble-stone appearance. Foreign bodies impregnated
in the wound bed and not removed completely at the
time of debridement or before application of graft also
incite a lot of foreign body reaction leading to fi brosis
and adherent scars and may appear as traumatic tattoos.
The donor sites of skin grafts and fl aps also add their
share of scars on the body. Covering of the scarred areas
with modifi cations of dress may be required.

4. Unstable areas: Areas which heal by epithelialization
from the graft margins lack dermis. This leads to their
frequent breakdown with the slightest of trauma and
day to day shearing forces. The areas over subcutaneous
bones and the ones over joints are also vulnerable.
Adherent scars may break down easily. Unstable areas
also form over joints when there are contractures and
patient tries to use the joint for full range of motion.

5. Contractures: These form due to secondary contraction
of grafts as well as due to unopposed actions of tendons
whose counterparts have been lost in avulsion injury.
The joints might have opened up as a result of injury
and damaged and may lead to joint deformity.

6. Distal edema: In avulsion injuries of extremities where
there is circumferential loss of skin and the grafts have
been applied all around, there is edema in the distal
limb due to poor lymphatic return and deep scarring.
It is desirable that these patients are forewarned of this
problem and advised to do massage of the limb from
distal to proximal, always wear pressure garments and

Skin Avulsion Injuries
151
avoid injury or infection as these may precipitate further
edema. Sometimes circumferential tightness may be
improved by longitudinal incision in the graft, very
much like fasciotomy and application of skin graft or a
fl ap. This may improve distal edema.
7. Loss of joint mobility: Absolute immobilization of joints
is required for successful graft ‘take’ and to avoid trauma
to recently applied grafts while active and passive joint
movements are desirable to avoid decreased range of
joint motion. There may be a compromise between the
two. A number of patients develop loss of nearby joint
mobility (joint stiffness) which may be signifi cant and
may need prolonged physiotherapy with or without
further reconstructive surgery. It may not be treatable at
all if the joint was exposed or traumatized in initial injury.
8. Loss of neurovascular structures and musculotendinous
units may lead to various functional and sensory
problems depending on the extent of loss and probability
of regeneration.
9. Fractures: A number of patients present to the surgeon
with fractures associated with avulsion injuries. These
fractures may be at the site of avulsion injury or else
unrelated at different site(s). The need for external fi xators
for the management of avulsion injury wound dictates
that an orthopedic surgeon and a reconstructive plastic
surgeon are together involved in the management of the
patient right from the beginning. The immobilization
required for fractures also complicates the management,
especially the mobility of joints, physiotherapy and
after care of grafted areas, etc. The fractures may also
lead to limb shortening.
10. Insensate areas: When the avulsion injury involves
sole or the palmar aspects of feet and hands, there are
problems related to sensation. The sensation does return
back over a period of one year or more depending upon
whether the coverage of these areas was done with
grafts or fl aps. With grafts, the sensation returns earlier
but is better in fl aps although slower to come back. In
case the nerves were lost during the avulsion injury, the
sensation may not return.
11. Unpadded areas: Since an avulsion injury takes away
the subcutaneous fat, areas in the body which need
padding for normal wear and tear and function, e.g.
gluteal region or heel pad or fi nger tips require surgical
intervention to restore the padding.
12. Loss of specialized structures like scalp, pinna, eyebrows,
testis, heel and sole, fi nger tip, etc.
13. Amputations: Patients may end up in amputations either
at the initial stages of treatment or else later on due to
constant morbidity, an amputation of the limb may be
considered better.
14. Malignant transformation: Marjolin’s ulcer can develop
in patients who have unstable scars with repeated break
downs over several years or decades (Figure 27). It is
advisable to treat all contracting bands and unstable areas
and allow the scars to become mature, soft and supple
before the treatment is called off. Additionally patient
must be advised to inform the clinician immediately if
any wound recurs.
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Types of Wounds and their Management
152
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• Genesis of Diabetic Foot Ulcer
• Impaired Wound Healing and Infection in Diabetes Mellitus
• Laboratory Investigation
• Economics of Treatment of Diabetic Foot
• Management
• Charcot Foot
Introduction
Our country has a diabetic population of over 42 million
which is highest in the world. Annual incidence of foot ulcer
is around four percent. Average healing time of foot ulcer is
four to six weeks. Seventy five to eighty percent of all non
traumatic amputations are done in diabetic patients.1
Genesis of Diabetic Foot Ulcer2
Intrinsic factors
Extrinsic factors
Bony prominence
Joint deformity
Callus
Altered tissue properties
Previous foot surgery
Neuro-osteoarthropathy
Inappropriate foot wear
Walking bare foot
Falls and accidents
Objects inside shoe
Activity level
Factors Which Precipitate Diabetic Foot Ulcer
(Figure 1)
1. Loss of sensation due to peripheral neuropathy. Normal
vibration threshold is < 15 ngh. In mild neuropathy, it is
15-25 ngh, moderate 25-40 ngh and in severe neuropathy,
it is > 40 ngh.
2. Decreased blood flow to legs occurs due to peripheral
vascular disease as a result of accelerated atherosclerosis
in diabetes mellitus.
3. Foot deformities leading to increased plantar pressure and
abnormal pressure points.
4. Past history of callus or foot ulcers.
5. Prior amputation.
6. Limited joint mobility.
7. Infection and cellulites of foot.
Risk Factors for Amputation
• Neuropathy – 78 percent
• Minor trauma – 77 percent
• Deformity – 63 percent
• Callus – 30 percent
• Ischemia – 35 percent
• Edema – 37 percent
Figure 1: Risk factors for diabetic foot ulcer
Medical Management of
Diabetic Ulcer
PG Raman
15
Chapter

Chapter 15
Medical Management of Diabetic Ulcer 
155
Schematic Diagram Showing Development
of Diabetes Foot Ulcer
Neuropathy
↓
Trauma
↓
Ulcer
↓
Impaired healing due to reduced blood flow
↓
Infection
↓
Leading to diabetic foot ulcer
Risk Factors for Peripheral Vascular Disease3
Modifiable
Non-modifiable
Increase BMI
Smoking
Elevated TG
Elevated fasting
blood glucose
Elevated LpA
Elevated APCB-100
Elevated viscosity
Increased platelets
aggregations
Poor and delayed follow-up
Increased age
Male gender
Menopause
Having peripheral arterial disease in
the contralateral leg
Risk Factors for Diabetic Neuropathy4
Modifiable
Non-modifiable
Hyperglycemic
Hypertension
Increased cholesterol
Smoking
Heavy alcohol intake
Old age
Longer duration of diabetes
mellitus
Greater height
Wagner’s Classification of Foot Ulcer5
Grade
0
No ulcer in a high risk foot
1
Superficial ulcer
2
Deep ulceration penetration up to tendon, bone or joint
3
Osteomyelitis or deep abscess
4
Localized gangrene
5
Extensive gangrene requiring major amputation.
Risk Categorization of Diabetic Foot Ulcer4
Category
Risk profile
Check-up frequency
0
No sensory neuropathy
Once a year
1
Sensory neuropathy
Every 6 months
2
Sensory neuropathy
with peripheral vascular
disease/deformities
Every 3 months
3
Previous ulcer/
amputation
Every 3 months
Impaired wound healing and
­infection in diabetes mellitus
Factors Contributing to Infection
in Diabetes
• Defective leukocyte bactericidal function
• Decreased phagocytosis
• Polymorph nuclear chemotaxsis is impaired
• Antibody mediated cellular cytotoxicity is impaired.
• Decreased enzyme activity of super oxide dismutase/
myeloperoxide lysozyme

Host factors contributing to wound infection are hyper­
glycemia, glycosuria, decreased skin and liver glycogen
levels, dehydration, electrolyte changes, ketone bodies, lactic
acidosis, catabolic state and negative nitrogen balance due to
insulin deficiency.
Nonulcer Pathologies
Skin infection, deformities of bone and nail pathology are
some nonulcer problems which provide a portal of entry for
infection.
Organism commonly involved in foot ­infection6 are:

1. Staphylococcus

2. Streptococcus

3. Gram-negative organism

4. Anaerobic infection (foul smelling)
For further details the reader is advised to refer to the next
chapter.

In diabetics, there is alteration in physiological processes
namely connective tissue formation, cellular activity and
growth factor activation. Diabetic ulcers are stuck in the
inflammatory phase of wound healing process. During this
delay there is cessation of epidermal growth and migration
over the wound surface. There is increased level of matrix
metallic proteinase which activates proteolytic activity and
inactivate growth factors. There is deficiency of growth factor,

Section 3
  Types of Wounds and their Management
156
cytokines in the wound. Impaired wound healing is due to
abnormal protein synthesis, cellular activity and growth factor
secretion. Growth factors like platelet derived growth factor
(PDGF) and fibroblast growth factor been found to be altered
or absent in diabetic foot ulcer.
Laboratory investigation
Scheme for Evaluation
1. Neuropathy evaluation:

– Sensory: Biothesiometry.

– Motor: Electrophysiological test

– Autonomic: Quantitative sweat test
2. Systolic ankle brachial index:

– Normal > 1.0

– Claudication > 0.7

– Severe ischemia with claudication > 0.05

– Gangrene with ulcer > 0.1
3. Transcutaneous PO2 on the dorsum of foot site on tropic
lesion 25 to 30 mm Hg indicate poor prognosis.
4. Doppler ultrasonography evaluation of large arteries.
5. Radiography for osteo articular disease and arterial
calcification.
6. Computerized foot mapping

• Can predict a high pressure area month before actual
pathological changes.

• Can detect sub-clinical pressure areas in already
ulcerated foot.

• Can even suggest design for insole. Can measure the
effectiveness of prescribed foot wear.
7. Sensitometer: It is an electric tuning fork which quantifies
neuropathy as follows:

Normal: 0–15 volts/microns

Mild: 15–25 volts/microns

Moderate: 25–35 volts/microns

Severe: 35–50 volts/microns
8. Semmes Weinstein 10 gm mono filament: It is the
simplest, cheapest and accurate for neuropathy.
9. Tuning fork is used to check vibration perception in the
feet.
10. Thermotop is used to check temperature perception.
11. Femoral arteriography.
12. Doppler study of femoral artery and its branches.
Economics of treatment of
­diabetic foot (figure 2)
Cost of treatment for complete healing7
Rough estimate of
cost
Type of lesion
Treatment
Direct cost in
US Dollars
Neuropathic ulcer
Ambulatory
56
Infected neuropathic foot
Ambulatory
165
Advanced diabetic foot
Salvage
1080
Advanced diabetic foot
Amputation
960
Advanced diabetic foot
salvage
Salvation
and then
amputation
2650
Neuro-ischemic foot
Bypass
1960
Management
It is a team approach between podiatrist, diabetologist, surgeon,
nurse and educator.
Principles of Management
• Off loading by wheel chair, crutches, walker, total contact
cast for long standing nonhealing noninfected planter
ulcer.
• Off loading, rest to affected foot, callus removal, eradication
and redistribution of weight bearing forces.
• Use of insoles giving cushioning to the feet and allow
distribution of planter pressure made up of micro cellular,
rubber, ethyl vinyl acetate or polyethylene foam. Needs to
be replaced three to six months. Wound dressing done by
gauze, impregnated gauze, cotton and packing strips.
Figure 2: Diabetic foot and associated problems

Chapter 15
Medical Management of Diabetic Ulcer 
157
3. Treatment of infections:
Staphylococcal/streptococcal
Nonlimb threatening infection
Polymicrobials
Limb threatening infection
Management of infection:14 In mild infection with limited
cellulitis—cephalexin, clindamycin, ciprofloxacin, oflaxacin,
linezolid can be used. If MRSA is grown, two of the following
oral therapies can be used—sodium fusidate, rifampicin,
trimethoprim, doxycycline with topical mupirocin.

In severe infection, patient has to be hospitalized and given
IV wide spectrum antibiotics. Piperacillin/tazobactum can be
given for 9-10 days.

Or Ampicillin/Sulbactum × 9 days

If admission of patient is not possible Ceftriaxone IM with
metrondiazole for one week is given.

Urgent surgical intervention is needed for infected
sloughy tissue, localized abscess and gas gangrene. Diabetic
osteomyelitis is to be treated surgically. Necrosis of foot has
grave implication and needs amputation (Figures 3 and 4).
4. Use of advanced wound care products
a. Recombinant PDGF-BD-Becaplermin: It is a potent
mitogen, chemotactic agent for connective tissue, stromal
cells and it helps to increase wound vascularization by
stimulating endothelial cells proliferation, movement and
tube formation.
b. Living skin equivalents:10 Biological skin substitutes
produced from fibroblasts and keratins available in
epidermal, dermal and composite forms LSE are
noninvasive which do not require anesthesia. Dermograft
and apligraph are used in this category.


Apligraf has both epidermal, dermal components but
lack in hair follicle, blood vessels and sweat glands.

The characteristic of an ideal dressing is to remove excess
of humidity, allow for gaseous exchange, provide thermal
insulation and prevent secondary infection.

Newer dressings include following materials (will be
discussed in later chapters):

1. Film, foam, nonadherent dressings, hydrogels, hydro­
colloids.

2. Growth factors like platelet derived growth factor,
epidermal growth factor, fibroblast growth factor,
insulin like growth factor, ester and apligraf.
The broad guidelines for management are:
1. Debridement: Remove nonviable tissue, remove all
necrotic, avascular tissue in order to achieve a red,
granulating wound bed. This is discussed in detail in
subsequent chapters.
2. Pressure offloading: Ulceration occurs in high areas of
insensate foot. Hence, reduction of pressure is needed by
using total contact casting.
Total Contact Casting9
Advantages
Disadvantages
Effective pressure reduction
Skill and time required for
application
Patient mobility is there
Secondary skin lesions due
to cast irritation
Inability to assess the wound
daily
Figure 4: Gangrene
Figure 3: Diabetic foot ulcer

Section 3
  Types of Wounds and their Management
158


Cytokines, growth factors, extra cellular matrix proteins,
protease inhibitors and vaso active compounds are also
used.
c. Microbiological control11
Topical Antimicrobial

– Povidone iodine is effective antibacterial

– Cadexomer iodine consists of microspheres formed
from a three dimension lattice of cross linked starch
chains

– Silver compound are used as antibacterial

– Mupirocin is active against gram positive bacteria,
including methicillin resistant staphylococcus aureus.
5. If arterial flow is defective, angioplasty is valuable and
improves, arterial flow in ischemic ulcer.
6. Osteomyelitis11 is usually associated with ulceration and
cellulitis in the initial stage X-ray may be normal but MRI
can detect early changes. If clinically, a sterile probe is
inserted into ulcer it penetrates bone. This test is 66 percent
sensitive and 85 percent specific.
7. Vacuum assisted closure12 – In this, VAC pump is applied
to create negative pressure to the ulcer through a tube
and foam sponge that can be applied to the ulcer over the
dressing and sealed with plastic film to create a vacuum to
improve vascularity and stimulate granulation tissue.
8. Hyperbaric oxygen13 – Therapy also reduces the number of
major amputation in ischemic diabetic foot. It accelerates
the healing of ischemic diabetic foot ulcer.
Charcot foot8 (figure 5)
Neuroarthropathy: It is painless, progressive arthropathy of
single or multiple joints caused by underlying neuropathy.
Affects often tarsal-metatarsal region followed by metatarso
phalanygeal joints and ankle subtalar joints. Precipitating factor
is minor trauma. It presents with hot swollen foot, as rocker foot
deformity and produces subluxation of tarsus downwards.

Charcot neuroarthropathy8 is a noninfectious progressive
joint destruction. There is a pathological fracture, joint
dislocation. Etiology is neuro traumatic or neurovascular.
Hyperemia due to autonomic neuropathy results in excessive
bone resorption, resulting in weakening of bone. Dorsalis
pedis pulsation is good. It passes through three clinical phases
namely acute coalescence and remodeling.

Acute phase: Presents with edema, erythema, local warmth
and joint crepitus. Coalescence begins when skin temperature
normalizes and joint crepitus diminishes. Remodeling occurs
in months to years and is characterized by joint stabilization.
Resolution of charcot neuroarthropathy result in deformed
foot with obvious bony prominences susceptible to ulceration.
Treatment
Complete immobilization for eight weeks and nonweight
bearing. Failure to immobilize the foot leads to rocker
bottom deformity. If the above measure fails to prevent joint
dislocation, arthrodesis of involved joints may provide stable
platform for ambulation.
Ten Commandments for Preventing
Diabetic Foot Ulcer (Figures 6 and 7)
Two minutes foot examination is a must daily for a diabetic
patient in order to prevent foot lesions:
• Look for ulcer, callus, blister, edema
• Check nails for fungal infection, in growing toe nails
• Identify foot deformity for prominent metatarsal heads,
claw toes, poor fitting shoes, walking pattern, find any
defect, treat and educate the patient.
ACKNOWLEDGMENT
I am thankful to Dr.A.Sundaram, Retd. Professor of Medicine,
Kilpauk Medical College, Chennai for providing me the
photographs on Diabetic Foot.
Table 1: The changes in the Charcot foot have been divided
into five stages10
Stage
Findings
0
1
2
3
4
Swollen, warm often painful foot
Periarticular cyst, erosion and diastasis
Joint subluxations
Joint dislocation and collapse of longitudinal arch of foot
Healed, stable end result
Figure 5: Charcot foot

Chapter 15
Medical Management of Diabetic Ulcer 
159
Figure 6: Ten commandments
Figure 7: Ten commandments note
REFERENCES
1. KK Suresh. Diabetic Foot in Type-2 Diabetes- Urban-Rural-
Microlab Publication; 2004. pp. 232-8.
2. Pendsey SP. Diabetic Foot, RSSDI Text Book of Diabetes
Mellitus; Edited by B.B.Tripathi; 2nd edn. Vol. 2;Chapter 64;
pp. 959-72.
3. Raman PG. The Diabetic Foot; Chapter 44 in Diabetes Mellitus;
3rd edn. AITBS Publisher; 2004. pp. 328-32.
4. AK Das, Thomas Mathew, Prasantha G. Neurological Com­
plication of Diabetes Mellitus; Edited by B.B.Tripathi and
H.B.Chandalia; 2nd edn. 2008;2:1065.
5. Wagner EW. The Dysvascular Foot a System for Diagnsosis
and Treatment; Foot Ankle 1981;2:64-7.
6. Grayson ML. Diabetic foot infections anti microbial therapy -
Infectious Disease Clinics of Nothern America - Philadelphia
PA WB Saunders; 1995. pp. 143-62.
7. Pendsey SP. Indian Scenario - The Diabetic Foot in Complications
of Diabetes in Indian Scenario Nidus, 1999; Diabetology
Initiative in Diabetology Proceedings.
8. Sanders LJ, Frykberg RG. Charcot Neuroarthropathy of
the Foot in Bowker JH Pfeifer MA Eds. Levin Oneal’s; The
Diabetic Foot 6th edn. St. Louis Mosby; 2000. pp. 467-82.
9. Nabuurs - Franssen Mlt Sleeqes R Huij Berts MS, et al. Total
Contact Casting of the Diabetic Foot in Daily Practice - a
Prospective follow up study Diabetic Care 2005;28(2):243-7.
10. Vevej A. Falanga V, Arun Strong DG, et al. Graft skin a human
equivalent is effective in the management of non infected
neuropathic diabetic foot ulcers - a prospective randomised
multicenter clinical trial diabetes care 2004;24(2):290-5.
11. Embil JM, Rose G, Trepman E, Math MC, et al. Oral anti-
microbial therapy for diabetic foot osteomyelitis. Foot Ankle
2006;207(10):771-9.
12. Arm Strong DG, Lavey LA. Negative pressure wound therapy
after partial diabetic foot amputation a multicenter RCT. Lancet
2005;366(9498):1704-10.
13. Kranke P, Bennett M, Roeckl Wiedmann I. Debuss. Hyper
Baric Oxygen Therapy for Chronic Wounds; Cochrane Data
Base Sept. Review 2004 (2) CD 004123.
14. Joseph WS, Lefrock JL. The pathogenesis of diabetic foot
infections immunopathy, angiopathy, neuropathy. Joint Foot
Surgery 1987;26:281-90.

• Pathophysiology of Infection
• Microbiology

– Clinical Evaluation of Infected Diabetic Foot

– Wound Cultures
• Assessing Severity of Infection
• Bone Infection Associated with
Diabetic Foot
• Treatment

– Treatment of Infection

– Topical Therapy

– Systemic Antibiotic Therapy

– Surgical Treatment

– Treatment of Osteomyelitis

– Adjunctive Therapies
INTRODUCTION
India is the world’s diabetes capital with an estimated 50.76
million people aged 20 to 79 years with diabetes.1 Worldwide,
it accounts for an amputation every 30 seconds.2 Fifteen
percent of all diabetics have a foot ulcer at least once in their
lifetime that gets infected with high morbidity and mortality.
The leg amputation rate is 15 times more in diabetic patients
and uncontrolled diabetes is the leading cause of proximal non-
traumatic amputations.3 Of all late complications of diabetes,
foot problems are probably the most easily preventable.
These include foot ulcers, gangrene, Charcot arthropathy and
neuropathic edema.4 Although not all diabetic foot ulcers are
initially infected but because of their anatomic location, they
easily become infected. This may start as a minor infection
and progress to become limb or life-threatening if not managed
properly specially in the presence of metabolic disturbances
associated with diabetes. Hence diabetic foot infections require
careful attention and coordinated management, preferably by
a multidisciplinary foot-care team including an infectious
diseases specialist or a medical microbiologist. Optimal
screening and management can potentially reduce morbidity,
hospitalization and incidence of major limb amputations.
Majority of the diabetic ulcers can be attributed to a clinical
triad of peripheral sensory neuropathy, trauma and foot
deformity. Other factors that may predispose to ulceration are
ischemia, callus formation, and edema. Flow chart 1 shows the
role of various factors in the etiology of diabetic foot ulcer.
PATHOPHYSIOLOGY OF INFECTION
A diabetic foot infection is defined as any inframalleolar
infection in a person with diabetes mellitus. This includes
paronychia, cellulitis, myositis, abscesses, necrotizing fasciitis,
septic arthritis, tendonitis, and osteomyelitis.5 The most
common and characteristic lesion, however, is the infected
diabetic “mal perforans” foot ulcer or neuropathic ulcer.6 Once
protective epidermal layer is breached, bacteria that colonize the
skin can enter dermal and subcutaneous tissues. Some evidence
suggests that wounds progress from uninfected to infected along
a continuum, with an increasing ‘Bacterial bioburden’ leading
to ‘critical colonization’ (100,000 bacteria per gram of tissue)
and ultimately overt infection.7 This infection may spread by
contiguous extension to involve deeper and more proximal
tissues including bone. Factors that may predispose diabetic
patients to infection in the foot are vascular insufficiency, poor
foot practice, fungal infections of skin and nails, obesity and
poor glycemic control (Flow chart 1).8
Diabetic Foot Infections
TD Chugh, Ashish Kumar Duggal, Shalini Duggal
16
Chapter

Chapter 16
Diabetic Foot Infections 
161
MICROBIOLOGY (Tables 1 and 2)
Aerobic gram-positive cocci are the predominant micro-
organisms that colonize and acutely infect breaks in the
skin. S. aureus and β-hemolytic streptococci (groups A, C,
G, and especially group B) are the most commonly isolated
pathogens.9 This is particularly true for patients presenting
with acute infections, and those who have not recently
received antibiotic therapy. As the wound becomes chronic;
and with multiple courses of antibiotics, colonizing flora
becomes polymicrobial with often 3 to 5 isolates/sample.
Facultative gram-negative bacilli (Proteus spp, Enterobacter
spp, Escherichia coli, and Klebsiella spp) are the predominant
aerobic pathogens besides usual gram-positive cocci.10
Among the obligate anaerobes, Peptostreptococcus spp,
Prevotella spp, and Bacteroides spp, including those of the
B. fragilis group, are recovered frequently. The frequency
of isolating anaerobic bacteria is greatest in patients with
severe infections, particularly those in whom infection
involves necrotic gangrenous tissue and amputation is often
required.11 Pseudomonas aeruginosa, Acinetobacter spp, and
other antibiotic-resistant facultative non-fermenting gram-
negative bacilli are common in chronically infected wounds
particularly when soaked or treated with wet dressings.6
Similarly,
Methicillin-resistant
Staphylococcus
aureus
(MRSA) is isolated from patients with chronically infected
ulcers that have persisted despite multiple prior courses
of antimicrobial therapy.12,13 These resistant bacteria are
acquired nosocomially or emerge from endogenous flora
during repetitive hospitalization and antibiotic treatment. This
has important clinical implication while selecting optimal
antimicrobial therapy.

The role of relatively avirulent bacteria, many of which are
part of skin flora (Staphylococcus epidermidis, enterococci,
viridans streptococci, and Corynebacterium spp) should
be interpreted in the clinical context. Percent frequency of
various bacterial pathogens from diabetic foot infections
varies widely.6
Clinical Evaluation of Infected Diabetic Foot
The evaluation of a patient with diabetic foot should include
local examination of the ulcer and evaluation of neurological
and vascular status of the limb. An adequate description of
ulcer characteristics: size, depth, appearance, location, nature
of secretions and odour should be noted. It is important to
differentiate between a neuropathic and ischemic ulcer.14
As mentioned earlier not all diabetic foot ulcers are infected
Flow chart 1: Pathophysiology of infection and ulceration in foot in a diabetic patient

Section 3
  Types of Wounds and their Management
162
and identification of infection in a chronic wound can be a
challenge since the clinical assessment for infection in chronic
wounds differs from acute wounds. In addition presence of
neuropathy and vascular disease in diabetics can alter the
physical signs of the ulcer. The warmth and hyperemia due
to neuropathy may be misinterpreted as cellulitis. Arterial
insufficiency can also alter the appearance of the foot and
obscure infection. Rubor may reflect vascular insufficiency
rather than inflammation, and conversely pallor may mute the
erythema of acute infection. Also, signs of systemic toxicity
generally do not accompany diabetic foot infections except in
very severe life-threatening infections. The diagnostic clinical
features of infection in diabetic foot ulcers are purulent
discharge, foul odour, crepitation, sinus tract and delayed
wound healing.6

Besides assessing for presence of infection it is important
to evaluate other factors that may influence the healing of
the wound. The goal is not only to determine the clinical
extent and microbiology of the wound but also the biology
or pathogenesis of the wound. Altered foot biomechanics,
vascular (especially arterial) disease, presence of neuropathy
and presence of any systemic consequences of infection,
should be taken into consideration.6
Wound Cultures
Culturing a clinically uninfected wound is unnecessary, unless
the purpose is to seek the presence of an epidemiologically
significant organism such as MRSA.15 In clinically infected
wound, specimen should always be obtained for culture to
identify causative organisms and guide antibiotic therapy.6
Unfortunately, clinicians often fail to obtain wound cultures,
including cases severe enough to warrant hospitalization. It
is argued that culturing a diabetic foot infection is futile as
foot ulcers, whether infected or not, will contain multiple
commensal or colonizing bacteria. In chronic wounds, culture
will usually grow mixed flora but even in these cases culture
results will help to tailor and constrain antibiotic regimens.
Table 1: Antimicrobials used in treatment of diabetic foot infections
Antimicrobial agent
Spectrum of activity
S.aureus*
Streptococci
Enterobacteriaceae
Pseudomonas
Anaerobes
Cloxacillin (O,P)
++++
+++
0
0
++
Amoxicillin-Clavulanate (O,P)
++++
++++
++
0
+++
Cephalexin (O)
++++
++++
++
0
++
Clindamycin (O,P)
+++
+++
0
0
++++
Trimethoprim/sulfamethoxazole (O,P)
+++
++
+++
0
+
Levofloxacin (O,P)
+++
+++
++++
++
+
Cefoxitin (P)
+++
+++
+++
0
+++
Ceftriaxone ( P)
+++
+++
++++
0
++
Ampicillin/sulbactam (P)
++++
++++
+++
0
++++
Linezolid (O,P)
Ticarcillin/clavulanate (P)
++++
++++
++
++++
++
Piperacillin/tazobactam (P)
++++
++++
++
++++
++
Ertapenem (P)
++
++
++++
0
++
Linezolid (O,P)
++++
++++
0
0
0
Imipenem-Cilastatin/Meropenem (P)
++++
++++
++++
++
+++
Metronidazole (O,P)
0
0
0
0
++++
O- Oral, P- Parenteral, * Glycopeptides (Vancomycin, Teicoplanin) and Linezolid to be considered for Methicillin resistant strains

Chapter 16
Diabetic Foot Infections 
163

It is important to obtain adequate and reliable specimens
for culture from foot ulcers. Cultures from superficial wounds
should be collected by rolling a cotton swab across the surface
of the ulcer after proper cleansing and debridement. However,
the hostile environment of the air filled cotton swab inhibits
the growth of anaerobes and fastidious organisms thereby
reducing the sensitivity of the culture. For collection of soft-
tissue specimens from an infected diabetic foot ulcer, cleanse
and debride the lesion, obtain specimens from the debrided
base by a curette or biopsy.6 If swabbing the debrided wound
base is the only available culture option, first thoroughly rinse
wound with normal saline. Then using a swab designed for
culturing aerobic and anaerobic organisms, rotate the tip in
an area of clean granulation tissue with enough pressure to
release tissue exudate for a period of five seconds. Transport
the swab as early as possible.6 Needle aspiration may be useful
for obtaining purulent collections or, perhaps, a specimen
from an area of cellulitis.6 Interpreting culture results requires
clinical correlation and judgment. If multiple organisms are
isolated the clinician must identify which pathogens require
specifically targeted therapy. In general, organisms isolated
from reliable samples that are the sole or predominant
pathogens on Gram-stain smear and culture are likely to
be true pathogens. Less virulent bacteria such as coagulase
negative staphylococci, enterococci and corynebacteria can
sometimes be ignored depending on the clinical condition.
Assessing Severity of Infection
Several classification systems have been proposed to assess
the severity of diabetic foot ulcers, but none of them is
universally accepted.
1. Wagner’s system as mentioned in the previous chapter
is the most commonly used since last 25 years but is
imprecise. It was developed for dysvascular foot and
contains all infections within a single grade (Grade 3).16
2. University of Texas classification takes into account the
depth of the ulcer, ischemia and infection.17 The limitations
are that it does not take into account the cross sectional
area of the ulcer although it has been seen that area of the
ulcer correlates with the final outcome.18 It does not also
consider the presence or absence of neuropathy. In spite of
these drawbacks it is easy to use in clinical practice, and is
being increasingly adopted as a means of describing ulcers
and for defining best management.
3. Lipsky has proposed a classification that utilizes depth
of a wound, presence of ischemia, presence of infection,
and systemic toxicity to designate severity of wound
infection.19
4. SAD classification consists of 5 elements: SAD (size, i.e.
area and depth), S (sepsis, i.e. infection), A (arteriopathy)
and D (denervation, i.e. neuropathy).20 However, because
of its complexity it is mainly used for clinical research
rather than routine practice.
5. PEDIS classification is the result of an attempt to
reach international consensus. It includes the same five
components as the SAD system, although using different
terms to create the acronym: Perfusion (ischemia), Extent
(area), Depth, Infection, Sensation (neuropathy).21
This classification has strict definitions for each of the
variables and is intended for use in prospective clinical
trials.
6. Infectious Diseases Society of America (IDSA) has
proposed a classification of the infection in diabetic foot
classifying the infection into mild, moderate and severe
which is quite similar to the grading of infection in PEDIS.6

Regardless of the classification used, the key factors to
be reviewed while assessing the severity of diabetic foot
ulcers are:

i. Depth and area of the ulcer: To be determined by
visually inspecting the ulcer to see which tissues are
involved and estimating the depth in millimeters.
Table 2: Proposed antibiotic therapy of diabetic foot infections
Severity of infection
Route
Recommended therapy
Alternative regimens
Mild Infection (IDSA) or
PEDIS Grade II
Oral
Amoxicillin+ Clavulanic acid
Clindamycin
Ofloxacin
Levofloxacin
Moderate Infection (IDSA)
or PEDIS Grade III
Parenteral
Switch to oral when
stable
Ampicillin+ Sulbactam
Linezolid+ Aztreonam
Ceftriaxone, Cefoxitin
Cefuroxime+ Metronidazole
Severe Infection (IDSA) or
PEDIS Grade IV
Prolonged
parenteral
Piperacillin+ Tazobactam+
Vancomycin*
Imipenem-Cilastatin
Flouroquinolones+ Clindamycin
* To be added in case of MRSA. Alternatively Teicoplanin or Linezolid can also be added.

Section 3
  Types of Wounds and their Management
164
ii. Presence of ischemia: Absent pulses or diminished
blood pressure in the lower limbs.
iii. Presence of infection.

These three factors have been found to correlate best with
the outcome. Although, neuropathy plays a significant role in
pathogenesis, its presence or absence does not really alter the
modality of treatment since offloading is part of treatment of
any foot ulcer.
Bone Infection associated with
diabetic foot
Up to two-thirds of diabetic patients with limb threatening
infections have osteomyelitis. It can occur by hematogenous
spread but more commonly it occurs by contiguous spread. Its
diagnosis is difficult because of several confounding features,
as typical symptoms may be masked by peripheral neuropathy
and radiological and clinical features can be confused with
diabetic neuro-osteoarthropathy and empiric antibiotic
therapy is usually started before its diagnosis is made. The
clinical criteria that suggest presence of osteomyelitis in an
infected diabetic foot ulcer are deep or long standing ulcer
especially if located over a bony prominence, large (>2 cm) or
deep (>3 mm) ulcer, poorly or non-healing ulcer (> 6 weeks of
antibiotic therapy and offloading), increased ESR (>70 mm)
or raised CRP, probe to bone (PTB) test in which a sterile
blunt metal probe is inserted into the wound till it contacts the
bony surface and visible bony surface.6 Probe to bone (PTB)
test has a low positive predictive value (50-60%) but a high
negative predictive value (95%) particularly in populations
with a low prevalence of osteomyelitis.22

Radiographic changes take at least two weeks to be
evident. The sensitivity of a plain X-ray is 55 percent and
specificity 75 percent. The characteristic changes include
focal osteopenia, cortical erosions, periosteal reaction and
sequestration of sclerotic bone.19 Any focus of bone destruction
beneath an ulcer should be considered osteomyelitis unless
proven otherwise. Imaging may be useful. Bone scan using
Technetium -99 is sensitive (~85%) but has a low specificity
(~45%) because they may show increased uptake of the
tracer with non-infectious bone disorders also. Leukocyte
scans are more specific (~75%) with the same sensitivity as
99Tc bone scans but they are costly, complicated and time
consuming.23 Magnetic resonance imaging (MRI) is the
diagnostic procedure of choice with a sensitivity of over 90
percent and specificity of 80 percent.24 Magnetic resonance
imaging (MRI) can also help in distinguishing osteomyelitis
from Charcot neuroarthropathy in difficult cases.

The gold standard for the diagnosis of osteomyelitis is
tissue specimen of bone for culture and histology.19 Specimens
can be obtained by open (during operative debridement) or
percutaneous biopsy. This not only confirms the diagnosis
but also helps in making an accurate decision about the
appropriate antibiotic therapy. Microbiological studies have
revealed that majority of cases are polymicrobial. S.aureus
is the most commonly isolated etiologic agent (~40%)
followed by S.epidermidis (~25%), streptococci (~30%) and
Enterobacteriaceae (~40%).23
Treatment
The principles of management include eradication of
infection, relieving the pressure, treatment of any vascular
insufficiency besides managing and improving glycemic
control.6 Flow chart 2 outlines the algorithm for management
of diabetic foot ulcers. A multidisciplinary approach should
be employed because of multifaceted nature of foot ulcers and
numerous comorbidities that can occur in these patients.
Treatment of Infection
Optimal treatment of infected diabetic foot ulcers depends on
the severity of infection of the ulcer. Treatment of clinically
uninfected diabetic foot ulcers is debatable. Some argue
that diabetic foot ulcers are extremely prone to infection
which may be difficult to diagnose in diabetics because of
associated neuropathy and vascular disease, and infection in
such conditions may lead to serious consequences. Moreover,
there is increasing evidence of the concept of “wound burden
or critical colonization”. Critical colonization (organisms >105
per gram of tissue) may impair wound healing.25 Unfortunately
very few clinical microbiology laboratories do quantitative
cultures. Furthermore, there is as yet scanty evidence that
treating critically colonized wounds hastens healing. Treating
such diabetic foot ulcers with antimicrobials would lead to
a dramatic increase in number of treatment courses with
associated increase in the cost of treatment and antibiotic
resistance. Infestions Diseases Society of America (IDSA)
does not recommend the use of antibiotics in uninfected
diabetic ulcers.6 Exceptions to this rule may be made in non
healing ulcers despite appropriate care. With epidemiologically
significant organism, e.g. MRSA, a brief, culture-directed
course of antibiotic therapy may be appropriate.6
Topical Therapy
Numerous topical medications and gels are promoted for
ulcer care. These include topical antimicrobials (neomycin,
bacitracin, polymyxin B), topical antiseptics (hexachlorophene,
povidone iodine, and chlorhexidine) and silver containing
dressings. There are two major concerns about these. These
may not diffuse into tissues and thus, it is advisable to use
these only in mild infected superficial ulcers and secondly
one should avoid using agents that are deleterious to wound

Chapter 16
Diabetic Foot Infections 
165
healing like povidone-iodine.5 Studies show that there is no
significant difference in the efficacies of these agents.26
Systemic Antibiotic Therapy
While antimicrobial therapy is a necessary step in the management
of the diabetic foot ulcers, it is rarely sufficient alone (Flow
chart 2). The important factors in the medical management are
selection of an appropriate antibiotic, route of administration and
duration of therapy. These decisions are guided by the severity,
extent and duration of ulcer, and associated comorbidities.
Besides treatment of infection, medical management consists
of correction of metabolic derangements which are often
associated with moderate-severe diabetic foot infections. Since,
hospitalization is the most expensive part of treating a diabetic
foot infection, deciding on its necessity requires consideration of
both medical and social issues.

Initial therapy is usually empirical and should be based
on severity of infection, recent microbiological data,
culture results or Gram-stained smear findings and previous
history of antibiotic usage. It is important to note that mild-
moderate infections particularly in antibiotic naive patients
are often monomicrobial and can be managed with narrow
spectrum antibiotics active against common aerobic gram-
positive bacteria. On the other hand, infections in patients
with chronically infected ulcers who have received multiple
courses of antibiotics or those with severe infections are
polymicrobial and broad spectrum antibiotics should be
used to adequately cover gram-positive and gram-negative
aerobes and anaerobes. Once definitive reliable culture
sensitivity results are available, initial antibiotic should be
revised to narrow the coverage to specific pathogens present
in the culture. Conversely in the absence of adequate clinical
improvement, despite coverage of cultured organisms, the
Flow chart 2: Alogrithm for management of a diabetic patient with a foot ulcer

Section 3
  Types of Wounds and their Management
166
antibiotic coverage should be augmented until an appropriate
response is achieved.
Treatment of Mild (PEDIS I-2) or Non-limb
Threatening Infections
These can be managed without hospitalization.6 Most non-
limb threatening infections are monomicrobial, with aerobic
gram-positive cocci predominating. Nevertheless gram-
negative organisms can be isolated from these patients
particularly those with chronic ulcers and repeated antibiotic
courses. Wound debridement should be done since it not
only reduces the bacterial burden but also promotes healing.
After obtaining cultures, oral antibiotic therapy can be
started empirically using agents with effective gram- positive
coverage. Newer fluoroquinolones (levofloxacin, gatifloxacin,
etc) are of particular use in these cases because of their high
oral bioavailability and excellent activity against both gram-
negative and gram-positive aerobes.5 After 48 to 72 hours
the patient should be reassessed to determine the response to
treatment. Antibiotic therapy should be adjusted according to
the culture results and clinical response. If no response is noted
after adequate therapy including offloading and debridement,
hospitalization for incision and drainage, intravenous
antibiotics and medical stabilization should be considered.6
Treatment of Moderate-severe (PEDIS I-3, 4)
Limb Threatening Infections
Most of the patients with moderate and severe infections
require hospitalization for surgical intervention, metabolic
control and intravenous antibiotics.6 Because many of these
patients are at an increased risk of a major or minor lower
extremity amputation, it is imperative that prompt and
aggressive treatment should be started immediately. Delays
in appropriate treatment and referral can result in more
proximate levels of amputation in 10 percent of these patients.
Polymicrobial involvement of aerobic gram-positive and
gram-negative bacilli, as well as anaerobic organisms should
be anticipated in moderate-severe infections. Accordingly,
empirical therapy for moderate and severe infections should
be started with broad spectrum agents with activity against
gram-positive cocci (including MRSA in locations where
this pathogen is common), as well as gram-negative and
obligate anaerobic organisms.6 Not every possible organism
needs to be covered initially, however, because gram-positive
organisms often predominate in these infections, therefore,
coverage primarily tailored against these organisms is
essential and may be clinically as effective as broad spectrum
agents especially in moderate infections when combined
with effective wound care and offloading.19 In a randomized
blinded trial, ampicillin-sulbactam therapy was not only as
effective as imipenem-cilastatin at the end of treatment, but
on initial evaluation of responses on day five the two regimens
also performed comparably.27 In more severe life-threatening
infections with systemic features, empirical broad spectrum
therapy that covers S.aureus, streptococci, Enterobacteriaceae
and B.fragilis are recommended.7 Moreover, no single agent
can cover all the organisms that may be seen in diabetic foot
infections. As a result combination therapy is often used in
particularly severe infections. To ensure adequate and prompt
tissue concentrations, therapy should be given parenterally,
at least initially. When culture and sensitivity results are
available, more specific therapy should be chosen. Narrower
spectrum agents should be preferred, but it is important to
clinically assess the response of the patient. If the lesion is
healing and the patient is tolerating the treatment, there may
be no reason to change the antibiotics even if some or all
of the organisms are resistant to the agent that were being
used.19 If the infection is worsening despite susceptibility of
the isolated bacteria to the chosen regimen, reconsider the
need for surgical intervention, or the possibility that fastidious
organisms particularly anaerobes are being missed.

The necessary duration of antibiotic therapy for diabetic
foot infections has not been well studied. It is important to
remember that the aim of antimicrobial therapy is to treat the
infection, not to heal the ulcer. Infectious Diseases Society of
America (IDSA) recommends that a one to two weeks course
of an antimicrobial is sufficient in mild-moderate infections,
while more complex and severe infections may require three
to four weeks of therapy.6 For osteomyelitis, the duration of
therapy largely depends on the degree of bone resection; when
the infected bone is not surgically resected, therapy should be
given for at least four to six weeks.6 Antibiotics can usually
be stopped when all signs and symptoms of infection have
resolved. Even if the ulcer has not fully healed after adequate
antibiotic therapy, antibiotics can in general be discontinued
when evidence of infection has resolved. Persistent ulcers
must be managed with wound care, including avoidance of
weight bearing, so that healing can be achieved and the ulcer
eliminated as a portal for later infection.28 Some patients who
have surgical metalwork at the site of infection, or who cannot
undergo surgical resection will require prolonged suppressive
antibiotic therapy.
Surgical Treatment
Most diabetic foot infections require some sort of surgical
intervention. The most common surgical procedure performed
in diabetic foot infections is debridement and preparation of the
wound bed. It is aimed at removing any eschar, other necrotic
tissue or foreign material, or surrounding callus. Debridement

Chapter 16
Diabetic Foot Infections 
167
helps to fully evaluate the wound, prepare the wound for
culture, allow penetration of any topical agents applied,
decreases the bacterial burden and promotes healing. Although
autolytic, enzymatic or chemical debridement may be used,
sharp debridement is the best method.29 Sharp debridement
can be done using a scalpel or scissors to remove the callus
and all undermining necrotic tissue. Regular (weekly) sharp
debridement is associated with rapid healing of ulcers as
compared to less frequent debridement, independent of other
factors.29 The presence of pus in an enclosed space will require
drainage. Similarly, fulminant soft tissue infections, such as gas
gangrene or necrotizing fasciitis, require urgent debridement
of involved tissue. Although, patients with these limb or life-
threatening infections are poor surgical risks because of the
associated metabolic abnormalities, early surgical intervention
in these patients has been shown to improve the outcome.
In some cases, amputation is the best or only option. Urgent
amputation is usually required only when there is extensive
necrosis or life-threatening infection. Elective amputation
may be considered for a patient who has recurrent ulceration
(despite maximal preventive measures), has irreversible loss
of foot function, or would require unacceptably prolonged
or intensive hospital care. When all or part of a foot has dry
gangrene, it may be preferable (especially for a patient for
whom surgery is a poor option) to let the necrotic portions
autoamputate. An ischemic limb may require revascularization
and this may be necessary prior to definitive antibiotic therapy
or surgical resection of the infected tissue or bone. In most
cases, ischemia is due to larger-vessel atherosclerosis, rather
than to “small-vessel disease”.30 Patients with noncritical
ischemia (e.g. those with an ankle to brachial artery blood
pressure index of 0.5–0.9) can usually be successfully treated
without a vascular procedure.6 For more-severe vascular
disease of the foot, many centers have reported successful use
of femoral-distal bypass procedures.
Treatment of Osteomyelitis
The presence of osteomyelitis underlying an ulcer impairs wound
healing and acts as a focus for relapse of soft tissue infection. The
need for surgical resection of the infected bone is controversial.
There are various reports which suggest that osteomyelitis of
the toe and foot is a surgical disease and medical management
alone is associated with poor outcome and limb loss.23, 30 But an
equal number of studies have shown that antibacterial therapy
alone induced remission in almost two-thirds of the patients.
So when it is feasible, surgical resection of the infected bone
in addition to antimicrobial therapy is the best option available.
When the affected bone is completely resected, the wound
may be treated as a soft tissue infection with antibiotics for one
to two weeks. If residual bone is left, the patient will require
four to six weeks of antibiotic therapy.6 However, in certain
situations surgical resection may not be possible at all. These
include: no acceptable surgical target, ischemia caused by
unreconstructable vascular disease, infection confined to the
forefoot, with minimal soft-tissue loss, and when patient and
healthcare professional agree that surgical management carries
excessive risk or is otherwise not appropriate or desirable.6 In
such cases prolonged antibiotic therapy for three to four months
may be required. In some patients when infection cannot be
cured, disease can be kept in remission with intermittent short
course or long-term oral suppressive antibiotic therapy. Many
clinicians also use antibacterial impregnated beads, despite the
fact their effectiveness has not been demonstrated in trials.31
Typically gentamicin, tobramycin or vancomycin may be used
in the beads.
Adjunctive Therapies
In spite of the best management, the healing rate in patients
with diabetic foot infections is often suboptimal. Therefore,
various adjunctive therapies have been advocated for the
treatment of diabetic foot ulcers: growth factors (platelet
derived, epidermal, TGF-β and vascular endothelial growth
factors), tissue engineered skins, acellular wound matrices,
G-CSF, and hyperbaric oxygen. The role of most of these
measures has not been adequately defined and is an area of
active clinical research. Amongst the adjuvant therapies
available, the role of recombinant human granulocyte colony
stimulating factor is particularly intriguing. A recent meta-
analysis found that using G-CSF in addition to antibiotic
therapy does not appear to accelerate the resolution of
infection but is associated with a decreased rate of lower limb
amputation and other surgical procedures.32 Recombinant
platelet derived growth factor is approved by the US Food and
Drug Administration for the treatment of neuropathic diabetic
foot ulcers.14 A review on the role of growth factors concluded
that recombinant platelet derived growth factor may be useful
in chronic non-healing neuropathic ulcers as compared to
other growth factors.33 It must, however, be emphasized that
none of the adjuvant therapies can substitute for well selected
antimicrobial therapy and appropriate surgical interventions.
Adjuvant therapies may be tried in cases where appropriate
therapy including surgical debridement and offloading fails to
reduce the size of the ulcer.
Conclusion
Diabetic foot is a largely preventable complication. It
is important to identify patients at risk for diabetic foot
particularly those with significant neuropathy and peripheral
vascular disease. All diabetic patients should undergo a

Section 3
  Types of Wounds and their Management
168
thorough foot examination, at least annually. In addition
diabetic patients should be taught about foot care practices.
American Diabetes Association annually publishes clinical-
practice recommendations on preventive foot care. The
treatment of diabetic foot requires a multidisciplinary
approach. It is critical to assess the vascular status of the limb
because an ischemic lesion can never heal. Besides appropriate
antimicrobial therapy, the role of surgical debridement
and pressure offloading is equally important which will be
discussed in subsequent chapters.
References
1. Joshi SR, Parikh RM. India--diabetes capital of the world:
now heading towards hypertension. J Assoc Physicians India.
2007;55:323-4.
2. Bajaj JS. Proceedings of the Eighteenth Round Table
Conference. In: Gupta SC, Sood OP (Eds), Diabetic
Retinopathy. Ranbaxy Science Foundation 2006. pp. 3-19.
3. Boulton AJ, Vileikyte L, Apelqvist J. The global burden of
diabetic foot disease. Lancet 2005;366:1719-24.
4. Williams G, Pickup JC. Handbook of Diabetes. 3rd edn.
Blackwell Publishing 2004. pp. 185-94.
5. Rao N, Lipsky BA. Optimizing antimicrobial therapy in
diabetic foot infections. Drugs. 2007;67(2):195-214.
6. Lipsky BA, Berendt AR, Deery HG, et al. IDSA Guidelines:
diagnosis and treatment of diabetic foot infections. 2nd, Clin
Infect Dis 2004;39:885-910.
7. Lipsky BA, Berendt AR, Embil J, De Lalla F. Diagnosing
and treating diabetic foot infections. Diabetes Metab Res Rev
2004;20:S56-S64.
8. Frykberg RG. Diabetic foot ulcers: pathogenesis and
management. Am Fam Physician. 2002;66(9):1655-63.
9. El-Tahawy AT. Bacteriology of diabetic foot. Saudi Med J
2000;21:344-7.
10. Pathare NA, Bal A, Talvalkar GV, Antani DU. Diabetic
foot infections: a study of micro-organisms associated with
the different Wagner grades. Indian J Pathol Microbiol
1998;41:437-41.
11. Karchmer AW. Microbiology and treatment of diabetic foot
infections. In: Veves A, Giurini JM, LoGerfo FW (Eds.) Diabetic
foot: medical and surgical management. Humana Press; 2002.
12. Hartemann-Heurtier A, Robert J, Jacqueminet S, et al. Diabetic
foot ulcer and multidrug-resistant organisms: risk factors and
impact. Diabet Med 2004;21:710-5.
13. Tentolouris N, Jude EB, Smirnof I, Knowles EA, Boulton AJ.
Methicillin-resistant Staphylococcus aureus: an increasing
problem in a diabetic foot clinic. Diabet Med 1999;16:767-71.
14. Boulton AJM, Kirsner RS, Vileikyte L. Neuropathic Diabetic
Foot Ulcers. N Engl J Med 2004;351:48-55.
15. Lipsky BA. A report from the international consensus on
diagnosing and treating the infected diabetic foot. Diabetes
Metab Res Rev 2004;20:(Suppl) 1:S68-S77.
16. Wagner FW Jr. The diabetic foot and amputation of the foot, in
Surgery of the Foot (Mann RA, Ed.), Mosby, St. Louis, 1986.
pp. 421-55.
17. Armstrong DG, Lavery LA, Harkless LB. Validation of a
diabetic wound classification system. The contribution of
depth, infection, and ischemia to risk of amputation. Diabetes
Care 1998;21:855-9.
18. Oyibo SO, Jude EB, Tarawneh I, et al. The effect of ulcer size
and site, patient’s age, sex and type and duration of diabetes on
the outcomes of diabetic foot ulcers. Diabet Med 2001;18:133-8.
19. Lipsky BA. Infectious problems of the foot in diabetic patients.
In: Bowker JH, Pfeifer MA. Levin, O’ Neal’s (Eds.) The
Diabetic Foot 6th edn. Mosby Inc; 2001.
20. Treece KA, Macfarlane RM, Pound P, Game FL, Jeffcoate WJ.
Validation of a system of foot ulcer classification in diabetes
mellitus. Diabet Med 2004;21:987-91.
21. Schaper NC. Diabetic foot ulcer classification system for
research purposes: a progress report on criteria for including
patients in research studies. Diabetes Metab Res Rev
2004;20:S90-S95.
22. Lavery LA, Armstrong DG, Peters EJ, Lipsky BA. Probe-to-
bone test for diagnosing diabetic foot osteomyelitis: reliable or
relic? Diabetes Care. 2007;30(2):270-4.
23. Lipsky BA. Osteomyelitis of the foot in diabetic patients. Clin
Infect Dis. 1997;25:1318-26.
24. Craig JG, Amin MB, Wu K, Eyler WR, van Holsbeeck MT,
Bouffard JA, et al. Osteomyelitis of the diabetic foot: MR
imaging-pathologic correlation. Radiology. 1997;203(3):849-55.
25. Kingsley A. The wound infection continuum and its application
to clinical practice. Ostomy Wound Manage 2003;49:1-7.
26. O’Meara SM, Cullum NA, Majid M, Sheldon TA. Systematic
review of antimicrobial agents used for chronic wounds. Br J
Surg. 2001;88(1):4-21.
27. Grayson ML, Gibbons GW, Habershaw GM, Freeman DV,
Pomposelli FB, Rosenblum BI, et al. Use of ampicillin/
sulbactam versus imipenem/cilastatin in the treatment of limb-
threatening foot infections in diabetic patients. Clin Infect Dis.
1994;18(5):683-93.
28. Consensus Development Conference on Diabetic Foot Wound
Care: 7-8 April 1999, Boston, Massachusetts. Diabetes Care
1999;22:1354-60.
29. Steed DL, Donohoe D, Webster MW, Lindsley L. Effect of
extensive debridement and treatment on the healing of diabetic
foot ulcers. J Am Coll Surg 1996;183:61-4.
30. Mader JT, Ortiz M, Calhoun JH. Update on the diagnosis
and management of osteomyelitis. Clin Podiatr Med Surg
1996;13:701-24.
31. Roeder B, Van Gils CC, Maling S. Antibiotic beads in the
treatment of diabetic pedal osteomyelitis. J Foot Ankle Surg
2000;9:124-30.
32. Lipsky BA, Berendt AR, Embil J, De Lalla F. Diagnosing
and treating diabetic foot infections. Diabetes Metab Res Rev
2004;20(Suppl 1):S56-64.
33. Bennett SP, Griffiths GD, Schor AM, Leese CP, Schor SL.
Growth factors in the treatment of diabetic foot ulcers. Br J
Surg 2003;90:133-46.

• Classification of Diabetic Foot Ulcer
• Anatomic Location of Foot Ulcers
• Causes of Foot Ulcers in Diabetics
• Assessment
• Investigation
• Management

– Dressing

– Surgical Debridement

– Skin Cover
• Rehabilitations
Introduction
Diabetes mellitus is a chronic disease in which there are
high levels of sugar in the blood. Diabetes is affecting more
than 200 million people in the world and too many of these
subjects suffer from diabetic foot ulcer, which many lead to
an amputation. Diabetes is affecting more than 20 million
Americans. Over 40 million Americans have prediabetes. The
International consensus on diabetic foot currently defines a
diabetic foot ulcer as a full thickness wound below the ankle
in patient with diabetes, irrespective of duration. Diabetes
is increasingly common, highest incidence being in India
probably due to western lifestyles and diet. Diabetes affects
almost all the systems of the body and reduces the immunity.
It changes the ability to fight against infections. Damage to
blood vessels because of diabetes results in less blood and
oxygen supply to feet. Because of this, small sores or breaks
in the skin may become deeper skin ulcers. The affected limb
may need to be amputated if these skin ulcers do not improve.
The condition worsens if ulcers get larger, or go deeper into
the subcutaneous tissue. Foot ulcers precede more than 80
percent of non-traumatic lower amputations.

The other major problem of diabetes is nerve involvement
leading to peripheral neuropathy and the blood supply to the
legs is hampered due to atherosclerotic lesions (peripheral
vascular disease). These, in turn, makes the patient insensate
to even minor injuries and pressure on the skin of the foot.
One may not notice a foot injury until severe damage or
infection develops. People with diabetic ulcers sometimes
need an amputation, if diabetes is not controlled and foot is
not managed properly. Diabetics develop foot ulcers due to a
number of following problems related to their feet.

• Infections

• Stiff deformities

• Peripheral neuropathy

• Peripheral vascular disease

• Ulceration

• Charcot neuropathic arthropathy

• Wrong foot wears

These further lead to serious complications which seriously
affect quality of life. These can lead to restricted mobility,
systemic ill-health, hospitalization and reduced lifespan. Ten
to fifteen percent of the 20 million individuals with diabetes
are at risk of developing diabetic ulcers. About 60 percent of
lower limb amputations occur in diabetics. The costs of caring
for people with diabetic foot disease are substantial.
Classification of Diabetic
Foot Ulcer
Many different classification systems have been reported in
the literature but the one developed by Wagner for grading
Surgical Management of
Diabetic Foot
Imran Ahmed
17
Chapter

Types of Wounds and their Management
Section 3
170
diabetic foot ulcer has been widely accepted (Table 1). This
classification takes into account presence or absence of
infection as well as depth and the presence of osteomyelitis
or gangrene of the tissue. This has five different grades which
help to intervene foot ulcer for proper management and tissue
replacement if required.
Anatomic Location of Foot Ulcers
The site of diabetic foot ulcers varies according to the
population and profession to which the patients belong. The
foot ulcer may occupy any part of the foot depending upon the
etiological factors but the most common ulcer sites were the
toes (dorsal and planter surface), followed by metatarsal heads
(Figures 1 to 3). The following data is from a prospective
study that reported foot ulcer site (Table 2).
Causes of Foot Ulcers In
­Diabetics
Smoking
Smoking any form of tobacco causes damage to the small
blood vessels in the feet and legs leading to ischemia and
necrosis of the part involved.
Figures 2A to C: Ulcer over toes and dorsum of foot
Table 1: Wagner diabetic foot ulcer classification system
Grade
Description
0
1
2
3
4
5
No ulcer, but high risk foot (deformity, callus,
insensitivities)
Superficial full thickness ulcer
Deeper ulcer, penetrating tendons, no bone
involvement
Deeper ulcer with bone involvement
Partial gangrene (e.g. toes, forefoot) osteitis
Gangrene of whole foot
Table 2: Anatomic site and outcome of diabetic foot lesions
Lesion site
Percentage
Toes (dorsal and planter surface)
Metatarsal heads, midfoot and heel
Dorsum of the foot
Multiple ulcer
51
28
14
07
Figures 1A and B: Ulcer over metatarsal heads
Infections
Minor trauma allows microorganisms to travel inside the
tissue and high blood sugar level favours rapid multiplication
of bacteria especially Staphylococcus.
Footwear
Poorly fitting shoes are one of the common causes of diabetic
foot ulcer problems especially in insensate foot.
B
A
B
C
A

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171
Nerve Damage
People with long-standing or poorly controlled diabetes are at
risk for having damage to the nerves in their feet. The medical
term for this is peripheral neuropathy and this acts as catalyst
to the damage.
Poor Circulation
Especially when poorly controlled, diabetes can lead to
accelerated hardening of the arteries or atherosclerosis. When
blood flow to injured tissues is poor, healing does not occur
properly.
Trauma to the Foot
Any trauma to the foot can increase the risk for a more serious
problem to develop.
Assessment
Prevention, early treatment and good aftercare can reduce
the burden of diabetic foot disease for diabetics themselves
and for the community. This requires good team working,
bringing together of the following specialists:
• Diabetologists
• Orthopedic foot and ankle surgeons
• Plastic surgeons
• Vascular surgeons
• Wound care specialists
• Bioengineers

Diabetics have many other potentially serious problems
which require detailed investigations like:
• Cardiovascular disease, including peripheral arterial
disease
• Renal disease
• Eye disease
• Increased susceptibility to infection

These may influence the feasibility, success and risks
of surgery and requires call for the involvement of many
specialists. However, a diabetic patient can contribute a lot to
their own treatment.
Investigation
Fasting blood glucose level—Diabetes is diagnosed if it
is higher than 126 mg/dl twice. Levels between 100 and
126 mg/dl are called impaired fasting glucose or prediabetes.
These levels are risk factors for type two diabetes.
Hemoglobin A1c
• Normal: Less than 5.7 percent
• Prediabetes: 5.7 to 6.4 percent

Diabetes: 6.5 percent or higher

Blood urea and electrolytes assess renal function and
may indicate potassium or sodium depletion secondary to
medication. Unless the patient is clinically ill further tests are
not usually required.

Routine white cell count, ESR and CRP can show
evidence of infection; diabetic control generally deteriorates
in the presence of infection.
Radiograph
Plain radiographs may show bone erosion, osteoporosis, new
bone formation or changes of chronic osteomyelitis.
• Standing hindfoot alignment view shows diabetic foot
deformities, especially after Charcot arthropathy (Figure 4)
• Standing lateral view shows rocker-bottom midfoot
deformity
• Standing dorso-plantar view plus an oblique view.
CT Scan
In very complex deformities, especially in the hind and
midfoot, a CT can give useful additional information.

Isotope bone scanning is fairly sensitive for infection but
not very specific; other nuclear medicine techniques such as
indium scanning or labeled white cell scanning are somewhat
more accurate but still not specific enough.

MRI and PET scanning with fluorodeoxyglucose have
emerged as the imaging techniques of choice over the last few
years. PET scanning obviously has an advantage where metal
implants are in place, but MRI is generally more available
and comparative studies have not shown a clear advantage for
either technique.
Management
Diabetic ulcers of foot often worsen due to chronic
lymphovenous insufficiency (Figure 5). It has been proved
Figures 3A and B: Multiple diabetic ulcer over dorsum
A
B

Types of Wounds and their Management
Section 3
172
that use of skin graft after radical debridement allows to
reduce the treatment complications and to improve the results
and the quality of patients life.

Infection in an ulcer can be difficult to treat because of:
• Polymicrobial infection
• Deficient immunity
• Ischemia
• Spread of infection along deep tissue planes
• Development of ostoemyelitis with dead bone

Diabetic ulcer complications are a leading cause of
hospitalization and amputation. Standard therapy involves
the use of dressings to protect the wound bed from trauma
and to absorb infected exudates. Bulky dressing is also used
for offloading high pressure from the wound bed. But these
measures are often deficient in healing all diabetic ulcers
when the patient’s own intrinsic wound-healing system is
insufficient. In such patients, skin replacement therapies are
second-line treatment options.

An infected foot should be elevated and broad-spectrum
antibiotics administered intravenously. Each unit needs to
develop their own antibiotic protocol with the help of the
microbiologist according to local organisms and sensitivities.
Improvement of the vascular inflow may improve the chance
of limb salvage.
Dressing
Dressing choice is not usually the first consideration when
treating a diabetic foot ulcer as in addition to pressure relief,
other measures including callus debridement, infection control
and adequate blood supply must be addressed if the ulcer is to
heal. Wound management is comprised of multilayer dressing
including Bactigrass (paraffin gauze and soframycin). Wound
management must be integrated into an effective program of
multidisciplinary care. There are lots of dressing agents like
Silver, iodine, hydrocolloid, alginate, hydrogel, promogran,
Hyalofill and biological dressings, etc. Dressing must never
be seen as an isolated treatment of the wound; rather it should
be a part of multifactorial apporoach to wound care.

VAC therapy: Negative-pressure dressings may improve
healing rates over conventional dressings, although the
evidence is not yet strong. Negative pressure optimizes blood
flow, decreases local tissue edema and removes excessive
fluid and proinflammatory exudates from the wound bed.
These physiological changes promote a moist wound healing
environment and may facilitate the removal of bacteria from
the wound (Figure 6). The technique is useful in wounds which
have failed other attempts at healing. However, this system is
not economical enough to be afforded by all patients.
Surgical Debridement
Surgery of the diabetic foot is indicated for deep infection or
for the treatment of recurrent abscesses or ulcerations or in
established deep infection where dressing and VAC are not
successful enough. The overall goal is complete healing of
Figure 4: Diabetic ulcer with Charcot arthropathy
Figure 5: Foot showing lymphovenous insufficiency
Figure 6: VAC therapy set for rapid granulation tissue

Surgical Management of Diabetic Foot 
Chapter 17
173
soft tissue and maximum preservation of functional anatomy
of the foot. The specific goals are:
1. To achieve and maintain the foot plantigrade, i.e functional
weight bearing
2. To restore and maintain an intact soft tissue envelope
3. To reduce the risk of foot loss.
The surgical debridement is of two types:
1. Regular/serial debridement: The usual signs of swelling,
rubor, heat and discharge may be obvious, but in an
ischemic foot with deficient function there is need to
decompress the wound to limit further ischemic damage
(Figures 7A to C). For diabetic foot, even a blister from
wearing a shoe that’s too tight can cause a lot of damage.
Regular debridement is done from time to time to unload
necrotic tissue until the wound become healthy for
secondary healing or skin cover. This is time consuming
and needs prolonged hospital stay and cannot assess the
status of the deeper structure. Diabetes decreases blood
flow therefore injuries are slow to heal the ulcer. Ulcer that
often require regular debridement are those classified as
grade 2 on Wagner scale, i.e abscess or soft tissue necrosis.


In a diabetic patient the infection is in multiple planes
especially in sole. If a knife is inserted into the ulcer,
copious pus comes out and it goes directly down to bone,
osteomyelitis is probably present. Ultimately, surgical
exploration is done to unload the infection from foot.
2. Radical debridement: Radical debridement is aggressive
debridement to remove all types of dead tissue under
magnification usually in single sitting under anesthesia
(Figure 8). Diabetic ulcers of foot, worsen due to chronic
lymphovenous insufficiency. It has been proved that radical
debridement will enhance the granulation tissue to come up
early. This is done in Wagner grade 3 and 4 with exposed
tendon, bone or joint. Radical debridement is necessary for
tissue healing as a damage control procedure preferably
before a reconstructive surgery to cover the defect. Use of
skin cover (graft or flap) after radical debridement allows
to reduce the treatment complications and to improve the
treatment results and the quality of patient’s life as well.
This may include amputation at various levels. Single or
multiple toe Ray(s) at one or multiple sittings (Figure 9A
to C). The levels of amputation may be either:
• Transverse amputations at the Lisfranc/midtarsal levels
• Hindfoot amputations such as Syme or Pirogoff
Figure 7A: Diabetic foot ulcer Wagner’s grade 2
for regular debridement
Figure 7B: After second sitting of debridement
Figure 7C: Multiple diabetic foot ulcers being drained
from dorsum and sole

Types of Wounds and their Management
Section 3
174

Foot complications and ulceration are well-known sequelae
to uncontrolled diabetes. Patients with chronic foot ulcers or
wounds resulting from surgical debridement of deep-space
infections are at continued risk for development of osteomyelitis
and potential amputation. Moreover, these wounds often
necessitate multiple outpatient clinic visits, daily dressing care,
and prolonged periods of nonweight bearing, all of which have
been shown to adversely affect the patient’s quality of life. After
a prudent period of wound-healing response early and aggressive
soft tissue reconstruction is in the patient’s best interest and is
crucial for resolution of the chronic non-healing wound.

Following are the advantages of radical debridement:
• Less hospital stay
• Economical
• Free from daily dressing
• Minimize amputations
Skin Cover
The diabetic foot ulcer may occupy any part of the leg and
foot. Skin cover depends upon the site and type of underlying
tissue. The site of ulcer could be weight bearing or nonweight
bearing and similarly underlying tissue could be a tendon or
bone or a muscle. However in majority of the cases, wound
closer techniques are utilized through local tissue available.
The primary determinant of primary or delayed primary closer
is the size and viability of the healthy soft tissue flaps. These
considerations for soft tissue closer after wound debridement
and bone resection are the same principle used for achieving
a stable, functional, healed foot in partial foot amputations. If
site is nonweight bearing then skin graft is the answer to the
problem and if it is weight bearing then to avoid breaking of
skin, a flap is superior to graft. Similarly if underlying tissue is
bone then graft becomes a contraindication. However, if ulcer
Figure 9A : Diabetic foot left wound over
dorsum
Figure 9B: Diabetic foot postradical
debridement
Figure 9C: Same foot after grafting
Figure 8: Wound for radical debridement
bed is made of soft tissue and contains good granulation then
again split skin graft is tissue of choice.
Skin Graft
Diabetic ulcers complications are a leading cause of
hospitalization and amputation. Ten to fifteen percent
of the 20 million individuals with diabetes are at risk of
developing diabetic ulcers. Standard therapy involves the
use of dressings to protect the wound bed from trauma and
to absorb exudates, offloading of high pressure on the wound
bed, e.g. by prescribing protective footwear, and wound bed
preparation to accelerate endogenous healing and to facilitate
the effectiveness of topically applied substances. But these
measures are often deficient to heal all diabetic ulcers when the

Surgical Management of Diabetic Foot 
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175
patient’s own intrinsic wound healing system is insufficient. In
this group of patients, skin replacement therapies are second
line treatment options (Figures 10A to C).

The following types of skin graft can be used to cover the
diabetic leg or foot ulceration to the patients of any age and in
any care setting:
• Autografts: Pinch, split thickness, or full thickness skin
grafts, cultured keratinocytes
• Allografts: Cultured keratinocytes or fibroblasts
• Xenografts: Nonhuman species
• Bioengineered skin

Diabetic foot and ankle soft tissue reconstruction poses a
difficult challenge to the treating surgeon, especially in cases
associated with previous infection or amputation. Maintenance
of a functional, plantigrade limb is important with regard to
prevention of persistent or recurrent cutaneous compromise
following diabetic limb salvage. Wound coverage by means
of application of a split thickness skin graft (STSG) is a useful
technique; however, donor site wounds require care during the
early postoperative period, and can pose a challenge to wound
healing themselves. Split thickness skin graft (STSG) is an
effective method of managing diabetic foot ulcers as, compared
with the conservative dressings. Bone and tendons exposure
in diabetic patients requires flap reconstruction to avoid major
limb amputation. However, for critical and unstable diabetic
patients, revascularization and flap reconstruction may not be
feasible. Skin grafts can be used in such a situation, and this
procedure has been evaluated in studies in terms of treatment
outcome. It reduces healing times and the length of hospital
stay, while donor-site morbidity was minimal. Dressing
comprises of multilayer dressing including Bactigrass (paraffin
gauze and soframycin). After skin grafting the dressing is
changed on third postoperative day and then redressed. In
the authors unit most of the patients with diabetic ulcer after
skin graft healed completely, except 5 percent had an ulcer
recurrence due to early non guarded ambulation. The mean
healing time and mean length of hospital stay are significantly
less in the grafted patients compared with the patients who are
undergoing dressing alone. Skin grafts also provide a simple
Figure 10A: Sloughed diabetic foot, wound over sole
Figure 10C: Same foot after application of split skin graft
Figure 10B: Sole after radical debridement

Types of Wounds and their Management
Section 3
176
Figure 12A: Diabetic foot right heel with Charcot joint
Figure 12B: Arthrodesis of ankle with grafting
wound location, illicit drug use, amputation history, Charcot
history, or preoperative infection. However, postoperative
graft complications were significantly associated with current
or previous smoking history23 Application of split-thickness
skin grafts with an appropriate postoperative regimen is a
beneficial procedure to achieve foot and ankle wound closure
in diabetic patients.

Taking adequate protection postoperatively for a maximum
of four weeks results in a higher healing rate. Graft skin may
be a very useful adjunct for the management of diabetic foot
ulcers that are resistant to the currently available standard of
care (Figures 12 to 14).
Figure 11A: Sloughed diabetic foot wound over dorsum
Figure 11B: Skin graft after radical debridement
method of wound coverage in nonweight bearing areas of the
foot. They may be harvested as partial thickness grafts and
applied to clean surgical wounds. Application of skin graft and
protection for a maximum of four weeks results in a higher
healing rate (Figures 11A and B). Skin grafting may be a very
useful adjunct for the management of diabetic foot ulcers that
are resistant to the currently available standard of care. It is an
effective method of managing diabetic foot ulcers as, compared
with the conservative dressings, it reduced healing times and
the length of hospital stay, while donor-site morbidity was
minimal. Surgical outcome was not significantly associated
with age, gender, race, hemoglobin HbAlc, wound size,

Surgical Management of Diabetic Foot 
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177
Skin Flap
Historically, the treatment of chronic foot wounds has centered
around aggressive debridement, pressure reduction and lately
the application of various flaps depending upon the wound
conditions. More recently, the use of reconstructive procedures
has been gaining support in reconstruction of foot and ankle as
an alternative to traditional offloading endeavors. Use of both
random and pedicle skin flaps offer many advantages over
conservative wound management. However, when dealing
with a wound on a weight bearing area that penetrates to the
fascia or beyond, it is much less likely to close by secondary
intention and yield a stable and durable envelope because of
the physical properties of the resulting scar.

Local flaps: The aim of the local skin flap is to cover the
nearby defect at earliest possible, after proper debridement
with minimum donor site morbidity. There is excellent
clinical efficacy of reverse lateral supramalleolar adipofascial
flap and skin grafting for one stage soft tissue cover around
ankle. Reconstruction using a reverse lateral supramalleolar
adipofascial flap and skin grafting was performed in diabetic
wounds.

Wounds with exposed bone are at high-risk for developing
osteomyelitis. Extended local wound care only increases
this risk. Rapid closure of the wound would be the treatment
of choice in these situations. One may provide wound
coverage via local and distant flaps, or by using muscle
flaps covered with a skin graft (Figures 15A to C). One may
utilize rotational, advancement and transpositional flap to
cover wounds with exposed subcutaneous tissue, tendon,
muscle or bone.
Figures 13A and B: (A) Diabetic foot right sole; (B) Split skin graft
A
B
Figures 14A and B: (A) Diabetic foot left lower leg;
(B) Diabetic foot left leg debridement and grafting
A
B
Figures 15A to C: (A) Diabetic foot with right heal defect; (B) Defect after debridement covered with medial planter artery flap;
(C) Same foot with healed defect at 3 months follow-up
B
C
A

Types of Wounds and their Management
Section 3
178
Pedicle Flaps
Finding appropriate soft-tissue to cover a wound located over
the middle or distal portion of the foot can be challenging.
A distally based sural fasciomusculocutaneous flap including
the sural nerve and a midline cuff of the gastrocnemius
muscle can be used for this purpose (Figures 16A and B).
This flap is designed on the proximal third of the posterior
calf and is nourished in a retrograde manner by the lower
peroneal septocutaneous perforators, through the vascular
axis of the sural nerve to the musculocutaneous perforators
of the gastrocnemius muscle. This is an important variant
of the sural neurocutaneous flap and it appears to be a good
alternative to free flaps for resurfacing the foot. Pedicle
flaps which contain a discreet and identifiable blood supply,
may be raised from soft tissue adjacent to or distant from
the wound defect. (Figures 17A to C). These flaps may
subsequently be used to provide coverage for plantar defects
of the forefoot and even the heel. One may use muscle flaps,
the main alternative to cutaneous flaps, in order to provide
well vascularized coverage over bone and to provide bulk
over a large defect. The abductor hallucis, the abductor digiti
minimi and the flexor digitorum brevis are often used to
provide coverage for hindfoot ulcers.
Free Flaps
The use of flaps with an intact blood supply is the essence
of plastic surgery. The ability to perform successful
microvascular repair of vessels as small as 1 mm enables
the transfer of composite tissue from its donor site basing
Figures 16A and B: (A) Diabetic foot right ankle; (B) Diabetic foot right ankle covered with sural flap
A
B
on an isolated vascular pedicle and the flap subsequently
revascularises with microvascular anastomosis. This is termed
microvascular free tissue transfer or free flap as the tissue is
transplanted from one part of the body to another. Free tissue
transfer can be indicated in diabetic foot for foot salvage when
local techniques are unsuccessful.

The associated morbidity and success rates are functions
of the surgical technique, the severity and the location of the
wound and the underlying healthy tissue status and vascularity
of the patients limb. Soft-tissue reconstruction of the feet
in diabetic patients with angiopathy, sensorial neuropathy,
and immunopathy is a complicated problem. Until the mid-
1980s, chronic foot ulcers in diabetic patients were treated
conservatively, because flap surgery was regarded as too
risky. However, in recent years, early debridement and flap
coverage have become popular reconstructive methods for
diabetic foot wounds. Several flap donor sites are available,
depending on the nature of the defect. LD (latissimus dorsi)
flap is a versatile flap available to cover the contour defect
and post bony resection defects over dorsum and heel (Figures
18A and B). The deep inferior epigastric artery perforator
(DIEP) flap is a relatively new flap that was developed as
a modification of the transverse rectus abdominis muscle
(TRAM) flap. ALT (anterolateral thigh) flap (Figures 19A
to D) or RAFF (radial artery forearm flap) can be raised on the
foot and leg, and used to repair defects on the weight bearing
and nonweight bearing surfaces of the foot. The advantage of
these flaps over healing by secondary intention is that their
tissue properties closely resemble those of the lost tissue, and
they will move harmonically with the surrounding soft tissue
during weight bearing.

Surgical Management of Diabetic Foot 
Chapter 17
179
Figures 17A and C: (A) Diabetic foot left heel debrided; (B) Diabetic foot left heel with cross leg flap;
(C) 2 months follow-up of same foot
C
B
A
Figures 18A and B: (A) Postdebridement diabetic foot defect; (B) Postoperative LD flap for defect
A
B
B
A
Figures 19A and B: (A) Preoperative planning for ALT flap; (B) Diabetic foot with Charcot joint

Types of Wounds and their Management
Section 3
180
Figures 19C and D: (C) Peroperative ALT flap harvesting; (D) Postoperative ALT flap for the same defect
Rehabilitations
Recurrence of foot ulcers can be prevented by using moulded
footwear, which provides effective load distribution. With
a diabetic foot, a blister from wearing a shoe that’s too tight
can cause a lot of damage. Diabetes decreases blood flow
therefore injuries are slow to heal. Therefore it is mandatory
to protect the affected/operated part by a suitable footwear
(Figures 20A and B). This habit of foot care not only helps
the patient but also prolongs the life of a graft or flap. Clinical
studies have shown that footwear and doctor prescribed
orthotics play an important role in diabetic foot care. Drew
footwear has removable insoles that can be replaced with
prescribed orthotics, which help reduce and redistribute
pressure and pressure points. The footwear has a wide shank
area to better accommodate the diabetic foot. Look for soft,
tumbled leathers that reduce irritation, and shoes that are lined
with deerskin or other soft, seamless materials. Diabetic shoes,
sometimes referred to as extra depth or therapeutic shoes, are
specially designed shoes, or shoe inserts, intended to reduce
the risk of skin breakdown in diabetics with coexisting foot
disease.

People with diabetic neuropathy in their feet may have
a false sense of security as to how much at risk their feet
actually are. An ulcer under the foot can develop in a couple of
hours. The primary goal of therapeutic footwear is to prevent
complications which can include strain, ulcers, calluses,
or even amputations for patients with diabetes and poor
circulation. In addition to meeting strict guidelines, diabetic
shoes must be prescribed by a physician and fit by a qualified
individual, such as a certified pedorthist. The shoes must also
be equipped with a removable orthotic. Foot orthotics are
devices such as shoe inserts, arch supports, or shoe fillers such
as lifts, wedges and heels. The diabetic shoes and custom-
molded inserts work together as a preventive system to help
diabetics avoid foot injuries and improve mobility.

Details of footwear and offloading techniques are mentioned
in another chapter and the reader is advised to refer to it.
Prevention of Diabetic Ulcer: It is important to re-emphasize
certain do’s and don’ts, as mentioned in previous chapters
also, as prevention of diabetic ulcer is better than its cure.
D
C
Do’s
• Inspect your feet daily for blisters, cuts and scratches.
• Always check between your toes.
• Wash your feet daily. Dry carefully.
• Avoid extreme temperatures. Test water with your hands or
elbow before bathing.
• Inspect the insides of your shoes daily for foreign objects,
and rough areas.
• For dry feet, use a very thin coat of lubricating oil such as
baby oil. Apply this after bathing and drying feet.
• Shoes should be fitted by a foot care specialist and be
comfortable at the time of purchase.
• See you physician regularly and be sure to have your feet
examined at each visit.
Don’ts
• Do not smoke.
• Do not soak your feet in hot water.
• Do not walk on hot surfaces such as sandy beaches or on
cement around swimming pools.
• Do not walk barefooted.
• Do not use chemical agents for the removal of corns and
calluses.
• Do not wear sandals with thongs between the toes.
• Do not cut corns or calluses; see your physician.
• Do not cross your legs. This can cause pressure on the
nerves and blood vessels.

Surgical Management of Diabetic Foot 
Chapter 17
181
Summary
Uncontrolled diabetes can not only involve the various organs
of the body but also lead to involvement of the leg and feet
in a variety of ways due to microangiopathy and peripheral
neuropathy leading to infection following even a minor trauma
to the foot. Diabetic ulcer complications are a leading cause
of hospitalization and amputation. Standard therapy involves
the use of dressings to protect the wound bed from trauma and
to absorb exudates, offloading of high pressure on the wound
bed, e.g. by prescribing protective footwear, and wound bed
preparation to accelerate endogenous healing and to facilitate
the effectiveness of topically applied substances. But these
measures are often deficient to heal all diabetic ulcers when the
Figures 20A and B: Protective and rehabilitative foot wear
patient’s own intrinsic wound healing system is insufficient. In
this group of patients skin replacement therapies are second line
treatment options. It is very important to recognize the severity
of the problem and go in for surgical intervention for a diabetic
foot ulcer at proper time to get the best from left over tissue.
Proper debridement and cover either in the form of skin graft
or a flap (local, regional or free) can reduce the morbidity to a
great extent. Split-skin grafting or flap cover following adequate
debridement, is an effective method of managing diabetic foot
ulcers as, compared with the conservative dressings. Therefore
timely management of these problems go a long way in
preventing further complications like amputations.
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• Management of DFU
• Microbiological control

– Wound Control

– VASHE Wound Cleansing Solution

– Debridement

– VAC

– PRP Gel

– O2 Misly

– LLLT

– Growth Factors

– Ozone Treatment

– Bagging

– Hyperbaric Oxygen Therapy
• Bioengineered Alternative Tissues
• Metabolic Control
• Vascular Control
• Mechanical Control—Offloading
Introduction
Foot ulcers in diabetic patients are common. It is estimated that
15 percent of diabetes patients will develop diabetic foot ulcer
(DFU) once in their life time, and approximately 14 percent of
diabetic ulcers lead to amputation.1 Unless a prompt, rational,
multidisciplinary approach to therapy is taken.

Factors that affect development and healing of diabetic
patients’ foot ulcers include the degree of metabolic control,
the presence of ischemia or infection, and continuing trauma
to feet from excessive plantar pressure or poorly fitting shoes.
Appropriate wound care for diabetic patients addresses
these issues and provides optimal local ulcer therapy with
debridement of necrotic tissue and provision of a moist
wound-healing environment.

A wide variety of advanced treatments for diabetic foot
ulcers, such as topical growth factors, bioengineered skin grafts,
vacuum assisted closure (VAC) therapy, and hyperbaric oxygen
therapy (HBOT), are available commercially now in India, and
clinical studies of these products have shown some evidence of
improved healing compared to standard wound care.2

During the prolonged healing process of a chronic wound,
rapid and accurate evaluation of the healing progress is
critical so that unsuccessful treatments can be discontinued
and alternate treatments be initiated as soon as possible.3,4
Management of DFU
It includes control at many levels, some of which have already
been discussed earlier.
A. Microbiological control
B. Wound control
C. Metabolic control
D. Vascular control
E. Mechanical control

F. Educational control.
Microbiological Control
Certain principles should be followed while giving antibiotics
when diabetic foot infection cases are suspected. These have
already been described in the previous chapters. Most of the
diabetic foot infections are poly microbial. So broad spectrum
antibiotic are to be used for longer duration. Because of
immunopathy there is a poor immune response in diabetics
hence normal skin commensals can cause serious infection.
Wide spectrum of antibiotics should always be used even at
initial presentation because it is impossible to predict type and
no. of microorganisms clinically, there is no way of predicting-
rapidly ascending or life threatening diabetic foot infection and
triopathy of DM reduces local resistance to invading bacterias.5
Ashok Damir
18
Chapter
Recent Advances in Management
of Chronic Non-healing Diabetic
Foot Ulcers