Principles and Practice of Wound Care

Dressings and Topical Agents in Wound Care 
Chapter 9
85
bibliography
1. Boateng JS, Matthews KH, Stevens H, Eccleston GM. Wound
Healing Dressings and Drug Delivery Systems: A Review. J
Pharm Sci. 2008;97(8):2892-923.
2. Chaby G, et al. Dressings for acute and chronic wounds: A
systematic review. Arch Dermatol. 2007;143(10):1297-304.
3. Eaglstein WH, Davis SC, Mehle AL, et al. Optimal use of
an occlusive dressing to enhance healing. Arch Dermatol.
1988;124:392-5.
4. Falanga V. Occlusive wound dressings. Why, when, which?
Arch Dermatol. 1988;124:872-7.
5. Fonder MA, et al. Treating the chronic wound: A practical
approach to the care of nonhealing wounds and wound care
dressings. J Am Acad Dermatol. 2008;58:185-206.
6. Fonder MA, Mamelak AJ. Lazarus GS, Chanmugam A.
Occlusive Wound Dressings in Emergency Medicine and
Acute Care. Emerg Med Clin N Am. 2007;25:235-42.
7. García-Gubern CF, Colon-Rolon L, Bond MC Essential
Concepts of Wound Management. Emerg Med Clin N Am.
2010;28:951-67.
8. Goldberg SR, Diegelmann RF. Wound Healing Primer. Surg
Clin N Am. 2010;90:1133-46.
9. Hess CT. When to use gauze dressings. Adv Skin Wound Care.
2000;13:266-8.
10. Kannon GA, Garret AB. Moist wound healing with occlusive
dressings. Dermatol Surg. 1995;21:583-90.
11. Lee CK,Hansen SL Management of Acute Wounds. Surg Clin
N Am. 2009;89:659-76.
12. Lio PA, Kaye ET Topical Antibacterial Agents. Infect Dis Clin
N Am. 2009;23:945-63.
13. Límová M. Active Wound Coverings: Bioengineered Skin and
Dermal Substitutes. Surg Clin N Am. 2010;90:1237-55.
14. Mahaffey PJ. Something old, something new in wound
dressings. BMJ. 2006;332(7546):916.
15. Moreira ME, Markovchick VJ. Wound Management. Emerg
Med Clin N Am. 2007;25:873-99.
16. Nakamura Y, Daya M. Use of Appropriate Antimicrobials in
Wound Management. Emerg Med Clin N Am. 2007;25:159-76.
17. Panuncialman J, Falanga V The Science of Wound Bed
Preparation. Surg Clin N Am. 2009;89:611-26.
18. Rohrich R (Ed): Current concepts in wound healing. Plast
Reconstr Surg. 2006;117(7S):1S.
19. Rumalla VK, Borah GL. Cytokines, growth factors, and plastic
surgery. Plast Reconstr Surg. 2001;108:719-33.
20. Strecker-McGraw MK, Jones TR, Baer DG. Soft Tissue
Wounds and Principles of Healing. Emerg Med Clin N Am.
2007;25:1-22.
21. Tatsioni A, Balk E, Donnell TO, Lau J. Usual Care in the
Management of Chronic Wounds: A Review of the Recent
Literature. J Am Coll Surg. 2007;205(4):617-24.
22 Teller P, White TK. The Physiology of Wound Healing:
Injury Through Maturation. Surg Clin N Am. 2009;89:
599-610.

• Techniques of Wound Closure
• Suturing Techniques
• Suturing Needles
• Sutures
• Newer Methods of Wound Closure

– Adhesives, Staples, Adhesive Tapes
• Skin Grafting
Introduction
Wound has been an enigma for the mankind which has been
obsessed about knowing it all and doing all it can to achieve
wound healing.

Wound closure can be achieved in one of three ways.
Primary wound closure is the fastest type of closure, and
results in healing by primary intention. Wounds that heal by
primary closure have a small, clean scar. Surgical incisions,
cuts, and small cutaneous wounds usually heal by primary
closure. This method is usually adopted in acute wound up to
48 hours old (Figures 1A and B).

Secondary wound closure, which leads to healing by
secondary intention, describes the healing of a wound in
which the wound edges cannot be approximated. Secondary
closure requires a granulation tissue matrix to be built to fill
the wound defect. This type of closure requires more time and
energy than primary wound closure, and creates more scar
tissue (Figure 2).

Occasionally, wounds are closed by delayed primary closure,
(healing by tertiary intention). Delayed primary closure is a
combination of healing by primary and secondary intention,
and is usually done for wounds which are contaminated or
have presented late. Here, the closure of wound is usually done
between five to seven days.

Though there are many methods, as mentioned above, to
achieve wound closure, however, primary wound closure
takes utmost priority if achievable. The prerequisites for
primary wound closure include:
• Clean healthy wound
• Minimal tension on the opposed skin margins
• Appropriate suture material availability.
Techniques of Wound Closure
1. Suturing: In primary wound closure the skin edges of the
wound are sutured together to close the defect. Whenever
possible and practical, primary wound closure is the best
way to close an acute open wound. This may be immediate,
as seen in surgically created or clean lacerated wounds. Here
scarring is minimized or it may be delayed primary, in which
the wound is prepared by debridement and regular dressings
and subsequently closed if the edges can be apposed without
tension. This usually takes four to five days.
2. Skin grafting: Is indicated for defects wherein there is
tissue loss and the margins cannot be approximated. In
this procedure a piece of skin is taken from another site
on the body and transferred to the defect. These are of two
types split thickness skin grafts (STSGs) and full thickness
skin grafts (FTGs). Skin grafts are used in places where
the wound bed has good vascularity, is free of infection
and incase there is exposed muscle or tendon with
intact paratenon, bone with periosteum or cartilage with
perichondrium.
VK Tiwari, Anshumali Mishra
Surgical Closure of Wounds
10
Chapter

Surgical Closure of Wounds 
Chapter 10
87
3. Flaps: Skin flaps are indicated for wounds or defects where
bone without periosteum, tendon without paratenon or
cartilage without perichondrium are exposed. This tissue
carries its own blood supply from the donor area and is
used in places where vascularity of the bed is doubtful or
not available.
Advantages of Primary Wound Closure
• Simplifies wound care for the patient with only suture line
to care for wound heals quickly and painlessly
• Vital underlying structures if any are protected
• Minimizes scarring and has better cosmetic outcome.
Contraindications of primary wound closure:
• Wound with devitalized tissue or with tissue of doubtful
viability even after debridement.
• Acute wounds where colonization is suspected such as bite
wounds.
• Wound with embedded foreign particles which can not be
removed.
• If skin margins on apposition are under tension.
• If there is dead space under the skin.
The two important components of primary wound closure are:
1. Suturing technique
2. Suture material.
Suturing Technique
Basic Principles
• Good approximation of wound edges is paramount to
proper wound closure.
• The wound edges must not only be aligned but also
everted. Eversion ensures that dermal elements of the skin
are apposed which is vital for wound healing.
• In most body areas except the face, sutures should be
placed 3 to 4 mm apart from the wound margin and 5 to 10
mm apart from each other.
• With simple sutures the knots of the sutures are to be placed
away from the opposed edges of the wound.
• Skin handling must be as atraumatic as possible.

The suturing techniques described below form the core of
suturing. Other types of suture techniques are a modification
of these basic techniques.
Simple Suture
Simple suture or everting interrupted suture: Insert the needle
at 90° to the skin. The needle should exit through the opposite
side equidistant to the wound edge and directly opposite to the
Figure 2: Results of secondary closure of a wound due to loss of
tissue in face leading to extensive scarring
Figures 1A and B: (A) Clean cut over lip; (B) Primary closure done
A
B

General Principles for Wound Management
Section 2
88
initial insertion. Equal amount of tissue should be opposed on
both sides. All knots should be placed on the same side with
wound edges everted (Figures 3A and B).
Simple running suture: This method entails similar technique
to that of a simple suture without a knotted completion after
each throw. This suture technique has the disadvantage of
causing excess tension and strangulation at the suture line if
too tight, which leads to compromised blood flow at the skin
edges (Figure 4).

Another variant of this suture is the simple locking suture.
This allows for greater accuracy in skin closure. Here the
running suture end is drawn through a preformed loop before
completion of the suture to form the locked pattern. This
technique is usually used for scalp closure (Figure 5).

Both the above sutures, i.e. simple running and locking
suture have the advantage of a more water tight closure of
Figures 3A and B: Simple interrupted sutures
Figure 5: Locking suture
A
B
Figure 4: Continuous or running suture
the wound when compared to the simple interrupted suture
but the down side is the fact that in case of wound infection
the entire wound will need to be opened in running sutures
whereas removal of one or two sutures may suffice in case of
the interrupted sutures.
Mattress Sutures
There are two types of mattress sutures:
1. Vertical mattress
2. Horizontal mattress.
Vertical Mattress
In this suture pattern the needle is inserted 1.5 cm from the
wound edge in the right side and passes through the wound

Surgical Closure of Wounds 
Chapter 10
89
then drawn out 1.5 cm from the left side of the wound. The
needle is reinserted 0.75 cm from the left side (medial to the
site from where it was withdrawn) passes through the wound
and is again drawn 0.75 cm from the wound edge (medial
to the first bite). This suture is used in areas of skin tension.
It may be used even in subdermal layers and aids in skin
eversion . The disadvantage of this type of suture is the use of
extra quantities of suture material and poor aesthetic result as
compared to the simple suture (Figures 6A to C).
Horizontal Mattress
In this type of suture the entrance and exit sites for the needle
are at the same distance from the wound edge forming a
rectangular plane. The needle is inserted from one side taken
out from the other. It is then reinserted at point approximately
0.5 cm away in the same line as the previous entry point
taken across the wound and taken out from the skin on the
opposite side again in the same line of the previous entry point
0.5 cm away and the knot is tied. This type of suture has the
disadvantage of interfering with the blood supply of the skin
edges and usually reserved to be used in muscles or in deeper
planes (Figures 7A and B).
Subcuticular Sutures
These sutures are placed intradermally in either simple or
running fashion.The needle is placed horizontally in the
dermis 1 to 2 mm from the wound edge. It is not passed
through the skin edge. The knot is buried in the simple suture
technique and the technique allows for minimization of the
tension over the wound edges. In the continuous subcuticular
stitch, the suture ends can be taped to the skin surface without
knotting (Figures 8A and B).
A
B
C
Figures 6A to C: Vertical mattress suture
Figures 7A and B: Horizontal mattress suture
B
A

General Principles for Wound Management
Section 2
90
Other Suture Techniques
• Half-buried mattress suture (Gille’s suture): Used to close
wounds that are angled or Y-shaped without appreciably
compromising blood supply to the wound tip (Figure 9).

The corner stitch is a variation of the horizontal mattress
stitch. The needle enters the skin on one side of the obtuse
angle of the wound, passes through the deep dermis of the
corner flap, and is reinserted through the dermis of the other
side of the obtuse wound angle. It finally re-emerges through
the epidermis on the side of the obtuse angle, adjacent to the
initial entry point.
• Pulley suture: The pulley suture is a modification of the
vertical mattress suture. When pulley sutures are used, a
vertical mattress suture is placed, the knot is left untied,
and the suture is looped through the external loop on the
other side of the incision and pulled across. At this point,
the knot is tied. This new loop functions as a pulley,
directing tension away from the other strands. The pulley
suture facilitates greater stretching of the wound edges and
is used when additional wound closure strength is desired.
• Far near—near far pulley stitch: Another stitch that serves
the same function as the pulley suture is the far-near near-
far modification of the vertical mattress suture. The first
loop is placed approximately 4 to 6 mm from the wound
edge on the far side and approximately 2 mm from the
wound edge on the near side. The suture crosses the suture
line and re-enters the skin on the original side at 2 mm from
the wound edge on the near side. The loop is completed,
and the suture exits the skin on the opposite side 4 to 6 mm
away from the wound edge on the far side. This placement
creates a pulley effect.

The other important constituent of achieving primary
closure is the suture material and the type of needles used to
achieve a near perfect closure for the given circumstances.
Figure 9: Half-buried suture
Suturing Needles
These may be classified on the basis of the parts of the needle
as follows:
1. Eye

a. Closed eye needle: Resembles a household needle.
Suture ends need to be passed through the eye is
traumatic for the tissues.

b. Swaged-on-needle (eyeless or atraumatic): Permanently
attached to the suture. Less traumatic to the tissues as
less suture passes through the tissues on each round.
2. Body or shaft

a. Straight or long stemmed needle.
Figures 8A and B: Subcuticular suture
B
A

Surgical Closure of Wounds 
Chapter 10
91

b. Curved needle: ¼, 3/8, ½, or 5/8 of a circle are common
shapes used in these type of needles.
3. Point of shaft

a. Conventional cutting: Point is sharp and cutting and is
provided at the concave surface.

b. Reverse cutting: The cutting edge here is provided on
the convex surface to minimize tissue trauma.

c. Taper cut needle: The point of the needle is cutting but
the body is round.

d. Noncutting (round tip) needle: The point is round and
the body is oval. It causes minimal tissue trauma and is
usually used for tissues such as mucosa and muscle.
SUTURES
The history of sutures begins more than 2,000 years ago with
first records of eyed needles. Indian plastic surgeon Susruta
(380–450AD) described sutures made from flax hemp and
hair. During the same time jaws of black ant were used as
surgical clips in bowel surgery. In 30 AD, the roman celsus
again described the use of sutures and clips. Galen further
propogated the use of silk and catgut as suture material. The
first synthetic sutures were developed in 1950s and further
development has led to creation of various forms.

An ideal suture material should be strong, should have
no intrinsic memory, should be easily sterilizable, should be
completely inert and should be easily producible. All these
qualities are not available in any one suture material and
hence an appropriate suture material is to be chosen for a
given situation.
Classification of Sutures
Sutures may be classified on the basis of:
• Origin

– Natural, e.g. silk, catgut

– Synthetic, e.g. prolene (polypropylene) and vicryl
(polygalactin).
• Durability

– Absorbable, e.g. catgut and vicryl

– Nonabsorbable, e.g. nylon and prolene
• Number of filaments

– Monofilament, e.g. catgut, nylon, prolene

– Multifilament, e.g. vicryl, silk.

The above examples are representative apart from
these various other synthetic materials such as monocryl
(Polyglecaprone), maxon (Polyglycolide-trimethylene carbo­
nate), PDS (polydiaxone) dexon (polyglycolic acid), novafil
(polybutester) and PTFE (polytetra fluroethylene) may be used
on appropriate occasions. Steel wires have also been used in
the past as sutures but today their mention is largely historical.

Absorbable sutures are applicable to a wound that heals
quickly and needs minimal temporary support. Their purpose
is to alleviate tension on the wound edges. Absorbable sutures
lose their tensile strength before complete absorption. Catgut
can last four to five days in terms of tensile strength. In chromic
form it can last up to three weeks. Vicryl (polygalactin) and
Dexon (polyglycolic acid) maintain tensile strength for 7 to
14 days although complete absorption takes several months.
maxon (Polyglycolide-trimethylene carbonate) and PDS
(polydiaxone) are considered long term absorbable sutures
maintaining tensile strength for several weeks and requiring
several weeks for complete absorption.

Nonabsorbable sutures have varying tensile strengths
and may be subject to some kind of degradation. Silk has
the lowest strength and nylon has the highest. Prolene
(polypropylene) sutures are comparable to nylon in strength.
Novafil (polybutester) is a suture appreciated for its elastic
properties.

Considerations for choosing suture material are as follows:
Physical Properties
Durability: Durabilty of the suture in the wound is affected
by many factors like blood supply of the wound and infection.
Tissues with good blood supply or presence of infection will
get rid of the suture materials rapidly, so materials with low
absorption rates should be used. Rate of healing and tension of
the suture line affect the choice of suture material too.

Handling ability and knot security: Good suture material
should have good handling ability, minimal capillarity and
good knot security. For example, though prolene and nylon are
very strong sutures they require extra throws to secure knot in
place.

Sterilization: Gamma irradiation adversely affects poly-
gycolic acid and polypropylene. Autoclaving of any suture
more than three times has also been found to significantly
reduce suture strength. Ethylene oxide gas is suitable method
of sterilization of all sutures.

Biological properties: Atraumatic needles with synthetic
monofilament sutures are preferred in most cases as they reduce
tissue reaction which ensues as a result of traumatization of
tissues by the needle dragging of suture material and chemical
nature of the suture. Also these sutures have less chances of
getting impregnated with micro-organisms.
NEWER WOUND CLOSURE TECHNIQUES
These include:
1. Adhesives
2. Staples
3. Adhesive tapes.

General Principles for Wound Management
Section 2
92
Adhesives: Use of surgical adhesives can simplify skin
closure because certain problems inherent to suture use can
be avoided. Problems (e.g. reactivity, premature reabsorption)
can occur with sutures and lead to an undesirable result, both
cosmetically and functionally. Several adhesives have been
developed to alleviate this problem and to facilitate wound
closure. One substance, cyanoacrylate, has been used for 25
years and easily forms a strong flexible bond (Figure 10).

Octyl-2-cyanoacrylate (Dermabond, ethicon, somerville,
NJ) is the only cyanoacrylate tissue adhesive approved by
the U.S. Food and drug administration (FDA) for superficial
skin closure. Octyl-2-cyanoacrylate should only be used
for superficial skin closure and should not be implanted
subcutaneously. Subcutaneous sutures are used to take the
tension off the skin edges prior to applying the octyl-2-
cyanoacrylate. Subcutaneous suture placement aids in everting
the skin edges and minimizing the chances of deposition of
cyanoacrylate into the subcutaneous tissues.

Fibrin-based tissue adhesives can be created from
autologous sources or pooled blood. They are typically used
for hemostasis and can seal tissues. Although they do not have
adequate tensile strength to close skin, fibrin tissue adhesives
can be used to fixate skin grafts or seal cerebrospinal fluid
leaks. Commercial preparations such as Tisseel (Baxter)
and Hemaseel (Hemacure) are FDA-approved fibrin tissue
adhesives made from pooled blood sources.

Staples: Staples provide a fast method for wound closure
and have been associated with decreased wound infection
rates. Staples are composed of stainless steel, which has been
shown to be less reactive than traditional suturing material.
The act of stapling requires minimal skin penetration, and,
thus, fewer microorganisms are carried into the lower skin
layers. Staples are more expensive than traditional sutures and
also require great care in placement, especially in ensuring the
eversion of wound edges. However, with proper placement,
resultant scar formation is cosmetically equivalent to that of
other techniques (Figure 11).

Adhesive tapes: Closure using adhesive tapes or strips
was first described in France in the 1500s, when pare devised
strips of sticking plaster that were sewn together for facial
wounds. This method allowed the wound edges to be joined
and splinted. The porous paper tapes (e.g. steri-strips) in use
today are reminiscent of these earlier splints and are used to
ensure proper wound apposition and to provide additional
suture reinforcement. These tapes can be used either with
sutures or alone. Often, skin adhesives (e.g. mastisol, tincture
of benzoin) aid in tape adherence (Figure 12).
SKIN GRAFTING
Definition: Skin graft is defined as a part of skin transferred
from one portion of the body to another without its blood
supply.
Figure 10: Adhesive used for closure of wound
Figure 11: Staples used for wound closure
Figure 12: Steri-strips used for wound closure

Surgical Closure of Wounds 
Chapter 10
93
Classification of skin grafts:
• Based on the anatomy skin grafts can be classified as
follows:

1. Partial thickness or split thickness skin graft: It
includes epidermis and part of dermis. Though
they can survive on less vascularity from the bed,
they have greater tendency for contraction. These
are most effective for coverage of post-traumatic
raw areas. Donor sites of split thickness grafts heal
spontaneously by re-epithelialization from epithelial
cells lining the hair follicles and sweat glands within
10 to 21 days. These can be reharvested once the
wound epithelializes.

2. Full thickness grafts: Include epidermis with entire
dermis and are approximately 0.88 to 1mm thick.
They require better vascular bed for survival as well
as good vascularity from the margins. They undergo
minimal contraction. Their sensory recovery is better
than that of split skin graft. They have no role to
play in coverage of raw areas but have an important
role to play in covering areas following contracture
release. The donor areas for full thickness grafts
cannot resurface spontaneously because of lack of
epithelial elements. The defect needs to be closed
primarily. Therefore, they are not used for large
defects, instead are used for small defects only.
• Based on thickness the partial or split thickness grafts can
be further categorized into three types:

1. Thin split thickness graft: Which has a thickness of
0.20 to 0.25 mm or 0.008 to 0.01 inch (Figures 13 A
and B).

2. Intermediate thickness graft: Which has a thickness
of 0.25 to 0.5 mm or 0.012 to 0.016 inch (Figures 14
A and B).

3. Thick split thickness graft: Which has a thickness of
0.6 to 1 mm or 0.30 to 0.45 inch (Figure 15).

By and large, for all wounds, grafts should be thin because
their ‘take’ is better. However, because they undergo greater
contraction, thicker grafts (intermediate thickness) are
preferred for regions like face especially eyelids and lips so
that they contract less postoperatively. In children and elderly,
usually thin grafts are harvested as the dermis is thin.
• Based on size and technique of harvesting split skin grafts
they are classified into following types:

1. Pinch grafts: Pinch grafts are ‘small deep ‘grafts’
which are not used at present because of the extremely
ugly scarring of the donor site. The donor area chosen,
therefore, is a hidden area usually the thigh or groin.
The procedure involves lifting the skin with a needle
and a 0.5 cm fragment is cut to obtain a graft which is
thicker in the centre and tapering towards the edges.
The resulting wounds can even be closed primarily.
The grafts are transferred to the wound at regular
intervals, distance between them being about 5 mm.
This method is now of historical importance only.

2. Stamp grafts: Stamp graft are split thickness
grafts which, after harvesting, are cut as square or
rectangular pieces of skin of different sizes. They
are also applied directly to the wound and held in
place with occlusive dressings. The intervening areas
between the stamps heal by epithelialization from
the margins of the graft. As a result, these areas tend
to hypertrophy and give unsightly scars. This method
may be of use in case of very extensive raw areas.

3. Sheet grafting: It is the most widely used at present as
the grafts can now be easily harvested with the help
of the latest modified humby skin grafting knife or
dermatome. Large sheets about 10 cm wide or more
Figures 13A and B: (A) Thin split skin graft—note the almost nonexistent dermis in the graft;
(B) Note the very fine and multiple bleeding points in the donor area
B
A

General Principles for Wound Management
Section 2
94
can be procured easily and they can cover large raw
areas. This gives good aesthetic results especially
on the face. These sheets can be meshed to increase
their size to cover larger areas.

4. Meek grafting: It is being used lately. This was
originally described in 1958 by an American surgeon,
CP Meek. The procedure involves using a special
spray called ‘meek adhesive’ with which a small
piece of graft is adhered to a prefolded gauze which
has an expansion ratios of 1:3, 1:4, 1:6 and 1:9. When
this is applied to a raw area this produces a regular
distribution of autograft islands with a ninefold
expansion. This requires a very small donor areas
and the graft islands were evenly placed in a regular
pattern. The epithelialization and hospitalization
time is reported to be shorter with this technique,
compared to the mesh graft method. This method is
preferred in extensive burns where the donor areas
are very limited.
Donor Areas
Skin grafts can be harvested from any area of the body
including scalp and chest and abdomen if there is scarcity
of donor areas. The most common sites whenever available
are the lower limbs and upper limbs. The thigh is the most
commonly used in lower limb especially the anteromedial
and anterolateral thigh. While harvesting grafts from a hairy
region, it is important to take thin grafts as thicker grafts
contain undesirable hair follicles which lead to hair growth in
the recipient area.

The donor areas of split skin graft heal in 10 to 21 days.
The donor areas are dressed by application of paraffin gauze
which may or may not be antibiotic impregnated followed
by gauze and then gamgee pads and a compressive bandage.
This bandage usually gets loosened up in two weeks and
gauze falls off when opened in three weeks as majority
of the superficial donor area re-epithelializes by 12 days.
The other dressings which have been used for donor areas
include collagen dressings, biobrane and opsite. All these
have been found to reduce pain, act as a barrier to bacteria,
fasten healing and reduce the bulk of dressing. However,
they are very costly.
Technique of Harvesting Split Skin Graft
Once the donor site has been selected, the graft can be
harvested under general anesthesia, regional nerve blocks
Figure 15: Thick split thickness skin graft—the white thick dermis
included in the graft and thicker and fewer bleeding points are visible
in the donor area
Figures 14A and B: Intermediate thickness skin graft—note the thickness of dermis in the graft and the fine innumerable
bleeding points in the donor area
B
A

Surgical Closure of Wounds 
Chapter 10
95
or even local anesthesia. Infiltration of local anesthesia with
adrenaline reduces the amount of blood loss from the donor
area apart from prolonging the duration of the effect of the
local anesthesia. The area is lubricated with vaseline or
paraffin and saline. An assistant gives traction to the skin from
one end of the donor site while the operating surgeon gives
traction from the opposite side. Wooden/ metallic Gabbroo
graft boards are frequently used for applying the traction. The
knife is placed parallel to the surface of skin and then moved
‘to and fro’ with moderate pressure and gradually moved
ahead with moderate speed till a long sheet is removed. The
width of the graft harvested can be adjusted according to the
area available (Figures 16A and B).

In case of dermatome, it is kept on the skin surface at an
angle of 30 to 45° and the throttle is pressed and the dermatome
advanced flat to the skin with gentle downward pressure.
Once the sheet of graft is harvested, the dermatome is angled
upwards and lifted off the donor site cutting the graft.
Meshing of Graft
The principle behind meshing a graft is to gain expansion by
making incisions parallel to the longitudinal axis of the graft
and the maximum advantage of meshing is gained when the
long axis of the meshes parallel the stress lines of the area to be
grafted.This can be achieved both manually by using an 11 no.
blade or by a mesher in which the carrier with the graft can be
pulled through the mesher with the help of a handle or lever. By
adjusting the lengths of the cuts, the resulting size of the graft
can be changed and expansion of 1.5 to 9 times the original size
can be gained. Minimal expansion should be used depending on
the availability of the skin graft in relation to the size of the raw
areas .The successful use of mesh grafts in covering extensive
raw areas has proved its worth (Figures 17 and 18).
Advantages
The advantages of meshing are as follows:
It expands the graft—
1. Discharge can escape through the gaps in the graft so that
the accumulated discharge does not lift the graft off the
wound surface.
2. The meshing gives a larger edge for production of new
epithelial cells than the stamp grafts or strip grafts. A
meshed graft conforms better to the wound surface. When
the slits are made, the edges of the slits curl towards the
dermal surface because of the inelastic epidermis and
elastic dermal layer. When this mesh is applied to the raw
area, both undersurface as well as the edges of the skin
bridges adhere to the recipient bed. This allows for greater
total contact of graft to the wound.
3. The raw areas seen within the mesh heals by the epithelium
migrating from the slit margins and this takes only a few
Figures 16A and B: (A) Anterolateral and anteromedial aspect of thigh—the most common site for harvesting graft; (B) Technique for
harvesting skin graft with Humby’s knife
B
A
Figure 17: Hand meshing of graft

General Principles for Wound Management
Section 2
96
Application of Graft
Before the application of the graft to the wound bed it has to
be ensured that proper hemostasis is achieved especially if
the unhealthy granulation tissue on the wound bed has been
excised with a scalpel. Hemostasis is achieved by using
adrenaline saline soaked (1 in 2,00,000) gauze pieces with
pressure dressing or even by fibrin glue which is being used
of late (TisselR). The graft is then spread over the wound
with the help of graft spreader or with the back of forceps
ensuring that the edges of the graft are properly spread out
as these have a tendency to roll over. This can then be held
in place with suture or surgical staples if areas are small or
with fibrin glue and this is covered with nonadherent gauze.

In the past it was a routine to do an occlusive dressing
after any split skin grafting because it was considered that
pressure over a graft was essential for its ‘take’. However
with time and experience with different techniques it has been
clearly demonstrated that a graft can ‘take’ satisfactorily over
granulating areas as long as it is not mechanically displaced
or lifted off from its bed by hematoma or pus formation and
that occlusive dressings are not a must. Areas like the anterior
chest, abdomen and back of trunk where constant motion
during respiration may displace the grafts by producing
shearing between the dressing and the wound bed are better
treated by exposure method after applying the graft. This is
also true if dressings are used as in the limbs, it is imperative
to give an even gentle compression dressing with proper
immobilization of the extremity. The general principle is
to immobilize a joint above and below the grafted area to
minimize limb movements and thus avoid shearing forces.

Postoperative care and dressing: After the fourth day,
usually the time by which the grafts have adhered fairly well
to the wound bed, change over to treatment by dressings is
advisable.The second dressing change can then be done
at 7 days postgrafting and dried up graft overlapping the
normal skin can then be debrided and exposed dressing can
be changed to a closed dressing which will be less bulky.
Thereafter, the dressing can be changed as often as required
till the areas heal completely. Sutures or staples, if applied, can
be removed on the third dressing. Immobilization of joints can
be discontinued after 7 days, once the grafts have taken up and
some movements of joint can then be allowed during dressing
change to avoid stiffening of the joints. Proper physiotherapy
with full range of movements should be resumed only after all
dressings are removed and healing is complete.

Once the wounds have completely healed, the grafts have
to be kept lubricated with some oil massage and require a
continuous pressure using pressure garments which prevent
inter-graft hypertrophy. In lower limbs, the pressure support
is essential for 3 months. This can be given by crepe bandage
or pressure garments. Apart from preventing hypertrophy in
grafts, they also prevent venous congestion and breakdown in
A
Figures 18A and B: (A) Graft being meshed by passing it through
the mesher; (B) Meshed graft being applied on raw area
B
days as the raw areas within the mesh are always less
than 5 mm wide. It is well known that epithelium spreads
rapidly from the edge of the defect for a distance of 5 mm
and thereafter it spreads very slowly.
4. Meshed graft can be easily placed in close proximity
to the wound surface in case of uneven or convoluted
surfaces.
5. It is easier to express out a hematoma or seroma from under
the surface of the graft without disrupting the entire graft if
it is meshed.
Disadvantages
The disadvantages of meshing are:
1. The checkered board pattern or cobblestone appearance
can be displeasing especially in aesthetically important
areas like face.
2. The secondary epithelium in the meshed area is not of the same
quality as the grafted skin and this is visible for rest of life.

Surgical Closure of Wounds 
Chapter 10
97
the graft. They have to be worn throughout the day and night
especially during ambulation.
Summary
Achieving an early and healthy closure of wound is the primary
aim in wound care. There are different methods of achieving
closure, either by suturing, staples, adhesives or by grafting or
flap corner. It is up to be the treating specialist to judiciously
use the right technique at the right time in orders to give good
results.
Bibliography
1. Bailey and Love’s short practice of surgery, 25th edn.
2. F Charles Brunicardi, Dana K Anderson, Timothy R Billar,
David L Dunn, John G Hunter, Jefferey B.
3. K Rajagopal Shenoy, Anitha Nileshwar. Manipal Manual of
Surgery, 3rd edn, 2010.
4. Morris PJ, Wood WC. Oxford Textbook of Surgery, 2nd edn.
Oxford University Press, New York, 2000.
5. Sabiston Textbook of Surgery. David C Sabiston, Courtney M.
Townsend.
6. Schwartz Principal of Surgery, 9th edn.

• Classification of Surgical Wounds
• Definition of SSI
• Epidemiology and Microbiology
• Reducing the Risk of Surgical Site Infections
Introduction
The principles of antisepsis by Joseph Lister and Pasteur’s germ
cell theory in the 19th century have led to a better understanding
in the etiopathogenesis of postoperative wound infection.
Despite improvements in operating room practices, instrument
sterilization methods and better surgical technique, surgical
site infections (SSIs) remain a major cause of postoperative
morbidity and delay in discharge from the hospital.
Classification of surgical
wounds
The surgical wound classification system can be divided into
the following four categories:

Class I—clean: Uninfected operative wound with no inflam-
mation and in which the respiratory, gastrointestinal, genital and
urinary tracts were not entered. Clean wounds are closed at
surgery and, if necessary, drained with closed drainage.

Class II—clean-contaminated: Wound in which the
respiratory, GI, genital or urinary tract(s) were entered under
controlled conditions but without unusual contamination or
spillage of contents.

Class III—contaminated: Open, fresh accidental wound
or an operation with a major break in aseptic technique (e.g.
open cardiac massage) or gross spillage from the GI tract.
Also included are incisions in which acute, nonpurulent
inflammation is found.

Class IV—dirty or infected: Old wounds with dead
tissue and those that involve existing clinical infection or a
perforated bowel, suggesting that the pathogens causing the
postoperative infection were present in the wound before the
surgery.
DEFINITION OF SSI
Surgical site infection: It is defined as either an incisional
or organ/space infection occurring within 30 days after an
operation or within 1 year if an implant is present, and at least
one of the following:
• Purulent drainage, with or without laboratory confirmation,
from the superficial incision
• Organisms isolated from an aseptically obtained culture of
fluid or tissue from the superficial incision
• At least one of the following signs or symptoms of
infection—pain or tenderness, localized swelling, redness,
or heat
• Diagnosis of superficial incisional SSI by the surgeon or
attending physician.

Incisional SSIs are further divided into superficial incisional
SSI (that only involves skin and subcutaneous tissue) and deep
incisional SSI (those involving deeper soft tissue, including
fascia and muscle layers).

Organ/space SSI are those infections which occur within
30 days after the operation if no implant is left in place or
within one year if implant is in place and the infection appears
Vinod K Malik, Ashish Dey
Surgical Site Infection: Preventive
Strategies
11
Chapter

Surgical Site Infection: Preventive Strategies 
Chapter 11
99
to be related to the operation and infection involves any part
of the anatomy (e.g. organs or spaces), other than the incision
(Figure 1).
Epidemiology and Microbiology
Epidemiology
The effects of surgical site infections can be judged by the fact
that in U.S. out of 40 million inpatient surgical procedures
each year; 2 to 5 percent is complicated by surgical site
infections. This prolongs the hospital stay by 7.4 days on an
average.

Organisms associated with SSIs vary with the anatomic
location of the operation and the procedure performed.
The most common organisms isolated from SSIs are
Staphylococcus aureus (coagulase negative staphylococci),
Enterococcus species and Escherichia coli. For most SSIs, the
source of the pathogen(s) are endogenous and comes from the
patient’s skin, mucous membranes or bowel. Exogenous SSI
pathogens are occasionally responsible and include aerobic
staphylococci and streptococci. These organisms mostly come
from members of the surgical team (e.g. hands, nose or other
body parts), contaminated surfaces in the operating room,
even the air; and contaminated instruments, surgical gloves or
other items used in surgery.

At the end of surgery, bacteria and other microorganisms
contaminate all surgical wounds, but only a small number
of patients actually develop a clinical infection. Whether an
infection actually occurs depends on the number of bacteria
entering the wound, type and virulence of the bacteria and the
host defense mechanisms.

Other factors affecting rates of SSIs include obesity, malnut­
rition, associated comorbidities and immuno­compromised
states.
REDUCING THE RISK OF SURGICAL
SITE INFECTIONS
In 1999, CDC issued a number of guidelines for reducing the
risk of SSIs. They can be grouped as follows:
Operating Room Measures
Although all guidelines regarding Intraoperative operating
room ventilation may not be financially possible they should
be adhered to as much as possible.
Ventilation
1. Positive-pressure ventilation in the operating room with
respect to the corridors and adjacent areas should be
maintained.
2. A minimum of 15 air changes per hour, of which at least 3
should be fresh air should be ensured.
3. Air should be introduced at the ceiling, and exhaust near
the floor.
4. Operating room doors should be kept closed except as
needed for passage of equipment, personnel and the patient.
5. The number of personnel entering the operating room
should be limited to necessary personnel.
Cleaning and Disinfection of Environmental
Surfaces

When visible soiling or contamination with blood or
other body fluids of surfaces or equipment occurs during
an operation, a disinfectant should be used to clean the
affected areas before the next operation.
Sterilization of Surgical Instruments
1. All surgical instruments should be sterilized according to
published guidelines.
2. Flash sterilization should be performed only for patient
care items that will be used immediately (e.g. to reprocess
an inadvertently dropped instrument). It should not be used
for reasons of convenience, as an alternative to purchasing
additional instrument sets, or to save time.
Preoperative Measures
a. Method of hair removal: In a Cochrane review that
included eleven RCTs that compared hair removal (using
either depilatory cream or razors) with no hair removal
Figure 1: Cross section of abdominal wall depicting CDC SSI
classifications

General Principles for Wound Management
Section 2
100
showed no statistically significant difference between the
groups in terms of surgical site infections. It also showed
that there were statistically significantly more SSIs when
people were shaved rather than clipped. There was also
no difference in SSIs when patients are shaved or clipped
one day before surgery or on the day of surgery. The
recommendations, therefore are:
1. Hair should not be removed preoperatively unless the
hair at or around the incision site interferes with the
operation.
2. If hair is removed, it should be removed immediately
before the operation, preferably with electric clippers.
b. Serum blood glucose: Levels should be adequately
controlled in all diabetic patients.
c. Stopping use of tobacco: Products should be encouraged
preoperatively. Patients should be instructed to abstain
from smoking for at least 30 days before elective
operation.
d. The incision site: Should be thoroughly washed and cleaned
to remove gross contamination before performing antiseptic
skin preparation. Whenever possible, all infections remote
to the surgical site should be identified and treated before
elective operation. An appropriate antiseptic agent for
skin preparation should be used (Table 1). Wide prepping
of the proposed incision site with antiseptic solution
preoperatively helps keep microorganisms from migrating
into the wound (breakthrough) if the site towels or drapes
become wet during surgery.
Hand/Forearm Antisepsis for Surgical
Team Members
1. Nails should be kept short.
2. A preoperative surgical scrub should be performed for at
least 2 to 5 minutes using an appropriate antiseptic. The
hands and forearms should be scrubbed up to the elbows.
3. Wearing of hand or arm jewelry should be discouraged.
Surgical Attire
1. A surgical mask that fully covers the mouth and nose
should be worn throughout the operation.
2. A cap or hood that fully covers the hair on the head and
face should be worn when entering the operating room.
3. Surgical gowns and drapes that are wet are ineffective
barriers and should be avoided. Scrub suits that are visibly
soiled, contaminated and/or penetrated by blood or other
potentially infectious fluids should be changed.
Asepsis and Surgical Technique
1. Principles of asepsis when placing intravascular devices
(e.g. central venous catheters), spinal or epidural anesthesia
catheters, or when dispensing and administering intravenous
drugs should be adhered to.
2. Good surgical technique is indispensable as it minimizes
tissue trauma, controls bleeding, eliminates dead space,
removes dead tissue and foreign bodies, uses minimal
Table 1: Characteristics of antiseptic solutions and suggested application
Antiseptic
Mechanism of action
Antimicrobial coverage
Onset
Duration
Application
Aqueous-
iodophor
Free iodine-protein,
DNA damage
Excellent for gram +ve
bacteria, good for gram −ve,
fungi, virus, mycobacteria
Intermediate
2 hours
2-step scrub and
paint
Aqueous-CHG
Disrupts membranes
Excellent for gram +ve, good
for gram –ve and virus, fair for
fungus, poor for mycobacteria
Intermediate
6 hours
2-step scrub and dry,
repeat
Alcohol-iodophor
Denatures protein, free
iodine-protein, DNA
damage
Improved gram –ve,
mycobacteria activity
Rapid
48 hours
1-step paint, dry
time, minimum of
3 min on hairless
surface
Alcohol-CHG
Denatures protein,
disrupts membranes
Improved gram −ve,
mycobacterial, fungal activity
Rapid
48 hours
Dry site: 30-sec
scrub, moist site:
2-min scrub dry time,
minimum of 3 min on
hairless surface
CHG—chlorhexidine gluconate.

Surgical Site Infection: Preventive Strategies 
Chapter 11
101
suture and maintains adequate blood supply and
oxygenation. Specifically, it is important to handle soft
tissue gently to avoid crushing that can result in tissue
necrosis. Electrocautery should be used sparingly to
control bleeding because it leaves behind dead tissue that
is more likely to become infected.
3. Absorbable suture should be used whenever possible
because permanent suture, especially silk suture, reduces
the number of bacteria necessary to cause infection.
4. Closed suction drains that exit through a separate stab
wound helps prevent accumulation of tissue fluid in
the dependent portion of the wound. Preventing this is
especially important in obese patients and may reduce
SSIs. Passive drains, such a penrose drain, exiting through
the bottom of the incision should not be used.
Antimicrobial Prophylaxis
1. A prophylactic antimicrobial agent should be used only
when indicated, and selected based on its efficacy against
the most common pathogens causing SSI for a specific
operation and published recommendations. There is
no general recommendation for antibiotic prophylaxis
in soft tissue and cutaneous procedures. It is routinely
used in thoracic, vascular and biliary procedures. In case
of most operations of the GI tract including colorectal
surgery, prophylaxis is recommended. Role of antibiotic
prophylaxis in laparoscopic cholecystectomy still needs to
be determined.
2. The initial dose of prophylactic antimicrobial agent
should be administered by the intravenous route and
timed such that a bactericidal concentration of the drug is
established in serum and tissues when the incision is made.
Therapeutic levels of the agent in serum and tissues should
be maintained throughout the operation and until a few
hours after the incision is closed.
3. The use of antibiotics preoperatively can reduce the rate
of infection, particularly wound infections, after certain
operations. For most procedures, an inexpensive, first-or
second-generation cephalosporin, which has a moderately
long half-life and is active against staphylococci and
streptococci, has been effective when given intravenously
(IV) 30 minutes before surgery.
4. Also, third-and fourth-generation cephalosporins should
not be used for routine surgical prophylaxis because they
are expensive, their spectrum of activity includes organisms
rarely encountered in elective surgery and their widespread
use may promote the emergence of resistance.

Other factors like prolonged preoperative hospitalization
exposes patients unduly to hospital flora including multidrug-
resistant organisms. prompt postoperative discharge reduces
the risk of infection, provided patients are able to take care
of themselves at home. A combined effort between the health
care providers including hospital staff and nursing personnel
can go a long way in preventing surgical site infections and
reducing the burden of health care costs to a great extent.
bibliography
1. Hemani ML, Lepor H. Skin preparation for the prevention
of surgical site infection: which agent is best? Rev Urol Fall
2009;11(4):190-95.
2. Mangram AJ. Guideline for Prevention of Surgical Site
Infection, 1999 (Infection Control and Hospital. Epidemiology
20 April 1999: 250-80.

• Epidemiology

– Incidence

– Augmentation Mammoplasty: Yeasts
• Pathogenesis Including Risk Factors
• Clinical Features of Fungal SSI
• Diagnosis
• Management

– Treatment Failure

– Invasive Aspergillosis
Introduction
Surgical site infections (SSI) are defined as bacterial or fungal
infections of the tissue, organ, or spaces, surgical wounds,
exposed by surgeons during performance of an invasive
procedure. The majority of SSIs are bacterial (70%), followed
by fungi (20%), viral and anaerobic (10%) causes. Fungal
SSIs are related to 3 factors: degree of microbial (yeast)
contamination of wound during surgery (major abdominal
surgery), duration of procedure, host factors. Fungi cause
nosocomial infections in surgical patients as: part of
polymicrobial infections, fungemia, rare aggressive soft tissue
infections, opportunistic infections.1,2

The ubiquity of fungi in environment coupled with
suppression of normal bacterial flora promotes fungal
super-infection in these patients. Invasive fungal infections
are missed owing to lack of clinical awareness and similar
presentation as bacterial infection coupled with paucity of
mycology laboratories. Though the diagnosis of invasive
fungal infection is difficult clinically and microbiologically,
as there is no general consensus about what signs, symptoms
and cultures define a fungal infection. But thankfully the
treatment is specific and results are dramatic, therefore,
early diagnosis and treatment of these mycoses are crucial.3,4
Furthermore, the morbidity and mortality (47%) are high,
healthcare costs is increased due to prolonged hospital stay,
patient dissatisfaction and higher resource utilization, thus
warranting early diagnosis. 1,2

Furthermore, emergence of resistance in non-albicans
Candida spp., unusual yeasts and molds in fungal wound
infection complicates the scene.6 Very recently, azole
resistance in C. albicans has been observed, leaving very few
fungi susceptible to antifungal drugs, warranting antifungal
susceptibility in such patients.6,7
Epidemiology
Incidence
Recently, a certain dynamic in the epidemiology of fungal
organisms has been observed despite the introduction of new
treatment modalities.8-12 The spectrum of fungal infections
include Candida spp., other yeasts, Aspergillus spp.,
Zygomycetes, Dematiceous fungi and other molds. Additionally,
other species such as Aspergillus, Fusarium, Mucor, Rhizopus
with an aggressive and invasive growth pattern are also
observed.8,13,14

Common causes of fungal infections are Candida spp.
(C. albicans, non-albicans Candida spp., other yeasts like
Cryptococcus neoformans, Rhodiola, Trichosporon, etc.),
Aspergillus spp, Zygomycete (Rhizopus, Mucor spp.), Dimor-
phic fungi (Histoplasma capsulatum, Coccidioides immitis, etc.),
Chromoblastomycosis (Fonsecaea pederosii, Cladophialophora
spp., Phialophora spp.), Phaeohyphomycosis (Exophiala,
Alternaria, Curvularia spp.), other molds (Fusarium,
Penicillium, Scedosporium spp.)1,3-6,14-31
Malini Capoor
Fungal Wound Infections:
­Diagnosis and Management
12
Chapter

Fungal Wound Infections: ­Diagnosis and Management 
Chapter 12
103
Fungi specific surgical intensive care conditions (in non-
neutropenic patients)1-38 include the following:

Blood stream infections (Fungemia): Candida spp., other
yeasts, invasive aspergillosis.

Bone marrow transplant patients: Invasive Aspergillosis
especially observed in patients with prolonged granulopenia
in hematology-oncology units without HEPA filters or laminar
flow.

Liver transplant: Candida spp., Cryptococcus neoformans.

Other
solid
organ
transplant:
Phaeohyphomycosis,
Aspergillus spp., Zygomycetes.

Skin and soft tissue infections: (transplant rejection,
diabetes mellitus, rheumatoid arthritis, Autoimmune, COPD):
Zygomycetes, Aspergillus spp., Chromomycosis.

Pancreatitis- fungal infection with Candida spp, other
yeasts, Phaehyphomycosis.

Carcinoma bladder, stomach, colon: Candida, Aspergillus,
Cryptococcus, Histoplasma, Coccidioides, etc.

Traumatic amputation (contact with soil and water):
Scedosporium, molds.

Burn wound: Candida spp., Less common: Mold (Aspergillus,
Zygomycetes, Fusarium spp.).
Augmentation Mammoplasty: Yeasts
Most invasive fungal infections in surgical patients are
caused by Candida spp, Aspergillus and less commonly by
Cryptococcus or other yeasts and molds.15 Candida spp.
has emerged as the fourth most common cause of blood
stream infections. All the more, invasive candidiasis (IC) has
emerged as a frequent complication in surgical critically-ill
patients. Approximately, one-third of patients with recurrent
gastrointestinal perforations, anastomotic leakages or acute
necrotizing pancreatitis develop intra-abdominal IC.16
Candida spp., which are normal commensal of gastrointestinal
tract are usually isolated from intra-abdominal sources. It is
considered an important secondary invader in patients with
acute necrotizing pancreatitis.6,17-20 Amongst Candida spp.
C. albicans, C. tropicalis, C. glabrata have been isolated
from SSIs. Non-albicans Candida species have been found
to be increasingly resistant against common antimycotic
substances.1,6,7
Pathogenesis Including Risk
­Factors
Virulence of the microbial agents, host resistance, and factors
about the wound are the determinants of the infection after
surgery. Risk factors related to patients for development of
fungal SSIs are old age, carcinoma, immunosuppression,
obesity, diabetes mellitus, chronic inflammatory process,
malnutrition, peripheral vascular disease, anemia, radiation,
chronic skin disease, carrier state of organisms and recent
surgery.1 Patients with carcinoma have increased risk of
developing SSIs due to damage of the skin and mucous
membranes, impairment of the immune system, tumor-
associated
abnormalities,
decreased
nutrition,
major
surgical intervention, chemotherapy and radiation therapy,
opportunistic infection. Immunosuppression occurs from
the use of corticosteroids, chemotherapy, radiation therapy,
surgery, hematopoietic stem cell transplantation, or the cancer
itself. The growth of tumors can disrupt natural barriers,
replace the normal cells in the bone marrow, compress nearby
normal tissues, and can decrease blood flow or cause an
obstruction and release inhibitory factors.22

The role of major surgery as a cause of immunosuppression
is crucial as within hours of surgery, researchers have noted
decreases in immune function due to anesthetic agents,
disruption of the skin and mucous membranes, the length
of hospitalization, the extent of the surgery, the duration of
the operation, the amount of bleeding during surgery, the
nutritional state of the patient, prior cancer treatment of the
surgical area, antimicrobials, and other associated medical
problems.22

Common causes of fungal infections in cancer patients
(bladder, stomach, colon carcinoma) are predominantly
Candida spp, followed by Aspergillus, Cryptococcus,
Histoplasma, Phycomycetes, and Coccidioides. These
infections can be serious, and in some cases, fatal. In a prior
study it was observed that Candida albicans was the fungi
predominantly isolated from abdominal incision specimens.22

Nutrition is a critical determinant of immune responses and
malnutrition the most common cause of immunodeficiency
globally. Protein-energy malnutrition is associated with a
significant impairment of cell-mediated immunity, phagocyte
function, complement system, secretory immunoglobulin A
antibody concentrations, and cytokine production.23 Patients
with head injury suffering from severe malnutrition exhibit
serious complications at the time of admission as well as
during rehabilitation treatment.24 Endocrine diseases such as
diabetes mellitus, Cushing syndrome, hypoparathyroidism,
hypothyroidism, and polyendocrinopathy are associated with
increased susceptibility to infection.25 The mechanism by
which diabetes mellitus is believed to raise infection rates is
through increased tissue glucose, altered yeast adhesion, and
decreased phagocytosis, opsonization defects and CD4+ and
NK cell defects.25 Recent studies have observed abnormalities
of signal transduction mechanisms in which insulinopenia
and other factors, such as circulating immune complexes, are
involved.26

Researchers are linking elevated glucose levels with
potential infectious outcomes.27 Physiological processes to

General Principles for Wound Management
Section 2
104
combat foreign agents are potentially impaired during periods
of hyperglycemia. Immune function and the inflammatory
response, for example, are impaired when they are needed
most (e.g. during recovery from surgical procedures).27
Antimicrobial usage is another factor that influences the
acquirement of fungal infections. Antimicrobials damage the
ecology of microorganisms in the bowel and on body surfaces,
permitting the overgrowth of Candida and undesirable
bacteria.28

In cases of burns, fungal infections most commonly occur
after the second week of thermal injury, usually following
a period of burn wound colonization with fungi found in
the surrounding environment and or in the case of Candida
spp from patient’s own gastrointestinal or upper respiratory
tract.1,5 The risk factors for acquiring fungal infection in burns
are: age of burns, total burn size, body surface area (30-60%),
full-thickness burns, inhalational injury, prolonged hospital
stay, late surgical excision, open dressing, artificial dermis,
central venous catheters, antibiotics (imipenem, vancomycin,
aminoglycosides), steroid treatment, long-term artificial
ventilation, fungal wound colonization, hyperglycemic
episodes and other immunosuppressive disorders.1,2,,8-11,21

For pancreatitis specific factors implicated are: Prolonged
ICU stay, central venous catheters, total parenteral nutrition,
broad-spectrum antimicrobials, Candida colonization).

For soft tissue fungal infection the risk factors are transplant,
leukemia, chronic obstructive airway disease, rheumatoid
arthritis, collagen vascular disorder, immunosuppression.

In broader terms SSIs are divided into SSIs in neutropenic
and non-neutropenic patients for management purposes
(covered in medical management).
Clinical features of fungal
­Surgical site infections (SSIs)39-43
Candidemia or fungemia may be suspected in patients
with persistent fever, unresponsiveness to broad-spectrum
antibacterial therapy, deteriorating medical or surgical
condition and repeated imaging (X-ray, USG/CT scan)
showing a mycotic lesion.39 In critically-ill patients with more
than 2 to 3 risk factors or host factors the surgeon should
strongly suspect fungal infection, as these are the patients who
would benefit from timely antifungal therapy.44

Invasive Aspergillosis (IA)41: Invasive aspergillosis is
seen in 10 to 20 percent of hematological malignancy patient,
in 20 to 30 percent of lungs, heart transplant patients. It is
in 30 percent cases a hospital acquired infection and in 70
percent it is community acquired infection. It is considered as
nosocomial infection if it observed at more than 1 week after
admission or <2 weeks after discharge. Its clinical features are
fever, cough, dyspnea, pleuritic chest pain, hemoptysis, etc.
A strong clinical suspicion is made in patients with persistent
fever and pulmonary infiltrates despite broad-spectrum
antimicrobials.

The predisposing factors are leukemia, lymphoma,
chemotherapy, steroid, HIV, transplant (lung, bone marrow,
heart). On imaging (CT scan) nodules, cavitatory infiltrates,
focal infiltrates, lung consolidation may be seen. It has a very
high mortality of 30 to 95 percent.

Soft tissue fungal infection: Soft tissue SSI fungal
infection may present as nodules, ulcerative lesions, indolent,
locally, aggressive or systemic infection with cutaneous
manifestations.

Fungal infections in burns: Patients with chronic burns
with fever despite >7 to 15 days of broad-spectrum antibiotics
and with more than 15 days of ICU stay. Patients with local
signs and symptoms of fungal wound infection like separation
of eschar, partial thickness burn converting into full thickness
burn, blackening of tissue, worsening of wound with cellulitis
or necrotizing fasciitis.39,40 Figures 1A and B depicts a typical
fungal wound invasion patient (a) before treatment. (b) after
treatment.

Orthopedic fungal infection: Nonhealing orthopedic wound.
Diagnosis
Candidemia or fungemia: One or more blood culture for
Candida spp. isolated from patients with clinical signs and
symptoms of infection (i.e. patients with blood culture positive
or blood culture and site culture (surgical site, urine, precious
fluid or other site) positive. Fungal blood culture can be
done by conventional method in biphasic bottle (brain-heart-
infusion agar/brain heart-infusion broth) and by automation in
BacT Alert 3D (Biomerieux, France) bottle.

Beta-glucan assay: Beta-glucan is an antigen present in
Candida, Aspergillus and other fungal cell wall. It is a rapid
antigen detection test.

Pan-fungal Polymerase Chain Reaction: Pan-fungal
PCR targets the ribosomal RNA present in fungi. It can be
performed on blood and sterile fluids specimen. It is a rapid,
but costly test available in reference laboratories only.

Invasive Aspergillosis, chronic necrotizing aspergillosis41:
Demonstration of organism can be done in tissue, i.e.
bronchoalveolar lavage (BAL). Direct staining on the samples
is done by Gram’s stain, potassium hydroxide (KOH) mount
and histopathological examination by periodic acid Schiff’s
(PAS) stain and tissue reaction is studied by hematoxylin and
eosin stain. Culture of the various samples on Sabouraud’s
dextrose agar (SDA) sputum, BAL, tissue gives a positivity
of (8-34%), 40, (45-62%), respectively. For, BAL, Blood
(Serum) galactomanan assay has a specificity of 50 to
95 percent.

Fungal Wound Infections: ­Diagnosis and Management 
Chapter 12
105

Allergic broncho pulmonary aspergillosis (ABPA): This
condition presents more frequently in general medicine or
respiratory medicine. Level of total IgE should be more than
1014 IU/ml or 2-fold rise in base line titer. A positive serology
results for Aspergillus antibody IgG or IgE is also diagnostic.
An intradermal test will give wheal and flare response and a
characteristic chest radiograph.

Soft tissue infection: The soft tissue biopsy is sent in
normal saline or aspirate for fungal culture and biopsy for
histopathological examination in formalin. Direct KOH
mount may show yeasts or hyaline or pigmented hyphae with
fungal elements-sclerotic bodies. Fungal culture on SDA will
depict the yeast or mold etiology. Figure 2A shows Growth of
Candida tropicalis on Sabourauds dextrose agar; Figure 2B
shows Budding yeast cells of Candida spp. (Grams stain 400
X). Figure 3 is a slide of periodic acid stain showing PAS
positive budding yeast cells. A mold Mucor is depicted in
Figure 4. Lactophenol cotton blue mount showing sporangium
borne on stolon from aseptate hyphae. Fusarium solani (mold)
growth is depicted in Figure 5.

Necrotizing pancreatitis: The samples include preoperative
aspirated/necrotic tissue from the pancreas, postoperative
Figure 2A: Growth of Candida tropicalis on
Sabourauds dextrose agar
Figure 2B: Budding yeast cells of Candida spp.
(Grams stain 400X)
Figures 1A and B: (A) A patient with all systemic and local (blackening and separation of eschar) signs and symptoms of infection and not
improving on antibacterials, biopsy showing typical fungal burn wound invasion; (B) Same patient showing healthy wound tissue after 21 days
of successful antifungal therapy and was later on taken for grafting
A
B

General Principles for Wound Management
Section 2
106
drain effluent and blood. The centrifuged deposit, drain
effluents or necrotic tissue are processed by direct microscopy
(10% KOH mount and Gram’s stain) and for culture on SDA.
The diagnosis of a true Candida infection of pancreatic tissue
is considered to be positive when yeast cells are seen and
grown in pure or mixed culture from necrotic tissue during
necrosectomy/aspirated sample from the pancreas collected
under the guidance of ultrasonography. The diagnosis of a
possible Candida infection of pancreatic tissue is considered
when Candida spp. were isolated from abdominal drain
effluents (atleast 2 lavage samples) in postoperative patients
with acute pancreatitis without Candida in pre/postoperative
samples. Thus the diagnosis of Candida pancreatitis is based
on the isolates of Candida from pancreatic tissue during
surgery. A culture of drain effluents is less reliable and it
may reflect contamination. However, in an emergency, ideal
circumstances are rare.29
Intra-abdominal Candidiasis
Intra-abdominal abscess with Candida spp. isolated in pure
or mixed culture Peritonitis: Peritonitis usually presents with
fever, abdominal pain, tenderness, ileus and leukocytosis
(WBC count >109 cumm/L) with isolation of Candida in
the peritoneal fluid from laparotomy or drain effluents (in
mixed bacterial and fungal cultures), Candida was regarded
as pathogen when recovered from blood or in increasing
amounts in serial culture in absence of clinical improvement
despite appropriate surgical and antibacterial therapy.16

Candida urinary tract infection (UTI): Candida present in
>105 CFU/ml with pyuria and fever without other focus and
or with local symptoms and sign of infection.

Postoperative
surgical
wound
infection:
Candida
isolated from a biopsy specimen or purulent discharge.
Histopathological examination of tissue: Demonstration of
fungal invasion in dermis and blood vessels.

Burns: Deep tissue biopsy sent in normal saline for Gram’s
stain, KOH mount and culture. Demonstration of fungi can be
done in direct examination and culture.

Histopathological examination of tissue: Demonstration of
fungal invasion in dermis and blood vessels.

PCR (Polymerase chain reaction): Pan-fungal PCR
available in reference laboratory (Figure 7).
Figure 5: Growth of Fusarium solani
Figure 3: PAS positive fungal elements (periodic acid
Schiff’s stain, 400X)
Figure 4: Lactophenol cotton blue mount showing sporangium borne
on stolon from aseptate hyphae (Mucor spp.), 450X

Fungal Wound Infections: ­Diagnosis and Management 
Chapter 12
107
Management
The management of invasive fungal infection is broadly
divided into neutropenic and non-neutropenic surgical patients.
Neutropenic patients are given antifungal prophylaxis.

Fungal culture should be sent multiple times and from
multiple sites and one should specifically ask for Candida
speciation and antifungal susceptibility (Figures 6A to C).
Intra treatment culture should also be sent. The treatment
duration is 2 to 6 weeks, depending upon the last negative
fungal culture.

Management of Candidemia in non-neutropenic surgical
patient42-44, i.e. (Candidemia, Tissue aspirate invasive
candidiasis, Candida isolated from sterile sites tissue, aspirate,
precious fluids). The recommended duration of therapy for
candidemia without obvious metastatic complication is for 2
weeks after documented clearance of Candida from the blood
stream (Blood culture: sterile) and resolution of symptoms
attributable to candidemia. The duration of therapy is guided by
every alternate day blood culture and tissue biopsy performed
at least twice. The intravenous or central venous catheter
removal is strongly recommended for non-neutropenic patients
with candidemia. Transition or change of drug is recommended
on confirmation of isolates susceptibility. For infection due to
Candida species likely to be susceptible to azoles (C. albicans)
or a mild infection or patients who are less critically ill and
have had no recent azole exposure, an azole, e.g. fluconazole
(loading dose of 800 mg (12 mg/kg body wt) followed by 400
mg (6 mg/kg/daily) is recommended. The treatment schedule
may be altered as per the antifungal susceptibility report, as
there is emergence of azoles resistance in C. albicans.6

For moderately severe to severe illness amphotericin B
deoxycholate (AmB-d at 0.5 mg/kg), lipid formulation of
AmB (LfAm B(3-5 mg/kg)) or an echinocandin (caspofungin,
micafungin) is preferred. An echinocandin (Caspofungin:
loading dose of 70 mg, then 50 mg daily, micafungin: 100 mg
daily, anidulafungin: loading dose of 200 mg, then 100 mg
daily). As per 1DSA guidelines echinocandin is recommended
for patient with moderately severe to severe illness or patients
who have recent azole exposure, hepatorenal toxicity, azole
resistant Candida spp. Transition from an echinocandin
to fluconazole is recommended in patients with moderate
to severe illness or patients who have isolates susceptible
to azoles. Clear advantages of echinocandins over other
antifungal drugs is low toxicity (since their site of action-
fungal cell walls is not present in humans and it has limited
drug interactions). Furthermore, it acts on intrinsically
resistant Candida spp. like C. krusei, C. glabrata, etc.

Voriconazole is administered at a dosage of 400 mg (6 mg/
kg) twice daily for 2 doses and then 200 mg (3 mg/kg) twice
daily thereafter, but it offers little advantage over fluconazole
and is recommended as step down oral therapy for selected
cases of candidiasis due to voriconazole susceptible C. krusei,
C. glabrata.

Surgical debridement is indicated in all cases of SSIs like
burns, soft tissue infection.

Candidemia in neutropenic patients: Amphotericin
B (AmB-d or LAmB) or an echinocandin (caspofungin,
micafungin or anidulafungin) in aforementioned doses is
recommended.
Figure 7: Real-time PCR machine used for Pan-fungal assay
Figures 6A to C: Antifungal susceptibility of (A) yeast and (B) mold by E-strip MIC method (C) by broth microdilution
A
B
C

General Principles for Wound Management
Section 2
108

Recommended duration of therapy for candidemia without
persistent fungemia or metastatic complications is for 2
weeks after documented clearance of Candida from the blood
stream, resolution of symptoms attributable to candidemia
and resolution of neutropenia.

Antifungal prophylaxis in solid-organ transplant recipients:
For solid-organ transplant as recepient, fluconazole 400 mg
daily or LF-AmB for 7 to 14 days is recommended as
postoperative antifungal prophylaxis for liver, pancreas,
small bowel transplant recipients. For patients hospitalized
in the ICU, fluconazole 400 mg is recommended for high-
risk patient in adults that have a high incidence of invasive
candidiasis. For stem cell transplant recepients with
neutropenia, fluconazole 400 mg or posicoanazole 200 mg or
micafungin in 50 mg daily is recommended during the period
of risk of neutropenia. Treatment for chronic disseminated/
heptosplenic candidiasis, the therapy should be continued for
several months, until the lesions have calcified or disappeared
radiologically. Fluconazole 400 mg daily is recommended
for clinically stable patients for several months or AmB for 2
weeks followed by fluconazole.

Treatment for osteoarticular Candida infection: For
osteomyelitis, fluconazole 400 mg daily for 6 to 12 months or
LF-AmB at doze of 3 to 5 mg/kg daily for 2 weeks followed
by fluconazole at a dosage of 400 mg daily for 6 to 12 months
is recommended. Alternatives include an echinocandin or
AMB-d at a dosage of 0.5 to 1 mg/kg daily for atleast 2 weeks
followed by fluconazole. Surgical debridement is indicated in
all cases. For infection involving a prosthetic device, device
removal in recommended for all cases.

Treatment for central nervous system candidiasis in adults:
Removal of infected ventricular devices is recommended. LF-
AmB at a dosage of 3 to 5 mg/kg body wt daily, with or without
flucytosine at a dosage of 25 mg/kg 4 times a daily. Fluconazole
at a dosage of 400 to 800 mg daily is recommended as step-
down therapy. Therapy should continue until all signs and
symptoms, CSF abnormalities and radiological abnormalities
have resolved.

Treatment of urinary tract infection by Candida spp.: In
asymptomatic UTI, treatment is not required. If risk factors
like invasive urologic procedures are present in asymptomatic
patients, then fluconazole 200 to 400 mg for two weeks is
given. If symptomatic UTI is present then oral fluconazole
200 to 400 mg or Amphotericin B is given for 2 weeks.

Suppurative thromboplebitis: Amphotericin B, fluconazole
or an echinocandin is given.
Treatment Failure
1. Death 7 to 14 days after diagnosis of candidemia
2. Persistent fever >5 days after AFT
3. Recurrence of fever after 2 consecutive afebile days on
AFT

Follow the Candida score in critically-ill patients44
Invasive Aspergillosis
Prevention: Itraconazole prophylaxis just after lung, bone
marrow and heart transplant. Environment control (HEPA or
laminar flow in granulocytopenic patients) and surveillance
from time to time is recommended.

Especially in non-neutropenic patients in cases of mold
infection in epidemiology-history of new building construction
near ward, (200 m) should be ellicited.

Other drugs recommended are voriconazole, caspofungin.

Orthopedic non-healing wound/amputation: Therapy is
instituted depending upon isolate. In case it is mycetoma,
ketoconazole and topical ketoconazole powder, or itraconazole
is recommended.

Pancreatitis (polymicrobial): Antibacterial and antifungal
therapy is advocated.

Transplant patients: (Solid-organ): Amphotericin is advisable
as Ist line prophylaxis and itraconazole and fluconazole as
follow-up. For transplant of kidney lipid formulation of
amphotericin B or voriconazole is recommended.

Soft tissue infection: Infection is tailored to infection type
and requires team approach of surgeon and expert infectious
disease consultant.

Group I: Locally aggressive infection—radical excision
with systemic AFT

Group II: Indolent infections—surgical control with or
without AFT

Group III: Cutaneous manifestation of systemic infection—
systemic AFT

Zygomycetes- Amphotericin B

Chromomycosis: Itraconazole and surgical excision if
Phaeohyphomycosis and Ampnotericin B is recommended.

Hyalohyphomycosis: Amphotericin B is included.

Burn wound: Depending upon the isolate AFT is given
similarly as candidemia.
Conclusion
As immunosuppression (especially cell-mediated immunity)
is a risk factor for fungal infections, and fungal infections
represent one of the most rapidly increasing health care
infections coupled with a significant mortality rate,31 clinicians
must be aware of fungal infections that may develop in this at-
risk group, particularly after surgery involving older, pediatric
age-group and immunosuppressed patients.

The pertinent literature cites Candida species as an
important etiological agent. In the last two decades, incidence

Fungal Wound Infections: ­Diagnosis and Management 
Chapter 12
109
of Candida infection has shown a shift from Candida albicans
to other Candida species.32-37 Changing epidemiologic
patterns has seen the emergence of non-albicans strains34 often
associated with resistance to azole antifungal agents,35 which
has implications on patient management. Recently published
standards of care36 advocate that all Candida species isolated
from sterile sites and all species from high-risk patients should
be identified at the species level and antifungal susceptibility
is crucial in overall management of critically-ill surgical
patients.
References
1. Demet Kaya, Canan Aldirmaz Agartan, Muhterem Yucel.
Fungal Agents as a Cause of Surgical Wound Infections: An
Overview of Host Factors Volume: 19 Publication Date: Aug
01 2007 Sidebars_in_article: Issue: 8.
2. Dunn DL, Bellman JG. Surgical infections. In: Brunicardi FC,
Andersen DK, Billiar TR, Dunn DL, Hunter JG, Pollack RE,
(Eds.) Schwartz’s Principles of Surgery. 8th edn. New York,
NY: McGraw Hill; 2005.pp.109-127.
3. Mousa HA. Fungal infection of burn wound in patients with
open and occlusive treatment methods. Eastern Mediterranean
Health J 1999;5:333-6.
4. Tsoutsos D, Tsati E, Metaxotos N, Keramidas E, Rodopoulou
S, Ioannovich J. Extensive burn injury complicated by
mucormycosis: A case report. Annals of Burns Fire Disasters
2001;16:1-2.
5. Gupta N, Hague A, Lattif AA, Narayan RP, Mukhopadhyay
G, Prasad R. Epidemiology and molecular typing of Candida
isolates from burn patients. Mycopathologia 2005;158:397-
405.
6. Chakrabarty A, Chatterjee SS, Rao KLN, et al. Recent
experience with fungemia: change in species distribution and
azole resistance. Scand J Infect Dis 2009;41:275-84.
7. Pfaller MA, Diekema DJ, Messer SA, Boyken L, Hollis RJ.
Activities of fluconazole and voriconazole against 1,586
recent clinical isolates of Candida species determined by broth
microdilution, disk diffusion and E-test method: Report form
the ARTEMIS Global Antifungal Susceptibility Program,
2001. J Clin Microbiol 2003;41:1440-6.
8. Greenhalgh DG, Saffle JR, Holmes JH 4th, Gamelli RL,
Palmieri TL, Horton JW, Tompkins RG, Traber DL, Mozingo
DW, Deitch EA, Goodwin CW, Herndon DN, Gallagher JJ,
Sanford AP, Jeng JC, Ahrenholz DH, Neely AN, O’Mara MS,
Wolf SE, Purdue GF, Garner WL, Yowler CJ, Latenser BA,
American Burn Association Consensus Conference on Burn
Sepsis and Infection Group: American Burns Association
Consensus Conference to define sepsis and infection in burns.
J Burn Care Res 2007;28:776-90.
9. Mathew BP, Nath M. Recent approaches to antifungal therapy
for invasive mycoses. Chem Med Chem 2009;4:310-23.
10. Dries DJ. Management of burn injuries - recent developments
in resuscitation, infection control and outcomes research.
Scand J Trauma Resusc Emerg Med 2009;17:14.
11. Struck MF. Scandinavian Journal of Trauma, Resuscitation and
Emergency Medicine 2009;17:51doi:10.1186/1757-7241-17-51.
12. Macedo JLSD, Santos JB. Bacterial and fungal colonization of
burn wounds. Braz J Infect Dis 2005;100(5):535-9. 20.
13. Stone HH. Aspergillus infection of the burn wound. Journal of
Trauma 1979;19:765-7.
14. Paz RN, Strahilevitz J, Shapiro M, Keller N, Goldshmied-Reoven
A, Yarden O, Block C, Polacheck J. Clinical and epidemiological
aspect of infectious caused by Fusarium spp.: A collaborative
study from Israel. J Clin Microbiol 2004; 42:3456-61.
15. Holzheimer RG, Dralle H. Management of mycoses in surgical
patients- review of the literature. Eur J Med Res 2002;7(5):
200-26.
16. Senn L, Eggimann P, Ksontini R, Pascual A, Demartines N,
Bille J, Calandra T, Marcheti O. Caspofungin for prevention
of intra-abdominal candidiasis in high-risk surgical patients.
Intensive Care Med. 2009;9:1405-8.
17. Sandevan P, Qvist H, Skorlund E, Giercksky KE. The
NORGAS group and the Norwegian study group. Significance
of Candida recovered from intra-operative specimens in
patients with intra-abdominal specimens in patients with intra-
abdominal perforations. Crit Care Med 2002;30:541-7.
18. Grewe M, Tsiotos GG, de-Leon EL, Sarr MG. Fungal infection
in acute necrotizing pancreatitis. J Am Coll Surgeons 1999;
188:408.
19. Waele JJD, Vogelaers D, Blot S, Colardyn F. Fungal infections
in patients with severe acute pancreatitis and the use of
prophylactic therapy. Clin Infect Dis 2003;37:208-13.
20. Calandra T, Marchetti O. Clinical trials of anti-fungal
prophylaxis among patients undergoing surgery. Clin Infect
Dis 2004: 39 (suppl 4):S185-92.
21. Ballard J, Edelman L, Saffle J, Sheridan R, Kagan R, Bracco
D, et al. Multicentre Trials Group. American Burn Association.
J Burn Care Res 2008;29:213-21.
22. American Cancer Society. Infections in individuals with
cancer. What are infections? Available at:
org/docroot/eto/content/eto_1_2x_infections_in_individ....
Accessed: August 16, 2006.
23. Chandra RK. Nutrition and the immune system: an introduction.
Am J Clin Nutr 1997;66(2):460S-3S.
24. Dénes Z. The influence of severe malnutrition on rehabilitation
in patients with severe head injury. Disabil Rehabil.
2004;26(19):1163-5.
25. Scheinfeld NS, Lambiase MC, Vaughan TK, Lehman DS, Allan
J. Candidiasis, cutaneous. Available at:
com/derm/topic67.htm. Accessed: August 16, 2006.
26. Moutschen MP, Scheen AJ, Lefebvre PJ. Impaired immune
responses in diabetes mellitus: analysis of the factors and
mechanisms involved. Relevance to the increased susceptibility
of diabetic patients to specific infections. Diabete Metab.
1992;18(3):187-201.
27. Aragon D, Ring CA, Covelli M. The influence of diabetes
mellitus on postoperative infections. Crit Care Nurs Clin North
Am. 2003;15(1):125-35.
28. Fungi and Disease. Symbiotic yeasts—Candida albicans.
Available at:
Accessed: August 16, 2006.

General Principles for Wound Management
Section 2
110
29. Chakrabarty A, Rao P, Tarai B, Shivaprakash MR. Candida in
acute pancreatitis. Surg Today 2007;37:207-11.
30. Weinberger M, Sacks T, Sulkes J, Shapiro M, Polacheck
I. Increasing fungal isolation from clinical specimens:
experience in a university hospital over a decade. J Hosp
Infect. 1997;35(3):185-95.
31. Pfaller MA, Diekema DJ. Role of sentinel surveillance
candidemia: trends in species distribution and antifungal
susceptibility. J Clin Microbiol. 2002;40(10):3551-7.
32. Pfaller MA, Diekema DJ, Jones RN, et al. International
surveillance of bloodstream infections due to Candida
species: frequency of occurrence and in vitro susceptibilities
to fluconazole, ravuconazole, and voriconazole of isolates
collected from 1997 through 1999 in the SENTRY antimicrobial
surveillance program. J Clin Microbiol. 2001;39(9):3254-9.
33. Pfaller MA, Jones RN, Doern GV, et al. Bloodstream infections
due to Candida species: SENTRY antimicrobial surveillance
program in North America and Latin America, 1997–1998.
Antimicrob Agents Chemother. 2000;44(3):747-51.
34. Pfaller MA, Jones RN, Messer SA, Edmond MB, Wenzel RP.
National surveillance of nosocomial blood stream infection due
to species of Candida other than Candida albicans: frequency of
occurrence and antifungal susceptibility in the SCOPE Program.
SCOPE Participant Group. Surveillance and Control of Pathogens
of Epidemiologic. Diagn Microbiol Infect Dis. 1998;30(2):121-9.
35. Pfaller MA, Jones RN, Messer SA, Edmond MB, Wenzel RP.
National surveillance of nosocomial blood stream infection due
to Candida albicans: frequency of occurrence and antifungal
susceptibility in the SCOPE Program. Diagn Microbiol Infect
Dis. 1998;31(1):327-32.
36. Pfaller MA, Jones RN, Doern GV, Sader HS, Hollis RJ,
Messer SA. International surveillance of bloodstream
infections due to Candida species: frequency of occurrence
and antifungal susceptibilities of isolates collected in 1997 in
the United States, Canada, and South America for the SENTRY
Program. The SENTRY Participant Group. J Clin Microbiol.
1998;36(7):1886-9.
37. Ribes JA, Vanover-Sams CL, Baker DJ. Zygomycetes in
human disease. Clin Microbiol Rev 2000;13:236-301.
38. Burdge JJ, Reo F, Iyers L. Noncandidal fungal infections of
burn wound. J Burn Care Rehab 1988;9:599-1.
39. Mandell, Douglas, Bennet’s Principles and Practice of
Infectious Diseases, 6th edn. Elsevier Churchill Livingstone;
2005.pp.2997-3012.
40. Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn
wound infections. Clin Microbiol Rev 2006;19:403-34.
41. Patterson TF, Kiirkpatrick WR, White M, et al. Invasive
aspergillosis: disease spectrum, treatment practices and
outcomes. 13 Aspergillus Study Group. Medicine (Baltimore)
2000;30:696-709.
42. Pappas PG, Kauffman CA, Andes D, et al. Clinical practice
guidelines for the management of candidiasis: 2009 update by
the Infectious Diseases Society of America. Clin Infect Dis
2009:48: IDSA candida.
43. Hoy JF. Antifungal Drugs (Part IV) Butterworth Heinemenn.
In: Kucer’s the use of Antibiotics: A Clinical Review of
Antibacterial, Antifungal and Antiviral Drugs Oxford, UK;
1997:
44. Leon C, et al. Prospective, cohort, observational, multicentre,
surveillance study of fungal infection and colonization in
intensive care unit (ICU) settings 73 medical-surgica-ICUs of
70 teaching hospitals in spain between May 1998 and January
1999. Critical Care Med 2006;34:730-7.

Types of Wounds
and their
Management
3
Section

(Trang không có chữ)

Introduction
Crush injuries are caused by compressive force applied
between two hard surfaces to the limbs. The compressive force
may be associated with other damaging forces like shearing
stress, high temperature or rough surface of the compressing
element. The tissues under compression suffer direct damage
proportional to the magnitude and duration of compression
and the surface characteristics of the compressing agent.
Tissues distal to the compression suffer from ischemia due to
direct injury to the vessels or secondary to edema.

Crush injuries occur to the limbs in road traffic accidents,
industrial accidents or when they get trapped under falling
rubble in massive building collapses and during natural
disasters like earthquakes. In the last group of patients the
wounds themselves may become life-threatening if long time
elapses before extrication of the crushed limb when it could
lead to the development of crush syndrome. The other major
complication of the crush injuries to the limbs is the onset of
the compartment syndrome. In this chapter we deal with the
emergency care of such injuries to prevent these two major
problems and discuss technical considerations influencing
reconstruction of these injuries. Management of the skeletal
injuries accompanying crush injuries of the limbs depends
upon the bone and the type of fracture and is beyond the scope
of this chapter.
Crush Syndrome in Limb Injuries
Crush syndrome refers to the group of systemic symptoms a
patient manifests when a limb is trapped for extended periods
of time usually beyond four to six hours. The three key
components are hypovolemia, cardiac arrhythmias and renal
failure. It is difficult to provide a time limit of compression
for its occurrence or the size of the body part that should be
trapped in the injury. If the compression is very proximal
in the lower limb, crush syndrome can occur with shorter
periods of time, while crush syndrome has been noted even
when the part involved has been just the foot or the hand.
Crush syndrome has to be differentiated from compartment
syndrome in which the muscles in a specific osteofascial
compartment suffer ischemia and the changes are restricted
to the contents of the compartment. It does not produce any
significant systemic problems.

When the limb gets trapped there is direct injury to the
tissues compressed and distal to the compression the muscles
suffer reduced blood supply. Ischemia promotes the cells to
switch over to anaerobic metabolism which produce lactic
acid as the end product. With continued ischemia the cell
permeability increases leading to the leak of potassium and
toxic products like lactic acid, myoglobin and purines into the
extracellular spaces in the tissues distal to the compression.
As long as the compression persists the patient may even be
Crush Injuries of Limbs
S Raja Sabapathy, Praveen Bhardwaj
13
Chapter
• Crush Syndrome in Limb Injuries

– Management of Crush Syndrome

– Compartment Syndrome in Crush Injuries
of the Limbs

– Vessel Injury in Crush Injuries of the Limbs

– Injury to Musculotendinous Units and Nerves in Crush
Injuries of the Limbs
• Wound Management in Crush Injuries of the Limbs

Section 3
  Types of Wounds and their Management
114
stable and alert, but the moment the compression is relieved
the toxic products that enter the circulation may prove life-
threatening. Hyperkalemia could cause cardiac arrhythmias
and even cardiac arrest, myoglobin blocks the renal tubules
causing renal failure and purines cause respiratory distress
and liver damage.
Management of Crush Syndrome
Aggressive management of the patient before and after extri-
cation is important.1 The patient is assessed and an intravenous
access is to be established and fluid is run to prevent hypov-
olemia. Normal saline is preferred and potassium containing
fluids like Ringer’s lactate are to be avoided. High oxygen
concentration is given. Hyperkalemia is the most important
life-threatening entity and it is monitored by ECG and must be
aggressively managed. Progressive hyperkalemia can result in
identifiable changes in the ECG. These include peaking of the
T wave, flattening of the P wave, prolongation of the PR inter-
val, ST segment depression, prolongation of the QRS complex,
and, eventually, progression to a sine wave pattern. Ventricular
fibrillation may occur at anytime during this progression. Con-
tinuous ECG monitoring is a must. These offer the physician
providing medical control a more complete assessment of the
patient when determining care, both in the field and hospital.

Mild and moderate hyperkalemia is treated by measures to
drive potassium from extracellular to intracellular compart-
ment. 50 ml of 8.4 percent sodium bicarbonate is infused over
a period of 5 minutes. It can be repeated after 30 minutes.
Onset of action is almost instant but the effect lasts for only
15 to 30 minutes. Another option is glucose – insulin infu-
sion. It takes about 20 to 30 minutes to act. When glucose is
taken into the cells by insulin it takes potassium along with it.
Beta agonists like Albuterol (used in asthma) can help in the
reuptake of potassium by the cells. In life-threatening situa-
tions 10 ml. of calcium gluconate is given over 2 to 3 minutes
with ECG monitoring. It acts within 5 minutes. This can be
repeated after 30 minutes if ECG changes persist.

Myoglobin crystallizes in acidic urine and causes tubular
necrosis and renal failure. Preventive measures are maintaining
a high urine output and alkalinizing the urine. Evidences for the
use of mannitol are equivocal. Loop diuretics like frusemide
are to be avoided since they may be harmful in that they may
acidify the urine. In life-threatening situations one needs to be
prepared for emergency amputation of the involved part.

These set of symptoms are not exclusive for patients
with crush syndrome, but also be exhibited by patients who
undergo revascularization of a major limb amputation with
prolonged ischemia period and they should also be similarly
be managed.2 Missed prolonged application of the tourniquet
beyond six hours can result in symptoms of crush syndrome
and might even require amputation to save the life of the
individual.3
Compartment Syndrome in Crush Injuries
of the Limbs
Compartment syndrome occurs in crush injuries and it could
leave very debilitating functional sequelae. It could be due to
direct occlusion of the arteries beneath the zone of compression
causing ischemia and swelling of the muscles, rupture of vessels
causing bleeding in the tissue planes or progressive swelling
that occurs over a period of time due to the injury. A series of
events occur which leads to progressive damage to the muscles
and nerves in the compartment. The symptoms first start with
pain, leading onto loss of function and paralysis. Absence of
pulse is a positive sign but palpable pulses can be present in a
full blown compartment syndrome. Diagnosis must be clinical
in most instances. Pain and resistance to passive stretch of the
muscles involved in the compartment and par esthesia of the
fingertips or toes are the important signs which should alert
the physician of the impending compartment syndrome to take
action. The presence of these two signs is enough to initiate
action.

The tight dressings if any are first removed to the level of
the skin. Fractures and dislocations if any are reduced. If these
measures do not improve the situation there must not be any
hesitancy in decompressing the compartment. In the forearm
there are 4 compartments: the superficial and deep flexor, the
extensor and the compartment enclosing the muscles of the
mobile wad (Figure 1). The upper limb compartments are
interrelated and decompression of the flexor compartment in
most instances relaxes other compartments. This is unlike the
situation in the lower limb where each compartment must be
individually decompressed.

Decompression of the forearm must include the decom-
pression of the carpal tunnel. The incision for carpal tunnel re-
Figure 1: The compartments of the forearm as shown in the cross-
section at the proximal forearm level

Chapter 13
Crush Injuries of Limbs 
115
Figure 3: Crush injury of the forearm. Decompression of the forearm
from the carpal tunnel, revealed proximal avulsion of the flexor
muscles. All these avulsed muscles had to be excised and the wound
closed primarily. Note the continuity of the nerves
A
B
Figures 4A to C
C
lease is extended horizontally to the ulnar side at the wrist and
then extended proximally in a curvilinear fashion (Figure 2).
The idea is to have skin cover for the nerves and vessels after
decompression since it will not be possible to close the wound
after fasciotomy. Unless very obvious, excision of muscles
are not done primarily (Figure 3). Hemostasis is achieved, the
skin wounds are not closed and an above elbow plaster slab is
applied. Movement of the fingers is encouraged and the pro-
gress noted. The wound is inspected every 24 hours and when
appropriate skin grafting may be done.

Sometimes the hand is very edematous and the compart-
ments may need to be released. If missed the intrinsic muscle
contracture develops. The thenar, hypothenar, and the inter-
osseous muscles are decompressed by the incisions shown
(Figures 4A to J). When hand alone is decompressed carpal
tunnel decompression must also form a part of it.

Decompression must be done early before the muscle death
occurs. Beyond 24 hours after the onset of the compartment
syndrome one has to rethink before decompressing the
forearm. If the muscles are unyielding to passive stretch
muscle death would have occurred. Opening the forearm
exposes the dead muscles and they get infected. The median
and ulnar nerves may be lost due to exposure. It is preferable
not to decompress the forearm at that stage. A full blown out
Volkmann’s ischemic contracture will develop and it has to
be secondarily reconstructed. In the event the compartment is
opened, radical debridement and flap cover is needed to keep
the options of later reconstruction open.

Compartment syndrome can occur even in open fractures
and Blick found the incidence to be 9 percent in their series
of 198 acute open tibial fractures.4 Commonly, it occurs in
Figure 2: markings for the forearm fasciotomy

Section 3
  Types of Wounds and their Management
116
D
E
F
Figures 4D to I
G
H
I

Chapter 13
Crush Injuries of Limbs 
117
proximal tibial fractures and a high index of suspicion and
frequent observation is necessary to prevent the complications.
The leg has four compartments—anterior, superficial posterior,
deep posterior and the peroneal compartments. Anatomically
all are independent of one another and each compartment
has to be specifically released during decompression. This is
unlike the condition in the forearm where flexor compartment
release may help reduce the pressures in other compartments.

Fasciotomy of the leg is done using the two incision technique,
an anterolateral incision decompressing the anterior and lateral
compartments and a posteromedial incision decompressing the
deep and superficial posterior compartments. The anterolateral
incision is made halfway between the tibial crest and the
fibula. The incision overlies the anterior intermuscular septum
and usually a 15 cm long incision is required. Transverse
incision is made over fascia and the intermuscular septum
identified. After identifying the septum a nick is made in the
deep fascia over the anterior compartment midway between
the septum and tibial crest. Fascia release is done with a blunt
tip scissor. Proximally the scissor should be pointing towards
the patella and distally towards the center of ankle. The lateral
compartment is similarly released in line with the fibula shaft
and the scissor pointing towards the lateral malleolus in order
to stay posterior to the superficial peroneal nerve which exits
from lateral compartment about 10 cm above lateral malleolus
and courses into anterior compartment.

The posteromedial incision is made about 2 cm posterior to
the medial palpable edge of the tibia. Usually a 15 cm incision
is required for adequate decompression. The saphenous vein and
nerve are just anterior to the incision and need to be identified
and retracted anteriorly. The fascia is divided with a blunt tip
scissor and the superficial posterior compartment is released. The
soleus originating from the proximal third of the tibia and fibula
covers the proximal portion of deep posterior compartment.
The soleus bridge is detached and retracted to expose the fascia
overlying the flexor digitorum longus and tibialis posterior
which comprise the deep posterior compartment. The fascia
overlying the flexor digitorum longus is divided to release the
deep posterior compartment. The neurovascular bundle lying
between the tibialis posterior and soleus is protected. Wounds
are generally left open and later closed or grafted.
Vessel injury in Crush Injuries of the limbs
Blunt trauma accounts for 5-10 percent of major vascular
injuries to the limbs.5 The presence of a fracture or dislocation
increases the risk. Blunt injuries are often more severe than
penetrating injuries due to trauma to adjacent structures.
The risk of eventual limb amputation is higher with blunt
mechanisms of injury and crush injuries than with vessel
injuries accompanying penetrating trauma or gunshots. This
is mostly because of late diagnosis and the accompanying
severe damage to other tissues. In proximal limb injuries
revascularizations after a warm ischemia of longer than 6 hours
has a very high-risk of severe morbidity and even mortality.

Diagnosis of a vascular injury is by a high degree of
suspicion on the part of the clinician and proper clinical
examination. These are considered to be the ‘hard signs’, of a
vascular injury which requires intervention.
• Bruit or thrill: These are present in only 45 percent of
patients with an arteriovenous fistula
• Active or pulsatile hemorrhage
• Pulsatile or expanding hematoma
• Signs of limb ischemia and elevated compartment
pressure including the 5 “P’s:” Pallor, paresthesia, pulse
deficit, paralysis, and pain on passive extension of the
compartment. Pain on passive extension is the earliest and
most sensitive physical finding.
• Diminished or absent pulses: This is not a sensitive
prognostic finding, as up to 25 percent of patients with
major vascular injuries requiring repair have normal pulses
distal to the injury.

The presence of “hard” signs of vascular injury has a 92-
95 percent sensitivity for injuries requiring intervention. The
vast majority of patients exhibiting the “hard” signs require
intervention with a positive predictive value of 95 percent. So
with these signs itself we can explore the wound for vascular
injury. Of all the signs of critical ischemia, we value the
Figures 4A to J: the hand of a 9-year-old boy with compartment
syndrome after a compression injury. (A to C) The hand was insensate
and the dorsal skin shows blisters; (D) shows the metacarpal fractures
of all fingers; (E and F) Showing the release done by decompression
of the carpal tunnel, thenar muscles and the interosseous muscles;
(G) Stabilization of the fractures by K-wires and (H to J) Showing the
good function achieved
Figure 4J

Section 3
  Types of Wounds and their Management
118
sign of pain on passive extension of the fingers as the most
sensitive and base our clinical decision on that alone.

The following “soft” signs are much less useful in predicting
or excluding major vascular injuries that require intervention.
The positive predictive value of “soft” signs indicating
abnormal findings on an arteriogram is only 35 percent. The
vast majority of these lesions do not require emergent repair.
• Hypotension or shock
• Neurologic deficit due to primary nerve injury occurs
immediately after injury. In contrast, ischemic neuropathy
is delayed in onset, developing within minutes to hours
after injury.
• Stable, non-pulsatile or small hematoma
• Proximity of the wound to major vascular structures.

The type of injury to the major vessels could be rupture
or in continuity thrombus. While arteries suffer in continuity
damage, veins frequently rupture. The bleeding that ensues
from ruptured vessels may result in compartment syndrome.
Absence of palpable pulses in the injured limb when pulses
are palpable in other limbs excludes shock and must make
the clinician suspect vessel injury. In the upper limb in closed
injuries the hand held Doppler is run along the course of
the brachial artery in the arm and at the elbow. If there is
an abrupt stop of the signal at any point in the course of the
vessel, it almost always signifies vessel injury at that level.
With that single clinical finding we have explored the arm
and elbow on many occasions and there has been no negative
exploration. Usually it is a segmental thrombus at the level
of compression (Figures 5A to E). The favored treatment is
excision of the injured segment and direct repair and if that is
not possible, reconstruction with a vein graft is done. Resection
of the injured segment and reconstruction is preferred over
embolectomy. On opening up the resected segment of the
artery, the intima very often is found to be damaged. Hence,
embolectomy has higher risk of re-thrombosis and in a crush
injury significant level of anticoagulation may not be advised.

In the upper limb collateral circulation is better and limb
survival may be possible if the brachial artery alone is injured
in a penetrating trauma and there is no significant skeletal
injury. Nevertheless if facilities exist and suitable skill
levels are available in the team or in the vicinity it is better
to explore. Revascularization brings in pulsatile flow into the
distal part, increases the survival of the injured structures,
keeps the local reconstruction options like local flaps open
and promotes healing. In the lower limb there is no significant
collateral circulation in proximal vessel injuries and vessel
repair is advised in all cases. Injuries to the popliteal artery
in crush injuries around the knee joint are notorious for being
missed. Injury to the single vessel, distal to the bifurcation of
the brachial into radial and ulnar and distal to the trifurcation
of the popliteal into anterior and posterior tibial and peroneal
vessels are compatible with survival of the limb.

Conventional angiography remains the criterion standard for
evaluation of vascular injuries in trauma patients. A part from
the cost and the less than 1 percent risk of major complication
inherent with the procedure, we feel the main disadvantage is the
delay in getting the patient to the operation table for surgery due
to the angiogram. It is our practice to opt for surgery in all cases
where ‘hard signs’ are present. Time is at a premium when a
major limb vessel is injured and when definite clinical signs are
present it is preferable not to waste time in angiography. Only
1-1.5 percent of proximity angiograms performed in patients
lacking “hard” signs of vascular injury reveals injuries that
require intervention. We do angiography in cases who present
late to know the amount of collaterals in the limb. Duplex
ultrasound is a useful investigation to know the integrity of the
vessels but it very much operator dependent.

Multidetector helical CT (MDCT) angiography is emerging
as a highly sensitive method of diagnosing arterial injuries when
compared with conventional angiography and surgical exploration
as criterion standards.6 A study by Seamon et al demonstrated a
sensitivity and specificity of 100 percent for clinically significant
injury using 16-slice and 64-slice technology.7

Higher-resolution 64-slice MDCT angiography and greater
institutional experience will further improve the diagnostic
accuracy of the modality. In comparison with conventional
angiography, MDCT angiography is considerably faster,
less expensive and less invasive, and does not require the
involvement of interventional radiology. Studies support
MDCT angiography as the diagnostic study of choice for blunt
and penetrating vascular trauma patients who have do not have
obvious indications for immediate operative intervention.8
Injury to Musculotendinous units and
Nerves in Crush injuries of the limbs
In crush injuries the damage occurs as rupture of the muscles
or avulsion at the musculotendinous junction. Mid substance
rupture of the tendons is rare. Injured muscles can be sutured,
while repair of the rupture at the musculotendinous junction
is difficult. Before suturing, all the muscle fibers attached to
the distal tendon segment has to be excised since the muscles
attached to the distal tendon cannot get revascularized.
Retaining those muscle attachments lead to infection. After
debridement an effort is made to trace the tendinous fibers
that have retracted into the proximal segment and if available
are sutured to the distal segment. If no tendinous fibers are
available in the proximal segment, the distal tendon is weaved
into the proximal muscles and held by nonabsorbable sutures.

Nerves are usually in continuity in crush injuries, unless
there is an additional element of rotation or avulsion involved
in the mechanism of injury. They may suffer neuropraxia or
more severe damage depending upon the nature and duration
of the crush element. If the nerve is in continuity, conservative

Chapter 13
Crush Injuries of Limbs 
119
A
B
C
D
E
Figures 5A to E: Crush injury of the left elbow resulting in dislocation:
(A and B) Radial and ulnar pulses were not palpable and there
was abrupt stop of signals at the elbow in a hand held Doppler;
(C) Exploration revealed in continuity thrombus in the brachial artery;
(D) the resected segment of the artery showing intimal tear and (E)
The brachial artery repaired with a vein graft
management is advised. It is essential that the nerve is well
covered with viable soft tissue and it lies on a good vascular
bed. Nerves do not stand exposure too long and it can lead to
sloughing of the nerve. Post-debridement the exposed nerve
can be covered with collagen sheets to keep it moist. It could
buy time of about 24 to 48 hours to provide soft tissue cover.9

Loss of nerve function immediately after the injury is
directly related to the injury. Late loss of nerve function is due
to ischemia of the nerve. This could be in the immediate post-
injury phase with the onset of compartment syndrome or later
due to the fibrosis of surrounding structures. Hypovascular
structures result in severe degrees of fibrosis and hence, it is
imperative that muscles of doubtful viability around the nerve
are excised at the time of debridement and ensure that the
nerve lies on a good vascular bed.

Nerve injury management takes priority since the ultimate
function of the salvaged limb depends upon the status of the
nerves. If there is a segmental defect of the nerve, the ends are
marked and the location of the proximal and distal ends of the
nerve are specifically entered in the operation notes for easier
identification during secondary reconstruction. The nerve ends
could be kept in non-anatomical location for easy access.

Section 3
  Types of Wounds and their Management
120
Wound Management in Crush
­injuries of the Limbs
Wounds in crush injuries may be attention seeking that one
may tend to look into that first. Patients with even with crush
injuries of the limbs must go through the same protocol of
ABC of resuscitation and assessment. The wounds must then
be debrided. The principles and technique of debridement
are detailed in an earlier chapter. Debridement of a crushed
wound needs more experience to decide the extent of the
tissues to be excised. This is because there will be areas of
differential levels of severity of injury. This is particularly true
of muscles and subcutaneous fat. Part of the muscle may be
hypovascular and the ensuing edema and pressure may reduce
the blood flow even further. So tight closures are to be avoided
and it may be safer to perform closure after 48 hours if the
skin edges do not come together without tension. Most of the
time, the crush injuries need soft tissue cover and the special
considerationsin providing them are given below.
• Skin grafting of raw areas secondary to crush injuries:
Normally the muscles are longitudinally aligned and
individual muscles held together by thin fascia which
facilitates muscle gliding. When the limb gets crushed the
individual muscle bellies get separated from one another
and lie freely. If the overlying skin is lost the raw area
might need skin grafting. In such situations even though
the muscles may be viable it will be prudent to wait for
about 48-72 hours by which time the individual muscle
bellies get stuck together. Primary grafting will have a
slightly increased risk of loss of skin graft. It is also partly
due to the increased oozing from the tissues (Figure 6).
• Flap cover to raw areas secondary to crush injuries: For
success in providing flap cover one need to ensure two
things. Firstly the skin to which the flap is attached must
be viable and secondly all the muscles retained are viable
and debridement is perfect. If the margin of the skin that
is chosen for the inset of the flap is not viable the flap
gets detached and there is the risk of exposure of critical
structures. If the debridement is inadequate infection
develops under the flap. For these two reasons performing
primary flap cover in crush injuries needs more skill and
judgment which comes with experience. In crush injuries
where critical structures like vessel anastomosis sites or
nerve repair sites are exposed, providing flap cover is an
emergency. In other situations similar outcomes can be
achieved by providing flap cover within 72 hours as when
it is done primarily.
• Providing flap cover to part of the raw areas: In some
instances the crush injury may result in extensive raw
area, the complete coverage of it with a flap may prove
difficult. Most of the times if the raw area is examined
part of it would only will definitely need flap cover and
the rest can be covered with skin graft. Thus, if we divide
the raw area into critical and noncritical areas, and plan
for flap cover only to the critical areas, planning the flap
and its execution will become simpler. While planning
the flap, future reconstructive needs also must be thought,
of most common error is in not providing flap cover to
areas in the lines of future tendon transfers or where one
needs to put in tendon or nerve grafts. So another flap has
to be provided prior to secondary reconstruction which is
essential for increasing the functionality of the hand. This
can be avoided from planning the whole reconstruction and
not just think for that day.
• Insetting the flap into raw areas: It is easier to inset the
flap to the skin. When we provide flap cover to part of the
raw area, the insetting has to be done to raw area which is
technically demanding. Horizontal mattress sutures have
to be taken in such a way that the free edge of the flap is
attached flush to the raw area. Normally the pedicle flaps
are divided by 3 weeks. If the inset is to the raw area, it will
be prudent to delay the flap before division.
Summary
Crush injuries are on the increase due to the changing lifestyles
and mode of transport in most countries. Management needs
high skill levels and could stress the infrastructure of any unit.
Optimal results are achieved by adhering to the protocols
and preventing complications. The main complication which
one has to avoid is infection. This is achieved by early and
efficient resuscitation, radical debridement and early soft
tissue cover.
Figure 6: Crush injury of the thigh with circumferential loss of skin.
Though the raw area would take skin graft, primary grafting cannot be
done because the muscle bellies are separated. Graft take is better
when they get adherent and form a unit

Chapter 13
Crush Injuries of Limbs 
121
References
1. Sever MS, Vanholder R, Lameire N. Management of Crush-
Related injuries after Disasters. N Engl J Med. 2006;354:1052-
63.
2. Sabapathy SR, Venkatramani H, Bharathi RR, Dheenadhaya-
lan J, Bhat VR, Rajasekaran S. Technical Considerations and
Fun­ctional outcome of 22 Major Replantations (The BSSH
Douglas Lamb Lecture, 2005). J Hand Surg. 2007;32B:488-
501.
3. Klenerman L. The Tourniquet in Surgery. J Bone Joint Surg Br.
1962;44:937-43.
4. Blick SS, Brumback RJ, Poka A, Burgess AR, Ebraheim NA.
Compartment syndrome in open tibial fractures. J Bone Joint
Surg Am. 1986;68:1348-53.
5. Rathlev N. Peripheral vascular injuries: clinical presentation.
Medscape E ref: Accessed on Nov 29th 2011.
6. Hood DB, Weaver FA, Yellin AE. Changing perspectives in
the diagnosis of peripheral vascular trauma. SeminVasc Surg.
1998;11:255-60.
7. Seamon MJ, Smoger D, Torres DM, Pathak AS, Gaughan JP,
Santora TA. A prospective validation of a current practice: the
detection of extremity vascular injury with CT angiography. J
Trauma. 2009;67:238-43.
8. Miller-Thomas MM, West OC, Cohen AM. Diagnosing
traumatic arterial injury in the extremities with CT angiography:
pearls and pitfalls. Radiographics. 2005;25(Suppl 1):S133-42.
9. Venkatramani H, Sabapathy SR. Collagen sheets as temporary
wound cover in major open fractures before definitive flap
cover. Plast Reconstr Surg. 2002;110:1613-4.

• Types of Avulsion Injuries
• Mechanism of Production of Avulsion Injury
• Clinical Features
• Management

– Controversies or Alternatives?
• Avulsion Injury of Specialized Structures
• Some other Avulsions
• Outcome of Avulsion Injuries: Early and Late
INTRODUCTION
Avulsion injuries are a malady of the 20th century1 which has
spilled over into the new millennium. Slack (1952)2 described
them as ‘injuries caused by modern road transport unknown
a few decades ago’. These are commonly due to high speed
rotating machinery in industry and agriculture or due to
friction from rubber tyres in ‘run over’ accidents in the ever
increasing vehicular traffi c on the roads. Thus, these injuries
are one of the hazards of modern industrial development and
road transport.3 The earliest reference to this injury is by
Farmer of Toronto.4,5 The word avulsion comes from Latin,
avellere, ab –‘from or away’ and vellere – ‘to pluck or pull’,
‘to tear off forcibly’. Oxford English Dictionary defi nes it
as “the action of pulling off, plucking out or tearing away,
forcible separation”.6 Thus, the distinguishing feature of an
avulsion injury is that the skin and subcutaneous tissues are
peeled off the underlying tissues as a fl ap (Figure 1). These
injuries have been referred to in literature by different names
by different authors as “roller wringer injury”, “pneumatic
tyre torsion avulsion injury”, “friction injury”2 or “degloving
injury” based on the mechanism or the presenting features.
In many patients, the avulsed skin is attached distally and
disrupted proximally and often rolled down the extremity
like a glove, hence the name ‘degloving injuries’. Degloving
injuries, described by MacCollum in 19387 as ‘Wringer Arm’
were common during the use of wringer washing machines.8-11
He described a complex traction-compression injury to skin,
subcutaneous tissue and muscles of the arm that resulted from
compression by the rollers of the clothes wringer of non-
automatic washing machines.12 It was primarily an injury of
infants and children and caused crushing and avulsion of the
skin with fractures being infrequent. Franz and Root (1975)12
described 90 cases of which 68 were less than 10 years of
age. The introduction of automatic appliances with safety
mechanisms has decreased the frequency of these upper limb
Figure 1: Avulsion injury of thigh, showing a lacerated wound with
undermining. The skin has been raised as a fl ap
Skin Avulsion Injuries
Arun Goel
14
Chapter

Skin Avulsion Injuries
123
injuries due to this cause at least.13 However, as the pathology
and the management is essentially the same, Innis (1957)3
preferred to use the term “avulsion injury” for all these cases.

These injuries vary from small lacerations with undermining
but completely preserved circulation to massive ones with
avulsion of skin, subcutaneous tissues, deep fascia, muscles,
tendons, nerves2,14 and vessels with or without fractures of
underlying bones and completely absent circulation in the
avulsed tissues. (Figures 2A and B). In addition, the avulsed
tissues may be healthy and in one piece or crushed, devitalized
and in multiple pieces. Thus, their management and outcome
cannot be uniform.15 Each patient requires a different approach
and modalities of treatment and consequently has different
morbidity patterns and outcome. Saad (1970)14 and Murray
(1990),16 in their historical reviews on the subject, recognized
the need of combining two specialties of orthopedic and
plastic surgery combining to treat these injuries to obtain a
fully functional limb provided there are no factors which limit
reparative surgery.
TYPES OF AVULSION INJURIES
Classically avulsion injuries have been divided into two types:
1. Anatomical or revealed or external type
2. Physiological or concealed or internal type.

Slack (1952)2 called them as open and closed varieties
respectively with former being more common while the latter
being rare.
The anatomical type: Anatomical avulsion injuries are the
most commonly seen type. There is an open wound over most
of the area with additional undermining around the periphery
of the wound. Thus, the extent of damage is revealed at the fi rst
inspection and careful examination of the wound (Figure 3).
The skin and subcutaneous tissues may be healthy or crushed
and mutilated. There may be damage to deeper soft tissues
including lacerations and crushing of muscles, avulsion of
neurovascular bundles and even fractures of underlying
bone(s) may be present. The wounds in these types of injuries
are generally heavily contaminated and demand meticulous
wound toiletry.
The physiological type: This injury is most commonly seen
in individuals run over by heavy vehicles, particularly buses
and trucks. They are easily overlooked and may be a source of
morbidity if not diagnosed early and correctly.17 In this atypical
and uncommon type of injury due to shearing forces, there is
an extensive detachment of the skin and subcutaneous tissues
from the deeper tissues of the extremity with a very small or
Figures 2A and B: Extensive avulsion injury of foot with multiple fractures, exposed tendons, gangrenous toes and necrosis of whole of sole
Figure 3: Extensive avulsion injury of the lower limb. The extent of
injury is obvious on inspection

Types of Wounds and their Management
124
almost no wound. The detachment leads to disruption of vessels
perfusing the skin and subcutaneous tissues. In addition, the
vascular network of the avulsed skin fl aps also gets disrupted
due to the extreme tension created by the shearing strain. Both
these effects combine to produce ischemic necrosis of the
avulsed tissues. The limb appears almost normal except for
the marks of vehicular tyres and scattered ecchymotic patches.
There may be bagginess and unnatural mobility of the skin.
Later, there may be an extensive hematoma (Figures 4 and
5). The extent of avulsion at this stage is highly deceptive
and can involve the whole limb. There may be associated
fractures. The shock may be greater than can be explained
by other so-called obvious injuries. Since the severity of
injury is usually grossly underestimated at the time of initial
evaluation, the consequences are generally highly disastrous.
Over a period of several days, necrosis of large areas of skin
and subcutaneous tissues occurs leading to pus formation,
generalized septicemia and death. If it is not recognized early,
skin necrosis may be found on removal of any plaster cast
which was applied. This may have medicolegal implications
that bandaging and splintage were in no way responsible.
MECHANISM OF PRODUCTION OF
AVULSION INJURY
All the avulsion injuries in the body do not occur by the same
mechanism although the end result is same viz. laceration with
undermining of skin and subcutaneous tissues with no regard
to its blood supply. If there were no undermining, even an
extensive laceration would not have been of much consequence,
requiring just simple suturing. Similarly, just extensiveness
of undermining is not important. The undermining has to be
without any regard to its vascular supply. Thus, while the whole
of scalp may be undermined safely by a surgeon with just one
superfi cial temporal artery intact, in a traumatic avulsion of
the scalp there may be minimal or no perfusion because of the
absence of any such big named vessel in its attachment to the
body. Similarly, whole of the forearm skin can be raised on
radial artery and its venae comitantes as is routinely done while
raising a radial forearm fl ap. In a traumatic case, the whole
of avulsed fl ap may necrose because of absence of perfusion.
Again, during abdominoplasty whole of the abdominal skin
up to costal margins superiorly and mid axillary line on either
side is raised through an incision just above the groins. No
necrosis occurs. In surgically created fl aps, there is no insult to
the perpendicular vessels coming from the longitudinal axial
vessels and supplying the subdermal plexus. Contrary to this,
in an avulsed fl ap, there is a severe insult to these vessels which
are stretched as the direction of force is at right angles to them.
Moreover, while surgically undermined tissues are healthy,
the avulsed tissues may be crushed, heavily contaminated,
burnt, devitalized and in multiple pieces.3 In limbs, the avulsed
tissues may be proximally, distally, medially or laterally
based. Knowledge of vascular anatomy of the region can tell
us the extent to which even non-proximally based fl aps can
also survive. Thus, the disruption of the perfusion of skin and
subcutaneous tissues is the essence of an avulsion injury.

Avulsion injuries, in a given region, generally occur due to
similar mechanisms and in similar planes in different patients.
Thus, scalp avulsions occur due to entanglement of long hair
in rotating machinery. These avulsions occur through loose
areolar plane and may take away pinna and eyebrows as well.
Figures 4A to C: Please note the several, large areas of bluish discoloration of the skin without any skin wound and increased girth of right
lower limb in a patient with history of road traffi c accident with a heavy vehicle. Suspicion of closed avulsion injury?

Skin Avulsion Injuries
125
The penoscrotal avulsions occur as the patients’ loose clothing
becomes entangled in rotating machinery (e.g. rotating belt
of fl our grinding machine). The clothing then twists and is
stripped off carrying the loose elastic skin of the male external
genitalia with it. Because of the native elasticity of the genital
skin, usually only the skin and dartos layers are avulsed
leaving the corpora, urethra and testicles exposed. Degloving
injuries of the abdominal wall alone are extremely rare
because the area lacks a bony framework to counteract the
reactive external force. Sonmez et al. (2002)18 reported a case
of roller machine injury where the abdominal skin between
costal arches and suprapubic area up to the iliac crests at the
sides was torn off as a degloving injury of anterior abdominal
wall with rectus fascia underneath being intact.

In extremities, the mechanism is different. They are
commonly due to friction from rubber tyres in “run over”
accidents although not all “run over” accidents produce
degloving. John Boyd Dunlop, a veterinary surgeon in
Belfast, reinvented the pneumatic tyre for the tricycle of
his son.19 Prendiville and Lewis (1955)19 called this injury
“pneumatic tyre torsion avulsion injury”, which is a more
correct description than Slack’s (1952)2 “friction injury”.
Subsequently, the development of transport based on pneumatic
tyre changed the whole scenario of road traffi c accidents and
the types of injuries sustained by the victims (Figures 6A
and B) A lesion directly associated with the pneumatic tyre,
viz. the pneumatic tyre torsion avulsion friction injury was
“born”, where the skin of the limb is torn apart from the deeper
structures due to it being trapped between the pneumatic tyre
of a vehicle and the road.

Heavy, slow moving vehicles with large tyres like buses,
trucks and cars have been suggested as being the most likely
cause of this injury, perhaps because the victim is more
likely to come into contact with tyres than other parts of the
vehicle.1 (Figures 7 and 8). Essentially, this injury causes an
avulsion of the skin and subcutaneous layer with separation in
a plane outside the deep fascia and rupture of the perforating
musculocutaneous vessels.2 When the vehicle is moving, the
tyre and the road both act in the same direction to drag the
skin from the limb. The skin may remain intact producing a
closed avulsion injury or else rupture on the opposite side,
producing a revealed type of avulsion injury. The force
primarily responsible for the injury is “shearing” force. If
the wheel of the vehicle continues to move and runs over the
limb, fractures may occur and a crushing injury is produced.
If the wheel is locked under braking, the limb may be pushed
ahead of the wheel with friction from road and tyre producing
a severe twisting force on the skin around the mid axis of the
limb. The skin may rupture at any point and friction burns
may also occur. The skin may retain some attachment as a
pedicle or else may be detached completely. Lower limbs are
Figures 5A to C: (A) Large areas of bluish discoloration of skin of
left thigh with a small patch of parchment like-eschar but intact skin
gave rise to suspicion of concealed avulsion injury. (B) On incising
the eschar, suspicion was confi rmed. (C) Please note the undermining

Types of Wounds and their Management
126
most commonly involved, the upper limb being the next most
common. Trunk including pelvis is generally involved along
with the limbs. The limb injuries are commonly associated
with other injuries like head injury or intraabdominal injury
etc. Pelvic fractures may be associated with urethral injuries
especially in males while extensive avulsions of lower back
and perineal regions demand diverting colostomy for their
management adding to the morbidity.

Arnez, Khan and Tyler (2010)20 categorized the soft tissue
trauma of limbs into four types in order to prognosticate the
injury as a whole.

Pattern 1: Limited degloving with abrasion/avulsion. The
loss of soft tissue is as a result of abrasive force with little
undermining of the remaining skin edges. Majority of these
cases occur over bony prominences leading to exposed bone
and joint. Most of these cases need fl ap cover.

Pattern 2: Noncircumferential degloving. The majority
of the skin is present as a fl ap with an extensive area of
undermining. The undermining is usually in a single plane,
between deep fascia and subcutaneous tissue. After excision
of dead and devitalized tissue, skin grafting (or sometimes
fl ap cover) is required and primary healing may be expected.

Pattern 3: Circumferential single plane degloving. Whether
closed or open type, the plane of avulsion is single, usually
between deep fascia and subcutaneous tissue.

Pattern 4: Circumferential multi-plane degloving. In
addition to avulsion as in pattern 3, there is opening up of
muscle bundles and bone may be exposed. These cases suffer
from the greatest degree of tissue disruption and lowest rate of
primary healing. Several stages of reconstruction are usually
required.
CLINICAL FEATURES
Avulsion injuries or degloving injuries affects individuals
of all age groups and both the sexes. These can involve
one or more of the many regions of the body from head to
toes. There can be an avulsion of scalp, pinna, eyelids,
lips, upper extremity (especially dorsum of hand and ring
fi nger), penoscrotum, lower torso (front and back) and lower
extremity (including sole and heel pad). The avulsion injuries
Figures 6A and B: Pneumatic rubber tyre, “the mother of road traffi c
avulsion injuries”
Figures 8A and B: Please note the tyre marks on the skin
Figure 7: The tyre of a large vehicle and the road move in the same
direction (towards left in the picture) with the bursting of skin on other
side (right in this picture)

Skin Avulsion Injuries
127
of the scalp and penoscrotal region are commonly due to
involvement in a rotating machinery while that of upper
and lower extremity and torso are mostly due to road traffi c
accidents. The avulsion injuries of the lower torso and lower
extremity may be associated with fractures of the pelvis,
femur or tibia/fi bula. The upper extremity avulsions may also
involve fractures of long bones. Crush-avulsion injuries of the
hand and feet are common with involvement of skeleton of
hand/foot in addition to avulsion of skin and tendons.21

Soon after injury, the avulsed skin fl ap may appear normal
in color or dusky in the distal most regions. The plane of
avulsion is not uniform even in a particular patient. Thus, in
a scalp avulsion which usually occurs through loose areolar
tissue, there may be pulling off of the periosteum as well at
some places. Similarly, in a lower limb avulsion, one part of
the avulsed fl ap may contain deep fascia while at other places
even periosteum (especially of shin) may also come off. In a
penoscrotal avulsion, even testis (testes) may be avulsed and
lost. In hand and foot, paratenon may be avulsed leading to
bare tendons.

There may be large areas of avulsed skin fl aps which are
badly traumatized and of doubtful viability or even clearly
useless. Similarly, the bed may be clean and uncontaminated,
moderately contaminated or may be heavily impregnated with
foreign material. Depending upon the plane of separation, the
under surface of the avulsed fl ap shows subcutaneous fat with
areas of deep fascia, muscle(s), tendon(s), etc. Fluid collection
and thrombosed vessels may also be seen. If the patient presents
very late or has been wrongly treated by simple suturing of the
avulsed fl aps, the latter may be black and obviously necrotic
with foul smelling fl uid and pus underneath and patient toxic
or may be in frank septicemia. The patient may also present
with absent avulsed tissues which might have been lost in the
machinery or at the site of accident on the road side and were
either not retrievable or not retrieved by the accompanying
person(s) due to any reason. Such patients simply present with
open wounds (raw areas). In both of the above situations, the
wound bed is generally uneven with loose fat and separated
muscle bundles.

It is a common mistake committed by the novice surgical
residents to suture back the avulsed pedicled fl aps.22 This is
specially so if the fl ap has a proximally based pedicle and/or
a large pedicle. Actually the size of this attachment is not as
important as the forceful injury caused to avulsed skin. The
arteries resist trauma more than the veins and the lymphatics
and the former may be less important than the latter. The
veins are more easily injured;progressive venous thrombosis
occurs and the lymphatics become inadequate to drain the
tissue fl uids and edema occurs. Thus, it is the poor venous
and lymphatic drainage rather than poor arterial supply which
leads to the death of the traumatized avulsed pedicled fl aps.22
Thus, whenever, avulsed fl aps are simply returned back to
their original bed and sutured, eventual sloughing of a part or
whole can occur.
MANAGEMENT
The appropriateness of primary treatment decides the
morbidity, mortality and disability with respect to the outcome
of millions of injuries occurring worldwide. The treatment of
avulsion injuries can be discussed under two major headings,
viz. general and local.

General: As is true for all injuries, wherever required,
control of airway and bleeding, resuscitation from shock,
examination for other life-threatening and non life-threatening
injuries requiring immediate attention, administration of
tetanus prophylaxis, maintenance of sterile techniques,
splinting of fractures, etc takes precedence over local wound
management.

Local: In the last 60 years, the treatment of extensive
avulsion injuries has made great advances. The appreciation of
detailed vascular anatomy of various regions, the availability
and use of external fi xators to stabilize associated fractures,
the use of microsurgical techniques and last but not the least,
cooperation of the plastic and orthopedic surgeons14,16,23 right
from the beginning have all made dramatic improvements
in the outcome. The fi rst successful replacement of avulsed,
but otherwise undamaged, fl aps as a full thickness skin graft
was reported by Farmer of Toronto in 19394,5 who described
four cases, three following automobile accidents and one a
domestic wringer injury. His treatment consisted of excision
of all the avulsed skin. The wound was thoroughly debrided
and cleansed using antiseptic fl uids. The avulsed skin was
treated by removal of all the subcutaneous fat and then sewn
accurately back into position. Quilting sutures were also used
and multiple perforations were made into the graft which was
then dressed with fi rm pressure. Slack (1952)2 advocated
the use of full thickness skin from the avulsed specimen
discarding only the directly traumatized areas. Coryllos et al.
(1960)24 reported the case of a 9-year-old boy with avulsion
injury of whole leg from knee to ankle. He carried out excision
of the whole of avulsed skin in a single piece, defatted it and
applied it as a free full thickness graft. Three-fourths of this
survived while the areas with skin loss were secondarily split
skin grafted.

Avulsion injuries may be localized requiring individual
solutions, for say, dorsum of hand/foot, heel/sole pad,
penoscrotal region, etc. In generalized injuries, the problem is
more of resurfacing and closing the large raw area.25 Because
of the large number of permutations and combinations of
the extent of avulsion injuries at various sites in different
patients, one must have a clear understanding of how to

Types of Wounds and their Management
128
approach these injuries. In addition, the approach may have
to be modifi ed by other life threatening injuries which may
take precedence over avulsion injury of a limb. Very grossly
speaking, the local management requires debridement of
the wound and provision of skin cover.21,26 Based on local
conditions and the general condition of the patient, Lehr and
Fitts (1969)6 advised one of the fi ve methods of treating these
patients, viz.
1. Debridement alone: This may be required in patients with
other associated life threatening injuries which require
more attention and is the minimum which has to be done in
every case.
2. Debridement and excision of the avulsed tissues with
primary or secondary closure of the wound: This will be
done in cases where debridement leaves a wound which can
be safely closed either primarily or secondarily in a week’s
time. Avulsion of lips, eyelids, partial scalp avulsions, etc.
need primary closure if possible. Avulsions due to human
or animal bites can be closed secondarily.
3. Debridement and excision of avulsed tissue with the use
of excised tissue as a free full thickness skin graft for
the wound closure: This technique is followed where the
avulsed tissues are available and useful for harvesting skin
graft. Immediate or delayed (5–7 days) application of graft
can be done.
4. Debridement and excision of avulsed tissue and the use
of a split thickness skin graft to close the wound: This
technique is followed where the avulsed tissues are not
available for harvesting skin graft. Immediate or delayed
application of graft can be done.
5. Debridement and excision of avulsed tissue and the use of
a pedicled/free fl ap to close the wound: This is necessary
in cases where important vital structures like tendons
(e.g. on dorsum of hand), blood vessels or neurovascular
structures are exposed and will dry up without immediate
cover with disastrous consequences. All sorts of fl aps in
the armamentarium of a plastic surgeon have been used for
various patient needs.

The concept of debridement was introduced by Pierre-
Joseph Desault (1744–95) and this was widely put into practice
by his pupil Dominique Jean Larrey (1766–1842) when he
accompanied Napoleon in his campaign.14 Debridement
includes shaving around the wound, cleansing of the skin
with detergent solution like savlon, fl ushing of the wound
with copious amounts of sterile water or saline and removal
of all the dead and necrotic tissues and impregnated foreign
material (road or farm or industrial debris).

Prendiville and Lewis (1955)19 classifi ed the patients of
avulsion injuries into three types, viz.
1. Patients admitted within a few weeks referred to as
primary or “delayed primary”.

2. Patients presenting with granulating wounds after the
slough has separated.

3. Patients presenting with late deformities due to this
injury.

When a patient is fi rst seen in emergency within a few
hours of injury, there are two possibilities, namely:
A. The avulsed tissues are not on the patient’s body, or
B. The avulsed skin is still attached to the body with a small
or a large pedicle.
A. In case they are absent, they may not have been brought
along with the patient because they got entangled
in the machinery and were lost or they fell off at the
site of mishap and no one retrieved them, etc. In cases
where the tissues have been brought along with the
patient, they may be reimplantable with microsurgical
techniques or they may be unfi t for reimplantation. These
reimplantation procedures are generally attempted for
scalp, pinna and testis (very rarely associated with
penoscrotal avulsions). This is because of various
reasons, viz.

i. They are highly specialized structures with their loss
leading to great physical morbidity and psychological
trauma.

ii. They are either very diffi cult or not at all possible to
reconstruct.

iii. They are reimplantable because of favorable vascular
plane of avulsion and anastomosis of a single vascular
pedicle can completely restore the circulation.
For limbs and penoscrotum, avulsed skin fl aps
are generally not reimplanted using microsurgery
because they are, as a rule, not reimplantable. This
is because the named large vessel supplying them
is sub-fascial in the septal planes while the avulsed
fl aps are suprafascial. Hence, they do not contain
any vessel which, when anastomosed, will supply
the whole avulsed fl ap. For those scalp avulsions
which are unfi t for microsurgical re-implantation and
for limb avulsions, the avulsed tissues may or may
not be fi t to provide full/split thickness skin grafts.
Distally based avulsed penile skin, when simply
stitched back, has consistently given poor results
with complete failure.

Waikakul (1997)21 attempted revascularization of deglo-
ving injuries of limbs in selected cases with good quality
avulsed fl aps. After debridement, veins of the fl ap at the distal
end were anastomosed to muscular arteries in the bed and
once fl ow was established, the veins at the proximal end were
anastomosed to veins in the bed. Up to 6 veins were required.
Good results were seen in several cases.

In patients where the avulsed tissues are not available
or they are unfi t for reimplantation, the wound is debrided

Skin Avulsion Injuries
129
and skin cover provided, either immediately or after the
granulations develop, using skin grafts. If delayed grafting
is considered, the wound is dressed daily with an antiseptic
solution (e.g. povidone iodine, eusol, etc). Over a period of
time (up to 2–3 weeks), depending upon the thoroughness
of the surgical debridement done/possible at the time of
admission, extensiveness of the foreign material in the wound,
extent of opening up of muscle bundles or neurovascular
structures separated from the bed (as bow strings), etc. the
wounds become smooth, contoured areas with healthy
granulation tissue. In these patients split skin grafts may have
to be harvested from other areas of body only as the grafts
harvested from avulsed tissues may not be viable for complete
“take”. Partial or full thickness skin grafts harvested from
the specimen brought along have been used immediately or
refrigerated at 4°C and applied up to a week later when either
the wounds become healthy or the dead tissues have declared
themselves and have been debrided.27 The skin grafts may be
stitched, fi xed to the bed and dressed by traditional techniques.
Use of VAC (vacuum assisted closure) therapy, also called
negative pressure wound therapy (NPWT) has also been
reported for graft application in degloving injuries of hand
and foot.28,29 Considerable edema and free fl uid that would
have normally collected under the graft with the potential of
impairing graft ‘take’ gets evacuated.

The early provision and restoration of a good skin cover is
very essential to: (1) Prevent wound infection, pain of repeated
dressings and loss of fl uids, electrolytes and proteins. It allows
early return to work. It also minimizes scarring, recurrent
ulceration, distal edema and loss of function. (2) Bony union
either by natural process or by surgical intervention can occur
only in a healed wound. (3) Secondary reconstructive surgery
in the form of tendon or nerve grafting, arthrodesis, etc. can be
done with best results.
B. In case the avulsed tissues are still attached to the body,
the pedicled avulsed tissues have been subjected to
one of the three possibilities by different individuals as
described below:

i. They have been sutured back as if they were just
simple lacerations. In spite of the recognition of the
problem for over last 60 years, many young surgeons
keep repeating the error while the lesson is learnt by
watching the sutured degloved skin become dead
and necrotic over next several days. This practice
is to be strongly condemned.3,30 Except for very
small undermined lacerations with broad, generally
proximally based pedicles or avulsed favorably
to the direction of vascular pedicle, this type of
treatment is bound to be a failure. Patients with
extensive avulsions of the lower limbs have been
treated in this way, leading to massive necrosis of
avulsed tissues, with formation of pus underneath
and septicemia and death of the patient. Even when
the avulsed fl aps appear fully viable because of
very limited undermining, it may not be desirable to
stitch them completely. This is because the edema
of the underlying muscles due to trauma may cause
pressure on the compromised circulation leading to
their partial necrosis. Rather, they may be loosely
approximated with a few tacking sutures and the
wound lightly dressed and observed every 24 hours
till clear evidence of its survival or necrosis.

ii. They have been completely excised as if they were
totally dead and useless.3,19,31 This radical thinking
leads to extensive debridement of all the avulsed
tissues so that no undermined areas exist. This is not
a good approach and illogical27 as a large amount
of salvageable tissues are unnecessarily discarded
(present author’s view as well). The recipient sites
require large split skin grafts/fl aps from uninjured
limbs and other areas with extensive morbidity. An
extensively degloved skin, though avascular and
destined to die if left to itself, is still viable and
can survive if used as a free skin graft.5,32 Even in
most severe cases, rarely will the avulsed skin be
so badly traumatized that it cannot be used as a free
graft.33 This is because dermal vascular pattern of
capillaries remain intact, thereby allowing the skin
to be replaced as full thickness graft. After defatting,
the graft is thoroughly irrigated with saline and
antimicrobial solutions.

iii. They have been carefully debrided with conservation
of all viable tissues. This intermediate course involves
the debridement of all the nonviable areas carefully
while preserving the tissues which are well perfused
and expected to remain viable. For this approach
to be followed, it is a must that one can distinguish
the live from dead areas. This middle path is most
appealing as well as bound to give good results with
minimum of morbidity (present author’s approach).

Thus, accurate assessment of the extent of the area lacking
circulation is desirable. Markedly abraded and contused skin
will probably not survive. Viability of the avulsed skin fl ap is
very diffi cult to determine clinically.13 It must be noted that
the methods discussed below are actually extrapolated from
the techniques we generally use for fl aps raised electively
based on the knowledge of vascular supply. Unfortunately
skin that has been avulsed by rough trauma cannot be assessed
accurately with these techniques.22,34 With gentle handling of
tissues as in elective surgery, one does not expect any damage
to the venous and lymphatic drainage. At the fi rst sight, the
severity and extent of damage to skin circulation may not be

Types of Wounds and their Management
130
particularly striking, but there is failure of the skin to blanch
when digital pressure is applied, with return of color when
the pressure is released.24,27,31 This test is, however, not very
accurate and interpretation requires experience. When a skin
edge is present, there is no dermal bleeding. Both these show
absence of circulation.

To assess perfusion of avulsed tissues, Fluorescein
(resorcinolphthalein) test has been used.35-37 Even though,
this dye was introduced into clinical practice more than 80
years back and it has been advocated as a reliable test for
fl ap viability, somehow it has not been commonly used by
reconstructive surgeons and certainly not in the acute trauma
setting. It is administered intravenously in a dose of 15
mg/kg in 200 ml of saline over a period of 10 minutes. On
examination under ultraviolet light, the normally perfused
skin clearly fl uoresces, while the avascular skin does not.
Unfortunately, diffi culty arises in areas where the damage is
partial and more help is needed. Such areas show a mottled
pattern of fl uorescence. The margins of an avulsed skin
fl ap are likely to necrose at least superfi cially and are best
considered as frankly ischemic areas.1 It must be remembered
that although fl uorescein fl uoresces well in the test tube, it
needs experience to know which tissues will survive.

A fairly accurate tourniquet blush test has been described to
assess the viability.25,38 The involved extremity is elevated for
one minute. A tourniquet is infl ated around the thigh or upper
arm. The limb is then lowered and the tourniquet defl ated. The
return of a pink color to the fl ap is looked for. This is the result
of the infl ux of blood into dilated capillaries. Where arterial
supply is insuffi cient, such areas remain pale (white). Where
venous congestion and thrombosis exists, the areas become
purple. Both pale and purple areas are ultimately destined to
become necrotic. The point to which good pink color returns,
is an indication of the future line of demarcation. The viable
tissues can be left while the nonviable ones are excised.

Another practical way of distinguishing viable from non-
viable areas, utilized by the present author, is as follows. A few
tacking sutures of thick silk (No.1 or 1/0) are applied to the
avulsed fl ap which is restored anatomically. The whole avulsed
fl ap is then thoroughly cleaned and draped as one does for
taking split skin grafts. Intermediate thickness split skin grafts
are then harvested from the whole of the undermined area and
dermal bleeding patterns are noted. The sutures are removed
and all the areas which show absent or doubtful dermal
bleeding are then excised immediately while the undermined
areas which show good bright red dermal bleeding are
considered viable and salvageable. The skin grafts harvested
from the avulsed areas can then be used to provide cover to
the raw areas created after thorough debridement. The grafts
can also be refrigerated at 4° Celsius and applied up to a week
later when good granulations have developed and hemostasis
has occurred. A by-product of this technique is availability of
larger size of grafts as compared to the size of recipient area.
These grafts can be meshed and expanded as well.

Use of SpO2 skin electrodes may offer a method of assessing
the adequacy of blood supply to an avulsed skin fl ap.30

After the grafts have been applied and the all the raw
areas healed, massage of the graft and scars with bland
oils and creams is started. Pressure therapy in the form
of crepe bandages initially and pressure garments later is
given to prevent hypertrophic scar formation and hasten
graft maturation. Passive and active joint movement is also
instituted gradually to attain complete range of motion.
Fractures of bones, etc. may not allow these measures to be
started at appropriate time or with appropriate vigor.

Patients presenting with granulating raw areas with
almost no slough require skin coverage with split skin grafts
harvested from the available and appropriate donor sites in the
body. As these patients did not have the facility for treatment
by a competent person to deal with this type of injury, it is
possible that these patients are anemic and hypoproteinemic
which needs to be treated. In addition, the wound bed is to
be prepared by a few regular wet to dry dressings done by
the surgeon himself while waiting for the wound bed culture-
sensitivity reports to be available. Once the culture reports are
available and the patient is fi t for anesthesia, skin grafting is
done with patient being administered appropriate antibiotic
cover. Some areas may need fl ap cover for they are not
graftable or else require fl ap because of their specialized skin,
e.g. sole or heel pad, dorsum of hand which will need tendon
grafting later.
Controversies or Alternatives?
To use Split Thickness Skin Grafts (SSG) or Full
Thickness Skin Grafts (FTG) from Avulsed Flaps?
Both SSG and FTG have their own advantages and
disadvantages. FTGs have the advantage of good color and
texture match but their chances of complete ‘take’ are poorer
in less than optimal conditions. FTGs require uncompromised
vascularity and are ordinarily reserved for acute uncontami-
nated wounds of small size.39 Because of their severe primary
contraction (up to 40%) and tendency to curl up, they require
suturing to themselves or to bed. The bed has to be thoroughly
debrided and complete hemostasis achieved. They can only
be harvested from avulsed fl aps.2,24,27,40 Harvesting of FTGs
from the avulsed fl aps has been done by various methods.41
“Defatting” the skin to get a real FTG with scissors is a
tedious and prolonged process while scraping may damage
the very undersurface of the graft which has to revascularize
from the bed by joining of the capillaries. Gibson and Ross

Skin Avulsion Injuries
131
(1965)32 developed a mechanical dermatome to cut free grafts
of any desired thickness up to 11 inches broad from the skin
that has become detached. On weighing all the pros and cons,
the FTGs do not offer any substantial advantage over SSGs in
the management of avulsion injuries. Farmer (1939, 1943)4,5
suggested FTG’s but many authors have found the results to
be poor. Prendiville and Lewis (1955)19 advocated the use of
split skin grafts applied after one week of initial debridement
as the avulsed skin was too severely damaged to be of use.
Innis (1957)3 too advocated the use of SSG, immediately to
prevent granulation tissue formation. The SSGs have much
less primary contraction and have far more chances of ‘take’
even in less than ideal situations. They can be just spread on
raw areas without sutures as they show minimal tendency
to curl up. They can be harvested from avulsed fl aps as well
as from patient’s uninjured sites. They can be considered as
the reconstructive surgeons’ best friend in coverage of large
wounds. They have withstood the test of time, with the whole
of last century being the testimony to that (Figures 9A to D).
Debridement—Conservative or Radical?
The debridement can be conservative or radical. If radical,
there are always chances of salvageable tissues going down
the drain. On the other hand, if conservative, there are chances
that some compromised tissues which are not frankly necrotic
have been left in the wound and these may necrose in ensuing
few days due to thrombosis, infection, etc. It is also possible
Figures 9A to D: (A and B) Extensive avulsion injury of right lower extremity with loss of skin from groin to foot;
(C and D) Completely resurfaced with split skin grafts

Types of Wounds and their Management
132
that some dead tissues have been left intentionally to avoid
injury to/drying up of the important underlying structures or
else prevent denuding the bone.

There are greater chances of graft ‘take’ after radical
debridement as compared to conservative debridement.
However, a radical debridement on the day of injury may
also expose some structures like tendons, bones, nerves and
vessels, etc which may demand immediate fl ap cover. This
may or may not be feasible due to extensiveness of the defect.
All these may require a general anesthesia for which the
patient may or may not be fi t due to other associated injuries.

Conservative debridement, on the other hand, is possible
without anesthesia and is often dictated by the poor general
condition of the patient or other associated injuries.
Conservative debridement saves all the tissues possible, leads
to lesser contour problems and lesser need for fl ap cover.
However, there is an increased early morbidity in the form of
more dressings and delayed recovery.
Skin Grafting Immediately or after Granulations
have developed?
There is no doubt that graft ‘take’ is far better, if grafting is
done on healthy granulating wound, when wound culture-
sensitivity reports are available and appropriate systemic
chemotherapy has been started and antimicrobials applied
locally. The raw area is also a smooth surface as compared
to the one immediately after debridement when the surface is
irregular and uneven due to separation of muscle bundles, cut
edges of muscles, areas with subcutaneous fat, some tenting
of neurovascular pedicles, traumatic tattoos, etc. In addition,
there is no problem of hemostasis in healthy granulating
wounds (Figures 10 to 18).

However, healthy granulations in these traumatized patients
do not form in the usual 5 to 6 days as in surgically created
wounds. It may take 2 to 3 weeks in heavily contaminated and/or
conservatively debrided cases. More radical the debridement,
earlier it will be a healthy granulating wound. During this
period, any grafts harvested from avulsed tissues are bound
to become useless. Moreover, there remain all the attendant
problems of infection, pain, loss of plasma proteins through
oozing wounds, massive dressings for such large wounds, etc.
Some of these problems can be minimized by use of one of the
various skin substitutes available. With immediate application
of autografts, these problems are minimized but there are graft
losses at various places requiring repeat grafting procedure(s).
Contour defects, muscle herniations are more with immediate
application of grafts.
Use of Flaps: Immediate or Delayed?
Most avulsions, especially of lower limbs are very extensive.
They neither require fl aps nor do we have such large fl aps
available in the body. Only the areas, where a fl ap cover is
absolutely essential, are covered with fl aps. Even in these areas,
in the acute setting, it is the split skin graft and wet dressings
Figures 10A to C

Skin Avulsion Injuries
133
Figures 10A to H: (A and B) Extensive avulsion injury of left thigh and gluteal region in a young female with opening up of muscle bundles.
No skin grafting is possible; (C and D) Conservative management being done with great reduction in raw area and smooth healthy granulating
wound devoid of any undermining; (E) Early result after split skin grafting; (F to H) Result after fi ve years. Please note the nice contours
Figures 10D to H
D