Principles and Practice of Wound Care

History and Healing
34
MANAGEMENT
“An ounce of prevention is better than tons of cure”. This old
saying holds true for scars as well. Various therapies used for
scar improvement area as follows:
Nonsurgical

1. Pressure therapy

2. Silicone sheets/gel

3. Massage

4. Splintage

5. Corticosteroids

6. Inhibitors of gene transfer

7. Flavonoids

8. Lasers

9. Radiotherapy
10. Cryotherapy
11. Intralesional antimetabolites
12. Others like anti-infl ammatory, antihistamine, calcium
antagonist drugs
13. Skin fi llers
14. Tattooing.
Pressure Therapy7-9
Pressure therapy has been the preferred conservative manage-
ment for both the prophylaxis and treatment of hypertrophic
scars and keloids since the 1970s. Currently, pressure garments
are predominantly used for the prophylaxis of hypertrophic
burn scar formation. The mechanism of action of pressure
therapy remains poorly understood; however, possible
mechanisms are decreased collagen synthesis attributable
to limiting of the supply of blood, oxygen and nutrients
to the scar tissue and increased apoptosis. It is generally
recommended that pressure be maintained between 24 and 30
mm Hg for 6 to 12 months for this therapy to be effective;
however, this advice is largely empiric. Electron microscopy
has demonstrated a reduction in the cohesiveness of collagen
fi bres in pressure treated scars (Figures 9A and B).
Silicone Gel Sheeting9,10
Topical silicone gel sheeting has been a well-established
treatment for management of scars since its introduction in
the early 1980s, and its therapeutic effects on predominantly
hypertrophic scars have been well documented. Current
opinion suggests that occlusion and hydration are the likely
mechanisms of therapeutic action of silicone gel sheeting
rather than an inherent antiscarring property of silicone.
Silicone sheets are recommended to be worn for ≥12 hours
Figures 9A and B: Tailor made pressure garments for post burn
scars on dorsum of both hands
B
A
and/or one day for at least two months beginning two weeks
after wound healing. Silicone gel is favored for areas of
consistent movement, where sheeting will not conform, and
should be applied twice daily (Figures 10A and B).
Intralesional Corticosteroid Injections
Since the mid-1960s intralesional steroid injections have
gained popularity as one of the most common approaches
to attenuate hypertrophic scar and keloid formation, while
topical administration of corticosteroid-containing creams
has been used with only varying success. Most of the known
effects of corticosteroids are thought to result primarily
from its suppressive effects on the infl ammatory process
in the wound , and secondarily from diminished collagen
and glycosaminoglycan synthesis, inhibition of fi broblast
growth and enhanced collagen and fi broblast degeneration.
Two or three injections of triamcinolone acetonide (TAC, 10
to 40 mg/ml) are usually suffi cient, although occasionally
injections are continued for 6 months or more. Response rates

Scars Following Wound Healing
35
Figures 10A and B: Silicone gel sheet application (A) over scar
following excision of nevus after stitch removal (B)
A
B
have been highly variable, with fi gures ranging from 50 to 100
percent, and a recurrence rate of 9 to 50 percent. An important
fi nding was that intralesional corticosteroid injections, when
used alone, have the most effect on younger keloids, which
can become completely fl attened. In older scars and keloids,
corticosteroids can soften and fl atten the scars only to some
extent and can provide symptomatic relief (Figures 11A to C).

Injections may be used alone or combined with other
therapies, of which the combination with cryotherapy or
surgery are the most widely used modalities in clinical practice.
Side effects include dermal atrophy, telangiectasia and pain
at the site of injection. Despite relatively few randomized,
prospective studies, TAC remains a fi rst-line therapy for the
treatment of early keloids and a second-line therapy for the
treatment of early hypertrophic scars if other easier treatments
have not been effective.
Figures 11A to C: (A) Keloid in ears after ear piercing. (B) Intralesional
steroid injection being given. (C) Keloid regressed in size after four
injections
B
C
A

History and Healing
36
Cryotherapy
Cryotherapy is believed to induce vascular damage that may
lead to anoxia and ultimately tissue necrosis.

Cryotherapy alone results in keloid fl attening in 51 to
74 percent of patients after two or more sessions, and it is
benefi cial for the management of severe acne scars. If
given directly before the administration of intralesional
TAC injections, it has been observed to give better results.
Limitations include the delay of several weeks required for
postoperative healing and the commonly occurring side effect
of permanent hypopigmentation. Other side effects include
hyperpigmentation, moderate skin atrophy, and pain.

As a result, cryotherapy is generally limited to management
of very small scars. Recently, the intralesional-needle
cryoprobe method has been assessed in the treatment of
hypertrophic scars and keloids, and has been demonstrated
to have increased effi cacy compared with that obtained with
contact/spray probes and shorter re-epithelialization periods.
Radiotherapy
Superfi cial X-rays, electron-beam therapy and low- or
high dose–rate brachytherapy have been used with good
results in scar reduction protocols, primarily as adjuncts
to surgical removal of keloids. The effects of radiation on
keloids are thought to be mediated through inhibition of
neovascular buds and proliferating fi broblasts, which result
in decreased collagen production. Electron beam irradiation
is usually started 24 to 48 hours after keloid excision, and
the total dose is limited to 40 Gy over the course of several
administrations to prevent side effects such as hypo- and
hyperpigmentation, erythema, telangiectasia and atrophy.
However, because radiation entails a risk of carcinogenesis,
particularly in areas such as the breast and thyroid, it should
be used with caution.
Flavonoids
Flavonoids (quercetin and kaempferol) are found in well-known
topical scar creams, such as Mederma skin care gel (Merz
Pharmaceuticals, Greensboro, NC, USA) and Contractubex gel
(Merz Pharma, Frankfurt, Germany). So far, effi cacy studies
testing the ultimate benefi t of these fl avonoid-containing topical
scar creams have provided controversial data.
Laser Therapy
Since the introduction of laser treatment for keloids in the mid-
1980s, the therapeutic use of different lasers with different
wavelengths has been investigated, and success has varied.
Until today, the most encouraging results have been obtained
with the 585 nm pulsed-dye laser (PDL), which has been
recognized as an excellent therapeutic option for the treatment
of younger hypertrophic scars and primarily keloids.

Nonoverlapping laser pulses at fl uences ranging from
6.0 to 7.5 J/cm2 (7 mm spot) or from 4.5 to 5.5 J/cm2 (10
mm spot) have been recommended for the treatment of
hypertrophic scars and keloids. Two to six treatments may be
necessary to successfully improve scar resolution, including
scar color, height, pliability and texture. By causing local
ischemia via destroying blood vessels, 585 nm PDL therapy
is believed to induce neocollagenesis, collagen-fi ber heating
with dissociation of disulfi de bonds and subsequent collagen-
fi ber realignment, and decreased fi broblast proliferation as
well as release of histamine and other factors that infl uence
fi broblast activity. Adverse effects include transient hyper-
or hypopigmentation and blistering. Hyperpigmentation has
been reported with a frequency of 1 to 24 percent. The most
common adverse side effect of 585 nm PDL treatment is
postoperative purpura, which can persist for seven to ten days.
Inhibitors of Gene Transfer
5-fl uorouracil and Mitomycin–C are antimetabolites which
block DNA synthesis and transcription through competitive
inhibition of thymidylate synthesis, thus inhibiting proliferation
of cells. They are likely to be helpful in scar control though
there are not many studies to show the long term results.
Usually a single application after wound closure is said to be
effective.

5–fl uorouracil 50 mg/ml intralesional injection two to three
times per week in review of multiple studies is found to be
effective for keloids and hypertrophic scars. It shrinks the
keloids safely without causing tissue atrophy or telengiectasia
and if combined with corticosteroids and pulsed dye laser
produces superior results in shrinking keloids than either of them
used alone. The only known side effects are hyperpigmention
and wound ulceration. Intralesional interferon alpha-2b (1.5
million IU twice daily for 4 days) also reduces keloid size by
50 percent and prevents its postsurgical recurrence. But the
only limitation is the injection pain and expense.
Anti-infl ammatory Agents
Recently some studies have shown that topically applied
salicylates reduce infl ammation in scars thus reducing pain
and itching in scars. Use of topical aspirin can precipitate
hypersensitivity reaction in asthmatic patients so its use
should be made under physician’s guidance.

Scars Following Wound Healing
37
Antihistamines
They are usually used to reduce pruritis in hypertrophic scars
but has been seen to exert antifi brotic effects as well because
of anti-infl ammatory response especially seen with H1
blockers. They are also known to inhibit collagen synthesis.
Thus they reduce scar growth rate. The most commonly used
antihistamine agents are diphenhydramine (Benadryl, Pfi zer),
Chlorpheniramine (Avil), Fexofenidine (Allegra, Aventis) and
Loratidine.
Calcium Antagonists
Calcium antagonists or calcium channel blockers like verapamil,
trifl uperazine and Tamoxifen which is a protein kinase inhibitor
have been found to induce collagenase production and thus
degradation of scar tissue. This effect is mediated by interruption
of the basic cellular G-protein signal transduction path which
regulates the fi broblast behavior. Studies have shown that both
intralesional injection and topical application of Verapamil are
effective in inducing scar degradation.
Skin Fillers
Skin fi llers are used to mask scars as in acne scars or depressed
atrophic scars. The various fi llers used can be classifi ed as:
1. Biological

a. Autologous fat

b. Collagen
2. Synthetic Fillers

a. Hyaluronic acid

b. Poly-l-lactic acid

c. Calcium hydroxyapatite

d. Polymethyl methacrylate
Tattoing
To camoufl age a pale white or hypopigmented scar, it can be
tattooed by injecting pigment into it with a needle so as to
match it to the surrounding skin.
Surgical Modalities
1. Excision

a. Shave excision

b. Simple excision

c. Serial excision
2. Z-plasty
3. W-plasty
4. Geometric broken line closure (GBLC)
5. Dermabrasion
6. Local fl aps
7. Subcision
Shaving and Split Skin Grafting
This is done for large raised scars like hypertrophic scars. This
is generally done by skin grafting knife and hypertrophied tis-
sue is shaved off till the layer of healthy dermis is reached. This
is then covered with a thin spilt skin graft (Figures 12A to C).
Simple Excision (Fusiform Excision)
Best for small scars that are wide or depressed and which lie
near to relaxed skin tension lines. Angle at the end of incision
needs to be less than 30 degrees.
Serial Excision
It is based upon the ability of skin to stretch over time. This
procedure can move scar to a better anatomic location.
It can also be used for reducing grafted areas. Surgical
excision is a common management option for hypertrophic
scars and keloids involving a small area, in combination
with postoperative silicone gel sheets and steroid injection
(Figures 13A and B).
Subcision
Subcutaneous incision, or subcision, for the treatment of
depressed scars was fi rst described in 1995. 22-gauge needle is
inserted into the superfi cial fat with the bevel up just adjacent
to the scarred area.

The needle is turned so that the bevel is perpendicular to the
skin surface, and the needle is moved back and forth in a fanning
motion to break up the fi brous tissue that is depressing the scar.
Audible rasping and popping is observed as the underside of the
dermis is released from its subcutaneous attachment.

Orentreich and Orentreich described two mechanisms
including release of tethers that bind down the scar and
reactive formation of new connective tissue.
Z-plasty
Z-plasty is a technique for scar irregularization that is parti-
cularly useful for correcting scar contractures. This technique
involves the transposition of triangular fl aps on opposite ends
of the scar. The end result is lengthening and changing the
orientation of the original scar. Z-plasties can also be used
consecutively along the entire length of a scar to allow for
redistribution of forces and camoufl age into surrounding
RSTLs. The angle of the triangular arm can be adjusted to

History and Healing
38
Figures 13A and B: Post burn keloid involving helical rim of ear
initially treated with steroid injections and later excised and primarily
closed with good resulted
B
A
Figures 12A to C: (A) Post burn hypertrophic scar on forearm and
wrist; (B) Excised with Watson’s knife till healthy dermis; (C) Thin split
skin graft applied to the defect to get a good result
A
B
C
achieve the desired amount of scar lengthening. The “classic”
Z-plasty uses a 60 degrees angle and results in 75 percent scar
lengthening (Figures 14A and B).

Depending on the angle chosen, a Z-plasty can lengthen
a contracted scar by as little as 25 percent (with a 30 degree
angle), or as much as 75 percent (with a 60 degrees angle). In
each case, the limbs of the Z-plasty are identical in length to
the central arm (scar). The direction of the new scar will be at
an angle (x + 30) from the old one. Therefore, a 30 degrees

Scars Following Wound Healing
39
Figures 14A and B: (A) Line diagramme showing z-plasty with different angles giving different gain in length.
(B) Clinical picture for the same, to realign scar according to RSTL’s
Z-plasty will rotate the scar 60 degrees, a 45 degrees Z-plasty
will rotate 75 degrees, and a 60 degrees Z-plasty will rotate 90
degrees, i.e. be perpendicular.

A long, linear scar can be broken up with multiple
Z-plasties, which can better camoufl age its appearance among
relaxing skin tension lines. Z-plasty therefore serves three
purposes as far as improving the ultimate scar is concerned 1.
it lengthens a linear contracting scar, 2. it breaks up a straight
line scar thus dispersing it, 3. it realigns the scar within the
lines of minimal tension. All these help in improving the
appearance of the fi nal scar (Figures 15A and B).
Geometric Broken Line Closure or GBLC
Geometric broken line closure or GBLC (Figure 16) is an
excellent technique of scar revision that creates an “irregularly
irregular” scar without affecting the length of the scar. The
geometry of the resultant scar is less predictable by the
casual obsever’s eye and thus frequently goes unnoticed. This
technique is particularly well suited for scars that traverse broad
fl at surfaces such as the cheek, malar, and forehead regions. The
design of a GBLC is a series of random, irregular, geometric
shapes cut from one side of a wound and interdigitated with the
mirror image of this pattern on the opposite side. The length of
the geometric shapes is between 5 and 7 mm.
Dermabrasion
Dermabrasion was the most commonly used plastic surgery
procedure for smallpox marks on the face in the early 1970’s
and 1980’s. Now it is most commonly used for post acne scars.
The principle of this procedure is the inter-island contraction
phenomenon (Converse and Rob and Smith, 1944), which
leads to dermal tightening in the normal inter-island skin
which cause smoothness and tightening of the overall skin,
thereby giving an optical illusion which makes the deep and
apparently hyperpigmented scars appear shallow and normal
color. It is done by either a mechanical dermabrader or a skin
rasp. The ablative carbon-dioxide laser resurfacing produces
the same results and is gradually replacing the mechanical
dermabrader.

Strict postoperative compliance in the form of avoiding
sun exposure are very essential in this procedure to achieve
good results, otherwise the chances of hyperpigmentation
especially in the darker skins is very high.
Tissue Expansion
Tissue expander is based on the physical properties of creep
and stress relaxation of the skin. It is used for excising large
unsightly scars especially burn scars in face, neck, chest and
abdomen. The expander is made of silicone and are available
in different shapes and sizes. The size and shape of expander to
be used depends upon the available normal skin in the adjacent
area.It is placed in the adjacent normal skin, below subcutaneous
plane and expanded with saline on a weekly or biweekly basis
through a self sealing port till the required expansion is achieved,
i.e. the expanded skin can be transposed after excising the scar
completely and achieving a primary closure without any tension
on the suture line (Figures 17A to C).
B
A

History and Healing
40
Figures 17A to C: (A) Post burn scarring in lower face and neck with
tissue expander placed. (B) Expanded neck skin pulled up to cover
defect after excising entire scar. (C) Lateral view postoperatively
B
C
A
Figures 15A and B: (A) Multiple scarp on check in different direction.
(B) Scar revision done by introducing z-plasty to realign the scar
B
A
Figure 16: Geometric broken line closure

Scars Following Wound Healing
41
SUMMARY
The end result of any wound healing is a scar. Therefore all
necessary steps need to be taken for rapid wound healing in
order to minimize scarring. Similarly steps have to be taken after
scar formation to reduce its visibility. In Indian skin because
of the higher melanin content chances of hyperpigmentation
and hypertrophy of scars is very common. Therefore the
main emphasis is on taking preventive measures to avoid
unsatisfactory scars immediately after wound healing. The
protocol for management of scars is as follows:
1. Tensionless suturing techniques during closure of wounds
and early suture removal followed by suture line support in
the form of adhesive tapes (Ethistrips/steristrips).
2. Early excision and coverage of deep dermal wounds
especially burns so as to avoid hypertrophy.
3. Following excision of hypertrophic scars or keloid,
peroperative wound edge corticosteroid injection is
imperative. If required, thereafter, monthly injections into
scar line for three to six months usually helps.
4. Postoperative care–After ten days of healing regular appli-
cation of occlusive dressing in the form of silicone gel sheet
along with pressure garments over the gel sheet is a must for
all scars for atleast 22 hours in a day, up to minimum of three
to six months. The remaining time is adjusted for twice or
thrice a day massage with coconut oil or any emmolient cream.
Massage with creams containing onion extract with heparin
and allantoin (Contractubex R) has also given good results.
5. Patient is advised to avoid sun exposure and to use sunscreen
lotions for atleast six months especially if dermabrasion or
laser resurfacing has been done in exposed areas.
6. For any scar given over a joint, splintage of the joint in a
position in which there is no tension on the scar line, is
given for three weeks. This avoids widening or stretching
of the scar.
REFERENCES
1. Berman B, Bieley HC Keloids. J Am Acad Dermatol.
1995;33:117-23.
2. Peacock EE Jr, Madden JW, Trier WC. Biologic basis for the
treatment of keloids and hypertrophic scars. South Med J.
1970;63:755-60.
3. Mancini RE, Quaife JV. Histogenesis of experimentally
produced keloids. J Invest Dermatol. 1962;38:143-81.
4. International Clinical Recommendations on Scar Management
Thomas A. Mustoe.
5. Hypertrophic Scarring and Keloids: Pathomechanisms and
Current and Emerging Treatment Strategies by Gerd G Gauglitz.
6. Review of Scar Scales and Scar Measuring Devices by Regina
Fearmonti, MD, a Jennifer Bond, PhD, a Detlev Erdmann,
MD, PhD, a and Howard Levinson, MD.
7. Ward RS. Pressure therapy for the control of hypertrophic scar
formation after burn injury. A history and review. J Burn Care
Rehabil. 1991;12:257-62.
8. Van den Kerckhove E, Stappaerts K, Fieuws S, et al. The
assessment of erythema and thickness on burn related scars
during pressure garment therapy as a preventive measure of
hypertrophic scarring. Burns. 2005;31:696-702.
9. Mustoe TA , Cooter RD , Gold MH, et al. International clinical
recommendations on scar management. Plast and Reconst
Surg. 2002;110:560-9.
10. Momeni M, Hafezi F, Rahbar H, Karimi H. Effects of silicone
gel on burn scars. Burns. 2009;35:70-4.

• Contused and Lacerated Wounds
• Bruise, Contusion and Hematoma
• Puncture Wounds
• Bite Wounds
• Traction and Avulsion Injuries
• Crush Injuries and Compartment Syndrome
• Ulcer
• Healing of Wounds
INTRODUCTION
Definition
Wound is a separation or break in continuity of skin, mucous
membrane or tissue caused by physical, chemical or biological
insult.
Classification
In order to simplify the management of wounds it is important
to categorize them into different groups so that a treatment
protocol can be formed for each section. There are various
ways of classifying the wounds. However, the simplest
classification was the one proposed by Rank and Wakefield
who divided them into tidy and untidy wounds.

Tidy wounds are inflicted by sharp instruments and contain
no devitalized tissue, e.g. surgical incisions, cuts from glass.
Fractures are uncommon and most can be closed primarily.

Untidy wounds are result from crushing, tearing, avulsion,
vascular injury or burns and contain devitalized tissue.
Fractures are common, requires wound excision with delayed
healing. However, the different types of wounds can also be
classified based on various other means like:
1. Cause

• Traumatic (sharp/blunt)

• Iatrogenic (surgical)

• Burns (thermal, electrical, chemical).
2. Length of time since formation

• Acute (< 6 weeks)

• Chronic (> 6 weeks)
3. Depth

• Superficial: Above subdermis

• Deep: Traverses subdermis.
4. Site

• Midline laparotomy, Lanz, suprapubic, thoracotomy.
5. Complexity

• Simple: Skin and subcutaneous tissue without tissue loss

• Complex: Significant tissue loss or devitalization,
communicates with deeper structures, e.g. internal
organs, joint spaces.

• Complicated: Wounds with superimposed complica­
tions, i.e. infection, hematoma, ischemia or compartment
syndrome.
6. Mode of injury

• Abrasion: Outer layer of skin is involved

• Ulceration: Defect in epithelial lining

• Incisions: By sharp objects

• Lacerations: By blunt objects

• Degloving injury: Laceration in which skin is sheard
away from underlying fascia.
7. Contamination and risk of postoperative infection

• Clean wound (class 1)

• Clean/contaminated wound (class II)

• Contaminated wound (class III)

• Dirty wound (class IV).
RS Mohil
Classification of Wounds
5
Chapter

Classification of Wounds 
Chapter 5
43
Classification Based on Presumed Amount of
Contamination at Time of Surgery (Table 1)
Clean wound (class I) include those in which no infection
is present; only skin microflora potentially contaminate the
wound and no hollow viscus is entered. Class I D wounds are
similar except that a prosthetic device (e.g. mesh or valve) is
inserted.

Clean/contaminated wounds (class II) includes those in
which hollow viscus such as the respiratory, alimentary or
genitourinary tracts with indigenous bacterial flora is opened
under controlled circumstances without significant spillage of
contents.

Contaminated wounds (class III) includes open accident
wounds encountered early after injury, those with extensive
introduction of bacteria into a normally sterile area of body
due to major break in sterile technique (e.g. gross spillage of
viscus contents such as from the intestine).

Dirty wound (class IV) includes traumatic wounds in
which a significant delay in treatment has occurred and in
which necrotic issue is present.

Appropriate postoperative management of incision includes
covering of the incision site with sterile dressing for 24-48
hours, beyond 48 hours it is unclear whether an incision must
be covered by dressing or whether showering or bathing is
detrimental to healing. Delayed primary skin closure or
incision left open to heal by secondary intention is done if it is
considered that the surgical site is heavily contaminated, e.g.
class III and class IV wounds.
Contused and Lacerated Wounds
Lacerated wounds are those in which the fibers, instead of
being divided by a cutting instrument, have been torn asunder
by some violence capable of overcoming their force of
cohesion. The edges of such wounds, instead of being straight
and regular, are jagged or unequal. The term contused is
applied to wounds occasioned by some blunt instrument or
surface which has violently struck a part of the body. Once
the cutting instrument has gone deep into dermis, there is
less resistance in the subcutaneous tissue and may extend
to a considerable depth. These wounds greatly resemble
one another, and as they require nearly the same kind of
treatment it is better to class them together. While evaluating
such a wound it is important to assess the integrity of the
underlying arteries, nerves, muscles, tendons and ligaments.
The principles of management remain the same as with any
wound, i.e. proper assessment, local care including cleaning
and repair of damaged structures with closure of wound
depending on the local conditions (Figure 1).
Bruise, Contusion and Hematoma
Closed blunt injury results in bruise or contusion. There
is bleeding in tissue with discoloration of overlying skin
without its breach. When the bleeding is sufficient it results
in hematoma. Initially, this will be liquid but will clot in
minutes to hours. After few days the hematoma will liquefy
again. Bruises require sometime to clear. Hematoma requires
Table 1: Classification of wounds based on contamination at time of surgery
Classification
Description
Infective Risk (%)
Clean (Class I)
Uninfected operative wound
No acute inflammation
Closed primarily
Respiratory, gastrointestinal, biliary, and urinary tracts not entered
No break in aseptic technique
Closed drainage used if necessary
<2
Clean-contaminated (Class II)
Elective entry into respiratory, biliary, gastrointestinal, urinary
tracts and with minimal spillage
No evidence of infection or major break in aseptic technique
Example: appendicectomy
<10
Contaminated (Class III)
Nonpurulent inflammation present
Gross spillage from gastrointestinal tract
Penetrating traumatic wounds <4 hours duration
Major break in aseptic technique
About 20
Dirty-infected (Class IV)
Purulent inflammation present
Preoperative perforation of viscera
Penetrating traumatic wounds >4 hours duration
About 40

History and Healing
Section 1
44
treatment if it is large or causing pressure symptoms (e.g.
intracranially) or if it gets infected. Blunt injuries may cause
variety of fat injuries on the face, breast or buttocks causing
lump formation. This may be important in breast where it
may masquerade as a breast lump. On face this may persist
as lumpiness for a prolonged period of time. Fat fracture
in buttock area may cause necrosis and this resolves with
an indentation of overlying skin. Bruise require no specific
treatment and no treatment has been proven to be of any value.

Most hematomas resolve without any scarring. A hematoma
may require aspiration if it is causing pressure symptoms, like
intracranially or in a cosmetically sensitive site. One has to wait
for some days for the hematoma to liquefy before it can be
aspirated by a wide bore needle (Figure 2).
Puncture Wounds
A puncture wound is  caused by an object piercing the skin
and  creating a small hole. Some punctures are just on the
surface. Others can be very deep, depending on the source and
cause. Common causes of puncture wounds are wood splinters,
pins, nails, and glass. Puncture wounds may also be caused by
objects such as scissors and knives. Almost any sharp object
can potentially cause a puncture wound. A puncture wound
from any cause becomes infected because the object that caused
the wound may carry bacteria or spores of tetanus into the skin
and tissue. There is not much to examine on the surface but the
depth may vary. Radiological test may be required to locate any
radiopaque object. This should be done with surface markers
in two planes for proper localization. Treatment is usually by
wound irrigation, antibiotics and tetanus immunization. Gross
foreign objects should be removed but too much exploration
may cause more tissue damage. Deep seated abscess may form
after 24-48 hours and will require drainage. Management of
puncture wounds in neck, thorax and abdomen will require a
more aggressive approach if there is a breach in deep fascia,
pleura or peritoneal cavity, respectively.

Needle stick injuries are a serious concern especially
in the health care workers. There is a risk of transmitting
hepatitis B, C and HIV due to improper disposal of infected
needles. Although, the risk of transmitting the disease by this
mode is low, health care workers must be immunized against
hepatitis B. In case of exposure to HIV infected needles,
immediate first aid by washing with soap and water and local
antiseptic should be done. Antiretroviral treatment based on
NACO guidelines should be started immediately; preferably
within 12 to 24 hours and continued for a minimum of 3
weeks. Serial blood testing is done for HIV virus at 3 and 6
months from the exposure date to rule out infection.
Bite Wounds
Most bite wounds are inflicted by pet dogs and cats and cause
minor injuries that do not require medical care. Some bite
wounds, however, become infected; pain at the wound site
appears 8 to 24 hours after the bite, with cellulitis and purulent
drainage. Seemingly minor bites can penetrate a tendon
sheath, joint capsule, bone, or nerve, resulting in serious
complications. The jaws of a large dog can exert more than
450 pounds of pressure per square inch, resulting in a crush
injury with lacerations, avulsions, and puncture wounds.
An estimated 15 to 20 percent of dog bite wounds become
infected. Mixed organisms, both aerobes and anaerobes, have
been cultured from dog bite wounds. The most common
aerobes are Pasteurella multocida, Staphylococcus species,
alpha-hemolytic streptococci, Eikenella corrodens, and
Capnocytophaga canimorsus. Anaerobes include Actinomyces,
Fusobacterium, Prevotella, and Porphyromonas species.
Figure 1: Lacerated wounds of face
Figure 2: Blunt injury to face resulting in a hematoma leading
to discoloration of overlying skin

Classification of Wounds 
Chapter 5
45

An infected dog bite wound manifests as cellulitis with a
gray, malodorous discharge. A typical P. multocida infection
causes an intense inflammatory reaction in less than 24
hours. Signs of infection, such as lymphangitis, fever, or
adenopathy, are present in less than 20 percent of cases. If
the tooth penetrates a joint or the periosteum, osteomyelitis
may follow. Systemic complications such as tetanus or rabies
are possibilities with these bites. Infection with C. canimorsus
may result in fulminant sepsis, disseminated intravascular
coagulation, and renal failure.

More than half of all cat bites and scratches result in
infection. Septic arthritis and osteomyelitis are seen more
often with cat bites than with dog bites. P. multocida is part
of the normal flora in 70 to 90 percent of cats and is the
pathogen found in the majority of cat bite infections. The list of
possible bacteria in cat bites is similar to that in dog bites. Cat-
scratch disease is a possible late consequence of cat bites and
scratches. The infection presents with a primary erythematous
inoculation papule 3 to 10 days following the injury. The
papule is followed by adenitis and fever. The infection, caused
by Afipia felis and Bartonella henselae, is usually self-limiting
and resolves in less than 2 months. Severe infections may be
treated with tetracycline.

Human bites: Human bites cause more serious infections
than dog and cat bites because the human oral flora contains
multiple species of aerobic and anaerobic bacteria. The most
common infectious organisms found with human bites are
Viridans streptococci, Staphylococcus aureus, Eikenella corr­
odens, Haemophilus influenzae, and beta-lactamase-producing
bacteria. Infection varies from cellulitis to osteomyelitis or
septic arthritis.

Human bites are categorized as either occlusal injuries or
clenched-fist injuries. The occlusal injury is inflicted by actual
biting. Clenched-fist injuries are sustained when the closed fist
hits a person’s teeth, often during a fight. Clenched-fist injuries
are considered more serious because the metacarpophalangeal
joint is in flexion during a punch, which allows a tooth to
penetrate the joint space. Bone, joints, or tendons are then
inoculated with organisms. When the hand is extended, the
tendons retract and the infection is carried beneath the skin
surface. The wound looks small and the injury is often ignored
until pain and infection develop.

Local care involves cleansing of the wound with soap or
a quaternary ammonium compound and water. Debridement
by removal of all eschar and foreign bodies should be done
and the wound should be copiously irrigated with saline. Soap
has antiviral properties and may provide some rabies virus
prophylaxis. Antibiotic solutions are not useful and may result
in increased tissue irritation.

Clinically infected wounds, puncture wounds, and wounds
older than 24 hours should be left open. Controversy exists
regarding whether wounds without signs of infection that
present within 8 hours of injury should be closed. Suturing
may predispose a significant minority of patients to infection.
Leaving the wound open or only approximating the edges with
adhesive strips to diminish the defect and employ a delayed
primary closure may be a better option. If well cleaned before
closure, bites of the head, neck, arms, and legs may be closed
with less risk of infection. Hand bites should be left open or
loosely approximated to allow drainage. If anaerobic bacteria
are present, the closed wound may develop serious infection
and abscess formation. Many surgeons will close face wounds
to limit scarring. The face has an excellent blood supply and
edema rarely develops. With copious irrigation and use of
prophylactic antibiotics, closures in the face usually heal well
(Figure 3).

Although antibiotics have not been shown to prevent
infections after bite wounds, they are recommended for almost
all high-risk wounds such as deep punctures, those being
repaired surgically, and bites involving the hand. Patients
with diabetes, vascular disorders, prosthetic heart valves,
splenectomy, or other immunocompromising conditions
should receive antibiotics routinely. Antibiotic should be
chosen for its ability to cover common pathogens. Prophylactic
antibiotic therapy ranges from 3 to 5 days, for cellulitis, the
treatment is continued for 10 to 14 days. Complications such
as osteomyelitis mandate longer treatment.

Patients must be closely followed and re evaluated in 24
to 48 hours after initiating antibiotic treatment. A failure to
respond should be referred for diagnostic alternatives and
surgical evaluation for debridement or drainage. An increase
in pain, edema, or cellulitis or suspicion of possible extension
into a bone or joint warrants hospital admission.
Figure 3: Dog bite leading to loss of major portion of ear in a child

History and Healing
Section 1
46
Traction and Avulsion Injuries
Avulsion injuries are open injuries in which there has been
a severe degree of tissue damage. Such injuries occur when
hands or limbs are trapped in moving machinery, such as in
rollers producing a degloving injury. Degloving injury caused
by shearing forces that separate tissue planes, rupturing there
vascular supply resulting in tissue ischemia. This occurs
most frequently between subcutaneous tissue and deep
fascia. Degloving injury can be localized or circumferential
and open or closed. It can be in just subcutaneous plane or
multiple planes involving deeper structures like muscle and
bone. Similar injuries occur due to run over road traffic
accidents, in which friction from rubber tyres will avulse skin
and subcutaneous tissue. The overlying skin can be pinched
easily and will undergo necrosis due to vascular disruption.
The skin may be removed with underlying fat and reapplied as
full thickness graft. Avulsion injuries of hand and feet require
immediate flap cover using microvascular grafts with skin and
muscle cover (Figures 4 and 5).
Crush Injuries and Compartment
Syndrome
When a part of the body is caught between two objects that
are being pushed together by a high pressure, the resulting
squeeze will leave that person with a crush injury (Figure 6).
Most often accidental, crush injuries are responsible for
broken bones, severe bruising, bleeding, lacerations and
compartment syndrome. Crush injuries are common in car
accidents, earthquakes, bomb blast, etc. In many cases of
crush injuries, compartment syndrome will take place which
is a serious condition that involves increased pressure in a
muscle compartment. Increased pressure in the area is due to
bleeding exudates and increased interstitial pressure. As the
interstitial pressure rises above capillary perfusion pressure it
leads to further ischemic injury and swelling. This will press
on the muscles, blood vessels, and nerves leading to permanent
injury to the muscle and nerves. While most common in crush
injuries to the legs, compartment syndrome can occur in any
part of the body that is crushed and trapped between two
objects for too long.

The hallmark symptom of compartment syndrome is severe
pain on passive stretching of muscle. Loss of distal pulsation
is not a feature of compartment syndrome but vessel injury.
Other features which may be noted may include decreased
sensation, paleness of skin or swollen and shiny skin.

To confirm the diagnosis, direct measurement of the pressure
in the compartment has to be done. This is done using a needle
attached to a pressure meter into the compartment. The needle is
inserted into the affected area. Specific pressure measurements
will lead to a diagnosis of compartment syndrome.
Figure 5: Avulsion injury over dorsum and plantar aspect of foot
Figure 6: Crush/friction injury thigh due to truck tyre running over it
(Tyre marks are grossly visible)
Figure 4: Severe avulsion injury over thigh and gluted region

Classification of Wounds 
Chapter 5
47

Surgery is needed to relieve the pressure by making long
longitudinal cuts through the skin and fascia. Individual
compartments must be relieved by separate incisions. When
the muscles and tissues are deprived of blood for too long
after a crush injury accident occurs, besides nerve damage
the victim will experience muscle death. Reperfusion of such
tissues by fasciotomy may lead to renal failure because of
released myoglobulins blocking the renal tubules. The wounds
can be left open (covered with a sterile dressing) and closed
during a second surgery, usually 48-72 hours later. Skin grafts
may be needed to close the wound. If a cast or bandage is
causing the problem, the dressing should be loosened or cut
down to relieve the pressure.
Ulcer
Definition: An ulcer is any breach in an epithelial surface.
Majority of skin lesions are called wounds and primarily
are divided into acute and chronic, the difference being the
time period during which they have been in existence and/
or their tendency to heal properly or not. Etiology is not
taken into account when applying the definitions of chronic
versus acute. The traditional definition of wounds and ulcers
was based primarily on etiology, where a wound (now called
an acute or surgical wound) is said to be caused by violence
(e.g. an outside force such as a bullet, a surgical incision) and
an ulcer, presently called a chronic “wound” was defined as
being caused by some kind of internal etiology (e.g. venous
hypertension with its secondary consequences to skin
integrity) (Figure 7).

Difference between wound and ulcer: However, in the
medical community virtually all skin lesions now are called
wounds (diabetic, venous, pressure, surgical, fungating carci­
noma, traumatic, etc.). Generally, the term wound is not used
in relation to the injuring mechanism anymore. Whether
the primary tissue breakdown is internal or caused by an
external force is not taken into account either, nor are other
physiological aspects. A chronic wound is defined as one that
has been in existence for more than 3 weeks or that has failed
to proceed through an orderly and timely process to produce
anatomic and functional integrity or proceed through the repair
process without establishing a sustained and functional result.

Pathogenesis: If an ulcer is defined as a gradual disturbance
of tissues by an underlying (and thus internal) etiology/
pathology and a wound (as in trauma) as an acute disturbance
of tissues by an external force, the observed differences in
appearance, demographics, anatomical locations, physiology
and pathology, as well as the required medical interventions,
possible medical options and outcomes become a great deal
more logical.

The difference in etiologies is reflected in the histological
and biochemical composition of the wound. Metalloproteinases
(MMPs) are produced by many different types of cells, and
when tissue is injured, they begin to break down several
components of the damaged extracellular matrix, which is
a necessary step prior to the influx of “rebuilding” cells and
humoral compounds. Metalloproteinases (MMPs) activity is
counterbalanced by tissue inhibitors of metalloproteinases
(TIMPs). In an ulcer (as well as during the development of a
hypertrophic scar) the balance between MMP activity (over
expressed) and TIMP activity (relatively under expressed) is
disturbed. One of the consequences of all these imbalances
in MMPs and TIMPs in an ulcer is inhibition of angiogenesis
and continuous breakdown of the extracellular matrix. Many
compounds, such as metalloproteinases (MMPs) are not active
in resting, non-damaged tissue.

The physiological difference between a wound and a
trauma is illustrated by the number of stromal cells expressing
MMP-1 and MMP-3, which is greater in chronic than in acute
lesions. In contrast, MMP-10 is not detected in the dermis
of ulcers. Tissue inhibitors of metalloproteinases (TIMP-1)
expression near the basement membrane is positive in acute,
but not in chronic, lesions.

Cytokine profiles in ulcers differ from those in trauma.
There is a major difference in the levels of epithelial growth
factor, tumor necrosis factor-α (TNF-α), transforming growth
factor-β (TGF-β) and insulin-like growth factor 1 (IGF-1),
in fluid obtained from a healing incision, compared to fluid
obtained from ulcers. There is also a significant difference in
protease levels.

The imbalance in “destroying and rebuilding” forces, as
well as the disruption in signaling pathways, confirm the
chronically inflamed status of an ulcer, which indeed is caused
by an underlying etiology/pathology.
Figure 7: Ulcers on lower leg

History and Healing
Section 1
48
Clinical Relevance
The difference in etiology and mechanism of injury also
guides the differences in treatment; wounds usually are
treated to heal by primary intention (through suturing, the use
of flaps, etc.). Ulcers, even deep ones, usually are treated with
a variety of dressings, heal by secondary intention and have a
much poorer tendency to heal unless the underlying etiology
is treated. Surgical wound bed preparation usually entails
more rigorous and aggressive excision than traditional ulcer
debridement with curette, scissors, and/or enzymes.

Ulcers can be changed into acute wounds by treating,
and sometimes removing, the underlying etiology (e.g.
compression/saphenous vein ablation in venous leg ulcers).
This in itself may lead to significant changes in wound bed
properties and healing tendencies since the chronic nature of
the ulcer is reversed. In addition, sometimes an ulcer can be
treated by extensive (surgical) debridement or excision and
primarily closure with a graft or a flap.

Conversion of a wound into an ulcer may also occur,
for example a pretibial laceration in an elderly patient with
diabetes or severe venous hypertension may turn into an
ulcer with poor healing tendencies. A Marjolin’s ulcer
(carcinomatous degeneration) of a burn scar is an example of
late term conversion.

Some skin lesions fit neither a wound (trauma) nor an ulcer
category, but their clinical behavior usually strongly favors
many or all other aspects of one of these two categories. For
example, infectious lesions such as necrotizing fasciitis are
neither caused by an underlying etiology nor the consequence
of an external force; still, clinical behavior (rapid and serious
systemic morbidity, leading to death without intervention)
and treatment approach is similar to that of a major skin
trauma. Toxic epidermal necrolysis is caused by an underlying
etiology (i.e. drug anaphylaxis) but is not chronic in nature
and treatment is quite often performed in surgically oriented
institutions, such as burn centers.

Making the etiology-based distinction between wound and
ulcer based not on how long they have been in existence but
on what has caused it may be useful and clinically relevant.
Healing of Wounds
Healing is a complex process but, in principle, all lesions go
through similar steps: hemostasis, inflammation, proliferation
and remodeling, again with similar cellular and humoral contri-
butions. Certain lesions more or less skip some of the sequential
steps by themselves: surgical, sutured incisions do not develop a
visible granulating surface. In other lesions, such as full thickness
burns, surgical intervention (excision and grafting) is used to
avoid the regular healing sequence (granulation) and to speed up
closure. The pathophysiology of wound healing has already been
discussed in detail in previous chapters.
Category 1
One of the simplest examples of wound repair is the healing
of a clean, uninfected surgical incision approximated by
surgical sutures. This is referred to as primary union, or
healing by first intention (Figure 8). The incision causes only
focal disruption of epithelial basement membrane continuity
and death of a relatively few epithelial and connective tissue
cells. As a result, epithelial regeneration predominates over
fibrosis. A small scar is formed, but there is minimal wound
contraction. The narrow incisional space first fills with fibrin-
clotted blood, which is rapidly invaded by granulation tissue
and covered by new epithelium.

Within 24 hours, neutrophils are seen at the incision margin,
migrating toward the fibrin clot. Basal cells at the cut edge of
the epidermis begin to show increased mitotic activity. Within
24 to 48 hours, epithelial cells from both edges have begun to
migrate and proliferate along the dermis, depositing basement
membrane components as they progress. The cells meet in the
midline beneath the surface scab, yielding a thin but continuous
epithelial layer. By day 3, neutrophils have been largely
replaced by macrophages, and granulation tissue progressively
invades the incision space. Collagen fibers are now evident at
the incision margins, but these are vertically oriented and do
not bridge the incision. Epithelial cell proliferation continues,
yielding a thickened epidermal covering layer.

By day 5, neovascularization reaches its peak as granulation
tissue fills the incisional space. Collagen fibrils become more
abundant and begin to bridge the incision. The epidermis
recovers its normal thickness as differentiation of surface
cells yields a mature epidermal architecture with surface
keratinization.

During the second week, there is continued collagen
accumulation and fibroblast proliferation. The leukocyte
infiltrate, edema, and increased vascularity are substantially
Figure 8: Primary suturing of a lacerated wound to achieved
healing by first intention

Classification of Wounds 
Chapter 5
49
Figure 9: Laceration over check presented after 48 hours with
edematous gaping edges—treated by delayed primary union
Figure 10: Wound over lateral aspect of foot left for secondary healing.
Granulation tissue appeared with dressing which can now be covered
with skin graft
diminished. The long process of “blanching” begins,
accomplished by increasing collagen deposition within
the incisional scar and the regression of vascular channels
architecture with surface keratinization.
Category 2
If the wound edges are not reapproximated immediately,
delayed primary wound healing transpires (Figure 9). This type
of healing may be desired in the case of contaminated wounds.
By the fourth day, phagocytosis of contaminated tissues is
well underway, and the processes of epithelization, collagen
deposition, and maturation are occurring. Foreign materials
are walled off by macrophages that may metamorphose into
epithelioid cells, which are encircled by mononuclear leukocytes,
forming granulomas. Usually, the wound is closed surgically at
this juncture, and if the “cleansing” of the wound is incomplete,
chronic inflammation can ensue, resulting in prominent scarring.
Category 3
A third type of healing is known as secondary healing or
healing by secondary intention. In this type of healing, a
full-thickness wound is allowed to close and heal. Secondary
healing results in an inflammatory response that is more
intense than with primary wound healing. In addition, a larger
quantity of granulomatous tissue is fabricated because of
the need for wound closure (Figure 10). Secondary, healing
results in pronounced contraction of wounds. Fibroblastic
differentiation into myofibroblasts, which resemble contractile
smooth muscle, is believed to contribute to wound contraction.
These myofibroblasts are maximally present in the wound
from the 10th to 21st days. This is followed by accumulation
of extracellular matrix (ECM) and formation of a large scar.
Category 4
Epithelization is the process by which epithelial cells migrate
and replicate via mitosis and traverse the wound. This
occurs as part of the phases of wound healing, which are
discussed in sequence of events in wound healing. In wounds
that are partial thickness, involving only the epidermis and
superficial dermis, epithelization is the predominant method
by which healing occurs. Wound contracture is not a common
component of this process if only the epidermis or epidermis
and superficial dermis are involved.
Bibliography
1. Adrian Barbul. Wound healing. In: Brunicardi FC, Dana
KA, Timothy RB, David LD, John GH, Raphael EP (Eds).
Schwartz’s Principles of Surgery. 8th edn. New York: Mc Graw
Hill; 2005. pp. 223-48.
2. David J Coleman. Wounds, tissue repair and scars. In: Russell
RCG, Norman SW, Christopher JK B (Eds). Bailey and Love’s
Short practice of Surgery. 24th edn. London: Arnold; 2004.
pp. 84-94.
3. Michael G Franz. Wound Healing. In: Gerad M Doherty (Ed).
Current diagnosis and treatment surgery, 13th edn. New Delhi:
Tata McGraw Hill; 2010. pp. 47-58.
4. Tissue Repair: Regeneration, Healing, and Fibrosis. In: Kumar,
Abbas, Fausto, Mitchell (Eds). Robins basic pathology. 8 edn.
New York, Elsevier- Saunders; 2007. pp. 59-79.

General Principles
for Wound
Management
2
Section

(Trang không có chữ)

• Definition
• Origin
• Importance
• Principles

– Tissue

– Infection/Inflammation

– Moisture

– Edge of Wound

– Preparing the Wound Bed
DEFINITION
Wound bed preparation (WBP) can be defined as the process
of removing local barriers which may facilitate healing and
provide a more efficient means of wound management.

Wound bed preparation is an essential process to obtain
maximum benefits from today’s advanced wound care products.
Preparing the wound bed can be achieved by the removal of
barriers. Removing these barriers may accelerate healing or
facilitate the effectiveness of other therapeutic measures.1
ORIGIN
Dr Vincent Falanga and Dr Gary Sibbald initially developed
concept of WBP in the United States and Canada from their
extensive experience in the treatment of chronic wounds.

It has subsequently gained momentum with key opinion
leaders who have discussed and expanded the concept at
international conferences and symposia around the world.1
IMPORTANCE
Wound bed preparation identifies the major components for
chronic wound care and organizes these components to create
a purposeful approach to wound care interventions, utilizing
current medical standards and practices.

It also has the potential to ensure that maximum benefits
are derived from advanced wound care products to overcome
the barriers to wound improvement.

The major barriers that must be overcome to achieve
optimal wound closure in chronic wounds are necrotic burden,
bacterial imbalance, excessive levels of exudate, biochemical
and cellular dysfunction.1
PRINCIPLES
The principles of wound bed preparation can be summarized
by the acronym - ‘TIME’. TIME stands for:
T - Tissue (Non-viable or Deficient)
I
- Infection or Inflammation
M - Moisture Imbalance
E - Edge of Wound (Non-advancing or Undermined).

The ‘TIME’ principles provide a systematic approach to
the management of wounds.

‘TIME’ is based on intervention in four clinical areas and
leads to an optimal well vascularised wound bed that facilitates
the effectiveness of other therapeutic measures.1
T - Tissue (Non-viable or Deficient)
Management of Necrosis
The most obvious marker of a chronic wound is the presence
of necrotic tissue, which can be both a focus for bacteria and a
barrier to healing. Debridement occurs naturally within wounds
and studies indicate that if this process is accelerated then
RK Chittoria
Wound Bed Preparation
(Guidelines of International Advisory
Board for WBP)
6
Chapter

General Principles for Wound Management
Section 2
54
healing will be more rapid. Various methods for debridement
are:
• Surgical
• Sharp
• Larval
• Enzymatic
• Autolytic
• Mechanical
• Chemical.

Sharp and surgical debridement rapidly remove necrotic
tissue and reduce the bacterial burden, but also carry the greatest
risk of damage to viable tissue and require high levels of
technical skill. Enzymatic, chemical, mechanical and autolytic
debridement is frequently regarded as safer options, although the
risk to the patient of ongoing wound complications is greater.2
I - Infection or Inflammation
Restoration of Bacterial Balance
Assessment of the impact of bacterial load on a wound is often
difficult. All chronic wounds harbor bacteria. However, whilst
some wounds are contaminated, others are colonized and
some are infected. What defines the level of bacterial burden
is the presence of replicating microorganisms within a wound,
the bacterial load, the virulence of the microorganism and the
host reaction. This can be expressed as:

Infection = dose × virulence
host resistance

Experimental evidence suggests that a bacterial load of
between 105 and 106 organisms per gram in a wound bed,
irrespective of the organism, will adversely affect wound healing.
For some more virulent organisms, however, a lower level may
cause infection. Bacterial colonization is three dimensional and
infection can, and often does, extend into the deep compartment
of the wound; surface swabs may not therefore give a true
reflection of the bacterial burden and may need to be augmented
by tissue culture. Therapy should reflect the clinical status of
the wound and not be based on culture results alone. Over time,
the bacterial status of the wound will vary and it is important
to recognize the changes that indicate wound deterioration and
respond to them quickly. These may include increasing exudate,
pain, odor, bleeding or tissue fragility.2 Table 1 highlights the
methods of restoring bacterial balance.
M - Moisture
Management of Exudate
Chronic wound fluid differs from that of acute wounds and
excess exudate has an adverse effect on wound healing. Even
in the presence of clean healthy-looking granulation tissue,
technologically advanced healing enhancements such as
growth factors and bioengineered skin will perform badly
if exudate is not controlled. Exudate from chronic wounds
has been shown to slow down or block the proliferation of
key cells in the wound healing process such as keratinocyte,
fibroblasts and endothelial cells. This action interferes with
growth factor availability and inactivates essential matrix
material. Exudate results in a loss of protein to the host, can
damage the surrounding healthy skin, and is also an excellent
culture medium for bacterial growth. The presence of edema
often increases the volume of exudate produced by chronic
wounds. Exudate management consists of two related phases
of direct and indirect management:
1. Direct

– Use of absorbent dressings

– Use of compression and/or elevation to eliminate fluid
from the wound site.

– Use of topical negative pressure (TNP) with devices
such as the VAC—vacuum assisted closure.
2. Indirect

– Control of infection or bacterial load

– Control of edema by systemic therapy such as the
treatment of heart failure

– Use of immunosuppressant or steroids to control
inflammatory exudate from wounds such as pyoderma
gangrenousum, vasculitic or rheumatoid ulcers.2
E - Edge of Wound (Non-advancing or
Undermined)
Correction of Cellular Dysfunction and Restora-
tion of Biochemical Balance Within a Wound
Normal wound healing in an acute wound is highly coordinated
with rapid choreographed changes in specific cell populations
occurring as the wound progresses from injury through repair
and remodeling to healing. This process is impaired in chronic
Table 1: Restoration of bacterial balance
• Recognize importance of bacterial load: Contamination,
colonization, infection
• Monitor the impact of bacteria on healing: Pain, exudate,
bleeding, odor, systemic effects
• Treat the wound appropriately

– Wound debridement

– Antimicrobial dressings: containing povidone iodine/
iodine (e.g. inadine, iodosorb/Iodoflex) or silver (e.g.
acticoat, actisorb silver, flamazine)

– Increase frequency of dressing changes

– Systemic antibiotics

– Anti-inflammatories
• Address host systemic factors

Wound Bed Preparation 
Chapter 6
55
diabetic ulcers. There is evidence that cells within chronic
ulcers become senescent (old, unresponsive and unable to
divide) and are unresponsive to certain messengers such
as cytokines and growth factors, which cause phenotypic
dysregulation. The prolonged inflammatory response seen in
chronic ulcers delays wound closure. In addition, the extended
exposure of the cellular matrix to chronic wound fluid may
affect cellular activity in a wound bed and result in cellular
senescence. Failure of wound edge migration, which is believed
to be linked to an inhibition of normal programmed cellular
death (apoptosis) within fibroblasts and keratinocyte, has been
suggested by Falanga to be related to healing times. These
and other abnormalities in fibroblasts have been demonstrated
by others in a variety of chronic wound types and have been
linked to senescence within the wound fibroblast population.
This may explain why the use of topical growth factors may
not always be effective and indicates that the use of single
topical agents without correction of the underlying cellular
dysfunction is unlikely to be the answer to the management
of chronic wounds. The superficial appearance of a wound
can be misleading. In the same way, all that glitters is not
gold, all that is red is not healthy. Biopsy of such wounds
frequently shows expression of excessive protein molecules
derived from the circulation such as fibrin and fibrinogen.
It has been hypothesized by Falanga that these and other
macromolecules may bind growth factors and other wound
messengers, so, freezing the wound in a debrided, but non-
healing, red state. This emphasizes the importance of, and
distinction between, debridement, which simply refers to
the removal of necrotic tissue from the wound bed, and total
wound management as envisaged in the principles of WBP,
which aims to address the four key areas defined in acronym
‘TIME’ (Table 2).3
Table 2: TIME – The principles of wound bed preparation
Clinical
observations
Proposed
pathophysioloy
WBP clinical
actions
Effect of WBP
actions
Clinical outcome
T
Tissue
(Non-viable or
deficient)
Defective matrix and cell
debris impairment
- Debridement (episodic
or continuous) can
be autolytic, sharp,
surgical, enzymatic,
mechanical or
biological
- Biological agents
Restoration of wound
base and functional
extra-cellular matrix
proteins
Viable wound base
I
(Infection or
inflammation)
High bacterial counts or
prolonged inflammation
- ↑Inflammatory cytokines
- ↑Protease activity
- ↓Growth factor activity
- Remove infected foci
- Topical/Systemic
antimicrobials
- Anti-inflammatories
- Protease inhibition
Low bacterial counts or
prolonged inflammation
- ↓ Inflammatory
cytokines
- ↓ Protease activity
- ↑ Growth factor activity
Bacterial balance
and reduced
inflammation
M
(Moisture
imbalance)
- Desiccation slows
epithelial cell migration
- Excessive fluid causes
maceration of wound
margin
- Apply moisture
balancing dressings
- Compression
- Negative pressure
or other methods of
removing fluid
- Restored epithelial cell
migration
- Desiccation avoided
- Edema, excessive fluid
controlled
- Maceration avoided
Moisture balance
E
Edge of wound
(Non-advancing
or undermined)
- Non-migrating
keratinocytes
- Non-responsive wound
cells
- Abnormalities in
extra-cellular matrix
or abnormal protease
activity
- Re-assess cause or
consider corrective
therapies
- Debridement
- Skin grafts
- Biological agents
- Adjunctive therapies
- Migrating keratinocytes
- Responsive wound
cells
- Restoration of
appropriate protease
profile
Advancing edge of
wound

General Principles for Wound Management
Section 2
56
Table 3: Preparing the wound bed
Treat the cause
1. Assess the patient for healing ability. Adequate blood supply must be present and host factors (coexisting
diseases, drugs) must all be considered.
2. Correct treatable cause of tissue damage.
Patient centered
concerns
1. Make the patient part of the decision making process. Pain and quality of life should be documented and
should form part of the treatment plan.
2. Provide education and support for patient centered care to increase coherence with a treatment process.
Local wound care
1. Assess and monitor the wound history and physical characteristics (location, size, base, exudate,
surrounding skin, staging and pain).
Debridement
1. Debride healable wounds, remove necrotic and non-viable tissue (surgical, autolytic, enzymatic and
mechanical). Non-healable wounds should have only non-viable tissue removed and active debridement
to bleeding tissue is contraindicated.
Persistent
inflammation and
bacterial balance
1. Assess the wound for bacterial balance, infection or persistent inflammation.
2. Use only non-sensitizing topical antibacterial agents for local symptoms and signs of increased bacterial
burden.
3. Use systemic antibiotics if symptoms or signs of infection extend beyond the wound margin or the ulcer
probes to bone.
4. For persistent inflammation, topical and systemic anti-inflammatories should be considered based on
superficial, local or systemic disease process.
Moisture balance
1. Cleanse wounds with normal saline and water. The use of topical antiseptics should be reserved for
wounds that are non-healable or those in which the local bacterial burden is of greater concern than the
stimulation of healing.
2. Select appropriate dressings for local moisture balance to stimulate granulation tissue and re-
epithelialization.
Edge effect
1. Evaluate expected rate of wound healing to determine if treatment is optimal. If sub-optimal healing is
noted, re-assess the cause and patient centered concerns.
2. Use active wound therapies (biological agents, skin grafts, adjunctive therapies) when other factors have
been corrected and if healing still does not progress.
Overall
1. For improved outcomes, education and evidence base must be tied to interdisciplinary teams with the
cooperation of health care systems.
Preparing the Wound Bed (Table 3)4
Preparing the wound bed includes treatment of underlying
cause, patient centered concerns, local wound care, debridement,
correction of persistent inflammation, bacterial balance, moisture
balance and treatment of wound edge (Table 3). These will be
discussed in detail in subsequent chapters.
SUMMARY
Wound bed preparation (WBP) provides a structured and
systematic approach to the management of nonhealing ulcers like
that of diabetic foot. The removal of barriers through the principles
of ‘TIME’ should facilitate endogenous healing. Debridement,
reduction of bioburden and exudate management is collectively
referred to as wound bed preparation (WBP). It is these processes
that prepare the wound bed to support the activities necessary
for wound healing. All practitioners who are, or will, become
involved in both assessing patients for, and initiating techniques
relevant to wound bed preparation (WBP), should understand
the need to remove these barriers.5,6
CONCLUSION
Wound bed preparation is a continuous process that requires
skill and an understanding of the patient, the underlying cause
of the wound and the wound environment. The method or
methods used for WBP will depend upon the patient, the type
of wound and the healthcare setting in which treatment is
undertaken (Flow chart 1). The prolonged inflammation and
cellular senescence seen in chronic wounds may also adversely
affect the efficacy of new, high technology products such as
hyaluronic acid, growth factors, protease modulators and
bioengineered skin products. It is suggested that appropriate
WBP is necessary to improve the clinical effectiveness of
these new, and frequently costly, technologies.

Wound Bed Preparation 
Chapter 6
57
Flow chart 1: Algorithm of wound bed preparation

General Principles for Wound Management
Section 2
58
REFERENCES
1. Falanga V. Classifications for wound bed preparation and
stimulation of chronic wounds. Wound Repair Regen.
2000;8(5):347-52.
2. Falanga V. Introducing the concept of wound bed preparation.
Int Forum Wound Care. 2001;16(1):1-4.
3. Dow G, Browne A, Sibbald RG. Infection in chronic wounds:
controversies in diagnosis and treatment. Ostomy Wound
Manage. 1999;45(8):23-7,29-40; quiz 41-2.
4. Sibbald RG, Williamson D, Orsted HL, Campbell K, Keast D,
Krasner D, Sibbald D. Preparing the wound bed - debridement,
bacterial balance, and moisture balance. Ostomy Wound
Manage. 2000;46(11):14-35.
5. Sibbald RG. What is the bacterial burden of the wound bed
and does it matter? In: Cherry GW, Harding KG, Ryan TJ, ed.
Wound Bed Preparation. London: Royal Society of Medicine
Press Ltd. 2001.pp.41-50.
6. Davey ME, O’Toole GA. Microbial biofilms: from ecology to
molecular genetics. Microbiol Mol Biol Rev. 2000;64(4):847-67.

• Definition
• Classification
• Etiopathogenesis
• Clinical Features
• Management

– Medical

– Surgery

– Assessment and Exploration

– Debridement

– Wound Closure

– Dressing and Skin Substitute

– Monitoring
Restoration of function and physical integrity with the
minimum deformity and without infection.
—Westaby, 1985
Introduction
Acute life-threatening wounds presents a spectrum of issues
that not only prevent their ultimate closure but also pose an
immediate threat to the life. The issues include type, etiology,
anatomic location and surgical techniques to deal with such
wounds. Advice on clinical practice and treatment options
cannot be prescriptive because of the wide range of injury
patterns and settings, but an understanding of the general
principles can guide clinical management. Recent advances in
dressing, debridement techniques and surgical repertoire allow
the modern surgeon to address any wound of any complexity.
Definition
Life-threatening wounds are those wounds that pose both
immediate as well as delayed risk to life. These include:
1. Faciomaxillary wounds (Figure 1)
2. Open chest wounds
3. Severe crush wounds of extremities (Figure 2)
4. Open abdominal wounds (Figure 3).

The immediate risk is due to underlying organ damage or
severe exsanguinations and delayed death is due to infection
and sepsis. These also cause lot of morbidity in terms of
prolonged hospital stay, wound infection, loss of limb,
cosmetic disfigurement and loss of function.
Classification
There are different ways of classifying traumatic wounds. They
can be classified based on anatomical location, surface area of
involvement or into simple or complex wounds depending on
their location, size, involved anatomical structures and bio-
burden.1

Based on integrity of the integument traumatic wounds can
be broadly classified into:
a. Closed wound (Figure 4)
b. Open wound. (Figures 1 to 3)
Closed Wound
The result of blunt forces that do not break the integrity of
skin. These include contusion and hematomas. These are
characterized by injury to blood vessels contained within
the dermis and causes localized swelling and pain. There
can be significant blood loss and limb threat due to injury to
underlying vessels and supportive structures.
Open Wound
There is a break in the integrity of the skin. Patient is at risk for
external bleeding and contamination with the bacteria, which
Sushma Sagar, Krishna Asuri, Maneesh Singhal
Initial Management of Life-­
threatening Wounds
7
Chapter

General Principles for Wound Management
Section 2
60
Figure 1: Faciomaxillary wound
Figure 2: Crushed extremity wound
Figure 3: Open abdominal wounds
Figure 4: Closed torso wound

Initial Management of Life-threatening Wounds 
Chapter 7
61
may lead to infection. Open wound may be the first indicator
of a deeper, more serious injury, such as fracture or ruptured
or lacerated organ. These wounds can be further classified as
follows:
Incised wounds
Made by a clean cut of a sharp
instrument, such as a sharp knife.
Lacerated
wounds
Made by an object that tears tissues,
producing jagged, irregular edges, such
as glass, jagged wire, or a blunt knife.
Puncture wounds
Made by a pointed instrument, such as
an ice pick, bullet, or nail (Figure 5).
Avulsion wounds
Made by strong shearing forces and
friction that can result in significant
tearing and destruction of tissues, e.g.
degloving injury (Figure 6).
Burn wounds
Caused by thermal, chemical, or
electrical injury to the skin (Figure 7).
Amputations
Involved the cutting away from the body
of a limb or protruding structure
(Figure 8).
Etiopathogenesis
The mechanisms of acute wounds include penetrating or blunt
trauma, various environmental exposures such as chemical
substances and extremes of temperature. Traumatic wounds
can be subdivided into blunt or penetrating trauma.
Blunt Trauma
This type of trauma can result in a large area of destruction, the
extent of which is not always obvious. Crush, degloving and
avulsion injuries fall into a similar category. It is difficult to
determine the extent of tissue viability on initial examination.
In these situations the mechanism of injury translates into a
larger anatomic zone based on direct tissue destruction and
microvascular injury. These types of injuries require thorough
exploration and subsequent vigilance to identify the zones of
injury. The ‘‘zones of injury’’ is divided into three areas: the
zone of necrosis, the zone of stasis and zone of hyperemia.
Penetrating Trauma
Results in destruction of soft tissues with variable amount
of underlying tendon, nerve, bone or vascular disruption and
inflicted either by sharp objects or missile injuries. Damage is
caused by several mechanisms such as laceration and crush,
shock waves and cavitation.

Numbers of injuries (such as amputations) involve more
than one mechanism of injury.
Figure 5: Puncture wound on neck
Figure 6: Avulsion wound of finger
Clinical features
Traumatic wounds can present as isolated or in combination
with other organ injuries. They can present as simple cuts
or abrasion or as limb/life-threatening extensive degloving or
amputation. The severity of the wound is determined by the area
of involvement and injury of underlying structures including
nerve, vessels, bone and other organs. Life-threatening wounds
in the maxillofacial region can present with acute airway threat,
in the thoracic region they can present as open pneumothorax, in

General Principles for Wound Management
Section 2
62
wounds frequently act as ‘‘distracters’’ making one pay more
attention to the “Gross” appearing wound rather than immediate
life-threatening problem. The initial assessment includes:
A—Airway maintenance with cervical spine protection
B—Breathing and ventilation
C—Circulation with hemorrhage control
D—Disability: neurological status
E—Exposure/Environmental control: completely undress the
patient but prevent hypothermia.

Some of the life-threatening wound such as excessively
bleeding wounds may require immediate compression
dressing as part of “C” stabilization.

Once the patient has been stabilized and his hemodynamic
status is well under control then a secondary survey including
a head to toe examination with detailed evaluation of all the
external as well as internal injuries can be undertaken. A detailed
evaluation, both clinical and radiological, should be undertaken
to exclude associated bony, tendon, nerve and vascular injury.
Presence of these injuries may alter the course of treatment.

The “golden” period for treatment of traumatic wounds has
been defined at six hours which is based on the laboratory and
clinical studies on the doubling time of bacterial colonization
progressing to an invasive infection and from clinical outcomes
describing the decreased risk for infection after debridement
within that window of time. Though the golden period serves
as a guideline to acute wound treatment but practical realities
(e.g. operating room time, delayed presentation) may impede
this principle.
Surgery
The surgical management of traumatic wounds can be discussed
under the following headings:
• Assessment and exploration
• Wound debridement
Figure 7: Electric burn
Figure 8: Amputation of foot
the abdomen as evisceration and in the limb as vascular injury,
mangled limb or amputation. The wounds can involve all the
variables in the initial assessment of the trauma victim.
A—Airway – Severe maxillofacial trauma
B—Breathing – Due to underlying lung injury or pneumothorax
C—Circulation – Due to associated blood loss both external
and internal
D—Disability – Due to the possible associated underlying
traumatic brain injury
E—Exposure and environment – Due to involvement of the
extremities.
Evaluation
The initial evaluation of all trauma patients should follow
the universal language of ATLS irrespective of the nature
of injury and assessment should always be done in line
of ABCDE. Patient should have a chest X-ray and X-ray
pelvis along with a FAST (Focused assessment sonography
in trauma) scan done as part of the primary survey protocol.
Once the patient has been stabilized he can be subjected to
special investigation for further evaluation of the wound,
underlying and associated injury. These investigations can
include a NCCT (Noncontrast computed tomography) face,
CECT (Contrast enhanced computed tomography) chest
and abdomen, CT-angiography and peripheral limb X-rays.
However, most of the local injuries like tendon and nerve can
be evaluated only on exploration of the wound.
Management
Medical
The management of life-threatening wound should always begin
with primary survey and simultaneous resuscitation. Large open

Initial Management of Life-threatening Wounds 
Chapter 7
63
• Wound closure
• Dressings
• Monitoring for complications.
Assessment and Exploration
When acute wounds involves underlying structure, is too large
to close primarily and requires special instrumentation, proper
exploration with a full delineation of the anatomy and extent
of injury is required in the operating room. The exploration
includes defining the extent of injury (zone of injury), the
identification of key anatomic structures and defining the
extent of infection or necrosis.

At the skin and subcutaneous level, the edges need to be
examined for vascularity and the amount of undermining/
internal degloving determined. Non-viable skin appears
dusky without capillary refill and does not bleed with
excision. Subcutaneous fat should appear yellow and
globular. Necrotic fat is dull in appearance and is gray/brown
to black in color. Adjuncts to assessment include fluorescein
dye, dermofluorometry, surface temperature readings,
photoplethysmography, ultrasound Doppler flow meters, laser
Doppler, and transcutaneous PO2 monitors fluorescein has
proven to be a consistent and reliable method to determine
skin viability. Obtaining clear exposure of the underlying
anatomy should be of prime importance. The incisions should
be designed so as to provide adequate exposure, maintain skin
vascularity and creation of simple flaps for closure.

Muscles should be explored and tested for viability.
Compartment syndrome should be recognized and adequate
aggressive fasciotomy to be done. Loss of contractility
on stimulation, change of color to dark red or absence
of bleeding is a sign of myonecrosis. Tendon should be
identified and repaired either immediately or tagged for
future repair. Any underlying vascular injury should be
identified and either coagulated or repaired immediately if
responsible for the vascularity of the limb. Nerve should
also be identified and tagged for primary repair or for
future grafting. Bone should also be assessed for viability
and presence of fracture.
Debridement
“Debridement is the most fundamental principle in surgical
wound bed preparation before closure” – plastic surgery dictum.

Operative wound debridement should be systematic and
thorough. It involves removal of all devitilized, infected and
necrotic tissue from the wound. Multiple wound debridements
may be necessary to achieve wound stability depending on the
necrotic and infectious burden.

There are different ways and techniques for wound
debridement:
1. Sharp debridement
2. Irrigating systems
3. Debridement by hydroscision
4. Debridement by sequential dressings.

Sharp debridement: Remains standard of surgical debride­
ment. It is usually accomplished using scalpel/scissors or
cutting cautery till viable tissue is reached.

Irrigating systems: Often used in wounds with large
bacterial load. They provide a way to nonsurgically remove
debris and lessen bacterial load. This irrigation can be
accomplished under pressure using high pressure systems
like PULSER VAC. They usually serve as adjuncts to sharp
debridement.2

Debridement by hydroscision: Hydroscision (Versajet,
Largo, Florida) has entered the foray of tools in surgical
debridement. By simultaneously cutting and removing tissue
with water through high pressure opening, it acts as a good
debridement tool. It is very useful in concavities and tight
spaces.3
Wound Closure
The reconstructive ladder is a useful way to plan the closure of
any wound. It is a logical sequence to regain form and function
as the anatomy of the defect dictates. One should however
remember that this ladder is just a guideline and one can move
up or down the ladder as per the requirement of the wound.
1. Primary closure
2. Delayed primary closure
3. Closure by secondary intention
4. Skin grafting
5. Local flaps
6. Distant flaps
7. Free tissue transfer
8. Innovative techniques (VAC) (Figure 9).

Primary closure: Most often used for simple laceration in
which the wound is closed in layers. Tension, potential infection
and indeterminate zone of injury preclude primary closure.
Advantages include simplicity and best healing potential.
Disadvantage includes potential wound infection. Primary
closure can be accomplished by clips, staples, skin tapes.

Delayed primary closure: This is usually done for
minimally contaminated wounds. After initial cleaning and
debridement of the wound it is left open and then closed
primarily after four to five days.

Closure by secondary intention: It is the most straightforward
approach to allow the wound to close spontaneously after an
adequate debridement, allowing the wound to form granulation

General Principles for Wound Management
Section 2
64
tissue and heal from inside out. However, it is associated with
a prolonged healing time, dressing changes and a suboptimal
scar.

Application of plastic surgery principles to trauma have
revolutionized the management of acute traumatic wounds.

Skin grafting4: If the defect cannot be closed primarily
then the next step is placement of a skin graft. Skin graft is a
sheet of epidermis and varying amounts of dermis, harvested
from a donor site, and transplanted to another area of the
body. Homografting and heterografting of skin has extreme
importance in providing temporary skin cover, especially in
extensive and deep burns and trauma. Skin grafts can be split
thickness (SSG) or full thickness (FTG) depending on the
amount of dermis included in the graft.

Split skin grafts (Thiersch grafts) can be thin, intermediate
or thick depending on the amount of dermis (Figure 10). It is
mandatory for skin grafts to be placed on a vascularized bed.
A surface which granulates rapidly will easily take a graft,
and on the contrary, surfaces such as bare bone, cartilage
and tendon (devoid of periosteum, perichondrium and para-
tenon, respectively) will not accept a skin graft. A skin graft
“takes” poorly on an irradiated bed, on adipose tissue, on
long-standing ischemic granulations and over extremities of
diabetic patients with atherosclerotic changes. Besides a good
bed, the skin graft should be properly immobilized to avoid
shearing, and there should be no obvious infection (bacterial
count to be < 105 per gram of tissue) or hematoma under it.
The graft can either be applied immediately or can be stored
and applied in a delayed manner depending on the general
status and associated injuries of the patient. The methods for
storing a skin graft are:
1. Refrigeration: At a constant temperature of 4°C, skin grafts
wrapped in a saline gauze may be stored for two to three
weeks.
2. Freezing: Skin grafts can be stored up to six months at
–80°C. Grafts stored in this manner have to be cryo-
preserved in 15 percent glycerol to prevent crystallization
of water in the cells. Grafts remain viable during this period.
3. Freeze drying: Grafts can be freeze dried in vacuum and
then stored at room temperature for very long periods.
Lyophilized grafts like these are non-viable, but they serve
as valuable adjuncts in providing temporary skin cover.

Skin flaps5-7: Plastic surgeons have added a new dimension
to anatomy by focussing on minute blood vessels that supply
the skin. Hitherto insignificant, the blood supply to a muscle
and the overlying skin territory or the underlying bone
segment that it can support has assumed importance.

There are two main patterns of blood supply to the skin:
1. A major blood vessel lying deep to the muscle gives off
perforator-musculocutaneous branches which reach the
dermal-subdermal plexus of skin. This is by far the most
common pattern. Skin flaps raised on this system are random
Figure 9: VAC dressing
Figure 10: Skin graft

Initial Management of Life-threatening Wounds 
Chapter 7
65
pattern flaps8 and critical to their survival is preservation
of dermal-subdermal plexus of blood vessels. This can be
ensured by raising the skin flap with a reasonable amount of
subcutaneous fat. The maximum surviving length of such
a flap is dependent on the vascular perfusion pressure. A
rough guide to safe flap dimensions is to have 1:1 ratio of
length to breadth. These dimensions may only be exceeded
in head and neck region or after prior delay procedures.
2. The other pattern has a large blood vessel giving off a direct
cutaneous artery which lies superficial to the muscle and
has branches which reach the dermal-subdermal plexus.
Skin flaps based on this system are axial pattern flaps
and they must include the full thickness of subcutaneous
tissue. The vascular territory of the axial vessel determines
the length of the flap. A random pattern paddle of skin can
be added at the distal end for additional length. Venous
drainage of such flaps is via dermal venous plexus and the
paired venae comitantes. There are only limited axial flap
territories on the body and they include the forehead flap,
deltopectoral flap, groin flap, hypogastric flap, etc.

Local flaps: Local flaps can be classified on the basis of
movement.

Advancement flaps: These are flaps of choice for small
defects. Simple advancement flap requires excision of skin
triangles (Burrow’s triangles) at the base of the flap. A V-Y
advancement of skin is also carried out in some situations.

Rotation and transposition flaps: These flaps pivot
around a point to move into a defect. The defect is generally
triangulated. The donor defect can be closed primarily or split
skin grafted. Previously, it was thought that these flaps are
different entities to close a triangulated defect, but it has been
shown that both the flaps are just ends of the spectrum of a
single flap template.
Distant Flaps
Direct: A pedicled flap is placed directly on the defect in the
first stage and detached after three to four weeks, e.g. cross
finger flap, groin flap, deltopectoral flap.

Indirect: This is a multistaged procedure, e.g. tube flap,
jump flap. Rarely, if ever, employed these days. If skin from
abdomen had to reach the leg, it would be first tubed on the
abdomen, then placed on wrist and finally made to reach the
defect with base on the wrist. Reconstruction would take
several months.

Free flaps: Axial flaps, myocutaneous flaps, fasciocutane-
ous flaps, perforator flaps, omentum, jejunum, bone, etc. can
be transferred to recipient site by microvascular techniques
after completely detaching from the donor area. Reconstruc-
tion can be accomplished in a single stage.

Innovative techniques (VAC): Vacuum assisted closure
(VAC) is a recent innovative technique for wound closure.
It has the potential advantage of containment of effulent and
protection of perifistulous tissue, increased granulation and
wound contraction compared to saline-soaked gauze and
accelerated wound healing (Figure 9).9,10
Dressing and Skin Substitutes
Biologic dressings and synthetic skin substitutes can provide
temporary cover to an open wound. These materials have
come to play a vital role in the management of patients with
extensive burns and as well as traumatic wounds where donor
sites are limited. Biological substitutes like homografts,
heterografts and amnion have been in use for over a century
and several synthetic skin substitutes have now been modelled
after these biological materials. Although, split skin grafting
is a relatively simple, reliable, practical and immensely
successful procedure, there are several advantages of using a
skin substitute, even if purely on a temporary basis.11
Advantages of Skin Substitutes
It temporarily covers extensive raw areas, thereby converting
open wounds to closed ones.
• It temporarily obviates the need to harvest graft in a patient
who may not be fit to undergo surgery.
• It protects tendons, nerves, and vessels from dessication.
• It prevents exudative protein and red cell loss from the wound.
• By providing physical cover it prevents evaporative loss of
water, and, therefore, conserves heat.
• It prevents bacterial proliferation.
• By covering exposed nerve endings it decreases wound
pain, and therefore, permits joint movement.
• It prepares the wound for autologous skin grafting.
Ideal Skin Substitute
Skin is a very intricate organ with great anatomic and
functional diversity, and therefore, it is not surprising that
till today no skin substitute has been developed that closely
matches natural skin. The following properties are desirable
in a skin substitute:
• It should adhere well to the wound surface.
• It should be easy to apply and remove without causing pain.
• It should conform well to the wound irregularities.
• It should be impermeable to microorganisms.
• It should be elastic enough to stretch during joint movement
without losing adherence.
• It should be non-toxic and non-antigenic.
• It should be inexpensive, easy to procure and store.

Homografts12-14: These are biological dressings of first
choice and a gold standard against which other skin substitutes
are evaluated. Homografts can be harvested from live donors

General Principles for Wound Management
Section 2
66
and used fresh or they can be taken from cadavers and used
following a period of refrigeration. Cadavers from whom
homografts are taken should be free from skin infections,
malignancy, hepatitis virus and HIV virus. Skin banks allow
the availability of homografts off the shelf. A homograft
“takes” exactly like an autograft. It survives for three to ten
weeks before getting rejected by the body’s immune response.
Subsequent crops of homografts survive for even shorter
period because of “priming” of the immune system.

Heterograft: The earlier widespread acceptability of
heterografts was primarily due to the limitations in the
availability of homografts. Porcine graft is considered to have
a close resemblence to human skin. They adhere poorly to the
wound bed. These grafts do not ‘take’ in the classical sense, as
vessel to vessel union between the graft and the bed does not
occur. The grafts get lost by progressive degenerative necrosis
before rejection occurs. They are available frozen-irradiated
or freeze dried. Freeze dried grafts are less antigenic.

Amnion: Amnion is another biological dressing which
is readily available and quite inexpensive. It exerts an
angiogenic effect which increases the capillary density of
the wound bed. Its adherence to the surface is poor. Amnion
dessicates and spontaneously separates from the wound bed,
therefore, it needs to be covered by an occlusive dressing.
Amnion can be stored for two to three days in sterile bottles
containing 0.25 percent sodium hypochlorite solution. Either
the amniotic side or the chorionic side can be applied, and the
dressings are changed every 72 hours.

Collagen: It is available as sheets, strips, powder and
sponge. It can be bonded to other materials to form bilaminate
or trilaminate structure. Though it has low antigenicity,
collagen is rapidly degraded on the wound surface, and
therefore, the dressing are changed every 72 hours.

Synthetic skin substitutes15: Earlier, unilamellar synthetic
skin substitutes (e.g. polymers of polyvinyl alcohol and
polyvinyl chloride films) were used. They were not pliable
enough to conform to the irregularities of the wound surface
and their permeability characteristics promoted subsurface
seroma formation. Later bilamellar structures were formed
which function effectively as skin substitutes. The thin outer
layer (epidermal analog) should have pores <5 m to make it
permeable to only water and not bacteria. The thicker inner
layer (dermal analog) should have pores of 80 m size to allow
the ingrowth of fibrovascular tissue from the wound surface
to form a biologic union. Biobrane is one such membrane
which consists of a collagen–gel dermal analog and a silastic
epidermal analog. Bacterial counts under Biobrane are 1/10th
of those found under a cadaveric homograft. If submembrane
suppuration does not occur, Biobrane need not be removed
and it separates itself as the wound re-epithelializes.
Monitoring for Complications
A number of complications can develop in traumatic wounds.
1. Hemorrhage and Hematoma—can be either primary or
secondary
2. Infection—presents as spreading erythema of the skin around
the incision line, local pain local edema, heat pyrexia, increased
exudate /suppuration, abscess formation, lymphangitis,
cellulitis, loss of function of a limb and septicemia
3. Dehiscence
4. Evisceration
5. Sinus
6. Fistula
Prognosis
Final outcome in these patients depends on various factors
such as mode of injury, time of arrival to hospital after injury,
associated comorbidities and initial care given. The triad of
hypothermia, acidosis and coagulopathy often goes unnoticed
is the major cause of mortality in major trauma patients.
Summary
1. A holistic approach to assessment and management of
surgical and acute wounds is essential.
2. Surgical and acute wound management focuses on
restoration of function and physical integrity with the
minimum deformity and without infection.
3. Modern wound dressings have a role to play, as they appear
to reduce pain, reduce patients’ length of stay.
References
1. Nakajima H, Fujino T, Adachi S. A new concept of vascular
supply to the skin and classification of skin flaps according to
their vascularization. Ann Plast Surg.1986;16(1):1-19.
2. Mathes SJ, Hansen SL. Flap Classification and Applications.
In: Mathes SJ. Plastic Surgery. General Principles. 2nd edn.
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3. Manchot C. The Cutaneous Arteries of the Human Body. In:
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Kopers, 1889. New York: Springer-Verlag; 1983.
4. Milton SH. Pedicled skin-flaps: the fallacy of the length: width
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Williams and Wilkins. 1997;19-28/Chapter 4.
14. Hirigoyen MB, Blackwell KE, Zhang WX, Silver L, Weinberg
H, Urken ML. Innovations in traumatic wound management.
Plast Reconstr Surg. 1997;99(3):763-73.
15. Casanova R, Iribarren O, Grotting JC, Vasconez LO. Skin
grafting past and present. Ann Plast Surg. 1988;20(2):112-6.

• Evolution of Concepts—Serial Debridement vs Radical
Debridement
• Technique of Debridement
• Role of Wound Swabs
• Role of Antibiotics and Tetanus Prophylaxis
• Pitfalls in Debridement
• Other Methods of Debridement

– Hydrosurgical Debridement

– Maggots for Debridement
INTRODUCTION
The term debridement comes from the French word
“desbrider”, meaning “to unbridle”. It was probably fi rst used
as a medical term by surgeons working several hundred years
ago in war zones, who recognized that grossly contaminated
soft tissue wounds had a better chance of healing (and the
soldier surviving) if the affected tissue was surgically removed
to reveal a healthy bleeding wound surface. French surgeons
Desault (1744-1795) and his pupil Larrey (1766-1842) are
credited with popularizing the procedure and introducing the
term “debridement”.1 Modern wound excision as is advocated
today was probably fi rst described by Milligan (1915) who was
a British surgeon in the First World War.2 Later Trueta (1944)
described the operation of wound excision in considerable
detail.3 A modern defi nition of debridement is the removal of
dead or necrotic tissue and foreign material from and around a
wound to expose healthy tissue. The practice of wound care and
concept of debridement has kept pace with our understanding
of the pathophysiology of wound healing and mirrored the
increased capability of providing soft tissue cover.

Two factors on which the functional outcome of a major
injury depends upon are one, whether the wound heals by
primary intention and second, whether the wound gets infected
or not. Both are dependent upon the quality of debridement
performed. Debridement is the key to successful outcome in
open fracture management. Court Brown when discussing
open fracture management said that “it is likely that the
prognosis of an open tibial fracture is governed mainly by the
adequacy of the initial debridement and the skill with which
the soft tissues are treated”.4
EVOLUTION OF CONCEPTS—
SERIAL DEBRIDEMENT VS RADICAL
DEBRIDEMENT
As defi ned earlier, debridement is the removal of dead or
necrotic tissue and contaminants from and around a wound to
expose healthy tissue. This is based on what we remove. With
the introduction of microsurgical free fl aps and our enhanced
capacity to cover large soft tissue defects, the focus shifted to the
timing of cover. Lister and Scheker5 based on Godina’s6 work
introduced the concept of emergency free fl aps whereby the
post-debridement defects were covered within 24 hours. This
was introduced on the basis, that earlier the wound cover was
achieved the lesser are the chances of infection and secondary
loss of critical structures due to exposure and desiccation.
For early cover to be successful, it was mandatory that the
debridement was of high quality and this introduced the concept
of primary radical debridement. To perform emergency free fl ap,
the surgeon had to be confi dent that whatever remained in the
wound was viable. Here the concept is based on what is retained.

Earlier, serial debridement was practiced whereby extensively
crushed and contaminated wounds were debrided and was
S Raja Sabapathy
Debridement—Preparing the
Wound Bed for Cover
8
Chapter

Debridement—Preparing the Wound Bed for Cover
CHAPTER 8
69
revisited for debridement every 24 or 48 hours until one felt that
the bed was fi t for soft tissue cover. Serial debridement had some
disadvantages. It required more visits to the operating room.
There was the potential risk of increased rate of infection acquired
at the time of dressing changes. Further if bare bone, tendons
and nerves are exposed in the wound they could be lost due to
desiccation. Whatever technique was used to keep the wound
moist, it was diffi cult to avoid desiccation. On the other hand,
radical primary debridement had the potential disadvantage of
excess removal of tissue which could have possibly survived.
The surgeon has to base his judgment while debriding by
assessing the tissues involved and the benefi ts of early coverage
versus the possible loss due to exposure and infection.

Barring electrical burns and few very badly contaminated
wounds, it is possible to confi dently perform primary radical
debridement and proceed to early soft tissue cover (Figures
1A to G).
TECHNIQUE OF DEBRIDEMENT
There are three essential prerequisites to perform a good
debridement. First, it must be done under good anesthesia
and good illumination. Second, the surgeon should use loupe
magnifi cation during the procedure. Third, which is applicable
for debridement of limb wounds is that debridement has to be
performed under tourniquet.

Local anesthesia can be used only in limited situations
where the wounds are small and superfi cial. In contaminated
wounds, it has the potential disadvantage of opening up
tissue planes for infection to spread in. While opportunities
for utilizing local infi ltration anesthesia are limited, regional
nerve blocks are favored, particularly in the limbs. This
enables the comfortable use of tourniquet.

The outcome has been found to be better when loupe
magnifi cation is used for debridement. This is attributed
Figures 1A to G: (A) An abrasive injury to the left foot in a road traffi c accident resulting in a
highly contaminated wound with loss of skin and soft tissue on the medial aspect of the leg,
abrasive injury to the bones with open joints; (B) The wound after debridement; (C) Skeletal
stabilization after wound debridement; (D and E) Harvested free latissimus dorsi muscle fl ap
before and immediately after transfer and (F and G) Long-term result with the boy comfortable
with independent weight-bearing walking

General Principles for Wound Management
SECTION 2
70
the wounds during debridement and it has been found effective
and economical (Figure 3).

After preliminary washing of the wound with autoclaved
water, the ragged skin margins are fi rst excised. If the wound
is not degloved, a narrow rim of skin excision is enough. With
sharp dissection, the surface of the wound is then excised to
reveal a fresh healthy surface. This is called wound excision.
The debrided skin edges are not allowed to fall back on the
undebrided wound surface until debridement is complete.
Care is taken to inspect all intermuscular planes which have
been violated for possible contaminants.
not only for its role in identifying contaminants, but also in
distinguishing the viable and non-viable margins in critical
structures and increased accuracy in hemostasis.

While the fi rst-two mentioned prerequisites fi nd easy
acceptance, the use of tourniquet still remains to be questioned
by some people. The author is very convinced of its role
for the following reasons: (1) When debridement is started
without tourniquet control, the moment the skin edges are
incised blood, covers the wound making everything look
bright red and it is possible that deeper parts of the wound
and intermuscular planes escape attention. (2) Patients with
major injuries have already suffered considerable blood
loss and debridement of an extensive limb injury without
tourniquet would involve signifi cant loss of blood which
could be stressful to the patient (Figure 2). (3) Identifi cation
and preservation of important structures like nerves and
blood vessels are easier done in a blood less fi eld and there
is potential risk of injuring them when debridement is done
without tourniquet. With practice, identifi cation of viable and
non-viable tissues under tourniquet poses no problem.

The technique of debridement has been well described by
Godina6 and Gupta et al.7 The following is a summary of their
description with the addition of points which we have found
useful in our work. Before starting debridement, the vascular
status of the limb and the integrity of sensation is examined
and documented. Under appropriate anesthesia, the tourniquet
is elevated to about 150 mm Hg above systolic pressure
with limb elevation. If the wound is very contaminated
preliminary irrigation of the wound is done to wash away
gross contamination. Irrigation must be relied only to remove
gross contamination. It is not effective to clear away ingrained
dirt. Sharp dissection is required to remove ingrained dirt.

Various solutions have been recommended for cleaning
wounds. Conventionally normal saline is favored as it is
an isotonic solution and does not interfere with the normal
healing process. There is an unresolved debate about using tap
water, boiled cool water versus normal saline and antibiotic
containing solutions. Fernandez and Griffi ths8 reviewed
randomized and quasi randomized controlled trials identifi ed
by electronic searches of Cochrane Wounds Group Specialized
Register (June 2007), MEDLINE (1996–2007), EMBASE
(1980–2007), CINAHL (1982–2007) and Cochrane Controlled
Trials Register (issue 3; 2007) and came to the conclusion that
there was no evidence that using potable tap water to cleanse
acute wounds increases infection. The use of isotonic saline,
distilled water and boiled water for cleansing open fractures
also did not demonstrate a statistically signifi cant difference
in the number of fractures that were infected. In the absence of
potable tap water, boiled and cooled water as well as distilled
water can be used as wound cleansing agents. It is the practice
of the author’s team to use autoclaved water for irrigation of
Figure 2: Tourniquet is applied for the debridement of all limb wounds
and even in a circumferential raw areas, a sterile tourniquet is used to
debride as much of the wound as possible under tourniquet to reduce
blood loss
Figure 3: Bottles of sterile autoclaved and cooled water are prepared
everyday for irrigation of the wounds during debridement in the
author’s unit

Debridement—Preparing the Wound Bed for Cover
CHAPTER 8
71

In the operative fi eld under tourniquet, it is simple to
distinguish between healthy and damaged tissue. The basic
elements of such judgment are appearance and consistency.
Healthy tissue in the exsanguinated limb is bright and
homogeneous in color. Subcutaneous tissue is yellow, the
muscles are bright red and the tendons and fascia have a white
and shiny appearance. Damaged tissue is recognized by the
presence of foreign bodies, irregular tissue consistency and
irregular distribution of dark red stains which are hematomas.
All such altered tissue is removed with a knife. The edge of
debridement should be in healthy tissue. Denuded tendon,
if not frayed, should be cleaned. Disrupted tendons can be
sutured or fi xed with a suture to the surrounding tissue for
late reconstruction. If the muscles are avulsed proximally and
are hanging loosely from their distal tendon attachment, the
muscles attached to the hanging tendons must be excised. They
are not viable muscles and cannot become viable even if the
limb is revascularized. The tendons are retained in case they
are needed for later utilization in tendon transfers. Exposed
bones are irrigated and mechanically cleansed with bone
rongeurs. Nerves are the only structures where debridement is
not radical. Those parts that are destroyed without any doubt
are removed and ends marked for later reconstruction. In the
case of vessels and nerves when they are badly contaminated,
with patience, it will be possible to fi nd a plane just superfi cial
to their surface and excise the contaminated tissue. This we call
as skeletonization of the longitudinal structures (Figures 4A
to J). In this way, debridement differs from en bloc excision
practiced during malignancy resection.

Judgment regarding the extent of skin excision becomes
diffi cult when there is an element of avulsion. When there is
skin avulsion as in degloving injuries, the excision is dependent
upon the extent and direction of degloving and the possible
presence of feeding perforators at the base. When the margin
of degloved skin is incised if there is bright red blood in the
subdermal level then the skin fl ap would survive. Dark color
bleeding in the subcutaneous plane is not an encouraging sign.
That skin would probably not survive and if it is not critical can
be removed primarily. If it is covering a vital structure, it can
be retained with a defi nite plan for inspection 48 hours later.

The plane of degloving is always superfi cial to the fascia.
Due to the lack of contribution from the fascial plexus of
vessels, the subdermal plexus becomes the predominant blood
supply of the degloved skin fl ap. The extent of survival will
depend upon the contribution to this plexus from the base.
Sometimes certain areas of degloved skin may just have the
dermis (Figures 5A and B). Those areas will surely necrose in
a few days and cannot be relied to cover important structures.
If the degloved fl ap is based on intermuscular septum, the
chances of a perforator being present is higher and the extent
of fl ap survival is more. Due to the paucity of perforators and
the usual pattern of injury, the loss of skin is more extensive
in degloving injuries of the lower limb than the upper limb.

In circumferential degloving injuries, the same principles
apply. The fl ap is trimmed up to the level of good bright
subdermal bleeding. Proximally based fl aps have higher
chances of survival than the distally based fl aps. In instances
where both ends are attached, it is our practice to debride
the inner surface and retain the strip after debridement for a
second look 48 hours later. When retained on day one, the fl ap
functions as a conduit for some venous drainage and reduces
the bleeding in the immediate postoperative phase. Strips with
both proximal and distal attachments have a higher extent of
survival than fl aps based either proximally or distally.

At the completion of wound excision, if the debridement
has been done under tourniquet, it is released and viability of
the remaining tissues is assessed. If there are any areas devoid
of blood supply, the wound is debrided again. If necessary,
tourniquet can be infl ated again.

At the completion of debridement, special care is taken
for hemostasis. Even while performing wound excision
under tourniquet, all open vessels as they appear need to be
coagulated. This is important because if the resultant raw area
is large, blood loss could be very severe in the postoperative
period when the blood pressure stabilizes. In circumferential
degloving injuries after skin excision, the distal skin margins
need special attention. Even minor vessels in the distal wound
skin margin can profusely bleed in the postoperative period.
They need to be coagulated at the end of debridement.

The postdebridement raw area is covered with non-
absorbent dressing and suitable amount of padding depending
Figure 4A

General Principles for Wound Management
SECTION 2
72
Figures 4B to G

Debridement—Preparing the Wound Bed for Cover
CHAPTER 8
73
Figures 4A to J: (A) Crush injury of the right forearm with open
comminuted fractures of the both bones of the forearm with
distal avascularity; (B) Shows gross contamination with mud; (C)
Examination under anesthesia reveals distally avulsed muscles and
loose bone fragments which need to be removed; (D and E) Show
the concept of skeletonization of longitudinal structures whereby intact
median and ulnar nerves are meticulously debrided and preserved;
(F) Skeletal stabilization done by creating a one bone forearm prior to
revascularization; (G and H) Long term result with function of the hand
and 4; (I and J) Show the preoperative and postoperative radiographs
upon the expected soakage from the wound. When the outer
most dressing gets soaked then it is no longer a closed wound.
If bare bone or tendons are exposed then they could be
covered by collagen sheet to keep them moist.9 This could be
done only when one is confi dent of good debridement, since
we would be converting it into a closed wound.

If the involved part is a limb, then it has to be splinted and
kept elevated. The operation notes must specifi cally record the
structures injured and the level of the distal and proximal cut
ends of vital structures. This is essential to avoid unnecessary
long exploratory incisions during secondary reconstruction.
ROLE OF WOUND SWABS
The role of wound swabs in management of open injuries
is controversial. There are reports stating the usefulness of
quantitative wound cultures in management of open wounds10
but Valenziano et al11 in 2002, performed a prospective study
to fi nd whether primary wound cultures predict which wounds
will become infected, and whether bacterial growth on primary
wound cultures correlates with bacteria cultured from infected
wounds. Initial aerobic and anaerobic cultures of the wound
of 117 consecutive open extremity fractures were obtained
before any intervention. The results of these cultures were
correlated with the development of a wound infection, and if
an infection occurred, the organism grown from the infected
wound was compared with any organism grown from the
primary wound cultures. Of the initial cultures, 76 percent
(89/117) did not demonstrate any growth, while the other
24 percent (28/117) only grew skin fl ora. There were only 7
(6%) wound infections, and 71 percent (5/7) initially did not
grow any organisms. Of the isolates that grew from the initial
cultures, none were the organisms that eventually led to wound
infections. Based on these fi ndings they concluded that the use
of primary wound cultures in open extremity injuries has no
value in the management of patients suffering with long bone
open extremity fractures.11

Lee J12 at the University of California while analyzing
the effi cacy of cultures in the management of open fractures
Figures 4H to J

General Principles for Wound Management
SECTION 2
74
Figures 5A and B: (A) Crush injury of the leg with degloving resulting
in a distally based non-viable skin fl ap; (B) The inner view of the
degloved fl ap showing that the plane of degloving is superfi cial to the
fascia and in many places it contains only the skin
in 245 cases concluded that “pre-debridement and post-
debridement bacterial cultures from open fracture wounds are
of essentially no value, and it is recommended that they not be
done”.12 Kreder and Armstrong13 at University of Washington
also found questionable role of perioperative cultures in open
pediatric lower-extremity fractures.

In the author’s unit wound swabs are done for patients who
are admitted secondarily with infection and for patients who get
infected to know the antibiotic sensitivity profi le of the infecting
organism. We do not do predebridement or postdebridement
wound swabs for open fractures primarily seen by us.
ROLE OF ANTIBIOTICS AND TETANUS
PROPHYLAXIS
Antibiotics have been found to be benefi cial in most of the
studies on open injuries. Patzakis and Wilkins14 found that the
pre-operative administration of appropriate antibiotics was
the most important factor in determining the rate of wound
infection in association with open fractures.14 Gosselin et
al15 in Cochrane systematic review concluded that antibiotics
reduce the incidence of early infections in open fracture of the
limbs. There is no universal agreement on which antibiotic
should be given; how many agents or combinations required
and the duration of the antibiotic therapy. Patzakis et al16 in
their prospective, randomized, double-blind study comparing
single-agent antibiotic therapy and combination therapy in
open fracture wounds concluded that a single-agent antibiotic
therapy with ciprofl oxacin is effective in treatment of Type
I and Type II open fracture wounds. However, for Type III
wounds, ciprofl oxacin alone is not recommended. Possibly one
can use fl uoroquinolones in combination therapy, specifi cally
as an alternate to an aminoglycoside. Hauser et al17 in their
review on the effects of prophylactic antibiotic administration
on the incidence of infections complicating open fractures
concluded that a short course of fi rst generation cephalosporins,
begun as soon as possible after injury, signifi cantly lowers
the risk of infection when used in combination with prompt,
modern orthopedic fracture wound management. There is
insuffi cient evidence to support other common management
practices, such as prolonged courses or repeated short courses
of antibiotics, the use of antibiotic coverage extending to
gram-negative bacilli or clostridial species, or the use of local
antibiotic therapy such as beads. In the author’s unit 1.5 gm of
cefuroxime is given intravenously for antibiotic prophylaxis.

Tetanus prophylaxis is important to avoid rare but life
threatening clostridium infection. Tetanus can occur after
minor, seemingly innocuous injuries though the wounds which
are prone for tetanus are—greater than 8 to 24 hours from
injury to treatment, barnyard contamination and devitalized
tissue.18 If the patient is fully immunized in past but has not
received booster for over 5 years, then should receive 0.5 ml
of tetanus toxoid IM. Any patient who has not received full
course of immunization should not only receive tetanus toxoid
but also should receive passive immunization with 250 units
of human tetanus immune globulin IM or 4 units/kg body
weight in pediatric population.18
PITFALLS IN DEBRIDEMENT
Penetrating Wounds
The need for anesthesia, good lighting, exposure, use of
magnifi cation and tourniquet does not vary with the size of

Debridement—Preparing the Wound Bed for Cover
CHAPTER 8
75
the wound. Penetrating wounds may be taken lightly with
disastrous consequences (Figure 6). Penetrating wounds need
opening up and excision of the tract if consistent good results
are to be obtained. Piercing injuries in the hand and feet injure
mobile structures at different levels which on movement
create closed space for anaerobic infection to set in. A classic
example is the injury by the tooth to the metacarpal head in a
clenched fi st position. It requires full opening of the tract and
debridement. The same principles apply when dealing with
the piercing injuries caused by sticks, iron rods and impaling
injuries. The risk of infection is directly related to the extent
of the contamination present in the injuring element. Even if
the offending object has been removed, the tract needs to be
debrided.
Closed Degloving Injuries
The mechanism of squeeze by a moving object can result in a
closed degloving injury. The plane of degloving is superfi cial
to the fascia similar to the open degloving injury. On
presentation, there might just be a transverse laceration either
at the proximal or the distal end. It might present a picture of
a deceptively simple injury (Figures 7A to F). The injury is
recognized by the loose feel of the skin and the subcutaneous
collection of blood. If there are associated abrasions,
infection is a serious possibility. Often closed circumferential
degloving injuries in the lower limb, end up with total loss of
the degloved area. Patients must be warned of this possible
sequence on arrival.
Retaining Non-viable Critical Structures
Reconstruction of long segment, loss of bones, tendons or
nerves are major secondary procedures. Ultimate functional
outcome and time taken to achieve it are unfavorable when
compared with primary repair. This fact and the prospect of
diffi cult reconstruction many times tilt the decision of the
surgeon to retain non-viable or questionably viable critical
structures. If for any reason such bones and tendons are not
covered early, they do not stand desiccation and they become
non-viable. Covering non-viable structures with a vascular
fl ap cannot make them viable. They are the common cause
of infection under the fl ap and occurrence of long standing
sinuses. The way to prevent is to achieve early soft tissue
cover. Prior to fl ap cover the dead tissues need to be excised.
Bone pieces without soft tissue attachment should be removed.
Cortical bones without soft tissue attachment do not act like
bone grafts. Though excision might result in a bigger defect,
ultimately the healing time is shorter with good debridement,
appropriate soft tissue cover to achieve primary healing and
secondary reconstruction.
Figure 6: Result of fulminant infection after sustaining a knife stab
wound during surgery of an infected wound in a surgeon’s index fi nger,
which ultimately needed ray amputation. All penetrating injuries need
to be debrided and the tract excised
Debridement in Diabetic Patients
Toe amputations are common in diabetics. Subsequent to
toe amputations, often proximal infections occur in the foot
necessitating revision amputations. A common cause for this
is the proximal migration of the infected tendon ends. The
divided tendon ends in a closed space facilitates anaerobic
infection. Contamination also occurs along the whole tract as
the tendon ends migrate proximally. To prevent this during
debridement, a proximal longitudinal incision is made in the
line of the tendon, the tendon is divided and it is withdrawn
distally (Figures 8A to E).
OTHER METHODS OF DEBRIDEMENT
Hydrosurgical Debridement
One of the recently introduced modality of debridement
is hydrosurgical debridement (Versajet). Water dissection
works by using a high-pressure jet of sterile saline that
travels parallel to the wound and creates a Venturi effect, thus
enabling the selective removal of necrotic tissues without
dissemination of contaminants. The advantage claimed over
surgical debridement is the selectivity of tissues since in
surgical debridement some healthy collateral tissue might also
be removed and its capability of removing deeply ingrained
contaminants. Proponents claim that its use allows expeditious
reconstruction of the wound with skin grafts or fl aps while
avoiding infection and injury to vital structures.19,20

General Principles for Wound Management
SECTION 2
76
Figures 7A to F: (A) Crush injury of the leg with burst wound in the upper part of the leg, with the distal part of the skin showing spotty areas
of depression signifying deep damage; (B) Shows extensive degloving injury which needs to be opened for debriding; (C) Opening reveals
extensive damage to muscles which might have been missed had the skin wound not been explored; (D) The status after debridement and
(E and F) Long term result after skin grafting

Debridement—Preparing the Wound Bed for Cover
CHAPTER 8
77
Maggots for Debridement
Debridement by maggots is termed as biological debridement.
Ambroise Pare was the fi rst person to document the benefi cial
effects of larvae in supportive wounds.21 It should be
considered as a therapeutic option in the management of certain
diffi cult wounds especially when the patients are not suitable
for surgical intervention or have declined it.21 They act by
secretion of proteolytic enzymes and antibacterial substances,
their effects on epidermal growth factor and interleukin-6
Figures 8A to E: (A) A diabetic great toe ulcer with the patient showing
toxic symptoms; (B to D) The common cause is the tracking of pus
along the long fl exor tendons which need to be opened for debridement
and the tendons divided proximally and withdrawn into the wound and
the tract washed prior to closure of the stump; (E) The wounds went
on for uneventful healing

General Principles for Wound Management
SECTION 2
78
and ingestion and digestion of bacteria and necrotic tissue.21
Maggots also help to sterlize wounds by local production of
ammonium and sodium bicarbonate that shifts an acidic pH
of the wound fl uid to alkaline, and this limits the growth of
bacteria regardless of their resistance to antibiotics.22 Maggots
are placed on the wound after protecting the wound edges to
prevent larvae from crawling beyond the edge. They have
to be replaced every two to three days. The debridement is
painless, but the sensate patient can feel the larvae moving.22
CONCLUSION
An important outcome determinant of healing of any wound
is the effi cacy of debridement. Though it is an undisputed
fact, still most of the complications in wound healing are due
to poor debridement. Surgical debridement still continues to
be the preferred and most effi cient method of debridement
of post-traumatic and most of the post-infective wounds.
Numerous pharmaceutical agents that have come up and other
ancillary methods of debridement at most times are not the
primary technique of debridement. Hence, every surgeon must
be well trained in the art of debridement which is essential for
primary wound healing or is a preparatory step for defi nitive
wound cover in the event of soft tissue loss.
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4. Court-Brown CM. Open tibial fractures. In: Court-Brown CM,
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Orthop Trauma. 2010;24:e66-8.
20. Vanwijck R, Kaba L, Boland S, Gonzales Y, Azero M, Delange
A, Tourbach S. Immediate skin grafting of sub-acute and
chronic wounds debrided by hydrosurgery. J Plast Reconstr
Aesthet Surg. 2010;63:544-9.
21. Turkmen A, Graham K, McGrouther DA. Therapeutic
applications of the larvae for wound debridement. J Plast
Reconstr Aesthet Surg. 2010;63:184-8.
22. Pomahac B, Hirsch T, Eriksson E. Wound management. In:
Guyuron B, Eriksson E, Persing J. (Eds). Plastic surgery-
indications and practice, (1st edn) UK, Saunders: Elsevier;
2009.pp.27-36.

• Wound Healing
• Classification of Wounds in Relation to Wound Closure
• Rationale behind Wound Dressings
• Classification of Wound Dressings

– Inert Dressings

– Active Dressings
• Topical Agents in Wound Healing

– Antimicrobials

– Growth Factors

– Matrix Forming agents

– Enzymes
Introduction
Wounds are common in surgical practice. A wound occurs
when there is a disruption of the surface epithelium with
variable loss of the underlying tissue. The etiology of wounds
is varied. The normal reparative mechanism of the human
body ensures that most of the wounds heal within a span
of time. However, when the normal response mechanism is
altered, wounds tend to become long standing and chronic.
Wound care techniques have been documented since 1500 BC
in ancient Egypt and Greece where lint was used as a fibrous
base, animal grease as a protective barrier, and honey as a
topical antibiotic. In 150 AD, the Greek surgeon, Galen of
Pergamum, while working with a Roman gladiator’s cuts,
first addressed the fact that the wound should be kept moist
to ensure adequate healing. In this chapter the mechanism of
wound healing will be mentioned briefly with the classification
of wounds and dressing materials along with the indications
for their use will be discussed in detail. The method of use of
wound dressings will also be explained along with care of the
wound during the healing phase.
Wound Healing
Pathophysiology of wound healing has been discussed in depth
in an earlier chapter already. However, there are two important
concepts to understand the mechanism that the body uses to
repair tissue loss. One mechanism is tissue repair and the other
is tissue regeneration. In tissue repair there is an effort of injured
tissues to restore their normal function and structural integrity
after injury. Because of the need of rapid return to function,
the repair sometimes results in scar formation. However in the
case of tissue regeneration there is complete restoration of tissue
integrity with no scar formation. Even though the ideal situation
in wound healing is tissue regeneration, in most instances there is
scar formation due to tissue repair.

In tissue repair, there are three stages namely:
a. Inflammatory phase
b. Proliferative phase
c. Remodeling phase
Inflammatory Phase
During this phase, there is an influx of neutrophils due to
the chemical mediators secreted by the damaged tissues.
Vasodilation occurs to improve the wound bed vascularity.
Proliferative Phase
As the name implies, there is formation of collagen matrix,
new blood vessels and epithelial cells. The key clinical feature
is that the epithelial cell proliferation and migration occurs
from the edges of the wound and the rate of epithelization is
directly related to the moistness of the wound.
Mohit Sharma, Deepak Balasubramanian
Dressings and Topical Agents
in Wound Care
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General Principles for Wound Management
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80
Remodeling Phase
The collagen deposited in the proliferative phase is remodeled
by the fibroblasts and there is deposition of contractile proteins
which is responsible for the wound contracture. The key issue
is that the width of the wound is a better predictor of wound
healing than the length.
Classification of wounds
in relation to wound closure
As mentioned in an earlier chapter, wounds are classified
based on the etiology of the wounds and the infective state of
the wound. This is necessary to plan the wound closure and
the dressings for the wound.
1. Class I – Clean wounds. Example—Operative wounds.
2. Class II – Clean contaminated wounds. Example—Visceral
surgeries.
3. Class III – Contaminated wounds: fresh traumatic wound
from clean source.
4. Class IV – Dirty-infected: traumatic wounds from dirty
source.
5. Unclassified.

Clean wounds do not require aggressive cleaning and
dressings due to adequate repair mechanisms in place. However,
contaminated wounds require cleaning and debridement,
dressings and correction of local infection and systemic
issues.
Types of Wound Closures
The type of the wound (clean vs contaminated) has a direct
bearing on the wound closure. There are three types of wound
closures namely:
a. Primary repair
b. Secondary repair
c. Tertiary repair

In primary closure, the wounds are closed immediately with
simple suturing, skin grafting or flap closure. It is commonly
done after a surgery or in clean wounds. Secondary closure
is done in highly contaminated wounds. Such wounds will
heal by re-epithelization and there will be scar formation and
contracture. A variation of this technique is the delayed primary
closure otherwise called tertiary repair. A contaminated
wound is initially treated by repeated debridement, antibiotics
(local or systemic), for several days. When the infection has
subsided, the wound is ready for closure with the conventional
techniques.

It is in the secondary or tertiary repairs, that wound dressings
play a vital role in promoting healing and epithelization and
reducing the pathogenic load in the wound bed.
Management of Wounds
There are 3 important steps in wound management:
Step 1: Assess
Step 2: Treat
Step 3: Reassess

Assessment includes etiology, wound and patient
assessment. Treatment includes cleaning, debridement and
wound dressings. Once these initial steps are completed the
wound and patient have to be reassessed to ensure adequate
and proper healing.
Wound Bed Preparation
Chronic wounds need to be converted to healing wounds prior
to application of dressings and topical agents. This process
is called wound bed preparation. One must remember the
‘TIME’ factors – namely tissue (viable vs nonviable), infection
(infected vs noninfected), moisture and edge (advancing
vs undermining) of the wound. These factors have to be
corrected by debridement and antibiotics prior to initiation of
wound dressings. This has already been discussed in detail in
an earlier chapter.
Rationale behind wound
dressings
When dressing the wound, we aim to cover the wound
surface (occlusive dressing). In 1962, Winter demonstrated
in animal experiments that wounds covered with occlusive
dressings re-epithelialized nearly twice as fast as similar
wounds left exposed to air. These have been confirmed in
humans. Occlusive dressings promote keratinocyte migration
and subsequent wound re-epithelialization. Also moisture-
retaining dressing materials do not cling to the wound bed.
This causes less pain and facilitates removal. Also there is
no damage to the regenerating epithelium. Wound fluid from
acute, uninfected wounds stimulates fibroblast, keratinocyte,
and endothelial cell proliferation. Occlusive dressings increase
cell proliferation and activity by retaining an optimum level of
wound exudate, which contains vital proteins and cytokines
produced in response to injury. These facilitate autolytic
debridement of the wound and promote healing. Also, the
hypoxic microenvironment in the wound created by occlusive
and semi-occlusive dressings has been shown to stimulate
wound angiogenesis and collagen synthesis.

Earlier there were fears that occlusive dressings would
promote wound infection by retaining pathogens. But
experiments have showed that it is not true. Because of the
low pH created on the wound surface by occlusive dressings,
bacteria does not grow leading to a reduction in infection.

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Aim of Wound Dressing
1. Hemostasis.
2. Promote healing and re-epithelization.
3. Prevent wound contamination.
4. Immobilize an injured body part and physical support.
5. Provide pain relief.
Characteristics of Ideal Dressing
1. Create a moist environment and remove exudates.
2. Impermeable to bacteria.
3. Nontoxic and nonallergenic.
4. Comfortable and conformable.
5. Infrequent changes.
6. Cost effective.
7. Easy removal.
8. Transparent to allow for wound inspection.
9. No damage to the peri-wound skin.
Layers of Dressings
Typically dressings usually have three layers namely:
1. Contact layer – The layer in contact with the wound surface.
2. Absorbing layer – To absorb the exudate from the wound.
3. Binding layer – The outermost layer which holds the dressing
together (bandage).
Classification of wound
­dressings
The US FDA (1999) recommends the following classification
for dressings (Table 1):
1. Nonresorbable (gauze, sponge).
2. Occlusive dressings.
3. Hydrophilic/absorptive.
4. Hydrogels.

Functionally, the nonresorbable are ‘inert’ dressings whereas
the other three are ‘active’ dressings. One must note that the
classic FDA classification is difficult to adhere to while describing
these dressings as the newer dressings have combined properties.
Inert Dressings (Gauze): Nonresorbable
Traditional wound dressings included gauze materials. These
materials are inert dressings which do not contribute ‘actively’ to
the wound healing process. Gauze can be applied to the wounds
as ‘dry’ dressings or ‘wet’ dressings. Dry gauze dressings though
absorptive tend to cling on to the wound surface. During removal
they can be painful and potentially damage the regenerating
epithelium resulting in delayed healing. Soaking the gauze
in physiological solutions (saline, Hartmann’s solution) can
ameliorate these problems, but reduce the absorptive capacity
of gauze and necessitates frequent change in the dressings.
However, recently we have paraffin impregnated gauze dressings
which can be used to create a moist environment for the wound
healing. On the whole, any gauze dressing does require a tertiary
layer (bandage) to hold it together. These gauze dressings are
universally available, easy to handle and relatively inert on
wound surfaces. But from a wound healing perspective, they do
not contribute to the process and this lead to the development of
active dressing materials.
Active Dressing Materials
Most of the active dressing materials used today rely on
the principle of providing a moist environment for wound
healing. Most of them are semipermeable dressings (allow for
the exchange of gas and vapors).
a. Occlusive dressings: Films, hydrocolloids and foams
come under this group. Films are polyurethane sheets
which are semipermeable. They are nonabsorbing and
form a sterile layer impermeable to bacteria. They are ideal
for surgical wounds and should not be used on exudative
wounds. Hydrocolloids contain sodium carboxymethyl
cellulose. These dressings are hydrophilic. This dressing
interacts with the wound surface forming a gelatinous mass
over the wound. This layer helps in autolytic debridement
of the necrotic tissue and helps in epithelial migration. Also
this layer prevents adhesion of the dressing to the wound
surface making it easy to remove. Commercial preparations
of hydrocolloids have an external hydrophobic layer which
acts as a dressing and retains the moisture. Foam dressings
are composed of polyurethane which has air bubbles.
They are absorptive and can be used for dressing cavities
(spreadable form). Their absorptive power is slightly more
than hydrocolloids and hence can be used in moderate to
severe exudative wounds.
b. Hydrophilic/absorptive: These dressings absorb exudates
from the wounds. Even though gauze and cotton products
perform the same function, they are not active dressings.
The currently available active hydrophilic dressing is
alginate which contains alginic acid extracted from
seaweed. The alginate dressings also interact with the
ulcer surface forming a hydrophilic layer which helps in
autolysis of necrotic tissue and promotes healing. They can
be used on heavily exudating wounds as well, a property
which is different from hydrogels or foam dressings.

General Principles for Wound Management
Section 2
82
Table 1: Wound dressings
S.No
Name
Indications
Advantages
Disadvantages
1.
Nonreabsorbable
(gauze)
Most wound types
Easily available, cheap. Good
absorbing capacity.
Sticks to the wound. Painful
during change. Can damage
epithelium. Not truly occlusive.
Require frequent change
2.
Films
Superficial wounds and
surgical sites
Occlusive dressing.
Impermeable to bacteria
Nonabsorbent, hence not
useful in exudative wounds
3.
Foams, colloids
Exudative wounds and
cavities
Form an ‘autolytic’ layer to
remove debris
Need exudates to function,
hence not suitable for dry
wounds
4.
Hydrophilic (alginate
dressings)
Highly exudative wounds
Form an ‘autolytic’ layer to
remove debris
Cannot be used in sites
of anaerobic infection/dry
wounds
5.
Hydrogels
Dry and necrotic wounds
Moisture contributing
Can cause maceration of
peri-wound skin. Very minimal
absorptive capacity.
c. Hydrogels: They are three dimensional structures containing
either polyethylene oxide or carboxymethyl cellulose with
greater than 90 percent water. Because of this high water
content, these dressings can contribute moisture to the
wound and hence can be used to soften dry, black necrotic
tissue in the wound bed. There is formation of a gel layer as
well which further contributes to autolysis. However, care
should be taken when using it in areas where the peri wound
skin is macerated or unhealthy as it might worsen due to the
water moisture contributing effect of this dressing. They can
be used only in minimally exudating wounds.
Topical agents in wound healing
Topical agents are applied on the wound surface in majority
of the dressings. They are beneficial in reducing the adherence
of the dressings (in cases of dry inactive dressings) and also
serve to form the ‘occlusive’ layer to maintain a low oxygen
tension and promote healing. They can be classified as:
1. Antimicrobials (antibiotics, antiseptics & super oxidized
solutions).
2. Growth promoting agents.
3. Matrix forming agents.
4. Topical debriding agents (enzymes).
Antimicrobials (Antibiotics and antiseptics)
One of the commonly used topical agents for dressing include
topical antimicrobials. They can be classified to topical
disinfectants (antiseptics) and antibiotics.

Antiseptics work by contact destruction of the pathogenic
organisms. They have a rapid action but poor residual effect.
Also these antiseptics are not suitable for open wounds as
they are detrimental to fibroblasts and epithelium. Currently,
their role is best reserved for surgical site cleaning of intact
skin. Routine wound irrigations with these substances are
now not recommended. The common antiseptics that we use
are povidone iodine (10%), sodium hypochlorite and acetic
acid. Povidone iodine (10% commercially available) should
not be used as such as it is toxic to fibroblasts. In the event of
use for wound irrigation, it has to be diluted to atleast 1:10 in
saline. Sodium hypochlorite solution (EUSOL or Edinburgh
University solution of lime) is one of the earliest disinfectants
used in hospitals. It is a chlorinated lime solution and can be
used to moisten the gauze dressings. It is an oxidizing agent
and has action against bacteria and virus. It is not available
commercially and is usually prepared in the hospital itself.
The drawbacks of EUSOL are the very short shelf life and
frequent need to prepare the fresh solution. Also it is difficult
to standardize the strength in the hospital settings. There is
a potential to cause blistering in some individuals and it is
preferred that a half strength solution to be used as a wound
dressing. Recently OXUM, a superoxidized, nontoxic, non-
irrigating, no rinse dermal wound irrigant solution is being
used as a topical agent in wound care. It does not require any
preparation or dilution. It also facilitates debridement of the
wound. It is available as a spray to allow for uniform application
during each dressing change. Since, it is commercially
available, the strength is uniform and standardized; this is not
possible with EUSOL solutions.

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The above solutions act by producing reactive ions which
destroy the pathogenic organisms. However, as mentioned
earlier these solutions are detrimental to the normal fibroblasts
and epithelial cells. The drawback of these contact antiseptics
is that their activity is reduced in the presence of pus and
blood.

Topical antibiotics are the recommended agents for topical
application today. The various agents available are:
a. Mupirocin: Mupirocin is a topical antibiotic obtained
from Pseudomonas fluorescens. It works by the reversible
inhibition of bacterial isoleucyl- tRNA synthetase. This
causes arrest of bacterial cell wall synthesis.


Mupirocin is effective against aerobic gram-positive
cocci, especially S. aureus. However, it has limited activity
against gram-negative bacteria. It is available as a two
percent ointment. Recently there have been concerns on
the development of mupirocin resistant strains of bacteria.
b. Neomycin: Neomycin is an aminoglycoside obtained
from Streptomyces fradiae. It binds to the 30S subunit of
the bacterial ribosome and inhibit protein synthesis. It is
effective on S. aureus and gram negative bacteria. Its activity
is limited on P. aeruginosa, streptococci and anaerobes. It
is available as 20 percent neomycin sulfate in petrolatum,
and is widely used by itself and in combination with other
antibiotics, such as bacitracin and polymyxin B. One word
of caution, there is a risk of development of allergic contact
dermatitis with the use of neomycin and this can lead to
damage of the normal intact peri-wound skin.
c. Bacitracin: Bacitracin is a polypeptide produced by
Bacillus subtilis. Bacitracin A is the form most commonly
used, often formulated as 20 percent bacitracin zinc
in petrolatum. It acts by combining with C55-prenol
pyrophosphate, a constituent of the bacterial cell wall, thus
blocking cell wall formation. It has good activity against
gram positive organisms. However, as with neomycin,
there is a risk of development of contact dermatitis.
d. Topical silver agents: Topical agents containing silver
have been used as wound dressings for the last 100 years.
Silver nitrate and silver sulfadiazine are two commonly
used preparations and the commercially available
preparation (1%) is a combination of the two. Unlike
topical antibiotics, topical silver is bacteriostatic and its
activity is directly proportional to the amount of silver
present in it. The mechanism of action is denaturing of the
nucleic acids. It has activity against S. aureus, Enterococci
and to a lesser extent Pseudomonas. However, there are
certain disadvantages with older topical silver agents
namely inactivation of the antimicrobial activity, with
a need for frequent application. Also these agents can
induce inflammation in the wound site. To overcome these
problems, newer dressings with impregnated nanocrystal
silver particles are being marketed (Acticoat-Smith &
Nephew). These are barrier dressings which prevent
wounds especially burn wounds from contamination. They
provide sustained release of silver into the wound for up
to seven days and can be left for about a week. Studies
comparing Acticoat with other silver containing dressings
indicate better antimicrobial activity and fewer side effects.
Growth Factors
Growth factors are cytokines which accelerate cellular
growth. They do so by acting on the cellular receptors and
inducing mitosis. Knighton in 1986 first demonstrated the
beneficial effects of using topical autologous platelet derived
wound healing factors (PDWHF) for the treatment of chronic
wounds. Most of the growth factors which are essential for
wound healing are produced and stored in the platelets.

Currently, there are various growth factors of interest in
wound healing and the ones which have been experimentally
studied include:
1. Platelet-derived growth factor (PDGF).
2. Fibroblast-derived growth factor (FGF).
3. Epidermal growth factor (EGF, including the neu
differentiation factor).
4. Tumor necrosis factor (TNF).
5. Granulocyte-macrophage colony-stimulating factor (GM-
CSF).
6. Insulin-like growth factor (IGF).
7. Transforming growth factors (TGF).
8. Keratinocyte growth factor.

However, only two classes are currently being used
clinically. They are:
a. Recombinant human platelet derived growth factor isoform
BB: The platelet derived growth factor is a potent mitogenic
agent belonging to the PDGF/VEGF family. It is produced
primarily in the platelets where it is stored and released
when required. It is a dimeric glycoprotein with two
isoforms namely PDGF AA, PDGF BB. Earlier platelet rich
plasma (PRP) containing PDDF obtained from autologous
blood (Autologel®, Safeblood®) was applied on the wound.
Now, the isoform BB is commercially available. Currently
it is the only topical growth factor approved by the US
Food and Drug Administration for the treatment of chronic
wounds and chronic diabetic ulcers. It acts by promoting the
chemotactic recruitment and proliferation of cells involved
in wound repair. There is a resultant increase in fibroblasts,
extracellular matrix and inflammatory cells in the wound site
which promotes healing. Currently it can be used for chronic
ulcers, decubitus ulcers and neuropathic lower limb ulcers in
combination with debridement and moist wound dressings.
However, it should not be used in infected wounds or when