Principles and Practice of Wound Care

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This type of debridement is particularly useful in handling
deep and tunnelling wounds where debridement with other
technique is difficult.8
VersajetTM
For optimum wound care good debridement is a key.
Hydrodissection in recent years has gained popularity in the
surgical debridement of ulcers. Smith and Nephew‘s (Hull,
UK) Versajet Hydrosurgery System was recognized by the
Wall Street Journal’s 2006 for Technology Innovation Awards.

Versajet™ a hydrosurgery tool, allows precise and
controlled surgical debridement. Versajet is a hydrosurgery
system where razor thin saline jet is used to optimize surgical
debridement.
Mechanism of Action
This innovative wound debridement system is in essence a
Venturi effect based instrument:

A high velocity stream of sterile saline jets across the
operating window and into an evacuation collector. Because
of the Venturi effect, a localized vacuum is created across the
operating window. This holds and cuts targeted tissue while
aspirating debris from the site. As the hand piece travels
tangentially over the soft tissue surface it creates a smooth
wound bed while maximizing dermal preservation. The
tissue-preserving technique reduces time to closure which
may reduce overall treatment costs9-11 (Figure 3).

In comparison with other methods of surgical debridement
the Versajet is highly selective in its ability to specifically
isolate eschar and also useful when debriding other irregular
surface areas of the body such as the toes, fingers and
perineum. Versajet debridement enables efficient removal of
necrotic tissue with maximal preservation of viable dermal
tissues necessary for re-epithelization. There is rapid wound
healing with better cosmetic outcomes.
Biodebridement or Maggot Treatment
The practice of using Maggots of flies to heal wounds has
been around for centuries. In the pre-antibiotic era, physicians
noted that larvae would debride wounds of necrotic tissue
and greatly improve the prognosis for disease. Larvae work
continually to remove the dead tissue and cleanse it of bacteria
while leaving the viable cells alone. Medicinal maggots of
Lucilia sericata (Figure 4) (Green Bottle fly) are used for
debriding the dead necrotic and infected tissue of wound.
Beauty of these Maggots is that they do not eat or disturb
normal host tissue.
Figure 3: Venturi effect
Figure 4: Lucilia sericata (Green Bottle fly)
Mechanisms of Action
The exact mechanism is unknown, however studies indicate
that it may be a combination of the below mentioned proposals.
Studies has shown that larvae can cleanse a wound of gram
positive, gram negative, aerobic and anaerobic bacteria and
they are very effective in eradicating MRSA. Maggots quickly
debride necrotic lesions and promote the formation of healthy
granulation tissue.

Benefits of Maggot’s therapy are good debridement
with removal of dead necrotic tissue and elimination of
infection.12,13

Shortcomings of Maggot’s therapy are that medicinal
Maggots are costly and difficult to get. They have a short shelf
life, patients can have uncomfortable crawling sensation and
once Maggots move out of dressing they can create a lot of
nuisance.

Types of Wounds and their Management
Section 3
186
pressure settings vary between 40 to 80 mm Hg and 125
mm Hg negative pressure removes exudates, reduces edema,
promotes perfusion and granulation tissue formation and
draws wound edges together14 (Figure 5).

Subatmospheric pressure application causes physical
contraction of complicated wounds and removes toxins,
excess interstitial fluid, and slough from the wound bed,
thereby optimizing the wound environment for angiogenesis
and resultant granulation tissue formation.
VAC or NPWT Device Comprises (Figure 6)

1. Granufoam dressing

2. Plastic tubing

3. Canister

4. Computerized treatment unit.

After cleaning and debriding the wound a special
granufoam dressing is applied over wound which is connected
S.No.
Indications
1.
Infected or sloughy wounds
2.
Necrotic area on diabetic foot
3.
Necrotizing fasciitis
4.
Infection with MRSA
S.No.
Contraindications
1.
Fistulae
2.
Wounds that connect with vital organs such as
brain
3.
Wounds near cavities, e.g. abdomen, thorax
4.
Wounds near large blood vessels
Contraindications for Maggot’s Treatment
Vacuum Assisted Closure/Negative
Pressure Wound Therapy
Negative pressure wound therapy (NPWT) was originally
introduced in the form of wound vaccum assisted closure
(VAC) by kinetic concepts, Inc. (San Antonio, TX) in 1995.
This technology has been widely embraced in surgical
and surgical subspecialty arenas, and is used worldwide.
VAC therapy must be used as part of an individualized,
comprehensive treatment plan and is indicated for both acute
and chronic wounds.
Principle
The technology consists of computer-controlled application
of subatmospheric pressure to a wound via a reticulated
hydrophobic polyurethane or polyvinyl alcohol sponge under
an occlusive dressing, with subsequent removal of wound
exudate by an electromechanical pump. Recommended
Figure 5: Principle of VAC therapy
Figure 6: VAC machine
Indications for Maggot’s Treatment
S.No.
Proposed mechanism of action of Maggot therapy
1.
Actual ingestion of the tissue by the larvae
2.
Physical presence of the larvae increasing the exudate
from the host which washes out the bacteria
3.
Larvae secretion of proteolytic enzymes which liquefy
the necrotic tissue
4.
Secretions from the larvae changing the wound pH
5.
Larval secretions promoting healing
6.
Bacteria being destroyed in the larval alimentary tract
due to antibacterial substances
7.
The crawling action of the larvae stimulating granulation
tissue.

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187
to special computerized treatment unit with a plastic tubing.
This computerized treatment unit applies 125 mm Hg
negative pressure to wound which draws exudates, etc. into
a special canister attached to the unit. VAC therapy helps in
reducing edema, exudates and bacterial load and also helps
in regeneration of granulation tissue and neovascularization.15
The reader is advised to refer to the chapter on RNPT for more
details.
Autologel-Autologus Platelet
Rich Plasma Gel
This new modality for wound healing is based upon principle
of platelets containing components and properties for wound
healing and plasma containing fibrin matrix.

Procedure: Depending upon the size of ulcer, around 5 to
30 ml patient’s blood is centrifuged and platelet rich plasma
(PRP) is separated. This PRP is taken into a syringe having
different reagents [Thrombin (CaCl2) and Vitamin C], which
activate platelets and make gel consistency. This is known as
autologel. This gel like material is applied over wound twice
a week for 12 weeks and it was observed by Vickie R. Driver
et al that 68.4 percent of those wounds which were treated
with autologel healed in comparison to 42.9 percent of control
wounds.16
O2 Misly
In response to the need for more effective wound healing,
IYIA Technologies (IYIA Technologies, Inc.San Marcos,
California) developed the O2 Misly Wound Treatment System
(WTS) device for wound care.
Principle
O2 Misly delivers hyperoxia treatment to wound followed by
a humidmist, to which the physician can add his/her choice
of antibiotic therapies. The mist opens microcapillaries and
encourages blood flow, and the oxygen bath then encourages
blood vessel growth.

Adequate tissue oxygenation and hydration promotes
revascularization and collagen deposition. To aid in fighting
infections, anti-bacterial mist helps. It is used as an adjunctive
therapy to standard wound care.17 After cleaning and
debriding the wound patient puts his lower limb in a canister
of O2 Misly machine and wound is exposed to 4 cycles of 100
percent O2(5 min each) alternatively with vapor of water and
antibiotic (10 min each). This therapy is given twice a week
for 12 to 20 weeks. Ubbink DT et al found that in comparison
to standard wound care, proportion of healed wounds with use
of O2 Misly were 200 percent better at 12 to 20 weeks.18
Low Level Laser Therapy (Figure 7)
Laser is light amplification by stimulated emission of radiation.
There have been lot of medical indications of using laser and
one indication is nonhealing diabetic foot ulcer.
Mechanism of Action
Wound is exposed to low level laser therapy (LLLT)
which stimulates metabolic process. Low level laser
activates microcirculation and macrophages. By activating
microcirculation it helps in oxygen transport and more
drug molecules are brought to the tissue and by activating
macrophages it helps in killing microbes. Martinez-Sanchez
G et al found low level laser therapy very effective in healing
of chronic non-healing diabetic foot ulcer.19
Growth Factors
The term growth factor refers to a naturally occurring protein
capable of stimulating cellular proliferation and cellular
differentiation. There are different types of growth factors
which are involved in wound healing.
Growth Factors Involved in Wound Healing
United States FDA has so far approved only two types of
growth factors for use in chronic wounds.

They are platelet derived growth factor (PDGF) and
epidermal growth factor (EGF).

Most commonly used Plermin® (rh PDGF BB, recombinant
human platelet derived growth factor) has chemotactic, mito
Figure 7: Low level laser therapy (LLLT) unit

Types of Wounds and their Management
Section 3
188
Therapeutic Principles
Several therapeutic principles are made use of in HBOT as
discussed later in another chapter on HBOT.

However in case of diabetic foot ulcers, the therapeutic
principle of HBOT lies in its ability to drastically increase
partial pressure of oxygen in the tissues of the body. The oxygen
partial pressures achievable using HBOT are much higher than
those achievable while breathing pure oxygen at normobaric
conditions (i.e. at normal atmospheric pressure). A related effect
is the increased oxygen transport capacity of the blood. Under
normal atmospheric pressure, oxygen transport is limited by
the oxygen binding capacity of hemoglobin in red blood cells
and very little oxygen is transported by blood plasma. Because
the hemoglobin of the red blood cells is almost saturated with
oxygen under atmospheric pressure, this route of transport
cannot be exploited any further. Oxygen transport by plasma,
however is significantly increased using HBOT as the stimulus.

Patient is placed in monoplace/multiplace HBO chamber and
he breaths 100 percent oxygen under increased (2 to 3 times)
atmospheric pressure for 90 to 120 minutes. This increases
tissue oxygen tension, angiogenesis, fibroblast proliferation,
collagen deposition and enhanced bacterial killing.21-24 This
treatment is given for 5 days a week and a total of such 20 to 40
treatments are given depending upon size and severity of wound.
Improved wound healing and reduced rate of amputations were
observed in significant no. of cases of DFU by Stone JA et al.25
Disadvantages
Hyperbaric oxygen therapy is expensive. Although it may cost
up to 250 to 1000US $ per treatment in America but in metro
cities like Delhi it costs @ Rs.30,000/-to 40,000/- per 10
treatments. However, this expense should be viewed in light
of the total costs associated with therapeutic failure: the costs
for osteomyelitis, amputation, and subsequent rehabilitation.
S. No.
Growth factors
1.
Epidermal growth factor (EGF)—US FDA approved
2.
Platelet derived growth factor (PDGF)—US FDA
approved
3.
Hepatocyte growth factor (HGF)
4.
Vascular endothelial growth factor (VEGF)
5.
Fibroblast growth factor 1 and 2 (FGF 1, 2)
6.
Transforming growth factor-α (TGF-α)
7.
Transforming growth factor-β (TGF-β)
8.
Keratinocyte growth factor (KGF)
Figure 8: Ozone therapy
genic, angiogenic, and stimulatory effects and helps in wound
healing if used in noninfected superficial wounds.20
Ozone Treatment
Ozone is “active oxygen”. It is triatomic allotrope of oxygen
formed by recombination of oxygen atoms. It is a colorless
pungent-odor gas.
Mechanism of Action
It has been suggested that ozone can activate the antioxidant
system, influence the level of glycemic index and some
markers of endothelial cell damage, improve glycemic
control, prevent oxidative stress damage, normalize levels of
organic peroxides, and activate superoxide dismutase.19

Ozone disinfects, oxidizes, deodorizes and decolorizes.
Ozone is very strong oxidant and is found to be more than
3000 times powerful disinfectant than chlorine.
“Bagging”
Peripheral ozone therapy is very effective for badly-infected
and non-healing ulcers like chronic diabetic foot ulcers.
Technique of giving peripheral ozone therapy is known as
“Bagging”. That means after preparing the wound, limb is
covered with a plastic bag and a tube from ozone generator is
tightly secured in upper portion of bag. Wound is exposed to
ozone for 20 to 30 minutes.

Initially higher concentration (60–90 ug/ml) is used to control
infection and later on lower concentration (30–40 ug/ml) is used
for wound healing (Figure 8).
Hyperbaric Oxygen Therapy
Hyperbaric oxygen (HBO) therapy means exposing patient to
100 percent oxygen under increased atmospheric pressure.

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HBOT is no longer a new technology, yet its use even in
modern centers is uncommon at best. Costs and logistics seem
to be a continued impediment to patient access.
Bioengineered Alternative
Tissues
In recent years there is growing interest in human and animal
‘‘skin’’ products for the non-healing wounds in the lower
extremity. Bioengineered alternative tissue (BAT) products
promote the conversion of a stagnant wound to an acute
wound and are used in different wound types and at different
wound stages than an autogenous skin graft procedure.26
Categorization
Not all BAT products are the same. Each product has been
specifically designed to interact with the wound environment
in a unique way; however, some broad categories can assist in
the proper selection of a BAT product.

The first category is ‘‘living tissue’’. These products are
derived from living cell cultures which contain human living
keratinocytes or fibroblasts embedded within the product.
Generally, these products should be reserved for superficial
wounds. For example, apligraf, dermagraft, laser skin, epicel
and orcel.

The second category is ‘‘bioactive adjuncts.’’ These products
function as tissue scaffolds that allow for a supportive structural
environment for cellular ingrowth. They generally should
be used for deeper wounds in which the base of the wound
can be built-up. For example integra, oasis, gammagraft and
graftjacket. Sequential application of different BAT products
or repeated applications of the same product may be necessary
to ultimately close a wound. Only two most commonly used
BAT products in the living tissue category, i.e. apligraf and
dermagraft are being discussed in detail in this chapter.
Apligraf
Whenever size of wound is large and it is superficial and well
granulated, it needs skin grafting. Skin graft can be natural
skin grafts or bioengineered grafts. Apligraf is bioengineered
epidermis and dermisgraft, developed from foreskin of
newborn. Indication of using apligraf are chronic nonhealing
(non-infected) DFU26 or superficial venous ulcers.27
Dermagraft
Dermagraft is obtained from growing, living allogeneic
fibroblasts on a polyglactin mesh. Similar to apligraf, fibroblasts
are obtained from neonatal foreskin and after implantation,
remain viable and continue to secrete matrix proteins and growth
factors. The polyglactin mesh is biodegradable and is reabsorbed
after 3 to 4 weeks. Dermagraft has been reported to have positive
efficacy in healing wounds in the lower extremity.28,29
Metabolic Control
Controlling blood sugar and other general parameters
are equally important for comprehensive management of
chronic nonhealing diabetic foot ulcer. If wound is small and
superficial one can use oral hypoglycemic agents (OHAS) for
controlling blood sugar in type II DM. Patient should be put
on insulin if wound is large, infected, necrotic and patient
has septicemia, looks toxic and or has diabetic ketoacidosis.
DKA should be treated and hydration should be maintained.
Patients nutrition especially hypoproteinemia, needs to be
taken care of.
Vascular Control
In all patients of DFU all peripheral pulses need to be
palpated like dorsalis pedis, posterior tibial, popliteal and
femorals. If two or more than 2 arteries are impalpalpable
and or ABI(Ankle Brachial Index) is low, peripheral vascular
Doppler and angiography is required, if need arises.

If arterial occlusion is less than 10 cm, then different options
available are intra-arterial thrombolysis, endarterectomy and
angioplasty which can be conventional balloon angioplasty
with or without stents (Figure 9). Sub-intimal angioplasty,
lasers angioplasty and rotablaters for hard plaque.

If arterial occlusion is more than 10 cm then different
types of vascular grafts (natural or synthetic ) are applied to
bypass the occlusion and to achieve good circulation distal to
occlusion leading to healing of ulcer.
Mechanical Control—OffLoading
Offloading is the cornerstone of managing chronic non-healing
diabetic foot ulcer which is most of the time overlooked
by clinicians.30-32 Inspite of using different modalities of
treatment as mentioned above, if proper offloading of the
wound is not done, one will not be able to achieve ultimate
target that is complete healing of diabetic foot ulcer.
Mechanism of Action
Whenever we walk all of our body weight is transmitted to
earth through both of our feet and at the time of walking our
peak plantar pressure increases to 600 kilopascals. Purpose of
offloading the diabetic foot ulcer is to offload, i.e. to remove
away load of our body from the foot ulcer. TCC and other

Types of Wounds and their Management
Section 3
190
offloading methods reduce peak plantar pressures, increase
the surface area of the foot for forefoot and midfoot and
allows pedal ulcers to heal rapidly.

Depending upon site, size and severity of wound, patient
may be advised either complete bedrest or may be advised
using different offloading devices. It should be emphasized
to the patient not to bear weight until wound is completely
healed. Every step taken will delay the wound healing until
otherwise optimal offloading is instituted.

Different offloading devices could be crutches, wheel
chair, different types of offloading shoes, scotch cast boot,
removable cast walker (RCW) and air cast walker which is
the latest in the armamentarium.

Total contact cast (TCC) is just like applying plaster around
fracture of foot or leg. TCC can be made of Plaster of Paris
(POP) or fiberglass (Figure 10). Although best offloading is
achieved by TCC but it is cumbersome, time consuming and
needs expertise and one can not follow the growth of wound.
Most of these shortcomings of TCC can be overcome by using
ITCC, i.e. instant total contact cast which was developed by
Dr David G Armstrong, et al of Chicago.
Summary
Most common cause of hospitalization in diabetics is diabetic
foot problems. Since number of diabetics is increasing, hence
different complications related to diabetes are also increasing
including non-healing diabetic foot ulcers.

Minor ulcer can lead to amputation so one should be
cautious from the beginning. Newer and more advanced
techniques are now available for better wound care including
VAC therapy, hyperbaric oxygen therapy, growth factors,
bioengineered skin grafts, Maggot’s therapy, etc.

If diabetic foot ulcer is not improving one should refer the
case to podiatrist or specialist.

The holistic care of diabetic foot ulcer patients requires
a multidisciplinary team approach. Apart from blood sugar
control, treatment of ulcer involves debridement, offloading,
appropriate dressings, vascular maintenance and infection
control.
References
1. Reiber GE, Lipsky BA, Gibbons GW. The burden of diabetic
foot ulcers. Am J Surg. 1998;176(2A Suppl):5S-10S. 
2. Sibbald RG, Orsted HL, Coutts PM, Keast DH. Best practice
recommendations for preparing the wound bed: update
2006. Adv Skin Wound Care. 2007;20(7):390-405
3. Goldman RJ, Salcido R. More than one way to measure a
wound: an overview of tools and techniques. Adv Skin Wound
Care. 2002;15(5):236-43.
4. Jessup RL. What is the best method for assessing the rate of
wound healing? A comparison of 3 mathematical formulas. Adv
Skin Wound Care. 2006;19(3):138-46.
5. Benjamin A. Lipsky, Levin O’Neal’s. Textbook of “The
Diabetic Foot”, 6th edn. 2001. pp. 475-6.
6. McKenna, et al. Biochem J 1988;254:685-92.
7. Selkon JB, Cherry GW, Wison JM, Huges MA. Evaluation
of hypochlorous acid washes in the Tt. of Ch. Venous Ulcers.
J Wound Care. 2006;15:33-37.
8. Martin E. Wendelken, et al. A closer look at ultrasonic
Debridement,Volume23-issue8-August 2010.
9. Granick MS, et al. “Efficacy and cost-effectiveness of a high-
powered parallel waterjet  for wound debridement”. Wound
Repair and Regeneration. 2006;14:394-7.
10. Cubison CS, et al. “Dermal preservation using the Versajet.
Hydrosurgery system for debridement of pediatric burns”.
Burns. 2006;32:714-20.
11. Mosti G, et al. “The debridement of chronic leg ulcers by means
of a new, Fluidjet - Based Device”. Wounds. 2006;18:227-37.
Figure 9: Balloon angioplasty with stent placement
for arterial occlusion
Figure 10: Different types of offloading shoes

Recent Advances in Management of Chronic Non-healing Diabetic Foot Ulcers 
Chapter 18
191
12. Weil GC, Simon RJ, Sweadner WR. A Biological,
Bacteriological and Clinical Study of Larval or Maggot
Therapy in the Treatment of Acute and Chronic Pyogenic
Infections. American Journal of Surgery. 1933;19(1):36-48.
13. Sherman RA. Cohort study of maggot therapy for treating
diabetic foot ulcers. Diabetes Care. 2003;26(2):446-51.
14. Zgonis T, Stapleton JJ, Girard-Powell VA, et al. Surgical
management of diabetic foot infections and amputations.
AORN. 2008;87(5):935-46.
15. Morykwas MJ, et al. Stat of basic research and physiologic
foundation, plastic and Reconstructive Surgery. 1117
Supplement:121S-126, 2006.
16. Vickie R Driver, Jason Hanft, Carelyn P. Fylling Judy m
Beriou. Autologel Diabetic Foot Ulcer Study Group,Ostomy/
Wound Management 2006;52:68-87
17. Adrian Pelkus. Foot ulcers succumb to a new healing system.
Diabetes Health.com, June/July 2007.
18. Ubbink DT, Vermeulen H, Lubbers MJ. Local wound care:
evidence based treatments and dressings. Ned Tijdscher
Geneeskd. 2006;150:1165-72.
19. Martinez-Sanchez G, Al-Dalain SM, Menendez S, Re L,
Giuliani A, Candelario-Jalil E, Alvarez H, Fernandez-M.
Therapeutic efficacy of ozone in patients with diabetic foot.
Eur J Pharmacol. 2005;523:151-61.
20. David L. Steed MD. The Diabetic Ulcer Study Group and from
the University of Pittsburgh, Presbyterian University Hospital,
Pittsburgh. Journal of Vascular Surgery. 1995;21:71-81.
21. Cianci P, Hunt TK. Adjunctive hyperbaric oxygen therapy in
treatment of diabetic foot wounds. In: Levin ME, O’Neal LW,
Bowker JH, (Eds). The Diabetic Foot. 5th edn. St Louis, Mo:
Mosby-Year Book; 1993.
22. Abidia A, Laden G, Kuhan G, et al. The role of hyperbaric
oxygen therapy in ischaemic diabetic lower extremity ulcers: a
double-blind randomised-controlled trial. Eur J Vasc Endovasc
Surg. 2003;25(6):513-8. 
23. Kalani M, Jörneskog G, Naderi N, Lind F, Brismar K (2002).
“Hyperbaric oxygen (HBO) therapy in treatment of diabetic foot
ulcers. Long-term follow-up”.  J. Diabetes Complicat.  16  (2):
153-158. doi:10.1016/S1056-8727(01)00182-9 PMID12039398
24. Morrey BF, Dunn JM, Heimbach RD, Davis J. Hyperbaric
oxygen and chronic osteomyelitis. Clin Orthop. 1979;144:121-7.
25. Stone JA. HBO Rx facilitates healing of chronic foot ulcers in
patients with diabetes. Diabetes Care. 2010;33(5):998-1000.
26. Attinger CE, et al. Clinical approach to wounds: debridement and
wound bed preparation including the use of dressings and wound-
healing adjuvants. Plast Reconstr Surg. 2006;117 (Suppl.):72S.
27. Alvarez OM, Fahey CB, Auletta MJ, Fernandez-Obregon
A.  A novel treatment for venous leg ulcers.  J Foot Ankle
Surg. 1998;37(4):319-24.
28. Hanft JR, Surprenant MS. Healing of chronic foot ulcers in
diabetic patients treated with a human fibroblast-derived
dermis. J Foot Ankle Surg. 2002;41(5):291-9.
29. Newton DJ, Khan F, Belch JJF, et al. Blood flow changes in
diabetic foot ulcers treated with dermal replacement therapy. J
Foot Ankle Surg. 2002;41(4):233-7.
30. Nick Martin, et al. A guide to offloading, the diabetic foot.
Podiatry Today. 2005;18(9):74.
31. David G Armstrong. Offloading the diabetic foot wound, a
randomized clinical trial. Diabetes Care. 2001;24(6):1019-22.
32. David G Armstrong, Stephanie Wu. Offloading the diabetic
foot wound, clinical care of diabetic foot, ADA Publication.
2005. pp. 52-60.

• Definition
• Classification of Leg Ulcers

– Arterial Ulcers

– Venous Ulcers
• Clinical Presentation

– Arterial Ulcers

– Venous Ulcers

– Mixed Ulcers
• Diagnosis
• Management of Chronic Leg Ulcers

– Tissue Management

– Infection Offloading

– Moisture

– Edge of Wounds

– VAC
• Surgery

– Venous Ulcers

– Arterial Ulcer Management
Introduction
Wound healing practices have been recorded from the time of
Smith Papyrus in 1700 BC. Vascular ulcer or wounds of the
nontraumatic variety are chronic and their far reaching effects
are a challenge for both the patient and the practitioner who
attempts their care and management and is augmented by a
paucity of evidence based treatment strategies.

Vascular ulcer care is one of the most unglamorous aspect
of vascular surgery, but, the morbidity and costs to the patient
along with psychological implications are too enormous to be
overlooked. The mixture of advancing life span leading to older
age group patients, increasing weight and prevalence of diabetes
and venous insufficiency due to altered lifestyle habits have led to
an increase in these chronic debilitating wounds who have been
inadequately treated over protracted courses. An attempt has
been made to outline the current concepts concerning treatment
of chronic wounds focusing on fundamental treatment principals
for management of arterial, venous, and mixed wound.
DEFINITION
Chronic wounds are defined as wounds, which have failed
to achieve anatomic and functional integrity over a period of
three months.1

The most commonly encountered chronic wound is the lower
extremity ulcer: these are generally vascular or diabetic in nature
and account for up to 98 percent of all lower extremity wound.2
CLASSIFICATION OF LEG ULCERS

1. Arterial

2. Venous

3. Vasculitic

4. Neoplastic

5. Neuropathic

6. Mixed.
This chapter deals with only arterial and venous ulcers.
Arterial Ulcers
Arterial ulcers are ischemic ulcers developing due
to either progressive or sudden interruption of blood
supply to the tissues and skin leading to ulceration. The
progressive atherosclerotic disease leads to thickening of
the endothelium with endothelial dysfunction. This leads
to decreased nutrient transfer, leukocyte trapping and
activation, resulting in both hypoxic as well as leukocyte
activation cascade injury to the tissues leading to their
breakdown and ulceration.
Vascular Ulcers
Rajiv Parakh, Anurag Agarwal
19
Chapter

Vascular Ulcers 
Chapter 19
193
Venous Ulcers
The pathogenesis of venous ulcers is complex and multi-
factorial. The various factors that are indicated work either
alone or in synergy with others. Venous stasis, however, is the
main factor leading to the overall cascade of event which lead
to venous ulceration.

a. Venous HTN: Sustained elevation of ambulatory venous
pressure due to either valvular dysfunction or calf
muscle pump weakness.3-5

b. Leukocyte trapping and activation: Leads to release
of proteolytic enzymes and of free radicals leading to
tissue damage.6,7 Release of cytokinines (TNF, IL-1)
and leukotrienes8 with margination of WBC leads to
oxygen deprivation9 and thus leads to ulceration.

c. Fibrin cuff: Fibrinogen leaking into dermis leads to
the formation of fibrin cuff by fibrin deposition around
dermal vessels.9 This cuff further acts as a barrier to
oxygen and nutrients which leads to ulceration.10,11

d. AV shunting: One recent hypothesis is of AV shunting
in venous disorders which leads to venous ulcers.12 This
theory is supported by presence of increased oxygen
saturation in venous blood, premature venous filling with
increased cutaneous blood flow on angiography, but,
decreased capillary density in cutaneous vasculature.

e. Miscellaneous: Varicose studies have shown a relation­
ship between obesity, chronic venous insufficiency (CVI)
and popliteal venous compression. This may be the
underlying cause of previously unexplainable incidence
of venous ulcer presentation.
CLINICAL PRESENTATION
Vascular leg ulcers typically manifest as arterial, venous or
mixed variety.
Arterial Ulcers (Figures 1A and B)
Patients usually present with complaints of a painful nonhealing
ulcer on dorsum of foot or toes and the pain characteristically
increases at night and is relieved by dependency. Most of the
signs and symptoms of chronic limb ischemia are present, like
pale shiny skin, loss of hair and absent pulses. The ulcers have
initially an irregular edge which progresses to a well defined
punched out appearance, base contains grayish unhealthy
granulation tissue that bleeds very little or not at all on curettage
or debridement and may deepen to bare tendons/bones.
Venous Ulcers (Figures 2 and 3)
Patients usually give a history of heaviness in leg by
evening and may have characteristic varicosities, swelling
Figures 1A and B: Arterial ulcer
Figure 2: Venous ulcer gaiter area
A
B
and venous dermatitis. These ulcers are commonly noted in
“gaiter” region of legs—located circumferentially around
the lower leg from approximately mid calf to just below
medial and lateral malleolus. These ulcers are larger but

Types of Wounds and their Management
Section 3
194
shallower than other ulcers. All venous stasis ulcers have a
moist granulating base, irregular border and oozes venous
blood when handled. Surrounding skin has signs of venous
dermatitis. Mild pain is relieved by elevation. They may
be multiple or single and if left untreated, may involve the
entire circumference.
Mixed Ulcers (Figure 4)
Clinically, the history has components from arterial, venous
and diabetic infection leading to ulceration. They are difficult
to heal due to associated edema, cellulitis and thrombophlebitis
along with the underlying cause of diabetes without vascular
disease.
DIAGNOSIS
All patients with a leg ulcer should be examined for arterial
disease. Despite their characteristic location and appearance,
a detailed clinical examination to identify and distinguish an
arterial from venous ulceration cannot be over emphasized.
The key to successful healing begins with the accurate
identification of the etiology of the disease.

The usual protocol is to take a detailed history including
initiating factors, medical history, past history and ulcer
treatment history. This is followed by a complete clinical
examination of the peripheral pulses, presence of varicose
veins or venous insufficiency and to note any evidence of
neurological deficits or connective tissue disorders.

Thereafter, a complete blood count, ankle-brachial
pressure index (ABI), postocclusive reactive hyperemia
(PORH), transcutaneous partial pressure of oxygen (TcPO2)
and a complete biochemical profile is done. Depending on the
results, a duplex evaluation (arterial/venous) is the first and
best noninvasive investigation carried out and gives maximum
primary information regarding the disease and the further
course of action. Arterial ulcers may further necessitate the
need for a CT/MR angiography or a conventional angiography
to diagnose and treat the vascular deficit, which is the cause of
the ulceration. A radionuclide venography may be indicated to
assess a post-thrombotic limb for recanalization.

Radiographs, bone scans and bone biopsy are indicated if
osteomyelitis of the underlying bone is suspected.
MANAGEMENT OF CHRONIC LEG ULCERS
The management of vascular ulcers can be divided into general
and specific treatment options/guidelines (Flow chart 1).
Whatever the etiology of the ulcer, general wound management
principals exist for a wide variety of chronic wounds.1 The
TIME acronym promoted by wound healing society is a simple
and comprehensive method for defining and addressing the
principal elements associated with impaired wound healing.13
T–Tissue, I–Inflammation/Infection, M–Moisture Balance,
E–Edge.
Tissue Management
The first step is to remove the local impediments to wound
healing by removal of devascularized tissue, necrotic material
and excessive bacterial burden.13 This involves a thorough yet
judicious debridement preserving vital tissues and ridding the
accumulated impediments.

Numerous modalities are present and include chemical
agents, sharp surgical instrument, mechanical devices – curette,
ultrasonic curettage, enzymes–collagenase and papain urea
derivatives, autolytic debridement dressings like hydrocolloid,
occlusive dressing . Sharp debridement is preferred in venous
Figure 3: Venous ulcer
Figure 4: Mixed ulcers

Vascular Ulcers 
Chapter 19
195
ulcers whereas radical debridement in arterial insufficiency
should be performed only after revascularization.
Infection Offloading
Decreasing bio burden to subinfection levels facilitates control
of local and systemic inflammatory mediators. A culture
sensitivity is essential to guide appropriate therapy.14 Surgical
debridement and topical antibiotics are effective in local
control. Systemic antibiotics are of minimal use in granulating
wounds.15 Use of silver containing dressing has increased
but randomized control trials do not demonstrate significant
increase in healing.16

Ultrasonic wound debridement is a new technique that
involves removal of biofilm by an ultrasonic probe and is
an economical, relatively painless procedure that is done
on an out-patient basis and promotes wound healing rates
(Figures 5 and 6).
Flow chart 1: Algorithm for management of chronic by ulcers (Source: Eplasty 2009 open surgery)

Types of Wounds and their Management
Section 3
196
Moisture
Maintenance of a moist but not macerated environment is
accepted as the best topical environment for open wounds.
Edge of Wounds
Wound healing progress and the condition of the wound
should be regularly monitored. An appropriate therapeutic
response should demonstrate a decrease in ulcer size. Surgical
procedures can be done for providing definitive closure or
treating underlying cause. Exposed functional elements like
tendons, bone or neurovascular structures prompt urgent
surgical intervention. No definite evidence exists that supports
decrease in healing times for venous ulcer treatment by skin
grafts. Free flap reconstruction after thorough excision,
debridement and bacterial control has shown to accelerate
healing17 only if no vascular compromise is present.
Figure 5: Pre-USG debridement
Figure 6: Post-USG debridement
Figure 7: Pre-VAC wound
Figure 8: Post-VAC 2 weeks
Vaccum Assisted Closure (VAC)
It is an innovative technique using negative pressure for closure
of chronic wounds. It consists of placing an open-cell foam
dressing into the wound cavity and applying controlled pressure
(usually 125 mm Hg below ambient pressure). VAC helps by
removing chronic edema and increasing localized blood flow
thereby resulting in enhanced formation of granulation tissue.
A few small studies have suggested the superiority of VAC to
saline gauze dressings18 and VAC maybe used as an adjunct
treatment modality (Figures 7 to 9).
Surgery
Surgery has its place in two specific conditions:

1. Correction of arterial insufficiency/venous hypertension

a. Open bypass of diseased occluded/stenosed arteries

b. Endovascular
reconstruction-angioplasty
and/or
stenting

Vascular Ulcers 
Chapter 19
197

c. Varicose veins and perforator incompetence surgery,
e.g. Endovenous laser ablation therapy (EVLT) and
Radio-frequency ablation (RF Ablation Therapy)

d. Ultrasound guided foam sclerotherapy for superficial
varicosities

2. Treatment of ulcer per se

a. Debridement

b. Skin grafting

c. Free flap coverage.
Predictive factors for wound healing:

1. Duration

2. Size

3. Fibrinous bed

4. Lipodermatosclerosis

5. Venous ring

6. Total knee replacement, total hip replacement

7. ABI <0.8.
Venous Ulcers
These ulcers should be debrided of necrotic and fibrinous
material to allow a healthy granulation tissue to develop.

In the absence of apparent local infection antibiotics have
little role to play. Low concentration iodine and hydrogen
peroxide can be used as debriding agents.19 Moist saline gauze
are used for initial management, but, moisture retentive dressings
are preferred. Moisture retentive dressings help debride necrotic
tissue, relieve pain and reduce the frequency of dressing change
and are cost effective. Limb elevation over at least 45 degree (or
above heart level) is advocated to venous insufficiency patient
along with advise to avoid prolonged standing.

The main stay in venous ulcer management is compression
therapy. Aim is to achieve an external pressure between
30 to 40 mm Hg at the ankle to prevent capillary transudate.
However, an ABI of 0.8 or more is essential for safely applying
the compression. The healing rate depends on ulcer size but 65
to 70 percent heal in six months. Five year recurrence of healed
ulcer can be as high as 40 percent. Surgery for varicose veins
may be beneficial, cumulative and may prevent recurrence.

Ulcer recurrence can be prevented by graduated elastic
stockings.

Compression stockings are the main stay for chronic
venous ulcer treatment. The aim is to increase healing by
improving venous return and reducing edema in the area.20,21
A number of compression dressings are available viz. Elastic,
non elastic, single or multilayered systems and compression
stockings. Elastic compression dressings maintain pressure
during working and resting phases. Elastic stockings are
contraindicated in arterial disease as they may further
decrease flow by compressing the diseased arteries. Single and
multilayer systems exert their action by delivering constant
compression or graded pressures respectively. Thereby, they
decrease edema and increase venous return with possible
reversal of venous hypertension and thus promote healing.
Drugs like pentoxyphilline and micronized purified flavonoid
fractions (Daflon) or calcium dobesilate (OSIL/DOBESIL)
are used to increase venous tone and thus decrease venous
stasis. Antiplatelet agents like aspirin, clopidogrel are used as
adjunctive and supportive therapies.
Arterial Ulcer Management
In daily wound care, sharp debridement is not recommended
and compression is contraindicated. The main stay of treatment
is surgical with aim being towards restoring blood supply. An
optimal control of associated factors such as hyperlipidemia,
hypertension and cessation of smoking along with exercise
program is included in management plan.

Apart from the general principles of wound management
as detailed above, certain specific modalities are detailed
below.
Cilastazol: Used for intermittent claudication but not for
ulcer treatment. However, it helps improve pain free walking
distance and thus exercise program.
Anticoagulants
Anticoagulants like warfarin and heparin/LMWH are used to
increase collateral circulation and prevent thrombus formation
in diseased vessels.
Antiplatelet Agents
Asprin is the most commonly used agent along with
clopidogrel.
Figure 9: VAC machine

Types of Wounds and their Management
Section 3
198

Antiviscosity agents like pentoxyphilline have a limited
role.
Antihyperlipidemic Agents
Statins are used and have a role in reducing plaque formations.
Hyperbaric Oxygen (HBO)
Its main indication are in diabetic foot and arterial insufficiency
treatment. Hundred percent O2 at 2 to 3 times atmospheric
pressure at sea levels can result in arterial oxygen tension in
excess of 2000 mm Hg and arterial oxygen tension in tissues
of almost 400 mm Hg. HBO treatment for 90 to 120 min are
used. However, it is expensive and unnecessary in simple well
perfused wounds. It is best used in hypoxic or ischemic wound.
Conclusion
Vascular ulcer treatment is a taxing and challenging aspect of
vascular surgery. The main stay of treatment depends on a good
history, clinical evaluation coupled with accurate diagnosis
via the various modalities and initiation and maintenance of
the treatment specific to the etiology of the disease.

Care should be given by well trained caregivers and should
be judicious and with patience. Strict adherence to the principles
of wound management is essential to achieve successful wound
healing without recurrence. Our patients deserve optimum
healing at affordable costs using readily available options to
treat, avoid complications and prevent recurrences.
references
1. Mustoe TA, O’Shaugnessy K, Kloeters O. Chronic wound
pathogenesis and current treatment strategies: a unifying
hypothesis. J Plast Reconstr Surg. 2006;117:35-41.
2. Wound healing society. Guidelines for the best care of chronic
wounds. Wound Repair Regen. 2006;14:647-710.
3. Welch HJ, Young CM, Semegran AB, et al. Duplex assessment of
venous reflux and chronic venous insufficiency: the significance
of deep venous reflux. J Vasc Surg. 1996;24:755-62.
4. White JV, Katz ML, Cisek P, Kreithen J. Venous outflow of the
leg: anatomy and physiologic mechanism of the plantar venous
plexus. J Vasc Surg. 1996;24:819-24.
5. Norgren L. Chronic venous insufficiency—a well known
disorder with many question marks. Angiology. 1997;48:23-6.
6. Kirsner RS, Eaglstein WH, Kerdel FA. Split-thickness skin
grafting for lower extremity ulceration. Dermatol Surg. 1997;
23:85-91.
7. Coleridge Smith PD, Scurr JH, Dormandy JA. Causes of venous
ulceration: a new hypothesis. Br Med J. 1988;296:1693-727.
8. Scott HJ, Coleridge Smith PD, Scurr JH. Histologic study of
white blood cells and their association with lipodermatosclerosis
and venous ulceration. Br J Surg. 1991;78:210-1.
9. Browse NL, Burnand KG. The cause of venous ulceration.
Lancet. 1982;ii:243-54.
10. Chaetle TR, Scott HJ, Scurr JH, Coleridge Smith PD. White
cells, skin blood flow and venous ulcers. Br J Dermatol.
1991;125:288-90.
11. Scott TE, LaMorte WW, Gorin DR, Menzoian JO. Risk factors
for chronic venous insufficiency: a dual case-control study. J
Vasc Surg. 1995;22:622-8.
12. Malanin K. About the pathophysiology of venous leg ulcera­
tion. JAAD. 2002;47:157-8.
13. Ayello EA, Dowsett C, Schultz GS, et al. TIME heals all
wounds. Nursing. 2004;34:26-41.
14. Sibbald RG, Williamson D, Orsted HL. Preparing the wound
bed-debridement, bacterial balance and moisture balance.
Ostomy/Wound Manage. 2000;46:14-35.
15. Diehr S, Hamp A, Jamieson B. Do topical antibiotics improve
wound healing? J Fam Pract. 2007;56:140-4.
16. Vermeulen H, van Hattem JM, Storm-Versloot MN, Ubbink
DT. Topical silver for treating infected wounds. Cochrane
Database Syst Rev. 2007;24(1):CD005486.
17. Kumins NH, Weinzweig N, Schulter JJ. Free tissue transfer
provides durable treatment for large nonhealing venous ulcers.
J Vasc Surg. 2000;32:848-54.
18. Evans D, Land L. Topical negative pressure for treating chronic
wounds. Cochrane Wounds Group. Issue 1. 2001. Date of Most
Recent Update: 28-11-2000.
19. McKenna PJ, Lehr GS, Leist P, Welling RE. Antiseptic
effectiveness with fibroblast preservation. Ann Plast Surg.
1991;27(3):265-8.
20. Kramer SA. Compression wraps for venous ulcer healing: a
review. J Vasc Nurs. 1999;17:89-97.
21. Cherry GW, Hoffman D, Cameron J, Poore SM. Bandaging
in the treatment of venous ulcers: an European view. Ostomy
Wound Manage. 1996;42:13S-18S.

• Pathogenesis
• Histopathology
• Classification
• Clinical Manifestation
• Management
INTRODUCTION
Vasculitis means inflammation of blood vessels within the
body and it presents on the surface of skin with a variety of
physical signs. The various types of vasculitis, their clinical
manifestations and classification is based on the common
problem affecting different layers of vessel wall. The role of
neutrophils, lymphocytes and the granulomatous processes
in the evolution of the disease further explains the reasons
for delayed healing and thus contributing to chronicity and
recurrences. The various syndromes manifest as cutaneous
signs of a number of different underlying conditions triggered
by a variety of etiological agents and modified by the host, who,
because of their own individuality behave idiosyncratically
which makes the diagnosis of these conditions difficult.
Etiology
The various conditions leading to the inflammation of blood
vessels in the body can be elicited as follows:
1. Infections

– Bacteria (Meningococcus, M. leprae)

– Viruses (Varicella zoster)

– Rickettsia

– Fungi (Aspergillus, Mucor)
2. Connective tissue/autoimmune disorders

– Primary—small and medium vessel, e.g. rheumatoid
arthritis, SLE, cryoglobulinemia, Sjögren’s, infla­
mmatory myopathies.
3. Drugs

a. NSAIDs

– Aspirin, Phenylbutazone, Cox inhibitors

b. Antibiotics

– Fluoroquinolones, ampicillin, erythromycin, sulfon­
amides

c. Antihypertensives

– ACE inhibitors, hydralazine

d. Diuretics

– Furesamide, thiazides

e. Antiepileptic

– Carbamazepine, phenytoin

f. Rheumatological

– Allopurinol, methotrexate, sulfasalazine
4. Miscellaneous

Radiocontrast, vaccines, azathoprine, malignancies, irrita­
ble bowel disease, antitumor necrosis factor.
PATHOGENESIS
Vascular manifestations in many diseases show identical
pictures which makes differentiation difficult. The most
common findings are leukocytic infiltration and areas of
necrosis in all layer of blood vessels which are severely
disrupted by the deposition of “fibrinoid”, a mixture of fibrin
degradation product and other proteins.1

There are various triggering factors for the disease process.
Such triggers include direct injury to endothelium by viruses
and bacteria as well as the activation of complement system
Vasculitic Ulcer
Rakesh Kain
20
Chapter

Types of Wounds and their Management
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200
by immune complexes, leukotrienes and fibrin degradation
products. The role of oxygen free radicals has also been
established. In vasculitis following injury to the blood vessel,
it leaks and since the endothelial lining is damaged at various
levels, such a vessel is vulnerable to subsequent injury and
it readily collects more immune complexes and is unable
to clear fibrin. This complex mechanism involves type III
hypersensitivity reaction which is immune complex mediated
like autoantibodies/foreign antigens. Other mechanisms
involved are IgM/IgG mediated compliment activation with
release of inflammatory mediators like cytokines which are
responsible for cell wall destruction.

Immune mechanism may occur through the action of
complement protein or through nonspecific receptors (non-
specific or innate immunity) or it may proceed through
the engagement of highly specific receptors or T and B
lymphocytes (e.g. specific immunity).

The T and B-lymphocytes generate their effect through
use of gene segment for variable extent of development of
cellular and humoral immunity. The CD4 and CD8 cells
bear receptors that recognize peptide fragments of antigens
embedded in MHC molecule. Protein antigens are engulfed
to form a phagolysosome in which degradation to peptide
occurs with the help of proteolytic enzymes. The adhesion of
lymphocytes to the surface of the endothelial cells is the first
step during inflammation which is increased in the presence of
cytokines –IL-1 and tumor necrosis factor.2

Breakdown of normal immune response is discussed in
term of hypersensitivity like anaphylactic reaction, antibody
mediated cytotoxic hypersensitivity, and immune complex
mediated hypersensitivity and delayed type hypersensitivity.
In an overview, the immune system protects against infection
by recognizing microorganism whether they are from outside
the body or from hosts own body and disposing them off.3
Disorder in this process may lead to pathologic autoimmunity.

Other type of hypersensitivity reactions associated with
vessel wall destruction are:
1.
Type I–Churg-Strauss
syndrome (CSS)
(↑IgE, Eosinophilia)
2.
Type II–Wegener’s
granulomatosis (WG),
microscopic polyangiitis
(MPA)
(Antibody, Antineutrophil
cytoplasmic antibody)
3.
Type III–Kawasaki
disease (KD)
(Lymphocytic infiltration)

Type II and Type III are the most common mechanisms.

Vasculitis typically affects the 50-400 mm vessels of the
vasanervosum, leading to randomly distributed ischemia
along the course of nerve. This in turn leads to a distinctive
picture of multiple mononeuropathy as a frequent but not
invariable clinical consequence of vasculitis. The diagnosis of
vasculitic neuropathy is usually made by biopsy or histological
confirmation.
Histopathology
At the site of inflammation capillaries proliferate and venules
thicken to resemble arteries. A thick walled vessel infiltrated
by white cells may be assumed to be a vein or lymphatics
and deeper vessels tend to hypertrophied due to gravitational
stasis.

In capillaries—there is reduction of diameter but they are
often dilated in foot venules in leg which leads to skin changes
and ulcer formation because of associated gravitationally
induced venous pathology.4

Lymphatics—there is increase plexus of lymphatics in
dermis. The characteristic features are presence of valve
and elastin fibers in the vessel wall. Fibrosclerosis of wall of
lymphatics is not uncommon in the lower limb. Inflammation
of such vessels may be mistakenly labelled as vasculitis or
even arteritis. Such vessels are found at dermoepidermal
junction and participate in nodular vasculitis.

Arteries—show
fibrinoid
changes
without
cellular
infiltration of vessel wall. They have several layers of muscles
cells and an internal elastic lamina which becomes wavy.
Terminal arteriole and venule have no internal elastic lamina,
with irregular layer of ill differentiated perivascular cells
surrounding the endothelium. Smooth muscle layer in media
is very sensitive to ischemia within two hours of anoxia.

Red cell are widely dispersed and islands of red cells
scattered through out the inflamed area. Mast cell deposition
is also noticed around vessels. Neutrophils aggregation is the
prominent feature of vasculitis. The leukocyte migration is
enhanced by cytokine A and B and it has been identified that
chromosome 4 is responsible for A and chromosome 17 for B.5

In allergic granulomatosis, the predominant infiltration is
by eosinophils. They are usually found early and attacked by
antigen antibody complexes.

Platelets adhere to endothelium with release of vasoactive
agents that influence all aspects of endothelial and smooth cell
behavior.

Granuloma formation is a late feature which includes
histiocytes and giant cells. Giant cells represent a reduction of
the phagocytic potential of a tissue. Incomplete degradation
of antigen due to hypoxia or excess antibody is one cause of
granulomas.

Renal lesions are found in various forms of systemic
vasculitis. The microscopic form of periarteritis nodosa
involves small vessels vasculitis and immunofluorescence
may reveal the deposition of IgG and IgM by C3.6

Vasculitic Ulcer 
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201

The vasculopathic reaction pattern includes a clinically
heterogeneous group of diseases, which have in common the
pathological changes in blood vessels. The important features
of this reaction are: (1) Perivascular infiltrate, (2) Presence
of fibrin, (3) Presence of endothelial swelling, (4) Increased
fibrohistiolytic cells and acid mucopolysaccharide in dermis.

Some dermatopathologist insist on the presence of fibrin
within the cell and vessel wall and consider it as an essential
feature for diagnosis, because similar feature of perivascular
infiltrate of inflammatory cell may resolve in the wall of the
vessels and also show extravasations of fiber.
CLASSIFICATION
Classification of primary vasculitis is made on the basis of
size of vessel involved as given in Table 1.
Types of Vasculitis
1. Chronic lymphocytic vasculitis
2. Leukocytoclastic (hypersensitivity) vasculitis
3. Leukemic vasculitis
4. Vasculitis in granulomatosis
5. Wegener’s granulomatosis
6. Giant cell (temporal arteritis).
CLINICAL MANIFESTATION
Patient presents with single or multiple painful ulcers with
variable degree of infection depending upon immunity
status. Involvement of small vessels leads to superficial
ulcers while that of medium vessels leads to deep ulcers.
Healing is from periphery and scab formation is a
constant feature of cutaneous panarteritis nodosa (Figures
1A to D). While in connective tissue disorder related
RA (CTDS-RA) the edges of ulcers are punched out
(Figures 2A to E). In Wegener’s granulomatosis and Churg-
Strauss syndrome the lesions are papulonecrotic type
predominantly over extensor surfaces of leg and forearm and
they can be differentiated from rheumatoid nodules where no
ulceration forms.

Vasculitis affects small vessels such as capillaries, arteries
of limbs, medium size renal, coronary and hepatic arteries
or even large vessels like aorta. Patients normally present
with fever, fatigue, weight loss, muscle and joint pain, loss
of appetite, neuralgia, etc. Sometimes associated features
with various syndromes like Behçet’s syndrome present with
genital ulcers, eye inflammation and acne like skin eruptions
(Figures 3A to C).

Presentation of Churg-Strauss syndrome also known as
allergic granulomatous disorder affect the pulmonary vessels
and therefore leads to respiratory problems. Giant cell arthritis
is associated with weakness and neuropathy. The temporal
artery vasculitis is most frequently associated with visual loss.7

Cryoglobulinemia may be associated with rashes over skin
of lower limb.

The frequent involvement of the coronary arteries with
atherosclerosis is also of concern. Arterial ulcers often affect
the toes or shin or occur over pressure points. Arterial ulcers
are often seen in elderly. These patients often present with a
history of intermittent claudication or a rest pain, which is
usually relieved by dependent position. Some patients report
that in order to ease the pain in their limbs they have to sit on
the edge of the bed and dangle their legs. Skin appearance as
dark and shiny with hair fall is the most common progression
of disease. The patient medical history is often positive
for smoking and other risk factors for atherosclerosis like
hypertension, hyperlipidemia, and diabetes. A history of minor
trauma to the leg initiating the ulcer is frequently reported.

Vasculitic ulcers: Vasculitic ulcers are related to numerous
underlying
etiologies
including
autoimmune
disease,
rheumatoid arthritis and other inflammatory conditions. Leg
Table 1: Classification of vasculitis as per size of vessels
Large size vessels
Medium size vessels
Small size vessels
Takayasu’s
Gaint cell arteritis (GCA)
Cogan’s disease
Behcet’s disease
Polyarteritis nodosa
Cutaneous PAN
Buerger’s
Kawasaki
Primary CNS angiitis
Immune complex
Goodpasture’s
Cut. LCA
HSP
Urticarial vasculitis
Ess. Cryoglobulinemia
Antineutrophil cytoplasm antibodies (ANCAs)
Associated vasculitis
Wegener’s granulomatosis
Microscopic polyangiitis
Churg-Strauss syndrome
Renal vasculitis

Types of Wounds and their Management
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202
ulcers are the recognized manifestation of cutaneous vasculitis
in connective tissue diseases (CTDs) including rheumatoid
arthritis (RH). Since the potential cause for an acute focal
deficit are numerous, therefore a detailed history and physical
examination is required to determine the nature of defect.

A typical vasculitic ulcer is deep and has circular or
well-demarcated “punched out” margins. The ulcer base is
covered with a black, dry necrotic material with minimal
or poor granulation tissue (Figures 2A to D). Other findings
include weak or absent peripheral pulses, dependent rubor and
elevational pallor of the foot, and thickened nails. The skin
of the affected leg is often shiny, atrophic, dry, and cold to
the touch. Examination of the leg should include palpation
of pulses, and determination of range of hip, knee, and ankle
movements. Involvement of these articulations with an
inflammatory process may explain the pain, which should
be differentiated from pain caused by arterial insufficiency.
Reduced mobility because of arthritis is a factor that is known
to prevent healing of ulcers.

The physical examination should include a careful cardiac
evaluation to detect vascular disease.

IgE autoantibody however has been found in autoimmune
disease and although there is no proof that they mediate any
autoimmune disease but may be found in case of vasculitis8
where there is development of mononeuropathy and polyneu­
ropathy.

The characteristic of ulcer is a painful inflammatory lesion
with variable extent of necrosis. To arrive at the diagnosis,
the clinician must perform a thorough history and physical
examination, and order relevant investigative studies. Unusual
causes of leg ulcers must be considered in the differential
diagnosis. Good management of chronic leg ulcers depends
Figures 1A to D: (A) Typical appearance of vasculitic lesion in PAN; (B) Close up view of the same lesion in lower leg; (C) Appearance
of vasculitic lesion over calf; (D) Lesions healed after treatment with rituximab (Photo courtesy: Dr Lalit Duggal, Consultant, Ganga Ram
Hospital, New Delhi, India)
A
B
C
D

Vasculitic Ulcer 
Chapter 20
203
on correction of identified underlying conditions, long-term
multidisciplinary care effort, and integrating traditional and
new wound-healing technologies.
A
C
Figures 2A to E: (A) Vasculitis in case of inflammatory arthritis;
(B) Vasculitic lesions over thighs; (C and D) Vasculitis involving upper
limb; (E) Vasculitic ulcers resolving after treatment with steroids
(Photo courtesy: Dr Lalit Duggal, Consultant, Sir Ganga Ram Hospital,
New Delhi, India)
E
B
D
Diagnosis
Investigation in a case of vasculitis involves assessment for
systemic involvement with findings suggesting involvement

Types of Wounds and their Management
Section 3
204
of vessel, its size, type of the inflammatory infiltrate,
granulomatous infiltration and necrosis.
a. Thorough history including chronicity of symptoms, food,
allergies, medications, connective tissue diseases (CTDs),
infections, malignancies.
b. Complete physical examination including oropharynx and
cutaneous ulcers.

Initial assessment of patient with leg ulcers: Initial
laboratory investigations may include a complete blood
cell count (to rule out underlying hematologic disorders),
erythrocyte sedimentation rate (which is elevated in patients
with many diseases including connective tissue diseases and
associated vasculitic ulcers, and infectious processes), and
fasting blood glucose. Serum albumin and transferrin levels
are very helpful in assessing the nutritional status in elderly
patients. Most of the information about the etiology of leg
ulcers is obtained from the patient’s history and physical
examination. If arterial insufficiency is suspected, with the use
of a hand-held Doppler the physician can assess the arterial
system in the lower extremities. Guided by the medical
history and physical examination, some specific laboratory
investigations and procedures can be performed to identify
the cause of atypical leg ulcers like vasculitis. Significantly
elevated antinuclear antibodies, rheumatoid factors, or other
more specific immunologic tests may tend to support the
diagnosis of vasculitic process. Serologic tests for syphilis,
or polymerase chain reaction for Mycobacterium DNA may
be performed on specimens from an ulcer suspected of being
of mycobacterial origin (e.g. erythema induratum of Bazin:
Mycobacterial panniculitis with subsequent ulceration usually
involving the calves). Cryoglobulins may be associated
with hepatitis C and leg ulceration. Therefore, hepatitis C
serologies and serum level of cryoglobulins may be helpful
tests. Like cryoglobulins, cryofibrinogens may be associated
with recurrent leg ulcers, especially if there is a history of
worsening of symptoms with exposure to cold.9
The various findings which are an indicator for vasculitis are:
1. Measurement of cryoglobulins: After midnight fasting blood
sample, plasma is examined for cryofibrinogen and serum
for cryoglobulins.
2. Diastolic blood pressure more than 90 mm Hg.
3. Elevated BUN more than 40 mg/dl and creatinine more than
1.5 mg/dl.
4. Arteriographic abnormalities: Arteriogram of affected limb
or part of body showing aneurysm or occlusion of arteries
not due to atherosclerosis, evidence of fibromuscular
abnormalities.
5. Biopsy of small or medium sized artery shows infiltration with
PMN cells, granulocyte and mononuclear leukocytes in the
cell wall.
6. Viral hepatitis markers: Presence of hepatitis B virus surface
antigen in serum may be detected in some cases.
7. ANA, RF, ANCA, C3 and C4.
Investigating Vasculitic Ulcers10
1. Noninvasive investigations
2. Invasive investigations
Noninvasive Methods of Investigating Leg Ulcers
Certain noninvasive methods are useful to confirm the
diagnosis of venous ulcers and clarify the anatomical and
functional defect. This will help determine further diagnostic
and therapeutic strategies.
1. Color Duplex ultrasound scanning which is becoming the
de facto standard for evaluation of venous obstruction is
used to assess the location and extent of reflux.
2. Ankle brachial index (ABI): The ABI is a basic test, which
can be performed at the initial office visit. Severe ischemia
may occur at less than 0.5.11 In patients with arterial media
calcification (mostly diabetics) the ABI may be elevated
(>1.3) due to incompressible vessels. Arterial Duplex
ultrasound is also used to assess the leg arterial system, and
information regarding areas of stenosis is obtained using
this technique. Patients with severe arterial insufficiency,
e.g. ABI<0.5 or severe areas of arterial stenosis documented
on Duplex ultrasound should be referred to a vascular
surgeon.


The ankle brachial index (ABI) is determined by
dividing the ankle systolic pressure by the brachial systolic
pressure obtained at the same time. This will provide an
objective estimate of arterial insufficiency, and will help in
making the decision as to whether compression therapy is
appropriate. The ABI of a normal artery ranges from 0.9 to
1.2.12
3. Plethysmography: With measurements taken at the thigh,
calf, ankle, metatarsal, and digital levels will assess
disease progression through volume recordings, which
are quantified through the pulse volume recorder. This
procedure measures the small volume changes that occur
in tissues during systole.
4. Transcutaneous pressure of oxygen (TcPO2) is used to help
determine the degree of microvascular perfusion, which
reflects the metabolic state of the limb. It may be measured
with an oxygen electrode coupled directly to the skin of the
foot or leg. The limb is adequately perfused when TcPO2
is 30 mm Hg. TcPO2 measurements are also obtained to
assess improvement after hyperbaric oxygen therapy.
5. Plain radiographs: To rule out osteomyelitis are suggested
when there is sinus tracking or when probing to bone is
possible.8 It is important to evaluate underlying blood
flow characteristics and determine the need for surgical
consultation. Low ABI and TcPO2 significantly increase the
odds ratio of amputation in diabetics.13 Ulcers that probe

Vasculitic Ulcer 
Chapter 20
205
to bone should be considered osteomyelitic until proven
otherwise. Radiographs will usually show characteristic
changes such as translucency corresponding to areas
of osteolysis. One should keep in mind that even in the
presence of osteomyelitis, constitutional symptoms and
leukocytosis may be lacking in immunocompromised and
some diabetic patients.
6. More specific tests such as white blood cell scans are more
sensitive than bone or gallium scan.14 In a comparative
study of 107 patients, Sonmezoglu et al.14 found that
99mTc-labelled ciprofloxacin (Infecton) has a better
specificity for bacterial infections than WBC scans in
detecting infectious foci in bones and joints.
Invasive Investigations
1. Arteriography and venography: May be performed as
an investigational procedure prior to valvular surgery.
Lower extremities arteriography is indicated in patients
with ischemic rest pain, intolerable claudication,
impending gangrene, or the presence of nonhealing ulcers
of suspected arterial origin.
2. Wound tissue biopsy and quantitative culture: Because
leg ulcers are neither sterile nor need to be sterile to heal,
a quantitative bacterial culture is more specific, and should
be performed once wound infection is suspected.14 This is
performed by curetting or taking biopsy from the bed of the
ulcer. Quantitative biopsy is the current gold standard for
assessing the quality and quantity of microbial pathogens
within a wound. Quantitative biopsies containing greater
than 105 organisms per gram of tissue are considered
significant, and systemic antibiotic therapy should be
considered. Punch or wedge biopsy capture medium size
vessels at level of subcutaneous fat and it should be from
borders of ulcerated lesions with skin of nonulcerated site.
Shave biopsy is not recommended.
MANAGEMENT
When a wound fails to heal after three to four months of
conventional treatment, biopsy of the ulcer edge (either
excisional or multiple punch biopsy techniques) should be
performed to rule out malignancy. The most common type
of cancer developing in chronic wounds is squamous cell
A
B
C
Figures 3A to C: (A and B) Vasculitic lesion in Behçet’s syndrome;
(C) Tongue lesion in Behçet’s syndrome (Photo courtesy: Dr Lalit
Duggal, Consultant, Ganga Ram Hospital, New Delhi, India)

Types of Wounds and their Management
Section 3
206
carcinoma. Pyoderma gangrenosum is a noninfective ulcer,
which usually presents with undermined borders. It may be
associated with inflammatory bowel disease, inflammatory
arthropathies, or myeloproliferative disorders. Appropriate
workup for associated disease should be considered in patients
with pyoderma gangrenosum. Patients with leg ulcers are prone
to developing contact dermatitis to dressings. When necessary
a patch testing should help determine specific allergens. Some
dermatopathologist insist on the presence of fibrin within the
cell and vessel wall, that’s a controversial issue to consider it
as essential feature for diagnosis. Because similar feature of
perivascular infiltrate of inflammatory cells may resolve in the
wall of the vessels which show extravasation of fiber.

Management includes treatment of various causes of vas­
culitis also. The current therapies include surgical interven­
tion in limited form because of underlying inflammatory pro­
cess, altered healing process and complications secondary to
etiology. Sometime conservative care like local wound care,
wound healing modulation and prevention of further progres­
sion of ulcer is useful.15 Once underlying cause of vasculitis
is identified, specific therapy must be started and ulcer is ad­
dressed by prevention of further damage, infection and im­
portant underlying structures should be preserved. Splintage
for the prevention of soft tissue contracture and joint position­
ing is advised which reduces progression and shortens future
complications. Physiotherapy of joints as advised by special­
ist may be started. Immunomodulation definitively has an im­
portant place in management provided specific cause has been
identified and has been addressed.

In management of histologically proven RA associated
vasculitis rituximab is administered as intravenous application at
intervals of 14 days accompanied by continuous treatment with
methotrexate, leflunomide and prednisolone. The efficacy and
safety of rituximab in the treatment of refractory SLE related
vasculitis has been shown in some studies (Figure 1D).16,17

Ulcers due to cryofibrinogenemia may be treated with an
anabolic steroid, stanozolol (Winstrol®). Iloprost® is a stable
prostacycline analogue which has been successfully used to
treat Reynaud’s phenomenon and digital ulcers associated with
CTD’s.18 The iloprost is administered for 6 to 8 hours daily and
continued for 21 to 28 days. Immunosuppressive therapy is also
indicated in severe necrotizing vasculitis (RAnv). Complete
ulcer healing can be achieved within six weeks of commencing
therapy while rapid improvement may occur in some patients.

A double blind placebo controlled iloprost therapy for RA
leg ulcers is already under way.18

While in many cases of polyarteritis nodosa and micro­
scopic polyangiitis (MPA) pulse methyl prednisolone and
glucocorticoids with azathioprine has been found effective
(Figure 2E). Plasma exchange and glucocorticoids give satis­
factory improvement in antineutrophils cytoplasm antibodies
(ANCAs) associated vasculitis.

In patients with the history of recurrent DVT, screening
for selected acquired and inherited risk factors for deep vein
thrombosis may be appropriate.5,19 Exercise programs, the use
of compression stockings, smoking cessation and avoidance
of estrogen therapies can greatly reduce risks of recurrent
DVT. Long-term anticoagulation may be necessary in these
patients.19

The available armamentarium for wound care includes over
two thousand wound dressing products and elastic compression
wraps. Chronic leg ulcer treatment options have been expanded
by alternatives available to treating these wounds. These
alternatives include hyperbaric oxygen therapy, bioengineered
skin
substitutes,
recombinant
platelet-derived
growth
factors and vacuum assisted wound closure.20 Surgery with
revascularization remains the treatment of choice for chronic
ischemic leg ulcers. In the absence of vascular compromise,
up to 90 percent of neuropathic ulcers will heal with proper
ulcer debridement, treatment of infection, saline wet-to-dry
dressings, and relief of weight from the ulcerated area.
Treatment Protocol for Vasculitic Ulcer
1. Guidelines

– Treat primary cause

– Support healing

– Protect from further trauma

– Prevent contamination

– Relieve pain
2. General care: Avoid venous stasis and cold exposure

– Bed rest

– Elevation of limb

– Warmth

– Avoid trauma

Ulcer dressing

– Keep wound moist

– Hypoxia—occlusive dressings

– Superficial wounds—low adherent dressings

– Deeper ulcers—absorbent hydrocolloid dressings

– Indolent ulcers—slow release iodine dressings

– Compression bandage

– Injection around ulcer edge of triamcinolone in selected
cases
3. Hypersensitivity vasculitis—usually self-limiting on removal
of insult/antigen

– Treat infections

– Remove suspected drug

– Malignancy—removal of primary tumor

– Autoimmune disease—immunosuppression

– Plasmapharesis

– IV prostacycline (RA, PSS)
4. Hypersensitivity (Idiopathic)

– Indomethacin

– Colchicine

– Dapsone

– Antihistamine
Contd...

Vasculitic Ulcer 
Chapter 20
207
Summary
Leg ulcers of atypical presentation or those that fail to heal
should alert the clinician to consider uncommon etiologies.
Leg ulcers are very common and physicians should be familiar
with the common methods used for their diagnosis and
management. Some laboratory investigations may be helpful
and can be ordered as part of the baseline work up. Unusual
leg ulcers need more specific tests. Treatment of these ulcers
requires primarily treatment of the etiology and secondarily
the local treatment of the lesions which may be the same in
almost all conditions.
References
1. Hoeanz Necke W, Zjpel M, Gue Nova E, et al. Vascular veins in
patients with mixed krogelo dysplastic and myeloproliferative
syndrome. J Eur Caca Dermatol Venereol. 2008;(1):110-2.
2. Hans, Dochs, Edward Smith CI, Puck Jen Nifer M. Primary
Immunodeficiency disease: a molecular and genetic approach.
Oxford University Press Inc; 1999.
3. Mudder G, Lee DK. Case presentation: xenograft resistance
to protease degradation in a vasculitic ulcer. Int J Low Extrm.
Wounds. 2009;8(3):157-61.
4. Ryan TJ Ed. Microvascular injury: London: Edward Arnold;
1976. p. 418.
5. Triantaphyllopoulos DC, Triantaphyllopoulos E. Fibrin
deposition and growth of connective tissue. Thrombus Diathes
Hemorrhage. 1969;21:144-50.
6. Atlas of Diagnostic Immunohistopathology: Lawrence D.True,
Juan Rosai; 17.28-54.
7. Olivers Amores B, Torralbam Perez Calrose, An Sist Sanit
navar. Rare complication in patient with Giant cell arteritis.
2010;33(3):327-30.
8. Lahita G, Robert, et al. Textbook of Autoimmune Disease:
Lipincot and Williams; 2000. pp. 549-56.
9. Mahabir RC, Taylor CD, Benny WB, Dutz JP, Snelling CF.
Necrotizing
Cutaneous
Cryoglobulinemic
Vasculopathy.
Plastic and Reconstructive Surgery. 2001;107(5):1221-4.
10. McCarthy SA, KuzuI Gattr KC. Heterogeneity of endothelial
cell and its role in organ preference for tumour metastasis.
Tends Pharmacol Sci. 1991;12:462-7.
11. John H, Stone, David B, Hell Mann. Rheumatic Disease
Clinics of North America; Vasculitis a Collection of Pearls and
Myths. 2001;617-728.
12. Champion RH, Burjon JL, Burns DA, Breathnach SM.
Textbook of Dermatology. Blackwith science. 1998;3:2073-6.
13. Caputo GM, Cavanaugh PR, Ulbrecht JS, Gibbons GW,
Karchmer AW. Assessment and management of foot disease in
patients with diabetes. N Engl J Med. 1995;332:854-60.
14. Sonmezoglu K, Sonmezoglu M, Halac M, Akgun I, Turkmen C,
Onsel C, Kanmaz B, Solanki K, Britton KE, Uslu I. Usefulness
of (99m)Tc-Ciprofloxacin (Infecton) Scan in Diagnosis of
Chronic Orthopedic Infections: Comparative Study with (99m)
Tc-HMPAO Leukocyte Scintigraphy. J Nucl Med 2001;42(4):
567-74.
15. Eugene D, Srandness JR, Arina Van Breda. Vascular Disease,
Surgical and Interventional Therapy. Churchill Livingstone.
1994;2:1-31.
16. Assmann G, Pfreunds Chuh M, Voswinkel J. Rituximab in
patients with rheumatoid arthritis and vasculitis associated
cutaneous ulcers. Clin Exp Rheumatol. 2010;28(57):81-3.
17. Lui NL, Thumboo J, Fong KY. A case of refractory vasculitis
ulcer in systemic lupus erythematosus patients responding to
rituximab and hyperbaric oxygen therapy. Int J Rheum Dis
2009;12(4):366-9
18. Veale DJ, Muir AH, Morley KD, Belch JJF. Treatment of
vasculitic leg ulcers in connective tissue disease with iloprost:
Clinical Rheumatology,Volume 14, Number 2, 187-190, DOI:
10.1007/BF02214941.
19. David Weedon. Textbook of Skin Pathology. Churchill
Livingstone; 1997. pp. 22-258.
20. Efrati S, Bergan J, Fishlev G, Tishler M, Golik A. Hyperbaric
oxygen therapy for nonhealing vasculitic ulcers. Clin Exp
Dermatol. 2006;12-7: EPUB2006 July 27.

– Steroids + colchicine

– Pain relief—NSAIDs + Opioids


Or Bupivacaine
5. Primary vasculitis

• Cutaneous


– Steroids + cyclophosphamide, azathioprine


– Methotrexate, MMF

• Systemic


– Pulse steroids + Immunosuppressants


– Rituximab (Anti-CD20)
6. Newer local approaches

– Platelet derived growth factor

– Epidermal growth factor

– Nerve growth factor
7. Large ulcers which fail to respond to conservative measures
require skin graft.
Contd...

• Burn Wound Classifi cation
• Pathology of Burn Wound Healing

– Proliferative Phase

– Remodeling Phase

– Histopathology of Burn Wound
• Aims of Burn Wound Care
• Management

– First Aid in Burns

– Initial Care of Burn Patient

– Local Wound Care
INTRODUCTION
Skin is the largest organ covering a surface area of 1.5 to 2.0 sq
m in an adult. Burns is defi ned as any injury to the skin due to
heat, electric current, radiation or chemicals. The survival of a
moderate to extensively burned patient depends on the successful
management of the burn wound. The main aim of burn wound
management as in any wound is closure of the wound as soon
as possible. However, in burns, the immunocompromised status
of the patient along with the large surface area wounds exposes
the patient to the risk of infection. The focus therefore remains
on avoiding wound infection with the help of topical antibiotic
dressings till the wounds heal or they are excised.

Though exposure method was being advocated earlier in
certain areas like face, perineum, etc. or even in extensive
burns, but keeping the wound surface dry leads to dessication
which impedes cell migration across wound surface and hence
retards healing. Therefore, exposure or open method is no
longer considered appropriate. Instead the emphasis has now
shifted to moist wound healing. Moisture over wound surface
allows: (1) Epithelial cells to migrate and spread; (2) Activity
of growth factors and surface proteolytic enzymes to remove
devitalized tissue and (3) Better oxygen and nutrient delivery.

Prior to managing burn wound it is important to understand
the mechanism of wound healing in burns but before we delve
into the details of burn wound healing it is also essential to
know the depth of injury in burns.
BURN WOUND CLASSIFICATION
Burns is classifi ed not only on the basis of etiology but by the
depth of skin and percentage body surface area involved.1-3
History has revealed many classifi cations for burns as
advocated by different surgeons. The classifi cation based on
depth of skin involvement has prognostic signifi cance as it
infl uences the time taken for a burn wound to heal. Though
burn involves both epidermis and dermis, the classifi cation of
burn depth is based on dermal thickness involvement which
can range from partial to full thickness. Burn wound can be
broadly categorized into two groups:
1. Partial thickness burns: Which can heal on their own
with conservative treatment within three weeks time
because some amount of dermis is spared with its viable
epidermal elements in hair follicles, sweat and sebaceous
glands. They are further divided into superfi cial (involving
superfi cial papillary dermis) and deep partial thickness
burns (involving papillary as well as reticular dermis).
2. Full thickness burns: In full thickness burns since whole of
the dermis is involved, spontaneous epithelialization is not
possible due to lack of epidermal adnexal elements. Hence
these require skin grafting for healing.

Another clinical classifi cation used to defi ne depth of burn
is the degree of burns4 (Table 1).

Epidermal burn is termed as fi rst degree burn (Figures 1A
and B).
Healing and Management
of Burn Wound
Sujata Sarabahi, VK Tiwari
21
Chapter

Healing and Management of Burn Wound
209
Table 1: Anatomical classifi cation of burns into 4 degrees
Burns
Involvement
Features
Depth
First degree
(Sun Burn)
Epidermis
Erythema (Hyperemia) only
Very painful
Heals in 3-5 days with no scars at all
Partial thickness
Second degree
Superfi cial dermal or
superfi cial partial thickness
Epidermis and
papillary dermis
Extremely painful Blister/vesicle formation—when
deroofed it exposes a wet, glistening pink dermis
which blanches on pressure indicating a rich capillary
arborization in superfi cial dermis
Partial thickness
Deep dermal or deep partial
thickness
Epidermis, papillary
dermis and part of
reticular dermis
Hair not pulled out easily
Heals in 10-15 days with minimal sacrring, more of
pigmentary changes
Less painful, Waxy
White appearance which does not blanch on
pressure. No bullae or blisters.
Can give a fallacious erythematous look or pinkish
white look because of fi xation of erythrocytes which
leak out of damaged capillaries. So blanching test is
important to differentiate superfi cial and deep dermal
burns if red looking areas.
Partial thickness
Hair follicles are easily pluckable signifying
devitalization
Heals in 3-5 weeks with severe hypertrophic scarring
and tendency for contracture formation
Third degree
Entire thickness of skin
Painless inelastic, translucent, parchment like eschar
with visible thrombosed vessels shining through the
dead s kin
Full thickness
Never heal on their own and require skin grafting
High-risk of contracture if not grafted
Fourth degree
Skin, subcutaneous
tissue, muscle,
carbonization of limb or
gangrene
Thick eschar to gangrene
Full thickness
Figure 1A: Schematic diagram showing the depth of injury in fi rst
degree burn involving epidermis only
Figure 1B: First degree burn in lower leg seen as only a
reddish discoloration of skin with very severe pain

Types of Wounds and their Management
210
Figure 2A: Schematic diagram showing depth of injury in superfi cial
second degree burns involving epidermis and papillary dermis
Figure 2B: Blister over foot indicating second degree superfi cial
scalds over dorsum of foot
Figure 3A: Schematic diagram showing depth of injury in deep
second degree burns extending till reticular dermis
Figure 3B: Deep second degree burns involving forearm and hand
with typical waxy white appearance
Figure 4A: Schematic diagram showing full thickness or third degree
burns involving the entire epidermis and dermis

Partial thickness burn is synonymous with second degree
burns which is further subgrouped into superfi cial and deep
second degree burn depending on the depth of dermis involved
(Figures 2A and B and 3A and B).

Full thickness burn is synonymous with third degree burn.
(Figures 4A and B).

Burns which extend beyond dermis to involve the
underlying muscle, bone and interstitial tissue are termed as
fourth degree burn (Figures 5A and B).
Clinical Presentation
Partial thickness burns involving dermis may be superfi cial
dermal or deep dermal. The superfi cial dermal burns which
involve the papillary layer of dermis are typically pink and
moist (Figure 6), whereas deep dermal burns involve the
reticular layer and are dry and pearly (waxy) white in color
(Figure 7). Full thickness burns (Figure 8), as the name
indicates, involve the whole of epidermis and dermis and
Figure 4B: Third degree burns over shoulder with parchment-like
eschar and visible thrombosed vessels

Healing and Management of Burn Wound
211
Figure 6: Superfi cial partial thickness or second degree burn with
typical wet glistening pink surface after deroofi ng the blister, which
blanches on pressure. These heal in 10-15 days
Figure 7: Deep partial thickness or second degree burn in forearm
characterized by whitish eschar which does not blanch on pressure
and deep full thickness burns on hand
Figure 8: Full thickness burns in arm with translucent eschar and
thrombosed cutaneous veins shining through the eschar
Figure 5B: Electric contact burns over limb usually presents with
fourth degree burn with damage extending till the bone
Figure 5A: Schematic diagram indicating depth of injury
in fourth degree burn extending beyond the skin to
involve underlying muscle and bone
appear parchment like with visible, thrombosed subcutaneous
veins. As the sensory end organs are concentrated in the skin,
the presence of sensation (tested by pinprick) in the burnt
area indicates that the skin is viable and the burn is partial
thickness whereas absence of sensation indicates full thickness
burns. Similarly, easy removal of hair (by pulling) indicates
deeper burns whereas inability to pull out hairs indicates
otherwise. Deeper a burn injury, greater is the loss of hair
follicles, sebaceous and sweat glands. In very deep dermal
burns, their number may be very small and any superimposed
bacterial infection can convert a partial thickness wound into
a full thickness wound hampering the process of spontaneous
healing. Thus, it is imperative to prevent this conversion by
appropriate wound care.

Types of Wounds and their Management
212
PATHOLOGY OF BURN WOUND
HEALING5,6
Healing of a burn wound is primarily by secondary intention
which involves two processes—epithelialization and contrac-
tion.

As with any wound healing the primary phases remain
the same even following burns, i.e. infl ammatory phase,
proliferative phase followed by remodeling and scar
formation. Each of these phases have been described in detail
in chapter on pathology of wound healing. It is the second and
third phase which is of signifi cance in burns as it is actually
responsible for the healing.
Proliferative Phase
Involves re-epithelialization, angiogenesis and fi broplasias.
Re-epithelialization restores the epidermis which forms the
permeability barrier. In partial thickness burns it involves
keratinocyte migration from remaining skin appendages and
wound edges. This is followed by proliferation of keratinocytes
which migrate and then cover the wound (Figure 9). As a result
of contact inhibition the migration stops and keratinocytes
attach themselves to the underlying substratum to reconstitute
the basement membrane and fi nally differentiate to form a
stratifi ed epidermis.

Within seven to nine days after re-epithelialization, the
basement membrane zone forms which serves as attachment
site for keratinocytes on its superior aspect and to the dermis
on the undersurface.
Dermal Reconstitution
The dermis is reconstituted by fi broplasias and angiogenesis.
Fibroplasia involves proliferation of fi broblasts and production
of collagen and other matrix proteins which constitute
the granulation tissue. Angiogenesis involves new vessel
growth from activated endothelial cells. These participate in
the formation of granulation tissue and supply oxygen and
nutrition to growing tissues.
Remodeling Phase
The extracellular matrix consisting of fi brous structural
proteins, i.e. collagen and elastin which soon gets organized
around epithelial cells, endothelial cells and smooth muscle
cells. The collagen fi bers constitute 80 percent of the normal
human dermis and are the principle proteins providing
structure, strength and stiffness to dermal tissue. During
early wound healing phases it is collagen type III which is
predominant. But over a period of one year or longer there
is degradation of type III collagen and it is replaced by type
I collagen. The fi nal phase of wound healing is resolution
where the extracellular matrix remodels and the scar tissue is
formed and contraction of wound also takes place when the
fi broblast assume a myofi broblast phenotype.

Superfi cial burns heal by epithelialization alone whereas
deeper burns close by epithelialization and wound contraction
both.7 In all partial thickness burns (other than fi rst degree
epidermal burns), the epidermis is completely destroyed.
However, the epidermal appendages, i.e. the hair follicles,
sweat glands and sebaceous glands are spared. It is from these
surviving epithelial structures that the epithelium spreads
rapidly to provide a new intact epithelial surface which is
elastic and supple. In case of deep dermal burns the majority
of the dermis and all sebaceous glands are destroyed and
only deeper parts of hair follicles or sweat glands survive. If
they are left to heal for themselves, as the eschar separates,
epithelial buds emerge from the site of these remaining
epidermal appendages and from these tiny islands the new
epidermis proliferates over the wound surface (Figure 10).
As this re-epithelialization is very slow, the healed skin
shows hypertrophic scarring because of excessive collagen
production by the fi broblasts and decreased degradation of
collagen. These hypertrophic scars also have a larger number
of myofi broblasts within them which have an inherent
contractile property. These contracting myofi broblasts in
Figure 9: Re-epithelialization of superfi cial dermal burns by keratinocyte
migration from remaining skin appendages and wound edges

Healing and Management of Burn Wound
213
the deeper dermis therefore cause a piling up of the scar as
it is forced outwards and may also cause joint contractures
and distortion of structures (Figure 11). The details of the
pathogenesis of hypertrophic scarring and keloid formation
are discussed elsewhere in the book and the reader is advised
to refer to the chapter on scars following wound healing.

Pigmentary changes8,9 in healed skin are also seen
following burns though the nature and extent of pigmentary
changes are not always predictable. Still it is cause of concern
to the patients.The usual observation is that hyperpigmentation
occurs after superfi cial burns whereas hypopigmentation/
depigmentation are seen following deeper burns (Figures 12A
Figure 10: Superfi cial second degree burns almost healed except at
the center. Epithelial buds emerge from the site of these remaining
epidermal appendages and from these tiny islands the new epidermis
proliferates over the wound surface
Figure 11: Hypertrophic scarring from deep dermal burns healing
spontaneously by dressings leading to severe extension contracture
at wrist
Figure 12A: Hypopigmented scarring following burns, though
pigmentation reappears after some time which can be seen as spots
that gradually enlarge and intermingle
Figure 12B: Hyperpigmentation in a post burn scar on thigh
and B). The pathophysiology for these pigmentary changes
can be explained if the anatomy of normal skin is understood.
The color of normal skin is determined by the number of
melanocytes, the amount of melanin synthesized and its
distribution and transfer to a keratinocyte. The melanocytes
contain organelles, melanosomes, in which melanin is
synthesized and then transferred to keratinocyte via cell to cell
contact between melanocyte and keratinocyte. This is called
the epidermal–melanin unit.

In case of superfi cial burns, the superfi cial layer of
keratinocytes and melanocytes are destroyed but the
melanocytes in the deeper layers of epidermis and dermis are

Types of Wounds and their Management
214
still intact. They become overactive in response to the trauma
of burns and stimulus of healing and probably synthesize
more melanin. This leads to hyperpigmentation. This is also
affected by the innate skin color, sun responsiveness of the
individual’s skin and amount of ultra violet light exposure.

In case of deeper burns there are only few melanocytes left
in the deeper layers of dermis. Therefore, there is a defi ciency
of melanin causing hypopigmentation or depigmentation in
these areas after they heal. Only the residual melanocytes
lining the intact hair follicles in the depth of the dermis migrate
upwards to the basal layer of surface regenerating epidermis
and give color to the healed skin which is defi cient compared
to surrounding healthy skin.
Histopathology of Burn Wound
Histologically the local effects of burn can be divided into
three zones of tissue damage as given by Jackson in 19534
(Figures 13A and B).
1. Zone of coagulation: It is the central zone with complete
coagulative necrosis of the tissue cells which become
completely nonviable. This area of tissue damage cannot
recover with any kind of treatment.
2. Zone of stasis: It surrounds the zone of coagulation and
results from signifi cant reduction in microcirculation
following damage to arterioles,venules and capillaries.This
zone can recover if adequate resuscitation and wound care
is given which further allows healing of the burn wound.
However, in case resuscitation is inadequate, this zone can
get converted to a zone of coagulative necrosis.
3. Zone of hyperemia: It is the outermost zone surrounding
the zone of stasis and results from vasodilatation. This
eventually recovers following adequate resuscitation with
passage of time.
AIMS OF BURN WOUND CARE
The basic aims of local burn wound care are:1
1. Debridement: To clean debris and particles from the wound
in order to improve healing. Thermal injury involves
necrosis of skin and subcutaneous tissues to varying
depths which results in formation of eschar which releases
chemical mediators which damage local capillaries and
epithelial elements though they also stimulate leukocytes
to digest debris. As a result, if this necrotic tissue is not
removed early, it prolongs infl ammation and retards
epithelialization and hence healing of wounds. Debridement
involves washing and gradual removal of loose debris and
necrotic tissue and handling of blisters, which is usually
done bedside or in the dressing room without anesthesia.
2. To prevent damage to remaining viable epithelium and to
prevent damage to regenerating, delicate neoepithelium
–by applying a moist nonadherent dressing. Whenever a
burn wound is exposed to air dehydration of tissue occurs
and the process of reversal of zone of stasis as mentioned
earlier is reduced resulting in deep partial or full thickness
loss of skin. Zawaki (1987)10 showed that when drying
of burn wound is prevented, epithelium migrates towards
surface around the necrotic hair follicles as soon as
circulation in the viable tissue returns.Winter11 showed
that the scab which forms over an exposed wound inhibits
the migration of keratinocytes ultimately impairing wound
healing. On the other hand Zawaki12,13 demonstrated that
occlusive dressings which do not allow wound to dry also
allow the tissue to retain its viability.
3. To produce an environment which inhibits microbial
growth: Burn wound is initially sterile and this sterility
has to be maintained by taking all aseptic precautions and
using some topical antimicrobial agent while dressing. Any
Figure 13A: Jackson’s three zones of damage in burn wound
Figure 13B: The three zones of damage shown clinically: (a) Central
zone of coagulation, (b) Zone of stasis and (c) Zone of hyperemia

Healing and Management of Burn Wound
215
superimposed bacterial infection can convert a superfi cial
or partial thickness burn into a deep or full thickness burn.
4. To encourage slough separation by natural means.
5. To allow free drainage of exudates from the wound and
prevent them from coming in contact with the environment
by using good absorbent dressing material.
6. Oxygenation of tissues to be maintained: Following
burns, the blood supply to the burn wound is reduced
because of edema and impaired circulation leading to poor
oxygenation of tissues. This reduced tissue oxygenation
not only impairs wound healing but also favors bacterial
invasion of the wound. The result is that the wound heals
poorly and with excessive scarring. To counter this, some
burn centers have used hyperbaric oxygen to assist wound
healing. However, it has not been used widely.2,3

Simpler measures can also be taken to ensure adequate
oxygenation of burn wounds: (a) The burned extremities
should be elevated, (b) Constricting dressings and casts
should be avoided, (c) Early escharotomies/fasciotomies
should be done to avoid compartment syndrome in case of
circumferential full thickness burns, (d) Early ambulation
with full range of joint motions to be started and
(e) Removal of dead tissue.
7. To immobilize the injured area in order to reduce pain,
especially the extremities should be immobilized in a
functional position.
8. To prevent development of bacteremia and septicemia.

The primary objective therefore in treating a partial
thickness burn injury is to provide an environment which
inhibits microbial growth and at the same time promotes
wound healing. On the other hand, the aim while treating a
full thickness burn is early removal of dead tissue, preventing/
minimizing and localizing infection to the burn wound and
closure of raw area at the earliest with skin grafts.
MANAGEMENT
First Aid in Burns
First aid to a burn patient is generally provided by the individual
present with the patient at the site of accident that time,which
may be a relative or friend or even an unknown persons.
Therefore, it is essential for every individual to know the fi rst
aid steps to be taken for handling a burn patient as the timely
help can reduce the severity of the injury to a great extent. It
includes certain do’s and don’ts which are elicited here.
Initial Care of Burn Patient1,2
Before starting to manage the wounds one needs to assess
the percentage of the total body surface area burned which
is easily done either by the ‘rule of nine’ in adults (Figure
14) or ‘rule of fi ve’ (Figure 15) in children. If the area of
burn is scattered it may be diffi cult to assess the percentage
using these rules as it may lead to overestimation of the area.
In those cases the palm of the patients hand is taken as one
percent total body surface area (TBSA) and is used to measure
the total burnt area (Figure 16). Lund and Browder chart gives
the surface area as per the age of the patient and is being used
universally the world over in all burn units for calculation of
percentage burns in different age groups (Table 2).

For all major and most moderate burns, patient needs to
be kept fi rst in the Intensive Care Unit (ICU) where there
are proper monitoring facilities. The airway and ventilation
is to be assessed fi rst especially in face burns or smoke
inhalation. Oxygen should be started in all such cases. If there
is respiratory distress and ABG is abnormal, patient should be
intubated. IV fl uids should be started immediately to restore
circulation.

For pain management in major burns usually morphine or
pethidine is given IV.

Tetanus immunization is to be given in the form of tetanus
toxoid or TIG if indicated. The use of antacids is controversial.
Do’s
• Stop the burning process—victim to drop on ground and roll
on surface
• Use water or sand to douse fi re
• ABC of resuscitation—check for airway, breathing, circulation
• Cool burnt area especially if extremity under running tap
water or in a bucket full of tap water till burning sensation
disappears
• If patient is unconscious think of smoke inhalation or
associated head injury and maintain patent airway
• Cover the part with a clean cloth or sterile polyethylene drape
• If patient is conscious give salt—sugar solution to patient
orally
• Shift patient to appropriate burn care facility
• In case of electric burn switch off the source of electricity and
move the source of electricity away from the injured person
by using nonconducting object like wood or plastic.
• In case of chemical burns—fl ush chemicals from skin surface
with running tap water for 15 min or more. In case the burning
chemical is a powder,brush it off the skin before fl ushing with
water. Clothes and jewellery soaked in chemicals should be
removed.
Don’ts
• Do not immerse severe large burns or whole body in cold
water
• Do not use ice as it can cause cold injury and damage skin
further
• Do not forcefully remove clothes adherent to burnt skin
• Do not apply any local agents like gentian violet, mercuro-
chrome, toothpaste to the wound as it interferes with
evaluation of burn depth and extent
• Do not break blisters
• Do not cover burnt area with cotton wool
• In electric burn do not pour water over the patient to douse
fi re and do not touch the injured person.

Types of Wounds and their Management
216
It was a standard teaching to give antacids prophylactically to
avoid curling’s ulcer (peptic ulcer). Usually ranitidine 50 mg
IV 8 hourly is given in adults or pantaprazole 40 mg once a
day.Though now it is believed that by giving antacids, the acid
barrier is broken which allows translocation of bacteria across
the gut.

Prophylactic antibiotics are not used in all admitted patients
with major burns because the wounds are sterile at admission.
Their use is to be restricted to only a few cases which will be
discussed later.

Patient is to be kept in a warm environment where
maintenance of room temperature and humidity is essential
Figure 15: Rule of fi ve used to calculate percentage
surface area burnt in children
Figure 14: Rule of nine used to calculate percentage
body surface area burnt in adults
Table 2: Lund and Browder’s chart showing changes in body surface area (%) with age

Infant
Age 1 yr
Age 5 yr
Age 10 yr
Age 15 yr
Adult
Head
19
17
13
11
9
7
Neck
2
2
2
2
2
2
Anterior trunk
13
13
13
13
13
13
Posterior trunk
13
13
13
13
13
13
Buttock
2.5
2.5
2.5
2.5
2.5
2.5
Perineum
1
1
1
1
1
1
Thigh
5.5
6.5
8
8.5
9
9.5
Leg
5
5
5.5
6
6.5
7
Foot
3.5
3.5
3.5
3.5
3.5
3.5
Upper arm
2.5
2.5
2.5
2.5
2.5
2.5
Lower arm
3
3
3
3
3
3
Hand
2.5
2.5
2.5
2.5
2.5
2.5
Figure 16: Palmar surface of hand with fi ngers closed, both in adults
and children is taken as 1% TBSA burnt for easy calculation in small
burns or when burn wounds are scattered

Healing and Management of Burn Wound
217
for treatment. All extensive burns are to be kept in a room
with temperature >26 degree C (26 – 32 degree C) and relative
humidity 60 to 65 percent.

Loss of skin in burns results in increased water and heat
loss. These losses are directly proportional to burn size. Large
volume of fl uid and electrolytes are lost from the burn surface
and they need to be replaced during the fi rst 12 to 24 hours
to maintain circulatory volume and thus prevent acute renal
failure. In burns <20 percent of BSA, fl uids can be replaced
orally but in >20 percent burns in adults and >10 percent in
children, I/V fl uids are a must. The main aim of resuscitation
is to maintain tissue perfusion to the zone of stasis and so
prevent the deepening of burn.

The ideal fl uid for replacement is plasma because the fl uid
lost in the extravascular spaces in burns resembles plasma in
its contents. But since plasma is not readily available, it is not
the fl uid of choice. Today’s teaching is to give crystalloids
because of their easy availability everywhere and economic
feasibility. Therefore in crystalloids, the fl uid of choice is
ringer lactate as it is a balanced electrolyte solution. The aim of
fl uid resuscitation is to have an alert, cooperative patient with a
good urine output.There are several formulae used in different
burns units all over the world to calculate the fl uid requirement
(Table 3). All patients need to be weighed prior to transfer to
ward in order to calculate fl uid requirement as all formulae are
based on body weight and body surface area burned.

The most common formula used is Parkland formula or
modifi ed Brook’s formula. In subsequent 24 hours, evaporative
losses from burned surface are replaced at 1 ml/kg/percent
burn daily and in then colloids are given in a volume of 0.3 to
0.5 ml/kg/percent burn to correct plasma volume.

Though there are many new invasive and noninvasive
methods available to monitor the resuscitation of a burn
patient, the simplest and most practical method is to check the
urine output on an hourly basis. An indwelling Foley’s catheter
should be place to monitor urine output. A minimum urine
output of 0.5 ml/kg/hr in adults and 1 ml/kg/hr in children
should be maintained to ensure adequate resuscitation.This
is an accurate method for monitoring burn resuscitation in
majority of the cases.

Apart from the supportive care, the proper wound
management per se will help in the spontaneous healing of the
partial thickness burn wounds and successful resurfacing of
the full thickness wounds.
Local Wound Care14,15
The patient should be shifted to the specifi ed dressing room
where the wound can be managed with all aseptic precautions.
This is important because immediately following burns the
skin surface is sterile as all surface bacteria are killed by the
heat. One should avoid introducing exogenous bacteria to the
wound by all means in order to avoid burn wound infection. All
the loose nonviable tissues should be removed with minimum
trauma. The area should be thoroughly washed with savlon®
and then normal saline to remove all the debris (Figure 17).
Only after thorough debridement, a proper appraisal of depth
of burns can be done and it should be properly charted in
the “Burn Chart” for future reference (Figure 18). This chart
contains detailed observations of the wound along with any
surgical procedure performed. Any change in burn wound
depth can also be charted in the same form at a later date
to follow the progress of the burn wound. All encircling
bracelets, rings and other jewellery on the person of the burn
victim should be removed because they can act as tourniquet
once edema sets in, causing distal ischemia.
Table 3: Crystalloid therapy (in adults)
Name
Formula (Ringer lactate)
Timing
Colloid
Parkland formula
4 ml/kg/%BSA RL
Half in fi rst 8 hrs , half in next 16 hrs
None
Modifi ed Brooke’s formula
2 ml/kg/% BSA of RL + 2500 ml 5% D
Half in fi rst 8 hrs and half in next 16 hrs
None
Hyperosmolar solution
Monafo’s formula
3.37 ml/kg/% BSA of hypertonic saline
(This gives 0.7 mEq Na /kg/% BSA in 48 hrs)
In 48 hours
None
Figure 17: Debridement of all dead skin tags and large blisters

Types of Wounds and their Management
218
Management of Blisters
While very small blisters (< 5 cm) may be allowed to be kept
intact, the larger blisters (> 5 cm) run the risk of rupture at
the time of initial dressing or else may get ruptured in odd
situations and the burn wound gets contaminated. It is very
diffi cult to keep blister fl uid sterile for a long time and so it has
been advocated to at least aspirate them with a needle to allow
the blister membrane to stick to the wound. Other workers
consider the blister skin as dead and necrotic tissue and hence
de roof the blister and dress the wound (Figure 19). In children,
it is preferable to rupture the blisters because they are bound to
get ruptured soon due to their uncontrolled activity.
Figure 18: Burn chart which is used in the author’s unit

Healing and Management of Burn Wound
219
Escharotomy
In full thickness circumferential burns of limbs, neck and
chest, the tight dry eschar with underlying edema may
produce a tourniquet effect leading to vascular compromise of
distal extremities and respiratory impairment respectively. To
diagnose distal vascular compromise, the following clinical
signs and symptoms are looked for: cyanosis of distal unburned
skin, delayed capillary fi lling in nails of fi ngers or toes distal
to circumferential burns in limbs, paresthesias or deep tissue
pain. All these signs warrant a second look at the burn wound
and diagnosis can be confi rmed by a colour Doppler to look
for arterial fl ow in distal palmar arch for upper limb and
posterior tibial artery in lower limb. These circumferential
burns are treated by performing an escharotomy wherein
an incision is made through the full thickness of the eschar
releasing the constricting effect and thus, decompressing the
underlying structures and improving the distal blood supply
(Figures 20A to D). In case escharotomy does not give
adequate decompression, as in case of high voltage electrical
injury where the muscles are also involved leading to edema
under the deep fascia and raising the compartment pressure,
the incision has to be extended till the underlying deep fascia
(fasciotomy) in order to release the compartment pressure.

In case of electrical burns when there is edema of the
muscles which increases the compartment pressures,
fasciotomy is required. In these cases, the skin of the limb
may be unburnt and requires local anesthesia before giving
the fasciotomy incisions in different compartments. At times,
the carpal tunnel has to be opened in the hand to release
the pressure on the nerves. In that case, the incision can be
extended over the forearm as an ‘S”-shaped incision over the
fl exor aspect of the forearm and extensor aspect of forearm.
Figure 19: Fluid-fi lled blister incised with blade with all aseptic
precautions and protein rich fl uid is expressed out. Deroofi ng may or
may not be done depending on the size
Figure 20A: Incisions used for escharotomy and
fasciotomy in limbs and chest
Figure 20B: Dorsal of hand with markings for fasciotomy incisions
Figure 20C: Escharotomy incisions given in chest for full thickness
circumferential burns of chest to allow full expansion of chest

Types of Wounds and their Management
220
Fasciotomy incisions should be given from proximal to
distal direction so that the pressure is released gradually and
immediately profuse bleeding does not occur and interfere
with the incisions (Figures 21A and B).
Conservative Management
After cleansing, the wounds are dabbed dry with sterile
gauze and then the appropriate method of further wound
management is selected, i.e. exposure method (open method)
or closed method (occlusive method) of dressing. In most
patients, neither of these methods used alone is ideal for local
care and frequently both methods are used in different areas of
the body in the same patient for best results.
Exposure or Open Technique3
It is especially useful for burns of face and perineum which
cannot be adequately dressed. Extensive non-salvageable
burns more than 90 percent TBSA may also be managed by this
method decreasing the requirement for manpower, material and
cost. This technique consists of placing the patient on a clean,
dry, sterile sheet after cleaning and debriding the wounds. The
wounds are left exposed to air without any topical agents or
any covering agents. The drying process, however, may retard
the spread of epithelium which is faster under moist conditions.
For deeper wounds, open treatment may be less satisfactory as
the dry eschar takes a long time to separate. This method is not
very suitable for wounds over joints as the scabs over a joint
surface may crack repeatedly and bleed.

A modifi cation of the open technique is to apply a thin
layer of antibiotic ointment over the wounds after cleansing
and drying them daily, especially on the face. Sometimes an
antimicrobial impregnated nonadherent gauze like tulle or
Figure 20D: Escharotomy incision in full thickness circumferential
burns in an infant to prevent circulatory impairment
Figure 21B: Flexor aspect of same arm
Figure 21A: Fasciotomy incisions given in electric contact burn
in upper limb to prevent compartment syndrome and subsequent
gangrene in the limb (Extensor aspect)
paraffi n gauze is used on exposed wounds and this gauze acts
as a wick to transport the exudates to the gauze surface where
it dries up forming a scab. The advantage with this technique
is that the scab does not adhere to the wound and the gauze
can be removed easily without the risk of bleeding from the
wound or else damage to the newly formed epithelium.

If the burned area is superfi cial partial thickness, the
whole scab/gauze begins to separate after a week or so and
this is trimmed gently and repeatedly with scissors and fi nally
comes out in 15 to 21 days to leave a well healed skin surface.
For patients treated by exposure method, a strict aseptic
environment, appropriate maintenance of the environmental
temperature and humidity is very important . This is because
leaving the wounds exposed increases the evaporative losses
as well as substantial body heat loss and increases the risk of
contamination of wounds. To compensate for this, the ambient

Healing and Management of Burn Wound
221
temperature must be maintained in the range of 28 to 32°C
and humidity to about 40 percent.
The advantages of open method are:
• Wound examination is easier
• Earlier detection of wound infection
• Early physiotherapy
• Easier control of hyperpyrexia, and
• Wound environment is not conducive for bacterial
colonization.
The disadvantages of open method are:
• Delay in eschar separation
• Evaporative losses increase
• Chances of hypothermia are more because of loss of body
heat, and
• Not possible where isolation is not available.

Therefore, the only indication for use of exposure technique
is in case of burns of face, perineum and genitalia.
Occlusive Dressing or Closed Technique
This method is most useful for patients who are treated on
outpatient basis, patients who need to be transported from
one centre to another, circumferential burns of extremities
and torso, in infants and children and uncooperative adults.
Occlusive dressings are avoided in burns of face and neck and
perineal burns.
The advantages of occlusive dressings are:
• It reduces evaporative losses
• Provides a mechanical barrier to prevent bacteria from
contaminating the wounds
• Absorbs exudates from the wound surface
• Assures maintenance of functional position in burned
extremities
• Maintains moist environment which encourages epitheliali-
zation
• Patient is more comfortable
• Provides splintage to joints thus preventing contractures.

Normally speaking, all fresh burn wounds are sterile because
the heat kills all the surface pathogens.The only organisms
present are those present deep in the skin appendages and
these are not very pathogenic. Some of these organisms may
come to the surface or the burn wound may get contaminated
from the environment. Once the wounds have been dressed,
presence of exudates in the dressings, warmth and lack of
light under the dressing provide an ideal environment for
proliferation of organisms after they gain entry to the skin
surface or through the dressings, resulting in infection. The
risk of wound contamination can be decreased by using either
of the following:
A. Antimicrobial agents
B. Biological or synthetic skin substitutes.
Topical Antimicrobial Agents
The antibacterials used for burn wound dressing have a dual
purpose—fi rst to control any organisms on the surface of the
burn wound and secondly to prevent entry of new organisms
from the exterior.

By the end of fi rst week post burn, the deeper surface
of eschar especially around the hair follicles shows active
proliferation of organisms which can penetrate into deeper
tissues and adjacent viable tissue as well, if not controlled.
This can again be checked by the application of surface
antibacterial creams which have a good eschar penetration.
The deeply burned areas are avascular5 which not only provide
a favourable environment for bacterial proliferation but also
prevent penetration of antibiotics administered systemically
and thus, ineffective delivery of antibiotic to the burn wound
surface to fi ght the surface contamination. This is better
tackled by topical antibacterial agents and obviates the need
for systemic antibiotics. It is very important to understand
that topical therapy does not sterilize the burn wound. It only
controls the bacterial proliferation and confi nes it within the
limits of the burn wound.
Criteria for a Good Antimicrobial Agent
1. It should have a broad spectrum of activity which includes
organisms which are most commonly isolated from the burn
wound, e.g. Pseudomonas aeruginosa, Staphylococcus
aureus, Klebsiella and enterococci, etc.
2. Ideally the topical agent should penetrate the eschar and
yet not be signifi cantly absorbed systemically.
3. There should be minimal emergence of resistance amongst
organisms against the agent. If there is high frequency
of acquired resistance against the substance being used,
the effi cacy of the agent decreases and resistant strains
produced are also more virulent.
4. It should cause minimum or no discomfort to the patient.
5. It should be economical and easily available.
6. It should have minimal side effects. Though majority of
the agents do get absorbed systemically, their use has to
be restricted for only certain specifi c established infections
and on the smallest possible wound areas.
7. It should be economical as in many areas of the world, cost
is the primary factor which affects selection of the agent.
8. Application should be simple and easy.

The topical antimicrobial agents, most frequently used
for burn wound dressings, are discussed below. As any one
agent is not uniformly effi cacious in all the cases, it may be
necessary to substitute it with a different agent on all or part
of the wounds during the course of treatment at different
times.16-20

Types of Wounds and their Management
222
One Percent Silver Sulfadiazine
It is the most commonly used agent used for burn dressing
in the form of a water soluble cream base at one percent
concentration.It is also the most effective in terms of
antibacterial control, patient comfort and compliance and
is used for closed dressings. Its action is bacteriostatic
due to both silver ion which acts on the bacterial cell wall
inducing structural changes and sulfadiazine moiety which is
a competitive inhibitor of para-aminobenzoic acid (PABA),
a metabolic precursor, when they are released at the wound
surface by gradual dissociation. It has to be applied as a 0.5 to
1 cm thick layer once or twice a day.

Advantages: It is an odorless cream and painless on
application. It is highly effective against gram-negative bacteria
especially Pseudomonas because it delays colonization. It
can be applied easily and action lasts for 24 hours. Tissue
penetration is moderate. It can be used for both open and
closed dressings.

Disadvantage: Causes transient leukopenia which resolves
spontaneously. It forms a proteinaceous gel called
‘Pseudoeschar’ on the wound surface after application. It also
inhibits epithelial regeneration.
Silver Nitrate Solution
Is used as a 0.5 percent solution. It is bacteriostatic and action
is due to the free silver ion and is effective against common
microbial fl ora especially gram-negative bacteria. Eight to ten
layers thick gauze is soaked in the solution and applied to the
wounds and have to be wetted every two hours.

Advantages: It is bacteriostatic and is effective against
a wide bacterial spectrum as well as fungal organisms. Its
application is painless with no known hypersensitivity. Its use
decreases evaporative water loss from burn wounds.

Disadvantages: It has limited tissue penetration and
therefore is ineffective in established wound infection. Its
application causes black staining of skin and clothes.

There are severe electrolyte derangements noticed with
its use. Use of distilled water as a vehicle for application of
silver nitrate leads to a markedly hypotonic solution and it
causes absorption of large volumes of distilled water into the
tissues and eventually into the blood stream. At times because
of systemic absorption, it can even cause hypochloremia and
hyponatremia especially in infants and children.This can be
prevented by giving large quantities of sodium chloride orally
or intravenously.

Some of the gram-negative bacteria especially enterobacter
cloacae metabolize nitrate ion to nitrite which when absorbed
through the wound results in methemoglobinemia. Though it
is a rare complication, it has to be suspected if there is cyanosis
or slate gray discoloration of skin without any pulmonary
injury and arterial blood is brown in color even though
PaO2 is normal. Diagnosis can be confi rmed by estimating
methemoglobin levels in the blood. Management of this
condition includes withdrawal of silver nitrate dressing and
intravenous administration of reducing agents like methylene
blue or ascorbic acid.2

0.5 percent silver nitrate remains the fi rst line topical agent
in many burn centres around the world. The best use of silver
nitrate is in case the patient is seen within a few hours of burns
and silver nitrate therapy is started immediately. If there is
a delay of several days and the burn wound has deteriorated
because bacterial sepsis has supervened or is impending, silver
nitrate will not be effective as it does not penetrate tissues
effectively. It can only act on the surface fl ora. In these cases,
other agents with better penetrating ability should be used.
Mafenide Acetate or Sulfamylon
It is used in 11.1 percent concentration cream base.Its active
against most gram-positive and gram-negative organisms
including Pseudomonas and Clostridium. It is bactericidal in
action. It is applied as a 3 to 5 mm thick layer over the wound
and it actively penetrates the burn wound and minimal amount
is left on wound surface after 3 hours14 and after 10 hours,
the tissue level is below the concentration required to inhibit
bacterial growth. Therefore, to maintain therapeutic levels of
the agent in the wound, it has to be reapplied after 12 hours.

Advantages: It has potent antibacterial action with a very
good penetration of burn eschar. Therefore its main use is in
established or incipient wound sepsis. It is also the agent of
choice for chondritis following burns of the ear.

Disadvantages: Application of mafenide is associated
with signifi cant pain which is probably because of its high
osmolarity and hygroscopic effect of the sulfonamide
suspension. The painful sensation persists for several minutes,
thereby earning its nickname of ‘white lightning’. The most
signifi cant complication with the use of topical mafenide
is metabolic acidosis because of its carbonic anhydrase
inhibiting property.

Despite its disadvantages, mafenide is still the best topical
agent for control of established burn wound infection.18,19
Its use should be reserved for short duration of time and
withdrawn before signifi cant side effects become evident.
Soframycin
Is very useful for small areas.

Disadvantage: If used liberally in extensive burns, its
absorption can lead to renal toxicity.

Healing and Management of Burn Wound
223
Chlorhexidine and Povidone Iodine
Though they have a broad spectrum of action, they have only
limited use because of their use in small burns only. If used
in larger areas they get absorbed and lead to hepatic and renal
toxicity. Chlorhexidine is painful to apply also.
Furacin (Nitrofurazone)
Has bactericidal action against both gram-negative and gram-
positive organisms.

Advantage: It penetrates rapidly through eschar. There
is low resistance to this agent. Use is restricted for MRSA
infection of burn wound.

Disadvantage: It is not effective against Pseudomonas.
Causes discomfort on application.

Can cause renal failure on systemic absorption if used in
large amounts.
Silver Impregnated Dressings
Recently newer products have been launched in the market
like acticoat® (Smith and Nephews) and biatin® Ag which
have revolutionized the antimicrobial barrier dressing because
they contain nanocrystalline silver which delivers silver
rapidly to the wounds for rapid onset of action to control
infection and then gradually over a sustained period of time so
that the dressing needs to be changed every three to fi ve days
only. The decreased frequency of dressing change decreases
the chances of exposing the burn wound to infection from
external environment (Figures 22A to C). Some silver staining
of the wounds is noticed with this dressing material but it is
temporary without any adverse effects.
Figure 22A: Patient admitted with burn wound sepsis in which
superfi cial wounds turned deep
Figure 22B: Nanocrystalline silver dressing (Acticoat)®
applied to the wounds
Figure 22C: Final result in the same patient when the wounds
improved and were grafted
Growth Factors21
Various growth factors are now being used in clinical trials
for wound healing though their effi cacy has not yet been
fully established. Epidermal growth factor (EGF)23,24 is one
of the recombinant cytokine growth factor which has been
successfully used in treating burn wounds. There have been
trials of using EGF alone or EGF in combination with silver
sulfadiazine cream EPIGROF®[Marksons]. Their use has
shown marginal improvement in burn wound healing when
compared to silver sulfadiazine alone.

Types of Wounds and their Management
224
Skin Substitutes
The main purpose of local care with antimicrobial creams, non-
stick vaseline gauze and gamgee pad dressings in superfi cial
burns is to prevent infection and injury to the regenerating
neoepithelium till epithelialization from the surviving
epidermal appendages is complete. It is during this period
that the burn wounds can also be covered with biological
dressings and skin substitutes to reduce pain, evaporative
loss of fl uids, exudative loss of electrolytes and proteins and
to prevent infection by preventing contamination. Once the
epithelialization is complete, the biological dressings and skin
substitutes either comes out of their own or are peeled off. In
full thickness burns wound closure is achieved by application
of autografts over the raw areas after the dead skin comes
out either spontaneously or by excisional surgery. However
in extensive burns, because of defi ciency of donor areas the
wounds need to be covered temporarily with some biological
dressing material or skin substitute till autografts are available.
There are various types of biological dressings and skin
substitutes.22-25 An ideal skin substitute should be inexpensive,
readily available, nonantigenic, sterile, durable, fl exible and
permeable enough but not allow excessive water loss. At the
same time, it should provide an effective barrier to microbes.
Skin substitutes can be either biological or synthetic.
Biological Skin Substitutes
1. Amniotic membrane:26 Re-epithelialization of the partial
thickness skin injury is facilitated by covering the wound
with an amniotic membrane.4,9,10 Both human and bovine
amnion has been used as a dressing material. Amnion is
readily available, inexpensive and can cover large areas.
Although it does not get vascularized, it provides an
excellent temporary cover for a few days and enhances re-
epithelialization in clean second degree burns or donor areas
of split skin grafts. It also enhances epithelial ingrowth from
the wound margins in full thickness wounds. It exerts an
angiogenic effect as well which increases capillary density
of the wound bed. As it does not get vascularized, it does
not get rejected by the body; thereby, allowing its repeated
use. Amnion can be stored for 2 to 3 days in sterile bottles
containing 0.25 percent sodium hypochlorite solution. It
relieves pain, avoids discomfort during dressing change,
reduces oozing and protects underlying regenerating
epithelium.
2. Collagen dressing:27 Collagen dressings are being used
primarily now for superfi cial as well as deep dermal wounds
because of excellent healing seen with their use. Collagen
is hydrophilic and very suitable for cell adhesion. It has
very low antigenicity. It is commercially manufactured and
is readily available in the market as preserved wet as well
as dried sheets.6 The method of application is same as for
amniotic membrane. The wet collagen sheet is rinsed in
normal saline and spread over cleaned wounds. Thereafter,
it is left exposed to get dry and sticks fi rmly to the wound.
In case of dry collagen sheets the surface of the wound
is wet with saline before application of the collagen sheet
and then covered with a dressing of gauze and gamgee.
In second degree superfi cial dermal burns epithelisation
occurs under the collagen sheet. When healing is complete,
the dried collagen automatically falls off (Figures 23A to
C). Thus, it provides good biological temporary cover in
superfi cial and deep partial thickness burns. It also reduces
pain and evaporative losses and forms a barrier for micro-
organisms and thus minimizing the chances of wound
infection.
Figure 23B: Collagen dressing applied to the wounds
Figure 23A: Scalds in a 5-year-old child leading to
superfi cial dermal burns

Healing and Management of Burn Wound
225
Figure 23C: All wounds almost healed after two dressings
in eight days
3. Homografts:28,29
Nonavailability
of
artifi cial
skin
mandates salvage of major burns by homografts. Skin
allografts have also been used extensively for preparing
the wounds for grafting. Cadavers are used as source for
homografts because of availability of large skin banks in
western countries. However, due to nonavailability of skin
banks and lack of public education about skin donations
the surgeons of developing countries procure homografts
from live donors—preferably near relatives. In our
experience, the homografts are mostly required in patients
with 50 to 70 percent burns in whom early excision is not
always possible due to obvious reasons and they are treated
conservatively till all second degree burns have healed
and the third degree burns start granulating. Thereafter,
the important areas are covered with whatever autografts
are available and the rest are covered with homografts.
Once these grafts settle (10-12 days), the patient’s general
condition improves fast. The homografts get vascularized
or ‘take’ exactly like an autograft. They survive for 3 to
10 weeks before getting rejected by the body’s immune
system. They should be removed from the wound before
the signs of rejection appear as the rejection reaction can
deteriorate the condition of the wounds. For the coverage
of resultant raw areas, autografts can be easily reharvested.
4. Heterograft (xenografts): As homografts are diffi cult to
procure, surgeons have used skin procured from porcine or
bovine or canine sources. However, the xenografts do not
get vascularized and hence, their tissue adherence property
is poor and not much effective in preventing bacterial
proliferation.
Synthetic Skin Substitutes
The synthetic skin substitutes are now easily available “Off
the shelf”, but they lack property of adhesion and hence sub-
membrane suppuration is common. But they reduce the pain
and evaporative losses from the wounds.
• Biobrane (Winthrop Pharmaceuticals-Santa Ana, CA): It is
a two layered temporary, synthetic skin substitute. The outer
layer is composed of ultrathin layer of silicon rubber which
is semipermeable and permits the exit of water vapours but
prevents entry of bacteria from the exterior. The inner layer
is tightly woven nylon fabric. Both layers have porcine
collagen peptides covalently bonded which allows the sheet
to adhere to the wound by integration of tissues without
causing infl ammation. The collagen is slowly replaced with
host tissue. Biobrane is translucent allowing observation
of wound healing through it. It is elastic and confi rms to
irregular surfaces. When donor sites for autografts are
available, the silicon sheet is removed and autografts are
applied. It should preferably be removed in about two weeks
to prevent fi broblast ingrowth into the mesh.
• Transcyte (Advanced tissue sciences, La Jolla, California):
It is a bilaminate synthetic, temporary skin substitute. The
dermal layer is composed of a layer of collagen synthesized
by human neonatal fi broblasts cultured on a nylon mesh.
The epidermal analogue is made up of silicone. It is better
than cadaveric skin as it can be easily removed with less
bleeding and leads to equal or better take of autografts.
There is no apparent immune mediated rejection.
• Omniderm (Omikron Scientifi c Ltd., Rehovat, Israel): It is
a temporary synthetic skin cover which is thin, transparent
and fl exible membrane of polyurethane. It is hydrophilic,
absorbs water and is elastic in nature. It is permeable to
liquid and can be used as an interface for skin grafting (as
a layer between graft and the dressing). It allows water
vapour to evaporate and allows antibiotics to permeate
inside.
• Apligraf (Graftskin) (Organogenesis Inc., Canton, MA):
This is composed of two layers, viz., the epidermal layer
made of human foreskin derived neonatal keratinocytes
and the dermal layer made of neonatal fi broblasts seeded
in bovine Type 1 collagen lattice. This has been shown to
improve the cosmetic results when applied over widely
meshed grafts.
• Opsite/Clingfi lm/Via-fi lm: It is a synthetic adhesive
moisture/vapor permeable dressing made up of modifi ed
polyvinyl chloride. Although it is permeable to water
vapour, it is impermeable to bacteria. The permeability

Types of Wounds and their Management
226
to water is low; at times can lead to collection under this
dressing. Pain relief, lack of bulky dressings and early
healing are the advantages.
• Integra (Integra Life Sciences Corporation, NJ): (Figures
24A to E) This is a synthetic, bi-laminate product designed
to provide permanent skin cover, with outer epidermal
substitute made up of silicone (polysiloxone polymer)
layers which controls moisture loss from the wound
bed. The deeper dermal analogue is made up of bovine
tendon collagen cross linked with glycosaminoglycan
(chondroitin-6-sulfate, derived from shark cartilage). With
its use the dermal layer is infi ltrated by fi broblasts. This
is followed by capillary invasion which vascularises the
dermis and leads to deposition of collagen by fi broblasts
and the dermal matrix gradually bio-integrates with the
wound. The silicone layer separates out in two to four
weeks time when a thin split skin graft coverage shall be
required to cover the neo-dermis.

Integra has been used since 1981 (Burke et al.) and
subsequent trials have concluded that hypertrophic scarring
was less, late contractures were rare and artifi cial skin grafted
areas demonstrated growth with the growth of the child.
Alloderm: It is decellularized allograft dermis. It is
prepared by a special biochemical process to make the human
Figure 24C: The appearance of integra after three weeks the dermal
element gets integrated with the underlying bed which can be seen
through the shining silicone sheet
Figure 24D: The overlying silicone sheet removed after three weeks
to show the vascularized dermis over which skin graft can be applied
Figure 24A: Postburn scar contracture over dorsum of the hand
Figure 24B: Scar excised completely to release all contracting
elements and artifi cial skin (Integra) or integrated dermal skin
substitute, which is a bilaminate skin substitute applied on the raw
area created after excision of scar

Healing and Management of Burn Wound
227
dermis acellular. It is used as a dermal transplant in deep
second degree and third degree burns. Donors are screened for
HIV 1 and 2, HBV, HVC, HTLV 1 and syphilis serologically.
Then the material is freeze dried and stored. After wound
excision the dermal matrix is grafted on to the fresh wound
and covered with split skin graft. There are fewer incidences
of infl ammation and infection.

Cultured keratinocytes (Epidermal cells):30,31 In this
technique a culture medium of fetal calf serum is used to
grow keratinocytes into confl uent sheets of epidermis which
are usually two to eight layers thick. By regular sub culturing,
a three square centimetre can be expanded fi ve thousand times
yielding almost enough epithelium to cover the whole body
surface of an adult human. This level of expansion requires
sophisticated labs and a large number of staff and is routinely
impracticable.
Cultured allogenic keratinocytes: This has the advantage
of unlimited supply and is immediately available. Cultured
epidermal allografts have been successfully used even after
cryopreservation. Initially the survival of this allograft was
thought to be because of elimination of langerhans cells
during the cultivation process which is assessed by a lack of
HLA-DR expression. Indefi nite cell survival in the allograft
is controversial, the long term wound healing is suggested to
be due to the residual host keratinocytes whose growth and
migration is stimulated by cultured allografts. The disadvantage
is that it still carries the possibility of disease transmission.
Dressing Technique
There are different types of dressings used at different stages
in conservative burn wound management in order to achieve
different goals. The main aim of dressing is to:
• Decrease evaporative losses
• Prevent and control colonization of wounds by bacteria
• Isolate the burn wound from the other sources of
contamination
• Maintain an environment which promotes epithelialization
of the partial thickness wounds.

The primary dressing in all acute burn wounds which is
done as a routine in the authors unit is as follows:

The technique of dressing a burn wound is very important
for the fi nal outcome of burn wound treatment program. All
burn dressings should be done with proper aseptic precautions
to prevent wound contamination. All doctors and nursing
staff should be properly gowned and gloved. Majority of
the dressings can be performed without general anesthesia.
Usually sedation with opioid analgesics (e.g. morphine ) is
adequate.

A satisfactory burn dressing is one which can absorb all
the fl uid exuded from the burn wound and distributed evenly
throughout so that there is no collection of the exudate on the
wound surface.

The innermost layer of occlusive dressing consists of
a layer of an antimicrobial agent over which a wide mesh
gauze impregnated with paraffi n or petroleum jelly is applied.
This tulle grass is nonadherent so that pain and trauma to
the regenerating neoepithelium can be minimized at the
time of change of dressing. After the nonadherent gauze and
antimicrobial agent is applied, multiple layers of gamgee pads,
depending on the expected amount of exudate, are applied and
kept in place with gentle compression bandage. This dressing
prevents edema formation, splints the wound and facilitates
absorption of discharge. However, it should not be constricting
in any way. This outer layer of the dressing should be porous
to allow evaporation of water and prevent inner layers from
becoming soggy as that encourages microbial growth (Figures
25A to D).

The superfi cial dermal burns usually heal within three
weeks with this type of dressing (Figures 26A and B). The
fi rst dressing can be left on for three to fi ve days provided
there is no soakage and smell in the dressing and subsequently
at three days interval. If there is any soakage, pain, fever
and smell, the dressing should be changed immediately and
more frequently till the wound condition improves. By three
weeks post burn most of the superfi cial dermal burns heal.
It is also easy at this time to identify wounds which are full
thickness. For superfi cial dermal burns, similar dressings can
be continued at infrequent intervals till healing is complete. It
is the deep dermal and full thickness burns in which there is
a lot of slough and the type of dressing needs to be changed
as per the requirements of the wound to assist in removal of
slough. The nonadherent dressing with silver sulfadiazine or
mafenide is continued till loosening of the eschar although
Figure 24E: Thin skin graft applied over the dermis is
completely taken up–one year postoperative picture
E

Types of Wounds and their Management
228
separation of slough is slow with use of these antimicrobials.
If the eschar is still adherent at 21 days, late surgical excision
of eschar can be considered as an option.

Once the eschar is loosened, it is debrided mechanically
and the remaining nonviable tissue is best removed by
repeated dressings with Eusol. This is a wet to dry type of
dressing which involves direct application of eusol soaked
gauze followed by dry gauze and bandage. Eusol is a good
desloughing agent. Eusol (Edinburgh University solution)
contains the following:
• Calcium hypochlorite
1 part by weight
• Boric acid
1 part by weight
• Water
80 parts by weight

If patient complains of pain, it can be diluted with normal
saline to half or quarter strength. Gauze well soaked in Eusol
and lightly squeezed out is directly applied to the wound
without any paraffi n gauze or any other nonadherent layer
and covered further by gamgee and bandage. Since this is an
adherent dressing, it has to be soaked well with normal saline
on removal during dressing change to avoid pain. Ideally eusol
dressings should not be allowed to dry for greater effi cacy.
The action of hypochlorite is transient so it is advised to repeat
the dressing 3 to 4 times a day. As this is not practicable, the
dressing is changed on daily basis. Although the action of
eusol has not been studied by any clinical trial, it has been
used by surgeons for decades and found to be very effective.

Enzymatic debridement using various enzyme preparations
(e.g. collagenase—salutyl) has been tried from time to time
with the assumption that the enzyme can digest the dead tissue
and help in earlier removal of eschar. Unfortunately, it does
Figure 25A: Burn wound is fi rst cleaned and debrided
Figure 25B: One percent SSD is applied to the clean wound over
paraffi n gauze
Figure 25C: Next layers of gauze are applied over the wound
surface
Figure 25D: Over the gauze a layer of gamgee is wrapped followed
by a fi rm compressive bandage

Healing and Management of Burn Wound
229
not prepare the bed to accept graft as it does not stimulate
granulation tissue formation and may even form a neoeschar.
Till date none of the enzymatic preparations have been found
to have much practical value.22

Once the slough is cleared off the wound surface, another
change in the type of dressing which promotes granulation
tissue formation is required. For this simple wet dressing
in the form of saline gauze is helpful. This includes a layer
of paraffi n gauze over which saline soaked gauze is applied
directly to the wound followed by gamgee and bandage.
These gauze compresses have to be in continuous contact with
the burn wound and should be wet at all times and replaced
preferably twice or thrice a day. As this is not practically
feasible, at least once daily dressing is essential. These wet
dressings help in development of healthy granulating wounds
ready for skin grafting. Wet dressings provide continuous
drainage and thus prevent pocketing and abscess formation.
These are continued till the patient is fi t to be taken up for
grafting.
Preparation of Wound for Grafting
A couple of days prior to grafting, the paraffi n gauze is omitted
from the dressing so as to make the raw surface non greasy for
better adherence of skin graft.

The condition of the granulation tissue is quite suggestive
of the wound preparation for grafting. A healthy bed which is
ready for grafting shows clean red granulations devoid of any
necrotic areas and does not bleed readily on touch (Figures 27
A and B). If the wound looks angry red and granulation tissue is
Figure 26B: Wounds healed completely in 10 days
Figure 26A: Scalds leading to superfi cial dermal burns
Figure 27A: Postacid burn raw area with healthy granulation tissue
fi t for grafting
Figure 27B: Three months after skin grafting of the wounds

Types of Wounds and their Management
230
very fragile and bleeds readily on touch with unhealthy copious
discharge, it is suggestive of beta-hemolytic Streptococcus
infection (Figure 28). This is the only true contraindication for
skin grafting of wound. Since Streptococcus is still found to be
sensitive to penicillin and other antibiotics, systemic penicillin
should be started immediately and continued till swab culture
is negative for this bacterium. If the granulation tissue appears
slimy it is suggestive of Staphylococcus infection (Figure 29)
In these cases, systemic antibiotics, based on wound swab
culture-sensitivity data are administered and local dressings are
done with anti-staphylococcal agents like fucidin, mupirocin,
etc. skin grafting is done only after Staphylococcus aureus is
cleared.

If there is edematous, hypertrophic granulation tissue,
gentle compressive dressings using crepe bandages should be
done to reduce edema. Local steroid cream is also effective.
Bluish green pus discharge from the wound suggests
Pseudomonas growth (Figure 30). In these cases, dressing
with one percent acetic acid solution is very effective or else
mafenide can be used. Pale granulation tissue suggests anemia
and should be corrected by blood transfusions.

Once granulation tissue appears, swab cultures are always
taken to look for microbial growth and its sensitivity pattern
to various antibiotics before taking up the patient for skin
grafting. Growth of betahemolytic Streptococcus is an absolute
contraindication for grafting. Initial ‘take’ of graft followed by
loss after a few days with an eaten up appearance is typically
indicative of Staphylococcus infection (Figure 31). To prevent
further loss of graft, action has to be taken immediately as
advised above. Sometimes the burn wounds are neglected and
Figure 28: Angry red wound with fragile granulation tissue bleeding
profusely on touch and forming hemorrhagic bullae indicating
streptococcal infection which is an absolute contraindication for
grafting. Penicillin is very effective in these cases
Figure 29: Slimy dirty granulation tissue with copious discharge
indicating staphylococcal infection
Figure 30: Greenish discoloration of wound surface indicating
Pseudomonas colonization of wound
Figure 31: Loss of skin grafts due to MRSA infection

Healing and Management of Burn Wound
231
Figure 32A: Old neglected postburn raw area with fi brosed
bed and no granulation
Figure 32C: One month postgrafting of the same area
Figure 32B: This wound needs to be excised to remove the
unhealthy tissue so that skin graft can be applied to the raw area
they turn into chronic fi brosed wounds. These wounds cannot
be prepared by dressing alone and require excision of the
fi brotic bed till healthy soft and supple vascular bed is reached
before application of split skin graft (Figures 32A to C).
Surgical Excision of Burn Wound
Types of excision
1. Tangential excision: It is used typically for deep dermal
burns. In this technique, the wound is excised with
Watson’s skin grafting knife till healthy viable dermis is
reached over which split skin graft is applied immediately.
2. Sequential excision: It is also used for deep burns in which
Watson’s skin grafting knife is used to sequentially excise
all necrotic tissue until viable tissue is encountered which
can be either viable deep dermis or viable fat or fascia.
This area is also immediately skin grafted. This technique
is most effective for mixed deep dermal and full thickness
burns in which sequential excision helps in saving the
viable dermis or fat which would otherwise be sacrifi ced if
the entire burned area were to be removed with a surgical
blade.
3. Suprafascial full thickness excision: It is indicated for full
thickness burn wounds. In this, full thickness of burned
skin with subcutaneous tissues is excised with a surgical
knife till the deep fascia. This can be immediately grafted
because fascia is a healthy bed for graft ‘take’.
4. Subfascial excision: It involves excising till deep to the
deep fascia, thus reaching the muscles. In these cases, the
chances of graft ‘take’ are poorer compared to suprafascial
excision.
5. Escharectomy and delayed skin grafting: This was
practiced earlier for partial and full thickness burns in
which the nonviable eschar is excised with a skin grafting
knife till minimal bleeding bed is encountered. This bed
is, then, covered with a biological dressing and reassessed
after 48 to 72 hours to look for remaining dead tissue which
is again excised and dressed till healthy granulation tissue
appears. This is secondarily grafted. It is suitable for cases
where primary excision cannot be done due to medical
reasons or associated injuries.

Tangential excision:32-34 This is indicated for deep dermal
wounds. In tangential excision burnt dermis is excised with
modifi ed Humby’s skin grafting knife/dermatome. Since
excision is done tangential to the wound and multiple thin
slices of the tissue are excised till viable bleeding tissue is
reached, the method of excision is called tangential excision.

Tangential excision is usually done between 3rd and 5th
day following burns. The rationale for not doing it earlier is
to give adequate time for resuscitation especially in extensive
burns and to avoid unnecessary excision of deeper tissues

Types of Wounds and their Management
232
where perfusion is restored after resuscitation is completed.
Excision is not done after fi ve days because there is a
signifi cant bacterial colonization of wound by then which may
inhibit graft ‘take’. After seven days, there is softening of the
surface of wound which makes excision technically diffi cult.
Technique of Excision
First step is to map and mark the area of deep dermal burn to
be excised.The skin grafting knife is set to take thick split skin
graft. Saline is used to keep the area wet and helps in easy
movement of knife. Slices of burned tissue are excised till
viable tissue with brisk bleeding is encountered. Viable dermis
appears shiny white in color with multiple bleeding points.
Small deeper (3rd degree) burnt areas in the deep dermal
burn wound may be excised tangentially till viable bright
yellow fat is exposed and nonviable brown fat is completely
excised. ‘Take’ of skin graft over the fat is relatively poorer
as compared to that on viable dermis.Thin skin graft is then
applied immediately over all the excised areas after proper
hemostasis (Figures 33A to D).
Advantages
Early excision has been advocated as one of the major factors
for reducing the incidence of wound infection and sepsis in
past three decades.35 Various authors have shown that have
shown that burn wound excision signifi cantly reduces bacterial
Figure 33A: Deep dermal burn wound over thigh
Figure 33B: Area to be excised marked and being tested for
sensations
Figure 33C: Tangential excision of the dead dermis
with Watson’s knife
Figure 33D: Two weeks postoperative picture (after graft application)

Healing and Management of Burn Wound
233
colonization (Barret and Herndon36 2003). Chances of sepsis
increase if excision is delayed by more than fi ve days. Desai37 et
al. (1990) have advocated that near-total excision of large burn
within fi rst 24 hours reduces blood requirement and morbidity
also. Experience of the surgeon and facilities available at the
center where excision is done is important. Less than 20 percent
TBSA excision is relatively safer than excising larger areas.
If treated with excision and grafting burn patients appear to
have fewer infectious wound complications, a shorter hospital
stay and full functional recovery may be achieved within two
weeks. Whereas in the conventional method, de-sloughing
alone requires three weeks and the shortest possible time for
full healing is therefore about fi ve weeks.
SUMMARY
The primary cause of morbidity and mortality following
an extensive burn injury has always been the burn wound
infection. Hence early closure of wound can eliminate not
only the risk of infection but also the risk to life in extensive
burns.Meticulous estimation of the extent and depth of burn at
the outset,is necessary for planning the wound management as
the healing of the burn wound depends on the depth of injury.
Superfi cial burns tend to heal with conservative management,
whereas deeper burns need some operative intervention for
faster healing.

Even though a fresh burn wound is sterile, use of topical
antimicrobial agents or skin substitutes in burn wound care
can prevent or minimize burn wound infections and sepsis
especially in small and superfi cial burns, although there is no
risk for burn sepsis. However, as these cases are treated on
an outpatient basis, they can be used to prevent conversion of
superfi cial wounds to deep wounds.

On the other hand wound excision and skin grafting
is an established method of treatment for deep dermal,
indeterminable depth and deep burns. Excisional surgery
has led to reduced overall morbidity signifi cantly and to
some extent, burn wound sepsis and mortality. It has also led
to reduced cost of treatment, reduced wound related pain,
better functional result, early rehabilitation and reduced
long term morbidity with reduced time away from work.
Scarring (hypertrophy, contractures) is also much less if
wound is closed early and there is reduction in the need for
reconstructive procedures. Hence early closure of burn wound
should be the primary aim when treating deep burns.
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