Principles and Practice of Wound Care

Miscellaneous
Section 4
436

There are various types of collagen which are present in
different types of scars. Proliferative phase also involves
the regeneration and migration of endothelial cells,
neovascularization and epithelialization. All these processes
are actively regulated by cytokines like TGF-β, EGF
(epidermal growth factor), KGF (keratinocyte growth factor)
and FGF-7.6,13,14 The phase of contraction overlaps and is also
intimately related to the proliferative and remodeling phases.
In this phase the edges of the wound contract centrally.
The process of contraction occurs by true shortening of the
collagen matrix in the wound bed as well as by adjacent
tissues being pulled into the wound. Here myofibroblasts
described by Gabbiani, et al13,15 play an important role. It
remains debatable whether the wound bed contracts or the
healing surface contracts. The degree of contraction depends
upon the origin and location of the wound, whether the closure
is primary or secondary, the presence or absence of infection,
type of supporting structure under the wound, etc.

The remodeling phase involves maturation of the wound
bed and the healed surface. Healing of a wound occurs by
laying down of collagen and epithelialization. A balance is
struck between laying down of collagen and its degradation.
The collagen changes to type I collagen over a period of time
in which the ground substance is less and collagen cross
linking increases.6,13 The remodeling of the wound goes
on for months to years before one can say that the healing
of the wound has been completed. More details about the
pathophysiology of wound healing is given in earlier chapters
and the reader should refer to them.
Metabolic Response to Injury
There are two phases of metabolic response to any trauma–
first is the “Ebb phase” which is a phase of traumatic shock
which lasts for a short period of hours or days. This is the
phase of reduced metabolism or a state of shock. The second
phase is the ‘flow phase’ which is a period of hypermetabolism
which lasts for a longer period.

The magnitude of these two phases of metabolism depends
upon the degree of trauma. In minor trauma, both the phases
may be very short and the wound heals quickly. However in
major trauma or multiple wounds the phases will be much
more prolonged. An understanding of the metabolic response
to the injury and nutritional support required, become very
important. There is an increased body energy consumption
and depletion of body nutrients.16-18
Role of nutrients
in wound ­healing
Carbohydrates in Wound Healing
Carbohydrates are energy producing nutrients. They provide
energy for proliferation of cells which are required during
proliferative phase of post-trauma wound healing. Recently
it has been proven that carbohydrates act as communication
markers when they convert into glycoproteins or glycolipids.
These glycoproteins also play a critical role in many structural,
lubricant, transport, immunologic, hormonal and enzymatic
activities19,20 (Table 2).
Problems Related to Excess Carbohydrate Intake
Carbohydrates are essential in the diet for maintenance
of good health. Excessive intake of high sugar containing
carbohydrates can have an adverse effect on the health in
general (by promoting obesity)21 as well as on wound healing.
Ludwig et al suggested that foods with high glycemic index,
induce hormonal and metabolic changes which leads to over
eating and may cause diabetes mellitus,22 which can promote
wound infection and adverse outcome.23 Diabetic patients
with wounds should take special precautions to regulate
carbohydrate intake and glycemic status throughout the period
of wound healing. Obesity may cause diabetes mellitus,
hypertension and coronary artery disease and eventually poor
wound healing.
Table 2: Roles of key macronutrients in wound healing
Nutrient
Specific compound
Contribution in wound healing
Proteins
Amino acids
Needed for platelet function, neovascularization, lymphocyte formation, fibroblast proliferation,
collagen synthesis and wound remodeling.
Required for certain cell-mediated responses, including phagocytosis and intracellular killing
of bacteria.
Gluconeogenic precursors.
Carbohydrates
Glucose
Energy substrate of leukocytes and fibroblasts.
Fats
Fatty acids
Cholesterol
Serve as building blocks for prostaglandins and isoprostanes that are inflammatory mediators;
energy source for some cell types.
Are constituents of triglycerides and fatty acids contained in cellular and subcellular membranes.

Role of Nutrition in Wound Healing 
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Fat and Fatty Acids in Wound Healing
There is an exponential increase in energy requirement during
the healing of wounds. This increase is proportionate to
the size of the wound, the depth of the wound, presence or
absence of dead tissue, infection, associated complications,
etc. This requires increase in calorie intake over REE. The
requirement is much more in severely injured, burned victims
or critically ill patients with hypermetabolic states.24,25
The stress causes release of stress hormones, e.g. glucagon,
cortisol, catecholamines, etc. These hormones result in
protein catabolism and lipolysis to meet the increased calorie
requirement. During stress, fat and fatty acids remain the
major source of energy supply. Therefore exogenous fat and
fatty acid production from adipose tissue remain the main
source of energy for wound healing and are the potential
modulators of the healing response.

The essential fatty acids play an important role in modulation
of inflammation and the immune response.26-28 There are
many contradictory reports on the role of fatty acids on wound
healing. One of the studies concluded that essential fatty acids
are not necessary for skin wound repair.29 It is clear from many
studies that antioxidants that have been shown to reduce lipid
peroxidation and modify the effect of fatty acids are vitamin C,
vitamin E, selenium compounds and α-lipoic acid.30-33

The effect of fatty acids on wounds varies depending upon
the stage of wound healing, the type of wound and its location.
In early stage of wound healing, the anti-inflammatory effect
of omega-3-fatty acids may delay wound healing34 (Table 2).
Effect of Inadequate Fat Intake on
Wound Healing
Inadequate fat intake or fat malabsorption results in deficient
fat assimilation and the body has to depend upon protein and
carbohydrates for its energy requirement. If there is a negative
nitrogen balance, it would delay wound healing.35 In another
scenario, in patients on parenteral nutrition, if not given
enough fat, the glucose inhibits the release of fatty acids from
adipose tissue, resulting into fatty acid deficiency.36
Effect of Excess Fat Intake on Wound Healing
Excess of fat may neither harm nor benefit healing wounds.
However an excess of polyunsaturated fat (w-PuFA)
could impact the immune system. Excess of w-PuFA may
cause immunosuppression. This may compromise the
fight against infection. In critically ill patients like burn
patients, high fat content should be avoided as it may cause
immunosuppression.37
Protein and Wound Healing
In experimental models38-43 it has been shown that:
• In healthy conditions, cell proliferation does not match
with protein synthesis. Rate of protein synthesis in the
epidermis is ten times more than that in the dermis.
• Insulin combined with glucose and amino acid
supplementation improves the skin and muscle protein
metabolism.
• During short-term changes in nutritional status, the skin
protein metabolism is maintained dynamically.
• In cases of chronic or prolonged malnutrition associated
with protein malnutrition, collagen synthesis is reduced.
• Whenever there is a wound there is a negative nitrogen
balance in the adjacent skin tissue due to protein loss from
the wound surface.

These findings indicate that protein metabolism plays
a vital role in wound healing. Hence nutritional support,
modulation of anabolic factors and addition of nutrients in
food are important. A positive protein balance in the skin
would accelerate the wound healing process. It has been
demonstrated that wound healing can be improved with
protein supplementation as it decreases muscle catabolism,
increases fibroblast activity, increases collagen synthesis and
improves immune response44-46 (Table 2).
Effect of Low Protein Diet on the Wound
Protein synthesis is the key factor in wound healing. Deficiency
of protein affects every stage of the healing process. It impedes
fibrin formation, impairs laying down of collagen, fibrous
tissue formation, phases of contraction and remodeling.47,48
Hypoalbuminemia <3 gm/dl causes edema which can result in
decreased oxygen delivery to the wound site. Wound healing
is significantly delayed when serum albumin is less than
2.5 gm/dl49,50 Normal wound healing cannot occur at serum
albumin levels <2.0 gm/dl.51

It has been shown that wounds in animals with deficient
protein intake heal with a scar which is weaker in strength as
compared to the group receiving adequate proteins.52
Requirement of protein increases in the following situations:
• Surgical/trauma patients
• Major surgery (10% increase)
• Multiple trauma patients may need as high as 75 percent
more protein
• Burn and stress have the greatest impact and increase the
protein need by 75 to 100 percent.53
• It is difficult to quantify the exact additional requirement
for a specific wound. However this can be decided based
on periodic assessment.

Miscellaneous
Section 4
438
Effect of High Protein Diet on Wound Healing
High protein diet enhances wound healing. This has been
proven in healing of truncal pressure ulcers. After ingestion of
high protein diet in a group of patients with pressure ulcer, the
area of pressure ulcer decreased significantly as compared to
the group receiving low protein diet.54

Conventionally high protein food is prescribed for patients
with wounds. The aim is to maintain a positive nitrogen
balance. Exogenous dietary protein is used for structural and
functional protein synthesis. Recommended protein intake for
various clinical conditions is given in Table 3.

The aim of protein supplementation is to minimize net
protein catabolism and to promote wound healing preserving
the lean body mass. Protein intake of >1.5 gm/kg/day has
not been shown to be advantageous, rather it can result in
an increased concentration of urea and ammonia. It may
also induce low grade metabolic acidosis and subsequently
a decreased renal tubular reabsorption of calcium, leading
to increased cell mediated bone resorption and osteoporosis.
Therefore in patients with major wounds, a comprehensive
evaluation of the clinical parameters, organ function especially,
visceral proteins, renal function, blood urea nitrogen and
urinary urea nitrogen and glucose tolerance should be carried
out to formulate the feeding regimen.
Amino Acids and Wound Healing
There are a few amino acids which play a key role in wound
healing. Glutamine and arginine are important amongst them.
Glutamine
Glutamate is the precursor of glutamine. It is the primary
fuel for rapidly proliferating cells apart from being a nitrogen
carrier. It is also a precursor of several important metabolic
agents, including glutathione, arginine, taurine DNA and
RNA.

Glutamine is a nonessential amino acid which can become
‘conditionally essential’ in certain circumstances like trauma,
stress, surgery, etc.55 Glutamine is a 5-carbon amino acid with
two amino moieties. This is the most abundant amino acid in
the human body. This accounts for 30 to 50 percent of all the
amino acids and is mainly responsible for transportation of
nitrogen in the blood.

Clinical studies have shown that glutamine level decreases
in cases of trauma, sepsis and stress. It has also been shown
that glutamine supplementation helps in wound healing and
reduces the incidence of infection.56 During proliferative
phase of wound healing, α-ketoglutarate is taken up by the
cells in the wounds by unmediated diffusion process.57 Here
glutamine forms the main energy source instead of glucose.58
In in vitro studies, glutamine stimulates synthesis of collagen
in fibroblast cultures59 and it has a dose dependant effect on
collagen gene expression.60

There are many contradictory reports about the role of
glutamine and its true efficacy in the process of wound healing.
The results of glutamine supplementation in surgical and burn
patients have not been uniform. However, at present majority
of studies have found that glutamine has a positive role to
play in wound healing. In a systematic review, high dose of
glutamine (>2 gm/kg/day) is said to reduce complications
including mortality and morbidity in patients with wounds.61
There is no ideal dose of glutamine as there are no established
guidelines yet. The doses used are as follows:

Oral dose – 0.3 to 0.5 gm/kg/day × 30 days

IV dose – 0.57 gm/kg/day × 30 days
Arginine
This is a nonessential amino acid that plays a key role in protein
and amino acid synthesis. Adequate tissue arginine appears to
be essential for efficient wound repair and immune function.62

Arginine is considered important for collagen synthesis and
deposition during growing age as well as in wound healing.
During growing age, arginine is important for connective
tissue protein synthesis and in wounds, it synthesizes
reparative connective tissue. A clinical study has documented
increased collagen deposition in healing wounds following
supplementation with 30 gm of arginine/day × 14 days. In
another study, it was shown that the predominant effect of
arginine in wound healing is to enhance wound collagen
deposition63-65 and not an enhanced inflammatory effect or
epithelialization.

A diet containing nine percent of total protein as arginine
has been shown to be beneficial for wound healing, to reduce
the infection rate of wounds and to reduce the hospital stay.66
Table 3: Recommended protein intake for specific clinical conditions
Clinical condition
(g/kg/day)
Healthy adult
0.8–1
Healthy neonate
2.20
7–12 months
1.20
1–3 years
1.05
4–8 years
0.95
9–13 years
0.95
14–18 years
0.85
Severe pressure ulcer
1.25–1.5
Burns (adult)
1.2–1.5
Burns (children)
2.5–3.0

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439

Normal individuals can be given high doses of arginine,
however, a careful monitoring is required in hepatic and renal
compromised patients. It may cause hyperkalemia in some
patients.
Vitamins and Wound Healing
The role of different vitamins in wound healing is given under
Table 4.
Vitamin B and Wound Healing
Vitamin B and its various components play a vital role in
every phase of wound healing. They act like coenzymes and
also interact with each other. These water soluble vitamins are
important for synthesis and interlinking of collagen fibers;
for proper energy metabolism and tissue synthesis. The
myofibroblasts which are responsible for wound contraction
are dependent upon B vitamins. During every phase of wound
healing the energy consumption is well regulated by these
vitamins.67 Similarly all anabolic activities require adequate
supply of all the necessary vitamins. They also improve the
immunological response to infection and help in clearing
necrotic tissue. Hence the need to provide different types of
vitamin B in greater quantity orally or parenterally to even
uncomplicated, ill patients for faster wound healing.68 In short
the B vitamin play a monumental role in wound healing.
Vitamin C
Vitamin C plays a key role in collagen synthesis; as it is
necessary for hydroxylation of proline and lysine residues in
procollagen which in turn forms collagen. Hydroxyproline also
stabilizes the collagen-triple-helix structure.69 Vitamin C also
improves immune function by enhancing neutrophil motility
and lymphocyte transformation; increases angiogenesis
and functions as a powerful antioxidant.70,71 Ascorbic acid
is necessary for the physiological response to any stress.72
Wounds, burns and surgical trauma may cause decrease
in plasma ascorbic acid, hence vitamin C is an essential
supplement for wound management protocol. It has been
shown to improve healing even in an ischemic wound model.73

Though vitamin C is essential for many metabolic
functions of the body, its storage is poor in the human
body. Elderly, drug abusers, alcoholics, undernourished
individuals; patients with prolonged hospitalization, severe
illness and even adults with poor intake are prone to ascorbic
acid deficiency.74-76

Ascorbic acid deficiency not only causes abnormal collagen
fibers, but also alterations of intracellular matrix manifesting
Table 4: Roles of key micronutrients in wound healing
Nutrient
Specific compound
Contribution to wound healing
Vitamins
Vitamin C
Hydroxylates proline and lysine in collagen synthesis.
Free radical scavenger.
Is a necessary component of complement that functions in immune reactions and increases
defense against infections.
Vitamin B complex
Serve as cofactors of enzyme systems.
Required for antibody formation and white blood cell function, essential for nucleic acid
metabolism.
Vitamin A
Enhances epithelialization of cell membranes.
Enhances rate of collagen synthesis and cross-linking of newly formed collagen.
Antagonizes the inhibitory effects of glucocorticoids on cell membranes.
Vitamin D
Necessary for absorption, transport and metabolism of calcium. Indirectly affects
phosphorus metabolism.
Vitamin E
Free radical scavenger.
Vitamin K
Needed for synthesis of prothrombin and clotting factors VII, IX, and X. Required for
synthesis of calcium-binding proteins.
Minerals
Zinc
Stabilizes cell membranes; Is an enzyme cofactor needed for cell mitosis and cell
proliferation in wound repair.
Iron
Needed for hydroxylation of proline and lysine in collagen synthesis.
Enhances bactericidal activity of leukocytes and hemoglobin oxygen transport to wounds.
Copper
Integral part of the enzyme lysyl oxidase, which catalyzes formation of stable collagen
cross-links.

Miscellaneous
Section 4
440
as cutaneous lesions, poor endothelial cell adhesion and
decreased tensile strength of fibrous tissue.77

Normal daily intake of vitamin C should be 20 to 30 mg/
day to maintain the total body pool of 2.3 gm.78 However
low intake for more than six months affects wound healing.
Otherwise it is compensated from the body pool.

Considering the importance of vitamin C, its supplementation
is appropriate in the management of wounds. It may be given
in low or high dosage even in nondeficient individuals. Dosage
of 500 to 1000 mgm/day in two divided doses may be adequate
for smaller wounds. For larger wounds 1 to 2 gm/day should
be given.79 Safety profile for vitamin C is good; however
hypervitaminosis may lead to oxalate renal stones.
Vitamin A
Vitamin A is required for epithelial growth, glycoprotein and
proteoglycan synthesis, cellular immunity and inflammatory
reaction.80-87 Levenson et al have suggested that it enhances
early inflammatory phase by monocyte and macrophage
stimulation at the wound site, modulates collagenase activity,
supports epithelial cell differentiation and stimulates the
immune response.88,89 There are a large number of experimental
and clinical studies out lining the important roles of vitamin
A. It increases collagen content and its strength in cutaneous
wounds, tendon and intestinal repair90,91 It can accelerate
fibroblast maturation and multiplication of fibroblast receptors
for epidermal growth factors.90,92 Deficiency of this fat soluble
vitamin causes delayed wound healing, impairs epithelialization,
retards collagen synthesis, compromises wound contraction
and cross-linking of newly formed collagen.93-95

Vitamin A has also been reported to correct nonsteroid
induced postoperative immune depression96 and improves
survival in surgically induced abdominal sepsis.88

In experimental studies, vitamin A supplementation was
found to increase collagen cross linkage and wound breaking
strength.97,98 Research supports the role of perioperative
vitamin A supplementation in immunocompromised patients
with sepsis or those on steroid treatment. Hypervitaminosis
should be avoided as it affects the liver and the cornea. It is
known to have a teratogenic effect too.
Vitamin D
In experimental studies in rats, topical application of
1,25-dihydroxyvitamin99 D3 was found to significantly
accelerate healing of full thickness cutaneous wounds.98
It was also found to increase the wound breaking strength
and improve epithelialization.100 It has also been reported
to stimulate the synthesis of fibronectin and enhance the
maturation of macrophages to promote wound healing101,102
Deficiency of vitamin D results in impaired healing besides
growth retardation in children, low bone mineral density and
increased incidence of fractures.
Vitamin E
Vitamin E is considered very important by lay public for
healing and for prevention of scars. But these claims have not
been supported by scientific studies. Scientific reports suggest
that vitamin E has a negative impact on wound healing.103
Vitamin E is an antioxidant and has anti-inflammatory
properties. It alters prostaglandin production by inhibiting
phospholipase A2 activity, resulting in decreased collagen
production and decreased inflammation. Most authors agree
that high doses of vitamin E leads to delayed wound healing.104
This antiproliferative effect however, might be beneficial in
the prevention of hypertrophic scar or keloid.105
Vitamin K
Vitamin K does not have any direct role in wound healing.
Vitamin K is important for coagulation which is a prerequisite
for hemostasis. This may be considered as its indirect role in
wound healing. Deficiency of vitamin K will result in bleeding,
delayed clotting, hematoma formation which predisposes to
infection, delayed tissue repair and poor wound healing.
Trace Elements in Wound Healing
Like many vitamins, trace elements do not directly affect wound
healing. They serve as cofactors or are part of cytokines or
enzymes which are essential for healing. Disturbances in the level
of these trace elements also does not usually occur independently.
Almost always it is associated with some metabolic or nutritional
deficiency. When it comes to wound healing zinc, copper and
iron are the most important trace elements (Table 5).
Zinc
Zinc is an essential trace element for DNA synthesis, cell
division and protein synthesis.106 All these functions are
important elements of wound repair and healing. Zinc
deficiency is associated with deranged fibroblast proliferation
and delayed epithelialization resulting in poor wound healing
and decreased breaking strength of experimental wounds.107
It also impairs cellular and humoral immunity, resulting in
increased susceptibility to infections.

Zinc supplementation is required in zinc deficient
individuals. Zinc deficiency is quite common in general
population, more so in critically ill, injured or burn patients
and in patients with chronic venous ulceration.108,109 Zinc

Role of Nutrition in Wound Healing 
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441
supplementation of 5 to 30 mgm daily (average 15 mgm/day)
has been recommended, perioperatively. Higher amount may
be needed in cases of zinc deficiency and conditions leading
to zinc depletion.
Iron
Iron is an essential cofactor in the replication of DNA. Iron
is involved in production of deoxyribonucleotides which is
required for DNA synthesis. Iron deficiency may impair
wound healing.110 Increased iron free radicals may be
responsible for persistent inflammation, increased connective
tissue destruction and lipid peroxidation, which creates a
hostile environment for wound healing.111
Copper and Magnesium
Copper is a cofactor and catalyzes the cross-linking of collagen
and strengthens the collagen framework.112 It also stimulates
angiogenesis and may in turn accelerate wound healing.113
In in vitro model, copper and zinc were found to stimulate
integrins expressed by the basal layer keratinocytes, which
play an important role in healing.114 Magnesium in humans,
enhances the mechanical properties of a scar.110

Chromium, iodine, manganese, molybdenum and selenium
have secondary importance in wound healing.
Other Dietary Supplements for Wound
Healing
Bromelain
Bromelain is a set of proteolytic enzymes derived from
pineapple plant Ananans comosus. Early studies showed that
oral bromelain caused reduction in edema, bruising, pain
and healing time after trauma or surgery.115-118 Its analgesic
effect may be because of the anti-inflammatory property of
bromelain rather than any direct analgesic property.119 It is
claimed that bromelain also prevents aggregation of blood
platelets in patients with high platelet aggregation values.120
However this has not been proved in human subjects.121,122
Researchers recommend that oral administration before
surgery should be advised with caution till further studies
document its role.
Table 5: Trace elements primary and secondary roles in wound healing
Elements
Role in wound healing
Copper
Cofactor for ceruloplasmin
Maintains iron utilization
Oxidase necessary for the formation of transferrin (carrier of iron)
Associated with the maintenance of normal synthetic rates for RBCs and WBCs
Iron
Helps in oxygen transport
Cytochrome content—normal cellular respiration; ATP storage through iron coupling reactions
T-cell immunity and cognitive function roles
Zinc
Functions with many enzymes, e.g. carbonic anhydrase, alkaline phosphatase, lactic acid dehydrogenase,
alcohol dehydrogenase, RNA and DNA polymerases, and superoxide dismutase
Helps in wound healing, increases oxygen affinity, synthesis of nucleic acid, glutathione and connective tissue
It is collagen precursor and component of bone
Chromium
Maintains protein, carbohydrate, and lipid metabolism
Glucose tolerance factor (GTF)—cofactor with insulin
Important in peripheral nerve function
Iodine
Incorporation into thyroid hormones (T3 and T4)
Regulates cellular metabolism, temperature, and normal growth
Manganese
Activator for several enzymes—glycotransferase activation (mucopolysaccharides formation)
Found in association with vitamin K deficiencies—glycotransferase activation in prothrombin synthesis
Found in association with squalene—precursor of cholesterol and sex hormones
Found in association with protein synthesis, carbohydrate and lipid metabolism
Molybdenum
Constituent of aldehyde oxidase, sulfite oxidase, and xanthine oxidase
Causes increased mobilization of copper from tissue
Increases urinary excretion
Selenium
Component of glutathione peroxidase (antioxidant)
Protects the cell from lipid oxidation
Functions with and substitute for vitamin E

Miscellaneous
Section 4
442
Glucosamine
Glucosamine is believed to regulate the production of
hyaluronic acid by fibroblasts during the proliferative stage
of wound healing, which in turn stimulates the proliferation
and migration of fibroblasts and epithelial cells.123 For faster
wound healing, oral glucosamine before and after surgery or
trauma might be indicated. This is believed to enhance the
healing process and possibly reduces scarring.
Nutrition and Wound Healing in Infants
and Elderly (at the Extremes of Age)
Normal human adults have adequate reserve to meet
emergency situations. Simple wounds heal without the need
for any supplementations without any complication. However,
in patients who are very young or very old, additional
supplementation may be required for proper healing because
of relatively poor reserves.
Nutrition in Children
Neonates and children have a higher baseline energy
requirements. Resting energy requirement in neonates is
about three folds that of adults and normal requirement is 120
kcal/kg/day, because the body growth substantially increases
the energy requirement in this age.

The increased metabolic demands and limited body
reserves require early and larger nutritional support in children
with trauma or wounds (normal requirement in children is ~70
kcal/kg/day). Micronutrients like vitamins and trace elements
are usually deficient in the diet of children, hence they should
be supplemented adequately.

Wound healing in children is quite different from that in
normal adults. On one side children have a greater potential
for wound healing, they have less serious and fewer medical
illnesses commonly. On the other side wound healing in
infants and small children is characterized by the immaturity
of the multiple systems involved in the healing process.124
Young children have an underdeveloped immune system.
Immunocompetence takes time to develop following exposure
to antigens over a period of time. The skin of children is less
protective, causing risk of infection which delay further
wound healing because of compromised immune response.125

Nutrition plays a significant role in wound healing in
infants. Children have limited protein reserve and during
wound healing the demand for protein increases (Table 3).
Similarly because of limited glycogen reserve, carbohydrate
supplementation is essential during wound healing. Excessive
carbohydrates should be used with caution as this may result
in osmotic diarrhea.126

Apart from the macronutrients, one should assess the need
for micronutrients especially vitamins A, B, C, D, iron, zinc
and folate.
Nutrition in Elderly Patients
As age increases, there is a progressive decrease in total
energy expenditure and hence requirement. There is no
growth as in children, basal metabolic rate is less and energy
expenditure due to physical activities is decreased. Decrease
in energy requirement is 165 kcal/day per decade in males and
103 kcal/day per decade in females.127 Protein supplementation
of elderly patients significantly enhances healing of pressure
ulcers. This improvement is correlated with the amount of
dietary protein intake.128

In elderly most of the micronutrients are deficient. There
is a risk of deficiency of vitamin B12, poor absorption of iron,
folate and calcium.129,130

Elderly have a lower rate of protein synthesis, are often
mildly immunocompromised and frequently suffer from
micro and macronutrient deficiencies. They are likely to have
comorbid conditions which may interfere with wound healing.
Like children, elderly patients are also at a risk of becoming
malnourished quickly. After trauma or illness these patients
have deficiency of nutrients in spite of having nutritional
reserve. Correction of nutritional deficiency as and when
detected, benefits these patients and accelerates wound healing.
Order and Supply
Hospitalized patients are at risk of having dietary deficiency of
nutrients important for wound healing despite ordering for an
adequate menu providing for sufficient nutrients. Hence, more
attention is required towards education and encouragement
for optimum nutritional supplementation.131
Conclusion
Nutritional status is the key to the well being of the patient
as nutrition plays a vital role in the healing process of the
wound. Ignoring nutrition may prolong the process of wound
healing.
Summary
Nutritional status of the patient has a major influence on the
outcome of trauma. Wound healing is faster and better in a
physiologic environment conducive to tissue regeneration
and repair. There should be a holistic approach to the
management of the patient rather than concentrating only on
the wound. Promotion of good nutrition is recommended,

Role of Nutrition in Wound Healing 
Chapter 36
443
more so in the population at risk for nutritional deficiency like
elderly, severely injured, smokers, patients with prolonged
hospitalization, etc. The dictum should be “healthy diet is
essential for healthy living”.
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• An Overview on Role of Physiotherapist in Wound Healing
• Role of Exercise Therapy in Wound Healing
• Role of Electrical Stimulation in Wound Healing

– General Effects of Electrical Stimulation

– Theories on Relation between Skin and Electric Current

– Indications for Electrical Stimulation

– Mechanism of Action

– Method of Application

– General Physiological Effects
• Effects of Electrical Stimulation in Each Phase of Wound
Healing
• Contraindications
• Role of Ultrasonic Therapy in Wound Healing

– General Effects of Ultrasonic Therapy

– Method of Application

– Contraindications

– Effects of Ultrasonic Therapy on Wound Healing
• Ultraviolet Therapy in Wound Healing

– Method of Application

– General Effects of Ultraviolet Therapy

– Contraindications
• Laser Therapy in Wound Healing

– Method of Application

– General Effects of Low Level Laser and Effects on Wound
Healing
• Role of Hydrotherapy in Wound Healing
INTRODUCTION
Physiotherapy means physiotherapeutic system of medicine
which includes examination, treatment, advice and instruction
to any person for the purpose of or in connection with movement
dysfunction, bodily malfunction, physical disorder, disability,
healing and pain from trauma and disease, physical and
mental conditions using physical agents including exercises,
mobilization, manipulation, mechanical and electrotherapy
activity and devices. In other words, it includes the diagnosis,
treatment and prevention of physical illness by physical
means.1 Here, the emphasis is on the role of physiotherapy in
wound healing, for which methods like electrical stimulation,
ultrasonic therapy, laser therapy, ultraviolet therapy and
hydrotherapy are discussed.

As mentioned in earlier chapters, normal wound healing is
interrupted by factors like:
• Infection
• Reduced blood perfusion
• Lack of moisture
• Some medications like corticosteroid, indomethacin
• Few topical applications, e.g. iodine
• Constant pressure
• Lack of proper nutrition
• Immunodeficiency
• Smoking
• Necrotic tissue.

Presence of any one of the above factors can hamper
the normal healing process and convert the healing wound
to a chronic nonhealing wound. A wound which has not
healed for more than 30 days is considered as nonhealing
wound according to the Center for Medicare and Medicaid
Services (CMMS).2 Nonhealing wounds are seen mainly as
a complication of some disease, injury or aging. The various
conditions leading to a chronic nonhealing wound could be
any of the following:
• Circulatory disease
• Metabolic disease
• Nutritional deficits
• Trauma
• Inadequate tissue perfusion
Ram Shanmugam
Role of Physiotherapy
in Wound Healing
37
Chapter

Section 4
  Miscellaneous
448
• Excess inflammation
• Postspinal cord injury especially in elderly patients.
The commonly seen chronic wounds and their distribution on
body are as follows:
• Arterial insufficiency ulcers are seen on the foot, malleoli,
joints of toe, medial side of lower leg and lateral side of foot
• Venous insufficiency ulcers are seen frequently on medial
side of lower leg and above ankle
• Diabetic ulcers are seen on plantar aspect of foot, heel,
lateral side of foot, weight bearing area of metatarsal head
• Pressure sores seen on ischial tuberosities, heel, sacrum,
greater trochanter and malleoli.
AN OVERVIEW ON ROLE OF
­PHYSIOTHERAPIST IN WOUND
­HEALING
Nonhealing wound can affect a patients normal life in the
following manner:
• It prolongs hospital stay
• It prevents independent activities of daily living (ADL)
• It increases risk of limb loss, which may take the patient to
the different level of amputation rehabilitation.
• It interrupts rehabilitation process in achieving any target.

The physiotherapist has an important role to play during
wound healing both, at early stage by using alternate means
of wound management principles in nonhealing wounds and
at a later stage during the process of restoring a patient’s
functional independency and mobility which restores the
normalcy in patient’s life. This is achieved by both exercise
therapy and electrotherapy. Before going into the details of the
role of these modalities in wound healing, it is important to
understand that a physiotherapist, being a medical professional
is more frequently visiting and also closely working with the
patient, and therefore has a bigger role to play in prevention
and treatment by other basic means like:
• Patient education regarding sensory loss
• Education to patient’s relatives regarding

– Turning

– Positioning
• Use of mattress: Water mattress, split mattress or air
mattress
• Use of orthoses: To prevent direct weight bearing on the
wound surface in case of foot ulcers by means of

– Adding cushion to the insole

– Removing the weight bearing contact area of the ulcer
in the inner sole of the shoe

– A patellar weight bearing orthoses where the sole of
the foot does not touch the inside floor of the shoe thus
maintaining a noncontact weight bearing.
• Cryotherapy: Ice cubes are applied directly on the wound
for a period of less than two minutes prior to the treatment
session with low level laser therapy and followed by wound
dressing. The vasodilation followed by vasoconstriction
created by ice is believed to increase the rate of wound
healing.
ROLE OF EXERCISE THERAPY IN
WOUND HEALING
Unlike electrotherapy, which uses many modalities in wound
healing, exercise therapy is a hands on practice, which is not
done on the wound surface. Exercise therapy mainly aims
at treating the underlying clinical illness such as paralysis
and joint stiffness. When it is combined with electrotherapy
modalities, the outcome is better. There are three main types
of exercise therapy.
1. Therapeutic massage: It is done in the affected part of
the body but not on the surface of the wound. It involves
many techniques such as effleurage performed distal to the
wound and towards the nearby lymphatic nodes, which
decreases edema by promoting lymphatic drainage and
thumb and finger kneading tends to break adhesions in
the soft tissues around the wound. This massage increases
blood supply at the local level and also increases lymphatic
drainage. Icecubes are used too while massaging directly
on the wound prior to the treatment session with low level
laser therapy and is followed by wound dressing.


Contraindications include skin infections, hyperpyrexia,
underlying vascular disease, benign and malignant conditions
and varicose veins. It is not a preferred mode of exercise
therapy in infected wounds.
2. Exercises: Passive or active assisted or active range
of motion and strengthening exercises are prescribed
according to the patient’s muscle power and neurological
status. Therapeutic exercises in the affected part of body
will mobilize the joints, increase muscle power and
bring increased vascularity at the local level and thereby
improves the functional ability to use the limb and make
the patient mobile.
3. Hydrotherapy: Involves performing exercises under water.
It is a type of graded exercise which is intended to increase
the muscle power in paralytic conditions by using buoyancy
of water. In this process it keeps the wound moist which is
necessary for the wound to heal faster and wash away the
debris in the surface of the wound. Details about its use in
wound healing is given later in this chapter.
ROLE OF ELECTRICAL STIMULATION
IN WOUND HEALING
For many centuries current has been used in wound healing,
like once a charged gold leaf was used in the past in this field.
Its electrochemical influence is believed to augment wound

Chapter 37
Role of Physiotherapy in Wound Healing 
449
healing. Early in the 20th century many studies had suggested
that it had a positive effect in producing granulation tissue.
Aluminum foil, polyethylene films and other metals had also
been tried. Of late, a lot of work has been done on the role
of electrical stimulation in wound healing in terms of its
application, dosage and effects.

Definition: Electrical stimulation is defined as the use of an
electrical current to transfer energy to the wound. It primarily
affects the nerves, muscle, hematoma and edematous tissue.
General Effects of Electrical Stimulation
• Pain relief
• Improved local circulation
• Reduction of edema
• Improves the range of motion of joints
• Maintain soft tissue glide
• Modification of scar tissue or adhesions.
Theories on Relation between Skin and
Electric Current
Skin Battery Theory
In 1945, it was discovered that there is a positive potential
present in the intact skin adjacent to the wounded tissue. When
wound healing is completed the positive potential ceases.

The surface of the skin was found to be holding negative
charge with respect to the inner layers of the skin and
especially hairless regions having more potentials. It is
believed that the skin battery is located in the epidermis and
that this phenomenon is driven by sodium-ion pump. Moist
wound environment ensures that there is a current flow across
especially when externally current is applied, which augments
wound healing.
Current of Injury Theory
A “current of injury” is generated between skin and the
underlying tissues whenever there is break in the skin. This
continues until the tissues are repaired. Healing of the injured
tissues is arrested when this current does not flow. The wound
moisture is an indispensible factor for this current to flow. The
application of electrical stimulation is aimed at mimicking this
current and that subsequently fastens the wound healing process.
Vascular Interstitial Closed Circuit
It was proposed by Nordenstrom that human body has
bioelectric circuits and current is contained in the vascular
bundle. This bioelectricity is conducted through five
components—the walls of blood vessels, the plasma, the
tissue matrix, interstitial fluid and electrical junctions, the first
and third acting as insulated components and the second and
fourth components are conductors.

The difference in the resistance between vessel wall and
interstitial fluids creates a potential. An injury which produces
the charge has the power to switch on this potential current,
and then the effects follows on.
Indications for Electrical Stimulation
• Pressure ulcers stage 1 through 4
• Diabetic ulcers due to pressure, insensitivity and
avascularity
• Venous ulcers
• Traumatic wounds
• Surgical wounds
• Ischemic ulcers
• Vasculitic ulcers
• Donor sites
• Burn wounds.
Mechanism of Action of Different Currents
Available for Electrical Stimulation
Low voltage constant microamperage direct current (CMDC)
of 200 to 1000 µa has been proved even histologically to be
of good value in this field by many researchers (Wolcott and
colleagues).3

The cathode here produces bactericidal effect which can
be considered as an adjunct to debridement. Because it is
proved to have sclerolytic ability to solubulize thrombus and
necrotic tissue. The anode has the opposite reaction which is
also believed to aid in closure of wound and producing a scar.

Iontophoresis: This process involves introducing ions into
tissues by placing the same polarity ion under the electrode.
The anode can repel either zinc or histamine into the wound,
when constant direct current is applied. When combined with
10 minutes of hydrotherapy preceeded by debridement, it
proved to be of good value as an increase in blood flow is
seen.

Low voltage pulsed microamperage current which is less
than 1.0 mA has also been proved to be augmenting wound
healing in the past.
High voltage pulsed monophasic current has also been used
in the past and proved useful in wound healing. It is considered
to be equally effective as CMDC and is a low cost treatment.
Low voltage pulsed milliamperage current has been used
from a TENS device in the past by Kaada.4 When applied
to the ipsilateral hand in a leg ulcer case, it was found to
improve the microcirculation in the ipsilateral lower limb

Section 4
  Miscellaneous
450
through mechanisms like stimulation of central serotonergic
link which inhibits sympathetic vasoconstriction; stimulation
and release of vasointestinal polypeptide into the plasma and
activation of segmental axon reflex leading to vasodilatation.
Patients of Raynaud’s disease, reflex sympathetic dystrophy
and CREST syndrome were said to be benefited most.
Key points by which electrical stimulation works
on wound healing
• Modifying endogenous bioelectricity
• Activation of inflammatory cells
• Presence of electrode breakdown products
• Attraction of connective tissue cells
• Enhancing cell replication
• Enhancing cell biosynthesis
• Inhibition of infectious microorganisms.
Method of Application
Before applying electrical stimulation,the standard wound
management is followed,the necrotic tissues are removed by
debridement or by dressings which keep the wound moisture
retained,as dry necrotic tissue does not allow the currents
to pass in the wound. For cleaning, use of topical agents for
bacteria and fungi and use of systemic antibacterial drugs
are continued alongside the antibacterial effects of electrical
stimulation.

Electrical stimulation is delivered through a machine which
has two conductive electrodes, the cathode and the anode,
which are applied to the skin. The electrodes are wrapped
in a gauze piece and made wet to enable them to conduct
electricity.

One electrode is applied on the wound and the other on
the area adjacent to the wound. The method of application
of electrodes in sacral ulcer (Figures 1A and B), ulcer in
the dorsum of the foot (Figures 2A and B) and the wound
in plantar surface of the foot (Figures 3A and B) are shown
below. The cathode is applied over the wound for the first
three sittings and then the polarity is changed,for the rest of
the sittings. There are usually 5 sittings in a week and each
session may last up to 30 minutes.
Foot Bath for Plantar Ulcers
The affected foot is placed in a tub which contains water and
electrodes are attached to the prescribed areas and current is
introduced (Figure 4).
General Physiological Effects
Effects on Cutaneous Oxygen Supply
The value of transcutaneous partial pressure of oxygen
(tc PO2) was improved after the application of electrical
stimulation, even in conditions which are known to slow
down wound healing process like diabetes, and spinal cord
injury, according to Dodgen and associates.
Bacteriocidal Effects
It was proved that the cathodal stimulation with CMDC has
resulted in reduced growth of Escherichia coli, Pseudomonas
aeruginosa and Staphylococcus aureus (Rowley). It is said
Figures 1A and B: Electrical stimulation in used for sacral ulcer
A
B

Chapter 37
Role of Physiotherapy in Wound Healing 
451
that the DC stimulation attacked organisms with electrons and
suppressed diffusion regulating mechanisms. The reason for
this was probably due to attraction of phagocytic macrophages
to the infected wound tissues.

Galvanotaxis, i.e. attraction of cells towards anode or
cathode has also been well supported by the researchers in
the past. It is said that macrophages move toward the cathode
and neutrophills migrate towards both the electrodes. The
bacteriocidal effect at cathode is attributed to the phagocytic
macrophages and leukocytes attracted towards the infected
tissues.

Alternatively, it is also believed that the increased numbers
of neutrophiles could have contributed to the process due to
increased blood flow.
Pain Relief
It can be explained through the pain gate theory where
substance P is secreted following application of electrical
stimulation, which ultimately blocks the conduction of pain
signals. As the pain reduces, the range of motion of the nearby
joint and surrounding muscle strength is also improved as a
result of electrical stimulation applied to the wounds.
Effects of Electrical Stimulation in Each
Phase of Wound Healing5-8
The various phases of wound healing are influenced by the
electrical stimulation in the following manner:
Inflammatory Phase
• Initiates the wound repair process by its effect on the
current of injury site
• Increases blood flow—as a result of stimulation of capillary
in growth into the wound, i.e. angiogenesis. Therefore,
there is definite increase in microcirculation
• Promotes phagocytosis
• Enhances tissue oxygenation
A
B
Figures 3A and B: Electrical stimulation used in plantar ulcer
B
Figures 2A and B: Electrical stimulation is used for healing of ulcer over ankle and dorsum of foot
A

Section 4
  Miscellaneous
452
• Reduces edema from reduced microvascular leakage
• Attracts and stimulates fibroblasts and epithelial cells
• Stimulates DNA synthesis
• Controls infection
• Solubilizes blood products including necrotic tissue.
Proliferative Phase
Fibroblasts normally migrate into the healing wound, mostly
seen in proliferative phase. It is proved that electrostatic fields
influence this fibroblastic activity thereby increasing both
DNA synthesis and collagen synthesis when fibroblast culture
is exposed to electrostatic field.
• Stimulates fibroblasts and epithelial cells
• Stimulates DNA and protein synthesis
• Increases ATP generation
• Improves membrane transport
• Produces better collagen matrix organization
• Stimulates wound contraction.
Epithelialization Phase
• Stimulates epidermal cell reproduction and migration
• Produces a smoother, thinner scar.
Contraindications to Electrical Stimulation
• Osteomyelitis
• Neoplasm
• Individual allergy
• In situ cardiac pacemakers and other electronic implants
• Areas related to control of cardiac and respiratory function.
ROLE OF ULTRASONIC THERAPY IN
WOUND HEALING
Application of therapeutic ultrasound to the wound has proved
effective in both open and closed wounds. It is applied with
a coupling medium directly on the wound and its effects are
both thermal and nonthermal.5,7
General Effects of Ultrasonic Therapy
The nonthermal effects are acoustic cavitation and micro-
streaming. Rhythmic contraction and expansion of gaseous
pockets produces cavitation in the tissues and it is believed that
ionic channels are activated by them. Microstreaming occurs
as a result of cavitation and it increases calcium conductance
which is necessary for collagen secretion.

Micromassage results when longitudinal compression
waves produces compression or rarefaction of cells and
results in movement of interstitial fluid. Stretching of scars
and adhesive tissue is much easier after achieving this effect.

The thermal effects are increased blood supply and
increased WBC migration which in turn decreases pain and
inflammation.
Method of Application
The equipment has an oscillator, circuits, and the applicator.
(Figure 5). It provides ultrasonic waves of both 1 mHz and
3 mHz frequency. The 1 mHz is usually preferred for wound
healing purpose. 3 mHz is suitable for superficial wounds
whereas 1 mHz is used for wound extending deeper.

The treatment area should not be more than 1.5 times of
the active surface of the applicator. Duration of treatment
should be 2 minutes to each area and the total time could be
around 5 to 10 min. This can be increased by 30 seconds in
subsequent sittings.

Intensity of 1.5 to 2.0 watts/sqcm is generally considered
adequate for wound healing.

Overdose results in increase of symptoms.
Contraindications of Ultrasonic Therapy
• Malignancy
• Acute infection
• Ischemic areas and vascular diseases
• Acute sepsis
• Cardiac disease
• Radiotherapy
• DVT
• Electronic or artificial implants
Figure 4: Foot bath for plantar ulcers along with electrical stimulation

Chapter 37
Role of Physiotherapy in Wound Healing 
453
• Areas over gonads, spinal cord, eyes and pregnant uterus.

Phonophoresis: It is proved that when pharmacologically
active agents are introduced as coupling medium, ultrasound
aids their entry to the tissues. This method is called
phonophoresis. Methyl nicotinate, histamine, lidocaine and
hydrocortisone are some of these agents that can be introduced
into tissues with ultrasound.
Effects of Ultrasonic Therapy on Wound
Healing
The various phases of wound healing are effected by
ultrasound therapy in the following manner:
Inflammatory Phase
• Increases the fragility of lysosome membranes and
enhances the release of the enzymes
• Stimulates histamine release from mast cells
• Increases calcium ion transport into mast cells.
Proliferative Phase
• Affects fibroblast activity and angiogenesis to accelerate
tissue repair
• Accelerates wound contraction by its effects on fibroblasts
and factors released from macrophages
• Myofibroblasts developed from fibroblasts resemble muscle
cell, which contracts by the application of ultrasound
• Stimulates endothelial cell activity
• In ischemic muscle, new capillaries are developed and
circulation restored.
Remodeling Phase
• Improves mechanical properties of scar tissue
• The fiber arrangement is more regular which looks like
uninjured dermis.
ULTRAVIOLET THERAPY IN WOUND
HEALING
In electromagnetic spectrum, the ultraviolet rays are in
between visible light and X-rays. They have been used for
therapeutic purpose, for many years.7,9
• They are divided into three bands, i.e. UVA (315–400 nm)
• UVB (280–315 nm)
• UVC (< 280 nm).
Method of Application
Typically, for an infected wound a lamp generally known as
kromayer lamp source of UV rays is used to irradiate the focal
area. The dose which is used to produce erythema is called E1
dose. It is given by the bulb after analysis. It can be found out
by using test area in the forearm of the patient at 90 cm distance
and based on the results of that, the E3 or E4 dose is calculated
(E2 = E1 × 2.5, E3 = E1 × 5, E4 = E1 × 10). Generally, the base
of the wound is treated with E4 dose and the wall with E3.

The wound is cleaned with a sterile gauze and the lamp is
kept 90° to the wound surface area and the lamp can be placed
close to the wound surface, but should not touch it. A quartz
rod is attached with the lamp for shelving sore or sinus. A lint
cloth is kept on the wound and is cut open only in area of the
wound to enable the exposure of the wound to the UV rays,
and protects other adjacent areas from UV. The patient and
the therapist should be wearing special goggles to protect eyes
from UV radiation.

Indications to ultraviolet therapy are the same as for
electrical stimulation in wound healing.
General Effects of Ultraviolet Therapy
• Erythema
• Pigmentation
• Thickening of the epidermis
• Peeling
• Production of vitamin D
• Solar elastosis and aging
• Can be carcinogenic.
Effects of UV Rays in Wound Healing
It is suggested through clinical studies that UVA and UVB
rays increase wound healing. Its mechanism of action starts
Figure 5: Ultrasonic therapy equipment (Courtesy: Medison’s
medical technologies)

Section 4
  Miscellaneous
454
with initiating an inflammatory response with vasodilatation
which increases oxygen delivery to the tissues and increased
capillary permeability which is followed by exfoliation and
tissue repair. This facilitates the transport of fibroblasts like
components to fasten tissue healing. The response begins
approximately 4 hours after irradiation and maximum effect
at approximately after 10 hours.

It has also been proved that the UV rays have a
debridement effect on the wounds (removes the infected
slough) by enhancing WBC accumulation and lysosomal
activity. It also stimulates formation of a cytokine that helps
in epithelialization. A filter like blue uvial glass or cellophane
is used to allow only UVA to access the wounds.In case of
noninfected wound, especially during granulation stage, a
progression of dosage is unnecessary.

Its use in infected wounds and its bacteriocidal effect is very
significant. Studies have shown that UVC is capable of killing
broad spectrum of microorganisms, and resistant bacteria as
well. It is believed that the nuclear functioning of bacteria
is inhibited with inhibition of DNA synthesis following UV
session which leads to cessation of the responses controlled
by nucleus which ultimately results in killing of the bacteria.
Infected wounds, necrotic wounds and other nonhealing
wounds are normally benefited by UV irradiation. Other
advantages include ease of administration and its affordability.
Contraindications
Include cardiac, renal and hepatic abnormalities, systemic
lupus erythematosus (SLE), hyperthyroidism, TB, diabetes,
herpes simplex and skin diseases/infections.
LASER THERAPY IN WOUND HEALING
Laser stands for light amplification by stimulated emission
of radiation. The effects of laser application are due to their
photochemical and biostimulatory effect and not the thermal
effects of the light. Amongst the high and low power lasers
available for therapeutic use, the low power laser is indicated
for wound healing purpose, i.e. less than one milliwatts per
square cm. The laser light is monochromatic and travels in
step with one other and are almost parallel. The laser of power
is 1 mW or less is considered as low level or cold laser. The
helium-neon laser is low energy cold laser since it does not
generate heat. The concentration of the power in a particular
area is called as power density.
General Effects of Low Level Laser and
­Effects on Wound Healing7,9
Decreasing inflammation, control of pain and thus healing wound
are generally considered as the nonthermal effects of low level
laser. The physiological activity of tissues is excited by this weak
stimulus, reduced by strong stimuli and stops by very strong
stimuli. Generally, laser is believed to relieve pain by decreasing
the conduction velocity of sensory nerves. Increase in the number
of T-cells after irradiation is a proven fact and thus laser stimulates
immune system and brings out an effective response. Relieving
primary myospasm which is protective in nature is also seen
as an effect of laser treatment. This relief is achieved through
vasodilation, thus it is effective in reducing inflammation also.
Increase in the level of collagen synthesis is shown after laser
irradiation especially in fresh injuries. It was found by Abertgers
and coworkers that the messenger RNA transcription rate of the
collagen gene is accelerated after laser therapy.

Collectively, though researchers are still trying to elaborate
this topic with more justifications about laser’s role in wound
healing, Cold lasers are definitely believed to be promoting
wound closure and nerve regeneration.

Indications are the same as for other electrotherapy
modalities in wound healing.
Method of Application
Generally, the power output is in milliwatts which is fixed
for the machines. The power per unit area is a significant
parameter and it is high with the contact technique. The
outcome after dividing power output by size of the treatment
head, normally varies between 0.1 and 0.125 square cm.

Energy is recorded in joules = power output × irradiation
time. The pulse repetition rate may vary from two to many
thousand Hz. The helium-neon laser has a head component
which is held at 90° on the wound. For chronic wounds 40
pps of lower pulse rate is considered better. The beam given
is interrupted in nature for superficial wounds. The pulse rate
given is 80 pps and the power density is 20 mW/square cm.
An average of 15 min per day, 5 days a week for 10 to 12
weeks protocol gives good results in nonhealing wounds.

There are two techniques of application, contact and non
contact techniques. In wound healing, contact technique is
used for the wound margins, with doses up to 2J per square
cm, generally considered to be 1J per point, approximately.
The non contact technique is used for wound bed, where
the head is held not more than 0.5 to 1 cm from the tissue
for maintaining aseptic measures and avoid painful contact
with an average dosage of 4J per square cm, which can
be increased to a maximum of 10J per square cm. In non-
contact application the inverse square law applies and thus
there is reduction in irradiation. The single probe fiber optic
applicator is also used, after mapping the wound bed to equal
sized squares and each area is treated individually.

Some scanning devices are used to promote hands off
treatment method and there are also cluster units which have
an array of diodes in a single unit. Each may operate at many

Chapter 37
Role of Physiotherapy in Wound Healing 
455
different wavelengths.It can be used in extensive ulcers, for
better accessibility to deeper areas and is time efficient. Thus,
a multisource array which has an output of 500 mW used for
a period of two minute on a bed sore of 12 square cm has an
energy density of 5J per square cm.

Contraindications: Treatments over the eye, hemorrhage,
skin sensitive to light, pregnant uterus and malignant tumors
are contraindicated for laser therapy.
ROLE OF HYDROTHERAPY IN WOUND
HEALING
It is one of the oldest therapies used in wound healing and involves
using water for therapeutic purpose.7,9 Generally, exercises are
prescribed in water in case the purpose is to strengthen muscles
or increase range of motion. But in wound healing, many forms
of hydrotherapies are used like the whirlpool therapy, pulsatile
lavage, jet irrigation and irrigation with a syringe.

Amongst all, the whirlpool therapy is popularly used
along with carefully chosen turbulence and temperature of
water varies for each type of wound and patient. Various
antimicrobial agents can be mixed to the water to counter
bacteria’s in case of the infected wound. Povidone iodone
diluted solution and sodium hypochlorite has proved effective
against microorganisms.

In whirlpool therapy, the extremity or the body is immersed
in the water which has prescribed temperature and turbulence.
It is normally used twice daily to improve softening and
removal of eschar and necrotic tissue. It is found to be very
effective when combined with post therapy saline dressings.
The benefits are to keep the wound wet, tissue hydration,
remove debris and drainage, improve blood circulation and
oxygen delivery and softens tissues.

Treatment time of maximum five minutes is used in case
of arterial wounds and the water’s temperature is kept neutral.
In case of pressure sores and other wounds also neutral
temperature is preferred. For venous ulcers water is used at
80 to 90°F temperature. Painful, dark eschar and large surface
wounds respond to hydrotherapy better.

Contraindications include DVT, major system failure,
incontinence, dry gangrene and poor neurological response
from patient.

Wounds with red appearance due to presence of granulation
tissues and epidermal cells can get damaged with agitation. So
they are better managed with dressing. Excessive temperature
and turbulence may harm regenerating wounds in skin grafts
and flaps.

Pulsatile lavage is combination of pulse irrigation and
suction to clean wounds and remove debris. It works effectively
in deeper wounds and aids the growth of granulation tissue. It
has a spray gun and normal saline is delivered under pressure
and concurrently aspirated by negative pressure via a tube
made up of plastic. Both the pressures can be controlled by
the therapist. The pressure can be increased for infected and
necrotic wounds. The suction pressure varies from 60 to 120
mm Hg and impact pressure less than 15 psi (4–6 psi for clean
wounds and 10–12 for necrotic wounds) are applicable. Low
pressures are preferred for clean wounds.

The nerves and blood vessels exposed in the wound are
carefully avoided from direct pressure and high pressure
should not be used in malignancy and over grafts and on
growing tissues.
SUMMARY
This chapter has discussed many types of currents used in
electrical stimulation and its benefits in nonhealing wounds.
The size of the electrodes and dosage of the currents used in
wound healing have been discussed in the available literature,
and has great scope in the future. The clinical relevance of
electrical stimulation in wound healing is well proved and it
is an integral part of wound healing in contemporary clinical
methods.

The potentially beneficial effects of ultrasonic therapy
is very valuable when used correctly, especially in the
inflammatory phase. And although LASER is a relatively
new form of light after the conventionally used infrared and
ultraviolet rays, a lot of research work is going on for the
same, to consolidate its place in wound healing, though it is
already well accepted in this area as the future of light therapy.

All forms of hydrotherapy chosen for a wound are
considered very practical in maintaining wound moisture.

Conclusively, the methods explained here and some more
recent and latest methods of physiotherapy to enhance wound
healing process, have already been consciously chosen
methods in the recent times which are truly proving to be the
alternative to conventional wound healing methods.
references
1. The act of the Delhi council for physiotherapy and occupational
therapy, 2001.
2. Andrew J Robinson, Lynn Snyder-Mackler. Electrical stimu­
lation to augment healing of chronic wounds in clinical
electrophysiology by Wolters Kluver, 3rd edn 2007.pp.275-300.
3. Wolcott LE, et al. Accelerated healing of skin ulcers by
electrotherapy, preliminary Clinical results. South Med J.
1969;62:795.
4. Kaada B. Promoted healing of chronic ulceration by TNS,
VASA. 1983;12:262.
5. Luther C Kloth, Joseph M Mcculloch, Jeffrey A Feeder. Chapter
12, 13 and 14, wound healing: alternatives in management, F A
Davis company, 1990.pp.221-9.

Section 4
  Miscellaneous
456
6. Shiela Kitchen,Sarah Basin. Chapter 21, Electrical stimulation
for wound healing in Clayton’s electrotherapy,10th edn, Prison
India Publishers; 1996.pp.323-48.
7. Judith A Schilling. Chapter 9 Therapeutic modalities in Wound
care made incredibily easy, Mccan, 195-211.
8. Jhon Low BA, Ann Reed. Electrotherapy explained principles
and practice. Butterworth Heinemann, 3rd edn, 2000, Chapter
6,7,13,14.
9. Michelle H Cameron. Chapter 8 and 12 in Physical agents in
rehabilitation from research to Practice, Saunders, St. Louis
Missouri, 2nd edn, 2003.

• Definition of Hyperbaric Oxygen
• History
• Mechanism of Oxygen Transport in

Hyperbaric Oxygen Therapy
• Role of Oxygen in Wound Healing
• Therapeutic Effects of Hyperbaric Oxygen
• Hyperbaric Oxygen Therapy Protocol
• Hyperbaric Oxygen Therapy in Wounds
• Side Effect and Complications
Introduction and Definition
of Hyperbaric Oxygen
Wound healing is a process which involves a sequence of
successful cellular and biochemical chain of events and any
disruption in this process will lead to a nonhealing ulcer or a
chronic wound.

Hyperbaric oxygen therapy (HBOT) is a method of
administering a higher dose of oxygen at an increased
atmospheric pressure. The Undersea and Hyperbaric Medical
Society describes HBOT as “the inhalation of 100 percent
oxygen while the entire patient is enclosed within a chamber
at pressures of at least 1.4 atmosphere absolute (ATA) or
greater.”1 The pressure chamber can accommodate either one
person (monoplace) or multiple people (multiplace) (Figures
1 and 2). The topical application of oxygen to a wound by
enclosing a body part is not recognized as a hyperbaric therapy.
History
Hyperbaric oxygen therapy as a treatment modality has been
used to assist healing in chronic wounds for about 50 years.
HBOT was used to treat decompression sickness in 1940s. In
1950s and 1960s, promising results were achieved in cases of
carbon monoxide poisoning, gangrene and anemic states with
HBOT treatment and it was from 1960s onwards that its use in
wound healing was noticed. Next few decades saw skepticism
to HBOT due to lack of adequate scientific validation of efficacy
and safety.2 Last two decades has witnessed a renewed interest
in this field with animal studies, clinical trials and numerous
scientific publications.3,4 Currently HBOT is recognized and
used as a primary treatment for decompression illness, air
embolism and carbon monoxide poisoning. It is regarded as
an adjunctive therapy for hypoxic wounds and compromised
skin grafts and flaps. Its role in hypoxic neurological illnesses
and ENT problems is under evaluation.5
Mechanism of oxygen transport
in Hyperbaric Oxygen Therapy
At normal atmospheric pressure, hemoglobin is 95 percent
saturated and 100 ml of blood carries 19 ml of oxygen
bound to hemoglobin. At this pressure oxygen in solution,
i.e. oxygen bound to plasma is meager 0.32 ml/100 ml of
blood. Inhalation of 100 percent hyperbaric oxygen has
dual effect. Hundred percent oxygen rapidly saturates the
hemoglobin, and the excess starts dissolving in plasma. At
2 ATA, the amount of oxygen dissolved in plasma is 4.4
ml/100 ml which increases to 6.8 ml/100 ml at 3 ATA. This
additional oxygen in solution is almost sufficient to meet
Ashish Rai, Sameek Bhattacharya
Hyperbaric Oxygen Therapy
in Management of Wounds
38
Chapter

Miscellaneous
Section 4
458
tissue needs without contribution from oxygen bound to
hemoglobin and is responsible for most of the beneficial
effects of HBOT.4,6 The increased plasma oxygen diffuses
directly through the hypoxia gradient from the adjacent
healthy tissues to the wound and aids in healing. Because
the oxygen is in solution, it can reach areas where red
blood cells may not be able to pass and can also provide
tissue oxygenation in the setting of impaired hemoglobin
concentration or function.7
Role of Oxygen in Wound Healing
A chronic wound is interruption in continuity of the body’s
surface that requires a prolonged time to heal, does not heal, or
recurs.8 Despite various etiologies, the common denominator
in many wounds is tissue hypoxia. An insufficient supply of
oxygen can sometimes support basal tissue maintenance, but
is not enough to allow tissue proliferation for wound healing.
Wound healing is a dynamic process. The central portion of
a wound has relative hypoxia as compared to surrounding
tissues with normal perfusion. This produces an oxygen
gradient from the peripheral tissues towards the center of the
wound. The central hypoxic zone, therefore, creates a demand
for oxygen and engages the peripheral tissue to provide
oxygen to support the healing process through angiogenesis.9
HBOT acts primarily by augmenting the oxygenation of
periwound tissues and thus elevating the oxygen gradient
and enhancing oxygen flow from the peripheral tissues to
the central hypoxic zone.10 This is the reason why in cases
of macrovascular disease HBOT has no beneficial effect.11
Although arterial oxygen partial pressure in major vessels
increases significantly but due to poor perfusion, its benefit
is not extended to the peripheral tissues. However, in cases of
microvascular disease, high oxygen tension pushes significant
amount of oxygen peripherally and improves periwound
oxygenation.
Therapeutic effects of
Hyperbaric Oxygen
Reduction of Carboxy Hemoglobin’s Half-
Life in Carbon Monoxide Poisoning3,4,6
Hyperbaric oxygen therapy is the treatment of choice for CO
poisoning. It displaces carbon monoxide from hemoglobin
and reduces the half-life of carboxy hemoglobin from four to
five hours to two hours or less.
Mechanical Effect in Decompression Illness
and Air Embolism3,4,6
Hyperbaric oxygen therapy causes elevation of hydrostatic
pressure of oxygen in the blood. This increases the partial
pressure of gases and causes a reduction in the volume
of gas-filled spaces in cases of arterial gas embolism and
decompression illness.
Wound Healing12-15
The role of HBOT in wound healing can be attributed to the
combined effect of various changes induced by hyperbaric
oxygen.
• Angiogenesis
• Fibroblast proliferation and synthesis of collagen
• Vasoconstric tion and reduction of edema
• Down regulation of inflammatory cytokines.
Figure 2: Patients receiving HBOT
Figure 1: Monoplace chamber for HBOT

Hyperbaric Oxygen Therapy in Management of Wounds 
Chapter 38
459
Bactericidal/Bacterostatic Effect16-18
Hyperbaric oxygen is bactericidal for anaerobic organisms
and is bacterostatic for the aerobic ones. The mechanism
of action is attributed to enhanced antibacterial activity by
macrophages and PMN cells. This effect of HBO is utilized
in treating gas-gangrene, compartment syndrome and crush
injuries where there is severe anaerobic environment within
tissues.
Activation of Dormant Neuronal Tissues in
Neurological Illnesses19-21
It probably acts by activating the dormant cells at the periphery
of the ischemic lesions in cerebral palsy, spinal cord injury,
etc. However, the modality is under evaluation and trials.
Free Radical Generation12,22
Free radical generation is the cause of many side effects related
to HBOT. The reactive oxygen species (ROS) generated with
HBOT mediate O2 toxicity, which encompasses pulmonary
injuries, central nervous system effects manifested by grand
malseizures, and ocular effects such as reversible myopia.
Indications (as Listed by the Undersea and
Hyperbaric Medicine Society)23
The following indications are approved uses of hyperbaric
oxygen therapy as defined by the Hyperbaric Oxygen Therapy
Committee:
1. Gas or air embolism
2. Carbon monoxide poisoning
3. Clostridal myositis and myonecrosis (Gas gangrene)
4. Crush injury, compartment syndrome and other traumatic
ischemias
5. Decompression sickness
6. Enhancement of healing in selected problem wounds
7. Necrotizing soft tissue infections
8. Osteomyelitis (Refractory)
9. Delayed radiation injury (Soft tissue and bony necrosis)
10. Skin grafts and flaps (Compromised)
11. Thermal burns
12. Exceptional blood loss (Anemia)
13. Intracranial abscess.
Contraindication
Absolute contraindications
• Pneumothorax
• Patient undergoing therapy with drugs: Doxorubicin,
cisplatin, bleomycin, disulfiram, sulfamylon
• Relative contraindications
• COPD, asthma
• Claustrophobia
• Pregnancy
• Seizures
• Eustachian tube blockade/obstruction, URTI
• Patient on pacemaker.
Hyperbaric Oxygen
Therapy Protocol24,25
Most therapy is given at two or three ATA and the average
duration of therapy is 60 to 90 minutes. Number of sessions
may vary from three to five for acute conditions to 50 to 60
for radiation illnesses. A typical HBOT session lasts for 90
minutes during which the patient is placed in a monoplace or
multiplace chamber with 100 percent oxygen delivery at 2 to
2.5 ATA. Each session is divided into three hyperbaric periods
of 30 minutes and two ‘air breaks’ of five minutes each, in
between.

There is experimental evidence that repeated ‘on-off’
exposures produce a better environment for wound healing
when compared to oxygen or air at normobaric pressure.
Hyperbaric Oxygen therapy
in Wounds
Problem Wounds15,26-34
Diabetic Wound, Venous Ulcers, Arterial
Ulcers, Pressure Ulcer
Hyperbaric oxygen is not a primary therapy for wound
management. It is used as an adjunctive therapy to normal
wound care measures in difficult, chronic wounds. Its role
in problem wound is due to positive effect of hyperbaric
oxygen on angiogenesis and infection control. However, not
all chronic wounds will respond favorably to HBOT and a
practitioner must rigorously select the patients who will be
maximally benefited from the therapy. A simple and quick
means to ascertain this is by the Doppler study of the affected
limb to visualize obstruction in major blood vessels and
measurement of transcutaneous pressure of oxygen in peri-
wound area. Studies have shown that there is poor response
to HBOT in cases of ischemia due to macrovascular disease.
However, there are other studies which show that HBOT
reduces the rate of amputation in limbs with absent distal
pulses.28 In absence of clear data, it may be inferred that for
large vessel obstruction, angioplasty or revascularization
surgery must be attempted wherever possible before starting
HBOT.29,30 However, in situations where corrective surgery
is not possible due to high operative risk, comorbidity, etc.
HBOT can still be employed.

Miscellaneous
Section 4
460
Figure 3: Chronic osteomyelitic wound over thigh

Measurement of transcutaneous pressure of oxygen,
TcPO2, is another noninvasive technique for selecting the
patients who will be benefited most by hyperbaric therapy.31,32
Level of TcPO2, in periwound area, both while normal
breathing and on HBOT is obtained. Patients with significant
hypoxia in spite of HBOT will in all probability not respond
to HBOT.33,34
Necrotizing Soft Tissue Infection35-37
Necrotizing soft tissue infection includes crepitant anaerobic
cellulitis, progressive bacterial gangrene, necrotizing fasciitis,
and nonclostridial myonecrosis. It may result from single or
mixed strains of bacteria and is more common in diabetics
and immune-compromised patients. Necrotizing infection
leads to soft tissue hypoxia, impaired neutrophil activity and
occlusive endarteritis. Surgical debridement and antibiotics
is the cornerstone of the treatment. Studies have shown that
adjunctive therapy with HBO reduces the risk of mortality and
also fewer debridement.
Compromised Skin Grafts and Flaps38-41
Initial skin graft survival depends upon a viable bed for
oxygen and nutrient supply. Normally skin graft and flap
do well without any added oxygen augmentation. The role
of HBOT in skin graft and flap is in two scenarios, either to
improve a hypoxic recipient bed prior to grafting or salvaging
an ischemic flap compromised by vascular insufficiency. In
a chronic, hypoxic bed the therapy is prolonged to include
preoperative as well as postoperative period. Studies have
shown that in compromised flaps, better results are seen in
flaps with arterial insufficiency as compared to venous or
mixed insult.
Radiation Ulcers42-44
The basic physiology of this process is a progressive
obliterative endarteritis with resultant hypoxia and tissue
ischemia. Radiation injury can be classified into soft tissue
and bony (osteoradionecrosis) types. Hyperbaric oxygen
therapy has positive role in both types of injuries.
Refractory Osteomyelitis45,46
In refractory osteomyelitis, anaerobic organisms are the
major culprit. Hyperbaric oxygen has a direct bactericidal/
bacterostatic action which is understandably more potent
against anaerobes. It also augments the efficacy of antibiotics
and promotes wound healing. These effects of HBO are utilized
in treatment of refractory osteomyelitis (Figures 3 and 4).
Burns25,47
A burn wound comprises of zones of necrosis, stasis and
hyperemia from within outwards. The conversion of zone of
stasis to zone of necrosis depends upon many adverse factors,
which includes hypovolemia, hypoxia, edema, infection,
etc. Adjunctive HBO therapy offsets the progression of burn
injury by reducing hypoxia and edema and its possible role in
infection control. The beneficial effect of HBOT in burns is
most evident when treatment is started early, possibly within
24 hours. Poor general condition of the patient, detailed
monitoring and large fluid resuscitation makes patients of
Figure 4: Same wound after 38 sessions of HBOT

Hyperbaric Oxygen Therapy in Management of Wounds 
Chapter 38
461
critical burns less likely candidate for HBOT. Practically,
role of hyperbaric oxygen therapy is for patients with less
extensive burn which are deep dermal in nature.
Side effect and
complications12,22,48,49
Oxygen in high doses is toxic to normally perfused tissues, in
particular the brain and lungs. Therefore, it is not possible to
expose patients to HBO for longer than one to two hours on a
regular basis. HBOT is associated with some risk of adverse
effects including damage to the ears, sinuses and lungs due to
high oxygen pressure, transient myopia, claustrophobia and
oxygen poisoning.

When used in standard protocols hyperbaric oxygen
therapy is safe. The most common complain may be slight pain
in the ears due to a blocked Eustachian tube. Pneumothorax,
air embolism, retrolental fibroplasia, cataract and transient
reversible myopia are rare complications encountered after
prolong HBO therapy. Fire safety protocol must be strictly
followed as malfunctioning electrical equipment in presence
of 100 percent oxygen is a recipe for disaster.
Conclusion
Hyperbaric oxygen therapy is an evolving specialty. As
number of hospitals using hyperbaric chamber are growing,
more and more medical specialties are coming under the realm
of this modality. As a plastic surgeon, knowledge of HBOT
may help us from being a hapless bystander in dealing with a
difficult wound or assist us in treating burns patient with CO
poisoning or in healing of deep dermal wounds.
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1. The Undersea and Hyperbaric Medical Society. Definition of
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10. Sheffield PJ. Tissue oxygen measurements with respect to soft-
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Miscellaneous
Section 4
462
27. Salvage of the problem wound and potential amputation with
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economic analysis. J Hyperbaric Med. 1988;3:127-41.
28. Goldman RJ. Hyperbaric oxygen therapy for wound healing
and limb salvage: a systematic review. PMR. 2009;1(5):
471-89.
29. Tan SG, Ong HS, Teoh MK. Early experience of limb salvage
in critical leg ischaemia. Singapore Med J. 1998;39:406-11.
30. Kalra M, Glovicski P, Bower TC, et al. Limb salvage after
successful pedal bypass grafting is associated with improved
long term survival. J Vasc Surg. 2001;33:6-16.
31. Padberg FT, Back TL, Thompson PN, et al. Transcutaneous
oxygen (TcP02) estimates probability of healing in the ischemic
extremity. J Surg Res. 1996;60(2):365-9.
32. Bunt TJ, Holloway GA. TcP02 as an accurate predictor of
therapy in limb salvage. Ann Vasc Surg. 1996;10(3):224-7.
33. Warriner RA, Fife CE. Diabetes watch: what you should
know about using HBOT in diabetic wounds. Podiatry Today.
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34. Lavan FB, Hunt TK. Oxygen and wound healing. Clinics in
Plast Surg. 1990;17(3):463-72.
35. Riseman JA, Zambons WA, Curtis A, et al. Hyperbaric
oxygen for necrotising fascitis reduces mortality and need for
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36. Bouachour G, Cronier P, Gouello JP, Toulemonde JL, Talha A,
Alquier P. Hyperbaric oxygen therapy in the management of
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37. Brown DR, Davis NL, Lepawsky M, Cunningham J, Kortbeek
J. A multicenter review of the treatment of major truncal
necrotizing infections with and without hyperbaric oxygen
therapy. Am J Surg. 1994;167:485-9.
38. McFarlane RM, Wermuth RE. The use of hyperbaric oxygen to
prevent necrosis in experimental pedicle flaps and composite
skin grafts. Plast Reconstr Surg. 1966;37:422-30.
39. Tan CM, Im MJ, Myers RA, Hoopes JE. Effect of hyperbaric
oxygen and hyperbaric air on survival of island skin flaps. Plast
Reconstr Surg. 1974;73:27-30.
40. Kaelin CM, Im MJ, Myers RA, et al. The effects of hyperbaric
oxygen on free flaps in rats. Arch Surg. 1990;125:607-9.
41. Perrins DJF. Influence of hyperbaric oxygen on the survival of
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42. Bennett M, Feldmeier J, Hampson N, Smee R, Milross C. Hyper-
baric oxygen therapy for late radiation tisue injury (Cochrane
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therapy in osteoradionecrosis. Can J Plast Surg. 1997;5(4):221-9.
44. Feldmeirer JJ, Heimbach RD, Davolt DA, et al. Hyperbaric
oxygen and the cancer patient, a survey of practice patterns.
Undersea and Hyperbaric Medicine1993;20(4):337-45.
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Therapy. Orthopedic Review. 1987;XIV(11):829-33.
47. Cianci P, Sato R. Adjunctive hyperbaric oxygen therapy in the
treatment of thermal burns: a review. Burns 1994;20(1):5-14.
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Press; 1970. pp.49-54.

Index
Page numbers followed by f refer to figure and t refer to table
A
Acromioclavicular joint 255f
Active dressing materials 81
Acute radiation changes 239f
Adipofascial extension of fasciocutaneous
flap 359f
Adriamycin extravasation 342f, 345f
Advantages of
primary wound closure 87
RNPT in skin grafting 425
skin substitutes 65
Air-fluidized bed 290f
Amino acids and wound healing 438
Amniotic band in baby NICU 391f
Amputation
injury of left hand 375f
of foot 62f
Anatomic location of foot ulcers 170
Ancient method of suturing wound 4f
Anhidrosis 275
Ankel defect 369f
Antegrade fasciocutaneous flap for
middle-third defect 354f
Anterolateral and anteromedial aspect of
thigh 95f
Anthracyclines 341
Antibiotics 246
in necrotizing fasciitis 310t
Anticoagulants 197
Antidotes in chemotherapeutic
drug extravasations 341
Antihistamines 37
Antihyperlipidemic agents 198
Anti-inflammatory agents 21, 36
Antimicrobial prophylaxis 101
Antiplatelet agents 197
Appearance of vasculitic lesion over
calf 202f
Application of
graft 96
porous mold and suction system to
wound 404f
Arginine 438
Arterial ulcer 192, 193, 193f, 459
management 197
Arthrodesis of ankle with grafting 176f
Aseptate hyphae 106f
Assessing severity of infection 163
Atrophic scar 29f
Augmentation mammoplasty 103
Autologel-autologus platelet rich
plasma gel 187
Avulsion
injury
dorsum of foot 372f
of gluteal region 140f
of thigh 122f
over dorsum and plantar aspect of
foot 46f
of palmer skin 145f
of sole 147f
wound of finger 61f
Axial flaps 381
B
Baby with birth injury 397f
Ballistic injury 348
Balloon angioplasty 190f
Bilateral
deltopectoral flaps 328f
gluteal rotation flaps 297f
gracilis myocutaneous flaps 249f
ischial sores 296f
Bioengineered alternative tissues 189
Biological skin substitutes 224
Bite wounds 44, 315
Bleeding 327, 333
Blood supply 275
Blunt trauma 61
Bone infection associated with
diabetic foot 164
Boyden’s chamber with millipore filter 13f
Brachial plexus 324f
Brachytherapy cannulae 252f, 264f
Breast
cancer 337f
implant failure after radiotherapy 269f
Bronchopleural fistula 265f
Budding yeast cells of Candida spp 105f
Burn wound 214
care 214
classification 208
healing 212
C
Calcium antagonists 37
Cancer of male breast 327f
Carbohydrate 433
in wound healing 436
Carotid artery 325f
Causes of
foot ulcers in diabetics 170
malodor 326
Cellular dysfunction and restoration of
biochemical balance within
wound 54
Central
venous access device 339
zone of coagulation 214f
Characteristics of
ideal dressing 81
malignant wounds 328
Charcot foot 158, 158f
Chemical burns 389
Chemo-extravasation 336
Chemoport extravasation 339f
resolved 339f
Chest wall tumor-chondrosarcoma 268f
Chlorhexidine 223
Chronic
extravasation ulcer 346f
in upper arm 346f
osteomyelitic wound over thigh 460f
radiation dermatitis 241f
ulcers 21
Circulation 350
Circumferential avulsion injury of right
thigh and popliteal region 137f
Classification of
diabetic foot ulcer 169
leg ulcers 192
surgical wounds 98
sutures 91
vasculitis 201t
wound 42
dressings 81
in relation to wound closure 80
Cleaning of wound 376
Clenched fist injuries 319
Closed
degloving injuries 75
technique 221
torso wound 60f
wound 59
Clostridial cellulitis and myonecrosis 312
Closure of wound 92f

Principles and Practice of Wound Care
464
Comparison of scar assessment scales 31t
Compartment
syndrome
after compression injury 117f
in crush injuries of limbs 114
of forearm 114
Complete traumatic amputation 378f
Complications of
pressure sores 295
wound healing 17
Compromised skin grafts and flap 460
Conservative wound management 291
Contraction of wounds 15
Contused and lacerated wounds 43
Cracker blast injury hand 379f
Criteria for good antimicrobial agent 221
Cross
leg fasciocutaneous flap 372f
section of abdominal wall depicting CDC
SSI classifications 99f
Crush injuries
and compartment syndrome 46
of forearm 115f
of leg with burst wound in upper part of
leg 76f
of limbs 113, 118
of right forearm 73f
Crush syndrome in limb injuries 113
Crushed extremity wound 60f
Cryotherapy 36
Crystalloid therapy 217t
Current of injury theory 449
D
Debridement
in diabetic patients 75
of wound 377
Decompression of Carpal-Tunnel 117f
Deep
dermal burn wound over thigh 232f
discharging ulcer 276f
Defect
after excision of sore 295f
in perenium after abdominoperineal
resection 267f
overlying dorsum of hand 342f
Degradation of extracellular matrix 15
Deltopectoral fasciocutaneous 253f
Denuded penis and testes 146f
Depth of injury in superficial second degree
burns 210f
Dermabrasion 39
Dermagraft 189
Dermal reconstitution 212
Development of
diabetes foot ulcer 155
malignancy in sacral pressure sore 297f
malignant wounds 323
neonatal skin 387
squamous cell carcinoma 151f
trophic ulcer 275
Diabetic
foot 156f, 420, 422
infections 160, 163t
left leg debridement and grafting 177f
left lower leg 177f
left wound over dorsum 174f
lesions 170t
postradical debridement 174f
right ankle 178f
right heel with charcot joint 176f
right sole 177f
ulcer 154, 154f, 157f, 158, 173f
with Charcot joint 179f
with right heal defect 177f
great toe ulcer 77f
neuropathy 155
ulcer with charcot arthropathy 172f
wound 459
Dietary supplements for wound
healing 441
Disease progression 307
Distal peroneal perforator flap 357f
Distant
flaps 381
pedicle flaps 368
Dorsal metatarsal first webspace flap 370
Dorsalis pedis artery flap 369
Draining sinus with infected implant
in situ 300f
Dressing
procedure 396
technique 227
Dry cracked skin 275f
E
Early salvage of brachytherapy
damage 252f
Economics of treatment of diabetic
foot 156
Edematous gaping edges 49f
Electric burn 62f
Electrical stimulation 449, 451f,
452, 452f
in used for sacral ulcer 450f
used in plantar ulcer 451f
Emergency local exploration 344
Epidermal stripping 389
Escharotomy 219
incisions 219f
Excised wall of ulcer 297f
Excoriation 334, 392
Exposed ankle joint 372f
Exposure 220, 350
Extensive avulsion injury 133f
of dorsum foot 373f
of foot with multiple fractures 123f
of lower limb 123f
Extensor digitorum brevis muscle flap 370
Extracellular matrix 14
Extravasation
injuries 389
in newborn 389f
of adriamycin 337f
of vincristine 337f
over wrist 338f
ulcer 337f, 344, 344f, 345f
covered with skin graft 345f
F
Facial vessels 256f
Faciomaxillary wound 60f
Factors influencing healing 16
Fascia lata graft 264f
Fasciocutaneous flap 355f, 372f
Fasciotomy incisions 219f, 220f
Fascitis of lower limb 309f
Fat and fatty acids in wound healing 437
Fimple interrupted sutures 88f
First aid in burns 215
Flap
planning 354
selection 353
Flavonoids 36
Foot
bath for plantar ulcers 450
defects 364
Forceps delivery 393f
Forearm fasciotomy 115f
Forefoot
defect 371f
sole ulcer 370f
Fournier`s gangrene 311, 311f, 312f329f
Fragile granulation tissue bleeding 230f
Free
radial
artery forearm flap 346
forearm flap 319f
tissue transfer 382
Frequency of operation 409
Full thickness skin grafts 130f
Fungal
surgical site infections 104
wound infections 102
Furacin 223
Fusiform excision 37
G
Gangrene 157f
of thumb 384f

Index 
465
Genesis of diabetic foot ulcer 154
Geometric broken line closure 39, 40f
Glucosamine 442
Glutamine 438
Gluteus maximus musculocutaneous
flap 296f
Gracilis
muscle 297f
myocutaneous flap 267f
Grading of ulcers 276t
Granulation tissue 49f
formation 14
Greek god of medicine 5f
Green bottle fly 185f
Groin flap 382f
cover 383f
Growth
factor inhibition 21
of candida tropicalis 105f
of fusarium solani 106
Gunshot
injury 374f
wounds 348
H
Half-buried suture 90f
Hand meshing of graft 95f
Harvesting graft 95f
Healing of wounds 48
Heel
advancement flap 367
avulsion 367f
ulcer with flap marking 366f
Hodgkin’s lymphoma 244f
Horizontal mattress suture 89f
Human bites 319
Hyperbaric oxygen 198, 457, 458
therapy 188, 247f
in management of wounds 457
in wounds 459
protocol 459
Hypertrophic scarring 213f
I
Ideal skin substitute 65
Immature scar 28f
Impact of malignant wounds 334
Indications for
electrical stimulation 449
Maggot’s treatment 186
Induction of granulation tissue
formation 402
Infected diabetic foot 161
Infection in diabetes 155
mellitus 155
Inhibitors of gene transfer 36
Intermediate thickness skin graft 94f
Intra-abdominal candidiasis 106
Intralesional
corticosteroid injections 34
steroid injection 35f
Intrinsic muscle paralysis 275
Invasive aspergillosis 108
Investigating vasculitic ulcers 204
Ischemic injuries 389, 390
Ischial sore 297f
J
Jackson’s three zones of damage in burn
wound 214f
K
Keloid in ears after ear piercing 35f
L
Lacerated wounds of face 44f
Laceration wound in neonate in NICU 393
Laminectomy dehiscence after
radiation 262f
Laser therapy in wound healing 454
Lateral calcaneal artery flap 368
Latissimus dorsi
muscle 254f
flap 69f, 261f
myocutaneous flap 246f, 251f, 255f,
268f, 269f
Layers of dressings 81
Limb salvage surgery 253
Linear hypertrophic scar 29f
Local muscle flaps 368
Locking suture 88f
Loss of skin
grafts due to MRSA infection 230f
soft tissue 384f
Low level laser therapy unit 187f
Lower posterior tibial perforators 355f
Lucilia sericata 185f
Lund and Browder’s chart 216t
M
Mafenide acetate 222
Maggot’s treatment 185, 186
Magnesium sulfate dressings 338f
Major keloids 30f
Malignancy destroying soft tissue and
bone 332f
Malignant
transformation 243
wounds 322, 323t, 328
Management of
blisters 218
chronic leg ulcers 194
crush syndrome 114
DFU 183
diabetic patient with foot ulcer 165
exudate 54
fibrotic wounds 21
malignant wounds 328
malodor 332
necrosis 53
radiation wounds 235
trophic ulcer on feet 274
upper extremity wounds 374
wounds 80
Manchester scar scale 33, 33t
Marjolin’s ulcer 151f
Matrix forming agents 84
Mattress sutures 88
Mature scar 28f
MCR footwear 281f
Medial plantar artery
based flap 366
flap 177f
Medical management of diabetic ulcer 154
Meningococcal sepsis 393f
Meshing of graft 95
Metacarpal fractures of all fingers 117f
Methods of
application 450, 452-454
debridement 75
delivery 237
wound closure 248
Microbiology of implant infection 299
Mixed ulcers 194, 194f
Multiple
diabetic ulcer over dorsum 171f
pressure sores 283f
sites of methylene blue injection 404f
Musculocutaneous flaps 382
Mutilating injury 384f
N
Nanocrystalline silver dressing 223
Necrosis of skin of entire dorsum of
hand 390f
Necrotic muscles of thigh and
abdomen 306f
Necrotizing fasciitis 304, 304f, 305t, 376
of perineum 311f
Necrotizing soft tissue infection 460
Neuropathic ulcer and ischemic ulcer 276t
Newborn with severe amniotic band
syndrome 391f
Newer wound closure techniques 91
Nitrofurazone 223
Non-clostridial anaerobic cellulitis 312
Noninvasive methods of investigating leg
ulcers 204

Principles and Practice of Wound Care
466
O
Observer scar assessment scale 32t
Occlusive
bites 319
dressing 221
Open
abdominal wounds 60f
comminuted fractures 73f
Operating room measures 99
Orthopedic device related infections 299
Orthopentogram panorouex 258f
Osseocutaneous fibular free flap 256f
Osteomyelitis of mandible 257f
Osteoradionecrosis 257
of clavicle 259f
of mandible 258f, 260f
Outcome of avulsion injuries 150
Oxygen transport in hyperbaric oxygen
therapy 457
Ozone
therapy 188f
treatment 188
P
Pain relief 451
Pathophysiology of
implant infections 300
infection 160
wound healing 435
Pectoralis major myocutaneous flap 254f,
260f
Pedicle flaps 178
Penetrating
trauma 61
wounds 74
Periodic acid Schiff’s stain 106f
Peripheral vascular disease 155, 420, 423
Postburn
hypertrophic scar on forearm and wrist 38f
keloid 38f
scarring in lower face and neck 40f
Postburn scar contracture over dorsum of
hand 226f
Postdebridement diabetic foot defect 179f
Posterior non-weightbearing heel 368
Postinfective wounds 376
Post-laminectomy dehiscence 261f
Postoperative ALT flap for same
defect 180f
Postsurgical wounds 376
Povidone iodine 223
Pre-emptive
postirradiation flap surgery 262
pre-radiation flap surgery 261
Preoperative ALT flap harvesting 180f
Preparation of wound for grafting 229
Preparing wound bed 56, 56t
Pressure
sores 283
therapy 34
ulcer 459
staging system 390t
Primary
breast reconstruction 269f
closure after vulvectomy 179f
squamous cell cancer of thyroid 327f
gland 327f
Principles of
management of radiation ulcers 247
VAC therapy 186f
wound bed preparation 55t
Promotion of wound healing 267
Protein 433
and wound healing 437
Pruritis 334
Puncture wound on neck 61f
R
Rabies infection 317t
Radial artery
fasciocutaneous forearm flap 256f
forearm
fasciocutaneous flap 264f
flap design 385f
flap reconstruction in oral
cavity 256f
free flap 385f
Radiation injury during radiotherapy 238
Radiation
osteitis 257f
ulcer 244f, 245f, 246, 460
Radical neck dissection 243f, 254f, 325
Radiotherapy for cancer penis 329f
Recent advances in
management of chronic non-healing
diabetic foot ulcers 183
wound
coverage 9
healing 19
Recommended vacuum pressure 409
Reconstruction of
extensive foot defects 370
foot defects 365
wound 377
Reconstructive breast surgery 264
Rectus abdominis myocutaneous flap 245f,
249f, 252f, 267f
Recurrence of STS in shoulder 255f
Recurrent
osteoradionecrosis of maxilla 260f
sacral chordoma 254f
Reduced bacterial count 403
Refractory osteomyelitis 460
Removal of
devitalized tissue from ulcer 184
spinal tumor 261f
Replanted hand dorsal aspect 378f
Restoration of bacterial balance 54, 54t
Retaining non-viable critical structures 75
Reticular dermis 210f
Retrograde adipofascial flap 356f
Reversal of lymphatic flow 403
Reverse sural artery flap 367
Right internal jugular vein 324f
Ring avulsion injury 145
RNPT in
fixation of skin graft 423
major
burns 420
trauma 412
minor
burns 418
injuries 412
open bone fractures 415
soft tissue trauma 412
Role of
antibiotics and tetanus prophylaxis 74
electrical stimulation in wound
healing 448
exercise therapy in wound healing 448
hydrotherapy in wound healing 455
key
macronutrients in wound healing 436t
micronutrients in wound healing 439t
nutrition in wound healing 432, 436
oxygen in wound healing 458
physiotherapy in wound healing 447
regulated negative pressure therapy in
wound healing 401
ultrasonic therapy in wound healing 452
wound swabs 73
Rotation flap 367
Rule of
five 216f
nine 216f
S
Sacral
chondrosarcoma 251f
pressure sore healed with split skin graft
295f
Sarcoma of breast 244
Scrotal abscess 311f
Self-care kit 277f
Serial excision 37
Severe
acute radiation 239f
avulsion injury 375f
over thigh and gluted region 46
crush injury 383f

Index 
467
limb threatening infections 166
pain 209f
Shaving and split skin grafting 37
Silicone gel sheet application 35f
Silver
impregnated dressings 223
nitrate solution 222
Simple
excision 37
suture 87
Skin
avulsion injuries 122
battery theory 449
cover 174, 279
fillers 37
flap 177, 366
graft 64f, 174, 368, 377
grafting of wounds 229f
substitutes 23, 224
Sloughed diabetic foot 175f
wound over dorsum 176f
Small pressure sore in back of neonate 389f
Soframycin 222
Soft tissue
infections 308t
sarcoma 250f
of forearm 264f
of shoulder 255f
Sole after radical debridement 175f
Spinal cord injury 283f
Split skin graft 177f
Squamous cell cancer of left buccal mucosa
326f
Stabilization of fractures by K-wires 117f
Staging of diaper dermatitis 392t
Staphylococcal infection 230f
Staples used for wound closure 92f
Stem cells 23
Sterilization of surgical instruments 99
Steri-strips used for wound closure 92f
Stony Brook scar evaluation scale 33
Subcutaneous tissue and fluid 343f
Subcuticular suture 89, 90f
Suction forces and acute bleeding 409
Sulfamylon 222
Superficial
dermal burns 224f, 229f
partial thickness 211f
temporal artery fasciocutaneous flap 260f
Supra
calcaneal defect 368f
malleolar flap 368
Sural neurofasciocutaneous flap for heel
defect 358f
Surgical
closure of wounds 86
debridement 172
excision of burn wound 231
intervention for pressure sores 293
management of diabetic foot 169
site infection 98
Suspicion of closed avulsion injury 124f
Suture tracks 16
Suturing
needles 90
technique 87
Synovial sarcoma of ilium 263f
Synthetic skin substitutes 225
Systemic antibiotic therapy 165
T
Tangential excision of dead dermis with
Watson’s knife 232f
Technique for harvesting skin graft with
Humby’s knife 95f
Technique of
debridement 69
excision 232
harvesting split skin graft 94
wound closure 86
Tensor fasciae latae musculocutaneous
flap 263f
Tetanus prophylaxis 377
Thenar muscles and interosseous
muscles 117f
Thermal injuries 389
Thick split thickness skin graft 94f
Thin split skin graft 93f
Tissue
cavitation 349
crushing 349
edema 403
engineering 23
expansion 39
management 194
Tongue
lesion in Behçet’s syndrome 205f
tumor 253f
Topical
antimicrobial 158, 221
pressure 403
therapy 164
Total contact casting 157
Trace elements primary and secondary roles
in wound healing 441t
Transposition of deltopectoral flap 253f
Traumatic wounds 374
Treatment for xerosis 246
Treatment of diabetic foot infections 162t
Treatment of
fasciotomy with RNPT 416
infection 164
necrotizing fasciitis 429
osteomyelitis 167
radiation induced wounds 245
ulcerations 344
Types of
avulsion injuries 123
suction applied for NPT 409f
vasculitis 201
vesicants 337
wound
closures 80
healing 16
Typical
appearance of vasculitic lesion in pan
202f
trophic ulcer 275f
U
Ulcer
over
metatarsal heads 170f
toes and dorsum of foot 170f
on lower leg 47f
Ultrasonic
debridement 184
therapy equipment 453f
Ultraviolet therapy 453
in wound healing 453
Underlying muscle and bone 211f
Unstable scar over shin of tibia 28
V
VAC
dressing 64f
machine 186f, 197f
therapy set for rapid granulation
tissue 172f
Vacuum assisted closure 196
device 279
Vancouver scar scale 31, 32t
Vascular
interstitial closed circuit 449
ulcers 192
Vasculitic
lesion
in Behçet’s syndrome 205f
over thighs 203f
ulcer 206
Vasculitis
in case of inflammatory arthritis 203f
involving upper limb 203f
Venous ulcers 193, 194f, 197, 459
Ventilation 99
Vertical mattress 88
suture 89f
Vessel injury in crush injuries of limbs 117
Vincristine extravasation 342f
Visual analog scale 31

Principles and Practice of Wound Care
468
Vitamin
A 440
B 439
C 439, 440
E 440
K 440
W
Wagner’s
classification of foot ulcer 155
diabetic foot ulcer classification system
170t
Watson’s knife 38f
Wound
bed preparation 53, 57, 80
cleaning 332
closure 63
control 184
culture 162, 377
dressing 22, 81, 82t
for radical debridement 174f
healing 11, 79, 458
malodors 324
management in crush injuries of limbs
120
Z
Zinc 440
Zone of hyperemia 214f
Z-plasty 37