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A Systematic Review on Classification, Identification, and Healing Process of

Burn Wound Healing

Article in The International Journal of Lower Extremity Wounds · June 2020

DOI: 10.1177/1534734620924857

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924857
research-article2020
IJLXXX10.1177/1534734620924857The International Journal of Lower Extremity WoundsAbazari et al

Original Review
The International Journal of Lower

A Systematic Review on Classification,

Extremity Wounds
1­–13
© The Author(s) 2020
Identification, and Healing Process of Article reuse guidelines:
sagepub.com/journals-permissions

Burn Wound Healing DOI: 10.1177/1534734620924857

https://doi.org/10.1177/1534734620924857
journals.sagepub.com/home/ijl

Morteza Abazari, MSc1 , Azadeh Ghaffari, PharmD, PhD1,

Hamid Rashidzadeh, MSc1, Safa Momeni Badeleh, PharmD1, and
Yaser Maleki, MSc2

Abstract
Because of the intrinsic complexity, the classification of wounds is important for the diagnosis, management, and choosing
the correct treatment based on wound type. Generally, burn injuries are classified as a class of wounds in which injury is
caused by heat, cold, electricity, chemicals, friction, or radiation. On the other hand, wound healing is a complex process,
and understanding the biological trend of this process and differences in the healing process of different wounds could
reduce the possible risk in many cases and greatly reduce the future damage to the injured tissue and other organs. The
aim of this review is to provide a general perspective for the burn wound location among the other types of injuries and
summarizing as well as highlighting the differences of these types of wounds with emphasizing on factors affecting thereof.

Keywords
wound, burn wound, classification, wound healing process, wound healing factors, instrumental wound identification

Introduction the articles were screened and abstracts of studies identified

In a minimalistic estimate and according to the World
Health Organization (WHO), American Burn Association,
and Centers for Disease Control and Prevention (CDC)
reports, annually about 1.1 million people in the United
States suffer from burn injuries and 486 000 people require
medical treatment. Approximately 50 000 of these burn
victims were admitted at 128 hospital burn centers, and
4500 and 10 000 deaths annually were reported as a result
of burn injuries and burn-related infections, respectively.
These numbers are several times higher for low- and mid-
dle-income countries.1-3 Accurate assessment of these
wounds is a critical task to provide the right diagnosis and
treatment. Classification of wounds by gathering the nec-
essary information along with knowledge of the wound
healing process can be useful for this purpose. In addition
to conventional methods, the recent development of instru-
mental techniques and spectroscopic analyses has been
used to evaluate and classify wounds. Many studies in this
field have shown that the specific capabilities of these
techniques can be used to collect and calculate the required
information for evaluating and classifying the wounds.4-6
from searches. The full text of articles was obtained if they
appeared to satisfy the inclusion criteria. Figure 1 shows the
flow diagram of steps and the number of trials identified
and selected for inclusion.
Classification
Wounds classification is very important from the point of
management, diagnosis, choosing the correct treatment,
needed time for wound healing, and anticipating the risks
and infections that may occur during the wound healing
process.7-9 To date, there is no standard and general classifi-
cation in this area. This is mainly because of different
causes, complexity, and large number of wounds, and over-
lapping of various subclasses of wound types. However, a
series of sporadic classifications in this field are provided in
books, journals, scientific articles, and related websites.10,11
These classifications have been proposed to classify a few
numbers of wounds based on effective parameters. These
1
Zanjan University of Medical Sciences, Zanjan, Iran
2
Institute for Advanced Studies in Basic Sciences. Zanjan, Iran

Corresponding Author:
Study Method Azadeh Ghaffari, School of Pharmacy, Zanjan University of Medical
Sciences, Next to Ayatollah Mousavi Hospital, Gavazang Boulevard,
First, the title of articles was searched from Google Scholar Zanjan 45139-56184, Iran.
database and related websites for years 1990 to 2019. Then, Email: aghaffari@zums.ac.ir
2 The International Journal of Lower Extremity Wounds 00(0)
Figure 1. Flow diagram for identification and selection of studies.
parameters include cause, color, location, etiology, wound
depth, contamination, duration of the wound healing, and so
on.5,12-18 In one embodiment, wound can be classified by the
integrity of skin, as shown in Figure 2, for burn wound. The
old and new system classifications of burn wound based on
depth are summarized in Table 1.
In the burn wound classification based on severity, inju-
ries are classified into 3 subclasses. This system is also
referred to as the ABA system (American Burn Association’s
Grading System), which includes patients who manifest
inhalation injury or have burn marks from high-voltage
electrical injury. In this system, the extent of injuries is
described by the percentage of the total body surface area
(%TBSA), which is caused by burn (Table 2).19-24
Healing Process of Burn Wound
Versus Other Wounds
Wound healing is a natural and normal response of the body
to its injuries. It is a complex and dynamic process for the
fast recovery of damaged tissues and normal function. This
process consists of 4 highly interconnected and overlapping
phases, which include hemostasis, inflammation, prolifera-
tion, and remodeling. Various biophysiological functions
and different predominant cells characterize these phases at
differing intervals and sometimes considerable overlapping
can occur.11,25-28 The proper sequence of these phases at a
specific time and continuation for a specific duration at an
optimal intensity is crucial for complete healing of wounds
(Figure 3). Key similarities and differences between burn
wound and other wounds are summarized in Table 3 and are
discussed in more detail below.
Hemostasis
Hemostasis is the shortest phase of the wound healing pro-
cess and refers to the mechanisms that eventually stops the
actual bleeding. It begins immediately on injury and is also
called the pro-inflammatory phase. In this phase, injury to
tissue causes a release of thromboxane A2 and prostaglan-
din 2-α from tissue injury to the wound bed causing a
potent vasoconstrictor response and the small vessels
within the wound constrict to provide hemostasis (vaso-
constriction). This vasoconstriction lasts 5 to 10 minutes
and is followed by vasodilation, a widening of blood ves-
sels, which peaks at about 20 minutes post wounding.
Vasodilation is the end result of factors released by plate-
lets and other cells (epidermal growth factor [EGF], fibro-
nectin, fibrinogen, histamine, platelet-derived growth
factor [PDGF], serotonin, and Von Willebrand factor).
Exposure of subendothelial collagen to platelets results in
platelet aggregation, degranulation, and activation of the
coagulation cascade. Platelet degranulation activates the
complement cascade, specifically C5, a potent neutrophils
chemotactic protein. Then, activation of clotting cascade
causes platelets to rapidly clump and adhere to connective
tissue at the cut end of a constricted vessel and form fibrin
clot (thrombus; Figure 2).29-31
Abazari et al
Figure 2. General classification of wounds and burn wounds.
This phase of wound healing is usually not considered in
burn wounds since the above-mentioned statements are dif-
ferent in burn wounds. There is no bleeding in the burn
wounds; hence, there is no homeostasis in the aforemen-
tioned concept to prevent bleeding in these types of wounds.
On the other hand, these effects in burn wounds consider-
ably vary depending on the severity of burns. In burn
wounds, immediately after burn, capillary permeability
increased, leading microvessels to lose its capacity to keep
fluids apart from the interstitial area. Loss of fluid and pro-
teins are intense and contemporary to shift in the ionic con-
tent of the cells (ischemia).15,32
Vasoconstriction in peripheral and splanchnic occurs, and
myocardial contractility is decreased, possibly due to release
of tumor necrosis factor-α. These changes, in association
with fluid loss from the burn wound, result in systemic
hypotension and end-organ hypoperfusion. This phase of
wound healing in burn wounds mostly depends on the depth
3
and burn zones. Jackson (1959) first described following 3
zones in the damaged burned tissue (Figure 4)32,33:
1. Zone of coagulation: This area is located in the cen-
tral part of the burn and characterized by complete
coagulative necrosis and irreversible tissue loss.
This zone occurs at the point of maximum damage,
and denaturation of the constituent proteins and loss
of plasma membrane integrity is observed, with a
necrosis visible at the center of injury.
2. Zone of stasis: This zone is located at the periphery
of the zone of coagulation. Sluggish tissue perfusion
ranging from critical capillary vasoconstriction to
ischemia could be observed in this area. The effects
created in this area have the potential to be recov-
ered after early and adequate resuscitation, and
proper wound care. Otherwise, they could be easily
transformed into necrosis by the additional and
4 The International Journal of Lower Extremity Wounds 00(0)

Table 1. The Old and New System Classifications of Burn Wound Based on Depth.
New system Superficial Superficial partial- Deep partial-thickness Full-thickness (third Full-thickness (fourth
(old system) (first degree) thickness (second degree) (second degree) degree) degree)

Etiology Ultraviolet light, very Scald (spill or splash), Scald (spill), flame, oil, Scald (immersion), Cause as for deep
short flash (flame short flash grease flame, steam, oil, partial-thickness
exposure) grease, chemical, high- burns
voltage electricity
Histology Epidermis only Epidermis and papillary Epidermis and reticular Epidermis and dermis; Involves fascia and
dermis, skin appendages dermis, most skin all skin appendages muscle and/or bone
intact appendages destroyed destroyed
Clinical features Erythema, dry Erythema, blisters; moist, Blisters (easily unroofed); Waxy white to leathery Black (dry, dull, and
(appearance) and pink or red; red and weeping; wet or waxy dry; variable gray to charred charred)
blanches with blanches with pressure color (patchy to cheesy and black; dry and
pressure white to red); does not inelastic; does not
blanch with pressure blanch with pressure
Sensation Painful Painful to air and Perceptive of pressure Deep pressure only Deep pressure only
temperature only (insensate) (insensate)
Healing time 3 to 6 days 7 to 20 days More than 21 days Never (no spontaneous Never (no
healing) spontaneous healing)
Scarring None Unusual; potential Severe (hypertrophic) risk Very severe risk of Eschar tissue (hard and
pigmentary changes, of contracture contracture, eschar inelastic)
moist, elastic tissue (hard and
inelastic)
Treatment Cleaning, cooling with Cleaning; cooling with Cleaning; topical agent; As for deep partial- Healing requires
running water or running water or a cold sterile dressing; possible thickness burns plus surgical intervention,
a cold compress, compress, topical agent; surgical excision and surgical excision functional
return of full sterile dressing, the grafting; earlier return of and grafting at the impairment
function return of full function function with surgery earliest possible time,
functional limitation
more common if not
grafted
Complication Increase the risk of Local infection, cellulites Possible skin grafting Possible amputation Amputation, gangrene,
skin cancer death
Schematic
appearance

accumulated insults such as decreased perfusion,
edema, and infection.
3. Zone of hyperemia: This area is located at the
peripheral of stasis zone and characterized by viable
cells and vasodilatation mediated by local inflam-
matory mediators. The tissues of this zone eventu-
ally recover completely unless complicated by
infection or severe hypoperfusion.
Inflammation
After hemostasis is achieved, local histamine release by the
activated complement cascade occurs due to the capillary
vasodilatation and leakage. Increased blood flow and vascu-
lar permeability of the vessels lead to the migration of
inflammatory cells to the wound site. The presence of for-
eign organisms activates complement C3, and its cascade of
nonenzymatic protein cleavage and interactions ultimately
leads to the bacterial lysis. Then, tissue injury with the
release of cytokines and other inflammatory mediators lead
to the recruitment of neutrophils to the site of the wound as
a second response cell. These cells are responsible for
engulfing and lysis of foreign organisms, debris scavenging,
complement-mediated opsonization, and bacterial destruc-
tion via oxidative burst mechanisms.27,29,32 The wastes gen-
erated from the activity of the neutrophils later phagocytosed
by macrophages or extruded with the eschar. Macrophages
from monocytes stimulated by fragments of the extracellular
matrix (ECM) protein secrete growth factors, enzymes, and
cytokines; promote phagocytosis of bacteria and foreign
materials; assist with autolytic debridement; and release
nitric oxide to kill bacteria. Macrophages also secrete EGF
and PDGF that initiate the formation of granulation tissue
and thus initiate the transition into the proliferative phase
Abazari et al 5

Table 2. Classification of Burn Wound Based on Severity or ABA System.

Type Agea Criteria Disposition

Minor Children <10% TBSA Outpatient management
Full-thickness <2% TBSA
Adults <15% TBSA
Full-thickness <2% TBSA
Elderly 10% TBSA
Full-thickness <2% TBSA
Moderate Children 15% to 20% TBSA Hospital admission
Full-thickness <10% TBSA
(noncritical areas)
Adults 15% to 25% TBSA
Full-thickness <10% TBSA
(noncritical areas)
Elderly 10% to 20% TBSA
Full-thickness <10% TBSA
(noncritical areas)
Major Children >20% TBSA Referral to a burn center
Full-thickness >10% TBSA
Burns in critical areasb
Complicated burnsc
Adults <25% TBSA
Full-thickness >10% TBSA
Burns in critical areasb
Complicated burnsc
Elderly <20% TBSA
Full-thickness >10% TBSA
Burns in critical areasb
Complicated burnsc

Abbreviations: ABA system, American Burn Association’s Grading System; TBSA, total body surface area.
a
Children, <10 year old; adult, <40 year old; elderly, >40 year old.
b
Critical areas include the face, hands, feet, and perineum.
c
Complications include inhalation injury, high-voltage electrical burns, associated major trauma, infants, elderly, and comorbid medical problems (eg,
diabetes mellitus).

and tissue regeneration. Lymphocytes infiltration and depo-
sition take place in the late inflammatory phase and remain
during the remodeling phase for weeks. T-helper/effector
and T-suppressor/cytotoxic lymphocytes with producing a
variety of lymphokines (such as INF-α and transforming
growth factor-β [TGF-β]) show distinct and different effects
on the wound healing process. It has been shown that
T-helper/effector lymphocytes are necessary for successful
wound healing and its depletion causes an impairment heal-
ing. On the other hand, T-helper/effector subsets with coun-
terregulatory effects regulate fibroblast replication and
collagen protein synthesis.34-36 Inflammation begins imme-
diately after wounding and lasts for 1 to 4 days. This phase
is vital in the wound care process, though if it goes on for too
long, it could actually prevent regeneration.30,37
The inflammatory response in thermal injury healing has
several distinct and specific differences with the normal
wound healing process. In the early phase of postburn
edema, the release of histamine, with its effect on vasocon-
striction, increases blood pressure in injury, with increasing
capillary permeability, causing decrees in intravascular
fluid and create hypovolemic shock, and leading to a
decrease in osmotic pressure with an effect on increased
protein leakage. Besides vasoactive histamine in these types
of wounds, increased activation of the kinin system has
been observed in this phase. Activation of the kinin system
leads to increased activation of the kallikrein-bradykinin
system but also has consequences on the complement cas-
cade, arachidonic acid cascade, and the coagulation fibrino-
lytic cascade.31 Increases in arachidonic acid cascade,
specifically prostaglandins, prostacyclin, and thromboxane
A2, have been observed, which result in perpetuation of
burn edema formation, vasoconstriction, and local ischemia
in burned tissue. C3 and C5a complement regulates poly-
morphonuclear leucocytes function. Monocytes in its active
form as macrophages secretes IL-1 and tumor necrosis
factor-α (TNF-α) and have an influence of the control of
remote functions (production of, eg, acute phase proteins,
IL-6, and fever). Mast cells besides secreting of vasoactiva-
tors and spasmogens, with releasing chemoattractants,
6 The International Journal of Lower Extremity Wounds 00(0)

Figure 3. General process for wound healing. Differences of process in burn wound highlighted in the text.

Table 3. Key Similarities and Differences Between Burn Wound and Other Wounds.

Differences Similarities Wound Healing Phase

Hemostasis  Vasoconstriction response
Inflammation  Histamine release and increased blood flow
and vascular permeability of the vessels
Proliferation  Releasing of migration and proliferation factors
 Reepithelialization and differentiation in the
basal layer of the wound edges
 Proliferation of fibroblast
Maturation  Leaving of fibroblast cells from the wound bed
 Collagen remodeling
 Contraction and scar formation
 No actual bleeding
 Depending on the depth, severity, and burn zones
 Different biophysiological functions and physiological
components
 Increased activation of the kinin system and
kallikrein-bradykinin system
 Different biophysiological functions
 Different cell recruitment and factors secretion
 Different physiological events orders and extensions
 Depending on the depth and severity of wounds
 Different physiological events orders and patterns
 Extent and outcome depend on the depth and
severity of the burn

directly contribute to the recruitment and interstitial migra-
tion of leucocytes. Immunosuppression because of severely
impaired lymphocytes is also seen in severe thermal injury.
Ultimately, the cellular response of burned tissue helps in
phagocytosis and cleaning of dead tissue and toxins from
the wound site.38,39
Proliferation
This phase begins in 4 days after injury and extends 14
days after injury. When the inflammation subsides, the
body releases several kinds of cells, including those that
are responsible for migration and proliferation. At this
phase, the wound site experiences several interconnected
processes (reepithelialization, angiogenesis, collagen syn-
thesize, and ECM formation) to restore the vascular net-
work and form granulation tissue. Reepithelialization
occurs by migration and differentiation of existing kerati-
nocytes in the basal layer of the wound edge and epithelial
stem cells from nearby hair follicles or sweat glands.38
Differentiation of keratinocyte takes place by 3 major MAP
kinase pathways that are activated by multiple stimuli such
Abazari et al
Figure 4. Jackson’s burn wound model.
as calcium influx, EGF, and TNF. The proliferation of kera-
tinocytes approximately 2 to 3 days after injury and forma-
tion of granulation tissue forms a barrier between the
wound and the environment (ie, reepithelialization) and
replace the matrix formed during the homeostasis phase.
Fibroblasts are major types of cells in this phase and prolif-
erate in the deeper parts of the wound and synthesize a
small amount of collagen, which acts as a scaffold for fur-
ther migration and proliferation of fibroblasts and ECM
production.40,41 Formation of new blood vessels, also called
as angiogenesis, takes place for supplying oxygen and
nutrients for wound repair. Migration and replication of
endothelial cells activated by some growth factors, for
example, vascular endothelial growth factor (VEGF),
PDGF, basic fibroblast growth factor (bFGF), and the ser-
ine protease thrombin in the wounds, result in the forma-
tion of new blood vessels. The proliferation phase extends
from 5 to 14 days and continues with the onset of the matu-
rational or remodeling phase. More details for this phase
could be found elsewhere.29,37
This phase of wound healing is approximately the same
for burn wounds and other types of wounds. Therefore, kera-
tinocyte migration from viable skin appendages in the dermis
(eg, hair follicles, sweat glands) initiate the reepithelializa-
tion in few hours after injury. This remains most dependent
on the depth and severity of wounds. In a first-degree burn
wound, the basement membrane remains intact and epithelial
cells migrate upward in the normal pattern. Intact progenitor
epithelial cells below the wound restore a normal layer of the
7
epidermis in 2 to 3 days. In deeper burn injuries, the base-
ment membrane has been damaged and then normal epider-
mal cells migrate from skin appendages and the wound
periphery reepithelialize the wound. After reepithelialization,
the proliferation of fibroblast restores connective tissue to
wound bed and membrane zone formation occurs between
dermis and epidermis. Angiogenesis and fibrogenesis con-
tinue to reconstruct dermal tissue, and collagen begin to be
deposited. Although rough scar and hard scabs could be
formed in this phase without a moist healing environment.
The contraction of the wound edge also begins in this phase
and continues in the maturation phase.31,33
Maturation
The last phase of wound healing is called maturation or
remodeling. This phase is approximately the same in all
wounds and can be last months or even years. During matura-
tion phase, fibroblast cells leave the wound bed and collagen
is remodeled in a more organized matrix. The transition of
granular tissue to scar takes place after 2 weeks of injury. The
contraction of the wound occurs because of mechanical ten-
sion and the differentiation of fibroblasts to myofibroblasts.
Cross-linking between collagen fibrils form to increase
mechanical tension or tensile strength, which aided with vita-
min C. Differentiation of fibroblasts to myofibroblasts by
activation of cytokines, for example, TGF-β, express α-
smooth muscle actin (SMA), and contract the wound.
Myofibroblasts are deposited in the ECM, secrete the ECM,
8 The International Journal of Lower Extremity Wounds 00(0)
and by secreting matrix metalloproteinases and tissue inhibi-
tors of metalloproteinases they could remodel this ECM.
Replacing of collagen III by collagen I in the ECM takes
place in this phase, which has higher tensile strength, though
it takes too long for deposition in the ECM. Ultimately, when
healing is complete, myofibroblasts undergo apoptosis.37
Angiogenesis for establishing new blood vessels and increas-
ing blood flow decline and eventually mature avascular and
acellular environment is formed. Recovery of skin compo-
nents such as hair follicles and sweat glands depends on
wound severity, and in serious injury, it could not be com-
pletely recovered. The healed tissue strength (scar tissue)
only achieve 70% to 80% of the original tensile strength after
1 year following the injury.29,42,43
Remodeling, contraction, and scar formation also occurs
in burn wounds. The extent and outcome of each of these
steps depend on the depth and severity of the burn. For
deeper and most severe burns, remodeling would take more
time, and skin contraction and scar formation would be
higher. In superficial burns, the overactive response of
melanocytes to burn trauma results in hyperpigmentation of
skin and hypopigmentation could be seen in the deeper
wound because of the destruction of melanocytes in the skin
appendages.44-47 In second-degree deep dermal and full-
thickness burns, if the duration of the wound takes too long
or wound left to heal of its own, the probability of hypertro-
phic scarring and contractures also would be high.15,31,32
Several biochemical components and biological events
are involved in each of the above-mentioned phases, which
ultimately lead to wound healing by acting in a sequential
and well-coordinated order. There is an organized overlap
in the components involved in each of the phases. The
breakdown of this sequence and overlap, as well as the
defect in the function of each of these components, leads to
incomplete wound healing and ultimately affects the impair
functional recovery in the healed wound. Comprehensive
information about these components and their origins, func-
tions, and effects are summarized elsewhere.27,38
Extrinsic Factors Affecting Burn
Wound Healing
In addition to the internal and physiological factors men-
tioned above, there are several external and extrinsic factors
that affect wound healing in general and the burn wound
healing in particular. In a general classification, these fac-
tors are categorized into 2 categories of local factors and
systemic factors. Local factors include infection, oxygen-
ation, foreign bodies, and so on. Systemic factors, in sum-
mary, include age and sex, obesity, sex hormones, ischemia,
and other cases. The role and effect of each of these factors
are summarized in Table 4. These factors are important for
achieving optimal wound healing in the shortest possible
time.24,39,48,49
Burn Wound Identification and
Classification by Instrumental
Techniques
Precise diagnosis of wounds, especially burn injuries,
requires structural and functional details. To this end, the
integration of conventional classification systems and new
methods such as instrumental techniques and using the cur-
rent knowledge about the wound healing process and its
effective factors can provide accurate identification and
classification of wounds in complicated situations. In some
cases, for example, in identifying superficial and full-thick-
ness injuries, an accurate assessment is easily achieved. But
sometimes, due to the fracture of the wound site and sur-
rounding tissues, the assessment of the wound is difficult.
For example, in identifying intermediate partial-thickness
wounds from deep partial-thickness. The latter usually
requires surgery, while the former will generally heal with
appropriate wound care. However, assessment of burn
depth and burn degree in this situation is limited to 60% to
75% even by experienced surgent.77-79
Among various instrumental techniques, laser Doppler
imaging (LDI) has been shown to stand out because of its
accuracy and clinical applicability. In this technique, the
perfusion index of the wound is measured by the Doppler
shift of the reflected laser light penetrating through the skin.
The blood perfusion and therefore perfusion velocity in the
superficial burn tissue are higher, compared with the normal
tissue and much lower in the deep burn tissue. On the other
hand, the blood perfusion increases with time due to the
start of metabolic processes in the burn wound. Therefore,
with measuring the perfusion index of the wound, identifi-
cation of burn depth and burn degree can be accomplished.
Many authors repeatedly measured the perfusion velocity.
The results showed that if the perfusion velocity of the burn
wound was 0 to 250 perfusion unit (PU), the burn was deep
and these patients should undergo surgery. If perfusion
velocity was 250 to 625 PU, the burn was superficial and
these referred for conservative treatment. In the latter case,
if perfusion velocity after later LDI decreased, the patient
will be referred to surgery, and if it remained >625, conser-
vative treatment is the chosen treatment, and finally, spon-
taneous epithelization of burn wounds will be appeared.
LDI is a noninvasive, painless, simple, and accurate tech-
nique (97% sensitivity), and it can reduce the length of stay
and cost of treatment with early diagnosis of burn depth.
This technique can be applied to another wound’s assess-
ment such as diabetic ulcers.78,80-82
Another technique for wound processing is Fourier
Transform Infrared spectroscopy (FTIR). In one study by
Mao, FTIR was applied along with the image processing
method and Raman spectroscopy (RS) for the evaluation of
chronic wounds (diabetics ulcer). In this method, the aver-
age spectrum of samples was used for the differentiation of
Abazari et al 9

Table 4. Factors Affecting Burn Wound Healing.

# Factors Description
Local factors Infection Cause wound colonization, invasion into subjacent tissue, progression in the destruction
of granulation tissue, visceral hematogenous lesions, leukopenia, hypothermia, and death.
Pronounce immune response, accompanied by sepsis or septic shock can be observed, which
results in hypotension and impaired perfusion of end organs, delay wound healing, longer
hospital stays, higher costs, and higher mortality.19,39
Oxygenation Essential for epithelialization, contraction, collagen maturation, and synthesis. Decreases edema
formation due to hyperoxic vasoconstriction and lead to phagocytic killing of bacteria. The
inspiration of pure oxygen or employing hyperbaric oxygen might delay wound healing due to
intensive vasoconstriction. The inspiration of HBO2 decreases mortality, lessen the need for
surgery, and reduce the length of hospital stay.50-52
Ischemia Creating hypoxia that is important in the stimulus of fibroblast growth and angiogenesis. It
causes malnourishment of wound tissues, lengthens and impairs wound healing.53 Contribution
of necrosis and apoptosis to cell death observed in the zone of ischemia.54
Edema May lead to obstruction of the venous and lymphatic return, and even severely reduce arterial
blood supply. Increase the risk of tissue ischemia and infection. Restriction of respiratory
movements in circumferential burns of the chest.55
Systemic Age Slower recoveries, delayed wound healing due to decreasing blood supply and relative hypoxia,
factors severe hypermetabolic response, ineffective inflammatory response due to less efficient
physiological functioning, longer hospitalization, and high cost in elder person were observed.
Also, an ineffective inflammatory response due to immature cells could be observed in a very
young person.56-59
Gender Different hormones in males and females cause different effects on the inflammatory response
and remodeling phase. Smaller TBSA, less severe injuries, higher mortality, and elder
complications are most common in women patients.60-62
Medications Drugs such as glucocorticoid steroids and nonsteroidal anti-inflammatory, besides decreasing
inflammation, could also decrease the production of collagen, delay wound healing, and
suppress the immune system. Inhibit the platelet action in aspirin, cell destruction, and
suppress the immune system in cancer chemotherapy, radiotherapy, and AIDS medications.48
Nutrition Proteins, vitamins (C and A), zinc, and iron are required in wound healing for enzyme activity
and collagen synthesizing and cross-linking. Malnourishing decreased collagen formation,
increases wound impair and delayed wound healing especially in elder people.63-65
Diseases Which affect blood, oxygen, and nutrient supply. Decrease the sensation, loss of appetite and
weight in diabetes, and malignancy.66,67
Smoking With the biological effects of nicotine such as inflammation or anti-inflammation, cell
proliferation, apoptosis, angiogenesis, and fibrosis,68 it interferes with the body’s immune
system, make vasocontraction and hypoxia, and delays wound healing. Other complications
including rupture of the wound, infection, necrosis, low tensile strength, and more likely to
have scarring.68,69
Alcoholism Increases the risk of wound infection by diminishing the body’s resistance and immune system to
bacteria and other harmful elements, detrimental to wound healing and increase mortality.70
Obesity Higher incidence of infection, higher oxygen requirement, and poor nutrition lead to long wound
healing time frame, impaired organ function in higher BMI pediatric patients, significantly
greater loss in bone mineral density, multiple organ failure, increased length of hospital stay,
and heightened requirement for exogenous insulin.71-73
Stress Psychological stress could be upregulated hormones, which reduces the levels of the pro-
inflammatory cytokines and influences immune cells. Restraint stress could further promote
wound hypoxia, causes a substantial delay in wound healing, and impairs wound healing.48,74-76

Abbreviations: TBSA, total body surface area; BMI, body mass index.

healing and nonhealing wounds. In healing wounds, FTIR
shows higher intensities at bands associated with collagen
and other proteins, while the nonhealing group shows
higher intensities at bands associated with red blood cells.6
In another study, Nogueira et al used FTIR for analyses of
the collagen fibers in the repair process of cutaneous
lesions.83 In another study, the structural characteristics of
collagen networks, such as the degree of fiber organization,
and the secondary structure of collagen (α-helices) were
obtained by FTIR and then used to monitor the collagen
10
deposition and differentiation of the collagen type in the
healing process along with histological analysis.84-86 Castro
et al used attenuated total reflection (ATR)-FTIR for bio-
chemical characterization of skin burn wound healing.
Spectral biomarkers of biological materials such as proteins
mid I and II bands, which related to conformational changes,
were used to monitor the protein’s activity in the switching
of wound healing process stages (proliferation to matura-
tion stage).87,88 In other studies, discrimination of healthy
and thermal injured tissues and burn injury classification
was performed by FTIR. More information in this regard
can be find elsewhere.89
Raman’s technique is another noninvasive technique that
has been extensively investigated for identifying degrees of
burn wounds. Rangaraju et al used optical coherent tomog-
raphy (OCT) and RS for distinguishing of superficial partial-
thickness, deep partial-thickness and full-thickness wounds.
OCT allows visualization of different skin layers, and polar-
ization-sensitive OCT (PS-OCT) can be used for the quanti-
tative determination of collagen with a decreased phase
retardation rate and correlated with burn depth.81,90 On the
other hand, the monitoring of biological molecules such as
nucleic acids, proteins, and lipids can be accomplished by
Raman spectral features of these molecules. In one study, RS
successfully applied to the evaluation of changes in the lipid
content of stratum corneum in human skin.33,91 This tech-
nique was also successfully used for the classification of
benign and malignant skin lesions with sensitivity between
95% to 99%.92 A previous study showed that RS has the
capability to extract hydration information from the skin,
which can be essential in burn wound assessment.93
Identification of burn-induced heterotopic ossification by
RS shows that RS has a potential modality in the assessment
of burn wound and burn degree categorization.94 Therefore,
integration of RS with other analytical methods, such as
FTIR, near-infrared spectroscopy (NIR), OCT, LDI, imag-
ing techniques, and other conventional methods can be very
useful in assessment and classification of the burn wound
and other skin lesions.
Discussion
Proper diagnosis of the wounds is the first and one of the
most important factors in the choosing of correct treatment,
which can effectively lead to perfect wound healing without
any complication. From this point, the classification of
wounds can lead to a proper diagnosis of the wounds.
However, there is no comprehensive classification for all
types of wounds, and sporadic classifications that are used
in the clinical practice are often incomplete and, in many
cases, do not take effective and key parameters. For exam-
ple, in the classification of burn wounds, the origin and
wound cause and effect of the wound bed moisture are not
included in the classifications, and mostly, the intensity,
The International Journal of Lower Extremity Wounds 00(0)
depth, and the old system’s classification are the basis of
clinical decision. Also, the conditions of the wound, includ-
ing the risk of infection and the type of infection, the wound
stage, and thus the type of proposed treatment protocol is
not very obvious. On the other hand, in the research works,
the wound classification is very superficial, typical, and
often these studies take place regardless of the parameters
involved in improving of these wounds, and only accounts
a number of routine and old accepted conditions. Therefore,
a comprehensive classification for all types of wounds is
necessary based on the factors and conditions of the wounds.
As a result, the available old and traditional classifications
can be collected and integrated into a comprehensive clas-
sification system and used as a standard protocol in the
clinical practices and research works.
One of the most important factors that affect the clas-
sification of the wounds is the special stage of wound
healing process, that is, which wound is present. Therefore,
it is crucial to understand the healing process of various
types of wounds from the biological and physiological
points. According to the differences of burn wounds with
other wounds, which was mentioned in the previous sec-
tion, the most important healing phase in these wounds is
the inflammation stage, which is the major part of the
wound healing process, and diverse mediators are involved
in this stage. Therefore, medical interventions are very
important at this stage, and any delay in the treatment at
this stage may lead to an incomplete wound healing or
scar and scab formation.
Using nondestructive, accurate, simple, and cost-effec-
tive techniques can reduce the duration of treatment and
lead to complete wound healing without any clinical com-
plications. However, the capability of each technique in
obtaining the special information for each case, the possi-
bility of using these techniques in the clinic and emergency
cases with appropriate accuracy and speed, and finally
appropriate sampling method for each technique should be
specified.
Conclusion and Future Prospect
In this review, the wound classification was evaluated based
on different parameters and its importance has been high-
lighted. Then, a number of systems used to evaluate burn
wounds and their principles and methods were described.
Despite the existence of a series of classification systems
for classifying these types of wounds, there is a vital need
for a comprehensive classification system in this area based
on different and effective factors. Next, the healing steps of
these wounds and medical interventions in different time-
lines should be specified for each class according to the
wound healing process and the involved factors. Finally,
these classifications should be applied in all medical centers
and clinics, as well as research centers. In the next section,
Abazari et al
a general insight on the wound healing process was dis-
cussed and the differences in burn wound healing with other
types of wounds were featured. Despite the proposed over-
all process for wound healing, different wounds have differ-
ent biological and physiological features, so further studies
are needed in this regard. Emerging new techniques in the
evaluation and classification of wounds provides a good
opportunity for the identification and treatment of wounds
more accurately. But the effectiveness of these techniques
in the clinic needs further studies in terms of application,
ease of use, and sampling methods.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
article.
Funding
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
ORCID iD
Morteza Abazari https://orcid.org/0000-0002-6425-0776
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