Standing Height

Published on April 2017 | Categories: Documents | Downloads: 33 | Comments: 0 | Views: 332
of 26
Download PDF   Embed   Report

Comments

Content

Standing Height


description / procedure: measurement the maximum
distance from the floor to the highest point on the
head, when the subject is facing directly ahead. Shoes
should be off, feet together, and arms by the sides.
Heels, buttocks and upper back should also be in contact with the
wall.


equipment required: stadiometer or steel ruler placed against a
wall



reliability: Height measurement can vary throughout the day, being
higher in the morning, so it should be measured at the same time of
day each time.



advantages: low costs, quick test


other comments: height or lack of height is an important attribute
for many sports.
Related Pages


see similar test: sitting height



other Anthropometric Tests



about body size testing

Body Mass / Weight


purpose: measuring body mass can be valuable for
monitoring body fat or muscle mass changes, or for
monitoring hydration level.


equipment required: Scales, which should be calibrated for
accuracy using weights authenticated by a government department
of weights and measures.



description / procedure: the person stands with minimal movement
with hands by their side. Shoes and excess clothing should be
removed.



reliability: To improve reliability, weigh routinely in the morning (12
hours since eating). Body weight can be affected by fluid in the
bladder (weigh after voiding the bladder). Other factors to consider
are the amount of food recently eaten, hydration level, the amount of
waste recently expelled from the body, recent exercise and clothing.
If you are monitoring changes in body mass, try and weigh at the
same time of day, under the same conditions, and preferably with no
clothes on. Always compare using the same set of scales.


advantages: quick and easy measurement when testing large
groups, with minimal costs.



other comments: measuring weight can be used as a measure of
changes in body fat, but as it does not take into account changes in

lean body mass it is better to use other methods of body
composition measurement.
Related Pages


other Anthropometric Tests



about body size testing

Wound Care Introduction
A wound is a break in the skin (the outer layer of skin is called the epidermis).
Wounds are usually caused by cuts or scrapes. Different kinds of wounds may be
treated differently from one another, depending upon how they happened and
how serious they are.
Healing is a response to the injury that sets into motion a sequence of events.
With the exception of bone, all tissues heal with some scarring. The object of
proper care is to minimize the possibility of infection and scarring.
There are basically 4 phases to the healing process:


Inflammatory phase: The inflammatory phase begins with the injury itself.
Here you have bleeding, immediate narrowing of the blood vessels, clot
formation, and release of various chemical substances into the wound that
will begin the healing process. Specialized cells clear the wound of debris
over the course of several days.



Proliferative phase: Next is the proliferative phase in which a matrix or
latticework of cells forms. On this matrix, new skin cells and blood vessels
will form. It is the new small blood vessels (known as capillaries) that give
a healing wound its pink or purple-red appearance. These new blood
vessels will supply the rebuilding cells with oxygen and nutrients to sustain
the growth of the new cells and support the production of proteins
(primarily collagen). The collagen acts as the framework upon which the
new tissues build. Collagen is the dominant substance in the final scar.
Remodeling phase: This begins after 2-3 weeks. The framework (collagen)
becomes more organized making the tissue stronger. The blood vessel
density becomes less, and the wound begins to lose its pinkish color. Over
the course of 6 months, the area increases in strength, eventually
reaching 70% of the strength of uninjured skin.





Epithelialization: This is the process of laying down new skin, or epithelial,
cells. The skin forms a protective barrier between the outer environment
and the body. Its primary purpose is to protect against excessive water
loss and bacteria. Reconstruction of this layer begins within a few hours of
the injury and is complete within 24-48 hours in a clean, sutured (stitched)
wound. Open wounds may take 7-10 days because the inflammatory
process is prolonged, which contributes to scarring. Scarring occurs when
the injury extends beyond the deep layer of the skin (into the dermis).

Synthetic wound dressings
Synthetic wound dressings originally consisted of two types; gauze-based dressings and paste
bandages such as zinc paste bandages. In the mid-1980s the first modern wound dressings
were introduced which delivered important characteristics of an ideal wound dressing:
moisture keeping and absorbing (e.g. polyurethane foams, hydrocolloids) and moisture
keeping and antibacterial (e.g. iodine-containing gels).
During the mid 1990s, synthetic wound dressings expanded into the following groups of
products:



vapour-permeable adhesive films










hydrogels
hydrocolloids
alginates
synthetic foam dressings
silicone meshes
tissue adhesives
barrier films
silver- or collagen-containing dressings

Silver containing dressings

Ideal wound dressing

No single dressing is suitable for all types of wounds. Often a number of different types of
dressings will be used during the healing process of a single wound. Dressings should perform
one or more of the following functions:



Maintain a moist environment at the wound/dressing interface











Absorb excess exudate without leakage to the surface of the dressing
Provide thermal insulation and mechanical protection
Provide bacterial protection
Allow gaseous and fluid exchange
Absorb wound odour
Be non-adherent to the wound and easily removed without trauma
Provide some debridement action (remove dead tissue and/or foreign particles)
Be non-toxic, non-allergenic and non-sensitising (to both patient and medical staff)
Sterile

Classification of wound dressings
Synthetic wound dressings can be broadly categorized into the following types.

Type

Properties

Passive
products

Traditional dressings that provide cover over the wound, e.g. gauze and
tulle dressings

Interactive
products

Polymeric films and forms which are mostly transparent, permeable to
water vapour and oxygen, non-permeable to bacteria, e.g. hyaluronic acid,
hydrogels, foam dressings

Bioactive
products

Dressings which deliver substances active in wound healing, e.g.
hydrocolloids, alginates, collagens, chitosan

Wound types and dressings

The following table describes some of the many different types of wound dressings and their
main properties.

Dressing type

Properties


Dressings can stick to the wound surface
and disrupt the wound bed when
removed



Only use on minor wounds or as
secondary dressings





Dressing does not stick to wound surface
Suitable for flat, shallow wound
Useful in patient with sensitive skin



E.g. Jelonet®, Paranet®



Sterile sheet of polyurethane coated with
acrylic adhesive
Transparent allowing wound checks
Suitable for shallow wound with low
exudate

Gauze

Tulle

Semipermeable
film




Hydrocolloids



E.g. OpSite®, Tegaderm®



Composed of carboxymethylcellulose,
gelatin, pectin, elastomers and adhesives
that turn into a gel when exudate is
absorbed. This creates a warm, moist
environment that promotes debridement
and healing
Depending on the hydrocolloid dressing
chosen can be used in wounds with light
to heavy exudate, sloughing or
granulating wounds
Available in many forms (adhesive or
non-adhesive pad, paste, powder) but
most commonly as self-adhesive pads







E.g. DuoDERM®, Tegasorb®

Hydrogels





Alginates



E.g. Tegagel®, Intrasite®





Composed of calcium alginate (a
seaweed component). When in contact
with wound, calcium in the dressing is
exchanged with sodium from wound
fluid and this turns dressing into a gel
that maintains a moist wound
environment
Good for exudating wounds and helps in
debridement of sloughing wounds
Do not use on low exudating wounds as
this will cause dryness and scabbing
Dressing should be changed daily



E.g. Kaltostat®, Sorbsan®



Designed to absorb large amounts of
exudates
Maintain a moist wound environment but
are not as useful as alginates or
hydrocolloids for debridement
Do not use on low exudating wounds as
this will cause dryness and scabbing




Polyurethane or
silicone foams





Hydrofibre

Composed mainly of water in a complex
network or fibres that keep the polymer
gel intact. Water is released to keep the
wound moist
Used for necrotic or sloughy wound beds
to rehydrate and remove dead tissue. Do
not use for moderate to heavily exudating
wounds



E.g. Allevyn®, Lyofoam®



Soft non-woven pad or ribbon dressing
made from sodium
carboxymethylcellulose fibres
Interact with wound drainage to form a
soft gel





Absorb exudate and provide a moist
environment in a deep wound that needs
packing

Collagens




Dressings come in pads, gels or particles
Promote the deposit of newly formed
collagen in the wound bed



Absorb exudate and provide a moist
environment

Different types of wounds and the different stages of a healing wound require different
dressings or combinations of dressings. The following table shows suitable dressings for
particular wound types.

Wound type

Dressing type


Paraffin gauze

Clean, medium-to-high
exudate (epithelialising)



Knitted viscose primary
dressing

Clean, dry, low exudate
(epithelialising)



Absorbent perforated plastic
film-faced dressing



Vapour-permeable adhesive
film dressing




Hydrocolloids
Foams



Alginates



Hydrocolloids



Hydrogels

Clean, exudating
(granulating)

Slough-covered

Dry, necrotic



Hydrocolloids



Hydrogels

The dressings may require secondary dressings such as absorbent pad and bandages.

Adverse effects of dressings
Wound dressings can cause problems, including:



Maceration (sogginess) of surrounding skin (change dressing frequently and use a
more absorbent dressing)




Irritant contact dermatitis (protect skin with emollient or barrier film)
Allergic contact dermatitis (uncommon: change dressing type, apply topical steroids)

Wound repair
Wound repair involves the timed and balanced activity of inflammatory,
vascular, connective tissue, and epithelial cells. All of these components
need an extracellular matrix to balance the healing process. Skin wounds
heal by the formation of epithelialized scars of different contraction ability
rather than by the regeneration of a true full-thickness tissue. To minimize
scar formation and to accelerate healing time, different wound dressings
and different techniques of skin substitution have been introduced in the
last decades.
Autologous skin grafting in the form of split- or full-thickness skin is still a
criterion standard. However, in many patients, this technique may not be
practicable for a variety of reasons, and the wound must be allowed to heal
by second intention. Moreover, in cases in which skin grafts are used, a
new wound is created on the donor side. Thus, eliminating a new wound to
close the old one and to close as many tissue defects as possible without
the risk of large area infection, necrosis, tissue hypertrophy, and
contraction, as well as deformation of wound borders, is a necessity. The

next important problem is to reduce or eliminate scar formation, particularly
in the field of large-surface wounds.
Traditional management of large-surface or deep wounds involves open
and closed methods. In the open method, the wounds are left in a warm,
dry environment to crust over, whereas, in the closed method, wounds are
covered with different kinds of temporary dressings and topical treatment,
including antibiotics, until healing by secondary intention. The early
removal of the dead tissue (eg, in burns) reduced pain, the number of
surgical procedures, and the length of the hospital stay.
The surgical intervention (ie, tangential excision of partial- or full-thickness
wound) followed by wound closure with autografts or temporary dressings
is one of the currently used methods. In large-surface, full-thickness
wounds, the wound can be excised down to the fat or the fascia,
particularly if infection is present. Excision to the fat induces the removal of
the subdermal plexus of blood vessels and decreases the take of
autografts because this tissue is less vascularized. Excision down to the
fascia induces better take of the autografts but has aesthetic
disadvantages.
Wound debridement can also be achieved by enzyme digestion of the
dead tissues. Proteolytic enzymes (eg, collagenases used topically) allow
a more specific destruction of necrotic tissues, while preserving viable
dermis and avoiding blood loss, but the treatment can be painful and can
increase the risk of local infection. In addition, it takes a long time to
achieve a clean wound bed.
Wound coverings
Currently available wound coverings can be divided into 2 categories: (1)
permanent coverings, such as autografts, and (2) temporary coverings,

such as allografts (including de-epidermized cadaver skin and in vitro
reconstructed epidermal sheets), xenografts (ie, conserved pig skin), and
synthetic dressings.
Conventional autograft (epidermis and a significant amount of dermis)
obtained from healthy skin areas is considered the optimum wound cover
in that its viability yields immediate take (incorporation into the wound bed)
and resistance to wound infection. However, harvesting of autograft
creates a second wound in the healthy tissue, a donor wound. This open
wound increases the risk of infection and fluid/electrolyte imbalance.
Repeated conventional harvests of autograft from a donor wound site can
result in contour defects or scarring. Optimizing the healing of both main
wounds and donor wounds becomes a later goal of patient management
and the development of different surgical dressings, which can be used
based on the principle of phase-adapted wound healing.
Most recently, developed wound dressings are in use only as temporary
dressings because of their synthetic or chemical components, limited
persistence on the wound surface, and foreign body character.
Primary closure versus second-intention treatment of skin punch biopsy
sites was evaluated in a randomized trial.1 Punch biopsy sites healed by
second intention appear at least as good as biopsy sites closed primarily
with sutures. Volunteers preferred suturing for 8-mm biopsy sites and had
no preference for 4-mm sites. Elimination of suturing of punch biopsy
wounds results in personnel efficiency and economic savings for both
patients and medical institutions.
The wounds had been dressed with petroleum jelly under an occlusive
dressing that consisted of gauze covered by a transparent dressing
(Tegaderm; 3M, St Paul, Minn) and were left in place for 3 days. After that
time, the gel foam was removed from the second-intention site and both

biopsy sites were cleansed with water to remove any exudate. Then, an
occlusive transparent dressing was reapplied to both sites. After this initial
dressing change, dressings were changed weekly or more often at the
volunteers' discretion until the biopsy sites were completely healed or
reepithelialized. Efficient wound dressings can be important for both small
and large wounds.
Some of the currently available surgical dressings used in dermatologic
and dermatosurgical practice are discussed.

CLASSIFICATION OF WOUNDS
Section 3 of 10
 Authors and Editors
 Introduction
 Classification of Wounds
 Wound Bed Preparation
 Autologous and Allogenic Skin Replacement
 Types of Dressings
 Acellular Dressings and Skin Substitutes
 Engineered Skin Dressings and Substitutes
 Perspectives
 References

Wounds encountered in surgical and dermatosurgical practice can be
classified according to their thickness, the involvement of skin or other
structures, the time elapsing from the trauma (breaking of skin continuity),
and their morphology. Additional classifications include factors that
determine how to close the wound, classification of how the wound heals,
and classification of the wound by bacterial contamination.
Thickness of the wound










Superficial wounds, involving only the epidermis and the dermis up to the
dermal papillae
Partial-thickness wounds, involving skin loss up to the lower dermis (Part
of the skin remains, and shafts of hair follicles and sweat glands are
leftover.)
Full-thickness wounds, involving the skin and the subcutaneous tissue
(Tissue loss occurs, and the skin edges are spaced out.)
Deep wounds, including complicated wounds (eg, with laceration of blood
vessels and nerves), wounds penetrating into natural cavities, and wounds
penetrating into an organ or tissue

Involvement of other structures




Simple wounds, comprising only 1 organ or tissue
Combined wounds (eg, in mixed tissue trauma)

Time elapsing from the trauma




Fresh wounds, up to 8 hours from the trauma
Old wounds, after 8 hours from trauma or skin discontinuity

Morphology














Excoriation or scarification, the most superficial type
Incised wound, mainly as a result of surgical intervention
Crush wound, made with a heavy blow of a cutting tool (eg, hatchet,
sword, sable)
Contused wound, the most common type of wound encountered in traffic
accidents
Lacerated wound, when fragments of tissue are torn away with a sharpedged object
Slicing wound (A classic example is detachment of epicranial epineurosis.)
Stab wound, made with a pointed tool or a weapon








Bullet wound
Bite wound
Poisoned wound

Factors that determine how to close the wound
















Type of wound
Size of wound
Location of wound (Poor vascular areas or areas under tension heal
slower than areas that are highly vascular.)
Age of wound (fresh surgical wounds vs chronic wounds)
Presence of wound contamination or infection (Bacterial contamination
slows down the healing process.)
Age of the patient (The older the patient, the slower the wound heals.)
General condition of the patient (Malnutrition slows down the healing
process.)
Medication (Anti-inflammatory drugs may slow down the healing process if
they are taken after the first several days of healing. After this period, antiinflammatory drugs should not have an effect on the healing process.)

Classification of how the wound heals





Healing by first (primary) intention (primary healing): The wound is
surgically closed by reconstruction of the skin continuity by simple
suturing, by movement (relocation) of skin fragments from the surrounding
area (flaps), or by transplantation of free skin elements (grafts) of different
thickness (eg, split- or full-thickness grafts). Primary healing is usually the
case in all wounds in which the anatomical location and the size allow the
skin continuity to be restored.
Healing by second intention (secondary wound healing): After wound
debridement and preparation, the wound is left open to achieve sufficient
granulation for spontaneous closure (reepithelialization from remaining
dermal elements [eg, hair follicle] or from wound borders). Secondary
healing is how abrasions or split-thickness graft donor sites heal.




Healing by third intention (tertiary wound healing [delayed primary
closure]): After wound debridement and preparation (ie, treatment of local
infection), the wound is left open and then closed by primary intention or
finally by surgical means of skin grafting. Tertiary healing is how primary
contaminated wounds or mixed tissue trauma wounds (eg, after
reconstruction of hard tissue) heal.

Classification of wound by bacterial contamination
The 4 types of surgical wounds are as follows: clean, clean contaminated,
contaminated, and dirty.










Clean wounds are usually wounds made by the doctor during an operation
or under sterile conditions. Only normally present skin bacteria are
detectable.
In clean-contaminated wounds, the contamination of clean wounds is
endogenous and comes from the environment, the surgical team, or the
patient's skin surrounding the wound.
In contaminated wounds, large contaminates infect the wound.
In dirty wounds, the contamination comes from the established infection.

In the daily praxis, the main objective for dermatologists,
dermatosurgeons, and surgeons is to transfer the wound from a
spontaneous stage to a surgical stage and to heal the wound by primary
intention. However, this is not always possible or practicable. In such
cases, wounds heal mostly by secondary intention, and the injured tissue
becomes healthy again; appropriate wound dressings are necessary to
give the wound an optimal environment to heal.

WOUND BED PREPARATION
Section 4 of 10
 Authors and Editors
 Introduction










Classification of Wounds
Wound Bed Preparation
Autologous and Allogenic Skin Replacement
Types of Dressings
Acellular Dressings and Skin Substitutes
Engineered Skin Dressings and Substitutes
Perspectives
References

Before any kind of wound dressing is applied, the wound should be
appropriately prepared to enhance both the effectiveness of the dressing
and the self-healing ability of the wound. To achieve optimal healing,
wounds must not be infected, they should contain as much vascularized
wound bed as possible, and they should be free of exudate.
Wound bed preparation in both acute wounds and chronic wounds is
currently a part of the overall wound healing cascade, including (1) local
blood coagulation, (2) vascular supply, (3) inflammation, (4) granulation
tissue formation and revascularization, (5) epithelialization, (6) wound
contraction, and (7) scar formation. However, the way of wound bed
preparation in acute wounds differs from that of chronic wounds. For
example, in acute wounds, debridement is an effective way to remove both
damaged tissue and potential bacteria. Once performed, the acute wound
should be clean and prepared to heal easily by primary intention. However,
in the case of chronic wounds, debridement is usually an ongoing process.
Unlike acute wounds, chronic wounds have what is termed necrotic burden
consisting of nonviable tissue and exudate. This is usually a result of many,
mostly long-standing local or systemic abnormalities, such as diabetes,
arterial or venous insufficiency, and local tissue compression, leading
pathogenetically to chronic wounds.

Drs Falanga2, Sibbald, and Harding introduced the concept of wound bed
preparation in the late 1990s. Wound bed preparation is defined as the
global management of the wound to accelerate endogenous healing or to
facilitate the effectiveness of other therapeutic measures, including wound
debridement, bacterial balance, and moisture balance. This concept leads
to more effective strategies to address the reasons why chronic wounds
fail to heal. Wound bed preparation as a strategy allows physicians to
break into individual components in various aspects of wound care, while
maintaining a global view of what they wish to achieve.
Chronic wounds have always been overshadowed by acute wounds.
Scientific breakthroughs and therapeutic measures would generally be
developed or envisioned first for wounds caused by trauma, scalpel, or
other types of acute injury. For instance, stimulation of reepithelialization by
dressings providing moist conditions was first observed experimentally in
acute wounds. The acceleration of healing by peptide growth factors was
first formally demonstrated in experimental acute wounds in animals.
These observations provided proof of principle for the effectiveness of
topically applied growth factors, and they led to testing and
commercialization of these agents in chronic wounds. Many other
examples exist, but the point is that knowledge accumulated about acute
injury has been the anchor on which one has relied for developing a
therapeutic strategy for chronic wounds.
The common error is to view wound bed preparation as the same as
wound debridement. In acute wounds, wound debridement is a good way
to remove necrotic tissue and bacteria. This is not the case for chronic
wounds, where much more than debridement needs to be addressed for
optimal results. Chronic wounds can be intensely inflammatory (eg, venous
ulcers) and, thus, produce substantial amounts of exudate that interfere
with healing or with the effectiveness of therapeutic products, such as

dressings, growth factors, and bioengineered skin substitutes. Therefore,
in the context of wound bed preparation, the concerns are not only the
removal of actual eschars and frankly nonviable tissue but also the
removal of the exudative component.
Another important aspect of chronic wounds, which make them different
from acute wounds in the context of wound bed preparation, is the possible
need for a maintenance debridement phase. Debridement, whether it is
performed by surgical, enzymatic, or autolytic means, is usually considered
a procedure or a therapeutic step with defined time frames. This may be
true of acute wounds that have become colonized and necrotic and, thus,
need to be revitalized. However, with chronic wounds, debridement is
generally unable to fully remove the underlying pathogenic abnormalities;
necrotic material, nonviable tissue, and exudate (ie, necrotic burden)
continue to accumulate.
Within the context of wound bed preparation, the notion of an initial
debridement phase followed by a maintenance debridement phase may be
adopted. For example, after the initial debridement of chronic wounds, a
temporary positive outcome on wound closure may be observed. However,
often, a healing arrest occurs, with a return to a poor wound bed. One
explanation may be that, because of the underlying and uncorrected
pathogenic abnormalities, necrotic tissue and exudate, which now cause
the healing arrest, continue to accumulate. Rather than always starting
from the beginning, with periodic debridement and exudate control, one
might consider a steady state removal of the necrotic burden that should
continue throughout the life of the wound.
In the concept of wound bed preparation, the biologic microenvironment of
chronic wounds has to be clearly understood. For example, after an
appropriate dressing is used, optimal compression therapy for edema
control in venous ulcers decreases the amount of exudate and, thus,

clears the macromolecules that may be trapping growth factors. Similarly,
correction of the bacterial burden decreases the possibility of infection, but
it also diminishes the ongoing inflammation that often characterizes many
chronic wounds. Some chronic wounds may be "stuck" in one of the
phases of the normal healing process, such as the inflammatory or
proliferative phase. Eliminating the bacterial burden by the use of
debridement, some antibacterial products, or adequate dressings can help
this situation.
As another example, appropriate debridement removes tissue and,
therefore, cells that have accumulated and are no longer responsive to
signals required for optimal wound healing. In this respect, fibroblasts from
chronic wounds, including venous and diabetic ulcers, have been shown to
become senescent and are unresponsive to certain growth factors. The
term cellular burden has been created to describe this phenomenon. When
a wound is debrided, this cellular burden is removed and wound
responsiveness is restored. In the future, some specially developed
chemical or biologic agents will probably help for normalizing such cells
rather than removing them.
In aiming at a well-vascularized wound bed, much can be achieved by
removing necrotic or fibrinous tissue, by controlling edema, by decreasing
bacterial burden, by performing compression therapy (especially for
venous ulcers), and by off-loading (in the setting of pressure-induced
ulcers). Further improvements in the vascularization of the wound bed can
also be achieved by applying growth factors (eg, platelet-derived growth
factor [PDGF]), by applying bioengineered skin, or even by using occlusive
dressings. Indeed, one of the most important effects of occlusive dressings
in chronic wounds, in addition to pain relief and absorption of exudate, may
be stimulation of granulation tissue formation. Some growth factors, not yet
available commercially, have the potential to greatly stimulate

angiogenesis. These agents include fibroblast growth factors (FGFs) and
vascular endothelial growth factor (VEGF).
Bioengineered skin and autologous or allogeneic skin can stimulate the
formation of granulation tissue and, perhaps indirectly, the process of
reepithelialization. Particularly noteworthy is the so-called edge effect
(migration of the wound's edge toward the wound's center) after the
application of bioengineered skin to previously unresponsive chronic
wounds. These clinical effects have been observed with bioengineered
skin and with simple keratinocyte sheets. It has been hypothesized that
these stimulatory effects are due to the synthesis and the release of certain
cytokines by the donor cells. However, the situation is probably highly
complex, with cross-talk developing between the donor cells and the
recipient resident wound cells. This cross-talk leads not only to the release
of cytokines but also to the recruitment of other cell types from surrounding
tissue and the circulation, to the formation of new blood vessels, and to the
laying down of a more ideal extracellular matrix.
The concept of wound bed preparation can help to recognize that chronic
wounds have a complex life of their own and that they are not simply an
aberration of the normal healing process. This concept allows examination
of the different components that need to be addressed in chronic wounds
and development of long-term strategies for the more complex issues that
lead to failure to heal.
The authors recommend the daily use of the concept of wound bed
preparation, which, together with an appropriately chosen wound dressing
or tissue substitute, will lead to more effective treatment of acute and
chronic difficult-to-treat wounds. Moreover, this area of wound care is also
critical to the assessment and evaluation of any new advanced wound
healing technologies.

AUTOLOGOUS AND ALLOGENIC SKIN
REPLACEMENT
Section 5 of 10
 Authors and Editors
 Introduction
 Classification of Wounds
 Wound Bed Preparation
 Autologous and Allogenic Skin Replacement
 Types of Dressings
 Acellular Dressings and Skin Substitutes
 Engineered Skin Dressings and Substitutes
 Perspectives
 References

Skin replacement using autologous grafts
The best way to cover large surface wounds is the transplantation of the
patient's own skin (ie, split-thickness skin grafts) from an adjacent
undamaged area that matches closely in terms of texture, color, and
thickness. This surgical procedure inflicts an injury on the donor site
analogous to a superficial second-degree burn, allowing spontaneous
healing in 2-3 weeks, usually without scarring.
Autograft is the method of choice to achieve definitive coverage of burned
skin with good quality of healed skin. This technique has been improved by
expanding the surface of the skin graft with a mesh apparatus, depending
on the needs of the patient. Recently, as much as 25-30 times expansion
has been described. However, excessive meshing usually results in healed
skin that is more susceptible to infections and has a basketlike pattern, a
major drawback for aesthetic appearance. An alternative is the Meek
island graft or sandwich graft. This method allows easier handling of widely

expanded autografts than meshed skin. In addition, because the autograft
islands are not mutually connected, failure of a few of them does not affect
the overall graft take. The Meek technique has been reported to be
superior to the mesh procedure for expansion ratios of more than 1:6.
In large surface burns, early closure of burn wounds with autologous skin
grafts is limited by the lack of adequate donor sites. A delay of 2-3 weeks is
necessary to wait for healing of donor sites before harvesting them again.
The split-skin graft from the initial donor site can usually be reharvested 23 times and healed autografted wounds. This coverage process is time
consuming and, thus, induces high risks of morbidity and mortality, mainly
due to bacterial invasion.
Cuono and coworkers3 proposed a 2-step procedure using composite
autologous-allogenic skin replacement (de-epidermized skin allografts for
dermis substitution and autologous, in vitro–reconstructed epidermis for
surface covering) in burns. Compton et al4, as well as Hefton and
coworkers5, preferred the use of both autologous, in vitro–reconstructed
and allogenic, in vitro–reconstructed epidermal grafts for large-surface
wounds.
Although the use of epidermal autografts has markedly advanced the
management of extensive burns and saved lives, this technique has major
limitations, as follows: (1) at least 3 weeks is needed for growth of cultured
epidermal sheets in the laboratory, thus delaying the coverage of wounds;
(2) epidermal sheets need to be grafted on a clean wound bed because
they are highly sensible to bacterial infection and toxicity of residual
antiseptics; (3) the success of the treatment strongly depends on the
dexterity of the laboratory and surgical teams, from the production of the
sheets to their graft and care after grafting because this material is very
fragile; (4) the regeneration of the dermal compartment underneath the
epidermis is a lengthy process, and skin remains fragile for at least 3 years

and usually blisters; and (5) the aesthetic aspect of the healed skin is less
acceptable than the one obtained with a split-thickness graft.
It was recognized early that any successful artificial skin or skinlike
material must replace all of the functions of skin and, therefore, consist of a
dermal portion and an epidermal portion. It was clinically apparent that a
deep burn or other deep and/or large-surface wounds could not be
completely closed promptly after injury by using the patient's available
autograft donor sites. Moreover, in certain clinical situations (eg, elderly
and young individuals), the donor sites themselves (if taken at standard
thickness) create new wounds that often take a long time to heal and
create additional metabolic stress, infection risk, and scarring.
Wound coverage with allogenic skin
One of the main differences between the cultured epidermal sheet and a
split-thickness autograft is the lack of the dermal structure from the
cultured autograftable sheets. The absence of dermis is perceived as the
major cause for a lower percentage of graft takes and higher fragility and
blistering after epidermal sheet transplantation compared to split-thickness
autograft. A dermal component protects the basal layer of the epidermis
and has a significant impact on the postgrafting biologic responses of the
epithelial cells to the differentiation and wound-healing processes.
After early debridement of deep and extensive burns, temporary closure of
the wound is usually achieved with cadaver allograft before autografting
with cultured epidermal sheets. Instead of completely removing cadaver
skin before sheet transplantation, an excision of allogeneic epidermis can
be performed with a dermatome to only maintain the allogeneic dermis on
the wound. Because nonliving dermis alone may not be rejected,
autologous cultured epidermal sheets can be grafted onto it, thus greatly
enhancing healing. Indeed, cultured epidermal sheets grafted onto

homograft dermis display early rete ridge development and anchoring fibril
regeneration, in addition to a graft take of 95%.
Knowing that devitalization of allografts reduces their antigenicity, the use
of allogeneic cadaver skin as a biologic dressing is now widely accepted
and is usually preferred to synthetic dressings. The preservation of
allografts can be performed by different techniques, such as freeze-drying,
glutaraldehyde fixation, or glycerolization.
Cryopreservation of homografts with glycerol is the most popular method
of cadaver skin processing because freeze-drying is too expensive and
glutaraldehyde fixation has proven less efficient. Moreover, skin
preservation can reduce the risk of virus transmission from skin grafting,
providing time to rid the donor skin of pathogens. Indeed, incubation of
cadaver skin for several hours at 37°C in glycerol displays a significant
virucidal and bactericidal effect. To provide sufficient cadaver skin instantly
accessible for the patient with a burn, skin banks, such as the Euro Skin
Bank in Beverwijk, The Netherlands, have been well developed through
the years. However, allogenic skin banking has a significantly higher cost
compared with xenogeneic skin banking and biologic dressings.

TYPES OF DRESSINGS
Section 6 of 10
 Authors and Editors
 Introduction
 Classification of Wounds
 Wound Bed Preparation
 Autologous and Allogenic Skin Replacement
 Types of Dressings
 Acellular Dressings and Skin Substitutes
 Engineered Skin Dressings and Substitutes
 Perspectives
 References

Until the early 1980s, only a few wound care products were available apart
from traditional dressings (eg, gauze-based products) and paste (eg, zinc
paste) bandages.
The first modern wound dressings introduced during the mid 1980s usually
combined 2 main characteristics: moisture keeping and absorbing (eg,
polyurethane foams, hydrocolloids) or moisture keeping and antibacterial
(eg, iod-containing gels).
During the mid 1990s, the group of surgical dressings expanded into the
well-recognized groups of products, such as vapor-permeable adhesive
films, hydrogels, hydrocolloids, alginates, and synthetic foam dressings.
Additionally, new groups of products, such as antiadhesive, mostly silicone
meshes; tissue adhesives; barrier films; and silver- or collagen-containing
dressings, were introduced. Finally, in the second half of the 1990s,
combination products and engineered skin substitutes were developed.
Until the end of 2002, many different dressings had been marketed (see
the Table below). Currently, the global tendency demonstrates decreasing
numbers of product categories approved both in Europe and in the United
States, making the wound dressing market more transparent.
The ideal wound dressing should have the following characteristics:










Provide mechanical and bacterial protection
Maintain a moist environment at the wound/dressing interface
Allow gaseous and fluid exchange
Remain nonadherent to the wound
Safe in use - Nontoxic, nonsensitizing, and nonallergic (both to the patient
and the medical personnel)


















Well acceptable to the patient (eg, providing pain relief and not influencing
movement)
Highly absorbable (for exuding wounds)
Absorb wound odor
Sterile
Easy to use (can be applied by medical personnel or the patient)
Require infrequent changing (if necessary)
Available in a suitable range of forms and sizes
Cost effective and covered by health insurance systems

Classic dressings (not all categories are discussed in this article) include
dry dressings and moisture-keeping dressings. Dry dressings include
gauze and bandages, nonadhesive meshes, membranes and foils, foams,
and tissue adhesives. Moisture-keeping dressings include pastes, creams
and ointments, nonpermeable or semipermeable membranes or foils,
hydrocolloids, hydrogels, and combination products.
Bioactive dressings include antimicrobial dressings, interactive dressings,
single-component biologic dressings, and combination products.
Skin substitutes include epidermal substitutes (autologous or allogenic),
acellular skin (dermis) substitutes (allogenic or xenogenic), autologous and
allogenic skin, and skin substitutes containing living cells.
Different types of wounds require different dressings or combinations of
dressings.

Sponsor Documents

Or use your account on DocShare.tips

Hide

Forgot your password?

Or register your new account on DocShare.tips

Hide

Lost your password? Please enter your email address. You will receive a link to create a new password.

Back to log-in

Close