Phẫu Thuật Tạo Hình (Tập 4): Chi Dưới, Thân Mình Và Bỏng – Neligan (2018)

464.e1
Reconstruction of specific areas
C
(C) Expander in forehead.
Fig. 20.24

465
Reconstruction of specific areas
cheek, which is critical to allow facial movements and expres-
sion. Full-thickness grafts exhibit less secondary contraction
and have an aesthetic result as compared to split skin grafts.
Also, they are better suited to areas where contracture would
result in distortion of the adjacent structures (e.g., lower
eyelids).
Tissue expansion
Tissue expansion has allowed reconstructive surgeons to
achieve functional and aesthetic goals that were previously
unobtainable. The expanded cervical, pectoral, and shoulder
skin has been used very effectively for burned cheek
resurfacing.
Flap cover
For small scars, ample local skin is available to be used as
flaps to replace the scar. For larger scars, the closest and best
available skin is that from the cervical region as it is very
similar to the residual cheek skin. For cheek resurfacing, neck
skin can be used in the form of cervicofacial flaps (medially,
laterally, or inferiorly based),138–140 cervicopectoral flaps,66,141
and angle rotation flaps.142 To improve the blood supply and
flap safety, a deep plane dissection below the superficial
muscular aponeurotic system (SMAS) and platysma has been
suggested.143
The other flaps which can be used for resurfacing the
cheeks are the pre-expanded supraclavicular artery flap,144
expanded lower trapezius flap,145 supraclavicular artery
island flap,146 supraclavicular prefabricated flap,147 the super-
ficial cervical artery flap,148 the deltopectoral flap, flaps from
chest wall, and the cervicothoracic prefabricated flap, which
may be pedicled or islanded and may be expanded.149,150
Rarely, in case of severe scarring in the neck and the chest,
one may have to opt for distant flaps or free flaps. Using
distant flaps/free flaps on the cheeks is the last choice as it
obliterates the contours of the face and hides the muscles of
facial animation. Radial artery forearm flap, thinned antero-
lateral thigh (ALT), scapular, and parascapular flaps have
been described for facial resurfacing.
Lips and perioral region
The lips are important for functional, aesthetic, emotional,
and sentimental reasons. The lip serves its many functions
and roles due to its unique anatomy, especially the perioral
sphincter muscle.151 The upper lip has an intricate anatomy
that includes the two lateral subunits, the philtral subunit,
and the vermillion with the Cupid’s bow. At the two junctions
of the upper and the lower lip is the modiolus, which is a
meeting ground of many facial muscles. Considering the
intricate anatomy of the upper lip, reconstruction of the lip to
its pre-burn appearance is exceedingly difficult.
One of the commonest reasons for microstomia is electrical
burns in children due to them biting on electrical wires.152 This
leads to microstomia due to commissure injury. Classifica-
tions have been described for these injuries that are aimed
towards describing the extent of the injury.153,154
Post-burn sequelae of the lips and perioral region include:
1. Minor hypertrophic scarring of the upper lip
2. Scarring with/without shortening of the upper lip
Surgical reconstruction of the deformed cheek remains a chal-
lenge because of deficiency of well-matched donor skin. This
problem becomes even graver when only one cheek is
deformed.
The cervical skin is most well matched, but it is limited in
mobility and size. Tissues transferred from the shoulder
region, chest wall, and areas distant from the face provide a
poor cosmetic match to the remaining facial skin.
Principally the following points should be kept in mind
while planning reconstruction of cheek defects:
1. Keep the aesthetic units in mind when planning
excision and resurfacing.
2. The skin used for replacing the cheek scar should be
thin, unscarred, and should reflect the facial expressions
when the patient animates.
3. When a third to half the cheek is to be reconstructed,
only the concerned area should be replaced. It can be
done by using cervicofacial flaps.
4. If more than half of the cheek needs reconstruction, one
should replace the entire esthetic unit of the cheek. This
can be successfully done by using expanded flaps from
the neck and the shoulder.
5. When grafts are used for resurfacing, the junctional
scars should be softened or erased at a later date by
W-plasty or dermabrasion.
6. The same holds true for the junction line between the
residual cheek and the cervical flaps.
7. Bulky flaps should be avoided as they bury the
expressions under them and the patient gets a mask-like
appearance.
8. If grafts are being used, the defect should be stretched
such that extra graft is inserted into the defect as later
there is sure to be graft contracture and reduction in size.
9. All possible ancillary measures should be used to
improve the scar as cheeks are our face to the world.
For resurfacing of cheek scars the following surgical strategies
are available:
Healing by secondary intention
This is the simplest method. It is useful for small (<1 cm),
superficial defects located in cosmetically inconspicuous areas
like below the sideburns, in patients with solar-damaged,
irregularly pigmented skin.
Primary closure and serial excision
This is the method of choice if excessive tension and distortion
of surrounding structures can be avoided. One should make
sure that scars are placed along minimal skin tension lines or
within natural skin contours such as the nasolabial or preau-
ricular folds.
Skin grafts
Skin grafts are an acceptable option in patients who have
significant comorbid conditions. Skin grafts can be used to
resurface less critical areas of the cheek (e.g., just below side-
burns) or the donor sites of flaps, which are used to resurface
more critical areas. The disadvantage is that skin grafts have
a patch-like appearance. Also, because of their innate contrac-
tion, grafts may limit the dynamism and suppleness of the

466
SECTION III
CHAPTER 20 • Management of the burned face
The addition of steroid injections or pulsed dye laser therapy
will frequently resolve these scars satisfactorily.2
Scarring with/without shortening of the upper lip
For small scars, excision and primary closure can be done or
local flaps can be done after excision of the hypertrophic
scars. In the main body of the lip, the scar should lie vertical,
whereas at the upper part (base of the nostril) the scar
should be horizontal. Any vertical scar or tight bands can be
released with Z-plasty. In major scarring where almost the
whole lip is scarred and short, the scar should be excised
and contracture released. The whole aesthetic subunit should
be excised. During excision and release, excessive overcor-
rection should not be attempted as it can lead to an elon-
gated, overhanging floppy upper lip. The bed that is created
to receive the graft should have the contours of
the philtral ridge as well as the dimple. This can be created
using the same scar tissue. Grishkevich describes leaving
behind a 4-mm ridge of scar tissue over the philtral ridges
and applying grafts on the philtral dimple and lateral
subunits to result in good contours of the upper lip.155
In females, resurfacing should be done with a full-thickness
graft from the postauricular region or supraclavicular region.
In males it would be better to bring in a hair-bearing
flap.156–160 Local flaps have also been described for upper lip
resurfacing like the nasolabial flap and facial artery muscu-
lomucosal flap.161,162
Lower lip ectropion with or without
mandible deformities
The deformity of the lower lip and chin complex (see Fig.
20.15
) is more often than not along with neck contractures
and is in the form of eversion of the lower lip, occasionally
with exposure of the teeth. It is very important to know
whether the ectropion is intrinsic or extrinsic. If intrinsic,
release of this lower lip contracture is by incising below the
lip in the labiomental groove with lateral darts. It is essential
to overcorrect as the lower lip ectropion tends to re-contract.
If the scar is very deep, one needs to be careful during the
deeper dissection to avoid making a buttonhole in the mucosa
from the anterior incision. When the scarring of the lower lip,
chin, and the neck is longstanding since childhood, the growth
of the mandible is affected. Because of the constant pull of the
scar, the symphyseal region grows inferiorly and the teeth
face downwards too. In such cases, the neck contracture and
the lower lip contracture should be released first. Once the
graft settles, the mandible and teeth deformities can be oper-
ated upon. One may have to consider resurfacing the chin
with a flap if mandible osteotomies are required and the scar
of skin graft is tight.
Microstomia
Post-burn microstomia may be intrinsic or extrinsic. Tight
bands running in the perioral region can restrict the mouth
opening. Release of these bands with Z-plasty will relieve the
microstomia. Scarring of the lips and the angle of the mouth
or the vermilion will lead to intrinsic microstomia. The angle
of the mouth moves medially and needs to be repositioned
laterally for function as well as aesthetics. The classic release
3. Lower lip ectropion without mandible deformities
4. Lower lip ectropion with mandible deformities
5. Microstomia
6. Macrostomia
7. Perioral scar bands
8. Pseudomicrogenia
9. Pigmentation issues.
Some salient principles that must be followed during post-
burn deformity correction of lips and perioral region are as
follows:
1. Recognize whether it is an intrinsic or extrinsic ectropion of
the lower lip: It is very important to know whether the
ectropion is intrinsic or extrinsic in nature. The lower lip
being a mobile structure with a free border, it is very
easily pulled by the surrounding tissues as they are
healing and may easily develop an ectropion or dental
show due to the tight scar below it. A neck contracture
going onto the chin can cause an extrinsic lip ectropion.
Releasing the neck contracture and excision of the
offending scar on the chin will reposition the lower lip.
2. Wait for scar maturity: If possible, in immature minor
scars and contractures of the lips, release should be
delayed until the scar matures. Aggressive scar massage
and lip exercises should be begun to help in scar
stretching. The addition of steroid injections or pulsed
dye laser therapy will frequently resolve these scars
satisfactorily.2
3. Full aesthetic subunit of the lip should be covered with a
graft. Total resurfacing of the upper lip should be
performed using a full-thickness skin graft.2
4. Always overcorrect a lower lip ectropion to avoid a
re-contracture.
5. Beware an elongated upper lip when releasing scars of the
upper lip.
6. In males the upper lip, chin and lower face should be
resurfaced with hair-bearing flaps.
7. Always reconstruct the philtral ridges and philtral dimple
while resurfacing the upper lip.
8. Pay attention to alignment of the vermilion as it is a key
element in an aesthetic lip.
9. Recreate the labiomental groove in lower lip and chin
scarring.
10. The oral commissure should be positioned at the mid-
pupillary line.
11. Restore function of the oral commissure by recreating an
adequate lip-seal and supple underlying musculature
for speech and mastication. Lip suspension procedures may
be required to avoid drooling after release of severe
contractures.
12. In the pediatric age group, a tight scar on the chin and lower
face should be excised and resurfaced even if it is not causing
a functional problem as growth of the mandible will be
hampered otherwise.
Minor hypertrophic scarring of the upper lip: When the patient
presents early with immature minor scars and contractures,
release should be delayed until the scar matures. Aggressive
scar massage and lip exercises should be begun to help in scar
stretching. Mouth opening exercises, blowing air forcefully
keeping lips closed, etc., goes a long way in stretching scars.

467
Reconstruction of specific areas
Perioral scar bands
These should be managed with Z-plasties, W-plasties, break-
ing the scar, and grafting or resurfacing with expanded skin.
Pseudomicrogenia
The contractile forces of the scar eliminate the normal concav-
ity between the junctions of lip and chin pad leading to chin
pad compression and “pseudomicrogenia”.23 This can be
taken care of by excising the whole scar on the chin. Resurfac-
ing can be with a full-thickness graft or expanded skin of
the neck.
Splints
Splints are an important part of management of lips and
perioral burns to avoid microstomia, and this may be occa-
sionally neglected as there are no ready-made solutions for
splints in this area. The therapist has to innovate to create
splints.170–173
Neck
Many classifications of neck contractures have been proposed,
aiming to describe the anatomy of the contracture, the func-
tion of the neck, and in planning the surgery.174–176 Airway
management is an important challenge for the anesthetist in
severe neck contractures. If available, fiberoptic intubation is
the safest method of intubation in these cases as it provides
direct visualization of the glottis.177 If not available, safe
techniques include releasing the neck contracture under
tumescent local anesthesia and intubating after release,178 or
one could also go ahead with the whole procedure under
tumescent anesthesia and give regional blocks in the thigh for
graft harvest.179,180
Airway problems
For linear contractures, release and resurfacing should be
by single, multiple, or double opposing Z-plasties, or an X
release. In very severe linear contractures the resultant flaps
of the incisions may not come together after achieving full
extension. These flaps should be sutured as far as they reach
on full extension, and the remaining raw areas should be
grafted. The advantage of this method of release is that the
grafts are interspersed with the Z flaps, and hence chances of
re-contracture are lower.
For bands, the release can be in the form of X release and
skin grafting or excision of the scar and advancement of the
lateral neck skin to cover the resultant raw area.
For broader contractures a full incisional or excisional
release should be done. The release may be by a single incision
with fishtailing of the incision or a bipedicle release can be
done with two horizontal incisions made parallel in the upper
and lower neck. Usually the resultant area is resurfaced with
a medium to thick split-thickness graft from the thigh or a
full-thickness graft. Postoperatively the neck needs to be
splinted for at least a year if a re-contracture is to be avoided.
It is for this reason that many surgeons advocate the use of
flaps as it obviates the need for splintage. Flaps that have been
used are neck advancement flaps, expanded neck flaps, supra-
clavicular flaps,181–183 and free flaps like thin ALT or scapular
and parascapular flaps.184–187
method as proposed by Converse in 1959 continues to be used
by most surgeons today. The external scar is released com-
pletely down to the buccal mucosa, saving the buccal mucosa.
Three flaps are created from the buccal mucosa and sutured
to the edge of the skin defect. The aim is to obtain full release
of the microstomia as well as displace the commissure later-
ally to its natural midpupillary line position.163 If the vermilion
is scarred and has a contracture, it can be released with
Z-plasty (Fig. 20.26). Different surgeons have suggested pro-
cedures like skin grafts, varieties of commissurotomies and
local flaps, nasolabial flaps, tongue flaps, and composite grafts
from the ear lobe.164–169
Macrostomia
This is a rare sequela of burn trauma. It can rarely occur if
there is tissue loss of the lips and angle of the mouth region
due to severe trauma like electrical burns. If the upper and
lower lips are both everted, the scar stretches both vermilions
and may rarely cause macrostomia if the angle region is not
scarred.
Fig. 20.26  (A) Microstomia due to accidentally drinking a chemical. (B) Full
mouth opening after microstomia release with Z-plasty.
A
B

467.e1
Reconstruction of specific areas
No description of neck contracture release can be considered
complete without adequate words being devoted to the
problem of anesthesia in cases of neck contractures. Airway
management in patients with neck burns is always a challenge
due to many factors like microstomia, limited neck extension,
reduced submandibular space, and tracheal deviation due to
scars in the neck. The procedure of giving anesthesia in a case
of neck contracture is as important as the procedure of release.
Prior to surgery it is a good idea to get an X-ray of the neck
done in the AP and lateral views. The AP view will inform us
about any deviation of the trachea due to a pull of the neck
scars, and the lateral view will give us information on any
kinking, narrowing, or pressure on the airway. An indirect
laryngoscopy during the preoperative evaluation by the
anesthetist will also help them plan in advance and be pre-
pared for difficulties during intubation. If available, fiberoptic
intubation is the safest method of intubation in these cases as
it provides direct visualization of the glottis.177 Prior to giving
any sedation or anesthetic agent the anesthetist should check
whether they can ventilate the patient with bag and mask.
Due to the scarring on the chin and neck, occasionally the
anesthetist does not get a hold on the mandible to be able to
stabilize it by the usual jaw thrust maneuver, and hence
ventilation may be ineffective in these cases. It would be more
prudent to attempt an awake fiberoptic intubation. For the
fiberoptic intubation, the endoscope is introduced after using
a lidocaine topical spray to reduce the gag reflex. The endo-
scope is then negotiated through the vocal cords under vision;
once this is accomplished, depending upon the amount of
space available, a bougie can be introduced past the cords
over which the endotracheal tube can then be threaded down
or an attempt can be made to introduce the endotracheal tube
directly under bronchoscopic vision. The endoscope is then
gently removed after confirming bilateral equal air entry over
the lung fields. If a fiberoptic bronchoscope is not available,
an attempt at awake intubation can be done with a readiness
for release of contracture under tumescent anesthesia. Another
safe method is to release the neck contracture under tumescent
local anesthesia and intubate after release.178 One could also
go ahead with the whole procedure under tumescent anesthe-
sia and give regional blocks in the thigh for graft harvest.179,180
The type of release and resurfacing will be decided according
to the type of contracture.

468
SECTION III
CHAPTER 20 • Management of the burned face
in Bangladesh. The face is the most frequently targeted
area in chemical assault, with the intention to maim and
disfigure.189 The physical effects of such chemical burns are
devastating, with blindness due to corneal perforation,190
nasal deformity, microstomia, and debilitating contractures
amongst the complications documented.191,192 Acid burns
differ in appearance and behavior from thermal burns. Esti-
mation of the percentage of burns is difficult as the chemical
is sprayed or thrown over the body and is distributed spot-
tily. The first aid should entail a detailed washing ritual with
copious amounts of running water or saline for a prolonged
period of about 45 minutes. This measure and early removal
of the chemical-soaked clothes worn by the victim can limit
the depth of burns. Application of topical antimicrobials that
stain is not recommended as they make wound depth assess-
ment difficult. It is recommended to cover the wound with
occlusive dressings until they are taken up for excision.
Superficial burns can be treated conservatively and be
expected to resolve within two weeks. Excision for deep
burns as early as feasible is the standard of care in acid
burns. However, despite expediently doing the excision, it
may still cause worse scarring than in thermal burns. Mor-
tality from acid burns is low, but morbidity is severe. It can
cause severe deformities and scarring of the face and body,
which is a social stigma. Women who have been traumatized
by acid throwing deserve deep empathy and greater efforts
towards aesthetic restoration to improve their self image and
confidence.
Future directions
Stem cells
In terms of use of stem cells in facial rejuvenation, the future
is already here. The use of cultured epithelial autograft (CEA)
for early coverage and speedy re-epithelization of burn
wounds has been described earlier. When adult bone marrow
derived MSCs were injected into fresh excised areas of deep
burns that would have otherwise become anhidrotic, the
sweat gland function was seen to recover in 2–12 months.193
Once treated and processed, the stromal vascular fraction
(SVF) obtained from liposuction aspirates has shown promise
to be used along with fat transfer to treat contour defects and
to improve the quality of post-burn scars.194
3D printing
This is a newer innovation using state of the art technology
in which scientists use a technique called scaffolding. Cells
from the patient’s tissues are layered onto three-dimensional
models of the organ to be created and grown in vitro in an
incubator. Tissue building information is fed into a computer
using bioprinting technology to generate cells for organogen-
esis.195 More studies are being now conducted to use human-
derived cartilage cells instead of the bovine counterpart to
reduce the chances of tissue immunorejection.196
Face transplantation
This is the final frontier in the reconstructive ladder where a
partial or total replacement of the human face is attempted by
transplant from a brain-dead donor. The world’s first partial
Technical pointers for a release of severe
neck contracture
The position of the patient is supine with a substantial bolster
support between the shoulder blades. This gives an adequate
neck extension. Head support should also be given with rings
as required still maintaining good extension. The arms are
strapped by the side of the patient and not abducted. After
the patient is under anesthesia, the whole scarred area is
infiltrated with tumescent solution. After waiting 10 min an
incision is made that is at the prominence of the contracture
where the scar seems stretched across maximum. If the con-
tracture is more towards the superior part of the neck, the
incision made should be such that post-release the upper flap
created should not slide up over the lower border of the
mandible. At both the lateral ends, a Y cut is made to fishtail
the incision. The depth of the incision should be such that all
scar tissue should be released. Platysma should be cut. If an
excisional release is being done, one should start excising the
scar from either the clavicular end or the mandibular end and
pick it up akin to how a full-thickness graft is raised. As the
surgeon proceeds with the release, counter-traction on the
supple bed by an assistant with a surgical mop makes separa-
tion of the scarred skin from the bed easier. The scar tissue
itself can be held by the surgeon with a strong allis or Kocher’s
clamp to be able to give traction. Excisional release is easier
and gives a superior aesthetic result, but it may not be a viable
option in patients who have a large amount of scarring as the
graft requirement is much more than an incisional release. To
check that the release is complete, neck lateral movements
should be checked. After full release the field can be covered
with sponges soaked in saline epinephrine solution. One
should wait for about ten minutes to wait for all minor bleed-
ing spots to stop oozing. Any leftover oozing can be coagulated
using bipolar cautery. Three sheets of medium-thickness
grafts should be harvested from the thigh. Wide sheets of
grafts can be harvested from the back of the thigh as well as
the medial thigh. The grafts are placed in a horizontal manner.
If possible the seam should lie in the submandibular region
and the supraclavicular region. Once the grafts are sutured in
place, a squirt of saline solution under the grafts helps to flush
out any minor hematomas. Long silk sutures placed along the
margins of the defect are used as tie-over sutures to keep the
fluffy dressing in place. The sutures should be tied over in a
horizontal direction. The neck is immobilized using a fabri-
cated plaster of Paris splint molded over the dressing or using
a rigid cervical collar. The dressing is done on the seventh
postoperative day. Postoperatively, a neck/chin pressure
garment should be worn with foam padding beneath to help
maintain uniform pressure over the contours of the neck. A
custom made Philadelphia collar helps to maintain the exten-
sion achieved by release over the next one year. Postoperative
use of moisturizers and exercises are also essential to keep the
grafts supple and to avoid a re-contracture.
Acid burns
An acid burn is a devastating injury seen more often due to
intentional vitriolage rather than due to industrial accidents
or accidents at home. A study by Das et al.188 studies the
epidemiology and management of acid burns in a burn unit

469
Conclusion
face transplant was carried out if France in 2005,197 and full
face transplant was achieved by Spain in 2010. Since then a
number of face transplants have been reported by Turkey,
France, United States, and Spain. Patients who could poten-
tially benefit from the procedure include those who have
devastating disfigurements due to trauma, burns, tumor, or
congenital disorders. The concept was proposed by Professor
Peter Butler of the Royal Free Hospital in 2002, who published
an article to this effect in the Lancet.198 This idea caused heated
ethical debates at the time and continues to do so in the
present day.
Patient selection is possibly the single most critical step
influencing the long-term outcomes of face allotransplanta-
tion. Microvascular surgeons with the necessary training and
transplant physicians with their four decades of experience of
solid organ transplant-related immunosuppression are set to
move the science forward. This has to be done taking ethical
and psychosocial issues into thorough consideration.199
Conclusion
The human face is crafted to perfection with balance and
harmony of features and symphony of movements. This estab-
lished divine ideal encourages the plastic surgeon to be tireless
and unrelenting in his pursuit for perfection in post-burn face
reconstruction. Despite major advances in treatment and
groundbreaking research, it is abundantly clear to the treating
surgeon that the element of nature taking its course is strong
in burn scars. This brings the focus back to preventive strate-
gies as the single most important factor that can reduce mor-
bidity in facial burns. Despite giant leaps in the field of research
to develop newer dressing materials and skin substitutes,
considerations of cost and global availability continue to keep
us engaged to try and develop low-cost strategies for wound
cover and tissue regeneration. No greater need and indication
exists for reconstructive intervention than in the burn patient
whose face is disfigured and scarred, who is deserted by his
own, and who hides his scars in shame. At the same time the
reconstructive surgeon should be ready to accept a certain
surgical outcome as the endpoint of the patient’s reconstruc-
tive journey beyond which further improvement is possible
only by psychosocial empowerment. Vocational rehabilitation
and burn survivor camps can provide this much-needed moral
thrust to the patient’s confidence and help them meet the
challenges thrown at them by life with a brave face.
Bonus content for this chapter can be found online at

Laser Doppler evaluation
Other skin substitutes
Versajet mode of action
Procedure of facial wound excision
Grafting post-excision
Acellular dermis
Xenograft
Matriderm and Integra
Cultured epithelial autograft
Ancillary measures
Factors affecting post-burn scarring
Classification of scalp defects
Options for individual areas
Canthal deformities
Symblepharon, entropion, blepharostenosis, and canalicular stenosis
Airway problems
Fig. 20.1 Woman with an acute facial burns less than 24 hours since burns.
Fig. 20.5 (A) 7-year-old child with facial burns due to firecrackers. Collagen
sheets have been applied. (C) Showing healing by day 7 with complete
separation of collagen sheet.
Fig. 20.6 (A,B) Thermoplastic splints for microstomia.
Fig. 20.7 (A) Old unattended facial burns with raw areas and contractures.
(B) Neglected burn presented to us about two weeks after burn, anterior view.
(C) Lateral view. (D) 6 months after grafting showing deformity of the left side
of face. (E) Lateral view.
Fig. 20.9 Eight months after release and split skin graft. (A) Anterior view.
(B) Left oblique view. (C) Right oblique view.
Fig. 20.10 (A–C) Eight years after neck release, patient presented for an
improved look.
Fig. 20.11 (A–C) One month after full-thickness graft.
Fig. 20.12 (A–C) Eight months after full-thickness graft.
Fig. 20.13 (A–C) One and a half years after full-thickness graft.
Fig. 20.15 (A) Minor deformity and scarring of the lower lip and chin complex.
(B) Pleasing appearance after resurfacing with full-thickness graft and
repositioning of the lip.
Fig. 20.16 (A) Scar over the left forehead and eyebrow. (B) Resurfaced with
expanded skin.
Fig. 20.18 (A) Alopecia of left temporal and parietal region. (B) With expander
in situ. The nose has been reconstructed with radial artery forearm flap.  
(C) Post-resurfacing.
Fig. 20.19 (A) Full-thickness electric injury with eschar on scalp. He had a
subdural hematoma that was evacuated by craniotomy at another hospital, and
10 days later the patient was sent to us for the dead necrotic skin and
management of burns. (C) The craniotomy bone was picked up, and the slough
over the dura was debrided. Seen here is the exposed dura after debridement of
dead tissue.
Fig. 20.20 (A) Upper third ear deformity. (B) Reconstruction with postauricular
skin and costal cartilage graft.
Fig. 20.24 (C) Expander in forehead.
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7. Monstrey S, Hoeksema H, Verbelen J, et al. Assessment of burn
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early surgical management for deep burns of the face.
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selected skin in regional aesthetic units. Br J Plast Surg.
1956;9:212–221.
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154. Small A. Early surgery for electrical mouth burns. AORN J.
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155. Grishkevich VM. Post-burn philtrum restoration. Burns.
2010;36:698–702.
156. Chang KP, Lai CS, Tsai CC, et al. Total upper lip reconstruction
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157. Hafezi F, Naghibzadeh B, Nouhi A. Facial reconstruction using the
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158. Hassanpour SE, Shariati SM. Simultaneous reconstruction of upper
and lower lip beside chin and nasal lobule: in a case of facial
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159. Kumar P. L-shaped scalp flap for moustache reconstruction in a
patient with an acid burn of the face. Burns. 1996;22:413–416.
160. Sakurai H, Soejima K, Takeuchi M, et al. Reconstruction of perioral
burn deformities in male patients by using the expanded frontal
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161. Pribaz JJ, Meara JG, Wright S, et al. Lip and vermilion
reconstruction with the facial artery musculomucosal flap. Plast
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162. Rudkin GH, Carlsen BT, Miller TA. Nasolabial flap reconstruction
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163. Converse J. Techniques for the repair of defects of the lips and
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164. Ayhan M, Aytug Z, Deren O, et al. An alternative treatment for
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165. Bakamjian V. Use of tongue flaps in lower-lip reconstruction. Br J
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166. Donelan MB. Reconstruction of electrical burns of the oral
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167. Grishkevich VM. Post-burn microstomia: anatomy and elimination
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179. Pawan A. Safe method for release of severe post burn neck
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181. Loghmani S, Eidy M, Mohammadzadeh M, et al. The
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184. Parwaz MA, Dalal R, Chakravarty B, Malik A. Free parascapular
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186. Upadhyaya DN, Khanna V, Kumar A, Kohli R. Our experience in
reconstructing the burn neck contracture with free flaps: are free
flaps an optimum approach? Indian J Burns. 2013;21:42–47.
187. Yang JY, Tsai FC, Chana JS, et al. Use of free thin anterolateral
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2002;110:39–46.
188. Das KK, Olga L, Peck M, et al. Management of acid burns:
experience from Bangladesh. Burns. 2015;41:484–492.
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197. Devauchelle B, Badet L, Lengele B, et al. First human face
allograft: early report. Lancet. 2006;368:203–209.
198. Hettiaratchy S, Butler PE. Face transplantation–fantasy or the
future? Lancet. 2002;360:5–6.
199. Pushpakumar SB, Barker JH, Soni CV, et al. Clinical considerations
in face transplantation. Burns. 2010;36:951–958.

SECTION III • Burns Surgery
21 
Burn reconstruction
Nelson Sarto Piccolo, Mônica Sarto Piccolo, and Maria Thereza Sarto Piccolo
SYNOPSIS
■ Major evolution in burn patient care in the last three decades has
allowed several positive changes in the treatment objectives.
■ Currently, the main objective of treatment of the burn patient is to
recover his/her quality of life and the patient’s social re-insertion.
■ It is best if the patient is treated in a facility with a dedicated
multidisciplinary team, acutely and during the reconstruction phase.
■ Reconstructive surgery planning starts during the acute phase or as
soon as the surgeon sees a patient in need.
■ Timely reconstructive surgery will guarantee the best results –
planning is based on need, scar maturation, and available surgical
techniques.
■ The patient should be treated as a whole – we do not treat wounds or
scars, we treat a person with wounds or scars.
Access the Historical Perspective section online at

Introduction
The major evolution that has occurred in burn patient care
over the past several decades has allowed several highly posi-
tive progressive changes in the treatment of these patients.
The main objective of treatment of the burned patient is
acutely life saving and then, secondarily, to recover the
patient’s quality of life.
Reconstruction, and its planning, must start when the
plastic surgeon has the initial contact with the burn victim.
Well-planned surgical care during the acute phase will ensure
a post-healing phase with fewer sequelae and complications.
This care must be accompanied by several other clinical
measures and by other professionals in the multidisciplinary
burn team, such as physiotherapists, occupational therapists,
dietitians, and psychologists, amongst others.
Frequent evaluations (and the ensuing therapeutic mea-
sures), treating the patient as a whole, and appropriate timing
for surgical intervention are paramount to the success of
treatment.
After healing, reconstructive surgical procedures will be
promptly indicated when functional loss or compromise are
encountered. If no dysfunction occurs, the authors favor
waiting for scar maturation prior to surgical intervention.
Procedures will range from skin grafting, local, distal or free
flaps, resurfacing with dermal regeneration templates, to
advancement of expanded tissue. We can also use fat grafting
and adipose-derived stem cells as a most effective ancillary
treatment for burn sequelae.
As these patients are usually submitted to a series or
sequence of procedures, and as the scar and the patient evolve,
there may be a need (or a request) for different/additional
procedures, and this very common occurrence must be well-
explained to the patient or their parents in advance. This is
necessary so that the patient and the patient’s family can have
realistic expectations of results and can also participate in the
treatment with a more informed attitude.
Increase in survival rates
Serious burn injuries will bring several risks for the patient,
who will need specialized and dedicated care in the
acute phase, during resuscitation, with intensive care life-
maintaining measures, pain management, frequent dressing
changes, early mobilization, surgery, and grafting.
The acute phase admission is usually followed by very long
periods of a highly complex rehabilitation phase with the
possibility of several immediate consequences such as hyper-
trophic scarring, retractions, sensorial alterations, limited
physical abilities, anxiety, depression, body image dissatisfac-
tion, and other difficulties that may hinder the patient’s return
to previous activities.1
After the major world conflicts of the first half of the twen-
tieth century – the two great wars – there was a growing

472
SECTION III
CHAPTER 21 • Burn reconstruction
surgeon involved in the process understands how these evalu-
ations and patient-reported outcome measures are derived as
well as appreciates the vertical nature of these measures
during follow-up visits.12
Evaluation questionnaires can be divided into generic and
specific. The health-related generic instrument that is most
used in the world is the Medical Outcomes Study 36-item Short-
Form Health Survey (SF-36). This is a multidimensional ques-
tionnaire composed of 36 items and 8 domains. Specific
instruments will be more advantageous than the generic since
they survey more relevant items, for the patient and for the
professional team.13,14
The Burn Specific Health Scale (BSHS) is an example of
a multidimensional specific instrument that approaches
several aspects of the treatment and rehabilitation results
within 114 items. It is the most utilized questionnaire in the
world for these purposes. It comprehends three modalities –
the Burn Specific Health Scale – Abbreviated (BSHS-A) with 80
items, validated by Munster and co-workers; the Burn Specific
Health Scale – Revised (BSHS-R), translated to the Portuguese
language and validated by Ferreira and co-workers, with 31
items and 6 domains, and the Burn Specific Health Scale – Brief
(BSHS-B) created by Kidal and co-workers, which is self-
applied with 40 items and 9 domains.
This last one, the BSHS-B, evaluates hand function and
sexuality, which are no less important domains in the evalu-
ation of the quality of life of these patients. This modality was
recently translated to the Portuguese language after been
validated and published. Others, such as the BurnSexQ-EPM/
UNIFESP, has also been translated into Portuguese and evalu-
ates psychological aspects of sexuality.15–23
Quality-of-life evaluation and
treatment phases
During the acute phase, the patient will be evaluated through
the SF-36, which will demonstrate the patient’s quality of life
before the accident, showing how the patient lived his day-
to-day activities before suffering a burn injury.
Upon discharge, a more specific instrument becomes neces-
sary, and the patient will be evaluated with the BSHS-Brief then
and at 3, 6, and 12 months. In a patient seeking reconstruction,
this routine is repeated every 6 months, which will then also
evaluate the results of the surgical reconstructive procedure.
The BSHS-Brief questionnaire is equally beneficial when
applied in patients who have been treated by us since the
accident as well as in those whom we meet after healing,
translating very important information that will aid in treat-
ment tailoring at that patient-specific moment. Changes can
then be identified in several domains, as for example, those
resulting from body image changes, which in turn will imme-
diately influence how the patient socializes or even relates
intimately to his or her partner from the sexuality standpoint.
This knowledge can help to elevate the final outcomes of
acute care and reconstructive stages of care.
Acute phase
A patient with acute burns that could eventually lead to
aesthetic and/or functional sequelae needs specialized treat-
ment protocols in a burn unit, and these should be instituted
as soon as possible after the accident.
interest in the pathophysiology of burn injuries and their
course. This promoted a great advancement in the clinical and
surgical treatment of the burn patient with a consequential
increase in burn patient survival. This increase in survival rate
brought a need for a more profound understanding of the
complex wound-healing process, since it became obvious to
all involved that treatment went well beyond life maintenance
measures.2,3
Efforts to obtain complete functional recovery of the burn
victim have evolved into several different objectives, with
quality of life and social reintegration as significant objectives.
During the past two decades, subjective patient evaluation via
patient-reported outcome measures has become a priority and
a guide, affecting treatment measures and evaluation and
occasionally leading to modifications of treatment protocols.4–7
The goal of treatment of a person with burn lesions is that
the multidisciplinary burn team make every possible effort to
bring this person back to his/her original “world” and way
of life previous to the accident. This is the reason why it is of
paramount importance that the patient be treated in a dedi-
cated burn center by a dedicated burn team – we do not treat
burn wounds or burn sequellae, we treat people with burn
wounds and/or with burn sequellae.
The plastic surgeon treating these people should preferably
be a member of a multidisciplinary burn team which works
with this objective.
Patient emotional status/evolution
It is believed that during the first year after the trauma,
approximately 13–23% of burn victims will present some
degree of depression – this percentage is significantly higher
than the general population incidence (which, surprisingly, is
up to 8.6% in some studies).8
Those patients with previously underlying psychological
instabilities will need more time as well as more intense/
prolonged psychological and surgical treatments in dedicated
burn services with a specialized burn team. Multicenter
studies aiming to improve results for this overall patient
population have also become a priority with the concomitant
development and evolution of treatment protocols.9
Body image changes
Dissatisfaction with one’s self image, such as changes in
overall appearance and function, will frequently lead the
patient to seek reconstructive surgical treatment. Surgical
planning must be shared with all members of the burn team
who will be, or are, involved in the patient’s treatment. The
main objective of treatment, during the acute or reconstruc-
tive phase, is that patients return to their usual life, within
their community, as soon as possible.10,11
Evaluating quality of life
Quality-of-life evaluation, after such a trauma, is a multidi-
mensional concept that requires instruments that are able to
capture local physical impairment and health changes in
general and that could be re-applied in the same person over
a long period of time. These instruments are generally referred
to as “questionnaires”. It is of utmost importance for the
success of each and every reconstruction effort that the plastic

472.e1
Historical perspective
Historical perspective4–51
On a report of clinics presented by Dr. Earl Padgett and staff
at the annual meeting of the American Society of Plastic and
Reconstructive Surgery in November 1946, they summarized
what they believed to be the key measures for a successful
treatment of a burn patient: proper early care when the patient
came immediately to them after the burn, proper intermediate
care previous to skin grafting, especially to the patient sys-
temically, and early skin grafting in amounts sufficient to
cover the denuded areas, in one operation if possible. Previ-
ous studies by Drs Lund and Browder and others had already
called attention to the great nutritional needs of these patients,
mostly regarding the massive protein and weight loss during
their treatment course. Tragedies like the Cocoanut Grove
disaster, two World Wars, and several other major conflicts
led to a need for more complete understanding of the burn
disease and how to accomplish wound closure as soon as
possible.
A.B. Wallace believed that the open exposure, “dry” method
would lead to a dry scab that would protect the wound from
invasion, prevent fluid and protein losses through the wound,
and work as a scaffold for new epithelium to form in less deep
burns; in deeper burns, as the scab sloughed in 3 weeks, the
wound could then be covered with skin grafts. Berkow’s
Formula, modified into a “rule of nines”, was then used to
calculate burn area, administering the proper fluid amount
according to the burn area, knowing that the most valuable
sign of progress and efficiency of treatment was, and is, a
satisfactory urinary output.
These conclusions led to a more standardized routine for
treatment of patients with burns, allowing then for the surgeon
to worry about how, and when, to close the burn wound,
promoting healing and survival. Homografts soon became the
gold standard for skin replacement and grafting on major
burns, usually obtained from a cadaver, but occasionally from
live donors (twins or relatives).
Dermatomes, using physical means or electric or nitrogen
power, became more and more popular, and as skin grafting
became the standard in treating the burn wound to attain its
closure, it then became a matter of when it should be applied.
Measures to expedite treatment, improving the overall status
of the patient, have allowed for earlier surgery, but probably
the main work in relation to accelerating burn wound closure
was developed by Zora Jazenkovic during the early 1950s,
who promoted the notion of early tangential excision fol-
lowed by immediate grafting. This way the wound was
promptly closed, greatly minimizing the risk of infection and
preventing wasting through an open burn wound.
As the lack of autologous skin is a most common situation,
and homograft is not always available, several researchers
have worked on a variety of skin substitutes and composite
tissues. This work was pioneered by Burke and Yannas, creat-
ing a dermal regenerating template in the 1970s, which very
quickly became popular for acute burn care as well as recon-
struction procedures.
Flaps soon became common procedures in burn reconstruc-
tion, aimed at covering exposed bone, tendons, nerves, carti-
lage, and deep tissue areas, particularly when these wounds
cannot be covered by other methods. Free tissue transfer
became as common as pedicled flap transfers in some services,
since skin and fasciocutaneous flaps are more common than
muscle-containing flaps. Free flaps offer an immediate solu-
tion, usually with much better contoured cosmetic result than
pedicled, bulky flaps. However, there is always the concern
of patient weight gain and gravity effects on the flap. Super-
thin flaps as well as prefabricated flaps became an alternative
and are used routinely by several services around the world.
After Radovan “re-introduced” tissue expanders (Neumann
in 1957 had tried a balloon in an ear reconstruction), skin
expansion became an excellent option for obtaining well-
vascularized local tissue with ideal texture and color, sensa-
tion, and thickness, while greatly minimizing donor area
defects. Although already in use for several decades, there is
still a high incidence of complications, and a most rigorous
routine must be applied in its usage.
Another major evolution in burn reconstruction is the
understanding that the patient must be treated as a whole and
there is a need for complete recovery, both psychological and
physical.

473
Clinical treatment
no, if any, excision of breast tissue and never excise the NAC,
even if there is doubt about its viability. When grafting, one
must place the graft sheets following the tension lines of the
skin, grafting each breast separately and avoiding “crossing”
the midline with the same graft sheet that was placed on the
breast, as these graft sheets must contour the breast according
to its shape and volume (Figs. 21.1 & 21.2).71,72
It is of utmost importance that the surgeon treating a
patient with acute burns understands and respects the skin
tension lines, applying the graft sheets transversely and per-
pendicular to the longitudinal axis of the extremity or trunk,
as well as in the neck, as hypertrophic scarring can be likely
in these patients if the graft sheets are placed longitudinally.
Aftercare
Changes in the scar or its appearance at the first visit
will define the treatment options and subsequent surgical
interventions.73–76 Pressure garments and devices are recom-
mended to most patients upon discharge. It has been our
experience that approximately 12% of patients wear these
garments for more than a year.
At 1 year post-healing, around 2.5–3.0% of patients will
wish to be submitted to reconstructive surgical procedures. A
current option for early treatment of hypertrophic scarring is
with sublesional fat grafting, with the aim of introducing the
benefits of adipose-derived stem cells and the factors con-
tained within the injected fat.77–84
Clinical treatment
Alternatives most frequently recommended range from pres-
sure garments and inserts to laser therapy, aimed at decreasing
hypertrophic scarring and its associated symptoms.
Important treatment measures are pharmacologic control
of the hypermetabolic response, early excision of deep areas,
immediate wound closure/resurfacing, early occupational
and physiotherapy, aggressive nutritional support, and the
immediate use of pressure as healing occurs.52 Adequate
wound care during the acute phase will determine initial
treatment success, which will greatly aid in future surgical
reconstruction planning.53–56
Burn wound excision
The excision of the burn wound has become the most impor-
tant surgical procedure in the treatment of an acute burn
patient with deep wounds, greatly decreasing the risk of
infection. Initially proposed by the Yugoslavian plastic
surgeon Zora Jazenkovic in the early 1950s, sharp tangential
excision consists of sequential removal of necrotic tissue in
relation to the wound surface.57,58 These damaged tissue layers
are sequentially removed until one obtains uniform and
diffuse bleeding, indicating local tissue viability.
This procedure has a very short learning curve, and the
experienced surgeon will notice tissue viability by its appear-
ance, thus experienced surgeons currently utilize tourniquets
and/or injection of vasoconstricting agents to minimize blood
loss. Although immediate coverage or resurfacing of the
excised wound would be the ideal measure, this is not always
possible, since commonly the patient has insufficient donor
areas, so alternatives are usually sought. In some parts of the
world, this is even harder to accomplish due the lack of avail-
ability of skin substitutes.59–62
Split-thickness autografts that are harvested from non-
burnt areas are the first option of choice. Burn wound excision
is typically performed in sequential steps, usually within 2- to
3-day intervals during the first week to 10 days of treatment.
Open burn wounds ideally should be covered with some sort
of biologic coverage or efficient topical agent and then grafted
in the next visit to the operating theater, during the ensuing
excision step in other areas of the wound (Fig. 21.1).
The first choice for local coverage when the patient does
not have enough donor areas would be cadaver skin. Xeno-
graft (pig or frog skin) or other biologic alternative can also
be used, although currently it has become common to resur-
face the wound with synthetic dermal regeneration templates,
which “close“ the wound, until the silicone layer is removed
or sloughs off, depending on the matrix being used. This may
take up to 3–4 weeks, allowing time for other areas to heal
and potentially become donor areas to yield thin split-
thickness skin grafts to complete the final epithelial coverage.
Other alternatives such as epidermal cell culture and even
more sophisticated composed tissue are also current, less
frequently used, alternatives.63–70 In summary, the burn wound
should be excised within 1 week of the accident and must be
closed or covered with the (local) best available tissue.
Anterior thorax excision
In some areas such as the breast, for example, there is a need
for specific surgical care when performing the excision. In
children, especially in females, the surgeon must identify and
protect the breast bud and the nipple–areola complex (NAC)
should not be removed, regardless of its appearance or wound
depth. Similarly, in older patients, there should be practically
Fig. 21.1  Patient 2 days after excision and grafting on thighs and right abdomen,
being excised on breasts – please note that although the burnt skin was excised
completely from the breast, the nipple–areola complex was not, regardless of the
burn depth.

474
SECTION III
CHAPTER 21 • Burn reconstruction
Another theory is that local hypoxia would decrease fibroblast
cohesiveness and the total amount of chondroitin-4-sulphate,
which coats collagen fibers and hinders collagenase activity.
Pressure therapy is considered the gold standard for the clini-
cal treatment of burn scars in most services around the
world.85–106
Silicone
Silicone is a dimethylsiloxane polymer gel applied over the
scar as a compressed or self-adherent sheet. The mechanism
of action on these scars is probably due to occlusion generat-
ing an increase in local temperature and keratinocyte hydra-
tion, modifying local inflammatory mediators and collagen
production as well as collagenase activity, improving scar
thickness, pain, itching, and appearance. It should be in
contact with the scar at least 12 hours per day, for 4–6 months.
We recommend starting its use 2 weeks after wound healing,
and that it be shaped along the scar to avoid depigmentation
and irritation of the normal surrounding skin.107–121
Steroids
Intralesional steroid injection inhibits fibroblast proliferation,
decreases local inflammatory process, inhibits TGF and (TGF-
β and IGF), decreases collagen and glycosaminoglycan
deposits, and increases collagenase activity. Triamcinolone is
generally used at up to 0.4 mg/kg injected at 3- to 6-week
intervals within the scar, avoiding sublesional injections. Side
effects can be hypopigmentation, telangiectasia, local necrosis
and ulceration, and local atrophy, which may last several
months or, more rarely, be permanent.122–133
Retinoids
Retinoids modulate scar fibroblast proliferation and collagen
production and organization, improving scar quality and
appearance. They induce apoptosis and immunoregulation
through inhibition of collagen type I gene TGF-β1-induced
expression, besides favoring epithelial growth. Concentra-
tions ranging from 0.025% to 0.1% are used to obtain hyper-
trophy decrease in 50–100% of cases. Its use can yield a
significantly improved result when associated with glycolic
acid, pressure garments, and silicone gel. Side effects include
photosensitivity, contact dermatitis, and skin atrophy.134–140
Laser
Pulsed dye laser (PDL) with a 585-nm wavelength has an
affinity for oxyhemoglobin (absorption peak at 542 nm),
leading to selective photothermolysis of cicatricial microcir-
culation, thus leading to thrombosis and ischemia, reducing
intracicatricial collagen. It may also hinder fibroblast prolif-
eration and type III collagen deposition through protein
kinases and apoptosis increase, TGF-β1 level decrease associ-
ated with increased metalloprotease 13 (collagenase 3) activity,
mastocyte content release (which affects collagen metabolism),
and through local heating breaks the bisulfate bridges favor-
ing collagen realignment. It also reduces erythema, itching,
and has been shown to improve scar thickness and texture.
Resulting treatment edema usually resolves in 48 hours, and
side effects may include local purpura, which may last several
days/weeks, and pigment changes, more frequent in
Pressure garments
Continuous pressure usually yields improvement of the
hypertrophic scar in color, texture, symptoms of pruritus, and
thickness in up to 65–85% of the scars. It possibly induces a
relative tissue ischemia; increases collagenase activity associ-
ated to MMP9 metalloprotease action, which favors regenera-
tion without scarring; and also decreases local metabolism.
A
Fig. 21.2  Acute appearance of a patient with third degree burn to the anterior
lateral chest (A) and after excision and grafting (B). One can easily note that the
graft sheets were placed following the local tension lines, resulting in multiple
directions of graft placement but following each individual area’s anatomic volume,
shape and disposition.
B

475
Surgical reconstruction
In patients with contractures across joints, we recommend
the surgical resection of the scar, as wide as necessary to
reach healthy tissue, and then resurfacing the area with the
best available substitute for that area. Currently, we greatly
favor the use of dermal regeneration matrix, followed by
autografts obtained from the scalp, at 8–10 thousandths of
an inch.179,180
Functional restrictions
Contractures can lead to severe functional restrictions, and we
believe that these must be approached in a descending order of
importance (according to the difficulties they produce). There-
fore we must treat those functional contractures that cause
greater difficulty/deformity first. Usually, we prioritize neck
contractures, warranting respiratory comfort for the patient,
but mainly ac hieving a supple neck during endotracheal intu-
bation for future procedures. We then approach periocular
and perioral defects, hands, genitals, axillae, elbows, and feet
as the following set of priorities (Fig. 21.3).181–185
Skin grafting
We limit the indication of full-thickness skin grafts to the
occasional facial reconstruction in eyelid(s), periorbital, or
perioral deformities. We prefer postauricular skin, where
possible. If there is not enough skin behind the ear or the ear
is absent, we will substitute this choice for supraclavicular
skin. These donor areas offer better color match, and a higher
proportion of collagen in these full-thickness grafts favors
more permanent and efficient results. Other uses of full-
thickness skin are extremely rare in our service.
We favor the use of split-thickness skin grafts, almost
always obtained from the scalp with an electrical dermatome
at the average thickness of ten-thousandths of an inch. For
this, the hair is shaved from almost the entire scalp area,
leaving a “rim” of 2 to 4 cm with intact hair. In both genders,
this “rim” will serve dual purposes: first, it will prevent the
surgeon inadvertently going into forehead or neck area while
harvesting the skin, leading to an undesired donor area scar
in these sites, and, in females, this residual hair is usually be
enough for the patient to cover the then short-haired donor
area, disguising this temporary aesthetic shortcoming with
a ponytail. Other advantages of the scalp as a donor area
is that the scalp skin is much thicker than other areas, with
a higher proportion of epidermal appendages embedded
on the thicker dermis, favoring a more prompt (re-)epithe-
lialization. This donor site area has practically no incidence
of hypertrophic scar, and it is naturally protected against the
sun, rarely presenting with a resulting discoloration.
Another advantage of utmost importance of this area is the
fact that for facial or neck resurfacing, this skin will retain the
donor area color that is identical to the entire cephalic segment.
This donor area is treated with an efficient topical agent on
a closed dressing, which is changed every 2 days until healing,
which usually occurs within 6 to 10 days. Due to this rather
rapid healing, we frequently use this donor area repeatedly
in the treatment of acute burns (Fig. 21.4).186
Tourniquet use
Operative tourniquets are frequently used to keep the extrem-
ity as exsanguinated as possible in order to minimize blood
dark-skinned patients. Hyperpigmentation must be treated
before the next treatment section since its energy may be
absorbed by melanin. Fractional photothermolysis (Fraxel,
1550 nm) can also be used.141–155
Surgical reconstruction
Adequate timing of surgical reconstructive procedures will
vary according to each patient. Immature scars require control
before their eventual surgical resection unless they are hinder-
ing the patient’s vital functions. The natural scar evolution as
well as the results of clinical scar manipulation measures will
dictate the treatment planning in those patients without
dysfunction. Surgical reconstructive procedures performed
through correct planning and appropriate timing will yield
better results.156–160
However, it is rather common for the patient or the patient’s
family to wish for immediate reconstruction and scar removal.
The plastic surgeon has a key role deciding which procedures
should/could be performed immediately after early healing, as
well as in the future planning of sequential surgical procedures.
In the literature, we frequently see discussions about the
“reconstructive ladder”, or a list of surgical procedures with
progressive complexity and operative difficulty, aimed at
obtaining the best results with the fewest number of surgical
interventions possible. Obviously, this logical tiered choice
can be applied to any case at hand.
In the treatment of scar contracture, we will use the simplest
technique that will yield the desired result. As these deformi-
ties are very frequently associated with lack of local tissue,
this can occasionally be solved with geometric flaps (Z-plasty,
rotation or advancement flaps) or attempts at replacing local
tissue with remote unburned tissue, such as skin grafting or
free flaps. In these cases, there is always the possibility of
resection of the involved area and resurfacing of the wound
with dermal regeneration templates. In those cases where
there is no scar contracture, our technique of choice is the use
of tissue expanders, always aiming for a complete as possible
removal of the scar.161–173
Currently, we restrict the use of free flaps for very specific
cases for a number of reasons: technical execution require-
ments, frequently flaps take on the appearance of a “pin
cushion”, flap (fasciocutaneous or muscle) volume can change
as the patient’s weight changes, and future implications for
flap viability when another surgeon takes over care and
potentially revises the flap without the knowledge of the
primary set of vascular anastomoses. Currently, our indica-
tion for free flap transfer will be in a patient who has suffered
a high-tension injury with exposure of distal forearm, hand,
or foot structures. Alternatively, we will use fat grafting and
deposition and/or dermal regeneration templates.174,175
Surgical planning must be individualized for each case and
adhere to indications and the patient’s wishes. The recon-
structive treatment of a burn patient with sequelae is usually
very long, intra-dependent of previous individual procedures
as well as, very frequently, subject to changes or evolution of
the patient’s desires. As surgeons, we must be very realistic
when considering what we can technically offer, also accept-
ing our occasional personal limitations before each presenting
patient – we should always obey medicine’s fundamental
principle: “primum non nocere” or “first, do no harm”.176–178

476
SECTION III
CHAPTER 21 • Burn reconstruction
practiced around the world. Not using the Esmarch bandage,
and consequently not emptying the superficial venous system,
is extremely advantageous for the reconstructive burn surgeon
and, consequently, for the patient.
When we do not empty the venous system and we inflate
the tourniquet, venous blood will be trapped within the non-
circulating vein. Doing so, as the incision is performed on
loss. This is used in procedures on the hand, forearm, distal
lower extremity, and foot, usually aimed at lesser blood loss
and at a “dry” operative field, in which local, critical structures
are better identified.
We would like to call the reader’s attention to the fact that
we do not recommend the usual “emptying” of the extremity
with the use of an Esmarch bandage, which is commonly
A
B
Fig. 21.4  (A–D) Split skin harvesting
sequence at the scalp – the area is
pre-injected with saline at a subgaleal
level temporarily transforming the scalp
on a more supple surface, which will
allow for a smoother dermatome
gliding. (The injected liquid is resorbed
in some hours, and its temporary
volume causes no distress to the
patient.)
C
D
Fig. 21.3  (A) Typical example of neck release
with local retraction segment resection and
resurfacing with dermal regeneration matrix,
followed by split-thickness autograft from the
scalp, 3 weeks after the original procedure
(complete eventual color match). (B) Results at 12
weeks.
A
B

477
Surgical approach
since, due to its proximity to the original band, a new flap
incision could hinder blood supply to the previously created
flaps of the “original” Z-plasty.188–190
Dermal regeneration matrix
These matrices allow host cell invasion and collagen substitu-
tion for host cell secreted collagen. The first matrix to be used
in burn care was created by a team of researchers lead by
Burke and Yannas in 1981. There are today a vast array of
products on the medical market with similar indications and
behavior.
When this tissue is applied to a live bed, this structure will
be integrated by the host usually within 21 days, when the
top layer is removed and the “new” dermis is autografted
with scalp split skin.
The objective of its use in the acute burn patient is the
coverage of the excised wound or excised scar, “saving” host
donor areas. It will also cover tendons and nerves without
hindering their functions. There may be a need for
re-intervention since in some patients the treated area may
still retract up to 60–70% (Fig. 21.6).191–197
Adipose-derived stem cells
Fat grafting has been used worldwide, taking advantage of
the benefits of adipose-derived stem cells (ADSCs) for regen-
erative purposes and their ability to differentiate into fat, bone
cartilage, muscle, and possibly other tissues. They also have
a great variety of regenerative and metabolic properties, as
well as growth factors (EGF, TGF-β, HGF, PDGF, BFGF, etc).
Fat on the lipoaspirate can be isolated and/or treated by
physical or chemical methods, in the operating room or later
in a laboratory set-up.
When treating burn scars, the objective is to decrease the
amount of hypertrophy (fibrosis), diminishing the scar thick-
ness and increasing scar malleability. We also use this tech-
nique with the aim of decreasing fibrosis around bone joints
and releasing tendon adhesions.198–218
Surgical approach
We harvest and prepare fat according to Coleman’s technique.
Fat is injected under the scar and its periphery. Injections are
repeated at 2- to 3-month intervals until complete hypertro-
phy control or another definitive procedure, such as scar
removal, is performed.
Operative technique219–221
Fat is obtained from the patient via liposuction of the abdomen,
thigh, knee, buttock, or other area. In adults or patients over
25 kg, suction is performed with a 10-cc syringe connected to
a 3-mm cannula with two 3-mm side openings distally. In
children, we prefer a 20-cc syringe and multiple microperfo-
rated cannulae, which will yield a relatively higher negative
pressure and a more efficient fat harvesting.
Fat is then centrifuged at 3.000 rpm for 3 minutes. The
upper oily phase and the lower, aqueous phase are discarded.
The central layer contains concentrated fat, growth and vaso-
dilating factors, and the stromal vascular fraction (SVF) and
is then transferred into 1-cc “insulin” syringes.
the usually extremely thick scar, the young as well as the
experienced surgeon will be able to do so with greater safety,
as explained below.
Very frequently, burn scar tissue, due to its fibrous con-
sistency, usually with visible bundles along the retraction
vectors, may be mistakenly confused by the novice (or by
the still insecure surgeon) with tendon tissue, mostly on the
hand and foot, where tendons are relatively smaller in rela-
tion to the proximal aspect, and then lead to a partial or eco-
nomic removal/incision of these scar tissues. So, when the
tourniquet is inflated directly, without exsanguination, these
will be very easily identified by their deep blue color, and in
the “incisional” sequence from the external world to deeper
structures on the extremities, there will be a scar of vari-
able thickness and appearance, and immediately under, the
veins are the most superficial structure, external to tendons,
nerves, and other noble, complex, structures. So, the surgeon
can continuously cut the scar, even if some retraction bands
look like tendinous structures, until he sees fat and veins
filled with blue, desaturated blood, when he/she will stop
with the certainty that nothing noble was incised, except for
the full-thickness of the deleterious scar (Fig. 21.5).187
Z-plasties
These geometric flaps are very frequently used and, when
properly indicated, will bring immediate aesthetic and func-
tional improvement.
The surgeon should always remember that cicatricial bands
are usually a consequence of abnormal collagen deposition
along a retraction/tension line, and in the same anatomic unit
there may be more than one dominating band or dominating
and secondary bands. When treating the main retraction band
with one or more Z-plasties, the surgeon may be surprised by
the immediate appearance of one or more parallel retraction
bands. Most unfortunately, very often, these second or third
bands cannot be treated similarly on the same intervention,
Fig. 21.5  Intraoperative picture of a dorsal hand procedure, without the previous
use of the Esmarch bandage. Please note the easily identified superficial “filled
veins”, consequently bringing comfort to the surgeon in relation to the certainty of
being in subcutaneous level (beyond the entire thickness of the scar) but not into
noble tissue level. If, on the contrary, these veins had been emptied by an Esmarch
bandage, they would be transparent and would not “alert” the surgeon.

478
SECTION III
CHAPTER 21 • Burn reconstruction
As many 16-gauge needle punctures as needed are made
through the skin on the periphery of the scar, and fat is pro-
gressively and uniformly injected under and in the immediate
periphery of the scar, using a 1.8 mm diameter cannula in a
retrograde fashion, using 20–30 passes/mL (Fig. 21.7).222,223
We frequently perform partial intralesional resections
(without reaching the subcutaneous tissue or normal skin
on the periphery) and subsequent fat injection, including
under the recently resected and sutured area. Marked
improvement can be seen with this technique when injected
along and under scar contracture after surgical release (Figs.
21.8–21.10).
Periarticular fibrosis
Fat injection can also be used in fracture lines of long bones
such as the tibia, fibula, ulna, radius, metacarpi, metatarsi,
and others, speeding healing as well as diminishing periar-
ticular fibrosis consequent to trauma to these structures (Figs.
21.11 & 21.12)
Tissue expansion224–232
Main advantages with this technique are the gain of
neighboring normal tissue, the reactive capsule, which war-
rants flap irrigation, and aesthetic and functional results.
Complications are well known and can be decreased dra-
matically with precise technique. Several expanders may
be needed, and the temporary growth deformity may be
an issue. Also, some patients may wish to have additional,
different procedures as the scar is sequentially removed
(Fig. 21.13).
Fig. 21.7  Skin puncturing with a 16-gauge needle and cannula introduction. Where
the scar is thicker, the surgeon can use the other hand to stabilize it, performing
multiple “passes” in a more secure way.
A
B
Fig. 21.6  Preoperative aspects (A,B)
and permanent functional result (at 2
years) after scar excision, substitution
for dermal regeneration matrix and
subsequent scalp skin autografting
(C,D) – the patient is able to write and
work with his hands.
C
D
Preoperative measures and surgical planning
There is a need for emotional and physical preparation of
the patient, tailoring planning to each individual case, as
tolerated.
The surgeon must plan enough undermining to accom-
modate the empty, flattened expander. Frequently, when

479
Surgical approach
Fig. 21.8  Demonstration of
intralesional resection and fat injection
under the suture line.
Fig. 21.9  Same patient as previous picture,
demonstrating the result after partial resections and
fat injections as shown above (5 sessions in 2
years).
ordering an implant from a catalog, one reads only length and
width, forgetting that height will be “added” to width when
the implant is flattened (even if one folds the implant sides
over itself, upon the first injection, it may open flat and
impinge against the sides) (Fig. 21.14).
When using more than one implant, we always use par-
tially overlapping tissue expanders.
Pre-conditioning of the area
In those patients for whom there is a need for expander place-
ment in tight areas (such as dorsum of the hand, wrist, distal
forearm, elbow, posterior knee, distal leg, foot dorsum, or
plantar area), we believe there is a need for preparation of
these areas before surgery.

480
SECTION III
CHAPTER 21 • Burn reconstruction
Fig. 21.11  (A–C) Foot X-rays taken during
healing time of a dorsal left foot friction/crush
wound. Note the “blurring” of articular spaces on
the tarsal joints on the left foot (B); note the
evolution with the “blurring” practically
disappearing on and around the joint spaces, 8
months post-cure (C), after 3 fat injections under
the cutaneous scar and around the articular
structures. Normal right foot X-ray shown for
comparison (A).
A
B
C
A
B
Fig. 21.10  (A) Preoperative
appearance, outlining area to be
resected intralesionally. (B) Two weeks
after fat injection and partial scar
resection. (C) 14 weeks and (D) 9
months after three injections. Please
note the suture line scar is practically
invisible even at long-term results.
C
D
We have created a routine protocol for these cases, aimed
at preparing the future expander site to receive and tolerate
the pressure of the deflated expander volume at the initial
placement operation and immediately postoperative.
In these areas, we inject normal saline with a 25-
gauge “butterfly” needle, thus creating a progressive hydro-
dissection of these areas approximating the pressure from
an inflated expander. These injections are performed at 2-day
intervals until half of the nominal volume is injected or the
entire area is undermined by the fluid injection, without local
blanching. One can also “push” the injected fluid to obtain
further undermining. If blanching occurs for more than

481
Surgical approach
A
B
Fig. 21.12  Same patient,
demonstrating a very elevated left foot
longitudinal arch (A), when compared
with the right foot (B); and with a
practically normal aspect, similar to the
right side, 8 months post-cure and 3 fat
injections (C,D).
C
D
A
B
Fig. 21.13  Typical example of
evolution of patient’s ambition. Results
after 3 expansions (A,C). Patient
“unhappy” with the result, with
“insufficient” breast projection requiring
breast implants (315 mL) (B,D).
C
D

482
SECTION III
CHAPTER 21 • Burn reconstruction
Fig. 21.14  Note that when the
expander is empty and flattened, it still
has a height and it “grows” to the
sides.
3–5 minutes, we will then add more preparation injections,
until blanching no longer occurs or rapidly disappears
(Fig. 21.15).
Operative procedure
A pocket is created through a small to moderate incision at
the border of the scar, undermining enough to fit the flattened,
empty expander(s). The injection site will be at a separate
cavity, usually on the opposite side of the scar. A continuous
suction drain is placed before the expander is inserted, exiting
through scar tissue. The expanders are placed in such a
manner that at least a third of its areas overlaps the next
expander.
Overlapping tissue expanders
To obtain a greater amount of expanded tissue, we have used
the technique of superimposing and stacking expanders at the
edges. Stacking and overlapping expanders in strategic areas
can markedly increase the amount of expanded skin. This,
however, should be performed with extreme caution when
expanding.
This is mostly advantageous in areas where it would be
desirable to advance tissue in more than one plane, such as
shoulders, neck, breast, etc. We inject into the expanders once
a week and frequently go beyond the nominal volume (up to
1.7×) (Fig. 21.16 & 21.17).
Reconstruction of the burned breast
Reconstruction of the burned breast can be initiated at any
time, in relation to scar maturation as well as in relation to the
patient’s age.
Male and female patients will, obviously, require different
planning. In male patients, we aim to recover the scar area
with normal, better quality tissue, searching for nipple–areolar
complex (NAC) symmetry in color, position, and size. In
female patients, we aim for similarity in shape, volume, mal-
leability, surface, and in NAC dimension, position, and shape.
In children, this consideration will persist until adult age is
reached, and repeated procedures may be necessary.
Reconstruction should not be delayed at any age, since the
scar envelope may restrict growth or positioning of the female
breast. As a second choice, in children, one may delay recon-
structive procedures if the scar is above the breast “equator”,
since the breast will grow, detaching its lower half from the
chest, and thrusting forward and upwards.
Conclusions
We believe that the reconstruction process of a burn victim
starts during the acute phase and that all patients must be
treated in specialized centers with a dedicated burn team.
Patient and family psychological preparation as well as
surgical planning explanations are a must for the success
of treatment. Self-applicable questionnaires before and after
surgery (Burn Specific Health Scale – Brief (BSHS-B) will
reveal satisfaction (or not) in relation to the obtained results.
Fat injection as an ancillary treatment for scars, particularly
over joints or around tendons, will favor a decrease in fibrosis
as well as thinning the scar, allowing for increased malleability
and movement.
When using tissue expanders, we believe that preoperative
preparation with pre-conditioning of tight areas with saline
expansion is of paramount importance to achieve successful

483
Conclusions
Fig. 21.15  Examples of preoperative
preparation of ankle and anterior chest
sites. Please note “blanching” on the
left lower group and its disappearance
within 3 minutes.
Fig. 21.16  Pictorial examples of different patients
demonstrating graphically and in reality, “L”- or
“V”-shaped superposed tissue expanders.
expansion. Also, geometric gain and advance of the expanded
flap in multiple planes can be significantly increased when
superposed tissue expanders in a “C”, “L”, or “V” shape or
in a “fallen dominoes” fashion are used.
Breast reconstruction can be initiated at any time (in rela-
tion to scar age and patient age).
The objective of treatment of a person with burn injuries or
sequelae is the patient’s psychosocial reinsertion, restoring, or
allowing for the best possible quality of life within the treat-
ment results (Fig. 21.18).
The burned patient must be considered as a whole not just
as a patient with isolated injuries. We do not treat burn
wounds or burn sequelae, we treat the person with burn
wounds and burn sequelae.
(The use of these pictures for this purpose have been autho-
rized by the patients or by their families.)

484
SECTION III
CHAPTER 21 • Burn reconstruction
Fig. 21.17  Patient previously treated
with side-by-side expanders; on the
last expansion, we used superposed
tissue expanders allowing for a
exponentially greater advancement,
maintaining underlying breast shape,
and its natural vertical and horizontal
curvatures, without deformity or
retraction.
Fig. 21.18  (A) Patient 1 year after flame burn, at
age 10. (B) After 4 expansions, the last one with 2
+ 2 “L”-shaped superposed tissue expanders, to
each lateral chest, completing the removal of the
scar, allowing for the breast mold to show. Second
pregnancy at 7 months, with 2-year-old daughter
– both children were breastfed from both breasts.
A
B
13. Ware JEJ, Sherbourne CD. The MOS 36 item short-form health
survey (SF-36). Med Care. 1992;30:473–483. This is the most important
tool to evaluate quality of life in general. It has become a must to be able
to evaluate the patient as a whole, so one can continue with specific tools
and re-evaluate the effects of the results on the patient’s quality of life.
19. Kildal M, Anderson G, Fugl-Meyer AR, et al. Development of a
Brief Version of the Burn Specific Health Scale (BSHS-B). J Trauma.
2001;51:740–746. This is the most used tool to specific evaluate the burn
patient – acutely and after initial burn care, rehabilitation, and later on
the patient’s reinsertion phase.
Access the complete reference list online at

485
Conclusions
59. Janzekovic Z. Once upon a time… How West discovered East.
J Plast Reconstr Aesthet Surg. 2008;61:240–244. Professor Zora
Janzekovic was a pioneer in burn surgery, detailing tangential excision
in the early 1950s, and only some decades later it was accepted around
the world – everybody in burn care should know her history.
67. Barret JP, Herndon DN. Effect of burn wound excision on bacterial
colonization and invasion. Plast Reconstr Surg. 2003;111:744–750.
Drs Barret and Herndon demonstrate the benefits of excision on burn
wounds, indicating that it should be performed in full-thickness burns.
73. Heimberg LJ, Fauerbach JA, Spence RJ, Hackerman F. Psychologic
factors involved in the decision to undergo reconstructive surgery
after burn injury. J Burn Care Rehabil. 1997;18:374–380. Drs
Fauerbach and colleagues have longed worked on aiding the patient back
to normal life – this is a relatively early paper that indicates the need for
continued efforts in doing so, using the best available tools.
106. Engrav LH, Heimbach DM, Rivara FP, et al. 12 year within-wound
study of the effectiveness of custom pressure garment therapy.
Burns. 2010;36:975–983.
157. Salisbury RE. Reconstruction of the burned hand. Clin Plast Surg.
2000;27:65–69. Professor Roger Salisbury can be quoted as saying
“there is no cookbook” for reconstructing the burn hand (as in other
areas) and describes how the surgeon can/should act, aiming at, what
it was then called, “the preburn lifestyle of the patient” – he could be
more current!
163. Cartotto R, Cicuto BJ, Kiwanuka HN, et al. Common postburn
deformities and their management. Surg Clin North Am.
2014;94:817–837. Professor Cartotto describes a series of approaches to
scar bands and lines, with views in relation to laser use and more
aggressive options such as transplants.
199. Klinger M, Marazzi M, Vigo D, Torre M. Fat injection for cases of
severe burn outcomes: a new perspective of scar remodelling and
reduction. Aesth Plast Surg. 2008;32:465–469. Marco Klinger showed
very early the benefits and fat grafting on burn scars – although we use
it more frequently (smaller intervals) today, his initial study was a
guideline for several surgeons around the world.
217. Coleman SR. The technique of periorbital lipoinfiltration. Oper Tech
Plast Reconstr Surg. 1994;1:120–126. Every plastic surgeon should be
familiar with Coleman’s technique for harvesting and preparing fat for
injection aiming at the benefits of the adipose-derived stem cells
contained on the fat concentrate.
224. Pasyk KA, Argenta LC, Austad ED. Histopathology of human
expanded tissue. Clin Plast Surg. 1987;14:435–445. The novice will
understand what happens during tissue expansion, facilitating future use
planning and comprehension of expansion abilities.

485.e1
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SECTION III
CHAPTER 21 • Burn reconstruction
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181. Kreulen M, Mackie DP, Kreis RW, Groenevelt F. Surgical release
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182. Onah II. A classification system for postburn mentosternal
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183. Malhorta R, Sheikh I, Dheansa B. The management of eyelid
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184. Orgill DP, Ogawa R. Current methods of burn reconstruction. Plast
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186. Wyrzykowski D, Chrzanowska B, Czauderma P. Ten years later
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187. Desai S, Prashantha PG, Torgal SV, Rao R. Fatal pulmonary
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188. Borges AF. Historical review of the Z and W plasty. Revision of
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189. Ivy RH. Who originated the Z plasty? (Charles Pierre
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Plast Reconstr Surg. 2014;72:150–154.

SECTION III • Burns Surgery
22 
Cold and chemical injuries and
management of exfoliative disorders,
epidermolysis bullosa, and toxic  
epidermal necrolysis
Stephen Milner
SYNOPSIS
■ Frostbite: is historically an injury of wartime, but is becoming more
frequent among the civilian population. Management is focused on
rewarming, preventing ischemia reperfusion injury, decreasing hypoxia,
and dampening of inflammatory mediators. Definitive treatment is
delayed until demarcation of the necrotic tissue is readily apparent.
■ Chemical burns: these result in deeper injury than thermal burns.
Classification has traditionally been based upon the mechanism of
action. Clothing, gloves, and other items in contact with the skin
should be removed quickly to minimize contact with the chemical.
Definitive management through excision and skin grafting may be
necessary. We also propose a new classification with an emphasis on
treatment modality.
■ Toxic epidermal necrolysis: erythema multiforme, Stevens–Johnson
syndrome (SJS), and toxic epidermal necrolysis (TEN) are a
continuum of the same disease spectrum. They have significant
morbidity and mortality risks. The mainstay of treatment is early
wound debridement and protection as well as intensive care, which are
most appropriately managed in a burn center. Mucosal complications
are common, and early involvement of ophthalmology is crucial.
■ Epidermolysis bullosa: is a congenital blistering skin condition that
results from defects in the system anchoring epithelium to the
basement membrane. Meticulous wound care is imperative to
preventing long-term complications such as scar contracture and
syndactyly. In addition, squamous cell carcinoma is a long-term
complication.
Frostbite
Baron Dominique Larrey, Napoleon’s military surgeon, first
described treatment of frostbite during the invasion of Russia
in 1812. He recognized the importance of rewarming and the
injurious effects of the freeze–thaw–freeze cycle.1,2 In addition,
during WWI, Munroe introduced prophylactic measures to
prevent frostbite. However, the term “frost-bite” was first
used by R.H. Jocelyn Swan, in 1915, who described symptoms
of paresthesia and pain. He advocated painting the wounds
with 2% iodine solution and delaying amputation until there
was demarcation of necrotic and viable tissues.3 These recom-
mendations remain true today.
Pathophysiology
When
the
temperature
falls
below
15°C,
an
auto-
thermoregulatory response causes cycles of vasoconstriction
and vasodilation to preferentially decrease blood flow
intermittently to the extremities in order to maintain core
body temperature. Prolonged hypothermia leads to persistent
vasoconstriction resulting in hypoxia, acidosis, stasis of blood
flow, and ultimately thrombosis.1,4
When tissue freezes, multiple mechanisms are initiated
that synergistically compound the injury. The formation of
extracellular ice crystals causes damage to cell membranes
resulting in a change in the osmotic gradient, leading to
intracellular dehydration and cell death. As the tissue tem-
perature continues to fall, formation of intracellular ice crystals
mechanically damages cells.1,4 Additionally, progressive
dermal ischemia causes endothelial injury, tissue hypoxia,
and thrombosis of blood vessels, which leads to a massive
inflammatory response (Fig. 22.1). This triggers the release
of prostaglandins and thromboxanes, which lead to further
vasoconstriction, platelet aggregation, and thrombosis.1,4
Treatment should be aimed at prevention, rewarming, increas-
ing blood flow, and blocking the release of inflammatory
mediators.
Clinical manifestations
Peripheral parts of the body, namely hands, feet, ears, nose,
and cheeks, are affected by frostbite.2 Risk factors include
alcoholism, being in the age group of 30–49 years, improper
clothing, homelessness, infection, diabetes, and smoking.
Frostbite can be can be classified as superficial or deep. In
superficial cases it presents clinically as numbness, a central
white plaque with surrounding erythema, or as blisters filled

487
Frostbite
made with the use non-steroidal anti-inflammatory drugs
(NSAIDs) and topical agents. Oral ibuprofen provides sys-
temic anti-prostaglandin activity, and topical Aloe vera, a
thromboxane synthetase inhibitor, can be applied to the
wounds. Injured extremities should be splinted and elevated
to minimize swelling. Prophylactic antibiotics are not indi-
cated, and tetanus toxoid should be administered according
to standard guidelines.
Immediate amputation should be avoided in order to allow
for proper demarcation of the wound. It is usual to wait a
period of more than 6–12 weeks for demarcation to become
apparent unless the patient develops wet-gangrene or sepsis
(Fig. 22.2).
Adjunctive therapies
Thrombolytic therapy has been shown to be a relevant treat-
ment option and multiple studies have been published on the
effectiveness of tissue plasminogen activator (rTPA). A reduc-
tion in digital amputation rates from 41% to 10% in those
patients receiving rTPA within 24 h of injury was reported by
Bruen et al.1,5
Summary
Frostbite, originally thought to be a disease of wartime, is
commonly seen in the civilian population. The pathogenesis
involves several synergistic mechanisms including intra- and
extracellular ice crystal formation, cell membrane rupture,
with clear fluid. Blisters usually develop within the first 24 h.
Deep frostbite manifests as bluish-purple discoloration and
hemorrhagic blisters (Fig. 22.1) that result in a hard, black
eschar and necrosis. Symptoms range from numbness, throb-
bing pain, and paresthesia to sensory loss and increased cold
sensitivity.4
Management
Before warming measures are implemented to the affected
areas, hypothermia must be corrected to a core temperature
above 35°C.5 The frostbitten area should be placed in a water
bath set at 38°C with an antiseptic solution. Optimal thawing
varies from 15 min to 1 h. Once the affected tissue becomes
pliable and appears a red/purple color, rewarming should be
stopped. As rewarming can be extremely painful, adequate
analgesia should be prescribed.
There is no convincing literature on the appropriate man-
agement of blisters with regard to drainage. Our protocol is
to debride the clear blisters and leave hemorrhagic ones intact.
An attempt to counter the inflammatory reaction should be
A
Fig. 22.1  Bluish-purple discoloration consistent with deeper injury.
B
Fig. 22.2  Demarcation of viable and non-viable tissue 6 weeks after initial injury.
A
B

488
SECTION III
CHAPTER 22 • Cold and chemical injuries; exfoliative disorders, epidermolysis bullosa, and TEN
and ischemia reperfusion injury. Classifications are similar to
those described in burn injury, i.e., superficial and deep.
Management should be focused on prevention, rewarming,
augmenting blood flow to decrease hypoxia, and inhibiting
the inflammatory response. In order to maximally preserve
tissue, definitive treatment should be delayed until demarca-
tion is seen between necrotic and viable tissue.6–9
Chemical burns
Incidence
Chemical burns represent the second most common cause of
hospital admission for patients with burns, second to thermal
injury.10 Although they represent a small proportion of burns,
approximately 10%, they account for up to 30% of all burn-
related deaths.11 The majority of patients are men, and acids
are the more common causative agents. Most take place in the
industrial setting; however; the incidence of domestic cases
has increased nearly three times in the last 20 years. Cement
burns make up approximately one-quarter of all chemical
burns.11,12 Factors that may influence the extension of the
chemical burn include the physical state of the chemical
(liquid, solid, or gas), mechanism of action (acid, base, or
another), concentration, strength (extreme pH < 2 or > 12), and
duration of exposure.10,12,13
Pathophysiology
Both chemical and thermal injuries involve denaturing of
proteins, and the wounds are often similar in appearance.
Whereas thermal injuries are produced by short-term expo-
sure to intense heat, chemical injuries are produced by con-
tinued exposure. Current classification dates back to 1974 to
the work of Carl Jelenko III, whereby chemicals were placed
in six broad categories based upon mechanism of action:
reducing agents, oxidizing agents, corrosive agents, proto-
plasmic poisons, desiccants/vesicants, and acids/bases.13 We
suggest a practical alternative whereby agents are listed as
acids, alkalis, those with specific antidotes, elemental metals,
vesicants, and inorganic compounds.
Treatment
A thorough history is essential to ascertain the responsible
agent and therefore expedite prompt treatment. All involved
clothing should be removed. Early and copious irrigation
with water has been shown to reduce the severity and the
length of hospital stay for most chemical injuries. The same
principles as those for thermal burns apply to the treatment
of chemical burns. Early excision and grafting of non-viable
tissue is advocated.12
Acids
Acids cause coagulation necrosis, which produces rapid tissue
changes including consolidation of loose connective tissue,
thrombosis of intramural blood vessels, ulceration, fibrosis,
and hemolysis of red blood cells. They typically produce a dry
eschar of varying colors from black to yellow, and treatment
includes removing any visible chemical and copious water
lavage.
Hydrochloric acid
Hydrochloric acid protonates skin proteins into chloride salts.
The acid will continue to denature protein as long as it is in
contact with the skin.
Sulfuric acid
Sulfuric acid has many industrial uses including lead–acid
batteries, fertilizer, and wastewater processing. It is highly
corrosive and causes damage via tissue dehydration and heat
production. The skin is blackened, forming a hard dry eschar
under which ulcers may form.
Chromic acid
Chromic acid is commonly used in the cleaning of other
metals. This pungent, viscous, yellow liquid is made up of the
active chemical metabolite chromic trioxide (CrO3) in a solu-
tion of strong sulfuric acid. Contact leads to protein coagula-
tion, blister formation, and ulceration. It reaches peak serum
levels by 5 h postinjury. Once in circulation, CrO3 binds
to hemoglobin and undergoes parenchymal uptake by the
kidneys, liver, bones, lungs, and spleen within the first 24 h.
It can be toxic to the kidney, leading to renal failure. Ingestion
causes gastroenteritis, vertigo, muscle cramps, and potentially
death. The lethal dose is 5–10 g. Primary treatment consists of
water lavage with a dilute solution of sodium hyposulfite,
followed by a rinsing with buffered phosphate solution made
up of 70 g of monobasic potassium phosphate and 180 g of
dibasic sodium phosphate in 850 mL of water. Systemic
manifestations are treated with 4 mg/kg of 2,3-dimercapto-1-
propanol given intramuscularly every 4 h for the first 48 h
followed by 2 mg/kg daily for 1 week.
Alkalis
Alkalis such as lime, sodium hydroxide, and potassium
hydroxide are common in household-cleaning solutions. The
mechanism of injury includes saponification of fat, dehydra-
tion of cells, and dissolving of proteins.12
Sodium hypochlorite
Sodium hypochlorite, household bleach, is a common cause
of chemical burns. It is a potent oxidizing agent in a strong
alkaline solution that causes protein coagulation. The active
metabolite is hypochlorous (OCL-), and toxicity arises from
its corrosive activity on skin and mucous membranes. The
severity of the injury is mostly dependent upon the concentra-
tion of the solution as opposed to the duration of exposure.
As little as 30 mL of 15% available chlorine concentration may
be lethal. Acid antidotes are not appropriate as they enhance
the release of chlorine.13 (See Fig. 22.3.)
Cement (calcium hydroxide)
Cement burns are a common injury that is classically seen
in patients kneeling in concrete. There are many constitu-
ents of cement; however, calcium oxide accounts for 65% of
the content in the most common mixtures. It acts as both
a desiccant and an alkali. Injury is caused when calcium
oxide reacts with water to become calcium hydroxide, which
causes liquefaction necrosis. Treatment consists of removing
all of the cement and clothing soaked in cement, followed by

489
Chemical burns
to potentially fatal arrhythmias.16,17 Treatment includes irriga-
tion, debridement, and application of a topical 2.5–5% calcium
gluconate gel to the affected area to neutralize the free fluo-
ride. The gel applications are continued every 4–6 h for 3–4
days.17 Treatment is deemed successful if pain is relieved. (See
Fig. 22.4.)8
Cover with oil
Phenol
Phenol is derived from coal tar. It was discovered in 1834 and
initially used for the treatment of sewage. It is an aromatic
hydrocarbon with antiseptic properties. Its antiseptic action
was first demonstrated by Lemaire in France in 1864 and
Lister in Scotland in 1867. It was initially recommended as an
antiseptic agent used in the operating room. In addition, Koch
demonstrated the germicidal action of phenol in 1881. Despite
showing initial promise, its role in medicine has become quite
limited to chemical face peels, nerve injections, and topical
anesthetics.
Acute phenol poisoning can occur by absorption through
the skin, and it has been shown that irrigation with copious
amounts of pure water allows for decontamination. Histori-
cally, phenol poisoning was treated with undiluted polyeth-
ylene glycol (PEG), which is still the best solvent. However,
setting up and treating using repeated sponging with lap pads
soaked in PEG can be time consuming. It is now recommended
to start irrigation with water while preparing for sponging
with PEG.
White phosphorus
White phosphorous is a yellow, waxy, translucent solid that
is used in a lot of weapons such as hand grenades and bombs
as well as in insecticides and fertilizers. On contact with the
skin it begins burning until it is oxidized or starved of oxygen
by immersion in water. It causes tissue injury by oxidizing
adjacent tissue, causing protein denaturation, and generating
a considerable amount of heat. Therefore it causes both chemi-
cal and thermal injury. The wounds are typically painful,
necrotic, yellow, and smell of garlic (Fig. 22.5).9 Treatment
includes removing all clothing, irrigating the area with saline
or water, and removing any visible particles. The wounds
should then be treated with saline or water soaked dressings
irrigation with water, and dressing with topical antimicrobial
creams.14,15
Those with specific antidotes
Calcium salts
Hydrofluoric acid burns
Hydrofluoric acid is commonly used in rust removers and
heavy-duty cleaners and has a dual mechanism on injury. It
produces direct corrosion of tissue due to production of free
hydrogen ions. Fluoride ions then bind to calcium and mag-
nesium to form insoluble salts, leading to life-threatening
hypocalcemia and hypomagnesemia. They inhibit NA-K
ATPase, leading to a massive potassium efflux, and they cause
direct activation of myocardial adenylate cyclase, which leads
Fig. 22.3  A typical example of a cutaneous burn to the bilateral lower extremities
caused by bleach.
A
B
Fig. 22.4  Hydrofluoric acid burn to fingers.

490
SECTION III
CHAPTER 22 • Cold and chemical injuries; exfoliative disorders, epidermolysis bullosa, and TEN
Lewisite
Lewisite (2-chlorovinyl-dichloroarsine) is associated with
immediate eye irritation and sneezing, salivation, and lacri-
mation. Non-lethal, chronic exposure may lead to arsenical
poisoning.
Mustard gas
Early symptoms of mustard gas exposure include ocular
burning and a sensation of suffocation. Erythema is seen after
4 h, and by 12–48 h blistering of the skin may occur accom-
panied by severe pruritus of the axilla and perineum. The
blisters tend to rupture, releasing amber colored serous fluid,
and result in painful, shallow ulcers. Greater exposure leads
to coagulative necrosis of the skin, corneal erosion, and nec-
rotizing bronchitis.
Halogenated oximes
Exposure to phosgene oxime has the immediate effect of
stinging. Within seconds, the affected area swells and begins
to blister. An eschar forms after 1 week; however, the healing
is often delayed for more than 2 months. It is extremely
painful if the eyes are affected and may result in blindness.
Inhalation leads to hypersecretion and pulmonary edema.
Treatment
Treatment of vesicants begins with removal of all clothing and
lavage of the exposed areas with copious amounts of water.
Those taking care of an exposed patient should be protected
suitably, and all contaminated clothing must be placed in
special bags. Blisters should be unroofed and dressed with
topical antimicrobials. However, silver sulfadiazine is incom-
patible with dimercaprol, which is a chelating agent that is a
specific antidote for lewisite poisoning. The mustard blister
fluid is harmless, but there is no antidote for mustard poison-
ing and affected eyes should be irrigated and treated with
antibiotics.12
Summary
Chemical burns, although uncommon, can cause serious
harm and are frequently fatal. A standard approach to treat-
ment includes removal of any involved clothing and copious
irrigation. It should be kept in mind that some chemicals have
specific antidotes.
Management of exfoliative disorders,
epidermolysis bullosa, and toxic
epidermal necrolysis
Erythema multiforme (EM), Stevens–Johnson syndrome (SJS),
and toxic epidermal necrolysis (TEN) once described as sepa-
rate entities, are now considered a continuum of bullous
disease syndromes differentiated only by the degree of epi-
dermal detachment. EM is a cutaneous hypersensitivity
reaction and is subclassified into minor and major forms.
EM minor is characterized by dusky erythematous “target”
lesions, which are symmetrically distributed on the extensor
surfaces of the limbs as well as the palms and soles of the feet.
and kept moist. Specific treatment includes irrigation with
0.5% copper sulfate. Copper sulfate causes the formation of a
black film of cupric oxide on the surface above the embedded
agent. This cupric oxide acts to impede oxidation and allows
for identification and removal of the white phosphorus.18
Others
Alkyl mercury agents
These compounds, such as ethyl and methyl mercuric phos-
phates, are primarily irritants; however, they may become
erythematous and blister, which may progress. Free mercury
within blisters can be absorbed and cause systemic effects.
They should therefore be debrided prior to washing with soap
and water and copious lavage. Systemic mercurial poisoning
is treated with chelating agents.
Elemental metals: metallic lithium, sodium,
potassium, or magnesium
Elemental metals are a rare exception to the water lavage
protocol. Applying water to these elements causes ignition
and leads to further thermal injury. Mineral oil should be used
to first coat the patient, followed by water lavage to remove
the particles of chemical embedded in the skin.
Vesicants
A vesicant is an agent that produces vesicles or blisters. They
were first used as a chemical warfare agent during WWI and
include nitrogen mustards, sulfur, lewisite, and halogenated
oximes. Severe exposure may lead to agranulocytosis or
aplastic anemia.12
Fig. 22.5  Phosphorus burn to the back.

491
Management of exfoliative disorders, epidermolysis bullosa, and toxic epidermal necrolysis
that TEN keratinocytes express lytically active FasL and
that the ligation of keratinocyte-expressed Fas leads to
apoptosis.
Cytotoxic T cells
The role of cytotoxic T cells occurs via granule-mediated
exocytosis of perforin and granzyme B. It was previously
thought that certain reactive drug metabolites induce a cell-
mediated cytotoxic immune response against the epidermis.
However, studies have shown that CD8+ T cells from the
blister fluid of patients with TEN reacted without restimula-
tion by the parent drug, but not against the metabolite.
Cytotoxic T cells kill autologous keratinocytes in a drug-
specific, perforin/granzyme-mediated pathway. Granulysin,
a cytolytic protein, which is produced by drug specific
CD8+ T cells and natural killer cells, has been identified as
an important factor for epidermal destruction. Its concentra-
tions in the blister fluid of TEN patients were four times
higher than those of other cytotoxic proteins. It was found
that by depleting granulysin, cytotoxicity was also greatly
reduced.24,25
Cytokines
Nassif et al. also contributed to the role of Fas–FasL interac-
tion. They found higher concentrations of IFN-γ, TNF-α, and
serum FasL in blisters of TEN patients than in control blister
fluid from burn patients. IFN-γ increases TNF-α and serum
FasL levels and causes keratinocyte activation. Fas expression
is not found on all subcorneal layers, but only on the epider-
mal basal keratinocytes.23
CD8+ T lymphocytes and macrophages that appear within
the epidermis are believed to mediate an autoimmune
response. Certain cytokines like TNF-α, which has been
identified within TEN blister fluid, are thought to contribute
to epidermal cell injury. Apoptosis, which occurs through
many different mechanisms, appears to be the final common
pathway of keratinocyte death.24,25
Blisters and bullae may or may not be present. EM major is
similar but includes the mucosal surfaces, most often the
mouth.19
SJS was initially reported in 1922 by American physicians,
Stevens and Johnson, who described an acute mucocutaneous
syndrome in two children who presented with cutaneous
lesions, stomatitis, and conjunctivitis. EM major has charac-
teristic target lesions that present in a symmetric acral distri-
bution and has a low morbidity and no mortality, whereas SJS
involves more widespread and central areas of skin and has
a high morbidity and occasional mortality.20
TEN is the most severe form of the exfoliative disorders
and is defined by the extent of the cutaneous involvement.
TEN, like EM major and SJS, also features mucosal involve-
ment and has a high associated morbidity and mortality.20,21
TEN was first characterized in 1956 by Lyell who described
four patients with skin blistering. Currently, SJS and TEN
represent a spectrum of acute life-threatening mucocutaneous
reactions,20 and they manifest histologically as disruption of
the dermal–epidermal junction. Involvement of more than
30% of the total body surface area defines TEN, whereas with
SJS less than 10% of the total body surface area is involved.
An associated prodromal phase, consisting of fever, malaise,
and flu-like symptoms, may occur after exposure to the incit-
ing agent. The syndrome may involve the mucosal surfaces
of the oropharynx, eyes, gastrointestinal tract, and tracheo-
bronchial tree. Nikolsky’s sign, the separation of the epidermis
with moderate digital pressure, may be present. Drug expo-
sure is the cause of 80% of TEN cases.22 The average mortality
rates for SJS and TEN are 1–5% and 25–35%, respectively.20,22
Epidemiology
SJS/TEN occurs rarely with an incidence rate quoted as 1–2
cases per million per year. They occur more frequently in
women, and the incidence increases with age. Certain patient
populations are at increased risk including certain types of
cancer, collagen vascular disease, and human immunodefi-
ciency virus.19,20
Medications are the causative agent in the majority of cases
with more than 100 drugs implicated. Certain high-risk medi-
cations have been identified and include sulfonamides, anti-
convulsants, allopurinol, and NSAIDs.
Pathophysiology
Epidermal cell death has been shown to result from epidermal
cell apoptosis. Proposed mechanisms involve Fas–FasL inter-
action, release of perforin and granzyme B from cytotoxic T
lymphocytes, and overproduction of T cell and macrophage
derived cytokines including interferon-gamma (IFN-γ) and
tumor necrosis factor-alpha (TNF-α).23–25 (See Fig. 22.6.)
Fas–FasL interaction
Epidermal cells express Fas on their cell surfaces. Fas ligand
(FasL) is expressed on T cells and natural killer cells. Viard
et al., in their landmark study in 1988, showed that serum
FasL elevation and FasL expression in the skin biopsy
specimens were present in patients with TEN and not in those
with drug-induced maculopapular rash or healthy controls.
It is thought that the serum FasL is due to the cleavage of
membrane-bound FasL on epidermal cells. They concluded
Fig. 22.6  Suggested pathophysiology of Stevens-Johnson syndrome/toxic
epidermal necrolysis (SJS/TEN). Cytotoxic T lymphocytes (CTLs) are activated
through antigen presentation by the antigen-presenting cell (APC). Cellular immune
reactions are directed at keratinocytes in a major histocompatibility class (MHC)
1-restricted manner. Activation of CTLs leads to production of various cytotoxic
proteins, including granulysin, perforin/granzyme B, Fas/Fas ligand, and cytokines,
which induce keratinocyte apoptosis and cell death. IFN-γ, interferon-gamma;
TNF-α, tumor necrosis factor-alpha; ROS, reactive oxygen species.
APC/
MHC 1
CTL
Perforin/granzyme B
Keratinocyte
apoptosis/cell death
Granulysin
TNF-α
IFN-γ
Fas/Fas ligand
ROS

492
SECTION III
CHAPTER 22 • Cold and chemical injuries; exfoliative disorders, epidermolysis bullosa, and TEN
the most commonly involved, causing severe pain, dysphagia,
and odynophagia and bleeding. Perhaps ophthalmologic
involvement is the most sinister form with conjunctival adhe-
sion and scarring, corneal ulceration and perforation, and
blindness. Genital, anorectal, and esophageal involvement
can also occur.26
Treatment
Current recommendations include cessation of causative
medications, early transfer to a burn center, and tissue diag-
nosis by full-thickness punch biopsy. Extensive involvement
of oral mucosa may require airway protection with intuba-
tion. Systemic corticosteroids and empiric prophylactic anti-
biotics have not been demonstrated to be of value. IVIG has
been studied as this blocks in vitro interaction of the Fas recep-
tor with FasL, an interaction that induces apoptosis, thus
preventing keratinocyte death. Initial reports were favorable
with higher survival rates; however, recent studies have not
been able to replicate those results.21,27,28 Wounds should be
treated with biologic, biosynthetic, or silver impregnated
dressings to decrease their frequency. Early enteral nutrition
is recommended. Ophthalmologic consultation is recom-
mended for patients with conjunctival involvement.
Some practitioners find the clinical scoring system known
as SCORTEN (SCORE of TEN) to be helpful in predicting
mortality. It is based on the following prognostic factors: age
>40 years, malignancy, total body surface area detached,
tachycardia >120 beats/min, serum urea >10 mmol/L, glucose
>250 mg/dL, and serum bicarbonate <20 mmol/L. Recent
studies show that day 3 scoring showed the best correlation
with patient survival.29
Summary
EM, SJS, and TEN are all part of a spectrum of bullous dis-
eases. Treatment should be aimed at keeping wounds clean
and dry, minimizing dressing changes, and supportive ICU
level of care. Although IVIG has been suggested to be helpful
in vitro, clinical reports fail to show similar results.
Epidermolysis bullosa
Epidermolysis bullosa (EB) represents a group of inherited
bullous disorders involving blistering of the skin due to
mechanical trauma. Subtypes are classified according to both
the morphologic features of the skin as well as the zone of the
basement membrane involved. There are four common forms
described: epidermolysis bullosa simplex, recessive dystro-
phic epidermolysis bullosa, recessive junctional epidermolysis
bullosa, and hemidesmosomal epidermolysis bullosa.
Epidemiology
EB occurs in 50 per million live births. The hallmark is the
formation of large, fluid-filled blisters that occur in response
to minor trauma, at birth or shortly thereafter. Blisters form
more commonly over weight-bearing surfaces and anatomic
areas of high wear and tear. This rare genetic disorder affects
all ethnic groups and races equally, and affects more than
100 000 Americans. The most common form is due to epider-
molysis bullosa simplex (90% of cases), the next is due to
recessive dystrophic epidermolysis bullosa (5% of cases), and
Clinical manifestations
Patients often initially present with fever and flu-like symp-
toms. Pain typically precedes cutaneous manifestations by a
few days. Macular eruptions appear first on the face and trunk
and then quickly spread throughout the rest of the body. The
lesions are flat, atypical targets or red, pupuritic macules. The
lesions evolve into flaccid blisters that result in extensive
sloughing of skin. Mucous membrane involvement may
precede or follow skin lesions and is almost always present.
Mucosal lesions begin with erythema and progress to erosions
and ulcers. Respiratory epithelium is involved in 25% of
patients with TEN. This may progress to acute respiratory
distress syndrome. The airway may also become acutely
compromised due to severe oral lesions and copious secre-
tions.20 (See Figs. 22.7 & 22.8.)
Mucosal involvement
Mucosal involvement involves blistering, sloughing, and
erosion of all mucosal surfaces. The lips and oropharynx are
Fig. 22.7  A patient with acute blistering in toxic epidermal necrolysis (TEN).
Fig. 22.8  A patient with resolving toxic epidermal necrolysis (TEN).

493
Management of exfoliative disorders, epidermolysis bullosa, and toxic epidermal necrolysis
abnormalities. Mucus membranes may be affected and result
in strictures.
Hemidesmosomal epidermolysis bullosa
Hemidesmosomal epidermolysis bullosa (HEB) produces
blistering at the hemidesmosomal level in the most superior
aspect of the basement membrane. The underlying common
mechanism is that defects in the anchoring system of the
epithelial tissues allow detachment, at a variable level, of the
skin with trauma.
Treatment
Management is limited to wound care and attempts to mini-
mize trauma. Avoidance of adhesives and compressive dress-
ings is important for prevention of blister formation. Future
therapies are aimed at molecular-based curative therapies.
Current research strategies being investigated include gene
therapy, fibroblast cell therapy, bone marrow stem cell therapy,
and protein therapy.30–36 Apligraf, a bilayered skin equivalent
derived from human keratinocytes and dermal fibroblasts
from neonatal foreskin, has shown favorable results.
Summary
EB represents a variety of rare, inherited bullous diseases. The
varying subtypes range from recurrent, small wounds to joint
contracture, strictures, and skin cancer. Management is aimed
at local wound care as well as minimization of traumatic
injury.
the last is due to junctional epidermolysis bullosa (1% of
cases).30,31
Epidermolysis bullosa simplex
Epidermolysis bullosa simplex (EBS) is defined as intraepi-
dermal skin separation. Dominantly inherited, EBS is not
associated with extracutaneous involvement. Fortunately,
lesions usually heal without scarring. The Weber–Cockayne
subtype is the most common form and is usually precipitated
by a traumatic event. The lesions tend to be mild and fre-
quently occur on the palms and soles of the feet and may be
accompanied by hyperhidrosis. A more severe form may be
characterized by generalized onset of blisters at birth.
Dystrophic epidermolysis bullosa
Dystrophic epidermolysis bullosa (DEB) represents a group
of diseases caused by a defect in the anchoring fibrils. There
may be dominant or recessive inheritance.
Recessive dystrophic epidermolysis bullosa (RDEB) is
due to mutations in the COL7A1 gene and is characterized
by skin separation in the lamina lucida or central base-
ment membrane. Characteristics of RDEB include chronic
blistering, decreased wound healing, joint contractures,
and strictures of the esophagus, pseudosyndactyly (mitten
hand deformity), corneal abrasions, and a shortened lifes-
pan30 (Fig. 22.9). Flexion contractures of the extremities are
common as well as nail and teeth involvement. Involvement
of the internal mucosa may result in esophageal strictures,
urethral and anal stenosis, phimosis, and corneal scarring.
Malabsorption may occur and result in failure to thrive.
Sequelae include life-threatening infections and develop-
ment of squamous cell carcinoma. Skin cancer occurs
most commonly in patients aged 15–35 years old and is
the most common cause of death in patients who survive
childhood.31
Recessive junctional epidermolysis bullosa
Recessive junctional epidermolysis bullosa (RJEB) occurs at
the sublamina densa within the basement membrane. RJEB
may be divided into lethal and non-lethal subtypes. Lethal
junctional epidermolysis bullosa is characterized by general-
ized blistering at birth and is due to a defect in the expression
of the anchoring filament glycoprotein laminin 5. The blisters
present with involvement of the mouth, eyes, and nares
and often have significant hypertrophic granulation. Severe
corneal, tracheobronchial, oropharyngeal, esophageal, rectal,
and genitourinary mucosa may be involved. Patients do not
survive past infancy. Non-lethal junctional epidermolysis
bullosa manifests as generalized blistering that clinically
improves with age. There may also be scalp, nail, and tooth
Fig. 22.9  An example of pseudosyndactyly in a patient with recessive dystrophic
epidermolysis bullosa (RDEB).
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4. Reamy BV. Frostbite: review and current concepts. J Am Board Fam
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494
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