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

390
SECTION II
CHAPTER 17 • Perineal reconstruction
complication rate ultimately led the manufacturer to with-
draw the device from the US market in 1999.48 Evolution
of this approach has continued in Europe where the device
is still available, but one meta-analysis has shown more
favorable results using an artificial bowel sphincter (Acticon
Neosphincter™, American Medical Systems, Minnetonka,
MN).49 All methods of sphincter preservation or reconstruc-
tion carry a significant (30–100%) risk of complications,
and a consensus is still not available on the best of these
alternatives. Despite these newer options, in a recent review
the traditional abdominal colostomy has been advocated
as still having the lowest complication rate for this group
of patients.
Postoperative care
The management of these patients follows the basic tenets of
surgical postoperative care. A key principle is to avoid exces-
sive pressure on the flap, as this can lead to venous congestion
and flap loss. The authors have the patients on bed-rest for
several days, followed by progressive ambulation. However,
the patients are instructed not to sit upright for several weeks.
Drains are typically placed in both the donor site and the
perineum. Deep venous thromboprophylaxis in the form of
sequential compression devices and subcutaneous heparin is
used. Nutrition must be optimized. The patient is seen regu-
larly by all involved teams postoperatively.
2000.46 In their transperitoneal approach, the rectus is har-
vested by taking down the posterior sheath. Therefore no
incisions were made in the anterior sheath, decreasing the risk
of hernia formation. More recently, Winters et al. reported on
the results of robotic total pelvic exenteration in conjunction
with a laparoscopic harvested rectus flap.47 Yet another
advancement is the use of the robot in rectus flap harvest.
Selber reported their experience with the Intuitive Surgical
robot, with harvest times of 45 minutes and incisions limited
to 3 ports, totaling 2 inches in length.54 As experience builds
in other disciplines with minimally invasive techniques, it is
likely that flap harvests will continue to be refined in plastic
surgery as well.
Special considerations –
sphincter reconstruction
For treatment of rectal cancers in patients seeking to avoid
colostomy, some centers have advocated resection with
sphincter reconstruction as a strategy. In such cases, functional
transfer using one or two gracilis muscles wrapped around
a perineal colostomy has been described with some
success, although the morbidity of this approach is high.55
Early authors in the 1950s encountered issues generating
resting sphincter tone when using a voluntary muscle
to perform an autonomic smooth muscle function. This
was addressed using an implantable electrical stimulator
(electrically stimulated dynamic graciloplasty), but a high
Fig. 17.18  Perforating vessels in the vicinity of the
perineum. Several flaps shown based on internal or
external pudendal vessels, and the profunda femoris and
medial circumflex femoral vessels. EPAP, external
pudendal artery perforator; IPAP, internal pudendal artery
perforator; MCFAP, medial circumflex femoral artery
perforator; PAP, profunda artery perforator.
External pudendal artery
Internal pudendal artery
Profunda artery
(deep femoral artery)
Medial circumflex femoral artery
Gracilis muscle
Adductor magnus
muscle
EPAP flap
A
B
C
MCFAP flap
PAP flap
IPAP flap

391
Outcomes, prognosis, complications
In contrast, when flaps are used, the small bowels are sepa-
rated from the radiated pelvic basin, which dramatically
reduces or eliminates all these major sequelae in every major
series.18,19,29,50 Complications remain at a significant incidence
of 5–33% overall, but these manifest a shift toward minor
complications. Still present are delayed wound healing at the
inset incisions, seromas, or superficial dehiscence or infection,
but none of these normally requires re-operation. Understand-
ing the vulnerabilities of the surgical site and the clinical
outcome data makes it possible to employ a reconstructive
plan that can limit complications and make perineal recon-
struction a relatively safe, reliable process.
Outcomes, prognosis, complications
It is important to emphasize that reconstruction of the
perineum cannot eliminate complications. In fact, multiple
series highlight complications even in the best of circum-
stances; what has improved with advances in the state of
surgical treatment has been the complication profile. In
earliest descriptions, extensive abdominoperineal resections
and exenterations were accompanied by significant mortality,
small bowel obstruction, small bowel fistulae, pelvic abscesses,
perineal hernias, and profound interstitial fluid losses through
what frequently became a chronic draining perineal wound.
11. Wee JT, Joseph VT. A new technique of vaginal reconstruction using
neurovascular pudendal-thigh flaps: a preliminary report. Plast
Reconstr Surg. 1989;83:701–709.
18. Nelson RA, Butler CE. Surgical outcomes of VRAM versus thigh
flaps for immediate reconstruction of pelvic and perineal cancer
resection defects. Plast Reconstr Surg. 2009;123:175–183. The largest
series of prospectively collected cases comparing abdominal vs thigh flap
reconstruction in perineal reconstruction, demonstrating most favorable
complication profile after abdominal flap use (M.D. Anderson Cancer
Center).
19. Butler CE, Gündeslioglu AO, Rodriguez-Bigas MA. Outcomes of
immediate vertical rectus abdominis myocutaneous flap
reconstruction for irradiated abdominoperineal resection defects.
J Am Coll Surg. 2008;206:694–703. Documented improvement in
outcomes using flaps in radiated perineal reconstruction.
20. Shibata D, Hyland W, Busse P, et al. Immediate reconstruction of
the perineal wound with gracilis muscle flaps following
abdominoperineal resection and intraoperative radiation therapy
for recurrent carcinoma of the rectum. Ann Surg Oncol. 1999;6:33–37.
Early evidence that flaps can reduce complication rate from 46% to 12%
in radiated perineal reconstruction.
29. Chessin DB, Hartley J, Cohen AM, et al. Rectus flap reconstruction
decreases perineal wound complications after pelvic
chemoradiation and surgery: a cohort study. Ann Surg Oncol.
2005;12:104–110. Documented improvement in outcomes using abdominal
flaps in radiated perineal reconstruction (Memorial Sloan-Kettering
Cancer Center).
31. Lee MJ, Dumanian GA. The oblique rectus abdominis
musculocutaneous flap: revisited clinical applications. Plast Reconstr
Surg. 2004;114:367–373. Variation in skin paddle design, expanding the
size and the reach of the rectus abdominis myocutaneous flap.
34. Whetzel TP, Lechtman AN. The gracilis myofasciocutaneous flap:
vascular anatomy and clinical application. Plast Reconstr Surg.
1997;99:1642–1652, discussion 1653–1655.
38. Wong S, Garvey P, Skibber J, Yu P. Reconstruction of pelvic
exenteration defects with anterolateral thigh-vastus lateralis muscle
flaps. Plast Reconstr Surg. 2009;124:1177–1185.
51. Lefevre JH, Parc Y, Kernéis S, et al. Abdomino-perineal resection for
anal cancer impact of a vertical rectus abdominis myocutaneus flap
on survival, recurrence, morbidity, and wound healing. Ann Surg.
2009;250:707–711.
Access the complete reference list online at

391.e1
References
References
1. Miles WE. Radical abdomino-perineal operation for cancer of
rectum and of pelvic colon. Br Med J. 1910;2:941.
2. Brunschwig A. Complete excision of pelvic viscera for advanced
carcinoma; a one-stage abdominoperineal operation with end
colostomy and bilateral ureteral implantation into the colon above
the colostomy. Cancer. 1948;1:177–183.
3. Altmeier WC, Culbertson WR, Alexander JW, et al. Primary closure
and healing of the perineal wound in abdominoperineal resection
of the rectum for carcinoma. Am J Surg. 1974;127:215–219.
4. Anderson R, Turnbull RB. Grafting the unhealed perineal wound
after coloproctectomy or Crohn disease. Arch Surg. 1976;111:
335–338.
5. Mathes SJ, Vasconez LO, Jurkiewcz MJ. Extensions and further
applications of muscle flap transposition. Plast Reconstr Surg.
1977;60:6–10.
6. Shaw A, Futrell JW. Cure of chronic perineal sinus with gluteus
maximus flap. Surg Gynecol Ostet. 1978;147:417–420.
7. Tobin GR, Day TG. Vaginal and pelvic reconstruction with distally
based rectus abdominis myocutaneous flaps. Plast Reconstr Surg.
1988;81:62–73.
8. Kroll SS, Pollock R, Jessup JM, Ota D. Transpelvic rectus abdominis
flap reconstruction of defects following abdominal-perineal
resection. Am Surg. 1989;55:632–637.
9. Palmer JA, Vernon CP, Cummings BJ, Moffat FL. Gracilis
myocutaneous flap for reconstructing perineal defects resulting
from radiation and radical surgery. Can J Surg. 1983;26:510–512.
10. Woods JE, Beart RW. Reconstruction of nonhealing wounds with
gracilis muscle flaps. Ann Plast Surg. 1983;11:513–516.
11. Wee JT, Joseph VT. A new technique of vaginal reconstruction using
neurovascular pudendal-thigh flaps: a preliminary report. Plast
Reconstr Surg. 1989;83:701–709.
12. Yu P, Sanger JR, Matloub HS, et al. Anterolateral thigh
fasciocutaneous island flaps in perineoscrotal reconstruction. Plast
Reconstr Surg. 2002;109:610–616.
13. Wang X, Qiao Q, Burd A, et al. Perineum reconstruction with
pedicled anterolateral thigh fasciocutaneous flap. Ann Plast Surg.
2006;56:151–155.
14. Vogt PM, Kall S, Lahoda LU, et al. The free “mutton chop” flap: a
fascio-musculocutaneous flap for the reconstruction of the entire
sacral and perineal area. Plast Reconstr Surg. 2004;114:1220–1224.
15. Wong DS. Reconstruction of the perineum. Ann Plast Surg.
2014;73(suppl 1):S74–S81.
16. Sinna R, Qassemyar Q, Benhaim T, et al. Perforator flaps: a new
option in perineal reconstruction. J Plast Reconstr Aesthet Surg.
2010;63:e766–e774.
17. Huang JJ, Chang NJ, Chou HH, et al. Pedicle perforator flaps
for vulvar reconstruction–new generation of less invasive
vulvar reconstruction with favorable results. Gynecol Oncol.
2015;137:66–72.
18. Nelson RA, Butler CE. Surgical outcomes of VRAM versus thigh
flaps for immediate reconstruction of pelvic and perineal cancer
resection defects. Plast Reconstr Surg. 2009;123:175–183. The largest
series of prospectively collected cases comparing abdominal vs thigh flap
reconstruction in perineal reconstruction, demonstrating most favorable
complication profile after abdominal flap use (M.D. Anderson Cancer
Center).
19. Butler CE, Gündeslioglu AO, Rodriguez-Bigas MA. Outcomes of
immediate vertical rectus abdominis myocutaneous flap
reconstruction for irradiated abdominoperineal resection defects.
J Am Coll Surg. 2008;206:694–703. Documented improvement in
outcomes using flaps in radiated perineal reconstruction.
20. Shibata D, Hyland W, Busse P, et al. Immediate reconstruction of
the perineal wound with gracilis muscle flaps following
abdominoperineal resection and intraoperative radiation
therapy for recurrent carcinoma of the rectum. Ann Surg Oncol.
1999;6:33–37. Early evidence that flaps can reduce complication rate from
46% to 12% in radiated perineal reconstruction.
21. Friedman JD, Reece GR, Liron Eldor L. The utility of the posterior
thigh flap for complex pelvic and perineal reconstruction. Plast
Reconstr Surg. 2010;126:146–155.
22. Monstrey S, Blondeel P, Van Landuyt K, et al. The versatility of the
pudendal thigh fasciocutaneous flap used as an island flap. Plast
Reconstr Surg. 2001;107:719–725.
23. Jurado M, Bazán A, Alcázar JL, Garcia-Tutor E. Primary vaginal
reconstruction at the time of pelvic exenteration for gynecologic
cancer: morbidity revisited. Ann Surg Oncol. 2009;16:121–127.
24. Gleeson NC, Baile W, Roberts WS, et al. Pudendal thigh
fasciocutaneous flaps for vaginal reconstruction in gynecologic
oncology. Gynecol Oncol. 1994;54:268–274.
25. Said HK, Bevers M, Butler CE. Reconstruction of the pelvic floor
and perineum with human acellular dermal matrix and thigh flaps
following pelvic exenteration. Gynecol Oncol. 2007;107:578–582.
26. Atik B, Tan O, Ceylan K, et al. Reconstruction of wide scrotal defect
using superthin groin flap. Urology. 2006;68:419–422.
27. Hallock GG. Scrotal reconstruction following fournier gangrene
using the medial circumflex femoral artery perforator flap. Ann
Plast Surg. 2006;57:333–335.
28. Ahmadzadeh R, Bergeron L, Tang M, et al. The posterior thigh
perforator flap or profunda femoris artery perforator flap. Plast
Reconstr Surg. 2007;119:194–200.
29. Chessin DB, Hartley J, Cohen AM, et al. Rectus flap reconstruction
decreases perineal wound complications after pelvic
chemoradiation and surgery: a cohort study. Ann Surg Oncol.
2005;12:104–110. Documented improvement in outcomes using abdominal
flaps in radiated perineal reconstruction (Memorial Sloan-Kettering
Cancer Center).
30. McAllister E, Wells K, Chaet M, et al. Perineal reconstruction after
surgical extirpation of pelvic malignancies using the transpelvic
transverse rectus abdominal myocutaneous flap. Ann Surg Oncol.
1994;1:164–168.
31. Lee MJ, Dumanian GA. The oblique rectus abdominis
musculocutaneous flap: revisited clinical applications. Plast Reconstr
Surg. 2004;114:367–373. Variation in skin paddle design, expanding the
size and the reach of the rectus abdominis myocutaneous flap.
32. Abbott DE, Halverson AL, Wayne JD, et al. The oblique rectus
abdominal myocutaneous flap for complex pelvic wound
reconstruction. Dis Colon Rectum. 2008;51:1237–1241.
33. McCraw JB, Massey FM, Shanklin KD, Horton CE. Vaginal
reconstruction with gracilis myocutaneous flaps. Plast Reconstr Surg.
1976;58:176–183.
34. Whetzel TP, Lechtman AN. The gracilis myofasciocutaneous flap:
vascular anatomy and clinical application. Plast Reconstr Surg.
1997;99:1642–1652, discussion 1653–1655.
35. Song YG, Chen GZ, Song YL. The free thigh flap: a new free flap
concept based on the septocutaneous artery. Br J Plast Surg.
1984;37:149–159.
36. Ali RS, Bluebond-Langner R, Rodriguez ED, Cheng MH. The
versatility of the anterolateral thigh flap. Plast Reconstr Surg.
2009;124(6 suppl):e395–e407.
37. Luo S, Raffoul W, Piaget F, Egloff DV. Anterolateral thigh
fasciocutaneous flap in the difficult perineogenital reconstruction.
Plast Reconstr Surg. 2000;105:171–173.
38. Wong S, Garvey P, Skibber J, Yu P. Reconstruction of pelvic
exenteration defects with anterolateral thigh-vastus lateralis muscle
flaps. Plast Reconstr Surg. 2009;124:1177–1185.
39. Woods JE, Alter G, Meland B, Podratz K. Experience with vaginal
reconstruction utilizing the modified Singapore flap. Plast Reconstr
Surg. 1992;90:270–274.
40. Hurwitz DJ, Swartz WM, Mathes SJ. The gluteal thigh flap: a
reliable, sensate flap for the closure of buttock and perineal
wounds. Plast Reconstr Surg. 1981;68:521–532.
41. Rubin JA, Whetzel TP, Stevenson TR. The posterior thigh
fasciocutaneous flap: vascular anatomy and clinical application.
Plast Reconstr Surg. 1995;95:1228–1239.
42. Pantelides NM, Davies RJ, Fearnhead NS, Malata CM. The gluteal
fold flap: a versatile option for perineal reconstruction following

391.e2
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CHAPTER 17 • Perineal reconstruction
anorectal cancer resection. J Plast Reconstr Aesthet Surg.
2013;66:812–820.
43. Bodin F, Dissaux C, Seigle-Murandi F, et al. Posterior perineal
reconstructions with “supra-fascial” lotus petal flaps. J Plast
Reconstr Aesthet Surg. 2015;68:e7–e12.
44. Bass LS, Karp NS, Benacquista T, Kasabian AK. Endoscopic harvest
of the rectus abdominis free flap: balloon dissection in the fascial
plane. Ann Plast Surg. 1995;34:274–279, discussion 279–280.
45. Friedlander LD, Sundin J. Minimally invasive harvesting of rectus
abdominis myofascial flap in the cadaver and porcine models. Plast
Reconstr Surg. 1996;97:207–211.
46. Greensmith A, Januszkiewicz J, Poole G. Rectus abdominis muscle
free flap harvest by laparoscopic sheath-sparing technique. Plast
Reconstr Surg. 2000;105:1438–1441.
47. Winters BR, Mann GN, Louie O, Wright JL. Robotic total pelvic
exenteration with laparoscopic rectus flap: initial experience. Case
Rep Surg. 2015;2015:835425.
48. Cera SM, Wexner SD. Muscle transposition: does it still have a role?
Clin Colon Rectal Surg. 2005;18:46–54.
49. Ruthmann O, Fischer A, Hopt UT, Schrag HJ.
Schließmuskelprosthese vs Ersatzmuskelplastik bei hochgradiger
Stuhlinkontinenz? Chirurg. 2006;77:926–938.
50. Lefevre JH, Parc Y, Kernéis S, et al. Abdomino-perineal resection for
anal cancer impact of a vertical rectus abdominis myocutaneus flap
on survival, recurrence, morbidity, and wound healing. Ann Surg.
2009;250:707–711.
51. Taylor GI, Corlett R, Boyd JB. The extended deep inferior epigastric
flap: a clinical technique. Plast Reconstr Surg. 1983;72(6):751–765.
52. Wagstaff MJ, Rozen WM, Whitaker IS, Enajat M, Audolsson T,
Acosta R. Perineal and posterior vaginal wall reconstruction with
superior and inferior gluteal artery perforator flaps. Microsurgery.
2009;29(8):626–629.
53. Combs PD, Sousa JD, Louie O, Said HK, Neligan PC, Mathes DW.
Comparison of vertical and oblique rectus abdominis
myocutaneous flaps for pelvic, perineal, and groin reconstruction.
Plast Reconstr Surg. 2014;134(2):315–323.
54. Pedersen J, Song DH, Selber JC. Robotic, intraperitoneal harvest of
the rectus abdominis muscle. Plast Reconstr Surg. 2014;134(5):
1057–1063.
55 Rulllier E, Zerbib F, Laurent C, Caudry M, Saric J. Morbidity and
functional outcome after double dynamic graciloplasty for anorectal
reconstruction. Br J Surg. 2000;87:909–913.

SECTION III • Burns Surgery
18 
Acute management of burn
and electrical trauma
Raphael C. Lee and Chad M. Teven
SYNOPSIS
■ Review of the pathogenesis of various burn-related injuries
■ Review of the classification and diagnosis and of cutaneous
burn injuries
■ Review of the first aid management of burn patients
■ Develop insight between extent of burn injury and physiologic
stress response
■ Review acute management of burn patients, including fluid,
nutritional, and wound care
■ Review state of the art wound management of burn patients
■ Learn indications for wound debridement, wound dressing
and splinting, and skin grafting
Access the Historical Perspective section online at

Epidemiology
Burn trauma incidence has a cyclical pattern with the peak
incidence during holidays and vacations. According to the
most recent statistics compiled by the World Health Orga-
nization and the World Fire Statistics Center (WFSC), fire
cause roughly 6.6 million major burn injuries and 400 000
deaths every year.1 In economically developed nations, 1–2%
of the population receives a burn injury annually and 10% of
those require professional medical attention. Roughly 10%
of those requiring medical attention have major burns that
require burn center management. Major burn trauma is a
disease of the poor and disabled, as the majority of cases
occur in poor neighborhoods and in low-income countries
where prevention programs are almost nonexistent. A practi-
cal indication of fire mortality risk is the international median
death rate which is 0.9–1.2 per 100 000 inhabitants by country.
In addition, the cost to society in terms of lost wages, acute
medical care, and rehabilitation is enormous. In 2009, the
WFSC noted that the cost of direct fire losses ranged from
0.06–0.26% of countries’ gross domestic product (GDP) and
the cost of indirect fire losses ranged from 0.002–0.95% of
countries’ GDP.
Risk factors
In addition to poverty, major burns are more common in
populations that have some predisposing factor such as
mental illness and substance abuse. For adults, predisposing
factors to burns include alcoholism, senility, psychiatric dis-
orders, and neurological disease such as epilepsy.2 Children
under 5 years old are also particularly vulnerable to burns.
Among all children, scald burns account for about two-thirds
of burn injuries. For children less than 5 years of age, they
account for 75% of all pediatric burns.
Aims of burn care
Rescue: Stop the burn injury process and provide life support.
Resuscitate: Immediate support must be provided for any
failing organ system.
Refer: After initial evacuation to emergency department, some
patients with burns may need transfer to a burn center for
multidisciplinary intensive care.
Resurface: Close open wounds as soon as possible.
Reconstruct: Replace damaged anatomic structure needed for
normal function.
Rehabilitate: Recover, as far as is possible, physical, emotional,
and psychological well-being.

392.e1
Historical perspective
Historical perspective
The capability to control fire (ca. 900,000 B.C.E.) provided
humans with enormous new capabilities and certainly
advanced our civilization. However, use of fire has taken its
toll on human suffering as well. Once the use of fire was
incorporated into daily life, accidental burns became an inevi-
table cause of injuries. Man began to identify botanicals for
soothing burn medications. As a result, humans have for mil-
lennia searched for various remedies to treat burns.
In the earliest medical handbook identified (ca. 3rd millen-
nium B.C.E.), an anonymous Sumerian physician documented
several burn remedies based on plant extracts. Fifteen hundred
years later (1534 B.C.E.), the Ebers papyrus described a topical
treatment for burns consisting of frog, mud, cow dung, ram’s
horn, lemon strips, and a variety of other ingredients. Around
600 B.C.E., Sushruta first described classic symptoms associ-
ated with severe burns including thirst and fever. He was also
the first to recommend surgical debridement for burns result-
ing in loose skin and flesh. The Old Testament (Leviticus
13:24–28) lists burn injury of the skin among other dermato-
logic illnesses.
In addition to many other topics, Hippocrates (460–377
B.C.E.) wrote extensively on burns. He recognized that signifi-
cant fluid loss occurred at the burned surface as fluid egressed
from blood vessels to form blisters. He also described several
aspects of burn management, including hydrating the patient,
topical treatments, and surgery for the most severe cases.
Perhaps most importantly, Hippocrates advocated that wound
care be performed in aseptic conditions and as quickly and
painless as possible.
Around 500 B.C.E., Chinese physicians were using a
mixture of tea leaves (tannic acid) to treat burns, but the oldest
preserved written Chinese scientific description of burn
wound treatment dates back to Hong Ge (281–341 C.E.). His
book Zhou Hou Fang (Prescriptions for Emergency) suggested
the topical application of two different prescriptions: old
(imperative) calcarea optionally blended with plant oil, or the
use of pig fat cooked with willow bark. The application of
these mixtures resulted in reduced numbers of wound infec-
tions and has to be regarded as the oldest preserved Chinese
description of an anti-infectious astringent to be used in
thermal injuries.
Years later, the 16th-century German physician Fabricius
Hildanus was the first to classify burns into three categories
that could be used to guide treatment. Around this time, the
French surgeon Paré also described areas of the body prone
to burn contracture and advocated for early excision of the
burn wound. Richter (1788) later wrote on the relationship
between burn wound size and prognosis. Debates would
continue for centuries about how to best classify and treat
burn wounds as well as about which factors – in addition to
burn wound size – must be considered when predicting
outcome.
Major advances were made in burn care in the 19th century.
The first dedicated burn center opened in 1848 when James
Syme, a burn surgeon at the Royal Infirmary in Edinburgh,
designated one building for all burn patients. Additionally,
physicians described excision of burnt tissue and skin graft-
ing, which led to an important publication in JAMA (1905)
advocating for early skin grafting. Physicians also began to
appreciate the importance of intravenous fluids in acute burn
management after Tappeiner (1881) demonstrated that burn
physiology results in a hemodynamic picture similar to that
of acute pancreatitis.
Arguably, the largest strides in burn care have been made
in the last century. Sentinel events such as the World Wars and
the discovery of antibiotics facilitated major change in medical
and surgical care of burns. During World War I, the British
plastic surgeon Sir Harold Gillies performed the first success-
ful autograft. His work also facilitated improved techniques
for tangential excision of burned skin, donor site harvest,
meshing of skin grafts, and the use of cadaveric grafts.
In the 1930s, the Yale-trained physician Frank Underhill
described burn shock, essentially an extreme form of hypovo-
lemic shock due to capillary leakage and the release of inflam-
matory mediators. Burn shock may result in decreased blood
pressures, inadequate tissue perfusion, and potentially death.
Stanley Levinson, a surgery resident in Boston at the time,
similarly observed that burn patients often lose fluids at a rate
incompatible with life. Therefore he advocated for adequate
fluid resuscitation as a cornerstone of acute burn care. This
early work resulted in various fluid resuscitation protocols
including the Parkland formula. Another important shift in
burn care was borne from Levinson’s comprehensive descrip-
tion of the pathology and effects of smoke-inhalation injury.
This research has led to advances in treating patients with
smoke-inhalation injury as well as the initiation of public
health safety measures to decrease the risk of smoke inhala-
tion including the development of smoke detectors.
Recent progress in burn care is largely the result of the
comprehensive treatment of burn patients in dedicated burn
units and a team approach to burn care. Multidisciplinary
teams consisting of plastic or general surgeons, intensivists,
psychiatrists or psychologists, nurses, dieticians, therapists,
pharmacists, social workers, and spiritual leaders are now the
standard at burn centers. In addition, a better understanding
of acute burn resuscitation, wound care management, and
early excision and skin grafting in severe burns has reduced
the mortality rate associated with burns.

393
Definition of burn injuries
Definition of burn injuries
Stedman’s medical dictionary list more than 22 types of burn
injury including thermal, chemical, electrical, friction, cement,
and other “burns”.3 The pathogenesis of these burn injuries is
quite different which causes some confusion. What they have
in common is that the injury process begins with damaging
molecular structure of tissue. Although the treatment of these
different injuries would have aspects in common, there are
differences that address the specific pathogenesis.
Thermal burns occur when the tissue temperature exceeds
the chemical bond energy thresholds stabilizing molecular
structure. This happens when tissue comes in contact with a
thermal energy source that results in heat transfer by conduc-
tion, convection, and/or radiation. When tissues are heated
to supraphysiologic temperatures for long enough, molecular
alterations result that do not spontaneously reverse. The
extent of tissue damage resulting from heat exposure depends
on the tissue type and recent history of heat exposure. Cells
have some capability to repair such molecular damage. The
amount of molecular damage tolerated by cells is dependent
on the history of trauma exposure. Cells adapt to repetitive
trauma by upregulating stress proteins that repair or remove
damaged molecules. In effect, tissue exposure to sub-lethal
injury increases cellular injury repair rates, thus allowing
tissues to subsequently survive greater thermal burn injury.
This is called thermal preconditioning. When the extent of
damage exceeds cellular repair capabilities, then loss of cell
and subsequent tissue viability results, which manifests as a
“burn”.4
The extent of thermal burn injury scales with both the
tissue temperature and duration of exposure (Fig. 18.1).
Characteristic molecular alterations include disruption of cell
membranes, aggregation of unfolded proteins, curling of col-
lagen and other structural macromolecules, activation of
degradative proteases, and dehydration. A basic comparison
across modes of cell injury due to burns can be appreciated
in Fig. 18.2. Cell membrane disruption is common to all forms
of trauma because membranes are the most vulnerable vital
cellular structure.5
Contact with electrical power sources may cause injury by
both thermal and non-thermal processes. The injury mode(s)
depend on the voltage, current capacity, and frequency of the
power source. In addition, other parameters such as the dura-
tion of electrical contact and the anatomic path of the current
through the body are deterministic. For example, although
static electrical shocks involve more than 1000 volts, they do
not injure tissue because the current is small and it only passes
on the outer surface of the body.
Frequency is a measure of how often the current changes
direction. The abbreviation “DC” (i.e., direct current) indicates
the current frequency to be zero (i.e., constant voltage), and
“AC” (i.e., alternating current) indicates that the current is
changing direction of flow (i.e., alternating polarity) with
time. Tissue damage can result from electrical energy at any
frequency in the electromagnetic spectrum (Table 18.1). But
the exact molecular details of the injury is quite frequency
dependent. The frequency of the change is measured in cycles
per second and is called Hertz (Hz). Commercial electrical
power usually operates in the 50–60 Hz range meaning it
changes direction every 8.4 milliseconds.
Radiation injury can result from either ionizing or non-
ionizing electromagnetic waves. Ionizing is higher energy and
shorter wavelength radiation. Ionizing radiation is absorbed
at the atomic level to disrupt the electron structure around
Fig. 18.1  The importance of both temperature and time in
determining the depth and extent of injury is illustrated by this
curve. The threshold for feeling pain precedes injury and sensation
is lost once all cutaneous pain receptors are burned. The data is
adapted from various models.
Pain threshold
2º
3º
Temperature (°C)
Depth of burn injury
Time (seconds)
1000
100
10
1
0.1
0.0
44
48
52
56
60
64
68
72
Table 18.1  Electrical shock by frequency
Frequency range
General
applications
Tissue injury
pathway
“Low”
(DC – 10 kilohertz)
Commercial electric
power; batteries.
Joule heating; cell
membrane
electroporation
“Radiofrequency”
(10 kilohertz to 10
megahertz)
Radio-communication;
diathermy;
electrocautery
Joule heating;
dielectric
heating of
proteins
“Microwave”
(10 megahertz to
10 gigahertz)
Microwave heating
Dielectric heating
of water
“Light and ionizing”
(1015 hertz and
higher)
Photo-optical and
ionizing irradiation
(ultraviolet, X-ray,
gamma, etc.)
Heating and
direct protein
damage;
oxidative
damage

394
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
Fig. 18.2  Schematic illustration of the different molecular
manifestations of thermal, electrical, and radiation burn
trauma.
+
S1
P1
+
+
+
-
--
-
+
P2
S2
+
+
+
-
-
-
-
+
P1
S1
+
+
+
-
-
-
-
+
+
+
+
-
-
-
-
+
+
+
+
-
-
-
-
+
+
+
+
--
-
-
Before injury
After thermal injury
After electrical injury
After radiation injury
P1
S1
+
+
+ +
-- --
P1
S1
+
++
+
-- --
P2
S2
+
+++
- -
-
-
+
S1
P1
+
+
+
-
--
-
+
P2
S2
+
+
+
-
--
-
+
P1
S1
+
+
+
-
--
-
A
B
C
molecules or atoms. This leads to chemical reactions that
damage. In tissue, water is the primary absorber. Ionizing
irradiation causes water and molecular oxygen to bind and
produce hydroxyl radicals with an unpaired electron in the
valence shell. Unpaired electrons on the outer shell are very
reactive with other biomolecules causing damage to DNA,
proteins, lipids, etc.
Burn trauma classification
Clinically, thermal burns are classified according to depth
of penetration from the epithelial surface into the tissue.
This stratification was historically labeled “degree of burn
wound”, but more recently by fractional thickness of injury
(Table 18.2).
Flash and flame burns
Although the mechanisms of “flash” and “flame” burns are
similar, there are some differences. Both flame and flash
phenomena pertain to hot, electricity-conducting gases ema-
nating from a fire that emit light and radiation. Typically, a
flame burn implies that an individual was exposed to flames
in an ongoing fire, whereas a flash burn implies that the
individual was exposed to an explosion (e.g., gasoline) or an
electrical arc (Fig. 18.3). Flash and flame burn injuries are very
common cause of adult burn admissions. Ambient air tem-
peratures associated with flash exposures are typically 10-fold
higher than flame exposures and have a significant radiation
heat energy component. Fortunately, flames and flashes are
composed of gases with very low heat capacity. Flash burns
usually result in less deep burns than flame burns because
flash heating is usually quite brief. In general, flash burn
depth relates the amount and type of fuel that explodes.
Unlike flash injuries, flame burns are often associated with
inhalational injury and other concomitant trauma.
Scald burns
Scald burns result from skin contact with hot liquid or steam.
Scald burn depth is often more difficult to clinically judge
than flame burn depth because it is a low temperature burn
(Fig. 18.4). Tissue structural changes are less noticeable com-
pared to flame burns. The depth of scald injuries are often not
apparent for 48–72 hours. The skin temperature changes in
scald burns depend on geographic location, being less severe
in high mountainous regions than at sea level. Unless super-
heated at high pressures, the maximum skin temperature
reached in scalding water can be 100°C. Because water has a
very high heat capacity and also cools by evaporation, the
duration of tissue contact with damaging temperatures
Fig. 18.3  Photograph of a gasoline flame burn to the neck and face illustrating the
non-uniform heat exposure corresponding to depth of injury from deep partial to
epidermal.

395
Definition of burn injuries
Fig. 18.4  Typical appearance of superficial skin burns from (A) low energy electical arc flash and (B) sunburn.
A
B
Table 18.2  Clinical presentation of thermal burn wounds
Depth of
burn
Skin
involvement
Examples
Signs
Sensation
Self-healing
capacity
Skin healing
time
Visible
scarring
Epidermal
burn
Epidermis
Brief flame or
flash;
Sunburn
Dry and red,
blanches with
pressure, no
blisters
Tender and
painful
when
exposed to
air.
Excellent with
use of
occlusive
dressing
Within 7 days
Unusual
Superficial
partial-
thickness
burn
Epidermis
and part of
the
papillary
dermis
Scald (spill or
splash),
short flash
Pale pink with
fine blistering,
blanches with
pressure
Very painful
Excellent with
proper
management.
Within 14 days
Can have
color match
defect.
Low to
moderate
risk of
hypertrophic
scarring
Deep
partial-
thickness
burn
Epidermis,
the entire
papillary
dermis
down to
reticular
dermis
Scald (spill),
flame, oil or
grease
Dark pink to
blotchy red,
capillary refill
sluggish to
none.
In child, may be
dark lobster
red with
mottling
May be painful
or reduced/
absent
sensation
Should not be
left to heal by
itself, but
instead
should
probably be
submitted to
surgery
14 to over 21
days
Moderate to
high risk of
hypertrophic
scarring
Full-
thickness
burn
Entire
thickness
of the skin
and
possibly
deeper
Scald
(immersion),
flame,
steam, oil,
grease,
chemical,
high-voltage
electricity
White, waxy or
charred, no
blisters, no
capillary refill.
May be dark
lobster red
with mottling
in child
Insensate
No healing
capacity and
as such
should
always be
submitted to
surgery
Never. Replaced
by scar and
contracture
Yes.

396
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
to voluntarily release the contact. Thus shock times are typi-
cally longer in low-voltage shocks with higher risk of cardio-
pulmonary arrest (i.e., electrocution). For high voltages (>1000
volts), electrical arcing initiates the electrical current flow
before mechanical contact. High-voltage electrical shocks are
associated with more severe extremity damage, but lower
rates of electrocution. Also, high-voltage contact arcs can
reach very high temperatures leading to corneal burns and
clothing ignition.
As the current passes through the body, injury may result
from either heat generation in the tissue or from strong electric
forces that rupture cell membranes. Electrical shock by com-
mercial electrical power can produce a range of neuromuscular
effects (Table 18.3). Of course, the most life threatening is the
immediate risk for cardiopulmonary arrest when the current
passes through the heart, especially during the myocardial
repolarization phase.
Factors that determine the relative contribution of heat
versus direct electrical damage include the amount of current,
anatomic location, and the contact duration. The type of cloth-
ing, use of protective gear, and the power capability of the
electrical source also make a difference. So knowing just the
voltage of contact is not enough to estimate the injury.
Because the epidermal layer of the skin is very resistive, it
is instantly destroyed in contact with electrical power sources
greater than 100 volts. Contact with commercial AC electrical
power does not cause “entrance” and “exit” wounds because
the current goes in and out of every contact point (Fig. 18.5).
If the skin is wet, extensive subcutaneous tissue damage can
occur without skin burns. For electrical shock injury, the skin
surface area damage is not reflective of the injury extent. The
damage is more volumetric and scattered along the current
path, often requiring CT or MR imaging to quantify (Fig. 18.6).
Peripheral nerve and skeletal muscle tissues are most
vulnerable to non-thermal damage during electrical shock.
Just 14–16 milliamperes of current passing through the
forearm induces tetanic contractions of muscles controlling
handgrip, which may prevent a person from voluntarily
releasing the electrical conductor (see Table 18.3). Joint dislo-
cations and fractures may result from the muscle spasm as
well. A current of 50 milliamperes or more passed through the
chest can result in cardiopulmonary arrest. Non-thermal
electric injury to nerves and muscles can occur in milliseconds
while taking seconds for burns to occur. Thus brief shocks
commonly result in neuromuscular function disturbances in
the absence of thermal burns.
Disruption of skeletal muscle membranes leads to release
of myoglobin and hemoglobin that enter the circulation and
muscle edema. Skeletal muscle damage and edema lead to
secondary compartment syndromes, leading to further
depends on factors like clothing or other vapor barriers. The
water temperature is also important. Skin surface contact with
60°C water creates a deep dermal burn in 3 seconds but will
cause the same injury in 1 second at 69°C. If the water contains
oils or lipids, as in soups, evaporation is slowed, resulting in
longer burn duration and a deeper skin injury.
Hot object “contact burns”
Contact burns occur when tissue is exposed to a hot, thermally-
conducting object (e.g., cooking pan or radiator). Burn depth
depends on the thermal energy storage capacity and thermal
conductivity of the object. Thus a hot metal rod would produce
a deeper burn than a hot plastic rod. Contact burn injuries are
often associated with workplace-related hand burns, patients
prone to seizures, and intoxicated individuals. They are also
seen in elderly people after a loss of consciousness; such a
presentation requires a workup of the cause of syncope.
Contact burns commonly result from mechanical contact with
hot metals, thermoplastic composites, glass, or coals in an
industrial setting. Because the heat energy transfer is large,
contact burns often involve full-thickness skin and subcutane-
ous tissue.
Tar and asphalt burns
Tar and asphalt burns occur in workers engaged in surfacing
pavement and roads, roofing, and other industrial applica-
tions. Tar is a wax and oil composite that is difficult to remove
from skin without causing injury. When hot tar makes contact
with skin, it solidifies and sticks. The tar usually retains suf-
ficient heat to produce prolonged heat transfer to the skin
resulting in deep skin burns. Once cooled, tar strongly adheres
to the tissues and is chemically damaging. In order to expedite
the cooling and solidification process one should apply cold
water. Often, the tar is cool by the time the patient arrives at
the medical facility. Injuries typically occur on the exposed
skin of the face and extremities, and the burn is of variable
depth ranging from deep partial to full thickness.
Electrical injury/“electrical burns”6,7
Extent of injury depends on the amount of current and the
anatomic path of the current. Contact with an electrical power
source results from both direct electrical force injury and heat
generation. Commercial electrical power operates in the
narrow frequency range of DC to 150 Hz. Electrical shocks in
this frequency range are clinically most common is the second
most common cause of workplace injury. Because of the
electrolytes content in tissue fluids, the body is a good con-
ductor of electricity. With wet skin, the DC resistance of a
current path from one hand to the other is about 1000 ohms
and from hand to both feet is about 750 ohms. At frequencies
greater than 100,000 Hz electrical power can radiate across air
gaps from the power source into the body. Microwave (109
Hz) and infrared heating (1019 Hz) used for cooking is a
common example (see Table 18.1).
Sometimes electrical shock injuries are categorized as low
or high voltage depending on whether the voltage is below
or above 1000 volts, respectively. Practically when the contact
voltage is less than 1000 volts, direct mechanical contact is
usually required to initiate current flow. Once mechanical
contact with the power source occurs, it is can be impossible
Table 18.3  Thresholds for electrical current effects
Threshold effect of 60 Hz current
(Path: hands to feet)
Threshold
current
(milliamps)
Tingling sensation/perception
1–4
“No let go” (i.e., skeletal muscle tetany)
16–20
Respiratory muscle paralysis
20–50
Ventricular fibrillation
50–120

397
Definition of burn injuries
clinical frostbite injury. Demographically, distal extremities,
ears, and other ambient air exposed areas of the face are
involved.8 Tissue tolerance to cold (above freezing) tempera-
tures is also very tissue type specific. Brain and cardiac func-
tion does not tolerate temperatures less than 21°C for more
than 20–30 minutes. Skin tolerates it better but not for more
than 19–24 hours. Freezing with ice formation in any tissue
creates a severe injury. Ice formation in tissues concentrates
electrolytes around proteins that leads to unfolding and
aggregation. Tissue freezing also dehydrates cells in addition
to promoting ice crystal propagation through cell membranes.
The thaw cycle also causes injury by osmotic rupture of tissue
cells. The majority of frostbite cases arise from homeless or
disabled populations in climates with cold winters. Ethanol
consumption predisposes to cold injury by vasodilatation and
rapid heat loss.8
Radiation burns
The most common cause of radiation burn is heavy sun
exposure. Sunlight produces a wide spectrum of radiating
energy from infrared to cosmic energies. In typical sunburn,
it is the heavy dose of the infrared heating and ionizing
ultraviolet (UV) that does the most damage. UV radiation
produces oxidative free radicals in the epidermis and dermis.
ischemic injury. Release of myoglobin from muscle into the
circulation and then into the urine is a characteristic feature
of severe electrical shock injury. Renal failure can result from
intrarenal aggregation of myoglobin. Direct electrical shocks
to the head may cause increased intracranial pressure as well.
Lightning is another common form of electrical shock.
Most of the lightning current passes around the body via the
lightning arc to ground. There are often superficial epidermal
burn marks that do not penetrate into the dermis. Cardiac and
central neurological arrest often occurs due to the magneti-
cally induced electrical currents. Because signs of brain
damage are unreliable, they cannot be used to guide CPR
efforts. In both high-voltage electrical contacts and lightning
strikes, ignition of the electrical arc can produce a strong
thermo-acoustic blast wave resulting in barotrauma. The flash
generated radiant heat injury associated with arc-mediated
electrical current can lead to eye injury. Table 18.1 presents a
classification of electrical injury according to frequency
regime.
Frostbite
Frostbite results from tissue exposure to lethally cold or freez-
ing temperatures. Loss of circulation, and the reperfusion
consequences on rewarming, are major pathogenic features of
Fig. 18.5  Appearance of a full-thickness electrical contact burns resulting from contact with AC electrical power. All contacts are entrance points and all are exit points
because the current is alternating direction of flow during the shock.
Fig. 18.6  MR imaging of an electrical injury to the scalp to visualize the extent of tissue damage and secondary edema formation.

398
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
unlikely to survive more than a few days. In the United States,
only 25% of burn-related deaths occur after the patient arrives
in the burn center. In remote locations without access to an
acute care medical center, death results from acute dehydra-
tion and hypothermia. In such locations, initial burn manage-
ment must control this dehydration and hypothermia until
the patient arrives at a hospital.
Zones of burn tissue injury
Skin burns resulting from contact with a heat source usually
result in a non-uniform injury depth (Fig. 18.8). The pattern
of thermal burns has been traditionally divided into three
zones: (1) coagulation, (2) stasis, and (3) hyperemia. The three
zones of a burn were initially described by Jackson, Topley,
and Cason in 1947.10
The zone of coagulation represents the most severely
burned tissue with extensive aggregation of intracellular and
extracellular matrix proteins, dehydration due to protein
coagulation, and loss of vascular perfusion. Historically, the
damage is thought to be irreversible and requires surgical or
enzymatic removal.
Moving away from the heat source contact area, the next
zone of injury is the zone of stasis, which is characterized by
cellular swelling, partial extracellular matrix denaturation,
and decreased vascular perfusion. Initial resuscitation timing
and strategy can influence the survival of tissue in the zone
of stasis. Additional insults, such as ischemia infection, or
edema, can push tissue in this zone toward necrosis. With
proper resuscitation and wound care, however, cell recovery
can occur and matrix molecular changes may be reversed.
The next adjacent zone is the zone of hyperemia. In this
outermost zone, vascular perfusion is increased in response
to inflammatory cytokines released from the zone of stasis.
When free radical scavenging mechanisms are exceeded,
damage occurs. It is rare that the burn depth is greater than
epidermal or superficial dermal. Clinical manifestations are
painful partial-thickness burns and blistering. Sunscreen
lotions absorb the UV and increase the amount of sun expo-
sure required to cause a burn. However, until recently they
did not totally shield the entire UV range. There is some
evidence that use of narrow-band (i.e., UVB) sunblock is
associated with other long-term consequences related to
prolonged exposure to DNA reactive irradiation outside of the
blocked UVB band.
Radiation injuries also occur from therapeutic, accidental,
space travel, or military use of ionizing irradiation. The
molecular target of the radiation depends on the type of radia-
tion.9 Most commonly, the damage is caused by generation of
hydroxyl (OH*) free radicals in oxygenated water. The higher
the water and oxygen in the tissue, the greater the radiation
injury to cells. Under conditions of tissue water and oxygen
content, doses of radiation less than 5 Gray (Joules/kilogram)
create protein and DNA cross-links that destroy the body’s
most rapidly dividing cell lines. Severe immune compromise
due to neutropenia and bleeding secondary to thrombocyto-
penia are seen over a period of 3–5 weeks. At higher levels of
exposure (30–100 Gy), the membranes of cells, even non-
proliferating nerves and muscle, are damaged leading to
tissue death within 6–24 hours. Non-ionizing radiation such
as that from a hot fire or an electrical arc can cause transfer of
thermal energy to the body by non-ionizing irradiation. This
is similar to infrared heating.
Deliberate burn injury
Up to 10% of pediatric burns are due to non-accidental injury.
Detecting these injuries is important, as many children who
are repeatedly abused eventually suffer a fatal injury. Usually
children less than 3 years old are affected. As with other
non-accidental injuries, the history and the pattern of injury
may arouse suspicion (Fig. 18.7). A social history is extremely
important. Abuse is more common in poor households with
single or young parents. Such abuse is not limited to children:
elderly and other dependent adults are also at risk, and a
similar assessment can be made in these scenarios.
Chemical injuries and burns
See Chapter 22 for details of chemical burns.
Clinical features of thermal burn injury
The skin is the largest organ of the body and serves multiple
functions essential to our survival including (1) transport
barrier against evaporative fluid and heat losses; (2) thermal
regulation; (3) immune barrier against microbes and foreign
chemicals; and (4) sensory receptors that provide information
about environment. Burn injuries often disrupt the skin barrier
functions, and the secondary effects of large burn injury result
in systemic stress responses.
Burn survival associated with burn injuries is strongly
dependent on the age of the patient, the percentage of the
body surface burned, and the presence or absence of smoke-
inhalation injury. Without the support of modern medical
facilities, individuals who suffer a major burn injury are
Fig. 18.7  The anatomic pattern of injury often provides clues to the cause of
injury. The burn tideline associated with sitting in a bath of hot water. The
non-burned in the center of the ring results from contact with the ceramic in the tub
that is a poor conductor of heat.

399
Clinical features of thermal burn injury
Fig. 18.8  (A) Flame burn on abdomen showing zones of injury. Dry full-thickness
thermal burn coagulation is in the upper aspect of the wound. Away from the
coagulation zone, the injury severity becomes progressively less. (B) Schematic
showing zones of injury in deep and superficial dermal burns.
Full thickness
Partial thickness
Superficial burn
A
Zone of coagulation
(necrosis)
Superficial dermal burn
Deep dermal burn
Zone of coagulation
(necrosis)
Zone of injury
(edema and stasis)
Zone of injury
(edema and stasis)
Zone of hyperemia
Zone of hyperemia
B

400
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
Histopathology in this zone reveals swollen cells and capil-
laries, suggestive of cell membrane disruption. The tissue here
will invariably recover unless the burn victim suffers pro-
longed hypotension and/or sepsis.
Estimating the depth of a skin burn on the basis of clinical
exam is difficult. The depth of a skin burn is not always
obvious initially, and experienced experts often disagree. This
is particularly true for scald or other low temperature burns
in patients with dark skin. Many methods have been proposed
to predict the depth of the injury immediately or soon after
injury (ultrasound examination, intravenous fluorescent
probes), but none has been as reliable as serial examination of
the wound. The final depth of the injury typically becomes
obvious 48–72 h after injury. Rarely, the thermal injury pene-
trates into the subcutaneous or deep tissue.
Local injury progression
Burn tissue damage activates inflammatory mediators, espe-
cially in the perfused subsurface, which degrade and extend
the volume of injury. Release of mitochondria, xanthine
oxidase, and other intracellular substances into the circulation
generates destructive reactive oxygen species in the tissue as
well as the local circulation. This causes thrombosis that
potentiates ischemic tissue necrosis. Both complement activa-
tion and intravascular stimulation of neutrophils add to small
vessel injury. Increased histamine activity, enhanced by the
catalytic properties of xanthine oxidase, further increases in
vascular permeability. As a general rule, the volume of tissue
necrosis after an uncomplicated burn injury progresses over
48 hours.
One important goal of resuscitation is to minimize the
injury extension. Edema formation often follows a biphasic
pattern. An immediate and rapid increase in the water content
of burn tissue is seen in the first hour after injury. A second
and more gradual increase in fluid flux of both the burned
skin and non-burned soft tissue occurs during the first 12–24 h
following burn trauma. The rate of progression of tissue
edema is dependent upon the adequacy of resuscitation that
is determined by both rate and composition of the fluid
administered.
Systemic injury progression
Thermal burn trauma produces an inflammatory cytokine
storm of local and system mediators that are released into the
circulation. These inflammatory cytokines mediate general-
ized stress responses including altered capillary permeability
and total body interstitial edema. This is mediated by numer-
ous vasoactive inflammatory mediators, including serotonin,
bradykinin, prostaglandins, and leukotrienes produced by
calcium influx into thermally disrupted cells. Inflammatory
cytokines also trigger generalized proteolysis, lipolysis, glu-
coneogenesis, and an increased metabolic rate. Severe burn
injury also depresses the function of the heart, large vessels,
and lungs.
Cardiovascular responses to the burn often result in
hypotensive shock once the burn reaches 20–30% of the
total body surface area (TBSA). Shock is a pathophysiologic
condition characterized by high sympathetic neurovascular
responses such that brain and cardiovascular perfusion is
prioritized over other tissues. Splanchnic vasoconstriction
and gut ischemia are features. Adding to this can be a delay
or inadequate fluid resuscitation resulting in increased hema-
tocrit values that increase the blood viscosity and hamper
perfusion.
As in the treatment of hypovolemic shock, the primary
initial therapeutic goal is to quickly restore vascular volume
and to preserve tissue perfusion to minimize tissue ischemia.
Burn shock is not easily or fully repaired by isotonic electro-
lyte fluid resuscitation. Large volumes of resuscitation solu-
tions maybe required to maintain vascular volume during the
first several hours after an extensive burn. Burn shock evolves
through a dynamic pathophysiologic process even if hypovo-
lemia is corrected. Increases in pulmonary and systemic vas-
cular resistance (SVR) occur despite adequate preload and
volume support. Such cardiovascular dysfunctions can further
exacerbate tissue ischemia resulting in a vicious cycle of
accelerating organ dysfunction. The critical concept in burn
shock is that massive fluid shifts can occur even though total
body water remains unchanged.
Hints and tips
• Thermal burn results in three distinct zones: coagulation,
stasis, and hyperemia.
• One goal of burn resuscitation is to maintain perfusion of
the zone of stasis.
• Major burns (>15–20% TBSA) require burn center
admission (see Box 18.1).
• Different burn mechanisms lead to different anatomic injury
patterns.
BOX 18.1  Burn injuries that should be referred to a burn unit
• Partial-thickness burns >10% TBSA and patients requiring burn
shock resuscitation
• Burns that involve the face, hands, feet, genitalia, perineum, or
major joints
• Deep partial-thickness burns and full-thickness burns in any age
group
• Circumferential burns in any age group
• Electrical burns, including lightning injury
• Chemical burns
• Burns with a suspicion of inhalation injury
• Burns of any size with concomitant trauma or diseases that
might complicate treatment, prolong recovery, or affect
mortality
• Diseases associated with burns such as toxic epidermal
necrolysis, necrotizing fasciitis, staphylococcal scalded child
syndrome, etc., if the involved skin area is 10% for children and
elderly and 15% for adults or any doubt of treatment
• Burned children in hospitals without qualified personnel or
equipment for the care of children
(Modified from: American Burn Association.)

401
Acute burn trauma management
■ The depth and TBSA of the burn, and therefore the
severity
■ Signs of inhalation injury (singed nasal hair, black carbon
in the sputum, or carbon in the oropharynx)
■ Any coexisting medical conditions (e.g., cardiac,
respiratory, or hepatic disease; diabetes; pregnancy; or
immunocompromised state)
■ Any predisposing factors that may require further
investigation or treatment (e.g., a burn resulting from a fit
or faint)
■ The possibility of non-accidental injury
■ The person’s social circumstances (e.g., ability to self-care
or need for admission).
The airway should be secured because upper airway obstruc-
tion can develop quickly. Smoke inhalation causes more than
50% of fire-related deaths. Patients sustaining an inhalation
injury may require aggressive airway intervention. Most
injuries result from the inhalation of toxic smoke; however,
super-heated air may rarely cause direct thermal injury to the
upper respiratory tract (see complications, below). Patients
who are breathing spontaneously and at risk for inhalation
injury should be placed on high-flow humidified oxygen.
Patients trapped in buildings or those caught in an explosion
are at higher risk for inhalation injury. These patients may
have facial burns, singeing of the eyebrows and nasal hair,
pharyngeal burns, carbonaceous sputum, or impaired menta-
tion. A progressive change in voice quality or hoarseness,
stridorous respirations, or wheezing may be noted. The upper
airway may be visualized by laryngoscopy, and the tracheo-
bronchial tree should be evaluated by flexible bronchoscopy.
Patients who have suffered an inhalation injury are also at risk
for carbon monoxide poisoning.
Chest radiography is not sensitive for detecting inhalation
injury. The pulse oximeter is not accurate in patients with
carbon monoxide poisoning because only oxyhemoglobin
and deoxyhemoglobin are detected. CO-oximetry measure-
ments are necessary to confirm the diagnosis of carbon
monoxide poisoning. Other pulmonary assessments include
arterial blood gas measurements and bronchoscopy. Patients
exposed to carbon monoxide should receive 100% oxygen
using a non-rebreather facemask.
The secondary survey must include assessment of the loca-
tion, depth, and fractional TBSA burned. Tetanus prophylaxis
should be administered as appropriate for immunization
history. Tetanus immunization or vaccine prophylaxis must
be administered according to standard practice guidelines,
particularly in elderly patients (Box 18.3).
Initial wound management
In the hospital setting, initial wound management is focused
on documenting the extent of injury, removing harmful
wound contaminants, reducing the rate of bacterial coloniza-
tion, and preventing evaporative water loss. Assessment of
burn depth and size on admission is important in making
decisions about fluid resuscitation requirements, type of
topical antimicrobial agents to use, splints, dressings, and
surgery (see Table 18.2).
Appropriate wound care reduces morbidity and mortality.
It also shortens the time for healing and return to normal
function and reduces the need for secondary reconstruction.
Acute burn trauma management
Initial evaluation and treatment in the field
Treatment of a burned patient starts with the removal of the
patient to a safe environment where first aid can be rendered.
In all cases (especially chemical or electrical injuries), care must
be taken to avoid personal injury by ensuring that the area is
safe and that appropriate protective clothing is worn. Basic
trauma victim life support protocols should be used to assess
and stabilize the patient. Top priority should be given to assess-
ing the airway, breathing, and circulation, and presence of any
coexisting injuries that may require more urgent treatment
than the burn. Clothing should be removed. If the burn occurred
in a closed space, inhalation injury should be ruled out by
inspecting the oropharyngeal airway for soot and carbon par-
ticulate. Supplemental oxygen is given if signs of hypoxia exist.
Substantial evidence demonstrates the beneficial effects
of cooling on reducing tissue damage and wound healing
time.11 Although immediate burn wound cooling is prefer-
able, application of cooling after a delay of more than half an
hour is still beneficial to the burn wound.11 While transporting
the patient to a medical center, cooling the burn wound by
wrapping in a hydrogel blanket or room temperature water-
soaked gauze is useful. Cooling for 20 minutes should achieve
near maximum benefit. However, systemic hypothermia and
hypotension must be avoided. The patient should be triaged
to a level 1 trauma center, stabilized, and then transported to
the nearest burn unit for definitive management (Box 18.2).
Initial hospital burn management
Once the patient arrives at the emergency room, the primary
survey should focus on the ABCs of trauma management (i.e.,
Airway, Breathing, and Circulation). It is also important to
exclude associated trauma and inhalation injury (see below).
Once the life-threatening problems are stabilized, a secondary
survey should be done including relevant history (i.e., time,
location, and circumstances of the injury), where the patient
was found, and their condition. Past medical and social
history, current medication usage, drug allergies, and tetanus
status should be determined. It is also important to consider
the possibility of non-accidental burns or scalding.
A thorough assessment of a person with a burn should then
take into account:
■ The type of burn (e.g., flame, scald, electrical, radiation,
or chemical)
BOX 18.2  Field management of a major burn
Perform an ABCDE primary survey:
A – Airway with cervical spine control
B – Breathing
C – Circulation
D – Neurological status and pain control
E – Environment (heat loss) control
F – Initiate fluid resuscitation

402
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
use of occlusive dressings, since epithelialization progresses
faster in a moist environment. Appropriate management of
blisters is a subject of debate. Topical antimicrobials are useful
if the patient is likely to be immune-compromised by a large
TBSA burn or other comorbid condition.
Optimal burn care requires early excision and grafting of
all burned tissue that raises the infection risk or will result in
problematic scars, so a good estimation of burn depth in the
first few days is crucial. The appearance of the wound – and
the apparent burn depth – changes dramatically within the
first 7–10 days. A burn appearing superficial on day 1 may
appear considerably deeper by day 3. For superficial burns,
wound closure with thin epithelium is expected within 14
days by regeneration of epidermis from keratinocytes within
dermal glands and hair follicles.
Deep partial-thickness burns
Deep partial-thickness burns cause total or near total destruc-
tion of dermal glands and hair follicles. Closure by epitheli-
alization takes much longer or does not occur. Distinguishing
between deep partial-thickness burns that are best treated by
early excision and grafting and superficial partial-thickness
burns that heal spontaneously is never simple by physical
examination. Many burn wounds have a mixture of superficial
and deep partial-thickness burns, making precise classifica-
tion of the entire wound difficult. They may initially seem
superficial, with blanching on pressure or sweating on bright
light exposure, but later progress to manifest fixed capillary
staining on re-examination after 48 h.
Some deep partial-thickness injuries will heal if the wound
environment is optimized to encourage endogenous healing.
This includes keeping it warm, moist, and at reduced micro-
bial colonization. Topical antimicrobials are important to use
because immune function in the damaged dermis is compro-
mised. Deep partial-thickness burns that require longer than
3 weeks to heal likely result in hypertrophic scars and scar
contractures. This often results in functional impairment.
Therefore large area deep partial-thickness burns, or those in
highly mobile or cosmetically sensitive areas, should be
excised as soon as possible to a viable depth and then skin
grafted.
Full-thickness injuries
Full-thickness burns involve all layers of the dermis and often
injure underlying subcutaneous adipose tissue as well. These
burns are usually insensate because of destruction of nerve
endings, but the surrounding areas are extremely painful. All
regenerative elements are non-viable, and the dehydrated
extracellular matrix will not support healing. Over days and
weeks if left in situ, eschar separates from the underlying
viable tissue, leaving an open, unhealed bed of granulation
tissue. Without surgical intervention, wound healing occurs
by eschar separation, granulation from the base, and wound
contraction, leaving severe contracture deformities. Unless
the burn wound is very small, optimum treatment of full-
thickness burns involves early excision and grafting.
Extremities should be examined for existence of circumfer-
ential burns with distal vascular compromise. This problem
is not to be confused with skeletal muscle compartment
syndromes. In pure muscle compartment syndromes, the
Epidermal (superficial) burns
These burns involve only the epidermis. They do not present
with blisters, but are hyperemic and tender. Sunburn is the
most common example. Over 2–3 days, the erythema and the
pain subside. Protective occlusive dressing changes is usually
all that is required, with analgesia and intravenous fluids for
extensive injuries. By about day 4, the injured epithelium
peels away from the newly healed epidermis underneath, a
process which is commonly seen after sunburn. By day 7,
healing is complete by regeneration from viable keratinocytes
within dermal glands and hair follicles. The patient should be
advised of measures to provide symptomatic relief, e.g., cover
with occlusive dressing like petrolatum gauze or hydrogels,
non-steroidal analgesia (e.g., ibuprofen), and avoid direct sun
exposure. First-degree burns are not considered in calculation
of the TBSA burned.
Superficial partial-thickness burns
These involve the epidermis and superficial dermis. Blistering
is a characteristic feature. The exposed superficial nerves
make these injuries painful. They leave behind epithelial-lined
dermal appendages including sweat glands, hair follicles, and
sebaceous glands. When thermal damaged superficial dermal
tissue is removed, epithelial cells migrate from the lining of
dermal glands and hair follicles, forming a new, fragile epi-
dermis on top of a thin residual dermal bed.
Most superficial facial burns close well with an initial
washing, immobilization, and proper physiologic dressing for
healing. Progression to a deeper burn is unlikely unless it is
allowed to dry, becomes edematous, and/or infected. Also,
systemic problems such as hypotension and sepsis from a
remote site may cause a partial-thickness wound to convert.
Treatment is aimed at preventing wound progression by the
BOX 18.3  Initial medical center management of a major burn
• Stop the burning process
• Rough estimate of % body surface area burned
• Establish peripheral intravenous access and start lactated
Ringer’s; in children, the interosseous route can be used for
fluid administration if intravenous access cannot be obtained
• Pain management as needed
• Catheterize patient or establish fluid balance monitoring
• Take baseline blood samples for investigation (full blood count;
urea and electrolyte concentration; clotting screen; blood group;
and save or cross-match serum)
• Electrical injuries:
•
12-lead electrocardiography
•
cardiac enzymes
• Inhalational injuries:
•
chest X-ray
•
arterial blood gas analysis
• Clean and dress wounds
• After completion of the primary survey, a secondary survey
should assess the depth and TBSA burned, reassess, and
exclude or treat associated injuries
• Arrange safe transfer to specialist burns facility

403
Acute burn trauma management
Quantifying the burn size12,13
For several reasons, it is important to accurately estimate the
fractional body surface area involved in a burn injury. It is
useful to guide the initial fluid resuscitation rate and deter-
mine whether the patient should be admitted to a burn center
or intensive care facility. For adults, Wallace’s “rule of nines”
is a simple and moderately accurate method of calculating
TBSA burned. However, the Lund and Browder chart is
slightly more accurate and widely accepted because it accounts
for the different body proportions in infants and children (Fig.
18.9). For all patients, burn diagrams and photographs of the
wounds should be placed in the medical record and updated
if the burn wound extends. More precise methods require
computer estimation (Fig. 18.10). The improved accuracy is
valuable for more precisely stratifying burn injuries when
investigating quality control or research outcomes.
Inhalation injury14–16
Upper and lower airway injuries can result from inhalation of
chemically reactive smoke and/or other products of combus-
tion. People burned in house or building fires are at high risk
for inhaling smoke or fumes. Thermal injury from the flame
or hot gases can damage the upper airway (supraglottic). This
results in burns of the lips and oropharynx, leading to edema
and airway obstruction. Heat rarely causes subglottic injury
unless the inhalant is hot steam. The products of combustion
peripheral pulses are not reflective of severity of muscle
perfusion compromise. With subtotal or total circumferential
burned skin contraction, the perfusion to all tissues in the
extremity at and distal to the site of compression are at risk
for ischemic necrosis. In most cases it is best to prophylacti-
cally incise or “release” the deep burn tissue at the time of
burn center admission to allow expansion and restoration of
distal perfusion. This mitigates the risk. In borderline cases
where it is not clear that vascular compromise will occur
after adequate resuscitation, monitoring of distal arterial
pulses is essential for early detection of ischemia. Doppler
monitoring of distal pulses is commonly used to monitor, but
this measurement is very qualitative. Pulse oximetry of digits
distal to the possible site of constriction is useful as well, but
changes in fingertip oxygenation occur late. Subcutaneous or
muscle compartment pressures should be measured if there
is doubt. Escharotomy should be performed for pressures
>30 mmHg.
Important special considerations
For patients with facial burns, fluorescent staining of the
cornea and ophthalmologic consultation are necessary. For
patients with genital burns a urethral catheter should be
placed. For patients with perineal burns a rectal catheter
should be placed. Specific burn circumstances such as chemi-
cal and electrical burn injuries may dictate further diagnostic
studies and treatments (see later).
Fig. 18.9  Estimation of burn size with the Lund and
Browder method. Body surface area calculations in
children must account for unique pediatric body
proportions, here with the Lund and Browder method.
a
b
c
b
c
b
c
b
c
a
Neck 1%
Hand 1.5%
Trunk 13%
Upper
arm 2%
Lower
arm 2%
Feet 1.75%
Neck 1%
Body part
0 yr
a = 1/2 of head
91/2
1 yr
81/2
5 yr
relative % of body surface area
61/2
10 yr
51/2
15 yr
Age
41/2
Hand 1.5%
Trunk 13%
Upper
arm 2%
Lower
arm 2%
Feet 1.75%
b = 1/2 of thigh
23/4
31/4
4
41/4
41/2
c = 1/2 of lower leg
21/2
21/2
23/4
3
31/4

404
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
degree of respiratory injury depends on the type and proper-
ties of the toxic gases and chemicals emanating from burning
carpets, furniture, and other domestic objects comprising the
smoke to which the patient is exposed.
A high index of suspicion is needed to manage these
patients. Inhalation victims may or may not have facial burns,
erythema of mucous membranes, and soot in the airways.
Examination of the pharynx for evidence of edema or particu-
late should be done as soon as possible after a patient is
extracted from a closed space fire. Stridor, difficulty speaking,
or history alone is enough to proceed with flexible bronchos-
copy (gold standard for diagnosing inhalation injury).
Inhalation injury results in bronchial edema and seques-
tration of fluid in pulmonary alveolae. A strong indication
that pulmonary edema is developing is when the resuscita-
tion fluid requirement to maintain urine output far exceeds
Parkland formula guidelines. The common clinical pattern
of significant inhalation injury is large fluid requirements,
high pulmonary artery pressures, and large ventilation–
perfusion O2 gradient. Early endotracheal intubation is
important in patients with upper airway or inhalation injury
to safeguard patency of the airway, to deliver mechanical ven-
tilatory support, and to provide aggressive pulmonary toilet
(Box 18.5).
are chemically reactive and are directly toxic to cells. The
resulting chemical injury causes edema, bronchospasm, and
bronchorrhea. The intrabronchial transudate is not cleared
because of loss of mucosal ciliary action and atelectasis and
potentially pneumonia follows. Bronchopulmonary inhala-
tion injury releases inflammatory mediators that also depresses
cardiac muscle function. Successful management involves
delicate fluid resuscitation to avoid pulmonary edema and
subsequent respiratory failure (Box 18.4).
Burn patients with inhalation injuries exhibit significantly
higher mortality rates than comparable TBSA burn patients
without inhalation injury. Consequences of smoke inhalation
account for more than 50% of fire-related deaths. Most smoke
inhalation victims are injured in closed space house fires. The
Fig. 18.10  Future burn charting will involve more precise digital technology and adjustable charts to match body morphology. (From Orgill, DP. Excision and skin grafting
of thermal burns. New Engl J Med. 2009;360:893–901.)
BOX 18.4  Signs of inhalational injury
• History of flame burns or burns in an enclosed space
• Full-thickness or deep dermal burns to face, neck, or upper
thorax
• Singed nasal hair
• Carbonaceous sputum or carbon particles in oropharynx

405
Acute burn trauma management
greater than 25%, myocardial ischemia, cardiac dysrhythmias,
or central neurological abnormalities. Hyperbaric oxygen is
also recommended for pregnant women and young children
with carboxyhemoglobin levels of ≥15%.
Cyanide intoxication
Nitriles, which contain hydrogen cyanide (HCN), are com-
monly used in industrial solvents, polyurethanes, and vinyl
plastic. They all release HCN during burning. HCN is rapidly
absorbed in lungs or skin and contributes to the morbidity
from smoke inhalation in industrial fires. Cyanide competi-
tively inhibits oxygen binding to hemoglobin and inhibits the
cytochromes of oxidative phosphorylation, resulting in cel-
lular energy depletion. Dicobalt edetate is known treatment
for massive cyanide poisoning in cases of ingestion or indus-
trial explosion. In cases of inhaled cyanide products, the
plasma concentrations of free cyanide is often low. Use of
dicobalt edetate to treat low cyanide levels is risky because it
is also toxic. A better approach is to use amyl nitrite inhalant
or sodium nitrite intravenously. They convert hemoglobin to
methemoglobin, which has a lower cyanide binding affinity.
Fluid resuscitation
Initiation of intravenous fluid administration should begin
immediately in major burn resuscitation. Establishment of
burn resuscitation IV fluid protocols should be reserved
for burns involving greater than 20% TBSA (Table 18.5). In
pediatric patients, fluid resuscitation should be initiated
in all infants with burns ≥10% TBSA and in older children
with burns ≥15% TBSA. Lactated Ringer’s solution with or
without colloid is the most commonly used fluid for burn
resuscitation.
Patients undergoing post-burn fluid resuscitation should
have a Foley catheter inserted in order to monitor urine
output. Urine output should be used as a measure of renal
perfusion and to assess fluid balance. In adults, a urine output
of 0.5–1.0 mL/kg per hour should be maintained.
The color and consistency of the initial urine in patients
with deep thermal burns or electrical injury should be moni-
tored. The urine may be dark red, indicating hemoglobinuria
or myoglobinuria. These heme-proteins can precipitate in the
renal collecting ducts resulting in renal failure. If so, then
osmotic or tubular diuretics should also be used to flush the
renal collecting ducts to avoid renal failure.
In elderly patients, patients with cardiorespiratory disease,
and patients who have delayed presentation, consider insert-
ing a central venous pressure line. This can play an important
part in the subsequent restoration of volume in a patient with
a severe burn. The risks of infection related to a central line
are small in the early stages. With current methods of line
management these risks are outweighed by the importance of
the line for monitoring and access.
Resuscitation fluid composition
Burn fluid resuscitation protocols vary considerably across
different burn centers. The amount of replacement fluid is
predicted from the extent of burn and size of the patient, and
fluid replacement should proceed at the same rate as the loss.
Fluid administered in excess of the capillary leak is excreted
by the kidney or results in increased hydrostatic pressure and
Carbon monoxide intoxication
Carbon monoxide (CO) is a combustion byproduct from the
burning of biomaterials such as petroleum products, coal, and
gas. CO binds to deoxyhemoglobin at 40 times greater affinity
than molecular oxygen (O2). It also binds to intracellular
proteins, particularly those involved in handling oxygen for
energy metabolism. These two effects lead to intracellular and
extracellular hypoxia and a shift to inefficient anaerobic
metabolism, resulting in metabolic acidosis. Closed space fires
often have high CO levels. CO toxicity can occur with or
without inhalation injury.
In the presence of carboxyhemoglobin, conventional elec-
trode blood gas analyzers display erroneously high values for
the calculated oxygen saturation and content. In these circum-
stances pulse oximetry is also inaccurate as it cannot differen-
tiate between oxyhemoglobin and carboxyhemoglobin and
may therefore give normal results.
A blood oximeter, however, accurately determines oxygen
saturation and content and also rapidly measures carboxyhe-
moglobin concentrations. However, under conditions of CO
intoxication, arterial blood gas analysis will reflect metabolic
acidosis and raised carboxyhemoglobin levels but may not
show hypoxia. Treatment is with 100% oxygen with a non-
rebreather facemask, which displaces carbon monoxide from
hemoglobin much faster than atmospheric oxygen.
The amount of carbon monoxide produced in a car engine
can cause fatal carbon monoxide poisoning without produc-
ing enough particulate matter to cause inhalation pneumoni-
tis. Also, some burning materials do not produce much CO.
The half-life of carboxyhemoglobin is ≈1 hour at an FIO2 near
100%.
Patients with carboxyhemoglobin levels greater than
25–30% have had clinically significant exposure to combus-
tion products and should be ventilated (Table 18.4). When
hyperbaric oxygen therapy is available, it can reduce the blood
half-life of carbon monoxide to 23 minutes. Hyperbaric oxygen
is recommended for patients with carboxyhemoglobin levels
BOX 18.5  Indications for intubation
• Erythema or swelling of oropharynx on direct visualization
• Change in voice, with hoarseness or harsh cough
• Stridor, tachypnea, or dyspnea
• Carbonaceous particles staining a patient’s face
Table 18.4  Clinical signs of carboxyhemoglobinemia
Carboxyhemoglobin levels
Symptoms
0–10%
Minimal (normal level in heavy
smokers)
10–20%
Nausea, headache
20–30%
Drowsiness, lethargy
30–40%
Confusion, agitation
40–50%
Coma, respiratory depression
>50%
Death

406
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
fundamental tasks in intensive care. A pulse rate ~110 beats/
min or less for adults usually indicates adequate volume,
with rates >120 beats/min usually indicative of hypovolemia.
Narrowed pulse pressure provides an earlier indication of
shock than systolic blood pressure alone.
Non-invasive blood pressure measurements by cuff are
inaccurate due to the interference of tissue edema and read
lower than the actual blood pressure. An arterial catheter
placed in the radial artery is the first choice, followed by the
femoral artery. The decision to perform invasive hemody-
namic monitoring requires careful consideration. The lack of
benefit associated with goal-directed supranormal therapy
has resulted in waning enthusiasm for the use of pulmonary
artery catheters.
Management of the burn wound
The priority in thermal burn wound management is to create
a physiologic environment for healing and reduce evapora-
tive losses. In a hospital setting, wounds should be washed
and debrided of contaminants and loose non-viable tissue.
For treatment of major burns or in cases of smaller deep
burns, topical antibiotics are useful to control microbial inva-
sion. This is followed by coverage with sterile dressings that
serve as an evaporative barrier and as an immobilizer. Extrem-
ity splints also help immobilize and are helpful to reduce
edema and pain. There is a wide range of wound products
that subserve these purposes. Preferences vary from institu-
tion to institution.
Some practical first aid tips can make a significance differ-
ence to the burn outcome. Small superficial burns are reduced
in severity by immediate rapid cooling with running cold
water for 5 to 10 minutes. Subsequent careful cleaning, immo-
bilization, and barrier protection are the next steps. Topical
extra interstitial edema. Lactated Ringer’s solution most
closely resembles the electrolyte content of normal body
fluids.
Today, the Parkland formula (and its variations) is the most
widely used burn resuscitation guideline. The Advanced
Burn Life Support curriculum supports the use of this formula
for initial resuscitation in burn injury. It is 4 mL/kg/% TBSA,
describing the amount of lactated Ringer’s solution required
in the first 24 h after burn injury. Starting from the time of
burn injury, half of the fluid is given in the first 8 h and the
remaining half is given over the next 16 h. As an example, by
the Parkland formula, a 70 kg patient with a 40% TBSA burn
receives (70 × 40 × 4) = 11,200 mL of lactated Ringer’s solution
during the first 24 h after the burn (approx. 470 mL/h).
Crystalloids are the resuscitation fluids of choice given the
lack of survival benefit and increased cost associated with
albumin and a meta-analysis comparing albumin to crystal-
loid that showed a more than doubled mortality rate with
albumin. Administration of albumin, and other colloids, are
usually avoided in the first 24 h post-burn, but may have a
role in severe burns (>50% TBSA) after the first 24 h.
Vital organ function monitoring
Heart rate and urine output are the primary modalities for
monitoring fluid therapy in patients with large burns although
there is a lack of evidence supporting them. Titrating intra-
venous fluid administration rate according to body weight is
commonly practiced. A minimum of 0.5–1.0 mL/kg per hour
urine output in adults and in children is recommended, but
1–2 mL/kg per hour urine output is preferred. Lesser hourly
urinary outputs in the first 48 h post-burn almost always
represent inadequate resuscitation. Hemodynamic monitor-
ing and treatment of deviation from normovolemia are the
Table 18.5  Fluid resuscitation formulae
Formula
Electrolyte
Colloid
Glucose
Colloid formulae
Brooke
Lactated Ringer’s at 1.5 mL/kg/% TBSA burn
0.5 mL/kg/% TBSA burn
2 L 5% dextrose
Evans
0.9% NaCl at 1 mL/kg/% TBSA burn
1 mL/kg/% TBSA burn
2 L 5% dextrose
Slater
Lactated Ringer’s 2 L/24 h
Fresh frozen plasma at
75 mL/kg/24 h
2 L 5% dextrose
Crystalloid formulae
Modified Brooke’s
Lactated Ringer’s at 2 mL/kg/% TBSA burn
Parkland
Lactated Ringer’s at 4 mL/kg/% TBSA burn
20–60% estimated plasma
volume
Titrated to urinary
output of 30 mL/h
Hypertonic saline formulae
Hypertonic saline solution
(Monafo)
Maintain Urine output at 30 mL/h
Fluid contains sodium 250 mmol/L
Modified hypertonic (Warden)
Lactated Ringer’s + 50 mmol/L NaHCO3 for
8 h to maintain UO at 30–50 mL/h
Lactated Ringer’s to maintain UO at
30–50 mL/h beginning 8 h post-burn
Dextran formula (Demling)
Dextran 40 in saline at 2 mL/kg/h for 8 h
Lactated Ringer’s titrated to maintain urine
output at 30 mL/h
Fresh frozen plasma at
0.5 mL/kg/h for 18 h
beginning 8 h post-burn

407
Acute burn trauma management
and discolors the wound, making it more difficult to evaluate
burn depth. This exudative process is associated with a tran-
sient leucopenia in some patients when it is used on large
open areas. A switch to a different topical agent for a few days
allows the white blood cell count to recover. Restarting silver
sulfadiazine rarely causes recurrent leucopenia. Silver sulfa-
diazine is best indicated for mid to deep partial-thickness
burns that clearly require excision and grafting.
Mafenide acetate is also commonly used and looks similar.
It has excellent eschar penetration and bacteriostatic action.
Use of mafenide acetate on full-thickness burns prevents
deeper infections. Often used on the ear, it helps against
infection of the cartilage. Systemic absorption of mafenide
acetate, when it is applied to large burns, produces a meta-
bolic acidosis by inhibition of carbonic anhydrase. The effect
is usually noted after 3–5 days. Use of the compound on
open wounds also causes pain on initial application. The pain
subsides after several minutes, but patients usually do not
like it.
Another topical dressing uses Dakin’s solution (0.25%
sodium hypochlorite), which is an oxidizing solution that
bleaches proteins and lipids. It is good for suppressing
bacterial and fungal proliferation but is not effective against
bacterial biofilms. Practically, it is useful as a three-times-
per-day gauze dressing to reduce devitalized tissue. Dakin’s
solution-soaked gauze is often alternated with topical
silver sulfadiazine to treat a wound heavily colonized with
bacteria.
Agents such as povidone-iodine solution and nitrofurazone
are still used but are becoming less popular. They are less
expensive to use. However, efficacy and side effects limit
acceptance. They are still widely used in many parts of the
world where access to more expensive agents is limited.
Fortunately, wound infections have decreased dramatically
during the last two decades largely due to a better under-
standing of their causes. Early tangential debridement and
coverage of the wound with skin have markedly decreased
the opportunity for burn wound infection. Despite meticulous
wound care, and even under the most sterile conditions, the
patient’s own microbial flora quickly colonizes and then
invades the non-perfused burned tissue. Only by removing
the devitalized burn tissue and providing stable coverage
is native immunity restored and risk of wound infection
reduced.
Wound dressings17
Standard burn dressing consists of petrolatum or wax impreg-
nated gauze, which effectively restores the transport barrier
function of the epidermis and helps to prevent adherence to
the wound. A topical antiseptic may be applied over this
followed by cotton wool or gauze to absorb the exudate.
Newer dressings have been introduced that are claimed to be
less adherent and allow less water to be lost by evaporation
from the wound while also protecting it from external patho-
gens. Some dressings are meant to provide temporary cover-
age while others are meant to be permanent. These may
further be classified into two groups:
■ Biologic dressings: These can be used either fresh or after
storage following preparation by freezing in liquid
nitrogen or rapid dehydration (lyophilization) and later
reconstitution with saline.
antibiotics are unnecessary unless there is contamination with
foreign material or large surface area involvement.
In wilderness situations well away from medical facilities,
the management priority for large surface area burn wound
care is the control of evaporative and heat losses until evacu-
ation. Cleaned and boiled leaves can block evaporative losses.
The inner cambium layer of plants or trees can also be used
to provide salicylates to control pain and reduce bacterial and
fungal growth.
Topical antimicrobials
In the hospital setting, some formulation of topical silver is
the most commonly used topical antibacterial. Historically,
silver nitrate, as a 0.5% solution, was widely used to deliver
silver ions. It is a liquid which can be poured into the gauze
dressings on the patient to saturate them. It has excellent
antibacterial properties but does not diffuse through eschar
well. Therefore it was not too effective in reducing coloniza-
tion beneath the eschar in deeper burns. Also, silver nitrate is
not very popular with burn center staff because it discolors
the bedding, floors, and uniforms. A more practical approach
is to use nanocrystalline silver coated dressings like Acticoat
(Fig. 18.11). When soaked in water, it releases mono- and
di-atomic silver ions, which can penetrate burn tissue and
provide broad-spectrum antibacterial coverage. This product
does not discolor the skin as silver nitrate does. The Acticoat
sheeting has enough silver to be effective for several days. It
has to be moistened with pure water occasionally to release
and transport the silver ions into the wound.
Silver, like many other transition metals, interferes with
bacterial energy metabolism. Other antimicrobial transition
metals clinically used are iodine, gold, titanium, platinum,
and zinc, to name a few. Silver ions are particularly well toler-
ated by tissue and rapidly cleared in the urine. Another silver
compound, silver sulfadiazine, is a very commonly used
antimicrobial ointment because it combines the antimicrobial
effects of silver and sulfur. It has intermediate eschar penetra-
tion and a large antibacterial spectrum. The antibacterial
activity lasts 8–10 h, and the dressings are changed once or
twice a day. Silver sulfadiazine causes an exudative reaction
Fig. 18.11  Application of a topical antimicrobial silver dressing (Acticoat) is
helpful to control bacterial proliferation in partial- to full-thickness burn injuries,
large surface area burns, heavily contaminated or immunocompromised patients.

408
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
(CEA) well. The rapidity of the engraftment process is likely
to depend on growth factors in the matrix material as much
as the wound bed on which it is placed.
Many burn centers do not routinely use dermal replace-
ments for extensive coverage of acute burns because of the
unpredictable engraftment rate. Large clinical trials have
not demonstrated a survival advantage with use of any of
these products or presented data to suggest that post-injury
function is improved. Therefore most surgeons use dermal
replacements for burn scar reconstruction when supplemental
dermis improves functional and cosmetic outcomes of the
grafting procedure and survival of the patient is not an issue.
The ability to grow and expand isogenic human keratino-
cytes in tissue culture has made survival possible for burn
injuries above 90% TBSA that would not have survived previ-
ously. No longer was an adjacent skin source a major limita-
tion for restoration of a keratinizing isogenic epithelial barrier.
In a landmark case in 1984, twin children with burns over
almost their entire bodies were treated at the Shriners Burns
Institute in Boston with cultured keratinocytes taken from a
small biopsy specimen of undamaged axillary skin. During
the course of their treatment, the keratinocytes were success-
fully expanded in tissue culture and used to resurface some
of their wounds. Survival of the patients was directly attrib-
uted to the use of the technique. Now several biotechnology
companies offer the service for a fee. Skin biopsy specimens
sent to the company are expanded in culture and returned to
the patient, usually in 2–3 weeks. The sheets of CEA are placed
directly onto a cleanly debrided wound bed. The grafts
survive well, and wounds close much faster than without
treatment.
Despite its theoretic advantages, CEA has not succeeded
in solving wound coverage needs of massively burned
patients. Covered by CEA, areas around joints and over
muscles, such as the face, have little motion and poor func-
tion. CEA placed directly on muscle or subcutaneous tissue
only gradually forms a basement membrane, in some cases
during 6 months. Often a mechanically fragile and unstable
epithelial barrier results, which requires replacement over
time.
Physiologic wound dressings
Similar products like Biobrane are also available. These com-
posite materials provide a matrix for vascular endothelial cell
ingrowth and establishment of perfusion beyond the wound
surface that effectively internalizes the wound surface. They
can provide physiologic wound control in large percentage
surface area burns while the process of autograft coverage
takes place. Biobrane is also used to provide a physiologic
environment for the healing of superficial burns and donor
sites.
If applied correctly, Biobrane usually adheres to the wound
bed. Left undisturbed, the dressing limits fluid loss and pre-
vents stimulation of the wound. Epidermal regeneration is
undisturbed beneath. The dressing falls off once the epithelial
layer completely heals underneath; much like a scab falls off
an open wound once it is healed. These materials work best
on superficial partial-thickness burn wounds and skin graft
donor sites that heal in 7–10 days. Placed on deeper wounds,
the materials adhere poorly and as foreign material serve as
a nidus for infection much like the burn eschar. These
■ Physiologic dressings: These consist of synthetic materials
such as polyethylene or silicone, which prevent
adherence to the wound, and plastic films, which reduce
evaporation and contamination.
Biologic wound dressings
Restoring immune defense boundaries to beyond the healing
wound requires restoration of vascular perfusion superficial
to the wound. This requires placement of a biologic dressing
on the wound that is capable on inducing vascular ingrowth
(Table 18.6). The most widely used biologic dressing remains
fresh or frozen human cadaveric split-thickness skin. Properly
handled, cadaveric skin remains viable and vascularizes
(“takes”) when it is placed on a healing wound bed. The
allograft’s dermal capillaries imbibe interstitial fluid, prolifer-
ate, and form channels with the wound bed 2–5 days after
grafting. The process is called inosculation. Once taken, the
wound beneath the allograft becomes sterile and less inflamed.
Of course, allografts contain foreign proteins that will
trigger an immunologic rejection. The immunosuppression
manifested in massively burned patients may delay the rejec-
tion process some, but eventually the grafts develop an
abundant inflammatory cell infiltrate and the epidermis dies
and sloughs from the patient. Loss of the epidermis requires
replacement with another set of cadaveric grafts, or, it is
hoped, the patient is ready for coverage with permanent
autologous tissue. Disease transmission from the donor to the
burn patient is possible but occurs rarely. After the epidermis
is lost, much of the allograft dermis is remodeled by host cells
and becomes permanent.
Porcine skin and freeze-dried human cadaveric skin were
once routinely used to cover burn patients. But they do not
take as well as properly preserved frozen cadaveric skin. Thus
they tend to detach from the wound bed during dressing
changes. However, they do help reduce evaporative fluid and
heat loss while they are attached to the burn wounds.
Over the past 30 years, both cellular and acellular tissue-
engineered biomaterials have served an increasing role in
burn wound coverage (Table 18.7). Acellular matrices of col-
lagen and proteoglycans were manufactured and marketed as
the first “artificial skin” and is now sold under the name
Integra. A thin porous polymer sheet, to serve as a barrier to
the air, covers the surface. Engraftment of the material takes
approximately 2 weeks, and any disturbance, such as exces-
sive movement, fluid accumulation under the material, or
infection, causes loss of the material. Once the matrix is
incorporated, the polymer sheeting is replaced with a thin
skin graft.
Replacement of lost dermis with Integra in deep partial- or
full-thickness burns during the initial treatment of the wound
may decrease the need for later reconstructive surgery by
improving the elasticity of the grafted skin. Despite the tech-
nical problems with these materials, the advantage of reduc-
ing functional and cosmetic deformities from scar contractures
makes their use worthwhile in many clinical situations.
AlloDerm is chemically treated human cadaver dermis
produced from skin allograft in which most non-cross-linked
proteins and lipids are removed. It is commercially available
as dermal replacement. As with Integra, however, the engraft-
ment process for the matrix is variable, and the matrix does
not support the attachment of cultured epidermal autograft

409
Acute burn trauma management
Table 18.6  Temporary skin substitutes
Product
Source
Layers
Category
Uses
Advantages
Disadvantages
Human
allograft
Human cadaver
Epidermis and
dermis
Cryostored
split-thickness
skin
Temporary dressing of
partial-thickness and
excised burns before
autografting or when there
is a lack of autograft
A bilayer skin providing epidermal
and dermal properties
Revascularizes maintaining
viability for weeks
Dermis incorporates
Antimicrobial activity
Epidermis will reject
Risk of disease transfer
Expensive
Need to cryopreserve
Gammagraft
Human cadaver
Epidermis and
dermis
Split-thickness
skin
Temporary dressing of
partial-thickness and
excised burns before
autografting or when there
is a lack of autograft
A bilayer skin providing epidermal
and dermal properties
Revascularizes maintaining
viability for weeks
Dermis incorporates
Epidermis will reject
Risk of disease transfer
Expensive
Store at room temperature
Human
amnion
Placenta
Amniotic
membrane
Epidermis
Dermis
Temporary dressing of
partial-thickness and
excised burns before
autografting or when there
is a lack of autograft
Acts like biologic barrier of skin
Decreases pain
Easy to apply, remove
Transparent
Difficult to obtain, prepare,
and store
Must change every 2 days
Disintegrates easily
Risk of disease transfer
Expensive
Pig skin
Xenograft
Pig dermis
Dermis
Dermis
Temporary dressing of
partial-thickness and
excised burns before
autografting or when there
is a lack of autograft
Good adherence
Decreases pain
More readily available compared
to allograft
Bioactive (collagen) inner surface
with fresh product
Less expensive than allograft
Does not revascularize and
will slough
Short-term use
Need to keep the fresh
product frozen
Oasis
Xenograft
Extracellular
wound matrix
from small
intestine
submucosa
Bioactive
dermal-like
matrix
Temporary coverage of
superficial partial-thickness
burns, although it has
been used for coverage of
autograft and for donor
Excellent adherence
Decreased pain
Provides bioactive dermal-like
properties
Long shelf-life, store at room
temperature
Relatively inexpensive
Mainly a dermal analogue
Incorporates and may
need to be reapplied
Transcyte
Allogenic dermis
Bilayer product
Outer: silicone
Inner: nylon
seeded with
neonatal
fibroblasts
Bioactive dermal
matrix
components
on synthetic
dermis and
epidermis
Temporary coverage of
superficial partial-thickness
burns, although it has
been used for coverage of
autograft and for donor
Bilayer analogue
Excellent adherence to a
superficial partial-thickness
burn
Decreases pain
Provides bioactive dermal
components
Maintains flexibility
Good outer barrier function
Need to store frozen until
use
Relatively expensive
Suprathel
Synthetic copolymer
of polylactide, and
ε-caprolactone
Monolayer
Synthetic
epidermis and
dermis
Temporary coverage of
superficial partial-thickness
burns, although it has
been used for coverage of
autograft and for donor
Long shelf-life, store at room
temperature
Relatively expensive
Not absorbent, requires
fairly frequent
replacement to obviate
pooling of exudate and
related problems

410
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
Table 18.7  Engineered skin substitutes or scaffolds
Product
Tissue of origin
Layers
Category
Uses
Advantages
Disadvantages
Apligraf
Allogenic
composite
Collagen matrix
seeded with
human
neonatal
keratinocytes
and fibroblasts
Composite:
epidermis
and dermis
Excised deep
partial-thickness
burn
Readily available
Expensive
Vascularizes slowly
No epithelial barrier
No antimicrobial
activity
Epicel
Autogenous
keratinocytes
Cultured
autologous
keratinocytes
Epidermis
only
Deep partial- and
full-thickness
burns >30%
TBSA
Readily available
Live cells
Expensive
Vascularizes slowly
No epithelial barrier
No antimicrobial
activity
Alloderm
Allogenic dermis
Acellular dermis
(processed
allograft)
Dermis only
Deep partial- and
full-thickness
burns
Readily available
Live cells
Expensive
Vascularizes slowly
No epithelial barrier
No antimicrobial
activity
Integra
Synthetic
Silicone outer
layer on bovine
collagen GAG
and shark
chondroitin
sulfate dermal
matrix
Biosynthetic
dermis
Full-thickness
burns; definitive
“closure”
requires skin
graft
Readily available
Live cells
Expensive
Vascularizes slowly
No epithelial barrier
No antimicrobial
activity
materials have no antimicrobial activity and therefore should
not be placed on a contaminated wound. Most of the newly
developed synthetic biologic dressings are used mainly in
developed countries because most of these products are
extremely expensive.
Non-operative wound closure
For major burn patients, it is worthwhile to place these
patients in protective isolation to limit contact with hospital-
based pathogens, such as multidrug-resistant organisms.
Despite these precautions, many have one or several bouts of
infection through the course of their treatment. The skin and
gut of the patient are common sources of microbial pathogens,
and no known therapy can eliminate these sources of infec-
tion. Contamination and then overgrowth of burn wounds by
pathogens causing a systemic picture of sepsis typically occur
2–3 weeks after injury. Early enteric feeding and early wound
coverage with skin greatly reduce the incidence of burn
wound infections.
Basically, most burn wounds eventually heal unless there
is infection, lack of blood flow (tissue ischemia), or inadequate
nutritional intake. Physiologic wound care helps minimize
the chance of infection and maximize healing. The daily dress-
ing changes in burn patients permit inspection of the wound
to assess the need for further interventions but, more impor-
tant, offer the chance to remove non-viable tissue. In burn
centers, the providers dedicate a large part of the time to
gently scraping off dead skin and proteinaceous debris that
have gathered since the last dressing. This leaves a healthy
bed for the migration of keratinocytes.
Conceptually, the approach to wound management is to
create a healing environment that attempts to mimic the in
utero environment of a fetal wound. Typically, the wound is
covered between dressings with a moist, antimicrobial cover-
ing to minimize microbial growth, fluid loss, and painful
stimuli and to maximize skin regeneration. Superficial partial-
thickness burns heal in a short time and with little pain or
contracture with warm, moist and bacteria-free dressings.
For small deep partial- or full-thickness burns that could
heal without causing functional limitations, the time for
healing can be more than several weeks with high risk of
infection. Fo r these wounds, it is far better to treat by surgical
debridement and coverage with skin grafts or an engineered
scaffold. For a deep burn over a small area or one with a
patchy distribution, the time for healing by secondary inten-
tion may be no longer than the healing of a skin graft. For
these wounds, surgical debridement and grafting may not be
appropriate. After all, it takes a skin graft 7–10 days to stabilize
on a wound and about the same amount of time for the donor
site to heal.
Operative wound closure18
The main goals of surgical treatment of patients with burns
are removal of damaged or devitalized tissue and replace-
ment with viable tissue. It is well established that early
removal of the necrotic tissue decreases wound infections and
mortality. The tissue undergoing necrosis incites a local and
systemic inflammatory response, serves as a growth medium
for pathogens, and delays wound healing. Early closure
reduces the time of inflammation. Open wounds lose heat and
fluids, contributing to the patient’s hyperdynamic and hyper-
metabolic state. To achieve early debridement and stable
permanent coverage of the wound, the surgeon must over-
come two main obstacles, the physical insult of the

411
Acute burn trauma management
The main limitation to removal of the burned tissue in large
burns is the need to limit blood loss during the debridement.
Blood platelet function often becomes less effective with
repeated blood transfusions. Although some units practice
large (>20% TBSA) debridement in one procedure, most burn
units limit each operative session to debridement of 10–20%
TBSA. This keeps blood replacement, fluid administration,
and anesthetic requirements within the range of stress toler-
ance. Tangential debridement involves cutting the skin tissue
at the depth of the dermal and subcutaneous capillary network
(Fig. 18.12). Historically, before modern pharmacologic agents
were available, tangential debridement of each square centi-
meter of burn would cause 1 mL of blood loss. Today, this
amount of bleeding is uncommon due to use of pressure
debridement process and, on occasion, the limited source of
replacement skin for permanent coverage of large surface area
burns.
Necrotic burn tissue is usually debrided in sequential
layers until all tissue appears viable. In obvious full-thickness
injuries, the burn can be excised to deep fascia in one stage to
reduce blood loss. Optimal timing to accomplish debridement
is within five days of injury to minimize blood loss. With
major burns, treatment is directed towards preservation of life
or limb, and large areas of deep burn must be excised before
the burnt tissue triggers multiple organ failure or becomes
infected. In such cases more superficial burns may be treated
with dressings until healing occurs late or fresh skin donor
sites become available.
Fig. 18.12  (A) Burn wound is marked prior to debridement. (B) Hand scald burn post-debridement.
(C) Using a Weck guarded knife for debridement of a hand scald burn.
A
B
C

412
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
dressings, hemostatic agents, electrocautery, avoidance of
agents that interfere with the coagulation, and subcutaneous
lactated Ringer’s injection beneath the burned tissue all
reduce blood loss. Although full-thickness excision to the
level of muscle fascia with electrocautery minimizes blood
loss, it requires skin grafts on fascia resulting in poor func-
tional and cosmetic results.
Autologous split-thickness skin grafts from unburnt areas
are the “gold standard” for definitive coverage of burn
wounds if enough donor sites are available (Fig. 18.13). When
available, the extremities, minus the hands and feet, are the
best areas for harvesting of skin grafts (Fig. 18.14). The trunk
is used next, but obtaining the grafts is technically more chal-
lenging because of contour irregularities. Tissue inflation with
lactated Ringer’s with 1 : 1 000 000 epinephrine allows harvest-
ing of thinner grafts and minimizes blood loss. Hair-bearing
scalp skin is a great but often underused donor site. The scalp
skin is thick and re-epithelializes rapidly owing to the density
of hair follicles. The scrotum can also be used. Regrowth of
the hair is rarely a problem; thus, the donor site is well cam-
ouflaged after healing.
Fig. 18.13  (A) Healed split-thickness graft. (B) Donor site.
A
B
Fig. 18.14  (A) Commonly used powered dermatome used to harvest skin grafts.
(B) Thin split-thickness autograft harvested.
A
B
Repeated harvesting of skin graft donor sites multiple
times is possible, but the donor site must allowed time to
regenerate between harvest procedures. Donor sites should
ideally be harvested from areas that optimize color match.
Non-meshed (“sheet”) grafts are preferred to improve the
cosmetic and functional result. Meshing the skin grafts allows
coverage of larger areas. Commercially available skin graft
meshers allow expansion ratio of the skin graft either 1.5 : 1 or
3 : 1. Meshing improves graft “take” and faster burn coverage;
the mesh pattern is permanent and unsightly. Sheet grafts are
often used on hands and faces, and over any future site for
intravenous central lines and tracheostomies to obtain rapid
cover.
Allografts (Table 18.6) and skin equivalents (Table 18.7)
have allowed rapid excisions of extremely large burns and
still achieve physiologic closure, with potentially lower mor-
tality in these injuries. Cultured epithelial autografts can also
be used to provide temporary burn wound closure while the
donor sites heal. The cultured cells can be applied as sheets
(available after 3 weeks) or in suspension (available within 1
week). A few burns units use these cells for superficial skin
loss or in combination with mesh graft to improve the cos-
metic result.

413
Acute burn trauma management
Burn wounds are typically debrided and covered with skin
grafts in one procedure. In large area burns, the patient may
undergo skin grafting a few days after debridement. Between
the time of excision and the skin grafting procedure, the
wounds are covered with a biologic dressing (Integra or
cadaver skin) (Fig. 18.15). Removing burned tissue reduces
physiologic stress. This allows the wound bed and the patient
to recover before harvesting the donor sites. Autograph skin
coverage begins as soon as the debridement is complete.
Although this is a more expensive approach to wound cover-
age, the improved functional outcome more than compensates
for the investment. Donor sites harvested a second time can
heal slowly, but the alternatives are limited in these patients
with large burns. Unfortunately, this approach is not feasible
in less developed countries.
A strategic plan directed toward achieving the best func-
tional outcome should be used in planning skin graft coverage
of large surface area burn patients. Most important is to cover
joints and intravenous access sites, thereafter grafting large
torso areas where skin grafts have a high probability for take
to decrease the surface area of the injury and reduce physio-
logic stress. Burns to the hands, neck, and face warrant special
consideration, however. To prevent excessive functional
impairment to these areas after the burn wounds are healed,
these areas should be grafted earlier rather than later. In full-
thickness burns to the hands, neck, and face, delay in grafting
will result in scar contractures and functional limitations that
are difficult to overcome. Thus deep burns to these areas
should be grafted early or closed with flaps so that range of
motion and hypertrophic scar management can be started
early (Box 18.6).
Management of tar burns19–21
Burns due to hot tar are difficult to manage because of the
difficulty in removing the tar without inflicting further injury
to the underlying burn. As it is difficult to remove the tar
rapidly and there is no pressing medical need to do so, it is
best to treat the injury as a deep burn with appropriate fluid
resuscitation or preparation for skin grafting as needed.
Removal of the tar is not essential, but it improves patient
comfort and allows early assessment of the underlying tissue
damage. This approach carries the risk of infection and the
potential conversion of a partial-thickness injury to a full-
thickness injury.
A
C
B
Fig. 18.15  (A) Integra acellular dermal matrix in place over a full-thickness
wound. (B) Well-vascularized Integra graft. (C) Coverage of Integra.
BOX 18.6  Techniques for burn scar reconstruction
• Without deficiency of tissue
•
Excision and direct closure
•
Local tissue rearrangement
• With deficiency of tissue
•
Serial excision and direct closure
•
Split and full-thickness skin autografts
•
Local/regional flaps
•
Distant flaps
•
Tissue expansion
•
Free flaps

414
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
imaging is often essential to determine the extent and location
of tissue damage. MRI without contrast is most accurate.
However, in the setting of a severely injured patient, soft-
tissue CT imaging is faster and more practical.
The surface area of burn usually does not factor into fluid
resuscitation for electrical injury patients unless they have
extensive skin burns as well. If the clinical exam indicates
a significant injury, a Foley catheter should be placed. If the
urine is clear, then fluid administration should be enough to
maintain urine output at 0.5–1 mL times kg body weight/
hour. After 3–4 hours, a judgement can be made about the
severity of injury and whether the intravenous fluids can be
reduced to maintain a baseline urine output of 20–30 mL/h.
If on the contrary the urine is dark colored due to myoglobin,
then intravenous fluid administered should be increased
to keep the urine output at 2 mL per kg body weight.
Sometimes an osmotic diuretic like mannitol is needed to
increase urine output. Alkalinizing agents (e.g., bicarbon-
ate) may prevent protein aggregation in the renal collecting
ducts. Once the urine is clear, then the fluid administration
can return to the level required to maintain a normal urine
output.
Skin burns are managed the same as thermal injuries. Deep
tissue injury, usually skeletal muscle, requires early diagnosis
of deep muscle injury locations, compartment pressure moni-
toring, fasciotomies, and debridement of non-viable tissue.
Manual testing of the compartment pressure is unreliable.
Various ways can be used to measure the pressure. Elevated
pressures over 30 mmHg requires fasciotomies of the fascia
and epimysial layers in the muscle. Escharotomies and other
releases needed to optimize perfusion should be done as soon
as feasible. Most electrical shocks involve the hand. When
hand edema is present, carpal tunnel Guyon’s canal releases
are needed. Doppler and pulse oximeter verification of perfu-
sion in distal tissue is needed.
A second look operation at 48–72 hours is needed for a
final muscle debridement. Deep wound cover with allograft
or composite, with an aim to preserve vital structures,
is indicated between debridements. Serial and multiple
debridements of wounds, including superficial and deep
muscles, must be performed, but nerves, tendons, joints
and bones, even if partially damaged, can be preserved.
Further assessment with time to guide reconstruction is
appropriate.
Large blood vessels that are damaged should be bypassed
by vascular grafting or removal. Injured nerves should be
decompressed by tunnel releases and kept physiologically
moist for later assessment. Allografts or biologic dressings can
be used for interim coverage until the second look procedure
and debridement are completed. If needed to fill dead space,
vascularized coverage is beneficial but may be technically
difficult to achieve in an unstable patient. The vascular
damage and resulting thrombotic phenomenon abates during
second week and tissues become less inflamed. This is the
time when tissues around the wound withstand manipulation
for a local, regional, axial, or free flap. The mortality rate of
patients who suffer high-energy electrical burns is high with
main cause of death being multi-organ failure.
Once wounds are closed, recovery of nerve and muscle
function becomes the next challenge. Nerve releases, nerve
grafts, and transfers are often necessary. Amputation and
replacement with a prostheses is often the most cost-effective
Numerous substances have been used in the past
with variable results, and selection of the appropriate agent
for the removal of adherent tar is still challenging. The deter-
gent surfactant copolymers like polyoxyethylene–sorbitan
or poloxamer 188, which are basically emulsifying agents
commonly used as a wax base, when applied will separate
the tar from the skin. Since they are water soluble, they easily
wash off.
Alternatively silver sulfadiazine, neosporin (with polyoxy-
ethylene sorbitan as a base), or polysorbate may be left under
the bandage on the tar-contaminated burn. The tar comes
away with the bandages when they are removed the next day.
With some of these agents, it is recommended to leave it on
for 12–48 h at a time until the tar has dissolved. Organic sol-
vents, such as alcohol, acetone, aldehydes, ether, gasoline, and
kerosene, are not recommended for removing tar from tissue.
When these emulsifiers above are not available, common
household agents, such as mayonnaise (15–30 min), butter
(20–30 min), sunflower seed oil (20–30 min), and baby oil
(1–1.5 h) placed on sterile gauze and onto the tar, should help
to remove tar without further tissue damage, over the afore-
mentioned time periods.
Mechanical debridement of tar burns is often painful,
relatively ineffective, and results in the removal of underly-
ing viable skin and hair follicles, thus extending the depth
and area of the dermal injury. In addition, a degree of auto-
debridement will occur. If the skin has a light coat of tar and
the patient does not complain about the underlying skin or
surrounding tissue, leaving the asymptomatic tar in place
may be acceptable.
Treatment of electrical injuries22–24
The majority of people that seek medical attention for electri-
cal shock have experienced brief contacts with an electrically
energized conductor. The presenting symptom is pain in the
sensory distribution of the shock, a small contact burn, and
perhaps soreness from falling. Very few have cardiac abnor-
malities. Electrical function of the heart should be assessed by
an electrocardiogram. It is common practice to continuously
monitor cardiac rhythm for the first 24 h after shock if the
current passed through the chest or if the patient reports
cardiac rhythm disturbance after the shock. This has proven
to be unnecessary. If there are no cardiac abnormalities on
admission, it is very unusual for it to develop. Fatal electrocu-
tions occur at the time of shock. Because of significant risk of
late onset neurological sequelae, these patients should follow-
up with a trauma specialist or neurologist.
Patients presenting with cardiac arrhythmias or full cardiac
arrest should undergo cardiac resuscitation procedures
according to standard criteria and will likely need agents to
reduce myocardial excitability in order to recover a functional
rhythm. Once resuscitated, these patients should be admitted
and evaluated for myocardial injury while being monitored
in an inpatient monitored bed or ICU setting for several days.
Patients that have suffered major electrical injuries from
high energy electrical power sources should be admitted to a
specialty burn center to undergo appropriate care. Vital organ
function should be stabilized as soon as possible. Thorough
evaluation to determine the full extent of injury throughout
the current path is the next priority while being constantly
monitored and receiving fluid resuscitation. Diagnostic

415
Acute burn trauma management
increased glucose production, insulin resistance, lipolysis,
and muscle protein catabolism. Without adequate nutritional
support, patients suffer delayed wound healing, decreased
immune function, and generalized weight loss. Many formu-
las predict the nutritional needs of patients on the basis of lean
body mass and percentage TBSA burned (Table 18.9). Increased
intake of both nutritional calories and protein are needed to
restore the deficit. Using the gut for providing nutrition has
several benefits including reduction of translocation of gut
microbes into the circulation.
Nutritional management29–35
Patients fed early have significantly enhanced wound healing
and shorter hospital stays. Meeting the extensive calorie
requirement by oral route alone is practically not possible in
the major burn patients. Enteral nutrition through nasogastric
or nasoduodenal transpyloric tubes are the preferred supple-
mentary route of providing calorie deficit to the acutely
injured burn patient. Patients with 20% TBSA burns will be
unable to meet their nutritional needs with oral intake alone,
and the transpyloric tube should be inserted at admission, as
it is better tolerated than if inserted after the return of peri-
stalsis. In the rare case that precludes use of the gastrointestinal
tract, parenteral nutrition should be used only until the
gastrointestinal tract is functioning.
Early enteral nutrition can relieve gastrointestinal damage
and maintain the integrity of intestinal mucosa after severe
burn. Gastrointestinal mucosal lesions take place during
ischemia and reperfusion period after severe burns. Early
enteral nutrition can relieve the ischemia and reperfusion
injury by means of increasing the ability of eliminating
oxygen free radical. The increase of intestinal permeability
is one of the early features of intestinal mucosal barrier
damage. Early enteral nutrition is an effective method to keep
a normal intestinal permeability through the maintenance
of blood circulation and the prevention of ischemia and
reperfusion injury of intestine. Parenteral nutrition requires
additional vascular access with its concomitant risks. It also
lacks the beneficial effects of gut mucosal stimulation and
protective effects against bacterial translocation and stress
hemorrhage.
The rigorous schedule of dressing changes for burn wound
care, operations, and rehabilitation sessions often interferes
with meals. Diminished appetite from high-dose analgesics
also contributes to poor feeding. Adequate nutritional support
is so critical to recovery from burn injury that most clinicians
will place feeding tubes in patients with inadequate oral
calorie intake despite the risk of aspiration pneumonia.
Much like fluid resuscitation, the exact nutritional require-
ments are debatable. The clinical response of the patient
remains the best indication of nutritional repletion during
recovery from the injury. The rapidity of epidermal regenera-
tion of superficial burns and donor sites and improving serum
nutritional parameters are the best indicators of adequate
nutrition. Measurement of the basal metabolic rate also guides
nutritional replacement therapy. Measuring weight loss and
gain during treatment is not useful because of the large fluid
shifts. Even with adequate nutritional support, most patients
lose muscle mass and weight. Optimizing nutrition to cover
nutrient utilization is the fundamental goal. Over- or under-
feeding increases the risks of complications.
and rapid approach to regaining productivity. Months after
wounds are closed, patients often develop neuromuscular
coordination problems, pain syndromes, and neuropsycho-
logical disorders that require a team approach to manage.
Treatment of radiation injury9,25
Treatment of sunburn injury is to immobilize to speed edema
resolution and apply a cool evaporative barrier. Dressings like
Xeroform, AquacelAg, or hydrogel sheeting are excellent
antimicrobial and evaporative barriers to maintain a physio-
logic environment for healing and substantially reduce
pain. Non-steroidal anti-inflammatory medications reduce
the inflammation and inflammation-driven pain.
Radiation-induced oxidative injury is the central mode
of injury in ionizing radiation-induced injury. Therefore the
administration of antioxidants, e.g., superoxide dismutase
(Cu/Zn/Mn-containing SOD), nitroxides (tempol), and
aminothiols (amifostine), represents a standard approach and
a first-line treatment in clinical therapies for ROI-mediated
injury. They scavenge free radicals, protecting cellular com-
ponents against oxidative damage. N-acetylcysteine (NAC) is
another thiol-containing antioxidant that replenishes cellular
levels of reduced glutathione, an endogenous antioxidant, as
well as scavenging aqueous phase free radicals. These mecha-
nisms allow NAC to serve as a radioprotectant against the
oxidative effects of gamma rays and other forms of ionizing
radiation.
At high radiation doses, it is very difficult to completely
block the effects of reactive oxygen intermediates (ROI) pro-
duction throughout the intracellular water. Consequently, in
parallel with the search for efficient antioxidants, sustained
research efforts are currently focused on identifying critical
targets of the ROIs at the cellular level and on developing
effective treatments for restoring these damaged cellular
components.
Effect of burn trauma on metabolism26–28
Extensive burns elicit a pronounced metabolic response to
trauma causing physiologic derangements leading to the
hypermetabolic state (Table 18.8). Over weeks post-burn, the
hypermetabolic response involves severe catabolism, nitrogen
depletion, and loss of lean body mass. This condition is associ-
ated with a progressive decline of host defenses that impairs
the immunologic response and can lead to sepsis. The burn
wound consumes large quantities of energy due the increased
cost of thermal homeostasis, maintaining host defense barri-
ers as well as protein biosynthesis.
Burn patients often increase the basal metabolic rate
50–100% of the normal resting rate. The main features include
Table 18.8  Percentage increase in metabolic rate versus
burn size
% Burn (TBSA)
Metabolic rate (% increase)
20
30
30
50
40
75
50
100
60
100

416
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
Table 18.9  Formulae for estimating calorie and protein needs
Formula
Age (years)
% TBSA burn
Calories (kcal) per day
Protein
Adults
Burke and
Wolfe
>18
Any
2 × BMR
Not calculated
Curreri
16–59
Any
(25 × body weight in kg) + (40 × % TBSA burn)
Not calculated
>60
Any
(20 × body weight in kg) + (65 × % TBSA burn)
Davies and
Liljedahl
>18
Any
(20 kcal × body weight in kg) + (70 kcal × % TBSA burn)
(1 g × body weight in
kg) + (3 g × % burn)
[>50% TBSA injuries are calculated as a 50% injury]
Galveston I
>18
(2100 kcal/m2 × TBSA) + (1000 kcal/m2 × % TBSA burn)
Not calculated
Ireton-Jones
>18
Any but must
be ventilator-
dependent
1784 − (11 × age in years) + (5 × weight in kg) + 244
(sex: male = 1; female = 0) + 239 (trauma: yes = 1;
no = 0) + 804
Not calculated
Modified
Harris-
Benedict
>18
<40
Male = 1.5 × ([66 + (13.7 × weight in kg) + (5 × height in
cm) − (6.8 × age))
1.5 g × weight in kg
Female = 1.5 × [655 + (9.6 × weight in kg) + (1.7 ×
height in cm) − (4.7 × age))
≥40
Male = 2 × ([66 + (13.7 × weight in kg) + (5 × height in
cm) − (6.8 × age))
2 g × weight in kg
Female = 2 × [655+(9.6 × weight in kg) + (1.7 × height
in cm) − (4.7 × age)
Children
Curreri Junior
0–1
Any
BMR + (15 kcal × % TBSA burn)
Not calculated
1–3
Any
BMR + (25 kcal × % TBSA burn)
Not calculated
4–15
Any
BMR + (40 kcal × % TBSA burn)
Not calculated
Davies Child
1–12
Any
(60 kcal × body weight in kg) + (35 kcal × % TBSA burn)
(3 g × body weight in
kg) + (1 g × % burn)
[>50% surface injuries are calculated as a 50% injury]
Galveston
Infant
0–1
Any
(2100 kcal/m2 × TBSA) + (1000 kcal/m2 × % TBSA burn)
Not calculated
Galveston II
1–11
Any
(1800 kcal/m2 × TBSA) + (1300 kcal/m2 × % TBSA burn)
Not calculated
Galveston
Adolescent
12–18
Any
(1500 kcal/m2 × TBSA) + (1300 kcal/m2 × % TBSA burn)
1 g nitrogen = 6.25 g protein; BMR, basal metabolic rate.
Nutrition formulae
The main features include increased glucose production,
insulin resistance, lipolysis, and muscle protein catabolism.
Without adequate nutritional support, patients have delayed
wound healing, decreased immune function, and generalized
weight loss. Many formulas predict the nutritional needs of
these patients on the basis of lean body mass and percentage
TBSA burned. Increased intake of both total calories and
protein (1.5–3 g of protein/kg/day) is needed to restore the
deficit. Much like fluid resuscitation, the exact nutritional
requirements are debatable. The clinical response of the
patient remains the best indication of nutritional repletion
during recovery from the injury.
Close glucose control of 80–110 mg/dL can be achieved
using an intensive insulin therapy protocol, leading to
decreased infectious complications and mortality rates.
Burn centers continue to use a variety of formulae to
estimate nutrient needs (see Table 18.9). The number of
energy estimation formulas has increased in recent years
with many developed for specific patient populations.
Burn-specific equations have been developed both for
pediatric and adult populations. A study compared 46 pub-
lished energy calculations with indirect calorimetry in burn
patients and found none precisely estimated calorie needs
and most demonstrated some inaccuracy for any given
patient.
Several studies propose the use of anabolic steroids or
growth hormone to reduce muscle catabolism and weight loss
during the injury and to enhance weight gain during recovery.
It appears that anti-catabolic and anabolic agents can mark-
edly diminish the net catabolism of burn injury during the
acute and recovery phases. These agents, in combination with
optimum protein intake, appear to be of significant benefit in
the metabolic management of the severe burn. Adequate
nutritional support from the beginning of acute care is critical
to burn patient survival.
Therapeutic strategies should aim to prevent body weight
losses of more than 10% of the patient’s baseline status because
more profound weight loss is associated with significantly

417
Complications
Complications
Skin graft loss
Loss of skin graft is the most common operative complica-
tion and is caused by inadequate immobilization, inadequate
wound debridement, or formation of blood clot beneath the
graft. Infection is usually the direct consequence of failed
graft take (Fig. 18.16). Thus careful placement of dress-
ings to immobilize the graft relative to the wound bed is
essential. Some burn surgeons spray freshly applied skin
grafts with fibrin sealant to help immobilize the graft and
accelerate vascular ingrowth. Unless carefully splinted, avoid
circumferential compression dressings on a grafted extremity.
Any movement in a grafted and circumferentially wrapped
extremity will generate shear stress between underlying
muscles and the overlying graft. Early graft inspection on
day 2–3 after grafting should be encouraged with removal of
any underlying hematoma. After day 3, capillary ingrowth
has occurred and would be interrupted by graft movement.
If examination shows that the skin grafts are grossly infected,
then microbiologic cultures can be performed and appropri-
ate antimicrobial therapy instituted.
Invasive wound infection
In burn patients, systemic antibiotic prophylaxis administered
in the first 4–14 days significantly reduces all-cause mortality
by nearly a half; limited perioperative prophylaxis reduces
wound infections but not mortality. Topical antibiotic prophy-
laxis applied to burn wounds, commonly recommended, had
no large beneficial effects. The methodologic quality of the
evidence is weak, however, so a large, robust randomized
controlled trial is now needed.
Wound infection should be suspected if the wound becomes
increasingly uncomfortable, tachycardic, painful, or malodor-
ous; if cellulitis is observed; or if the patient becomes febrile.
Several biopsies from suspicious areas in the burn wound
should be sent for microbiology. Since all wounds will be
colonized after a few hours, it is best to measure the density
of bacteria in the wound. This is called quantitative bacterial
culture. Some experience, clean instruments, and training is
worse outcomes. Known consequences of catabolic disorders
with loss of lean body mass above 10% include impaired
immune function and delayed wound healing. Lean body
mass reduction beyond 40% leads to imminent mortality.
Therefore complications of ongoing catabolism remain a
major cause of morbidity and mortality in severely burned
patients.
Pain control
The adverse sequelae of inadequate pain in the burn popula-
tion have been long recognized, yet control of pain remains
inadequate globally. The dynamic evolution of the pain both
centrally and peripherally, and the many factors that influence
pain perception, illustrate the need for a therapeutic plan that
is similarly dynamic and flexible enough to cope with the
facets of background, breakthrough, procedural, and postop-
erative pain. Regular, ongoing, and documented pain assess-
ment is key in directing this process.
Severe pain with burns is a major physiologic stress
that can have a negative impact on the patient’s recovery.
Often, bedside procedures require high doses of anxiolytic
and opiates. Particularly painful and anxiety-provoking is
the first dressing change after skin grafting. In addition to
significant pain, especially at the donor site, patients often
experience great anxiety as they confront their new graft
for the first time. Various approaches have been studied to
provide sedation, comfort, and pain control. Conventional
pharmacotherapy utilizes opioids for analgesia and ben-
zodiazepines for sedation. The risk of apnea may cause
the provider to err on the side of administering too little
drug. To combat this, some centers offer patient-controlled
analgesia (PCA) using propofol. PCS allows the patient to
self-titrate to the comfort level desired, which may have the
added benefit of allowing the patient to feel in control of the
situation.
In general, it is helpful to have an anesthesiologist or pain
specialist involved in the day-to-day management of burn
patients. Providers caring for burn patients should keep in
mind several key points in order to optimize pain control
during dressing changes: optimize nutrition and hydration to
stimulate the healing process; ensure the safety and comfort
of sedated patients both during and post-procedure by
frequently assessing pain level and vital signs; and control
acute pain during the most painful stages of dressing changes
(dressing removal and wound cleansing). Close monitor-
ing of respiratory status is required when consciousness is
diminished.
More emphasis on pain control not only helps the patient’s
psychological wellbeing but may significantly affect physical
outcome as well. Painful stimuli influence the release of a
number of circulatory factors that affect tissue perfusion,
immune system function, and wound healing. Effect manage-
ment of pain requires a working knowledge of pain neuro-
physiology and pharmacology. These skills are important for
burn care providers.
Patients without a substance abuse problem before the
injury typically do not develop opiate addiction even after
receiving high doses for prolonged periods, but physical
dependence often occurs after sustained treatment with
opiates. Gradually reducing the doses of opiates as pain
diminishes avoids opiate withdrawal.
Fig. 18.16  Appearance of an infected burn wound resulting in systemic sepsis and
loss of skin autografts and allografts.

418
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
syndrome. Patients presenting with burns of neck, thorax,
abdomen, extremities that are near circumferential, or greater
full-thickness burns are likely to have obstructed blood flow
to the extremity and require escharotomies. In extremities
there is impaired capillary refill and paresthesia, and increased
pain develops earlier than decreased pulses. Measurement of
muscle or tissue pressures with a manometer and Doppler
meter can be used to monitor tissue perfusion distal to the site.
If tissue pressures are high, surgical release maybe indicated.
If the pressures are moderately high, constant monitoring is
indicated. The orbit is a compartment limited to expansion
necessary to accurately perform the test. When the density of
bacteria in the wound exceeds 100 000 colony-forming units
per gram of tissue (equivalent to 105/gram), then host defense
mechanisms are no longer effective. This condition permits
invasive wound infection.
Treatment of invasive wound infections requires both
antibiotics and excision of all infected tissue. Empiric broad-
spectrum antibiotic treatment should be started after discus-
sion with the microbiology team. The antibiotic treatment
regime can be adjusted to be more specific according to the
rapid-slide Gram stain results obtained in a few hours from
the biopsy. In 24–48 hours, more specific identification of the
bacteria and its antibiotic sensitivities can be used to decide
on the antibiotic regime. The recommended choice of antibi-
otic is guided by the most likely cause of infection and local
patterns of antibiotic resistance should also be considered.
Adrenal insufficiency
Some degree of adrenal insufficiency occurs in up to 36% of
patients with major burns. Correcting for it is not as simple
as administering corticotropin. Probably due to the variation
in the stress responses across different patients, there is no
statistically resolved association between response to cortico-
tropin stimulation and survival. The clinical relevance of this
finding has not been established.
Circumferential limb compression with
vascular compromise
Patients may require escharotomies (Fig. 18.17), fasciotomies,
or both (Fig. 18.18) for the release of extremity compartment
Fig. 18.17  (A) Escharotomy lines and relevant anatomy.
(B) Hand escharotomy incisions.
A
B
Fig. 18.18  Volar escharotomy and extensive fasciotomies of the volar forearm and
hand with necrotic muscle debridement following electrical injury. The fasciotomy
extended into normal skin above and below the skin contracture. The fasciotomies
included the investing compartment fascia and epimysial layers.

419
Complications
Neutropenia
Transient leucopenia is common, primarily due to a decreased
neutrophil count. Maximal white blood cell depression occurs
several days after admission with rebound to normal a few
days later. Use of silver sulfadiazine has been associated with
this transient leucopenia; resolution is independent of contin-
ued silver sulfadiazine.
Sepsis36–39
Patients with large TBSA burns are immunosuppressed and
at increased risk for infections, especially of the wounds,
venous access sites, and lungs. Small injuries (<10% TBSA)
heal rapidly, and infections are rare. Clinical surveillance for
signs of infection is not simple because many burn patients
have a fever and altered white blood cell counts without infec-
tions. Many burn patients exhibit a low-grade fever in the first
week after injury due to chemical sepsis syndrome.
Common causes of infections in burn patient populations
arise from translocation of gut flora in physiologically stressed
patients and cross contamination. The first priority is to rule
out central venous catheter sepsis and change the line if it is
positive. Burn wounds become rapidly colonized with Gram-
positive bacteria, mainly staphylococci from hair follicles and
dermal glands. The moist burn eschar encourages microbial
growth. Gram-negative bacterial infections result from trans-
location from the gut because of reduced mesenteric blood
flow at the time of burn and subsequent insults. Finally, burn
patients can incur hospital-acquired infections common to
other patients in intensive care units, including intravascular
catheter-related infections and ventilator-associated pneumo-
nia, with an overall incidence of infection higher than that of
other patients in intensive care units.
Current guidelines for management do not recommend
continuous systemic antibiotic prophylaxis for burns patients,
indicating lack of evidence for efficacy and induction of
antibiotic resistance. A recent meta-analysis found that for
burn patients systemic antibiotic prophylaxis administered
over the first 4–14 days post-burn significantly reduced all-
cause mortality by nearly a half and limited perioperative
prophylaxis reduced wound infections but not mortality.39 In
addition, the study suggested that topical antibiotic prophy-
laxis applied to burn wounds, commonly recommended, had
no beneficial effects. Because of the difficulty of multicenter
clinical studies, methodologic quality of the data was weak,
and they concluded that prophylaxis could not be recom-
mended for patients with severe burns other than periopera-
tively and that there was a need for randomized controlled
trials to assess its use. Prophylactic antibiotics are adminis-
tered immediately prior to burn wound excision is commonly
performed as a treatment to prevent burn wound infection. It
is important to establish adequate blood levels at the time of
the incision.
Patients with large surface area burn injuries that have
failed coverage and remain open for long periods still develop
wound infections and ultimately succumb to infection. Isola-
tion of the patient in specialized unit beds along with infection
precautions by the healthcare workers (handwashing, gloves,
and gowns) reduces the transmission of pathogens from one
patient to another. A high level of suspicion for wound infec-
tion must be kept when the patient’s condition deteriorates
and may require lateral canthotomy to successfully reduce
intraocular pressure to normal.
Compartment syndromes
Compartment syndrome occurs when the tissue pressure
within an enclosed space is elevated above venous pressure. If
the pressure exceeds venous pressures, the result is decreased
blood flow within the fascial compartment, decreased tissue
oxygenation, and ischemia. Tissue hypoxia leads to intracel-
lular edema and increase in compartment pressure. The final
result without prompt treatment is tissue necrosis.
The occurrence of abdominal compartment syndrome
has a similar pathophysiology. Because of the vital organs
involved, it can become life-threatening. It often follows fluid
extravasation/edema in a major burn patient with severe
capillary leak. It is diagnosed by an intra-abdominal pressure
>20 mmHg and at least one new organ dysfunction. It is
associated with renal impairment, gut ischemia, and cardiac
and pulmonary malperfusion. Clinical manifestations include
tense abdomen, decreased pulmonary compliance, hypercap-
nia, and oliguria. Urine output monitoring is not sensitive or
specific enough to diagnose abdominal compartment syn-
drome. Careful monitoring and aggressive treatment should
be instituted to avoid this mortal complication. Appropriate
intravascular volume, appropriate body positioning, pain
management, sedation, nasogastric decompression if appro-
priate, chemical paralysis if required, and torso escharotomy
are all interventions to increase abdominal wall compliance
and decrease intra-abdominal pressures. Bladder pressure
monitoring should be initiated as part of the burn fluid resus-
citation protocol in every patient with 30% TBSA burn.
Patients who receive >250 mL/kg of crystalloid in the first
24 h may require abdominal decompression. Percutaneous
abdominal decompression is a minimally invasive procedure
that should be performed before resorting to laparotomy. If
less invasive maneuvers fail, decompressive laparotomy
should be performed in patients with abdominal compart-
ment syndrome that is refractory to other therapies.
Deep venous thrombosis
Deep venous thrombosis incidence ranges from 1% to 23% in
burn patients and deep venous thrombosis chemoprophylaxis
with heparin is recommended. Often coagulopathies develop
after multiple transfusions. Alteration in clotting parameters
can trigger intravascular thrombosis in low flow veins.
Systemic inflammatory response syndrome
There are standardized definitions for sepsis and infection-
related diagnoses in burn patients. Patients with large burns
have a baseline temperature reset to 38.5°C, and tachycardia
and tachypnea may persist for months. Continuous exposure
to inflammatory mediators leads to significant changes in the
white blood cell count, making leukocytosis a poor indicator
of sepsis. Use other clues as signs of infection or sepsis, such
as increased fluid requirements, decreasing platelet counts >3
days after burn injury, altered mental status, worsening pul-
monary status, and impaired renal function. The term “sys-
temic inflammatory response syndrome” should not be
applied to burn patients because patients with large burns are
in a state of chronic systemic inflammatory stimulation.

420
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
reduce the incidence of this problem. Venous clots in large
surface area burn patients serve as a rich culture media for
bacteria. Many major burn patients who require many weeks
of care require central venous lines at some point in their
treatment because peripheral access sites are usually limited.
Central line-related infections can cause major morbidity, and
constant attention is given to changing catheters once a line
infection is suspected. Septic thrombophlebitis is a common
complication of venous thromboembolism in burn patients. It
should be suspected and ruled out in burn patients with
unexplained signs of sepsis. The evaluation begins by inspect-
ing all sites of prior catheter access. Resection of the infected
vein is often required for effective therapy.
Rehabilitation40–44
Major burn injuries create indescribable challenges for the
patient to overcome. Alteration in body image, mechanical
disabilities, increased risk of further injury, and pain are just
a few of the problems. Burn trauma rehabilitation is the res-
toration of health and work capacity of a person incapacitated
by burn injury. Achieving success in burns rehabilitation is
often challenging.
Adaptation and regain of capability requires the invest-
ment of support groups, family, friends, and a multidisci-
plinary rehab team. Very few countries have the resources to
support that level of investment. But effective rehabilitation
can produce a gainfully employed and psychologically intact
person. Burn patients have to recover mobility and balance to
gain the confidence in their ability to work or engage in per-
sonal interactions.
Formulation of an optimal rehabilitation strategy begins in
the first few days after hospital admission. Before the wounds
are closed, therapy to prevent contractures by musculoskeletal
dynamic therapy, traction, and splinting is of paramount
importance especially for wounds surrounding joints. Splints
are made preoperatively and placed in the operating room at
the time of grafting. Some burn centers use hydrotherapy as
a part of physical therapy to range extremities while the
patient is in warm water. This reduces joint stiffness and pain.
Skilled physiotherapy is very important in the prevention
of the burn contractures. Because the competing factors con-
trolling scar and scar contracture as well as the incomplete
information, debates over whether to rest or mobilize healing
wounds continues. Recently, early motion has been strongly
advocated to avoid joint contractures. Injured upper and
lower extremities are elevated to allow adequate venous
drainage and to reduce edema.
Experienced judgment is required to recognize the stages
of wound healing and the relative importance of inflamma-
tion and mechanical tension in scar stimulation. A study has
demonstrated that starting good burn physiotherapy on post-
burn day 1 for non-grafted areas and post-burn day 3 for
skin-grafted areas resulted in only 6% burn contracture. Early
and proper splinting and stretching of flexion crease burns,
such as the neck, axilla, and antecubital areas, reduce the
extent of scar contractures and may prevent subsequent
functional deformities and the need for reconstruction.
Plan for continuation of physiotherapy treatment after
releasing the patient from hospital, for at least 18 months. In
the acute and post-healing stages of recovery, the move out of
rapidly. Wound cultures, particularly quantitative assessment,
and biopsies for histologic examination help confirm the
diagnosis and direct therapy. Prompt excision of necrotic or
infected tissue, appropriate topical treatment, and systemic
antimicrobial therapy are critical to survival of the patient.
The best clinical approach to prevent sepsis is to bolster
the immune system with early nutritional support and
re-establish the barrier function of the gut and skin. Treatment
with an antibiotic usually controls the infections but alters the
patient’s microbial flora. Should the patient remain at risk for
infections after the first infection is treated, a second, more
drug-resistant infection often occurs. Should the burn be large
enough that the patient remains at risk for a month or longer,
systemic fungal infections become a major clinical problem.
Treatment of fungal sepsis with less toxic fluconazole has
greatly increased the therapeutic options.
Ventilator management
Inhalation injury and respiratory complications are still one
of the major causes of mortality in severe burns. Ventilatory
support and airway management in this situation are often
challenging, and the need for prolonged endotracheal intuba-
tion is very common in patients affected by different degrees of
respiratory distress syndrome. Despite the use of high-volume
low-pressure cuffs, considerable controversy exists among
burn surgeons as to whether to convert endotracheal tubes
to tracheostomy in burns patients, particularly when ventila-
tor support is prolonged beyond two weeks or when other
airway complications occur, as many studies have recorded
high mortality and high tracheostomy complications.
The pathogenesis of these entities is still unclear, but the
combination of inhalation injury, infection, presence of an
endotracheal tube, and individual factors play an important
role in their development. Tracheostomies may provide a
good portal of entry for microorganisms into the respiratory
tract, with a high incidence of respiratory infection and sepsis.
In addition, feeding aspirations, obstructive abnormalities,
increased incidence of pneumonia and tracheo-innominate
fistulas have been reported as high-morbidity complications
of tracheostomies. Long-term sequelae are no less important.
Stenosis of the airway, dysphagia, alterations of speech,
tracheo-esophageal fistulas, and tracheomalacia can compro-
mise the favorable outcome of this selected group of patients.
Every effort should be made to maintain airway pressures at
the lowest range, in order to prevent tracheomalacia. Advan-
tages of tracheostomy include minimizing dead space, ease
of suctioning, presence of a more secure airway, and ease of
movement. Theoretically, it should prevent the appearance of
subglottic stenosis.
The use of low-pressure balloons in modern endotracheal
tubes has markedly decreased the incidence of tracheal
erosion and life-threatening tracheo-innominate artery fistu-
las. Tracheostomies are still useful so patients can be gradually
and safely weaned from prolonged dependence on mechani-
cal ventilation and to decrease injury to vocal cords.
Thrombophlebitis
Venous thrombosis is a common problem in major burn
patients, especially in the veins used for intravenous access.
Heparin prophylaxis is routinely used in burn centers to

421
Managing burn scar hypertrophy and contracture
manifest months after an electrical shock injury. These
problems are common even in patients who have low-energy
electrical shocks. In general, a multidisciplinary team of
neurologists, neuropsychologists working in collaboration
with the burn rehabilitation team is needed.41,42 Intense and
protracted physical and occupational therapy is required to
regain normal balance and coordination.
Fortunately, severe radiation skin injury is not common.
Wound closure with non-irradiated skin is required.25 The
non-irradiated cells in the autografted skin will gradually
improve the quality and healing capacity of surrounding
radiation-injured skin.9 Adipose transfer into radiation-injured
soft tissue has also been found to benefit radiated skin.25
Managing burn scar hypertrophy
and contracture45–50
The ideal scar is strong enough to subserve the mechanical
requirements and support epidermal functions. Ideally, just
enough scar forms for this purpose. However, the wounds of
burn patients often heal with excess (i.e., hypertrophic) scar-
ring. There is no quantitative definition of hypertrophic
scarring. Rather, the diagnosis is given to scars that are thicker
than necessary. Hypertrophic scar formation after burn wound
healing is a common obstacle to rehabilitation.
Several epigenetic causes of hypertrophic scarring are well
known and important to consider. Basically, prolonged wound
inflammation, dynamic tension (shoulders, chest, volar
forearm, and dorsal legs) on the wound, endocrine or hor-
monal factors associated with rapid growth, pregnancy, and
pigmented skin predispose to hypertrophic scar formation.
Factors that increase inflammation include wound infection,
prolonged healing by secondary intention, or immunologi-
cally foreign material present in the wound. It is postulated
that hypertrophic scars begin as the result of an injury to the
deep dermis. They are especially pronounced in wounds that
have a prolongation of the inflammatory and proliferative
phases of wound healing. The incidence of hypertrophic scars
following burn wound healing is close to 90%.
Hypertrophic scarring also occurs as the result of dynamic
mechanical skin tension acting on the healing wound. As a
result of mechanical tension, scars located on certain areas of
the body (e.g., sternum, deltoid, and upper back) are fre-
quently hypertrophic, the typical appearance of which can be
seen in Fig. 18.19. This anatomic dependency seems to cor-
relate with patterns of skin tension. The natural history of
hypertrophic scars is that they regress with time after injury,
leaving behind, however, an unsightly wide gap of thinned
dermis between wound edges.
A familial pattern in hypertrophic scarring is not described;
however, populations with higher skin melanin content are
known to have a higher incidence of hypertrophic scars. These
populations include people of African, Asian, and Hispanic
descent.
Hormonal influences are also known to be a factor, with
hypertrophic scarring often initiated at the start of puberty or
during pregnancy. Scar tissue cells are sensitive to the influ-
ences of the same growth factors that drive normal tissue
growth and development. Schierle reported an increase in
testosterone receptors in hypertrophic scars, which may
the burn center is the first defining point in a patient’s post-
burn life. In addition to physical considerations, wound
healing and recovery after burns is promoted by good nutri-
tion, for initial wound healing and long-term scar reduction.
Rehabilitation involves the whole burn team to collectively
encouraging the patient to live as normal a life as possible
between dressing changes and operations; the therapists take
the lead in maintaining muscle strength, joint range, and
activities of daily living.
In the chronic phase, the prevention and management of
hypertrophic scarring and contractures are significant issues.
Another important aspect of burn care is recognizing the
psychosocial needs of burn patients. To facilitate this, many
centers provide psychologists, social workers, and vocational
counselors as part of the multidisciplinary team. The physi-
ologic recovery of burn patients is divided into categories
(critical stage, acute stage, long-term rehabilitation), each with
unique psychosocial aspects to consider.
Psychological challenges in the critical stage are due to
over- and understimulation, an uncertainty about and a
struggle for survival, painful treatments, delirium and confu-
sion, and impaired communication. At this stage, physical
survival is the primary goal and psychological intervention
may be of little value. During the acute or restorative phase
of care, patients often display symptoms of depression and
anxiety. Patients may also exhibit grief, impaired sleep, and
acute stress disorder. Pharmacotherapy and counseling can
help patients during this stage.
After discharge from the acute rehab program, long-term
rehabilitation begins. There are several basic challenges to
overcome. Anxiety and depression are common issues. Learn-
ing to cope with a potential decrease in physical function (i.e.,
due to deconditioning and scarring) is also important. Psy-
chological factors such as sexuality and changed body image
also require supportive management. Post-traumatic stress
disorder is another common inexorable sequelae of burn
trauma that requires early intervention to contain its conse-
quences. Negative emotional interpersonal experiences only
add to the severity. The direct involvement of psychiatric
services is an invaluable aspect of burns rehabilitation.
Another post-healing concept is community outreach. It
was introduced to try to overcome the gap recognized at this
stage of recovery, to provide links with the community ser-
vices and local hospitals. Rehabilitation centers start integra-
tion back into society in a protected environment with other
people who had sustained physical trauma. They could
receive the help in returning to work, to the home, hobbies,
and to society, and if necessary return for “top up” help after
reconstructive surgery.
For children, reintroduction to society that usually centers
around school is more challenging especially during adoles-
cence. Children’s burn clubs go a long way in providing
confidence-building support before and after hospital dis-
charge. Issues related to a full return to the community, and
their solutions such as partnership with teachers, behavior
therapy, and adaptive equipment, may be outside the limits
of this chapter. However, follow-up recommendations,
including a more comprehensive checklist of potential areas
of need, may be helpful.
Electrical injury patients have particularly difficult reha-
bilitation challenges.41,42 Many of the widely reported neuro-
logical, neuromuscular, and neuropsychiatric complications

422
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
Fig. 18.19  (A) Hypertrophic burn scar 6 months after flame burn to chest and neck.
(B) Application of hydrogel or polymer sheeting sheeting to scar to increase
moisture content and comfort. (C) Scar appearance several months later.
A
B
C
contribute to the formation of these scars during adolescence.
Hypertrophic scars occur in 60% of burned children aged
under 5 years.
Hypertrophic scarring, unstable epithelium, and poor
skin elasticity often occur when deep burns are allowed to
heal without grafting. Initial therapy is focused on control-
ling scar pathogenesis. Effect treatments requires induction
of scar remodeling and softening. Topical non-steroidal
anti-inflammatory agents, anti-histamines, and other immu-
nomodulators are useful to downregulate scar inflammation,
which often persists long after the wound is epithelialized.
Ointments moisturize by blocking evaporation and reduce
harmful scratching of healed skin grafts.
Typically, the rehabilitation team (occupational and physi-
cal) evaluates and formulates a treatment plan early to mini-
mize scarring. Preventative therapy begins with pressure

423
Managing burn scar hypertrophy and contracture
hand and extremities, physical and occupational therapists
often use thermoplastic splints, serial casting, gel sheeting
inserts, and pressure to decrease hypertrophic scars and joint
contractures.
Major burn patients are known to be vitamin D deficient,
in part, resulting from the skin damage. Vitamin D is an anti-
inflammatory hormone that also regulates calcium metabo-
lism. Normal Vitamin D levels are essential for normal healing.
garments, moisturizers, anti-inflammatories, functional range
of motion, splinting, edema control, and scar treatments
while the scarring is in the immature phase, before it is hyper-
trophic or contracted. Hand scars are particularly important
to address early. They often require splinting, message and
range of motion exercises.
Management of mature scars that are hypertrophic on
presentation is another level of challenge. For burns of the
2. Demling RH. Burns. N Engl J Med. 1985;313:1389–1398. This article is
an excellent early review of burns and burn management. It details acute
resuscitation, burn-associated infection, metabolic aspects of burns, wound
healing, and more.
5. Despa F, Orgill DP, Neuwalder J, Lee RC. The relative thermal
stability of tissue macromolecules and cellular structure in burn
injury. Burns. 2005;31:568–577.
6. Lee RC, Parsons RW. Confusion in electrical trauma terminology.
Plast Reconstr Surg. 1992;89:1020–1021. This paper discusses the cellular
structure of tissue macromolecules during burn injury. The authors
suggest that strategies to minimize the damage in a burn injury should
include the stabilization of the cellular membrane and membrane-bound
ATPases.
7. Cancio LC, Lundy JB, Sheridan RL. Evolving changes in the
management of burns and environmental injuries. Surg Clin N Am.
2012;92:959–986. This review of electrical shock trauma details the
anatomic patterns of the resultant tissue injury from various modes of
electromagnetic exposure. Also, the physics of tissue injury due to power
lines, exposure to lightning and radio frequency, ionizing radiation, and
microwave is discussed.
10. Jackson D, Topley E, Cason JS, et al. Primary excision and grafting
of large burns. Ann Surg. 1960;152:167–189.
11. Nguyen N, Gun R, Sparnon A, et al. The importance of immediate
cooling – a case series of childhood burns in Vietnam. Burns.
2002;28:173–176.
12. Mankani MH, Kicska G, Lee RC. A three-dimensional computerized
burn chart – stage II: assessment of accuracy. J Burn Care Rehab.
1994;15:191–193.
18. Orgill DP. Excision and skin grafting of thermal burns. N Engl J
Med. 2009;360:893–901. The clinical problem associated with thermal
burns is reviewed. The author also discusses the benefits of skin grafting,
clinical evidence associated with it, clinical use, and adverse events.
23. Lee RC, Jang DJ, Hannig J. Biophysical injury mechanisms in
electrical shock trauma. Ann Rev Biomed Eng. 2000;2:477–510.
31. Venter M, Rode H, Sive A, et al. Enteral resuscitation and early
enteral feeding in children with major burns: effect on McFarlane
response to stress. Burns. 2007;33:464–471. This study discusses enteral
resuscitation and early enteral feeding in children with major burns. The
authors provide recommendations on the use of enteral resuscitation and
early enteral feeding based on the clinical scenario.
50. Edstrom LE, Robson MC, Macchiaverna JR, et al. Prospective
randomized treatments for burned hands: nonoperative vs.
operative. Preliminary report. Scand J Plast Reconstr Surg.
1979;13:131–135.
Access the complete reference list online at

423.e1
References
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an excellent early review of burns and burn management. It details acute
resuscitation, burn-associated infection, metabolic aspects of burns, wound
healing, and more.
3. Stedman TL. Illustrated Stedman’s Medical Dictionary, 24th ed.
Baltimore: Williams & Wilkins; 1982.
4. Lee RC, Astumian RD. The physicochemical basis for thermal and
non-thermal “burn” injury. Burns J. 1996;22:509–519.
5. Despa F, Orgill DP, Neuwalder J, Lee RC. The relative thermal
stability of tissue macromolecules and cellular structure in burn
injury. Burns. 2005;31:568–577. This paper discusses the cellular
structure of tissue macromolecules during burn injury. The authors
suggest that strategies to minimize the damage in a burn injury should
include the stabilization of the cellular membrane and membrane-bound
ATPases.
6. Lee RC, Parsons RW. Confusion in electrical trauma terminology.
Plast Reconstr Surg. 1992;89:1020–1021.
7. Cancio LC, Lundy JB, Sheridan RL. Evolving changes in the
management of burns and environmental injuries. Surg Clin N Am.
2012;92:959–986. This review of electrical shock trauma details the
anatomic patterns of the resultant tissue injury from various modes of
electromagnetic exposure. Also, the physics of tissue injury due to power
lines, exposure to lightning and radio frequency, ionizing radiation, and
microwave is discussed.
8. Su CW, Lohman R, Gottlieb LJ. Frostbite of the upper extremity.
Hand Clin. 2000;16:235–247.
9. Mettler FA, Voelz GL. Major radiation exposure – what to expect
and how to respond. N Engl J Med. 2002;346:1554–1560.
10. Jackson D, Topley E, Cason JS, et al. Primary excision and grafting
of large burns. Ann Surg. 1960;152:167–189.
11. Nguyen N, Gun R, Sparnon A, et al. The importance of immediate
cooling – a case series of childhood burns in Vietnam. Burns.
2002;28:173–176.
12. Mankani MH, Kicska G, Lee RC. A three-dimensional computerized
burn chart – stage II: assessment of accuracy. J Burn Care Rehab.
1994;15:191–193.
13. Tuch DS, Lee RC. Three-dimensional wound surface area
calculations with a CAD surface element model”. IEEE Trans Biomed
Eng. 1998;45:1397–1400.
14. Fujioka M, Yakabe A. Does inhalation injury increase the mortality
rate in burn patients? Investigation of relationship between
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2009;4:20–22.
15. Rabinowitz PM, Siegel MD. Acute inhalation injury. Clin Chest Med.
2002;23:707–715.
16. Thompson PB, Herndon DN, Traber DL, Abston S. Effect on
mortality of inhalation injury. J Trauma. 1986;26:163–165.
17. Orgill DP, Straus FH, Lee RC. The use of collagen-GAG
membranes in reconstructive surgery. Ann N Y Acad Sci.
1999;888:233–248.
18. Orgill DP. Excision and skin grafting of thermal burns. N Engl J
Med. 2009;360:893–901. The clinical problem associated with thermal
burns is reviewed. The author also discusses the benefits of skin grafting,
clinical evidence associated with it, clinical use, and adverse events.
19. Demling RH, Buerstatte WR, Perea A. Management of hot tar
burns. J Trauma. 1980;20:242.
20. Schiller WR. Tar burns in the southwest. Surg Gynecol Obstet.
1983;157:38–39.
21. Stratta RJ, Saffle JR, Kravitz M, et al. Management of tar and
asphalt injuries. Am J Surg. 1983;146:766–769.
22. Lee RC. Injury by electrical forces: pathophysiology, manifestations
and therapy. Curr Probl Surg. 1997;34:677–765.
23. Lee RC, Jang DJ, Hannig J. Biophysical injury mechanisms in
electrical shock trauma. Ann Rev Biomed Eng. 2000;2:477–510.
24. Brown C, Rhee P, Chan L, et al. Preventing renal failure in patients
with rhabdomyolysis: do bicarbonate and mannitol make a
difference? J Trauma. 2004;56:1191–1196.
25. Akita S. Treatment of radiation injury. Adv Wound Care (New
Rochelle). 2014;3:1–11.
26. Atiyeh BS, Gunn SW, Dibo SA. Metabolic implications of severe
burn injuries and their management: a systematic review of the
literature. World J Surg. 2008;32:1857–1869.
27. Wall-Alonso E, Schoeller DA, Schechter L, Gottlieb LJ. Measured
total energy requirements of adult patients with burns. J Burn Care
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28. Dickerson RN, Gervasio JM, Riley ML, et al. Accuracy of predictive
methods to estimate resting energy expenditure of thermally-
injured patients. J Parenter Enteral Nutr. 2002;26:17–29.
29. Chen Z, Wang S, Yu B, et al. A comparison study between early
enteral nutrition and parenteral nutrition in severe burn patients.
Burns. 2007;33:708–712.
30. Cahill NE, Dhaliwal R, Day AG, et al. Nutrition therapy in the
critical care setting: what is ‘best achievable’ practice? An
international multicenter observational study. Crit Care Med.
2010;38:395–401.
31. Venter M, Rode H, Sive A, et al. Enteral resuscitation and early
enteral feeding in children with major burns: effect on McFarlane
response to stress. Burns. 2007;33:464–471. This study discusses enteral
resuscitation and early enteral feeding in children with major burns. The
authors provide recommendations on the use of enteral resuscitation and
early enteral feeding based on the clinical scenario.
32. Hemmila MR, Taddonio MA, Arbabi S, et al. Intensive insulin
therapy is associated with reduced infectious complications in burn
patients. Surgery. 2008;144:629–637.
33. Pidcoke HF, Wanek SM, Rohleder LS, et al. Glucose variability is
associated with high mortality after severe burn. J Trauma.
2009;67:990–995.
34. Ritz MA, Fraser R, Tam W, et al. Impacts and patterns of disturbed
gastrointestinal function in critically ill patients. Am J Gastroenterol.
2000;95:3044–3052.
35. McAlhany JC Jr, Czaja AJ, Cathcart RS 3rd, et al. Histochemical
study of gastric mucosubstances after thermal injury: correlation
with endoscopic evidence of acute gastroduodenal disease.
J Trauma. 1975;15:609–612.
36. Greenhalgh JR, Saffle JH, Holmes RL, et al. American Burn
Association consensus conference to define sepsis and infection in
burns. J Burn Care Res. 2007;28:776–790.
37. Deitch EA, Winterton J, Li M, et al. The gut as a portal of entry
for bacteria: role of protein malnutrition. Ann Surg.
1987;205:681–692.
38. Ziegler TR, Smith RJ, O’Dwyer ST, et al. Increased intestinal
permeability associated with infection in burn patients. Arch Surg.
1988;123:1313–1319.
39. Avni T, Levcovich A, Ad-El DD, et al. Prophylactic antibiotics for
burns patients: systematic review and meta-analysis. Br Med J.
2010;340:c241.
40. Okhovatian F, Zoubine N. A comparison between two burn
rehabilitation protocols. Burns. 2007;33:429–434.
41. Chico M, Capelli-Schellpfeffer M, Kelley KM, Lee RC.
Management and coordination of post-acute medical care
for electrical trauma survivors. Ann N Y Acad Sci. 1999;
888:334–342.
42. Pliskin NH, Ammar AM, Fink JM, et al. Neuropsychological
changes following electrical injury. J Int Neuropsych Soc.
2006;12:17–23.
43. Salter RB. History of rest and motion and the scientific basis for
early continuous passive motion. Hand Clin. 1996;12:1–11.
44. Chen HC, Yang JY, Chuang SS, et al. Heterotopic ossification in
burns: our experience and literature reviews. Burns.
2009;35:857–862.
45. McDonald WS, Deitch EA. Hypertrophic skin grafts in burned
patients: a prospective analysis of variables. J Trauma.
1987;27:147–150.

423.e2
SECTION III
CHAPTER 18 • Acute management of burn and electrical trauma
46. Bombaro KM, Engrav LH, Carrougher GJ, et al. What is the
prevalence of hypertrophic scarring following burns? Burns.
2003;29:299–302.
47. Su C, Alizadeh K, Boddie A, Lee RC. The problem scar. Clin Plast
Surg. 1998;25:451–465.
48. Anzarut A, Olson J, Singh P, et al. The effectiveness of pressure
garment therapy for the prevention of abnormal scarring after burn
injury: a meta-analysis. J Plast Reconstr Aesthet Surg. 2009;62:77–94.
49. Kealey GP, Jensen KL, Laubenthal KN, et al. Prospective
randomized comparison of two types of pressure therapy
garments. J Burn Care Rehabil. 1990;11:334–336.
50. Edstrom LE, Robson MC, Macchiaverna JR, et al. Prospective
randomized treatments for burned hands: nonoperative vs.
operative. Preliminary report. Scand J Plast Reconstr Surg.
1979;13:131–135.

SECTION III • Burns Surgery
19 
Extremity burn reconstruction
Lorenzo Borghese, Alessandro Masellis, and Michele Masellis
SYNOPSIS
■ In electrical burn injuries, the patient’s condition often seems less
critical than it really is.
■ Always consider burn-induced compartment syndrome (BICS) when
limbs have extensive burns.
■ When performing escharotomy on the limbs, pay attention to
dangerous sites, such as the basilic or saphenous veins, and the radial
or tibial nerves.
■ The extremities are the most frequent areas affected by post-surgery
scar contractures. Correct positioning of articulations, good
management of scars, and postoperative care are mandatory.
■ The Z-plasty technique (in all its variations) remains one of the most
effective procedures for post-burn scar retractions.
■ Reconstructive surgery of burn sequelae often needs “imagination”.
Due to the presence of scars, to the damaged tissues, and to the lack
of good vessels, it is very hard to follow a single preoperative plan.
You need many arrows in your quiver.
Access the Historical Perspective section online at

third-degree burns, if not treated early and adequately in a
well-equipped burn specialized facility, can result in severe
burn-induced compartment syndromes (BICS), which can cause
death of viable tissues such as skin muscles and nerves and
even the loss of the extremity involved.3,4
Knee and elbow joints are often prone to severe damage
related to electrocution. In this type of accident, electricity
often finds its entry or exit point in one of these joints, causing
their explosion.
Extremities scarring often represents a challenge for the
plastic surgeon. About 50% of Z-plasties, as well as other
surgical techniques such as scar revision, involve the extremi-
ties. In developing countries, the percentage of scar retraction
causing disabilities is significant. This results in a grotesque
thoraco-brachial and brachio-antebrachial clinical picture, or
severe leg adhesions and contractures.
While the patient is hospitalized, physical and occupational
therapy is specifically aimed at maintaining mobility of the
major joints. Even if they are only marginally involved in the
accident, these parts are in fact often subject to arthritis,
dysplasia, and joint calcification, which are not easy to treat.
Thus the reconstruction of the extremities, which are a
person’s main means of self-sufficiency, is not simply a matter
of aesthetics but represents a real challenge for both the
surgeon and the patient. For the sake of clarity, the following
analysis will consider the upper and the lower extremities
separately.
Basic science/disease process
Electrical burns
In cases of electrocution, the upper extremities are almost
always involved, especially as entry or exit points of what is
known as the electric arc.15
The electric arc mainly involves the wrist, elbow, and ankle
joints with devastating effects on the joints themselves, the
nervous structures, and the muscular masses. Often the most
Introduction
The upper and lower extremities are often involved in burn-
related accidents. In particular, the arms, forearms, hands, and
legs are the most exposed areas, as they constitute the first
means of self-protection and are used to aid escape in
accidents.
Most burn-related accidents involving the extremities
occur at work, caused mainly by fire and electricity, and at
home where the majority of victims are babies.1,2 Extrem-
ity burns can be considered “difficult” burns, especially if
they are extensive circumferential burns. Deep second- and

424.e1
Historical perspective
Historical perspective
Many concepts such as early excision and grafting of small
burns can be traced to Lustgarten in 1891. The work of Allen
and Koch, in 1942, during the Second World War, focused on
the concept of closed dressings instead of the exposure tech-
nique in the care of burn patients.5 In the same period, many
authors (e.g., McCorkle and Silvani) described for the first
time the importance of early excision and grafting.6
Tangential excision preserving most of the viable tissue,
with immediate skin grafting, was suggested initially by
Janzekovic and colleagues in the early 1970s. They recom-
mended performing this procedure on the 2nd to 5th day
post-burn as the optimal time for best results, with less scar-
ring and good preservation of function.7
There was no official protocol until 1987, when, in Geneva,
seven burn surgeons from around the world agreed that full-
thickness burns of the hand and upper limb did better when
excised and grafted early, with better functional results, as a
result of earlier rehabilitation, and better aesthetic results
because of the reduced development of thick hypertrophic
scars. Early tangential excision of deep burns, followed by
skin grafting, is probably the most significant breakthrough
in recent years, leading to a reduction in the mortality rate in
burns >40% TBSA.8,9
In 2014, a new effective enzymatic debridement using
bromelain-derived pharmaceutical agent was released. It
allows the removal of the eschar early on admission day
preserving the non-injured dermis, leaving the viable tissue
for healing by epithelialization or autografting.10–14

425
Diagnosis/patient presentation
Diagnosis/patient presentation
Deep burns in the entire upper extremities are statistically
infrequent. Areas most often affected by burns are the hands
and the forearms. The involvement of any part of the upper
arms may have negative consequences distally to the burn,
even if the burn itself does not affect that area.
Patients affected by upper extremity burns often suffer
other associated traumas because of work-related accidents,
very frequent in this type of injury. An assessment of potential
fractures, amputations, wounds, blast, and crush injuries is
essential for planning subsequent reconstruction procedures.
The function of the shoulder joints must be carefully exam-
ined, and the nervous function of the median, ulnar, and
radial nerves should also be evaluated.24
After this first assessment, and after calculating the extent
and depth of the burn surface area, it is of fundamental
importance to assess whether an escharotomy is needed. This
is an emergency procedure that should be executed as soon
as possible with the objective to resolve/prevent the patho-
logic increased subcutaneous pressure that is the main
pathophysiology of electrical current-induced compartment
syndrome.
Fluid infusion and edema
Burn can be defined as a non-hemorrhagic hypovolemic shock
with loss of water, sodium, and plasma proteins but not of
corpuscular elements. In the first 24–48 h, fluid losses cannot
be stopped but only replaced, though early colloid adminis-
tration may attenuate it.
The objective of the treatment is to restore and preserve
tissue perfusion and avoid ischemia. One of the biggest
complications of burn shock is the increase of capillary perme-
ability throughout the organism due to the effects of heat on
the microcirculation. Edema reaches its maximum expression
within 8–12 h of the accident in minor burns and within
12–24 h in major ones.
These phenomena, caused by endothelial damage and
by hypoperfusion, lead to the liberation of vasoactive sub-
stances and cytotoxic free radicals, which in turn are respon-
sible for cellular edema and the generalized inflammatory
reaction.17,19
When burns exceed 20–30% of the total body surface area
(TBSA), even unburned areas develop edema owing to the
increase of vascular permeability secondary to hypoperfusion
and because of the plasma protein deficit.
The first choice “emergency solution” is an IV administra-
tion within the first 8 h of crystalloids (Ringer’s lactate). In
patients with extensive burns in whom it is not possible to
achieve adequate tissue perfusion, even by doubling the infu-
sion volume normally prescribed, it is possible to use hyper-
tonic solutions (Ringer’s lactate + 50 mEq of NaHCO3 +
40 mEq lactate). These solutions have to be used carefully,
monitoring natremia (which must never exceed 160 mEq/dL)
and plasma osmolarity. Note: hyperosmolar syndrome
induces kidney failure.
The administration of colloids is not effective in the first
8 h post-burn; later on, it is possible to infuse solutions of
albumin or fresh plasma. The quantity of colloids to infuse
has to be defined: one can calculate 0.5–1 mL/kg/% TBSA in
serious damage is to the wrist and ankle. Since the hands
and feet are the most frequent entry and exit points, the
wrist and ankle are the nearest points of electrical resistance.
The patient’s clinical condition on admission often looks
less critical than it really is, since the cutaneous lesions may
be misleading, with limited skin burn; in some other cases,
ample charred areas can be witnessed. These are the electric
current’s entry and exit points. However, the underlying
damage is always more extensive and may well involve the
muscular fasciae. This is because nerves and vessels are very
good conductors of electricity, and they may suffer damage
a few days after the accident. Venous thrombosis or ischemia
can be caused by internal destruction of the vessels catalyzed
by the electric current. Peripheral neurological damage
may occur with total destruction of the nerve (neurotmesis), if
close to the electricity entry and exit points, or with partial
axonal damage (axonotmesis), which often resolve in a few
months.16,17
In cases of high-voltage electrical burns (over 1000 volts),
muscles, bones, and nerve structures can be totally destroyed
and complete destruction of the major joints is common.18 In
such cases, intervention should be performed within 3–5 days
from the accident in order to save the affected joints and to
remove destroyed muscular tissue. Myoglobinuria is closely
linked to muscular damage, since the destruction of muscle
cell causes the release of myoglobin and in turn catalyses
myoglobinemia. This is a difficult condition to manage, and
the first sign of this pathology is the dark pink color of the
urine.19,20 An accurate diagnosis of myoglobinuria can be
provided only by serum differentiation between hemoglobin
and myoglobin.
All patients with myoglobinuria should be treated with
mannitol IV, bicarbonate IV, and Ringer’s lactate therapy in
order to obtain alkaline osmotic diuresis. This can minimize
the precipitation of the pigment at the level of the renal
tubules.
The damage caused by an electric current passing through
the body, especially if of high voltage, depends not only on
the characteristics of the electricity itself but also on the path
it follows and on the characteristics of the tissues affected by
the electricity. Even if adequate medical and surgical therapy
is available, the risk of amputation of an extremity remains
high, rated between 37% and 65%.16,21
From a surgical point of view, debridement of necrotic
tissue plays a fundamental role in the very first phase after
the electrical accident. As said, this can be very extensive
compared to the skin lesion. Reconstruction in these cases is
rarely limited only to skin graft coverage. It often also requires
vascular reconstruction, nerve grafts, and the transposition of
microvascular free flaps.
Vascular and neural reconstruction has to be carefully
monitored, since late electricity-related damage affecting
the neurovascular structures can occur even some days after
the accident and the surgical procedures, due to irreversible
endothelial damage, which affects small terminal vessels in
particular. Hence, it is preferable in such cases to postpone
the more complex reconstruction procedures.22 During the
acute phase, it is advisable to proceed by more limited
simple debridement and temporary skin coverage with
a free skin graft, isolating and preparing the vascular and
nervous structures that will be treated in a secondary surgical
stage.23

426
SECTION III
CHAPTER 19 • Extremity burn reconstruction
Full circumferential burns, or burns involving at least
three-quarters of the extremity’s circumference, are liable to
develop BICS. The clinical reaction that occurs when edema
develops during the first hours post-burn triggers a pressure
increase at the subcutaneous and at the muscular level of the
extremities. The expansion of the subcutaneous tissues is
blocked by the burned skin, which has no elasticity. After the
initial restriction of venous outflow, if proper treatment is not
given, there is the risk of a reduction in arterial flow, resulting
in ischemic tissue distally to the burn. It is important to
perform direct monitoring of compartment pressure or at least
the subcutaneous tissue all providing the very first sign of the
fresh plasma in the first 24 h, starting 8/10 h post-burn.
Elderly patients and those with extensive burns (>50%) main-
tain better hemodynamic stability and develop less edema,
thanks to the administration of colloids.
If no colloids have been used in the first hours after
the trauma and oncotic pressure remains low because of the
depletion of plasma proteins, it is necessary to return the
losses: the 5% albumin. Albumin demand during the second
24 h is 0.3–0.5 mL/kg/% TBSA, attempting to keep its blood
levels above 2 g/dL to reabsorb peripheral edema.
The volume of fluids indicated in the resuscitation of burn
patients depends on the gravity of the burn, the age and
general condition of the patient, and the presence of associ-
ated lesions. In patients with burns of more than 15% TBSA,
the quantity of fluid to provide has to be calculated on the
basis of the burned area and body dimensions (ABA Guide-
lines), being careful not to overload the patient, aggravating
the swelling with secondary edema to systems such as the
lungs, subcutaneous tissues and BICS, etc.3
Burn-induced compartment
syndrome (BICS)14
Deep second-degree and third-degree circumferential burns
can trigger a serious “burn-induced compartment syndrome”
(BICS) (Figs. 19.1–19.6, Box 19.1), which if not adequately
treated can easily result in the loss of the extremity involved.
Fig. 19.1  Anatomy of forearm escharotomy incisions.
A
B
Extensor digiti minimi
muscle and extensor
digitorum muscle
Extensor carpi
radialis tendon
Radius
Radial artery and
superficial branch
of radial nerve
Cephalic vein
Flexor carpi
radialis muscle
Palmar
fasciotomy
Dorsal
fasciotomy
Extensor carpi
ulnaris muscle
Posterior interosseous
artery and nerve
Ulna
Ulnar artery
Palmaris longus
muscle
Basilic vein
BOX 19.1  Emergency surgical procedures (with evidence of
procedures involving limbs)
• Releasing incisions
• Unavoidable amputations
• Early debridement, excision, and coverage
• Management of compartment syndrome
• Deep burn of the face
• Tracheotomy (inhalation injury)
• Pin hanging of the limbs
• Colostomy

427
Diagnosis/patient presentation
Fig. 19.2  Recommended sites for upper extremity and chest escharotomies.
Numbers 1 to 5 indicate dangerous incision sites.
A
B
4
5
1
2
3
Fig. 19.3  Recommended sites for lower extremity escharotomies. Numbers 1 to 5
indicate dangerous incision sites.
A
B
2
1
3
5
4
developing danger. Main clinical signs of initial compartmen-
tal syndrome are the 5 Ps: diminished Pulses in distal arteries;
Pallor and cold limb; initial intense Pain especially at passive
flexion–extension, which then may decrease following mus-
cular ischemia; under the subcutaneous Pressure the skin of
the hand or the foot is very tight; Paraesthesia.25 Screening
with Doppler ultrasound could be useful during initial assess-
ment, but this method cannot evaluate the exact compartment
pressure. If laboratory values give high levels of creatinine
phosphokinase (CPK), it may indicate severe muscle damage,
or ischemia.
Direct measurement of compartment/subcutaneous pres-
sure by hypodermic needle may provide the first measurable
sign of imminent, developing BICS. One of the most common
devices that allow a precise measurement of compartment
pressure is the Stryker Set. This device includes a monitoring
unit and a syringe with 3 mL of saline solution. The needle
is introduced into the subcutaneous tissue or the muscular
compartment that has to be monitored, and is flushed with
0.3 mL to re-equilibrate the pressure with interstitial fluids.
After a few seconds the pressure level in mmHg appears
on the monitoring unit. For measurements exceeding
35–40 mmHg (some claim even 30 mmHg), it is necessary
to perform an emergency escharotomy and sometime fasci-
otomy or even canal release even in the very first hours in
order to restore normal blood flow. In case of measures lower
than 30 mmHg, it is possible to administer non-steroidal anti-
inflammatory drugs combined with antioxidants to prevent
progression.26,27
This surgical procedure must involve all the burned tissues,
skin, fat, and sometimes fasciae, until decompression of the
compartment is observed. These escharotomies should follow
the recommended procedures and be performed before the
initial signs of either vascular (frozen hand) or neurological
deficits occur. In cutaneous burns, the muscular and neural
damages are secondary to the increased subcutaneous swell-
ing; thus an early escharotomy of the skin may prevent or
resolve BICS. In the later stages, when the muscles themselves
are ischemic, they swell and a fasciotomy is needed. Escha-
rotomies can be performed with an electrosurgical knife or a
scalpel, ensuring complete release of the muscles (see Figs.
19.4B & 19.5).
When treating the upper extremity, particular attention
should be paid to the blood flow through the cephalic and
basilic veins and superficial branch of the radial nerve at the
level of the wrist. In the most serious cases, it may be neces-
sary to perform complete decompression of the carpal tunnel
(see Figs. 19.1 & 19.2).
Escharotomy of the lower limb must be performed avoid-
ing the tibial anterior nerve, the medial saphenous vein and
nerve, the tibial posterior nerve, the fibular nerve, and the
external saphenous nerve but not directly over the tibial
plateau (see Figs. 19.3, 19.4, & 19.6).28
Recent reports indicate that an early on admission use of
bromelain-based (NexoBrid) debriding enzyme can resolve or
prevent BICS.10–14
Direct pressure measurement pre- and post-debridement/
escharotomy should be performed after any procedure to
ensure that the pressure did return to normal (Fig. 19.7).
Medication of the extremities should be carried out after
careful cleaning and debridement of the affected surface.

428
SECTION III
CHAPTER 19 • Extremity burn reconstruction
Fig. 19.4  (A) Anatomy of lower extremity escharotomy and fasciotomy incisions.
(B) Schematic of fascial release after escharotomy in the lower extremity.
Superficial
peroneal nerve
Fibula
Soleus
Lesser saphenous
vein and tendon
of gastrocnemius
Deep posterior
fasciotomy
Superficial
posterior
fasciotomy
Anteromedial
fasciotomy
Anterolateral
fasciotomy
Great saphenous vein
and saphenous nerve
Posterior tibial
artery and vein
and tibial nerve
Tibia
A
B
Early mobilization of the joints is recommended unless other-
wise specified. Nonadherent dressings such as Vaseline gauze
are indicated for all burn-affected areas. For areas affected
only superficially or at mid-dermal level, it is better to use
primary biologic dressings/medications such as Biobrane,
Mefix, or Aquacel-Ag to protect the exposed, raw wound bed
ensuring good epithelialization. In areas that are deeply
affected or clearly of third-degree, it is possible to proceed
with protective biologic dressings until the time comes for
surgical procedures. Early on admission enzymatic debride-
ment can remove the eschar and serve as an escharotomy
resolving/preventing BICS and preparing the patient for a
scheduled surgical autografting operation or engraftment of
skin substitute. During hospitalization it is fundamentally
important to keep the upper and lower extremities of the
patient in an elevated position in order to avoid the formation
of new edema and reduce existing edema.
Surgery of the burn areas that will remove dead tissues
(debridement) and cover the raw areas (engraftment) should
be performed as early as possible in order to prevent the
eschar-related inflammatory process. Inflammation that pro-
ceeds to granulation tissue formation leads to a greater inci-
dence of hypertrophic scars, weaker scar tissues, and delays
in prompt mobilization of the extremities.29,30

429
Diagnosis/patient presentation
Deep burned areas should be subjected to the earliest
debridement (surgical or enzymatic) and cover treatment as
soon as possible. Burns that do not heal within in 2 or 3 weeks
should also be considered for surgical treatment. Depending
on the burn area, regional or local anesthesia can be performed
in the extremities, but preferably only in patients with rela-
tively limited burn areas. The preferred treatment remains
early debridement and autologous skin graft.
Related trauma
The local trauma most frequently associated with burns is
bone fracture. In this case, close collaboration between the
plastic and orthopedic surgeons is essential in order to choose
the most appropriate surgical plan to follow. Stabilization
of fractures contiguous to deeply burned areas should be
performed early, preferably within the first 48 h after the
accident, before bacterial colonization can hamper orthopedic
Fig. 19.5  Upper extremity escharotomy and fasciotomy.
Fig. 19.6  Lower extremity escharotomy.
Fig. 19.7  (A) Admission, 4 hours post-injury, burns diagnosed as full-thickness,
compartment interstitial pressure measured 80 mmHg. NexoBrid enzymatic dressing
applied. (B) Immediately after removal of NexoBrid enzymatic dressing: pressure
reduced to 20 mmHg, eschar wiped away revealing viable deep dermis. (With the
courtesy of Prof Lior Rosenberg.)
A
B
action. It has frequently been reported that the early stabi-
lization of burn patients drastically decreases the onset of
complications.
Various related trauma should be treated contextually
or before their coverage with skin grafts, in order to avoid
re-opening already treated burn areas.
In the deepest burn areas, especially if the result of electro-
cution or if accompanied by related trauma, the explosion of
bones or tendons can occur, especially in major joints. This
condition imposes an additional priority in the planning of
the surgical procedures. The exposed tendons are liable to
rapid dehydration and consequent necrosis, and prompt
coverage is therefore essential. In the preparatory phase,
cadaver skin or biologic medications can be useful, while in
the surgical phase it is recommended to use dermal substitutes
(such as Integra, Matriderm, etc.), which allow the formation
of new tissue between the tendons and the grafted skin. Graft-
ing directly on the exposed tendons is counter-indicated in
terms of graft survival and functional results.

430
SECTION III
CHAPTER 19 • Extremity burn reconstruction
areas the necrotomy is more complex to perform. In deep or
electrical burns, it is possible to avulse the entire skin and
subcutaneous fat down to the muscular fascia in order to
reduce blood loss and avoid the risk of incomplete eschar
removal. Unlike the cutaneous dermis, the viable fat under-
neath is an unpredictable recipient bed for free skin grafts,
often necessitating preparatory procedures such as temporary
allo- or xenograft that, when removed a few days later, leaves
an adequately perfused recipient bed.33–36
During debridement of more superficially burned areas
that require surgical treatment, dermabrasion or hydrosurgery
(with instruments like VersaJet) provide useful support as
they minimize the waste of vital tissue and also permit careful
debridement in non-flat surfaces, such as the extremities.34
Recently a new rapid and effective enzymatic debride-
ment using bromelain-derived pharmaceutical gel-like agent
(NexoBrid) allows the removal of the entire eschar early on
admission day by a single, 4-hour, local application. This
enzymatic debridement does not harm viable tissues, pre-
serving the non-injured dermis, and has been found to act
as an enzymatic escharotomy tool. Being eschar-specific it
can be applied on all burns without committing to a specific
diagnosis of the burn depth: the enzyme will dissolve only
the dead eschar, leaving the viable tissue for healing by
epithelialization or autografting. Being a topical agent, it can
be easily applied by non-surgeons without initial burn depth
diagnosis, independent of any surgical facilities even on dif-
ficult areas such as extremities and joints (including axillae).
As in surgical debridement, the enzymatically debrided bed
needs immediate cover to protect it from desiccation but, as
much of the dermis is preserved, autografting is needed only
for full-thickness areas and most of the burns (>70%) can heal
spontaneously by epithelialization (see Fig. 19.7).10–14
Skin grafts
Skin grafts can be meshed with mesher 1 : 1 or 1.5 : 1, or even
larger 2–5 : 1 if the patient does not have donor areas. Meshing
the graft will facilitate adherence, drainage, and take besides
increasing in size. The elbow joint and the axillary and pop-
liteal cavities are preferably grafted with medium-thickness
skin, which provides greater elasticity and resistance in areas
subject to high mobility and trauma. All skin grafts should be
positioned considering the least relaxed skin tension lines in
order to obtain the aesthetically best results. In the specific
case of the arms, it is recommended to position the skin grafts
longitudinally for the best aesthetic outcome.
Skin grafts must be checked after 4–5 days and treated until
full recovery is completed.
Skin substitutes
Over the last decade, the use of dermal substitutes in acute-
phase burn surgery has become more frequent. In particular,
this technique is now used in acute-phase burn surgery in
cases of extensive deep burns with exposure of bones and
tendons.
The characteristics of an ideal skin substitute were defined
in 1978 by Tavis, but to date none of the available skin substi-
tutes fulfil all those criteria.
The currently available products (Integra, Matriderm,
allograft, Terudermis, etc.) have different characteristics, but
Also, exposed bone should be covered as early as possible,
even though resistance to exposure is much higher and more
easily resolved than in the case of tendons. Coverage can be
performed at a second stage utilizing rotation or free flaps.31
Patient selection
Plastic/burn surgeons possess all the necessary tools and
scientific know-how to treat burn patients. From intensive
care to the surgical phase, they should be able to take the best
decisions for the patient. He should decide the necessity,
extent, and timing of surgery and, in some cases, also the
choice to pursue a second intention healing process. The
preoperative care plan for scars is also crucial and should be
prepared by the same medical team that treated the patient
during the previous acute phase. The extremities are the most
frequent sufferers from post-surgery scar contractures, often
as a result of a lack of proper preventive scar modulation
measures (such as massage therapy, elastic compression, kinesi-
therapy, and splinting) aimed at preventing pathologic scar-
ring. An assessment of the affected areas will suggest to the
specialist whether to proceed with corrective measures or
engage in additional surgical interventions.
Considering that importance of normal walking, physical
autonomy, and self-dependence at home and work depend on
the complete rehabilitation of the affected areas, the main
objective of sequelae surgery is to re-establish the extremity’s
proper range of motion (ROM) and function.32
Treatment/surgical technique
Burn surgery can be subdivided into acute-phase surgery and
sequelae surgery. Acute-phase extremity surgery is not fun-
damentally different from surgery in any other part of the
body. Procedures such as fasciotomy, debridement, and cover-
age with autologous skin grafts, as previously described,
follow the surgical guidelines of acute-phase general burns
with special attention to prevention of BICS. Regarding
sequelae surgery of the extremities, it must be noted that the
majority of scar retractions here lead to disabilities, and local-
ized burn-related joint contracture may occur.17
Acute-phase surgery
BICS and emergency procedures such as escharotomy and
fasciotomy were largely dealt with in the foregoing section.
Focusing only on the extremities, the commonest surgical
procedures continue to be debridement and sheet or meshed
free-skin graft of autologous skin. These procedures should
preferably be performed as early as possible, i.e., before the
5th and 7th day post-injury. As previously said, some ad hoc
surgical variations may be necessary, depending on the type
of damage affecting the extremities and the kind of structures
involved. In order to limit bleeding and thus operate in a
condition of controlled hemostasis, tourniquet can be used.
This procedure facilitates extremity surgery, reducing blood
loss, but at the same time assessment of tissue viability and
the limiting tourniquet-time are challenging. Debridement
should be performed up to the viable tissues, after carefully
removing necrotic eschar and paying special attention to the
flexion–extension areas and the axillary hollow areas. In these

431
Treatment/surgical technique
imbibition phase (3–5 days) as it may interfere with the graft’s
venous outflow and final vascularization. For the same reason,
bulky gauzes, bolsters, and soft collars should not be used in
these areas.
Flaps
There is a general hesitancy to perform early free tissue
transfer in acute burns because of the concept of progressive
tissue necrosis following electrical and thermal burns. Occa-
sionally local flaps and free flaps may be utilized in primary
reconstruction after electrical injuries in forearm and legs.
Debridement in these areas often produces large tissue defects
or large bone exposition. Fascial flaps may provide good
coverage for the axilla and forearm. Recent studies have
looked at the use of free flaps in primary reconstruction and
found good results on the number of surgical procedures and
reduction in hospitalization.38
Joint reconstruction (Figs. 19.8 & 19.9)
High-voltage electricity (>1000 volts) flowing through the
extremities meets the point of maximum resistance in the
joints, and in such cases, severe damage involving all
the anatomic joint structures affected can be observed.
Joint reconstruction and coverage of exposed joints should
be managed early, in order to preserve as much functionality
as possible, together with the integrity of any viable tissue
that is still alive, and to prevent septic arthritis.
Articulation capsule and joint ligament apparatus recon-
struction has priority for surgery. In our experience the dermal
graft is an effective solution to this problem. Using a powered
or manual dermatome (Padgett drum dermatome, Humby,
Watson, Rosenberg, or others), a thin epidermal graft is har-
vested followed by harvesting of the dermal layer. The epi-
dermal layer is returned to cover the deep donor site defect.
The harvested dermis is then carefully shaped in relation to
the structures requiring reconstruction, whether an articula-
tion capsule or a ligament, and then finally grafted onto the
site. The fibroblast-rich grafted dermis realigns its elastic
fibers under the stimulation of the force applied to the joint.
This contributes to the reconstruction of strong vector tissue,
they all aim for the same objective: re-establishment of a layer
of dermis under a free skin graft. There is an ongoing debate
as to whether these newly formed tissues can be considered
dermis or not.
A fundamental prerequisite for valid results is that the
application should be onto vital tissue that is free of any
contamination or necrotic residue.
In acute burns of the extremities, the use of skin substitutes
is extremely effective in the treatment of critical areas (axilla,
elbow, popliteal cavity) and on exposed bones and tendons.
These products provide immediate coverage of the burned
area, resulting in reduced risk of infection or tissue necrosis,
and facilitate the regeneration of subcutaneous-like tissues
between the deep structures and the skin graft.
Applying dermal substitutes is usually easy. However,
when treating the extremities, some critical aspects should be
considered, such as range of movement, the autonomy of the
various segments, and perfect adherence between the product
and the wound bed. In the post-surgical period it is recom-
mended that the surgeon should be guided by the instructions
of the manufacturer of the product together with personal
experience.35–37
It is important to recall, however, that the commonest pos-
sible complication following their use in the acute phase is
infection, which can lead to complete loss of the skin grafts
applied in 30–40% of cases.
Negative pressure dressings (NPDs) (V.A.C., Renasys, etc.)
are often used for a few days as primary dressing for skin
grafts or skin substitute sheets. The use of negative pressure
devices improve the graft take, perform its better adherence
on the wound bed, prevent contamination, protect the graft
from traumas, and finally create a good environment for skin
graft taking or vascularization of skin substitute. It is possible
to use these devices on meshed and unmeshed skin grafts, on
single/double layer sheets with interposition of Vaseline
gauze between the graft and the NPD gauze/sponge. Many
authors suggest removing the dressing directly on the 6th/7th
postoperative day, but it is possible to do so before. We found
this kind of dressing very useful in critical areas such as
hollows, axilla, popliteal region, and neck, giving much more
stability and a perfect adhesion between the graft and the
wound bed, but it is safer not to use it beyond the graft
Fig. 19.8  (A) Knee joint space exposed secondary to high-voltage electrical burn. (B) Dermis harvested for joint reconstruction. (C) Dermal grafts incorporated into joint
capsule reconstruction. (D) Result after skin graft.
A
B
C
D

432
SECTION III
CHAPTER 19 • Extremity burn reconstruction
physical/occupational therapy, especially in burns involving
the extremities.
Burn patients who must stay many hours in bed may lie in
particular positions that can be defined as “antalgic”. These
are related to the great degree of pain suffered and to the
distressing situation the patients are dealing with. The joints
can easily lose their ROM if not properly treated.
Positioning the patient
The position of the patient should generally be supine with
the neck slightly stretched. In non-extensive burns, lateral
decubitus is also allowed.
The interposition of a thick surface (e.g., pillow, sheets) in
the interscapular area ensures slight hyperextension of the
neck. When necessary, it is desirable to use tutor collars.
Fig. 19.9  (A) The Padgett dermatome. (B) Dermal harvest with the Padgett
dermatome. Epidermal layer is adherent to the dermatome drum.
A
B
Fig. 19.10  Specialized compression garment.
which is a characteristic feature of healthy joint structure.39 In
case of lack of tissue for reconstruction, a polycaprolactone-
based polyurethane urea, like an Artelon patch, should be
used to reinforce the joint. It is an elastic sheet, built on well-
known chemical components cleared for use in medical
devices, that degrades non-enzymatically, and reinforces and
stabilizes the reconstructed joint.40
A selective debridement that leaves much of the native
deep dermis viable and intact over the joints may reduce the
need for such challenging surgical procedures.
Postoperative care
Burn injuries cause highly scar-related disabilities character-
ized by major hyperplasia and marked contraction of the skin
surface. The mobile segments of the extremities (axilla, elbow,
wrist, knee, ankle) are among the most critical for monitoring
in the post-surgical phase (Figs. 19.10 & 19.11; Table 19.1).
Many studies have dealt with the actual effectiveness of
post-surgical elastic compression and massage therapy, and
in normal clinical practice these procedures are routinely
performed to obtain the best results possible in terms of scar-
ring, range of motion (ROM), and function. The use of elastic
pressure garments for the extremities, silicone sheets or gel,
and splints are widely recommended from the earliest post-
operative stage in all centers specializing in burns treatment.
In addition to these devices, it is always advisable to perform
Fig. 19.11  Physical/occupational tasks to enhance post-burn mobility and
minimize contracture formation.