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156.e2
© Copyright 2012 Elsevier, Inc. All rights reserved.
50. Murray PR, Baron EJ, American Society for Microbiology. Manual
of clinical microbiology. 8th ed. Washington, D.C.: ASM Press;
2003.
51. Martyn J. Clinical pharmacology and drug therapy in the burned
patient. Anesthesiology. 1986;65(1):67-75.
52. Edwards-Jones V, Greenwood JE. What’s new in burn
microbiology? James Laing Memorial Prize Essay 2000. Burns.
2003;29(1):15-24.
53. Mandell GL, et al. Mandell, Douglas, and Bennett’s principles and
practice of infectious diseases. [Book review (E-STREAMS)] 2005;
6th:[2 v. (xxxviii, 3661, cxxx p.) ill. (some col.) 29 cm. + 1
CD-ROM (4 3/4 in.)]. Available from:
es0806_7/es0867_4196.html.
54. McEvoy GK, American Society of Health-System Pharmacists.
AHFS drug information essentials. Bethesda, MD: American Society
of Health-System Pharmacists; 2004:v.
55. Rybak MJ. The pharmacokinetic and pharmacodynamic properties
of vancomycin. Clin Infect Dis. 2006;42(Suppl 1):S35-S39.
56. Law EJ, Blecher K, Still JM. Enterococcal infections as a cause of
mortality and morbidity in patients with burns. J Burn Care
Rehabil. 1994;15(3):236-239.
57. Church D, et al. Burn wound infections. Clin Microbiol Rev.
2006;19(2):403-434.
58. Albrecht MC, et al. Impact of Acinetobacter infection on the
mortality of burn patients. J Am Coll Surg. 2006;203(4):546-550.
59. Patel JA, Williams-Bouyer NM. Infections in Burn Patients. In:
Feigin RD, ed. Feigin & Cherry’s textbook of pediatric infectious
diseases. Philadelphia, PA: Saunders/Elsevier; 2009:1139-1151.
60. Branski LK, et al. Emerging infections in burns. Surg Infect
(Larchmt). 2009;10(5):389-397.
61. Kunin CM, Bugg A. Binding of polymyxin antibiotics to tissues:
the major determinant of distribution and persistence in the
body. J Infect Dis. 1971;124(4):394-400.
62. Kunin CM, Bugg A. Recovery of tissue bound polymyxin B and
colistimethate. Proc Soc Exp Biol Med. 1971;137(3):786-790.
63. Baron S. Medical microbiology. 4th ed. Galveston, Tex.: University
of Texas Medical Branch at Galveston; 1996:xvii, 1273.
64. Woods GL. Diagnostic pathology of infectious diseases. Philadelphia:
Lea & Febiger; 1993:xiv, 656.
65. Becker WK, et al. Fungal burn wound infection. A 10-year
experience. Arch Surg. 1991;126(1):44-48.
66. Winn WC, Koneman EW. Koneman’s color atlas and textbook of
diagnostic microbiology. 6th ed. Philadelphia: Lippincott Williams
& Wilkins; 2006:xxxi, 1535, 30, 79 leaves of plates.
67. Pruitt Jr BA. Phycomycotic Infections. Probl Gen Surg. 1984;
664-678.
68. Sheridan RL. Sepsis in pediatric burn patients. Pediatr Crit Care
Med. 2005;6(3 Suppl):S112-S119.
69. Saliba F, Dupont B. Renal impairment and amphotericin B
formulations in patients with invasive fungal infections. Med
Mycol. 2008;46(2):97-112.
70. Walsh TJ, et al. Treatment of aspergillosis: clinical practice
guidelines of the Infectious Diseases Society of America. Clin
Infect Dis. 2008;46(3):327-360.
71. Moncrief JA. The status of topical antibacterial therapy in the
treatment of burns. Surgery. 1968;63(5):862-867.
72. Glasser JS, et al. Activity of topical antimicrobial agents against
multidrug-resistant bacteria recovered from burn patients. Burns.
2010;36(8):1172-1184.
73. Dai T, et al. Topical antimicrobials for burn wound infections.
Recent Pat Antiinfect Drug Discov. 2010;5(2):124-151.
74. Heggers JP. The use of antimicrobial agents. In: Krizek TJ, Robson
MC, eds. Clin Plast Surg. Philadelphia: Saunders; 1979:545-551.
75. Heggers JP, Robson MC. Quantitative bacteriology: its role in the
armamentarium of the surgeon. Boca Raton: CRC Press; 1991:139.
76. Moncrief JA. Topical antibacterial treatment of the burn wound.
In: Artz CP, Moncrief JA, Pruitt BA, eds. Burns, a team approach.
Philadelphia: Saunders; 1979:250-269.
77. Georgiade NG, Harris WA. Open and closed treatment of burns
with povidone-iodine. In: Polk HC, Ehrenkranz NJ, eds.
Therapeutic advances and new clinical implications: medical and
surgical antisepsis with batadine microbicides; the proceedings of the
symposium co-sponsored by the Departments of Surgery, Epidemiology,
and Public Health, University of Miami School of Medicine, Florida.
n.p.: Purdue Frederick Co.; 1972:x, 157.
78. Krizek TJ, et al. Topical therapy of burns: experimental evaluation.
Plast Reconstr Surg. 1967;39(3):248-255.
79. Buchvald J. An evaluation of topical mupirocin in moderately
severe primary and secondary skin infections. J Int Med Res.
1988;16(1):66-70.
80. Denning DW, Haiduven-Griffiths D. Eradication of low-level
methicillin-resistant Staphylococcus aureus skin colonization
with topical mupirocin. Infect Control Hosp Epidemiol. 1988;9(6):
261-263.
81. Rode H, et al. Bactericidal efficacy of mupirocin in multi-
antibiotic resistant Staphylococcus aureus burn wound infection.
J Antimicrob Chemother. 1988;21(5):589-595.
82. Acikel C, et al. Comparison of silver sulfadiazine 1%, mupirocin
2%, and fusidic acid 2% for topical antibacterial effect in
methicillin-resistant staphylococci-infected, full-skin thickness rat
burn wounds. J Burn Care Rehabil. 2003;24(1):37-41.
83. Kooistra-Smid AM, et al. Prevention of Staphylococcus aureus
burn wound colonization by nasal mupirocin. Burns.
2008;34(6):835-839.
84. Strock LL, et al. Topical Bactroban (mupirocin): efficacy in
treating burn wounds infected with methicillin-resistant
staphylococci. J Burn Care Rehabil. 1990;11(5):454-459.
85. Khundkar R, Malic C, Burge T. Use of Acticoat dressings in burns:
what is the evidence? Burns. 2010;36(6):751-758.
86. Brooks P, Phang KL, Moazzam A. Nanocrystalline silver (Acticoat)
for itch relief in the burns patient. ANZ J Surg. 2007;77(9):797.
87. Varas RP, et al. A prospective, randomized trial of Acticoat versus
silver sulfadiazine in the treatment of partial-thickness burns:
which method is less painful? J Burn Care Rehabil.
2005;26(4):344-347.
88. Supp AP, et al. Evaluation of cytotoxicity and antimicrobial
activity of Acticoat Burn Dressing for management of microbial
contamination in cultured skin substitutes grafted to athymic
mice. J Burn Care Rehabil. 2005;26(3):238-246.
89. Holder IA, et al. Assessment of a silver-coated barrier dressing
for potential use with skin grafts on excised burns. Burns.
2003;29(5):445-448.
90. Barret JP, et al. Topical nystatin powder in severe burns: a new
treatment for angioinvasive fungal infections refractory to other
topical and systemic agents. Burns. 1999;25(6):505-508.
91. Heggers JP, et al. The efficacy of nystatin combined with topical
microbial agents in the treatment of burn wound sepsis. J Burn
Care Rehabil. 1989;10(6):508-511.

©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00013-8
Operative wound management
Jong O. Lee, Manuel Dibildox, Carlos J. Jimenez, James J. Gallagher,
Syed Sayeed, Robert L. Sheridan, David N. Herndon
Skin grafting of granulation tissue following eschar separa­
tion has been replaced by operative intervention within days
of injury. Skin substitutes, dermal replacements, skin tissue
culture, and bioengineering are exciting and rapidly expand­
ing technologies that are already offering amazing results.
This chapter deals with the pathophysiology of the burn
wound, the scientific basis of wound excision, and the tech­
niques and technologies now available to burn surgeons.
Introduction
Surgery for burn injury is a key component to the multidis­
ciplinary care of the burn patient. Early excision and grafting
has dramatically changed the outcome and survival of the
burn patient. Burned tissue promotes an inflammatory
response at the junction of the eschar and the underlying
viable tissue. Bacterial proliferation in the eschar attracts
polymorphonuclear leukocytes that release large quantities
of proteolytic enzymes and inflammatory mediators. Subse­
quent enzymatic action results in separation of the eschar,
leaving granulation tissue. In large burns, the inflammatory
response at the burned site becomes systemic. Mediators
such as prostanoids, thromboxane, histamine, cytokines,
and tumor necrosis factor are produced and released from
the burn site. The serum levels of these mediators increase
proportionally as the surface area of burn increases. The
hypermetabolic response with increased protein catabolism,
increased energy expenditure, weight loss, poor wound
healing, and immune depression continues until the out­
pouring of mediators abates.1,2
Beneficial effects of operative
wound management
Early excision and skin grafting to achieve wound closure
have been shown to reduce infectious complications, reduce
the length of hospital stay, and improve survival in burned
patients of all ages. Children in particular have benefited
from more prompt and extensive surgical intervention.3,4
There has been a remarkable increase in the burn size associ­
ated with a 50% mortality risk over recent decades, such that
it is now unusual for a child to succumb to burn injury of
any size, even if it is associated with an inhalation injury
(Tables 13.1 and 13.2). Early prompt initiation of resuscita­
tion, nutritional support, proper critical care and treatment
of infection have also played a part in this achievement.
Early operative intervention, however, has contributed most
towards this major advance. Burke and colleagues reported
on results of total excision of full-thickness burns in 1974.5
They applied allografts to cover the wound after excision of
burn and controlled rejection by adding immunosuppres­
sants. Children with massive burns began surviving their
injuries where they had never previously done so. Improved
mortality, shorter hospital stay, and fewer metabolic compli­
cations were noted by others when early excision was retro­
spectively compared with late excision.6 When 32 children
with an average age of 7 years and mean burn size of 65%
total body surface area (TBSA) who underwent either total
excision or serial debridement were studied, mortality,
overall blood loss, and cumulative operating time were
equivalent.7 The early excision group, however, had their
length of hospital stay almost halved (97 ± 8 days vs 57 ± 5
days). Since that time, hundreds of children with burns
>30% TBSA treated with early excision have exhibited a
length of hospital stay less than 1 day/% TBSA burned.8
Tompkins and colleagues showed that mortality of adult
burn patients at Massachusetts General Hospital declined
from 24% in 1974 to 7% for 1979–1984 after prompt eschar
excision and immediate wound closure was instituted as
standard.9 This study was expanded to include 85 patients
aged 17–55 years.10 Those patients aged 17–30 years without
inhalation injury showed significantly reduced mortality if
treated by early excision (9%) than if treated conservatively
(45%). Patients with a concomitant inhalation injury or
aged over 30 years, however, derived no survival benefit
from early excision. In burned children, Xiao-Wu and col­
leagues showed that delays in excision of severe burn were
associated with longer hospitalization, delayed wound
closure, increased rates of invasive wound infection, and
increased incidence of sepsis.11
Munster and colleagues demonstrated a statistically sig­
nificant decrease in length of hospital stay that correlated
with a decrease in the interval between surgical interventions
over a 14-year period.12 Other variables, such as burn size,
inhalation injury, and age, remained static during this time;
they found that mortality rate decreased significantly whereas
burn indices remained constant. The average annual increase
in hospital charges for burn care grew to 9.6%, which was
substantially lower than the hospital as a whole (10.8%).
Active surgical intervention in burn care can be associated
with cost containment and fewer lives lost.
Elderly burn patients also have been shown to benefit
from an early surgical treatment. Deitch and colleague
operated upon consecutive patients with an average age
of 68 years and showed a reduction of 40% in mean length
of hospital stay compared to the national average, and
CHAPTER 13 
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Total Burn Care
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158
These are typically flame or contact burns. Heimbach and
colleagues observed that deep partial-thickness burns did
not convert to full-thickness burns when topical antimicro­
bials were used to control infection.20 Although these wounds
eventually healed after many weeks, they showed persistent
blistering, pruritus, hypertrophic scar formation, and poor
functional results. These observations prompted a prospec­
tive trial of early excision and grafting versus non-operative
treatment of burns of indeterminate depth of < 20% TBSA.21,22
Shorter hospitalization, lower cost, less time away from
work, but greater use of blood products, were seen in those
treated with early operation. Those patients treated non-
operatively required more late grafts for closure and also
developed more hypertrophic scars.
Tangential excision
Tangential excision removes burned skin while preserving
the underlying viable tissue. Body contours are better pre­
served than with fascial-level excision, and therefore this is
the standard method for small burns. The technique of tan­
gential excision was originally described by Janzekovic, who
observed that deep skin graft donor sites could be grafted
with thinner split-thickness skin graft taken from another
area.23 She then extended this concept to partial-thickness
burns by excising thin layers of burn until viable tissue was
reached (Fig. 13.1). Split-thickness skin grafts were imme­
diately applied. This technique of tangential excision and
autografting of partial-thickness burns was a major advance.
Prior to this time, only full-thickness burns were excised,
usually as a formal integumentectomy, taking subcutaneous
fat and accompanying lymphatics down to the underlying
layer of investing fascia (Fig. 13.2). Janzekovic analyzed the
results of the use of tangential excision in over 2000 patients.
She found that, compared to fascial excision, hospital length
of stay, pain, and reconstructive procedures were decreased.24
A number of different instruments can be used to perform
tangential excision. The Rosenberg knife, Goulian knife,
Watson knife, and the Versajet Hydrosurgery System water
dissector are used (Fig. 13.3).25 The Goulian knife and the
Watson knife are probably the most popular instruments for
tangential excision. If the burn depth is superficial, partial-
thickness burns are debrided to a white, shiny dermal surface
with punctate bleeding. In full-thickness burns, excision
continues layer by layer until viable subcutaneous tissue with
mortality was less than predicted.13 Many studies show that
early excision can be safely performed in the elderly, with
clear benefit of reductions in duration of hospitalizations
and the number of septic episodes.14–18
Hypertrophic burn scar formation is common, with dark-
skinned patients being more prone to its development.
However, the most important determinant of hypertrophic
scar is delayed wound healing. Deitch and colleagues have
shown that if wounds take more than 10 days to heal the
risk is significant, and it rises to 80% if healing is delayed
beyond 21 days.19 Surgery is therefore indicated for those
whose wounds fail to heal promptly. Operative treatment is
also an effective means of limiting the duration of pain that
burn patients must endure. Excisional therapy of the burn
wound is lifesaving, offers improved cosmetic and func­
tional results, is cost-effective, and more swiftly returns the
patient to their normal environment.
Techniques of burn wound excision
Excision of a small burn
Operative intervention is indicated without further delay
once a burn wound is determined to be ‘deep.’ ‘Deep’ burns
are those which are clearly either full-thickness or deep
partial-thickness burns unlikely to heal within 3 weeks.
Table 13.1  Mortality following burn over time for different age
groups, shown as the burn size at which 50% live or die – lethal
area 50 (la50)
Age [years]
LA50 (% TBSA)
1942–1952
1980–1991
1992–2004
0–14
49
98
99
15–44
46
70
88
45–64
27
46
75
>65
10
19
33
TBSA, percentage of total body surface area burned; LA50, lethal burn area for a
50% mortality.
1992–2004: Branski LK, Barrow RE, Herndon DN, unpublished data.
Table 13.2  Pediatric-specific mortality rates over time. Near-total early excision is the basis of these excellent results. Mortality and
pediatric burn patients, Shriners Burn Institute, Galveston, Texas
Years
Mortality sorted by burn size (% TBSA)
<20%
n
21–40%
n
41–60%
n
61–100%
n
1980–1985
<0.1%
889
1%
230
8%
105
33%
  95
1986–1990
<0.1%
571
1%
224
4%
117
19%
  88
1991–1995
<0.1%
522
2%
192
8%
  94
20%
  78
1996–2000
<0.1%
635
1%
222
3%
133
19%
114
2001–2004
2%
  83
2%
121
26%
  91
n, total number of patients admitted with respective burn size in given period.

Operative wound management
159
Fascial excision
In fascial excision, skin and subcutaneous tissue are removed
en bloc using electrocautery. This involves surgical removal
of the full-thickness of integument, including all the subcu­
taneous tissue, down to the layer of investing fascia. It is
a yellow glistening appearance is reached. Dullness, purple
discoloration, or thrombosed vessels indicate non-viable
tissue upon which grafts will fail, and deeper excision is
mandatory (Fig. 13.4). Grafts may take initially, but will
eventually fail. When excision is performed on limbs with
a pneumatic tourniquet, these features are especially
important.
Figure 13.1  (a–d) Schematic representation of tangential excision; sequential slices are taken until punctate hemorrhage is evident. (Adapted from Janzekovic Z.
A new concept in the early excision and immediate grafting of burns. J Trauma 1970 Dec; 10(12): 1103–8 with permission.)23
A
B
C
D
Figure 13.2  Fascial level excision using cutting diathermy and an
incorporated smoke evacuator.
Figure 13.3  A selection of hand-cutting dermatomes available for use for
tangential excision. Most have the ability to have the aperture set to the
desired depth while the Goulian has a large series of blade guards that are
changed.

Total Burn Care
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160
compared to 0.75 mL/cm2 excised if performed between
days 2 and 16 post burn. The blood loss dropped to 0.49 mL/
cm2 excised if the procedure was performed after the 16th
day. Overall mortality was 5% for an average burn size of
60% TBSA. Early excision had no adverse effect on mortality.
Very early excision led to a halving of blood loss for both
large and small burns26,27 (Fig. 13.5).
Other factors associated with increased blood loss during
excision of burns are older age, male gender, larger body size,
total area of full-thickness burns, high wound bacteria
counts, total area excised, and operative time.27
In the operating room, several techniques to reduce blood
loss during excision of burns can be employed. Adjunctive
measures to limit blood loss include tourniquets for
the extremities, pre-debridement tumescence with weak
epinephrine solutions, topical application of epinephrine
1 : 10 000–1 : 20 000, topical application of thrombin, fibrin
sealant, autologous platelet gel, calcium-enriched alginate
sheets, and immediate bandaging with delayed grafting.
The application of tourniquets to extremities is very effec­
tive at minimizing blood loss, especially for the hands and
fingers. As with tumescence, the lack of bleeding can make
the right depth of excision difficult to determine. To coun­
teract this, the tourniquet can be released briefly to check the
adequacy of excision and then reinflated. The larger vessels
are controlled by electrocautery or ligation and the wound
is covered with sheets of calcium alginate or sponges, which
are soaked in epinephrine solution. The tourniquet is
released after 5–8 minutes. The limb should then be held
elevated for about 10 minutes.
Tumescence with epinephrine containing saline can be
injected into the burn wound prior to excision. This tech­
nique is particularly useful for the trunk, scalp, and face;
1.6 mL of 1 : 1000 epinephrine (0.8 mL in pediatric patients)
is added to 500 mL of 0.45% normal saline solution. The
resulting local vasoconstriction will minimize blood loss.
One-way syringes, such as the Multi-Ad Fluid Dispensing
System or a pneumatic infuser, can make the injection
process easier (Fig. 13.6). Monitoring the patient’s hemody­
namics is necessary because the epinephrine may cause
performed to reduce blood loss when there is massive burn,
or in case of severe infection to control the source of infec­
tion. Fascial excision can limit the amount of blood loss
because control of the deeper perforating vessels is achieved,
bypassing the extensive capillary network present in the skin
and subcutaneous tissue. Fascial excision is also required for
those areas where subcutaneous tissue has been burned. The
advantages of this technique are that grafts take well on
fascia and blood loss is reduced.
Fascial excision is also indicated for life-threatening
invasive wound infection or sepsis, particularly with fungi
such as Aspergillus and Mucor, and also for large areas with
failed graft take in a critically ill patient with massive burns.
Episodes of sepsis lead to ischemic necrosis of subcutaneous
fat due to poor peripheral perfusion and microvascular
stasis. This becomes problematic in patients with very large
burns and leads to late graft loss, and these ischemic areas
become portals for invasive wound infection. The disadvan­
tages of fascial excision are lymphedema and contour
deformities.
Controlling blood loss
Excision of burns can result in considerable, if not massive,
blood loss. Tangential excision can lead to large blood loss
unless measures are taken to limit potential hemorrhage.
The simplest measure is to operate within 24 hours of injury.
Vasoactive metabolites, particularly the potent vasoconstric­
tor thromboxane, are in abundance during this time to limit
blood loss.26 Desai and colleagues showed in a prospective
trial of 318 pediatric patients with burns >30% TBSA that
early excision of burns is associated with an overall reduc­
tion in blood loss.26 The average blood loss per surface area
excised (mL/cm2) was compared at various postburn periods
of excision. The total blood loss during excision performed
within the first 24 hours after burn was 0.4 mL/cm2 excised,
Figure 13.4  A deep flame burn on the left thigh that is in the process
of being debrided. The wound has been tumesced with 1 : 1 000 000
epinephrine in normal saline and shows minimal bleeding. The lower part of
the wound demonstrates residual dead dermis with dull appearance and
staining from lyzed cells. The area just above demonstrates shiny yellow
living fat and (mostly) surviving shiny white dermis with a few patches
needing another slice.
Figure 13.5  Blood loss is almost halved by operating within 24 hours of
injury. (Adapted from Desai MH, Herndon DN, Broemeling L, Barrow RE, Nichols RJ Jr, Rutan
RL. Early burn wound excision significantly reduces blood loss. Ann Surg. 1990 Jun; 211(6):
753–9; discussion 759–62 with permission.)26
Blood loss (mL/cm2)
0.2
0.4
0.6
0.8
0
Postburn excision (days)
0–1
1–2
2–16
*
* Significantly different from 0–1
and >16 days at p<0.01
(ANOVA) N = 318
>16

Operative wound management
161
possible accumulation of seroma or hematoma that can
compromise the apposition of the graft to the wound bed.
Seroma or hematoma should be identified and removed by
‘rolling’ them out or by aspiration with 27 gauge needle. The
graft can be secured to the wound bed with quilting sutures
or the application of a bolster dressing, which can reduce
shearing of the graft. These grafts are best laid perpendicular
to the long axis of limbs, particularly across joint flexural
creases, which is in line with the general rule of placing
potential scars perpendicular to the dominant muscle con­
traction in the area. This will reduce the degree of contracture
if it occurs. Possible exceptions are the dorsum of the hand
and forearm, where some clinicians argue that longitudi­
nally placed grafts are cosmetically superior.
If burns are large and donor sites limited, autograft is
meshed. This allows the autograft to be expanded to cover a
wider area than its original size. The most common mesh
ratios are 2 : 1 and 4 : 1, although different ratios of expan­
sion can be employed. The main advantages of 2 : 1 meshed
autograft is the easy handling and application, and the exten­
sive network of slits that allows seroma or hematoma to
drain. The main disadvantage is that the diamond-shaped
interstices will leave a visible pattern once healed. Much
larger areas can be covered when autografts are meshed 4 : 1
or greater and widely expanded. This widely meshed skin
requires an overlay coverage of non-expanded allograft in a
sandwich pattern to decrease the risk of graft loss. These are
applied at 90° to the autograft in a sandwich pattern (Fig.
13.7).28 The difficult handling, the large interstices that take
considerable amount of time to heal by epithelialization, the
need for an allograft overlay, and the poor cosmetic result
limit the use of meshed autograft to massively burned
patients. Even in large burns, the face, neck, and hands are
grafted with sheet split-thickness skin graft.
The Meek technique, which was later modified by Kreis
and colleagues, is another tool to cover extremely large burn
surface areas.29,30 It uses autograft cut into small squares with
the aid of a dermatome and a cork board. These squares are
then passed onto prefolded pleated gauze that is expanded
in all four directions, leaving uniformly distributed islands
of autograft which are then applied to the wound bed. Ratios
of expansion can vary from 1 : 3 to 1 : 9. This technique has
similar disadvantages to 4 : 1 meshed autograft and requires
overlay with allograft.
Advances in wound closure
Dermal replacement
The flexibility, elasticity and strength of normal skin are
provided mainly by the dermis. Excision of full-thickness
burn removes the entire dermis. A layer of scar develops
between the graft and the underlying tissue which prevents
the healed skin from having the properties of normal skin.
The use of dermal replacement in the treatment of burns
brings new hope in providing the highly desired character­
istics of normal dermis. Integra is a dermal analog composed
of a porous matrix of cross-linked bovine collagen and glu­
cosaminoglycan that provides a scaffold for a cellular inva­
sion and capillary growth. This is placed over the wound bed
after excision. The matrix is fully incorporated into the
tachycardia and hypertension, which can worsen bleeding.
Another drawback of this technique is that the lack of bleed­
ing from the wound bed makes the adequacy of excision
difficult to assess.
When dealing with large areas of disrupted capillaries, one
of the most effective ways to safely limit blood loss is rapid
excision followed by coverage with epinephrine-soaked
sponges and compressive bandages.
Delayed grafting is used in some centers to limit blood
loss. If delayed grafting is undertaken, the wound bed
needs to be kept moist and clean. The wound can be covered
with bulky cotton dressings with tubing through the dressing
to the wound surface for continuous or intermittent irriga­
tion with antibiotic solution. The patient returns to the oper­
ating room within 24 hours and undergoes a second
procedure of procurement and application of skin grafts.
This may be a practical approach in cases of large excisions,
where coagulopathy can develop due to large blood loss or
hypothermia.
Techniques of wound closure
The standard treatment for a full-thickness burn is excision
and grafting. Once procured, the autograft can be used in
different ways depending on the amount of body surface
area that requires grafting.
Autografts are classified as full or split thickness depending
on the depth of dermal layer included. Full-thickness
autografts have better cosmetic results and reduced scarring
compared to split-thickness grafts because the dermis pro­
vides flexibility and elasticity. The main caveat is that the
increased amount of dermis in the full-thickness graft can
compromise its own viability during the imbibition, inoscu­
lation, and neovascularization phases of graft take. The
donor site completely devoid of dermis must be closed pri­
marily or grafted. Because of the reasons mentioned above,
split-thickness skin grafts are mainly used in the treatment
of extensive burn injuries.
If the burn is small, skin grafts can be applied as a ‘sheet’
and no meshing is performed. The advantages are better
cosmetic and functional outcome. The disadvantage is the
Figure 13.6  An infuser device.

Total Burn Care
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162
Figure 13.7  (a) Schematic representation
of ‘sandwich’ technique of allograft overlay.
(Adapted from Alexander JW, MacMillan BG, Law E,
Kittur DS. Treatment of severe burns with widely meshed
skin autograft and meshed skin allograft overlay. J Trauma.
1981 Jun; 21(6): 433–8 with permission.)28 (b) Sandwich
technique on the chest of a boy with massive
deep burn having a return surgery a week after
sandwich grafting. Most of the (fresh) allograft
has vascularized with one piece obviously whiter
than the rest. The mesh pattern of the underlying
widely meshed autograft is visible.
A
Allograft
Autograft
Excised
wound
B
wound bed in 2–3 weeks and a thin split-thickness autograft
is placed over it. Except for a possible increase in risk of
infections, its use is safe and effective.31 Engraftment is aided
by the use of negative-pressure dressings such as VAC Therapy
(Fig. 13.8).32
Another dermal analog available for the treatment of full-
thickness burns is Alloderm. This consists of cadaveric
dermis devoid of cells and epithelial elements. Its use is very
similar to that of other dermal analogs, and it has shown
favorable results.33
Cultured epidermal autograft
Cultured epidermal autograft (CEA) is an important tool in
the management of patients with massive burns. In full-
thickness burns involving more than 90% TBSA it may be
the only choice, given that procurement of the uninvolved
skin will not be sufficient to cover the patient’s wound.
Munster has shown that the use of CEA in the massively
burned patient reduced mortality.34 CEA involves obtaining
two 2 × 6 cm full-thickness specimens of unburned skin. The
skin is processed and cultured ex vivo in the presence of
murine fibroblasts that promote growth. The final product
takes approximately 3 weeks to be ready for grafting and
consists of sheets of keratinocytes, 2–8 cells thick; conse­
quently, shearing and blistering is common for many
months. Long-term survival of CEA is therefore particularly
problematic on the posterior surfaces of these massively
burned patients and goes some way towards explaining the
5–50% long-term CEA engraftment rates reported in the
literature. CEA applied to areas such as the back, buttocks,
posterior lower extremities, and other dependent areas is
prone to shearing and possible graft loss. Barret and col­
leagues compared the use of CEA with wide mesh autograft
and allograft overlay in a group of children with >90%
TBSA.35 Once healed, the CEA has a better cosmetic result
than healed 4 : 1 meshed autograft, but is associated with a
longer hospital stay and more reconstructive procedures.
Despite these limitations, including a substantial cost, series
from different burn centers have shown promising results.
When used in conjunction with allograft dermis, Sood and
colleagues reported a graft take of over 72%.36
Tissue engineering technology is advancing rapidly. Fetal
skin constructs have been recently successfully trialled and
the bilaminar cultured skin substitute is showing promise.37,38
Skin procurement
Many factors are considered when choosing the best donor
site. Donor sites represent new wounds that can add signifi­
cant morbidity to the patient: patients usually complain of
more pain at the donor site than at the burn wound or graft
area. Whenever possible, grafts that match the color of the
recipient area should be pursued. The face and neck should

Operative wound management
163
Figure 13.8  (a)-(c) Deep flame burn on a boy’s chest treated with early excision and Integra with
VAC. (d) The silicone layer being removed on day 12 ready for thin grafting with well-vascularized
dermal template underneath. (e) The pleasing final result.
A
B
C
D
eE
be grafted with skin procured from the area above the line
of the nipple for the best color match. Thigh, hip, and back
are commonly used as donor sites because the skin is flat for
easy procurement, and scars are easily covered under cloth­
ing. The scalp may represent an ideal donor site because it
is associated with less pain and rapid healing, given the rich
blood supply. The subsequent scar can be hidden after the
regrowth of hair.
Good-quality grafts of consistent depth are obtained by
use of an electric or pneumatic powered dermatome. The

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which in turn maintains a moist environment that allows
faster epithelial cell proliferation and migration. Other ben­
efits include minimizing pain, a barrier to bacterial contami­
nation, and prevention of protein loss. The main options
available are allograft, xenograft, and amnionic membrane.
Allograft, also known as homograft, is an effective tempo­
rary wound coverage after tangential or fascial excision.39 It
can be stored in a cryopreserved state for an extended period,
and becomes adherent and vascularized when applied to
viable wound beds. This process can serve as a test for wound
bed viability. Immune rejection takes place 3–4 weeks after
its application. When used to temporarily cover the face and
hands, it should be applied as a sheet graft to prevent the
formation of granulation tissue inside the interstices, which
can cause scarring and poor cosmetic outcome after defini­
tive autografting takes place.
Xenografts are another option for temporary wound cover­
age.40 Only those derived from porcine dermis are currently
available.41 Their main use is for partial-thickness burns after
superficial debridement, as well as for donor sites. As with
allograft, xenograft becomes adherent and provides many of
the benefits of having the wound covered, such as pain
control while the underlying wound bed epithelializes, but
it does not vascularize.
Sterilely processed amniotic membranes can also be used
to provide temporary coverage for superficial burns. Given
its flexibility and pliability, amnion is useful in irregular
surfaces such as the face. Even though it does not reduce
healing time or scarring, it provides some of the benefits of
wound coverage and reduces the number of dressing changes
required.42
Management of specific burns
Scald burns
Scald burns of small or moderate size have been shown to
be the exception to the general rule of early excision. Young
children who had scald burns up to 20% TBSA required less
area to be excised and had smaller blood loss if operated
upon in the second or third week post burn.43 A subsequent
prospective trial randomized 24 children to early or late
excision if their scald had caused burns of clinically indeter­
minate depth.44 No patient experienced a significant wound
infection or sepsis. Only half of the delayed excision group
ultimately required surgical intervention, and a significantly
smaller area of excision was necessary.
In light of the foregoing evidence, children with scald
burns <20% TBSA can be appropriately treated with a topical
antimicrobial such as silver sulfadiazine for about 2 weeks.
This approach needs to be balanced by the knowledge that
the longer a wound remains open, the greater the inflamma­
tory response and subsequent scarring. A number of tech­
niques are available to cover the partial-thickness burn.
When successful, they have the added advantage of eliminat­
ing a great deal of the pain associated with frequent dressing
changes. More superficial wounds can be covered by a poly­
urethane membrane such as Omiderm. The authors favor
Biobrane for smaller and more superficial wounds.45 Bio­
brane is a nylon/silicone bilaminated compo­site skin substi­
tute. At the time of the first wound dressing application, all
depth of the procurement can be precisely adjusted to the
desired thickness, usually between 0.006 and 0.018 inches.
Patients with extensive burns have few potential donor
sites. Anatomical regions that are usually spared and repre­
sent viable options for procurement are the axilla, the mons
pubis and the scrotum. Given the irregular topography,
tumescence can be used to obtain useful amounts of skin
graft. Although less optimal, the soles of the feet can also be
used in extreme circumstances. The first layer obtained is
discarded because it represents the stratum corneum, which
has no viable epithelial cells.
In severely burned patients, several operations will be
required for wound coverage as donor sites are limited. A
limiting factor to repeat grafting is the time to healing of the
donor sites. Healing at these sites comes from proliferation
and migration of the epithelial cells from the hair follicles,
the sweat glands, and the oil glands situated deep inside the
dermis.
Donor site management
After the skin graft has been procured, careful management
of the donor site wound is mandatory to expedite healing.
Smaller donor sites can be treated with occlusive or adherent
dressings such as Opsite or Biobrane. Another technique is
to use alginate sheets or hydrocolloid fiber dressings. These
have the advantage of promoting a moist wound healing
environment and may diminish donor site pain. The wounds
can be also covered with gauze impregnated with an oil-
based ointment. The most common examples are Xeroform
or a fabricated dressing containing olive oil, petrolatum,
lanolin, and the chemotactic agent Sudan red. Silver-
impregnated dressings such as Acticoat, Acticoat Absorbent
or Aquacel Ag seem to diminish bacterial overgrowth and
can be used directly on the donor site or as an intermediate
layer. Skin graft donor sites heal primarily by epithelializa­
tion from the remaining epithelial elements. The time to
healing depends on depth of procurement, the vascularity of
the donor site, wound management, and general patient
condition.
Dressings
After excision and grafting, the wounds are covered with
non-adherent dressings. At our institution, gauze impreg­
nated with a petrolatum-based ointment is used. This oint­
ment contains an antibacterial (Polymyxin/Bacitracin) and
an antifungal (Mycostatin). This is followed by the place­
ment of a thick layer of fluff gauze that is then covered with
an elastic bandage. With areas of the body prone to shearing,
such as the back and axilla, the application of a bolster dress­
ing can be beneficial. The application of negative-pressure
dressings such as VAC Therapy can also be useful to splint
and protect the grafts. Dressings are usually removed on
postoperative day 3 or 4. This time frame is normally suffi­
cient to allow for adherence of the graft to the wound bed.
Temporary skin substitutes
Providing wound coverage with skin substitute, even if it is
temporary, has many advantages. Wound coverage prevents
water and electrolyte losses as well as tissue desiccation,

Operative wound management
165
>70% TBSA. The incidence of failure due to infection rises
dramatically as the burn size tops 75% TBSA. First choice
would be to excise all burn wounds and start covering the
wound beds with autograft and the uncovered areas with
allograft. The patient is taken back to the operating room for
regrafting once used donor sites are healed.
Massive burns
The operating room
A very important perioperative issue for safe management of
a patient undergoing massive burn excision is the mainte­
nance of body temperature. The patient is usually completely
Figure 13.9  (a, b) High-voltage electrical flash burn treated by fascial
excision and Integra. Flat anterior surfaces are particularly amenable to use
of Integra.
aA
B
loose skin and blisters are removed to leave a clean, moist
surface. The material works by becoming densely adherent
to the exposed dermis, thereby acting as a neoepidermis. Lal
and colleagues reported no increase in infection rates using
Biobrane.46 If infections do occur, it is usually as a result of
non-adherence and accumulation of fluid. Some centers
have taken a middle road and use silver-impregnated dress­
ings such as Acticoat, with great success. This has the advan­
tage of having antimicrobial activity and only needs to be
changed every 3–7 days. A series of catheters are inserted
through the overlying dressing through which 5–10 mL of
water are instilled every 4–6 hours. Glycerol or cryopreserved
allograft or xenograft have also been used.
Large burns
Patients with deep burns >40% TBSA pose unique challenges
with many conflicting demands for available donor sites.
Near-total excision should be completed as soon as possible
in the first few days after injury. The back, buttocks, and
posterior thighs are covered with autograft taken at
8–10/1000, which is meshed at an expansion ratio of 4 : 1.
This is applied to the wound bed and spread wide. Irrigation
via a bulb syringe is useful to spread the thin, fragile graft
into the appropriate position. ‘Fresh’ allograft is the best
option as an overlay to protect autograft.
Consideration needs to be given to the use and extent of
dermal replacements such as Integra. Dermal replacement is
an expensive option, but one that leaves an excellent result.
Integra is a bilaminar composite that has a neodermis of
bovine collagen held in a matrix pattern with shark cartilage
chondroitin-6-sulfate. A layer of rubberized silicone is press
sealed onto this and acts as a neoepidermis. The abdomen,
anterior thigh, forearm, leg, and male chest are sites where
Integra can easily be applied (Fig. 13.9).
Meticulous surgical technique is essential. Topical epine­
phrine, direct pressure, compression wrapping, epinephrine
clysis, and electrocautery are the hemostatic methods of
choice. Integra is best held in place either by a VAC Therapy
or by attaching an elastic netting material (Surginet) over it.
A layer of Acticoat is frequently added in many centers.
Further protection is provided by layers of netting (bridal
veil, Conformant 2, Exudry). The neodermis is vascularized
from the underlying wound. This process takes 2–3 weeks
to complete. The neodermis often becomes a plum color due
to suffusion through the matrix of red cells from minor
hemorrhage. This is normal and should be left alone.
Hematoma or seroma can be aspirated with a 27 gauge
needle. Integra overlying the hematoma is best incised,
hematoma removed, and the edges stapled down.
The neodermis is ‘ready’ when it has a ‘straw’ color. Close
inspection under magnification will reveal telangiectatic
vessels dotted about. The second-stage operation involves
gentle removal of the silicone layer and application of 6/1000
inch autograft, which can be meshed up to an expansion of
3 : 1. CEA has been used as epidermal cover for Integra neo­
dermis.47 In sick patients with very large burns there is benefit
in performing staged, sequential replacement of the silicone
layer with thin, 1.5 : 1-meshed autograft. Engraftment and
graft survival seems to be more reliable in the long term and
the cosmetic result is enhanced. Debate continues regarding
the role of Integra in wound coverage of patients with burns

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infused albumin to maintain normal serum levels, and this
is an indication of the net positive protein balance.48 The
usual hospital stay of 42 days for a 30 kg patient with a 60%
TBSA burn was reduced to 32 days. This tremendous decrease
in length of hospital stay realized a net saving of 15% in
total costs. Salutary effects have also been documented in a
group of patients treated non-operatively. Mortality dropped
from 45% to 8%.49 Although it must be acknowledged that
two European studies in critically ill adults of mixed etiology
showed increased mortality among the GH-treated groups,
this experience has not been repeated in the massively
burned pediatric population in North America.50 Other ana­
bolic agents have shown promise as a means of speeding
wound healing in severely injured catabolic burn patients.51
Oxandrolone 20 mg/day has demonstrated a positive effect
on protein kinetics and wound healing in clinical trials.51,52
In oxandrolone-treated severely burned adults, donor site
wound healing was accelerated by 20% compared to non-
treated patients.51 Although these pharmacological agents
provide great support to the massively burned, they are only
an adjunct to early near-total excision and prompt wound
coverage.
Operative management of burns
in special areas
The hand
Survival after serious burns has improved dramatically over
the past 20 years.53 However, despite generally satisfying
long-term quality of life, many such patients will have sig­
nificant physical disabilities, many of which can be traced to
compromised hand function. If optimal function is to be
recovered after a very serious burn, proper acute care of the
injured hand is essential. These early efforts should be
directed at preservation of tissue, maintenance of normal
hand geometry, and developing a strategy for wound closure.
Escharotomy and fasciotomy
A critical part of the initial care of hand burn is to ensure
that soft tissues are well perfused. Decompression of high
tissue pressure from burn skin with edema is an area in
which early surgical intervention can make a tremendous
difference to the ultimate outcome. Hands at risk for ischemia
include those with circumferential or near-circumferential
burns, those with very deep burns, and any electrical injuries
involving high or intermediate-range voltage. It is important
to look at signs more subtle than the loss of a palpable pulse
in named arteries at the wrist. Mean arterial pressure in the
central system is three times higher than capillary pressure,
and blood flow may be maintained in these larger vessels
when flow in distal soft tissues is impaired. If the hand is
warm, soft, and has pulsatile flow detectable by Doppler in
the palmar arch and digital vessels, and a normal transmis­
sion pulse oximetry signal at the distal digit, then flow is
adequate. As flow is progressively impaired, the hand will
become firm and cool, with decreased Doppler flow and
loss of the pulse oximetry signal. Voluntary movement
will become difficult and the hand will assume a clawed
position. Decompression should be performed to prevent
exposed and has little intact skin, especially after donor skin
procurement, leading to rapid heat loss. A number of strate­
gies can be used to counteract heat loss and maintain nor­
mothermia. The operating room should be warmed to 32°C.
The latent heat of evaporation of water is 31.5°C. Above this
temperature, the energy source for evaporation will come
from the environment rather than the patient. Radiant
heaters are also helpful for perioperative thermoregulation.
Other adjunctive measures include the use of ‘space blan­
kets,’ aluminum foil coverings, plastic sheeting over the head
and face, and all intravenous fluids being given at 38°C
through a warming coil. Repeated applications of warm
sterile blankets or forced air warming systems are useful.
Irrigation fluids are used warm. In addition, insulating blan­
kets and active heating are available via either infrared or
ceramic heaters.
The burn operating room is an extension of the burn
intensive care unit. Large, heated (32°C), humid and well-lit
rooms are ideal for burn surgery. The procedures are long,
intense, and require multiple individual setups for different
types of equipment and instrumentation.
The ideal operating room environment should allow only
minimal evaporative loss from the patient. Filtered warm
water connections and pressurized gas connections should
be available to power shower heads, dermatomes and other
gas-driven instrumentation. The surgical bed should be posi­
tioned under supporting ceiling brackets or railings that
allow for the hanging of irrigation solutions and equipment.
This will also provide anchorage for suspension of extremi­
ties as needed during the operation. Reliable vascular access
is required, and these lines should be sutured securely to
prevent dislodgment during positioning of the patient.
The operation
Excision commences with the patient in the prone position.
Excision of the shoulders, back, buttocks, and upper thighs
is performed. Wide-meshed autograft with allograft overlay
is applied. If insufficient autograft is available, the excised
wound is covered with unexpanded, meshed fresh allograft.
Other alternatives include skin substitutes such as Integra,
xenograft, or cryopreserved allograft. Dermal replacement
material is prone to failure owing to infection in massive
burns, particularly on posterior surfaces, but can be used
selectively on anterior surfaces. In the case of allografts mul­
tiple layers of bulky gauze dressings are applied over the
antibiotic-impregnated gauze. Silk sutures are inserted in a
row along the posterior axillary lines and tied over the bulky
gauze dressing as a bolster to prevent shearing of grafts on
the back and buttocks. The patient is then placed in the
supine position. A tourniquet can be used on the limbs to
reduce blood loss during excision. Weak epinephrine clysis,
topical 1 : 10 000 epinephrine irrigation, topical thrombin
spray, epinephrine-soaked sponges, and direct application of
pressure are all techniques used to limit blood loss during
debridement.
As soon as donor sites are healed patients return to the
operating room for further autografting and replacement of
non-adherent allograft or infected skin substitute. In mas­
sively burned children, treatment with recombinant human
growth hormone (GH) showed that donor site wound
healing accelerated by 25%. GH-treated patients require less

Operative wound management
167
supplemented with subeschar injections of local anesthetic.
Some patients will require a general anesthetic in the operat­
ing room to have this procedure performed properly, espe­
cially if digital escharotomy is needed.
Fasciotomy may be needed for edema within the fascial
compartments of the forearm and hand. Clinically this is
often seen after high-voltage electrical injury or exceptionally
deep thermal injury. Upper extremity fasciotomy may
include volar and dorsal decompression, carpal tunnel
release, and dorsal hand fasciotomy. A curvilinear incision
is ideal for volar exposure of the compartments of the
forearm. This approach allows one to gain access to all indi­
vidual muscle bundles in the volar forearm and decompress
the carpal tunnel through a contiguous incision, and creates
a well vascularized flap of skin that will maintain coverage
over the median nerve at the wrist upon completion of the
fasciotomy. When needed, straight linear incisions are ade­
quate for exposure of the dorsal aspect of the forearm. Inter­
metacarpal incisions on the hand allow one to decompress
the intrinsic muscles of the hand if this is necessary.
Techniques of excision and grafting
It has become increasingly clear that allowing hand injuries
to heal by contraction over the course of many weeks gives
very poor long-term results.56 Surgery is indicated for any
deep dermal or full-thickness hand burn that will not
promptly heal within 3 weeks. Generally, this need is appar­
ent to an experienced examiner within 5 days of injury (Fig.
13.11). The skin of the dorsal hand is much thinner than
that of the palmar hand. It is quite common for circumfer­
ential hand burns to heal very well over their palmar aspect,
yet require grafting on the dorsal surface. There is general
agreement that earlier surgery is associated with a better
functional result and a decreased need for reconstructive
procedures.
Practical options for wound coverage include split-
thickness autograft, full-thickness autograft, and groin or
abdominal flaps. Split-thickness sheet autograft, generally
thick, is the optimal coverage for most hand burns.
otherwise avoidable ischemic injury. Pressure measurement
confirmation is generally not necessary if serial examinations
suggest diminished perfusion.
Escharotomy should be performed with electrocautery.
Longitudinally oriented medial and lateral incisions are
made through eschar on the arm and forearm (the former
being made anterior to the ulnar styloid to avoid injury to
the ulnar nerve), stopping at the metacarpophalangeal joints
of the first and fifth digits (Fig. 13.10a). The hand is then
re-examined for perfusion prior to performing hand and
digital escharotomies. Often, blood flow is enhanced ade­
quately by decompression of the arm, making additional
escharotomy unnecessary.
The efficacy and safety of digital escharotomies is debated.
One study demonstrated a reduced incidence of amputation
if digital escharotomies were performed on circumferentially
burned digits.54 However, particularly in small children,
improperly performed digital escharotomies can cause sig­
nificant injury, and therefore caution must be exercised.
When digital perfusion remains marginal or inadequate
despite decompression of the arm, forearm, and hand,
escharotomies of full-thickness burns of the digits should be
performed. Incisions are carefully made with pinpoint elec­
trocautery between the neurovascular bundle and the exten­
sors, avoiding both structures. A single longitudinal incision
is made on the radial aspect of the thumb and the ulnar
aspect of the digits. This places the incisions on the side of
the digit with the least functional importance, should the
digital nerve be exposed by separation of edematous tissue
after escharotomy. The central digital incision can be
extended proximally onto the dorsum of the hand between
the metacarpals to enhance decompression (Fig. 13.10b).
The line of incision along a given digit can be found by
putting the fingers in maximal flexion, marking the lateral
extensions of the flexor wrinkles and completing them to a
continuous line (Fig. 13.10c).55 Meticulous hemostasis is
maintained throughout the procedure and the success of
decompression is documented by Doppler examination.
Escharotomy can generally be performed at the bedside or
in the emergency department under moderate sedation
Figure 13.10  (a) Arm escharotomy (b) Hand escharotomy (c) Finger escharotomy. (Adapted from Figure 61.6ABC in Green DP, Pederson WC, Hotchkiss RN, et al. ed. Green’s
Operative Hand Surgery, Philadelphia: Elsevier/Churchill Livingstone; 2005: 2164.)
A
B
C

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Figure 13.11  Deep dermal burn of the dorsal hand which underwent excision and grafting. (a) Post-burn day 7. (b) 6 weeks post injury.
A
B
Full-thickness grafts are ideally reserved for palmar surface
burns, particularly deep wounds of limited extent, or for
reconstructive operations during the acute recovery phase.
Groin and abdominal flaps can be very useful when manag­
ing isolated fourth-degree injuries.
Deep partial- and full-thickness hand burns generally
require layered excision and autografting. These procedures
are ideally performed after exsanguination of the extremity
with an elastic wrap and inflation of a pneumatic tourniquet
on the arm to reduce blood loss. The excision is performed
sequentially until a bed of viable tissue is reached. Viability
is recognized by a pearly white moist dermis or the presence
of bright yellow subcutaneous fat without thrombosed small
vessels or extravascular hemoglobin. Recognition of viable
tissue in an exsanguinated extremity with a proximal pneu­
matic tourniquet is an acquired skill that greatly facilitates
low-blood-loss excisions. The hand is then placed in a snug
wrap of epinephrine-soaked gauze prior to deflation of the
pneumatic tourniquet. After some time has been allowed to
elapse for spontaneous hemostasis, definitive hemostasis is
secured with judicious use of pinpoint electrocautery. The
hand is covered with sheet autograft. Grafted hands are then
covered with a gentle compressive gauze wrap and placed in
a thermoplastic splint in functional position. Hands are
elevated and immobilized for 4 days prior to reinstituting
passive and active hand therapy.
Only about 15% of palmar burns require grafting, as the
palmar skin is much thicker than the dorsal skin. It is not
uncommon to wait 2–3 weeks for healing before a decision
to graft is made. Palmar burns that require grafting are
usually covered with thick, sheet split-thickness autograft if
the defect is large, and full-thickness grafts if the defect is
small. When the palm is deeply burned and loss of palmar
concavity and range is at risk, the hand is splinted with the
palm extended to minimize contracture, both during topical
care of the burn and following any surgery. Instep grafts have
been advocated for aesthetic reasons, but functional results
with full-thickness or thick split-thickness grafts are generally
excellent.
Hands are splinted in the position of function: the meta­
carpophalangeal joints at 70–90° of flexion, the interphalan­
geal joints in extension, the wrist in 20° of extension, and
the first webspace open. Special attention should be paid to
the fifth digit, as it is particularly prone to contractures that
result in fixed interphalangeal joint flexion. In the hand,
such failures of early closure may compromise the ability to
participate in early therapy and possibly compromise long-
term outcome or delay full recovery. Inadequate excision is
a particular risk, as most of these operations are performed
after inflation of a proximal pneumatic tourniquet. If this is
compromised by direct injury or subsequent desiccation and
rupture, the collateral bands will migrate volarward and the
proximal interphalangeal joint will be brought into a posi­
tion of flexion from which recovery may be impossible. In
some cases this unfortunate sequence of events can be pre­
vented by ensuring prompt coverage of the proximal inter­
phalangeal joint. If the depth of injury is such that the
integrity of the overlying extensor mechanism is threatened,
splinting in extension and placing axial Kirschner wires
across the joint for 2–3 weeks may facilitate healing, with

Operative wound management
169
resulting stability. If the overlying extensor mechanism is
frankly destroyed and the joint is open, a partially functional
joint can sometimes be salvaged by Kirschner wire fixation
for 2–3 weeks, which may allow granulation tissue to bridge
the open joint; this can subsequently be grafted.
Techniques to salvage length
in fourth degree burn
In the presence of fourth degree burn involving the underly­
ing extensor mechanism, joint capsule, and bone, manage­
ment can be more complex and less satisfying. Patients
with small overall surface area burns are candidates for
early debridement with groin or abdominal flap coverage
(Fig. 13.12).57 A common pattern is deep dorsal burn with
exposure of the proximal interphalangeal joints, and dorsal
phalanges with viable volar tissue. If these wounds are kept
moist and clean, and proper position maintained, often the
avascular tissue will be covered with granulation tissue,
which can then be grafted with an acceptable result. When
the extensor mechanism is exposed, proper geometry
during the time needed for granulation tissue formation is
critical. The resting hand position with metacarpophalan­
geal joints in flexion at 90°, extension of the interphalan­
geal joints, and the thumb abducted and externally rotated
in opposition to the fingers, is proper. Granulation tissue
formation may be facilitated by meticulously debriding
remnants of burned cortical bone. Positioning may not be
reliable when only splints are used. Kirschner wires can
be helpful to maintain the interphalangeal joints in the
proper position while metacarpophalangeal joint flexion is
maintained with the splints. Wires are passed axially
from the tip of the finger proximally, stopping when the
proximal interphalangeal joint is immobilized. Autograft­
ing is performed whenever possible, and exposed joints
and bones are allowed to granulate and subsequently are
covered with autograft (Fig. 13.13). Joints which remain
unstable after coverage is achieved are later fused by open
arthrodesis.
The scalp
Scalp and skull burns represent a major challenge. The loca­
tion of these injuries presents a complex scenario with the
possibility of injury to vital organs. These injuries can be
classified into two groups: those which are limited to soft
tissue and those that involve the calvarium. Acute surgical
management of the burned scalp can vary from a simple soft
tissue debridement and skin grafting to a management of
complicated calvarial injury.
Scalp burns without bony involvement are treated as any
other burn, with debridement and skin grafts or flap cover­
age.58 There are several classifications for cranial burn wounds
based on the depth and extent of the injury.59 Bone loss of
<2 cm usually heals by its own regenerative processes, espe­
cially in children. In adults, bone regeneration is more
unpredictable.60 The priority in the acute phase is to debride
the wound and provide coverage without compromise to the
adjacent tissues. The use of bone grafts or tissue expander is
deferred until after the acute burn has resolved. Surgical
debridement includes the removal of necrotic soft tissue and
A
B
Figure 13.12  Abdominal flap coverage of fourth degree dorsal finger
burns. (a) Deep dorsal burns and intraoperative positioning of the hand on
the abdomen. (b) Flaps in position. (c) Final result.
C

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13
170
Figure 13.13  Preservation of digital length in fourth degree dorsal burn of
the hand in a 9 year old boy with 85% TBSA burn. (a) Day 7 post-burn.
(b) Day 12 post-burn. (c) Day 61 post-burn.
A
B
C
bone, avoiding injury to the outer cerebral layers. The use of
a fine diamond-tipped drill allows for a controlled layered
removal of non-viable skull tissue.
The surgical excision stops at a depth that provides a foun­
dation for the application of skin graft. Central nervous
system infections are possible, and adequate antibiotic
prophylaxis should be considered. In case of observable cer­
ebrospinal fluid leaks, clotting agents such as thrombin
foam or gel are applied.
The face
Burns to the face can have potentially devastating conse­
quences. Attention to details, patience, skill of excision,
coverage and postoperative management are essential in the
preservation of vital functions and cosmesis.61 Burns to
the face have the potential to affect vital structures such as
the upper airway and vital sensory organs such as the eyes
and ears.

Operative wound management
171
There have been no large randomized outcome trials com­
paring early excision and grafting of the face compared to
grafting after eschar separation and granulation formation.
Most authors have applied the general principle of early
excision to prevent contractures and provide the best esthetic
outcome for the face, with a suggested maximal waiting
period of 18 days.62
Once a decision has been made to proceed with excision
and grafting, suitable donor sites should be evaluated. Site
selection and depth of donor skin needs careful considera­
tion. If at all possible, the donor skin should come from the
area above the line of the nipples for the best color match.
Skin grafts from the scalp provide excellent color match but
carry a risk of follicle transplantation and subsequent hair
growth in undesired locations if the donor skin is taken
thicker. An alternative site is to use the upper part of the back.
Unmeshed sheet graft is applied to the face. If donor sites are
limited, temporary coverage with unmeshed allograft is an
option while waiting for re-epithelialization of donor sites.
Excision of facial burns can be carried out using various
methods. The mainstay of excision remains the Goulian/
Weck knife. If there is any doubt as to the depth, tangential
excision with a Goulian knife is more appropriate, as pres­
ervation of any viable dermal elements is essential for
optimal results (Fig. 13.14). Previously described ‘water dis­
sectors’ such as the Versajet can also be used in areas of
contour for more controlled, precise excision avoiding
potential iatrogenic injuries.
Owing to the rich capillary networks in the face, large
amounts of blood may be lost at the time of the excision.
Epinephrine clysis is a sensible pre-emptive measure to
reduce blood loss.63,64 Epinephrine-moistened topical
sponges are helpful, as is topical thrombin. Electrocautery
on a low setting can be useful for accurate hemostasis.
Placement of grafts on the face should be carried out to
mimic esthetic units as much as possible. If large pieces of
autograft are obtained they should be placed as a single piece
along adjacent cosmetic units. For esthetic purposes the face
is divided into cosmetic units. (Fig. 13.15).65 In the central
horizontal plane, periorbital, nasal and upper cheek areas
may be grafted as a single esthetic unit.65 Grafts should be
taken as widely as possible so as to reduce the number of
seams between the grafts. The grafts can be secured with
staples, sutures, glues or fibrin sealant.
The use of fibrin sealant, a hemostatic adjunct and
adhesive underlay has been shown in controlled studies
to reduce seroma and hematoma formation as well as
minimizing the need for staples or sutures, with equal or
better outcome.66 Medical-grade glues such as 2-cyano-butyl
acrylate (Histoacryl) can be used to secure graft around the
edge and is an excellent adjunct to suturing.
Once the grafts are in place, tubes and lines should be
positioned away to avoid disruption of grafts. Septal tie can
be used to secure the endotracheal tube and rid the face of
the ties that inevitably rub on the grafts. Sheet grafts on the
face should be evaluated frequently for movement or fluid
collection, which may be drained with a small-gauge needle.
Some centers delay the autografting phase of the procedure
to reduce graft loss from hematoma formation. Temporary
wound closure with allograft is a good option if this course
is chosen.67
In regions of extensive soft tissue injury and no underlying
bony structure, such as the buccal area, consideration may
be made for acute flap coverage with regional or free tissue
transfer. If the sinuses become exposed, the dead space may
be filled using free vascularized omental transfers, as
described in cases of facial trauma.68
Eyelids
Deep burns to the eyelids should be excised and grafted
early. Deep burns to eyelids can result in cicatricial ectro­
pion, leading to incomplete closure of the lids, which inevi­
tably exposes the eyes to desiccation, corneal ulceration, and
ultimately threat to sight.69 Post-burn cicatricial ectropion is
a serious condition, with unconscious ventilated patients at
particular risk. Release of scars and full-thickness skin grafts
to the lower eyelids and split-thickness skin grafts to the
Figure 13.14  Tangential excision being applied with a Goulian knife to the
chin. Previous grafting had been largely successful. The instrument is useful
for small and tricky areas.
Figure 13.15  Esthetic units of the face. (a) Frontal view. (b) Lateral view.
(Adapted from McCauley RL, Obeng MK. Reconstruction of cheek deformities, In: McCauley
RL, ed. Functional and aesthetic reconstruction of burned patients. Boca Raton, Florida:
Taylor and Francis Group; 2005: 270.)
A
B

Total Burn Care
13
172
Perianal burns are seen in association with extensive burns
in adults and in scalded children. Early excision and grafting
is recommended to prevent bacterial colonization and infec­
tion. Some centers recommend diversion of the fecal stream
to aid healing and graft take.73 If graft failure occurs, it is
important to keep trying to achieve engraftment as perianal
circular contracture can result from prolonged healing by
secondary intention.
The breast
The scarring and disfigurement associated with breast burns
can be a source of significant psychological stress in develop­
ing girls and young women.74 All efforts should be made to
preserve the breast bud in a prepubescent girl and the breast
mound in a postpubertal woman. Small burns, especially
linear ones, may be excised and closed primarily or allowed
to form scar and later excised.
The nipple–areola complex, especially in women, requires
extra attention. In general, it is best left unexcised as healing
can occur from the deep glandular structures that are usually
preserved.
Conclusion
One of the most important components of modern burn
care is early operative wound management. The evidence is
clear that prompt excision and closure of burn wound is
lifesaving for massively burned patients. Skin substitutes and
dermal replacement have made operative wound care even
more appealing for providing temporary coverage in patients
with insufficient autograft and offer an attractive alternative
to topical antimicrobial therapy for partial-thickness wounds.
Further reading
Desai MH, Herndon DN, Broemeling L, et al. Early burn wound
excision significantly reduces blood loss. Ann Surg. 1990
Jun;211(6):753-759; discussion 759-62. (Paper on early burn
excision and decreased blood loss.)
Heimback DM, Warden GD, Luterman A, et al. Multicenter
postapproval clinical trial of Integra dermal regeneration template
for burn treatment. J Burn Care Rehabil. 2003 Jan-Feb;24(1):42-48.
(Paper on dermal regeneration template.)
Herndon DN, Barrow RE, Rutan RL, et al. A comparison of
conservative versus early excision. Therapies in severely burned
patients. Ann Surg. 1989 May;209(5):547-553; discussion 552-553.
Janzekovic Z. The burn wound from the surgical point of view. J
Trauma. 1975 Jan;15(1):42-62. (Classic paper on early excision and
immediate grafting.)
Sood R, Roggy D, Zieger M, et al. Cultured epithelial autografts for
coverage of large burn wounds in eighty-eight patients: the Indiana
University experience. J Burn Care Res. 2010 Jul-Aug;31(4):559-568.
(Paper on cultured epithelia autografts.)
Supp DM, Boyce ST. Engineered skin substitutes: practices and
potentials. Clin Dermatol. 2005 Jul-Aug;23(4):403-412.
upper lids should be undertaken as soon as the condition is
diagnosed.70 Eyelid involvement is common with extensive
facial burns. The natural reflex of blinking will protect the
eyelid margin and the cornea, exposing the skin of the upper
eyelids.
Ophthalmic lubricants should be applied frequently to
keep the eyes moist to prevent exposure keratitis, especially
in unconscious patients. If burn ectropion develops, early
tarsorrhaphy or release of contracted eyelids may be neces­
sary. Tarsorrhaphy can be carried out at the bedside. The
eyelid is injected with a combination of dilute epinephrine
and lidocaine. A U-stitch is placed using a fine non-
absorbable suture, and the upper and lower eyelids are
approximated on their medial and/or lateral portions. The
suture should be passed through material such as a rubber
pledget to prevent suture being pulled through skin. The
suture should incorporate the ridge of tarsus but not traverse
it. An adequate tarsorrhaphy will permit the passive closure
of the eyelids to protect the cornea.
Consideration should also be given to acute release of the
upper and lower eyelids if there is contraction of eyelids
leading to corneal exposure and irritation. This can be carried
out using local flaps, full-thickness skin grafts or split-
thickness skin grafts. Full-thickness loss may require recon­
struction using hard palate mucosa or acellular dermis as the
inner lining of the lid.71
Genital burns
When burn occurs in the genital region it can produce sig­
nificant morbidity and long-term consequences for mobility,
waste elimination and sexual dysfunction. Spontaneous
epithelialization will likely occur with scald burns in this
region owing to the rich supply of hair follicles and
appendages.
Recommendations for acute management include selec­
tive urethral catheterization. This will allow urinary collec­
tion and also stenting of the urethra in the case of
circumferential constricting burns.
Most partial-thickness burns of the scrotum will heal
spontaneously as scrotal skin is thick and contains multiple
hair follicles. Testicular function should be evaluated by
measuring stimulated testosterone levels.72 Small full-
thickness burns to the scrotum can be excised and closed
primarily. In full-thickness burns to the foreskin circumci­
sion is appropriate, as phimosis is a common sequela. Along
the shaft of the penis full-thickness burns can be excised
using a Goulian knife or Versajet, and grafted using unmeshed
split-thickness skin grafts.
Scald burns to the genitalia are best treated conservatively.
A deep burn to the glans penis may be best allowed to
demarcate or proceed to eschar separation and then graft
the resultant granulation tissue. Full-thickness burns to the
labia majora should be excised and grafted as a delayed
procedure.
Access the complete reference list online at

Operative wound management
172.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
References
1. Lee JO, Herndon DN. Modulation of the post-burn
hypermetabolic state. In: Cynober L, Moore FA, eds. Nutrition
and critical care. Switzerland: Nestec. 2003;(8):39-56.
2. Herndon DN, Tompkins RG. Support of the metabolic response
to burn injury. Lancet. 2004 Jun 5;363(9424):1895-1902.
3. Bull JP, Fisher AJ. A study of mortality in a burns unit: a revised
estimate. Ann Surg. 1954;139:269-274.
4. Muller MJ, Herndon DN. The challenge of burns. Lancet. 1994
Jan 22;343:216-220.
5. Burke JF, Bandoc CC, Quinby WC. Primary burn excision and
immediate grafting: a method for shortening illness. J Trauma.
1974 May;14(5):389-395.
6. Pietsch JB, Netscher DT, Nagaraj HS, et al. Early excision of major
burns in children: effect on morbidity and mortality. J Pediatr
Surg. 1985 Dec;20(4):754-757.
7. Herndon DN, Parks DH. Comparison of serial debridement and
autografting and early massive excision with cadaver skin overlay
in the treatment of large burns in children. J Trauma. 1986
Feb;26(2):149-152.
8. Herndon DN, Barrow RE, Rutan RL, et al. A comparison of
conservative versus early excision. Therapies in severely burned
patients. Ann Surg. 1989 May;209(5):547-553; discussion
552-553.
9. Tompkins RG, Burke JF, Schoenfeld DA, et al. Prompt eschar
excision: a treatment system contributing to reduced burn
mortality. A statistical evaluation of burn care at the
Massachusetts General Hospital (1974–1984). Ann Surg. 1986
Sep;204(3):272-281.
10. Thompson P, Herndon DN, Abston S, et al. Effect of early
excision on patients with major thermal injury. J Trauma. 1987
Feb;27(2):205-207.
11. Xiao-Wu W, Herndon DN, Spies M, et al. Effects of delayed
wound excision and grafting in severely burned children. Arch
Surg. 2002 Sep;137(9):1049-1054.
12. Munster AM, Smith-Meek M, Sharkey P. The effect of early
surgical intervention on mortality and cost-effectiveness in burn
care. 1978–91. Burns. 1994 Feb;20(1):61-64.
13. Deitch EA, Clothier J. Burns in the elderly: an early surgical
approach. J Trauma. 1983 Oct;23(10):891-894.
14. Deitch EA. A policy of early excision and grafting in elderly burn
patients shortens the hospital stay and improves survival. Burns.
1985 Dec;12(2):109-114.
15. Hara M, Peters WJ, Douglas LG, Morris SFl. An early surgical
approach to burns in the elderly. J Trauma. 1990 Apr;30(4):
430-432.
16. Scott-Conner CEH, Love R, Wheeler W. Does rapid wound closure
improve survival in older patients with burns? Ann Surg. 1990
Jan;56(1):57-60.
17. Hunt JL, Purdue CF. The elderly burn patient. Am J Surg. 1992
Nov;164(5):472-476.
18. Ikeda J, Sugamata A, Jumbo Y, et al. A new surgical procedure for
aged burn victims: applications of dermolipectomy for burn
wounds and donor sites. J Burn Care Rehabil. 1990 Jan-Feb;11(1):
27-31.
19. Deitch EA, Wheelahan TM, Rose MP, et al. Hypertrophic
burn scars: analysis of variables. J Trauma. 1983 Oct;23(10):895-
898.
20. Heimbach DM. Early burn excision and grafting. Surg Clin North
Am. 1987 Feb;67(1):93-107.
21. Ong YS, Samuel M, Song C. Meta-analysis of early excision of
burns. Burns. 2006 Mar;32(2):145-150.
22. Engrav LH, Heimbach DM, Reus JL, et al. Early excision and
grafting vs. nonoperative treatment of burns of indeterminant
depth: a randomized prospective study. J Trauma. 1983
Nov;23(11):1001-1004.
23. Janzekovic Z. A new concept in the early excision and immediate
grafting of burns. J Trauma. 1970 Dec;10(12):1103-1108.
24. Janzekovic Z. The burn wound from the surgical point of view.
J Trauma. 1975 Jan;15(1):42-62.
25. Klein MB, Hunter S, Heimbach DM, et al. The Versajet water
dissector: a new tool for tangential excision. J Burn Care Rehabil.
2005 Nov-Dec;26(6):483-487.
26. Desai MH, Herndon DN, Broemeling L, et al. Early burn wound
excision significantly reduces blood loss. Ann Surg. 1990
Jun;211(6):753-759; discussion 759-62.
27. Hart DW, Wolf SE, Beauford RB, et al. Determinants of blood loss
during primary burn excision. Surgery. 2001 Aug;130(2):396-402.
28. Alexander JW, MacMillan BG, Law E, Kittur DS. Treatment of
severe burns with widely meshed skin autograft and meshed skin
allograft overlay. J Trauma. 1981 Jun;21(6):433-438.
29. Meek CP. Successful microdermagrafting using the Meek-Wall
microdermatome. Ann J Surgery. 1958 Oct;96(4):557-558.
30. Kreis RW, Mackie DP, Vloemans AWFP, et al. Widely expanded
postage stamp skin grafts using a modified Meek technique in
combination with an allograft overlay. Burns. 1993 Apr;19(2):
142-145.
31. Heimback DM, Warden GD, Luterman A, et al. Multicenter
postapproval clinical trial of Integra dermal regeneration template
for burn treatment. J Burn Care Rehabil. 2003 Jan-Feb;24(1):
42-48.
32. McEwan W, Brown TL, Mills SM, et al. Suction dressings to secure
a dermal substitute. Burns. 2004 May;30(3):259-261.
33. Sheridan RL, Choucair RJ. Acellular allodermis in burn surgery:
1-year result of a pilot trial. J Burn Care Rehabil. 1998 Nov-
Dec;19(6):528-530.
34. Munster AM. Cultured skin for massive burns. A prospective,
controlled trial. Ann Surg. 1996 Sep;224(3):372-375; discussion
375-7.
35. Barret JP, Wolf SE, Desai MH, et al. Cost-efficacy of cultured
epidermal autografts in massive pediatric burns. Ann Surg. 2000
Jun;231(6):869-876.
36. Sood R, Roggy D, Zieger M, et al. Cultured epithelial autografts
for coverage of large burn wounds in eighty-eight patients:
the Indiana University experience. J Burn Care Res. 2010
Jul-Aug;31(4):559-568.
37. Hohlfeld J, de Buys Roessingh A, et al. Tissue engineered fetal
skin constructs for paediatric burns. Lancet. 2005 Sep 3-9;
366(9488):840-842.
38. Supp DM, Boyce ST. Engineered skin substitutes: practices and
potentials. Clin Dermatol. 2005 Jul-Aug;23(4):403-412.
39. Bondoc CC, Burke JF. Clinical experience with viable frozen
human skin and a frozen skin bank. Ann Surg. 1971 Sep;
174(3):371-382.
40. Song IC, Bromberg BE, Mohn MP, et al. Heterografts as biological
dressings for large skin wounds. Surgery. 1966 Apr;59(4):
576-583.
41. Sheridan RL, Thompkins RG. Skin substitutes in burns. Burns.
1999 Mar;25(2):97-103.
42. Branski LK, Herndon DN, Celis MM, et al. Amnion in the
treatment of pediatric partial-thickness facial burns. Burns. 2008
May;34(3):393-399.
43. Irei M, Abston S, Bonds E, et al. The optimal time for excision of
scald burns in toddlers. J Burn Care Rehabil. 1986 Nov-Dec;7(6):
508-510.
44. Desai MH, Rutan RL, Herndon DN. Conservative treatment of
scald burns is superior to early excision. J Burn Care Rehabil. 1991
Sep-Oct;12(5):482-484.
45. Barret JP, Dziewulski P, Ramzy PI, et al. Biobrane versus 1% silver
sulfadiazine in second-degree pediatric burns. Plast Reconstr Surg.
2000 Jan;105(1):62-65.
46. Lal S, Barrow RE, Wolf SE, et al. Biobrane improves wound
healing in burned children without increased risk of infection.
Shock. 2000 Sep;14(3):314-318; discussion 318-319.

Total Burn Care
13
172.e2
© Copyright 2012 Elsevier, Inc. All rights reserved.
47. Boyce ST, Kagan RJ, Meyer NA, et al. Cultured skin substitutes
combined with Integra artificial skin to replace skin autograft and
allograft for the closure of excised full-thickness burns. J Burn
Care Rehabil. 1999 Nov-Dec;20(6):453-461.
48. Gilpin DA, Barrow RE, Rutan RL, et al. Recombinant human
growth hormone accelerates wound healing in children with large
cutaneous burns. Ann Surg. 1994 Jul;220(1):19-24.
49. Singh KP, Prasad R, Chari PS, et al. Effect of growth hormone
therapy in burn patients on conservative treatment. Burns. 1998
Dec;24(8):733-738.
50. Ramirez RJ, Wolf SE, Barrow RE, et al. Growth hormone
treatment in pediatric burns: a safe therapeutic approach. Ann
Surg. 1998 Oct;228(4):439-448.
51. Demling RH, Orgill DP. The anticatabolic and wound healing
effects of the testosterone analog oxandrolone after severe burn
injury. J Crit Care. 2000 Mar;15(1):12-17.
52. Wolf SE, Thomas SJ, Dasu MR. et al. Improved net protein
balance, lean mass, and gene expression changes with
oxandrolone treatment in the severely burned. Annals of Surgery.
2003 Jun;237(6):801-810; discussion 810-811.
53. Rodeberg DA, Easter AJ, Washam MA, Housinger TA, Greenhalgh
DG, Warden GD. Use of a helium-oxygen mixture in the
treatment of postextubation stridor in pediatric patients with
burns. J Burn Care Rehabil. 1995 Sep-Oct;16(5):476-480.
54. Salisbury RE, Taylor JW, Levine NS. Evaluation of digital
escharotomy in burned hands. Plast Reconstr Surg. 1976
Oct;58(4):440-443.
55. Robson MC, Smith DJ Jr, VanderZee AJ, et al. Making the burned
hand functional. Clin Plast Surg. 1992 Jul;19(3):663-671.
56. Goodwin CW, Maguire MS, McManus WF, et al. Prospective
study of burn wound excision of the hands. J Trauma. 1983
Jun;23(6):510-517.
57. Hanumadass M, Kagan R, Matsuda T. Early coverage of deep hand
burns with groin flaps. J Trauma. 1987 Feb;27(2):109-114.
58. Spies M, McCauley RL, Mudge BP, et al. Management of acute
calvarial burns in children. J Trauma. 2003 Apr;54(4):765-769.
59. Habal MB. Burns of the skull and scalp and their clinical
management, In: McCauley RL, ed. Functional and aesthetic
reconstruction of burned patients. Boca Raton, Florida: Taylor and
Francis Group; 2005:227-233.
60. Jackson D. Burns of bone: can these bones live?: II. Results of 98
cases and discussion of treatment. Burns. 1975 Jul;1(4):356-372.
61. Villapalos JL, Jeschke MG, Herndon DN. Topical management of
facial burns. Burns. 2008 Nov;34(7):903-911.
62. Fraulin FO, Illmayer SJ, Tredget EE. Assessment of cosmetic and
functional results of conservative versus surgical management of
facial burns. J Burn Care Rehabil. 1996 Jan-Feb;17(1):19-29.
63. Huges WB, DeClement FA, Hensell DO. Intradermal injection of
epinephrine to decrease blood loss during split thickness skin
grafting. J Burn Care Rehabil. 1996 May-Jun;171(3):243-245.
64. Sheridan RL, Szyfelbein SK. Staged high-dose epinephrine clysis
is safe and effective in extensive tangential burn excisions in
children. Burns. 1999 Dec;25(8):745-748.
65. Acikel C, Peker F, Ulkur E. Skin grafting of the naso-orbital region
as a single aesthetic unit. Burns. 2001 Nov;27(7):753-757.
66. Foster K, Greenhalgh D, Gamelli RL, et al. FS 4IU VH S/D
Clinical Study Group. Efficacy and safety of a fibrin sealant for
adherence of autologous skin grafts to burn wounds: results of a
phase 3 clinical study. J Burn Care Res. 2008 Mar-Apr;29(2):
293-303.
67. Horch RE, Jeschke MG, Spilker G, et al. Treatment of second
degree facial burns with allografts–preliminary results. Burns.
2005 Aug;31(5):597-602.
68. Jurkiewicz MJ, Nahai F. The omentum: its use as a free
vascularized graft for reconstruction of the head and neck. Ann
Surg. 1982 Jun;195(6):756-765.
69. Barrow RE, Jeschke MG, Herndon DN. Early release of third-
degree eyelid burns prevents eye injury. Plast Reconstr Surg. 2000
Mar;105(3):860-863.
70. Astori IP, Muller MJ, Pegg SP. Cicatricial postburn ectropion and
exposure keratitis. Burns. 1998 Feb;24(1):64-67.
71. Jiaqi C, Zheng W, Jianjun G. Eyelid reconstruction with acellular
human dermal allograft after chemical and thermal burns. Burns.
2006 Mar;32(2):208-211.
72. Alghanem AA, McCauley RL, Robson MC, et al. Management of
pediatric perineal and genital burns: twenty-year review. J Burn
Care Rehabil. 1990 Jul-Aug;11(4):308-311.
73. Quarmby CJ, Millar AJ, Rode H. The use of diverting colostomies
in paediatric peri-anal burns. Burns. 1999 Nov;25(7):645-650.
74. Foley P, Jeeves A, Davey RB, et al. Breast burns are not benign:
long-term outcomes of burns to the breast in pre-pubertal girls.
Burns. 2008 May;34(3):412-417.

©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00014-X
Anesthesia for burned patients
Lee C. Woodson, Edward R. Sherwood, Asle Aarsland, Mark Talon,
Michael P. Kinsky, Elise M. Morvant
Introduction
Continuous improvements in burn care since World War II
have resulted in a steady increase in the rate of survival after
large burn injury.1 These improvements have been attributed
to aggressive fluid resuscitation, early excision and grafting
of burn wounds, more effective antimicrobials, advances in
nutritional support, and development of burn centers. The
development of specialized burn centers has allowed the
concentration and coordination of resources needed to
provide a multidisciplinary approach from the time of
admission, with the goal of not just maximizing survival but
of optimizing functional recovery as well.
Today, most patients who are in good health prior to
injury will survive a more than 80% total body surface area
(TBSA) burn if promptly treated in a modern burn unit. In
their study of risk factors for death following burn injuries
Ryan et al.2 identified three variables that can be used to
estimate the probability of death: age over 60 years, burns
over more than 40% of TBSA, and the presence of inhalation
injury. Mortality increased in proportion to the number of
risk factors present: 0.3%, 3%, 33%, or approximately 90%
mortality depending on whether zero, one, two, or three risk
factors were present, respectively. O’Keefe et al. observed an
approximately twofold higher risk of death in women aged
30–59 years compared to men with similar burns and age.3
Although it has been assumed that very young children are
also at increased risk of death from burn injuries, Sheridan
et al. found very low rates of mortality in children younger
than 48 months who had suffered large burns.4 An increased
risk of mortality has been consistently observed in elderly
burn patients. All organ systems are influenced by age-related
factors of variable expression that can reduce functional
reserve. However, aged patients represent a heterogeneous
group in terms of physiological reserve, with wide variation
in the presence of coexisting diseases and the difference
between chronological and biological age. Issues relating to
the treatment of burns in elderly patients have recently been
reviewed by Keck and colleagues.5 Most studies of mortality
associated with burns focus on patient condition prior to
burn center admission. Wang and colleagues examined the
association of features related to treatment and hospital
course with mortality among patients who had experienced
massive burns (>70% TBSA).6 In their series, only sepsis,
ventilator dependency and reduced platelet count were inde­
pendent predictors of mortality.
Major burn injury results in pathophysiological changes in
virtually all organ systems. Table 14.1 lists and Fig. 14.1
illustrates some of the challenges presented by the acutely
burned patient during the perioperative period. In addition
to the predictable challenges relating to airway management,
monitoring, and vascular access, patient positioning requires
close communication and teamwork. Burns involving poste­
rior areas may require turning the patient to the prone posi­
tion for optimal access (Fig. 14.1). Vascular catheters and
endotracheal tubes must be secured with confidence and due
care given these lifelines during patient turning.
Modern burn care depends on coordination of a multidis­
ciplinary team including surgeons, intensivists, nurse clini­
cians, nutritionists, rehabilitation therapists, pulmonary care
therapists, and anesthesia providers. Anesthetic manage­
ment is an important part of this multidisciplinary approach.
Anesthesia providers have highly developed skills and expe­
rience in airway management, pulmonary care, fluid and
electrolyte management, vascular access, and pharmacologi­
cal support of the circulation. These areas of clinical expertise
are all central to the care of patients with major burn inju­
ries. However, the effective use of this clinical expertise for
the care of burn patients requires knowledge of the patho­
physiological changes associated with burns and an under­
standing of the multidisciplinary approach to burn care, so
that perioperative care is compatible with the overall treat­
ment goals for the patient.
The current standard of surgical treatment calls for early
excision and grafting of non-viable burn wounds, which may
harbor pathogens and produce inflammatory mediators
with systemic effects resulting in cardiopulmonary compro­
mise. After an extensive burn injury, the systemic effects of
inflammatory mediators on metabolism and cardiopulmo­
nary function reduce physiological reserve, and the patient’s
tolerance to the stress of surgery deteriorates with time.
Assuming adequate resuscitation, extensive surgery is best
tolerated soon after injury when the patient is most fit.
Another advantage of early excision is that blood loss is less
when wound excision is performed soon after the initial
burn.7 However, it must be recognized that the initial resus­
citation of patients with large burns results in large fluid
shifts and may be associated with hemodynamic instability
and respiratory insufficiency. Reynolds et al.8 reported that
more than half of deaths after burn injuries occur due to
failed resuscitation. Some burn patients develop refractory
burn shock soon after injury and cannot be resuscitated.8
An important part of the preoperative evaluation is an
CHAPTER 14 
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Total Burn Care
14
174
Preoperative evaluation
In addition to the standard features of a preoperative evalu­
ation, the anesthetist should focus on certain burn injury-
related features that are associated with increased risk and
technical challenge when planning perioperative care of the
patient with acute burn injuries (Table 14.2). Because physio­
logical changes associated with the burn injury and their
resolution during healing are dynamic, the evaluation of the
acutely burned patient requires knowledge of the continuum
of these changes after the initial injury. The preoperative
evaluation must also be performed within the context of the
planned operative procedure, which will depend on the loca­
tion, extent, and depth of burn wounds, time after injury,
presence of infection, and existence of suitable donor sites
for autografting. It is important to know the mechanism of
injury, as this determines the quality of burn injuries and the
kinds of associated disorder the patient may present with.
As an example, a person burned in the enclosed space of a
house and a child who has suffered a scald burn would
present with very different associated injuries. As resuscita­
tion and the inflammatory response to injury are dynamic,
it is also important to know the time elapsed since injury.
Initial evaluation of the burn injury
Destruction of skin by thermal injury disrupts the vital func­
tions of the largest organ in the body. The skin provides
several essential protective and homeostatic functions (Table
14.3). Treatment of patients with burn injuries must com­
pensate for loss of these functions until the wounds are
covered and healed. As a barrier to evaporation of water, the
skin helps maintain fluid and electrolyte balance. Heat loss
through evaporation and loss of vasomotor regulation in
burned skin diminishes effective temperature regulation.
The skin’s barrier function also protects against infection by
invading organisms. Wound exudate rich in protein depletes
plasma proteins when large body surface areas are injured.
In addition to the loss of these important functions of the
skin, extensive burns result in an inflammatory response
with systemic effects that alter function in virtually all organ
systems. Perioperative anesthetic management depends on
an appreciation of these pathophysiological changes as
revealed by the preoperative evaluation.
Much of the morbidity and mortality associated with burn
injuries are related to the size of the injury. The extent of the
assessment of the quality of the resuscitation to be sure the
patient is adequately prepared to withstand the stress of
surgery.
Since the last edition of this book was published, Fuzaylov
and Fidkowski have reviewed the anesthetic management of
pediatric patients with major burn injuries.9 Patients suffer­
ing burn injuries also require surgical treatment for years
after the initial injury in order to correct functional and
cosmetic sequelae, and anesthetic management for recon­
structive burn surgery presents many special problems.10 This
chapter, however, will concentrate on the care of acute burn
patients. The acute phase of burn injury is defined as the
period from injury until the wounds have been excised,
grafted, and healed.
Table 14.1  Perioperative challenges in the acute burn patient
• Compromised airway
• Pulmonary insufficiency
• Altered mental status
• Associated injuries
• Limited vascular access
• Rapid blood loss
• Impaired tissue perfusion due to:
• Hypovolemia
• Decreased myocardial contractility
• Anemia
• Decreased colloid osmotic pressure
• Edema
• Dysrhythmia
• Impaired temperature regulation
• Altered drug response
• Renal insufficiency
• Immunosuppression
• Infection/sepsis
Figure 14.1  As illustrated in this photograph, anesthetic management of
the acute burn patient for excision and grafting of wounds presents
numerous challenges regarding monitoring, vascular access, temperature
regulation, and rapid blood loss. Prone positioning requires extra care to
assure vascular cannulas and the endotracheal tube are secure.
Table 14.2  Major preoperative concerns in acutely burned
patients
Age of patient
Extent of burn injuries (total body surface area)
Burn depth and distribution (superficial or full thickness)
Mechanism of injury (flame, electrical, scald, or chemical)
Airway patency
Presence or absence of inhalation injury
Elapsed time from injury
Adequacy of resuscitation
Associated injuries
Coexisting diseases
Surgical plan

Anesthesia for burned patients
175
Table 14.3  Functions of skin
1. Protection from environmental elements (e.g. radiation, mechanical
irritation or trauma)
2. Immunological – antigen presentation, antibacterial products (sebum),
barrier to entry of pathological organisms
3. Fluid and electrolyte homeostasis – helps maintain protein and
electrolyte concentrations by limiting evaporation
4. Thermoregulation – helps control heat loss through sweating and
vasomotor regulation of superficial blood flow
5. Sensory – extensive and varied sensory organs in skin provide
information about environment
6. Metabolic – vitamin D synthesis and excretion of certain substances
7. Social – appearance of skin has strong influence on image and social
interactions
Adapted from Williams WG, Phillips LG. Pathophysiology of the burn wound. In:
Herndon DN, ed. Total burn care, 1st edn. London: WB Saunders; 1996: 64.
burn injury is expressed as the total body surface area (TBSA)
burned. Estimates of TBSA burned are used to guide fluid
and electrolyte therapy and to predict surgical blood loss.
Initial estimates of the percentage of the skin’s surface that
has been burned can be quickly estimated by the so-called
‘Rule of Nines;’ estimates are modified for pediatric patients
because of age-related differences in body proportions. More
precise estimates of TBSA affected can be made using a
Lund–Browder chart (Fig. 14.2).
Knowledge of the burn depth is also critical to anticipating
physiological insult, as well as planned surgical treatment.
Partial-thickness burns may heal without scarring or deform­
ity and do not require surgical excision. Deeper partial-
thickness and full-thickness burns will not heal and require
surgical debridement and grafting, with associated surgical
blood loss.
With extensive wound excision or debridement large
amounts of blood can be lost rapidly. Adequate preparation
in terms of monitors, vascular access, and availability of
blood products is essential. Accurate estimates of blood loss
are crucial in planning preoperative management of burn
patients. Surgical blood loss depends on the area to be
excised (cm2), time since injury, surgical plan (tangential
vs fascial excision), and the presence of infection.7 Blood
loss from skin graft donor sites will also vary depending
on whether it is an initial or a repeat harvest. These
variables are valuable predictors of surgical blood loss,
which is a critical factor in planning anesthetic management
(Table 14.4).
Airway and pulmonary function
Special attention must be paid to the airway and pulmonary
function during preoperative evaluation. In the emergency
department burn patients may initially present with respira­
tory issues that demand immediate attention. In addition,
there is general recognition that smoke inhalation injury
increases morbidity and mortality for burn patients.11 The
presence of an inhalation injury in combination with a cuta­
neous burn increases the volume of fluid required for resus­
citation by as much as 44%, and this may contribute to the
increased hemodynamic instability seen in patients with
combined injury.12 Numerous studies have also shown an
increased incidence of pulmonary complications (pneumo­
nia, respiratory failure, or ARDS) in patients with burns
and inhalation injury compared to burns alone.13 Sequelae
of inhalation injury include upper airway distortion and
obstruction from direct thermal injury, impaired pulmonary
gas exchange due to effects of irritant gases on lower airways
and pulmonary parenchyma, and systemic effects of inhaled
toxins such as carbon monoxide (CO) or cyanide. These
three components of the inhalation injury have separate
time courses and pathophysiological consequences.
Burn injuries to the face and neck can distort anatomy and
reduce range of mobility in ways that make direct laryngos­
copy difficult or impossible. Specific alterations include
impaired mouth opening, edema of the tongue, oropharynx,
and larynx, as well as decreased range of motion of the neck.
The tissue injury and sloughing present after severe facial
burns may also make mask ventilation difficult.
Foley described findings of 335 autopsies performed on
patients who died from extensive burns.14 Intraoral, palatal,
and laryngeal burns were not uncommon among patients
with inhalation injuries. The most common sites of laryn­
geal injury were the epiglottis and vocal folds where their
edges were exposed. In contrast, thermal necrosis below the
glottis and upper trachea was not observed in any of these
patients. The lower airways are nearly always protected from
direct thermal injury by the efficiency of heat exchange in
the oro- and nasopharynx, unless the injury involves steam
or an explosive blast. This has been demonstrated in an
experimental model.15 Inhalation injury to the lower airways
and pulmonary parenchyma is due to the effect of toxic or
irritant gases.
Clinical suspicion of inhalation injury is aroused by the
presence of certain risk factors, such as history of exposure
to fire and smoke in an enclosed space, or a period of uncon­
sciousness at the accident scene, burns including the face and
neck, singed facial or nasal hair, altered voice, dysphagia,
oral and/or nasal soot deposits, or carbonaceous sputum.
The most immediate threat from inhalation injury is upper
airway obstruction due to edema. Early or prophylactic intu­
bation is recommended when this complication threatens.
However, exposure to smoke does not always lead to severe
injury, and in the absence of overt evidence of respiratory
distress or failure it may be difficult to identify patients who
will experience progressive inflammation and ultimately
require intubation of the trachea. In a retrospective study,
Clark et al. reported that 51% of their patients exposed to
Table 14.4  Calculation of expected blood loss
Surgical procedure
Predicted blood loss
<24 h since burn injury
0.45 mL/cm2 burn area
1–3 days since burn injury
0.65 mL/cm2 burn area
2–16 days since burn injury
0.75 mL/cm2 burn area
>16 days since burn injury
0.5–0.75 mL/cm2 burn area
Infected wounds
1–1.25 mL/cm2 burn area
Adapted from Desai et al. Early burn wound excision significantly reduces blood
loss. Ann Surg 1990; 221: 753–762.10

Total Burn Care
14
176
Figure 14.2  Modified from Lund and Browder. Chart used to calculate the surface area involved by burn. It takes into account that, as one grows from
infancy to adulthood, the relative surface area of the head decreases while the relative surface area of the lower extremities increases.
BURN DIAGRAM
Shriners Burns Institute – Galveston Unit
Burn Estimate – Age vs. area
Head
Neck
Anterior trunk
Posterior trunk
Right buttock
Left buttock
Genitalia
Right upper arm
Left upper arm
Right lower arm
Left lower arm
Right hand
Left hand
Right thigh
Left thigh
Right leg
Left leg
Right foot
Left foot
Birth–
1 year
19
2
13
13
2.5
2.5
1
4
4
3
3
2.5
2.5
5.5
5.5
5
5
3.5
3.5
1–4
years
17
2
13
13
2.5
2.5
1
4
4
3
3
2.5
2.5
6.5
6.5
5
5
3.5
3.5
5–9
years
13
2
13
13
2.5
2.5
1
4
4
3
3
2.5
2.5
8
8
5.5
5.5
3.5
3.5
10–14
years
11
2
13
13
2.5
2.5
1
4
4
3
3
2.5
2.5
8.5
8.5
6
6
3.5
3.5
15
years
9
2
13
13
2.5
2.5
1
4
4
3
3
2.5
2.5
9
9
6.5
6.5
3.5
3.5
Total
TBSA%
3°
2°
Adult
7
2
13
13
2.5
2.5
1
4
4
3
3
2.5
2.5
9.5
9.5
7
7
3.5
3.5
Age:
Sex:
Date of admission:
Type of burn:
Height (cm)
Weight (kg)
Body surface (m2)
Total burn (m2)
3° burn (m2)
3rd°
2nd°
Associated injuries/comments:
Flame
Electrical
Inhalation injury
Date of burn
Date completed
Completed by
Date revised
Revised by
Approved by
Scald
Chemical

Anesthesia for burned patients
177
airway and parenchymal injuries develop more slowly than
upper airway obstruction. Prior to resuscitation, clinical
signs and symptoms, chest X-ray, and blood gas analysis may
be within normal limits despite significant injury that even­
tually progresses to respiratory failure requiring intubation
and mechanical ventilation.24
Linares et al. studied the sequence of morphological
changes following smoke inhalation in an experimental
sheep model.25 They observed four discrete but overlapping
phases of injury, described as exudative, degenerative, prolif­
erative, and reparative. During the first 48 hours the exudative
phase was characterized by polymorphonuclear (PMN) infil­
tration, interstitial edema, loss of type I pneumocytes, and
damage to the tracheobronchial epithelium in the form of
focal necrosis, hemorrhage, and submucosal edema. The
degenerative phase occurred between 12 and 72 hours and
was characterized by progressive epithelial damage with
shedding of necrotic tissue and the formation of pseu­
domembranes and casts. Hyaline membranes developed
over alveolar surfaces. Macrophages began to accumulate to
begin absorption of necrotic debris. A proliferative phase was
described between days 2 and 7 during which type II
pneumocytes and macrophages proliferated. After the
fourth day reparative changes were observed, with regenera­
tion of epithelium from spared epithelium from the orifices
of glands.
Demling and Chen have provided a lucid description of
the pathophysiological changes following inhalation injury.26
Decreased dynamic compliance increases the work of breath­
ing. Increased closing volume and decreased functional
residual capacity lead to atelectasis and shunt, resulting in
hypoxia. Airways become plugged by sloughed epithelium,
casts, and mucus. Impaired ciliary action exacerbates the
airway obstruction by reducing the clearance of airway
debris. These changes lead to further shunting and allow
colonization and pneumonia. Treatment for inhalation
injury is empiric and supportive, with tracheal intubation
and mechanical ventilation. The application of aggressive
pulmonary toilet, high-frequency percussive ventilation, and
respiratory therapy protocols designed to mobilize obstruct­
ing debris have been found to be beneficial.27,28 The impor­
tance of strategies to limit ventilator-induced lung injury has
been recognized.29,30
Carbon monoxide (CO) and cyanide are two major toxic
components of smoke. The burn patient with evidence of
inhalation injury should be evaluated for the presence of
toxicity resulting from these compounds. CO binds hemo­
globin 200 times more avidly than oxygen.31 Therefore, CO
markedly impairs the association of oxygen with hemo­
globin and reduces oxygen-carrying capacity. CO also shifts
the oxyhemoglobin dissociation curve to the left, thereby
reducing the release of oxygen into tissues. These factors
result in decreased oxygen delivery to tissues and, at critical
levels, lead to anaerobic metabolism and metabolic acidosis.
Signs and symptoms of CO poisoning include headache,
mental status changes, dyspnea, nausea, weakness, and tachy­
cardia. Patients suffering CO poisoning have a normal PaO2
and oxygen saturation by routine pulse oximetry. They are
not cyanotic. Carboxyhemoglobin must be detected by CO
oximetry. Carboxyhemoglobin levels above 15% are toxic
and those above 50% are often lethal. The major treatment
approach is administration of 100% oxygen. Hyperbaric
smoke inhalation did not require intubation.16 Unnecessary
intubation in the presence of an inflamed laryngeal mucosa
risks further damage to the larynx and subglottic area.17,18
Traditional clinical predictors of airway obstruction have
been found to be relatively insensitive and inadequate for
identifying early severe airway inflammation, and often
underestimate the severity of the injury.19,20 More objective
criteria for evaluation of the risk of airway obstruction are
often needed. Hunt et al. found fiberoptic bronchoscopy to
be a safe and accurate method for diagnosis of acute inhala­
tion injury.21 They described observations of severe supra­
glottic injuries associated with mucosal edema obliterating
the piriform sinuses and causing massive enlargement of the
epiglottis and arytenoid eminence. Haponic et al. made
serial observations by nasopharyngoscopy in patients at risk
for inhalation injury and found distortions of the upper
airway described as compliant, edematous mucosa of the
aryepiglottic folds, and arytenoid eminences that prolapsed
to occlude the airway on inspiration.22 Progressive upper
airway edema in these patients was correlated with body
surface area burned, resuscitative volume administered, and
rate of infusion of resuscitative fluids. Traditional teaching
with the support of the American Burn Association has
encouraged early prophylactic endotracheal intubation
when risk factors for upper airway inhalation injury are
present. In response to what appeared to be a preventable
death associated with a prehospital intubation, Eastman and
colleagues at the Parkland Burn Center performed a retro­
spective study to identify the factors that led to prehospital
intubation of burn victims and, by examining the patients’
hospital courses, to determine which intubations were indi­
cated.23 Of 879 patients intubated prior to hospitalization
11.9% were extubated the day of admission and 41.4% were
extubated successfully within 48 hours of injury. This implies
that many patients were intubated without benefit. The
authors suggested that improved training of prehospital pro­
viders might reduce the number of unnecessary prehospital
intubations. Over the past two decades we have observed
serious morbidity and some deaths due to airway complica­
tions in patients intubated for transport (unpublished obser­
vations). Tracheal intubation is not a benign intervention
and should be employed only when there is a clear risk–
benefit advantage, especially in the context of transport
between facilities. For patients who are at risk for inhalation
injury but lack definitive indications for intubation, fiberop­
tic nasopharyngoscopy is effective in identifying laryngeal
edema. Serial examinations may help avoid unnecessary
intubations and at the same time identify progressive inflam­
matory changes and allow intubation before severe airway
obstruction and emergency conditions develop.17
The level of respiratory support must also be assessed. The
level of required support may range from supplemental
blow-by or mask oxygen to intubation and ventilation with
high positive end-expiratory pressure (PEEP) and FIO2.
Acute lung injury can occur from inhalation of chemical
irritants, systemic inflammation from burn wounds or dif­
ficulties with resuscitation, or ventilator-induced injury.
Common pathologies include upper thermal airway injury
with stridor, pulmonary parenchyma damage from chemical
irritants or inflammation, lower airway obstruction from
mucus plugs and epithelial casts, as well as pulmonary
edema due to acute lung injury or volume overload. Lower

Total Burn Care
14
178
hours.39 The forces responsible for this massive fluid shift
involve components of the Starling equilibrium,40
J
K
P
P
v
f
c
if
p
if
=
−
−
−
[(
)
(
)]
σ π
π
where Kf is the capillary filtration coefficient, Pc is the capil­
lary pressure, Pif is the interstitial hydrostatic pressure, σ is
the reflection coefficient for protein, πp is the plasma colloid
osmotic pressure, and πif the interstitial colloid osmotic
pressure.
The specific alterations include:
•
an increased microvascular permeability coefficient (kf
and σ) due primarily to the release of local and
systemic inflammatory mediators;
•
an increase in capillary hydrostatic pressure (Pc) due to
microvascular dilatation;
•
decreased interstitial hydrostatic pressure (Pif) due to
disruption in collagen binding;41
•
decreased intravascular oncotic pressure (πc) due to
leakage of protein from the intravascular space; and
•
a relative increase in interstitial oncotic pressure due to
a smaller decrease in interstitial oncotic pressure (πi)
compared to πc.
Burn injury is unique with regard to microcirculatory dys­
function. Perturbations occur in all of the Starling forces.
Marked edema formation in burn-injured skin occurs almost
instantaneously owing to a large negative interstitial hydro­
static pressure.42 Other hydraulic forces coupled with micro­
vascular permeability lead to the leakage of protein and fluid
into the interstitial space. Although fluid replacement therapy
is essential in treating hypovolemia, edema is worsened by
plasma protein dilution (reduction in plasma oncotic pres­
sure). The net effect of these changes is the development of
massive edema during the first 24–48 hours after thermal
injury and a concomitant loss of intravascular volume.
The hypotension associated with burn injury could also
be due to myocardial depression.43–47 Thermal injury stimu­
lates the release of inflammatory mediators such as tumor
necrosis factor α (TNFα), interleukin-1 (IL-1), and prosta­
glandins. TNFα and IL-1 are known to have myocardial sup­
pressant effects.48,49 Experimental animal models clearly
demonstrate cardiac depression.43–46 Clinical evidence of
myocardial depression is less characterized. Measurements
of cardiac function after burn injury often differ with respect
to time of injury, severity of injury, patient comorbidities,
monitor type, e.g. PA catheter, echocardiography, and the
sample size of the study.50–56 At our institution, we routinely
perform transesophageal echocardiography in severely
injured patients within the first 72 hours of admission. Our
observational data show that a significant percentage of
patients have severe systolic dysfunction, which is associated
with a prolonged ICU course (Fig. 14.3).57
If the patient survives the initial burn shock and is ade­
quately resuscitated, an inflammation induced hyperdy­
namic circulation develops. This state of massive inflammation
or systemic inflammatory response syndrome (SIRS) is char­
acterized by hypotension, tachycardia, a marked decrease in
systemic vascular resistance, and increased cardiac output.
SIRS has a continuum of severity ranging from the presence
of tachycardia, tachypnea, fever, and leukocytosis to refrac­
tory hypotension and multiple organ system dysfunction.
oxygen has also been used to treat acute CO poisoning, but
there is no general agreement on indications, treatment
parameters, or outcome benefits. The data have been reviewed
recently by Kealey.32 As a result, available data provide no
reliable evidence that hyperbaric oxygen reduces the inci­
dence of neurological sequelae of CO toxicity.
Cyanide is also a component of smoke, resulting from the
burning of certain plastic products.33 Cyanide directly
impairs the oxidative apparatus in mitochondria and reduces
the ability of cells to utilize oxygen in metabolism. These
alterations result in conversion to anaerobic metabolism and
the development of metabolic acidosis. Signs and symptoms
include headache, mental status changes, nausea, lethargy,
and weakness. Hydrogen cyanide levels above 100 ppm are
generally fatal.34,35
Treatment of cyanide toxicity begins with a high inspired
oxygen concentration, which may increase intracellular
oxygen tension sufficiently to cause non-enzymatic oxida­
tion of reduced cytochromes, or displace cytochrome oxidase
and potentiate the effects of administered antidotes. Phar­
macological intervention includes methemoglobin genera­
tors such as the nitrates (amyl nitrite inhalation 0.2 mL, or
sodium nitrite IV 10 mL of 3% solution for adults and 0.13–
0.33 mL/kg of 3% solution for children) and dimethylami­
nophenol (3.25 mg/kg) to increase methemoglobin levels.
Methemoglobin competes with cytochrome oxidase for
cyanide. However, excessive levels of methemoglobin lead to
reduced oxygen-carrying capacity and may be toxic. Direct
binding agents have a high affinity for cyanide. Di-cobalt
edetate (20 mL of 15% solution for adults or 0.3–0.5 mL/
kg of 15% solution for children) is extremely rapid in action
but has significant toxicity, whereas hydroxocobalamin
(adults 5–10 g or children 70 mg/kg), the precursor of
vitamin B12, has been shown to be safe, with few systemic
side effects; it is actively metabolized by the liver and avoids
renal absorption. Sulfur donors such as sodium thiosulfate
(adults 25 mL of 50% solution or children 1.65 mL/kg of
25 % solution) accentuate the body’s enzymatic conversion
of cyanide to thiocyanate in the presence of the mitochon­
drial enzyme rhodanese, reducing its toxicity and increasing
elimination.35,36
Effect of burn injury on circulation
Thermal injury has profound effects on the systemic circula­
tion. In particular, severe injury results in microcirculatory
derangements and cardiac dysfunction. Hemodynamic man­
agement is a major component of perioperative care. It is
critical for the anesthesiologist to assess the adequacy of
fluid resuscitation and the hemodynamic status of the
patient.
After massive thermal injury, a state of burn shock devel­
ops due to intravascular hypovolemia and, in some cases,
myocardial depression. This state of burn shock is character­
ized by decreased cardiac output, increased systemic vascular
resistance, and tissue hypoperfusion.37,38 Intravascular hypo­
volemia results from alterations in the microcirculation in
both burned and unburned tissues, leading to the develop­
ment of massive interstitial fluid accumulation. Cutaneous
lymph flow increases dramatically in the immediate post-
burn period and remains elevated for approximately 48

Anesthesia for burned patients
179
Recently, in a prospective, randomized study, the use of
plasma for volume resuscitation was shown to limit the
volume infused along with reducing intra-abdominal pres­
sure and abdominal compartment syndrome (see below).64
These outcome variables have not been used for comparing
crystalloid and colloid resuscitation in the past. With the
trend toward larger volumes for initial resuscitation it may
be that the use of colloid may be beneficial for larger injuries
requiring more volume.
The use of hypertonic saline, either alone or in conjunc­
tion with colloids, has been advocated by some in the initial
resuscitation of burned patients. Among the potential
benefits are reduced volume requirements to attain similar
levels of intravascular resuscitation and tissue perfusion
compared to isotonic fluids.65 Theoretically, the reduced
volume requirements would reduce the incidence of pulmo­
nary and peripheral edema, thereby reducing the incidence
of pulmonary complications and the need for escharotomy.
Hypertonic saline dextran solutions have been shown to
expand intravascular volume by mobilizing fluids from
intracellular and interstitial fluid compartments. Although
hypertonic saline dextran solutions transiently reduce initial
fluid requirements, there is a potential for a rebound in fluid
needs later in resuscitation owing to the sodium load.66,67
Therefore, most burn centers continue to use isotonic crystal­
loid fluids for initial resuscitation of patients in burn shock.
Several fluid resuscitation protocols that use various combi­
nations of crystalloids, colloids, and hypertonic fluids have
been developed (Table 14.5). Isotonic crystalloid is the most
commonly used fluid for resuscitation in US burn centers.
The most popular fluid resuscitation regimen, the Parkland
formula, uses isotonic crystalloid solutions and estimates the
fluid requirements in the first 24 hours to be 4 mL/kg/%
TBSA burned. However, many burn centers are administering
50% more fluid than the Parkland formula would predict.58
Crystalloid solutions generally provide adequate volume
resuscitation, but the large volumes that are needed result
in substantial tissue edema and hypoproteinemia. Con­
sequently, complications of over-resuscitation, including
abdominal compartment syndrome, pleural effusions,
pulmonary edema, fasciotomies and conversion of partial-
thickness lesions to full-thickness lesions are more frequently
observed. Explanation for this pattern of ‘fluid creep’ is
unclear.59,60 Clinical practice has changed in the last 30 years.
Patients are receiving higher amounts of opioids to treat pain
associated with thermal injury, which can cause vasodilation
and precipitate hypotension. Additionally, most clinicians
appreciate the dangers of hypovolemia; however, there is
limited education about the risks of administering too much
fluid. Thus, reliance on targeted or goal directed endpoints
for fluid resuscitation following severe thermal injury is
rarely practiced.
Resuscitation regimens that restore vascular volume losses
while reducing edema formation are continuously being
tested. Colloid and hypertonic fluids have shown efficacy in
treating other injuries. Overall, colloid resuscitation within
the first 24 hours of burn injury has not improved outcome
compared to crystalloid resuscitation.61,62 Furthermore, a
recent meta-analysis indicated that mortality is higher in
burned patients receiving albumin as part of the initial resus­
citation protocol, with a 2.4 relative risk of mortality com­
pared to patients receiving crystalloid alone.63 Because of the
added cost and the little established benefit, colloid solu­
tions have not been used routinely in the United States for
initial volume resuscitation in burned patients. However,
specific types of colloid regimen might yield different results.
Figure 14.3  Systolic function as measured by transesophageal
echocardiography is severely depressed in some patients with major burn
injuries. This myocardial depression has been associated with prolongation
of ICU stay. (From Kinsky et al. ESICM. 2009; 193: 6–228).
Length of ICU stay (days)
10
20
30
40
50
60
70
80
90
0
Ejection fraction %
>50%
p < 0.05
40–50%
<40%
Table 14.5  Formulas for estimating adult burn patient
resuscitation fluid needs
Colloid
formulas
Electrolyte
Colloid
D5W
Evans
Normal saline
1.0 mL/kg/%
burn
1.0 mL/kg/%
burn
2000 mL/24 h
Brooke
Lactated Ringer’s
1.5 mL/kg/%
burn
0.5 mL/kg
2000 mL/24 h
Slater
Lactated Ringer’s
2 liters/24 h
Fresh frozen
plasma
75 mL/kg/24 h
Crystalloid formulas
Parkland
Lactated Ringer’s
4 mL/kg/% burn
Modified
Brooke
Lactated Ringer’s
2 mL/kg/% burn
Hypertonic saline formulas
Hypertonic
saline solution
(Monafo)
Volume to maintain urine output at 30 mL/h
Fluid contains 250 mEq Na/liter
Modified
hypertonic
(Warden)
Lactated Ringer’s +50 mEq NaHCO3 (180 mEq Na/liter)
for 8 hours to maintain urine output at 30–50 mL/h
Lactated Ringer’s to maintain urine output at
30–50 mL/h beginning 8 hours postburn
Dextran
formula
(Demling)
Dextran 40 in saline – 2 mL/kg/h for 8 hours
Lactated Ringer’s – volume to maintain urine output at
30 mL/h
Fresh frozen plasma – 0.5 mL/kg/h for 18 hours
beginning 8 hours postburn

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180
and burn patients.77–79 The use of inotropes to attain supra­
physiological oxygen transport could be detrimental in some
cases. One study that used dobutamine to increase cardiac
output and increase oxygen delivery demonstrated increased
mortality.80 Dobutamine, like other inotropes, can increase
cardiac work and result in myocardial ischemia or myocar­
dial infarction. Selective use of inotropes is warranted. In
general, our practice is to use inotropic support in patients
with dilated cardiomyopathy and withhold it in patients
with risk factors for coronary artery disease. Estimating
preload in the acutely burned patient is quite challenging.
Filling pressures (central venous pressure and pulmonary
artery occlusion pressure) correlate poorly with circulating
blood volume, especially during positive-pressure ventila­
tion.81 Newer techniques estimate the volume of blood in
the thorax (intrathoracic blood volume, or ITBV) using
transcardiopulmonary thermodilution.82,83 This technique
has been used in burn patients during resuscitation. Holm
and colleagues observed that ITBV, but not central venous
and pulmonary capillary occlusive pressure, correlated with
cardiac index and oxygen delivery during fluid resuscitation
of burn patients.83 The use of ITBV to successfully restore
cardiac index in this series was associated with significantly
larger volumes than predicted by the Parkland formula.83
This technology is available commercially as the PiCCO
system (Pulsion Medical Systems, Munich, Germany). In
addition to ITBV this system also provides an estimate of
extravascular lung water and stroke volume variability, and
a continuous estimate of cardiac output and systemic vascu­
lar resistance.
Blood lactate and base deficit provide indirect metabolic
global indices of tissue perfusion. Lactic acid is a byproduct
of anaerobic metabolism and is an indicator of either inad­
equate oxygen delivery or impaired oxygen utilization. In the
absence of conditions such as cyanide poisoning or sepsis
that alter oxygen utilization at the cellular level, lactate pro­
duction serves as a useful marker of oxygen availability.
Serum lactate levels have served as a useful marker of fluid
resuscitation and tissue perfusion in burn patients.84 A recent
study showed serum lactate to be highly predictive of ade­
quate tissue perfusion. A serum lactate level <2 mmol/L in
the first 24–72 hours after burn injury correlated with
increased survival.85 Base deficit is another indirect indicator
of global tissue perfusion. The base deficit is calculated from
the arterial blood gas using the Astrup and Siggard–Anderson
nomograms. Although it is not directly measured, base
deficit provides a readily obtained and widely available indi­
cator of tissue acidosis and shock. Base deficit has been
shown to correlate closely with blood lactate and provides a
useful indicator of inadequate oxygen delivery. A retrospec­
tive study by Kaups et al. showed that base deficit was an
accurate predictor of fluid requirements, burn size, and mor­
tality rate.86
Lactate and base deficit serve as global markers of tissue
perfusion and oxygen delivery. However, in burn patients
tissue perfusion is not uniform. Perfusion of the splanchnic
beds is often sacrificed in order to maintain the perfusion of
heart, brain, and kidneys. The use of gastric intramucosal pH
(pHi) has been advocated as a measure of splanchnic per­
fusion. Several studies have shown that measurement of pHi
is useful in guiding resuscitation, and that low pHi is a pre­
dictor of organ failure and death.87 pHi is measured by gastric
Monitors for resuscitation
Several parameters have been used to assess the adequacy of
volume resuscitation in burned patients (Table 14.6). Unfor­
tunately, there is no single physiological variable that is
always reliable as an endpoint to guide resuscitation in acute
burn patients. The overall goal is early volume resuscitation
and establishment of tissue perfusion. Traditionally, urine
output (0.5–1 mL/kg/h) and normalization of blood pres­
sure (mean arterial blood pressure > 70 mmHg) have been
used as endpoints. However, these parameters alone do not
always indicate adequate tissue perfusion.68–70 Jeng and col­
leagues showed that attaining urine outputs > 30 mL/h and
mean blood pressures > 70 mmHg correlated poorly with
other global indicators of tissue perfusion, such as base
deficit and blood lactate levels.68 During shock, perfusion of
vital organs such as the heart and brain is maintained due
to the redistribution of blood flow from the splanchnic cir­
culation and other peripheral organs. Persistent hypoper­
fusion of these organ systems ultimately results in tissue
injury and contributes to multisystem organ dysfunction.
Therefore, the anesthesiologist should not base the cardio­
vascular assessment strictly on vital signs and urinary output.
Invasive cardiovascular monitors are not used routinely in
burned patients to guide volume resuscitation. Most patients
can be adequately resuscitated without their use. However, a
small subset of patients, such as those with underlying car­
diovascular disease or those who do not respond normally
to volume resuscitation – termed non-responders, may
benefit from invasive monitoring. Some investigations use
cardiac index and oxygen delivery to guide volume resuscita­
tion.71,72 One way in which shock can be defined is oxygen
debt. Bernard and colleagues have shown that patients sur­
viving large burn injuries had higher cardiac indices and
more effective oxygen delivery than non-survivors.73 Some
investigators have proposed the use of supranormal oxygen
delivery as a means of assuring adequate tissue perfusion.74,75
The preselected goals were a cardiac index of 4.5 L/m2 and
an oxygen delivery index of 600 mL/min/m2. These values
represent approximately 150% of normal cardiac index and
oxygen delivery values. Attaining supraphysiological cardiac
output and oxygen delivery has been shown to improve
outcome in some studies. Schiller and colleagues demon­
strated that maintaining a hyperdynamic hemodynamic
state using fluids and inotropes improved survival in burn
patients.76 However, other investigations, including a meta-
analysis, have shown that achieving supraphysiological
levels of cardiac output and oxygen delivery did not improve
mortality or reduce the incidence of organ failure in trauma
Table 14.6  Criteria for adequate fluid resuscitation
• Normalization of blood pressure
• Urine output (1–2 mL/kg/h)
• Blood lactate (<2 mmol/L)
• Base deficit (<−5)
• Gastric intramucosal pH (>7.32)
• Central venous pressure
• Cardiac index (Cl) (4.5 L/min/m2)
• Oxygen delivery index (DO2l) (600 mL/min/m2)

Anesthesia for burned patients
181
pressure: 50 mL of saline is instilled into the bladder through
the Foley catheter and the height of the saline column above
the symphysis pubis is measured (1.36 cm H2O = 1 mmHg).92
Conservative treatment of elevated intra-abdominal pressure
includes attempts to limit the volume of intravenous fluid
needed for resuscitation. The inclusion of plasma with
infused fluids has been found to reduce the volume required
and was associated with significantly lower intra-abdominal
pressures.64 In addition, adequate analgesia and sedation
should be achieved. Diuresis with furosemide and muscle
relaxants to reduce muscle tone have been used to reduce
intra-abdominal pressure. More invasive measures include
escharotomies,93 percutaneous peritoneal dialysis catheter
drainage,94 and laparotomy.90
Recently several clinicians have reported a specific type of
burn injury that has been associated with difficulties with
tonometry and can provide useful information regarding
tissue perfusion.
Formulae for resuscitation of burns provide an approxima­
tion of fluid needs, but volumes actually administered need
to be individualized for each patient. Although two patients
may each have 50% TBSA burns, it is not likely that their
physiologic responses will be equivalent. Several factors can
increase fluid requirements (Table 14.7). Deep full-thickness
burns require larger volume than partial-thickness injuries.
Likewise, extensive soft tissue damage from electrical burns
or crush injuries increases fluid needs. Inhalation injury can
also increase fluid requirements as much as 50%, as noted
above.12 These differences in wounds and fluid requirements
between patients make it very difficult at times to optimize
fluid administration. Because no single physiologic end­
point is always reliable, all available clinical information
must be examined and each variable evaluated within the
context of all the other variables.
As discussed, increased volumes of crystalloid solutions
are being used for resuscitation of burn patients.88 In many
cases as much as twice the volume recommended by the
Parkland formula is used. Edema is commensurate with
volume infused. During the preoperative evaluation atten­
tion must be paid to the degree to which edema produces
physiologic derangements. The edema can lead to compart­
ment syndrome of extremities or abdomen (Fig. 14.4).
Blindness due to ischemic optic neuropathy has been
reported as a complication of burn resuscitation.89 Increased
intra-abdominal pressure is a complication of vigorous fluid
resuscitation, which may be more common than generally
appreciated and may often explain difficulties with resuscita­
tion. Greenhalgh and Warden first described the association
of increased abdominal pressures and compartment syn­
drome with burn resuscitation.90 Ivy and colleagues prospec­
tively studied 10 adult patients presenting with >20% TBSA
burns and found that 70% of them had at least transient
intra-abdominal hypertension.91 Two of their patients with
>80% TBSA burns developed abdominal compartment syn­
drome requiring surgical decompression. Several studies
since then have described the common occurrence of
increased intra-abdominal pressure with large-volume burn
resuscitation. Increased intra-abdominal hypertension is
termed abdominal compartment syndrome when it is asso­
ciated with impaired respiration, circulation, and urine
output. Mechanical ventilation is impaired by pressure on
the diaphragm, circulation is impaired by restricted venous
return due to caval compression, and urine output is impaired
by compression of renal vessels. When this pattern presents
the patient should be examined for elevated intra-abdominal
pressure. This can be accomplished by measuring bladder
Table 14.7  Factors that may increase fluid needs for resuscitation
of patients with acute burn injuries
• Inhalation injury
• Delay in resuscitation
• Crush injury
• Electrical injury
• Large full-thickness burns
• Methamphetamine lab accidents
• Associated injuries
Figure 14.4  Large volumes of crystalloid solution required for resuscitation
of patients with extensive acute burns are associated with significant
edema. This can result in compartment syndromes of extremities, abdomen,
and the periorbital space. (a) Escharotomies can decompress compartments
and also improve thoracic compliance; (b) laparotomy may be required in
some cases of abdominal compartment syndrome when escharotomies do
not adequately decompress the abdomen.
A
B

Total Burn Care
14
182
volume status, and electrolyte concentrations; diuretic
therapy should also be noted. Scheduled doses of diuretics
may need to be continued during the perioperative period
to maintain urine output.
Metabolic changes associated with burn injury
Increased metabolic rate is the hallmark metabolic alteration
that takes place after thermal injury. The magnitude of hyper­
metabolism is influenced by the size of the burn wound,
medical management and the core body temperature of the
patient.107–111 Within the range of 30–70% TBSA burn injury,
hypermetabolism tends to be proportionate to the size of
the burn wound. With burns beyond this range, the hyper­
metabolism appears to plateau and only increases in smaller
increments as burn size increases.112 Sepsis can also increase
the metabolic response, as does the physiologic stress of
pain.109,113 It has been observed that modern treatment of
burn injuries with early excision and grafting ameliorates the
hypermetabolism.114 As mentioned earlier, burn patients
increase their metabolic rate in an effort to generate heat
according to an increased core temperature threshold set
point, which is influenced by the size of the burn (see Ther­
moregulation in burn patients, below). The recognition of
this fact has led to an increased awareness of the importance
of the ambient temperature in modulating the hypermetabo­
lism of the burn patient. Using indirect calorimetry in acute
patients with major burn injuries that are treated according
to current standards, resting energy expenditures that are
110–150% above predicted values are frequently measured.115
Resting energy expenditure typically increases as core body
temperature decreases below the new set point.116 Therefore,
it is critical to prevent significant decreases in core body
temperature in the operating room.
As a result of the hypermetabolic response, the burned
patient has an increased O2 consumption along with an
increased CO2 production that collectively causes increased
minute ventilation and demands a higher respiratory
effort.109 The anesthetic care of the acute burned patient must
accommodate these changes, and frequently this has to be
done in patients with compromised pulmonary function
due to burn and inhalation injuries.
According to the hypermetabolism, the caloric needs of
the burn patient are also increased. Furthermore, numerous
studies have shown that optimized nutritional care can not
only ameliorate the burn-associated state of catabolism and
immune suppression but can also improve wound healing.107
Oral or enteral feeding is recognized as optimal for the
burned patient. Frequently the acute burn patient has to be
fed continuously over extended periods. This is not only
because of the increased caloric needs but also because of
compromised gastric emptying and decreased intestinal
motility, which necessitates a slower feeding rate of critically
ill patients. If standard guidelines for perioperative fasting
are implemented, recurrent operative procedures can signifi­
cantly impinge on the nutritional needs of the patient and
ultimately cause a caloric deficit. To accommodate the nutri­
tional needs of the patient a continuation of duodenal nutri­
tion perioperatively has been advocated. Studies indicate
that not only is this procedure safe but it might also provide
for a favorable gut oxygen balance.117
resuscitation.95–97 There has been a dramatic increase in burn
injuries from explosions and fires related to methampheta­
mine production in illicit laboratories. Victims of these acci­
dents present unique challenges for a variety of reasons.
Substances used in methamphetamine production include
chemicals that are corrosive and toxic (e.g. anhydrous
ammonia, hydrochloric acid, red phosphorus, and ephe­
drine). Other ingredients are flammable (acetone, alcohol,
and gasoline) and explosions can coat the victims with all
these chemicals. As a result, in addition to the victim’s toxic
exposure, contacting incompletely decontaminated victims
of these accidents has injured first responders and hospital
workers.98,99 In addition to exposures described above, these
patients are usually intoxicated with methamphetamine, as
demonstrated by positive urine screen, and may have inhaled
toxic fumes such as phosphine gas. Santos et al. found the
incidence of inhalation injury to be twice as great in victims
of methamphetamine-related burns as in age- and burn-
matched controls.95 Among their patients requiring intuba­
tion for inhalation injury methamphetamine users also
required roughly twice as many ventilator days. Clinical
studies have consistently observed increased fluid require­
ments for resuscitation of methamphetamine patients.95,98
For example, Santos et al. found that resuscitation volumes
were 1.8 times greater for methamphetamine users with
burns than for controls.95 Methamphetamine users with
burns also experienced more behavioral problems. These
patients are more often agitated and require restraints.
Santos et al. reported that all their methamphetamine
patients required greater than normal doses of sedatives and
displayed what they referred to as ‘withdrawal-type syn­
drome,’ 95 possibly owing to withdrawal of methampheta­
mine from chronic users.
Effect of burn injury on renal function
Acute renal failure (ARF) is a relatively common complica­
tion following major burn injuries. The incidence of ARF
following burn injury has been reported to be as high as 40%
and is most dependent on the size and severity of the burn
and the presence of inhalation injury.100–103 The development
of ARF is a poor prognostic indicator. Jeschke and colleagues
reported a mortality of 56% in pediatric burn patients with
ARF.104 A recently reported Scandinavian study that analyzed
1380 adult burn patients reported an overall mortality rate
of 44.1% in patients with acute renal insufficiency, with a
mortality rate of 62.5% in those requiring renal replacement
therapy.103 Holm and colleagues observed that ARF could be
divided into early and late categories. Early ARF was defined
as occurring within 5 days of burn injury.105 The most
common apparent causes of early renal injury were hypoten­
sion and myoglobinuria. ARF occurring after 5 days of injury
was defined as late. Here, sepsis was the most common
cause, with a small number of cases resulting from the
administration of nephrotoxic drugs. Factors that will reduce
the incidence of ARF and, if it occurs, associated mortality,
include adequate fluid resuscitation, early wound excision,
and prevention of infection.106 Regardless of the cause, it is
critical to assess renal function in burn patients in order to
develop a comprehensive anesthetic plan. Important areas
of analysis include urine output, dialysis dependence,

Anesthesia for burned patients
183
ambient temperature as effectively as normal controls.124
This is likely due to the retained ability of burn patients to
sense changes in core temperature and transmit this infor­
mation to the central nervous system. Central control of
temperature is a complicated system that is not well under­
stood. The hypothalamus plays an important role in
temperature regulation, but the complete mechanism of
temperature control is likely to be multifaceted and is an
area of intense research. Regardless of the ultimate control
mechanisms, temperature control can be divided into three
main functions: threshold, gain, and maximum response
intensity.
Threshold encompasses a set point at which responses to
temperature change are initiated. In normal individuals the
threshold range is generally near 36.5–37.5°C. In burn
patients, the threshold set point is higher and the increase is
proportional to the size of the burn. The work of Caldwell
and colleagues predicts that the temperature set point will
increase by 0.03°C/% TBSA burn.125 This increase in tem­
perature threshold appears to be due to the hypermetabolic
state and the pyrogenic inflammatory mediators such as TNF,
IL-1, and IL-6 that are present after thermal injury. The ele­
vated temperature set point can be reduced by administra­
tion of indomethacin, which suggests that prostaglandins act
as final common mediators of this response.126,127
Gain describes the intensity of response to alterations in
temperature. In most cases the gain of thermoregulatory
responses is very high, with response intensity increasing
from 10% to 90% with only a few tenths of a degree change
in core temperature. This response is maintained in most
burn patients, resulting in a further increase in metabolic
rate.124 Burn patients respond with a brisk increase in heat
generation and metabolic rate in response to changes in core
body temperature.124 However, work by Shiozaki and col­
leagues has shown that burn patients who are slow to
respond to postoperative hypothermia are at increased risk
of mortality.128 The decreased responsiveness may be due, in
part, to tissue catabolism, poor nutrition, or sepsis. In addi­
tion, the response to relative hypothermia is characterized
by increased catecholamine release, tissue catabolism, and
hypermetabolism. These responses further stress burn
patients and reduce their ability to respond to their primary
injury.129
The most important efferent responses to hypothermia are
behavioral responses such as gaining shelter, covering up,
and seeking a more desirable ambient temperature. In the
At the time of the withdrawal of ventilator support and
extubation the metabolic state of the burn patient should be
considered. The characteristic catabolic state of major burn
injury spares no muscles109,118 and the respiratory muscles
are affected. Along with decreased muscle strength there is
frequently decreased pulmonary compliance, due not only
to the formation of scar tissue and pulmonary interstitial
changes but also to increased intra-abdominal content.
Burn-associated hepatomegaly along with gastrointestinal
retention can significantly impinge on respiratory reserves.119
Severe insulin resistance with hyperglycemia and concur­
rent hyperinsulinemia is a key feature of the metabolic alter­
ations of burn injury.108,109,113 It is well recognized that
critically ill patients with insulin resistance benefit from tight
glycemic control in the ICU,120 and these findings have been
expanded to the burn patient population.121 During the
intraoperative period the question is less studied. Although
the benefit of tight intraoperative glycemic control has been
documented in other patient populations,122 the risk versus
benefit during anesthesia has not been studied specifically
in burn patients.
Thermoregulation in burn patients
Maintenance of proper body temperature is an important
factor in the care of severely burned patients. The thermoreg­
ulatory system is controlled by three major components.
These are the afferent system, which senses changes in core
body temperature and transmits this information to the
brain; the central regulatory mechanisms located primarily
in the hypothalamus that process afferent input and initiate
responses; and the efferent limb, which mediates specific
biological and behavioral responses to changes in core body
temperature (Fig. 14.5). Temperature is sensed by Aδ and C
fibers present in peripheral tissues such as skin and muscle
as well as core tissues such as brain, deep abdominal tissues,
and thoracic viscera.123 The vast majority of afferent input
arises from the core tissues. Because the skin is in direct
contact with the environment, it senses immediate changes
in environmental temperature. However, the overall afferent
input of the skin and other peripheral tissues is estimated to
be only 5–20% of total afferent thermoregulatory input.123
Therefore, loss of skin following a burn injury is not likely
to markedly alter overall afferent input. Wallace and col­
leagues have shown that burn patients perceive changes in
Figure 14.5  Thermoregulatory control
mechanisms. Afferent input from a variety of
sites, most notably skin, central tissues, and brain,
are processed in the central nervous system.
Based on input, a variety of efferent
thermoregulatory responses are initiated.
(From Sessler DI. Temperature monitoring. In: Miller R, ed.
Anesthesia, 3rd edn. New York: Churchill Livingstone; 1990.)
Hypothalamus
Hypothalamus
Other part
of brain
Skin surface
Spinal cord
Deep central
tissues
Warm responses
Cold responses
Interthreshold
range
36.5
37.5
Active vasodilation
Sweating
Behavior
Vasoconstriction
Nonshivering

thermogenesis
Shivering
Behavior

Total Burn Care
14
184
blankets, using radiant heaters and forced air warming
devices, warming fluids and blood, and warming gases are
usually effective in maintaining core temperature if applied
aggressively. Ideally, hypothermia should be corrected prior
to transport to the operating room.131 Hypothermia revealed
in the preoperative evaluation may be due to inadequate
resuscitation or metabolic instability. Either situation may
predispose burn patients to intolerance of anesthetic drugs
or the stress of surgery.
In contrast to acutely burned patients, the development of
hypothermia may not be as serious a problem in severely
burned patients who have complete regrafting and present
for reconstructive surgery. Davis and colleagues132,133 reported
that cutaneous vasoconstriction is preserved in grafted skin.
Therefore, these patients are likely to have a temperature
response to anesthesia and the operating room environment
that is similar to that of non-burned patients. However, cuta­
neous vasodilation and heat dissipation are impaired in
grafted skin, which makes these patients more susceptible to
developing hyperthermia in warm environments. Therefore,
temperature should be monitored in these patients during
surgery, especially if warming devices will be employed in
their perioperative care.
Pharmacological considerations
General considerations
Burn injury and its treatment result in physiological changes
that may profoundly alter response to drugs. These changes
alter both pharmacokinetic and pharmacodynamic determi­
nants of drug response. Altered drug response in burned
patients may require deviation from usual dosages to avoid
toxicity or decreased efficacy.134 The complex nature of the
pathophysiological changes, interpatient variation in the
nature and extent of burn injuries, and the dynamic nature
of these changes during healing and recovery make it diffi­
cult to formulate precise dosage guidelines for burn patients.
However, an understanding of the systemic response to large
burn injuries can help predict when an altered drug response
can be expected and how to compensate.
The two distinct phases of cardiovascular response to
thermal injury can affect pharmacokinetic parameters in dif­
ferent ways. During the acute or resuscitation phase the rapid
loss of fluid from the vascular space due to edema formation
results in decreased cardiac output and tissue perfusion.
Volume resuscitation during this phase dilutes plasma pro­
teins and expands the extracellular fluid space, especially,
but not exclusively, around the burn injury itself. Decreased
renal and hepatic blood flow during the resuscitation
phase reduces drug elimination by these organs. Also,
decreased cardiac output will accelerate the rate of alveolar
accumulation of inhalation agents, which may result in
an exaggerated hypotensive response during induction of
general anesthesia.
After approximately 48 hours the hypermetabolic and
hyperdynamic circulatory phase is established, with increased
cardiac output, oxygen consumption, and core temperature.
During this phase, increased blood flow to the kidneys and
liver may increase clearance of some drugs to the point
where increased doses are required.135
acute post-burn setting most of these behaviors are impeded
by positioning, sedation, and inability to seek a more favo­
rable environment. Therefore, caregivers must be attentive to
the patient’s temperature and perception of cold so that
measures can be undertaken to optimize the patient’s tem­
perature. Cutaneous vasoconstriction is another important
mechanism for preserving heat and core body temperature.
In unburned persons a temperature gradient of 2–4°C exists
between skin and core tissues. This gradient is maintained
by cutaneous vasoconstriction. Without cutaneous vasocon­
striction, heat is redistributed from the core compartment to
the periphery. This heat is ultimately lost to the environ­
ment. Peripheral vasoconstriction minimizes temperature
redistribution and acts to maintain core body temperature.
This mechanism of heat preservation is lost after cutaneous
thermal injury and excision of large areas of skin, particu­
larly if cutaneous tissues are excised down to the fascial level.
The loss of skin facilitates the redistribution of core body
heat to the periphery and, ultimately, into the environment,
which places the burn patient at risk for core hypothermia.
Another mechanism of heat loss in burn patients is evapora­
tion. Burn patients can lose as much as 4000 mL/m2 burned/
day of fluids through evaporative losses.130 Mechanisms of
non-shivering heat production and shivering remain intact
in burn patients. However, shivering increases metabolic
requirements and is likely deleterious.
The induction of anesthesia results in relative ablation of
thermoregulatory mechanisms and puts the patient at further
risk for developing hypothermia. Patients under general
anesthesia exhibit a markedly decreased threshold for
responding to hypothermia (Fig. 14.6). This is particularly
important in burn patients, given their high temperature set
point and the deleterious effects of further stress responses
and hypermetabolism in this patient population. Most anes­
thetics reduce nonbehavioral responses to hypothermia,
such as vasoconstriction, non-shivering thermogenesis, and
shivering. Of course, behavioral responses are ablated during
general anesthesia. Therefore, it is the responsibility of the
intraoperative caregivers to monitor and maintain patient
temperature.
Actions such as maintaining higher ambient air tem­
perature, covering the extremities and head, applying warm
Figure 14.6  Effects of anesthesia on thermoregulatory mechanisms.
(From Sessler DI. Temperature monitoring. In: Miller R, ed. Anesthesia, 3rd edn. New York:
Churchill Livingstone; 1990.)
Normal
33
35
37
39
41°C
33
35
37
39
41°C
Vasoconstriction
Nonshivering
thermogenesis
Sweating
Vasodilation
Shivering
Vasoconstriction
Nonshivering
thermogenesis
Shivering
Sweating
Vasodilation
Anesthesia

Anesthesia for burned patients
185
increased glomerular filtration rates and reduced half-life of
tobramycin in burn patients.138 However, this was age
dependent, and patients over 30 years of age did not have
increased glomerular filtration or reduced half-life.
Burn patients may also experience altered drug clearance
due to novel excretion pathways. Glew et al. found that 20%
of a daily gentamicin dose was eliminated in the exudates
lost to wound dressings.139 In addition, rapid blood loss
during surgery may speed elimination of drugs when blood
loss and transfusion amount, essentially, to an exchange
transfusion.
Hepatic clearance of drugs with low extraction coefficients
is also sensitive to alterations in hepatic capacity (enzyme
activity). There is evidence of impairment of hepatic enzyme
activity in burn patients.114 Phase I reactions (oxidation,
reduction, or hydroxylation by the cytochrome P450 system)
are impaired in burn patients, whereas phase II reactions
(conjugation) seem to be relatively preserved.135 However,
these generalizations do not always produce predictable
alterations in pharmacokinetic parameters. For example,
contradictory observations of morphine clearance in burn
patients have been reported. Morphine metabolism is by
glucuronidation. This is a phase II reaction which is nor­
mally retained in thermally injured patients. Consequently,
morphine clearance has been reported unchanged as pre­
dicted or decreased.140,141 With so many variables involved,
such as hepatic blood flow, Vd, plasma proteins, multiple
drug exposure, and variation in burn injury, this inconsist­
ency is not surprising. The key to effective drug therapy in
burn patients is to monitor drug effects and carefully titrate
the dose to the desired effect.
Muscle relaxants
In terms of anesthetic management, the most profound
and clinically significant effect of burn injuries on drug
response relates to muscle relaxants. Burn injuries >25%
TBSA influence responses to both succinylcholine and the
non-depolarizing muscle relaxants. In burned patients, sen­
sitization to the muscle relaxant effects of succinylcholine
can produce exaggerated hyperkalemic responses severe
enough to induce cardiac arrest.142–144 In contrast, burned
patients are resistant to the effects of non-depolarizing
muscle relaxants.145–147 These changes are explained by
upregulation of skeletal muscle acetylcholine receptors.148–150
Martyn and Richtsfeld150 have recently reviewed the mech­
anisms of exaggerated hyperkalemic responses to succinyl­
choline. There are several disease states, including burns,
denervation, and immobilization, that are associated with
potentially lethal hyperkalemic responses to succinylcho­
line. The molecular mechanism appears to be both quantita­
tive and qualitative changes in skeletal muscle postsynaptic
nicotinic acetylcholine receptors. Animal and human studies
consistently demonstrate an association of increased
numbers of skeletal muscle acetylcholine receptors with
resistance to non-depolarizing muscle relaxants and
increased sensitivity to succinylcholine. In addition, the dis­
tribution of the new receptors is altered. Nicotinic receptors
are normally restricted to the neuromuscular synaptic cleft
but in these disease states new receptors are distributed
across the surface of the skeletal muscle membrane. The new
receptors are also a distinctly different isoform (α7AChR)
Many drugs are highly protein bound. Drug effects and
elimination are often related to the unbound fraction of the
drug that is available for receptor interaction, glomerular
filtration, or enzymatic metabolism. The two major drug-
binding proteins have disparate responses to burn injury.
Albumin binds mostly acidic and neutral drugs (diazepam
or thiopental) and is reduced in burn patients. Basic drugs
(pKa >8, propranolol, lidocaine, or imipramine) bind to
α-acid glycoprotein (AAG). AAG is considered an acute-
phase protein and its concentration may double after burns.
Because these drug-binding proteins respond in opposite
ways to thermal injury it can be expected that changes in
drug binding and function will depend on which of these
proteins has the highest affinity for the drug in question.
Martyn et al. observed decreased plasma albumin concentra­
tion and increased plasma AAG concentration in burn
patients.136 These observations were associated with an
increased unbound fraction for diazepam (bound by
albumin) and a decreased unbound fraction for imipramine
(bound by AAG).
Volume of distribution (Vd) can be changed by alterations
in either extracellular fluid volume or protein binding. Large
changes in both of these variables occur with thermal inju­
ries. Drugs with high protein binding and/or a Vd in the
range of the extracellular fluid volume may be associated
with clinically significant alterations of Vd in burned patients.
Vd is the most important determinant of drug response fol­
lowing a rapid loading dose. However, adjustments in dose
to compensate for altered Vd are indicated only when Vd for
the drug is small (<30 L) because with larger Vd only a small
fraction of the drug is present in the plasma.134
Clearance is the most important factor determining the
maintenance dose of drugs and can influence the response
to drugs given by infusion or repeated bolus during anesthe­
sia. Drug clearance is influenced by four factors:
•
metabolism;
•
protein binding;
•
renal excretion; and
•
novel excretion pathways.
The characteristic hepatic extraction of a particular drug
influences changes in its clearance that occur after thermal
injury. Drugs vary greatly in their extraction by the liver.
Hepatic clearance of drugs highly extracted by the liver
depends primarily on hepatic blood flow and is insensitive
to alterations in protein binding. Clearance of these drugs
may increase during the hyperdynamic phase when hepatic
blood flow is increased. In contrast, clearance of drugs that
have a low hepatic extraction coefficient is not affected by
changes in hepatic blood flow but is sensitive to alterations
in plasma protein levels.134 For these drugs it is the unbound
fraction that is metabolized. As above, changes in unbound
fraction depend on whether the drug is bound by albumin
or AAG. Changes in protein levels produce clinically signifi­
cant pharmacokinetic changes only for drugs that are highly
bound (>80%).137
During resuscitation, renal blood flow may be reduced and
renal excretion of drugs may be impaired. Later, during the
hypermetabolic phase, renal blood flow is increased as a
result of the elevated cardiac output. During this period
excretion of certain drugs can be increased to the point that
the dose may need to be increased. Loirat et al. reported

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14
186
ventilation may require emergency surgical airway access. A
cyclodextrin (Org 25969) has recently been tested in man as
a reversal agent with a novel mechanism of action for rocuro­
nium.160 Org 25969 has been specifically designed to encap­
sulate rocuronium. This agent has been found to rapidly
terminate neuromuscular blockade by rocuronium, theoreti­
cally by sequestering it from nicotinic neuromuscular recep­
tors. If this agent becomes approved for clinical use it may
provide a way to rapidly reverse muscle relaxation with
rocuronium and provide a more attractive choice for burn
patients when rapid sequence induction is indicated.
Responses to non-depolarizing relaxants are also altered
by burn injury. Three to five times higher doses are required
to achieve adequate relaxation.145 Resistance is apparent by
7 days after injury and peaks by approximately 40 days.
Sensitivity returns to near normal after approximately 70
days. Two reports described slight but measurable resistance
to nondepolarizing relaxants persisting for more than a year
after complete healing of the wounds. The mechanism of the
altered response appears to involve pharmacodynamic rather
than pharmacokinetic changes. Upregulated immature
receptors are less sensitive to non-depolarizing relaxants.
Burns >25% TBSA require higher total dose and greater
plasma concentrations of non-depolarizing blockers to
achieve a given level of twitch depression.146
Proliferation of acetylcholine receptors across the muscle
membrane has been used to explain both resistance to non-
depolarizing muscle relaxants and the exaggerated hyperka­
lemic response to succinylcholine.150 The observation of
resistance of a patient to metocurine for up to 463 days after
burn has been used to suggest that hyperkalemic responses
to succinylcholine also could persist for more than a year.147
However, no pathologic hyperkalemic responses to succinyl­
choline in burned patients have been reported more than 66
days after burns.153
In contrast to other non-depolarizing neuromuscular
blockers, mivacurium dosage requirements in pediatric
patients appear to be unchanged by burn injury.160,161 The
time to onset of drug action, degree of paralysis achieved by
a specific dose, and rate of infusion required to maintain a
given level of relaxation were all the same in burn patients
as values reported for non-burned control patients.161 Plasma
cholinesterase activity is reduced in burn patients.151 In a
study by Martyn, the observation of an inverse relationship
between plasma cholinesterase activity and recovery time
from 25% to 75% twitch tension suggests that reduction of
metabolic degradation of mivacurium may compensate for
other factors that induce resistance to relaxants.161 This
observation suggests that mivacurium can be administered
to burn patients in normal doses that would avoid cardio­
vascular perturbations associated with the larger doses of
other relaxants required in burn patients.
Anesthetic management
Airway management
If injuries do not preclude conventional airway management
(i.e. mask fit, jaw lift, and mouth opening), standard induc­
tion and intubation procedures are appropriate. Hu et al.
reported that gastric emptying was not delayed in patients
that has been referred to as an immature, extrajunctional, or
fetal receptor. The immature receptors are more easily depo­
larized by succinylcholine and their ion channel stays open
longer. The immature receptors are also strongly and persist­
ently depolarized by the metabolite of acetylcholine and
succinylcholine, choline. It has been suggested that the
hyperkalemic response to succinylcholine after burn or den­
ervation injury results when potassium is released from
receptor-associated ion channels across the entire muscle cell
membrane, rather than just the junctional receptors. Depo­
larization persists because the channels stay open longer and
the breakdown product of succinylcholine, choline, is also a
strong agonist for the immature receptors.
Cardiac arrest in burned patients after succinylcholine
administration was first reported in 1958.142 It was not until
1967, however, that an exaggerated hyperkalemic effect was
identified as the cause of this phenomenon.143,144 Several
clinical studies have documented exaggerated increases in
potassium concentrations after succinylcholine administra­
tion in burned patients. However, considerable individual
variability exists, and only a few patients in these series
developed dangerously high potassium levels. The size of the
increase was greatest about 3–4 weeks after injury. The earli­
est exaggerated hyperkalemic response described occurred 9
days after injury and normal responses were observed in the
remaining patients in this series for up to 14–20 days.151 The
shortest post-burn interval associated with succinylcholine-
induced cardiac arrest was 21 days.152 Controversy surrounds
recommendations regarding the safe use of succinylcholine
after burn injury. Various authors recommend avoidance of
succinylcholine at intervals ranging from 24 hours to 21 days
after burn injury.153,154 A series of letters to the editor of
Anesthesiology from experts in this area illustrates the contro­
versy surrounding this question.155–157 It was pointed out by
Martyn157 that at the time when the mechanism of the
cardiac arrest after succinylcholine was elucidated, surgical
treatment of burns was delayed for approximately 2 weeks
until the eschar spontaneously separated. As a result there
are few clinical data regarding potassium changes during this
early period. On the basis of indirect evidence from experi­
mental data, Martyn157 recommended avoidance of succinyl­
choline, starting 48 hours after injury. This seems rational
and prudent. Brown and Bell158 described supersensitivity of
burned pediatric patients to the relaxant effect of succinyl­
choline. They observed more than 90% depression of muscle
activity with 0.2 mg/kg succinylcholine without dangerous
hyperkalemia. Despite these observations, Brown and Bell
state that it is generally advisable not to use succinylcholine
in patients with large burns. The question remains: in the
presence of life-threatening laryngospasm in a burn patient,
is it acceptable to give a small dose of succinylcholine (e.g.
0.1 mg/kg) and accept a theoretical risk of hyperkalemia to
treat a real and immediate risk of anoxic brain injury? There
is not enough clinical evidence to answer this question con­
clusively, and it remains a matter of clinical judgment.
When rapid sequence induction and quick onset of paraly­
sis in burn patients is desired rocuronium is the drug of
choice. A dose of 1.2 mg/kg of this drug provided good
intubation conditions in 86 ± 20 seconds in burned
patients.159 The problem with this choice is that muscle
relaxation will persist for some time and precludes extuba­
tion after short cases, and difficulty with intubation and

Anesthesia for burned patients
187
with severe burns, so that a rapid sequence induction is not
necessary.162 However, attention should be paid to gastric
residuals during enteric feeding. The development of sepsis
can slow gastric emptying, which can result in retained fluids
in the stomach and risk of aspiration.
When burns include the face and neck, swelling and dis­
tortion may make direct laryngoscopy difficult or impossi­
ble. In addition, loss of mandibular mobility may impair
airway manipulation and make mask ventilation difficult.
Fiberoptic intubation while maintaining spontaneous venti­
lation is a safe and reliable technique under these condi­
tions. Fiberoptic intubation can be performed in awake
adults, but pediatric patients are unable to cooperate and
must be sedated. As most anesthetics cause collapse of pha­
ryngeal tissues and airway obstruction they are unsuitable
for fiberoptic intubation in patients whose airway would be
difficult to manage with a mask.163 Ketamine, however, is
unique among anesthetic drugs because it maintains spon­
taneous ventilation and airway patency.164,165
Ketamine anesthesia has been found to be safe and effec­
tive for airway management in infants with difficult airways
caused by congenital airway anomalies. Reports of successful
nasotracheal intubation in infants with congenital airway
malformations have been made both by manipulations
guided by fiberoptic nasopharyngoscopy and the conven­
tional technique of fiberoptic intubation with the endotra­
cheal tube mounted on the fiberscope.166,167 In the latter case
an ultrathin bronchoscope (2.7 mm) was required because
a larger fiberscope would not fit through the appropriately
sized endotracheal tube. To facilitate intubation under keta­
mine anesthesia, topical anesthesia of the larynx with lido­
caine prior to instrumentation of the larynx is advised.
Because the ultrathin bronchoscope lacks a working channel
for administration of topical lidocaine, fiberoptic intubation
with the 2.7 mm bronchoscope was preceded by nasopharyn­
goscopy with a 3.5 mm fiberscope for administration of
topical lidocaine. At SBH Galveston we have also found this
technique, using two fiberscopes, to be effective in infants
with burn injuries. Wrigley et al. evaluated the use of a
2.2 mm intubating fiberscope during halothane anesthesia
in ASA 1 or 2 children aged 6 months to 7 years.168 In this
series of 40 patients a number of complications were expe­
rienced, including laryngospasm and failure to achieve intu­
bation with the fiberscope. This experience is in contrast to
numerous reports of safe and effective airway management
with ketamine.
Securing an endotracheal tube in a patient with facial
burns presents a variety of problems, and numerous tech­
niques have been described.169 Tape or ties crossing over
burned areas will irritate the wound or dislodge grafts. A
useful technique to avoid these problems involves the use of
a nasal septal tie with one-eighth inch umbilical tape (Fig.
14.7). The umbilical tape is placed around the nasal septum
using 8 or 10 Fr red rubber catheters passed through each
naris and retrieved from the pharynx by direct laryngoscopy
and McGill forceps. A length of umbilical tape is tied to each
of the catheters; when the catheters are pulled back through
the nose, each end of the umbilical tape is pulled out of its
respective naris, producing a loop around the nasal septum.
Before securing with a knot, care should be taken to assure
that the uvula is not captured in the loop. A knot in the
nasal septal tie should be snug enough to prevent excessive
Figure 14.7  Nasotracheal tubes can be secured with confidence by tying
to umbilical tape tied in a loop around the nasal septum. (a) Red rubber
catheters (8 or 10 Fr) are passed through each naris, retrieved with McGill
forceps from the oropharynx, and each end of a piece of umbilical tape
is tied to the catheters. (b) When the catheters are pulled out of the nares,
the umbilical tape follows and, after laryngoscopy to assure the uvula
has not been trapped, a loop can be tied around the bony nasal septum.
(c) Umbilical tape can be used to secure the endotracheal tube to
this loop. This technique is very secure, avoids irritating facial burn wounds
or grafts, and leaves the surgical field free of tape or ties.
A
B
C

Total Burn Care
14
188
Systolic blood pressures obtained from the pressure at which
the pulse oximetry signal returns during cuff deflation has
also been found to be accurate.174
When blood loss is expected to be rapid and extensive,
blood pressure may change more rapidly than the interval
between cycles of non-invasive blood pressure measure­
ment. In this case an arterial catheter can provide direct and
continuous measurement of blood pressure. This monitor
can provide much more information regarding the patient’s
circulatory status than just systolic and diastolic blood pres­
sure. The arterial pressure waveform is influenced by preload,
contractility, and vascular tone. Perioperative variation in the
rate of rise of arterial pressure, the area under the pressure
wave, position of the dicrotic notch, and beat-to-beat altera­
tions in systolic pressure related to respiration all reflect
clinically significant hemodynamic changes.175 With experi­
ence, trends in these variables can help guide volume and
vasoactive therapy. Display of the beat-to-beat arterial pres­
sure allows measurement of systolic pressure variation (SPV).
SPV is the difference between maximum and minimum
systolic blood pressure during a single cycle of positive-
pressure mechanical ventilation. Several studies have corre­
lated SPV with cardiac output response to volume infusion.
Tavernier et al. reported that in septic patients on mechani­
cal ventilation SPV is a better predictor of left ventricular
ejection volume response to volume loading than either
pulmonary artery occlusion pressure or echocardiographic
measurement of left ventricular end-diastolic area.176 Meas­
urements are not as simple as merely ‘eyeballing’ the blood
pressure trace because several variables influence SPV, includ­
ing arrhythmias, tidal volume, and mechanical versus spon­
taneous ventilation. SPV provides a dynamic assessment of
the interaction of preload and cardiac output.177
Arterial blood sampling for blood gas analysis also pro­
vides valuable information regarding pulmonary function
and acid–base balance. Inadequate tissue perfusion may
manifest as metabolic acidosis despite apparently adequate
arterial and central venous blood pressures.
In patients with large burns a central venous catheter
serves several functions. Central venous pressure can be
useful for titrating blood and fluid administration. Blood
samples from a central vein are not truly mixed venous, but
trends in central venous oxygen tension can help identify
inadequate tissue perfusion. A central venous catheter
sutured into place also provides very secure intravenous
access and is an ideal route for administration of vasoactive
infusions. A pulmonary artery catheter is usually not required
for burn surgery. In some cases, however, the ability to more
closely monitor ventricular function and oxygen supply/
demand relationships may be helpful as when large doses
of inotropes or high PEEP is required. As described above, a
newer transpulmonary thermodilution catheter system is
also capable of estimating thoracic and end-diastolic cardiac
blood volumes. These measures of preload have been
reported to correlate better than filling pressures (central
venous pressure or pulmonary artery occlusion pressure)
with changes in cardiac index or oxygen delivery with fluid
volume administration.
Urine output is the most useful perioperative monitor of
renal function. Urine output of 0.5–1.0 mL/kg/h is often
recommended as an endpoint for fluid management in acute
burn patients. Adequate urine output is one measure of both
movement of the endotracheal tube but loose enough to
prevent ischemic necrosis of the underlying tissues.
Airway management using a laryngeal mask airway (LMA)
has also been used successfully during burn surgery for chil­
dren. McCall et al. reported their experience with 141 general
anesthetics administered to 88 pediatric burn patients.170
Nineteen (14.5%) of the procedures were complicated by
respiratory events such as unseating, desaturation, and
partial laryngospasm that required intervention. Two of
these events required intraoperative intubation without
sequelae, but all other events resolved with therapy. Interest­
ingly, the presence of preoperative respiratory problems or
face/neck burns did not predict intraoperative respiratory
problems. These authors suggest that, in patients with upper
airway mucosal injury, LMA airway management may help
avoid further laryngeal injury that might occur with intuba­
tion of the trachea.
Hagberg et al. published a case report describing the suc­
cessful use of an esophageal tracheal Combitube in a patient
undergoing elective surgery for burn scars involving the
mouth.171 The patient had a class IV oral airway by Samsoon
and Young’s modification of the Mallampati airway classi­
fication, and limited mouth opening. A translaryngeal
endotracheal tube was undesirable because tracheostomy
had resulted in subglottic stenosis, which could have been
exacerbated by an endotracheal tube. After induction with
fentanyl and propofol the Combitube was placed and the
patient was relaxed with rocuronium and mechanically
ventilated during the 60-minute procedure.
Perioperative monitors
As with any critically ill patient suffering from multiorgan
system involvement, the choice of monitors in a burned
patient will depend on the extent of the patient’s injuries,
physiological state, and planned surgery. In addition to the
preoperative pathophysiology associated with thermal inju­
ries, perioperative monitoring must be adequate to assess
rapid changes in blood pressure and tissue perfusion asso­
ciated with the massive blood loss that can accompany
excision of burn wounds. The minimum standards of the
American Society of Anesthesiologists require monitoring of
circulation, ventilation, and oxygenation. Standard monitors
include electrocardiography (EKG), measurement of sys­
temic blood pressure, pulse oximetry, capnography, and
inspired oxygen concentration. The ability to measure body
temperature should be readily available and is highly recom­
mended for the burn patient.
Standard EKG gel electrodes usually will not adhere to
burn patients because the skin is injured or covered with
antibiotic ointment. For acute burn surgery, surgical staples
and alligator clips are useful. Respiratory rate can be quan­
titated using bioimpedance from the EKG signal or from the
capnogram. Pulse oximetry in burn patients can be difficult
when transmission pulse oximetry sites are either burned or
within the operative field. Reflectance pulse oximetry has
been suggested as an alternative in these circumstances.172
However, an effective commercially available instrument has
been slow in development.
If direct arterial pressure monitoring is not necessary, a
blood pressure cuff can provide accurate measurements even
if placed over bulky dressings applied to an extremity.173

Anesthesia for burned patients
189
recommend avoiding the femoral site unless no other site is
available, as loss of limb, or limb length discrepancy in chil­
dren, is a devastating, if rare, complication.182
Other sites for arterial access include the dorsalis pedis,
posterior tibial, and temporal arteries, none used with great
frequency, and all distal enough to give inaccurate blood
pressure readings, particularly in hypotensive patients. Use
of the axillary artery has the disadvantages of a relatively
higher rate of infection and difficulty in maintaining correct
arm positioning for proper catheter function.183
The incidence of complications from arterial catheters has
been cited as anywhere from 0.4% to 11%, with the higher
rate seen most often in pediatric patients, particularly those
under 1 year of age.184–186 Early complications include bleed­
ing, which is usually easily controlled, and hematoma for­
mation, which is more common if the artery is transfixed
during cannulation, and is avoided by an adequate period
of pressure applied to the site if bleeding occurs. Damping
of the arterial waveform or clotting of the catheter is more
common with small catheters or small arteries; this can
be lessened somewhat by continuous heparin flushing
systems.185
The incidence of catheter-related infections with arterial
catheters is generally low, quoted at anywhere from 0.4% to
2.5% until 4 days’ duration. The incidence of infection grad­
ually increases to 10% by 7 days, but stays constant thereaf­
ter. This relatively low rate of infection in comparison to
central venous catheters confirms the clinical impression
that catheter-related infections are less commonly seen in
the high-flow arterial system.182,186
Vascular insufficiency of the distal extremity has been
reported at the rate of 3–4% of patients in whom arterial
catheters are placed.181 Fortunately, most cases of ischemia
resulting from vascular obstruction are evident immediately
and resolve when the catheter is removed. The risk of
ischemia can be minimized by selecting the smallest pos­
sible catheter that will give an accurate arterial waveform.181
There is a marked increase in the incidence of arterial vaso­
spasm when >50% of the vessel lumen is occluded by the
catheter.187 Predisposing factors to ischemia from arterial
obstruction include hypotension, the use of vasoconstric­
tors, prolonged catheterization, age under 5 years, and inser­
tion by cutdown.188 Indeed, most reports of chronic sequelae
have come in patients less than 1 year of age who were
hypotensive at the time of catheter insertion. Other less com­
monly reported complications from arterial catheters include
cutaneous damage, pseudo-aneurysm formation, and septic
arthritis of the hip.189–191
Central venous catheters are very useful for large-volume
resuscitation in patients with burns over 30% or more TBSA.
Normal anatomic landmarks can be totally obliterated. The
problem is compounded by the need for long-term access in
patients with large burns who are also at high risk for central
venous catheter infections and so will require frequent line
changes. Ultrasound guidance for placement of vascular
catheters has become more common. Technical improve­
ments in equipment have made image quality and ease of
use much better. There have been suggestions that ultra­
sound guidance be made a standard of care.192 However,
extensive scarring from burn wounds can degrade the ultra­
sound image. In these instances success and safety depend
on clinical skill and experience.
renal and global perfusion. When intraoperative transfusion
is planned, examination of the urine may be the only reli­
able indicator of a transfusion reaction, as signs and symp­
toms other than hematuria are masked by general anesthesia
or hemodynamic changes associated with burn surgery.
Myoglobinuria may also occur after burn injury, and in this
case a Foley catheter is necessary to monitor response to
therapy. Diuretic therapy for myoglobinuria or any other
indication will negate the usefulness of urine output as an
index of perfusion.
Vascular access
Securing adequate vascular access in the acutely burned
patient is one of the more technically challenging procedures
facing the anesthesia care team. In the pediatric age group
the task can be even more difficult. Skin sites for insertion
of vascular access catheters may be involved in the burn, and
regional anatomy is often distorted by burn, edema, or scar­
ring. Early in the course of an acute burn shock leads to
vasoconstriction, making cannulation of peripheral vessels
nearly impossible. Later, once the patient has had several
operative procedures, scarring in the area of access sites
makes their placement difficult as well. As burn patients
undergo multiple debridement procedures it is necessary to
attain vascular access many times in each patient. The need
for frequent catheter changes in an attempt to minimize
catheter-related sepsis increases the risk of mechanical com­
plications. The anesthesia care team is frequently involved
in the maintenance of adequate vascular access during the
period of acute care and therefore must be adept in their
placement. When a large portion of the surface area is
burned, it becomes necessary to insert catheters through
burned skin. If the burn is deep, it may have to be debrided
prior to line placement so that the catheter can be sutured
to viable tissue.
For the operative excision of a large burn wound, an arte­
rial catheter allows continuous blood pressure monitoring
in the face of sudden and sometimes massive blood loss as
well as during the titration of vasoactive drugs. It also
allows easy access to blood samples for arterial blood gases,
chemistries, and serial hematocrit determinations. For pedi­
atric patients with large burns, arterial monitoring is neces­
sary. A large number of patients have been cannulated
without complications. There is a relatively high rate of
arterial occlusion: 8% with 20-gauge catheters and 34%
with 18-gauge, but almost all completely recanalize.178 It is
often difficult to maintain a radial arterial catheter in burn
patients for more than 48 hours, particularly in children,
and, unfortunately, the hands and forearms are typically
involved in a large burn wound.
Accessing the femoral artery is easier in most patients,
particularly those in low perfusion states, because it is a
larger and more central vessel.179,180 The groin is often spared
from injury, even in a large burn, and placement of a catheter
in the femoral artery is not greatly affected by the presence
of edema.181 The duration of patency is longer than that of
a radial artery catheter, and the incidence of infection in a
femoral artery catheter is similar to that at any other loca­
tion, at about 1%.179 The risk of mechanical complications
is smaller than that of more peripheral arteries because
the arterial/catheter diameter ratio is larger. Still, some

Total Burn Care
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190
infection and the site of the central venous catheter, although
almost all studies agree that the incidence of infection is
lowest if the subclavian approach is used.195,203,204 Also,
all studies that compared single-lumen and multilumen
catheters found a lower rate of infection with single-lumen
catheters.193,204 Those that compared percutaneous catheter
placement with placement via cutdown technique found a
higher incidence of infection with cutdowns.204,205
Advances in vascular catheters that incorporate an antibi­
otic have improved the efficacy of these devices in reducing
the incidence of catheter-related bloodstream infections. A
prospective randomized trial examined the efficacy of two
types of central venous catheter that incorporate antibiotics:
one catheter releases silver ions continuously and the other
is impregnated with two antibiotics with different mecha­
nisms of action, rifampin and minocycline. Both catheters
were associated with low rates of catheter-related blood­
stream infections.206 Improvements in this technology would
provide two significant clinical advantages. Reduced coloni­
zation of central venous catheters will reduce bloodborne
infections, and reduced need for changes in vascular access
sites for infection control will reduce the incidence of
mechanical complications of catheter insertion.
Additional measures recognized by the CDC for
reducing catheter-related bloodstream infections include
maximum sterile barrier technique (cap, mask, sterile
gown, sterile gloves, and large sterile drape with a small
opening).207 A meta-analysis concluded that chlorhexidine
gluconate is superior to povidone-iodine for insertion-site
disinfection.208
The operative debridement of a large burn wound is
accompanied by rapid and sometimes considerable blood
loss. Critical hypoperfusion of vital organs begins to occur
when 20–30% of blood volume is lost.209 Irreversible shock
and cellular damage can begin within minutes, depending
on the continuing rate of loss. The achievement of a very
rapid fluid infusion rate is critical in the resuscitation of the
patient undergoing operative excision of the burn wound.
Clearly, adequate venous access to achieve rapid infusion
rates is imperative.
Flow through an intravenous catheter can be increased by
high-pressure gradients, tubes of large diameter and short
length, and the use of low-viscosity fluids. The most signifi­
cant variable is the radius of the tube, where changes result
in exponential changes in flow: doubling the diameter of
the tube increases flow 16-fold. There have been a number
of studies comparing flow rates of various catheters under
different conditions. Large-diameter short catheters maxi­
mize flow, as does a central venous location: flow is 20–40%
less in a peripheral vein than in a central vein for the equiva­
lent diameter and length of catheter. Peripheral veins add
resistance to flow before fluid is delivered to the central
compartment.210
Diluting one unit of packed red blood cells with 250 mL
of normal saline can increase the flow of the blood 10-fold.211
The application of a 300 mmHg pressure device to the blood
unit can increase the flow rate another seven times. The
diameter and length of the intravenous tubing system deliv­
ering fluid from the bag to the patient has profound effects
on the rate of fluid delivery. Large-bore trauma tubing with
an internal diameter of 5.0 mm allows fluid to flow three
Catheters placed in the subclavian vein have a lower risk
of infection than those placed in the internal jugular or
femoral veins, but carry a higher risk of mechanical compli­
cations during their placement.193 The internal jugular vein
is typically more difficult to access in burn patients with
facial and neck burns or edema, and is associated with a
higher infection risk. Additionally, it is a difficult position in
terms of patient comfort, particularly for pediatric patients.
The femoral vein is a large central vein that is usually easy
to cannulate. It has several advantages, including no risk of
pneumothorax, easier control of bleeding, less anatomic dis­
tortion due to edema, and the inguinal region is often spared
even in a large burn. Goldstein and others found femoral
venous catheters to be well tolerated in their pediatric burn
patients.194 In some studies the risk of catheter-related infec­
tion was higher in the femoral vein than at other vascular
access sites, and the risk of venous thrombosis is also quoted
by some authors as being greater.195–197
Patients with acute burn injury may be at increased risk of
thrombotic complication due to a hypercoagulable state
associated with systemic inflammatory response and vascu­
lar injury associated with cannulation attempts. Although
Barrett and colleagues found that complications due to
thrombosis were infrequent in their burn population,
thrombosis can result in severe morbidity and mortality.198
It has been very difficult to establish the true incidence of
central venous catheter-related infectious complications.
This of course makes it difficult to establish the most effec­
tive policies and procedures to reduce infections associated
with central venous catheters. The diagnosis of catheter-
related bloodstream infections is made when there are signs
and symptoms of infection and other sources of infection
are excluded. Patients with large burns have multiple poten­
tial sources of infection that may be difficult to exclude, and
the systemic inflammatory response to large burn injury
mimics the signs and symptoms of bloodstream infection.
Catheter-related infection in burn patients has been reported
to have an incidence as low as 2.5% and as high as 22.4%.199
One large study of 1183 burn patients and 1346 central
venous catheters showed that the incidence of catheter-
related infection was 19.5%, with a mortality of 14.1%.
These authors cite catheter-related infection as the second
most common cause of sepsis in burn patients after the burn
wound itself.200
As a result of these and other issues, controversy continues
regarding when vascular catheters should be changed and
whether or not changing the catheter over a guide wire
reduces the incidence of infection. For patients with large
burns and who experience a prolonged hospital course with
continuous central venous access, the risk of mechanical
complications increases with the number of new vascular
sites cannulated. Three large randomized trials demonstrated
no difference in the incidence of catheter-related infections
among groups who had lines placed at a new site every 7
days and groups who had their lines changed over a guide
wire every 7 days.195,201,202 At our hospital, in selected cases
where we would like to avoid cannulating a new site we will
change the catheter over a wire and culture the catheter tip.
If the culture is negative the catheter is left in place; if the
old catheter was colonized, we place a catheter in a new site.
There are conflicting data in relation to the incidence of

Anesthesia for burned patients
191
Selection of anesthetic agents
Many anesthetic agents have been used effectively for the
induction and maintenance of anesthesia in burn patients.
Intravenous agents can be used for both induction and
maintenance and the specific agent used will depend prima­
rily on the patient’s hemodynamic and pulmonary status, as
well as the potential difficulty in securing their airway. Keta­
mine has many advantages for use in the burn patient for
induction and maintenance of anesthesia. As an induction
agent, ketamine can be administered at a dose of 0.5–2.0 mg/
kg. Except in patients who are catecholamine depleted, keta­
mine generally preserves hemodynamic stability (Fig. 14.8).
In addition, ketamine preserves hypoxic and hypercapnic
ventilatory responses and reduces airway resistance.215 Com­
pared to other IV anesthetics, airway reflexes remain more
intact after ketamine administration. However, some risk of
aspiration remains. Patients who do not require ventilatory
support can be allowed to breathe spontaneously, which
provides an additional margin of safety should inadvertent
extubation occur. In fact, some clinicians have reported the
use of ketamine anesthesia without instrumentation of the
airway.216,217 Patients were allowed to breathe spontaneously
and the airway complication rate was comparable to that of
intubated patients. The use of intramuscular ketamine can
be beneficial in securing the airway in pediatric burn patients
or uncooperative adults who do not have vascular access.
Because ketamine preserves spontaneous ventilation and
times as fast as standard blood infusion set tubing with an
internal diameter of 4.4 mm, which is twice as fast as stand­
ard intravenous tubing with an internal diameter of 3.2 mm.
The large-bore trauma tubing allows fluid flow rates of
1200–1400 mL/min.212 Several large studies have shown
introducer catheters to be superior to all other devices for
the rapid infusion of blood and intravenous (IV) fluid. These
catheters are typically of large diameter, with thin walls and
no tapering, so that for any given catheter size the inner
diameter is largest.209,213,214 This finding holds especially true
for pediatric patients, in whom vessel size is limited. The
flow rate of a 4 Fr introducer catheter is greater than that of
a 16-gauge IV catheter. However, the 4 Fr introducer placed
by the Seldinger technique requires only a 21 gauge needle
to be inserted into the vein for its placement.
When planning vascular access for perioperative anesthetic
management it is important to be aware of and take into
account the patient’s hospital course. Choice of access site
should avoid vessels previously involved in complications
such as thrombosis or vascular injury. Note must be taken
of when existing catheters were placed, and what the local
convention is with regard to the timing of regular changes
of access sites for infection control. The patient’s hospital
course must also be considered when choosing a catheter.
Although introducers offer the greatest flow and may give
the anesthesiologist a sense of assurance, the patient may
require continuous vascular access for months of hospitali­
zation and may return for surgery weekly. Large vascular
introducers placed weekly will not be tolerated without com­
plications that may result in morbidity, and will limit access
sites for future surgery. The catheter should be large enough
to transfuse appropriately for the case, but much larger cath­
eters will increase risk without benefit.
Patient transport
The safe transport of a critically ill burn patient to and from
the operating room can be a formidable task. A methodical
approach will help to ensure patient safety and the seamless
maintenance of respiratory, hemodynamic, and general
support. Hemodynamic status should be optimized prior to
transport; pharmacological support may be required. The
American Society of Anesthesiologists standards mandate
evaluation, treatment, monitoring, and equipment appro­
priate to the patient’s medical condition for any transport.
Depending on the patient’s condition, simple observation
may be appropriate. Patients requiring supplemental oxygen
should be monitored by pulse oximetry. Hemodynamic
monitoring is guided by the patient’s hemodynamic status.
Sufficient battery power must be available for uninterrupted
monitor and infusion pump function during transport.
Airway supplies should be readily available, including a
full oxygen cylinder, a self-inflating Ambu bag with mask,
and intubation equipment. The patient’s airway and ventila­
tion as well as overall condition must be continually observed
by the anesthesia care team. Drugs for resuscitation should
accompany the patient on any transport. As discussed below,
hypothermia is poorly tolerated by patients with an acute
burn injury. It is imperative that patients be kept warm
during transport in order to avoid increasing oxygen con­
sumption and taxing limited metabolic reserve.
Figure 14.8  Heart rate, mean arterial pressure, and cardiac index changes
during a 15-minute period of ketamine administration to critically ill
patients. (From Nolan JP. Intravenous agents. In Grande CM, et al., eds. Textbook of
trauma anesthesia and critical care. St. Louis: Mosby Yearbook; 1993.)
Minutes after injection
Control
10–15
6–9
3–5
0–2
Heart rate
Mean arterial pressure
Cardiac index
beats/min
20
10
0
L/min/m2
5.0
2.5
0
mmHg
15
10
5
0

Total Burn Care
14
192
Scalp donor sites are particularly painful. Sensory nerves
to the scalp are superficial and easily blocked with injections
of local anesthetic, and this technique has been used for
awake craniotomy.219 Scalp blocks have been used with
success at our institution for donor sites in acute patients
(unpublished observation) and for scalp procedures in
reconstructive patients.220
Fluid management
Fluid management and blood transfusion for burn wound
excision can be quite challenging. Fluid administration
should be guided not only by intraoperative events but also
by previous hospital course and ICU treatment goals. If
early excision is performed during the first 24 hours, peri­
operative fluid management may involve the acute resusci­
tation and fluid needs will exceed replacement of shed
blood. Even after this period insensible fluid requirements
are increased by large open surfaces from excised wounds,
hypermetabolic state, and hyperthermia. However, early in
the hospital course patients are edematous owing to the
large amounts of crystalloid solutions administered during
resuscitation. At this time additional crystalloid adminis­
tered during the perioperative period may be poorly toler­
ated and may result in complications of compartment
syndrome in extremities or the abdomen. After the initial
period of resuscitation, ICU therapy may include vigorous
attempts to reduce edema, including the use of diuretics. If
the ICU staff have been administering diuretics to the
patient all week in order to reduce interstitial edema it is
not helpful when the patient receives several liters of fluid
in the operating room. Perioperative fluid management
must also take into account hypotonic clysis fluids that the
surgeons may inject to facilitate donor skin harvest with the
dermatome. In small children the volume of this fluid can
be in excess of 50 mL/kg.
Replacement of surgical blood loss during burn wound
excision and grafting can be just as challenging. During burn
surgery it is impossible to accurately estimate the amount of
shed blood, as blood is concealed beneath the patient, in
drapes, in sponges, or may be washed down a drain on the
operating table. As discussed above regarding the initial
resuscitation, there is no one physiological endpoint to
titrate volume replacement. Arterial pressure may be main­
tained by vasoconstriction despite significant hypovolemia,
central venous pressure is not a reliable index of preload,
changes in urine output and hematocrit lag behind rapid
reductions in blood volume, and metabolic acidosis may
indicate deficient perfusion but does not identify the specific
problem. All of these variables are useful, however, when
evaluated together. Although systolic blood pressure may be
within the normal range, alterations in the arterial waveform
and changes with the respiratory cycle may indicate hypovo­
lemia. Even though central venous pressure correlates poorly
with hemodynamic function, this variable is useful in deter­
mining whether volume administration will be tolerated by
the patient. If perfusion appears inadequate and central
venous pressure is low or normal, it is safe to give volume.
If central venous pressure is elevated, volume administration
may cause pulmonary edema.
The concept of transfusion trigger with regard to burn care
is discussed below. It must be remembered, however, that
induces dissociative anesthesia, it provides good conditions
for securing the airway by fiberoptic bronchoscopy. The addi­
tion of other anesthetic agents, particularly potent volatile
agents or opioids, should be avoided until the airway is
secured because these anesthetics depress respiratory drive
and relax pharyngeal muscles, thereby increasing the risk of
apnea, upper airway obstruction, or laryngospasm. Ketamine
can also be used, either alone or in combination with other
anesthetics, for maintenance of anesthesia either by infusion
or by intermittent bolus. Ketamine has potent analgesic
properties and is used extensively in the operating room as
well as for painful wound care and patient manipulations.
A drying agent such as glycopyrrolate (2–5 µg/kg) may be
given in combination with ketamine to reduce ketamine-
induced secretions. In addition, benzodiazepines are often
recommended in older children and adults to reduce the
incidence of dysphoria sometimes associated with ketamine
administration. Propofol is more commonly used for induc­
tion in patients returning for reconstructive procedures
rather than in the acute phase of injury, but is also some­
times chosen in patients with small burns and no evidence
of airway or facial involvement when direct laryngoscopy is
planned.
Volatile anesthetics may be used for both induction and
maintenance of anesthesia in burn patients. In pediatric
patients, mask induction with either halothane or sevoflu­
rane is commonly used if the patient does not have injuries
that may make airway manipulation difficult. In the acute
setting, an anesthetic technique involving nasotracheal intu­
bation after mask induction with halothane, nitrous oxide,
and oxygen has been described.218 Proponents particularly
emphasize avoiding the potential problems associated with
the ketamine-based technique. However, volatile agents
produce dose-dependent cardiac depression and vasodila­
tion. In addition, hypoxic ventilatory drive is ablated by
volatile anesthetics at low concentrations, and a dose-
dependent depression of hypercapnic drive also occurs.
However, as maintenance agents volatile anesthetics have
predictable washin and washout kinetics and provide a
useful adjunct to other agents when titrated to hemody­
namic and ventilatory parameters. Of the volatile agents,
nitrous oxide has the least impact on cardiovascular and
respiratory function and can serve as a useful component of
a balanced anesthetic if the patient’s oxygen requirements
permit.
Opioids are important agents for providing analgesia to
burn patients throughout the acute phase of injury and for
providing postoperative analgesia in patients undergoing
reconstructive procedures. The spectrum of opioids currently
available provides a wide range of potencies, durations of
action, and effects on the cardiopulmonary system. The
introduction of the ultrashort-acting narcotic remifentanil
provides additional flexibility in perioperative dosing. With
this drug, a primarily narcotic-based anesthetic can be pro­
vided to patients who may be intolerant of potent inhalation
agents without prolonging emergence. Regional anesthesia
can be used effectively in patients with small burns. In coop­
erative children or adults with injuries confined to the lower
extremities, epidural or intrathecal anesthesia may be used
if no contraindications exist. For upper extremity procedures,
brachial plexus block may be considered as the primary
anesthetic or as an adjunct for postoperative pain control.

Anesthesia for burned patients
193
in 3 hours, or ongoing blood loss of 150 mL/min. When
blood loss is this extensive coagulation factors are lost and
consumed as volume is replaced and/or diluted. Once devel­
oped, the resulting coagulopathy is difficult to treat and is
associated with serious morbidity and mortality. In the past,
ASA guidelines have recommended that the administration
of fresh frozen plasma (FFP) to replace surgical blood loss
be restricted to cases with microvascular bleeding and docu­
mented coagulation factor deficiency.226 In recent years these
traditional indications for FFP have been challenged. In a
computer simulation of exsanguinating traumatic hemor­
rhage, Hirshberg and colleagues predicted that this restrictive
use of FFP to treat massive hemorrhage was inadequate to
prevent or correct dilutional coagulopathy.227 With their
model early and aggressive use of FFP was needed to prevent
coagulopathy owing to dilution of coagulation factors. In
addition, a problem with the use of laboratory measure­
ments of coagulation function during massive hemorrhage
is that results cannot be provided in a timely fashion. Find­
ings from recent clinical studies have also supported the
early use of FFP in combination with packed red blood cells
to replace ongoing massive blood loss. In both civilian and
military patient populations a dose-dependent reduction in
mortality has been consistently observed when FFP is admin­
istered early in patients requiring massive transfusion.228,229
As a result, blood banks have adopted protocols to provide
blood components to support coagulation function (e.g.
FFP, platelets, and cryoprecipitate) when massive hemor­
rhage is diagnosed.230 These protocols were developed from
data obtained from trauma patients presenting in hemor­
rhagic shock. During surgical excision of burn wounds
attempts are made to replace blood loss as it occurs, rather
than after a state of hypovolemic shock has developed. Still,
the concept that coagulopathy is better prevented than
reversed seems to justify the adoption of a modification of
the treatment protocol used for massive traumatic hemor­
rhage when replacing extensive blood loss during burn
wound excision. As an example, in our institution, during
burn surgery intravascular volume is maintained with infu­
sion of colloid (hetastarch or albumin) and oxygen-carrying
capacity with packed red blood cells until 50% of the esti­
mated blood volume has been replaced. From that point on,
FFP is administered in a 1 : 1 ratio with packed cells to replace
continued blood loss.
Red blood cells also facilitate hemostasis. Through a rheo­
logical effect, red blood cells push platelets to the periphery
of the intravascular lumen, which increases their concentra­
tion at and interaction with the endothelium. Red cells may
also enhance hemostasis through effects on platelet bio­
chemistry and function.231
Massive transfusion can also be complicated by hypother­
mia and hypocalcemia. Hypothermia can contribute to
coagulopathy and is poorly tolerated by burn patients from
a metabolic standpoint. When large blood loss is anticipated
blood warmers capable of warming fluids at the flow rates
required to resuscitate massive hemorrhage (>100 mL/min)
must be available. Hypocalcemia can result from rapid
administration of blood products containing citrate (espe­
cially FFP). Hypocalcemia also impairs coagulation and, in
addition, interferes with vascular and myocardial contrac­
tion, which results in hypotension. The effects of hypocal­
cemia respond more rapidly to calcium chloride than
during rapid blood loss the hematocrit may change much
more slowly than the blood loss, and often blood must be
administered before the hematocrit falls below a specific
trigger.
Blood transfusion
The need for blood transfusion is usually not a major concern
during the immediate resuscitation phase in acutely burned
patients unless other coexisting trauma exists. Nevertheless,
a fall in plasma hemoglobin concentration can occur during
the acute resuscitative phase due to hemodilution and blood
loss from escharotomies and other invasive procedures.221
However, major blood loss is common when patients are
taken to the operating room for excision and grafting of burn
wounds. Desai and colleagues reported that the amount of
blood loss during burn wound excision is determined by the
age of the burn, the body surface area involved, and whether
infection is present (see Table 14.4).7 In general, more blood
loss was observed as the time from initial injury increased,
and if wounds were infected. Transfusion requirements
ranging from 0.45 to 1.25 mL of packed red blood cells
(PRBC) per cm2 burn area were reported. In another study,
Criswell and Gamelli222 reported an average transfusion rate
of 0.89 mL PRBC/cm2 burn area in a cohort of adult burn
patients. A study by O’Mara and colleagues showed an
average transfusion rate of 0.65 mL PRBC/cm2 in a hetero­
geneous group of burn patients.223
Controversy exists regarding transfusion triggers and
targets. Some authors advocate allowing hematocrit to drop
to 15–20% prior to transfusion in otherwise healthy patients
undergoing limited excision, and transfusing at a hematocrit
of 25% in patients with pre-existing cardiovascular disease.224
The same group proposed maintaining hematocrit near 25%
in patients with more extensive burns, and near 30% if the
patients have pre-existing cardiovascular disease. A small
study by Sittig and Deitch showed fewer transfused units and
no increase in adverse hemodynamic or metabolic effects in
patients transfused at a hemoglobin of 6–6.5 g/dL compared
to patients maintained at a hemoglobin near 10 g/dL.225
However, in general, few outcome data exist regarding the
optimum transfusion trigger for blood transfusion during
burn wound excision. Blood transfusion needs are best
assessed by evaluating the clinical status of the patient. Spe­
cifically, assessment of ongoing blood losses, preoperative
hemoglobin levels, vital signs, and evidence of inadequate
oxygen delivery, such as hypotension, tachycardia, acidosis,
and decreasing mixed venous oxygen tension, provide
important information regarding the patient’s oxygen
balance. Patients with coexisting cardiac and pulmonary
disease generally require higher oxygen-carrying capacity.
Overall, American Society of Anesthesiologists guidelines
indicate that blood transfusion is rarely required at a hemo­
globin of 10 g/dL or above and is almost always indicated at
a hemoglobin of less than 6 g/dL.226 For each patient, there­
fore, acceptable blood loss can be determined based on
pre-existing diseases, preoperative hematocrit (Hct), and the
patient’s estimated blood volume (EBV).
During excision of major burn wounds blood loss may
reach or exceed the patient’s blood volume. Various defini­
tions of massive hemorrhage have been used, but include
loss of one blood volume in 24 hours, 50% blood volume

Total Burn Care
14
194
Packed red blood cells
PRBCs are the most common means of replacing blood loss
during surgical procedures. Most of the plasma and platelets
are removed during processing so that PRBCs provide few
plasma components, clotting factors, or platelets. A unit of
PRBCs contains approximately 200 mL of red cells and
50 mL of residual plasma. A comparison of PRBC composi­
tion with whole blood is shown in Table 14.9. PRBCs provide
oxygen-carrying capacity and, when reconstituted with crys­
talloid or plasma, volume resuscitation. As described above,
red blood cells can enhance platelet function, and hemosta­
sis can be facilitated by correction of anemia.
Fresh frozen plasma
In the setting of burn injury, fresh frozen plasma (FFP) is
most commonly used to replace clotting factors during
massive blood transfusion. FFP will replace clotting factors
as well as proteins S and C by a factor of 2–3% per unit. The
use of FFP varies among different burn centers. Plasma is
calcium gluconate because the gluconate form requires
hepatic metabolism to release the ionized calcium. Other
transfusion reactions are described along with the individual
components.
Several means of reducing surgical blood loss may be
employed during burn wound excision, such as the use of
tourniquets on limbs and compression dressings at sites of
excision or skin graft harvesting.232 Tourniquets have been
shown to be effective for reducing blood loss during burn
wound excision.222 The drawbacks of tourniquet use are that
their effectiveness is limited to surgery on the extremities,
and that they may interfere with the surgical field. Pharma­
cological interventions that may reduce blood loss include
the use of epinephrine-soaked dressings or topical epine­
phrine spray to induce local vasoconstriction. Alternatively,
subcutaneous tissues may be infiltrated with epinephrine-
containing fluids. The use of epinephrine may be associated
with tachycardia and hypertension if significant amounts are
absorbed into the systemic circulation. However, some
studies have reported that the use of topical or subcutaneous
epinephrine in burn patients is not associated with an
increased incidence of side-effects or complications.233
However, the effectiveness of this approach is unclear. A
recent study showed that the use of topical epinephrine
spray or subcutaneous epinephrine infiltration did not result
in decreased blood loss during burn wound excision.234
However, the data were quite variable and the patients also
received topical thrombin. A larger study examining the
effects of subcutaneous epinephrine and topical thrombin
might clarify this issue. In a more recent study, Mzezewa and
colleagues reported that treatment with systemic terlipressin,
a vasopressin analog, reduced blood loss and transfusion
requirements in a cohort of pediatric and adult burn
patients.235 The authors did not report significant complica­
tions associated with this approach.
Blood components
Several blood components are available for replacement of
losses incurred during burn wound excision.
Whole blood
Whole blood consists of unfractionated blood and contains
all of the components of blood, including red blood cells,
plasma, platelets, and white blood cells; however, whole
blood stored for more than 24 hours does not contain func­
tional white blood cells or platelets (Table 14.8). One unit
of whole blood contains approximately 200 mL of red blood
cells and 250 mL of plasma. Whole blood is available in
some hospitals for large-volume blood transfusions (trauma,
liver transplantation, burns) and treatment of hypovolemic
shock. However, because of the scarcity of blood products in
most communities, whole blood is not readily available.
Fractionation of whole blood into its individual compo­
nents is a much more efficient and cost-effective means of
maximizing blood usage. When available, however, whole
blood provides an excellent means of volume expansion and
providing oxygen-carrying capacity in patients requiring
large-volume blood transfusion.
Table 14.8  Changes that occur during storage of whole blood in
citrate–phosphate–dextrose
Days of storage at 4°C
1
7
14
21
pH
7.1
7.0
7.0
6.9
PCO2 (mmHg)
48
80
110
140
Potassium (mEq/L)
3.9
12
17
21
2,3-Diphosphoglycerate (µmol/mL)
4.8
1.2
1
1
Viable platelets (%)
10
0
0
0
Factors V and VII (%)
70
50
40
20
Table 14.9  Comparison of whole blood and packed red blood cells
Value
Whole blood
Packed red
blood cells
Volume (mL)
517
300
Erythrocyte mass (mL)
200
200
Hematocrit (%)
40
70
Albumin (g)
12.5
4
Globulin (g)
6.25
2
Total protein (g)
48.8
36
Plasma sodium (mEq)
45
15
Plasma potassium (mEq)
15
4
Plasma acid (citric/lactic) (mEq)
80
25
Donor/recipient ratio
1 unit per
patient
1 unit every 4–6
patients

Anesthesia for burned patients
195
Complications of massive blood transfusion
Coagulopathy
Coagulopathy associated with massive blood transfusion is
due to thrombocytopenia or depletion of coagulation factors
by dilution or consumption. PRBCs are essentially devoid of
platelets, and whole blood stored for more than 24 hours
does not possess significant numbers of viable platelets.
Whole blood contains essentially normal levels of coagula­
tion factors, with the exception of the volatile factors V and
VIII. Because most plasma is removed from PRBCs they
provide a poor source of coagulation factors. Massive blood
loss and transfusion with PRBCs or whole blood results in
dilutional losses of both platelets and factors V and VIII.
Thrombocytopenia is the most common cause of non-
surgical bleeding after massive blood transfusion. In general,
15–20 units, or 2–4 volumes of blood or PRBCs, must be
transfused before bleeding due to thrombocytopenia will
develop (Fig. 14.9). Observed platelet counts usually remain
higher than calculated values owing to the release of platelets
from sites of sequestration. Bleeding due to thrombocyto­
penia usually develops when the platelet count drops below
50–100 000 platelets/µL. Replacement of platelets usually
requires transfusion of 6 units of whole blood platelets or 1
unit of single-donor platelets, as described earlier.
As discussed above, blood bank protocols have recently
been developed to provide coagulation factors earlier and
more aggressively to prevent rather than treat coagulopathy
associated with massive hemorrhage and transfusion. These
frozen within 6 hours of collection and each unit provides
approximately 250 mL of plasma containing normal levels
of all coagulation factors. A National Institutes of Health
consensus conference has recommended usage guidelines
for FFP (Table 14.10).
In the setting of massive blood transfusion, FFP adminis­
tration has been indicated if active bleeding exists and labo­
ratory evidence of coagulation factor depletion is shown.
As described above, recent experience with massive transfu­
sions associated with trauma in military and civilian patient
populations has provided justification for a more aggressive
and proactive use of FFP to prevent rather than treat
coagulopathy. When burn wound excision involves massive
hemorrhage a similar practice may benefit these patients
as well.
Platelets
Platelets are stored at room temperature to maximize viabil­
ity. The incidence of bacterial contamination increases expo­
nentially after 4 days. However, refrigerated platelets remain
viable for only 24–48 hours. Platelets are obtained from
either units of whole blood or by apheresis from a single
donor. ABO-compatible platelets, particularly if from a
single donor, should be used when possible because post-
transfusion viability is improved. One unit of whole blood
platelets contains approximately 5 × 1010 platelets in 50 mL
of plasma. Most commonly, 6 units of platelets are com­
bined into a single bag and transfused. A unit of single-
donor platelets contains about 30 × 1010 platelets suspended
in 200–400 mL of plasma. Therefore, 1 unit of single-donor
platelets is equal to about 6 units of whole blood platelets.
One unit of whole blood platelets will increase the platelet
count by 5000–10 000/µL.
Cryoprecipitate
Cryoprecipitate is prepared by thawing FFP at 4°C and col­
lecting the precipitate. Cryoprecipitate is rich in factors VIII
and XIII, fibrinogen, and von Willebrand factor. In the
setting of massive blood transfusion it is used primarily to
treat hypofibrinogenemia. Generally, cryoprecipitate is
administered when plasma fibrinogen levels fall below
100 mg/dL. One unit of cryoprecipitate will increase plasma
fibrinogen levels by 5–7 mg/dL.
Table 14.10  Indications for FFP according to National institutes of
Health guidelines
A. Replacement of isolated factor deficiencies (as documented by
laboratory evidence)
B. Reversal of warfarin effect
C. In antithrombin III deficiency
D. Treatment of immunodeficiencies
E. Treatment of thrombotic thrombocytopenia purpura
F. Massive blood transfusion (only when factors V and VIII are 25% of
normal)
G. Requirements for indications A and F would be a prothrombin and
partial thromboplastin time of 1.5 times normal
Figure 14.9  Calculated versus observed mean platelet counts in two
studies of platelet count after massive blood transfusion. (Reproduced with
permission from Reed RL, et al. Prophylactic platelet administration during massive
transfusion. Ann Surg 1986; 203: 46.)
300
200
100
100
50
50
0
0
10
20
30
40
50
Calculated
Observed
Platelet count
(× 103/µL)
Platelet count
(× 103/µL)
200
Units of blood transfused
0
0
10
20
30
40
50

Total Burn Care
14
196
tissue perfusion results in lactic acidosis. Generally, admin­
istration of sodium bicarbonate is not indicated. The
re-establishment of tissue perfusion and homeostasis is
much more important in re-establishing acid–base balance.
In contrast, many patients receiving massive blood transfu­
sion will develop a metabolic alkalosis during the post-
transfusion phase. This is due to the conversion of citrate to
sodium bicarbonate by the liver and is an additional reason
to avoid sodium bicarbonate administration during massive
blood transfusion, except in cases of severe metabolic acido­
sis (base deficit >12).
Altered oxygen transport
During the storage of blood, red blood cell 2,3-diphospho-
glycerate (DPG) levels decline. This results in a shift in the
oxyhemoglobin dissociation curve to the left. Under these
conditions, oxygen has a higher affinity for hemoglobin and
oxygen release at the tissue level is theoretically diminished.
In clinical practice, this alteration in oxygen affinity has not
been shown to be functionally significant.
Hypothermia
Rapid infusion of large volumes of cold (4°C) blood can
result in significant hypothermia, owing to the already
impaired thermoregulatory mechanisms in burn patients.
Potential complications of hypothermia include altered
citrate metabolism, coagulopathy, and cardiac dysfunction.
During large-volume blood transfusion in burn patients,
fluids should be actively warmed with systems designed to
effectively warm large volumes of rapidly transfused blood.
In addition, the room temperature should be elevated and
the patient’s extremities and head covered to minimize
heat loss. Body temperature should be maintained at or
above 37°C.
Pulmonary complications
Pulmonary edema is a potential complication of massive
blood transfusion. This may result from volume overload
and/or pulmonary capillary leak due to inflammation and
microaggregates present in transfused blood. Some studies
have indicated that the incidence of pulmonary edema is
more related to the patient’s underlying injury than to blood
transfusion per se. However, volume status should be moni­
tored closely during large-volume blood transfusion so that
volume overload may be avoided.
Transfusion reactions
Hemolytic transfusion reactions are a relatively rare but dev­
astating complication of blood transfusion. The incidence of
transfusion reactions is approximately 1 : 5000 units trans­
fused, and fatal transfusion reactions occur at a rate of
1 : 100 000 units transfused. Most severe reactions result from
ABO incompatibility. The most common cause of ABO-
incompatible blood being transfused is clerical error. There­
fore, most hospitals have developed policies that require
multiple checks of the blood prior to transfusion. A list of
blood types and associated circulating antibodies is shown
in Table 14.11. Massive hemolytic transfusion reactions
protocols organize communication between those directly
involved in the patient’s care and blood bank personnel to
provide coagulation factors including not only packed red
blood cells and FFP but, when indicated, platelets, cryopre­
cipitate, and recombinant activated factor VII.239 These pro­
tocols can facilitate more timely and effective management
of massive transfusion in order to reduce associated morbid­
ity and mortality.
Citrate toxicity
Citrate is universally used as an anticoagulant in the storage
of blood because of its ability to bind calcium, which is
required for activation of the coagulation cascade. Citrate
is metabolized by the liver and excreted by the kidneys.
Patients with normal liver and kidney function are able
to respond to a large citrate load much better than patients
with hepatic or renal insufficiency. During massive blood
transfusion citrate can accumulate in the circulation, result­
ing in a fall in ionized calcium.218 Hypocalcemia can result
in hypotension, reduced cardiac function, and cardiac
arrhythmias. Severe hypocalcemia can also result in clotting
abnormalities. However, the level of calcium required for
adequate coagulation is much lower than that necessary to
maintain cardiovascular stability. Therefore, hypotension
and decreased cardiac contractility occur long before coagu­
lation abnormalities are seen. During massive blood transfu­
sion it is generally prudent to monitor ionized calcium,
especially if hemodynamic instability is present in the
hypocalcemic patient.236
Potassium abnormalities
During the storage of whole blood or packed red cells, potas­
sium leaks from erythrocytes into the extracellular fluid and
can accumulate at concentrations of 40–80 mEq/L. Once the
RBCs are returned to the in vivo environment, the potassium
quickly reenters RBCs. However, during rapid blood trans­
fusion transient hyperkalemia may result, particularly in
patients with renal insufficiency. The transient hyperkalemia,
particularly in the presence of hypocalcemia, can lead to
cardiac dysfunction and arrhythmias. In patients with renal
insufficiency, potassium load can be minimized by the use
of either freshly obtained blood or washed PRBCs. Hypoka­
lemia can also result from massive blood transfusion due to
reentry of potassium into RBCs and other cells during stress,
alkalosis, or massive catecholamine release associated
with large-volume blood loss. Therefore, potassium levels
should be monitored routinely during large-volume blood
transfusions.
Acid–base abnormalities
During the storage of whole blood an acidic environment
develops due to the accumulation of lactate and citrate, with
a pH in the range of 6.5–6.7. Rapid transfusion of this acidic
fluid can contribute to the metabolic acidosis observed
during massive blood transfusion. However, metabolic aci­
dosis in this setting is more commonly due to relative tissue
hypoxia and anaerobic metabolism owing to an imbalance
of oxygen consumption and delivery. The anaerobic metabo­
lism that occurs during states of hypovolemia and poor

Anesthesia for burned patients
197
colleagues showed a significant correlation between the
number of blood transfusions and infectious complications
in burn patients.238 The most common source of major infec­
tion from blood products is hepatitis. Hepatitis C is the most
common offender, followed by hepatitis B. The incidence of
hepatitis C is approximately 3 in 10 000 units transfused. The
development of rigorous screening mechanisms has mark­
edly reduced the incidence of HIV infection to 1 in 200 000–
500 000 units transfused. Cytomegalovirus (CMV) has been
identified in blood products and could cause clinically sig­
nificant problems in immunocompromised burn patients.
However, the incidence of clinically important CMV infec­
tion is low in burn patients.
Postoperative care
Decisions regarding postoperative airway management and
support of ventilation depend on several factors. Extubation
is desirable as soon as it is indicated, but in burn patients,
for a number of reasons, it often may be even more impor­
tant not to extubate when it is not indicated. If the patient
came to the operating room intubated, the indication for
intubation must be determined. If the initial indication has
resolved, the decision to extubate depends on perioperative
events. Some patients with neck and facial burns are intu­
bated to protect the airway from obstruction by edema. Air
leaking around a deflated endotracheal tube cuff during
positive-pressure ventilation is an encouraging sign that the
airway may remain patent after extubation. The upper airway
can also be examined by direct laryngoscopy or with an
endoscope. In marginal cases the endotracheal tube can be
removed while an exchanger is left in the trachea. Another
technique is to extubate under direct vision with a broncho­
scope with an endotracheal tube already loaded on the bron­
choscope. Especially in small pediatric patients a common
reason for post-extubation stridor and failed extubation is
edematous and redundant mucosa over the arytenoid emi­
nences that obstruct the glottic inlet during inspiration. This
condition can be exacerbated by an endotracheal tube that
is too large, excessive patient movement due to inadequate
sedation and analgesia, reflux of acidic gastric contents, and
mechanical irritation due to compression of the posterior
laryngeal structures between the endotracheal tube and
gastric tubes. These irritants can also cause laryngomalacia
in pediatric patients. If laryngeal obstruction persists despite
attention to all these details, a short course of steroids is
result from destruction of transfused erythrocytes by circulat­
ing antibodies and complement. Many of the common signs
and symptoms of transfusion reactions, such as chills, chest
pain, and nausea, cannot be detected in the patient under
anesthesia. The most commonly recognized signs of transfu­
sion reaction in the anesthetized patient are fever, hypoten­
sion, hemoglobinuria, and coagulopathy. The cornerstones
of treatment are to stop the transfusion, protect the kidneys
with aggressive hydration and alkalinization of urine, and
treat existing coagulopathy.
Delayed hemolytic transfusion reactions can occur in
patients who have received prior blood transfusions and
result from a secondary immune response with production
of antibodies to blood antigens. This reaction can occur from
2 to 21 days after transfusion and should be suspected in
patients with unexplained decreases in hematocrit during
the postoperative period. Renal injury is less common than
in acute hemolytic reactions, but adequate hydration and
alkalinization of urine are usually indicated. Febrile reac­
tions are common following blood transfusion and are gen­
erally due to contaminating leukocytes and leukocyte
antigens present in transfused blood. Pure febrile reactions
usually do not require termination of the transfusion, but
the patient should be monitored closely to assure that a
more severe transfusion reaction is not developing.
In recent years the most common cause of mortality asso­
ciated with blood transfusion has been transfusion-related
acute lung injury (TRALI). TRALI is defined as a new acute
lung injury occurring within 6 hours of transfusion in a
patient without additional risk factors for acute lung injury.
The greatest risk of TRALI is associated with blood products
that contain large amounts of plasma, namely FFP and plate­
lets. As with ARDS, there are no specific therapies for TRALI
and management is supportive. It is difficult to recognize
TRALI in patients with major burns, as there are multiple
etiologies for acute lung injury and ARDS in these patients.
The risk of TRALI has been reduced by the institution of a
blood bank policy of minimizing preparation of plasma-rich
components (e.g. FFP and platelets) from donors who are
known to be or are at risk of becoming alloimunized against
leukocytes.237
Infection
Infection is a major problem in burn patients owing to dis­
ruption of the cutaneous barrier and immunosuppression.
Blood transfusion adds to the infection risk. Graves and
Table 14.11  Blood groups and cross-match
Blood group
Antigen on
erythrocyte
Plasma
antibodies
Incidence (%)
Whites
African-Americans
A
A
Anti-B
.40
27
B
B
Anti-A
11
20
AB
AB
None
4
4
O
None
Anti-A
Anti-B
45
49
Rh
Rh
42
17

Total Burn Care
14
198
Summary
Anesthetic management of the burn patient presents numer­
ous challenges. Anatomical distortions make airway man­
agement and vascular access difficult. Pathophysiological
changes in cardiovascular function range from initial hypo­
volemia and impaired perfusion to a hyperdynamic and
hypermetabolic state that develops after the resuscitative
stage. These and other changes profoundly alter the response
to anesthetic drugs. Effective anesthetic management will
depend on knowledge of the continuum of pathophysiologi­
cal changes, technical skills, proper planning, and availabil­
ity of proper resources. A team approach is necessary, keeping
in mind that perioperative management should be compat­
ible with ICU management and goals. This requires close
communication with other members of the burn care team
and is one of the most important principles of effective
anesthetic management of these challenging patients.
Further reading
Cancio LC, Chavez S, Alvarado-Ortega M, et al. Predicting increased
fluid requirements during the resuscitation of thermally injured
patients. J Trauma. 2004 Feb;56(2):404-413; discussion 413-414.
Fuzaylov G, Fidkowski CW. Anesthetic considerations for major burn
injury in pediatric patients. Paediatr Anaesth. 2009 Mar;19(3):
202-211.
Holm C, Melcer B, Horbrand F, et al. The relationship between
oxygen delivery and oxygen consumption during fluid
resuscitation of burn-related shock. J Burn Care Rehabil. 2000
Mar-Apr;21(2):147-154.
Jeschke MG, Chinkes DL, Finnerty CC, et al. Pathophysiologic
response to severe burn injury. Ann Surg. 2008 Sep;248(3):
387-401.
Kinsky MP, Guha SC, Button BM, et al. The role of interstitial starling
forces in the pathogenesis of burn edema. J Burn Care Rehabil.
1998 Jan-Feb;19(1 Pt 1):1-9.
Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in
acquired pathologic states: etiologic factors and molecular
mechanisms. Anesthesiology. 2006 Jan;104(1):158-169.
Muehlberger T, Kunar D, Munster A, et al. Efficacy of fiberoptic
laryngoscopy in the diagnosis of inhalation injuries. Arch
Otolaryngol Head Neck Surg. 1998 Sep;124(9):1003-1007.
often effective as long as concerns regarding burn wound
infection do not preclude their use (unpublished observa­
tions). Heliox has also been used successfully in this
situation.239
After transfer of monitors and ventilatory support in the
intensive care unit, a full report on the intraoperative anes­
thetic course is given, along with information about the
patient’s current condition and therapy. Laboratory studies,
including arterial blood gas, blood chemistries, renal
function tests, hematocrit, platelet count, and coagulation
studies, are sent soon after patient arrival to the intensive
care unit. These studies are particularly important if large
volumes of fluid were required in the operating room.
One of the most important issues in the immediate post­
operative period for burn patients is adequate analgesia and
sedation, particularly for the intubated and mechanically
ventilated patient. Debridement of burned tissue and the
harvesting of skin grafts are painful procedures that merit
ample analgesic doses in order to ensure patient comfort. It
is not uncommon for burn patients to be quite tolerant to
narcotic analgesics, especially after they have had several
operative procedures, and in this case larger doses than
normal are required.
Ongoing blood loss is unfortunately a common problem
after the excision and grafting of a large burn wound, even
when strict attention is placed on intraoperative hemostasis
by surgical personnel. A significant amount of shed blood
can be concealed in bulky burn dressings. The burn wounds
are necessarily excised down to bleeding tissue before skin
grafts are applied. Massive intraoperative transfusion adds to
the problem with dilutional thrombocytopenia and coagu­
lopathy. Diligent postoperative care is needed to continually
assess ongoing blood loss and transfuse additional blood
products as indicated by clinical course and laboratory
studies. Ongoing bleeding may manifest as hypovolemia
and hypotension even in the brief period of transport from
the operating room to the intensive care unit. Monitoring of
central venous pressure and urine output also helps in
guiding postoperative blood and fluid therapy.
Finally, burn patients must be recovered in a warm envi­
ronment. Postoperative hypothermia can result in vasocon­
striction, hypoperfusion, and metabolic acidosis. Radiant
heaters, blood and fluid warmers, warm blankets, heated
humidifiers for gas delivery, and high room temperature are
all useful in the postoperative period to provide warmth to
the recovering patient.
Access the complete reference list online at

Anesthesia for burned patients
198.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
References
1. Saffle JR. Predicting outcomes of burns. N Engl J Med. 1998 Feb
5;338(6):387-388.
2. Ryan CM, Schoenfeld DA, Thorpe WP, et al. Objective estimates
of the probability of death from burn injuries. N Engl J Med.
1998 Feb 5;338(6):362-366.
3. O’Keefe GE, Hunt JL, Purdue GF. An evaluation of risk factors
for mortality after burn trauma and the identification of
gender-dependent differences in outcomes. J Am Coll Surg. 2001
Feb;192(2):153-160.
4. Sheridan RL, Remensnyder JP, Schnitzer JJ, et al. Current
expectations for survival in pediatric burns. Arch Pediatr Adolesc
Med. 2000 Mar;154(3):245-249.
5. Keck M, Lumenta DB, Andel H, et al. Burn treatment in the
elderly. Burns. 2009 Dec;35(8):1071-1079.
6. Wang Y, Tang HT, Xia ZF, et al. Factors affecting survival
in adult patients with massive burns. Burns. 2010 Feb;36(1):
57-64.
7. Desai MH, Herndon DN, Broemeling L, et al. Early burn wound
excision significantly reduces blood loss. Ann Surg. 1990 Jun;
211(6):753-759; discussion 759-762.
8. Reynolds EM, Ryan DP, Sheridan RL, et al. Left ventricular failure
complicating severe pediatric burn injuries. J Pediatr Surg. 1995
Feb;30(2):264-269; discussion 269-270.
9. Fuzaylov G, Fidkowski CW. Anesthetic considerations for major
burn injury in pediatric patients. Paediatr Anaesth. 2009
Mar;19(3):202-211.
10. Woodson LC, Sherwood ER, Cortiella J. Anesthesia for
reconstructive burn surgery. Functional and aesthetic
reconstruction of burned patients. 2005.
11. Thompson PB, Herndon DN, Traber DL, et al. Effect on
mortality of inhalation injury. J Trauma. 1986 Feb;26(2):
163-165.
12. Navar PD, Saffle JR, Warden GD. Effect of inhalation injury on
fluid resuscitation requirements after thermal injury. Am J Surg.
1985 Dec;150(6):716-720.
13. Hollingsed TC, Saffle JR, Barton RG, et al. Etiology and
consequences of respiratory failure in thermally injured patients.
Am J Surg. 1993 Dec;166(6):592-596; discussion 596-597.
14. Foley FD. The burn autopsy. Fatal complications of burns. Am J
Clin Pathol. 1969 Jul;52(1):1-13.
15. Moritz AR, Henriques FC, McLean R. The effects of inhaled heat
on the air passages and lungs: an experimental investigation.
Am J Pathol. 1945 Mar;21(2):311-331.
16. Clark WR, Bonaventura M, Myers W. Smoke inhalation and
airway management at a regional burn unit: 1974–1983. Part I:
Diagnosis and consequences of smoke inhalation. J Burn Care
Rehabil. 1989 Jan-Feb;10(1):52-62.
17. Muehlberger T, Kunar D, Munster A, et al. Efficacy of fiberoptic
laryngoscopy in the diagnosis of inhalation injuries. Arch
Otolaryngol Head Neck Surg. 1998 Sep;124(9):1003-1007.
18. Colice GL, Munster AM, Haponik EF. Tracheal stenosis
complicating cutaneous burns: an underestimated problem. Am
Rev Respir Dis. 1986 Dec;134(6):1315-1318.
19. Clark CJ, Reid WH, Telfer AB, et al. Respiratory injury in the
burned patient. The role of flexible bronchoscopy. Anaesthesia.
1983 Jan;38(1):35-39.
20. Haponik EFLM. Acute upper airway obstruction in patients with
burns. Critical Care Rep. 1990;2:28-49.
21. Hunt JL, Agee RN, Pruitt BA. Fiberoptic bronchoscopy in acute
inhalation injury. J Truma. 1975;15:641-649.
22. Haponic EF, Meyers DA, Munster AM. Acute upper airway injury
in burn patients: Serial changes of flow-volume curves and
nasopharyngoscopy. Am Rev Respir Dis. 1987;135:360-366.
23. Eastman AL. Pre-burn center management of the burned airway:
Do we know enough? J Burn Care Res. 2010;31(5):701-705.
24. Lee JM, O’Connell DJ. The plain chest radiograph after acute
smoke inhalation. Clin Radiol. 1988;39:33.
25. Linares HA, Herndon DN, Traber DL. Sequence of morphologic
events in experimental smoke inhalation. J Burn Care Rehabil.
1989 Jan-Feb;10(1):27-37.
26. Demling RH, Chen C. Pulmonary function in the burn patient.
Semin Nephrol. 1993 Jul;13(4):371-381.
27. Mlcak RP, Suman OE, Herndon DN. Respiratory management of
inhalation injury. Burns. 2007 Feb;33(1):2-13.
28. McCall JE, Cahill TJ. Respiratory care of the burn patient. J Burn
Care Rehabil. 2005 May-Jun;26(3):200-206.
29. Dries DJ. Key questions in ventilator management of the
burn-injured patient (first of two parts). J Burn Care Res. 2009
Jan-Feb;30(1):128-138.
30. Peck MD, Koppelman T. Low-tidal-volume ventilation as a
strategy to reduce ventilator-associated injury in ALI and ARDS.
J Burn Care Res. 2009 Jan-Feb;30(1):172-175.
31. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med.
1998 Nov 26;339(22):1603-1608.
32. Kealey GP. Carbon monoxide toxicity. J Burn Care Res. 2009
Jan-Feb;30(1):146-147.
33. Tibbles PM, Perrotta PL. Treatment of carbon monoxide
poisoning: a critical review of human outcome studies
comparing normobaric oxygen with hyperbaric oxygen. Ann
Emerg Med. 1994 Aug;24(2):269-276.
34. Clark CJ. Measurements of toxic combustion products in fire
survivors. J R Soc Med. 1982;153:41-44.
35. Cummings TF. The treatment of cyanide poisoning. Occup Med
(Lond). 2004 Mar;54(2):82-85.
36. Hardman JG, Limbird LE. Goodman and Gilmans the
pharmacological basis of therapeutics, 10th ed. New York:
Pergamon; 2001:1892-1893.
37. Deitch EA. The management of burns. N Engl J Med. 1990 Nov
1;323(18):1249-1253.
38. Horton JW, Baxter CR, White DJ. Differences in cardiac
responses to resuscitation from burn shock. Surg Gynecol Obstet.
1989;168:201-213.
39. Zetterstrom H, Arturson G. Plasma oncotic pressure and plasma
protein concentration in patients following thermal injury. Acta
Anaesthesiol Scand. 1980 Aug;24(4):288-294.
40. Starling EH. On the absorption of fluids from the connective
tissue spaces. J Physiol. 1896 May 5;19(4):312-326.
41. Kinsky MP, Guha SC, Button BM, et al. The role of interstitial
starling forces in the pathogenesis of burn edema. J Burn Care
Rehabil. 1998 Jan-Feb;19(1 Pt 1):1-9.
42. Reed RK, Rubin K. Transcapillary exchange: role and importance
of the interstitial fluid pressure and the extracellular matrix.
Cardiovasc Res. 2010 Jul 15;87(2):211-217.
43. Baxter CR, Cook WA, Shires GT. Serum myocardial depressant
factor of burn shock. Surg Forum. 1966;17:1-2.
44. Maass DL, White J, Horton JW. IL-1beta and IL-6 act
synergistically with TNF-alpha to alter cardiac contractile
function after burn trauma. Shock. 2002 Oct;18(4):360-366.
45. Horton JW, Tan J, White DJ, et al. Selective decontamination of
the digestive tract attenuated the myocardial inflammation and
dysfunction that occur with burn injury. Am J Physiol Heart Circ
Physiol. 2004 Nov;287(5):H2241-H2251.
46. Horton JW. Left ventricular contractile dysfunction as a
complication of thermal injury. Shock. 2004 Dec;22(6):495-507.
47. Westphal M, Noshima S, Isago T, et al. Selective thromboxane
A2 synthase inhibition by OKY-046 prevents cardiopulmonary
dysfunction after ovine smoke inhalation injury. Anesthesiology.
2005 May;102(5):954-961.
48. Muller-Werdan U, Engelmann H, Werdan K. Cardiodepression
by tumor necrosis factor-alpha. Eur Cytokine Netw. 1998 Dec;
9(4):689-691.
49. Roberts AB, Vodovotz Y, Roche NS, et al. Role of nitric oxide in
antagonistic effects of transforming growth factor-beta and

Total Burn Care
14
198.e2
© Copyright 2012 Elsevier, Inc. All rights reserved.
interleukin-1 beta on the beating rate of cultured cardiac
myocytes. Mol Endocrinol. 1992 Nov;6(11):1921-1930.
50. Goodwin CW, Dorethy J, Lam V, et al. Randomized trial of
efficacy of crystalloid and colloid resuscitation on hemodynamic
response and lung water following thermal injury. Ann Surg.
1983 May;197(5):520-531.
51. Papp A, Uusaro A, Parviainen I, et al. Myocardial function and
haemodynamics in extensive burn trauma: evaluation by clinical
signs, invasive monitoring, echocardiography and cytokine
concentrations. A prospective clinical study. Acta Anaesthesiol
Scand. 2003 Nov;47(10):1257-1263.
52. Kuwagata Y, Sugimoto H, Yoshioka T, et al. Left ventricular
performance in patients with thermal injury or multiple trauma:
a clinical study with echocardiography. J Trauma. 1992
Feb;32(2):158-164; discussion 164-165.
53. Reynolds EM, Ryan DP, Sheridan RL, Doody DP. Left ventricular
failure complicating severe pediatric burn injuries. Journal of
Pediatric Surgery 1995;30:264–270.
54. Murphy JT, Horton JW, Purdue GF, et al. Evaluation of
troponin-I as an indicator of cardiac dysfunction after thermal
injury. J Trauma. 1998 Oct;45(4):700-704.
55. Minifee PK, Barrow RE, Abston S, et al. Improved myocardial
oxygen utilization following propranolol infusion in adolescents
with postburn hypermetabolism. J Pediatr Surg. 1989
Aug;24(8):806-810; discussion 810-811.
56. Etherington L, Saffle J, Cochran A. Use of transesophageal
echocardiography in burns: a retrospective review. J Burn Care
Res. 2010 Jan-Feb;31(1):36-39.
57. Kinsky JM, Woodson L, Sherwood E, Talon M, et al. Cardiac
dysfunction following large burn injury in children is
associated with increased length of icu stay. ESICM. 2009;193:
0006-00228.
58. Cartotto RC, Innes M, Musgrave MA, et al. How well does the
Parkland formula estimate actual fluid resuscitation volumes?
J Burn Care Rehabil. 2002;23(4):258-265.
59. Cancio LC, Chavez S, Alvarado-Ortega M, et al. Predicting
increased fluid requirements during the resuscitation of
thermally injured patients. J Trauma. 2004 Feb;56(2):404-413;
discussion 413-414.
60. Chung KK, Blackbourne LH, Wolf SE, et al. Evolution of burn
resuscitation in operation Iraqi freedom. J Burn Care Res. 2006
Sep-Oct;27(5):606-611.
61. Alderson P, Schierhout G, Roberts I. Colloids versus crystalloids
for fluid resuscitation in critically ill patients. Cochrane Database
Syst Rev. 2000.
62. Nguyen TT, Gilpin DA, Meyer NA, et al. Current treatment of
severely burned patients. Ann Surg. 1996 Jan;223(1):14-25.
63. Alderson P, Bunn F, Lefebve C. Human albumin solution for
resuscitation and volume expansion in critically ill patients.
Cochrane Database Syst Rev. 2000.
64. O’Mara MS, Slater H, Goldfarb IW, et al. A prospective,
randomized evaluation of intra-abdominal pressures with
crystalloid and colloid resuscitation in burn patients. J Trauma.
2005 May;58(5):1011-1018.
65. Guha SC, Kinsky MP, Button B, et al. Burn resuscitation:
crystalloid versus colloid versus hypertonic saline hyperoncotic
colloid in sheep. Crit Care Med. 1996 Nov;24(11):1849-
1857.
66. Elgjo GI, Poli de Figueiredo LF, Schenarts PJ, et al. Hypertonic
saline dextran produces early (8–12 hrs) fluid sparing in burn
resuscitation: a 24-hr prospective, double-blind study in sheep.
Crit Care Med. 2000 Jan;28(1):163-171.
67. Suzuki K, Ogino R, Nishina M, et al. Effects of hypertonic saline
and dextran 70 on cardiac functions after burns. Am J Physiol.
1995 Feb;268(2 Pt 2): H856-H864.
68. Jeng JC, Lee K, Jablonski K, et al. Serum lactate and base deficit
suggest inadequate resuscitation of patients with burn injuries:
application of a point-of-care laboratory instrument. J Burn Care
Rehabil. 1997 Sep-Oct;18(5):402-405.
69. Dries DJ, Waxman K. Adequate resuscitation of burn patients
may not be measured by urine output and vital signs. Crit Care
Med. 1991 Mar;19(3):327-329.
70. Wo CC, Shoemaker WC, Appel PL, et al. Unreliability of blood
pressure and heart rate to evaluate cardiac output in emergency
resuscitation and critical illness. Crit Care Med. 1993
Feb;21(2):218-223.
71. Schiller WR, Bay RC, Garren RL, et al. Hyperdynamic
resuscitation improves survival in patients with life-threatening
burns. J Burn Care Rehabil. 1997 Jan-Feb;18(1 Pt 1):10-16.
72. Holm C, Melcer B, Horbrand F, et al. The relationship between
oxygen delivery and oxygen consumption during fluid
resuscitation of burn-related shock. J Burn Care Rehabil. 2000
Mar-Apr;21(2):147-154.
73. Bernard F, Gueugniaud PY, Bertin-Maghit M, et al. Prognostic
significance of early cardiac index measurements in severely
burned patients. Burns. 1994 Dec;20(6):529-531.
74. Bishop MH, Shoemaker WC, Appel PL, et al. Prospective,
randomized trial of survivor values of cardiac index, oxygen
delivery, and oxygen consumption as resuscitation endpoints in
severe trauma. J Trauma. 1995 May;38(5):780-787.
75. Fleming A, Bishop M, Shoemaker W, et al. Prospective trial of
supranormal values as goals of resuscitation in severe trauma.
Arch Surg. 1992 Oct;127(10):1175-1179; discussion 1179-1181.
76. Schiller WR, Bay RC, Garren RL, et al. Hyperdynamic
resuscitation improves survival in patients with life-threatening
burns. J Burn Care Rehabil. 1997;18:10-16.
77. Heyland DK, Cook DJ, King D, et al. Maximizing oxygen
delivery in critically ill patients: a methodologic appraisal of the
evidence. Crit Care Med. 1996 Mar;24(3):517-524.
78. Gattinoni L, Brazzi L, Pelosi P, et al. A trial of goal-oriented
hemodynamic therapy in critically ill patients. SvO2
Collaborative Group. N Engl J Med. 1995 Oct 19;333(16):
1025-1032.
79. Durham RM, Neunaber K, Mazuski JE, et al. The use of oxygen
consumption and delivery as endpoints for resuscitation in
critically ill patients. J Trauma. 1996 Jul;41(1):32-39; discussion
9-40.
80. Hayes MA, Timmins AC, Yau EH, et al. Elevation of systemic
oxygen delivery in the treatment of critically ill patients. N Engl J
Med. 1994 Jun 16;330(24):1717-1722.
81. Hendenstierna. What value does the recording of intrathoracic
blood volume have in clinical practice. Intensive Care Med.
1992;18(3):142-147.
82. Kuntscher MV, Czermak C, Blome-Eberwein S, et al.
Transcardiopulmonary thermal dye versus single thermodilution
methods for assessment of intrathoracic blood volume and
extravascular lung water in major burn resuscitation. J Burn Care
Rehabil. 2003 May-Jun;24(3):142-147.
83. Holm C, Melcer B, Horbrand F, Worl H, et al. Intrathoracic
blood volume as an end point in resuscitation of the severely
burned: an observational study of 24 patients. J Trauma. 2000
Apr;48(4):728-734.
84. Porter JM, Ivatury RR. In search of the optimal end points of
resuscitation in trauma patients: a review. J Trauma. 1998
May;44(5):908-914.
85. Holm C, Melcer B, Horbrand F, et al. Haemodynamic and
oxygen transport responses in survivors and non-survivors
following thermal injury. Burns. 2000 Feb;26(1):25-33.
86. Kaups KL, Davis JW, Dominic WJ. Base deficit as an indicator for
resuscitation needs in patients with burn injuries. J Burn Care
Rehabil. 1998 Jul-Aug;19(4):346-348.
87. Robbins MR, Smith RS, Helmer SD. Serial pHi measurement as
a predictor of mortality, organ failure, and hospital stay in
surgical patients. Am Surg. 1999 Aug;65(8):715-719.
88. Engrav LH, Colescott PL, Kemalyan N, et al. A biopsy of
the use of the Baxter formula to resuscitate burns or do we do it
like Charlie did it? J Burn Care Rehabil. 2000 Mar-Apr;21(2):
91-95.

Anesthesia for burned patients
198.e3
© Copyright 2012 Elsevier, Inc. All rights reserved.
89. Pirson J, Zizi M, Jacob E, et al. Acute ischemic optic neuropathy
associated with an abdominal compartment syndrome in a burn
patient. Burns. 2004 Aug;30(5):491-494.
90. Greenhalgh DG, Warden GD. The importance of intra-
abdominal pressure measurements in burned children. J Trauma.
1994 May;36(5):685-690.
91. Ivy ME, Atweh NA, Palmer J, et al. Intra-abdominal hypertension
and abdominal compartment syndrome in burn patients. J
Trauma. 2000 Sep;49(3):387-391.
92. Ivatury RR, Sugerman HJ, Peitzman AB. Abdominal
compartment syndrome: recognition and management. Adv Surg.
2001;35:251-269.
93. Oda J, Ueyama M, Yamashita K. Effects of escharotomy as
abdominal decompression on cardiopulmonary function and
visceral perfusion in abdominal compartment syndrome with
burn patients. J Trauma. 2005;59(2):368-373.
94. Corcos AC, Sherman HF. Percutaneous treatment of secondary
abdominal compartment syndrome. J Trauma. 2001
Dec;51(6):1062-1064.
95. Santos AP, Wilson AK, Hornung CA, et al. Methamphetamine
laboratory explosions: a new and emerging burn injury. J Burn
Care Rehabil. 2005 May-Jun;26(3):228-232.
96. Warner P, Connolly JP, Gibran NS, et al. The methamphetamine
burn patient. J Burn Care Rehabil. 2003 Sep-Oct;24(5):275-278.
97. Danks RR, Wibbenmeyer LA, Faucher LD, et al.
Methamphetamine-associated burn injuries: a retrospective
analysis. J Burn Care Rehabil. 2004 Sep-Oct;25(5):425-429.
98. Mitka M. Meth lab fires put heat on burn centers. JAMA. 2005
Oct 26;294(16):2009-2010.
99. Cooper D, Souther L, Hanlon D. Public Health consequences
among first responders to emergency events associated with
illicit methamphetamine laboratories—selected states. JAMA.
1996–1999;284(21):2715-2716.
100. Davies MP, Evans J, McGonigle RJ. The dialysis debate: acute
renal failure in burns patients. Burns. 1994 Feb;20(1):71-73.
101. Davies DM, Pusey CD, Rainford DJ, et al. Acute renal failure in
burns. Scand J Plast Reconstr Surg. 1979;13(1):189-192.
102. Cameron JS. Disturbances of renal function in burnt patients.
Proc R Soc Med. 1969 Jan;62(1):49-50.
103. Mustonen KM, Vuola J. Acute renal failure in intensive care burn
patients (ARF in burn patients). J Burn Care Res. 2008 Jan-Feb;
29(1):227-237.
104. Jeschke MG, Barrow RE, Wolf SE, et al. Mortality in burned
children with acute renal failure. Arch Surg. 1998 Jul;133(7):
752-756.
105. Holm C, Horbrand F, von Donnersmarck GH, et al. Acute renal
failure in severely burned patients. Burns. 1999 Mar;25(2):
171-178.
106. Chrysopoulo MT, Jeschke MG, Dziewulski P, et al. Acute renal
dysfunction in severely burned adults. J Trauma. 1999
Jan;46(1):141-144.
107. Herndon DN, Tompkins RG. Support of the metabolic response
to burn injury. Lancet. 2004 Jun 5;363(9424):1895-1902.
108. Wolfe RR. Herman Award Lecture. 1996: relation of metabolic
studies to clinical nutrition—the example of burn injury. Am J
Clin Nutr. 1996 Nov;64(5):800-808.
109. Jeschke MG, Chinkes DL, Finnerty CC, et al. Pathophysiologic
response to severe burn injury. Ann Surg. 2008 Sep;248(3):
387-401.
110. Pereira CT, Herndon DN. The pharmacologic modulation of the
hypermetabolic response to burns. Adv Surg. 2005;39:245-261.
111. Jeschke MG, Finnerty CC, Kulp GA, et al. Combination of
recombinant human growth hormone and propranolol
decreases hypermetabolism and inflammation in severely
burned children. Pediatr Crit Care Med. 2008 Mar;9(2):209-216.
112. Wilmore DW, Long JM, Mason AD Jr, et al. Catecholamines:
mediator of the hypermetabolic response to thermal injury. Ann
Surg. 1974 Oct;180(4):653-669.
113. Jeschke MG, Mlcak RP, Finnerty CC, et al. Burn size determines
the inflammatory and hypermetabolic response. Crit Care.
2007;11(4):R90.
114. Hart DW, Wolf SE, Chinkes DL, et al. Effects of early excision
and aggressive enteral feeding on hypermetabolism, catabolism,
and sepsis after severe burn. J Trauma. 2003 Apr;54(4):755-761;
discussion 61-4.
115. Liusuwan RA, Palmieri TL, Kinoshita L, et al. Comparison of
measured resting energy expenditure versus predictive equations
in pediatric burn patients. J Burn Care Rehabil. 2005 Nov-
Dec;26(6):464-470.
116. Williams FN, Herndon DN, Jeschke MG. The hypermetabolic
response to burn injury and interventions to modify this
response. Clin Plast Surg. 2009 Oct;36(4):583-596.
117. Andel D, Kamolz LP, Donner A, et al. Impact of intraoperative
duodenal feeding on the oxygen balance of the splanchnic
region in severely burned patients. Burns. 2005 May;31(3):
302-305.
118. Hart DW, Wolf SE, Chinkes DL, et al. Determinants of skeletal
muscle catabolism after severe burn. Ann Surg. 2000
Oct;232(4):455-465.
119. Barrow RE, Hawkins HK, Aarsland A, et al. Identification of
factors contributing to hepatomegaly in severely burned
children. Shock. 2005 Dec;24(6):523-528.
120. Langouche L, Van den Berghe G. Glucose metabolism and
insulin therapy. Crit Care Clin. 2006 Jan;22(1):119-129, vii.
121. Pham TN, Warren AJ, Phan HH, et al. Impact of tight glycemic
control in severely burned children. J Trauma. 2005
Nov;59(5):1148-1154.
122. Ouattara A, Lecomte P, Le Manach Y, et al. Poor intraoperative
blood glucose control is associated with a worsened hospital
outcome after cardiac surgery in diabetic patients. Anesthesiology.
2005 Oct;103(4):687-694.
123. Sessler DI. Perioperative heat balance. Anesthesiology. 2000
Feb;92(2):578-596.
124. Wallace BH, Caldwell FT Jr, Cone JB. The interrelationships
between wound management, thermal stress, energy
metabolism, and temperature profiles of patients with burns.
J Burn Care Rehabil. 1994 Nov-Dec;15(6):499-508.
125. Caldwell FT Jr, Wallace BH, Cone JB. The effect of wound
management on the interaction of burn size, heat production,
and rectal temperature. J Burn Care Rehabil. 1994 Mar-Apr;
15(2):121-129.
126. Caldwell FT Jr, Graves DB, Wallace BH. Pathogenesis of fever in
a rat burn model: the role of cytokines and lipopolysaccharide.
J Burn Care Rehabil. 1997 Nov-Dec;18(6):525-530.
127. Caldwell FT Jr, Graves DB, Wallace BH. Chronic indomethacin
administration blocks increased body temperature after burn
injury in rats. J Burn Care Rehabil. 1998 Nov-Dec;19(6):501-511.
128. Shiozaki T, Kishikawa M, Hiraide A, et al. Recovery from
postoperative hypothermia predicts survival in extensively
burned patients. Am J Surg. 1993 Mar;165(3):326-330;
discussion 31.
129. Pereira CT, Murphy KD, Herndon DN. Altering metabolism.
J Burn Care Rehabil. 2005 May-Jun;26(3):194-199.
130. Zawacki BE, Spitzer KW, Mason AD Jr, et al. Does increased
evaporative water loss cause hypermetabolism in burned
patients? Ann Surg. 1970 Feb;171(2):236-240.
131. Vanni SM, Braz JR, Modolo NS, et al. Preoperative combined
with intraoperative skin-surface warming avoids hypothermia
caused by general anesthesia and surgery. J Clin Anesth. 2003
Mar;15(2):119-125.
132. Davis SL, Shibasaki M, Low DA, et al. Sustained impairments in
cutaneous vasodilation and sweating in grafted skin following
long-term recovery. J Burn Care Res. 2009 Jul-Aug;30(4):
675-685.
133. Davis SL, Shibaski M, Low DA, et al. Impaired cutaneous
vasodilation and sweating in grafted skin during whole body
heating. J Burn Care Res 2007;28:427-434.

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198.e4
© Copyright 2012 Elsevier, Inc. All rights reserved.
134. Jaehde U, Sorgel F. Clinical pharmacokinetics in patients with
burns. Clin Pharmacokinet. 1995 Jul;29(1):15-28.
135. Bonate PL. Pathophysiology and pharmacokinetics following
burn injury. Clin Pharmacokinet. 1990 Feb;18(2):118-130.
136. Martyn JA, Abernethy DR, Greenblatt DJ. Plasma protein
binding of drugs after severe burn injury. Clin Pharmacol Ther.
1984 Apr;35(4):535-539.
137. Blaschke TF. Protein binding and kinetics of drugs in liver
diseases. Clin Pharmacokinet. 1977 Jan-Feb;2(1):32-44.
138. Loirat P, Rohan J, Baillet A, et al. Increased glomerular filtration
rate in patients with major burns and its effect on the
pharmacokinetics of tobramycin. N Engl J Med. 1978 Oct 26;
299(17):915-919.
139. Glew RH, Moellering RC Jr, Burke JF. Gentamicin dosage in
children with extensive burns. J Trauma. 1976 Oct;16(10):819-
823.
140. Perry SI. Analgesia and morphine disposition in burn patients.
J Burn Care Rehabil. 1983;4:276-279.
141. Furman WR, Munster AM, Cone EJ. Morphine pharmacokinetics
during anesthesia and surgery in patients with burns. J Burn Care
Rehabil. 1990 Sep-Oct;11(5):391-394.
142. Moncrief JA. Complications of burns. Ann Surg. 1958 Apr;
147(4):443-475.
143. Tolmie JD, Joyce TH, Mitchell GD. Succinylcholine danger
in the burned patient. Anesthesiology. 1967 Mar-Apr;28(2):
467-470.
144. Schaner PJ, Brown RL, Kirksey TD, et al. Succinylcholine-induced
hyperkalemia in burned patients. 1. Anesth Analg. 1969 Sep-Oct;
48(5):764-770.
145. Martyn JA, Szyfelbein SK, Ali HH, et al. Increased d-tubocurarine
requirement following major thermal injury. Anesthesiology. 1980
Apr;52(4):352-355.
146. Martyn JA, Liu LM, Szyfelbein SK, et al. The neuromuscular
effects of pancuronium in burned children. Anesthesiology. 1983
Dec;59(6):561-564.
147. Martyn JA, Matteo RS, Szyfelbein SK, et al Unprecedented
resistance to neuromuscular blocking effects of metocurine with
persistence after complete recovery in a burned patient. Anesth
Analg. 1982 Jul;61(7):614-617.
148. Kim C, Fuke N, Martyn JA. Burn injury to rat increases nicotinic
acetylcholine receptors in the diaphragm. Anesthesiology. 1988
Mar;68(3):401-406.
149. Martyn JA, White DA, Gronert GA, et al. Up-and-down
regulation of skeletal muscle acetylcholine receptors. Effects on
neuromuscular blockers. Anesthesiology. 1992 May;76(5):822-
843.
150. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia
in acquired pathologic states: etiologic factors and molecular
mechanisms. Anesthesiology. 2006 Jan;104(1):158-169.
151. Viby-Mogensen J, Hanel HK, Hansen E, et al. Serum
cholinesterase activity in burned patients. II: anaesthesia,
suxamethonium and hyperkalaemia. Acta Anaesthesiol Scand.
1975;19(3):169-179.
152. McCaughey. Hazards of anesthesia for the burned child. Anesth
Soc J. 1962;9:220-233.
153. Yentis SM. Suxamethonium and hyperkalaemia. Anaesth Intensive
Care. 1990 Feb;18(1):92-101.
154. MacLennan N, Heimbach DM, Cullen BF. Anesthesia for major
thermal injury. Anesthesiology. Sept 1998;89:749-770.
155. Gronert GA. Succinylcholine hyperkalemia after burns.
Anesthesiology. 1999 Jul;91(1):320-322.
156. MacLenna N, Heimbach DM, Cullen BF. Succinylcholine
hyperkalemia after burns. Anesthesiology. 1999;91:320.
157. Martyn JA. Succunylcholine hyper-kalemia after burns.
Anesthesiology. 1999;91:321-322.
158. Brown TC, Bell B. Electromyographic responses to small doses of
suxamethonium in children after burns. Br J Anaesth. 1987 Aug;
59(8):1017-1021.
159. Han T, Kim H, Bae J, et al. Neuromuscular pharmacodynamics
of rocuronium in patients with major burns. Anesth Analg. 2004
Aug;99(2):386-392, table of contents.
160. Werba AE, Neiger FX, Bayer GS, et al. Pharmacodynamics of
mivacurium in severely burned patients. Burns. 1996 Feb;22(1):
62-64.
161. Martyn JA, Chang Y, Goudsouzian NG, et al Pharmacodynamics
of mivacurium chloride in 13- to 18-yr-old adolescents with
thermal injury. Br J Anaesth. 2002 Oct;89(4):580-585.
162. Hu OY, Ho ST, Wang JJ, et al. Evaluation of gastric emptying in
severe, burn-injured patients. Crit Care Med. 1993;21:527-531.
163. Esch O, Lang J, Herbert ME. Effects of propofol anesthesia and
nasal continuous positive airway pressure in humans
Anesthesiology. 1996;84:275-278.
164. Lang J, Herbert ME, Esch O. Magnetic resonance of the upper
airway: Ketamine preserves airway patency compared to
propofol anesthesia in human volunteers. Anesth Analg.
1997:542.
165. Wilson RD, Nichols RJ, McCoy NR. Dissociative anesthesia with
CI-581 in burned children. Anesth Analg. 1967 Nov-Dec;
46(6):719-724.
166. Alfery DD, Ward CF, Harwood IR, et al. Airway management for
a neonate with congenital fusion of the jaws. Anesthesiology.
1979 Oct;51(4):340-342.
167. Kleeman PP, Jantzen JP, Bonfils P. The ultra-thin bronchoscope
in management of the difficult paediatric airway. Can J Anaesth.
1987 Nov;34(6):606-608.
168. Wrigley SR, Black AE, Sidhu VS. A fibreoptic laryngoscope for
paediatric anaesthesia. A study to evaluate the use of the 2.2 mm
Olympus (LF-P) intubating fibrescope. Anaesthesia. 1995 Aug;
50(8):709-712.
169. Gordon JW. Burn Care protocols: anchoring endotracheal tubes
on patients with facial burns. J Burn Care Rehabil. 1987;8:233-
237.
170. McCall JE, Fischer CG, Schomaker E, et al. Laryngeal mask
airway use in children with acute burns: intraoperative airway
management. Paediatr Anaesth. 1999;9(6):515-520.
171. Hagberg CA, Johnson S, Pillai D. Effective use of the esophageal
tracheal Combitube following severe burn injury. J Clin Anesth.
2003 Sep;15(6):463-466.
172. Sheridan RL, Prelack KM, Petras LM, et al. Intraoperative
reflectance oximetry in burn patients. J Clin Monit. 1995
Jan;11(1):32-34.
173. Bainbridge LC, Simmons HM, Elliot D. The use of automatic
blood pressure monitors in the burned patient. Br J Plast Surg.
1990 May;43(3):322-324.
174. Talke P, Nichols RJ Jr, Traber DL. Does measurement of systolic
blood pressure with a pulse oximeter correlate with conventional
methods? J Clin Monit. 1990 Jan;6(1):5-9.
175. Murray WB, Foster PA. The peripheral pulse wave: information
overlooked. J Clin Monit. 1996 Sep;12(5):365-377.
176. Tavernier B, Makhotine O, Lebuffe G, et al. Systolic pressure
variation as a guide to fluid therapy in patients with sepsis-
induced hypotension. Anesthesiology. 1998 Dec;89(6):1313-1321.
177. Perel A. Assessing fluid responsiveness by the systolic pressure
variation in mechanically ventilated patients. Systolic pressure
variation as a guide to fluid therapy in patients with sepsis-
induced hypotension. Anesthesiology. 1998 Dec;89(6):1309-1310.
178. Slogoff S, Keats AS, Arlund C. On the safety of radial artery
cannulation. Anesthesiology. 1983 Jul;59(1):42-47.
179. Thomas F, Burke JP, Parker J, et al. The risk of infection related
to radial vs femoral sites for arterial catheterization. Crit Care
Med. 1983 Oct;11(10):807-812.
180. Gurman GM, Kriemerman S. Cannulation of big arteries in
critically ill patients. Crit Care Med. 1985 Apr;13(4):217-220.
181. Purdue GF, Hunt JL. Vascular access through the femoral vessels:
indications and complications. J Burn Care Rehabil. 1986;7:448-
450.