Chăm Sóc Và Điều Trị Bỏng Toàn Diện (Total Burn Care – Tập 5)

113.e4 11  •  Treatment of Infection in Burn Patients
159. Surawicz CM, Brandt LJ, Binion DG, et al. Guidelines for diagnosis,
treatment, and prevention of Clostridium difficile infections. Am J Gas­
troenterol. 2013;108(4):478-498, quiz 499.
160. Nassour I, Carchman EH, Simmons RL, Zuckerbraun BS. Novel
management strategies in the treatment of severe Clostridium dif­
ficile infection. Adv Surg. 2012;46:111-135.
161. Neal MD, Alverdy JC, Hall DE, Simmons RL, Zuckerbraun BS. Divert­
ing loop ileostomy and colonic lavage: an alternative to total abdomi­
nal colectomy for the treatment of severe, complicated Clostridium
difficile associated disease. Ann Surg. 2011;254(3):423-427, discus­
sion 427-429.
162. Anderson DK, Dunn DL, Hunter JG, Matthews JB. Schwartz’s Prin­
ciples of Surgery. New York: McGraw-Hill; 2015.
163. Chenoweth C, Saint S. Preventing catheter-associated urinary tract
infections in the intensive care unit. Crit Care Clin. 2013;29(1):19-32.
164. Leon-Villapalos J, Jeschke MG, Herndon DN. Topical management of
facial burns. Burns. 2008;34(7):903-911.
165. Templer J, Renner GJ. Injuries of the external ear. Otolaryngol Clin
North Am. 1990;23(5):1003-1018.
166. Reim M, Redbrake C, Schrage N. Chemical and thermal injuries of
the eyes. Surgical and medical treatment based on clinical and patho­
physiological findings. Arch Soc Esp Oftalmol. 2001;76(2):79-124.
167. Sherman RT. The prevention and treatment of tetanus in the burn
patient. Surg Clin North Am. 1970;50(6):1277-1281.
168. Larkin JM, Moylan JA. Tetanus following a minor burn. J Trauma.
1975;15(6):546-548.
169. Mzezewa S, Jonsson K, Sibanda E, Aberg M, Salemark L. HIV infec­
tion reduces skin graft survival in burn injuries: a prospective study.
Br J Plast Surg. 2003;56(8):740-745.
170. Moreira J. The burden of sepsis in critically ill human immunode­
ficiency virus-infected patients—a brief review. Braz J Infect Dis.
2015;19(1):77-81.

114
Operative Wound Management
MOHAMED E. ISMAIL ALY, MOAYAD DANNOUN, CARLOS J. JIMENEZ,
ROBERT L. SHERIDAN, and JONG O. LEE
12 
Improved mortality, shorter hospital length of stay, and
fewer metabolic complications were noted when early exci­
sion was retrospectively compared with late excision.7 In
another study, 32 children with an average age of 7 years
and mean burn size of 65% (TBSA) who underwent either
total excision or serial debridement were studied. Mortality,
overall blood loss, and cumulative operating time were
equivalent.8 The early excision group, however, had their
length of hospital stay almost halved (97 ± 8 days vs. 57 ±
5 days). Since then, hundreds of children with burns of
more than 30% TBSA treated with early excision have dem­
onstrated a hospital length of stay of less than 1 day/%
TBSA burned.9
Tompkins et al. demonstrated that mortality of adult
burn patients at Massachusetts General Hospital improved
from 24% in 1974 to 7% in the time period from 1979 to
1984 after implementation of prompt eschar excision and
immediate wound closure.10 This study was later expanded
to include 85 patients aged 17–55 years.11 Those patients
aged 17–30 years without inhalation injury showed signifi­
cantly reduced mortality of 9% if treated by early excision,
compared to 45% when treated conservatively. Patients
with a concomitant inhalation injury or aged over 30 years,
however, had no survival benefit from early excision.
In children with burn injuries, Xiao-Wu et al. showed
that delays in the excision of extensive burn were associ­
ated with longer hospitalization, delayed wound closure,
increased rates of invasive wound infection, and increased
incidence of sepsis.12
Munster et al. demonstrated a statistically significant
decrease in hospital length of stay correlating with a
decrease in the interval between surgical interventions over
a 14-year period.13 Other variables such as burn size, inha­
lation injury, and age remained unchanged during the
same time period; mortality rate decreased significantly.
Elderly burn patients have also been shown to benefit
from early excision. Deitch et al. demonstrated that early
surgical excision in patients with an average age of 68 led
to 40% reduction in mean hospital length of stay compared
to the national average and reduced mortality.14 Many
studies show that early excision can be safely performed in
the elderly with clear benefits of reducing hospital length
of stay and the number of septic episodes.15–19
Hypertrophic scar formation is common following burn
injuries, with dark-skinned patients more prone to hyper­
trophic scar development. However the most important
factor in the development of hypertrophic burn scars is
delayed wound healing. Deitch et al. demonstrated that in
wounds requiring more than 10 days to heal, the risk of
hypertrophic scarring is significant and rises to 80% if
healing is delayed beyond 21 days.20 Operative treatment
also limits the duration of pain caused by the burn wound.
Introduction
Surgery for burn injury is a key component to the multidis­
ciplinary care of the burn patient. It usually involves early
procedures such as escharotomy and fasciotomy when indi­
cated, followed by burn excision. Early intervention in the
form of early burn wound excision and grafting has dra­
matically changed the outcome and survival of the burn
patient.1
Following burn injuries, tissues affected, including skin,
promote an inflammatory response at the junction between
the eschar and the underlying viable tissue. The presence
of microorganisms within the eschar attracts polymorpho­
nuclear leukocytes that release large amounts of proteolytic
enzymes and inflammatory mediators. Subsequent enzy­
matic action results in separation of the eschar, leaving
granulation tissue. In large surface area burns, the inflam­
matory response at the burn injury site develops into a sys­
temic response.
Mediators such as prostanoids, thromboxane, histamine,
cytokines, and tumor necrosis factor are produced and
released from the burn site. The serum levels of these medi­
ators increase proportionally to the skin surface area of the
burn. The hypermetabolic response with increased protein
catabolism, increased energy expenditure, weight loss, poor
wound healing, and immune depression continues until the
outpouring of mediators abate.2,3
Advantages of Operative Wound
Management
Early excision and skin grafting to achieve wound closure
have been shown to reduce infection rates, reduce length
of hospital stay, and improve survival in burn patients.
Pediatric burn patients in particular have benefited from
timely surgical intervention.4,5 There has been a remark­
able increase in the total burn surface area (TBSA) associ­
ated with a 50% mortality risk over recent decades. It is
now fairly unusual for a child to succumb to burn injuries
of any size, even in association with an inhalation injury
(Tables 12.1 and 12.2). Early prompt fluid resuscitation,
appropriate critical care, nutritional support, and treat­
ment of infections have also played a major role in this
achievement.
Early operative intervention, however, remains the major
contributor to this major advance in burn care. In 1974,
Burke and colleagues reported on the results of total exci­
sion of full-thickness burns where allografts were applied to
cover burn wounds following excision; allograft rejection
was controlled using immunosuppressants.6

12  •  Operative Wound Management
115
TANGENTIAL EXCISION
Tangential excision, as a technique, is the meticulous
removal of burned skin while preserving underlying viable
tissue. Body contours are better preserved with tangential
excision than with fascial-level excision, which removes
underlying subcutaneous fat; hence, it is the standard exci­
sion technique for burns.
Tangential excision was originally described by Janze­
kovic, who observed that deep skin graft donor sites could
be grafted with thinner split-thickness skin grafts taken
from another area.23 Later she extended this concept to
partial-thickness burns by repeatedly excising thin layers of
the burned skin until viable tissue was reached (Fig. 12.1).
Then split-thickness skin grafts were immediately applied.
The technique of tangential excision and autografting of
partial-thickness burns was a major advance in burn care
at the time. Prior to its introduction, only full-thickness
burns were excised, including subcutaneous fat and accom­
panying lymphatics down to the underlying layer of invest­
ing fascia (Fig. 12.2). Janzekovic analyzed the results of the
use of tangential excision in more than 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 of the burn wound. The Goulian knife,
Watson knife, and the Versajet Hydrosurgery System are
used for tangential excision (Fig. 12.3).25 Deep partial-
thickness burns are debrided down to white, viable dermis
with punctate bleeding. In full-thickness burns, excision
continues layer by layer until viable subcutaneous tissue
with a yellow glistening appearance is encountered. Dull
yellow color, purple discoloration, or thrombosed vessels
indicate nonviable tissues that are not suitable for grafting
and require deeper excision (Fig. 12.4). When excision is
performed on limbs with a pneumatic tourniquet, these fea­
tures are particularly important.
There are noninvasive imaging tools available for predict­
ing burn depth and healing time in adult burns. These
include laser Doppler imaging (LDI), which is the current
gold standard; infrared thermography (IRT); and spectro­
photometric intracutaneous analysis (SIA). LDI uses a low-
intensity laser beam to scan across the tissue surface. Laser
is both absorbed and scattered by tissue matrix and the
blood flow in the vessels. Flux is then determined by process­
ing the photocurrent resulting from both absorbed and
scattered light. The device generates a colored map of the
Table 12.1  Mortality Following Burn Over Time for
Different Age Groups, Shown as the Burn Size at Which
50% Live or Die
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.
From Branski LK, Barrow RE, Herndon DN, unpublished data, 1992–2004.
Table 12.2  Pediatric-Specific Mortality Rates Over Time; Near-Total Early Excision Is the Basis of These Excellent Results.
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.
Mortality and pediatric burn patients, Shriners Burn Institute, Galveston, Texas.
In conclusion, early burn wound excision is lifesaving,
offers improved cosmetic and functional outcomes, and is
cost-effective.
Techniques of Burn
Wound Excision
EXCISION OF A SMALL BURN
Operative intervention is indicated without delay once the
burn injury is determined to be a “deep” injury. Deep burn
injuries are clearly either full-thickness or deep partial-
thickness burns that are unlikely to heal within 3 weeks
and are typically flame or contact burns. Heimbach et al.
noted that deep partial-thickness burns did not convert to
full-thickness burns when topical antimicrobials were used
to control infection.21 Although these wounds eventually
healed after several weeks, they showed persistent blister­
ing, pruritus, hypertrophic scar formation, and poor func­
tional outcomes. These observations prompted a prospective
trial of early excision and grafting versus nonoperative
treatment of indeterminate depth in burns of less than 20%
TBSA.22 Shorter hospitalization, lower cost, and reduced
time away from work, but greater use of blood products
were seen in patients treated with early excision. Those
patients treated nonoperatively required more late skin
grafting to achieve wound closure and developed more
hypertrophic scars.

12  •  Operative Wound Management
116
perfusion.27,28 SIA is used in the diagnosis of pigmented skin
lesions such as melanoma. It uses spectrally filtered images
using polarized light ranging from 400 to 1000 nm. A
complex set of mathematical algorithms determines the
melanin and hemoglobin content of the epidermis and pap­
illary dermis, then presents them in high-resolution images.
wound correlating with the extent of the injury. LDI can be
a useful tool in surgical decision-making in indeterminate-
depth burns.26
IRT uses the heat signature resulting from tissue perfu­
sion to predict the depth of burn injury. Superficial burns
retain a bright color compared to the surrounding normal
tissue due to increased perfusion, whereas deeper burns
appear darker in color due to decreased or lack of
A
B
C
D
Fig. 12.1  (A–D) Schematic representation of tangential excision; sequential slices are taken until punctate hemorrhage is evident (From Janzekovic Z.
A new concept in the early excision and immediate grafting of burns. J Trauma. 1970 Dec;10(12):1103–1108.)
Fig. 12.2  Fascial-level excision using cutting diathermy and an incor­
porated smoke evacuator.
Fig. 12.3  A selection of hand-cutting dermatomes available for use for
tangential excision. Most have the ability to set the aperture to the
desired depth, while the Goulian has a large series of blade changeable
guards.

12  •  Operative Wound Management
117
ischemic areas are transformed into portals for invasive
wound infection. The disadvantages of fascial excision are
lymphedema due to the interruption of the subcutaneous
lymphatics and contour deformities due to the loss of sub­
cutaneous fat.
CONTROLLING BLOOD LOSS DURING
BURN EXCISION
Excision of large burns can result in considerable, if not
massive, blood loss. Tangential excision can lead to large
blood loss unless measures are taken to limit hemorrhage.
The simplest measure is to operate within 24 h of the burn
injury. Vasoactive metabolites, in particular the potent
vasoconstrictor thromboxane, are in abundance during
this time to limit blood loss.32 Desai et al. demonstrated in a
prospective trial of 318 pediatric patients with burns of
more than 30% TBSA that early excision of burns is associ­
ated with an overall reduction in blood loss. The average
blood loss per surface area excised (mL/cm2) was compared
at various post-burn excision time points. The total blood
loss during excision performed within the first 24 hours
after burn was 0.4 mL/cm2 excised, 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 pro­
cedure was performed after the 16th day. Overall mortality
was 5% for an average burn size of 60% TBSA. Early exci­
sion had no adverse effect on mortality. Very early excision
led to a halving of blood loss for both large and small
burns32,33 (Fig. 12.5).
Other factors associated with increased blood loss during
excision of burns are old age, male gender, larger body size,
large full-thickness burns, high wound bacterial count,
total area excised, and operative time.33
Several techniques to reduce blood loss during burn
wound excision can be employed in the operating room.
Adjunctive measures to limit blood loss include tourniquets
for the extremities, pre-debridement tumescent infiltration
with epinephrine solutions, topical application of epineph­
rine 1: 10 000–1: 20 000, fibrin sealant, autologous platelet
The additional analysis of pigment available using SIA may
more accurately indicate the depth of burn compared with
perfusion alone.29
Ultrasounds with frequencies higher than 20 MHz have
shown promising results in quantitative assessment of burn
depth in animal models.30 Currently only LDI has been vali­
dated for use in burn depth assessment.29 It has been shown
to reduce wound healing time in patients requiring surgery
with a potential cost saving of about $1200 per patient.31
Unfortunately LDI costs in excess of $70,000 in addition to
annual servicing costs.
FASCIAL EXCISION
Skin and subcutaneous tissue are excised en-bloc using
electrocautery in fascial excision. This involves excision of
the full thickness of the integument, including all subcuta­
neous tissues down to the investing deep fascia. It is usually
performed to reduce blood loss in extensive burns or in cases
of severe infection to control the source of infection.
Fascial excision can limit the amount of blood loss
because control of the deeper perforating vessels is achieved
during the excision, bypassing the extensive capillary
network present in the skin and subcutaneous tissue.
Fascial excision is also required for areas where subcutane­
ous tissue has been involved in the burn injury. The advan­
tages of this technique include improved graft take on fascia
and reduced blood loss.
Fascial excision is also indicated in cases of life-threatening
invasive wound infection or sepsis, particularly fungal
infections such as Aspergillus and Mucor, and in cases of
failed graft take in extensive burns in critically ill patients.
Episodes of sepsis lead to ischemic necrosis of the subcuta­
neous fat due to poor peripheral perfusion and microvascu­
lar stasis. This represents a considerable problem in patients
with extensive burns leading to late graft loss, and the
Fig. 12.4  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 epi­
nephrine 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.
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
Fig. 12.5  Blood loss is almost halved by operating within 24 hours of
injury. (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):753–759; discussion 759–762.)

12  •  Operative Wound Management
118
application of skin grafts. This may be a practical approach
in cases of large surface area excision, where coagulopathy
can develop due to large blood loss or hypothermia. The
authors of this chapter adhere to a hemoglobin (Hgb)
threshold of 7 for transfusion. One study suggested a pos­
sible decrease in infection rate when compared to a more
liberal transfusion strategy.34
TECHNIQUES OF WOUND CLOSURE
Once procured, the autograft skin can be used in different
ways depending on the size of body surface area burned
that requires grafting.
Autografts are classified as full- or split-thickness depend­
ing on the depth of dermal layer included when harvesting
the skin. Full-thickness autografts have better cosmetic
results and reduced scarring compared to split-thickness
autografts because the dermis provides flexibility and elas­
ticity. The main caveat is that the increased amount of
dermis in the full-thickness autograft can compromise its
own viability during the imbibition, inosculation, and neo­
vascularization phases of graft take. The donor site com­
pletely devoid of dermis must be closed primarily or grafted.
Therefore, split-thickness skin grafts are mainly used in the
treatment of extensive burn injuries.
If the burn is small, skin grafts can be applied without
meshing as a “sheet.” The advantage of nonmeshed skin is
better cosmetic outcomes. The disadvantage is the possible
accumulation of seroma or hematoma underneath the skin
graft that can compromise the apposition of the skin graft
to the wound bed. Seroma or hematoma should be identi­
fied and removed by aspiration with a 25- or 27-gauge
needle. The skin graft can be secured to the wound bed with
quilting sutures or the application of a bolster dressing,
which can reduce shearing of the skin graft. These grafts
are best laid perpendicular to the long axis of limbs, particu­
larly across joint flexural creases, which is in line with the
general rule of placing potential scars perpendicular to the
dominant muscle contraction in the area, thus reducing
the degree of contracture if it occurs. Possible exceptions
are the dorsum of the hand and forearm, where one may
contend that longitudinally placed grafts are cosmetically
superior.
In large burns where donor sites are limited, autografts
are usually meshed. This allows the autograft skin to be
expanded to cover a wider area compared to its original size.
The most commonly utilized mesh ratios are 2 : 1 and 4 : 1,
although other ratios of expansion can be employed. The
main advantages of 2 : 1 meshed autograft skin is the ease
of handling and application and the extensive network of
slits that allows drainage of seroma or hematoma. The
main disadvantage is that the interstices 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 graft requires an overlay
coverage of nonexpanded allograft skin to decrease the risk
of graft loss, and this is applied over the autograft skin in a
sandwich pattern (Fig. 12.7).35 The large interstices, which
require a considerable amount of time to heal by epitheli­
alization; the need for an allograft skin overlay; and the less
desirable cosmetic result limit the use of 4 : 1 meshed auto­
graft skin to massively burned patients. Even in massive
gel, calcium-enriched alginate sheets, and immediate ban­
daging with delayed grafting.
The application of tourniquets to the extremities is a very
effective method of minimizing blood loss, especially for
excision of burns involving hands and digits. As with
tumescent infiltration, the absence of bleeding can make
the estimation of the right depth of excision difficult. To
counteract 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. Fol­
lowing the release of the tourniquet, the limb should be
elevated for about 10 min prior to graft application.
Tumescent solution made of epinephrine containing
saline can be injected into the burn wound prior to excision.
This technique is particularly useful for burn excision of
areas such as 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, and one-way
syringes, such as the Multi-Ad Fluid Dispensing System or
a pneumatic infuser, can make the injection process easier
(Fig. 12.6).
Monitoring the patient’s hemodynamics is necessary
because epinephrine may cause tachycardia and hyperten­
sion, which can worsen bleeding. Another drawback of this
technique is that the lack of bleeding from the wound bed
may make 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 or gauze and compressive bandages.
Delayed grafting after excision is used in some centers to
limit blood loss. In case of delayed skin grafting, the wound
bed needs to be kept moist and clean prior to skin grafting.
The wound can be covered with bulky cotton dressings with
tubes through the dressing to the wound surface for con­
tinuous or intermittent irrigation with antibiotic solution.
The patient returns to the operating room within 24 h and
undergoes a second procedure of procurement and
Fig. 12.6  An infuser device.

12  •  Operative Wound Management
119
treatment of burns can provide the highly desired charac­
teristics of normal dermis. Integra is a dermal substitute
composed of a porous matrix of cross-linked bovine colla­
gen and glucosaminoglycans providing a scaffold for cellu­
lar invasion and capillary growth. It is applied to the wound
bed following burn excision, and the matrix is fully incor­
porated into the wound bed in 2–3 weeks; then, thin split-
thickness autograft skin is applied. Except for a possible
increased risk of infections, the use of Integra is safe and
effective.38 Skin graft take is usually aided by the use of
negative-pressure wound therapy such as VAC Therapy
(Fig. 12.8).39
Another dermal analog available for the treatment of
full-thickness burns is Alloderm, consisting of cadaveric
dermis devoid of cells and epithelial elements. Its applica­
tions are similar to other dermal analogs, and it has shown
favorable results.40
CULTURED EPIDERMAL AUTOGRAFTS
Cultured epidermal autografts (CEA) remain 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 treatment available, given that procurement of
burns, the face, neck, and hands are still grafted with non­
meshed split-thickness skin graft due to the unacceptable
outcome of using widely meshed skin grafts in these areas.
The Meek technique, which was later modified by Kreis
et al., is another tool to cover extremely large burn surface
areas.36,37 It uses autografts cut into small squares with
the aid of a dermatome and a cork board. The squares
are then pressed onto prefolded pleated gauze that is
expanded in all four directions, leaving uniformly distrib­
uted islands of autograft skin that are then applied to the
wound bed. Ratios of expansion can vary from 3 : 1 to 9 : 1.
This technique has similar disadvantages to 4 : 1 meshed
autografts.
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, and the lack of the dermal
layer prevents the healed skin from having the properties of
normal skin. The use of dermal replacements in the
B
Allograft
Autograft
Excised
wound
A
Fig. 12.7  (A) Schematic representation of “sandwich” technique of allograft overlay. (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. (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): 433–438.)

12  •  Operative Wound Management
120
E
D
C
B
A
Fig. 12.8  (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.

12  •  Operative Wound Management
121
sites are limited. A limiting factor to repeat grafting is the
healing time of the donor sites. Donor site healing is a result
of migration and proliferation of the epithelial cells from
hair follicles, sweat glands, and sebaceous glands within the
dermis. Early re-epithelialization after a week can allow
reprocurement of thin split-thickness skin grafts from
donor sites.
MANAGEMENT OF DONOR SITE
Careful management of the donor site is required to expe­
dite wound healing. Smaller donor sites can be treated with
occlusive or adherent dressings such as Opsite or Biobrane.
Another technique is the use of alginate sheets or hydrocol­
loid dressings, which produce a moist environment that
promotes healing and diminishing pain. The wounds can
be also covered with gauze impregnated with an oil-based
ointment. The most common examples are Xeroform or
locally prepared dressing containing olive oil, petrolatum,
lanolin, and the chemotactic agent “Sudan red.” Silver-
impregnated dressings such as Acticoat, Mepilex Ag, or
Aquacel Ag seem to diminish bacterial overgrowth and can
be used directly on the donor site. The healing time of donor
sites depends on the depth of skin graft, vascularity of the
donor site, wound management, and general condition of
the patient.
DRESSINGS
After burn excision and skin grafting, the grafts are covered
with nonadherent dressings. At our institution, gauze
impregnated with a petrolatum-based ointment and a
mixture of an antibacterial (Polymyxin/Bacitracin) and an
antifungal (Mycostatin) is used. This is followed by the
placement of a layer of fluff gauze and an elastic bandage.
With areas of the body prone to shearing, such as the back
and axilla, the application of a bolster dressing to protect
the skin grafts can be beneficial. The application of negative-
pressure wound therapy can also be useful in splinting and
protecting the grafts. Dressings are usually removed on
postoperative day 3. This time frame is normally sufficient
to allow for adherence of the skin graft to the wound bed.
TEMPORARY SKIN SUBSTITUTES
Providing wound coverage with skin substitutes, even if it
is temporary, has many advantages. Wound coverage pre­
vents water and electrolyte losses as well as tissue desicca­
tion, therefore maintaining a moist environment that
allows faster epithelial cell migration and proliferation.
Other benefits include reducing pain, creating a barrier to
bacterial contamination, and preventing protein loss. Avail­
able temporary skin substitutes are either biological, such
as allografts, xenografts, or amniotic membrane, or artifi­
cial, such as Biobrane.
Allografts remain an effective temporary burn wound
coverage after excision if autograft skin is not available.48
Allograft skin can be stored in a cryopreserved state for
an extended period of time and become adherent and
vascularized when applied to a viable wound bed. This
process can also serve as a test for wound bed viability
after burn excision, with immune rejection occurring
the unburned skin will not be sufficient to cover the patient’s
wounds.
Munster has shown that the use of CEA in the massively
burned patient reduced mortality.41 CEA requires two 2 ×
6-cm full-thickness unburned skin specimens. The skin is
processed and cultured in vivo in the presence of murine
fibroblasts to promote growth. The culture is expanded over
a period of 3 weeks until thin sheets of keratinocytes, 2–8
cells thick, are available for grafting. Shearing and blister­
ing are common problems for many months following
application. The long-term survival of CEA in extensively
burned patients has been reported at between 5% and 50%
in the literature, and CEA applied to areas such as the back,
buttocks, and posterior lower extremities are prone to
shearing and graft loss. Barret et al. compared the use of
CEA with widely meshed autograft skin and allograft skin
overlay in a group of children with more than 90% TBSA.42
Once healed, the CEA has a better cosmetic result than
healed 4 : 1 meshed autograft skin but is associated with
longer hospital length of stay and increased number of
reconstructive procedures. Despite these limitations, includ­
ing substantial cost, series from different burn centers have
shown promising results when used in conjunction with
allograft dermis. Sood et al. reported a graft take rate of
greater than 72%.43
Tissue engineering technology is a rapidly advancing
field where fetal skin constructs have been successfully
introduced 44 and reproduced in vitro using genetic replica­
tion.45 Bilaminar cultured skin substitutes showed promis­
ing results,46 and, recently autologous engineered skin
substitutes reduced mortality and requirements for donor
skin in full-thickness burns of greater than 50% TBSA.47
SKIN PROCUREMENT
Many factors are considered when choosing the best donor
site for skin grafting. Donor sites represent new wounds that
would add significant morbidity to the patient; patients
usually complain of more pain at the donor site compared
to the burn wound or graft site. Whenever possible, skin
grafts should be obtained from donor sites matching the
color of the recipient area. The face and neck should be
grafted with skin obtained 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 faster healing, given the rich
blood supply. The subsequent scar can be hidden after the
regrowth of hair.
Good quality skin grafts of consistent depth are obtained
using an electric or pneumatic-powered dermatome. The
depth of the skin harvest can be precisely adjusted, with
thickness usually between 0.006 and 0.018 inches.
Patients with extensive burns have few potential avail­
able donor sites. Anatomical regions that are usually spared
and represent viable options for skin graft are the axilla, the
mons pubis, and the scrotum. Given the irregular topogra­
phy, tumescent fluid can be infiltrated to facilitate skin graft
procurement.
In extensively burned patients, multiple operations are
required to achieve complete wound coverage since donor

12  •  Operative Wound Management
122
EXTENSIVE BURNS
Patients with burns of greater than 40% TBSA pose unique
challenges with increased demands for donor sites, which
are of limited availability. Ideally, near-total excision should
be completed as soon as possible in the first few days follow­
ing injury, definitely within a week. The back, buttocks, and
posterior thighs are covered with autograft skin taken at
thickness between 0.008 and 0.010 inch and meshed at an
expansion ratio of 4 : 1. Allografts are the best option to
apply as an overlay to protect widely meshed autografts.
Consideration needs to be given to the use of dermal
replacement therapies (e.g., Integra). Dermal replacements
are an expensive option but produce good results in relation
to scarring. Integra is a bilaminar composite that has a neo-
dermis of bovine collagen held in a matrix pattern of shark
cartilage chondroitin-6-sulfate. A layer of rubberized sili­
cone is press sealed as a top layer. The abdomen, anterior
thigh, forearm, leg, and male chest are sites where Integra
can be easily applied (Fig. 12.9).
. The neo-dermis is vascularized from the underlying
wound bed, and the process takes 2–3 weeks to complete.
The neo-dermis often develops a pink or plum color due to
staining of the matrix during the vascularization process.
If hematoma or seroma develops, it can be aspirated with a
27-gauge needle, or the overlying Integra is incised, the
hematoma removed, and the edges are stapled down.
The neo-dermis is “ready” or adequately vascularized
when it has a straw color. Close inspection under magnifica­
tion will reveal widespread telangiectasia. The second-stage
operation involves gentle removal of the silicone layer and
application of 0.006-inch autograft skin, which can be
meshed up to an expansion ratio of 3 :1. CEA has been used
as epidermal cover for vascularized Integra neo-dermis.55
Debate continues regarding the role of Integra in wound
coverage of patients with burns of greater than 70% TBSA.
The incidence of failure due to infection rises dramatically as
the burn size approaches greater than 75% TBSA. The first
priority remains excision of all the burn wounds, wound
coverage with autografts, and application of allografts to
the remaining areas, with a return to the operating room
planned once used donor sites are healed.
The Operating Room
The burn operating room is usually an extension of the
burn intensive care unit. Large, heated, 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.
A very important perioperative issue for safe manage­
ment of a patient undergoing extensive burn excision is the
maintenance of body temperature. The patient is usually
completely exposed with little intact skin, particularly after
procurement of donor skin, leading to rapid heat loss. A
number of strategies can be used to counteract heat loss
and maintain normothermia. The operating room should
be warmed to 32°C, since the latent heat of water evapora­
tion is 31.5°C. Above this temperature, the energy source
for evaporation will come from the environment rather
than the patient. Radiant heaters are useful in perioperative
thermoregulation. Other adjunctive measures include the
use of space blankets, aluminum foil coverings, plastic
3–4 weeks after application. When allografts are used as
a temporary coverage to the face and hands, they should
be applied as sheet grafts. This prevents the formation of
granulation tissue between the interstices, which can cause
scarring and poor cosmetic outcome following definitive
autografting.
Xenografts are another option for temporary wound cov­
erage. Only porcine xenograft skin is currently available for
clinical use.49 Their main application is on partial-thickness
burns following superficial debridement, as well as on donor
sites. As with allografts, xenografts become adherent and
provide the benefits of temporary wound coverage, such as
pain control, while the underlying wound re-epithelializes,
but the xenograft does not vascularize.
Amniotic membrane can also be used to provide tempo­
rary coverage to superficial burns. Given its flexibility and
pliability, amniotic membrane is useful for application on
irregular surfaces such as the face. Despite not reducing
healing time or scarring, it provides some of the benefits of
wound coverage and reduces the number of dressing
changes required until healing is achieved.50
Management of Specific Types
of Burns
SCALD BURNS
Small or moderate size scald burns 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 on
in the second or third week post burn.51
A subsequent prospective trial randomized 24 children to
early or late excision if their scald burn was of clinically
indeterminate depth.52 There was no significant wound
infection or sepsis resulting from late excision. Only half of
the delayed excision group ultimately required surgical
intervention, and a significantly smaller area of excision
was necessary.
In light of the previous evidence, children with scald
burns of less than 20% TBSA can be appropriately treated
with a topical antimicrobial such as silver sulfadiazine for
about 2 weeks. This approach needs to be balanced with the
knowledge that the longer a wound remains open, the
greater the inflammatory response and subsequent scar for­
mation. A number of techniques are available to cover the
partial-thickness burn. When successful, they have the
advantage of reducing the pain associated with frequent
dressing changes. Biobrane is a useful dressing for smaller
and more superficial wounds.53
At the time of the first wound dressing application, all
loose skin and blisters are removed to leave a clean, moist
surface. Biobrane is a nylon/silicone bilaminated composite
skin substitute that becomes adherent to the exposed
dermis, thereby acting as a neo-epidermis. Lal et al. reported
no increase in infection rates using Biobrane.54 Infections
occur rarely as a result of nonadherence and accumulation
of fluid. Other alternatives include the use of silver-
impregnated dressings such as Acticoat, allografts, and
xenografts.

12  •  Operative Wound Management
123
normal serum levels, and this was an indication of the net
positive protein balance.56 The usual hospital length of stay
of 42 days for a 30 kg patient with a 60% TBSA burn was
reduced to 32 days. This remarkable decrease in length of
hospital stay produced a net saving of 15% in total hospital
costs, and mortality was reduced from 45% to 8%.57
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 extensively burned
pediatric population in North America.58 Other anabolic
agents have shown promise as a means of stimulating
wound healing in severely injured catabolic burn patients.59
Oxandrolone 20 mg/day has demonstrated a positive effect
on protein kinetics and wound healing in clinical trials.60,61
In oxandrolone-treated severely burned adults, donor site
healing was accelerated by 20% compared to nontreated
patients.59 Although these pharmacological agents provide
great support to the extensively burned patient, they are
only an adjunct to early near-total excision and prompt
wound coverage.
Operative Management of Burns
Involving Special Areas
THE HAND
Survival after serious burns has improved dramatically over
the past 30 years; however despite generally satisfactory
long-term quality of life, many patients will have significant
physical disabilities. Many of these disabilities can be traced
to compromised hand function following severe burn
sheets over the head and face, and heated intravenous fluids
at 38°C. Repeated applications of warm sterile blankets,
forced air warming systems, warm irrigation fluids, and
active heating via either infrared or ceramic heaters have
also been used.
The ideal operating room environment should allow only
minimal evaporative loss from the patient. Reliable vascular
access is required, and the central access lines should be
sutured securely to prevent dislodgment during patient
positioning.
The Operation
At our institution, excision commences with the patient in
the prone position, during which excision of the shoulders,
back, buttocks, and upper thighs is performed. Wide-
meshed autografts with allograft overlay are applied. If
insufficient autografts are available, the excised wound is
covered with allografts. Other alternatives include skin sub­
stitutes such as Integra, xenografts, or allografts. Dermal
replacement materials are prone to failure due to increased
rates of infection in extensive burns, particularly on dorsal
surfaces, but can be applied selectively on ventral surfaces.
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 skin grafts on the back and buttocks.
The patient is then placed in the supine position
As soon as donor sites are healed, patients return to the
operating room for further autografting and replacement of
nonadherent allografts or infected skin substitutes. In chil­
dren with considerably extensive burns, treatment with
recombinant human growth hormone (GH) demonstrated
donor site wound healing was accelerated by 25%. GH-
treated patients required less infused albumin to maintain
B
A
Fig. 12.9  (A,B) High-voltage electrical flash burn treated by fascial excision and Integra. Flat anterior surfaces are particularly amenable to use of Integra.

12  •  Operative Wound Management
124
amputation if digital escharotomies were performed on cir­
cumferentially burned digits.62 However, particularly in
small children, improperly performed digital escharotomies
can result in significant injury, and therefore caution must
be used. When digital perfusion remains inadequate despite
decompression of the arm, forearm, and hand, escharoto­
mies of full-thickness burns of the digits should be per­
formed. Longitudinal incisions are carefully made with
pinpoint electrocautery mid-laterally between the neuro­
vascular bundle and the dorsal extensors, avoiding both
structures. A single longitudinal incision is made on the
radial aspects of the thumb and little finger and the ulnar
aspects 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. 12.10B).
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. 12.10C).63 Meticulous hemostasis is
maintained throughout the procedure, and the outcome of
decompression is confirmed using Doppler.
Escharotomy can generally be performed at the bedside
or in the emergency department under moderate seda­
tion supplemented with sub-eschar injections of local
anesthetic. Some patients will require general anesthesia
in the operating room for the procedure to be performed
appropriately.
Fasciotomy might be required for edema developing
within the fascial compartments of the forearm and hand.
Clinically this is often seen following high-voltage electrical
injuries or exceptionally deep thermal injuries. Upper
extremity fasciotomy may include volar and dorsal decom­
pression, carpal tunnel release, and dorsal hand fasciotomy.
A curvilinear incision is ideal for volar exposure of the com­
partments of the forearm. This approach allows access to
all individual muscle bundles in the volar forearm. It also
allows decompression of the carpal tunnel through a
palmar extension of the incision, and creates a well-
vascularized skin flap to cover the median nerve at the wrist
injuries. If optimal function is to be restored after extensive
burn injuries, proper care of the injured hand is essential.
These early efforts should be directed at preservation of
tissue, maintenance of normal hand anatomy, and develop­
ment of a strategy for wound closure.
Escharotomy and Fasciotomy
A critical part of the initial care of hand burn is to maintain
soft tissue perfusion in the acute phase following the burn
injury. Decompression of high compartment pressure
caused by burned skin and tissue edema is an area in which
early surgical intervention can produce a remarkable differ­
ence to the final outcome of hand function. Hands at risk
of ischemia include circumferential or near-circumferential
burns, very deep burns, and any electrical injuries involv­
ing high- or intermediate-range voltage. It is important to
elicit clinical signs of ischemia subtler than the loss of pal­
pable pulse at the wrist. Mean arterial pressure in the
central vascular system is three times higher than capillary
pressure, and blood flow can be maintained in these vessels
despite impaired flow in distal soft tissues. If the hand is
warm, soft, and has pulsatile flow detectable by Doppler in
the palmar arch and the digital vessels, and it has a normal
pulse oximetry signal at the tip of the digit, then flow is
adequate. As flow becomes progressively impaired, the
hand will become firm and cold, with decreased Doppler
flow and loss of the pulse oximetry signal. Decompression
should be performed to prevent otherwise avoidable ische­
mic injury as a result of compartment syndrome. Pressure
measurement confirmation is generally not required if
serial examinations suggest diminished tissue perfusion.
Escharotomy should be performed using electrocautery.
Longitudinally oriented medial and lateral incisions are
made through eschar on the arm and forearm, stopping at
the metacarpophalangeal joints of the first and fifth digits
(Fig. 12.10A).
The hand is then re-examined for perfusion prior to per­
forming hand and digital escharotomies. If blood flow is
restored adequately following arm and forearm decompres­
sion, additional escharotomy may be unnecessary.
The efficacy and safety of digital escharotomies are
debatable. One study demonstrated a reduced incidence of
A
B
C
Fig. 12.10  (A) Arm escharotomy. (B) Hand escharotomy. (C) Finger escharotomy. (From fig. 61.6ABC in Green DP, Pederson WC, Hotchkiss RN, et al. ed.
Green’s operative hand surgery, Philadelphia: Elsevier/Churchill Livingstone; 2005:2164.)

12  •  Operative Wound Management
125
to reduce blood loss, and tangential excision is performed
until a bed of viable tissue is encountered. Viability is rec­
ognized by the appearance of a pearly white moist dermis,
punctate bleeding, or the presence of bright yellow subcu­
taneous fat without thrombosed small vessels or extravas­
cular blood staining. Recognition of viable tissue in an
exsanguinated extremity under tourniquet is an acquired
skill that greatly facilitates low-blood-loss excisions.
The hand is then wrapped in epinephrine-soaked gauze
prior to deflation of the pneumatic tourniquet. After
5–10 min to allow for spontaneous hemostasis, definitive
hemostasis is secured with careful use of pinpoint electro­
cautery. The hand is covered with sheet autograft skin.
Finally grafted hands are covered with a gentle compressive
gauze wrap and placed in a thermoplastic splint in position
of function. Hands are elevated and immobilized for 3–4
days prior to reinstituting passive and active hand therapy.
Only about 15% of palmar burns require grafting.
Because the palmar skin is much thicker than the dorsal
skin, it is not uncommon to wait for 2–3 weeks before a
decision to graft is made. Palmar burns that require skin
grafting are usually covered with thick, split-thickness
sheet autografts if the defect is large, and full-thickness
autografts if the defect is small. In deep palmar burn inju­
ries with loss of range of motion, the hand is splinted
with metacarpophalangeal joints (MCPJ) in exten­
sion, both during topical care of the burn and following
surgery. Skin grafts from the instep area have been advo­
cated for aesthetic reasons, but functional results with
full-thickness or thick split-thickness grafts are generally
acceptable.
upon completion of the fasciotomy. When needed, straight
linear incisions are adequate for decompression of the
dorsal aspect of the forearm, and inter-metacarpal incisions
on the hand allow decompression of the intrinsic muscles
of the hand.
Techniques of Excision and Grafting
It has become increasingly clear that allowing hand injuries
to heal by secondary intention over the course of many
weeks produces poor long-term aesthetic and functional
results.64 Usually surgery is indicated for any deep dermal
or full-thickness hand burn that will not promptly heal
within 3 weeks. This need is apparent to an experienced
examiner within 5 days of the injury (Fig. 12.11).
The skin on the dorsum of the hand is much thinner than
the palmar skin. There is a general consensus that earlier
surgery is associated with a better functional outcome and
a reduced need for reconstructive procedures in the future.
Different options for wound coverage include split-
thickness autografts, full-thickness autografts, and groin or
abdominal flaps. Split-thickness nonmeshed autograft is the
optimal coverage for most hand burns. Full-thickness grafts
are ideally reserved for palmar surface burns, particularly
deep wounds of limited extent, or for reconstructive opera­
tions. Groin and abdominal flaps can be useful when man­
aging isolated injuries with exposed tendons without
paratenon, exposed bone without periosteum, or exposed
neurovascular bundles.
Deep partial and full-thickness hand burns generally
require tangential excision and autografting. These proce­
dures are ideally performed under a pneumatic tourniquet
B
A
Fig. 12.11  Deep dermal burn of the dorsal hand that underwent excision and grafting. (A) Post-burn day 7. (B) 6 weeks post injury.

12  •  Operative Wound Management
126
for 2–3 weeks may facilitate healing with improved stability.
If the overlying extensor mechanism is damaged in an open
PIPJ, a partially functional joint can sometimes be salvaged
by K-wire fixation for 2–3 weeks, which may allow granula­
tion tissue to bridge the open joint; this can subsequently be
skin-grafted.
Techniques to Salvage Length in Fourth-Degree
Hand Burns
In the presence of fourth-degree burns involving the under­
lying extensor mechanism, joint capsule, and bone, man­
agement can be more complex with less satisfactory
outcomes. Patients with small surface area burns are can­
didates for early debridement with groin or abdominal flap
coverage (Fig. 12.12).65
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
Hands are splinted in the position of function: the MCPJ
at 70–90 degrees of flexion, the interphalangeal joints (IPJ)
in extension, the wrist in 20 degrees of extension, and the
thumb in palmar abduction and external rotation. Special
attention should be given to the position of the fifth digit
because it is particularly prone to flexion contractures
resulting in fixed IPJ flexion. In the hand, failure of early
wound closure may compromise the ability to participate in
early physical therapy and possibly compromise long-term
outcomes.
If the extensor mechanism is compromised by direct
injury or subsequent desiccation and rupture, the dorsal
collateral bands migrate volarly, and the proximal interpha­
langeal joint (PIPJ) develops a flexion contracture from
which recovery might be impossible. In some cases, this
unfortunate sequence of events can be prevented by ensur­
ing prompt coverage of the PIPJ. If the depth of injury com­
promises the extensor mechanism, splinting in extension
and inserting axial Kirschner wire (K wires) across the joint
C
B
A
Fig. 12.12  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.

12  •  Operative Wound Management
127
insertion can be helpful to maintain the IPJ position while
metacarpophalangeal joint flexion is maintained with the
splints. Wires are passed axially from the tip of the finger
proximally, stopping when the PIPJ is immobilized. Auto­
grafting is performed whenever possible, and exposed joints
and bones are allowed to granulate and subsequently are
covered with autograft skin (Fig. 12.13). Joints that remain
unstable following coverage are fused by open arthrodesis
at a later stage.
clean, with position of function maintained, often the avas­
cular tissue will granulate and can be skin grafted with an
acceptable result.
When the extensor mechanism is exposed, maintaining
the position of function during granulation tissue forma­
tion is critical to the final outcome. Granulation tissue for­
mation may be facilitated by meticulously debriding
remnants of burned cortical bone. Positioning may not be
reliable when only splints are used, therefore K-wire
C
B
A
Fig. 12.13  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.

12  •  Operative Wound Management
128
is more appropriate to preserve viable dermis, which is
essential for optimal results (Fig. 12.14).
Previously described “water dissectors” such as the Ver­
sajet Hydrosurgery System can also be used in areas of
contour for more controlled and precise excision, thus
avoiding potential injuries to viable deeper layers.
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 an appropriate pre-emptive measure to
reduce blood loss during facial excision.69,70 Epinephrine-
moistened topical sponges are helpful, and electrocautery
can be useful for accurate hemostasis.
Placement of skin grafts on the face should be carried out
with respect to aesthetic units, where sheet autografts are
placed to reconstruct an entire aesthetic unit. For aesthetic
purposes the face is divided into cosmetic units (Fig.
12.15),71 and the periorbital, nasal, and upper cheek areas
THE SCALP
Scalp and skull burns are a major challenge due to the loca­
tion of these injuries representing a complex wound with
the possibility of injury to underlying structures. These
injuries can be classified into two groups: injuries limited to
soft tissue and injuries that involve the calvarium. Surgical
management of the burned scalp can vary from simple soft
tissue debridement and skin grafting to management of
complicated calvarial bone injury.
Scalp burns without bony involvement are treated simi­
larly to any other burn, with debridement and skin grafts
or flap coverage.66 There are several classifications for scalp
burn wounds based on the depth and extent of the injury.
Calvarial burn that does not involve the inner table can be
managed by careful burring and skin grafting. The use of a
fine diamond-tipped drill allows controlled layer-by-layer
removal of nonviable bone without risking penetration into
the intracranial cavity. Complex defects involving full-
thickness bone loss with exposure of the dura will require
reconstruction using local, regional, or free flaps.
The use of bone grafts or tissue expanders is deferred
until after the acute burn phase. The priority is wound
debridement and adequate coverage without compromising
the underlying tissues. Surgical debridement includes the
removal of necrotic soft tissue and bone, avoiding injury to
the dura. Surgical excision stops at a viable layer to apply a
skin graft.
Central nervous system infections are a possible compli­
cation, and antibiotic prophylaxis should be considered
prior to the procedure.
THE FACE
Burns to the face can have potentially devastating conse­
quences to the patient and can adversely impact the patient’s
return to premorbid activity. Attention to details, adequate
excision, wound coverage and postoperative management
are essential in the preservation of vital functions and cos­
mesis.67 Facial burns can involve injuries to vital structures
such as the upper airway and sensory organs such as the
eyes and ears.
There have been no large randomized outcome trials
comparing early excision and grafting of the face compared
to grafting after eschar separation and granulation tissue
formation. Most authors have applied the general principle
of early excision to prevent contractures and provide the
best aesthetic outcome, with a suggested maximal waiting
period of 18 days.68
Once a decision has been made to proceed with excision
and grafting, site and thickness of donor skin need careful
consideration. If possible, the donor skin should be pro­
cured 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 if
taken too deeply and subsequent hair growth of the recipi­
ent site and alopecia of donor site. An alternative site is the
upper back.
Excision of facial burns can be performed using various
methods; the mainstay of excision remains use of the
Goulian/Weck knife. If there are any doubts regarding the
depth of the burn, tangential excision using a Goulian knife
Fig. 12.14  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.
A
B
Fig. 12.15  Aesthetic units of the face. (A) Frontal view. (B) Lateral view.
(From McCauley RL, Obeng MK. Reconstruction of cheek deformities. In:
McCauley RL, ed., Functional and aesthetic reconstruction of burned patients.
Boca Raton, FL: Taylor and Francis Group; 2005: 270.)

12  •  Operative Wound Management
129
GENITAL BURNS
Genital burns can produce significant morbidity and long-
term consequences for mobility, urine elimination, and
sexual function. Spontaneous epithelialization will likely
occur with scald burns in this region owing to the rich
supply of hair follicles and skin appendages.
Recommendations for acute management include selec­
tive urethral catheterization to allow urine collection and
urethral stenting in the case of circumferential constricting
burns.
Most partial-thickness burns of the scrotum will heal
spontaneously because scrotal skin is thick and contains
multiple hair follicles. Testicular function should be evalu­
ated by measuring stimulated testosterone levels if testicu­
lar injury is suspected.78
Small full-thickness burns to the scrotum can be excised
and closed primarily, and large full-thickness burns will
require skin grafting. Along the shaft of the penis, full-
thickness burns are excised using Goulian knife or Versajet
and grafted using unmeshed split-thickness skin grafts.
Full-thickness burns involving foreskin can be managed
with circumcision because phimosis is a common sequela.
Scald burns to the genitalia are best managed conserva­
tively because they are usually partial thickness and heal
with acceptable outcomes. Deep burns to the glans penis
may be allowed to demarcate and proceed to eschar separa­
tion, then the underlying granulation tissue is skin grafted
later. Full-thickness burns to the labia majora should be
excised and grafted as a delayed procedure to avoid scar
contractures in the long term.
Perianal burns are seen in association with extensive
burns in adults and in children with scald burns. Early exci­
sion and grafting is recommended to prevent bacterial colo­
nization and infection from fecal contamination. Some
centers recommend bowel diversion to aid healing and graft
take.79 If skin graft failure occurs, it is important to try
regrafting because prolonged healing time by secondary
intention can cause perianal circular contractures.
THE BREAST
The scarring and disfigurement associated with breast
burns can be a source of significant psychological stress in
developing girls and young women.80 All efforts should be
made to preserve the breast bud in prepubescent girls and
the breast mound in a postpubertal women. 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
particular attention; it is best left un-excised because 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 available
evidence is clear that prompt burn wound excision and
closure is lifesaving for massively burned patients. Skin sub­
stitutes and dermal replacement have made operative
are grafted as a single aesthetic unit.71 Grafts should be
taken as widely as possible to reduce the number of seams
between the grafts, then secured with sutures, glues, or
fibrin sealant.
The use of fibrin sealant, a hemostatic adjunct and adhe­
sive underlay, has been shown in studies to reduce seroma
and hematoma formation as well as minimize the need for
staples or sutures, producing equal or better outcome.72
Medical-grade glue such as 2-cyano-butyl acrylate (Histo­
acryl) can be used to secure the edges of skin grafts.
Once the skin grafts are secured in place, tubes and lines
should be positioned appropriately to avoid disruption of
the grafts. Nasal septal ties can be used to secure the endo­
tracheal tube and avoid facial ties that can disrupt the skin
grafts.
Sheet grafts on the face should be evaluated frequently
for fluid collection or hematoma, which can be drained with
a small-gauge needle. Some centers delay autografting the
face to reduce graft loss from hematoma formation. Tempo­
rary wound coverage with allografts remains a good option
until definitive coverage.73
In areas of extensive soft tissue injury with no underlying
bony injuries, such as the buccal area, acute reconstruction
with regional or free tissue transfer can be considered. If the
maxillary sinuses are exposed, the dead space may be filled
using free vascularized omental transfers, as described in
cases of facial trauma.74
EYELIDS
Deep burns to the eyelids should be excised and grafted early
because they can result in cicatricial ectropion, leading to
lagophthalmos, exposure keratitis, corneal ulceration, and,
ultimately, perforation leading to blindness.75 Post-burn
cicatricial ectropion is a serious complication, with uncon­
scious ventilated patients at particular risk. Release of burn
scars and full-thickness skin grafts to the lower eyelids and
split-thickness skin grafts to the upper lids should be under­
taken as soon as the condition is diagnosed.76
Ophthalmic lubricant drops and ointments should be
applied frequently to keep the eyes moist to avoid exposure
keratitis, especially in unconscious patients. If post-burn
ectropion develops, early tarsorrhaphy or release of the
contracted eyelids may be necessary.
Tarsorrhaphy can be carried out at the bedside under
local anesthesia. A U-stitch is placed using a fine non­
absorbable suture at the lid margin, anterior to the gray
line to avoid corneal irritation. The upper and lower
eyelids are approximated at their lateral and/or medial
portions. Lateral tarsorrhaphy is more commonly used.
The suture should be secured through material such as
a rubber pledget to prevent the suture from being pulled
through skin. The suture should incorporate the ridge of
tarsus but not traverse it, and an adequate tarsorrhaphy
will permit the passive closure of the eyelids to protect
the cornea.
Upper and lower eyelid releases can be carried out using
local flaps, full-thickness skin grafts, or split-thickness skin
grafts. Full-thickness eyelid defects require layered recon­
struction using hard palate mucosa or acellular dermis as
the inner lamella and split skin grafts or local skin flaps as
the outer lamella.77

12  •  Operative Wound Management
130
treatment. J Burn Care Rehabil. 2003;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;209(5):547-553, discussion 552–553.
Janzekovic Z. The burn wound from the surgical point of view. J Trauma.
1975;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;31(4):559-568. (Paper on cultured
epithelia autografts.)
Supp DM, Boyce ST. Engineered skin substitutes: practices and potentials.
Clin Dermatol. 2005;23(4):403-412.
wound care even more accessible in terms of providing tem­
porary wound coverage. This offers an alternative to topical
antimicrobial therapy and conservative management for
full-thickness wounds.
Complete references available online at

Further Reading
Desai MH, Herndon DN, Broemeling L, et al. Early burn wound excision
significantly reduces blood loss. Ann Surg. 1990;211(6):753-759, dis­
cussion 759–762. (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

130.e1
12  •  Operative Wound Management
29. Burke-Smith A, Collier J, Jones I. A comparison of non-invasive
imaging modalities: Infrared thermography, spectrophotometric
intracutaneous analysis and laser Doppler imaging for the assessment
of adult burns. Burns. 2015;41(8):1695-1707.
30. Lin YH, Huang CC, Wang SH. Quantitative assessments of burn
degree by high-frequency ultrasonic backscattering and statistical
model. Phys Med Biol. 2011;56(3):757-773.
31. Hop MJ, Stekelenburg CM, Hiddingh J, et al. Cost-effectiveness of laser
Doppler imaging in burn care in the Netherlands: a randomized con­
trolled trial. Plast Reconstr Surg. 2016;137(1):166e-176e.
32. Desai MH, Herndon DN, Broemeling L, et al. Early burn wound exci­
sion significantly reduces blood loss. Ann Surg. 1990;211(6):753-
759, discussion 759-762.
33. Hart DW, Wolf SE, Beauford RB, et al. Determinants of blood loss
during primary burn excision. Surgery. 2001;130(2):396-402.
34. Jeschke MG, Chinkes DL, Finnerty CC, et al. Blood transfusions are
associated with increased risk for development of sepsis in severely
burned pediatric patients. Crit Care Med. 2007;35(2):579-583.
35. 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;21(6):433-438.
36. Meek CP. Successful microdermagrafting using the Meek-Wall micro­
dermatome. Am J Surg. 1958;96(4):557-558.
37. Kreis RW, Mackie DP, Vloemans AW, Hermans RP, Hoekstra MJ.
Widely expanded postage stamp skin grafts using a modified Meek
technique in combination with an allograft overlay. Burns. 1993;
19(2):142-145.
38. Heimbach DM, Warden GD, Luterman A, et al. Multicenter postap­
proval clinical trial of Integra dermal regeneration template for burn
treatment. J Burn Care Rehabil. 2003;24(1):42-48.
39. McEwan W, Brown TL, Mills SM, Muller MJ. Suction dressings to
secure a dermal substitute. Burns. 2004;30(3):259-261.
40. Sheridan R, Choucair R, Donelan M, et al. Acellular allodermis in
burns surgery: 1-year results of a pilot trial. J Burn Care Rehabil.
1998;19(6):528-530.
41. Munster AM. Cultured skin for massive burns. A prospective, con­
trolled trial. Ann Surg. 1996;224(3):372-375, discussion 375-377.
42. Barret JP, Wolf SE, Desai MH, Herndon DN. Cost-efficacy of cul­
tured epidermal autografts in massive pediatric burns. Ann Surg.
2000;231(6):869-876.
43. Sood R, Balledux J, Koumanis DJ, et al. Coverage of large pediatric
wounds with cultured epithelial autografts in congenital nevi and
burns: results and technique. J Burn Care Res. 2009;30(4):576-586.
44. Hohlfeld J, de Buys Roessingh A, Hirt-Burri N, et al. Tissue
engineered fetal skin constructs for paediatric burns. Lancet.
2005;366(9488):840-842.
45. Pouyani T, Papp S, Schaffer L. Tissue-engineered fetal dermal matri­
ces. In Vitro Cell Dev Biol Anim. 2012;48(8):493-506.
46. Supp DM, Boyce ST. Engineered skin substitutes: practices and poten­
tials. Clin Dermatol. 2005;23(4):403-412.
47. Boyce ST, Simpson PS, Rieman MT, et al. Randomized, paired-site
comparison of autologous engineered skin substitutes and split-
thickness skin graft for closure of extensive, full-thickness burns. J
Burn Care Res. 2016;38(2):61-70.
48. Bondoc CC, Burke JF. Clinical experience with viable frozen human
skin and a frozen skin bank. Ann Surg. 1971;174(3):371-382.
49. Sheridan RL, Tompkins RG. Skin substitutes in burns. Burns.
1999;25(2):97-103.
50. Branski LK, Herndon DN, Celis MM, et al. Amnion in the treatment of
pediatric partial-thickness facial burns. Burns. 2008;34(3):393-399.
51. Irei M, Abston S, Bonds E, et al. The optimal time for excision of scald
burns in toddlers. J Burn Care Rehabil. 1986;7(6):508-510.
52. Desai MH, Rutan RL, Herndon DN. Conservative treatment of
scald burns is superior to early excision. J Burn Care Rehabil.
1991;12(5):482-484.
53. Barret JP, Dziewulski P, Ramzy PI, et al. Biobrane versus 1% silver
sulfadiazine in second-degree pediatric burns. Plast Reconstr Surg.
2000;105(1):62-65.
54. Lal S, Barrow RE, Wolf SE, et al. Biobrane improves wound healing
in burned children without increased risk of infection. Shock.
2000;14(3):314-318, discussion 318-319.
55. Boyce ST, Kagan RJ, Meyer NA, Yakuboff KP, Warden GD. The 1999
clinical research award. Cultured skin substitutes combined with
Integra Artificial Skin to replace native skin autograft and allograft
for the closure of excised full-thickness burns. J Burn Care Rehabil.
1999;20(6):453-461.
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9. Herndon DN, Barrow RE, Rutan RL, et al. A comparison of conserva­
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delayed wound excision and grafting in severely burned children. Arch
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intervention on mortality and cost-effectiveness in burn care, 1978-
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14. Deitch EA, Clothier J. Burns in the elderly: an early surgical approach.
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15. Deitch EA. A policy of early excision and grafting in elderly burn
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16. Kara M, Peters WJ, Douglas LG, Morris SF. An early surgical approach
to burns in the elderly. J Trauma. 1990;30(4):430-432.
17. Scott-Conner CE, Love R, Wheeler W. Does rapid wound closure improve
survival in older patients with burns? Am Surg. 1990;56(1):57-60.
18. Hunt JL, Purdue GF. The elderly burn patient. Am J Surg.
1992;164(5):472-476.
19. Ikeda J, Sugamata A, Jimbo Y, Yukioka T, Makino K. A new surgical
procedure for aged burn victims: applications of dermolipectomy for
burn wounds and donor sites. J Burn Care Rehabil. 1990;11(1):27-31.
20. Deitch EA, Wheelahan TM, Rose MP, Clothier J, Cotter J. Hypertrophic
burn scars: analysis of variables. J Trauma. 1983;23(10):895-898.
21. Heimbach DM. Early burn excision and grafting. Surg Clin North Am.
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22. Engrav LH, Heimbach DM, Reus JL, Harnar TJ, Marvin JA. Early
excision and grafting vs. nonoperative treatment of burns of
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23. Janzekovic Z. A new concept in the early excision and immediate
grafting of burns. J Trauma. 1970;10(12):1103-1108.
24. Janzekovic Z. The burn wound from the surgical point of view.
J Trauma. 1975;15(1):42-62.
25. Klein MB, Hunter S, Heimbach DM, et al. The Versajet water dis­
sector: a new tool for tangential excision. J Burn Care Rehabil.
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26. Park YS, Choi YH, Lee HS, et al. The impact of laser Doppler imaging
on the early decision-making process for surgical intervention in
adults with indeterminate burns. Burns. 2013;39(4):655-661.
27. Prindeze NJ, Fathi P, Mino MJ, et al. Examination of the early diag­
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28. Prindeze NJ, Hoffman HA, Ardanuy JG, et al. Active dynamic ther­
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56. Gilpin DA, Barrow RE, Rutan RL, Broemeling L, Herndon DN. Recom­
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58. Ramirez RJ, Wolf SE, Barrow RE, Herndon DN. Growth hormone
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59. Demling RH, Orgill DP. The anticatabolic and wound healing effects
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60. Wolf SE, Thomas SJ, Dasu MR, et al. Improved net protein balance,
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65. Hanumadass M, Kagan R, Matsuda T. Early coverage of deep hand
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calvarial burns in children. J Trauma. 2003;54(4):765-769.
67. Leon-Villapalos J, Jeschke MG, Herndon DN. Topical management of
facial burns. Burns. 2008;34(7):903-911.
68. Leon-Villapalos J, Eldardiri M, Dziewulski P. The use of human deceased
donor skin allograft in burn care. Cell Tissue Bank. 2010;11(1):
99-104.
69. Hughes WB, DeClement FA, Hensell DO. Intradermal injection of epi­
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Burn Care Rehabil. 1996;17(3):243-245.
70. Sheridan RL, Szyfelbein SK. Staged high-dose epinephrine clysis is safe
and effective in extensive tangential burn excisions in children. Burns.
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71. Acikel C, Peker F, Ulkur E. Skin grafting of the naso-orbital region as
a single aesthetic unit. Burns. 2001;27(7):753-757.
72. Foster K, Greenhalgh D, Gamelli RL, et al. 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;29(2):293-303.
73. Horch RE, Jeschke MG, Spilker G, Herndon DN, Kopp J. Treatment of
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131
Anesthesia for Burned Patients
LEE C. WOODSON, EDWARD R. SHERWOOD, MICHAEL P. KINSKY, MARK TALON,
CAROLINE MARTINELLO, and SUE M. WOODSON
13 
Patients suffering burn injuries often require surgical
treatment for years after the initial injury in order to correct
functional and cosmetic sequelae. Anesthetic management
for reconstructive burn surgery presents many special prob­
lems11 but this chapter 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.
Modern burn care depends on coordination of a multidis­
ciplinary team including surgeons, intensivists, nurse cli­
nicians, nutritionists, rehabilitation therapists, pulmonary
care therapists, and anesthesia providers. Rational and effec­
tive anesthetic management of acute burn patients requires
an understanding of this multidisciplinary approach 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 nonviable
burn wounds, which may harbor pathogens and produce
inflammatory mediators with systemic effects resulting in
cardiopulmonary compromise. After an extensive burn
injury, the systemic effects of inflammatory mediators on
metabolism and cardiopulmonary function reduce physi­
ological reserve, and the patient’s tolerance to the stress of
surgery deteriorates with time. Assuming adequate resusci­
tation, extensive surgery is best tolerated soon after injury,
when the patient is most fit. However it must be recog­
nized that the initial resuscitation of patients with large
burns results in large fluid shifts and may be associated
with hemodynamic instability and respiratory insufficiency.
Reynolds et al. reported that more than half of deaths after
burn injuries occur due to failed resuscitation.6
Effective anesthetic management of patients with exten­
sive burn injuries requires an understanding of the patho­
physiological changes associated with large burns and
careful preoperative evaluation to assure that resuscitation
has been optimized and an appropriate anesthetic plan has
been formulated.
Preoperative Evaluation
The preoperative evaluation of burn patients requires
knowledge of the continuum of pathophysiological changes
that occur in these patients from the initial period after
injury through the time that all wounds have healed. The
dramatic changes that occur in all organ systems following
burn injury directly affect anesthetic management. The fol­
lowing discussion will describe the pathophysiological
changes that occur in the acutely burned patient as they
relate to the preoperative evaluation. In addition to the
routine features of the preoperative evaluation, evaluation
of acute burn patients requires special attention to airway
Videos available at
Introduction
Continuous improvement in burn care since World War
II has 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. Today most patients with more than 80% total
body surface area (TBSA) burned will survive if promptly
treated in a modern burn unit with adequate resources. In
their study of risk factors for death following burn inju­
ries Ryan et al. identified three variables that can be used
to estimate the probability of death: age greater than 60
years, burns of more than 40% TBSA, and the presence
of inhalation injury.2 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.
The incidence of mortality is also influenced by significant
coexisting disease or delays in resuscitation. O’Keefe et al.
observed an approximately twofold higher death risk of
death in women aged 30–59 years compared with 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 One group that has not benefited as
much from advances in burn care is the elderly. The morbid­
ity and mortality (as expressed as lethal dose 50 for burns)
associated with serious burns in elderly patients has not
improved over the past three decades.5 Some burn patients
develop refractory burn shock soon after injury and cannot
be resuscitated.6
Major burn injury results in pathophysiological changes
in virtually all organ systems. Box 13.1 lists and Figs. 13.1
and 13.2 illustrate 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 posterior areas may require turning the
patient to the prone position for optimal access (Fig. 13.1).
Vascular catheters and the endotracheal tube must be
secured with confidence and due care given to these life
lines during patient turning. Several highly informative
reviews of anesthetic management for burn surgery have
been written during the past decade, each with its own
special areas of concentration.7–10

13  •  Anesthesia for Burned Patients
132
Box 13.1  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
Fig. 13.1  Many of the technical challenges regarding airway
management, intravenous access, application of monitors, tempera­
ture regulation, and expectation of extensive bleeding associated with
anesthetic care of patients with major burn injury.
Fig. 13.2  Occasionally patients requiring burn wound excision present
with special needs, as with this 3-day-old patient. Cardiovascular,
hepatic, and renal physiological systems are immature, and vascular
access adequate to keep up with extensive blood loss can be techni­
cally difficult.
Box 13.2  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
Box 13.3  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
management and pulmonary support, vascular access,
adequacy of resuscitation, and associated injuries. The
severely burned patient presents with numerous preopera­
tive concerns, as listed in Box 13.2. The preoperative evalu­
ation must be performed within the context of the planned
operative procedure, which will depend on the location,
extent, and depth of burn wounds; time after injury; pres­
ence of infection; and existence of suitable donor sites for
autografting.
INITIAL EVALUATION OF BURN INJURY
Destruction of skin by thermal injury disrupts the vital
functions of the largest organ in the body. The skin provides
several essential protective and homeostatic functions (Box
13.3). 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 impairment 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

13  •  Anesthesia for Burned Patients
133
must also be assessed. The level of required support may
range from supplemental blow-by or mask oxygen to intu­
bation 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 difficulties with resuscitation, or
ventilator-induced injury. Common pathologies include
upper airway thermal injury, pulmonary parenchyma
damage from chemical irritants or inflammation, and lower
airway obstruction from mucus plugs and epithelial casts,
as well as pulmonary edema due to acute lung injury or
volume overload. With very high levels of PEEP or peak
inspiratory pressure, it must be determined if the anesthesia
ventilator is adequate or if an ICU ventilator will need to be
brought to the operating room. If the patient is intubated
at the time of the preoperative evaluation, it is essential to
know what the indications for intubation were so that an
appropriate plan for postoperative support can be made.
There is general recognition that smoke inhalation injury
increases morbidity and mortality for burn patients.13 The
presence of an inhalation injury in combination with a
cutaneous burn increases the volume of fluid required for
resuscitation by as much as 44%.14 Numerous studies have
also shown an increased incidence of pulmonary complica­
tions (pneumonia, respiratory failure, or acute respiratory
distress syndrome [ARDS]) in patients with burns and inha­
lation injury when compared with burns alone.15 Sequelae
of inhalation injury include upper airway distortion and
obstruction from direct thermal injury as well as impaired
pulmonary gas exchange due to effects of irritant gases on
lower airways and pulmonary parenchyma. These two
components of the inhalation injury have separate time
courses and pathophysiological consequences.
Foley described the findings of 335 autopsies performed
on patients who died from extensive burns.16 Intraoral,
palatal, and laryngeal burns were not uncommon among
patients with inhalation injuries. The most common sites of
laryngeal 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 pro­
tected 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 demon­
strated in an experimental model.17 Inhalation injury to the
lower airways and pulmonary parenchyma is, therefore,
almost always 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, dyspha­
gia, oral and/or nasal soot deposits, or carbonaceous
sputum. The earliest threat from inhalation injury, aside
from asphyxia or systemic poisoning, is upper airway
obstruction due to edema. Early or prophylactic intubation
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
protein depletes plasma proteins when large body surface
areas are injured.
In addition to loss of important functions of the skin,
extensive burns result in an inflammatory response with
systemic effects that alter function in virtually all organ
systems. Preoperative evaluation of the burn patient is
guided largely by a knowledge of these pathophysiological
changes.
Much of the morbidity and mortality associated with
burn injuries are related to the size of the injury. The extent
of the burn injury is expressed as the TBSA burned. Esti­
mates of TBSA burned are used to guide fluid and electro­
lyte therapy and to estimate surgical blood loss. These
estimates can be made with Lund Browder charts developed
from age-specific nomograms (Fig. 13.3). Simplified “Rule
of Nines” charts are available in emergency departments
for rapid estimates of TBSA involvement. A knowledge of
the burn depth is also critical to anticipating physiological
insult as well as planned surgical treatment. First-degree or
superficial second -degree burns may heal without scarring
or deformity and do not require surgical excision. Deeper
second-degree and third-degree burns require surgical
debridement and grafting with associated surgical blood
loss.
Accurate estimates of blood loss are crucial in planning
preoperative management of burn patients. With extensive
wound excision or debridement, large amounts of blood
can be lost rapidly. Adequate preparation in terms of moni­
tors, vascular access, and availability of blood products is
essential. Surgical blood loss depends on area to be excised
(cm2), time since injury, surgical plan (tangential vs. fascial
excision; Fig. 13.4), and presence of infection.12 Blood loss
from skin graft donor sites will also vary depending on
whether it is an initial or repeat harvest. These variables are
valuable predictors of surgical blood loss, which is a critical
factor in planning anesthetic management (Table 13.1).
AIRWAY AND PULMONARY FUNCTION
Special attention must be paid to the airway and pulmonary
function during preoperative evaluation. Burn injuries to
the face and neck can distort anatomy and reduce range of
mobility in ways that make direct laryngoscopy difficult or
impossible. Specific alterations include impaired mouth
opening and 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
make mask ventilation difficult. Inhalation injury may
impair pulmonary gas exchange and lead to respiratory
insufficiency or failure. The level of respiratory support
Table 13.1  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

13  •  Anesthesia for Burned Patients
134
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
Fig. 13.3  Modified Lund and Browder for use at Shriners Hospital, Galveston. Relatively precise estimation of the percent of total body surface area
affected by burns is possible with the use of the chart, which normalizes areas of different surface structures with changes that occur with age. A more
rapid estimate can be made using a “Rule of Nines” chart that only distinguishes between infants and adults.

13  •  Anesthesia for Burned Patients
135
sheep model.26 They observed four discrete but overlapping
phases of injury described as exudative, degenerative, pro­
liferative, and reparative. During the first 48 hours the exu­
dative phase was characterized by polymorphonuclear
(PMN) infiltration, interstitial edema, loss of type I pneumo­
cytes, 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 formation of
pseudomembranes and casts. Hyaline membranes devel­
oped over alveolar surfaces. Macrophages began to accu­
mulate 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
regeneration of epithelium from spared epithelium from the
orifices of glands.
Several reviews provide lucid descriptions of pathophysi­
ological changes resulting from smoke inhalation.27–29
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 decreasing the clearance of airway
debris. These changes lead to further shunt and allow colo­
nization and pneumonia. Treatment for inhalation injury
is empiric and supportive with tracheal intubation and
mechanical ventilation. The application of aggressive pul­
monary toilet, high-frequency percussive ventilation, and
respiratory therapy protocols designed to mobilize obstruct­
ing debris are also highly beneficial. As with treating ARDS,
it has been suggested that reduced tidal volumes and
airway pressures may limit ventilator-induced lung injury
in patients with smoke inhalation injury.30,31 Recently,
however, Sousse et al. examined the effect of reduced tidal
volumes on clinical outcomes in patients with inhalation
injury requiring mechanical ventilation. Historical controls
et al. reported that 51% of their patients exposed to smoke
inhalation did not require intubation.18 Unnecessary intu­
bation in the presence of an inflamed laryngeal mucosa
risks further damage to the larynx and subglottic area.19,20
Traditional clinical predictors of airway obstruction
have been found to be poor predictors of airway compro­
mise in patients with risk factors for inhalation injury.21,22
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 diag­
nosis of acute inhalation injury.23 They described obser­
vations of severe supraglottic injuries associated with
mucosal edema obliterating the piriform sinuses and
causing massive enlargement of the epiglottis and aryte­
noid 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 com­
pliant, edematous mucosa of the aryepiglottic folds, and
arytenoid eminences that prolapsed to occlude the airway
on inspiration.24 Progressive upper airway edema in these
patients was correlated with body surface area burned,
resuscitative volume administered, and rate of infusion of
resuscitative fluids. For patients who are at risk for inhala­
tion injury but lack definitive indications for intubation,
fiberoptic nasopharyngoscopy is effective in identifying
impending airway compromise. Serial exams may help
avoid unnecessary intubations and at the same time iden­
tify progressive inflammatory changes and allow intubation
before severe airway obstruction and emergent conditions
develop.20
Lower airway and parenchymal injuries develop more
slowly than upper airway obstruction. Prior to resuscitation
clinical signs and symptoms relating to respiratory func­
tion, chest x-ray, and blood gas analysis may be within
normal limits despite significant injury that eventually pro­
gresses to respiratory failure requiring intubation and
mechanical ventilation.25
Linares et al. studied the sequence of morphological
changes following smoke inhalation in an experimental
B
A
Fig. 13.4  (A) An important determinant of bleeding is surgical technique. Here the burn wound is excised tangentially with a Watson knife down to
viable tissue, which is recognized by bleeding. (B) Bleeding during burn wound excision is less when the wound is excised down to the fascial layer,
as in this image. Notice also the thick gelatinous layer of edematous tissue beneath the burn wound compared with the unburned tissue at the left
of the image.

13  •  Anesthesia for Burned Patients
136
Sulfur donors such as sodium thiosulphate (adults 25 mL
of 50% solution or pediatrics 1.65 mL/kg of 25% solution)
accentuate the bodies’ enzymatic conversion of cyanide to
thiocyanate in the presence of the mitochondrial enzyme
rhodanese, thus decreasing its toxicity and increasing
elimination.36,37
EFFECT OF BURN INJURY ON CIRCULATION
Thermal injury has profound effects on the systemic circu­
lation, and hemodynamic management is a major compo­
nent of perioperative care. The skills and clinical experience
of anesthesiologists match very well with the needs of
patients presenting with serious burn injury, and anesthe­
siologists are often asked to participate in the initial resus­
citation. Patients may also require surgical intervention
such as escharotomy, fasciotomy, or wound excision during
the first 24 hours after injury; that is, during the initial fluid
resuscitation. Because of this, it is important for anesthesi­
ologists to understand the fundamentals of burn resuscita­
tion. It is also critical for the anesthesiologist to be able to
evaluate the quality of the resuscitation and assess the
hemodynamic status and physiological reserve of the
patient after the initial acute resuscitation. These require
familiarity with phasic changes in cardiovascular function
that follow major burn injuries.
During the first few days after a large burn injury there
is a biphasic change in cardiovascular function. With loss
of fluid from the vascular space, hypovolemia develops
quickly without aggressive replacement. This is associated
with decreased cardiac output and increased systemic resis­
tance. Over the next 2–3 days, if resuscitation is successful,
this pattern is reversed. A hyperdynamic pattern develops
with significantly elevated cardiac output and decreased
systemic vascular resistance. Evaluation of physiological
status and planning for perioperative care requires knowl­
edge of these changes.
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 charac­
terized by decreased cardiac output, increased systemic vas­
cular resistance, and tissue hypoperfusion.38,39 Intravascular
hypovolemia results from alterations in the microcircula­
tion in both burned and unburned tissues, leading to the
extensive loss of intravascular fluid to the interstitium.
Cutaneous lymph flow increases dramatically in the imme­
diate post burn period and remains elevated for approxi­
mately 48 hours.40 The forces responsible for this massive
fluid shift involve all components of the Starling equilib­
rium equation,41
J
K
P
P
v
f
c
if
c
i
=
−
−
−
[
)
)],
(
(
σ π
π
where Kf is the capillary filtration coefficient, Pc is the capil­
lary pressure, Pif is the interstitial hydrostatic pressure, σ s
the reflection coefficient for protein, πc is the plasma colloid
osmotic pressure, and πi the interstitial colloid osmotic pres­
sure. The specific alterations include:
■ Increase in microvascular permeability (kf and σ) due
primarily to the release of local and systemic inflam­
matory mediators;
were patients previously ventilated with tidal volumes of
15 mL/kg. Outcomes of these patients were compared with
current patients receiving 9 mL/kg. Patients in the group
with lower tidal volumes required fewer ventilator days and
had a lower incidence of atelectasis and ARDS.32 Where
the pathophysiology of ARDS relates primarily to alveolar
flooding with protein rich fluid, smoke inhalation injury
involves more small airway obstruction (cast and necrotic
debris) resulting in increased airway resistance, decreased
compliance, and V/Q mismatch. It may be that these two
disease processes require different treatments.
Carbon monoxide (CO) and cyanide are two major toxic
components of smoke. The burn patient with evidence of
smoke inhalation injury should be evaluated for the pres­
ence of toxicity resulting from these compounds. CO binds
hemoglobin 200 times more avidly than oxygen.33 There­
fore CO markedly impairs the association of oxygen with
hemoglobin and decreases oxygen-carrying capacity. CO
also shifts the oxy-hemoglobin dissociation curve to the left,
thus decreasing 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, weak­
ness, and tachycardia. 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 and, in severe cases, hyperbaric treatment to
increase the partial pressure of oxygen in blood.34
Cyanide is also a component of smoke, resulting from the
burning of certain plastic products.35 Cyanide directly
impairs the oxidative apparatus in mitochondria and
decreases the ability of cells to utilize oxygen in metabolism.
These alterations result in conversion to anaerobic metabo­
lism 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.36,37
Treatment of cyanide toxicity begins with a high inspired
oxygen concentration, which may increase intracellular
oxygen tension enough to cause nonenzymatic oxidation
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, intravenous 10 mL of 3% solution for
adults and 0.13–0.33 mL/kg of 3% solution for pediat­
rics) and dimethylaminophenol (3.25 mg/kg) to increase
methemoglobin levels. Methemoglobin competes with
cytochrome oxidase for cyanide. However excessive levels
of methemoglobin lead to decreased 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
pediatrics) is extremely rapid in action but has significant
toxicity, whereas hydroxocobalamin (adults 5–10 g or pedi­
atrics 70 mg/kg), the precursor of vitamin B12, has been
shown to be safe with few systemic side effects, is actively
metabolized by the liver, and avoids renal absorption.

13  •  Anesthesia for Burned Patients
137
develops over the following 2–3 days that is supported by a
variety of inflammatory mediators. This state of systemic
inflammation has been termed the systemic inflammatory
response syndrome (SIRS) and is characterized in burned
patients by tachycardia, a marked decrease in systemic vas­
cular resistance, and increased cardiac output. SIRS is
expressed as a continuum of severity ranging from the pres­
ence of tachycardia, tachypnea, fever, and leukocytosis to
refractory hypotension, and, in its most severe form, shock
and multiple organ system dysfunction. In thermally
injured patients, the most common cause of SIRS is the
burn itself; however, sepsis (SIRS with the presence of infec­
tion or bacteremia) is also a common occurrence.
As a result of these pathophysiological mechanisms,
burns involving more than 20% of the patient’s TBSA will
produce a state of burn shock. In patients with reduced
physiologic reserve this can occur with less extensive burns
(e.g., 10% TBSA burned). Initial survival from this insult
requires aggressive replacement of intravascular fluid. At
the same time overresuscitation can cause serious morbid­
ity which, in extreme cases, can be lethal. Several resuscita­
tion protocols utilizing various combinations of crystalloids,
colloids, or hypertonic fluids have been developed as guides
for administration of the large amounts of fluid needed by
patients with acute burns (Table 13.2). Alvarado and col­
leagues have provided a history of the evolution of these
protocols.57 As these authors point out, little theoretical
progress has been made in our understanding of burn
resuscitation since current protocols were introduced in the
1970s. As a result, considerable controversy continues
regarding such basic decisions as to what fluids to use or
what physiological variables to use to titrate volume replace­
ment. Whereas in the past colloid solutions were often
avoided during the first 24 hours after burn injury, colloids,
especially as albumin or plasma, are returning into favor.
Isotonic crystalloid is still the most commonly used fluid
for resuscitation in U.S. burn centers. The most popular
fluid resuscitation regimen, the Parkland Formula, uses iso­
tonic crystalloid solutions and estimates the fluid require­
ments in the first 24 hours to be 4 mL/kg per TBSA burned.
Another popular formula is the modified Brooke formula
recommending 2 mL/kg per TBSA burned. With both of
these protocols, half is given during the first 8 hours and
half given over the next 16 hours. The American Burn
Association “consensus formula” recommends resuscita­
tion with 2–4 mL/kg/TBSA burned.58
These formulas are only estimates, and fluid require­
ments will vary considerably among patients with similar
percentage of TBSA burned for a variety of reasons; rates
and volumes must be titrated according to the patient’s
response. Fluid administration is generally titrated to main­
tain mean blood pressure above 70 and urine output at
30–50 mL/h in adults and 0.5–1.0 mL/kg per hour in pedi­
atric patients. The use of invasive hemodynamic monitors
allows targeting of determinants of oxygen delivery, which
should intuitively lead to more physiologically precise resus­
citation. Such efforts, however, have not improved clinical
outcome and have generally resulted in more aggressive
fluid administration and consequent overresuscitation.59,60
When evaluating the quality of resuscitation, estimates
of fluid requirements based on these protocols can reveal
significant departure from predicted needs. Review of the
■ Increase in intravascular hydrostatic pressure (Pc) due
to microvascular dilatation;
■ Decrease in interstitial hydrostatic pressure (Pi);
■ Decrease in intravascular oncotic pressure (πc) due to
leakage of protein from the intravascular space
■ Relative increase in interstitial oncotic pressure due to
a smaller decrease in interstitial oncotic pressure (πi)
compared to intravascular oncotic pressure (πc).
The leakage of protein and fluid into the interstitial space
often results in a washout of interstitial colloid and mark­
edly increased lymph flow. The net effect of these changes
is the development of massive edema during the first 24–48
hours after thermal injury with a concomitant loss of intra­
vascular volume. The hypotension associated with burn
injury is also due, in part, to myocardial depression. It has
been 50 years since Baxter and colleagues first described
burn-induced cardiac dysfunction.42 They postulated that a
circulating depressant “factor” was present in the plasma,
resulting in reduced myocardial contractility. Since then,
numerous groups have confirmed similar findings.43,44
Although, this “factor” has not been specifically isolated,
cytokines including tumor necrosis factor-α (TNF-α), inter­
leukin 1-β (IL-1β), gut-derived factors from plasma and
mesenteric lymphatics, and other neurohumoral mediators
have been shown to reduce contractility and relaxation
properties of the heart.45-49 Both systemic activation and
local tissue levels of cytokine expression are responsible for
early burn-induced myocardial depression (first 2–6 hours)
that begins to resolve days within days after injury.47 There
is pronounced synergy among burn injury, sepsis, and
other forms of shock with regard to myocardial depression,
suggesting a common pathway(s) in cardiac dysfunction.
Clinically the incidence of myocardial dysfunction fol­
lowing severe burn injury and its related sequelae remain
somewhat controversial. Studies have often been small,
underpowered, and use differing methodologies, and data
have been collected at different time periods. Indirect assess­
ments of ventricular function throughout the acute resus­
citation period using right heart catheterization found that
left ventricular function was hypocontractile in the context
of high circulating catecholamine levels.6,50 On the other
hand, normal cardiac function has also been reported in the
initial resuscitation period following burn injury. Goodwin
et al., reported an increase in internal fiber shortening
using M-mode echocardiography following burn injury.51
Others reported similar findings at similar time after injury.52
More recently diastolic dysfunction in the resuscitation
period was found to be associated with increased cytokine
levels and death.53 Myocardial injury, indicated by increased
plasma troponin, has also been described and associated
with reduced stroke work and diastolic dysfunction.54
Autopsy data in burns show evidence of myocardial ische­
mia (30–60% cases, for all age groups), suggesting non–
coronary artery causes for ischemia.55 Myocardial ischemia
is likely from reduced supply (tachycardia) and increased
demand (tachycardia + contractility) due to catecholamine
surge and sympathetic activation. Thus cardiac dysfunc­
tion in the early (ICU) phase is likely due to myocardial
stunning since fibrosis would take longer (e.g., months).56
If the patient survives the initial burn shock and is ade­
quately resuscitated, a state of hyperdynamic circulation

13  •  Anesthesia for Burned Patients
138
patients.60 When administered specifically for the therapeu­
tic goal of limiting the volume necessary for resuscitation,
the use of colloid solutions is a rational choice for many
clinicians.
In a prospective randomized study, the use of plasma for
volume resuscitation was found to reduce volume infused
and weight gain along with intra-abdominal pressure and
the incidence of abdominal compartment syndrome (see
later discussion).66 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, with associated morbidity, it may be that the
use of colloid is beneficial for larger injuries. The use of
plasma during resuscitation may involve more than just
volume and increased colloid osmotic pressure. Kozar and
colleagues demonstrated that plasma but not crystalloid
resuscitation partially reverses hemorrhage-induced endo­
thelial damage in an experimental animal model.67 Restora­
tion of the endothelial glycocalyx may help recovery of the
capillary function and reduce fluid extravasation.
Crystalloid solutions alone provide adequate intravascu­
lar expansion without unacceptable complications in many
patients. However not all patients respond favorably to crys­
talloid resuscitation. Box 13.4 provides a list of a number
of factors that can significantly increase the volume of fluid
needed for resuscitation. For patients with these features,
and in other patients for unknown reasons, very large
volumes of crystalloid are needed to support blood pressure
and maintain urine output. In these cases the excessive
volume of fluid can result in dangerous morbidity, such as
abdominal compartment syndrome (Fig. 13.5). For example,
patients who receive more than 250 mL/kg during the first
24 hours are at risk for abdominal compartment syn­
drome.68 It is important to recognize when resuscitation is
difficult so that measures can be taken to limit morbidity.
patient’s physiological status provides evidence of over- or
underresuscitation. Crystalloid solutions generally provide
adequate volume resuscitation; however the large volumes
that are needed result in substantial tissue edema and
hypoproteinemia. In addition, a trend toward administra­
tion of more fluid than the Parkland Formula would predict
has been termed “fluid creep.”61 As mentioned earlier,
overresuscitation can be associated with serious morbid­
ity and even mortality. This has led to a search for inter­
ventions that can reduce the volume of fluid needed for
resuscitation.
Although colloid was included in earlier resuscitation
formulas, it was dropped during the 1970s. An overall
clinical benefit was difficult to demonstrate for colloid solu­
tions, especially when given during the first 12 hours after
injury. Pruitt and colleagues reported that the addition of
colloids to resuscitation fluid during the first 24 hours did
not increase the intravascular volume more than crystal­
loid fluid alone.62 It was also suggested that colloid use
could contribute to pulmonary edema during the post-
resuscitation period.51 Because of the added cost with
little established benefit, colloid solutions have not been
used routinely for initial volume resuscitation in burned
patients in the United States until recently. In 1998, a
highly publicized Cochrane meta-analysis concluded that
albumin administration increases mortality in critically ill
patients, including patients with severe burn injuries.63 As
relating specifically to burn-injured patients, there were
serious methodological flaws with this meta-analysis suf­
ficient for most clinicians to discount the Cochrane con­
clusion that albumin administration increases mortality
among burn patients.64,65 In a recent review, Saffle reported
that, in nearly all studies of burn resuscitation, the use
of colloid solutions has reduced the volume required as
well as the complications of overresuscitation in these
Table 13.2  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

13  •  Anesthesia for Burned Patients
139
earlier intervention. This study also emphasizes the hetero­
geneity of the burned patient population with regard to
response to treatment. This heterogeneity may also explain
in part why it has been difficult to show benefit from colloid
administration. It would be difficult to show benefit from an
intervention if it is given to a group of patients comprising
both responders and nonresponders.
The use of hypertonic saline, either alone or in conjunc­
tion with colloids, has also been advocated by some in the
initial resuscitation of burned patients. Among the poten­
tial benefits are reduced volume requirements to attain
similar levels of intravascular resuscitation and tissue per­
fusion compared to isotonic fluids.71 Theoretically, the
reduced volume requirements would decrease the incidence
of pulmonary and peripheral edema, thus 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 will tran­
siently decrease fluid requirements, there is potential for a
rebound in fluid resuscitation needs.72 Therefore most burn
centers continue to employ isotonic crystalloid fluids rather
than hypertonic solutions for initial resuscitation of patients
in burn shock.
Unfortunately there is no single physiological variable
that is always reliable as an end point to guide resuscitation
in acute burn patients. Several variables are used to assess
the adequacy of volume resuscitation in burned patients
(Box 13.5). The overall goal is early volume resuscitation
and establishment of tissue perfusion. Traditionally urine
output (0.5–1 mL/kg per h) and normalization of blood
pressure (mean arterial blood pressure of greater than
70 mm Hg) have been used as endpoints. However, some
studies indicate that these parameters may be poor predic­
tors of adequate tissue perfusion. Jeng and colleagues
showed that attaining urine outputs of greater than
30 mL/h and mean blood pressures of greater than
70 mm Hg correlated poorly with other global indicators of
tissue perfusion such as base deficit and blood lactate
levels.73 In order to maintain perfusion of vital organs such
as heart and brain, blood flow is often redistributed away
from splanchnic organs. Persistent hypoperfusion of these
organs ultimately results in tissue injury and may be a con­
tributing factor to multisystem organ dysfunction. Several
studies have shown that normalization of blood pressure,
heart rate, and urine output alone does not by itself
Extensive recent experience with burn injuries resulting
from military conflicts has produced protocols that include
administration of albumin for managing patients who do
not have an adequate response to appropriate volumes of
crystalloid fluid.69 Likewise many civilian burn centers have
adopted “colloid rescue” for patients with inadequate
response to resuscitation. Lawrence and colleagues70 evalu­
ated responses of burn patients as an hourly ratio (I/O) of
volume of fluid infused (mL/kg/%TBSA burned/h) to urine
output (mL/kg/h). Patients who responded favorably to
fluid administration maintained a ratio of less than 0.4, but
poor responders had progressively increasing ratios to a
maximum of 1.97. When patients were identified as poor
responders, 5% albumin was added to their resuscitation
fluid regimen. After addition of albumin each of the patients
responded with a prompt decrease in the I/O ratio for the
remainder of the resuscitation. In this study albumin rescue
was initiated more than 12 hours after injury. The authors
noted that these patients still received large volumes of fluid
and that this volume might have been reduced if colloid had
been given earlier. In the future it may be feasible to recog­
nize poor responders early during resuscitation to allow
Box 13.4  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
Fig. 13.5  Large volumes of crystalloid solution required for resuscita­
tion of patients with acute burns can result in compromise of circula­
tion in various compartments. Escharotomies or fasciotomies may be
required for extremities. Laparotomy may be required for abdominal
compartment syndrome when other measures do not adequately
decompress the abdomen.
Box 13.5  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)

13  •  Anesthesia for Burned Patients
140
muscle tone have been used to reduce intra-abdominal
pressure. More invasive measures include escharotomies,81
percutaneous peritoneal dialysis catheter drainage,82 and
laparotomy.79
Serious burns can also be caused by contact with caustic
or corrosive chemicals. An increasingly common specific
example is burns related to the illicit production of
methamphetamine.83–85 There has been a dramatic increase
in burn injuries from explosions and fires related to meth­
amphetamine production in illegal labs. Victims of these
accidents 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 phosphorous, and ephed­
rine). 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.86,87
In addition to exposures just described, these patients are
usually intoxicated with methamphetamine, as demon­
strated by positive urine screen, and may have inhaled toxic
fumes such as phosphine gas. Santos et al. found the inci­
dence of inhalation injury twice as great in victims of
methamphetamine-related burns as in age- and burn-
matched controls.85 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.85,86
For example, Santos et al. found that resuscitation volumes
were 1.8 times greater for methamphetamine users with
burns than for controls.85 In addition, methamphetamine
users with burns 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
syndrome.”85 This behavior may be due to withdrawal of
methamphetamine from chronic users.
EFFECT OF BURN INJURY ON RENAL FUNCTION
Acute kidney injury (AKI) is a very common and devastat­
ing complication of severe burn injuries. The incidence is
often estimated at 30% or more and can increase the mor­
tality in these patients to more than 80%.88 The risk of AKI
with burns increases with all the features intuitively associ­
ated with poor outcome. Despite improvements in critical
care, AKI continues to complicate burn care and increase
mortality. There have been some indications of an improve­
ment, however. Jeschke and colleagues have shown a
decrease in mortality in pediatric burn patients with ARF
to 56% since 1984.89 Also, Chung and colleagues found
that early application of continuous venovenous hemofil­
tration in patients with evidence of AKI, especially in the
presence of inhalation injury, improved survival compared
with conventional care that included hemodialysis after
more stringent criteria were met.90
The pathogenesis of AKI in burn patients is complex and
can involve a number of interconnected mechanisms. A
correlate with improved outcome.74,75 Therefore during the
preoperative assessment of the burn patient, the anesthesi­
ologist should not base the cardiovascular assessment on
one variable but use a more global approach to evaluating
the patient’s physiological status and reserve.
When vital signs and urine output are within normal
limits, measurements of metabolic function may provide
more subtle evidence of impaired perfusion. In burn
patients, tissue perfusion is not uniform. Perfusion of the
splanchnic beds may be sacrificed in order to maintain the
perfusion of heart, brain, and kidneys. 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 inadequate 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 level may be
a useful marker of oxygen availability.76 Wo and colleagues
found serum lactate to be the most predictive index of ade­
quate tissue perfusion, and a lactate level of less than
2 mmol/L in the first 24–72 hours after burn injury cor­
related with increased survival.75 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 a calcu­
lated and not directly measured variable, base deficit pro­
vides a readily obtained and widely available indicator of
tissue acidemia and shock. Base deficit has been shown to
correlate closely with blood lactate and provides a useful
indicator of inadequate oxygen delivery. A retrospective
study by Kaups et al. showed that base deficit was an accu­
rate predictor of fluid requirements, burn size, and mortal­
ity rate.77
Overresuscitation can also be a serious complication of
fluid administration to acute burn patients. Blindness due to
ischemic optic neuropathy has been reported as a complica­
tion of burn resuscitation.78 Greenhalgh and Warden first
described the association of increased abdominal pressures
and compartment syndrome with burn resuscitation.79
Several studies since then have described the common
occurrence of increased intra-abdominal pressure with
large-volume burn resuscitation. Intra-abdominal hyper­
tension is termed abdominal compartment syndrome when
it is associated with impaired respiration, circulation, and
urine output. Mechanical ventilation is impaired by pres­
sure 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 ele­
vated intra-abdominal pressure. This can be accomplished
by measuring bladder 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 of H2O = 1 mm Hg).80 Conservative treatment of
elevated intra-abdominal pressure includes attempts to
limit the volume of intravenous fluid needed for resusci­
tation. The inclusion of plasma with resuscitation fluids
has been found to reduce the volume required and was
associated with significantly lower intra-abdominal pres­
sures.66 When intra-abdominal hypertension occurs it can
be relieved to a degree by optimizing sedation and analgesia.
Diuresis with furosemide and muscle relaxants to reduce

13  •  Anesthesia for Burned Patients
141
The hypermetabolic pattern also increases caloric needs.
Numerous studies have shown that optimized nutritional
care not only can ameliorate the burn-associated state of
catabolism and immune suppression, but also can improve
wound healing.96 Oral or enteral feeding is recognized as the
optimal feeding route of the burned patient. Frequently the
acute burn patient is fed continuously over extended time
periods. 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. Each surgical procedure
requiring general anesthesia theoretically necessitates a
10-hour interruption of enteral nutritional support (fasting
for 8 hours preoperatively and 2 hours postoperatively). To
avoid this interruption of nutritional support, continuation
of feeding via a post-pyloric feeding tube has been used. One
study indicates that this practice provides a favorable gut
oxygen balance.100 Varon et al. reviewed records of 17
patients fed intraoperatively through post-pyloric feeding
tubes and 16 patients fasted for surgery. These patients had
an average of seven surgical procedures each.101 There were
no clinical adverse effects with intraoperative feeding, and
these patients met nutritional goals sooner than patients
fasted for surgery. Larger studies are necessary to establish
the safety of intraoperative feeding but many practitioners
consider this safe in the presence of a cuffed tracheal tube.
Severe insulin resistance with hyperglycemia and con­
current hyperinsulinemia is a key feature of the metabolic
alterations of burn injury.95 Critical care of burn patients
often involves parenteral nutritional support and may also
include insulin infusions. It is important to recognize these
interventions during the preoperative evaluation of the
burn patient in the ICU. Oxygen consumption and glucose
balance are altered when general anesthesia, muscle relax­
ation, and mechanical ventilation are employed. Increased
sympathetic tone due to the stress of surgical trauma can
also alter glucose production and insulin resistance. These
changes often result in significant changes in blood glucose
levels that require treatment.
THERMOREGULATION IN BURN PATIENTS
Maintenance of proper body temperature is an important
factor in the care of severely burned patients. The thermo­
regulatory system is controlled by three major components.
These include the afferent system that senses changes in
core body temperature and transmits this information to
the brain, the central regulatory mechanisms located pri­
marily in the hypothalamus that process afferent input and
initiate responses, and the efferent limb that mediates spe­
cific biological and behavioral responses to changes in core
body temperature (Fig. 13.6). Temperature is sensed by Aδ
and C fibers present in peripheral tissues such as skin and
muscle, as well as in core tissues such as brain, deep abdom­
inal tissues, and thoracic viscera. The vast majority of affer­
ent 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 thermoregula­
tory input.102 Therefore loss of skin following a burn injury
is not likely to markedly alter overall afferent input. Wallace
difference between AKI that occurs early after injury has
been distinguished from injury developing later.91 Early AKI
is associated with reduced renal blood flow resulting from
acute burn shock, whereas AKI that occurs later is associ­
ated with sepsis and exposure to nephrotoxic drugs. Early
AKI carries a worse prognosis than the late form.88 Con­
tinuous evaluation of the patient’s response to fluid resus­
citation is necessary for the early recognition and correction
of under- or overresuscitation to prevent early AKI.
Another mechanism of early AKI is caused by myoglo­
binemia resulting from rhabdomyolysis due to compart­
ment syndrome or electrical injury.92,93 Treatment of this
form of AKI is difficult. Brown and colleagues found that
rates of renal failure, dialysis, or mortality were not altered
by treatment of rhabdomyolysis with bicarbonate and man­
nitol.94 Early diagnosis and treatment of compartment syn­
drome or muscle damage due to electrical injury is,
therefore, critical to preventing its development.
The presence of renal failure complicates intraoperative
management. It seriously reduces the margin of error for
fluid replacement of blood loss. A central venous catheter
(CVC) to monitor filling pressure may be more useful in
these patients. Electrolyte balance, especially potassium,
should be watched closely and extra caution with dosage
and rate of administration of nephrotoxic drugs such as
antibiotics is needed.
METABOLIC CHANGES ASSOCIATED WITH
BURN INJURY
Increased metabolic rate is the hallmark of the metabolic
alterations that take place after thermal injury. The mag­
nitude of the hypermetabolism is influenced by the size of
the burn wound, how the burn patient is treated, and the
ambient temperature of the patient.95,96 Within the range
of 30–70% TBSA burn injury, the hypermetabolism tends
to be proportional to the size of the burn wound. With
burns beyond this range, the hypermetabolism appears to
plateau and only increases in smaller increments.97 Septic
complication is an important factor that can increase
the metabolic response, as does the physiologic stress of
pain. It has been observed that modern-day treatment of
burn injuries with early excision and closed-wound treat­
ment ameliorates this hypermetabolism.98 Burn patients
increase their metabolic rate in an effort to generate heat
according to a new threshold set point for the body tem­
perature that is influenced by the size of the burn (see the
section “Thermoregulation in Burn Patients”). The recog­
nition of this fact has led to an increased awareness of
the importance of the ambient temperature in modulating
the hypermetabolism of the burn patient. By indirect calo­
rimetry, patients with major burn injuries treated accord­
ing to current standards have resting energy expenditures
that are 110–150% above values recorded in nonburned
subjects.99
As a result of this hypermetabolic response, the acutely
burned patient has an increased O2 consumption along
with an increased CO2 production that demands a higher
respiratory effort. The anesthetic care of the acute burned
patient has to accommodate these changes, and frequently
this has to be done in patients with compromised pulmo­
nary function due to burn injury.

13  •  Anesthesia for Burned Patients
142
patients and decrease their ability to respond to their
primary injury.108
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 acute postburn setting, most of these behaviors are
impeded by positioning, sedation, and inability to seek a
more favorable 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 temperature. Cutaneous vasoconstriction is
another important mechanism for preserving heat and
core body temperature. In unburned persons, a tempera­
ture gradient of 2–4°C exists between skin and core tissues.
This gradient is maintained by cutaneous vasoconstriction.
Without cutaneous vasoconstriction, heat is redistributed
from the core compartment to the periphery. This heat is
ultimately lost to the environment. Peripheral vasocon­
striction minimizes temperature redistribution and acts to
maintain core body temperature. This mechanism of heat
preservation is lost with the loss of large areas of skin,
particularly if cutaneous tissues are excised down to the
fascial level. The loss of skin facilitates the loss of core body
heat into the environment and places the burn patient at
risk for core hypothermia. Another mechanism of heat loss
in burn patients is evaporation. Burn patients can lose as
much as 4000 mL/m2 burned per day of fluids through
evaporative losses.109 Mechanisms of nonshivering 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. 13.7). This is particu­
larly important in burn patients, given their high tempera­
ture set point and the deleterious effects of further stress
responses and hypermetabolism. Most anesthetics decrease
nonbehavioral responses to hypothermia such as vasocon­
striction, nonshivering thermogenesis, and shivering. Of
course, behavioral responses are ablated during general
anesthesia. Therefore, it is the responsibility of the
and colleagues have shown that burn patients perceive
changes in ambient temperature as effectively as normal
controls.103 This is likely due to the retained ability of burn
patients to sense changes in core temperature and transmit
this information to the central nervous system. Central
control of temperature is a complicated system that is not
well understood. The hypothalamus plays an important
role in temperature regulation, but the complete mecha­
nism 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.104 This increase in tem­
perature threshold appears to be due to the hypermetabolic
state and the presence of pyrogenic inflammatory media­
tors such as TNF, IL-1, and IL-6 that are present after
thermal injury. The elevated temperature set point can be
decreased by administration of indometacin, which sug­
gests that prostaglandins act as final common mediators of
this response.105,106
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.103 Burn patients respond with a brisk increase in heat
generation and metabolic rate in response to changes in
core body temperature.103 However work by Shiozaki and
colleagues has shown that burn patients who are slow to
respond to postoperative hypothermia are at increased risk
of mortality.107 The decreased responsiveness may be due,
in part, to tissue catabolism, poor nutrition, or sepsis. In
addition, the response to relative hypothermia is character­
ized by increased catecholamine release, tissue catabolism,
and hypermetabolism. These responses further stress burn
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
Fig. 13.6  Thermoregulatory control mechanisms. Afferent inputs 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.)

13  •  Anesthesia for Burned Patients
143
alveolar accumulation of inhalation agents, which may
result in an exaggerated hypotensive response during induc­
tion 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.112
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 a disparate response to burn injury.
Albumin binds mostly acidic and neutral drugs (diazepam
or thiopental) and is decreased 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. Since
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 pro­
teins has the highest affinity for the drug in question.
Martyn et al. observed decreased plasma albumin concen­
tration and increased plasma AAG concentration in burn
patients.113 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) is changed by alterations to
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 following a rapid loading dose. However adjust­
ments 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.111
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 anes­
thesia. Drug clearance is influenced by four factors: metabo­
lism, protein binding, renal excretion, and novel excretion
pathways. The characteristic hepatic extraction of a par­
ticular 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.111 For these drugs it is
the unbound fraction of the drug that is metabolized. As
noted, changes in unbound fraction depend on whether the
drug is bound by albumin or AAG. Changes in protein levels
produce clinically significant pharmacokinetic changes
only for drugs that are highly bound (>80%).114
intraoperative caregivers to monitor and maintain patient
temperature.
Actions such as maintaining higher ambient air tem­
perature, covering extremities and head, applying warm
blankets, utilizing 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.110 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.
Pharmacological Considerations
Burn injury and its treatment result in physiological
changes that may profoundly alter the response to drugs.
These changes alter both pharmacokinetic and pharma­
codynamic determinants of drug response. Altered drug
response in burned patients may require deviation from
usual dosages to avoid toxicity or decreased efficacy.111 The
complex nature of the pathophysiological changes and
interpatient variation in the nature and extent of burn
injuries, as well as the dynamic nature of these changes
during healing and recovery make it difficult to formulate
precise dosage guidelines for burn patients. However an
understanding of the systemic response to large burn inju­
ries 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
different ways. During the acute or resuscitation phase the
rapid loss of fluid from the vascular space due to edema
formation results in decreases of cardiac output and tissue
perfusion. Volume resuscitation during this phase dilutes
plasma proteins and expands the extracellular fluid space
especially, but not exclusively, around the burn injury itself.
Decreased renal and hepatic blood flow during the resusci­
tation phase reduces drug elimination by these organs.
Also, decreased cardiac output will accelerate the rate of
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
Fig. 13.7  Effects of anesthesia on thermoregulatory mechanisms.
(From Sessler DI. Temperature monitoring. In: Miller R, ed. Anesthesia, 3rd
edn. New York: Churchill Livingstone; 1990.)

13  •  Anesthesia for Burned Patients
144
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) that has been referred to as an imma­
ture, extrajunctional, or fetal receptor. The immature recep­
tors are more easily depolarized by succinylcholine, and
their ion channel stays open longer. The immature recep­
tors are also strongly and persistently depolarized by the
metabolite of acetylcholine and succinylcholine, choline. It
has been suggested that the hyperkalemic response to suc­
cinylcholine after burn or denervation injury results when
potassium is released from receptor-associated ion channels
across the entire muscle cell membrane rather than just
the junctional receptors. Depolarization 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 1958.119 It was not
until 1967, however, that an exaggerated hyperkalemic
effect was identified as the cause of this phenomenon.120,121
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 earliest exaggerated hyperkale­
mic 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.128 The shortest post-
burn interval of an association of succinylcholine with
cardiac arrest was 21 days when a 4-year-old patient expe­
rienced a fatal cardiac arrest during a fourth anesthetic
induction and intubation with succinylcholine. Contro­
versy has surrounded 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.129,130 A
series of letters from experts in this area to the editor of
Anesthesiology illustrates the controversy.131,132 It was
pointed out by Martyn that, at the time when the mecha­
nism of the cardiac arrest after succinylcholine was eluci­
dated, surgical treatment of burns was delayed for
approximately 2 weeks until the eschar spontaneously
separated.132 As a result, there are few clinical data regard­
ing potassium changes during this early period. On the
basis of indirect evidence from experimental data, Martyn
recommended avoidance of succinylcholine starting 48
hours after injury.132 This seems rational and prudent.
Brown and Bell described the super-sensitivity of burned
pediatric patients to the relaxant effect of succinylcho­
line.133 They observed more than 90% depression of muscle
activity with 0.2 mg/kg succinylcholine without danger­
ous hyperkalemia. Despite these observations Brown and
Bell state that it is generally advisable not to use succinyl­
choline 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 succinylcho­
line (e.g., 0.1 mg/kg) to relieve laryngospasm without full
paralysis and accept a theoretical risk of treatable hyperka­
lemia in order to treat a real and immediate risk of asphyxia?
Administration of a large dose of a nondepolarizing relax­
ant requires more time for onset than succinylcholine and
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
increased glomerular filtration rates and reduced half-life of
tobramycin in burn patients.115 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 clear­
ance 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.116 In addition, rapid blood
loss during surgery may speed the elimination of drugs
when blood loss and transfusion amount, essentially, to an
exchange transfusion.
Hepatic clearance of drugs with low extraction coeffi­
cients is also sensitive to alterations of hepatic capacity
(enzyme activity). There is evidence of impairment of
hepatic enzyme activity in burn patients.111 Phase I reac­
tions (oxidation, reduction, or hydroxylation by the cyto­
chrome P-450 system) are impaired in burn patients,
whereas phase II reactions (conjugation) seem to be rela­
tively preserved.112 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 that is normally retained in thermally injured
patients. Morphine clearance in burn patients has been
reported unchanged or decreased.117,118 With so many vari­
ables involved, such as hepatic blood flow, Vd, plasma pro­
teins, multiple drug exposure, and variation in burn injury,
this inconsistency is not surprising. The key to effective drug
therapy in burn patients is to monitor drug effects and care­
fully titrate the dose to the desired effect.
In terms of anesthetic management, the most profound
and clinically significant effect of burn injuries on drug
response relates to muscle relaxants. Burn injuries of more
than 25% TBSA influence responses to both succinylcho­
line and the nondepolarizing muscle relaxants. In burned
patients, sensitization to the muscle-relaxant effects of
succinylcholine can produce exaggerated hyperkalemic
responses severe enough to induce cardiac arrest.119–121
In contrast, burned patients are resistant to the effects of
nondepolarizing muscle relaxants.122–124 These changes are
explained by up-regulation of skeletal muscle acetylcholine
receptors.125–127
Martyn and Richtsfeld have recently reviewed the mech­
anisms of exaggerated hyperkalemic responses to succi­
nylcholine.127 There are several disease states, including
burns, denervation, and immobilization, that are associ­
ated with potentially lethal hyperkalemic responses to
succinylcholine. The molecular mechanism appears to be
both quantitative 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 recep­
tors with resistance to nondepolarizing muscle relaxants
and increased sensitivity to succinylcholine. In addition,
the distribution of the new receptors is altered. Nicotinic

13  •  Anesthesia for Burned Patients
145
hyperkalemic response to succinylcholine.127 The observa­
tion of resistance of a patient to metocurine for up to 463
days after the burn has been used to suggest that hyperka­
lemic responses to succinylcholine also could persist for
more than a year.123 However, no pathologic hyperkalemic
responses to succinylcholine in burned patients have been
reported more than 66 days after burns.129
In contrast to other nondepolarizing neuromuscular
blockers, mivacurium dosage requirements in pediatric
patients appear to be unchanged by the burn injury. The
time to onset of drug action, the degree of paralysis achieved
by a specific dose, and the rate of infusion required to main­
tain a given level of relaxation were all the same in burn
patients as values reported for nonburned control
patients.136 Plasma cholinesterase activity is reduced in
burn patients.137 In a study by Martyn, the observation of
an inverse relationship between plasma cholinesterase
activity and recovery time of 25–75% twitch tension sug­
gests that reduction of metabolic degradation of mivacu­
rium may compensate for other factors that induce
resistance to relaxants.136 This observation suggests that
mivacurium can be administered to burn patients in normal
doses that would avoid cardiovascular perturbations associ­
ated with required larger doses of other relaxants in burn
patients. It also illustrates the complex nature of altered
drug responses in burned patients.
Airway Management
If injuries do not preclude conventional airway manage­
ment (i.e., mask fit, jaw lift, and mouth opening), standard
induction and intubation procedures are appropriate. Hu
et al. reported that gastric emptying was not delayed in
patients with severe burns so that a rapid-sequence induc­
tion is not necessary.138 However, attention should be given
to gastric residuals during enteric feeding. 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 impossible.
In addition, loss of mandibular mobility may impair airway
manipulation and make mask ventilation difficult. Fiber­
optic intubation while maintaining spontaneous ventila­
tion is a safe and reliable technique under these conditions.
Fiberoptic intubation can be performed in awake adults
but pediatric patients are unable to cooperate and must be
sedated. Since most anesthetics cause the 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.139 Ketamine, however, is
unique among anesthetic drugs because it maintains spon­
taneous ventilation and airway patency.140
Ketamine anesthesia has been found safe and effective 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.141,142 In the latter
case an ultra-thin bronchoscope (2.7 mm) was required
produces total paralysis. There is not enough clinical evi­
dence to answer this question conclusively, and, at present,
it remains a matter of clinical judgment.
In some cases another clinical choice is now available
since the U.S. Food and Drug Administration (FDA) approval
of sugammadex in December 2015. Sugammadex is a rever­
sal agent with a novel and unique mechanism of action.
It is a cyclodextrin that irreversibly chelates aminosteroid
muscle relaxants by forming a 1 : 1 tight complex (encapsu­
lation) with the relaxant molecule, which reduces the con­
centration of the free drug in plasma below the minimum
necessary for muscle relaxation. A Cochrane review found
sugammadex to be an effective reversal agent without
evidence of increased frequency of adverse effects when
compared to neostigmine.134 In fact, sugammadex has been
found to provide more rapid recovery of more than 90%
twitch strength than either spontaneous recovery with suc­
cinylcholine or reversal with neostigmine.134 Sugammadex
has a lower affinity for pancuronium, and higher doses are
required for this agent than for rocuronium or vecuronium.
Although the frequency of adverse effects due to sugam­
madex has been very low, there have been some serious
complications associated with its administration, includ­
ing anaphylaxis and severe bradycardia requiring chest
compressions. Another more common issue relates to the
potential for sugammadex to inactivate hormonal contra­
ceptives. Female patients treated with contraceptives should
be advised to use an alternative form of contraception for a
period after receiving sugammadex.
As of this writing (January 2017), sugammadex has not
yet received FDA approval for pediatric patients, and most
reported pediatric data are in the form of case reports and
small studies. The clinical experience with sugammadex in
children has been reviewed by Tobias.135 Sugammadex has
been found to be an effective rescue agent in situations
where pediatric patients cannot be intubated or ventilated.
It has also proved useful in pediatric patients with neuro­
muscular diseases such as Duchenne muscular dystrophy
and myotonic dystrophy.135 In some situations rocuronium
might be an additional choice to relieve laryngospasm in an
acute burn patient when there is a risk of intubation or
ventilation impossibility if sugammadex is available since it
can reverse relaxation with rocuronium faster that sponta­
neous recovery from succinylcholine. Still, the onset of
action for rocuronium is slower than for succinylcholine.
Responses to nondepolarizing relaxants are also altered
by burn injury. Three- to fivefold greater doses are required
to achieve adequate relaxation.122 Resistance is apparent by
7 days after injury and peaks by approximately 40 days.
Sensitivity returns to 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. Up-regulated imma­
ture receptors are less sensitive to nondepolarizing relax­
ants. Burns of greater than 25% TBSA require higher total
dose and greater plasma concentrations of nondepolarizing
blockers to achieve a given level of twitch depression.124
Proliferation of acetylcholine receptors across the muscle
membrane has been used to explain both resistance to
nondepolarizing muscle relaxants and the exaggerated

13  •  Anesthesia for Burned Patients
146
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 movement of
the endotracheal tube but loose enough to prevent ischemic
necrosis of the underlying tissues. Nasal endotracheal tubes
are often avoided in ICUs due to concern for sinusitis.
However, nasogastric or nasal feeding tubes carry similar
risk. Over the past 25 years our hospital has had two
patients with suspected sinusitis. Sinus cultures from these
patients were negative for bacterial growth (unpublished
observations). The nasal endotracheal tube is much more
secure than an oral tube, better tolerated by the patient, and
the patient cannot occlude the nasal tube by biting it.
A red rubber catheter may also be used to secure an oral
endotracheal tube (Fig. 13.9). A red rubber catheter is
placed in a nostril and brought out the mouth by direct
laryngoscopy and MacGill forceps. A loop is formed which
the endotracheal tube is secured to with umbilical tape. This
is very secure and avoids ties around the neck, which can
irritate wounds and grafts, and the problem of changing
head circumference due to formation and resolution of
edema.
Airway management using a laryngeal mask airway 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.145 Nineteen (14.5%) of the procedures were com­
plicated by respiratory events such as unseating, desatura­
tion, and partial laryngospasm that required intervention.
Two of these events required intraoperative intubation
without sequelae, while all other events resolved with
therapy. Interestingly the presence of preoperative respira­
tory problems or face/neck burns did not predict intra­
operative respiratory problems. These authors suggest that,
in patients with upper airway mucosal injury, laryngeal
mask airway management may help avoid further
because a larger fiberscope would not fit through the
appropriate-sized endotracheal tube. To facilitate intuba­
tion under ketamine anesthesia, topical anesthesia of the
larynx with lidocaine prior to instrumentation of the larynx
is advised. Since the ultra-thin bronchoscope lacks a
working channel for administration of topical lidocaine,
fiberoptic intubation with the 2.7-mm bronchoscope was
preceded by nasopharyngoscopy with a 3.5-mm fiberscope
for administration of topical lidocaine. At SBH Galveston
we have also found this technique, utilizing two fiberscopes,
effective in infants with burn injuries. Wrigley et al. evalu­
ated the use of a 2.2-mm intubating fiberscope during halo­
thane anesthesia in ASA 1 or 2 children aged 6 months to
7 years.143 In this series of 40 patients, a number of com­
plications were experienced including laryngospasm and
failure to achieve intubation with the fiberscope. This expe­
rience is in contrast to numerous reports of safe and effec­
tive 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.144 Tape will not adhere to
burned skin and ties crossing over burned areas will irritate
the wound or dislodge grafts. In addition, if the head is
burned, especially if the patient has also required a large
fluid resuscitation, then during the first few days after
injury, the head is swelling due to edema formation or
shrinking as edema resolves. Under these conditions tape
surrounding the head will become loose or too tight within
hours. A useful technique to avoid these problems involves
the use of a nasal septal tie with one-eighth-inch umbilical
tape (Fig. 13.8). The umbilical tape is placed around the
nasal septum using 8 or 10 French red rubber catheters
that are 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, and,
when the catheters are pulled back through the nose, each
end of the umbilical tape is pulled out of its respective naris,
B
A
Fig. 13.8  A nasotracheal tube can be secured with confidence with a loop of umbilical tape around the bony nasal septum. (A) Red rubber catheters
have been passed through each naris and retrieved from the oropharynx using McGill forceps. A length of umbilical tape is then tied to each of the
catheters. When the catheters are pulled from the nose, the umbilical tape can be tied in a loop around the nasal septum. (B) Endotracheal tube,
nasogastric tube, and duodenal feeding tube are all secured in place after being tied to the septal bridal. When fastened in this manner the endotra­
cheal tube is very secure, and tape or ties do not irritate burn wounds of the face and neck.

13  •  Anesthesia for Burned Patients
147
capnogram. Pulse oximetry in burn patients can be difficult
when transmission pulse oximetry sites are either burned
or within the operative field. Reflectance pulse oximeter
probes are now available, and nasal clip probes are much
improved (Fig. 13.10 with oral red rubber).
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 extrem­
ity.147 Systolic blood pressures obtained from the pressure at
which the pulse oximetry signal returns during cuff defla­
tion have also been found to be accurate.148
When vasoactive infusion is needed or blood loss is
expected to be rapid and extensive, the blood pressure may
change more rapidly than the interval between cycles of
noninvasive blood pressure measurement. In this case an
arterial catheter can provide direct and continuous mea­
surement of blood pressure. This monitor can provide much
more information regarding the patient’s circulatory status
than just systolic and diastolic blood pressure. The arterial
pressure wave form is influenced by preload, contractility,
and vascular tone. Perioperative variation in the rate of rise
of arterial pressure, the area under the pressure wave, posi­
tion of the dicrotic notch, and beat-to-beat alterations in
systolic pressure related to respiration all reflect clinically
significant hemodynamic changes.149 With experience,
trends in these variables can help guide volume and vasoac­
tive therapy. Display of the beat-to-beat arterial pressure
allows measurement of systolic pressure variation (SPV)
laryngeal injury that might occur with intubation 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.146 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 endo­
tracheal tube was undesirable because tracheostomy had
resulted in subglottic stenosis that could have been exacer­
bated by an endotracheal tube. After induction with fen­
tanyl and propofol, the Combitube was placed and the
patient was relaxed with rocuronium and mechanically
ventilated during the 60 min procedure.
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 associ­
ated with the massive blood loss that can accompany exci­
sion 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 systemic blood pressure, pulse oximetry, capnography,
and inspired oxygen concentration. The ability to measure
body temperature should be readily available and is highly
recommended 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
Fig. 13.9  An oral endotracheal tube can be secured to a loop created
by a red rubber catheter (or similar device) passed through the nose
and brought out the mouth. When the endotracheal tube is fastened
to this loop there are no ties surrounding the head and neck which can
irritate burn wounds and disrupt grafts. Note also the nasal pulse oxim­
eter probe, which has undergone significant improvements recently.
Other sites for pulse oximetry, such as ears and fingers, are frequently
unavailable in patients with large burns.
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
Fig. 13.10  Heart rate, mean arterial pressure, and cardiac index
changes during a 15-min 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.)

13  •  Anesthesia for Burned Patients
148
to monitor response to therapy. Diuretic therapy for myoglo­
binuria or any other indication will negate the usefulness
of urine output as an index of global perfusion.
Vascular Access
Care of patients with major burn injury requires secure
vascular access for resuscitation, blood sampling, hemody­
namic monitoring, and intravenous medication. In patients
with large burns a CVC can serve several functions. Exten­
sive burns may preclude cannulation of peripheral veins. A
CVC sutured in place can provide secure access longer than
a peripheral catheter can be maintained. Multiport cathe­
ters can provide a monitor of CVP while infusing blood or
other fluids and can allow simultaneous infusion of incom­
patible drugs.
Vascular cannulation of acutely burned patients can be
one of the more technically challenging procedures facing
the burn care team. Anesthesiologists are often involved
in the management of vascular access for burn patients. In
the pediatric age group the task can be even more difficult.
Sites for percutaneous insertion of vascular catheters may
be involved in the burn and nonburned sites are often dis­
torted by burn wound, edema, or trauma. Early after burn
injuries burn shock is associated with hypovolemia and
vasoconstriction, which add to the difficulty. Later in the
hospital course debridement and scarring further distort
anatomy.
Because the systemic manifestations of wound infection
and SIRS mimic those of catheter-related bloodstream
infections, vascular catheters are changed to new sites
more often than in nonburned patients. In addition, CVCs
appropriate for ICU care are not always appropriate for
rapid infusion of fluid and blood products during surgery,
often necessitating placement of new catheters in the oper­
ating room. With hospitalization for major burns lasting
weeks and months, patients may need multiple cannula­
tions over a prolonged time period. With multiple techni­
cally difficult vascular cannulations over a prolonged period,
risks of infectious and mechanical complications are signifi­
cant. In addition to immediate mechanical complications of
line insertion, repeated cannulation of vessels can result in
thrombosis, which can be a source of embolic events, and
the vessel can be obliterated, causing venous stasis and lim­
iting future access. These considerations make it necessary
to minimize the number of cannulations as much as pos­
sible, especially for patients expected to have a long hospital
course. Infectious complications are as much a consider­
ation as mechanical complications in burn patients. Open,
possibly infected wounds near or at the insertion site as well
as bacteremia that may occur during wound care increase
the risk of line infection. Although it is commonly assumed
that arterial catheters are less susceptible to infection,
studies show that the rates are similar for arterial and
central venous catheters.152 However, since the risk of
mechanical complications for femoral arterial cannulation
is greater (see later discussion), the risk–benefit relationship
of changing sites or exchanging over a wire is less favorable
for arterial catheters than venous. There is no consensus,
and a great deal of variation exists between burn centers
regarding policies and procedures to minimize these risks.
and other measures sensitive to variation in stroke volume.
These dynamic measures of the interaction between preload
and stroke volume have been used to predict the response
to fluid volume administration. SPV is the difference
between maximum and minimum systolic blood pressure
during a single cycle of positive pressure mechanical venti­
lation. Several studies have correlated SPV with cardiac
output response to volume infusion. Tavernier et al. reported
that in septic patients on mechanical 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 ven­
tricular end diastolic area.150 When hemorrhage is brisk,
the decision to administer volume is not difficult. In other
cases during burn wound manipulation, hypotension and
other evidence of poor perfusion can occur in the apparent
absence of significant blood loss. Inappropriate fluid admin­
istration can cause hemodilution, increased cardiac filling
pressure, and fluid overload. Measurement of central
venous pressure (CVP) can indicate if there is room in the
intravascular space for volume administration, and dynamic
measures of fluid responsiveness can identify patients who
will respond to fluid loading with an increase in cardiac
output and tissue perfusion. The use of these dynamic mea­
sures of fluid responsiveness, as well as their limitations,
have been reviewed recently.151 However no single physio­
logical variable can be relied on to correct all deficiencies in
perfusion during burn wound debridement. Wound manip­
ulation can release inflammatory mediators and bacterial
products that alter myocardial compliance and contractility
as well as vascular tone. During challenging cases with
brisk bleeding volume replacement alone may not correct
hemodynamic deficiencies. It is necessary to monitor blood
gases, electrolyte changes, and urine output, as well as arte­
rial and central venous pressures. Inadequate tissue perfu­
sion may manifest as metabolic acidosis despite apparently
adequate arterial and central venous blood pressures.
Arterial blood sampling for blood gas analysis can also
provide valuable information regarding pulmonary func­
tion and ventilatory support, acid–base balance, and elec­
trolyte abnormalities. 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
CVC sutured into place also provides very secure intrave­
nous access and is an ideal route for administration of vaso­
active 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 in the
presence of pre-existing disease or when large doses of ino­
tropes or high PEEP is required.
Urine output is the most useful perioperative monitor of
renal function. Urine output of 0.5–1.0 mL/kg per hour is
often recommended as an end point for fluid management
in acute burn patients. Adequate urine output is one
measure of both renal and global perfusion. When intra­
operative transfusion is planned, examination of the urine
may be the only reliable indicator of a transfusion reaction
since signs and symptoms 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

13  •  Anesthesia for Burned Patients
149
Maintaining arterial catheters in burn patients presents
an additional challenge. Radial artery catheters are prob­
lematic because the hands are often burned, and it is diffi­
cult to maintain them over prolonged periods in burn
patients. As a result most burn centers rely on femoral
artery catheters when arterial cannulation is indicated.
Since the femoral artery is an end artery, mechanical injury
can lead to the devastating complication of the loss of lower
extremity tissue. For this reason it is essential to have a clear
indication for arterial cannulation (Table 13.3). In many
cases clinical decisions can be made with analysis of venous
blood samples rather than arterial blood.
Studies in nonburned patients have compared rates of
infection of different insertion sites. In nonburned patients
it is recommended that cannulas not be changed over a wire
to avoid infection.156 It is also recommended that catheters
not be changed in response to fever alone, and, when uni­
versal precautions are followed, catheters can be left in
place for prolonged periods. However in burn patients
requiring prolonged hospitalization it is often necessary to
utilize all available sites as catheters are rotated to fresh
sites. Also, the increased risk of line infection in patients
with burns and the confounding signs and symptoms of
systemic inflammation from the burn wounds that mimic
catheter-related bloodstream infection make it difficult to
follow guidelines established for nonburned patients.
Lozano and colleagues found 9.36 catheter-related infec­
tions per 1000 catheter days when vascular catheter sites
were changed only with signs of infection as per guidelines
from the U.S. Centers for Disease Control and Prevention
(CDC) but only 3.23 per 1000 catheter days when the sites
were routinely changed every 5 days. As a result, in most
burn centers, vascular insertion sites are changed more fre­
quently than in ICUs caring for nonburn patients. Many
centers will also change catheters over a wire and culture
the catheter tip after a certain period of time. If the tip is
colonized a new site can be cannulated. It is difficult to form
universal protocols for vascular access in burn patients
since they comprise such a heterogeneous group. Decisions
regarding site of cannulation and when to change sites are
influenced by multiple factors including which sites are
available, previous complications, surgical scheduling, ICU
management (e.g., need for total parenteral nutrition), and
evidence of infection (wound- or catheter-related). Inci­
dence of catheter infection increases when the insertion site
Early complications of the placement of venous catheters
include trauma, hematoma, bleeding, air embolus, pleural
effusion, pneumothorax, or pericardial tamponade. Late
complications include venous thrombosis, infection, and
infiltration. Complications of arterial catheters include
damage to adjacent structures, ischemia to distal tissues,
and infection.
Ultrasound-guided placement of vascular catheters is
now widely recommended.153,154 This technique has been
found to be faster and associated with fewer complications
than cannulation with anatomical landmarks. Few studies,
however, compare ultrasound-guided cannulation out­
comes with other techniques in burn patients. The combi­
nation of massive edema, hypovolemia, vasoconstriction,
and acoustic shadows from scars all degrade the ultrasound
image. Practitioners should not rely solely on one technique
but should be able to utilize multiple techniques including
ultrasound, anatomical landmarks, a palpable pulse, and
pencil Doppler signal to place vascular catheters.
When possible, if a percutaneous insertion site is involved
in the burn wound, it is best to have surgical debridement
accomplished before insertion. This facilitates both ease of
placement and infection control. Catheter selection must
take into account multiple clinical needs: blood sampling,
hemodynamic monitoring, rapid infusion of large volumes
of fluid and blood products, and infusion of medications
that may be incompatible with each other. A lumen large
enough to allow rapid infusion of volumes appropriate to
the patient’s size is necessary. When blood loss is expected
to be extensive, it is helpful to monitor CVP. Although CVP
correlates poorly with hemodynamic function in popula­
tions of patients, when hypotension or anemia occur,
knowledge of whether the CVP is high or low can help
decide if an inotrope is appropriate or if there is room in the
vascular space to increase the hematocrit quickly. In addi­
tion, ICU management may require a different catheter.
Some compromise or a change of catheters prior to trans­
port to the ICU may be needed.
In recent years peripherally inserted central catheters
(PICCs) have been used in burn patients. The advantages of
these devices over conventional CVCs are the ease of inser­
tion, reduced risk of some complications of CVCs, and
reduced cost. At the time of this writing the largest study
of complications associated with PICCs is by Austin and
colleagues who described their clinical experience with 53
patients and reviewed the literature.155 While the use of a
PICC avoids some risk of a CVC, such as pneumothorax or
hemothorax, the PICC carries its own unique risks. The
incidence of catheter-related infections may be similar for
PICCs and CVCs. Despite the use of antithrombotic prophy­
laxis upper extremity deep vein thrombosis (UEDVT) that
can lead to fatal embolic events has been associated with
PICC placement. Burn patients are often hypercoagulable
and, as a result, are at risk for occlusive and embolic events.
Austin et al. found symptomatic UEDVT in 5.5% of patients
with PICC lines in place.155 UEDVT associated with PICC
lines appears to increase with duration longer than 7 days
and with increasing diameter of the catheter. Austin and
colleagues describe the PICC as an accepted standard of
care for burn patients but not without risk. The decision of
whether to use a PICC or a conventional CVC must balance
the risks and benefits of these devices for each patient.
Table 13.3  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 (mm Hg)
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

13  •  Anesthesia for Burned Patients
150
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
patient transport; pharmacological support may be
required. The American Society of Anesthesiologists stan­
dards mandate evaluation, treatment, monitoring, and
equipment appropriate 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 oxime­
try. 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 venti­
lation, as well as overall condition, must be continually
observed by the anesthesia care team. Drugs for resuscita­
tion should accompany the patient on any transport. As
discussed earlier, 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 consumption and taxing limited metabolic reserve
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 pri­
marily on the patient’s hemodynamic and pulmonary
status as well as on the potential difficulty of securing the
patient’s airway. Ketamine has many advantages for use in
the burn patient for induction and maintenance of anesthe­
sia. 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, ketamine generally preserves
hemodynamic stability (Fig. 13.10). In addition, ketamine
preserves hypoxic and hypercapnic ventilatory responses
and reduces airway resistance.165 Compared to other IV
anesthetics, airway reflexes remain more intact after ket­
amine administration. Patients who do not require ventila­
tory support can be allowed to breathe spontaneously,
which provides an additional margin of safety should inad­
vertent extubation occur. In fact, some clinicians have
reported the use of ketamine anesthesia without instru­
mentation of the airway.166,167 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 of pediatric burn patients or uncooperative adults
who do not have vascular access. Because ketamine pre­
serves spontaneous ventilation and induces dissociative
anesthesia, it provides good conditions for securing the
airway by fiberoptic bronchoscopy. When using this
is in or near burn wounds.157 With limited sites available it
is tempting to leave catheters in unburned sites longer than
in sites through burn wounds. Decisions are best guided by
the general goals of minimizing infection and mechanical
complications but should be individualized for each patient’s
immediate needs.
Although arterial catheters are generally considered less
likely to be associated with infection, these catheters are
infected with a frequency similar to CVCs.152 There are
fewer sites for arterial cannulation, however, and the risk of
serious mechanical complications of femoral artery injury
are potentially greater than with venous catheters. As a
result, femoral arterial catheters are often left in place
longer than venous cannulas.
Delayed complications include infection and thrombosis,
which have been studied by many authors with often con­
flicting results. Many older studies recommend frequent
catheter changes to decrease the incidence of infection, but
several later studies show no increase in infection out to as
many as 7–10 days. Three large randomized trials demon­
strated 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 guidewire every 7 days.158–160 The incidence of mechani­
cal complications is lower with guidewire exchange rather
than changing to a new site.161
Vascular catheters that incorporate an antibiotic have
been found effective in reducing the incidence of catheter-
related bloodstream infections in burn patients. A prospec­
tive, randomized trial examined the efficacy of two types
of CVCs that incorporate antibiotics: one catheter releases
silver ions continuously, and the other is impregnated with
two antibiotics with different mechanisms of action, rifam­
picin and minocycline. Both catheters were associated with
low rates of catheter-related bloodstream infections.162 If
effective, these catheters can provide two significant clini­
cal advantages. Reduced colonization of CVCs will reduce
the risk of blood-borne infections, and reduced need for
changes in vascular access sites for infection control will
reduce the incidence of mechanical complications of cathe­
ter insertion. However, as with other clinical decisions with
burn patients, the data from studies in burn patients make
it difficult to form guidelines. Studies consistently show
decreased rates of bloodstream infection, but the rates of
infection between burn centers are greater than the effect
of using antibiotic-impregnated catheters.163,164 Moreover,
since catheters are changed much more frequently in
burn patients, often every 72 hours, and even earlier with
signs of infection, the cost benefit in burn patients is not
established.
When planning vascular access for perioperative anes­
thetic 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 complica­
tions 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 timing of regular changes
of access sites for infection control. The patient’s hospital
course must also be considered when choosing a catheter.
The catheter should be large enough to transfuse appropri­
ately for the case, but catheters much larger will increase
risk without benefit.

13  •  Anesthesia for Burned Patients
151
those with challenging airways, should be monitored
closely.
Regional anesthesia can be used effectively in patients
with small burns or those having reconstructive proce­
dures. In pediatric or adult patients having procedures con­
fined to the lower extremities, lumbar epidural or caudal
anesthesia can provide a useful adjunct for control of post­
operative pain. In cooperative adult patients with injuries
confined to lower extremities, epidural or intrathecal anes­
thesia may be used if no contraindications exist. For upper
extremity procedures, brachial plexus block may be consid­
ered as the primary anesthetic or as an adjunct for postop­
erative pain control.
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.172 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.173
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 pre­
vious hospital course and ICU treatment goals. If excision
is performed during the first 24 hours, perioperative fluid
management may involve acute resuscitation, 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 patients’ hospital
course, patients are edematous from the large amounts of
crystalloid solutions administered during resuscitation. At
this time additional crystalloid administered during the
perioperative period may be poorly tolerated 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 patients all week in order to
reduce interstitial edema, it is not helpful when the patient
receives several liters of fluid in the operating room. Periop­
erative fluid management must also take into account hypo­
tonic clysis fluids that the surgeons may inject subcutaneously
to facilitate donor skin harvest with the dermatome. In
small children the volume of this fluid can be in excess of
50 mL/kg. State of hydration and electrolyte balance must
be monitored carefully in order to maintain proper fluid
balance. Although it is important to avoid overhydration,
aggressive diuresis in the burn ICU may result in a patient
who presents to the operating room intravascularly hypo­
volemic despite extensive peripheral edema.
Replacement of surgical blood loss during burn wound
excision and grafting represents another challenge. Unlike
most general surgical procedures, during burn surgery it is
impossible to accurately estimate the amount of shed blood
during the procedure. Shed blood is not collected in suction
canisters where it can be measured. During burn surgery
shed blood is concealed beneath the patient, in drapes, in
technique, the addition of potent volatile agents should be
avoided until the airway is secured because these anesthet­
ics depress respiratory drive and relax pharyngeal muscles,
thus increasing the risk of apnea, upper airway obstruc­
tion, or laryngospasm. Ketamine can also be utilized, either
alone or in combination with other anesthetics, for mainte­
nance of anesthesia either by infusion or intermittent bolus.
Ketamine has potent analgesic properties and is used exten­
sively in the operating room as well as for painful dressing
changes and procedures such as line insertion. A drying
agent such as glycopyrrolate (2–5 µg/kg) may be given in
combination with ketamine to reduce ketamine-induced
secretions. Delirium during emergence from ketamine seda­
tion is more common in adults. This is often treated with
midazolam, but dexmedetomidine may be more effective
and also attenuates hypertensive and tachycardic effects of
ketamine.168 Dexmedetomidine also reduces the dose of ket­
amine required.169
Propofol is the most common intravenous induction
agent used in burn patients. Dose requirements for propofol
will vary over time after the initial burn injury. Initially,
with hypovolemia and reduced cardiac output, a lower dose
may be required but as the hyperdynamic circulatory
pattern develops the Vd and clearance rate for propofol are
increased enough to increase dose requirements.170
Volatile anesthetics may be used for both induction and
maintenance of anesthesia in burn patients. In pediatric
patients, mask induction with sevoflurane is commonly
used if the patient does not have injuries that may make
airway manipulation difficult. In the acute setting, an anes­
thetic technique involving nasotracheal intubation after
mask induction with halothane, nitrous oxide, and oxygen
has been described.171 The proponents particularly empha­
size avoiding the potential problems associated with the
ketamine-based technique. However volatile agents produce
dose-dependent cardiac depression and vasodilation. 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
wash-in and wash-out kinetics and provide a useful adjunct
to other agents when titrated to hemodynamic and ventila­
tory 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 anes­
thetic if the patient’s oxygen requirements permit.
Opioids are important agents for providing analgesia for
burn patients throughout the acute phase of injury and for
providing postoperative analgesia in patients undergoing
reconstructive procedures. The spectrum of opioids cur­
rently available provides a wide range of potencies, dura­
tions of action, and effects on the cardiopulmonary system.
Burn patients experience intense pain even in the absence
of movement or procedures, and opioids are the mainstay
for providing analgesia in the acute phase of burn manage­
ment. Selection of dosage must take into account the fact
that acute burn patients usually become tolerant to opioids
due to continuous and prolonged administration. Therefore
opioids should be titrated to effect in the acute burn patient.
Most opioids have little effect on cardiovascular function,
but they are potent respiratory depressants. Therefore the
ventilatory status of patients receiving opioids, particularly

13  •  Anesthesia for Burned Patients
152
of 6–6.5 g/dL compared to patients maintained at a hemo­
globin near 10 g/dL.178 However, in general, few outcome
data exist regarding the optimum transfusion trigger for
blood transfusion during burn wound excision. Assessment
of blood transfusion needs is best determined by evaluating
the clinical status of the patient; specifically, assessment of
ongoing blood losses, preoperative hemoglobin levels, vital
signs, and urine output. Metabolic evidence of inadequate
oxygen delivery such as acidemia and decreasing mixed
venous oxygen tension provide important information
regarding the oxygen balance in the patient. Patients with
coexisting cardiac and pulmonary disease generally require
higher oxygen-carrying capacity. Oxygen requirements will
be determined by the type and severity of coexisting condi­
tions. Overall American Society of Anesthesiologists guide­
lines indicate that blood transfusion is rarely required at a
hemoglobin of 10 g/dL or above and is almost always indi­
cated at a hemoglobin of less than 6 g/dL.179
During excision of large burn wounds, patients may
require one or more blood volumes of transfused blood to
replace intraoperative blood losses. Massive blood transfu­
sion can be associated with a variety of complications, and
the use of blood products is associated with significant
financial costs.175 Several means of decreasing surgical
blood loss during burn wound excision may be employed,
such as the use of tourniquets on limbs and compression
dressings at sites of burn wound excision or skin graft har­
vesting.180 Tourniquets have been shown to be an effective
strategy for decreasing blood loss during burn wound exci­
sion.176 The drawbacks of tourniquet use are that their
effectiveness is limited to surgery on the extremities and
they may interfere with the surgical field. Pharmacological
interventions that may decrease blood loss include the use
of epinephrine-soaked dressings or topical epinephrine
spray to induce local vasoconstriction. Alternatively subcu­
taneous 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 subcutane­
ous epinephrine in burn patients is not associated with an
increased incidence of side effects or complications.181
The effectiveness of this approach is, however, 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 exci­
sion.182 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, decreased
blood loss and transfusion requirements in a cohort of pedi­
atric and adult burn patients.183 The authors did not report
significant complications associated with this approach.
BLOOD COMPONENTS
Several blood components are available for replacement of
losses incurred during burn wound excision. These compo­
nents include whole blood, PRBCs, fresh frozen plasma
(FFP), platelets, and cryoprecipitates.
sponges, or may be washed down a drain on the operating
table. As discussed earlier regarding the initial resuscita­
tion, there is no one physiological end point to titrate volume
replacement. Arterial pressure may be maintained by vaso­
constriction despite significant hypovolemia, CVP 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 wave form and changes with the
respiratory cycle may indicate hypovolemia. Even though
CVP correlates poorly with hemodynamic function, this
variable is useful in determining if volume administration
will be tolerated by the patient. If the perfusion appears
inadequate and CVP is low or normal it is safe to give
volume. If CVP is elevated, volume administration may
cause pulmonary edema.
The concept of transfusion trigger with regard to burn
care is discussed in the next section. It must be remembered,
however, that during rapid blood loss the hematocrit may
change more slowly than the blood loss, and often blood
must be administered in anticipation of the hematocrit
falling 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. In fact, when the resuscitation is inadequate, the
hematocrit will be elevated. 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.174 However
major blood loss is common during excision and grafting of
burn wounds. Desai and colleagues reported that the
amount of blood loss during burn wound excision is deter­
mined by the age of the burn, the body surface area involved,
and whether infection is present (see Table 13.1).12 In
general, more blood loss was observed as the time from
initial injury increased and if wounds were infected. Trans­
fusion requirements ranging from 0.45 to 1.25 mL of
packed red blood cells (PRBCs) per cm2 burn area were
reported. In another study, Criswell and Gamelli reported
an average transfusion rate of 0.89 mL PRBC/cm2 burn
area in a cohort of adult burn patients.175 A study by
O’Mara and colleagues showed an average transfusion rate
of 0.65 mL PRBC/cm2 in a heterogeneous group of burn
patients.176
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 cardiovas­
cular disease.177 The same group proposed maintaining
hematocrit near 25% in patients with more extensive burns
and near 30% if the patients have pre-existing cardiovascu­
lar 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

13  •  Anesthesia for Burned Patients
153
provide oxygen-carrying capacity and, when reconstituted
with crystalloid or plasma, volume resuscitation.
Fresh Frozen Plasma
In the setting of burn injury, FFP is most commonly used
to replace clotting factors during massive blood transfu­
sion. FFP will replace clotting factors as well as protein S
and protein C by a factor of 2–3% per unit. The initial rec­
ommended volume is 10–15 mL/kg. The use of FFP varies
among different burn centers. Plasma is frozen within 6
hours of collection, and each unit provides approximately
250 mL of plasma containing normal levels of all coagula­
tion factors. In the setting of massive blood transfusion,
FFP administration is indicated if active bleeding exists
and laboratory evidence of coagulation factor depletion is
shown. A volume of 2–6 units is generally used depend­
ing on the severity of the coagulopathy. Some practitio­
ners argue that the use of FFP rather than crystalloid to
reconstitute PRBCs results in less interstitial edema during
the postoperative period and may enhance skin graft
survival.
In the past, guidelines recommended the use of FFP to
replace shed blood only for documented coagulopathy due
to reduced coagulation factors. Recent experiences with
both civilian and military trauma have led to more liberal
use of FFP, and, as a result, early and aggressive use of FFP
to treat massive hemorrhage has been associated with
decreased mortality.184,185 As a result, massive transfusion
protocols including early use of blood products other than
PRBCs to support coagulation (e.g., FFP, platelets, and cryo­
globulin) are now activated for trauma patients requiring
massive transfusion.186,187 Blood loss during extensive burn
wound excision often meets criteria for the diagnosis of
massive transfusion. The physiological status of trauma
patients presenting with hypovolemic shock, acidemia,
hypothermia, and coagulopathy, however, is different from
the post-resuscitation burn patient. Except in certain emer­
gencies burn patients should have their wounds debrided
when resuscitation is effective or in the post-resuscitation
period. Under these circumstances the patient is warm, has
adequate preload and oxygen-carrying capacity, adequate
or increased cardiac output, and no coagulation dysfunc­
tion. As a result, all features of the massive transfusion
protocol are not necessary initially. At our institution (Shri­
ners Hospital for Children, Galveston) shed blood is initially
replaced with colloid (2.5% albumin), and the HCt is allowed
to diminish to a target value appropriate for the patient
before PRBCs are administered. As a result of dilution, shed
blood contains a smaller mass of RBCs. When shed blood
reaches 50% of estimated total blood volume, it is then
replaced with PRBCs mixed with FFP. Transfusion of recon­
stituted whole blood in burned children has been shown to
be safe and efficacious.188 Only if microvascular bleeding
occurs along with thrombocytopenia and/or hypofibrino­
genemia are other blood products administered.
Platelets
Platelets are stored at room temperature to maximize viabil­
ity. The incidence of bacterial contamination increases
exponentially 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
Whole Blood
Whole blood consists of unfractionated blood and contains
all of the components of blood including red blood cells
(RBCs), plasma, platelets, and white blood cells. However
whole blood stored for more than 24 hours does not contain
functional white blood cells or platelets (Box 13.6). 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
to provide oxygen-carrying capacity in patients requiring
large-volume blood transfusion.
Packed Red Blood Cells
PRBCs are the most common means of replacing RBC loss
during surgical procedures. Most of the plasma and plate­
lets 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 com­
position with whole blood is shown in Table 13.4. PRBCs
Box 13.6  Indications for Arterial Cannulation
1. Expected blood pressure changes more rapid than the interval
between noninvasive measurements
2. Patient’s fragility and reduced physiological reserve (e.g.,
ischemic or valvular heart disease)
3. Requirement for vasoactive infusions (other than dobutamine)
4. Need for measurement of PaO2 for management of respiratory
support
5. Extremities unavailable for blood pressure cuff
Table 13.4  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

13  •  Anesthesia for Burned Patients
154
Citrate Toxicity
Citrate is universally used as an anticoagulant in the
storage of blood because of its ability to bind calcium that
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,
resulting in a fall in ionized calcium.192 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 coagulation abnormalities are seen. During massive
blood transfusion it is generally prudent to monitor ionized
calcium, especially if hemodynamic instability is present in
the hypocalcemic patient.
Potassium Abnormalities
During the storage of whole blood or packed red cells, potas­
sium leaks from erythrocytes into the extracellular fluid and
can accumulate to concentrations of 40–80 mEq/L. Once
the RBCs are returned to the in vivo environment, the potas­
sium quickly reenters RBCs. However, during rapid blood
transfusion, transient hyperkalemia may result, particu­
larly in patients with renal insufficiency.193 The transient
hyperkalemia, particularly in the presence of hypocalce­
mia, can lead to cardiac dysfunction and arrhythmias. In
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’s 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.
COMPLICATIONS OF MASSIVE BLOOD
TRANSFUSION
Coagulopathy
Coagulopathy associated with massive blood transfu­
sion is due to thrombocytopenia or depletion of coagu­
lation factors. PRBCs are essentially devoid of platelets,
and whole blood stored for more than 24 hours does not
possess significant numbers of viable platelets.189 Whole
blood contains essentially normal levels of coagulation
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 results in dilutional losses of platelets
and factors V and VIII, particularly when PRBCs alone
are utilized.
Thrombocytopenia is the most common cause of nonsur­
gical bleeding after massive blood transfusion.190 In general,
15–20 units, or 2–4 blood volumes of blood or PRBCs,
must be transfused before bleeding due to thrombocyto­
penia will develop (Fig. 13.11). Observed platelet counts
usually remain higher than calculated values due to the
release of platelets from sites of sequestration. Bleeding due
to thrombocytopenia usually develops when the platelet
count drops below 50,000–100,000 platelets/µL. Replace­
ment of platelets usually requires transfusion of 6 units of
whole blood platelets or 1 unit of single-donor platelets as
described earlier in this chapter.
Development of coagulopathy due to depletion of coagu­
lation factors is also possible during massive blood transfu­
sion. Significant prolongation of the prothrombin (PT) and
partial thromboplastin time (PTT) can result after transfu­
sion of 10–12 units of PRBCs in adults. It has been recom­
mended that FFP be given to correct dilutional coagulopathy
if the PT and PTT exceed 1.5 times normal levels.191 It is also
important to know the fibrinogen level in massively transfused
patients since hypofibrinogenemia can also result in prolon­
gation of the PT and PTT. Fibrinogen may be replaced using
cryoprecipitate.
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
Fig. 13.11  Calculated versus observed mean platelet counts in two
studies of platelet count after massive blood transfusion. (From Reed
RL, et al. Prophylactic platelet administration during massive transfusion.
Ann Surg. 1986;203:46.)

13  •  Anesthesia for Burned Patients
155
blood transfusion per se. However volume status should be
monitored closely during large-volume blood transfusion so
that volume overload may be avoided.
Transfusion-associated acute lung injury (TRALI) is a
relatively rare complication characterized by acute hypox­
emia and noncardiogenic pulmonary edema occurring
within 6 hours of blood transfusion.195 Although relatively
uncommon, TRALI is among the most common causes of
transfusion-related mortality.196 The pathogenesis is not
well understood but is thought to be related to transfusion-
associated inflammatory responses. Although the incidence
is higher in critically ill patients, specific risk factors are
difficult to identify and treatment is supportive. In cases of
transfusion-related lung injury, it is important to rule out
other causes of ARDS and the presence of transfusion-
associated volume overload (TACO).
Transfusion Reactions
Hemolytic transfusion reactions are a relatively rare but
devastating complication of blood transfusion. The inci­
dence of transfusion reactions is approximately 1 : 5000
units transfused, 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
transfusing ABO-incompatible blood 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 13.5. Massive hemolytic transfusion reactions
result from destruction of transfused erythrocytes by cir­
culating antibodies and complement. Many of the common
signs and symptoms of transfusion reactions, such as chills,
chest pain, and nausea, cannot be detected in a patient
under general anesthesia. The most commonly recognized
signs of transfusion reaction in the anesthetized patient
are fever, hypotension, hemoglobinuria, and coagulopathy.
The cornerstones of treatment are to stop the transfusion,
protect the kidneys with aggressive hydration and alkaliza­
tion of urine, and treat existing coagulopathy.197
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
patients with renal insufficiency, potassium load can be
minimized by the use of either freshly obtained blood or
washed packed RBCs. Hypokalemia 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 rou­
tinely 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 resulting from an imbal­
ance of oxygen consumption and delivery. The anaerobic
metabolism that occurs during states of hypovolemia and
poor tissue perfusion results in lactic acidosis.186 Generally,
administration of sodium bicarbonate is not indicated. The
re-establishment of tissue perfusion and homeostasis is a
much more important factor in re-establishing acid–base
balance. In contrast, many patients receiving massive blood
transfusion 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 addi­
tional reason to avoid sodium bicarbonate administration
during massive blood transfusion except in cases of severe
metabolic acidosis (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 dimin­
ished. 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.194 When added to the
already impaired thermoregulatory mechanisms in burn
patients this can result in clinically significant hypother­
mia. 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 in burn patients.
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
Table 13.5  Blood Groups and Cross-Match
Blood
Group
Antigen on
Erythrocyte
Plasma
Antibodies
Incidence (%)
Whites
African-Americans
A
A
Anti-B
0.40
27
B
B
Anti-A
11
20
AB
AB
None
4
4
O
None
Anti-A
45
49
Anti-B
Rh
Rh
42
17

13  •  Anesthesia for Burned Patients
156
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 bronchoscope with an
endotracheal tube already loaded on the bronchoscope.
Especially in small pediatric patients a common reason for
post-extubation stridor and failed extubation is edematous
and redundant mucosa over the arytenoid eminences that
obstruct the glottic inlet during inspiration (Fig. 13.12A,
video). This condition can be exacerbated by an endotra­
cheal tube that is too large, excessive patient motion due to
inadequate sedation and analgesia, reflux of acidic gastric
contents, and mechanical irritation due to compression of
the posterior laryngeal structures between the endotra­
cheal tube and gastric tubes. These irritants can also cause
laryngomalacia in pediatric patients (Fig. 13.12B). If laryn­
geal obstruction persists despite attention to all these details
a short course of steroids is often effective as long as con­
cerns regarding burn wound infection do not preclude the
use of steroids (unpublished observations.) Heliox has also
been used successfully in this situation.199
The decision to extubate must also take into consider­
ation the metabolic state and the burn-related decrease in
strength of the patient. Increased generation of CO2 must
be matched by increased minute ventilation and respiratory
effort. Work of breathing is often also increased by poor
pulmonary compliance and diaphragmatic elevation due to
hepatomegaly.200 At the same time skeletal muscle wasting
and decreased strength are also products of the catabolic
state.98 If the patient’s physiological reserve was marginal
preoperatively, it may be best to continue mechanical ven­
tilation until extubation criteria can be assessed objectively
in the ICU.
After transfer of monitors and ventilatory support in the
ICU, a full report of the intraoperative anesthetic course is
given, along with information about the patient’s current
condition and therapy. A chest radiograph may be needed
for vascular catheters placed in the OR to check the position
of an endotracheal tube if the patient will be ventilated
postoperatively. Laboratory studies, including arterial blood
gas, blood chemistries, renal function tests, hematocrit,
alkalization of urine are usually indicated. Febrile reactions
are common following blood transfusion and are generally
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.
Infection
Infection is a major problem in burn patients due to dis­
ruption of the cutaneous barrier and immunosuppres­
sion. Blood transfusion adds to the infection risk. Graves
and colleagues showed a significant correlation between
the number of blood transfusions and infectious compli­
cations in burn patients.198 The most common source of
major infection 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 markedly decreased the incidence of HIV
infection to 1 in 200,000–500,000 units transfused. Cyto­
megalovirus (CMV) has been identified in blood products
and could cause clinically significant problems in immuno­
compromised burn patients. However the incidence of clini­
cally important CMV infection 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. The
airway must be examined to be sure edematous pharyngeal
tissues will not cause obstruction of the airway when the
endotracheal tube is removed. Air leaking around a deflated
endotracheal tube cuff during positive pressure ventilation
B
A
Fig. 13.12  Dynamic obstruction of the upper airway in a pediatric patient with thermal injury of the larynx. Edematous tissues collapse and obstruct
during inhalation (A) but expand and allow exhalation (B).

13  •  Anesthesia for Burned Patients
157
first few hours postoperatively in order to maintain ade­
quate oxygen saturation. Airway support may also be nec­
essary initially in these patients until they are more alert
and responsive.
Finally, burn patients must be recovered in a warm envi­
ronment. Postoperative hypothermia can result in vasocon­
striction, hypoperfusion, and metabolic acidosis and
exaggeration of the hyperdynamic and catabolic metabolic
response to their injury. Radiant heaters, blood and fluid
warmers, warm blankets, heated humidifiers for gas deliv­
ery, and high room temperature are all useful in the post­
operative period to provide warmth to the recovering
patient.
Conclusion
Anesthetic management of the burn patient presents
numerous challenges. Anatomical distortions make airway
management and vascular access difficult. Pathophysiolog­
ical changes in cardiovascular function range from initial
hypovolemia and impaired perfusion to a hyperdynamic
and hypermetabolic state that develops after the resuscita­
tive stage. These and other changes profoundly alter
response to anesthetic drugs. Effective anesthetic manage­
ment will depend on knowledge of the continuum of patho­
physiological changes, technical skills, proper planning,
and availability of proper resources. A team approach is
necessary, keeping in mind that perioperative management
should be compatible with ICU management and goals. This
requires close communication with other members of the
burn care team, which is one of the most important prin­
ciples of effective anesthetic management of these chal­
lenging patients.
Complete references available online at

platelet count, and coagulation studies, are sent soon after
patient arrival to the ICU. These studies are particularly
important if massive transfusion was required in the oper­
ating 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. 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 coagulopa­
thy. Diligent postoperative care is needed to continually
assess ongoing blood loss and to transfuse additional blood
products as they are indicated by clinical course and labora­
tory studies. Postoperative bleeding can be concealed by
bulky burn dressings. Such bleeding may manifest as hypo­
volemia and hypotension even in the brief period of trans­
port from the operating room to the ICU. Monitoring of CVP
and urine output also help in guiding postoperative blood
and fluid therapy.
Adequate ventilation is essential in the postoperative
period in order to minimize hypoxemia and hypercarbia.
Blood gases and oxygen saturation can be used as guides to
ventilator management. Patients with inhalation injury
benefit not only from rational ventilator management but
also from a program of inhaled bronchodilators and muco­
lytics combined with judicious airway suctioning. Extu­
bated patients require supplemental oxygen for at least the

157.e1
13  •  Anesthesia for Burned Patients
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