Burns Neligan

SECTION III Burns Surgery
18
Acute management of burn/electrical injuries
Lars Steinstraesser and Sammy Al-Benna
SYNOPSIS
Acute management of burn injuries
! Learn assessment and classification of burn wounds, including
estimation of burn size and depth, and reduction of related Rescue: The aim is to get the individual away from the
morbidity and mortality. source of the injury and provide first aid.
! Gain an appreciation of stress response to acute burn injury, Resuscitate: Immediate support must be provided for any
including hemodynamic, metabolic, nutritional and immunologic failing organ system. This usually involves administering
sequelae. fluid to maintain the circulatory system but may also
! Learn initial management of the acute burn patients, including involve supporting the cardiac, renal, and respiratory
fluid resuscitation, nutritional support and wound care. systems.
! Learn wound management of burn patients including an Retrieve: After initial evacuation to an accident and emer-
understanding of wound healing, wound sepsis, topical gency department, patients with serious burns may need
antimicrobial agents, biological dressings, skin substitutes and transfer to a specialist burns unit for further care.
skin grafts. Resurface: The skin and tissues that have been damaged by
! Learn fundamental surgical principles in treatment of burn patients, the burn must be repaired. This can be achieved by
including wound debridement, wound dressing and splinting, skin various means, from simple dressings to aggressive
grafting and scar contracture release. surgical debridement and skin grafting.
! Burn rehabilitation, including physical/occupational therapy, Rehabilitate: This begins on the day a patient enters hospital
psychosocial support and reconstructive needs. and continues for years after he or she has left. The aim is
! Principles of management of special problems, including inhalation to return patients, as far as is possible, to their pre-injury
injuries, chemical burns, electrical injuries and toxic epidermal level of physical, emotional, and psychological wellbeing.
necrolysis. Reconstruct: The scarring that results from burns often leads
to functional impairment that must be addressed. The
operations needed to do this are often complex and may
Access the Historical Perspective section online at need repeating as a patient grows or the scars re-form.
http://www.expertconsult.com Review: Burn patients, especially children, require regular
review for many years so that problems can be identified
early and solutions provided.
Aims of burn care

Restore form: Return the injured areas to as close to
Epidemiology
normality as is attainable
The incidence of burn injuries varies from country to country,
Restore function: Optimize patients ability to perform typically peaking during the countrys holiday period.
activities of daily living at pre-injury level According to the most recent statistics compiled by the World
Restore feeling: Enable psychological and emotional Health Organization and the World Fire Statistics Center, fires
rehabilitation. caused 6.6 million major burn injuries and 400 000 deaths
2013, Elsevier Inc. All rights reserved.
Downloaded for Universidad Monterrey (udem@udem.edu) at Universidad de Monterrey from ClinicalKey.com by Elsevier on September 17, 2017.
For personal use only. No other uses without permission. Copyright 2017. Elsevier Inc. All rights reserved.
History 393.e1
Around 500 BCE, the Chinese were using a mixture of tea

History leaves (tannic acid) to treat burns, but the oldest preserved
written Chinese scientific description of burn wound treat-
Since man first learned to make fire (ca.500 000 BCE), fire was ment dates back to Hong Ge (281341 CE). His book Zhou Hou
metaphorically a multiedged sword. By controlling fire, man Fang (Prescriptions for Emergency) suggested the topical
could throw off many shackles but once the use of fire was application of two different prescriptions: old (imperative)
incorporated into daily life, accidental burns became an inevi- calcarea optionally blended with plant oil, or the use of pig
table cause of common and severe injuries. Man began to fat cooked with willow bark. The application of these mix-
search their environment for soothing burn medications. The tures resulted in reduced numbers of wound infections and
difficulties in the treatment of burns have been lamented by has to be regarded as the oldest preserved Chinese description
all writers for millennia. of an anti-infectious astringent to be used in thermal
About 4000 BCE the Shumerian civilization emerged upon injuries.
the flood plain of the lower reaches of the Tigris and Euphrates Paulus Aegineta (625690 CE) recommended applications
rivers. One of the greatest finds of archaeology was the ruins of moderately detergent materials, which were not definitely
of a library assembled in Nineveh by Ashurbanipal. The heating or cooling: Light earths mixed with vinegar to
library included a medical section with Shumerian medical prevent blisters from forming. Rhazes (850923 CE) of the
texts dealing with the diagnosis and bultiti (therapy) of burns Arabian School of Medicine introduced the popular white
written on tablets of moist clay in cuneiform script. An anony- ointment, composed of white lead, oil of roses and wax.
mous Shumerian physician, who lived toward the end of the Furthermore, he wrote about the effect of application of cold
3rd millennium BCE, prepared a tablet 9.5 16 cm in size and water in relieving the pain of an acute burn. Thus, Rhazes
wrote down a number of remedies for burns, based on plant advised rose water, cooled with snow, and Avicenna (980
extracts. This clay document, the oldest medical handbook 1037 CE) advocated icy water. Valesco de Tarenta of Montpellier
known to man, lay buried in the Nippur ruins for more than in his Textbook of Surgery (1490) described how to avoid syn-
5000 years, until it was excavated and taken to Philadelphia. dactyly in the burnt hands. Bouisson of Montpellier was the
The next data on the treatment of burns is recorded in Ebers originator of the exposure method in treating burns: in
Papyrus in 1500 BCE, where initial topical treatment of burns burns the ventilation can supersede other methods it sub-
was a frog warmed in oil and rubbed on the burned surface, stitutes dry for a moist surface diminishing the chances of
and later treatment included lemon strips in an oily lixture or infection.
black mud, boiled cow dung and goose. Par (15101590 CE) clearly described the differences
Sushruta Samhita (ca.800 BCE) used clarified butter mixed between second-degree and third-degree burns, early excision
with red ochre or the bark of a fig tree. He recommended of the burn wound, and those burns that frequently devel-
debridement of severe burns with loose skin and flesh. In oped contractures. One must be careful if burns affect the
the Sushruta Samhita, we find the first description of the clas- palpebres or the legs or the fingers or the throat or the axilla
sical symptoms of a typical burn case the enormous thirst or the joint of the knee or of the arm for these joints should
and fever are mentioned. The Old Testament (Leviticus 13: not stick together. Fabricius Hildanus (15601634 CE) wrote
2428) lists burn-injury of the skin among other dermatologi- the first book devoted entirely to burns: De Combustionibus
cal illnesses. (1607) and insisted that the classification of burns should be
Hippocrates (460377 BCE) wrote a whole chapter on burns a guide for treatment: Gradus et distributio combustionurn
in his book Peri Elkeon (About Ulcers). Burns were systemati- in tres species item ex quibus indicationes. A more extensive
cally described as kavma or pyrikafston. He realized the signifi- survey was written in 1622 by Hornung. Richard Wiseman in
cance of loss of fluids from the burn surface by pointing out 1676 wrote several chirurgical treatises and discussed
in his book Peri Himon (About Humors) that fluids (exu- splinting to avoid contractures. He advised refrigerants or
dates) coming out of the vessels are forming blisters, as in calefactive medicaments.
burn wounds, and should be emptied and advised as treat- Richter (1788) wrote on the relation between burn wound
ment, lots of fluids and diluted honey by mouth for the size and the patients prognosis. Edward Kentish (17691797)
patient. In his fourth book, Kat Iitrion (In the Medical in his essay on burns (1797) described warm stimulating rem-
Office), which is similar to the operating theater of todays edies for the treatment of frostbite. Baron Guillaume
medicine, he clarified local treatment of wounds under aseptic Dupuytren (17751835) classified burns into six degrees. Jean
conditions. He demonstrated that wound management and Petit wrote about burns in the Dictionare des Sciences Medicales,
dressing changes should be as quick as possible, painless, which was published in 1812. He clearly delineated three
comfortable, and presentable, while the bandage should be degrees of burns, based on depth, as erythema, blistering, and
soft, light, and clean. He urged his colleagues to work under full-thickness skin injury, including tendon or muscle. Samuel
as clean conditions as possible and to wear clean and properly Coopers surgical dictionary of 1830 referred to the three-
tailored garments. Finally, according to the Hippocratic degree classification based on inflammation and appearance,
Aphorisms, surgery remained the ultimate solution for treat- rather than burn depth.
ment, since what drugs do not cure, iron may cure; what iron In a landmark decision in 1848, Syme at the Royal Infirmary
doesnt. in Edinburgh designated one building for all burn cases, and
Pliny the Elder (2379 CE) used goats dung, gluebristles, this became known as the Burn Hospital. The 19th century
wax and bone marrow. Application of animals dung is still presented two basic important principles for the local treat-
popular in various parts of the world. Apart from the excision ment of burns. Pollock (18171897) used in 1871 skin grafts
of contracted scars described by Celsus, surgery had no place for burns, after Reverdins famous publication on skin graft-
in the treatment of burns in Greek and Roman medicine. ing technique in Paris in 1869.
393.e2 SECTION III 18 Acute management of burn/electrical injuries
In 1875, Joseph Lister recommended boric acid and carbolic and wrote an article in the Journal of the American Medical
acid for burn wounds to kill bacteria. In 1881, Tappeiner of Association advocating early skin grafting.
Munich studied autopsies of burn deaths and recognized the The first person to suggest excision of the burnt tissue was
concentration of blood, increased hemoglobin concentration, Lusgarten (1871), however, Wilms (1901) was the first to carry
and decreased blood and water volume. In spite of a speech it out, but he never grafted the excised areas. In Vienna,
by Robert Hornby in 1833 to the Royal Medical Society, in Weidenfeld and Zumbusch (1905) performed excision of
which he recognized burn shock as similar to shock seen with burnt areas in the acute period, either on admission or during
acute peritonitis, and in which he argued against bleeding the first 3 days. In 1968, Janekovi revived the idea of early
and purging, these practices persisted through the latter part excision of burnt tissue and immediate skin grafting and thus
of the 19th century. The appreciation by Tappeiner of burn laid the cornerstone to the contemporary principle of early
pathology, however, was a significant event. In 1905, Sneve tangential excision and early grafting.
noted the importance of intravenous saline for resuscitation
394 SECTION III 18 Acute management of burn/electrical injuries
every year.1 The burden of burn injury falls predominantly Thermal burns
on the worlds poor; 95% of fire-related burns occur in low-
Flash and flame burns
and middle-income countries where prevention programs
are almost nonexistent and open fires for cooking, lighting Flash and flame burn injuries are the most common cause of
or heating are commonplace. The average death rates are adult burn admissions. In general, flash burns reach progres-
about three fire deaths per 100 000 inhabitants and one fire sive layers of the dermis in proportion to the amount and kind
death per 100 fires. However, this average conceals a more of fuel that explodes. In contrast to flash injuries, flame burns
than 100-fold variation in death rates from country to country. are invariably deep dermal if not full-thickness because of
A better indication of typical fire risk is the median fire more prolonged exposure to intense heat and are often associ-
death rate per 100 000 inhabitants by country, which was 0.9 ated with inhalational injury and other concomitant trauma.
in 2004. In addition, the WFSC released fire-related death Patients whose bedding or clothes have been on fire rarely
data by country (from lowest to highest number of deaths per escape without some full-thickness burns.
100 000 person) from 20022004. The countries with the lowest
incidences include Singapore (0.08) and Switzerland (0.51). Scalds
Those with the highest include Finland (2.08) and Hungary Hot water scalds are the most common cause of pediatric burn
(2.10).The cost to society in terms of lost wages, vocational admissions. They also often occur in elderly people. The
rehabilitation, and need for long-term care is staggering. common mechanisms are spilling hot drinks or liquids or
Worldwide, severe burns cause disabilities that cost $80.2 being exposed to hot bath water (Fig. 18.1). The depth of scald
billion a year in lost productivity (wages and skills) alone; injury depends on the water temperature, the skin thickness
medical expenses would add millions more. Lost productivity and the duration of contact. Water at 60C creates a deep
costs the world billions of dollars annually. In 2009, the WFSC dermal burn in 3 s but will cause the same injury in 1 s at
noted that the cost of direct fire losses ranged from 0.060.26% 69C. Boiling water often causes a deep dermal burn, unless
of countries gross domestic product (GDP) and the cost of the duration of contact is very short. Grease and hot oils will
indirect fire losses ranged from 0.0020.95% of countries generally cause deep dermal or deeper burns.
GDP.
Males account for approximately two-thirds of the total Contact burns
costs of fire/burn injuries and females account for the remain- In order to get a burn from direct contact, the object touched
ing third. Fatal fire and burn injuries cost 2% of the total costs must either have been extremely hot or the contact abnor-
of all fatal injuries. Hospitalized fire and burn injuries are 1% mally long. The latter is a more common reason, and these
of the total cost of all hospitalized injuries. Nonhospitalized types of burns are commonly seen in people with epilepsy
fire and burn injuries cost 2% of the total cost of all non- or those who misuse alcohol or drugs. They are also seen
hospitalized injuries. in elderly people after a loss of consciousness; such a presen-
tation requires a full investigation as to the cause of the black-
out (Fig. 18.2). Contact burns commonly result from hot
metals, plastics, glass or hot coals. Burns from brief contact
Risk factors with very hot substances are usually due to industrial acci-
dents. Although generally small in size, contact burns are
Children under 5 years old are a vulnerable group, susceptible
to injury and especially to burns. The two most common
causes of burns are scalds and contact burns. The latter
play a minor role since they imply injury of small extent
and rarely require admission to hospital. On the other
hand, scalds are often accidents of such a severity that
hospitalization and resuscitation are required. In children,
scald burns accounted for about two-thirds of burn injuries
and in those <5 years old, scalds caused 75% of all burn
injuries, most commonly occurring in the kitchen. In adults,
predisposing factors to scalding include alcoholism, senility,
psychiatric disorders, and neurological disease such as
epilepsy.
Mechanisms of thermal injury

Types of burns
The body has very few specific protective and repair mecha-
nisms for thermal, electrical, radiation and chemical burns.
Heat changes the molecular structure of tissue and denatura-
tion of proteins is a common effect of all types of burns. The
extent of burn damage depends on the temperature of agent, Fig. 18.1 The burn wounds may give clues to the mechanism of injury. The burn
concentration of heat and the duration of contact. tideline associated with sitting in a bath of hot water.
Epidemiology 395
Burns due to hot tar are difficult to manage because of the

difficulty in removing the tar without inflicting further injury
to the underlying burn. As it is difficult to remove the tar
rapidly and there is no pressing medical need to do so, it is
best to treat the injury as a deep burn with appropriate fluid
resuscitation or preparation for skin grafting as needed.
Removal of the tar is not essential but it improves patient
comfort and allows early assessment of the underlying tissue
damage. This approach carries the risk of infection and the
potential conversion of a partial thickness injury to a full
thickness injury.
Numerous substances have been used in the past with vari-
able results and selection of the appropriate agent for the
removal of adherent tar is still challenging. Polyoxyethylene
sorbitan, an emulsifying agent commonly used as a base in
ointments, separates the tar from the skin and, as it is water
soluble, easily washes off.2
Alternatively silver sulfadiazine, neosporin ointment (with
polyoxyethylene sorbitan as a base), polysorbate or De-Solv-It
(a citrus petroleum distillate with surfactant and lanolin) may
be left on the burn, which is then bandaged. The tar comes
away with the bandages when they are removed the next day.
These may be used by themselves or in combination with an
antibiotic ointment.3 With some of these agents, it is recom-
mended to leave it on for 1248 h at a time until the tar has
dissolved.
Organic solvents, such as alcohol, acetone, aldehydes,
Fig. 18.2 Direct contact burn.
ether, gasoline and kerosene have had limited use. Some of
these substances are relatively ineffective, have a slow solvent
action, which requires continual rubbing and repeated appli-
cations and can induce further local tissue damage as well as
challenging in that the injury tends to be deep dermal or full the possibility of systemic toxicity through absorption, so
thickness. these are not recommended for removing tar.
Common household agents, such as mayonnaise (15
Tar 30 min), butter (2030 min), sunflower seed oil (2030 min),
Tar is usually used as a protective coating in surfacing pave- and baby oil (11.5 h) placed on sterile gauze and onto the
ment and roads, roofing and other industrial applications. It tar, have been promoted to remove tar effectively, rapidly
is made from distillates of petroleum and is composed of and without further damage, over the aforementioned
long-chain hydrocarbons and waxes, which have a high time periods. When large amounts of tar are present, the
boiling point. The boiling points of paving tar and roof tiling technique may need to be repeated. The burn depth can
tar are 140C and 232C, respectively. Hence, accidents involv- then be evaluated and managed by early surgical interven-
ing tar, tend to be associated with deeper burns. tion if required. Organic, nonsterile agents are easy to
When tar splatters, it cools rapidly to between 93C and acquire and are available in large quantities, but they carry
104C before landing. When hot tar makes contact with the the risk of promoting wound infection or allergic reaction.
skin it cools, solidifies and sticks. The tar usually retains suf- Bacterial or fungal growth can occur if the tar is not com-
ficient heat to produce a significant burn by prolonged heat pletely removed and the organic agent is not completely
transfer to the skin. Once cooled, the tar quickly hardens and rinsed off.
adheres to the skin. The aim of first aid at the scene is to Mechanical or manual debridement is painful, relatively
reduce the effects of thermal insult. In order to expedite the ineffective, and results in the removal of underlying viable
cooling and solidification process one should apply cold skin and hair follicles, thus extending the depth and area of
water. Often, the tar is cool by the time the patient arrives at the dermal injury. In addition, a degree of autodebridement
the medical facility. If not, the tar should be actively cooled to will occur. Debriding is a balance between removing the
terminate thermal damage with room temperature water and tar and exposing the injured skin for evaluation and treat-
prevent the further spread of the tar. Care must be taken not ment. Judgment should be exercised as to how much debride-
to develop hypothermia in major burns and adherent tar ment is appropriate in the emergency setting, as extensive
should not be removed in the field, but only by qualified debridement may require moderate-to-deep sedation. If the
personnel at a medical facility. The injuries are typically over skin has a light coat of tar and the patient does not complain
the exposed skin of the face and extremities and the burn is about the underlying skin or surrounding tissue, leaving the
of variable depth but is often deep second degree or third asymptomatic tar in place may be acceptable.4 It has been
degree. Tar which has just been heated is sterile, skin is not. reported that early excision and grafting may be required in
So, colonization of the wound from the surrounding intact some patients and this will decrease the hospitalization times.
skin may develop. Tar that is part of an obvious burn, blister, or tissue loss should
be removed and conjunctival tar, should be removed by an can occur with significant electrical burns. This multiorgan
ophthalmologist. injury (e.g., heart, kidney, nerves, eyes) must be promptly
identified, controlled and treated. In addition, it is important
Chemical burns to note that high voltage electrical injuries resemble a crush
See Cold and chemical injury to the upper extremity, Chapter syndrome and require suitable decompression. Therefore, the
20 for details of chemical burns. degree of tissue damage is more extensive than that perceived
on initial examination due to the progressive and continuing
Electrical burns tissue necrosis. In high-voltage injuries, the victim usually
Thermal injury due to electrical current is defined as tissue does not continue to grasp the conductor. Often, these patients
injury by exposure to supraphysiological electrical currents are thrown away from the electric circuit, which leads to
(Table 18.1). Electrical burns (Figs 18.3, 18.4) are classified as traumatic injuries (e.g., multiple orthopaedic injuries, cranio-
high voltage (1000 V), low voltage (<1000 V), flash burn (in encephalic trauma). As a result of these associated injuries,
which there is no electrical current flow through the body of these patients must be considered as polytraumatized.
the patient) and burns caused by lightning. Despite great advances in the treatment modalities of elec-
Low voltage injuries rarely cause significant damage trical injuries in the recent decades, the magnitude of the
beyond a small deep partial thickness burn at contact points. problem remains very high both for the victim and the treat-
High-voltage injuries are more apt to cause deep tissue ing surgeon. Most of them succumb to it due to systemic
destruction. In fact, most electrical burns are work related (i.e., effect; many of those who survive, lose one or more limbs and
construction workers, linemen, utility and electrical workers). present with complicated defects involving different tissues
Typically, high-voltage injury causes extensive skin injury at different parts of the body. These wounds are often poten-
with necrosis at the contact point and deeper structures, tially life-threatening and some are functionally disabling.
resulting in a large area of necrosis. The electricity flows The contact wounds are usually present at the entry and
through the tissues and generates heat, which damages them. exit points and the injuries are more severe at these two
The resistance of tissues increases gradually from nerves to points. The terminology of entry and exit point, however, is
vessels, muscles, skin, tendons, fat and bone. Bones are more an archaic term for the simple reason that they are applicable
resistant to the flow of electricity, producing the highest to direct current, whereas in an alternate current the exit point
amount of heat with the same current, in accordance with the becomes the entry (re-entry) point also. The resultant damage
Joule effect. Because of this phenomenon, multi-organ injury is more severe.
The victims of electrical burns show certain specific fea-
tures with regard to therapy and the evolution of the pathol-
ogy. The very nature of electrical burns is its vascular damage
Table 18.1 Physiologic effects of different electrical currents
leading to progressive tissue necrosis, often seen in skin and
Effect current (milliamps) muscles. Soft tissue damage in the extremities can precipitate
compartment syndrome requiring fasciotomy. This results
Tingling sensation/perception 14 in a gross limitation on manipulation of local tissues for
Let-go current 39 reconstruction.
The damage to the tissues is three-dimensional with the
Skeletal muscle tetany 1620 current producing extensive necrosis of the tissues at different
Respiratory muscle paralysis 2050 levels from skin to bone. The site and extent of tissue necrosis
can be clearly identified by 99 T Cm-MDP bone scans. The
Ventricular fibrillation 50120
optimal management of these wounds therefore has evolved
Fig. 18.3 Electrical burn wounds. Fig. 18.4 Entry site for an electrical burn.
Pathophysiology 397
into a plan of early primary debridement, suitable decompres- and pathologic alterations to the abdominal viscera. Therefore,
sion, including fasciotomy, an aggressive but cautious revi- these injuries of the abdomen warrant early exploration to
sion debridement and early skin cover, often composite, with determine whether there is injury of the viscera. Distribution
an aim to preserve vital structures. Serial and multiple debri- of intravenously injected fluorescein dye may prove helpful
dements of wounds, including superficial and deep muscles in demarcating devascularized bowel.
must be performed but nerves, tendons, joints and bones even
if denatured can be preserved as they can partially regenerate Nonaccidental burns
if covered with vascularized skin.
Aggressive treatment including surgical debridement of Up to one-tenth of pediatric burns may be due to non-
devitalized tissues, or those with doubtful viability, frequently accidental injury. Detecting these injuries is important as up
exposes vital structures in patients who have suffered high- to one-third of children who are repeatedly abused die.
voltage burns. The problem of high risk wounds warranting Usually children less than 3 years old are affected. As with
priority in providing an early and emergency cover com- other nonaccidental injuries, the history and the pattern of
pounded with paucity and limitations of choice of procedures injury may arouse suspicion. A social history is extremely
throw a great challenge to the surgeon. These require a higher important. Abuse is more common in poor households with
necessity of flaps when compared with other burn groups, single or young parents. Such abuse is not limited to children:
due to the characteristic compromising of deeper structures. elderly and other dependent adults are also at risk and a
High complication rates are reported with electrical injury similar assessment can be made in these scenarios.
including partial or complete flap failure. This fact, associated
with the need to preserve the vital organs and structures like
vessels, bones, tendons and nerves justifies the aforemen-
tioned cautious reconstructive approach with serial examina-
Pathophysiology
tion and debridement prior to a definitive surgery. The The skin is the largest organ of the body. While not very active
vascular damage and resulting thrombotic phenomenon metabolically, the skin serves multiple functions essential to
abates during second week and tissues become healthy. This our survival, functions that are compromised in the presence
is the time when tissues around the wound withstand manip- of a burn. These functions include: (1) Thermal regulation and
ulation for a local, regional, axial or free flap. The mortality prevention of fluid loss by evaporation. (2) Hermetic barrier
rate of patients who suffer high-voltage burns ranges from 0 against infection. (3) Sensory receptors that provide informa-
to 21.7%; their main cause of death is multiorgan failure section about environment.
ondary to sepsis of cutaneous origin.5,6 The skin is divided into three layers: (1) Epidermis: This is
Myonecrosis, with severe myoglobinemia as a result of a the outermost layer of skin composed of cornified epithelial
massive muscular destruction can lead to acute renal failure, cells. Outer surface cells die and are sloughed off as newer
despite aggressive volemic replacement. As the extent of cells divide at the stratum germinativum. The outer epider-
injury cannot be quantified as in a cutaneous burn, fluid mal layer provides critical barrier functions and is composed
resuscitation must be adjusted to urine output. The treatment of an outer layer of dead cells and keratin, which present a
of myoglobinuria includes initial stabilization and resuscita- barrier to bacterial and environmental toxins. The basal epi-
tion of the patient while concomitantly attempting to preserve dermal cells supply the source of new epidermal cells. (2)
renal function. Early aggressive fluid replacement is beneficial Dermis: This is the middle layer of skin composed of primarily
in minimizing the occurrence of renal failure. While osmotic connective tissue. It contains capillaries that nourish the skin,
diuretics (e.g., mannitol) and alkalinizing agents (e.g., bicar- nerve endings, and hair follicles. The inner dermal layer has
bonate) are considered the standard of care in preventing a number of essential functions, including continued restora-
acute renal failure in patients with myoglobinuria, there is tion of the epidermis. The dermis is divided into the papillary
little clinical evidence to support the use of these agents.7 dermis and the reticular dermis. The former is extremely bio-
Cardiac dysfunction, such as atrial fibrillation or supra- active; the latter, less bioactive. This difference in bioactivity
ventricular arrhythmias, are observed in up to one-third of within the dermis is the reason that superficial partial-
patients who suffered from electrical burns. Electrical func- thickness burns generally heal faster than deeper partial-
tion of the heart should be assessed by an initial electrocardio- thickness burns; the papillary component is lost in the deeper
gram and continuous cardiac rhythm monitoring for the burns. (3) Hypodermis: This is a layer of adipose and connec-
first 24 h after injury. According to the majority of publica- tive tissue between the skin and underlying tissues.
tions, these complications are transitory and no patients were Much of the treatment of burns is predicated on the depth
noted to have developed late cardiac complications. Chronic and extent (percentage total body surface area, TBSA) of the
complications that persist after the hospitalization period, initial burn injury. In this way the severity can be clarified and
include the occurrence of peripheral nerve injuries, mainly the treatment designed. The classification of burn depths
sensory deficits such as dysesthesias and paraesthesias and should be referred to as:
cataracts.
Epidermal burn
A wide spectrum of abdominal visceral complications
Superficial partial thickness burn
occur following high-voltage electrical injury. These injuries
result either from direct injuries to intra-abdominal structures Deep partial thickness burn
from the contact points over the abdomen or are a result of Full thickness burn.
current passing through the abdominal viscera from more It is critical to understand the clinical implications of accu-
distant entrance and exit wounds. In treating high-voltage rate evaluation of the injury so that consistent and timely
electric accidents, anticipate the entire spectrum of anatomic therapy can be instituted.
Burn injuries of the skin result in both local tissue destruc- dermal structures. One major component of burn shock is the
tion and systemic responses. Loss of the normal skin barrier increase in total body capillary permeability. Direct thermal
function causes the common complications of burn injury. injury results in marked changes in the microcirculation. Most
These include infection, loss of body heat, increased evapora- of the changes occur locally at the burn site, when maximal
tive water loss, and change in key interactive functions such edema formation occurs at about 812 h post-injury in smaller
as touch and appearance. burns and 1224 h post-injury in major thermal injuries. The
rate of progression of tissue edema is dependent upon the
adequacy of resuscitation.
Local response The temperature of the heat source and the length of
exposure determine the extent of tissue destruction (time-
The three mechanisms by which energy is transferred are temperature curve). Patients burned by higher temperatures
conduction, convection and radiation. All of these mecha- (molten metal, hot grease, or flammable clothing) have deeper
nisms affecting heat transfer may deliver heat to, or away burns than those burned with hot water. The effect also varies
from, living tissues. Sustained temperatures result in cellular over different types and parts of the body. The result of heat
dysfunction and early denaturation of protein. As the tem- injury is affected by variables such as skin thickness. The
perature or the time of exposure increases, cell damage thicker, glabrous skin of the palms and soles is more resistant
increases. to full-thickness injury than is the thinner skin of the eyelid
Excessively high temperatures cause graded tissue injury or dorsum of the hand. Infant skin is also thinner than adult
radiating from the point of contact and become progressively skin and more likely to sustain full-thickness injury from the
less severe at the periphery. The increased temperature kills same temperature.
cells in the immediate area and coagulates and denatures the The depth of any injury is not always obvious initially, and
surrounding extracellular matrix proteins (zone of coagula- observers often disagree. Many methods have been proposed
tion). Circulation to this area ceases immediately. The area to predict the depth of the injury immediately or soon after
surrounding the injury is characterized by decreased tissue injury (ultrasound examination, intravenous fluorescent
perfusion (zone of stasis). The tissue in this zone is potentially probes), but none has been as reliable as serial examination of
salvageable. The main aim of burn resuscitation is to increase the wound over time. The final depth of the injury typically
tissue perfusion here and prevent any damage becoming irre- becomes obvious 4872 h after injury. Very rarely does the
versible. Additional insults, such as prolonged hypotension, thermal injury penetrate into the subcutaneous or deep tissue.
infection, or edema, can convert this zone into an area of
complete tissue loss. With proper wound care, however, these
pathophysiological changes may be reversed. The zone of Systemic response
stasis is surrounded by a zone of hyperemia. In this outermost
zone, tissue perfusion is increased. The tissue here will invari- The release of cytokines and other inflammatory mediators at
ably recover unless there is severe sepsis or prolonged hypop- the site of injury has a systemic effect once the burn reaches
erfusion. The three zones of a burn were described by Jackson 30% TBSA. Cutaneous thermal injury greater than one-third
in 1947. These three zones of a burn are three-dimensional, of the TBSA invariably results in the severe and unique
and loss of tissue in the zone of stasis will lead to the wound derangements of cardiovascular function called burn shock.
deepening as well as widening. Shock is an abnormal physiologic state in which tissue per-
Primary tissue loss in burn injury occurs as a result of fusion is insufficient to maintain adequate delivery of oxygen
protein denaturation secondary to thermal, chemical, electri- and nutrients and removal of cellular waste products.
cal, friction, or ultraviolet radiation induced insults. This Unresuscitated burn shock correlates with increased hemat-
process is rapidly followed by activation of toxic inflamma- ocrit values in burned patients, which are secondary to fluid
tory mediators, especially in the perfused subsurface. Oxidants and electrolyte loss after burn injury. Increased hematocrit
and proteases further damage skin and capillary endothelial values occurring shortly after severe burn injury result from
cells, potentiating ischemic tissue necrosis Burn wound con- fluid and protein translocation into both burned and non-
version is also attributed to the secondary consequences of burned tissues.
burn injury. Sequelae such as edema, infection, and altered Burn shock is a complex process of circulatory and micro-
perfusion promote progression of injury beyond the degree of circulatory dysfunction that is not easily or fully repaired by
initial cell death. Burn-induced disruption of collagen cross- fluid resuscitation. Severe burn injury results in significant
linking abolishes the integrity of osmotic and hydrostatic hypovolemic shock and substantial tissue trauma, both of
pressure gradients, resulting in local edema and larger scale which cause the formation and release of many local and
fluid shifts. In addition, damage to cell membranes results in systemic mediators. Burn shock results from the interplay of
a dynamic cascade of inflammatory mediators that exacerbate hypovolemia and the release of multiple mediators of inflam-
already abnormal cell-to-cell permeability, worsening fluid mation with effects on both the microcirculation and the func-
regulation and systemic inflammatory responses. At the tion of the heart, large vessels and lungs. Subsequently, burn
molecular level, both complement activation and intravascu- shock continues as a significant pathophysiologic state, even
lar stimulation of neutrophils result in the production of cyto- if hypovolemia is corrected. Increases in pulmonary and sys-
toxic oxygen free radicals. Increased histamine activity, temic vascular resistance (SVR) and myocardial depression
enhanced by the catalytic properties of xanthine oxidase, occur despite adequate preload and volume support. Such
causes progressive local increases in vascular permeability. cardiovascular dysfunctions can further exacerbate the whole
Toxic byproducts of xanthine oxidase, including hydrogen body inflammatory response into a vicious cycle of accelerat-
peroxide and hydroxyl radicals, appear to directly damage ing organ dysfunction.
Pathophysiology 399
Hypovolemia and fluid extravasation Mediators of burn injury

Burn injury causes extravasation of plasma into the burn Apart from the burn shock mechanism already described,
wound and the surrounding tissues. Extensive burn injuries burn injury produces a veritable cornucopia of local and cir-
are hypovolemic in nature and characterized by the hemody- culating mediators that are produced in the blood or released
namic changes similar to those that occur after hemorrhage, by cells after thermal injury. These mediators clearly play
including decreased plasma volume, cardiac output, urine important, but complex roles in the pathogenesis of edema
output, and an increased systemic vascular resistance with and the cardiovascular abnormalities of burn injury. Osteo-
resultant reduced peripheral blood flow. However, as opposed muscular proteolysis, lipolysis, gluconeogenesis, increased
to a fall in hematocrit with hemorrhagic hypovolemia, due to metabolic rate, and a severe systemic inflammatory response
transcapillary refill an increase in hematocrit and hemoglobin are induced by local infections or surgical procedures. The
concentration will often appear even with adequate fluid increased vascular permeability post-burn is mediated by his-
resuscitation. As in the treatment of other forms of hypovo- tamine and numerous vasoactive substances, including sero-
lemic shock, the primary initial therapeutic goal is to quickly tonin, bradykinin, prostaglandins, leukotrienes, and platelet
restore vascular volume and to preserve tissue perfusion to activating factor. Hyper-metabolism is mediated by hormones
minimize tissue ischemia. The critical concept in burn shock such as catecholamines, glucagon, and particularly cortisol.
is that massive fluid shifts can occur even though total body
water remains unchanged. What actually changes is the
volume of each fluid compartment, intracellular and intersti-
tial volumes increasing at the expense of plasma volume and
blood volume. In extensive burns (>25% TBSA), fluid resusci- Hints and tips
tation is complicated not only by the severe burn wound
edema, but also by extravasated and sequestered fluid and A burn results in three distinct zones: coagulation, stasis,
protein in nonburned soft tissue. Large volumes of resuscita- and hyperemia
tion solutions are required to maintain vascular volume The aim of burns resuscitation is to maintain perfusion of
during the first several hours after an extensive burn. Multiple the zone of stasis
formulae have been published with variations in both the Systemic response occurs once a burn is greater than 30%
volumes per weight suggested and the type or types of crys- of total body surface area
talloid or crystalloid-colloid combinations administered to Different burn mechanisms lead to different injury patterns.
approximate the fluid need of a burn patient. To date, no
single recommendation has been distinguished as the most
successful approach. A detailed description of various formu-
lae appears later in this chapter. It should be emphasized that
blind adherence to any formula can result in overresuscita- Initial evaluation and treatment
tion and thereby to massive volume overload and edema. All
formulae represent only a rough guideline to estimate the Treatment of a burned patient starts at the scene of injury with
fluid need. Successful fluid resuscitation has to be adapted to the safe removal of the patient from the cause of the burn. In
the clinical need and to the monitoring (urinary output, suf- all cases (especially if chemical or electrical burns), care must
ficient mean arterial pressure). Data suggest that despite fluid be taken to avoid personal injury by checking the area is safe
resuscitation normal blood volume is not restored until 24 and that appropriate protective clothing is worn if necessary.
36 h after large burns. Edema formation often follows a bipha- Priority should be given to assessing the persons airway,
sic pattern. An immediate and rapid increase in the water breathing, and circulation, and presence of any coexisting
content of burn tissue is seen in the first hour after burn injury. injuries which may require more urgent treatment than the
A second and more gradual increase in fluid flux of both the burn. Belts, clothes, jewelry and watches that can retain heat
burned skin and nonburned soft tissue occurs during the first and cause constriction should be removed and the patient
1224 h following burn trauma. kept aware. An inhalation injury should be assumed and
The tissues in ischemic areas can potentially be salvaged airway should checked and oxygen given. Heat can be dissi-
by proper resuscitation in the initial stages and by proper pated from the burn wound by cooling with water but cold
burn wound excision and antimicrobial therapy in the conva- water and ice should not be used as they can cause rapid
lescent period. Underresuscitation can convert this area into hypothermia. A quick assessment should be made for associ-
deep dermal or full-thickness burns in areas not initially ated trauma and the patient transported to the nearest burn
injured to that extent. Reevaluation of these threatened areas unit for definitive management (Box 18.1, Fig. 18.5).
over the first several days is used to determine when the first Once the patient arrives at the emergency room, an evalu-
burn excision should be performed (i.e., when the depth of ation of the Airway, Breathing, and Circulation (the ABCs)
burn has become apparent and decisions about which areas should receive first priority (Box 18.2). It is also important to
are deep dermal or full thickness are clear). exclude associated trauma. The history should include the
A new area of interest with immediate resuscitation is the time, location and circumstances of the injury, where the
use of negative pressure dressings on affected areas. Animal patient was found, and their condition (Box 18.3). Past medical
models and early clinical work suggest that this treatment and social history, current medication usage, drug allergies,
may limit the conversion of zones of hyperemia to zones of and tetanus status should be rapidly determined. It is also
ischemia by removing edematous fluid and allowing salvage important to consider the possibility of nonaccidental burns
of areas that would otherwise need excision and grafting. or scalding (Box 18.4).
Box 18.1 Burn injuries that should be referred to a burn unit Box 18.2 Initial assessment of a major burn
1. Partial thickness burns >10% TBSA and patients requiring burn Perform an ABCDEF primary survey:
shock resuscitation A Airway with cervical spine control
2. Burns that involve the face, hands, feet, genitalia, perineum, or B Breathing
major joints
C Circulation
3. Deep partial thickness burns and full thickness burns in any age
D Neurological disability
group
E Exposure with environmental control
4. Circumferential burns in any age group
F Fluid resuscitation
5. Electrical burns, including lightning injury
Assess burn size and depth
6. Chemical burns
Establish good intravenous access and give fluids (in children,
7. Burns with a suspicion of inhalation injury
the interosseous route can be used for fluid administration if
8. Burns of any size with concomitant trauma or diseases which intravenous access cannot be obtained)
might complicate treatment, or prolong recovery, or affect
Give analgesia
mortality
Catheterize patient or establish fluid balance monitoring
9. Diseases associated to burns such as toxic epidermal necroly-
sis, necrotizing fasciitis, staphylococcal scalded child syndrome Take baseline blood samples for investigation (full blood count;
etc., if the involved skin area is 10% for children and elderly and urea and electrolyte concentration; clotting screen; blood group;
15% for adults or any doubt of treatment and save or cross-match serum)
10. Any patients with burns and concomitant trauma (such as Electrical injuries
fractures) in which the burn injury poses the greatest risk of 12-lead electrocardiography
morbidity or mortality. In such cases, if the trauma poses the Cardiac enzymes (for high tension injuries)
greater immediate risk, the patient may be initially stabilized in a Inhalational injuries
trauma center before being transferred to a burn unit. Physician Chest X-ray
judgment will be necessary in such situations and should be in Arterial blood gas analysis
concert with the regional medical control plan and triage Dress wound
protocols
After completion of the primary survey, a secondary survey
11. Any type of burns if any doubt about the treatment should assess the depth and TBSA burned, reassess, and
12. Burned children in hospitals without qualified personnel or exclude or treat associated injuries
equipment for the care of children Arrange safe transfer to specialist burns facility.
13. Burn injury in patients who will require special social, emotional,
or long-term rehabilitative intervention
14. Suspected nonaccidental injury.
Modified from: European Burns Association. European Practice Guidelines A thorough assessment of a person with a burn should then
for Burn Care & Guidelines for the Operations of Burn Units; 2002:5562; take into account:
Resources for Optimal Care of the Injured Patient; 1999; Committee on Trauma,
American College of Surgeons; 1999.
The type of burn (e.g., flame, scald, electrical, or chemical)
The depth and extent of the burn, and therefore the
severity
The risk of inhalation injury (singed nasal hair, black
carbon in the sputum, or carbon in the oropharynx)
(Box 18.5)
Any coexisting medical conditions (e.g., cardiac,
respiratory, or hepatic disease; diabetes; pregnancy; or
immunocompromised state)
Any predisposing factors which may require further
investigation or treatment (e.g., a burn resulting from a fit
or faint)
The possibility of nonaccidental injury
The persons social circumstances (e.g., ability to self-care
or need for admission).
The airway should be secured because upper airway
obstruction can develop quickly (Fig. 18.6). Smoke inhalation
causes more than 50% of fire-related deaths. Patients sustain-
ing an inhalation injury may require aggressive airway inter-
vention (Fig. 18.7). Most injuries result from the inhalation of
toxic smoke; however, super-heated air may rarely cause
direct thermal injury to the upper respiratory tract (see com-
plications, below). Patients who are breathing spontaneously
and at risk for inhalation injury should be placed on high-flow
humidified oxygen. Patients trapped in buildings or those
caught in an explosion are at higher risk for inhalation
injury. These patients may have facial burns, singeing of the
Fig. 18.5 Burns patients often have other injuries that require attention. eyebrows and nasal hair, pharyngeal burns, carbonaceous
Pathophysiology 401
Box 18.3 Key points of a burn history Box 18.5 Signs of inhalational injury
Exact mechanism History of flame burns or burns in an enclosed space

Nature of injury (scald, flame, flash, contact, electrical, chemical) Full thickness or deep dermal burns to face, neck, or upper
How did it come into contact with patient? thorax
What first aid was performed? Singed nasal hair
What treatment has been started? Carbonaceous sputum or carbon particles in oropharynx.
Is there risk of concomitant injuries (such as fall from height,
road traffic crash, explosion)?
Inhalational injuries
Is there risk of inhalational injuries (did burn occur in an enclosed
space)?
If possible, the nature of burning materials (furniture, poly-
urethane foam, polyvinyl chloride, etc.)
Exact timings
The time elapsed from burn/injury/smoke inhalation to arrival in
hospital
How long was patient exposed to energy source? or
How long was the patient exposed to smoke?
How long was cooling applied?
When was fluid resuscitation started?
Scalds
What was the liquid?
Was it boiling or recently boiled?
If tea or coffee, was milk in it?
Was a solute in the liquid? (Raises boiling temperature and
causes worse injury, such as boiling rice)
Is there any suspicion of nonaccidental injury?
Electrocution injuries
What was the voltage (high or low)?
Was there a flash or arcing?
Contact time
Chemical injuries Fig. 18.6 The airway must be secured early in cases of airway involvement.
What was the chemical?
Box 18.4 Indicators of possible nonaccidental burns or scalds
Delay in seeking help

Historical accounts of injury differ over time
History inconsistent with the injury presented or with the
developmental capacity of a child
Past abuse or family violence
Inappropriate behavior/interaction of child or caregivers
Glove and sock pattern scalds
Scalds with clear-cut immersion lines
Absence of splash marks in a scald injury. A child falling into a
bath will splash; one that is placed into it may not
Burns to palms, soles, genitalia, buttocks, perineum
Is there sparing of flexion creases that is, was child in fetal
position (position of protection) when burnt? Does this correlate
to a tideline of scald that is, if child is put into a fetal position,
do the burns line up?
Doughnut sign, an area of spared skin surrounded by scald. If
a child is forcibly held down in a bath of hot water, the part in
contact with the bottom of the bath will not burn, but the tissue
around will
Symmetrical burns of uniform depth
Restraint injuries on upper limbs
Other signs of physical abuse bruises of varied age, poorly
kempt, lack of compliance with healthcare (such as no
immunizations) Fig. 18.7 Inhalation injury necessitates aggressive airway interventions, here
nasopharyngeal suction.
sputum, or impaired mentation. A progressive change in

voice quality or hoarseness, stridorous respirations, or wheez- A A
ing may be noted. The upper airway may be visualized by
laryngoscopy, and the tracheobronchial tree should be evalu-
ated by bronchoscopy. Chest radiography is not sensitive for 1
1
detecting inhalation injury. Patients who have suffered an
inhalation injury are also at risk for carbon monoxide poison-
ing. The pulse oximeter is not accurate in patients with carbon 2 13 2 2 13 2
monoxide poisoning because only oxyhemoglobin and deox-
yhemoglobin are detected. Co-oximetry measurements are 1 1 1 1
necessary to confirm the diagnosis of carbon monoxide poi- 1 1 1 1
soning. Other pulmonary assessments include arterial blood 2 2
1
gas measurements and bronchoscopy. Patients exposed to
carbon monoxide should receive 100% oxygen using a nonre- B B BB B
breather facemask.
Burn assessment C C C C
1 1 1 1
After completion of the primary survey, a secondary survey
must include assessment of the depth and TBSA burned
Age 01 1 3 5 7
(Figs 18.818.10).
A of head 9% 8% 7% 6% 6%
Diagnosis/patient presentation B of one thigh 2% 3% 3% 4% 4%
Accurate assessment of burn depth on admission is important C of one leg 2% 2% 2% 2% 2%

in making decisions about dressings and surgery (Table 18.2).
Fig. 18.9 Body surface area calculations in children must account for unique
pediatric body proportions, here with the Lund and Browner method.
Age 01 14 59 1014 15
A of head 9% 8% 6% 5% 4%
B of one thigh 9% 8% 6% 5% 4%
C of one leg 9% 8% 6% 5% 4%
9% Adult body % of total
A A
3% 3% 1% Part BSA
1%
1% Adult Front Arm 9%
18%
2% 2% 2% 2%
Head 9%
13% 13%
Back
18% Neck 1%
1% 1% 1% 1% Leg 18%
2% 2%
Anterior trunk 18%
1%
1% 1% 1% 1% 18% 18%
Posterior trunk 18%
4% 4% 4% 4%
B B B B
C C C C
3% 3% 3% 3%
1% 1% 1% 1%
Fig. 18.10 Estimation of burn size with Wallaces rule of nines: head and neck,
9%; each arm, 9%; anterior torso, 18%; posterior torso, 18%; each leg, 9%;
Fig. 18.8 Estimation of burn size with the Lund and Browner method. (From: genitalia/perineum, 1%. BSA, body surface area. (From: Herndon DN, ed. Total Burn
Herndon DN, ed. Total Burn Care, 2nd edn. Edinburgh: Elsevier.) Care, 2nd edn. Edinburgh: Elsevier.)
Table 18.2 Typical findings in burn injuries

Depth of Skin Healing
burn involvement Example Signs Sensation % TBSA capacity Healing time Scarring
Epidermal Epidermis UV light, very Dry and red, May be Should not be Should be left Within 7 days No scarring
burn short flash, blanches with painful calculated to heal by
sunburn pressure, no in the extent itself
blisters of the
burned
surface area
Superficial Epidermis and Scald (spill or Pale pink with fine Usually Part of the % Should be left Within 14 days Can have color
partial part of the splash), short blistering, extremely burned area to heal by match defect.
thickness papillary flash blanches with painful itself Low to moderate
burn dermis pressure risk of
hypertrophic
scarring
Deep partial Epidermis, the Scald (spill), Dark pink to blotchy May be Part of the % Should not be 14over 21 days Moderate to
thickness entire flame, oil or red, may be with painful or burned area left to heal high risk of
burn papillary grease large blisters, no reduced/ by itself, but hypertrophic
dermis capillary refill absent instead scarring
down to sluggish to none. sensation should
reticular In child, may be probably be
dermis dark lobster red submitted to
with mottling surgery
Full Entire Scald White, waxy or No Part of the % No healing Does not heal Will scar
thickness thickness of (immersion), charred, no sensation burned area capacity and spontaneously,
burn the skin and flame, steam, blisters, no as such grafting
possibly oil, grease, capillary refill. should needed if
deeper chemical, May be dark lobster always be >1 cm
Burn assessment
high-volt red with mottling submitted to
electricity in child surgery.
403
Box 18.6 Burn reconstruction priorities
Urgent and important procedures

Deformities affecting vital function (e.g., airway, oral continence,
protection of the eye, and hand function)
Compression/entrapment or neurovascular bundles
Severe contractures
Important procedures
Restoration of function (e.g., joint contractures)
Progressive deformities that prevent performing of activities of
daily living not correctable by nonsurgical rehabilitation
Desirable procedures
Aesthetics (e.g., pigmentation changes, textural irregularities)
Contractures causing discomfort
Resurfacing (e.g., unstable epithelium).
However, the burn wound is a dynamic living environment

that will alter depending on both intrinsic factors (such as
release of inflammatory mediators, bacterial proliferation)
and extrinsic factors (such as dehydration, systemic hypoten-
sion, cooling). There is much evidence to demonstrate the
beneficial effects of cooling on reducing tissue damage and Fig. 18.11 Epidermal burn. Sunburn.
wound healing time. Although immediate cooling is prefer-
able, even a 30 min delay in application of cooling is still
beneficial to the burn wound but the application of cooling fluids for extensive injuries (Fig. 18.12). By about day 4, the
60 min after injury, does not demonstrate any benefit.8 Tetanus injured epithelium peels away from the newly healed epider-
prophylaxis must be considered wherever there is tissue mis underneath, a process which is commonly seen after
damage, and particularly in elderly patients. It is therefore sunburn. By day 7, healing is complete by regeneration from
important to review the wound at regular intervals until undamaged keratinocytes within skin adnexae. The patient
healing. should be advised of measures to provide symptomatic relief,
Optimum treatment of the wound reduces morbidity and, e.g., take a cool bath or shower; apply topical emollients;
in larger injuries, mortality. It also shortens the time for apply cold compresses; take simple analgesia (e.g., paraceta-
healing and return to normal function and reduces the need mol or ibuprofen); maintain adequate hydration to prevent
for secondary reconstruction (Box 18.6). When epithelializa- heat exhaustion or heat stroke.
tion is delayed beyond 3 weeks, the incidence of hypertrophic
scarring rises. Hypertrophic scars occur in 60% of burned Superficial partial thickness burns
children aged under 5 years. Optimal burn care requires early
excision and grafting of all burns that will produce hyper- These affect the epidermis and superficial dermis. Blistering
trophic scars (typically those that will not or have not healed is common. The exposed superficial nerves make these inju-
within 3 weeks of the injury), so an accurate estimation of ries painful. Healing is expected within 14 days by regenera-
burn depth is crucial. Early grafting of those burns that have tion of epidermis from keratinocytes within sweat glands and
not healed at three weeks has been shown to improve the hair follicles (Figs 18.13, 18.14). First-degree burns are not
result, but because of delays in the referral process, all injuries, considered in calculation of the TBSA burned.
which show no sign of healing by 10 days, should be referred They do not extend entirely through dermis and leave
for assessment. The appearance of the wound and the appar- behind epithelial-lined dermal appendages including sweat
ent burn depth changes dramatically within the first 710 glands, hair follicles, and sebaceous glands (Figs 18.13, 18.14).
days. A burn appearing shallow on day 1 may appear consid- When dead dermal tissue is removed, epithelial cells migrate
erably deeper by day 3. This demarcation of the burn is a from the surface of each dermal appendage to other epithelial
consequence of thrombosis of dermal blood vessels and the cells from neighboring appendages, forming a new, fragile
death of thermally injured skin cells. Superficial burns may epidermis on top of a thin residual dermal bed. The rate of
convert to deeper burns due to infection, desiccation of the regeneration depends on the density of these skin adnexae:
wound, or the use of vasoactive agents during resuscitation thin hairless skin (inner arm, eyelids, etc.) heals more slowly
from shock. than thick or hairy skin (back, scalp, and face). Most superfi-
cial facial burns heal well with watchful neglect. Progression
Epidermal burns to a deeper burn is unlikely but can occur if the wound dries
out or becomes infected or the patient becomes systemically
These burns involve only the epidermis. They do not blister, unwell or hypotensive. Treatment is aimed at preventing
but are red and quite painful (Fig. 18.11). Over 23 days, the wound progression by the use of antimicrobial creams and
erythema and the pain subside. Supportive therapy is usually occlusive dressings, since epithelialization progresses faster in
all that is required, with regular analgesia and intravenous a moist environment. There is considerable disagreement
Burn assessment 405
Depth assessed (appearance, bleeding, capillary refill, sendation)
Superficial (epidermal) Superficial partial thickness Deep partial thickness Full thickness
Dress with tulle gras and gauze Dress with tull gras and gauze,
Obvoius deep dermal injury? Yes
if extensve until healed (usually reassess in 48 hours
within 1 week)
Requires surgery, preferably

Likely to heal within 23 weeks? No
within 5 days, unless < 1cm2
in area in a nonessential area
Yes No Dress with tulle gras and gauze,

reassess after 48 hours
Signs of improvement
or healing?
Low exudate? High exudate?
No Yes
Might be suitable for Hypafix Contaminated or signs

wash dressing daily and take Requires surgery refer Redress and review
of infection?
off with oil in 1 week to burns unit every 2 days
Unhealed at 2 weeks?
No Yes
Continue with tulle gras or Apply antimicrobials (such as

Bactigras and review every silver sulfadiazine cream,
2 days until nhealed antibiotics) Need to refer
Fig. 18.12 Protocol for the management of burn wounds.
regarding the management of blisters, but there is weak evi- and superficial partial thickness burns that heal spontane-
dence from one controlled study that leaving blisters intact ously is not always straightforward, and many burn wounds
results in fewer burns becoming colonized with bacteria at have a mixture of superficial and deep partial thickness
10 days, compared with aspiration or de-roofing (15% v burns, making precise classification of the entire wound
73% v 78%). difficult (Fig. 18.12). They may initially seem superficial, with
All superficial partial thickness burns should heal with blanching on pressure, but have fixed capillary staining on
supervised neglect but, outcome can be improved by appro- re-examination after 48 h. With deeper burns, the density of
priate management. If the burn wound has not healed within the appendages (and hence islands of regeneration) contribut-
14 days of injury, the depth has probably been assessed incor- ing to healing is less, appendages so the burn takes longer to
rectly and referral should be made to a burns unit. heal, the scarring is more severe and associated with contrac-
tion. Therefore, if these injuries are extensive or in functional
Deep partial thickness or cosmetically sensitive areas, they are better excised to a
viable depth and then skin grafted to reduce morbidity and
These wounds are the most difficult to assess and treat. to speed return to normal function. Some deep partial thick-
Nevertheless, distinguishing between deep partial thickness ness injuries will heal if the wound environment is optimized
burns that are best treated by early excision and grafting to encourage endogenous healing. This includes keeping it
Fig. 18.13 Patient with inhalational injury must be intubated before the onset of Fig. 18.15 Full thickness scald injury of the hand.
oropharyngeal edema.
Fig. 18.16 Full thickness bilateral lower limb burns.
Fig. 18.14 Superficial partial thickness burns of the face. these injuries, and healing only occurs from the edges and is
associated with considerable contraction. Full-thickness burns
involve all layers of the dermis and often injure underlying
warm, moist, and free of infection. If infection is prevented subcutaneous adipose tissue as well. Burn eschar is structur-
and spontaneous healing is allowed to progress, these burns ally intact but dead and denatured dermis. Over days and
will heal in 39 weeks. Deep partial thickness burns that weeks if left in situ, eschar separates from the underlying
require longer than 3 weeks to heal routinely produce hyper- viable tissue, leaving an open, unhealed bed of granulation
trophic scars, frequently lead to functional impairment, even tissue. Without surgery, they can heal only by wound contrac-
with physical therapy and provide only a thin epithelial cov- ture with epithelialization from the wound margins. Some
ering that remains fragile for many weeks or months. full-thickness burns involve not only all layers of the skin, but
also deeper structures such as muscle, tendon, ligament and
Full thickness injuries bone. All such injuries should therefore be excised and grafted
unless they are <1 cm in diameter in an area where function
Full-thickness or third-degree burns involve all layers of the would not be compromised (Fig. 18.12).
epidermis and dermis and may destroy subcutaneous struc- Careful calculation of the burn injured TBSA is necessary
tures (Fig. 18.15). They appear white or charred (Fig. 18.16). to guide fluid resuscitation. For adults, Wallaces rule of
These burns are usually insensate because of destruction of nines is a simple and accurate method of calculating TBSA
nerve endings, but the surrounding areas are extremely burned (Fig. 18.11). However, in children, the Lund and
painful. All regenerative elements have been destroyed in Browder chart is more accurate as it accounts for the different
Burn assessment 407
A B
Fig. 18.17 (A,B) Burned genitalia should be catheterized in both sexes.
body proportions in infants and children (Figs 18.9, 18.10). For and therefore present sporadically. The type of respiratory
all patients burn diagrams and photographs of the burn injury sustained is influenced, in large part, by the magnitude
wounds should be placed in the medical record and updated of exposure, as well as the type and properties of the toxic
if the burn wound extends. gases and chemicals comprising the smoke to which the
Extremities should be examined for signs of circumferen- patient is exposed.10
tial burns and signs of compartment syndrome. Compartment Injury can occur to the airway during a fire or explosion
pressures can be measured and escharotomy should be per- and greatly complicate the cutaneous burn injury. Patients
formed for pressures >40 mmHg and considered for those caught in an enclosed, smoke-filled space are at risk for inha-
>25 mmHg. Fasciotomies may also be performed for electrical lation injury. They may or may not have facial burns, ery-
burns where the deep muscular compartments are effected, thema of the mucous membranes, and soot in the airways.
for diagnostic purposes such as accessing deeper tissues, Thermal injury from the flame or hot gases can damage the
evaluating the condition of the underlying muscles with upper airway (supraglottic). This results in burns of the lips
direct observation and determining the extent of muscle and oropharynx, leading to edema and airway obstruction.
necrosis. For patients with facial burns, fluorescent staining Heat rarely causes subglottic injury. The products of combus-
of the cornea and ophthalmological review are necessary. tion, though cooled by the time they reach the lungs, act as
For patients with genital burns a urethral catheter should be direct irritants to the lungs, leading to bronchospasm, inflam-
placed (Fig. 18.17). For patients with perineal burns a rectal mation, and bronchorrhea. The ciliary action of pneumocytes
catheter should be placed. Specific burn circumstances such is impaired, exacerbating the situation. The inflammatory
as chemical and electrical burn injuries, may dictate further exudate created is not cleared, and atelectasis or pneumonia
diagnostic studies and treatments (see later). Tetanus prophy- follows. Acute responses to inhalation injury cause a release
laxis should be considered. of inflammatory mediators, the effects of which are not limited
to the lung and bronchus but also affect systemic vascular
Inhalation injury resistance. Furthermore, intravascular volume deficiency
which frequency leads to reduced cardiac output and stroke
Smoke inhalation causes more than 50% of fire-related deaths. volume, occurs due to increased permeability of the capillary
Smoke inhalation principally affects the respiratory system, bed and substantial interstitial fluid accumulation. This hypo-
and constitutes a major cause of mortality and morbidity in volemic condition requires excessive fluid resuscitation,
burn patients. Patients with inhalation injuries are associated which could cause an overload of cardiopulmonary function
with higher mortality rates than patients without inhalation during the refilling phase. The situation can be particularly
injury. Inhalation injuries are likely to cause a patients condi- severe in asthmatic patients.
tion to weaken and to result in an increased mortality rate, Carbon monoxide binds to deoxyhemoglobin with 40 times
but many patients with inhalation injury are also likely to the affinity of oxygen. It also binds to intracellular proteins,
sustain more severe cutaneous burns, which can also cause particularly the cytochrome oxidase pathway. These two
death.9 Smoke inhalation has been recognized for many years effects lead to intracellular and extracellular hypoxia. In the
but it is only relatively recently that its significance in substan- presence of carboxyhemoglobin, conventional electrode blood
tially increasing the mortality in patients who also have cuta- gas analysers display erroneously high values for the calcu-
neous burns has been quantified these disasters are fortunately lated oxygen saturation and content, giving the unwary a
infrequent and contribute only a small percentage to the false sense of security. In these circumstances pulse oximetry
annual overall mortality from smoke inhalation and burns. is also inaccurate as it cannot differentiate between oxyhemo-
Most smoke inhalation victims are injured in domestic fires globin and carboxyhemoglobin, and may therefore give
Table 18.3 Signs of carboxyhemoglobinemia Box 18.7 Indications for intubation

Carboxyhemoglobin levels Symptoms
Erythema or swelling of oropharynx on direct visualization
Change in voice, with hoarseness or harsh cough
010% Minimal (normal level in heavy
Stridor, tachypnea, or dyspnea
smokers)
Carbonaceous particles staining a patients face after a burn in
1020% Nausea, headache an enclosed space.
2030% Drowsiness, lethargy
3040% Confusion, agitation
4050% Coma, respiratory depression in the hemoglobin available for oxygen transport can be
>50% Death dangerous.
There is no effective treatment of inhalation injury other
than supportive care, there is a real lack of motivation to
develop a truly reliable test. The early accurate diagnosis of
the condition has little therapeutic implication. Pulmonary
normal results (Table 18.3). A blood oximeter, however, injury results in sequestration of fluid in the lungs. When
accurately determines oxygen saturation and content and fluid resuscitation for the visible cutaneous thermal injury
also rapidly measures carboxyhemoglobin concentrations. far exceeds the predicted amount, inhalation injury should
However, arterial blood gas analysis will reveal metabolic be suspected. Decreasing fluid intake in these patients
acidosis and raised carboxyhemoglobin levels but may not may decrease extravasation of fluid in the pulmonary paren-
show hypoxia. Treatment is with 100% oxygen with a non- chyma, but the need to maintain intravascular volume
rebreather facemask, which displaces carbon monoxide from and tissue perfusion may be more important. In significant
bound proteins six times faster than does atmospheric oxygen. inhalation injury, fluid requirements are large, pulmonary
For instance, the amount of carbon monoxide produced in a capillary leakage is significant, and impairment of gas
car engine can cause fatal carbon monoxide poisoning without exchange is inevitable. Early endotracheal intubation is
producing enough particulate matter to cause chemical pneu- important in patients with upper airway or inhalation injury
monitis. Conversely, patients can inhale significant smoke and to safeguard patency of the airway, to deliver mechanical
have normal carboxyhemoglobin levels because of the rapid ventilatory support, and to provide aggressive pulmonary
clearance of carbon monoxide from the blood after adminis- toilet (Box 18.7). To date, we can provide only supportive care
tration of oxygen during transport. Direct laryngoscopy and for pulmonary failure from inhalation injury because no effec-
bronchoscopy more accurately assess airway injury but can tive therapy has been identified for prevention or treatment
still be misleading. A nuclear medicine study with technetium of the damage to the alveoli by the inhaled toxins. Hyperbaric
Tc99m uptake in the lung can also be used for diagnostic oxygen treatment has been used for acute carbon monoxide
purposes. Noninvasive management can be attempted, with poisoning from smoke inhalation. Hyperbaric therapy is
nebulizers and positive pressure ventilation with some posi- rarely practical and has not been proved to be advantageous.
tive end-expiratory pressure. However, patients may need a It takes longer to shift the carbon monoxide from the cyto-
period of ventilation, as this allows adequate oxygenation and chrome oxidase pathway than from hemoglobin, so oxygen
permits regular lung toileting. The typical adult respiratory therapy should be continued until the metabolic acidosis has
distress syndrome picture of inhalation injury may not be cleared.
manifested as altered pulmonary gas exchange and chest
radiographic changes for several hours to days after injury.
Patients with carboxyhemoglobin levels greater than 25
30% indicate a significant exposure to fumes but are not
always predictive of inhalation injury but should be venti-
Management of moderate
lated. Hyperbaric oxygen therapy reduces the half-life of to severe burns
carbon monoxide to 23 min. Hyperbaric oxygen is recom-
mended for patients with carboxyhemoglobin levels greater Initiation of fluid resuscitation should precede initial wound
than 25%, myocardial ischemia, cardiac dysrhythmias, or neu- care. In adults, IV fluid resuscitation is usually necessary
ropsychiatric abnormalities. Hyperbaric oxygen is also recom- in burns involving >20% TBSA. In pediatric patients, fluid
mended for pregnant women and young children with resuscitation should be initiated in all infants with burns
carboxyhemoglobin levels of 15%. of 10% TBSA and in older children with burns 15% TBSA.
Dicobalt edetate is standard treatment for massive cyanide Two large-bore IV lines should be placed and fluid should
poisoning in cases of ingestion or industrial accident. It may be given. Intraosseous line placement may be required in
not be appropriate, however, for patients who have inhaled children in the proximal tibia or the distal femur. Lactated
smoke as poisoning by inhalation is limited, with no further Ringers solution is the most commonly used fluid for
absorption after respiratory arrest or rescue. In the presence burn resuscitation. Urine output should be used as a measure
of low plasma concentrations of free cyanide dicobalt edetate of renal perfusion and to assess fluid balance. In adults, a
itself can be toxic. A better approach is to use sodium nitrite, urine output of 0.51.0 mL/kg per hour should be main-
which converts hemoglobin to methemoglobin, though in a tained. Patients with significant burns should have a Foley
patient whose oxygen delivery is already compromised by catheter inserted in order to monitor urine output. The color
a high carboxyhemoglobin concentration a further decrease and consistency of the initial urine in patients with severe
Management of moderate to severe burns 409
flame or high voltage electrical burns should be noted. The in increased hydrostatic pressure and extra interstitial edema.
urine may already be black, indicating hemoglobinuria or All fluid is therefore administered at a constant rate, and fluid
myoglobinuria, or both. This is of prognostic importance for boluses are avoided. Lactated Ringers solution most closely
subsequent renal function. In elderly patients, patients resembles normal body fluids. Factors that influence fluid
with cardiorespiratory disease, and patients who have requirements during resuscitation besides TBSA burn include
delayed presentation consider inserting a central venous burn depth, inhalation injury, associated injuries, age, delay
pressure line. This can play an important part in the subse- in resuscitation, need for escharotomies/fasciotomies, and
quent restoration of volume in a patient with a severe use of alcohol or drugs. The Parkland formula has been
burn. The risks of infection related to a central line are renamed the Consensus formula because it is the most widely
small in the early stages. With current methods of line used resuscitation guideline. The Advanced Burn Life Support
management these risks are outweighed by the importance curriculum supports the use of the Consensus formula for
of the line for monitoring and access. A nasogastric (NG) resuscitation in burn injury. It is 4 mL/kg/% TBSA, describ-
tube should be placed in patients with burns involving 20% ing the amount of lactated Ringers solution required in the
TBSA in order to prevent gastric distention and associated first 24 h after burn injury. Starting from the time of burn
emesis. injury, half of the fluid is given in the first 8 h and the remain-
ing half is given over the next 16 h. As an example, by the
Parkland formula, a 70 kg patient with a 40% TBSA burn
Resuscitation formulae receives (70 40 4) = 11 200 mL of lactated Ringer solution
during the first 24 h after the burn (approx. 470 mL/h).
Sufficient resuscitation to prevent burn shock is the single Crystalloids are the resuscitation fluids of choice given the
most important therapeutic intervention in burn treatment lack of survival benefit and increased cost associated with
but due to a lack of evidence-based literature, burn resuscita- albumin and a meta-analysis comparing albumin to crystal-
tion remains an area of clinical practice driven primarily by loid showed a more than doubled mortality rate with albumin.
local custom of treating burn units.11 Fluid replacement is Albumin is contraindicated in the first 24 h post-burn, but
based on the observation that fluid loss from the vascular may have a role in severe burns (>50% TBSA) after the first
space occurs at a constant rate during the first day after injury. 24 h. Hypertonic saline has also had disappointing results,
The amount of replacement fluid is predicted from the extent with a quadrupled increase in renal failure and twice the
of burn and size of the patient, and fluid replacement should mortality of patients given lactated Ringers solution.
proceed at the same rate as the loss (Table 18.4). Fluid admin- Hypertonic saline does not routinely have a place in burn
istered in excess of the leak is excreted by the kidney or results resuscitation.
Table 18.4 Fluid resuscitation formulae

Formula Electrolyte Colloid Glucose
Colloid formulae
Brooke Lactated Ringers at 1.5 mL/kg/% 0.5 mL/kg/% TBSA burn 2 L 5% dextrose
TBSA burn
Evans 0.9% NaCl at 1 mL/kg/% TBSA burn 1 mL/kg/% TBSA burn 2 L 5% dextrose
Slater Lactated Ringers 2 L/24 h Fresh Frozen Plasma at 2 L 5% dextrose
75 mL/kg/24 h
Crystalloid formulae
Modified Brookes Lactated Ringers at 2 mL/kg/%
TBSA burn
Parkland Lactated Ringers at 4 mL/kg/% 2060% estimated plasma Titrated to urinary
TBSA burn volume output of 30 mL/h
Hypertonic saline formulae
Hypertonic saline solution Maintain UO at 30 mL/h
(Monafo) Fluid contains sodium 250 mmol/L
Modified hypertonic (Warden) Lactated Ringers + 50 mmol/L NaHCO3 for
8 h to maintain UO at 3050 mL/h
Lactated Ringers to maintain UO at
3050 mL/h beginning 8 h post-burn
Dextran formula (Demling) Dextran 40 in saline at 2 mL/kg/h for 8 h Fresh Frozen Plasma at
Lactated Ringers titrated to maintain urine 0.5 mL/kg/h for 18 h
output at 30 mL/h beginning 8 h post-burn
Monitoring also causes pain on initial application. The pain subsides after
several minutes, but patients usually do not like it.
Heart rate and urine output are the primary modalities Another topical dressing is Dakin solution (0.25% sodium
for monitoring fluid therapy in patients with large burns hypochlorite). This is good for a wet-to-dry dressing for minor
although there is a lack of evidence supporting them. Reliance debridement of the wound surface. It is particularly useful if
on hourly urine output as the sole index of optimum resu- a skin graft smells or looks infected.
scitation sharply contrasts with the lack of clinical studies Silver nitrate, as a 0.5% solution, is applied as a wet
demonstrating the ideal hourly urine output during resusci- dressing. It has excellent antibacterial properties but causes
tation (Fig. 18.17). A minimum of 0.51.0 mL/kg per hour discoloration of the skin and all the surrounding clothing
urine output in adults and in children is recommended but and bedding. A newer version marketed as Acticoat contains
12 mL/kg per hour urine output is preferred. Lesser hourly gauze material impregnated with a silver compound. This
urinary outputs in the first 48 h post-burn almost always product does not discolor the skin as silver nitrate does. The
represent inadequate resuscitation. Hemodynamic monitor- dressing does not have to be removed. Instead, it is moistened
ing and treatment of deviation from normovolemia are the occasionally to release the active ingredient into the wound.
fundamental tasks in intensive care. A pulse rate ~110 beats/ Agents such as povidone-iodine solution and nitrofura-
min in adults usually indicates adequate volume, with rates zone are still used in some burn units but less and less often.
>120 beats/min usually indicative of hypovolemia. Narrowed The need to use multiple agents once one has failed is becom-
pulse pressure provides an earlier indication of shock than ing less common. Burn wound infections have decreased dra-
systolic blood pressure alone. matically during the last 2 decades not from better topical
Noninvasive blood pressure measurements by cuff are dressings but from a better understanding of the causes of
inaccurate due to the interference of tissue edema and read burn wound infection. Early tangential debridement and
lower than the actual blood pressure. An arterial catheter coverage of the wound with skin have markedly decreased
placed in the radial artery is the first choice, followed the opportunity for colonization of the burn eschar. Despite
by the femoral artery. The decision to perform invasive meticulous wound care, and even under the most sterile con-
hemodynamic monitoring requires careful consideration. The ditions, the patients own microbial flora quickly colonizes
lack of benefit associated with goal-directed supranormal and then invades the burn eschar. Only by removing the dead
therapy has resulted in waning enthusiasm for the use of tissue and providing stable coverage is the risk of wound
pulmonary artery catheters. The most applicable cardiac infection eliminated.
output-related variable to manipulate in burn patients is
preload. Pulmonary artery occlusion pressure and central Wound dressings
venous pressure are not good indicators of preload. As long
as other signs of adequate tissue perfusion are normal, the The standard burn dressing consists of gauze impregnated
temptation to normalize filling pressures should be avoided. with soft paraffin, which helps to prevent adherence to the
The use of end points demonstrating the adequacy of oxygen wound. A topical antiseptic may be applied over this followed
delivery has not yet found a place in the management of burn by cotton wool or Gamgee to absorb the exudate. Newer
shock. dressings have been introduced that are claimed to be less
adherent and allow less water to be lost by evaporation from
Management of the burn wound the wound while also protecting it from external pathogens
(Box 18.8). These may be classified into two groups:
Topical ointments 1. Biological dressings: These can be used either fresh or after
storage following preparation by freezing in liquid
Many ointments serve as good temporary coverings for the nitrogen or rapid dehydration (lyophilization) and later
wounds between dressing changes. The simplest is just a reconstitution with saline.
petroleum-based antibiotic ointment such as bacitracin; but
2. Physiological dressings: These consist of synthetic materials
for sizable burns, most clinicians use some preparation with
such as polyethylene or silicone, which prevent
a stronger bactericidal or bacteriostatic action.
adherence to the wound, and plastic films, which reduce
Silver sulfadiazine is the most common ointment used. It
evaporation and contamination.
has intermediate wound penetration and a good antibacterial
spectrum. The antibacterial activity lasts 810 h, and the
dressings are changed twice a day. Silver sulfadiazine causes Biological wound dressings
transient leucopenia in some patients when it is used on large The most widely used biologic dressing remains fresh or
open areas. A switch to a different topical agent for a few days frozen human cadaveric split-thickness skin. Properly
allows the white blood cell count to recover. Restarting silver handled, cadaveric skin remains viable and revascularizes
sulfadiazine rarely causes recurrent leucopenia. (takes) when it is placed on a healthy wound bed. The
Mafenide acetate is also commonly used and looks similar. dermal capillaries of the graft fill with blood and then develop
It has excellent eschar penetration and bacteriostatic action. nutrient flow 25 days after grafting by inosculation, just
Use of mafenide acetate on full-thickness burns prevents like autologous split-thickness grafts. The cadaveric skin
deeper infections. Often used on the ear, it helps against infec- functions very much like autologous grafts, decreasing fluid
tion of the cartilage. Systemic absorption of mafenide acetate, loss, lowering local pathogen growth, and decreasing painful
when it is applied to large burns, produces a metabolic acido- stimuli during dressing changes. The need for frequent dress-
sis by inhibition of carbonic anhydrase. The effect is usually ing changes decreases, and the overall effect on the patients
noted after 35 days. Use of the compound on open wounds hyperdynamic state is beneficial. However, just as Medawar
Box 18.8 Characteristics of the ideal temporary skin substitute Box 18.9 Characteristics of the ideal permanent skin substitute
Nonantigenic Bilayer structures with biologic dermal analogue and either

Durable synthetic or biologic epidermal analogue
Flexible Rapid and excellent adherence properties
Prevents water loss Easily applied and secured to an excised wound
Barrier to micro-organisms Minimum wait period from time of burn to availability of skin
Drapes well substitute
Rapid and firm wound adherence Bilayer tissue containing both epidermal and dermal eliminates
to best replicate normal skin
Easy to secure
Rapid incorporation
Relieves pain
Cannot transmit disease
Grows with a child
Good functional and cosmetic result
Can be applied in one operation
Inexpensive.
Hemostatic
Stimulates wound healing
Optimizes healing environment
Does not cause hypertrophic tissue response
Easy to remove when wound has re-epithelized or is ready for
grafting cultured epidermal autograft (CEA) are placed directly onto
Cannot transmit disease a cleanly debrided wound bed. The grafts survive well, and
Inexpensive wounds close much faster than without treatment.
Long shelf-life Despite its many advantages, CEA does not address all of
Can be used off the shelf the wound problems facing massively burned patients. Unlike
Does not require refrigeration. split-thickness skin, the epithelial cultures contain no dermal
matrix tissue. Typically, the CEA is placed on debrided full-
thickness burns that lack any dermal elements. Because the
dermis provides the elastic quality of the skin, healed wounds
described in his Nobel Prize-winning studies in the 1940s, that lack dermis have little give and are stiff. Covered by CEA,
cadaveric skin undergoes first-set rejection 12 weeks after areas around joints and over muscles, such as the face, have
grafting. The immunosuppression found in massively burned little motion and poor function. The dermis also provides the
patients may delay the rejection process some, but eventually foundation for the formation of the basement membrane
the grafts develop an abundant inflammatory cell infiltrate between the epidermis and dermis. CEA placed directly on
and the epidermis dies and sloughs from the patient. Loss of muscle or subcutaneous tissue only gradually forms a base-
the epidermis requires replacement with another set of cadav- ment membrane, in some cases during 6 months. The base-
eric grafts, or, it is hoped, the patient is ready for coverage ment membrane serves an important attachment function,
with permanent autologous tissue. Disease transmission from and epidermis lacking a well-formed basement membrane
the donor to the burn patient remains a theoretical concern. blisters and shears easily. Reopening of a healed wound is
Interestingly, all burn surgeons have observed over the years common after application of CEA.
that the dermis of the cadaveric graft frequently remains Growth of CEA is slow and expensive. A biopsy specimen
attached to the wound bed and is eventually incorporated must be obtained from the patient, and growth of the CEA
into the wound. takes several weeks. Several centers have used cultured epi-
Porcine skin and freeze-dried human cadaveric skin do dermal allograft to treat burn wounds with varying success.
not have the same properties as fresh or properly preserved Because the donor keratinocytes are taken from discarded
frozen cadaveric skin (Table 18.5). These other skin substitutes neonatal foreskins from circumcisions, cultured epidermal
do not revascularize and therefore easily detach from the allografts can be available at any time and are much less
wound bed during dressing changes. Whether these materials expensive to produce. However, the engrafted cells undergo
decrease fluid loss or have antimicrobial effects is debated. rejection just as cadaveric skin grafts do. The cells work best
The ability to grow and expand human keratinocytes in as temporary coverage in partial-thickness wounds where a
tissue culture was a major advance in wound treatment (Table supply of autologous keratinocytes is available to replace the
18.6). No longer was an epidermal source a major limitation allografts after rejection.
for restoration of the epithelial barrier. In a landmark case in Dermal replacements offer better functional results once
1984, twin children with burns over almost their entire bodies they are incorporated in the wound, but engraftment rates
were treated with cultured keratinocytes taken from a small have been a problem (Box 18.9). Replacement of lost dermis
biopsy specimen of undamaged axillary skin. During the in deep second-degree or third-degree burns during the initial
course of their treatment, the keratinocytes were successfully treatment of the wound with these materials may decrease the
expanded in tissue culture and used to resurface some of their need for later reconstructive surgery. These dermal replace-
wounds. Survival of the patients was directly attributed to the ments may prevent the extensive scarring and associated poor
use of the technique. Now several major burn centers have skin elasticity often seen in burns covered with thin skin
laboratory facilities to culture keratinocytes. Several biotech- grafts. Despite the technical problems with these materials,
nology companies offer the service for a fee. Skin biopsy the advantage of preventing functional and cosmetic deformi-
specimens sent to the company are expanded in culture and ties from scar contractures makes their use worthwhile in
returned to the patient, usually in 23 weeks. The sheets of many clinical situations.
412
SECTION III 18 Acute management of burn/electrical injuries
Table 18.5 Temporary skin substitutes

Product Tissue of origin Layers Category Uses Advantages Disadvantages
Human Human cadaver Epidermis and Split thickness Temporary dressing of A bilayer skin Epidermis will reject
allograft dermis skin partial thickness and providing epidermal Difficult to obtain and store
excised burns before and dermal properties Risk of disease transfer

autografting or when Re-vascularizes Expensive
there is a lack of maintaining viability for Need to cryopreserve
autograft weeks
Dermis incorporates
into the wound
Antimicrobial activity
Human Placenta Amniotic Epidermis Temporary dressing of Acts like biologic Difficult to obtain, prepare
amnion membrane Dermis partial thickness and barrier of skin and store
excised burns before Decreases pain Need to change every 2 days
autografting or when Easy to apply, remove Disintegrates easily
there is a lack of Transparent Risk of disease transfer
autograft Expensive
Pig skin Pig dermis Dermis Dermis Temporary dressing of Good adherence Does not revascularize and
Xenograft partial thickness and Decreases pain will slough
excised burns before More readily available Short-term use
autografting or when compared to allograft Need to keep the fresh
there is a lack of Bioactive (collagen) product frozen
autograft inner surface with
fresh product
Less expensive than
allograft
Biobrane Synthetic with Bilayer product Synthetic Temporary coverage of Bilayer analog Relatively expensive
added outer silicone epidermis and superficial partial Excellent adherence to Has very little direct
denatured Inner nylon dermis thickness burns, a superficial partial bioactivity
bovine collagen mesh with although it has been thickness burn Difficult to remove if left in
added used for coverage of Decreases pain place over 2 weeks
collagen autograft and for donor Maintains flexibility Not as good for deep partial
Easy to store with long and full thickness burns
shelf-life

Oasis Xenograft Extracellular Bioactive Dermal Temporary coverage of Excellent adherence Mainly a dermal analogue
wound matrix like Matrix superficial partial Decreased pain Incorporates and may need
from small thickness burns, Provides bioactive to be reapplied
intestine although it has been dermal like properties
submucosa used for coverage of Long shelf-life, store at

autograft and for donor room temperature
Relatively inexpensive
Transcyte Allogenic Dermis Bilayer product Bioactive Dermal Temporary coverage of Bilayer analogue Need to store frozen till use
Outer Matrix superficial partial Excellent adherence to Relatively expensive
silicone Inner Components thickness burns, a superficial partial
nylon seeded on Synthetic although it has been thickness burn
with neonatal dermis and used for coverage of Decreases pain
fibroblasts epidermis autograft and for donor Provides bioactive
dermal components
Maintains flexibility
Good outer barrier
function
Duoderm Synthetic Monolayer Synthetic Temporary coverage of Long shelf-life, store at Adhesive layer barrier to
hydrocolloid epidermis and superficial partial room temperature diffusion of exudate from the
dressing dermis thickness burns, Relatively inexpensive wound so that most of the
although it has been fluid never diffuses through
used for coverage of the adhesive layer;
Management of moderate to severe burns

autograft and for donor No transpiration of fluid to
the atmosphere
The adhesive is aggressive
to the intact perilesional skin
so that on removal this skin
may be traumatized
Loss of adhesion in a day or
two due to fluid accumulation
Provides a favorable
environment at the wound
locus for the growth of
harmful anaerobic bacteria
413
414
SECTION III 18 Acute management of burn/electrical injuries
Table 18.5, Temporary skin substitutescontd


Opsite Synthetic Monolayer Synthetic Temporary coverage of Long shelf-life, store at Not absorbent
elastomeric epidermis and superficial partial room temperature requires fairly frequent
polyurethane dermis thickness burns, Relatively inexpensive replacement to obviate
film although it has been pooling of exudate and
used for coverage of related problems
autograft and for donor The adhesive is aggressive
may be traumatized
Suprathel Synthetic Monolayer Synthetic Temporary coverage of Long shelf-life, store at Relatively expensive
copolymer of epidermis and superficial partial room temperature Not absorbent
polylactide, dermis thickness burns, requires fairly frequent
trimethylene although it has been replacement to obviate
carbonate and used for coverage of pooling of exudate and
-caprolactone autograft and for donor related problems
Tegaderm Synthetic Monolayer Synthetic Temporary coverage of Long shelf-life, store at Not absorbent
elastomeric epidermis and superficial partial room temperature requires fairly frequent
polyurethane dermis thickness burns, Relatively inexpensive replacement to obviate
film although it has been pooling of exudate and
used for coverage of related problems
autograft and for donor The adhesive is aggressive
may be traumatized
Table 18.6 Permanent skin substitutes

Apligraf Allogenic Collagen matrix seeded Composite: Excised deep Readily Expensive
Composite with human neonatal Epidermis partial thickness available Vascularizes slowly
keratinocytes and and burn No epithelial barrier
fibroblasts Dermis No antimicrobial activity
OrCel Allogenic Collagen sponge Composite: Skin graft donor Readily Expensive
Composite seeded with human Epidermis site. Excised available
neonatal and deep partial Live cells Vascularizes slowly
keratinocytes and Dermis thickness burn No epithelial barrier
fibroblasts No antimicrobial activity
Epicel Autogenous Cultured autologous Epidermis Deep partial and Readily Expensive
keratinocytes keratinocytes only full thickness available
burns >30% Live cells Vascularizes slowly
TBSA No epithelial barrier
No antimicrobial activity
Alloderm Allogenic dermis A cellular Dermis Dermis only Deep partial and Readily Expensive
(processed allograft) full thickness available
burns Live cells Vascularizes slowly
No epithelial barrier
No antimicrobial activity
Integra Synthetic Silicone outer layer on Biosynthetic Full thickness Readily Expensive
bovine collagen GAG dermis burns; definitive available
and shark closure requires Live cells Vascularizes slowly
chondroitin sulfate skin graft No epithelial barrier
dermal matrix No antimicrobial activity
The first product available on the market for dermal matrix The rapidity of the engraftment process is likely to depend on
was Integra. The matrix is composed of undenatured bovine the vascularity of the matrix material as much as the wound
collagen and shark chondroitin sulfate, a proteoglycan. A thin bed on which it is placed. AlloDerm placed over the wound
Silastic sheet, to serve as a barrier to the air, covers the surface. and covered with a split-thickness skin graft acts as an extra-
When it is placed on a wound, the material is incorporated cellular dermal matrix. The matrix is incorporated into the
and serves as a scaffold for infiltration and growth of fibrob- final thickness of the skin. Studies on the long-term results of
lasts and capillaries. Engraftment of the material takes wounds treated with AlloDerm are under way.
approximately 2 weeks, and any disturbance, such as exces- Most burn centers, including the authors, do not use
sive movement, fluid accumulation under the material, or dermal replacements for extensive coverage of acute burns
infection, causes loss of the material. Once the matrix is incor- because of the unpredictable engraftment rate. Large clinical
porated, the Silastic membrane is removed, and the material trials have not demonstrated a survival advantage with use
is covered by epidermis. CEA placed on Integra does not of any of these products or presented data to suggest that
survive, and no one seems to know the explanation. After the postinjury function is improved. Therefore, most surgeons
Silastic is removed, the manufacturer recommends use of a use dermal replacements for burn scar reconstruction when
thin split-thickness skin graft to cover the wound to establish supplemental dermis improves functional and cosmetic out-
the epidermis. An obvious disadvantage of this method is the comes of the grafting procedure and survival of the patient is
long time from excision of the burn wound to final epithelial not an issue.
coverage. When multiple areas need skin grafting, this delay
may be no more than waiting for donor sites to re-epithelialize.
In addition, use of only thin split-thickness skin reduces donor Physiological wound dressings
site problems and hastens donor site healing. So far, no one Synthetic materials are often used to cover wounds but have
has demonstrated a survival advantage with the use of other limitations. If they are applied correctly, they usually
Integra, but many clinicians believe that its use on extensive adhere to the wound bed. Left undisturbed, the dressing
full-thickness wounds definitely improves the final functional limits fluid loss and prevents stimulation of the wound.
results. Epidermal regeneration is undisturbed beneath. The dressing
AlloDerm is the other commercially available dermal falls off once the epithelial layer completely heals underneath,
replacement made from freeze-dried human dermis obtained much like a scab falls off an open wound once it is healed.
from cadaveric split-thickness skin. As with Integra, however, These materials work best on superficial second-degree burn
the engraftment process for the matrix is variable, and the wounds and skin graft donor sites that heal in 710 days.
matrix does not support the attachment of CEA well. Placed on deeper wounds, the materials adhere poorly and as
foreign material serve as a nidus for infection much like the

burn eschar. These materials have no antimicrobial activity
and therefore should not be placed on a contaminated wound.
Most of the newly developed synthetic biologic dressings are
used mainly in developed countries because most of these
products are extremely expensive.
Conservative versus surgical therapy

All wounds eventually heal if they are left alone unless there
is infection, lack of blood flow (tissue ischemia), or inadequate
nutritional intake. Meticulous wound care helps minimize the
chance of infection and maximize healing. The daily dressing
changes in burn patients permit inspection of the wound to
assess the need for further interventions but, more important,
offer the chance to remove dead tissue that is a nidus for
infection. The burn nurse dedicates a large part of the time
to gently scraping off dead skin and proteinaceous debris
that have gathered since the last dressing. This leaves a Fig. 18.18 Equipment for tangential excision. Silver knife; Watson modification of
healthy bed for the migration of keratinocytes. Typically, the the Humby knife and air powered dermatome.
wound is covered between dressings with a moist, antibacte-
rial covering to minimize microbial growth, fluid loss, and
painful stimuli and to maximize skin regeneration. Superficial
and delays wound healing. Even after removal of the dead
partial thickness burns heal in a short time with wound treat-
tissue, pathogens colonize the wound and enter the patients
ment only. For deep partial or full burns, the time for healing
blood stream to seed distant sites. Open wounds leak proteins
can be extensive and risks of infection greater. For these
and fluids and continue to be painful. All these factors con-
wounds, it is far better to treat by surgical debridement
tribute to the patients hyperdynamic and hypermetabolic
and coverage with skin grafts or cultured epidermis. For a
state. To achieve early debridement and stable permanent
deep burn over a small area or one with a patchy distribution,
coverage of the wound, the surgeon must overcome two main
the time for healing by secondary intention may be no longer
obstacles, the extreme physical insult of the debridement
than the healing of a skin graft. For these wounds, surgical
process and the limited source of replacement skin for perma-
debridement and grafting may not be appropriate. After all,
nent coverage of large surface area burns.
it takes a skin graft 710 days to stabilize on a wound and
The burn eschar is shaved tangentially or excised to deep
about the same amount of time for the donor site to heal.
fascia. From the surgical viewpoint, the best time to graft
Ideally, all wounds should have epithelial cover within 3
burns is within five days of injury to minimize blood loss,
weeks to minimize scarring, but in practice the decision
and injuries that are obviously deep at presentation must be
whether to refer a patient must be made by day 10 to achieve
referred early. With major burns, treatment is skewed towards
this.
preservation of life or limb, and large areas of deep burn must
be excised before the burnt tissue triggers multiple organ
Surgery failure or becomes infected (Fig. 18.19). In such cases more
superficial burns may be treated with dressings until healing
Aggressive but carefully timed removal of burnt tissue and occurs late or fresh skin donor sites become available.
replacement with definitive wound cover is the key to sur- The main limitation to removal of the dead skin in large
vival and return to function. Early excision and grafting have burns is severe physiologic disturbance caused by rapid and
been shown to reduce pain, shorten hospital stay, and acceler- copious blood loss as a consequence of skinning patients over
ate return to normal function in moderate injuries. The coagu- an extensive area. In adults, blood loss reaches 100 mL for
lated tissue from third-degree burns does not easily separate every 1% TBSA of skin debrided. Although some units prac-
from the wound bed until very late, and the thick layers of tice large (>20% TBSA) debridement in one procedure, most
dead tissue retard epithelial regrowth and harbor pathogens. burn units limit each operative session to debridement of
Removal requires sharp debridement with a knife (tangential) 1020% TBSA. This keeps blood replacement, fluid adminis-
(Fig. 18.18). Because of the intensely painful stimuli and the tration, and anesthetic needs to levels that can be addressed
likelihood of a large quantity of blood loss from the debride- by the operating room team in a timely fashion. Tangential
ment, these procedures are typically done in the operating debridement involves cutting the skin tissue at the depth of
room. the dermal and subcutaneous capillary network. Because of
The main goals of surgical treatment of patients with deep the local inflammatory response in the burn, these capillaries
burns are debridement of the burn and placement of stable are usually well dilated by the time of excision. After excision,
permanent skin coverage. Many studies have demonstrated blood loss can be torrential, and it is difficult to imagine such
that early removal of the dead tissue and aggressive measures extensive hemorrhage until one participates in such a proce-
to re-establish the epithelial barrier decrease wound infections dure. Clinical studies estimate that tangential debridement of
and mortality. The dead tissue continues to incite an inflam- each square centimeter of burn causes 1 mL of blood loss.
matory response, serves as a growth medium for pathogens, Thus, in an adult, excision of each 1% TBSA of burn averages
Fig. 18.19 Debridement may lead to exposed joints. Exposed elbow joint after Fig. 18.20 Pneumatic tourniquets can minimize blood loss and improve vision
debridement of a full thickness burn. during surgery.
100 mL of bleeding. Debridement of a 20% TBSA burn results

in 2000 mL or 4 units of whole blood loss. Tourniquet use
on extremities, pressure dressings, electrocautery, hemostatic
agents, avoidance of agents that interfere with the coagula-
tion, and subcutaneous injection of the burn with dilute epine-
phrine all limit blood loss but not completely (Fig. 18.20).
Full-thickness excision of the burn to the level of muscle fascia
with electrocautery limits blood loss. The loss of such a sig-
nificant amount of soft tissue requires skin grafts on muscle
fascia and has poor functional and cosmetic results. The best
method to control blood loss is to limit each debridement
session to about 1020% TBSA. The patient and the anesthe-
siologist better tolerate this amount of blood loss.
Timely coverage of the debrided wounds depends on
available sources of autologous skin. Autologous split-
thickness skin grafts from unburnt areas are the gold stand-
ard for definitive coverage of burn wounds if enough donor
sites are available. When available, the extremities, minus the
hands and feet, are the best areas for harvesting of skin grafts.
The trunk is used next, but obtaining the grafts is technically Fig. 18.21 Dermatome harvest of a split thickness skin graft.
more challenging because of contour irregularities (Fig. 18.21).
The scalp is a great but often underused donor site. The scalp
skin is thick and re-epithelializes rapidly owing to the density
of hair follicles (Fig. 18.22). Tissue inflation of the scalp gives
better quality of skin graft. It is even possible to harvest skin preferred to improve the cosmetic and functional result (Figs
grafts from the scrotum after tissue inflation (Fig. 18.23). 18.24, 18.25). If donor sites are sparse, however, or the wound
Regrowth of the hair is rarely a problem; thus, the donor site bed is likely to bleed profusely (because excision is carried out
is well camouflaged after healing. late, for instance) then the graft is perforated with a mesher
Repeated harvesting of skin graft donor sites multiple to allow expansion (Figs 18.2618.28). Although this improves
times increases the amount of skin available, but the donor graft take, where the wound bed is bleeding after tangential
site must heal between harvest procedures, and these areas excision, the mesh pattern is permanent and unsightly (Fig.
typically bleed more on the second harvest. Most important, 18.29). Unmeshed sheet graft is used on hands and faces, and
the site has limited potential for recovery as more and more over any future site for intravenous central lines and trache-
of the dermis and hair follicles are taken for the graft. ostomies to obtain rapid cover. Where unburnt split skin
Eventually, the donor site can become a full-thickness wound donor sites are in very short supply, there are two possible
itself. Thickness is usually tailored to the depth of excision to solutions:
obtain good cosmesis, although thinner grafts are thought to
contract more. Donor sites should ideally be harvested adja- 1. Rotation of donor sites is practised, and unexcised burn
cent to the injury to improve color match, and sheet graft is covered with antimicrobial creams
Fig. 18.22 (A) Intraoperative tissue expansion

to allow harvest of split thickness skin grafts
A B from the scalp. (B) Expanded scalp allows
harvest of split thickness skin grafts.
Fig. 18.23 (A) Inflation tissue expansion of the

scrotum to allow skin graftings when donor sites
A B are lacking. (B) Harvesting a split thickness skin
graft from an inflated scrotum.
2. The excised wound is resurfaced with a temporary

covering until donor sites have regenerated and can be
re-harvested.
Examples of a temporary covering are cadaveric allograft
from an unrelated donor, xenograft, synthetic products, and
cultured epithelial autograft (Fig. 18.30). Development of syn-
thetic products has allowed us to excise extremely large burns
and still achieve physiological closure, with potentially lower
mortality in these injuries. Cultured epithelial autografts also
permits us to extend the available donor sites. The cultured
cells can be applied as sheets (available after 3 weeks) or in
suspension (available within 1 week). A few burns units use
these cells for superficial skin loss or in combination with
mesh graft to improve the cosmetic result.
Wounds are debrided and covered with skin grafts in one
procedure if blood loss is acceptable. In large area burns, the
patient may undergo skin grafting a few days after debride-
ment to allow time for the debrided wounds to stop bleeding
Fig. 18.24 Suprathel on superficial partial thickness burns. and for the patient to recover from the blood loss. Harvesting
Fig. 18.26 Meshing a split thickness graft.
Fig. 18.25 Healed lower limb donor sites.
Fig. 18.28 The use of sponge and staples is a fast and easy technique to
immobilize the skin graft but patients often find the removal of staples painful.
Fig. 18.27 Split skin graft applied to the debrided burn wound.
of skin grafts, although less bloody than tangential debride-

ment of the burn, still results in significant blood loss. Between
the time of excision and the skin grafting procedure, the
wounds are covered with a biologic dressing (pig or cadaver
skin) or a topical wound dressing. Should the patient need
several debridement sessions to remove all of the burns, deb-
ridement can be alternated with grafting sessions to achieve
staged coverage of each debrided area before going on to the
next burned area. This strategy delays the complete removal
of all burned tissue, leading to some increased risk of burn Fig. 18.29 Healing split thickness graft.
A B
Fig. 18.30 (A,B) Application of a sheet of cultured epidermal autograft.
Fig. 18.31 Excised full thickness being reconstructed with local flaps.
wound infection. An alternative method is to dedicate the Fig. 18.32 Local pivot flaps to cover exposed tendo Achillis after a cement burn.
early sessions to debridement of the burns and coverage with
a biologic dressing. When all wounds are debrided, skin graft-
ing is performed. This method results in the most rapid should be grafted earlier rather than later. In full-thickness
removal of all necrotic tissue. With burn wounds of more than burns to the hands, neck, and face, delay in grafting can result
50% TBSA, there are inadequate donor sites; alternating deb- in excess scarring and functional limitations that are difficult
ridement with grafting affords time for the donor sites to to overcome. The scarring can make the rehabilitation of the
re-epithelialize before they are harvested again. Donor sites patient very problematic. Thus, deep burns to these areas
harvested a second time can heal slowly, but the alternatives should be grafted early or closed with flaps to form healthy
are limited in these patients with large burns. The use of cul- tissue (Figs 18.3118.33) so that range of motion and hyper-
tured autologous epidermis for patients with more than 50% trophic scar management can be started early.
TBSA burns has helped because it is a ready and abundant
source of autologous epithelium for patients with limited
donor sites. Summary of burn wound treatment
A logical algorithm should be used in skin grafting of (Box 18.10)
patients with large surface area burns. Most important for
survival of the patient is to decrease the surface area of the Superficial wounds should heal by regeneration within 2
injury, so in the absence of other restrictions, the largest area weeks. They should be cleaned, dressed, and reviewed on
of burn should be excised and grafted first, such as the trunk, alternate days to optimize the wound healing environment.
then the lower extremity, followed by the upper extremity. Any burn not healed within 2 weeks should be referred for
Burns to the hands, neck, and face warrant special considera- assessment.
tion, however. To prevent excessive functional impairment to Deep partial thickness burns are unlikely to heal within 3
these areas after the burn wounds are healed, these areas weeks. The incidence of unsightly hypertrophic scarring rises
Metabolism/nutrition 421
A B Fig. 18.33 Pedicled radial forearm flap to cover

an open elbow joint.
Box 18.10 Techniques for burn reconstruction Table 18.7 Percentage increase in metabolic rate versus
burn size
Without deficiency of tissue
% Burn (TBSA) Metabolic rate (% increase)
Excision and primary closure
Plasty techniques 20 30
With deficiency of tissue
30 50
Serial excision and primary closure
Split and full thickness skin autografts 40 75
Dermal templates and split skin autografts 50 100
Plasty techniques
Local flaps 60 100
Regional flaps
Distant flaps
Tissue expansion Table 18.8 Catabolism-induced complications relative to loss of
Free flaps. lean body mass
Lean body
mass (% loss) Complication Mortality (%)
from 33% to 78% if healing is delayed from 36 weeks. 10 Impaired immunity; increased 10
Therefore, these injuries should also be excised and grafted infection
within the first 510 days.
20 Decreased healing; failure to 30
Full thickness injuries have no regenerative elements left.
wean
Unless they are very small they will take weeks to heal and
undergo severe contraction. They should be referred for 30 Too weak to sit; pressure 50
surgery as early as possible. sores; pneumonia
Clean wounds can be dressed with a nonadherant primary 40 Death, usually from 100
dressing such as tulle gras or Mepitel and an absorbent sec- pneumonia
ondary dressing such as gauze or Gamgee Tissue. Antimicrobial
agents are added where infection is likely (perineum, feet) or
heavy colonization is evident on the dressings or invasive approach to the nutritional management is essential for the
infection is suspected. survival of burn patients. Extensive burns elicit a pronounced
metabolic response to trauma causing physiological derange-
ments leading to the hyper-metabolic state (Table 18.7).12 The
Metabolism/nutrition hyper-metabolic response is accompanied by severe catabo-
lism and a loss of lean body mass and also by a progressive
Nutritional therapy plays a key role in the overall manage- decline of host defenses that impairs the immunological
ment of the burns patient and the aggressive dynamic response and leads to sepsis (Table 18.8). The burn wound
consumes large quantities of energy during the healing benefit. The mortality in the burns patients especially above
process due to the large population of inflammatory cells and 40% TBSA burns managed by appropriate nutrition has been
the production of collagen and matrix by fibroblasts. Severe found to be decreased because of decrease in negative nitro-
burn results in profound metabolic alterations, which include gen balance and better wound healing leading to decreased
increasing nitrogen loss, malnutrition and hypermetabolism. graft losses and improved immunity causing a decrease in
Catabolism as a response to thermal trauma only can be infections.
modulated, not completely reversed. Much of the morbidity Burn injury can increase the basal metabolic rate 50100%
and mortality after major burns may be attributed to this of the normal resting rate. The main features include increased
alteration. Nutritional therapy plays a key role in the overall glucose production, insulin resistance, lipolysis, and muscle
strategy for burned patients.13 Post-burn, the metabolic and protein catabolism. Without adequate nutritional support,
catabolic responses are prolonged in severity and time course, patients have delayed wound healing, decreased immune
lasting weeks to months in contrast to the days and weeks function, and generalized weight loss.14 Many formulas
observed in other injuries. Extensive nutritional support to predict the nutritional needs of these patients on the basis of
meet the increased energy expenditure is essential for the lean body mass and percentage TBSA burned. Increased
survival of burn patients. Effective provision of the required intake of both total calories and protein (1.53 g of protein/
amount of calories can be provided with oral, enteral or kg per day) is needed to restore the deficit. Much like fluid
parenteral route. resuscitation, the exact nutritional requirements are debata-
Controlling the stress response to burn injury alters ble. The clinical response of the patient remains the best indi-
the metabolic abnormalities (Boxes 18.1118.13).Optimizing cation of nutritional repletion during recovery from the injury.
nutrition to match nutrient utilization is essential. Controlling The rapidity of epidermal regeneration of superficial burns
the catabolic response is the next key treatment measure. It and donor sites and improving serum nutritional parameters
appears that anticatabolic and anabolic agents can markedly are the best indicators of adequate nutrition. Measurement of
diminish the net catabolism of burn injury during the acute the basal metabolic rate also guides nutritional replacement
and recovery phases.12 These agents, in combination with therapy. Measuring weight loss and gain during treatment is
optimum protein intake, appear to be of significant benefit in
the metabolic management of the severe burn.
Therapeutic strategies should aim to prevent body weight
losses of more than 10% of patients baseline status because Box 18.12 Systemic response to the release of cytokines and other
more profound weight losses are associated with significantly inflammatory mediators at the site of injury once the burn reaches
25% of total body surface area
worse outcomes. Known consequences of catabolic disorders
with loss of lean body mass above 10% include impaired Cardiovascular changes: Capillary permeability is increased,
immune function and delayed wound healing. Lean body leading to loss of intravascular proteins and fluids into the
mass reduction beyond 40% leads to imminent mortality. interstitial compartment. Peripheral and splanchnic vasoconstric-
Therefore, complications of ongoing catabolism remain a tion occurs. Myocardial contractility is decreased, possibly due
major cause of morbidity and mortality in severely burned to release of tumour necrosis factor. These changes, coupled
with fluid loss from the burn wound, result in systemic hypoten-
patients. In addition to optimizing nutrient intake, anticata- sion and end organ hypoperfusion.
bolic and anabolic agents that may counteract the stress Respiratory changes: Inflammatory mediators cause bronchocon-
response to injury or illness may be of significant clinical striction, and in severe burns adult respiratory distress syndrome
can occur.
Metabolic changes: The basal metabolic rate increases up to
three times its original rate. This, coupled with splanchnic
Box 18.11 Bodys response to injury hypoperfusion, necessitates early and aggressive enteral feeding
to decrease catabolism and maintain gut integrity.
Emergent Phase (Stage 1) Immunological changes: Nonspecific down regulation of the
immune response occurs, affecting both cell mediated and
Pain response
humoral pathways.
Catecholamine release
Tachycardia, tachypnea, mild hypertension, mild anxiety
Fluid Shift Phase (Stage 2)
Length 1824 h
Begins after Emergent Phase Box 18.13 Major metabolic abnormalities with response to burn
Reaches peak in 68 h stress response
Damaged cells initiate inflammatory response
Increased catabolic hormones (cortisol and catechols)
Increased blood flow to cells
Decreased anabolic hormones (human growth hormone and
Shift of fluid from intravascular to extravascular space due to testosterone)
leaky capillaries causing massive edema
Marked increase in metabolic rate
Hypermetabolic Phase (Stage 3)
Sustained increase in body temperature
Last for days to weeks Marked increase in glucose demands and liver gluconeogenesis
Large increase in the bodys need for nutrients as it repairs itself Rapid skeletal muscle breakdown with amino acid use as an
Resolution Phase (Stage 4) energy source (counter to normal nutrient channeling)
Scar formation Lack of ketosis, indicating that fat is not the major calorie source
General rehabilitation and progression to normal function. Unresponsiveness of catabolism to nutrient intake.
Metabolism/nutrition 423
not useful because of the large fluid shifts. Even with ade- Early enteral nutrition can relieve gastrointestinal damage,
quate nutritional support, most patients lose muscle mass and and maintain the integrity of intestinal mucosa after severe
weight. Several studies propose the use of anabolic steroids burn. Gastrointestinal mucosal lesions take place during
or growth hormone to reduce muscle catabolism and weight ischemia and reperfusion period after severe burns. Early
loss during the injury and to enhance weight gain during enteral nutrition can relieve the ischemia and reperfusion
recovery. injury by means of increasing the ability of eliminating
oxygen free radical. The increase of intestinal permeability is
one of the early features of intestinal mucosal barrier damage.
Nutrition Early enteral nutrition is an effective method to keep a normal
The goal of resuscitation is not only to maintain stable circu- intestinal permeability through the maintenance of blood
lation, but also to improve the hypoxic state of the tissues and circulation and the prevention of ischemia and reperfusion
cells. Patients fed early have significantly enhanced wound injury of intestine.13,16 Parenteral nutrition requires additional
healing and shorter hospital stays.15 Meeting the extensive vascular access with its concomitant risks. It also lacks
calorie requirement by oral route alone is practically not pos- the beneficial effects of gut mucosal stimulation and its pro-
sible in the major burn patients. Enteral nutrition through tective effects against bacterial translocation and stress hem-
nasogastric or nasoduodenal transpyloric tubes are the pre- orrhage. Early enteral nutrition is superior to parenteral
ferred supplementary route of providing calorie deficit to the nutrition in the early stage after burn. It might be a more
acutely injured burn patient. Patients with burns 20% TBSA effective route to preserve the secretion and motility of gas-
will be unable to meet their nutritional needs with oral intake trointestinal tract, lower intestinal ischemia and reperfusion
alone and the transpyloric tube should be inserted at admis- injury, reduce intestinal permeability, decrease plasma endo-
sion, as it is better tolerated than if inserted after the return of toxin and inflammatory mediators, and maintain mucosa
peristalsis. In the rare case that precludes use of the gastroin- barrier function.
testinal tract, parenteral nutrition should be used only until
the gastrointestinal tract is functioning. Nutrition formulae
Tube feedings also have an advantage over regular oral
intake. Patients with large surface area burns need to consume Burn centers continue to use a variety of formulae to estimate
large amounts of food to satisfy their nutritional requirements nutrient needs (Table 18.9).17 The number of energy estim-
(Fig. 18.34). The rigorous schedule of dressing changes, ation formulas has increased in recent years with many
operations, and rehabilitation sessions interferes with meals. developed for specific patient populations.17 Burn-specific
Diminished appetite from high-dose analgesics also contrib- equations have been developed both for pediatric and
utes to poor feeding. Adequate nutritional support is so criti- adult populations. A study compared 46 published energy
cal to recovery from burn injury that most clinicians will place calculations with indirect calorimetry in burn patients and
feeding tubes in patients with inadequate oral calorie intake found none (including, Curreri, Davies, HarrisBenedict,
despite the risk of aspiration pneumonia. Muir and Wilmore formulae) precisely estimated calorie
needs and most demonstrated some degree of bias.18 In
addition, formulas published before 1980 often overestimated
300 energy needs.18 Burn centers continue to use a variety of
methods to monitor nutritional status though there appears
Stress response Rehabilitation response to be less agreement regarding some methods than in years
Muscle gain, g
(catabolic phase) (anabolic phase) past.

200
Add anabolic agent

Gain 9 kg
Endocrine and glucose monitoring
100 Injury
Strict glucose control of 80110 mg/dL can be achieved using
Gain 9 kg an intensive insulin therapy protocol, leading to decreased
10 20 30 Nutrition and exercise
0 infectious complications and mortality rates.19,20
10 20 30 40 50 60 70 80 90
Time, days Hepatic protein monitoring
100
Hepatic proteins (albumin, transferrin, prealbumin) have a
Muscle loss, g
Lose 9 kg role acute phase reactants, and are profoundly affected by

200 fluid status and by metabolic stress, both of which are key
Injury components of the hypermetabolism present after a burn
resolved injury and therefore have limited use in the measure of nutri-
300
tional status in burn injuries.
Anabolic steroids
400
Severe burn injuries induce a hypermetabolic response, which
Fig. 18.34 The role of metabolic state in determining the rate of restoration of lean leads to catabolism. Oxandrolone, a synthetic derivative of
body mass. testosterone, has been used in adult patients with severe
Table 18.9 Formulae for estimating calorie and protein needs

Age
Formula (years) % TBSA Burn Calories (kcal) per day Protein
Adults
Burke and >18 Any 2 BMR Not calculated
Wolfe
Curreri 1659 Any (25 body weight in kg) + (40 % TBSA burn) Not calculated
>60 Any (20 body weight in kg) + (65 % TBSA burn)
Davies and >18 Any (20 kcal body wt in kg) + (70 kcal % TBSA burn) (1 g body wt in
Liljedahl [>50% TBSA injuries are calculated as a 50% injury] kg) + (3 g %
burn)
Galveston I >18 (2100 kcal/m2 TBSA) + (1000 kcal/m2 % TBSA burn) Not calculated
Ireton-Jones >18 Any but must be 1784 (11 age in years) + (5 weight in kg) + 244 Not calculated
ventilator- (sex: male = 1; female = 0) +239 (trauma: yes = 1;
dependent no = 0) + 804
Modified >18 <40 Male = 1.5 ([66 + (13.7 weight in kg) + (5 height in 1.5 g weight in kg
Harris-Benedict cm) (6.8 age))
Female = 1.5 [655+(9.6 weight in kg) + (1.7 height
in cm) (4.7 age))
40 Male = 2 ([66 + (13.7 weight in kg) + (5 height in 2 g weight in kg
cm) (6.8 age))
Female = 2 [655+(9.6 weight in kg) + (1.7 height in
cm) (4.7 age)
Muir >18 <20 35 kcal/kg 1.5 g/kg
2029.9 40 kcal/kg 2.0 g/kg
3039.9 50 kcal/kg 3.0 g/kg
4050 60 kcal/kg 4.0 g/kg
Wilmore >18 Any Use nomograms to calculate BMR, % change in Adjust nitrogen/total
BMR, energy requirements calorie to 1 : 150
30 20002200 kcal/m2 15 g nitrogen/m2
Toronto >18 Any 4343 + (10.5 % TBSA burn) + (0.23 calorie Not calculated
intake) + (0.84 Harris-Benedict energy
expenditure) + (114 mean body temperature
(C)) (4.5 days post-burn)
Children
Curreri Junior 01 Any BMR + (15 kcal % TBSA burn) Not calculated
13 Any BMR + (25 kcal % TBSA burn) Not calculated
415 Any BMR + (40 kcal % TBSA burn) Not calculated
Davies Child 112 Any (60 kcal body weight in kg) + (35 kcal % TBSA (3 g body wt in
burn) kg) + (1 g %
[>50% surface injuries are calculated as a 50% injury] burn)
Galveston Infant 01 Any (2100 kcal/m2 TBSA) + (1000 kcal/m2 % TBSA burn) Not calculated
Galveston II 111 Any (1800 kcal/m TBSA) + (1300 kcal/m % TBSA burn)
2 2
Not calculated
Galveston 1218 Any (1500 kcal/m TBSA) + (1300 kcal/m % TBSA burn)
2 2
Adolescent
1 g nitrogen = 6.25 g protein; BMR, basal metabolic rate.
Rehabilitation 425
thermal injury to enhance lean body mass accretion, restore

body weight, and accelerate wound healing. In clinical Box 18.14 Physiotherapy and occupational therapy treatments
studies, oxandrolone 10 mg orally twice daily improved Regular physiotherapy several times per day
wound healing, restored lean body mass, and accelerated Starting physiotherapy from 1st day of patients admission and
body weight gain. During the rehabilitation period, oxan- as early as the 3rd day of grafting25
drolone therapy with adequate nutrition and exercise Early chest physiotherapy to prevent remove secretions and
improved lean body mass, increased muscle strength, and prevent atelectasis
restored body weight.21 Burn patients recieving oxandrolone Exercise and stretching therapy to prevent joint contracture
regain weight and lean mass two to three times faster than Ankle pump exercise several times per day
with nutrition alone.22 Prevention of muscular atrophy with passive and active (with and
without load) exercises electrical stimulation
Ambulation as soon as possible
-blockade Education of the patients family to help the patient and the burn
care professionals
-blockers after severe burns decrease heart rate, resulting in Consideration and prevention of secondary complications (e.g.,
reduced cardiac index and decreased supraphysiologic ther- frozen shoulder, scoliosis, etc.)
mogenesis.23 In children with burns, treatment with pro- Use of splinting and modalities (e.g., ultrasound) based on
pranolol during hospitalization attenuates hypermetabolism patients need to protecting the skin grafts and preventing the
and reverses muscle-protein catabolism. Propranolol is given burn scar
to achieve a 20% decrease in heart rate of each patient com- Encourage activities of daily living with emphasis on fine
pared with the 24-h average heart rate immediately before movements and joint mobilization.
administration.23
Amino acids
Research into glutamine and arginine has proliferated in or mobilize injuries.26 Recently, early motion has been strongly
recent years with equivocal results. Both nutrients have been advocated but it is important to recognize the stages of wound
demonstrated to improve outcomes such as length of stay, healing and to arrange a balance between rest and exercise. A
infection rate, mortality in critically ill patients including burn study has demonstrated that starting good burn physiother-
patients. A review of randomized trials, systematic reviews apy on day 1 for not grafted areas and day 3 for skin grafted
and guidelines concluded that glutamine therapy in burns is areas resulted in only 6% burn contracture.25 In addition, the
promising but the safety and efficacy of long-term use along results of this study indicated the following factors that could
with the best route and dosage is debatable.24 help to decrease the burn-injured complications:
1. To consider the joint position during immobilization
phase after graft
Rehabilitation 2. To decrease the immobilization phase after graft
3. To increase the interval of physiotherapy treatment per
Rehabilitation is the restoration to health and work capacity day and also to organize the aim of physiotherapy based
of a person incapacitated by burn injury. Burns rehabilitation on the patients needs
is often challenging and has several other dimensions, entail-
4. To pay extra attention to some areas, e.g., shoulder, neck,
ing much more than the sole aim of preventing scarring. Burn
fingers and face.
patients have to recover full use not only of their injured
part(s) but of their whole body and they have to recover con- To achieve these, everyone, including patients, must have
fidence in their ability to work and enjoy life. a clear understanding of the aims of physiotherapy and the
Rehabilitation starts on the day of injury. The treatment of following points could be considered for decreasing the burn-
burns is generally divided into an acute and a chronic period. injured complications:
Anticipation and treatment of problems resulting from the 1. To have a team activity with emphasis on psychological
injury and edema prevent many subsequent complications. It and nutritional supports
progresses through grafting and healing to discharge from the 2. To consider the continuation of physiotherapy treatment
ward, integration into society and through the sometimes after releasing the patient from hospital, for at least 18
endless period of reconstructive surgery to a point when, months
either the patient has had enough or the surgeon suggests
3. To use pressure garment before starting the keloid
he can do no more, and usually it is the former.
The acute period is defined as the period from the occur- 4. To use a suitable cream for itching.
rence of the burn to complete wound coverage. The chronic In the acute and post-healing stages of recovery, the move
period has been arbitrarily defined as the period from comple- out of the ward is the first defining point in a patients post-
tion of wound coverage to maturity of the scar. During the burn life. In addition to physical considerations, wound
acute phase, prevention of contractures by physical therapy, healing and recovery after burns is promoted by good nutri-
traction and splinting is of paramount importance (Box tion, for initial wound healing and long term scar reduction.
18.14).25 Physiotherapy is very important in the prevention of Rehabilitation involves the whole burn team in encouraging
the burn contractures and also, to show the effectiveness of the patient to live as normal a life as possible between dress-
the teamwork. There have been debates over whether to rest ing changes and operations; the therapists take the lead in
Fig. 18.36 Silicone and pressure garment therapy for burn rehabilitation.
Fig. 18.35 Burn patient positioning and pressure management are important for and plastic facemasks to decrease hypertrophic scars and joint
rehabilitation. contractures. There is a need for intensive post-healing reha-
bilitation, both for adults and for children, particularly as it
will increasingly be possible to keep alive, and to heal, burns
maintaining muscle strength, joint range and activities of of a much greater percentage of body area. Childrens burn
daily living (Fig. 18.35). clubs go a long way in providing confidence-building support
In the chronic phase, the prevention of hypertrophic scar- after discharge from the ward, so the children are at present
ring and contractures become major concerns. Throughout in a better position than adults, however there is still a need
treatment, the social and emotional rehabilitation of burn for intensive rehabilitation in high trauma rehabilitation
patients is a prime concern. Pressure garments, have pitfalls centers independent of burn centers.
in their use and the importance of careful fitting, constant Many can manage well with physiotherapy and occupa-
wearing of the garments and the appropriate use of pressure tional therapy. Another post-healing team concept is outreach.
paddings is essential. It is obvious that close supervision is It was introduced to try to overcome the gap recognized at
essential, particularly for children. this stage of recovery, to provide links with the community
The rehabilitation therapist (occupational and physical) services and local hospitals. Rehabilitation centers start inte-
evaluates and formulates a treatment plan and begins func- gration back into society in a protected environment with
tional range of motion, splinting, edema control, and scar other people who had sustained physical trauma. They could
modulation as needed. Hands are a primary concern, espe- receive the help in returning to work, to the home, hobbies
cially deep burns of the dorsal surface. They receive immedi- and to society, and if necessary return for top up help after
ate range of motion and splinting (Fig. 18.36). Although reconstructive surgery.
survival takes precedence in the critically ill patient, physical Psychological factors such as sexuality and changed body
and occupational therapy objectives are always kept in mind. image require careful management. Adaptation to long-term
Irrespective of the patients general condition, injured upper disability should be integrated into the rehabilitation treat-
and lower extremities are elevated to allow adequate venous ment plan as well as the assessment of post-traumatic stress
drainage and to reduce edema. Much of the functional limita- disorder as the potential to develop this disorder exists owing
tions to burned areas depend on the outcome of skin grafts, to the often distressing nature of many of these injuries. The
the local tissue healing factors, and the baseline state of the input of psychological services is an invaluable aspect of
patient. Nonetheless, the quality and availability of therapists, burns rehabilitation.
especially in burn injuries of the upper extremities, have been In addition, reintroduction to society and work may
shown to influence the outcomes of surgical interventions. In provide several challenges to a burns survivor. Issues related
some circumstances, treatment by good therapists decreases to a full return to the community, and their solutions such as
the need for surgical treatment. Early and proper splinting behaviour therapy, occupational rehabilitation, and adaptive
and stretching of flexion crease burns, such as the neck, axilla, equipment may be outside the limits of this chapter. However,
and antecubital areas, reduce the extent of scar contractures follow-up recommendations, including a more comprehen-
and may prevent subsequent functional deformities and the sive checklist of potential areas of need, may be helpful.
need for reconstruction.
During the recovery phase of the burn injury, rehabilitation Pain control
therapy is even more important, often occupying the majority
of the patients treatment time. Limitations to activities of The adverse sequelae of inadequate pain in the burn popula-
daily living, strengthening and increasing of muscle mass, tion have been long recognized, yet control of pain remains
and even cosmetic results of burn scars are under the influ- inadequate globally. The dynamic evolution of burn pain both
ence of the therapists. The therapists provide pressure gar- centrally and peripherally, and the many factors which influ-
ments, thermoplastic splints, serial casting, silicone inserts, ence pain perception illustrate the need for a therapeutic plan
Rehabilitation 427
in the pharmacological treatment of every burn patient.

Box 18.15 Pharmacological methods of burn pain management Nonpharmacological methods of pain control can play an
Opioid analgesics important role in suitable patients but resources vary widely
between units.
Morphine: gold standard opioid drug
Severe pain with burns is a major physiologic stress that
Oxycodone: less hallucinations and histamine-induced itching
than morphine can have a negative impact on the patients recovery. A person
Fentanyl: rapid onset, potent, short acting synthetic opiate. with burns has exposed functioning nerve endings. Dressing
Provides good procedural analgesia but potent respiratory changes and bedside debridement often require high doses of
depressant opiates and sedatives. The availability of reversal agents for
Remifentanil: ultra-short acting opiate, useful only as an infusion benzodiazepines has improved the safety of combining these
for the management of short bursts of previous pain and to drugs with opiates. Close monitoring of respiratory status is
assist with weaning from mechanical ventilation required when consciousness is diminished. Short-acting
Alfentanil: shorter acting than fentanyl and thus favored as the agents such as barbiturates and lipid-soluble agents also
opiate of choice for control of procedural burn previous pain require careful monitoring with use. Ketamine, combined
both as a sole agent and in combination with propofol
with a sedative like midazolam, provides pain control with
Alfentanil: undergoes hepatic metabolism to inactive, nontoxic
metabolites which are renally cleared. Safest strong opioids in little respiratory depression.
severe renal impairment. More emphasis on pain control not only helps the patients
Methadone. psychological wellbeing but may significantly affect physical
Simple analgesics outcome as well. Some clinical evidence and common sense
Paracetamol
suggest that adequate analgesia may limit the overall hyper-
Non-steroidal anti-inflammatory drugs (NSAIDs) metabolic and catabolic state. Painful stimuli influence the
Other drugs
release of a number of circulatory factors that affect tissue
perfusion, immune system function, and wound healing.
Gabapentin
Further research should help delineate the negative or posi-
Ketamine
tive effect of modulating pain.
Clonidine
Patients without a substance abuse problem before the
Benzodiazepines
injury typically do not develop opiate addiction even after
Amitriptyline
receiving high doses for prolonged periods, but physical
Lignocaine by intravenous infusion
dependence often occurs after sustained treatment with
Entonox
opiates. Gradually reducing the doses of opiates as pain
diminishes avoids opiate withdrawal.
Patients with a history of substance abuse present special
problems. Heroin users require much larger doses of opiates
which is similarly dynamic and flexible enough to cope with to achieve the same analgesic effects. Methadone can be used
the facets of background, breakthrough, procedural and post- for long-acting pain relief and to prevent opiate withdrawal.
operative pain. Regular, ongoing and documented pain Alcoholic patients risk alcohol withdrawal and delirium
assessment is key in directing this process. tremens. Benzodiazepines prevent discomfort and the poten-
Before prescribing any drug to a burn patient, the clinician tial for progression to life-threatening delirium tremens and
must have an understanding of the altered pharmacokinetic seizure. Skillful pain management can contribute greatly to
state resulting from well-described pathophysiological wound healing and rehabilitation efforts and should be given
changes that follow burn injury. During the first 48 h, a high priority in the comprehensive treatment of the burn
decreased organ blood supply will reduce clearance of drugs, patient.
but the subsequent hypermetabolic phase (48 h after injury)
is associated with increased clearance. Variations in levels of
acute phase plasma proteins lead to changes in drug binding
Complications (Box 18.16)
and free fractions available for end action. The volume of
distribution of a drug may be further affected by alterations Skin graft loss
in total body water. Using regular and repeated pain assess- Loss of skin graft is the most common operative complication
ment to quantify the effect of analgesic agents reduces the and is caused by hematoma, infection and graft shear. Early
impact of these changes. Doses vary widely between indi- graft examination should be encouraged with removal of any
viduals and over time with the same individual. underlying hematoma. After day 3, capillary ingrowth has
The family of opioid analgesics provides the backbone of occurred and would be interrupted by graft movement. If
analgesia to burn patients (Box 18.15). Together, they provide examination shows that the skin grafts are grossly infected,
an excellent range of potencies, duration of actions and routes then quantitative microbiological cultures can be performed
of administration. However, they must be used judiciously as and appropriate topical antimicrobial therapy commenced. It
side-effects may be clinically relevant and furthermore, recent is very important that skin grafts are carefully immobilized
data has implicated them as being capable of inducing pain with bolsters or splinting to prevent graft shear.
NMDA receptor antagonist such as ketamine and gabapentin
are increasingly recognized as useful adjuncts, capable of Infected burn
marked opiate sparing effects in this population. The simple
analgesic paracetamol (acetaminophen) has both anti-pyretic Infection should be suspected if the wound becomes incre-
and opioid-sparing properties and justly deserves its place asingly uncomfortable, painful, or smelly; if cellulitis is
Radial sensory
branch
Ulnar nerve Radial nerve
Cephalic vein
Common peroneal nerve
Common peroneal nerve

Fig. 18.37 Pseudomonas aeruginosa infection of burn wounds.
Posterior tibial vessels Short saphenous vein

Sural nerve
Box 18.16 Potential complications during acute burns management
Respiratory distress from smoke inhalation or a severe chest

Fig. 18.38 Escharotomy lines and relevant anatomy.
burn
Fluid loss, hypovolemia and shock
Infection
Increased metabolic rate
Increased plasma viscosity and thrombosis to serum cortisol increases in response to stimulation. The
Vascular insufficiency and distal ischemia from a circumferential clinical relevance of this finding has not been established.
burn of limb or digit
Muscle damage from an electrical burn may be severe even with
minimal skin injury; rhabdomyolysis may cause renal failure
Compartment syndrome
Poisoning from inhalation of noxious gases released by burning Pathophysiologically, any process that results in elevated
(e.g., cyanide poisoning due to smouldering plastics) pressure in a closed fascial compartment can cause a compart-
Hemoglobinuria and renal damage ment syndrome (Figs 18.38, 18.39). Compartment syndrome
Scarring and possible psychological consequences. occurs when the tissue pressure within an enclosed space is
elevated to the extent that there is decreased blood flow
within the space, decreasing tissue oxygenation and impair-
ing metabolic function. The final result without prompt treat-
observed; or if the person develops a fever (Fig. 18.37). A swab ment is cellular death. Extremity compartment syndromes
from the burn wound should be sent for microbiology. can also result from extensive edema formation. Patients may
Treatment may require wide excision of all infected tissue and require escharotomies, fasciotomies, or both for the release of
administration of antibiotics. Empirical antibiotic treatment extremity compartment syndrome. Patients with circumferen-
should be started after discussion with the microbiology tial full-thickness burns (neck, thorax, abdomen, extremities)
team and the antibiotic treatment later changed according to are also at risk of requiring escharotomies (Figs 18.4018.46).
the results from the swab. The recommended choice of In extremities there is impaired capillary refill, paraesthesia,
antibiotic is guided by the most likely cause of infection and increased pain develop earlier than decreased pulses. The
and local patterns of antibiotic resistance should also be orbit is a compartment limited to expansion and may require
considered. lateral canthotomy to successfully reduce intraocular pressure
to normal.
Adrenal insufficiency Abdominal compartment syndrome is a life-threatening
situation associated with fluid extravasation/edema and
Absolute adrenal insufficiency occurs in up to 36% of patients fluid resuscitation. It is defined as intra-abdominal pressure
with major burns, but there is no association between response >20 mmHg and at least one new organ dysfunction. It is
to corticotropin stimulation and survival. Those with >30% associated with renal impairment, gut ischemia, and
TBSA burns have higher cortisol levels but may be resistant cardiac and pulmonary malperfusion. Clinical manifestations
Rehabilitation 429
Fig. 18.39 Hand escharotomy incisions: (A,C) lateral view, (B) dorsal view.
Fig. 18.40 Escharotomy for full thickness burn. It must extend into normal tissue.
Fig. 18.41 Circumferential full thickness burns require escharotomy. It is not

always possible to site intravenous access in unburnt tissue.
A B
Fig. 18.42 Hand escharotomies.
A B C
Fig. 18.43 Zigzag escharotomy incisions help prevent straight line scar contractures which may require secondary reconstruction.
A B
Fig. 18.45 (A) Periocular escharotomies. (B) Temporal and periocular

escharotomies.
Fig. 18.44 Escharotomy incision of the lower limb in the midaxial line between the
flexor and extensor surfaces.
include tense abdomen, decreased pulmonary compliance,

hypercapnia, and oliguria. Urine output monitoring is not
sensitive or specific enough to diagnose abdominal compart-
ment syndrome. Careful monitoring and aggressive treatment
should be instituted to avoid this mortal complication.
Appropriate intravascular volume, appropriate body posi-
tioning, pain management, sedation, nasogastric decompres-
sion if appropriate, chemical paralysis if required, and
torsoescharotomy are all interventions to increase abdominal
wall compliance and decrease intra-abdominal pressures.
Bladder pressure monitoring should be initiated as part of the
burn fluid resuscitation protocol in every patient with 30%
TBSA burn. Patients who receive >250 mL/kg of crystalloid
in the first 24 h may require abdominal decompression. Fig. 18.46 Any circumferential burn of the face, scalp, thorax, abdomen, penis or
Percutaneous abdominal decompression is a minimally inva- extremity may require early escharotomy for deleterious compressional effects of
sive procedure that should be performed before resorting to the burn eschar.
Rehabilitation 431
The use of drugs to prevent stress-related gastric bleeding

in critically ill surgical cancer patients is common. Occult
bleeding in the adult burn population is also very common.
However, clinically important bleeding, as defined by the
need for blood transfusions or a significant alteration in the
vital signs, occurs in 0.66% of patients. Because of marked
improvements in early resuscitation and oxygenation, correc-
tion of fluid and acidbase imbalances, improvements in the
care of the critically ill (including early enteral nutrition), as
well as early prophylactic treatment with antacids, H2b antag-
onists, proton pump inhibitors or sucralfate and early enteral
feedings have greatly decreased the incidence of this devastat-
ing problem. Aggressive nutritional support has probably
helped with ulcer healing and also prevents acalculous
cholecystitis.
Fig. 18.47 Extensive escharotomies and decompressive laparotomy. Heterotopic ossification

The transformation of primitive mesenchymal cells in the sur-
laparotomy. If less invasive maneuvers fail, decompressive rounding soft tissue to mature lamellar bone is termed hetero-
laparotomy (Fig. 18.47) should be performed in patients with topic ossification (HO). HO is a pathologic condition that
abdominal compartment syndrome that is refractory to other adversely affects a subpopulation of burn patients. The inci-
therapies and the reported mortality rates for decompressive dence of HO in a general burn population is reported to be
laparotomy is as high as 100%. between 1% and 3%. HO after burns commonly occurs around
major joints. Elbow, shoulder, and hip are the most commonly
affected joints, in that order of frequency. HO is characterized
Deep venous thrombosis by progressive abnormal soft tissue and periarticular bone
Deep venous thrombosis incidence ranges from 1% to 23% in formation that encroaches upon the joint, eventually causing
burn patients and deep venous thrombosis chemoprophylaxis decreased range of motion and functional disability, pain in
is recommended. the involved joint and limb, and possibly nerve entrapment.
The etiology and pathogenesis of HO in burn patients is not
Gastrointestinal complications understood. It usually occurs in patients with large (generally
>20% TBSA) and/or full-thickness burns, but HO has occa-
Gastrointestinal (GI) complications (e.g., gastric and intestinal sionally been reported in burns under 10% TBSA. HO also
motor dysfunction as well as stress-related mucosal disease usually occurs in burned extremities, but it is sometimes
[SRMD]) frequently occur in burn patients and adversely found in areas remote from the injured site. HO seems to be
affect patient outcomes. Gastrointestinal motor dysfunction related to the extended time to wound closure and genetic
may predispose patients to impaired enteral nutrition and predisposition. Patients who require a longer time to defini-
pulmonary aspiration of gastric contents.27 Stress-related tive burn excision and skin grafting tend to demonstrate a
mucosal damage an acute erosive gastritis occurs in many greater incidence of HO than patients who undergo successful
burn patients in ICUs and may develop within 24 h of admis- early excision and grafting. HO also appears to be related
sion.28 The incidence of SRMD varies widely given the popu- to movement at the affected joints. However, the exact
lation of patients studied and the definition of bleeding used. relationship is unclear. Patients who are completely immobi-
Upper gastrointestinal tract mucosal injury detected by lized and patients who receive aggressive physical/
endoscopy is extremely common in the burns population, and occupational therapy seem to both be at greater risk for the
stress-induced gastritis and ulceration can be shown to be development of HO. A combination of immobilization, an
endoscopically evident in up to 78% of adult burn patients. active inflammatory state, hypermetabolism, and local trauma
Stress induced ulcers of the stomach and duodenum in very and hemorrhage from over-vigorous physiotherapy are thus
extensively burned patients are due to a defect in the mucosal putative causative events. Other contributing factors may
barrier to secreted acid. The cause of this defect is related include vascular stasis, tissue hypoxia, infection, deep venous
partly to mucosal ischemia which is aggravated by hypoten- thrombosis, high dietary protein intake, and abnormal calcium
sion, sepsis and hypoxia. metabolism. Sometimes, it is difficult to differentiate HO from
Occult bleeding in the adult burn population is also very scar contracture by clinical symptoms and signs. Physicians
common. The incidence of clinically important GI bleeding, should keep the diagnosis of HO in mind when burn patients
defined as overt bleeding complicated by hemodynamic complain of decreased ROM in their elbow joints. X-ray is a
instability, decrease in hemoglobin, and/or need for blood fast and economical tool for diagnosis of HO. Other diagnos-
transfusion, from SRMD in the this population is about 16%. tic tools include CT, magnetic resonance imaging (MRI), bone
In addition, the morbidity associated with this type of scan and ultrasound.
severe ulceration and bleeding can increase the length of The treatment of HO is largely conservative with surgery
stay in the ICU by up to 8 days, and mortality is as much as in combination with rehabilitation reserved for patients who
four-fold higher than it is in ICU patients without this do not respond to less invasive measures, or who have severe
complication. HO.29,30 Adjuvants to surgical excision include perioperative
radiation therapy and/or injection of corticosteroids. Attempts Gram-negative bacterial infections result from translocation
to prevent HO in burn patients have focused on early wound from the colon because of reduced mesenteric blood flow at
closure, early mobilization, gentle passive and active range of the time of burn and subsequent insults. Furthermore, there
motion exercises, and pharmacologic therapy with salicylates, are several immune deficits in burns patients, including
warfarin, and/or biphosphates. impaired cytotoxic T lymphocyte response, myeloid matura-
tion arrest causing neutropenia, impaired neutrophil function,
and decreased macrophage production. Finally, burns patients
Heparin-induced thrombocytopenia can incur hospital acquired infections common to other
Early thrombocytopenia occurs in the post-burn course in patients in intensive care units, including intravascular cath-
patients with extensive injury. Problems after burn injury such eter related infections and ventilator associated pneumonia,
as pulmonary infections, multiorgan failure, sepsis, and with an overall incidence of infection higher than that of other
bleeding disorders accentuate this trend. Careful observance patients in intensive care units.
for thrombocytopenia after the first week of hospitalization Antibiotic prophylaxis reduces all cause mortality among
will alert the practitioner to make the diagnosis in burn patients in intensive care but injudicious use of antibiotics
patients. Although the incidence of heparin-induced throm- merely eliminates the patients normal flora and allows resist-
bocytopenia is relatively low, the complications are major and ant organisms to grow; therefore, prophylactic antibiotics are
include arterial and venous thromboses and increased number rarely used. Therefore, current guidelines for management do
of surgeries. not recommend systemic antibiotic prophylaxis for burns
patients, stating lack of evidence for efficacy and induction of
antibiotic resistance. A recent systematic review and meta-
Inflammation analysis found that in burns patients, systemic antibiotic
prophylaxis administered in the first 414 days significantly
There are standardized definitions for sepsis and infection-
reduced all cause mortality by nearly a half and limited peri-
related diagnose in burn patients. Patients with large burns
operative prophylaxis reduced wound infections but not mor-
have a baseline temperature reset to 38.5C, and tachycardia
tality.32 In addition, they concluded that topical antibiotic
and tachypnea may persist for months. Continuous exposure
prophylaxis applied to burn wounds, commonly recom-
to inflammatory mediators leads to significant changes in the
mended, had no beneficial effects. Unfortunately, the meth-
white blood cell count, making leukocytosis a poor indicator
odological quality of the data was weak and they concluded
of sepsis. Use other clues as signs of infection or sepsis such
that prophylaxis could not be recommended for patients with
as increased fluid requirements, decreasing platelet counts >3
severe burns other than perioperatively and that there was a
days after burn injury, altered mental status, worsening pul-
need for randomized controlled trials to assess its use.
monary status, and impaired renal function. The term sys-
However, these patients are often fragile, and delayed
temic inflammatory response syndrome should not be applied
treatment of real infections risks severe episodes of sepsis
to burn patients because patients with large burns are in a
leading to multisystem organ failure. Treatment is often
state of chronic systemic inflammatory stimulation.31
initiated empirically before a specific organism is isolated.
Patients with large enough wounds and with enough time
Neutropenia ultimately develop life-threatening infections that must be
treated. Unfortunately, treatment of one organism often leads
Transient leucopenia is common, primarily due to a decreased to colonization by resistant organisms and additional infec-
neutrophil count. Maximal white blood cell depression occurs tions. Bacteria, such as staphylococci and pseudomonas,
several days after admission with rebound to normal a few resistant to many antibiotics and fungus are pathogens
days later. Use of silver sulfadiazine has been associated with commonly found in burn patients late in the course of treat-
this transient leucopenia; resolution is independent of contin- ment. These organisms are more difficult and risky to treat.
ued silver sulfadiazine. Waiting until there is good clinical evidence of an infection
before initiating treatment may delay the infection by resist-
Infection ant organisms.
The majority of burn patients have a low-grade fever but no
Patients with large TBSA burns are immunosuppressed and source of infection in the first week after injury. Contamination
at increased risk for infections, especially of the wounds, and then overgrowth of burn wounds by pathogens causing a
venous access sites, and lungs. Small injuries (<10% TBSA) systemic picture of sepsis typically occur 23 weeks after
heal rapidly, and infections are rare. Monitoring at-risk injury. Early debridement of the necrotic burn tissue and cov-
patients for infection can be a problem because many burn erage with skin greatly reduce the incidence and morbidity of
patients have a fever and altered white blood cell counts burn wound infections. Patients with large surface area burns
without infections. that remain open for long periods still develop wound infec-
In burns patients infections arise from multiple sources. tions, have poor healing, and ultimately succumb to infection.
Any infection in a burn patient should be considered to be Isolation of the patient in specialized unit beds along with
from the central venous catheter until proven otherwise and infection precautions by the health care workers (handwash-
the catheter should be changed.31 Burn wounds become ing, gloves, and gowns) reduces the transmission of pathogens
rapidly infected with Gram-positive bacteria, mainly staphy- from one patient to another but does not protect patients from
lococci, that are normal deep inhabitants of the sweat their own pathogens (skin and gastrointestinal tract). A high
glands and hair follicles exposed by the burn. The moist, level of suspicion for wound infection must be kept when the
vascular burn eschar further encourages microbial growth. patients condition deteriorates rapidly. Daily observation of
Rehabilitation 433
the wounds by trained personnel is critical even after perma- Patients with cutaneous burns have a high incidence of
nent skin grafts are placed. Wound cultures, particularly quan- pulmonary infection even without lung injury from smoke
titative assessment, and biopsies for histologic examination inhalation. The skin injury increases interstitial fluid in the
help confirm the diagnosis and direct therapy. Prompt exci- lung, and the lung is at risk from pathogens in the blood and
sion of infected and necrotic tissue, appropriate topical treat- the respiratory tree. Chest radiographic changes, purulent
ment, and systemic antimicrobial therapy are critical to sputum production, and microbiologic results help determine
survival of the patient. when and what to treat. Patients are at risk for pulmonary
Great emphasis is placed on the isolation and protection of infection until the burn wounds are covered. Evidence of a
burn patients from environmental pathogens. It is worthwhile pulmonary infection should be treated aggressively with pul-
to place these patients in protective isolation to limit contact monary toilet and broad-spectrum antibiotics. A more narrow
with hospital-based pathogens, such as multidrug-resistant spectrum antibiotic can be selected after sputum or pulmo-
organisms. Despite these precautions, most severely injured nary lavage culture results are obtained. Mechanical ventila-
patients have one or several bouts of infection through the tion support may be needed in cases of severe pulmonary
course of their treatment. The skin and gut of the patient compromise to augment gas exchange and to decrease the
harbor pathogens, and no known therapy can eliminate labor of respiration for the patient. On occasion, patients
these sources of infection for long. The best treatment is to develop adult respiratory distress syndrome marked by
bolster the immune system and re-establish the barrier func- worsening hypoxemia, hypercapnia, and lung compliance.
tion of the gut and skin. Suspected or proven infections Supportive treatment with supplemental oxygen, positive
warrant treatment with systemic antimicrobial medications. end-expiratory pressure, and high-frequency ventilation is
Treatment with an antibiotic usually controls the infections effective in most patients. High-dose steroids have been used
but alters the patients microbial flora. Should the patient in cases of refractory pulmonary failure but have not been
remain at risk for infections after the first infection is treated, shown to be effective. Many patients intubated for more than
a second, more drug resistant infection often occurs. Should a month benefit from a tracheostomy. The use of low-pressure
the burn be large enough that the patient remains at risk for balloons in modern endotracheal tubes has markedly
a month or longer, fungal infections become a serious threat. decreased the incidence of tracheal erosion and life-threatening
Treatment with less toxic fluconazole has greatly increased the trachea-innominate artery fistulas. Tracheostomies are still
therapeutic options, but many patients still eventually require useful so patients can be gradually and safely weaned from
amphotericin. prolonged dependence on mechanical ventilation and to
Inhalation injury and respiratory complications are still decrease injury to vocal cords.
one of the major causes of mortality in severe burns. Ventila- Long-term vascular access plays a vital role in the manage-
tory support and airway management in this situation is ment of burn patients, in which a reliable vessel to access
often challenging, and the need for prolonged endotracheal for medications (e.g., antimicrobials and analgesics), blood
intubation is very common in patients affected of different draws, fluid administration and sometimes for arterial pres-
degrees of respiratory distress syndrome. Despite the use sure monitoring is needed. Although the lines have been
of high-volume low-pressure cuffs, considerable controversy highly valued by patients and parents, they carry with them
exists among burn surgeons as to whether to convert endotra- inherent risks (Table 18.10). Most of these problems occur
cheal tubes to tracheostomy in burns patients, particularly either at the time of insertion, such as a pneumothorax, or
when ventilatory support is prolonged beyond two weeks while the line is in place, such as a line infection. Regular
or when other airway complications occur, as many studies monitoring following insertion or removal of a vascular access
have recorded high mortality and high tracheostomy line is mandatory for the early recognition and treatment of
complications. any associated complications. Peripheral lines should be used
The pathogenesis of these entities is still unclear, but the initially whenever sites are available. These lines can become
combination of the inhalation injury, infection, presence of the infected with blood-borne pathogens or from the skin punc-
endotracheal tube and individual factors play an important ture site. The diagnosis should be suspected when the patient
role in the development of this complications. Tracheostomies
may provide a good portal of entry for microorganisms into
the respiratory tract, with a high incidence of respiratory
Table 18.10 Complications of peripheral and central-line
infection and sepsis. Cross-colonization of the respiratory
insertion
tract from the wound exists, but it does not show a direct
relationship with cross-infection. In addition, feeding aspira- Early Late
tions, obstructive abnormalities, increased incidence of pneu-
monia and trachea-innominate fistulas have been reported as Hematoma Thrombophlebitis
high morbidity complications of tracheostomies. Long-term Venous laceration Infection
sequelae are no less important. Stenosis of the airway, dys-
Arterial puncture Chylothorax
phagia, alterations of speech, trachea-esophageal fistulas and
tracheomalacia can compromise the favorable outcome of this Hemothorax Horners syndrome
selected group of patients. Every effort should be made to Air embolism Pseudoaneurysm
maintain airway pressures at the lowest range, in order to
prevent tracheomalacia. Advantages of tracheostomy include Pneumothorax Arteriovenous fistula
minimizing dead space, ease of suctioning, presence of a more Pleural effusion Thrombosis
secure airway and ease of movement. Theoretically, it should
Dysrhythmias Embolism
prevent the appearance of subglottic stenosis.
develops fever, leucocytosis, or thrombocytopenia or when thermoneutral environment (~30C). During hydrotherapy, in
organisms are grown from blood cultures. Septic throm- the operating room, and in the burn unit, keep the room tem-
bophlebitis should be suspected in all burn patients with perature at ~30C to reduce heat loss and decrease metabolic
unexplained infections, and all sites of prior catheter rate.
access must be carefully inspected. Many of these patients
require central venous lines at some point in their treatment Secondary sclerosing cholangitis
because peripheral access sites are usually limited. Central
line-related infections can cause major morbidity, and con- There are increasing reports in the literature regarding second-
stant attention is given to changing catheters once a line ary sclerosing cholangitis (SSC).11 Sepsis and shock cause
infection is suspected. endothelial and bile duct injury also through translocation of
bacteria and endotoxins into the portal blood and into the bile
ducts. Following cholangitis, post-inflammatory biliary stric-
Hypertrophic scar tures may develop. Moreover, burn injuries in particular can
induce selective vasoconstriction of hepatic arterial blood
Hypertrophic scar formation after burn wound healing is a flow. This additional hepatic ischemia and critical reduction of
major problem. Hypertrophic scarring, unstable epithelium, hepatic oxygen delivery may lead to sclerosing cholangitis.
and poor skin elasticity often occur when deep wounds are Treatment options for patients with SSC are limited. Long-
allowed to heal without grafting. Deep wounds, treated con- term results of several trials in patients with sclerosing
servatively, tend to develop problems more frequently than cholangitis suggest an improvement in clinical symptoms
superficial wounds because the extended period of inflamma- and liver function tests after regular endoscopic treatment
tion elicits a fibrotic response. Early skin grafting of these (sphincterotomy, stenting, extraction of as many of the biliary
deep wounds shortens the period of healing and inflamma- casts as possible, continuous flushing of the bile ducts with
tion and avoids some of the later problems of hypertrophic saline solution through endoscopic nasobiliary drainage).
scarring. Both pressure garment and silicone therapy are asso- Ursodeoxycholic acid treatment, in combination with repeated
ciated with a reduction of hypertrophic scar formation after endoscopic interventions and opening of bile duct stenoses,
burn injury. may further improve both survival and the clinical outcome of
patients with sclerosing cholangitis. It is recommended that
Hypothermia biliary infection should be treated with antibiotics at doses
high enough that effective concentrations of the drug are
The serious side-effects of hypothermia cannot be overstated. reached in the bile. The combination of endoscopic and medical
Strategies to vigorously prevent hypothermia include a treatment may result in transient clinical and biochemical
warmed room, warmed inspired air, warming blankets, and improvements; however, the progressive destruction of the
countercurrent heat exchangers for infused fluids. Metabolic biliary tree cannot be prevented. If end-stage liver disease
responses can be minimized by treating the patient in a develops orthotopic liver transplantation is indicated.
Access the complete reference list online at http://www.expertconsult.com

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SECTION III Burns Surgery

Aims of burn care

2013, Elsevier Inc. All rights reserved.

Around 500 BCE, the Chinese were using a mixture of tea

Mechanisms of thermal injury

Burns due to hot tar are difficult to manage because of the

Hypovolemia and fluid extravasation Mediators of burn injury

Exact mechanism History of flame burns or burns in an enclosed space

Box 18.4 Indicators of possible nonaccidental burns or scalds

Delay in seeking help

sputum, or impaired mentation. A progressive change in

Accurate assessment of burn depth on admission is important C of one leg 2% 2% 2% 2% 2%

Table 18.2 Typical findings in burn injuries

Box 18.6 Burn reconstruction priorities

Urgent and important procedures

However, the burn wound is a dynamic living environment

Depth assessed (appearance, bleeding, capillary refill, sendation)

Requires surgery, preferably

Yes No Dress with tulle gras and gauze,

Low exudate? High exudate?

Might be suitable for Hypafix Contaminated or signs

Continue with tulle gras or Apply antimicrobials (such as

Fig. 18.12 Protocol for the management of burn wounds.

Fig. 18.16 Full thickness bilateral lower limb burns.

Fig. 18.17 (A,B) Burned genitalia should be catheterized in both sexes.

Table 18.3 Signs of carboxyhemoglobinemia Box 18.7 Indications for intubation

Table 18.4 Fluid resuscitation formulae

Nonantigenic Bilayer structures with biologic dermal analogue and either

Table 18.5 Temporary skin substitutes

excised burns before and dermal properties Risk of disease transfer

Product Tissue of origin Layers Category Uses Advantages Disadvantages

submucosa used for coverage of Long shelf-life, store at

Management of moderate to severe burns

Table 18.5, Temporary skin substitutescontd

Product Tissue of origin Layers Category Uses Advantages Disadvantages

Table 18.6 Permanent skin substitutes

foreign material serve as a nidus for infection much like the

Conservative versus surgical therapy

100 mL of bleeding. Debridement of a 20% TBSA burn results

Fig. 18.22 (A) Intraoperative tissue expansion

Fig. 18.23 (A) Inflation tissue expansion of the

2. The excised wound is resurfaced with a temporary

Fig. 18.26 Meshing a split thickness graft.

Fig. 18.25 Healed lower limb donor sites.

of skin grafts, although less bloody than tangential debride-

Fig. 18.30 (A,B) Application of a sheet of cultured epidermal autograft.

A B Fig. 18.33 Pedicled radial forearm flap to cover

(catabolic phase) (anabolic phase) past.

Add anabolic agent

Lose 9 kg role acute phase reactants, and are profoundly affected by

Table 18.9 Formulae for estimating calorie and protein needs

thermal injury to enhance lean body mass accretion, restore

in the pharmacological treatment of every burn patient.

Ulnar nerve Radial nerve

Common peroneal nerve

Common peroneal nerve

Posterior tibial vessels Short saphenous vein

Respiratory distress from smoke inhalation or a severe chest

Fig. 18.41 Circumferential full thickness burns require escharotomy. It is not

Fig. 18.42 Hand escharotomies.

Fig. 18.45 (A) Periocular escharotomies. (B) Temporal and periocular

include tense abdomen, decreased pulmonary compliance,

The use of drugs to prevent stress-related gastric bleeding

Fig. 18.47 Extensive escharotomies and decompressive laparotomy. Heterotopic ossification