Điều Trị Bỏng Toàn Diện (Bản Expert Consult)

Total Burn Care
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n Air and oxygen are drawn through vaporizer by
negative pressure generated by the patient’s
inspiration.
n Airflow in the vaporizer is guided by a rotary (PAC)
or sliding (TAA) valve.
n For ventilation in a controlled mode, a combination
of the Impact 754 Eagle ventilator and the PAC
system is used in the field.101
Anesthesia machines with controlled ventilation modes
for field use (mostly military) include the following:
•
Ohmeda (FAM) Model 885A
n Portable-circuit system
n Weighs 55 lb (25 kg)
n Powered by bottled O2
n Has a multiagent vaporizer with a Vernitrol
anesthetic flow calculator
n Has no modern ventilation modes
•
Draeger Narkomed M
•
Weighs 103 lbs. (47 kg)
•
Variable-bypass vaporizer
•
Limited by high oxygen consumption.
The biggest disadvantage of the drawover systems and FAM
885A is their failure to meet ASA safety standards. Therefore,
training with the devices in ordinary or military hospitals is
difficult and possible only with connection to the safety and
monitoring systems of standard anesthesia machines.
Another drawback is that single-agent temperature- and
pressure-compensated vaporizers are generally used today.
Therefore, anesthesia providers do not have experience with
Vernitrol-type vaporizers. Future systems must be widely
used in civilian hospitals and properly adapted to field use.
The main advantage will be that anesthesia personnel will
already be familiar with the features of the device, such as
displays, alarms, and service. Getting acquainted with a
device only in a disaster is useless and dangerous.
An example of this new generation of anesthesia machine,
which is now used in the US and by several European armies,
is described below:
•
Draeger Fabius Tiro M
n Electrically powered (no gas for power)
n Weighs 198 lb (90 kg), including the container
n >45 min on battery, including the monitor
n All necessary safety systems and alarms
n Many critical-care ventilation modes
n Can be connected to an oxygen generator.
Critical care transport ventilators
and ICU ventilators
During disasters a discrepancy may exist between the number
of available ICU ventilators and the number of severely
injured patients who cannot be ventilated with simple rescue
service transport ventilators. High-end critical care transport
ventilators, which are mainly used for intraclinical critical
care transport, are lightweight and easily moved to the triage
areas and frontline hospitals. They have battery capacities of
4–6 hours and can be used both independently and con­
nected to a central gas system. They can be used not only for
transport, but also as temporary substitutes for missing ICU-
ventilator capacity, if necessary.
metamizol, and NSAIDs, is helpful. In addition, because
considerable psychological stress occurs, anxiolytic drugs
such as benzodiazepines (e.g., midazolam, lorazepam) and
stomach mucosa-protecting agents should be administered.
Postoperative adverse effects, especially prolonged effects
of anesthetics and relaxants, must be anticipated. Respira­
tion, hemodynamics, urinary output, and temperature must
be closely monitored. Hypothermia and blood loss must be
prevented.
Oxygen
During disasters, O2 requirements rise rapidly. Delivering
small bottles of liquid O2 is logistically difficult owing to
constraints imposed by bottle weight, the space they occupy,
and their need to be refilled. Even hospitals’ large bulk liquid
oxygen systems may be damaged or inaccessible. In such
cases, alternatives must be implemented as soon as possible.
Portable bulk systems (1000–5000 L of liquid oxygen) or
mobile cylinder banks are helpful, but often unavailable in
disasters.
Two other options are portable and non-portable oxygen
generators, often used in military field hospitals. If electrical
power is present, oxygen generators can deliver oxygen with
>93% purity. They can be connected to patients or ventila­
tors. With a booster system to provide enough pressure,
oxygen generators can be used to refill oxygen tanks.
For work to proceed safely in the face of diminished
resources, a sufficient supply should be organized, the right
connections must exist between the systems, different
systems should be rechecked during exercises, and actual
oxygen needs should be evaluated to minimize wasted gas.100
Anesthesia machines and ventilators
Anesthesia machines and ventilators in the field must have
the following characteristics:
•
Robust
•
Lightweight
•
Operate in extreme temperatures
•
Suited to air service.
They should also meet the following criteria:
•
Need as little fuel for power as possible
•
Be ready for use quickly
•
Be easy to use
•
Require little maintenance
•
Have an extended battery capacity
•
Be able to ventilate in modern ventilation modes
•
Meet safety standards of the American Society of
Anesthesiologists (ASA) or of Directive 2007/47/EC of
the European Parliament and of the Council.
Anesthesia machines
Forward surgical teams from the US and British Armies use
drawover anesthesia systems:
•
Ohmeda Universal Portable Anesthesia Complete
(PAC) or TriService Anesthesia Apparatus (TAA; Penton
Ltd, UK)
n The main advantage is the low weight (5 lbs or
2.3 kg).

Burn management in disasters and humanitarian crises
75
authorities, foundations, and non-profit organizations. They
organize blood donations, process blood products, test the
donations, and manage distribution to hospital blood banks.
Standardization of blood products, tight regulation by
health authorities, general donor shortages, and economic
struggles have led to a higher turnover of products and an
optimization of inventories. Cost-cutting has prevailed in
nearly all developed countries, leading to the shutdown of
several blood centers and the establishment of large, central­
ized facilities housing production, testing, and IT services.
This actually increases the total processing time. In some
countries, testing and IT are centralized to one national site
or even outsourced internationally. This may pose a threat
to the healthcare system if a facility shuts down or otherwise
malfunctions.
Blood centers may collect, process, and test blood; however,
they generally distribute blood products and provide addi­
tional services (e.g., platelet apheresis) to hospital blood
banks, which are responsible for the immunohematologic
and clinical services. Disaster management and mitigation
plans may exist in well-managed regional and national
blood services but are mostly focused on anticipated threats
such as pandemics (e.g., H1N1 influenza) and on the disin­
tegration of vital core facilities (e.g., IT services, nucleic acid-
testing laboratories). Burn disasters are often absent from
these plans. Blood centers are rarely consulted by emergency
systems or hospitals, nor are they integrated into hospitals’
communication pathways and disaster plans.
What happens at blood centers
in burn disasters?
Hospital blood banks possess a certain inventory, usually no
more than the amount of blood products needed for 2–3
normal days, including additional units for major trauma.
Burn disasters immediately deplete the available stocks
and lead to urgent requests to the local blood center. Triaging
mass casualties, especially in burn disasters, results in the
dissemination of patients to different trauma centers, so that
multiple hospital blood banks are involved. High-volume
and high-priority requests concentrate in a spiraling sequence
on one blood center, which is greatly strained to coordinate
the distribution to its hospital blood banks.
Supplies are usually sufficient to meet the urgent first
requests, but many blood centers hold only enough blood
products to meet the regular demand of 1 week or less. Burn
disasters are characterized by the urgent need for platelet
products and erythrocyte concentrates in the early phase.
A blood center’s stocks may be depleted within hours –
platelets first, and then erythrocyte concentrates. Plasma
products are sufficiently available, even in bigger disasters.
Because it takes at least 24 hours and as long as 3 days
after a donation to produce blood products, a quick start to
regain the required amount of blood products may go awry
in an already strained blood center. Deliveries from other
blood centers and national coordination may be a big help
in mitigating the center’s own insufficiency.
More often, a blood center acts without information about
the disaster and the estimated need for blood products.
Communication between emergency services and blood
centers is rare, and hospitals have no coordinated system to
inform the blood center.
•
Transport ventilators, such as the Uni-Vent Impact 754
Eagle, Draeger Oxylog 3000, and Weinmann Medumat
Transport System
n Weigh 10–13 lb (4.5–6 kg)
n Adequate monitoring of respiratory digital data and
curves
n Adequate safety systems and alarms
n Easily connected with transport units, such as LSTAT
and Mobi Doc system
n Offer most of the new ventilation modes.
Providing this extended level of anesthesia and ventilator
care requires high-level logistics and organization. In devel­
oped countries this should eventually be achievable in most
disasters. It will be much harder in countries where resources
and infrastructure are insufficient even without a disaster. In
this case, only rapid, structured outside help through federal,
military, or international rescue organizations can mitigate
the crisis.
Blood transfusion
Transfusion’s role in burn disasters
Adequate blood products are important for primary and
sustained life support. Few publications have described the
responsiveness and efficacy of transfusion services in catas­
trophes and disasters. Blood supply has been mentioned as
being scarce in the first and prolonged phases of disaster
mitigation.16 However, the 9/11 terror experience showed
that an uncoordinated surge in blood donation may gener­
ate an unusual drop in patient supply several weeks later.102
Managing blood in disasters and catastrophes is tricky,
and may be complicated by public pressure and poor
communication.103
Transfusion in burns
Blood loss may occur in combined injuries, but also in
severe burn injuries involving large TBSAs. Full-thickness
burns may cause blood loss that is correlated with TBSA.104,105
A TBSA >10% acutely lowers erythrocytes because of thermic
hemolysis and microthrombosis.106 Concomitant CO poi­
soning may further reduce the remaining oxygen transport
capacity of erythrocytes. The loss of red cell volume and
oxygen transport capacity cannot be estimated correctly in
these circumstances (CO intoxication, thermic hemolysis,
and microthrombosis), and fluid resuscitation can obscure
the available red cell mass. Sufficient oxygen delivery to
peripheral tissue is important for hypermetabolic patients
who may need surgery (e.g., escharotomies) and repeated
dressings.107–110 Platelets may be required in the acute phase
and subsequent treatment. Correct transfusions of leukocyte-
reduced blood products are a prerequisite in managing
transfusions in burns.106
Organization of blood transfusion services
Modern transfusion medicine has silently changed its organ­
izational background in recent years without being noticed
by the public and other medical personnel. Blood centers
serve specific areas and are run by the Red Cross, national

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victims is unclear, as is the number of beds available in burn
centers. Although a surge capacity is defined, it still allows
a burn center to distribute patients to other burn centers.
However, a challenge remains: can the distributing center
prepare patients in time?
Such situations call for resource-rich jurisdictions, with
many burn centers, many burn beds, and many staff. The
actual availability of burn beds varies between states. One
can usually assume that burn beds are in short supply and
high demand. Whatever the advantages of this approach to
safety and sufficient primary care and stabilization, they are
lost when the number of victims is so high that quality
standards cannot be maintained. Burn centers must first treat
many patients with less severe burns, thereby tying up staff
who are needed for the severely burned. In special cases,
combination injuries (e.g., mechanical injuries) are to be
expected and may necessitate transfer to a trauma unit. BATs
and BSTs can back up local teams to improve capacities. If
the influx greatly exceeds surge capacity, the ability to triage
and stabilize patients according to ABLS criteria will depend
on the recruitable staff. Even in the US, many burn centers
have fewer than 15 beds112 and even fewer ICU beds. Not
even the full staff of small centers can treat 30 or 40 severely
burned patients, perform secondary triage according to ABA
policy, and prepare them for transport in time.
Until this triage occurs, the patients must be kept in a suit­
able environment. The feasibility of this policy in smaller
burn centers has yet to be demonstrated. Surge capacity is
important because it is a number that must be considered
in planning. The ABA definition – 50% more than the usual
capacity – gives each center a planning dimension, which
must be funded before it can be realized.
Transferring patients elsewhere can be reasonable even for
burn centers, because surge capacity cannot be maintained
for long. Medical vanity should never be a reason to avoid
transferring patients elsewhere. Burn centers are usually not
empty, and their size is adapted to normal needs. Transfer­
ring patients whose treatment has already begun from a burn
center to a hospital’s non-burn units gives the impression
that no burn center was needed, or provokes fears that
the ensuing treatment in other units will be insufficient.
Workload above the normal capacity causes complications,
including hygienic problems within the unit, endangering
patients and increasing costs.29
Primary treatment in trauma centers
without burn units
Trauma centers will always be part of disaster responses, and
as victims go to the nearest hospitals by themselves these
trauma centers will be part of the response. Trauma centers,
being much more numerous than burn centers, can more
easily cope with primary treatment for an unknown number
of casualties.113
Although primary care for burns is part of ATLS procedure,
many emergency doctors, trauma surgeons, and other
medical personnel throughout the world do not seem to be
experienced in the primary treatment of burns. This is true
even in military organizations.32 Therefore, trauma centers
without burn units need support from experts and seem to
be the place where BSTs and BATs can be most effective.
More serious is the effect of mass media on blood dona­
tion. Blood donation is very well known among the media
and the public, and blood services often use the media to
boost donations. The media focus early attention on blood
centers and provoke the public’s urgent desire to help. Blood
donation is the commonest way to ease tension if the public
feels powerless about the disaster’s cause and/or effect. This
is most pronounced after acts of terror, when blood centers
are confronted with a mass of potential donors and some­
times do not need that much blood. They may be quickly
overwhelmed when faced with such a surge of potential
donors.
Strategies
During mass casualties, strategies in early burn treatment
differ mainly in the degree of treatment before admission to
a burn center and in the initial goal of transport. Strategies
can differ by country, depending on the resources available.
Medical outposts as extended treatment areas
Usually, the first place to assemble burn victims is an in-field
collection or treatment point. Keeping burn victims at this
site until the definitive place of treatment is known is impos­
sible, because the number and severity of injuries will not
be known during the first hours and resources will be insuf­
ficient. Longer stay in advanced medical outposts or collec­
tion points is also linked to greater hypothermia.
BSTs and BATs at the scene
In some mass casualty plans, triage and primary care in the
field are supported by BATs or BSTs.111 Reports of different
events show6 that triage in the field usually starts late and that
many victims arrive at hospitals long before actions at the
incident site have become structured. Therefore, BAT teams
must be on standby for deployment within minutes, and
information about the incident must be instant and exact.
Even when deployed very early, BATs usually are too late, at
least for those victims who have already been transported.
Burn center criteria for mass casualties
Individual medicine criteria for admitting patients to burn
centers are rather extensive. The German-Speaking Associa­
tion for Burn Treatment and the European Burns Association
have guidelines stating that burns in functionally and/or
aesthetically important areas should be treated in burn
centers regardless of degree and extent. According to ABA, all
third-degree burns should be treated in burn centers. Com­
pliance with these guidelines is not possible during mass
casualties and disasters. The available burn beds must be
filled by victims who will get the maximum advantage from
burn center treatment.
Primary transfer to burn centers
Patients should be transported to the best place for the best
treatment available. These are normally burn centers.
However, at the time of a mass casualty the number of

Burn management in disasters and humanitarian crises
77
infections, stays in ICUs and burn centers are prolonged,
mortality rises, and costs increase. When patients from coun­
tries with multiresistant bacteria are taken to a burn center,
this can be the beginning of a long-lived fight against such
infections.117 Although the increased number of nurses and
other medical specialists can usually be sustained over a
longer period by adding new resources, this cannot be done
with burn specialists. Their number is limited, and no center
has too many. Therefore, after some weeks, burnout is to
expected in those working additional shifts without respite.29
Distributing burn victims among more centers to avoid
danger both to patients and staff would be more effective.
This distribution can take place only when clear regulations
exist for compensating costs, regulations regarding the
uninsured, and a humanitarian understanding of this
procedure.
Burn bed availability (Fig. 5.5)
The US has 1825 burn beds. A national electronic registry of
availability is in development. In Europe, burn beds, espe­
cially in small countries, are very few, so that international
cooperation is necessary. Few data exist on the real avail­
ability of burn beds in the case of a disaster. Germany
has the highest ratio of burn beds to population. In the
Enschede fireworks explosion, Germany could offer 19 burn
ICU beds, out of 127 for adults and 15 for children.118
National burn bed bureaus exist in Germany and the UK,
and there are networking facilities for cooperation (e.g., the
Mediterranean Burns Club).
The European Union has a ‘Community Mechanism for
Civil Protection,’ which regulates disaster support among
states both in and outside the Union. This covers sending
disaster relief staff to countries with disasters, but does not
address transferring victims to other countries. There are
exchange treaties between some countries, and there is actual
cross-border hospitals cooperation. However, there is no
general regulation of these processes.
BSTs and BATs act as experts and can provide support to
other surgeons. Because they are not busy with details, but
with directing treatment for many others, they can use
the trauma center’s surgical and staff resources to improve
results. They can also help determine the extent and severity
of burns for central data collection, and for distribution to
burn centers or other hospitals as well as guarantee adequate
primary care.
Referring the most severely burned patients
to burn centers first
Referring only the most severely burned patients to burn
centers first is of little use, as demonstrated in the case of
Pope Army Air Field, where many futile patients diverted the
center’s resources. Burn beds are scarce and must be reserved
for victims with the best chance of survival. ABA has pub­
lished a benefit–resource ratio table to optimize triage to
burn centers. To enable the optimum distribution of patients
to burn centers, one must know the number and qualities
of beds available, as well as the number and severity of
patients needing burn beds. Because this number is not
known in the first hours of an incident, the distribution to
burn centers cannot properly be planned during this time.
Primary distribution to local primary
responder hospitals
BATs or BSTs provide support to primary responder hospi­
tals, guiding resuscitation and primary care as well as deliver­
ing data for centrally directed casualty distribution, after
considering the number of burn beds available nationally
and internationally. Transport to the definitive place of care
is organized from the primary responder hospitals. BATs or BSTs
are necessary for this strategy to work well. Telemedicine
might help in this process.114–116
Tiered response
A tiered response is crucial for an effective response during
a burn disaster. In ABA plans, this is a national response
directed by intrastate and interstate cooperation of burn
centers with military assistance under Department of Home­
land Security governance. In other countries, especially in
Europe, where there are many small countries without the
resources, the tiered response can necessitate international
cooperation. This strategy requires advance preparation so
that certain basic information is clear. Problems will arise
without international agreements for such cooperation,
without knowledge of international burn bed availability,
and in funding treatment in another country without
knowledge of patients’ insurance status.
Allocating and distributing more burn patients
This strategy is important to avoid overwhelming single burn
units and treating patients in relatively understaffed units.
High-capacity utilization in burn units increases difficulties
through intensive resource use.
Cross-infections can be expected to increase, and
patients’ safety will easily be negatively affected. With these
Figure 5.5  Investigation of free burn beds in neighbouring states following
the Enschede fireworks explosion, in which at least one individual was
severely burned. Courtesy of OOEN/Archiv.

Total Burn Care
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certain treatment methods may arise because of religion (e.g.,
use of pig skin or frog skin). Knowledge of and adaptation to
local cultural habits is often necessary for success.
Armed conflict
Armed conflict falls into two main categories:
•
Conflicts between militaries
•
Asymmetric conflict, in which a severe disparity of
power and strategies exists between opponents (e.g., an
army against terrorists).
The rate of burn injuries in armed conflicts depends on
the technical standard of the armies. The number of burn-
related deaths has remained fairly constant since World War
I until the 1991 Gulf War. The use of tanks, battleships, air­
craft, and armored vehicles increases burn casualties. In the
1973 Arab–Israeli War, which involved many tanks, 70% of
tank casualties included burns. Burn injuries range from 10%
to 30% of all casualties.89 Combination injuries (e.g., blast
injuries with burns) are frequent.
Treatment in the field
Field treatment occurs under different conditions, so that
evacuation times vary greatly. Early shock treatment is the
most important parameter for survival. A patient with
massive burn injuries who does not undergo resuscitation
until more than 4 hours after injury has almost no chance
of survival. The necessity of starting sufficient resuscitation
is countered by the logistical problem of carrying great
amounts of fluids during battle.
Care under fire is usually buddy aid or given by a combat
lifesaver. Burning must be stopped, and resuscitation must
begin. In the conscious patient, oral rehydration fluid can be
self-administered or given by the buddy or combat lifesaver.
The unconscious patient should be moved to a safe location
as soon as the tactical situation permits.
In the second step, tactical field care, IV access is gained and
resuscitation with RL is begun. Otherwise, hypertonic resus­
citation and/or oral fluids should be considered. The initial
fluid requirement can be reduced by 80% by an initial
30-minute infusion of 4 mL/kg hypertonic 7.5% saline–
dextran and then of RL to maintain urine output. A rebound
should be expected after 6–8 hours.86 Too rapid an infusion
for 2 minutes causes hyperosmolarity and hypernatremia,
with possible cardiac arrhythmia.126
Thomas89 suggests starting resuscitation with IV admini­
stration of 250 mL hypertonic saline solution and continu­
ing with ORS as an oral bolus of 4 mL/kg every 20 minutes
to maintain a good gastric emptying rate and to satisfy fluid
requirements. ABA suggests the same where IV therapy is
logistically impossible.47
New technical equipment allows easy IO application,
which can provide large amounts of fluid. For hypertonic
saline solutions IO seems unsuitable, as soft tissue and bone
necrosis have been observed after some days.127
Education, awareness, and preparedness
Recent burn disasters have raised the degree of alertness
worldwide for mass burn injuries. Ongoing wars and
Burn bed registries are necessary for quickly ascertaining
how many patients can be treated in an area. These registries
should include the different burn bed types, whether they
are intensive care beds with or without the ability to warm
patients, and whether there are non-ICU beds. Asking each
individual center how many beds are free for use during
an incident is too time-consuming: an online system is
preferable.
Humanitarian crisis
A humanitarian crisis is an event or series of events causing
critical threats to health, safety, or human wellbeing, usually
over a wide area. For burn injuries, armed conflicts and
natural disasters are the likeliest forms. Natural disasters
can not only be directly linked to fire (as in wildfires), but
can also cause burn injuries through atypical use of energy.
For example, burn incidence rises when people are not accus­
tomed to open fire but need it because their electricity source
has failed. The same happens when people try to obtain
electricity by throwing wires over power lines. After a severe
storm, the increased use of emergency internal combustion
generators and internal combustion power saws increases
burn injuries and burns related to fire accelerants.119
In disasters and humanitarian crises, burn and other
medical treatment can often begin only after minimal infra­
structure and order have been established. Medical work can
be dangerous where there is looting or political or religious
rivalry.120 Therefore, cooperation with security forces, at least
in the early stages, can be necessary.121 Minimum require­
ments for work are shelter, safe water, food, and electricity.122
One of the basic problems in medical aid work during dis­
asters and in low-resource countries is sterility. That is, there
is usually a high rate of infections with hepatitis and HIV,
which must not be spread.123
Burns can be categorized into the following three main
types:
•
Those that can be treated with minimal efforts
(e.g., by clean dressings and available analgesics).
•
Those that are not survivable without specialized
care. Special care must be established, and success will
depend on the degree of medical care given.
•
Those that cannot be treated successfully in this
environment. Patients must be transported to facilities
where successful treatment can be performed and is
funded. Otherwise, these patients are deemed futile,
and ‘comfort care’ must be provided.
Preparing medical systems for burn treatment can be aided
by history, which provides an overview of prognosis com­
bined with special measures. At the end of World War II, only
50% of patients survived >40% TBSA.124 After treatment
for shock was initiated, topical antibacterial treatment with
silver-containing products reduced the mortality rate. Early
excision and feeding lowered it further. Early tangential exci­
sion, introduced by Janžekovič, was the next step in reducing
mortality.125 Thus, success depends on the degree of logistics
and the infrastructure that can be built up to allow the use of
special techniques. The feasibility of safe blood support and
wound technologies (e.g., use of cadaver skin as a temporary
skin substitute) also influences the prognosis. Problems with

Burn management in disasters and humanitarian crises
79
burn disasters, and surgeons are not the only personnel to
be trained. Escharotomy must be taught, training must
occur, and this training must be repeated if preparedness is
to be maintained.
Acknowledgments
The authors wish to thank Mr Forrest Adam Sumner for
working tirelessly to put this article into clear, understand­
able English, and Ms Christina Haller, who assisted him in
making the authors’ meaning intelligible. We would also like
to thank the Austrian Red Cross for their support.
Further reading
Disaster management and the ABA Plan. J Burn Care Rehabil. 2005
Mar;26(2):102-106.
Jordan MH, Mozingo DW, Gibran NS, et al. Plenary Session II:
American Burn Association Disaster Readiness Plan. J Burn Care
Rehabil. 2005 Mar;26(2):183-191.
Potin M, Senechaud C, Carsin H, et al. Mass casualty incidents with
multiple burn victims: rationale for a Swiss burn plan. Burns. 2010
Sep;36(6):741-750.
Saffle JI. The phenomenon of ‘fluid creep’ in acute burn resuscitation.
J Burn Care Res. 2007 May;28(3):382-395.
Swedish Emergency Management Agency. Crisis Communication
Handbook. 2008.
Thomas SJ, Kramer GC, Herndon DN. Burns: military options and
tactical solutions. J Trauma. 2003 May;54(5 Suppl):S207-S218.
terrorist attacks, along with several indoor fires, have shown
that preparedness for such events is necessary. No-one is
immune to such risks. The question is not whether such
disasters will occur, but when they will occur and how we
can cope.
Preparedness requires plans. It also requires staff,
stuff, and structure (the three ‘S’s). Plans include interna­
tional disaster plans, national disaster plans, coordinated
disaster plans at state level, and local disaster plans for
locales and institutions. Structure is the national or inter­
national health system. Stuff is emergency supplies ready
for disasters. Staff is medical, paramedical, rescue, and
technical relief organizations. Legal preconditions must be
established on the basis of these plans, and resources must
be planned and funded. Both planning and execution
require money, which is an investment in a society’s future
and security.
Burn societies can aid this procedure, as ABA does, as they
comprise experts in these fields. Planning without the experts
in burn treatment is futile. However, on their own, burn
experts rarely make sufficient plans for mass casualties,
which is not usually part of their expertise. Military organiza­
tions can serve as examples, with their participation in
war operations and their routine drills. Disaster drills for
hospitals and rescue organizations must be realistically
performed.
Education in burn treatment (e.g., ABLS, EMSB) is essen­
tial for coping effectively with mass casualties – not only for
medical staff but also for hospital administrations, who
must provide sufficient support. Burn surgeons are rare in
 
Access the complete reference list online at

Burn management in disasters and humanitarian crises
79.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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Care of outpatient burns
C. Edward Hartford
Introduction
During the past four decades there has been a remarkable
improvement in the outcome of burn injuries and a progres­
sive decline in its incidence. In the United States, this process
began with the development of specialized burn treatment
units, the first at the Medical College of Virginia, now the
Virginia Commonwealth University Medical Center, and
then at the US Army Institute of Surgical Research, Brooke
Army Medical Center, San Antonio, Texas, both in 1947.
There are now 125 units/centers in the USA.1 The improve­
ment in outcome in the treatment of burn patients acce­
lerated following the formation of the American Burn
Association in 1967. According to the American Burn Asso­
ciation’s 2007 Fact Sheet, using information derived from a
variety of sources, each year, in the USA, there are now
approximately 500 000 individuals who sustain a burn
injury requiring treatment from healthcare professionals.2
The annual incidence of burn victims has declined from an
estimated 1 million each year during the 1960s. Fagenholz
and colleagues documented a decrease in the incidence of
visits to Emergency Departments for burns during the period
1993–2007.3 Currently, among those who sustain a burn,
approximately 40 000 are admitted to hospitals for their care
and there are approximately 4000 fire- and burn-related
deaths each year.2 Therefore, thermal trauma typically results
in an injury of low mortality in which the majority of care
can be safely rendered in an ambulatory setting.
The outcome of burns treated in the outpatient setting is
usually good. If, however, care is suboptimal, protracted
morbidity or compromised function can result. The goals of
therapy are to minimize pain and the risk of infection,
achieve timely wound healing, preserve physical function,
minimize cosmetic deformity, and affect physical and psy­
chosocial rehabilitation in the most expeditious manner.
Who can be managed as an outpatient?
When a patient with a burn is first evaluated, information is
immediately available from which an accurate prognosis can
be derived. For instance, a valuable easily remembered esti­
mate of the probability of death from burn injury was pub­
lished in 1998.4 Using stepwise logistic regression analysis
of 1665 patients, the authors identified three risk factors for
death: age greater than 60 years; burns on more than 40%
of the total body surface area (TBSA); and, the presence of
inhalation injury. The mortality prediction for the presence
of none of these risk factors is 0.3%; for the presence of one
risk factor it is 3%; for two it is 33%; and, for all three it is
approximately 90% (actual, 87%).
In addition to these risk factors, there are other factors –
and a huge dose of common sense – which help determine
the initial treatment venue. These include depth of the burn;
premorbid diseases; and, co-morbid factors such as associ­
ated trauma, distribution of the burn, and injuring agent.
When outpatient care is an option the patient’s social
situation needs to be assessed. In some instances, it may
be prudent to initiate care in a hospital so that potential
complicating medical problems can be sorted out or the
possibility of non-accidental trauma can be excluded.
Age
Patients between 5 and 20 years of age have the most favo­
rable survival outcome from burns. The LA50 (percentage of
total body surface area at which 50% of the patients live and
50% die) for this age cohort is 94.5% TBSA of burn.5 Younger
individuals, especially infants, have an increase in morbidity
as well as mortality from burn injury. In this age group, child
abuse or neglect must be included in the psychosocial analy­
sis.6,7 The peak incidence of non-accidental burn injury is
13–24 months of age.8 Burns that are particularly suspicious
are those whose appearance suggests an injury from a ciga­
rette, hot iron, or immersion in hot water. The latter injury
is identified by a stocking/glove distribution of the burn
and a sharp linear demarcation between the burned and
unburned skin (Fig. 6.1). Scalding which has occurred in an
institution or in the presence of a caregiver other than one
who has a biological relationship to the victim should also
heighten one’s suspicion. Even with trivial injury, if the burn
was sustained under suspicious circumstances or the history
does not correspond with the nature or distribution of the
burn, the patient should be admitted to a hospital for their
protection. Cases of suspected abuse, neglect or bad parent­
ing must be referred to the appropriate social services agency.
The author has become aware that in some instances being
investigated for non-accidental trauma, the actual cause was
from bad parenting and not done with malicious intent.
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00006-0
CHAPTER 6 
Access the complete reference list online at

Total Burn Care
6
82
Browder (Table 6.1).10 A helpful adjunct in estimating the
area of burn is to use the surface area of the patient’s hand.
This area, which approximates 1% of the TBSA, includes the
palm together with the fingers and thumb extended and
adducted.
Any burned patient who requires intravenous fluid resus­
citation should be admitted to a hospital. This includes
adults and older children with burns in excess of 15% of the
body surface area, as well as younger children (under 5 years
of age) and infants with burns in excess of 10% of the body
surface area.11 In some instances, due to premorbid dehydra­
tion caused by physical activity, an arid or semi-arid climate,
alcohol, or diuretics, some patients with smaller burns may
need supplemental intravenous fluids for optimal care. In
the author’s practice, patients with small area burns that
need intravenous fluid are often held for several hours or
overnight in an observation area in the Emergency Depart­
ment until their pain is controlled and fluid needs are met.
Then care can often be continued as an outpatient.
Depth of the burn
The deeper the burn the worse is the prognosis. However,
depth of small-area burns is less important in determining
the need to initiate care in a hospital than the extent of
the burn.
When a burn is first evaluated it is often difficult to deter­
mine its depth. The superficial injury of sunburn or its equiv­
alent is easy to identify. Likewise, it is easy to discern a
waxen, dry, inelastic, insensate, cadaveric-appearing wound
as a full-thickness burn. However, it is difficult to distinguish
the subtle differences between a superficial partial-thickness
burn, which will heal spontaneously within 3 weeks, and a
deeper partial-thickness burn that will take longer to heal.
This is especially true for weeping wounds in which the
blisters have ruptured. Initially, these wounds appear super­
ficial and are perfused. However, with time, as the injured
small blood vessels in the wound thrombose, the wound
takes on an ischemic, cadaveric appearance of a deeper
injury.12,13 This change does not reflect invasive infection but
merely the natural evolution of the wound.
Premorbid diseases
Preexisting medical conditions often have a profound influ­
ence on the clinical course and outcome of a burn injury.
While any medical disorder may have an adverse effect, there
are a number of conditions that occur frequently among the
burned and which may play a significant role in causation or
outcome. For instance, any condition or habit that alters an
individual’s mental state may lead to a burn injury. These
include seizure disorders, senility, and psychiatric illnesses
as well as the use of sedatives, controlled substances, illegal
and recreational drugs, and alcohol. These usually obligate
hospital admission. Medical conditions that are known
to enhance morbidity of patients with burns include renal
failure, congestive heart failure, cardiac dysrhythmias, hyper­
tension, chronic obstructive pulmonary disease, diabetes
mellitus, sequelae of alcoholism, morbid obesity, conditions
which require the use of steroids, and other diseases which
compromise the immune system.14 The clinical status of any
of these disorders must be determined and their potential
However, when investigated, for a variety of reasons, e.g.
immigration status, prior felony conviction, previous report
to or concern of the local county authorities, the individual
lied about the details of how the injury occurred. In a more
unusual instance, a third person tries to protect the perpetra­
tor, e.g. a mother protecting her daughter, when the daughter
was the perpetrator of the injury to a child. Any patient over
the age of 70 years with burns is in danger of dying regardless
of the extent of the burn. The LA50 for this age group is 29.5%
TBSA of burn.5 Therefore, admitting the older patient to a
hospital to assess their response to the injury can prove
invaluable before treatment is continued as an outpatient.
Extent of the burn
The larger the percent of body surface area involved by the
burn, the worse the prognosis. The percent of the body
surface area can be roughly estimated by using the ‘rule of
nines’9 or more accurately by the technique of Lund and
Figure 6.1  (a,b) Two cases of non-accidental trauma with immersion
pattern scald burns. Note the sharp transverse linear demarcation between
the burned and unburned skin.
A
B

Care of outpatient burns
83
Distribution of the burn
The location of the burn may have a profound effect on the
patient’s activities of daily living, and dictate the setting in
which the patient receives care. For instance, the edema
from a small-area superficial burn of the face may result in
swelling of the eyelids, hampering the patient’s vision
(Fig. 6.2), or burns that involve the lips or the oral cavity
may inhibit efficient oral alimentation. Likewise, burns of
the hands, feet, or those involving the perineum or adjacent
areas may severely limit an individual’s autonomy. While
burns in these areas may not necessarily demand care in
a hospital, there must be consideration of the assistance
available to the patient when contemplating outpatient
ambulatory care.
Because of fluid flux into the tissues beneath a burn,
patients with circumferential burns of an extremity are in
danger of ischemia of underlying and distal tissues from
increased tissue pressure.18 Except for those with very super­
ficial burns all patients with circumferential burns of an
extremity should be monitored for evidence of elevated
tissue pressure. Since the clinical signs of compartment syn­
drome and ischemia in a burned extremity are unreliable,19
the author advocates measuring the tissue pressure by a
direct method and uses the Stryker® Intracompartment Pres­
sure Monitoring System. A tissue pressure above 40 mmHg
Table 6.1  Burn estimate – age versus area
Area
Birth–1 year
1–4 years
5–9 years
10–14 years
15 years
Adult
2°
3°
TBSA%
Head
19
17
13
11
9
7
Neck
2
2
2
2
2
2
Ant. trunk
13
13
13
13
13
13
Post. trunk
13
13
13
13
13
13
R. buttock
2.5
2.5
2.5
2.5
2.5
2.5
L. buttock
2.5
2.5
2.5
2.5
2.5
2.5
Genitalia
1
1
1
1
1
1
R. U. arm
4
4
4
4
4
4
L. U. arm
4
4
4
4
4
4
R. L. arm
3
3
3
3
3
3
L. L. arm
3
3
3
3
3
3
R. hand
2.5
2.5
2.5
2.5
2.5
2.5
L. hand
2.5
2.5
2.5
2.5
2.5
2.5
R. thigh
5.5
6.5
8
8.5
9
9.5
L. thigh
5.5
6.5
8
8.5
9
9.5
R. leg
5
5
5.5
6
6.5
7
L. leg
5
5
5.5
6
6.5
7
R. foot
3.5
3.5
3.5
3.5
3.5
3.5
L. foot
3.5
3.5
3.5
3.5
3.5
3.5
Total
Reproduced with permission from Surg Gynecol Obstet10 (now J Am Coll Surg).
influence on the outcome assessed before determining
whether the patient can be safely managed as an outpatient.
Co-morbid disorders
Respiratory complications
Inhalation injury and carbon monoxide poisoning substan­
tially magnify the burned patient’s risk and may occur even
with no or trivial cutaneous injury.15,16 In addition, upper
airway obstruction can be caused by the edema produced
from burns of the oropharynx or the flux of fluid into the
soft tissues of the upper airway resulting from deep burns of
the face and/or neck. The full-blown adverse sequelae of
these complications may not be immediately apparent.17
Therefore, if the history of the accident or distribution of
burns suggests any of these three complications, a period of
monitored observation is warranted. Overnight observation
is usually sufficient.
Associated trauma
Burns frequently occur with other forms of trauma. If the
burn involves only a small area of the body, the associated
trauma will dictate whether a patient needs to be admitted
to a hospital.

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84
Chemicals
Although chemicals cause tissue damage by chemical reac­
tions and not from heat, by tradition, the care of those
injured by chemicals is by burn surgeons. Brushing off dry
chemicals or copious lavage with water of wet chemicals is
the appropriate emergency treatment.23,24 No one knows
how long lavage should be continued, but up to 1 h has
been recommended.25 One guide is the presence of pain. The
supposition is that, as long as there is pain, the chemical
remains active and continues to cause damage.
In some instances, there are specific antidotes for the pain
caused by a chemical. For example, with hydrofluoric acid,
the injured tissues should be injected with calcium gluco­
nate.26 Hydrofluoric acid also serves as a good example of
the many chemicals that are absorbed into the body with
the potential to cause organ injury. Exposure of concentrated
hydrofluoric acid to as little as 3% of the body surface area
can result in a fatal dysrhythmia from hypocalcemia caused
by the binding of calcium by the absorbed fluoride ion.27
Since it is impossible to remember the systemic sequelae of
all the chemicals to which an individual might be exposed,
the physician should identify the chemical and seek infor­
mation from the local poison control center.
After emergency local wound care, the treatment of the
residual wound from a chemical is the same as the treatment
for any wound.
Social circumstances
Patients whose injuries may be non-accidental need to be
admitted to a hospital for their protection.
Before a patient is discharged from emergency care, the
physician should ascertain that there are satisfactory resources
available for supervision and care, and a way in which the
patient can readily access medical care. Therefore, the dis­
tance the patient lives from care needs to be taken into
consideration. For outpatients a visiting nurse can be invalu­
able in providing wound care and monitoring for wound
complications, as well as assessing the patient’s physical
progress and social situation.
Treatment
Cooling the burn
The first objective in burn wound care is to dissipate the
heat. As long as the temperature in the tissues is above 44°C
injury continues.28 The first step is to remove the source of
heat. Both clinical and experimental evidence indicate a ben­
eficial effect from immediate active cooling of the wound to
dissipate heat.29 Cool tap water or saline at about 8°C
(46.4°F) applied in any practical manner (e.g. compress,
lavage, or immersion) is as effective as any other product or
method.30–32 Colder substances, such as ice, may be detri­
mental.33 The period of time that is required for active
cooling is brief.34 Typically, by the time most patients present
for care, the tissues have cooled spontaneously.
Active cooling also has several potential advantages beyond
dissipation of heat. First, cooling stabilizes skin mast cells,
decreasing histamine release and, thereby, decreasing edema
of the wound. Second, in the first several hours after the
is the indication for surgical decompression of the injured
limb. Alternatively, a Doppler ultrasonic flow meter can be
used to assess the circulatory status of the extremity.19 A
muffled first arterial sound and/or the absence of the second
arterial sound is regarded as sufficient evidence of pathologi­
cal elevation of the tissue pressure.
Burns across joints do not, for that reason alone, require
admission to a hospital.
Injuring agent
Electricity
Patients exposed to low-voltage electricity, arbitrarily defined
as less than 1000 volts (the most frequent source being
household currents of 110 or 220 volts), are in danger of
dying at the accident scene from a cardiac dysrhythmia,
usually ventricular fibrillation.20 Following low-voltage
electrical exposure, the most frequent residual electrocardio­
graphic abnormality is a non-specific change in the ST-T
wave segment21 and the most troublesome dysrhythmias are
among the atrial fibrillation-flutter group.22 If the electrocar­
diogram is normal or becomes normal during observation,
the chances of a subsequent dysrhythmia or cardiac arrest
are virtually nil.
The tissue damage from low levels of electrical energy is
usually small and most patients do not need to be admitted
to a hospital. Occasionally, however, the damage to a child’s
lip, tongue, gums, and dentition from sucking on a defective
energized electrical cord may preclude efficient oral alimen­
tation. In this circumstance, hospital admission to establish
satisfactory oral intake is probably wise. With an electrical
burn of the lip, the injury is often deep enough to cause
necrosis of the superior or inferior labial artery. The injured
artery is prone to rupture between the fourth and seventh
post-burn day. Therefore, the patient or caregiver must be
warned of this possibility and instructed on the first aid
measures for hemorrhage control.
Patients who sustain tissue damage from contact with
high-voltage electricity generally require admission.
Figure 6.2  Swelling caused by a burn that healed spontaneously without
scar. For several days the edema of the eyelids prevented the patient from
seeing.

Care of outpatient burns
85
Those who advocate removal of blistered skin cite
laboratory studies that show that the blister fluid exhibits
several potentially detrimental effects.43 Immune function is
depressed by impairment of polymorphonuclear leukocytes
and lymphocytes. Blister fluid adversely affects neutrophil
chemotaxis, opsonization, and intracellular killing. Inflam­
mation is enhanced by the presence of metabolites of ara­
chidonic acid in the blister fluid. A plasmin inhibitor in the
blister fluid decreases vascular patency. Finally, blister fluid
may provide a medium for the growth of bacteria. Based on
these considerations, the case can be made that blistered skin
should be removed to facilitate healing.
Conversely, this author recommends leaving burn blisters
intact. Blisters form in the stratum spinosum layer of the
epidermis. An intact blister usually indicates a superficial
partial-thickness wound, which will heal spontaneously
within 3 weeks. If, under these circumstances, the blistered
skin is removed, the wound is converted from an absolutely
painless one to a painful open wound exposed to coloniza­
tion by bacteria and potential infection.42 An infection in a
burn wound covered by an intact blister rarely, if ever, occurs.
Therefore, this author prefers to leave blisters intact, and
recommends that they be dressed for protection and not
necessarily covered with medication.
If the blister remains intact and the wound is a superficial
partial-thickness burn, spontaneous resorption of the fluid
will usually begin in less than 1 week. The blistered skin will
gradually wrinkle and collapse onto the healing wound
surface. If the blister has ruptured, often the devitalized skin
can be used as a protective dressing for the wound. Whether
the blistered skin has remained intact or it has been used as
a protective cover, at about the 10th day post-burn, the
author inspects the underlying wound to determine its
potential for healing spontaneously within the next 10 days.
If it is unlikely that the wound will heal spontaneously
within that time, surgical intervention to facilitate wound
closure is undertaken.
Persistence of the blister, with no signs of spontaneous
resorption of the fluid after 7–10 days, usually signifies that
the underlying wound is either a deep partial-thickness or
full-thickness wound.
There is often concern about large blisters in locations that
limit range of motion or interfere with an efficient dressing.
This concern most often occurs with a heat contact burn on
the palm of the hand, a common injury among toddlers.
Since contraction is a property of healing of all wounds, this
author prefers to decompress these blisters, leaving the blis­
tered skin to protectively cover the wound. Then the palm,
the thumb, and fingers can be dressed to be maintained in
full extension with gentle pressure on the web spaces and
the digits in moderate abduction until the danger of contrac­
tion is past. This is accomplished by several dressing methods.
The hand can be immobilized in full palmar extension using
an occlusive dressing consisting of triple antibiotic ointment
on Adaptic® and padded with dressing sponges, including in
the web spaces to maintain moderate abduction of the digits,
and incorporating these dressings in a wrap of Coban®. A
more secure technique is to use semi-rigid casting tape,
referred to as ‘Soft Cast’ (3M™ Health Care, St. Paul, MN).
This material consists of a polyurethane resin incorporated
in a knitted fabric. Exposure to water activates the resin with
a set time of 3–4 min. Curing is completed in about 10 more
injury, cooling is an effective way of controlling the pain of
partial-thickness burns.35,36 In cooling for pain control, cool,
but not ice-cold,37,38 moist compresses are applied to the
painful wound. This method is applicable in the manage­
ment of virtually all patients whose wounds can be safely
cared for in an ambulatory setting. Because of the limited
surface area of burn among most of those patients treated as
outpatients, the detrimental systemic effects of active cooling,
e.g. hypothermia from accelerated heat loss, should not
occur. However, since water conducts heat 23 times faster
than air, it makes good sense to monitor the patient’s core
temperature during active cooling of the wound. A limit to
the surface area that is cooled is arbitrary, but a practical
limit is about 10% of the TBSA.
Pain control
Burn wounds are painful. The most severe pain occurs with
partial-thickness wounds devoid of epidermis. Initially it is
intense and can prove to be unbearable. The pain spontan­
eously moderates after several hours but intensifies when
wounds are manipulated during dressing changes, wound
care, and physical activity. While eschar-covered burns may
be insensate, when the eschar separates spontaneously or is
removed, the exposed viable tissues are painful when cut
into, cauterized, or manipulated.39
Narcotics are typically used as first-line treatment. In the
emergency setting, small incremental doses of morphine can
be given intravenously and titrated to effect. Subsequently,
acetaminophen with codeine or oxycodone or similar analge­
sics, alone or in combination, are usually effective. Provided
alteration of platelet function is not a concern, nonsteroidal
anti-inflammatory drugs (NSAIDs) can be used. Analgesics
can be supplemented with short-acting benzodiazepines,
such as midazolam, to enhance sedation and provide anxioly­
sis. Most patients will require supplemental analgesics for
wound dressing changes, physical therapy, and sleep.
Clearance of these classes of drugs is accelerated among
those who regularly abuse alcohol or controlled sub­
stances.40,41 Therefore, remarkable amounts of analgesics and
sedatives may be required.
If a patient’s pain cannot be controlled by oral medication,
the patient may need to be admitted to a hospital. In the
hospital setting, effective pain control can usually be
obtained by the patient-controlled analgesia method. Even
with patient-controlled analgesia, supplemental analgesia
and sedation will often be required when wound dressings
are changed.
Topically applied or injected local anesthetics are not
recommended in the management of burns.
Local burn wound care
Loose, devitalized tissue is gently trimmed away, a practice
known as épluchage. This process should not cause pain or
bleeding.
Blisters
Recommendations for the management of blisters are varied
and range from leaving blisters intact,42 to removing the
blistered skin immediately,43 or delaying removal.44

Total Burn Care
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86
in all areas, even around the eyes. According to the manu­
facturer it effectively removes contaminants from wounds
without inducing tissue trauma.
In the treatment of burns from tar and asphalt, after
cooling to dissipate heat, the solidified tar and asphalt can
be removed by solvents that have a close structural affinity
to these substances. Therefore, substances related to petrola­
tum (an oleaginous colloid suspension of solid microcrystal­
line waxes in petroleum oil) are effective. Medi-Sol™ Adhesive
Remover is a citrus-based non-toxic, non-irritating Category
I Medical Device solvent authorized by the FDA for use on
the skin. It is an effective product for the removal of tar
and asphalt.45 It can be obtained from Orange-Sol Medical
Products Division (1400 N Fiesta Blvd, Bldg. 100, Gilbert,
AZ 85233–1000, phone 480–497–8822) or by using an
internet search for ‘Medi-Sol.’ Medi-Sol™ Adhesive Remover
is liberally applied and then removed by gentle wiping.
Polysorbates alone or in combination with topical antibiot­
ics46 and topical antibiotics in petrolatum base47 can be used
minutes. It can be removed by unwrapping or cutting it with
a bandage scissors without the need to use a traditional cast
saw. This is a tremendous advantage when treating young
children. The technique for applying the ‘Soft Cast’ is shown
in Figure 6.3. The author keeps these casts in place for inter­
vals of 3, 4, 7 (the most frequent interval), or 10 days, repeat­
ing the application as long as necessary to prevent contraction
of the healing skin.
Cleansing the wound
For cleansing and to remove residual dirt, the wound can be
gently washed with room temperature or tepid (100°F)
normal saline or sterile water with a mild, bland soap. Anti­
septic solutions should not be used. The author’s service uses
Shur-Clens® Skin Wound cleanser, which is composed of
poloxamer 188 (polyethylene-polypropylene glycol), a sur­
factant, 20%, and USP water, 80%. Shur-Clens® is a sterile
cleansing solution designed for use on wounds of the skin
A
B
C
D
Figure 6.3  ’Soft’ casting technique to maintain optimal extension of the hand. (a) Heat contact burns of the palm and tips of fingers. (b) Wound dressed
with Adaptic® and triple antibiotic ointment. (c) Kling® wrap started by securing it around the wrist. (d) Kling® wrap threaded between fingers to prevent
interdigital web formation.

Care of outpatient burns
87
E
F
G
H
(e) A strip of Webril™ is placed in the thumb/index finger web space preparatory to laying a strip of Plaster-of-Paris to maintain optimal
abduction of the web space. (f) Application of the Plaster-of-Paris strip in the thumb/index finger web space while holding the metacarpal phalangeal joint
of the thumb in optimal abduction. Because the metacarpal phalangeal joint of children is fragile, special care needs to be taken to avoid hyperextension of
it. (g) Soft Cast® wrap being applied while maintaining thumb, thumb/index finger web space in optimal abduction and fingers in full extension until the
Soft Cast® material sets. (h) Dressing being completed with a wrap of Coban®.
Figure 6.3, cont’d
but are less effective, and repetitive applications are usually
required.
Topical agents
There is a long tradition of applying substances to burn
wounds in an attempt to prevent infection.48 A large variety
of antiseptics, antibiotics, and topical antibacterial (antimi­
crobial) agents have been advocated. Most of these agents
have adverse local or systemic effects, or impede wound
healing, or both. Additionally, there is no published evi­
dence that the use of any topical agent designed to prevent
or control infection will favorably influence the outcome of
small burns.49–51 In spite of this, many physicians feel obli­
gated to apply one of these agents to the wound. All pub­
lished comparative studies show no advantage of these
agents over petrolatum-impregnated gauze.52 However, if the
treating physician believes that the use of a topical antimi­
crobial agent is desirable, and most do, there are several
choices. Among topical antibacterial agents introduced for
the treatment of burns during the past five decades, 1% silver
sulfadiazine has been the most popular. However, its silver
component makes it an antiseptic and, therefore, an inher­
ent property is delay in wound healing. In comparative
studies of partial-thickness burn wounds covered with
dressings that do not contain antiseptics, e.g. TransCyte®,3
Biobrane®,53 and collagenase ointment with polymyxin B
sulfate/bacitracin powder,54 1% silver sulfadiazine delayed
spontaneous reepithelialization of the wound. However, if
the wound surface is covered with eschar, 1% silver sulfadi­
azine, among topical antiseptics recommended for burn
wounds, has the fewest side effects and is probably the
current best recommendation. If the patient is allergic to
sulfa products, silver sulfadiazine should not be used.

Total Burn Care
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88
once or twice daily, or more frequently as needed, particu­
larly in a dry climate. Bacitracin has activity against Gram-
positive bacteria. Occasionally it causes a contact dermatitis
that impedes wound healing.
Since one purpose of dressings is to absorb drainage, the
thickness of the dressing is determined by the amount of
drainage generated between dressing changes. In weeping
superficial partial-thickness wounds, the amount of drainage
is greatest soon after the injury. As the character of the wound
changes and healing begins, drainage decreases. Lint-free,
coarse mesh gauze, usually starting with about 20 thick­
nesses, is preferred by the author.
The dressing is held in place with a gauze bandage (e.g.
Kling® or Kerlix®) wrapped with sufficient tightness to hold
the gauze in place but not so tightly as to impede circulation.
Many use Flexinette® to secure the dressing. Stockinette,
semi-impervious to liquid, can be used as an outer layer to
help prevent the drainage from soaking through the dress­
ing. As an alternative, a cohesive flexible bandage (Coflex®,
Coban®, Cowrap™) can be used as an outer layer to hold a
dressing securely in place and prevent drainage from seeping
through. Joints are dressed to facilitate range of motion and
fingers are dressed separately. However, among infants and
young children, an effective way to hold the hand and fingers
in extension is with a multilayer covering of one of the cohe­
sive flexible bandages. This kind of a dressing functions as a
‘soft’ splint.
The frequency with which dressings are changed is arbi­
trary and dictated by the volume of drainage or the physical
condition of the dressing. Recommendations range from
twice daily, to as infrequently as once a week. Those who
advocate twice-daily dressing changes do so based on the use
of topical antimicrobials whose half-life is about 8 h. Those
who use petrolatum, antibiotic combinations in ointment,
or bismuth-impregnated petrolatum gauze recommend less-
frequent dressing changes, some extending the period to as
long as 5 or 7 days.52,55
For inpatients, the author prefers once-daily or every other
day dressing changes to permit inspection and cleansing of
the wound. Moreover, among inpatients after about 24–
48 h, wound dressings are often saturated or disheveled.
Daily dressing changes may be used in the care of outpa­
tients even if the patient or another layperson is responsible
for the inspection, cleansing, and redressing of the wound.
Cleansing of the wound can often be incorporated into
general body cleansing each day. The person responsible for
wound care should be instructed in the clinical manifesta­
tions of wound infections.
In the management of burns among pediatric outpatients,
the author now has an extensive and satisfying experience
with the use of triple antibiotic ointment and dressing
changes done at 3-, 4- or even 7-day intervals. In many
instances these dressings are changed and the progress of
healing checked at clinic visits. Therefore, parents do not
need to deal with the disquieting chore of changing their
child’s dressings and inflicting pain on them.
Biologic wound dressings
The author does not believe it is necessary or advantageous
to use human cadaver allografts, xenografts, or allogenic
amnion in the management of burn patients who qualify
Because sulfonamides are known to increase the possibility
of kernicterus, silver sulfadiazine is not used on pregnant
women, nursing mothers, and infants less than 2 months of
age. Because silver sulfadiazine impedes epithelialization, it
should be discontinued when healing partial-thickness
wounds are devoid of necrotic tissue and evidence of reepi­
thelialization is seen.
Alternatively, there has been increasing interest in the use
of combinations of antibiotics in ointment for the treatment
of small-area burns. These drugs have no clinically dis­
cernible detrimental effect on wound healing. These anti­
microbial combinations include triple antibiotic ointment
(neomycin, 3.5 mg/g; bacitracin zinc, 400 units/g; and poly­
myxin B sulfate, 5000 units/g) and Polysporin (polymyxin
B sulfate, 10 000 units/g; and bacitracin zinc, 500 units/g).
These antibiotic combinations have efficacy against the
Gram-positive cocci and some of the aerobic Gram-negative
bacilli that most frequently colonize small burn wounds.
Occasionally, small superficial pustules caused by yeast
develop on the surrounding uninjured or newly regenerated
skin. Discontinuing the antimicrobial agent usually results
in clearing of these lesions. The use of a topical antibiotic
ointment usually decreases or eliminates the unpleasant
odor often associated with the use of petrolatum-impregnated
gauze alone. The author now uses these agents almost exclu­
sively in the management of small-area burns when a topical
antimicrobial is used.
Dressing the wound
Because there are virtually no objective studies on the subject,
dogmatic recommendations for dressing small burn wounds
cannot be made.
Dressings serve three purposes:
1. To absorb drainage;
2. To provide protection and a measure of isolation of the
wound from the environment; and
3. To decrease wound pain.
In most instances the author prefers to dress wounds and
makes the following suggestions.
Superficial partial-thickness burns, the equivalent of
sunburn, with intact epidermis, require neither topical
medication nor a dressing.
For relatively small superficial partial-thickness burns
devoid of epithelium, it is generally conceded that topical
antibacterial agents are not necessary.49–51 Non-medicinal
white petrolatum-impregnated fine mesh or porous mesh
gauze (Adaptic®), or fine mesh absorbent gauze impregnated
with 3% bismuth tribromophenate in non-medicinal petro­
latum blend (Xeroform®) are satisfactory wound covers. If
the burn is deeper and contains adherent necrotic tissue, a
topical antimicrobial agent may be used.
For practical reasons, most burns of the face are treated
without dressing. These wounds may also be treated without
topical medication, allowing the wounds to dry and form a
crust. Because the dry wound is often uncomfortable and
heals more slowly than moist wounds, many physicians
prefer to use a thin layer of bland ointment combined with
a topical antibiotic, e.g. Baciquent® (bacitracin in anhydrous
lanolin, mineral oil, and white petrolatum). The ointment
is applied to the wound after gentle cleansing with water

Care of outpatient burns
89
Hydrocolloid dressings
Hydrocolloid dressings are described as wafers, powders, or
pastes composed of materials such as gelatin, pectin, and
carboxymethyl-cellulose. They provide a moist environment
favorable for wound healing and a barrier against exogenous
bacteria. In comparison to wounds treated with 1% silver
sulfadiazine, those treated with hydrocolloid occlusive dress­
ings had more rapid wound healing, less pain, and needed
fewer dressing changes.61,62 As a result, the cost of care was
lower. Hydrocolloid dressings have been effective in the
treatment of small-area partial-thickness burns and are espe­
cially useful in the terminal phase of spontaneous healing
of small burns. There are a number of products made by
different manufacturers that are probably suitable, e.g.
Cutinova® Thin (Beiersdorf-Jobst), DuoDerm® CGF Border
Sterile Dressing (ConvaTec), RepliCare® Hydrocolloid Dress­
ing (Smith & Nephew, Inc.), and Restore® Wound Care
Dressing (Hollister). Hydrocolloid dressings may be left in
place for several days at a time.
Other wound dressing/covering materials
Publications are replete with technologic advances and inno­
vations for wound dressings with the purported goal of
enhancement of spontaneous wound healing or protection
of the wound until it can be closed with skin grafts or with
tissue-engineered delivery systems which contain cultured
autogenous keratinocytes with or without fibroblasts.57 This
effort resulted in several available products, including: Tissue
Tech autograft system (Fidia Advanced Biopolymers S.r.l.,
Padua, Italy); Hyaff-NW (Fidia Advanced Biopolymers S.r.l.);
Laserskin (Fidia Advanced Biopolymers S.r.l.); Apligraft
(Organogenesis, Canton, MD); Epicell CEA (Genzyme,
Cambridge, MA); Integra (Johnson and Johnson, Ratingen,
Germany; Integra Life Sciences Corporation, Plainsboro NJ,
USA); Alloderm (Life Cell Corporation, Woodlands, TX);
Terumo (Terumo, Tokyo, Japan);63 and, Pelnac (Kowa
Company, Tokyo, Japan).64 While the results of use of these
products may be encouraging, a major limitation in their use
is undoubtedly their high cost. However, among most of
those treated as outpatients the area of burn wound requir­
ing skin grafts is relatively small. Therefore, the use of these
products is unnecessary and standard techniques of surgical
wound debridement and skin grafting suffice. Most of the
clinical information about the efficacy of these products is
anecdotal. However, information in medical publications
can be accessed through the cost-free National Library of
Medicine’s online service: On the
search screen use the name of the product and burns as the
subjects.
Elevation of the burned part
One of the most effective ways to reduce the incidence of
infection in burns is to eliminate edema from the burned
part. Burn injury elicits a flux of fluid into the tissues imme­
diately subjacent to the wound. Additionally, there is a great
tendency for the patient to hold the injured part immobile
in a dependent position. To eliminate edema, the injured
part should be exercised regularly and, when not in use,
maintained slightly above the level of the heart. Merely
for ambulatory care. However, in certain circumstances,
amniotic membranes may be plentiful and therefore
useful.
Allogenic amnion
Allogenic amnion, the innermost layer of the fetal mem­
brane, has been used as a biologic wound dressing since
1910.56 Although fragile and technically difficult to handle,
allogenic amnion is particularly effective when used as a
protective dressing on partial-thickness burn wounds. It also
has a good track record when used to protect and preserve a
clean excised wound for subsequent autogenous skin graft­
ing.57 When harvested, amniotic membranes are invariably
contaminated and carry a biologic risk that can never be
totally eliminated. The amnion is washed, sterilized with
gamma irradiation and preserved in glycerol, by lyophiliza­
tion or deep freezing. The risk of biologic transmission can
be diminished by systematic serologic testing of the donor
for syphilis, AIDS, and hepatitis at the time of harvesting the
membrane and 6 months later.57
Synthetic tissue-engineered wound dressings
The use of synthetic wound coverings is becoming more
popular in the treatment of superficial partial-thickness burn
wounds. The purported advantages are less pain, use of less
pain medication, shorter wound healing time, improved
compliance with scheduled outpatient visits, and lower
costs.
Biobrane®
There are two prospective randomized clinical trials of small
numbers of patients that show that in the treatment of super­
ficial partial-thickness burns the use of Biobrane® results in
less pain, a lower pain medication requirement, and shorter
healing time when compared to those patients treated with
1% silver sulfadiazine.58,59
Biobrane® is a bilayer fabric composed of an inner layer
of knitted nylon threads coated with porcine collagen and
an outer layer of rubberized silicone, pervious to gases
but not to liquids and bacteria.60 Wounds on which Bio­
brane® is to be applied must be carefully selected. They
must be fresh, not infected, free of eschar and debris, moist,
have a sensate surface, and demonstrate capillary blanching
and refill. It is applied snugly to the cleansed wound overlap­
ping itself or fixed to unburned skin with sterile strips of
adhesive tape. The key to the successful use of Biobrane® is
adherence to the wound. Therefore, the burned area must be
dressed and splinted, especially across a joint, to prevent
shearing of the Biobrane® from the wound surface. Satis­
factory adherence usually occurs in about 4 days. If, at
follow-up, the Biobrane® is found to be loose, the non-
adherent area can be trimmed away and new Biobrane®
applied. If sterile fluid accumulates beneath the synthetic
dressing, it can be aspirated. However, if the fluid is purulent,
the Biobrane® must be opened to permit complete drainage.
Biobrane® is left intact until the wound has reepithelialized.
Then it can be gently teased away. If the wound surface has
even a thin veneer of residual necrotic tissue, Biobrane® will
not adhere.

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90
spontaneous healing will occur within 3 weeks. Among
wounds in which the subtle differences between superficial
and deep partial-thickness burns are not initially discernible,
by 2 weeks after injury it is usually apparent whether or not
the wound will heal spontaneously within the next 7–10
days. At about 10 days after injury, those wounds which are
devoid of necrotic tissue and have evidence of squamous
reepithelialization will usually heal spontaneously within
the desirable time frame. The beginning of reepithelializa­
tion can be detected by seeing tiny opalescent islands of
epithelium scattered throughout the wound. Inspection with
a magnifying lens is helpful.
Infection and use of systemic antibiotics
There is no evidence that systemic antibiotic prophylaxis will
decrease the incidence of infection in small burn wounds.70
Antibiotics should be used only when there is evidence of
infection.
The burn itself elicits inflammation. Therefore, the early
manifestation of infection in the wound may be quite subtle.
Mild erythema, edema, pain, and tenderness, all classic signs
of infection, may be present without infection. However,
when these manifestations increase over baseline, especially
in the presence of lymphangitis and fever, treatment for
infection should be instituted. Mainstays of treatment for
infection include elevation and rest of the infected wound
to control swelling and systemic antibiotic therapy. If the
infection progresses the patient should be admitted to a
hospital and antibiotics given intravenously.
Infections in the outpatient setting are usually caused by
common skin flora. Those most frequently implicated are
staphylococci. If there is evidence of infection, a culture of
the surface of the wound should be obtained to identify the
offending organism and narrow the spectrum of antibiotic
therapy. While some burn care physicians advocate the use
of burn wound biopsy quantitative culture rather than a
wound surface culture,71 the author has not found biopsy
cultures to be necessary in the treatment of outpatient burns.
Among patients with burns treated in an ambulatory
setting, it is quite unusual to develop systemic sepsis.
However, patients should be instructed to take their tem­
perature twice daily, once in the morning shortly after they
get up from sleep, and again late in the afternoon before
they eat supper. Localized infection will be reflected in fever
in the afternoon or evening. Sustained fever is suggestive of
systemic sepsis. Temperatures above 38°C, especially if
accompanied by symptoms of malaise and anorexia, should
be reported to the physician and the patient called in for an
examination.
A change in the appearance of the wound during the first
several days is more likely to result from a decrease in per­
fusion of the wound than from wound infection. This occurs
as the blood vessels injured by heat clot off. This is fre­
quently observed with scald burns. Any further burn wound
discoloration, such as the appearance of gray or black spots,
especially if there are other manifestations of infection,
should raise concern for invasive infection. This rarely occurs
among those treated as outpatients. However, if it does
occur, the patient should be admitted to a hospital, the
wound biopsied for histologic and microbiological studies,72
and treatment for infection instituted.
elevating a leg off the floor to the level of the hip when in
the sitting position is not sufficient. Holding the burned
forearm flexed and dependent in a sling will enhance edema.
Specific instructions and a demonstration of the proper posi­
tion should be explicit. Patients with small burns who expe­
rience persistent edema beyond 3 days are spending too
much time with the part dependent.
The most efficient position for the injured part is just
slightly above the level of the heart. To elevate the burned
part higher does not further enhance removal of excess tissue
fluid. However, for every incremental elevation of the part
there is an incremental decrease in the arterial perfusion
pressure.65
When burns involve the lower extremity, walking and
holding the leg in the dependent position often elicit severe
pain. To diminish this effect, support, such as with a rub­
berized elastic bandage (Ace Bandage®), or a cohesive flex­
ible bandage, which the author prefers, applied from the
level of the toes to above the burn, should be used. This
will also aid in reducing the accumulation of edema during
walking.
Instructions and follow-up care
Before patients are released from emergency care, they are
instructed in wound care, positioning, physical therapy, the
clinical manifestations of infection, a convenient way to
access medical care (usually by telephone), and they are
given pain medication.
The authors often examine patients within the next several
days. This allows re-inspection of the wound, assessment of
the patient’s compliance with instructions, and reinforce­
ment of the principles of wound care. Often, because of pain
during emergency care, the patient is distracted from fully
understanding instructions. If concern remains, more fre­
quent visits are scheduled until the physician is certain that
care is being followed appropriately. After that, the patient
can be seen at weekly intervals.
Definitive wound closure
A primary objective in burn care is to have all wounds healed
within 1 month. Usually, this goal is easily achieved in an
ambulatory setting. Burn wounds that heal spontaneously
from the depth of the wound within 3 weeks have an excel­
lent result. When this occurs, the skin functions normally
with good elasticity, a nil incidence of hypertrophic scarring
(scars that are red, raised, and indurated), and little, if any,
alteration in pigmentation. The longer spontaneous healing
takes, the worse the result. With longer healing periods, there
is an increasing likelihood of developing hypertrophic scar­
ring66 and unsightly alterations in pigmentation. In addi­
tion, wounds that take a very long time to heal spontaneously
may have unstable epithelium.
It is the surgeon’s responsibility to make certain that burn
wounds either heal spontaneously or are closed surgically in
a timely fashion. If it is apparent that a wound will not heal
spontaneously within 3 weeks, a better outcome67,68 can
usually be anticipated by surgically removing the residual
necrotic tissue and any granulation tissue by tangential exci­
sion69 and applying a skin graft. In many instances it is
obvious immediately or within several days as to whether

Care of outpatient burns
91
Step 4: Hydroxyzine 0.5 mg/kg/dose PO q 6 h and
cyproheptadine 0.1 mg/kg/dose PO q 6 h and
diphenhydramine 1.25 mg/kg/dose PO q 6 h. Alternate
medication so that patient is receiving one itch medicine
every 2 h while awake.
Phillips and Robson82 advocate using penicillin in pruritus
management. They observed that post-burn hypertrophic
scars were much more frequently colonized with beta-
hemolytic streptococcus, Staphylococcus aureus, and Staph.
epidermidis compared to matched healed wounds without
hypertrophic scarring. Therefore, to decrease the inflamma­
tion caused by these microorganisms, a root cause of itching,
they used the following regimen: low-dose oral penicillin,
250 mg twice daily, to control the beta-hemolytic streptococ­
cus, and aloe vera cream applied topically. As noted above,
aloe vera has both anti-inflammatory and antimicrobial
properties.
Traumatic blisters in reepithelialized wounds
As the wounds reepithelialize, the delicate thin layer of epi­
thelium is fragile and easily damaged. Itching and other mild
forms of trauma may cause small blisters. Patients need to
be cautioned about this potential and assured that the
epithelium will gain strength and that this will not be a
long-term problem. If these blisters rupture, leaving small
superficial wounds, the wounds may be left exposed to form
a crust. Alternatively, Adaptic® or Xeroform® and a light
dressing or one of the hydrocolloid wafer products may
be used.
Rehabilitative physical care
Measures to preserve strength and restore function should
be incorporated into the initial treatment plan.83 Before
leaving emergency care, the patient’s physical activity should
be discussed and a program for range of motion exercises
and muscle strengthening outlined, both verbally and in
writing.
At each subsequent follow-up visit, function and strength
should be assessed. If there is lack of compliance or if the
patient’s function begins to deteriorate, the patient should
be referred for supervised physical or occupational therapy,
or both. If the injury extends across a joint, or involves the
hand or distal portion of the lower extremity, it is advisable
to have therapists involved from the outset. When there are
burns of the face that have the potential for facial dysfunc­
tion, it may be prudent to have the patient evaluated and
treated by a speech pathologist.
The potential for development of contractures and hyper­
trophic scars among the burned treated as outpatients is the
same as for those treated as inpatients.83 The principles of
prevention and treatment of these complications apply in
both settings.
Outpatient treatment of moderate
and major burns
Some patients classified as having moderate or even major
burn injuries (Table 6.2)84 are suitable for treatment in the
ambulatory setting.85 The purported advantages include less
Burns, even minor ones, are regarded as tetanus-prone
wounds.73 Tetanus prophylaxis should be provided unless
the patient has received tetanus immunization within the
previous 5 years.74
Pruritus
Itching is an annoying, often unrelenting manifestation of
healing and healed burn wounds.
Most burn patients develop pruritus. The incidence is
higher among children. The lower extremities are most fre­
quently affected and more frequently than the upper. The
face is seldom involved.75
Post-burn itching interferes with everything. Scratching
often results in repetitive superficial wounding of both skin
grafted and spontaneously healed wounds. Triggered and
enhanced by environmental extremes, especially heat, physi­
cal activity, and stress, pruritus is most intense in the period
immediately after wounds are healed. In most instances, it
gradually diminishes and eventually stops. There are a few
patients in whom it persists beyond 18 months. Patients
with prolonged and chronic itching may harbor a psycho­
genic component.
The sensation of itch is most likely a primary sensory
modality rather than, as widely held in the past, a forme
fruste of pain.76 Histamine, whose synthesis is known to be
increased in healing and inflamed wounds,77 as well as
bradykinin and a series of endopeptides, have all been impli­
cated in the genesis of itching.78,79 Because the precise mech­
anism of pruritus is not known, the likelihood is that there
are multiple causative factors.
Since there are no controlled trials defining the best treat­
ment, management is by trial and error. However, antihista­
mines, cool compress, and lotions are the cornerstones of
most attempts to relieve burn-related itching. The antihista­
minic diphenhydramine hydrochloride is the most fre­
quently prescribed first treatment.80 This drug has an added
benefit of providing mild sedation. Other antihistamines,
such as cyproheptadine hydrochloride, may also be tried.
Analgesics of any kind may be helpful by altering perception
of itching in the central nervous system. Combinations of
antihistamines and analgesics may be tried. Hydroxyzine
hydrochloride, a drug used to provide relief from anxiety and
emotional tension, is used by many to help ameliorate
itching. Many patients find comfort in an air-conditioned
environment. Cool compresses also may temporarily inter­
rupt the itching cycle. A variety of topical agents, including
aloe vera,81 which has anti-inflammatory and antimicrobial
properties, and skin moisturizing creams, such as Elta®, Vase­
line Intensive Care®, Eucerin®, Nivea®, mineral oil, cocoa
butter, and even lard, have been effective. Any odorless
lotion free of alcohol is probably helpful. In addition, many
patients prefer loose, soft clothing made from cotton.
The staff at the Shriners Burns Hospital, Galveston, Texas,
uses the following protocol for the treatment of itching:
Step 1: Use moisturizing body shampoo and lotions.
Step 2: Diphenhydramine 1.25 mg/kg/dose PO q 4 h
scheduled.
Step 3: Hydroxyzine 0.5 mg/kg/dose PO q 6 h and
diphenhydramine 1.25 mg/kg/dose PO q 6 h. Alternate
medication so that patient is receiving one itch medicine
every 3 h while awake.

Total Burn Care
6
92
cost, less chance of exposure to antibiotic-resistant microor­
ganisms, and a more psychologically comfortable environ­
ment for the patient. In spite of these benefits, caution
should be exercised in selecting patients with moderate and
major thermal injury for early discharge from the hospital.
On the other hand, as convalescence progresses, many of
these patients can have the terminal phase of their acute
burn care completed safely as outpatients.
The conditions that need to be met in order to consider
ambulatory care for any patient include: intravenous fluid
resuscitation must be completed; there must be no ongoing
complication; there must be no wound or systemic manifes­
tation of sepsis; adequate enteral nutrition must be estab­
lished; and pain control must be satisfactory with medication
taken by mouth. Additionally, arrangements need to be
made for wound care and physical and/or occupational
therapy.
Further reading
Hartford CE. The bequests of Moncrief and Moyer: an appraisal of
topical therapy of burns – 1981 American Burn Association
presidential address. J Trauma. 1981;21:827-834.
Matsen III FA. Compartmental Syndromes. New York: Grune & Stratton;
1980.
Moritz AR, Henriques Jr FC. Studies of thermal injury II. The relative
importance of time and surface temperature in the causation of
cutaneous burns. Am J Pathol. 1947;23:695-720.
Ryan CM, Schoenfeld DA, Thorpe WP, et al. Objective estimates
of the probability of death from burn injuries. N Engl J Med.
1998;338:362-366.
Table 6.2  Classification of burn severity
Minor burn
≤15% TBSA in adults
≤10% TBSA in children and the elderly
≤2% TBSA full-thickness burn in children or adults without cosmetic or
functional risk to eyes, ear, face, hands, feet, or perineum
Moderate burn
15–25% TBSA in adults with <10% full-thickness burn
10–20% TBSA partial-thickness burn in children under 10 and adults over
40 years of age, with <10% full-thickness burn
≤10% TBSA full-thickness burn in children or adults without cosmetic or
functional risk to eyes, ears, face, hands, feet, or perineum
Major burn
≥25% TBSA
≥20% TBSA in children under 10 and adults over 40 years of age
≥10% TBSA full-thickness burn
All burns involving eyes, ears, face, hands, feet, or perineum that are likely
to result in cosmetic or functional impairment
All high-voltage electrical burns
All burn injuries complicated by major trauma or inhalation injury
All poor-risk patients with burn injury
TBSA, total body surface area.
 
Access the complete reference list online at

Care of outpatient burns
92.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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management of the deeply burned hand. J Trauma. 1976;16:593-
598.
69. Janzekovic Z. A new concept in the early and immediate grafting
of burns. J Trauma. 1970;10:1103-1108.
70. Durtschi MB, Orgain C, Counts GW, et al. A prospective study of
prophylactic penicillin in acutely burned hospitalized patients.
J Trauma. 1982;22:11-14.
71. Loebl EC, Marvin JA, Heck EL, et al. The method of quantitative
burn-wound biopsy cultures and its routine use in the care of the
burned patient. Am J Clin Pathol. 1974;61:20-24.
72. Pruitt BA Jr. The diagnosis and treatment of infection in the burn
patient. Burns Incl Thermal Inj. 1984;11:79-91.
73. Larkin JM, Moylan JA. Tetanus following a minor burn. J Trauma.
1975;15:546-548.
74. Committee on Trauma, American College of Surgeons. A Guide
to Prophylaxis against Tetanus in Wound Management, 1984 revision.
Philadelphia: American College of Surgeons; 1984.
75. Bell L, McAdams T, Morgan R, et al. Pruritus in burns: a
descriptive study. J Burn Care Rehabil. 1988;9:305-308.
76. Herndon JH Jr. Itching: the pathophysiology of pruritus. Int J
Dermatol. 1975;14:465-484.
77. Kahlson G, Rosengren E. New approaches to the physiology of
medicine. Physiol Rev. 1968;48:155-196.
78. Keele CA, Armstrong D. Substances Producing Pain and Itch.
London: Edward Arnold; 1964:297-298.
79. Robson MC, Jellema A, Heggers JP, et al. Care of the Healed Burn
Wound: A Prospective Randomized Study. San Antonio, TX:
American Burn Association; 1980:94 (Abstract).
80. Gordon MD. Pruritus in burns. J Burn Care Rehabil. 1988;9:305-
311.
81. Heimbach DM, Engrav LH, Marvin J. Minor burns: guidelines
for successful outpatient management. Postgrad Med. 1981;69:22-
32.
82. Phillips LG, Robson MC. Comments from Detroit Receiving
Hospital, Detroit, Michigan. J Burn Care Rehabil. 1988;9:
308-309.
83. Helm PA, Kevorkian G, Lushbaugh M, et al. Burn injury:
rehabilitation management in 1982. Arch Phys Med Rehabil.
1982;63:6-16.
84. Guidelines for service standards and severity classification in the
treatment of burn injury. Appendix B to Hospital Resources
Document. ACS Bulletin. 1984;69:25-28.
85. Warden GD, Kravitz M, Schnebly A. The outpatient management
of moderate and major thermal injury. J Burn Care Rehabil.
1981;2:159-161.

Pre-hospital management,
transportation and emergency care
Ronald P. Mlcak, Michael C. Buffalo, Carlos J. Jimenez
Introduction
Advances in trauma and burn management over the past
three decades have resulted in improved survival and reduced
morbidity from major burns. The cost of such care, however,
is high; it requires conservation of resources such that only
a limited number of burn intensive care units with the capa­
bilities of caring for such labor-intensive patients can be
found – hence regional burn care has evolved. This region­
alization has led to the need for effective pre-hospital man­
agement, transportation, and emergency care. Progress in the
development of rapid, effective transport systems has resulted
in marked improvement in the clinical course and survival
for victims of thermal trauma.
For burn victims, there are usually two phases of transport.
The first is the entry of the burn patient into the emergency
medical system with treatment at the scene and transport to
the initial care facility. The second phase is the assessment
and stabilization of the patient at the initial care facility and
transportation to the burn intensive care unit.1 With this
perspective in mind, this chapter reviews current principles
of optimal pre-hospital management, transportation, and
emergency care.
Pre-hospital care
Prior to any specific treatment, a patient must be removed
from the source of injury and the burning process stopped.
As the patient is removed from the injuring source, care
must be taken so that a rescuer does not become another
victim.2 All caregivers should be aware of the possibility
that they may be injured by contact with the patient or the
patient’s clothing. Universal precautions, including wearing
gloves, gowns, masks, and protective eye wear, should be
used whenever there is likely contact with blood or body
fluids. Burning clothing should be removed as soon as pos­
sible to prevent further injury.3 All rings, watches, jewelry,
and belts should be removed as they can retain heat and
produce a tourniquet-like effect with digital vascular
ischemia.4 If water is readily available, it should be poured
directly on the burned area. Early cooling can reduce the
depth of the burn and reduce pain, but cooling measures
must be used with caution, since a significant drop in body
temperature may result in hypothermia with ventricular
fibrillation or asystole. Ice or ice packs should never be
used, since they may cause further injury to the skin or
produce hypothermia.
Initial management of chemical burns involves removing
saturated clothing, brushing the skin if the agent is a powder,
and irrigation with copious amounts of water, taking care
not to spread chemical on burns to adjacent unburned areas.
Irrigation with water should continue from the scene of
the accident through emergency evaluation in the hospital.
Efforts to neutralize chemicals are contraindicated due to the
additional generation of heat, which would further contrib­
ute to tissue damage. A rescuer must be careful not to come
in contact with the chemical, i.e. gloves, eye protectors, etc.
should be worn.
Removal of a victim from an electrical current is best
accomplished by turning off the current and by using a non-
conductor to separate the victim from the source.5
On-site assessment of a burned patient
Assessment of a burned patient is divided into primary and
secondary surveys. In the primary survey, immediate life-
threatening conditions are quickly identified and treated.
The primary survey is a rapid, systematic approach to iden­
tify life-threatening conditions. The secondary survey is a
more thorough head-to-toe evaluation of the patient. Initial
management of a burned patient should be the same as for
any other trauma patient, with attention directed at airway,
breathing, circulation, and cervical spine immobilization.
Primary assessment
Exposure to heated gases and smoke from the combustion
of a variety of materials results in damage to the respira­
tory tract. Direct heat to the upper airways results in
edema formation, which may obstruct the airway. Initially,
100%-humidified oxygen should be given to all patients
when no obvious signs of respiratory distress are present.
Upper airway obstruction may develop rapidly following
injury, and the respiratory status must be continually mon­
itored in order to assess the need for airway control and
ventilator support. Progressive hoarseness is a sign of
impending airway obstruction. Endotracheal intubation
should be done early before edema obliterates the anatomy
of the area.3
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00007-2
CHAPTER 7 
Access the complete reference list online at

Total Burn Care
7
94
blanket to minimize heat loss and to control temperature
during transport.
Transport to hospital emergency department
Rapid, uncontrolled transport of a burn victim is not the
highest priority, except in cases where other life-threatening
conditions coexist. In the majority of accidents involving
major burns, ground transportation of victims to a hospital
is available and appropriate. Helicopter transport is of great­
est use when the distance between an accident and a hospital
is 30–150 miles or when a patient’s condition warrants.10
Whatever the mode of transport, it should be of appropriate
size, and have emergency equipment available as well as
trained personnel, such as a nurse, physician, paramedic, or
respiratory therapist.
Assessment at the initial care facility
The assessment of a patient with burn injuries in a hospital
emergency department is essentially the same as outlined
for a pre-hospital phase of care. The only real difference is
the availability of more resources for diagnosis and treat­
ment in an emergency department. As with other forms of
trauma, the primary survey begins with the ABCs, and the
establishment of an adequate airway is vital. Endotracheal
intubation should be accomplished early if impending res­
piratory obstruction or ventilatory failure is anticipated,
because it may be impossible after the onset of edema fol­
lowing the initiation of fluid therapy. Securing an endotra­
cheal tube may be difficult because traditional methods
often do not adhere to burned skin, and tubes are easily
dislodged. One method of choice includes securing an
endotracheal tube with woven tape, umbilical cord, under
the ears as well as over the ears.11 While doing assessments
and making interventions for life-threatening problems in
the primary survey, precautions should be taken to maintain
cervical spine immobilization until injuries to the spine can
be ruled out.
Following a primary survey, a thorough head-to-toe evalu­
ation of a patient should be done. This includes obtaining a
history as thorough as circumstances permit. The history
should include the mechanism and time of the injury and a
description of the surrounding environment, such as whether
injuries were incurred in an enclosed space, the presence of
noxious chemicals, the possibility of smoke inhalation, and
any related trauma. A complete physical examination should
include a careful neurological examination, as evidence of
cerebral anoxic injury can be subtle. Patients with facial
burns should have their corneas examined with fluorescent
staining. Routine admission laboratories should include a
complete blood count, serum electrolytes, glucose, blood
urea nitrogen (BUN), and creatine. Pulmonary assessment
should include arterial blood gases, chest X-rays, and
carboxyhemoglobin.12
Emergency treatment at the initial care facility
All extremities should be examined for pulses, especially
with circumferential burns. Evaluation of pulses can be
assisted by use of a Doppler ultrasound flowmeter. If pulses
The patient’s chest should be exposed in order to ade­
quately assess ventilatory exchange. Circumferential burns
may restrict breathing and chest movement. Airway patency
alone does not assure adequate ventilation. After an airway
is established, breathing must be assessed in order to insure
adequate chest expansion. Impaired ventilation and poor
oxygenation may be due to smoke inhalation or carbon
monoxide intoxication. Endotracheal intubation is neces­
sary for unconscious patients, for those in acute respiratory
distress, or for patients with burns of the face or neck
which may result in edema which causes obstruction of
the airway.3 The nasal route is the recommended site of
intubation. Assisted ventilation with 100%-humidified
oxygen is required for all intubated patients.
Blood pressure is not the most accurate method of moni­
toring a patient with a large burn because of the pathophy­
siologic changes which accompany such an injury. Blood
pressure may be difficult to ascertain because of edema in
the extremities. A pulse rate may be somewhat more helpful
in monitoring the appropriateness of fluid resuscitation.6
If a burn victim was in an explosion or deceleration acci­
dent, there is the possibility of a spinal cord injury. Appro­
priate cervical spine stabilization must be accomplished
by whatever means necessary, including a cervical collar to
keep the head immobilized until the condition can be
evaluated.
Secondary assessment
After completing a primary assessment, a thorough head-to-
toe evaluation of a patient is imperative.7 A careful determi­
nation of trauma other than obvious burn wounds should
be made. As long as no immediate life-threatening injury or
hazard is present, a secondary examination can be performed
before moving a patient; precautions such as cervical collars,
backboards, and splints should be used.8 Secondary assess­
ment should examine a patient’s past medical history, medi­
cations, allergies, and the mechanisms of injury.
There should never be a delay in transporting burn victims
to an emergency facility due to an inability to establish
intravenous (IV) access. If the local/regional emergency
medical system (EMS) protocol prescribes that an IV line is
started, then that protocol should be followed. The Ameri­
can Burn Association recommends that if a patient is less
than 60 min from a hospital, an IV is not essential and can
be deferred until a patient is at a hospital. If an IV line is
established, Ringer’s lactate solution should be infused at:
•
14 years and older: 500 mL LR per hour
•
6–14 years old: 250 mL LR per hour
•
5 years and younger: 125 mL LR per hour.
Pre-hospital care of wounds is basic and simple, because
it requires only protection from the environment with an
application of a clean dressing or sheet to cover the involved
part. Covering wounds is the first step in diminishing pain.
If it is approved for use by local/regional EMS, narcotics may
be given for pain, but only intravenously in small doses and
only enough to control pain. Intramuscular (IM) or subcu­
taneous routes should never be used, since fluid resuscita­
tion could result in unpredictable patterns of uptake.4 No
topical antimicrobial agents should be applied in the field.4,9
The patient should then be wrapped in a clean sheet and

Pre-hospital management, transportation and emergency care
95
sedation using electrocautery. Midaxial incisions are made
through the eschar but not into subcutaneous tissue of the
eschar in order to assure adequate release. Limbs should be
elevated above the heart level. Pulses should be monitored
for 48 h.12
If pulses are still present, but appear endangered, chemical
escharotomy with enzymatic ointments (Accuzyme, colla­
genase, Elase) can be effective. Enzymatic escharotomy in
hand burns may be preferred since surgical incisions risk
exposure of superficial nerves, vessels, and tendons. Enzy­
matic escharotomy is indicated only during the first 24–48 h
post-burn, and it should be used only in combination with
a topical antimicrobial agent or sepsis can occur. With enzy­
matic escharotomy, there is usually a spike in temperature,
which subsides after the enzyme is removed.
Evaluation of wounds
After the primary and secondary surveys are completed and
resuscitation is underway, a more careful evaluation of burn
wounds is performed. The wounds are gently cleaned, and
loose skin and in large wounds blisters greater than 2 cm
are debrided (see Ch. 6). Blister fluid contains high levels
of inflammatory mediators, which increase burn wound
ischemia. The blister fluid is also a rich media for subsequent
bacterial growth. Deep blisters on the palms and soles may
be aspirated instead of debrided in order to improve patient
comfort. After burn wound assessment is complete, the
wounds are covered with a topical antimicrobial agent and
appropriate burn dressings or a biological dressing is applied.
An estimate of burn size and depth assists in making a
determination of severity, prognosis, and disposition of a
patient. Burn size directly affects fluid resuscitation, nutri­
tional support, and surgical interventions. The size of a burn
wound is most frequently estimated by using the Rule-of-
Nines method (Fig. 7.2). A more accurate assessment can be
made of a burn injury, especially in children, by using the
Lund and Browder chart, which takes into account changes
brought about by growth (Fig. 7.3).4,9 The American Burn
Association identifies certain injuries as usually requiring a
referral to a burn center. Patients with these burns should be
treated in a specialized burn facility after initial assessment
and treatment at an emergency department. Questions about
specific patients should be resolved by consultation with a
burn center physician (Box 7.1).4,13
Fluid resuscitation
Establishment of IV lines for fluid resuscitation are necessary
for all patients with major burns including those with inha­
lation injury or other associated injuries. These lines are best
started in the upper extremity peripherally. A minimum of
two large-caliber IV catheters should be established through
non-burned tissue if possible, or through burns if no
unburned areas are available. The ABLS 2010 Fluid Resus­
citation Formula of Ringer’s lactate solution should be
infused at 2 mL/kg/% total body surface area (TBSA) which
is burned.1,4,9 Children must have additional fluid for
maintenance.14
Taking into account the increased evaporative water loss
in the formula for fluid resuscitation for pediatric patients,
the initial resuscitation should begin with 5000 mL/m2/%
Figure 7.1  Possible escharotomy sites. (a) Chest escharotomy site.
(b) Escharotomy site on finger. (c) Lower limb escharotomy. (Fig. 7.1a
Reproduced from Herndon DN, Desai MH, Abston S, et al. Residents Manual. Galveston:
Shriner’s Burns Hospital, and the University of Texas Medical Branch 1992:1-17.)
A
B
C
are absent, the involved limb may need urgent escharotomy
for release of the constrictive, unyielding eschar (Fig. 7.1). In
circumferential chest burns, escharotomy may also be neces­
sary to relieve chest wall restriction and improve ventilation.
Escharotomies may be performed at the bedside under IV

Total Burn Care
7
96
TBSA burned/day + 2000 mL/m2/BSA total/day 5% dextrose
in Ringer’s lactate. This formula calls for one-half of the total
amount to be given in the first 8 h post-injury with the
remainder given over the following 16 h (Box 7.2).14
All resuscitation formulas are designed to serve as a guide
only. The response to fluid administration and physiologic
tolerance of a patient is the most important determinant.
Additional fluids are commonly needed with inhalation
injury, electrical burns, associated trauma, and delayed resus­
citation. The appropriate resuscitation regimen administers
the minimal amount of fluid necessary for maintenance of
vital organ perfusion; the subsequent response of the patient
over time will dictate if more or less fluid is needed so that
the rate of fluid administration can be adjusted accordingly.
Inadequate resuscitation can cause diminished perfusion
of renal and mesenteric vascular beds. Fluid overload can
produce undesired pulmonary or cerebral edema.
Urine output requirements
The single best monitor of fluid replacement is urine output.
Acceptable hydration is indicated by a urine output of more
than 30 mL/h in an adult (0.5 mL/kg/h) and 1 mL/kg/h in
a child. Diuretics are generally not indicated during an acute
resuscitation period. Patients with high-voltage electrical
burns and crush injuries with myoglobin and/or hemo­
globin in the urine have an increased risk of renal tubular
obstruction. Sodium bicarbonate should be added to IV
fluids in order to alkalinize the urine, and urine output
should be maintained at 1–2 mL/kg/h as long as these pig­
ments are in the urine.1,4 The addition of an osmotic diuretic
such as mannitol may also be needed to assist in clearing
the urine of these pigments.
Additional assessments and treatments
Decompression of stomach
To combat the problem of gastric ileus, a nasogastric tube
should be inserted in all patients with major burns in order
to decompress the stomach. This is especially important for
patients being transported at high altitudes.13 Additionally,
all patients should be restricted from taking anything
by mouth until after the transfer has been completed.
Figure 7.2  Estimation of burn size using the Rule-of-Nines. (From: Advanced
Burn Life Support Providers Manual. Chicago, IL: American Burn Association; 2010.)
Adult body
Part
Arm
Head
Neck
Leg
Anterior trunk
Posterior trunk
% of total
BSA
9%
9%
1%
18%
18%
18%
Child body
Part
Arm
Head and neck
Leg
Anterior trunk
Posterior trunk
% of total
BSA
9%
18%
14%
18%
18%
9%
1%
Front
18%
Front
18%
Back
18%
Back
18%
18%
18%
18%
9%
9%
14%
14%
9%
9%
Box 7.1  Criteria for transfer of a burn patient to a burn center
•
Second-degree burns greater than 10% total body surface area
(TBSA)
•
Third-degree burns
•
Burns that involve the face, hands, feet, genitalia, perineum, and
major joints
•
Chemical burns
•
Electrical burns including lightning injuries
•
Any burn with concomitant trauma in which the burn injuries
pose the greatest risk to the patient
•
Inhalation injury
•
Patients with pre-existing medical disorders that could complicate
management, prolong recovery, or affect mortality
•
Hospitals without qualified personnel or equipment for the care of
critically burned children.
Reproduced from the Advanced Burn Life Supporters Manual. Chicago, IL:
American Burn Association; 2005.
Box 7.2  Burn fluid resuscitation formula
Fluid administration – Ringer’s lactate:
First 24 h
•
5000 mL/m2 burn + 2000 mL/body area m2, administer half in 8 h
and the remaining half in 16 h.
Second 24 h
•
3750 mL/m2 + 1500 mL/body area m2, administer half in 8 h and
the remaining half in 16 h.
Adjust the above rates to maintain a urine output of 1 mL/kg/h.
Reproduced with permission from: Herndon DN, Rutan RL, Rutan TC. Management
of the pediatric patient with burns. J Burn Care Rehabil 1993; 14(1):3-8.

Pre-hospital management, transportation and emergency care
97
Transferring a burn patient
The appearance of burn skin is rather obvious and has the
potential to mask or cover any other potential injuries that
the burn patient could have. The burn patient is a trauma
patient with burns and should be promptly and effectively
evaluated to include other potential injuries. It is important
to establish effective communication between the trans­
ferring unit and the receiving center.
Once the need to transfer the patient is identified, the
transferring process begins. The doctor-to-doctor referral
process starts with the initial care facility. Available phone
numbers and doctor information should be available to
centers that should promptly call and ask for all the informa­
tion needed for the transfer.
The referring physician should give a brief and concise
history of the event that includes the time of injury and all
resuscitation efforts prior to the call. The ABCs of trauma
resuscitation should be discussed and the most current vital
signs and physical examination findings should be pre­
sented. The accepting facility should then fill out an intake
form that details all the information. Understanding of the
patient’s current status is needed for a successful and
un­eventful transfer. It is imperative that physicians partici­
pate in the process adding to the already available informa­
tion gather by other personal.
Decompression of the stomach is usually necessary because
an anxious, apprehensive patient will swallow considerable
amounts of air and distend the stomach. Narcotics also
diminish peristalsis of the gastrointestinal tract and result in
distension.
A patient must be kept warm and dry
Hypothermia is detrimental to traumatized patients and can
be avoided or at least minimized by the use of sheet and
blankets. Wet dressings should be avoided.
Pain
The degree of pain experienced initially by the burn victim
is inversely proportional to the severity of the injury.8 No
medication for pain relief should be given intramuscularly
or subcutaneously. For mild pain, acetaminophen 650 mg
orally every 4–6 h may be given. For severe pain, morphine,
1–4 mg intravenously every 2–4 h, is the drug of choice,
although meperidine (Demerol) 10–40 mg by IV push every
2–4 h may be used.10 Recommendations for tetanus prophy­
laxis are based on the patient’s immunization history. All
patients with burns should receive 0.5 mL of tetanus toxoid.
If prior immunization is absent or unclear, or if the last
booster was more than 10 years ago, 250 units of tetanus
immunoglobulin is also given.4
Figure 7.3  Estimation of burn size using the Lund and
Browder method.
Age
0–1
1–4
5–9
10–14
15
A – ½ of head
9½%
8½%
6½%
5½%
4½%
B – ½ of one thigh
9½%
8½%
6½%
5½%
4½%
C – ½ of one leg
9½%
8½%
6½%
5½%
4½%
Adult
3½%
3½%
3½%
3½%
3½%
3½%
A
A
B
B
C
C
B
B
C
C
1½%
1½%
1½%
1½%
1½%
1½%
1½%
1½%
2½%
2½%
4¾%
4¾%
4¾%
4¾%
1¾%
1¾%
1%
1%
1%
13%
13%
2%
2%
2%
2%
1¾%
1¾%

Total Burn Care
7
98
patient and reveals a specific diagnosis or condition. While
standard e-mail works and is offered free of charge by service
providers such as Yahoo, Gmail, Comcast and many others,
vendors of secure messaging networks are quick to point out
multiple deficiencies (Box 7.3).
Whether or not electronic communication is encrypted or
secure, physicians should guard against getting lulled by
the casual nature of e-mail which, unlike a conversation or
phone call, is not erased from a computer’s hard drive when
deleted and is potentially discoverable in litigation.
Transportation guidelines
The primary purpose of any transport teams is not to bring
a patient to an intensive care unit but to bring that level of
care to the patient as soon as possible. Therefore, the critical
time involved in a transport scenario is the time it takes to
get the team to the patient. The time involved in transporting
a patient back to a burn center becomes secondary. Com­
munication and teamwork are the keynotes to an effective
transport system.
When transportation is required from a referring facility
to a specialized burn center, a patient can be fairly well
stabilized before being moved. Initially, the referring
facility should be informed that all patient referrals require
physician-to-physician discussion. Pertinent information
needed include: patient demographic data; time; date; cause
and extent of burn injury; weight and height; baseline vital
signs; neurological status; laboratory data; respiratory status;
previous medical and surgical history, and allergies.
A referring hospital is informed of specific treatment pro­
tocols regarding patient management prior to transfer. To
ensure patient stability, the following guidelines are offered:
•
Establish two IV sites, preferably in an unburned upper
extremity, and secure IV tubes with sutures.
•
Insert a Foley catheter and monitor for acceptable urine
output (30 mL/h adult; 1 mL/kg/h child.
•
Insert a nasogastric tube and ensure that the patient
remains NPO.
•
Maintain body temperature between 38 and 39.0°C
rectally.
•
Stop all narcotics.
Transferring a patient without the needed information can
potentially lead to bad outcomes and or unnecessary expense.
For example, a burn patient with an underlying anoxic brain
injury could be transferred to a burn center, when instead
the diagnosis of brain death could have been done at the
initial care facility.
Physicians have the availability of accessing patient
information utilizing different technologies. Although a
doctor-to-doctor phone call is preferred by many, today’s
technology allows patient data including pictures, labora­
tory results as well as any other clinical information needed
to further assess the patient’s needs.15 While some physi­
cians still prefer the immediacy of the telephone, secure
electronic messaging tools are beginning to supplement
phone calls and beepers to facilitate communication among
physicians.15,16
Privacy and security issues
Perhaps the most fundamental choice physicians must
make when selecting tools to communicate electronically
with each other and with patients is how they will manage
the privacy and security of the information exchanged.
The HIPAA (Health Insurance Portability and Accountabil­
ity Act) is ‘technology-neutral,’ in that it does not require any
set form of encryption or information safeguarding, and is
‘scalable,’ in that it allows small practices to do what they
can afford to do without requiring them to purchase expen­
sive communication security systems.15–17
For electronic communication, the physician should have
an informed consent form signed by each patient specific to
the form of communication being used, such as e-mail. The
form should verify the patient’s e-mail address; should
discuss the security risks involved, e.g. that other parties on
the patient’s end might have access to their e-mail accounts,
and that standard (unencrypted, non-secure) e-mail can be
intercepted by unintended parties; should discuss allowable
content of the communication; and should include a provi­
sion to hold the physician harmless if security is breached.
While there is no private right of action under the HIPAA,
i.e. a patient cannot sue physicians for breach of HIPAA’s
privacy or security provisions, the federal agencies that
oversee the HIPAA have recently announced plans to step-up
their audits, and they could conduct an inquiry if a patient
filed a complaint. Federal investigations seem more likely to
focus on hospitals than physician offices. Carelessness could
also have legal repercussions. For example, information
could be sent to the wrong recipient because of failure to
verify the address field before sending the message. Physi­
cians using standard e-mail should take as many practical
safeguards as possible to minimize liability exposure. This
could include a privacy and security disclaimer footer
on each e-mail; requesting the patient’s permission before
continuing to respond to certain issues by e-mail; limiting
the amount of medical detail in the messages, password-
protecting e-mail access on office and home workstations, as
well as on portable devices, such as PDAs and Blackberries,
in case they are lost.
Another way to alleviate security or HIPAA compliance
concerns is to leave out ‘protected health information’ (PHI)
in standard e-mail: data that both personally identifies a
Box 7.3  Deficiencies of electronic mail services for
the transmission of medical information
•
Lack of encryption or authentication
•
Can be used by anyone to access a physician if they simply know
the physician’s e-mail address
•
Have no ‘terms of service’ or legal disclaimers to protect
physicians
•
Can easily expose patient e-mail addresses and identities to
unintended third parties
•
Can breach patient privacy by using employer e-mail networks
•
Offer no charge capture function
•
Have no template or medical records features
•
Lack of consistency with HIPAA or medical liability insurance
company standards.

Pre-hospital management, transportation and emergency care
99
•
For burns less than 24 h old, only use lactated Ringer’s
solution. The staff physician will advise on the infusion
rate, which is calculated based on the percentage of
total body surface area burned.
Following physician-to-physician contact and collection of
all pertinent information, the physicians will make recom­
mendations regarding an appropriate mode of transporta­
tion. The options are based on distance to a referring unit,
patient complexity, and comprehensiveness of medical care
required. Options include:
•
Full medical intensive care unit transport with a
complete team, consisting of a physician, a nurse, and
a respiratory therapist from the burn facility
•
Medical intensive care transport via fixed wing or
helicopter with a team from a referring facility
•
Private plane with medical personnel to attend patient
•
Commercial airline
•
Private ground ambulance
•
Transport van with appropriate personnel.
Transport team composition
Because stabilization and care for a burned patient is so
specialized, team selection is of the utmost importance.
Traditionally, these patients were placed in an ambulance
with an emergency medical technician and transported with
few efforts made to stabilize the patient prior to transfer.
As levels of care and technology have evolved, the need
for specialized transport personnel has been increasingly
observed. Today most transport teams are made up of one
or more of the following healthcare members: a registered
nurse, a respiratory therapist, and/or a staff physician or
house resident. Because a large number of burned patients
require some type of respiratory support due to inhalation
injury or carbon monoxide intoxication, the respiratory
therapist and nurse team has proven to be an effective com­
bination. The background and training of nurses and thera­
pists differ in many ways, so such a team provides a larger
scope of knowledge and experience when both are utilized.
Team members ideally should be cross-trained so that each
member can function at the other’s level of expertise.
Training and selection
Since the transport team will work in a high-stress environ­
ment, often with life or death consequences, these individu­
als must be carefully selected. The selection process should
involve interviews with a nursing administrator, a director of
respiratory therapy, and a medical director of a transport
program.
Minimum requirements for transport team members
should include:
•
Transport nurse qualifications:
 a registered nurse;
 minimum of 6 months burn care experience;
 current cardiopulmonary resuscitation (CPR)
certification;
 advanced cardiac life support (ACLS) or pediatric
advanced life support (PALS) certification;
 ability to demonstrate clinical competency;
 observe two transports;
 a valid passport for international response.
•
Transport respiratory therapist qualifications:
 registered respiratory therapist with 6 months burn
care experience;
 licensed by appropriate regulatory agency as a
respiratory care practitioner;
 have current BLS;
 ACLS or PALS certification;
 ability to demonstrate clinical competency;
 observe two transports;
 demonstrate a working knowledge of transport
equipment;
 a valid passport for international response.
Because all of the care rendered by a transport team outside
a hospital is given as an extension of care from a transporting/
receiving facility, specific steps must be taken to protect staff
and physicians from medical liability and to provide consist­
ent care for all patients. Strict protocols are used to guide all
patient care; team members should be in constant commu­
nications with an attending physician regarding a patient’s
condition and the interventions to be considered. Team
members must be proficient at a number of procedures,
which may be needed during transport or while stabilizing
a patient prior to transport. To keep up with current techno­
logy and changes, team members should be included in
discussions of recent transports and current management
techniques, so that they can discuss patient care issues,
receive ongoing in-service education, and participate in a
review of the quality of transports.
Modes of transportation
Once the need for transport of a burned patient is estab­
lished, the decision must be rendered concerning what
type of transportation vehicle is to be used (Table 7.1).
There are two models of transport commonly used: ground
(ambulance/transport vehicle); air (helicopter, fixed wing),
or a combination of both. Factors to be considered when
selecting a mode of transportation are the condition of the
patient and the distance involved. The level of the severity
of the burn mandates the speed with which the team must
arrive in order to stabilize and transport a patient.18
Ground transport
Ground transport should be considered to cover distances of
70 miles or less; however, sometimes a patient’s condition
may require air transport, particularly helicopter transport,
even though the distance is within the 70-mile range. The
ground transport vehicle should be modified with special
equipment needed for intensive care transport, and there
must be enough room to comfortably seat team members
and equipment.
Air transport
Air transport is used primarily when long distances or the
critical nature of an injury separate a team from a patient.
Air transport, however, does present its own unique set of
problems. Aviation physiology is a specialty unto itself, and

Total Burn Care
7
100
can be reached should be evacuated prior to an increase in
altitude. Intrathoracic air and gastric air must be removed via
functional chest tubes or nasogastric tubes and periodically
checked during transport. Other factors that should be con­
sidered during air transport are reduced cabin pressure,
turbulence, noise and vibration, changes in barometric
pre­ssure, and acceleration/deceleration forces. Physiologic
changes which affect a patient and team members include
middle ear dysfunction, pressure-related problems with
sinuses, air expansion in a gastrointestinal tract, and motion
sickness. Utilizing transport vehicles that have pressurized
cabins can reduce or eliminate most of these problems.22
Helicopters and fixed wing aircraft
Helicopters and fixed wing aircraft both have advantages and
disadvantages related to patient care. Helicopters are widely
used for short-distance medical air transport. Medical heli­
copters, because they are usually based on hospital premises,
have no need to use airport facilities or ambulance services
and, thereby, reduce team response time. Helicopters are
able to land close to a referring hospital. Additionally, heli­
copters provide ease in loading and unloading patients and
equipment.18 The disadvantages of helicopter transport
include its limited range, usually less than 150 miles23 and
its non-pressurized cabin which limits the altitude at which
patients can be safely carried. The low-altitude capabilities
also subject the aircraft to variability in weather (i.e. fog,
rain, and reduced visibility); therefore, helicopter flights
experience much more interference due to the weather.
Other disadvantages include noise, vibrations, reduced air
speed, small working space, lower weight accommodation,
and high maintenance requirements.18
When long distances must be traveled (more than
150 miles) or when increased altitude is necessary, fixed
wing aircraft are considered as a viable mode of transport
for patients. The advantages of using fixed wing aircraft
include: long range capabilities, increased speed, ability to
fly in most weather conditions, control of cabin pressure and
temperature, larger cabin space, and more liberal weight
restrictions. Disadvantages of fixed wing aircraft include the
need for an airport with adequate runway length, difficulty
in loading and unloading patients and equipment, and the
pressure of air turbulence and noise.
Equipment
Because medical equipment used in intensive care units
has evolved tremendously in the last 10 years, there is no
reason that these advances should not be extended to the
equipment which is used in a transport program. The
transport team must be able to provide ICU level care
whenever needed. Most hospitals are well stocked and able
to provide necessary supplies for initial patient stabiliza­
tion and resuscitation; however, specialty items relating to
the care of burn patients may not be present or adequate
to meet the needs of burn victims. It is imperative that
adequate equipment be available to handle any situation,
which may arise during a transport process (Fig. 7.4). Extra
battery packs and electrical converters on fixed wing air­
craft are recommended due to long transport times and
delays caused by unforeseeable circumstances of weather
or logistics.
the gas laws play an important role in air transport and must
be taken into consideration.
Dalton’s law states that in a mixture of gases, the total
pressure exerted by the mixture is equal to the sum of the
pressures each would exert alone.19 This is important when
changing a patient’s altitude because as altitude increases,
barometric pressure decreases. The percentage of nitrogen,
oxygen, and carbon dioxide remain the same, but the partial
pressures exert change.20
Altitude is an important factor in the oxygenation of a
transported patient and constant monitoring by a team is
required under such circumstances. Boyle’s law states that
the volume of gas is inversely proportional to the pressure
to which it is subject at a constant temperature. This gas law
significantly affects patients with air leaks and free air in the
abdomen, because as altitude increases, the volume of air in
closed cavities also increases.21 For this reason, all air that
aC, complete team (doctor, nurse, respiratory therapist); N, nurse; RT, respiratory
therapist.
Table 7.1  Transport criteria: mode and team composition, burns
≤6 days post-burn
Weight
(kg)
% Burn
Distance
(miles)
Teama
Transport
mode
≤3
Any
≤75
C
Van, helicopter
76–250
C
Turboprop
airplane
≥251
C
Learjet
3.1–20
≤10
≤75
N-RT
Van, helicopter
76–500
N-RT
Commercial
flight or
turboprop
airplane
≥501
N-RT
Commercial
airplane or
Learjet
>10
≤75
C
Van, helicopter
76–250
C
Turboprop
airplane
≥251
C
Learjet
≥20
≤20
≤75
N
Commercial
flight or
turboprop
airplane
76–500
N-RT
≥501
N-RT
Commercial
airplane or
Learjet
>20
≤75
N
Van, helicopter
76–500
C
Turboprop plane
≥501
C
Jet
If any of the following criteria exist, the transport shall be changed to the fastest
mode with a complete team:
•
depressed mental status;
•
drug depression;
•
respiratory support;
•
unstable cardiovascular system;
•
presence of associated diseases;
•
decreased urine output/unresponsiveness to appropriate fluid administration;
•
absent or marginal venous access;
•
hypothermia unresponsive to corrective measures.

Pre-hospital management, transportation and emergency care
101
in-flight use by the US Air Force. The transport ventilator
weighs 1.5 pounds (0.68 kg), can be set to provide respira­
tory rates of between 6 and 250 breaths per minute, and
provides tidal volumes of between 5 and 1500 cc. This ven­
tilator is powered entirely by oxygen and requires no electri­
cal power. All timing circuit gases are delivered to the patient
so that operation of the ventilator does not consume addi­
tional oxygen. The I : E ratios are preset at the factory from
1 : 1 at frequencies of 250 cycles per minute to 1 : 5 at a rate
of 6 cycles per minute. As a result, breath stacking and unde­
sired over inflation due to air trapping may be avoided.25
Stabilization
One of the primary reasons for a specialized transport team
is to be able to transport a patient in as stable condition as
possible. Current practice has evolved to embrace the concept
that events during the first few hours following burn injury
may affect the eventual outcome of the patient; this is espe­
cially true with regard to fluid management and inhalation
injury. Stabilization techniques performed by the transport
team have been expanded to include procedures that are
usually not performed by nursing or respiratory personnel.
Such techniques include interpreting radiographs and labo­
ratory results and then conferring with fellow team members,
referring physicians, and the team’s own medical staff in
order to arrive at a diagnosis and plan for stabilization. The
transport team may perform such procedures as venous can­
nulation, endotracheal intubation, arterial blood gas inter­
pretation, and management of mechanical ventilators. Team
members may request new radiographs, in order to assess
catheter or endotracheal tube placement or to assess the
pulmonary system’s condition. Team members may aid in
the diagnosis of air leaks (pneumothorax) and evacuate the
pleural space of the lung by needle aspiration as indicated.
All of these procedures may be immediately necessary and
life-saving. Cross-training of all team members to be able to
perform the others’ jobs is recommended in order to safe­
guard patients in the event that any team member becomes
incapacitated during transport. All these skills can be learned
via experience in a burn intensive care unit, through formal
training seminars, and via a thorough orientation program.
Mature judgment, excellent clinical skills, and the ability to
function under stress are characteristics needed when select­
ing candidates for a transport program.
Patient assessment prior to transport
to a specialized burn care unit from a
referring hospital
Initial assessment upon arrival of a flight team should
include a list of standard procedures for determining a
burned patient’s current condition. First, a thorough review
of the patient’s history concerning the accident and past
medical history must be done. This process provides the
transport team with an excellent base from which to begin
to formulate a plan of action. The patient will certainly have
been diagnosed by a referring physician; however, a transport
team often finds problems overlooked in initial evaluations.
Since burn care is a specialized field, modes of treatment
Portable monitor
A portable ECG monitor capable of monitoring two pressure
channels should accompany all patients in transport. This
allows for continuous monitoring of heart rate, rhythm, and
arterial blood pressure. The second pressure channel may be
used for patients with a pulmonary artery catheter or those
who need intracranial pressure monitoring. This monitor
should be small and lightweight but able to provide a display
bright enough to be seen from several feet away. The monitor
should have its own rechargeable power supply which con­
tinuously charges while connected to an alternating current
(AC) power supply. One suitable unit is the Protocol Systems
Propaq 106 portable monitor. This monitor has two pressure
channels; it provides a continuous display of ECG, heart rate,
systolic, diastolic, and mean blood pressure; it can display
temperature and oxygen saturation; and it is also capable of
operating a non-invasive blood pressure cuff. High and low
alarms for each monitored parameter can be set, silenced, or
disabled by a trained operator.
Infusion pump
Continuous delivery of fluids and pharmacological agents
must not be interrupted during transport. Infusion pumps
can be easily attached to stretchers and are usually capable
of operating for several hours on internal batteries. These
devices should have alarms to warn of infusion problems
and should be as small and lightweight as possible.
Ventilator
Size, weight, and oxygen consumption are the primary con­
cerns in selecting transport ventilators. A weight under
5 pounds (2.2 kg) is desirable, and a ventilator’s dimensions
should make it easy to mount or to place on a bed. Orienta­
tion of controls should be along a single plane, and inadvert­
ent movement of dials should be difficult.24 The ventilator
breathing circuit and exhalation valve should be kept simple,
and incorrect assembly should be impossible. One type
of transport ventilator that has become popular is the
TXP transport ventilator. The TXP transport ventilator (Per­
cussionaire Corporation, Sand Point, ID) is a portable
pressure-limited time-cycled ventilator and is approved for
Figure 7.4  Typical equipment used in transport of a patient.

Total Burn Care
7
102
understand and anticipate the condition of the patient.
Additionally, all treatments, including invasive procedures,
must be recorded, along with a patient’s response to these
interventions.
Summary
Burn injuries present a major challenge to a healthcare team,
but an orderly, systematic approach can simplify stabiliza­
tion and management. A clear understanding of the patho­
physiology of burn injuries is essential for providing quality
burn care in the pre-hospital setting, at the receiving health­
care facility, and at the referring hospital prior to transport.
After a patient has been rescued from an injury-causing
agent, assessment of the burn victim begins with a primary
survey. Life-threatening injuries must be treated first, fol­
lowed by a secondary survey, which documents and treats
other injuries or problems. Intravenous access may be estab­
lished in concert with logical/regional medical control and
appropriate fluid resuscitation begun. Burn wounds should
be covered with clean, dry sheets; and the patient should
be kept warm with blankets to prevent hypothermia. The
patient should be transported to an emergency room in the
most appropriate mode available.
At the local hospital, it should be determined if a burn
patient needs burn center care according to the American
Burn Association Guidelines. In preparing for organizing a
transfer of a burn victim, consideration must be given to the
continued monitoring and management of the patient
during transport. In transferring burn patients, the same
priorities developed for pre-hospital management remain
valid. During initial assessment and treatment and through­
out transport, the transport team must ensure that the
patient has an adequate airway, breathing, circulation, fluid
resuscitation, urine output, and pain control. Ideally, trans­
port of burn victims will occur through an organized,
protocol-driven plan, which includes specialized transport
mechanisms and personnel. Successful transport of burn
victims, whether in the pre-hospital phase or during inter-
hospital transfer, requires careful attention to treatment
priorities, protocols, and details.
Further reading
American Burn Association. Advanced Burn Life Support Providers
Manual. Chicago, IL: American Burn Association; 2010.
American Burn Association. Radiation injury. Advanced Burn Life
Support Manual: Appendix 1. Chicago, IL: American Burn
Association; 2010.
Brooks RG, Menachemi N. Physician’s use of email with patients:
factors influencing electronic communication and adherences to
best practices. J Med Internet Res. 2006;8(1):e2.
Herndon DN, Rutan RL, Rutan TC. Management of the pediatric
patient with burns. J Burn Care Rehabil. 1993;14(1):3-8.
Mandl KD, Kohane IS, Brandt AM. Electronic patient-physician
communication: problems and promise. Ann Intern Med.
1998;129(6):495-500.
may vary greatly outside the burn treatment community.
Frequently, a referring hospital is not well versed in the treat­
ment of burn victims and should not be expected to display
the expertise found among clinicians who work with such
patients’ everyday. Thus, the next step in stabilizing a burn
patient is a physical assessment done by a transport team.
These procedures should always be performed in the same
order and in a structured fashion. Assessment of a burn
patient begins with the ABCs of a primary survey, including
airway, breathing, circulation, cervical spine immobilization,
and a brief baseline neurological examination. All patients
should be placed on supplemental oxygen prior to transport
in order to minimize the effects of altitude changes on oxy­
genation. Two IV lines should be started peripherally with a
16-gauge catheter or larger. Ideally, IV lines should be placed
in non-burned areas but may be placed through a burn if
they are the only sites available for cannulation. Intravenous
lines should be sutured in place because venous access may
not be available after the onset of generalized edema. The
fluid of choice for initial resuscitation is lactated Ringer’s
solution.
In addition to initial stabilization procedures, blood
should be obtained for initial laboratory studies if not
already done. Initial diagnostic studies include hematocrit,
electrolytes, urinalysis, chest X-ray, arterial blood gas, and
carboxyhemoglobin levels. Any correction of laboratory
values must be done prior to transfer and verified with repeat
studies. Electrocardiographic monitoring should be insti­
tuted on any patient prior to transfer. Electrode patches may
be a problem to place because the adhesive will not stick to
burned skin. If alternative sites for placement cannot be
found, an option for monitoring is to insert skin staples and
attach the monitor leads to them with alligator clips. This
provides a stable monitoring system, particularly for the agi­
tated or restless patient who may displace needle electrodes.
A Foley catheter with an urometer should be placed to accu­
rately monitor urine output. Acceptable hydration is indi­
cated by a urine output of more than 30 mL/h in an adult
(5 mL/kg/h) and at least 1 mL/kg/h in a child.
With the exception of escharotomies, open chest wounds,
and actively bleeding wounds, management during trans­
port consists of simply covering wounds with a topical anti­
microbial agent or a biological dressing. Wet dressings are
contraindicated because of the decreased thermoregulatory
capacity of patients sustaining large burns and the possibility
of hypothermia. To combat the problem of a gastric ileus,
a nasogastric tube should be inserted in all burn patients
in order to decompress the stomach. This is especially
important for patients being transferred at high altitudes.
Hypothermia can be avoided or minimized by the use of
heated blankets and/or aluminized Mylar space blankets.
The patient’s rectal temperature must be kept between 37.5
and 39.0°C.
A clear, concise, chronological record of the mechanism of
injury and assessment of airway, breathing, and circulation
should be kept in the field and en route to the hospital.
This information is vital for a referring facility to better
 
Access the complete reference list online at

Pre-hospital management, transportation and emergency care
102.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
References
1. Boswick JA, ed. The Art and Science of Burn Care. Rockville, MD:
Aspen; 1987.
2. Dimick AR. Triage of burn patients. In: Wachtel TL, Kahn V,
Franks HA, eds. Current Topics in Burn Care. Rockville, MD: Aspen
Systems; 1983:15-18.
3. Wachtel TL. Initial care of major burns. Postgrad Med.
1989;85(1):178-196.
4. American Burn Association. Advanced Burn Life Support Providers
Manual. Chicago, IL: American Burn Association; 2010.
5. American Burn Association. Radiation injury. Advanced Burn Life
Support Manual. Appendix 1. Chicago, IL: American Burn
Association; 2010.
6. Bartholomew CW, Jacoby WD. Cutaneous manifestations of
lightning injury. Arch Dermatol. 1975;26:1466-1468.
7. Committee on Trauma, American College of Surgeons. Burns.
In: Advanced Trauma Life Support Course Book. Chicago: American
College of Surgeons; 1984:155-163.
8. Rauscher LA, Ochs GM. Pre-hospital care of the seriously burned
patient. In: Wachtel TL, Kahn V, Franks HA, eds. Current Topics in
Burn Care. Rockville, MD: Aspen Systems; 1983:1-9.
9. Goldfarb JW. The burn patient, Air Medical Crew National Standards
Curriculum. Phoenix: ASHBEAMS; 1988.
10. Marvin JA, Heinback DM. Pain control during the intensive care
phase of burn care. Crit Care Clin. 1985;1:147-157.
11. Mlcak RP, Helvick B. Protocol for securing endotracheal tubes in a
pediatric burn unit. J Burn Care Rehabil. 1987;8:233-237.
12. Herndon DN, Desai MH, Abston S, et al. Residents manual.
Galveston: Shriners Burns Hospital, and the University of Texas
Medical Branch; 1992:1-17.
13. Collini FJ, Kealy GP. Burns: a review and update. Contemp Surg.
1989;34:75-77.
14. Herndon DN, Rutan R, Rutan T. Management of the pediatric
patient with burns. J Burn Care Rehabil. 1993;14(1):3-8.
15. Fotsch E. Online physician communication. Physician’s News
Digest 2008. Online. Available:
16. Mandl KD, Kohane IS, Brandt AM. Electronic patient-physician
communication: problems and promise. Ann Intern Med.
1998;129(6):495-500.
17. Brooks RG, Menachemi N. Physician’s use of email with patients:
factors influencing electronic communication and adherences to
best practices. J Med Internet Res. 2006;8(1):e2.
18. Roy LR, Cunningham W. Transport. Neonatal and Pediatric
Respiratory Care. St Louis, MO: Mosby; 1988:321.
19. McPhearson SP. Respiratory Therapy Equipment. 3rd ed. St Louis,
MO: Mosby; 1986.
20. US Navy Flight Surgeons’ Manual. US Government publication;
1968.
21. Jacobs B. Emergency Patient Care, Pre-hospital Ground and Air
Procedures. New York: Macmillan; 1983.
22. McNeil EL. Airborne Care of the Ill and Injured. New York: Springer-
Verlag; 1983.
23. Federal Regulations for Pilots. Government publication; 1987.
24. Branson RD. Intrahospital transport of critically ill, mechanically
ventilated patients. Respir Care. 1992;37:775-793.
25. Johannigman JA, Branson RD, Cambell R, et al. Laboratory and
clinical evaluation of the MAX transport ventilator. Respir Care.
1990;35:952-959.

Pathophysiology of burn shock
and burn edema
George C. Kramer
Introduction and historical notes
Cutaneous thermal injury involving more than one-third of
the total body surface area (TBSA) invariably results in the
severe and unique derangements of cardiovascular function
known as burn shock. Shock is an abnormal physiologic
state in which tissue perfusion is insufficient to maintain
adequate delivery of oxygen and nutrients and removal of
cellular waste products. Before the nineteenth century, inves­
tigators demonstrated that after a burn, fluid is lost from the
blood and blood becomes thicker; and in 1897, saline infu­
sions for severe burns were first advocated.1,2 However, a
more complete understanding of burn pathophysiology was
not reached until the work of Frank Underhill.3 He demon­
strated that unresuscitated burn shock was associated with
increased hematocrit values in burned patients, which are
secondary to fluid and electrolyte loss after burn injury.
Increased hematocrit values occurring shortly after severe
burn were interpreted as a plasma volume deficit. Cope and
Moore4 showed that the hypovolemia of burn injury resulted
from fluid and protein translocation into both burned and
non-burned tissues.
Animal and clinical studies have established the impor­
tance of fluid resuscitation for burn shock. Investigations
have focused on correcting the rapid and massive fluid
sequestration in the burn wound and the resultant hypo­
volemia. The peer-reviewed literature contains a large
experimental and clinical database on the circulatory and
microcirculatory alterations associated with burn shock and
edema generation in both the burn wound and non-burned
tissues. During the last 50 years, research has focused on
identifying and defining the mechanisms and effects of the
many inflammatory mediators produced and released after
burn injury.5
Burn shock is a complex process of circulatory and micro­
circulatory dysfunction that is not easily or fully repaired by
fluid resuscitation. Severe burn injury results in significant
hypovolemic shock and substantial tissue trauma, both of
which cause the formation and release of many local and
systemic mediators.6–8 Burn shock results from the interplay
of direct tissue injury, hypovolemia, and the release of mul­
tiple mediators of inflammation, with effects on both the
microcirculation and the function of large vessels, heart and
lungs. Subsequently, burn shock continues as a significant
pathophysiologic state, even if hypovolemia is corrected.
Increases in pulmonary and systemic vascular resistance
(SVR) and myocardial depression occur despite adequate
preload and volume support.8–12 Such cardiovascular dys­
functions can further exacerbate the whole body inflam­
matory response into a vicious cycle of accelerating organ
dysfunction.7,8,13 Hemorrhagic hypovolemia with severe
mechanical trauma can provoke a similar form of shock.
This chapter examines our current understanding of the
pathophysiology of the early events in burn shock, focusing
on the many facets of organ and systemic effects resulting
directly from hypovolemia and circulating mediators. Inflam­
matory shock mediators, both local and systemic, that
are implicated in the pathogenesis of burn shock include
histamine, serotonin, bradykinin, nitric oxide, oxygen free
radicals and products of the eicosanoid acid cascade, pros­
taglandin, thromboxane, tumor necrosis factor, and inter­
leukins. Additionally, certain hormones and mediators of
cardiovascular function are elevated severalfold after burn
injury; these include epinephrine, norepinephrine, vaso­
pressin, angiotensin II, and neuropeptide-Y. Other media­
tors and unknown factors yet to be defined are also involved.
Understanding the complex mechanism of the pathophysi­
ologic actions of these mediators may be of great relevance
when optimally effective therapies are designed. The hope
is that improved early treatment of burn shock, perhaps
through individualized fluid resuscitation protocols and
methods of mediator blockade, can be developed to
ameliorate the severity of organ dysfunction. Effective burn
resuscitation and treatment of burn shock remains a
major challenge in medicine.
Hypovolemia and rapid edema formation
Burn injury causes extravasation of plasma into the burn
wound. Extensive burn injuries are hypovolemic in nature
and characterized by hemodynamic changes similar to those
that occur after hemorrhage, including decreased plasma
volume, cardiac output, and urine output; and an increased
systemic vascular resistance with resultant reduced periph­
eral blood flow.6,8,14–16 However, as opposed to a fall in hema­
tocrit with hemorrhagic hypovolemia due to transcapillary
refill, an increase in hematocrit and hemoglobin concentra­
tion will often appear despite fluid resuscitation. As in the
treatment of other forms of hypovolemic shock, the primary
initial therapeutic goal is to promptly restore vascular volume
and to preserve tissue perfusion in order to minimize tissue
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00008-4
CHAPTER 8 
Access the complete reference list online at

Total Burn Care
8
104
formation was rapid, with over 50% occurring in the first
hour, maximum water content was not present until 12–24
hours after burn injury.
Normal microcirculatory fluid exchange
An understanding of the physiologic mechanisms of the
rapid formation of burn edema requires an understanding
of the mechanisms of microvascular fluid balance. Under
physiologic steady-state conditions blood pressure in capil­
laries causes a filtration of fluid into the interstitial space.
Filtered fluid may be partially reabsorbed into the circulation
at the venous end of capillaries and venules, but the bulk of
the filtrate is removed from the interstitial space by lym­
phatic drainage.24–26 Fluid transport across the microcircula­
tory wall in normal and pathological states is quantitatively
described by the Landis–Starling equation:
J
K
P
P
v
f
c
if
p
if
=
−
(
) −
−
(
)
[
]
σ π
π
This describes the interaction of physical forces that govern
fluid transfer between vascular and extravascular compart­
ments. Jv is the volume of fluid that crosses the microvascu­
lature barrier. Kf is the capillary filtration coefficient, which
is the product of the surface area and hydraulic conductivity
of the capillary wall; Pc is the capillary hydrostatic pressure;
Pif is the interstitial fluid hydrostatic pressure; πp is the colloid
osmotic pressure of plasma; πif is the colloid osmotic pres­
sure of interstitial fluid; σ is the osmotic reflection coeffi­
cient. Edema occurs when the lymphatic drainage (JL) does
not keep pace with the increased Jv (Fig. 8.1).
Mechanisms of burn edema
Analyzing the factors that connect the physiological deter­
minants of transmicrovascular fluid flux (i.e. the Landis–
Starling equation) shows that edema forms with increased
ischemia. However, burn resuscitation is complicated not
only by severe burn wound edema, but also by extravasated
and sequestered fluid and protein in non-burned soft tissue.
Large volumes of resuscitation solutions are required to
maintain vascular volume during the first several hours after
an extensive burn. Data suggest that despite fluid resuscita­
tion normal blood volume is not restored until 24–36 hours
after large burns.17
Edema develops when the rate by which fluid is filtered
out of the microvessels exceeds the flow in the lymph vessels
draining the same tissue mass. Edema formation often
follows a biphasic pattern. An immediate and rapid increase
in the water content of burn tissue is seen in the first hour
after burn injury.15,18 A second and more gradual increase in
fluid flux of both the burned skin and non-burned soft tissue
occurs during the first 12–24 hours after burn injury.7,18 The
amount of edema formation in burned skin depends on the
type and extent of injury15,19 and on whether fluid resuscita­
tion is provided, as well as the type and volume of fluid
administered.20 Fluid resuscitation elevates blood flow and
capillary pressure, thereby contributing to further fluid
extravasation. Without sustained IV replacement of vascular
fluid losses edema formation is somewhat self-limited, as
tissue blood flow and capillary pressure decrease. Edema
formation in thermally injured skin is characterized by an
extremely rapid onset. Tissue water content can double
within the first hour after burn.15,21 Leape found a 70–80%
increase in water content in a full-thickness burn wound 30
minutes after burn injury, with 90% of this change occurring
in the first 5 minutes.16,22,23 There was only a modest increase
in burn wound water content after the first hour in non-
resuscitated animals. In resuscitated animals or animals with
small wounds, adequate tissue perfusion continues to ‘feed’
the edema for several hours. Demling et al.18 used dichro­
matic absorptiometry to measure edema development
during the first week after an experimental partial-thickness
burn injury on one hindlimb in sheep. Although edema
Figure 8.1  The Landis–Starling equation.
Kf, σ
Jv
Pif
Pc
COPc
COPp
Capillary
Proteoglycan
Lymph
flow
Cell–collagen
attachment
integrin α2β1
Collagen
bundles
Hyaluronan
Capillary hydrostatic
pressure
Interstitial fluid
pressure
Plasma colloid
osmotic pressure
Interstitial fluid
colloid osmotic
pressure
Net capillary
filtration

Pathophysiology of burn shock and burn edema
105
studies using the vascular occlusion technique in the
scalded hindlimb of dogs, Pc doubled from ~25 mmHg to
~50 mmHg during the first 30 minutes after burn injury,
and slowly returned to baseline over 3 hours.47
Interstitial hydrostatic pressure (Pif)
An initially surprising, but now well-verified, finding is that
Pif in dermis becomes extremely negative after thermal injury.
Using micropipettes and a tissue oncometer, Lund19 reported
that dermal Pif was rapidly reduced from its normal value of
−1 mmHg to less than −100 mmHg in isolated non-perfused
samples of skin. This large negative interstitial hydrostatic
pressure constitutes a powerful ‘suction force’ or imbibition
pressure, adding to the elevated capillary pressure in promot­
ing microvascular fluid filtration. In vivo measurements
show a temporary reduction of −20 to −30 mmHg; the less
negative Pif in vivo is due to the continued tissue perfusion
and fluid extravasation that relieves the imbibition pressure.
After resuscitation, Pif was reported increased to a positive
value of 1–2 mmHg in one study.48,49 On the other hand,
Kinsky50 reported a continued negative pressure providing a
partial explanation for the sustained edema for the first four
hours post injury. During the first several days post burn
injury tissue volume and hydration are greatly elevated, with
a slight decrease or no change in Pif. By definition this implies
an elevated interstitial compliance, which is likely to be the
main mechanism that sustains burn edema.
The size of the decrease in Pif establishes it as the factor
predominantly responsible for both the initial rapid devel­
opment of edema and the sustained edema. The mechanism
for the large decrease in Pif is due, at least in part, to the
release of cellular tension exerted on the collagen and micro­
fibril networks in the connective tissue via the collagen-
binding β1-integrins. The integrins are transmembrane
adhesion receptors that mediate cell–cell and cell–matrix
adhesion, thereby allowing the glycosaminoglycan ground
substance, which is normally underhydrated, to expand and
take up fluid.58 The magnitude of the reduction in Pif is also
observed in several non-burn inflammatory reactions (48/80
and PAF). However, these mediator-induced changes are
milder, with a lowering of Pif to −5 to −10 mmHg. The much
greater decrease in burn injury versus mediator-induced
inflammation suggests additional mechanisms in burn
Kf, Pc or πif, and with decreased Pif, σ and πp. Burn edema is
unique in its rapidity compared to other types of edema,
because it is only in burn edema that all of these variables
change significantly in the direction required to increase
fluid filtration. Each Starling variable is discussed indi­
vidually below. For perspective, the normal imbalance or
net filtration pressure across the microvascular wall is
only 0.5–1 mmHg. Thus an increased pressure gradient of
1 mmHg increases filtration two- to threefold, and an
increase of 10 mmHg would increase filtration 10–20-fold.
Capillary filtration coefficient (Kf)
Burn injury causes direct and indirect mediator-modulated
changes in the permeability of the blood–tissue barrier of
the capillaries and venules. Arturson and Mellander27 showed
that, in the scalded hindlimb of dogs, Kf immediately
increased two to three times, suggesting that the hydraulic
conductivity (water permeability) of the capillary wall
increased. Kf is a function of both hydraulic conductivity and
the capillary surface area. Thus, local vasodilation and micro­
vascular recruitment contribute to the increased Kf in addi­
tion to increased hydraulic conductivity. Measuring Kf and
the rate of edema formation (Jv) allowed Arturson and Mel­
lander to determine the changes in transcapillary forces nec­
essary to account for the increased capillary filtration. Their
calculations indicated that a transcapillary pressure gradient
of 100–250 mmHg was required to explain the extremely
rapid edema formation that occurred in the first 10 minutes
after a scald injury. They concluded that only a small fraction
of the early formation of burn edema could be attributed to
the changes in Kf and permeability. They further suggested
that osmotically active molecules generating sufficiently
large osmotic reabsorption pressures are released from burn-
damaged cells. This hypothesis was never confirmed, and
subsequent studies described below show that such large
increases in filtration force could be attributed to increased
Pc, and particularly to a large decrease in Pif (Table 8.1).
Capillary pressure (Pc)
In most forms of shock capillary pressure decreases as venous
pressure decreases and less arterial pressure is transferred to
the capillary due to arteriolar vasoconstriction. However, in
Table 8.1  Effect of burn injury on changes in the Starling equation variables
Variable
Normal or baseline
Post-burn
Δ
References
Pc
~25 mmHg
~50 mmHg
↑ ~25 mmHg
47
ΠP
20–28 mmHg
15 to 18 mmHg
↓ ~10 mmHg
51, 52
Pi
−2 to 0 mmHg
~100 mmHg non-resuscitated
non-perfused skin and −5 mmHg perfused skin
↓ ~100 mmHg
↓ 3–5 mmHg
19, 53–55
Πif
10–15 mmHg
13–18 mmHg in burn wound
↓ and with resuscitation hypoproteinemia in non-burned skin
↑ ~3 mmHg
52, 54, 55
σ
~0.9
~0.5
↓ ~0.4
47, 56, 57
Kf
~0.003 mL/min/
mmHg/100 g (leg)
↑ 2–5×
27, 57

Total Burn Care
8
106
colloid osmotic pressure in lymph from burned skin initially
increases 4–8 mmHg after burn injury.56 However, more
direct measurements of πif using wick sampling14,20,52,64 or
tissue sampling techniques14,25 show only modest initial
increases in πif of 1–4 mmHg in the early non-resuscitated
phase of burn injury. With resuscitation, πp falls and then πif
decreases, as the protein concentration of capillary filtrate
remains less than that of plasma despite an increased perme­
ability. The osmotic reflection coefficient, σ, decreases with
burns, but never equals zero, thus protein concentration in
filtrate is less than in plasma even in burned skin.56 Com­
pared to non-burned skin the πi remains significantly higher
in the burn wound, supporting the view that sustained
increases in protein permeability contribute to the persist­
ence of burn edema.14,25,50 However, compared with the large
changes in Pc and particularly Pif, increased capillary protein
permeability is not the predominant mechanism for the
early rapid rate of edema formation in injured skin.48
Non-burned tissue
Generalized edema in soft tissues not directly injured is
another characteristic of large cutaneous burns. Brouhard
et al.65 reported increased water content in non-burned skin
even after a 10% burn, with the peak edema occurring 12
hours post burn. Arturson reported an increased transcapil­
lary fluid flux (lymph flow) from non-burned tissue and a
transient increase in permeability, as measured by an increase
in the lymph concentration of plasma protein and macro­
molecular dextran infused as a tracer.15,21,59 Harms et al.56
extended these findings by measuring changes in lymph flow
and protein transport in non-injured soft tissue for 3 days
after injury. They found that skin and muscle permeability
(flank lymph from sheep) were elevated for up to 12 hours
post burn for molecules the size of albumin and immu­
noglobulin G, but the microvascular permeability of the
lung (lymph for caudal mediastinal node) showed no
increase. Maximum increased lymph flow and tissue water
content were observed to correlate with the severe hypopro­
teinemia that occurred during the early resuscitation period
of a 40% burn injury in sheep.8,61 The sustained increase in
water content and the elevated lymph flow of the non-
burned tissue after the return of normal permeability is likely
the result of the sustained hypoproteinemia.51,56,59,60
Demling and colleagues66 suggested that the edema could
be partially attributed to alterations in the interstitial
structure. They suggested that interstitial protein washout
increases the compliance of the interstitial space and that
water transport and hydraulic conductivity across the entire
blood–tissue–lymph barrier increased with hypoproteine­
mia. Several clinical and animal studies have established that
maintaining higher levels of total plasma protein concentra­
tion can ameliorate the overall net fluid retention and
edema.7,67 Non-burn edema can also be moderated by infu­
sion of non-protein colloids such as dextran, if the colloid
osmotic gradient is increased above normal.8,61 However, it
is not known whether either the correction of hypoproteine­
mia or the use of either albumin or dextran leads to improved
clinical outcome. It has been reported that the use of colloids
has no beneficial effect on edema in the burn wound.50,61
Use of hypertonic saline formulations as initial fluid
edema. These mechanisms remain to be identified, but may
result from the direct physical destruction of the connective
tissues by heat.
Osmotic reflection coefficient (σ)
The osmotic reflection coefficient is an index of the propor­
tion of the full osmotic pressure generated by the concentra­
tion gradient of plasma proteins across the capillary wall. A
σ = 1.0 represents a membrane impermeable to protein; σ =
0 represents a membrane that is completely permeable to
protein. In skin, the normal σ of albumin is reported to be
0.85–0.99.25,59 Increased capillary permeability to protein
causes a reduced σ, an effective reduction in the reabsorptive
oncotic gradient across the capillary wall and a resulting
increase in net fluid filtration. Lymph sampled from burned
skin has shown elevated protein concentrations consistent
with the large and sustained increases in capillary permeabil­
ity,15,56,59 whereas a transient and smaller increase in capillary
permeability occurs over 8–12 hours following injury in
other soft tissue not directly burned.56 Pitt et al.47 estimated
the σ for skin from dog hindpaw using a lymph washdown
technique and reported a normal σ of 0.87 for albumin and
a reduction to 0.45 after scald injury.
Plasma colloid osmotic pressure (πp)
The normal plasma protein concentration of 6–8 g/dL, and
its associated πp of 25–30 mmHg, produces a significant
transcapillary reabsorptive force counterbalancing other
Starling forces that favor filtration.14,25 Plasma colloid
osmotic pressure decreases in non-resuscitated burn injured
animals as protein-rich fluid extravasates into burn wounds,
and a significant volume of protein-poor transcapillary
reabsorption comes from non-burned tissue, such as skel­
etal muscle.14,51,52,60 Plasma is further diluted and πp is
further reduced after crystalloid resuscitation. Zetterstrom
and Arturson found that πp was reduced to half of the
normal values in burn patients; πp can decrease so rapidly
with resuscitation that the transcapillary colloid osmotic
pressure gradient (πp – πif) will approach zero or even
reverse to favor filtration and edema.51,52 Although it is
likely that some hypoproteinemia is inevitable after major
burn injury, animal and clinical studies using early colloid
resuscitation produce higher levels of πp than with crystal­
loid resuscitation alone.7,60,61 The degree of hypoproteine­
mia and reduced πp were reported to correlate with the total
volume of crystalloid solutions.60 Initial therapy with colloid
solution has always been advocated by some clinicians,7 but
the majority wait 8–24 hours after injury, reasoning that
some normalization of microvascular permeability in
injured tissue must occur before colloid therapy is cost
effective.8 In recent years there appears to be greater use of
albumin therapy earlier for burn resuscitation, and there is
new evidence for improved outcomes with albumin resus­
citation of burns.62,63
Interstitial colloid osmotic pressure (πif)
The πif in skin is normally 10–15 mmHg or about one-half
that of plasma.14,25 Experimental studies in animals using
lymph as representative of interstitial fluid suggest that the

Pathophysiology of burn shock and burn edema
107
Inflammatory mediators of burn injury
A veritable cornucopia of local and circulating mediators are
produced in the blood or released by cells after thermal
injury. These mediators clearly play important but complex
roles in the pathogenesis of edema and the cardiovascular
abnormalities of burn injury. Many mediators alter vascular
permeability and transcapillary fluid flux, either directly or
indirectly, by increasing the microvascular hydrostatic
pressure and surface area via the arteriolar vasodilation
superimposed on an already altered membrane. The exact
mechanism(s) of mediator-induced injury are of considera­
ble clinical interest, as this understanding would allow for
the development of pharmacologic modulation of burn
edema and shock by mediator inhibition. Unfortunately,
strategies directed at mediator blockage have only been effec­
tive in small localized burn wounds and have had little
clinical impact for care of patients with major burns.
Histamine
Histamine is a key mediator responsible for the early phase
of increased microvascular permeability seen immediately
after burn. Histamine causes large endothelial gaps to tran­
siently form as a result of the contraction of venular endothe­
lial cells.28 Histamine is released from mast cells in thermally
injured skin; however, the increase in histamine levels and
its actions are only transient. Histamine also can cause the
rise in capillary pressure (Pc) by arteriolar dilation and
venular contraction. Statistically significant reductions in
localized edema have been achieved with histamine blockers
and mast cell stabilizers when tested in animal models.28
Friedl et al.30 demonstrated that the pathogenesis of burn
edema in the skin of rats appears to be related to the interac­
tion of histamine with xanthine oxidase and oxygen radicals.
Histamine and its metabolic derivatives increased the cata­
lytic activity of xanthine oxidase (but not xanthine dehydro­
genase) in rat plasma and in rat pulmonary artery endothelial
cells. In thermally injured rats, levels of plasma histamine
and xanthine oxidase rose in parallel, in association with the
increase in uric acid. Burn edema was greatly attenuated by
treating rats with the mast cell stabilizer cromolyn, comple­
ment depletion, or the H2 receptor antagonist cimetidine,
but was unaffected by neutrophil depletion.29,34,82 Despite
encouraging results in animals, beneficial antihistamine
treatment of human burn injury has not been demonstrated,
although antihistamines are administered to reduce the risk
of gastric ulcers.
Prostaglandins
Prostaglandins are potent vasoactive autacoids synthesized
from the arachidonic acid released from burned tissue and
inflammatory cells, and contribute to the inflammatory
response of burn injury.36,83 Activated macrophages and neu­
trophils infiltrate the wound and release prostaglandin as
well as thromboxanes, leukotrienes and interleukin (IL)-1.
These wound mediators have both local and systemic effects.
Prostaglandin E2 (PGE2) and leukotrienes LB4 and LD4
increase microvascular permeability both directly and indi­
rectly.84 Prostacyclin (PGI2) is produced in burn injury and
therapies for burn shock can greatly reduce initial volume
requirements and net fluid volume (infused in minus urine
out).68,69 However, a rebound of fluid requirements and net
fluid can occur after early use of hypertonics and colloids.61,68
Retrospective analyses of patients correlating early albumin
use with fluid requirements show significant volume sparing
during the first post-burn day, but after 48 hours the effect
is less apparent.70
Altered cellular membranes and
cellular edema
In addition to a loss of capillary endothelial integrity, thermal
injury also causes change in the cellular membrane. In skel­
etal muscle cellular transmembrane potentials decrease away
from the site of injury.10 It would be expected that the directly
injured cell would have a damaged cell membrane, increas­
ing sodium and potassium fluxes and resulting in cell swell­
ing. However, this process also occurs in cells that are not
directly heat-injured. Micropuncture techniques have dem­
onstrated partial depolarization in the normal skeletal
muscle membrane potential of −90 mV to levels of −70 to
−80 mV; cell death occurs at −60 mV. The decrease in mem­
brane potentials is associated with an increase in intracel­
lular water and sodium.71–73 Similar alterations in skeletal
membrane functions and cellular edema have been reported
in hemorrhagic shock71,73 and in cardiac, liver, and endothe­
lial cells.74–76 Action potentials become dampened or non-
existent, with likely delays in signal propagation in nerves,
brain, skeletal muscle, heart, diaphragm, and gastrointesti­
nal organs. Encephalopathy, muscle weakness, impaired
cardiac contractility and gut dysfunction are associated with
major burn injury, and may be due in part to reduced mem­
brane potentials. Early investigators of this phenomenon
postulated that a decrease in ATP levels or ATPase activity
was the mechanism for membrane depolarization. However,
more recent research suggests that it may result from an
increased sodium conductance in membranes, or that an
increase in sodium–hydrogen antiport activity is the primary
mechanism.72,75 Resuscitation of hemorrhage rapidly restores
depolarized membrane potentials to normal, but resuscita­
tion of burn injury only partially restores the membrane
potential and intracellular sodium concentrations to normal
levels, demonstrating that hypovolemia alone is not totally
responsible for the cellular swelling seen in burn shock.77 A
circulating shock factor(s) is likely to be responsible for the
membrane depolarization.78–80 When plasma from a burn-
injured animal is superfused to an isolated muscle pre­
paration, membrane depolarization occurs. Further, the
depolarization can be reversed by changing the superfusion
to normal plasma or saline.77 Surprisingly, the molecular
characterization of such circulating factors have not been
elucidated, suggesting that it has a complex and perhaps
dynamic structure. Data suggest a large molecular weight,
> 80 kDa.81 Membrane depolarization may be caused by
different factors in different states of shock. Very little is
known about the time course of the changes in membrane
potential in clinical burns. More importantly, we do not
know the extent to which the altered membrane potentials
affect total volume requirements and organ function in burn
injury, or even shock in general.

Total Burn Care
8
108
burn edema when methysergide was given to dogs prior to
burn injury, but claimed that this was not attributable to
blunting of the regional vasodilator response. Zhang et al.
reported a reduction in skin blood flow after methysergide
administration to burned rabbits.93
Catecholamines
Circulating catecholamines epinephrine and norepinephrine
are released in massive amounts after burn injury.7,94,95 On
the arteriolar side of the microvessels these agents cause
vasoconstriction via α1-receptor activation, which tends to
reduce capillary pressure, particularly when combined with
the hypovolemia and the reduced venous pressure of burn
shock.28 Reduced capillary pressure may limit edema and
induce transcapillary refill and autoresuscitation of protein-
poor interstitial fluid reabsorbed from non-burned skin,
skeletal muscle, and visceral organs, especially in under-
resuscitated burn shock. Even in non-resuscitated animals,
plasma protein concentration falls. Further, catecholamines,
via β-agonist activity, may also partially inhibit increased
capillary permeability induced by histamine and bradyki­
nin.28 These potentially beneficial effects of catecholamines
may not be operative in directly injured tissue, and may also
be offset in non-burned tissue by the deleterious vasocon­
strictor and ischemic effects. The hemodynamic effects of
catecholamines will be discussed later in the chapter.
Oxygen radicals
Oxygen radicals play an important inflammatory role in all
types of shock, including burn. These short-lived elements
are highly unstable reactive metabolites of oxygen; each one
has an unpaired electron, making them strong oxidizing
agents.96 Superoxide anion (O2
–), hydrogen peroxide (H2O2),
and hydroxyl ion (OH–) are produced and released by acti­
vated neutrophils after any inflammatory reaction or reper­
fusion of ischemic tissue. The hydroxyl ion is believed to be
the most potent and damaging of the three. The formation
of the hydroxyl radical requires free ferrous iron (Fe2) and
H2O2. Evidence that these agents are formed after burn injury
is the increased lipid peroxidation found in circulating red
blood cells and biopsied tissue.29,96,97 Demling98 showed that
large doses of deferoxamine (DFO), an iron chelator, when
used for resuscitation of 40% TBSA in sheep, prevented sys­
temic lipid peroxidation and reduced the vascular leak in
non-burned tissue, while also increasing oxygen utilization.
However, DFO may have accentuated burned tissue edema,
possibly by increasing the perfusion of burned tissue.
Nitric oxide (NO) generated simultaneously with the
superoxide anion can lead to the formation of peroxynitrite
(ONOO–). The presence of nitrotyrosine in burned skin
found in the first few hours after injury suggests that pero­
xynitrite may play a deleterious role in burn edema.99 On
the other hand, the blockade of NO synthase did not reduce
burn edema, whereas treatment with the NO precursor
arginine does reduce burn edema.100 NO may be important
for maintaining perfusion and limiting the zone of stasis in
burn skin.101 Although the pro- and anti-inflammatory roles
of NO remain controversial, it would appear that the acute
beneficial effects of NO generation outweigh any deleterious
effect in burn shock.
is also a vasodilator, but also may cause direct increases in
capillary permeability. PGE2 appears to be one of the more
potent inflammatory prostaglandins, causing postburn
vasodilation and increased microvascular surface area in
wounds, which when coupled with the increased microvas­
cular permeability amplifies edema formation.85,86
Thromboxane
Thromboxane A2 (TXA2) and its metabolite, thromboxane B2
(TXB2) are produced locally in burn wounds by platelets.28
Vasoconstrictor thromboxanes may be less important in
edema formation; however, by reducing blood flow they can
contribute to a growing zone of ischemia under the burn
wound and can cause the conversion of a partial-thickness
wound to a deeper, full-thickness wound. The serum level of
TXA, and TXA2/PGI2 ratios are significantly increased in burn
patients.37 Heggers showed the release of TXB2 at the burn
wound, which was associated with local tissue ischemia,
while thromboxane inhibitors prevented the progressive
dermal ischemia associated with thermal injury and throm­
boxane release.35,87 The TXA2 synthesis inhibitor anisod­
amine also showed beneficial macrocirculatory effects by
restoring the hemodynamic and rheological disturbances
towards normal. Demling88 showed that topically applied
ibuprofen (which inhibits the synthesis of prostaglandins
and thromboxanes) reduces both local edema and prosta­
noid production in burned tissue without altering systemic
production. On the other hand, systemic administration of
ibuprofen did not modify early edema, but did attenuate the
postburn vasoconstriction that impaired adequate oxygen
delivery to tissue in burned sheep.38 Although cyclooxgenase
inhibitors have been used after burn injury, no convincing
benefit, nor their routine clinical use have been reported.
Kinins
Bradykinin is a local mediator of inflammation that increases
venular permeability. It is likely that bradykinin production
is increased after burn injury, but its detection in blood or
lymph can be difficult owing to the simultaneous increase
in kininase activity and the rapid inactivation of free kinins.
The generalized inflammatory response after burn injury
favors the release of bradykinin.89 Pretreatment of burn-
injured animals with aprotinin, a general protease inhibitor,
should have decreased the release of free kinin, but no effect
on edema was noted.90 On the other hand, pretreatment
with a specific bradykinin receptor antagonist was reported
to reduce edema in burn wounds in rabbits91 (Table 8.2).
Serotonin
Serotonin is released early after burn injury.32 This agent is
a smooth-muscle constrictor of large blood vessels. Antise­
rotonin agents such as ketanserin have been found to reduce
peripheral vascular resistance after burn injury, but not to
reduce edema.32 On the other hand, pretreatment with
methysergide, a serotonin antagonist, reduces hyperemic or
increased blood flow response in the burn wounds of rabbits
and reduces burn edema.91 Methysergide did not prevent
increases in the capillary reflection coefficient or permeabil­
ity.92 Ferrara et al.92 found a dose-dependent reduction of

Pathophysiology of burn shock and burn edema
109
prevented all pulmonary lipid peroxidation and inflamma­
tion. This suggests that the release of oxidants from burned
tissue was in part responsible for local burn edema, as well
as systemic inflammation and oxidant release.97 The failure
of neutrophil depletion to protect against the vascular per­
meability changes and the protective effects of the xanthine
oxidase inhibitors (allopurinol and lodoxamide trometh­
amine) suggests that plasma xanthine oxidase is the more
likely source of the oxygen radicals involved in the forma­
tion of burn edema. These oxygen radicals can increase vas­
cular permeability by damaging microvascular endothelial
cells.29,30 The use of antioxidants has been extensively inves­
tigated in animals, and some clinical trials suggest benefit.
Antioxidants (vitamin C and E) are routinely administered
to patients at many burn centers. High doses of antioxidant
ascorbate (vitamin C) have been found to be efficacious in
reducing fluid needs in burn-injured experimental animals
when administered postburn.104–106 Super-high doses (10–
20 g/day) of vitamin C were shown to effectively reduce
Antioxidants, namely agents that either bind directly to the
oxygen radicals (scavengers) or cause their further metabo­
lism, have been evaluated in several experimental studies.102,103
Catalase removes H2O2 and superoxide dismutase (SOD),
lessens radical O2
–, and is reported to reduce the vascular
loss of plasma after burn injury in dogs and rats.29,102
The plasma of thermally injured rats showed dramatic
increases in levels of xanthine oxidase activity, with peak
values appearing as early as 15 minutes after thermal injury.
Excision of the burned skin immediately after the injury
significantly diminished the increase in plasma xanthine
oxidase activity.29,30 The skin permeability changes were
attenuated by treating the animals with antioxidants (cata­
lase, SOD, dimethyl sulfoxide, dimethylthiourea) or an iron
chelator (DFO), thereby supporting the role of oxygen radi­
cals in the development of vascular injury as defined by
increased vascular permeability.29 Allopurinol, a xanthine
oxidase inhibitor, markedly reduced both burn lymph flow
and levels of circulating lipid peroxides, and further
Table 8.2  Cardiovascular and inflammatory mediators of burn shock
Mediators
Central cardiovascular effects
(at high concentrations)
Load tissue effects
References
Histamine
↓ Blood pressure
Hypovolemia
Arteriolar dilation; Venular constriction
↑ Blood flow
↑ Permeability
28–34
Prostaglandin E2 (PGE2)
↓ Systemic arterial and pulmonary arterial
blood pressure
Vasodilation
↑ Blood flow
↑ Permeability
28, 35, 36
Prostacyclin (PG12)
↓ Blood pressure
↑ Permeability
28
Leukotrienes
  LB4
  LD4
Pulmonary hypertension
28
Thromboxane A2 (TXA2)
Thromboxane B2 (TXB2)
GI ischemia
Pulmonary hypertension
Vasodilation
↑ Blood flow
↑ Permeability
35, 37–39
Bradykinin
↓ Blood pressure
Hypovolemia
Vasodilation, ↑ Permeability
28, 33
Serotonin
↑ Permeability
32
Catecholamines
  Epinephrine
  Norepinephrine
↑ Heart rate
↑ Blood pressure
↑ Metabolism
Vasoconstriction (receptors); Vasodilation (β2
receptors in muscle); block ↑ permeability due to
histamine & bradykinin via β receptors
28, 31, 40, 41
Oxygen radicals:
  Superoxide
  Anion (O2
−)
  Hydrogen peroxide (H2O2)
  Hydroxyl Ion (OH−)
  Peroxynitrite (ONOO−)
Cardiac dysfunction
Tissue damage
↑ Permeability
28–30, 42
Platelet aggregation factor
↑ Blood pressure
Vasoconstriction
43–45
Angiotensin II
GI ischemia
↑ Blood pressure
Vasoconstriction
46
Vasopressin
GI ischemia
↑ Blood pressure
Vasoconstriction
46
Enhanced microvascular blood flow typically increases capillary surface area.
Permeability typically refers to protein permeability of the microvascular exchange vessels, which is often linked to hydraulic conductivity.

Total Burn Care
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110
ameliorate or inhibit the fluid extravasation induced by
thermal injury. Topically applied local anesthetic lidocaine/
prilocaine cream has been reported to be effective in reduc­
ing albumin extravasation in small burns in experimental
animals.113 The inositol triphosphate analog α-trinositol has
also been reported to be effective in reducing postburn
edema when administered after injury.114–116 Even though
α-trinositol showed promising effects in animal experiments
and also seemed to reduce pain in pilot clinical projects, its
clinical application is not reported.
Hemodynamic consequences of acute burns
The cause of reduced cardiac output (CO) during the resus­
citative phase of burn injury has been the subject of consid­
erable debate. There is an immediate depression of cardiac
output before any detectable reduction in plasma volume.
The rapidity of this response may result from impaired elec­
trical activity of cardiac nerves and muscle and increased
afterload due to vasoconstriction. Soon after injury a devel­
oping hypovolemia and reduced venous return undeniably
contribute to the reduced cardiac output. The subsequent
persistence of reduced CO after apparently adequate fluid
therapy, as evidenced by restoration of arterial blood pres­
sure and urinary output, has been attributed to circulating
myocardial depressant factor(s), which possibly originates
from the burn wound.11,12 Demling et al.18 showed a 15%
reduction in CO despite aggressive volume replacement pro­
tocol after a 40% scald burn in sheep. However, there are
also sustained increases in catecholamine secretion and ele­
vated systemic vascular resistance for up to 5 days after burn
injury.94,111 Michie et al.117 measured CO and SVR in anesthe­
tized dogs resuscitated after burn injury. They found that CO
fell shortly after injury and then returned toward normal;
however, reduced CO did not parallel the blood volume
deficit. They concluded that the depression of CO resulted
not only from decreased blood volume and venous return,
but also from an increased SVR and from the presence of a
circulating myocardial depressant substance. After the resus­
citation phase of burn shock, patients can have supranormal
CO. This is associated with a hypermetabolic state and sys­
temic inflammatory response syndrome (SIRS).
Myocardial dysfunction
Myocardial function can be compromised after burn injury
due to the right heart overload and direct depression of
contractility shown in isolated heart studies.118,119 Increases
in the afterload of both the left and the right heart result
from elevations in SVR and PVR. Stroke volume and CO can
be maintained despite contractile depression by augmented
adrenergic stimulation, albeit at a cost of increased myocar­
dial oxygen demands. The right ventricle has a minimal
capacity to compensate for increased afterload. In severe
cases, desynchronization of the right and left ventricles is
deleteriously superimposed on a depressed myocardium.120
Kinsky121 demonstrated both systolic and diastolic dysfunc­
tion in burn-injured children during the first few weeks post
injury. Burn injury >45% TBSA can produce intrinsic con­
tractile defects. Several investigators reported that aggressive
early and sustained fluid resuscitation failed to correct left
volume requirements in one clinical trial, but were ineffec­
tive in others, albeit with somewhat different doses.107,108
High-dose vitamin C has not received wide clinical use.
Platelet aggregation factor
Platelet aggregation (or activating) factor (PAF) can increase
capillary permeability and is released after burn injury.44,90
Ono et al.44 showed in scald-injured rabbits that TCV-309
(Takeda Pharmaceutical Co Ltd., Japan), a PAF antagonist,
infused soon after burn injury, blocked edema formation in
the wound and significantly inhibited PAF increase in the
damaged tissue in a dose-dependent manner. In contrast, the
superoxide dismutase content in the group treated with
TCV-309 was significantly higher than that of the control
group. These findings suggest that the administration of
large doses of a PAF antagonist immediately after injury may
reduce burn wound edema and the subsequent degree of
burn shock by suppressing PAF and superoxide radical
formation.
Angiotensin II and vasopressin
Angiotensin II and vasopressin or antidiuretic hormone
(ADH), are two hormones that participate in the normal
regulation of extracellular fluid volume by controlling
sodium balance and osmolality through renal function and
thirst.28 During burn shock sympathetic tone is high and
volume receptors are stimulated, and both hormones are at
supranormal levels in the blood. Both are potent vasocon­
strictors of terminal arterioles with less effect on the venules.
Angiotensin II may be responsible for the selective gut and
mucosal ischemia, which can cause translocation of endo­
toxins and bacteria and the development of sepsis and even
multiorgan failure.109,110 In severely burn-injured patients
angiotensin II levels were elevated two to eight times normal
in the first 1 to 5 days after injury, with peak levels occurring
on day 3.111 Vasopressin had peak levels of 50 times normal
upon admission and declined towards normal over the first
5 days after burn injury. Along with catecholamines, vaso­
pressin may be largely responsible for increased system vas­
cular resistance and left heart afterload, which can occur in
resuscitated burn shock. Sun et al.46 used vasopressin-
receptor antagonists to improve hemodynamics and survival
time in rats with burn shock, whereas vasopressin infusion
exacerbated burn shock.
Corticotropin-releasing factor
Corticotropin-releasing factor (CRF) has proved to be effica­
cious in reducing protein extravasation and edema in burned
rat paw. CRF may be a powerful natural inhibitory mediator
of the acute inflammatory response of the skin to thermal
injury.112
Other approaches to pharmacological
attenuation of burn edema
Multiple reports on edema-reducing strategies using known
burn mediator-blocking agents have been discussed above.
However, there are other hypothesized approaches to

Pathophysiology of burn shock and burn edema
111
the result of increased blood viscosity secondary to the
hemoconcentration.
Hilton and others performed experiments in anesthetized
dogs in which infusion of various peripheral vasodilators
improved CO after burn injury.117,134 They demonstrated a
reduction in the peripheral vascular resistance and aug­
mented CO after verapamil, but the myocardial force of
contraction remained depressed. Pruitt et al. examined in a
group of burn patients the hypothesis that increased sympa­
thetic activity contributes to CO reduction.135 They showed
a higher CO with treatment using the vasodilator hydrala­
zine along with the reduced SVR.
There are several organs particularly susceptible to
ischemia, organ dysfunction and organ failure when burn
resuscitation is delayed or inadequate. These include the
kidney and the gastrointestinal tract. Renal ischemia can
result directly from hypovolemia and increased sympathetic
tone, but elevations in serum free hemoglobin, and particu­
larly myoglobin, correlate with increased renal failure.136,137
Renal failure rates have declined dramatically owing to
standardized regimens of adequate fluid therapy, but when
therapy is delayed or associated with hypotension acute
renal failure is not uncommon.136,137
An occult hypoxia can result from vasoconstriction of
the gastrointestinal tract, which can occur despite appar­
ently ‘adequate’ resuscitation.110,138 Bacterial and endotoxin
translocation that reduces mucosal pH and can contribute
to the development of sepsis is a consequence of visceral
ischemia.
Cerebropathy is not uncommon after large cutaneous
burns, particularly in children, but the exact cause remains
unclear. Studies in anesthetized sheep subjected to a 70%
TBSA scald show that cerebral autoregulation is well main­
tained in the immediate postburn period, but six hours after
resuscitation increased cerebral vascular resistance reduced
cerebral blood flow 50%.139
Edema in non-burned tissue
Lungs
In large burns there is a pronounced increase in pulmonary
vascular resistance (PVR) that corresponds with the increased
SVR.8,61 Pulmonary edema is not an uncommon finding and
occurs more often after than during the fluid-resuscitation
phase of burn injury. Increased capillary pressure secondary
to the increased PVR occurs with both pre- and postcapillary
vasoconstriction and may contribute to pulmonary edema
formation. Pulmonary wedge pressure is increased more
than left atrial pressure after experimental burn injury owing
to postcapillary venular constriction.61,140 It is likely that
some degree of left heart failure also contributes to the
increased capillary pressure. However, hypoproteinemia may
be the greatest contributing factor to postburn pulmonary
edema.141 Analysis of lung lymph sampled in large animal
models after 40% TBSA injury showed no evidence of
increased capillary permeability, although rat studies suggest
that albumin sequestration increases in the lungs after a 30%
cutaneous scald.29 Clinical studies of burn-injured patients
suggest that in the absence of inhalation injury the lungs do
not develop edema,142,143 a finding that is consistent with
the little or no change in the microvascular permeability of
the lung and the fact that lung lymph rate may increase
ventricular contractile and compliance defects.119,120,122 These
data suggest that hypovolemia is not the sole mechanism
underlying the myocardial defects observed with burn shock.
Serum from patients failing to sustain a normal CO after
thermal injury have exhibited a markedly negative inotropic
effect on in vitro heart preparations, which may be due to
the circulating shock factor described above.77,123 In other
patients with large burn injuries and normal cardiac indices,
little or no depressant activity was detected.
Traber and colleagues studied intact, chronically instru­
mented sheep after a 40% TBSA flame burn injury and
smoke inhalation injury, and after smoke inhalation injury
alone. They found that contractile force was reduced after
either burn injury or inhalation injury alone.124,125 Horton
et al.126 demonstrated decreased left ventricular contractility
in isolated, coronary-perfused guinea pig hearts harvested
24 hours after burn injury. This dysfunction was more pro­
nounced in hearts from aged animals and was not reversed
by resuscitation with isotonic fluid. It was largely reversed
by treatment with 4 mL/kg of hypertonic saline dextran
(HSD), but only if administered during the initial 4–6 hours
of resuscitation.127,128 These authors also effectively amelio­
rated the cardiac dysfunction of thermal injury with infu­
sions of antioxidants, arginine and calcium channel
blockers.129–131 Cioffi and colleagues,132 in a similar model,
observed persistent myocardial depression after burn when
the animals received no resuscitation after injury. As opposed
to most studies, Cioffi reported that immediate and full
resuscitation totally reversed abnormalities of contraction
and relaxation after burn injury. Murphy et al.133 showed
elevations of a serum marker for cardiac injury, troponin I,
for patients with a TBSA > 18%, despite good cardiac indices.
Resuscitation and cardiac function studies emphasize the
importance of early and adequate fluid therapy and suggest
that functional myocardial depression after burn injury may
not occur in patients receiving prompt and adequate volume
therapy.
The primary mechanisms by which burn shock alters
myocardial cell membrane integrity and impairs mechanical
function remain unclear. Oxygen-derived free radicals
may play a key causative role in the cell membrane dysfunc­
tion that is characteristic of several low-flow states. Horton
et al. showed that a combination therapy of free radical
scavengers SOD and catalase significantly improved burn-
mediated defects in left ventricular contractility and relaxa­
tion when administered along with adequate fluid
resuscitation (4 mL/kg per percent of burn). Antioxidant
therapy did not alter the volume of fluid resuscitation
required after burn injury.129
Increased systemic vascular resistance and
organ ischemia
Cardiac output may remain below normal after adequate
volume replacement in burn patients and experimental
animals. After burn injury sympathetic stimulation and
hypovolemia result in the release of catecholamines, vaso­
pressin, angiotensin II, and neuropeptide-Y.46,111 These
agents cause contraction of the arteriolar smooth muscle,
which is systemically manifested by increased afterload and
SVR. The increased SVR after burn injury is also partly

Total Burn Care
8
112
or surgery, but the condition in the absence of abdominal
injury is known as secondary ACS.158 Severely burn-injured
patients are at risk for this development owing to increas­
ingly large volumes of resuscitation fluid, decreased abdomi­
nal wall compliance due to eschar, increased capillary
permeability with leakage of large plasma volumes, and
massive edema formation.
Summary and conclusion
Thermal injury results in massive fluid shifts from the circu­
lating plasma into the interstitial space, causing hypovo­
lemia and swelling of the burned skin. All the Starling forces
change to favor fluid extravasation from blood to tissue.
Rapid edema formation is predominantly due to the devel­
opment of strongly negative interstitial fluid pressure and to
a lesser degree by an increase in microvascular pressure and
permeability. When burn injury exceeds 20–30% TBSA there
is also edema formation in non-injured soft tissues. The type
of fluid used to resuscitate alone with the timing and total
volume infused imparts these fluid shifts.
Secondary to the thermal injury there is release of inflam­
matory mediators and stress hormones. Circulating media­
tors deleteriously increase microvascular permeability and
alter cellular membrane function, by which water and
sodium enter cells. Circulating mediators also favor renal
conservation of water and salt, impair cardiac contractility
and cause vasoconstriction. This further aggravates ischemia
due to combined hypovolemia and cardiac dysfunction. The
end result of this complex chain of events is decreased intra­
vascular volume, increased systemic vascular resistance,
decreased cardiac output, end-organ ischemia, and meta­
bolic acidosis. Without early and full resuscitation therapy
these derangements can result in acute renal failure, organ
dysfunction, cardiovascular collapse, and death. Early exci­
sion of the devitalized tissue appears to reduce the local
and systemic effects of mediators released from burned
tissue, thereby reducing the progressive pathophysiologic
derangements.
Edema in the burn wound, and particularly in the non-
injured soft tissue, is increased by resuscitation. Edema likely
contributes to decreased tissue oxygen diffusion and further
ischemic insult to already damaged cells, with compromised
blood flow increasing the risk of infection. Research should
continue to define better treatments that ameliorate the burn
edema and vasoconstriction that exacerbate tissue ischemia.
The success of this research will require the identification
of key circulatory factors that alter capillary permeability,
cause vasoconstriction, depolarize cellular membranes, and
depress myocardial function. Hopefully, cellular or systemic
methods to prevent the release or block the activity of spe­
cific mediators can be developed and reduce the morbidity
and mortality burn injury.
Further reading
Button B, Baker RD, Vertrees RA, et al. Quantitative assessment of
a circulating depolarizing factor in shock. Shock. 2001;15(3):
239-244.
Cancio LC, Chavez S, Alvarado-Ortega M, et al. Predicting increased
fluid requirements during the resuscitation of thermally injured
considerably to prevent interstitial fluid accumulation. Pul­
monary dysfunction associated with inhalation injury is dis­
cussed in a separate chapter.
Edema and abdominal compartment
syndrome
Prompt and adequate fluid resuscitation has undoubtedly
improved the outcome of burn-injured patients. The Park­
land formula for burn resuscitation, introduced by Baxter
and Shires in 1968, has been the cornerstone of early burn
care.123 Despite the treatment advances of burn surgery,
massive edema of burned and non-burned tissues continues
to be a repercussion of large-volume fluid resuscitation.
There is a physiological conflict that exists in the balance
between the edema process and hypovolemia. Edema results
from the massive efflux of intravascular fluid to the intersti­
tial space owing to altered Starling forces. As hypovolemia is
treated with crystalloid infusions, edema can continue to
increase.
Although the guidelines for burn resuscitation have
changed little, fluid management has changed over the past
two decades. Engrav and associates144 compiled data from
seven burn centers. The results included 50 patients with 43
± 21% TBSA burns, 16 of whom had documented inhalation
injuries. The authors found that 58% of patients with large
burns received volumes that greatly exceeded the formula
proposed by Baxter. Their patients received close to 6 mL/
kg/%TBSA (2 mL/kg/%TBSA more than the Parkland
formula). Urine output also exceeded clinical targets (0.5–
1 mL/kg/h) in 64% of patients. Friedrich and associates145
found that their patients admitted in the year 2000 received
twice the resuscitation volume as those admitted in the
1970s. In yet another report, the Parkland formula was
exceeded in 84% of the burn-injured patients treated.146 A
meta-analysis of 23 burn-resuscitation trials (1980–2003)
using crystalloid burn resuscitation produced similar find­
ings.147 Mean fluid infused (5.0 ± 1.2 mL/kg/%TBSA) and
mean urinary outputs (1.2 ± 0.4 mL/kg/h) were both over
the burn resuscitation guidelines, suggesting that well over
half of all burn patients may be over-resuscitated.
This trend of providing fluid in excess of the Parkland
formula has been termed ‘fluid creep’.148 Over-resuscitation
and its resulting edema are not without consequences. The
problems of the over-resuscitated burn patient may include
eye injuries due to elevated orbital pressures,149 pulmonary
edema,150,151 the need for prolonged mechanical ventilation,
or tracheostomy,152 graft failure or the need for fasciotomy
of uninjured extremities153 due to massive edema.
A life-threatening complication of edema seen with
increasing frequency is abdominal compartment syndrome
(ACS).154,155 Intra-abdominal pressure (IAP) >30 cmH2O is
defined as intra-abdominal hypertension (IAH). ACS is sus­
tained IAH in association with a clinically tense abdomen
combined with ventilation aberrations due to elevated pul­
monary inspiratory pressures or oliguria despite aggressive
fluid resuscitation. Owing to a cascade of pathophysiological
events, ACS is often fatal. The syndrome typically leads to
multiple organ dysfunction, characterized by impaired renal
and hepatic blood flow, bowel ischemia, pulmonary dys­
function, depressed cardiac output, and elevated intracranial
pressures.156,157 ACS can occur after major abdominal trauma

Pathophysiology of burn shock and burn edema
113
patients. Journal of Trauma Injury Infection & Critical Care.
2004;56(2):404-413.
Ivatury RR, Diebel L, Porter JM, et al. Intra-abdominal hypertension
and the abdominal compartment syndrome. Surgical Clinics of
North America. 1997 Aug;77(4):783-800.
Lawrence A, Faraklas I, Watkins H, et al. Colloid
administration normalizes resuscitation ratio and ameliorates
 
Access the complete reference list online at

‘fluid creep’. Journal of Burn Care & Research. 2010
Jan-Feb;31(1):40-47.
Lund T, Wiig H, Reed RK, et al. A ‘new’ mechanism for edema
generation: strongly negative interstitial fluid pressure causes
rapid fluid flow into thermally injured skin. Acta Physiol Scan.
1987;129:433-435.

Pathophysiology of burn shock and burn edema
113.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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