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474
S. M. Roberts et al.
hypothermia include severity of injury, environmental conditions, and medical care provided by EMS. All phases of
trauma care should be analyzed to minimize the cause or
worsening of hypothermia by the trauma team.
Several patient factors inuence the likelihood of a patient
developing hypothermia. Risk of hypothermia is increased in
patients with less muscle and fat, due to decreased ability of
fat to insulate [4]. Medical conditions can increase the likelihood of developing hypothermia if they interfere with thermoregulation or total body heat production. Such conditions
include hypoglycemia and low caloric intake that decrease
the shivering response and heat production and chronic skin
conditions and burns that increase total body heat loss.
Additionally, decreased activity and alcohol or drug use
causing vasodilation can interfere with a patient’s ability to
conserve heat [1]. Age, young and old, can also predispose to
hypothermia. Children are susceptible due to increased body
surface area to body mass, increased metabolic rate, and
small amount of subcutaneous tissue. Older adults are susceptible due to loss of subcutaneous fat, nutritional deciencies, and chronic medical conditions that impair the body’s
ability to maintain heat production.
Common hospital factors that exacerbate hypothermia for
trauma patients include exposure for examination, administration of room temperature uids, medications that affect
the body’s ability to thermoregulate, hypovolemia, and cavitary exposure during surgery [3].
Pathophysiology
Trauma-induced shock leads to anaerobic metabolism,
which results in reduced ATP synthesis and decreased hydrolysis of ATP to ADP, ultimately decreasing heat production
[3]. When the body is exposed to cold temperature, in order
to preserve core body temperature, the body’s initial response
is peripheral vasoconstriction [4]. This allows the blood to be
more centrally located, therefore decreasing heat loss to the
environment. Impairment in the threshold for vasoconstriction may occur after trauma [3]. Trauma patients have
decreased heat production as a result of low perfusion of
muscles and might experience heat loss through radiation,
conduction, or evaporation through exposed body cavities if
they require surgery.
of mild hypothermia (35–32°C) include increased shivering and muscle tone, cool skin due to vasoconstriction, and
social withdrawal [1, 3, 4]. Moderate hypothermia
(32–28°C) characteristics include cessation of shivering,
confusion, apathy, slurred speech, loss of ne motor skills,
and loss of consciousness. Severe hypothermia (<28°C)
signs consist of severe bradycardia, dilated pupils, hypotension, cardiac conduction abnormalities, loss of deep tendon reexes and voluntary motion, decreased or cessation
of respiratory rate, and cardiac arrest. The risk of cardiac
arrest increases as the core body temperature decreases
below 32°C and is increasingly common below 28°C.Heart
rate and blood pressure can be variable for hypothermic
patients, and absence of respiratory and cardiac activity is
not uncommon for hypothermic patients who eventually
recover. Since hypothermic patients can have severely
depressed respiratory rate and heart rate, the trauma team
must carefully assess the patient to avoid missing signs of
respiratory or cardiac activity.
Systemic Manifestations ofHypothermia
Hypothermia leads to many systemic consequences and
impairs the normal function of organs. Cardiac effects
include reduction of cardiac output and cardiac conduction
abnormalities (ventricular brillation, more common below
28°C, and asystole below 25°C). Nonspecic EKG changes
occur and include J (Osborn) waves (upward deection after
the QRS complex [1]), bradycardia, atrial brillation with
slow ventricular response, and prolongation of PR, QRS, and
QT intervals [7]. Additional cardiovascular effects include
vasoconstriction and hypotension with low organ ow status
[6]. Nervous system effects include behavioral changes, disorientation, amnesia, apathy, ataxia, dysarthria, pupil dilation, pupil nonreactivity, and decreased or absent reexes.
Respiratory consequences include bradypnea and respiratory
acidosis. Endocrine responses include an initial increase in
the stress hormones of cortisol, catecholamines, and thyroxin to increase metabolic rate to maintain core body temperature. These mechanisms cease to be effective with the
progression of hypothermia.
Lethal Triad (Diamond) Component
Signs ofHypothermia
Signs of hypothermia can be broken into different categories based on body temperature, although there is no specic cut- off temperature where one event may occur.
Effects of hypothermia are inuenced by many factors,
including age, comorbidities, and associated injuries. Signs
The lethal triad consists of acidosis, hypothermia, and coagulopathy and is associated with high mortality [3]. The recent
change to lethal diamond also adds hypocalcemia. Recent
changes in trauma resuscitation for patients with hemorrhagic
shock involve moving away from crystalloid resuscitation
and towards “Damage Control Resuscitation” (DCR) [1].
This method involves a restrictive use of crystalloid uids and
54 Hypothermia andtheTrauma Team
475
early administration of balanced ratios of packed red blood
cells, fresh frozen plasma, and platelets (1:1:1). This approach
interrupts the lethal triad and has been associated with
improved outcomes in severely injured patients. Hypothermia,
acidosis, hypocalcemia and coagulopathy all interact with
one another in a vicious cycle worsening the coagulopathy.
The goal of DCR is to avoid the start of the cycle or to reverse
its progression [8]. Hypothermia and acidosis are generally
corrected with resuscitation, while coagulopathy is harder to
correct. Coagulopathy is exacerbated by excessive crystalloid
administration, hypothermia impairs the clotting cascade, and
metabolic acidosis in trauma patients occurs from hypoperfusion due to massive blood loss and impairs clotting enzyme
activities [9]. Commonly in severe trauma, the combination
of acidosis, hypothermia, and hypotension worsens due to
ongoing bleeding [8]. This then exacerbates the patient’s
shock, including worsening acidosis and hypothermia, thus
leading to a vicious cycle of the lethal triad components.
Inuence ofHypothermia onCoagulation
Traumatic injury is a leading cause of death, and uncontrolled bleeding from coagulation defects is one of the leading causes of potentially preventable mortality [9]. The lethal
triad components are important contributors to coagulation
defects after trauma. In a bleeding trauma patient, impaired
hemostasis occurs as a result of disproportionally impaired
coagulation, anti-coagulation, and brinolysis. Traumainduced coagulopathy (TIC) is primarily due to blood loss
from injury, hemodilution from crystalloid administration,
and development of hypothermia and acidosis. Hypothermic
patients have a prolonged PT and PTT, which are independently associated with increased blood transfusion and
higher mortality. Thromboelastography (TEG) is a test of
whole blood coagulation and provides information on speed
of clot formation and growth, clot strength, and whether the
clot is maintained or broken down [10]. TEG can differentiate the mechanism of coagulopathy and guide blood product
administration [11].
Fibrinolysis occurs as a result of tissue factor exposure
after trauma, through a pathway coagulation factor consumption [9]. Traumatic injury and shock-related hypoperfusion
are the two most important initiators of early coagulopathy
after trauma. In the resuscitation phase, metabolic acidosis
and hypothermia can develop alongside hemodilution from
resuscitative uids; this further impairs the existing coagulopathy from the traumatic injury. Acidosis inhibits thrombin
generation and propagation and increases brinogen degradation, and hypothermia inhibits thrombin generation and
impairs brinogen synthesis [8]. Hypothermia decreases
enzymatic activity of clotting factors and impairs platelet
aggregation, resulting in hypo-coagulation [1, 3].
Several days after the traumatic event and TIC, there is a
transition from hypo-coagulation to hyper-coagulation [9].
Systemic levels of cytokines (IL-1, IL-6, and TNF [12])
increase, leading to endothelial cell activation (with cytokines and thrombin), resulting in a gradual transition of
endothelial cell phenotype from antithrombotic to prothrombotic. Activation of the endothelial cells downregulates
thrombomodulin and brinolysis, and brinogen levels
increase [9]. Overall, a prothrombotic environment develops
and puts the patient at risk for thrombotic events, often
requiring heparin or other anticoagulant medications.
Treatment
Identifying hypothermia is the rst step in management and
appropriate treatment. All members of the trauma team
should be aware of the classic clinical presenting signs of
hypothermia and be able to identify hypothermia when present. Diligent screening for core body temperature should be
performed initially and throughout management in order to
detect, prevent, and treat further temperature loss [3].
Aggressive measures should be taken to prevent loss of body
heat and increase the core body temperature [1]. Hypothermia
can be present on initial presentation, or it can develop secondary to progressing injury or iatrogenically.
Prior to hospital arrival, the treatment care team should
focus on improving the patient’s core body temperature. In
order to prevent heat loss, the patient should be removed
from the cold environment, have wet clothing removed, and
be covered with warm blankets or an external warming
device. This will prevent further temperature loss in the
trauma resuscitation area while the patient undergoes further
evaluation and treatment. Utilization of blood warmers in the
trauma resuscitation area is critical for resuscitation, as the
most efcient method to prevent hypothermia for patients
receiving substantial amounts of crystalloid and blood is by
warming the products before infusion. Popular uid infusers
include the Belmont and Level 1, which both allow for infusing large amounts of warmed uids.
Methods ofRewarming
There are various warming modalities for a hypothermic
patient, and the appropriate technique is selected based on
core body temperature, clinical condition, available
resources, and the experience of the trauma team [1]. From
least to most invasive, the modalities are passive external
rewarming, active external rewarming, and active internal
rewarming. Generally, the modalities selected for a particular patient are correlated with that patient’s degree of hypothermia: passive external rewarming for mild hypothermia
476
S. M. Roberts et al.
(35–32°C), active external rewarming for moderate hypothermia (32–28°C), and active internal rewarming for severe
hypothermia (<28°C) [4]. Passive rewarming involves placing the patient in an environment that reduces heat loss and
relies on the patient’s intrinsic thermoregulatory mechanisms
to generate heat. Active rewarming involves supplying additional sources of heat energy to the patient [1]. Passive
rewarming is utilized for mild hypothermia, while active
rewarming is utilized for moderate and severe hypothermia.
Passive external warming techniques consist of removal
of cold, wet clothing with replacement of dry clothing and
blankets, and transfer from a cold environment to a warm
environment. The temperature in the trauma resuscitation
area should be increased to maintain a warm ambient temperature and minimize body heat loss.
Active external rewarming involves insulation with heating pads, external convection heaters like heat lamps, thermal caps, warm packs to areas of high vascular ow, warm
blankets, and external devices such as a Bair Hugger or other
warmed forced-air blankets.
Active internal rewarming includes warmed IV uids and
blood products, heated humidied oxygen or air, warm uid
lavage through nasogastric tubes for intragastric, urinary
bladder irrigation, chest tubes for thoracic lavage, peritoneal
lavage, and extracorporeal blood warming. Massive transfusions have been associated with marked hypothermia and
elevated risk of cardiac arrest [13]. Studies have shown a
decrease in core body temperature of 0.5–1.0°C after transfusion of 500mL of cold blood [14]. Crystalloid solutions
should be warmed to 39°C before administration. Various
extracorporeal rewarming methods exist and yield rapid
rewarming (1.5–10° per hour) but are more difcult to manage. Implementing these various and often simultaneous
rewarming techniques requires attention and effort from all
team members. Organization and communication between
the team must be maintained to ensure adequate rewarming.
Afterdrop
Afterdrop is a phenomenon observed after rewarming has
started in a hypothermic patient, most commonly moderate to
severe hypothermia, that consists of an additional decrease in
core body temperature once rewarming has been initiated [6].
External rewarming causes peripheral vasodilation and return
to the heart of cold peripheral blood with acidemia accumulated from the extremities. Afterdrop can trigger severe hypotension or lethal arrhythmias such as ventricular brillation.
Cardiac Arrest andRole ofCPR
Hypothermic cardiac arrest includes ventricular brillation, ventricular tachycardia without pulse, pulseless electrical activity, and asystole. Cardiac irritability begins
around 33°C [1], and when the core body temperature of
an injured patient decreases 1.3 °C, the probability of
adverse cardiac events increases twofold [14]. Clinical presentation of severely hypothermic patients is challenging to
distinguish from clinical signs of death, including absence
of pulse, respiration, or consciousness and with dilated or
nonreactive pupils and muscle rigidity [15]. This overlap
necessitates critical attention from team members during
the exam. These patients should be resuscitated and treated
aggressively, as many dysrhythmias will correct with
rewarming alone [7].
Hypothermic patients often require prolonged, highquality CPR, and cardiac activity should be continuously
monitored [6]. Debrillation is the best method to treat
lethal arrhythmias or cardiac arrest. Cardiac arrhythmias
often don’t respond to debrillation until core body temperature is greater than 30°C.Cardiac drugs and debrillation are generally ineffective in the presence of acidosis,
hypoxia, and hypothermia. As such, these methods should
be delayed until the patient’s core body temperature is at
least 28–30°C [1].
Resuscitation Progression
During rewarming, the patient’s temperature should be taken
repeatedly to identify if the temperature is decreasing, indicating the need for a different or more aggressive warming
technique. Coagulopathy may develop or worsen in hypothermic patients; monitor for this complication early since it
is difcult to reverse. Lab tests can help monitor rewarming
process, with poor prognosis indicators consisting of hyperkalemia, hypernatremia, and elevated ammonia and lactate
[16]. Recommended key factors in guiding treatment include
level of consciousness, intensity of shivering, and hemodynamic stability [6].
The well known saying for hypothermia exists: “You’re
not dead until you’re warm and dead.” It’s necessary to fully
rewarm hypothermic patients before pronouncing death [4].
Resuscitation should be continued in a hypothermic patient
until the core body temperature is greater than 30–32°C, and
there are still no signs of apparent life [7].
54 Hypothermia andtheTrauma Team
477
Prognosis
Several retrospective studies have shown an independent
relationship between mortality and hypothermia after trauma
[3]. It has been proposed that the mortality prediction related
to hypothermia is likely in co-existence with acidosis and
coagulopathy. Hypothermic fatalities in general had a lower
average body temperature, higher injury severity score, and
increased blood transfusion requirement. Increased morbidity associated with hypothermia includes a higher risk for
organ dysfunction and risk factor for surgical site infections
in trauma laparotomies.
Team Dynamics
Eect onTrauma Team Dynamics
The purpose of a trauma team is to provide advanced simultaneous care from various specialties to severely injured
patients [5]. Trauma teams have been shown to improve survival rates for severely injured patients, through reduction of
resuscitation time and reduced time to CT scan, ED discharge, and OR.Similar to other trauma cases, hypothermic
patients require the same concepts, organization, and uidity
that make trauma teams so effective. Important team dynamics that have been specically identied for hypothermia
situations include closed-loop communication and a healthcare team with clear denition of roles [16].
The initial phase of hospital care in the trauma resuscitation area is where most preventable problems occur [5].
Common problems include errors or delays in diagnosis or
treatment and failing to perform diagnostic or therapeutic
measures at the appropriate time with the right frequency or
in the proper order. Additional problems include unfamiliarity with the trauma scenario, disorganization of the team, and
failure to prioritize complexity of issues. These problems can
be addressed by formal teaching and simulations for trauma
team members to familiarize them with recognizing and
managing hypothermic patients.
Hypothermia in a severely injured patient is a highly
demanding clinical challenge, due to effect of injury severity
and associated bleeding complications that is often found in
these patients [17]. Team members should be knowledgeable
about common pitfalls associated with treating hypothermia,
so they can try to avoid or more quickly mitigate them. Some
common pitfalls include excessive exposure of the patient,
failure to infuse warm blood and uids, and failure to activate the Massive Transfusion Protocol (MTP) quickly. In
order to limit exposure, the patient should immediately be
covered with external warming devices such as a Bair hugger. Fluid warmers such as Belmont or Level 1 should be
available, nearby, and properly functioning for immediate
use. Trauma teams should be aware of the lethal triad and
activate the MTP as soon as possible. Education and established protocols for the trauma team surrounding these common pitfalls are essential to improve care.
For hypothermic patients, it’s important that they are
transported to a hospital that has the appropriate treatment
capabilities. Mortality decreases if the patient is brought to a
hospital with specialized trauma services, especially if completed in less than 60minutes [16]. Proper notication and
hand- off from the prehospital team to the hospital team is
also important. The prehospital team should ensure that the
hospital team is aware of the incoming hypothermic patient,
the patient status, and current interventions to improve efciency of care.
Eect onResuscitation
Steps to caring for a hypothermic patient involve: prioritizing ABCDE, appropriately measuring the core body temperature, applying appropriate rewarming techniques, and
managing complications of hypothermia such as arrhythmias.. In the primary survey, the trauma team should be
aware of the potential for severely decreased respiratory
rates and pulse. The trauma team should be mindful of the
potential for arrhythmias or cardiac arrest and attach the
patient to a cardiac monitor or debrillator. Trauma team
members should be aware of common complications of
hypothermia, such as the lethal triad. It’s important to recognize which rewarming techniques are most practical with
the timing of the initial assessment, such as less invasive
techniques started while the patient is still being assessed.
Monitoring the patient during rewarming with repeating
core body temperature measurements, secondary surveys,
and complications is critical to assess rewarming progress
and further interventions. The trauma team should be aware
that resuscitation may take several hours in a hypothermic
patient. Knowing the sequence of treatment events for the
care of hypothermic patients is important for the trauma
team to know and be efcient [18]. This can be practiced
through simulations to improve familiarity and efciency
for trauma teams.
Conclusion
To prevent mortality in hypothermic patients, it’s essential
for team members to be attentive to hypothermia as part of
the lethal triad and other complications of hypothermia. It is
imperative that the trauma team recognize hypothermia and
aggressively address it to improve outcomes.
478
Key Points
1. Hypothermia is best managed by prevention, so
prevention should be emphasized.
2. The lethal triad consists of hypothermia, acidosis,
and coagulopathy. Hypothermia worsens coagulopathy, and in a trauma patient causes hypocoagulation initially and shifts to hyper-coagulation
after several days.
3. Rewarming techniques for hypothermia are categorized into passive external rewarming, active external rewarming, and active internal rewarming.
Techniques are utilized based on severity of
hypothermia.
4. Trauma team dynamics play an essential role in the
successful outcome of a hypothermic patient, particularly in recognizing the hypothermia and the
sequence of management.
References
1. Stewart RM.ATLS: advanced trauma life support student course
manual. 10th ed. Chicago: American College of Surgeons; 2018.
2. Gjeraa K, Moller TP, Ostergaard D.Efcacy of simulation-based
trauma team training of non-technical skills: a systematic review.
Acta Anaesthesiol Scand. 2014;58:775–87.
3. Soreide K. Clinical and translational aspects of hypothermia in
major trauma patients: from pathophysiology to prevention, prognosis and potential preservation. Injury. 2014;45:647–54.
S. M. Roberts et al.
4. Fudge J. Preventing and managing hypothermia and frostbite
injury. Sport Health. 2016;8(2):133–9.
5. Georgiou A, Lockey DJ.The performance and assessment of hospital trauma teams. Scand J Trauma Resusc Emerg Med. 2010;18:66.
6. Avellanas Chavala ML, Ayala Gallardo M, Soteras Martinez I,
Subirats BE.Management of accidental hypothermia: a narrative
review. Med Intensiva. 2019;43(9):556–68.
7. McCullough L, Arora S.Diagnosis and treatment of hypothermia.
Am Fam Physician. 2004;70(12):2325–32.
8. Samuels JM, Moore HB, Moore EE.Damage control resuscitation.
Chirurgia. 2017;112(5):514–23.
9. Martini WZ. Coagulation complications following trauma. Mil
Med Res. 2016;3:35.
10. Gentilello LM, Pierson DJ. “Damage control” approach to trauma
surgery. Am J Respir Crit Care Med. 2001;163(3):604–7.
11. Jeger V, Zimmermann H, Exadaktylos AK.The role of thromboelastography in multiple trauma. Emerg Med Int. 2011;2011:895674.
12. Grignani G, Maiolo A.Cytokines and hemostasis. Haematologica.
2000;85:967–72.
13. Horosz B, Malec-Milewska M.Methods to prevent intraoperative
hypothermia. Anaesthesiol Intensive Ther. 2014;46(2):96–100.
14. Wei C, Yu Y, Chen Y, Wei Y, Ni X.Impact of warming blood transfusion and infusion toward cerebral oxygen metabolism and cognitive
recovery in the perioperative period of elderly knee replacement. J
Orthop Surg Res. 2014;9:8.
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setting: an emergency medicine simulation scenario. Cureus.
2017;9(12):e1998.
16. Hilmo J, Naesheim T, Gilbert M. “Nobody is dead until warm and
dead”: prolonged resuscitation is warranted in arrested hypothermic victims also in remote areas– a retrospective study from northern Norway. Resuscitation. 2014;85:1204–11.
17. Kirkpatrick AW, Chun R, Brown R, Simons RK.Hypothermia and
the trauma patient. Can J Surg. 1999;42(5):333–43.
18. Jensen KO, Jensen JM, Sprengel K.Practicability of avoiding hypothermia in resuscitation room phase in severely injured patients. J
Med Eng Technol. 2015;39(4):223–5.
Burns
AdamPadalko, RaePauleneSpiwak,
andSarveshLogsetty
55
Burns are devastating injuries that result in signicant shortterm and long-term impact. They are non-discriminatory in
their incidence, however are overrepresented in marginalized
populations [1]. Their care requires specialized knowledge
in acute management, surgical techniques, inpatient and outpatient care, and extensive long-term multidisciplinary
involvement by a trained burn care team. This chapter will
discuss initial management, a team-based approach to recovery and burn prevention, with an emphasis on appropriate
resource utilization.
Incidence
Burns are the fourth most common type of trauma worldwide [2]. According to Statistics Canada, an average of 110
Canadians died yearly from burns, and ten times that number
were admitted to hospital for re-related injury [3].
Fortunately, advancements in acute management and burn
care have decreased the mortality rate, with less than 4% of
burns admitted to burn centers proving to be fatal [4]. A low
mortality rate emphasizes the growing importance of postburn recovery and long-term follow-up with psychosocial
support and resources and a specialized multidisciplinary
burn care team.
Etiology
Thermal injuries (ame/scald) are the most common cause
of burn injury; however, chemicals, electricity, or cold may
also result in burn injuries. Table 55.1 outlines unique
causes of burn injuries, as well as important considerations
with each.
A. Padalko
Department of Family Medicine, Max Rady College of Medicine,
Rady Faculty of Health Sciences, University of Manitoba,
Winnipeg, MB, Canada
e-mail: umpadala@myumanitoba.ca
R. P. Spiwak
Department of Surgery, Max Rady College of Medicine, Rady
Faculty of Health Sciences, University of Manitoba,
Winnipeg, MB, Canada
e-mail: Rae.Spiwak@umanitoba.ca
S. Logsetty (*)
Department of Surgery, Psychiatry, Children’s Health, Max Rady
College of Medicine, Rady Faculty of Health Sciences, University
of Manitoba, Winnipeg, MB, Canada
e-mail: Logsetty@umanitoba.ca
© Springer Nature Switzerland AG 2025
L. Marshall Gillman, S. Widder (eds.), Trauma Team Dynamics, https://doi.org/10.1007/978-3-031-86312-7_55
479
480
Baux ScoreTBSAAge =+
()
Table 55.1 Cellular mechanism, treatment, and clinical pearls relating to burn mechanisms
Etiology Mechanism Treatment Clinical pearls
Chemical Acidic—Coagulation necrosis
Alkali—Liquefaction necrosis
Electrical When tissue conducts electricity,
the heat generated causes thermal
injury to tissue in addition to
direct electrical damage
Cold Ice crystal formation in tissue,
microvascular occlusion, and
tissue anoxia
Limit duration of contact
Flush with warm water for 20–30min
Obtain information from Material Safety Data Sheet
regarding systemic toxicity
May require timely fasciotomies to prevent compartment
syndrome
Ensure EKG monitor and indwelling bladder catheter in
addition to acute burn care
Volume resuscitation to prevent acute renal failure in
those with myoglobinuria
Place injured area in circulating water at 38–40°C until
thawed
Be wary of reperfusion syndrome, which may occur on
rewarming (characterized by acidosis, hyperkalemia,
local edema)
Do not attempt to neutralize
chemical, may cause exothermic
reaction and further tissue damage
Remove powders before irrigating
Normal overlying tissue may
co-exist with deep muscle
necrosis, maintain a high degree
of clinical suspicion
Avoid dry heat for reperfusion as
injury is often insensate and
risking further thermal injury
A. Padalko et al.
Prognosis
Major predictors of mortality in burn injuries include age,
total body surface area (TBSA), and presence of an inhalation injury [5, 6]. The Baux score allows timely estimation of
the chance of mortality secondary to burn injury using age
and % TBSA.Revision of the Baux score includes the presence of an inhalation injury to modify mortality risk.
ModifiedBaux ScoreTBS AAge Inhalationinjury =++
∗
17
Recent literature has evaluated the utility of the modied
Baux score compared with alternative prediction models
(Baux, APACHE II, Smith, Ryan, ABSI score) [7, 8]. The
modied Baux score remains an accurate and efcient way
of predicting mortality in burn survivors [9]. While the Baux/
Revised Baux scores remain valid prediction models of burnrelated mortality, this is not a 1:1 relationship. The improvements in care mean that the Baux scores at which mortality
is estimated to be 50% has moved up to 110 and the Baux
score at which 100% mortality is predicted is 160 [10].
Initial Management: “ABCDE” Approach
Initial management of burn injuries is critical to limit the
extent of the burn injury, stabilize the patient, and appropriately triage for further management. It is important to obtain
information regarding the event as early as possible. Burns
can be associated with other forms of traumatic injury. This
can be an obvious association, such as in a motor vehicle/
airplane crash or less obvious as in a house re where a propane tank exploded. As standard trauma practice, a primary
survey is indicated in the acute setting. Using a structured
approach ensures consistency and efciency: airway, breath-
ing, circulation, disability, and exposure. The major difference in burn injury compared to other traumatic injuries is
the response to injury is directly linked to the inammatory
response to the burn. This link to inammation means that
some of the life-threatening sequelae may take time to evolve
and should be considered in managing the acute burn injury.
The Airway must be evaluated immediately to assess for
an inhalation injury or edema from direct thermal injury.
Evaluate the oropharynx with any degree of clinical suspicion for compromise. Maintain a low threshold for initiation
of endotracheal intubation, especially in those with >40%
TBSA burn injuries or co-occurring inhalation injury. Be
aware that there is a synergistic rise in inammatory response
when an integumentary burn occurs combined with inhalation injury [11]. This increased inammation results in
increased uid resuscitation requirements and subsequent
formation of edema.
Breathing concerns are often the result of smoke
inhalation- related hypoxia, carbon monoxide poisoning, or
the consequences of chemical and particulate injury to the
lung parenchyma. Prompt supplemental oxygen is warranted. A chest escharotomy should be considered if the
patient has a signicant full-thickness burn injury that
restricts chest wall motion impeding ventilation and oxygenation. One should suspect carbon monoxide poisoning with
burns that occur in a closed space or if there is an altered
level of consciousness. Diagnosis is conrmed with measurement of carboxyhemoglobin levels (HbCO). Treat carbon monoxide poisoning with high-ow 100% oxygen via
non-rebreathing mask if not intubated. The role of Hyperbaric
Oxygen (HBO) therapy is controversial. A randomized controlled trial by Weaver etal. suggests [12] that there may be
long-term cognitive benet from HBO; however, a signicant portion of the population studied had low carboxyhemoglobin levels raising questions about the applicability of the
ndings. In addition, availability of a readily accessible
hyperbaric chamber and limitations on the ability to safely
mL RL patient weight kg TBSA of deep partial
×
()
×
55 Burns
481
monitor and resuscitate a multi-injured patient while in most
chambers signicantly limit its potential application.
Parenchymal smoke inhalation injury results from smoke
particulate and chemical matter settling in distal bronchioles,
causing inammation and diminished clearance and increasing inammation and risk of pneumonia. History of exposure to smoke in a closed space for an extended period of
time should increase suspicion of inhalation injury. Chest
radiograph and arterial blood gas determination are initial
steps of evaluation. Treatment requires supportive management; height of the bed should be elevated 30 degrees to
decrease neck and chest wall edema. Prophylactic intubation
should be considered in those with an associated signicant
burn injury (>40% TBSA) in co-occurrence with an inhalation injury. Controlled laboratory studies have shown that
under-resuscitating these individuals does not minimize the
edema and may worsen the overall response [13].
Circulating volume needs to be maintained to counteract
the ongoing losses secondary to capillary leak due to inammation. Failure to replace uids has the potential to compromise end-organ perfusion and lead to burn shock.
Resuscitation uid should be initiated in all deep partial or
full-thickness injuries greater than 20% TBSA.The endpoint
of resuscitation is to maintain adequate perfusion; most frequently assessed through hourly urine output. Choosing
Wisely Canada recommends against the routine use of uid
administration in burns <15% TBSA [14]. Oral uids and
maintenance therapy are appropriate for minor burns.
Clinical correlation is recommended. Two large-caliber
intravenous lines in the upper extremities are the preferred
method of administration for warmed isotonic crystalloid
solution, such as Ringer’s Lactate. Central venous access or
intraosseous infusion may be a second option. Note that
large-volume resuscitation with normal saline is not recommended due to the possibility of hyperchloremic metabolic
acidosis.
The American Burn Association: Advanced Burn Life
Support (ABLS) course recommends calculating the burn
resuscitation with 2cc/kg/%TBSA and titrating to a urine
output of 0.5cc/kg/%TBSA in adults and 1cc/kg/%TBSA in
children [15].
2
%iickness burns half administered
and full th
in the first eight hours
An indwelling catheter must be placed for monitoring
urine output and assessment of organ perfusion, with a target
of 0.5mL/kg/h for adults. Children <30kg require a maintenance uid of D5W+½ NS IV in addition to parkland with
the goal urine output of 1ml/kg/h for children 1–2years old,
and 2mL/kg/h for children <1year old. Dramatic changes in
uid rate should be avoided, instead, adjust uid rate of uids at 10–20% maximum each hour to titrate to optimal urine
.
output. Patients should be monitored with electrocardiography for any cardiac rhythm disturbances, as these may be a
sign of hypoxia or electrolyte disturbances [15]. Patients
with co-existing either acute or chronic renal insufciency
make resuscitation and monitoring that much more complex.
In these populations alternate endpoints for resuscitation
must be considered including central venous pressures, pulse
pressure variability, serial base decit, and lactate levels,
among others. There is currently no evidence to support the
use of colloids (e.g., albumin) during early resuscitation. The
role of albumin in later resuscitation is controversial with
some retrospective data suggesting that the resuscitation
uid given can be decreased with the use of albumin after
18–24 h [16]. There has not been an effect on mortality
observed with the use of albumin.
Disability refers to neurologic status and gross deformities. Level of consciousness may be assessed through neurological exam. Findings of altered level of consciousness may
indicate smoke inhalation, carbon monoxide toxicity, substance abuse, hypoxia, exacerbation of secondary medical
conditions, or excessive anesthesia. A thorough secondary
survey with complete history is helpful to discriminate the
cause. Be cautious with burn-injured persons with altered
consciousness who have limited history; they should be
assessed for other physical trauma (i.e., closed head injury).
Anesthesia should be adequate to alleviate patient pain
intolerance; however, Choosing Wisely Canada recommends
that opioids be co-administrated with adjunctive agents such
as acetaminophen and NSAIDs. Daily reassessment is
needed to minimize opioid overuse. In addition, neuropathic
pharmacotherapy and physical and psychological interventions should be optimized [14]. If NSAIDs are used, remember to use adequate gastric ulcer prophylaxis, and consider
avoiding if there is a recent history of ulcers.
Exposure of the patient is necessary to delineate the extent
of burn injury and assess for any co-occurring injuries.
Clothing should be removed to stop the burning process, and
patients should be warmed to minimize losses.
A thorough secondary survey should be used to complete
a full medical history and physical exam to evaluate the
injury. Physical exam ndings noted should include extent of
the burned skin (% TBSA), depth of the injury, anatomic
location, and evidence of other non-burn injuries.
Classication
Classication of burn injuries is based on the depth, as outlined in Table55.2. Depth of burn depends on etiology, temperature of offending agent, contact time, and skin thickness.
Sensation can be an important physical exam nding to history, and burn depth is important to guiding wound care and
evaluating the utility of surgical management.
482
Table 55.2 Classication of burn injuries
Affected layers Characteristics
Supercial Epidermis Erythematous,
Painful
Sensate
Does NOT blister
Supercial partial Epidermis and papillary dermis Moist, blistered, homogenously pink
Hypersensitive
Blanchable
Deep partial Epidermis, papillary, and reticular dermis Dryer, red
Non blanchable
Insensate to light touch
Full thickness Epidermis and all layers of dermis Leathery, waxy, gray coloration
Painless, dry, pale
A. Padalko et al.
Fig. 55.1 Supercial partial thickness
Supercial partial thickness (Fig.55.1):
Full thickness (Fig.55.4)
Estimation of partial- and full-thickness burn injury is done
using percentage of Total Body Surface Area (TBSA) and the
“Rule of 9’s.” This allows the adult body to be anatomically
split into areas that represent TBSA percentages in fractions of
9’s. Smaller burn injuries or those extending beyond anatomical zones may be estimated with the “Palm” method, where
the patient’s volar hand surface with digits extended but
together represents 1% TBSA of burn injury. Children are proportionally different than adults, with proportionately larger
heads and smaller lower extremities. Burn extent in children
should be estimated using the “Palm” method.
Fig. 55.2 Deep partial thickness.Deep partial thickness (a). Note: the
non-blanching erythema (Fig.55.2)
Fig. 55.3 Deep partial thickness (b). Note the mixed pictures, with
central areas of near full thickness (Fig. 55.3)
55 Burns
483
Deeper burn injuries may require excision/grafting. In the
interim [17], it should be noted that not all silver dressings are
equally effective in antimicrobial activity [18]; the dressing
chosen should be discussed with the regional burn center.
Nutrition
Fig. 55.4 Full thickness
Admission
Admission should be considered for burn injuries that are:
• Signicant (>10% TBSA) partial thickness
• Full thickness of sufcient size to require surgery
• Sensitive areas (face, hands, feet, perineum, or genitals)
• Special etiology (electrical, chemical, tar)
• Immunocompromised or co-morbid patients (require specialized medical, rehabilitation, or psychosocial care)
Choosing Wisely Canada has outlined a set of recommen-
dations to encourage mindful use of resources when outlining
admission orders and treating burn injuries. First, early systemic antibiotics should not be administered prophylactically,
as this encourages growth of antimicrobial-resistant organisms which can limit antimicrobial dressings at a later time
[14]. Wound swabs and antibiotics should be used when sus-
picious of a wound infection. Next, correcting hypoalbuminemia is not recommended, as this is often the normal result of
the hypermetabolism, protein loss, and impaired synthesis
associated with the burn injury. Instead, diet and nutrition
should be optimized. Lastly, patients should not have routine
blood work or chest radiographs unless these will be critical
in guiding clinical management. Daily reassessment should
be performed to examine the necessity of these orders [14].
Dressings
Burn wound care aims to protect the injury, promote a moist
environment for burn wound healing, and prevent infections.
Topical antimicrobials in conjunction with non-adherent
dressings are standard [17].
Supercial burn wounds do not require antimicrobial
dressings as the protective skin layer has not been compromised. For deeper wounds while waiting for the wound to
demarcate, antimicrobial dressings are recommended. These
dressings can consist of topical antibiotic ointments or silvercontaining dressings. Supercial partial requires antimicrobial treatment with a non-adherent dressing, such as
polysporin ™ with an adaptic™ dressing.
Burn injuries result in a hypermetabolic response and associated insulin resistance [19]. Energy requirements increase in
proportion with TBSA of burn injury [20]. With larger burns
patients may require more than 30 Kcal/Kg/day of total
energy and 2.5 grams/Kg/day of protein. Inadequate nutrition has been associated with impaired wound healing and
increased length of stay [19]. Burns <20% TBSA should be
placed on a high protein, high energy diet with a daily multivitamin. Burns >20% require high protein tube feeds, a daily
multivitamin, vitamin C, and zinc. In addition, frail elderly
patients or those with bilateral hand burns may also require
tube feeds. Metabolic carts can help calculate caloric requirements in large burns and multi-injured patients.
Multidisciplinary Recovery
Survivors of burn injury face a prolonged and difcult recovery. Immediate post-injury challenges include adequate
resuscitation, pain management, adapting to physical disgurement, regaining function, and managing co-morbid conditions. Long-term challenges include physical rehabilitation,
social reintegration, developing healthy coping mechanisms,
being connected with community, and nancial supports [21,
22].
Rehabilitation with physical and occupational therapy
prevents physical dysfunction and reduction of muscle mass
and leads to improved functional recovery [23]. Early consultation is recommended for assessment and timely
decisions regarding splints, exercises, and contracture risk
with burn anatomy.
Recent literature outlines the underutilization of mental
health screening and connection with psychosocial resources
in Canadian burn centers [24]. Survivors of burn injuries
have higher rates of mental disorders, substance abuse, suicide attempt, and physical illness after burn injury [21].
Consultation with psychiatric services familiar with burn
survivors and routine screening for mental health risk factors
are indicated in burn survivors.
Burn injuries are known to be overrepresented in those
with adverse social determinants and psychosocial obstacles
[25]. Connection of these individuals with appropriate
resources should be considered, which may necessitate the
involvement of social work familiar with community
supports.