Advanced Trauma Life Support ATLS Student Course Manual 2018

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APPENDIX B n Hypothermia and Heat Injuries
virtually all cases. Dehydration, low physical fitness,
lack of acclimation, sleep deprivation, and obesity
increase the likelihood of developing exertional
heat stroke.
Pathophysiology
Through multiple physiological responses that help
balance heat production and dissipation, the human
body is able to maintain a core body temperature of
about 37°C (98.6°F) despite being exposed to a wide
range of environmental conditions. Heat is both
generated by metabolic processes and gained from
the environment.
The first response to an elevated core temperature
is peripheral vasodilation, increasing loss through
radiation. However, if the ambient air temperature
is greater than the body temperature, hyperthermia
is exacerbated. Sweating is required to dissipate heat
when the ambient temperature exceeds 37°C (98.6°F).
Ambient temperature and relative humidity can affect
the efficiency of heat dissipation. The average person
can produce 1.5 L of sweat per hour, increasing to 2.5
L in well-trained athletes. Cutaneous vasodilatation
may increase peripheral blood flow from 5% to up to
20% of total cardiac output.
The efferent information sent to the temperaturesensitive
neurons in the preoptic anterior hypothalamus
results in a thermoregulatory response. This response
includes not only autonomic changes, such as an
increase in skin blood flow and sweating, but also
behavioral changes such as removing clothing or
moving to a cooler area. Proper thermoregulation
depends on adequate hydration. The normal
cardiovascular adaptation to severe heat stress is
to increase cardiac output up to 20 L/min. This
response can be impaired by salt and water depletion,
cardiovascular disease, or medication that interferes
with cardiac function (like beta blockers), resulting
in increased susceptibility to heat stroke. When the
normal physiological response fails to dissipate heat,
the core body temperature increases steadily until it
reaches 41°C to 42°C (105.8°F to 107.6°F), or critical
maximum temperature.
At the cellular level, exposure to excessive heat can
lead to denaturation of proteins, phospholipids, and
lipoprotein, and liquefaction of membrane lipids. This
results in cardiovascular collapse, multi-organ failure,
and ultimately death. A coordinated inflammatory
reaction to heat stress involves endothelial cells,
leukocytes, and epithelial cells in an attempt to
protect against tissue injury and promote healing.
A variety of cytokines are produced in response to
endogenous or environmental heat. Cytokines mediate
fever and leukocytosis, and they increase synthesis
of acute phase proteins. Endothelial cell injury and
diffuse microvascular thrombosis are prominent
features of heat stroke, leading to DIC. Fibrinolysis
is also highly activated. Normalization of the core
body temperature inhibits fibrinolysis, but not the
activation of coagulation. This pattern resembles that
seen in sepsis.
Heat stroke and its progression to multi-organ
dysfunction are due to a complex interplay among
the acute physiological alterations associated with
hyperthermia (e.g., circulatory failure, hypoxia, and
increased metabolic demand), the direct cytotoxicity of
heat, and the inflammatory and coagulation responses
of the host.
Management
In treating heat injuries, pay special attention to
airway protection, adequate ventilation, and fluid
resuscitation because pulmonary aspiration and
hypoxia are important causes of death. Initially,
administer 100% oxygen; after cooling, use arterial
blood gas results to guide further oxygen delivery.
Patients with an altered level of consciousness,
significant hypercapnia, or persistent hypoxia should
be intubated and mechanically ventilated. Obtain
arterial blood gas, electrolytes, creatinine, and blood
urea nitrogen levels as early as possible. Renal failure
and rhabdomyolysis are frequently seen in patients
with heat stroke. Have a chest x-ray performed. Use
standard methods to treat hypoglycemia, hyperkalemia,
and acidosis. Hypokalemia may become apparent
and necessitate potassium replacement, particularly
as acidemia is corrected. Seizures may be treated
with benzodiazepines.
Prompt correction of hyperthermia by immediate
cooling and support of organ-system function are
the two main therapeutic objectives in patients with
heat stroke.
Rapid cooling improves survival. The goal is to
decrease body temperature to < 39°C within 30 minutes.
Start cooling measures as soon as practical at the scene
and continue en route to the emergency department.
Water spray and airflow over the patient is ideal in
the prehospital setting. Alternatively, apply ice packs
to areas of high blood flow (e.g., groin, neck, axilla).
Although experts generally agree on the need for rapid
and effective cooling of hyperthermic patients with heat
stroke, there is debate about the best method to achieve
it. The cooling method based on conduction—namely,
immersion in iced water started within minutes of
the onset of exertional heat stroke—is fast, safe and
effective in young, healthy, and well-trained military
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