Thermal Trauma

Definition
Burns are injuries of skin or other
tissue caused by thermal, radiation,
chemical, or electrical contact.
Burns cause between 3000 and 4000
deaths/yr in the US and about 2
million physician visits.

Etiology
Thermal Burns may result from any
external heat source (flame, hot
liquids, hot solid objects, or,
occasionally, steam). Fires may also
result in toxic smoke inhalation

Etiology
Radiation burns most commonly
result from prolonged exposure to
solar ultraviolet radiation but may
result from prolonged or intense
exposure to other sources of
ultraviolet radiation (eg, tanning
beds) or from exposure to sources of
x-ray or other nonsolar radiation

Etiology
Chemical burns may result from
strong acids, strong alkalis (eg, lye,
cement), phenols, cresols, mustard
gas, phosphorus, and certain
petroleum products (eg, gasoline,
paint thinner).
Skin and deeper tissue necrosis
caused by these agents may
progress over several hours.

Etiology
Electrical burns result from heat
generation and electroporation of cell
membranes associated with massive
current of electrons.
Electrical burns may cause extensive
deep tissue damage to electrically
conductive tissues, such as muscles
and nerves, despite minimal apparent
cutaneous injury.

Pathophysiology
Burns cause protein denaturation
and thus coagulative necrosis.
Around the coagulated tissue,
platelets aggregate, vessels
constrict, and marginally perfused
tissue (known as the zone of stasis)
can extend the injury.
Around the zone of stasis, tissue is
hyperemic and inflamed.

Pathophysiology
Damage to the normal epidermal
barrier allows bacterial invasion and
external fluid loss; damaged tissues
often become edematous, further
enhancing volume loss.
Heat loss can be significant because
thermoregulation of the damaged
dermis is absent, particularly in
wounds that are exposed.

Burn Depth
First Degree
Limited to the epidermis

Burn Depth
Second Degree
Superficial partial thickness
Superficial partial-thickness burns involve
the papillary (more superficial) dermis.
These burns heal within 1 to 2 wk and rarely
scar.
Healing occurs from epidermal cells lining
sweat gland ducts and hair follicles; these
cells grow to the surface, then migrate
across the surface to meet cells from
neighboring glands and follicles.

Burn Depth
Deep partial thickness
Deep partial-thickness burns involve the
deeper dermis and take 2 wk to heal.
Healing occurs only from hair follicles, and
scarring is common and may be severe.

Second Degree

Burn Depth
Third degree
Full-thickness (3rd-degree) burns extend
through the entire dermis and into the
underlying fat.
Healing occurs only from the periphery;
these burns, unless small, require
excision and skin grafting.

Third Degree

Complications
Burns cause both systemic and local
complications.
The major factors contributing to
systemic complications are
breakdown of skin integrity and fluid
loss.
Local complications include eschars
and contractures and scarring.

 Systemic
The greater the percentage of BSA involved, the
greater the risk of developing systemic
complications.
Risk factors for severe systemic complications and
mortality include all of the following:
Burns of > 40% of BSA
Age > 60 yr or < 2 yr
Presence of simultaneous major trauma or smoke
inhalation

The most common systemic complications are

hypovolemia and infection.

Complications
Hypovolemia, causing hypoperfusion of
burned tissue and sometimes shock, can
result from fluid losses due to burns that are
deep or that involve large parts of the body
surface; whole-body edema from escape of
intravascular volume into the interstitium and
cells also develops.
Hypoperfusion of burned tissue also may
result from direct damage to blood vessels or
from vasoconstriction secondary to
hypovolemia.

Complications
Infection, even in small burns, is a
common cause of sepsis and
mortality, as well as local
complications.
The most common pathogens are
streptococci and staphylococci
during the first few days and gramnegative bacteria after 5 to 7 days;
however, flora are almost always
mixed.

Complications
Metabolic abnormalities
hypoalbuminemia
hemodilution
Dilutional electrolyte deficiencies can
develop; they include hypomagnesemia,
hypophosphatemia, and hypokalemia.
Metabolic acidosis may result from
shock.
Rhabdomyolysis or hemolysis

Complications
Hypothermia may result from large
volumes of cool IV fluids and
extensive exposure of body surfaces
to a cool emergency department
environment, particularly in patients
with extensive burns.
Ileus is common after extensive
burns.

Complications
Local
Eschar :stiff, dead tissue caused by deep
burns.
Scarring and contractures

Symptoms and Signs

First-degree burns
These burns are red, blanch markedly
and widely with light pressure, and are
painful and tender.
Vesicles or bullae do not develop.

Symptoms and Signs

Superficial partial-thickness burns
These burns blanch with pressure and
are painful and tender.
Vesicles or bullae develop within 24 h.
The bases of vesicles and bullae are
pink and subsequently develop a
fibrinous exudate.

Symptoms and Signs

Deep partial-thickness burns:
These burns may be white, red, or
mottled red and white.
They do not blanch and are less painful
and tender than more superficial burns.
A pinprick is often interpreted as
pressure rather than sharp.
Vesicles or bullae may develop; these
burns are usually dry.

Symptoms and Signs

Full-thickness burns:
These burns may be white and pliable,
black and charred, brown and leathery,
or bright red because of fixed Hb in the
subdermal region.
Hairs can be pulled easily from their
follicles.
Vesicles and bullae usually do not
develop.

Diagnosis
The rule of nines assesses the
percentage of burn and is used to
help guide treatment decisions
including fluid resuscitation and
becomes part of the guidelines to
determine transfer to a burn unit.

Treatment
IV fluids for burns > 10% BSA
Wound cleaning, dressing, and serial
assessment
Supportive measures
Transfer or referral of selected patients
to burn centers
Surgery and physical therapy for deep
partial-thickness and full-thickness
burns

Initial Treatment
Treatment begins in the prehospital
setting.
The first priorities are the same as for
any injured patient:
ABC (airway, breathing, and circulation).
An airway is provided, ventilation is
supported, and possible associated smoke
inhalation is treated with 100% O2.
Ongoing burning is extinguished, and
smoldering and hot material is removed.

First Priorities
All clothing is removed.
Chemicals, except powders, are flushed
with water; powders should be brushed
off before wetting.
Burns caused by acids, alkalis, or
organic compounds (eg, phenols,
cresols, petrochemicals) are flushed with
copious amounts of water continuing for
at least 20 min after nothing of the
original solution seems to remain.

Intravenous Fluids
IV fluids are given to patients in
shock or with burns > 10% BSA.
A 14- to 16-gauge venous cannula is
placed in 1 or 2 peripheral veins
through unburned skin if possible.
Venous cutdown, which has a high
risk of infection, is avoided.

Initial Wound Care

After analgesia, the wound is cleaned
with soap and water, and all loose
debris is removed.
After the wound is cleaned and is
assessed by the final treatment
provider, burns can be treated
topically.

Initial Wound Care

Tetanus toxoid booster
Escharotomy
Topical treatment may be with
antimicrobial salves, commercial
dressings incorporating silver, or
biosynthetic wound dressings.

Electrical Injuries

 Electrical injury is damage caused by

generated electrical current passing
through the body.
Symptoms may include skin burns,
damage to internal organs and other
soft tissues, cardiac arrhythmias, and
respiratory arrest.
Diagnosis is by history, clinical
criteria and selective laboratory
testing.
Treatment is supportive, with
aggressive care for severe injuries.

Pathophysiology
Traditional teaching is that the severity of electrical
injury depends on Kouwenhoven's factors:
Type of current (direct [DC] or alternating [AC])
Voltage and amperage (measures of current strength)
Duration of exposure (longer exposure increases injury
severity)
Body resistance
Pathway of current (which determines the specific tissue
damaged)

However, electrical field strength, a newer concept,

seems to predict injury severity more accurately.

Symptoms and Signs

Burns may be sharply demarcated on
the skin even when current
penetrates irregularly into deeper
tissues.
Severe involuntary muscular
contractions, seizures, ventricular
fibrillation, or respiratory arrest due
to CNS damage or muscle paralysis
may occur.

Symptoms and Signs

Brain, spinal cord, and peripheral
nerve damage may result in various
neurologic deficits.
Cardiac arrest may occur without
burns in bathtub accidents

Treatment

Shutting off current

Resuscitation
Analgesia
Sometimes cardiac monitoring for 6
to 12 h
Wound care

Lightning Injuries

 Lightning injuries include cardiac

arrest, loss of consciousness, and
temporary or permanent neurologic
deficits; serious burns and internal
tissue injury are rare.
Diagnosis is clinical; evaluation
requires ECG and cardiac monitoring.
Treatment is supportive.

Symptoms and Signs

The electrical charge can cause:
Asystole or other arrhythmias
Symptoms of brain dysfunction, such as
loss of consciousness, confusion, or
amnesia.
Keraunoparalysis: paralysis and
mottling, coldness, and pulselessness of
the lower and sometimes upper
extremities with sensory deficits; the
cause is probably sympathetic nervous
system injury.

Symptoms and Signs

Minor skin burns in a punctate or
feathered, branched pattern,
Tympanic membrane perforation,
Cataracts.

Sepsis & Septic Shock

 Sepsis, severe sepsis, and septic

shock are inflammatory states
resulting from the systemic response
to bacterial infection.
In severe sepsis and septic shock,
there is critical reduction in tissue
perfusion.
Common causes include gramnegative organisms, staphylococci,
and meningococci.
Acute pancreatitis and major trauma,
including burns, may manifest with

 The inflammatory reaction typically

manifests with 2 of the following:
Temperature > 38 C or < 36 C
Heart rate > 90 beats/min
Respiratory rate > 20 breaths/min or
Paco2< 32 mm Hg
WBC count > 12,000 cells/L or <4,000
cells/L or > 10% immature forms

 Severe sepsis is sepsis accompanied

by signs of failure of at least one
organ.
Cardiovascular failure by hypotension,
Respiratory failure by hypoxemia,
Renal failure by oliguria,
Hematologic failure by coagulopathy.

 Septic shock is severe sepsis with

organ hypoperfusion and
hypotension that are poorly
responsive to initial fluid
resuscitation.

Etiology
Most cases of septic shock are caused by
hospital-acquired gram-negative bacilli or
gram-positive cocci and often occur in
immunocompromised patients and patients
with chronic and debilitating diseases.
Rarely, it is caused by Candida or other
fungi.
A unique form of shock caused by
staphylococcal and streptococcal toxins is
called toxic shock

Predisposing factors
diabetes mellitus;
cirrhosis;
leukopenia, especially that associated with
cancer or treatment with cytotoxic drugs;
invasive devices, including endotracheal
tubes, vascular or urinary catheters,
drainage tubes, and other foreign materials;
prior treatment with antibiotics or
corticosteroids.

Pathophysiology
The pathogenesis of septic shock is not
completely understood.
An inflammatory stimulus (eg, a bacterial
toxin) triggers production of
proinflammatory mediators, including
tumor necrosis factor and IL-1.
These cytokines cause neutrophilendothelial cell adhesion, activate the
clotting mechanism, and generate
microthrombi.

Pathophysiology
They also release numerous other
mediators, including leukotrienes,
lipoxygenase, histamine, bradykinin,
serotonin, and IL-2.
They are opposed by antiinflammatory mediators, such as IL-4
and IL-10, resulting in a negative
feedback mechanism.

Pathophysiology
Initially, arteries and arterioles dilate,
decreasing peripheral arterial resistance;
cardiac output typically increases.
This stage has been referred to as warm
shock.
Later, cardiac output may decrease, BP
falls (with or without an increase in
peripheral resistance), and typical
features of shock appear.

Symptoms and Signs

fever,
tachycardia,
tachypnea;
BP remains normal.

Symptoms and Signs

As severe sepsis or septic shock develops, the
first sign may be confusion or decreased
alertness.
BP generally falls, yet the skin is paradoxically
warm.
Oliguria (< 0.5 mL/kg/h) is likely to be present.
Later, extremities become cool and pale, with
peripheral cyanosis and mottling.
Organ failure causes additional symptoms and
signs specific to the organ involved.

Diagnosis
Sepsis is suspected when a patient
with a known infection develops
systemic signs of inflammation or
organ dysfunction.
History, physical examination, and
tests, including urinalysis and urine
culture, serial blood cultures, and
cultures of other suspect body fluids.

Diagnosis
Blood levels of procalcitonin and Creactive protein are elevated in
severe sepsis and may facilitate
diagnosis, but they are not specific.
CBC, ABGs, chest x-ray, serum
electrolytes, lactate levels or
sublingual PCO2, and liver function

Diagnosis
At the onset of septic shock, the WBC
count may initially decrease to < 4000/L,
and PMNs may be as low as 20%.
However, this situation reverses within 1
to 4 h, and a significant increase in both
the total WBC count to > 15,000/L and
PMNs to > 80%
A sharp decrease in platelet count to
50,000/L is often present early.

Diagnosis
Hyperventilation with respiratory
alkalosis
Serum HCO3 is usually low, and
serum and blood lactate levels
increase.

Prognosis
Overall mortality in patients with
septic shock is decreasing and now
averages 40%.
Once severe lactic acidosis with
decompensated metabolic acidosis
becomes established, especially in
conjunction with multiorgan failure,
septic shock is likely to be irreversible
and fatal.

Treatment
Fluid resuscitation with 0.9% normal
saline
O2
Broad-spectrum antibiotics (modified
by culture results)
Drainage of abscesses and excision
of necrotic tissue
Normalization of blood glucose levels
Replacement-dose corticosteroids