Problem 2

Susan Natalia

Burns
Burns are injuries to the skin resulting from
contact with heat, electrical current, radiation,
or chemical agents.
The young and elderly are more likely to
sustain deep burns because their skin is
generally thinner than that of adults.

Epidemiology

The bodys response to a burn

Zone of coagulation
This occurs at the point of maximum damage. In this zone
there is irreversible tissue loss due to coagulation of the
constituent proteins.
Zone of stasis
The surrounding zone of stasis is characterised by decreased
tissue perfusion. The tissue in this zone is potentially
salvageable.
Zone of hyperaemia
In this outermost zone tissue perfusion is increased. The tissue
here will invariably recover unless there is severe sepsis or
prolonged hypoperfusion.

BURN INJURY (33)

BURN INJURY (34)

superficial 0

BURN INJURY (35)

superficial 0

BURN INJURY (36)

deep 0

BURN INJURY (37)

Burn
Injury to the skin activation of complex
hematologic cascades, include the clotting and
compliment system local activation and
recruitment of inflammatory cells a large number
of inflammatory mediators or cytokines
The accumulation of leukocytes, red blood cells, and
platelets in the blood vessels of the injured area
results in the formation of microthrombi, which
further reduce local perfusion.

Burn
Prostaglandins, histamine, bradykinin permeability
of blood vessels hypoperfusion secondary
fluid shifts from intravascular into interstitial space
edema
Denatured proteins accumulate as a result of
exposure to heat stress response heat shock
proteins help attenuate the production of
proinflammatory cytokines ( TNF-, IL-1, IL-6 ) which
tend to increase the extent of the burn injury

Burn
Regeneration of the damaged epidermis : the basal
layer of cells from the uninjured adjacent epidermis
can give rise to reepithelialization of the burn, limited
to 1 cm from the wound edges.
With large burns, regenerative epidermal cells comes
from the dermal skin appendages : hair follicles and
sebaceous glands.

A : Allergies
M : Medication
P : Past illnesses
L : Last meal
E : Events/environment

Treatment

Burn

 Pemberian nutrisi dititikberatkan pd jumlah kalori & protein.

Sgt diharapkan kalori yg masuk > 60% dr perhitungan.

COMPLICATION

The following are some complications

of some moderate and severe burns:
Dehydration : Skin damage from burns fluid
due to excessive evaporation, the entry of fluid into
the bullae were formed on second degree burns,
and discharge from the III degree scald burns.
Shock develops if dehydration is severe (see Shock).

 Chemical imbalances can result from

extensive burns.
Destruction of muscle tissue (rhabdomyolysis)
sometimes occurs with deep third-degree
burns.
The muscle tissue myoglobin(one of the
muscle's proteins) into the blood If present in
high concentrations harms the kidneys.

 Infection can complicate burn wounds.

Sometimes the infection can spread
throughout the bloodstream and cause severe
illness or death.
Thick, crusty surfaces (eschars) are produced
by deep third-degree burns. Eschars can
become too tight, cutting off blood supply to
healthy tissues or impairing breathing.

Oliguria
Which induces stress hormones and
mediators (angiotensin, aldosterone,
vasopressin) less blood flow to the kidneys
decreased plasma flow and filtration rate
renal failure

paralytic ileus
severe burns paralytic ileus
Acute phase: intestinal peristalsis decreased
or stopped due to shock
Phase mobilization: persitalsis may decline
due to lack of potassium ions

Contracture
Contracture is a complication of wound healing,
especially burns. Contracture is a kind
scar that is formed from the remaining healthy skin
around the wound, which attracted to the other
side of the wounded skin.
Contractures were exposed to layers of muscle and
tendon tissue can lead to limited movement.

Inhalation trauma
Damage is caused primarily by inhaled toxins.
Heat is dispersed in the upper airways, whereas the cooled
particles of smoke and toxins are carried distally into the
bronchi.
Smoke inhalation increase blood flow in the bronchial
arteries to the bronchi along with edema formation and
increases in lung lymph flow
The edema increased lung neutrophils primary
mediators of pulmonary damage neutrophils release
proteases and oxygen free radicals

Inhalation trauma
1st : acute pulmonary insufficiency severe
signs of pulmonary failure from the time of injury
asphyxia, CO poisoning, bronchospasm,
upper airway obstruction

2nd : occurs 72-96 hours after injury hypoxia,

development of diffuse lobar infiltrates
3rd : clinical bronchopneumonia dominates
occur 3-10 days after inhalation injury
expectoration of large mucous casts formed in
the tracheobronchial tree

Inhalation trauma

Electrical burn
Electrical current enters a part of the body, such
as the fingers or hand proceeds through
tissues with the lowest resistance to current,
generally the nerves, blood vessels, and muscles
the current then leaves the body at a
grounded area, typically the foot
Low-voltage injury is similar to thermal burns
without transmission to deeper tissues; zones of
injury extend from the surface into the tissue
which causes only local damage.

Electrical burn
The syndrome of high-voltage injury consists of
varying degrees of cutaneous burn at the entry
and exit sites, combined with hidden destruction
of deep tissue
Initial evaluation : cardiopulmonary resuscitation
initial ECG findings are abnormal or there is a
history of cardiac arrest continued cardiac
monitoring + pharmacologic treatment of any
arrhythmias the most serious derangements
the first 24 hours

Chemical burn
Accidental, cleaners, industrial exposure
The degree of tissue damage, as well as the
level of toxicity, is determined by the chemical
nature of the agent, the concentration of the
agent, and the duration of skin contact

Chemicals cause their injury by protein

destruction,
with
denaturation,
oxidation,
formation of protein esters, or desiccation of the
tissue

SIRS

Systemic inflammatory response

syndrome (SIRS)
At least two of the following conditions:
Oral temperature of >38 C or <35 C,
Respiratory rate of >20 breaths/min or partial
pressure of arterial carbon dioxide (Paco2) of <32
mm Hg
Heart rate of >90 beats/min
Leukocyte count of >12,000/dL or <4000/dL or
>10% bands

 Sepsis: SIRS that has a proven or suspected

microbial source
Severe sepsis: sepsis with one or more signs of
organ dysfunction, hypoperfusion, or
hypotension, such as metabolic acidosis, acute
alteration in mental status, oliguria, or adult
respiratory distress syndrome

 Septic shock: sepsis with hypotension that is

unresponsive to fluid resuscitation plus organ
dysfunction or perfusion abnormalities as
listed for severe sepsis
Multiple organ dysfunction syndrome (MODS):
dysfunction of more than one organ, requiring
intervention homeostasis

Pathophysiology
Stage I :
Following an insult, local cytokine is produced
with the goal of inciting an inflammatory
response, thereby promoting wound repair and
recruitment of the reticular endothelial system

 Stage II
Small quantities of local cytokines are released
into the circulation to improve the local response.
This leads to growth factor stimulation and the
recruitment of macrophages and platelets. This
acute phase response is typically well controlled
by a decrease in the proinflammatory mediators
and by the release of endogenous antagonists; the
goal is homeostasis

 Stage III
If homeostasis is not restored, a significant
systemic reaction occurs. The cytokine release
leads to destruction rather than protection. A
consequence of this is the activation of numerous
humoral cascades and the activation of the
reticular endothelial system and subsequent loss
of circulatory integrity. This leads to end-organ
dysfunction