Susan Problem2

8/10/2019 Susan Problem2

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Problem 2

Susan Natalia


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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.


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Epidemiology


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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.


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BURN INJURY (33)


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superficial0

BURN INJURY (34)


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superficial0

BURN INJURY (35)


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deep0

BURN INJURY (36)


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0

BURN INJURY (37)


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Burn

Injury to the skin

activation of complexhematologic 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.


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Burn

Prostaglandins, histamine, bradykinin

permeabilityof 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 ofproinflammatory cytokines ( TNF-, IL-1, IL-6 ) which

tend to increase the extent of the burn injury


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Burn

Regeneration of the damaged epidermis : the basallayer 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.


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A : Allergies

M : Medication

P : Past illnesses

L : Last meal

E : Events/environment


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Treatment


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Burn


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Pemberian nutrisi dititikberatkan pd jumlah kalori & protein.

Sgt diharapkan kalori yg masuk > 60% dr perhitungan.


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COMPLICATION


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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).


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Chemical imbalances can result from

extensive burns.

Destruction of muscle tissue (rhabdomyolysis)

sometimes occurs with deep third-degree

burns.

The muscle tissuemyoglobin(one of the

muscle's proteins)into the bloodIf present inhigh concentrationsharms the kidneys.


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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 tohealthy tissues or impairing breathing.


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Oliguria

Which induces stress hormones and

mediators (angiotensin, aldosterone,

vasopressin)less blood flow to the kidneys

decreased plasma flow and filtration raterenal failure


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paralytic ileus

severe burnsparalytic ileus

Acute phase: intestinal peristalsis decreased

or stopped due to shock

Phase mobilization: persitalsis may decline

due to lack of potassium ions


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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.


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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 bronchialarteries to the bronchi along with edema formation and

increases in lung lymph flow

The edema increased lung neutrophils primary

mediators of pulmonary damage

neutrophils releaseproteases and oxygen free radicals


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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


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Inhalation trauma


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Electrical burn

Electrical current enters a part of the body, suchas 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 agrounded area, typically the foot

Low-voltage injury is similar to thermal burnswithout transmission to deeper tissues; zones of

injury extend from the surface into the tissue

which causes only local damage.


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Electrical burn

The syndrome of high-voltage injury consists ofvarying 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 cardiacmonitoring + pharmacologic treatment of any

arrhythmias the most serious derangements

the first 24 hours


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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


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SIRS

S i i fl


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Systemic inflammatory response

syndrome (SIRS)

At least two of the following conditions:

Oral temperature of >38 C or 20 breaths/min or partial

pressure of arterial carbon dioxide (Paco2) of 90 beats/min

Leukocyte count of >12,000/dL or 10% bands


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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


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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


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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


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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 controlledby a decrease in the proinflammatory mediators

and by the release of endogenous antagonists; the

goal is homeostasis


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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 thereticular endothelial system and subsequent loss

of circulatory integrity. This leads to end-organ

dysfunction

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