Mita-pemicu 2 Kgd

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Classifications



Burn depth classification

Depth Appearance Surface Sensation Time to healing

1st

degree Epidermis Pink or red Dry Painful Days

2nd degree

(partial-thickness)

-Superficial

-Deep

Epidermis +

pars papilare

Epidermis +

pars retikulare

Pink, clear

blister

Pink,

hemorrhagic

blister, red

Moist

Moist

Painful

Painful

14-21 days

Weeks, or may

progress to 3rd

degree, require

graft

3rd degree (full-

thickness)

Epidermis +

dermis

White, brown Dry Insensate Require excision

4th degree Skin,

subcutaneos

fat, muscle,

bone

Brown,

charred

Dry Insensate Require excision



Depth of Burn

• Superficial Burn

• Partial Thickness Burn

• Full Thickness Burn



Burn Depth

• Superficial Burn:

1st Degree Burn

– Signs & Symptoms

• Reddened skin

• Pain at burn site

• Involves only

epidermis



Burn Depth

• Partial-ThicknessBurn: 2nd DegreeBurn

–Signs & Symptoms• Intense pain

• White to red skin

• Blisters

•Involves epidermis& dermis



Burn Depth

• Full-Thickness Burn:

3rd Degree Burn

– Signs & Symptoms

• Dry, leathery skin(white, dark brown, or

charred)

• Loss of sensation (little

pain)

• All dermal

layers/tissue may be

involved



Determining Severity of Injury

• Size (surface area)

• Depth

• Prior status of health of victim

• Age

• Location of burn

• Severity of associated injury



Classifications of burn injury

First-degree burns

• Painful, red, dry, and blanch with pressure

• Typically occur secondary to prolonged exposure tolow-intensity heat or short-duration flash exposure to aheat source

• Only a superficial layer of epidermal cells is destroyed

• They slough (peel away from healthy tissue underneaththe wound) without residual scarring

• Usually heal within 2 to 3 days



Second-degree burns• Superficial partial-thickness burns

a) Characterized by blisters

b) Commonly caused by skin contact with the following:

(1) Hot but not boiling water

(2) Other hot liquids

(3) Explosions producing flash burns

(4) Hot grease(5) Flames



c) Injury extends through the epidermis to the

dermis

(1) Basal layers of the skin are not destroyed

(2) Skin regenerates within a few days to a

week



d) Edematous fluid infiltrates dermal-epidermal junction, creating blisters

e) Intact blisters provide a seal that protects the

wound from infection and excessive fluid lossf) Injured area is usually red, wet, and painful, andmay blanch when tissue around the injury iscompressed

g) In the absence of infection these woundsgenerally heal without scarring, usually within 14days



2) Deep partial-thickness burns

a) Depth of burn involves the basal layer of the dermis

(1) Sensation in and around the wound may be diminishedbecause of the destruction of basal-layer never endings

b) Depending on the degree of vascular injury, wound mayappear red and wet, or white and dry

c) Major complications are wound infection and subsequentinfection



d) If uncomplicated, injury generally heals within

3 to 4 weeks

e) Skin grafting may be necessary to promote

timely healing and to prevent scar tissue

formation

(1) Scar tissue may severely restrict joint

movements and cause persistent pain and

disfigurement



Third-degree burns

1) Because the entire thickness of the epidermisand dermis is destroyed, skin grafts arenecessary for timely and proper healing

2) Injury is characterized by coagulation necrosis ofcells and appears pearly white, charred, orleathery

3) Definitive sign is a translucent surface in thedepths of which thrombosed veins are visible

4) Eschar is present in these injuries



5) Sensation and capillary refill are absent because smallblood vessels and nerve endings are destroyed

a) Often results in large plasma volume loss, infection,and sepsis

6) Natural wound healing may produce contracturedeformity and severe scarring

7) Surgical intervention with skin grafting is necessary to:

a) Close full-thickness woundsb) Minimize complications

c) Allow restoration of maximal function



Burn Severity

http://emcrit.org/030-064/056-thermal.burn.htm









Rule s of Nine



Lund & Browder Chart

http://www.medstudentlc.com/uploaded_images/Lund%20Browder%20Rakel.gif





Pathophysiology

• Limit cell tolerance

• ≤ 44oC no significant damage

•> 51

o

C

tissue damage is very great speed• > 70oC although cellular damage in a very

short period of exposure



Area burns

• Coagulation area area cells have been

damaged, the maximum damage points

• Static area damage and leakage of blood

vessels, are impaired perfusion, there are cells

that can still be saved

• Hyperemia area consists of cells damaged

and less money to complete recovery



Pathogenesis

Increased capillary permeability

Isotonic fluid & protein transudation into extracapsuler

Reduction in circulating plasma volume

Edema Curah output ↓ Peripheral vascular resistance↑



SYSTEMIC RESPONSE

Due to the release of cytokines and other inflammatory mediators at the site of injury

Cardiovascular

changes

• Capillary permeability ↑ loss of intravascular proteins and fluids

into the interstitial compartment

•Peripheral and splanchnic vasoconstriction occurs

• Myocardial contractility is << (due to release of TNF-α)

• These changes, coupled with fluid loss from the burn wound, result in

systemic hypotension and end organ hypoperfusion hypovolemic

shock

Respiratory changes • Inflammatory mediators bronchoconstriction

• In severe burns, ARDS can occur

Metabolic changes • BMR ↑ > 3x normal

• This, coupled with splanchnic hypoperfusion, necessitates early and

aggressive enteral feeding to decrease catabolism and maintain gutintegrity

Immunological

changes

• Non-specific down regulation of the immune response occurs,

affecting both cell mediated and humoral pathways



Body’s Response to Burns

• Emergent Phase (Stage 1) – Pain response

– Catecholamine release

– Tachycardia, Tachypnea, Mild Hypertension, Mild Anxiety

• Fluid Shift Phase (Stage 2) – Length 18-24 hours

– Begins after Emergent Phase

• Reaches peak in 6-8 hours

– Damaged cells initiate inflammatory response

• Increased blood flow to cells

• Shift of fluid from intravascular to extravascular space

– MASSIVE EDEMA

– “Leaky Capillaries



Body’s Response to Burns

• Hypermetabolic Phase (Stage 3)

– Last for days to weeks

– Large increase in the body’s need for nutrients

as it repairs itself

• Resolution Phase (Stage 4)

– Scar formation

– General rehabilitation and progression tonormal function



Diagnose

• Calculation extensive burns and deep burns

• Lab and radiology tests (Chest X-Ray)



Diagnostic

Anamnesis

• History of trauma / exposure

to the heat source (flame, hot

water, hot oil, chemicals,

electricity, radiation)• History trapped in a confined

space

• History of exposure to a blast

•History of falls from a certainheight after exposure to heat

sources

Physical examination

• Primary Survey : ABC

• Secondary Survey

Embed also:

1. The degree and extent of burns

2. Causes burns

3. As well as the problems that exist

at the time of the first inspection,

the example problem:

- inhalation injury

- Eskar around his chest

- shock



• Lab. blood examination of peripheral blood (hemoglobin,

hematocrit, leukocyte count, platelet count), blood gas analyzer,

function system / organ (metabolic function, liver, kidney)

• Lab.urin urine specific gravity, pH, sediment

•Microbiological culture and resistance with the material from thewound, where entry intravenous line and catheter urine

• Radiology photo upright piston AP / half sit for pulmonary

evaluation:

– Detection of the ARDS and pulmonary edema (usually done after

the fifth day)



Laboratory

• Hb, Ht pd every 8 hours the first 2 days and

then every 2 days to 10 days

• Liver and kidney function every week

• Examination of electrolytes each day duringthe first week.

• Examination of blood gases when

breathing> 32x/menit• Tissue culture on days I, III, VIII.



Laboratory

• hemoglobin, hematocrit, electrolit (do as soon aspossible to repair the body fluids)

• Complete blood

• Renal function (BUN and creatinine)

• Liver function

• Blood gas analysis with carboxy hemoglobin levels(HbCO2)

•Profiles of blood clots

• Analysis of urine

• Creatine phosphokinase (CPK) and myoglobin urine



Treatment



Treatments Based on the Degree ofSeverity



Systemic Complications

• Infection

– Greatest risk of burn is infection

• Organ Failure

– Release of myoglobin

• Special Factors

– Age & Health

• Physical Abuse

– Elderly, Infirm or Young



Prognosis

• Will depend on depth of burn and the bodysurface area affected.

• Superficial burns usually heal within two

weeks without surgery.• Risk factors for death include age over 60

years, more than 40% of body surface areaaffected and inhalation injury.

• Death may result from severe extensive burnsor electric shock.



Chemical burns

• Can result from exposure to acidic, alkaline orpetroleum products.

• Alkali burns tend to be deeper and more seriousthan acid burns.

• Immediately flush away the chemical with largeamounts of water for at least 20 to 30 minutes(longer for alkali burns). Alkali burns to the eyerequire continuous irrigation during the first eight

hours after the burn.• If dry powder is still present on the skin, brush it

away before irrigation with water.



Electrical burns

• Are often more serious than they appear on thesurface.

• Rhabdomyolysis results in myoglobin release, whichcan cause acute renal failure. If the urine is dark, start

therapy for myoglobinuria immediately.

• Fluid administration should be increased to ensure aurinary output of at least 100 ml/hour in the adult.

• Metabolic acidosis should be corrected by maintainingadequate perfusion and adding sodium bicarbonate.



Inhalation Injury

Toxic Inhalation Synthetic resin combustion

Cyanide & Hydrogen Sulfide

Systemic poisoning

More frequent than thermal inhalation burn

Carbon Monoxide Poisoning Colorless, odorless, tasteless gas

Byproduct of incomplete combustion of carbon products

Suspect with faulty heating unit 200x greater affinity for hemoglobin than oxygen

Hypoxemia & Hypercarbia



Inhalation Injury

• Airway Thermal Burn – Supraglottic structures absorb heat and prevent lower airway

burns

• Moist mucosa lining the upper airway

– Injury is common from superheated steam

– Risk Factors

• Standing in the burn environment

• Screaming or yelling in the burn environment

• Trapped in a closed burn environment

– Symptoms

• Stridor or “Crowing” inspiratory sounds

• Singed facial and nasal hair

• Black sputum or facial burns

• Progressive respiratory obstruction and arrest due to swelling

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