BURN INJURY

Tutor 17
Learning Issues

1. Anatomy of upper limb g. Management

(nerve, muscle, bone, joint, h. Grades

vascular)
3. Post Burn Scar and
2. Burn Injuries contracture
a. Definition
4. BHP PHOP CRP
b. Comorbid
c. TBSA
d. Etiology
e. Mechanism
ANATOMY OF UPPER LIMB
Regions
Bones
MUSCLE
Vein
Innervation
Definition of Burn Injury
A burn is an injury to the skin or other organic tissue primarily caused by heat or due to
radiation, radioactivity, electricity, friction or contact with chemicals. Skin injuries due to
ultraviolet radiation, radioactivity, electricity or chemicals, as well as respiratory damage
resulting from smoke inhalation, are also considered to be burns.
2c. Burn Type

Classification:

Then : 1st degree to 4th degree

Now :

1. Superficial burns (first-degree)

2. Partial thickness burns (second degree)
3. Full-thickness burns (third degree to fourth degree).
Superficial Burns (First Degree)
● Depth : Epidermis (superficial)
● Red
● Sometimes painful
Superficial Burns (First Degree)
Partial Thickness Burns (Second Degree)
● Depth : Dermis (superficial)
● Red
● Blistered
● Swollen
● Very Painful
● Heals spontaneously (does not require
grafting for closure)
● No granulation tissue
Partial Thickness Burns (Second Degree)
Full-Thickness Burns (Third Degree)
● Depth : Subcutaneous
● Whitish
● charred or translucent
● no pin prick sensation in burned area
● Burn requiring closure by excision and
grafting
● Develop granulation tissue
Full Thickness Burns (Third Degree)
Full Thickness Burns (Fourth Degree)
2d. Etiology

A. Thermal Burn Injury

B. Chemical Burn Injury
C. Electrical Burn Injury
D. Radiation burn injury
A. Thermal Burn Injury
1. Scalds

Resulted from heated fluids such as boiling water or steam.

Mostly: first or second degree burns, but third degree
burns can result, especially with prolonged contact

70% of burns in children are caused by scalds.

They also often occur in elderly people.
The common mechanisms: ● spilling hot drinks, soup, or other liquid
● exposed to hot bathing water

Scalds tend to cause superficial to superficial dermal burns

A. Thermal Burn Injury
2. Flame Burns

Direct contact with fire

Flame burns comprise 50% of adult burns.

They are often associated with inhalational injury and

other concomitant trauma.

Flame burns tend to be deep dermal or full thickness.

A. Thermal Burn Injury
3. Contact Burn

Direct contact with hot solid materials , such as : Metal, coal, muffler, etc
extremely hot object
getting burn from direct contact
abnormally long contact
The latter is a more common reason.
Commonly seen in : ● people with epilepsy
● misuse alcohol or drugs.
● elderly people after a loss of
consciousness
Usually due to industrial accidents.
Contact burns tend to be deep dermal or full thickness.
B. Chemical Burn Injury
Result of industrial accidents but may occur with household chemical products.

These burns tend to be deep, as the corrosive agent continues to cause

coagulative necrosis until completely removed.

Alkalis
> Acids Common cause: Cement, Hydrofluoric acid

Hydrofluoric acid, widely used for glass etching and in the manufacture of
circuit boards, causes a continuing, penetrating injury.
Must be neutralised with calcium gluconate, either applied topically in a
gel or injected into the affected tissues.
The initial management of all chemical burns is the same irrespective of the agent.

● All contaminated clothing must be removed, and the area thoroughly irrigated.
● Often best achieved by showering the patient.
● Has been shown to limit the depth of the burn.
● Litmus paper can be used to confirm removal of alkali or acid.
● Eye injuries should be irrigated copiously and referred to an ophthalmologist.
C. Electrical Burn Injury
An electric current will travel through the body from one point to another, creating
“entry” and “exit” points. The tissue between these two points can be damaged by
the current.

Some 3-4% of burn unit admissions are caused by electrocution injuries.

The amount of heat generated, and hence the level of tissue damage, is equal to
0.24×(voltage)2×resistance.

The voltage is therefore the main determinant of the degree of tissue damage,
and it is logical to divide electrocution injuries into those caused by low voltage,
domestic current and those due to high voltage currents.
Low Voltage Domestic electricity

“True”high tension injuries

High
Voltage “Flash”injury
Domestic electricity
Low voltages tend to cause small,
deep contact burns at the exit and
entry sites.

The alternating nature of

domestic current can interfere
with the cardiac cycle, giving rise
to arrhythmias.
True”high tension injuries
Occur when the voltage is 1000 V or greater.

There is extensive tissue damage and often limb loss. Usually a

large amount of soft and bony tissue necrosis.

Muscle damage gives rise to rhabdomyolysis, and renal failure may

occur with these injuries.

This injury pattern needs more aggressive resuscitation and

debridement than other burns.

Contact with voltage greater than 70 000 V is invariably fatal.

“Flash”injury
occur when there has been an arc of current from a high tension voltage
source.

The heat from this arc can cause superficial flash burns to exposed body
parts, typically the face and hands.

However, clothing can also be set alight, giving rise to deeper burns.

No current actually passes through the victim’s body.

A particular concern after an electrical injury is the need for cardiac
monitoring.

There is good evidence that if the patient’s electrocardiogram on

admission is normal and there is no history of loss of consciousness,
then cardiac monitoring is not required.

If there are electrocardiographic abnormalities or a loss of

consciousness, 24 hours of monitoring is advised.
D. Radiation Burn Injury
caused by exposure to radioactive substances or sunlight for a long time.
 2f. Mechanism : Pathophysiology
Skin’s functions that lost when skin are burned :
- Epidermal layer : maintenance of fluid and electrolyte homeostasis
→ patient dehydration
- Dermal layer : strength, flexibility, and control internal body temperature
→ patient covered with blanket, heat loss, worsen inadequate perfusion

Burn wounds are initially clean but are rapidly colonized by endogenous and
exogenous bacteria.

Bacteria multiplication → release protease → eschar liquefaction & separation →

wound healing → if wounds >40% → systemic infection

Body response to wound : 1. Local response

2. Systemic response
1. Local Response

- Occur when total amount of heat that absorbed > what can body compensate
- In molecular level :
Protein degradation (40°) → activate complement → inflammation → mediators
release (cytokines, histamine, prostaglandin)

Mediators
a. Cyokines :
Margination of leukocyte to injured site → platelet contribute to hemostasis → local
thrombosis → vasoconstriction → local ischemia

b. Histamine :
Vasodilation → ↑ vascular permeability → edema
c. Prostaglandin : pain
 Zone of Burn Injury

1. Zone of coagulation:
- point of maximum damage
- Irreversible tissue loss
- Coagulative necrosis

2. Zone of stasis:
- Moderate degree of damage
- Characterized by decreased tissue perfusion
(ischemia)
- Potentially salvageable (survive/full necrosis)

3. Zone of hyperemia:
- characterized by increased tissue perfusion
(blood supply)
- Always recovered
 2. Systemic Response

The release of inflammatory mediators (cytokines, histamine, prostaglandin) at

the site of injury has a systemic effect once the burn reaches 30% of TBSA

- ↑ capillary permeability → loss of intravascular proteins

Cardiovascular & fluids into interstitial compartment
changes - Peripheral & splanchnic vasoconstriction
- ↓ myocardial contractility : due to release of TNF-α
- Systemic hypotension & hypoperfusion : due to fluid
loss

- Inflammatory mediators cause

bronchoconstriction Respiratory Changes
- severe burns can cause adult respiratory
distress syndrome
 - BMR increases up to 3x
Metabolic Changes - Splanchnic hypoperfusion causes early &
aggressive enteral feeding (to decrease
catabolism & maintain gut integrity.
Non-specific down regulation of the immune
response occurs, affecting both cell mediated and Immunological Changes
humoral pathways
 PATOGENESIS DARI LUKA BAKAR

RIP Anakin 1 like for 1 pray

 Etiologinya (menurut “Hudak Gallo (1996)”)

APA sih luka bakar itu ? 1. Termal (Basah & Kering)

2. Listrik (Tegangan tinggi & Petir)
“Luka bakar adalah kerusakan atau 3. Kimia
kehilangan jaringan yang disebabkan kontak 4. Radiasi (X-ray)
dengan sumber panas (Misal : Api, air panas, 5. Sun burn
bahan kimia, listrik, radiasi, bahkan sumber
dingin)”

FAKTOR YANG MEMPENGARUHI “SEVERITY”

1. Kedalaman
2. Jumlah kulit yang terbakar
3. Umur
4. Penyakit kronis / kesehatan secara menyeluruh
5. Bagian tubuh yang terbakar
6. Inhalasi asap
PENYEBAB LUKA BAKAR

“Luka bakar disebabkan oleh Kehilanga cairan karena “peningkatan

perpindahan energi dari “sumber panas” ke permeabilitas pembuluh darah dapat
tubuh melalui “konduksi atau radiasi”. Bagian mengakibatkan tubuh kehilangan “Natrium, air,
kulit yang terkena adalah Epidermis, dermis, klorida, kalium, & proein plasma”, lalu terjadi
maupun subkutan. Luka bakar menyebabkan “edema” fan dapat berlanjut pada “Syok
pula turunnya integritas kulit yang dapat pula Hipovolemik”
memicu “infeksi” oleh mikroorganisme.

Menurunnya aliran intravaskuler menyebabkan “aliran plasma ke ginjal dan

GFR (Glomerular Filtration Rate) menurun” sehingga saluran urin
meningkat. Jika “restitusi cairan” tidak cukup ke ginjal, maka dapat
menyebabkan “gagal ginjal”
KLASIFIKASI LUKA BAKAR BERDASARKAN
KEDALAMANNYA I
1. Luka bakar derajat I (Superfisial)

Luka bakar teringan dimana kerusakannya hanya mencapai bagian epidermis. Kulit tampak
kering, kemerahan (vasodialatasi). Dan nyeri karena ujung saraf sensorik “teriritasi”. Umumnya
karena sengatan sinar “matahari”.

2. Luka bakar derajat II (Dermis)

Meliputi “epidermis” dan “sebagian dermis”, elemen epitel (Sel epitel basal, kelenja sebasea,
kelenjar keringat, & folikel rambut) masih bersisa, tampak “pucat dan kemerahan” (karena
kerusakan “kapiler & ujung saraf” pada dermis), serta timbul “Bulla” akibat “permeabilitas ‘kapiler’
yang meningkat”.
KLASIFIKASI LUKA BAKAR BERDASARKAN
KEDALAMANNYA II
3. Luka bakar derajat III

Luka bakar ini merusak bagian “epidermis dan dermis”. Selain itu, luka ini
juga merusak “tulang, otot, serta tendon”. Warna luka bakar “putih” & tidak
terasa apapun karena ujung saraf bebas hancur.
TIPE LUKA BAKAR II

1. Tipe A

Kerusakan mengenai bagian “superficial dermis”, “Apendensis kulit” masih utuh,

menyebabkan perubahan warna kulit yang mencolok, jarang menyebabkan parut hipertrofik.
Biasanya karena “tumpahan air panas”.

2. Tipe B

Kerusakan hampi mengenai seluruh bagian “dermis”, luka tampak“bercak putih & pink”
perbedaan aliran darah (Putih : gk ada aliran darah, Pink : Sedikit aliran darah), serta sering
terjadi “parut hipertrofik & kontraktur”
FASE-FASE LUKA BAKAR

1. Fase “Akut”

Permasalahn utama “fase Akut” adalah “airway, breathing, & circulation”. Terjadi pula
“gangguan keseimbangan dan elektrolit” karena cedra termal. “Fase syok”.

2. Fase “Sub-akut”
a. Proses inflamasi yang disertai “eksudasi & kebocoran”
b. SIRS (“Sistemik inflamation respons syndrome”) & Sepsis (karena “Infeksi”)
c. Penguapan cairan tubuh (menyebabkan gangguan metabolisme)
3. Fase lanjut

Setelah terjadi penutupan luka, muncul deformitas seperti “jaringan parut hipertrofik, kleoid,
serta gangguan pigmentasi.
LUKA BAKAR LISTRIK I
“LUKA BAKAR LISTRIK” ADALAH LUKA BAKAR YANG DIESBABKAN OLEH KONTAK LANGSUNG
DENGAN BENDA YANG BERARUS LISTRIK

Kerusakan jaringannya disebabkan oleh beberapa hal :

1. “Sumber listrik” (Kontak dengan badan, dialirkan lewat bagian tubuh dengan resistensi renda, lalu
keluar lewat tubuh yang kontak dengan bumi)

Kerusakan tergantung organ yang dilewatinya :

A. Jantung (Fibrilasi ventrikel)

B. Otak (Ensefaloti)
C. Otot (Rabdomiolisis)
D. Ginjal (Gagal ginjal)
LUKA BAKAR LISTRIK II
2. Loncatan energi yang ditimbulkan di udara, berupa “Api”
3. Kerusakan jaringan yang lambat tapi pasti karena kerusakan pembuluh darah
(Trombosis & Oklusi kapiler) disepanjang tubuh yang dialiri
LUKA BAKAR KIMIA
“LUKA BAKAR KIMIA” ADALAH LUKA BAKAR PADA ORGAN LUAR MAUPUN DALAM TUBUH
YANG DISEBABKAN OLEH BAHAN-BAHAN KIMIA YANG MERUPAKAN “ASAM KUAT ATAU BASA
KUAT” DAN ZAT PRODUKSI “PETROLEUM”

Biasanya disebabkan oleh “asam kuat”. Luka bakar ini dapat menyebabkan kerusakan jaringan yang
hebat sehingga menyebabkan diskonfigurasi luka sehingga luka sulit sembuh & terbentuk jaringan parut
yang tebal.

1. Asam Kuat (Nekrosis koagulasi protein, menghambat proliferasi sel, toksisitas sistemik, nyeri)
2. Basa Kuat (Nekrosis koagulasi protein & jaringan, dehidrasi sel, serta denaturasi protein & kolagen)
Pathogenesis of burn Shock

CNS Adrenalin Alfa-adrenoreceptor of precapillaries

Hypoperfusion of Vasoconstriction
organs and tissue

Acidosis Blocking of alfa-adrenoreceptor

Paretic dilatation
Increased capillary
“hydrostatic pressure”
Capillary leak
syndrome
Management of Burns
Essential Management Points:
- Stop the burning

- ABCDE

- Determine the percentage area of burn (Rule of 9’s)

- Good IV access and early fluid replacement

A airway

B breathing → beware of inhalation and rapid airway compromise

C circulation → fluid replacement

D disability → compartment syndrome

E exposure → percentage area of burn

• The severity of the burn is determined by:

- Burned surface area

- Depth of burn

- Other considerations
Depth of Burn
The American Burn Association burn center transfer criteria are as follows: [22]

● Second- or third-degree burns greater than 10% total body surface area (TBSA) in patients younger than 10
years or older than 50 years [29]
● Second- or third-degree burns greater than 20% TBSA in persons of other age groups
● Second- or third-degree burns that involve the face, hands, feet, genitalia, perineum, or major joints
● Third-degree burns greater than 5% TBSA in persons of any age group
● Electrical burns, including lightening injury
● Chemical burns [30, 31]
● Inhalational injury [20]
● Burn injury in patients with preexisting medical disorders that could complicate management, prolong
recovery, or affect mortality
● Any patients with burns or concomitant trauma (eg, fracture) in which the burn injury poses the greatest
risk of morbidity or mortality: In such cases, if the trauma poses the greater immediate risk, the patient
may be treated initially in a trauma center until stable before being transferred to a burn center. Physician
judgment is necessary in such situations and should be in concert with the regional medical control plan
and triage protocols. [22]
● A lack of qualified personnel or equipment for the care of children (transfer to facility with these qualities)
[32]

● Burn injury in patients who require special social/emotional and/or long-term rehabilitative support,
including cases involving suspected child abuse or substance abuse [33, 34]
Resuscitation

The Parkland or Baxter formula, consists of 3 to 4 mL/kg/% burn of lactated

Ringer’s, of which half is given during the first 8 hours after burn and the
remaining half is given over the subsequent 16 hours

Specific pediatric formulas have been described, but the simplest approach
is to deliver a weight-based maintenance IV fluid with glucose
supplementation in addition to the calculated resuscitation fluid with
lactated Ringer’s.

Intravenous fluid resuscitation for patients with burns greater than 20% of
total body surface area (children with burns >15% of total body surface area)
should be titrated to mean arterial pressure (MAP) greater than 60 mmHg
and urine output greater than 30 mL/h.
Actual administrated fluid volumes typically exceed volumes predicted by
standard formulas. Those patients receiving higher fluid volumes were at
increased risk of complications and death.

High-dose ascorbic acid (Vitamin C), plasmapheresis, bedside thoracic

ultrasound, cardiac function and volume status determination
Transfusion
Blood transfusions are considered to be immunosuppressive, which is one
explanation for the common responses seen to blood transfusions, such as
increased infection and shorter time to recurrence after oncologic surgery

Data recommend that blood transfusions be used only when there is an

apparent physiologic need
Wound Care

FIRST AID

• If the patient arrives at the health facility without first aid having been given, drench the burn thoroughly
with cool water to prevent further damage and remove all burned clothing.

• If the burn area is limited, immerse the site in cold water for 30 minutes to reduce pain and oedema
and to minimize tissue damage.

• If the area of the burn is large, after it has been doused with cool water, apply clean wraps about the
burned area (or the whole patient) to prevent systemic heat loss and hypothermia.

• Hypothermia is a particular risk in young children.

• First 6 hours following injury are critical; transport the patient with severe burns to a hospital as soon
as possible.
INITIAL TREATMENT

• Initially, burns are sterile. Focus the treatment on speedy healing and prevention of infection.

• In all cases, administer tetanus prophylaxis.

• Except in very small burns, debride all bullae. Excise adherent necrotic (dead) tissue initially and
debride all necrotic tissue over the first several days.

• After debridement, gently cleanse the burn with 0.25% (2.5 g/litre) chlorhexidine solution, 0.1% (1
g/litre) cetrimide solution, or another mild water-based antiseptic.

• Do notuse alcohol-based solutions.

• Gentle scrubbing will remove the loose necrotic tissue. Apply a thin layer of antibiotic cream (silver
sulfadiazine).

• Dress the burn with petroleum gauze and dry gauze thick enough to prevent seepage to the outer
layers.
Outpatient Management Inpatient Management

Patient and family Initial evaluation and

education resuscitation

Wound cleansing Initial wound excision

and biologic closure
Choice of topical or
membrane dressing [39] Definitive wound closure

Pain control Rehabilitation and

reconstruction.
Early return instructions

Follow-up clinic visits

Long-term follow-up care

 Daily treatment
• Change the dressing daily (twice daily if possible) or as often as necessary to
prevent seepage through the dressing. On each dressing change, remove any loose
tissue.

• Inspect the wounds for discoloration or haemorrhage, which indicate developing

infection.

• Cellulitis in the surrounding tissue is a better indicator of infection.

• Give systemic antibiotics in cases septicaemia. (Pseudomonas aeruginosa infection

often results in septicaemia and death. Treat with systemic aminoglycosides.)

• Administer topical antibiotic chemotherapy daily. Silver nitrate (0.5% aqueous), silver
sulfadiazine (1% miscible ointment), or Mafenide acetate (11% in a miscible ointment)
Treat burned hands with special care to preserve
function.

− Cover the hands with silver sulfadiazine and place them in loose polythene
gloves or bags secured at the wrist with a crepe bandage;

− Elevate the hands for the first 48 hours, and then start hand exercises;

− At least once a day, remove the gloves, bathe the hands, inspect the burn and
then reapply silver sulfadiazine and the gloves;

− If skin grafting is necessary, consider treatment by a specialist after healthy

granulation tissue appears.
 Healing Phase
• Apply split thickness skin grafts to full-thickness burns after wound excision or the
appearance of healthy granulation tissue.

• Burn scars undergo maturation, at first being red, raised and uncomfortable. They
frequently become hypertrophic and form keloids. They flatten, soften and fade with
time, but the process is unpredictable and can take up to two years.

• Burn scars on the face lead to cosmetic deformity, ectropion and contractures about
the lips. Ectropion can lead to exposure keratitis and blindness and lip deformity
restricts eating and mouth care. Consider specialized care for these patients as skin
grafting is often not sufficient to correct facial deformity.
Nutrition

• Patient’s energy and protein requirements will be extremely high due to the
catabolism of trauma, heat loss, infection and demands of tissue regeneration. If
necessary, feed the patient through a nasogastric tube to ensure an adequate
energy intake (up to 6000 kcal a day).

• Anaemia and malnutrition prevent burn wound healing and result in failure of skin
grafts. Eggs and peanut oil and locally available supplements are good.
 Skin Graft
1. What is skin graft?
Skin Grafts are used to mainly to help in wound healing. Skin grafting is a procedure
whereby a part of the skin is harvested from and transferred to another part in order
to help wound healing. The blood supply of the skin tissue from its site of origin is not
harvested in a skin graft. Several tissues can be transferred and not only the skin.
Other tissues that can be grafted include: bone grafts, cartilage grafts, tendon grafts,
nerve grafts, muscle grafts, fat grafts and many others.
2. Uses of skin graft
● To aid in wound healing
● To restore normal function of the skin tissue
● To restore normal anatomy (make the part of the body look normal even when
the function is not restored. This is for cosmetic reasons) this could occur
following burns
● To prevent skin contractures
● To release a contracture or relieve pain due to contracture or compression
3. Classification of skin grafts based on thickness of the
skin tissue harvested
● Full Thickness skin graft or (Wolfe skin graft)
● Partial or Split Thickness skin graft- this is further classified into Thin partial thickness skin graft (also
known as Thiersch skin graft), Intermediate partial thickness skin graft and Thick partial thickness skin
graft.

4. Skin Graft Recovery Time and Stages of Healing

● Stage of Imbibition: Plasmatic imbibition is responsible for survival for 2-3 days until angiogenesis occurs
● Stage of Inosculation: This occurs in day 3; cut ends of the vessels under the dermis begin to form
connection with those of the beds.
● Stage of Angiogenesis: By day 5 new blood vessels grow into graft and graft become vascularized
Skin Graft Ilustration
BHP
❏ Informed consent untuk pemeriksaan yang akan dilakukan secara fisik atau
lab
❏ Menjelaskan dengan simpati tentang kondisi yang dialami oleh pasien dan
mengenai luka parut
❏ Memberi penjelasan tentang langkah pengobatan yang akan dilakukan
❏ Menjelaskan tentang komplikasi yang bisa terjadi
PHOP
❏ Mengedukasi masyarakat tentang luka bakar dan pertolongan pertama yang
harus dilakukan jika terkena
❏ Mengedukasi masyarakat penyebab luka bakar dan cara menghindarinya
❏ Memberi edukasi tentang pengelolaan luka parut yang betul
 CRP
An estimated 265.000 deaths occur each year from fires alone, with more deaths
from scalds, electrical burns, and other forms of burns

Over 96% of fatal fire-related burns occur in low- and middle-income countries. In
addition to those who die, millions more are left with lifelong disabilities and
disfigurements, often with resulting stigma and rejection