First degree:

Includes only the outer layer of skin, the epidermis Skin is usually red and very painful Equivalent to superficial sunburn without blisters Dry in appearance Healing occurs in 3-5 days, injured epithelium peels away from the healthy skin Hospitalization is for pain control and maybe fluid imbalance

Second degree: Can be classified as partial or full thickness.

Partial thickness o Blisters can be present o Involve the entire epidermis and upper layers of the dermis o Wound will be pink, red in color, painful and wet appearing o Wound will blanch when pressure is applied o Should heal in several weeks (10-21 days) without grafting, scarring is usually

minimal Full thickness

o Can be red or white in appearance, but will appear dry. o Involves the destruction of the entire epidermis and most of the dermis o Sensation can be present, but diminished o Blanching is sluggish or absent o Full thickness will most likely need excision & skin grafting to heal

Third degree:

All layers of the skin is destroyed Extend into the subcutaneous tissues Areas can appear, black or white and will be dry Can appear leathery in texture Will not blanch when pressure is applied No pain

Burns are classified according to the total body surface area (TBSA) involved, the depth of burn, and the presence or absence of inhalation injury.

First Second (Superficial or Deep)

Third (Full Thickness)

Depth (how deep the burn is)

Epithelium Epithelium and top aspects of the dermis

Epithelium and dermis

How the wound looks

No blisters; dry pink Moist, oozing blisters; Moist, white, pink, to red

Leathery, dry, no elasticity; charred appearance

Causes Sunburn, scald, flash flame

Scalds, flash burns, chemicals

Contact with flame, hot surface, hot liquids, chemical, electric

Level of Pain (sensation)

Painful, tender, and sore

Very painful Very little pain, or no pain

Healing Time Two to five days; peeling

Superficial: five to 21 days. Deep: 21-35 days

Small areas may take months to heal; large areas need grafting.

Scarring No scarring; may have discoloration

Minimal to no scarring; may have discoloration

Scarring present

The TBSA burned is calculated using the rule of nines (Figure 76-1). In adults, each upper extremity and the head and neck are 9% each of the TBSA, the lower extremities and the anterior and posterior aspects of the trunk are 18% each of the TBSA, and the perineum and genitalia are 1% of the TBSA. Children have a larger proportion of body surface area contributed by the head and neck relative to the surface area of the lower extremities. The Lund-Browder chart can be used to estimate the TBSA in children

Burn depth is classified according to the degree of injury in the epidermis, dermis,

subcutaneous fat, and underlying structures (Table 76-1). First-degree burns are confined to

the epidermis, are painful and erythematous, and do not result in scarring. Second-degree or

partial-thickness burns are classified further as superficial and deep. Superficial second-

degree burns are erythematous and painful, spontaneously heal in 7–14 days, and may result

in skin discoloration. Deep second-degree burns appear pale and mottled but remain painful

to pinprick, heal in 14–35 days by reepithelialization, and often result in severe scarring.

Third-degree or full-thickness burns are characterized by eschar that is painless and black,

white, or cherry red and result in scarring and some limitation of function. Fourth-degree

burns involve organs beneath the skin, such as muscle and bone; require complete excision;

and result in limited function.

Classification Depth of Injury Appearance/Sensation Outcome First degree Epidermis Erythematous No scarring Painful Second degree (partial thickness)

Superficial Epidermis and superficial dermis

Erythematous Painful

Heals in 7–14 days Skin discoloration

Deep Epidermis and into deep dermis

Pale, mottled Painful to pinprick

Heals in 14–35 days Severe scarring

Third degree (full thickness)

Epidermis, dermis, and into subcutaneous fat

Leathery eschar (black, white, or cherry red) Painless

Requires excision Scarring with some limitation of function

Fourth degree Epidermis; dermis; subcutaneous fat; and into muscle, fascia, or bone

Brown, charred Painless

Requires excision Limitation of function

Inhalation injury

The critically ill burn patient has multiple mechanisms in addition to smoke inhalation that

may contribute to lung injury such as sepsis, Ventilator-Induced Lung Injury (VILI) or a

systemic inflammation in response to burns.

Inhalation injury may describe pulmonary trauma caused by inhalation of thermal or

chemical irritants.

1) heat injury which is restricted to upper airway structures except in the case of steam jet

exposure, suhu yang sgt panas memicu penutupan laring dan suhu yang panas itu sendiri

mengakibatkan massive swelling of the tongue, epiglottis, and aryeepiglottic folds with

obstruction pertimbangkan intubasi

2) local chemical irritation throughout the respiratory tract Smoke-related toxins

membahayakan epithelial and capillary endothelial cells pada jalur pernafasan risiko

trakeobronkitis. Respiratory failure may occur from 12 to 48 hours after smoke exposure.

Characteristics are decreased lung compliance, increased ventilation perfusion mismatch, and

increase in dead space ventilation.

3) systemic toxicity as may occur with inhalation of carbon monoxide or cyanide

carboksihb susah dideteksi, namun half-life of carboxyhemoglobin is 250 minutes for the

victim breathing room air dan dapat dikurangi to 40 to 60 -minutes with inhalation of 100%

oxygen.

Diagnosis

Physical findings including facial injury, singed nasal hairs, soot in the proximal airways,

carbonaceous sputum production and changes in voice fiberoptic bronchoscopy

Treatment

- bronkoskopi

Aggressive use of bronchoscopy is highly effective in removing foreign particles and

accumulated secretions that worsen the inflammatory response and may impede ventilation.

- Immediate management of carbon monoxide toxicity is administration of normobaric

oxygen by means of a nonrebreather reservoir facemask supplied with high flow oxygen or

100% oxygen by means of an artificial airway. HATI2: Carbon monoxide exposure can

exacerbate angina and cause cardiac injury even in persons with normal coronary arteries.

Thus, exposed patients may require cardiovascular investigation including electrocardiogram

and measurement of cardiac enzymes. Hyperbaric oxygen has potential complications

including barotrauma, tympanic membrane disruption, seizures and air embolism.

- Cyanide is produced by combustion of natural or synthetic household materials including

synthetic polymers, polyacrylonitrile, paper, polyurethane, melamine, wool, horsehair and

silk. Ingestion of cyanide products produces metabolic acidosis which is also seen in

burn patients during resuscitation.

Sulit dideteksi juga karena CN normal diproduksi in vitro oleh SDM dalam jumlah kecil. A

popular cyanide antidote kit utilizes a series of reactions with oxidation of hemoglobin to

methemoglobin which binds cyanide forming cyanomethemoglobin. As

cyanomethemoglobin dissociates, free cyanide is converted to thiocyanate by hepatic

mitochondrial enzymes using colloidal sulfate or thiosulfate. Thiocyanate is then excreted in

the urine. European data suggests treatment of cyanide poisoning with chelating agents such

as dicobalt edetate or hydroxycobalamin.

- A significant number of patients with smoke inhalation will develop pneumonia in

association with mechanical ventilation. High Frequency Oscillatory Ventilation (HFOV)

supports the lung at a mean airway pressure above that used in conventional ventilation.

Airway Pressure Release Ventilation (APRV) uses continuous positive airway pressure

applied at a high level with intermittent releases of airway pressure.

Terapi medikamentosa

- beta agonis

The use of inhaled agents targeting beta-adrenoreceptors may help ameliorate this

bronchoconstriction. Nebulized epinephrine & nebulized albuterol.

- Pulmonary blood flow

Tujuan:

1. diminishing bronchial arterial blood flow and thus, 2. decreasing the flow of systemic

inflammatory mediators to the lung

- inhaled nitric oxide (NO) decreased ventilation/perfusion mismatch, decreased

shunting, and decreased pulmonary hypertension

- Anticoagulants (Airway casts are formed by a combination of sloughed epithelial cells,

mucus, inflammatory cells, and fibrin)

- combination of aerosolized heparin and recombinant human antithrombin

- tissue plasminogen activator (TPA)

- The combined heparin/lisofylline group had decreased shunt and less of an increase

in alveolar-arterial oxygen tension gradient after a smoke inhalation injury.

Antiinflammatory agents

- intinya menghambat thromboxane A2 OKY-046 as a thromboxane synthase

inhibitor decreased pulmonary thromboxane, and in turn had decreases in

pulmonary vascular resistance and less of a decrease in cardiac output.

- Free oxygen radicals also trigger inflammation during inhalation injury. Nebulized

gamma-tocopherol

- Sistem parasimpatis mengaktifkan sekresi Ach bekerja pada reseptor

muskarinik untuk konstriksi otot polos pada sal napas dan mengaktifasi kelenjar

submukosa. Pake : muscarinic antagonist tiotropium bromide.

1. zona koagulasi cedera paling parah.

Pada zona ini terdapat jaringan yang

irreversibel karena koagulasi dan protein

konstituen

2. Zona stasis sekitar daerah ini

ditandai dengan berkurangnya perfusi

jaringan. Berpotensi mati. Kalau ada

keadaan hipotensi berkepanjangan,

infeksi, edema area complete loss.

3. hiperemis perfusi meningkat. Dapat pulih kcl bila ada sepsis parah dan hipoperfusi

berkepanjangan.

Cardiovascular changes—Capillary permeability is increased, leading to loss of

intravascular proteins and fluids into the interstitial compartment. Peripheral and splanchnic

vasoconstriction occurs. Myocardial contractility is decreased, possibly due to release of

tumour necrosis factor. These changes, coupled with fluid loss from the burn wound, result in

systemic hypotension and end organ hypoperfusion.

Respiratory changes—Inflammatory mediators cause bronchoconstriction, and in severe

burns adult respiratory distress syndrome can occur.

Metabolic changes—The basal metabolic rate increases up to three times its original rate.

This, coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral

feeding to decrease catabolism and maintain gut integrity.

Immunological changes—Non-specific down regulation of the immune response occurs,

affecting both cell mediated and humoral pathways.

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 TBSA 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 TBSA Age > 60 yr or < 2 yr Presence of simultaneous major trauma or smoke inhalation

Infection, even in small burns, is a common cause of sepsis and mortality, as well as local complications. Impaired host defenses and devitalized tissue enhance bacterial invasion and growth. The most common pathogens are streptococci and staphylococci during the first few days and gram-negative bacteria after 5 to 7 days; however, flora are almost always mixed.

Metabolic abnormalities may include hypoalbuminemia that is partly due to hemodilution (secondary to replacement fluids) and partly due to protein loss into the extravascular space through damaged capillaries. Dilutional electrolyte deficiencies can develop; they include hypomagnesemia, hypophosphatemia, and hypokalemia. Metabolic acidosis may result from shock, bisa juga dari inhalasi sianida. Rhabdomyolysis or hemolysis can result from deep thermal or electrical burns of muscle or from muscle ischemia due to constricting eschars. Rhabdomyolysis causing myoglobinuria or hemolysis causing hemoglobinuria can lead to acute tubular necrosis and renal failure.

Local:

Eschar is stiff, dead tissue caused by deep burns. A circumferential eschar, which completely encircles a limb (or sometimes the torso), is potentially constricting. A constricting eschar limits tissue expansion in response to edema.

Scarring and contractures result from healing of deep burns. Depending on the extent of the scar, contracture deformities can appear at the joints. If the burn is located near joints (particularly in the hands), in the feet, or in the perineum, function can be severely impaired. Infection can increase scarring.

Debridement: Suatu tindakan eksisi pada luka bakar yang bertujuan untuk membuang jaringan nekrosis maupun debris yang menghalangi proses penyembuhan luka dan potensial terjadi/berkembangnya infeksi; sehingga merupakan tindakan pemutus rantai respon inflamasi sistemik dan maupun sepsis.

c. Indikasi Operasi Debridement luka bakar diindikasikan pada luka bakar yang dalam misalnya luka bakar deep-dermal dan subdermal. Luka bakar yang dalam ini ditandai dengna permukaan yang keputihan, merah, kecoklatan, kuning atau bahkan kehitaman dan tidak adanya capillary refill ataupun sensibilitas kulit.

Balutan awal harus dipertahankan selama 3-7 hari, kecuali timbul rasa sakit, berbau, basah.

Bila proses eksudasi tidak berlebihan, biasanya penilaian hasil, sekaligus penggantian balutan

dapat dikerjakan dalam waktu 5-7 hari pasca bedah. Sebaliknya, dengan eksudasi yang

berlebihan; terlihat sebagai balutan yang jenuh, dalam 24-48 jam pertama pasca bedah dapat

dilakukan pergantian balutan.