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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.