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Minggu, 18 Desember 2011

ACUTE BURN


Oleh : Dr. Mgs. Roni Saleh, SpB-SpBP(K)

I. Phatophysiology
A.The severity of the burn is determined by temperatur and length of exposure to the heat source.
B.Skin has a large water conten; therefore, it overheats slowly and cools slowly.
C.Heat continues to penetrate deeper tissue layers even after the external heat source is removed. Immediate cooling may reduce underlying tissue temperature, but it has a limted role in large burns because it may reduce the patient’s core temperature.

D. Three areas of injury
1.Central “zone of coagulation”: Nonviable, irreversibly injured tissue.
2.Middle “zone of stasis”: Initially characterized by dilated blood vessels and capillary diffusion. After 24 to 28 hours, dilated capillaries become occluded, with resulting conversion of this zone of tissue to coagulation. Injury in this zone may be reversible with appropriate treatment (cooling, fluid resuscitation, critical care).
          Outer “zone of hyperemia”: Composed mostly of viable, edematous tissue.

E.Progressive changes in microcirculation
1.There is an initial, sudden decrease in blood flow.
2.Arteriolar vasodilation follows.
3.Increase capillary permeability leads to edema formation, which is greatest at 8 to 12 hours.
4.Endogenous mediators (histamine, serotonin, kinins) increase capillary permeability, leaking protein into the intersitial space.
5.Hypoproteinemia decreases intravascular oncotic pressure, resulting in a shift of fluid into the interstitium (i.e., “third spacing”)

II. Initial management
A.History
1.Identity the source: Hot liquid, chemicals, flame, superheated air/steam, explosion, etc.
2.Duration and location of exposure: Closed space; potential for smoke inhalation
3.Concomitant drug or alcohol ingestion
4.Associated injury mechanism: Esplosion, jump/fall, motor vehicle crash, etc.


B. Airway and breathing
1.Early intubation
a.Frequently necessary to prevent airway obstruction due to progressive airway edema.
b.Most patients with extensive (>50%) burns requre intubation
c.Use humidified oxygen.
2.Chest and abdominal wall burns can severely limit chest wall excursion and impair ventilation.  Escharotomies may be necessary 


C.Circulation
1.Intravenous access:  Ideally, several peripheral large-bore intravenous lines should be place through nonburned tissue.  Central lines are the next best option.
2.Intravenous fluid administration
a.Isotonic salt solutions are used for resuscitation and maintenance.
b.Glucose should be avoided.  Burn patients are frequently  glucose intolerant and hyperglycemic due to the stress response. The resulting osmotic diuresis can lead to spuriously high urine output.
D.Disability : A rapid, thorough baseline neurologic examination should be performed.  This is especially important in the setting of blunt trauma, head injury, carbon monoxide exposure, and/or the need for sedation.


E.Initial wound care
1.Stop the burning process
a.Flame burns: smoldering or burning materials must be extinguished and removed, since they can retain heat and exacerbate the burn injury.  Irrigate the wounds with normal saline if any foreign material remains.
b.Chemical burns: Remove all clothing and begin gentle, copious irrigation with warm normal saline.  Avoid the use of neutralizing solutions.
2.Cover: Clean, dry, nonadherent dressings are used to protect the wound and prevent hypothermia.
3.Analgesia.
4.Tetanus prophylaxis.
5.Prophylactic intravenous antibiotics are not indicated.
6.Criteria for admission to a burn center.
a.If 10 to 40 years old: Greater than 15% total body surface area (TBSA) second-degree burns or greater than 3%. TBSA third-degree burns should be treated on an inpatient basis.
b.If younger than 10 years or older than 40 years: Greater than 10% TBSA second-or third-degree burns.
c.Burns involving the face, hands feet and/or perineum
d.Circumferential extremity burns.
e.Electrical burns

III. Inhalation Injury

A.Etiology
1.Chemical irritants in smoke affect the distal airways, resulting in an intense inflammatory response, which can lead to adult respiratory distress syndrome (ARDS) and/or systemic inflammatory response syndrome (SIRS).
2.Direct thermal injury: inhalation of superheated air or water vapor can cause a thermal burn to the airway mucosa.
3.Oropharyngeal and supraglottic edema caused by thermal injury can progress to airway obstruction
B.Evaluation
1.Maintain a high index of suspicion.
2.Signs and symptoms
a.History of burn in a closed space
b.Presence of facial burns and/or oral carbon deposits.
c.Singed facial hair/nares, hoarseness, or wheezing.
d.Unconsciousness.
3.Nasopharyngoscopy: Can be used to directly evaluate the larynx and vocal cords for injury.
4.Bronchoscopy: Via the endotracheal tube, if symptoms warrant.
C.Treatment
1.Intubation, mechanical ventilation
a.Early intubation is essential. Patients with inhalation injury often present as conscious, awake, and comfortable initially.  Upper airway edema can progress rapidly to complete airway obstruction.
b.Ventilator management goals: Maximize oxygenation while avoiding oxygen toxicity (keep FiO2 <0.7) and barotrauma.
2.Bronchodilators: Useful in treating bronchospasm associated with smoke inhalation.
3.Steroids: Have not been shown to be beneficial in avoiding pulmonary complications with burns
D.Carbon Monoxide (CO) poisoning
1.CO is generated by fire.  When inhaled and absorbed, it preferentially binds with hemoglobin, displacing oxygen and blocking oxygen binding sites, causing a substantial reduction in oxygen delivery.
2.Signs and symptoms
a.Pulse oximetry is unreliable
b.Cherry red skin
c.Hypoxemia
d.Mental status changes or a history of a loss of consciousness
e.Persistent acidosis in the presence of normovolemia
3.CO level
a.May be normal or minimally elevated, even with significant exposure.
b.20% to 40% Associated with severe neurologic symptoms.
c.Greater than 60% Commonly fatal
4.Treatment
a.100% oxygen administration: Displaces CO from hemoglobin
b.Hyperbaric therapy: Consider if the patient is at risk for CO exposure and has mental status changes

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