07 Burns

Chemical Injury

Chemical burns are typically due to either a strong acid or an alkali.

Alkali and acid burns present differently.

Alkali burns are usually full thickness and cause the skin to appear pale and feel slippery.

On the other hand, acid burns are usually partial-thickness. Patients usually develop erythema and erosion.

Alkali and acid burns are treated with tap water and surgery if necessary.

Burns should be irrigated with tap water before arriving to the emergency department.

Water may not completely resolve an alkali burn, in which case, surgery will be necessary.

Unlike the treatment of other acidic burns, hydrofluoric acid burns should be covered with calcium gluconate gel.

Polyethylene glycol, in addition to water irrigation, may be used to treat a phenol burn by increasing the latter’s solubility.

Electric

Electric shock and burn occurs via current flow through the body.

Young men and children are disproportionately injured.

Both the type of current and the amount of voltage affect the extent of damage from a shock.

The skin is a barrier to injury from electric shock. However, wet skin and breaks in the skin both reduce this resistance.

Electric shocks cause general, neurologic, orthopedic, and cardiovascular clinical findings.

• General clinical findings: Pain, fatigue, and headache.

• Neurologic clinical findings: Nervous irritability, seizures, deafness, and blindness.

• Orthopedic clinical findings: Shoulder dislocation and femoral neck fractures, for example.

• Cardiovascular clinical findings: ectopic beats, sinus tachycardia, bradycardia, atrial fibrillation, asystole, and ventricular fibrillation.

• Electrical burns to internal organs may be hidden by small external burn

• Skin necrosis and sloughing may not occur for days.

• Third spacing of fluid occurs with internal organ injury.

• Rhabdomyolysis can occur.

Electrical shocks are managed by freeing the patient from the current either by turning off the power, severing the wire, or by prying them or hitting them away with a non-conductive material (e.g. wooden board).

Cardiac and ventilatory statuses should be checked immediately. CPR must be initiated if necessary.

Electrical burns are treated conservatively.

Give an intravenous infusion of crystalloid solutions if the patient is in circulatory shock. Acidosis may require the infusion of intravenous bicarbonate therapy. Mannitol may be given to those with very low urine output. A fasciotomy may be necessary, but the full extent of an electrical burn may not be apparent until 7-10 days after the burn.

Burns

Severe burns disrupt the skin barrier and create an avascular, immunologically poor, protein-rich substrate for the growth and proliferation of bacteria and fungus. Immediately after a severe burn, gram-positive organisms (eg, Staphylococcus aureus) from hair follicles and sweat glands dominate; after more than 5 days, most infections are due to gram-negative organisms (eg, Pseudomonas aeruginosa) or fungi (eg, Candida).

Wound infections are common, and patients with large surface area (>20%) burns are at highest risk. The earliest sign is usually a change in appearance (partial-thickness injury turns into a full-thickness injury) of the wound or the loss of a viable skin graft. Burn wound sepsis can develop rapidly and is associated with some or all of the following systemic findings:

• Temperature less than 36.5 C (97.7 F, as in this patient) or more than 39 C (102.2 F)

• Progressive tachycardia (>90/min)

• Progressive tachypnea (>30/min)

• Refractory hypotension (systolic blood pressure <90 mm Hg)

Oliguria, unexplained hyperglycemia, thrombocytopenia, and mental status changes are also common. Diagnosis requires quantitative wound culture (>105 bacteria/g of tissue) and biopsy for histopathology (to determine tissue invasion depth). Treatment involves empiric, broad-spectrum intravenous antibiotics (eg, piperacillin/tazobactam, carbapenem) with the addition of potential coverage for methicillin-resistant Staphylococcus aureus (eg, vancomycin) or multidrug-resistant Pseudomonas aeruginosa (eg, an aminoglycoside). Local wound care and debridement are usually necessary.

Initial Management

The initial management of burn injuries is identical to the management of all trauma patients - airway, breathing and circulation must always be secured first. Burn victims are at high risk for respiratory compromise because the supraglottic airway, which efficiently exchanges heat with inhaled air, is very susceptible to direct thermal injury and acute obstruction by edema and blistering. (In contrast, the subglottic airway is protected from injury by reflexive closure of the vocal cords upon exposure to extremely hot air.) Clinical indicators of thermal and smoke inhalation injury include: burns on the face, singeing of the eyebrows, oropharyngeal inflammation, blistering or carbon deposits, carbonaceous sputum, stridor, carboxyhemoglobin level >10%, and a history of confinement in a burning building. All burn victims should be treated initially with high-flow oxygen via a non-rebreather mask, though caregivers should maintain a low threshold for intubation in any patient with physical evidence of thermal damage to the upper airway. A key reason for early intubation is that progressive airway edema may preclude intubation later in the patient's clinical course, potentially necessitating an emergent surgical airway.