Incidence: Electric Burns of the lip are the most common electric injury in children.^1,2 In comparison with flame and scald burns, electric burns are seen infrequently.¹ The Brooke Army Medical Center Burn Unit, Fort Sam Houston, Texas reports to see approximately three patients per year.^3,4 The Children's Hospital, Columbus, Ohio shows 3% of their burn patients to have electrical burns that usually involve the commissure of the mouth.¹

Age group: The majority of the patients is younger than three years.5 Roughly at four to six months infants start to explore their environment by grasping objects and inserting them in their mouth.  Etiology and Pathophysiology: The extent of tissue damage is related to the type of current passing through the tissue.6 Exposure to 110-220V household lines is generally not fatal but can cause arrhythmias. With 220V cutaneous burns are more severe and cause more significant damage to structures deep to the skin. Tissue destruction increase with increasing amperage.

Fig1. Three year old girl with electric burn on lip two weeks post-injury, notice that eschar (necrotic wound tissue)has been lost.  Photo courtesy Dr. MaryJo McGuire

Alternating current at low voltage is more dangerous than direct current. Alternating current produces tetanic spasm, freezing the patient to the power source with subsequent prolongation of contact. Low cycle household lines (50-60 Hz) are more dangerous than high cycle commercial currents. The lower the tissue resistance the more extensive the injury. Nerve, blood vessels, and muscle offer the least resistance and show greatest destruction. Tendon, fat and bone have the highest resistance. The moist and highly vascular lip mucosa offers very little resistance to electric current.⁶ Children with electric burns should have a thorough systemic evaluation. If the subject is well grounded the current may flow through the body and cause cardiac arrhythmias. Renal injury may result from direct damage or through myoglobinuria caused by breakdown products at the site of injury. Neurologic damage may involve peripheral nerves. Cerebral damage can become evident as long as two years later.^7,8

Electrical injuries to the mouth are most commonly caused by "live" extension or appliance cords. The pool of saliva in the labial sulcus or the moist mucosa act as a conductor for the electric current. The tissue injury results from direct thermal changes at the entrance and exit site. Temperatures can reach as high as 3000°C (5400°F).⁶ These burns are usually full thickness burns involving deep muscle destruction. The damage to the nerve tissue frequently causes anesthesia or paresthesia.⁹ Blood vessels are cauterized and little or no hemorrhage is present. Unfortunately spontaneous arterial bleeding can occur during the first three weeks.^4,5,6 The burn most often invades both upper and lower lip and the oral commissure. After six hours the surrounding tissue becomes edematous and the prior to that well delineated wound margin becomes irregular. Edema, paresthesia, and tissue destruction contribute to drooling. The necrotic tissue, known as eschar, separates in two to three weeks (see Fig1.), resulting in a well demarcated ulceration, that will be filled from below by granulation tissue.⁶ The later period of healing will be characterized by scar formation, contracture, and microstomia.⁶

Contracture and scar formation: The sphincter activity of the orbicularis oris muscle contributes to the contracture of the wound and the development of microstomia. Contracture and hyperplastic scar formation though are well known and frustrating sequelae of burn injuries.¹⁰ Healing burn wounds are characterized by a marked increase in vasculature, fibroblasts, and collagen deposition. The newly formed collagen fibers become compact and disorganized, maintaining the wound in a shortened position. Following the scar formation the collagen is less compact, but continues to hold the wound in a shortened position. Two observations in burn wounds are (1) The position of comfort is the position of contracture (2) The burn wound will shorten until it meets an opposing force.¹⁰ These wound shortening mechanisms can be combated by traction, splinting, and exercise. Existent contracture and scar formation can be treated with constant pressure above capillary pressure. The scar is most responsive to this treatment during the first three to six months following healing.¹⁰

Management: Upon presentation a prompt evaluation for patency of airway and adequate breathing and circulation is necessary.⁶ Admission to the hospital is recommended by several sources^4,6, whereas others believe patients can betreated on outpatient basis.⁵ Complete H&P, EKG, hematologic evaluation, electrolyte determination, urinalysis, and coagulation profile should be done.⁶ The patient needs to be monitored for signs of shock, cardiorespiratory collapse, or late hemorrhage. Tetanus prophylaxis should be assured in all cases of electric burns to the oral cavity.^1,6 Most authors recommend prophylactic antibiotic coverage.^1,4,6 Proper nutrition is paramount to proper healing. Nasogastric tubes can be indicated in severe cases. From a nutritional standpoint children represent a high risk population. Under normal circumstances children are gaining weight and growing on a daily basis. Weight loss cannot be accepted as a normal result of an oral burn injury.⁶

The local wound care is instituted immediately with warm saline rinses and peroxide irrigation. Topical antibiotics (Bacitracin®) can be applied. The sloughing eschar should not be disturbed.⁶ The placement of a splint can prevent wound contracture.^{2,5,6,9,11,12} The goal is to preclude the need for corrective surgery.

The splint should be placed prior to the proliferation of granulation tissue. The design of the splint holds the commissures at a constant tension opposing the contracting forces of the scar tissue. Different designs can be used, depending on the age and the compliance of the patient. If enough teeth are erupted fixed appliances can be used. Otherwise extraoral splints or facemasks may be indicated. Compliance is a major factor since the maturation of burn scars may last from three months to three years. Early contractures can be corrected with expansile removable appliances. Silverglade reports expansions of over 20mm without patient discomfort.⁵

Splint appliances maintain the intercommissure dimension. In partial-thickness burns no surgery may be necessary. In more severe full-thickness circumoral burns procedures can be limited to a single operation instead of multiple surgical follow-up interventions.⁵

References

1. Harmel RP, Vane DW, King DR: Burn Care in Children: Special Considerations, Clin Plast Surg 13:1, 95-105, 1986

2. Pitts W, Pickrell K, Quinn G., Massengill R: Electrical burns of lips and mouth in infants and children, Plast Reconstr Surg 44:471-479, 1969

3. Taylor PH, Pugsley LQ, Vogel EH: The intriguing electrical burn, J Trauma 2:309, 1962

4. McMaughan GW, Brooke Army Medical Center Burn Unit, personal communication

5. Silverglade D, Ruberg RL: Nonsurgical management of burns to the lips and commissures, Clin Plast Surg 13:1, 87-94, 1986

6. Hirschfeld JJ, Assael LA: Conservative management of electric burns to the lips of children, J Oral Maxillofac Surg 42:197-202, 1984

7. Esses SI, Peters WJ: Electrical burns: ponnophysiology and complications, Canadian J Surg 24:11, 1981

8. Ugland OM: Electrical burns: a clinical and experimental study with special reference to peripheral nerve injury, Scand J Plast Reconstr Surg 2:141, 1967

9. McDonald RE: Dentistry for the child and adolescent, 6th ed. Mosby 1994

10. Larson DL, Abston S, Willis B, Linares H, Dobrkovsky M, Evans EB, Lewis SR: Contracture and scar formation in the burn patient, Clin Plast Surg 1:4, 653-666, 1974

11. Silverglade D: Splinting electrical burns utilizing a fixed splint technique: a report of 48 cases, J Dent Children 50:455-458, 1983

12. Richardson DS, Kittle PE: Extraoral management of a lip commissure burn, J Dent Children 48:352-356, 1981

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