Non-fire facial trauma

Cold injury of the maxillofacial region

In deep exposure to low temperatures, the management tactics depend on the degree of tissue damage.

Grade III injuries are characterized by the formation of an eschar. Local therapy aims at its rapid rejection — for this, a 5% iodine tincture is used. To avoid purulent complications, the wound is regularly sanitized with antiseptics. An important anatomical feature: facial frostbites are treated using an open method until granulations appear. Only after the rejection of necrotic masses and the formation of a granulating surface does one switch to closed management, applying moist-drying dressings with antiseptics until complete epithelialization.

Grade IV injuries are accompanied by irreversible loss of tissues and entire anatomical structures of the face, which subsequently requires complex reconstructive surgery.

All patients with frostbite must receive tetanus antitoxin administration. It should be remembered that areas of the face subjected to cold injury permanently acquire thermal hypersensitivity — the risk of re-frostbite remains high even with minimal exposure to the cold.

Pathogenesis and clinical presentation of chemical burns

Aggressive chemical agents (acids, alkalis, heavy metal salts) disrupt microcirculation in the surrounding tissues, which is why such wounds heal much slower than thermal injuries. The depth of destruction directly depends on the concentration, temperature of the substance, and duration of its contact with the skin.

Burns caused by acids and heavy metal salts They provoke protein breakdown and rapid dehydration, leading to the formation of coagulative (dry) necrosis.

• Sulfuric acid: produces a thermochemical effect (with heat release), forming a brown or white eschar against the background of severe edema and hyperemia. Fumes, posing a threat of inhalation injuries.
• Nitric acid: acts more aggressively than sulfuric. Leaves a greenish-yellow eschar that is completely painless upon palpation.
• Hydrochloric acid: concentrated causes yellow necrosis, weak causes blisters.
• Hydrofluoric acid: insidious with a latent period of 4 to 6 hours. Then acute pain occurs, blisters with a gelatinous bottom appear. Tissue destruction continues even after removing the reagent from the surface.

Alkali burns (caustic soda, caustic potash) Alkalis split protein structures and saponify fats, forming liquefactive (wet) necrosis. The surface is covered with a loose dirty-white eschar. Unlike acids, alkalis penetrate much deeper, act longer, and do not form a demarcation wall. Destroyed tissues accumulate the chemical, forming toxic albuminates that continue to corrode tissues for several days. Strong alkalis can completely dissolve nails, hair, and muscles.

Emergency care for chemical injuries

The key task at the pre-hospital stage is to immediately remove the reagent, reduce its concentration, and cool the tissues. The basic method is copious washing of the wound under running water for 20–30 minutes.

Critical exceptions (when water is contraindicated):

1. Aluminum compounds (triethylaluminum, diethylaluminum hydride) — ignite upon contact with water. They must be washed off with alcohol, gasoline, or kerosene.
2. Concentrated sulfuric acid and quicklime — enter into an exothermic reaction with water, which adds a severe thermal burn to the chemical one.

Special case: the area affected by hydrofluoric acid must be washed continuously for 3 to 5 hours to flush out deeply penetrated fluoride ions.

Applying neutralizing solutions before arriving at the hospital is not recommended. Wasting time preparing them will worsen destruction, and a mistake in identifying the chemical agent will lead to unpredictable reactions.

Inpatient treatment and neutralization

In a clinical setting, chemical neutralization is mandatory.

• For acids on the face, compresses of 2–5% sodium bicarbonate are used.
• To neutralize hydrofluoric acid, the affected area is treated with a 10–20% ammonia solution (1–3 minutes), then rinsed with water, repeating the cycle. Compresses with magnesium oxide and glycerin are also effective.
• For alkalis, weak (1–2%) solutions of acids—citric or acetic—are used.

If the patient arrives late, pastes containing neutralizers are applied to the wound. If signs of systemic poisoning (resorptive intoxication) appear, specific antidotes and infusion therapy are administered.

Primary surgical debridement (PSD) of the face

PSD is a set of surgical measures that creates an optimal environment for regeneration. As N.I. Pirogov wrote, the essence of the intervention lies in transforming a bruised wound into a clean incised one.

Objectives of facial PSD:

1. Management of life-threatening conditions (bleeding, shock, asphyxia).
2. Prevention of infectious complications.
3. Preservation of vital functions (speech, chewing, swallowing).
4. Minimization of cosmetic defects and disfigurement.

Assistance begins right in the emergency department. Victims undergo sanitary processing and strict medical triage. First, patients with asphyxia, uncompensated shock, or profuse bleeding are taken to the operating table. Second, individuals with massive destruction of the facial skeleton and soft tissues are operated on. Patients with minor injuries await care in the third queue.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathophysiology of resorptive intoxication in extensive chemical burns.
• Providing care for combined inhalation injuries caused by acid vapors.
• Methods of reconstructive plastics in the loss of facial tissues (grade IV frostbite).
• Specific antidotes used in toxicology for chemical burns.

Other topics in the section "Chapter 11. Non-ballistic and ballistic facial injuries. Thermal and radiation lesions of the maxillofacial region (V.V. Afanasyev)"

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