Do not limit the examination of a patient with a significant chemical acid burn to the skin because acids may cause respiratory and mucous membrane irritation as well. Furthermore, skin absorption of some compounds may occur and result in systemic signs and symptoms.
With the exception of hydrofluoric acid, strong acids produce coagulation necrosis from the denaturation of proteins in the superficial tissue. Injury severity is related to the physical characteristics of the acid. Most substances with a pH <2 are strong corrosives. Other important tissue-damaging properties of acids include concentration, molarity, and complexing affinity for hydroxyl ions. The higher each of these factors is, the greater is the tissue damage. Contact time with the skin is the most important chemical burn feature that healthcare professionals may alter. For example, instantaneous skin decontamination of 18M sulfuric acid will cause no burn, but a 1-minute exposure can cause full-thickness skin damage.
The dilute (<40%) acetic acid solution found in hair-wave neutralizer solutions is perhaps the most common cause of chemical burns to the scalp in women. Prolonged contact, especially with an already damaged scalp, can cause a partial-thickness burn that heals slowly and is prone to infection. Initial treatment is copious water irrigation. Oral antibiotics should be prescribed if the scalp burn has created open skin lesions.
Phenol (carbolic acid), a corrosive organic acid used widely in industry and medicine, denatures proteins and causes chemical burns characterized by a relatively painless white or brown coagulum. Paradoxically, dilute phenol penetrates tissue more readily than the concentrated form. Systemic absorption may result in life-threatening cardiac dysrhythmias or seizures. The unpleasant, acrid odor of phenol, detecTable in air at 0.047 parts per million, and its low volatility help prevent airborne exposure. Although commercially available in concentrations up to 90%, even dilute solutions of 1% to 2% phenol may cause a burn if contact is prolonged or extensive. Chemically related phenolic compounds that induce skin damage include cresol, creosote, and cresylic acid.
Coagulation necrosis of the involved area is common. Necrotic tissue may delay absorption temporarily, but phenol may become entrapped under the eschar. Remove contaminated clothing and begin water irrigation immediately. Water lavage alone may not be totally effective, because the necrotic coagulum inhibits water penetration to the deeper layers.
Decontamination is more effective by the use of an undiluted polyethylene glycol solution of molecular weight 200 to 400 or by a gentle wash with isopropyl alcohol. Adequate supplies of either irrigation solution should remain stored for such use. Either irrigation solution reduces the extent of cutaneous corrosion and also decreases systemic toxicity. An isopropyl alcohol rinse is equivalent to polyethylene glycol in removing phenol.3 The advantage of isopropyl alcohol is its ready availability. If neither polyethylene glycol nor isopropyl alcohol is available in adequate supplies, large volumes of water should be used.
Chromium hexavalent compounds (Cr6+) are powerful oxidizers. The chromate ion in chromic acid produces a chronic penetrating ulcerating lesion of the skin. Associated signs and symptoms of chromic acid exposure are conjunctivitis, lacrimation, and ulceration of the nasal septum. Systemic chromium toxicity can cause liver or renal failure, GI bleeding, coagulopathy, and CNS disturbances. Significant symptoms may occur after only 1% to 2% body surface area burns. A 10% body surface area cutaneous burn caused by chromic acid can be fatal due to systemic toxicity. Any acute skin exposure to chromic acid should be treated with copious water irrigation and observation for systemic effects. Aggressive excision is the best method for prevention of systemic effects because depth of the burn is difficult to determine and absorption of chromium may continue after irrigation.4
Formic acid in 60% solution is used by acrylate glue makers, cellulose formate workers, and tanning workers. Formic acid produces coagulation necrosis of the skin. Systemic effects, including decreased respiration, anion gap metabolic acidosis, and hemolysis have been reported.5 Treatment includes immediate decontamination and irrigation with water. Systemic toxicity may require intravenous sodium bicarbonate for the metabolic acidosis or exchange transfusions for severe hemolysis.
HYDROCHLORIC AND SULFURIC ACIDS
The dermal toxicity of hydrochloric acid and sulfuric acid is so well recognized that early decontamination and water irrigation usually prevent severe burns to the skin. These acids can burn the skin dark brown or black. Toilet bowl cleaners may contain 80% solutions of sulfuric acid, and some drain cleaners may be 95% to 99% sulfuric acid solutions. Munitions, chemical, and fertilizer manufacturers commonly use 95% to 98% sulfuric acid solutions in their industrial processes. Automobile battery fluid is 25% sulfuric acid. Most household bleaches are only 3% to 6% hypochlorite solutions, which, although acidic, cause little damage unless they are in contact with skin for a prolonged time. Treatment is the same as for formic acid burns.
Hydrofluoric acid is used in the production of high-octane fuel, etching and frosting glass, semiconductors, microelectronics/microinstruments, germicides, dyes, plastics, tanning, and fireproofing material and is used in cleaning stone and brick buildings. It is also a very effective rust remover.
Unlike other acids, hydrofluoric acid penetrates deeply and will cause progressive tissue loss. It produces burns in two ways. First, hydrogen ions cause direct cellular damage as other acids do through protein denaturation. Second, free fluoride ions scavenge intracellular cations, such as calcium and magnesium, disrupt cellular membranes, and inhibit the sodium/potassium/ATPase. This leads to systemic hypocalcemia, hypomagnesemia, and hyperkalemia. Locally, free fluoride ions cause spontaneous depolarization of nerve tissue and severe pain. Pain will persist until all free fluoride ions have been neutralized.
The dermal effects may not be immediately noted and appear to be more related to the concentration of hydrofluoric acid than to the duration of exposure. Solutions >50% produce immediate pain and tissue destruction. Solutions <20% may not produce signs and symptoms until 12 to 24 hours after exposure. The skin often develops a blue-gray appearance with surrounding erythema.
The treatment of hydrofluoric acid burns consists of two phases. The first, immediate phase is copious water irrigation of the affected skin for 15 to 30 minutes. This may be the only treatment that is needed if the hydrofluoric acid solution is <20% concentration, the duration of exposure was very brief, and decontamination is begun immediately. Severe, persistent pain denotes a more serious injury requiring the second phase of treatment.
The second phase of treatment is aimed at replacing calcium and magnesium and detoxifying the enzyme-poisoning fluoride ion. Two ions—calcium (Ca2+) and magnesium (Mg2+)6—bind the fluoride ion and curtail its toxic effects. However, the overwhelming clinical experience to date has been with calcium gluconate, so it is the agent of choice. Calcium gluconate can be administered as a topical preparation, subcutaneous/intradermal injection, or intra-arterial infusion. A calcium gluconate gel made with a water-soluble lubricant is generously applied to the affected skin. The topical preparation is made by mixing 3.5 grams of calcium gluconate powder in 5 oz of water-soluble lubricant, or 25 mL of 10% calcium gluconate in 75 mL of water-soluble lubricant. Calcium chloride or calcium carbonate can be substituted if no calcium gluconate is available. The main limitation of topical therapy is the impermeability of the skin to calcium, and therefore, topical therapy is limited to use in mild, superficial burns. Most importantly, topical therapy should not delay intradermal or intra-arterial injections for severe burns.
Treatment with intradermal injection of a 10% calcium gluconate solution through a 27-gauge needle into the hydrofluoric acid–burned skin is a very effective treatment. A typical dose of 0.5 mL of 10% calcium gluconate per square centimeter of burned skin is recommended. Pain relief is nearly immediate, and, indeed, the elimination of pain may be used as a guide for further therapy. Recurrence of pain indicates the need for further therapy. Unfortunately, injection therapy has several disadvantages: (1) only limited amounts of calcium are delivered to the tissue; (2) hyperosmolarity and inherent toxicity of free calcium ions cause more pain initially, and more tissue damage is possible if calcium is not bound to fluoride; (3) vascular compromise can result if too much fluid is injected, especially into digits; and (4) rapid penetration of hydrofluoric acid beneath the nail requires nail removal to administer the calcium gluconate into the nail bed adequately. Acute hydrofluoric acid contamination of the hands, feet, digits, or nails requires consultation with a medical toxicologist and plastic surgeon.
Intra-arterial infusion of calcium gluconate may be used to prevent tissue necrosis and stop the pain associated with hydrofluoric acid burns.7 This should be performed as soon as possible after the initial burn, preferably within 6 hours of insult. Place an intra-arterial catheter in the appropriate vascular supply (the brachial artery if the entire hand is affected) and connect to a three-way stopcock to which is attached an arterial pressure-monitoring device and the infusion syringe of calcium gluconate. A 50-mL syringe may be filled with 10 mL of a 10% calcium gluconate solution and 40 mL of 5% dextrose in water and infused over 4 hours. The arterial pressure-monitoring device ensures that the catheter has not dislodged from the lumen of the cannulated artery. Repeat infusion may be needed if pain recurs within 4 hours. Intra-arterial infusion avoids the disadvantages of local infiltration therapy, but it has its own disadvantages: it is an invasive vascular procedure that (1) may result in arterial spasm or thrombosis, (2) requires more time and hospital resources, and (3) requires experience in the technique.
Inhalation of hydrofluoric acid can cause immediate or delayed pulmonary injury. All cases of suspected inhalation injury should be admitted for observation even if asymptomatic. Nebulized calcium gluconate may be attempted in these cases, but no controlled studies exist for its use. The solution is made by adding 1.5 mL of 10% calcium gluconate solution into 4.5 mL of sterile water or saline and is administered by nebulizer.
Ocular exposure to hydrofluoric acid requires water irrigation for at least 30 minutes and requires emergent ophthalmologic consultation. An animal study suggests that calcium-containing irrigation fluids for eye exposures may be harmful.8 Therefore, standard eye irrigation practices should be used. The possibility of severe injury and eye necrosis should not be taken lightly. In severe ocular exposures, systemic absorption is possible as well.
Systemic toxicity from dermal hydrofluoric acid exposure can result in ventricular fibrillation as a result of systemic acidosis, hyperkalemia, hypomagnesemia, and hypocalcemia. In major hydrofluoric acid burns, immediately administer IV calcium and magnesium, using standard slow IV rates, before laboratory results are available. Once patients develop hypocalcemia or hypomagnesemia, it is very difficult to restore these electrolyte deficiencies. Cardiac monitoring, IV access, and electrolyte monitoring should be performed in all cases of significant hydrofluoric acid dermal burns (Table 217-6).
TABLE 217-6Options for Treatment of Hydrofluoric Acid Skin Burns ||Download (.pdf) TABLE 217-6 Options for Treatment of Hydrofluoric Acid Skin Burns
Copious irrigation for 15–30 min immediately.
Application of calcium gluconate gel, 25 mL of 10% calcium gluconate in 75 mL of water-soluble lubricant.
Further treatment options as dictated by patient response:
Dermal injection of 10% calcium gluconate at the rate of 0.5 mL/cm2 of skin surface using a small-gauge needle.
Arterial infusion over 4 h (40 mL of 5% dextrose in water with 10 mL of 10% calcium gluconate).
Consider supplemental magnesium and calcium IV.
Methacrylic acid, found in many artificial nail cosmetic products, can produce severe dermal burns, usually in preschoolers. Emergency treatment is copious water irrigation.
Nitric acid is used in industry for casting iron and steel, electroplating, engraving, and fertilizer manufacturing. Upon contact with skin, nitric acid can produce tissue damage by oxidation and may turn the skin yellowish as it is burned. Emergency treatment consists of copious water irrigation and standard burn care (see chapter 216, "Thermal Burns").
Oxalic acid is used for leather tanning and blueprint paper. Oxalic acid binds calcium and prevents muscle contraction. The wounds should be irrigated with water, and IV calcium may be required. Serum electrolytes and renal function should be evaluated, and cardiac monitoring should be instituted after serious dermal exposure.