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Hydrofluoric acid burns

American Family Physician, April, 1992 by Dinu G. Mistry, David J. Wainwright

Hydrofluoric acid is widely used in both industrial and household settings. The acid may cause insidious burns that can be very destructive. If the burns are not treated appropriately, the continued action of the free fluoride ion leads to liquefaction necrosis of the affected soft tissues, bony erosion and, ultimately, potentially lethal hypocalcemia. Immediate and copious irrigation, followed by topical, subcutaneous or intra-arterial administration of calcium carbonate, minimizes the extent of injury. In major exposure to hydrofluoric acid, management includes serum electrolyte and electrocardiographic monitoring, as well as aggressive repletion of calcium deficiency.

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Hydrofluoric acid, one of the strongest inorganic acids known, has been in industrial use since its ability to dissolve silica was recognized in the late 17th century.[1] While the acid is still employed in glass etching and frosting, it is also used in the production of semiconductors and fluorocarbons. Hydrofluoric acid is an ingredient in several household products, most notably rust removers, aluminum brighteners and heavy-duty cleansers.[1-3]

Pathophysiology

Although hydrofluoric acid is a corrosive agent, its hydrogen ion plays a relatively insignificant role in the pathophysiology of burns. The acid does produce caustic injury to skin, but it causes less surface damage than equimolar solutions of stronger acids such as hydrochloric and sulfuric acids.[4]

The fluoride ion is the primary agent responsible for the prolonged destruction seen in hydrofluoric acid burns. Once the skin is traversed, the fluoride ion is liberated and penetrates freely through the underlying tissues. Most fluoride salts are soluble and thus freely dissociable; only magnesium and calcium form neutralizing, insoluble fluoride salts that precipitate within the tissues. As cellular calcium is bound and immobilized, cell death and liquefaction necrosis ensue. The resultant ionic shifts, particularly of potassium, are thought to be responsible for the excruciating pain associated with hydrofluoric acid burns.

If not fully bound in the more superficial tissues, the free fluoride ion will progress to decalcify bone, cause systemic hypocalcemia and induce potentially lethal cardiac arrhythmias.[1-5] While these manifestations are relatively rare, they have been reported with burns involving as little as 8 percent of the total body surface area.[6]

Symptoms

Clinically, the two hallmarks of hydrofluoric acid burns are the delayed onset of symptoms and the severe pain. Hydrofluoric acid concentrations of 20 percent or less may take up to 24 hours to produce clinical evidence of injury. Concentrations of 20 to 50 percent cause symptoms one to eight hours after exposure, while burns due to concentrations greater than 50 percent usually become symptomatic within one hour. Only maximally concentrated hydrofluoric acid (99 percent) has an immediate effect.

As in all chemical burns, the extent of injury depends on the concentration of the agent, the duration of exposure, the surface area involved and the resistance of the tissue.[4] Household preparations, which generally contain very weak concentrations of hydrofluoric acid, are particularly dangerous. With delays of as much as 24 hours before symptoms appear, these exposures can result in considerable tissue loss. In addition, since exposure and symptoms often are not temporally related, the etiology of the injury may be confusing.

In hydrofluoric acid burns, the skin in the exposed area initially appears erythematous. With more severe burns (longer exposure or stronger concentration), the skin assumes a putty-gray color, and a cheesy, yellow substance accumulates beneath the skin as the salts begin to precipitate. Blisters filled with turbid fluid may develop. Without therapy, the injury will progress to full-thickness skin loss with decalcification of underlying bone.

Systemic manifestations of hydrofluoric acid burns stem primarily from hypocalcemia.[1,2,4] Surprisingly small exposures to concentrated hydrofluoric acid can lead to systemic effects. If left untreated, a burn with as little as 7 mL of 99 percent hydrofluoric acid can theoretically bind all of the available calcium in a 70-kg (154-lb) man.[2] The hypocalcemia is "silent," because it does not typically produce tetany; only the serum calcium level and the electrocardiogram (with the ECG showing a prolonged QT interval) are reliable indicators. In addition, the hypocalcemia of hydrofluoric acid burns induces cardiac arrhythmias that are particularly resistant to treatment.[6]

Finally, ingestion of hydrofluoric acid and inhalation of its vapor can lead to life-threatening complications. Hydrofluoric acid vapor produces caustic burns with severe swelling of the oropharynx and tracheobronchial tree, occasionally necessitating tracheostomy. Inhalation injuries are also associated with a characteristic late-onset pulmonary edema. Ingestion of hydrofluoric acid leads to rapid absorption of the fluoride ion. The initial symptoms of nausea, vomiting, abdominal pain and diarrhea may progress to symptoms of acute systemic fluoride toxicity, such as hypocalcemia, ventricular fibrillation, pulmonary edema and seizures.[7]

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Hydrofluoric acid burns

American Family Physician, April, 1992 by Dinu G. Mistry, David J. Wainwright

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