Hydrofluoric Acid Poisoning
Kennon Heard
Introduction
Hydrofluoric acid (HF) is a commonly encountered industrial reagent that is available in concentrations from 6% to 90%. It is used for the production of fluorocarbons, etching glass, and silicone, and as a household rust-removal agent. Sodium fluoride is used as a rodenticide and also as a preservative in blood collection tubes. A related compound, ammonium bifluoride is used in rust removers, commonly found in commercial car washes.
Mechanism of Action
HF (pKa = 3.8) is a weak acid. Hence, compared with other acids, it is relatively less ionized at any given pH. This allows HF to penetrate more deeply into tissue and to be more readily absorbed into the systemic circulation than other acids. Once absorbed, it disassociates and the fluoride anion binds to divalent cations, forming insoluble salts (primarily calcium fluoride, fluorapatite, and magnesium fluoride). This results in tissue and systemic hypocalcemia and hypomagnesemia. Fluoride also directly poisons several enzymes and cellular transport proteins. High-concentration HF exposures result in rapid onset of local pain and tissue injury with or without systemic toxicity, whereas low-concentration exposures can result in life-threatening hypocalcemia and hypomagnesemia, with minimal or absent local corrosive effect.
Dermal Exposure
Clinical Manifestations
While most dermal exposures will result in minor symptoms or superficial chemical burns, systemic toxicity may occur following dermal exposure. Symptoms may be delayed for 24 hours or more following low-concentration (< 20% HF) exposure, and there is often severe pain with minimal skin abnormalities. Symptoms can develop within several hours of exposure to medium concentrations (20% to 50% HF). While the initial injury is not always visible, patients exposed to medium-concentration products often go on to have erythema, blanching, or necrosis of the involved area. High-concentration (> 50% HF) exposures result in the immediate injury expected after exposure to concentrated acids. Patients may develop full- or partial-thickness injury that includes tissue necrosis and eschar formation [1].
Evaluation and Treatment
Laboratory studies are not indicated for small, low-concentration dermal exposures. However, exposure to products containing more than 50% HF that involve more than 1% of the skin or exposure to any HF product that affects more than 5% of the skin can cause hypocalcemia, so patients with these burns should have serum calcium levels monitored, as described in the systemic toxicity section below [2].
The most important step in treatment is decontamination by irrigating the affected area for at least 15 minutes as quickly as possible. In one large case series of exposures, many of which involved concentrations of greater than 40% HF, immediate irrigation produced excellent outcome in the majority of patients [3]. Hexafluoride, an irrigating solution developed to bind fluoride, does not appear to offer any improvement over water irrigation [4].
After irrigation, apply a 2.3% to 2.5% calcium gluconate preparation in a water-soluble gel to the exposed areas for at least 30 minutes or until symptoms resolve [5]. This treatment often remains effective if it is delayed several hours after symptoms develop [6]. The role of topical therapy following high-concentration exposures is less well defined, but it is recommended [7].
If pain is not relieved by topical therapy, regional intra-arterial or intravenous calcium perfusion should be initiated. The major drawback of intra-arterial perfusion is the requirement for arterial catheterization. Brachial, radial, and femoral catheterization have all been described. Following cannulation, monitor arterial waveform to assure that the catheter remains patent and properly placed within the artery. If there is any question as to adequate placement, perform arteriography prior to infusing calcium. Flushing the catheter with heparin may help keep the catheter patent [2]. The largest case series reported infusion of 50 mL of 2.5% calcium gluconate in saline over 4 hours [2]. It is not uncommon to have to repeat the dose several times over a 12- to 24-hour period.
Regional perfusion using a Bier block may allow treatment without arterial cannulization. Some clinicians advocate this technique before proceeding to intra-arterial administration. This technique requires venous cannulation in the affected extremity. The extremity is exsanguinated by elevation and compression with an Esmarch bandage. The blood pressure cuff should be inflated to a pressure 100 mm Hg above systolic pressure and remain up for 15 to 20 minutes following calcium administration. The usual dose is 40 mL of a 2.5% calcium gluconate solution [8]. The cuff is then gradually deflated over 5 minutes. Pain is usually relieved within minutes of the calcium administration.
If the affected area is not an extremity, calcium can be directly injected into the burn. The most common method is injection of 0.3 to 0.5 mL per cm2 of 2.5% calcium gluconate. Calcium chloride should not be used as it can cause tissue injury. Excision of exposed tissue is not recommended.
