Hydrofluoric acid is commonly used in industry and dermal exposure causes deeply-penetrating painful soft tissue injury and also local and sometimes systemic fluoride toxicity. Treatment includes local burn care and topical and/or parenteral calcium.
Hydrofluoric acid (HF) is commonly used in numerous industrial processes, including oil refining, silicon and glass etching, refrigerant production, fluoropolymer production, and aluminum metal production. HF is also used as a brick and stone cleaner, rust remover, and wheel cleaner. Although most HF exposure is occupational, some products containing HF are available for retail purchase, and nonoccupational exposure does occur.
HF is a weak acid (pKa = 3.17) in dilute aqueous solution and exists primarily in the non-ionized form. Compared with strong acids that exist primarily in the ionized form, HF in dilute solutions is better able to penetrate the skin barrier and diffuse into local soft tissues, where it causes injury. Strong acids cause only direct caustic injury (coagulative necrosis, which typically spares the underlying soft tissues), but HF causes caustic skin injury due to its acidity and also injures underlying soft-tissue due to penetration of the fluoride ion.
In aqueous intracellular and extracellular spaces, fluoride complexes with divalent cations (calcium, magnesium), forming insoluble calcium fluoride and magnesium fluoride. Formation of these insoluble salts promotes the release of more fluoride ion from HF (per Le Chatelier’s principle). The removal of calcium and magnesium from solution results in local hypocalcemia and hypomagnesemia, which can cause cellular dysfunction and cell death. With sufficient exposure, systemic hypocalcemia and hypomagnesemia may occur, resulting in cardiac arrhythmias. In addition, the fluoride ion itself may be arrhythmogenic.
Time to symptom-onset from time of exposure varies and is inversely related to the concentration of HF. Exposure to concentrated preparations (> 50% HF) results in immediate pain and tissue damage due to the direct caustic effect on the skin or mucous membranes. This effect is partly due to a marked increase in the acidity of HF at high concentrations and HF homoassociation resulting in an increase in disassociated protons. Conversely, exposure to dilute preparations (< 20% HF) may not result in pain or clinical findings for several hours after the exposure because cellular dysfunction and death caused by local hypocalcemia and hypomagnesemia take time to develop.
HF exposure may be dermal, ocular, oral, or inhalational. The most common route of occupational exposure to HF is dermal.
Symptoms and Signs of Hydrofluoric Acid Exposure
Symptoms and signs of hydrofluoric acid exposure vary depending on the route of exposure.
Dermal
Pain is typically the first symptom to manifest after dermal exposure and precedes signs of chemical burns, such as erythema (1st degree), edema and bullae formation (2nd degree), or gray-white discoloration (3rd degree). Pain is often more severe than expected based on apparent dermal involvement. If the fingers and nail beds are burned, the nails may remain intact, and pain may be severe despite apparent absent or minimal involvement of the nails and skin.
Oral
Oral occupational exposure to HF is less common but may occur when aqueous solution containing HF is stored in unmarked containers (eg, water bottles). Nonoccupational oral HF exposure may result from attempts at self-harm or exploratory ingestion by young children.
Ingestion of dilute HF solution may result in oropharyngeal erythema and edema and gastrointestinal irritation; ingestion of a small volume may be asymptomatic. Ingestion of concentrated HF solution results in hemorrhagic gastritis and pulmonary toxicity similar to inhalational exposure.
Inhalational
Inhalational exposure to HF most commonly results in upper airway and chest pain (described as burning), cough, and shortness of breath. Patients may also report nausea, vomiting, and headache and a burning sensation in skin exposed to HF vapor. Time to symptom-onset is inversely proportional to the airborne concentration of HF. Pharyngeal erythema and edema may be present, as may wheezing, rales, and respiratory distress. With more severe inhalational exposure, patients may develop hemorrhagic alveolitis with hemoptysis or acute hypoxemic respiratory failure (adult respiratory distress syndrome [ARDS]), which may be fatal.
Systemic
Dermal, oral, or inhalational HF exposure may result in systemic fluoride toxicity (ocular exposure has not been implicated in systemic toxicity). Onset of systemic toxicity is more rapid after oral HF exposure because systemic absorption is more rapid after oral exposure than dermal exposure. Dermal exposure to concentrated HF solution may result in systemic fluoride toxicity even when the body surface area involved is small.
Systemic fluoride toxicity is marked by hypocalcemia, hypomagnesemia, and impaired cardiac contractility. Hyperkalemia may also occur. Cardiac arrhythmias including polymorphic ventricular tachycardia (torsades de pointes), ventricular fibrillation, and asystole may occur. Coagulopathy may result from hypocalcemia.
Ocular
Ocular exposure to HF may result from a splash injury involving an aqueous solution or from gaseous HF. Mild (more dilute) exposure may cause eye pain, conjunctival injection, and chemosis and may not manifest for hours after the exposure. If the exposure is more concentrated, onset of symptoms is more rapid; corneal coagulative necrosis may occur, and the globe may rupture.
Diagnosis of Hydrofluoric Acid Exposure
Clinical evaluation
Electrolyte levels
Diagnosis of problems due to hydrofluoric acid exposure begins with a thorough history and physical examination. Physicians should obtain information about potential exposure in the last 24 hours, including route and duration of exposure, concentration of HF, other chemicals in the formulation, and use of personal protective equipment (PPE).
There is no specific test for HF poisoning; however, hypocalcemia (ideally measured as ionized calcium), hyperkalemia, hypomagnesemia, and elevated serum fluoride (if available) may suggest that systemic exposure has occurred. Except for the most minor burns, patients are usually admitted to the hospital for monitoring for systemic toxicity and for any indicated treatments.
Pulmonary function testing is not necessary to do immediately but, if done, may detect a restrictive lung disease pattern.
If pulmonary edema is suspected, a chest x-ray and other appropriate testing (eg, pulse oximetry) are done. If the fingers are burned, x-rays are taken promptly to check for bone damage.
If systemic exposure is possible, electrocardiography is done to check for the effects of hypocalcemia (eg, a prolonged QT interval) and hyperkalemia (peaked T waves, widening of the QRS interval, flattening of the P wave, sine wave pattern).
Endoscopy should generally be done for oral ingestion, and consultation with gastroenterology and/or otorhinolaryngology should be obtained.
Prognosis for Hydrofluoric Acid Exposure
Prognosis depends on the route of hydrofluoric acid exposure.
Dermal
Prognosis after mild dermal HF exposure is good if the patient is promptly evaluated and treated. As with other chemical burns, symptoms typically resolve over a period of days to weeks, depending on the severity of the burn.
Oral
Patients who have ingested a dilute HF solution may develop reversible oropharyngeal or gastrointestinal (GI) irritation or may remain asymptomatic and have a benign prognosis. Ingestion of concentrated HF solution may result in fatal GI hemorrhage or systemic fluoride toxicity, which may be fatal. If patients with severe GI burns survive, long-term sequelae including strictures may develop.
Systemic
Patients with systemic fluoride toxicity are at high risk of cardiac arrhythmia and hypotension.
Inhalational
Prognosis after inhalational exposure depends on the intensity and chronicity of exposure. If inhalational exposure is mild to moderate, symptoms may resolve spontaneously over a period of hours to days. More intense exposures may result in persistent upper airway irritation (reactive upper airways dysfunction syndrome [RUDS]) or pulmonary irritation (reactive airways dysfunction syndrome [RADS]) that persists for months to years. Chronic occupational HF exposure may result in a bronchial hyperreactivity syndrome called "potroom worker’s asthma". Serial pulmonary function tests may be used to monitor RADS and bronchial hyperreactivity in workers exposed to HF.
Ocular
If ocular exposure is mild, conjunctival irritation and chemosis (which typically occurs) resolves over a period of several days, and no long-term sequelae are anticipated. If exposure is more severe, corneal injury or sloughing may result in chronic conjunctivitis, corneal opacification or vascularization, glaucoma, or keratitis sicca.
Treatment of Hydrofluoric Acid Exposure
Various treatments depending on type of exposure
Prompt decontamination if applicable
Dermal
Topical calcium is applied until pain is relieved.
All but the most minor or superficial exposures require transfer to a burn center for possible surgical intervention, including skin grafting, debridement of necrotic tissue, fasciotomy, and amputation.
Oral
A GI specialist should be consulted about possible endoscopy.
Systemic
Patients with systemic fluoride toxicity should be admitted to an intensive care unit for cardiac monitoring, serial electrocardiography and, if depressed cardiac contractility is suspected, echocardiography. Serial measurement of calcium, magnesium, potassium, and phosphate levels is done and treated as required.
Fluoride ions are eliminated by hemodialysis. Hemodialysis should be considered for patients with systemic toxicity, although such patients may be too clinically unstable to have the procedure.
Inhalational
standard interventions for ARDS, including positive pressure ventilation, use of high positive end-expiratory pressure, and proning.
Ocular
Prompt decontamination is most important. Irrigation at a workplace eyewash station should be followed by continued irrigation en route to the hospital. Continued irrigation in an emergency department may be done using normal saline or sterile water applied to the affected eye or eyes using a Morgan lens. Irrigation with at least 2 to 3 liters of fluid is recommended. Ocular irrigation with calcium-containing solutions, which are irritating and may create corneal injury, should not be used. Consultation with an ophthalmologist should be obtained in the acute care setting, and ophthalmology follow-up should be arranged.
Prevention of Hydrofluoric Acid Exposure
Various organizations (eg, Occupational Safety and Health Administration [OSHA], National Institute for Occupational Safety and Health [NIOSH]) provide recommendations for minimizing the risk of exposure to hydrofluoric acid. These recommendations include
Providing workers with information about the hazards specific to HF before they handle it
Limiting the time workers are exposed to HF
Requiring workers to wear a properly functioning fume hood and appropriate personal protective equipment (PPE), such as goggles, disposable gloves, and acid-resistant apron
Requiring workers to wear long pants, long sleeves, and closed-toe shoes
Equipping the work area with a safety shower and eye wash station
Storing HF properly
Key Points
Dermal, oral, inhalational, and ocular exposures to hydrofluoric acid may occur in the workplace.
Symptoms begin immediately after exposure to concentrated HF formulations but may be delayed by several hours after exposure to dilute HF formulations.
Surface burns and the complexation of calcium or magnesium with the fluoride ion in HF results in local hypocalcemia and hypomagnesemia, which cause cellular dysfunction and death.
Treat dermal burns and severe pain due to dermal exposure with dermal, subcutaneous, or intra-arterial calcium; transfer almost all patients with burns to a burn center.
For oral exposures, use an orogastric or nasogastric tube to empty the stomach as soon as possible; ingestion of concentrated HF solution is toxic as well as caustic and can be fatal.
Admit patients with systemic fluoride toxicity (which may be due to dermal, oral, or inhalational exposure) to an intensive care unit for serial monitoring and support, and treat them with IV magnesium and calcium and, if needed, vasopressors.
After ocular exposure, irrigate the eyes immediately, continuously, and thoroughly and arrange consultation and follow-up with an ophthalmologist.
