Don't Get Burned by Hydrofluoric Acid Toxicity

Hydrofluoric acid is found in a variety of products and used in multiple industries, so exposure, while not exceedingly common, is not rare. Know how to treat HF toxicity and prevent contamination among the health care team managing these injuries.

Hydrofluoric acid (HF) is used in a variety of industries, including plastic, dye, semiconductor, and fertilizer manufacturing, beer fermentation, and in petroleum production. It is also found in rust remover, various pesticides, refrigerants, car wash cleaning products, and detergents.1-4

Most HF burns occur in the occupational setting, although toxicity from household products is also reported. Cutaneous exposures are most common, especially to the fingers and hands. Hydrofluoric acid toxicity may also result from ingestion or inhalation.2

Dilute aqueous HF is a weak acid, but at concentrations greater than 20%, severe and potentially lethal burns can occur. Hydrofluoric acid behaves as a strong acid at concentrations > 50%. Burns covering even a small surface area can be fatal.2 Unlike strong acids, HF is highly penetrative due to primarily being in the non-dissociated state, causing deep tissue destruction via liquefactive necrosis and allowing for easy entry into the systemic circulation.1,2,5 Once within the tissues, the fluoride ion complexes with calcium and magnesium, causing their depletion. Hyperkalemia results from increased cellular permeability and inhibition of the Na+/K+ pump. Neuron depolarization and severe pain result from these electrolyte abnormalities.1 Fluoride also causes myocardial irritability, predisposing to dysrhythmia.2

In 2017, 676 HF exposures were reported to U.S. poison centers. There was 1 fatality and an additional 6 that resulted in life-threatening signs and symptoms.6 In the past, there have been several masscasualty incidents involving HF. In 2012, 8 tons of HF leaked from a chemical plant in South Korea, killing several and affected thousands. There were 2 separate incidents in China in 2014. A rust remover leak injured 48 people, and a tanker truck collision resulted in several deaths and more than 250 injuries.7

Clinical Presentation
The classic finding of HF toxicity is pain out of proportion to the exam.1 The discomfort is often described as severe throbbing.8 The National Institutes of Health classifies HF burns based on the concentration of the product. In exposures to concentrations > 50%, there will be immediate pain and tissue damage, which may include erythema, blistering, ulceration, underlying bone damage, and tenosynovitis.

Systemic toxicity develops more slowly and can manifest as nausea, vomiting, abdominal pain, renal failure, hepatic failure, seizure, hypotension, dysrhythmia, or heart failure. Electrolyte abnormalities (hypocalcemia, hypomagnesemia, and hyperkalemia) are common.2

Coagulopathy may develop secondary to hypocalcemia. The combination of coagulopathy and chemical burns may lead to hemorrhage.2 Necrotic lesions of the kidneys and myocardium have been observed on autopsy.9

Systemic toxicity is also likely following ingestion or inhalation.1,10 Gastrointestinal (GI) and pulmonary toxicity, including bronchospasm and pulmonary edema, may develop.2 Tissue destruction and pain usually occur within 1-8 hours after exposure to HF concentrations of 21-50%. Some systemic toxicity is possible, but typically less severe than what is observed at higher concentrations. At concentrations < 20%, signs and symptoms may be delayed up to 24 hours. The toxic effects of lower-concentration exposures are generally confined to the affected areas; systemic toxicity is unlikely.2

Diagnostic Testing
Patients with significant HF exposures require continuous cardiac monitoring. A 12-lead EKG should also be obtained to evaluate for dysrhythmia and interval abnormalities. Prolongation of the QTc interval is one of the best indicators of systemic HF toxicity; symptoms of hypocalcemia (eg, tetany) are often absent.10 Serial electrolyte levels should be measured, and more significant exposures warrant more frequent laboratory testing, as often as hourly in large or concentrated exposures.1,2

Pain relief is the primary indicator of treatment success. Multiple treatment algorithms have been proposed, but there is no consensus on management.2 However, there are steps that are universally recommended.

Irrigation: As with any chemical burn, the first step is to immediately irrigate with water for 15-30 minutes to remove and dilute the acid.1 Irrigation will not effectively remove HF that has already penetrated into deeper tissue.2

Calcium gluconate gel (topical): Application of topical calcium gluconate gel turns the fluoride into an insoluble salt, preventing further absorption. This reduces the amount of tissue destruction and systemic toxicity. It is reasonable to initially apply the gel to affected areas every 30 minutes. Once pain is controlled, the frequency can be reduced to every 4 hours. Consider filling an examination glove with gel to treat hand burns.9 Commercially-prepared calcium gluconate gels are available. Alternatively, homemade gel can be prepared by combining 100 mL of waterbased lubricant with 2.5 g of calcium gluconate.1,10 The majority of HF burns can be effectively treated with topical calcium gluconate, despite its relatively poor skin penetration.7

Calcium gluconate infiltration: Local infiltration allows for much greater skin penetration than topical application can provide, and its use should be considered for significant burns. Infiltration is generally unnecessary for exposures of < 20% HF. Infiltration is performed with a small gauge needle, e.g. 25- or 27-gauge. Inject approximately 0.5 mL/cm2 of 5% calcium gluconate into the affected skin and subcutaneous tissue.1,2 For finger injuries, do not exceed 0.5 mL per phalanx to prevent an excessive rise in compartment pressure.1

Calcium gluconate, intravenous: Calcium gluconate should be administered intravenously following significant exposures and in cases of hypocalcemia. Intravenous calcium gluconate decreases pain and prevents extension of the burn to deeper tissues.2 For extremity burns, regional intravenous calcium gluconate may be administered via Bier block. In this technique, a tourniquet is placed proximal to the burn, and calcium gluconate is administered intravenously distal to the tourniquet. One approach is to inject 10 mL of 10% calcium gluconate diluted in 30–40 mL of normal saline and maintain for 20– 25 minutes.11 This regional technique may be complicated by electrolyte abnormalities and dysrhythmia once the tourniquet is released, so cardiac monitoring and serial laboratory tests are essential. Fortunately, because most victims are young and otherwise healthy, significant systemic complications are rare.8

Calcium gluconate, arterial: Arterial injection of calcium gluconate has a high incidence of complications, e.g. arterial spasm, necrosis, dysrhythmia, and vasculitis. Some experts recommend that this procedure only be done via angiography, making it less practical for ED use. There is no demonstrable benefit when compared to intravenous calcium gluconate for most HF exposures. Intra-arterial calcium is theoretically advantageous in severe burns affecting tissues with clear arterial distribution and in small spaces that cannot accommodate large volumes of locally- infiltrated calcium. Cardiac monitoring is essential when administering calcium intra-arterially.2

Techniques for elimination of fluoride: Hemodialysis should be considered in patients with refractory hypocalcemia and/or hyperkalemia. Diuresis and urine alkalinization may also enhance the elimination of fluoride.1-2

Non-Skin/Dermal Exposures

This form of exposure is very rare. If it suspected, concurrent inhalational exposure should also be considered. Hydrofluoric acid is rapidly absorbed by the GI tract, leading to vomiting, abdominal pain, hemorrhage, perforation, and systemic effects.2 

Anhydrous HF boils at room temperature, and aqueous HF releases fumes that can lead to inhalational exposure.2 Consider the possibility of inhalational exposure in any patient with HF burns to the face, head, or neck, as well as in burns sustained in confined spaces. Inhalational injuries may also occur following exposures involving greater than 5% of the body surface area, in burns from concentrated (ie, > 50%) HF solutions, and in patients who are not properly decontaminated in a timely fashion.10 Inhalation may cause fever, chills, pulmonary edema, hemorrhage, chest discomfort, cyanosis, and wheezing. Obtain chest radiography and provide supplemental oxygen in these patients. Consider nebulized calcium gluconate (2-3%), positive pressure ventilation, and intubation in more severe cases.2 

Ocular exposure is an ophthalmologic emergency. As with any ocular chemical burn, irrigation is the immediate priority. Remove contact lenses, if present, after brief irrigation, and then resume irrigation.10 Consider administration of calcium gluconate (1-10%) eye drops.1 Instill 1-2 drops every 2-3 hours into the affected eye(s). Hydrofluoric acid rapidly penetrates into the anterior chamber; immediate aqueous humor removal and replacement is commonly required despite aggressive irrigation. Ophthalmology must be consulted for ocular exposures.2 

HF easily penetrates the nail, and removal is generally required to apply calcium gluconate gel to the affected nailbed.1

Provider Safety
Health care professionals must take precautions to avoid contaminating themselves while caring for HF victims. The use of "double gloving" is recommended in case a glove has microscopic pinholes. Providers should also consider the use of additional personal protective equipment, including eye protection and gowns.8


  • HF is found in a variety of products and used in multiple industries.
  • Burns to the upper extremity and hand are most common and may cause severe pain.
  • HF is lipophilic, enabling it to cause deep burns and systemic toxicity.
  • Systemic toxicity is mostly due to electrolyte abnormalities, including hypocalcemia, hypomagnesemia, and hyperkalemia.
  • Important diagnostic tests for HF burn victims include EKG and serial electrolyte measurements.
  • Most HF burns can be successfully treated with topical calcium gluconate.
  • Resolution of pain is a good indicator of treatment efficacy.
  • If topical application of calcium gluconate is not effective, consider local infiltration, intravenous injection (including regional injection using Bier block), and arterial injection.
  • There are specific methods used to manage non-skin exposures to HF (gastrointestinal, inhalation, ocular, etc.).

1. McKee D, Thoma A, Bailey K, Fish J. A review of hydrofluoric acid burn management.  Plast  Surg. 2014;22(2):95-98.
2. Xingang W, Zhang Y, Liangfang N, et al. A review of treatment strategies for hydrofluoric acid burns: current status and future prospects. Burns. 2014;40:1447-1457.
3. Genuino H, Opembe N, Njagi E, McClain S, Suib S. A review of hydrofluoric acid and its use in the car wash industry. J Industr Engineering Chemistry. 2012;18:1529-1539.
4. Hatzifotis M, Williams, A, Muller M, Pegg S. Hydrofluoric acid burns. Burns. 2004;30:156-159.
5. Burd A. Hydrofluoric acid – revisited. Burns. 2004;30;720-722.
6. Gummin DD, Mowry JB, Spyker DA, Brooks DE, Osterthaler KM, Banner W. 2017 annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 35th annual report. Clin Toxicol. 2018 Dec 21:1-203.
7. Zhang Y, Wang X, Sharma K, et al. Injuries following a serious hydrofluoric acid leak: First aid and lessons. Burns. 2015;41:1593-1598.
8. Dunser M, Öhlbauer M, Rieder J, et al. Critical care management of major hydrofluoric acid burns: a case report, review of the literature, and recommendations for therapy. Burns. 2014;30;391-398.
9. Marx C, Trautmann S, Halank M, Weise M. Lethal intoxication with hydrofluoric acid. Crit Care. 2005;9(Suppl):407.
10. Kirkpatrick J, Burd D. An algorithmic approach to the treatment of hydrofluoric acid burns. Burns. 1995;21:495-499.
11. Graudins A, Burns MJ, Aaron CK. Regional intravenous infusion of calcium gluconate for hydrofluoric acid burns of the upper extremity. Ann Emerg Med. 1997 Nov;30(5):604-7.

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