EMS, Disaster Medicine, Toxicology

Hydrofluoric Acid Related Injuries and Illness for First Responders

The 2020 siege on the U.S. Capitol shows that even peaceful protests can turn violent.

Emergency physicians, tactical medical providers, and other first responders are tasked with taking care of those who become injured or ill in such gatherings. Hydrofluoric acid (HF) was likely used in incidents of vandalism during protests in Portland, Oregon this past year.1 Accidental or intentional exposure of law enforcement officers (LEO), other first responders, protestors, and bystanders to HF acid should therefore be planned for by emergency personnel especially given the complexity of treatment and the potentially fatal nature of HF toxicity. This article reviews the literature regarding the presentation, pathophysiology, and treatment of the chemical burns and systemic effects associated with HF.

Hydrofluoric acid is an inorganic acid historically used for its corrosive properties in domestic and industrial settings. More recently, HF is being used at low levels in the manufacture of cleaning supplies, rust removers, fertilizer, pesticides, and some plastics.2 Indeed, most of our knowledge about HF exposures comes from occupational exposures. HF is most commonly encountered as a colorless liquid similar to water in appearance or as a gas. It has a strong, irritating odor though may reach levels capable of causing harm to humans without a noticeable odor. Even small quantities of HF can cause life-threatening burns and systemic effects.3 Diagnosis of systemic toxicity may be delayed, as HF liquid often appears innocuous and symptoms of exposure may not present immediately. Delays in treatment may result in devastating consequences for the patient.

Mechanism of Injury
HF acid toxicity can occur via contact with skin or eyes, inhalation, or ingestion. All of these initial contacts can lead to severe local and possibly systemic effects.

HF toxicity results from the weak HF acid penetrating deep into the skin and underlying tissue before dissociating into hydrogen and fluoride ions allowing fluoride anions into fascia, muscle, bone and the circulatory system.4 Fluoride anions sequester calcium, magnesium and manganese cations causing precipitous drops in these levels. Local and systemic hyperkalemia may ensue as cell membrane permeability to potassium is increased by local calcium depletion. Counterintuitively, hypokalemia may result as well, though the mechanism is not clearly understood.  Hypocalcemia, hypomagnesemia and hyper and hypokalemia may lead to fatal dysrhythmias. Fluoride ions are believed to be directly toxic to myocardial cells by inhibiting adenylate cyclase. Locally, fluoride ions are also thought to directly inhibit Na+/K+ pumps, which adds to the local hyperkalemia with resultant neuronal depolarization and significant pain. HF is highly lipophilic causing liquefactive necrosis of deeper tissues resulting in the hallmark finding of HF burns: “pain out of proportion to exam.”

Clinical Manifestations
Clinically, the toxicity of HF exposure is directly proportional to:

  1. Concentration of HF
  2. Duration of exposure
  3. Immediacy and adequacy of first aid measures, such as irrigation
  4. Extent of body surface area exposed.

Unfortunately, outside of an occupational or household exposure, such as in an intentional attack, the concentration may not be known.

Cutaneous exposure:  HF causes local injury via two primary mechanisms: as immediate burns and as delayed burns with skin penetration.5 At high HF concentrations (>50%), the hydrogen ion causes a corrosive burn similar to other acid burns, with immediately visible tissue damage,2 immediate pain followed by the development of grey areas, necrosis or ulceration. Late manifestations may include tenosynovitis and osteolysis.

At lower HF concentrations, which represent a majority of HF burns, immediately visible tissue destruction does not occur and there may be no initial evidence of chemical burn.  Symptoms may be delayed up to 24 hours. Immediate burns and pain from high HF concentration exposures may actually have a better prognosis as lower concentration asymptomatic burns may go undetected till severe local and systemic effects are already widespread.

Inhaled HF leads to symptoms related to local irritation, upper airway edema, non-cardiogenic pulmonary edema, reactive airway disease, and systemic absorption. Symptoms include mouth and throat pain, stridor, wheezing and dyspnea.

Ingested HF is less common and often the result of accidental or intentional ingestion of low HF concentration household products.6 Clinical manifestations related to local irritation include burning in the throat, esophagitis, gastritis, hemorrhagic pancreatitis, small bowel edema with resulting nausea abdominal pain, vomiting, gi bleeding, liver failure. Ingestion is often associated with rapid mortality but may result in systemic toxicity among those who don't die immediately.

Systemic HF toxicity can be difficult to manage. The systemic effects of HF are primarily related to potentially massive electrolyte disturbances, mainly hypocalcemia, hypomagnesemia, acidosis, fluorosis, and hyper or hypokalemia. Such disturbances can lead to severe alterations in renal, hepatic, and cardiac function.7 Along with the symptoms associated with the mechanism of exposure, patients may present with systemic symptoms such as headaches, seizures, paresis, coma, hypotension, and cardiac arrhythmias. Signs of systemic HF toxicity include prolonged QT, cardiac failure, renal failure, coagulation disorders, rhabdomyolysis.8 These may be acute or late findings. Although toxicity is less likely to occur in minor cutaneous exposures involving very low concentrations of HF9 the provider must remain vigilant for systemic effects even in this situation. For instance, consider the case of a patient with 3% BSA splash exposure to 20% HF who received immediate irrigation and calcium gluconate treatment and yet suffered cardiac arrest related to severe electrolyte imbalance.10

Systemic toxicity is a feared complication of acute HF exposure, especially in the potential setting of attacks against first responders, terrorist attacks, accidental exposures, riots, and protests. In these settings, patients may not readily be aware of their contact and decontamination and treatment might be delayed.  For this reason, first responders must be acutely aware of the possibility of exposure and all patients require rapid assessment.

As always, tactical assessment must precede treatment. Assessment of scene and tactical safety for the medical provider should occur, followed by ABCs. Patients should be triaged based on severity of injuries and if HF exposure is suspected, the provider must begin immediate decontamination with water or normal saline (NS).

Local pain can be used as a gauge of severity of exposure and HF concentration in unknown situations and helps guide triage and treatment. If the patient experiences severe, immediate pain, exposure to >50% HF should be suspected. If pain is delayed initially but develops within hours, HF concentration between 20-50% should be suspected. If local pain develops 12 to 24 hours after exposure, suspect HF concentrations <20%. Exposure to >50% HF of any amount is of significant concern for life-threatening electrolyte abnormalities; >5% TBSA with any concentration of HF is similarly higher risk for life-threatening electrolyte abnormalities.

Prehospital Treatment Principles

  1. Skin irrigation with tap water should be initiated immediately to dilute and remove HF from the skin. Lavage should be performed for 20-30 minutes. Delay of lavage until arrival to the hospital results in significantly more full-thickness injury, increased likelihood of systemic effects as well as a hospital stay that is twice as long compared with those who received immediate first aid measures after HF chemical injury.11 Make sure all jewelry is removed and skin underneath is irrigated.
  2. Following irrigation, calcium gluconate gel should be applied to the affected skin in order to bind the cutaneous free fluoride ions and prevent penetration into the deeper tissues.11 Because calcium ions have poor tissue penetration, the gel can only neutralize fluoride ions on the surface or the superficial skin layers. The gel can be purchased or made by mixing a water-soluble lubricant with a calcium gluconate solution or calcium gluconate powder (75 mL lubricant plus 25 mL of 10% calcium gluconate or 100 mL of lubricant plus 2.5 g of calcium gluconate powder).12 This gel must be massaged into the affected area. Application of the gel should occur every 30 min initially and tapered down to every 4 hours until pain relief is achieved.13 Since there is such poor penetration of calcium into the deeper tissues, DMSO has been used as an agent to improve absorption. There is currently no consensus on use of DMSO, but this remains an option in contemporary literature.14 The person applying the gel must wear gloves to avoid self-contamination. One trick of the trade for treating hand exposures is to place the calcium gel in a large surgical glove then have the patient place their hand inside the glove.
  3. Inhalational exposure can be treated with nebulized 2.5% calcium gluconate. (1.5 mL of 10% calcium gluconate in 4.5 mL of NS nebulized)
  4. For ingested HF, the conscious patient should be encouraged to drink large amounts of water to dilute the HF followed by several glasses of milk or several ounces of Maalox, Mylanta or crushed Tums. Do NOT induce vomiting.
  5. Institute immediate cardiac monitoring. A 12 lead EKG should be obtained to look for QT prolongation.
  6. If severe systemic toxicity is suspected, immediately administer IV calcium and magnesium. There is low risk for hypercalcemia or hypermagnesemia with this approach.
  7. The eye is highly susceptible to HF exposure. The most important therapy is immediate irrigation. Contacts should be removed, and eyes should be irrigated with 1 liter of water or preferably normal saline. This can be administered using a nasal cannula setup or Morgan lenses for eye irrigation. A 1% calcium gluconate solution for follow-up irrigation has been suggested in some articles, but this treatment is controversial and may cause worsening irritation. Prompt ophthalmological consultation should occur.

Field Considerations
In preparation for treating hydrofluoric acid exposures in the field, the tactical medical provider should remain alert for the possibility of HF exposure. Consider beforehand having access to a water supply for decontamination and carrying 10% calcium gluconate that can be readily mixed in the field. 10% calcium gluconate comes in 10 mL, 50 mL, and 100 mL plastic vials and does not require refrigeration. Normal saline and water-soluble lubricant should be carried so the provider can mix nebulized, and topical calcium treatments as needed.



Calcium gluconate 10%



Topical gel

25 mL

75 mL water soluble lubricant



1.5 mL

4.5 mL NS

If possible, mass decontamination with copious water should be performed on all victims as soon as possible. If there is a mass casualty situation, patients with immediate severe pain after exposure are likely to have had exposure to higher concentrations >50% of HF and may be considered for more involved antidotes.

Emergency Department Treatment Principles

  1. If not already performed in the field, decontaminate as above.
  2. Other important considerations in HF burns include chemical injury to the nails. Fluoride ions readily passes through the nail plate and cause significant damage to the subungual tissues and could lead to systemic absorption, however finger and toenails block decontamination water and binding calcium gluconate from reaching the underlying tissue. Removal of the fingernail or drilling may be required to facilitate application of calcium gel to the underlying tissue.
  3. Clinical evidence of hypocalcemia is often absent; therefore, patients who are high risk for HF exposure must be placed on cardiac monitoring and evaluated for prolonged QT interval and arrhythmias with electrocardiogram.12
  4. High-exposure groups and when severe systemic toxicity is suspected warrant immediate parenteral calcium and magnesium replacement even before the serum calcium and magnesium levels are determined. As mentioned above, it is rare to cause hypercalcemia or hypermagnesemia in this setting since total body stores of these ions are often severely depleted.
  5. Ionized calcium, magnesium and potassium must be emergently and frequently monitored in cases of suspected systemic toxicity. Other labs to consider obtaining include venous or arterial blood gas monitoring, kidney function and liver function tests.
  6. Proven hypocalcemia requires calcium gluconate infusion parenterally and frequent (hourly) serum calcium monitoring.15
  7. Treat hyperkalemia as per usual.
  8. In suspected systemic HF toxicity it is beneficial to maintain normal acid base status. In patients with systemic fluoride toxicity or metabolic acidosis, alkalization of urine by administering parenteral sodium bicarbonate improves excretion of fluoride and may help normalize acid-base status.
  9. Consider hemodialysis to reduce both fluoride and potassium levels, and to treat persistent hypocalcemia despite calcium infusion especially in patients with decreased renal function.
  10. If ingestion occurred recently, gastric lavage via NG tube may be of benefit. Risk of gastric or esophageal perforation must be balanced against the risk of death from systemic absorption. The provider placing the NG is at risk of dermal or inhalation exposure related to the procedure so proper PPE is a must.
  11. Calcium gluconate injections have been widely adopted for use on moderate to severe HF burns as it has been shown to reliably reduce pain.16 Indications include a central hard grey area with surrounding erythema and throbbing severe pain despite management with irrigation and gel. Infiltration is thought to be unnecessary for burns with HF concentrations ≤20%. A 27-gauge needle can be used to inject a 5% to 10% calcium gluconate solution into subcutaneous tissue beneath the burn. It is recommended to inject no more than 0.5 mL/cm2of burn surface area, as infiltration has been associated with increased compartment pressure and necrosis. Compartments should be monitored closely after injection. Edelman et al were first to describe this and set a limit of 0.5 mL per phalanx with repeated injections preferred.17
  12. For patients with severe HF burns with unrelenting pain despite aggressive calcium gel topical therapy, typically of the digits or other poorly distensible areas that will not tolerate intradermal injection, intra-arterial calcium infusion has been used; this management technique may be associated with complications, including artery spasm and bleeding, ulnar nerve palsy relating to position of immobilization, median nerve palsies secondary to hematomas, and carpal tunnel syndrome.2 It is traditionally used for digital burns of the hand as the fingers are poorly distensible and may not tolerate local injection, but has also been described for the face and lower extremities. Intra-arterial calcium infusion was first described by Kohnlein and Achinger in 1978, in which they used angiogram to guide the route of infusion to the radial, ulnar, or brachial artery and then infused 50 mL of 4% calcium gluconate given over a 4-hour period.18 This cycle was repeated every 12 hours until the patient was free from pain. This protocol has since been adapted with decreased complication rates. In this procedure, an artery such as the radial artery, proximal to the burns is cannulated. Placement of the cannula should be confirmed by angiography, although an arterial line with good wave form placed on first attempt without any difficulty could be assumed to be usable as well. 10 mL of 10% calcium gluconate is added to 40 mL of either D5W or NS (resulting in a 2% calcium gluconate solution) and infused interarterially over 4 hours. This treatment may need repeated for recurrent pain.19

Hydrofluoric acid (HF) chemical burns are an important consideration in patients seeking medical treatment with signs of chemical injury following riots and violent protests. The hallmark physical exam finding in HF burns is “pain out of proportion to exam” though the exposed may be completely asymptomatic initially. Serious systemic toxicity can occur with even small cutaneous exposures. Alongside the normal field medical assessment and treatments, every known or suspected exposure should have immediate and thorough skin irrigation with water for 20-30 minutes followed by application of calcium gluconate topical gel. Providers should consider inhaled calcium gluconate for patients with signs of inhalational exposure. Ingestions should be treated with decontamination and dilution by drinking copious water and antacids.  Eye exposure should be treated with immediate irrigation. Patients with signs of toxicity should be empirically treated with IV calcium gluconate and magnesium pending lab evaluation. Patients require prompt EKG and cardiac monitoring for dysrhythmias and prolonged QT interval. Once lab is available, serum electrolyte levels, liver and renal function, venous or arterial blood gas should be obtained urgently, and electrolytes must be repeated hourly at a minimum.

We would like to thank and acknowledge the contributions of Amber Adams, PharmD, and Courtney Olesky, PharmD, in describing the packaging, handling and other aspects in the field use of calcium gluconate.


  1. Ettlin, Galen. “Search on for Old Town Graffiti Vandal Using Acid to Etch Images.” KGW8, 25 May 2020, www.kgw.com/article/news/local/search-for-old-town-graffiti-vandal/283-5d688a8e-3823-438a-a001-da152e6526c0. 
  2. McKee D, Thoma A, Bailey K, Fish J. A review of hydrofluoric acid burn management. Plast Surg. 2014;22(2):95-98.
  3. “CDC - The Emergency Response Safety and Health Database: Systemic Agent: Hydrogen Fluoride/Hydrofluoric Acid - NIOSH.” Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health (NIOSH), 12 May 2011, www.cdc.gov/niosh/ershdb/EmergencyResponseCard_29750030.html. 
  4. Rega, Paul P. Ciottone's Disaster Medicine, by Gregory P. Ciottone, Elsevier, 2016, pp. 680–684. 
  5. Bajraktarova-Valjakova E, Korunoska-Stevkovska V, Georgieva S, et al. Hydrofluoric Acid: Burns and Systemic Toxicity, Protective Measures, Immediate and Hospital Medical Treatment. Open Access Maced J Med Sci. 2018;6(11):2257-2269. Published 2018 Nov 20.
  6. Kao W, Dart RC, Kuffner E, Bogdan G. Ingestion of Low-Concentration Hydrofluoric Acid: An Insidious and Potentially Fatal Poisoning. Annals of Emergency Medicine. 1999; 34(1): 35-41
  7. Mclvor M. Delayed fatal hyperkalemia in a patient with acute fluoride intoxication. Ann Emerg Med. 1987;16:118–20
  8. Wang X, Zhang Y, Ni L, You C, Ye C, Jiang R, Liu L, Liu J, Han C. A review of treatment strategies for hydrofluoric acid burns: current status and future prospects. Burns. 2014 Dec;40(8):1447-57. 
  9. Burd A. Hydrofluoric acid burns: Rational treatment. J Burn Care Res. 2009;30:908.
  10. Wu ML, Deng JF. Survival after hypocalcemia, hypomagnesemia, hypokalemia and cardiac arrest following mild hydrofluoric acid burn. Clin Toxico. 2010;48(9):953-955
  11. Leonard L, Scheulen J, Munster A. Chemical burns: Effect of prompt first aid. J Trauma. 1982;22:420–3
  12. Holstege C, Baer A, Brady W. The electrocardiographic toxidrome: The ECG presentation of hydrofluoric acid ingestion. Am J Emerg Med. 2005;23:171–6.
  13. Kirkpatrick J, Burd D. Hydrofluoric acid burns: A review. Burns. 1995;21:483–93
  14. Hatzifotis M, Williams A, Muller M, Pegg S. Hydrofluoric acid burns. Burns. 2004;30(2): 156-159
  15. Kirkpatrick J, Burd D. An algorithmic approach to the treatment of hydrofluoric acid burns. Burns. 1995;21:495–99.
  16. Ohata U, Hara H, Suzuki H. 7 cases of hydrofluoric acid burn in which calcium gluconate was effective for relief of severe pain. Contact Dermatitis. 2005;52:133–7.
  17. Edelman P. Hydrofluoric acid burns. Occup Med. 1986 Jan-Mar;1(1):89-103.
  18. Kohnlein H, Achinger R. A new method of treatment of hydrofluoric acid burns of the extremities. Chir Plast. 1982;6:297–305.
  19. Su, Mark. Goldfrank's Toxicologic Emergencies, by Lewis R. Goldfrank, Appleton & Lange, 1998, pp. 1374–1379. 

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