Hydrofluoric (HF) acid, one of the strongest inorganic acids, is used mainly for industrial purposes (eg, glass etching, metal cleaning, electronics manufacturing). Hydrofluoric acid also may be found in home rust removers. Exposure usually is unintentional and often is due to inadequate use of protective measures.
Hydrofluoric acid burns are a unique clinical entity. Dilute solutions deeply penetrate before dissociating, thus causing delayed injury and symptoms. Burns to the fingers and nail beds may leave the overlying nails intact, and pain may be severe with little surface abnormality.
Severe burns occur after exposure of concentrated (ie, 50% or stronger solution) hydrofluoric acid to 1% or more body surface area (BSA), exposure to hydrofluoric acid of any concentration to 5% or more BSA, or inhalation of hydrofluoric acid fumes from a 60% or stronger solution. The vast majority of cases involve only small areas of exposure, usually on the digits.
A unique feature of HF exposure is its ability to cause significant systemic toxicity due to fluoride poisoning.
The two mechanisms that cause tissue damage are corrosive burn from the free hydrogen ions and chemical burn from tissue penetration of the fluoride ions.
Fluoride ions penetrate and form insoluble salts with calcium and magnesium. Soluble salts also are formed with other cations but dissociate rapidly. Consequently, fluoride ions release, and further tissue destruction occurs.
Systemic toxicity occurs secondary to depletion of total body stores of calcium and magnesium, resulting in enzymatic and cellular dysfunction, and ultimately in cell death. Majority of deaths are resulting from cardiac arrhythmias that were precipitated by hypocalcaemia and consequent hyperkalemia.[1, 2]
More than 1000 cases of hydrofluoric acid exposure are reported annually. Actual incidence rate is unknown.
In a review of 15 years' experience with hydrofluoric acid burns at one center, hydrofluoric acid burns accounted for 35 (17%) patients out of 205 who were admitted for chemical burns; all of these patients were men.[3]
Males are affected more commonly by hydrofluoric acid burns, which reflects occupational patterns.
The majority of hydrofluoric acid exposures occurs in adults.
Prognosis varies depending on burn severity and site. Poor prognosis follows fluoride inhalation.
Local effects of hydrofluoric acid burns include tissue destruction and necrosis. Burns may involve underlying bone. Systemic fluoride ion poisoning from severe burns may be associated with hypocalcemia, hyperkalemia, hypomagnesemia, and sudden death. Deaths have been reported from concentrated acid burns to as little as 2.5% BSA.
Time of exposure to onset of symptoms is related to the concentration of the hydrofluoric acid, as follows:
Pain typically is described as deep, burning, or throbbing. Pain often is disproportionate to apparent skin involvement.
Obtain a history of potential exposure to cleaning solutions within the last 24 hours, to include the following:
Weaker solutions penetrate before dissociating. Surface involvement in these cases is minimal and may be absent.
Three categories of appearance include the following:
Patients with inhalation burns may develop acute lung injury presenting with the following:
Ocular burns may present with severe pain.
Complications are as follows:
Evaluate electrolyte status.[4] Severe disturbances can occur, especially the following:
Obtain chest a radiograph if pulmonary edema is suspected. If burns to the fingers exist, perform digital radiographs to evaluate bone integrity.
Cardiac monitoring with electrocardiography is necessary if burn is significant. Arrhythmias are a primary cause of death. Monitor for QT prolongation from hypocalcemia or signs of hyperkalemia.
Treatment of hydrofluoric acid burns includes basic life support and appropriate decontamination, followed by neutralization of the acid by use of calcium gluconate or hydrofluoric-specific agent such as Hexafluorine, if available. If exposure occurs at an industrial site, obtain and transport any available treatment literature.[5]
Assess and manage acute life-threatening conditions in the usual manner. Emergency Medical Services (EMS) personnel should use gloves, masks, and gowns, if necessary.
Remove soiled clothing. Initially decontaminate by irrigation with copious amounts of water.
Ice packs on the affected area may alleviate symptoms by retarding diffusion of the ion.
If calcium gluconate gel or specific agent (eg, Hexafluorine) is available, apply liberally to the affected area.[6]
For digital burns, if calcium gluconate gel is not available, the fingers may be soaked in magnesium hydroxide–containing antacid preparations (eg, Mylanta) en route to a medical facility. Retain gel/antacid in a latex glove if practicable, and the gloved hand may be immersed in iced water.
Treat inhalation injuries with oxygen and 2.5% calcium gluconate nebulizer.
Control pain with opioid agents.
Transport the patient to the nearest appropriate medical facility.
Remove soiled clothing.
Decontaminate by irrigation with copious amounts of water.
Assess and manage life-threatening conditions as with any other cause.
Commence comprehensive monitoring for significant exposures.
With any evidence of hypocalcemia, immediately administer 10% calcium gluconate IV.
Cutaneous burns
Apply 2.5% calcium gluconate gel to the affected area. If the proprietary gel is not available, constitute by dissolving 10% calcium gluconate solution in 3 times the volume of a water-soluble lubricant (eg, KY gel). For burns to the fingers, retain gel in a latex glove.
If pain persists for more than 30 minutes after application of calcium gluconate gel, further treatment is required. Subcutaneous infiltration of calcium gluconate is recommended at a dose of 0.5 mL of a 5% solution per square centimeter of surface burn extending 0.5 cm beyond the margin of involved tissue (10% calcium gluconate solution can be irritating to the tissue).
Do not use the chloride salt because it is an irritant and may cause tissue damage.
Burns to the digits [7]
Local infiltration of digits is not recommended because of pain, disfigurement, and potential complications. Alternative treatment methods follow.
IV regional calcium gluconate: 10-15 mL of 10% calcium gluconate plus 5000 units of heparin diluted up to 40 mL in 5% dextrose. Use a Bier ischemic arm block technique to infuse the solution intravenously. Release the cuff when any of the following conditions first occur: (1) pain from the digits resolves, (2) the cuff becomes more painful than the burn, or (3) 20 minutes of ischemic time elapses. Treatment can be repeated after 4 hours if needed. Continuous ECG and clinical monitoring are essential during this procedure.
Intra-arterial calcium gluconate: Place an arterial catheter in the radial or brachial artery to perfuse the affected digits. Infuse a solution of 10 mL of 10% calcium gluconate in 40 mL of 5% dextrose over a 4-hour period. Follow with further infusions repeated after 4-8 hours, if necessary. Several treatments may be needed. Exercise great care to ensure that the catheter is appropriately placed intravascularly (ie, by continuous waveform analysis), as tissue necrosis and digit loss have occurred following extravasation of calcium salts. Continuous ECG and clinical monitoring are essential during this procedure.
Digital block with local anesthetics may be an alternative for pain control in patients with delayed presentation after exposure to low concentration HF.
Administer opioids for additional pain control.
Ocular burns
Generously irrigate with sterile water or saline for at least 5 minutes. Local anesthetic may be required. If pain persists, irrigate with a 1% solution of calcium gluconate, which is made by diluting the 10% solution in 10 times the volume of normal saline. Do not use undiluted 10% calcium gluconate.
Calcium salts are very irritating to the eye, and urgent ophthalmologic consultation should be requested prior to the irrigation with 1% calcium gluconate solution.
Inhalation burns
Exposures to the head and neck should arouse suspicion of pulmonary involvement. If any doubt is present, admission for observation is advised. Specific treatment includes the following:
Provide 100% oxygen by mask, 2.5% calcium gluconate by nebulizer with 100% oxygen, continuous pulse oximetry, ECG, and clinical monitoring.
Acute lung injury is treated along conventional lines, as needed.
Oral ingestion
Despite concerns of perforation, consider gastric lavage with calcium chloride (ie, 20 mmol calcium in 1000 mL normal saline solution) early in overdose. In isolated HF exposure, lavage should be performed through a nasogastric tube.
One series of autopsies performed on decedents who had received calcium chloride lavage after hydrofluoric acid ingestion demonstrated hemorrhagic gastritis; however, no evidence of perforation was revealed.
Secure the airway prior to gastric lavage.
Admission to a burn service or ICU may be required if burns are extensive or if any clinical, laboratory, or electrocardiographic evidence of complications is present.
Subcutaneous injection of growth factors is being explored as part of initial treatment for skin burns beyond chelation therapy.[8, 9]
Consultation with specialty units may be required depending on individual circumstances.
Most burns are a result of inadequate use of safety devices. Patient education is important to prevent recurrences.
Patients are suitable for discharge only when pain has been controlled adequately. Patients with serious exposures can be discharged once electrolytes return to normal, arrhythmias are absent, and ECG is normal, provided other complications are managed adequately.
Patients with finger burns can be discharged with calcium gluconate gel on the affected digits. Instruct patients to keep affected digits in a latex glove for 24 hours to maximize gel penetration.
Prudence requires physicians to provide follow-up care with all patients after 24 hours, at least by telephone.
The goal of pharmacotherapy is to reduce morbidity and prevent complications.
Clinical Context: Calcium gluconate moderates nerve and muscle performance and facilitates normal cardiac function. For systemic hypocalcemia, it can be given intravenously initially. For topical pain, it can be applied as a water-soluble gel mixture. For intravenous, intra-arterial, or ocular administration, please refer to the discussion in Treatment.
Clinical Context: Calcium chloride manages underlying hypocalcemic effects.
The major pharmacologic intervention is with calcium gluconate. Depending on the clinical situation, it may be used in a gel, intravenously, intra-arterially or used to irrigate ocular burns.
Grade 1 hydrofluoric (HF) acid burns of the fingertips. The patient has severe pain (maximum middle digit) with only minimal redness of the nail beds.
Grade 3 hydrofluoric (HF) acid burns of the fingertips. Note how the nailbed and tip of the fingers have severely been injured, but the nails show no damage.
Grade 1 hydrofluoric (HF) acid burns of the fingertips. The patient has severe pain (maximum middle digit) with only minimal redness of the nail beds.
Grade 3 hydrofluoric (HF) acid burns of the fingertips. Note how the nailbed and tip of the fingers have severely been injured, but the nails show no damage.
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