| Patient Education |
|
Click here for patient education.
|
|
You are in: eMedicine Specialties >
Emergency Medicine > ENVIRONMENTAL
Hydrofluoric Acid Burns
Article Last Updated: Aug 7, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 12  
Author: Garry Wilkes, MBBS, Director, Emergency Medicine, Adjunct Associate Professor, Edith Cowan University, Department of Emergency Medicine, Bunbury Health Service
Editors: Edward A Michelson, MD, Program Director, Associate Professor, Department of Emergency Medicine, University Hospital Health Systems in Cleveland; John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital; Richard Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Author and Editor Disclosure
Synonyms and related keywords:
HF acid, HF acid burns, HF acid exposure, hydrofluoric acid exposure, hydrofluoric acid burns
Background
Hydrofluoric (HF) acid, one of the strongest inorganic acids, is used mainly for industrial purposes (eg, glass etching, metal cleaning, electronics manufacturing). HF acid also may be found in home rust removers. Exposure usually is accidental and often is due to inadequate use of protective measures.
HF 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) HF acid to 1% or more body surface area (BSA), exposure to HF acid of any concentration to 5% or more BSA, or inhalation of HF acid fumes from a 60% or stronger solution. The vast majority of cases involve only small areas of exposure, usually on the digits.
Pathophysiology
The 2 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.
Frequency
United States
More than 1000 cases of HF exposure are reported annually. Actual incidence rate is unknown.
Mortality/Morbidity
- Local effects 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.
Sex
Males are affected more commonly, which reflects occupational patterns.
Age
The majority of exposures occur in adults.
History
- Time of exposure to onset of symptoms is related to the concentration of the HF acid.
- Solutions of 14.5% immediately produce symptoms.
- Solutions of 12% may take up to an hour to produce symptoms.
- Solutions of less than 7% may take several hours before onset of symptoms, resulting in delayed presentation, deeper penetration of the undissociated HF acid, and a more severe burn.
- Concentrated solutions cause immediate pain and produce surface burns similar to those produced by other common acids (eg, erythema, blistering, necrosis).
- Pain typically is described as deep, burning, or throbbing.
- Pain often is disproportionate to apparent skin involvement.
- Obtain history of potential exposure to cleaning solutions within the last 24 hours, to include the following:
- Duration of exposure
- Concentration of acid
- Use of protective measures
- Other agents in the solution
- Symptoms of hypocalcemia
- Tetany
- Chvostek sign
- Trousseau sign
- Cardiac arrhythmias
- Additionally, obtain history of medications and intercurrent illness that predispose patient to hypocalcemia or hypomagnesemia.
Physical
- Weaker solutions penetrate before dissociating.
- Surface involvement in these cases is minimal and may be absent.
- Three categories of appearance include the following:
- Grade 1 - A white burn mark and/or erythema and pain
- Grade 2 - A white burn mark and/or erythema and pain, plus edema and blistering
- Grade 3 - A white burn mark and/or erythema and pain, edema, and blistering, plus necrosis
- Patients with inhalation burns may develop acute pulmonary edema.
- Ocular burns may present with severe pain.
Burns, Chemical
Burns, Ocular
CBRNE - Lung-Damaging Agents, Chlorine
Toxicity, Fluoride
Lab Studies
- Electrolytes - Severe disturbances can occur, especially the following:
- Hypocalcemia
- Hypomagnesemia
- Hyperkalemia
Imaging Studies
- Radiographs
- Obtain chest x-ray (CXR) if pulmonary edema is suspected.
- If burns to the fingers exist, perform digital x-rays to evaluate bone integrity.
Other Tests
- Electrocardiogram
- Cardiac monitoring is necessary if burn is significant.
- Arrhythmias are a primary cause of death.
- Monitor for QT prolongation from hypocalcemia or signs of hyperkalemia.
Prehospital Care
Treatment for HF acid burns includes basic life support and appropriate decontamination, followed by neutralization of the acid by use of calcium gluconate. If exposure occurs at an industrial site, obtain and transport any available treatment literature.
- 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 is available, apply liberally to the affected area.
- 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.
- Transport the patient to the nearest appropriate medical facility.
Emergency Department Care
- 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.
- 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 10% solution per square centimeter of surface burn extending 0.5 cm beyond the margin of involved tissue. Do not use the chloride salt because it is an irritant and may cause tissue damage.
- Burns to the digits: 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.
- 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.
- 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
- Provide 100% oxygen by mask, 2.5% calcium gluconate by nebulizer with 100% oxygen, continuous pulse oximetry, ECG, and clinical monitoring.
- Pulmonary edema is treated along conventional lines, as needed.
- Despite concerns of perforation, consider gastric lavage with calcium chloride (ie, 20 mmol calcium in 1000 mL normal saline solution) early in overdose. One series of autopsies performed on decedents who had received calcium chloride lavage after HF acid ingestion demonstrated hemorrhagic gastritis; however, no evidence of perforation was revealed. Secure the airway prior to gastric lavage.
Consultations
Consultation with specialty units may be required depending on individual circumstances.
- Toxicologist
- Burn surgeon
- Intensive care specialist
- Ophthalmologist
- Hand surgeon
- Gastroenterologist (following ingestions)
The goal of pharmacotherapy is to reduce morbidity and prevent complications.
Drug Category: Pharmacologic antidote
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.
| Drug Name | Calcium gluconate (Kalcinate) |
|---|
| Description | Moderates nerve and muscle performance and facilitates normal cardiac function. For systemic hypocalcemia, can be given IV initially, and calcium levels maintained with high calcium diet. Some patients will require oral calcium supplementation.
For topical pain, can be applied as a water-soluble gel mixture.
For IV, intra-arterial, or ocular administration, please refer to discussion in Treatment. |
|---|
| Adult Dose | May apply 2.5-5% calcium gluconate to affected area; repeat prn pain; if not available commercially, can be prepared by simple 3:1 (for 2.5%) or 1:1 (for 5%) dilution of a 10% IV solution in a water-soluble surgical gel or similar sterile base |
|---|
| Pediatric Dose | Apply as in adults |
|---|
| Contraindications | Documented hypersensitivity; renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity |
|---|
| Interactions | May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels |
|---|
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
|---|
| Precautions | Caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia; monitor serum calcium level when calcium gluconate is given parenterally |
|---|
| Drug Name | Calcium chloride |
|---|
| Description | Manages underlying hypocalcemic effects. |
|---|
| Adult Dose | Initial dose: 1-2 g (1-2 ampules) IV slow push of 10% calcium chloride solution (10 mL each); repeat doses to obtain desired serum calcium level; for severe poisoning, may need to give multiple grams for the first several hours |
|---|
| Pediatric Dose | 20-25 mg/kg IV push of calcium chloride; repeat prn; may need massive doses with severe poisoning |
|---|
| Contraindications | Documented hypersensitivity; ventricular fibrillation not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease |
|---|
| Interactions | Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate |
|---|
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
|---|
| Precautions | Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure |
|---|
Further Inpatient Care
- 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.
Further Outpatient Care
- 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.
- Prudence requires physicians to provide follow-up care with all patients after 24 hours, at least by telephone.
Deterrence/Prevention
- Most burns are a result of inadequate use of safety devices.
- Patient education is important to prevent recurrences.
Complications
- Airway compromise
- Systemic fluorosis
- Pulmonary edema
- Electrolyte abnormalities
- Arrhythmias
- Scarring
- Loss of digits
- Corneal perforation
- Blindness
Prognosis
- Prognosis varies depending on burn severity and site.
- Poor prognosis follows fluoride inhalation.
Medical/Legal Pitfalls
- Several features of HF acid burns may lead to delayed or missed diagnosis.
- Significant delays may occur between exposure and onset of symptoms.
- Marked pain in the absence of significant surface dermal injury should raise suspicion of HF acid burns.
- HF acid penetrates fingernails and burns the pulp beneath without destroying the nails. Adequate treatment of these cases requires removal of the nails and/or IV and/or intraarterial infusion of calcium gluconate.
- Severe burns may produce severe electrolyte disturbances and arrhythmias. These must be monitored expediently and corrected.
- All exposures to the head and neck may be associated with respiratory burns. Keep patients for observation with that possibility in mind.
- Although 10% calcium gluconate is the agent of choice for counteracting most sites of exposure, irrigate burns to the eye with 1-2% dilute solution.
- Dislodgement of intra-arterial catheter may result in extravasation of calcium salts and subsequent tissue necrosis and/or digit loss.
Thank you to those clinicians who have shared their experience with this uncommon, clinically distinct and sometimes challenging condition to treat.
| Media file 1:
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. |
 |  View Full Size Image | |
Media type: Photo
|
| Media file 2:
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. |
 | View Full Size Image | |
Media type: Photo
|
- Bertolini JC. Hydrofluoric acid: a review of toxicity. J Emerg Med. Mar-Apr 1992;10(2):163-8. [Medline].
- Chan BS, Duggin GG. Survival after a massive hydrofluoric acid ingestion. J Toxicol Clin Toxicol. 1997;35(3):307-9. [Medline].
- Dunn BJ, MacKinnon MA, Knowlden NF, et al. Topical treatments for hydrofluoric acid dermal burns. Further assessment of efficacy using an experimental piq model. J Occup Environ Med. May 1996;38(5):507-14. [Medline].
- Graudins A, Burns MJ, Aaron CK. Regional intravenous infusion of calcium gluconate for hydrofluoric acid burns of the upper extremity. Ann Emerg Med. Nov 1997;30(5):604-7. [Medline].
- Greco RJ, Hartford CE, Haith LR Jr, et al. Hydrofluoric acid-induced hypocalcemia. J Trauma. Nov 1988;28(11):1593-6. [Medline].
- Hatzifotis M, Williams A, Muller M, Pegg S. Hydrofluoric acid burns. Burns. Mar 2004;30(2):156-9. [Medline].
- Henry JA, Hla KK. Intravenous regional calcium gluconate perfusion for hydrofluoric acid burns. J Toxicol Clin Toxicol. 1992;30(2):203-7. [Medline].
- Kono K, Watanabe T, Dote T, et al. Successful treatments of lung injury and skin burn due to hydrofluoric acid exposure. Int Arch Occup Environ Health. Jun 2000;73 Suppl:S93-7. [Medline].
- Mayer TG, Gross PL. Fatal systemic fluorosis due to hydrofluoric acid burns. Ann Emerg Med. Feb 1985;14(2):149-53. [Medline].
- McIvor ME, Cummings CE, Mower MM, et al. Sudden cardiac death from acute fluoride intoxication: the role of potassium. Ann Emerg Med. Jul 1987;16(7):777-81. [Medline].
- Nguyen, L. T.Mohr, W. J., 3rdAhrenholz, D. H.Solem, L. D. Treatment of hydrofluoric acid burn to the face by carotid artery infusion of calcium gluconate. J Burn Care Rehabil. Sep-Oct 2004;25:421-4. [Medline].
- Ryan JM, McCarthy GM, Plunkett PK. Regional intravenous calcium--an effective method of treating hydrofluoric acid burns to limb peripheries. J Accid Emerg Med. Nov 1997;14(6):401-4. [Medline].
- Shewmake SW, Anderson BG. Hydrofluoric acid burns. A report of a case and review of the literature. Arch Dermatol. May 1979;115(5):593-6. [Medline].
- Soderberg K, Kuusinen P, Mathieu L, Hall AH. An improved method for emergent decontamination of ocular and dermal hydrofluoric acid splashes. Vet Hum Toxicol. Aug 2004;46(4):216-8. [Medline].
- Vance MV, Curry SC, Kunkel DB, et al. Digital hydrofluoric acid burns: treatment with intraarterial calcium infusion. Ann Emerg Med. Aug 1986;15(8):890-6. [Medline].
- Velvart J. Arterial perfusion for hydrofluoric acid burns. Hum Toxicol. Apr 1983;2(2):233-8. [Medline].
- Wilkes GJ. Intravenous regional calcium gluconate for hydrofluoric acid burns of the digits. Emerg Med (Aust). 1993;5:155-8.
- Wilkes GJ, Morel DG. Hydrofluoric acid burns of the hands. In: Abstracts of the 6th International Conference on Emergency Medicine. Sydney. 1996.
Hydrofluoric Acid Burns excerpt Article Last Updated: Aug 7, 2007
|
