Tag Archives: calcium gluconate

Hydrofluoric Acid: The Burn that keeps on Burning

Authors: Brian Murray, DO (@bpatmurray, EM Senior Resident, SAUSHEC, USAF) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

screen-shot-2016-12-04-at-5-29-47-pmA 40-year-old man presented to the Emergency Department with the complaint of pain to his right hand. Three-hours prior he had been using rust remover to clean the air-conditioning unit in his house. Now the patient has exquisite pain to his distal thumb, index finger, and middle fingers.

screen-shot-2016-12-04-at-5-30-09-pm

Figure 1 A & B: Two images of the affected fingers showing A) the bluish hue of the blanched right index finger with incisions used to relieve the pressure of local infusion of 10% calcium gluconate into the tips of the fingers and B) the arterial catheter placed for arterial infusion of 10% calcium gluconate.

Introduction

Hydrofluoric acid (HF) is one of the most dangerous corrosive inorganic acids due to its ability to destroy body tissue.1 It is well known for its ability to dissolve silica and glass and is used in numerous industrial processes (e.g. glass etching, brick cleaning, microchip etching, electroplating, and leather tanning) and even as an active ingredient in several household chemicals such as rust remover, aluminum brighteners, and heavy-duty cleaners.2 Industrial HF can be as concentrated as 100%, termed anhydrous, while the household variants are usually no more concentrated than 10-40% HF. However, due to the local, and potentially systemic effects of HF, even dilute HF has the potential to cause significant morbidity and mortality.3 From 2011 – 2014 the American Association of Poison Control Centers reported over 2000 HF exposures and 4 deaths.4,5,6,7 Deaths have been reported with exposures of 100% HF covering as little as 2.5% total body surface area.8 One of these deaths was due to the ingestion of 1 oz of dilute 1.92% HF which caused severe fluorosis, hypocalcemia, and ultimately death due to ventricular fibrillation.4

Pathophysiology/Toxicity

HF burns are more damaging and serious than other acidic burns because it causes tissue damage through two distinct mechanisms. The first, common to all acids, is by the rapid release of hydrogen ions and subsequent tissue dehydration and coagulation necrosis.9 HF is a weak acid with a pKa of 3.20. By comparison, the pKa of citric acid if 3.13 and the pKa of sulfuric acid is <-2 (considered a strong acid),10 and HF is approximately 1000 times less disassociated than equimolar strong acids such as hydrochloric acid.11 This acidic burn generated by free hydrogen ions is relatively insignificant compared to its second mechanism: the release of the highly reactive free fluoride ion, F, after the uncharged HF molecule penetrates deeply into the underlying tissue.9 The F causes liquefaction necrosis and creates strong bonds with calcium and magnesium forming the insoluble salts CaF2 and MgF2. Potassium ions are released from the peripheral nerve endings in response to Ca2+ depletion, which produces the severe pain classically associated with HF exposure.2

The severity of the burn is a product of the concentration, the surface area involved, and the time of exposure. Because HF is a weak acid, there may be a delay of up to several hours with dilute concentrations.9 Concentrations exceeding 50% almost always result in immediate pain due to the corrosive action of hydrogen ion disassociation.12 This delay can lead to deep penetration of HF before exposure is identified, increasing exposure time and tissue damage due to the F ion. This also allows for greater potential for systemic toxicity. Systemic symptoms occur from hypocalcemia and hypomagnesemia in response to systemic fluorosis after the absorption of a significant amount of HF. However, a significant amount is a relative term as massive exposure and death can result from as little as a 1% total body surface area from a >50% hydrofluoric acid solution, or exposure of >5% total body surface area of hydrofluoric acid of any concentration.13 When death does occur, it is typically due to dysrhythmia secondary to profound hypocalcemia and hypomagnesemia,14 as well as hyperkalemia caused by an efflux of potassium ions from cells due to hypocalcemia.15

Aside from dermal toxicity, patients can be poisoned though inhalation/pulmonary, ingestion/gastrointestinal, and ocular routes as well. Patients exposed to very low-concentration HF fumes may experience minor respiratory tract irritation,16 while inhalation of more concentrated fumes can lead to throat burning and shortness of breath leading to hypoxia and systemic hypocalcemia.17 Given the high propensity for evaporation, especially in concentrations greater than 60% which have boiling points around or below room temperature, inhalation injury should be assessed in all patients with cutaneous burns, especially those with exposures that involve the head and neck.18  Clothing soaked in HF can also produce deadly concentrations of inspired HF.19 Frequently, pulmonary exposures are also associated with ocular exposures, and as such patients should be evaluated for occult HF ocular injuries.11

Ingestion of any concentration of HF causes significant gastritis, and patients will promptly develop pain and vomiting. Systemic symptoms and death nearly always follow due to the high surface area involved, the extended time of contact, and the high degree of absorption, although actual absorption occurs rapidly along with the development of systemic symptoms and fatal dysrhythmias.2 Patients may present with altered mental status, airway compromise, and dysrhythmia.11 There is one case report of a person who ingested 8% HF, suffered multiple episodes of ventricular fibrillation, and was successfully resuscitated.20 This is the exception and not the norm, as ingestion of HF is almost universally fatal.2,11

Ocular exposures to HF typically cause more extensive damage to ocular tissue than other acids.21 HF, either by liquid splashes or exposure to HF gas, causes corneal and conjunctival epithelial denuding, leading to stromal corneal edema, conjunctival ischemia, sloughing, and chemosis. Fluoride ions penetrate deeply within the anterior chamber leading to corneal opacification and necrosis of the anterior chamber structure.2 Usually the effects are noted within one day, however case reports have noted situations where corneal damage was not apparent until 4-days post exposure.22 Long-term complications include corneal ulcers.11

Evaluation

All exposures should be discussed with a toxicologist.  Initial evaluation consists of a thorough history and physical, particularly to the chemical used (to help in identification of the HF concentration), the time of exposure, and the area of exposure.2 Laboratory evaluation of patients poisoned with HF consists of monitoring serum electrolytes, particularly ionized calcium, magnesium, and potassium.23 Additionally, as toxicity progresses, a venous blood gas may be useful, as metabolic acidosis may develop.  An ECG should be obtained and trended over time to assess for clinically significant hypocalcemia (prolonged QT interval) and hyperkalemia (peaked T-waves). Serum fluoride levels can be obtained, but will often lag behind clinically significant levels.11

Treatment

The first treatment that should be performed, as with any chemical exposure, is removing soaked clothing and copious irrigation with water.1,9 This would ideally be performed immediately upon contact with HF, helping to reduce the risk of acidic burn and deeper penetration, but it will have some benefit even if performed later.

Cutaneous Exposures

There are three levels of treatment specific for HF burns. The first is to topically apply a 2.5% calcium gluconate slurry, which is made by mixing 3.5 gm of calcium gluconate in 5 oz of a water based lubricant such as Surgilube® or K-Y Jelly®. This treatment has excellent efficacy at preventing further tissue damage and decreasing pain, especially if used soon after the exposure. Putting a glove over the exposed hand when using the calcium slurry can help keep the gel in place and prevent loss of the calcium. It has limited ability to penetrate to deeper tissues and only helps to neutralize superficial HF.1,2,9

If topical calcium is not effective at treating the patient’s pain after 30 minutes and the area of tissue damage continues to increase, local infiltration with 5-10% calcium gluconate, not exceeding 0.5 ml per cm2 of affected body surface area, is used (the only currently available dosing recommendation in the literature).2,9,11,13 This method is more effective at treating deeper exposures. Calcium gluconate is used instead of calcium chloride, as calcium chloride is irritating and toxic to local tissue. If infiltration is going to be performed in the pads of the fingers, a prophylactic fasciotomy is recommended to prevent compartment syndrome from the injection of a large amount of fluid into a small compartment.1,2,9

If the pain is still not controlled, intra-arterial infusion of 10 ml of 10% calcium gluconate or calcium chloride (in 40-50 ml 5% dextrose) over 4 hours will allow large amounts of calcium to be delivered directly to the damaged tissue, and this infusion can be repeated until the patient is pain free.2,9,24

Systemic calcium and magnesium depletion should be treated by replacing the depleted electrolytes.9

Ocular Exposures

The most important step in the treatment of ocular HF exposure is early irrigation with 1L normal saline, lactated ringer solution, or sterile water. The use of 1% calcium gluconate eye drops is controversial, with some reports showing benefit.25,26,27,28,29  However, it can also be irritating to the eye and toxic to subconjunctiva, and sufficient evidence to support its recommended use over saline irrigation alone is lacking.2,11 Prompt ophthalmologic evaluation is essential after irrigation.

Ingestion Exposures

Ingestion of HF is almost universally fatal11 and are frequently associated with dermal exposure and inhalation exposures. If the ingestion occurred <2 hours prior to evaluation, it is recommended to pass a nasogastric tube for decontamination.13 The addition of 10% calcium gluconate to the lavage fluid may help neutralize the remaining fluoride ions that have not yet absorbed.13,30 Aggressive systemic therapy is indicated, and gastroenterology evaluation is necessary to address local tissue damage.11

Inhalation Exposures

The primary treatment for inhalation exposures is 4ml of nebulized 2.5-5% calcium gluconate.31,32 This is a benign therapy and is recommended to be given to all patients with symptomatic inhalational exposures.33 Attention should be paid to the patient’s airway and ability to maintain adequate oxygen saturation, as tracheobronchopulmonitis and local edema may impair both.34 Corticosteroids and antibiotics are not routinely recommended for all patients and should only be administered in coordination with a Medical Toxicologist.35 The systemic absorption of fluoride from inhalation exposures is extremely rapid and carries a high risk of systemic toxicity, even from relatively dilute concentrations.36

Case Outcome

The chemical was compound the patient was using was Condenser Coil Brightener and Cleaner (compound 90-920) that he had purchased online.  90-920 contains 10% HF solution, and therefore the patient did not begin to feel pain until 3 hours post exposure. Topical calcium and local infusion of calcium were not sufficient to control his pain and an intra-arterial catheter was placed and an infusion of 10% calcium gluconate was started. The patient was admitted to the burn ICU, where he eventually required excision of the tips of his fingers due to tissue necrosis. He otherwise experienced an uneventful recovery.

Pearls

  • The F ion causes significant tissue damage and pain through formation of insoluble salts and calcium depletion.
  • Even small burns with concentrated HF can lead to significant systemic toxicity and death.
  • Electrolytes, VBG, and ECG are necessary in the evaluation.
  • The Toxicology service must be consulted.
  • Treatment with 2.5% topical calcium gluconate, 0.5 ml/cm2 of 10% calcium gluconate, and 10ml of 10% calcium gluconate or chloride in 40-50 ml 5% dextrose over 4 hours may be needed to neutralize the F

 

References/Further Reading

  1. Anderson WJ, Anderson JR. Hydrofluoric acid burns of the hand: mechanism of injury and treatment. The Journal of hand surgery. 1988;13(1):52–7.
  2. Kirkpatrick JJ, Enion DS, Burd DA. Hydrofluoric acid burns: a review. Burns. 1995 Nov;21(7):483–93.
  3. Department of Health and Human Services. NIOSH Skin Notation Profiles: Hydrofluoric Acid. CDC. 2011. Accessed online: https://www.cdc.gov/niosh/docs/2011-137/ on 18 Nov 2016
  4. Bronstein AC, Spyker DA, Cantilena LR Jr, Rumack BH, Dart RC. 2011 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 29th Annual Report. Clinical Toxicology. 2012 Dec 7;50(10):911–1164.
  5. Mowry JB, Spyker DA, Cantilena LR Jr, Bailey JE, Ford M. 2012 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 30th Annual Report. Clinical Toxicology. 2013 Dec 8;51(10):949–1229.
  6. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report. Clinical Toxicology. 2014 Oct 6;52(10):1032–283.
  7. Mowry JB, Spyker DA, Brooks DE, McMillan N, Schauben JL. 2014 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 32nd Annual Report. Clin Toxicol (Phila). 2015;53(10):962–1147.
  8. Tepperman PB. Fatality due to acute systemic fluoride poisoning following a hydrofluoric acid skin burn. J Occup Med. 1980;22:691-2.
  9. Bertolini JC. Hydrofluoric acid: a review of toxicity. J Emerg Med. 1992;10(2):163–8.
  10. “Appendix C: Dissociation Constants and pKa Values for Acids at 25°C”, appendix 3 from the book Principles of General Chemistry (v. 1.0) Accessed at: http://2012books.lardbucket.org/books/principles-of-general-chemistry-v1.0/s31-appendix-c-dissociation-consta.html on 10 November 2016
  11. Su M. Hydrofluoric Acid. In: Goldfrank’s Toxicologic Emergencies, 10e. 2016.
  12. Sheridan RL, Ryan CM, Quinby WC, Blair J, Tompkins RG, Burke JF. Emergency management of major hydrofluoric acid exposures. Burns. 1995 Feb;21(1):62–4.
  13. Hatzifotis M, Williams A, Muller M, Pegg S. Hydrofluoric acid burns. Burns. 2004 Mar;30(2):156–9.
  14. Yamaura K, Kao B, Iimori E, Urakami H, Takahashi S. Recurrent ventricular tachyarrhythmias associated with QT prolongation following hydrofluoric acid burns. Journal of Toxicology: Clinical Toxicology. 1997 Jan 1;35(3):311-3.
  15. Mclvor ME, Cummings CE, Mower MM, Wenk RE, Lustgarten JA, Baltazar RF, Salomon J. Sudden cardiac death from acute fluoride intoxication: the role of potassium. Annals of emergency medicine. 1987 Jul 31;16(7):777-81.
  16. Lee DC, Wiley JF II, Synder JW II. Treatment of inhalational exposure to hydrofluoric acid with nebulized calcium gluconate. J Occup Med. 1993;35:470.
  17. Wing JS, Brender JD, Sanderson LM et al. Acute health effects in a community after a release of hydrofluoric acid. Arch Environ Health. 1991;46:155–160.
  18. MacKinnon MA. Hydrofluoric acid burns. Dermatologic clinics. 1988 Jan;6(1):67-74.
  19. Mayer L, Guelich J. Hydrogen fluoride (HF) inhalation and burns. Archives of Environmental Health: An International Journal. 1963 Oct 1;7(4):445-7.
  20. Stremski ES, Grande GA, Ling LJ. Survival following hydrofluoric acid ingestion. Ann Emerg Med. 1992;21:1396–1399.
  21. McCulley JP, Whiting DW, Petitt MG, Lauber SE. Hydrofluoric acid burns of the eye. J Occup Med. 1983;25:447–450.
  22. Hatai JK, Weber JN, Doizaki K. Hydrofluoric acid burns of the eye: report of possible delayed toxicity. Journal of Toxicology: Cutaneous and Ocular Toxicology. 1986 Jan 1;5(3):179-84.
  23. Greco RJ, Hartford CE, Haith Jr LI, Patton ML. Hydrofluoric acid-induced hypocalcemia. Journal of Trauma and Acute Care Surgery. 1988 Nov 1;28(11):1593-6.
  24. Vance MV, Curry SC, Kunkel DB, Ryan PJ, Ruggeri SB. Digital hydrofluoric acid burns: treatment with intraarterial calcium infusion. YMEM. 1986 Aug;15(8):890–6.
  25. Bentur Y, Tannenbaum S, Yaffe Y, Halpert M. The role of calcium gluconate in the treatment of hydrofluoric acid eye burn. Ann Emerg Med. 1993;22:1488–1490.
  26. Dunser MW, Ohlbauer 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. 2004;30:391–398.
  27. Hatzifotis M, Williams A, Muller M, Pegg S. Hydrofluoric acid burns. Burns. 2004;30:156–159.
  28. Trevino MA, Herrmann GH, Sprout WL. Treatment of severe hydrofluoric acid exposures. Journal of Occupational and Environmental Medicine. 1983 Dec 1;25(12):861-3.
  29. Bentur Y, Tannenbaum S, Yaffe Y, Halpert M. The role of calcium gluconate in the treatment of hydrofluoric acid eye burn. Annals of emergency medicine. 1993 Sep 30;22(9):1488-90.
  30. Caravati EM. Acute hydrofluoric acid exposure. The American journal of emergency medicine. 1988 Mar 1;6(2):143-50.
  31. 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. 2000;73(suppl):S93–S97.
  32. Lee DC, Wiley JF II, Synder JW II. Treatment of inhalational exposure to hydrofluoric acid with nebulized calcium gluconate. J Occup Med. 1993;35:470.
  33. Dunser MW, Ohlbauer 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. 2004;30:391–398.
  34. Upfal M, Doyle C. Medical management of hydrofluoric acid exposure. Journal of Occupational and Environmental Medicine. 1990 Aug 1;32(8):726-31.
  35. Flood S. Hydrofluoric acid burns. American family physician. 1988;37(3):175-82.
  36. Watson AA, Oliver JS, Thorpe JW. Accidental death due to inhalation of hydrofluoric acid. Medicine, Science and the Law. 1973 Oct 1;13(4):277-9.