Mastering Minor Care: Hydrofluoric Acid Exposure

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Background

Fig 1. Hydrofluoric Acid Burn (Courtesy of Dr. Watchorn cc-SA 3.0 https://commons.wikimedia.org/wiki/File:61569264_jamesheilman-224x2991.jpg)

Fig 1. Hydrofluoric Acid Burn (Courtesy of Dr. Watchorn cc-SA 3.0 https://commons.wikimedia.org/wiki/File:61569264_jamesheilman-224x2991.jpg)

Emergency departments in the United States treat nearly 3.5 million upper extremity injuries annually, with 38% involving the fingers [1]. Frequently, hand and finger injuries are triaged to the fast track area: fingertip injuries, lacerations, paronychias…. Many of these patients present with self-evident exams and injury patterns. A few serious hand injuries, though, can present with subtle findings on the initial exam — emergency physicians must beware the missed diagnosis, because those exams will evolve and worsen: high-pressure injection injuries were recently reviewed in Nov 2020 by Life in the Fast Lane, and below we review hydrofluoric (HF) acid exposures. HF exposures present as hand/digit injuries in more than half of cases [2,3]. In this article we review the epidemiology, mechanisms of injury, and therapy for hydrofluoric (HF) acid exposures.

Epidemiology: Who is at risk?

  • Hydrofluoric acid exposures occur in industrial settings, including semiconductor manufacturing, and are generally higher-risk due to higher concentrations [4]

  • More frequent are exposures in commercial or residential settings with cleaning products, especially those targeted to air conditioners, rust removal, tires, or aluminum. [3]

  • A risk factor for a missed diagnosis is an unlabeled secondary container: A retrospective review of US Poison Center data from 2007-2017 found 45,512 cases of exposure to a xenobiotic (substance that is foreign to the body) after transfer to a secondary container; while most cases were nontoxic, HF acid accounted for 6 out of 23 (26%) deaths reported in this review [5]. In particular, unintended ingestion in a secondary container has also been described in more detail as a case report [6].

  • While uncommon, exposures warranting admission are not rare: Over a 15-year period, Parkland Hospital (Dallas, TX) reported 17% of all acute chemical burn admissions were for HF [3].

  • Reviews of poison-related fatalities show both pediatric and adult deaths are reported; example fatal exposures include a patient with a 2.5% TBSA burn from 100% HF and ingestion of 1oz of 1.92% dilute HF due to fatal arrhythmia [7,8].

Mechanisms of Injury and Toxicity: What is a toxic HF exposure?

  • Toxicity is a function of concentration, surface area of exposure, and duration of contact (until complete decontamination)

  • >50% concentration will cause immediate severe pain, whereas <20% may have delayed recognition (and therefore a risk for more prolonged contact time) [9]

    • HF is initially a weak acid, leading to delayed recognition of the initial burn as the pain is not as severe initially [9].

  • At high concentrations (HF>50%), the effect of H+ ions in driving coagulative necrosis is an important mechanism of tissue damage (as with any strong acid)

  • The lipophilic nature and weak acid of HF allows it to penetrate deep into tissue, where a liquefactive necrosis can develop through effects of F- driving tissue damage – this is one of the distinctive mechanisms for HF injury compared to other acids [4].

  • Systemic disruptions can develop as F- ions act as profound scavengers for Mg++ and Ca++ resulting in hypomagnesemia and hypocalcemia [2]. Hypocalcemia may stimulate an efflux of potassium ions from cells resulting in hyperkalemia, and animal studies suggest a significant possible role for hyperkalemia. [10]

  • Both a widened QRS and lengthened QTc can be seen [6]. Cardiac arrhythmias are the primary cause of death in hydrofluoric acid exposures [11].

Therapy: What should we do to treat HF acid exposures

FIG 2. Summary of Therapies

FIG 2. Summary of Therapies

Therapy should begin as soon as possible, including in the pre-hospital environment.

1) Decontamination and Irrigation are the first priority

  • Remove affected clothes

  • Vinyl or rubber gloves and eye protection are essential if assisting

  • Latex can be penetrated by HF so latex gloves are not sufficient [3]

  • Irrigate with tepid water extensively

  • Large area of exposure or saturated clothes should undergo shower decontamination

  • Eye exposure should include extensive irrigation (including consideration of Morgan lens) and emergent ophthalmology consultation

  • Hexofluorine®, a proprietary product intended for HF exposure, has not shown benefit in settings relevant to EPs. Although, industry-funded studies have shown benefit in an ex vivo model of an ultra-acute exposure (20 seconds) [12,13].

In general, do not “play chemist” with acid exposures – exothermic neutralization reactions can be harmful and decontamination with irrigation is the key first step.

2) Topical Calcium Therapy

Calcium is the mainstay of directed therapy: Calcium ions complex free fluoride ions to prevent further toxicity in addition to helping the electrolyte derangements

  • Mix 3.5g of Calcium gluconate with 5 ounces of a water-soluble lubricant to reach 2.5% Calcium gluconate slurry

  • Do not use calcium chloride

  • For hands, can use a glove to apply topical occlusive dressing on the patient’s hands

  • Nail removal is controversial

  • Each administration of topical calcium should be for 30 minutes. Topical calcium administration can be repeat up to every four hours for inadequate pain relief [14]

  • Topical calcium therapy may be adequate therapy for brief, small, time-limited exposures

3) Invasive Local Calcium Therapy

  • Subcutaneous therapy

    • Multiple indications have been proposed but most focus on inadequate pain relief [14]

    • Subcutaneous therapy is more likely to be necessary if HF concentration is >20%

    • 10% calcium gluconate should be used [9]

    • Extreme care should be taken to avoid worsening excessive pressure leading to pressure necrosis distally, with some authors recommending prophylactic palmar fascioties of digits [14]

    • A 27g or 30g needle is used to infiltrate subcutaneously beginning from the periphery of the lesion with a dose of 0.5cc / cm2 (as initially described by Dibbell and colleagues) [14]

  • Intravenous therapy

    • Sometimes deference entirely in favor of intra-arterial therapy but is recommended by some authors (with proximal tourniquet application) as an intermediate step in extremity injuries before attempting IA therapy; 10mL of 10% Calcium Gluconate with Heparin 5000u has been described [2]

  • Intra-arterial therapy

    • Described for high-concentration exposures to digits, although one case report of external carotid artery cannulation has been described [15]

    • As originally described, required an arteriogram to identify the vessel serving the affected area

    • Complications can include hematomas and nerve palsies

    • Intra-arterial therapy should be completed in consultation with a burn and/or hand surgeon

    • 10 to 15 mL of 10% calcium gluconate in 40 mL of Ringer's lactate may be given via an arterial line in the affected extremity over three hours [16]

 4) Systemic Therapy for Systemic Toxicity

  • Risk factors for systemic toxicity: exposure to concentration >50%, exposure of >5% TBSA with any concentration, or inhalation or ingestion of HF directly [3,4].

  • If you have these risk factors, you are no longer “Mastering Minor Care” and are outside the scope of this review, but there are a few items that should be considered while are arranging the appropriate disposition of this patient:

    • Do not wait for a calcium level before beginning calcium therapy if there is a suspected large exposure or if there are electrocardiographic changes. Proceed with calcium gluconate and consider placement of central line for use of calcium chloride.

    • In cases of systemic toxicity 4 grams of IV magnesium should be administered over 20 minutes.

Less common therapies

Ocular, inhalational, and gastrointestinal injuries are all sites of exposure with unique recommendations beyond the typical cutaneous exposure.

  • Ocular therapy: One-time prolonged saline irrigation, with pain control and pH testing as goals. Discuss repeat therapy with ophthalmologist, due to risk of worsened corneal ulcers [9]

  • Inhalational therapy: Can attempt nebulized calcium gluconate for symptomatic exposure, as recently described for a mass event in South Korea with an 8-ton HF spill [17]

  • Gastrointestinal therapy: Rare but reported in the literature.[6] Some authors suggest having patients drink water, milk, or 10% calcium gluconate slurry [2]

AUTHORED BY Adam Gottula, MD and Bennett Lane, MD, MS

Dr. Gottula and Dr. Lane are PGY-4’s in Emergency Medicine at the University of Cincinnati

POST and peer editing BY SHAN MODI, MD

Dr. Modi is a PGY-4 in Emergency Medicine at the University of Cincinnati

FACULTY EDITING BY EDward Otten, MD, FACMT, FAWM

Dr. Otten is a Professor of Emergency Medicine and Director of Toxicology at the University of Cincinnati

References:

  1. Ootes D, Lambers KT, Ring DC. The Epidemiology of Upper Extremity Injuries Presenting to the Emergency Department in the United States. HAND. 2012;7(1):18-22. doi:10.1007/s11552-011-9383-z

  2. Wang X, Zhang Y, Ni L, et al. A review of treatment strategies for hydrofluoric acid burns: Current status and future prospects. Burns. 2014;40(8):1447-1457. doi:10.1016/j.burns.2014.04.009

  3. Stuke LE, Arnoldo BD, Hunt JL, Purdue GF. Hydrofluoric Acid Burns: A 15-Year Experience: J Burn Care Res. 2008;29(6):893-896. doi:10.1097/BCR.0b013e31818b9de6

  4. McKee D, Thoma A, Bailey K, Fish J. A review of hydrofluoric acid burn management. 2014;22(2):4.

  5. Carpenter JE, Murray BP, Moran TP, Dunkley CA, Layer MR, Geller RJ. Poisonings due to storage in a secondary container reported to the National Poison Data System, 2007–2017. Clin Toxicol. Published online October 20, 2020:1-7. doi:10.1080/15563650.2020.1833026

  6. Holstege C, Baer A, Brady WJ. The electrocardiographic toxidrome: the ECG presentation of hydrofluoric acid ingestion. Am J Emerg Med. 2005;23(2):171-176. doi:10.1016/j.ajem.2004.04.032

  7. Murray B, Long B. Hydrofluoric Acid: The Burn that keeps on Burning. EMDocs.net. Published December 5, 2016. Accessed November 2, 2020. http://www.emdocs.net/hydrofluoric-acid-burn-keeps-burning/

  8. Bronstein AC, Spyker DA, Cantilena LR, Green JL, Rumack BH, Dart RC. 2010 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 28th Annual Report. Clin Toxicol. 2011;49(10):910-941. doi:10.3109/15563650.2011.635149

  9. Bertolini JC. Hydrofluoric acid: A review of toxicity. J Emerg Med. 1992;10(2):163-168. doi:10.1016/0736-4679(92)90211-B

  10. Mclvor ME, Cummings CE, Mower MM, et al. Sudden cardiac death from acute fluoride intoxication: The role of potassium. Ann Emerg Med. 1987;16(7):777-781. doi:10.1016/S0196-0644(87)80573-5

  11. Yamaura K, Kao B, Iimori E, Urakami H, Takahashi S. Recurrent Ventricular Tachyarrhythmias Associated with QT Prolongation Following Hydrofluoric Acid Burns. J Toxicol Clin Toxicol. 1997;35(3):311-313. doi:10.3109/15563659709001218

  12. Höjer J, Personne M, Hultén P, Ludwigs U. Topical Treatments for Hydrofluoric Acid Burns: A Blind Controlled Experimental Study. J Toxicol Clin Toxicol. 2002;40(7):861-866. doi:10.1081/CLT-120016957

  13. Burgher F, Mathieu L, Lati E, et al. Part 2. Comparison of emergency washing solutions in 70% hydrofluoric acid-burned human skin in an established ex vivo explants model. Cutan Ocul Toxicol. 2011;30(2):108-115. doi:10.3109/15569527.2010.534748

  14. Kirkpatrick JJR, Enion DS, Burd DAR. Hydrofluoric acid burns: a review. Burns. 1995;21(7):483-493. doi:10.1016/0305-4179(95)93254-H

  15. Nguyen LT, Mohr WJ, Ahrenholz DH, Solem LD. Treatment of Hydrofluoric Acid Burn to the Face by Carotid Artery Infusion of Calcium Gluconate: J Burn Care Rehabil. 2004;25(5):421-424. doi:10.1097/01.BCR.0000138288.15403.BA

  16. Wedler V, Guggenheim M, Moron M, K??nzj W, Meyer VE. Extensive Hydrofluoric Acid Injuries: A Serious Problem: J Trauma Inj Infect Crit Care. 2005;58(4):852-857. doi:10.1097/01.TA.0000114528.15627.65

  17. Choe MSP, Lee MJ, Seo KS, et al. Application of calcium nebulization for mass exposure to an accidental hydrofluoric acid spill. Burns. 2020;46(6):1337-1346. doi:10.1016/j.burns.2020.02.015