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Goldfrank's Toxicologic Emergencies, 11e

Chapter 104: Hydrofluoric Acid and Fluorides Mark K. Su

FIGURE 104–1.

HISTORY AND EPIDEMIOLOGY

Hydrofluoric acid has been known for centuries for its ability to dissolve silica. The Nuremberg artist

Schwanhard is given credit for the first attempt in 1670 to use HF vapors to etch glass.47 Today, hydrofluoricacid (HF) is widely used throughout industry. In addition to glass etching, HF is used in brick cleaning,etching microchips in the semiconductor industry, electroplating, leather tanning, rust removal, and the

cleaning of porcelain.47 From 2011 to 2015, the American Association of Poison Control Centers (AAPCC)reported 2,761 single-substance exposures to HF and 6 deaths (Chap. 130). The hands are the commonestpart of the body injured. Exposures to HF o�en occur as unintentional occupational hazards. The actualnumber of work-related poisonings from HF appears di�icult to quantitate because of limitations inInternational Classification of Diseases (ICD) medical coding and the lack of notification of regional poison

control centers by worksites.10

Hydrofluoric acid is also the commonest cause of fluoride poisoning, although other forms of fluoride,including sodium fluoride (NaF), ammonium bifluoride (NH4HF2), and sodium or zinc fluorosilicate, also

produce significant toxicity. Historically, NaF was used as an insecticide, rodenticide, an antihelminthic forswine, and a delousing powder for poultry and cattle. Ammonium bifluoride is mainly used in industrialinorganic chemistry, especially in the processing of alloys and in glass etching. Other fluoride salts are widelyused in, for example, the steel industry, drinking water, toothpaste additives, electroplating, lumbertreatment, and the glass and enamel industries.

The widespread use of HF and fluoride-containing compounds results in significant toxicity. In 1988, an oilrefinery in Texas released a cloud of hydrogen fluoride gas that resulted in 939 people seeking hospital

treatment and 94 of these patients requiring admission.100 The petroleum industry has since been plagued

by similar HF incidents.100 In 2015, Washington State reported one death and 48 occupational HF burns

associated with car and truck washing between 2001 and 2013.78 Sodium fluoride was responsible for thepoisoning of 263 people and 47 fatalities when it was mistaken for powdered milk and unintentionally

combined with scrambled eggs.55 Following ingestion, this and other fluoride salts are converted to HF invivo, resulting in significant fluoride toxicity.

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CHEMISTRY

Hydrofluoric acid is synthesized as the product of gaseous sulfuric acid and calcium fluoride, which is

subsequently cooled to a liquid.56 Aqueous HF is a weak acid, with a pKa of 3.17; as such, it is approximately

1,000 times less dissociated than equimolar hydrochloric acid, a strong acid. Hydrofluoric acid generallyranges in concentrations from 3% to 40%, for use in both industry and the home. Anhydrous HF is highlyconcentrated (>70%) and used almost exclusively for industrial purposes. Hydrofluoric acid has uniqueproperties that can cause life-threatening complications following seemingly trivial exposure.

Sodium fluoride is commonly synthesized by the reaction of sodium hydroxide (NaOH) with HF, with

subsequent purification by recrystallization. Sodium fluoride is highly water soluble and readily dissociates.4

To synthesize ammonium bifluoride (NH4HF2), ammonium fluoride (NH4F) is first formed by the reaction of

ammonium hydroxide (NH4OH) with HF. Ammonium fluoride is then converted to bifluoride by dehydrating

the aqueous solution.

Fluorine is the most electronegative element in the Periodic Table of the Elements owing to its relativelylarge number of protons in the nucleus compared to its molecular size, and the minimal amount of screeningor shielding by inner electrons. Other halides possess lesser electronegative properties. Consequently, the

corresponding anion of fluorine, the fluoride ion (F−), is a weak base because it possesses only a limitedability to donate its electrons. Liberation of the fluoride ion from the previously mentioned compounds isbelieved to be the major determinant of toxicity.

PATHOPHYSIOLOGY

Exposures to HF occur via dermal, ophthalmic, inhalation, oral, and rectal routes.18 A permeability coe�icient

of 1.4 × 10−4 cm/sec allows HF to penetrate deeply into tissues prior to dissociating into hydrogen ions and

highly electronegative fluoride ions.34 These fluoride ions avidly bind to extracellular and intracellular stores

of calcium (Ca2+) and magnesium (Mg2+), depleting them, and ultimately leading to cellular dysfunction and

cell death.11,54,64 The alteration in local calcium homeostasis causes neuroexcitation and accounts for thedevelopment of neuropathic pain. Furthermore, ischemia related to calcium dysregulation–mediated

localized vasospasm is likely an additional contributory factor to the development of pain.42,91

Formation of insoluble calcium fluoride (CaF2) is proposed as the etiology for both the precipitous fall in

serum calcium concentration and the severe pain associated with tissue toxicity. There are several theoriesregarding the actual fate of calcium and fluoride ions in tissues. In vitro evidence suggests that fluorapatite isformed in the presence of phosphate and hydroxyapatite, which is a more likely pathway for disposition of

the fluoride ion.11 Fluorapatite, like calcium fluoride, is insoluble and its formation contributes to the clinicalfindings recognized following HF toxicity.

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Fluoride also binds magnesium and manganese ions and there is in vitro evidence that this interferes withmany enzyme systems. In the anhydrous form, the high concentration of hydrogen ions in HF also produces acaustic burn similar to that caused by strong acids (Chap. 103). The minimal lethal oral dose in humans is

approximately 5 to 10 g of NaF.5

CLINICAL EFFECTS

Local E�ects

Dermal

The extent of tissue injury following dermal exposure is determined by the volume, concentration, andcontact time with the tissues. Following dermal exposure, the concentration of HF is directly related to the

onset of pain at the contact site.31,56,90 High concentrations (>20%) cause immediate pain with visible tissue

damage.84 Exposure to household rust-removal products (6% and 12% HF) is o�en associated with a typical

latency of several hours, before pain develops.31,85,95,96 The initial site of injury typically appears relativelybenign despite significant subjective complaints of pain. Over time, the tissue becomes hyperemic, withsubsequent blanching and coagulative necrosis. As calcium complexes precipitate, a white discoloration of

the a�ected area appears74 (Fig. 104–1). Ulceration is dependent on the concentration and duration of

contact.27,48,57 If more than 2.5% of the body surface area (BSA) is burned with highly concentrated HF, life-

threatening systemic toxicity should be expected.20,71,73,84,90 Small body surface area exposures to lowconcentrations (<20%) typically do not result in life-threatening systemic toxicity, although fatalities have

resulted with dermal exposures to concentrated HF covering less than 5% body surface area.89

FIGURE 104–1.

Severe injury to the fingers resulted from exposure to hydrofluoric acid. Note the arterial line in place foradministration of calcium. (Used with permission from the Fellowship in Medical Toxicology, New YorkUniversity School of Medicine, New York City Poison Center.)

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Gastrointestinal

Intentional ingestion of concentrated HF (or other fluoride salts) causes significant gastritis yet o�en sparesthe remainder of the gastrointestinal tract. Patients promptly develop vomiting and abdominal pain.Although systemic absorption is rapid and almost invariably fatal, there is at least one report of a patient whoingested a low concentration (8%) of HF and su�ered multiple episodes of ventricular fibrillation but was

successfully resuscitated.87 Following HF ingestion, patients o�en present with altered mental status, airway

compromise, and dysrhythmias.13,55,59,87

Ophthalmic

Hydrofluoric acid results in more extensive injury to the eye than most other acids.65 Ophthalmic exposuresfrom liquid splashes or hydrogen fluoride gas rapidly denudes the corneal and conjunctival epithelium, and

lead to stromal corneal edema, conjunctival ischemia, sloughing, and chemosis.47 Fluoride ions penetrate

deeply to a�ect anterior chamber structures.47 The e�ects are usually noted within one day.47 Other possiblefindings include corneal revascularization, recurrent epithelial erosions, and, sometimes,keratoconjunctivitis sicca (dry eye) develops as a long-term complication with subsequent corneal

ulcers.7,65,80

Pulmonary

Patients with inhalational exposures present with a variety of signs and symptoms depending on theconcentration and exposure time. Thirteen oil refinery workers exposed to a low-concentration HF mist

experienced minor upper respiratory tract irritation.52 By contrast, in a mass inhalational exposure to HF,

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throat burning and shortness of breath were among the more common chief complaints.100 Some of thesepatients developed hypoxemia and hypocalcemia and had altered pulmonary function tests. Stridor,wheezing, rhonchi, and erythema and ulcers of the upper respiratory tract were described. Eye pain was alsonoted, reinforcing the fact that ophthalmic injury o�en accompanies inhalational and/or dermal

exposures.52,62,79,100

ASSESSING SEVERITY OF SYSTEMIC EFFECTS

Significant systemic toxicity occurs via any route of exposure because of the ability of HF to penetrate tissues.The potential for systemic toxicity is an important consideration in management necessitating rapid

decontamination and treatment.12,16,33,83,84,92,93 Fatal exposures to HF by any route share the similarfeatures of hypocalcemia, hypomagnesemia, and, in many cases, hyperkalemia as preterminal

events.4,13,19,23,33,56,59,66,67,90 In some circumstances, the hypocalcemia severely disrupts the coagulation

cascade, resulting in significant anticoagulation, even on postmortem examination.59,69,70

Fatalities from HF occur as a result of either sudden-onset myocardial conduction failure or ventricularfibrillation. Although the evidence regarding the mechanism of myocardial irritability is inconclusive,electrolyte disturbances that lead to ventricular dysrhythmias including ventricular fibrillation are the most

likely primary cause of death in patients with severe systemic fluoride poisoning.20,72,84,90,104 Although one

postmortem human case reveals significant structural myocardial injury,63 interestingly, histologic

abnormalities of the myocardium do not occur in canine models of HF poisoning.25,69

Systemic fluoride toxicity results in hypocalcemia, by mechanisms not fully elucidated. Fluoride causescalcium ions to accumulate intracellularly, leading to an e�lux of potassium ions into the extracellular

space.25,54,69 One in vitro study performed with human erythrocytes demonstrated that fluoride inhibition of

Na+,K+-ATPase and Na+,Ca2+ exchange leads to an increase in intracellular calcium.68 The subsequenthyperkalemia alters the automaticity and resting potential of the heart, leading to fatal dysrhythmias (Chap.

15).66 Dogs treated with quinidine, a potassium e�lux blocker, are protected from lethal doses of intravenous

NaF.25 Likewise, amiodarone, which also blocks potassium e�lux has demonstrable e�icacy in both in vitro

and in vivo models of fluoride toxicity.88 However, e�icacy in humans has not been studied. Furthermore, the

mechanism of toxicity is likely much more complicated.106 A child with systemic fluoride toxicity, who wasappropriately replenished with calcium, and had normal electrolytes still experienced nonfatal ventricular

fibrillation.12,106 Perhaps this is because serum potassium, calcium, and magnesium concentrations only

partly represent tissue concentrations.11,12,25,66,67 Furthermore, HF directly impairs myocardial function.Rabbits exposed to topical HF over 2% of their total body surface area developed focal necrosis of myocardial

fibers, as well as significant elevations in cardiac enzymes that persisted for almost 5 days a�er injury.105

Assessing Severity of Clinical Exposures. Historical and clinical features of an exposure usually determinewhich HF exposures are life-threatening. All oral and inhalational exposures are potentially fatal, as should

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burns of the face and neck, regardless of HF concentration. Inhalational exposure should be assumed for allpatients with skin burns of greater than 5% body surface area, any exposure to HF concentrations greater

than 20%, and head and neck burns.46 Patients presenting with altered mental status directly related to HFare critically ill and necessitate rapid therapy.

Hydrofluoric acid concentrations greater than 20% have potential for significant toxicity in any patient, even

if only a small surface area is exposed.61 As a general rule, patients who experience severe pain withinminutes of contact are most likely exposed to a very high concentration of HF and their condition should beexpected to rapidly deteriorate. Some otherwise well-appearing patients have a precipitous demise withoutany clinical manifestations of hypocalcemia. Furthermore, it is possible that systemic toxicity will occurfollowing seemingly minimal exposure. A 36-year-old man was exposed to 20% HF over a 3% BSA and

subsequently developed hypocalcemia, hypomagnesemia, and cardiac arrest 16 hours later.102 A 2-year-oldgirl ingested some “fingers full” of an ammonium bifluoride glass etching cream and had prolonged

hypocalcemia refractory to calcium gluconate up to 24 hours a�er ingestion.58 Consequently, patients willrequire prolonged electrolyte and cardiac monitoring following significant fluoride exposures.

DIAGNOSTIC TESTING

No monitoring or testing is required for uncomplicated small BSA exposures to low concentrations of HF.Diagnostic testing for systemic fluoride poisoning is currently based on monitoring of serum electrolytes.

Calcium, magnesium and potassium concentrations should be serially monitored.33 As systemic toxicity

progresses, a metabolic acidosis will likely develop necessitating a venous or arterial blood gas analysis.11

Serum fluoride concentrations are not readily available in a clinically relevant time frame. Although a serumfluoride concentration of 0.3 mg/dL was reported as fatal, one patient survived with a serum fluoride

concentration of 1.4 mg/dL.90,106

Electrocardiographic findings of both hypocalcemia (prolonged QT interval) and hyperkalemia (peaked T

waves, etc) are o�en reliable indicators of toxicity (Chap. 15).4,16,33,36,41,70,90 In fact, ECG findings of peakedT waves from hyperkalemia preceded the onset of ventricular dysrhythmias in reported cases, thus

potentially serving as a marker of severe fluoride toxicity.12,67 It should be noted that in some cases of HF

poisoning, hypokalemia is reported26,32,102 and for unclear reasons, are specifically related to sodium

fluoride toxicity.97

MANAGEMENT

General

For patients with more than localized exposure to low concentration (<20%) HF or any exposures to highconcentration (>50%) HF, the mainstay of management is to prevent or limit systemic absorption, assess forsystemic toxicity, and rapidly correct any electrolyte imbalances. Intravenous access should be obtained. An

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ECG should be obtained and examined for dysrhythmias and signs of hypocalcemia, hypomagnesemia, andhyperkalemia. The patient should be attached to continuous cardiac monitoring and have a rapidassessment of serum electrolyte concentrations.

Rapid airway assessment and protection should occur early in patients with inhalation or ingestion,respiratory distress, ingestion with vomiting, or burns significant enough to cause a change in mental statusor phonation. If an unstable patient requires intubation, the depolarizing neuromuscular blocking agent,succinylcholine, should not be used because of potential hyperkalemia.

For patients with less significant dermal exposures, studies have focused on alternatives to irrigation withwater or saline as decontamination techniques. The compound “hexafluorine” is promoted for dermal and

ophthalmic decontamination of HF splashes.60,86 Hexafluorine is a proprietary name whose chemicalformula is not disclosed and papers that report success have strong ties to the manufacturer. In a controlledand blinded experimental study, Hexafluorine treatment was less e�ective than irrigation with water

followed by the application of topical calcium.40 In a follow-up animal study, water irrigation was as e�ective

as Hexafluorine in preventing systemic toxicity from HF.43 At this time, until further objective data areavailable, we do not recommend the use Hexafluorine for initial decontamination of patients with HFexposures.

An iodine-containing preparation was evaluated in a guinea pig model of HF-induced burns and found to be

associated with significant reductions in ulceration area.101 Iodine is hypothesized to inhibit apoptosis and

has protective e�ects against burns from various alkylating agents, including mustard gas.101 Becauseexperience with iodine treatment of human HF burns is lacking, it cannot be recommended at this time.

The most important therapy for skin exposures is the rapid removal of clothing and irrigation of the a�ected

area with copious amounts of water or saline, whichever is more readily available.2,51,53,57

One report describes a woman who was dying from severe HF toxicity who was treated by amputation of thea�ected limb, and survived. Although this may be an alternative measure for patients who are critically illand demonstrate an inadequate response to all other therapeutic modalities, we do not recommend such

aggressive measures.15,49

Dermal Toxicity

Several therapeutic options have been studied in animal models for treatment of topical HF burns.Unfortunately, many study designs use histologic or subjective wound inspection as outcome

parameters,17,75 some with unblinded inspection.14,29,49,51,72 These animal models do not address theclinically important parameters of pain reduction, cosmesis, and functionality (Antidotes in Depth: A32).

We recommend that a topical calcium gel be applied to the a�ected area. A commercial gel is available in theUnited States but an acceptable substitute is reasonable and easily prepared. This is accomplished by mixing

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3.5 g of calcium gluconate powder in 150 mL of sterile water-soluble lubricant, or 25 mL of 10% calcium

gluconate in 75 mL of sterile water-soluble lubricant.2,17,46 If calcium gluconate is unavailable, it is

reasonable to use calcium chloride or calcium carbonate in a similar formulation.21 This topical therapy forsevere and non–life-threatening toxicity scavenges fluoride ions. A�er irrigation, we recommend a gelsolution of calcium carbonate or gluconate be applied directly to the a�ected area or mixed directly into asterile surgical glove and then placed on the patient’s burned hand for 30 minutes. Two case series report

limited success with this therapy.2,21 Some patients describe prompt and dramatic relief of pain.Alternatively or simultaneously, analgesics are recommended orally or parenterally as needed, but preferablynot to the point of sedation, because local pain response is used to guide therapy. Digital nerve blocks withsubcutaneous lidocaine or bupivacaine is also reasonable for patients with significant pain presenting 12 to24 hours a�er the injury from a low concentration of HF and with no systemic signs of toxicity since that time

topical calcium salts are unlikely to be e�ective.28 An animal study examining the e�icacy and mechanism oftopical calcium gel therapy found that the fluoride ion concentration in the calcium gel was significantlyhigher than non–calcium-containing gel controls. Although this was a limited study, these animals also had adecrease in urinary fluoride ion concentration as compared to controls, suggesting less overall tissue

absorption of the HF.51 Delivery of calcium transcutaneously is enhanced by various means. In a rodent studyof HF burns, iontophoretic (facilitated transport using an electromotive force) delivery of calcium ions

appeared to increase calcium concentrations in vitro and improve pathologic changes in vivo.103 Significantlimitations to this study are time to administration of therapy and feasibility in patients with complex

burns.81 Human data are lacking. Dimethyl sulfoxide (DMSO) mixed with topical calcium salts facilitates thetransport of calcium ions through the skin to penetrate deeply into the tissues. Dimethyl sulfoxide also is

able to act as a scavenger of free radicals, thus limiting inflammation and ongoing injury.36 Although one

group of authors advocates for the combined use of DMSO and calcium,36 concerns remain over reported

adverse e�ects of DMSO.47 There are currently inadequate data to support the routine use of DMSO in thetreatment of HF burns.

Three other therapies have had variable success in human exposures: the appli cation of calcium viaintradermal, intravenous, and intraarterial routes. If topical gel therapy fails within the first few minutes ofapplication, intradermal therapy with dilute calcium gluconate is a reasonable next step. Unfortunately, thistreatment has limited usefulness and is not recommend in nondistensible spaces such as fingertips.Histologic studies in animal models demonstrate that 10% calcium chloride solution is damaging to the

tissues and is not recommended.28,35 The preferred method is to approach the wound from a distal point of

injury and inject intradermally no more than 0.5 mL/cm2 of 5% calcium gluconate. Although one author

recommends a palmar fasciotomy whenever this method of treatment is used in the hand,2 this practice isnot recommended unless a compartment syndrome is present. The potential for iatrogenic injury exceedsthe potential benefit of injections in the hand. The limits of intradermal injection include the potential toincrease so�-tissue damage without adequate relief, infection, and inadequate space to safely inject withoutcausing a compartment syndrome.

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E�ective pain relief is especially problematic for nailbed involvement, leading some authors to suggestremoval of the nail. This approach has some advantages in accessing the a�ected area; however, it is apainful procedure that is o�en cosmetically undesirable and the outcome is not always significantlyimproved. We therefore do not routinely recommend this procedure.

If the wound is large or on a section of the fingerpad or an area that is not amenable to intradermal

injections, intraarterial calcium gluconate is the next most reasonable step.95 This procedure deliverscalcium directly to the a�ected tissue from a proximal artery. Placement should be ipsilateral and proximalto the a�ected area, usually in the radial or brachial artery. The method of obtaining access is debated.Because of the potential to damage the endothelial lining of the artery, and because extravasation can havepotentially devastating consequences, angiographic confirmation or direct visualization of the vessel wasformerly recommended. This practice is still prudent if cannulation of the artery is expected to be di�icultbecause of prior surgery or if an anatomic deformity is suspected. If the arterial line is carefully placed in asingle attempt, and a good confirmatory arterial tracing is obtained, the infusion can be started. Werecommend adding 10 mL of 10% calcium gluconate to either 40 mL of D5W (dextrose 5% in water) or 0.9%

sodium chloride solution infused continuously over 4 hours.1,2,76,85,94,95 This results in a 2% calciumgluconate solution. An animal model examined the e�ect of undiluted 10% calcium gluconate intraaortically.Although the model did not involve exposure to HF, there was significant tissue injury in the vessel wall as

compared to a 2% calcium gluconate solution.28 Calcium chloride has also been used successfully, althoughthe potential for vessel injury and extravasation are significant and there is no defined benefit over calcium

gluconate.94,107 The complications associated with the use of intraarterial calcium infusion in several caseseries were relatively benign, and include transient radial artery spasm, hematoma, inflammation at the

puncture site, and a fall in serum magnesium concentration.82,95 A�er the infusion is initiated, patientstypically experience significant pain relief. Patients requiring an arterial line for treatment should beadmitted to the hospital, as the majority will require more than one treatment, and some patients require as

many as 5 separate infusions of calcium gluconate. Although wounds may require débridement,2 someauthors suggest that following intraarterial calcium infusion, tissue can be salvaged that initially would not

have been considered viable.96 There are no reported cases of clinically significant hypercalcemia followinginfusion as the total dose infused is quite low, although serum calcium concentrations were not routinelyrecorded in some cases.

Magnesium salts are an alternative or adjunctive therapy to the administration of calcium salts for patientswith dermal HF burns. Application of magnesium hydroxide and magnesium gluconate gel show histologic

evidence of e�icacy in rabbit models of dermal HF burns.17 Two other animal models of intravenous

magnesium for dermal HF burns also suggest e�icacy in terms of wound healing.24,99 Magnesium wassuggested as an antidote for fluoride poisoning because magnesium fluoride is more water soluble than

calcium fluoride and magnesium is readily excreted by the kidneys.100 However, these magnesium modelsinadequately address the disadvantage of magnesium salt solubility, and both topical and intravenousmagnesium therapy remain incompletely evaluated in humans and therefore is not routinely recommended.

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Another reported therapy for localized HF poisoning is an intravenous Bier block technique that uses 25 mL

of 2.5% calcium gluconate. In one case, the e�ects lasted 5 hours and there were no adverse events.39 In 2other cases of patients exposed to HF, a 6% calcium gluconate solution administered using this procedure

resulted in rapid and complete analgesia with minimal tissue necrosis.82 Although the intravenous Bier blocktechnique is not reported as being used in a substantial number of patients, it is reasonable, particularly

when intraarterial infusion is problematic.82 Further data are required before this therapy is routinelyrecommended.

We rountinely observe all patients with digital exposures to HF over 4 to 6 hours, as the pain o�en recurs andreapplication of the gel or an alternative therapy will be necessary. Even if successful pain control isachieved, the patient will require specialized follow-up and wound care.

Inhalational Toxicity

Patients exposed to a low concentration of HF and treated with 4 mL of a 2.5% nebulized calcium gluconate

solution demonstrated a subjective decrease in irritation with no adverse e�ects.52 Another reportdemonstrated a good outcome following nebulization of a 5% calcium gluconate solution in a patient with an

inhalational exposure.50 Because nebulized calcium gluconate is a relatively benign therapy, we recommendthat all patients with symptomatic inhalational exposures to any concentration of HF be administered a

dilute solution of calcium gluconate.30

Ingestions

In patients with intentional ingestions of HF, gastrointestinal decontamination poses a dilemma. Induction ofemesis is potentially harmful and therefore contraindicated. Because aqueous HF is a weak acid, the risk ofperforation by passage of a small nasogastric tube may be lower than the risk of death from systemic

absorption.4,59 In the acidic environment of the stomach, more of the weak acid solution remainsnonionized, thus penetrating the gastric mucosa and causing rapid systemic poisoning. Moreover, activatedcharcoal is unlikely to adsorb the relatively small fluoride ions. Although placement of a nasogastric tube toperform gastric lavage is clearly associated with risks to the patient, insertion of a nasogastric tube isbeneficial under specific circumstances if done safely and in a timely manner. Consequently, gastricemptying via a nasogastric tube is reasonable in the absence of significant spontaneous emesis because

these exposures are almost universally fatal.4,13,59,70 Health care providers should exercise extreme cautionduring this procedure because secondary dermal or inhalational exposures to the provider is possible in theabsence of appropriate personal protective equipment. If there is a possibility of inhalation by the provider,the area should be well ventilated. Acceptable forms of hand protection include gloves made of nitrile, butylrubber, polyvinyl chloride, or Neoprene. Latex gloves should not be used.

Following ingestion, we recommend a solution of a calcium or magnesium salt be administered orally assoon as possible to prevent HF penetration into the stomach and to provide an alternative source of cationsfor the damaging electronegative fluoride ions.

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When comparing the e�icacy of calcium to magnesium salts, calcium is better than magnesium in reducing

the bioavailability of fluoride as described in a murine model.38 Magnesium citrate in a standard catharticdose, magnesium sulfate, or any of the calcium solutions can be administered orally to prevent absorption(Antidotes in Depth: A16). Although intuitive, evidence for the benefit of oral calcium or magnesium salts islimited. In a mouse model of oral HF toxicity, administration of calcium- or magnesium-containing solutions

did not change average survival time.37 The study results, however, were limited because the calcium andmagnesium salts were premixed together with the HF during administration, thus being an inadequatemodel for the study of HF ingestion. In another study, the survival rate of mice poisoned with NaF was

significantly greater when treated with either high doses of oral CaCl2 or MgSO4.45 Given the current

information, we recommend oral calcium salts for oral ingestion; however, if calcium salts are unavailable,magnesium salts are reasonable should be given.

Ophthalmic Toxicity

Patients with ophthalmic exposures should have each eye irrigated with 1 L of 0.9% sodium chloride

solution, lactated Ringer solution, or water.65 Although there are limited data, repetitive or prolonged

irrigation appears to worsen outcome.65 A complete ophthalmic examination should be performed a�er thepatient is deemed stable, and an ophthalmology consultation should be obtained (Chap. 24). One casereport demonstrated a good outcome following ocular HF exposure with the use of 1% calcium gluconate

eye drops.7 Although 2 reviews also recommend the use of 1% calcium gluconate for this purpose,30,36

calcium salts tend to be irritating to the eye and this therapy is not adequately studied; consequently, use isnot recommended at this time. There is no role for gel therapy or ophthalmic injection for these patients,because most calcium and magnesium salts are potentially toxic to ophthalmic tissues and may actually

worsen outcome.6,65

Systemic Toxicity

If there is a clinical suspicion of severe toxicity, the immediate intravenous administration of both calciumand magnesium salts is recommended. Calcium gluconate is preferred over calcium chloride because of therisks associated with extravasation (Antidotes in Depth: A32). Patients o�en require several grams of calcium

to treat severe HF toxicity.33 We recommend that intravenous magnesium be administered to adults as 20 mLof a 20% magnesium sulfate solution (4 g) over 20 to 30 minutes. An approach that uses intravenous calciumor magnesium, and local calcium or magnesium gels to limit absorption protects against life-threateninghypocalcemia and hyperkalemia. Because of the numerous adverse e�ects of systemic fluoride poisoning,administration of calcium and magnesium salts alone is o�en insu�icient in improving survival from

systemic fluoride poisoning.22 Furthermore, an animal model of hydrogen fluoride toxicity found that

maintaining a normal acid–base balance was protective against HF toxicity.98 Moreover, in a study of patientsreceiving enflurane, an inhalational anesthetic metabolized by the liver to fluoride ions, urine alkalinization

improved the excretion of fluoride.77 Thus, it is beneficial to correct any significant acidemia with hydration

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and IV sodium bicarbonate (calcium salts and sodium bicarbonate cannot be mixed). Because standardtreatment for systemic fluoride toxicity includes administration of calcium salts and sodium bicarbonate,hyperkalemia is simultaneously addressed.

Treatment with large quantities of calcium and magnesium do not generally result in significant

hypercalcemia or hypermagnesemia.30 Several explanations are proposed. First, in systemically HF-poisonedpatients, total body calcium and magnesium stores are severely decreased so that large doses are requiredfor adequate repletion. In addition, most patients who are exposed to HF are young and healthy, with intact

kidney function.30 Administration of calcium also results in antidiuretic hormone antagonism on renaltubular reabsorption resulting in polyuria which facilitates the urinary excretion of calcium and

magnesium.30

Because most of the fluoride ions are eliminated renally,8,44,51,83 hemodialysis is reasonable in patients withsevere HF poisoning and acute kidney injury. There are several reported cases of successful clearance of

fluoride ions via hemodialysis, with one case also using continuous venovenous hemodialysis.3,8,9 Becausethe reported clearance rate did not di�er significantly from normally functioning kidneys, it is unclearwhether hemodialysis alters outcome in patients with normal kidney function. Furthermore, prolongedhemodialysis, beyond the standard 4-hour course, is unnecessary for most patients unless they have kidney

failure.3

Although the use of quinidine, a potassium channel blocker, is protective in dogs,69 it has not been studied orused in humans, and at this time cannot be recommended, but in the presence of life-threatening ventriculardysrhythmias, quinidine (or any other class III antidysrhythmic) is reasonable.

SUMMARY

Although HF has a pKa of 3.17 and is considered a weak acid, it causes local and systemic toxicity because offluoride binding to cations.

Dermal exposure to HF causes severe pain, o�en before any physical manifestations are evident.

In patients with greater than 2.5% BSA HF burns we recommend periodic assessment of serum calcium,magnesium, and potassium concentrations. Admission is required for prolonged electrolyte and cardiacmonitoring.

Therapy for local toxicity includes topical calcium and magnesium salts and systemic analgesia. In somecases, intradermal or intraarterial administration of calcium is required.

Therapy for systemic toxicity includes all treatments for local toxicity plus intravenous calcium andmagnesium salts, sodium bicarbonate, and potentially hemodialysis.

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Baltazar  RF, et al. Acute fluoride poisoning leading to fatal hyperkalemia. Chest. 1980;78:660–663. [PubMed: 7418496]

Baselt  RC. Disposition of Toxic Drugs and Chemicals in Man . 9th ed. Seal Beach, CA; BiomedicalPublications; 2011.

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