The Poison Control Center

Hydrofluoric Acid

John Caterfino, RPh, Tox Talk 1996, Vol. 7 Issue 1

Introduction
Cases
Pathophysiology
Dermal exposure
Exposure by other routes
Ocular exposures
Oral/ingestion exposure
Pulmonary/inhalation exposures
Rectal exposure
Systemic intoxication/systemic fluorosis
Summary
References

Introduction

Recognizing the hallmarks of a hydrofluoric acid (HF) burn can be difficult. A working knowledge of the mechanisms of injury involved in exposures to HF is necessary for all emergency care providers. In 1994, the American Association of Poison Control Centers documented over 1370 exposures to HF. Two-thirds of these cases required treatment in health care facilities.1 An emergency physician confronted with a patient complaining of intense pain after a chemical exposure where the severity of pain does not correlate with the clinical findings should consider the possibility of an HF exposure. Recognition of an HF burn is perhaps the most important factor in preventing deep local or systemic injury.4 Rapid decontamination and treatment are necessary to avoid deep tissue damage, liquefaction necrosis, bone destruction due to decalcification, and systemic fluorosis.2,3,4

HF is a significantly corrosive inorganic acid. It is produced by reacting sulfuric acid and calcium fluoride in a heated environment: CaF2 (s) + H2SO4 (l) 2 HF (g) + CaSO4 (s).22

The resultant gas is then purified and condensed into a highly corrosive fuming, nearly colorless liquid. In industrial settings, HF is utilized in the production of fluoride compounds, as a catalyst in the petrochemical development of hi-octane fuels, in the manufacture of plastics and dyes and in semiconductor research.5 Commercially, hydrofluoric acid solutions are employed to frost or etch crystal or glass and in the development of silicone chips.6 Products available to the general public include rust removal agents and aluminum or chrome cleaning agents.7,8

Other industrial uses of hydrofluoric acid include metal refining, mineral processing, and the desulfurization of oil.23 Despite the fact that hydrofluoric acid is used in a wide variety of industries, it is extremely toxic. Human exposure to hydrofluoric acid may produce serious or life-threatening effects, depending on the route of exposure, the extent of exposure and the concentration of the acid. Specialized treatment is required for hydrofluoric acid exposure because of the unique toxicities of this substance.

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Cases

Case 1

A 59 year old male spilled 74 percent hydrofluoric acid on his left arm and both legs while at work. Exposed areas were immediately irrigated with normal saline for 15 minutes followed by the application of benzalkonium chloride. The patient presented to the emergency room 30 minutes after the exposure complaining of severe pain of the exposed tissue. Physical exam revealed an awake and alert man with 20 percent body surface area burns to his left arm and both legs with evidence of tissue necrosis. Calcium gluconate gel was applied to the exposed areas followed by infiltration of 19 vials of calcium gluconate 10 percent at 0.5 ml./cm2 with 95 percent pain relief. Vital signs showed a normal blood pressure with a heart rate of 60-80 beats per minute. Electrocardiogram(ECG) was unremarkable except for an occasional sinus bradycardia of 60 beats per minute. Pertinent laboratory values 2.5 hours following the exposure were: total calcium, 6 mg./dl.; magnesium, 1.2 mEq./l.; and potassium, 4.7 mEq./l. An infusion of calcium gluconate was started at 10 mEq./hour and the patient received a total of 80 mEq. of calcium gluconate IV. Repeat total calcium was 10 mg./dl. At this point the patient was stabilized and transferred to a burn unit at a local hospital. Upon arrival to the burn unit the patient's total calcium was 12.6 mg./dl. and remained within normal limits for the remainder of the hospital course. The patient was placed on dicloxocillin and ciprofloxacin three days following the exposure due to infection and possible cellulitis. Five days post-exposure the patient was ambulatory and still receiving applications of calcium gluconate gel with dressing changes and Tylenol as needed for pain.

Case 2

A 57 year old male presented to his private physician with severe pain and erythema of the distal portions of several fingers on both hands. Twenty-four hours prior to this visit, the patient had been using an aluminum brightener which he claimed contained "an acid". He had spilled some on his fingers and under his nails. The physician called the poison control center to identify the contents of the product. Since the metal cleaner contained hydrofluoric acid 5-10 percent, the patient was referred to the burn unit of a local hospital for treatment of hydrofluoric burns.

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Pathophysiology

As with all inorganic acids, the dissociation of hydrogen ions causes the initial corrosive burns, which vary in severity depending on the concentration of the specific acid and the duration of contact. A unique characteristic of HF is the ability of the fluoride ion to penetrate deeply into tissue. This penetration leads to damage that is much more severe than the initial corrosive burn. Fluoride ions bind with calcium and magnesium to form insoluble salts which produce cell death and necrosis as cellular metabolism is disrupted. The resulting hypocalcemia causes an extracellular potassium shift, with the hyperkalemia then causing nerve stimulation and extreme pain. Serious systemic toxicity has developed upon exposure to HF, regardless of the route of the exposure.9 In summary, HF exposures result in biphasic injury — dehydration and coagulation necrosis — penetration of tissue by fluoride ion scavenging for cations.2,10,11

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Dermal exposure

Hydrofluoric acid burns are most commonly seen on the fingers. The initial presentation can vary from mild redness with severe pain to blistering second and third degree burns. The blisters may become filled with a cheese-like necrotic tissue that may progress to ulcerations, full thickness tissue loss and even the loss of fingers. HF rapidly penetrates the skin and enters the systemic circulation causing hypocalcemia, hyperkalemia, hypoxia and tremor. The severe pain may be due to the hypocalcemia causing a potassium shift and nerve stimulation. The lower the concentration of the HF acid, the more the onset of pain is delayed.4,9,12

Dermal exposure to hydrofluoric acid causes extensive tissue damage, unlike that which results from exposure to any other inorganic acid.23 Hydrofluoric acid produces tissue injury by two mechanisms.15 As the acid comes into contact with the skin, the fluoride ion dissociates from the hydrogen ion. The hydrogen ion causes coagulation of surface tissue, which eventually appears as a grayish white area surrounded by erythema.16 Fluoride ions freely penetrate the skin and continue into deeper tissues, causing cellular death and liquefaction necrosis of soft tissue.22,15 Neutralization of fluoride ions occurs when fluoride complexes with calcium and other divalent cations in the tissues, forming an insoluble salt. Unneutralized ions may penetrate to the bone, causing decalcification and bone erosion. Left untreated, hydrofluoric acid burns may increase in size and depth for days to weeks.22

Individuals with hydrofluoric acid burns have described the pain as "deep burning," "unbearable" and "excruciating."15 The temporal relationship between the acid exposure and the development of pain is concentration dependent.25 With hydrofluoric acid concentrations of less than 20 percent, pain and erythema may be delayed for up to 24 hours. The patient described in case 2 did not develop pain until the day after exposure to a 5-10 percent hydrofluoric acid concentration. At concentrations of 20-50 percent, pain will generally begin within one-eight hours. Immediate pain and tissue destruction occur with hydrofluoric acid concentrations of greater than 50 percent, as was seen in the patient described in case 1.

Immediate treatment is required for the patient with dermal exposure to hydrofluoric acid, in order to limit the depth and extent of tissue damage.23 As initial emergency measures, the victim's clothing should be removed without contaminating unexposed body areas or other individuals.16 The contaminated area should be irrigated with copious amounts of water for at least fifteen minutes. Patients with burns due to hydrofluoric acid should be referred to an emergency department where thorough decontamination and electrolyte and ECG monitoring are available. Burns involving greater than 50-100 cm2 are serious and require hospitalization.16

Several types of treatment for dermal burns are currently recommended. These include topical therapy, intradermal calcium injections and intraarterial calcium infusion. The rationale for the use of topical preparations is to apply a divalent cation that will bind to form a insoluble salt, thus limiting percutaneous penetration of the fluoride ion.15 Calcium gluconate gel 2.5 percent is a topical treatment for hydrofluoric acid burns. This product is not commercially available in the United States, but may be prepared by mixing calcium gluconate powder and a water soluble gel such as K-Y Jelly. Treatment consists of rubbing the gel into the burned area four to six times a day for three to four days.16

Other topical treatments include the use of quaternary ammonium compounds and magnesium oxide/magnesium sulfate paste. One topical therapy is the immersion of the exposed area in an iced solution of a quaternery ammonium compound such as 0.2 percent benzethonium chloride (Hyamine) or 0.13 percent benzalkonium chloride (Zephiran).23 A total of four to six hours of immersion may be necessary for complete relief of pain. Care must be taken to avoid frostbite. Magnesium oxide paste has been suggested as an alternative to calcium gluconate gel.15 Bracken et al. compared the use of 0.13 percent benzalkonium chloride solution, 2.5 percent calcium gluconate gel and 30 percent magnesium sulfate/6 percent magnesium oxide paste to a control (water) for treating dermal burns induced by 70 percent hydrofluoric acid.26 In this study, calcium gluconate gel was the only agent effective in limiting the extent of the burn. However, others have found the quaternary ammonium compounds to be effective and practical for the treatment of hydrofluoric acid burns in the industrial setting.22, 23 The Poison Control Center's current recommendation is to apply 2.5 percent calcium gluconate gel topically to all burned areas until the patient is symptom free.

Intradermal calcium injections are required for burns that do not respond to topical therapy, for extensive burns or when treatment delay has occurred.23,16 A 27 to 30 gauge needle is used to inject a 10 percent calcium gluconate solution into the burn.22 No greater than 0.5 ml. of solution should be injected per cm2, in order to avoid pressure necrosis.24 Injections should be extended 0.5 cm. beyond the affected area. Pain relief is generally considered the endpoint of treatment; therefore, most physicians will avoid the use of local anesthetics.23 Short acting general anesthetics or regional nerve blocks are sometimes used during treatment. Both patients described in cases 1 and 2 were treated with intradermal calcium gluconate injections and were pain free after treatment.

Successful treatment of hydrofluoric acid burns of the fingers with intraarterial infusions of calcium salts has been reported.15 A 1.66 percent solution of calcium gluconate or calcium chloride was infused slowly into the radial or brachial artery over four hours. The patients was retreated if pain returned within four hours after the end of the infusion. This method of treatment assures adequate delivery of calcium to all affected areas of the fingers and avoids pressure necrosis that may develop from intradermal injections of the fingers. Furthermore, there is no need to remove the patient's nails with this route of administration, which is most beneficial with burns involving the fingers. However, intraarterial infusions may induce arterial spasm, thus reducing the blood supply to the distal extremity. Because of the potential hazards of this method of calcium administration, it is not commonly used. However, it may be considered when a patient does not respond to maximum intradermal calcium injections.23

Onset of pain and HF concentration

HF concentration (percent) Time of onset of pain
0 - 20 24 hours
20 - 50 1-8 hours
> 50 < 1 hour

The distinct characteristics of hydrofluoric acid burn include: intense pain that may be delayed in onset for hours and that, without treatment, may last for days; the formation of tough coagulated skin; tissue destruction that, without treatment, is progressive and a strong affinity for subungal tissues that have no protective stratum corneum.11,13

Current treatment of dermal HF exposures involves decontaminating the skin and detoxifying the fluoride ion by providing available cations to form insoluble salts. Copious irrigation with water should begin immediately. Time is critical due to the rapid penetration of fluoride into tissues. Immediate irrigation may be adequate for brief exposures to dilute solutions. However, as the onset of pain is delayed, most exposures to dilute solutions of HF go undetected for several hours. Consequently, penetration of deep tissues and cellular damage has already occurred by the time the pain causes the patient to seek medical attention.

Calcium can limit percutaneous penetration of the fluoride ion by promoting the formation of calcium fluoride, an insoluble salt. Calcium can be introduced by topical administration, local infiltration or intra-arterial perfusion.4,8,13

The topical treatment of choice is a 2.5 percent calcium gluconate gel. Applied frequently and liberally, it has proven effective in decreasing the severity of the burns. Because skin is impermeable to calcium, DMSO can be added to enhance permeability.13 When the gel is not available, it can be compounded using 3.5 grams of calcium gluconate powder and 150 mL of a water soluble lubricant.13,14 An alternative therapy is a 33 percent calcium carbonate gel compounded using 6.5 grams of calcium carbonate tablets and 20 mL. of a water soluble lubricant.3 Either gel may be secured with an occlusive dressing, such as a surgical glove.

The second method of treatment is subcutaneous infiltration achieved by injecting a 10 percent calcium gluconate solution via a 27 to 30 gauge needle with a maximum delivery of 0.5 mL. solution per cm2 of affected area.12 Some sources suggest using a 5 percent solution to decrease the amount of tissue irritation and scarring, especially on the face.13 The endpoint of the infiltration is pain relief, which is almost immediate. If the pain recurs, the procedure may be repeated. If the pain is extreme, nerve block anesthesia may be used before the infiltration; however, a valuable guide to the endpoint of therapy would be lost.

There are several disadvantages to the local infiltration of calcium, especially if the digits are involved:

The intra-arterial perfusion of calcium is primarily used when the digits are affected. While this method provides more calcium than infiltration, it is not shown to be superior. The procedure involves the identification of the arterial supply of the affected area and the insertion of an intra-arterial catheter as close as possible to the affected area. Its placement should be confirmed by an arteriogram. The calcium solution is then infused over four hours. The solution may be 10 mL. of 10 percent calcium gluconate in 40-50 mL. of 5 percent dextrose in water, which may be repeated in four hours if pain returns. An alternative therapy suggests 10 mL. of 20 percent calcium gluconate in 40 ml. of normal saline via the radial or ulnar artery, which may be repeated in 12 hours or 20 mL. of 20 percent calcium gluconate in 80 mL. of normal saline via the brachial artery, which may be repeated in 12 hours.9,10,13 This procedure will relieve pain and restore color to blanched skin, but in order to prevent necrosis, it must be performed within six hours post-exposure.13,14

Topical preparations

Commercially available: 2.5 percent calcium gluconate gel (orphan drug) -H-F Gel - LTR Pharmaceuticals - Calcium Gluconate Gel - 2.5 percent - Paddock.

Compounded in-house: to yield 2.5 percent calcium gluconate gel mix 3.5 grams calcium gluconate powder in 150 mL. of a water soluble lubricant. To yield 33 percent calcium carbonate gel mix 6.5 grams calcium carbonate (crushed tablets) in 20 mL. of a water soluble lubricant.

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Exposure by other routes

Other routes of exposure to hydrofluoric acid include ocular exposure, inhalation and ingestion of hydrofluoric acid. A unique case of accidental rectal administration of hydrofluoric acid has been described.27 Exposure by these routes also requires specialized treatment and monitoring for signs of systemic fluorosis.

Ocular exposures

Hydrofluoric acid is more damaging to the eye than any other acid due to the ability of the fluoride ion to penetrate deep into tissue. Furthermore, the severity and extent of the damage is concentration dependent. A 0.5 percent solution may produce mild conjunctival ischemia and corneal edema that resolves in about 10 days. Exposure to an 8 percent solution may produce severe ischemia and corneal edema still evident after 65 days. A 20 percent solution can produce immediate and total corneal clouding. Ocular exposures to HF are quite painful and associated with several complications, such as decreased visual acuity, perforation of the eye, uveitis, conjunctival scarring and lid deformities.19 Treatment involves immediate and copious irrigation of the eye for at least 30 minutes or until the pH of the cul de sac fluid is normal. An ophthalmic anesthetic agent should be used to ease the pain and allow for a longer irrigation.4 Only simple irrigation with water or normal saline has proven nontoxic and able to decrease corneal epithelial loss and corneal inflammation. Some sources indicate repeated irrigations may even lead to an increased frequency of corneal ulceration. A thorough ophthalmic exam must be done once the irrigation is completed.6,13

Various treatments have been proposed for hydrofluoric acid burns of the eye. Most of these have been based on treatments which are effective for hydrofluoric acid burns of the skin.28 However, because of the sensitivity of the human eye, many of these agents are too irritating to be instilled in the eye, even in a dilute form. McCulley et al. investigated the effect of water, isotonic sodium chloride, isotonic magnesium chloride, lanthanum chloride, isotonic calcium chloride, 0.2 percent benzethonium chloride (Hyamine) and 0.03 percent benzalkonium chloride (Zephiran) on the normal rabbit eye and on the rabbit eye exposed to hydrofluoric acid.6 Applications of 20 percent and 50 percent ointments of magnesium salts, as well as subconjunctival injections of 10 percent calcium gluconate were also evaluated. The majority of these agents produced severe injury in the normal rabbit eye and were excluded from further testing. The only agents that appeared to have a therapeutic effect without extending corneal ulceration and other damage produced by the hydrofluoric acid were a single 30 minute irrigation with water, isotonic sodium chloride solution and isotonic magnesium chloride solution. Therefore, these investigators recommend that only those solutions be used to irrigate the eye exposed to hydrofluoric acid. However, the Allied Chemical Company, a large supplier of hydrofluoric acid, recommends an initial irrigation with water, followed by irrigation with a 1percent calcium gluconate solution for 15 minutes to two hours depending on the severity of the burn.23 This solution was not included in the investigation by McCully and associates. The Poison Control Center only recommends irrigation with water or saline.

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Oral/ingestion exposure

Hydrofluoric acid ingestion requires immediate action. Nausea, vomiting and abdominal pain may occur before systemic toxicity becomes apparent.18 Use of Syrup of Ipecac is contraindicated because HF is extremely caustic and the onset of systemic toxicity is rapid. Dilution with milk may bind some of the fluoride. Due to the severity of systemic fluoride toxicity, cautious gastric lavage with a soft, flexible nasogastric tube should be considered up to 90 minutes post-ingestion. It may be beneficial to add 10 percent calcium gluconate to the lavage fluids, either water or normal saline, to bind the available fluoride. While this procedure may risk perforation of the esophagus or the stomach, the risk should be weighed against that of systemic toxicity.8,13 It is also essential to protect the airway and monitor for gastric hemorrhage or perforation and for signs of systemic fluorosis.

As with hydrofluoric acid exposures by other routes, the patient who has ingested hydrofluoric acid is at risk for hypocalcemia and other complications of systemic fluorosis. Therefore, careful monitoring for these complications must accompany treatment.23 Ingestion of hydrofluoric acid will cause burns of the mouth, esophagus, and stomach.23 Milk or water should be administered to the patient immediately to dilute the acid.29 The ingestion of several ounces of milk of magnesia may be beneficial, particularly with dilute concentrations of acid.23,29 The administration of sodium bicarbonate orally is contraindicated because the heat of neutralization may cause additional thermal injury. Care must be taken to avoid over dilution, as this may lead to vomiting and further tissue injury.

Emesis with Syrup of Ipecac is contraindicated. The use of gastric lavage for acid exposures is controversial. Since acids do not produce their damage immediately, treatment should be aimed toward preventing further injury. Gastric lavage following an acid exposure involves the risk of esophageal or gastric perforation, however, some authors feel that gastric lavage with a small diameter nasogastric tube is warranted to remove any acid in the stomach to prevent further damage and to prevent systemic complications.30

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Pulmonary/inhalation exposures

Inhaled HF is extremely irritating. It can produce transient coughing and choking followed by an asymptomatic period lasting from a few hours to a day or two. After the asymptomatic period there may be coughing, dyspnea, cyanosis and possibly pulmonary edema. Exposures may result in months or years of pulmonary symptoms (e.g., hoarseness, coughing) and epistaxis. However, there have been no documented long-term changes in pulmonary function. Inhalation exposures are most serious when there is an explosive release of high concentrations of hydrofluoric acid. In such cases there is the danger of rapid atelectasis, hemorrhage and death within 2.5 hours post exposure.13

Treatment for inhalation exposures include removal of the victim to fresh air and decontamination of the skin and clothing. If any respiratory signs or symptoms occur, the patient should be given humidified air or oxygen and transported to a health care facility. An initial chest X-ray and arterial blood gases should be done. Monitoring the victim for laryngeal edema, pneumonitis, pulmonary edema or hemorrhage and systemic toxicity may be necessary for up to 48 hours. Occupational toxicology texts mention the use of nebulized calcium gluconate as a first line treatment.16,17 Chemical plants employ this measure and the patient may arrive with this treatment in progress.4 In 1993, the Poison Control Center documented 12 cases in which nebulized calcium was started at the site of exposure and no patients experienced any ill effects from this therapy.18 More documentation is needed on the safety and effectiveness of this measure.

Concentrated aqueous hydrofluoric acid and anhydrous hydrofluoric acid vaporize readily at room temperature.23 Inhalation of hydrofluoric acid fumes will produce burns of the lips, oral and nasal mucosa, pharnyx, trachea, and bronchi.16,29 Edema, resulting in airway obstruction, may complicate the injury produced by the acid. Obstruction of the airway generally requires endotracheal intubation or tracheostomy.16 The patient with inhalation burns should be placed on 100% oxygen. A 2.5-3 percent solution of calcium gluconate may be administered to the patient by nebulizer with intermittent positive pressure.23,16 Pulmonary edema may develop within minutes or may be delayed up to 24 hours after exposure.21 The administration of high-dose parenteral steroids has been recommended.23 The development of bronchospasm may be controlled by bronchodilators.

Significant inhalation of hydrofluoric acid may result in systemic fluorosis and these patients should be monitored for signs and symptoms of systemic intoxication/fluorosis.

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Rectal exposure

Accidental rectal insertion of a substance containing a unknown concentration of hydrofluoric acid in a patient who was intoxicated with cocaine has been reported.27 The patient presented 36 hours after the exposure complaining of excruciating abdominal and perianal pain. Total calcium concentration on admission was 8.7 mg./dl. The patient was initially treated with subcutaneous injections of 10 percent calcium gluconate and lidocaine HCl 1 percent into the perianal area without pain relief. Total calcium concentration on day 3 and 5 was 8.2 mg./dl. and 8.6 mg./dl. respectively. Laparotomy revealed a perforation in the sigmoid colon. The delay in treatment necessitated the surgical removal of necrotic tissue and the placement of a colostomy.

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Systemic intoxication/systemic fluorosis

Any type of exposure to HF may result in systemic toxicity. Burns to body surface areas as low as 2.5 percent have been associated with systemic effects.20 The interval between the exposure and fatal consequences can be brief. Life threatening electrolyte imbalances, such as hypocalcemia, hypomagnesemia, hyponatremia, hyperkalemia and/or hyperphosphatemia, which lead to arrhythmias, especially ventricular fibrillation and asystole, can occur within 30 minutes. These imbalances are due to fluoride binding to calcium and magnesium to form insoluble salts and to fluoride inhibiting sodium and potassium ATPase. Fluoride also binds to and inhibits metal-containing enzymes, such as those involved in glycolysis. Hypovolemic or cardiogenic shock and lactic acidosis may also develop due to pulmonary and/or gastrointestinal bleeding or as the result of arrhythmias.

The treatment of significant HF exposure should include protecting the airway, establishing intravenous access and providing cardiac monitoring. Lethal arrhythmias due to electrolyte imbalances, acidosis or hypoxia may develop very quickly.13 Antiarrhythmic agents and a defibrillator should be readily available. Electrolytes should be monitored immediately and parenteral calcium and magnesium may be administered empirically in anticipation of such arrhythmias. Acidosis may be treated with sodium bicarbonate as guided by arterial blood gases and a slight alkalosis may help increase the renal clearance of fluoride.9 Hypotension may necessitate the use of volume expanders and vasopressors. Aggressive fluid replacement can aid in maintaining a high GFR for rapid elimination of fluoride. If the systemic fluoride ion concentration is elevated,13,20,21 it may be necessary to follow up for several months to rule out any chronic effects on the major organ systems. Dialysis may be considered to remove the fluoride and potassium,7,9,13 but its value has not been documented. Reported life threatening exposures have progressed so rapidly that initiation of this therapy was not possible. In any significant exposure the patient should be observed for 24-48 hours.

A fatal case of systemic fluorosis has been reported after sustaining burns involving hydrofluoric acid over 10% of body surface area.21 This patient developed hypocalcemia and ventricular arrhythmias despite aggressive calcium replacement.21 In addition, hypomagnesemia, hypoxemia and acute renal failure developed. Findings on autopsy included pulmonary edema and hemorrhage, myocardial necrosis and proteinaceous debris in the renal tubules. Frequent serum calcium determinations and continuous ECG monitoring for prolongation of the Q-T interval should be used to detect the development of hypocalcemia.23,16 The patient described in case 1 developed hypocalcemia that responded to aggressive calcium replacement. Calcium may be replaced by slow intravenous infusion of calcium gluconate.23 Other electrolyte abnormalities such as hypomagnesemia and hyperkalemia are possible. Monitoring parameters for systemic fluorosis should include electrolytes, ECG, arterial blood gas determinations, liver function tests, blood urea nitrogen, serum creatinine, and urine output.23,16

Due to its unique characteristics, any HF exposure requires prompt decontamination and treatment. Treatment begins with rapid recognition of the HF burn. Many HF exposures go unrecognized until the patient is aware of the pain. Pain is a late sign and deep tissue injuries may already be an issue when the patient seeks treatment. Timely interventions may avoid protracted injury.

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Summary

Hydrofluoric acid is an extremely dangerous chemical that is capable of producing severe tissue damage, systemic complications and even death after exposure. For this reason, hydrofluoric acid should be used only by individuals who are knowledgeable about its effects, and who employ adequate measures to prevent exposure. The patient in case 2 knew only that the substance he had spilled on his fingers contained "an acid." An exposure such as this could have been prevented by the use of protective gloves, had the patient understood the hazards associated with hydrofluoric acid use. Fortunately for this patient, treatment with intradermal calcium gluconate was successful. His injuries resolved without systemic complications or the need for further treatment. However, the patient described in case 1 developed both local tissue damage as well as systemic symptoms which required aggressive treatment with intradermal and intravenous calcium gluconate.

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References

  1. Litovitz TL, Felberg L, Soloway RA, Ford M, Geller R. 1994 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med.1995 Sep;13(5):551-97.
  2. Shewmake SW, Anderson BG. Hydrofluoric acid burns. A report of a case and review of the literature. Arch Dermatol 1979 May;115(5):593-6.
  3. Chick LR, Borah G. Calcium carbonate gel therapy for hydrofluoric acid burns of the hand. Plast Reconstr Surg 1990 Nov;86(5):935-940.
  4. MacKinnon MA. Hydrofluoric acid burns. Dermatol Clin 1988 Jan;6(1):67-74.
  5. Bentur Y, Biran I, Miller B. Evaluation of the efficacy of 1% calcium gluconate in the treatment of hydrofluoric acid (HF) eye burn. Clin Toxicol 1995;33:5:(abstract) 535.
  6. McCulley JP, Whiting DW, Petitt MG, Lauber SE. Hydrofluoric acid burns of the eye. J Occup Med 1983 Jun;25(6):447-450.
  7. Stremski ES, Grande GA, Ling LJ. Survival following hydrofluoric acid ingestion. Ann Emerg Med 1992 Nov;21(11):1396-9.
  8. Mistry DG, Wainwright DJ. Hydrofluoric acid burns. Am Fam Physician 1992 Apr;45(4):1748-1754.
  9. Bertolini JC. Hydrofluoric acid: a review of toxicity. J Emerg Med 1992 Mar-Apr;10(2):163-168.
  10. Conway EE Jr, Sockolow, R. Hydrofluoric acid burn in a child. Pediatr Emerg Care1991 Dec;7(6):345-7.
  11. Henry JA, Hla KK. Intravenous regional calcium gluconate perfusion for hydrofluoric acid burns. J Toxicol Clin Toxicol 1992;30(2): 203-7.
  12. Dibbell DG, Iverson RE, Jones W, Laub DR, Madison MS. Hydrofluoric acid burns of the hand. J Bone Joint Surg Am 1970 Jul;52(5):931-936.
  13. Caravati EM. Acute hydrofluoric acid exposure. Am J Emerg Med 1988 Mar;6(2):143-50.
  14. El Saadi SM, Hall AH, Hall PK, Riggs BS, Augenstein WL, Rumack BH. Hydrofluoric acid dermal exposure. Vet Hum Toxicol 1989 Jun;31(3):243-7.
  15. Vance MV, Curry SC, Kunkel DB, Ryan PJ, Ruggeri SB. Digital hydrofluoric acid burns: treatment with intraarterial calcium infusion. Ann Emerg Med 1986 Aug;15(8):890-6.
  16. Trevino MA, Herrmann GH, Sprout WL. Treatment of severe hydrofluoric acid exposures. J Occup Med 1983 Dec;25(12):861-3.
  17. Sullivan and Kruger:
  18. Lee DC, Wiley JF 2nd, Snyder JW 2nd. Treatment of inhalation exposure to hydrofluoric acid with nebulized calcium gluconate. J Occup Med. 1993 May;35(5):470.
  19. Grant WM. Toxicology of the Eye. Charles C Thomas, Publisher. Fourth edition, 1993;788- 790.
  20. Tepperman PB. Fatality due to acute systemic fluoride poisoning following a hydrofluoric acid skin burn. J Occup Med 1980 Oct;22(10):691-2.
  21. Mayer TG, Gross PL. Fatal systemic fluorosis due to hydrofluoric acid burns. Ann Emerg Med 1985 Feb;14(2):149-53.
  22. Browne TD. The treatment of acid skin burns. Occup Health (Lond) 1974 Jun;26(6):224-5.
  23. Allied Chemicals. Hydrofluoric acid exposure. Recommended medical treatment.
  24. White JW Jr. Hydrofluoric acid burns. Cutis 1984 Sep;34(3):241-4.
  25. Stencel JR, Tobin JS. Hydrofluoric acid burn: latent period was key factor. Am Ind Hyg Assoc J 1987 Jul;48(7):A451-452.
  26. Bracken WM, Cuppage F, McLaury RL, Kirwin C, Klaassen CD. Comparative effectiveness of topical treatments for hydrofluoric acid burns. J Occup Med 1985 Oct;27(10):733-9.
  27. Foster DE, Barone JA. Rectal hydrofluoric acid exposure. Clin Pharm 1989 Jul;8(7):516-8.
  28. Hatai JK, Weber JN, Doizaki K. Hydrofluoric acid burns of the eye: report of possible delayed toxicity. J Toxicol-Cut Ocular Toxicol 1986;5:179-184.
  29. Brunelli(ed.). Hydrofluoric acid. Tox Talks (Blue Ridge Poison Center) 1988;1(2).
  30. Penner GE. Acid Ingestion: toxicology and treatment. Ann Emerg Med 1980 Jul;9(7):374-9.

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