CASE REPORT

hydrofluoric acid, ingestion

Survival Following Hydrofluoric Acid Ingestion From the Department of Emergency Medicine, Hennepin County Medical Center, * and Hennepin Regional Poison Center,t Minneapolis, Minnesota.

Ernest S Stremski, MD *t

Gregory A Grande, RPh, CSPIt Louis J Ling, MD, FACEP, ABMT *t

Received for publication November 22, 1991. Revision received March 2, 1992. Accepted for publication April 24, 1992. Presented at the AACT/AAPCC/ ABMT/CAPCC Annual Scientific Meeting in Toronto, Ontario, Canada, September-October 1991.

Systemic toxicity after significant dermal exposure to hydrofluoric acid includes rapid development of hypocalcemia and hyperkalemia, leading to ventricular fibrillation. Similar dysrhythmias have occurred in patients after ingestion of sodium fluoride-containing compounds. Ingestion of hydrofluoric acid could induce similar cardiac toxicity; however, reported cases of hydrofluoric acid ingestion rarely have been described, and the rapid death of these patients has not allowed verification of this hypothesis. On two separate occasions, a 70-year-old woman ingested up to 2 oz of a 8% hydrofluoric acid-containing solution. Recurrent ventricular fibrillation with concurrent hypocalcemia and hypomagnesemia complicated her first episode, whereas a more aggressive administration of calcium and magnesium may have prevented dysrhythmias in the second episode. Survival from ventricular fibrillation after hydrofluoric acid ingestion has not been reported previously and suggests a role for aggressive empiric calcium and magnesium replacement. [Stremski ES, Grande GA, Ling LJ: Survival following hydrofluoric acid ingestion. Ann Emerg/WedNovember 1992;21:1396-1399.] INTRODUCTION Industrial-strength hydrofluoric acid compounds (more than 20% hydrofluoride) are used in petroleum processing, glass and computer chip etching, and fluoridated hydrocarbon production. However, products containing hydrofluoric acid are also available for consumer use. These include rustremoval agents in solution or as gels (6% to 8% hydrofluoride) and aluminum and chrome cleaning solutions (2% to 8% hydrofluoride). Systemic absorption of fluoride anion from hydrofluoric acid leads to complexation of positive-charged cations as calcium and magnesium. *,2 Tiffs may occur in the setting of hydrofluoric acid burns 3-5 or ingestion 6 and result in the development of serum hypocalcemia (less than 0.62 mmol/L; normal, 2.23 to 2.57 mmol/L 7) or hypomagnesemia3, 4 (less than 0.65 mmol/L; normal, 0.65 to 1.05 mmol/LT). Fluoride intoxication also may result in the extracellular release of erythrocyte potassium, leading to serum hyperkalemia 8 (more than 6.5 mmol/L). 9-11 Hypocalcemia, hypomagnesemia, and/or hyperkalemia after significant fluoride absorption leading to refractory ventricular fibrillation is the suspected cause of death.

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CASE

REPORT

A 70-year-old woman was witnessed by her husband to d r i n k two swallows of a rust-removal agent containing 8% hydrofluoric acid. She immediately complained of mouth and throat pain, which was followed by spontaneous emesis. Twenty minutes after this ingestion, she had a blood pressure of 102/64 mm Hg; pulse, 140; and respirations, 24. She was alert and complaining of throat and midsternal chest pain yet in no distress. She a r r i v e d in the emergency d e p a r t m e n t approximately 40 minutes after ingestion. Her pulse was 152 and irregular and blood pressure was 81/49 mm Hg. She had no further episodes of emesis, n o r did she demonstrate drooling or oral pharyngeal burns. Breath sounds were equal bilaterally, and there was no stridor. Her abdomen was soft and nontender. She remained alert and oriented without exhibiting tetany. The initial 12-lead ECG revealed atrial fibrillation with nonspecific ST segment depressions and a corrected QT interval of 0.382 second. Oxygen was started, an IV line was established, and blood was obtained for l a b o r a t o r y studies. Oral fluids were not administered because caustic gastrointestinal i n j u r y was suspected due to the nature of the agent and the patient's initial complaints. One hour after ingestion, the patient's total serum calcium level was 6.6 mg/dL (1.65 mmol/L; normal, 2.23 to 2.57 mmol/L). Twenty milliliters of 10% calcium gluconate was administered intravenously (100 m g = 9.3 mEq calcium p e r ampule), and an additional 200 mg (18.6 mEq) of calcium gluconate was added to the existing 1 L of IV lactated Ringer's. A star repeat of the total serum calcium was 1.57 mmo]/L. The patient's blood pressure decreased to 62/40 mm Hg as she remained in atrial fibrillation with a ventricular rate of more than 140. After attempted cardioversion, she deteriorated into ventricular fibrillation. She was intubated and received an additional 200 mg (18.6 mEq) calcium plus 1 mg epinephrine and 100 mg lidocaine IV. The patient then was defZbrillated successfully to a normal sinus rhythm with pulse of 103 and blood pressure of 113/60 mm Hg. At this point, her serum potassium was 4.0 rmnol/L (normal, 3.3 to 4.9 mmol/LT), total serum calcium was 1.57 mmol/L, and magnesium was 0.45 mmol/L. The corrected QT interval now measured 0.440 second. In the next two hours, after the patient's admission to the ICU, she was defibrillated 22 times for ventricular fibrillation. During this period, an additional 500 mg (46.5 mEq) calcium gluconate IV and 1 g magnesium sulfate IV (8 mEq magnesium) were administered. She was maintained on a lidocaine drip at a rate of 4 rag/hr. Total serum calcium increased to 2.05 retool/L, and serum magnesium increased to 0.55 mmol/L. The patient had received 30 mEq KC1, and sermn potassium was 3.3 mmol/L. During the next two hours, she required defibrillation seven times and received an additional 100 mg (9.3 mEq) calcium gluconate, 8 mEq magnesium, and 30 mEq KC1. Seven hours after ingestion, she had a

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normal sinus rhythm with pulse of 98 and blood pressure of 138/70 mm Hg. The corrected QT interval was 0.392 second. At this point, the patient's total serum calcium was 2.24 mmol/L, magnesium was 0.85 mmol/L, and potassium was 4.3 mmo]/L. The patient then remained hemodynamically stable and was extnbated successfully. She had no cardiac history, and myocardial infarction was ruled out by serial ECG and cardiac enzymes. Endoscopy was performed approximately 48 hours after ingestion. The examination revealed esophageal erythema and edema without localized burns or perforations. There was diffuse gastritis and a normal duodenum. Significant gastrointestinal bleeding did not develop. She then was transferred to an inpatient psychiatry service. On the day after her discharge, the patient was witnessed again by her husband to have ingested two swallows of the same rust-removal agent. She had immediate emesis and complaints of mouth and throat pain. On presentation to the ED she was alert with blood pressure of 126/76 mm Hg; pulse, 80; and respirations, 24. There were no oral lesions, drooling, or stridor. Cardiac and neurological examinations were normal. The 12-lead ECG revealed a normal sinus rhythm without ST segment changes and a corrected QT interval of 0.435 second. IV administration of 9.3 mEq calcium, 8 mEq magnesium, and 75 mg lidocaine was started immediately. Serum laboratory results obtained after this revealed total serum calcium of 1.97 retool/L, magnesium of 0.80 mmo]/L, and potassium of 4.0 mmol/L. During the next seven hours, the patient received an additional 65.1 mEq calcium and 32 mEq magnesium as intermittent venous boluses. Serum potassium remained within the normal range, and there was no further decrease in total calcium or magnesium. With the exception of unifocal p r e m a t u r e ventricular contractions, no dysrhythmias developed. By eight hours after admission, total serum calcium was 2.25 mmol/L, magnesium was 1.15 retool/L, and potassium was 4.0 mmol/L. Fluoride levels were not available for either hospitalization. Repeat endoscopy revealed findings similar to those seen after the first ingestion. Neurological examination at discharge was unchanged from that at admission. DISCUSSION

Severe metabolic derangement, including hypocalcemia, 3-5,12,t3 hyperkalemia, 9-11 and hypomagnesemia, 3,a has been documented after significant fluoride exposure and absorption. A r a p i d onset of lethal dysrhythmias may occur if such abnormalities are not corrected. Although the pathophysiology of these changes is not understood fully, they most likely occur secondary to the effect of free fluoride anion. In tissue, hydrofluoric acid will dissociate into free H+ cations and F anions. 3 The binding of free F - anions to free Ca 2+ and Mg z+ forms insoluble salts and may occur at a rate that exceeds the ability to mobilize bone calcium and magnesium into serum. 12 Fluoride anion may inhibit the Na +, K+-ATPase

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enzyme of the cell membrane, leading to a massive potassium efflux. 9 Five fatal cases of ventricular fibrillation have occurred after development of 3% to 22% third-degree total body surface burns from concentrated hydrofluoric acid (more than 50%) exposure. Hypocalcemia (0.55 to 1.15 mmol/L) was present in all five eases. 3,4,9,12,13 Minimum serum calcium levels were achieved between one and 11 hours after exposure and, in some cases, occurred after initial IV calcium replacement.a,9,14 Ventricular fibrillation occurred at the time of reaching the trough serum calcium level. In two cases, hypomagnesemia also was documented during fibrillation (0.6 mmol/L for each)3, 4 (Table). Two cases of survival have been reported after the development of hypocalcemia in men b u r n e d with 60% hydrofluoric acid. Minimum total serum calcium levels of 0.875 or 1.15 mmol/L developed within two hours in patients with 3% or 22% total body surface area b u r n s , respectively. Serum magnesium of 0.65 mmol/L was r e p o r t e d for one patient. The total amount of administered calcium was 113 mEq (18.6 mEq i n t r a d e r m a l and 94.4 mEq IV) in the first patient. A total of 266.7 mEq of calcium (9.3 mEq i n t r a d e r m a l and 257.4 mEq IV) was administered to the second patient. Ventricular fibrillation did not develop in either case. 12 Manoguerra and Neuman described a 29-year-old man who developed r e s p i r a t o r y arrest and asystole within one hour of ingesting a hydrofluoric acid-containing rust-removal agent. 6 Total serum calcium at the time of death was 0.77 mmol/L despite administration of 81 mEq IV elemental calcium (CAC12).6 All r e p o r t e d ingestions of hydrofluoric acid have resulted in fatality. 15 Autopsy findings of patients who ingest hydrofluoric acid-containing products include full-thickness esophageal burns with perforation and severe hemorrhagic gastritis with gastric perforation, is This patient did not develop severe gastrointestinal burns. There may be two reasons for this. In each case, her witnessed ingestion was reported as only two swallows that were followed by immediate emesis, possibly limiting the amount of p r o d u c t in the stomach. Gastric injury, as seen in this patient, is induced more often than esophageal injury after ingestion of acidic compounds. 16 Rust-removal agents now contain 6% to 8% hydrofluoric acid, which was decreased from 10% to 12% hydrofluoride as of 1981.17 Table. Development of metabolic abnormalities after burns from concentrated hydrofluoric acid Age (yr) Adult 4 6113 199 233 6212

Burn (% Total Body % Hydrofluoric Total Serum Time after SurfaceArea) Acid Calcium(mmol/L) Exposure(hr) 3 8 7 10 22

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> 50 70 > 50 70 60

0.55 0.87 1.15 0.82 0.62

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2 3.5 6 11 t

Patients who ingest hydrofluoric acid-containing compounds require immediate interventions. Theoretically, the oral administration of milk or other calcium-containing p r e p a r a t i o n s may r e t a r d fluoride absorption. However, patients may present with symptoms compatible with severe caustic injury and manifest contraindications for oral intake. Stabilization of an airway is of p r i m a r y importance if there is clinical evidence of u p p e r airway burns or obstruction. Other life-threatening symptoms that require immediate stabilization include hypovolemic shock from gastrointestinal bleeding and cardiac dysrhythmias. Endoscopy should follow after patient stabilization. Blood should be obtained for stat determination of serum calcium, magnesium, and potassium levels. Because of the r a p i d development of hypocalcemia and hypomagnesemia, empiric IV administration of calcium and magnesium should begin. Patients also may require immediate treatment of hyperkalemia. Empiric dosing with IV calcium and magnesium after fluoride ingestion has not been studied. IV calcium (37.2 to 65.3 mEq) was administered during the first hour after severe hydrofluoric acid burns in two patients. Neither developed dysrhythmias during that time period, n In the second hospitalization of our patient, 9.3 mEq calcium (1 ampule of 10% calcium gluconate) and 8.3 mEq magnesium sulfate (1 g) were administered (along with lidocaine) during the first hour after ingestion. Unlike her first episode, in which a similar quantity of ingestion occurred, dysrhythmias did not develop. There appears to be a definite risk of further lowering of the serum calcium level despite administration of IV calcium. These patients also are at risk of hyperkalemia.8,9012 Early administration of calcium can antagonize the a b n o r m a l cardiac effects of hyperkalemia. 7 Frequent assessment of serum calcium, magnesium, and potassium levels as well as continual cardiac monitoring are necessary for optimal management of electrolyte abnormalities. Hemodialysis may be used after excessive fluoride absorption to remove fluoride anion and correct abnormal serum chemistries. 8,1° Serum fluoride levels (normal, 0.01 m m o l / L ) J although not as readily available as serum calcium, magnesium, or potassium levels, also can be useful in determining therapy. There are numerous acute life-threatening events that may occur after small ingestions of a hydrofluoric acid-containing compound. Of p r i m a r y importance is stabilization of a secure airway if there are manifestations of u p p e r airway burns and obstruction. Hypotension may result from gastrointestinal bleeding, necessitating vigorous volume resuscitation. Severe and prolonged electrolyte abnormalities may lead to refractory ventricular fibrillation. Immediate and frequent assessments of electrolytes plus continual cardiac monitoring are required. Empiric IV administration of calcium (9.3 mEq = 1 ampule calcium gluconate) and magnesium (8 mEq = 1 g magnesium sulfate) should begin. This quantity of initial administration can only be speculated by this case

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report. Antiarrhythmic agents and/or cardioversion-dcfibrillation may be necessary should dysrhythmias develop. After patient stabilization, gastrointestinal endoscopy should be performed in patients who exhibit signs of caustic injury.

2. Bracken W, Cuppage F, McLaury R, et al: Comparative effectiveness of topical treatments for hydrofluoric acid burns. J OccupMad 1985;27:79-85.

SUMMARY

3. Mayer T, Gross P: Fatal systemis fluorosis due to hydrofluoric acid burns. Ann Emerg Mad 1985;14:113-117.

A 70-year-old woman drank a rust-removal agent containing 8% hydrofluoric acid. Despite ventricular fibrillation and cardiac arrest, she made a full cardiac and neurologic recovery. She also required no surgical interventions for her degree of gastric caustic injury and subsequently was transferred to psychiatry services. The emergency physician should be aware of the hydrofluoric acid-containing products that are readily available to the consumer. While dermal injury and its management have been well described, 1 life-threatening injury may occur should these products be ingested.

REFERENCES 1. Caravati E: Acute hydrofluoric acid exposure, Ann EmergMad 1988;6:143-149.

4. Tepperman P: Fatality due to acute systemic fluoride poisoning following a hydrofluoric acid skin burn. J OccupMed1980;22:691-692. 5. Abkurah A, Moser A, Baird C, et al: Acute fluoride poisoning. JAMA 1972;222:816-817, 6. Manoguerra A, Neuman T: Fatal poisoning from acute hydrofluoric acid ingestion. Am J EmergMad 1986;4:362-363. 7. Dunagan CW, Ridner ML: Manual of Medical Therapeutics,ed 26. Boston, Little, Brown and Co, 1989, p 505-506. 8. Mclvor M, Cummings C, Mower M, et el: Sudden cardiac death from acute fluoride intoxication: The role of potassium. Ann EmergMad 1987;16:777-781. 8. Mclvor M: Belayed fatal hyperkalemia in a patient with acute fluoride intoxication. Ann EmergMad 1987;16:1t8-120. 10. Yolken R, Konecy P, McCarthy P: Acute fluoride poisoning, Pediatrics 1976;58:90-93. 11. Baltazaar R, Mower M, Reider R, et al: Acute fluoride poisoning leading to fatal hyperkalemia. Chest1980;78:660-662. 12. Grace R, Hartford C, Haith L, et al: Hydrofluoric acid induced hypocalcemia. J Trauma1988;28:1593-1596. 13. Mullett T, Zoeller T, Bingham H, et al: Fatal hydrofluoric acid cutaneous exposure with refractory ventricular fibrillation. J Bum CareRehabf11987;8:216-219. 14. Burke W, Ulrich H, Phillips R: Systemic fluoride poisoning resulting from a fluoride skin burn. J OecupMad 1973;15:39-41. 15. Menchel S, Dunn W: Hydrofluoric acid poisoning. JAm ForensMad Pathol 1984;5:245-248. 18. 6oldfrank LR, Flomenbaum NE (eds): Goldfrank's ToxicologicEmergencies,ed 4. NonNalk, Connecticut, Appleton and Lange, 1990, p 770-771. 17.Rumack BH, Spoerke DS (eds): POISONDEXInformationSystem. Denver, Micromedex, Inc (edition expires 2/28/92). Address for reprints: Ernest S Stremski, MD Children's Hospital of Wisconsin Division of Emergency Medicine MS 677 9000 West Wisconsin Avenue Milwaukee, Wisconsin 53226

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Survival following hydrofluoric acid ingestion.

Systemic toxicity after significant dermal exposure to hydrofluoric acid includes rapid development of hypocalcemia and hyperkalemia, leading to ventr...
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