eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Fluoride

Geofrey Nochimson, MD, Consulting Staff, Department of Emergency Medicine, Sentara Careplex Hospital

Updated: Dec 2, 2008

Introduction

Background

Fluoride toxicity is characterized by a variety of signs and symptoms. Poisoning most commonly occurs following ingestion (accidental or intentional) of fluoride-containing products. Symptom onset usually occurs within minutes of exposure.

Fluoride is found in many common household products, including toothpaste (eg, sodium monofluorophosphate), vitamins, dietary supplements (eg, sodium fluoride), glass-etching or chrome-cleaning agents (eg, ammonium bifluoride), and insecticides and rodenticides (eg, sodium fluoride). Historically, most cases of fluoride toxicity have followed accidental ingestion of insecticides or rodenticides.

Pathophysiology

Fluoride has several mechanisms of toxicity. Ingested fluoride initially acts locally on the intestinal mucosa. It can form hydrofluoric acid in the stomach, which leads to GI irritation or corrosive effects. Following ingestion, the GI tract is the earliest and most commonly affected organ system.

Once absorbed, fluoride binds calcium ions and may lead to hypocalcemia. Fluoride has direct cytotoxic effects and interferes with a number of enzyme systems; it disrupts oxidative phosphorylation, glycolysis, coagulation, and neurotransmission (by binding calcium). Fluoride inhibits Na⁺/K⁺ -ATPase, which may lead to hyperkalemia by extracellular release of potassium. Fluoride inhibits acetylcholinesterase, which may be partly responsible for hypersalivation, vomiting, and diarrhea (cholinergic signs). Seizures may result from both hypomagnesemia and hypocalcemia. Severe fluoride toxicity will result in multiorgan failure. Central vasomotor depression as well as direct cardiotoxicity also may occur. Death usually results from respiratory paralysis, dysrhythmia, or cardiac failure.

Frequency

United States

In 2006, the American Association of Poison Control Centers reported 22,168 exposures involving toothpaste with fluoride.¹

Only 313 cases were actually treated in the emergency department. Moderate effects were seen in 45 cases. No cases of major adverse effects or death were reported.¹

In 2006, 1802 exposures involving multiple vitamins with fluoride were reported.¹

Only 61 cases were treated in the emergency department with no moderate or major effects noted.¹

Mortality/Morbidity

One death from ingestion of fluoride toothpaste was reported to the American Association of Poison Control Centers in 2002.

No deaths were reported in 2006.¹

• Death may result from ingesting as little as 2 g of fluoride in an adult and 16 mg/kg in children. Symptoms may appear with 3-5 mg/kg of fluoride.
• Estimated toxic dose for fluoride ingestion is 5-10 mg/kg.
• Estimated lethal dose is 5-10 g (32-64 mg/kg) in adults and 500 mg in small children.

Age

Children younger than 6 years account for the vast majority of the cases. In 2006, this age group had a total 21,064 exposures, while adults 19 years and older had only 982 exposures.¹

• Infants and children usually have accidental exposures.
• Adults usually have intentional exposures.

Clinical

History

• Determine the exact nature and time of exposure or ingestion. Query patient, bystanders, paramedics, and family members regarding specifics of exposure or ingestion.

Physical

• Gastrointestinal signs predominate
  • Hypersalivation
  • Nausea
  • Vomiting
  • Diarrhea
  • Abdominal pain
  • Dysphagia
  • Mucosal injury
• Electrolyte abnormalities
  • Hypocalcemia
  • Hypomagnesemia
  • Hyperkalemia
  • Hypoglycemia
• Neurologic effects
  • Headache
  • Tremors
  • Muscular spasm
  • Tetanic contractions
  • Hyperactive reflexes
  • Seizures
  • Muscle weakness
• Cardiovascular
  • Widening of QRS
  • Various arrhythmias
  • Shock
  • Cardiac arrest

Causes

• The most common type of exposure is ingestion of products that contain fluoride. To obtain the exact name of the product and how much was ingested is extremely important.
• Toothpaste contains 1 mg/g of fluoride as sodium monofluorophosphate. This fluoride formulation has low solubility and is generally nontoxic.
• The toxic effects following large ingestions of the following products usually are limited to GI discomfort.
  • Toothpaste
  • Oral hygiene products
  • Insecticide
  • Rodenticide
  • Dietary supplements
  • Automobile wheel-cleaning products
  • Glass-etching products

Differential Diagnoses

Workup

Laboratory Studies

The following studies may be indicated for suspected fluoride toxicity:

• Serum electrolytes
  • Hyperkalemia
  • Hypocalcemia
  • Hypomagnesemia
  • Hypoglycemia
• Electrocardiogram and cardiac monitoring
  • Effects of hyperkalemia (peaked T waves, widened QRS, bradycardia, atrioventricular [AV] nodal blockade)
  • Effects of hypocalcemia (prolonged corrected QT interval [QTc])
• Serum and urine fluoride levels are not available for ED evaluation.
• Perform a Dextrostix evaluation (fingerstick) on all patients with seizure and altered mental status because of the risk for hypoglycemia with systemic fluoride toxicity.

Treatment

Prehospital Care

Place patients with a known significant ingestion of fluoride on a cardiac monitor and initiate an IV line. Administer calcium IV to patients who present with cardiac dysrhythmias.

Emergency Department Care

• Provide cardiac monitoring.
• Hypocalcemia may be detected.
• Perform gastric aspiration and lavage. Small-bore nasogastric tube aspiration, followed by lavage, is recommended because of the potential severity of this ingestion and the ineffective absorption of fluoride by activated charcoal. Lavage with milk or a solution containing calcium or magnesium hydroxide (eg, milk of magnesia) is theoretically attractive but has not been proven beneficial. Some recommend lavaging with 1-5% calcium chloride solution to bind fluoride in the stomach.
• Gastric aspiration and lavage are most effective when instituted within 1 hour of ingestion.
• Administer milk, calcium carbonate, and aluminum- and magnesium-based antacids (eg, hydroxides) to bind fluoride.
• Activated charcoal is not helpful. Fluoride does not bind to charcoal. Activated charcoal still is recommended for those with intentional ingestions when a polysubstance overdose is possible.
• Correct calcium deficiencies with IV calcium chloride.

Consultations

• Consult a toxicologist or poison control center for acute management recommendations.
• Psychiatric consultation is necessary after medical clearance.

Medication

Goals of therapy are to reduce toxicity and prevent complications.

Electrolytes

Calcium chloride is administered to correct hypocalcemia that may result from fluoride poisoning. Calcium chloride provides 3 times more calcium than calcium gluconate on an equal-volume basis and is preferred (despite greater tissue toxicity if extravasation occurs).

Calcium chloride

Manages underlying hypocalcemic effects caused by fluoride poisoning.

Dosing

Adult

Initial dose: 1-2 g (1-2 ampules) IV slow push of 10% calcium chloride solution (10 mL each); repeat doses to obtain desired serum calcium level; for severe poisoning, may need to give multiple grams for the first several hours

Pediatric

20-25 mg/kg IV push of calcium chloride; repeat as necessary; may need massive doses with severe poisoning

Interactions

Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate

Contraindications

Ventricular fibrillation not associated with hyperkalemia; digitalis toxicity, hypercalcemia, renal insufficiency, cardiac disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure

Calcium gluconate (Kalcinate)

Moderates nerve and muscle performance and facilitates normal cardiac function. For systemic hypocalcemia, agent can be given IV initially, and then calcium levels can be maintained with high calcium diet. Some patients will require oral calcium supplementation. For topical pain, agent can be applied as a water-soluble gel mixture.

Dosing

Adult

May apply 2.5-5% calcium gluconate to affected area; repeat as often as required for pain control; if not available commercially, prepare as a simple 3:1 (for 2.5%) or 1:1 (for 5%) dilution of a 10% IV solution in a water-soluble surgical gel or similar sterile base

Pediatric

Apply as in adults

Interactions

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels; interactions likely not significant for calcium administered via topical route

Contraindications

Renal calculi, hypercalcemia, hypophosphatemia, renal or cardiac disease, and digitalis toxicity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia; monitor serum calcium when calcium gluconate is administered parenterally

Follow-up

Further Inpatient Care

Further inpatient care for those with fluoride ingestion include the following:

• Correct electrolyte abnormalities, especially hyperkalemia and hypocalcemia.
• Hemodialysis is used for critically ill patients that are refractory to all other forms of treatment.
• Cardiac arrhythmias are difficult to treat because they do not respond to lidocaine, cardioversion, or defibrillation.

Deterrence/Prevention

• Keep all dangerous household products out of reach of small children.

Prognosis

• Patients may be discharged if asymptomatic and ingestion is less than 3 mg/kg by accurate history.
• If a patient presents with persistent signs and symptoms, admit to a monitored bed.
• Monitor and watch patients in the ED for 6 hours before possible discharge.
• Delayed clinical presentation of significant exposures is quite common.

Patient Education

• For excellent patient education resources, visit eMedicine's Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Poisoning and Poison Proofing Your Home.

Miscellaneous

Medicolegal Pitfalls

• Failure to appreciate potential severity of this exposure

References

1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol (Phila). Dec 2007;45(8):815-917. [Medline]. [Full Text].

2. Augenstein WL, Spoerke DG, Kulig KW, et al. Fluoride ingestion in children: a review of 87 cases. Pediatrics. Nov 1991;88(5):907-12. [Medline].

3. Eichler HG, Lenz K, Fuhrmann M, Hruby K. Accidental ingestion of NaF tablets by children--report of a poison control center and one case. Int J Clin Pharmacol Ther Toxicol. Jul 1982;20(7):334-8. [Medline].

4. Gessner BD, Beller M, Middaugh JP, Whitford GM. Acute fluoride poisoning from a public water system. N Engl J Med. Jan 13 1994;330(2):95-9. [Medline].

5. Kao WF, Deng JF, Chiang SC. A simple, safe, and efficient way to treat severe fluoride poisoning--oral calcium or magnesium. J Toxicol Clin Toxicol. 2004;42(1):33-40. [Medline].

6. Klasaer AE, Scalzo AJ, Blume C, et al. Marked hypocalcemia and ventricular fibrillation in two pediatric patients exposed to a fluoride-containing wheel cleaner. Ann Emerg Med. Dec 1996;28(6):713-8. [Medline].

7. McIvor ME. Acute fluoride toxicity. Pathophysiology and management. Drug Saf. Mar-Apr 1990;5(2):79-85. [Medline].

8. Schneir A, Clark RF, Kene M, Betten D. Systemic fluoride poisoning and death from inhalational exposure to sulfuryl fluoride. Clin Toxicol (Phila). Jun 16 2008;1-5. [Medline].

9. Shulman JD, Wells LM. Acute fluoride toxicity from ingesting home-use dental products in children, birth to 6 years of age. J Public Health Dent. Summer 1997;57(3):150-8. [Medline].

10. Vance M. Fluoride poisoning. In: The Clinical Process of Emergency Medicine. Vol 1. 1991:507-9.

Keywords

fluoride poisoning, fluoride toxicity, fluoride ingestion, toothpaste, sodium monofluorophosphate, dietary supplement, sodium fluoride, glass-etching agent, chrome-cleaning agent, ammonium bifluoride, insecticide, rodenticide 

Contributor Information and Disclosures

Author

Geofrey Nochimson, MD, Consulting Staff, Department of Emergency Medicine, Sentara Careplex Hospital
Geofrey Nochimson, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

David C Lee, MD, Research Director, Department of Emergency Medicine, Assistant Professor, North Shore University Hospital and New York University Medical School
David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Michael J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center
Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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