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Emergency Medicine > TOXICOLOGY
Toxicity, Fluoride
Article Last Updated: Jan 8, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 10
Author: Geofrey Nochimson, MD, Consulting Staff, Department of Emergency Medicine, Sentara Careplex Hospital
Geofrey Nochimson is a member of the following medical societies: American College of Emergency Physicians
Editors: David C Lee, MD, Research Director, Department of Emergency Medicine, Assistant Professor, North Shore University Hospital and New York University Medical School; John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital; Michael J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center; 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; 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
Author and Editor Disclosure
Synonyms and related keywords:
fluoride poisoning, toothpaste, sodium monofluorophosphate, dietary supplement, sodium fluoride, glass-etching agent, chrome-cleaning agent, ammonium bifluoride, insecticide, rodenticide, fluoride toxicity, fluoride ingestion
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), 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 2004, the American Association of Poison Control Centers reported 24,180 exposures involving toothpaste with fluoride.
Only 440 cases were actually treated in the emergency department.
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 2004.
- 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 2004, this age group had a total 21,890 exposures, while adults 19 years and older had only 1213 exposures.
- Infants and children usually have accidental exposures.
- Adults usually have intentional exposures.
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
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Lab Studies
- 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.
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.
Goals of therapy are to reduce toxicity and prevent complications.
Drug Category: 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).
| Drug Name | Calcium chloride |
| Description | Manages underlying hypocalcemic effects caused by fluoride poisoning. |
| Adult Dose | 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 h |
| Pediatric Dose | 20-25 mg/kg IV push of calcium chloride; repeat as necessary; may need massive doses with severe poisoning |
| Contraindications | Ventricular fibrillation not associated with hyperkalemia; digitalis toxicity, hypercalcemia, renal insufficiency, cardiac disease |
| Interactions | Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate |
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
| Precautions | Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure |
| Drug Name | Calcium gluconate (Kalcinate) |
| Description | 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. |
| Adult Dose | 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 Dose | Apply as in adults |
| Contraindications | Renal calculi, hypercalcemia, hypophosphatemia, renal or cardiac disease, and digitalis toxicity |
| 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 |
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
| Precautions | Caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia; monitor serum calcium when calcium gluconate is administered parenterally |
Further Inpatient Care
- 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
Medical/Legal Pitfalls
- Failure to appreciate potential severity of this exposure
- 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].
- 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].
- 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].
- 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].
- 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].
- McIvor ME. Acute fluoride toxicity. Pathophysiology and management. Drug Saf. Mar-Apr 1990;5(2):79-85. [Medline].
- 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].
- Vance M. Fluoride poisoning. In: The Clinical Process of Emergency Medicine. Vol 1. 1991:507-9.
Toxicity, Fluoride excerpt Article Last Updated: Jan 8, 2007
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