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Hydrofluoric Acid

Hydrofluoric Acid
3.Oct.2022-Expires: 7 days - Do not archive



Hydrofluoric Acid 


Inorganic Acid


Intervention Level


Medical assessment in an emergency department is recommended for:
- Dermal exposure to any concentration of hydrofluoric acid where calcium gluconate gel has not been given as a first aid procedure, even if asymptomatic
- Dermal exposure to any solution of greater than 6% hydrofluoric acid, regardless of whether calcium gluconate gel has been administered
- Any patient developing pain, erythema, or swelling at the exposure site at any time following dermal exposure to hydrofluoric acid


Medical assessment in an emergency department is recommended for:
- Any hydrofluoric acid ingestion


Medical assessment in an emergency department is recommended for:
- Symptomatic cases


Medical assessment in an emergency department is recommended for:
- All eye exposures to hydrofluoric acid liquids
- All symptomatic eye exposures to hydrofluoric acid vapors

Observation Period

Observation at Home

The patient can be observed at home in the event of:
Dermal exposures to:
- Solutions of less than 6% hydrofluoric acid, involving very small areas of skin, but where the area has been decontaminated and calcium gluconate gel has been given as a first aid treatment
- Where the exposure is via inhalation, serious symptoms are unlikely to develop and medical assessment is unlikely to be required
However, if the following symptoms develop the patient should seek medical attention:
Mild cough
Throat/nasal irritation
Dyspnea or breathing difficulty

Medical Observation

If medical observation is required the patient should be monitored for 12 hours following exposure for the onset or worsening of symptoms.[1]
If the patient is asymptomatic and has a normal ECG and serum calcium concentration (without calcium administration), they can be:[1]
- Discharged into the care of a reliable observer, or
- Referred for psychological assessment (if the exposure was intentional)

Admission Criteria

Admission to an intensive care environment is recommended:
Those developing hypocalcemia following any route of exposure.
- Any patient who requires intraarterial infusion of calcium
- Patients with a significant percentage of body surface area affected
- Any patient ingesting a concentrated hydrofluroic acid solution (>50%)
- Patients suffering:
Breathing difficulty
Pulmonary signs



The personal protection and safety of the attending personnel must be considered at all times, during the treatment of patients exposed to hydrofluoric acid.
The treatment of all hydrofluoric acid exposures focuses on preventing systemic absorption, evaluating the degree of systemic toxicity and rapidly correcting electrolyte abnormalities. Following systemically toxic doses of hydrofluoric acid, the initial emergency stabilization involves monitoring for and correcting hypocalcemia, which may lead to severe hypotension, seizures or dysrhythmias, if left untreated. Blood pressure and ECG should also be closely monitored and IV access secured immediately.
Skin exposures should be decontaminated firstly with water and then treated with calcium gluconate gel. Although gastrointestinal decontamination is not recommended, patients can be given water, or preferably milk, to rinse the mouth out.
The mainstay of the supportive care focuses on the prevention and treatment of hypocalcemia. Monitor serum electrolyte levels (particularly calcium and magnesium) for evidence of hypocalcemia and hypomagnesemia. Patients should also be observed for symptoms secondary to the onset of hypocalcemia, i.e. hypotension, seizures or dysrhythmias. Administer IV calcium gluconate to replace calcium, if plasma levels are depleted or in the presence of secondary effects. Correct any hypomagnesemia and/or hyperkalemia using standard procedures. Hyperkalemia and metabolic acidosis may be severe enough to warrant urgent hemodialysis, if not responsive to standard treatment measures.
All ocular exposures are potentially severe and will require immediate copious irrigation with water or normal saline for at least 30 minutes. Application of ice packs during any transportation to medical facilities has been suggested. Examination with a slit-lamp microscope and fluorescein stain to assess the injury is recommended for all exposures. The patient should always be referred to an ophthalmologist.
Emergency Stabilization
Enhanced Elimination
Supportive Care
Fluid and electrolytes


Ensure Adequate Cardiopulmonary Function

Ensure the airway is protected if compromised (intubation may be necessary).
Establish secure intravenous access in ingestions, inhalational exposures, and large dermal exposures (>3% body surface area).

Severe Hypocalcemia

Severe hypotension, seizures or dysrhythmias indicate severe hypocalcemia. Whilst it is preferable to document reduced serum ionized calcium, in the presence of these effects intravenous calcium is warranted even without serum test results.[2]

Emergency Monitoring

Blood pressure
Serum ionized calcium
Serum electrolytes including:



Decontamination is not recommended.
Immediate rinsing out of the mouth with water, or preferably milk, may benefit. Oral fluids should be avoided due to the risk of vomiting, with attendant risks of aspiration and re-exposure of the esophagus to this corrosive substance.
Activated charcoal is not indicated as it does not adequately adsorb this substance and will impair visibility if endoscopy is required.
Nasogastric aspiration, gastric lavage, and whole bowel irrigation are contraindicated. No benefit has been demonstrated from these procedures, and there is significant risk of perforation during gastric intubation.
Emesis is contraindicated due to both risks of re-exposure of the esophagus to the corrosive substance and/or aspiration, and the increased intraluminal pressure produced by emesis.


Irrigate Skin Immediately

Remove contaminated clothing or jewelry. Flush the affected area with water as soon as possible. Continue to irrigate until all of the contaminant is removed. Further treatment will then be required to address signs and symptoms.
The personal protection and safety of the attending personnel must be considered at all times during the treatment of patients.

Apply Calcium Gluconate Gel

A 2.5% calcium gluconate gel massage should be performed. Continue massaging into the burned skin for a minimum of 30 minutes and for as long as the pain persists. For digital exposures place the gel in a latex glove and put this on the affected hand.
If no gel is available, mix calcium gluconate (10 mL of 10%) with KY jelly (10 g) and apply, or use a calcium or magnesium solution for soaking the affected area.
Sometimes pain persists for up to four hours.

Remove Blisters

All blisters should be removed and the underlying tissues cleaned. The blister fluid is generally contaminated and it is contraindicated to leave the blisters intact.
Removal of nails SHOULD BE AVOIDED if periungual or ungual tissues are involved. Pain at these sites will usually respond well to either intra-arterial or regional intravenous calcium therapy.
Any excision of affected tissue should be avoided.


Immediate copious irrigation with water or normal saline for at least 30 minutes is required. Application of ice packs during any transportation to medical facilities has been suggested. Examination with fluorescein and slit-lamp to assess the injury is recommended for all exposures.
The patient should always be referred to an ophthalmologist.
Further injury may be reduced with application of a 1% solution of calcium gluconate in saline.[3] This is used to wash the eye for a further 5 to 10 minutes (after the initial immediate irrigation), and thereafter as drops every 2 to 3 hours for 48 to 72 hours, or as long as clinically indicated.
The personal protection and safety of the attending personnel must be considered at all times during the treatment of patients.


Remove the patient from the exposure. If respiratory symptoms such as shortness of breath are present, administer oxygen and provide additional support if necessary.


Calcium Gluconate

Calcium gluconate is the antidote for hypocalcemia caused by systemic toxicity and for the treatment of localized dermal burns. Historically other agents including iced quaternary ammonium compounds, magnesium salts, and calcium carbonate have been used, but these were less effective than calcium gluconate in the treatment of burns.
Hexafluorine is a commercial product designed for hydrofluoric acid decontamination. While it has been claimed in case reports and an ex vivo study published by the manufacturer to be beneficial in reducing burns and systemic toxicity,[4][5][6][7] animal studies have not shown a benefit over flushing with water and application of calcium gluconate in either reducing local burns or systemic toxicity.[8][9] Further research is required before advocating its use.
Intravenous administration of calcium, to prevent the depletion of plasma calcium or to replace it, is one of the mainstays of management. Administration should be considered if a systemically toxic dose is suspected or if symptoms of hypocalcemia occur. When given IV through a peripheral venous catheter, the gluconate salt must be used.

It is better to document serum ionized calcium level prior to treatment. However, if severe hypocalcemia is suspected and seizures, tetany, life-threatening hypotension or cardiac arrhythmia are present, intravenous calcium is warranted without these results.[2] Untreated hypomagnesemia will render hypocalcemia refractory to therapy.[10]


Calcium gluconate is indicated for hydrofluoric acid toxicity following:
- Hydrofluoric acid ingestions
- A burn area greater than 2.5% of body surface area
- Development of symptoms indicative of hypocalcemia
- Pain persisting more than 30 minutes after commencing continuous calcium gluconate gel massage
- Any exposure to high concentration solutions greater than 20%

Dose and Administration

Initial Calcium Dose
Calcium gluconate dose:
0.6 to 1.0 mL/kg of 10% solution by slow IV push[11]
10 to 30 mL of 10% solution diluted in 150 mL 5% dextrose administered IV over 10 minutes[2]
The effect of IV calcium will subside after about 2 hours and maintenance infusion may be required.
Maintenance Calcium Infusion
Calcium gluconate maintenance infusion dose:
Dose yet to be established
Add 100 mL 10% calcium gluconate to 900 mL of 5% dextrose and infuse at 50 mL/h (47 mg calcium ion). Titrate infusion rate against effect - minimum infusion time is 4 to 6 h.[12]
Rate should be based on serial (2 to 6 hourly) ionized calcium measurements and resolution of manifestations of hypocalcemia. ECG monitoring is recommended. Importantly any existing abnormalities in magnesium, potassium, and pH must be corrected simultaneously. Untreated hypomagnesemia will make hypocalcemia refractory to therapy.[10]


Patients receiving digoxin or digoxin-like compounds should be monitored very closely as calcium may precipitate potentially fatal digitalis toxicity.[12][13]
Use of calcium gluconate is preferable to calcium chloride, which is an acidifying salt.[14]
Note: calcium gluconate (9% calcium ion) contains one third the calcium content of calcium chloride (27% calcium ion).

Adverse Effects

If calcium salts are administered too rapidly, bradycardia, vasodilation, hypotension, dysrhythmias and cardiac arrest may occur.

Calcium chloride can be irritating to veins and may cause tissue destruction if extravasation occurs. It should be administered through central venous access.

Dermal Exposures

Following dermal exposures to digits specialized approaches to the administration of calcium gluconate should be considered. This is due to the increased success that these specialized approaches offer at enhancing the distribution of calcium gluconate to the affected tissues. If symptoms of hypocalcemia and/or if severe hypotension, seizures or arrhythmia exist, IV calcium gluconate should be administered.
The primarily treatment should be with regional intravenous calcium gluconate administered as a Bier’s block; if this fails intra-arterial calcium gluconate should be used.


The onset and severity of symptoms is concentration dependent. Hydrofluoric acid is moderately corrosive by ingestion, inhalation, skin and eye exposure, and can cause systemic toxicity via all routes. Unlike more corrosive acids, it may not cause immediate localized pain and tissue damage when individuals are exposed to concentrations less than 50%. Local symptoms may be delayed and should be monitored for following exposures to low concentration formulations.
Systemic symptoms of hypocalcemia, hypomagnesemia, hyperkalemia, pulmonary edema, metabolic acidosis, ventricular dysrhythmias and death may occur following ingestion or large dermal exposures.[15][16]

Onset/Duration of Symptoms

The onset and severity of symptoms may vary depending on the concentration and the route of exposure. Following exposure to low concentration formulations localized symptoms may be delayed, while onset of local and systemic symptoms may be rapid following high concentration exposures. Pain may be delayed and may not be proportional to the size of the visible injury. This may result in delayed triage or medical diagnosis on presentation to hospital. Without appropriate treatment, burns can continue to increase in surface area for 4 to 7 days.[17]

Hydrofluoric acid primarily produces tissue damage by the dissociation of fluoride ions into the tissues. This is a relatively slow process, compared to the corrosive action of other acids. Hypocalcemia, hypomagnesemia and acidosis may occur within 1 to 2 hours following large dermal exposures or ingestions of hydrofluoric acid.

Routes of Exposure

Hydrofluoric acid is moderately corrosive by ingestion, inhalation, skin and eye exposure. Systemic toxicity can occur from all routes of exposure, but is most likely following ingestions or significant dermal exposures to concentrated formulations.

Following any exposure to hydrofluoric acid systemic toxicity is possible and may be delayed; a cautious approach must be applied in all cases.

Severity of Poisoning

Following an exposure to hydrofluoric acid, mild symptoms are associated with local effects, while moderate or severe symptoms are an indication of systemic toxicity or an exposure to a concentrated formulation.
Mild Hydrofluoric Acid ToxicityModerate Hydrofluoric Acid ToxicitySevere Hydrofluoric Acid Toxicity
Decalcification of the bone
Cardiac dysrhythmias
Metabolic acidosis
Hepatic damage
Cardiac arrest


Chronic ingestion or inhalation can lead to fluorosis.[18]

Weight loss
Discoloration of teeth


[1] Murray L, Daly F, Little M, Cadogan M. Toxicology handbook. 2nd ed. Sydney, Australia: Churchill Livingstone; 2011. p. 240-3
[2] Reber PM, Heath H 3rd. Hypocalcemic emergencies. Med Clin North Am 1995 Jan; 79 (1): 93-106.
[3] Trevino MA, Herrmann GH, Sprout WL. Further evaluation of hydrofluoric acid burns of the eye: Author’s response [letter]. J Occup Med 1984 Jul; 26 (7): 483, 486.
[4] Yoshimura CA, Mathieu L, Hall AH, Monteiro MG, de Almeida DM. Seventy per cent hydrofluoric acid burns: delayed decontamination with hexafluorine® and treatment with calcium gluconate. J Burn Care Res 2011 Jul-Aug; 32 (4): e149-54.
[5] Soderberg K, Kuusinen P, Mathieu L, Hall AH. An improved method for emergent decontamination of ocular and dermal hydrofluoric acid splashes. Vet Hum Toxicol 2004 Aug; 46 (4): 216-8.
[6] Mathieu L, Nehles J, Blomet J, Hall AH. Efficacy of hexafluorine for emergent decontamination of hydrofluoric acid eye and skin splashes. Vet Hum Toxicol 2001 Oct; 43 (5): 263-5.
[7] Burgher F, Mathieu L, Lati E, Gasser P, Peno-Mazzarino L, Blomet J, Hall AH, Maibach HI. Part 2. Comparison of emergency washing solutions in 70% hydrofluoric acid-burned human skin in an established ex vivo explants model. Cutan Ocul Toxicol 2011 Jun; 30 (2): 108-15.
[8] Hojer J, Personne M, Hulten P, Ludwigs U. Topical treatments for hydrofluoric acid burns: a blind controlled experimental study. J Toxicol Clin Toxicol 2002; 40 (7): 861-6.
[9] Hultén P, Höjer J, Ludwigs U, Janson A. Hexafluorine vs. standard decontamination to reduce systemic toxicity after dermal exposure to hydrofluoric acid. J Toxicol Clin Toxicol 2004; 42 (4): 355-61.
[10] Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 8: advanced challenges in resuscitation: section 1: life-threatening electrolyte abnormalities. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000 Aug 22; 102 (8 Suppl): I217-22.
[11] Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 10: pediatric advanced life support. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000 Aug 22; 102 (8 Suppl): I291-342.
[12] Bushinsky DA, Monk RD. Electrolyte quintet: Calcium. Lancet 1998 Jul 25; 352 (9124): 306-11.
[13] Erdmann E, Reuschel-Janetschek E. Calcium for resuscitation? Br J Anaesth 1991 Aug; 67 (2): 178-84.
[14] Gilman AG, Rall TW, Nies AS, Taylor P, editors. Goodman and Gilman’s the pharmacological basis of therapeutics. 8th ed. New York: Pergamon Press; 1990. p. 1523.
[15] Stremski ES, Grande GA, Ling LJ. Survival following hydrofluoric acid ingestion. Ann Emerg Med 1992 Nov; 21 (11): 1396-9.
[16] Klasaer AE, Scalzo AJ, Blume C, Johnson P, Thompson MW. Marked hypocalcemia and ventricular fibrillation in two pediatric patients exposed to a fluoride-containing wheel cleaner. Ann Emerg Med 1996 Dec; 28 (6): 713-8.
[17] Seamens CM, Seger DL, Meredith T. Hydrofluoric acid. In: Ford MD, Delaney KA, Ling LJ, Erickson T. Clinical toxicology. Philadelphia (PA): WB Saunders; 2001. p. 1019-26.
[18] Budavari S, editor. The Merck index. 12th ed. Whitehouse Station (NJ): Merck & Co; 1996. p. 820.

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