Hydrofluoric acid (HF) is commonly used in numerous industrial processes, including oil refining, silicon and glass etching, refrigerant production, fluoropolymer production, and aluminum metal production. HF is also used as a brick and stone cleaner, rust remover, and wheel cleaner. Although most HF exposure is occupational, some products containing HF are available for retail purchase, and nonoccupational exposure does occur.
HF is a weak acid (pKa = 3.17) in dilute aqueous solution and exists primarily in the non-ionized form. Compared with strong acids that exist primarily in the ionized form, HF in dilute solutions is better able to penetrate the skin barrier and diffuse into local soft tissues, where it causes injury. Strong acids cause only direct caustic injury (coagulative necrosis, which typically spares the underlying soft tissues), but HF causes caustic skin injury due to its acidity and also injures underlying soft-tissue due to penetration of the fluoride ion.
In aqueous intracellular and extracellular spaces, fluoride complexes with divalent cations (calcium, magnesium), forming insoluble calcium fluoride and magnesium fluoride. Formation of these insoluble salts promotes the release of more fluoride ion from HF (per Le Chatelier’s principle). The removal of calcium and magnesium from solution results in local hypocalcemia Hypocalcemia Hypocalcemia is a total serum calcium concentration 8.8 mg/dL ( 2.20 mmol/L) in the presence of normal plasma protein concentrations or a serum ionized calcium concentration 4.7 mg/dL ( 1.17... read more and hypomagnesemia Hypomagnesemia Hypomagnesemia is serum magnesium concentration 1.8 mg/dL ( 0.70 mmol/L). Causes include inadequate magnesium intake and absorption or increased excretion due to hypercalcemia or drugs such... read more , which can cause cellular dysfunction and cell death. With sufficient exposure, systemic hypocalcemia and hypomagnesemia may occur, resulting in cardiac arrhythmias Overview of Arrhythmias The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial... read more . In addition, the fluoride ion itself may be arrhythmogenic.
Time to symptom-onset from time of exposure varies and is inversely related to the concentration of HF. Exposure to concentrated preparations (> 50% HF) results in immediate pain and tissue damage due to the direct caustic effect on the skin or mucous membranes. This effect is partly due to a marked increase in the acidity of HF at high concentrations and HF homoassociation resulting in an increase in disassociated protons. Conversely, exposure to dilute preparations (< 20% HF) may not result in pain or clinical findings for several hours after the exposure because cellular dysfunction and death caused by local hypocalcemia and hypomagnesemia take time to develop.
HF exposure may be dermal, ocular, oral, or inhalational. The most common route of occupational exposure to HF is dermal.
Symptoms and Signs of Hydrofluoric Acid Exposure
Symptoms and signs of hydrofluoric acid exposure vary depending on the route of exposure.
Pain is typically the first symptom to manifest after dermal exposure and precedes signs of chemical burns, such as erythema (1st degree), edema and bullae formation (2nd degree), or gray-white discoloration (3rd degree). Pain is often more severe than expected based on apparent dermal involvement. If the fingers and nail beds are burned, the nails may remain intact, and pain may be severe despite apparent absent or minimal involvement of the nails and skin.
Oral occupational exposure to HF is less common but may occur when aqueous solution containing HF is stored in unmarked containers (eg, water bottles). Nonoccupational oral HF exposure may result from attempts at self-harm or exploratory ingestion by young children.
Ingestion of dilute HF solution may result in oropharyngeal erythema and edema and gastrointestinal irritation; ingestion of a small volume may be asymptomatic. Ingestion of concentrated HF solution results in hemorrhagic gastritis and pulmonary toxicity similar to inhalational exposure.
Inhalational exposure to HF most commonly results in upper airway and chest pain (described as burning), cough, and shortness of breath. Patients may also report nausea, vomiting, and headache and a burning sensation in skin exposed to HF vapor. Time to symptom-onset is inversely proportional to the airborne concentration of HF. Pharyngeal erythema and edema may be present, as may wheezing, rales, and respiratory distress. With more severe inhalational exposure, patients may develop hemorrhagic alveolitis with hemoptysis Hemoptysis Hemoptysis is coughing up of blood from the respiratory tract. Massive hemoptysis is production of ≥ 600 mL of blood (about a full kidney basin’s worth) within 24 hours. Most of the lung’s blood... read more or acute hypoxemic respiratory failure Acute Hypoxemic Respiratory Failure (AHRF, ARDS) Acute hypoxemic respiratory failure is defined as severe hypoxemia (PaO2 (See also Overview of Mechanical Ventilation.) Airspace filling in acute hypoxemic respiratory failure (AHRF) may result... read more (adult respiratory distress syndrome [ARDS]), which may be fatal.
Dermal, oral, or inhalational HF exposure may result in systemic fluoride toxicity (ocular exposure has not been implicated in systemic toxicity). Onset of systemic toxicity is more rapid after oral HF exposure because systemic absorption is more rapid after oral exposure than dermal exposure. Dermal exposure to concentrated HF solution may result in systemic fluoride toxicity even when the body surface area involved is small.
Systemic fluoride toxicity is marked by hypocalcemia Hypocalcemia Hypocalcemia is a total serum calcium concentration 8.8 mg/dL ( 2.20 mmol/L) in the presence of normal plasma protein concentrations or a serum ionized calcium concentration 4.7 mg/dL ( 1.17... read more , hypomagnesemia Hypomagnesemia Hypomagnesemia is serum magnesium concentration 1.8 mg/dL ( 0.70 mmol/L). Causes include inadequate magnesium intake and absorption or increased excretion due to hypercalcemia or drugs such... read more , and impaired cardiac contractility. Hyperkalemia Hyperkalemia Hyperkalemia is a serum potassium concentration > 5.5 mEq/L (> 5.5 mmol/L), usually resulting from decreased renal potassium excretion or abnormal movement of potassium out of cells. There are... read more may also occur. Cardiac arrhythmias including polymorphic ventricular tachycardia (torsades de pointes), ventricular fibrillation, and asystole may occur. Coagulopathy may result from hypocalcemia.
Ocular exposure to HF may result from a splash injury involving an aqueous solution or from gaseous HF. Mild (more dilute) exposure may cause eye pain, conjunctival injection, and chemosis and may not manifest for hours after the exposure. If the exposure is more concentrated, onset of symptoms is more rapid; corneal coagulative necrosis may occur, and the globe may rupture.
Diagnosis of Hydrofluoric Acid Exposure
Diagnosis of problems due to hydrofluoric acid exposure begins with a thorough history and physical examination. Physicians should obtain information about potential exposure in the last 24 hours, including route and duration of exposure, concentration of HF, other chemicals in the formulation, and use of personal protective equipment (PPE).
There is no specific test for HF poisoning; however, hypocalcemia (ideally measured as ionized calcium), hyperkalemia, hypomagnesemia, and elevated serum fluoride (if available) may suggest that systemic exposure has occurred. Except for the most minor burns, patients are usually admitted to the hospital for monitoring for systemic toxicity and for any indicated treatments.
Pulmonary function testing is not necessary to do immediately but, if done, may detect a restrictive lung disease pattern Restrictive disorders Airflow and lung volume measurements can be used to differentiate obstructive from restrictive pulmonary disorders, to characterize severity, and to measure responses to therapy. Measurements... read more .
If pulmonary edema is suspected, a chest x-ray and other appropriate testing (eg, pulse oximetry) are done. If the fingers are burned, x-rays are taken promptly to check for bone damage.
If systemic exposure is possible, electrocardiography is done to check for the effects of hypocalcemia Diagnosis (eg, a prolonged QT interval) and hyperkalemia ECG Hypokalemia is serum potassium concentration 3.5 mEq/L ( 3.5 mmol/L) caused by a deficit in total body potassium stores or abnormal movement of potassium into cells. The most common cause is... read more (peaked T waves, widening of the QRS interval, flattening of the P wave, sine wave pattern).
Endoscopy should generally be done for oral ingestion, and consultation with gastroenterology and/or otorhinolaryngology should be obtained.
Prognosis for Hydrofluoric Acid Exposure
Prognosis depends on the route of hydrofluoric acid exposure.
Prognosis after mild dermal HF exposure is good if the patient is promptly evaluated and treated. As with other chemical burns, symptoms typically resolve over a period of days to weeks, depending on the severity of the burn.
Patients who have ingested a dilute HF solution may develop reversible oropharyngeal or gastrointestinal (GI) irritation or may remain asymptomatic and have a benign prognosis. Ingestion of concentrated HF solution may result in fatal GI hemorrhage or systemic fluoride toxicity, which may be fatal. If patients with severe GI burns survive, long-term sequelae including strictures may develop.
Patients with systemic fluoride toxicity are at high risk of cardiac arrhythmia and hypotension.
Prognosis after inhalational exposure depends on the intensity and chronicity of exposure. If inhalational exposure is mild to moderate, symptoms may resolve spontaneously over a period of hours to days. More intense exposures may result in persistent upper airway irritation (reactive upper airways dysfunction syndrome [RUDS]) or pulmonary irritation (reactive airways dysfunction syndrome [RADS]) that persists for months to years. Chronic occupational HF exposure may result in a bronchial hyperreactivity syndrome called "potroom worker’s asthma". Serial pulmonary function tests may be used to monitor RADS and bronchial hyperreactivity in workers exposed to HF.
If ocular exposure is mild, conjunctival irritation and chemosis (which typically occurs) resolves over a period of several days, and no long-term sequelae are anticipated. If exposure is more severe, corneal injury or sloughing may result in chronic conjunctivitis, corneal opacification or vascularization, glaucoma, or keratitis sicca.
Treatment of Hydrofluoric Acid Exposure
Various treatments depending on type of exposure
Prompt decontamination if applicable
Calcium and magnesium salts
Immediate decontamination should be done, including removing contaminated clothing or work gear and flushing the affected areas with water for 15 minutes. After decontamination, 2.5% calcium gluconate or calcium carbonate gel should be applied to the affected area and covered with an occlusive nonadherent dressing (for finger injuries, gel can be placed in a surgical glove put on the patient's hand). Application of the soluble calcium salt to areas exposed to HF results in complexation of calcium with fluoride, which forms soluble calcium fluoride. This reaction results in a fluoride concentration gradient that favors the diffusion of HF out of the body and into the gel.
Topical calcium is applied until pain is relieved.
If pain persists despite application of topical calcium or if the patient was exposed to concentrated HF solutions, calcium gluconate may be given by subcutaneous or intra-arterial injection. Calcium chloride should not be given by these routes because tissue necrosis is a risk.
For subcutaneous injection, 0.5 mL of 5% calcium gluconate per square centimeter can be infiltrated. Iatrogenic compartment syndrome is a risk in small tissue compartments (eg, the hand). If those areas are affected, risks and benefits of calcium infiltration should be weighed. No more than 0.5 mL of solution should be injected per digit.
For intra-arterial administration, 50 mL of 2% calcium gluconate can be infused into the artery perfusing the affected area over a 4-hour period. Risks of arterial cannulation should be considered when deciding whether to do this procedure.
All but the most minor or superficial exposures require transfer to a burn center for possible surgical intervention, including skin grafting, debridement of necrotic tissue, fasciotomy, and amputation.
Gastric emptying with an orogastric (OG) or nasogastric (NG) tube should be done as soon as possible after an oral HF exposure. Gastric emptying is unlikely to be beneficial if >1 hour has elapsed since the ingestion. The same OG or NG tube may be used to deliver calcium or magnesium salt to the GI tract, although evidence of its benefit is limited. As with other caustic ingestions, activated charcoal is contraindicated.
A GI specialist should be consulted about possible endoscopy.
Patients with systemic fluoride toxicity should be admitted to an intensive care unit for cardiac monitoring, serial electrocardiography and, if depressed cardiac contractility is suspected, echocardiography. Serial measurement of calcium, magnesium, potassium, and phosphate levels is done and treated as required.
Treatment of systemic fluoride toxicity includes calcium and magnesium salts, given IV, to replenish calcium and magnesium lost from complexation with fluoride. IV fluids, and vasopressor and/or inotropic support are given for depressed cardiac contractility. Magnesium sulfate may be given as a loading dose of 4 to 6 g IV over 60 minutes, followed by 2 to 4 g/hour infusion. Patients should be monitored for hypotension and respiratory depression. Calcium gluconate may be given as a loading dose of 6 g IV over 60 minutes, followed by infusion of 0.5 mEq/kg/hour. If a central venous catheter is available, calcium chloride may be used instead of calcium gluconate at a loading dose of 2 g, followed by infusion of 0.5 mEq/kg/hour. If hypocalcemia or hypomagnesemia persist or recur, loading doses of both magnesium and calcium may be repeated. Amount of supplementary electrolytes to administer should be guided by real time blood testing.
Sodium bicarbonate may be given IV for acidemia, although few studies address its efficacy.
Fluoride ions are eliminated by hemodialysis. Hemodialysis should be considered for patients with systemic toxicity, although such patients may be too clinically unstable to have the procedure.
Inhalational exposure may be treated with nebulized calcium gluconate; 2.5% and 5% calcium gluconate can be given as intermittent or continuous treatments. Patients with wheezing and bronchospasm can also be treated with a nebulized beta agonist (eg, albuterol), nebulized ipratropium, and oral or IV corticosteroids. Patients with ARDS-like symptoms may be treated with standard interventions for ARDS Treatment Acute hypoxemic respiratory failure is defined as severe hypoxemia (PaO2 (See also Overview of Mechanical Ventilation.) Airspace filling in acute hypoxemic respiratory failure (AHRF) may result... read more , including positive pressure ventilation, use of high positive end-expiratory pressure, and proning.
Prompt decontamination is most important. Irrigation at a workplace eyewash station should be followed by continued irrigation en route to the hospital. Continued irrigation How To Cleanse, Irrigate, Debride, and Dress Wounds Wound hygiene (eg, cleansing, irrigation, and debridement), including thorough examination of the wound and surrounding tissues, promotes uncomplicated healing of traumatic skin wounds and is... read more in an emergency department may be done using normal saline or sterile water applied to the affected eye or eyes using a Morgan lens. Irrigation with at least 2 to 3 liters of fluid is recommended. Ocular irrigation with calcium-containing solutions, which are irritating and may create corneal injury, should not be used. Consultation with an ophthalmologist should be obtained in the acute care setting, and ophthalmology follow-up should be arranged.
Prevention of Hydrofluoric Acid Exposure
Various organizations (eg, Occupational Safety and Health Administration [OSHA], National Institute for Occupational Safety and Health [NIOSH]) provide recommendations for minimizing the risk of exposure to hydrofluoric acid. These recommendations include
Providing workers with information about the hazards specific to HF before they handle it
Limiting the time workers are exposed to HF
Requiring workers to wear a properly functioning fume hood and appropriate personal protective equipment (PPE), such as goggles, disposable gloves, and acid-resistant apron
Requiring workers to wear long pants, long sleeves, and closed-toe shoes
Equipping the work area with a safety shower and eye wash station
Having calcium gluconate available for skin treatment
Storing HF properly
Providing all areas where HF is used with spill-response equipment (eg, dry magnesium sulfate, spill control pads, sodium bicarbonate solution)
Dermal, oral, inhalational, and ocular exposures to hydrofluoric acid may occur in the workplace.
Symptoms begin immediately after exposure to concentrated HF formulations but may be delayed by several hours after exposure to dilute HF formulations.
Surface burns and the complexation of calcium or magnesium with the fluoride ion in HF results in local hypocalcemia and hypomagnesemia, which cause cellular dysfunction and death.
Treat dermal burns and severe pain due to dermal exposure with dermal, subcutaneous, or intra-arterial calcium; transfer almost all patients with burns to a burn center.
For oral exposures, use an orogastric or nasogastric tube to empty the stomach as soon as possible; ingestion of concentrated HF solution is toxic as well as caustic and can be fatal.
Treat patients with inhalational exposure with nebulized calcium gluconate; treat patients who have had a more concentrated exposure and who have ARDS-like symptoms with the usual treatments for ARDS.
Admit patients with systemic fluoride toxicity (which may be due to dermal, oral, or inhalational exposure) to an intensive care unit for serial monitoring and support, and treat them with IV magnesium and calcium and, if needed, vasopressors.
After ocular exposure, irrigate the eyes immediately, continuously, and thoroughly and arrange consultation and follow-up with an ophthalmologist.
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