Hydrofluoric Acid Exposure

Hydrofluoric acid (HF) is a weak acid that penetrates tissue as the undissociated molecule, then dissociates to release fluoride ions that bind calcium and magnesium, forming insoluble salts. This causes deep liquefactive necrosis, hypocalcaemia, hypomagnesaemia, hyperkalaemia and cardiac arrhythmias. Sources are glass etching, rust removal, aluminium brightening, semiconductor manufacture, petroleum refining, and household wheel and rust cleaners.

The severity depends on concentration and area. Concentrations over 50 percent cause immediate pain and visible burns; concentrations of 20 to 50 percent cause pain after 1 to 8 hours; concentrations below 20 percent can cause pain after up to 24 hours.

Exposure of more than 1 percent of body surface area to concentrated HF, or any ingestion or inhalation, may be lethal because systemic fluoride toxicity can cause cardiac arrest even with small burns.

Early, aggressive calcium treatment prevents deep necrosis, and early death is from ventricular dysrhythmia.

• Dermal: severe, disproportionate, throbbing pain, often delayed by hours for dilute solutions; erythema, blanching, blistering, grey white necrotic areas, subungual injury.
• Ocular: pain, conjunctival injection, corneal opacification and ulceration, perforation.
• Inhalation: cough, wheeze, stridor, haemoptysis, pulmonary oedema, laryngospasm.
• Ingestion: oropharyngeal and oesophageal burns, vomiting, haematemesis, abdominal pain, haemodynamic collapse.
• Systemic: tetany, carpopedal spasm, paraesthesia, weakness, QT prolongation, torsades, ventricular fibrillation, hypotension.
• Red flags: pain out of proportion, burns over more than 1 percent body surface area, ingestion, inhalation, QTc over 500 ms.

• Diagnosis is clinical: contact history and pain out of proportion to visible burn.
• Serum ionised or total calcium (hypocalcaemia is the key marker; ionised calcium below 1.1 mmol/L), magnesium (below 0.7 mmol/L), potassium (hyperkalaemia from cell necrosis), and fluoride (not available urgently).
• Continuous ECG monitoring: prolonged QTc, peaked T waves, ventricular ectopy; repeat ECG every 2 hours initially.
• Arterial blood gas for acidosis; renal and liver function for fluoride toxicity.
• Eye: fluorescein staining, pH, slit lamp examination.
• Chest radiograph and spirometry for inhalation.
• Exclude other corrosive acids and alkalis, and thermal burns.

• Remove clothing and jewellery; irrigate skin with running water for at least 5 minutes (not longer if calcium gel is quickly available), and then apply calcium.
• Topical: calcium gluconate 2.5 percent gel (2.5 g in 100 g water soluble lubricating jelly) applied thickly with gloves, massage and reapply every 15 minutes until pain stops, usually for 30 to 60 minutes. If gel is not available, mix 3.5 g calcium gluconate (35 mL of 10 percent solution) with 150 mL of water soluble lubricant.
• Persistent pain after 30 to 60 minutes: infiltrate 10 percent calcium gluconate subcutaneously, 0.5 mL per square centimetre of affected skin, using a 30 gauge needle; do not use calcium chloride (causes tissue necrosis); avoid infiltrating fingers beyond 0.5 mL to avoid vascular compromise. For digit burns or deep or hand burns: regional intra arterial calcium gluconate 10 mL of 10 percent in 40 mL of 5 percent glucose infused over 4 hours via a radial or brachial arterial line, repeated if pain returns.
• Eyes: irrigate with normal saline for 30 minutes or longer using a Morgan lens; calcium gluconate 1 percent eye drops can be given, but do not use calcium gel in eyes; urgent ophthalmology review.
• Inhalation: humidified oxygen, nebulised calcium gluconate 2.5 percent (1.5 mL of 10 percent calcium gluconate in 4.5 mL normal saline) every 4 hours until symptoms resolve, salbutamol 2.5 to 5 mg nebulised as needed.
• Systemic toxicity, or burns over 1 percent body surface area, ingestion, or inhalation: intravenous calcium gluconate 10 percent, 10 to 20 mL (children 0.5 mL/kg) over 10 minutes with ECG monitoring, repeated to restore normal ionised calcium and QTc; then infusion of 10 percent calcium gluconate 50 to 100 mL in 500 mL of 5 percent glucose over 4 to 6 hours; large amounts (over 200 mL of calcium gluconate in 24 hours) may be needed.
• Magnesium sulfate 2 g (8 mmol) intravenously over 20 minutes if magnesium is under 0.7 mmol/L, then repeat as indicated.
• Hyperkalaemia: avoid suxamethonium; treat with calcium, insulin 10 units with 25 g glucose, and salbutamol 10 mg nebulised.
• Ingestion: give milk or calcium carbonate antacids 2 g orally; do not induce vomiting; endoscopy within 12 to 24 hours.
• Surgery: debridement or excision of necrotic tissue after resuscitation, and for nail bed burns; analgesia with intravenous morphine 0.05 to 0.1 mg/kg every 4 hours as needed.
• Monitoring: admit for at least 24 hours when concentration is over 20 percent, there is ingestion or inhalation, or burns exceed 1 percent body surface area; monitor ECG, calcium, magnesium and potassium every 2 hours initially.
• Prevention: protective gloves, face shield, and calcium gluconate gel at each workplace using HF.