Hydrofluoric acid burn

S K Leung 梁時勁， D V K Chao 周偉強

HK Pract 2002;24:541-545

Summary

Hydrofluoric acid is widely used in many industrial setting and its diluted form is also used as household and commercial rust removers. It is a dangerous substance that can cause severe cutaneous burns as well as possible systemic and lethal toxicity with the unique characteristic of delayed presentation. The severity and onset of symptoms after hydrofluoric acid depend on the concentration, duration of exposure, and area of exposure (body surface area). Treatment modality of hydrofluoric acid burn includes decontamination, topical therapy, local infiltrative therapy, intravenous and intra-arterial infusion administration of calcium. Every health care professional should be aware of the characteristic delayed presentation and also the possible systemic toxicity of this problem.

摘要

氫氟酸廣泛用於各種工業場所，稀釋後還用做家庭和工業除劑。這是一種危險物質，能引起嚴重的局部或全身皮膚燒傷，還可能導致致命的遲發性全身性中毒。中毒症狀出現的時間和嚴重性取決於其濃度、接觸時間和接觸的體表面積。氫氟酸中毒的處理 方法包括清除毒物、局部治療、局部滲透療法、靜脈和動脈鈣劑輸液治療。每個醫務人員都應了解其遲發性中毒的特點以及發生全身性中毒的可能。

Introduction

Hydrofluoric acid is known to be one of the most caustic and corrosive inorganic acids. It is widely used in many industrial settings including microcircuit manufacturing, control of fermentation in breweries, glass etching, petrochemical manufacturing processes, catalysts of organic acids and refrigerant. In its diluted form, it is a good agent for removing rust stains from fabrics and thus used as household and commercial rust removers.¹ According to the American Association of Poison Control Centres National Collection System, there were 1366 exposures to hydrofluoric acid in year 2000, among them, 1354 cases were accidental, and 1 case died.²

Despite its widespread usage, many people including some health care professionals are not aware that hydrofluoric acid is a dangerous substance that can cause severe cutaneous burns as well as possible systemic and lethal toxicity. Tepperman reported as little as 2.5% body surface area burn from 70% hydrofluoric acid resulted in death.³

This article highlights some unique features of hydrofluoric acid and the treatment regimens for hydrofluoric acid burn.

Pathophysiology

Hydrofluoric acid (HF) is a watery colourless to green liquid with an irritating odour and is soluble in water. Its anhydrous form is one of the most acidic substances known. It has a great affinity for water and will produce considerable heat as it dissolves in water. HF dissociation produces free hydrogen and fluoride ion (H⁺ and F^-). The free hydrogen ion (H⁺) produces dehydration and corrosion of tissues just like other organic acids. However, it is the free fluoride ion (F^-) that causes the unique systemic toxicity in the following ways: Firstly, it will bind with tissue cations (e.g. calcium and magnesium) and form insoluble salts. The insoluble salts precipitate within tissues and also cause hypocalcaemia, release of cellular potassium and intense stimulation of nerve endings.⁴ Secondly, it inhibits Na-K-ATPase system, which increases the release of potassium from the erythrocyte, resulting in hyperkalaemia.⁵ Thirdly, it activates tissue adenylate cyclase, which increases cyclic adenosine mono-phosphate, resulting in myocardial irritability and the potential for refractory dysrhythmias.⁶ Lastly, it also inhibits acetylcholinesterase, with resulting acetylcholine excess and causes gastrointestinal symptoms.⁵

Clinical features

Dermatological effect

Hydrofluoric acid burn can cause both local and systemic effect. For the local dermatological effect, it has a unique characteristic of delayed presentation. Due to the affinity of the fluoride ions, few free hydrogen ions exist in dilute solutions. Thus, unlike most other acid burn, it causes little or no initial pain on exposure to a dilute solution. This delay of presentation allows more time for the acid to penetrate the skin and mucous membranes, causing more severe destruction and liquefaction necrosis.⁴ It results in the characteristically excruciating pain that is usually out of proportion to the appearance of the burn. Other conditions like limb ischaemia and necrotising fasciitis can also present with limb pain without significant physical sign.

The severity and onset of symptoms after hydrofluoric acid burn depends on the concentration, duration of exposure, and area of exposure (body surface area). According to "The National Institute of Health - Division of Industrial Hygiene", hydrofluoric acid burns are classified into three classes:⁷

1. Concentration less than 20%: pain and erythema may be delayed up to 24 hours, often not reported until significant tissue damage has occurred.

2. Concentration from 20% to 50%: pain and erythema may be delayed for 8 hours, often not reported until tissue injury has occurred.

3. Concentration more than 50%: may cause immediate severe pain, erythema with apparent tissue destruction and life threatening sequelae.

Systemic effect

The systemic toxicity following hydrofluoric acid exposure involves the heart, neuromuscular junctions, central nervous system and electrolyte disturbance. It must be borne in mind that life threatening systemic toxicity can occur with minimal external tissue damage. Systemic toxicity has been reported after ingestion, inhalation and skin burn.

Hydrofluoric acid exposure can cause severe hypocalcaemia, hypomagnesaemia, hyperkalaemia and metabolic acidosis. Cardiotoxic effects including prolonged QT interval (associated with hypocalcaemia), cardiac dysrhythmias and even cardiac arrest have been reported. It was postulated it is the hypomagnesaemia, hypocalcaemia and hyperkalaemia that lead to myocardial irritability and refractory arrhythmias. The cardiotoxicity may also be due to the direct toxic effect of the fluoride ions on the myocardium.⁸ The neuromuscular effects include seizure due to hypocalcaemia and direct toxic effect of fluoride ions to the central nervous system. Physical evidence of hypocalcaemia such as tetany and Trousseau and Chvostek signs are often absent.⁴ Hydrofluoric acid burn may also cause decalcification and corrosion of the bone beneath the area of a severe dermal burn.

Patients thought to be at high risk for systemic hypocalcaemia are those with more than 1 per cent body surface area exposure to >50% solution, or those with >5% body surface area exposure to any concentration of solution, or inhalation of a >60% solution.⁹

Treatment

Topical therapy, local infiltrative therapy, intravenous and intra-arterial infusion of calcium have all been used to treat hydrofluoric acid burn. The concentration of acid, time and duration of exposure, and the possibility of systemic toxicity should determine the choice of treatment.¹⁰

Dermal decontamination

The most important thing for any chemical burn is to remove all exposed clothing in order to limit the duration of exposure. The same applies to hydrofluoric acid burn. The exposed area should be irrigated with copious amounts of water or crystalloid solution for at least 30 minutes.⁵ Remember to take necessary precautions to prevent secondary exposure to health care providers during the procedure.

Topical treatment

Topical calcium gel is an effective primary treatment after decontamination of hydrofluoric acid burn. A 2.5% calcium gluconate gel can be made by mixing 3.5 gram of calcium gluconate with 5 ounces of a water soluble lubricant such as K-Y jelly.¹¹ The gel is massaged into the affected area after water irrigation to relieve the pain and the treatment is repeated at least every 4 hours. Surgical gloves filed with gel are useful for hand burns.¹⁰ The relief of pain is a useful indicator to the treatment efficacy. If the pain persists, more aggressive therapy is indicated.

Besides calcium gluconate gel, magnesium chloride and quaternary ammonium salts can also be used as topical therapy. However, studies found no significant advantage when compared to calcium gluconate gel.^12,13

Infusion therapy

If both topical and infiltration treatment fail, infusion therapy is the choice of treatment. The therapy can be intravenous or intra-arterial.

(1) Intravenous calcium infusion

Ten millilitres of 10% calcium gluconate solution diluted with 30 to 40mL of 5% dextrose solution is infused via an intravenous cannula, which is placed on the dorsum of affected hand. Ischaemia is maintained for 25 minutes by inflating the sphygmomanometer to 100mm Hg and then the pressure is gradually lowered over 3 to 5 minutes.¹⁵ The maximum amount of injection should be 15mL of 10% calcium gluconate.¹⁶ It is considered successful if the pain is relieved during the hour following treatment. If not so, intra-arterial infusion should be considered.

(2) Arterial calcium infusion

Intra-arterial therapy is considered when intravenous therapy cannot relieve the pain. It is also considered if the burn is extensive, if it involves the palmar surface of the hand or more than one digit, or if the removal of more than one nail is necessary.¹⁷ The intra-arterial catheter is placed in either the brachial, radial, or ulnar artery in close proximity to the site of the burn. 10mL of 10% calcium gluconate in 40mL saline is infused over 4 hours via the radial or ulnar artery (if brachial artery is used, 20mL of 20% is infused in 80mL saline instead).¹⁸ Digital subtraction arteriography may be used to confirm catheter placement. If the pain persists or recurs within 4 hours, another dose can be given after 4 hours. It can be repeated until the patient is pain free for more than 4 hours.¹⁹

Intra-arterial therapy can deliver calcium more evenly. It also has the advantage of providing a larger amount of calcium without increasing the tissue pressure and compromising circulation in swollen tissues.¹⁹

Fingernail removal

The issue of nail removal when periungual tissues are involved is a controversial one. Nail removal is probably not necessary if the concentration is <10%. For more concentrated solution, the nailplate can be split, lifted or totally removed to facilitate decontamination and calcium infiltration therapy.²⁰ The intra-arterial therapy can prevent the removal of nail.

Surgical treatment

For patients with extensive burn damage over a small surface area or refractory hypocalcaemia, immediate excision of the affected skin may be indicated.²¹ Also, debridement or excision of necrotic tissue can allow better topical infiltration.

Systemic toxicity

For patients with extensive injury, it is necessary to monitor the ECG continuously and check serial calcium, magnesium and potassium levels. They should be managed in the hospital under close monitoring. As soon as any ECG or clinical signs of hypocalcaemia are discovered, aggressive treatment with intravenous calcium should be started while awaiting the serum calcium levels. Since fluoride is excreted mainly through the kidneys, it is important to maintain a good urine flow. Haemodialysis or cation exchange resins may be needed for severe cases.⁴

Conclusion

Hydrofluoric acid has the potential to cause significant injury due to the unique toxicity of the dissociated fluoride ion. Calcium therapy (either topical or infusion) is the mainstay of the treatment plan. Every health care professional should be aware of the characteristic delayed presentation and also the possible systemic toxicity of this problem.

Moreover, hydrofluoric acid is widely used in both industrial and domestic setting. As family physicians, we have the responsibility to promote safety at work and in the home. This can be achieved through patient education on occupational and domestic safety measures. We can also educate those at risk patients on the acute management of accidental burns. After all, prevention is the best treatment.