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Intra-arterial infusions in the treatment of hydrofluoric acid burns
440
Burns (1985) 11,44C-443
Printedin
GreatBritain
Intra-arterial infusions in the treatment hydrofluoric acid burns
of
S. P. Pegg, S. Siu and G. Gillett Burns Unit, Royal Brisbane
Hospital,
Australia
Summary
Burns due to hydrofluoric acid are uncommon, but are severe injuries. The mode of action is discussed briefly and the routine management of these patients is outlined. The use of intra-arterial infusions of calcium gluconate is stressed, and case reports are given to support its use. INTRODUCTION
BURNS due to hydrofluoric acid are uncommon since only six patients with such injuries have been admitted during the last 1900 admissions to the Burns Unit of the Royal Brisbane Hospital. Previous epidemiological surveys (Pegg, 1972; Pegg et al., 1975) recorded no burns due to hydrofluoric acid. However, the frequency of such burns appears to be increasing especially in the petroleum industry (Heddle, 1984), and undoubtedly many are treated well in first aid stations in industry and never attend hospital. There is, however, conflict in the literature regarding the treatment of these burns, which mainly involves the use of calcium gluconate in various forms. At the 5th International Congress on Burn Injuries in Stockholm, Sweden, Koehnlein et al. (1978) reported the use of intra-arterial infusions of calcium gluconate to treat hydrofluoric acid burns of limbs. This was an exciting breakthrough in this extremely painful burn and our use of this technique with two patients fully supports the method described. Hydrofluoric acid as used in industry is available as a liquid with varying concentrations up to 70 per cent. It is used for etching glass, as the primary component of rust removing agents; as a catalyst in alkylation units in the petroleum
industry, and in many other industries such as the semi-conductor, plastic and dye industries. It is often transported by road over long distances necessitating careful precautions. The acid is a fuming corrosive liquid which boils at 20” C, giving off a white pungent, irritating vapour. It produces burns via the hydrogen ion and the fluorine ion penetrates the skin and subcutaneous tissues, destroying them until precipitated as calcium or magnesium fluoride. This can be by natural tissue Mg or Ca compounds or by those administered medically. The fluorine ion penetrates the horny layer of the skin and moves to the deeper tissues. The material may pass through the nail without altering its appearance, causing severe pain and blanching, later followed by haemorrhage. The fluorine ions produce liquefaction necrosis of the subcutaneous tissue and unless it is neutralized with the formation of the salts of calcium and/or magnesium, it will continue its destructive process and cause the loss of the affected tissue such as the distal phalanx of the finger (Fig. 1). (Blunt, 1964). Pain is intense and immediate with strong concentrations, and intense but delayed perhaps for several hours with weak solutions. The vapour is also intensely irritating to the lungs and conjunctivae, and may itself produce skin burns. Breathing strong vapour for more than a few minutes may be fatal. With weak solutions, the lung effects due to pulmonary oedema may be delayed for several hours. With skin burns, it is usually the pain that brings the patient to medical attention. On the skin surface, it may cause erythema followed by blistering, progressing to white areas of coagulation and later black necrosis. Cases of such severity as that reported by
Pegg et al.: Hydrofluoric acid burns
441
I;in. acid burns to fingers. showing marked ._ I, Hvdrotluoric _ involving the distal interphalangeal joint
Heddle (1984) are rare. The active fluorine ion binds with calcium ions, causing depletion of body calcium. It binds strongly with serum calcium rendering attempts at haemodialysis useless. There is strong evidence that fluorosis, acute or chronic, kills also by the inhibition of several metabolic enzymes (Heddle, 1984). CASE HISTORIES Case
1
A 27-year-old man presented to the Royal Brisbane Hospital in July. 1980 at 1 a.m., complaining of severe pain in his right hand. He gave a history that he had been using SO per cent hydrofluoric acid 12 h prior to presentation at the Casualty Department for cleaning the oxide off a metal boat. Whilst using the acid, he had noticed pain in his hand and this was allayed by washing with cold water. He used the acid for 1 h. Two hours later the pain had increased and was unrelieved by copious washing and local application of a barrier cream. His pain was predominantly in the palmar aspect of his hand and the nail bed of his fingers. On examination. he was in marked distress. with erythema and oedema of his right hand. The erythema extended on the palmar aspect to the level of the wrist joint with more marked involvement of his fingers and on the dorsal aspect marked involvement of his nail beds. He was treated by an intra-arterial infusion of 30 ml of IO per cent calcium gluconate given via a brachial artcry line using a pressurized giving set. The intra-arterial calcium gluconatc gave immediate relief associated with a burning sensation to his hand. He complained of come residual pain in the tips and pulp of his fingers. This was injected with IO per cent calcium gluconate subcutaneously and his nails were removed to allow
tissue necrosis into and
proper infiltration of his nail bed. This relieved all his pain and his hand was placed in soaks of a quaternary ammonium compound. He was admitted to hospital for observation; he remained pain free in hospital until 24 h later, when he again developed pain in the tips of his fingers which was relieved by subcutaneous injection of 10 per cent calcium gluconate to the 3rd and 4th fingers of his hand. He had a further episode of pain 24 h later on his right thumb tip which again was relieved by subcutaneous injection of calcium gluconate. X-ray examination of his hand on day 3 after admission showed no areas of atopic calcification. with normal bone consistency and no areas of bony erosion. He was discharged on day 4 and was followed up as an outpatient and regained complete and full recovery of his hand.
Case 2 A 25-year-old man presented at the Casualty Department of this hospital in February, 1981 at 8p.m. He had been using a 30 per cent solution of hydrofluoric acid to clean a metal boat’s hold some 6 h previously. He had noticed pain developing in his right hand some 2 h after the USC of this solution and this was not relieved by washing with water. On presentation at the hospital, he was in moderate distress with an erythema tous right hand but with no pain under his nails. he was given 30ml of IO per cent calcium gluconate via a brachial intra-arterial line and had immediate relief of his symptoms. He refused hospital admission and discharged himself, pain free, and has been lost to follow UP.
TREATMENT The what
affinity
for
determines
calcium the
and
treatment
magnesium of burns
ions
is
due
to
442
hydrofluoric acid. The rapid precipitation of fluorine ions is the primary aim with skin burns. This leads to immediate relief of pain, and the destructive action will cease. Once absorption has taken place, treatment is by systemic methods, that is, by local injection, the oral route or, as in the cases presented, the intra-arterial route to perfuse the area. In pulmonary damage, respiratory support and systemic methods are the only methods applicable. In eye injury, the tear mechanism is supported by drops to aid the protective mechanism. First Aid
As neutralization of fluorine ions is so essential, first aid is of paramount importance and is the reason why many minor cases, adequately treated, do not reach hospital (Pearcy, 1981). Skin Exposure. For skin exposure, irrigate vigorously with water, removing clothing, and preferably use a shower rather than a bath, which may spread the acid, As soon as possible after washing, vigorously for about 1 min apply calcium gluconate gel and massage the gel into the contaminated areas until the pain is relieved for at least 15 min, or medical attention is available. If the gel is not available continue washing in warm water. If more than 1 per cent of the body surface area is involved, give six calcium tablets in water by mouth. Magnesium sulphate paste can be used but calcium gluconate gel is preferable. Eye Exposure. Wash well with water for at least
10min then instil a few drops of 1 per cent calcium gluconate. Medical Treatment Skin Exposure. As pain is the indicator
of acid activity, local anaesthetic injections should not be used. As long as pain persists, calcium gluconate gel should be massaged into the affected area. If a thick necrotic coagulum has formed, this should be excised and gel massaged into the base of the wound. If the pain does not respond to this then a 10 per cent solution of calcium gluconate shoutd be injected under the burn, taking care not to inject so much that the circulation will be jeopardized. If the burn is in a suitable site, such as a limb, or hand or foot, then an intra-arterial infusion (Koehnlein et al., 1978) of 10 ml of 20 per cent calcium gluconate in 40 ml of normal saline infused over 4 h, should be considered. This can be repeated twice in 24 h. If pain recurs
Burns (1985) Vol. 11INo. 6
later, especially in burns from dilute acid then the gel, or injections may need to be repeated. If finger or toe nails are involved, they may show no change. Severe pain under the nails is an indication for removal of the nails involved, under local or general anaesthesia, and treatment with gel or injection continued. Magnesium sulphate paste can be used instead of calcium gluconate gel but generally is not as effective (Kleinert et al., 1976). In large skin burns, systemic administration of calcium and/or magnesium may be necessary (Pearcy, 1981). Calcium tablets should be given orally in water every 2 h on the way to hospital. Frequent electrolyte monitoring, or clinical signs of hypocalcaemia may indicate the need for intravenous calcium and/or magnesium. Profound hypocalcaemia may occur in the absence of clinical tetany and ECG monitoring should be instituted. Eye Exposure. Instillation of 1 per cent calcium gluconate drops may need to be repeated, with fluorescein staining to show cornea1 ulceration. An ophthalmologist should examine these patients. Inhalation injury should be suspected in all cases
due to the ready vaporization of the acid. If collapse occurs, cardio-pulmonary resuscitation will be needed and humidified oxygen support, and treatment to prevent hypocalcaemia. Delayed pulmonary oedema may occur requiring support with humidified 100 per cent oxygen and ventilation. The use of intermittent high concentrations of oxygen may prevent the onset of pulmonary oedema. PREVENTION
In areas where hydrofluoric acid is used, routines for treating these burns should be worked out, with information booklets, and water for vigorous irrigation readily available. Calcium gluconate gel (2.5 per cent), calcium gluconate eye drops (1 per cent), and calcium gluconate tablets should be readily available in the workplace, and gel should be kept in the home of vulnerable workers, in case delayed burns occur. Burns units, likely to treat such patients should be alerted as to the problems of these burns (Pearcy, 1981). DISCUSSION
Burns due to hydrofluoric acid are not common, but, when they occur, cause severe pain and
Pegg et al.: Hydrofluoric acid burns
damage. The majority are minor, but more severe injuries do occur (Heddle, 1984). The pattern of treatment at the vital first aid level, and the medical treatment are now more standardized, as given above. A forward step has been the use of intra-arterial infusions (Koehnlein et al., 1978). As in the two cases cited above, this has been a valuable adjunct, enabling calcium gluconate to be readily available for locally absorbed fluorine ions. If systemic symptoms were to occur, this would be of further help in systemic treatment. Obviously such an infusion is of use only when a large artery to the area is readily available. In the case cited by Heddle, involving the face, then this method of infusion could not be readily applied. No doubt, better methods of treatment will be developed in the future. However, we found that intra-arterial infusion of calcium gluconate gave immediate relief of pain, and cessation of the effects of hydrofluoric acid burns. CONCLUSIONS At present, the mainstay of treatment depends on prevention with worker education, rapid adequate first aid and prompt efficient medical
443
treatment. It is considered that intra-arterial fusion has a valuable place in the treatment burns due to hydrofluoric acid.
inof
REFERENCES Blunt C. P. (1964) Treatment of hydrofluoric acid skin burns by injection with calcium gluconate. Ind. Med. Surg. 33, 869. Heddle S. B. (1984) Hydrofluoric acid burns; an updating of patho-physiology and management. The Bulletin and Clinical Review of Burn Injuries 1, (3), 21.
Kleinert H. E. and Bronson J. L. (1976) Hydrofluoric acid burns of the hand. Medical Times 104, (12), 77. Koehnlein H. E.. Seitz H. D., Achinger R. et al. (1978) Abstracts of 5th International Congress on Burn Injuries, Stockholm, Sweden. Pearcy L. H. D. (1981) 6th Annual Meeting of A.N.Z.B.A., Perth, West Australia. Pegg S. P. (1972) Adult burns: a three year survey with assessment of Sulfamylon. Med. J. Am. 1, 350. Pegg S. P., Gregory J. J., Hogan P. G. et al. (1979) Epidemiological patterns of adult burn injuries. Burns 5, 326. Paper accepted 15 April 1985.
Correspondence should be addressed to: Dr S. P. Pegg. Royal Brisbane Hospital, Herston Road. Herston 4029, Queensland, Australia.
Burns (1985) 11,44C-443
Printedin
GreatBritain
Intra-arterial infusions in the treatment hydrofluoric acid burns
of
S. P. Pegg, S. Siu and G. Gillett Burns Unit, Royal Brisbane
Hospital,
Australia
Summary
Burns due to hydrofluoric acid are uncommon, but are severe injuries. The mode of action is discussed briefly and the routine management of these patients is outlined. The use of intra-arterial infusions of calcium gluconate is stressed, and case reports are given to support its use. INTRODUCTION
BURNS due to hydrofluoric acid are uncommon since only six patients with such injuries have been admitted during the last 1900 admissions to the Burns Unit of the Royal Brisbane Hospital. Previous epidemiological surveys (Pegg, 1972; Pegg et al., 1975) recorded no burns due to hydrofluoric acid. However, the frequency of such burns appears to be increasing especially in the petroleum industry (Heddle, 1984), and undoubtedly many are treated well in first aid stations in industry and never attend hospital. There is, however, conflict in the literature regarding the treatment of these burns, which mainly involves the use of calcium gluconate in various forms. At the 5th International Congress on Burn Injuries in Stockholm, Sweden, Koehnlein et al. (1978) reported the use of intra-arterial infusions of calcium gluconate to treat hydrofluoric acid burns of limbs. This was an exciting breakthrough in this extremely painful burn and our use of this technique with two patients fully supports the method described. Hydrofluoric acid as used in industry is available as a liquid with varying concentrations up to 70 per cent. It is used for etching glass, as the primary component of rust removing agents; as a catalyst in alkylation units in the petroleum
industry, and in many other industries such as the semi-conductor, plastic and dye industries. It is often transported by road over long distances necessitating careful precautions. The acid is a fuming corrosive liquid which boils at 20” C, giving off a white pungent, irritating vapour. It produces burns via the hydrogen ion and the fluorine ion penetrates the skin and subcutaneous tissues, destroying them until precipitated as calcium or magnesium fluoride. This can be by natural tissue Mg or Ca compounds or by those administered medically. The fluorine ion penetrates the horny layer of the skin and moves to the deeper tissues. The material may pass through the nail without altering its appearance, causing severe pain and blanching, later followed by haemorrhage. The fluorine ions produce liquefaction necrosis of the subcutaneous tissue and unless it is neutralized with the formation of the salts of calcium and/or magnesium, it will continue its destructive process and cause the loss of the affected tissue such as the distal phalanx of the finger (Fig. 1). (Blunt, 1964). Pain is intense and immediate with strong concentrations, and intense but delayed perhaps for several hours with weak solutions. The vapour is also intensely irritating to the lungs and conjunctivae, and may itself produce skin burns. Breathing strong vapour for more than a few minutes may be fatal. With weak solutions, the lung effects due to pulmonary oedema may be delayed for several hours. With skin burns, it is usually the pain that brings the patient to medical attention. On the skin surface, it may cause erythema followed by blistering, progressing to white areas of coagulation and later black necrosis. Cases of such severity as that reported by
Pegg et al.: Hydrofluoric acid burns
441
I;in. acid burns to fingers. showing marked ._ I, Hvdrotluoric _ involving the distal interphalangeal joint
Heddle (1984) are rare. The active fluorine ion binds with calcium ions, causing depletion of body calcium. It binds strongly with serum calcium rendering attempts at haemodialysis useless. There is strong evidence that fluorosis, acute or chronic, kills also by the inhibition of several metabolic enzymes (Heddle, 1984). CASE HISTORIES Case
1
A 27-year-old man presented to the Royal Brisbane Hospital in July. 1980 at 1 a.m., complaining of severe pain in his right hand. He gave a history that he had been using SO per cent hydrofluoric acid 12 h prior to presentation at the Casualty Department for cleaning the oxide off a metal boat. Whilst using the acid, he had noticed pain in his hand and this was allayed by washing with cold water. He used the acid for 1 h. Two hours later the pain had increased and was unrelieved by copious washing and local application of a barrier cream. His pain was predominantly in the palmar aspect of his hand and the nail bed of his fingers. On examination. he was in marked distress. with erythema and oedema of his right hand. The erythema extended on the palmar aspect to the level of the wrist joint with more marked involvement of his fingers and on the dorsal aspect marked involvement of his nail beds. He was treated by an intra-arterial infusion of 30 ml of IO per cent calcium gluconate given via a brachial artcry line using a pressurized giving set. The intra-arterial calcium gluconatc gave immediate relief associated with a burning sensation to his hand. He complained of come residual pain in the tips and pulp of his fingers. This was injected with IO per cent calcium gluconate subcutaneously and his nails were removed to allow
tissue necrosis into and
proper infiltration of his nail bed. This relieved all his pain and his hand was placed in soaks of a quaternary ammonium compound. He was admitted to hospital for observation; he remained pain free in hospital until 24 h later, when he again developed pain in the tips of his fingers which was relieved by subcutaneous injection of 10 per cent calcium gluconate to the 3rd and 4th fingers of his hand. He had a further episode of pain 24 h later on his right thumb tip which again was relieved by subcutaneous injection of calcium gluconate. X-ray examination of his hand on day 3 after admission showed no areas of atopic calcification. with normal bone consistency and no areas of bony erosion. He was discharged on day 4 and was followed up as an outpatient and regained complete and full recovery of his hand.
Case 2 A 25-year-old man presented at the Casualty Department of this hospital in February, 1981 at 8p.m. He had been using a 30 per cent solution of hydrofluoric acid to clean a metal boat’s hold some 6 h previously. He had noticed pain developing in his right hand some 2 h after the USC of this solution and this was not relieved by washing with water. On presentation at the hospital, he was in moderate distress with an erythema tous right hand but with no pain under his nails. he was given 30ml of IO per cent calcium gluconate via a brachial intra-arterial line and had immediate relief of his symptoms. He refused hospital admission and discharged himself, pain free, and has been lost to follow UP.
TREATMENT The what
affinity
for
determines
calcium the
and
treatment
magnesium of burns
ions
is
due
to
442
hydrofluoric acid. The rapid precipitation of fluorine ions is the primary aim with skin burns. This leads to immediate relief of pain, and the destructive action will cease. Once absorption has taken place, treatment is by systemic methods, that is, by local injection, the oral route or, as in the cases presented, the intra-arterial route to perfuse the area. In pulmonary damage, respiratory support and systemic methods are the only methods applicable. In eye injury, the tear mechanism is supported by drops to aid the protective mechanism. First Aid
As neutralization of fluorine ions is so essential, first aid is of paramount importance and is the reason why many minor cases, adequately treated, do not reach hospital (Pearcy, 1981). Skin Exposure. For skin exposure, irrigate vigorously with water, removing clothing, and preferably use a shower rather than a bath, which may spread the acid, As soon as possible after washing, vigorously for about 1 min apply calcium gluconate gel and massage the gel into the contaminated areas until the pain is relieved for at least 15 min, or medical attention is available. If the gel is not available continue washing in warm water. If more than 1 per cent of the body surface area is involved, give six calcium tablets in water by mouth. Magnesium sulphate paste can be used but calcium gluconate gel is preferable. Eye Exposure. Wash well with water for at least
10min then instil a few drops of 1 per cent calcium gluconate. Medical Treatment Skin Exposure. As pain is the indicator
of acid activity, local anaesthetic injections should not be used. As long as pain persists, calcium gluconate gel should be massaged into the affected area. If a thick necrotic coagulum has formed, this should be excised and gel massaged into the base of the wound. If the pain does not respond to this then a 10 per cent solution of calcium gluconate shoutd be injected under the burn, taking care not to inject so much that the circulation will be jeopardized. If the burn is in a suitable site, such as a limb, or hand or foot, then an intra-arterial infusion (Koehnlein et al., 1978) of 10 ml of 20 per cent calcium gluconate in 40 ml of normal saline infused over 4 h, should be considered. This can be repeated twice in 24 h. If pain recurs
Burns (1985) Vol. 11INo. 6
later, especially in burns from dilute acid then the gel, or injections may need to be repeated. If finger or toe nails are involved, they may show no change. Severe pain under the nails is an indication for removal of the nails involved, under local or general anaesthesia, and treatment with gel or injection continued. Magnesium sulphate paste can be used instead of calcium gluconate gel but generally is not as effective (Kleinert et al., 1976). In large skin burns, systemic administration of calcium and/or magnesium may be necessary (Pearcy, 1981). Calcium tablets should be given orally in water every 2 h on the way to hospital. Frequent electrolyte monitoring, or clinical signs of hypocalcaemia may indicate the need for intravenous calcium and/or magnesium. Profound hypocalcaemia may occur in the absence of clinical tetany and ECG monitoring should be instituted. Eye Exposure. Instillation of 1 per cent calcium gluconate drops may need to be repeated, with fluorescein staining to show cornea1 ulceration. An ophthalmologist should examine these patients. Inhalation injury should be suspected in all cases
due to the ready vaporization of the acid. If collapse occurs, cardio-pulmonary resuscitation will be needed and humidified oxygen support, and treatment to prevent hypocalcaemia. Delayed pulmonary oedema may occur requiring support with humidified 100 per cent oxygen and ventilation. The use of intermittent high concentrations of oxygen may prevent the onset of pulmonary oedema. PREVENTION
In areas where hydrofluoric acid is used, routines for treating these burns should be worked out, with information booklets, and water for vigorous irrigation readily available. Calcium gluconate gel (2.5 per cent), calcium gluconate eye drops (1 per cent), and calcium gluconate tablets should be readily available in the workplace, and gel should be kept in the home of vulnerable workers, in case delayed burns occur. Burns units, likely to treat such patients should be alerted as to the problems of these burns (Pearcy, 1981). DISCUSSION
Burns due to hydrofluoric acid are not common, but, when they occur, cause severe pain and
Pegg et al.: Hydrofluoric acid burns
damage. The majority are minor, but more severe injuries do occur (Heddle, 1984). The pattern of treatment at the vital first aid level, and the medical treatment are now more standardized, as given above. A forward step has been the use of intra-arterial infusions (Koehnlein et al., 1978). As in the two cases cited above, this has been a valuable adjunct, enabling calcium gluconate to be readily available for locally absorbed fluorine ions. If systemic symptoms were to occur, this would be of further help in systemic treatment. Obviously such an infusion is of use only when a large artery to the area is readily available. In the case cited by Heddle, involving the face, then this method of infusion could not be readily applied. No doubt, better methods of treatment will be developed in the future. However, we found that intra-arterial infusion of calcium gluconate gave immediate relief of pain, and cessation of the effects of hydrofluoric acid burns. CONCLUSIONS At present, the mainstay of treatment depends on prevention with worker education, rapid adequate first aid and prompt efficient medical
443
treatment. It is considered that intra-arterial fusion has a valuable place in the treatment burns due to hydrofluoric acid.
inof
REFERENCES Blunt C. P. (1964) Treatment of hydrofluoric acid skin burns by injection with calcium gluconate. Ind. Med. Surg. 33, 869. Heddle S. B. (1984) Hydrofluoric acid burns; an updating of patho-physiology and management. The Bulletin and Clinical Review of Burn Injuries 1, (3), 21.
Kleinert H. E. and Bronson J. L. (1976) Hydrofluoric acid burns of the hand. Medical Times 104, (12), 77. Koehnlein H. E.. Seitz H. D., Achinger R. et al. (1978) Abstracts of 5th International Congress on Burn Injuries, Stockholm, Sweden. Pearcy L. H. D. (1981) 6th Annual Meeting of A.N.Z.B.A., Perth, West Australia. Pegg S. P. (1972) Adult burns: a three year survey with assessment of Sulfamylon. Med. J. Am. 1, 350. Pegg S. P., Gregory J. J., Hogan P. G. et al. (1979) Epidemiological patterns of adult burn injuries. Burns 5, 326. Paper accepted 15 April 1985.
Correspondence should be addressed to: Dr S. P. Pegg. Royal Brisbane Hospital, Herston Road. Herston 4029, Queensland, Australia.