[Necrotizing pancreatitis after formic acid and hydrofluoric acid burns].
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Hydrofluoric acid is a colourless or almost colourless, fuming liquid having a highly caustic and corrosive effect on organic tissue. Many kinds of hydrofluoric acid in concentrations are used in Industrial processes and laboratory uses because of its useful chemical properties. Hydrofluoric acid causes severe and painful burns to the skin and eyes. In this paper, the immediate symptoms, the typical treatments in the literature, first aid and therapy of hydrofluoric acid burns are reviewed.
Hydrofluoric acid exposures to the skin can produce severe, progressive burns. Medical treatment of these burns is aimed at neutralizing the free fluoride ion, which is felt to be responsible for burn progression. Both calcium and magnesium will form complexes with free fluoride and have been used as topical or intradermal treatments in the past. This study evaluated the efficacy of intravenous magnesium sulfate for the treatment of hydrofluoric acid burns and compared this treatment to controls and burns treated with intradermal calcium gluconate in a rabbit model. Both treatments demonstrated a reduction in burn area over time, wound depth, healing time and final scar area compared to controls. The intravenous magnesium treatment showed trends toward improved outcome compared to the intradermal calcium treatment in all parameters evaluated, but these differences did not reach statistical significance. This investigation found intravenous magnesium to be an effective method for treating hydrofluoric acid burns. Intravenous magnesium may have significant utility for treating hydrofluoric acid burns that are not amenable to current therapies.
INTRODUCTION: Hydrofluoric acid is a fluoride-substituted compound used in the chemical industry. Burns and hypocalcaemia result from ingestion or contact with the skin or mucosal membranes. We observed burns and skin necrosis on the hands after home use of low-concentration hydrofluoric acid. CASE REPORT: A 57-year-old woman consulted in February 1994 for oedema, erythema and very painful burns of the palms of both hands. The day before, she had used a home-made furniture cleanser containing 5 p. 100 hydrofluoric acid. At admission, calcium and radiography of the two hands were normal. She was given a topical application of 5 p. 100 calcium chloride. The clinical course was favourable with squamation of both palms then necrotic lesions of the pulp on the 1st, 2nd and 3rd fingers. DISCUSSION: Such exposure in a household situation is unusual. Hydrofluoric acid has two dangerous mechanisms of action. First it is a caustic substance producing late-onset burns and secondly hypocalcaemia results from precipitation of insoluble calcium fluoride. The risk of hypocalcaemia is greatest when a large area of the skin is exposed. Prognosis depends on early treatment based on prevention of hypocalcaemia by abundant washing of the teguments and permanent application of a 5 p. 100 calcium gluconate solution associated with local skin treatments. Careful follow-up is required with regular calcium chemistries.
Hydrofluoric acid burns are characterized by progressive tissue destruction and severe pain. Fluoride ion chelators, such as salts of calcium and magnesium, have been used to treat these burns. This study was designed to compare the efficacy of several treatment methods that involve the use of these salts. Standard hydrofluoric acid burns were produced on the shaved hindquarters of rats. After being rinsed with water, the chemical burns were treated by one of seven experimental methods. The progress of the chemical burn damage was observed for 1 week by measuring the surface areas of the burns. Calcium gluconate burn jelly, 20% calcium gluconate in water, and 50% aqueous dimethyl sulfoxide did not significantly slow the spread of the burn area. However, subcutaneous injections of calcium gluconate or magnesium sulfate and topical applications of calcium gluconate in a solution of dimethyl sulfoxide significantly slowed the progress of the burns during the first 24 hours and enhanced tissue recovery for the remainder of the observation period. These results indicate that subcutaneous injections of magnesium or calcium salts appear to be more effective than conventional topical applications in the treatment of hydrofluoric acid burns. More significantly, topically applied calcium gluconate combined with a penetration enhancer, such as dimethyl sulfoxide, is as effective as injection treatments in reducing damage caused by hydrofluoric acid.
Hydrofluoric acid is used in a variety of industries and poses a considerable medical hazard. The dual mechanism of injury makes hydrofluoric acid burns among the most severe and lethal seen. Prompt treatment with copious irrigation, iced benzethonium or benzalkonium soaks, calcium gluconate gel application and calcium gluconate injections may well prove to be lifesaving.
Hydrofluoric acid burns are usually due to accidental exposure. Deep tissue injury may result, damaging nerves, blood vessels, tendons, and bone. Concentrated hydrofluoric acid may cause immediate pain; dilute solutions may result in a delay of symptoms for many hours. Symptoms are usually out of proportion to the observed injury. Appropriate first aid and medical management can dramatically affect the prognosis. Local treatment consists of copious water lavage and the application of topical neutralization agents. For more severe exposures, calcium gluconate injection or intraarterial infusion of calcium gluconate may be indicated as well. Life-threatening alterations of electrolytes can occur, with ensuing arrhythmias. Inhalation, ingestion, and ocular exposures require specialized treatment and referral.
Hydrofluoric acid is widely used in both industrial and household settings. The acid may cause insidious burns that can be very destructive. If the burns are not treated appropriately, the continued action of the free fluoride ion leads to liquefaction necrosis of the affected soft tissues, bony erosion and, ultimately, potentially lethal hypocalcemia. Immediate and copious irrigation, followed by topical, subcutaneous or intra-arterial administration of calcium carbonate, minimizes the extent of injury. In major exposure to hydrofluoric acid, management includes serum electrolyte and electrocardiographic monitoring, as well as aggressive repletion of calcium deficiency.
Hydrofluoric acid (HF) injuries have a potential for both systemic toxicity as well as severe tissue destruction. We present an algorithm for the management of HF burns. This algorithm addresses these issues emphasizing the differences between major and minor cutaneous burns, and includes the approach to inhalation, ingestion and eye injuries. Although algorithms can never be complete, we hope this algorithm will be used as an aid in the clinical management of these patients.
Hydrofluoric acid burns create unique problems that require specialized treatment to prevent serious sequelae. The most important factors to remember are the delay in the onset of signs and symptoms related to concentration of acid and the penetration and destruction of tissues by fluoride ions, which bind calcium and magnesium cations with subsequent serious systemic effects. In this article, an attempt has been made to describe these factors and to offer recommended treatment protocols which, if appropriately applied, can offset the destructive nature of HF burns. Several methods of treatment have been offered, and it is recommended that one or more be used according to circumstances. The most important initial point in treatment is the recognition that an HF burn has occurred. Then, with a clear understanding of the mechanisms of injury, one can properly manage such a burn. It is hoped that this report will assist the practitioner in dealing with this potential serious and complex problem.
Hydrofluoric acid (HF) burns are characterized by progressive tissue necrosis and severe pain. Numerous topical treatments have been proposed, yet few have been studied experimentally. The present study was designed to examine the comparative efficacy of recommended treatments. Hair on the hind legs of rats was removed and 48 hours later 70% HF was applied. Calcium gluconate, Zephiran (benzalkonium chloride), A + D Ointment, aloe gel, and magnesium ointment were applied topically and burn development was monitored. Calcium gluconate significantly reduced burn size as early as one hour after application. Significant protection continued for seven days after the single application. The other treatments were not effective in decreasing or delaying HF burn development. The results indicated that calcium gluconate ointment was the most effective topical treatment for HF burns.
Hydrofluoric acid (HF) causes severe skin burns which often progress in severity despite physiologic neutralization. The currently accepted therapy is the subcutaneous injection of calcium (Ca) gluconate to precipitate the residual free fluoride ion. Magnesium (Mg) also forms an insoluble fluoride salt and is less tissue irritating than Ca. This study compared the effects of subcutaneous injection of saline, Ca gluconate, Mg acetate (MgAc), and Mg sulfate (MgSO4) on lesions resulting from HF burns in rats. Burns treated with either Mg compound healed 3.7 +/- 1.7 days faster (p less than 0.05) developed less severe lesions (p less than 0.01) and exhibited left untreated or treated with saline. There was no difference in the incidence of infection between the study groups. The effects of burns treated with calcium were statistically similar to the control groups. This study suggests that Mg may be more effective than Ca in minimizing the duration, depth, and progression of dermal HF burns.
Hydrofluoric acid is used for different purposes in industry and in the home as a rust remover. Most exposures are accidental and may result in severe superficial and deep tissue injury as well as systemic toxicity. There is uncertainty regarding the optimal treatment of hydrofluoric acid eye injury. A patient in whom a solution of 49% hydrofluoric acid induced a large corneal erosion is described. Repeated instillation of 1% calcium gluconate eye drops combined with the conventional treatment of acid eye burns resulted in a complete and quick recovery.
Although hydrofluoric acid burns are frequent, fatality is rare. In the case of massive exposure, the prognosis is generally poor. We present two fatal cases resulting from extensive exposure to hydrofluoric acid which produced acute systemic metabolic acidosis with profound hypocalcemia and hypomagnesemia. Both patients died within three hours after the exposure. The current knowledge of treatment for severe hydrofluoric acid burns is reviewed and the importance of prevention and prompt recognition for proper treatment is emphasized.
Exposure to hydrofluoric acid is serious and many times fatal. We have reported the case of a man who was totally immersed in a 10% hydrofluoric acid solution. A multidisciplinary approach to management was important to his ultimate recovery.
BACKGROUND: Hydrofluoric acid ingestion is known to have a very high mortality rate secondary to the rapid development of hypocalcemia and fatal arrhythmias. CASE REPORT: A 33-year-old man ingested an estimated dose of hydrofluoric acid 6 times that considered to be lethal. The patient survived with minimal morbidity despite having multiple ventricular fibrillation arrests. His survival is attributed to early, high dose calcium therapy given via the nasogastric and intravenous routes.
Quantitation of 5-methylcytosine in DNA after acid hydrolysis has been inaccurate because deamination of cytosine and 5-methylcytosine occurs during the hydrolysis procedure. There is little information in the literature regarding the use of hydrofluoric acid (HF) for DNA hydrolysis and we have therefore undertaken a systematic study of this process. The deoxyribonucleotides of cytosine and 5-methylcytosine were shown not to undergo detectable levels of deamination during prolonged periods (up to 24 h) at 80 degrees C in 48% HF. Kinetic studies show that the release of purine and pyrimidine bases was complete by 4 h under these conditions. Analysis of the 5-methylcytosine content of DNA from various tissues gave levels that were very close to the values reported in the literature. This method is ideally suited for the determination of the overall cytosine methylation levels in DNA.
Hydrofluoric acid is used extensively as an industrial cleaning agent for metals and glass. Many workers are injured by cutaneous contact of the acid with exposed skin surfaces, particularly hands. Hydrofluoric acid burns are characterized by delayed onset of symptomatology with skin ulceration, and severe pain may be of extended duration. Treatment of hydrofluoric acid burns traditionally has consisted of local infiltration or intraarterial injections of calcium solutions. These injections are painful and frequently require retreatment. A new treatment utilizing a topical gel of calcium carbonate is described. Nine patients have been treated for hydrofluoric acid burns of the hand with calcium carbonate gel applied topically and covered with occlusive glove dressings. A gel slurry is compounded from calcium carbonate tablets and K-Y Jelly. Fingernails of the affected fingers are removed if a subungual burn is obvious. The gel is put into a surgeon's glove and placed over the burned hand. The patient replaces the glove and slurry every 4 hours for 24 hours. After the first day, the glove is discontinued unless there is resumption of painful symptoms. Full range of motion is encouraged during this interval. The calcium carbonate gel technique was successfully utilized in nine patients with no further need for injection therapy. In these patients, pain relief was obtained within 4 hours of treatment, with no further progression of skin ulceration. No reconstructive procedures were required in any patient, and only one patient did not return to full-duty work within 1 week. There were no long-term sequelae from burns treated with this topical therapy, except one patient, who presenting 24 hours after the burn, developed a digital tip neuroma that was excised.