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Hydrofluoric acid has widespread uses in industry and at home. Its mechanism of toxicity is the basis of a specific treatment. Cutaneous burns are the most common form of toxicity and the consequences can be catastrophic. Its insidious presentation can delay any therapeutic action, except if the physician is aware about it. A case report underlines the beneficial action of the intra-arterial infusion of calcium gluconate.
Recently, porcelain veneer restoratives have been introduced to the general practice, and their clinical performances have been confirmed through many longterm clinical investigations. It is expected that porcelain veneer restorations will perform successfully in esthetic, conservative and abhesive dentistry. It is an well known fact that the micro-mechanical bonding strength at the porcelain-resin interface which is achieved through the application of hydrofluoric acid to the porcelain surface is quite a strong bonding mechanism. However, there are very few studies reporting on the acid treatment of porcelain surfaces. The authors have been studying the influence of hydrofluoric acid on porcelain surfaces, and in our previous report we reported, the degrees of corroded porcelain treated with different concentrations of hydrofluoric acid for different durations of application. In the present study, shear bonding strength was measured between resin cements and porcelain surfaces treated with different concentrations (4, 6, 8%) of hydrofluoric acid and for different durations (1 to 24 min.), and the appropriate treatment of porcelain surfaces with regard to the bonding strength was determined. The results obtained were as follows. 1. As the treating time increased with any concentration (4, 6, 8%) of hydrofluoric acid, corrosion of the porcelain surface became more intense. Hardly any evidence of corrosion was observed on any porcelain surface treated for one minute, so it seems that the treatment of porcelain surfaces using 4 to 8% hydrofluoric acids should be continued for over three minutes. 2. Observation of the surface profile by SEM showed no significant differences between the surfaces treated for 3, 6, 12 and 24 minutes. 3. It was not clear as to how the differences of hydrofluoric acid concentrations (4, 6, 8%) plus the differences in the kinds of porcelain (Super Porcelain AAA, NORITAKE Co. Ltd., VMK 68, Vita Zahnfabrik Gmbh & Co., Cosmotech Porcelain, G-C Co. Ltd.) had affected the differences in the amount of corrosion. 4. Regarding to the shear bonding strength at the porcelain-resin cement interface, in comparison with control specimens which were only sandblasted, about all two to three times higher bonding strength were obtained in specimens treated with any concentration (4, 6, 8%) of hydrofluoric acids and for any duration between 3 to 24 minutes. Specimens treated for one minute were an exception.
STUDY OBJECTIVE: To compare topical preparations of magnesium and calcium in the treatment of dermal hydrofluoric acid burns. DESIGN: A randomized, blinded, controlled animal model study. SETTING: Animal care facility. TYPE OF PARTICIPANTS: New Zealand rabbits. INTERVENTIONS: Each rabbit was burned with hydrofluoric acid at four sites along the thoracolumbar spine. Equimolar amounts of calcium gluconate, magnesium gluconate, and a magnesium hydroxide antacid were added into a lubricating jelly. The jelly alone was a control preparation. After a water rinse, the burns were massaged with the gels for 1 minute five times; at 4 and 20 minutes and at 1, 4, and 24 hours. Each rabbit served as its own control by receiving all four treatments. MEASUREMENTS AND MAIN RESULTS: Burn diameter and burn surface area diminished over time, but there were no statistically significantly differences among the treatments. Burn ranking and burn rating of severity also did not demonstrate differences. The histologic analysis of the burns, however, demonstrated that calcium gluconate-treated burns were less severe and more superficial than the control and magnesium gluconate-treated burns; the magnesium hydroxide antacid-treated burns were not statistically different compared to the calcium gluconate-treated burns. CONCLUSION: Topical calcium gluconate is an efficacious treatment for dermal hydrofluoric acid burns. Further research is needed to determine the role of magnesium-containing antacids in the treatment of hydrofluoric acid burns.
Two male cleaning workers aged 62 (patient 1) and 28-(patient 2) presented with red, swollen, aching hands and fingers. At the first interview, the fingers of the right hand of both patients were swollen from the proximal interphalangeal joint to the tip of the finger. The fingers were red and intensely painful. The bleach that both patients used contained 9.5% hydrofluoric acid, and therefore we diagnosed their symptoms as those of burns caused by this agent. We subcutaneously injected 8.5% calcium gluconate into the affected fingers and dressed them with gauze soaked in cooled 0.025% benzethonium chloride. The patients did not use gloves at work, neither of them knew that the cleaning fluid contained dilute hydrofluoric acid, and they were unaware of the danger of this agent. They had not received proper education about the care and handling of poisons and deleterious substances such as hydrofluoric acid. The doctors who had examined the patients in the emergency ward overlooked the possibility of hydrofluoric acid burns, although they suspected chemical burns and confirmed the trade name of the cleaning agent. In addition, although the patients presented with intense pain, no white areas of coagulation and blistering, or surrounding erythemas, which are characteristic symptoms of such burns, were evident. The component of the cleaning agent was described on the container label in very small print. Had the words "poison" and "hydrogen fluoride" been printed in large characters, the examining doctors in the emergency ward would probably not have overlooked the presence of hydrofluoric acid, and the patients would perhaps have been more careful when using it. Hydrofluoric acid can be easily obtained by anyone through the Internet, although general consumers could not obtain industrial quantities. Therefore, the number of burn patients who are not familiar with hydrofluoric acid may increase in the future.
Numerous reports of poisonings due to various fluoride salts and also to hydrofluoric acid have appeared in the literature. Hydrofluoric acid, which is recognized as a strong acid, is expected to cause severe burns following acute exposure. This case is reported because the expected burns were not observed, but the laboratory analysis (a blood fluoride concentration of 13 mg/L) supported the ruling of death due to ingestion of hydrofluoric acid.
Reasons and frequencies of hydrofluoric acid burns have been investigated during our work in the toxicological information centre (1987/88) and by means of the patients treated in the last five years in our ICU: Almost all of the cases are due to accidental hurts (29/30). About 3/4 of the accidents (22/30) happened during occupational exposure. One third of the patients (10/30) have been exposed to hydrofluoric acid fume and 18/30 suffered from percutaneous burns especially of the distal parts of the upper limbs. Oral intoxications are rare (2/30). The observed quotes of the information centre are equivalent to those of our own patients (eight cases from 1984 to 1989). Hydrofluoric acid burns are treated with calcium. Concerning the frequent burns of the limbs, the intraarterial therapy proved good and prevailed during the last years over the classical infiltration therapy. Only early treatment avoids necroses. Unfortunately the particularity of this percutaneous intoxication is often misunderstood.
STATEMENT OF PROBLEM: Fracture of porcelain is a relatively common clinical misfortune. Recent research has indicated that strong bonds can be formed between composite and dental porcelain. Porcelain surfaces are etched with hydrofluoric acid and treated with silane coupling agents before composite application. The question is how exposed dentin may react to etching with hydrofluoric acid. PURPOSE: This investigation examined the effect of 9.5% buffered hydrofluoric acid, of 36% o-phosphoric acid alone and in combination on the surface structure of cut human dentin. MATERIAL AND METHODS: Human molar teeth were sectioned in approximately 0.8-mm thick slices and treated with different acids or their combinations. Application periods were 10, 60, and 180 seconds. Specimens were processed for SEM and for energy-dispersive x-ray (EDX) microanalysis. RESULTS: The smear layer on the surface of sectioned dentin was not completely removed by hydrofluoric acid alone and that a dense amorphous precipitate was formed on the peritubular zone. Starlike structures in dentinal tubules were visible. EDX analysis revealed different fluoride content on the treated surface, dependent on the etchant used. CONCLUSION: Topical application of hydrofluoric acid appeared to provide a dentinal surface with an amorphous precipitate of fluoride. This layer may be important both for resistance of dental caries in dentin and for bonding reactions.
Since years, ion exclusion chromatography (ICE) has been the standard method to separate strong acid analyte anions from concentrated weak acid matrices such as hydrofluoric acid (HF). In this work, the commercially available IonPac ICE-AS 1 column was used to separate trace levels of chloride, nitrate, sulfate and phosphate from HF solutions at 20% (w/w). The efficiency of the separation was studied in more detail using techniques such as ion chromatography (IC), inductively coupled plasma optical emission spectrometry (ICP-OES) and ICP-mass spectrometry (ICP-MS). For 20% (w/w) HF solutions and at a water carrier flow-rate of 0.50 ml/min, the cut window was set from 8.5 to 14.5 min. Under these conditions, analyte recoveries of better than 90% were obtained for chloride, nitrate and sulfate, but only about 75% for phosphate. The HF rejection efficiency was better than 99.9%. It was found that the ICP techniques, measuring total element levels and not species, yielded significantly higher recoveries for phosphorus and sulfur compared to IC. Evidence will be given that part of the added phosphorus (approximately 15% for an addition of 10 mg PO4/kg) is present as mono-fluorophosphoric acid (H2FPO3). In the case of sulfate, the difference between IC and ICP-MS could be attributed to an important matrix effect from the residual HF concentration.
Burns caused by exposure to hydrofluoric acid are occurring with ever-increasing frequency due to the wide use of this acid in industry and research. Such burns are characterized by severe progressive tissue destruction and excruciating pain resulting from the unique properties of the freely dissociable fluoride ion. The subungual tissues are especially susceptible to the destructive effects of hydrofluoric acid. The proper treatment of hydrofluoric acid burns requires prompt recognition and the institution of specific therapeutic measures by the attending physician.
STUDY OBJECTIVE: To gather preliminary data on the safety and efficacy of IV magnesium in a rat model of hydrofluoric acid burns. MODEL: Forty-seven anesthetized male rats (200 to 300 g) received a standardized burn with 52% hydrofluoric acid. INTERVENTIONS: Animals were anesthetized with 30 to 50 mg/kg ketamine IM and 1 to 3 mg/kg xylazine IM. A standardized chemical burn was created by topical application of 52% hydrofluoric acid. The rats were divided into four treatment groups: group 1 received no treatment; group 2 received intradermal injection of 10% calcium gluconate; group 3 received 80 mg/kg MgSO4 IV; and group 4 received 160 mg/kg MgSO4 IV. After the rats were killed, the burn lesions were excised and examined by a pathologist to determine the grade of burn (which was equal to the clinical degree of burn). MEASUREMENTS AND MAIN RESULTS: Microscopic examination of the burns revealed differences among the four groups. Five of 13 group 1 rats (37%) died within 24 hours of burn initiation. Of group 1 survivors, 50% had grade 2 burns, and the other 50% had grade 3 burns. In group 2, eight of 11 rats (73%) had grade 3 burns. Twenty-five percent of group 3 rats (three of 12) had grade 3 burns, and only 9% of group 4 rats (one of 11) had grade 3 burns. Only the difference in the rates of grade 3 burns for groups 2 and 4 was statistically significant. Although not statistically significant, burns in groups 3 and 4 tended to be smaller in diameter than burns in groups 1 and 2. CONCLUSION: High-dose IV magnesium sulfate reduces the severity of hydrofluoric acid burn compared with conventional intradermal calcium gluconate therapy. Early deaths appeared to be prevented by both calcium and magnesium therapies.
BACKGROUND: Calcium gluconate gel, applied after initial rinsing with water, has a documented effect as first aid treatment for hydrofluoric acid burns. Hexafluorine is a novel liquid compound developed especially for emergency decontamination of hydrofluoric acid eye and skin exposures. However, scientific documentation of the effect of Hexafluorine is insufficient. This study was undertaken to compare Hexafluorine with water rinsing plus topical calcium and with water rinsing alone. METHODS: Thirty-five Sprague-Dawley rats were anesthetized and their backs shaved. Four filter papers 10 mm in diameter were soaked in 50% hydrofluoric acid and applied on the shaved area of each rat for 3 minutes. Thirty seconds later, the acid-exposed skin areas were rinsed with 500 mL Hexafluorine for 3 minutes (group H, n = 10), 500 mL water for 3 minutes (group W, n = 10) or 500 mL water for 3 minutes followed by a single application of 2.5% calcium gluconate gel (group Ca, n = 10), or received no treatment (controls, n = 5). The animals were closely observed for 5 days. Daily at 4 P.M. each of the four burns on every rat was rated on a modified Draize scale graded from 0 to 5 (0 = no visible injury, 1 = diffuse erythema, 2 = distinct erythema, 3 = distinct erythema plus wounds or discolored spots, 4 = distinct erythema plus wounds or discolored areas covering >50% of the burn, 5 = a necrotic wound covering the whole burn). The mean of the four scores was then calculated for each animal and day. The rating procedure was performed by one laboratory assistant who was unaware of the treatment given. Kruskal-Wallis analysis was used to evaluate possible differences between treatment groups on each of the 5 days. If the p-value obtained was <0.05, correction for multiple comparisons was made. RESULTS: The mean severity score in group H was significantly higher than that in group Ca on days 2 and 3. Moreover, Hexafluorine showed a consistent trend towards a worse outcome, both in comparison to water plus topical calcium and to water rinsing alone. CONCLUSION: Based on these observations it is concluded that water rinsing followed by topical calcium should remain the standard first aid treatment for skin exposure to hydrofluoric acid.
We observed seven patients who presented consecutively with hydrofluoric acid hand burns. The clinical characteristics of these patients and the course of their disease and treatment are reviewed. Dermatologists should be aware that a hydrofluoric acid burn constitutes a dermatologic emergency. Specialized treatment is required to prevent topical, system, and even lethal toxic effects.
A 20% solution of hydrofluoric acid (HF) was applied to the skin of rats and a biomedical observation of the tissues and sera was made. Flushing with running water was effective for HF burns. By applying 2.5% calcium gluconate jelly, concentrations of fluoride in the urine and the tissues surrounding the injured region were reduced. Thus, the results proved that irrigation with running water and jelly applications were evaluated as the most effective therapy among various methods tested for HF burns.
A case report of accidental hydrofluoric acid burns that involve dermal tissue of the hand is presented. Prompt medical treatment for this accident resulted in minimal disfigurement and minimal paresthesia and disability. Protocols for essential treatment and precautions for personnel working in dental laboratories where hydrofluoric acid is used have been discussed.
The production of hydrofluoric acid (HF) and its use have increased remarkably due to the rapid development of the electronic and petrochemical industries. HF has a highly corrosive and penetrating action when it comes in contact with organic material, including body tissue. When burns are caused by a high concentration of HF, fatal cases have been reported, even when the contact with HF is only for a short time or on a small area of the body. The causes of death have been reported to be lung edema, mineral disturbance and systemic injury. But no pathological experiments have been reported. In the present study, experiments of HF burns using mice (d.d.Y., 6w, male) were performed, mainly histopathologically and ultramicroscopically. Histological examination revealed that thrombosis occurred in the lung, and that the group in which mice had more thrombi showed a higher death rate. Thrombosis in the lung may be one of the main causes of death by hydrofluoric acid burns. Other organs showed no significant change. Ultrastructural examination of the lungs, revealed that the thrombi were seen in the capillary of the alveolar septa much more than in the pulmonary arteries and were mainly composed of platelets. The endothelial cells in the lungs were injured and had condensed cytoplasm, intracellular edema, or dilation of the intercellular gap. The basement membrane of the capillary was sometimes bared between the strongly condensed endothelial cells, but no platelets directly touched the membrane. Moreover, that no platelets directly touched the subendothelial tissue and the mechanism of the platelet aggregation is interesting. Platelet aggregation was thought to have resulted from the unbalance between thrombogenic factors and antithrombogenic factors in the blood above the surface of endothelial cells caused by endothelial injury. Endothelial cells in the lungs were assumed to be injured by fluoride, directly or indirectly, because the group which showed higher fluorine contents in the lungs showed more severe injury to the endothelial cells and because the fluorine contents in the lung increased much more than that in the other organs which had no thrombi.
OBJECTIVE: To compare the effects of different kind of methods in the management of hydrofluoric acid burn in early postburn stage in rabbits. METHODS: Thirty-three rabbits were inflicted with burn by 55% of hydrofluoric acid covering 5% TBSA, and were randomly divided into 3 groups, i.e. A (n = 13, with 5 ml.kg(-1).h(-1)of isotonic saline intravenous infusion), B (n = 10, with isotonic saline and 50 g/L of calcium gluconate infusion in dose of 20 mg/kg at different time points), and C (n = 10, with the same treatment as B group, and with excision of burn wound at 0.5 post burn hour) groups. The serum levels of fluorine and calcium were determined before and after various postburn hours, and the mortality rate was statistically analyzed. RESULTS: (1) The serum level of fluorine in A (8.37 +/- 2.62 mg/L) and B (8.59 +/- 2.25 mg/L) groups reached the peak value at 1 postburn hour (PBH), which was 107 times higher than that before the burn injury. The serum level of fluorine in B group was significantly lower than that in A group at 24 PBH (P < 0.05), while that in C group declined to (6.20 +/- 0.23) mg/L, which was obviously lower than that in A and B groups (P < 0.01). (2) The serum calcium level declined after burns, reaching the lowest level at 8 to 12 PBH. and began to increase at 24 PBH. Compared with normal calcium value, the serum level of calcium in A, B and C groups declined to as much as 46%, 32% and 26%, respectively. Statistically significant difference was found between C and B groups (P < 0.01). (3) The mortality rate in the three groups within 72 PBH were 30.8%, 12.5% and 0.0%, respectively. CONCLUSION: Early removal of burn area and calcium supplementation could help quickly decrease blood fluorine, reverse the fatal hypocalcemia and the multiple systemic toxic injury in rabbits inflicted with hydrofluoric acid injury.
Hydrofluoric acid is a strong inorganic acid. It is used commercially in a number of industrial settings. Injuries sustained from this acid are infrequent and the management of such cases is therefore not well known. Tissue destruction caused by this acid is rapid and severely painful and may result in disfigurement if treatment is not instituted promptly. Methods of management of hydrofluoric acid burns are still controversial and no single type of therapy has yet been determined. The patient was managed according to the guideline in the literature, but, in the presence of severe digital oedema, intra-arterial infusion of gluconate was performed. This resulted in rapid relief of pain and prevention of continuing tissue destruction.
PURPOSE: To evaluate the repair bond strength of a laboratory processed composite treated with hydrofluoric acid gels of different acid concentrations and for various etching times and repaired with a flowable composite. METHODS: 75 specimens of a laboratory composite (Targis) were prepared in a split metal mold and stored for 24 hours in an incubator at 37 degrees C and 100% relative humidity. The laboratory composite surfaces were then etched for 5, 10, 15, 30, and 60 seconds using three hydrofluoric acid concentrations (5%, 8%, and 9.5%). The repair composite (Tetric Flow) was light-cured in two increments for 40 seconds each in an inverted, truncated cone mold. Storage conditions of specimens before debonding were 24 hours at 37 degrees C and 100% relative humidity. Tensile bond strengths were determined using a testing machine at a crosshead speed of 0.5 mm/minute. A two-way ANOVA was used to determine significant differences. Failure sites were classified. The morphological aspects of the etched composite surfaces were evaluated qualitatively by scanning electron microscopy. RESULTS: There were no differences in the repair bond strengths with respect to the three different acid concentrations or the five etching times tested. The minimum etching time to observe an etched pattern was at 60 seconds with the highest concentration of hydrofluoric acid (9.5%).