HF Burns Research Articles

Chitosan-based hydrogels to treat hydrofluoric acid burns and prevent infection.

There is an urgent need for treatments for hydrofluoric acid (HF) burns and their derivative problems that prevent hydrogen ion dissociation and fluoride ion binding to tissues. This study evaluated the ability of chitosan-based hydrogels combined with a buffer solution containing either boric acid or Tris and calcium gluconate (CHS-BA-CG and CHS-Tris-CG) to repair HF burn wounds and prevent wound infections. We assessed calcium release rates and biocompatability and constructed a mouse HF burn model to assess the tissue repair effects of the hydrogels. Finally, we performed disc diffusion tests from burn tissue and quantified the bacterial counts to assess the anti-infection properties of the hydrogels. Calcium was gradually released in the CHS-BA-CG and CHS-Tris-CG groups (73% and 43%, respectively, after 48h). The cell viabilities at 48h after HF burn in these groups were significantly higher than those in the phosphate-buffered saline (PBS) and CG-treated groups. Histopathological evaluation showed a clear boundary between the epidermal and dermal layers in both CHS-BA-CG and CHS-Tris-CG-treated groups, indicating their effectiveness in tissue repair. In the disc diffusion test, CHS-BA-CG and CHS-Tris-CG exhibited larger inhibition zones against Acinetobacter baumannii than those for PBS and CG. The bacterial counts on HF burn wounds were significantly lower in the CHS-BA-CG and CHS-Tris-CG-treated groups than those in the PBS and CG-treated groups. The in vitro studies demonstrated the biocompatibility and antimicrobial effects of the CHS-BA-CG and CHS-Tris-CG hydrogels. Both gels also demonstrated tissue repair and anti-infection effects. Thus, chitosan-based hydrogels may be candidates for HF burn therapy.

The effect of calcium gluconate with natural extracts on skin toxicity of hydrofluoric acid

Hydrofluoric acid (HF) is a highly corrosive acid. The conventional treatment for HF burn is topical application of calcium gluconate (CG). Our study aimed to assess the synergistic effects of natural extracts (Centella asiatica, Portulaca oleracea, and blueberry extracts) in combination with CG in healing HF induced burn wound. We investigated the effects of different topical CG formulations with natural extracts using cell proliferation assay, western blot, reverse transcription- polymerase chain reaction, human skin equivalent model (HSEM), and mouse model. Topical CG formulations with natural extracts showed better recovery from HF burns shown by greater collagen expression in the dermal fibroblast model, HSEM and mouse model. Our study demonstrated that CG in combination with natural extracts show superior wound healing in treating HF burn compared to CG monotherapy.

Clinical significance of urinary fluoride levels in patients with hydrofluoric acid burns

ObjectiveWe investigated the urinary fluoride level in patients with hydrofluoric acid (HF) burns of different severities and explored the clinical significance of these levels in the diagnosis of acute HF burn. MethodsData from 260 patients with HF burns were collected from the Department of Burns, Zhejiang Quhua Hospital, between July 2006 and June 2016. According to burn severity, patients were divided into non-poisoning, mild poisoning, moderate poisoning, and severe poisoning groups. In addition, 25 healthy controls were recruited from fluorine chemical companies. The urinary fluoride level was measured using a fluoride-selective electrode and values were compared amongst groups. The urinary fluoride level was also measured periodically after exposure to investigate dynamic changes in the moderate and severe poisoning groups. ResultsUrinary fluoride levels were 0.32–520.0mg/L (n=260) on admission to the emergency department, and 182 patients had levels >1.7mg/L. The levels in controls and the non-poisoning group were lower than in the other two groups, and increased significantly with an increase in severity. Thirty-three patients were admitted 4h after injury; of these patients, fluoride levels were significantly higher in those with severe poisoning than in those with moderate poisoning. Levels peaked 4h after injury and then dropped and returned to normal 6days after injury. ConclusionUrinary fluoride level can be used for the early diagnosis of HF burns and to determine the severity of fluoride poisoning, which is crucial for early treatment.

Analysis on clinical characteristics of 316 patients with hydrofluoric acid burns

Objective: To investigate the clinical characteristics of patients with hydrofluoric acid (HF) burns. Methods: Clinical data of 316 patients with HF burns admitted to Zhejiang Quhua Hospital from January 2004 to December 2016 were retrospectively analyzed. Patients were divided into non and mild poisoning group (NMP, n=157), moderate poisoning group (MP, n=120), and severe and fatal poisoning group (SFP, n=39) based on the severity of poisoning. Occurrences of hypocalcemia, hypomagnesemia, hypokalemia, and hyperkalemia of patients within 24 hours after admission were recorded. Values of emergency urinary fluoride of patients on admission were recorded. Values of urinary fluoride of patients admitted to hospital in 4 hours post injury in groups MP and SFP at post injury hour 4, 12, and 24 and on post injury day 2, 3, 4, 5, 6, and 7 were also recorded. Electrocardiographic abnormalities of patients within 24 hours after admission were recorded. Data were processed with chi-square test, Kruskal-Wallis H test, and Mann-Whitney U test. Results: (1) Hypocalcemia, hypomagnesemia, and hypokalemia occurred in some patients in each of the three groups, but no patient had hyperkalemia. Taking serum calcium namely total serum calcium as reference, the incidence rate of hypocalcemia of patients in group NMP was close to that in group MP (χ(2)=0.05, P>0.05). The incidence rate of hypocalcemia of patients in group SFP was significantly higher than that in group NMP or group MP (χ(2)=10.53, 7.92, P<0.01). The incidence rates of hypokalemia in the three groups were close (χ(2)=0.63, P>0.05). Taking serum ionized calcium as reference, the incidence ratio of hypocalcemia of patients in group NMP was close to that in group MP (χ(2)=0.01, P>0.05), while there were statistically significant differences in incidence ratio of hypocalcemia of patients between group SFP and each of group NMP and group MP (χ(2)=4.66, 4.47, P<0.05). Taking serum calcium as reference, the incidence rate of hypocalcemia of patients was 7.3% (23/316). Taking serum ionized calcium as reference, the incidence rate of hypocalcemia of patients was 60.0% (42/70), which was significantly higher than that of taking serum calcium as reference (χ(2)=113.74, P<0.01). The incidence rates of hypomagnesemia of patients in groups MP and NMP were close (χ(2)=0.02, P>0.05). The incidence rate of hypomagnesemia of patients in group SFP was significantly higher than that in group NMP or group MP (χ(2)=14.69, 9.94, P<0.01). (2) The urinary fluoride levels were tested in 288 patients, with the value of emergency urinary fluoride of patients on admission 0.2-590.0 mg/L. The values of urinary fluoride of 202 patients were above the normal value. The values of emergency urinary fluoride of patients in groups NMP, MP, and SFP were 2.15 (1.11, 4.30), 5.89 (1.72, 14.25), and 36.0 (13.2, 103.2) mg/L, respectively. The values of emergency urinary fluoride of patients in groups MP and SFP were significantly higher than the value in group NMP (χ(2)=23.28, 66.03, P<0.01). The value of emergency urinary fluoride of patients in group SFP was significantly higher than that in group MP (χ(2)=39.23, P<0.01). The value of urinary fluoride of 33 patients admitted to hospital within 4 hours post injury in groups MP and SFP reached the top at 4 hours post injury and then gradually declined, which returned to normal on about 5 days post injury. The values of urinary fluoride of patients in group SFP at 4, 12, and 24 hours post injury and on 2, 3, 4, 5, 6, and 7 days post injury were significantly higher than those in group MP (Z=-4.28, -4.15, -3.81, -4.21, -2.48, -2.06, -2.31, -2.68, -3.03, P<0.05 or P<0.01). (3) Twenty-seven patients had electrocardiographic abnormality. There were 12 patients with T wave changes (the most common), 8 patients with ST-T changes, 6 patients with ventricular arrhythmias, 6 patients with conduction block, and 1 patient with broadened QRS waveform. There was no patient with prolonged Q-T interval. The ratios of patients with the above electrocardiographic abnormalities in group SFP were higher than those in group NMP and group MP. Conclusions: Clinical manifestations of patients with HF burn are hypocalcemia, hypomagnesemia, hypokalemia, and electrocardiographic abnormality. In addition to routine serum electrolyte and electrocardiogram monitoring, the levels of serum ionized calcium and urinary fluoride can be helpful to evaluate the severity of illness of the patients.

Epidemiology of Work-Related Hydrofluoric Acid Exposure in Western Zhejiang Province, China

Background: Hydrofluoric acid (HF) burns are one of the most frequent chemical burns in western Zhejiang province of China, and most of them are work-related. This study documents the epidemiology of HF burns in the region using burn data from a local specialized hospital. Results from this survey will assist in the planning of prevention strategies for high-risk occupations and groups. Methods: A 13 y retrospective analysis was conducted including all patients with work-related HF exposure admitted to the Department of Burns and Plastic Surgery, Zhejiang Quhua Hospital, Zhejiang Province, China, between January 2004 and December 2016. Information obtained from eligible patients included sex, age, education, season distribution, type and nature of enterprise, cause of HF injury, and HF concentration. Data regarding time lag from injury to medical treatment, burn sites and sizes, accompanying injuries, treatments, and prognosis were also assessed. Results: A total of 316 patients (294 males, 22 females; average age: 39.5 ± 10.31 y) were admitted for work-related HF burns. These patients were divided into the FI group (170 patients) and the NFI group (146 patients). The incidence of HF burn injury has increased gradually over the last 13 y period, although several slight fluctuations were observed in several years. There was a significant difference in education level between the FI and NFI groups. Compared to the state-owned enterprises, private enterprises seemed to contribute most of the work-related HF injuries. These HF injuries were caused by varying concentrations of HF solution. The average concentration of HF in the FI group was significantly higher than that in the NFI group. However, the time lag from injury to medical treatment in the FI group was shorter than that in the NFI group. The most common burn sites in the FI group were the head, neck, arms, and legs, while the hand was the most frequently involved site in the NFI group. The average burn area was significantly larger in the FI group than the NFI group. In terms of accompanying injuries, there were higher rates of morbidity in the FI group than the NFI group. Accordingly, the FI group showed a higher poisoning severity score than the NFI group. Fifty-two patients underwent surgery, including 31 from the NFI group and 21 from the FI group. Most of the surgeries involved early eschar excision and skin grafting performed in the ER, while most surgeries, including amputation and flaps, were performed in patients in the NFI group. More sequelae were observed in the NFI group. Conclusions: Work-related HF burns are preventable. The high morbidity of HF burns in western Zhejiang Province is related to the industrial structure of the area. The related enterprises and local authorities are encouraged to launch and upgrade their safety policies, as well as to provide the necessary occupational education and training to high-risk populations based on the differences in characteristics of the FI and NFI groups. Strategies focusing on the production, transportation, and usage of HF should be enhanced immediately.

Hydrofluoric acid burns in the western Zhejiang Province of China: a 10-year epidemiological study.

BackgroundChemical burns caused by hydrofluoric acid (HF) frequently occur in the Western Zhejiang Province. This study aimed to investigate the epidemiological characteristics of HF burns within this region.MethodsA 10-year retrospective analysis was conducted using data from all inpatients with HF burns. These patients were treated at the Department of Burns and Plastic Surgery at our hospital between January 2004 and December 2013. Information obtained for each patient included sex, age, occupation, burn location, burn cause, and the hazard category of the chemical which caused the burn. Data regarding wound site and size, accompanying injuries, serum electrolyte levels, operations, length of hospital stay, and mortality were also assessed.ResultsA total of 201 patients (189 males, 12 females; average age: 38.33 ± 10.57 years) were admitted due to HF burns. Over the 10-year period, the morbidity of HF burns in the past 10 years showed a gradual increase, which paralleled the development of local fluoride industries. Most HF injuries were work related and distributed in working-age patients. Aqueous HF solutions, especially highly concentrated ones, were the most common chemical cause of HF burns. Moreover, inappropriate operation, machine problems, and inadequate protection were identified as the leading causes of HF burns in the workplace. The burn area was <5% of TBSA in more than 90% of patients, and the most common burn sites were the head, neck, and upper extremities. Approximately 17% of patients underwent surgical operation. Accompanying injuries should be detected and treated correctly in a timely manner. Lastly, electrolyte imbalances, such as hypocalcaemia, hypomagnesaemia, and hypokalaemia, occurred frequently in patients with HF exposure; however, hyperkalaemia was not encountered in this study.ConclusionBased on the epidemiological results for HF burns in this region, the related enterprises and local authorities should be encouraged to upgrade management policies and to provide necessary occupational hazard education and safety training for high-risk occupations within high-risk working populations. Furthermore, the enhancement of hazardous chemicals management is also needed. Finally, for patients with HF exposure, early and correct pre-hospital triage, treatment and consequent in-hospital treatment and procedures should also be improved.

Optical coherence tomography analysis of hydrofluoric acid decontamination of human cornea by mannitol solution

PurposeTo evaluate the efficacy of mannitol solution as a decontamination agent on the chemical burn of the human corneas. MethodsEight donor corneas from an eye bank were exposed to 25μl of 2.5% hydrofluoric acid (HF) solution on a filter paper for 20s. Three eyes were rinsed with 1000ml of mannitol 20% for 15min immediately after removal of the filter paper, 3 other were rinsed with sodium chloride (NaCl) 0.9% (1000ml for 15min) and two eyes were not rinsed. Microstructural changes were monitored in the time domain by optical coherence tomography (OCT) imaging for 75min. ResultsNaCl reduced the penetration depth to approximately half the thickness of the cornea at 15min; scattering within the anterior cornea was higher than that for the unrinsed eye. With mannitol, no increased scattering was observed in the posterior part of the corneal stroma within a time period of 1h after rinsing. OCT images revealed low-scattering intensity within the anterior stroma at the end of the rinsing period. ConclusionIn eye bank human corneas, mannitol proved to be an efficient agent to decontaminate HF burn.

Occupational Hydrofluoric Acid Injury from Car and Truck Washing--Washington State, 2001-2013.

Exposure to hydrofluoric acid (HF) causes corrosive chemical burns and potentially fatal systemic toxicity. Car and truck wash cleaning products, rust removers, and aluminum brighteners often contain HF because it is efficient in breaking down roadway matter. The death of a truck wash worker from ingestion of an HF-based wash product and 48 occupational HF burn cases associated with car and truck washing in Washington State during 2001-2013 are summarized in this report. Among seven hospitalized workers, two required surgery, and all but one worker returned to the job. Among 48 injured workers, job titles were primarily auto detailer, car wash worker, truck wash worker, and truck driver. Because HF exposure can result in potentially severe health outcomes, efforts to identify less hazardous alternatives to HF-based industrial wash products are warranted.

Hydrofluoric Acid Exposure

A 21-year-old male was admitted to the emergency department with bleeding skin burns. He had been exposed to 70% hydrofluoric acid (HF) through his nitrile hand gloves during an etching glass procedure at work. He had painful lesions, which included bleeding skin abrasions due to second-degree burns on the first and second fingertips on the right hand, and white spots on the left first finger, which covered approximately 0.1% of the surface (Figures 1a-d). Electrocardiography was performed and electrolyte levels were determined. After washing with water, 10% calcium gluconate was administered intravenously and 5 mL was injected around the border of the wounds for analgesia and detoxification. The pain was reduced, and six weeks later, his wounds had fully healed. Upon tissue penetration, hydrofluoric acid dissociates into hydrogen and fluoride ions, the latter of which is toxic.1, 2, 3 HF burn treatment aims to neutralize the fluoride ions with calcium and magnesium ions. Figure 1 (a) Hydrofluoric acid burns on the right and left hands. (b) Hydrofluoric acid did not penetrate the finger, but non-hemorrhagic white lesions were seen on the left thumb (mid metaphalangeal). (c, d) Bleeding fields due to second-degree burns by hydrofluoric ... Massive exposure to HF constitutes a life threatening situation. A 50% hydrofluoric acid solution covering as little as 1% of the total body surface (160 cm2) area or exposure to HF of any concentration covering 5% of the total body surface area can be life threatening.[1] Calcium gluconate injections provide fluoride detoxification and improve pain. Intravenous calcium gluconate and locally administered subcutaneous injections are recommended to resolve the pain of the exposed skin area.

Chemical burn injury due to hydrofluoric acid: a case of successful management without hexafluorine

We report an employee working in glass manufacturing who suffered a burn, induced by hydrofluoric acid (HF) as a result of an explosion of an acid container. The patient was admitted to our burn center with second and third degree burn injuries over 5% of his body. The burn improved completely and dramatically without application of hexafluorine because he presented to our burn center expeditiously. The primary goal of all treatment modalities is to prevent deep tissue injury, decomposing fluoride ion chemically. In the treatment of such burns, the wound area should be washed with plenty of water, preferably with bottled water. In addition, the compounds of calcium and magnesium applied topically and hexafluorine have a role in the treatment, where available. Training programs, including first-aid teams, should be prepared for this programs, including first-aid teams, should be prepared for this in order to reduce or prevent the mortality and morbidity associated with HF burns. Keywords: Hydrofluoric acid, Burns, Hexafluorine

A review of hydrofluoric acid burn management

Hydrofluoric acid (HF) causes a unique chemical burn. Much of the current treatment knowledge of HF burns is derived from case reports, small case series, animal studies and anecdotal evidence. The management can be challenging because clinical presentation and severity of these burns vary widely. Plastic surgeons managing burn patients must have a basic understanding of the pathophysiology, the range of severity in presentation and the current treatment options available for HF burns. The present article reviews the current understanding of the pathophysiology and systemic effects associated with severe HF burns. Furthermore, it distinguishes between minor and life-threatening HF burns and describes several of the basic techniques that are available to treat patients with HF burns.

Hydrofluoric acid HF burn injuries decontamination in ex vivo human eye and skin models

Hydrofluoric acid HF burn injuries decontamination in ex vivo human eye and skin models

Hydrofluoric Acid Burns: Rational Treatment

I commend the message underlying the article by Stuke et al.1 An interest in extravasation injuries2 preceded my interest in hydrofluoric acid (HF) burns. Many years ago, I was asked to see a renal patient who had had an intravenous extravasation of 10% calcium gluconate, a hyperosmolar agent that causes devastating tissue destruction. Subsequently, I was referred my first case of HF burn affecting the right (dominant) hand of a glass worker. I was presented with a patient with a tense swollen thenar eminence by a pleased looking emergency physician holding a 5-ml syringe and a half empty vial of 10% calcium gluconate. It was with extreme alarm that I decompressed the thenar eminence with hyaluronidase. The dismayed doctor showed his manual that described subcutaneous infiltration with 10% calcium gluconate for hand HF burns. This stimulated the most extensive and intellectually rigorous review of the published literature pertaining to HF burn and their management.3 We also developed a series of algorithms for treating cutaneous, inhalation, ingestion, and eye burns involving HF.4 It is interesting to note that the management we recommended in 1995 is the one supported by the clinical experience of the Parkland Memorial team. Another published algorithm for HF burns appeared in an article from Brisbane.5 This detailed a series of algorithms based on supposed clinical experience and the “novel” use of dimethyl sulfoxide, although we had discussed this fully in our previous review.3 Our commentary to that article points out other fundamental and misleading statements regarding HF burns.6 I have had to express caution about the dangers of intraarterial infusion following reports in other journals, including The Journal of Burn Care and Rehabilitation.7,8

Hydrofluoric Acid Burns: A 15-Year Experience

Hydrofluoric acid (HF) is a strong inorganic acid commonly used in many domestic and industrial settings. It is one of the most common chemical burns encountered in a burn center and frequently engenders controversy in its management. We report our 15 year experience with management of HF burns. We reviewed our experience from 1990 to 2005 for patients admitted with HF burns. Primary treatment was with calcium gluconate gel. Arterial infusion of calcium and fingernail removal were reserved for unrelenting symptoms. There were 7944 acute burn admissions to our center during this study period, 204 of which were chemical burns. HF burns comprised 17% of these chemical burn admissions (35 patients). All were men, with a mean burn size of 2.1 +/- 1.5% (range, 1-6%) and hospital stay of 1.6 +/- 0.7 days (range, 0-3 days). The most common seasonal time of injury was in the summer. Twelve patients (34%) were admitted to the intensive care unit for a total of 14 intensive care unit days, primarily for arterial infusions. Ventilator support was not required in any patient. No electrolyte abnormalities occurred. All burns were either partial thickness or small full thickness with no operative intervention required and no deaths. The upper extremity was most commonly involved (29 patients, 83%). The most common cause was air conditioner cleaner (8 patients, 23%). HF is a common cause of chemical burns. Although hospital admission is usually required for vigorous treatment and pain control, burn size is usually small and does not cause electrolyte abnormalities, significant morbidity, or death.

Intra-Arterial Calcium Gluconate Treatment After Hydrofluoric Acid Burn of the Hand

Hydrofluoric acid (HF) is a colorless corrosive acid used in different industrial branches. Exposure to HF typically results from spills, and most often the hand or fingers are involved. Tissue damage through cutaneous HF exposure occurs through corrosive burns due to the free hydrogen ions and through skin penetration of the fluoride ions, causing a depletion of calcium in the deep tissue layers, ultimately leading to cell death and tissue necrosis. Treatment of HF burns consists of thoroughly flushing the exposed area with water and applying calcium gluconate gel to the skin. If topical treatment does not suffice, subcutaneous injections, as well as intravascular--both intravenous and intra-arterial--calcium gluconate therapy, have been advocated. We report for the first time a case of HF burn of the hand and digits associated with vasospasm. Pain and vasospasm were successfully treated by repeated intra-arterial calcium gluconate injection. We conclude that intra-arterial calcium gluconate injection is a successful and well-tolerated therapy for HF burn associated with Raynaud's syndrome. Intra-arterial injection allows for well-controlled delivery of therapy as well as assessment of the vascular status.

Analysis of hydrofluoric acid penetration and decontamination of the eye by means of time-resolved optical coherence tomography

So far the study of chemical burns has lacked techniques to define penetration kinetics and the effects of decontamination within biological structures. In this study, we aim to demonstrate that high-resolution optical coherence tomography (HR-OCT) can close this gap. Rabbit corneas were exposed ex vivo to 2.5% hydrofluoric acid (HF) solution, and microstructural changes were monitored in the time domain by OCT imaging. HF application and penetration resulted in shrinkage of the corneal thickness, interpreted as a result of osmolar changes and of loss of water-binding capacity, and a substantial increase in OCT signal amplitudes. The effectiveness of different rinsing solutions on the chemical burn was also evaluated. With tap water and with 1% calcium gluconate, the deep corneal stroma remained clear until the end of the rinsing period but became opaque afterwards. With Hexafluorine ®, the cornea remained clear for 60 min after rinsing ceased. We conclude that HR-OCT can assist in the clinical evaluation of an ex vivo eye irritation test, and that decontamination of an HF burn using Hexafluorine ® is efficient.

Percutaneous penetration of uranium in rats after a contamination on intact or wounded skin

The aim of this work is to assess in vivo in a hairless rat model, the percutaneous diffusion of uranium through intact or wounded rat skin. Six types of wounds were simulated by excoriation and burns with 10 N HF, 2, 5 and 14 N HNO3 and 10 N NaOH on anaesthetised hairless rats. Percutaneous penetration through wounded skin towards blood and subsequent urinary excretion of uranium was followed in vivo during 24 h. The influence of the physicochemical form (solution or powder) of uranyl nitrate (UN) on its percutaneous diffusion was also investigated. UN, even as a powder, can diffuse through intact skin. The presence of uranium in blood is more persistent and its urinary elimination is slower after an HF burn than after an HNO3 burn. Excoriation increases dramatically percutaneous absorption of UN. Thus, percutaneous diffusion of UN is largely dependent on skin barrier integrity with a particular importance of stratum corneum.

7 cases of hydrofluoric acid burn in which calcium gluconate was effective for relief of severe pain

We report 7 cases of chemical burns due to hydrofluoric acid (HF). The patients suffered from severe pain. However, the pain was relieved after treatment with calcium gluconate. 6 out of the 7 cases were men. At the accidental exposures, all the patients had been engaged in washing or cleaning work and received burns on their hands and/or fingers. In one case, the forearm was also involved. During such work, all the patients had used rubber gloves, but the gloves had pinholes. For the treatments, 4% calcium gluconate jelly was applied in 5 cases and 4 of 7 were subcutaneously injected with 8.5% calcium gluconate. The involved nails were removed in 5 cases. It is concluded that physicians should provide calcium gluconate jelly and subcutaneous injections to treat an HF burn and should not hesitate to remove the involved nails. To prevent chemical burn due to HF, education and reeducation of workers regarding the hazard of this chemical are necessary.

Hydrofluoric acid burns

Objective: The purpose of this article is to report our experience with hydrofluoric acid (HF) burns and to present our management guidelines for these burns, which include a novel way of delivering calcium combined with dimethyl sulphoxide (DMSO) for cutaneous burns. Method: We reviewed our institutional experience from 1977 to 1999 for patients presenting with burns caused by hydrofluoric acid and collected data on age, sex, burn size, anatomical site, method of contact, surgical procedure, and outcome. Results: Of a total of 2310 admissions, 42 HF burns patients were identified during the study period. The average age was 34 years. There were 35 males and 7 females. Seventy-four percent of cases received burns to the upper limb. Median burn size was 1% of the total body surface area. Seventeen percent of patients required a surgical procedure. In 24% of cases, the method of contact was work related and 40% were injured using cleaning products at home or on boats. No deaths were recorded. Conclusion: HF injury is uncommon but problematic burns often requiring surgery. Recommended management: In cases of cutaneous exposure, treatment should commence immediately with 30 min lavage followed by application dimethyl sulphoxide 50% + calcium gluconate 10% in surgical jelly. If hand or forearm is affected, regional intravenous calcium ‘Bier’s block’ using 40 ml 10% calcium gluconate with 5000 U heparin in total final volume of 40 ml may be indicated. Subcutaneous infiltration may be indicated for elsewhere at 0.5 ml/cm 2 burn of 10% calcium gluconate. Persisting pain may require nail removal or arterial calcium infusion.

Hexafluorine vs. standard decontamination to reduce systemic toxicity after dermal exposure to hydrofluoric acid.

Dermal exposure to hydrofluoric acid (HF) may cause severe burns and systemic toxicity. Hexafluorine (Prevor, France) is a product marketed as an emergency decontamination fluid for HF skin and eye exposures. Documentation concerning Hexafluorine is scanty, and a recent study indicates that its ability to reduce HF burns is at most equal to that of water. The present study was conducted to evaluate Hexafluorine's capacity to reduce HF-induced systemic toxicity. Sprague Dawley rats were anesthetized, catheterized in the left femoral artery, and shaved on their back. A filter paper (3.5 x 6 cm) was soaked in 50% HF and applied on the back of each rat for 3 min. Thirty seconds after removal of the paper, a 3-min rinsing with either 500 mL Hexafluorine (group H), 500 mL water (group W), or 500 mL water followed by a single application of 2.5% calcium gluconate gel (group Ca) was carried out. Blood samples were analyzed for ionized calcium and potassium (before injury and 1, 2, 3, and 4 h after) and also for ionized fluoride (1, 2, and 4 h after injury). The animals developed hypocalcemia, hyperkalemia, and hyperfluoridemia after the HF exposure. The only significant difference observed among the groups was in serum potassium at 1 h between group Ca and group W. However, there was a constant trend toward milder hypocalcemia and less pronounced hyperkalemia in group Ca compared to the other groups. There were no differences in the electrolyte disturbances between the Hexafluorine-treated animals and those treated with water only. Five of 39 animals died before completion of the experiment as a result of the HF exposure, one from group Ca and two from each of the other two groups. In this experimental study, decontamination with Hexafluorine was not more effective than water rinsing in reducing electrolyte disturbances caused by dermal exposure to hydrofluoric acid.