To read the full-text of this research, you can request a copy directly from the authors.
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.
To read the full-text of this research, you can request a copy directly from the authors.
... Le tableau 1 ci-dessous décrit par ailleurs les principaux signes et symptômes associés. . Il y a alors apparition d'une nécrose liquéfiante profonde . ...
... Il y a alors apparition d'une nécrose liquéfiante profonde . Suivant la modification de la perméabilité membranaire causée par l'hypocalcémie, une hyperkaliémie peut survenir [5,6]. ...
... Puis, ces désordres électrolytiques vont mener aux manifestations systémiques suivantes : dysrythmies cardiaques (fibrillation ventriculaire, torsades de pointes), tétanie, convulsions, etc.  Le fluor causerait également une toxicité directe sur les cellules myocardiques en entraînant l'activation de l'adénylate cyclase. Ceci augmenterait l'adénosine monophosphate cyclique intracellulaire et pourrait accroître le risque d'arythmies [5,7]. ...
Les brûlures à l'acide fluorhydrique présentent un danger, et elles peuvent menacer la vie des victimes de ce type de brûlure. Comme des produits domestiques ou industriels en contiennent, une mauvaise utilisation de ces produits peut entraîner un accident de travail. Étant donné ses caractéristiques physicochimiques, l'acide fluorhydrique cause des brûlures profondes aux tissus et peut provoquer des anomalies électrolytiques engendrant des troubles du rythme cardiaque. Les professionnels de la santé doivent donc être en mesure de reconnaître la présentation clinique de l'exposition à cette substance toxique afin d'éviter les complications. L'irrigation à l'eau, l'application topique de calcium, l'administration parentérale de calcium (sous-cutanée, au moyen d'un bloc régional intraveineux, intra-artérielle) et les interventions chirurgicales font partie de l'arsenal thérapeutique potentiellement requis dans le traitement des patients souffrant d'une brûlure causée par cet acide, selon leur présentation clinique.
... The degree of injury to a finger due to HFA exposure can be determined by the density of HFA and what appropriate action has been taken at the time of exposure [3,4]. Higher density of HFA will cause more damage that could result in systemic effects . ...
... The degree of injury to a finger due to HFA exposure can be determined by the density of HFA and what appropriate action has been taken at the time of exposure [3,4]. Higher density of HFA will cause more damage that could result in systemic effects . However, even if the HFA is of low density, the degree of damage can be serious if there is insufficient first aid or if the tissue has been exposed for a long time. ...
... No evidence-based guideline is currently available for surgery time or method. Treatments for fingers remain controversial [4,5]. Here, we share our center's methods to care for patients whose digits were exposed to HFA. ...
Occupational injuries to digits due to hydrofluoric acid (HFA) are frequently encountered. They have distinctive features, including intense pain, progressive tissue necrosis, and possible bone erosion. To minimize tissue damage, it is of great importance to execute prudent preoperative assessment and determine the correct surgical modality to reconstruct and maintain the function of the hand. However, proper protocols for fingers have not been presented in previous studies. Eight cases with HFA burn to digits were presented to the emergency room. Wounds were immediately irrigated with saline, calcium gluconate was applied topically to block destructive effects of fluoride ions. Blisters that could lead to progressive tissue destruction were debrided. A fish-mouth fasciotomy was performed and prostaglandin was administered intravenously to maintain maximal distal circulation. Wounds were evaluated daily for apparent demarcation for 6 or 7 days. Digits were reconstructed with free sensate second toe pulp-free flap to provide sufficient padding for the fingertip. All patients showed excellent recovery with stable flaps with acceptable external contour, durable soft tissue padding, and full range of motion of affected joints. In conclusion, when a patient is admitted due to HFA exposure to the finger, early treatment including irrigation, topical neutralizers, and fasciotomy are of great importance to minimize tissue damage. In addition, a physician should wait at least 7days until the degree of damage to the tissue can be classified so that the physician can decide whether aggressive debridement should be proceeded. In case of deep layer injuries of weight bearing portions such as finger pulp, reconstruction techniques utilizing durable tissues such as partial second toe pulp free flap should be employed.
... Cloudy and creamy blisters may gradually occur, with ulcers and tissue necrosis developing in the final stage [2,3]. HF burns are currently managed by removing HF, preventing systemic toxicity, applying supportive treatment, and managing local infection . The common treatment methods include flushing with normal saline, the application of topical calcium ointments, the injection of calcium solutions, and even the surgical removal of affected parts. ...
... The CG gel is suitable as a first-aid treatment for injuries due to its easy administration; however, both the gel and calcium penetrate poorly into tissue, which also limits their use for treating fluoride ions in deep tissues . Although local tissue damage could be addressed, water flushes and neutralizers may not prevent systemic toxicity [4,12]. ...
... After 48 h, the cells in the CG group appeared slender and with an unclear nucleolus and showed significantly decreased cell viability compared to those in the other two groups. In theory, the CG gel could address dissociated fluoride ions on the cell surface and prevent cell death . However, some data have indicated that the CG gel does not adjust pH values; thus, it could not block hydrogen ion penetration into deep tissue. ...
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 48 h). The cell viabilities at 48 h 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.Graphical abstract
... Hydrofluoric acid (HFA) is an inorganic acid commonly used in both domestic and industrial settings for cleaning agents, fertilizer production, and many other uses [1,2]. In the household, HFA can be found in products such as silverware cleaner and herbicides. ...
... On a systemic level, HFA releases fluoride ions that bind to calcium and magnesium, leading to hypocalcemia and hypomagnesemia, respectively. As a result, HFA can lead to significant systemic effects such as hypotension, cardiac arrhythmias, and cardiac failure . ...
... HFA burns are uncommon but unique among chemical burns in that they can cause visually mild burns with significant deep tissue injury and systemic toxicity through a variety of mechanisms. The majority of medical literature discussing these burns is derived from case reports, small case series, animal studies, and anecdotal evidence . ...
Hydrofluoric acid burns are uncommon but unique among chemical burns in that they can cause visually mild burns with significant deep tissue injury and systemic toxicity through multiple mechanisms. We present the case of a patient who presented with bilateral hydrofluoric acid burns to his hands from aluminum brightener. The patient had been using an aluminum brightener with a hydrofluoric acid concentration of 10% for several months at work. On emergency department presentation, the patient endured significant tenderness to his hands and fingers. The patient suffered no serious complications, had no concerning lab or electrocardiographic findings, and was treated symptomatically with calcium gluconate gel. He was discharged home after successful symptom resolution with proper return precautions and instructions on how to safely use hydrofluoric acid containing products. Although not a very common cause of burns, acute care of these burns requires specific knowledge which is imperative for emergency personnel.
... The tissue damage and the degree of toxicity are determined by the acid concentration, the exposure time, the contaminated body surface area, the time elapsed between exposure and decontamination i.e. hospital care , , , and person's age as well , . ...
... Corrosive burns are similar to those provoked by other acids: they occur immediately, with visible tissue destruction, grey areas, ulceration or necrosis, followed by intense pain . The latter is caused by cytotoxic fluoride anion responsible for local and systemic toxicity when HF acid products with high, as well as with low concentrations have been used , . The fluoride ion is very small and diffuses readily in the aqueous media . ...
... Subsequently, the cell membrane's permeability to potassium is increased resulting in local hyperkalemia. High lipid affinity induces liquefaction necrosis and cellular death, thus destructing the nerve and blood vessels, tendons, bone structures and all other tissues , . These effects are due to the presence of fluoride ion and differ from other acids, in which the feature of the free hydrogen cations to provoke coagulative necrosis, which retards the further penetration into the tissues, is expressed , . ...
BACKGROUND: Hydrofluoric acid is a commonly used chemical in many industrial branches, but it can also be found as an ingredient in household products such as cleaning agents. Possessing high corrosive potential, HF acid causes burns and tissue necrosis, while when absorbed and distributed through the bloodstream, its extremely high toxic potential is expressed. Acute symptoms are often followed by pain, particularly in the case of skin burns, which intensiveness does not often correlate with the expressiveness of the clinical findings. Even exposure to low-concentrated solutions or gasses, or low-doses of high-concentrated acid, may provoke delayed systemic disorder which may eventually have a lethal outcome.
AIM: Therefore, having information regarding the possible hazardous effects of hydrofluoric acid usage, a variety of symptoms, as well as a treatment approach, is of great importance in the case of HF exposure.
METHODS: Available scientific articles published in literature databases, scientific reports and governmental recommendations from the internet websites, written in English, using the following search terms “Hydrofluoric acid, skin burns, eye injury, ingestion, inhalation, systemic toxicity, decontamination, antidote, medical treatment” have been reviewed.
RESULTS: This review is useful not only for physicians but for everyone who may come in contact with a person exposed to HF acid.
CONCLUSION: It highlights the mechanism of action, presents the acute and chronic symptoms, personal and general protective measures and devices that should be used, as well as decontamination procedures, immediate, antidote and hospital medical treatment.
... The latter step is responsible for the hallmark severe pain of HF burns, which is a result of local hyperkalemia secondary to calcium depletion by binding of the fluoride ions to the tissue calcium ions 6 . The morbidity of the burn is directly proportional to the concentration of HF, the duration of exposure, and the appropriate emergency measures taken after contact with the acid 1,7 . The main objective in the treatment for HF burns is to neutralize the fluoride ions into insoluble salts as much as possible before they penetrate deeper into the tissue 8 . ...
... Fluoride ions being highly permeable and lipophilic, easily penetrates the tissue and binds to the divalent cations calcium and magnesium depleting the local storage of these ions 5,9,20 . Local calcium depletion increases membrane permeability to potassium resulting in local hyperkalemia and depolarization which is responsible for progressive liquefaction necrosis, bone decalcification and the "pain out of pro- portion", a hallmark excruciating pain in HF burns 1,8,21 . Therefore, immediate emergency actions are important in minimizing damage, with the first step being thorough washing of the affected area with ample running water 5,9,22 . ...
... Kono et al. 27 reported a profound electrolyte imbalance including hypocalcemia, hyponatremia in the animals exposed to 50% HF. Our animal experiment protocol was exposure of 20% HF for 5 min, as exposure to higher concentrations of HF in real life may require more than topical treatment 1,7,8 . The mice treated with CGF-3 showed complete recovery of wound after 7 d of treatment. ...
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.
... The potassium channel is forced open by calcium-dependent inhibition on Na + /K + -ATPase, which causes hyperkalemia. Myocardial adenylate cyclase is activated by fluoride ions, which increases cAMP and stimulates the myocardium, inducing refractory and fatal arrhythmia . ...
... A review of several journals of emergency medicine [2,4,5] showed that patients exposed to high-concentration HFA died from fatal arrhythmia within 1 hr in many reported cases. In the present case, the patient's general condition quickly worsened after the injury. ...
... Chemical burns from hydrofluoric acid cause immediate tissue destruction through 2 mechanisms: corrosive hydrogen ion activity causes immediate tissue destruction, and fluoride ions cause liquefaction necrosis to deep tissues . The morbidity of the chemical burn is directly proportional to the concentration, duration of exposure, and timeliness of treatment . ...
... Chemical burns from hydrofluoric acid cause immediate tissue destruction through 2 mechanisms: corrosive hydrogen ion activity causes immediate tissue destruction, and fluoride ions cause liquefaction necrosis to deep tissues . The morbidity of the chemical burn is directly proportional to the concentration, duration of exposure, and timeliness of treatment . Chemical injuries involving the eyes and eyelids can result in severe sequelae including exposure keratopathy. ...
Severe chemical burns can damage the periocular area causing exposure keratopathy and resulting in ocular pain, foreign body sensation, epiphora, photophobia, and vision loss. A custom fit large diameter therapeutic scleral lens can protect the ocular surface by preventing desiccation and providing immediate improvement in comfort. This case describes the management of a patient with extensive chemical burn with complete lid loss and exposure keratopathy who has maintained excellent visual acuity and comfort with therapeutic scleral lens use.
... 5,59 Even though HF etching can effectively improve the bond strength between glass ceramics and resin cements, it is a dangerous, toxic and highly corrosive inorganic acid. 10,59 HF at high concentrations (>50%) can cause severe morbidity and death, 4,30 although at low concentrations (about 5%), it may already pose a risk to the human body. 14 In addition, studies have reported that surface treatment with HF etching increases ceramic roughness by the presence of microporosities, which in turn may act as sources of crack initiation and lead to weakening of the mechanical properties of glass ceramics. ...
... It is important to highlight the better performance of the E&P 20s + 5min protocol over HF5 + SIL in such a scenario, since hydrofluoric acid is a hazardous substance. 4,10,14,30,59 However, the E&P 20s + 5min group can be considered a time-consuming protocol. The etching time recommended by the manufacturer (E&P 20s + 40s) is more clinically friendly, and both treatments presented similar long-term bond strengths. ...
Purpose: To evaluate the effect of different etching times of a self-etching ceramic primer on the microshear bond strength (µSBS) and topographic surface pattern of a lithium-disilicate glass-ceramic.
Materials and methods: Ceramic slices were subjected to an in-lab simulation of CAD/CAM milling and randomly allocated to 10 groups (n = 35) considering two factors: "surface treatment" in 5 levels - one control group (5% hydrofluoric acid + silane application [HF5+SIL]), and 4 experimental groups using ceramic etching/primer (Monobond Etch & Prime, E&P) with different passive application times (40 s, 2 min, 5 min, or 10 min); and "aging" factor in 2 levels - short-term (after 24 h), or long-term (storage for 180 days + 12,000 thermal cycles). Composite cement cylinders were built and µSBS tests were run in a universal testing machine. The failure patterns were categorized, and complementary analyses with SEM and Atomic Force Microscopy (AFM) were performed.
Results: The groups showed statistically similar bond strengths in the short term (range 22.4 to 25.1 MPa). However, only the E&P 20s+40s (19.3 MPa) and E&P 20s+5min (21.5 MPa) groups maintained stable bond strength in the long term, and HF5+SIL (17.1 MPa) presented statistically significantly lower values than did E&P 20s+5min. The failure pattern was predominantly adhesive. The increased application time of the ceramic primer promoted greater dissolution of the glass matrix; thus, the E&P 20s+10min group presented the most complex surface characteristics in the fractal dimension analysis.
Conclusion: The self-etching ceramic primer can be used as an alternative to classical conditioning with HF plus silane, promoting stable bond strength for etching times of 40 s or 5 min of passive application.
Keywords: CAD/CAM; adhesion; fractal dimension; glass ceramic; surface treatments; topographical changes.
... Acids cause tissue coagulation and collagen shrinkage, however, the binding of the ocular proteins to acids, creates a buffering effect, resulting in the prevention of deeper penetration of the agent. Trifluoroacetic acid and hydrofluoric acid are exceptions since they cause deeper injury by hydrogen and fluoride ions they own . ...
Ocular trauma affecting the anterior segment of the eye including conjunctiva, cornea, sclera, iris, and lens may be chemical, mechanical, or thermal. Although the eyelids and tear film layer act as a barrier for mild traumas, severe traumas need thorough evaluation and prompt management to prevent catastrophic complications, such as vision or globe loss. The initial treatment approaches to chemical injuries of the eye, abrasion, foreign body and lacerations in the conjunctiva, cornea and sclera, hyphema, secondary glaucoma, and traumatic cataract along with the examination with imaging techniques and history taking tips are going to be discussed in this chapter.
... It is well-established that HF is capable of causing significant local toxicity via chemical burns, as well as potentially lethal systemic toxicity following large dermal, or oral, exposures. 9 Dissociated fluoride ions aggressively bind to extracellular and intracellular calcium and magnesium, resulting in local cell death, and potential cardiac toxicity secondary to hypocalcemia and hypomagnesemia. Perhaps less well-known is similar potential for systemic toxicity associated with exposure to AB-containing products. ...
... Although these methods provide short-step approaches to 1, they have several disadvantages from the viewpoint of cost/safety of reagents. In particular, 3 is still expensive and concentrated aqueous HF is notoriously toxic (Mckee et al., 2014). We report here a safe, low-cost, two-step method for the synthesis of 1a using calcium carbide CaC 2 (7) as an ethynyl group source. ...
Stannylation of calcium carbide followed by Sn–hypervalent iodine(III) exchange reaction cleanly afforded the electrophilic ethynylating agent ethynyl(phenyl)-λ3-iodane in high yield. This two-step method uses very inexpensive materials and is readily operable without any special precautions.
... CaCO 3 dispersions were added first and D-Glucono-δ-lactone (GDL) solutions were afterwards added dropwise, using a micro-pipette. GDL was chosen, as it is already used in some medical products, where it serves as irrigation solution to prevent clogs in bladder catheters and is applied for hydrofluoric acid burn management in the form of calcium gluconate gels [38,39]. The initial concentrations of CaCO 3 dispersions were 20, 50 and 80 mM and corresponding GDL solutions always had twice the concentration (40, 100 and 160 mM respectively), leading to the final values seen in table 1. ...
Many different biofabrication approaches as well as a variety of bioinks have been developed by researchers working in the field of tissue engineering. A main challenge for bioinks often remains the difficulty to achieve shape fidelity after printing. In order to overcome this issue, a homogeneous pre-crosslinking technique, which is generally applicable to all alginate-based materials, was developed in this study. With this technique it was possible to markedly enhance the printability of a 2 % (w/v) alginate solution, without using a higher polymer content, fillers or support structures. It was possible to print 3D porous scaffolds with a height of around 5 mm. Furthermore, the rheological behavior of different pre-crosslinking degrees was studied. Shear forces on cells as well as the flow profile of the bioink inside the printing nozzle during the process were estimated. A high cell viability of printed NIH/3T3 cells embedded in the novel bioink of more than 85 % over a time period of two weeks could be observed. Furthermore, also the Young's Modulus of selected hydrogels, as well as the chemical characterization of alginate in terms of M/G ratio and molecular weight, were determined.
... They form insoluble salts with calcium and magnesium, but soluble salts are also formed with other cations, which dissociate rapidly releasing more fluoride ions, which cause further tissue destruction and delayed symptoms and signs. These acids thus cause tissue damage by two mechanisms, corrosive burn by the free hydrogen ions and chemical burn by tissue penetration of the fluoride ions . ...
Chemical eye injury (CEI) is an acute emergency which can threaten sight and life. These commonly occur at home or the workplace with the former being generally mild and the latter more severe and bilateral. Major workplace accidents involve other parts of the body and can be associated with inhalation or ingestion of the chemical. Alkali injuries cause damage by saponification of tissue and deeper penetration as a consequence. Acid injuries cause rapid coagulation of tissue, which impedes penetration and limits damage. Irritants such as alcohols, cause superficial epithelial denudation. Severe chemical insult can affect all anterior segment structures causing iris, pupil and lens abnormalities. Eye pressure is variably affected and can be low or high or start as one and rapidly change to the other. Chorioretinal changes in the form of vasculopathy are seen and ascribed to be secondary to anterior segment inflammation rather than due to the direct effect of CEI. Final outcome related to structure and function is determined by the injurious agent, duration of exposure, nature of treatment and the rapidity with which it is instituted. Prevention of further damage by profuse and prolonged eye wash, after ascertaining pH of both eyes, together with exploration and removal of all particulate matter, is the key. Other management principles include a complete and thorough assessment, control of inflammation, facilitation of healing and prevention and management of sequelae and complications. Intraocular pressure is often forgotten and must be assessed and managed. Management often requires a multidisciplinary approach.
... First, the contaminated clothing should be quickly removed and the skin wiped with clean gauze, rinsed with a 4 % solution of sodium bicarbonate, and then with saline (14,15). Thorough debridement of the wound should follow, and then an early escharotomy and delayed skin graft in case of deep wounds (16,17). These steps are critical, since early escharotomy can remove the surface of the tissue that contains monochloroacetic acid and reduce further corrosion of the tissue. ...
The patient, a 45-year-old male chemical factory worker, was burned by monochloroacetic acid discharged from a ruptured pipe. The patient was merely flushed with water and did not leave the workplace immediately. As a result, he suffered local burn symptoms, which gradually worsened. Two and a half hours after the accident, he developed symptoms of systemic poisoning, such as lethargy and dyspnoea. After a thorough debridement of the wound surface and subsequent skin grafting combined with early glucocorticoid therapy and haemofiltration, a satisfactory result was achieved, and the patient eventually recovered. With the widespread use of monochloroacetic acid in China, incidents of poisoning with this chemical are becoming increasingly common, with more than 100 cases reported in the past ten years in China alone.
... One of the main approaches involves chemical etching of the TiO 2 surface using hydrofluoric acid after the anodization process [19,20]. Unfortunately, this technique relies on an environmentally hazardous chemicals, which can cause severe fluoride-related health conditions . Another widely used method is ultrasonication, where mechanical forces break the top-layer nanograss structures [22,23]. ...
A single-step anodic fabrication of TiO2 nanotubes (TNT) without a surface layer of nanograss was attained in electrolytes containing diethylenetriamine-pentaaceticacid (DTPA) as chelating agent. The role of DTPA concentration and anodization voltage on the final TNT morphology was studied. We discuss chemical aspects of the DTPA effect over the surface of TNTs as well as the physical properties of TNT samples prepared under several anodization conditions. We demonstrate that the DTPA concentration has a significant effect on the final surface morphology of TNTs, leading to a surface free of nanograss. Furthermore, we propose a mechanism that explains this phenomenon.
... Bur grinding (BG) in composites and acid etching in ceramics are standard procedures for enhancing bond strength and removing contaminated surfaces in repair process (Akyil, Yilmaz, Karaalioglu, & Duymus, 2010;Kirmali, Kapdan, Harorli, Barutcugil, & Ozarslan, 2015). However, tissue contact with HF may cause severe burns (McKee, Thoma, Bailey, & Fish, 2014). Therefore, using HF for intra-oral repair of the restorations has a potential risk. ...
This study intended to compare the repair bond strength of computer‐aided design/computer‐aided manufacturing (CAD/CAM) blocks consisting of resin and feldspathic ceramics following different surface treatments using the microtensile bond strength (μTBS) test. Ten specimens were prepared with 4 mm height for Vita Enamic (VE), Lava Ultimate (LU), Vita Mark II (VM), and thermocycled (10,000 cycle, 5–55°C). Each material was categorized into one of five subgroups according to following surface treatments: (a) bur grinding (BG), (b) hydrofluoric acid etching (HF), (c) neodymium‐doped yttrium aluminum garnet (Nd:YAG or NY), (d) erbium‐doped yttrium aluminum garnet (Er:YAG or EY), and (e) erbium, chromium‐doped yttrium, scandium, gallium, and garnet (Er,Cr:YSGG or ECY) laser conditioning. After surface treatment procedures, specimens were properly restored to 4 mm high with a micro‐hybrid composite resin. Bar specimens (1 × 1 × 8 mm) were obtained using a low‐speed cutting machine and then thermocycled (10,000 cycle, 5–55°C). The μTBS was tested at 1 mm/min crosshead speed, and failure modes were evaluated. Data were analyzed with two‐way ANOVA and post hoc Tukey tests. LU‐BG showed significantly higher μTBS (32.94 ± 5.80 MPa) compared to LU‐laser groups (p < .05). VE‐BG showed significantly higher μTBS (22.06 ± 4.26 MPa) compared to other VE groups (p < .05). Among the laser groups, the NY laser produced the lowest (p < .05) μTBS for LU (13.42 ± 3.44 MPa) and VE (2.27 ± 0.85 MPa), while EY showed the highest (p < .05). Laser‐treated VM groups were all prefailured. VM‐HF produced a higher μTBS (18.73 ± 3.75 MPa) than VM‐BG (5.05 ± 1.76 MPa) (p < .05).
... Se utiliza ampliamente en agentes de limpieza, removedores de óxido, en la industria de semiconductores y para la fabricación de fertilizantes, pesticidas y algunos plásticos. Los efectos sistémicos están relacionados principalmente con alteraciones electrolíticas, principalmente hipocalcemia, pero también con hipomagnesemia, acidosis, fluorosis e hiperpotasemia, que pueden provocar alteraciones de la función renal, hepática y cardiaca . ...
Las enfermedades pueden generar un desequilibrio de electrolitos como parte de su fisiopatología, al igual que los medicamentos usados crónicamente y algunas sustancias tóxicas disponibles en nuestro medio. A pesar de todos los datos estadísticos existentes, la incidencia global de los trastornos electrolíticos secundarios a fármacos o sustancias tóxicas permanece desconocida, y, posiblemente, subregistrada; por lo tanto, el objetivo de esta revisión es analizar los trastornos electrolíticos que causan algunos medicamentos y sustancias tóxicas, y describir el mecanismo a través del cual se producen las alteraciones, en particular, del sodio, potasio, magnesio, calcio y fósforo, con el fin de alertar a los profesionales de la salud en el momento de enfrentarse a este tipo de condiciones en su práctica clínica. El conocimiento de los efectos adversos relacionados con medicamentos y tóxicos es importante para prevenir, identificar y gestionar de forma eficaz, complicaciones que son potencialmente peligrosas. Esta revisión pretende ser un referente de apoyo para los profesionales de la salud en estas situaciones.
... This inorganic chemical is one of the most dangerous acids known. At concentrations >40%, skin contact with small amounts of HF can cause a corrosive burn, which immediately results in severe tissue destruction (McKee et al., 2014). Moreover, HF is highly lipophilic and quickly penetrates deep into tissue. ...
Pollen analysis is one of the most important methods to reconstruct past climate change and to understand prehistoric and early historic human-environment interactions. Every study based on fossil pollen assemblages from sedimentary archives starts with the preparation of collected sample material. The most widely employed protocols to concentrate pollen involve the use of several chemicals including hydrofluoric acid (HF), which is extremely hazardous to human health. As an alternative to HF, we have tested the reliability of dense media separation using two non-toxic substances, sodium polytungstate (SPT) and lithium heteropolytungstate (LST). Our test, which is based on five different samples representing different palaeoenvironmental archives partly revealed statistical disagreement between HF-treated samples and those treated by SPT and LST. In most cases, the observed differences in taxa proportions of the SPT and LST samples are unidirectional. In general, they do not appear to be pollen-taxa-specific but sample-specific thus probably linked to properties associated with the respective study material. However, sample comparison indicates that SPT-based dense media separation produces pollen concentrates that are statistically more comparable to those obtained by protocols based on HF-treatment. Discrepancies between both methods were also recognised for pollen concentrations and generally support the sample-specific character of dense media separation performance as suggested by the pollen proportion comparison. To verify the observed significant differences in pollen proportions and concentrations and to understand the factors that control them, further studies based on a larger number of test samples are required. In addition, we evaluated the effect of ultrasonic-aided fine sieving to bi-saccate pollen types. Our results indicate that this commonly used method to remove clays may lead to fragmentation of bi-saccate pollen into corpora and sacci, thus making identification more complicated. Although more time-consuming, we recommend to use less destructive differential centrifugation as an alternative, if indicated by preliminary tests.
... La toxicité du fluor est due d'abord à la perturbation de l'équilibre électrolytique, principalement l'hypocalcémie, mais aussi l'hypomagnésémie, l'hyperkaliémie, l'acidose, ou encore la fluorose, pouvant induire une IR, hépatique ou cardiaque (McIvor 1987;McKee et al. 2014;Sanz-Gallen et al. 2001). ...
L’uranium (U) et le fluor (F) sont des substances néphrotoxiques naturelles et anthropogéniques auxquelles la population peut être exposée quotidiennement. Cependant, leurs effets à faibles doses restent méconnus et des études précédentes suggèrent qu’une exposition chronique à de faibles doses pourrait induire une réponse adaptative (RA). Afin de mettre en évidence cette RA rénale in vivo, un protocole d’exposition prime à faibles doses suivie d’un traitement challenge néphrotoxique a été mis en place. Une première étude dose-réponse aiguë a permis de définir nos conditions challenge, avec des doses néphrotoxiques de 5 et 7.5 mg/kg d’U et de F, et un temps d’analyse de 72h post-injection. Pour l’étude de la RA, les souris ont été contaminées 6 mois via l’eau de boisson à des doses prime d’U (0, 10, 20 et 40 mg/L) ou de F (0, 15, 30 et 50 mg/L), puis traitées aux concentrations « challenge ». Une RA est observée aux doses respectives de 20 et 50 mg/L d’U et de F, avec un retour à la normale de l’expression et de la sécrétion de biomarqueurs de néphrotoxicité KIM-1 et CLU en comparaison aux animaux non pré-exposés. Une diminution de l’apoptose ou de l’expression in situ de VCAM est observée chez les animaux pré-exposés respectivement à 20 mg/L d’U ou à 50 mg/L de fluor, concentrations auxquelles la RA a été identifiée. L’autophagie, la réponse UPR et le recrutement de cellules inflammatoires sont des mécanismes induits par l’U alors que seule la réponse UPR est induite par le F. Cependant, nos résultats ne permettent pas de les identifier comme des mécanismes impliqués dans la RA, car ces derniers sont induits avec ou sans préexposition. En conclusion, cette étude montre l’existence d’une RA dans le cadre d’une exposition chronique à de faibles doses d’U ou de F chez la souris, avec l’induction de mécanismes adaptatifs tels que la régulation de l’apoptose et de l’inflammation. Ces résultats permettent de mieux appréhender les effets de faibles expositions chroniques chez l’Homme, et d’apporter de nouvelles connaissances pour la radioprotection de l’Homme.
A right-hand-dominant 55-year-old male automotive mechanic presented 24 hours following a hydrofluoric acid burn to the volar left thumb. Despite the severity of soft tissue injury, the neurovascular bundles were intact. Although a free toe-pulp flap is often described to cover volar digit defects, the resultant 6- × 4-cm full-thickness injury of the thumb was too large to be adequately covered by a toe-pulp flap or other commonly used local flaps from the ipsilateral hand. The authors used a superficial circumflex iliac artery perforator (SCIP) flap to reconstruct the volar surface of the thumb from the tip to the metacarpophalangeal joint. They used an arterial anastomosis with the princeps pollicis artery so that the anastomosis was well outside the zone of injury. The patient recovered from the procedure without event and was discharged home on postoperative day 5. At his 2-week postoperative visit, protective sensation with diminished light touch was intact. The authors conclude that the SCIP flap is a technically challenging but versatile, thin flap with minimal donor site morbidity that can be used to resurface the volar aspect of the thumb. The SCIP flap is a valuable resource for the hand surgeon confronted with larger soft tissue defects of the hand.
1 Zusammenfassung 1.1 Hintergrund und Ziele Ziel dieser Arbeit war die Untersuchung des klinischen Langzeitergebnisses adhäsiv befestigter Leuzit-Glaskeramik Inlays und Onlays 14 Jahre nach Eingliederung am Patienten. Bei der Bewertung lag der Fokus dabei vor allem auf der Klebefuge der indirekten Restaurationen. 1.2 Methoden Zwischen 2003 und 2005 wurden 83 Leuzit-Glaskeramik Inlays und Onlays (IPS Empress, Ivoclar Vivadent, Schaan, Liechtenstein) bei 30 Patienten adhäsiv unter Kofferdam eingesetzt. Zur Befestigung wurden zwei verschiedene Vorgehensweisen gewählt: Die Restaurationen der Gruppe 1 (RelyX™ Unicem = RX; n = 43) wurden mit dem selbstadhäsiven Befestigungskomposit RelyX™ Unicem (3M, Seefeld, Deutschland) eingesetzt. In Gruppe 2 (Variolink® II Low = SV; n = 40) wurden die Zähne konventionell mittels Phosphorsäureätzung und Mehrschritt-Adhäsivsystem (Syntac, Ivoclar Vivadent) vorbehandelt. Anschließend wurden die Restaurationen mit Variolink® II Low (Ivoclar Vivadent) befestigt. Die Inlays und Onlays wurden für die vorliegende Arbeit nach 14 Jahren von zwei kalibrierten Zahnärzten nachuntersucht und das klinische Langzeitergebnis anhand modifizierter USPHS-Kriterien bewertet. Zur qualitativen mikromorphologischen Untersuchung der Klebefuge unter dem Rasterelektronenmikroskop wurden über Präzisionsabformungen Replikamodelle auf Polyurethanbasis hergestellt. Patientenbezogene Daten wie Beschwerden oder postoperative Hypersensitivitäten wurden ebenfalls erfasst. Die statistische Analyse erfolgte mit dem Programm IBM SPSS® für Windows, Version 21. 1.3 Ergebnisse und Beobachtungen In der vorliegenden Studie konnten nach 14 Jahren 54 der ursprünglich 83 eingegliederten Inlays und Onlays (≈ 65%) nachuntersucht werden. Zehn der 54 Restaurationen mussten innerhalb der 14 Jahre ersetzt werden. Vier davon wurden bis zum 14-Jahre-Recall als insuffizient bewertet. Die sechs anderen Restaurationen wurden erst bei der 14-Jahre-Nachuntersuchung als erneuerungsbedürftig klassifiziert. Dies entspricht insgesamt einer Verlustquote von 11% nach Kaplan-Meier. Die Gründe für den Austausch waren Bulkfrakturen der Keramik (n = 7), eine Fraktur der Zahnhartsubstanz und Randfrakturen (n = 2). Die Randfrakturen wurden adhäsiv repariert, ohne dass ein Austausch der Restaurationen erfolgen musste. Die restlichen 25 Restaurationen konnten nicht einbezogen werden, da die Patienten nicht zur Nachuntersuchung erschienen. Vier der Inlays/Onlays wurden nach der 4-Jahres-Nachuntersuchung ersetzt, weitere sechs wurden zum Zeitpunkt der 14-Jahre-Nachuntersuchung als Verlust bewertet und kamen sowohl in der RX Gruppe (n = 2) als auch in der SV Gruppe (n = 4) vor. Gruppe 2 (SV) zeigte statistisch signifikant bessere Ergebnisse bezüglich der Farbanpassung und Oberflächenrauigkeit der Klebefuge (Mann-Whitney U-test, p < 0,05). Die Integrität der Restaurationen in den jeweiligen Gruppen (RX ≈ 78 %, SV ≈ 61 %) selbst wurde überwiegend positiv mit alpha 1 oder 2 bewertet. Alle Patienten (≈ 97%) hatten über 14 Jahre keine postoperativen Beschwerden. 1.4 Schlussfolgerung Im Rahmen dieser Untersuchung zeigten beide Verbundmaterialien zufrie-denstellende Langzeitergebnisse. Zwischen den beiden untersuchten Vorgehensweisen der adhäsiven Befestigung gab es außer bei der Farbanpassung und Oberflächenrauigkeit der Klebefuge nach 14 Jahren keine signifikanten Unterschiede.
Background: Hydrofluoric acid (HF) is an extremely dangerous weak inorganic acid, which can produce extensive burn lesions, depending especially on the solution concentration and exposure time, systemic toxicity occurring in patients with large burn areas, high concentration of acid or an extensive time of exposure. The subcutaneous inﬁltration and intravenous administration of calcium gluconate is essential for preventing dyselectrolytemia and severe pain appearance. Case summary: A 26-year-old man patient presented to our hospital after a hydrofluoric burn, secondary to an occupational accident. At the scene, the wound was irrigated with fresh water and topical calcium gluconate was applied. In the Emergency Department, we started the intravenous calcium gluconate administration, and in the Burn Unit it was injected subcutaneously and the pain was thus diminished. A prolonged QT interval was identiﬁed upon admission that has been corrected over the next few days. Particularly, the serum pseudocholinesterase levels were within normal range. The local treatment involved repeated copious lavage with sterile water and Betadine solution, the evolution being rapidly favorable with the burn lesions completely healed in the next week. Conclusion: HF burns are a very special type of chemical burn taking into account that exposure to a small quantity of solution can be life threatening and that the immediate treatment is mandatory in order to maximize the outcome. It is of vital importance that any medical facility had a chemical burn protocol.
Hydrofluoric acid is a caustic compound found in a wide variety of items for household and industrial uses. Dermal exposures can be visually unimpressive on presentation but still have fatal complications. This case review includes a description of a patient presenting with a dermal hydrofluoric acid burn that was effectively treated with topical calcium gluconate gel. Also highlighted are the challenges faced with recognizing the severity and appropriately treating dermal hydrofluoric acid burns in the emergency department.
Critical illnesses, including sepsis, cancer cachexia and burn injury, invoke a milieu of systemic metabolic and inflammatory derangements that ultimately results in increased energy expenditure leading to fat and lean mass catabolism. Burn injuries present a unique clinical challenge given the magnitude and duration of the hypermetabolic response in comparison to other forms of critical illness, which drastically increase the risk of morbidity and mortality. Skeletal muscle metabolism is particularly altered as a consequence of burn-induced hypermetabolism as it primarily provides a main source of fuel in support of wound healing. Interestingly, muscle catabolism is sustained long after the wound has healed, indicating that additional mechanisms beyond wound healing are involved. In this review, we discuss the distinctive pathophysiological response to burn injury with a focus on skeletal muscle function and metabolism. We first examine the diverse consequences on skeletal muscle dysfunction between thermal, electrical and chemical burns. We then provide a comprehensive overview of the known mechanisms underlying skeletal muscle dysfunction that may be attributed to hypermetabolism. Lastly, we review the most promising current treatment options to mitigate muscle catabolism, and by extension improve morbidity and mortality, and end with future directions which have the potential to significantly improve patient care.
Etched fiber Bragg gratings (EFBGs) have been widely employed for refractive index (RI) measurements that can be used to monitor sugar consumption during the fermentation of alcoholic beverages. EFBGs are obtained by removing the cladding of a fiber Bragg grating, which is traditionally performed by a chemical attack with hydrogen fluoride, an extremely hazardous corrosive substance that causes severe wounds and even death. To overcome such drawbacks, this technical note presents a simple, practical, and low cost method for the diameter reduction of single mode optical fibers by mechanical polishing, employing a small scale computer numerical control device and an ad hoc 3D-printed rod. The sensor probe obtained was tested using sucrose aqueous solutions with RIs between 1.333 and 1.394, measured in an Abbe refractometer. The results show a linear shift of the Bragg wavelength with respect to RI with a correlation of 0.928.
Since 2016 there has been a 20-fold increase in known burns injury from personal mobility device (PMD) related fires. The root cause is the failure of high-density lithium ion (Li-ion) battery packs powering the PMDs. This failure process, known as thermal runaway, is well documented in applied science journals. Importantly, the liberation of hydrogen fluoride from failing Li-ion batteries may contribute to unrecognized chemical burns. A clinical gap in knowledge exists in the understanding of the explosive nature of Li-ion batteries. We reviewed the electrochemical pathophysiology of a failing Li-ion cell as it impacts clinical management of burn injuries. This retrospective study was carried out in two major institutions in Singapore. All admitted PMD-related burns and follow up appointments were captured and reviewed from 2016 - 2020. Thirty patients were admitted to tertiary hospitals, 43% of patients were in the pediatric population and 57% were adult patients, aged from 0.3 to 77 years. TBSA of burns ranged from 0 to 80% with a mean 14.5%. 73% of cases presented with inhalation injury, 8 of whom did not suffer any cutaneous burns. 50% of patients sustained both cutaneous and inhalation burn injuries. 27% of patients sustained major burns of >20% TBSA, with 2 in the pediatric group. Mortali ty rate was 10% from PMD-related fires. This cause of burn injury has proven to be fa tal. Prevention of PMD-related fires by ensuring proper battery utilization, adherence to PMD sanctions for battery standards and public education is vital to reducing the morbidity and mortality of this unique type of thermal injury.
Although chemical burns are relatively uncommon, they can be particularly challenging to treat because of the wide variety of chemicals involved. Since each chemical has a unique injury pattern and potential-associated systemic toxicity, it is important to have a set of general principles of management. These principles include self-protection from the injurious agent, early detection of airway involvement, removal and dilution of the chemical, identification of potential systemic toxicity, limited use of neutralizing agents, and careful ocular assessment. Hydrofluoric acid burns are one of the more common, but highly dangerous chemical burns that do require early intervention with a neutralizing agent in addition to application of the above-mentioned principles.
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 (HF) is a highly dangerous substance with a wide range of industrial as well as domestic applications. It is unique in both the severity of the cutaneous burns it may produce, and its potential for systemic and occasionally lethal toxicity. The literature on the treatment of HF injuries is extensive, though occasionally confusing and often contradictory, with no coherent management policy emerging. In this paper we present a comprehensive account of the evolution of therapy, drawing on clinical reports and experimental studies.
Chemical burns to the lower extremity can be disabling and of serious consequence if not managed properly. The severity and rapid onset of the burns caused by hydrofluoric acid after initial contact make this a highly dangerous substance. The potential severity of injury and the following complications make it a chemical of which all physicians should have a basic understanding.
Hydrofluoric acid readily penetrates the skin and mucous membranes, causing deep tissue layer destruction. Dermal exposure can produce hypocalcaemia, hypomagnesaemia, hyperkalaemia, cardiac dysrhythmias and death. We report the case of a 52-year-old man who presented hypocalcaemia and hypomagnesaemia due to occupational dermal contact with hydrofluoric acid. Hypocalcaemia and hypomagnesaemia were corrected by i.v. administration of calcium gluconate and magnesium sulphate.
Hydrofluoric (HF) acid has numerous uses both in industry and the home. HF burns are characterized by intense pain, progressive tissue damage and significant systemic effects. Pain may be prolonged because the fluoride ion remains active despite irrigation of the burn. Subcutaneous infiltration of calcium gluconate is the local treatment of choice. We present a case of hydrofluoric acid burn from rust remover that was effectively treated by topical calcium gluconate baths. A calcium gluconate solution can be prepared with material available in most hospitals and may be readily administered in this fashion. Early recognition and appropriate treatment of hydrofluoric acid burns will provide symptomatic relief and minimize tissue damage.
: Exposure to hydrofluoric acid can cause severe skin damage via both corrosive and chemical means. Dermatologists should be aware of the various clinical presentations and knowledgeable of how to manage such patients. A case of a man with exposure of the hands after use of a consumer product containing hydrofluoric acid is presented. The presentation may vary depending on the concentration and duration of exposure. Patients experiencing exposure are at risk of serious complications, including death, resulting from electrolyte abnormalities. Information regarding the source of exposure will allow the physician to better predict the patient's course. The use of immediate flushing with water and the use of topical calcium gluconate can prevent extensive damage to the area of exposure and potentially fatal complications that may occur. More extensive burns may necessitate more invasive therapies. The treatment and the management and monitoring of such cases will allow for more optimal outcomes.
After studying this article and accompanying Supplemental Digital Content, the participant should be able to: 1. Explain current burn-prevention strategies and criteria for referral to a burn center. 2. Summarize the current advances made in the critical care of acute burn patients. 3. Outline the recent developments in burn depth assessment and burn wound dressing technology. 4. Describe the common psychosocial aspects of postburn rehabilitation.
Burn patients require interdisciplinary care in which the plastic surgeon plays a prominent role. Appropriate referral, assessment, treatment, and posttreatment supports are essential to achieving favorable outcomes following burn injury. The authors reviewed the current literature on epidemiology, prevention, referral criteria, critical care, wound assessment, wound dressings, and psychosocial aspects of burn injury. Recent advances in burn care are highlighted and have been made possible through ongoing collaborative epidemiologic, clinical, and basic biomedical research. A systematic interdisciplinary approach to the evaluation and treatment of acute burn injuries is pivotal to providing patients with the greatest chance of functional recovery. Plastic surgeons treating burn patients must remain current in a wide variety of areas, ranging from critical care to psychosocial rehabilitation.
Based on animal experiments we describe a method of treating H.F. burns of the hand by intraarterial perfusion with calcium gluconate as close to the lesion as possible. We prefer this to intraarterial injection as advised by others because we have treated a series of 13 consecutive cases and know of many others in other hospitals with always yielding good results. We therefore advice the use of this therapy for H.F. burns as the best method available at present.
Although hydrofluoric (HF) acid burns may cause extensive tissue damage, severe systemic toxicity is not common after mild dermal exposure.
A 36-year-old worker suffered a first-degree burn of 3% of his total body surface area as a result of being splashed on the right thigh with 20% HF acid. Immediate irrigation and topical use of calcium gluconate gel prevented local injury. However, the patient developed hypocalcemia and hypomagnesemia, hypokalemia, bradycardia, and eventually had asystole at 16 h post-exposure, which were unusual findings. He was successfully resuscitated by administration of calcium, magnesium, and potassium.
This report highlights a late risk of HF acid dermal exposure.
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.
Fluoride poisoning is a potentially severe environmental hazard for children. A case of fluoride poisong is presented which was manifested by severe hypocalcemia, ventricular arrhythmias, and respiratory failure. Treatment of this poisoning, including peritoneal dialysis, is discussed. The kinetics of fluoride distribution as measured in this patient suggest a rapid binding of ingested fluoride to bone, followed by gradual release and excretion. Peritoneal dialysis resulted in no significant fluoride removal.
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.
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.
Among patients exposed to hydrofluoric acid the potentially lethal effect of calcium depletion induced by binding with fluoride ion has not been well reported. Three patients exposed to hydrofluoric acid had acute fluoride poisoning with serum calcium levels equal to or below 4.1 mgm/dl. Treatment included administration of large amounts of calcium, both intravenously and by subsechar injection, to replenish the biologically active calcium and to bind fluoride. This report describes successful treatment of two survivors, apparently the first two, of severe hypocalcemia caused by hydrofluoric acid.
Generally, chemical burns of the skin, both acid and caustic, are best treated initially by irrigating with copious amounts of water. Subsequently the burn is managed as one would treat a thermal burn. An exception may exist when skin burn is caused by hydrofluoric acid (HF), especially in its anhydrous form. HF is a commonly used catalyst in the petrochemical industry. The following report concerns a life-threatening burn from anhydrous HF.
Significant local and systemic toxicity may occur from hydrofluoric acid by all routes of exposure. Prompt decontamination by removal from the source and copious irrigation of eyes and skin are essential to reduce morbidity and mortality. Ingestion of small amounts of HF can lead to rapid systemic poisoning and death. Calcium gluconate therapy has become the preferred method of detoxifying the fluoride ion, although its efficacy is based mainly on anecdotal reports and poorly controlled clinical studies. Therefore, more basic research is needed to elucidate the pathophysiology of local toxicity and the best therapeutic modalities to limit injury. All significant exposures should be evaluated by health care personnel familiar with the potential toxicity of this compound.
Chemical burns sustained in the microelectronics industry consist mostly of injuries to the skin of the hand and face. The injuries are caused by splashes, holes in gloves, or accidental use of a chemical improperly. The chemical burns of the face primarily involve splashes. Employee education and the ability to intervene swiftly are the foundations of prevention of serious injury. Every facility using hydrogen fluoride should be certain that they have current treatment protocols reviewed by someone with expertise in this area. Furthermore, companies should not assume that all local physicians are knowledgeable about hydrogen fluoride and should educate them as well.
Hydrofluoric acid is one of the strongest inorganic acids and is used extensively in industry and research. It differs from other acids in that the fluoride ion readily penetrates the skin, causing destruction of deep tissue layers and even bone. Authors have previously described numerous topical treatments. This report describes one method of treatment emphasizing immediate skin cleansing and the application of calcium gluconate gel, which is followed by calcium gluconate subcutaneous injections when necessary. An accurate occupational history and physical examination are important aspects of patient assessment. Prompt treatment resulted in relief of pain and a satisfactory clinical result in all cases. A significant delay in treatment was responsible for permanent impairment in 2 of 14 patients.
A 19-year-old man presented with acute fluoride poisoning. Initially his serum electrolytes were normal, but two hours later he developed ECG evidence of hyperkalemia followed by refractory ventricular fibrillation, suggesting that hyperkalemia may be important in the cardiotoxicity of acute fluoride intoxication. Treatment of fluoride-induced hyperkalemia consists of removal of fluoride from the body by dialysis, binding fluoride with aluminum or calcium, or enhancing fluoride excretion by inducing a metabolic alkalosis. Direct treatment of the hyperkalemia with glucose, insulin, and bicarbonate is ineffective. Quinidine may be an effective therapy for the hyperkalemia and ventricular irritability, but is as yet untested in human beings.
Chemical burns account for a relatively small proportion of the patients treated within a burn center; however, certain characteristics of these injuries, particularly in the initial stages of treatment, justify their separate consideration and review. Thirty-five patients were treated in the Baltimore Regional Burn Center from July 1976 through June 1980, with 14 different agents involved. The majority of injuries were work related; however, 20% were the result of assault. All patients received copious water lavage as primary therapy. In approximately one half of the patients this was begun as a first-aid measure at the scene of the accident. Compared to the group which did not receive lavage until admission to the hospital, the patients receiving appropriate first aid showed significantly less full-thickness injury and more than twofold shorter hospital stay, indicating the importance of public and industrial medical awareness of the role of immediate copious lavage. The problems of systemic toxicity with and specific therapy for certain agents is discussed with particular attention given to an unusual case involving cutaneous absorption of dichromate.
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 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.
To determine the effect of continuous intra-arterial calcium gluconate infusion therapy on patients suffering from hydrofluoric acid dermal burns of the digits, clinical treatment was performed prospectively on 10 patients from January 1997 to December 1998 at the burn care unit of Kaohsiung Medical University Hospital. An arterial catheter was inserted transcutaneously through the radial artery of the involved hand. After confirmation of the proper position of the catheter, calcium gluconate was infused continuously with an ambulatory infusion pump. Rapid pain relief was achieved immediately after infusion. The rate of infusion was then tapered down gradually, and treatment was completed with no major therapeutic complication. All injured digits of these 10 patients were successfully salvaged with good cosmetic appearance and complete functional preservation. Compared with other conventional therapies, continuous intra-arterial calcium gluconate infusion therapy proved to be a safe, rapid, simple, portable, and effective method for treating hydrofluoric acid dermal burns.
A young female suffered burns to her hand after the ignition of gas from a compressed air duster. After debridement and dressing, the patient continued to have pain out of proportion to injury that was refractory to intravenous morphine. The material safety data sheet revealed that the chemical used was 1,1-difluoroethane. High temperatures can cause decompensation to form hydrofluoric acid. Calcium gluconate gel was applied topically to the patient's burns, which caused prompt and complete relief of her pain. A review of different compressed air duster products revealed that the main ingredient in each was a halogenated hydrocarbon. Although not considered flammable, all products have warnings regarding the possibility of ignition under various circumstances. Ignition of the gas in compressed air cleaners not only can cause flame burns, it can also cause chemical damage from exposure to hydrogen and fluoride ions. Prompt recognition and treatment is necessary to prevent severe injury.
Hydrofluoric acid (HF) is highly corrosive substance often used in industrial processes. HF burns to the skin cause local tissue injury. Systemic hypocalcemia may ensue, with the potential to produce life-threatening arrhythmias. Medical treatment consists of local application of topical calcium gels, subcutaneous injection of calcium gluconate, and intravenous or intra-arterial infusion of calcium gluconate. Calcium gluconate infusions have been used for HF burns on distal extremities and digits. We report a case of HF burn to the face that was treated by the use of calcium gluconate infusion via the external carotid artery.
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.
The clinician can approach the poisoned patient using the toxidrome system of toxin identification; this approach makes use of findings noted on the physical examination, highlighting the importance of abnormalities in blood pressure, heart rate, respiratory effort, body temperature, mental status, pupillary size, skin color, diaphoresis, and gastrointestinal sounds. Such a method provides structure and guidance to the clinical evaluation, providing the clinician with rapid diagnostic information and suggesting urgent management issues. A case of hydrofluoric acid poisoning is used as an example of this diagnostic approach. The patient demonstrated systemic toxicity accompanied by oral irritation and electrocardiographic abnormality (QRS complex widening and QT interval prolongation). The constellation of these findings suggested the possibility of a caustic agent (history and examination) with potential effect on potassium and calcium metabolism (electrocardiographic abnormalities). Such a constellation strongly suggested hydrofluoric acid as the culprit toxin.
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.
We report an autopsy case of a man who suffered accidental chemical burns following exposure to 60% hydrofluoric acid. The extent of the burns covered about 30% of his body surface, and cardiopulmonary arrest occurred about 30min after the exposure. At autopsy, the skin of the affected area showed greenish gray or black coloring with thin circumferential erythema, and this discoloration extended as far as the periosteum of the skull. However, such discoloration was not found on the mucosa of the airway or the gastrointestinal tract. Microscopically, severe liquefactive necrosis was already evident on the skin. Elastic fibers within the dermis were completely lost, and the entire wall of large vessels within the subcutaneous layer was already severely affected. Blood analysis in the emergency room showed hypocalcemia, and the levels of fluoride ions in the postmortem blood and urine showed extremely high values. However, fewer fluoride ions were detected from the lung tissue. The present case suggests that the hydrofluoric acid had immediately penetrated down into the deep layer of the skin, thereby involving the large vessels present within the subcutaneous layer. These pathological findings of the skin seen in the present case explain the mechanism behind the rapid dissemination of fluoride ions which entered the bloodstream from damaged arteries, resulting in the development of acute toxicity.
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.
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.
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.
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.
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.