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Burns caused by exposure to hydrofluoric acid require immediate First Aid and specific therapeutic measures by the first available physician. Based on a review of the literature the following outline of therapy is proposed.
A 30-year-old man sustained exposure of his eyes, face, and neck involving 4% of body surface area to hydrofluoric acid. He was treated with immediate lavage and topical calcium gluconate. Because free fluoride ions from ocular and facial exposures can form complexes with body stores of calcium and magnesium, the patient was transferred to a burn unit for cardiac and electrolyte monitoring. He was also treated with calcium gluconate skin injections, pulmonary nebulizer therapy, and topical antibiotics and corticosteroids. In another case, a 25-year-old man with less severe exposure to hydrofluoric acid was treated as an outpatient with topical antibiotics, corticosteroids, and cycloplegia. If an ophthalmologist is the first to treat a patient with chemical exposure, the history of hydrofluoric acid exposure must be obtained, and the burn team and other medical specialists must be quickly consulted to avoid potentially fatal complications.
Polysaccharide P (poly P) of canine coagulase-positive staphylococci contains glycerol, glucose, glucosamine, muramic acid, phosphate, and the usual peptidoglycan amino acids, but does not cross-react serologically with standard teichoic acids. Products from hydrolyses in hydrofluoric acid and alkali contained phosphates of glycerol and glucose as well as combinations of these, but neither glucosyl-glycerol units nor glucosamine-phosphates were observed. The teichoic acid of poly P is probably a polymer of a repeating unit consisting of alternating glycerol, phosphate and glucose.
The treatment of hydrofluoric acid burns by injection, as it is recommended by many authors, does not give a satisfactory outcome in cases in which the fingers are involved. In these cases the treatment might be dangerous. However good results are seen after early excision of the burned area and covering the defect with split thickness skin grafts. In a case report the typical course and treatment is demonstrated.
Topical therapy with 2.5% calcium gluconate gel is considered as the "first-aid" treatment of accidental hydrofluoric acid skin burns. The efficacy of three different gel formulations varying in the amount and/or nature of their gelling and moisturizing agents was experimentally evaluated. Thirty male Wistar-Han rats (250 g) were exposed to 60 mul of 40% hydrofluoric acid for 2 minutes on two spots (4 cm) of skin under pentobarbital anesthesia. One lesion was massaged with 1 g of gel (10 rats/type of gel) at 3 minutes; 30 minutes; 1 hour; 1 hour, 30 minutes; 2 hours; 3 hours; and 4 hours after injury. During the next 3 days, rats received a single daily application of gel. The other lesion for each rat remained untreated (control). From day 1 after injury to the end of the study (day 17), gel therapy reduced the number of extensive (-66%), severe (-44%), and moderate (-34%) lesions (P < .0001). It reduced (P < .001) the median Area Under the Curve day 0-17 of burn injury from 34.0 (25th to 75th percentile: 18.2-44.5; untreated lesions) to 17.7 (7.0-26.7); overall, there was three cases of treatment failure. At day 17, full wound recovery was obtained in 14 cases by gel therapy compared with 6 in the absence of treatment. The efficacy of the three gel formulations was comparable for all evaluated parameters. Repeated applications of a 2.5% calcium gluconate gel is an efficient treatment of experimental 40% hydrofluoric acid skin burn; few differences were observed between evaluated gel formulations.
Previous publications on treatment of hydrofluoric acid exposures have given insufficient emphasis to immediate skin cleansing and prompt restitution of both serum and tissue calcium ion levels. Use of calcium gluconate topically as a 2.5% gel, in eyes as a 1% solution, and by nebulizer as a 2.5% or 3% solution has improved treatment results. Ten percent calcium gluconate solution may be given intravenously as indicated for hypocalcemia. Proper application of the calcium gluconate gel immediately after thorough washing of localized skin burns will produce relief of pain similar to that achieved by subcutaneous infiltration of 5% calcium gluconate solution. This may be used as an end-point for adequacy of treatment.
A 35-year-old man attempted suicide by subcutaneous self-administration of hydrofluoric acid (5 cc of a domestic rust removal solution containing 7% hydrofluoric acid). A burn 9 x 7 cm in diameter immediately appeared at the injection site (left forearm and fold of the elbow). In the emergency department, the burn was copiously washed with isotonic solution and treated with cutaneous and subcutaneous injections of magnesium chloride, 10% solution of calcium gluconate, and 2% xylocaine, then continuously maintained under topical treatment with calcium gluconate. Seven hours after injection, the patient was severely hypocalcemic (Ca+2 0.64 mmol/L). Ten hours after injection, in addition to the persistent hypocalcemia (Ca+2 0.81 mmol/L), hyponatremia (123 mmol/d), hypokalemia (3.4 mmol/L), and hypochloremia (95.6 mmol/L) had developed. The hypocalcemia was corrected with infusion of calcium gluconate (8.92 mEq of Ca+2 as total amount). The patient underwent surgical intervention 7 days after admission, followed by several interventions of plastic surgery.
We report a fatal case of hydrofluoric acid (HF) ingestion with suicidal intent. Quantitation using an ion-selective electrode for fluoride in fresh bile, gastric contents, kidney, liver, skeletal muscle, urine, and vitreous humor yielded 6.5, 39.0, 10.0, 6.0, 4.5, 5.0, and 4.5 ppm, respectively. In addition to the unfixed specimens, fluoride ion was measured in the following fixed tissue: brain, heart, kidney, liver, pancreas, stomach, and heart. Tissues were measured directly and/or by using the technique of standard addition. Fluoride concentrations using either method were found to be comparable. Fluoride concentration in fresh tissue was consistent with toxicity, although the urine fluoride concentration was in the range observed for asymptomatic workers exposed to fluoride in air. Fixed tissue preparations revealed fluoride concentrations consistent with nonexposure, whereas examination of the formalin fixative revealed fluoride concentrations only slightly higher than negative control formalin. We conclude that fixed tissues are inappropriate for fluoride determination. This is the first case we are aware of that provides fluoride concentrations in skeletal muscle in a fatality involving HF ingestion.
Hydrofluoric acid (HF) produces a unique chemical burn due to tissue penetration by fluoride ion. Fluoride ion interferes with calcium activity in a variety of cell membranes and calcium-dependent processes, resulting in severe pain and deep tissue destruction. The currently accepted methods of treating HF burns include application of topical soaks or ointments with calcium or magnesium salts for minor burns and local injection of calcium gluconate for more severe burns. Digital burns also may require nail removal and direct injection into the nail bed. We present the cases of a series of patients with moderate to severe HF burns involving one or more fingers who were treated with selective intraarterial calcium infusion of dilute (1.66%) calcium salts. All patients had excellent relief of symptoms and marked improvement of the burn lesions following one to three four-hour infusions of calcium chloride or calcium gluconate. One patient required subsequent surgical intervention for grafting of a full-thickness burn, and one patient developed transient spasm at the site of percutaneous arterial line insertion. Intraarterial calcium infusion for the treatment of HF burns of the fingers provides many therapeutic advantages, including elimination of painful calcium injection directly into fingertips, avoidance of debilitating procedures such as fingernail removal, and assurance that all affected cells are receiving adequate amounts of calcium to replenish depleted stores and to complex with remaining free fluoride ion.
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.
A chemical-plant worker sustained hydrofluoric acid burns during cleaning procedures. Intra-arterial perfusion and intralesional injections of calcium gluconate solution prevented progression of the burns into deeper tissue layers.
Several topical treatments for hydrofluoric acid dermal burns (Zephiran, calcium acetate and magnesium hydroxide antacid soaks, and calcium gluconate gel) were assessed for efficacy in a pig model. Gross appearance and histopathology of treated and untreated burn sites were evaluated. For superficial burns, Zephiran was most effective; calcium acetate, magnesium hydroxide antacid, and calcium gluconate gel were less effective. For deep burns, gross observations showed that calcium acetate and Zephiran were most efficacious, whereas histopathology indicated comparable efficacy of Zephiran, calcium acetate, and calcium gluconate gel for all skin layers. Magnesium hydroxide antacid demonstrated efficacy only for the subdermis. The clinically beneficial effects of both Zephiran and calcium gluconate gel were affirmed. Although results suggest that calcium acetate and magnesium-containing antacids may be beneficial for human hydrofluoric acid dermal burns, these are not established clinical treatments.
A case of suicidal ingestion of hydrofluoric acid is presented. Death of the victim while in police custody was one of the more unique aspects of the case. This is the sixth case of poisoning of this type reported in Dade County. Clinical, pathological, and toxicological aspects of fluoride poisoning are discussed.
A case of hydrofluoric acid (HF) burns of the eye is reported and a review is presented of our investigation into the mechanism of HF toxicity in ocular tissues. A number of therapeutic procedures that have been successful in the treatment of HF skin burns were studied in the rabbit for use in the eye. Immediate single irrigation with water, normal saline or isotonic magnesium chloride solution is the most effective therapy for ocular HF burns. Extrapolation of other skin burn treatments to use in the eye is unacceptable due to the toxicity of these agents in normal eyes and the additive damage caused in burned eyes.
BACKGROUND: Case reports have identified hydrofluoric acid (HF) as causing fatal work injury, and HF has both local and systemic toxicity. Surveillance for HF-related mortality is problematic because of the lack of unique coding for this acid in hospital records and vital statistics. METHODS: We identified HF-related fatal work injuries investigated by the Occupational Safety and Health Administration (OSHA) for 1984-94 from coding of Hazardous Substance 1460 (HF) and requested case investigation files under the Freedom of Information Act. We attempted to identify HF-related deaths in the US for the same period through literature case reports, the Consumer Product Safety Commission, and the American Association of Poison Control Centers (AAPCC). RESULTS: For the 11 year period, OSHA investigated nine deaths in eight incidents which involved HF. Four deaths were from skin contact with concentrated HF, and five deaths involved both skin contact and inhalation of vapor. Unsafe work practices were factors in all of the deaths. Calcium chloride or gluconate was noted to have been administered to five of the nine victims. Calcium was administered 90 min after exposure to two victims, and more than 6 h after exposure to a third. We were able to establish that the regional poison control center had been contacted in regard to only one victim. For the period 1984-94, we were able to identify no additional deaths from CPSC reports, one additional death from AAPCC annual reports, and four other deaths from case reports in the medical literature. CONCLUSIONS: For the period of this study, OSHA records identified the greatest number of HF-related fatalities. The limited information in the records suggest that some victims did not receive appropriate medical care, nor was the regional poison center contacted regarding care. The full extent of health problems related to HF could be better quantified if usual surveillance sources, such as vital records, included unique coding for this acid.
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.
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.
A case of accidental oral poisoning with hydrofluoric acid in an adult is presented. The patient ingested the product from a drinking glass, mistaking it for water, and died approximately 90 minutes after the exposure. Severe acidemia and hypocalcemia were present, which resulted in refractory asystole. A plasma fluoride determination showed an extremely high fluoride level.