Hydrofluoric Acid Burn Management – Case Presentation

1 Department of Plastic Surgery and Reconstructive Microsurgery, Emergency Clinical Hospital, Bucharest, Romania 2 Clinical Department No. 14, „Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania 3 Department of Internal Medicine, Emergency Clinical Hospital, Bucharest, Romania 4 Clinical Department No. 5, „Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania 5 Department of Urology, „Dr. Carol Davila” Emergency University Central Military Hospital, Bucharest, Romania 6 Clinical Department No. 3, „Carol Davila” University Medicine and Pharmacy, Bucharest, Romania 7 Department of Anesthesiology and Intensive Care, Emergency Clinical Hospital of Bucharest, Romania Corresponding author: Tiberiu Paul NEAGU, Department of Plastic Surgery and Reconstructive Microsurgery, Emergency Clinical Hospital, 8th Floreasca Avenue, 1st District, 01446, Bucharest, Romania. E-mail: dr.neagupaul@gmail.com Abstract

gic and cardiac disturbances 2 , due to fl uoride ions binding with usual ions. Apparently, these ions manifest direct toxicity on myocardial cells due to the fact that they inhibit the adenylate cyclase, therefore, the serum electrolyte levels monitoring is mandatory 3 .
In the department of emergency, the infi ltration of subcutaneous tissue with calcium gluconate solution may reduce the pain. If the burn is localized on the hand, palmar fasciotomy may be taken into consideration, seeing that the infusion of calcium gluconate may cause compartment pressure and necrosis, especially in fi ngers. Intra-arterial calcium infusion is also used in patients with severe HF burns of fi ngers, face and lower extremities 2 .
Immediate surgical excision of the burn areas may be performed if systemic toxicity develops, requiring the maximum intensive care treatment in order to remove the source of fl uoride ions 6 . It also involves irrigation of the burn area with water for at least 15-30 minutes, which prevents rapid skin penetration 2 . Surgical treatment involves blisters debridement, eschars excision, and multiple debridement with auto grafting the defects or using allograft and xenograft for unclean wound bed 6 .

CASE PRESENTATION
A 26-year-old man patient presented to our hospital after a hydrofl uoric burn, secondary to an occupational accident, in an industrial building. He was working with a hydrofl uoric acid solution when drops with a concentration of 17% HF slipped over his left arm. At the scene, the coworkers irrigated the wound with water and applied topical calcium gluconate. In the emergency department, the intravenous infusion of calcium

INTRODUCTION
Medical treatment of hydrofl uoric acid (HF) exposure is highly specialized, many physicians not being familiar with the appropriate management. HF is an extremely dangerous weak inorganic acid, due to fl uoride ions in its structure, being largely used as an industrial raw material, industrial cleaning agent and in household cleaning 1 .
Th e HF concentration is essential for the initial assessment and treatment. It is important to know that the exact concentration of HF and the exposure duration in order to immediately initiate the correct treatment and thus to minimize the patient morbidity and mortality 1 . HF can produce burns in the liquid or vaporous state. Burns larger than 160 cm 2 have serious systemic toxicity 1 . Low concentrations of HF (<20%) are less dangerous and acidic, compared to high concentrations (>20%) which can be deadly and must be immediately treated 2 .
Consisting with the fi ndings of Kirkpatrick and Burd et al. 3 and Upfal and Doyle 4 , the severity rises in some cases, like a concentration >50% HF is, an exposure more than 5% of the body area, inhalation or ingestion of HF 4 . Th e poisoning severity can also rise if there is an increased duration of exposure 5 .
HF skin burns elicit severe pain in the aff ected area 1 , probably related to the released hydrogen and fl uoride ions in contact with normal cations (calcium, magnesium) 5 . Hydrogen ions cause a deep corrosive burn with serious complications, and the fl uoride ions cause liquefaction necrosis 2 .
ECG trace showed a slightly prolonged QT interval ( Figure 2) and the blood gas test revealed a mild metabolic acidosis. Th e calcium, sodium and potassium levels and the ECG trace were monitored all over the admission period, with blood gas tests performed every 2 to 4 hours in the fi rst few days. In addition to the normal burn therapy protocol, the calcium gluconate solution was continuously infused (Figure 3). As HF poisoning can alter serum pseudocholinesterase levels, we measured them specifi cally and in our case and the values were within normal limits. Th e local treatment involved copious lavage with sterile water and Betadine solution, the evolution being rapidly favorable with the burn lesions completely healed over the next week (Figure 4-6). Th e serum calcium levels were constantly monitored for adjusting the calcium gluconate infusion rate, with the QT interval normalizing and maintaining a normal value through the admission period (Figure 7). Th e treatment was stopped after 7 days when the calcium levels returned to normal value. Th e evolu-gluconate was started, after a rapidly evaluation and monitoring. Th e local exam revealed an erythematous lesion localized in the anterior-intern distal part of the left arm, of about 10/10 cm, with moderate pain, normal mobility, sensitivity, pulse and distal capillary refi ll, but with erythematous and edematous skin adjacent to the burn. Calcium gluconate was immediately injected subcutaneously in the involved area (Figure 1). Th e patient was conscious, hemodynamically and respiratory stable and the burn area was almost painless. After the admission in the Burn Unit, we started the standard examination, like serial ECG, chest X-ray, arterial blood tests and permanent monitoring. Th e recorded    induce various symptoms, especially nausea, vomiting, abdominal pain, convulsions, hypotension, cardiac arrhythmias and cardiac failure 7 . However, in our case, the exposure time was short and the treatment very prompt, therefore the systemic manifestation was faded.
Studies have shown that calcium replacement must begin even before the serum calcium levels are determined. If serum hypocalcaemia is already present, the appropriate treatment involve intravenous calcium gluconate infusion, hemodialysis if the potassium and fl uoride serum levels are very high or to treat refractory hypocalcemia 4 . For our patients, calcium gluconate infusion was started in the emergency department and after that, it was immediately injected subcutaneously in the aff ected area, reducing the pain intensity.
Clinical evidence of hypocalcaemia is not usually present, thus, ECG monitoring is important, in order to show the presence of a prolonged QT interval or arrhythmias and to prevent fatal events 2 .
It is well known that an important aspect in managing patients with hydrofl uoric acid burn involve absorption prevention to minimize tissues destruction 8 . HF rapidly penetrates the tissues because it is a lipophilic molecule. Zhang Y, Tepperman and al. emphasize the fact that there are some areas, like neck and face, where the HF can be quickly absorbed into systemic circulation with consecutive poisoning and death 9,10 . Th erefore, wound irrigation with water and topical application of calcium gluconate at the scene was a decisive element for our patient favorable outcome 11 .
Regarding fl uoride excretion, it happens via the kidney, with half of the HF concentration being eliminated during the fi rst 24 hours after exposure. However, tion was favorable and the patient was discharged into the surgical ward after 8 days of intensive care staying.

DISCUSSION
In this type of burn lesions, the patient outcome is strictly related with the HF concentration, the exposure duration and the immediate and correct treatment 2 . Th is chemical burn can be lethal if the treatment is delayed or inappropriate, the systemic poisoning being the most dangerous component of HF burns. It can   ximize the outcome. Topical, subcutaneous and intravenous calcium plays a decisive role in HF burn treatment. Surgical intervention is required only in cases with extensive burn lesions.
Regarding the extent of the chemical burns, it is very important for the medical staff to understand the importance of rapid management of these types of chemical burns and we strongly recommend that a chemical burn protocol must exist in any medical facility.
Compliance with ethics requirements: Th e authors declare no confl ict of interest regarding this article. Th e authors declare that all the procedures and experiments of this study respect the ethical standards in the Helsinki Declaration of 1975, as revised in 2008 (5), as well as the national law. Informed consent was obtained from all the patients included in the study.
it is well known that these ions have toxic eff ects on the nephrons, with consecutive inhibition of sodium and chloride. Stimulating kidney function using diuretics to obtain an increased urine volume is usually used in cases with important systemic toxicity 12 . In case of systemic poisoning, there are some reported case about the use of continuous renal replacement therapy for removing the circulatory fl uoride and for correcting acidbase and electrolyte disturbances 13 .

CONCLUSIONS
HF burns are a very special type of chemical burn. It must be taken into consideration that exposure to a very small amount of solution can be life threatening, especially through cardiac arrhythmias, therefore the immediate treatment being mandatory in order to ma-