Potassium fluoride,anhydrous
           Potassium fluoride,extra pure
           Potassium fluoride,Granular
           Silicon Dioxide
           Hydrofluoric acid
           Synthetic Cryolite
           Potassium Fluoaluminate
           Ammonium bifluoride
           Potassium Bifluoride
           Aluminium fluoride
           Sodium fluoride
           Potassium Fluorosilicate
           Fluorosilicic Acid
           Sodium silicofluoride
           Potassium Hydroxide Flakes
           Magnesium Fluoride
           Magnesium fluorosilicate
           Barium Fluoride
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Hydrofluoric acid causes tissue destruction by two primary mechanisms:

At concentrations >50%, Hydrofluoric acid acidity increases dramatically and it then behaves like a strong acid. The hydrogen ion causes a corrosive burn similar to other acid burns – this damage occurs immediately and results in visible tissue destruction. However, for low-concentration HF burns – which represent the large majority of HF burns – immediate corrosive destruction does not occur in any significant manner and there may be no immediate pain or tissue destruction.

The second, more significant mechanism of tissue destruction is caused by fluoride ions. Liquefaction necrosis of deeper tissues is unique to Hydrofluoric acid because the acid is highly lipophilic and readily penetrates deep into tissue. The molecule then wreaks havoc as it releases its acidic hydrogen ion and fluoride ion in the presence of cations such as calcium and magnesium. This often-delayed reaction is responsible for the ‘pain out of proportion’ to physical examination findings, a result believed to be related to the local hyperkalemia effect secondary to calcium binding. Cell membrane permeability to potassium is increased by local calcium depletion; in addition, fluoride ions are believed to directly inhibit Na+K+ pumps. Both result in local hyperkalemia, neuronal depolarization and intense pain.

Objective: To investigate the effect of early rabbits after hydrofluoric acid burn treated in different ways. Methods: 33 rabbits were used 550 g / L of hydrofluoric acid 5% TBSA burn wounds were randomly divided into three groups. Group A with 13 rabbits, vein infusion of isotonic saline 5 ml * kg-1 * h-1; group B contains 10 rats administered isotonic saline at the same time in different time points intravenous injection 50 g / L calcium gluconate, each 20 mg / kg; group C contan 10 rabbits, with treatment group B and 0.5 h after injury to surgical excision. each group of rabbits were before injury and post-injury time points blood pumping blood detection fluorine, calcium, mortality statistics results ( 1) a, group B after 1.0 h blood injury in rabbits fluorine concentration peak, respectively (8.37 ± 2.62), (8.59 ± 2.25) mg / L, group B is 107 times the pre-injury value .24.0 h in group B lower than in group a (P <0.05) .C 1.0 h after injury group significantly decreased serum concentrations of fluorine (6.20 ± 0.23) mg / L, with a, B group, the difference was statistically significant (P <0.01). ( 2) each group of rabbits serum calcium concentration decreased after injury, 8.0 or 12.0 h for the low value of comparison with the previous injury, when 12.0 h a group decreased by 46%, 32% decline in group B, group C decreased 26% group C and a, group B, the difference was statistically significant (P <0.01) .24.0 h after serum calcium concentration in each group began to rise. (3) a, B, C group of rabbits within 72 h mortality rates were 30.8 %, 12.5%, 0.0%, after the conclusion of hydrofluoric acid burn in rabbits using calcium + escharectomy surgery, the body can quickly reduce blood concentrations of fluorine, reversing fluorosis fatal hypocalcemia and multi-system toxicity damage.