a) Thoroughly irrigate skin immediately after exposure. Patients with early decontamination do well. Patients with pain should be treated with topical calcium therapy. TOPICAL - Treat with calcium gluconate or carbonate gel (1 g calcium gluconate in 40 g (about 40 mL) water-soluble lubricant = 2.5% gel; alternative is 10 10-g tablets crushed to fine powder + 20 mL water-soluble lubricant mixed into a slurry; apply thin coat to burn, then place hand in glove containing 10 mL slurry for 4 hours). SUBCUTANEOUS - Inject 0.5 mL/cm(2) with 10% calcium gluconate for topical treatment failures (not commonly used).
b) Do not use calcium chloride for bier block procedures. Calcium chloride is irritating to the tissues and may cause injury.

a) Patients with pain not responding to topical calcium can be treated with regional venous or arterial perfusion. These methods are particularly effective for fluoride exposures involving the digits. BIER BLOCK - Inject IV 10 to 40 mL calcium gluconate in 50 mL normal saline for 20 minutes. ARTERIAL - 10 to 20 mL of 10% calcium gluconate in 50 mL D5W. Infuse over 4 hours via radial or brachial artery. The arterial catheter may be placed in normal position (not inverted).
b) Do not use calcium chloride for bier block procedures. Calcium chloride is irritating to the tissues and may cause injury.

a) PREHOSPITAL: For dermal exposure, remove clothing and irrigate skin thoroughly with water.
b) HOSPITAL: Irrigate exposed skin. Remove all exposed clothing and jewelry taking necessary precautions to prevent secondary exposure to health care providers. Irrigate exposed areas promptly with copious amounts of water for at least 30 minutes.

a) CASE REPORT: Two children developed systemic fluorosis, hypocalcemia, prolonged QTc interval and ventricular fibrillation after ingesting a solution containing 15.9% ammonium bifluoride (Klasner et al, 1996). Ventricular dysrhythmias developed 3 and 3.5 hours after exposure in these children.
b) Fluoride ingestion has caused arrhythmias consistent with hyperkalemia (Baltazar et al, 1980).
c) CASE REPORT: After ingesting ammonium bifluoride in Armor All Quicksilver Wheel Cleaner (Clorox), a 3-year-old girl experienced bradycardia, a bradysystolic arrest, and hypoxemia. She died approximately 90 minutes postingestion (Mullins et al, 1998).
d) CASE REPORT: Another child developed dysrhythmias including ventricular fibrillation and torsades de pointes after ingesting Rust Bust'R (Core Products) (less than 30% ammonium bifluoride). She died approximately 4 hours postingestion (Klasner et al, 1998).

a) CASE REPORT: A 2.5-year-old boy developed increased salivation, rhonchi and tracheal inflammation after ingesting a solution containing 15.9% ammonium bifluoride (Klasner et al, 1996).
b) CASE REPORT: A 3-year-old girl died approximately 90 minutes after ingesting ammonium bifluoride in Armor All Quicksilver Wheel Cleaner (Clorox). Severe pulmonary hemorrhage, and hemorrhagic necrosis of the pharynx, esophagus, and stomach were noted on postmortem examination (Mullins et al, 1998).
c) Inhalation of ammonium bifluoride can severely irritate and burn the nose, throat and lungs, causing epistaxis, cough, wheezing and dyspnea((NJFS, 2003))

a) Fluoride ingestion may first stimulate, then depress respirations. Death may occur from respiratory paralysis.

a) CNS depression may develop after ingestion (HSDB , 2001).
b) CASE REPORT: Two children developed systemic fluorosis, hypocalcemia, and became unresponsive after ingesting a solution containing 15.9% ammonium bifluoride (Klasner et al, 1996).

a) Paralysis may develop after ingestion (HSDB , 2001).

a) CASE SERIES: Two children developed mental status changes, marked hypocalcemia, and ventricular fibrillation after ingestion or inhalation of ammonium bifluoride in Armor All Quicksilver Wheel Cleaner (Clorox) (Klasner et al, 1996).

a) Fluoride poisoning with stomach pain, weakness, convulsions, collapse and death may occur following very high exposure((NJFS, 2003)).

a) Ammonium bifluoride is a corrosive (due to hydrogen fluoride release) and may cause corrosive effects if it comes in contact with the oral or gastrointestinal mucosa ((NJFS, 2003)).
b) CASE REPORT: A 3-year-old girl developed a gastric ulcer after ingesting a solution containing 15.9% ammonium bifluoride (Klasner et al, 1996).

a) Salivation may develop if ingested (BJ Dabney , 1993).
b) CASE REPORT: A 2.5-year-old boy developed increased salivation after ingesting a solution containing 15.9% ammonium bifluoride (Klasner et al, 1996).

a) Vomiting and nausea may occur if ingested ((NJFS, 2003)).

a) Bloody diarrhea may develop if fluoride is ingested (Heifetz & Horowitz, 1986; BJ Dabney , 1993).
b) CASE REPORT: A 3-year-old girl developed a gastric ulcer and guaiac positive stools after ingesting a solution containing 15.9% ammonium bifluoride (Klasner et al, 1996).
c) CASE REPORT: A 3-year-old girl died approximately 90 minutes after ingesting ammonium bifluoride in Armor All Quicksilver Wheel Cleaner (Clorox). Severe pulmonary hemorrhage, and hemorrhagic necrosis of the pharynx, esophagus, and stomach were noted on postmortem examination (Mullins et al, 1998).

a) Abdominal pain or cramping may be seen if ingested (Monsour et al, 1984; Eichler et al, 1982).
b) Fluoride poisoning with stomach pain, weakness, convulsions, collapse and death may occur following very high exposure((NJFS, 2003)).

a) Reduction of serum calcium can decrease clotting ability.

a) In experiments where rabbits were given repeated doses, red blood cell counts and hemoglobin levels were lowered (Bogacheva, 1971).

a) Ammonium bifluoride is a corrosive chemical and can cause burns to any tissue with which it comes in contact((NJFS, 2003)).
b) Exposure may cause an unusual large, pustular skin rash which appears similar to ballooning of the skin. This effect is neither a primary reaction nor an allergic dermatologic reaction (Fisher, 1959). Depending on the concentration of fluoride present, the development of pain and redness may be delayed after skin exposure. Untreated burns that may initially appear trivial can progress as fluoride ion penetrates more deeply causing progressive tissue destruction.
c) CASE REPORT: Two children (8-month-old twins) presented with erythema, edema, and scaling of their neck and upper chest area, following dermal contact with a rust remover containing ammonium bifluoride that was used to remove oral iron solution stains from their feeder bibs. Following treatment with topical steroids and discontinuation of using the rust remover as a cleaning agent, the rash resolved and did not recur (Toledo et al, 2013).

a) Muscle spasms and weakness may occur after ingestion (BJ Dabney , 1993). The blood calcium decreases, causing an increase in skeletal muscle excitability, hyperactive reflexes, painful spasms, weakness, and tetanic contractures 3 to 5 hours after fluoride ingestion (Arena, 1979).
b) Fluoride poisoning with stomach pain, weakness, convulsions, collapse and death may occur following very high exposure((NJFS, 2003)).

a) Perform serial ECGs and cardiac monitoring for moderate to severe dermal exposures and any ingestion exposure. Follow QTc prolongation as a marker for hypocalcemia/hypomagnesemia and risk for dysrhythmias.

a) Hydrofluoric acid containing test solutions were prepared by dissolving sodium fluoride in hydrochloric acid to produce three solutions, each with a pH of 4.5 (solution I), 4.0 (solution II), or 2.1 (solution III).
b) The solutions provide a source of calcium that reacts with hydrofluoric acid producing calcium fluoride.
c) The table below illustrates the percentage of fluoride removed by calcium fluoride formation in vitro.
d) Additional in vitro studies are needed to confirm the safety and efficacy of these agents for gastric lavage in human fluoride poisoning.

a) ADULT DOSE: 1 g (10 mL of 10% solution) IV infused over 5 minutes; may repeat after 10 minutes (Jones & Flanagan, 2004; Saxena, 1989; Anon, 2000).
b) PEDIATRIC DOSE: 10 to 25 mg/kg (0.1 to 0.25 mL/kg) per dose up to a maximum single dose of 5 mL (500 mg) IV infused over 5 minutes; may repeat after 10 minutes (Jones & Flanagan, 2004; Barkin, 1986; Anon, 2000).
c) CALCIUM FOR INJECTION is available as three salts; calcium chloride, calcium gluconate, and calcium gluceptate.
d) While the other salts may be used, calcium chloride is the preferred salt for resuscitation since it directly delivers ionized calcium, whereas the other salts must be hepatically metabolized to release ionized calcium (Chameides, 1988). However, other studies have suggested that hepatic metabolism may not be required for calcium gluconate (Martin et al, 1990).
e) Calcium chloride is very irritating, and is ideally given via a central venous catheter. It may cause hypotension and bradycardia. Calcium salts are incompatible with bicarbonate (Chameides, 1988; Saxena, 1989; Anon, 2000).

a) ADULT: 1 to 2 g diluted in 250 mL D5W or NS and infused IV, may be repeated as necessary.
b) PEDIATRIC: 25 to 50 mg/kg IV infusion over 30 to 60 minutes; repeat dose as necessary; max 2 g/dose (Kleinman et al, 2010; Manrique et al, 2010; Haque & Saleem, 2009)

a) ECG changes include peaked T waves in the precordial leads, prolongation of the PR interval and QRS duration, progressive flattening of the P wave, merging of the QRS complex with the T wave to produce a continuous sine wave appearance, and ventricular fibrillation or asystole (Martin et al, 1986; Smith et al, 1985).
b) ECG manifestations of hyperkalemia and/or a serum potassium concentration of 7.5 mEq/L or greater indicates a medical emergency and requires aggressive therapy and continuous cardiac monitoring.
c) Fluoride-induced hyperkalemia, once developed, may be irreversible. Therapeutic intervention to prevent development of elevated serum potassium is essential. Note: the beta-adrenergic receptor and the calcium channel do NOT appear to have major roles in fluoride-induced hyperkalemia. Early aggressive therapy with glucose, insulin and/or sodium bicarbonate prior to the development of hyperkalemia was ineffective in dog studies; however, quinidine was shown effective in preventing the K+ efflux from cells and preventing cardiotoxicity in fluoride-toxic dogs. Therapeutic doses of other antidysrhythmics, such as lidocaine, were not effective. Propranolol worsened fluoride-induced cardiotoxicity (Cummings & McIvor, 1988; McIvor & Cummings, 1987).
d) In an in-vitro model of human erythrocytes, the potassium channel blockers, amiodarone and quinidine, attenuated fluoride-induced hyperkalemia. The authors recommended further in-vivo studies to determine whether amiodarone can enhance survival in fluoride poisoning (Su et al, 2003).
e) Death is usually the result of delayed sudden cardiovascular collapse with ventricular fibrillation associated with electrolyte imbalances (hypocalcemia, hypomagnesemia, hyperkalemia). If sudden death is avoided in the first 24 hours, prognosis is good, although recovery may be prolonged. In dog studies, increase in serum potassium levels began at approximately 2 hours postexposure and began to rise exponentially at 6 hours postexposure. Maintain normal or alkalotic pH. Cation exchange resins or dialysis may be the only effective means in which to reverse fluoride-induced hyperkalemia (Cummings & McIvor, 1988; McIvor & Cummings, 1987; McIvor et al, 1987).

a) Intravenous calcium has no effect on circulating potassium levels, but it antagonizes cardiac toxicity in patients demonstrating cardiac signs and/or symptoms of hyperkalemia.
b) ADULT DOSE: 1 g (10 mL of 10% solution) IV infused over 5 minutes; may repeat after 10 minutes (Jones & Flanagan, 2004; Saxena, 1989; Anon, 2000).
c) PEDIATRIC DOSE: 10 to 25 mg/kg (0.1 to 0.25 mL/kg) per dose up to a maximum single dose of 5 mL (500 mg) IV infused over 5 minutes; may repeat after 10 minutes (Jones & Flanagan, 2004; Barkin, 1986; Anon, 2000).
d) CALCIUM FOR INJECTION is available as three salts; calcium chloride, calcium gluconate, and calcium gluceptate.
e) While the other salts may be used, calcium chloride is the preferred salt for resuscitation since it directly delivers ionized calcium, whereas the other salts must be hepatically metabolized to release ionized calcium (Chameides, 1988). However, other studies have suggested that hepatic metabolism may not be required for calcium gluconate (Martin et al, 1990).
f) Calcium chloride is very irritating, and is ideally given via a central venous catheter. It may cause hypotension and bradycardia. Calcium salts are incompatible with bicarbonate (Chameides, 1988; Saxena, 1989; Anon, 2000).

a) Administer intravenous sodium bicarbonate to shift potassium intracellularly. Expect 0.5 to 1 mEq/L reduction in serum potassium for each 0.1 unit rise in blood pH.
b) A standard syringe contains 50 mL of 8.4% solution, 1 mEq/mL, 50 mEq/syringe.
c) ADULT DOSE - 50 mL (50 mEq) intravenously over 5 minutes, repeated at 20 to 30 minute intervals.
d) PEDIATRIC DOSE - 1 to 2 mL/kg/dose (1 to 2 mEq/kg/dose) intravenously every 2 to 4 hours or as required by pH (Barkin, 1986). The onset is 15 minutes, the duration of action 1 to 2 hours (Ellenhorn, 1997).

a) Enhances intracellular potassium shift.
b) ADULT DOSE - Administer 25 grams of dextrose (250 mL of a 10% solution) intravenously over 30 minutes, and then continue the infusion at a slower rate.
c) Ten units of regular insulin are given subcutaneously or added to the infusion.
d) ALTERNATIVELY, 50 mL of a 50% dextrose solution with 5 to 10 units of regular insulin may be administered intravenously over 5 minutes.
e) Typically, this regimen will lower serum potassium by 1 to 2 mEq/L within 30 to 60 minutes with the decrease lasting for several hours.
f) PEDIATRIC DOSE - 0.5 to 1 gram/kg/dose followed by 1 unit of regular insulin intravenously for every 4 grams of glucose infused; may repeat every 10 to 30 minutes (Barkin, 1986).
g) HYPEROSMOLARITY - It must be remembered that 50% dextrose, and even 25% dextrose, are very hyperosmolar and may be sclerosing to peripheral veins (Chameides, 1988); administration of hypertonic solutions via central lines is preferred, if possible.

a) AMIODARONE/INDICATIONS
b) AMIODARONE/ADULT DOSE
c) AMIODARONE/PEDIATRIC DOSE
d) ADVERSE EFFECTS

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) Examination at that time revealed chemotic and hyperemic conjunctiva and sloughing of nearly all of the corneal epithelium. The patient was treated with 1% calcium gluconate drops (3 drops every 3 hours for 2 days), topical cycloplegia and antibiotics and a mild pressure patch. The epithelial defect healed over the next 4 days and eye exam was normal at 3 months.

a) ANIMAL STUDY - Following experimental 50% HF burns to the nude backs of rats, one group of rats was treated with iontophoresis of calcium chloride with constant voltage at 1.5V and electric current at 20-30 microamps at first, then increased to 100-120 microamps within 5 minutes; total treatment, 30 minutes. Burn areas of this group were reduced significantly when compared to untreated rats, those treated with calcium gluconate jelly, and rats treated with intradermal and subcutaneous calcium gluconate injections. Transdermal transport of calcium appeared to be enhanced in stripped skins by iontophoresis. No adverse effects were observed in normal skins. Limitations of iontophoretic treatment include number of lesions that can be treated simultaneously and size of the lesion (patches are small and unable to cover large areas). Use of iontophoretic delivery of calcium in humans is currently not recommended (Yamashita et al, 2001).

a) ANIMAL STUDIES - Various eye treatments were tried on animals to determine the most effective method to bind the fluoride ion.
b) ANIMAL STUDIES - Following a 20 second exposure of 2.5% HF to rabbit corneas, different rinsing solutions were evaluated (tap water, 1% calcium gluconate, and Hexafluorine(R)). Rinsing commenced 25 seconds after burning and continued for 15 minutes. High resolution optical coherence tomography (OCT) was used to measure changes in corneal thickness and HF penetration. Both tap water and 1% calcium gluconate rinses showed initial reduction in HF penetration, but full corneal penetration was seen once the rinses ended. The Hexafluorine(R) rinse showed no increased HF penetration within 1 hour after rinsing, suggesting superior efficacy to the other rinses (Spoler et al, 2008).

a) Exposure to dilute solutions (6% to 11%) hydrofluoric acid is best treated by immediately washing all exposed areas with copious amounts of water or crystalloid solution (lactated ringer's or normal saline) for at least 30 minutes while removing all potentially contaminated clothing and jewelry. Take necessary precautions to prevent secondary exposure to health care providers. Carefully evaluate for ocular damage when dermal exposure involves the face.
b) Exposure to dilute ammonium bifluoride solutions may result in delayed signs and symptoms of ocular damage. If ocular exposure has occurred, the patient should be evaluated by an ophthalmologist after appropriate decontamination. Calcium gluconate or calcium carbonate gel applied topically to the affected area has been associated with relief of pain at the site of exposure. Systemic toxicity or severe tissue damage is unlikely to occur with small surface area exposures to dilute solutions. Aggressive therapy with calcium gluconate infiltration or calcium gluconate arterial perfusion are not likely to be necessary and may increase tissue damage.

a) Dermal exposure to fluoride can produce hypocalcemia, hypomagnesemia, hyperkalemia, cardiac dysrhythmias, and death (Tepperman, 1980; Yamaura et al, 1997).

a) Thoroughly irrigate skin immediately after exposure. Patients with early decontamination do well. Patients with pain should be treated with topical calcium therapy. TOPICAL: Treat with calcium gluconate or carbonate gel (1 g calcium gluconate in 40 g (about 40 mL) water-soluble lubricant = 2.5% gel; alternative is 10 10-g tablets crushed to fine powder + 20 mL water-soluble lubricant mixed into a slurry; apply thin coat to burn, then place hand in glove containing 10 mL slurry for 4 hours). SUBCUTANEOUS: Inject 0.5 mL/cm(2) with 10% calcium gluconate for topical treatment failures (not commonly used).
b) Do not use calcium chloride for bier block procedures. Calcium chloride is irritating to the tissues and may cause injury.

a) Patients with pain not responding to topical calcium can be treated with regional venous or arterial perfusion. These methods are particularly effective for HF exposures involving the digits. BIER BLOCK: Inject IV 10 to 40 mL calcium gluconate in 50 mL normal saline for 20 minutes. ARTERIAL: 10 to 20 mL of 10% calcium gluconate in 50 mL D5W. Infuse over 4 hours via radial or brachial artery. The arterial catheter may be placed in normal position (not inverted).
b) Do not use calcium chloride for bier block procedures. Calcium chloride is irritating to the tissues and may cause injury.

a) ADULT: 1 to 2 g diluted in 250 mL D5W or NS and infused IV, may be repeated as necessary.
b) PEDIATRIC: 25 to 50 mg/kg IV infusion over 30 to 60 minutes; repeat dose as necessary; max 2 g/dose (Kleinman et al, 2010; Manrique et al, 2010; Haque & Saleem, 2009)

a) AMIODARONE/INDICATIONS
b) AMIODARONE/ADULT DOSE
c) AMIODARONE/PEDIATRIC DOSE
d) ADVERSE EFFECTS

a) SUMMARY

a) Hexafluorine(R), an amphoteric, hypertonic, polyvalent compound, was developed in France for decontamination of hydrofluoric acid (HF) eye and skin exposures. In a series of eye and skin occupational exposures with either 40% HF or a mixture of 6% HF and 15% nitric acid, Hexafluorine(R) was used as emergent decontamination within 2 minutes following exposure. None of the workers who were exposed experienced any chemical burns or sequelae. There was no need for any other treatment besides the Hexafluorine(R) decontamination and none of the workers lost work time (Mathieu et al, 2001).
b) In another series of occupational exposures, involving 16 workers who experienced ocular and dermal splashes with either 70% HF or a mixture of 6% HF and 15% nitric acid, Hexafluorine(R) decontamination occurred within 1 minute of exposure in 12 of the workers. Three workers who were exposed to the 6% HF/15% nitric acid mixture received decontamination 1 hour postexposure. Immediate pain relief was reported either during or after Hexafluorine(R) decontamination in all HF-exposed workers. No severe burns or permanent sequelae were reported in any of the workers and 12 of the 16 workers did not require any further treatment following the initial decontamination with Hexafluorine(R). The mean lost work time was less than 1 day (Soderberg et al, 2004).
c) In a rat study, a 50% HF solution was applied to the shaved backs of rats via a soaked filter paper for a 3 minute period. Thirty seconds after removal of the filter paper, the animals were either rinsed with 500 mL Hexafluorine(R) over a 3 minute period, or rinsed with water followed by calcium gluconate 2.5% gel, or rinsed with water only, or given no treatment. A consistent trend toward poorer results with Hexafluorine(R) was observed (Hulten et al, 2004; Hojer et al, 2002). Hall et al (2003) have disagreed with the findings of this study, stating that a 3 minute 50% HF contact time followed by a 30 second delay until decontamination is unrealistic in actual workplace exposures and would negate the effectiveness of any decontamination method (Hall et al, 2003).

a) Regional intravenous infusion of calcium gluconate, using a technique similar to the Bier block, is a therapeutic option if fluoride burns of forearm, hand, or digits as adjunct to topical therapy or if topical therapy is unsatisfactory (Ryan et al, 1997; Henry & Hla, 1992) (Graundins et al, 1997; Isbister, 2000).
b) An intravenous cannula is inserted into a vein in the dorsum of the affected hand. The superficial veins of the extremity are exsanguinated by raising the arm for about 5 minutes. This can also be accomplished by application of an Esmarch bandage. When exsanguination is complete the sphygmomanometer cuff is inflated to just above the systolic blood pressure to prevent the arm refilling with blood. The arm is then lowered or the Esmarch bandage removed. Ten to 20 mL of 10% calcium gluconate solution diluted to 30 to 40 mL with 0.9% saline solution is infused. Ischemia is maintained for 25 to 30 minutes; the blood pressure cuff is then sequentially released over 5 minutes.
c) Intravenous therapy is considered successful if there is absence of pain and tenderness during the hour following treatment. Intraarterial calcium infusion should be considered in cases in which pain or tenderness persists at exposure sites.
d) ANIMAL STUDY: Williams et al (1994) compared intravenous magnesium sulfate treatment with intradermal calcium gluconate treatment in HF-burned rats (Williams et al, 1994).
e) Rats treated with magnesium sulfate (80 mg/kg) experienced fewer severe burns (1 of 11 surviving rats; 1 died) than controls (4 of 8 surviving rats; 5 died) or those treated with intradermal calcium (7 of 9 surviving rats; 1 died).
f) Intravenous magnesium sulfate (0.2 mEq bolus over 2 minutes, followed by 0.2 mEq/kg/hr for 4 hours) diminished burn scars and lessening healing time in rabbits with HF burns (Cox & Osgood, 1994). Calcium gluconate infiltration (0.5 mL of 10% solution) was as effective in diminishing burn scars and healing time in this model.

a) Intraarterial calcium infusion for digital fluoride burn is also a therapeutic option and should be considered if regional intravenous calcium gluconate is ineffective. This method should be used on severe distal extremity burns by those physicians who are comfortable with the technique and have experience in the treatment of HF burns (Isbister, 2000).
b) Several studies have evaluated arterial perfusion of 10 to 20% calcium salt (CALCIUM GLUCONATE or CALCIUM CHLORIDE) solutions to treat distal upper extremity HF burns (Kohnlein & Achinger, 1982; Velvart, 1983; Vance & Curry, 1986; Siegel & Heard, 1992). Intra-arterial infusion should be continued until pain does not recur (Tournoud et al, 1999). In general, pain relief was obtained and wound healing required 2 to 4 weeks.
c) A long catheter is inserted percutaneously into the radial artery using standard aseptic technique. Intra-arterial catheter placement is confirmed by pressure transducer and oscilloscope. If the burn involves only the thumb, index, or long fingers, the catheter is advanced only a few centimeters proximally in preparation for digital subtraction arteriography. If the burn involves the ring or small fingers, the catheter is advanced proximally into the brachial artery because access to the ulnar circulation is necessary.
d) Following satisfactory placement of the arterial line, digital subtraction arteriography is performed to identify the origin of vascular supply to digits involved. Once the tip of the catheter is in the desired location, a dilute preparation of calcium salts (10 mL of a 10% solution mixed in 40 to 50 mL 5% dextrose) is infused with a pump apparatus into the catheter over 4 hours. Generally, calcium gluconate is used, although calcium chloride may be used in a similar manner. The patient should be observed closely during the infusion period for progression of symptoms and potential complications of the procedure, such as alterations of distal vascular supply.
e) Following the 4 hour infusion, the arterial line is maintained in place in the usual manner while the patient undergoes an observation period. If typical fluoride pain returns within 4 hours, a second calcium infusion is repeated. This cycle is repeated until the patient is pain free 4 hours following completion of the calcium infusion.
f) EFFICACY - The efficacy of this method is difficult to determine since adequate controls were absent in all reports. This technique avoids the painful injections and nail removal required with infiltration therapy. It is able to deliver more calcium ions to the injured tissue. It has not been proven to give superior results to the infiltration technique, however, and requires an invasive vascular procedure, an infusion pump, and hospital admission.
g) Complications associated with intra-arterial calcium infusion, include transient ulnar nerve palsy (believed due to the armboard used for infusion), and median nerve palsy from to hematomas from multiple arterial punctures (Siegel & Heard, 1992).
h) Continued tissue destruction and associated pain (due to penetration of free fluoride ion into affected tissue) may be minimized by subcutaneous administration of CALCIUM GLUCONATE to form an insoluble (inactive) fluoride salt (Blunt, 1964). This procedure is NOT recommended for digital areas (fingers or toes) unless the physician is experienced with the technique, due to potential for tissue injury from increased pressure.
i) CALCIUM CHLORIDE should NOT be used for intra-arterial infusions or local injection because it is irritating and may cause tissue injury.
j) INDICATIONS - Local infiltration with CALCIUM GLUCONATE may be considered if (1) fluoride exposure results in immediate tissue damage or (2) erythema and pain persist following adequate irrigation (NOTE: Pain and erythema may be delayed up to 24 hours post exposure depending on the concentration of fluoride).
k) Infiltrate each square centimeter of the affected (painful) dermis and subcutaneous tissue with about 0.5 mL of 10% CALCIUM GLUCONATE using a 30 gauge needle. Repeat as needed to control pain (Matsuno, 1996).
l) CAUTION - Avoid administering large volumes of subcutaneous CALCIUM GLUCONATE, as this will result in decreased tissue perfusion and potential necrosis. Exposure of subungual tissue to concentrated hydrofluoric acid often necessitates removal of the nail in order to adequately decontaminate the nailbed and relieve pain (Mayer & Guelich, 1963; Wetherhold & Shepherd, 1965; Dibbell et al, 1970). In general, regional infusion is preferred to local injection in the hand or foot.

a) Harris et al (1981) evaluated the efficacy of subcutaneous and intradermal injections of magnesium salts (10% acetate and sulfate) in rats dermally exposed to HF. In this study, the magnesium salts effectively minimized the depth and progression of the HF burn but further studies are needed before these salts can be routinely recommended (Harris et al, 1981).
b) Burkhart et al (1992) found that magnesium gluconate in water soluble lubricant gel (K-Y Jelly(R)) was less effective than calcium gluconate in preventing deep layer skin damage in HF-exposed rabbit skin (Burkhart et al, 1992).

a) Soaking the burn in a quaternary ammonium compound solution has been recommended (Wetherhold & Shepherd, 1965) (Reinhart et al, 1966), and although successful it is uncomfortable to the patient and difficult to use in awkward or large areas.
b) In a porcine model of hydrofluoric acid burns topical application of iced benzalkonium chloride (17%) was more effective than topical calcium gluconate gel (2.5%), calcium gluconate injections (5% or 10%), topical calcium acetate (10%) soaks, or benzethonium chloride soaks in reducing the gross size and severity of skin lesions produced after a 9 minute exposure to 38% hydrofluoric acid (Dunn et al, 1992). Calcium acetate soaks (10%) were most effective in reducing the gross size and severity of lesions produced after 15 minutes exposure to 38% hydrofluoric acid.
c) In the same study benzalkonium chloride (17%) soaks, calcium acetate (10%) soaks, calcium gluconate gel (2.5%), and calcium gluconate injection (5%) were all effective in reducing the histologic severity of injury, while benzethonium chloride soaks were less effective and 10% calcium gluconate injection increased the severity of injury (Dunn et al, 1992).

a) ANIMAL STUDY - In an animal study, it was determined that postexposure treatment with an iodine ointment was efficacious upon hydrofluoric acid-induced skin burns. Statistically significant reductions of 76% and 68% in ulceration areas were noted at intervals of 5 and 10 minutes between exposure and treatment; however, a weaker effect was observed at a longer time interval of 15 minutes (a 56% reduction in the ulceration area). It was speculated that the protective effect of iodine may be derived from its ability to inhibit apoptosis or proteinase activity crucial for the evolution of skin damage. The authors suggested the therapeutic usage of these iodine preparations for hydrofluoric acid-induced skin burns (Wormser et al, 2002).

a) In patients with extensive skin damage over a small surface area and refractory hypocalcemia, immediate excision of the affected skin may be indicated. Packing the wound with benzalkonium chloride solution until calcium status is stable, followed by split-thickness skin grafting, has been recommended (Buckingham, 1988).
b) In patients without refractory hypocalcemia, immediate excision is not recommended unless necrotic tissue necessitates debridement. A conservative initial approach with local calcium injections has been suggested (Craig, 1964).

a) Exposure of the subungual (nailbed) tissue to fluoride is particularly painful and difficult to decontaminate. Nail removal is probably not necessary for exposures to concentrations of less than 10%; more concentrated solutions may produce tissue necrosis. The nail plate can be split, lifted, or totally removed in cases of severe exposure to facilitate decontamination and calcium therapy (Roberts et al, 1989). This disfiguring procedure may not be necessary when regional intravenous or intraarterial calcium salt treatment is initiated in a timely manner.

a) Plasma FLUORIDE concentrations in normal subjects range from 0.01 to 0.2 milligram/liter (Kiss, 1987).
b) Survival has been reported with serum FLUORIDE levels of 3.4 milligrams/liter in an untreated adult (Saady & Rose, 1988), and 14.7 milligrams/liter in a treated adult (Baselt & Cravey, 1989).