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) 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) In a study of 409 occupational exposures to hydrofluoric acid reported to 6 Texas Poison Centers during 2000 to 2010, ocular irritation/pain and red eyes were observed in 46 (11.2%) and 14 (3.4%) patients, respectively. Route of exposures included dermal (69.4%), inhalation (21%), ocular (12%), and oral (3.7%). Overall, 51.6% of exposures were not serious. Calcium therapy was used in 234 cases (57.2%) (Forrester, 2012).
b) Hydrofluoric acid was a severe eye irritant in humans using the standard Draize test (RTECS , 2001).
c) Conjunctival injection and chemosis may develop after splash exposure (Sadove et al, 1990; Bentur et al, 1993). A severe bilateral keratoconjunctivitis was reported following a splash injury with 3% HF; symptoms resolved following frequent eye rinses and antiinflammatory and cycloplegic eye drops (Garrido et al, 2001; Sanz-Gallen et al, 2001).

a) Progressive vascularization and scarring of the corneal stroma are induced in rabbits with ocular HF burns (Carney et al, 1974).

a) Hypocalcemia and hypomagnesemia with associated QTc prolongation and torsades de pointes and ventricular dysrhythmias including bigeminy, ventricular tachycardia, refractory ventricular fibrillation, and cardiac arrest have been reported following ingestion and dermal exposure. Cardiac toxicity generally manifests within 6 hours of an exposure (Dalamaga et al, 2008; Wedler et al, 2005; Cordero et al, 2004; Speranza et al, 2002; Stremski et al, 1991; Mullett et al, 1987; Tepperman, 1980; Greco et al, 1988; Buckingham, 1988; Manoguerra & Neuman, 1986; Bordelon et al, 1993; Klasner et al, 1996; Hung et al, 1998; Perry, 2001). In a case of ingestion of one cupful of rust removal agent, a 35-year-old developed obvious tented T wave on ECG, followed by an extreme high T wave due to a relative hyperkalemia; this resolved following treatment with calcium gluconate injections, calcium carbonate via NG tube and an insulin injection (Yu-Jang et al, 2001). In another case of ingestion of 8 oz of rust remover, an 82-year-old woman developed ventricular fibrillation, possibly precipitated by a long QT interval secondary to hypocalcemia, approximately 6 hours after the ingestion (Rivera et al, 2002).
b) CASE REPORT: A 46-year-old man developed severe fluoride intoxication and recurrent ventricular fibrillation 3.5 hours following occupational exposure of 71% hydrofluoric acid to 7% of his total body surface area. Following immediate parenteral administration of calcium and magnesium sulfate, his serum electrolyte levels normalized; however, a urine sample, obtained 8 hours postexposure, showed a fluoride concentration of 5800 mcmol/L (upper reference limit is 105 mcmol/L). Hemodialysis was performed and, 8 hours later, the patient's urine fluoride concentration had decreased to 3850 mcmol/L and his ventricular fibrillation had resolved. Thirty hours postexposure, continuous veno-venous hemodialysis (CVVHD) was started and continued for 48 hours. Two hours following the end of CVVHD treatment (80 hours post-exposure), his urine fluoride concentration was 260 mcmol/L. One month postexposure, the patient was discharged (Bjornhagen et al, 2003).
c) CASE REPORT: A 65-year-old man, who received third degree burns to 5% of his total body surface area after being splashed in the face with hydrofluoric acid solution, complained of chest pain 5 minutes postexposure. Thirty minutes after the accident, he developed cardiopulmonary arrest. Initial laboratory tests revealed hypocalcemia and hyperkalemia (4.9 mg/dL and 6.2 mEq/L, respectively). Despite aggressive resuscitative measures, the patient died 1.5 hours after the accident (Takase et al, 2004).
d) CASE REPORT: After being splashed on the right thigh with 20% hydrofluoric acid, a 36-year-old man experienced a 3% total body surface area first-degree burn. He immediately washed and applied 2.5% calcium gluconate gel to the affected area. On presentation, all serum electrolytes were normal, and he had mild leukocytosis and mild metabolic acidosis. Despite treatment with a bolus injection of 10% calcium gluconate and 20% magnesium sulfate, he developed sinus bradycardia (50 to 56 beats/min) in the ICU. At this time, he was administered 10% calcium gluconate and 15% potassium chloride. Approximately 16 hours after exposure, he lost consciousness with tetany of right upper limb for about 1 minute. An ECG revealed progressive bradycardia and ventricular arrest. At this time, laboratory analysis revealed hypocalcemia (calcium, 6.9 mg/dL), hypomagnesemia (magnesium, 1.41 mg/dL), and hypokalemia (potassium, 2.6 mmol/L). Following resuscitation and treatment with IV 10% calcium chloride, 10% calcium glucose, 20% magnesium sulfate, and 15% potassium chloride, he was stabilized and returned to sinus bradycardia, which persisted from 9 to 49 hours postexposure. Overall, 112 mEq IV calcium, 97.2 mEq IV magnesium, and 142 mEq of IV and oral potassium were administered and he gradually recovered and was discharged after 4 days of hospitalization (Wu et al, 2010).

a) Histologic myocardial damage has been described in fatal oral and dermal exposures (Mayer & Gross, 1985; Greendyke & Hodge, 1964).
b) CASE REPORT: A 59-year-old man with a history of coronary artery disease died from myocardial infarction after he sustained an 11% body surface area burn from 70% HF complicated by hypotension, respiratory failure and hypocalcemia (Lopez et al, 1994).

a) CASE REPORTS

a) CASE REPORT: A 47-year-old man presented to the ED with nausea, weakness, and pleuritic chest pain 1 hour after ingesting blue liquid thought to be a sports drink. He had difficulty swallowing and his oropharynx appeared erythematous without edema or ulceration. An initial ECG revealed sinus tachycardia with a QRS complex of 110 ms and prominent T-waves and an arterial blood gas indicated metabolic acidosis (pH 7.28, pCO2 29, pO2 209, HCO3 13). Initial laboratory values indicated a potassium level of 5.7 mmol/L, a calcium level of less than 4 mmol/L, and a magnesium level of 0.7 mmol/L. A repeat ECG, conducted 30 minutes later, showed QRS complex widening (152 ms), QT interval prolongation (742 ms), and peaked T-waves. The patient's metabolic acidosis and electrolyte and cardiac abnormalities resolved within 12 hours after receiving supportive treatment (4 grams calcium gluconate, 2 grams calcium chloride, 10 grams magnesium sulfate, 400 mEq sodium bicarbonate, and 15 mmol sodium phosphate IV). Further evaluation, using flame ionization and atomic absorption, identified the ingested liquid as hydrofluoric acid (Holstege et al, 2005).

a) In dog studies, death following HF exposure was usually the result of delayed sudden cardiovascular collapse with ventricular fibrillation that combined with irreversible hyperkalemia, and was unresponsive to vasopressors (Cummings & McIvor, 1988; McIvor & Cummings, 1987; McIvor et al, 1987).

a) Dyspnea is common following inhalation. Bronchospasm may occur (Wing et al, 1991; Sadove et al, 1990).
b) HYPOXIA occurred in 17.4% of patients with oxygenation measurement following a HF spill (Wing et al, 1991).
c) PULMONARY FUNCTION TESTS: Abnormalities included decreased FEV1 in 42.3% and decreased FEV1/FVC in 16.9% of patients with PFTs tested following a HF spill (Wing et al, 1991).
d) In a study of 409 occupational exposures to hydrofluoric acid reported to 6 Texas Poison Centers during 2000 to 2010, dyspnea was observed in 23 (5.6%) patients. Route of exposures included dermal (69.4%), inhalation (21%), ocular (12%), and oral (3.7%). Overall, 51.6% of exposures were not serious. Calcium therapy was used in 234 cases (57.2%) (Forrester, 2012).
e) CASE REPORT: Following inhalation of fumes from a glass etching cream for approximately one hour, a 41-year-old man presented to the emergency department with throat irritation, burning chest pain, and dyspnea. The glass etching cream, that the patient was using to remove scratches from his glasses, was found to contain 28% to 39% ammonium bifluoride and sodium bifluoride. At presentation his vital signs were normal, oxygen saturation was 100%, laboratory data (ie, CBC, electrolytes, renal and hepatic function) were within normal limits, there were no ECG abnormalities (QRS 84, QTc 440), and a chest x-ray indicated clear lungs. Physical exam revealed pharyngeal erythema. Treatment was initiated with 2.5% nebulized calcium gluconate resulting in immediate improvement in symptoms; however, continued recurrence of pain and dyspnea necessitated a total of 4 rounds of therapy over a 12-hour period. During therapy, the patient's QTc interval peaked at 458; however, he became asymptomatic, with normal ECG intervals, and was discharged (Kessler et al, 2015).

a) Hemorrhagic pulmonary edema has been observed after significant inhalation, ingestion, and dermal exposures (Watson et al, 1973) Mayer & Guelich, 1986; (Chan et al, 1987; Manoguerra & Neuman, 1986; Kleinfeld, 1965; Takase et al, 2004).
b) CASE REPORT/PEDIATRIC: A 7-year-old girl with dermal exposure to 70% hydrofluoric acid and burns over 10% total body surface area, (serum calcium level 5.5 mg/dL) suffered hypotension, pulmonary edema and four cardiac arrests requiring extensive resuscitation. She was pronounced dead approximately 6 hours after the exposure (Speranza et al, 2002).

a) Severe chemical pneumonitis may occur following inhalation (Klasner et al, 1996).
b) CASE REPORT - Death due to severe pulmonary lesions occurred 3 hours after sustaining an inhalation and dermal injury (Chela et al, 1989).

a) CASE REPORT: One case of tracheobronchitis occurring several days after a dermal exposure has been reported (Braun et al, 1984). Respiratory injury in the form of tracheitis has been reported following inhalation and possible ingestion (Klasner et al, 1996). Immediate upper airway irritation and shortness of breath have been reported following a one minute inhalation exposure to fumes from an anhydrous hydrofluoric acid spill in an enclosed room (Boyer et al, 2000).

a) In a study of 409 occupational exposures to hydrofluoric acid reported to 6 Texas Poison Centers during 2000 to 2010, cough was observed in 29 (7.1%) patients. Route of exposures included dermal (69.4%), inhalation (21%), ocular (12%), and oral (3.7%). Overall, 51.6% of exposures were not serious. Calcium therapy was used in 234 cases (57.2%) (Forrester, 2012).

a) AIRWAY OBSTRUCTION may occur after ingestion or inhalation secondary to laryngeal edema.

a) CASE REPORT: Larynx, trachea, and bronchial tree burns were reported in a fatal case of HF inhalation (Chela et al, 1989).

a) CASE REPORT: A 26-year-old woman experienced burning of her eyes, nose, and mouth, chest tightness, and dyspnea approximately 2 minutes following exposure to hydrofluoric acid fumes while using a rust remover (containing an aqueous solution of 8% to 9% hydrogen fluoride) to clean a toilet bowl. Over the next several weeks, she continued to have persistent wheezing, particularly with exertion. Ultimately the patient was diagnosed with reactive airways dysfunction syndrome that was attributed to her exposure to the rust remover (Franzblau & Sahakian, 2003).

a) CASE SERIES: Three soldiers presented with dyspnea that progressed to acute lung injury and hypoxemic respiratory failure after an automatic fire suppression system in their military vehicle was damaged by a rocket-propelled grenade, releasing hydrogen fluoride gas. Despite supportive care, all 3 patients died within 24 hours of exposure. Several weeks later, 2 more soldiers presented with dyspnea after similar exposure to hydrogen fluoride gas. Both patients were treated with nebulized sodium bicarbonate in the prehospital setting. Both patients developed respiratory failure and acute lung injury and were treated with nebulized calcium chloride every 4 hours, IV calcium boluses, and positive pressure ventilation. The first patient gradually recovered following supportive care and was extubated a week after injury. The second patient developed hospital acquired pneumonia and received tracheostomy. He also recovered gradually and was removed from mechanical ventilation 3 weeks after injury (Zierold & Chauviere, 2012).
b) CASE REPORT - A 65-year-old man developed dyspnea that progressed to respiratory failure after being severely sprayed in the face with liquefied hydrogen fluoride. Despite resuscitative measures, the patient developed cardio-pulmonary arrest and died approximately 1 hour and 40 minutes post-exposure. Initial laboratory analysis showed a potassium level of 6.2 mEq/L and a calcium level of 4.9 mEq/L (albumin correction value 5.1). An autopsy revealed facial necrosis, gray and green membranes of the lips, conjunctiva, and nose, exfoliated and turbid corneas bilaterally, and severely congestive and edematous lungs bilaterally (Dote et al, 2003).
c) CASE REPORT - A 40-year-old man who experienced inhalation exposure to hydrofluoric acid (HF) while retrieving a machine part from a container containing concentrated HF and sulfuric acid presented 9 hours after the exposure with severe hypoxia and metabolic acidosis (pH 7.31, HCO3 17). The patient was intubated and treated with nebulized calcium gluconate 2.5%. The patient's recovery was complicated by respiratory failure, multiple pneumonias, a pulmonary embolus, and pulmonary hypertension. Twelve weeks after exposure, the patient was breathing via a tracheostomy and was transferred to a rehabilitation center (Tsonis et al, 2008).

a) In a study of 409 occupational exposures to hydrofluoric acid reported to 6 Texas Poison Centers during 2000 to 2010, headache was observed in 16 (3.9%) patients. Route of exposures included dermal (69.4%), inhalation (21%), ocular (12%), and oral (3.7%). Overall, 51.6% of exposures were not serious. Calcium therapy was used in 234 cases (57.2%) (Forrester, 2012).

a) Spontaneous vomiting is common following exposure (Klasner et al, 1996). Ingestion of hydrofluoric acid may cause painful necrotic lesions of the oral mucosa and the GI tract depending on concentration.
b) Persistent nausea, vomiting, and diarrhea were reported following dermal exposure to 70% hydrofluoric acid (Wedler et al, 2005).

a) Hemorrhagic gastritis may occur following significant ingestions (Menchel & Dunn, 1984; Manoguerra & Neuman, 1986; Kleinfeld, 1965).

a) Significant gastrointestinal burns are NOT expected after taste ingestions of low concentration products, but may occur after ingestion of high concentrations (greater than 20%) or deliberate ingestions (i.e., suicidal attempts by adults) of large amounts of low or high concentration products. Caustic injury to the esophagus, stomach and duodenum with sloughing and necrosis has been reported following ingestions (Menchel & Dunn, 1984; Chela et al, 1989; Kao et al, 1999; Chu et al, 2001). In one case, ingestion of about 50 mL of a rust removal agent (12% HF and 16% ammonium bifluoride) resulted in severe erosive esophagitis and gastritis (Chu et al, 2001).
b) A 43-year-old man developed nausea, vomiting, abdominal pain, electrolyte abnormalities, and cardiac dysrhythmias after intentionally ingesting a rust remover containing hydrofluoric acid. Despite aggressive resuscitative measures, the patient died 8 hours post-ingestion. Autopsy findings showed the presence of severe erosive cheilitis, glossitis, esophagitis, and gastritis (Cordero et al, 2004).

a) HEMORRHAGIC PANCREATITIS has been reported at autopsy following ingestion (Menchel & Dunn, 1984).

a) RECTAL

a) CASE REPORT: A 51-year-old man who fell into a tank containing 10% to 12% hydrofluoric acid and anhydrous ammonia developed elevated transaminase levels (AST and LDH between 1,000 and 1,400 International Units/L) for the first few days after injury (Sadove et al, 1990). These effects were likely secondary to the patient's overall condition rather than primary liver injury. Values returned to normal by 25 days postexposure.

a) Metabolic acidosis is an important marker of fluoride toxicity, and is likely to be an important determinant of the subsequent course. Metabolic acidosis increases the tissue/intracellular delivery of fluoride and decreases renal elimination of fluoride.
b) CASE REPORT: Oral ingestion resulted in severe acidosis and death in one case (Manoguerra & Neuman, 1986).
c) CASE REPORT: Metabolic acidosis was described in a 60-year-old man with extensive chemical burns following a splash exposure of 70% hydrofluoric acid solution while it was being unloaded from a tanker (pH 7.21, pO2 150 mmHg, pCO2 26 mmHg, HCO3 15 mEq/L) (Chan et al, 1987).
d) CASE REPORT/PEDIATRIC: A 14-month-old boy who sustained 11% body surface area full thickness burns from a product that contained between 8% and 23% hydrofluoric acid developed hypotension and recurrent ventricular fibrillation associated with hypocalcemia and acidosis (pH 7.31) (Bordelon et al, 1993).
e) CASE REPORT: Metabolic acidosis (pH 7.28, pCO2 29, pO2 209, HCO3 13) occurred in a 47-year-old man who ingested blue liquid thought to be a sports drink. Further evaluation of the liquid, via flame ionization and atomic absorption, identified it as hydrofluoric acid. The patient recovered with supportive care (Holstege et al, 2005).
f) CASE REPORT - Metabolic acidosis (pH 7.31, HCO3 17) occurred in a 40-year-old man who experienced inhalation exposure to hydrofluoric acid (HF) while retrieving a machine part from a container containing concentrated HF and sulfuric acid. He presented 9 hours after the exposure with severe hypoxia requiring intubation. The patient's recovery was complicated by respiratory failure, multiple pneumonias, and a pulmonary embolus. Twelve weeks after exposure, the patient was breathing via a tracheostomy and was transferred to a rehabilitation center (Tsonis et al, 2008).
g) CASE REPORT: Mild metabolic acidosis with respiratory compensation (pH: 7.414; PO2: 105 mmHg; PCO2: 30.5 mmHg; HCO3: 19.1 mmol/L) and a 3% total body surface area first-degree burn developed in a 36-year-old man after being splashed on the right thigh with 20% hydrofluoric acid. He immediately washed and applied 2.5% calcium gluconate gel to the affected area. On presentation, all serum electrolytes were normal, and he had mild leukocytosis. He later developed hypocalcemia, hypomagnesemia, hypokalemia, bradycardia, and asystole 16 hours after exposure. Following resuscitation and treatment with IV 10% calcium chloride, 10% calcium glucose, 20% magnesium sulfate, and 15% potassium chloride, he was stabilized and returned to sinus bradycardia, which persisted from 9 to 49 hours postexposure. Overall, 112 mEq IV calcium, 97.2 mEq IV magnesium, and 142 mEq of IV and oral potassium were administered and he gradually recovered and was discharged after 4 days of hospitalization (Wu et al, 2010).

a) In a study of 409 occupational exposures to hydrofluoric acid reported to 6 Texas Poison Centers during 2000 to 2010, dermal irritation/pain, erythema/flushing, and edema were observed in 206 (50.4%), 74 (18.1%), 26 (6.4%) patients, respectively. Route of exposures included dermal (69.4%), inhalation (21%), ocular (12%), and oral (3.7%). Overall, 51.6% of exposures were not serious. Calcium therapy was used in 234 cases (57.2%) (Forrester, 2012).

a) SUMMARY: Brief dermal exposure to products with less than 20% hydrofluoric acid typically does not cause clinically apparent burns (Perry, 2001). Hydrogen fluoride burns may cause little initial pain, especially with low concentration forms of the acid. It readily penetrates the skin and mucous membranes. The associated hydrogen fluoride penetrates into the deep subdermal layers and causes severe destruction and liquefaction necrosis. Insidious onset of erythema progressing to vesiculation, ulceration, and finally tissue necrosis occurs. Eventually a characteristically severe throbbing pain sets in, which may not be adequately controlled by parenteral narcotics. The pain is thought to result from the release of cellular potassium and intense stimulation of nerve endings (Clayton & Clayton, 1994; Iverson et al, 1971; Dibbell et al, 1970; CHEMINFO , 1990; Edinburg & Swift, 1989; Asvesti et al, 1997; Garrido et al, 2001; Mangion et al, 2001).
b) INCIDENCE - RETROSPECTIVE STUDY: 219 patients exposed to dilute hydrofluoric acid (6% to 11%) reported symptoms of dermal swelling, redness, or both (55%), blistering (5%), blackish discoloration beneath the fingernail (5%), and pain without dermal changes (27%). Onset of symptoms reported occurred from 0.5 to 24 hours after exposure (El Saadi et al, 1989).
c) Fatal systemic poisoning following the absorption of fluoride from a hydrogen fluoride burn involving 2.5% of body surface has been reported. A burn of less than 50 cm(2) maybe treated on an outpatient basis if vital areas are not involved. A burn involving a 50 to 100 cm(2) area requires hospitalized treatments. A burn that exceeds an area of 100 cm(2) should be treated in facilities with an intensive care unit (Clayton & Clayton, 1994).
d) PERMANENT SEQUELAE: CASE SERIES: In a study of 14 patients with hydrofluoric acid burns of the hand, 2 patients developed permanent impairment that was associated with a delay in diagnosis and appropriate treatment. All patients were treated with immediate flushing with water for 15 minutes, calcium gluconate gel 2.5% massaged into burned skin for at least 30 minutes, and subcutaneous injections of 10% calcium gluconate into the affected area if pain persisted (Anderson & Anderson, 1988).
e) Depending on the severity of the burn, signs and symptoms may include erythema, central blanching with peripheral erythema, swelling, vesiculation, serous crusting, ulceration, blue-gray discoloration, and necrosis (Hathaway et al, 1996a).
f) In a study of 409 occupational exposures to hydrofluoric acid reported to 6 Texas Poison Centers during 2000 to 2010, burns (2nd-3rd degree) were observed in 35 (8.6%) patients. Superficial burns were observed in 70 (17.1%) patients. Route of exposures included dermal (69.4%), inhalation (21%), ocular (12%), and oral (3.7%). Overall, 51.6% of exposures were not serious. Calcium therapy was used in 234 cases (57.2%) (Forrester, 2012).
g) CASE REPORT: A 65-year-old man received third-degree burns to his face after being splashed in the face with a solution of hydrofluoric acid while cleaning pipes. He complained of chest pain and, 30 minutes after the accident, developed cardiopulmonary arrest. Despite aggressive resuscitative measures, the patient died 1.5 hours after the accident. Autopsy findings showed that the chemical burn on his face extended to both ears with the affected area a greenish-gray color. Both temporal bones were also dyed a greenish-gray color (Takase et al, 2004).
h) CASE REPORT: Following accidental dermal exposure to 70% hydrofluoric acid, a 29-year-old man received chemical burns over approximately 15.5% of his total body surface area. He developed persistent nausea, vomiting, and diarrhea, and severe hypocalcemia exhibiting as generalized tetany. He continued to deteriorate clinically, developing QT interval prolongation which progressed to cardiac arrest. Despite cardiopulmonary resuscitation, the patient died 1.5 hours postexposure (Wedler et al, 2005).
i) CASE REPORT: After being splashed on the right thigh with 20% hydrofluoric acid, a 36-year-old man experienced a 3% total body surface area first-degree burn. He immediately washed and applied 2.5% calcium gluconate gel to the affected area. On presentation, all serum electrolytes were normal, and he had mild leukocytosis and mild metabolic acidosis. He later developed hypocalcemia, hypomagnesemia, hypokalemia, bradycardia, and asystole 16 hours after exposure. Following resuscitation and treatment with IV 10% calcium chloride, 10% calcium glucose, 20% magnesium sulfate, and 15% potassium chloride, he was stabilized and returned to sinus bradycardia, which persisted from 9 to 49 hours postexposure. Overall, 112 mEq IV calcium, 97.2 mEq IV magnesium, and 142 mEq of IV and oral potassium were administered and he gradually recovered and was discharged after 4 days of hospitalization (Wu et al, 2010).

a) An intradermal injection of approximately 5 mL of a rust removal solution containing 7% HF resulted in a severe chemical burn with necrotic eschar formation and systemic effects of severe, resistant hypocalcemia, hyponatremia, hypokalemia, and hypochloremia (Gallerani et al, 1998).

a) BONE DECALCIFICATION: The fluoride ion may cause decalcification and corrosion of bone beneath the area of dermal burn. Bone destruction is extremely painful (Dibbell et al, 1970; Matsuno, 1996).

a) CHRONIC FLUOROSIS, characterized by bone pain, osteosclerosis of long bones, and calcification of ligaments has been reported after chronic occupational exposure to HF fumes (Largent et al, 1951; Waldbott & Lee, 1978; White, 1980).

a) Rhabdomyolysis, with elevated CPK levels, has been reported following dermal exposures (Sanz-Gallen et al, 2001; Sadove et al, 1990).
b) CASE REPORT: A 51-year-old man who fell into a tank containing 10% to 12% hydrofluoric acid and anhydrous ammonia developed elevated CPK levels (40,000 International Units/L) for the first few days after injury (Sadove et al, 1990). Values had returned to normal by 25 days after exposure.

a) Pre- and post-implantation mortality was reported in one rat study, where a dose of 470 mcg/m(3) were administered by inhalation route to females at 1 to 22 days of pregnancy (RTECS , 2000).

a) Perform serial ECGs and cardiac monitoring for moderate to severe exposures. Follow QTc prolongation as a marker for hypocalcemia 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).
f) Doses of up to 113 mEq of calcium have been used to successfully to treat hydrofluoric acid burns. A dose of 266.7 mEq used in one case resulted in hypercalcemia (Greco et al, 1988).

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 HF 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 HF 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.
c) Doses of up to 113 mEq of calcium have been used to successfully treat hydrofluoric acid burns. A dose of 266.7 mEq used in one case resulted in hypercalcemia (Greco et al, 1988).

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 HF 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 HF 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 HF 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) HF 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 HF).
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 HF 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.

1) A 70-year-old woman survived 2 separate ingestions of up to 2 ounces of a rust removal agent containing 12% hydrofluoric acid following aggressive calcium and magnesium replacement to prevent or treat the development of cardiac arrhythmias (Stremski et al, 1991).
2) Oral ingestion of an unknown rust remover resulted in death within 90 minutes. The calcium level upon arrival to the emergency department was 3.1 mg/dL with a plasma fluoride of 35.2 mg/L. Post mortem findings included hemorrhagic pulmonary edema and gastritis, without ulceration (Manoguerra & Neuman, 1986).
3) A 33-year-old man reportedly ingested 100 ml of 10% HF. He presented to the ED with hematemesis and abdominal pain. His blood pressure decreased to 84/63 and the patient was given IV calcium chloride. His initial serum calcium level was 1.91 mmol/L (ionized 0.78 mmol/L). He developed ventricular fibrillation (VF) and was defibrillated and given 10 mL of 10% calcium chloride and 1 gram of magnesium sulfate. He suffered 5 additional VF arrests. He survived after dialysis for renal failure. A CT scan of the abdomen suggested edema of the stomach and small bowel (Chan & Duggin, 1997).

1) A 40-year-old man who experienced inhalation exposure to hydrofluoric acid (HF) while retrieving a machine part from a container containing concentrated HF and sulfuric acid presented 9 hours after the exposure with severe hypoxia and metabolic acidosis (pH 7.31, HCO3 17). The patient was intubated and treated with nebulized calcium gluconate 2.5%. The patient's recovery was complicated by respiratory failure, multiple pneumonias, a pulmonary embolus, and pulmonary hypertension. Twelve weeks after exposure, the patient was breathing via a tracheostomy and was transferred to a rehabilitation center (Tsonis et al, 2008).

1) Profound hypocalcemia (total serum calcium 3.5 mg/dL, ionized calcium 1.7 mg/dL) occurred 6 hours after an 8% body surface area burn with 70% hydrofluoric acid (Mullett et al, 1987). This patient died from refractory ventricular fibrillation.
2) Profound hypocalcemia (3.5 mg/dL and 4.1 mg/dL) was successfully treated with aggressive parenteral and subeschar calcium injections in a 38-year-old man with a 2.5% body surface area burn with 60% HF and a 50-year-old man with a 22% body surface area burn with 70% HF, respectively (Greco et al, 1988).
3) A 48-year-old man developed erythema and second-degree burns to 3.5% of his body surface area following dermal exposure to 70% HF. He immediately showered and applied 5% calcium gluconate gel, and arrived at the hospital 45 minutes later; ECG showed QTc prolongation and ventricular tachycardia. Initial total and ionized calcium levels were 5.6 mg/dL and 0.8 mmol/L, respectively. Other lab tests revealed hypokalemia (2.1 mmol/L) and hypomagnesemia (0.25 mmol/L). All electrolyte abnormalities were corrected with IV replacement, and cardiac rhythm returned to sinus rhythm approximately 20 hours post admission. A full recovery without sequelae was reported (Dalamaga et al, 2008).

1) IMMERSION
2) RECTAL ADMINISTRATION

1) A 14-month-old child with hydrofluoric acid burns over 11% of his body suffered cardiac arrest in association with severe hypocalcemia and hyperfluoridemia. The child survived following treatment including topical, sub-eschar, and intravenous calcium gluconate administration (Bordelon et al, 1993).
2) A 7-year-old girl with dermal exposure to 70% hydrofluoric acid and burns over 10% total body surface area, (serum calcium level 5.5 mg/dL) suffered hypotension, pulmonary edema and four cardiac arrests requiring extensive resuscitation. She was pronounced dead approximately 6 hours after the exposure (Speranza et al, 2002).

1) Home irrigation and emergency department irrigation was performed in all cases. Treatment included antibiotics (2/8), steroids (1/8), and 10% calcium gluconate (1/8) for relief of pain.

1) The burn was copiously washed with isotonic solution and treated with cutaneous and subcutaneous injections of magnesium chloride, 10% calcium gluconate solution and 2% Xylocaine. Plastic surgery interventions were later required. The patient developed severe and persistent hypocalcemia 7 hours after the incident followed by hyponatremia, hypokalemia, and hypochloremia (Gallerani et al, 1998).

a) Lethal plasma fluoride concentrations following ingestion of hydrofluoric acid have ranged from 8.3 to 56.2 mg/L (Curry, 1962; Manoguerra & Neuman, 1986; Menchel & Dunn, 1984); however, fluoride levels of 2.6 mg/L from other sources have resulted in fatalities (Baselt, 2000).
b) Blood and vitreous humor concentrations of fluoride ions in a fatality from a hydrofluoric acid splash accident were 0.98 mEq/L and 0.63 mEq/L, respectively (Hung et al, 1998).
c) Background fluoride levels are less than 0.1 mg/L (Manoguerra & Neuman, 1986).
d) Following a suicidal ingestion of an unknown quantity of a 10% hydrofluoric acid and 25% ammonium bifluoride solution, a 43-year-old male was found dead. Blood fluoride concentration was reported to be 13 mg/L (Bost & Springfield, 1995).
e) A serum fluoride level of 2 mg/L was reported in an 82-year-old woman more than 6 hours after ingestion of 8 ounces of a rust remover. Urine fluoride level was 72.46 mg/L (Rivera et al, 2002).
f) Post-mortem fluoride concentrations from a 43-year-old man, who intentionally ingested a 10 fluid ounce bottle of rust remover containing hydrofluoric acid solution, are as follows (Cordero et al, 2004):
g) CASE REPORT - A 65-year-old man, who received third degree burns to 5% of his total body surface area after being splashed in the face with hydrofluoric acid solution, complained of chest pain 5 minutes post-exposure. Thirty minutes after the accident, he developed cardiopulmonary arrest. Initial laboratory tests revealed hypocalcemia and hyperkalemia (4.9 mg/dL and 6.2 mEq/L, respectively). Despite aggressive resuscitative measures, the patient died 1.5 hours after the accident. Post-mortem analyses of the serum, urine, and fluids of the pericardium and thoracic cavity showed elevated fluoride concentrations (6.38, 6.60, 6.17, and 5.37 mg/dL, respectively) (Takase et al, 2004).
h) CASE REPORT - Ionized fluoride concentrations in the heart, thoracic cavity, and urine inside the bladder of a 65-year-old man, following a fatal inhalation exposure of liquefied hydrogen fluoride, were 61 mcg/mL, 54 mcg/mL, and 66 mcg/mL, respectively (Dote et al, 2003).
i) CASE REPORT - The post-mortem fluoride concentrations in the gastric contents, urine, and heart blood of a 29-year-old man, following dermal exposure of 70% hydrofluoric acid, were 1.7 mg/L, 15 mg/L, and 14 mg/L, respectively (Wedler et al, 2005).

1) Hydrogen fluoride, as F

a) TWA: 3 ppm (2.5 mg/m(3))
b) STEL:
c) Ceiling: 6 ppm (5 mg/m(3)) [15-minute]
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

a) IDLH: 30 ppm
b) Note(s): Not Listed

a) 8-hour TWA:

a) 8-hour TWA:3 ppm
b) Acceptable Ceiling Concentration:
c) Acceptable Maximum Peak above the Ceiling Concentration for an 8-hour Shift:
d) Notation(s): Not Listed

a) 32 ppm
b) Male, 100 mg/m(3) for 1M -- NOSE,EYE,ACID