1 Official Newsletter of the Utah Poison Control Center IN THIS ISSUE TOXICOLOGY TODAY A program of the University of Utah College of Pharmacy 2011 • VOLUME 13 • ISSUE 2 TODAY by Nicole Hendriksen, PharmD Illustrative Case A 35 year-old man received severe burns on his face and neck following an exposure to 100% hydrofluoric acid (HF). Upon arrival to the local hospital he was conscious and oriented and had no evidence of oral or upper airway damage. Following skin irrigation with with co- pious amounts of water for 20 minutes, calcium gluconate 2.5% gel was applied to the burns. Laboratory evaluation revealed an elevated WBC and a serum fluo- ride of 1,980 ug/l and urinary fluoride 7.17 mg/L. Serum and uri- nary fluoride remained elevated for 2 weeks. Serum calcium concen- tration was normal. He slowly improved with topical calcium gluco- nate treatment and the burns resolved within 3 months of exposure. 1 Introduction In 2009 the Ameri- can Association of Poison Control Centers reported 1017 exposures to hydrofluoric acid with 86% of those being unintentional. Of the exposures reported, 65% were treated in a health care facility, 228 resulted in a moderate or major outcome and 3 resulted in death. 2 Uses Hydrofluoric acid is commonly used in rust removers and in etching and glass polishing. HF is also used in the manufacture of metals and silicon semiconduc- tor chips. Products with dilute solutions of HF between 0.6-12% are available to the public in rust-removers and alumi- num cleaning products. Properties HF is a weak acid and is approximately 1000 times less dissoci- ated than an equimolar concentration of hydro- chloric acid, yet it can be extremely corrosive and must be handled with care. Mechanism of Toxicity HF penetrates deeply into tissues where the fluoride ion binds to divalent cations, such as calcium and magnesium, interfering with their physiologic functions. Severe pain, tissue necrosis, bone destruc- tion and life-threatening electrolyte imbalances can occur as calcium and magnesium become compromised. Con- centrated HF is caustic enough to cause skin injury, but more dilute forms, concentrations less than 20%, usually are not associated with severe burns. Clinical Presentation e onset and extent of injury is dependent upon the concentra- tion and volume of the product, and the dura- tion of contact with the skin. Weak solutions of 20% or less may present with pain, erythema and edema at the site of exposure that is delayed up to 24 hours; while solutions of greater than Treatment of Hydrofluoric Acid Burns Outreach Education: Use Only As Directed Poison Pearls: Bath Salts Arsenic & Arsine Meet the UPCC Staff: Marilyn Redd 50% immediately produce burns characterized by intense pain, coagulated skin at the burn site and tissue destruction. System- ic toxicity has been seen with high concentration exposures involving 2.5% of body surface. Ocular exposures to HF are more damaging than ocular exposures to other acids because of HF’s abil- ity to penetrate into tissues. HF destroys the corneal and conjunctival epithe- lium, and leads to corneal edema, conjunctival isch- emia, sloughing, and swell- ing. Additionally, HF can penetrate deeper into the anterior chamber structures and cause necrosis. 3 Inhalation of HF may cause effects ranging from mild upper respiratory irritation to pneumonitis and pulmonary edema. Patients may present with cough, dyspnea, wheezing or stridor. HF ingestions may cause corrosive injury to the mouth, esophagus and stomach. Patients quickly develop vomiting and ab- dominal pain and may also present with altered mental status, airway compromise and dysrrhythimas. Systemic toxicity has been associated with inges- tion, inhalation and dermal exposures to hydrofluoric acid. Systemic toxicity manifests as hypocalcemia, hypomagnesemia and hyperkalemia that can lead to cardiac arrhythmias and death. Patients at higher risk for hypocalcemia include: any ingestion of HF, exposure to 50% or greater concentration HF, exposure to more than 5% of the body surface area or inhalation of vapors from 60% or greater concentration of acid. 4 (cont. on pg. 2) Photo Credit: David Royle TREATMENT OF HYDROFLUORIC ACID BURNS
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1
Official Newsletter of the Utah Poison Control Center
I N T H I S I S S U E
TOXICOLOGY TODAY A program of the University of Utah College of Pharmacy
2011 • VOLUME 13 • ISSUE 2
T O D A Y
by Nicole Hendriksen, PharmD
Illustrative CaseA 35 year-old man
received severe burns on his face and neck following an exposure to 100% hydrofluoric acid (HF). Upon arrival to the local hospital he was conscious and oriented and had no evidence of oral or upper airway damage. Following skin irrigation with with co-pious amounts of water for 20 minutes, calcium gluconate 2.5% gel was applied to the burns. Laboratory evaluation revealed an elevated WBC and a serum fluo-ride of 1,980 ug/l and urinary fluoride 7.17 mg/L. Serum and uri-nary fluoride remained elevated for 2 weeks. Serum calcium concen-tration was normal. He slowly improved with topical calcium gluco-nate treatment and the burns resolved within 3 months of exposure.1
IntroductionIn 2009 the Ameri-
can Association of Poison Control Centers
reported 1017 exposures to hydrofluoric acid with 86% of those being unintentional. Of the exposures reported, 65% were treated in a health care facility, 228 resulted in a moderate or major outcome and 3 resulted in death.2
UsesHydrofluoric acid is
commonly used in rust removers and in etching and glass polishing. HF is also used in the manufacture of metals and silicon semiconduc-tor chips. Products with dilute solutions of HF between 0.6-12% are available to the public in rust-removers and alumi-num cleaning products.
Properties HF is a weak acid
and is approximately 1000 times less dissoci-ated than an equimolar
concentration of hydro-chloric acid, yet it can be extremely corrosive and must be handled with care.
Mechanism of Toxicity HF penetrates deeply
into tissues where the fluoride ion binds to divalent cations, such as calcium and magnesium, interfering with their physiologic functions. Severe pain, tissue necrosis, bone destruc-tion and life-threatening electrolyte imbalances can occur as calcium and magnesium become compromised. Con-centrated HF is caustic enough to cause skin injury, but more dilute forms, concentrations less than 20%, usually are not associated with severe burns.
Clinical PresentationThe onset and extent
of injury is dependent upon the concentra-tion and volume of the product, and the dura-tion of contact with the skin. Weak solutions of 20% or less may present with pain, erythema and edema at the site of exposure that is delayed up to 24 hours; while solutions of greater than
Treatment of Hydrofluoric Acid BurnsOutreach Education: Use Only As DirectedPoison Pearls: � Bath Salts � Arsenic & Arsine
Meet the UPCC Staff: Marilyn Redd
50% immediately produce burns characterized by intense pain, coagulated skin at the burn site and tissue destruction. System-ic toxicity has been seen with high concentration exposures involving 2.5% of body surface.
Ocular exposures to HF are more damaging than ocular exposures to other acids because of HF’s abil-ity to penetrate into tissues. HF destroys the corneal and conjunctival epithe-lium, and leads to corneal edema, conjunctival isch-emia, sloughing, and swell-ing. Additionally, HF can penetrate deeper into the anterior chamber structures and cause necrosis.3
Inhalation of HF may cause effects ranging from mild upper respiratory irritation to pneumonitis and pulmonary edema. Patients may present with cough, dyspnea, wheezing
or stridor. HF ingestions may
cause corrosive injury to the mouth, esophagus and stomach. Patients quickly develop vomiting and ab-dominal pain and may also present with altered mental status, airway compromise and dysrrhythimas.
Systemic toxicity has been associated with inges-tion, inhalation and dermal exposures to hydrofluoric acid. Systemic toxicity manifests as hypocalcemia, hypomagnesemia and hyperkalemia that can lead to cardiac arrhythmias and death. Patients at higher risk for hypocalcemia include: any ingestion of HF, exposure to 50% or greater concentration HF, exposure to more than 5% of the body surface area or inhalation of vapors from 60% or greater concentration of acid.4
(cont. on pg. 2)
Photo Credit: David Royle
TREATMENT OF HYDROFLUORIC ACID BURNS
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TOXICOLOGY TODAY A publication for Health Professionals.
O U T R E A C H E D U C A T I O N
Did you know…Prescription drug overdoses are the number one cause of injury-related deaths in Utah, killing more people each year than car crashes – Utah Health News, April
28, 2010. In 2009 poisoning became the lead-ing cause of unintentional injury death in the US – Injury Facts, 2011 Edition.
In January 2009, the Utah Pharmaceutical Drug Crime Project (UPDCP) was convened to address the growing problem of prescrip-tion drug abuse in Utah. As a public-private, multidisciplinary partnership, UPDCP in-volves over 20 local, state and federal experts in the fields of substance abuse prevention and treatment, law enforcement, environ-mental quality, medicine, human services, the judiciary and public health, as well as legisla-tors and prosecutors.
UPDCP set the following goals with regard to prescription drugs in Utah:
ʶ Reduce availability for abuse ʶ Increase the perception of risk to include the physical and psychological harmful effects as well as legal sanctions
ʶ Change the public’s attitude toward be-ing less tolerant of the non-medical use of pharmaceutical drugs
The Utah Poison Control Center partici-pates on the UPDCP Public Awareness and Training Subcommittee. Members of this committee worked with a local advertising agency to create a public awareness campaign to educate Utahns about the safe use, storage and disposal of prescription pain medications.
The campaign, “Use Only As Directed,” originally developed under the 2008 Pre-scription Pain Medication Management & Education Program, kicked off in February 2011. UPDCP adopted the same slogan and
took over the task of making consumers more aware of the dangers of improperly using, storing or throwing away prescription drugs. Several TV and radio ads were launched in February and an information brochure was developed. In April, billboards were posted across the state that focused on safe storage and disposal. Campaign materials may be viewed at www.useonlyasdirected.org.
The proper use, storage and disposal of prescription pain medications can do much to correct the problems associated with misuse and abuse of these medicines. For the safety of your family, neighbors, friends, and environment, please use, store and dispose of your prescription pain medications “only as directed.”
(cont. from pg. 1) Hydrofluoric Acid
TreatmentDermal Exposures:Initial management involves immediate removal of contaminated clothing and washing of the area with running water for at least 15 minutes. For exposures to hands that result in visible burns a burn, or hand surgeon should be consulted.
Following decontamination, calcium gluconate gel 2.5% should be applied to af-fected areas. Application should be repeated as often as necessary to eliminate pain. The gel may be covered with a surgical glove or an occlusive dressing to enhance penetration. If calcium gluconate is not available, calcium chloride or calcium carbonate can be used to prepare a topical gel. Quarternary ammonium compounds such as benzalkonium chloride (Zephiran®) may be used in the treatment of HF burns. Magnesium has been suggested as an alternative treatment for HF burns. However, data regarding its efficacy compared to calcium are mixed.5, 6
If pain doesn’t improve with topical calcium gluconate application, subcutane-ous injections of calcium gluconate should
be considered. Intra-dermal calcium injec-tions can be used in patients who do not get adequate pain relief from topical calcium
treatments. For subcutaneous treatment a 5% calcium gluconate solution can be injected into the exposed skin at about
0.5 cm peripheral to the burn. The maximum amount injected is 0.5 mL of solution per cm2 of exposed skin. Injection into areas
with limited tissue space, such as fingers, is not recommended as infiltration of too much fluid may lead to a compartment syndrome and tissue necrosis.7, 8 Ten percent calcium gluconate injections have been studied with mixed effects. Dunn reported a negative effect in tissues when 10% calcium gluconate injections were compared to 5% calcium gluconate injections and topical preparations of calcium, benzalkonium chloride (Zephi-ran®) and benzethonium chloride; while Seyb found 10% calcium injections to be more beneficial than topical preparations of cal-cium in animal models.9, 10 Calcium chloride should never be used for infiltration as it can be corrosive and cause further tissue damage.
Intravenous infusions of calcium gluco-nate utilizing a Bier block technique can be considered if pain does not resolve with topical preparations or if intra-dermal injec-tions are problematic (e.g fingertips). This technique has had variable success.11, 12 A case
series of seven patients showed four treat-ment successes, one partial success and two treatment failures after intravenous calcium gluconate infusions.13 Intravenous infusions are less technically demanding, possibly less hazardous and easier to perform in emergency departments than intra-arterial infusions.Intra-arterial calcium injections:
Intra-arterial administration of calcium gluconate is effective for larger surface areas of burn or for burns to the hand when intra-dermal infiltration cannot be employed; however, this technique is more technically demanding. Intra-arterial therapy should be reserved for severe burns and should only be employed by individuals experienced with its use. Intra-arterial calcium gluconate has been associated with complications such as nerve palsy, arterial spasms and hematomas. Ocular:
Prompt irrigation of the eye with copious amounts of water or saline for 15 to 30 min-utes is the most important step. After irriga-tion consult an ophthalmologist. McCulley compared irrigation and subconjunctival in-jection with water, normal saline, magnesium chloride, lanthanum chloride, 0.2 percent benzethonium chloride, 0.3 percent benzalko-nium chloride, and magnesium ointments in a rabbit model. Single irrigations with water, normal saline or magnesium (cont. on pg. 3)
USE ONLY AS DIRECTED CAMPAIGN
Photo Courtesy of Calgonate®
3 TOXICOLOGY TODAY www.utahpoisoncontrol.org
P O I S O N P E A R L S
(cont. from pg. 2) Hydrofluoric Acidchloride were the only treatments that provided therapeutic benefit without toxic effects. Multiple irrigations were associated with an increase in ulceration.3 Calcium solutions are not routinely used because they are irritating and have not been well studied. Inhalation:
Inhalation exposure should be suspected for patients who are exposed to high concen-trations of hydrofluoric acid and for patients with burns to the face or neck. Anecdotal reports suggest that nebulized calcium gluco-nate may be helpful for patients with inhala-tion exposures.14,1 Nebulized 2.5% calcium gluconate is thought to be relatively benign. Therefore, it is recommended for all patients who show respiratory symptoms following HF exposure. Treatment of Systemic Effects:
For patients at high risk for hyocalcemia, early replacement of calcium is important. Twenty mL of 10% calcium gluconate should be given IV while awaiting serum calcium results. Patients at risk for systemic toxicity should receive have serial monitoring of electrolytes along with ECG monitoring for signs of hypocalcemia, hypomagnesemia and hyperkalemia. Serial calcium concen-trations should be monitored and calcium supplementation given to normalize calcium concentrations.
SummaryHydrofluoric acid dermal exposures gener-
ally result in local tissue damage, but larger exposures can lead to systemic toxicity and death. Treatment involves rapid decon-tamination and administration of calcium gluconate formulations to bind fluoride ions and prevent tissue injury and electrolyte disturbances.
References1. Kono K, Watanabe T, Dote T et al. Successful treatment of lung
injury and skin burn due to hydrofluoric acid exposure. Int Arch Occup Environ Health 2000; 73 supplement: S93-S97.
2. Bronstein AC, Spyker DA, Cantilena LR, et al. 2009 annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 27th Annual Report. Clin Toxicol 2010; 48:979–1178.
3. McCulley J, Whiting D, Petitt M et al. Hydrofluoric acid burns of the eye. J Occup Med 1983; 25(6):447-450.
4. Greco R, Hartford C, Haith L et al. Hydrofluoric acid-induced hypocalcemia. J Trauma 1988; 28:1593-1596.
5. Bracken W, Cuppage F, McLaury R, et al. Comparative effective-ness of topical treatments for hydrofluoric acid burns. J Occup Med 1985; 27:33-739.
6. Burkhart K, Brent J, Kirk M et al. Comparison of topical magne-sium and calcium treatment for dermal hydrofluoric acid burns. Ann Emerg Med 1994; 24:9-13.
7. Caravati EM. Acute hydrofluoric acid exposure. Am J Emerg Med 1988; 6:143-149.
8. Kirkpatrick J and Burd D. An algorithmic approach to the treat-ment of hydrofluoric acid burns. Burns 1995; 21:495-499.
9. Dunn B, MacKinnon M, Knowlden N et al. Hydrofluoric acid dermal burns; An assessment of treatment efficacy using an experi-mental pig model. J Occup Med 1992; 34: 902-909.
10. Seyb S, Noordhoek L, Botens S et al. A study to determine the efficacy of treatments for hydrofluoric acid burns. J Burn Care Rehabil 1995; 16: 253-257.
11. Ryan J, McCarthy G and Plunkett P. Regional intravenous calcium- an effective method of treating hydrofluoric acid burns to limb peripheries. J Accid Emerg Med 1997;14:401-404.
12. Isbister G. Failure of intravenous calcium gluconate for hydroflu-oric acid burns. Ann Emerg Med 2000; 36(4):398-399.
13. Graudins A, Burns M and Aaron C. Regional intravenous infu-sion of calcium gluconate for hydrofluoric acid burns of the upper extremity. Ann Emerg Med 1997; 30(5): 605-607
14. Lee D, Wiley J and Synder J. Treatment of inhalational exposure to hydrofluoric acid with nebulized calcium gluconate. J Occup Med 1993; 35:470.
BATH SALTSEliza Johnson, MDEmergency Medicine Resident
When I first heard of people snorting bath salts, I thought it was kids’ stuff, like snorting Pixie Stix in 6th grade. However, it is quickly becoming apparent that “bath salts” are no more kids’ stuff than they are adjuncts to help you relax in a soothing hot tub. As one of the latest trends in designer drugs, substances referred to as “bath salts” have been found to contain mephedrone or methylenedioxypyrovalerone (MDPV). Related to amphetamines, both of these substances act as stimulants with hallucino-genic properties. Clinical presentation is usually similar to sympathomimetic drugs and often accompanied by hallucinations and
paranoid delusions. These products are sold in truck stops, gas stations, head shops, and websites with product names such as Ivory Wave, Vanilla Sky, and Red Dove. Effects typically last a few hours but may linger up to 3 or 4 days. Treatment is symptomatic; benzodiazepines seem effective for many of the sympathomimetic symptoms. Effec-tive February 25, 2011, Utah House Bill 23 enacted criminal penalties for the possession, distribution, and administration of both synthetic cannabinoids (Spice) and bath salts. As more states and countries enact laws prohibiting these substances, designer drug manufactures will surely create new “legal” highs to circumvent the law. In this escalat-ing game with new designer drugs, rumor has it that “plant food” may be the next street name for a “legal” drug of abuse.
ACUTE ARSENIC AND ARSINE POISONINGCaroline Vines, MDEmergency Medicine Resident
A distinction should be made between acute arsenic and arsine poison-ing. The classic presenting complaints after oral ingestion of arsenic are gastrointestinal; including nausea, vomiting, diarrhea, and abdominal pain. Arsenic is cor-rosive to the GI tract and can cause a diffuse, watery, cholera-like diarrhea. Cardiac effects may also be seen including tachycardia, hy-potension, QT prolongation, and ventricular dysrhythmias. A subacute peripheral neu-ropathy that progresses from a stocking-glove distribution occurs days to weeks after expo-sure and may mimic Guillan-Barre syndrome. In the acute setting, any organ system can be affected and in severely poisoned patients, confusion, encephalopathy, seizure, or coma may predominate.
Acute arsine poisoning occurs through the inhalational route, usually in an industrial setting such as metal smelting. The classic triad of arsine gas exposure is abdominal pain, followed by gross hematuria, and jaundice. The pathology of arsine poisoning is related to arsine induced hemolysis. The gross “hematuria” is actually a black or coca-cola colored urine and is related to hemoglo-bin and RBC breakdown products. The skin discoloration may actually be more orange than what is seen in classic jaundice.
Arsenic ingestion can be confirmed with a spot or 24 hour urine test. The most common cause of a positive arsenic result is recent seafood ingestion. Speciation can be performed to differentiate non-toxic organic forms of arsenic caused by seafood from inorganic toxic forms. In severe cases of acute arsenic poisoning, treatment should not be delayed for confirmatory testing.
The treatment for acute arsenic poisoning is supportive and chelation therapy. Decon-tamination rarely plays a role unless the inges-tion was recent and arsenic is detected on abdominal film, in which case whole bowel irrigation may be helpful. Chelation is indi-cated in a) severely symptomatic patients with confirmed ingestion; b) symptomatic patients with urinary arsenic (cont. on pg. 3)
THANK YOUThe Utah Poison Control Center expresses its sincere thanks to the health care professionals, public health officials and toxicology colleagues that
work together to treat and prevent poisonings.
UTAH POISON CONTROL CENTER STAFF
M E E T T H E U P C C S T A F F
ʶ Side effects associated with Potassium Iodide include allergic reactions, hypothyroidism, nausea, vomiting, diarrhea, rashes, and inflammation of salivary glands.
ʶ Long-term use, usually more than one year, of Proton Pump Inhibitor (PPIs) drugs (e.g., omeprazole, lansoprazole) have been associated with low serum magnesium levels.
MARILYN REDD became a PIP (Poison Information Providers) on the UPCC team in October 2009. She just finished her third year at the University of Utah, College of Pharmacy and is looking forward to clerkships during her fourth year. She was born and raised on a farm in Mon-ticello, UT, and loves to go home to the clear blue
skies and crisp country air during school breaks. Marilyn enjoys run-ning and cycling and has competed in two triathlons. Her more relax-ing hobbies include baking, crocheting, embroidering, and catching up with each of her five sisters. The follow-up calls she enjoys most are those in which she can hear the relief in the voice of a concerned par-ent when their child is completely fine after a poison exposure.
E M P L O Y M E N TThe UPCC is recruiting for the Assistant Director-Clinical position. This position is a member of the poison center management team and directly supervises approximately 12 specialists in poison information. For additional details, please see our website at www.utahpoisoncontrol.org/employment.
(cont. from pg. 2) Arsenic & Arsine > 50 mcg/L; or c) anyone with a urinary arsenic > 200 mcg/L. Di-mercaprol, commonly known as British anti-lewisite (BAL), is the parenteral chelation agent of choice in the US. However, it is poorly tolerated with a narrow therapeutic index and is administered IM in peanut oil. Succimer, or DMSA, is a hydrophilic analog of dimer-caprol that is administered by mouth but this may not be tolerated in severely poisoned patients. Chelation is not indicated in acute arsine poisoning and treatment is hydration, supportive care and possibly exchange transfusion.
Bibliography1. Caravati EM, Arsenic and Arsine Gas. In: Dart RC, ed. Medical Toxicology 3rd Edition. Philadelphia, PA: Lip-
pincott Williams & Wilkins; 2004:1393-1401.2. Muckter H, et al. Are we ready to replace dimercaprol (BAL) as an arsenic antidote? Hum Exp Toxicol 1997;
