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Walter Reed Army Medical Center

Washington, DC

JAMES J. JELINEK, MAJ MC

Dept of Radiology

Walter Reed Army Medical Center

KATHLEEN MCHALE, LTC, MC

Dept of Orthopedics

Walter Reed Army Medical Center

MEGAN ADAMSON, MD

Human Genetics Branch

National Institute of Child Health and

Human Development

National Institutes of Health

Bethesda, MD

SONDRA W. LEVIN, MD

Dept of Pediatrics

Walter Reed Army Medical Center

Human Genetics Branch

National Institute of Child Health and

Human Development

REFERENCES

1. Weismann-Netter R, Stuhl L. D’une ost#{233}opathie cong#{233}nitale #{233}ventuellement familiale. Presse Med. 1954;62:1618-1622 2. Amendola MA, Brower AC, Tisnado J.

Weismann-Netter-Stuhl syndrome: toxopachyosteose diaphysaire

tibio-peron-iere.Am J Roentgenol. 1980;135:1211-1215

3. Robinow M, Johnson GF. The Weismann-Netter syndrome.

Am J Med Genet. 1988;29:573-579

4. Hoefnagel D. Malformation syndromes with mental defi-ciency. Birth Defect.s. 1969;2:11-15

5. Keats T, Alavi M. Toxopachyost#{233}ose diaphysaire tibio-p#{233}r-oni#{233}re (Weismann-Netter syndrome). Am J Roentgenol. 1970;109:568-574

6. Breuzard J, Tixier P, Sallet J. A propos des incurvations non rachitiques des membres inf#{233}rieurs: deux nouveaux cas de toxo-pachy-ost#{233}ose diaphysaire tibio-p#{233}roni#{233}reobserves chez l’adulte. Societe Med Hosp Paris. 1960;76:165-171 7. Krewer B. Dysmorphiejambi#{232}re de Weismann-Netter

(toxo-pachyost#{233}ose diaphysaire tibio-peroni#{232}re) chez deux vrais jumeaux. Presse Med. 1961;69:419-420

8. Larcan A, Cayotte JL, Gaucher A, Bertheau JM. La

toxo-pachyost#{233}ose de Weismann-Netter (a propos d’une nouvelle observation). Ann Med Nancy. 1963;2:1724-1732

9. Weismann-Netter R, Rouaux V. Toxopathyost#{233}ose diaphy-saire tibio-peroniere (R. Weismann-Netter et L. Stuhl) chez deux soeurs. Presse Med. 1956;64:790

10. Greulich WW, Pyle SI. Radiographic Atlas of Skeletal

De-velopment of the Hand and Wrist. 2nd ed. Stanford, CA: Stanford University Press; 1959

Cyanide

Poisoning

From

a

Cosmetic

Nail Remover

Delayed cyanide toxicity is illustrated in the case

of a 23-month-old child who ingested Super Nail

Nail Off. This product has 98% to 100% acetonitrile

and is used to remove sculptured nails. When

in-gested or inhaled by mammals, acetonitrile, an

ali-phatic nitrile, is metabolized to cyanide.’5. Several deaths following inhalation of acetonitrile in

indus-trial settings have been reported.6’7 Ingestion of

acetonitrile has resulted in only one reported

death.8 We present the following case to alert

pri-mary care physicians to the delayed cyanide toxicity of this product.

CASE REPORT

A previously well 23-month-old boy was seen in the emergency department 12 hours after the ingestion of

appproximately 60 mL of Super Nail Nail Off. The

pa-Received for publication Jul 27, 1990; accepted Sep 5, 1990. Reprint requests to (J.D.L.) Dept of Pediatrics, Children’s Hos-pital of Wisconsin, 9000 Wisconsin Aye, MS 756, Milwaukee, WI 53226.

PEDIATRICS (ISSN 0031 4005). Copyright © 1991 by the American Academy of Pediatrics.

tient had vomited three times 6 hours postingestion, but

otherwise he did not appear ill.

In the emergency department, the patient’s rectal tem-perature was 35.6#{176}C,blood pressure 96/60 mm Hg, pulse rate 144 beats per minute, and respiratory rate 40 breaths

per minute. Examination results were within normal

limits. Fundoscopic examination results were normal. No

bitter almond smell was noted. Laboratory results

re-vealed the following values: pH, 7.43; sodium, 136 mEg]

L; potassium, 4.2 mEciJL; carbon dioxide, 21.2 mEgJL;

chloride, 102 mEg]L; and anion gap, 13. Blood was drawn for determination ofcyanide level. Eight liters per minute

of oxygen by mask was initiated and the patient was

admitted.

Twenty-four hours postingestion the patient began

having staring episodes and was not responding to his

mother. At that time, vital signs were as follows: heart

rate, 130 beats per minute; blood pressure, 110/50 mm

Hg; and respiratory rate, 30 breaths per minute. Exami-nation results otherwise were within normal limits. Oxy-gen saturation by pulse oximetry was 93% on 8 L/min of

oxygen by mask. The low oxygen saturation prompted

the administration of amyl nitrite. A broken ampule was held under the patient’s nose, but the patient’s condition did not change.

A chest roentgenogram was normal. Arterial blood gas analyses revealed the following values: pH, 7.43; Pco2, 26.4 mm Hg; Po2, 167.6 mm Hg; HCO,, 17 mEgjL; and oxygen saturation, 99%. Lactic acid concentration was 50.1 mg/dL and methemogbobin level was 0.7 g/dL. Fur-ther treatment was then given, including activated

char-coal with magnesium citrate and intravenous sodium

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338 PEDIATRICS Vol. 88 No. 2 August 1991

sodium thiosulfate, lactic acid level decreased to 14.2 mgI dL (normal 4.0 to 15.0 mg/dL), and arterial blood gas values were as follows: pH, 7.42; Pco,, 33.8 mm Hg; Po,, 435.8 mm Hg; HCO,, 21.8 mEgJL; and oxygen saturation,

99.9%. At approximately 25 hours postingestion, blood

was again drawn for determination of cyanide level. During his hospital course, the patient received sodium thiosulfate every 4 hours for five doses. During this time, the patient’s level of consciousness returned to normal and the pulse oximeter readings were 95% to 98% while he was breathing room air. The patient was discharged

on the third hospital day. Whole-blood cyanide levels

were later received and were 2.1 g/mL 12 hours post-ingestion and 3.8 g/mL 25 hours postingestion.

DISCUSSION

To our knowledge, this is the sixth reported case of acetonitrile ingestion resulting in cyanide

toxic-ity. Summary of these six cases is given in the

Table. The first case was a 26-year-old man who

ingested 40 g of acetonitrile in a suicide attempt.9

Coma, shock, and respiratory failure required

an-tidote treatment. The second case was a

39-year-old woman who also attempted suicide. Antidote

treatment

was given over

3 days.’#{176}The third case

was a 2-year-old child who ingested Nailene Glue

Remover, which contains 84% acetonitrile. Coma

was rapidly reversed with antidote treatment.” The

last three children ingested Super Nail Nail Off.

Case four required only supportive care despite a

potentially lethal cyanide level.8

The fifth case was a 16-month-old boy who

in-gested 15 to 30 mL of Super Nail Nail Off and

vomited 20 minutes postingestion.8 Poison center

was contacted, but no treatment was recommended

because the product was mistaken for an

acetone-containing nail polish remover. Respiratory distress

developed after he was put to bed. The patient was

left to sleep and was found dead 12 hours after

ingestion.

Oral median lethal dosages of acetonitrile in

an-imals are 177 mg/kg in guinea pigs, 200 mg/kg in

young rats, and 1.7 to 8.5 g/kg in adult rats.’ We

do not believe these lethal doses are applicable to

children because of the wide range, even in the

same animal species. Serum levels of greater than

3.0 sg/mL are potentially lethal,’2 but as in our

case levels may not be immediately available.

Be-cause

lethal doses are unknown and cyanide levels

may not be rapidly determined, we suggest hospital

admission and initiating supportive care for

asymp-tomatic children who ingest acetonitrile.

Vomiting was present in the six patients

ingest-ing acetonitrile. Vomiting also occurs with

inges-tion

of

acetone-containing nail polish removers.

Other symptoms of acetone toxicity include

beth-argy, slurred speech, ataxia, stupor, coma, and

res-piratory depression.’3 These are similar to the

symptoms of cyanide toxicity, which include

con-fusion, nausea, vomiting, tachycardia, coma,

con-vulsions, and cardiovascular collapse.’2 Therefore,

it is critical that these two nail remover products

not be considered the same despite similar uses and

toxic symptoms.

The smell of bitter almonds was not noticed in

any of the above cases. The three physicians caring

for the case presented can smell bitter almonds,

unlike one-half of the general population. Another

physical finding of cyanide poisoning is equally red

retinal veins and arteries. This was not noted in

our case and was not documented in the cases

previously reported.

With acetonitrile ingestion, symptoms of cyanide

toxicity develop over a latency period. During this

period, oxidative metabolism of acetonitrile via the

cytochrome P-450-dependent hepatic microsomal

enzyme system occurs and cyanide is slowly

re-leased.4’5 This latency period is reported to be 3 to

4 hours and as long as 12 hours. For this reason,

the patient may not seek medical care for hours

after ingestion, as occurred in our patient. Despite

the likelihood of a delay in seeking medical care

and no specific data on acetonitrile binding to

ac-tivated charcoal, activated charcoal and a cathartic

is recommended.8 For those patients who present

early, lavage instead of ipecac is recommended

be-cause symptoms of altered consciousness can

de-velop rapidly.

Noting the difference between the oxygen

satu-ration of the pulse oximeter vs arterial blood gases

can be a diagnostic aid in patients who present with altered consciousness and respiratory insufficiency

from unknown cause. The oxygen saturation from

arterial blood gases is calculated from the measured

P02. The Po2 is not affected by the presence of

dysfunctional hemoglobin (cyanhemogbobin) and,

therefore, the calculated oxygen saturation is

nor-mal in cyanide toxicity.’2 However, the measured

oxygen saturation via pulse oximeter is lower

be-cause some of the hemoglobin (cyanhemoglobin) is

not

carrying oxygen. When the oxygen saturation

difference between the arterial blood gas and pulse

oximeter is 5 or greater, a dysfunctional hemoglobin

is suspected.’2 If amyl nitrate is administered prior

to determining the oxygen saturation difference,

methemoglobin instead of cyanhemogbobin

ac-counts for the difference. Our patient’s oxygen

sat-uration per pulse oximeter was determined before

nitrate therapy and the oxygen saturation

differ-ence was

6. Although our patient’s oxygen

satura-tion difference supports cyanide toxicity, an in vitro study questions the ability of instruments presently

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www.aappublications.org/news

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(4)

340 PEDIATRICS Vol. 88 No. 2 August 1991

used to detect a significant oxygen saturation

dif-ference secondary to cyanhemoglobin.’4 Other

measurements that may suggest cyanide poisoning

include an elevated venous P02, an elevated

meas-ured venous oxygen saturation, or a small

arterial-central venous measured oxygen saturation

differ-ence.

Standard cyanide antidotal therapy (amyl

ni-trite-10% sodium nitrite-25% sodium thiosulfate)

is possibly less effective for acetonitrile than for

inorganic cyanide poisoning.’5 Sodium thiosulfate

combines with available cyanide to form the

non-toxic thiocyanate, which is excreted in the urine.

Nitrite induces methemoglobin, which has greater

affinity for cyanide than hemoglobin. Therefore,

nitrites are recommended for acute inorganic

cya-nide toxicity, whereas sodium thiosulfate alone may

be preferred for prolonged release of cyanide from

acetonitrile. For this reason, our patient was not given sodium nitrite. However, if the patient’s

con-dition is not improving with sodium thiosulfate

alone, nitrite therapy should be administered. An

additional nitrite antidotal mechanism besides

met-hemoglobin induction has been postulated.’6 Other

cyanide antidotes not approved for use in the

United States include hydroxocobalamin and

di-cobalt ethylenediaminetetraacetic acid.’2

Acetonitrile is present in the following fingernail

cosmetic products: Super Nail Nail Off, Nailene

Salon Quality Glue Remover, Artificial Nail Tip

and Glue Remover, Super Nail Wrap Off Instant

Glue Dissolver, Super Nail Tip Off, Super Nail

Glue Off, and Ardell Instant Glue Remover.8 These

products are marketed to professional beauty

op-erators,

but they are available to the general public.

Each product is packaged in a non-child-resistant

bottle that

contains

a

potentially lethal amount of acetonitrile. Child-resistant caps will become

man-datory in 1991 (telephone communication with Dr

Tony Litovitz, Medical Director, National Capital

Poison Center, Washington, DC. August, 1990).

Mistaking these products for acetone-containing nail polish

removers

can

lead to delay

in

life-saving

therapy.

ACKNOWLEDGMENT

We thank Frances Sommer for her assistance in the

preparation of this manuscript.

REFERENCES

JOSEPH D. LOSEK, MD

ALICE L. ROCK, MD

RHONDA R. BOLDT, MD

Dept

of

Pediatrics

Medical College of Wisconsin Children’s Hospital of Wisconsin Milwaukee

1. Pozzani UC, Carpenter CP, Palm PE, Weil CS, Nair JH III. An investigation of the mammalian toxicity of acetonitrile. J Occup Med. 1959;1:634-642

2. Willhite CC, Smith RP. The role of cyanide liberation in the acute toxicity of aliphatic-nitriles. Toxicol Appl Phar-macol 1981;59:589-602

3. Tanii H, Hashimoto K. Studies on the mechanism of acute toxicity of nitriles in mice. Arch Toxicol. 1984;55:47-54 4. Freeman JJ, Hayes EP. Microsomal metabolism of

aceto-nitrile to cyanide. Biochem PharmacoL 1988;37:1153-1159 5. Freeman JJ, Hayes EP. The metabolism of acetonitrile to

cyanide by isolated rat hepatocytes. Fundam AppI Toxicol. 1987;8:263-271

6. Amdur ML. Accidental group exposure to acetonitrile. J Occup Med. 1959;1:627-633

7. Dequidt J, Furon D, Wattel F, et a!. Acetonitrile poisoning: report of a fatal case. J Eur Toxicol. 1974;7:91-97

8. Caravati EM, Litovitz TL. Pediatric cyanide intoxication and death from an acetonitrile-containing cosmetic. JAMA. 1988;260:3470-3473

9. Jaeger A, Tempe JD, Porte A, Stoeckel L, Mantz JM. Acute voluntary intoxication by acetonitrile. Acta Pharmacol Tox-icoL 1977;41(suppl):340. Abstract

10. Turchen SG, Manoguerra AS. Severe cyanide poisoning following suicidal ingestion ofacetonitrile. Vet Hum ToxicoL 1989;31:356. Abstract

11. Kurt TL, Day LC, Reed WS, Gandy W. Cyanide poisoning from sculpted nail remover. Vet Hum ToxicoL 1989;31:339. Abstract

12. Hall AH, Rumack BH. Clinical toxicology of cyanide. Ann Emerg Med. 1986;15:1067-1074

13. Gamis AS, Wasserman GS. Acute acetone intoxication in a pediatric patient. Pediatr Emerg Med. 1988;4:24-26

14. Curry SC, Patrick HC, Bond GR, Hall AH. Cyanide does

not produce a hemoglobin oxygen saturation gap. Vet Hum ToxicoL 1989;31:379

15. Willhite CC. Inhalation toxicology of acute exposure to aliphatic-nitriles. Clin ToxicoL 1981;18:991-1003

16. Johnson WS, Hall AH, Rumack BH. Cyanide poisoning successfully treated without ‘therapeutic methemoglobin levels.’ Am J Emerg Med. 1989;7:437-440

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1991;88;337

Pediatrics

JOSEPH D. LOSEK, ALICE L. ROCK and RHONDA R. BOLDT

Cyanide Poisoning From a Cosmetic Nail Remover

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1991;88;337

Pediatrics

JOSEPH D. LOSEK, ALICE L. ROCK and RHONDA R. BOLDT

Cyanide Poisoning From a Cosmetic Nail Remover

http://pediatrics.aappublications.org/content/88/2/337

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American Academy of Pediatrics, 345 Park Avenue, Itasca, Illinois, 60143. Copyright © 1991 by the

been published continuously since 1948. Pediatrics is owned, published, and trademarked by the

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