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
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 casewas 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 levelsmay 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 saturationdifference 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 oxygensatura-tion difference supports cyanide toxicity, an in vitro study questions the ability of instruments presently
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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 becomeman-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 delayin
life-savingtherapy.
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
PediatricsMedical 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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JOSEPH D. LOSEK, ALICE L. ROCK and RHONDA R. BOLDT
Cyanide Poisoning From a Cosmetic Nail Remover
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