Prolonged Seizures due to
Contact and
Inhalation Exposure to Camphor A Case Cdr. R. R.
Skoglund, M:C. U.S.N., Lcdr. L. L. Ware, Jr., M.C. U.S.N., Capt. J. E. Schanberger, M.C. U.S.N.
CAMPHOR
POISONING as a distinct has been known for the past 20 y~ars;’1 entity yet the quantities of over-the-counter preparations’ with questionable therapeutic effectiveness allo~~f accidental poisonings seen in children to continue. Sibert3 in 1973 reports that 9.5 per cent of all hospitalizations due to accidental poisoning in the 6-month to 5-year age period were due to camphor poisoning. In 1973, approximately 500 cases were reported in the United States.4 The most common route of camphor poisoning is by oral îngestion.Butit has been reported through other routes such as întranasal by instillation of nasal drops con-
search
‘
From the
that inhalation of induce clinical references. Indeed, a
states
camphorated vapor poisoning but gives no
can
Department of Pediatrics and Clinical
Investigation Center, Naval Regional Medical Center, San Diego, California 92134. Supported in part by the Bureau of Medicine and Surgery Clinical Investigation Program. Correspondence to: Cdr. R. R. Skoglund, M.C. U.S.N., Department of Pediatrics, Naval Regional Medical Center, San Diego, CA 92134. The opinions or assertions expressed herein are those of the authors and are not to be construed as official or as reflecting the views of the Navy Department or the naval service at large.
of’ English
medical literattire failed
to
reports of camphor poisoning secondary to vapor inhalation or by skin absorjJtion. ~’e here present such a case with resultant seizures upon exposure to camphor by these two routes. uncover
taining camphor, intraperitoneal by injection, by transplacental trans-
and mother-to-fetu,5 fer.5-7 J acobziner8
Report
Case E.
Report H.,
7!i!lz-year-old
a
white
boy,
came
to
pediatric neurology clinic For seizure follow-up. He had had normal growth and development
our
until age
15
months
when he had crawled
through spirits-cif-carn~hon ’s~illeci by a sibling. The preparation contained I’0 per cent camphor. Over the ensuing 48 hours, the child became progressively ataxic and had some brief generalized major motor seizures. After Iztaspitalization, the seizures persisted for two days despite appropriate phenobarbital therapy. Over a 15-day period, he siwvly im~ro~Ted--from severe recurrent shaking of extremities with position changes while bedridden, to ambuiation with ataxic gait. His birth weight was 6 lb 10 oz. He was delivered by a breech presentation to a 23-year-old female gravida-4, para-2, aborts-1. No Apgar scores are reported. The mother stated that the baby was lethargic at birth, but with vigorous stimulation spontaneous breathing began. He was discharged from the nursery with his mother. at four days of age. Growth and development recorded by a pediatrician were normal; immunizations were up-to-date. He had not been ill in the months preceding admission for the present illness.
901
Downloaded from cpj.sagepub.com at Purdue University on April 12, 2015
Laboratory data at hospitalization at 1 ~ months inrlucled normal blood chemistry levels, normal, complete blood count (CBC), and normal radiographs of skull, chest, and long bones. Lumbar puncture revealed clear fluid, protein 34 mg%, cells-none, cultures-no growth. Electroencephalogram (EEG) displayed diffuse spikewave activity bilaterally; which disappeared in two subsequent EEG examinations. Recovery in motor and mental function was complete. The 15 month old boy
was
discharged
He had when a
no
on
phenobarbital.
further seizures until
a
year later
camphorated vaporizer preparation containing 4.81 per cent camphor was given by
the mother to relieve symptoms of an acute afebrile upper respiratory illness. Concurrent with this inhalant exposure, a brief major motor seizure occurred. The camphor source was removed. The boy had had no further seizures during 5 years of control with phenobarbital. This drug was discontinued over the past year, without recurrence of seizures. The occurrence of seizures only with two camphor exposures a year apart indicate a specific sensitivity to this agent.
Discussion This case is a unique example of how skin surface absorption and later inhalation of a toxin can be related to a serious alteration in cerebral function. Camphor is a pleasant-smelling hydroaromatic compound of the terpene group. Gastrointestinal absorption is rapid, producing symptoms in as little time as 5 minutes Once ingested, inhaled, or absorbed, products of camphor are conjugated in the liver to produce an inactive substance which is excreted in the urine. Camphorated oil is 20 per cent camphor in cottonseed oil. The lethal dose of camphor in a one-year-old child is said to be I gm-the content of one teaspoon of camphorated oil. In adults, 2 gm produce toXiCity.3 The toxicology rating for camphor sets a human lethal dose at 50 mg t0500mg/kg.lO This is a &dquo;class 4-very toxic rating. 112 Neurologic changes from camphor ingestion include anxiety, confusion, depression, headache, dizziness, hallucinations, facialtwitching, convulsions, and coma. Eye findings include dilated pupils, strabismus and peculiar optic movements, and amblyopia.
Gastrointestinal symptoms are more comthan neurologic manifestations. With
mon
ingestion, gastrointestinal symptoms may have an immediate ‘onset:.3 Fatty changes in the liver and kidney can also occur pathologically.5 Recovery is usually complete within 48 hours, though our patient had a more prolonged phase. Death, reported up to five days after ingestion,’ is usually due to respiratory failure. The efficacy of treatment has never been documented in controlled series. The literature advises removal of stomach contents by emesis or lavage, and to avoid instilling digestible oil or alcohol which promotes absorption .2 -1 No specific antidote is available, so attention to symptomatic care is vital. Treatment of seizures with anticonvulsants is an obvious adjunct to symptomatic care. The use of barbiturate for this purpose has been shown to prevent convulsions and to protect against neural damage in experimental animals.5It has the additional theoretical advantage of activating liver enzymes.9 In the most critical situations lipid dialysis has been successfully empl
Contact and
Inhalation Exposure to Camphor A Case Cdr. R. R.
Skoglund, M:C. U.S.N., Lcdr. L. L. Ware, Jr., M.C. U.S.N., Capt. J. E. Schanberger, M.C. U.S.N.
CAMPHOR
POISONING as a distinct has been known for the past 20 y~ars;’1 entity yet the quantities of over-the-counter preparations’ with questionable therapeutic effectiveness allo~~f accidental poisonings seen in children to continue. Sibert3 in 1973 reports that 9.5 per cent of all hospitalizations due to accidental poisoning in the 6-month to 5-year age period were due to camphor poisoning. In 1973, approximately 500 cases were reported in the United States.4 The most common route of camphor poisoning is by oral îngestion.Butit has been reported through other routes such as întranasal by instillation of nasal drops con-
search
‘
From the
that inhalation of induce clinical references. Indeed, a
states
camphorated vapor poisoning but gives no
can
Department of Pediatrics and Clinical
Investigation Center, Naval Regional Medical Center, San Diego, California 92134. Supported in part by the Bureau of Medicine and Surgery Clinical Investigation Program. Correspondence to: Cdr. R. R. Skoglund, M.C. U.S.N., Department of Pediatrics, Naval Regional Medical Center, San Diego, CA 92134. The opinions or assertions expressed herein are those of the authors and are not to be construed as official or as reflecting the views of the Navy Department or the naval service at large.
of’ English
medical literattire failed
to
reports of camphor poisoning secondary to vapor inhalation or by skin absorjJtion. ~’e here present such a case with resultant seizures upon exposure to camphor by these two routes. uncover
taining camphor, intraperitoneal by injection, by transplacental trans-
and mother-to-fetu,5 fer.5-7 J acobziner8
Report
Case E.
Report H.,
7!i!lz-year-old
a
white
boy,
came
to
pediatric neurology clinic For seizure follow-up. He had had normal growth and development
our
until age
15
months
when he had crawled
through spirits-cif-carn~hon ’s~illeci by a sibling. The preparation contained I’0 per cent camphor. Over the ensuing 48 hours, the child became progressively ataxic and had some brief generalized major motor seizures. After Iztaspitalization, the seizures persisted for two days despite appropriate phenobarbital therapy. Over a 15-day period, he siwvly im~ro~Ted--from severe recurrent shaking of extremities with position changes while bedridden, to ambuiation with ataxic gait. His birth weight was 6 lb 10 oz. He was delivered by a breech presentation to a 23-year-old female gravida-4, para-2, aborts-1. No Apgar scores are reported. The mother stated that the baby was lethargic at birth, but with vigorous stimulation spontaneous breathing began. He was discharged from the nursery with his mother. at four days of age. Growth and development recorded by a pediatrician were normal; immunizations were up-to-date. He had not been ill in the months preceding admission for the present illness.
901
Downloaded from cpj.sagepub.com at Purdue University on April 12, 2015
Laboratory data at hospitalization at 1 ~ months inrlucled normal blood chemistry levels, normal, complete blood count (CBC), and normal radiographs of skull, chest, and long bones. Lumbar puncture revealed clear fluid, protein 34 mg%, cells-none, cultures-no growth. Electroencephalogram (EEG) displayed diffuse spikewave activity bilaterally; which disappeared in two subsequent EEG examinations. Recovery in motor and mental function was complete. The 15 month old boy
was
discharged
He had when a
no
on
phenobarbital.
further seizures until
a
year later
camphorated vaporizer preparation containing 4.81 per cent camphor was given by
the mother to relieve symptoms of an acute afebrile upper respiratory illness. Concurrent with this inhalant exposure, a brief major motor seizure occurred. The camphor source was removed. The boy had had no further seizures during 5 years of control with phenobarbital. This drug was discontinued over the past year, without recurrence of seizures. The occurrence of seizures only with two camphor exposures a year apart indicate a specific sensitivity to this agent.
Discussion This case is a unique example of how skin surface absorption and later inhalation of a toxin can be related to a serious alteration in cerebral function. Camphor is a pleasant-smelling hydroaromatic compound of the terpene group. Gastrointestinal absorption is rapid, producing symptoms in as little time as 5 minutes Once ingested, inhaled, or absorbed, products of camphor are conjugated in the liver to produce an inactive substance which is excreted in the urine. Camphorated oil is 20 per cent camphor in cottonseed oil. The lethal dose of camphor in a one-year-old child is said to be I gm-the content of one teaspoon of camphorated oil. In adults, 2 gm produce toXiCity.3 The toxicology rating for camphor sets a human lethal dose at 50 mg t0500mg/kg.lO This is a &dquo;class 4-very toxic rating. 112 Neurologic changes from camphor ingestion include anxiety, confusion, depression, headache, dizziness, hallucinations, facialtwitching, convulsions, and coma. Eye findings include dilated pupils, strabismus and peculiar optic movements, and amblyopia.
Gastrointestinal symptoms are more comthan neurologic manifestations. With
mon
ingestion, gastrointestinal symptoms may have an immediate ‘onset:.3 Fatty changes in the liver and kidney can also occur pathologically.5 Recovery is usually complete within 48 hours, though our patient had a more prolonged phase. Death, reported up to five days after ingestion,’ is usually due to respiratory failure. The efficacy of treatment has never been documented in controlled series. The literature advises removal of stomach contents by emesis or lavage, and to avoid instilling digestible oil or alcohol which promotes absorption .2 -1 No specific antidote is available, so attention to symptomatic care is vital. Treatment of seizures with anticonvulsants is an obvious adjunct to symptomatic care. The use of barbiturate for this purpose has been shown to prevent convulsions and to protect against neural damage in experimental animals.5It has the additional theoretical advantage of activating liver enzymes.9 In the most critical situations lipid dialysis has been successfully empl
