Bromate Poisoning From Hair Permanent Preparations

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Reprint requests to (B.L.W.) Department of Pediatrics, 2040 Ridgewood Dr, NE, Atlanta, GA 30322.

1. Burr ML: Does infant feeding affect the risk of allergy?

Arch Dis Child 1983;58:561-565

2. Hide DW, Guyer BM: Clinical manifestations of allergy related to breast and cows’ milk feeding. Arch Dis Child

1981;56:172-175

3. Hide DW, Guyer BM: Cows milk intolerance in Isle of Wight infants. Br J Clin Pract 1983;37:285-287

4. Cogswell JJ, Alexander J: Breastfeeding and eczema! asthma. Lancet 1982;1:910

5. Fergusson DM, Horwood U, Shannon FT: Asthma and

infant diet. Arch Dis Child 1983;58:48-51

6. Zach M, Erben A, Olinsky A: Croup, recurrent croup, allergy and airways hyper-reactivity. Arch Dis Child 1981;56:336-341

7. Saarinen UM, Kajosaari M, Backman A, et al: Prolonged breast feeding as prophylaxis for atopic disease. Lancet

1979;2:163-166

8. Downham MAPS, Scott R, Sims DG, et al: Breast feeding protects against respiratory syncytial virus infection. Br MedJ 1976;2:274-6.

9. Stuart CA, Twiselton R, Nicholas M, et al: Passage of cows’ milk protein in breast milk. Clin Allergy 1984;14:533-535

Bromate

Poisoning

From

Hair

Permanent

Preparations

Potassium bromate is a tasteless, odorless, and colorless chemical found in the neutralizing solu-tion of cold wave home hair permanents and profes-sional solutions. Toxic ingestions of this substance were initially reported during the 1940s and 1950s and are characterized primarily by gastrointestinal symptoms, hearing impairment, and acute renal failure.’ Although many manufacturers have now substituted less toxic substances as neutralizers, use of potassium bromate in some hair permanent solutions continues, and poisonings from this sub-stance still occur.24

Because renal failure from potassium bromate intoxication may be severe, dialysis may be

neces-sary for replacement of renal function. Moreover, a major toxicology reference presently suggests that “if readily available, the prompt use of hemodialysis or peritoneal lavage may serve to remove absorbed but unreacted bromate in significant amounts.”1 However, because of limited clinical experience, the

optimal time for initiating dialysis is not well de-fined, and more data are needed to determine the role of dialysis in the early management of this condition.

We have recently encountered four children with

accidental potassium bromate ingestion. The pur-pose of this report is to analyze the clincal course, therapy, and outcome of these cases and to review the literature in order to formulate improved guide-lines for the use of dialysis.

CASE REPORTS

Case I

A two-year-old boy was observed to drink “a swallow” of home cold wave hair permanent neutralizer (Soft and

Free, M & M Products, Atlanta) containing 10% to 12%

potassium bromate. He was given water and milk and

began vomiting 15 minutes later. Because vomiting

con-tinued for more than six hours, he was taken to the Pediatric Emergency Clinic at Grady Memorial Hospital where the findings on physical examination were normal,

with the exception of lethargy. The initial BUN value

was 20 mg/dL and the serum creatinine value was 0.7

mg/dL (Table). Gastric lavage was performed, followed

by administration of activated charcoal and one

intrave-nous dose of 10% sodium thiosulfate. He had no sponta-neous voiding for approximately 26 hours after

admis-sion. Following a dose of furosemide, urine output grad-ually increased. The peak BUN value was 67 mg/dL and

the peak creatinine value was 3.7 mg/dL on the second and third days of hospitalization, respectively, with

re-turn to normal values (18 and 0.4 mg/dL, respectively)

and adequate urine output by the fifth day of hospitali-zation. The child is now 3 years of age and his mother

reports apparently normal speech and hearing.

Case 2

A 17-month-old boy drank approximately 30 mL of

hair-neutralizing solution (Cosmopolitan Curl, Bronner Brothers, Atlanta) containing bromate and began vom-iting approximately one-half hour later. He was taken to

the Pediatric Emergency Clinic at Grady Memorial

Hos-pital, where he appeared lethargic, but the results of his

physical examination were otherwise normal. The initial

BUN value was 11 mg/dL and the creatinine value was

0.6 mg/dL (Table). Study of RBC morphology revealed the presence of schistocytes. Urinalysis results were 2+ protein, 1+ glucose, and normal microscopic findings.

Gastric lavage was performed, followed by administra-tion of activated charcoal. He was given 10 mL of 20%

sodium thiosulfate intravenously, two hours after inges-tion, and was admitted for observation.

On the second and third days of hospitalization, the

BUN reached a peak value of38 mg/dL and the creatinine

a peak value of 2.7 mg/dL, and no spontaneous urine

output was noted for 12 hours. Furosemide was admin-istered with good response. Thereafter, renal function

improved, and by the fourth hospital day the BUN value had decreased to 26 mg/dL and the creatinine value to

0.5 mg/dL. He is now 28 months of age and his mother

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Bromide*

(mg/dL)

TABLE. Laboratory Values

Patient No. Age (mo) Hospital Day BUN (mg/dL) Creatinine (mg/dL) 1 2 3 4 32 17 19 19 1 2AM PM 3AM PM 4 5 1 2 3AM PM 4 5 1 2 3 1 5 6 8t 9 13 15 22 20 31 43 58 67 50 18 11 31 33 38 29 26 14 19 15 29 124 132 119 77 64 91 25 0.7 2.6 3.7 3.5 2.9 1.0 0.4 0.6 2.3 2.7 1.4 0.9 0.5 0.5 0.5 0.5 2.4 7.7 8.4 10.2 7.7 4.2 2.6 0.7 Hct (%) 39 38 37 42 26 18.6 6.0 5.9

CThree patients had measurements of serum bromide concentration. Bromate

measure-ments were not available.

t Dialysis initiated. :1:Dialysis discontinued.

976 PEDIATRICS

Vol. 76 No. 6 December

1985

Case 3

An 18-month-old boy, playing with patient 2, ingested an unknown amount of hair-neutralizing solution con-taming bromate. He began to vomit approximately 30 minutes after ingestion and had one episode of hemate-mesis. Upon arrival at Grady Memorial Hospital, he was

lethargic but otherwise his physical examination findings

were normal. Gastric lavage was performed, followed by

administration of activated charcoal, and he was admit-ted for observation. He did not receive sodium thiosulfate. Laboratory values on admission were: BUN, 14 mg/dL; creatinine, 0.5 mg/dL; serum bicarbonate, 17 mg/dL

(Ta-ble). His hospital course was uneventful with mainte-nance of normal urine output and no change in the BUN and creatinine concentrations. He has been lost to follow-up, and the status of his hearing is unknown.

Case 4

An 18-month-old boy ingested approximately 60 to 90 mL of professional cold wave neutralizer (Soft and Free,

M & M Products, Atlanta). Vomiting ensued, and 30

minutes after the ingestion he was taken to a local

emergency room. Consultation from the regional Georgia Poison Control Center indicated that the neutralizer

contained bromate. Gastric lavage and activated charcoal

were administered, and the infant was admitted to the hospital. However, during subsequent management, the neutralizer was erroneously thought to contain bromideS rather than bromate. His physical examination findings on admission were normal. His laboratory values (Table)

were: WBC count, 36,600 with 73 neutrophils, 18 band

cells, seven lymphocytes, and two monocytes; hematocrit, 42%; hemoglobin, 14.1 g/dL; BUN, 29 mg/dL; serum creatinine, 2.4 mg/dL. He was started on intravenous

fluids and sodium bicarbonate. On his third day of hos-pitalization, a regular diet was attempted but was

discon-tinued because of vomiting. On the fifth day, he was noted to be lethargic with cessation of spontaneous void-ing. Laboratory studies revealed a metabolic acidosis with a pH of 7.24; BUN, 124 mg/dL; creatinine, 7.7 mg/dL.

On the sixth day, the regional Georgia Poison Control

Center was again consulted and the distinction between bromide and bromate poisoning was recognized. Twenty milliliters of 10% sodium thiosulfate was given

intrave-nously. On the seventh day after ingestion, he was

trans-ferred to Henrietta Egleston Hospital for Children.

The physical examination findings revealed an alert

boy with mild periorbital and pedal edema and an Il/VI systolic ejection murmur. The initial laboratory studies

were as follows: serum sodium, 142 mEqJL; potassium,

6.8 mEcijL; chloride, 89 mEqjL; bicarbonate, 18 mEcijL; BUN, 139 mg/dL; creatinine, 9.9 mg/dL; WBC count,

10,000/id; hematocrit, 25%; hemoglobin, 8.2 g/dL; retic-ulocyte count, 0.3%. Hemoglobin electrophoresis was nor-mal and the serum haptoglobin value was 227 mg/dL (elevated).

Peritoneal dialysis was initiated on the day of admis-sion and continued for seven days. The hematocrit value decreased to 22% and a transfusion of packed RBCs was

administered. Renal nuclear scan, performed eight days after ingestion, showed depressed uptake and no

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tion of isotope. Spontaneous voiding resumed on the

ninth day following ingestion, after 96 hours of anuria

and two days of dialysis. The initial urine specimen showed 4+ protein and 60 to 70 WBCs per high-power field. Results of a hearing test performed by an audiology

consultant in the intensive care unit were normal.

Four weeks after ingestion, recovery appeared com-plete. A urinalysis was normal. The BUN value was 20 mg/dL and the creatinine value was 0.7 mg/dL.

DISCUSSION

Bromate is a highly toxic substance that has resulted in fatal poisoning,4’5 deafness,24 or irre-versible renal failure.6 Because few cases of bromate

poisoning have been reported in the medical liter-ature, the toxicity of this substance is not widely recognized. In a recently reported case2 and in one case described here, confusion with the consider-ably less toxic bromide ion delayed diagnosis and postponed appropriate therapy.

Several manufacturers of hair permanent prepa-rations now substitute less toxic substances than potassium bromate in the neutralizer solutions, eg,

sodium perborate and sodium hexametaphosphate.’

However, the two products responsible for the

poi-sonings in our patients still include bromate in both home and professional solutions, and a third prod-uct resulted in poisoning in a recent case from California.2 Moreover, bromate is reportedly still widely used in other countries such as Japan.4

Thirteen cases of bromate poisoning have been reported previously in children2’3’5’7’2 with one death due to acute renal failure prior to the avail-ability of dialysis.5 Twenty Japanese cases involv-ing adults were recently reviewed,4 and one other

adult case has been reported from Korea.6 Among the adults, there were nine deaths, most of which were suicides.

The toxic dose of potassium bromate has not

been established, but doses as small as 2 oz of a 2%

solution have caused serious poisonings in

chil-dren.’ The toxic effects usually manifest within one

hour of ingestion with gastrointestinal symptoms including nausea, vomiting, epigastric pain, and occasionally diarrhea and hematemesis; no

long-term gastrointestinal sequelae have been reported.’ CNS depression usually follows and may be of variable severity. Three of 13 pediatric patients had seizures,2’5”2 and a fourth suffered transient loss of consciousness.7 Most of the others, including each of our four patients, experienced only mild CNS depression, and there have been no reports of

long-term sequelae. Hematologic effects of bromate

tox-icity have included anemia reported in four chil-dren, including severe microangiopathic anemia in one2; the latter case presented findings similar to the hemolytic uremic syndrome. Our case 4

dem-onstrated similar findings, although the evidence for hemolysis was inconclusive. We observed

dys-morphic RBCs (schistocytes) in one of our

remain-ing three patients, none of whom had significant anemia.

In contrast to the reversible toxic manifestations

described above, potentially irreversible conse-quences of bromate poisoning include hearing loss and renal failure. Permanent sensorineural hearing loss has been reported in two pediatric patients.2’3 Although no obvious sequelae were described in most of the other pediatric cases, hearing outcome was not specifically mentioned. Among the four children in the present report, hearing tests dem-onstrated no abnormalities in one, and follow-up reports from their mothers suggested intact hearing

and speech development in two others. No infor-mation was available for the remaining child (who was the mildest case clinically). Among adults, deaf-ness was reported in 17 of 20 cases from Japan, with onset of irreversible damage occurring between four and 16 hours following ingestion.4 Experimen-tally, injection of bromate into guinea pigs produced

deafness, attributed to cochlear damage, within one to 24 hours, depending on the dose administered.4

In nine of 13 children in previous reports and in

three of four children in the present study acute renal failure developed. Among these 12 children with renal failure, one died prior to the availability of dialysis; three underwent acute peritoneal di-alysis, with good recovery in one (our case 4) and only partial recovery in two2’3; the remaining eight recovered without dialysis. In addition, a recent report from Korea described an 18-year-old woman who presented ten days following bromate ingestion

with permanent deafness and irreversible renal fail-ure requiring maintenance hemodialysis.6 Patho-logic studies have demonstrated tubular necrosis and interstitial edema during the acute stage and progressive interstitial fibrosis and mononuclear

infiltrates in chronic cases.3’5’6

Present recommendations for therapy of bromate ingestion”13 can be summarized as follows: (1) In-duce vomiting and/or perform gastric lavage.

La-vage with a 2% solution of sodium bicarbonate has been suggested to prevent the formation of hydro-bromic acid’3; lavage with oral thiosulfate should be avoided’; (2) administer a demulcent; (3) admin-ister sodium thiosulfate (10 to 50 mL of a 10% solution) intravenously, to reduce absorbed bro-mate to the relatively innocuous bromide ion; (4)

correct dehydration, shock, electrolyte, or acid-base

disturbance with appropriate intravenous glucose and electrolyte solutions.

In addition, should oliguria ensue despite optimal

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he-REFERENCES

1. Gosselin RE, Hodge HC, Smith RP, et al: Clinical Toxicology of Commercial Products: Acute Poisoning, ed 4, Section III. Baltimore, Williams & Wilkins, 1976, pp 66-68

2. Gradus (Ben-Ezer) D, Rhoads M, Bergstrom LB, et al: Acute bromate poisoning associated with renal failure and deafness presenting as hemolytic uremic syndrome. Am J Nephrol

i984;4:i88-i91

3. Quick CA, Chole RA, Mauer SM: Deafness and renal failure due to potassium bromate poisoning. Arch Otolaryngol

i975;iOl:494-495

4. Matsumoto I, Morizono T, Paparella MM: Hearing loss following potassium bromate: Two case reports. Otolaryngol Head Neck Surg 1980;88:625-629

5. Dunsky I: Potassium bromate poisoning. Am J Dis Child

1947:74:730-734

6. Oh SH, Lee HY, Chung SH, et al: Acute renal failure due to potassium bromate poisoning. Yonsei Med J

1980;21:106-109

7. Parker WA, Barr JR: Potassium bromate poisoning. Br Med J i951;i:i363-1364

8. Benson GI: Potassium bromate poisoning. Br Med J

i951;i:i5i6

9. Kitto W, Dumars KW: Potassium bromate poisoning. J Pediatr 1949;35:197-200

10. Knappenberger RC: Potassium bromate poisoning. J Pediatr

1952;40:i05-i08

1 1. Robertson HF, Flothow MW Jr, Kissen MD: Potassium bromate poisoning. J Pediatr 1950;36:24i-243

12. Thompson HC, Westfall SW: Potassium bromate poisoning: Report of a case due to ingestion of a “cold wave” neutralizer.

J Pediatr 1949;34:362-364

13. Poisindex, microfiche. Denver, Micromedix Inc, November

1984, frames H 10 and I 10

No reprints available.

PEDIATRICS (ISSN 0031 4005). Copyright ( 1985 by the American Academy of Pediatrics.

978 PEDIATRICS Vol. 76 No. 6 December 1985

moglobin concentration should be monitored and transfusions of packed RBCs administered as

nec-essary.

The following conclusions may be formulated regarding the role of dialysis: (1) Most accidentally poisoned children, treated with the measures out-lined above, will recover without sequelae in the absence of dialysis; (2) dialysis should be instituted for established acute renal failure that does not begin to remit within 48 hours of onset; (3) the role

of dialysis for the prevention of nephrotoxicity or ototoxicity is presently untested. No patient with bromate ingestion reported to date has received dialysis therapy earlier than 48 hours following ingestion. Because ototoxicity is probably complete by 24 hours,4 dialysis is unlikely to prevent this

complication in patients presenting after this pe-nod of time. Moreover, the rapid onset of ototox-icity suggests that peritoneal dialysis, being rela-tively inefficient, would not be useful prophylacti-cally. The prophylactic value of hemodialysis re-quires confirmation but, when expertise in the

treatment of infants and children is available, might be considered in patients presenting in the early hours following suspected ingestion of a large quantity of bromate. Unfortunately, objective as-sessment of the amount of bromate absorbed is not presently possible; blood levels of bromide have not

correlated with the severity of intoxication,2 and

bromate levels have not been reported. Accordingly, the decision whether to perform early hemodialysis must presently rely on clinical judgment as to the

severity of the intoxication.

BARRY L. WARSHAW, MD MELODY C. CARTER, MD

LEONARD C. HYMES, MD BARBARA

S.

BRUNER, MD ALBERT P. RAUBER, MD Department of Pediatrics

Emory University School of Medicine

Atlanta

Acute

Lithium

Poisoning

in a

Child

With

Dystonia

Lithium is commonly used to treat bipolar de-pression in adults. Several recent studies demon-strate the efficacy of the drug for certain behavioral and affective disorders in children.’ There is also evidence that lithium may be therapeutic in a di-verse group of clinical problems including premen-strual syndrome, neutropenia, cluster headaches,

certain movement disorders, and syndrome of

in-appropriate antidiuretic hormone secretion.26

Thus, it appears that lithium use will increase, resulting in its greater availability for accidental poisoning. Currently, this is a rare event. A recent

literature review disclosed no reports of single-dose intoxications either in childhood or manifesting as

dystonia. The following is a description of a child who presented with dystonia associated with lith-ium ingestion. Signs of lithium toxicity and the causes of acute dystonia are reviewed.

CASE REPORT

A.B., a previously healthy 3#{189}-year-old, 15-kg, girl in-gested 300 mg of lithium carbonate mixed in orange juice. The medication was noticed missing eight hours later.

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1985;76;975

Pediatrics

BRUNER and ALBERT P. RAUBER

BARRY L. WARSHAW, MELODY C. CARTER, LEONARD C. HYMES, BARBARA S.