Acute Fluoride Poisoning

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ARTICLES

(CONTINUED)

Acute

Fluoride

Poisoning

Robert Yolken, M.D., Philip Konecny, M.D., and

Paul McCarthy,

M.D.

From time Departnment of Pediatrics, Yale (Tnicersity School of Medicine, New !-Iacen, Gonnectictit

ABSTRACT. Fluoride poisoning is a potentially severe

environniental hazard for children. A case of fluoride

poisoning is presented which was manifested by severe

hpocalcemnia, ventricular arrhythmias, and respirator

fail-nrc. Treatnient of this poisoning, including peritoneal

dial-sis, is disctmssed. The kinetics of fluoride distribution as

mneasured Ili this patient suggest a rapid bimidimig of ingested

fluoride to bone, followed by gradual release and excretion.

Peritoneal dialysis resulted in no significamit fluoride

removal. Pediatrics, 58:90-93, 1976, FLUORIDE, POISONING,

HYPOCALCEMIA, COMA.

Poisoning

from

both

organic

and

inorganic

fluoride compounds was recognized as a clinical

entity

in the

early

part

of this

century.

Over

112 fatal

cases

were

reported

by

1935,

most

occurring

from suicide attempts with rodent poison or when sodium fluoride was mistaken for sugar, salt, or

baking

soda.’2

Such

errors

have

occasionally

led

to

mass

poisonings,

the

largest

of

which

was

in

1943

when

163 inmates

of

a state

prison

were

poisoned,

with

47 fatalities.

Although

fluorides

have

been

removed

from

most

rodenticides,

they

are

still

present

in

a

nuniber

of

comniercial products. The following report describes a child

with

acute

fluoride

poisoning

resulting

from

ingestion

of

a laundry

powder.

Some

aspects

of

fluoride

kinetics

and

therapy

of this

condition

are

discussed.

CASE REPORT

A 2#{189}-year-old black girl was brought to the emergency

roomn because of progressive vomiting and lethargy which

had started six hours before admission. Physical examination

revealed a comatose child who responded only to deep pain.

Respiratory rate was 6 to 8 breaths/mm. Blood pressure and

temperature were normal. Generalized twitching and

disconjugate gaze with coarse horizontal nystagmus were

present; Chvostek and Trousseau signs were absent. No

ulcerations were noted in the oropharynx and no cutaneous

burns or petechiae were present. A soft systolic ejection

murmur was heard at the left sternal border.

Past history revealed that the child was being followed for

an asymptomatic ventricular septal defect and for mild

developmental delay, thought to be due to an inadequate

family situation. She was receiving no medications.

Although the possibility of ingestion was originally denied

by the mother, repeated questioning revealed that prior to

becoming ill the child had been playing with a laundry

powder. The mother had obtained this material from a

commercial laundry. This powder was identified as “Rayline

Brand Laundry Sour” (manufactured by BASF Wyandotte

Corporation, Wyandotte, Michigan), a whitener sold only to

commnercial laundries. This contained sodium silicofluoride

(NaSF) as its major ingredient. Gastric lavage was

performed, yielding viscous yellow material.

(Received August 21; revision accepted for publication

November 17, 1975.)

ADDRESS FOR REPRINTS: (R.Y.) Department of

Pediat-rics, New York Hospital-Cornell Medical School, New York,

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URINARY

FLOURIDE

(mg/I)

‘

SERUM

FLOURIDE

(mg/I)

.-

---. - - - 4-. - -

-.‘...----___

;PNHITH*H

Ifs

rcaIcium1

15 CCL2 L

GIuciate

I

luses

Peritlmeal Dialysis

L

CaOH Louoge

1

5 VFIB

El

-- --

-_______

I

I I I I I I I I I I

0 20 30 40 50 60 10 80 90 100

HOURS AFTER INGESTION

ARTICLES

91

10

5

0

SERUM

Ca++(mgo,o)

10

“,#{248},-

a..,

FIG. 1. Clinical course of patient. Dashed line, urinary fluoride (mg/liter); broken line, serum fitmoride (mug/liter): solid line, serum

calcium (mg/100 ml); CaCL, 0.3-gm boluses of calcium chloride; VFIB, eight episodes of ventricular fibrillatiomi treated 1w

direct-current cardioconversion.

Materials and Methods

Total fluoride was measured in body fluids by an Orion

fluoride specific electrode with a corning PH meter. All

samples were frozen and read less than five days after they

were obtained. All samisples were diluted at least 1:1 with

TISAB (total ionic strength and buffer). Peritoneal dialysis

was carried out with a commercially prepared dialysis

SOltItiOli (Peridial) using one-hour equilibration times and an

average volume of 500 ml. Calcium chloride was added to

the dialysate to obtain a calciumn concentration of 10 mg/ 100

1511. Fluoride content of the dialysate was 0.17 mg/liter.

The total amisount of fluoride in the vascular system was

calculated assuming a blood volume of 80 nil/kg and a serum

to whole blood fluoride distribution of 7:10 and a hematocrit

of 35%.’ Fluoride clearance was calculated according to the

formula UV/p and corrected to 1.73 sq mu with P and U being

the mean plasma and urine fluoride concentrations when a

steady state was reached, and V being the average urine

voltmmiie during that period.

Laboratory Data

I:’. I)

Complete l)lOOd count, blood glucose, and spinal fluid

were nor,iial. The BUN was 31 mg/100 ml. Urimialysis

revealed 2+ protein and 40 RBC/high-power field. Serum

electrolyte values were: sodium, 138 mEq/liter; potassium,

6.7 mEq/liter; l)icarl)onate, 13 miiEq/liter; aIld chloride. 107

niEq/liter. Serum calciimmii was :3.4 miig/ 100 m,il. Initial

electrocardiogram demonstrated normal sintms rhvthni with

Q-T interval of 0.52 seconds. T-waves were peaked and

inverted in the chest leads. A chest X-ray filmii showed a right upper lobe infiltrate.

Hospital Course

Shortly after admissiomi, the patient developed acute

respiratory failure; assisted ventilation was required for the

next 48 hours. Three hours after admission, she developed

repeated episodes of ventricular tachycardia amid fibrillation.

These were treated with intravemiously administered

lido-caine and eight separate courses of direct current

cardiover-sion. Hypocalcemia was treated with three 0.3 gIll

intrave-noims infusions of 10% calciumii chloride followed 1w a

continuous imifusion of calciumn gltmconate (Fig. 1). She was

treated with orally administered 0.1% calcium hydroxide

(lime water) and aluminnmi hydroxide b nasogastm-ic ttmbe.

Penicillin, kanamvcin, and dexaniethasone were given for

presumed aspiration 1)mietmmiionia.

Nimse hours after admission peritoneal dialysis was

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titted using a dialysate solution with a calcium concentration

of 10 mg/100 miil amid continued for 48 hours. Six hours after

dialysis was begun the serum calcium had increased to 13

mg/100 ml and the intravenously given calcium gluconate

infusion was stopped.

The patient became responsive 18 hours after admission

and returned to full consciousness two days later. Her renal

function and urinalysis returned to normal. She developed no

mucosal burns or ulcerations. ECG, chest X-ray film, and

upper gastroimitestimial examination were normal at

dis-charge. Her course subsequent to discharge has been

uneventful except for an episode of viral pneumonitis. She

has been free of seizures, and developmental examination

eight mnonths following discharge demonstrated normal

progress.

Fluoride values

Serum fluoride level six hours after ingestion was 14 mg/

liter, an extremely high value (Fig. 1). Fatalities have

occurred frequently at senim levels above 3 mg/liter. Serum

fluoride dropped quickly to 1.8 mg/liter 11 hours after

admission and was less than 0.1 mg/liter 21 hours after

ingestion. Urinary fluoride excretion amounted to 24.8 mg

over the first three days following ingestion with the urine

fluoride concentration remaining relatively constant during

that period. Average fluoride clearance was 98 ml/min/1.73

sq m and the creatanine clearance was 80 ml/min/1.73 sq m.

Penitoneal dialysis was ineffective as the total amount of

fluoride removed by this procedure was less than 0.2 mg over

two days. This was less than 1.5% of the fluoride excreted in

the urine during the same period.

DISCUSSION

Fluoride

excess

adversely

affects

many

organ

systems: Ingestion of fluoride salts invariably causes irritation of the gastrointestinal tract,

leading

to

abdominal

pain

and

vomiting.2

Fluo-ride

contact

with

the

skin

can

produce

burns

through which significant absorption can then

occur.” Inhalation can cause inflammatory

changes

in

the

lungs

which

may

progress

to

pulmonary emphysema.”

Systemic

absorption

affects

body

metabolism

in

a variety

of

ways.

The

ion

binds

to

circulating

calcium causing severe hypocalcemia, tetany, and

cardiac

arrhythmias.’#{176}

In

addition,

fluoride

appears

to

exert

a

direct

toxic

effect

on

the

central

nervous

system

leading

to stupor

and,

at

times,

frank

coma

with

subsequent

respiratory

failure.’ ‘#{149}12

It may be difficult to establish a diagnosis of

fluoride poisoning in a comatose patient when a

history

of

ingestion

cannot

be

obtained.

Low

serum

calcium

and

prolonged

Q-T

interval

on the

electrocardiogram,

when

associated

with

vomit-ing

and

a depressed

level

of consciousness,

may

suggest fluoride poisoning.

Once the diagnosis of fluoride poisoning has

been

made,

further

absorption

of

fluoride

from

the

gastrointestinal

tract

can

be

decreased

by

gastric

lavage

with

a dilute

solution

of

calcium

hydroxide or calcium chloride followed by

instal-lation of aluminum hydroxide gel into the

gastrointestinal

tract.

Such

treatment

removes

fluoride directly from the stomach and decreases

the

absorption

by

forming

poorly

absorbed

calcium

and

aluminum

fluoride

salts.’

:t.4

Care

should

be

taken

to prevent

gastric

from

coming

into

prolonged

contact

with

skin

as

serious

burns

may

ensue.’2

Hypocalcemia,

which

invariably

accompanies

significant fluoride intoxication, can be treated

with initial intravenous infusions of calcium chlo-ride to bring the serum calcium tip to a normal level. This may be followed by a continuous

infusion

of

150 ml/sq

m/24

hr

of

10%

calcium

gluconate.’5

Careful

monitoring

of calcium

levels

is required.

Fluoride intoxication often leads to cardiac and

respiratory

abnormalities.

Our

patient

required

direct

current

cardioversion

eight

times

for

ventricular

arrhythmias.

Since

arrhythrnias

are

known to occur up to 72 hours following

inges-tion,

careful

cardiac

monitoring

is required

for

that

period

of time.’2

Fluoride

is primarily

removed

from

the

body

by means of renal excretion.’#{176}m7 In our patient

the

average

fluoride

clearance

was

98 cc/min/

1.73

sq m, a clearance

similar

to that

reported

in

the

literatureJ’2’T

Over

a three-day

period,

24.8 mg

of fluoride

were

removed,

an

amount

corre-sponding

to

two

times

the

initial

amount

of

fluoride in the vascular system. Although there

was

a rapid

initial

disappearance

of fluoride

from

the

blood

with

the

serum

concentration

falling

from

14 mg/liter

to 1 mg/liter

over

the

nine-hour

period following admission, the urinary

con-centration

of

fluoride

remained

elevated

to

15 mg/liter

for

three

days

following

ingestion.

These

kinetics

suggest

that

there

is initial

rapid

binding

of

fluoride

to

a body

store,

presumably

bone,”

followed

by a gradual

release

and

excretion

in the

urine.

The

rate

of

release

is sufficiently

slow

so

that

toxic

levels

of fluoride

do

not

recur.

In our case we attempted to enhance fluoride removal by the use of peritoneal dialysis;

however,

this

resulted

in no significant

removal

of.

fluoride.

In

fact,

the

fluoride

level

of the

effluent

was

less

than

the

level

of

the

bottled

dialysate

solution,

which

had

evidently

been

prepared

from

fluoridated

water.

It can

be

concluded

that

pen-toneal

dialysis

is not

indicated

in the

management

of acute

fluoride

poisoning.

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ARTICLES

93 in

their

patient

was

not

significantly

different

than

what

we

saw.

Thus,

in

the

presence

of

normal renal function, maintenance of an ade-quate urine output is

the

most

effective

way

to

assure removal of fluoride from

the

body.

Hemo-dialysis may have an additive effect but would be

most

useful

in a patient

with

compromised

renal

function.”

REFERENCES

1. Rohoelmn K: Fluoride Intoxication: A Clinical Hygiene

Study. London, HK Lewis & Co Ltd, 1937.

2. Waldbott GL: Acute fluoride intoxication. Acta Med

Scand 174(suppl 400): 1, 1963.

3. Lidbeck WL, Hill TB, Beeman JA: Acute sodium

fluoride poisoning. JAMA 14:862, 1943.

4. Greendyke RM, Hodge HC: Accidental death due to

hydrofluoric acid.

J

Forensic Sci 9:383, 1943.

5. Singer L, Armstrong WD: Measurement of fluoride ion.

Anal Chemn 31:105, 1959.

6. Carlson LH, Armstrong WD, Singer L: Distribution and

excretion of radiofluoride in the human. Proc Soc

Exp Biol Med 104:235, 1960.

7. Chen PS, Smith FA, Garner DE: Renal clearance of

fluoride. Proc Soc Exp Biol Med 92:879, 1956.

8. Burke WJ, Hoegg UR, Phillips RE: Systemic fluoride

poisoning resulting from a fluoride skin burn.

I

Occup Med 15:39, 1973.

9. Machle W, Thamann F, Kitzmniller K: The effects of the

inhalation of hydrogen fluoride.

J

Industr Hyg

16:129, 1934.

10. Rabmowitch JM: Acute fluoride poisoning. Can Med

Assoc

J

52:345, 1945.

11. Waldbott GL: Fluoride in clinical medicine. Int Arch

Allergy 20(suppl): 1, 1962.

12. Abukurah AR, Moser AM, Baird CC, et al: Acute sodium

fluoride poisoning. JAMA 222:816, 1972.

13. Gleason M, Gosselin R, Hodge H, Smith R: Clinical

Toxicology of Commercial Products, ed 3.

Balti-more, Williams & Wilkins, 1969.

14. Maletz L: Report of a fatal case of F poisoning. N EngI

J

Med 213:370, 1935.

15. Bruck E: Etiology manifestations of disorders of calcium

metabolism

in children.

Q

Rev Pediatr 16:102,

1961.

16. Juncus

J, Donadio

J: Renal

failure and fluorosis. JAMA 222:783, 1972.

17. Berman LB, Taves DR: Fluoride excretion in normal

and uremic humans. Clin Res 21:100, 1973.

18. Berman LB. Taves DR, Mitra 5, Newmark K: Inorganic

fluoride poisoning: Treatment by hemodialysis. N

Engl

J

Med 289:922, 1973.

19. Knepshield

J,

Schreinar G, Lowenthal D, Gelfand M:

Dialysis of poisons and drugs-annual review. Trans

AM Soc Artif Organs 19:590, 1973.

ACKNOWLEDGEMENT

We wish to thank Drs. Howard Pearson for his thoughtful

reading of the manuscript, Tom Dolan for his help in the

clinical management of the patient, and Norman Hyatt for

performing the fluoride determinations and Mrs. Gretchen Umbach and Mrs. Dorothy Page for secretarial assistance.

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1976;58;90

Pediatrics

Robert Yolken, Philip Konecny and Paul McCarthy

Acute Fluoride Poisoning

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