Primary Meningococcal Conjunctivitis

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104

PEDIATRICS

Vol.

60 No.

1 July

1977

angular

vein

and

ophthalmic

veins,

and

also

the

ethmoidal

veins,

to

the

cavernous

sinus

(Fig.

3).’

The

sinus,

in

turn,

communicates

with

the

meninges.

Second,

Moxon

and

associate?

pro-duced

H. influenzae

type

b meningitis

in

infant

rats

by

intranasal

inoculation

of

the

organism.

Fluorescein-labeled

specific

antiserum

demon-strated

the

apparent

bacterial

route

to

be

nasal

mucosa penetration with subsequent entry into

the

lymphatics

and

the

systemic

circulation.

Meningeal

spread

then

occurred

from

the

dorsal

longitudinal and lateral dural sinuses.

Third,

lymphatics from the superior meatus drain

intra-cranially.2

Fourth,

direct

invasion

can

occur

during

surgery,

from

fracture,

by local

erosion,

or

from congenital defects.

Fifth,

pathways

along

perineural

sheaths

have

been

suggested;

the

olfactory

fibers

proceed

intracranially

via

the

cril)riform plate. In the present case, it is not known whether the meningitis developed after therapy was initiated or whether the meningitis

had

been

present

before

therapy,

requiring

time

to become

manifest.

Fearon

et

al.

have

studied

43 cases

of abscess

of the

nasal

septum

seen

at the

Hospital

for

Sick

Children

in Toronto.

Two

of these

patients

subse-quently acquired meningitis, and

Staphylococcus

aureus

was

isolated

from

one

of the

patients

who

had

been

treated

with

penicillin,

streptomycin,

and

sulfadiazine,

Larchenko’

reported

one

case

of

meningoencephalitis in 105 cases of nasal septal

abscess.

A

ten-year

chart

review

from

the

Childrens

Hospital

of Los

Angeles

produced

only

three

cases

of abscess

of the

nasal

septum.

Only

the

present

case

was

complicated

by

meningitis.

ADDRESS FOR REPRINTS: (H.T.W.) Childrens Hospital of Los Angeles, P.O. Box 54700, Terminal Annex, Los Angeles, CA 90054.

REFERENCES

1. DeWeese DD, Saunders WH: Textbook of Otolaryngol-ogy, ed 4. St Louis, CV Mosby Co, 1973, pp 218, 230.

2. Fearon B, McKendry JB, Parker

J:

Abscess of the nasal septum in children. Arch Otolaryngol 74:408,

1961.

3. Lutovac M, Ercegovac N, Ledic S: Brain abscess after resection of the nasal septum. Srp Arh Celok Lek 95:959, 1967.

4. Glasenapp GB, Freitag G: Beitrag zu rhinogenen endo-kraniellen komnplikationen. Z Laryngol Rhinol Otol 52:897, 1973.

5. Larchenko RM: On abscesses of the nasal septum in children. Vestn Otorhinolaringol 23:46, 1961. 6. Surkov VK: The veins of the nasal septum with regard to

the formation of hematomas and abscesses. Vestn Otorhinolaringol 25: 14, 1963.

7. Fry HJ: The pathology and treatment of haematoma of the nasal septum. Br

J

Plast Surg 22:331, 1969. 8. Moxon ER, Smith AL, Averill DR, Smith DH:

Haemo-philus influenzae meningitis in infant rats after intranasal inoculation.

J

Infect Dis 129:154, 1974. 9. McCasky CH: Rhinogenic causes of brain abscess.

Laryngoscope 61:460, 1951.

ACKNOWLEDGMENT

The authors acknowledge the expertise in clinical manage-ment and helpful suggestions contributed by Dr. Seymour

Cohen.

They also thank Dr. Vaclav Klement and Ms. Heidi Lewis-Wiettling for translating references from the Russian

and

German literature.

CONCLUSIONS

Abscess

of

the

nasal

septum

is an

important

consideration in the differential diagnosis of

conditions

such

as nasal

obstruction,

hematoma

of

the

nasal

septum,

nose

pain,

and

swollen

nasal

turbinates.

Surgical

drainage

and

antibiotic

coverage

should

be

initiated

as soon

as the

diag-nosis

of

abscess

of

the

nasal

septum

is made

to

prevent

severe

deformities.

Intracranial

compli-cations

can

become

apparent

even

after

appro-priate

therapy

has

been

initiated.

ROLAND

D.

EAvEY,

M.D.

MOHAMMED MALEKZAKEH,

M.D.

HARRY T. WRIGHT, JR.,

M.D.,

M.P.H.

Department

of Pediatrics,

University

of Southern

California,

School

of Medicine,

and

Childrens

Hospital

of

Los

Angeles

I1os

Angeles,

California

Primary

Meningococcal

Conjunctivitis

Primary

meningococcal

conjunctivitis

is a rare

disorder

with

clinical

characteristics

that

are

similar

to

those

of

gonococcal

conjunctivitis.

Although

infections

of the

conjunctivas

occur

as

unusual

complications

of meningococcemia,

pri-mary

meningococcal

conjunctivitis

has

been

reported

even

less

frequently.

We

recently

observed

a patient

with

primary

meningococcal

conjunctivitis.

This

case

reinforces

the

need

for

bacteriological

identification

of

the

etiologic

agent

in acute

conjunctivitis

to avoid

mismanage-ment.

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EXPERIENCE AND REASON 105

CASE REPORT

A 9#{189}-year-old white girl had a red eve of three hours’ duration. While riding her bicycle, she noted increased tearing, followed quickly by yellow conjunctival discharge and minimal lid edema. There was no pain, photophobia, history of trauma, or known exposure to conjunctivitis.

Examination at that time revealed a normal child except for her right eye. The conjunctivas were red and edematous, with much yellow exudate. Erthema, tenderness, and warmth were present in both lids, and extended approxi-matelv 2 cm onto the right cheek. There was minimal edema of the eyelids and no edema of the cheek. The cornea, anterior chamber, and hindus were normal.

Gram stain of the exudate revealed man polmorphonti-clear leukocytes and a moderate miumber of Cram-negative diplococci. The exudate was cultured on chocolate agar, and the patient was placed on oral phenoxmethl penicillin, 250 mg four times a day, and Neosporin ophthalmic solution topically every four hours.

At 48 hours, the eye culture was reported to be yielding Gram-negative diplococci. The patient was contacted by telephone and reportedly was well, with clearing of the conjunctivitis. On the fifth day, results of physical examina-tion, which included the previously involved eye, were normal. All therapy was discontinued and the patient has continued to do well.

The original conjunctival culture yielded Xc’i.s.scria ,,eflin-gitidis group C. Antibiotic sensitivity tests (agar dilution) revealed the organism to be resistant to sulfisoxazole (> 10 sg/ml) and inhibited by neomycin (> 5 gig/mI and < 10 sg/ ml). Other antibiotics were not tested. The identity and group of the organism were confirmed (Laboratory Division, North Carolina State Board of Health). Eye culture from the second visit yielded no organism, but a nasopharyngeal culture yielded group C N. ;neningitidis, which also was resistant to sulfisoxazole.

DISCUSSION

Forty

cases

of primary

meningococcal

conjunc-tivitis

have

been

reported.’

The

incidence

of this

disease

is difficult

to

establish

because

of

prob-lems

inherent

in culturing

for

Neisseria

and

the

possibility

of

confusing

N. ineningitidis

with

N. gonorrhoeae,

particularly

in

the

earlier

litera-ture.24

The

acute

onset

of

unilateral

purulent

conjunctivitis

in our

patient

was

similar

to that

in

most

of the

cases

previously

reported.

Subsequent

systemic

infection

was

seen

in 10%

of the

patients,

two

with

sepsis

and

two

with

meningitis.

Most

of

the

patients

were

children

and

young

adults;

a male

predominance

was

noted

in

one

series.’

The

disease

also

has

been

reported

in

a

5-day-old

infant

with

ophthalmia

neonatorum.7

The

treatment

of meningococcal

conjunctivitis

varies

greatly

in different

reports;

the

results

have

been

quite

good

even

when

topical

therapy

was

used

alone.’’7

However,

the

patient

reported

by

Dillman6

did

not

respond

to three

days

of

sulface-tamide

ointment

and

fulminating

meningococ-cemia

occurred

(sensitivities

of

this

organism

were

not

reported).

Because

of

this

risk

of

systemic

infection,

topical

antibiotics

should

only

be

used

as

an

adjunct

to

systemic

therapy

with

penicillin

or a suitable

alternative.

Few

local

complications

of

meningococcal

conjunctivitis

were

reported.

Of

the

40 cases

of

primary

infection,

there

were

six

corneal

ulcers

that

healed

without

sequelae.’2

Only

one

patient

was

reported

with

a

residual

corneal

opacity.

Eye

involvement

has

been

reported

in

0.9%

of

cases of systemic meningococcal infection

(46

of

5,151

patients

from

five

combined

series).5

In this

situation, panophthalmitis with varying degrees

of destruction

of

the

cornea,

retina,

uveal

tract,

and

vitreous

has

been

reported.

In

our

patient,

we

were

impressed

by

the

involvement of the cheek below the eye. This

seemed

to be

more

than

a local

reaction

and

was

interpreted

as

cellulitis.

The

reports

noted marked

lid

edema

and

discoloration,’T

but

none

mentions

the

presence

of soft

tissue

infec-tion.

While

this

must

be

most

uncommon,

the

meningococcus is probably capable of causing cellulitis.i

Meningococcal

conjunctivitis

resembles

gono-coccal

conjunctivitis

both

in the

clinical

presenta-tion

as an acute

bacterial

conjunctivitis

and

in the

finding

of

Gram-negative

diplococci

on

staining

of

the

exudate.

Culture

for

identification

of

the

organism

is

needed

because

of

the

different

epidemiologic implications of these two

Neisseria

species, and because of

the

potential

sociologic

impact

of the

diagnosis.

Family

conflict

may

be

generated

by

the

suggestion

that

a child

has

a

venereal

disease.2

Gram’s

stain

of

conjunctival

exudate is useful in guiding initial therapy, but bacteriological studies should be relied upon to

determine

the

etiologic

agent

and

the

suscepti-bility

to antibiotics.

DALE ALAN NEWTON,

M.D.

WILLIAM GRADY \VILSON,

M.D.

Department of Pediatrics,

School

of Medicine,

University

of North

Carolina

Chapel

Hill,

North

Carolina

ADDRESS FOR REPRINTS: (D.A.N.) Tarboro Clinic, P.O. Box 40, Tarboro, NC 27886.

REFERENCES

1. Shuttleworth FN, Benstead JG: Primary meningococcal ophthalmia. Br Med

J

2:568, 1947.

2. Stuart RD, McWalter D: Primary meningococcal conjunctivitis in children. Lancet 1 :246, 1948. 3. Lewis N, Ferris AA: A case of primary meningococcal

conjunctivitis. Med

J

Aust 1:621, 1948.

4. Gray JDA, Lambert BA: Meningococcal conjunctivitis. Br Med

J

1:17, 1949.

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106

PEDIATRICS

Vol.

60 No.

1 July

1977

5. Miller H: Nei.sseria meningitidis isolated from case of

acute conjunctivitis. Public Health Rep 70:1010, 1955.

6. Dillman CE: Meningococceniia following meningo-coccal conjunctivitis. South Med

J

60:456, 1967. 7. l-Iansnian D: Neonatal meningococcal conjunctivitis. Br

Med

J

1:748, 1972.

8. \\‘illianis DN, Ceddes AM: Meningococcal meningitis comiplicated by pericarditis, panophthalmitis, and arthritis. Br Med

J

2:93, 1970.

9. Ploy-Song-Sang Y, Winkle RA, Phair JP: Neisseria

mcningitidis cellulitis. South Med

J

65:1243, 1972.

Transitory

Cataracts

in Children

With

Diabetes

Mellitus

One

of

the

most

common

visual

complaints

seen

ill

diabetes

is transitory

refractive

changes.

This

abnormality

affects

all

age

groups

equally’

and

has

been

reported

in

6%

to 34%

of patients.2’

Diabetic

myopia is associated

with

marked

hperglyceniia, whereas hyperopia usually de-velops as the blood sugar level returns to normal

in

response

to

therapy.4

The

“true”

diabetic

cataract

is now

a rare

cause

of blurred

vision

in

children

and

young

adults

with

diabetes.5

Very

few

instances

of

transitory

cataracts,

however,

have

been

documented,

and

those

observed

are

found priI1arily in the ophthalmological

litera-ture.

For

these

reasons,

we

are

reporting

in

the

pediatric

literature

two

new

cases

of

transitory

cataracts.

We

will

also

discuss

temporary

lens

opacities

in the

light

of more

recent

biochemical

knowledge.

CASE REPORTS

Case 1

A 15-year-old white boy was admitted to the University of Missouri Medical Center in April 1974 in severe diabetic ketoacidosis. Poldipsia, polyphagia, and polyuria began about six weeks prior to admission to the hospital. During this period of time, he gradually lost 5 to 6 kg. Three weeks after the onset of symptoms he had a pruritic rash about his waist which was thought to be from contact with poison ivy. He was given oral prednisone 5 mg every six hours for seven days. About t\Vo weeks prior to admission he had blurred vision. Upon exanination, an optometrist found no refractive error. The evening before admission to the medical center, he was taken to a local hospital and was found to have severe ketoacidosis. The diagnosis of overt diabetes was made and he was given parenteral fluids and 30 units of regular insulin

intramuscularly and transferred to the medical center for further evaluation and treatment.

On admission, the boy was severely dehydrated and undernourished. His height was 177.5 cm (about 2 SD above mean for age) and his weight was 55.5 kg (about 2 SD below expected weight for height). No other abnormal physical findings were found.

Initial laboratory findings were blood sugar level, 550 mg/ dl; elevated senim acetone level; bicarbonate level, 12 mEq/ liter; potassium level, 3.7 mEq/liter; and chloride level, 107 mEq/Iiter. His hemoglobin level was 16.7 mg/dl with a hematocrit value of 48%. Urine revealed 5% glucose, a strongly positive test for acetone, and a negative test for protein.

The patient was given 0.45% saline at a rapid rate (300 ml/ hr) for a few hours, and then glucose and potassium were added to the intravenous (IV) fluid. He was given 4,000 ml of fluid per square meter for the first 24 hours. After an initial dose of 2 units/kg of regular insulin, the patient received 0.5 to 0.25 mits/kg of regular insulin every four to six hours until his ketonuria cleared and his blood sugar level decreased to less than 200 mg/dl.

Within 24 hours, dehydration had been corrected and laboratory findings had reverted to normal limits, except for minimal transient hyperglycemia and glycosuria. After 36 hours, he was eating four small nieals at six-hour intervals. Regular insulin was administered prior to each meal and dosage was adjusted on the basis of repeated urine examina-tions. After the first few days, the patient received a 2:1 mixture of NPH: regular insulin. Two thirds of the total daily dose was given one-half hour before breakfast and the remaining one third of the same mixture was given one-half hour before the evening meal. At the same time, his caloric distribution was changed to a three mueal-three snack schedule and his caloric intake was gradually increased from 2,400 to 3,000 calories a day. He had no insulin reactions and his urine remained sugar-free. His total insulin requirement during the next three weeks gradually decreased from 78 to 30 units daily.

On the fourth day of hospitalization, the child again complained of blurred vision. Ophthalmological consultation revealed decreased visual acuity (20/40 in both eyes). Bilateral lamellar cataracts at the depth of the posterior Y suture were found. By the 15th day after admission, his vision had become normal and the patient’s visual acuity made it easy for him to reconstruct a model V-8 engine. An ophthal-mological examination revealed that his vision had returned to 20/20 in both eyes. Bilateral lamellar cataracts persisted (b ehind posterior Y suture) but were much less dense. By the end of the third week, the ophthalmological examination revealed no detectable abnormality.

Case 2

A 10-year-old white girl was admitted to the University of Missouri Medical Center in May 1975 in diabetic ketoacido-sis. History revealed the gradual development of polydipsia and polyuria for a few weeks with increased sleepiness and onset of nausea and abdominal pain two days prior to admission. On the day of admission to the hospital, her local physician found glycosuria, a blood sugar value of over 2,000 mg/dl, a strongly positive test for serum acetone, and a senim bicarbonate level of 7.3 mEq/liter. Arrangements were made to transfer the child to the medical center for further evaluation and treatment.

On admission, she was lethargic and hyperventilating. There was niinimiial response to painful stimuli. She was moderately dehydrated and had bilateral otitis media. Her

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1977;60;104

Pediatrics

Dale Alan Newton and William Grady Wilson