LETFERS TO THE EDITOR 159
3. Mitchell, R. S.: Control of tuberculosis. New
Eng.
J.
Med., 276:842, 1967.EDITOR’S Noi-#{128}: Dr. Turner commented as
fol-lows:
With reference to the letter by Drs. Brick-man, Beaudry, and Wise, I would reply that I agree in part with their declaration of the rela-tive lack of infectivity of primary pulmonary tuberculosis. There also is little doubt that un-der therapy such infectivity may be quickly
minimized.
One should, however, point out that, on the
basis of the finding of tubercle bacilli in gastric washings, there is a potential for infection. In
our paper, such potential was cited as an added argument for the routine use of isonia-zid, which use those physicians endorse in their letter.
J.
A. PETER TURNER, M.D.The Hospital for Sick Children
555 University Avenue
Toronto 2, Ontario
Hearing Loss after Maternal Rubella: Need for Accurate Diagnosis of Maternal Infection
To nm EDITOR:
Borton and Stark, in their recent paper,’ de-signed a study to describe hearing loss
secon-dary to maternal rubella. Having been
inti-mately’ involved in the surveillance of maternal
rubella for the past 18 months, I must seriously
question the validity of their case finding pro-cedure. Unless the two Illinois state agencies
are remarkable exceptions, the case records
ex-amined by the authors have dubious value as
documents of clinical merit. This type of data often becomes increasing nebulous with each successive transcription. The diagnosis of ma-temal rubella by a physician, in the absence of frank arthralgia and/or arthritis, or serologic
confirmation, must be held circumspect. In the
absence of a rubella epidemic, and/or the two above parameters of infection, the diagnosis of maternal rubella is notoriously inaccurate in my experience.
One would assume by the date that the
orig-inal manuscript was submitted, that the major
part of this investigation was carried out in 1968. Since the mean age was 6 years 1 month, at least one half of the children studied proba-bly acquired their gestational illness prior to the 1964 rubella epidemic (unless the age
dis-than 6 year age group.) Prior to 1964, there
was minimal interest and knowledge in the
ten-atogenic effect of maternal rubella among
physicians at large. Diagnostic acumen was
probably less “sensitized” toward establishing the correct diagnosis.
Of the 80 subjects, 33.7% were diagnosed
as having at least one additional congenital ab-normality associated with rubella syndrome;
the highest incidence of associated abnormali-ties was found in those subjects whose mothers experienced rubella during the first month of
pregnancy. Of the congenital abnormalities
enumerated by the authors, only congenital heart disease and cataracts are rather
specif-ically characteristic for the syndrome. The
ac-tual incidence of these two abnormalities
would be elucidating. Two large studies2’3 have revealed that ocular abnormalities,
con-genital cardiac lesions, and hearing loss occur
with almost equal frequency in rubella
syn-drome, secondary to first trimester maternal
ru-bella.
The author’s findings have considerable im-portance regarding prognostication of hearing deficits secondary to maternal rubella and
di-agnosis of congenital rubella infection based on certain hearing loss patterns. The potential
im-portance of their observations demands a more
accurate diagnosis of gestational rubella.
DAVID W. REYNOLDS, M.D.
Division of Epidemiology
Oklahoma State Health Department
3400 N. Eastern
Oklahoma City, Okkihoma 73105
REFERENCES
1. Borton, T. E., and Stark, E. W. : Audiological
findings in hearing loss secondary to maternal
rubella. Pwriucs, 45:225, 1970.
2. Cooper, L. Z. : Rubella: A preventable cause of
birth defects. In Bergsman, D., ed. :
Intraute-rine Infections, Birth Defects Original Article
Series, Vol. IV, No. 7., December, 1968, New York: National Foundation, March of Dimes.
3. Members of the Baylor Rubella Study Group:
Rubella: Epidemic in retrospect. Hosp. Pract.,
2:27, 1967.
EDITOR’S NOTE: Drs. Stark and Borton
corn-mented as follows:
In general, the critical comments of Dr.
Reyn-olds concerning the validity of case finding in
maternal rubella are well taken. Some,
how-ever, are ambiguous and worthy of response. First, Dr. Reynolds suggests that the case
“un-160 LETFERS TO THE EDITOR
able exceptions . . .“ because the data “often
become increasingly nebulous with each
suc-cessive transcription.” The state agencies
in-volved are indeed remarkable and Dr.
Reyn-olds’s stated reason for lacking confidence in the case records is unintelligible to us. The rec-ords used in the investigation contained
origi-nal medical reports from pediatric and otologic
consultants and no transcription was involved. Second, Dr. Reynolds states that the clinical
diagnosis of rubella by a physician “must be held circumspect” (Webster defines the word
as ‘cautious’) , and that the diagnosis of rubella
in the absence of frank arthralgia and/or
ar-thritis, serologic confirmation or a rubella
epi-demic “is notoriously inaccurate in my experi-ence.” This, of course, is opinion and not a
statement of fact. Circumspect, perhaps;
al-though we suppose that pediatricians and
otol-ogists who make such diagnoses think of them-selves as being competent. But where does the literature tell us that we must have Dr.
Reyn-olds’s criteria in order to make such a
diagno-sis? It is well known, for example, that a signif-icant number of cases of maternal rubella are
seen in years other than the so-called epidemic
years (as of March 31, there were 1485
re-ported cases of rubella in downstate Illinois alone in 19681) . In addition, having only been at this business for 18 months, by his own
ad-mission, hardly qualifies Dr. Reynolds’s almost
cavalier rejection of rubella diagnosis over a period of some 230 years, from 1740 when the disease was first described through 1963 when
serologic confirmation became plausible. A
clinical diagnosis still has value in any area of
medicine, even in the diagnosis of maternal ru-bella. It is unreasonable to assume that the children used in the study were not products of rubella positive mothers simply because
sero-logic data were not available.
Third, Dr. Reynolds suggests that the 1964 epidemic “sensitized” physicians to making a
“correct” diagnosis which, he implies, they were not doing before. Again, this is an opinion and not a statement of fact. Indeed, serologic diagnosis is still not the common rule and it
could be argued, plausibly, that the 1964 epi-demic taught us little in this regard.
Fourth, Dr. Reynolds mentions two large studies which report that congenital heart
le-sions, ocular abnormalities, and hearing loss “occur with almost equal frequency in the ru-bella syndrome . . .“ Hearing loss has been
shown to be the most common sequela of
mater-nal rubella by a number of authors.26 More-over, deafness can occur as a single sequela of maternal rubella, and does so more often than when other defects are present. Our findings
were in agreement with the results of these studies.
The reference to maternal rubella in a
child’s history, no matter how poorly defined
serologically, warrants follow-up before critical periods of speech, language, and cognitive
de-velopment. The action approach is to confirm
normal hearing early and accurately if there is
any index for suspicion and not to fall into the
trap of considering that such children would have normal hearing until proven otherwise.
The authors are grateful for the criticism,
some of which has considerable merit for all in-volved in clinical reporting. Hopefully our re-port will be outdated by more precise data from centers with explicitly defined
popula-tions of postmaternal rubella children who
have been studied in a prospective manner.
EARL W. STARK, PH.D.
THOMAS E. BORTON, M.A. Hearing Clinic
University of Illinois Urbana-Champaign, Illinois 61820
REFERENCES
1. State of Illinois. Illinois Department of Public Health : Division of Preventive Medicine
Weekly Report. April 12, 1968.
2. Jackson, A. D. M., and Fisch, L. : Deafness
fol-lowing maternal rubella. Results of a
prospec-five investigation. Lancet, 2: 1241, 1958. 3. Campbell, M.: Place of maternal rubella in the
aetiology of congenital heart disease. Brit. Med. J., 1:691, 1961.
4. Lundstrom, R. : Rubella during pregnancy. A
follow-up study of children born after an epi-demic of rubella in Sweden, 1959, with
addi-tional investigation of prophylaxis and
treat-ment of maternal rubella. Acta Pediat.,
(Suppl. 133), 51:1, 1962.
5. Green, R. H., Balsamo, M. R., Giles, J. P., Krugman, S., and Mirick, C. S. : Studies of
the natural history and prevention of rubella. Amer. J. Dis. Child., 110:348, 1965.
6. Plotkin, S. A., Cochran, W., Lindquist, J. M., Cochran, G. G., Schaffer, D. E., Scheie, H. G.,
and Furukawa, T. : Congenital rubella
syn-drome in late infancy. J.A.M.A., 200:435,
1967.
7. Bell, J.: On rubella in pregnancy. Brit. Med. J.,
1:686, 1959.
8. Manson, M. M., Logan, C. W., and Loy, R. M.:
LETFERS TO THE EDITOR 161
pregnancy. Reports on Public Health and
Medical Subjects, Number 101, Ministry of
Health, Her Majesty’s Stationary Office, 1960.
9. Barr, B., and Lundstrom, R. : Deafness following maternal rubella; Retrospective and
Prospec-tive studies. Acta Otolaryng., 53:413, 1961.
Azathioprine (Imuran) in Treatment
of Hepatic Failure
To ma EDITOR:
The article “The Critically Ill Child: Acute
Hepatic Failure” (PEIMATRICS, 45:93, 1970) by
Dr. Trey failed to mention one drug that has been recently used as an adjunct to
chemother-apy of acute hepatic failure in children.
Aza-thioprine (Imuran) in the dosage of 50 to 100 mg per day has been utilized in this disease to suppress any auto-immune factors that may
contribute to the destruction of hepatic tissue or in the prevention of regeneration of hepatic cells.
I have recently treated a 6-year-old child
with severe hepatic failure and impending
coma (somnolence and liver flap) secondary to
infectious hepatitis. This child received all the
general and specific therapies outlined in your
excellent article. Ascites was a major problem
during the acute stage of the disease and large
doses of spironolactone and albumin were ad-ministered. The recuperative stage was
short-ened appreciably by the combined use of aza-thioprmne and corticosteroids. The child, at the present time, has been home for 2 months and
is on decreasing doses of azathioprine with completely normal liver function studies.
One interesting finding noted during this
child’s hospitalization was the almost complete
absence of SGOT, SGPT, and transaminase
during the most acute phase of her disease and
the subsequent rise in these enzymes as
re-covery occurred. At the present time this child
is asymptomatic and her physical examination
and all liver function tests are normal. She is
taking 12.5 mg of Azathioprine daily and I plan to gradually stop the drug within the next
2 months.
KENNETH A. DEITCHER, M.D.
3 Lockrow Avenue
Albany, New York 12205
EDITOR’S NOTE: Dr. Trey comments as follows:
In reply to the interesting case report of Dr. Deitcher, I am not aware of the use of
aza-thioprine in patients in fulminant hepatic
fail-ure who have had previously normal liver func-tions and have developed this condition
acutely. It has been used in patients with
chronic active hepatitis. The patient in
fulmi-nant hepatic failure is subject to many
compli-cations and the addition of this
immunosup-pressive agent may mask some of these. This is
the reason I would be unwilling to advocate its use at this time. The course of severe hepatic failure is variable, as I have stressed in the
re-view, and difficult to predict. We have seen
normal SGOT’s and SGPT’s during the course
of the disease. The values of these enzymes are not related to the patient’s prognosis.
CHARLES TREY, M.D.
Fulminant Hepatic Failure Surveillance
Study
Boston City Hospital Boston, Massachusetts 02118
Cephalosporium Meningitis
To THE EDITOR:
I find it necessary to comment on the paper
“Cephalosponium Meningitis” (PEDIATRICS,
44:749, 1969) in order to emphasize a word of
caution to physicians who may encounter
pa-tients under circumstances similar to those
de-scribed by Drs. Papadatos, Pavlatou, and Alex-iou.
The patient reported was a newborn infant
who on day 15 of life became irritable, listless, and refused feedings. In the absence of abnor-mal physical findings, the cerebrospinal fluid was examined and found to be slightly
xantho-chromic with 20 white blood cells per cu mm,
and with normal chemical constituents. The
diagnosis of cephalosporium meningitis “was
suspected by the morphological features of yeast-like organisms with long fine filaments
on direct smears in two separate cerebrospinal fluid specimens and confirmed by two cerebro-spinal fluid cultures.” The infant received 50
infusions of amphotericin B over a 60-day
pe-nod and was described as having a “normal
course” subsequent to the initiation of therapy. One must question the etiologic relationship between the organism isolated in culture, the agent visualized on smears of the cerebrospinal fluid, and the disease process in the patient.
