LETTERS TO THE EDITOR
792
Co,,u,nciit.s’ time Contents of PEDIATRICS or alit, tOJ)iC of general interest are incited. Queries aimcl answers iia#{231}be exchanged between correspondents. Letters accepted for publication will
iOt be subjected to editorial alteration except as to proper form. The Editor reserves time right to publish re/)/ze.s to letters one! to solicit responses from authors 00(1 others.
Thi.v column has been established to provide a forum for all members of time profession for
cxciwnge of information aimcl views. Statements and opinions expressed in letters are those of
time authors arid do not represent the official /)o.Sition of the American Academq of Pediatrics, lime. ,or its Coi;m lflitt(’(’S.
Erythroblastosis Fetalis
To nm EDITOR:
I should hike to comment on the
conclu-sions of Giblett, Varela, and Finch
(PEDI-ATRICS, 17:37, 1955), which appeared to me
to be poorly fouinded. Their reasoning is
based omi time assuimmiption that a 2-week-old
immfant with a imemoglobimm level between 6
amid 8 gm. is suffering frommi anoxia to the
cx-tent that he shouthd normally be producing
red cells at a rapid rate. I doubt that this
assumption is correct, even in part, and they
have presemited no data on
nonerythnoblas-totic infants to suipport it. Therefore their
conclusions are not validi, in my opinion.
They made one interesting
observation-the apparent normal uptake of iron without
its sumbsequment appearance in the circulating
imemoglobin. Timis should be followed up.
There was another paper which should
not have gone uinchallenged this long, by
Jones et a!. (PEmAnrncs, 14:346, 1954). While
I d!isagnee with muich in this paper, the
point I wouildi like to emphasize is that if
careful observation jim time first 5 days
re-veals no abnormal neurohogic signs it is
)ractically certain that the child will have
ho sequehae of any kind. Since the parents
are usumally fairly well informed, and almost
invariably worried aboumt the possibility of
permanent brain damage, it is sheen cruelty
to hedge in the slightest when making a
prognosis on the apparemmtl intact infant.
I personally kmmow of no case in which there
imas been penmnammemmt damage of any kind
traceable to the enythroblastosis in an
in-fant who seemed all right during the first
5 days.
There is a still more glaring error in the
paper by Hyman and Sturgeon (PEDIAmIc5,
16: 15, 1955) where they say “we still
con-sider it possible that Rh-positive blood (for
exchange transfusion of Rh-incompatibility
erythrobiastosis) may have certain
thena-peutic advantages.” If people have such
dangerous thoughts they should keep them
to themselves rather than displaying them in
public. On their own admission the authors
have not done a controlled trial of such
therapy; indeed I doubt that they would
dare to do so. I hope you will forgive me
for saying that I think it was an impontant
editorial error to have allowed suich a foolish
statement to appear in print.
FRED H. ALLEN, JR., M.D.
Boston, Massachusetts
To THE EDITOR:
We are happy to explain more fully our
stand in respect to the point raised by Dr.
Allen. It is stated that “our reasoning is
based on the assumption that a 2-week-old
infant with a hemoglobin level between 6
and 8 gm. is suffering from anoxia to the
extent that he should normally be
produc-ing red cells at a rapid rate.” This
state-ment was considered “poorly founded” and
it was “doubted that this assumption is
cor-rect even in part The nature of the
objection raised by Dr. Allen is not entirely
clear. Is exception taken to this type of
rca-soning because it is believed that: (1)
new-bonn infants cannot respond to the stimulus
of anoxia; (2) a hemoglobin level of 6 gm.
is not necessarily accompanied by anoxia,
or (3) the age of the infant is important in
R.tIcs/IOORBC 2
3000
Morrow
Erythrold 15,000 Count
-
20 40 60 50 00 DaysA.Chanq.s in Hb.concentration, ritlculocytws and morrow #{149}rythroldcount In a normal niwborn
Is
Hg. 6
(gm./IOOcc.) 4 2 7
R.tics/IOOROC 3 p. d’
0’ , , , I
20 40 60 80 00 Days
B. Eryttiropoletic activity In on Infant with cyanotic h#{149}ortdlssoss 21
2:
IC Hg.
(gm./lOOcc.)
R.tics/I00 RBC
II _,
9 ,i I’
7 i .,
!
-- - #{149}--- ---20 40 60 80 00 Days
C. Hb. concentration and retlculocyte levels Is on untronsfused Infant with erythroblastosis
LETTERS TO THE EDITOR I1.3
We will emidleavor to aimswer these points.
It is gemmerally accepted that when the
in-fammt goes from time anoxic intrauterine
en-viroimment to mmormal atmospheric
comidi-tions, there is a temporary depressioim of enythnopoiesis. However, when the
hemo-globin drops to a critical level, the red cell
marrow is stimulated to increased activity.
Is
H. 6
(m./IOOcc.) 14 2
mass at birth to fall to a critical level. That
the marrow of the newborn infant is
capa-ble of responding to the stimulus of anoxia
has been clearly demonstrated by Rudolpim
et a!. (PEDIATRICS, I 1:454, 1953) and
Gaird-ncr et a!. (op. cit.) who report on babies
with severe congenital heart disease with
markedly decreased arterial oxygen
sattmra-Fi;. 1. After Gairdner et al. (op. cit.) and Hyman and Sturgeon (op. cit.).
In Figtmre 1A, adapted from the report of
Gairdlnen et al. (Arch. Dis. Childhood,
27:214, 1952), is indicated the interrelation
of erythropoietic activity and the arterial
hemoglobin level in the normal infant. Such
evidence immdicates that the normal infant
rarely, if ever, has a imemoglobin level of
less than 10 gm./100 ml.
It Votmldl appear likely that the tinme
nela-tiomisimil) of marrow response omm time pant of
the nonmmmal infant marrow is due to the
in-tenval required for time expanded red cell
tion and a persistent polycythemia. Thmes
infants did not develop the usual postnatal
drop in red cells and reticumlocytes (Fig. 1B).
The infant with hemolytic disease of time
newborn also has mmeed for active
enythno-poiesis shortly after birth since the
imemo-globin level may drop rapidly. The active
erythropoiesis which occurs in these anemic
children during time first 2 to 3 weeks
of life is well illuistnated by the reports of
Pickles (Haemolytic Disease of the
794 LETTERS TO THE EDITOR
Hvmmman amid Sturgeomm (PEDIATRICS, 16:15, 1955) (Fig. 1C).
Thus, mmmarrow response as a result of
aimoxia or anemia may occur during the first few weeks of life wlmemmever the stimulus becomnes of sufficient degree. It seems likely
that time greater anemia reacimed in infants
with erythnobiastosis before marrow
re-sponse is mmmanifest by reticulocytosis
(Des-forges et a!. : Blood, 10:802, 1955), may be
ascribed to the rapid! fall in hemoglobin and
the time lag within the marrow for delivery
of miew cells to the blood. While the
theoretical qumestion migimt be raised as to
whether a decrease in oxygen carrying
ca-pacit of time blood represents anoxia, in
our practical thinking it is impossible to
make any differentiation in the way the
marrow responds to these two if they be
diffenemmt.
1mmtime case report uimder discussion
(Gib-hett Ct al. : PEDrAmIcs, 17:37, 1956) the
imemoglobin level oven a 50-day period
de-scended on several occasiomms to less than
7 gm. withoumt reticulocytosis. Thus, in spite
of a persistent anemia which would provide
ample stimulus for erythnopoiesis in the
nor-mal child, there was no evidence of
mar-row activity until the child was nearly 2
months old. We could only conclude that
the bone marrow was depressed in the face
of an adequate stimulus. The lack of
re-spomise in this child has been ascribed to the
effect of antibody on time erythroid marrow
for reasons discussed in oumr report.
ELO GIBLETT, M.D. C. A. FINCH, M.D.
Seattle, Washington
To mm EDITOR:
Although I was riot first author on either
of the second or third paper referred to by
Dr. F. A. Allen, Jr. in his letter to you of
February 6, 1956, I sincerely appreciate the
opportunity of submitting a reply. Dr.
Allemm’s letter, as I interpret it, contains two
types of cniticismmi, one scientific and the
other edhtonial. First, it appears he finds
some of time conclumsions, ideas or both
cx-pressed in those papers are scientifically
unsoumnd. In the second place he indicates
therefore “an important editorial error.”
I should like to deal first with Dr.
Allen’s challenge to the paper of Dr. M. H.
Jones et al. (PEDIATRICS, 14:346, 1954). In
that paper the number of patients studied
is definitely stated, “100”; the length of
fol-low-up is clearly given, “6 months to 5
years.” The criteria for assessing the
integ-nity of the central nervous system during
the newborn period are listed amid the
method of classification is given. In the
fol-low-up age range the growth and
develop-ment of the infants and children was
ob-served in our cerebral palsy and child
de-velopment clinics. A considerable
propor-tion of the paper is devoted to a
descrip-tion of the methods employed in those
clinics for the evaluation of the children.
The results of these studies were tabulated
in detail in Tables I and II. The data, I
be-lieve, were thus presented in accordance
with acceptable scientific standards. This
form of presentation permits the critical
reader to re-examine the data if he so
wishes. The conclusions stated in the last
paragraphs of the discussions and the
sum-mary are supported by the data. It is
pointed out in the discussion moreover that
our data and interpretations were consistent
with the independent data presented by
Molhison and Walker (Lancet, 1:429, 1952)
and Armitage and Mollison
(J.
Obst. &Gynaec. Brit. Emp., 60:605, 1953). At the
time of preparing our paper we could find
no data supporting the opposite conclusion;
but only statements to the contrary, such
as the one by Vaughn, Allen and Diamond
(Pimimics, 6:706, 1950), which we cited
in our paper.
Similar statements continued to appear in
the literature, A. R. Jones, Diamond and
Allen (New England
J.
Med., 250:324, 1954)state “In a follow-up study of a considerable
number of infants who have had
erythro-blastosis fetalis, with a comparison of their
intellectual capacities with that of their
olden siblings, we found no evidence of
im-pairment of intelligence (or of nmoton
abil-ity). These infants have been observed
closely, however, during the neonatal period
