Indian J Pediatr (2010) 77:1049–1050
DOI 10.1007/s12098-010-0161-7
CORRESPONDENCE
Hyponatremia in Birth Asphyxia—Cause or Effect?
Vibeke Moen & Lars Irestedt
Received: 4 June 2010 / Accepted: 17 June 2010 / Published online: 7 September 2010
# Dr. K C Chaudhuri Foundation 2010
Sir,
We were greatly interested to read the recent article
Electrolyte Status in Birth Asphyxia by Basu and coau-
thors [1]. Their results, however, leave some questions
unanswered.
The authors conclude that babies with perinatal asphyxia
develop hyponatremia and hypocalcemia soon after birth in
proportion to the severity of asphyxia. However, as blood
samples were collected immediately after birth, we can
assume that the electrolyte status of the newborn also
represents intrauterine electrolyte status shortly before birth.
The low serum sodium values observed in asphyxiated
babies could imply that hyponatremia contributes to the
development of asphyxia, and therefore, factors contribut-
ing to the development of fetal hyponatremia should be
examined.
What policies regarding oral intake/intravenous fluids
were adopted during labour? Particularly, did the mothers
V. Moen (*)
Department of Anaesthesiology and Intensive Care,
County Hospital,
S-39185 Kalmar, Sweden
e-mail: vibekem@ltkalmar.se
L. Irestedt
Section of Anaesthesiology and Intensive Care,
Department of Physiology and Pharmacology,
Karolinska Institute,
S-17177 Stockholm, Sweden
of the asphyxiated babies receive large amounts of fluid,
and what about oxytocin administration?
As many as 30 of the 50 asphyxiated babies were
delivered by cesarean section. What were the indications
for caesarean section? What methods of anaesthesia were
used? And what kinds and volumes of intravenous fluids
were administered to the mothers during cesarean section,
prior to delivery? Were there any differences in serum
sodium values in the asphyxiated babies delivered by
caesarean section and vaginal delivery?
Serum potassium levels tended to be higher in hypona-
tremic, asphyxiated newborns. This could be explained by a
lower pH in the asphyxiated babies, but cord pH is not
mentioned. Was cord blood not examined for pH at birth?
Calcium levels were also lower in the asphyxiated,
hyponatremic newborn. Dilutional hyponatremia also
causes lower albumin levels, and as a result, lowering in
calcium levels. Only analysis of ionised calcium would
show the true calcium levels.
In a recent study, we found hyponatremia to be quite
common during longer lasting labours, and hyponatremia
developed after administration of quite moderate oral and
intravenous fluid volumes [2]. We did not observe any
asphyxiated babies in our study, but case reports of
hyponatremia with severe consequences for mothers and
infants have been published [3]. We therefore hope that
Basu and coauthors can answer our questions, as this might
shed useful information on this important topic.
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References
1. Basu P, Som S, Das H, Choudhouri N. Electrolyte status in birth
asphyxia. Indian J Pediatrics. 2010;77:259–62.
2. Moen V, Brudin L, Rundgren M, Irestedt L. Hyponatremia
complicating labour—rare or unrecognised? A prospective obser-
vational study. BJOG. 2009;116:552–61.
3. Johansson S, Lindow S, Kapadia H, Norman M. Perinatal water
intoxication due to excessive oral intake during labour. Acta
Paediatr. 2002;91:811–4.
Author’s Reply
Sir,
First of all we thank Dr. Moen, MD for taking interest in
our article. We must point out that the aim of our study was
to see the electrolyte status in asphyxiated newborn just
after their birth. We expected that the findings of our study
could help in better management of asphyxiated neonates.
We have not found any literature or standard text book
citing hyponatremia as the cause of perinatal asphyxia.
Rather few literatures have demonstrated clearly in separate
studies that hyponatremia and hypocalcemia are the con-
sequences of perinatal asphyxia [1, 2]. In our study we
demonstrated that the hyponatremia and hypocalcemia
occur simultaneously in such neonates and they also have
significant correlation with their severity of asphyxia,
irrespective of their intra or post partum origin. Oxytocin
was administered to mothers of 6% of total number of cases
in scheduled therapeutic doses as per protocol available
with the labour room.
The Correspondent probably overlooked that we have
excluded cases whose mothers had pre and post delivery
electrolyte abnormalities. The indications of caesarean section
were decreased scores of foetal biophysical profiles, suspected
intrauterine asphyxia or development of early foetal distress.
All the mothers who were delivered by caesarean section
received either spinal anaesthesia or epidural analgesia. All of
them received fluid during operation as per standard anaes-
thetic protocol. All other mothers delivered vaginally also
received fluid as per standard obstetric protocol. In none of the
cases any fluid or medication was given in excess of available
guideline. From different literatures and from our study we
found that a large percentage of the asphyxiated babies were
delivered by caesarean section [3]. So, it was our aim also to
find electrolyte status in those asphyxiated neonates soon
after birth. If some outcome of electrolyte status is influenced
by standard interventions during delivery or operations, the
electrolyte status we found in babies after such deliveries
Indian J Pediatr (2010) 77:1049–1050
invariably indicated that they require some definite manage-
ments and caesarean asphyxiated babies are in greater
numbers than their normally delivered counterpart. So, we
do not found it is necessary to give special importance to
draw a line between normally delivered and caesarean
babies.
All the standard text books and literatures explained that
perinatal asphyxia and metabolic acidosis go hand in hand.
So, cord blood pH was not considered in our study. This study
never aimed at finding out the aetiology of the abnormalities
in electrolyte status in asphyxiated babies. May be acidosis is
one of the contributor of increased potassium level in cases.
May be the transient hyperinsulinism which sometimes
develop in perinatal asphyxia influence the potassium level
among cases [4]. We hope researchers are seriously thinking
to find the etiologic correlations between electrolyte changes
and perinatal asphyxia and from the correspondent’s letter it
is clear that we have raised such queries in others mind. This
might be a success of our study. We do not know what
literature guided the correspondent to state that in birth
asphyxia, dilutional hyponatremia causes lower albumin
level. Correction of total calcium level for albumin level is
only done when it is so indicated. And perinatal asphyxia is
never such indication. So we do not find it necessary to
estimate albumin.
Pallab Basu, DCH, MD1, Sabyasachi Som, DCH, MD2,
Harendranath Das, MD 3 and Nabendu Choudhuri, MD,
MNAMS, PhD4
1
Department of Biochemistry, Nil Ratan Sircar Medical College
and Hospital, Kolkata - 700014. E-mail: dr.pallab_basu@rediffmail.
com.
2
Department of Pediatrics, Burdwan Medical College and
Hospital, Burdwan - 713101.
3
Department of Biochemistry, B. I. N., Kolkata - 700020.
4
Power House Para, Burdwan - 713101.
References
1. Gupta BD, Sharma P, Bagla J, Parakh M, Soni JP. Renal Failure in
Asphyxiated Neonates. Indian Paediatrics 2005;42:930.
2. Jajoo D, Kumar A, Shankar R, Bhargava V. Effect of birth asphyxia
on serum calcium levels in neonates. Indian J Pediatr 1995 Jul-
Aug; 62(4):455-9.
3. Bader D, Gozal D, Weinger-Abend N, Berger A, Lanir A. Neonatal
urinary uric acid/creatinine ratio as an additional marker of perinatal
asphyxia. Eur J Pediatr 1995;154:748.
4. Clark W, O’Donovan D. Transient hyperinsulinism in asphyxiated
newborn infant with hypoglycaemia. Am J Perinatol 2001 Jun;
18(4):175-8.