1
93
urine and, her random blood glucose (RBS with the glu-
cometer) was now 19.7mmol/L.
poorly documented when it does occur.
She continued on normal saline at 15% deficit minus
anti-shock. A repeat RBS an hour later showed
Neonatal diabetes can also cause neonatal hyperglycae-
mia. It is defined as persistent hyperglycaemia occurring
in the first months of life, lasting for more than 2 weeks
1
7.3mmol/L. At this point she was commenced on solu-
3
7
ble insulin at 0.05IU/kg/hr as hourly boluses. Intrave-
nous Ceftazidime was commenced and 2hourly RBS
estimations continued. Nine hours after admission RBS
dropped to 12.6mmol/L; at this time intravenous fluids
were changed to 4.3% dextrose in 0.18 saline. Two
hours later, blood glucose dropped to 9.8mmol/L and
remained between 7.8 and 10.4mmol/L over the next 8
hours. Insulin studies were not done as facilities for this
are unavailable in this environment.
and requiring insulin for management. It is considered
distinct from autoimmune type 1 DM, which manifests
8
after the first 3 to 6 months of life. It is a rare disorder,
7
occurring in only 1:500,000 live births, and may be
9
permanent or transient with/without recurrences. The
condition was first described in the infant son of a physi-
cian who presented with polydypsia, polyphagia, polyu-
3
ria, dry skin after birth. It is characterised by hypergly-
caemia, glycosuria, hypoinsulinnaemia and absent or
minimal ketonuria. Babies are usually full term, small
for gestational age, and de1s0cribed as having an aged
appearance and alert facies. Babies with the transient
form respond to insulin with normalization of growth
and weight rgd ain, and remission is usually apparent by
At 38hr on admission, her clinical condition was found
to have deteriorated, with temperature instability, dimin-
ished peripheral pulses, and worsening peripheral perfu-
sion in spite of adequate hydration. Blood sugar fluctu-
ated between 11.0 and 15.9mmol/L. At this point we
assumed that Systemic Inflammatory Response Syn-
drome had set in and started her on dopamine at 5µg/kg/
min. The two-hourly blood glucose estimation and intra-
venous insulin continued. From about the 47 hour on
admission, blood glucose was noted to have begun to
decline, falling to 8.0mmol/L; at that time the insulin
dose was skipped. She died at the 63 hour on admission
and it was noted that the final two readings before her
demise were within normal limits (3.6mmol/L and
11
about the 3 month of life. In majority of cases, the
child relapses at about the age of puberty (median age
1
1
14 years) with type 2 (nonautoimmune) diabetes.
Growth and development however remain normal. In the
permanent form (about half of babies presenting 1w2 ith
neonatal diabetes), insulin therapy is needed for life.
In the case of the neonate highlighted, she presented
with clear features of failure to thrive, with sepsis and
dehydration. In majority of instances, in our clinical
experience, the result of a random blood sugar done at
admission would usually require for hypoglycaemia to
be corrected. The finding of hyperglycaemia in the dia-
betic range is indeed a rare occurrence, and for that rea-
son insulin is not one of the usual drugs in the NICU
emergency arsenal.
2
.8mmol/L).
A post-mortem lumbar puncture revealed bloody CSF
on macroscopic appearance. Microscopically, RBC were
3
numerous, 30 WBC/cmm with 20% lymphocytes and
8
0% PMN, no growth on culture. Her parents unfortu-
nately declined a post mortem.
Treatment of the underlying cause is usually sufficient
to correct hyperglycaemia in neonates with transient
neonatal hyperglycaemia. Unfortunately in this case, we
lost the opportunity to arrive at a definitive diagnosis/
arrive at a definite cause of the hyperglycaemia as the
baby gave in early into the primary pathology, and we
lacked the capacity to run serum insulin assay. Rever-
sion of her blood glucose to near normal levels termi-
nally was more likely due to a terminal hepatic insuffi-
ciency.
Discussion
Hyperglycaemia is thought to be associated with a num-
ber of primary pathologic conditions [infection, as-
phyxia, hyperosmolality (following hyperosmolar feeds
or hype2r,n5 atraemic dehydration), seizures, respiratory
2
distress] and drugs [steroids, β agonists, phenytoin,
5
theophylline, intravenous glucose infusion] used in the
neonatal period. It is also more common in the preterm
and intrauterine growth restricted (IUGR) infant, as they
6
appear to have a reduced capacity for insulin secretion.
Conclusion
In clinical practice, hyperglycaemia mostly occurs fol-
lowing the introduction of glucose containing intrave-
nous fluids, and responds appropriately to a reduction in
the glucose concentration of the infusion. The evidence
for hyperglycaemia occurring with or as a complication
Hyperglycaemia, though not a primary diagnosis on its
own, is capable of worsening morbidity and mortality. It
therefore needs to be handled as a separate entity with
insulin therapy. In the case highlighted, while not giving
total credence to the hyperglycaemia, it is certain that it
contributed to poor outcome. As has been previously
stated, it is more common for hypoglycaemia to be the
co-morbid finding at admission of most sick neonates.
The finding of hyperglycaemia, demonstrated here, fur-
ther buttresses the need for random blood sugar estima-
tion to become part of routine admission work-up.
5
of other clinical entities are few; Nalini et al working
with 1171 neonates found a prevalence of 0.94%
(
prevalence in very low birth weight babies was 2.9%),
in this environment documentation of the occurrence of
hyperglycaemia occurring with/complicating primary
morbidities is nonexistent. Give the frequency of neona-
tal illness, it is either this problem does not occur, or is