Neonatal thyrotoxicosis is a rare disorder, and still rarer is its
co-occurrence with early onset neonatal sepsis. Thyroid dysfunction,
both hypothyroidism and hyperthyroidism, can alter a range of immune
functions including chemotaxis, phagocytosis, production of reactive
oxygen species, and cytokine production [1].
A 31-week-old appropriate for gestational age, baby
girl weighing 1420 g was born to gravida 2 mother by precipitate labor.
Mother was an unbooked case and presented to our hospital in labor with
meconium stained amniotic fluid. Apgar scores were 7 and 8 at 1 and 5
minute, respectively. On admission baby had severe respiratory distress
with Silverman Anderson score of 8. She was noted to have tachycardia
with a heart rate of 198/per minute. Due to non-availability of
ventilator, she was manually ventilated for 6 hours. We kept the
differential diagnosis of early onset sepsis, respiratory distress
syndrome and meconium aspiration syndrome. She received injectable
ampicillin and gentamicin and provided supportive care. On
investigation, her total leucocyte count was 3675×109/L, platelets 8900
× 109/L and procalcitonin levels 7.28 µg/L (normal, less than 0.5 µg/L).
Chest X-ray showed cardiomegaly and bilateral clear lung fields.
Blood culture grew Enterococcus faecalis sensitive to ampicillin
and gentamicin.
After 6 hours of age baby showed improvement and was
shifted to continuous positive airway pressure (CPAP). However, she was
noted to have persistent tachycardia, with heart rates ranging from
180-210 per minute without any evidence of poor tissue perfusion.
Electrocardiogram showed sinus tachycardia. Echocardiography
demonstrated structurally normal heart. Detailed examination of baby
revealed a swelling over anterior aspect of neck. The eyes of the baby
were prominent. Baby appeared irritable and hyperalert. Mother gave
history of neck swelling for 3 months and tremors prior to delivery. She
had exophthalmos and tachycardia. Thyroid profile of baby on day 3 of
life in venous blood showed triiodothyronine (T3) levels of 315.4 ng/dL,
thyroxine (T4) levels of 19.5 µg/dL and thyroid stimulating hormone
(TSH) levels of <0.01 mU/mL. Mother’s thyroid profile showed a free T3
value of 10.2 pmol/L, free T4 value of 80.4 pmol/L and TSH value of
<0.01 mU/mL. Ultrasound of neck of the baby showed bulky thyroid gland
with altered echotexture, suggestive of thyroiditis. TSH receptor
antibody levels in baby were 37.75 IU/L (normal, less than 1.75
IU/L).The final diagnosis was early onset sepsis with neonatal
thyrotoxicosis.
We started oral propranolol 2 mg/kg/day in three
divided doses along with methimazole 0.5 mg/kg/day in three divided
doses from day 3. Tachycardia settled after 72 hours of treatment
following which propranolol was tapered. Thyroid function tests were
repeated after 7 days of starting methimazole which showed no
significant improvement, hence dose of methimazole was increased. On
follow-up at 6 weeks and 3 months of age, baby showed normal growth and
development. Thyroid functions normalized by 18 weeks of age.
Methimazole dose was tapered and stopped. Baby tolerated methimazole
well and did not show any adverse drug reaction.
In the present case, neonatal thyrotoxicosis
coexisted with early onset sepsis which made diagnosis challenging.
Although, free T4 could not be done in the postnatal period in the index
case, rest of the investigations and clinical examination findings of
the mother and baby were suggestive of neonatal thyrotoxicosis. Thyroid
hormones are known to act as modulators of immune response [1] and it is
possible that thyrotoxicosis predisposed the baby to early onset sepsis.
The clue to diagnosis of thyrotoxicosis was persistent tachycardia in
the absence of any known cause, such as tachyarrhythmia or shock.
Previous studies on pregnant women with
thyrotoxicosis showed that women treated earlier in pregnancy were more
likely to be euthyroid at delivery and had better pregnancy outcomes
[2]. Uncontrolled thyrotoxicosis in pregnancy is associated with
abortion, prematurity, low birthweight, and stillbirth [2]. Polak, et
al. [3] reported clinical manifestations on 10 neonates with congenital
thyrotoxicosis. Nine of them were due to autoimmune causes. Tachycardia
was the commonest sign followed by goiter and hyperexcitability. Our
patient responded well to treatment. Tachycardia settled first, followed
by hyperexcitability. Neck swelling gradually reduced in size on
follow-up but eye signs persisted longer. Thyroid function returned to
normal by 4.5 months of age. The present case shows the rare occurrence
of neonatal sepsis with congenital thyrotoxicosis, and highlights the
importance of maternal history and examination in making correct
neonatal diagnosis.
1. Vito PD, Incerpi S, Pedersen JZ, Luly P, Davis FB,
Davis PJ. Thyroid hormones as modulators of immune activities at the
cellular level. Thyroid. 2011;21:879-90.
2. Davis LE, Lucas MJ, Hankins GDV, et al.
Thyrotoxicosis complicating pregnancy. Am J Obstet Gynecol.
1989;160:63-70.
3. Polak M, Legac I, Vuillard E, Guibourdenche J,
Castanet M, Luton D. Congenital hyperthyroidism: The fetus as a
patient. Horm Res. 2006;65:235-42.