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Neonatal Thyrotoxicosis
1.
2.
3. Case Summary
Gara ; was born at 20th January 2020
• A term Boy delivered ( 2kg ) by Caesarean
section and The baby was discharged home on
exclusive breast milk feed.
• The baby had progressive weight loss, which
led to the introduction of formula milk with
no recovery.
4. • The gestation was unknown until 16 weeks
and was followed in the high-risk consultation
due to gestational diabetes, which was poorly
controlled by Endocrinologist and the mother
had emotional liability was followed by
Psychatry specialist but with out benefits.
• During pregnancy the mother complained of
increase fetal movement and on follow up by
ultrasound; the fetus had IUGR.
5. Farther History …..
• A newborn ( male ) at 25 days of age
presented because of irritability, poor weight
gain, flushing and sweating.
• Nothings were significant in history apart
from Family History
• Father 49 years ; COPD on medication.
• Mother 32 years old (cousins) with gestational
diabetes.
6. physical examination
• The physical examination revealed a
malnourished infant (weight 1700g) with a
great irritability, hyperhidrosis and an ocular
protrusion.
• He also had tachycardia (HR>165 ppm) with a
normal blood pressure.
7. • The child was admitted to Hevi pediatric
teaching hospital under close surveillance.
8. On further enquiry
• By close observation and contentious
assessment of patient regarding history,
physical examination and farther
investigations
• Mather with emotional lability
• Fetus with IUGR
• Neonate with irritability and sweating
9. Differential diagnosis
o neonatal sepsis
o congenital heart diseases
o Hyperthyroidism
o congential viral infection,
o tachyarrythmia.
o narcotic withdrawal syndrome
o infantile colic
10. Investigations
• The blood work revealed
• low level of TSH 0.01 mUI/L (range value (RV)
0.70–18.10),
• high level of free thyroxine (FT4) 6.91 ng/dL (RV
0.66–2.36) and
• high level of TRABS 22.50 IU/L (RV <1.0 IU/L).
• The cervical ultrasound and echocardiogram
were normal.
• Mother investigations revealed: low TSH, high
FT4.
12. Treatment
• The patient started treatment with propranolol
and methimazole with clinical improvement and
normalization of the thyroid hormone levels.
• Mother : thyrotoxicosis and referred to adult
Endocrinologist.
13. Outcome and follow-up:
• The baby was discharged at 33 days of life,
medicated with propranolol and methimazole
until 2 and 4 months, respectively.
• The thyroid function normalised during the
Hospital stay and TRABs(thyrotropin receptor
antibody) were negative at 4 months of age.
• Now the child is euthyroid (FT4 1.18 ng/dL
and TSH 1.703 μUI/mL) without any treatment
and with excellent development and growth.
14. Lessons
• Neonatal Thyrotoxicosis should be considered
in any Fetus with IUGR & Neonate with
irritability and weight loss.
The maternal history may give you a clue for
neonatal condition and vice versa is correct.
We recommend and support Thyroid function
test for all newborn as a part of newborn
screening program
15. Some theory
• Neonatal hyperthyroidism is a rare but
potentially fatal condition.
• Between 1% and 5% of the offspring of
women with Graves disease will be diagnosed
with thyrotoxicosis, which equates to 1 in
10,000 to 1 in 50,000 newborns.
16. ETIOLOGY
Immune causes:
• In most cases, the cause is transplacental passage of
thyroid-stimulating immunoglobulin (TSI) from a
mother with Graves disease.
• In these infants, thyrotoxicosis may be anticipated by
knowing the mother’s thyrotropin receptor antibody
(TRAb) level in the third trimester and/or cord blood
levels.
• but it also has been described in women with
Hashimoto thyroiditis.
Rare nonimmune causes of neonatal thyrotoxicosis is
due to genetic disorder.
17. Clinical features of Fetal thyrotoxicosis
• In pregnancies affected by maternal
thyrotoxicosis, both stillbirths and preterm births
are increased. Other features include:
• Goiter.
• Tachycardia and dysrhythmias
• Hydrops
• Abnormally increased activity
• Premature bone ossification
• Oligohydramnios
• Intrauterine growth restriction
18. Clinical features of neonatal thyrotoxicosis
• Small for gestational age, Preterm birth
• Goiter
• Central nervous system signs, including irritability and restlessness
• Eye signs, including lid retraction, periorbital edema, and proptosis
• Cardiovascular signs, including tachycardia, which may progress to
tachyarrhythmia and cardiac failure
• Hypermetabolism presenting as flushing and sweating, avid
feeding, diarrhea, excess weight loss, and failure to thrive
• Hepatosplenomegaly, Lymphadenopathy, Thrombocytopenia,
coagulopathy, Jaundice and liver disease.
• Craniosynostosis, Microcephaly and advanced bone age
19. Treatment of neonatal thyrotoxicosis
• The main treatment is with a thionamide,
either carbimazole (750 mg/kg per day—
single daily dose until euthyroid,then
gradually reducing to a maintenance dose of
30% to 60% of the initial dose) or
• propylthiouracil (2.5–5 mg/kg twice daily
until euthyroid, then gradually reducing to a
maintenance dose of 30% to 60% of the initial
dose).
20. Treatment of neonatal thyrotoxicosis
• Both block the synthesis but not the release of
thyroid hormones; so a response may not be
seen until the thyroid hormone store in the
colloid is depleted.
• Propylthiouracil also blocks the peripheral
conversion of T4 to T3, but because of the risk of
hepatic failure, carbimazole (methimazole) would
be the preferred drug.
• Carbimazole also has the advantage of a once-
daily dose, but there is a risk of agranulocytosis.
21. • Iodine suppresses thyroid hormone synthesis and
has a prompt effect on blocking the release of
thyroid hormones.
• It is recommended in a very thyrotoxic infant (ie,
one with significant cardiovascular and/or
hypermetabolic signs).
• Either saturated potassium iodide (48 mg/drop,
1 drop/ day) or
• Lugol solution(5%potassium iodide,8mg/drop,1–
3 drops/day) may be used.
Treatment of neonatal thyrotoxicosis
22. • b-blockers (propranolol) are effective at
controlling the symptoms caused by
adrenergic stimulation.
• The goal is to reduce the heart rate to safe
levels.
Treatment of
neonatal
thyrotoxicosis
23. • The severely thyrotoxic infant may be treated
with corticosteroids (prednisolone 2 mg/kg
per day), which suppresses the deiodination
of T4 to T3 and compensates for the
hypermetabolism of endogenous steroids by
the excessive levels of thyroid hormones.
Treatment of
neonatal
thyrotoxicosis
24. Follow up
• Infants receiving treatment require regular monitoring
(biweekly to start with, reducing to weekly, then
alternate weeks once stable) of thyroid function to
ensure accurate treatment and prompt reduction,
followed by discontinuation of the ATD once TRAb is
cleared from the circulation to prevent iatrogenic
hypothyroidism.
• T3 tends to be disproportionally more elevated thanT4
in cases of thyrotoxicosis caused by direct thyroid
activity; therefore, T3 measurements (if available) can
aid accurate adjustments in ATDs.
25. Duration of neonatal thyrotoxicosis
• Thyrotoxicosis in infants of mothers with
Graves disease resolves with the clearance of
TRAb from the infant’s circulation.
• This generally takes 3 to 12 weeks, but may be
more than 36 months
26. Breast feeding of mother on ATDs
• Both propylthiouracil and carbimazole
(methimazole) may be detected in human milk.
• Propylthiouracil is highly protein bound, and
therefore is at a lower concentration in the milk
compared with methimazole.
• Thyroid function and later neurodevelopment
remain normal with maximal daily doses of 20 mg
methimazole or 450 mg propylthiouracil, and
therefore breastfeeding is regarded as safe with
maternal ATD use at or below these doses.
27. PROGNOSIS
• Normalization of thyroid function is usually
rapid after initiation of therapy in thyrotoxic
infants.
• There are few data on long-term outcomes.
• Historically, mortality has been reported to be
as high as 25%.
• It is there for essential that high-risk infants
are kept under close review.
28. THANKS FOR YOUR
ATTENTION
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