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Transcript
NEONATE BORN TO MOTHER
WITH GRAVE’S DISEASE


Baby boy born at 24 weeks gestation,
weight 559G
Mother 25year,G6 P4 Ab1 LC4.

Known case of Grave’s disease, with
uncontrolled thyrotoxicosis since 1999…non
compliant on treatment (PTU/Inderal). No
PNC.

With pre-eclampsia, abruption- severe
decelerations-Emergency C-section.
NICU COURSE
Maternal TSI on Sept 2003: 212%
(Normal 0 - 129%)
• Resuscitated at birth Apgars 3,6 & 8.Ventilated
….given curosurf and transferred to ICN on
portable ventilator

• On exam, baby 24 weeks gestation AGA

Systemic exam WNL. No evidence of
goiter/exophthalmos. Initially had heart rates in
160-170 but later normalized.
MANAGEMENT IN NICU

Hypoperfusion/hypotension/metabolic
acidosis needing NS bolus x 2 and
inotrope support.

D2-3 echo showed PDA…treated with
Indomethacin

Head sono…no IVH. Drug screen normal
THYROID CHEMISTRIES
Infant values
Day -1
Day -7
T4,free
(0.6-1.70)
TSH
(0.4-5)
T3,total
(70-204)
1.26
0.45
0.07
0.01
124
97
PRESENT CONDITION


Presently baby on IMV, being treated for
evolving lung disease…diuretics and steroid
nebulization
On TPN and NG feeds.
OBSTETRIC HISTORY






7/96 40wks
9/97 40wks
11/01 31wks
9/03 36wks
12/00 15wks
7/04 24wks
9lbs NSVD
7lbs NSVD
2lbs NSVD
3lbs NSVD
miscarriage
1.2lbs CS
Dallas
Mexico
Thomason
Thomason
Thomason
BABY WITH NEONATAL
THYROTOXICOSIS





Baby No.3 was born at Thomason in 2001
Preterm 31 wks SGA , BW:1130 G
No prenatal-care. Presented 1 hour prior to
delivery.
Had fetal bradycardia/abruptio.
Ventilated
CLINICAL
FEATURES/COURSE




IUGR. Microcephaly, Bone age noted to
be advanced.
Had persistent tachycardia
Baby had fluctuating levels of T4 and T3.
Treated with Lugol’s iodine, Inderal and
PTU
THYROID CHEMISTRY
2001 Day 1
Day 10
Day 14
T4
>6
2.6
TSH < 0.1
<0.1
<0.1
T3
570
81
0.7
264
COURSE AFTER DISCHARGE




Discharged at 2 m with T4 :0.6 and T3 :69.
Stopped meds prior to discharge.
Had initially weight loss which later
improved.
At 2 m age had seizures. F/Up thyroid tests
were normal.
Head scan/MRI July 2004 showed non
communicating hydrocephalus
THYROTOXICOSIS IN
NEONATE
Typically a transient hyperthyroidism
 1 in 70 Grave’s affected pregnancies.
 Mortality :up to 25%
Etiology
 Placental transfer : Thyroid-stimulating
immunoglobulins. Maternal antibodies
wane over 2-3 months

MATERNAL TBII
TSH binding inhibiting immunoglobulin
Levels > 70% predictive neonatal
thyrotoxicosis
 Role of stimulatory and inhibitory
immunoglobulins
 Duration of disease depends on
concentration, degradation rate and
presence or absence of inhibitory Ab

BABIES AT RISK






Raised level of TBII in pregnancy
TBII not assessed
Thyotoxicosis in 3rd trimester
Thionamide required in 3rd trimester
Family H/O TSH receptor mutation
Evidence of fetal thyrotoxicosis
POINTS TO CONSIDER





Mother with Grave’s disease may not have
thyrotoxicosis and may be euthyroid or
hypothyroid.
Exposure to anti-thyroid drugs in-utero may delay
symptoms
Newborn Screening with T4-radioimmune assay,
can detect raised levels of T4
Positive assay for Thyroid stimulating
immunoglobulins….confirmatory
Consider narcotic withdrawal
CLINICAL FEATURES OF
NEONATAL THYROTOXICOSIS








Hyperirritability
Tachycardia
Goiter
Exophthalmos
LBW and weight loss
CHF
Craniosynostosis/ advanced bone
age/microcephaly…psychomotor retardation
Jaundice/thrombocytopenia
APPROACH TO BABY OF
MOTHER WITH GRAVES
DISEASE
Babies at risk
Cord blood fT4,TSH,TSI + examination
If high risk repeat fT4,TSH & exam
Age 2-7 days
In all babies repeat fT4,TSH and exam
Age 10-14 days
Hypothyroid. Repeat fT4/TSH
Treat with thyroxine if confirmed
Hyperthyroid
PTU/carbimazole
iodide+/Propanolol+/Normal.No treatment
TREATMENT






Should biochemical abnormality in absence
of symptoms be treated?
Thionamides block hormone synthesis
PTU 5-10mg/kg/d in 3 divided doses
Carbimazole 0.5-1.5mg/kg/d
Lugol’s iodine (8mg/drop) 1-3 drops/D
Iopanoic acid/sodium ipodate, Propanolol,
Prednisolone–in refractory cases
TREATMENT (CONTINUED)




Exchange transfusions…to reduce TSI
levels
Baby on treatment for thyrotoxicosis is
reviewed weekly until stable, then every 2
weeks and drug dose reduced.
Usually treated for 4-8 weeks.
Thyrotoxicosis secondary to mutations of
TSH receptor require ablative treatment
with surgery.
SUMMARY



Possibility of fetal thyrotoxicosis must be kept
in all mothers with a history of Grave’s disease
regardless of thyroid status/treatment.
Thyroid stimulating immunoglobulins (TSI)
persist even after thyroid surgery/radioablation
in mother.
Neonatal thyrotoxicosis secondary to TSIs is a
transient disorder, limited by clearance of
maternal antibodies
SUMMARY (CONTINUED)


In neonates signs of thyrotoxicosis may be
delayed due to effect of maternal antithyroid drugs or effect of blocking
antibodies. Cases reported as late as 45
days.
TSH binding inhibitor Ig levels from mother
and from neonate correlate well with
neonatal thyrotoxicosis.