NEONATE BORN TO MOTHER WITH GRAVE

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• NEONATE BORN TO MOTHER WITH GRAVES DISEASE
• Baby boy born at 24 weeks gestation, weight 559G
• Mother 25year,G6 P4 Ab1 LC4.
• Known case of Graves disease, with uncontrolled
  thyrotoxicosis since 1999non compliant on
  treatment (PTU/Inderal). No PNC.
• With pre-eclampsia, abruption- severe
  decelerations-Emergency C-section.

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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.

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MANAGEMENT IN NICU

• Hypoperfusion/hypotension/metabolic acidosis
  needing NS bolus x 2 and inotrope support.
• D2-3 echo showed PDAtreated with Indomethacin
• Head sonono IVH. Drug screen normal

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THYROID CHEMISTRIES
Infant values Day -1 Day -7
T4,free (0.6-1.70) 1.26 0.45
TSH (0.4-5) 0.07 0.01
T3,total (70-204) 124 97
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• PRESENT CONDITION
• Presently baby on IMV, being treated for evolving
  lung diseasediuretics and steroid nebulization
• On TPN and NG feeds.

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OBSTETRIC HISTORY

• 7/96 40wks 9lbs NSVD Dallas
• 9/97 40wks 7lbs NSVD Mexico
• 11/01 31wks 2lbs NSVD Thomason
• 9/03 36wks 3lbs NSVD Thomason
• 12/00 15wks miscarriage
• 7/04 24wks 1.2lbs CS Thomason

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BABY WITH NEONATALTHYROTOXICOSIS

• Baby No.3 was born at Thomason in 2001
• Preterm 31 wks SGA , BW1130 G
• No prenatal-care. Presented 1 hour prior to
  delivery.
• Had fetal bradycardia/abruptio.
• Ventilated

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CLINICAL FEATURES/COURSE

• IUGR. Microcephaly, Bone age noted to be
  advanced.
• Had persistent tachycardia
• Baby had fluctuating levels of T4 and T3.
• Treated with Lugols iodine, Inderal and PTU

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THYROID CHEMISTRY
2001 Day 1 Day 10 Day 14
T4 0.7 gt6 2.6
TSH lt 0.1 lt0.1 lt0.1
T3 264 570 81
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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

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THYROTOXICOSIS IN NEONATE

• Typically a transient hyperthyroidism
• 1 in 70 Graves affected pregnancies.
• Mortality up to 25
• Etiology
• Placental transfer Thyroid-stimulating
  immunoglobulins. Maternal antibodies wane over
  2-3 months

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MATERNAL TBII

• TSH binding inhibiting immunoglobulin
• Levels gt 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

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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

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POINTS TO CONSIDER

• Mother with Graves 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

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CLINICAL FEATURES OF NEONATAL THYROTOXICOSIS

• Hyperirritability
• Tachycardia
• Goiter
• Exophthalmos
• LBW and weight loss
• CHF
• Craniosynostosis/ advanced bone
  age/microcephalypsychomotor retardation
• Jaundice/thrombocytopenia

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APPROACH TO BABY OF MOTHER WITH GRAVES DISEASE
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• 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
• Lugols iodine (8mg/drop) 1-3 drops/D
• Iopanoic acid/sodium ipodate, Propanolol,
  Prednisolonein refractory cases

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TREATMENT (CONTINUED)

• Exchange transfusionsto 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.

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SUMMARY

• Possibility of fetal thyrotoxicosis must be kept
  in all mothers with a history of Graves 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

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SUMMARY (CONTINUED)

• In neonates signs of thyrotoxicosis may be
  delayed due to effect of maternal anti-thyroid
  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.

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