Clinical Guideline



St. Peter’s Hospital, Neonatal Unit

Management of infants born to mothers with thyroid disease in pregnancy

Introduction

The thyroid hormones have profound effects on growth, neurological development, metabolism and cardiovascular status.

• Under the influence of TRH, TSH stimulates thyroid to synthesise T4, T3

• Only fT4, fT3 is active (= 1% of the total)

• fT4 is deiodinated to fT3 which is 3-4 times more potent

The thyroid gland in the fetus develops @ 3-4/40 GA but produces little thyroid hormone until 12/40. The fetus is dependent on the small amounts of T4 that can cross the placenta during the first trimester. During the second trimester the hypothalamic-pituitary axis becomes functional (by 20/40) and the TSH rises along with T3 from the thyroid gland. The full maturation of the hypothalamo-pituitary-thyroid feedback system happens in the third trimester. Therefore when babies are born the thyroid levels are a reflection of the fetal thyroid production.

At birth there is a TSH surge which results in high T4 and T3 levels. These return gradually to normal infant levels by 7-14 days of life

• Maternal TSH & T3 do not cross the placenta (poor permeability and placenta deiodinases)

• T4 crosses the placenta during the first trimester but this reduces significantly with increasing gestational age. At term only if the fetus is athyroid, a small amount of T4 can cross the placenta.

• Carbimazole, propythiouracil, thyroid stimulating immunoglobulins (TSIs) and thyroid inhibitory antibodies cross the placenta.

Maternal Hypothyroidism

• Establish the aetiology (e.g. history, maternal notes, Winpath or contact GP)

• Maternal hypothyroidism :

1. Secondary to congenital aplasia/ hypoplasia,

There is only a slightly increased risk of hypothyroidism to the baby.

Blood spot test will suffice.

2. Secondary to Hashimoto thyroiditis

Maternal inhibiting antibodies (& rarely stimulating antibodies) can cross the placenta.

Infant can develop transient hypothyroidism and rarely hyperthyroidism

Clinical review & TFTs on day 10-14 (usually as ward attender).

3. Secondary to treatment for Graves’ disease

Maternal Thyroid stimulating immunoglobulins (TSIs) continue to be produced even after ablation or radioiodine and cross the placenta.

Infant is at risk of thyrotoxicosis and should be managed as below:

Maternal hyperthyroidism

The prevalence of Graves’ disease in pregnant women is 2/1000. However the incidence of neonatal hyperthyroidism in the literature varies between 1 in 4000 to 1 in 50 000 deliveries.

Neonatal hyperthyroidism is usually secondary to maternal Graves’ disease with transplacental passage of TSIs*. Not all infants whose mothers’ had hyperthyroidism in pregnancy carry the same risk of developing thyrotoxicosis.

Infants at increased risk for thyrotoxicosis:

• Increased TSI levels in pregnancy

• Thyrotoxic mother in 3rd trimester

• Family history of TSH receptor mutation

These infants should be managed as below:

[pic]

* TSI: thyroid stimulating immunoglobulins

** If cord blood is insufficient or not taken; observe the newborn for 24hrs and take TFTs day 10-14. Earlier results, if not from cord blood, will reflect the newborns’ TSH surge.

Signs of thyrotoxicosis:

• Background history of fetal tachycardia

• Irritability, jitteriness, and restlessness

• Poor feeding

• Tachycardia and arrhythmia (can lead to cardiac failure)

• IUGR, goitre and non- immune hydrops.

• Systemic and pulmonary hypertension

• Eye signs may be present in the absence of maternal exophalmos

Treatment:

• Discuss with consultant first.

• Anti thyroid drugs, +/- iodine, +/- b-blockers

• Close FU

References:

• A L Ogilvy-Stuart, Neonatal thyroid disorders; ADC Neonatal Ed 2002

• Shiri B et al, Neonatal thyroid function; neoReviews 2010

• Besancon A et al, Management of neonates born to women with Graves’ disease: a cohort study; Eur J Endocrinol 2014

• Stagnaro- Green A et al, Guidelines of the American Thyroid association for the diagnosis and management of thyroid disease during pregnancy and postpartum,Thyroid 2011;21:1081-1125

• British Thyroid Association, UK guidelines for the use of thyroid function tests, July 2006

• Banakar, M.Formosa, Serum thyroid function tests in neonates of mothers with thyroid disease, Int J Biol Med Res 2010; 1:76-78

• Barbesino, Tomer, Clinical utility of TSH Receptor antibodies, J Clin Endocrinol Met.June.2013

• Laurberg et al, Guidelines for TSH receptor antibody measurements in pregnancy; European Journal of Endocrinology 1998

• Tamaki H,Amino N, Universal predictive criteria for neonatal overt thyrotoxicosis requiring treatment; Am. J Perinatol.1988;5:152-158

• Girling J, Thyroid disease in pregnancy; TOG 2008;10;237-243

• Skuza KA, Sills IN, Prediction of neonatal hyperthyroidism in infants born to mothers with Graves disease, J Pediatr. Feb 1996

• Zakarija M, McKenzie JM, Pregnancy associated changes in the thyroid stimulating antibody of Graves disease and the relationship to neonatal hyperthyroidism,; J Clin Endocrinol Metab, Nov 1983

Guideline written by Dr S Leontiadi, Neonatal SpR August 2014

Supervision by Dr. Peter Reynolds Neonatal Consultant

Reviewed and approved by Neonatal Clinical Management Group August 2014

Review Date August 2019

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Neonatal Intensive Care Unit

Clinical Guideline

Mother with active or inactive hyperthyroidism

or

Family history of TSH receptor mutation

Check maternal TSI* levels during pregnancy

TSIs more than 3 fold increase

or

History of TSH receptor mutation

TSIs low or absent

Risk for thyrotoxicosis is negligible

Take cord blood for TFTs**

Observe in postnatal ward for 24 hours

Discharge with information leaflet

If clinically well at 24 hours

Discharge with information leaflet

Repeat TFTs day 10-14

If clinically unwell

Admit to NICU

Seek expert advice

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