NEONATAL GRAVES

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1.    

Source:Nelson Textbook of Pediatrics 21e


        What is neonatal graves disease?
·        The transplacental transfer of TRSAbs from mother to fetus results in Graves diseases in neonates.
 
2.     What are the conditions of such illness?
·        Maternal untreated Graves
·        Mother treated with radioiodine and surgery can develop
·        Mother treated for Graves with ATDS
 
·        Sometimes neonates of mother’s with Hashimotos thyroiditis can develop Graves disease.
 
3.     What is the presentation of neonatal thyrotoxicosis in neonate born to mother receiving ATDs?
·        They present after 3-7 days after the ATDs are metabolized in newborn.
·        Sometimes after some weeks if TRBAbs are also present.
 
4.     Does neonatal thyrotoxicosis occur in all neonates of Graves disease mother?
No. Only 2% DEVELOP.
Some predisposing factors are:
·        Elevated serum titers of TRSAb (more than 3 times the upper limit of normal) or
 
·        History of a prior child with neonatal thyroid dysfunction.
 
5.     How and when should be monitor the fetus dueing intrapartum period?
In 3rd trimester and fetal tachycardia and goiter should be evaluated.
 
6.     Neonatal Graves disease typically remits spontaneously within 6-12 wk but
can persist longer, depending on the titer and rate of clearance of the TRSAbs.(and TRBAbs, if present).


7.     Rarely, classic neonatal Graves disease may not remit but persist for several yr or longer. These children typically have a family history of Graves disease. In these infants, the transfer of maternal TRSAbs exacerbates
the infantile onset of autonomous Graves disease.


8.     How do the new born present?
·        LBW and IUGR
·        prematurity
·        Goiter may be present
·        stare,
·        periorbital edema,
·        retraction of the eyelids,
·        hyperthermia,
·        irritability,
·        diarrhea,
·        feeding difficulties,
·        tachycardia, heart failure, hypertension,
·        hepatomegaly, splenomegaly, cholestasis, jaundice,
·        Thrombocytopenia, and
·        hyperviscosity
 
9.     LAB IX
·        Low TSH and high total and free thyroid hormones.
·        TRSAbs are markedly elevated at birth and typically resolve within 3 mo of life.
 
If symptoms and signs are not immediately recognized and treated, cardiac failure and death can occur.
 
Craniosynostosis and developmental delay can be permanent sequelae of the hyperthyroidism
 
                                                                             
10. How do we treat?
·        Methimazole (0.5-1.0 mg/kg/24 hr given every 12 hr)
·        Oral or intravenous administration of a nonselective β- adrenergic blocker such as propranolol to decreases sympathetic hyperactivity.
 
 
11. How do we treat refractory cases?
In refractory cases, Lugol solution or potassium iodide (1-2 drops per day) can be added.
The first dose of iodide should be given at least 1 hr after the 1st dose
of ATD to prevent the iodide from being used for further thyroid hormone
synthesis.
 
If thyrotoxicosis is severe and progresses to heart failure, parenteral
fluid therapy, corticosteroids, and digitalization may be indicated.
 
Once serum thyroid hormone levels begin to decrease, antithyroid medications should be gradually tapered to keep the infant euthyroid.
 
12.  In most of the cases neonatal thyrotoxicosis remits by 3 months of age but in few cases it may result in permanent hyperthyroidism.
 
13.Usually such cases have family H/o hyperthyroidism.
 
14.  TSHR gene mutation can cause neonatal Graves disease.
 
15. How does resistance to thyroid hormone present?
·        They can present with hypo or hyperthyroidism.
 
·        They are often associated with ADHD in children.
 
·        LAB
    Normal or elevated TSH
    High T3 and T4
 
 
·        NO SPECIFIC TREATMENT


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