RT Book, Section
A1 Bianchi, Diana W.
A1 Crombleholme, Timothy M.
A1 D'Alton, Mary E.
A1 Malone, Fergal D.
SR Print(0)
ID 1106397349
T1 Goiter
T2 Fetology: Diagnosis and Management of the Fetal Patient, 2e
YR 2015
FD 2015
PB McGraw-Hill Education
PP New York, NY
SN 978-0-07-144201-5
LK obgyn.mhmedical.com/content.aspx?aid=1106397349
RD 2024/04/19
AB Key  PointsGoiter  in  the  fetus,  a  rare  condition,  can  occur  as  part  of  a  hypothyroid,  hyperthyroid,  or  euthyroid  state.Hypothyroid  fetal  goiter  may  be  secondary  to  transplacental  passage  of  antithyroid  medication,  iodine  deficiency,  iodine  intoxication,  transplacental  passage  of  antithyroid  antibodies,  congenital  metabolic  disorders  of  thyroid  hormone  synthesis,  or  hypothalamic-pituitary  hypothyroidism.Congenital  hypothyroidism  is  a  serious  condition,  which  if  not  treated  in  the  first  3  months  of  life  is  likely  to  result  in  irreversible  mental  retardation.Hyperthyroid  fetal  goiter  is  most  often  caused  by  transplacental  passage  of  a  thyroid-stimulating  IgG  antibody  from  the  mother.  Such  antibodies  are  present  in  approximately  95%  of  women  with  Graves  disease.Thyroid-stimulating  antibody  levels  in  Graves  disease  may  not  reflect  maternal  thyroid  status  because  they  are  detectable  in  women  who  are  clinically  hyperthyroid,  euthyroid,  or  hypothyroid.The  typical  sonographic  appearance  of  a  fetal  goiter  is  a  symmetric,  homogenous  mass  in  the  anterior  neck,  with  an  echogenic  consistency,  and  with  some  lobulation.The  diagnosis  of  fetal  goiter  is  rarely  made  prior  to  24  weeks’  gestation.  The  fetal  neck  may  be  hyperextended  and  the  trachea  and  esophagus  may  become  compressed  or  displaced  resulting  in  polyhydramnios.It  is  extremely  important  to  thoroughly  evaluate  and  treat  a  fetal  goiter.Because  ultrasound  methods  of  differentiating  between  hypothyroidism  and  hyperthyroidism  may  not  be  reliable,  fetal  cord  blood  sampling  may  be  required.  Amniotic  fluid  thyroid  hormone  values  may  not  be  reliable.If  fetal  hypothyroidism  is  diagnosed,  intra-amniotic  injection  with  levothyroxine  will  be  required.Little  information  is  available  to  guide  patient  counseling  regarding  the  antenatal  natural  history  of  fetal  goiter.  The  clinical  course  will  depend  on  whether  or  not  the  fetus  is  hyperthyroid,  euthyroid,  or  hypothyroid.Serial  sonographic  surveillance  is  suggested  due  to  the  fact  that  fetal  goiter  may  be  associated  with  polyhydramnios,  intrauterine  growth  restriction,  hydrops,  and  intrauterine  fetal  demise.A  neonatologist  should  be  present  in  the  delivery  room  because  problems  securing  an  airway  may  be  encountered.  In  the  most  severe  cases  of  fetal  goiter,  the  ex  utero  intrapartum  treatment  (EXIT)  procedure  may  be  needed  to  maximize  the  ability  to  promptly  secure  an  airway  at  delivery.There  is  little  data  available  to  counsel  patients  on  the  long-term  prognosis  of  antenatal  fetal  goiter.