management of thyroid diseases in pregnancy

1. Amal S
Final MBBS
Department of Surgery

2. Changes during pregnancy
Hyperthyroid
Hypothyroid
Postpartum thyroid disease
Thyroid cancer
Euthyroid with autoimmune thyroid disease

3. Increase in thyroid-binding globulin
secondary to an estrogenic stimulation of TBG
synthesis and reduced hepatic clearance of TBG ;
two to threefold
levels of bound proteins, total thyroxine, and
total triiodothyronine are increased and
resin triiodothyronine uptake (RT3U) is decreased
begins early in the first trimester, plateaus
during midgestation, and persists until shortly
after delivery decrease in its hepatic clearance,
estrogen-induced sialylation
free T4 and T3 increase slightly during the first trimester
in response to elevated hCG. decline to nadir in
third trimester

4. Human chorionic gonadotropin (hCG)
•intrinsic thyrotropic activity
•begins shortly after conception, peaks
around gestational week 10,declines to a nadir
by about week 20
•directly activate the TSH receptor partial inhibition
of the pituitary gland
•transient decrease in TSH between Weeks 8 and 14
mirrors the peak in hCG concentrations
•20% of normal women, TSH levels decrease to
less than the lower limit of normal

5. Physiologic Change
Thyroid-Related
Consequences
↑ Serum thyroxine-binding globulin ↑ Total T4
and T3
; ↑ T4
production
↑ Plasma volume ↑ T4
and T3
pool size; ↑ T4
production; ↑ cardiac output
D3 expression in placenta and (?)
uterus
↑ T4
production
First trimester ↑ in hCG ↑ Free T4
; ↓ basal thyrotropin;
↑ T4
production
↑ Renal I-
clearance ↑ Iodine requirements
↑ T4
production; fetal T4
synthesis
during second and third trimesters
↑ Oxygen consumption by
fetoplacental unit, gravid uterus, and
mother
↑ Basal metabolic rate; ↑
cardiac output

7. 0.2% of pregnancies
prevalence 0.1% to 0.4%, with 85% Graves’ disease
•Single toxic adenoma, multinodular toxic goiter, and
subacute thyroiditis
•gestational trophoblastic disease,viral thyroiditis and
tumors of the pituitary gland or ovary (struma ovarii)
TSH is depressed and fT4 and fTI are increased.
The RT3U that normally is decreased in
pregnancy is increased in hyperthyroidism.

8. serum TSH value <0.01 mU/L and also a
high serum free T4 value
may be difficult to determine the cause
•thyroid radionuclide imaging is contraindicated
in pregnant women.
Measurement of thyrotropin receptor antibody
(thyroid stimulating immunoglobulins)  Graves'
disease during pregnancy
Transient hyperthyroidism in hyperemesis
gravidarum and gestational transient thyrotoxicity
(GET)

9. Severe maternal hyperthyroidism
-increased risk of stillbirth
-preterm delivery
-intrauterine growth restriction
-Preeclampsia
-heart failure
-spontaneous abortion
-Fetal thyroid hyperfunction or hypofunction caused
by TSHRAbs
-Fetal goiter from excessive antithyroid drug treatment
-Neonatal thyrotoxicosis
-Increased perinatal and maternal mortality
-Decreased IQ of offspring because of excessive use
of antithyroid drugs

10. Hyperemesis gravidarum
•severe nausea and vomiting
•absence of goiter and ophthalmopathy, and absence
of the common symptoms and signs of hyperthyroidism
•Normalization of T4 levels by midgestation.
•Treatment is supportive care

11. -First trimester
-Related to hCG stimulation of the thyroid gland
-Symptoms of hyperthyroidism and elevated free T4 levels.
-The thyroid gland usually is not enlarged
-Resolution of symptoms parallels the decline in hCG levels
-Usually resolves spontaneously by 20 weeks’ gestation
beyond 20 weeks,repeat evaluation for other causes

12. Hydatidiform mole & choriocarcinoma.
High serum hCG concentrations and abnormal
hCG isoforms
55 to 60 percent had clinically evident hyperthyroidism
normal thyroid gland and few symptoms of thyroid
hormone excess.
 A diffuse goiter ophthalmopathy is not present
Nausea and vomiting may predominate

13. Associated with osteoporosis, cardiovascular morbidity,
and progression to overt thyrotoxicosis and thyroid failure.
Not associated with adverse pregnancy outcomes
Does not warrant treatment.

14. Activity level fluctuate during gestation, with :
exacerbation during the first trimester
gradual improvement during the latter half.
exacerbation shortly after delivery
Clinical scenarios:
•stable Graves’ disease receiving thionamide
therapy with exacerbation during early pregnancy.
•in remission with a relapse of disease.
•without prior history diagnosed with Graves’
disease de novo during pregnancy.

15. Diagnosis
•difficult :hypermetabolic symptoms in normal pregnancy
•thyroid examination:
goiter suppressed serum TSH level and usually
elevated free and total T4 serum concentrations.
Complications related to the duration and control
of maternal hyperthyroidism
Autoantibodies mimic TSH can cross the placenta
and cause neonatal Graves’ disease

16. Pregnancy outcome in Graves’ Disease
-preterm labor
-preeclampsia
-stillbirth
-small for gestational age
-congenital malformations unrelated to thionamide therapy
-Mother may have thyroid-stimulating hormone-binding
inhibitory immunoglobulin (TBII)
-Neonatal Thyrotoxicosis

17. •obstetric emergency
•extreme metabolic state
•10% of pregnant women with hyperthyroidism
•high risk of maternal cardiac failure.
•fever, change in mental status, seizures, nausea,
diarrhea, and cardiac arrhythmias.
•inciting event (eg, infection, surgery, labor/delivery)
and a source of infection
•treatment immediately, even if serum free T4, free T3,
and TSH levels are not known.
•untreated thyroid storm can be shock, stupor, and coma.

18. Thionamides
Beta blockers
Iodides
Surgery
Subtotal thyroidectomy :
Second trimester, before gestational week 24
prepared with a β-adrenergic blocking agent and
a 10 to 14 day course of potassium iodide.

19. Elevated serum TSH concentration:2.5% of pregnancies
In iodine-sufficient environment
Hashimoto’s thyroiditis
prior radioactive iodine treatment
surgical ablation of Graves’ disease

20. Diagnosis
Symptoms masked by the hypermetabolic state of
pregnancy.
20% to 30% overt hypothyroidism develop symptoms :
weight gain, lethargy,decrease in exercise capacity,
and intolerance to cold,constipation,hoarseness,
hair loss,brittle nails, dry skin, goiter, or delay in
the relaxation phase of the deep tendon reflexes
Elevated serum TSH concentration
Central hypothyroidism do not manifest an elevated
serum TSH level.

21. Pregnancy outcome
Depends on the severity of disease and adequacy
of treatment.
Gestational hypertension in overtly hypothyroid women
Overt hypothyroid vs subclinical disease:
•increased use of cesarean section because of fetal
distress
•placental abruption, anemia, andpostpartum
hemorrhage increased rates of miscarriage,
preeclampsia,placental abruption, growth restriction,
prematurity and stillbirths
Fetuses are at risk for impaired neurologic development
low-birth-weight neonates

22. CLINICALLY:
TSH can be elevated with or without suppressed
levels of free T4.
antithyroid autoantibodies are present
elevated creatine phosphokinase, cholesterol,
and liver function tests.
5% to 8% prevalence of hypothyroidism in type I
diabetes mellitus and women who have type I
diabetes have a 25% risk of developing postpartum
thyroid dysfunction

23. normal free T4 level
elevated TSH above the upper limit of
reference range (4.5–10.0mIU/L)
TSH in the first half of pregnancy is 3.0 mIU/L
Prevalence of subclinical hypothyroidism 2–5%
Increased risk of placental abruption and preterm birth
2–5% progress to overt hypothyroidism each year

24. Normal TSH
Free T4 below 0.86 ng/dl.
In the first half of pregnancy,prevalence 1.3%.
Not associated with adverse perinatal outcome

25. 1. For newly diagnosed hypothyroid women,
initial levothyroxine dosage is based on
severity of hypothyroidism.
2. For overt hypothyroidism, administer 2
mcg/kg/d. If TSH is < 10 mU/L, initial dose of
0.1 mg/d may be sufficient.
3. For previously diagnosed hypothyroid women,
monitor serum
TSH every 3–4 weeks during first half of
pregnancy and every 6 weeks thereafter.
4. Adjust levothyroxine dosage to maintain serum
TSH ≤ 2.5 mU/L.
5. Monitor serum TSH and total T4 levels 3–4
weeks after every dosage adjustment. When
levothyroxine dosage achieves equilibrium,
resume monitoring TSH alone

26. Autoimmune disorder with a self-limited
hyperthyroid phase within one year after parturition.
Presentations
•Transient hyperthyroidism alone
•Transient hypothyroidism alone
•Transient hyperthyroidism followed by
hypothyroidism and then recovery.
Can also occur after spontaneous or induced abortion
3 to 16 percent.

27. Distinguished from Graves' hyperthyroidism,
hyperthyroidism in postpartum thyroiditis is usually
mild (both clinically and biochemically),
Thyroid enlargement is minimal
Graves' ophthalmopathy is absent.
By re-evaluation in three to four weeks: postpartum
thyroiditis improved

28. Antithyroids :no role.
Hypothyroid :may require treatment and some
significant rate of residual hypothyroidism
Recommend: maintain thyroxine until
childbearing is complete, with an attempt to
wean off medication 1 year after the last delivery

29. 60% Graves’ disease in the reproductive years;
postpartum onset
Euthyroid patients with Graves’ disease with TSI
Increased risk of developing recurrent Graves’
disease if antithyroid medication was withheld
TSIs differentiate postpartum Graves’ disease from
postpartum thyroiditis with a hyperthyroid component.

30. Thyroid tumors ;most common endocrine neoplasms.
Thyroid cancer accounts for 1% of all cancers. ¾
women; 1/2 reproductive years.
Diagnosis :biopsy ,Serum TSH and free T4
levels,ultrasonography & Fine needle aspiration .
Radionucleotide scanning is contraindicated during
pregnancy.
Malignant or suspicious for papillary cancer, surgery
at the earliest safe period
No evidence that pregnancy causes a reactivation of
thyroid cancer or that exposure to radioactive iodine
poses a risk to future pregnancies
Maintained on thyroid replacement therapy with

32. Increased risk for spontaneous miscarriage,
subclinical hypothyroidism, and postpartum thyroiditis
Increase in serum TSH levels
Presence of antithyroid antibodies
Lack of thyroidal reserve in response to the
stimulatory effects of pregnancy.

33. 1. Recommend initiating levothyroxine therapy in women
with antithyroid antibodies before pregnancy, if TSH
level is greater than 2.5 mU/L.
2. Serum TSH should be monitored throughout
pregnancy in all antithyroid antibody–positive women
3. Maintain the TSH concentration at 2.5 mU/L or less.

34. 1. Kronenber; Williams Textbook of Endocrinology
2. Williams textbook of Gynaecology and
Obstetrics
3. Jounal of Thyroid disorders