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Thyroid disorders in pregnancy
This document discusses thyroid disorders in pregnancy. It notes that thyroid disorders are common in pregnancy, affecting 1-2% of pregnancies with overt disease and 3-5% with subclinical disease. Thyroid screening and treatment in pregnancy can help improve outcomes for both mother and baby, though guidelines vary on who and when to screen. The document reviews thyroid changes in pregnancy, screening recommendations, treatment of hypothyroidism and hyperthyroidism, and complications like postpartum thyroid dysfunction.
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Thyroid disorders in pregnancy
- 1. Thyroid disorders in pregnancy DrAjay SDhawle AssociateProfessor,OBGY JNMCSawangi
- 2. • Thomas Whartonin 1656 gave the thyroid gland its modern name (meaning oblong shield ), because… • he thought that the gland fills the vacant spaces and • contributes to the shape and beauty of the neck, especially in women!!!
- 3. Ice-Breakers Do you screenfor Thyroid disorders in pregnancy? In whom? What cut-offs do you use?
- 4. Introduction • Common duringpregnancy • Recent knowledge: affect perinatal outcomes • Overt thyroid disease: 1-2% • Subclinical disease much more common : 3-5% • Not a single entity but a spectrum • Paucity of good research, recommendations based on limited research
- 5. The year 1999… Haddowand colleagues • children born to untreated mothers had IQ scores that were 7 points lower than treated peers, and 19% had IQ scores less than 85 compared with 5% of treated. • Findings supported by Pop et al: found impaired psychomotor function in 22 infants (age 10 months) whose mothers had had low FT4 at 12 weeks of gestation, compared with 194 infants whose mothers had normal readings Increasing pressure on Obgyns to screen and treat despite uncertainty whether such
- 7. Thyroid during pregnancy 4Changes • Increase in Estrogen: increased TBG, decreased Free T4 • HCG rise: Structural similarity with TSH: increase in T4/ T3, decrease in TSH • Increased peripheral metabolism of thyroid hormones: Placenta: type II /III deiodinases Fetus dependent on Type II for T4 T3 • Decline in availability of iodide related to increased renal clearance and overall losses to the fetus and placenta
- 8. •The pattern ofchanges in serum concentrations of thyroid function studies and hCG according to gestational age. •The shaded area represents the normal range of TBG, T4, TSH or free T4 in the nonpregnant woman.
- 9.
- 10. Thyroid function testingin Pregnancy • Uncertainty regarding reference ranges for thyroid tests • Variability by gestational age, number of fetuses, population studied, laboratory, and testing method • Whom to screen? • When to screen? • How to screen? • What Cut-offs? • Role of thyroid antibody testing
- 11. The 4 problemswith screening • A first problem concerns the validity and normal reference limits of serum TSH and free T4 measurements in pregnancy • Still unclear today as to what degree of maternal T4 lowering must be reached – and during how long? – for thyroid function abnormalities to be associated – beyond doubt – to detrimental effects on the neuro- psychological development in the offspring
- 12. • Does treatmentof Subclinical disease alter outcomes? • The last question concerns the future implementation of consensus guidelines. The existence of guidelines raises the issue of liability
- 14. Universal versus Selective screening •A $ 64000 Question • Endocrinologists versus the Obstetricians
- 16. Whom to gowith? The ITS (Indian Thyroid Society) • “All antenatal mothers should be screened at the first antenatal visit using TSH” • “Ideally, screening should be carried out at the pre- pregnancy evaluation or as soon as pregnancy is confirmed” • India: Higher incidence of thyroid antibody positivity, uncertainty of universal iodine supplementation: Universal screening makes sense!!!
- 17.
- 18. When totreat? ATA Guideline: •“All women where the Sr TSH> 10 mIU/l, • when Sr TSH > 2.5mIU/l + Low FT4 / TPO Ab +” • a first trimester TSH < 2.5 mIU/l : no further testing TES guideline: • Treat all cases where St TSH > 2.5mIU/l in I trimester > 3.0 mIU/l in II/III trimester ITS guideline: • All pregnant women with subclinical hypothyroidism targeting upper limit of normal ref ranges
- 19. Repeattesting in pregnancy? •ATA/ TES: Regular thyroid monitoring for euthyroid antibody positive women • ITS: Every trimester in Anti-thyroid antibody positive euthyroid women
- 20. Risk factors:“Specific screening” •Symptomatic • Family history of thyroid disease • History of postpartum thyroid disease • Type 1 diabetes mellitus • Recurrent spontaneous abortions • Unexplained intrauterine fetal demise • Otherautoimmunedisorders Vitiligo / Addison’s disease /Pernicious anemia Multiple sclerosis/ Rheumatoid arthritis Sjögren’sdisease Vaidya et al (2007) Only risk based screening is likely to miss one thirds of the total cases
- 22. Hypothyroidism and Pregnancy •Overt Hypothyroidism: Low FT4, High TSH • Subclinical Hypothyroidism: High TSH, normal FT4 • Subclinical Hypothyroxinemia: Low FT4, normal TSH • Women with subclinical hypothyroidism are more likely than euthyroid women to have antibodies for TPO: 31% compared with 5%. & • Half of these women progress to hypothyroidism within next 8 years.
- 23. Pregnancy Complications in96 Women With Overt or Subclinical Hypothyroidism as Reported by Davis, Leung, and Their Colleagues
- 24. Principles of treatment •I trimester: 30-50% increased dose requirement • Preconception counseling: an opportunity to educate, optimize treatment, and provide an additional 25-mg prescription of levothyroxine to start with a positive pregnancy test. • Newly diagnosed cases: Starting dose of Levo thyroxin= 1 to 2mg/kg/d • An initial dose ranges between 100 and 150 mg/d with adjustments in 25- to 50-mg increments
- 25. • Reassess TSH4 to 6 weeks later • Treatment goal in pregnancy :TSH = 0.5 and 2.5 mU/L. • Once stable, TSH can be checked every 8 weeks. • The bioavailability of levothyroxine can be affected by medications or foods. Carafate, cholestyramine, ferrous sulfate, and calcium carbonate reduce its absorption. • Phenytoin and carbamazepine increase its clearance. In addition, pregnant patients should space their levothyroxine and prenatal vitamin by 2 to 3 hours.
- 26. • Postpartum :levothyroxine dose requirement decreased. • Prediagnosed patients: prepregnancy dose. • Newly diagnosed hypothyroidism during pregnancy: decrease their dose by 30% (often a decrease of 25mg). • TSH should be reassessed at 6 weeks postpartum.
- 28. Hyperthyroidism in Pregnancy •Less than 1% (0.2%) of pregnant women • Signs overlap with pregnancy symptoms • Few high-quality studies to guide the management of hyperthyroidism in pregnancy • Treatment advisable : adversely affects a number of pregnancy outcomes. • Subclinical hyperthyroidism (TSH is low but FT4 is normal) : does not affect pregnancy outcomes and treatment is unnecessary
- 29. Associatedcomplications • Spontaneous abortion •Minor congenital anomalies • Preeclampsia • Preterm birth, • LBW • Abruption • Neonatal thyroid dysfunction and • Perinatal mortality. Maternal complications of uncontrolled hyperthyroidism are primarily related to • thyroid storm • Arrhythmia and c • Congestive heart failure.
- 30. Pregnancy Outcomes in239 Women With Overt Hyperthyroidism as Reported by Davis, Kriplani, Millar, and Their Colleagues
- 31. Principles of management •Treatment & adequate metabolic control : associated with improved pregnancy outcome. • Goal : to keep the patient euthyroid, with the FT4 at the upper limit of normal range so as not to cause fetal or neonatal hypothyroidism • Propylthiouracil : drug of first choice because it partially inhibits the conversion of T4 to T3 and crosses the placenta less readily than methimazole. • Although not proven, methimazole used in early pregnancy has been associated with esophageal and choanal atresia as well as aplasia cutis in the fetus.
- 32. • All antithyroidmedications cross the placenta and can cause iatrogenic fetal hypothyroidism • A typical PTU dose: 300 to 450 mg/d given in 3 oral doses of 100 to 150 mg each. • β-Adrenergic blockers inhibit conversion of T4 to T3 ; used as an adjunct to reduce tachycardia, palpitations, and tremors. • Propranolol 20 to 40 mg orally every 8 to 12 hours may be used while awaiting response to the antithyroid medications. • PTU dose adjustments are based on FT4 or FT4I testing performed every 3 to 4 weeks. TSH is not helpful in treatment monitoring because it remains low. • Improvement in symptoms occurs after 3 to 4 weeks of treatment but a full response may take 8 weeks.
- 33. Role of Surgery •Indications: severe refractory hyperthyroidism intolerance of medications agranulocytosis noncompliance or malignant thyroid cancer. • Ideally, surgery is delayed until postpartum • During pregnancy : best accomplished in the second trimester
- 34. • Other concerns: airway management and recurrent laryngeal nerve injury. • Surgical risks of total thyroidectomy include 2% to 4% risk of injury of the recurrent laryngeal nerve and 1% risk of hypoparathyroidism following inadvertent resection of parathyroid glands. • Complications, costs, and length of stay associated with thyroid surgery may be increased in pregnancy. • Thyroidectomy for Graves disease with subsequent discontinuation of antithyroid medications can lead to fetal hyperthyroidism if thyroid-stimulating antibodies are present.
- 35. • The fetusshould be monitored for signs of hypothyroidism by clinical examination for growth and fetal heart tones for baseline bradycardia. • Approximately 10% of those exposed to PTU will develop fetal or neonatal hypothyroidism. • Ultrasound is not routinely recommended but has been advocated by some to assess fetal biometry and for evidence of fetal goiter. • A fetal goiter can be suspected if there is a symmetric paratracheal mass, neck hyperextension, and polyhydramnios.
- 37. Thyroid Storm • Rarebut Critical medical complication • Acute exacerbation of thyrotoxicosis in poorly controlled/ undiagnosed cases • Presentation: unexplained fever, tachycardia neurologic changes, arrhythmias, and cardiac failure • Lab values: typical Hyperthyroid+ Leukocytosis transaminitis and hypercalcemia • Inciting causes: infection, surgery, medical complications, preeclampsia, and delivery
- 38. Do NOT Intervene on behalfof the fetus, until maternal stabilization
- 39. Post partum Thyroiddysfunction • An autoimmune disorder, occurs at 13 to 19 weeks postpartum • Affects 1 in 12 women worldwide, and is usually associated with psychiatric symptomatology • Is strongly associated with antithyroid peroxidase antibodies (TPOAbs). • Premawardhana and colleagues found that 10% of women are TPOAbs-positive in the first trimester; of these, 50% develop PPTD. • Upto 25% of Type I DM patients: PPTD
- 40. • Of thewomen with PPTD, 20% to 30% develop permanent hypothyroidism, and an additional 30% to 40% develop it by 7 years. • In contrast, only 5% of women without PPTD progress to overt disease by 7years. • Women with a history of postpartum thyroiditis should be monitored annually for hypothyroidism and treated accordingly
- 41. Screening for PPTD? •Proponents argue that PPTD is highly prevalent, linked to considerable morbidity, is easily diagnosed with relatively inexpensive tests, and is easy to treat effectively. • Critics note the lack of consensus on the best screening test (thyroid function test versus TPOAbs) , optimal timing of screening (early pregnancy or postpartum), and lack of high-quality, prospective cost-benefit analyses.
- 42. Summary • Thyroid diseaseis common in pregnancy. • Hypo and hyperthyroidism :adverse pregnancy outcomes, and treatment may improve these. • Untreated hypothyroidism during pregnancy: impaired intellectual development in childhood. • Routine screening for thyroid disease in women without risk factors is NOT (Yet) recommended or accepted practice. • Whether subclinical thyroid disorders are associated with adverse pregnancy or childhood outcomes, or whether treatment is beneficial: UNCLEAR
- 43.
Editor's Notes
- #5 Until recently, thyroid dysfunction was thought to have little influence on pregnancy as long as it was treated, and management was straightforward. That was before case control studies in prominent journals suggested an association between even subclinical hypothyroidism and impaired neonatal neurodevelopment.1–4
- #6 Pop and associates2 found impaired psychomotor function in 22 infants (age 10 months) whose mothers had had FT4 below the 10th percentile at 12 weeks of gestation, compared with 194 infants whose mothers had normal readings Haddow JE, Palomaki GE, Allan WC, et al. Maternalthyroid defi ciency during pregnancy and subsequent neuropsychological development of the child [see comment]. N Engl J Med. 1999;341:549–555. Pop VJ, Kuijpens JL, van Baar AL, et al. Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy [see comment]. Clin Endocrinol. 1999;50:149–155. Two studies published in 2006 also suggest that maternal free thyroxine levels in the first trimester of pregnancy correlate with impaired neonatal behavior at 3 months, and impaired mental development at ages 6, 9, and 12 months. Kasatkina EP, Samsonova LN, Ivakhnenko VN, et al. Gestational hypothyroxinemia and cognitive function in offspring. Neurosci Behav Physiol. 2006;36:619–624. Kooistra L, Crawford S, van Baar AL, Brouwers EP, Pop VJ. Neonatal effects of maternal hypothyroxinemia during early pregnancy. Pediatrics. 2006;117:161–167.
- #10 The placenta transfers a small amount of maternal T3and T4. This maternally derived thyroid hormone supports fetal development during critical organogenesis. Production of T4by the fetus is detectable by 14 weeks’ gestational age Full fetal thyroid activity is present by midgestation and concentrations of thyroid hormone increase until term Importantly, although overt maternal thyroid failure during the first half of pregnancy has been associated with several pregnancy complications and intellectual impairment in offspring, 12–15 it is currently less clear whether milder forms of thyroid dysfunction have similar effects on pregnancy and infant outcomes
- #11 Although pregnancy-induced changes in thyroid physiology and their effects on laboratory interpretation have long been known, uncertainty remains regarding reference ranges for thyroid tests Adding to the difficulty of setting reference ranges, the median TSH is lowest in the first trimester, with wider variation than in later trimesters. 12,13 Some have proposed using gestational age–specific nomograms for TSH reported as multiples of the median, similar to the reporting of analytes used in aneuploidy screening programs; however, this is not yet clinically available. A large population-based study of pregnant women defined the reference range (2.5–97.5th centile) for TSH in the first half of pregnancy as 0.08 to 2.99 mU/L.
- #13 A third unresolved issue concerns subclinical thyroid disorders associated with pregnancy (both hypo- “SCH” and hyperthyroidism “SCHR”). There is some evidence that SCHR – which is primarily related to GTT – has no detrimental effect on the pregnancy outcome (22). This is not the case for SCH, as various arguments (more or less direct or indirect) exist to suggest a possible relationship between mild thyroid insufficiency and a poorer pregnancy outcome (23).
- #15 Proponents of routine screening argue that it may limit health risks to children and save money in the long run, and they point out that thyroid disease is easy to treat with pills. Opponents note that no cost-benefi t analysis has been performed, the benefits of treating mild disease are unclear, and screening a large population could be a significant expense ($40–100 per person) and would necessitate a lifelong commitment to daily medication in asymptomatic patients
- #16 American College of Obstetricians and Gynecologists, Committee on Practice Bulletins. ACOG Practice Bulletin. Clinical management guidelines for obstetrician-gynecologists. Number 37, August 2002 (replaces practice Bulletin Number 32, November 2001). Thyroid disease in pregnancy. Obstet Gynecol 2001;98(5 Pt 1):879–88. US Preventive Services Task Force. Screening for thyroid disease, topic page. Rockville (MD): Agency for Healthcare Research and Quality; 2004. Available at: http://www.ahrq.gov/clinic/uspstf/uspsthyr.htm. Accessed December 28, 2009. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Evaluation and Treatment of Hyperthyroidism and Hypothyroidism. AACE thyroid task force. Endocr Pract 2002;8(6). 2006 Amended version. Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf. Accessed December 31, 2009. UK Guidelines for the Use of Thyroid Function Tests. The Association for Clinical Biochemistry, British Thyroid Association, and British Thyroid Foundation. Available at: http://www.british-thyroid-association.org/info-for-patients/Docs/TFT_ guideline_final_version_July_2006.pdf; 2006. Accessed December 31, 2009 Abalovich M, Amino N, Barbour LA, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2007;92(8 Suppl):S1–S47
- #20 Repeat testing in those who come out with normal results in the first test*
- #23 In contrast, TPO antibodies are no more common in women with isolated hypothyroxinemia than in women with normal thyroid function. This finding causes some to question the significance of isolated hypothyroxinemia as a pertinent biologic entity.
- #29 Recognition of hyperthyroidism during pregnancy can be elusive because signs overlap with pregnancy symptoms such as nausea and vomiting, increased appetite, heat intolerance, insomnia, changes in bowel habits, fatigue, and irritable or anxious mood.
- #33 Occasionally doses of 600 mg daily are necessary.
- #34 Subtotal or near-total thyroidectomy is the surgical management for women with complications of severe refractory hyperthyroidism, intolerance of medications, agranulocytosis, noncompliance, or malignant thyroid cancer. Ideally, surgery is delayed until postpartum, but it can be performed in pregnancy when necessary. If surgery is required during pregnancy it is best accomplished in the second trimester to avoid possible anesthesia complications such as potential teratogenicity and preterm birth.
- #35 Other concerns regarding thyroid surgery in pregnancy are airway management and recurrent laryngeal nerve injury. Surgical risks of total thyroidectomy include 2% to 4% risk of injury of the recurrent laryngeal nerve and 1% risk of hypoparathyroidism following inadvertent resection of parathyroid glands. Complications costs, and length of stay associated with thyroid surgery may be increased in pregnancy. Thyroidectomy for Graves disease with subsequent discontinuation of antithyroid medications can lead to fetal hyperthyroidism if thyroid-stimulating antibodies are present.
- #37 Thyroid nodules occur in 1% to 2% of young women. The chance of having a palpable thyroid nodule increases with age. Among reproductive-age women, most palpated nodules of the thyroid are benign. Evaluation of a thyroid nodule includes a serum TSH and an ultrasound assessment of the neck and thyroid gland. Multinodular goiter is defined as the presence of 2 or more nodules. Thyroid nodules are described as functional or nonfunctional depending on whether they produce thyroid hormone. Functional nodules are less likely to be malignant, but this is not absolute. Autoimmune thyroid diseases may increase the risk of thyroid cancer, and coexistent Graves disease or Hashimoto thyroiditis must be considered if the serum TSH is low or high, respectively. Fine-needle aspiration of thyroid nodules during pregnancy is recommended to exclude cancer if they are growing, suspicious (microcalcifications, hypoechoic, increased vascularity, infiltrative margins), or larger than 1 cm. 15,65 Management of hyperthyroidism in pregnancy resulting from a hyperfunctioning solitary nodule or multinodular goiter consists of antithyroid medications, b-adrenergic blockers, and thyroid surgery
- #39 A high index of suspicion, low threshold for evaluation, and prompt treatment are essential to avoid adverse outcomes. Intensive monitoring may require intensive care unit admission, especially if there is evidence of cardiac decompensation. Initial stabilization requires intravenous fluid and electrolyte replacement. Once the diagnosis is established or highly likely, an antithyroid medication must be started to block further production of T4. The maternal heart rate should be controlled. b-Adrenergic blocking agents also impede the conversion of T4to T3. Iodine blocks release of T4and can be commenced after an initial 1 to 2 hours of stabilization with the antithyroid medication. Corticosteroids are often given to further reduce the peripheral conversion of T4to T3. Specific recommendations for medications and doses vary slightly in the literature but most have thionamide,b-adrenergic blockers, corticosteroids, and iodide in common (Fig. 3). Supportive therapy may be needed to treat fever and hypoxia. Maternal telemetry, central monitoring, and arterial monitoring may be indicated, depending on clinical circumstances. The inciting factor should be sought and treated if possible. Consultation with an endocrinologist and an obstetrician familiar with the management of critically ill pregnant women is appropriate. If the fetus is of a viable gestational age, fetal monitoring should be considered. Intervention on behalf of the fetus should not be undertaken until the maternal condition is stabilized, because vaginal or cesarean delivery may exacerbate thyroid storm.
- #40 These findings have generated considerable controversy about routine screening for PPTD.