Thyroid Disease I: Hyperthyroidism in Pregnancy

2020 ◽  
Author(s):  
Robert B. Martin ◽  
Brian Casey

Thyroid physiologic adaptations in pregnancy may be confused with pathologic changes. Human chorionic gonadotropin rises early in pregnancy, stimulating thyrotropin secretion and suppressing thyroid stimulating hormone. These chemical changes are often seen in hyperemesis gravidarum and gestational transient thyrotoxicosis. Therefore, mild thyrotoxicosis may be difficult to differentiate from early pregnancy thyroxine stimulation.  However, overt hyperthyroidism usually includes classic symptoms seen outside of pregnancy in addition to suppressed TSH and T4 levels. Treatment includes thionamides propylthiouracil and methimazole.  Thyroid ablation is contraindicated in pregnancy. Often, in affected women, the fetus is euthyroid, but neonates can develop hyper or hypothyroidism with or without a goiter. Lastly, thyroid storm, though rare, is life threatening. Often presenting as a hypermetabolic state with cardiomyopathy and pulmonary hypertension, it generally results from decompensation from preeclampsia, anemia, sepsis, or surgery.  Treatment requires intensive care level management, with initiation of thionamides, iodine, and beta blockers.   This review contains 2 figures, 4 tables and 38 references. Keywords: Thyroid-releasing hormong, thyroid-stimulating hormone, thyromegaly, thyroid-stimulating immunoglobulins, thryotoxicosis, thionamides, thyroid storm

2021 ◽  
Vol 14 (7) ◽  
pp. e243159
Author(s):  
Yudianto Budi Saroyo ◽  
Achmad Kemal Harzif ◽  
Beryliana Maya Anisa ◽  
Fistyanisa Elya Charilda

A thyroid storm (or thyroid crisis) is an emergency in endocrinology. It is a form of complication of hyperthyroidism that can be life-threatening. Inadequate control of hyperthyroidism in pregnancy could develop into thyroid storm, especially in the peripartum period. We present a woman came in the second stage of labour, with thyroid storm, superimposed pre-eclampsia, acute lung oedema and impending respiratory failure. Treatment for thyroid storm, pre-eclampsia protocol and corticosteroid was delivered. The baby was born uneventfully, while the mother was discharged after 5 days of hospitalisation. Delivery is an important precipitant in the development of thyroid storm in uncontrolled hyperthyroidism in pregnancy. Although very rare, it can cause severe consequences. Diagnosis and treatment guidelines for thyroid storm were available and should be done aggressively and immediately. Uncontrolled hyperthyroidism should be prevented by adequate control in thyroid hormone levels, especially before the peripartum period.


2018 ◽  
Vol 2018 ◽  
pp. 1-4 ◽  
Author(s):  
Anna Walch ◽  
Madeline Duke ◽  
Travis Auty ◽  
Audris Wong

We present a case of a 39-year-old G8P6 Pacific Islander woman who at 15+5 weeks’ gestation had an out-of-hospital cardiac arrest secondary to profound hypokalaemia which was associated with severe hyperemesis gravidarum (HG). Her clinical course after arrest was complicated by a second 5-minute cardiac arrest in the Intensive Care Unit (ICU) (pre-arrest potassium 1.8), anuric renal failure requiring dialysis, ischaemic hepatitis, and encephalopathy and unfortunately fetal demise and a spontaneous miscarriage on day 2 of admission. Despite these complications, she was discharged home 4 weeks later with a full recovery. Following a plethora of inpatient and outpatient investigations, the cause of her cardiac arrest was determined to be profound hypokalaemia. The hypokalaemia was presumed second to a perfect storm of HG with subsequent nutritional deficiencies causing electrolyte wasting, extracellular fluid (ECF) volume reduction, and activation of the renin-angiotensin-aldosterone axis (RAAS). This combined with the physiological changes that promote potassium wasting in pregnancy including volume expansion, increased renal blood flow, increased glomerular filtration rate, and increase in cortisol contributed to the patient having a profoundly low total body potassium level. This diagnosis is further strengthened by the fact that her pre- and post-pregnancy potassium levels were within normal limits in the absence of supplementary potassium. This case highlights the potentially life-threatening electrolyte imbalances that can occur with HG and the importance of recognising the disease, comprehensive electrolyte monitoring, and aggressive management in pregnancy.


2016 ◽  
Vol 9 (3) ◽  
pp. 126-129 ◽  
Author(s):  
Helen Robinson ◽  
Philip Robinson ◽  
Michael D’Emden ◽  
Kassam Mahomed

Background First-trimester care of maternal thyroid dysfunction has previously been shown to be poor. This study evaluates early management of thyroid dysfunction in pregnancy in Australia. Methods Patients reviewed by the Obstetric Medicine team for thyroid dysfunction from 1 January 2012 to 30 June 2013 were included. Data were collected on gestation at referral from the patient’s general practitioner to the antenatal clinic, information provided in the referral letter, thyroid function tests and thyroid medications. Results Eighty-five women were included in the study. At the time of general practitioner referral to antenatal services, 19% of women with preexisting thyroid disease had no thyroid function tested. Forty-three percent had an abnormal thyroid-stimulating hormone defined as being outside the laboratory-specific pregnancy reference range if available, or outside the level of 0.1–2.5 mIu/L in the first trimester, 0.2–3.0 mIu/L in the second trimester and 0.3–3.0 mIu/L in the third trimester. Only 21% of women increased their thyroxine dose prior to their first antenatal clinic review. Conclusion This study highlights that a significant proportion of women with known thyroid disease either have untested thyroid function in the first trimester or a thyroid-stimulating hormone outside of levels recommended by guidelines.


2018 ◽  
Vol 35 (2) ◽  
pp. 241
Author(s):  
KhaledN Elfayoumy ◽  
MahmoudF Midan ◽  
WalaaM El-Bassiony ◽  
AhmadA Al-Metwally

2005 ◽  
Vol 1 (1) ◽  
pp. 97-104
Author(s):  
John H Lazarus

Pregnancy has marked effects on thyroid physiology and autoimmune thyroid disease tends to ameliorate through gestation due to the general immunosuppression seen in pregnancy. There is a need for trimester-specific thyroid hormone reference ranges. Hyperthyroidism in pregnancy – usually due to Graves' disease – is not common but, if the patient is compliant, a good outcome can be expected for both mother and child if treatment with anti-thyroid drugs (propylthiouracil is preferred) is instituted. Thyroid-stimulating hormone receptor antibody should be measured at 36 weeks in such patients in order to predict the possibility of neonatal hyperthyroidism. Transient gestational hyperthyroidism is often associated with hyperemesis gravidarum and thyroid function should be checked in patients severely affected by this condition. Radioiodine therapy is contraindicated in pregnancy but thyroid surgery may be performed safely in the second trimester. Autoimmune thyroiditis and Graves’ hyperthyroidism occur quite commonly in postpartum women.


2014 ◽  
Vol 430 ◽  
pp. 33-37 ◽  
Author(s):  
Jonathan P. Bestwick ◽  
Rhys John ◽  
Aldo Maina ◽  
Varvara Guaraldo ◽  
Mohammed Joomun ◽  
...  

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A929-A929
Author(s):  
Hind Alameddine ◽  
Gurunanthan Palani ◽  
Kidmealem Zekarias

Abstract Untreated or inadequately treated overt hyperthyroidism in pregnancy can have devastating consequences for both mother and fetus. At the same time antithyroid drugs (ATDs) are known for their teratogenic effect and should be avoid when possible; once the diagnosis of hyperthyroidism is made in a pregnant woman, attention should be focused on determining the etiology of the disorder and whether it warrants treatment. Here, we report a case of hyperemesis gravidarum patient presenting with significant elevation of thyroid hormones and a review on diagnosis and management of gestational transient thyrotoxicosis. A 33-year-old female, G4P3 at 8 weeks pregnant admitted for nausea and vomiting. Thyroid labs showed TSH < 0.01 (Reference: 0.4-4.0mU/L) and free T4 is 3.53 (Reference: 0.76-1.46ng/dl). Patient was discharged on antiemetics with a diagnosis of hyperemesis gravidarum. She was re-admitted at 9 weeks pregnant with ongoing nausea and vomiting. She had palpitations, fatigue and reported 15 pound weight loss in 2 weeks. Past medical history included thyroid hormone abnormality noted during pregnancies of 2011 and 2017. Physical exam was significant for tachycardia and diffusely enlarged thyroid gland. Repeat labs showed TSH <0.01, free T4 5.81, total T3 of 317 (Reference: 60-181ng/dl). Thyroid ultrasound showed multiple nodules. Considering significant elevation in free T4 and total T3; empiric therapy with propylthiouracil was recommended. Patient declined anti-thyroid therapy. TSI and TRH antibodies came back later as negative. Patient was treated with enteral feeding for hyperemesis gravidarum. Thyroid labs 3 weeks later improved; FT4 down to 1.63 and TT3 down to 250. Patient delivered healthy baby at 40 weeks of gestation. Although the differential diagnosis of thyrotoxicosis in pregnancy includes any cause that can be seen in a nonpregnant patient, the most likely causes for hyperthyroidism in pregnancy are gestational thyrotoxicosis (GTT) with or without hyperemesis gravidarum or Graves’ disease. GTT is described as an hCG-mediated hyperthyroidism that occurs in the first trimester of pregnancy; it is generally asymptomatic with mild biochemical hyperthyroidism. Distinguishing true overt hyperthyroidism from GTT in a setting of hyperemesis gravidarum is challenging. The absence of clinical signs of hyperthyroidism and negative thyroid antibodies supports the diagnosis of GTT. T3 tends to be disproportionately elevated more than T4 in patients with overt hyperthyroidism. HCG level has not been found to be useful in distinguishing between GTT and GD. Overt hyperthyroidism is treated using anti-thyroid drugs (ATD) whereas supportive therapy without ATD is the accepted standard of treatment of patients with hyperemesis gravidarum and GTT. More studies addressing the best management of these group of patients is needed.


2011 ◽  
Vol 26 (S1) ◽  
pp. s155-s155
Author(s):  
M.J. Van veelen ◽  
L. Yurtsever ◽  
M. Baggen ◽  
E.A. Dubois

CaseA 20-year-old woman was referred to the emergency department with rapid acceleration of complaints of palpitations, fever, diarrhea, and agitation that had been present for several weeks. During physical examination, the patient was uncomfortable and restless with a tachycardia of 170/minute, and a fever of 38.5 °C. Palpation of the neck revealed a small ventral, painless, solid elastic mass, more prominent on the right side, clinically suspicious for goiter. An electrocardiograph showed an atrial flutter of 150/min. Initial laboratory results showed an erythrocyte sedimentation rate of 35 mm/hour (0–20 mm/hour) and urine analysis tested positive for ketones.Outcome and TreatmentThe patient was presumed to be suffering from a thyroid storm. She was treated promptly with Propranolol 160 mg and Thiamazole 30 mg twice daily at the emergency department. She was admitted to the Cardiac Care Unit for observation of the heart rhythm, which slowed down to 110/minute the same day and her condition improved clinically. The following day her laboratory result confirmed the diagnosis with a thyroid-stimulating hormone of < 0.01 mIU/L (0.4–4.0 mIU/L) and a free thyroxine (T4) of > 75 pmol/l (10–22 pmol/l). Eventually, she was diagnosed with Graves Disease.DiscussionThyroid storm is an acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones. The adult mortality rate is high (90%) if early diagnosis is not made and the patient is left untreated. Therefore, in case of clinical suspicion for thyroid storm, it is critical to start prompt treatment with Beta blockade and Thiamazole before the diagnosis can be confirmed biochemically.


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