Thyroid Storm In Pregnancy Case Study

Thromboembolic complications of thyroid storm

T Min1, S Benjamin2 and L Cozma2

[1] ST4 Diabetes and Endocrinology, Princess of Wales Hospital, Bridgend CF31 1RQ, UK

[2] Consultant Diabetes and Endocrinology, Princess of Wales Hospital, Bridgend CF31 1RQ, UK

Endocrinology, Diabetes & Metabolism Case Reports, 1 2014, EDM130060, 10.1530/EDM-13-0060.

Summary

Thyroid storm is a rare but potentially life-threatening complication of hyperthyroidism. Early recognition and prompt treatment are essential. Atrial fibrillation can occur in up to 40% of patients with thyroid storm. Studies have shown that hyperthyroidism increases the risk of thromboembolic events. There is no consensus with regard to the initiation of anticoagulation for atrial fibrillation in severe thyrotoxicosis. Anticoagulation is not routinely initiated if the risk is low on a CHADS2 score; however, this should be considered in patients with thyroid storm or severe thyrotoxicosis with impending storm irrespective of the CHADS2 risk, as it appears to increase the risk of thromboembolic episodes. Herein, we describe a case of thyroid storm complicated by massive pulmonary embolism.

Learning points

  • Diagnosis of thyroid storm is based on clinical findings. Early recognition and prompt treatment could lead to a favourable outcome.

  • Hypercoagulable state is a recognised complication of thyrotoxicosis.

  • Atrial fibrillation is strongly associated with hyperthyroidism and thyroid storm.

  • Anticoagulation should be considered for patients with severe thyrotoxicosis and atrial fibrillation irrespective of the CHADS2 score.

  • Patients with severe thyrotoxicosis and clinical evidence of thrombosis should be immediately anticoagulated until hyperthyroidism is under control.

Background

Thyroid storm is rare and can be life threatening with a mortality rate of 10–20%; hence, it is important to recognise it early and to initiate appropriate treatment. Atrial fibrillation is a common clinical feature of hyperthyroidism and thyroid storm. However, hyperthyroid status is not taken into account while considering anticoagulation for atrial fibrillation. Studies have demonstrated that hyperthyroidism; especially thyroid storm, is associated with an increased risk of thromboembolic events.

Case presentation

A 50-year-old man was referred to the medical take with a history of increasing confusion and shortness of breath. He had a background history of schizophrenia, which was well controlled with antipsychotics. He has never smoked and is a teetotaller. No significant past medical history or family history was noted. Within a few hours of assessment, he became agitated and restless.

On examination, he appeared very anxious and had fine tremors in hands, exophthalmos and a diffusely enlarged goitre. He was in atrial fibrillation with heart rate of 165 beats/min, hypotensive with blood pressure of 90/54 mmHg and hypoxic requiring high-flow oxygen to maintain oxygen saturation of 92–94%. He had a raised jugular venous pressure (JVP), mild ankle oedema and equal air entry to both lung fields. A bedside echocardiogram revealed a dilated right ventricle and pressure overload in the right ventricle. A clinical diagnosis of pulmonary embolism was made. As he was in a peri-arrest state, he was thrombolysed as per local hospital protocol. Subsequently, computed tomography pulmonary angiogram (CTPA) confirmed the diagnosis of pulmonary embolism, and he was moved to intensive therapy unit (ITU) for further management.

Thyroid function test showed him to be severely thyrotoxic. On Burch & Wartofsky (1) scoring, he obtained a score of 75: delirium, 20; unexplained jaundice, 20, tachycardia of more than 140 beats/min; 25, atrial fibrillation and ten, suggesting that he was in thyroid storm. A score of 45 or more suggests thyroid storm.

Investigation

Investigation revealed deranged liver function, normal kidney function and severe thyrotoxicosis with suppressed thyroid-stimulating hormone (TSH) concentration of <0.03 mU/l, free thyroxine (T4) concentration of 71.4 pmol/l and free triiodothyronine (T3) concentration of 27.4 pmol/l. The concentration of TSH receptor antibody was markedly elevated at 38.2 U/l (<1.0). Atrial fibrillation with a rapid ventricular response (heart rate of 165 beats/min) was noted on ECG (Fig. 1).

Figure 1

Initial electrocardiogram (ECG) at presentation to the emergency room: heart rate 160 beats/min and atrial fibrillation.

Bedside echocardiogram demonstrated globally impaired left ventricle function, dilated right ventricle and pressure overload on the right side of the heart. Subsequent CTPA confirmed multiple bilateral pulmonary emboli (Fig. 2a and b).

Figure 2

(a) Axial CTPA illustrating a filling defect at the bifurcation of the main pulmonary artery (pointed by black arrow) as well as clots bilaterally (pointed by two white arrows). (b) Coronal view of CTPA showing a large filling defect in the left pulmonary trunk (pointed by white arrow).

Treatment

He remained in the ITU. Treatment with i.v. steroid and 20 mg OD carbimazole was initiated. Anticoagulation with low-molecular-weight heparin (1.5 mg/kg per day enoxaparin) was continued.

Outcome and follow-up

The patient made a significant recovery after a week of ITU stay. He was discharged with advice to continue using carbimazole 20 mg OD and enoxaparin 1.5 mg/kg per day s.c.. Repeat thyroid function test done 4 weeks after carbimazole treatment revealed completely suppressed TSH concentration of <0.03 mU/l with normal free T4 concentration of 16.4 pmol/l and normal free T3 concentration of 4.8 pmol/l.

Discussion

Thyroid storm is rare and can be life threatening with a mortality rate of 10–20%; hence, it is important to recognise it early and initiate appropriate treatment. The cause for thyrotoxicosis in thyroid storm is likely due to Graves' disease; however, it occurs with other forms of thyrotoxicosis.

The diagnosis of thyroid storm is based on clinical findings. Burch & Wartofsky (1) developed a scoring system based on clinical criteria in 1993. A score between 25 and 44 is suggestive of impending thyroid storm and a score >44 is suggestive of thyroid storm. More recently, Akamizu et al. (2) have formulated diagnostic criteria based on the review of clinical manifestations, namely CNS, cardiovascular, gastrointestinal and hepatic manifestations and multi-organ failure. The prerequisite for the diagnosis of thyroid storm is a definite biochemical evidence of thyrotoxicosis. In the study carried out by Akamizu et al., a 10% mortality rate was reported for thyroid storm and the presence of multi-organ failure was an independent prognostic factor for death. A higher incidence of irreversible neurological defects including psychosis was observed in this cohort.

Precipitating factors for thyroid storm are poor compliance with medications, delayed treatment, infection, radioiodine therapy, trauma, surgical procedures and cardiovascular events. Individuals at a risk of developing thyroid storm are elderly, individuals with mental health issues, pregnant women, individuals with Addison's disease and individuals with alcohol abuse.

The pathophysiology of thyroid storm is unclear; the hypothesis suggested is an increase in free T3 concentrations and increase in β-adrenergic receptor activation. There is usually a precipitating event that sets off the thyroid storm. There is no clear cut-off level for free T4 or free T3 to predict severe thyrotoxicosis. What is important is to recognise the severity of thyrotoxicosis and treat the patient appropriately.

Previous studies have reported that hyperthyroidism is associated with a hypercoagulable state. There are case reports of sinus, cerebral thrombosis and deep vein thrombosis (3) in patients with thyrotoxicosis. The hypercoagulable state may be multifactorial and be linked to an increase in the activity of factor VIII, Von Willebrand factor and tissue plasminogen activator inhibitor-1 (4). A 5-year follow-up study carried out by Lin et al. (5) to assess the risk of pulmonary embolism in hyperthyroid patients found a 2.3 times greater increase in the risk of pulmonary embolism after removing the confounding factors using Cox model hazard regression.

Atrial fibrillation is a clinical feature of hyperthyroidism with an estimated prevalence rate of 10–20% in patients with thyrotoxicosis (2)(6)(7); however, in thyroid storm, a 30–40% occurrence rate of atrial fibrillation has been observed and 50% of patients who died due to thyroid storm have been reported to be in atrial fibrillation (2). About 10–40% of hyperthyroid patients with atrial fibrillation have been found to have arterial thrombosis (8). There is no consensus with regard to the initiation of anticoagulation for atrial fibrillation in severe thyrotoxicosis. Anticoagulation is not routinely initiated if the risk is low on the CHADS2 score; however, this should be considered in patients with thyroid storm or severe thyrotoxicosis with impending storm irrespective of the CHADS2 risk, as it appears to increase the risk of thromboembolic episodes.

Declaration of interest

The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding

This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

Patient consent

Written informed consent was obtained from the patient for publication of the case report and accompanying images.

Author contribution statement

T Min was responsible for case note review and literature search and wrote the case report; S Benjamin reviewed the patient in the ward and while visiting the outpatient clinics and L Cozma was responsible for discussion and literature review.

References

1

Burch HB, & Wartofsky L 1993 Life-threatening thyrotoxicosis. Thyroid storm. Endocrinology and Metabolism Clinics of North America. 22: 263

2

Akamizu T, Satoh T, & Isozaki O 2012 Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid. 22: 661–679.(doi:10.1089/thy.2011.0334)

3

Squizzato A, & Romualdi E 2007 Clinical Review: Thyroid dysfunction and effects on coagulation and fibrinolysis: a systematic review. Journal of Clinical Endocrinology and Metabolism. 92: 2415–2420.(doi:10.1210/jc.2007-0199)

4

Stuijver DJ, van Zaane B, Romualdi E, Brandjes DP, Gerdes VE, & Squizzato A 2012 The effect of hyperthyroidism on procoagulant, anticoagulant and fibrinolytic factors: a systematic review and meta-analysis. Thrombosis and Haemostasis. 108: 1077. doi:10.1160/TH12-07-0496)

5

Lin HC, Yang LY, & Kang JH 2010 Increased risk of pulmonary embolism among patients with hyperthyroidism: a 5-year follow-up study. Journal of Thrombosis and Haemostasis. 8: 2176–2181.(doi:10.1111/j.1538-7836.2010.03993.x)

6

Petersen P, & Hansen JM 1988 Stroke in thyrotoxicosis with atrial fibrillation. Stroke. 19: 15–18.(doi:10.1161/01.STR.19.1.15)

7

Sawin CT, Geller A, Wolf PA, Belanger AJ, Baker E, Bacharach P, Wilson PW, Benjamin EJ, & D'Agostino RB 1994 Low serum thyrotropin concentrations as a risk factor for atrial fibrillation in older persons. New England Journal of Medicine. 331: 1249–1252.(doi:10.1056/NEJM199411103311901)

8

Bar-Sela S, Ehrenfeld M, & Eliakim M 1981 Arterial embolism in thyrotoxicosis with atrial fibrillation. Archives of Internal Medicine. 141: 1191. doi:10.1001/archinte.1981.00340090087019)

Impending thyroid storm in a pregnant woman with undiagnosed hyperthyroidism

A case report and literature review

Yushan Ma, MS,a,bHao Li, MS,a,bJin Liu, MD,c,Xuemei Lin, MD,a,b, and Hui Liu, MSa,b

Monitoring Editor: Fabio Comim.

aDepartment of Anesthesiology, West China Second University Hospital

bKey Laboratory of Birth Defects and Related Diseases of Women and Children

cDepartment of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Correspondence: Jin Liu, Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan, China (e-mail: moc.361@4180uilnijucs); Xuemei Lin, Department of Anesthesiology, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China (e-mail: moc.361@ucsniliemeux).

Author information ►Article notes ►Copyright and License information ►

Received 2017 Sep 17; Revised 2017 Dec 20; Accepted 2017 Dec 20.

Copyright © 2018 the Author(s). Published by Wolters Kluwer Health, Inc.

This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0

Abstract

Rationale:

Thyroid storm is a rare complication during caesarean section of patients with hyperthyroidism. It occurs abruptly, with a high mortality rate if not recognized immediately and aggressively treated. Herein, we reported a case of impending thyroid storm during a caesarean section.

Patient concerns:

A healthy 23-year-old woman with undiagnosed hyperthyroidism underwent an emergency caesarean section under general anesthesia. After tracheal extubation, the patient exhibited abnormal tachycardia, agitation, sweating, and hyperpyrexia.

Diagnoses:

The clinical manifestation and the following thyroid function test indicate a high index of suspicion for impending thyroid storm.

Interventions:

Hydrocortisone and esmolol were intravenously administered immediately. Propylthiouracil and propranolol were orally administered after the patient regained complete consciousness.

Outcomes:

Due to our immediate recognition and aggressive treatment, more serious manifestations of thyroid storm were avoided.

Lessons:

Good antenatal care is very important for pregnant women, and they should be generally screened for thyroid disorders, especially if the resting heart rate is >100 beats/min and weight increases are inconsistent with gestational age. When hyperthyroidism is suspected, drugs that excite the sympathetic nerves or promote the release of histamine should not be used during caesarean section.

Keywords: emergency caesarean section, hyperthyroidism, pregnancy, thyroid storm

1. Introduction

Thyroid storm is a rare complication of hyperthyroidism, which can be life threatening, with a high mortality rate of 10% to 30% if not recognized immediately and aggressively treated.[1] According to the degree of systemic decompensation, it can be divided into 2 stages: the early stage (impending storm) and the actual crisis (thyroid storm).[2] Currently, there are no uniform diagnostic criteria for impending storm. In most cases, Burch and Wartofsky's[2] Point Scale is used. It is generally believed that the impending storm is the intermediate stage of hyperthyroidism that finally develops into thyroid storm. Caution is advised if the original symptoms of hyperthyroidism suddenly aggravate, such as temperature 38°C to 39°C, pulse 120 to 159 beats/min, accompanied by sweating, nausea, irritability, etc. The impending storm is reversible, if it can be diagnosed early and actively treated. If the situation continues to deteriorate, with temperature >39°C, pulse >160 times/min, accompanied by consciousness disorders (delirium, lethargy, coma, etc), it is diagnosed as thyroid storm. The occurrence of thyroid storm is associated with numerous precipitants, including surgery, trauma, delivery, and infection, especially those accompanied by undiagnosed and untreated hyperthyroidism.[2,3] Pregnant women with hyperthyroidism are more likely to develop thyroid storm.[4,5] Herein, we reported a case of impending thyroid storm during an emergency caesarean section. We also performed a literature review on the management of thyroid storm or impending thyroid storm.

2. Case report

This study was approved by the Ethics Committee of West China Second University Hospital of Sichuan University. Written informed consent was obtained from the patient for publication of this report.

A 23-year-old, gravida 1, para 0 woman was admitted to the antenatal ward of our hospital, due to tachycardia of the fetus and premature rupture of membranes. She was at 36 weeks and 4 days of gestation and had no unusual medical or family history. She had a regular prenatal examination during pregnancy at another medical institution, and no obvious abnormality was detected. But there was no report of thyroid function test in her record. Physical examination revealed her weight as 57.5 kg, height as 158 cm, temperature of 36.8°C, blood pressure (BP) of 132/88 mm Hg, and heart rate (HR) of 118 beats/min. The fetal position was left sacrum anterior, and the fetal HR was 150 to 200 beats/min. Regular uterine contraction was present. Vaginal examination showed meconium-stained amniotic fluid, and ultrasound revealed a fetus younger than the gestational age. The obstetrician diagnosed fetal distress in utero, which required immediate termination of pregnancy. Thus, an emergency caesarean section was performed under general anesthesia to expedite delivery.

After simple preoperative visit and airway assessment, anesthesia was induced with ketamine 60 mg, propofol 120 mg, and suxamethonium 100 mg in rapid sequence, followed by tracheal intubation. The fetus was delivered 3 min after incision, with Apgar scores of 10 at both 1 and 5 minutes. The weight of the newborn was 2250 g, and body length was 46 cm. Sufentanil 15 μg along with atracurium 25 mg which was immediately administered. Anesthesia was maintained with sevoflurane 3% and remifentanil 0.15 μg/kg/min. The patient experienced tachycardia at 110 to 120 beats/min during the surgery, with BP of 115 to 125/75 to 85 mm Hg. The operation was uneventful and lasted 45 minutes. Sufentanil 5 μg was given toward the end of the surgery, while simultaneously terminating the use of sevoflurane and remifentanil. The patient's HR reached 130 beats/min during tracheal extubation after the patient was able to respond to commands. Another dose of sufentanil 5 μg and additional midazolam 2 mg were intravenously given. Intravenous esmolol was administered intermittently to control the tachycardia. However, the patient's HR continuously increased, and peaked at 160 beats/min. Additionally, the patient exhibited a respiratory rate of 25 breaths/min, BP of 135 to 145/95 to100 mm Hg, agitation, coupled with profound sweating. However, the patient was able to respond to commands and denied having palpitations, shortness of breath, or postoperative pain. Meanwhile, her temperature reached 38.2°C. Thyroid palpation was performed, which revealed a slightly enlarged thyroid. Notably, when the thyroid was touched, the patient's HR increased. The release of thyroid hormone by touching the thyroid gland may be responsible for this phenomenon. A thyroid function test was immediately conducted to establish a definitive diagnosis. Simultaneously, hydrocortisone 100 mg was administered by intravenous drip, and esmolol 0.15 mg/kg/min was intravenously pumped. The HR was maintained between 130 and 140 beats/min. The patient was then transferred to the intensive care unit (ICU) for further treatment. The thyroid function test revealed triiodothyronine (T3) 8.15 nmol/L (normal range: 0.93–3.7), thyroxine (T4) >387.0 nmol/L (normal range: 58.1–173), free triiodothyronine (FT3) 18.81 pmol/L (normal range: 3.5–6.5), free thyroxine (FT4) 70.22 pmol/L (normal range: 11.5–22.7), thyroid-stimulating hormone (TSH) 0.005 mIU/L (normal range: 0.55–4.78), and thyroid globulin antibody (TGAb) 173.8 IU/mL (normal range: <60). Therefore, hyperthyroidism was definitively diagnosed. After the patient was completely conscious, propylthiouracil 100 mg and propranolol 10 mg were administered orally 3 times daily, and the patient's HR gradually decreased to <100 beats/min. The patient was transferred out of the ICU after 3 days and discharged from the hospital 3 days later.

The thyroid function test of the newborn at 5 days after birth revealed T3 4.84 nmol/L (normal range: 1.4–2.5), T4 318.9 nmol/L (normal range: 105–213), TSH 0.007 mIU/L (normal range: 1.7–9.1), and TGAb 113 IU/mL (normal range: <60). Neonatal hyperthyroidism was diagnosed. Propylthiouracil 5 mg was administered orally 3 times daily for 8 weeks. The repeat thyroid function test was normal. The mother continued to take propylthiouracil after discharge. One year later, her thyroid function test showed normal FT3, FT4, TT3, and TT4 levels, but TSH was reduced to 0.05 mIU/L.

3. Discussion

Hyperthyroidism is a rare complication, occurring in 1 to 4/1000 pregnant women,[6] with 85% of these cases resulting from Graves’ disease.[7] Untreated and inadequately controlled thyrotoxicosis is correlated with miscarriage, stillbirth, prematurity, pre-eclampsia, maternal congestive heart failure, low birth weight, and intrauterine growth restriction.[8–10] Maternal serum thyrotrophin receptor antibody (TRAb) due to Graves’ hyperthyroidism can cross the placenta and stimulate the fetal thyroid, resulting in fetal hyperthyroidism, with signs of intrauterine growth restriction and an increased fetal HR,[11] as seen in our patient.

Treatment of hyperthyroidism does not increase the likelihood of an adverse perinatal outcome, but is an independent risk factor for cesarean section.[12] However, symptoms of hyperthyroidism, including tachycardia, hyperhidrosis, and anxiety can also occur during a normal pregnancy.[7] Moreover, because of the bias towards a Th2 immune state in pregnant women accompanying tolerance of the fetus, symptoms of hyperthyroidism during pregnancy can be alleviated.[13] Therefore, there is considerable difficulty in diagnosing hyperthyroidism during pregnancy without thyroid function test. Our patient had no history of hyperthyroidism and was not previously screened for thyroid function during pregnancy. Thus, when she was admitted to the emergency ward of our hospital, the obstetrician focused on the fetal distress and could not differentiate if the tachycardia of the fetus was caused by maternal disease, such as maternal hyperthyroidism.

The symptoms of hyperthyroidism are often worsened by the precipitating events, ultimately leading to thyroid storm.[3,4] Patients with hyperthyroidism during pregnancy are 10 times more likely to develop a thyroid storm than in the nongestation period.[5] Various stress conditions, such as surgery, childbirth, infection, pre-eclampsia, induced labor, diabetic ketoacidosis, etc, can induce maternal thyroid storm. Therefore, the choice of anesthetic technique and drugs for caesarean section are particularly important in pregnant women with hyperthyroidism. As compared to neuraxial anesthesia, general anesthesia can avoid the stimulation of patients via invasive preoperative manipulation. However, narcotic drugs should be carefully chosen, and the use of anesthetics that could excite the sympathetic nerves and release histamine should be avoided. Ketamine is a potent analgesic with lighter respiratory depression. In spite of ketamine's avid transfer from the placenta, it does not lead to reduced Apgar scores in the neonate, making it a part of the small group of drugs that are approved for the induction of caesarean section.[14] However, ketamine obviously activates sympathetic function via inhibiting neuronal noradrenaline (NA) uptake at the sympathetic nerve endings,[15] and spontaneously evokes NA release, which is exocytosis-independent and insensitive to NA transport.[16] In addition, histamine concentrations increase dramatically when atracurium is administered at ≥0.5 mg/kg, which exerts positive inotropic and chronotropic effects on the H2 receptors of the myocardia and increases the HR.[17,18] We speculate that the use of atracurium and ketamine in our patient may have been a key factor for inducing the impending thyroid storm.

For surgery patients, the symptoms of thyroid storm may be atypical due to the effects of narcotic drugs. If a patient's hemodynamics drastically change and the increase of arterial pressure or HR is inconsistent with the depth of anesthesia, thyroid storm should be considered. However, other hypermetabolic conditions should be differentiated from thyroid storm, such as malignant hyperthermia (MH) and inadequate analgesia. In our case, sufentanil was intravenously given twice at the end of the operation and the patient denied any postoperative pain. Most MH patients developed signs of muscle rigidity and higher carbon dioxide,[19] which did not occur in our patient. Therefore, thyroid storm was highly suspected. Thyroid storm can be divided into 2 stages: the early stage (impending storm) and the actual crisis (thyroid storm).[20] In 1993, precise criteria for thyroid storm were defined by Burch and Wartofsky[2] based on the patient's clinical symptoms, including thermoregulatory and cardiovascular dysfunction, gastrointestinal–hepatic dysfunction, and central nervous system disturbance. Our patient exhibited abnormal tachycardia, agitation, sweating, and hyperpyrexia after extubation, with a high index of suspicion for thyroid storm. However, the patient's temperature did not exceed 39°C, and there was no vomiting, diarrhea, psychosis, stupor, or coma. The Burch and Wartofsky score of the patient was 45 implying that she was still in the stage of impending thyroid storm. But if not recognized in time and treated properly, it might have developed into a thyroid storm. As thyroid storm occurs abruptly and with a high mortality rate, people who are highly suspected of impending storm should be treated as thyroid storm. Thyroid function should be examined to establish a definite diagnosis. Meanwhile, antithyroid drugs, such as propylthiouracil, a saturated solution of potassium iodide or β-blockers, should be aggressively used to reverse the thyrotoxicosis. In addition, other multimodality treatment should be provided, including corticosteroid therapy, abundant oxygen, volume resuscitation, effective temperature control with antipyretics or cooling blankets, and correction of electrolyte imbalance.[7,20] In the present case, due to immediate recognition and aggressive treatment, we effectively controlled the condition and avoided more serious symptoms of thyroid storm.

Notably, our patient exhibited some unusual phenomena during the third trimester of pregnancy, despite the absence of thyroid function test results. According to the prenatal examination records, the patient's weight only increased by about 1500 g in the last 7 weeks. Her HR maintained at 100 to 120 beats/min in the past 2 months. Bulimia, hyperhidrosis and anxiety were also considered to be normal by the patient and her previous obstetrician. The neglect of these symptoms led to the missed diagnosis of hyperthyroidism. Inadequate preoperative preparation resulted in the occurrence of impending thyroid storm during the operation.

4. Conclusions

Herein, a pregnant woman with undiagnosed hyperthyroidism who developed impending thyroid storm was reported. Good antenatal care is very important for pregnant women, and they should be generally screened for thyroid disorders, especially if the resting HR is >100 beats/min and weight increases are inconsistent with gestational age. When hyperthyroidism is suspected, drugs that excite the sympathetic nerves or promote the release of histamine should not be used during caesarean section. Once symptoms similar to thyroid storm occur, aggressive treatment should be administered without hesitation to prevent worsening of the condition.

Footnotes

Abbreviations: BP = blood pressure, FT3 = free triiodothyronine, FT4 = free thyroxine, HR = heart rate, ICU = intensive care unit, MH = malignant hyperthermia, NA = neuronal noradrenaline, T3 = triiodothyronine, T4 = thyroxine, TGAb = thyroid globulin antibody, TRAb = thyrotrophin receptor antibody, TSH = thyroid-stimulating hormone.

YM and HL contributed equally to this work.

The authors have no conflicts of interest to disclose.

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