Thyroid storm is a rare and serious complication of pregnancy which can lead to spontaneous abortion, preterm delivery, preeclampsia and cardiac failure. It is also associated with high maternal and foetal mortality if not diagnosed and managed promptly. The diagnosis of thyroid storm in pregnancy can pose significant challenges due to its presentation being similar to other pregnancy-related complications. We present a patient who developed thyroid storm at 29 weeks of pregnancy, which resulted in pre-term delivery, cardiac failure and thyroidectomy. We discuss the treatment of thyroid storm in pregnancy, the decision making involved in proceeding to thyroidectomy or to use radio-iodine, and foetal thyroid status in thyrotoxicosis.
KeywordsThyroid storm, placental abruption, thyroidectomy, stress-induced cardiomyopathy, radioiodine
Case reportA 29-year-old pregnant woman presented with symptoms of lower back pain and vaginal bleeding. She was 29 weeks pregnant (gravida 2, para 2) with no previous antenatal history. Her past medical history included iron-deficiency anaemia, hypertension and a familial history of type II diabetes mellitus. On examination, the patient's vital signs were as follows: temperature 37.4 C; heart rate 140 beats/min; blood pressure 140/80 mmHg; respiratory rate 40 breaths/ min; SpO 2 94% while breathing air. Vaginal examination revealed blood-stained mucus in the vagina and a dilated cervix of 2 cm. Her initial chest radiograph (CXR) showed some opacification at both the left and right base ( Figure 1); however, in view of her high body mass index (>30), and sudden increase in her tachypnoea, a computed tomography pulmonary angiogram (CTPA) was arranged to investigate for potential pulmonary emboli. While the CTPA was being arranged, her cardiotocography (CTG) monitoring became 'non-reassuring' and emergency caesarean section was undertaken. This took place under general anaesthesia given her respiratory distress.On induction of anaesthesia with sodium thiopental and suxamethonium, she developed hypertension of 220/120 mmHg and atrial fibrillation (AF) with a rapid ventricular response of 180 beats/min. This was treated by increasing the depth of anaesthesia, intravenous amiodarone 300 mg and magnesium sulphate 20 mmol, following which she reverted to sinus rhythm at a rate of 130 beats/min. She required an FiO 2 of 0.55 and Positive end-expiratory pressure (PEEP) 10 cm H 2 O to maintain adequate oxygenation, and her compliance appeared reasonable with manual ventilation not being difficult. She was found to have a placental abruption, though the operative blood loss was estimated at 1.5 L which was less than expected. Thick meconium was noted at the time of delivery. She received transfusion of six units of packed red blood cells, four units of fresh-frozen plasma, and two units of cryoprecipitate guided by her estimated blood loss and the pre-operative full blood count and coagulation studies: Hb 100 g/L; white cell count (WCC) 28.7