Hyperthyroidism during pregnancy is a relatively rare event and is usually best managed medically with thionamide medications.1 Poor control of hyperthyroidism during pregnancy is associated with a host of issues, including intrauterine fetal demise, hypertensive disorders of pregnancy, preterm delivery, low birth weight, intrauterine growth restriction, and maternal congestive heart failure.2 One of the most feared sequelae of hyperthyroidism is thyroid storm, which carries a mortality rate of approximately 10% to 30%.3 Numerous precipitating factors for thyroid storm have been identified: surgery, trauma, infection, and delivery.4 Patients who develop thyroid storm present several challenges to anesthesiologists, including hemodynamic instability and medication management. Here, we present the anesthetic management for a pregnant woman whose delivery was complicated by signs and symptoms consistent with thyroid storm. The patient provided written consent for the use of her health information for publication.
Our patient is a 32-year-old gravida 5 para 0 woman who presented to the labor and delivery unit of our hospital in preterm labor at 25 weeks gestation. Her medical history was notable for well-controlled type II diabetes mellitus (glycated hemoglobin [A1c] = 6.5%) and Graves’ disease, which had been recently diagnosed after her primary care physician noted thyromegaly and tachycardia on examination at her initial prenatal appointment. She was prescribed methimazole and referred to an endocrinologist; however, she stated that she never made an appointment with an endocrinologist and reported taking the methimazole intermittently.
On admission to labor and delivery, her vital signs were notable for sinus tachycardia with rates of 120–130 beats per minute (bpm), mildly elevated blood pressures, and normothermia. Given her history of poor compliance with her antithyroid therapy, thyroid laboratory studies were sent and revealed a decreased thyroid-stimulating hormone (TSH) of 0.02 µIU/mL (normal range: 0.1–2.5 µIU/mL), increased free T4 of 2.6 ng/dL (normal range: 0.7–1.9 ng/dL), and increased T3 of 272 ng/dL (normal range: 80–180 ng/dL) but normal total T4 (Figure 1). An electrocardiogram was also performed revealing sinus tachycardia. After an endocrinology consultation, the dose of methimazole was increased, and betamethasone was given to accelerate fetal lung maturity. In addition, she was placed on nifedipine for tocolysis; however, this was discontinued on the day of admission given an exacerbation of persistent maternal tachycardia. The patient was assessed by the obstetric anesthesia team on admission, and various anesthetic options including epidural, spinal, and general anesthesia were discussed, pending her clinical and obstetric course. Her airway examination revealed a Mallampati II airway with no obvious thyromegaly or airway displacement.
Approximately 30 hours into her admission, the patient had a preterm premature rupture of membranes and began to have painful contractions. Fetal heart rate monitoring revealed recurrent variable and late decelerations. On consultation with the obstetric team, and given the likelihood of impending operative delivery, a combined spinal–epidural anesthetic was performed. After rupture of membranes, she was subsequently expectantly managed by the obstetric team.
Nineteen hours after rupture of membranes, the decision was made to proceed with urgent cesarean delivery for nonreassuring fetal heart tracing. At this time, the patient’s temperature was 99.2°F, heart rate was 120 bpm, and blood pressure was 148/79 mm Hg. The patient’s epidural catheter was dosed with 2% lidocaine with epinephrine, and surgical anesthesia was obtained. She was given preoperative antibiotics of cefazolin 2 g and azithromycin 500 mg. During the procedure, the patient’s epidural catheter was dosed with 4 mg of morphine for postoperative pain control; she also received 4 mg of ondansetron for nausea and a single dose of 10 mg of ephedrine for a blood pressure of 108/54 mm Hg. She received an oxytocin infusion at a rate of 300 mIU/min after the delivery of the fetus and no additional uterotonic medications. Surgery was uncomplicated, with an estimated blood loss of 700 mL, and the patient received 2000 mL of crystalloid intraoperatively. On arrival to the postanesthesia care unit (PACU), the patient’s temperature was 99.2°F, heart rate was 109 bpm, and blood pressure was 157/70 mm Hg (Figure 2). Thirty minutes later, the anesthetic team was notified of increase in temperature to 101.8°F, heart rate of 143 bpm, and blood pressure of 171/84 mm Hg. The patient was mildly agitated and noted shortness of breath, but her oxygen saturation (Spo2) was 100% on room air. She reported no nausea and was not diaphoretic. The patient was given several bolus doses of esmolol with transient decreases in heart rate and was started on an esmolol infusion. Heart rate decreased from approximately 140 to <120 bpm as the esmolol infusion was titrated. An arterial catheter was placed to closely monitor blood pressure, and an additional peripheral intravenous line was placed. Hemorrhage was deemed unlikely because a complete blood count demonstrated a hemoglobin of 9.8 g/dL and there was no evidence of ongoing bleeding. The patient was started on antibiotic therapy for possible chorioamnionitis (white blood cell count was 13,400 cells/μL), but given the rapid onset of her symptoms, the intensive care and endocrinology teams were consulted for concern of thyroid storm. The patient was started on corticosteroids immediately in the PACU (hydrocortisone 100 mg every 8 hours) and saturated solution of potassium iodide (5 drops every 6 hours). Once the patient was normotensive with resolution of tachycardia, the decision was made to transfer the patient to the medical intensive care unit for further monitoring.
The patient’s clinical condition improved in the intensive care unit, and her thyroid hormone levels began to normalize over the following days (Figure 1). Preeclampsia remained a concern, but the patient demonstrated normal urine protein/creatinine ratios during her admission. Endocrine surgery was consulted for thyroidectomy; however, the patient initially refused surgery and was discharged on medical management 3 days later. Ultimately, she underwent total thyroidectomy in postpartum month 4 and has been under close management by her endocrinologist for thyroid hormone supplementation.
Hyperthyroidism, as well as thyroid storm, can be challenging to diagnose in the parturient. Many symptoms of hyperthyroidism—tachycardia, hyperhidrosis, and anxiety—can occur during a normal pregnancy.1 Moreover, in the setting of delivery, blood loss and hormonal changes can further obscure thyrotoxic symptoms, further precluding prompt diagnosis of thyroid dysfunction. There are no broadly accepted diagnostic criteria for thyroid storm; however, the Burch–Wartofsky Point Scale is often used.4 This diagnostic system makes use of thermoregulatory dysfunction (pyrexia), cardiovascular dysfunction (tachycardia, atrial fibrillation, and congestive heart failure), gastrointestinal dysfunction (abdominal pain and jaundice), and central nervous system disturbance (agitation and delirium) to assess for the presence and severity of thyroid storm (Table). Fortunately, in our patient, a history of poorly controlled Graves’ disease increased suspicion for thyroid storm as a cause of her hemodynamic instability. Using the Burch–Wartofsky Point Scale, our patient had a score of 60, indicating likely thyroid storm. Prompt diagnosis and treatment of her condition resulted in a favorable patient outcome.
Intrapartum and immediate postpartum management of hyperthyroidism necessitate a multidisciplinary approach to patient care. In our case, we were aware that the patient was noncompliant with her antithyroid medication before delivery and, as such, the endocrinology service had already been involved with the patient to outline first steps to be taken in the event of potential postpartum thyroid storm. On arrival to the PACU, detailed discussion was held among the obstetric, anesthesia, and nursing teams to review concerning signs and symptoms. When hyperthermia ensued, as noted above, there was prompt evaluation and initiation of treatment. Key tenets of management in these situations are appropriate hemodynamic monitoring with intra-arterial line placement, adequate intravenous access for resuscitative measures, antiarrhythmic therapy with β-adrenergic receptor blockade, and administration of corticosteroids to limit peripheral conversion of thyroid hormone.5 Our team utilized the β-blocker esmolol initially because it was both readily available and could be easily titrated; the patient was subsequently switched to propranolol, which has the additional benefit of blocking the peripheral conversion of inactive T4 to the active form of T3. Of note, antithyroid medications are safe to continue during the postpartum period in the setting of breastfeeding. A recent review6 noted that: “Continuation of breastfeeding is safe and should be encouraged in hyperthyroid mothers taking [antithyroid drugs, ATDs], whether these are ATDs being continued after gestation or indeed ATD treatment initiated in the postpartum period.” There is some concern about the hepatotoxic effects of propylthiouracil, so many experts recommend using low-to-moderate methimazole doses as a first-line therapy in lactating mothers. Indeed, our patient was discharged and subsequently managed on a moderate dose of methimazole.
Delivery has long been recognized as a precipitating factor for thyroid storm, although only a small number of case reports describe its diagnosis in the postpartum period,7,8 none of which are in the anesthesiology literature. As anesthesiologists become increasingly involved with the perioperative management of the surgical patient, an understanding of the treatment of conditions such as thyroid storm is paramount. With this case report, we intend to create awareness of a rare but serious diagnosis in the postpartum patient and the challenges it presents for the obstetric anesthesiologist. Such a diagnosis is important to consider in the hemodynamically unstable postpartum patient, even in those without a history of thyroid dysfunction.
Name: Jack M. Peace, MD.
Contribution: This author helped draft and edit the manuscript, obtain consent from the patient, and perform the chart review.
Name: Matthew G. Hire, MD.
Contribution: This author helped care for the patient and edit the manuscript.
Name: Feyce M. Peralta, MD.
Contribution: This author helped participate in the care of the patient and edit the manuscript. She is also a mentor for the above trainees.
This manuscript was handled by: Mark C. Phillips, MD.
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