Video Clips on DVD
- 13-1
PowerPoint Discussion of Management of Thyroid Storm
- 13-2
Discussion with Dr. Sibai on Acute Management of a Patient with Thyroid Storm
Thyroid storm is a rare but potentially lethal complication of uncontrolled hyperthyroidism during pregnancy. The estimated incidence is 1% to 2% of pregnant women with hyperthyroidism. It is a life-threatening condition that usually develops in patients with poorly controlled disease in association with one or more of the factors listed in Table 13-1 .
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Case 1: Thyroid Storm
A 32-year-old in the 24th week of her fourth pregnancy arrives at the emergency department complaining of cough and congestion; shortness of breath; and swelling in her face, hands, and feet; diarrhea; and racing heart. The swelling and shortness of breath have become worse over the past 2 weeks, and she had several episodes of bloody vomiting the day before her visit. In addition, she had a 15-pound weight loss during the past 2 weeks. The patient says she has not experienced any leakage of fluid, vaginal bleeding, or contractions. She reports good fetal movement.
Physical findings revealed exophthalmia and an enlarged thyroid with a nodule on the right side, as well as bilateral rales, tachycardia, tremor, and increased deep tendon reflexes. The blood pressure was 170/111, pulse of 125 beats per minute (bpm), and temperature of 99° F. Laboratory tests revealed thyroid-stimulating hormone (TSH) of <0.01 IU/L (normal, 0.35 to 5.50), free T 4 (FT 4 ) of 5 ng/dL (normal, 0.8 to 11.8), free T 3 (FT 3 ) of 842 pg/dL (normal, 230 to 420), thyroid-stimulating immunoglobulin (TSI) 234% (normal <125), and thyroid peroxidase antibody (TPo) of 984 IU/mL (normal, 0 to 35). Complete blood count, platelet count, liver enzymes, and metabolic profile were all normal. Pulse oximetry was 90%, chest x-ray revealed bilateral pulmonary edema and pleural effusions, and electrocardiogram (ECG) revealed sinus tachycardia. A computed tomography (CT) scan of the chest showed bilateral pleural effusions indicative of high-output cardiac failure. Thyroid ultrasonography (US) revealed a diffusely enlarged thyroid gland with a right-sided mass.
Fetal heart rate (FHR) was in the 170s, with normal variability and occasional variable deceleration ( Fig. 13-1 ). Fetal US was consistent with the estimated gestational age and showed adequate amniotic fluid and no gross fetal anomalies and no evidence of fetal cardiac failure.
A diagnosis of thyroid storm was made, and the patient received propylthiouracil (PTU) 800 mg orally as a loading dose followed by 200 mg every 6 hours. One hour later she received Lugol’s solution. In addition, she received 2 mg IV propranolol followed by 2 mg as needed, and dexamethasone 2 mg IV every 6 hours. Because of congestive heart failure, she received IV doses of furosemide, and for severe hypertension she received IV labetalol. As her symptoms diminished, fetal tachycardia resolved ( Fig. 13-2 ). The patient’s (FT 4 ) level began to decline, consistent with appropriate treatment, and she was discharged home and instructed to continue PTU and labetalol and to follow up at the endocrinology and high-risk obstetric clinics as soon as possible.
The patient did not follow this advice. Consequently, she presented at 33 5/7 weeks in a hypertensive crisis (blood pressure 182/125 mm Hg), with symptoms similar to those she first exhibited plus acute pulmonary edema. Laboratory testing again revealed hyperthyroidism, with hemoconcentration (hematocrit 43%), elevated liver enzymes (AST, ALT, and bilirubin), and proteinuria of 2+ on dipstick. Chest x-ray revealed pulmonary edema. She was treated accordingly. Because of active labor and diagnosis of severe preeclampsia, she was given IV magnesium sulfate and IV labetalol to control severe hypertension. During labor, FHR revealed repetitive late decelerations ( Fig. 13-3 ) and emergency cesarean section was performed. A male infant was delivered, weight 2390 g, Apgar scores 9 at 1 minute and 9 at 5 minutes. Cord gases revealed pH of 7.21, P co 2 of 63 mm Hg, HCO 3 of 26 mmol/L, and base deficit of –3.2 mmol/L.
