Thyroid Storm With Concurrent Covid-19 Infection in a Pediatric Patient

Abstract

Listen

Translate article

Title: Thyroid Storm with Concurrent COVID-19 Infection in a Pediatric Patient Background: A 16-year-old boy with recently diagnosed hyperthyroidism developed acute worsening of palpitations, tremor, diaphoresis, and shortness of breath in the setting of COVID-19 infection. There is increasing evidence of a relationship between COVID-19 and thyroid disease possibly due SARS-COV-2 use of ACE2 and the transmembrane protease serine 2 (TMPRSS2), which are highly expressed in the thyroid gland, to infect host cells.1 Clinical Case: Patient was diagnosed with hyperthyroidism after presenting to PCP with tremor, palpitations, and weight loss with a TSH <0.02 mIU/L and FT4 6.86 ng/dL on day 0. No treatment was initiated and he was referred to outpatient endocrinology clinic. On day 2, he developed mild URI symptoms which improved by day 4.On day 5, he developed acute worsening of tremor, palpitations, and weakness and presented to the ED where he was febrile to 38.4 C, tachycardic to 161 BPM, and hypertensive to 139/91 mmHg. Initial laboratory evaluation was significant for TSH <0.02 mIU/L, FT4 6.64 ng/dL and COVID-19 nucleic acid amplification test positivity. FT3 was >20.0 pg/mL and TRAB was 20.68 IU/L consistent with Graves’ disease. He met diagnostic criteria for thyroid storm with a score of 45 points using the Burch and Wartofsky scoring system based on the presence of thermoregulatory dysfunction (10 points), cardiovascular dysfunction (25 points) and precipitant history (10 points). Patient was admitted to a pediatric ICU and started on methimazole 20 mg every 8 hours, potassium iodide 250 mg every 8 hours, propranolol 40 mg every 8 hours, and hydrocortisone 50 mg every 8 hours with resolution of fever, tachycardia, and hypertension. He was noted to have left ventricular hypertrophy with progressive, asymptomatic ST elevation/nonspecific repolarization changes on electrocardiogram (ECG). Echocardiogram was normal. B-natriuretic peptide and serial troponin were normal. On day 6, inflammatory markers and coagulation studies were reassuring against concurrent multisystem inflammatory syndrome in children. Potassium iodide was discontinued on day 6 and hydrocortisone was discontinued on day 8.Repolarization abnormalities persisted throughout his admission with appearance of prominent U waves and borderline QT prolongation, however no significant arrhythmias were noted. On day 9 FT4 was 1.99 ng/dL and FT3 was 4.8 pg/mL; he was discharged home in stable condition Conclusion: This is the first reported case of COVID-19 infection as presumed precipitant of thyroid storm in a pediatric patient with cardiac findings. [1] Scappaticcio, L., Pitoia, F., Esposito, K., Piccardo, A., & Trimboli, P. (2020). Impact of COVID-19 on the thyroid gland: an update. Reviews in endocrine & metabolic disorders, 1–13. Advance online publication. https://doi.org/10.1007/s11154-020-09615-z