ESPE Abstracts

Background: Thyrotoxic crisis is a rare, emergent complication of paediatric hyperthyroidism. A rare neurological manifestation of thyrotoxicosis is thyroid myopathy.

Objective and hypotheses: We report the case of a female teenager who presented to the Emergency Department with thyrotoxic crisis and lower extremity weakness. Our objective is to discuss the course of thyrotoxic crisis and review potential rare neurological manifestations of thyrotoxicosis and their non-thyroid differential.

Method: History: this 15 year-old African American female was diagnosed with Graves’ disease at age 14 and had a history of poor methimazole compliance and previous thyrotoxic crisis complicated by mild pulmonary hypertension. History also included asthma and chronic lower extremity weakness of uncertain aetiology. 5 days prior to admission, she developed fever and congestion and progressed to shortness of breath, sweating, dizziness, palpitations, weight loss, abdominal pain, vomiting, and diarrhoea. Exam: Her exam showed tachycardia (170 bpm), hypertension (147/81 mmHg), mild symmetric exophthalmos, a diffuse non-tender goitre (transverse diameter 6 cm bilaterally) with thyroid bruit, hyperdynamic precordium, and 3+ DTRs in legs. Despite professed lower extremity weakness, neurological examination revealed muscular deconditioning but normal lower extremity tone, strength, and gait. Work-up: Laboratory workup showed TSH <0.01 mIU/l (0.5–4.8), FT₄ >7.77 ng/ml (0.93–1.6), FT₄ by dialysis 15 ng/dl (0.8–1.7), T₃ 471 ng/dl (80–185), T₄ 23.6 μg/dl (4.9–13), and TrAB 34 IU/l (0–1.75). EKG showed sinus tachycardia with a normal ECHO. Clinical management: She received loading doses of propylthiouracil (PTU) 500 mg and hydrocortisone (HC) 300 mg and scheduled PTU 200 mg, atenolol 25 mg, potassium iodide 250 mg, and HC 100 mg.

Results: Clinical symptoms improved over 2 days. TFTs decreased to FT₄ 6.63 ng/dl and T₃ 123 ng/dl 5 days later after increase in PTU dose, and she was switched to methimazole (MMI). Final labs showed FT₄ 1.53 ng/dl, T₃ 203 ng/dl, and T₄ 7.6 μg/dl. Lumbar spine imaging and rheumatologic workup were negative. Her severe reported weakness was absent on neurological examination and was deemed to be consistent with conversion disorder with weakness, attributed in part to a conflictive maternal relationship, rather than thyrotoxic myopathy. She was discharged to an inpatient rehabilitation facility on MMI 20 mg daily and atenolol with plan for thyroidectomy.

Conclusion: Our patient presented with thyrotoxic crisis, which was attributed to a combination of Graves’ disease, MMI noncompliance, and stress. Her course included prolonged elevated thyroid hormone levels, possibly due to early escape from the Wolff-Chaikoff effect. Thyrotoxic myopathy is a rare cause of muscle weakness in hyperthyroid patients and should be considered in the differential diagnosis for all thyrotoxic patients complaining of muscular weakness; however, in this case, the aetiology of the weakness was cognitive rather than neurological. Finally, few cases of thyrotoxic crisis have been described in children and adolescents. As in adults, prompt diagnosis and management may prevent cardiovascular collapse and CNS dysfunction, but early escape from Wolff-Chaikoff effect may make treatment more complex.