How to Stop a Thyroid Storm When the Liver Is Bad: A Case Report and Literature Review

Abstract

Introduction: Patients with thyroid storm and resistance or contraindications to conventional medications may receive plasmapheresis until they have the definitive therapy. Case Presentation: A 42 years old lady with no past medical history was brought by the EMS with palpitations, shortness of breath, vomiting, and profuse diarrhea. She was found to have an atrial flutter with low blood pressure, received synchronized cardioversion, but unfortunately, she developed ventricular tachycardia, tonic-clonic seizure and went to pulseless electrical activity (PEA). Upon examination, the patient was intubated, heart rate of 200 beats/min, blood pressure of 80/60 on vasopressors. She had exophthalmos and icteric eyes. Neck examination revealed palpable goiter. There was bibasal fine cracked and mild lower limb edema. Laboratory showed FT4 39 (11.6-21.9 pmol/L), FT3 5 (3.7- 6.4 pmol/L), and TSH <0.01 (0.3-4.2 mIU/L). Burch- Wartofsky’s score was 55/140. Her presentation was suggestive of Graves’ disease with thyroid storm. Further labs showed high liver enzymes, high INR, ammonia as well as high creatinine. She was started on IV hydrocortisone and cholestyramine. Thionamides were contraindicated due to liver impairment. Extracorporeal membrane oxygenation (ECMO) was initiated for cardiopulmonary support and continued for 6 days. TSH receptor antibodies result was pending, thus a thyroid uptake scan was done while the patient connected to ECMO to confirm the diagnosis. Thyroid scan showed increased uptake suggestive of grave’s disease despite iodine contrast received for CT scan chest two days back. After 5 sessions of plasmapheresis, FT3 2.8, and FT4 30, Lugol’s iodine started and she underwent total thyroidectomy. She was successfully extubated and thyroxine replacement was started after normalization of thyroid hormones Discussion: The raised liver enzymes (shock liver) were a barrier to thioamides. With the contraindication to antithyroid medications, plasmapheresis was a rapid and safe option before thyroidectomy. The mechanism of plasmapheresis is to eliminate thyroid hormones, TSH-receptor antibodies, and cytokines. The current guidelines lack clear indications, the timing of initiation, and patient selection for plasmapheresis. Conclusion: Plasmapheresis should be considered as a stabilising measure, especially when patients cannot tolerate conventional medications. Plasmapheresis leads to rapid decline in thyroid hormone levels, providing a window to treat definitively with thyroidectomy.