Thyroid Storm with Multiorgan Failure Treated with Plasmapheresis

Abstract

Background Thyroid storm is a severe manifestation of thyrotoxicosis and can present with multiorgan failure. First line treatment of thyroid storm is directed towards decreasing thyroid hormone production and peripheral conversion of T4 to T3, and treating adrenergic symptoms. When medical therapy fails, plasmapheresis is an alternative treatment option. Here we present a patient with thyroid storm and multiorgan failure who was treated with plasmapheresis. CaseA 50-year-old male with a history of hyperthyroidism, hypertension, and congestive heart failure presented to another hospital with fever and altered mentation. He was found to have pneumonia on imaging and was started on antibiotics. He developed shock complicated by atrial fibrillation with rapid ventricular rate which was treated with amiodarone. He was transferred to our hospital for further management. On arrival, TSH was <0.01 mIU/L, free T4 was >7 ng/dL and total T3 was 358 ng/dL. The endocrinology team determined he was in thyroid storm. His medical treatment of thyroid storm was aggressively titrated to maximal therapy. His hospital course was complicated by transaminitis, respiratory failure requiring intubation, shock requiring vasopressor support, kidney failure requiring continuous renal replacement therapy, and heart failure. Despite maximal anti-thyroid therapy, he had not improved clinically and T4 and T3 remained markedly elevated. A 4-day course of plasmapheresis was initiated resulting in marked lowering of T4 and T3 and clinical stability. ConclusionWhile current guidelines for plasmapheresis for thyroid storm recommend individualized decision making, no further clarification is provided on who would be a good candidate for the procedure. We present a patient with thyroid storm and multiorgan failure who was treated with plasmapheresis after failing maximal medical therapy. Given the significant improvement seen with plasmapheresis, endocrinologists should consider this mode of treatment earlier in the course of thyroid storm when patients are not improving with medical therapy alone.

Apathetic Thyroid Storm with Cardiorespiratory Failure, Pulmonary Embolism, and Coagulopathy in a Young Male with Graves’ Disease and Myopathy

“…TPE improves the thyroid storm by rapidly removing the large molecular weight substances like thyroid hormones, TSH receptor antibodies, catecholamines, and cytokines [ 51 ]. Similarly, TPE would help to replace the thyroid-binding proteins.…”

“…Fresh frozen plasma (FFP) is preferred as the replacement fluids compared to albumin, as it contains higher levels of TBG to bind to thyroid hormones [ 51 ]. Absolute indication for TPE is acute liver failure associated with thyroid storm, whereas relative indication is lack of clinical improvement after 24–48 hours of ATDs, β -blockers, corticosteroids, and inorganic iodide, treatment of triggers, and complications [ 51 ]. Moreover, when ATDs are not effective or contraindicated, TPE is used as a bridge to control the thyroid hormones until the curative treatment is introduced [ 5 ].…”

Neonatal Outcomes of Pregnancies Complicated by Maternal Hyperthyroidism

“…Among newborns with mothers who had thyroid antibodies, the median time of TFT normalization was longer at 46.6 days (95% CI, 20.6 to 39.4) compared to newborns whose release of thyroid hormone. 16 The hypermetabolic state is characterized by hemodynamic instability, manifesting as tachycardia, tachypnea, fever and hypertension. Neurologically, babies appear irritable with wide open eyes, jitteriness and difficulty in sleeping.…”

Тиреотоксический Криз: Современные Представления, Подходы К Диагностике И Лечению

“…Еферентна терапія (зазвичай плазмаферез, рідшегемосорбція чи діаліз) дає хворому реальний шанс завдяки швидкій елімінації з кров'яного русла надлишку ТГ та інших токсичних метаболітів; через це рекомендується багатьма фахівцями та експертами за умови прогресування поліорганної (особливо печінкової) недостатності [4,5,13]. Щоправда, існують застереження, які стосуються ефекту «рикошету» з повторним підйомом концентрацій ТГ, додаткового навантаження на систему кровообігу, впливу високих доз гепарину на зв'язування ТГ з транспортними протеїнами та ризику тромбоцитопенії [3].…”