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Myxedema Coma: Improving Outcomes With Prompt Recognition and Therapy

Background: Myxedema coma, a misnomer for severe hypothyroidism, is a rare endocrine emergency with an incidence of 1.08 cases per million people per year and a high mortality rate ranging from 30-50%. A delay in diagnosis and treatment worsens the prognosis and increases morbidity and mortality. De...

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Detalles Bibliográficos
Autor principal: Parihar, Aisha
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8089968/
http://dx.doi.org/10.1210/jendso/bvab048.1927
Descripción
Sumario:Background: Myxedema coma, a misnomer for severe hypothyroidism, is a rare endocrine emergency with an incidence of 1.08 cases per million people per year and a high mortality rate ranging from 30-50%. A delay in diagnosis and treatment worsens the prognosis and increases morbidity and mortality. Delayed management often leads to decompensation, presenting as uncontrolled persistent hypothermia, severe electrolyte derangements, and a potential for ventilator requirement needing ICU care. We present a patient in hypothyroid crisis who was promptly managed in a non-ICU setting who demonstrated a relatively early improvement in vital signs, thyroid lab values, and return to baseline mental status. Clinical Case: A 75 year old female with past medical history of hypothyroidism, atrial fibrillation, hypertension, coronary artery disease, depression, tardive dyskinesia, and dementia presented to the hospital in the month of December due to confusion after a mechanical fall that resulted in a head laceration requiring multiple stitches. Trauma work up included a CT scan of the head that was negative. On presentation, patient was also hypothermic, bradycardic, hypotensive, and lethargic with an altered mental status. Sepsis work up was negative. TSH was checked on day of admission and found to be significantly elevated to > 100 mcIU/mL, consistent with severe hypothyroidism. Free T4 and total T3 levels were low. Patient was immediately given intravenous levothyroxine 300 mcg followed by oral levothyroxine 125 mcg daily. In addition, intravenous hydrocortisone 100 mg every 8 hours was started until adrenal insufficiency was ruled out with a normal cortisol level. Upon discussion with family, it was learned that patient had not been taking her home medications indicating non-compliance to thyroid replacement therapy as the etiology for her hypothyroid crisis. Within a day of initiating therapy, TSH levels drastically improved with a reduction by 50%. Bradycardia, hypotension, and hypothermia resolved as well. In three days, patient’s mentation improved back to baseline and TSH, free T4, and total T3 continued to normalize. Conclusion: This case demonstrates how prompt recognition of hypothyroid crisis and immediate therapy can lead to early improvement in outcomes such as reversibility of mental status, normalization of vital signs and lab values, prevention of escalation of care to an ICU setting, and overall morbidity and mortality.