Oral Levothyroxine Treatment in Lithium Intoxication- Induced Myxedema Coma: A Case Report.

IF 0.8 Q4 EMERGENCY MEDICINE
Po-Hsuan Kao
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Abstract

Lithium intoxication-induced myxedema coma, a rare but dangerous condition of severe hypothyroidism, can be easily misdiagnosed in patients without history of hypothyroidism. The objective of this case report is to describe a lithium-treated patient who presented to emergency department with obtundation and moderate hypothermia and was diagnosed with myxedema coma and lithium toxicity. A 64-year-old female presented to the emergency department with obtundation and hypothermia. The patient had the past history of stage-III chronic kidney disease, bipolar-type schizoaffective disorder, hypertension, and hyperlipidemia, and she had received long-term lithium therapy for the schizoaffective disorder. Bradycardia with hypotension developed after a few hours of admission and thyroid function revealed thyroid-stimulating hormone 53.1 nIU/mL and free T4 (FT4) 0.11 ng/dL, and the serum lithium level was 2.54 mmol/L. Therefore, diagnosis of lithium intoxication-induced myxedema coma was made, and the patient was managed with oral form of levothyroxine (LT4) (loading dose of 400 mcg followed by 100 mcg per day), intensive fluid therapy, empirical antibiotics, mechanical ventilation, and inotropic agents; lithium had been discontinued since admission. The patient weaned from the mechanical ventilation and inotropic support at day 4 of admission and by day 6, the patient's consciousness had fully recovered; on day 9, the serum lithium level was 0.37 mmol/L. The patient's FT4 recovered to the normal range (0.96 ng/dL) on day 15. In patients with no history of hypothyroidism or neck surgery and radiation therapy, lithium intoxication can be the single contributor to myxedema coma, which can be treated with oral form of LT4 as thyroid replacement therapy with instant and intensive supportive care. However, further study is needed to compare the outcomes of the patients with myxedema coma treated by oral and intravenous LT4.

口服左旋甲状腺素治疗锂中毒致黏液水肿昏迷1例。
锂中毒引起的黏液水肿昏迷是一种罕见但危险的严重甲状腺功能减退症,在没有甲状腺功能减退史的患者中很容易被误诊。本病例报告的目的是描述一位接受锂治疗的患者,他以昏厥和中度低温就诊于急诊科,并被诊断为黏液水肿昏迷和锂中毒。一名64岁女性因失水和体温过低被送往急诊科。患者既往有iii期慢性肾脏疾病、双相型分裂情感性障碍、高血压和高脂血症病史,并因分裂情感性障碍接受了长期锂离子治疗。入院数小时后出现心动过缓伴低血压,甲状腺功能:促甲状腺激素53.1 nIU/mL,游离T4 (FT4) 0.11 ng/dL,血清锂水平2.54 mmol/L。因此,诊断为锂中毒引起的黏液水肿昏迷,并给予口服左旋甲状腺素(LT4)(负荷剂量为400 mcg,随后为100 mcg / d)、强化液体治疗、经验抗生素、机械通气和肌力药物;自入院以来已停止使用锂。患者于入院第4天脱离机械通气和肌力支持,第6天意识完全恢复;第9天,血清锂水平为0.37 mmol/L。患者FT4在第15天恢复到正常范围(0.96 ng/dL)。在没有甲状腺功能减退或颈部手术和放疗史的患者中,锂中毒可能是造成黏液水肿昏迷的唯一原因,可使用口服LT4作为甲状腺替代疗法,并给予即时和强化的支持治疗。然而,需要进一步的研究来比较口服和静脉注射LT4治疗黏液水肿昏迷患者的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of acute medicine
Journal of acute medicine EMERGENCY MEDICINE-
CiteScore
0.80
自引率
0.00%
发文量
20
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