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黏液性水肿昏迷:对旧有危机的新审视。

Myxedema coma: a new look into an old crisis.

作者信息

Mathew Vivek, Misgar Raiz Ahmad, Ghosh Sujoy, Mukhopadhyay Pradip, Roychowdhury Pradip, Pandit Kaushik, Mukhopadhyay Satinath, Chowdhury Subhankar

机构信息

Institute of Post-Graduate Medical Education & Research, Calcutta 700020, India.

出版信息

J Thyroid Res. 2011;2011:493462. doi: 10.4061/2011/493462. Epub 2011 Sep 15.

Abstract

Myxedema crisis is a severe life threatening form of decompensated hypothyroidism which is associated with a high mortality rate. Infections and discontinuation of thyroid supplements are the major precipitating factors while hypothermia may not play a major role in tropical countries. Low intracellular T3 leads to cardiogenic shock, respiratory depression, hypothermia and coma. Patients are identified on the basis of a low index of suspicion with a careful history and examination focused on features of hypothyroidism and precipitating factors. Arrythmias and coagulation disorders are increasingly being identified in myxedema crisis. Thyroid replacement should be initiated as early as possible with careful attention to hypotension, fluid replacement and steroid replacement in an intensive care facility. Studies have shown that replacement of thyroid hormone through ryles tube with a loading dose and maintenance therapy is as efficacious as intravenous therapy. In many countries T3 is not available and oral therapy with T4 can be used effectively without major significant difference in outcomes. Hypotension, bradycardia at presentation, need for mechanical ventilation, hypothermia unresponsive to treatment, sepsis, intake of sedative drugs, lower GCS and high APACHE II scores and Sequential Organ Failure Assessment (SOFA) scores more than 6 are significant predictors of mortality in myxedema crisis. Early intervention in hypothyroid patients developing sepsis and other precipitating factors and ensuring continued intake of thyroid supplements may prevent mortality and morbidity associated with myxedema crisis.

摘要

黏液性水肿危象是一种失代偿性甲状腺功能减退的严重危及生命的形式,死亡率很高。感染和停用甲状腺补充剂是主要的诱发因素,而在热带国家体温过低可能并非主要因素。细胞内T3水平低会导致心源性休克、呼吸抑制、体温过低和昏迷。通过仔细询问病史并着重检查甲状腺功能减退的特征和诱发因素,以低怀疑指数来识别患者。黏液性水肿危象中越来越多地发现心律失常和凝血障碍。应尽早开始甲状腺替代治疗,在重症监护病房要特别注意低血压、液体补充和类固醇补充。研究表明,通过鼻胃管给予负荷剂量并进行维持治疗来替代甲状腺激素与静脉治疗一样有效。在许多国家,无法获得T3,口服T4治疗可有效使用,且结果无重大显著差异。就诊时出现低血压、心动过缓、需要机械通气、对治疗无反应的体温过低、败血症、服用镇静药物、格拉斯哥昏迷评分较低以及急性生理与慢性健康状况评分系统(APACHE II)和序贯器官衰竭评估(SOFA)评分超过6分是黏液性水肿危象死亡率的重要预测指标。对发生败血症和其他诱发因素的甲状腺功能减退患者进行早期干预,并确保持续服用甲状腺补充剂,可能会预防与黏液性水肿危象相关的死亡率和发病率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be18/3175396/a77b6ed82bc2/JTR2011-493462.001.jpg

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