Ragaller M, Quintel M, Bender H J, Albrecht D M
Institut für Anästhesiologie und operative Intensivmedizin, Fakultät für klinische Medizin Mannheim, Universität Heidelberg.
Anaesthesist. 1993 Mar;42(3):179-83.
Myxedema coma is characterized by severe lack of thyroid hormones, unconsciousness and serious restriction of vital functions. The mortality rate still ranges between 50 and 80%. In patients with inapparent hypothyroidism myxedema coma occasionally follows surgery, anesthesia or severe infection. A case of myxedema coma following surgery is reported. CASE REPORT. A 46-year-old woman was anesthesized for hip replacement. The intraoperative cardiovascular situation was characterized by hypotension and tachycardia. On the first postoperative day, unexpectedly a cardiac arrest occurred. Resuscitation with high doses of epinephrine was successful. There was no evidence of myocardial infarction, hypoxia and pulmonary embolism as causative factors for cardiac arrest. A pulmonary artery catheter was inserted and showed low cardiac output. Catecholamines and intravascular fluids were administered without hemodynamic improvement. In the next 5 days pneumonia was followed by ARDS and acute renal failure. After successful treatment of these complications the patient remained in deep coma. An intracerebral disease could be excluded by computerized tomography. Evaluation showed low thyroid hormones (T3; T4) and elevated TSH. The diagnosis of a myxedema coma was assumed. After failure of oral therapy with L-thyroxine (0.025-0.05 mg/day) for 10 days, intravenous therapy with 0.5 mg L-thyroxine was performed. Thirty-six hours later the patient regained consciousness, without cardiac complications. The patient progressed uneventfully under oral therapy with 0.1 mg L-thyroxine and was discharged from the hospital 6 weeks later. DISCUSSION. Pathophysiology and symptomatology of a case of postoperative myxedema coma are described (Tables 1-4). In this patient, the following symptoms occurred: low thyroid hormones (T3; T4), elevated TSH, deep coma, decreased ventilatory response to CO2, diminished myocardial contractility under catecholamine stimulation, impaired renal water excretion. After failure of oral substitution of L-thyroxine, intravenous therapy had to be performed in spite of the high risk of further cardiac complications in this patient. This led to complete recovery with normal neuropsychological and cardiopulmonary parameters. CONCLUSION. Myxedema coma is a rare complication in postoperative care, but in cases of inexplicable unconsciousness thyroid failure should be excluded. If myxedema coma is evident, intravenous therapy with L-thyroxine should be performed under the conditions of extended monitoring.
黏液性水肿昏迷的特征是甲状腺激素严重缺乏、意识丧失和重要功能严重受限。死亡率仍在50%至80%之间。在隐匿性甲状腺功能减退患者中，黏液性水肿昏迷偶尔继发于手术、麻醉或严重感染。本文报告一例术后黏液性水肿昏迷病例。病例报告。一名46岁女性接受髋关节置换手术麻醉。术中心血管情况表现为低血压和心动过速。术后第一天，意外发生心脏骤停。大剂量肾上腺素复苏成功。没有证据表明心肌梗死、缺氧和肺栓塞是心脏骤停的病因。插入肺动脉导管显示心输出量低。给予儿茶酚胺和血管内液体治疗，但血流动力学无改善。在接下来的5天里，患者发生肺炎，随后出现急性呼吸窘迫综合征（ARDS）和急性肾衰竭。成功治疗这些并发症后，患者仍处于深昏迷状态。计算机断层扫描排除了脑内疾病。评估显示甲状腺激素（T3；T4）水平低，促甲状腺激素（TSH）升高。考虑诊断为黏液性水肿昏迷。口服左甲状腺素（0.025 - 0.05毫克/天）治疗10天无效后，给予静脉注射0.5毫克左甲状腺素治疗。36小时后患者恢复意识，无心脏并发症。患者在口服0.1毫克左甲状腺素治疗下病情平稳进展，6周后出院。讨论。描述了一例术后黏液性水肿昏迷的病理生理学和症状（表1 - 4）。该患者出现了以下症状：甲状腺激素（T3；T4）水平低、TSH升高、深昏迷、对二氧化碳的通气反应降低、儿茶酚胺刺激下心肌收缩力减弱、肾排水功能受损。口服左甲状腺素替代治疗无效后，尽管该患者有进一步发生心脏并发症的高风险，但仍必须进行静脉治疗。这使得患者完全康复，神经心理和心肺参数恢复正常。结论。黏液性水肿昏迷是术后护理中一种罕见的并发症，但在出现无法解释的意识丧失情况时，应排除甲状腺功能减退。如果黏液性水肿昏迷明确，应在加强监测的条件下进行静脉注射左甲状腺素治疗。
