Oke Ibiyemi O, Mughees Waneeza, Patel Hinal, Oladunjoye Olubunmi, York Eugene
Internal Medicine, Reading Hospital - Tower Health, West Reading, USA.
Internal Medicine, Drexel University College of Medicine, Philadelphia, USA.
Cureus. 2021 May 19;13(5):e15129. doi: 10.7759/cureus.15129.
Osmotic demyelination syndrome (ODS) is a clinical syndrome seen following aggressive correction of severe hyponatremia. Chronic alcohol use, malnutrition, and electrolyte derangement are additional risk factors promoting the demyelination in ODS. A 49-year-old female with a history of untreated mood disorder, hypertension, alcohol, and tobacco abuse presented to the emergency department (ED) with a three-month history of generalized body weakness. She also had a history of recurrent falls, difficulty walking, inadequate food and water intake, progressively worsening jaundice, and confusion which started about the same time. Her vital signs were normal; some of the significant physical examination findings were: sclera icterus, abdominal distension, bilateral pedal edema, hand tremors, rotary nystagmus, paraparesis, 1+ bilateral knee jerk, and absent bilateral ankle jerk. She had moderate hyponatremia, mild hypokalemia, deranged liver function test with a cholestatic pattern and transaminitis, hypoalbuminemia, elevated ammonia, lipase, in keeping with alcoholic liver disease and acute pancreatitis. In the ED, she received a normal saline infusion, and her serum sodium rose by just 6 mmol/L within the first 24 hours. She had drainage of her ascitic fluid and treatment with thiamine, folic acid, prednisone, lactulose, rifaximin, furosemide, spironolactone, and Ceftriaxone with improvement in clinical and laboratory abnormalities. Her lower extremity weakness persisted despite physical therapy, prompting neurologic evaluation. MRI of the lumbar spine showed an old compression fracture and lumbar spinal stenosis, while MRI brain findings were consistent with Osmotic demyelination. At the time of discharge to a rehabilitation facility, her serum sodium was 132 mmol/L, but her leg weakness persisted. Although rare, ODS can occur in the setting of moderate hyponatremia if there are additional risk factors that lower the threshold for demyelination.
渗透性脱髓鞘综合征（ODS）是在严重低钠血症得到积极纠正后出现的一种临床综合征。长期饮酒、营养不良和电解质紊乱是促使ODS发生脱髓鞘的其他危险因素。一名49岁女性，有未治疗的情绪障碍、高血压、酗酒和吸烟史，因全身乏力3个月就诊于急诊科（ED）。她还有反复跌倒、行走困难、食物和水摄入不足、黄疸进行性加重以及大约同时开始出现的意识模糊病史。她的生命体征正常；一些重要的体格检查发现包括：巩膜黄染、腹胀、双侧足背水肿、手部震颤、旋转性眼球震颤、双下肢轻瘫、双侧膝反射1+、双侧踝反射消失。她有中度低钠血症、轻度低钾血症，肝功能检查结果异常呈胆汁淤积型并伴有转氨酶升高，低白蛋白血症，氨、脂肪酶升高，符合酒精性肝病和急性胰腺炎。在急诊科，她接受了生理盐水输注，血清钠在最初24小时内仅升高了6 mmol/L。她接受了腹水引流，并接受了硫胺素、叶酸、泼尼松、乳果糖、利福昔明、呋塞米、螺内酯和头孢曲松治疗，临床和实验室异常情况有所改善。尽管进行了物理治疗，她的下肢无力仍持续存在，促使进行神经学评估。腰椎MRI显示陈旧性压缩性骨折和腰椎管狭窄，而脑部MRI结果符合渗透性脱髓鞘改变。在转至康复机构时，她的血清钠为132 mmol/L，但腿部无力仍持续存在。尽管罕见，但如果存在降低脱髓鞘阈值的其他危险因素，ODS可发生于中度低钠血症的情况下。
