Kawajiri K, Matsuoka Y, Kan M
Department of Neurosurgery, Saiseikai Ibaraki Hospital, Osaka, Japan.
No Shinkei Geka. 1992 Sep;20(9):1003-7.
A case of cerebral salt wasting syndrome secondary to head injury is reported here. A 4-year-old boy was admitted to our hospital with head injury. Neurological examination revealed no abnormal findings other than consciousness disturbance. Plain skull X-ray demonstrated a linear fracture of the bilateral parietal bones, and CT scan demonstrated subarachnoid hemorrhage of the tentorium of the cerebellum. He gradually improved, but on the 6th day deterioration of consciousness developed. At that time CT scan demonstrated no abnormal findings. Biochemical analysis showed hyponatremia (116mEq/L) with increased natriuresis. Although a high dose of NaCl was supplied, serum sodium levels did not normalize. So we suspected that SIADH might be causing the hyponatremia, and water restriction was started. He lost 1 kg in body weight over 3 days, but serum sodium levels remained low (118mEq/L) with increased natriuresis. We found that the hyponatremia was caused by cerebral salt wasting syndrome, so we treated the patient with fludrocortisone acetate. Consciousness disturbance improved two days after the medication with fludrocortisone acetate, and serum sodium levels became normal (137mEq/L) on the 27th day. The administration of fludrocortisone acetate was able to be stopped two months after admission, and then the patient was discharged without any neurological deficits. We discussed in detail the diagnosis and the treatment of cerebral salt wasting syndrome.
本文报告1例继发于头部损伤的脑性盐耗综合征。一名4岁男孩因头部损伤入院。神经系统检查除意识障碍外未发现异常。头颅X线平片显示双侧顶骨线性骨折,CT扫描显示小脑幕下蛛网膜下腔出血。他逐渐好转,但在第6天意识恶化。当时CT扫描未发现异常。生化分析显示低钠血症(116mEq/L)伴尿钠增加。尽管补充了高剂量的氯化钠,但血清钠水平未恢复正常。因此我们怀疑抗利尿激素分泌异常综合征可能导致低钠血症,于是开始限制水摄入。他在3天内体重减轻了1kg,但血清钠水平仍低(118mEq/L)且尿钠增加。我们发现低钠血症是由脑性盐耗综合征引起的,因此我们用醋酸氟氢可的松治疗该患者。使用醋酸氟氢可的松治疗两天后意识障碍改善,第27天血清钠水平恢复正常(137mEq/L)。入院两个月后能够停用醋酸氟氢可的松,随后患者出院,无任何神经功能缺损。我们详细讨论了脑性盐耗综合征的诊断和治疗。