Berendes E, Scherer R, Schuricht G, Rol R, Hengst K
Abteilung für Anasthesie und operative Intensivemedizin, Clemenshospital Münster.
Anasthesiol Intensivmed Notfallmed Schmerzther. 1992 Nov;27(7):445-8.
A thirty-year-old male patient suffered subarachnoidal haemorrhage from an angioma positioned in the cranio-cervical transition. After rebleeding twice the patient developed a hydrocephalus internus malresorptivus and excessive natriuresis and polyuria, accompanied by depressed renin activity and extremely low aldosterone plasma levels. Neither fluid restriction and sodium substitution, nor administration of hydro-chlorothiazide/indomethacin affected natriuresis and polyuria. It was only after treatment with fludrocortisone-acetate/hydrocortisone that hyponatraemia and polyuria were resolved. At the same time a ventriculo-peritoneal shunt was applied. Differential diagnosis excluded the syndromes of inadequate antidiuretic hormone secretion, renal and cerebral diabetes insipidus, osmotic receptor hypofunction, chronic renal dysfunction and tubular necrosis. Natriuresis and polyuria developed under dexamethasone therapy. Since patient history, physical examination and laboratory criteria could not explain the electrolyte and fluid imbalance, this might be attributed to the hydrocephalus. Similar disturbances have been reported from other patients with intracranial disorders. Mechanical pressure exercised on the hypothalamus might cause the disturbance of fluid and sodium balance. Assuming a cerebral salt wasting syndrome, a putative natriuretic factor coming from the brain or an imbalance in the cerebral renin-angiotensin-system, as described in rats and dogs, must be discussed.
一名30岁男性患者因位于颅颈交界处的血管瘤发生蛛网膜下腔出血。在两次再出血后,患者出现了内吸收不良性脑积水、高钠尿症和多尿,伴有肾素活性降低和醛固酮血浆水平极低。限制液体摄入和补充钠,以及使用氢氯噻嗪/吲哚美辛均未影响钠尿症和多尿。仅在使用醋酸氟氢可的松/氢化可的松治疗后低钠血症和多尿才得以缓解。同时进行了脑室-腹腔分流术。鉴别诊断排除了抗利尿激素分泌不足综合征、肾性和中枢性尿崩症、渗透受体功能减退、慢性肾功能不全和肾小管坏死。在接受地塞米松治疗期间出现了钠尿症和多尿。由于患者病史、体格检查和实验室检查标准均无法解释电解质和液体失衡,这可能归因于脑积水。其他患有颅内疾病的患者也有类似的紊乱情况报道。对下丘脑施加的机械压力可能导致液体和钠平衡紊乱。假设存在脑性盐耗综合征,必须讨论来自大脑的假定利钠因子或大鼠和狗中所描述的脑肾素-血管紧张素系统失衡。