Vingerhoets F, de Tribolet N
Service de Neurochirurgie, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Acta Neurochir (Wien). 1988;91(1-2):50-4. doi: 10.1007/BF01400528.
This prospective study is based on 256 patients with severe brain injury. Six patients (2.3%) developed the clinical picture of inappropriate secretion of antidiuretic hormone (SIADH): 3 in the first 3 days following the injury, 3 after more than a week. Their ADH plasmatic level were measured by radio-immunoassay. In the former, many factors, largely iatrogenic, can explain the increased secretion of ADH we found and which is then definitely "appropriate". It should be prevented by fluid restriction. In the latter, we found adequately low ADH levels, when the hypo-osmolarity is taken into account. Here, the aetiology seems to be a renal salt loss, eventually in relation to a natriuric factor (e.g. atrial natriuretic factor), justifying the term: "Cerebral salt wasting syndrome". With the resistance to fluid restriction, the treatment still remains a problem.
这项前瞻性研究基于256例重度脑损伤患者。6例患者(2.3%)出现抗利尿激素分泌不当综合征(SIADH)的临床表现:3例在受伤后的头3天内出现,3例在1周多后出现。通过放射免疫测定法测量他们的血浆抗利尿激素水平。在前者中,许多因素(很大程度上是医源性的)可以解释我们发现的抗利尿激素分泌增加的情况,而这种增加随后肯定是“适当的”。应通过限制液体摄入来预防。在后者中,考虑到低渗状态时,我们发现抗利尿激素水平足够低。在这里,病因似乎是肾盐丢失,最终可能与利钠因子(如心钠素)有关,这就解释了“脑性盐耗综合征”这一术语。由于对液体限制有抵抗性,治疗仍然是一个问题。