Peruzzi W T, Shapiro B A, Meyer P R, Krumlovsky F, Seo B W
Department of Anesthesia, Northwestern University Medical School, Chicago, IL.
Crit Care Med. 1994 Feb;22(2):252-8. doi: 10.1097/00003246-199402000-00016.
To define the occurrence rate, time course, and potential etiologic factors of hyponatremia in patients with acute spinal cord injury.
Analysis of data obtained from a retrospective review of medical records and from a systematized, prospective database pertaining to patients with spinal cord injury.
A university hospital with a federally funded regional spinal cord injury center and a dedicated spinal cord injury intensive care unit.
Two hundred eighty-two patients admitted between January 1, 1988 and December 31, 1989 with acute (< 24-hr duration) spinal cord or vertebral column injury.
None.
The mean age of patients was 36.7 +/- 17.6 (SD) yrs; 225 (80%) of the patients were male and 57 (20%) were female. Hyponatremia, when it occurred, developed at a mean time of 6.4 +/- 6.7 days postadmission, reached its nadir at 8.7 +/- 8.8 days, and occurred in 28% of those patients with cervical injuries, 34% with thoracic injuries, and 27% with lumbar injuries (p = NS). Logistic regression analysis demonstrated that the type of spinal cord injury (Frankel class: range is A = complete neurologic lesion to E = no neurologic lesion) was the strongest predictor of hyponatremia. The occurrence rate of hyponatremia was as follows: Frankel class-A 62%; Frankel class-B 48%; Frankel class-C 41%; Frankel class-D 23%; Frankel class-E 16% (p < .0001).
The prevalence of hyponatremia in acute spinal cord injury is much higher than in the general medical or surgical patient population. This abnormality usually occurs within the first week postinjury. The most significant predictor of hyponatremia is the type rather than the level of spinal cord injury. The potential etiological factors are many and these factors are probably interrelated. The pathophysiological mechanisms that result in hyponatremia must be explored so that this occurrence and its consequences can be prevented.
确定急性脊髓损伤患者低钠血症的发生率、病程及潜在病因。
对医疗记录进行回顾性分析，并对脊髓损伤患者的系统化前瞻性数据库中的数据进行分析。
一家拥有联邦政府资助的地区脊髓损伤中心和专门的脊髓损伤重症监护病房的大学医院。
1988年1月1日至1989年12月31日期间收治的282例急性（病程<24小时）脊髓或脊柱损伤患者。
无。
患者的平均年龄为36.7±17.6（标准差）岁；225例（80%）为男性，57例（20%）为女性。低钠血症发生时，平均发生时间为入院后6.4±6.7天，最低点出现在8.7±8.8天，28%的颈椎损伤患者、34%的胸椎损伤患者和27%的腰椎损伤患者发生低钠血症（p=无显著性差异）。逻辑回归分析表明，脊髓损伤类型（Frankel分级：范围从A=完全神经损伤到E=无神经损伤）是低钠血症最强的预测因素。低钠血症的发生率如下：Frankel A级62%；Frankel B级48%；Frankel C级41%；Frankel D级23%；Frankel E级16%（p<0.0001）。
急性脊髓损伤患者低钠血症的患病率远高于普通内科或外科患者群体。这种异常通常发生在受伤后的第一周内。低钠血症最显著的预测因素是脊髓损伤的类型而非损伤水平。潜在病因众多，且这些因素可能相互关联。必须探索导致低钠血症的病理生理机制，以便预防这种情况及其后果。
