颅脑损伤患者血浆ADH测定的临床意义

目的 :探讨颅脑损伤病人血浆抗利尿激素 (ADH)的变化 ,以及与低钠血症发生的机制。方法 :血浆ADH采用放射免疫分析 (RIA) ,血BUN、Cr测定采用酶法 ,血Na 、尿Na 测定采用离子电极法 ,随机对 75例单纯颅脑损伤病人伤后 1、7、1 4、2 1d血浆ADH进行测定 ,同时对血Na 测定值 <1 30mmol/L的 4 3例颅脑损伤并发低钠血症的病人血浆中ADH、BUN、Cr及 2 4h尿Na 进行测定。结果 :颅脑损伤后 1d、7d、1 4d三组中ADH含量明显高于对照组 (P <0 .0 1 ) ,伤后第 2 1d病人ADH含量较对照组差异无显著性 (P >0 .0 5 )。颅脑损伤并发低血钠症的病人 ,需要应用脱水剂 ,其ADH变化较不一致。 4 3例中A组 1 9例 ,系仍在使用脱水剂期间 ,测其ADH与对照组无差异性 (P >0 .0 5 ) ,与血钠浓度亦无相关性 (r=0 .2 0 )。B组 1 6例 ,停用脱水剂后出入量平衡 ,其ADH水平明显高于对照组 ,与血钠浓度呈负相关 (r=- 0 .6 7)。C组 8例 ,停用脱水剂后出量明显大于入量 (每天差额 >5 0 0ml)其ADH水平明显低于对照组 ,与血钠浓度呈正相关 (r=0 .87)。三组低钠血症病人 2 4h尿钠浓度明显高于对照组 (P <0 .0 1 )。结论 :颅脑损伤后ADH改变随情况而异。一般说来 ,ADH在伤后即升高 ,以后逐渐下降至正常 ,但亦有一些病例ADH反而降低 ,导致类似

Clinical Significance of Determination of Plasma Antidiuretic Hormone Levels in Patients with Head Injury

Objective To investigate the change of plasma levels of ADH and its relationship with hyponatremia in patients with cranio-cerebral injury. Methods Plasma ADH levels were measured with RIA in 30 controls and 75 cases of head injury (without hyponatremia) on d1,d7,d14 and d21 after admission. Serum BUN, Cr(with enzyme method), plasma ADH levels and 24h urinany sodium contents (with ion-electrode method) were also measured in another 43 cases of head injury with serum sodium concentrations below 130mmol/L. Results In the 75 patients without hyponatremia the plasma ADH levels rose abruptly on d1 and remained significantly higher than those in controls ( P <0.01) until d21 when the levels again dropped to approaching normal (vs controls, P >0.05). In the other 43 patients who were complicated with hyponatremia and required dehyderation therapy (Na <130mmol/L), the plasma ADH levels varied. Group A ( n=19 ) patients were still on diuretics; the plasma ADH levels were not much different from those in controls ( P >0.05) and were not correlated to sodium levels ( r=0.20 ). Group B patients ( n=16 ) had their diuretics withdrawn with balanced water intake and output. The plasma ADH levels were significantly higher then those in the controls ( P <0.01) and were negatively correlated to the sodium levels ( r=-0.67 ). The remaining 8 patients (Goup C) had water output exceeding intake over 500ml/day. The plasma ADH levels were significantly lower than those in controls with positive correlation to sodium levels ( r=0.87 ). The 24h urinary sodium contents in all these three groups were significantly higher than those in the controls ( P <0.01). Conclusion Plasma ADH levels changes after head injury vary under different conditions. Generally speaking, the levels increased after injury immediately and gradually returned to normal. However, in some cases low ADH levels with even diabetes-insipidus-like syndrome may occur, requiring therapeutic use of posterior pituitary hormone.