颅脑创伤后并发低钠血症118例诊疗分析

目的探讨颅脑创伤后并发低钠血症的临床特点及中枢性低钠血症的诊治经验。方法回顾性分析2005年1月至2011年1月我院神经外科收治的118例并发低钠血症的颅脑创伤患者的临床资料,通过临床表现及实验室检查明确诊断,探索有效的治疗方案。结果本组治愈103例(87.3%),死亡15例(12.7%),其中放弃治疗2例,死于各种并发症13例,无低钠血症死亡病例。轻中型、重型及特重型颅脑损伤患者的中重度低钠血症发生率分别为37.0%、54.3%和76.2%(χ2=7.296,p=0.026);三种类型颅脑损伤患者的低钠血症持续时间超过8天的发生率分别为48.1%、50.0%和85.7%(χ2=9.220,p=0.010)。诊断为脑性盐耗综合征(CSWS)22例(18.6%),抗利尿激素不适当分泌综合征(SIADH)7例(5.9%),营养性低钠血症89例(75.5%)。CSWS组和SIADH组中血钠浓度与营养性低钠血症组相比无显著性差异(t=-0.896,p=0.609);血浆ADH及血浆渗透压与营养性低钠血症组相比存在显著性差异(t≥130.31,p0.05)。结论颅脑损伤越重,发生中重度低钠血症可能性越大,低钠血症持续时间越长。CSWS组血浆ADH显著低于营养性低钠血症组,SIADH组血浆ADH显著高于营养性低钠血症组,CSWS组和SIADH组血浆渗透压均低于营养性低钠血症组。CSWS和SIADH是导致颅脑创伤后低钠血症的主要原因,两者在发病机制、临床诊断及治疗方面都存在明显区别。早期诊断,及时明确类型,针对性积极治疗,可有效降低患者致残率和致死率,改善预后。

Diagnosis and treatment of hyponatremia associated with traumatic brain injury: an analysis of 118 cases

Objective To analyze the clinical features of hyponatremia associated with traumatic brain injury (TBI) and investigate the experience in the diagnosis and treatment of central hyponatremia.Methods A retrospective analysis was performed on the clinical data of 118 TBI patients with hyponatremia admitted to the Department of Neurosurgery in our hospital from January 2005 to January 2011. The diagnosis was confirmed through clinical manifestations and laboratory examinations, and the effective treatment strategy was explored.Results Among the 118 cases, 103 (87.3%) were cured, and 15 (12.7%) died, including 2 cases due to abandoning treatment and 13 cases due to various complications ( without hyponatremia). The incidence rates of moderate or severe hyponatremia in patients with mild or moderate TBI, severe TBI, and extremely severe TBI were 37.0%, 54.3%, and 76.2%, respectively (χ²=7.296, P=0.026); the proportions of individuals with a duration of hyponatremia more than 8 days in the three groups of patients were 48.1%, 50.0%, and 85.7%, respectively (χ²=9.220, P=0.010). Twenty-two cases (18.6%) were diagnosed as cerebral salt wasting syndrome (CSWS), 7 cases (5.9%) as syndrome of inappropriate antidiuretic hormone secretion (SIADH), and 89 cases (75.5%) as nutritional hyponatremia. There was no significant difference in serum sodium concentration between patients with nutritional hyponatremia and those with CSWS or SIADH (t=-0.896, P=0.609); compared with those with nutritional hyponatremia, patients with CSWS or SIADH had significantly different plasma antidiuretic hormone (ADH) level and plasma osmotic pressure (t≥130.31, P<0.05).Conclusions The risk of developing moderate or severe hyponatremia and the duration of hyponatremia rise as the severity of TBI increases. The plasma ADH level of patients with CSWS is significantly lower than that of patients with nutritional hyponatremia, but the plasma ADH level of patients with SIADH is significantly higher than that of patients with nutritional hyponatremia. The plasma osmotic pressure of patients with CSWS or SIADH is lower than that of patients with nutritional hyponatremia. CSWS and SIADH are the main factors leading to hyponatremia associated with TBI, and the pathogenesis, clinical diagnosis, and treatment differ significantly between CSWS and SIADH. Early diagnosis, timely typing, and symptomatic comprehensive treatment can reduce the disability rate and mortality in patients and improve their prognosis.