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     

颅脑外伤后并发低钠血症的危险因素分析

目的探讨颅脑外伤患者并发低钠血症的发生机制及危险因素,以期为其早期预测及预防提供参考。方法回顾性分析2016年6月至2019年6月我院收治的185例中型和重型颅脑外伤患者的临床资料,包括导致低钠血症的不同病因、损伤类型、性别、格拉斯哥昏迷(GCS)评分、手术、脑水肿、颅底骨折和穿透性性损伤等;采用单因素χ^2检验和多因素Logistic回归分析探究颅脑外伤后并发低钠血症的危险因素。结果所有患者中,80例出现低钠血症,其中钠盐摄入不足、利尿剂过量使用47例,抗利尿激素分泌失调综合征19例,脑性耗盐综合征14例。低钠血症更多发生在脑挫裂伤、蛛网膜下腔出血和弥漫性轴索损伤患者中,差异具有统计学意义(P<0.05)。单因素χ^2检验结果显示,GCS评分(P=0.000)、脑水肿(P=0.000)、颅底骨折(P=0.000)、穿透性损伤(P=0.001)是颅脑外伤后并发低钠血症的相关因素。多因素Logistic回归分析结果显示,GCS评分(P=0.006)、脑水肿(P=0.006)、颅底骨折(P=0.000)、穿透性损伤(P=0.015)是颅脑外伤后并发低钠血症的危险因素。结论脑挫裂伤、蛛网膜下腔出血、弥漫性轴索损伤、GCS评分≤8分、脑水肿、颅底骨折和穿透性损伤的颅脑外伤患者更易发生低钠血症,应早期关注患者血清钠水平,明确病因及时纠正,防止病情恶化。     

脑性盐耗综合征的发病机制及钠代谢中枢的解剖位置

目的 探讨脑性盐耗综合征的发病机制及临床问题.方法 2007年7月至2012年7月治疗脑性盐耗综合征9例.依照患者补盐量与尿量有无直线回归关系将病例分为2组,对其补盐量、尿量、每日尿量/补盐量的均数做两样本t检验.结果 9例均治愈,其中6例补盐量与尿量有直线回归关系,P ＜0.05；3例补盐量与尿量无直线回归关系,P＞0.05.有直线回归关系组与无直线关系组相比:补盐量前者大于后者(P＜0.001)；尿量前者大于后者(P＜0.001)；但2组单位补盐量所对应的尿量(尿量/补盐量)不相等(P＞0.05).结论 脑性盐耗综合征患者补盐量与尿量的直线回归关系,补盐后肾脏排钠增加,因此,钠代谢中枢的解剖位置可能是以下丘脑为主,包括额叶、侧裂周围脑组织的广泛区域.     

抗利尿激素分泌不当综合征与脑性盐耗综合征

中枢性低钠血症是一种颅内疾病所致的常见电解质紊乱,发病机理有所争论,可分为抗利尿激素分泌不当综合征(SIADH)和脑性盐耗综合征(CSWS),它们有很多相似之处但不尽相同.SIADH以水潴留,ADH不适当分泌导致的稀释性低钠为特点,而CSWS则以原发性尿钠增多导致血容量不足和真性缺钠为特征.SIADH应该限水治疗,而CSWS则需要补液补盐治疗.补盐速率不当可导致严重的神经系统并发症,因此对急慢性低钠血症的补盐速率有一定的规则.     

抗利尿激素分泌不当综合征与脑性盐耗综合征

中枢性低钠血症是一种颅内疾病所致的常见电解质紊乱 ,发病机理有所争论 ,可分为抗利尿激素分泌不当综合征 (SIADH)和脑性盐耗综合征 (CSWS) ,它们有很多相似之处但不尽相同 .SIADH以水潴留 ,ADH不适当分泌导致的稀释性低钠为特点 ,而CSWS则以原发性尿钠增多导致血容量不足和真性缺钠为特征 .SIADH应该限水治疗 ,而CSWS则需要补液补盐治疗 .补盐速率不当可导致严重的神经系统并发症 ,因此对急慢性低钠血症的补盐速率有一定的规则 .     

轻度颅脑损伤急性期的免疫学反应

作者检查259例病人,其中脑震荡154例,轻度脑挫伤105例.采用改进的生物学检查方法,测定血浆中抗利尿激素含量的动力学改变.同时还选择血清备解素、血清总蛋白及球蛋白、C-反应蛋白、IgG、IgA、IgM等非特异性免疫成分做了检查.作者分别于伤后1～2、3～4、7～9及13～15天测定血浆抗利尿激素的含量.测定结果证实,脑挫伤病人抗利尿激素指数始终高于对照组,而脑震荡病人的两个年龄组于     

急性颅脑损伤患者血浆神经肽和电解质水平变化及其临床意义

目的: 探讨颅脑损伤急性期血浆精氨酸血管加压素(AVP)、血管紧张素Ⅱ(AngⅡ)和电解质水平的变化。方法: 根据GCS评分将78例急性颅脑损伤患者分为轻度组、中度组和重度组,测定各组患者损伤后第1、3、7 d 血浆 AVP和AngⅡ水平,入院当天同时测定血浆电解质。另外选择正常对照组41例相比较。结果: 与正常对照组相比,颅脑损伤患者AVP和AngⅡ明显增高(P<0.01),颅脑损伤越重,上述指标升高越明显,损伤后第3 d达高峰。颅脑损伤患者血钾、血钙浓度降低(P<0.01),其下降程度与颅脑损伤严重程度相关,轻型颅脑损伤组与对照组比较无显著差异。颅脑损伤后血钠水平无明显变化。结论: 血浆AVP和AngⅡ水平的改变可作为判断颅脑损伤严重程度的指标;血钾与血钙降低可以作为颅脑损伤患者病情判断的指标。     

输入新鲜冰冻血浆治疗颈脊髓损伤后低钠血症

背景：课题组考虑到新鲜冰冻血浆在临床上有综合治疗的价值,如抗休克、免疫、止血和解毒等,并能纠正胶体渗透压。如果在限水、补钠的同时补充新鲜冰冻血浆能提高脊髓损伤患者血钠水平,将为临床治疗脊髓损伤后低钠血症找到一个新的突破点。 目的：建立家兔颈脊髓损伤并发低钠血症动物模型,观察输入新鲜冰冻血浆治疗颈脊髓损伤并发低钠血症的疗效。 方法：健康成年家兔60只,采用改良ALLen氏打击法制作家兔颈脊髓损伤模型,将幸存且合并低钠血症的40只家兔随机分为2组,对照组20只,实验组20只,再按取标本时间不同依次分为1,3,6,10,15 d组,共10组,每组4只。实验组家兔出现低钠血症后每24 h静脉输入20 mL新鲜冰冻血浆(即1 d组输入1次,3 d组输入3次,6 d组输入6次,10 d组输入10次,15 d组输入15次)。对照组家兔每24 h静脉输入20 mL生理盐水。各组动物分别于术前及输入血浆后24 h采取标本分别进行血清钠离子及脊髓组织钠离子测定。 结果与结论：①术后3 d和术后6 d时实验组及对照组家兔的平均血钠浓度较术前明显降低(P < 0.05)。术后10,15 d时实验组血钠浓度升高,而对照组血钠水平持续下降,与实验组血钠水平比较差异有显著性意义(P < 0.05)。②术后3,6 d时实验组及对照组家兔脊髓组织钠浓度较空白对照组明显升高(P < 0.05)。实验组输入血浆10 d后脊髓组织钠浓度逐渐恢复,而对照组脊髓组织钠浓度持续升高,与实验组脊髓组织钠浓度比较差异有显著性意义(P < 0.05)。结果可见颈脊髓损伤后易并发低钠血症,输入新鲜冰冻血浆对颈脊髓损伤并发低钠血症的纠正有一定作用。     

蛛网膜下腔出血急性期血浆脑钠素与低血钠关系初探

目的:探讨蛛网膜下腔出血（SAH）急性期血浆脑钠素（BNP）含量与低钠血症的关系。方法:用放射免疫检测法测定36例SAH急性期患者病程0～2d（Ⅰ期）、7～9d（Ⅱ期）和>14d（Ⅲ期）血浆BNP含量。Ⅱ期还测定抗利尿素（ADH）、心钠素（ANP）和去甲肾上腺素（NA）血浆浓度。结果:22例低钠血症（血钠浓度<135mEq/L）各期血浆BNP浓度与对照组有显着差异。低钠血症者Ⅱ期血浆BNP浓度显着高于Ⅰ期、Ⅲ期（P<0.05）.Ⅱ期患者中,伴低钠血症者血浆NA浓度高于血钠正常者（P<0.05）,而两者血浆ADH、ANP浓度无显着差异。结论:血浆BNP与低血钠间可能有一定关系;NA可能与BNP分泌有关。     

颅脑损伤高渗性非酮症糖尿病液体疗法的护理

高渗性非酮症糖尿病昏迷(HNDC)是一种继发于重型颅脑损伤等疾患的并发症.纠正高渗透压状态关键是液体疗法.本文对颅脑损伤并发HNDC 8例患者用液体疗法护理体会,认为静脉内输入低渗盐水可防止发生静脉内溶血及血压下降;胃管内注水结合静脉补给生理盐水有助于改善高渗状态,应用喂饲泵可以防止引起返流及胃潴留;使用小剂量胰岛素时可用微量泵持续静注,但需防止低血糖的发生.本组病人经过细致的观察和护理后本组病人血糖、血钠、血浆渗透压均控制在稳定水平.     

Cerebral salt wasting treated with fludrocortisone in a 17-year-old boy

Cerebral salt wasting is characterized by inappropriate natriuresis and volume contraction with associated cerebral pathology. It is distinct from the syndrome of inappropriate antidiuretic hormone secretion, which is characterized by inappropriate retention of free water. We report a patient with a porencephalic cyst who developed cerebral salt wasting. His initial treatment was supplementation of water and salt, which did not improve natriuresis or volume contraction. Fludrocortisone administration effectively managed the cerebral salt wasting.     

脑性盐耗综合症

1　概述神经外科病人术后常出现低钠血症 ,尤其是鞍区肿瘤术后更为常见。以往将其统统归因于抗利尿激素分泌不当综合症 (ｓｙｎｄｒｏｍｅｏｆｉｎａｐｐｒｏｐｒｉａｔｅａｎｔｉｄｉ ｕｒｅｔｉｃｈｏｒｍｏｎｅｓｅｃｒｅｔｉｏｎ ,ＳＩＡＤＨ) ,但近些年来另一种与ＳＩＡＤＨ病因完全不同的 ,也可以引起低钠血症的综合症渐渐受到人们的重视 ,这就是脑性盐耗综合症 (ｃｅｒｅｂｒａｌｓａｌｔｗａｓｔｉｎｇｓｙｎｄｒｏｍｅ ,ＣＳＷＳ)。ＣＳＷＳ的主要临床表现为低钠血症、尿钠增高和低血容量 ,而ＳＩＡＤＨ是正常血容量或血容量增加的…     

114例多发伤合并低钠血症临床分析

目的 探讨多发伤舍并低钠血症的病因、发病机理、诊断和治疗。方法 回顾性总结114例多发伤合并低钠血症患者的临床表现、实验室检查结果，分析病因、分型和治疗方法。结果 114例患者中，39例（34．2％）因外伤后血浆大量丢失或强力利尿致血钠丢失过多引起，6例（5．3％）固外伤后长时间禁食及不恰当补液致血钠摄入不足引起，9例（7．9％）系外伤后高血糖或应用甘露醇等引起高渗性低钠，SIADH28例（24．6％），CSWS23例（20．1％），肾功能不全等9例（7．9％）。在治疗原发病的基础上，针对上述因素分别采用补充钠盐，补充血吝量，限制液体入量，应用激素等不同治疗方法，110例（96，5％）得到纠正。4例（3，5％）死亡，取得良好效果。结论 在治疗多发伤同时，应注意低钠血症发生的相关因素，做到早发现、早治疗以免产生严重后果。     

Two cases of cerebral salt wasting syndrome developing after cranial vault remodeling in craniosynostosis children

Hyponatremia has been recognized as an important postoperative metabolic complication after central nervous system (CNS) operations in children. If not appropriately treated, the postoperative hyponatremia can cause several types of CNS and circulatory disorders such as cerebral edema, increased intracranial pressure. The postoperative hyponatremia after CNS surgery has been considered as one of the underlying causes of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). In some cases, however, the cerebral salt wasting (CSW) syndrome has been detected. CSW syndrome is far less well-known than SIADH and also different from SIADH in diagnosis and treatment. It causes an increase in urine output and urine sodium after a trauma of CNS and dehydration symptoms. The appropriate treatment of CSW syndrome is opposite the usual treatment of hyponatremia caused by SIADH. The latter is treated with fluid restriction because of the increased level of free water and its dilutional effect causing hyponatremia, whereas the former is treated with fluid and sodium resuscitation because of the unusual loss of high urinary sodium. Early diagnosis and treatment of CSW syndrome after CNS surgery are, therefore, essential. We made a diagnosis of CSW syndrome in two craniosynostosis children manifesting postoperative hyponatremia and supplied them an appropriate amount of water and sodium via intravenous route. The hyponatremia or natricuresis of the children improved and neurologic and circulatory sequelae could be prevented.     

Cerebral salt wasting syndrome after calvarial remodeling in craniosynostosis

Hyponatremia and increased urine output after calvarial remodeling have been noted in pediatric patients with craniosynostosis. If not treated properly, patients develop hypoosmotic conditions that can lead to cerebral edema, increased intracranial pressure, and collapsed circulation. Postoperative hyponatremia after central nervous system surgery is considered as the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Recently, however, cerebral salt wasting syndrome (CSWS) instead of SIADH has been reported frequently. CSWS is associated with a decreased serum sodium level, increased urinary sodium level, increased urine output, decreased ECF volume, increased atrial natriuretic peptide (ANP) level, and increased brain natriuretic peptide (BNP) level. We experienced nine patients with craniosynostosis who underwent calvarial remodeling. By postoperative day 1, the ANP and BNP levels increased by 3-6 folds compared with the preoperative levels. They returned to the normal levels by postoperative day 5. The ADH level was within the normal range even after operation. The urinary sodium level increased in all patients by postoperative day 1 and 3. But the serum sodium level, and serum and urine osmolarity were normal due to appropriate replacement of sodium and fluid. After calvarial remodeling, the potential development of CSWS should be considered and distinguished from SIADH. The patients with CSWS require normal saline resuscitation and should prophylactically receive normal saline.     

Hyponatremia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women

Severe hyponatremia developed after elective surgery in 15 previously healthy women who subsequently either died or had permanent brain damage. The mean age was 41 years (range, 22 to 66), and the preoperative serum sodium level was 138 mmol per liter. All the patients recovered from anesthesia, but about 49 hours after surgery, when the average plasma sodium level was 108 mmol per liter, grand mal seizures, followed by respiratory arrest requiring intubation, developed in all 15. At that time, the urinary sodium level and the osmolality averaged 68 mmol per liter and 501 mOsm per kilogram, suggesting inappropriate secretion of antidiuretic hormone. In 10 of 15 patients, an acute cerebral vascular disorder was suspected, leading to a delay in treatment and multiple diagnostic studies, including CT scanning, cerebral angiography, and open-brain biopsies. The net postoperative fluid retention was 7.5 liters, and when correction of the serum sodium level was initiated, the rate of correction was less than 0.7 mmol per liter per hour. Histologic studies of the brain in five patients were not diagnostic, and no patient had any evidence of central pontine myelinolysis on the basis of autopsy, brain biopsy, or CT scanning. Seven patients recovered from coma after the serum sodium level was increased to 131 mmol per liter, but coma recurred two to six days later and ended in either death or a persistent vegetative state. Overall, 27 percent of the patients died, 13 percent had limb paralysis, and 60 percent were left in a persistent vegetative state.     

Severe hyponatraemia: investigation and management in a district general hospital

AIMS: To study the incidence, investigation, and management of severe hyponatraemia (serum sodium < 120 mmol/litre) over a period of six months in a district general hospital. METHODS: The laboratory computer was used to identify all inpatients who had a serum sodium concentration of less than 120 mmol/litre over a six month period. The records of these patients were reviewed for the relevant demographic, clinical, and laboratory data, in addition to diagnosis, treatment, and outcome of hospitalisation. RESULTS: Forty two patients were studied, with a female to male ratio of 2 : 1. Nine patients had central nervous system symptoms, and four of these patients died in hospital. Only 14 patients had their urinary electrolytes and/or osmolality checked. A diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was mentioned in eight patients, sometimes without checking their urinary electrolytes or osmolality. Twenty one patients died in hospital. The patients who died did not have lower serum sodium values or a higher rate of correction of hyponatraemia, but they all suffered from advanced medical conditions. CONCLUSIONS: The possible cause of hyponatraemia should always be sought and that will require an accurate drug history, clinical examination, and assessment of fluid volume, plus the measurement of urinary electrolytes and osmolality in a spot urine sample. The diagnosis of SIADH should not be confirmed without the essential criteria being satisfied. The current or recent use of diuretics is a possible pitfall in the diagnosis of SIADH. The rate of serum sodium correction of less than 10 mmol/day is probably the safest option in most cases.     

Syndrome of inappropriate antidiuretic hormone secretion in a patient with large cell neuroendocrine carcinoma

The syndrome of inappropriate antidiuretic hormone secretion has only been reported in a few patients with large cell neuroendocrine carcinoma (LCNEC); however, it has never been reported in a patient with LCNEC of the lung, whose serum sodium levels were normalized after surgical resection of the mass. A 63-year-old male presented with a two-day history of dizziness and recent memory loss. On admission, his serum sodium level was 113 mEq/L with a serum osmolality of 236 mosm/kg, a urine osmolality of 441 mosm/kg, and a urine sodium level of 65 mEq/L. His chest computed tomography revealed a 2.7×2.3 cm-sized mass in the left lower lobe. After surgical removal of the mass, his serum sodium concentrations were normalized, and histopathology of the mass revealed LCNEC.