SIADH

摘要： 目的:讨论重度颅脑损伤患者伤后出现中枢性低钠血症的类型、各自临床特征及治疗.方法:选取2015年9月至2018年6月期间潍坊医学院附属医院神经外科收治的71例重度颅脑损伤的患者出现中枢性低钠血症的临床表现及相关电解质检查,分析其特点、总结治疗经验.结果:大多数中枢性低钠血症患者,明确SIADH或CSWS后,分别经过各自严格补钠标准后,血钠恢复至正常,出院随访54例患者,均未再出现因不明原因导致头痛、恶心呕吐、意识混乱、嗜睡、癫痫、昏迷等相应症状,复查血电解质未见低钠.结论:重度颅脑损伤后发生中枢性低钠血症时由于发病机制的差别,治疗措施亦有差别,血容量评估是鉴别SIADH或CSWS的重要依据,及时形成有效的治疗措施,可明显改善患者的治疗效果,缩短患者的恢复时间,改善患者的预后.

摘要： 总结小细胞肺癌合并SIADH的治疗及护理.回顾性分析2014年1月～2016年1月收治的小细胞肺癌合并SI ADH患者的临床特征、治疗及护理.2014年1月～2016年1月共收治小细胞肺癌患者46例,伴有SIADH者31例,发生率为67.6％,经积极处理,治愈好转18例,未治愈患者自动出院5例,死亡8例.及时、有效、恰当的补钠,积极治疗原发病,去除相关诱因,给予针对性的护理措施,加强专科护理及基础护理等,对改善小细胞肺癌合并抗利尿激素分泌失调综合征(SIADH)有积极的意义.

摘要： 主要探讨窒息新生儿发生抗利尿激素异常分泌综合症（SIADH）内在和外在原因及相应的防治对策，以进一步提高危重新生儿的抢救存活率，降低病死率。

摘要： Objective: Hyponatremia is the most common electrolyte imbalance. The initial treatment decision is based on clinical evaluation of patient volume status but an accurate assessment is difficult, particularly differentiating mild hypovolemia from euvolemia. The aim of this study is to examine if biomarkers are valuable in the early determination of volume status and SIADH diagnosis. Methods: Blood samples were collected from an unselected patient population at entry to the Emergency Department. If the plasma sodium level (P-Na) was ≤125 mmol/L, the sample was frozen for further analysis. Mid-regional pro-atrial natriuretic peptide (MR-proANP), proadrenomedullin (MR-proADM), C-terminal prepro-vasopressin (copeptin), pro-endothelin-1 (proET-1) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were analysed. A comprehensive assessment of volume status and underlying causes was made after discharge blinded for biomarker results. Results: A total of 81 patients were included. A well substa ntiated volemic state (hypo/eu/hypervolemia) was established in 72 patients (mean age 76 years, 65% women, median P-Na 119 mmol/L). A significant association was observed between MR-proANP levels and volemic state (p = 0.0001). Data was specifically analysed with respect to distinguishing hypo- from euvolemia (n = 59) using logistic regression. In a crude analysis, MR-proANP was significantly related to euvolemia (OR: 2.54 per SD of MR-proANP, 95% CI 1.32 - 4.86, p = 0.005) and remained so after the multivariate backward elimination model (OR: 2.45 per SD of MRproANP, 95% CI 1.22 - 4.91, p = 0.012.), whereas the other studied biomarkers were not. Copeptin levels were not associated with a diagnosis of SIADH. Conclusions: MR-proANP may be of value in early determination of volume status in hyponatremic patients.

摘要： Background: Post-operative hyponatremia occurs after 30% of orthopedic surgeries, increasing morbidity, mortality and hospital length of stays and hospital costs. The cause of the hyponatremia can be varied, hard to diagnose and impact management. The goal of this study was to determine the causes of post-operative orthopedic hyponatremia and to evaluate the accuracy with which nephrologists and internists interpret the data. Methods: This was a retrospective chart review of patients >21 years old on the adult total joint service who developed postoperative hyponatremia. A hyponatremic order set was developed and patient fluid status was charted by the presence or absence of edema in non-surgical extremities. The patients were treated by their managing physicians. After one year, data on 51 patients were assembled and sent to three nephrologists and three internists to analyze and diagnose the etiology of the hyponatremia. Results: The most common causes of post-operative hyponatremia were hypovolemia (33.7%), the syndrome of inappropriate antidiuretic hormone, SIADH (32.4%), hypotonic fluid (8.2%), acute kidney injury (5.2%) and medications (5.9%). The interrater agreement, measured by kappa coefficient, was moderate (0.43;95% CI 0.34, 0.53) for the nephrologists and fair (0.38;95% CI 0.30, 0.46) for the internists. Conclusions: The majority of post-operative hyponatremia following total joint surgery in adults is from hypovolemia and SIADH. The treatment for these is very different: the first requires fluid resuscitation and the latter, free water restriction. Due to an interplay of peri-operative factors, the diagnosis can be difficult for both internists as well as nephrologists.

摘要： 低钠血症是最常见的电解质紊乱类型,其完整定义不仅包含血浆钠离子浓度≤135 mmol/L,还应包括机体水含量相对增多及肾脏清除自由水能力下降而造成的血钠降低[1-3]。Wald等[4]将低钠血症定义为社区获得性低钠血症及医院获得性低钠血症,并对53 236例成年患者进行为期7年的随访,结果显示有37.9%及38.2%的被调查者出现社区获得性低钠血症及医院获得性低钠血症,两者均与死亡

摘要： 目的：总结临床药师参与脑外伤后SIADH的治疗与体会。方法：通过临床药师参与脑外伤后SIADH诊疗方案的改进，体现临床药师作用。结果：临床药师提供的诊疗方案合理，促进了患者的康复。结论：临床药师参与临床药物治疗，结合患者病情，发挥自身优势，协助临床优化治疗方案，保障了药物在临床使用的安全、合理、有效。

摘要： 目的：：探究与分析颅脑损伤并发低钠血症的临床发病表现与诊疗手段。方法：选取我院自2011年11月至2012年11月收治的低钠血症患者60例，将其作为临床研究对象，对其采用综合疗法进行治疗，观察并记录临床疗效。结果：各血钠浓度患者治愈率无明显差异，P>0.05，不具有统计学意义。而该组患者的总治愈率高达91.67%，其余5例患者治疗3天后，自动放弃治疗后出院，仅占8.33%。结论：行综合疗法治疗颅脑损伤并发低钠血症的临床效果较为显著，大部分患者的血钠恢复正常，临床工作人员能对此类患者给以密切的检测并采取积极有效的治疗方案，以提升患者的生存质量。

摘要： 目的：探讨重型颅脑损伤患者合并中枢性低钠血症的病因、诊断及治疗。方法：回顾性分析重型颅脑损伤后合并中枢性低钠血症患者50例的临床表现及实验室指标，分析其治疗方法。结果：发生中枢性低钠的50例患者中，15例诊断为抗利尿激素分泌失调综合征（SIADH），35例诊断为脑性盐耗综合征（CSWS）。经过针对性治疗，除2例患者死于脑疝，1例死于多器官功能衰竭，1例放弃治疗自动出院外，其他46例患者经过治疗后，低钠血症均能恢复正常。结论：SIADH和CSWS的发病机制及治疗措施不同，对其进行正确诊断并进行针对性的治疗才能纠正中枢性低钠血症。

摘要： 低钠血症在蛛网膜下腔出血(subarachnoid hemorrhage SAH)后有1/3到1/2的患者会发病,是常见的电解质及水平衡紊乱.低血症钠常由抗利尿激素分泌不当综合征(SIADH)或者脑耗盐综合征(CSWS)引起,或者两者的组合.本文从低钠血症的发生机制、诊断及治疗进行综述.

摘要： 本文介绍了颅脑损伤后脑性盐耗综合征(cerebralsaltwastingsyndromeCSWS)的临床表现及其实验室诊断标准，介绍了具体的治疗方案及其疗效。

摘要： 本文介绍了颅脑损伤后脑性盐耗综合征(cerebralsaltwastingsyndromeCSWS)的临床表现及其实验室诊断标准，介绍了具体的治疗方案及其疗效。

摘要： 本文介绍了颅脑损伤后脑性盐耗综合征(cerebralsaltwastingsyndromeCSWS)的临床表现及其实验室诊断标准，介绍了具体的治疗方案及其疗效。

摘要： 本文介绍了颅脑损伤后脑性盐耗综合征(cerebralsaltwastingsyndromeCSWS)的临床表现及其实验室诊断标准，介绍了具体的治疗方案及其疗效。

摘要： 抗利尿激素分泌异常综合征（ＳＩＡＤＨ），是颅脑术后严重并发症。该文总结６例ＳＩＡＤＨ的救治体会。一、临床资料脑出血４例，脑瘤１例，颅内血肿１例。术后边３￣１０天出现低血钠临床表现，严重者形成脑疝。化验血钠均＜１３０ｍｍｏｌ／Ｌ，血渗＜２７０ｍｍｏｌ，尿钠＞８０ｍｍｏｌ／２４ｈ。二、讨论１、ＳＩＡＤＨ发病机制是ＡＤＨ释放过多而ＡＣＴＨ相对不足导致水潴留，低血钠低血渗，形成脑水肿。２、ＳＩＡＤＨ诊断（１）原发病，如脑外伤等。（２）临床表现。（３）化验，这是主要依据。３、ＳＩＡＤＨ的治疗，补充高渗盐水、脱水利尿，限制入量，控制原发病等要综合治疗才能尽快使病情好转。

摘要： 抗利尿激素分泌异常综合征（ＳＩＡＤＨ），是颅脑术后严重并发症。该文总结６例ＳＩＡＤＨ的救治体会。一、临床资料脑出血４例，脑瘤１例，颅内血肿１例。术后边３￣１０天出现低血钠临床表现，严重者形成脑疝。化验血钠均＜１３０ｍｍｏｌ／Ｌ，血渗＜２７０ｍｍｏｌ，尿钠＞８０ｍｍｏｌ／２４ｈ。二、讨论１、ＳＩＡＤＨ发病机制是ＡＤＨ释放过多而ＡＣＴＨ相对不足导致水潴留，低血钠低血渗，形成脑水肿。２、ＳＩＡＤＨ诊断（１）原发病，如脑外伤等。（２）临床表现。（３）化验，这是主要依据。３、ＳＩＡＤＨ的治疗，补充高渗盐水、脱水利尿，限制入量，控制原发病等要综合治疗才能尽快使病情好转。

摘要： 抗利尿激素分泌异常综合征（ＳＩＡＤＨ），是颅脑术后严重并发症。该文总结６例ＳＩＡＤＨ的救治体会。一、临床资料脑出血４例，脑瘤１例，颅内血肿１例。术后边３￣１０天出现低血钠临床表现，严重者形成脑疝。化验血钠均＜１３０ｍｍｏｌ／Ｌ，血渗＜２７０ｍｍｏｌ，尿钠＞８０ｍｍｏｌ／２４ｈ。二、讨论１、ＳＩＡＤＨ发病机制是ＡＤＨ释放过多而ＡＣＴＨ相对不足导致水潴留，低血钠低血渗，形成脑水肿。２、ＳＩＡＤＨ诊断（１）原发病，如脑外伤等。（２）临床表现。（３）化验，这是主要依据。３、ＳＩＡＤＨ的治疗，补充高渗盐水、脱水利尿，限制入量，控制原发病等要综合治疗才能尽快使病情好转。