颈髓损伤后水电解质紊乱30例临床分析

目的:探讨颈髓损伤后电解质紊乱的临床特点及诊断治疗。方法:回顾30例颈髓损伤患者(完全性损伤15例,不完全性损伤15例)血压、心率、血清钠、血清钾、血浆渗透压、尿量及24h尿钠排出量等资料。结果:23例患者于伤后2～8d出现低钠血症,其中完全性损伤15例全部出现,发生率100%,1例患者并发抗利尿激素分泌异常综合征。根据血钠水平,经采用控制每日水量、补钠治疗10～21d后,23例均治愈,血钠平均恢复至138(135～142)mmol/L,血浆渗透压、尿钠均正常。结论:低钠血症是颈髓损伤后极为常见的并发症,但并发抗利尿激素分泌异常综合征十分少见;机体内抗利尿激素不适当分泌,导致的稀释性低钠血症可能是颈髓损伤继发低钠血症的发生机制之一。严格控制入液量及补钠为主要治疗方法。     

颅脑损伤并发抗利尿激素分泌异常综合征的临床特点分析

目的 研究颅脑损伤并发抗利尿激素分泌异常综合征的病因、发病机制、临床特点及治疗方法.方法 回顾性分析16例颅脑损伤并发抗利尿激素分泌异常综合征患者的临床表现、实验室检查,分析抗利尿激素分泌异常综合征的临床特点.结果 16例颅脑损伤合并抗利尿激素分泌异常综合征均具有以下临床特点:低钠血症、低血浆渗透压、尿渗透压与血浆渗透压之比＞1.治愈15例,死亡1例.结论 颅脑损伤并发抗利尿激素分泌异常综合征的发病机制与治疗措施不同于低钠血症,早期诊治能降低颅脑损伤患者的病残率和病死率.     

颈髓损伤抗利尿剂激素分泌异常致低钠血症的护理

目的探讨颈髓损伤抗利尿激素分泌异常性低钠血症治疗和护理。方法通过58例颈损伤后抗利尿激素分泌异常综合征低血钠症护理,严格控制液体摄入水量,口服精盐胶囊、静脉补给高渗盐水等治疗。结果58例中46例,经上述治疗症状缓解,血钠、尿钠恢复正常。7例并发肺感染及中枢高热,因病情严重而死亡。5例不能有效控制摄入量,20 d尚恢复。结论及时测定血钠、尿钠,有效地纠正低钠和严密观察病情,严格控制入水量,是治疗颈髓损伤利尿激素分泌异常综合征较有效的方法。     

颈髓损伤抗利尿剂激素分泌异常致低钠血症的护理

目的探讨颈髓损伤抗利尿激素分泌异常性低钠血症治疗和护理.方法通过58例颈损伤后抗利尿激素分泌异常综合征低血钠症护理,严格控制液体摄入水量,口服精盐胶囊、静脉补给高渗盐水等治疗.结果58例中46例,经上述治疗症状缓解,血钠、尿钠恢复正常.7例并发肺感染及中枢高热,因病情严重而死亡.5例不能有效控制摄入量,20 d尚恢复.结论及时测定血钠、尿钠,有效地纠正低钠和严密观察病情,严格控制入水量,是治疗颈髓损伤利尿激素分泌异常综合征较有效的方法.     

颅脑损伤并发抗利尿激素异常分泌综合征临床分析

目的探讨颅脑损伤并发抗利尿激素异常分泌综合征的临床特点和治疗效果。方法选择我院2003年10月至2009年10月颅脑损伤合并抗利尿激素异常分泌综合征患者26例,分析以上患者的临床表现,同时给予补钠治疗。结果本组26例患者经过相应补钠治疗后,意识状态逐渐好转,在1周内血钠浓度开始升高,1个月后,所有血钠均达到正常。随访时间为5个月至1年,血钠恢复正常。根据格拉斯哥预后积分（GOS评分）进行疗效评定：良好14例,中残9例,重残2例,1例因严重肺感染而死亡。结论颅脑损伤后患者出现低钠血症时,及时确定产生低钠血症的原因,给予相应治疗,这是治疗抗利尿激素异常分泌综合征的关键。     

颈髓损伤患者抗利尿激素分泌异常综合征的特征

目的：探讨抗利尿激素分泌异常综合征(SIADH)在颈髓损伤时的发病原因、机制及诊断和治疗。方法：对发生在颈髓损伤中的58例SIADH患者临床资料进行分析总结。实验室检查：血清Na^+&;lt;130mmol／L，其中8例&;lt;120mmol／L，为脊髓损伤严重、年老及病程长者。尿Na^+在37～63mmol／L，其渗透压在410～980mmol／L。结果：58例患者中，51例经增加盐摄入、适量补充盐溶液及严格限制摄水量，低钠血症于伤后两三周恢复；7例因中枢性高热及病情严重，水摄入量不能有效控制，其中2例因病情严重死亡，另5例病情控制缓慢，其中1例患者于伤后9个月后再度出现低钠血症，经治疗后1周内恢复。结论：SIADH的发生率与颈髓损伤程度呈正相关。SIADH的诊断依赖于低钠血症、尿渗透压高于血渗透压、抗利尿激素(ADH)分泌增多、血容量增加。根据其发病特点，严格限制摄水量和及时补充钠盐可以安全有效地治疗本症。     

颅脑损伤并发中枢性低钠血症的诊断和治疗

目的:探讨颅脑损伤并发中枢性低钠血症的病因、发病机制、诊断及治疗方法.方法:对我院2000年1月～2008年6月收治的84例颅脑损伤并发中枢性低钠血症临床资料进行回顾性分析.结果:本组有抗利尿激素异常分泌综合征(SIADH)24例,脑性盐耗综合征(CSWS)60例,血钠均<130 mmol/L,最低107 mmol/L,血浆渗透压<270 mOsm/L,尿钠均>80 mmol/24h.中心静脉压<6 cmH2O 60例,>12 cmH2O 24例.除15例因重度颅脑损伤死于脑功能衰竭外,其余患者低钠血症均得以纠正,治愈时间为2～4周.结论:对颅脑损伤患者应密切监测血钠浓度,SIADH和CSWS发病机制与治疗措施不同,及时正确地诊治可改善预后,降低病死率.     

急性颈髓损伤并发低钠血症的诊治及护理

总结了41例急性颈髓损伤并发低钠血症患者的诊治及护理特点.包括早期密切观察患者的生命体征、意识状态、脱水症状等临床表现;严密监测电解质、血浆渗透压、尿渗透压、尿比重及24 h尿量、抗利尿激素(ADH)、血浆肾素活性、醛固酮等生化指标;及时准确地评估及诊断;给予积极的心理护理、正确的治疗干预.认为早期发现及正确诊治急性颈髓损伤后低钠血症十分重要,应当提高护理人员对低钠血症的认识,积极进行护理干预及正确的治疗对于纠正低钠血症、改善患者的预后尤为关键.     

1例肺癌并发抗利尿激素分泌失调综合征的护理体会

抗利尿激素分泌失调综合征（ syndrome of inappropriate an?tidiuretic hormone，SIADH）是抗利尿激素（ ADH）未按血浆渗透压的调节而分泌异常增多，导致体内水分潴留、尿钠排出增加以及稀释性低钠血症等一系列临床表现的综合征［1］。此综合征最早由Schwartz在1957年报道，随着医学的发展，发现并发SI?ADH的疾病有80多种，其中肺癌是并发SIADH 的常见原因之一。本科室2014年4月14日收治1例肺癌并发SIADH的患者，经过2周多的治疗和护理，患者的病情得到明显缓解，血钠浓度恢复正常。现将护理情况报道如下。     

颈髓损伤患者抗利尿激素分泌异常综合征的特征

目的:探讨抗利尿激素分泌异常综合征(SIADH)在颈髓损伤时的发病原因、机制及诊断和治疗。方法:对发生在颈髓损伤中的58例SIADH患者临床资料进行分析总结。实验室检查:血清Na <130mmol/L,其中8例<120mmol/L,为脊髓损伤严重、年老及病程长者。尿Na 在37～63mmol/L,其渗透压在410～980mmol/L。结果:58例患者中,51例经增加盐摄入、适量补充盐溶液及严格限制摄水量,低钠血症于伤后两三周恢复;7例因中枢性高热及病情严重,水摄入量不能有效控制,其中2例因病情严重死亡,另5例病情控制缓慢,其中1例患者于伤后9个月后再度出现低钠血症,经治疗后1周内恢复。结论:SIADH的发生率与颈髓损伤程度呈正相关。SIADH的诊断依赖于低钠血症、尿渗透压高于血渗透压、抗利尿激素(ADH)分泌增多、血容量增加。根据其发病特点,严格限制摄水量和及时补充钠盐可以安全有效地治疗本症。     

急性颈髓损伤患者的水钠代谢变化及其机制

背景大多数急性颈髓损伤患者可继发严重的水钠代谢紊乱,但其发生机制还不清楚.目的研究急性完全性颈髓损伤患者继发的水钠代谢紊乱及尿中前列腺素PGE 2排出量的相应变化,探讨颈髓损伤患者继发水钠代谢紊乱的发生机制.设计以诊断为依据的病例对照研究.地点、对象和方法实验在北京大学第三医院骨科完成,研究对象为完全性颈髓损伤(CSCI)组患者28例,其中男19例,女9例;年龄(37.14±9.39)岁;对照组为同期骨科住院的非脊髓损伤和急性创伤患者18例,男13例,女5例,年龄(38.11±11.89)岁.检测两组水钠代谢和尿前列腺素PGE2的变化.主要观察指标两组血压心率、血电解质、尿量、液体入量以及尿电解质排出量的变化,尿前列腺素PGE 2的变化.结果CSCI组血Na+浓度[(132.70±3.20)mmol/L]低于对照组(t=2.01,P＜0.01),低钠血症发生率为92.9%;CSCI组尿量(3610±761)mL/d,Na+排出量(473.7±169.4)mmol/d均高于对照组(分别为t=2.01,P＜0.01;t=2.08,P＜0.05);血压、心率均低于对照组(t=2.01,2.01,P＜0.01);24 h尿PGE 2排出量高于对照组(t=2.04,P＜0.01).结论颈髓损伤后交感神经系统抑制,血压降低,肾血流量减少,肾皮质缺血缺氧,继而刺激肾脏前列腺素合成增多,产生利钠利尿作用,可能是颈髓损伤继发低钠血症的发生机制之一.     

颈髓损伤后抗利尿激素分泌异常综合征的护理

目的探讨颈髓损伤抗利尿激素分泌异常综合征(syndrome of inappropriate secretion of antidiuretic hor-mone,SI-ADH)的护理方法。方法回顾性分析山东大学附属省立医院创伤骨科2006年4月至2010年3月收治的20例SIADH患者的临床资料,总结其护理方法。结果 20例SIADH患者血钠浓度为115～130mmol/L,症状持续时间为2～8d。经治疗,18例患者的低血钠症获得及时纠正,血钠水平恢复正常,临床有效率为90%。结论颈髓损伤患者护理中应重视观察血清电解质、尿钠等,对已发生的SIADH首先要明确诊断,并采取及时有效的治疗方法,大多数患者在短期内都可以得到纠正。     

Difference in solute excretion during correction of hyponatremic patients with cirrhosis or syndrome of inappropriate secretion of antidiuretic hormone by oral vasopressin V2 receptor antagonist VPA-985.

VPA-985 is an orally active, competitive vasopressin V(2) receptor antagonist that in normal human beings increases water excretion without affecting solute excretion. Whether solute excretion is affected in patients with hyponatremia resulting from inappropriate secretion of antidiuretic hormone (SIADH) or from cirrhosis treated with VPA-985 is unknown. Six hyponatremic patients with SIADH and 5 hyponatremic patients with cirrhosis with ascitis (CWAs) were treated with 50 or 100 mg VPA-985 twice daily. Evolution of creatinine, urea, uric acid, sodium, potassium, and osmotic clearance were determined. Volume hormones (plasma renin [PR], aldosterone, antidiuretic hormone [ADH], atrial natriuretic factor [ANF]) were also determined before and after treatment. In patients with SIADH, serum sodium concentration (SNa) was generally corrected in 1 day (SNa: 126 +/- 4.5 mmol/L at t = 0 hours and 133 +/- 5.6 mmol/L at t = 24 hours) and associated with a decrease in sodium excretion (from 82 +/- 22 mmol/24 hours to 45 +/- 21 mmol/24 hours; P < 0.05) without modification in potassium excretion. Despite an increase in diuresis (from 0.84 +/- 0.2 ml/min to 1.46 +/- 0.4 ml/min) urea and uric acid clearances decreased. Urine osmolality decreased from 414 +/- 148 mOsm/kg H(2)O to 209 +/- 55 mOsm/kg H(2)O. Volume hormones did not change. In the CWAs the rise of SNa was more progressive (SNa: 126 +/- 2.8 mmol/L at t = H0 to 133 +/- 4.9 mmol/L at t = 48 hours) and parallel to an augmentation in sodium excretion (from 23 +/- 18 mmol/24 hours to 65 6 60 mmol/24 hours the second day of VPA administration). The higher sodium excretion was also connected with a progression in potassium excretion (from 22 6 7 mmol/24 hours to 36 +/- 18 mmol/24 hours). The increase in diuresis under VPA from 0.42 +/- 0.2 mL/min to 1.7 +/- 0.9 mL/min resulted in a higher urea clearance. Urine osmolality decreased from 509 +/- 142 mOsm/kg H(2)O before VPA to 194 +/- 106 mOsm/kg H(2)O after VPA. ADH increased in CWAs treated with VPA, from 1.9 +/- 1.2 pg/mL to 5.3 +/- 2.8 pg/mL (P <.05) while other volume hormones did not change. VPA-985 is a highly effective drug in the short-term management of hyponatremic patients with SIADH or CWAs. SNa correction is associated with urinary sodium retention in SIADH, whereas in CWAs a mild increase in sodium excretion is observed.     

手术治疗无骨折脱位颈脊髓损伤合并抗利尿激素分泌失调综合征的疗效观察

[目的]探讨手术治疗无骨折脱位颈脊髓损伤合并抗利尿激素分泌失调综合征(syndrome of inappropriate secretion of antidiuretic hormone,SIADH)的疗效.[方法]回顾性分析2010年9月至2014年9月本院骨科诊治的26例无骨折脱位颈脊髓损伤患者,术前患者Frankel分级:A级12例,B级及以下14例.所有患者均接受椎管减压手术治疗,采用Franke脊髓损伤分级及日本骨科协会评分(Japanese Orthopaedic Association Scores,JOA)评估脊髓损伤程度,并观察伤后并发SIADH的时间及疗效.[结果]26例患者均获得随访,随访时间26(12～37)个月,末次随访时Frankel分级:A级8例,B级及以下18例;末次随访时JOA评分为(11.6±3.1)分,JOA评分改善率为78.2％.患者出现SIADH的时间为伤后(4～10)d,恢复时间为(28.4±13.8)d.[结论]手术治疗无骨折脱位颈脊髓损伤患者安全可靠,但围手术期并发的SIADH应重视,补钠并控制入液量能有效地治疗SIADH.     

Etiology and management of hyponatremia in neurosurgical patients

Hyponatremia is the most common electrolyte disorder encountered in neurosurgical patients. The aggressive treatment of hyponatremia in this group is critical, as hyponatremia can lead to mental status changes, seizures, vasospasm, cerebral edema, and even death. When it occurs, it represents a failure of one of several homeostatic mechanisms that tightly regulate serum sodium. In these patients, hyponatremia is most commonly due to the syndrome of inappropriate antidiuretic hormone (SIADH) or cerebral salt wasting (CSW). It can be problematic to differentiate between these 2 as they share key features, including low serum sodium, low serum osmolality, a higher urine osmolality than serum osmolality, and an elevated urinary sodium concentration. Furthermore, distinctions between CSW and SIADH, namely extracellular fluid (ECF) volume and total sodium balance, are often difficult to establish. Syndrome of inappropriate antidiuretic hormone is characterized by a volume-expanded state, whereas CSW is characterized by a volume-contracted state. Determining the exact cause remains a clinical imperative as the treatment for each is different. The rate at which serum sodium is corrected must be attended to, as rapid shifts in serum sodium pose potential risk of cerebral pontine myelinolysis.     

男性急性颈髓损伤病人的水钠代谢紊乱及相关激素变化

目的研究男性急性完全性颈髓损伤患者继发的水钠代谢紊乱及有关的内分泌变化,探讨颈髓损伤继发低钠血症的发生机制。方法男性颈髓损伤组(简称男性CSCI组)19例,男性对照组14例,研究其水钠代谢变化,放免检测血浆肾素活性(PRA)、抗利尿激素(ADH)浓度及血清睾丸酮浓度。结果与对照组比较,男性CSCI组血钠浓度降低,此外还有多尿、尿钠排出增多以及液体入量低于尿量等变化(P<0.05);CSCI组PRA、血浆ADH及血清睾丸酮浓度均低于对照组。结论男性颈髓损伤患者其伤后血清睾丸酮浓度下降,可能对其继发性的低钠血症有一定的促发作用。     

颅脑损伤并发抗利尿激素异常分泌综合征机制和临床分析

目的：探讨颅脑损伤并发抗利尿激素异常分泌综合征（SIADH）机制。临床特征及治疗转归。方法：回顾分析总结1992年1月-2001年2月我院收治的23例颅脑损伤并发SIADH资料，23例均有临床表现，CT及实验室检查完整资料。结果：23例均有不同程度的脑挫裂伤和低钠，低氯血症，低渗血症及高尿钠症，其中19例早期诊断，预后好，4例误诊误治，预后差。结论：SIADH是由于下丘脑直接或间接损伤所致，临床特征为难以纠正的低钠，低渗血症，治疗关键是严控摄入水量。适量补盐，将血钠控制在安全水平（125mmol/L)以上。     

SIADH and hyponatremia with theophylline

OBJECTIVE: To report a case of possible theophylline-induced hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH). CASE SUMMARY: An 88-year-old man developed severe symptomatic hyponatremia (serum sodium 112 mEq/L) associated with inappropriate natriuresis (urinary sodium 58 mEq/L) temporally related to the initiation of theophylline. The patient fulfilled the criteria for the diagnosis of SIADH after all other causes of hyponatremia were excluded. Furthermore, no other drugs or conditions that could have evoked SIADH were found. DISCUSSION: Theophylline has rarely been associated with hyponatremia. A thiazide-like action of the drug on the stimulation of SIADH could be the underlying mechanism for SIADH. CONCLUSIONS: Theophylline should be considered as a possible cause of hyponatremia.     

Management of hyponatremia

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.     

Tolvaptan for the treatment of hyponatremia secondary to the syndrome of inappropriate antidiuretic hormone secretion

Hyponatremia is prevalent in hospitalized patients and predicts a poor prognosis. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is perceived as one of the most frequent causes of hyponatremia. Traditionally, chronic hyponatremia has been treated with fluid restriction and demeclocycline. However, these treatment options have been unsatisfactory due to problems with treatment compliance and/or safety concerns. In recent years, several vasopressin-receptor antagonists, the vaptans, were introduced into clinical practice. One of these vaptans – tolvaptan – is an oral vasopressin V2-receptor antagonist that induces free water excretion without increasing sodium excretion. Few studies have assessed the role of vaptans in treating hyponatremia in a population with only SIADH. Current data shows that vaptans may safely correct mild or moderate hyponatremia in patients with SIADH. However, further clinical trials are needed to determine the optimal dosing, proper monitoring and adequate precautions for the use of vaptans in this patient population.