鞍区肿瘤术后低钠血症的临床分析

目的 探讨鞍区肿瘤手术后并发低钠血症的病因、发病机制、诊断和治疗方法.方法 回顾性分析我院2004年1月至2008年12月诊治的鞍区肿瘤手术后并发低钠血症21例患者临床资料.结果 19例患者诊断为脑性盐耗综合征,2例诊断为抗利尿激素分泌异常综合征.经相应治疗后,全部患者低钠血症纠正.结论 鞍区肿瘤手术后易发生低钠血症,包括脑性盐耗综合征和抗利尿激素分泌异常综合征,前者主要是补钠和补充血容量,后者需限水治疗.中心静脉压监测对其诊治有指导意义.     

鞍区肿瘤术后低钠血症的临床处理

目的探讨鞍区肿瘤手术后并发尿崩症以及低钠血症的病因、发病机制、诊断、治疗经验。方法回顾分析37例鞍区肿瘤术后尿崩症以及低钠血症患者,通过其临床表现及实验室检查确立诊断,总结有效的治疗方法。结果37例中临床诊断脑性盐耗综合征27例,抗利尿激素分泌异常综合征10例,均恢复良好。结论鞍区肿瘤术后易并发严重的尿崩症及低钠血症,绝大多数为脑性盐耗综合征,应与抗利尿激素分泌异常综合征相区别,抗利尿、补充血容量和补盐治疗效果满意。     

神经外科患者术后低钠血症诊断及治疗

目的:探讨神经外科患者术后低钠血症的常见病因、发病机理、鉴别诊断和治疗方法。方法:回顾性分析180例神经外科术后低钠血症患者的临床表现、实验室检查结果,根据病因分为4种类型并分别采用不同的治疗方法。结果:180例低钠血症患者中营养性或利尿性低钠血症70例,脑性盐耗综合征57例,抗利尿激素分泌异常综合征35例,尿崩症18例。所有患者的低钠血症均得到纠正,取得良好效果。结论:营养性和利尿性低钠血症给予补钠即可,脑性盐耗综合征患者需要补充钠盐,同时补足血容量,抗利尿激素分泌不当综合征患者则需要限水治疗。尿崩症患者应用激素替代治疗。     

中枢性低钠血症42例临床分析

目的探讨中枢性低钠血症的诊断和治疗特点。方法回顾性分析2007年6月至2012年6月收治的42例中枢性低钠血症患者的诊断和治疗资料。结果脑性耗盐综合征35例,抗利尿激素分泌不当综合征7例,治愈41例,1例转院治疗死亡。结论中枢性低钠血症常发生于严重脑外伤及鞍区肿瘤术后的患者,脑性耗盐综合征与抗利尿激素分泌不当综合征临床症状相似,治疗方法不同。严格监测水盐平衡,早期发现和鉴别中枢性低钠血症的分型,及时进行针对性个体化治疗,能有效防止严重的神经系统及循环系统并发症。     

鞍区肿瘤术后并发抗利尿激素异常分泌综合征的诊治

目的 探讨鞍区肿瘤术后并发抗利尿激素异常分泌综合征（SIADH）的病因和发病机制、诊断和鉴别诊断及治疗。方法 对本院神经外科近20年间61例并发SIADH患者进行回顾性临床分析。结果 鞍区肿瘤术后并发SIADH早期，可先出现尿量减少、尿比重升高，易被忽视；增大皮质醇药物剂量或予ACTH，限水补钠等治疗有效。结论 及时发现SIADH有助于此病的及早治疗。     

鞍区肿瘤术后中枢性低钠血症的护理

目的：总结鞍区肿瘤术后中枢性低钠血症的护理经验。方法：对我科近4年鞍区肿瘤术后并发中枢性低钠血症的58例患者护理进行回顾性分析。结果：56例恢复正常，1例死于严重肺部感染，1例自动出院。结论：掌握鞍区肿瘤术后易出现抗利尿激素分泌不当综合征和脑性耗盐综合征两种类型的发病机理和鉴别护理，控制补盐、补液的均衡速度，注意维持血容量及电解质的平衡是护理的关键。     

鞍区肿瘤术后低钠血症的临床处理

目的探讨鞍区肿瘤手术后并发尿崩症以及低钠血症的病因、发病机制、诊断、治疗经验.方法回顾分析34例鞍区肿瘤术后尿崩症以及低钠血症患者,通过其临床表现及实验室检查确立诊断,总结有效的治疗方法.结果除1例患者继发细胞毒性脑水肿、肢体瘫痪、记忆、定向神经功能低下外,其余33例病人恢复良好.结论鞍区肿瘤,特别是垂体肿瘤切除术后易发严重的尿崩症以及低钠血症,绝大多数为脑性耗盐综合征,应与抗利尿激素分泌不当综合征相区别,均匀适度及时地补盐,补充血容量,适度抗利尿治疗效果满意.     

蛛网膜下腔出血并低钠血症60例的常见病因探讨

目的:探讨蛛网膜下腔出血并低钠血症的常见病因.方法:对60例蛛网膜下腔出血并低钠血症的临床资料进行分析.结果:60例低钠血症中因利尿剂使用不慎引起46例,补钠不足7例.脑性盐耗综合征5例,抗利尿激素异常分泌综合征2例.结论:因补钠不足或利尿剂使用不慎引起的低钠血症予补钠即可,抗利尿激素异常分泌综合征引起者应以限水为主,脑性盐耗综合征引起者需采取综合治疗措施.     

脑性盐耗综合征的观察与护理

重型颅脑损伤和鞍区肿瘤术后病人易发生脑性盐耗综合征（CSWS）,临床表现为意识状态改变、低钠血症、高钠尿症、低血容量,这些表现极易于抗利尿激素不适当分泌综合征（SIADH）相混淆,而SIADH的限水治疗与CSWS的补水=补钠疗法相对立,护士必须熟练掌握CSWS的临床观察和实验室检查,密切观察病情变化,定时监测血、尿电解质,渗透压及尿量,尿比重,准确记录24h出入量,为尽早明确诊断提供可靠的临床资料。以便及时有效地予以治疗。     

颅脑损伤后中枢性低钠血症的诊治

目的:分析颅脑损伤并发中枢性低钠血症的临床特点、诊断和治疗。方法:回顾分析近10年收治的25例颅脑损伤后中枢性低钠血症的临床资料。结果:本组抗利尿激素分泌异常综合征11例,治愈8例,死亡3例;脑耗盐综合征14例,治愈12例,死亡2例。结论:抗利尿激素分泌异常综合征和脑耗盐综合征的发病机制、临床表现和治疗都不相同,早期诊断和治疗可以降低病人的死亡率。     

颈髓损伤后水电解质紊乱的临床诊断治疗

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、钾、血浆渗透压、尿量及24ｈ尿钠排出量等资料：23例患者于伤后2－8天出现低钠血症，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 结果 根据血钠水平,经采用控制每日水量、补钠治疗5－14天后，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.     

异基因造血干细胞移植后的抗利尿激素分泌失调综合征

目的提高异基因造血干细胞移植（allo-HSCT）后的抗利尿激素分泌失调综合征（SIADH）的认识,探讨其病因及诊疗方法。方法报道1例慢性粒细胞性白血病患者行allo-HSCT后发生SIADH的诊疗经过。结果患者在移植后第5d发生超急性移植物抗宿主病,予糖皮质激素治疗后控制．移植后第18d出现烦躁、抽搐等中枢神经系统症状,出现严重的低钠血症,并呈进行性下降,血渗透压明显下降,尿钠及尿渗透压明显升高,血渗透压小于尿渗透压,诊断SIADH,予以限制人液量,补充钠盐,及其他对症治疗后血钠有所上升,但中枢神经系统症状无好转,患者家属要求自动出院。结论allo-HSCT后SIADH罕见,起病隐匿,病情发展迅速,早期的正确诊断和治疗有利于改善其预后。     

Citalopram-associated SIADH

OBJECTIVE: To report a case of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with use of citalopram in an elderly male patient and to review the English-language literature for any previous reports of SIADH or hyponatremia caused by citalopram. CASE SUMMARY: An 87-year-old Filipino man was admitted to the hospital reporting malaise, confusion, dizziness, and falls approximately 3 weeks following an increase in his citalopram dosage from 10 to 20 mg/d. On physical examination, the patient was euvolemic and had no evidence of malignancy, cardiac, renal, or hepatic disease. Pertinent laboratory test results revealed hyponatremia, serum hypoosmolality, urine hyperosmolality, and elevated urine sodium concentration, leading to a diagnosis of SIADH. Citalopram was discontinued and fluid restrictions were instituted. The patient was discharged after his serum sodium increased from 122 to 128 mEq/L and he reported increased strength and decreased confusion. Five days after discharge, the patient denied experiencing any new falls, weakness, confusion, or lethargy. His serum sodium measured that day was 131 mEq/L; 2 months later, it was 135 mEq/L. DISCUSSION: We report the seventh case of citalopram-induced hyponatremia published in the English language and the second in a man. Review of the cases demonstrated that the onset of citalopram-induced hyponatremia or SIADH ranged from 6 to 20 days. Potential risk factors for SIADH due to citalopram included advanced age, female gender, concomitant use of medications known to cause SIADH or hyponatremia, and, possibly, higher citalopram doses. CONCLUSIONS: Elderly patients receiving citalopram should be monitored for signs and symptoms of SIADH, especially in the first few weeks of therapy, in the presence of risk factors, and during dose escalation.     

Cerebral salt wasting syndrome

There is significant evidence to show that many patients with hyponatremia and intracranial disease who were previously diagnosed with SIADH actually have CSW. The critical difference between SIADH and CSW is that CSW involves renal salt loss leading to hyponatremia and volume loss, whereas SIADH is a euvolemic or hypervolemic condition. Attention to volume status in patients with hyponatremia is essential. The primary treatment for CSW is water and salt replacement. The mechanisms underlying CSW are not understood but may involve ANP or other natriuretic factors and direct neural influence on renal function. Future investigation is needed to better define the incidence of CSW in patients with intracranial disease, identify other disorders that can lead to CSW, and elucidate the mechanisms underlying this syndrome.     

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.     

中枢性低钠血症的临床鉴别分析

目的分析中枢性低钠血症临床鉴别要点及治疗方法。方法回顾性分析脑外伤及脑出血病程中并发中枢性低钠血症29例患者的临床资料。结果 16例确诊为脑性盐耗综合征(CSWS),13例确诊为抗利尿激素分泌不当综合征(SIADH)。其中CSWS患者经过治疗后11例低钠血症得到纠正,5例死亡;SIADH患者经过治疗后12例低钠血症得到纠正,1例死亡。结论脑外伤及脑出血患者病程中易出现中枢性低钠血症,而CSWS及SIADH是中枢性低钠血症常见的病因,CSWS与SIADH病理机制不同,临床上易延误诊断,由于二者的治疗方法不同,并且直接关系到患者的预后,所以,正确的诊断在临床上非常重要。     

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。     

Comparison of hyponatremia and SIADH frequency in patients with tick borne encephalitis and meningitis of other origin

Aim The aim of the study was the evaluation of frequency and origin of hyponatremia in tick borne encephalitis (TBE) in comparison to non-TBE viral meningitis and bacterial meningitis. Methods A total of 124 patients aged 18–80 years, with TBE were included to the study. The mild form of TBE was diagnosed in 59 patients, while the severe form was diagnosed in 65 patients. The first control group (VMG) consisted of 72 patients with viral meningitis, but excluded TBE. The second control group (BMG) consisted of 16 patients diagnosed with bacterial meningitis. Results Hyponatremia was diagnosed in 55 (44.4%) patients with TBE. In 12 (9.7%) patients (mean age 56.6?±?19.9 years; 9 men, 3 women) syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was diagnosed. In VMG hyponatremia was diagnosed in 7 (9.7%) patients. In the age group?<35 years and in the age group of 50–64 years the frequency of hyponatremia and SIADH was higher in TBE than in VMG (p?Conclusions (1) Hyponatremia is a common disorder in TBE and is more frequent than in other viral types of meningitis, especially in young patients (相似文献