口服盐胶囊治疗脑性盐耗综合征患者的护理

对9例脑性盐耗综合征患者进行静脉补钠和口服盐胶囊治疗,结果患者血清电解质紊乱及时纠正.提出严密观察神经系统及低血容量症状,及时监测水、电解质平衡状况;静脉补钠时,注意补液量及速度;口服盐胶囊时,做好健康教育,防止并发症发生,同时动态调整静脉补钠量和口服盐胶囊量是获得满意疗效的关键.     

自制食盐胶囊纠正鞍区肿瘤术后脑性盐耗综合征的效果

目的探讨简便、实用的口服补钠方法,提高患者口服补钠的依从性。方法将60例鞍区肿瘤术后并发脑性盐耗综合征的患者随机分成观察组和对照组各30例。两组均在静脉补钠的基础上每日经口摄入12g食盐,对照组将12g食盐配制成食盐水口服,观察组将12g食盐做成食盐胶囊口服。观察两组患者服盐的口感、口服补盐的依从性及不良反应。结果观察组服盐的口感和依从性显著优于对照组(P<0.05,P<0.01),但胃部灼痛发生率显著高于对照组(P<0.01)。结论食盐胶囊口服补钠的口感好、服用方便,患者口服补钠的依从性高。但在口服盐的过程中要严密观察患者的胃肠道不良反应。     

慢性肾病患者的盐敏感性及限盐干预的临床研究

目的:了解慢性肾病患者盐敏感性特点,使限盐干预个体化,并更趋合理、及时和安全。方法:采用急性口服盐水负荷及速尿排钠缩容试验,对70例无水肿及血压增高的慢性肾病患者及40例健康对照者进行盐敏感性检测,按Sullivan标准判断盐敏感者,并对70例慢性肾病患者实施限盐干预。结果:(1)慢性肾病患者盐敏感检出率显著高于健康受试者(P<0.01)。在慢性肾病患者中,盐敏感检出率还与肾小球滤过功能有关(P<0.05);(2)盐敏感者存在肾脏排钠障碍,且慢性肾病组较健康对照组更为突出(P<0.05);(3)慢性肾病盐敏感者限盐后血压显著降低,并与限盐剂量呈量效关系,而盐不敏感者,未见血压降低。结论:慢性肾病患者在未发生血压增高及水肿时,应检测其盐敏感性,对盐敏感者应及早进行限盐干预,这对慢性肾衰竭(CRF)的早期防治将起到有益的作用,而盐不敏感者,无需严格限盐。     

低钾型周期性麻痹患者心电监护下补钾效果观察

目的探讨以心电监护T波的改变指导低钾型周期性麻痹（HOPP）患者补钾的可行性，以预防和减少高血钾发生。方法将98例HOPP患者随机分为对照组和观察组各49例，遵医嘱口服氯化钾（10ml／h）和静脉补钾（40mmol／h）。观察组T波恢复正常时。停止口服补钾并调慢静脉补钾滴速至10mmol／h；对照组肌力恢复4级时，停止口服和静脉补钾。结果治疗后观察组血钾浓度显著低于对照组（P〈0．05）；高血钾（〉5．5mmol／L）发生率及高钾心电图发生率显著低于对照组（P〈0．05．P〈0．01）。结论心电监护T波的改变可为HOPP患者补钾治疗提供更为科学、更有价值的信息。     

重型颅脑损伤后脑性盐耗综合征12例

目的探讨重型损伤病人并发脑性盐耗综合征的病因、发病机制、诊断及治疗经验。方法回顾性分析重型颅脑损伤后发生脑性盐耗综合征的12例病人，通过其临床表现及实验室指标明确诊断，确定有效的治疗方法。结果经过治疗，10例病人低血钠症状恢复，2例死亡。结论低血钠、高尿钠、低血容量及意识状态改变是脑性盐耗综合征的诊断依据，补液及补盐治疗安全有效。     

急性颈髓损伤后的低钠血症

[目的]探讨急性颈髓损伤后低钠血症的病因、发病机制、诊断和治疗。[方法]回顾性分析2004年-2006年收治的急性颈髓损伤后低钠血症患者15例的临床资料。[结果]全组患者入院24—72h内血钠低于130mmol／L，其中5例低于120mmol／L。14例尿钠40—68mmol／L，1例尿钠为148mmol／L；尿渗透压420～980mmol／L，12例患者经适当的补盐和限制水摄入量治疗，低钠症状2～3周内改善；2例发热患者因发热不能严格限制水摄入，其中1例2个月后恢复，另1例失访；1例患者补盐限水后病情加重，调整治疗方案后恢复。[结论]颈髓损伤越重，损伤后低钠血症发生率越高；颈髓损伤后低钠血症多由抗利尿激素分泌异常综合征引起；血钠浓度，血、尿渗透压等是诊断依据；适当补充钠盐和液体量是有效的治疗方法。     

急性完全性颈髓损伤并发低钠血症的早期有效防治

目的探讨急性完全性颈髓损伤后并发低钠血症的有效预防与治疗。方法采用前瞻性方法,选择自2013-01—2015-05诊治的急性完全性颈髓损伤81例,入院后随机分为2组,A组40例入院后根据体重(以kg为单位)每日需钠量立即给予1/3~1/2量口服补钠,发现低钠血症后给予静脉补钠,以30 ml/h的速度静脉滴注,并根据尿量限制液体入量。B组41例入院后不口服补钠,在发现低钠血症后再行静脉补钠。结果 42例(51.9%)发生低钠血症,其中A组15例(37.5%),B组27例(65.9%);A组低钠血症发生率明显低于B组,差异有统计学意义(χ2=6.520,P=0.011)。发生低钠血症时间距伤后3~15 d,平均9 d;低钠血症持续时间11~25 d,平均18 d。A组意识障碍发生率(χ2=4.419,P=0.036)、血氧饱和度降低发生率(χ2=4.125,P=0.042)、非心源性肺水肿水泡痰发生率(χ2=5.239,P=0.022)明显低于B组,差异有统计学意义(P0.05)。结论急性完全性颈髓损伤可并发严重低钠血症,在颈髓损伤后早期采取预防性干预措施,早期发现及时纠正低钠血症对于改善预后具有极其重要的意义。     

静脉补铁对肾性贫血促红细胞生成素的治疗效果

目的比较静脉补铁与口服补铁对慢性肾脏疾病患者使用促红细胞生成素（EPO）治疗贫血的效果。方法选择58例初次使用铁剂及EPO治疗慢性肾功不全的透析患者。试验前检查每位患者的血红蛋白（Hb）、红细胞比容（Hct）、血清铁（SI）、血清铁蛋白（SF）、总铁结合力（TIBC）、转铁蛋白饱和度（TSAT）。Hct〈33％作为贫血指标。将患者随机分为静脉补铁组（30例）和口服补铁组（28例），静脉补铁组予以低分子右旋糖酐氢氧化铁复合物注射液（科莫非）100mg，每周2次；口服组予以右旋糖酐铁225mg／d。两组均予以EPO10000单位／周，皮下注射。4周后复查上述指标。结果试验结束时，静脉补铁组各项铁参数指标明显高于口服补铁组；静脉补铁组贫血改善较口服服补铁组好，两组Hb和Hct上升有明显差异。结论在使用EPO的同时，静脉补铁较口服补铁能更快、更好地改善肾性贫血。     

多系统萎缩合并抗利尿激素分泌不当综合征患者的护理

对1例多系统萎缩合并抗利尿激素分泌不当综合征患者,给予严格限水、适当补钠、抗感染、降高热等治疗及护理;同时加强安全防护、心理护理及康复训练;强化出院指导。结果患者住院13 d好转出院;随访半年,肺部炎症吸收,膀胱造瘘定期换药,未发生泌尿系感染,体温随环境温度变化波动于38℃左右;长期常规口服盐胶囊。提出针对罕见、复杂疾病患者,兼顾疾病、心理、安全、早期康复训练的综合防护措施是有效治疗的保障。     

颅脑损伤后中枢性低钠血症临床诊治分析

目的探讨中枢性低钠血症的临床诊断及治疗方法。方法回顾性分析48例颅脑损伤后中枢性低钠血症患者的临床资料。结果8例患者因重型颅脑损伤在住院期间2周内死亡,40例患者低钠血症在1—3周内得到纠正。结论中枢性低钠血症包括脑性耗盐综合征和抗利尿激素分泌不当综合征两种类型。其临床表现相似,但处理原则相反。脑性耗盐综合征的治疗原则以补盐、补水、恢复血容量及维持钠的平衡为目的。而抗利尿激素分泌不当综合征的治疗原则是以限制入水量、降低血容量、使血钠恢复正常为目的。     

Salt sensitivity of blood pressure in non-dialysis patients with chronic kidney disease

Background: Chronic kidney disease (CKD) is a world-wide public health problem. Hypertension is both a cause and a complication of CKD, and a risk factor for progression of kidney disease. The effect of salt intake on blood pressure (BP) and the salt sensitivity in non-dialysis patients with CKD were studied. Methods: One hundred and thirty non-dialysis patients with CKD were enrolled in the present study. Daily urinary excretion of sodium (representative of daily sodium intake) and BP was monitored in conditions of original eating habits. Estimated glomerular filtration rate (eGFR) was measured by the creatinine clearance (Ccr). Results: There was a linear positive relationship between the salt intake and systolic blood pressure (SBP) (β?=?0.250, p?=?0.004). It had been found that the log of BP/24-h urinary sodium (salt sensitivity index) had linear relationship with the log of eGFR (β_syst?=??0.364, p?=?0.000, β_diast?=??0.345, p?=?0.000, respectively). Multi-stepwise regression analysis showed SBP was mainly influenced by salt intake and eGFR. There was a negative correlation between diastolic blood pressure (DBP) and age. Conclusion: These results demonstrated a linear relationship between the salt intake and SBP in non-dialysis patients with CKD. The salt sensitivity of BP rose with the decline of renal function.     

Salt and the newborn kidney

Renal function differs in term infants from that in adults, with lower glomerular filtration rate (GFR) and reduced proximal tubular reabsorption of sodium (Na) and water: nevertheless, it is adequate for their needs. This is not true of very preterm infants in whom hyponatraemia is common. Animal studies have shown that Na⁺, K⁺-ATPase and the Na⁺/K⁺ exchanger are poorly expressed at birth with rapid postnatal rises. Cell receptors for hormones that influence tubular Na transport are less numerous in the premature infant than later in life: intracellular second messenger systems may also be immature. The low GFR is due to vasoconstriction and may be necessary to prevent water and electrolyte wasting due to tubular overload. The hyponatraemia of prematurity could, in principle, be due either to Na loss or water excess and can be prevented either by giving additional Na or by restricting water intake. Na supplementation causes relative volume expansion (VE), water restriction volume contraction (VC); this is demonstrated by the effect of the two approaches on weight gain and on the levels of vasoactive hormones in the blood. We argue that moderate VE is more physiological than VC, both in attempting to simulate intrauterine conditions and in consideration of the infant's nutritional needs. The much less common complication of hypernatraemia is usually due to abnormal water loss and should be prevented by increasing water intake appropriately. The above applies to well, preterm babies: sick preterm infants are much more variable in their Na and water requirements than well infants of comparable gestation and weight and each needs an individually tailored regimen based on frequent clinical assessment and laboratory measurement.