慢性肺心病并发低钠血症72例分析

目的 探讨慢性肺心病并发低钠血症的发病因素及预防措施。方法 对72例慢性肺心病并发低钠血症患者的临床资料进行回顾性分析。结果 低钠血症发生率为33．3％，合并低渗性脑病者易误诊为肺性脑病。结论 慢性肺心病易并发低钠血症，临床上应提高认识及时纠正。     

慢性肺源性心脏病急性加重期并发低钠血症58例临床分析

慢性肺源性心脏病(肺心病)急性加重期易合并许多并发症,低钠血症是常见的并发症之一,易与肺性脑病混淆.尤其是中、重度低钠血症,因其直接关系到病人特别是重危病人的预后,若不及时诊断和治疗,可明显增加病人的病死率.我科2004年1月-2006年12月,共收治慢性肺心病186例,其中合并低钠血症58例(31.2%),现将其临床资料分析报道如下.     

肺心病合并低渗性脑病46例临床分析

目的探讨肺心病合并低渗性脑病的病因、临床表现及防治措施。方法回顾性分析我院1999年1月～2005年10月确诊的46例肺心病合并低渗性脑病患者的临床资料。结果46例患者中,33例于3～6d内血电解质紊乱逐渐纠正,临床症状逐渐消失;13例（28．26％）经抢救无效死亡。结论肺心病合并低渗性脑病的病因复杂,临床表现无特异性症状,控制原发病,预防并早期治疗低渗性脑病尤其重要。     

慢性重型肝炎低钠血症的临床分析

慢性重型肝炎合并低钠血症临床多见,严重低钠血症可导致脑水肿,诱发或加重肝性脑病,致病情恶化、甚至死亡.严重低钠血症可作为判断预后的一项指标.现将我院2001年至2005年收治的37例慢性重型肝炎合并低钠血症的临床资料进行有关分析.     

肺心病急性加重期并神经精神症状28例临床分析

探讨肺心病急性加重期发生神经神症状的原因，表现及防治措施，方法对２８例肺心病急性加重期患者并神经精神症状进行分析。结果肺脑病最多见（１９例），低钠血症或低渗性脑病（１５例）次之。结论对肺心病急性加重期肺性脑病及低钠血症应予重视。     

肺性脑病并发急性肺梗塞的临床护理

肺心病急性加重期由于缺氧、二氧化碳潴留极易发生 型呼吸衰竭 ,合并肺性脑病时临床上可表现为一系列精神症状。肺心病患者因长期慢性缺氧 ,引起血液红细胞继发性增多 ,血流缓慢 ,导致全血粘度明显增加 ,老年患者常合并脑动脉硬化 ,极易发生脑梗塞。肺心病并发急性脑梗塞多半来势凶猛 ,急需采取有效措施治疗护理。为提高对并发急性脑梗塞的临床认识 ,本文就急性脑梗塞的 5例患者进行临床特点及护理措施探讨 :1　临床资料我科 1999年 10月～ 2 0 0 0年 6月收治肺心病急性加重期合并肺性脑病者 19例 ,其中并发急性脑梗塞 5例。男 4例 ,女 1例…     

慢性肺源性心脏病与低钠血症

肺心病常并发水电解质平衡紊乱,其中又以低钠血症较为多见。国内资料报道,肺心病合并低钠血症发生率接近50％。肺心病合并低钠血症的轻、中度患者多数没有明显的临床症状,不需要特殊处理;而水、电解质重度紊乱的患者则往往出现严重的意识障碍,临床常误诊为肺性脑病,甚至延误治疗。我院1996年至1998年共收治肺心病病人174例,其中合并低钠血症的60例,占肺心病病人的34.5％。总结分析如下。     

老年肺心病并发低渗性脑病患者的护理要点

文献报道36％～43％的肺原性心脏病(肺心病)患者并发低渗性脑病。低渗性脑病的临床表现无特异性，易被临床忽视。1999年12月-2003年12月，我们共收治肺心病合并低渗性脑病患者237例，现将护理体会报告如下。     

肺心病急性发作期合并低渗性脑病40例临床分析

目的对肺心病合并低渗性脑病患者诊断及治疗加以总结,提高对本病的认识。方法从诊断和治疗方面分析1995年1月~2005年6月我科收治的40例肺心病合并低渗性脑病患者。结果40例患者治愈好转34例,死亡6例,存活率达85%。结论肺心病合并低渗性脑病宜早期诊断,积极纠正电解质紊乱,并注意与肺性脑病鉴别。     

老年慢性心力衰竭伴低钠性脑病患者的治疗与预后

目的 探讨老年慢性心力衰竭伴低钠性脑病患者的治疗与预后.方法 对3例不同程度老年慢性心力衰竭伴低钠性脑病患者进行治疗,并分析其预后.结果 30例老年慢性心力衰竭并发低钠性脑病患者,予以慢性心力衰竭标准化治疗、低钠血症标准化治疗和低钠性脑病标准化治疗.结果 心功能治疗有效患者28例,其中显效20例.低钠血症和低钠性脑病治疗使试验室指标恢复正常,以及临床症状消失患者28例.另外2例患者治疗无效,终因顽固性心衰伴重度低钠血症和低钠性脑病死亡.结论 老年慢性心力衰竭伴低钠性脑病患者一旦诊断明确,经及时规范化治疗可获得良好预后.     

以低钠血症为首发表现的肺癌临床分析

目的探讨以低钠血症为首发表现肺癌的临床表现、诊断和治疗。方法分析8例以低钠血症为首发表现肺癌的临床表现、诊断过程和转归。结果难以纠正的低钠血症是SIADH的一大特点，临床表现无特异性。结论当出现难以纠正的低钠血症时，应考虑到肺癌的可能性，应用多种方法明确诊断，以避免漏诊、误诊，早期诊断是治疗本病的关键。     

慢性阻塞性肺疾病急性发作与低钠血症的关系

目的探讨慢性阻塞性肺疾病（COPD）急性发作患者发生低钠血症的病因及治疗的重要性。方法70例COPD住院患者,其中ICU患者加例,普通病房患者50例,观察其血钠情况,可能发生低血钠的原因及酸碱失衡的情况,并分析其中的关系。结果COPD急性发作的ICU患者低钠血症发生率明显高于普通病房,与病情严重程度存在明显的相关性。结论低钠血症病因复杂,与疾病的发展程度及医源性因素有关,在综合治疗原发病的基础上,应定期检测血电解质并给予及时处理,以降低死亡率。     

肺心病急性加重期并发低钠血症49例分析

目的探讨肺心病急性加重期并发低钠血症的发病因素、临床特征及防治措施。方法对49例肺心病急性加重期低钠血症患者的临床资料进行回顾性分析。结果肺心病的低钠血症发生率为31.41%,中、重度低钠血症主要并发混合性电解质异常,并易误诊为肺性脑病。结论应提高对肺心病急性加重期低钠血症的重视。     

小细胞肺癌合并低钠血症的临床特点研究

目的:探讨小细胞肺癌(SCLC)患者合并低钠血症的临床表现及其预后的关系。方法:收集我院2001年1月至2011年12月明确诊断为SCLC患者180例,比较初治时血钠正常患者(A组)与合并低钠血症患者(B组)临床分期、血钠水平、临床症状、病情进展程度和疗效。结果:SCLC合并低钠血症的发生率为12.2%。总体中位生存期是8.89个月,A组患者的1年和2年生存率分别为77.8%(123/158)和22.8%(36/158),而B组患者的1年和2年生存率分别为22.7%(5/22)和4.5%(1/22),2组比较差异有统计学意义(P=0.001 8)。2组SCLC患者血钠值水平存在统计学差异[(142.11±2.12)mmol/L比(111.22±2.67)mmol/L,P0.05];B组出现胸腔积液和多部位转移的比例显著高于A组(54.5%比9.5%和31.8%比8.9%,均P0.05)。结论:SCLC合并低钠血症的发生率为10%左右,并发低钠血症的SCLC患者可能预后更差。     

高龄低钠血症患者的临床特点及防治

目的 探讨高龄低钠血症患者的临床特点及发生原因,为临床防治低钠血症提供理论依据。方法 选择我院老年科住院的80岁以上低钠血症患者(高龄低钠组)33例,分别对其临床特点进行逐项统计,并对其中25例患者进行24 h尿钠排泄量测定。同时选择80岁以上非低钠血症患者(高龄对照组)34例及60-79岁非低钠血症患者(老年对照组)31例同样测定24 h尿钠排泄量作为对照。结果 (1)高龄低钠组患者患冠心病、高血压病及糖尿病的比率高,可能是肾动脉硬化而保钠及保钾能力减退和尿钠排泄增多的原因之一;(2)钠盐摄入不足及高渗混合奶使体内钠过多消耗是导致部分高龄患者发生低钠血症的重要原因之一;(3)大量出汗也是导致低钠血症的原因之一;(4)利尿剂的应用是导致高龄患者发生低钠血症的原因之一。结论 高龄低钠组患者是多因素的综合结果。对不能自由进食的高龄患者应保证足够的钠盐摄入,对有发热多汗及应用利尿剂的患者应适当增加钠盐摄入。     

慢性心力衰竭伴低钠血症患者102例临床分析

目的 探讨3%氯化钠治疗慢性心力衰竭伴低钠血症患者的临床疗效.方法 对102例慢性心力衰竭(纽约心功能分级Ⅲ-Ⅳ级)伴低钠血症患者,给予限水、扩张血管、强心、利尿、血管紧张素转换酶抑制剂/血管紧张素II受体拮抗剂等常规治疗外,同时给予3%氯化钠.比较治疗前后患者的心功能分级、治疗效果及血钠水平.结果 102例患者治疗后,心功能恢复至Ⅰ级39例,心功能恢复至Ⅱ级47例,心功能Ⅲ级11例,心功能Ⅳ级5例.与治疗前心功能Ⅲ级45例,Ⅳ级者57例比较,差异有统计学意义(χ2=150.26,P＜0.05).治疗后显效58例,37例有效,7例无效,总有效率93.1%.治疗后心功能Ⅲ级、Ⅳ级患者的血钠分别(139.4±22.6) mmol/L、(138.2±23.3)mmol/L,与治疗前心功能Ⅲ级、Ⅳ级患者的血钠(122.9±20.5)mmol/L、(120.5±26.8)mmol/L比较,差异有统计学意义(t=2.02、2.04,均P＜0.05).结论 合理利尿、适当补充钠盐有助于减少慢性心力衰竭伴低钠血症患者不良事件的发生,改善患者预后.

Abstract：

Objective To summarize the clinical experience of 3% sodium chloride in treatment of chronic heart failure with hyponatremia. Methods The 102 patients suffering from chronic heart failure with hyponatremia were treated with water limit, vasodilator, cardiotonic, diuretics, angiotensin-converting enzyme inhibitor, angiotensin Ⅱ receptor antagonist and 3% sodium chloride. Cardiac functional capacity classification (NYHA), treatment effect and hyponatremia level were compared between pre- and post- treatment. Results After treatment, heart function was statistically different as compared with that of pre-treatment (χ2=150.26, P＜0.05). The 58 cases showed distinct effect, 37 cases moderate effect, 7 cases no effect, and the percentage of total effect was 93.1%. The hyponatremia of patients with different level of heart function were (139.4±22.6) mmol/L, (138.2±23.3) mmol/L, the difference had a statistics significance compared with pre-treatment hyponatremia which were (122.9±20.5) mmol/L, (120.5±26.8) mmol/L (t=2.02, 2.04, P＜0.05). Conclusions Proper diuresis and sodium salt supplement could help to reduce the malignant risk of the patients suffering from chronic heart failure with hyponatremia and to improve the prognosis.     

The Management of Hyponatremia in Cirrhosis: Should it Be Pharmacologic?

Hyponatremia is a common complication of patients with advanced cirrhosis that is associated with increased morbidity and mortality. Patients with cirrhosis may develop two types of hyponatremia: hypovolemic or hypervolemic hyponatremia. Hypervolemic hyponatremia is the most frequent type of hyponatremia that develops in patients with advanced liver disease and is the consequence of impairment in the renal capacity to eliminate solute-free water. The pathogenesis of these increased solute-free water retention involves several factors, but the most important one is a non-osmotic hypersecretion of vasopressin. The treatment of choice for hypervolemic hyponatremia is fluid restriction. Vaptans, drugs that are selective antagonists of vasopressin V2 receptors, emerged as the first pharmacological treatment of hypervolemic hyponatremia in cirrhosis with promising results. However, satavaptan was withdrawn from development for safety reasons and tolvaptan is not recommended in patients with liver disease. Therefore, currently there is no effective and safe pharmacological approach available for the management of hypervolemic hyponatremia in cirrhosis.     

Hyponatraemia is an independent predictor of in-hospital mortality

BackgroundHyponatraemia increases morbidity and mortality, but the extent to which this condition influences mortality independently of other contributing factors is unclear.Materials and methodsAll hyponatremic patients admitted to the internal medicine department during a six month period were included. Medical records were reviewed and patients' demographics, underlying disease, cause of hyponatremia and in-hospital deaths were noted. Control group consisted of patients with normonatremia admitted to the same department during the same period matched 1:1 by sex, age and underlying disease. Difference in in-hospital mortality rate between the study and control groups was tested by chi-square test. Baseline demographics, underlying diseases, cause of hyponatremia and state of hyponatremia correction as possible risk factors for mortality were tested in a multivariate analysis.ResultsThe baseline cohort of all admitted patients consisted of 2171 patients. Hyponatraemia was found in 278 (13%) patients (160 females and 118 males). The three most common causes of hyponatremia included gastrointestinal loss (52 patients), decreased oral intake (47 patients), and dilution hyponatremia (45 patients). The in-hospital mortality rate in the hyponatremic group was significantly higher compared with the control group (22% vs 7%, respectively; OR 3.75, 95% CI 2.17–6.48, p < 0.0001). In a multivariate analysis age above 65 years, dilution hyponatremia, decreased oral intake as etiologic factors of hyponatremia, and unsuccessful hyponatremia correction were independent factors associated with increased mortality.ConclusionHyponatraemia represents independent factor associated with in-hospital mortality. Age above 65 years, failure to correct hyponatremia and some specific etiologic factors of hyponatremia are related to increased mortality.     

Hyponatremia and SARS-CoV-2 infection: A narrative review

A novel rapid spreading and changing virus called SARS-CoV-2 appeared in Wuhan city in December 2019. It was announced by the World Health Organization (WHO) as a pandemic disease in March 2020. It commonly presents with respiratory symptoms; however, it may be asymptomatic. Electrolyte abnormalities are not uncommon features of SARS-CoV-2 infection. Hyponatremia is one of these electrolyte disturbances among SARS-CoV-2 patients, and it may produce symptoms such as weakness and seizure as the initial presenting symptoms. The underlying mechanism(s) of hyponatremia due to SARS-CoV-2 infection is (are) not established.The aim of this review is to evaluate the possible mechanism of hyponatremia in patients with COVID-19. Understanding and categorizing the hyponatremia in these patients will lead to better treatment and correction of the hyponatremia.A review of the literature between December 2019 and March 2022 was conducted searching for the possible reported mechanism(s) of hyponatremia in SARS-CoV-2.Although SIADH is the commonly reported cause of hyponatremia in SARS-CoV-2 infection, other causes such as diarrhea, vomiting, and kidney salt loss must be considered before SIADH.