连续性静脉-静脉血液滤过治疗急性严重低钠血症

目的 :探讨应用连续性静脉 静脉血液滤过 (CVVH)治疗急性严重低钠血症 (ASH)的疗效。　 方法 :6例ASH患者 ,基础病变分别为慢性肾功能衰竭 3例 ,急性肾衰 (ARF)、妊娠子痫及骨折手术后各 1例。患者血钠均低于 115mmol/L。采用中心静脉留置导管建立血管通路行CVVH。滤器为AN69及AV60 0各 2例 ,HF12 0 0及FH66各 1例 ,每 2 4h更换一次。应用低分子肝素抗凝。　 结果 :CVVH平均治疗时间为 5 9 7(45 6～ 86)h。CVVH治疗中 ,患者血流动力学稳定 ,存活率 10 0 % ,6例意识模糊 ,其中 5例在治疗 12h后意识有所好转 ,2 4h对疼痛有反应 ,3 6h意识清楚 ;3例嗜睡及谵妄在治疗 2 4h后症状消失 ;1例抽搐在治疗 2 4h后症状消失 ;1例昏迷 96h后神志完全恢复正常 ,视乳头水肿消退 ,视网膜平复 ,一周后视力恢复正常。 6例中 3例转入维持性血液透析 ,3例完全康复。CVVH治疗后 ,6h、2 4h及 48h血Na+ 分别上升至 (115 0± 2 7)mmol/L、(12 9 2± 4 1)mmol/L、(140 3± 1 6)mmol/L ;纠正速度分别为 (2 5± 0 4)mmol/L·h-1、(1 2± 0 1)mmol/L·h-1及 (0 82± 0 10 )mmol/L·h-1。CVVH开始后 6h、2 4h及 48h血渗透质量摩尔浓度分别为 (2 45 0± 5 5 )Osmmol/kg、(2 72 7± 7 1)Osmmol/kg、(2 95 0± 4 2 )Osmmol     

重型颅脑损伤并发中枢性低钠血症的诊断与治疗

目的探讨重型颅脑损伤并发中枢性低钠血症的诊断与治疗方法。方法回顾性分析2005-2008年我科收治的38例重型颅脑损伤并发中枢性低钠血症患者的诊断与治疗方法。结果22例抗利尿激素不适当分泌综合征患者20例血钠恢复正常。2例死于肺部感染。16例脑性盐耗综合征患者15例血钠恢复正常,1例死于颅内感染。结论正确区分脑性盐耗综合征和抗利尿激素分泌不当综合征是保证有效治疗的关键。     

Cost-effectiveness of Tolvaptan for Euvolemic or Hypervolemic Hyponatremia

Purpose

Tolvaptan is clinically effective in increasing serum sodium concentrations for patients with euvolemic or hypervolemic hyponatremia. Appropriate treatment of hyponatremia may reduce the risk of death, hospital resource utilization, and economic burden. The aim of this study was to estimate the cost-effectiveness of tolvaptan treatment in patients who need to be hospitalized for treatment and monitoring of euvolemic or hypervolemic hyponatremia.

Methods

A decision-analytic model was constructed to assess the clinical and economic impact of tolvaptan compared with placebo during a 1-month treatment period. The probabilities, utility weights, resource utilization, and costs in the model were derived from clinical trials, survey research, and the Korean National Health Insurance database. Cost analysis was performed from the perspective of the South Korean health care setting in 2012 Korean won (KRW). The model outcome was the incremental cost per quality-adjusted life-year gained. In addition, subgroup analysis was performed to identify the cost-effectiveness in case of tolvaptan treatment only for patients with marked hyponatremia. Deterministic and probabilistic sensitivity analyses were performed on key model parameters and assumptions.

Findings

The total cost per patient was KRW 1,826,771 for tolvaptan treatment and KRW 2,281,926 for placebo. The quality-adjusted life-years for treatment with and without tolvaptan were 0.0481 and 0.0446, respectively. The base-case analysis revealed that tolvaptan was a more effective and less expensive strategy compared with placebo. In the subgroup analysis, this trend was more apparent in case of tolvaptan treatment only for patients with marked hyponatremia. The robustness of the results was confirmed by using deterministic and probabilistic sensitivity analyses.

Implications

This cost-effectiveness analysis found that the use of tolvaptan was less expensive and more effective than treatment without tolvaptan in patients with euvolemic or hypervolemic hyponatremia.     

急性脊髓损伤患者并发低钠血症的危险因素分析及护理

目的探讨急性脊髓损伤患者并发低钠血症的危险因素,以提供针对性的护理干预措施,提高护理质量,改善患者预后。方法回顾性分析121例确诊为急性脊髓损伤患者,根据有无并发低钠血症将患者分为两组,分析年龄、性别、损伤平面、完全截瘫、损伤严重程度、精神状态、甘露醇使用、激素使用、高热、腹泻、合并感染、合并颅脑损伤及血糖、血钾值等指标对其发生的影响,采用单因素分析和Logistic多元回归分析。结果脊髓损伤患者低钠血症发生率为43.8%,多因素Logistic回归模型分析显示:高热、合并颅脑损伤是低钠血症发生的独立危险因素(P<0.05)。结论高热和合并颅脑损伤是急性脊髓损伤患者并发低钠血症的独立危险因素。应针对危险因素早期加强护理评估和护理干预,降低急性脊髓损伤后低钠血症的发生率。     

中枢性低钠血症的诊断及治疗

目的探讨中枢性低钠血症的诊断及处理方法。方法回顾性分析我院神经外科从1995年1月至2005年2月收治的42例中枢性低钠血症患者的诊断及治疗方法。结果除3例患者因原发性脑干损伤在伤后5d内死亡外,其余患者的低钠血症均在1～4周内得到纠正。结论中枢性低钠血症包括脑性盐耗综合征(CSWS)和抗利尿激素分泌异常综合征(SIADH)两种类型,其临床表现相似,而处理原则相反。CSWS的治疗原则是以补盐、补水达到恢复血容量及维持钠的平衡为目的;SIADH的治疗原则是以限制水入量、降低血容量,使血钠恢复正常为目的。     

慢性重型病毒性肝炎并低钠血症治疗的动态观察

目的 :探讨慢性重型病毒性肝炎患者低钠血症的治疗。方法 :对 4 6例慢性重型病毒性肝炎并低钠血症及腹水患者给予补钠治疗 ,观察血钠、尿钠、腹水钠、2 4h尿量的变化。结果 :随着血钠水平的提高 ,尿钠浓度、2 4h尿量随之提高 ,腹水钠浓度较稳定。结论 :对慢性重型病毒性肝炎低钠血症患者及时足量补钠是重要的辅助治疗措施     

Water Intoxication in a Schizophrenic Patient with Rhabdomyolysis

Abstract: We report a case of water intoxication in a 54-year-old female schizophrenic patient with rhabdomyolysis. She had been admitted to a mental hospital, and treated with spiperone 6 mg daily. On August 3, 1992, the coma following a convulsion occurred. Laboratory data initially showed marked hyponatremia and hypochloremia with decreased serum potassium, and a gradual increase in serum creatine phosphokinase (CPK). The elevation in serum CPK with marked hyponatremia observed in the present patient was probably caused by excessive drinking of water. In this patient, the CPK elevation revealed the rhabdomyolysis.     

Vasopressin, oxytocin, corticotrophin-releasing factor, and sodium responses during fluoxetine administration in the rat

Hyponatremia has been observed in elderly patients treated with the selective serotonin reuptake inhibitor (SSRI) fluoxetine. The pathogenesis of this effect is not known, but enhanced release of vasopressin (VP) and its renal actions may be a possible mechanism. Excess secretion of VP in combination with large fluid intake is known to induce hyponatremia. We determined if chronic fluoxetine administration in association with liberal fluid intake will induce hyponatremia via enhanced release of VP. We used a previously described model in which fluid intake is forced by administering rats a nutritionally balanced liquid diet. Male Sprague-Dawley rats in groups of 10 were randomized to solid and liquid diets, and each diet group administered daily ip injections of fluoxetine (10 mg/kg) or saline for 10 d. Water was given ad libitum to all groups. Daily weight, fluid and food intake, and urine output were measured. On d 10, rats were killed by rapid guillotine decapitation 1–3 h after injection. Trunk blood was collected for measurements of plasma VP and oxytocin (OT) and serum sodium (Na), BUN, creatinine, and glucose. Pituitary glands were assayed for VP and OT content. VP mRNA in the paraventricular and supraoptic nuclei (PVN and SON) and corticotrophin-releasing factor (CRF) mRNA in the PVN were measured by in situ hybridization histochemistry. Fluid intake was significantly higher in groups maintained on liquid vs solid diet (p < 0.0001), as was urine output (p < 0.0001). Fluoxetine-treated rats gained significantly less weight than placebotreated rats (p = 0.01), in keeping with fluoxetine’s anorexigenic properties. However, no significant differences were found among the groups in Na, plasma VP or OT, pituitary VP or OT, or PVN CRF or VP mRNA levels. We conclude that administration of fluoxetine to laboratory rats in the dose and duration used in this study does not significantly affect hypothalamic expression, pituitary stores, or peripheral secretion of VP.     

The Syndrome of Self-Induced Water Intoxication in Psychiatric Patients

Abstract: This is a report on six psychiatric patients who indulged in excessive ingestion of water and subsequently developed tonic-clonic seizures in the course of the underlying mental disorders. On the basis of the DSM-III criteria, they were diagnosed as follows: schizophrenic disorder, 4; schizoaffective disorder, 1; borderline personality disorder, 1. The levels of serum electrolytes were estimated during five episodes of seizures in three patients. Hyponatremia was a consistent finding (serum sodium: mean = 120.6 mEq/liter). Plasma osmolality and plasma levels of arginine vasopressin (AVP) were determined during two episodes in two patients. The inappropriately high circulating levels of AVP relative to plasma hypoosmolality were documented. However, the response to the overnight fluid deprivation and acute water load during the period of no seizures in two patients revealed no evidence of the persistent SIADH, suggesting the temporal association of hyponatremic encephalopathy with inappropriate AVP secretion. It is not conclusive whether the transient SIADH is the cause or the consequence of hyponatremic encephalopathy, although a delusion or an auditory hallucination could play a critical role in drinking water excessively in three patients.     

Atrial natriuretic polypeptide in patients with subarachnoid haemorrhage due to aneurysmal rupture

Summary Measurement of plasma alpha-humanANP (ANP) and antidiuretic hormone (ADH) in 28 cases with aneurysmal subarachnoid haemorrhage (SAH) was carried out, and then compared with control subjects who were infused with hypertonic saline.In cases with hyponatremia (HN), statistical correlation between control subjects and cases without HN was not evident with regards to ANP and plasma osmolality (Posm), excreted fraction of filtrated sodium (FENa) and urinary Na/K. Furthermore, they secreted supernumerarilly in spite of HN.Cases with HN were further subdivided into two groups, they were those cases with negative total sodium balance at the time of appearance of HN, and those cases without total negative sodium balance. In the former, central venous pressure had a tendency to decrease, however, secretion of ANP and ADH was statistically not different in either groups.It appears that ANP regulated urinary sodium excretion against an osmotic or sodium load acts as a maintenance of homeostasis as an osmotic regulator. Cases with HN in which secretion of ADH was physiological, ANP secreted supernumerarilly in spite of hypoosmonaemia and hypovolaemia.Our findings may contribute to a better understanding of the pathophysiological processes leading to hyponatremia in cases with cerebral disorders, and may help to improve the treatment possibilities.