颅脑肿瘤术后电解质及皮质醇激素改变的临床分析
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摘要
目的分析颅脑肿瘤手术后连续5天水电解质尤其是血钠的改变,皮质醇(cortisol)及促肾上腺皮质激素(ACTH)的改变,探讨低钠血症的发生率及其严重程度、术后皮质醇功能障碍与肿瘤类型、手术方式及年龄的相关性。
方法对2010年5月～2012年1月入住中南大学湘雅医院神经外科颅脑肿瘤患者的临床资料进行回顾性分析。收集进行了术前术后电解质和皮质醇检测的242例病例,术前血钠、皮质醇及ACTH均在正常范围内,术后第1天～术后第5天每日监测电解质,连续监测5天,术后在使用任何皮质醇激素类药物之前测血皮质醇及ACTH,并进行术前与术后皮质醇及ACTH的比较。所有病例记录24小时尿量及术后的补液方式,部分术后低钠血症的病例,为指导治疗进行中心静脉压(CVP)的测定。
结果242例颅脑肿瘤患者中出现术后低钠血症者为119例,占总人数的49.17%。肿瘤类型、手术方式及年龄可影响术后低钠血症的发生率,但不能影响术后低钠血症的严重程度,术后低钠血症发生的高峰时间在不同类型肿瘤之间并无明显差别,大约在术后第3.88±1.116天。术后皮质功能障碍的发生率为59.4%,术后皮质功能障碍在不同颅脑肿瘤类型之间有显著性差异,开颅手术皮质功能障碍的发生率(68.30%)高于经鼻蝶鞍区肿瘤切除术(52.00%),但无统计学意义(P=0.058),不排除样本量不足所致。
结论颅脑肿瘤术后易发生低钠血症和皮质功能障碍,<20岁颅咽管瘤行开颅手术的患者最易发生低钠血症,不同年龄患者因不同类型颅脑肿瘤行不同方式的手术后,低钠血症的严重程度均一致,低钠血症病例中部分可出现抗利尿激素分泌不恰当综合征(SIADH)和脑耗盐综合征(CSWS),进行中心静脉压以及尿渗透压的测定可予以鉴别。若诊断为SIADH,予以限液治疗,若为CSWS,治疗上则以补充血容量及补钠为主。开颅手术术后皮质功能障碍发生率较经鼻蝶鞍区切除术高,但无统计学意义,治疗上予以补充ACTH或外源性糖皮质激素。
Objective To analyze the electrolyte after brain tumor surgery for five days, especially the change of serum sodium, cortisol and ACTH, discuss the incidence of hyponatremia, the severity of hyponatremia and the correlation with tumor type, surgical approach and age.
Method To retrospective analyzed the data of patients with cerebral tumor who admitted to the Central South University of XiangYa Hospital neurosurgery in May2010to January2012.242cases had done the preoperative and postoperative electrolyte and cortisol testing. Preoperative serum sodium monitoring was all normal, the cortisol and ACTH within the normal range. Monitoring electrolyte in the postoperative1-5days continuously. Monitoring serum cortisol and ACTH before used any cortisol drug. Every patient should note the24hours urine volume and the fluid replacement way after operation. In some postoperative hyponatremia cases, central venous pressure determination was used to guide the treatment.
Result119cases were diagnosed of postoperative hyponatremia in242cases of patients with brain tumor, accounting for49.17%of the total number of people. The type of cerebral tumor, surgical procedure and age produced an effect on the occurrence of postoperative hyponatremia, but not the severity of hyponatremia. There was no significant difference between the several types of cerebral tumor in the peak time of postoperative hyponatremia, about in the3.88±1.116th day after operation. The occurrence of postoperative cortical dysfunction was59.4%. The cerebral tumor type can influence the postoperative cortex dysfunction. The incidence of cortical dysfunction for craniotomy(68.30%) is higher than nose sellar tumor resection(52.00%), but no statistical significance(P=0.058). The reason is lack of sample size.
Conclusion Hyponatremia and cortical dysfunction are easily happened after cerebral tumor surgery. The patients with craniophary-ngioma who are younger than20years old used craniotomy are more likely to get hyponatremia. The patients with different ages using the different surgical methods to treat the different types of cerebral tumor, the severity of hyponatremia is consistent. Some cases of hyponatremia is SIADH and CSWS, according to the postoperative blood volume and the balance of sodium metabolism to identify. If it is SIADH, limit the amount of liquid intake to treat this condition. Add volume and sodium can correct CSWS. The craniotomy is more likely to cause cortical dysfunction, but there is no statistical significance. The treatment is ACTH or exogenous glucocorticoid.
方法对2010年5月～2012年1月入住中南大学湘雅医院神经外科颅脑肿瘤患者的临床资料进行回顾性分析。收集进行了术前术后电解质和皮质醇检测的242例病例,术前血钠、皮质醇及ACTH均在正常范围内,术后第1天～术后第5天每日监测电解质,连续监测5天,术后在使用任何皮质醇激素类药物之前测血皮质醇及ACTH,并进行术前与术后皮质醇及ACTH的比较。所有病例记录24小时尿量及术后的补液方式,部分术后低钠血症的病例,为指导治疗进行中心静脉压(CVP)的测定。
结果242例颅脑肿瘤患者中出现术后低钠血症者为119例,占总人数的49.17%。肿瘤类型、手术方式及年龄可影响术后低钠血症的发生率,但不能影响术后低钠血症的严重程度,术后低钠血症发生的高峰时间在不同类型肿瘤之间并无明显差别,大约在术后第3.88±1.116天。术后皮质功能障碍的发生率为59.4%,术后皮质功能障碍在不同颅脑肿瘤类型之间有显著性差异,开颅手术皮质功能障碍的发生率(68.30%)高于经鼻蝶鞍区肿瘤切除术(52.00%),但无统计学意义(P=0.058),不排除样本量不足所致。
结论颅脑肿瘤术后易发生低钠血症和皮质功能障碍,<20岁颅咽管瘤行开颅手术的患者最易发生低钠血症,不同年龄患者因不同类型颅脑肿瘤行不同方式的手术后,低钠血症的严重程度均一致,低钠血症病例中部分可出现抗利尿激素分泌不恰当综合征(SIADH)和脑耗盐综合征(CSWS),进行中心静脉压以及尿渗透压的测定可予以鉴别。若诊断为SIADH,予以限液治疗,若为CSWS,治疗上则以补充血容量及补钠为主。开颅手术术后皮质功能障碍发生率较经鼻蝶鞍区切除术高,但无统计学意义,治疗上予以补充ACTH或外源性糖皮质激素。
Objective To analyze the electrolyte after brain tumor surgery for five days, especially the change of serum sodium, cortisol and ACTH, discuss the incidence of hyponatremia, the severity of hyponatremia and the correlation with tumor type, surgical approach and age.
Method To retrospective analyzed the data of patients with cerebral tumor who admitted to the Central South University of XiangYa Hospital neurosurgery in May2010to January2012.242cases had done the preoperative and postoperative electrolyte and cortisol testing. Preoperative serum sodium monitoring was all normal, the cortisol and ACTH within the normal range. Monitoring electrolyte in the postoperative1-5days continuously. Monitoring serum cortisol and ACTH before used any cortisol drug. Every patient should note the24hours urine volume and the fluid replacement way after operation. In some postoperative hyponatremia cases, central venous pressure determination was used to guide the treatment.
Result119cases were diagnosed of postoperative hyponatremia in242cases of patients with brain tumor, accounting for49.17%of the total number of people. The type of cerebral tumor, surgical procedure and age produced an effect on the occurrence of postoperative hyponatremia, but not the severity of hyponatremia. There was no significant difference between the several types of cerebral tumor in the peak time of postoperative hyponatremia, about in the3.88±1.116th day after operation. The occurrence of postoperative cortical dysfunction was59.4%. The cerebral tumor type can influence the postoperative cortex dysfunction. The incidence of cortical dysfunction for craniotomy(68.30%) is higher than nose sellar tumor resection(52.00%), but no statistical significance(P=0.058). The reason is lack of sample size.
Conclusion Hyponatremia and cortical dysfunction are easily happened after cerebral tumor surgery. The patients with craniophary-ngioma who are younger than20years old used craniotomy are more likely to get hyponatremia. The patients with different ages using the different surgical methods to treat the different types of cerebral tumor, the severity of hyponatremia is consistent. Some cases of hyponatremia is SIADH and CSWS, according to the postoperative blood volume and the balance of sodium metabolism to identify. If it is SIADH, limit the amount of liquid intake to treat this condition. Add volume and sodium can correct CSWS. The craniotomy is more likely to cause cortical dysfunction, but there is no statistical significance. The treatment is ACTH or exogenous glucocorticoid.
引文
[1]姚冰,王丽丽,等.颅脑肿瘤术后低钠血症89例临床分析.辽宁医学杂志,2007,21(5)：298-230
[2]廖二元.内分泌代谢病学.人民卫生出版社,2012,5
[3]宋泓敏,李栋友,等.低钠血症80例临床分析.中国全科医学,2006,9,(12)：1019-1020
[4]曾剑平,张国斌,林志雄,等.儿童颅咽管瘤全切术后并发症的诊治.中国神经肿瘤杂志,2011(03)
[5]漆松涛,陈状,方陆雄,等.颅咽管瘤全切术后钠代谢紊乱及处理.中国临床神经外科杂志,2004(03)
[6]黄小平,陈建良,张清平,等.脑胶质瘤146例手术效果及预后因素分析.中国神经肿瘤杂志,2006(03)
[7]郭芳,王亚东,陈劲草.开颅术后低钠血症的治疗。中国临床神经外科杂志,2007(64)
[8]王建华,邵明海。颅内肿瘤1628例临床分析。医师进修杂志,2005(16)
[9]周国胜,张新中.鞍区肿瘤的显微手术治疗进展.新乡医学院学报,2005,2(22)：174-176
[10]Yamaki T, Tano oka A, Takahashi A, et al. Cerebral salt wasting syndrome distinct from the syndrome of inappropriate secretion of antidiuretie hormone(SIADH)[J]. Acta Neurochir,1992.115 (3-4):15-162
[11]Schwartz WB, Bennett W, Curelop S, et al. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone.Am J Med,1957.23:527
[12]Gonzales-Portillo G, Tomita T. The syndrome of inappropriate secretion of antidiuretic hormone:an unusual presentation for childhood craniopharyngioma: report of three cases [J].J Neurosurg,1998.42(4):917-921
[13]陆永建,李明昌.重型颅脑损伤和术后中枢性低钠血症及相关激素的分泌异常[J].中华神经医学杂志,2005.4(4)：424-426
[14]Nelson PB, Seif SM, Maroon JC, et al. Hyponatremia in intracranial disease: perhaps not the SIADH.J Neurosurg,1981.55:938
[15]Ciiper WC, Green IJ, Wang S, Cerebral salt wasting associated with Guillain-Bsrr syndrome. Arch Intern Med,1965.116:113
[16]Goldbery M, Handler JS. Hyponatremia and renal wasting of sodium in patients with malfunction of the central nervous system. N Engl J Med,1960.263:1037
[17]Roca-Ribas F, Ninno JE, Gasperin A, et al. Cerebral salt wasting syndrome as a postoperative complication after surgical resection of acoustic neuroma[J]. Otol Neurotol,2002.23:992-995.
[18]Harrigan MR. Cerebral salt wasting syndrome [J].Crit Care Clin,2001. 17(1):125-138
[19]Yamamoto N, Miyamoto N, Seo H, et al. Hyponatremia with high plasma ANP level-report of two cases with emphasis on the pathophysiology of cerebral salt wasting. No-Shinkei-Geka,1987.15:1019
[20]De Bold AJ, Borenstein HB, Veress AT, et al. A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats.Life Sci, 1981.28:89
[21]sotani E, Suzuki R, Tomita K, et al. Alterations in plasma concen-trations of natriuretic peptides and antidiuretic hormone after subarachnoid hemorrhage[J].Stroke,1994.25:2198-2203
[22]姚国杰,龚杰,马廉亭,等.重型颅脑损伤后脑性盐耗综合征20例.中华创伤杂志,1999.15(4)：269
[23]Dibona GF. Neural Control of renal function in health and disease.Clin Auton Res,1994.4:69
[24]Ishikawa S, Saito T, Kaneko K, et al. Hyponatremia responsive to fludrocortisone acetate in elderly patients after head injury [J].Ann Intern Med, 1987.106:187-191.
[25]张天锡.颅脑损伤.见：江基尧,朱诚,主编.现代颅脑损伤学.上海：第二军医大学出版社,1999.403-404
[26]Steele A, Gowrishankar K, Abrahson S, et al. Postoperative hyponatremia despite near-isotonic saline infusion:a phenomenon of desalination[J].Ann Intern Med,1997.126:20-25
[27]Streefkerk JO, Zwieten PA, Vasopressin receptor antagonists:pharmacological tools and potential therapeutic agents. Auton Autacoid Pharmacol,2006.26: 141-148
[28]Gowrishankar M, Lin SH, Mallie JP, et al. Acute hyponatremia in the perioperative period:insighs into its pathophysiology and recommendations for management[J]. Clin Nephol,1998.50:352-360
[29]戴炯,李善泉.颅脑手术后并发脑性盐耗损综合征的诊疗分析.上海第二医科大学学报,2004,24(12)：1053-1055
[30]陈瑛,刘建民,赵红燕,等.急性肾上腺皮质功能减退症伴低钠血症的临床分析.上海交通大学学报(医学版),2008,3
[1]Elhassan EA, Schrier RW. Disorders of extracellular volume. In:Floege J, Johnson RJ, Feehally J, eds. Comprehensive clinical nephrology,2010.85-99
[2]Hoorn EJ, Lindemans J, Zietse R. Development of severe hyponatraemia in hospitalized patients:treatment-related risk factors and inadequate management. Nephrol Dial Transplant,2006.21(1):70-76
[3]Goh KP. Management of hyponatremia. Am Fam Physician,2004. 69(10):2387-2394
[4]Anderson R.J. Hospital acquired hyponatraemia. Kidney International,1986. 29:1237-1247
[5]Upadhyay A, Jaber BL, Madias NE. Incidence and prevalence of hyponatremia. Am J Med,2006.119(7):30-35
[6]Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta,2003.337:169-172
[7]Siregar P. The risk of hyponatremia in the elderly compared with younger in the hospital inpatient and outpatient. Acta Med Indones,2011.43(3):157-160
[8]Baylis P.H. Thompson C.J. Osmoregulation of vasopressin secretion and thirst in health and disease. Clinical Endocrinology,1988.29:549-576
[9]McKenna K. Thompson C.J. Osmoregulation in clinical disorders of thirst appreciation. Clinical Endocrinology,1998.49:139-152
[10]Kokko J.P. Rector F.C. Countercurrent multiplication system without active transport in inner medulla:new model. Kidney International,1972.2:214-223
[11]Nielsen S, Agre P. The aquaporin family of water channels in kidney. Kidney International,1995.48:1057-1068
[12]Knepper M.A, Wade J.B, Terris J, et al. Renal aquaporins. Kidney International, 1996.49:1712-1717
[13]Nielsen S, Marples, D, et al. Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. Proceedings of the National Academic Sciences of the U.S.A,1995.92:1013-1017
[14]Lankford S.P, Chou C-L, et al. Regulation of collecting duct water permeability independent of cAMP-mediated AVP response. American Journal of Physiology,1991.261:554-F566
[15]DiGiovanni S.R, Nielsen S, et al. Regulation of collecting duct water channel expression by vasopressin in Brattleboro rats. Proceedings of National Academic Sciences of the U.S.A,1994.91:8984-8988
[16]Ecelbarger C, Nielsen S, et al. Role of renal aquaporins in escape from vasopressin induced antidiuresis in rat. Journal of Clinical Investigation,1997. 99:1859
[17]Yamanoto N, Miyamoto N, et al. Hyponatraemia with high plasma atrial natriuretic peptide levels. Report of two cases with emphasis on the pathophysiology of cerebral salt wasting syndrome. Neurologica Surgica,1987. 15:1019-1023
[18]Berendes E, Walter M, Cullen P. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid hemorrhage. Lancet,1997.349:245
[19]Beck T.R, Dunn M.J. The relationship of vasopressin and renal prostaglandins. Mineral and Electrolyte Metabolism,1981.6:46-59
[20]Inoue M, Crofton J.T, Share L. Interactions between brain acetylcholine and prostaglandins in control of vasopressin release. American Journal of Physiology,1991.261:420-426
[21]Carney S, Morgan T, Ray C, Thompson L. Effect of calcitonin on urine concentration in the rat. American Journal of Physiology,1983.244:432-435
[22]DeRouffignac C, Elalouf J.M. Effects of calcitonin on the renal concentrating mechanism. American Journal of Physiology,1983.245:506-511
[23]Elalouf J.M. Sari D.C. Effects of glucagon and parathyroid hormone on the loop of Henle of rat juxtamedullary nephrons. Kidney International,1986. 29:807-813
[24]Mandell I.N, DeFronzo R.A, Robertson G.L. Role of plasma vasopressin in the impaired water diuresis of isolated glucocorticoid defficiency in the rat. Kidney International,1980.17:186-195
[25]Oelkers W. Hyponatraemia and inappropriate secretion of antidiuretic hormone in patients with hypopituitarism. New England Journal of Medicine,1989. 321:492
[26]Kimura T, Ota K, et al. Plasma vasopressin and atrial natriuretic hormone levels in hypopituitarism with and without hydrocortisone treatments:responses to an acute water load. Acta Endocrinologica Copenhagen,1992.126:217-223
[27]Elhassan EA, Schrier RW. Disorders of extracellular volume. In:Floege J, Johnson RJ, Feehally J, eds. Comprehensive clinical nephrology.4th ed. St. Louis:Elsevier Saunders,2010.85-99
[28]Andersen R.J, Chung H.M, Kluge R, Schrier R.W. Hyponatraemia:a prospective analysis of its epidemiology and the pathogenetic role of vasopressin. Annals of Internal Medicine,1985.102:164-168
[29]Katz M.A. Hyperglycaemia induced hyponatraemia ± calculation of expected serum sodium depression. New England Journal of Medicine,1973. 289:843-844
[30]Sonnenblick M., Friedlander Y, Rosin A. Diuretic induced hyponatraemia. Chest,1993.103:601-606
[31]VanAssen S, Mudde A.H. Severe hyponatraemia in an amiloride/ hydrochlorothiazide-treated patient. Netherlands Journal of Medicine,1999. 54:108-113
[32]Ishikawa S, Kim J.K, Schrier R.W. Effects of arginine vasopressin antidiuretic and vasopressor antagonists in glucocorticoid and mineralocorticoid deficient rats. In:Schrier R.W, eds. Vasopressin,1995.171-180
[33]Peters J.P, Welt K.G., et al. A salt wasting syndrome associated with cerebral disease. Transactions of the Association of American Physiology,1950. 63:57-64
[34]Bartter F.C, Schwartz W.B. The syndrome of inappropriate antidiuretic hormone. American Journal of Medicine,1967.42:790-806
[35]Tomida M, Muraki M, Uemura K, Yamasaki K. Plasma concentration of brain natriuretic peptide in patients with subarachnoid hemorrhage. Stroke,1998. 8:1584-1587
[36]Damaraju S.C, Rajshekhar V, Chandy M.J. Validation study of a central venous pressure-based protocol for the management of neurosurgical patients with hyponatraemia and natriuresis. Neurosurgery,1997.40:312-317
[37]Schrier R.W, Fassett R.G. Pathogenesis of sodium and water retention in cardiac failure. Renal Failure,1998.20:773-781
[38]Schrier R.W, Martin P.Y. Recent advances in the understanding of water metabolism in heart failure. Advances in Experimental Medicine and Biology, 1998.449:415-426
[39]Abraham W.T, Lauwaars M.E, Kim J.K, Pena R.L, Schrier R.W. Reversal of atrial natriuretic peptide resistance by increasing distal tubular delivery in patients with decompensated cirrhosis. Hepatology,1995.22:737-743
[40]Villarreal D, Freeman R.H. Atrial natriuretic factor and the renin-angiotensin system in the regulation of sodium balance:longitudinal studies in experimental heart failure. Journal of Laboratory and Clinical Medicine,1991.118:515-522
[41]Moe G.W, Forster C, DeBold A.J, Armstrong P.W. Pharmacokinetics hemodynamic, renal and neurohormonal effects of atrial natriuretic factor in experimental heart failure. Clinical Investigative Medicine,1990.13:111-118
[42]Martin P.Y, Schrier, R.W. Pathogenesis of water and sodium retention in cirrhosis. Kidney International,1997.51:43-49
[43]Asahina Y, Izumi N, Enomoto N, Sasaki S, Fushimi K, Marumo F. Increased gene expression of water channel in cirrhotic rat kidneys. Hepatology,1995. 21:169-173
[44]Xu D.L, Martin P.Y, Ohara M, et al. Upregulation of aquaporin water channel expression in chronic heart failure in rats. Journal of Clinical Investigation, 1997.99:1500
[45]Montengro J, Gonzalez O, Saracho R, Aguirre R, Gonzalez O, Martinez I. Changes in renal function in primary hypothyroidism. American Journal of Kidney Disease,1996.27:195-198
[46]Skowsky W.R, Kikuchi T.A. The role of vasopressin in the impaired water excretion of myxedema. American Journal of Medicine,1978.64:613
[47]Ojamaa K, Balkman C, Klein, I. Acute effects of triiodothyronine on arterial smooth muscle cells. Annals of Thoracic Surgery,1993.56:61
[48]Raff H. Interactions between neurohypophysial hormones and the ACTH±adrenocortical axis. Annals of the New York Academy of Sciences, 1993.689:411-425
[49]Erkut Z.A, Pool C, Swaab D.F. Glucocorticoids suppress corticotropin releasing hormone and vasopressin expression in human hypothalamic neurons. Journal of Clinical Endocrinology and Metabolism,1998.83:2066-2073
[50]Mora A, Enriquez R, Lacueva F, Gonzales E. Severe hyponatraemia and hypopituitarism. Nephron,1995.70:139-140
[51]Kamoi K, Ebe T, Kobayashi O, et al. Atrial natriuretic peptide in patients with the syndrome of inappropriate antidiuretic hormone secretion and with diabetes insipidus. Journal of Clinical Endocrinology and Metabolism,1990. 70:1385-1390
[52]Shimizu K, Nakano S, et al. Ectopic atrial natriuretic peptide production in small cell lung cancer with the syndrome of inappropriate antidiuretic hormone. Cancer,1991.68:2284-2288
[53]Gross A.J, Steinberg S.M, et al. Atrial natriuretic factor and arginine vasopressin production in tumor cell lines from patients with lung cancer and their relationship to serum sodium. Cancer Research,1993.53:67-74
[54]Satchell S.C, Connaughton M. Inappropriate antidiuretic hormone secretion and extreme rises in creatinine kinase following MDMA ingestion. British Journal of Hospital Medicine,1994.51:495
[55]Holden R., Jackson M.A. Near fatal hyponatraemic coma due to vasopressin oversecretion after ecstasy. Lancet,1996.347:1052
[56]Verbalis J.G. Adaptation to acute and chronic hyponatraemia:implications for symptomatology, diagnosis and therapy. Seminars in Nephrology,1998. 18:3-19.
[57]Sterns R.H, Baer J, Ebersol S, Thomas D. Organic osmolytes in acute hyponatraemia. American Journal of Physiology,1993.264:833-836
[58]Ayus J.C, Wheeler J.M, Arieff A.I. Postoperative hyponatraemic encephalopathy in menstruant women. Annals of Internal Medicine,1992. 117:891-897
[59]Marples D, Christensen S, Christensen E.I, Neilsen S. Lithium induced downregulation of aquaporin-2 water channel expression in rat kidney medulla. Journal of Clinical Investigation,1995.95:1838-1845
[60]Yamamura Y, Ogawa H, Chihara T, et al. OPC-21268, an orally effective, nonpeptide vasopressin Ⅵ receptor antagonist. Science,1991.252:572-574
[61]Saito T, Ishikawa S, Abe K, et al. Acute aquaresis by the nonpeptide arginine vasopressin(AVP) antagonist OPC-31260 improves hyponatemia in patients with syndrome of inappropriate secretion of antidiuretic hormone(SIADH). J Clin Endocrinol Metab,1997.82:1054-1057
[62]Hirano T, Yamamura Y, Nakamura S, et al. Effects of the V2-receptor antagonist OPC-41061 and the loop diuretic furosemide alone and in combination in rats. J Pharmacol Exp Ther,2000.292:288-294
[63]Gheorghiade M, Gattis WA, O'Connor CM, et al. Vasopressin V2 receptor blockade with tolvaptan versus fluid restriction in the treatment of hyponatremia.Am J Cardiol,2006.97:1064-1067
[64]Gross P, Verbalis J, Berl T, et al. Hyponatremia management with a once-daily, oral vasopressin V2 receptor antagonist for up to one year:first report of the tolvaptan SALT 2 study. American Society of Nephrology Congress,2005. 121-126
[65]Lee CR, Watkins ML, Patterson H. Vasopressin:a new target for the treatment of heart failure. Am Heart J,2003.146:9-18
[66]Gheorghiade M, Niazi I, Ouyang J, et al. Vasopressin V2-receptor blockade with tolvaptan in patients with congestive heart failure:results from a double blind, randomized trial. Circulation,2003.107:2960-2966
[67]Gheorghiade M, Konstam MA, Udelson JE, et al. Vasopressin receptor blockade with tolvaptan in chronic heart failure:differential effects in normonatremic and hyponatremic patients. J Am Coll Cardiol,2002.39:171
[68]Udelson JE, O'Brien T, Sequeira R, et al. Vasopressin receptor blockade in patients with congestive heart failure:results from a placebo controlled, randomized study comparing the effects of tolvaptan, furosemide and their combination. J Am Coll Cardioll,2002.39:156
[69]Gerbes AL, Gulberg V, Gines P, et al. Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist:a randomized, double blind multicenter trial. Gastroenterology,2003.124:933-939
[70]Vaprisol (conivaptan hydrochloride injection) prescribing information. Astellas Pharma US,2007.67-72
[71][71] Streefkerk JO, Zwieten PA, Vasopressin receptor antagonists: pharmacological tools and potential therapeutic agents. Auton Autacoid Pharmacol,2006.26:141-148
[72]Ghali JK, Koren MJ, Taylor JP, et al. Efficacy and safety of oral conivaptan:a V1A/V2 antagonist, assessed in a randomized, placebo controlled trial in patients with euvolemic or hypervolemic hyponatremia. J Clin Edocrinol Metab,2006. 91:2145-2152
[73]Greenberg A, Verbalis JG. Vasopressin receptor antagonists. Kidney,2006.69: 2124-2130
[74]Fernandez-Varo G, Ros J, Cejudo-Martin P, et al. Effect of the V1/V2-AVP receptor antagonist, conivaptan, on renal water metabolism and systemic hemodynamics in rats with cirrhosis and ascites. J Hepatol,2003.38:755-761
[75]Gross P, Reimann D, Henschkowski, et al. Treatment of severe hyponatremia: conventional and novel aspects. J Am Soc Nephrol,2001.17:10-14
[76]Lemmens-Gruber R, Kamyar M. Vasopressin antagonists. Cell Mol Life Sci, 2006.63:1766-1779
[77]Wang X, Gattone V, Harris PC, et al. Effectiveness of vasopressin V2 receptor antagonists OPC-31260 and OPC-41061 on Polycystic Kidney Disease Development in the PCK Rat. J Am Soc Nephrol,2005.16:846-851
[78]Sterns RH. Overview of the treatment of hyponatremia. In:Emmet M, Forman JP, eds. Uptodate, Waltham, MA,2011
[79]Musch W, Decaux G. Treating the syndrome of inappropriate antidiuretic hormone with isotonic saline. Quarterly Journal of Medicine,1998.91:749-753
[80]Reeder R.F, Harbaugh R.E. Administration of intravenous urea and normal saline for the treatment of hyponatraemia in neurosurgical patients. Journal of Neurosurgery,1989.70:201-206
[81]Cluitmans F.H, Meinders A. Management of severe hyponatraemia:rapid or slow correction. American Journal of Medicine,1990.88:1054-1057
[82]Mickel H.S, Oliver C.N, Starke-Reed P.E. Protein oxidation and myelinolysis occur in brain following rapid correction of hyponatraemia. Biochemical and Biophysical Research Communications,1990.172:92-97
[83]Adams R.A, Victor M, Mancall E.L. Central pontine myelinolysis:a hitherto undescribed disease occuring in alcoholics and malnourished patients. Archives of Neurology,1959.81:154-172
[84]Schrier RW, Bansal S. Diagnosis and management of hyponatremia in acute illness. Curr Opin Crit Care,2008.14(6):627-634
[85]Adrogue HJ, Madias NE. Primary care:Hyponatremia. New Engl J Med,2000. 342:1581-1589
[2]廖二元.内分泌代谢病学.人民卫生出版社,2012,5
[3]宋泓敏,李栋友,等.低钠血症80例临床分析.中国全科医学,2006,9,(12)：1019-1020
[4]曾剑平,张国斌,林志雄,等.儿童颅咽管瘤全切术后并发症的诊治.中国神经肿瘤杂志,2011(03)
[5]漆松涛,陈状,方陆雄,等.颅咽管瘤全切术后钠代谢紊乱及处理.中国临床神经外科杂志,2004(03)
[6]黄小平,陈建良,张清平,等.脑胶质瘤146例手术效果及预后因素分析.中国神经肿瘤杂志,2006(03)
[7]郭芳,王亚东,陈劲草.开颅术后低钠血症的治疗。中国临床神经外科杂志,2007(64)
[8]王建华,邵明海。颅内肿瘤1628例临床分析。医师进修杂志,2005(16)
[9]周国胜,张新中.鞍区肿瘤的显微手术治疗进展.新乡医学院学报,2005,2(22)：174-176
[10]Yamaki T, Tano oka A, Takahashi A, et al. Cerebral salt wasting syndrome distinct from the syndrome of inappropriate secretion of antidiuretie hormone(SIADH)[J]. Acta Neurochir,1992.115 (3-4):15-162
[11]Schwartz WB, Bennett W, Curelop S, et al. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone.Am J Med,1957.23:527
[12]Gonzales-Portillo G, Tomita T. The syndrome of inappropriate secretion of antidiuretic hormone:an unusual presentation for childhood craniopharyngioma: report of three cases [J].J Neurosurg,1998.42(4):917-921
[13]陆永建,李明昌.重型颅脑损伤和术后中枢性低钠血症及相关激素的分泌异常[J].中华神经医学杂志,2005.4(4)：424-426
[14]Nelson PB, Seif SM, Maroon JC, et al. Hyponatremia in intracranial disease: perhaps not the SIADH.J Neurosurg,1981.55:938
[15]Ciiper WC, Green IJ, Wang S, Cerebral salt wasting associated with Guillain-Bsrr syndrome. Arch Intern Med,1965.116:113
[16]Goldbery M, Handler JS. Hyponatremia and renal wasting of sodium in patients with malfunction of the central nervous system. N Engl J Med,1960.263:1037
[17]Roca-Ribas F, Ninno JE, Gasperin A, et al. Cerebral salt wasting syndrome as a postoperative complication after surgical resection of acoustic neuroma[J]. Otol Neurotol,2002.23:992-995.
[18]Harrigan MR. Cerebral salt wasting syndrome [J].Crit Care Clin,2001. 17(1):125-138
[19]Yamamoto N, Miyamoto N, Seo H, et al. Hyponatremia with high plasma ANP level-report of two cases with emphasis on the pathophysiology of cerebral salt wasting. No-Shinkei-Geka,1987.15:1019
[20]De Bold AJ, Borenstein HB, Veress AT, et al. A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats.Life Sci, 1981.28:89
[21]sotani E, Suzuki R, Tomita K, et al. Alterations in plasma concen-trations of natriuretic peptides and antidiuretic hormone after subarachnoid hemorrhage[J].Stroke,1994.25:2198-2203
[22]姚国杰,龚杰,马廉亭,等.重型颅脑损伤后脑性盐耗综合征20例.中华创伤杂志,1999.15(4)：269
[23]Dibona GF. Neural Control of renal function in health and disease.Clin Auton Res,1994.4:69
[24]Ishikawa S, Saito T, Kaneko K, et al. Hyponatremia responsive to fludrocortisone acetate in elderly patients after head injury [J].Ann Intern Med, 1987.106:187-191.
[25]张天锡.颅脑损伤.见：江基尧,朱诚,主编.现代颅脑损伤学.上海：第二军医大学出版社,1999.403-404
[26]Steele A, Gowrishankar K, Abrahson S, et al. Postoperative hyponatremia despite near-isotonic saline infusion:a phenomenon of desalination[J].Ann Intern Med,1997.126:20-25
[27]Streefkerk JO, Zwieten PA, Vasopressin receptor antagonists:pharmacological tools and potential therapeutic agents. Auton Autacoid Pharmacol,2006.26: 141-148
[28]Gowrishankar M, Lin SH, Mallie JP, et al. Acute hyponatremia in the perioperative period:insighs into its pathophysiology and recommendations for management[J]. Clin Nephol,1998.50:352-360
[29]戴炯,李善泉.颅脑手术后并发脑性盐耗损综合征的诊疗分析.上海第二医科大学学报,2004,24(12)：1053-1055
[30]陈瑛,刘建民,赵红燕,等.急性肾上腺皮质功能减退症伴低钠血症的临床分析.上海交通大学学报(医学版),2008,3
[1]Elhassan EA, Schrier RW. Disorders of extracellular volume. In:Floege J, Johnson RJ, Feehally J, eds. Comprehensive clinical nephrology,2010.85-99
[2]Hoorn EJ, Lindemans J, Zietse R. Development of severe hyponatraemia in hospitalized patients:treatment-related risk factors and inadequate management. Nephrol Dial Transplant,2006.21(1):70-76
[3]Goh KP. Management of hyponatremia. Am Fam Physician,2004. 69(10):2387-2394
[4]Anderson R.J. Hospital acquired hyponatraemia. Kidney International,1986. 29:1237-1247
[5]Upadhyay A, Jaber BL, Madias NE. Incidence and prevalence of hyponatremia. Am J Med,2006.119(7):30-35
[6]Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta,2003.337:169-172
[7]Siregar P. The risk of hyponatremia in the elderly compared with younger in the hospital inpatient and outpatient. Acta Med Indones,2011.43(3):157-160
[8]Baylis P.H. Thompson C.J. Osmoregulation of vasopressin secretion and thirst in health and disease. Clinical Endocrinology,1988.29:549-576
[9]McKenna K. Thompson C.J. Osmoregulation in clinical disorders of thirst appreciation. Clinical Endocrinology,1998.49:139-152
[10]Kokko J.P. Rector F.C. Countercurrent multiplication system without active transport in inner medulla:new model. Kidney International,1972.2:214-223
[11]Nielsen S, Agre P. The aquaporin family of water channels in kidney. Kidney International,1995.48:1057-1068
[12]Knepper M.A, Wade J.B, Terris J, et al. Renal aquaporins. Kidney International, 1996.49:1712-1717
[13]Nielsen S, Marples, D, et al. Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. Proceedings of the National Academic Sciences of the U.S.A,1995.92:1013-1017
[14]Lankford S.P, Chou C-L, et al. Regulation of collecting duct water permeability independent of cAMP-mediated AVP response. American Journal of Physiology,1991.261:554-F566
[15]DiGiovanni S.R, Nielsen S, et al. Regulation of collecting duct water channel expression by vasopressin in Brattleboro rats. Proceedings of National Academic Sciences of the U.S.A,1994.91:8984-8988
[16]Ecelbarger C, Nielsen S, et al. Role of renal aquaporins in escape from vasopressin induced antidiuresis in rat. Journal of Clinical Investigation,1997. 99:1859
[17]Yamanoto N, Miyamoto N, et al. Hyponatraemia with high plasma atrial natriuretic peptide levels. Report of two cases with emphasis on the pathophysiology of cerebral salt wasting syndrome. Neurologica Surgica,1987. 15:1019-1023
[18]Berendes E, Walter M, Cullen P. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid hemorrhage. Lancet,1997.349:245
[19]Beck T.R, Dunn M.J. The relationship of vasopressin and renal prostaglandins. Mineral and Electrolyte Metabolism,1981.6:46-59
[20]Inoue M, Crofton J.T, Share L. Interactions between brain acetylcholine and prostaglandins in control of vasopressin release. American Journal of Physiology,1991.261:420-426
[21]Carney S, Morgan T, Ray C, Thompson L. Effect of calcitonin on urine concentration in the rat. American Journal of Physiology,1983.244:432-435
[22]DeRouffignac C, Elalouf J.M. Effects of calcitonin on the renal concentrating mechanism. American Journal of Physiology,1983.245:506-511
[23]Elalouf J.M. Sari D.C. Effects of glucagon and parathyroid hormone on the loop of Henle of rat juxtamedullary nephrons. Kidney International,1986. 29:807-813
[24]Mandell I.N, DeFronzo R.A, Robertson G.L. Role of plasma vasopressin in the impaired water diuresis of isolated glucocorticoid defficiency in the rat. Kidney International,1980.17:186-195
[25]Oelkers W. Hyponatraemia and inappropriate secretion of antidiuretic hormone in patients with hypopituitarism. New England Journal of Medicine,1989. 321:492
[26]Kimura T, Ota K, et al. Plasma vasopressin and atrial natriuretic hormone levels in hypopituitarism with and without hydrocortisone treatments:responses to an acute water load. Acta Endocrinologica Copenhagen,1992.126:217-223
[27]Elhassan EA, Schrier RW. Disorders of extracellular volume. In:Floege J, Johnson RJ, Feehally J, eds. Comprehensive clinical nephrology.4th ed. St. Louis:Elsevier Saunders,2010.85-99
[28]Andersen R.J, Chung H.M, Kluge R, Schrier R.W. Hyponatraemia:a prospective analysis of its epidemiology and the pathogenetic role of vasopressin. Annals of Internal Medicine,1985.102:164-168
[29]Katz M.A. Hyperglycaemia induced hyponatraemia ± calculation of expected serum sodium depression. New England Journal of Medicine,1973. 289:843-844
[30]Sonnenblick M., Friedlander Y, Rosin A. Diuretic induced hyponatraemia. Chest,1993.103:601-606
[31]VanAssen S, Mudde A.H. Severe hyponatraemia in an amiloride/ hydrochlorothiazide-treated patient. Netherlands Journal of Medicine,1999. 54:108-113
[32]Ishikawa S, Kim J.K, Schrier R.W. Effects of arginine vasopressin antidiuretic and vasopressor antagonists in glucocorticoid and mineralocorticoid deficient rats. In:Schrier R.W, eds. Vasopressin,1995.171-180
[33]Peters J.P, Welt K.G., et al. A salt wasting syndrome associated with cerebral disease. Transactions of the Association of American Physiology,1950. 63:57-64
[34]Bartter F.C, Schwartz W.B. The syndrome of inappropriate antidiuretic hormone. American Journal of Medicine,1967.42:790-806
[35]Tomida M, Muraki M, Uemura K, Yamasaki K. Plasma concentration of brain natriuretic peptide in patients with subarachnoid hemorrhage. Stroke,1998. 8:1584-1587
[36]Damaraju S.C, Rajshekhar V, Chandy M.J. Validation study of a central venous pressure-based protocol for the management of neurosurgical patients with hyponatraemia and natriuresis. Neurosurgery,1997.40:312-317
[37]Schrier R.W, Fassett R.G. Pathogenesis of sodium and water retention in cardiac failure. Renal Failure,1998.20:773-781
[38]Schrier R.W, Martin P.Y. Recent advances in the understanding of water metabolism in heart failure. Advances in Experimental Medicine and Biology, 1998.449:415-426
[39]Abraham W.T, Lauwaars M.E, Kim J.K, Pena R.L, Schrier R.W. Reversal of atrial natriuretic peptide resistance by increasing distal tubular delivery in patients with decompensated cirrhosis. Hepatology,1995.22:737-743
[40]Villarreal D, Freeman R.H. Atrial natriuretic factor and the renin-angiotensin system in the regulation of sodium balance:longitudinal studies in experimental heart failure. Journal of Laboratory and Clinical Medicine,1991.118:515-522
[41]Moe G.W, Forster C, DeBold A.J, Armstrong P.W. Pharmacokinetics hemodynamic, renal and neurohormonal effects of atrial natriuretic factor in experimental heart failure. Clinical Investigative Medicine,1990.13:111-118
[42]Martin P.Y, Schrier, R.W. Pathogenesis of water and sodium retention in cirrhosis. Kidney International,1997.51:43-49
[43]Asahina Y, Izumi N, Enomoto N, Sasaki S, Fushimi K, Marumo F. Increased gene expression of water channel in cirrhotic rat kidneys. Hepatology,1995. 21:169-173
[44]Xu D.L, Martin P.Y, Ohara M, et al. Upregulation of aquaporin water channel expression in chronic heart failure in rats. Journal of Clinical Investigation, 1997.99:1500
[45]Montengro J, Gonzalez O, Saracho R, Aguirre R, Gonzalez O, Martinez I. Changes in renal function in primary hypothyroidism. American Journal of Kidney Disease,1996.27:195-198
[46]Skowsky W.R, Kikuchi T.A. The role of vasopressin in the impaired water excretion of myxedema. American Journal of Medicine,1978.64:613
[47]Ojamaa K, Balkman C, Klein, I. Acute effects of triiodothyronine on arterial smooth muscle cells. Annals of Thoracic Surgery,1993.56:61
[48]Raff H. Interactions between neurohypophysial hormones and the ACTH±adrenocortical axis. Annals of the New York Academy of Sciences, 1993.689:411-425
[49]Erkut Z.A, Pool C, Swaab D.F. Glucocorticoids suppress corticotropin releasing hormone and vasopressin expression in human hypothalamic neurons. Journal of Clinical Endocrinology and Metabolism,1998.83:2066-2073
[50]Mora A, Enriquez R, Lacueva F, Gonzales E. Severe hyponatraemia and hypopituitarism. Nephron,1995.70:139-140
[51]Kamoi K, Ebe T, Kobayashi O, et al. Atrial natriuretic peptide in patients with the syndrome of inappropriate antidiuretic hormone secretion and with diabetes insipidus. Journal of Clinical Endocrinology and Metabolism,1990. 70:1385-1390
[52]Shimizu K, Nakano S, et al. Ectopic atrial natriuretic peptide production in small cell lung cancer with the syndrome of inappropriate antidiuretic hormone. Cancer,1991.68:2284-2288
[53]Gross A.J, Steinberg S.M, et al. Atrial natriuretic factor and arginine vasopressin production in tumor cell lines from patients with lung cancer and their relationship to serum sodium. Cancer Research,1993.53:67-74
[54]Satchell S.C, Connaughton M. Inappropriate antidiuretic hormone secretion and extreme rises in creatinine kinase following MDMA ingestion. British Journal of Hospital Medicine,1994.51:495
[55]Holden R., Jackson M.A. Near fatal hyponatraemic coma due to vasopressin oversecretion after ecstasy. Lancet,1996.347:1052
[56]Verbalis J.G. Adaptation to acute and chronic hyponatraemia:implications for symptomatology, diagnosis and therapy. Seminars in Nephrology,1998. 18:3-19.
[57]Sterns R.H, Baer J, Ebersol S, Thomas D. Organic osmolytes in acute hyponatraemia. American Journal of Physiology,1993.264:833-836
[58]Ayus J.C, Wheeler J.M, Arieff A.I. Postoperative hyponatraemic encephalopathy in menstruant women. Annals of Internal Medicine,1992. 117:891-897
[59]Marples D, Christensen S, Christensen E.I, Neilsen S. Lithium induced downregulation of aquaporin-2 water channel expression in rat kidney medulla. Journal of Clinical Investigation,1995.95:1838-1845
[60]Yamamura Y, Ogawa H, Chihara T, et al. OPC-21268, an orally effective, nonpeptide vasopressin Ⅵ receptor antagonist. Science,1991.252:572-574
[61]Saito T, Ishikawa S, Abe K, et al. Acute aquaresis by the nonpeptide arginine vasopressin(AVP) antagonist OPC-31260 improves hyponatemia in patients with syndrome of inappropriate secretion of antidiuretic hormone(SIADH). J Clin Endocrinol Metab,1997.82:1054-1057
[62]Hirano T, Yamamura Y, Nakamura S, et al. Effects of the V2-receptor antagonist OPC-41061 and the loop diuretic furosemide alone and in combination in rats. J Pharmacol Exp Ther,2000.292:288-294
[63]Gheorghiade M, Gattis WA, O'Connor CM, et al. Vasopressin V2 receptor blockade with tolvaptan versus fluid restriction in the treatment of hyponatremia.Am J Cardiol,2006.97:1064-1067
[64]Gross P, Verbalis J, Berl T, et al. Hyponatremia management with a once-daily, oral vasopressin V2 receptor antagonist for up to one year:first report of the tolvaptan SALT 2 study. American Society of Nephrology Congress,2005. 121-126
[65]Lee CR, Watkins ML, Patterson H. Vasopressin:a new target for the treatment of heart failure. Am Heart J,2003.146:9-18
[66]Gheorghiade M, Niazi I, Ouyang J, et al. Vasopressin V2-receptor blockade with tolvaptan in patients with congestive heart failure:results from a double blind, randomized trial. Circulation,2003.107:2960-2966
[67]Gheorghiade M, Konstam MA, Udelson JE, et al. Vasopressin receptor blockade with tolvaptan in chronic heart failure:differential effects in normonatremic and hyponatremic patients. J Am Coll Cardiol,2002.39:171
[68]Udelson JE, O'Brien T, Sequeira R, et al. Vasopressin receptor blockade in patients with congestive heart failure:results from a placebo controlled, randomized study comparing the effects of tolvaptan, furosemide and their combination. J Am Coll Cardioll,2002.39:156
[69]Gerbes AL, Gulberg V, Gines P, et al. Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist:a randomized, double blind multicenter trial. Gastroenterology,2003.124:933-939
[70]Vaprisol (conivaptan hydrochloride injection) prescribing information. Astellas Pharma US,2007.67-72
[71][71] Streefkerk JO, Zwieten PA, Vasopressin receptor antagonists: pharmacological tools and potential therapeutic agents. Auton Autacoid Pharmacol,2006.26:141-148
[72]Ghali JK, Koren MJ, Taylor JP, et al. Efficacy and safety of oral conivaptan:a V1A/V2 antagonist, assessed in a randomized, placebo controlled trial in patients with euvolemic or hypervolemic hyponatremia. J Clin Edocrinol Metab,2006. 91:2145-2152
[73]Greenberg A, Verbalis JG. Vasopressin receptor antagonists. Kidney,2006.69: 2124-2130
[74]Fernandez-Varo G, Ros J, Cejudo-Martin P, et al. Effect of the V1/V2-AVP receptor antagonist, conivaptan, on renal water metabolism and systemic hemodynamics in rats with cirrhosis and ascites. J Hepatol,2003.38:755-761
[75]Gross P, Reimann D, Henschkowski, et al. Treatment of severe hyponatremia: conventional and novel aspects. J Am Soc Nephrol,2001.17:10-14
[76]Lemmens-Gruber R, Kamyar M. Vasopressin antagonists. Cell Mol Life Sci, 2006.63:1766-1779
[77]Wang X, Gattone V, Harris PC, et al. Effectiveness of vasopressin V2 receptor antagonists OPC-31260 and OPC-41061 on Polycystic Kidney Disease Development in the PCK Rat. J Am Soc Nephrol,2005.16:846-851
[78]Sterns RH. Overview of the treatment of hyponatremia. In:Emmet M, Forman JP, eds. Uptodate, Waltham, MA,2011
[79]Musch W, Decaux G. Treating the syndrome of inappropriate antidiuretic hormone with isotonic saline. Quarterly Journal of Medicine,1998.91:749-753
[80]Reeder R.F, Harbaugh R.E. Administration of intravenous urea and normal saline for the treatment of hyponatraemia in neurosurgical patients. Journal of Neurosurgery,1989.70:201-206
[81]Cluitmans F.H, Meinders A. Management of severe hyponatraemia:rapid or slow correction. American Journal of Medicine,1990.88:1054-1057
[82]Mickel H.S, Oliver C.N, Starke-Reed P.E. Protein oxidation and myelinolysis occur in brain following rapid correction of hyponatraemia. Biochemical and Biophysical Research Communications,1990.172:92-97
[83]Adams R.A, Victor M, Mancall E.L. Central pontine myelinolysis:a hitherto undescribed disease occuring in alcoholics and malnourished patients. Archives of Neurology,1959.81:154-172
[84]Schrier RW, Bansal S. Diagnosis and management of hyponatremia in acute illness. Curr Opin Crit Care,2008.14(6):627-634
[85]Adrogue HJ, Madias NE. Primary care:Hyponatremia. New Engl J Med,2000. 342:1581-1589
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