脑性耗盐综合征的诊断和治疗进展

低钠血症是神经科重症患者最常出现的电解质紊乱。脑性耗盐综合征（CSW）是由颅内疾病引起的肾性失钠导致的低钠血症和细胞外液的丢失。其发病机制仍末完全清楚。除一些利钠因子的作用外，交感神经反射在CSW中也发挥了作用。CSW和（抗利尿激素分泌异常综合征）SIADH的鉴别存在困难，关键在予容量的状态。排除一些其他的原因也非常必要。治疗有赖于液体的支持和盐的平衡。盐皮质激素在一些复杂的病例中可能有用。     

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。     

脑出血术后低钠血症相关因素分析

目的探讨脑出血术后低钠血症的相关因素、诊断和治疗。方法对82例脑出血术后低钠血症患者监测血生化、血气分析、尿比重、尿钠等;记录24 h出入水量;限水治疗。结果抗利尿激素分泌不当综合征(SIADH)6例,脑性耗盐综合征(CSWS)36例。结论脑出血术后低钠血症与脱水、利尿所致排钠大于摄入有关,而难治性低钠血症应考虑CSWS和SIADH存在,并给予鉴别和相关治疗。     

颈脊髓损伤并发低钠血症的临床分析

目的探讨颈脊髓损伤并发低钠血症的诊断、治疗和机制。方法收集65例颈脊髓损伤并发低钠血症的患者的临床资料,其中男42例,女22例;年龄19~74岁,平均53.6岁。Frankel分级,A级21例,B级15例,C级16例,D级12例,E级0例。分析其临床表现、辅助检查和临床处理,分为三种类型分别给予不同的治疗方法。结果单纯性低钠血症7例,抗利尿激素异常分泌综合征患者45例,脑耗盐耗综合征患者12例。采取相应的治疗方法后65例低钠血症患者均得到纠正。结论颈脊髓损伤并发低钠血症病因可能是单纯低钠血症、抗利尿激素异常分泌综合征、脑耗盐耗综合征等不同类型,治疗时需加以鉴别,根据不同的病因采取不同的治疗方法。     

急性颈髓损伤并发低钠血症的治疗

目的探讨急性颈髓损伤并发低钠血症的发病机制和治疗方法。方法回顾性分析本院2002年1月至2008年5月收治的187例颈髓损伤病人的临床资料,其中112例并发低血钠症。结果本组低钠血症发生率为59.89%（112/187）。颈髓损伤到出现低钠血症的时间平均为5.9±3.6天。血钠降至最低到血钠开始回升的时间为20.9天±11.6天。经补液、补钠等治疗。死亡2例,愈110例。结论低钠血症是急性颈髓损伤的常见并发症,其发病机制可能与抗利尿激素分泌异常综合征（SIADH）及脑耗盐综合征（CSWS）有关。低钠血症的严重程度和颈髓损伤平面及颈髓损伤程度相关,低钠血症的发生率与感染相关。     

重型颅脑损伤后中枢性低钠血症的临床分析

目的探讨颅脑损伤并发中枢性低钠血症的临床特点与治疗方法。方法回顾性分析2004年7月至2011年7月收治的12例颅脑损伤后并发中枢性低钠血症,通过其临床表现及实验室检查结果明确诊断,确定治疗方法。结果除1例特重型颅脑损伤死于肺部感染．11例病人血钠均恢复至正常水平。治疗时间为7-27天,平均13．8天。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,早期诊治能降低颅脑损伤病人的病残率和病死率。     

颅脑外伤后脑盐耗综合征

脑盐耗综合征(cerebral salt wastingsyndrome,CSWS)是颅脑外伤患者低钠血症的重要原因之一,重要发生在重伤或特重伤患者中,合并CSWS的颅脑外伤患者,其死亡率明显增高[1,2].本文就近年来有关CSWS的研究进展综述如下.     

两种钠盐饮食对肝硬化腹水并低钠血症的临床研究

目的:探讨肝硬化腹水并低钠血症患者在不同钠盐饮食时对腹水消退及其并发症的影响。方法:将100例肝硬化腹水并低钠血症患者随机分为两组:限钠组50例,给予低盐饮食。不限钠组50例,饮食除正常钠盐外,据血钠值适当补充钠盐。比较两组患者腹水消退时间,发生肝性脑病、肝肾综合征及循环衰竭的发生率。结果:不限钠饮食组腹水消退时间明显缩短,发生肝性脑病、肝肾综合征及循环衰竭的发生率明显低于限钠饮食组。结论:肝硬化腹水并低钠血症患者,不限钠饮食及适当补充钠盐利于腹水消退,能减少各种严重并发症,起到良好的治疗效果。     

以低钠血症为首发表现的肺癌一例

肺癌的临床表现多种多样，其中以低钠血症为首发表现的抗利尿激素分泌失调综合征（syndrome of inappropriate secretion of antidiuretic hormone, SIADH）并不多见。我院于2008年10月17日收治了1例以顽固性低钠血症为首发表现的肺癌患者，现报道如下。     

肝硬化失代偿期低钠血症相关因素分析及护理

目的 探讨肝硬化失代偿期发生低钠血症的相关因素及护理措施。方法 从护理的角度对96例肝硬化失代偿期低钠血症患者的临床资料进行由顾性分析。结果 96例肝硬化患者失代偿期低钠血症的诱发因素主要为摄入不足与排出过多、利尿剂使用不当、长期低钠饮食和多次放腹水。不同程度低钠血症患者肝性脑病、肝肾综合征的发生率及预后比较．差异有显著性意义（P〈0．05。P〈0．01）。结论 临床护理工作中需密切注意肝硬化失代偿期低钠血症的各项相关因素。根据不同原因进行心理护理和饮食指导．加强治疗中用药观察和护理．预防肝性脑病和肝肾综合征的发生。     

Cerebral salt wasting versus SIADH: what difference?

The term cerebral salt wasting (CSW) was introduced before the syndrome of inappropriate antidiuretic hormone secretion was described in 1957. Subsequently, CSW virtually vanished, only to reappear a quarter century later in the neurosurgical literature. A valid diagnosis of CSW requires evidence of inappropriate urinary salt losses and reduced "effective arterial blood volume." With no gold standard, the reported measures of volume depletion do not stand scrutiny. We cannot tell the difference between CSW and the syndrome of inappropriate antidiuretic hormone secretion. Furthermore, the distinction does not make a difference; regardless of volume status, hyponatremia complicating intracranial disease should be treated with hypertonic saline.     

Syndrome of inappropriate antidiuresis and cerebral salt wasting syndrome: are they different and does it matter?

The syndrome of inappropriate antidiudresis (SIAD) and cerebral salt wasting (CSW) are similar conditions with the main difference being the absence or presence of volume depletion. The two conditions may be indistinguishable at presentation, as volume status is difficult to assess, which can lead to under-diagnosis of CSW in patients with central nervous system (CNS) disease. Carefully conducted studies in patients with CNS disease have indicated that CSW may be more common than SIAD. CSW may be differentiated from SIAD based on the persistence of hypouricemia and increased fractional excretion of urate following the correction of hyponatremia. Hyponatremia should be prevented if possible and treated promptly when discovered in patients with CNS disease as even mild hyponatremia could lead to neurological deterioration. Fluid restriction should not be used for the prevention or treatment of hyponatremia in hospitalized patients with CNS disease as it could lead to volume depletion especially if CSW is present. 0.9% sodium chloride may not be sufficiently hypertonic for the prevention of hyponatremia in hospitalized patients with CNS disease and a more hypertonic fluid may be required. The preferred therapy for the treatment of hyponatremia in patients with CNS disease is 3% sodium chloride.     

Cerebral salt wasting and elevated brain natriuretic peptide levels after traumatic brain injury: 2 case reports

BACKGROUND: Historically, hyponatremia in patients with varying brain diseases was termed cerebral salt wasting. Hyponatremia secondary to CSW was reported to be a distinct entity from SIADH, with the distinguishing feature of decreased extracellular fluid volume. Brain natriuretic peptide, a peptide with natriuretic, vasorelaxant, and aldosterone-inhibiting properties, was recently implicated in aneurysmal SAH patients with CSW. Here, we describe 2 cases of CSW in TBI patients with elevated BNP levels. This phenomenon has not been previously described. CASE DESCRIPTION: Two patients with TBI and hyponatremia were subject to analysis. Central lines were placed to assess volume status. Levels of BNP were measured at the onset of hypertonic saline infusion. Electrocardiogram and cardiac enzyme studies were performed to assess cardiac function. Serial imaging was performed to assess the extent of brain injury. CONCLUSIONS: These patients with TBI had findings consistent with CSW with elevated BNP levels in the setting of normal cardiac function. In both cases, a high BNP level was observed after declining plasma Na levels despite aggressive hypertonic saline infusion. High BNP levels may be associated with CSW. Further studies are necessary to establish a causative role for BNP in TBI-induced CSW.     

A method to estimate urinary electrolyte excretion in patients at risk for developing cerebral salt wasting

OBJECT: Two major criteria are necessary to diagnose cerebral salt wasting (CSW): a cerebral lesion and a large urinary excretion of Na+ and Cl- at a time when the extracellular fluid (ECF) volume is contracted. Nevertheless, it is difficult for the physician to confirm from bedside observation that a patient has a contracted ECF volume. Hyponatremia, although frequently present, should not be a criterion for a diagnosis of salt wasting. A contracted ECF volume is unlikely if there are positive balances of Na+ and Cl-. The goal of this study was to assess the accuracy of calculating balances for Na+ plus K+ and of Cl- over 1 to 10 days in an intensive care unit (ICU) setting. METHODS: A prospective comparison of measured and estimated quantities of Na+ plus K+ and of Cl- excreted over 1 to 10 days in 10 children and 12 adults who had recently received a traumatic brain injury or undergone recent neurosurgery. Plasma concentrations of electrolytes were recorded at the beginning and end of the study period. The total volumes infused and excreted and the concentrations of Na+, K+, and Cl- in the infusate were obtained from each patient's ICU chart. The electrolytes in the patients' urine were measured and calculated. Correlations between measured and calculated values for excretions of Cl- and of Na+ plus K+ were excellent. CONCLUSIONS: Mass balances for Na+ plus K+ and for Cl- can be accurately estimated. These data provide information to support or refute a clinical diagnosis of CSW. The danger of relying on balances for these electrolytes measured within a single day to diagnose CSW is illustrated.     

The role of fludrocortisone in a child with cerebral salt wasting

Cerebral salt wasting (CSW) is a syndrome of hyponatremia due to excessive natriuresis described in patients with central nervous system insult. We present a 29-month-old black male with tuberculous meningitis who developed CSW with depressed mineralocorticoid activity. The patient required hypertonic saline and ionotropic support. Mineralocorticoid supplementation effectively treated CSW. Received October 20, 1997; received in revised form and accepted February 18, 1998     

Cervicothoracolumbar spinal epidural abscess and cerebral salt wasting

BACKGROUND CONTEXT: Spinal epidural abscess (SEA) is a rare infectious disease. However, if left unrecognized and untreated, the clinical outcome of SEA can be devastating. PURPOSE: To report a rare clinical presentation of a cervicothoracolumbar SEA with cerebral salt wasting (CSW). STUDY DESIGN: Case report. METHODS: Clinical history, physical and laboratory findings, and magnetic resonance imaging studies of a patient with cervicothoracolumbar SEA and CSW. RESULTS: We report the case of a 15-year-old boy with cervicothoracolumbar SEA complicated with CSW and treated with conservative methods. CONCLUSIONS: In conclusion, CSW can be seen at the follow-up period of the SEA and the clinicians must be aware of this entity.     

Acute symptomatic hyponatremia and cerebral salt wasting after head injury: an important clinical entity.

Hyponatremia is a well known complication of traumatic and nontraumatic cerebral injury, often related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Nonetheless, it also can be associated with a different entity, the syndrome of cerebral salt wasting (CSW). The authors report the case of a 4.5-year-old boy presenting with major head injury who at day 6 after admission had generalized tonic-clonic seizures caused by severe acute hyponatremia (serum sodium level, 119 mmol/L) and signs of dehydration. Despite initial isotonic rehydration, hyponatremia persisted because of excessive renal salt losses and concomitant enormous water losses, necessitating increasing amounts of sodium, up to 160 mmol/kg/d, and large amounts of intravenous fluids, up to 27 L/d. Highly increased levels of atrial natriuretic peptide (ANP) confirmed the diagnosis of CSW. The occurrence of a CSW has to be recognized early in the clinical course for adequate treatment and remains one of the important differential diagnosis of SIADH in hyponatremic states in patients with cerebral disorders, especially after head injury.     

Nephritic edema

Nephritic edema results from the primary retention of salt. Acute glomerulonephritis is the prototypical form of the disorder. The stimulus for the salt retention arises within the kidney by an unknown mechanism. As effective arterial blood volume (EABV) was normal at the start of the disease process, it becomes expanded as salt and water are added to it. The pathophysiological sequelae of this process are compared with those which follow the salt retention of congestive heart failure (CHF). The latter is a syndrome in which salt retention is secondary, driven by the contraction of EABV which is at the heart of CHF. Finally, mechanisms responsible for the salt retention of nephrosis are considered. It is possible, and even likely, that most patients with nephrotic edema have primary salt retention, rather than secondary edema. If this view is correct, salt is retained not because of urinary protein loss and its consequent hypoalbuminemia, but rather because of the glomerulopathy which caused the syndrome in the first place.     

Cerebral salt-wasting syndrome. We need better proof of its existence.

It is widely believed that the cerebral salt-wasting syndrome (CSWS) exists as an entity distinct from the syndrome of inappropriate ADH secretion, and that it is characterized by evidence of severe renal salt wasting that results in volume depletion and hyponatremia. Proof of the existence of CSWS as an entity requires documentation of renal salt wasting and volume depletion. The present review has been undertaken to examine the evidence that the CSWS is a separate entity. In this effort, we have discussed various methods of documentation of volume depletion, and then reviewed reported cases of CSWS to determine whether volume depletion and renal salt wasting have been clearly demonstrated. Our review has led us to conclude that not one case of purported CSWS has demonstrated clear evidence of volume depletion and renal salt wasting. If renal salt wasting had been proven in these cases, we would conclude that the likely site of renal salt transport was the proximal tubule. The proximal site of salt transport defect has been suggested by the absence of hyperreninemia and hypokalemia, which would be a distinguishing feature of Bartter's syndrome and Gitelman's syndrome.