Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na⁺)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na⁺] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema. It is possible that excessive administration of electrolyte-free solutions and high doses of insulin may increase the risk of this complication. While there are some data to suggest that brain cell size is disturbed during acute uremia, additional work is necessary to clarify the role of cerebral cell volume regulation during acute and chronic uremia.     

颅脑损伤合并高钠血症63例临床分析

目的：探讨颅脑损伤后合并高钠血症的临床治疗及高钠血症对预后的影响。方法回顾分析该院2007年1月-2014年12月间收治的重型颅脑损伤合并高钠血症63例患者临床资料,对比血钠高低对死亡率的影响,对比控制尿量组与非控制尿量组血钠恢复时间。结果轻度高钠组、中度高钠组、重度高钠组分别有17例、24例、22例,各组的死亡率分别为29.4%、45.8%、63.6%,轻度高钠组与重度高钠组间相比,差异有统计学意义(P<0.05)。控制尿量组28例,非控制尿量组18例,两组的血钠恢复正常所需的平均天数分别为(4.57±1.86)、(6.38±1.49),两组相比差异有统计学意义(P<0.05)。结论颅脑损伤合并高钠血症血钠值越高,死亡率越高,除常规治疗外,控制尿量可明显缩短血钠恢复的时间。     

Early Sodium and Fluid Intake and Severe Intraventricular Hemorrhage in Extremely Low Birth Weight Infants

Hypernatremic dehydration is an important cause of intracranial hemorrhage. A possible association of intraventricular hemorrhage (IVH) with hypernatremia and/or high sodium intake has been suggested in preterm infants. To investigate the associations of early fluid and sodium intake or serum sodium concentrations with severe intraventricular hemorrhage (IVH) in extremely low birth weight (ELBW) infants, we reviewed the medical records of 169 inborn ELBW infants. Daily fluid and sodium intake, urine output, weight loss and serum sodium concentration during the first 4 days of life were obtained. Patients were divided into the severe IVH (grade 3/4) and the control (no or grade 1/2 IVH) group. The maximum serum sodium concentration and the incidence of hypernatremia did not differ between the two groups. Related to the fluid balance and sodium intake, the risk for severe IVH was strongly associated with total fluid and sodium intake during the initial four days of life. With respect to the fluids other than transfusion, severe IVH can be discriminated only by sodium intake but not by fluid intake. Large randomized controlled trials are required to clarify the causal relationship between the early sodium intake and severe IVH in ELBW infants.

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呼吸监护病房老年患者高钠血症的临床分析

目的 探讨老年危重患者高钠血症与病情变化及预后的关系。方法 回顾2002年5月-2003年10月呼吸监护病房所有老年高钠血症患者临床资料．并用统计学方法对上述资料进行分析。结果 189例患者中高钠血症26例，发生率13．76％。高钠血症患者中死亡14例．病死率53．85％。在气管插管病例中高钠血症发生率为70．37％。发生高钠血症时急性生理学和慢性健康状况(APACHE)Ⅱ评分显著高于入监护室24小时的APACHEⅡ评分，同时肾功能也有一定影响，血肌酐值明显升高。高钠血症中死亡组与存活组比较，血钠水平有显著差异。结论 高钠血症是老年危重患者较常见的并发症，在气管插管患者发生率更高，且预后差。因此要重视老年危重患者高钠血症的发生。     

A new quantitative approach to the treatment of the dysnatremias

Rapid correction of the dysnatremias can result in significant patient morbidity and mortality. To avoid overly rapid correction of the dysnatremias, the sodium deficit equation, water deficit equation, and Adrogue–Madias equation are frequently utilized to predict the change in plasma sodium concentration ([Na⁺]_p) following a therapeutic maneuver. However, there are significant limitations inherent in these equations. Specifically, the sodium deficit equation assumes that total body water (TBW) remains unchanged. Similarly, when using the Adrogue–Madias equation, the volume of infusate required to induce a given [Na⁺]_p is determined by dividing the target [Na⁺]_p by the result of this formula. This calculation also assumes that TBW remains constant. In addition, neither of these equations are applicable in the management of symptomatic syndrome of inappropriate antidiuretic hormone secretion (SIADH) because they fail to consider the subsequent increase in sodium excretion following the administration of infusate. Furthermore, in the treatment of hypernatremia, the water deficit equation is only applicable if the hypernatremia is caused by pure water loss. In hypernatremia caused by hypotonic fluid losses, the water deficit equation does not provide any information on the differential effect of infusates of variable [Na⁺] and [K⁺] on the [Na⁺]_p. Finally, all these equations fail to consider any ongoing Na⁺, K⁺, or H₂O losses. Taking all these limitations into consideration, we have derived two new equations which determine the volume of a given infusate required to induce a target [Na⁺]_p. These equations consider the mass balance of Na⁺, K⁺, and H₂O, as well as therapy-induced changes in TBW. The first equation is applicable to both hypernatremia and hyponatremia. The second equation is applicable to the management of severe symptomatic SIADH requiring intravenous therapy.     

Acute peritoneal dialysis as both cause and treatment of hypernatremia in an infant

This report describes a 4-month-old infant with multisystem organ failure who developed severe hypernatremia (sodium 168 mEq/l) due to rapid free water removal associated with acute peritoneal dialysis instituted for fluid overload. The current report describes the pathophysiology of the hypernatremia, and its correction by low-sodium hypertonic peritoneal dialysis without compromising ultrafiltration or supplementing with free water. Although peritoneal dialysis can cause hypernatremia, a modified solute concentration in the dialysate can treat the hypernatremia successfully. Received: 2 January 2001 / Revised: 24 April 2001 / Accepted: 24 April 2001