Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperg...Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypo-volemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium defcit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the frst component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fuid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtainedby the corrected sodium concentration, which representsa calculated value of the serum sodium concentrationthat would result from reduction of the serum glucoseconcentration to a normal level.展开更多
文摘Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypo-volemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium defcit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the frst component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fuid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtainedby the corrected sodium concentration, which representsa calculated value of the serum sodium concentrationthat would result from reduction of the serum glucoseconcentration to a normal level.
