Hypertonicity: Clinical entities, manifestations and treatment

Abstract

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 hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, 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 first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level.

Keywords: Hyperglycemia; Hypernatremia; Hypertonicity; Osmotic diuresis; Water diuresis.

Figure 1

Diagnosis of hypovolemic and euvolemic hypernatremia. UOsm: Urine osmolality; USL: Urine solute load; GI: Gastrointestinal; DDAVP: Desmopressin; DI: Diabetes insipidus; Osm: Osmolality.

Figure 2

Effect on [Na]_S of varying volumes of infusate containing varying total monovalent cation concentration (sum of sodium plus potassium concentrations) in a patient with initial body water of 40 L and [Na]_S1 of 150 mmol/L.

Figure 3

Effect on [Na]_S of varying 24-h urinary volume containing varying total monovalent cation concentration (sum of sodium plus potassium concentrations) in a patient with initial body water of 40 L and [Na]_S1 of 150 mmol/L infused with the same volume (2.4 L) of 5% dextrose in water, or “half-normal” saline ([Na]_S3 = 77 mmol/L) or “normal” saline ([Na]_S3 = 154 mmol/L).

Figure 4

Increase in tonicity for the same degree of hyperglycemia (100 mmol/L) at various states of extracellular volume.

Figure 5

Increase in tonicity expressed as a percent of the increase in serum glucose concentration in progressive hyperglycemia.

Figure 6

Mean values of [Na]_S, [Glu]_S and serum tonicity in hyperglycemia in patients on chronic dialysis. The figure shows the mean values of [Na]_S, [Glu]_S and tonicity in 148 episodes of severe episodes of severe hyperglycemia treated only with insulin infusion[40]. A: Values recorded at presentation with hyperglycemia; B: Values predicted by the corrected [Na]_S[47]; C: Values of observed [Na]_S and [Glu]_S and calculated tonicity at the end of treatment when [Glu]_S had declined to desired levels. Tonicity was calculated as [Glu]_S + 2 × [Na]_S in A, B and C. The average level of tonicity after treatment predicted by the use of predicted [Na]_S (B) was very close to the corresponding measured level (C).