Porth's Essentials of Pathophysiology, 4e

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Disorders of Fluid, Electrolyte, and Acid–Base Balance

C h a p t e r 8

Manifestations of Hyponatremia and Hypernatremia

TABLE 8-4

Hyponatremia

Hypernatremia

LaboratoryValues

LaboratoryValues

Serum sodium <135 mEq/L (135 mmol/L)

Serum sodium >145 mEq/L (145 mmol/L)

Decreased serum osmolality

Increased serum osmolality

Dilutional decrease in blood components, including hematocrit, blood urea nitrogen (BUN)

Increased concentrations of blood components, including hematocrit, BUN Compensatory Mechanisms Increased thirst Increased ADH with oliguria and high urine specific gravity Decreased Intracellular Fluid Dry skin and mucous membranes Decreased tissue turgor Decreased salivation and lacrimation Elevated body temperature

Hypo-osmolality and Movement ofWater into Muscle and Neural Tissue  Muscle cramps and weakness  Depressed deep tendon reflexes  Headache  Disorientation  Lethargy  Seizures and coma (severe hyponatremia) Gastrointestinal Tract

Hyperosmolality and Movement ofWater out of Neural Tissue Headache Disorientation and agitation Decreased reflexes Seizures and coma (severe hypernatremia)

 Anorexia, nausea, vomiting  Abdominal cramps, diarrhea

ADH, antidiuretic hormone.

Symptoms include apathy, lethargy, and headache, which can progress to disorientation, confusion, gross motor weakness, and depression of deep ten- don reflexes. Seizures and coma occur when serum sodium levels reach extremely low levels. 22 These severe effects, which are caused by cerebral edema, may be irreversible. Treatment. The treatment of hyponatremia is determined by the underlying cause, severity, and timing of onset. 21–23 When hyponatremia is caused by water intoxication, lim- iting water intake or discontinuing medications that con- tribute to SIADH may be sufficient. The administration of a saline solution orally or intravenously may be needed when hyponatremia is caused by sodium deficiency. Symptomatic hyponatremia (i.e., neurologic manifesta- tions) may be treated with hypertonic saline solution and a loop diuretic, such as furosemide, to increase water elim- ination. This combination allows for correction of serum sodium levels while ridding the body of excess water. The vasopressin receptor antagonists (vaptans) may be used in the treatment of euvolemic hyponatremia. 22,23 The treatment of severe hyponatremia varies depending on the timing of the onset of the disorder. Cells, particularly those in the brain, tend to defend against changes in cell volume caused by changes in ECF osmolality by increasing or decreasing their concentration of organic osmotically active mol- ecules (called osmolytes ) that can’t cross the cell

membrane. 22,25 In the case of prolonged water intoxi- cation (greater than 48 hours), brain cells reduce their concentration of osmolytes as a means of preventing an increase in cell volume. 22 It takes several days for brain cells to restore the osmolytes lost during hypona- tremia. Thus, treatment measures that produce rapid changes in serum osmolality may cause a dramatic decrease in brain cell volume. One of the reported effects of rapid treatment of hyponatremia, called the osmotic demyelination syndrome, is characterized by destruction of the myelin sheath of the axons passing through the brain stem. 22,23,25 This syndrome can cause serious neurologic injury and sometimes death. In per- sons with acute-onset hyponatremia (i.e., onset within 48 hours), in whom cerebral adaptation has not had time to occur, rapid correction is less likely to result in osmotic demyelination. Hypernatremia Hypernatremia is characterized by a serum sodium level above 145 mEq/L (145 mmol/L) and a serum osmolal- ity greater than 295 mOsm/kg H 2 O. 3 Because sodium and its attendant anion is functionally an impermeable solute, hypernatremia increases ECF tonicity, causing movement of water out of the ICF, resulting in cellular dehydration. 3,26–28 As with hyponatremia, hypernatremia can present as an euvolemic state, in which water from the ICF is