Sodium Imbalance
The major cation (90%) in extracellular fluid (ECF), sodium is the main factor responsible for ECF concentration. Increases or decreases in ECF sodium concentrations greatly affect ECF volume and distribution. Sodium controls the distribution of water throughout the body and regulates ECF volume. It also plays an important role in the transmission of nerve impulses for muscle contraction.
Hyponatremia refers to an excess of body water relative to sodium; it isn’t synonymous with sodium depletion. Sodium loss is just one state in which hyponatremia may occur. Hypernatremia refers to a deficit of body water relative to sodium. Thirst seems to be the major defense mechanism against hypernatremia.
Although the body requires only 2 to 4 g of sodium per day, most Americans consume 6 to 10 g per day (mostly sodium chloride, as table salt), excreting excess sodium through the kidneys and skin. Under the influence of antidiuretic hormone (ADH) and aldosterone, the kidneys primarily regulate ECF sodium balance.
Causes
Hyponatremia usually results from defective urine dilution caused by either an excessive loss of sodium or an excessive gain of water. Specific causes of hyponatremia include:
excessive perspiration, fever, or excessive GI loss of water and electrolytes due to vomiting, suctioning, fistulas, or diarrhea. When such losses decrease circulating fluid volume, increased secretion of ADH promotes maximum water reabsorption, which further dilutes serum sodium. Combined with too much free water intake, these factors are especially likely to cause hyponatremia.
diuretic therapy, most commonly thiazides
excessive drinking of water (psychogenic polydipsia) or infusion of I.V. dextrose in water without other solutes, particularly during stress
endocrine disorders, such as adrenal gland insufficiency and moderate-to- severe hypothyroidism
chronic illnesses, such as cirrhosis of the liver and heart failure
syndrome of inappropriate antidiuretic hormone (SIADH) secretion, resulting from central nervous system disorders, such as head injury or cerebrovascular accident; nonmalignant pulmonary diseases such as tuberculosis; neoplasms with ectopic ADH production such as oat cell lung tumors; or certain drugs, such as chlorpropamide and clofibrate.
Hypernatremia results from a sodium gain in excess of water or, most commonly, by a water loss in excess of sodium. It may also result from water loss alone. Specific causes of hypernatremia include:
severe insensible water losses that aren’t replaced, such as in patients with fever, hyperventilation, or extensive burns
severe renal water losses as in patients with acute diabetes insipidus
severe vomiting and diarrhea, causing water loss that exceeds sodium loss; serum sodium levels rise, but overall ECF volume decreases
excess adrenocortical hormones as in patients with Cushing’s syndrome
water loss in excess of sodium due to diaphoresis, if the patient can’t drink
administration of high-protein feedings without adequate water supplement (due to urea diuresis)
sodium excess, such as administration of excessive amounts of hypertonic sodium chloride infusions to obtunded patients who can’t drink, or inadvertent introduction of hypertonic sodium chloride solution into maternal circulation during therapeutic abortion.
Thirst is such a strong drive that severe, persistent hypernatremia only occurs in people who can’t respond to thirst voluntarily, such as patients with sedativeinduced confusion or those who have been restrained. A disturbance of the thirst mechanism is rare.
Complications
States of severe hyponatremia or hypernatremia may result in seizures, coma, and permanent neurologic damage.
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