endocrine and metabolic disorders
Hyponatremia
Etiology of Hyponatremia
). Note that the ECF volume is not the same as effective plasma volume. For example, decreased effective plasma volume may occur with decreased ECF volume (as with diuretic use or Shock ), but it may also occur with an increased ECF volume (eg, in Sometimes, a low serum sodium measurement is caused by an excess of certain substances (eg, glucose, lipid) in the blood (translocational hyponatremia, pseudohyponatremia) rather than by a water-sodium imbalance. (See also Volume Depletion .) Deficiencies in both total body water and total body sodium exist, although proportionally more sodium than water has been lost; the sodium deficit causes hypovolemia. In hypovolemic hyponatremia, both serum osmolality and blood volume decrease.Vasopressin(antidiuretic hormone [ADH]) secretion increases despite a decrease in osmolality to maintain blood volume. The resulting water retention increases plasma dilution and hyponatremia. Extrarenal fluid losses,such as those that occur with the losses of sodium-containing fluids as in protracted vomiting, severe diarrhea, or sequestration of fluids in a 3rd space (see table), can cause hyponatremia typically when losses are replaced by ingesting plain water or liquids low in sodium (see table) or by hypotonic IV fluid. Significant ECF fluid losses also cause release ofvasopressin, causing water retention by the kidneys, which can maintain or worsen hyponatremia. In extrarenal causes of hypovolemia, because the normal renal response to volume loss is sodium conservation, urine sodium concentration is typically<10 mEq/L (< 10 mmol/L). resulting in hypovolemic hyponatremia may occur with Addison Disease , thiazide diuretic therapy, osmotic diuresis, or salt-losing nephropathy. Salt-losing nephropathy encompasses a loosely defined group of intrinsic renal disorders with primarily renal tubular dysfunction. This group includes 20 mEq/L [> 20 mmol/L]). Urine sodium concentration may not help in differentiation when Metabolic Alkalosis (as occurs with protracted vomiting) is present and large amounts of bicarbonate are spilled in the urine, obligating the excretion of sodium to maintain electrical neutrality. In metabolic alkalosis, urine chloride concentration frequently differentiates renal from extrarenal sources of volume depletion. Diureticsmay also cause hypovolemic hyponatremia. Thiazide diuretics, in particular, decrease the kidneys’ diluting capacity and increase sodium excretion. Once volume depletion occurs, the nonosmotic release ofvasopressincauses water retention and worsens hyponatremia. Concomitant hypokalemia shifts sodium intracellularly and enhancesvasopressinrelease, thereby worsening hyponatremia. This effect of thiazides may last for up to 2 weeks after cessation of therapy; however, hyponatremia usually responds to replacement of potassium and volume deficits along with judicious monitoring of water intake until the drug effect dissipates. Older patients may have increased sodium diuresis and are especially susceptible to thiazide-induced hyponatremia, particularly when they have a preexisting defect in renal capacity to excrete free water. Rarely, such patients develop severe, life-threatening hyponatremia within a few weeks after the initiation of a thiazide diuretic. Loop diuretics much less commonly cause hyponatremia. In euvolemic (dilutional) hyponatremia, total body sodium and thus ECF volume are normal or near-normal; however, TBW is increased. Primary polydipsia can cause hyponatremia only when water intake overwhelms the kidneys’ ability to excrete water. Because normal kidneys can excrete up to 25 L urine a day, hyponatremia due solely to polydipsia results only from the ingestion of large amounts of water or from defects in renal capacity to excrete free water. Patients affected include those with psychosis or more modest degrees of polydipsia plus renal insufficiency. Euvolemic hyponatremia may also result from excessive water intake in the presence of Addison Disease , The Syndrome of Inappropriate ADH Secretion (SIADH) (SIADH) is another cause of euvolemic hyponatremia. Euvolemic hyponatremia can occur quite rapidly during transurethral resection of the prostate, cystoscopic or hysteroscopic procedures when hypotonic fluid is used as an irrigant. Early recognition is critically important since brain edema can be caused by rapid development of hypotonicity. Bipolar electrocautery, which uses isotonic irrigation solutions, is preferred over monopolar electrocautery which uses hypotonic solutions.. When hypotonic fluid must be used, limited irrigation volume, low infusion pressure and limited duration of surgery is used to minimize absorption. If prearranged thresholds of hypotonic irrigant absorption are exceeded (1000 to 2000 mL, depending upon body weight) the procedure should be aborted. Hypervolemic hyponatremia is characterized by an increase in both total body sodium (and thus ECF volume) and total body water with a relatively greater increase in TBW. Various edematous disorders, including Heart Failure (HF) and The antidiuretic effect ofvasopressinon the kidneys Direct impairment of renal water excretion byangiotensin II Decreased glomerular filtration rate (GFR) Stimulation of thirst byangiotensin II Urine sodium excretion is usually<10 mEq/L (<10 mmol/L), and urine osmolality is high relative to serum osmolality. ) in patients with normal cardiac, hepatic, renal, adrenal, and thyroid function. Syndrome of Inappropriate ADH Secretion (SIADH) is associated with myriad disorders (see table 50% of hospitalized patients with Immune system . Among the many potential contributing factors are Administration of medications that impair renal water excretion Administration of hypotonic fluids Impaired renal function Nonosmoticvasopressinrelease due to intravascular volume depletion In addition, adrenal insufficiency has become increasingly common among AIDS patients as the result of cytomegalovirus adrenalitis, mycobacterial infection, or interference with adrenal glucocorticoid and mineralocorticoid synthesis byketoconazole. SIADH may be present because of coexistent pulmonary or central nervous system infections. Hyponatremia frequently occurs in patients with brain pathology, including concussion, intracranial hemorrhage, encephalitis, meningitis, and CNS tumors. It is most commonly due to Syndrome of Inappropriate ADH Secretion (SIADH) or less commonly glucocorticoid deficiency. However, cerebral salt wasting has been recognized by some as a separate entity affecting a small group of these patients, especially those with 