BRAUN, DO, Madigan Army Medical Center, Tacoma, Washington CRAIG H. BARSTOW, MD, Womack Army Medical Center, Fort Bragg, North Carolina NATASHA J. PYZOCHA, DO, Madigan Army Medical Center, Tacoma, Washington Am Fam Physician. Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders are associated with an increased risk of morbidity and mortality. Plasma osmolality plays a critical role in the pathophysiology and treatment of sodium disorders. Hyponatremia and hypernatremia are classified based on volume status (hypovolemia, euvolemia, and hypervolemia). Sodium disorders are diagnosed by findings from the history, physical examination, laboratory studies, and evaluation of volume status. , which increases following the administration of oral salt. We analyze the use of an oral salt load followed by furosemide for the acute/short-term treatment of euvolemic SIADH hyponatremia. Methods: Retrospective analysis of nine patients with SIADH-induced hyponatremia and moderate hyponatremic encephalopathy receiving 45 g of oral salt, followed 3 h later by 20 mg furosemide i.v. Serum sodium levels (SNa), serum potassium (SK), and urinary sodium (UNa) were measured at baseline, and 1216 h following salt administration. All blood pressure levels were below 130/85 mm Hg before and after salt administration. In six out of nine patients, a SNa level was available from 24 h or less previously (PSNa). Conclusions: The oral administration of 45 g of salt followed by furosemide was useful for the acute/short-term treatment of euvolemic SIADH-hyponatremia in our patients. However, this therapy should not be attempted in severe hyponatremia, since a minimum 4 mmol/l SNa rise was not assured.
Treat underlying cause and give IV isotonic saline. It is important to note that sudden restoration of blood volume to normal will turn off the stimulus for continued ADH secretion. This can cause a sudden and dramatic increase the serum sodium concentration and place the patient at risk for so-called "central pontine myelinolysis" (CPM). That disorder is characterized by major neurologic damage, often of a permanent nature. Because of the risk of CPM, people with low volume hyponatremia may eventually require water infusion as well as volume replacement. Doing so lessens the chance of a too rapid increase of the serum sodium level as blood volume rises and ADH levels fall. In people who are volume depleted, i.e., their blood volume is too low, ADH secretion is increased, since volume depletion is a potent stimulus for ADH secretion. As a result, the kidneys of such patients recover water and produce a fairly concentrated urine. Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality.
Hypoosmolar hyponatremia is a condition where hyponatremia associated with a low plasma osmolality. The term "hypotonic hyponatremia" is also sometimes the plasma osmolarity is low, the extracellular fluid volume status may be in one of three states low volume, normal volume, or high volume. INTRODUCTION. Hyponatremia is an occasional but potentially fatal complication of diuretic therapy. Virtually all cases of severe diuretic-induced hyponatremia have been due to a thiazide-type diuretic.