The abnormality chosen is:

HYPONATREMIA, a serum sodium level less than 135 mEq/L. This is the most comon electrolyte abnormality in clinical medicine, and is a common consequence of diuretic therapy (along with hypochloremia and metabolic alkalosis).  Most cases are mild and asymptomatic.  Sympotms develop as the sodium level decreases and may include weakness, lethargy, nausea, headache, obtundation, seizures, coma and death. The sodium value is considered critical when it is less than 120 mEq/L. While correction of a critically low sodium value is imperative, it is important not to become overly aggressive unless the symptoms dictate heroic measures. Rapid correction of hyponatremia may result in central pontine myelinolysis with resultant irreparable neurologic damage that manifests clinically as spastic tetraparesis, pseudobulbar paralysis (dysphagia, dysarthria, tongue weakness, and emotional lability) and/or the locked-in syndrome (intact consciousness but an inability to respond in anyway except vertical gaze or blinking). Women of child bearing age suffer worse outcomes than do their male counterparts. Hyponatremia associated with hypoxia is an emergent condition and requires prophylactic intubation.

The differential diagnosis for hyponatremia is extensive and since determining the serum osmolality helps narrow the differential diagnosis, this is the first step in the work up to determine the underlying etiology. The serum osmolality should be measured, and then calculated via the following formula:

The normal range for serum osmolality is 280 to 295 mOsm/kg. If the measured osmolality is greater than the calculated value by more than 10 mOsm/kg, this is consistent with the presence of an unmeasured osmotically active serum solute such as ethanol, mannitol or methanol. Hypertonic (elevated plasma osmolality >295) hyponatremia is associated with mannitol therapy or hyperglycemia. Isotonic (normal osmolality 280 to 295) hyponatremia is seen with marked hyperproteinemia or hyperlipidemia.  The differential for hypotonic (low plasma osmolality <280) hyponatremia is extensive.  Hypotonic hyponatremia may also be associated with a normal or elevated serum osmolality if elevated levels of othe solutes (ethanol or urea) are present.

Determination of the volume status helps to narrow the differential diagnosis of hypotonic hyponatremia.  Hypovolemic hypotonic hyponatremia (positive orthostatic vital signs, dry mucous membranes, FENa<1, anuria or oliguria) results from vomiting, diarrhea, laxative abuse, nasogastric suctioning, renal disease, salt-wasting nephropathy, solute diuresis, or aggressive diuretic therapy. In this group of patients, the urinary sodium from a random sample may be helpful as a low urinary sodium should be expected in hypovolemia except in the case of diuretic usage/abuse or salt wasting nephropathy. Hypervolemic hypotonic hyponatremia (edema, respiratory crackles, ascites) resuts from congestive heart failure, nephrotic syndrome, cirrhosis, or renal failure with volume overload. Euvolemic hypotonic hyponatremia results from severe hypothyroidism, Addison's disease, SIADH, psychogenic polydipsia, beer potomania, tea and toast syndrome, exercise-associated hyponatremia, and medications. Cerebral salt wasting occurs secondary to excessive release of brain natriuretic peptide in such conditions as subarachnoid hemorrhage, tuberculous meningitis, and status post brain surgery.

Hypokalemia may cause or exacerbate hyponatremia and therefore should be corrected and the serum sodium rechecked afterwards. Hyponatremia is also commonly associated with thiazide diuretic therapy in elderly patients and during the postoperative period for many patients, especially following TURP or hysteroscopy.

Hyperglycemia causes an increase in the serum osmolality. In this instance, the serum sodium may be corrected via the following equation:

If the corrected serum sodium is within the normal range, then the etiology is entirely hyperglycemia and correction of the elevated blood sugar will normalize the serum sodium. If the corrected sodium is still hyponatremic, then a second etiology for the low sodium should be considered.

Prolonged endurance athletics such as marathons and triathalons can lead to a condition of excercise-associated hyponatremia. The etiology of which may be due to either pain associated SIADH or excessive ingestion of water during the competition without replacement of solutes. Alcoholics (beer potomania) and the elderly (tea and toast syndrome) may develop hyponatremia as a result of poor solute intake via their diets.

Therapy for most cases of hyponatremia will be treatment of the underlying etiology. When there is associated hypoxia, this represents an emergent condition and intubation is indicated. Therapy for symptomatic patients is with hypertonic saline (3%) infusion at a rate of 1 mL/kg/hr. Hypertonic saline may be co-administered with furosemide if the urine osmolality is greater than 300 mOsm/kg as this limits the expansion of the extracellular fluid volume. Serum sodium should be monitored every hour during correction and the rate of correction should not exceed 1 to 2 mmol/L/hr and no more than 10-12 mmol/L/day. Hyponatremic patients who are seizing or show signs of impending brain stem herniation may be treated with 3% saline IV at 2-3 mL/kg/hr initially. If overcorrection occurs, patients may be given intravenous 5% dextrose or desmopressin to lower the sodium level. Asymptomatic patients with hypovolemia may be treated with intravenous isotonic saline whereas euvolemic patients may respond to fluid restriction. Vasopressin receptor antagonists (intravenous conivaptan and oral tolvaptan) are available for the treatment of hyponatremia secondary to SIADH, CHF, or ascites due to cirrhosis. Asymptomatic thiazide induced hyponatremia may be treated by discontinuing diuretic therapy and correcting hypovolemia and hypokalemia. Elderly patients with poor dietary habits may be treated with oral sodium bicarbonate therapy or demeclocycline (300-600 mg orally BID).