Physiology of Hyponatremia Hyponatremia results from either the excessive intake or inability to excrete free water. Water intake  dilutional fall in plasma osmolality  suppression of ADH. Plasma osmolality is elevated OR effective circulating volume is low  ADH secretion Normals can excrete over 10 L of free water a day.

Differential Diagnosis Conditions in which ADH levels are elevated: 1. Volume depletion (vomiting, diarrhea, hemorrhage, profuse sweating) 2. CHF, cirrhosis (effective volume depletion) 3. Diuretic use 4. Adrenal insufficiency 5. SIADH

Differential Diagnosis Conditions in which ADH levels are suppressed: 1. Advanced renal failure 2. Primary polydipsia 3. Low dietary solute intake 4. Beer potomania Pseudohyponatremia—rare 1. High Sosms: hyperglycemia, mannitol 2. Normal Sosms: hyperlipidemia, hyperproteinemia

Workup History and PE are focused on volume status Later on, pattern recognition helps –The elderly lady on a tea and toast diet who is also taking a diuretic –The cirrhotic with worsening ascites, edema Early on, be complete with the evaluation: send UA (specific gravity is the poor man’s Sosm); serum osmolality, urine osmolality, urine electrolytes Urine electrolytes give another assessment of volume status (Na+ should be <10 in volume depletion, unless on diuretic), K+ handling

Workup A normal or elevated Uosm (above 100) in the setting of low Posms makes the diagnosis of SIADH. --usually Na+ is >40 --usually Creatinine is normal --normal acid-base, K+ handling Low Uosm (less than 100) seen in primary polydipsia, poor solute intake

Workup Distinguishing hypovolemia/diuretic induced from SIADH (or presence of both): --Urine Na+ usually low --PE reveals signs dehydration --Creatinine may be elevated --hold diuretic and hydrate; if the Urine Na+ rises to above 40 and the Uosms remain above 100 the patient also has SIADH.

Treatment Goal: to prevent cerebral edema and encephalopathy (lethargy, obtundation, seizures, coma, arrest) while preventing central pontine myelinolysis (correcting sodium too rapidly.) More rapid therapy (1.5 to 2 mEq per hour) can be used in the first few hours if there is serious cerebral dysfunction. Otherwise, maximum rate of elevation: mEq during the first 24 hours and 18 mEq/L in the first two days.

Ways to Raise Serum Sodium Water restriction—chronic primary therapy for hyponatremia in edematous states (CHF, cirrhosis) and in SIADH SIADH in the acute setting must be treated with IVF that exceeds the Uosm (NS or hypertonic saline) In volume depletion—use normal saline

Calculation of the Sodium Deficit TBW times the net sodium gain 0.5 times the weight in kilos for women, 0.6 for men Example of 50 kg female, sodium of 122 So, if we wish her sodium to be raised by 12 mEq in the first 24 hours: x 50 kg x 12 = 300 mEq Hypertonic saline contains roughly 1 mEq of sodium per 2 cc, so 600 cc should be given over 24 hours (25 cc/hour)

Ddx of SIADH CNS: head trauma, neurosurgery, psychiatric illness, stroke, infection Tumor: ectopic ADH due to small cell Ca of the lung (most common), also seen in bronchogenic Ca, pancreatic Ca, neuroblastoma (rarer) Drugs: Carbamazepine, chlorpropamide, highdose IV cyclophosphamide, SSRIs Major surgery Pulmonary disease (particularly pneumonia)