Hyponatremia

Hyponatremia is the most common electrolyte abnormality encountered in the hospital. It primarily signifies a problem with water, not salt.

Etiology: Net gain of electrolyte free water relative to the body's stores of Na and K. This can occur in three volume states:

1) Hypovelemic State: ADH is appropriately released resulting in the retention of water in the kidneys. There is relatively more water retention than sodium retention resulting in hyponatremia. The urine osmolality will be high and urine sodium will be low. Thiazide diuretics are also common culprits of chronic hyponatremia.

2) Euvolemic State:

• SIADH: ADH is inappropriately released by many mechanisms including pain response, nausea/vomitting, CNS disturbance, pulmonary disease, medications (anti-depressants, anti-convulsants, MDMA/ectsasy)
• Tumour producing ADH
• Endocrine abN (hypothyroidism, adrenal insufficiency)
• Low solute diet (tea and toast, beer potomania)
• Psychogenic polydipsia.

3) Hypervolemic State: Low effective circulating volume i.e. cirrhosis, heart failure.

Severity:
The degree of severity is inversely proportional to the serum Na and the time frame over which the change occurred. The risk of hyponatremia is inversely proportional to the Serum Na, with serum Na less than 120mmol/L considered severe. Symptoms are non-specific, including lethargy, headache, confusion, seizures and decreased LOC. Patients with seizures and decreased LOC, secondary to low Na, should have their serum Na corrected quickly (see treatment below). However patients with chronically low serum Na, do not need to be corrected quickly and may in fact be harmed by over correction.

Patients with chronically low serum [Na] develop shifts in the intracerebral osmoles to coompensate for the chronically low serum [Na]. Therefore, if a rapid correction of serum [Na] occurs, this can result in a sudden shift of water extracellularly, putting patients at risk of osmotic demyelinating syndrome (ODS) or cerebral pontine myelinolysis (CPM). Patients who are elderly, malnourished and hypokalemic are at the highest risk. In the case of rapid correction (8mmol/day or more), the serum Na must be decreased quickly to prevent the development of ODS/CPM. Treatment includes administering hypotonic IV fluids and giving DDAVP to increase serum ADH.

Diagnosis:
1) Start by confirming hyponatremic hyponatremia by doing a serum osmolality. Rule out hypertonic hyponatremia caused by other osmoles (hyperglycemia, mannitol)

2) Assess volume status: hypervolemic, hypovolemic, euvolemic

3) Confirm volume status with urine lytes:

• Hypovolemic: High urine osmolality greater than 300mOsm. Low excretion of urine Na less than 20. 
• Euvolemic: Normal urine Na, normal urine osmolality.
• Keep in mind if pt is on Lasix, urine Na may be high!

Treatment of Hyponatremia:
1) Severe Hypo Na: Treat with hypertonic saline 3% (513 mOsm). Give 100cc 3%NS over 10 minutes, this should increase serum [Na] by 2meq. This can be repeated twice every 10 minutes. Pateints should be treated until symptoms resolve (i.e. seizures). Furosemide can be given reduce volume expansion and prevent shutting off of ADH and diuresis.

2) Non-severe hypovolemic HypoNa: A safe range for improving sodium is 6-8mEq/24 hrs. Patients should be monitored for urine output, repeat serum lytes and urine lytes Q4hr as they receive IV fluids. A sign of aquaresis is the sudden production of large amounts of dilute urine. If this occurs, to prevent rapid correction of serum [Na], DDAVP can be given 2-4mcg IV. Some insititutions advocate for giving DDAVP up front, however as long as close care is taken to detect aquaresis early, giving up front DDAVP can be avoided.

3) SIADH = restrict fluid to less than 1.5L per day, and consider salt tabs.

Please refer to the following recently published article on Hyponatremia in JASN: http://jasn.asnjournals.org/content/23/7/1140.full.pdf+html?sid=c14ec703-91e2-4d5e-966e-eef3e9aa8ac5