Classifying Hyponatremia by Symptoms and Sodium Concentration.

Urine Osmolality

Low urine osmolality (<100 m Osm/kg water).
Normal or High Urine Osmolality (> 100 m Osm/kg water)


MedCalc: Hyponatremia & Hypernatremia, recommended in Pocket Medicine

Excellent Article from AAFP, 2015: Diagnosis and Management of Sodium Disorders: Hyponatremia and Hypernatremia

Algorithm for the Evaluation of Hyponatremia, AAFP 2015

Treatment for Severe Symptomatic Hyponatremia, AAFP 2015

Algorithm for Hypotonic Hyponatremia from Pocket Medicine, 4th Edition

* “Hypertonic saline, 3% normal saline is only given in the ICU and you need a central line to give it”, per doctor Wagner

TBW = Total Body Water; TBS=Total Body Sodium

Pathophysiology of Hyponatremia

Excess of water relative to sodium; almost always due to increased ADH. The increased ADH may be appropriate (e.g. when there is hypovolemia or hypervolemia with decrease EAV) or the increased ADH may be inappropriate (SIADH)

Workup of hyponatremia

Step 1: Get a history. Is this acute or chronic? Chronic means > 48h.
Step 2: Symptom severity. Is the patient symptomatic or asymptomatic? Is patient malnourished, an alcoholic, has cirrhosis, older females on thiazides, hypoxia, hypokalemia? Any of these increases the risk of neurologic complications.
Step 3: Check Volume Status.
Step 4: Measure Plasma Osmolality. Hypotonic hyponatremia is the most common scenario. Hypertonic hyponatremia (when there is an excess of another osmole, e.g. glucose, mannitol) that draws water intravascularly. For each 100mg/dl increase in glucose >100, there will be a decrease in [Na+] of about 2.4mEq. That’s why in DKA for example, you have to use this formula to correct the sodium. Isotonic hyponatremia is a rare lab artifact from hyperlipidemia or hyperproteinemia.
Hypotonic hyponatremia is divided into three types based on volume status.

Info in the following table is excerpted from Pocket Medicine

TBW TBS  Causes & Treatment
Hypovolemic hypotonic hyponatremia TBW  ↓↓ TBS
  • Renal losses ( UNa >20 mEq/L, FENa > 1%): Diuretics, salt-wasting nephropathy, cerebral salt wasting, mineralocorticoid deficiency.
  • Extrarenal losses (UNa < 10 mEq/L, FENa < 1%): GI losses (eg, diarrhea, vomiting), third-spacing (eg, pancreatitis), inadequate intake, insensible losses

Treatment: Volume repletion with normal saline. When the volume is replete, the low blood volume which was the stimulus for ADH production will be removed. The kidneys will again start excreting free water and serum sodium will quickly go back to normal.

Euvolemic  hypotonic hyponatremia

Also called Isovolemic…

↑TBW No change in TBS Here there is an increase in the TBW relative to total body Na (which doesn’t change).

  • SIADH (Multiple things cause SIADH)
  • Endocrinopathies: increased ADH activity is seen in glucocorticoid deficiency  (co-secretion of ADH & CRH) and hypothyroidism (↓CO & ↓GFR)
  • Psychogenic polydipsia (Uosm < 100, ↓ Uric Acid), usually requires intake 12 L/d
  • Low solute:“tea & toast”;“beer potomania”
  • Reset Osmostat: chronic malnutrition (decreased intracellular osmoles) or pregnancy (hormonal effects) lead to ADH physiology reset to regulate a lower [Na]serum

** Here, you have mostly free water going into the intravascular space. Most of it is going to be redistributed into the ECF and ICF by osmosis leaving the patient isovolumic.

Treatment: Free water restriction + treat underlying cause

Hypervolemic hypotonic hyponatremia ↑↑TBW  ↑TBS
  • CHF ( decreased CO leads to decreased EAV; UNa < 10 mEq/L, FENa <1%)
  • Cirrhosis (splanchnic arterial vasodilation and ascites lead to decreased EAV; UNa <10 mEq/L, FENa  <1%)
  • Nephrotic syndrome (hypoalbuminemia → edema → decreased EAV; UNa < 10 mEq/L, FENa < 1%)
  • Advanced renal failure (diminished ability to excrete free H2O; UNa > 20 mEq/L). Also, Acute Renal Failure can cause this.

 Treatment: Free water restriction, sodium restriction, and restrict all fluids.

Primary polydipsia = Psychogenic polydipsia;
Effective arterial volume (EAV)

If hypervolemic: Consider a daily dose of Lasix 40-80IV if giving a lot of NS.

“The cause of hyponatremia can be determined in part by how the patient’s kidneys are responding to the condition. If the urine is appropriately dilute, then the most likely cause of hyponatremia is excessive water intake or inadequate solute intake. Conversely, if the urine is concentrated, the patient may be hypovolemic, or have the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The relative volume of the patient’s extravascular fluid will help determine how to proceed with treatment. Spot urine sodium or serum uric acid levels can be used to help ascertain whether the patient is hypovolemic, euvolemic, or hypervolemic.

No treatment specific to hyponatremia is required when the serum osmolality is either normal or elevated. Both iso-osmolar hyponatremia and hyperosmolar hyponatremia are due to an overabundance of another osmole such as glucose, mannitol, or contrast dye. These situations are often referred to as pseudohyponatremia.” The ABFM

Watch this 5 minute Summary Video which is part 4 of a great series by MED CRAM