Hyponatremia

A Tactical Framework for the Wards

When you get a consult for hyponatremia, your job isn’t to memorize every cause — it’s to think like the kidney. Hyponatremia is not a sodium problem. It’s a water problem. Your task is to figure out whether ADH is on, whether it should be on, and whether the patient’s water intake, solute load, or kidney handling explains the imbalance.

Step 1: Confirm It’s True Hyponatremia

1. Check serum osmolality.

2. Normal osmolality (280–295) means pseudohyponatremia, often from severe hyperlipidemia or hyperproteinemia (e.g. multiple myeloma).

3. Hyperosmolar hyponatremia (osmolality >295) means translocational hyponatremia, most often from hyperglycemia or mannitol.

4. Low osmolality (<275) means true hypotonic hyponatremia, and you proceed to the next step.

Step 2: Determine if ADH Is On or Off Using Urine Osmolality

The next goal is to determine whether ADH is shown on or off. It’s impossible to measure ADH directly, so we use urine osmolality as a surrogate marker.

Uosm < 100 mOsm/kg means ADH is off — the kidneys are making maximally dilute urine. The problem is too much water intake or too little solute load.

Causes: primary polydipsia, beer potomania, “tea and toast” diet.

Management: restrict water and increase protein/salt intake.

Uosm > 100 mOsm/kg means ADH is on. Now you determine why it’s on.

Step 3: Interpret Urine Sodium and Clinical Context

1. Urine sodium tells you if the kidney believes the body is volume depleted.

2. UNa < 20 mmol/L indicates sodium avidity from hypoperfusion (GI losses, third spacing, heart failure, cirrhosis).

3. UNa > 30 mmol/L means the kidney is not conserving sodium and ADH is inappropriately active. Common causes include SIADH, adrenal insufficiency, and thiazide diuretics.

4. Loop diuretics do not cause hyponatremia.

5. Step 4: Calculate the Urine Electrolyte Free-Water Ratio

6. Whenever you send urine studies, obtain urine sodium, potassium, and osmolality. These tell you how the kidney is handling salt and water at that particular moment in time.

7. Urine electrolyte ratio = (urine Na + urine K) / plasma Na.

8. If ratio < 1, the kidney is excreting free water (dilute urine).

9. If ratio > 1, the kidney is retaining free water (concentrated urine, ADH effect).

Step 5: Assess Severity, Chronicity, and Contributing Factors

Ask whether the patient is symptomatic (confusion, lethargy, seizures, coma). Hyponatremia developing acutely is rare; assume chronic unless proven otherwise.

Ask the patient how often this happens and whether they are on thiazide diuretics or any medications that can cause SIADH. They should look up a list of SIADH-inducing medications on UpToDate.

Take a food history and estimate daily protein intake. If the patient eats more than 80 grams of protein per day, low solute intake is unlikely to be the cause.

Assess for nausea, vomiting, or pain (all increase ADH release), diarrhea (causes volume and sodium loss), and any pulmonary processes such as pneumonia that could trigger ADH.

Step 6: Management Strategy

Symptomatic or Severe Hyponatremia (Na < 120 or with seizures, coma, or significant lethargy)

1. Give 3% hypertonic saline: 100 mL IV over 10 minutes; may repeat up to 3 times if seizures persist. The goal is to raise the sodium by 4-6 mmol/L. 

2. If not actively seizing but severely hyponatremic, consider continuous infusion (e.g., 15–30 mL/hr) with sodium checks every 2–4 hours.

3. If there is concern for rapid water diuresis (for example, if you expect the patient to start making large volumes of dilute urine once volume replete or underlying cause reverses), give Desmopressin (DDAVP) 1 µg IV every 8 hours.

4. The DDAVP “clamp” works by keeping ADH artificially active so that the kidney does not suddenly start excreting large amounts of free water. This prevents rapid sodium correction and osmotic demyelination. It allows you to control sodium rise using measured hypertonic saline and free water rather than being at the mercy of the patient’s physiology. It is generally safer to err on the side of giving DDAVP early if the patient appears to be recovering or producing more urine.

5. The target correction rate for chronic hyponatremia is 6–8 mmol/L in 24 hours.

6. If overcorrection occurs, reverse with D5W and/or additional DDAVP.

Risk factors for osmotic demyelination can be remembered with the acronym SHAAM:

S = Serum sodium <105

H = Hypokalemia (raising potassium raises sodium via the Edelman equation)

A = Alcoholism

A = Alcoholic liver disease

M = Malnutrition

Patients with any of these risk factors are at higher risk of demyelination and should be corrected even more cautiously.

The goal of the first 12 hours, if the patient is asymptomatic, is to keep the sodium level stable. Even if you think you know the cause, you do not yet know how their body will respond to intervention. By the end of 24 hours, aim for a rise of 4–6 mmol/L, not exceeding 6–8 mmol/L total in 24 hours.

Hypovolemic Hyponatremia (Uosm > 100, UNa < 20)

1. Treat with isotonic saline (0.9%) to restore intravascular volume. This suppresses ADH and allows water excretion. Only give isotonic saline after the 12-hour mark since we don’t know how the patient tends to handle salt and water in the first 12 hours. 

2. Be cautious with hypertonic saline, as repletion of intravascular volume may suddenly suppress ADH and cause rapid water diuresis with overcorrection.

Euvolemic Hyponatremia (SIADH, Hypothyroidism, Adrenal Insufficiency)

1. Treat the underlying cause and restrict free water (<1 L/day).

2. Increase solute intake using salt tablets, protein, or urea. As a general equivalence, 15 grams of oral urea provides a solute load similar to 50 grams of dietary protein or about seven or eight 1-gram salt tablets.

3. 100 mL of 3% saline provides about 3 grams of sodium chloride.

4. If refractory, consider a loop diuretic with salt supplementation or a vasopressin antagonist such as tolvaptan.

Hypervolemic Hyponatremia (Heart Failure, Cirrhosis)

1. Fluid restrict, limit sodium intake, and use loop diuretics to offload water.

2. Optimize management of the underlying condition.

Step 7: Monitoring

1. Recheck sodium every 2–4 hours during active therapy.

2. Track urine output, urine osmolality, and urine electrolytes. A sudden fall in Uosm or a urine (Na+ + K+)/plasma Na ratio < 0.5 indicates the kidney has begun excreting free water and sodium may rise quickly.

3. Maintain strict intake and output records.

4. Stop correction or give D5W if sodium rises faster than planned.

5. Step 8: When to Involve Nephrology

6. Consult nephrology for sodium <120, for hyponatremia with unclear cause or neurologic symptoms, for rapid or unpredictable sodium changes, for SIADH not responsive to fluid restriction, or for complex cases requiring DDAVP clamp management.

Physiologic Logic Recap

1. Confirm true hypo-osmolar state.

2. Uosm < 100 means ADH off and the problem is too much water or too little solute.

3. Uosm > 100 means ADH on and you check urine sodium and the story.

4. Severe or symptomatic cases need 3% saline ± DDAVP clamp.

5. Use urine (Na + K)/plasma Na ratio to assess current renal handling of water.

6. Correct slowly, deliberately, and always think about the underlying mechanism of hyponatremia.

7. Hyponatremia management is controlled physiology. Measure, interpret, and act deliberately — and always respect the brain’s pace of adaptation.