Best Case Ever Discussion

Treatment Algorithm

Management Discussion

2. Defend the Intravascular Volume

In order to defend the intravascular volume a determination an assessment of the patient’s volume status must occur. Is the patient hypovolemic, euvolemic or hypervolemic?

Although volume status is difficult to assess with any accuracy at the bedside, a clinical assessment with attention to the patient’s history, heart rate, blood pressure, JVP, the presence of pedal and sacral edema, the presence of a postural drop (helpful in Dr. Etchell’s opinion) and point-of-care ultrasound (POCUS) is usually adequate to make a rough determination of whether the patient is significantly hypovolemic (requiring fluid resuscitation) or significantly hypervolemic (requiring fluid restriction +/- diuretics).

In a patient who is hypovolemic and hyponatremic, the priority is to restore adequate circulating volume. In particular, restoring adequate circulating volume takes priority over any concerns that the hyponatremia might be corrected too rapidly and lead to osmotic demyelination syndrome.

When selecting the type of fluid for restortation of adequate circulating volume in the hypovolemic/hyponatrmemic patient, be mindful of the sodium concentration of the fluid that you have chosen. Ringer’s lactate has a sodium concentration of 128mmol/L which will be more isotonic to the hyponatremic patient. Although never shown in clinical studies, administering Ringer’s lactate will likely result is a slower rise in serum serum sodium than Normal Saline, and therefore have a lower risk of potentiating osmotic demyelination syndrome. Ringer’s lactate is therefore recommended by our experts as the fluid of choice for resuscitation of the hypovolemic/hyponatremic patient.

The management of hypervolemic hyponatremia centers on sodium restriction, water restriction and diuretics.

Euvolemic patients with hyponatremia have an appropriate volume status, and so do not require any particular treatment to defend intravascular volume, and management should concentrate on preventing worsening hyponatremia.


3. Prevent Worsening Hyponatremia

Once you have correctly identified and managed the baseline volume status of the patient through either volume resuscitation or diuresis, the goal becomes preventing further exacerbation of the hyponatremia. This is achieved through strict fluid restriction and saline locking the IV. It is extremely important to communicate this to the patient family and healthcare team. Water can literally kill your patient with hyponatremia!


4. Prevent Rapid Overcorrection: The Rule of 100s

It is important to understand that the fluid itself that you have given to your patient is not the cause of a rapid increase in the serum sodium, but rather, the free water diuresis that results shortly afterwards. Monitoring the urine output will be the deciding factor in preventing over-correction and possible complications. Therefore, to prevent rapid over-correction:

  1. Insert a foley catheter and monitor ins and outs
  2. If urine output >100cc/hour, send STAT urine osmolarity and urine sodium
  3. If urine osmolarity<100, consider administering 1 microgram DDAVP IV
  4. Continue following steps 2-3 as per urine output


Indication for DDAVP in patients with hyponatremia

The situation in which our experts recommend administering IV DDAVP 1 microgram in the ED to prevent osmotic demyelination syndrome is in the hypovolemic patient with hyponatremia who has been given IV chrystalloid for emergency management of pediatric seizuresvolume replacement and now has a high urine output >100cc/hr and urine osmolarity <100mosm/L.


Correcting Hyponatremia: The Rule of 6s

“Six in six hours for severe symptoms, then stop. Six a day makes sense for safety.”

The rule of 6s can be helpful in guiding your correction of hyponatremia. “Six in six hours for severe symptoms and then stop” implies that if you need to rapidly increase serum sodium due to a neurologic emergency do not correct more than 6mmol. “Six a day make sense for safety” implies that you should not exceed an increase of sodium of more than 6mmol/day. While different sources will cite different ranges, targeting six is a conservative approach. If you overshoot by one or two mmol then you will still be well within the safe range.


5. Ascertain the Cause of Hyponatremia

Dr. Baimel’s Practical Approach to the Differential Diagnosis of Hyponatremia

  1. Look at chief complaint: look for conditions which can increase output or decrease intake such as vomiting and diarrhea, pain or altered level of awareness
  2. Review Medication List: look for those that cause SIADH, especially thiazide diuretics and SSRIs; patients who have been on chronic steroids may have adrenal insufficiency
  3. Evaluate PMHx: Look for history of end organ failure (CHF, liver failure and renal failure) or cancers (a cause of SIADH)
  4. Lab work: glucose (hyperglycemia), potassium (hyperkalemia may suggest adrenal insufficiency), TSH (hypothyroidism)

Correcting Hypokalemia Can Help Improve Hyponatremia


  • 1 tab of 20meq of KDur tid (preferred by our experts)
  • KCl elixir 10mmol q4H PO or NG
  • Ringers lactate 50mL/hr IV + 40KCl/hr


Complications of Hyponatremia

Cerebral Edema

Cerebral edema should be considered in all patients with either severe hyponatremia or a rapid lowering of serum sodium concentration and altered level of consciousness.

Measurement of the optic nerve diameter with point-of-care ultrasound (POCUS), and a CT scan of the head may show effacement of the sulci as a surrogate of cerebral edema.

Video on how to perform ocular ultrasound for optic nerve diameter By Minh LeCong

If you suspect cerebral edema, administer 3% hypertonic saline as described above.


Osmotic Demylination Syndrome (ODS)

Formerly known as Central Pontine Myelinolysis, ODS is a devastating condition which can occur after rapid over-correction of hyponatremia. It is a clinical diagnosis with a delayed presentation up to 7 days after the rapid correction. The symptoms can vary and are dependent on which anatomical structure in the brain demyelinates.

ODS most commonly affects the pons, however other structures can be affected including the cerebellum or basal ganglia. Commonly described symptoms include ataxia, quadriplegia, cranial nerve palsies, and the ‘locked-in’ syndrome.

Risk factors for ODS:

  • elderly
  • malnourished state
  • chronic severe hyponatremia
  • hypokalemia


Management of the Patient with Hyponatremia who has been Over-corrected

The scenario we all dread seeing in a hyponatremic patient occurs when a repeat serum sodium level comes back dramatically higher than expected. The management of over-correction of hyponatremia is similar to the general approach to hyponatremia:

  1. Defend the intravascular volume
  2. Prevent the sodium from increasing any further
    • Fluid restriction: make the patient NPO and stop IV fluids
    • Give DDAVP 1 microgram IV
  3. Consult Nephrology

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