47M with mutism p/w AMS, profound weight loss and found to have marked hypernatremia
- Approach to hypernatremia
- Consider free water loss (renal, GI, insensible loss)
- Reduced access to free water (dementia)
- Hypertonic intake (3% NS, ocean water)
- Diabetes insipidus implies impaired urinary water reabsorption and therefore urine osms are inappropriately lower than serum osms.
- Determine acute versus chronic
- Calculate free water detect
- If acute correct over 24 hours
- If chronic correct 10mEq/day
- Reassess frequently
Approach to hypernatremia
The principles of treatment in hypernatremia are similar to those in hyponatremia and therefore it also important to determine:
- Acute (< 24 hours) versus chronic (> 24 hours)
- Acute: correct over 24 hours
- Chronic: correct by 10mEq/24 hours
- Why? With aggressive repletion of free water, there is a risk of cerebral edema. This risk is less than that of aggressive correction of hyponatremia (–> osmotic demyelination syndrome) but is more likely in patients with higher initial Na
- Symptomatic versus asymptomatic
Details of correction of chronic hypernatremia
- Step 1: use the (1) patients’ weight (2) current sodium and (3) goal sodium (usually 10mEq less than current sodium) to calculate the free water deficit for the day.
- Step 2: divide the free water deficit/24 hours and infuse D5 H20 at that rate
- Frequently recheck your Na and adjust your rate by starting back at step 1
*Consider making the patient NPO to ensure accuracy of free H20 intake (especially initially).
*In patients with DI, their free water clearance via the kidneys may be dynamic. Therefore, monitoring the urine osm (along with renal or endocrine) is important.
- For patients with concomitant hypovolemia obtain second PIV (if possible) and bolus PRN (e.g. soft blood pressures)
- Separating the treatment of hypovolemia from addressing your free water deficit will help maintain better control of your sodium correction.