Chronic hypernatremia
-Patient with chronic hypernatremia. Unlikely to be acute hypernatremia.
–DDx hypernatremia.
Admit to Med/Surg
Order/Review: Urine osmolality, urine sodium, plasma osmolality at the same time. CBC, CMP
Check volume status with vital signs, orthostatic vitals, JVP, Skin turgor, BUN, CR.
Consider CT head to r/o brain lesion.
Consider CXR and UA with UCx.
Calculate free water deficit
–Free Water Deficit (FWD)
Note: The FWD does is not constant but will change moving forward. It doesn’t include ongoing free water losses.
Tx of the chronic hypernatremia
-Restore access to water or give daily requirement of water (≥ 1L/day)
-Replace free water: D5 Water IV at a rate of 1.35 mL/hr. x pt.’s weight in kg, or about 70 mL/hr. in a 50 kg pt. and 100 mL/hr. in a 70 kg pt.
-Treatment goal:The tx goal for this chronic hypernatremia regimen is to lower the serum sodium by 10 meq/L in 24 hours or 0.4mEq/L/hr (12 meq/L in 24hrs is considered the maximum safe limit, and we have chosen 10 meq/L in 24 hours to increase safety). The rate of decrease of Na should not exceed 0.5 mEq/L/hr to avoid cerebral edema.
–Sodium correction Rate
Monitoring treatment
BMP q4h for the first day. Remeasure the serum sodium q4hrs for the first day of tx. If the repeat serum sodium indicates that the target rate of correction has been attained, then the freq of measurement can be reduced in most patients to q12 to 24 hours.
If the target rate of correction has not been attained (the rate of correction is either too fast or too slow), then the infusion rate should be modified, and the serum sodium should be remeasured 4hrs after the modification has taken place.
Will watch Na + and K+ levels and if hypokalemia or hyponatremia, will replace the electrolyte in IVFs as needed.
Will watch out for hyperglycemia since pt on D5.
If hyperglycemia occurs, will switch to D2.5 Water to avoid high glucose that may cause osmotic diuresis and electrolyte free water losses.
| The approach above is a four-step approach to treating pt hypernatremia:
1. Estimate the magnitude of the water deficit. |
“Central diabetes insipidus (CDI) may occur with severe cases of traumatic brain injury (TBI), and is thought to result from injury to the hypothalamic/pituitary area of the brain (SOR A). This is manifested by the development of hypernatremia and polyuria during the post-injury period. Treatment with desmopressin reduces the attendant water loss and may prevent further brain injury. TBI patients with CDI have a higher mortality rate, probably because their injuries are more severe. One study showed hypernatremia to be a possible (but not definite) independent risk factor for higher mortality among TBI patients, even after accounting for those who developed CDI (SOR B).
It is a common practice to use hypertonic saline to relieve cerebral edema in TBI patients, but it has not yet been determined whether hypertonic saline has a role in the development of hypernatremia, and if so, whether this has a deleterious effect independent of other factors. Hypernatremia most consistently corresponds to the development of central diabetes insipidus in patients with TBI, not to the severity of cerebral edema. Other factors contributing to hypernatremia include dehydration and volume status, and side effects of other medications (SOR C).
Mannitol is an osmotic diuretic commonly used to reduce cerebral edema. It results in reduced renal reabsorption of water and sodium. The net effect on serum sodium is variable, but it does not consistently increase sodium concentration (SOR C).” The ABFM