inpatient / nephrology


Last Updated: 1/21/2023

# Hypernatremia

-- ABCs: 
if Na >160 and AMS, consider ICU for close monitoring and q1-2 lab draws
-- Chart Check: h/o DI, dementia, substance use, immobility, brain pathology
-- Can't Miss: *** sepsis, cause of patient havign AMS or being found down (stroke, seizure, syncope, etc)
-- Admission Orders: CBC, BMP, Calcium, serum and urine Osm
-- Initial Treatment to Consider: fluids to correct FWD

-- History: *** long-term care facility, dementia, immobile, diuretic use
-- Clinical: *** fevers, AMS, N/V/D, polyruia/polydipsia
-- Exam: *** volume assessment, AMS, hyperreflexia, weakness
-- Data: *** Free-water Deficit (FWD), calcium
-- Etiology: decreased access to free water, AMS, decreased thirst drive, diabetes insipidus, post-ATN, loop diuretics, hyperCa, insensible losses, N/V/D

The patient's HPI is notable for ***. Exam showed ***. Labwork and data were notable for ***. Taken together, the patient's presentation is most concerning for ***, with a differential including ***.

-- Monitoring: ***BMP q ***; Strict I/O
-- Send urine Osm if c/f renal mechanism or DI - will be <600-800
-- If e/o DI - renal consult to trial desmopressin to distinguish central vs peripheral (cental will respond, nephrogenic will not)

-- Free Water: *** (PO, free water flush, D5W IV) to address FWD of *** plus *** of expected insensible losses
-- if c/f DI, Consider Na restriction <2g per day

The current free water deficit is ***. Accounting for insensible losses, we should continue to replete with *** at a rate of *** in order to decrease the sodium level *** over 24 hours.

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If You Remember Nothing Else

Hypernatremia is most commonly caused by poor PO intake and/or insensible losses.  In general, hypernatremia is rarely the sole cause of presenation, and is usually a result of another process; it may be a reflection of either poor PO intake or insensible losses secondary to other acute illnesses like infection/sepsis or a fall 2/2 intoxication, syncope or seizures. You should calculate the free water deficit and replete via D5W. Never bolus free water, but instead give it as a maintenance fluid with a goal to correct 8-12 over a 24 hour period. A complication of rapid correction is cerebral edema, but this is rarely seen in adults. If you accidentally bolus free water, touch base with renal consultants to discuss giving hypertonic 3% saline to re-correct. If the hypernatremia does not correct with replacement of free water, you can begin thinking about other etiologies like diabetes insipidus.

Clinical Pearls

  • Hypernatremia is caused by free water loss in excess of sodium loss
  • Two major mechanisms maintain plasma osmolarity between 275 and 290: Thirst and secretion of ADH. When these mechanisms malfunction, dysnatremias occur
  • It is very rare to overcorrect in adults, but the feared complication is cerebral edema
  • When calculating the FWD, the target Na should be the goal Na in 24 hours (about 8-12 lower than it is at the time of calculation)
  • Shortcut FWD in L = (current Na - goal Na in 24 hours)/3
  • Insensible losses are about 700-900cc per day usually - more if diarrhea, vomiting, burns, fevers
  • Loop diuretics wash out the renal medullary concentration gradient, which is crucial for free water reabsorption. Without the gradient, free water is lost in urine, leading to hypernatremia. In contrast, thiazides do not affect the medullary concentration gradient
  • ADH is secreted from the posterior pituitary and acts in the renal collecting ducts
  • Central DI will respond to vasopressin whereas nephrogenic will not

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