Hypernatremia

BASICS

DESCRIPTION

Serum sodium (Na) concentration >145 mEq/L (1)
Usually represents a state of hyperosmolality (1)
Na concentration reflects balance between total body water (TBW) and total body Na. Hypernatremia occurs from deficit of water relative to Na.
Hypernatremia results from net water loss or, more rarely, from primary Na gain (1).
May exist with hypo-, hyper-, or euvolemia, although hypovolemia is by far most common type
- Hypovolemic: occurs with a decrease in TBW and a proportionately smaller decrease in total body Na
- Euvolemic: no change in TBW with a proportionate increase in total body Na
- Hypervolemic: increase in TBW and a proportionately greater increase in total body Na
It has been shown to be an indicator for higher mortality in critically ill patients and patients with chronic kidney disease (CKD) (2)[B].

EPIDEMIOLOGY

Incidence

More common in elderly and young
Occurs in 1% of hospitalized elderly patients (3)
Seen in about 9% of ICU patients (3). Gastroenteritis with diarrhea is the most common cause of hypernatremia in infants.
Women are at an increased risk due to decreased TBW, as compared with men.

ETIOLOGY AND PATHOPHYSIOLOGY

Pure water loss (total body Na normal) resulting from the following:
- Adipsia/hypodipsia (e.g., impaired thirst regulation, decreased access to water) (4)
- Nephrogenic diabetes insipidus (DI) (congenital or due to renal dysfunction, hypercalcemia, hypokalemia, medication-related, particularly lithium)
- Central DI (due to head trauma, stroke, meningitis) (3)
- Increased insensible water loss (e.g., fever, hyperventilation, hypermetabolic state, heat exposure, newborns under radiant warmers)
Hypotonic fluid loss (total body Na decreased) resulting from the following:
- Loss of fluid containing relatively more water than Na (e.g., excessive sweating, severe burns)
- Urinary loss
  - Osmotic diuresis: hyperglycemia, mannitol
  - Diuretics, especially loop diuretics
  - Diabetes mellitus, particularly new presentation/decompensated
  - Post acute tubular necrosis (ATN) or post obstructive diuresis
  - Intrinsic renal disease
- Gastrointestinal loss
  - Diarrhea, especially in children
  - Vomiting, nasogastric (NG) lavage
  - Enterocutaneous fistula
Excess Na (increase in total body Na) resulting from the following:
- IV NaCl or NaHCO3 during cardiopulmonary resuscitation, metabolic acidosis, or hyperkalemia (3)
- Sea water ingestion
- Excessive use of NaHCO3 antacid.
- Incorrect infant formula preparation
- Intrauterine NaCl for abortion
- Excessive Na in dialysate solutions
- Disorders of the adrenal axis (Cushing syndrome, Conn syndrome, congenital adrenal hyperplasia)
- Tube feeding

With acute hypernatremia, the rapid decrease in brain volume can cause rupture of the cerebral veins, leading to focal intracerebral and subarachnoid hemorrhages and possibly irreversible neurologic damage (5).
Genetics
Some forms of DI may be hereditary.

RISK FACTORS

Patients at increased risk include those with an impaired thirst mechanism or restricted access to water, as well as those with increased water loss
Infants/children
Elderly patients (may also have a diminished thirst response to osmotic stimulation via an unknown mechanism)
Patients who are intubated/have altered mental status.
Diabetes mellitus
Prior brain injury
Surgery
Diuretic therapy, especially loop diuretics
Lithium treatment

GENERAL PREVENTION

Treatment/prevention of underlying cause
Properly prepare infant formula and never add salt to any commercial infant formula.
Keep patients well hydrated.

COMMONLY ASSOCIATED CONDITIONS

Gastroenteritis
Altered mental status
Burns
Hypermetabolic conditions
Head injury
Renal dysfunction

DIAGNOSIS

HISTORY

Excessive thirst, nausea, vomiting, diarrhea, oliguria, polyuria
Fever, myalgia, muscle weakness
Neurologic symptoms common: altered mental status, seizure (especially if rapid development of hypernatremia), twitching, lethargy, irritability, coma, anophthalmos
Severe symptoms are likely to occur with acute increases in plasma Na levels or at concentrations >160 mEq/L.
Obtain list of current and recent medications.
Review recent illnesses and activities.

PHYSICAL EXAM

Sinus tachycardia, hypotension, orthostatic hypotension, poor O2 saturation
Dry mucous membranes, cool/gray skin
Neurologic abnormalities: lethargy, weakness, focal deficits (in cases of intracerebral bleeding/lesion), confusion, coma, seizures

DIFFERENTIAL DIAGNOSIS

DI
Hyperosmotic coma
Salt ingestion
Hypertonic dehydration
Hypothyroidism
Cushing syndrome

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

Serum Na, potassium, BUN, creatinine, calcium, and osmolality (serum lithium if appropriate)
Urine Na and osmolality
- DI: urine osmolality (usually <300 mosmol/kg) < serum osmolality, and urine Na usually low normal/slightly low (due to dilution) (4)
- Osmotic diuresis: urine osmolality intermediate, urine Na low/low-normal, total daily osmole excretion high
- Salt ingestion: increased urine osmolality (above 600 mosmol/kg) and high urine Na
- Hypertonic dehydration: increased urine osmolality and decreased urine Na
Serum glucose
Special tests for DI
- Water deprivation test: In DI, urine osmolality does not increase as it normally should when hypernatremic.
- Antidiuretic hormone (ADH) stimulation: distinguishes central versus nephrogenic DI
  - Urine osmolality does not increase after ADH or desmopressin (DDAVP) in nephrogenic DI.
Head CT/MRI in DI to rule out craniopharyngioma, other brain tumor or masses, or median cleft syndrome

Diagnostic Procedures/Other
History, physical, laboratory studies, family history for central DI

TREATMENT

GENERAL MEASURES

The treatment of hypernatremia involves treating the underlying cause and correcting the water deficit.
Goal for corrected Na is 145 mEq/L (1).
Speed of correction depends on symptom severity/rate of development of hypernatremia. Avoid rapid correction to prevent development of cerebral edema if chronic hypernatremia (>24 hours):
- Maximum of 0.5 mEq/L/hr or 10 mEq/L/day (6)[C]
- May correct at up to 1 mEq/L/hr if acute hypernatremia (<24 hours) (1)
Treat volume depletion first, then hypernatremia:
- Restore intravascular volume with IV fluids to normalize serum Na levels.
Replace water orally if patient is conscious.
Important formulas in determining rate of fluid administration
- TBW = coefficient wt (kg), where coefficient = 0.6 for children, 0.5 for nonelderly women and elderly men, 0.45 for elderly women
- Calculated free water deficit (liters) = TBW [1- (Na_t/Na_m)], where Na_t = target Na+, and Na_m = measured Na+. Note: wt = weight in kilograms.
- Change in serum Na per 1 L infusate = [(infusate Na + infusate K) - serum Na]/[TBW + 1]
Account for ongoing fluid losses during calculation of rate of fluid administration.
Dialysis can be considered if acute kidney injury is present concomitantly and if conventional treatment has failed (7)[B].

MEDICATION

First Line

See "General Measures" for overall approach.
Volume depletion: Use isotonic fluids initially if signs of hemodynamic compromise, then change to hypotonic fluids when stable:
- Hypotonic fluids (0.45% NaCl or dextrose 5% in water)
  - Important not to decrease serum Na by >10 mEq/L/day to prevent cerebral edema (4)[C]
Hypervolemia: Give furosemide along with hypotonic fluids. Dose varies depending on desired urine output. Loop diuretics with fluid restriction worsen hypernatremia (4)[C].
Central DI
- DDAVP acetate: Use parenteral form for acute symptomatic patients, and use intranasal or oral form for chronic therapy (4).
- Free water replacement: may use 2.5% dextrose in water if giving large volumes of water in DI to avoid glycosuria
- May consider sulfonylureas/thiazide diuretics for chronic, but not acute, treatment
Nephrogenic DI
- Treat with diuretics and NSAIDs.
- Lithium-induced nephrogenic DI: hydrochlorothiazide 25 mg PO BID or indomethacin 50 mg PO TID, or amiloride hydrochloride 5 to 10 mg PO BID (8)
Precautions
- Rapid correction of hypernatremia can cause cerebral edema, central pontine myelinosis, seizures, or death (9).
- Hypocalcemia and more rarely acidosis can occur during correction.
- DI: High rates of dextrose 5% in water can cause hyperglycemia and glucose-induced diuresis.

Second Line

Consider NSAIDs in nephrogenic DI.
Modalities requiring further investigations
Continuous renal replacement therapy (CRRT): Multiple case reports and case series have shown success and safety in using CRRT to treat hypernatremia in critically ill patients with CHF and severe burns (7,10).

ISSUES FOR REFERRAL

Underlying renal involvement associated with hypernatremia would benefit from a nephrology referral.

INPATIENT CONSIDERATIONS

Admission Criteria/Initial Stabilization
Symptomatic patient with serum Na >155 mEq/L requires IV fluid therapy.
IV Fluids
Refer to "Medication" section.
Nursing
Bed rest until stable or underlying condition resolved/controlled
Discharge Criteria
Stabilization of serum Na level and symptoms are minimal.

ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

Frequent reexams in an acute setting
Frequent electrolytes and blood glucose: initially q4-6h
Urine osmolality and urine output in DI
Ensure adequate ingestion of calories because patients may ingest so much water that they feel full and do not eat.
Measure ongoing losses of water and solute and replace as needed.
Daily weights

DIET

Ensure proper nutrition during acute phase.
After resolution of acute phase, may want to consider Na-restricted diet for patient
Low-salt, low-protein diet in nephrogenic DI

PATIENT EDUCATION

Patients with nephrogenic DI must avoid salt and drink large amounts of water.

PROGNOSIS

Most recover but neurologic impairment can occur.

COMPLICATIONS

CNS thrombosis/hemorrhage
Seizures
Mental retardation
Hyperactivity
Chronic hypernatremia: >2 days duration has higher mortality
Serum Na >180 mEq/L (>180 mmol/L): often results in residual CNS damage
More common if rapid development of hypernatremia

REFERENCES

11 Adrogu © HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493-1499.22 Kovesdy CP, Lott EH, Lu JL, et al. Hyponatremia, hypernatremia, and mortality in patients with chronic kidney disease with and without congestive heart failure. Circulation. 2012;125(5):677-684.33 Bagshaw SM, Townsend DR, McDermid RC. Disorders of sodium and water balance in hospitalized patients. Can J Anaesth. 2009;56(2):151-167.44 Hannon MJ, Finucane FM, Sherlock M, et al. Clinical review: disorders of water homeostasis in neurosurgical patients. J Clin Endocrinol Metab. 2012;97(5):1423-1433.55 Sterns RH. Disorders of plasma sodium-causes, consequences, and correction. N Engl J Med. 2015;372(1):55-65.66 Al-Absi A, Gosmanova EO, Wall BM. A clinical approach to the treatment of chronic hypernatremia. Am J Kidney Dis. 2012;60(6):1032-1038.77 Huang C, Zhang P, Du R, et al. Treatment of acute hypernatremia in severely burned patients using continuous veno-venous hemofiltration with gradient sodium replacement fluid: a report of nine cases. Intensive Care Med. 2013;39(8):1495-1496.88 Libber S, Harrison H, Spector D. Treatment of nephrogenic diabetes insipidus with prostaglandin synthesis inhibitors. J Pediatr. 1986;108(2):305-311.99 Mastrangelo S, Arlotta A, Cefalo MG, et al. Central pontine and extrapontine myelinolysis in a pediatric patient following rapid correction of hypernatremia. Neuropediatrics. 2009;40(3):144-147.1010 Park HS, Hong YA, Kim HG, et al. Usefulness of continuous renal replacement therapy for correcting hypernatremia in a patient with severe congestive heart failure. Hemodial Int. 2012;16(4):559-563.

ADDITIONAL READING

Waite MD, Fuhrman SA, Badawi O, et al. Intensive care unit-acquired hypernatremia is an independent predictor of increased mortality and length of stay. J Crit Care. 2013;28(4):405-412.

CODES

ICD10

E87.0 Hyperosmolality and hypernatremia

ICD9

276.0 Hyperosmolality and/or hypernatremia

SNOMED

39355002 Hypernatremia (disorder)
12403008 Chronic hypernatremia (disorder)
7405009 Acute hypernatremia
72452005 Cerebral hypernatremia

CLINICAL PEARLS

Occurs from water deficit in comparison to total body Na stores
Common causes include dehydration, DI, impaired access to fluids
Determine if the patient has hypervolemic, euvolemic, or hypovolemic hypernatremia in the differential diagnosis of etiology; most commonly hypovolemic; other entities rare
Avoid rapid correction of hypernatremia to prevent development of cerebral edema when hypernatremia is chronic (goal rate is 10 meq/L in 24 hours).
Use hypotonic fluids unless patient has hemodynamic compromise, which necessitates use of isotonic fluids.
Use oral replacement in conscious patients if possible.
Use the estimated water deficit, desired rate of correction, and estimation of ongoing free water losses to calculate a fluid repletion regimen.

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