Hypernatremia
Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Serum sodium greater than 145 mEq/L (see Box 5.5).
Incidence
A.Up to 80% of hypernatremia is hospital acquired. Only 0.1% to 1.4% of hypernatremia is present on admission.
B.Overall inpatient incidence is 1% to 5%, and incidence in critically ill patients is 9% to 26%.
C.Hypernatremia is associated with increased length of stay and is an independent predictor of mortality (increased >40%).
D.Populations at increased risk.
1.Extremes of age (infants and elderly), especially patients with pulmonary or urinary tract infections.
2.Restricted access to water.
3.Altered mental status/neurological illness.
4.Chronic debilitating illnesses associated with impaired thirst/dehydration.
Pathogenesis
A.Reflects a water deficit relative to total body sodium.
B.Can occur in hypovolemic, euvolemic, and hypervolemic patients.
C.Causes plasma hypertonicity (effect of plasma on cells that causes cells to shrink).
D.Almost always requires reduced intake of water with or without loss of the normal thirst response. Otherwise, individuals’ normal thirst would encourage them to drink a sufficient amount to correct plasma hypertonicity.
BOX 5.5
Sodium in Humans
- Normal serum concentration 135 to 145 mEq/L.
- Most abundant extracellular cation.
- The majority of total body sodium is found in cells and plasma water. Additional bound sodium is found (and can accumulate) in bone, cartilage, and connective tissue.
- Plasma sodium is approximately the same as interstitial sodium.
- Sodium does not cross the blood–brain barrier, but plasma sodium levels and tonicity of plasma affect brain cells.
- Changes in serum sodium concentration typically reflect changes in water balance rather than actual changes in total body sodium.
E.Hypovolemic hypernatremia: Represents a pronounced water deficit with a mild sodium deficit and requires impaired thirst or decreased intake of water in addition to losses.
F.Euvolemic hypernatremia: Represents a pure body water deficit.
G.Hypervolemic hypernatremia: Represents minimal decrease or no change in total body water (TBW) with an increase in total body sodium.
H.Acute salt poisoning: Large intake of sodium (whether accidental or intentional), resulting in a rapid rise in sodium and subsequent severe hypertonicity.
Predisposing Factors
A.Alterations in thirst.
B.Volume depletion.
C.Hyperglycemia.
D.Certain brain tumors such as pituitary tumors.
Subjective Data
A.Common complaints/symptoms.
1.Vary depending on cause, severity, and rate of development of hypernatremia.
a.Altered skin turgor commonly found in hypovolemic or euvolemic hypernatremia.
b.Signs of volume overload: Hypervolemic hypernatremia.
2.Spectrum of neurological symptoms: Beginning with irritability, dizziness, fatigue, lethargy, and confusion; can progress to seizures and coma.
3.Other symptoms: Nausea, vomiting, and generalized muscle weakness.
4.Polyuria.
a.Definition: 3 L or more per day.
b.Urine output exceeding 5 to 10 L per day indicates antidiuretic hormone (ADH) deficiency (as in diabetes insipidus [DI]); these affected patients often crave ice.
5.Acute salt poisoning: High fever, intracranial hemorrhage, seizures, and coma.
Physical Examination
A.Physical examination to assess volume status.
1.Check skin, mucous membranes, heart, lungs, jugular venous distension (JVD), edema.
2.Assess blood pressure and orthostatic changes.
3.Determine weight changes.
B.Neurological assessment (initial and ongoing).
Diagnostic Tests
A.Serum sodium.
B.Complete chemistry panel to assess causes.
C.Serum osmolality.
D.Spot urine osmolality (measured).
1.Greater than 300 mOsm/kg: Urine is concentrated and hypertonic but not necessarily because of sodium. This indicates a relative increase in solute compared to water.
2.Less than 100 mOsm/kg: Urine is dilute and hypotonic. This indicates a relative increase in water and/or decrease in solute.
E.Spot urine sodium.
1.Less than 20 mEq/L: Renal sodium retention as in low effective arterial blood volume.
a.Common with extra-renal volume losses.
2.Greater than 20 to 30 mEq/L: Renal-related losses of electrolytes (sodium).
a.Common with loop diuretics, osmotic diuresis, or hyperglycemia.
b.Post-AKI diuresis and post obstructive diuresis.
F.Determination of patient volume status.
1.Consider volume assessment to be unreliable initial diagnostic criteria but is necessary when interpreting hypernatremia-related lab tests.
2.Review and calculate history of fluid intake and output.
Differential Diagnosis
A.Hypovolemic hypernatremia.
1.Water and salt deficit.
2.Renal losses (Urine sodium >20 mEq/L).
a.Loop diuretics (spot urine osmolality <100 mOsm/kg [hypotonic]).
b.Post-obstructive or post-acute kidney injury (AKI) diuresis.
c.Osmotic diuresis: Hyperglycemia, mannitol, urea (enteral tube feedings; spot urine
osmolality >300 mOsm/kg or 24-hour urine osmolality >1,200 mOsm/kg).
3.Extrarenal losses: Urine sodium less than 20 mEq/L; urine osmolality greater than 300 mOsm/kg (hypertonic).
a.Gastrointestinal losses such as vomiting, diarrhea (i.e., acute infectious, osmotic [enteral tube feedings]), nasogastric suctioning, or enterocutaneous fistula.
b.Skin losses: Perspiration, burns, or severe wounds.
B.Euvolemic hypernatremia.
1.Pure water deficit; body sodium preserved.
2.Renal losses: Hypotonic urine (urine osmolality/plasma osmolality <1).
a.DI: Inadequate ADH release (spot urine osmolality <100 mOsm/kg).
i.Central DI: Congenital, head trauma, post neurosurgical surgery, neoplasms, infiltrative disorders (i.e., sarcoidosis), hypoxic encephalopathy, bleeding, infection, aneurysm, meningitis/encephalitis.
b.Gestational DI: Peripheral degradation of ADH.
c.Nephrogenic DI (hereditary): Inadequate renal response to ADH.
i.X-linked nephrogenic DI.
ii.Autosomal recessive nephrogenic DI.
d.Acquired nephrogenic DI: ADH independent urine concentrating defect.
i.Hypercalcemia or hypokalemia.
ii.Medication-induced: Lithium, vasopressin V2 receptor antagonists, demeclocycline, amphotericin B, methoxyflurane, or foscarnet.
iii.Chronic kidney diseases (i.e., medullary cyst disease, sickle cell disease, amyloidosis, Sjögren’s syndrome).
iv.Bartter’s syndrome.
v.Malnutrition.
3.Extrarenal losses: Hypertonic urine (urine osmolality/plasma osmolality >1).
a.Insensible losses.
i.Cutaneous: Fever, sweating, burns, or increased ambient temperature.
ii.Respiratory: Tachypnea or mechanical ventilation.
b.Decreased water intake.
i.Primary hypodipsia.
ii.Reset osmostat.
iii.Decreased access to water (i.e., altered mental status, iatrogenic).
iv.Water loss intracellular (i.e., seizures, extreme exercise).
C.Hypervolemic hypernatremia.
1.Increased sodium intake (TBW and sodium can be variable).
2.Iatrogenic causes.
a.Sodium administration (e.g., normal saline, 3% saline, or sodium bicarbonate) via intravenous or oral routes.
b.Hyperalimentation.
3.Mineralocorticoid excess.
4.Medications: Lithium, demeclocycline, glyburide, amphotericin, colchicine, vinblastine, and others.
5.Hypertonic dialysis.
6.Salt ingestion.
Evaluation and Management Plan
A.Initial goal: To replace free water deficit and prevent ongoing water loss.
1.Assess volume status.
2.Calculate water losses and exact replacement necessary to avoid overcorrection.
a.TBW for lean men is usually 60% of weight in kilogram, and for lean women is usually 50% of weight in kilogram. TBW is lower (approximated to 45%) in obese patients because of adipose tissue. Elderly patients also have a lower TBW (commonly estimated around 50%).
b.Free water deficit (L) = Normal TBW × [140 mEq/l / (Current NAPlasma) – 1].
3.Choose appropriate replacement fluid and initial rate of repletion based on acuity and degree of hypovolemia.
4.Estimate ongoing water losses: Renal and extrarenal.
5.Choose an appropriate replacement fluid based on sodium level and underlying cause/diagnosis.
6.Choose replacement rate based on water losses.
B.Hypovolemic hypernatremia.
1.Step 1—Replace intravascular volume deficit (plasma volume deficit) with isotonic crystalloids within the first several hours. The goal is stable hemodynamics.
2.Step 2—Replace total free water deficit/loss over 3 to 4 days (include ongoing losses).
a.Calculate free water deficit (as previously noted).
b.Choose hypotonic replacement fluid.
i.0.45% NaCl IV (1/2 of the volume given is water).
ii.Water (D5NS, D5W, oral/gastric tube water).
c.Replacement rate.
i.Acute rise in sodium (hypernatremia developed over <48 hours).
1)Rapid water replacement/correction over 24 hours.
ii.Chronic rise in sodium (hypernatremia developed over >48 hours; NOTE: If unknown whether hypernatremia is acute or chronic—treat as chronic).
1)Maximum rate for sodium correction = 10 mEq/l per day over 2 to 3 days.
2)Less than 6 mEq/L per day in elderly patients.
d.Monitor fluid intake and output closely.
e.With low sodium intake, do not allow sodium intake to exceed output as this will exacerbate hypernatremia.
f.Determine and treat the underlying cause.
g.Perform neurological checks frequently.
h.Monitor sodium levels every 4 hours, then daily.
i.Monitor all electrolytes and replace as indicated.
j.Initially monitor closely in an intensive care setting.
3.Step 3—Replace ongoing water losses.
a.Choose fluid with less sodium than current urine concentration.
b.Monitor sodium at least daily.
c.Monitor fluid intake and output closely.
d.Give a low salt diet.
4.Step 4—Monitor/replace other electrolyte losses due to polyuria (e.g., hypokalemia, bicarbonate).
C.Euvolemic and hypervolemic hypernatremia.
1.Step 1—If necessary, correct water deficit (as previously noted).
2.Step 2—Monitor fluid intake and output closely. Low salt diet. Do not allow sodium intake to exceed output as this will exacerbate hypernatremia.
3.Step 3—Define/treat underlying cause.
a.Review medications.
b.Consider desmopressin (dDAVP) for central DI (synthetic ADH analog; also increases factor VIII and von Willebrand factor levels—monitor for clotting) at ONE of the following doses.
i.0.05–0.6 mg BID PO.
ii.1–2 mcg BID IV.
iii.10–20 mcg BID intranasal.
c.Perform neurological checks frequently.
d.Monitor sodium levels every 4 hours then daily.
e.Monitor all electrolytes and replace as indicated.
f.Initially monitor closely in an intensive care setting.
4.Step 4—Treat other electrolyte and acid–base disorders.
D.Acute salt poisoning—rapid rise in sodium.
1.Give a rapid infusion of water to correct at a rate of 1 mEq/L per hour.
2.Consider hemodialysis for sodium correction.
3.Closely monitor and avoid overcorrection.
Follow-Up
A.Follow-up depends on the nature of the underlying condition.
B.Hypernatremia needs to be corrected and maintained.
Consultation/Referral
A.Consult nephrology to help regulate hypernatremia.
B.Consult neurosurgery if central DI is responsible for hypernatremia.
Special/Geriatric Considerations
A.Increased age: Decline in TBW, decreased urinary concentrating ability, and impaired thirst; thus, elderly patients lack the same defenses against hypernatremia as younger patients.
Bibliography
Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). Treatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62(16), 1663–1682. doi:10.2146/ajhp040300
Lindner, G., Funk, G. C., & Schwarz, C. (2007). Hypernatremia in the critically ill is an independent risk factor for mortality. American Journal of Kidney Diseases, 50, 952. doi:10.1053/j.ajkd.2007.08.016
Sterns, R. H. (2015). Disorders of plasma sodium. The New England Journal of Medicine, 372(1), 55–65. doi:10.1056/NEJMc1501342