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Diagnosis and Management of Sodium Disorders: Hyponatremia and Hypernatremia
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Diagnosis and Management of Sodium Disorders: Hyponatremia and Hypernatremia
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Diagnosis and Management of Sodium
Disorders: Hyponatremia and Hypernatremia
MICHAEL M. BRAUN, DO, Madigan Army Medical Center, Tacoma, Washington
CRAIG H. BARSTOW, MD, Womack Army Medical Center, Fort Bragg, North Carolina
NATASHA J. PYZOCHA, DO, Madigan Army Medical Center, Tacoma, Washington
Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders
are associated with an increased risk of morbidity and mortality. Plasma osmolality plays a critical role in the patho-
physiology and treatment of sodium disorders. Hyponatremia and hypernatremia are classified based on volume
status (hypovolemia, euvolemia, and hypervolemia). Sodium disorders are diagnosed by findings from the history,
physical examination, laboratory studies, and evaluation of volume status. Treatment is based on symptoms and
underlying causes. In general, hyponatremia is treated with fluid restriction (in the setting of euvolemia), isotonic
saline (in hypovolemia), and diuresis (in hypervolemia). A combination of these therapies may be needed based on the
presentation. Hypertonic saline is used to treat severe symptomatic hyponatremia. Medications such as vaptans may
have a role in the treatment of euvolemic and hypervolemic hyponatremia. The treatment of hypernatremia involves
correcting the underlying cause and correcting the free water deficit. (Am Fam Physician. 2015;91(5):299-307. Copy-
right © 2015 American Academy of Family Physicians.)
H
More online yponatremia is a common elec- a worse prognosis in patients with liver cir-
at http://www. trolyte disorder defined as a rhosis, pulmonary hypertension, myocardial
aafp.org/afp.
serum sodium level of less than infarction, chronic kidney disease, hip frac-
CME This clinical content 135 mEq per L.1-3 A Dutch sys- tures, and pulmonary embolism.1,8-10
conforms to AAFP criteria tematic review of 53 studies showed that the
for continuing medical
prevalence of mild hyponatremia was 22.2% Etiology and Pathophysiology
education (CME). See
CME Quiz Questions on in geriatric hospital wards, 6.0% in nongeri- The most common classification system for
page 284. atric wards, and 17.2% in the intensive care hyponatremia is based on volume status:
Author disclosure: No rel- unit.2 The prevalence of severe hyponatremia hypovolemic (decreased total body water with
evant financial affiliations. (serum sodium level less than 125 mEq per L) greater decrease in sodium level), euvolemic
Patient information:
▲
A handout on this topic, was 4.5%, 0.8%, and 10.3%, respectively. It is (increased total body water with normal
written by the authors estimated that hyponatremia occurs in 4% to sodium level), and hypervolemic (increased
of this article, is avail- 7% of the ambulatory population, with rates total body water compared with sodium).11
able at http://www.aafp.
of 18.8% in nursing homes.2-4 Plasma osmolality has a role in the patho-
org/afp/2014/0000/
p000-s1.html. Access to Hyponatremia is associated with increased physiology of hyponatremia. Osmolality
the handout is free and morbidity and mortality.1-6 In patients with refers to the total concentration of solutes in
unrestricted. heart failure who undergo cardiac surgery, water. Effective osmolality is the osmotic gra-
Scan the QR code below hyponatremia increases rates of postoperative dient created by solutes that do not cross the
with your mobile device complications, length of hospital stay, and cell membrane. Effective osmolality deter-
for easy access to the mortality.5,6 Mild hyponatremia in the ambu- mines the osmotic pressure and the flow of
patient information hand-
out on the AFP mobile site. latory setting is associated with increased water.11 Plasma osmolality is maintained by
mortality (hazard ratio = 1.94) compared strict regulation of the arginine vasopressin
with normal sodium levels.3 Patients who (also called antidiuretic hormone [ADH]) sys-
develop hyponatremia during hospitalization tem and thirst. If plasma osmolality increases,
have increased mortality rates compared with ADH is secreted and water is retained by the
those who have hyponatremia on admission.7,8 kidneys, thus decreasing serum osmolality.
It is unclear if hyponatremia is a marker for If plasma osmolality decreases, ADH also
poor prognostic outcomes or merely a reflec- decreases, resulting in diuresis of free water
tion of disease severity. Its presence suggests and a return to homeostasis.12,13
March 1, 2015
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, SORT: KEY RECOMMENDATIONS FOR PRACTICE
Evidence
Clinical recommendation rating References Comments
In patients with severe symptomatic hyponatremia, the rate of sodium C 13, 14 Consensus guidelines based on
correction should be 6 to 12 mEq per L in the first 24 hours and 18 mEq systematic reviews
per L or less in 48 hours.
A bolus of 100 to 150 mL of hypertonic 3% saline can be given to correct C 13, 14 Consensus guidelines based on
severe hyponatremia. small studies
Vaptans appear to be safe for the treatment of severe hypervolemic and C 14 Consensus guidelines based on
euvolemic hyponatremia but should not be used routinely. observational studies
Chronic hypernatremia should be corrected at a rate of 0.5 mEq per L per C 33 Expert opinion
hour, with a maximum change of 8 to 10 mEq per L in a 24-hour period.
A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented
evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort.
Diagnostic Approach to Hyponatremia hyperproteinemia, mannitol use, or laboratory errors.
Symptoms of hyponatremia depend on its severity and on Osmolality remains unchanged, and patients are usually
the rate of sodium decline. Gradual decreases in sodium euvolemic.12,13 A corrected sodium calculation is needed
usually result in minimal symptoms, whereas rapid in the setting of hyperglycemia (eTable A).
decreases can result in severe symptoms. Polydipsia,
muscle cramps, headaches, falls, confusion, altered men- Hypovolemic Hyponatremia
tal status, obtundation, coma, and status epilepticus may There are numerous causes of hypovolemic hyponatre-
indicate the need for acute intervention. Most patients mia (Table 1).11-13 Patients typically have signs and symp-
with hyponatremia are asymptomatic, and hyponatremia toms associated with volume depletion (e.g., vomiting,
is noted incidentally. Volume status should be assessed to diarrhea, tachycardia, elevated blood urea nitrogen–
help determine the underlying cause11,13 (Figure 111-16). to-creatinine ratio). Urinary sodium levels are typically
The diagnostic workup should include a history and less than 20 mEq per L unless the kidney is the site of
physical examination with specific attention to cardiac, sodium loss. Fractional excretion of sodium is often inac-
cancer, pulmonary, surgical, endocrine, gastrointestinal, curately elevated in patients receiving diuretics because of
neurologic, and renal histories (Table 1).11-13 Diuretics, diuretic-induced natriuresis; fractional excretion of urea
carbamazepine (Tegretol), and selective serotonin reup- can be utilized in these patients instead. Fractional excre-
take inhibitors can cause hypovolemia; therefore, medi- tion of urea less than 35% is more sensitive and specific
cations should be reviewed. Alcohol and illicit drug use for diagnosing prerenal azotemia in this setting.18 Treat-
(especially beer and 3,4-methylenedioxymethamphet- ment generally consists of volume repletion with isotonic
amine [“Ecstasy”]) can cause hyponatremia.11-13 Athletes (0.9%) saline, occasional use of salt tablets, and treat-
should be asked about training regimens because high ment of the underlying condition.13,14 Monitoring of urine
endurance activities can lead to hyponatremia. output is recommended because output of more than 100
Laboratory tests include a complete metabolic panel and mL per hour can be a warning sign of overcorrection.14
urinary sodium and creatinine levels.11,13 Serum osmolal-
ity and fractional excretion of sodium should be calcu- Euvolemic Hyponatremia
lated (eTable A). Measurement of thyroid-stimulating Euvolemic hyponatremia is most commonly caused by
hormone, urinary uric acid, adrenocorticotropic hor- SIADH, but can also be caused by hypothyroidism and
mone, plasma cortisol, and brain natriuretic peptide may glucocorticoid deficiency. Euvolemia is diagnosed by
be considered in select patients to rule out other causes.13 findings from the history and physical examination, low
The diagnosis of reset osmostat (a variation of syndrome serum uric acid levels, a normal blood urea nitrogen–
of inappropriate antidiuretic hormone secretion [SIADH] to-creatinine ratio, and spot urinary sodium greater than
in which ADH secretion occurs despite low plasma osmo- 20 mEq per L. Diuretic therapy can artificially elevate
lality) may be aided using fractional excretion of urate urinary sodium, whereas a low-salt diet can artificially
(uric acid) in nonedematous patients who have hypona- lower urinary sodium, thus clouding the diagnosis of
tremia that does not respond to usual treatment.17 hypovolemia vs. euvolemia. Treatment generally con-
sists of fluid restriction and correcting the underlying
Pseudohyponatremia cause. Fluid restriction should be limited to 500 mL
Pseudohyponatremia occurs when seemingly low sodium less than the daily urinary volume.13 Salt and protein
levels are actually normal. Causes include hyperglycemia, intake should not be restricted. Predictors of failure with
300 American Family Physician www.aafp.org/afp Volume 91, Number 5 ◆ March 1, 2015
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