HYPONATREMIA

DEFINITION

Hyponatremia, defined as a serum sodium

concentration below 135 mmol/L, is one of the
most frequently encountered electrolyte
disorders.
 INCIDANCE AND PREVALANCE

Hypo-osmolality is one of the most common disorders of

fluid and electrolyte balance encountered in hospitalized
patients.
Similarly high incidences have been reported in patients
with specific disease states, including patients with heart
failure (HF) and cirrhosis; reports from recent trials and
registries suggest that hyponatremia is seen in up to 27%
of patients admitted with acute HF, and that up to 50% of
patients with cirrhosis and ascites are found to be
hyponatremic.
Even with these more stringent criteria, incidences from
7%-53% have been reported in institutionalized geriatric
patients.
 CLASSIFICATION AND DIAGNOSIS OF
HYPOTONIC HYPONATREMIAS
The following sections will describe the diagnostic criteria,
common etiologies, and pathophysiologies of the 3 major
classifications of hypotonic hyponatremia based on the
patients ECF volume status:
Hypovolemic hyponatremia,
Euvolemic hyponatremia, and
Hypervolemic hyponatremia.
 HYPOVOLEMIC HYPONATREMIA

Hyponatremia with volume depletion (hypovolemia) can

arise in a variety of settings. Because intravascular volume
cannot be easily measured directly, volume depletion is
diagnosed clinically from the history, physical examination,
and laboratory results.
Patients with clinical symptoms or signs of volume
depletion (eg, vomiting and diarrhea, orthostatic decreases
in blood pressure and increases in pulse rate, dry mucus
membranes, and decreased skin turgor) should be
considered to be hypovolemic, unless there are alternative
explanations for these findings.
 EUVOLEMIC HYPONATREMIA

Most patients with hyponatremia are clinically euvolemic

because of the high prevalence of SIADH. Euvolemia is
generally diagnosed clinically from the history, physical
examination, and laboratory results.
Patients without clinical signs of volume depletion (eg,
orthostatic decreases in blood pressure, decreased skin
turgor, increases in pulse rate, dry mucus membranes) or
volume expansion (eg, subcutaneous edema, ascites)
should be considered to be euvolemic absent other
evidence suggesting an abnormal ECF volume status.
 HYPERVOLEMIC HYPONATREMIA

Hyponatremia with ECF volume excess can arise in a

variety of diseases. Because intravascular volume cannot
be easily measured directly, volume excess is a clinical
diagnosis made from the history, physical examination, and
laboratory results.
Patients with signs of volume overload (eg, subcutaneous
edema, ascites, pulmonary edema) should be considered to
be hypervolemic, unless there are alternative explanations
for these findings.
 ETIOLOGIES

Hypovolemic Euvolemic Hypervolemic

hyponatremia Hyponatremia Hyponatremia
Gastrointestinal Syndrome of Heart Failure
disease Inappropriate Cirrhosis
Exercise- Antidiuretic Acute Kidney
associated Hormone Injury, Chronic
hyponatremia Secretion Kidney Disease,
Diuretic Therapy Nephrogenic and Nephrotic
Cerebral Salt Syndrome of Syndrome
Wasting Inappropiate Anti-
Minealocorticoid Diuresis
Deficiency Glucocorticoid
Deficiency
Hypothyroidsm
Exercise
Associated
Hyponatremia
Low Solute Intake
Primary
Polydipsia
 PATHOPHYSIOLOGY

The principal mechanisms of water and sodium homeostasis in

the body are controlled by hypothalamic osmoreceptors, which
regulate the secretion of ADH and perception of thirst.
When osmoreceptors sense slight increases in plasma tonicity,
ADH is released from the posterior pituitary, causing increased
kidney tubule permeability, increased water reabsorption, and
formation of more concentrated urine.
In older adults, osmoreceptors are hypersensitive compared with
younger adults, as shown by hypertonic fl uid administration and
water deprivation tests.The same phenomenon can be observed
by administering metoclopramide to stimulate vasopressin,
resulting in signifi cantly higher ADH release in older adults.
Hypersensitivity of these mechanisms along with increased time
to excrete excess water predispose older adults to hyponatremia.
 Structural changes in the aging kidney
also can contribute to the
development of hyponatremia. These
changes include glomerular sclerosis
of the superficial cortex, tubular
atrophy, interstitial fibrosis, and
hyalinosis of the arterioles. This leads
to functional declines including
decreases in glomerular fi ltration rate
(GFR), creatinine clearance, renal
plasma fl ow, and the ability to dilute
and concentrate filtrate.
Normally, older adults are able to
compensate for these changes and
sustain a normal balance of
electrolytes. However, illness or injury
may potentiate loss of electrolyte
homeostasis and lead to dysnatremias
and volume dysregulation
 RISK FACTORS

Risk factors for hyponatremia in older adults include

administration of hypotonic fl uid, low dietary sodium
intake, low-sodium enteral nutrition formulas for primary
nutrition, previous brain injury, age, and idiopathic SIADH.
Whites and Hispanics appear to be at higher risk than
African Americans.5 Thiazide diuretics and selective
serotonin reuptake inhibitors are more likely to cause
hyponatremia in older adults than in younger adults.2
Clinicians must take steps to avoid promoting hyponatremia
in older adults because of these structural and functional
alterations, comorbid conditions, and medications that can
lead to fl uid and sodium dysregulation.
 DIAGNOSTIC
Urine osmolality can help clinicians differentiate between impaired
excretion of water versus normal but excessive water excretion as
in polydipsia.
Serum osmolality measures the bodys electrolyte-water balance
and can differentiate between true and pseudohyponatremia.
Urinary sodium concentration can help differentiate hypovolemic
hyponatremia from hyponatremia secondary to SIADH.
CBC count with differential, basic metabolic panel, and renal and
liver function tests can help identify comorbidities and their
potential causes.
TSH and cortisol response to ACTH can evaluate for SIADH as a
potential cause of hyponatremia.
Serum uric acid and urea concentrations can identify
hypouricemia associated with SIADH.
A brain CT or MRI and chest radiographs may reveal cerebral
edema, demyelination, pulmonary congestion as a potential cause
of SIADH, or cerebral salt wasting.
INITIAL TREATMENT OF HYPONATREMIA BASED
ON PATIENT VOLUME STATUS

Euvolemic
Restrict fluids
Prescribe loop diuretics and saline infusions to replace urinary sodium
losses
Prescribe demeclocycline and vasopressin receptor antagonists
Enhance solute intake if patient has poor nutritional status
Discontinue medications associated with SIADH
Treat underlying conditions associated with SIADH
Treat endocrinopathies (for example, hypothyroidism)
Hypervolemic
Restrict fl uids and sodium
Prescribe loop diuretics
Treat underlying conditions
Hypovolemic
Prescribe IV isotonic saline
Discontinue diuretics
Replace mineralocorticoid deficiencies
 TREATMENT

Acute hyponatremia Acute onset of symptomatic

hyponatremia can be a medical emergency leading
to cerebral edema, brain herniation, and
cardiopulmonary arrest, and requires rapid
correction with 3% hypertonic saline.7 If the
patient is hypervolemic because of heart failure or
underlying cardiovascular disease, also administer
a loop diuretic to avoid volume overload.4,7,10
Closely monitor patients receiving hypertonic
saline for extracellular volume status, neurologic
symptoms, and serum sodium trends to avoid rapid
overcorrection
 TREATMENT

Chronic hyponatremia Patients with chronic hyponatremia are

unlikely to present with serious signs and symptoms. If they do,
carefully tailor sodium correction to reverse serious signs and
symptoms only and avoid overcorrection. Too-rapid correction of
chronic hyponatremia with hypertonic saline can cause excessive
loss of intracellular water, cell shrinkage, and osmotic demyelination
syndrome (damage to the myelin sheaths covering axons of the
brainstem, which can lead to permanent neurologic damage).
Patients with osmotic demyelination syndrome may show improved
mental status initially, accompanied by neurologic declines, paresis,
flaccid paralysis, dysarthria, dysphagia, hypotension, and possible
death. Patients who are malnourished; abuse alcohol; have
hypokalemia, burns, or advanced liver disease; and older women on
thiazide diuretics have much lower thresholds for osmotic
demyelination and should be corrected much more slowly
 CONCLUSION

Hyponatremia is a complex condition that demands a

systematic approach to diagnosis and management.23 In
older adults, hyponatremia is one of the most common
electrolyte imbalances and is associated with increased
mortality. Careful attention to common causes, clinical
presentation, laboratory diagnosis, and appropriate
treatment will help practitioners safely reverse this
potentially life-threatening condition. The primary
treatment for hyponatremia is to identify and correct
underlying causes and, if necessary, correct sodium
imbalances slowly to lessen the chance of neurologic
disease. Vasopressin antagonists have emerged as
promising new treatments that may improve outcomes