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Hyponatremia
Authors

Helbert Rondon1; Madhu Badireddy2.

Affiliations
1 University of Pittsburgh
2 Christus Santa Rosa Hospitals

Last Update: January 31, 2022.

Continuing Education Activity

Hyponatremia is defined as a serum sodium concentration of less than 135 mEq/L but can vary to a small extent in
different laboratories. Hyponatremia is a common electrolyte abnormality caused by an excess of total body water
when compared to total body sodium content. Edelman discovered that serum sodium concentration does not depend
on total body sodium but the ratio of total body solutes (e.g., total body sodium and total body potassium) to total
body water. Hyponatremia represents an imbalance in this ratio where total body water is more than total body
solutes. This activity explains when this condition should be considered on differential diagnosis, articulates how to
properly evaluate for this condition, and highlights the role of the interprofessional team in caring for patients with
this condition.

Objectives:

Review the causes of hyponatremia.

Describe the pathophysiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and its
association with hyponatremia.

Summarize the treatment of hyponatremia.

Outline the importance of enhancing care coordination among the interprofessional team to ensure proper
evaluation and management of hyponatremia.

Access free multiple choice questions on this topic.

Introduction
Hyponatremia is defined as a serum sodium concentration of less than 135 mEq/L but can vary to some extent
depending upon the set values of varied laboratories.[1] Hyponatremia is a common electrolyte abnormality caused by
an excess of total body water in comparison to that of the total body sodium content. Edelman approved of the fact
that serum sodium concentration does not depend on total body sodium but is determined by the ratio of total body
solutes (e.g., total body sodium and total body potassium) to total body water.[2] Hyponatremia represents an
imbalance in this ratio where total body water is more than total body solutes. Total body water (TBW) has two main
compartments, extracellular fluid (ECF) accounting for one-third and intracellular fluid (ICF), accounting for the
remaining two-thirds. Sodium is the major solute of ECF and potassium for ICF.

Etiology

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The etiology of hyponatremia can be classified based upon the volume status of the extracellular fluid. As mentioned
earlier, sodium is the major solute of extracellular fluid (ECF). Based upon the volume of ECF, a patient can be
classified into hypovolemic, euvolemic, or hypervolemic.[3]

Physiological stimuli that cause vasopressin release in adjunct with increased fluid intake can cause hyponatremia.
Hypothyroidism and adrenal insufficiency may contribute to an increased release of vasopressin. Physiological stimuli
for vasopressin release include loss of intravascular volume (hypovolemic hyponatremia) and the loss of effective
intravascular volume (hypervolemic hyponatremia).

Causes of Hypovolemic Hyponatremia (TBW decreases more than a decrease in total body sodium) [4]

Gastrointestinal fluid loss (diarrhea or vomiting)

The third spacing of fluids (pancreatitis, hypoalbuminemia, small bowel obstruction)

Diuretics

Osmotic diuresis (glucose, mannitol)

Salt-wasting nephropathies

Cerebral salt-wasting syndrome (urinary salt wasting, possibly caused by increased brain natriuretic peptide)

Mineralocorticoid deficiency

Causes of Hypervolemic Hyponatremia (TBW increases greater than an increase in total body sodium) [5]

Renal causes (acute renal failure, chronic renal failure, nephrotic syndrome)

Extrarenal causes (congestive heart failure, cirrhosis)

Iatrogenic

Causes of Euvolemic Hyponatremia (TBW increase with stable total body sodium)

Nonosmotic, pathologic vasopressin release may occur in the setting of normal volume status, as with euvolemic
hyponatremia.

Causes of euvolemic hyponatremia include:

Drugs, as mentioned below.

Syndrome of inappropriate antidiuretic hormone (SIADH)

Addison's disease

Hypothyroidism

High fluid intake in conditions like primary polydipsia; or potomania, caused by a low intake of solutes with
relatively high fluid intake

Medical testing related to excessive fluids such as a colonoscopy or cardiac catheterization[6][7][8]

Iatrogenic

Many drugs cause hyponatremia and the most common include:

Vasopressin analogs such as desmopressin and oxytocin

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Medications that stimulate vasopressin release or potentiate the effects of vasopressin such as selective
serotonin-reuptake inhibitors and other antidepressants morphine and other opioids

Medications that impair urinary dilution such as thiazide diuretics

Medications that cause hyponatremia such as carbamazepine or its analogs, vincristine, nicotine, antipsychotics,
chlorpropamide, cyclophosphamide, nonsteroidal anti-inflammatory drugs

Illicit drugs such as methylenedioxymethamphetamine (MDMA or ecstasy).[6]

Epidemiology
Hyponatremia is the most common electrolyte disorder, with a prevalence of 20% to 35% among hospitalized
patients. The incidence of hyponatremia is high among critical patients in the intensive care unit (ICU) and also in
postoperative patients. This is more common in elderly patients due to multiple comorbidities, multiple medications,
and a lack of access to food and drinks.[9]

Pathophysiology
Thirst stimulation, antidiuretic hormone (ADH) secretion, and handling of filtered sodium by kidneys maintain serum
sodium and osmolality. Normal plasma osmolality is around 275 mOsm/kg to 290 mOsm/kg. To maintain normal
osmolality, water intake should be equal to water excretion. The imbalance of water intake and excretion causes
hyponatremia or hypernatremia. Water intake is regulated by the thirst mechanism where osmoreceptors in the
hypothalamus trigger thirst when body osmolality reaches 295 mOsm/kg. Water excretion is tightly regulated by
antidiuretic hormone (ADH), synthesized in the hypothalamus, and stored in the posterior pituitary gland. Changes in
tonicity lead to either enhancement or suppression of ADH secretion. Increased ADH secretion causes reabsorption of
water in the kidney, and suppression causes the opposite effect. Baroreceptors in the carotid sinus can also stimulate
ADH secretion, but it is less sensitive than the osmoreceptors. Baroreceptors trigger ADH secretion due to decreased
effective circulating volume, nausea, pain, stress, and drugs.[10]

Hypertonic Hyponatremia (Serum osmolality of greater than 290 mOsm/kg)

Hyperglycemia

Mannitol

Isotonic Hyponatremia (Serum osmolality between 275 mOsm/kg and 290 mOsm/kg)

Pseudo-hyponatremia is a laboratory artifact. It is usually caused by hypertriglyceridemia, cholestasis

(lipoprotein X), and hyperproteinemia (monoclonal gammopathy, intravenous immunoglobulin [IVIG]). Two-
thirds of clinical labs in use still use indirect ion-selective electrode technology, and therefore this problem is
still present.

Nonconductive irrigant solutions: these solutions contain mannitol, glycine, or sorbitol, and are used in
urological and gynecological procedures such as transurethral resection of the prostate (TURP).[11]

Hypotonic Hyponatremia (Serum osmolality of less than 275 mOsm/kg)

Hypotonic hyponatremia represents an excess of free water. This excess free water can be caused by two mechanisms:

Increased free water intake: The patient drinks a large volume of free water (greater than 18 L/day or greater
than 750 mL/h) that overwhelms kidney capacity to excrete free water. Examples of this are psychogenic
polydipsia, marathon runners, water drinking competitions, and ecstasy.

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Decreased free water excretion: Patients drink a normal volume of free water, but the kidneys cannot excrete
the water for some reason.

There are three mechanisms involved in the inability of kidneys to excrete water:

1. High ADH activity: Three different mechanisms can cause high ADH:

Decreased effective arterial blood volume (EABV): antidiuretic hormone (ADH) is released when there is a
reduction of 15% or more of the EABV. This occurs with hypovolemia (e.g., vomiting, diarrhea), decreased
cardiac output (e.g., heart failure), or vasodilation (e.g., cirrhosis).

SIADH: ADH is secreted autonomously. Four general causes of this are brain disorders, lung disorders, drugs
(e.g., SSRI), and miscellanea (e.g., nausea and pain).

Cortisol deficiency: Cortisol exerts an inhibitory effect on ADH release. When cortisol is decreased, ADH
is released in large amounts. Adrenal insufficiency is the cause of this mechanism.[12]

2. Low glomerular filtration rate (GFR): a low glomerular filtration rate would impair the kidney's ability to get rid of
water. Typical examples are acute kidney injury (AKI), chronic kidney disease (CKD), and end-stage renal disease
(ESRD).

3. Low solute intake: Patients on a regular diet consume 600 mOsm to 900 mOsm of solute per day. Solutes are
defined as substances that are freely filtered by the glomeruli but have a relative or absolute difficulty in being
reabsorbed by the tubules in relationship to water. The main solutes are urea (which comes from the metabolism of
proteins) and electrolytes (e.g., salt). Carbohydrates do not contribute to solute load. In steady-state conditions, solute
intake is equal to urine solute load. Therefore, it is expected that these patients also excrete 600 mOsm to 900 mOsm
of solute in the urine. Urine volume, and hence water excretion, is dependent on the urine solute load. The more solute
one needs to excrete, the larger the urine volume one needs to produce. The less solute one needs to excrete, the
smaller the urine volume one needs to produce. Patients who eat a low amount of solute per day (e.g., 200
mOsm/day), on steady-state conditions, will also excrete a low amount of solute in the urine, and therefore they will
do it in a smaller volume of urine. This decreased urine volume will limit the capacity of the kidneys to excrete water.
Typical examples of this are beer potomania and the tea-and-toast diet.

SIADH (Syndrome of inappropriate antidiuretic hormone secretion) [13]

This is a condition where inappropriate secretion of ADH despite normal or increased plasma volume causes impaired
water excretion by the kidney leading to hyponatremia. SIADH is a diagnosis of exclusion, as there is no single test to
confirm the diagnosis. Patients are hyponatremic and euvolemic.[14]

Causes of SIADH include

Any central nervous system (CNS) disorder,

Ectopic production of ADH (most commonly small cell carcinoma of the lung),

Drugs (carbamazepine, oxcarbazepine, chlorpropamide, and multiple other drugs),

HIV,

Pulmonary diseases (pneumonia, tuberculosis),

Postoperative patients (pain medicated)

Treatment includes fluid restriction and the use of vasopressin 2 receptor inhibitors.[12][15][12][15][12]

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History and Physical

Symptoms depend upon the degree and chronicity of hyponatremia. Patients with mild-to-moderate hyponatremia
(greater than 120 mEq/L) or gradual decrease in sodium (greater than 48 hours) have minimal symptoms. Patients
with severe hyponatremia (less than 120 mEq/L) or rapid decrease in sodium levels have multiple varied symptoms.
[16]

Symptoms can range from anorexia, nausea and vomiting, fatigue, headache, and muscle cramps to altered mental
status, agitation, seizures, and even coma.[17]

Apart from symptoms, a detailed history taking to include a history of pulmonary and CNS disorders, all home
medications, and social history (increased beer intake or use of MDM or ecstasy) is very important.

Physical examination includes assessing volume status and neurological status. 

Patients with neurological symptoms and signs need to be treated promptly to prevent permanent neurological
damage.[18]

Evaluation
The following steps may be performed while evaluating a patient with suspected hyponatremia[19]:

Step 1: Plasma Osmolality (275 mOsm to 290 mOsm/kg)

It can help differentiate between hypertonic, isotonic, and hypotonic hyponatremia.

True hyponatremic patients are hypotonic.

If the patient is hypotonic, then go to step 2.

Step 2: Urine Osmolality

Urine osmolality less than 100 mOsm/kg indicates primary polydipsia or reset osmostat.

Urine osmolality greater than 100 mOsm/kg usually indicates a high ADH state, go to step 3.

Step 3: Volume Status (ECF status)

Hypovolemic vs euvolemic vs hypervolemic.

If the patient is hypovolemic, then proceed to step 4.

Step 4: Urine Sodium Concentration

Urine sodium less than 10 mmol/L indicates extrarenal loss of fluid (remote diuretic use and remote vomiting).

Urine sodium greater than 20 mmol/L suggests renal loss of urine (diuretics, vomiting, cortisol deficiency, and
salt wasting nephropathies).

Other tests that might help in differentiating the causes include

Serum thyroid-stimulating hormone (TSH)

Serum adrenocorticotropic hormone (ACTH)

Serum urea

Liver function tests

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Chest X-ray or computed tomography (CT) scan of the chest

CT scan of the head

Treatment / Management
Treatment of hyponatremia depends upon the degree of hyponatremia, duration of hyponatremia, the severity of
symptoms, and volume status.

Acute Symptomatic Hyponatremia

Severely symptomatic hyponatremia: Administer 3% sodium chloride; 100 mL intravenous (IV) bolus (repeat
up to twice if symptoms persist).

Mild to moderately symptomatic hyponatremia: 3% Sodium chloride, slow infusion (use sodium deficit formula
to calculate the rate of infusion but recalculate rate with frequent sodium monitoring).

Chronic Asymptomatic Hyponatremia

Hypovolemic hyponatremia: Isotonic fluids administration and holding of any diuretics.

Hypervolemic hyponatremia: Treat underlying condition, restrict salt and fluids, and administer loop diuretics.

Euvolemic hyponatremia: Fluid restriction to less than 1 liters per day.

Drugs: Selective vasopressin 2 receptor antagonists are being used recently. They increase the excretion of water in
the kidneys without affecting sodium, thereby increase serum sodium levels. These medications are used in patients
with euvolemic and hypervolemic conditions (except liver failure) if the above measure does not help.[20][21]

The goal of correction: Correct sodium by no more than 10 mEq/L to 12 mEq/L in any 24 hour period.

Risk factors for osmotic demyelination syndrome (ODS): Hypokalemia, liver disease, malnutrition, alcoholism.

Limits of Correction

High-risk for ODS: less than 8 mEq/L in any 24 hour period

Average-risk for ODS: less than 10 mEq/L in any 24 hour period

In the absence of false laboratory hyponatremia, pseudo hyponatremia, and lack of hypovolemic state, including
postural hypotension, the next step is to measure the urine sodium and osmolarity. In the low urinary sodium of less
than 100 mOsm/kg and absence of rapid water consumption, the potential for a high fluid, low protein diet, including
beer potomania, should be examined. In patients with severe hyponatremia of less than 120 mEq/L, the chronicity of
the hyponatremia should be considered. Accordingly, in severe, chronic hyponatremia, intravenous 3 percent saline at
a rate of 15 to 30 mL/hour should be initiated. In some patients, desmopressin (dDAVP) should also be administered
to prevent overly rapid correction.

Three percent saline can be safely infused via a peripheral vein, and so far, vascular thrombosis and extravasation
injuries have not been reported. However, some centers have policies against the peripheral infusion of hypertonic
saline. In these circumstances, central vein infusions or infusion of a lower concentration with higher infusion rates
are required.  Tolvaptan is indicated in hyponatremia associated with high anti-diuretic hormone (ADH) activity.

Fluid restriction is adequate for patients who have normovolemic hypotonic hyponatremia. Some patients with the
syndrome of inappropriate antidiuretic hormone secretion (SIADH) who are malnourished may need a high protein
intake, which increases the solute load for renal excretion, resulting in more free water removal. Laboratory findings

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in patients with SIADH reveal hyponatremia (plasma sodium level of less than 135 mEq/L) and low serum osmolality
(less than 280 mOsm/kg). Moreover, patients with SIADH have increased urinary sodium levels (greater than 20
mMol/L) and urine osmolality (generally above 100 mOsm/L).[22]

Differential Diagnosis
True hyponatremia is associated with hypo osmolality. Conditions causing hyperosmolar hyponatremia and iso-
osmolar hyponatremia (pseudo-hyponatremia) should be differentiated first.[23]

Hyperglycemia

Mannitol overdose

Hyperlipidemia

Hyperproteinemia

Differential Diagnosis for Hypo-Osmolar Hyponatremia

Gastroenteritis

Diuretic use

Congestive heart failure

Liver failure

Psychogenic polydipsia

Renal causes

SIADH

Adrenal crisis

Hypothyroidism

Prognosis
Prognosis in patients with hyponatremia depends on the severity of hyponatremia and the underlying condition
causing it. Prognosis is poor in patients with severe hyponatremia, acute hyponatremia, and elderly patients.[24]

Complications
If left untreated or inadequately treated, patients with hyponatremia can develop rhabdomyolysis, altered mental
status, seizures, and even coma.

Rapid correction of chronic hyponatremia (greater than 10 mEq/L to 12 mEq/L of sodium in 24 hrs) can lead to
osmotic demyelination syndrome.

Osmotic demyelination syndrome, formerly known as central pontine myelinolysis is a complication of rapid

correction sodium in patients with chronic hyponatremia.[25] In patients with hyponatremia, the brain adapts to a fall
in serum sodium level, without developing cerebral edema, in about 48 hours. As a result, patients with chronic
hyponatremia are mostly asymptomatic. Once the brain adapts to low serum sodium, the rapid correction of sodium
leads to osmotic demyelination syndrome. Clinical manifestations are typically delayed by few days and
comprise several irreversible neurological symptoms, including seizures, disorientation, and even coma. "Locked-in"

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syndrome occurs in severely affected patients. These patients are awake but unable to move or can communicate with
the help of their eyes only.[26]

Consultations
It is imperative to consult a nephrologist in a patient with severe hyponatremia or a rapid decrease in sodium or
persistent hyponatremia.

Cardiology and gastroenterology consultation might be necessary for patients with congestive heart failure and
hepatic failure, respectively.

Deterrence and Patient Education

Patients with hyponatremia should be followed closely at discharge by both the primary care provider and nephrology.
Follow up labs are ordered as needed, and patients needing fluid restriction should be educated appropriately.[27]

Pearls and Other Issues

Hyponatremia is a common electrolyte abnormality.

Hyponatremia can range from an asymptomatic condition to a life-threatening condition.

Hyponatremia can occur with hypovolemic or hypervolemic or euvolemic states.

Common causes include diuretics, vomiting, diarrhea, congestive heart failure, renal, and liver disease.

Degree, duration of hyponatremia, along with the severity of symptoms, determine the management algorithm
and the rapidity to correct sodium.

Do not correct the hyponatremia by more than 10 mEq/L to 12 mEq/L in 24 hours except in patients with severe
symptoms and rapidly decreased sodium levels.

Too rapid correction of the sodium levels can lead to the osmotic demyelinating syndrome.

Enhancing Healthcare Team Outcomes

Hyponatremia is a common electrolyte abnormality. Sodium levels need to be closely monitored, as this could lead to
life-threatening complications if left untreated. This is even more important in patients with renal disease and those
who are on diuretics. Good interprofessional communication between the primary care provider and a nephrologist is
imperative to keep a close eye on sodium level and its proper correction as and when needed.

Review Questions

Access free multiple choice questions on this topic.

Comment on this article.

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