D i s o rd e r s o f So d i u m

Aaron Alindogan, MD, Ryan Joseph, DO, DTM&H*

KEYWORDS

Hypernatremia
Hyponatremia
Sodium
Hypertonic saline

Osmotic demyelination syndrome
SIADH

KEY POINTS

Evaluating the patient’s volume status is critical to helping ascertain the possible cause for
the sodium imbalance.

Rapidity of the development of the patient’s sodium imbalance and if the patient has
symptoms will often drive the management of the patient.

Patients with severe symptoms require rapid treatment to prevent permanent neurologic
sequelae.

If hypertonic saline therapy is not readily available, you can use 8.4% sodium bicarbonate
as an acceptable alternative.

Preventing overcorrection should be foremost on the emergency clinician/s mind when
managing sodium imbalance. Have a low threshold to check sodium levels more
frequently while correcting.

INTRODUCTION

Dysnatremias are one of the most common electrolyte disturbances that present to
the emergency department, with hyponatremia being the most common electrolyte
abnormality in the United States. Between 3 and 6 million patients per year present
to a clinical setting with hyponatremia and somewhere between 12% and 20% of pa-
tients admitted from the emergency department have a sodium imbalance.1,2 One
study found that hypernatremia was found in 2% of patients and hyponatremia was
found in 10% of patients presenting to the emergency department.3 Severe hyperna-
tremia and hyponatremia are associated with considerable morbidity and mortality,
and even mild hyponatremia is associated with worse outcomes when it complicates
other conditions such as heart failure.4
Hyponatremia is defined as a serum sodium level of less than 135 mmol/L, and
hypernatremia is defined as a serum sodium level of greater than 145 mmol/L.
Because sodium is the most abundant cation in extracellular fluid, it is the primary

Department of Emergency Medicine, UTHSCSA, Floyd Curl Drive, MC 7736, San Antonio, TX
78229, USA
* Corresponding author.
E-mail address: [email protected]

Emerg Med Clin N Am 41 (2023) 697–709

https://doi.org/10.1016/j.emc.2023.06.003 emed.theclinics.com
0733-8627/23/Published by Elsevier Inc.

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698 Alindogan & Joseph

determinant of plasma osmolality. As a result, any derangements in sodium can affect

the balance of cations, anions, and overall plasma osmolality resulting in potential
ramifications clinically, specifically the central nervous system (CNS).
The difference between a minor symptom and a life-threatening condition caused
by an imbalance of sodium is often a consequence of the rapidity of change in sodium
concentration, not necessarily the overall deficit. Severity of sodium imbalance de-
pends on the patient’s symptoms because the serum level does not always correlate
to the patient’s symptoms. Therefore, it is important to understand that, although
total-body salt content may be abnormal, the vast majority of dysnatremias originate
from a primary imbalance in electrolyte-free water intake and loss. The perturbation in
water balance rather than the salt content is commonly the problem.

Physiology
The body maintains a delicate balance of water for its physiologic processes. Ulti-
mately, the body’s water is governed by solute concentrations or tonicity, particularly
sodium, which serves as a marker for plasma tonicity. When this balance sways and
sodium concentration changes, the CNS is often affected first and the most signifi-
cantly. Moreover, depending on the rate of change, symptoms can range anywhere
from asymptomatic to catastrophic and life threatening.
Plasma osmolality is a ratio of plasma solutes and plasma water. Simply, it can be
estimated as follows:

½Glucose ½BUN
Posm 5 2½Na 1 1
18 2:8
Plasma tonicity factors only those solutes that do not easily traverse across cell
membranes (ie, sodium salts); therefore, this can be thought of as the effective plasma
osmolality. Even more simply, it is the same equation without factoring in urea, as urea
also equilibrates freely across cell membranes.

½Glucose
Plasma tonicity 5 2½Na1
18
Plasma tonicity, or the effective plasma osmolality, is largely regulated by the renal
system, antidiuretic hormone (ADH), and the thirst response to regulate relative free
water intake. The regulation of salt and water can be accomplished independently
as one can consume foods with increased or decreased salt and/or drink water. In or-
der to maintain the physiologically normal range of 275 to 295 mOsm/L of water, the
posterior pituitary gland is highly sensitive to osmolality fluctuations and may secrete
ADH.5 More specifically, the hypothalamic nuclei are sensitive to changes in serum
osmolality within 1% to 2%.5 Because serum osmolality decreases (this is most often
in cases of polydipsia), the posterior pituitary will not secrete ADH, the nephrons will
not resorb free water, and the urine will become more diluted (ie, increased urine
osmolality).5,6 Conversely, because serum osmolality increases (ie, in cases of dehy-
dration), the posterior pituitary will secrete ADH, which causes a multitude of meta-
bolic effects in order to increase water reabsorption and decrease diuresis, thus
concentrating the urine. ADH affects increased expression of aquaporin-2 receptors
to capture water in the luminal collecting ducts of the nephrons. Furthermore, through
vasoconstriction, ADH can decrease blood flow in the renal medulla. This allows for an
increased hypertonicity surrounding the loop of Henle, increasing water reabsorption.7
Other factors may also stimulate ADH release. These include hypovolemia, drugs,
pain, emotional stress, nausea, pregnancy, menstruation, hypoglycemia, severe

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 Disorders of Sodium 699

hypoxemia and hypercapnia, and distribution into the body’s “third space” (ie, sepsis,
severe burns, trauma).6,8–10
Finally, although ADH regulates water retention, the body’s thirst mechanism can
control how much free water is allowed into system. Separate from diuresis, whether
through ventilation, evaporation of sweat for bodily cooling, or water lost in stool, the
body will also lose free water through insensible losses. This is estimated to be 40 to
800 mL per day.11 Thirst prevents against dehydration more so than ADH.6 Its
threshold is a slightly higher threshold of plasma osmolality than ADH.12 In this way,
one can view thirst as the marker for the upper limit of osmolality and ADH release
the lower limit. Proper functioning of these mechanisms optimizes the body’s fluid bal-
ance and maintains water homeostasis. Therefore, anything that interferes with either
function disrupts the delicate fluid balance and leaves the patient to risks of devel-
oping hyponatremia and hypernatremia and the subsequent symptoms associated
with them.

HYPONATREMIA

Defined as a serum sodium level less than 135 mmol/L, hyponatremia is the most
common electrolyte disorder found in any medical setting.13 In cases of hyponatremia,
the most common cause is hemodilution rather than loss of total sodium. Specifically,
it is most commonly due to a failure to secrete free water. The emergency clinician
ought to recognize and respect this pathologic condition because even the mild cases
of hyponatremia can increase mortality in patients both inpatient and outpatient and
increase morbidity in hospitalized patients.14–17

Presentation
Patients who present with hyponatremia have variable clinical presentations. Although
hyponatremia often presents asymptomatically, hyponatremia with sodium less than
125 mmol/L often present with signs and symptoms that reflect neurologic dysfunc-
tion usually due to cerebral edema.18,19 The severity of symptoms typically depends
on the rate of reduction rather than the serum sodium level. Common complaints
are usually broken into 2 categories: mild and severe. Mildly symptomatic patients
commonly complain of headache, nausea, vomiting, lethargy, and confusion. Un-
treated, it may progress severe symptoms that include severe confusion, seizure,
coma, and death.
In cases of chronic hyponatremia, the brain has 2 steps in protecting itself, thus
decreasing the severity of symptoms. First, cerebral edema causes an increased inter-
stitial hydrostatic pressure, which yields a net flow of fluid from the brain tissue and
into the cerebrospinal fluid.20 Second, in its attempt to prevent cerebral edema, the
brain will draw out other solutes in an effort to neutralize the osmotic gradient and
decrease swelling.4 Patients with sodium concentrations less than 120 mmol/L
most commonly present with nausea and vomiting, which is not usually associated
with severe adverse outcomes.21 However, when presenting with acute hyponatremia
or acute on chronic cases, nausea, and vomiting can portend life-threatening cerebral
edema.

Evaluation and Diagnosis

Making the diagnosis comes from evaluating the patient’s serum sodium level from
bloodwork, usually a basic metabolic panel or comprehensive metabolic panel.
Once the emergency clinician recognizes a patient is hyponatremic, the next step is
to determine the possible cause for hyponatremia. Common causes of hyponatremia

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700 Alindogan & Joseph

are found in Table 1. Additionally, it is important to ascertain the patient’s volume sta-
tus and plasma osmolality because true hyponatremia is due to a hypoosmolar state.
Cases of hypertonic hyponatremia occur when serum osmolality exceeds 290 mOsm/
kg and isotonic hyponatremia between 275 and 290 mOsm/kg. Hypertonic hyponatre-
mia is most often due to another solute increasing, contributing to the calculated num-
ber, such as cases of severe hyperglycemia; these solutes too act as osmotic forces
causing fluid shifts. In cases such as diabetic ketoacidosis or hyperosmolar hypergly-
cemia, the abundance of serum glucose acts as an osmotic force, drawing free water
out of the cell and into the extracellular space, and thus decreasing the relative con-
centration of serum sodium while increasing serum tonicity. Other common causes
include administration of hypertonic agents, such as mannitol or hypertonic saline
(HTS), which are critical in the acute management of patients with sudden increases
of intracranial pressure, that is, traumatic intracranial hemorrhage and hemorrhagic
strokes.22 Given the patient’s plasma osmolality and calculated osmolality, the clini-
cian can then determine if there is a concurrent osmolar gap at play. The presence
of a wide osmolar gap will lead to osmotic diuresis in the patient and further decreased
plasma sodium concentrations.
In normal patients, the plasma water consists of approximately 93% of the volume,
with the remaining 7% being attributed to fats and proteins.23 Isotonic hyponatremia
can be seen in pseudohyponatremia, which is a laboratory artifact in processing the
blood sample for its sodium concentration. Most commonly, the cause is due to
severely elevated cholesterol.24 Other causes of pseudohyponatremia include hyper-
triglyceridemia, obstructive jaundice, which can cause extreme levels of cholesterol
and lipoprotein-X, and myeloma and subsequent hyperproteinemia.25,26 These pa-
tients will have unchanged concentrations of plasma water sodium and osmolality.
They will largely be asymptomatic with respect to their hyponatremia and require no
acute or emergent interventions.
Most commonly, hyponatremia is seen in hypotonic states. Hypotonic hyponatre-
mia will have serum osmolality less than 275 mOsm/kg. There are several types of hy-
potonic hyponatremia: hypervolemic, euvolemic, and hypovolemic hyponatremia. It is
important to note that other classification systems also exist, such as classifications
according to the body’s ability to excrete dilute urine. Typically, measurement of urine
sodium can elucidate the hypotonic hyponatremia variant, that is, high urine sodium
generally points to hemodilution as the culprit.8 Therefore, the variant is likely hypovo-
lemic hyponatremia. However, given the setting of the emergency department, volume
status can be assessed quickly to provide further medical decision-making. For
example, a dehydrated or hypovolemic patient’s kidneys will respond by retaining

Table 1
Common causes of hyponatremia

Hypervolemic Euvolemic Hypovolemic hyponatremia

hyponatremia hyponatremia SIADH Vomiting
Heart failure Drugs Diarrhea
Hepatic failure Primary polydipsia Exercise induced
Renal failure Beer potomania Diuretics (thiazides most commonly)
Nephrotic syndrome Hyperglycemia Cerebral salt wasting syndrome
Hypothyroidism
Adrenal insufficiency
Hypokalemia
Diet

Abbreviation: SIADH, syndrome of inappropriate antidiuretic hormone excretion.

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 Disorders of Sodium 701

sodium and the water that follows. Consequently, urine sodium should be lower.
Therefore, in states of hypotonic hyponatremia, if the urine sodium is greater than
20 mEq/L, the likely culprit is nephrogenic in etiology. Initial workup should also
include the comprehensive metabolic panel, thyroid stimulating hormone (TSH),
cortisol, and urine sodium. As discussed above, when the body has a low effective
circulating volume, that is, a state of intravascular depletion, it will retain water thus
concentrating the urine. When there is impairment of water excretion, urine osmolality
will be elevated.23 Except in cases of polydipsia and the “tea and toast” diet or beer
potomania, wherein the urine osmolality will be less than 100 mOsm/kg, hyponatremic
states will typically be greater than 200 mOsm/kg. With this methodology, one can
elucidate or at least narrow down the differential diagnosis.
In states such as congestive heart failure, liver failure and subsequent cirrhosis,
and nephrotic syndrome, the effective arterial blood volume is decreased due to
decreased cardiac output, congestion with subsequent vasodilation, or protein
loss.27 ADH is secreted in response to decreased osmolality, causing sodium
and water reabsorption while decreasing free water secretion. These patients will
“third space” the fluids, mainly redistributing the fluid into the interstitial space
and cause hypervolemic hyponatremia. They will present with edema and seem
“volume up.”
In hypovolemic hyponatremia, patient will seem dry or “volume down” on examina-
tion. They will often lack edema on examination and skin turgor may be poor. If the
urine sodium is elevated, this may be due to renal losses in cases of diuretic use,
salt wasting, or adrenal insufficiency. If it is decreased, one should suspect extrarenal
losses, as in cases of gastroenteritis.
In euvolemic hyponatremia, which is the most common variant of true hyponatre-
mia, evaluation of volume status can be unclear. Most of these cases are due to syn-
drome of inappropriate antidiuretic hormone excretion (SIADH). Other causes include
psychogenic polydipsia and drug-induced hyponatremia. In some disease states,
ADH may be secreted despite normal or increased plasma volume. Common condi-
tions manifesting as SIADH include malignancy, central nervous system disorders,
drugs, HIV, tuberculosis, and pneumonia.27 However, SIADH is a diagnosis of exclu-
sion. Since Bartter and Schwartz first described the syndrome, the diagnostic criteria
have not changed: hypoosmolality (<275 mosm/kg); hyperosmolar urine (>100 mosm/
kg); euvolemia; increased urine sodium (>20 mEq/L); and no diuretic use or evidence
of thyroid or adrenal disease.28

Management
Management depends on the patient’s symptoms and rapidity of development of the
hyponatremia, if able to be elicited from the patient’s history. Acute hyponatremia is
defined as a sodium level of less than 135 mmol/L that develops during a period of
48 hours. The short course is not enough time for cells to adapt to the new extracellular
tonicity, which may result in cerebral edema. If it is known that the hyponatremia has
been present longer than 48 hours, then it is considered chronic.13 Chronic hyponatre-
mia, however, is oftentimes asymptomatic because the cells have had time to adapt to
the extracellular environment. Intervening may cause the dreaded complication of os-
motic demyelination syndrome (ODS).13
The management of hyponatremia should be individualized based on the patient’s
specific clinical condition, underlying causes, and comorbidities. The approach to
treatment of hyponatremia depends on multiple factors, which includes duration,
severity (degree), and severity of symptoms. Concentrations between 130 and 134
mEq/L and between 120 and 129 mEq/L are defined as mild and moderate

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702 Alindogan & Joseph

hyponatremia, respectively. Once concentrations decline less than 120 mEq/L, it is

considered severe hyponatremia.13
Especially in cases of chronic hyponatremia, some patients may present asymp-
tomatically or with vague symptoms despite having moderate-to-severe hyponatre-
mia. Although the acuity and the degree of sodium derangement are both important
considerations for the clinician, guidelines now support that emergent intervention
is more governed by the severity of the patient’s symptoms. Mild-to-moderate hypo-
natremia may have relatively nonspecific symptoms to include headache, fatigue,
nausea, vomiting, dizziness, gait disturbances, forgetfulness, confusion, and muscle
cramps. More severe symptoms include seizures, obtundation, coma, and respiratory
arrest.
Patients with severe symptoms warrant emergent management. Rapidly increasing
the serum sodium is paramount to prevent permanent neurologic damage. The goal
should be to increase the serum sodium by 2 to 4 mEq/L until symptoms abate as
rapidly as possible.29 This can be achieved by infusion of 100 mL boluses (or 5 mL/
kg in children) of 3% HTS up to a maximum of 3 boluses.30 If HTS is not readily avail-
able, 8.4% sodium bicarbonate ampules from the code cart can be used as an
acceptable alternative. Ampules of 50 mL of 8.4% sodium bicarbonate contain almost
6% sodium and is effectively equal to 100 mL of HTS. If the serum sodium increases
adequately and symptoms persist, consider another cause other than hyponatremia.
Experts have long debated the appropriate correction rate for mildly symptomatic
hyponatremia. From multiple studies, it has been well established that correction of
the sodium level should not occur quicker than 10 to 12 mEq/L per 24 hours, with
some conservative experts stating the correction should not occur faster than 6
mEq/L per 24 hours to prevent complications.31,32 Both United States and European
guidelines now recommend a correction limit of 10 mmol/L per day regardless of chro-
nicity and advise frequent monitoring response to treatment.31,33 Where they diverge
is in their recommendations for managing overcorrection. Although both recommend
using vasopressin or free water to address overcorrection, they differ on when one
should intervene. Per the United States guidelines, if the limit is reached in a patient
whose baseline sodium was greater than 120 mmol/L, then correction is likely unnec-
essary. If the baseline was less than 120 mmol/L, then the clinician ought to relower
the sodium. The European guidelines suggest relowering if the limit of correction
has been surpassed, regardless of initial baseline concentration.31
Both guidelines recommend the use 3% HTS for the treatment of symptomatic
hyponatremia. The United States guidelines still holds slightly differing intervention
recommendations in terms of acute versus chronic hyponatremia; however, they
recommend for mild symptoms 3% HTS as a continuous infusion at 0.5 to 2 mL/kg
per hour.31 Comparatively, the European guidelines recommend 3% HTS bolus
150 mL over 20 minutes once.31 There is a recent study that compares bolus therapy
and continuous infusion, and it found that both were equally effective but that the
bolus therapy had a lower incidence of overcorrection requiring relowering therapy.34
Except in hypovolemic hyponatremia, both the US and European guidelines recom-
mend fluid restriction as first-line therapy for management of chronic euvolemic and
hypervolemic hyponatremia. Vaptans, which block vasopressin type 2 receptors to
cause free water loss or aquaresis, is suggested as second-line therapy for SIADH
(or euvolemic hyponatremia) and hypervolemic hyponatremia in the United States.33
However, vaptans may cause liver toxicity as well as overcorrection.31,35,36 For this
reason, the European guidelines do not recommend it for moderate hyponatremia
and recommend against it in severe cases and in hypervolemic hyponatremia.
Instead, the European second-line for SIADH includes loop diuretics. Nevertheless,

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 Disorders of Sodium 703

in most patients, correction of the underlying medical conditions will usually correct
the hyponatremia.31
In chronic hypovolemic hyponatremia, volume expansion is the mainstay of treat-
ment. Fluid resuscitation must be initiated and any underlying problem causing the
volume depletion must be corrected. As the intravascular volume is restored, ADH
secretion drops, renal function improves, and excess free water can be excreted.31
Most commonly, the initial fluid used is 0.9% normal saline. Guidelines suggest the
clinician may use isotonic saline alone (United States) or also balanced crystalloid
(European).31,33
Disposition depends on the patient’s symptoms. If the patient is severely symptom-
atic, they warrant ICU admission. Mild symptoms with moderate to severely
decreased serum sodium levels warrant admission to the floor depending on the hos-
pital protocols for serum sodium levels. Asymptomatic patients or patients with mildly
decreased sodium levels can often be discharged with close follow-up.
Complications
Cerebral edema
As stated previously, patients with severe hyponatremia can develop cerebral edema
because of water moving from the extracellular to the intracellular compartment
because of a difference in effective osmolality between brain and plasma. This usually
occurs when hyponatremia develops rapidly, and the brain has had too little time to
adapt to its hypotonic environment.31 Patients particularly at risk for this include post-
menopausal women, women on thiazide diuretics, children, psychiatric patients with
polydipsia, and hypoxemic patients.32 Once treatment of hyponatremia has
commenced, it is important to watch electrolyte levels closely, checking every 2 hours
if needed to help guide medical therapy. All these measures are to prevent the
dreaded complication known as osmotic demyelination syndrome.
Osmotic demyelination syndrome
ODS is the iatrogenic irreversible clinical syndrome of neurologic symptoms that oc-
curs after too rapid a correction of serum sodium.19 This severe complication is
caused by exceeding the safe limits of serum sodium correction, which as stated pre-
viously, is 10 to 12 mEq/L in a 24-hour period.19 This syndrome is postulated to be
caused by rapid swelling of the brain and nervous system tissue parenchyma during
fluid shifts because the tissue cannot adapt quickly enough to the changing osmo-
lality. Symptoms of osmotic demyelination syndrome include fluctuating levels of con-
sciousness or confusion, behavioral changes, dysarthria, and dysphagia, with the
worst symptoms being seizures, “locked-in syndrome” (devastating permanent con-
dition where all the voluntary muscles are paralyzed aside from the eyes), and death.
This condition can take anywhere from 2 to 6 days to develop and, thus, will often not
be clinically apparent while the patient is still in the emergency department. Therefore,
it is incumbent on the emergency clinician to be very meticulous when it comes to the
treatment of hyponatremia to prevent rapid overcorrection to prevent this condition.

HYPERNATREMIA

Defined as a serum sodium of greater than 145 mmol/L, hypernatremia is less com-
mon than hyponatremia, and it is most commonly due to excess water loss. However,
it can also be caused by the intake of salt without water or the administration of HTS
solutions. The vast majority is diagnosed in hospitalized patients but, according to one
population-based study, 0.2% of patients with hypernatremia were diagnosed in the
emergency department.37 The clinical manifestations of acute hypernatremia are

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704 Alindogan & Joseph

caused by an increase in serum sodium and osmolality causing water movement out
of brain cells and into the extracellular space subsequently causing brain cells to
shrink. Similar to hyponatremia, hypernatremia is associated with a higher mortality,
especially with other comorbid conditions.38

Presentation
The symptoms of acute hypernatremia are most attributable to the rapidity of change
of the serum sodium levels, not necessarily the overall sodium excess (or free water
deficit). The cause of hypernatremia is usually evident on clinical presentation and,
as stated previously, it most often occurs when water loss outpaces replacement.3
Alternatively, acute hypernatremia can be induced by large amounts of salt ingestion
or it can be iatrogenic in the case of administration of hypertonic sodium containing
solutions. The most common initial symptoms include thirst, dry mucous membranes,
and decreased urine output. Again, the central nervous system is the most sensitive to
changes in serum osmolality and is usually the most affected. Therefore, as the con-
dition progresses, more pronounced neurologic signs and symptoms may emerge,
including, restlessness, irritability, confusion, lethargy, muscle twitching, and seizures.
Severe hypernatremia can lead to neurologic complications such as altered mental
status, hallucinations, coma, and even death, if left untreated. The shrinking of brain
cells can cause intracerebral hemorrhage because of tearing of cerebral blood ves-
sels. The severe manifestations of hypernatremia usually are not present until the
serum sodium increases more than 158 mEq/L and values greater than 180 mEq/L
are associated with a very-high mortality rate.18

Evaluation and Diagnosis

As with hyponatremia, the first step when evaluating a patient with hypernatremia is to
determine the cause and then the volume status of the patient. See Table 2 for common
causes of hypernatremia. Hypovolemic hypernatremia is usually caused by decreased
water intake in patients with limited access to free water; however, it can also be due to
the inability to detect or respond to the sensation of thirst. Primary adipsia or hypodipsia
is caused by damage to the hypothalamic osmoreceptors. Patients with hyperglycemic
hyperosmolar syndrome are clinically dehydrated and have a relative hypernatremia
due to the hyperglycemia-induced eunatremia on laboratory work. Correction of sodium
based on the glucose levels will often reveal the true sodium level. Hypervolemic hyper-
natremia is usually iatrogenic in nature from the administration of hypertonic solutions or
from the improper preparation of solutions for enteral or parenteral feeding or peritoneal
dialysis. Euvolemic hypernatremia most often develops in diabetes insipidus (DI) in
which the body does not respond to ADH either centrally or peripherally. Therefore,
the patient continues to make maximally dilute urine with low urine osmolality. Causes

Table 2
Common causes of hypernatremia

Hypervolemic Euvolemic hypernatremia Hypovolemic hypernatremia

hypernatremia Diabetes insipidus Dehydration due to decreased
Hypertonic solution water intake
administration Prolonged hyperglycemia
Hyperglycemic hyperosmolar
syndrome
Osmotic diarrhea
Hyperaldosteronism

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 Disorders of Sodium 705

of DI are divided into 2 categories: central and nephrogenic. Central DI, also known as
arginine vasopressin deficiency, can be caused by trauma, pituitary surgery, and malig-
nancies but is most commonly idiopathic. Arginine vasopressin deficiency is character-
ized by a decrease in the release of ADH resulting in a variable degree of polyuria. About
30% to 50% of cases are idiopathic and are associated with the destruction of the hor-
mone secreting cells in the hypothalamic nuclei.39 Nephrogenic DI, also known as argi-
nine vasopressin resistance, is most commonly caused by renal disease, medications,
and genetic disorders.

Management
The approach to the treatment of hypernatremia is relatively straightforward given that
the range of causes is less than that for hyponatremia. The most important factors to
consider are whether the increase was acute or chronic, and the severity of
symptoms.
Acute hypernatremia is defined as a serum sodium level of greater than 145 mEq/L,
which develops during a period of less than 48 hours. If it is known that the hyperna-
tremia developed during a period of greater than 48 hours, or if the duration is un-
known, then it is considered chronic.40
Unstable patients should have their hypernatremia corrected during a minimum of
48 hours to decrease the likelihood of seizures, permanent brain damage, or even
death, which can occur in the setting of rapid correction with hypotonic fluids. The
serum sodium should not decrease by more than 8 to 15 mEq/L in a given 8-hour
period.41 The use of isotonic fluids (0.9% normal saline or lactated ringers) to restore
plasma volume is optimal because it is still likely hypotonic compared with the patients’
serum and is less likely to result in too rapid of overcorrection. However, the serum so-
dium must be closely monitored to prevent overcorrection, leading to additional neuro-
logic problems.6 If the correction does occur too rapidly, or if the patient begins to show
signs of cerebral edema or hyponatremia, the fluid replacement should immediately
stop and the patient should be treated for hyponatremia, with fluid restriction.
Stable patients will have less symptoms and a lower associated mortality because it
relates to their sodium levels. In these chronic cases, the brain goes into self-
preservation mode and produces idiogenic osmoles that allows relative maintenance
of brain cell hydration. In an asymptomatic patient, correction of the serum sodium level
should occur slowly, at a rate of no greater than 0.5 mEq/L/h and no more than 8 to 15
mEq/L per day.40 The specific treatment of hypernatremia is tailored to the nature of the
cause. If the patient is asymptomatic and has normal renal function, then the clinician
can wait for natural excretion. If the patient’s renal function is impaired, then excess so-
dium may need to be removed by dialysis. In patients with adipsia or hypodipsia, pa-
tient, caregiver, and family education is of paramount importance.

Complications
Cerebral edema
Rapid correction of hypernatremia can lead to a shift of water into brain cells, causing
cerebral edema. This can result in neurologic symptoms such as seizures, altered
mental status, focal neurologic deficits, and even coma. To prevent this, a gradual
and controlled correction of sodium levels is important.

Osmotic demyelination syndrome

Overly rapid correction of sodium levels, particularly in cases of chronic hypernatre-
mia, can cause the destruction of myelin in the brainstem, leading to a condition called
central pontine myelinolysis or osmotic demyelination syndrome. This condition can

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result in a range of neurologic symptoms, including paralysis, dysarthria, dysphagia,

and other motor deficits.
Fluid overload
Inappropriate administration of fluids or excessive water replacement can lead to fluid
overload, especially in patients with compromised cardiac or renal function. This can
result in pulmonary edema, congestive heart failure, or exacerbation of existing edem-
atous conditions.
Electrolyte imbalances
Correcting hypernatremia can affect the balance of other electrolytes, such as potas-
sium and magnesium. Rapid shifts in electrolyte levels can lead to cardiac arrhyth-
mias, neuromuscular abnormalities, and other complications.
To minimize the risk of these complications, it is crucial to closely monitor the pa-
tient’s serum sodium levels, fluid balance, and clinical status during the treatment of
hypernatremia. The correction of sodium levels should be gradual and tailored to
the individual patient’s needs.

SUMMARY

Sodium imbalances are a common occurrence in the emergency department.

Although recognition and diagnosis are relatively straightforward, discovering the
cause and management should be approached systematically. The most important
history items to ascertain is if the patient has symptoms and how long this imbalance
has taken to develop. Treatment rapidity depends on severity of symptoms with the
most rapid treatment occurring in only the severely symptomatic. Overcorrection
has dire consequences and must be approached in a careful and systematic fashion
in order to prevent these devastating consequences.

CLINICS CARE POINTS

Evaluating the patient’s volume status is critical to helping ascertain the possible cause for
the sodium imbalance.

Rapidity of the development of the patient’s sodium imbalance and if the patient has
symptoms will often drive the management of the patient.

Patients with severe symptoms require rapid treatment to prevent permanent neurologic
sequelae.

If HTS therapy is not readily available, you can use 8.4% sodium bicarbonate as an acceptable
alternative.

Preventing overcorrection should be foremost on the emergency clinician/s mind when
managing sodium imbalance. Have a low threshold to check sodium levels more
frequently while correcting.

DISCLOSURE

The authors have no financial disclosures.

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