October Sodium Disorders

Sodium Disorders In The October 2012
Volume 14, Number 10

Emergency Department: Authors
Camiron L. Pfennig, MD
A Review Of Hyponatremia
Assistant Professor of Emergency Medicine, Director of Undergraduate
Medical Education, Vanderbilt University Medical Center, Nashville, TN
Corey M. Slovis, MD
And Hypernatremia Professor and Chair, Department of Emergency Medicine, Vanderbilt

University Medical Center; Medical Director, Nashville Fire Department
and International Airport, Nashville, TN
Peer Reviewers
Abstract
Keith A. Marill, MD
Assistant Professor, Harvard Medical School; Emergency Department
Identifying and correcting sodium abnormalities is critical, since Attending Physician, Massachusetts General Hospital, Boston, MA
suboptimal management potentially leads to substantial morbid- Christopher J. Rees, MD
ity and mortality. Manifestations of hyponatremia, which is one Clinical Instructor in Emergency Medicine, Perelman School of
Medicine, University of Pennsylvania School of Medicine; Attending
of the more common electrolyte abnormalities in clinical medi- Physician, Emergency Department, Pennsylvania Hospital,
cine, depend on multiple factors, including the chronicity of the Philadelphia, PA
symptoms, the absolute level of sodium, and the patient’s overall CME Objectives
health. In symptomatic hyponatremia, emergency clinicians must Upon completion of this article, you should be able to:
understand the importance of determining the proper rate of so- 1. Describe the pathophysiology and complications of hyponatremia
dium correction in order to avoid encephalopathy, cerebral edema, and hypernatremia.
and death. Hypernatremia is most often due to unreplaced water 2. Differentiate the 3 types of hypernatremia and describe the
general treatment approach in hypernatremia.
that is lost from the gastrointestinal tract, skin, or the urine. Acute 3. Distinguish the 4 general categories of hyponatremia and
symptomatic hypernatremia should be corrected rapidly, while describe the treatment algorithm for each category of
chronic hypernatremia is generally corrected more slowly due to hyponatremia.
the risks of brain edema during treatment. Special circumstances Prior to beginning this activity, see “Physician CME Information” on the
do exist in sodium management, and every patient’s presentation back page.
should be evaluated in clinical context.
Editor-in-Chief Medical Center, University of North Charles V. Pollack, Jr., MA, MD, Stephen H. Thomas, MD, MPH International Editors
Andy Jagoda, MD, FACEP Carolina School of Medicine, Chapel FACEP George Kaiser Family Foundation
Peter Cameron, MD
Professor and Chair, Department of Hill, NC Chairman, Department of Emergency Professor & Chair, Department of
Academic Director, The Alfred
Emergency Medicine, Mount Sinai Medicine, Pennsylvania Hospital, Emergency Medicine, University of
Steven A. Godwin, MD, FACEP Emergency and Trauma Centre,
School of Medicine; Medical Director, University of Pennsylvania Health Oklahoma School of Community
Professor and Chair, Department Monash University, Melbourne,
Mount Sinai Hospital, New York, NY System, Philadelphia, PA Medicine, Tulsa, OK
of Emergency Medicine, Assistant Australia
Editorial Board Dean, Simulation Education, Michael S. Radeos, MD, MPH Jenny Walker, MD, MPH, MSW
University of Florida COM- Assistant Professor of Emergency Assistant Professor, Departments of Giorgio Carbone, MD
William J. Brady, MD
Jacksonville, Jacksonville, FL Medicine, Weill Medical College Preventive Medicine, Pediatrics, and Chief, Department of Emergency
Professor of Emergency Medicine,
of Cornell University, New York; Medicine Course Director, Mount Medicine Ospedale Gradenigo,
Chair, Resuscitation Committee, Gregory L. Henry, MD, FACEP
Research Director, Department of Sinai Medical Center, New York, NY Torino, Italy
University of Virginia Health System, CEO, Medical Practice Risk
Emergency Medicine, New York
Charlottesville, VA Assessment, Inc.; Clinical Professor Ron M. Walls, MD Amin Antoine Kazzi, MD, FAAEM
Hospital Queens, Flushing, New York
of Emergency Medicine, University of Professor and Chair, Department of Associate Professor and Vice Chair,
Peter DeBlieux, MD
Michigan, Ann Arbor, MI Robert L. Rogers, MD, FACEP, Emergency Medicine, Brigham and Department of Emergency Medicine,
Louisiana State University Health
FAAEM, FACP Women’s Hospital, Harvard Medical University of California, Irvine;
Science Center Professor of Clinical John M. Howell, MD, FACEP
Assistant Professor of Emergency School, Boston, MA American University, Beirut, Lebanon
Medicine, LSUHSC Interim Public Clinical Professor of Emergency
Medicine, George Washington Medicine, The University of Scott Weingart, MD, FACEP
Hospital Director of Emergency Hugo Peralta, MD
University, Washington, DC; Director Maryland School of Medicine, Associate Professor of Emergency
Medicine Services, LSUHSC Chair of Emergency Services,
of Academic Affairs, Best Practices, Baltimore, MD Medicine, Mount Sinai School of
Emergency Medicine Director of Hospital Italiano, Buenos Aires,
Faculty and Resident Development Inc, Inova Fairfax Hospital, Falls Alfred Sacchetti, MD, FACEP Medicine; Director of Emergency Argentina
Church, VA Assistant Clinical Professor, Critical Care, Elmhurst Hospital
Francis M. Fesmire, MD, FACEP Dhanadol Rojanasarntikul, MD
Department of Emergency Medicine, Center, New York, NY
Professor and Director of Clinical Shkelzen Hoxhaj, MD, MPH, MBA Attending Physician, Emergency
Thomas Jefferson University, Medicine, King Chulalongkorn
Research, Department of Emergency Chief of Emergency Medicine, Baylor Senior Research Editor
College of Medicine, Houston, TX Philadelphia, PA Memorial Hospital, Thai Red Cross,
Medicine, UT College of Medicine,
Scott Silvers, MD, FACEP Joseph D. Toscano, MD Thailand; Faculty of Medicine,
Chattanooga; Director of Chest Pain Eric Legome, MD
Chair, Department of Emergency Emergency Physician, Department Chulalongkorn University, Thailand
Center, Erlanger Medical Center, Chief of Emergency Medicine,
Medicine, Mayo Clinic, Jacksonville, FL of Emergency Medicine, San Ramon
Chattanooga, TN King’s County Hospital; Professor of Suzanne Peeters, MD
Regional Medical Center, San
Nicholas Genes, MD, PhD Clinical Emergency Medicine, SUNY Corey M. Slovis, MD, FACP, FACEP Ramon, CA Emergency Medicine Residency
Assistant Professor, Department of Downstate College of Medicine, Professor and Chair, Department Director, Haga Hospital, The Hague,
Emergency Medicine, Mount Sinai Brooklyn, NY of Emergency Medicine, Vanderbilt Research Editor The Netherlands
School of Medicine, New York, NY Keith A. Marill, MD University Medical Center; Medical Matt Friedman, MD
Assistant Professor, Harvard Medical Director, Nashville Fire Department and Emergency Medical Services Fellow,
Michael A. Gibbs, MD, FACEP International Airport, Nashville, TN
School; Emergency Department Fire Department of New York, New
Professor and Chair, Department
Attending Physician, Massachusetts York, NY
of Emergency Medicine, Carolinas
General Hospital, Boston, MA
Accreditation: EB Medicine is accredited by the ACCME to provide continuing medical education for physicians. Faculty Disclosure: Dr. Pfennig, Dr. Slovis, Dr. Marill, Dr. Rees,
Dr. Jagoda, and their related parties report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational
presentation. Commercial Support: This issue of Emergency Medicine Practice did not receive any commercial support.
Opening Cases EM physicians, including yourself. He is protecting
his airway and has a bounding radial pulse, but he is
An 88-year-old woman with history of moderate demen- confused, has edema of the fingers and wrists, and is
tia presents via ground ambulance for irritability and vomiting. He has normal skin turgor and color. His
increased weakness after having 2 weeks of cough and running partner states that he had a mild viral ill-
vomiting at her extended care facility. She was found ness all week but made sure to stop at every water stop
febrile and confused during morning nursing rounds. during the race to try to remain hydrated. The medic
Her past medical history is significant for recent cere- establishes IV access, and vital signs reveal a blood
brovascular accident with residual left-sided weakness pressure 103/60 mm Hg, pulse 121 beats per minute,
and chronic kidney disease. Current medications include temperature 38°C, and oxygen saturation 100% via
metformin, hydrochlorothiazide, metoprolol, and aspirin. nonrebreather mask. The paramedic you are working
Her vital signs on arriving in the ED are blood pressure with suspects dehydration and tells you that he plans
98/63 mm Hg, pulse 95 beats per minute, respiratory to aggressively rehydrate the athlete with 2 L of normal
rate 24 breaths per minute, oral temperature 38.3°C, saline. Fortunately, you have a different plan.
and oxygen saturation 95% on 2 L nasal cannula. On
physical exam, she is frail and appears dehydrated, Introduction
with intermittent confusion. Her pulmonary exam is
remarkable for crackles at the right base with mild dif- Disorders of sodium are the most common electro-
fuse abdominal discomfort. Her chest x-ray shows right lyte disturbance in clinical medicine. Most sodium
middle lobe pneumonia. Blood is obtained, and a serum disorders are mild and require no acute therapy.
chemistry panel shows sodium 152 mEq/L, potassium Patients with heart failure, patients taking diuret-
4.0 mEq/L, chloride 108 mEq/L, bicarbonate 14 mEq/L, ics, and the elderly population are the patients most
BUN 55 mg/dL, creatinine 1.7 mg/dL, and glucose 131 likely to be seen in the emergency department (ED)
mg/dL. The nurse asks you what IV fluids you want and with relatively minor degrees of sodium disorders
how fast . . . that typically require minor medication adjustments;
A 22-year-old graduate student with new-onset sei- however, emergency clinicians must recognize and
zure activity arrives in the ED from her dormitory. The treat these electrolyte abnormalities when indicated,
paramedics state that her roommate called the ambulance because severe hypernatremia and hyponatremia
because of the patient’s altered behavior and vomiting are both associated with significant morbidity and
that had been worsening over the past 5 hours. The mortality. Most deaths from sodium abnormalities
roommate also reported that she had mild asthma but no are due to an underlying disease process; however,
other medical problems and that she took no daily medi- recognizing and treating the abnormality can maxi-
cations. Multiple empty beer cans were found scattered mize good outcomes and may attenuate complica-
around the dorm room, but no empty pill bottles were tions of the underlying process. Delays in treatment
seen. On EMS arrival, the patient began seizing, and 2 or inadequate treatment of both severe hypernatre-
doses of diazepam, 1 mg each, were administered with no mia and hyponatremia can be dangerous and even
improvement. She arrived in the ED with intermittent life threatening.
tonic clonic seizure activity without return to baseline
between events. Her vital signs on arrival are blood Critical Appraisal Of The Literature
pressure 106/44 mm Hg, pulse 135 beats per minute,
respiratory rate 14 breaths per minute, oral temperature An Ovid MEDLINE® search for randomized con-
36.7°C, and oxygen saturation 90% on 100% oxygen trolled trials was performed using the search terms
via nonrebreather mask. Her finger-stick glucose is 154 hyponatremia and hypernatremia. Studies within the
mg/dL. Her seizures persist, despite another 10 mg of past 12 years were reviewed for practice-changing
lorazepam and 20 phenytoin sodium equivalents (PE)/ trials. A total of 36 randomized controlled tri-
kg of fosphenytoin. The patient is intubated with no als were identified, including 1 landmark animal
difficulties while a levetiracetam infusion is prepared. A study. These results were added to a prior search
friend of the patient arrives and reports that the patient performed 18 months ago that used the same
had been drinking alcohol and using ecstasy at a party. terms with a search span back to 1985. This prior
At that point, blood chemistries return, revealing a search provided more than 300 articles. A total
sodium 104 mEq/L, potassium 2.9 mEq/L, chloride 112 of 91 review articles published since 2000 in the
mEq/L, bicarbonate 16 mEq/L, BUN 51 mg/dL, creati- English language focused on the adult population.
nine 1.5 mg/dL, and glucose 159 mg/dL. You realize In addition, The National Guideline Clearinghouse
that the patient’s hyponatremia needs to be emergently and the Cochrane Database of Systematic Reviews
corrected, but you wonder: how fast is too fast? were queried.
A 33-year-old man collapses at mile 22 of his
first full marathon (26.2 miles) and is rushed to the
emergency medical tent staffed by EMS providers and
Emergency Medicine Practice © 2012 2 www.ebmedicine.net • October 2012

Etiology And Pathophysiology vascular, and neurologic complications. Hypernatre-
mia results from the disequilibrium of the balance
Volume And Osmolarity Regulation: The between water intake and/or the combined water
Simplified Basics loss from renal excretion and respiratory, skin, and
There are many complex physiological interactions gastrointestinal sources. Under normal conditions,
involved in maintaining normal serum sodium, water intake and losses are matched. To maintain
osmolality, and euvolemia. Regulation of osmolar- salt homeostasis, the kidneys adjust urine concentra-
ity is predominantly based on the hypothalamus tion to match salt intake and loss.
monitoring and adjusting plasma osmolarity via the Most hypernatremic patients have either an
secretion of antidiuretic hormone (ADH). If osmo- impaired sense of thirst or no access to water. Thus,
larity increases by a small amount, ADH is secreted the elderly, infants, patients in coma or with men-
to retain body water (along with an increased sense tal impairment, and those who are intubated and
of thirst for water) and lower serum osmolarity. paralyzed are at highest risk for this disorder.2,3
Conversely, if a patient’s osmolarity falls, ADH is Other patients at high risk of hypernatremia may
not secreted and free water is excreted to raise serum have other underlying medical diseases including
osmolarity. Derangement in ADH can result from Conn syndrome, sickle cell disease, or various can-
inappropriate secretion, as in the syndrome of inap- cers. Conn syndrome is characterized by increased
propriate antidiuretic hormone secretion (SIADH), aldosterone secretion leading to hypernatremia,
in which ADH is secreted even as total body water suppressed plasma renin activity, hypertension, and
(TBW) is normal. This increased ADH secretion hypokalemia.
results in hypo-osmolarity, excess TBW, and resul- Hypernatremia can be divided into 3 physi-
tant hyponatremia. Conversely, the body becomes ologic pairings. (See Table 1.) Diabetes insipidus (a
volume depleted in diabetes insipidus, no ADH is disorder leading to hypernatremia with low TBW
released, and TBW dramatically decreases, leading and normal total body sodium) can lead to life-
to hypernatremia. threatening hypernatremia with multiple causes.4
Volume is regulated by a number of mecha- (See Table 2, page 4.)
nisms, but the most important is the stimulation of
the renin-angiotensin system in the kidney. When
intravascular volume falls, the renin-angiotensin Table 1. Types Of Hypernatremia
system is stimulated and aldosterone is released Hypovolemic hypernatremia: decreased total body sodium and
from the adrenal gland, resulting in increased decreased TBW
glomerular reabsorption of sodium in exchange for • Heat illness
increased excretion of potassium and hydrogen. • Increased insensible losses: burns, sweating
The increased sodium reabsorption will cause more • Gastrointestinal loss: diarrhea, protracted vomiting, continuous
water to also be reabsorbed by the kidney. If too gastrointestinal suction
• Osmotic diuresis: glucose, mannitol, enteral feeding
much circulating volume is sensed by the atria, na-
triuretic peptides are released, resulting in a diure- Euvolemic hypernatremia: normal total body sodium and
decreased TBW
sis. Derangements in this system are best typified
• Diabetes insipidus
by adrenal insufficiency where there is suboptimal
• Neurogenic
or no aldosterone secretion, resulting in volume
• Elderly with “reset” osmostat
contraction and hyponatremia in association with • Hypothalamic dysfunction
elevations in potassium and a nongap metabolic • Suprasellar or infrasellar tumors5
acidosis. An increase in aldosterone, as seen in • Renal disease
Cushing syndrome, does not usually cause hyper- • Drugs (amphotericin, phenytoin, lithium, aminoglycosides, me-
natremia, due to other compensatory mechanisms. thoxyflurane)
Nonetheless, hypokalemia and a metabolic alkalo- • Sickle cell disease
sis do occur as the distal exchange site aggressively Hypervolemic hypernatremia: increased total body sodium and
reabsorbs sodium in exchange for the excretion of increased TBW
potassium and hydrogen. • Salt tablet ingestion
• Salt water ingestion6
Hypernatremia • Saline infusions
• Saline enemas
Hypernatremia is defined as serum sodium > 145
• Intravenous sodium bicarbonate
mEq/L and is often associated with morbidity and • Poorly diluted interval feedings
mortality. It is very uncommon in previously normal • Primary hyperaldosteronism
patients, and in adults it is almost exclusively due • Hemodialysis
to a TBW deficit.1 The hyperosmolar state associ- • Cushing syndrome
ated with hypernatremia alters a variety of cellular • Conn syndrome
functions, which contributes to metabolic, cardio- Abbreviation: TBW, total body water.
October 2012 • www.ebmedicine.net 3 Emergency Medicine Practice © 2012

Hyponatremia Pseudohyponatremia
Hyponatremia is defined as serum sodium con- In pseudohyponatremia, serum sodium levels may
centration of < 135 mEq/L. It has been associated be artificially low due to increased levels of plasma
with increased mortality, increased length of hos- proteins or lipids or due to increased serum con-
pitalization and need for extended care admission, centrations of osmotically active chemicals such
gait imbalance and falls, rhabdomyolysis, and bone as glucose and mannitol.10 The phenomenon of
fractures.8 Consequently, hyponatremia has also pseudohyponatremia is explained by the increased
been linked to increased healthcare costs.9 The most percentage of large molecular particles relative to
common causes of symptomatic severe hyponatre- sodium. These large molecules do not contribute to
mia in adults are the following: plasma osmolality (resulting in a state in which the
• Therapy with thiazide diuretics relative sodium concentration is decreased), but the
• SIADH overall osmolality remains unchanged. In addition,
• Polydipsia in psychiatric patients emergency clinicians should always consider blood
• Unintentional water intoxication draw or laboratory errors as a possible etiology of
• Patients recovering postoperatively a patient’s hyponatremia, especially if the blood
sample was drawn near an infusion site using D5W
Gastrointestinal fluid loss, ingestion of dilute (5% dextrose in water) or D5½NS (5% dextrose in
baby formula, and accidental ingestion of excessive half-normal saline) or when a very abnormal sodium
water are the main causes of severe hyponatremia in level is reported in an otherwise healthy patient.
infants and children.
Most patients presenting to the ED with hypona-
tremia are asymptomatic and do not require emer-
gent therapy; however, if symptoms are present,
the emergency clinician must be prepared to initiate
Table 3. The 4 Categories Of Hyponatremia
treatment immediately. Symptoms are based both on Pseudohyponatremia
the degree of hyponatremia as well as how acutely • Hyperglycemia
the drop in sodium occurred. Patient presentations • Hyperlipidemia
vary from headache, lethargy, and vomiting to dis- • Hyperproteinemia (multiple myeloma, macroglobulinemia)
• Laboratory or blood draw errors
orientation, seizures, encephalopathy, and death.
Hyponatremia has many causes that are sub- Hypovolemic hyponatremia (decreased TBW and sodium, with
divided based on the patient’s volume status. The a relatively greater decrease in sodium)
• Body fluid losses
causes of hyponatremia fall into 4 general categories:
Sweating, vomiting, diarrhea, GI suction
(1) pseudohyponatremia, (2) hypovolemic hypo-
l
• Third spacing
natremia, (3) hypervolemic hyponatremia, and (4) Bowel obstruction, burns
euvolemic hyponatremia. (See Table 3.)
l
• Renal causes
l
Diuretics, mineralocorticoid deficiency, osmotic diuresis, renal
tubular acidosis, salt-wasting nephropathies
Hypervolemic hyponatremia (increased total body sodium with
a relatively greater increase in TBW)
Table 2. Common Causes Of Diabetes • Heart failure
Insipidus • Chronic renal failure
• Hepatic failure/cirrhosis
Central
Euvolemic hyponatremia (increased TBW with near-normal
• Idiopathic origin
total body sodium)
• Familial disease
• SIADH
• Neurosurgery or trauma
• Drugs causing SIADH, including diuretics, barbiturates, car-
• Cancer
bamazepine (Carbatrol®, Epitol®, Tegretol®), chlorpropamide
• Hypoxic encephalopathy
(Diabinese®, Insulase®), clofibrate (Atromid-S®), opioids, SSRIs,
• Infiltrative disorders
tolbutamide (Orinase®, Tol-Tab®), vincristine (Oncovin®)
• Supraventricular tachycardia
• Psychogenic polydipsia
• Anorexia nervosa
• Beer potomania
Nephrogenic
• Hypothyroidism
• Chronic renal insufficiency
• Adrenal insufficiency
• Polycystic kidney disease
• MDMA (ecstasy)
• Lithium toxicity7
• Accidental or intentional water intoxication
• Hypercalcemia
• Hypokalemia
Abbreviations: GI, gastrointestinal; MDMA, 3,4-methylenedioxy-
• Tubulointerstitial disease
methamphetamine; SIADH, syndrome of inappropriate antidiuretic
• Heredity
hormone secretion; SSRIs, selective serotonin reuptake inhibitors;
• Sickle cell disease
TBW, total body water.

Hyperglycemia is sometimes considered a cause include SIADH, psychogenic polydipsia,12 beer po-
of pseudohyponatremia; however, it actually causes tomania,13 hypothyroidism, diuretic use in patients
a dilutional hyponatremia by pulling water into the with mild congestive heart failure, and accidental or
vascular space by osmosis, as glucose is osmotically intentional water intoxication. These patients do not
active. One formula that is commonly used to correct present with edema because most of the increased
serum sodium levels based on the degree of a pa- body water is intracellular and not intravascular.
tient’s hyperglycemia advocates adding 1.6 mEq/L to Patients prescribed various psychiatric medica-
the measured sodium for every 100 mg/dL of glucose tions including selective serotonin reuptake inhibi-
above 100 up to about 400, then 4 mEq/L should be tors (SSRIs) and carbamazepine can develop hypo-
added for every additional 100 mg/dL.11 It may be natremia, likely secondary to excess water intake.
easier for a busy emergency clinician to remember The mechanism by which SSRIs cause hyponatre-
that the maximum fall for every 100 mg elevation in mia is thought to be secondary to development of
blood glucose is about 2.0 to 2.5 mEq/L of sodium. SIADH. Hyponatremia without edema has also been
described in patients after the use of the recreational
Hypovolemic Hyponatremia drug ecstasy (3,4-methylenedioxymethamphet-
Hypovolemic hyponatremia—hyponatremia in as- amine, or MDMA).14 Factors that may contribute
sociation with dehydration—occurs when there is to hyponatremia following ecstasy ingestion most
decreased extracellular volume combined with an commonly include excessive fluid intake secondary
even greater loss of sodium. Hyponatremia second- to central polydipsia and fluid third-spacing. Beer
ary to body fluid losses must be differentiated from potomania is a specific hypo-osmolality syndrome
low sodium secondary to renal losses. Body fluid related to consumption of beer, which is poor in
losses include vomiting, diarrhea, sweating, gastro- solutes and electrolytes.
intestinal suction, and “third spacing,” as in patients SIADH is an important cause of hyponatremia
with bowel obstruction, burns, or intra-abdominal that occurs when normal control of ADH secretion is
sepsis. Hypovolemic hyponatremia due to renal lost and ADH is secreted independent of the body’s
causes includes diuretic use, mineralocorticoid need to conserve water. The process results from
deficiency, renal tubular acidosis, and salt-wasting excess ADH production that causes TBW to increase,
nephropathy. Hypovolemic hyponatremia can be diluting the body’s sodium and causing the serum
further exacerbated when fluid losses are replaced sodium to decrease. The excessive release of ADH is
with hypotonic saline. most commonly from the posterior pituitary gland
Clues to the underlying cause of hypovolemic but can also be from other ectopic sources including
hyponatremic dehydration may be obtained by eval- the lung. Patients with SIADH have inappropriately
uating the patient’s serum bicarbonate, chloride, and concentrated urine despite the presence of a low
potassium levels. Hyponatremic patients who have serum osmolality and normal circulating blood vol-
concomitant hypochloremia, alkalosis, and hypoka- ume. Patients with SIADH have excess TBW but no
lemia likely have hyponatremia due to protracted signs of edema, ascites, or heart failure because most
vomiting or prolonged gastric suction. A normal gap of the increased body water is intracellular and not
metabolic acidosis should alert emergency clinicians intravascular. In general, patients with SIADH have
that diarrhea may be the cause of a patient’s dehy- normal acid-base status, normal potassium balance,
dration and hyponatremia. Hyperkalemia with a and normal adrenal function.
normal gap acidosis may be an important clue to an The 3 most common causes of SIADH are the fol-
underlying diagnosis of adrenal insufficiency. lowing: (1) pulmonary lung masses and infections, (2)
central nervous system disorders, and (3) drug use.
Hypervolemic Hyponatremia (See Table 4, page 6.) Lung cancers (especially small
Hypervolemic hyponatremia—hyponatremia with cell cancer), pneumonia, and tuberculosis can lead to
increased extracellular volume—occurs when SIADH. Central nervous system infections, masses,
sodium and water are retained but water retention and psychosis can also cause SIADH. There are a
exceeds sodium retention. On physical examination, large number of medications associated with SIADH,
most of these patients present with edema. Hypona- the most common of which are thiazide diuretics,
tremia with increased total body sodium occurs in narcotics, lithium, oral hypoglycemics, barbiturates,
patients with congestive heart failure, chronic renal antineoplastics, and antiepileptics.
failure, and hepatic failure secondary to hypoperfu-
sion of the kidneys, causing high aldosterone secre- Differential Diagnosis
tion and decreased free water excretion.
Both hypernatremia and hyponatremia can pres-
Euvolemic Hyponatremia ent with very vague complaints involving multiple
The final category of hyponatremia includes patients organ systems, which leads to a broad differential
who are euvolemic but have increased TBW. The diagnosis. Common complaints with mild to moder-
most common causes of this type of hyponatremia

ate sodium abnormalities include irritability, nausea, Hypernatremia
weakness, abdominal pain, lethargy, confusion, and Hypernatremia is a disease seen predominantly
tachypnea. These vague complaints can also be seen in the elderly, but it can also be seen in patients
in hypothyroidism, hypoglycemia, viral illnesses, who depend on others to provide them with water,
psychiatric illnesses, and other electrolyte abnor- including infants, intubated patients, and persons
malities. In more extreme cases of hyponatremia with mental debilitation.16,17 Hypernatremia should
and hypernatremia, patients may present with head be considered as part of the differential in breastfed
injury after a fall or a seizure, and the differential infants in the first weeks of life and elderly patients
diagnosis may include seizure, polysubstance abuse, who are institutionalized; however, most patients
cerebrovascular accident, and cardiac emergencies. will also have multifactorial etiologies leading to
severe hypernatremia.18
Prehospital Care Patients with hypernatremia often present with
nonspecific symptoms such as irritability, nausea,
Prehospital management of suspected sodium weakness, abdominal pain, lethargy, and tachypnea.
abnormalities is difficult, since serum levels are not Patients or caregivers may have noted polyuria or
generally known in the field. In cases of confirmed polydipsia, or patients may have obvious signs of
hyponatremia in endurance athletes, prehospital extrarenal fluid losses. Other patients may have no
providers can consider initiating treatment with 3% complaints at all. The degree of dehydration may
hypertonic saline if part of a pre-established protocol be underestimated because intravascular volume is
or by Medical Control. Nonetheless, in the cases of maintained. In severe cases of hypernatremia, coma,
both hyponatremia and hypernatremia, prehospital convulsions, pulmonary edema, and shock due to
providers will most likely be treating symptoms of severe intracellular fluid loss can develop rapidly.
the underlying electrolyte abnormality. Hypernatremia should be considered in any patient
presenting with altered mental status, especially
Emergency Department Evaluation individuals with severe mental retardation or head
injury as well as in bedridden patients who have no
Presenting complaints of sodium disorders are access to water.
generally vague, so there must be a high index of
suspicion in order to consider the diagnosis. Most Hyponatremia
patients will be diagnosed with hyponatremia or hy- The signs and symptoms of hyponatremia correlate
pernatremia only after a laboratory value has been with the rapidity at which hyponatremia develops,
returned; however, focused history taking and home and they increase as sodium levels decline. Nonspe-
medication review can be helpful in guiding the di- cific signs of hyponatremia include anorexia, nau-
agnosis.15 In addition, it is important to understand sea, vomiting, and generalized weakness. Acutely
some common presenting signs and symptoms as hyponatremic patients whose sodium drops to < 120
well as common underlying disease patterns that mEq/L over 24 to 48 hours may present with severe
often cause sodium abnormalities. neurologic findings including confusion, seizures,
cerebral edema, coma, or brainstem herniation.
Table 4. Most Common Causes Of Syndrome Determining the hydration status of the patient may
Of Inappropriate Antidiuretic Hormone help establish the etiology of the hyponatremia and
Secretion help direct subsequent treatment. The diagnosis of
hypovolemic hyponatremia is more likely in the
Lung Conditions
• Cancer (especially small cell)
patient with diminished skin turgor, decreased capil-
• Pneumonia lary refill, dry mucous membranes, and orthostasis.
• Tuberculosis On the other hand, the patient with jugular venous
• Abscess distension, peripheral edema, or pulmonary con-
Central Nervous System Disorders gestion is much more likely to have hypervolemic
• Infection (meningitis, brain abscess) hyponatremia. Patients presenting with SIADH or
• Mass (tumor, subdural hematoma) other euvolemic hyponatremia will not present with
• Postoperative edema because most of the increased body water is
• Cerebrovascular accident intracellular and not intravascular.
• Psychosis (with psychogenic polydipsia)
Drugs Diagnostic Studies
• Thiazide diuretics
• Narcotics
Hypernatremia
• Oral hypoglycemics
• Barbiturates In patients with concern for hypernatremia, serum
• Antineoplastics osmolarity as well as urine sodium concentration
• Antiepileptics and osmolality should be obtained in addition to

routine serum chemistries. In adults, the degree of as furosemide (Delone®, Furocot®, Lasix®), has not
hypernatremia almost always equals the TBW defi- been recently administered, as these will increase
cit. The patient’s TBW deficit can be estimated by urinary sodium losses. It is essential that adrenal in-
using the following formula: sufficiency be considered when a dehydrated patient
has both hyponatremia and hyperkalemia.
TBW deficit = TBW x [(serum Na/140) - 1] Comparing the serum osmolality to the urine
osmolality may help diagnose the cause of the pa-
A patient’s TBW is usually calculated by multi- tient’s hyponatremia. The serum osmolality should
plying the patient’s body weight in kilograms times normally mirror the patient’s volume status. Thus,
0.6; however, due to body fat differences based on a volume-contracted dehydrated (hyperosmolar)
the age and sex of the patient, it is more accurate to patient should have a concentrated urine with high
use the correction factors listed in Table 5. osmolality and a volume-overloaded (hypo-osmo-
For example, a 78-year-old male patient weigh- lar) patient should have a very dilute hypo-osmolar
ing 60 kg is brought to the ED with altered mental urine. If a hyponatremic hypo-osmolar patient has
status. He is found to have a serum sodium of 160 a nonmaximally dilute urine and is wasting so-
mEq/L. The patient’s TBW deficit is: dium, SIADH should be suspected. Similarly, if a
hyperosmolar hypernatremic patient has a dilute
(0.5 x 60 kg) X (160/140) – 1 = 30 X (1.143 - 1) = urine (and is wasting free water), diabetes insipi-
4.29 (4290 mL) dus should be expected.
Hyponatremia Treatment
In order to determine whether the etiology of the
hyponatremia is secondary to renal causes, a spot Hypernatremia
urinary sodium and/or urinary chloride should be The treatment of hypernatremia has 3 interdepen-
obtained. Patients with hypovolemic hyponatremia dent goals:
due to renal causes will have elevated urine sodium 1. Quickly correct underlying shock, hypoperfu-
levels > 20 mEq/L, as their kidneys cannot retain sion, or significant hypovolemia with normal
sodium or chloride. Thus, their kidneys are inap- saline;
propriately wasting sodium even in the face 2. Treat the underlying cause of hypernatremia
of hyponatremia. On the other hand, patients (such as fever, vomiting, diarrhea, or diabetes
with hypovolemic hyponatremia due to nonrenal insipidus); and
causes typically have a low urinary sodium or chlo- 3. Carefully lower the serum sodium level, usually
ride (< 20 mEq/L) as they try to retain solute. Thus, by replacing the body’s total water deficit.
these patients are appropriately retaining sodium
due to their hyponatremia. Patients with euvolemic Until hypoperfusion and hypovolemia are cor-
hyponatremia typically have a urinary sodium con- rected, homeostatic mechanisms for sodium balance
centration > 20 mEq/L secondary to volume expan- will promote sodium resorption to maintain intra-
sion caused by water retention. Patients with hyper- vascular volume, even at the expense of the serum
volemic hyponatremia secondary to congestive heart sodium concentration.
failure or cirrhosis have urine sodium levels < 20 The rate of correction in hypernatremia is
mEq/L due to renal hypoperfusion, whereas those extremely important to minimize complicating the
with renal causes of hypervolemic hyponatremia patient’s care and avoid life-threatening cerebral
or with SIADH have sodium levels > 20 mEq/L, as edema and seizures. There are no data to suggest
their kidneys are not retaining sodium. that the etiology of the hypernatremia alters the
When interpreting serum sodium levels, always likelihood of developing osmotic demyelination
consider the possibility of sampling error if the with overly rapid correction. The rate of correction
reported value does not seem consistent with the pa- of hypernatremia must be taken into account before
tient’s presentation, and confirm that a diuretic, such deciding on the most appropriate therapy for any
patient with hypernatremia.
In adult patients who have developed hyper-
Table 5. Correction Factors For Calculating natremia over a short period of time due to sodium
Body Water Deficit loading, rapid correction at 1 to 2 mEq/L/h by
lowering serum sodium is relatively safe.19,20 None-
Population Correction Factor
theless, in patients with chronic hypernatremia
Children and adult males Total body weight (kg) x 0.6
or in cases where the duration of hypernatremia
Adult females Total body weight (kg) x 0.5 is unknown, rapid correction of the water deficit
Elderly males Total body weight (kg) x 0.5 should be avoided. In this patient population, slow
Elderly females Total body weight (kg) x 0.45 correction of hypernatremia over a period of 2 to 3

Clinical Pathway For Management Of Hypernatremia
In The Emergency Department
Hypernatremia
Serum sodium > 145
mEq/L
Hypovolemic
• TBW decreased Euvolemic Hypervolemic
• Total body sodium decreased • TBW decreased • TBW increased
• Total body sodium • Total body sodium
normal increased
• Urine osmolality > 600 • Urine osmolality 300-

mOsm/kg 600 mOsm/kg • Urine osmolality usually
• Urine sodium < 20 • Urine sodium > 20 < 300 mOsm/kg Urine sodium > 20 mEq/L
mEq/L mEq/L • Always less than
plasma osmolality
• Insensible losses • Osmotic diuresis • Cushing syndrome

Diabetes insipidus
• GI losses • Hyperglycemia • Conn syndrome
• Burns • Mannitol • Primary hyperaldoste-
• Heat illness • Urea Reverse underlying ronism
• Enteral feeds causes (Class I) • Salt ingestions
Hemodynamically stable? NO • Standard resuscitation

guidelines (0.9% NS IV) Removal of excess
Adequate thirst?
YES (Class I) sodium; consider D5W
• When hemodynami- and diuretics
cally stable, initiate YES
NO
Sodium elevation acute? correction
• IV fluids that are

YES Drink fluid to replace urine
NO hypotonic compared to
losses
serum sodium (Class I)
• Desmopressin (Class
Rapid lowering of serum Slow correction over
II)
sodium 1-2 mEq/L/24h period of 48 h at no more
(Class I) than 0.5 mEq/L/h or 10-
12 mEq/L/24h (Class I)
Abbreviations: D5W, 5% dextrose in water; GI, gastrointestinal; IV, intravenous; NS, normal saline, TBW, total body water.
Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.
Class I Class II Class III Indeterminate tatives from the resuscitation
• Always acceptable, safe • Safe, acceptable • May be acceptable • Continuing area of research councils of ILCOR: How to De-
• Definitely useful • Probably useful • Possibly useful • No recommendations until velop Evidence-Based Guidelines
• Proven in both efficacy and • Considered optional or alterna- further research for Emergency Cardiac Care:
effectiveness Level of Evidence: tive treatments Quality of Evidence and Classes
• Generally higher levels of Level of Evidence: of Recommendations; also:
Level of Evidence: evidence Level of Evidence: • Evidence not available Anonymous. Guidelines for car-
• One or more large prospective • Nonrandomized or retrospective • Generally lower or intermediate • Higher studies in progress diopulmonary resuscitation and
studies are present (with rare studies: historic, cohort, or case levels of evidence • Results inconsistent, contradic- emergency cardiac care. Emer-
exceptions) control studies • Case series, animal studies, tory gency Cardiac Care Committee
• High-quality meta-analyses • Less robust randomized con- consensus panels • Results not compelling and Subcommittees, American
• Study results consistently posi- trolled trials • Occasionally positive results Heart Association. Part IX. Ensur-
tive and compelling • Results consistently positive Significantly modified from: The
Emergency Cardiovascular Care ing effectiveness of community-
Committees of the American wide emergency cardiac care.
Heart Association and represen- JAMA. 1992;268(16):2289-2295.
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2012 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

Clinical Pathway For Management Of Hyponatremia
In The Emergency Department
Hyponatremia
Sodium < 135 mEq/L
Serum osmolality?
High, due to: Normal, due to: Low (contracted)

Low (hypotonic)
• Hyperglycemia • Pseudohyponatremia hypovolemic
• Mannitol • Hyperlipidemia
• Paraproteinemia
• Blood draw/laboratory
error Extracellular fluid volume?
Renal losses Extrarenal losses High (expanded) hyper- Limited fluid shift (eu-
• Diuretics • Diarrhea volemic volemic)
• Osmotics • Vomiting • CHF • SIADH
• Renal tubal acidosis • Burns • Cirrhosis • Hypothyroidism
• Cerebral salt wasting • Sweating • Nephrotic syndrome • Secondary adrenal
• Primary adrenal insuf- • Blood loss • Toxemia of pregnancy insufficiency
ficiency • Third spacing • Renal failure • Psychogenic polydipsia
• Beer potomania
• Tap water enema
• MDMA (ecstasy) usage
• Treat underlying cause • Treat underlying cause Treat with: Treat with:
(Class I) (Class I) • Fluid restriction • Elimination of underly-
• Trial of volume expan- • Trial of volume expan- (Class I) ing cause (Class I)
sion with 0.9% NS sion with 0.9% NS • Sodium restriction • Free water restriction
(Class I) (Class I) (Class I) (Class I)
• 3% hypertonic saline • 3% hypertonic saline • Diuretics (CHF) • Hypertonic saline
(severe) (Class II) (severe) (Class II) (Class II) (Class II)
• Consider potassium • Vaptans (Class II) • Vaptans (Class II)
repletion (diuretics) • Albumin (cirrhosis) • Demeclocycline (Class
(Class II) (Class III) indeterminate)
• Paracentesis (cirrhosis)
(Class III)
• Hemodialysis (renal
failure) (Class III)
Note: Treatments are listed in order from most recommended to consideration.

Abbreviations: CHF, congestive heart failure; MDMA, 3,4-methylenedioxymethamphetamine; NS, normal saline; SIADH, syndrome of inappropriate
antidiuretic hormone secretion.

days has been recommended, at no more than 0.5 described with rapid correction of sodium. Central
mEq/L/h or 10 to 12 mEq/L/24h.19 nervous system damage due to hyponatremia may
Typically, patients can be started on normal be caused by cerebral edema and increased intracra-
saline for volume replacement until they are he- nial pressure, by osmotic fluid shifts during overly
modynamically stable and then changed to half- aggressive treatment, or both. When subjected to
normal saline at 100 mL/h once their vital signs a hyponatremic environment, neurons become
have normalized. The treatment of central diabetes depleted of sodium and potassium as they attempt
insipidus with desmopressin (DDAVP®), a syn- to limit their own osmolarity to prevent intracellu-
thetic analogue of ADH available in subcutaneous, lar fluid shifts that would lead to cerebral edema. If
intranasal, and oral preparations, is an effective fluid therapy raises extracellular sodium levels too
means of improving polyuria. Table 6 shows the quickly, fluid is pulled out of neurons and diffuse
most common dosing regimens. demyelination may occur, leading to flaccid paraly-
For fluid-overloaded patients with hypernatre- sis and, often, death due to this osmotic demyelin-
mia, the proper therapy is water administration or ation syndrome.21
its parenteral equivalent, D5W, in conjunction with While reports of sodium disturbances leading
furosemide. This combination achieves negative so- to demyelination syndromes were being published,
dium balance with neutral or negative fluid balance. reports were also being made claiming that severe
hyponatremia itself could cause life-threatening
Hyponatremia brain damage. As of today, the rate at which pro-
Treatment of hyponatremia must be guided by the found hyponatremia should be corrected is the focus
patient’s clinical presentation, severity of symptoms, of continued clinical debate. There is no consensus
estimated duration of illness, fluid status, and un- about the optimal treatment of symptomatic hypo-
derlying etiology for the sodium disturbance. There natremia. In his well-known 1990 article, Tomas Berl
are 2 groups of hyponatremic patients that will discusses the difficult clinical dilemma that physi-
require treatment with either normal saline or hy- cians face with patients presenting with symptom-
pertonic saline. The 2 groups include patients with: atic hyponatremia because of the different clinical
(1) severe but asymptomatic hyponatremia with a guidelines and lack of true consensus.22 There is a
sodium level ≤ 110 mEq/L, and (2) acute symptom- very fine line between correcting the sodium too
atic hyponatremia with a sodium level < 120 mEq/L. quickly versus too slowly, and inappropriate man-
Most patients presenting to the ED with hypona- agement can be devastating.
tremia are stable and require no emergent therapy; Fortunately, over the past few years, we are
however, asymptomatic patients who have severe coming closer to a consensus regarding the optimal
hyponatremia with serum sodium levels of ≤ 110 treatment of hyponatremia. There is agreement
mEq/L and those who have acute alterations in among physicians that correction should occur at a
mental status, seizures, or new focal findings due to sufficient pace and magnitude to reverse the mani-
hyponatremia with serum levels < 120 mEq/L need festations of hypotonicity, but not so rapid and large
immediate intervention. Table 7 presents the sodium to pose a risk of developing osmotic demyelination.
concentration of various infusates. The following In patients with chronic hyponatremia, neurologic
equation is helpful to estimate the effect of 1 L of any sequelae are more likely to occur with rapid rates of
infusate on serum sodium: sodium correction.23,24
Change in serum Na+ (mEq/L) = (infusate Na+

(mEq/L) - serum Na+ (mEq/L) / (TBW + 1)

For the past 30 years, the treatment of hypo- Table 7. Characteristics Of Infusates
natremia has remained controversial. In the early Infusate Infusate Na+ Extracellular Fluid
1980s, central pontine myelinolysis, now more accu- (mEq/L) Distribution (%)
rately labeled as osmotic demyelination syndrome, was 3% hypertonic 513 100
saline
0.9% NS 154 100
Table 6. Desmopressin Dosing LR 130 97

½NS 77 73
Intranasal 5-40 mcg/qd or divided q8-12h
0.2% NaCl + 34 55
Oral Initially 0.05 mg q12h D5W
Effective range: 0.1-1.2 mg divided q8-12h
D5W 0 40
Subcutaneous 2-4 mcg/qd, divided q12h
Abbreviations: D5W, 5% dextrose in water; LR, lactated Ringer; NS,

Abbreviation: q, every. normal saline.

A prospective study looking at neurological manage the most severe manifestations of hypona-
outcomes with serial magnetic resonance imaging tremia.27 In a prospective observational study of 58
in hyponatremic patients found that the correction patients with euvolemic acute symptomatic severe
rate of hyponatremia plays a significant role in the hyponatremia, administration of 100 mL of 3% hy-
pathogenesis of pontine lesions in individuals with pertonic saline resulted in a mean increase in serum
profound hyponatremia who undergo large in- sodium of 2 mEq/L.31 Studies have also shown that
creases in sodium concentration as a result of severe infusing 3% saline at a rate of 1 to 2 mL/kg/h re-
initial hyponatremia.25 A comparative multicenter sults in an increase in serum sodium of 1 mEq/L/h
study evaluating 64 patients concluded that patients to 2 mEq/L/h.32
with severe chronic hyponatremia are most likely to Potassium deficits must also be replaced ag-
avoid neurologic complications when their electro- gressively when treating hyponatremic patients. If
lyte disturbance is corrected slowly.26 patients are retaining volume and not diuresing ad-
After weighing the available evidence, Adrogue equately, furosemide can be used. Many authorities
and Madias recommended a targeted rate of correc- recommend concomitant furosemide, although some
tion that does not exceed 8 mEq/L on any day of recommend avoiding it or reserving it for patients
treatment.19 Remaining within this target, the initial with extracellular fluid volume expansion.19
rate of correction can be 1 to 2 mEq/L/h for several Patients may be able to make full neurologic re-
hours in patients with severe symptoms. In order to coveries from osmotic demyelination syndrome with
minimize the likelihood of osmotic demyelination the re-induction of hyponatremia in these extreme
syndrome, it is essential that symptomatic patients cases.33,34 In patients with refractory hyponatremia,
with severe hyponatremia not have their serum so- demeclocycline (Declomycin®) induces nephrogenic
dium levels rise by any more than a total of 10 to 12 diabetes insipidus and helps to correct hyponatre-
mEq/L within the first 24 hours.27 In a multicenter mia in a dosage of 600 to 1200 mg daily.35
trial of patients with hyponatremia, no neurologic
complications were observed in patients corrected Hypovolemic Hyponatremia
by < 12 mEq/L/24h or by < 18 mEq/L/48h.28 Treatment of hypovolemic hyponatremia begins
Most cases of osmotic demyelination syndrome with rehydration. Hypotensive, dehydrated patients
occur in the alcoholic, malnourished, and elderly are volume resuscitated with normal saline, but once
population, although this devastating side effect can they are hemodynamically stable, the infusion rate
occur in healthy, young patients as well. Patients is slowed. Typically, the normal saline is started at
with osmotic demyelination syndrome develop a 500 to 1000 mL/h until the blood pressure is stable
flaccid paralysis, dysarthria, dysphagia, and hypo- and then slowed to 200 mL/h with frequent sodium
tension. If a patient develops these symptoms dur- checks. If the sodium is < 120 mEq/L, the sodium
ing therapy, stop all sodium-containing fluids and should only be allowed to rise by an average of 0.5
administer D5W immediately to temporarily lower mEq/h and 10 to 12 mEq/d.27 It is also essential to
serum sodium levels. Reversal of symptoms has treat the underlying cause of hyponatremia.
been shown, experimentally, in numerous animal
studies and also in 3 human case reports.29 Hypervolemic Hyponatremia
For relatively asymptomatic patients with Normal saline and hypertonic saline can cause
sodium values of 115 to 135 mEq/L, a trial of free pulmonary edema in the hypervolemic hypona-
water restriction to < 0.8 L/d to 1.25 L/d can be tremic patient. Fluid and sodium restriction is the
attempted. This includes all fluids, including water preferred treatment of patients with hypervolemic
contained in food and medications. Serum sodium hyponatremia. Patients with congestive heart
level should be measured at regular intervals to look failure contributing to their hyponatremia will usu-
for improvement. ally benefit from diuretics that will increase water
In more-severe cases, when the sodium is secretion and cause vasodilation to improve cardiac
≤ 120 mEq/L and the patient has either alterations output.36 In patients with liver failure, consider
in mental status, focal neurological findings, or sei- utilizing albumin and diuretics and performing
zures, hypertonic saline is indicated.27,28 A consen- a paracentesis to improve the underlying pathol-
sus statement in 2005 suggested that 3% hypertonic ogy. Hemodialysis is an alternative in patients with
saline be used for symptomatic patients, either renal impairment and will be required in signifi-
as a 100 mL (513 mEq of Na+/L) rapid infusion cantly hyponatremic renal failure patients with
followed by 100 mL/h or at a rate of 1 to 2 mL/ volume overload. When dispositioning the patient,
kg/h.30 If a second bolus is required, an additional it is important to discuss water restriction with the
100 mL of the 3% solution may be administered inpatient service because it may make the largest
over the next 50 minutes. Correction of hypona- impact in these patients’ long-term care.
tremia by 4 to 6 mEq/L within 6 hours, with bolus
infusions of 3% saline if necessary, is sufficient to

Euvolemic Hyponatremia Special Circumstances
The mainstay of treatment for euvolemic hyponatre-
mia is free-water restriction. As the hypo-osmolality Exercise-associated hyponatremia (EAH) is the
in SIADH results from a relative abundance of water occurrence of hyponatremia during or up to 24
in the intracellular and extracellular volumes and hours after prolonged physical activity. EAH is
is maintained by a reduced ability to excrete water, defined by a serum or plasma sodium concentra-
the restriction of oral free water intake is usually the tion < 135 mEq/L. Approximately 5% to 30% of
most effective therapy and was recommended by a endurance cyclists, triathletes, and runners may
2007 expert panel on hyponatremia.27 Nonetheless, develop hyponatremia during their events, and
the use of water restriction is insufficient to treat although most will be asymptomatic, life-threat-
acute severe hyponatremia, and it is not recom- ening hyponatremia can occur and fatalities have
mended as the sole intervention in severely symp- been reported.41,42 Several risk factors have been
tomatic hyponatremia in which a more rapid correc- identified for the development of EAH, including
tion rate is necessary. The only definitive treatment exercise duration > 4 hours, female gender, low
of SIADH is elimination of its underlying cause. In body weight, excessive drinking during the event,
cases of hyponatremia associated to oxcarbazepine preexercise dehydration, nonsteroidal anti-inflam-
(Trileptal®) and other antiepilepsy medications, all matory agents, and lack of heat acclimation. In the
cases resolved spontaneously when the drug treat- majority of athletes that develop EAH, there is an
ment was stopped.37 increase in TBW relative to that of total body ex-
Somewhat surprisingly, the use of normal changeable sodium, leading to a dilutional effect.
saline in patients with SIADH may cause the se- The incidence of EAH was very rare prior to
rum sodium to decrease even more, as free water is 1981, when there was a movement that encouraged
retained and hypertonic urine is excreted; however, athletes to consume as much fluid as possible during
a trial of normal saline may be considered when try- races; however, excessive water and sports beverage
ing to differentiate between a hypovolemic patient intake is not the sole explanation for the develop-
and a euvolemic patient. From a study of a series of ment of EAH.
17 patients with chronic SIADH, Musch and Decaux Ideally, medical facilities would be able to
concluded that the infusion of 0.9% normal saline rapidly assess sodium at the end of an endurance
raises the serum sodium when the urine osmolality event, but recognizing EAH by clinical criteria is
is < 530 mOsm/L.38 If a patient is symptomatic due often necessary if equipment is not available. As
to a rapid decrease in serum sodium concentration, emergency clinicians, it is important to be familiar
treatment with hypertonic saline is recommended. with the differences between dehydration and EAH,
Demeclocycline and lithium are rarely utilized in the as the inappropriate administration of fluids can be
treatment of SIADH due to their many side effects devastating.43 The spectrum of EAH ranges from
and nephrotoxicity. Rapid correction of hyponatre- bloating, nausea, vomiting, edema (particularly of
mia can be obtained via hemodialysis. To minimize ring fingers and wrists), and headache all the way
the risks of osmotic demyelination syndrome, he- to hyponatremic encephalopathy that develops as
modialysis is reserved for patients with documented a result of cerebral edema leading to altered men-
renal failure and is utilized in a very careful manner. tal status, seizures, pulmonary edema, and death.
A 2007 expert panel assessed the potential con- More commonly, dehydrated athletes have poor skin
tributions of aquaretic nonpeptide small-molecule turgor, excessive thirst, sunken eyes, and postural
arginine vasopressin receptor antagonists, also hypotension. EAH often becomes symptomatic after
known as vaptans, to hyponatremia therapies.27 the event, as water continues to be absorbed from
Currently, intravenous conivaptan (Vaprisol®) and the gastrointestinal tract.
oral tolvaptan (Samsca®) are FDA approved for use Medical providers at endurance events need
in the treatment of euvolemic and hypervolemic to be aware of EAH and avoid incorrectly diagnos-
hyponatremia. In 2 multicenter randomized double- ing dehydration and erroneously beginning normal
blind placebo-controlled trials known as the SALT-1 saline infusions. The specific treatments will depend
and SALT-2 clinical trials, the efficacy of tolvaptan on the clinical presentation of the patient. Most
was evaluated in patients with euvolemic or hyper- athletes with mild, asymptomatic hyponatremia
volemic hyponatremia and was found to increase that would likely be recognized only on laboratory
serum sodium concentrations at day 4 and day 30 testing will improve with fluid restriction, until they
more than placebo.39 In addition, a recent single-cen- spontaneously diurese. The definitive treatment for
ter study retrospectively examined 18 patients who EAH encephalopathy is immediate administration
were hyponatremic due to SIADH who were treated of a 100 mL bolus of 3% intravenous saline. If the
with conivaptan. The study found that 66.7% of the patient is not clinically improving after the initial
patients had an absolute increase in serum sodium bolus, the athlete can be treated with up to 2 addi-
of at least 4 mEq/L within 24 hours.40 tional 100 mL 3% NaCl bolus infusions at 10-minute

Risk Management Pitfalls For Sodium Emergencies
1. “The extended-care facility sent the elderly 6. “The patient presented from her dormitory
patient here for treatment of her urinary tract with seizure activity, and her sodium was
infection.” found to be 131 mEq/L. I began intravenous
Often, the elderly patient cannot provide a fluid replacement to correct her hyponatremia,
good history on arrival to the ED. Always check but I didn’t evaluate her for meningitis.”
electrolytes in elderly patients with underlying Mild to moderate hyponatremia (sodium 125
medical problems. mEq/L to 135 mEq/L) does not cause altered
mental status or seizures. Look for another
2. “The patient was significantly dehydrated from cause.
her gastrointestinal illness, so 2 large-bore IVs
were established, and I ran normal saline in on 7. “A diabetic patient presented via ground EMS
the pressure bag as fast as possible.” with altered mental status and tachycardia.
Never correct sodium disorders too rapidly. Her venous blood gas, obtained immediately,
Be aware that normal saline is not always revealed a blood sugar of 650 mg/dL and a
the initial fluid of choice in hyponatremia or sodium of 118 mEq/L.”
hypernatremia. Hyperglycemia can cause hyponatremia; correct
the glucose elevation, not the sodium fall. The
3. “After the marathon, the runner presented to body tries to maintain stable osmolarity in the
the medical tent complaining of headache and setting of profound hyperglycemia.
nausea. The medic gave her a 32-ounce bottle
of water and a 16-ounce bottle of sports bever- 8. “The patient’s sodium improved from 120
age and told her to drink them both quickly.” mEq/L on arrival to 130 mEq/L at the time
Always consider hyponatremia in any runner the admission request was initiated. She was
or endurance athlete with altered mental status. transferred to the observation area to await her
After a long endurance event, altered behavior, bed upstairs in the medical wing. The nurse
nausea, vomiting, and headache may not be called me to report that the patient was sig-
secondary to dehydration. nificantly hypotensive and having stroke-like
symptoms. “
4. “The patient is currently undergoing chemo- Always check sodium hourly in patients with
therapy for lung cancer and presented to the severe hyponatremia.
ED with cold-like symptoms. She was found to
have a sodium of 116 mEq/L. On review of her 9. “He came to the ED with a blood sugar that
records, her sodium at her last oncology clinic was very elevated, but his serum sodium was
visit, 2 weeks prior, was 119 mEq/L.” normal.”
Never raise serum sodium by more than 10 to 12 A significantly hyperglycemic patient with a
mEq/d in patients with chronic hyponatremia. normal sodium level is very dehydrated and has
hypernatremic dehydration.
5. “The patient presented with fatigue, weakness,
diarrhea, loss of appetite, and weight loss. Her 10. “He was brought to the ED from a bar because
sodium was found to be 126 mEq/L on evalua- his friends were concerned that he had some-
tion. She said she had been craving salty foods thing slipped into his drink. They informed
for the past month and had also noticed some the emergency clinician that, although he
significant hair loss.” drinks frequently, he had never acted this
Always consider adrenal insufficiency drunk before.”
in hyponatremia patients who are either Remain cautious when diagnosing alcohol
dehydrated, acidotic, and/or hyperkalemic. intoxication without further evaluation. Sodium
abnormalities frequently occur in heavy alcohol
abuse and MDMA (ecstasy) dependence.

intervals.44 In this special population of hypona- Disposition
tremic patients, the emergency clinician can assume
that the hyponatremia is acute and be comforted by Disposition of patients with hypernatremia or hy-
the fact that there are no reported cases of osmotic ponatremia will vary for each individual patient de-
demyelination syndrome with aggressive treatment pending on the severity of symptoms, the etiology of
of EAH.30 After initial stabilization, either in the field the underlying cause of the electrolyte abnormality,
or in the hospital, EAH can be treated with standard the degree of sodium abnormality, and the patient’s
hyponatremia protocols. response to treatment.
In all patients with hyponatremia and hyperna-
Controversies And Cutting Edge tremia, the cause should be identified and treated.
Some conditions, such as congestive heart failure or
Multiple literature sources continue to state that the use of diuretics, are obvious causes of hyponatre-
there is controversy in the management of hypona- mia. Other causes, such as SIADH and endocrine de-
tremia; fortunately, fluid management strategies are ficiencies, usually require further evaluation before
becoming more standardized in emergency medi- identification and appropriate treatment.
cine. Newer agents, such as the vaptans, have shown Patients who are asymptomatic or those with
promising results and may be useful in the treatment mild symptoms can often be discharged home to
of hyponatremia. Hyponatremia is increasingly rec- follow up closely with primary care providers. Some
ognized as an independent prognostic marker that patients with underlying cardiac disease or endo-
adversely affects morbidity and mortality in heart crine abnormality will require expert consultation
failure.45 Current research is looking at the addi- and likely admission, while patients with unstable
tion of vaptans to a standard heart failure treatment vital signs, altered mental status, or seizure activity
regimen in hyponatremic patients and whether they may require intensive care admission.
may offer additional survival benefits. The effi- The prognosis for hyponatremia generally
cacy of vaptans may be beneficial as an adjunctive depends on the underlying etiology causing the
therapy and may prevent hyponatremia in cases of sodium disturbance. In general, acute hyponatremia
EAH as well.46,47 that occurs in < 48 hours is more dangerous than
It remains uncertain whether sodium distur- hyponatremia that develops slowly over time. In the
bances are a marker of poor prognosis or an active general adult hospitalized population, Anderson
contributor to adverse outcomes, but evidence of et al found that mortality rates were 60-fold higher
direct adverse effects on multiple organ systems con- in patients with even asymptomatic hyponatremia
tinues to emerge in the medical literature.45 compared to patients with normal sodium levels.46
Patients with hypernatremia often have other seri-
ous comorbidities, so it is difficult to precisely evalu-
ate mortality directly due to hypernatremia; how-
ever, delays in treatment or inadequate treatment
Time- And Cost-Effective increase both morbidity and mortality, especially in
Strategies elderly patients.48
1. Do not treat sodium abnormalities in a patient Summary

when the finding is incidentally discovered in a
laboratory draw in a completely asymptomatic Sodium abnormalities can be a challenging issue
patient with mild sodium abnormalities. in the ED because they are often difficult to man-
2. Water restriction may be the only necessary age appropriately in both the acute and the chronic
intervention in some patients with sodium phase. It is important to not only be able to differen-
abnormalities. tiate between the 4 categories of hyponatremia and
3. Be cautious when prescribing medications—es- the 3 types of hypernatremia but also to understand
pecially diuretics—for elderly patients, in order the treatment approach in the emergency setting.
to avoid potential sodium disturbances and Physical examination findings are vague, but patient
their complications. history often leads to considering sodium disorders
4. Educate ancillary staff on blood draw tech- in the differential diagnosis. Acute symptomatic
niques to avoid false hyponatremia from a blood hyponatremia, whether self-induced, drug-related,
sample drawn near an infusion site using D5W or hospital-acquired, is a medical emergency that
or D5½NS. demands immediate recognition and intervention.
5. Inform the community about the risks of exer- Inappropriate correction of sodium abnormali-
cise-associated hyponatremia and the important ties can rapidly lead to morbidity and mortality. It
preventative recommendations to avoid serious remains uncertain whether dysnatremia is a marker
illness and hospitalization. of poor prognosis or an active contributor to adverse

outcomes, but evidence of direct adverse effects on To help the reader judge the strength of each ref-
multiple organ systems is emerging. erence, pertinent information about the study will be
included in bold type following the reference, where
Case Conclusions available. In addition, the most informative referenc-
es cited in this paper, as determined by the authors,
Your elderly patient had multiple medical concerns that re- are noted by an asterisk (*) next to the number of the
quired emergent evaluation. You diagnosed her with severe reference.
hypernatremia, likely secondary to her underlying disease
1. Huang WY, Weng WC, Peng TI, et al. Central pontine and
processes, combined with a lack of access to free water. In extrapontine myelinolysis after rapid correction of hypona-
addition to her pneumonia, she had been having gastroin- tremia by hemodialysis in a uremic patient. Ren Fail. 2007;
testinal losses from vomiting, along with her known under- 29(5):635-638. (Case report)
lying renal insufficiency. On arrival, she was hypotensive 2. Adler SM, Verbalis JG. Disorders of body water homeo-
and febrile. You immediately established 2 large-bore IVs, stasis in critical illness. Endocrinol Metab Clin North Am.
2006;35(4):873-894. (Review)
placed her on 2 L oxygen via nasal cannula, and obtained a 3. Jacobson J, Bohn D. Severe hypernatremic dehydration and
finger-stick blood glucose. You began her management by hyperkalemia in an infant with gastroenteritis secondary
correcting her hypoperfusion and hypovolemia with a 500- to rotavirus. Ann Emerg Med. 1993;22(10):1630-1632. (Case
mL NS bolus followed by a second 500-mL NS bolus for report)
her persistent hypotension after the pulmonary exam and 4.* Verbalis JG. Diabetes insipidus. Rev Endocr Metab Disord.
2003;4(2):177-185. (Review)
confirmation of her past medical history. You then began 5. Loh JA, Verbalis JG. Disorders of water and salt metabolism
treatment of the underlying causes of her hypernatremia associated with pituitary disease. Endocrinol Metab Clin North
with antipyretics, antiemetics, and antibiotics for her fever, Am. 2008;37(1):213-334. (Review)
vomiting, and pneumonia, respectively. After 2 NS boluses, 6. Casavant MJ, Fitch JA. Fatal hypernatremia from saltwater
her vital signs normalized, and slow correction of hyperna- used as an emetic. J Toxicol Clin Toxicol. 2003;41(6):861-863.
(Case report)
tremia was initiated with ½NS at 100 mL/h over 48 hours 7. Trepiccione F, Christensen BM. Lithium-induced nephrogen-
as an inpatient. ic diabetes insipidus: new clinical and experimental findings.
Your grad student patient was suffering from hypo- J Nephrol. 2010;2 (Suppl 16):S43-S48. (Review)
natremia likely secondary to the use of MDMA (ecstasy) 8. Chawla A, Sterns RH, Nigwekar SU, et al. Mortality and
at the party. On arrival, she was having seizure activity serum sodium: do patients die from or with hyponatremia?
Clin J Am Soc Nephrol. 2011; 6(5):960-965. (Comprehensive
that was unresponsive to benzodiazepines, so you secured retrospective review of 53 medical records after 45,693
her airway with endotracheal intubation, confirmed bilat- patient reviews)
eral breath sounds, and established 2 large-bore IVs. You 9. Callahan MA, Do HT, Caplan DW, et al. Economic impact of
rechecked her blood glucose and administered naloxone. hyponatremia in hospitalized patients: a retrospective cohort
She did not have any improvement, so you administered study. Postgrad Med. 2009;121(2):186–191. (Retrospective
cohort study, 7573 patients)
100 mL of 3%NS over 10 minutes, followed by a second 10. Turchin A, Seifter JL, Seely EW. Clinical problem-solving.
bolus of 100 mL of the 3% solution en route to the ICU. Mind the gap. N Engl J Med. 2003;349(15):1465-1469. (Case
The patient’s sodium was slowly corrected over 72 hours, report)
and she was successfully extubated and hemodynamically 11. Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: evaluat-
stable on hospital day 3. ing the correction factor for hyperglycemia. Am J Med. 1999;
106(4):399-403. (Journal article)
Based on the athlete’s normal skin turgor and color, 12. Cheng JC, Zikos D, Skopicki Ha, et al. Long-term neurologic
the edema of his upper extremities, the lack of hyperther- outcome in psychogenic water drinkers with severe symp-
mia, and reports that he had been drinking water at every tomatic hyponatremia: the effect of rapid correction. Am J
race stop, you suspected EAH and sent him to the ED. Med. 1990;88(6):561-566. (Review)
In the ED, his serum sodium level was found to be 112 13. Hettema ME, Halma C. Beer drinker’s hyponatremia: a case
report. Neth J Med. 1999; 54(3):105-107. (Case report)
mEq/L, and a 100-mL bolus of 3% IV NS was immedi- 14. Holmes SB, Banerjee AK, Alexander WD. Hypona-
ately initiated. The patient continued to be confused and traemia and seizures after ecstasy use. Postgrad Med J.
vomiting, and a second 100-mL 3% NS bolus infusion 1999;75(879):32-33. (Case report)
was given, after which, his mental status began to clear. 15.* Buckley MS, Leblanc JM, Cawley MJ. Electrolyte distur-
An NS infusion at a rate of 200 mL/h was started, and he bances associated with commonly prescribed medications
in the intensive care unit. Crit Care Med. 2010;38(6 Suppl):
was discharged 12 hours later, feeling well. S253-S264. (Review)
16. Palevsky PM, Bhagrath R, and Greenberg A. Hypernatremia
References in hospitalized patients. Ann Intern Med. 1996;124(2):197-203.
(Journal article)
17. Price TG, Kallenborn JC. Infant hypernatremia: a case report.
Evidence-based medicine requires a critical ap- J Emerg Med. 2000;19(2):153-157. (Case report)
praisal of the literature based upon study methodol- 18. Holley AD, Green S, Davoren P. Extreme hypernatraemia: a
ogy and number of subjects. Not all references are case report and brief review. Crit Care Resusc. 2007;9(1):55-58.
equally robust. The findings of a large, prospective, (Case report)
19.* Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med.
randomized, and blinded trial should carry more
2000;342(21):1581-1589. (Review)
weight than a case report. 20.* Kaplan LJ, Kellum JA. Fluids, pH, ions and electrolytes. Curr

Opin Crit Care. 2010;16(4):323-331. (Review) tremia: evidence from 2135 weighed competitive athletic
21. Pirzada NA, Ali II. Central pontine myelinolysis. Mayo Clin performances. Proc Natl Acad Sci USA. 2005;102 (51):18550-
Proc. 2001;76(5): 559-562. (Case report) 18555. (Comparative study)
22.* Berl T. Treating hyponatremia: damned if we do and damned 43. Glace B, Murphy C. Severe hyponatremia develops in a
if we don’t. Kidney Int. 1990;37(3):1006-1018. (Journal article) runner following a half-marathon. JAAPA. 2008;21(6):27-29.
23. Sterns RH. Severe symptomatic hyponatremia: treatment and (Case report)
outcome. A study of 64 cases. Ann Intern Med. 1987;107(5):656- 44. Hew-Butler T, Ayus JC, Kipps C, et al. Statement of the
664. (Retrospective chart review; 64 patients) Second International Exercise-Associated Hyponatremia
24.* Sterns RH, Nigwekar SU, Hix JK. The treatment of hypona- Consensus Development Conference, New Zealand, 2007.
tremia. Semin Nephrol. 2009;29(3):282-299. (Review) Clin J Sport Med. 2008;18: 111-121. (Consensus development
25.* Brunner Jennifer, Redmond JM, Haggar AM, et al. Central conference statement)
pontine myelinolysis and pontine lesions after rapid cor- 45. Siegal AJ, Verbalis JG, Clement S, et al. Hyponatremia in
rection of hyponatremia: a prospective magnetic resonance marathon runners due to inappropriate arginine vasopressin
imaging study. Ann Neurol. 1990;27(1): p. 61-66. (Prospective secretion. Am J Med. 2007;120(5):461. (Journal article)
study; 13 patients) 46. Anderson RJ, Chung HM, Kluge R, et al. Hyponatremia: a
26.* Sterns RH, Cappuccio JD, Silver SM, et al. Neurologic se- prospective analysis of its epidemiology and the pathogenet-
quelae after treatment of severe hyponatremia: a multicenter ic role of vasopressin. Ann Intern Med. 1985;102(2):164-168.
perspective. J Am Soc Nephrol. 1994;4(8):1522-1530. (Multi- (Prospective analysis)
center retrospective study; 64 patients) 47. Pokaharel M, Block CA. Dysnatremia in the ICU. Curr Opin
27.* Verbalis JG, Goldsmith SR, Greenberg A, et al. Hyponatremia Crit Care. 2011;17(6):581-593. (Review)
treatment guidelines 2007: expert panel recommendations. 48. Chua M, Hoyle GE, Soiza RL. Prognostic implications of
Am J Med. 2007;120(11)Suppl:S1-S21. (Practice guideline) hyponatremia in elderly hospitalized patients. Arch Gerontol
28.* Lien YH, Shapiro JI. Hyponatremia: clinical diagnosis and Geriatr. 2007;45(3):253-258.
management. Am J Med. 2007; 120(8):653-658. (Review)
29. Sterns RH, Hix JK, Silver S. Treatment of hyponatremia. Curr
Opin Nephrol Hypertens. 2010;19(5):493-498. (Review) CME Questions
30. Hew-Butler T, Almond C, Avus JC, et al. Consensus statement
of the 1st international Exercise-Associated Hyponatremia
Consensus Development Conference, Cape Town, South
Take This Test Online!
Africa 2005. Clin J Sport Med. 2005;15(4):208-213. (Review)
31. Bhaskar E, Kumar B, Ramalakshmi S. Evaluation of a proto- Current subscribers receive CME credit absolutely
col for hypertonic saline administration in acute euvolemic free by completing the following test. Monthly on
symptomatic hyponatremia: a prospective observational line testing is now available for current and archived
trial. Indian J Crit Care Med. 2010;14(4):170-174. (Prospective
observational cohort study; 58 patients)
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32. Ellison DH, Berl T. Clinical practice. The syndrome of inap- receive your free CME credits. Each issue includes
propriate antidiuresis. N Engl J Med. 2007;356(20):2064-2072. 4 AMA PRA Category 1 CreditsTM, 4 ACEP Category
(Journal article) 1 credits, 4 AAFP Prescribed credits, and 4 AOA
33. Gankam Kengne F, Soupart A, Pochet R, et al. Re-induction Category 2A or 2B credits.
of hyponatremia after rapid overcorrection of hyponatremia
reduces mortality in rats. Kidney Int. 2009;76(6): 614. (Journal
article)
34. Soupart A, Ngassa M, Decaux G. Therapeutic relowering of
the serum sodium in a patient after excessive correction of
hyponatremia. Clin Nephrol. 1999;51(6):383. (Case report)
35. Janicic N, Verbalis JG. Evaluation and management of hypo-
osmolality in hospitalized patients. Endocrinol Metab Clin
North Am. 2003;32(2):459-481. (Review)
36. Goldsmith SR. Current treatments and novel pharmacologic
treatments for hyponatremia in congestive heart failure. Am J
Cardiol. 2005;95(9) Suppl 1:14-23. (Journal article)
1. An 89-year-old male with a history of demen-
37. Caillaud E, Gates J. Iatrogenic causes of hyponatraemia.
Epilepsia. 2002;43:(suppl 8):150. (Journal article) tia presents to the ED with confusion and
38. Musch W, Decaux G. Treating the syndrome of inappropriate vomiting. On evaluation in the ED, his vital
ADH secretion with isotonic saline. QJM. 1998;91(11): 749- signs are stable, but he is lethargic and disori-
753. (Chart review; 17 patients) ented. Further history was unobtainable on
39. Schrier RW, Gross P, Gheorghiade M, et al for the SALT
arrival. Laboratory evaluation is remarkable
Investigators. Tolvaptan, a selective oral vasopressin
V2-receptor antagonist, for hyponatremia. N Engl J Med. for a sodium of 165 mEq/L, potassium of 4.6
2006;355:2099-2112. (Multicenter randomized double-blind mEq/L, chloride of 118 mEq/L, bicarbonate of
placebo-controlled trials; 448 patients) 28 mEq/L, BUN of 31 mg/dL, and creatinine of
40. Velez JC, Dopson SJ, Sanders DS, et al. Intravenous conivap- 1.1 mg/dL. Urine-specific gravity is 1.030. His
tan for the treatment of hyponatraemia caused by the syn-
hypernatremia is most likely due to:
drome of inappropriate secretion of antidiuretic hormone in
hospitalized patients: a single-centre experience. Nephrol Dial a. Lack of free water intake and secondary
Transplant. 2010;25:1524–1531. (Chart review; 18 patients) dehydration
41. Hew TD, Chorley JN, Cianca, JC, et al. The incidence, risk fac- b. Central diabetes insipidus
tors, and clinical manifestations of hyponatremia in marathon c. Diuretic medications
runners. Clin J Sport Med. 2003;13(1):41-47. (Journal article)
d. Nephrogenic diabetes insipidus
42. Noakes T, Sharwood K, Speedy D, et al. Three independent
biological mechanisms cause exercise-associated hypona-

2. Which class of diuretics is most likely to lead 7. A 73-year-old female presents to the ED with
to hyponatremia? diarrhea, vomiting, and fever for 2 days. Her
a. Carbonic anhydrase inhibitors vital signs in triage include a temperature
b. Potassium-sparing diuretics of 39.4°C, pulse of 117, and blood pressure
c. Loop diuretics of 100/51 mm Hg. She appears dehydrated
d. Thiazide diuretics with dry mucous membranes. Her abdominal
examination is remarkable for mild diffuse
3. Which of the following is the most likely to tenderness with no rebound or guarding. On
cause pseudohyponatremia? laboratory evaluation, she has a sodium of 156
a. Rhabdomyolysis mEq/L, potassium of 4.1 mEq/L, chloride of
b. Hepatic failure 118 mEq/L, bicarbonate of 19 mEq/L, BUN of
c. Renal failure 30 mg/dL, creatinine of 1.6 mg/dL, and glucose
d. Hyperlipidemia of 71. Urine osmolality is 800 mOsm/kg, and
serum osmolality is 330 mOsm/kg. Which of
4. How much would the emergency clinician the following statements is true?
expect a patient’s sodium to increase after re- a. This is most likely diabetes insipidus
ceiving 100 cc of 3% hypertonic saline intrave- b. Intravenous D5W should be the initial fluid
nously? of choice
a. 1.0 mEq/L c. Free water deficit is 1.7 L
b. 2.0 mEq/L d. Intravenous NS should be the initial fluid of
c. 3.5 mEq/L choice
d. 4.0 mEq/L
8. If a patient develops flaccid paralysis, dysar-
5. A 45-year-old female patient with history of thria, dysphagia, and hypotension during the
Conn disease presents with a sodium of 150 treatment of hyponatremia, what is the initial
mEq/L. She weighs 70 kg. What is her calcu- therapy of choice?
lated TBW deficit? a. D5W bolus
a. 2.3 L b. ½NS bolus
b. 2.5 L c. D5NS at 100 mL/hour
c. 2.8 L d. NS at 2x maintenance
d. 3.0 L
9. A 68-year-old woman with a history of small
6. A 50-year-old women with a history of type cell lung cancer is brought in for headache
2 diabetes, coronary artery disease, and end- and fatigue for the past 2 days. She is awake
stage renal disease presents to the ED with and alert, with normal vital signs, and has a
generalized weakness and decreased appetite. nonfocal neurologic examination with a serum
She was last dialyzed 6 days ago, and she also sodium of 127 mEq/L. What is the appropriate
ran out of her insulin 6 days ago. She is slight- management of her hyponatremia?
ly hypertensive, but otherwise her vitals are a. Free water restriction
stable and physical examination is unremark- b. Hypertonic saline bolus
able. Laboratory results reveal a serum sodium c. Intravenous furosemide
of 126 mEq/L, serum potassium of 5.3 mEq/L, d. NS bolus
serum chloride of 103 mEq/L, serum bicarbon-
ate of 18 mEq/L, and glucose of 750 mg/dL. 10. A runner is brought in after collapsing during
ECG and chest x-ray are unremarkable. Which a race. She has been careful to drink both water
of the following is the next best appropriate and sports electrolyte beverages at each mile
treatment? marker. She is confused and combative despite
a. Immediate hemodialysis 10 mg of diazepam. What is the most appropri-
b. Restrict free water to correct hyponatremia ate treatment after she suffers a tonic-clonic
c. Restart home subcutaneous insulin regimen seizure?
d. Initiate intravenous insulin therapy a. 5% dextrose solution
b. Fosphenytoin
c. Hypertonic saline
d. Lorazepam

Coming Soon In
Emergency Medicine Practice
Emergency Medicine Approach to An Evidence-Based Review Of
the Evaluation and Treatment of Transient Ischemic Attack
Pulmonary Embolism
AUTHORS:
AUTHORS: MATTHEW S. SIKET, MD, MS
Instructor, Department of Emergency Medicine,
AMY CHURCH, MD, FAAEM, FACEP Stroke Research Fellow (SPOTRIAS), Department of
Assistant Professor of Emergency Medicine Neurology, Massachusetts General Hospital And
and Residency Program Director, University of Harvard Medical School, Boston, MA
Medicine and Dentistry of New Jersey: Robert JONATHAN EDLOW, MD
Wood Johnson Medical School, New Brunswick, Professor of Medicine, Harvard Medical School; Vice
New Jersey Chair of Emergency Medicine, Beth Israel Deaconess
Medical Center, Boston, MA
MATTHEW TICHAUER, MD
Department of Emergency Medicine, University A transient ischemic attack (TIA) may seem
of Medicine and Dentistry of New Jersey: Robert underwhelming to patients and providers, but
Wood Johnson Medical School, New Brunswick, it should always be considered a true medical
New Jersey emergency. Caused by temporary focal central
nervous system hypoperfusion, a TIA is often a
In the United States, it is estimated that between
warning of an impending stroke. Patients presenting
600,000 and 900,000 individuals will suffer from
to the emergency department with a TIA are at the
acute pulmonary embolism each year, with an
highest risk of stroke within the next 48 hours, and it
estimated 200,000 to 300,000 hospital admissions,
is critically important for the emergency practitioner
many from the emergency department. Despite
to recognize this opportunity to initiate primary
decades of research on the topic, the diagnosis
stroke prevention strategies. Since the last issue of
remains elusive in many situations, and the fatality
Emergency Medicine Practice on TIA in 2008, there
rate remains high. This issue of Emergency Medicine
have been numerous studies focusing on improved
Practice will present a succinct review of the current
risk stratification and early management strategies in
evidence guiding the emergency medicine approach
TIA. This issue will serve as a practical, evidence-based,
to the diagnosis and treatment of pulmonary
up-to-date review of TIA for the emergency clinician.
embolism. Key to this approach is the idea of risk
stratification: using factors from the history and
physical examination as well as key diagnostic
results to guide both the work up and treatment
for the individual patient you are caring for. The
pathophysiology of disease, decision support tools
used both in the evaluation for pulmonary embolism
and in assessing the severity of disease, and current
treatment options will be discussed.

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October Sodium Disorders

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Sodium Disorders In The October 2012

Volume 14, Number 10

And Hypernatremia Professor and Chair, Department of Emergency Medicine, Vanderbilt

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• Urine osmolality > 600 • Urine osmolality 300-

• Insensible losses • Osmotic diuresis • Cushing syndrome

Hemodynamically stable? NO • Standard resuscitation

• IV fluids that are

Class Of Evidence Definitions

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High, due to: Normal, due to: Low (contracted)

Note: Treatments are listed in order from most recommended to consideration.

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Change in serum Na+ (mEq/L) = (infusate Na+

Table 6. Desmopressin Dosing LR 130 97

Abbreviations: D5W, 5% dextrose in water; LR, lactated Ringer; NS,

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1. Do not treat sodium abnormalities in a patient Summary

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