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Hyponatremia: When It Rains, It Pours!


Kim A. Noble, PhD, RN, CPAN
HYPONATREMIA is a common electrolyte abnormality,
with an estimated prevalence of 1528% of inpatients in
the acute care setting.1,2 Hyponatremia, or a serum sodium level of ,135 meq/L, is found in patients with a variety of clinical disorders, including cirrhosis, heart
failure, surgical irrigation or fluid administration, trauma,
and neuroendocrine disorders.2 It is also associated with
the syndrome of inappropriate antidiuretic hormone followed by the administration of selective serotonin reuptake inhibitors.3
Perianesthesia nurses care daily for hospitalized patients,
and a good understanding of the physiologic effects of
fluid and electrolyte abnormalities is imperative. Surgical
patients may be denied oral intake and arrive at the surgical suite after receiving intravenous fluid replacement as
their only intake. Numerous pre-existing medical disorders may also place a patient at risk for complications
that result from electrolyte abnormalities. Rapid assessment and treatment by the perianesthesia nurse may
reverse the neurologic sequela associated with hyponatremia, decline in serum sodium (Na1).
Sammy Sodium (S.S.) is a 72-year-old male who was admitted to the hospital with a four-day history of abdominal
pain, nausea, and vomiting. Sam reported frequently sipping water between bouts of nausea to moisten his
mouth. He has a surgical history of an abdominal aortic aneurism resection and three incisional hernia repairs in the
last 18 months, with the insertion of mesh for a recurrent
incisional hernia. S.S. has a past medical history of renal
insufficiency, poorly-controlled hypertension, and hyperlipidemia. His daily medications include losartan (Cozaar,
E.I. du Pont de Nemours and Company, Wilmington, DE),
simvastatin (Zocor, Merck & Co, Whitehouse Station,
NJ),4 and a diuretic. In the emergency department, orders
for Sam included allowing nothing per mouth to rule out
Kim A. Noble, PhD, RN, CPAN, is an Assistant Professor at Temple
University, Philadelphia, PA.
Address correspondence to Dr Kim A. Noble, Department of
Nursing, Temple University, 3307 N Broad St, Philadelphia, PA
19140; e-mail address: knoble@temple.edu.
2009 by American Society of PeriAnesthesia Nurses.
1089-9472/09/2402-0011$36.00/0
doi:10.1016/j.jopan.2009.01.009
124

a bowel obstruction. Admission electrolytes included:


Na1 141 mEq/L; Cl 98 mEq/L; K1 3.1 mEq/L. S.S.s medications were held because his blood pressure was 112/73
and vital signs were stable. He was ordered opioids as
needed for pain. Sam also was ordered to receive an intravenous solution (IV) of D512 NS with 20 mEq of potassium
chloride (KCl) at 125 mL per hour.
S.S. continued with abdominal distention, absent bowel
sounds, pain, and vomiting for 48 hours. He refused a nasogastric tube (NGT) insertion, reporting a very bad experience with that tube after his abdominal aortic
aneurism repair. Lab work was monitored, with the only
identified abnormalities of: Na1 of 128 mEq/L; K1 3.1
mEq/L. His IV solution was changed to 0.9% normal saline
solution. On day 3, he had improvement in his pain and
minimal bowel sounds were present. He was started on
clear liquids, consuming several liters of water in the first
hour to quench his thirst. Sam began reporting severe
abdominal pain, additional fluids were with withheld,
and he was sent to radiology for an abdominal ultrasound
to rule out a recurrent bowel obstruction. He received an
additional bolus of fluid to fill his bladder and complete
the ultrasonic testing.
S.S. presented to the surgical suite for resection of an incarcerated bowel. Anesthesia and surgery began as planned.
He was induced with 100% oxygen, midazolam 2 mg, fentanyl 2 mL, propofol 200 mg, and succinylcholine for
rapid-sequence induction. Anesthesia was maintained
with nitrous oxide, sevoflurane, vecuronium, and morphine sulfate 6 mg, given in divided doses during the final
hour of the procedure. His blood pressure was slightly labile during induction and he was treated with a fluid bolus.
S.S. had a small bowel resection for necrotic bowel with an
end-to-end anastomosis. He was reversed with pyridostigmine and glycopyrrolate and extubated without difficulty.
Sam received 3,200 mL of lactated Ringers solution for
a procedure that took approximately two hours. His blood
loss for the procedure was 350 mL and urine output via urinary catheter was 360 mL. A NGT was inserted under anesthesia and drained 200 mL of dark, bilious material
during the surgical procedure. S.S. was transported to
the Phase I Postanesthesia Care Unit (PACU) with 4 L of
oxygen via nasal cannula.
Journal of PeriAnesthesia Nursing, Vol 24, No 2 (April), 2009: pp 124-127

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Sam arrived in the Phase I PACU stuporous, confused, and


minimally compliant with direct commands. His speech
was slow and he was complaining of a headache and
blurred vision. Admission vital signs were: blood pressure
158/88; heart rate 92 beats per minute with frequent multifocal premature ventricular contractions and occasional
couplets noted; RR 28 and snoring; temperature 97.4 F,
oxygen saturation 93%. A head position change was
used and the snoring resolved and bilateral clear breath
sounds were auscultated. Sam was noncompliant with repeated commands to take a deep breath, but his oxygen
saturation was adequate. His midline abdominal dressing
was dry and intact. His NGT was connected to low continuous wall suction and was draining minimal amounts of
dark green fluid. There were no audible bowel sounds.
S.S.s urinary catheter was intact and draining sufficient
amounts of clear drainage. Compression boots and peripheral pulses were bilaterally intact.
Anesthesia was consulted and present condition
reported. During the anesthesia evaluation, S.S. was unresponsive to loud verbal and light tactile stimuli and then
began having tonic-clonic movements. His airway was
supported, his oxygen was increased to 6 L/min via the
nasal cannula, and safety measures were instituted. His
seizure lasted approximately three minutes and then he
was again unresponsive. Orders were received for diazepam 2.55 mg as needed to control seizure activity and
stat electrolyte analysis. S.S.s Na1 was 112 mEq/L, Cl
81 mEq/L, and K1 2.9 mEq/L. S.S. was treated with a hypertonic saline (3%) and intermittent piggyback doses
of KCl replacement as needed and, once cleared by anesthesia, S.S. was transported to intensive care. In 48 hours,
S.S.s Na1 was 137 mEq/L, Cl 102 mEq/L, and K1 4.3
mEq/L. Sam made a full recovery and was discharged after
a 10-day hospital stay.

The Physiologic Consequences of


Hyponatremia
Abnormalities in electrolytes may negatively impact the
function of many systems; however, neurologic symptoms are frequently the first to be encountered and
directly correlated to the degree of neuronal damage.
This disorder was originally believed to affect all individuals equally, but research has demonstrated a 25-fold
increase in the risk of permanent neurologic injury after
hyponatremia in women between menarche and menopause. Children have also been found to be at increased
risk, and for all affected individuals, rapid diagnosis and
treatment are key for the prevention of permanent neurologic injury.5
Hyponatremia and dilution of serum osmolarity depress
the function of the central nervous system and can lead
to irritability. The central nervous system depression,
termed encephalopathy, is because of the movement of

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water from the interstitial space into the neuronal cells.


This cerebral edema occurs because the increased intake
of water dilutes the extracellular fluid. The neuronal cells
have a higher osmolarity than the dilute interstitium and
water is passively pulled into the cells toward the
higher solute concentration.6 As the cells swell, their ability to rapidly process and transmit impulses decreases.
The symptoms of hyponatremia are first manifested as
confusion and a slight decrease in cognition. As the disorder progresses, the patient may report headache, weakness, and tremors. The increase in cellular irritability
also predisposes the patient with a decreased serum
Na1 to generalized tonic-clonic seizure activity. The risk
of seizures is an ominous sign and is associated with
serum sodium levels below 115 mEq/L or when the hyponatremia has a rapid onset.5 If the cerebral edema has
a rapid onset and progression, the patient is also at risk
for increased intracranial pressure and herniation.
If the development of hyponatremia is gradual, the brain
has the time required to compensate or adapt, termed
regulatory volume decrease.5 There are two mechanisms used by the intracranial cells to adapt to a diluted
extracellular environment. The early compensatory
mechanism for cellular edema is caused by the increase
in pressure associated with fluid entry. As the intracellular
hydrostatic pressure increases, the fluid moves out of the
cells and into the cerebrospinal fluid and is then returned
to the venous circulation. The cells also attempt to
decrease the osmotic gradient, or the difference in the
concentration of solutes between the intracellular and extracellular fluids, by the movement of ions Na1, K1, and
Cl, out of the cells. This adaptive process takes approximately three hours for equilibration.5 The second form of
intracranial cell adaptation to a dilute extracellular environment is the outward movement of osmotically active
particles such as amino acids. Again, this compensation
is time dependent and cerebral edema, which occurs
over less than 48 hours, can overwhelm this compensatory mechanism, rendering it ineffective.5 The intracranial cellular compensation has been correlated with
a decrease in the insulating myelin coating of the axons
of neurons. As the osmotically active ions and amino
acid are displaced from the cells, they impact the support
cells surrounding the neurons, called glia, causing a degeneration of the myelin coating formed by glial cells.
This loss of myelin, termed central pontine myelinolysis,7 is also associated with alcoholism, severe liver disease, and brain injury.5

Treatment for Hyponatremia


Rapid diagnosis of hyponatremia may be made with
serum electrolyte and osmolarity measurements. For
persons with severe hyponatremia, serum Na1 levels
,115 mEq/L, the administration of a hypertonic solution

KIM A. NOBLE

126

of 3% normal saline with close monitoring of urine output


and serum electrolytes is recommended.7 It is recommended that serum Na1 levels are not increased more than
812 mEq/L in the first 24 hours. Loop diuretics can
also be used to assist with the excretion of excess water.3

Implications for the PACU Patient


Perianesthesia nursing can be very challenging because
assessment is conducted rapidly as the patient is admitted
and report is received from the anesthesia care provider.
The assessment is conducted in an ongoing fashion
throughout the patients stay in the Phase I and Phase II
PACU, and any detected abnormalities are reported to
the anesthesia care provider and treatment orders are
received. A thorough understanding of the physiologic
implications of electrolyte abnormalities allows the perianesthesia nurse to anticipate, assess, and assist in the
rapid treatment of the highly time-dependent disorder
of hyponatremia.
Alteration in Neurologic Function
A rapid neurologic screen is completed concurrently with
the admission procedure into the Phase I PACU. Confusion may accompany the patient emerging from general
anesthesia but should clear rapidly with reorientation
from the nurse.8 A complaint of a headache is also a relatively common finding but should be explored further. If
confusion is persistent despite redirection, there is need
for a more comprehensive neurologic examination and
immediate reassessment to screen for other possible
causes. Confusion is a vague symptom and there are
many factors that may contribute to its development. Topping the list of possible causes of confusion is hypoxemia,
which necessitates a detailed airway and respiratory reassessment. Other possible causes of confusion include
hypotension with decreased cerebral perfusion, hypoglycemia, and possible medication reaction, either from anesthetics given during the surgical procedure or
withdrawal such as from alcohol or benzodiazepines.8
Sams seizure activity placed heightened importance on
his confusion and headache. The immediate priority of
a patient exhibiting seizure activity is maintenance of an
open airway and ventilatory support as indicated. Of secondary importance is patient safety for the protection of
head or body movements in a confined area. Seizure activity usually is of short duration and the anesthesia care provider is notified immediately. Benzodiazepines are the
drug of choice for the treatment of seizure activity4 and
should be available for immediate administration. The
determination of the cause of the seizure activity is also
imperative and necessitates additional patient assessment
and immediate blood sugar and laboratory analysis as indicated. Finally, the anticipation and prevention of future

seizures would also be a priority for S.S.s Phase I PACU


care.
Alteration in Respiratory Function
A rapid respiratory assessment is completed upon admission to the Phase I PACU, including rate and expansion of
ventilation, auscultation of breath sounds, and measurement of oxygen saturation. Another high priority is the
maintenance of a patients airway during the seizure. Seizures rapidly deplete intracranial resource, increasing the
use of adenosine triphosphate by 250% and oxygen consumption by 60%.6 Seizures also lead to increased blood
flow to the brain by 250%6 and can lead to devastating
consequences for patients with increased intracranial
pressure. The provision of high-flow oxygen to the
patient with a seizure is important, but the use of
a mask is discouraged because of the risk of vomiting
and aspiration. Airway support and suction should be provided as indicated.
Alteration in Fluid and Electrolyte Balance
The availability of venous access is required for the rapid
administration of needed medications. Once S.S.s lab
work is available, the IV will be used for the administration of hypertonic saline, diuretics, and KCl as ordered
and indicated. Careful monitoring of fluid intake and
urinary output is indicated. Communication of current
status to the anesthesia care provider is always important, as is the receipt and delivery of physician orders.
Alteration in Cardiovascular Function
Continuous cardiac monitoring is used for any patient recovering from general anesthesia. S.S.s ventricular ectopy
is of concern and can be due to hypoxemia or decreased
serum potassium levels. Both possible causes should be
explored, and when the low serum K1 result is reported
by the laboratory, correction with KCl supplementation is
indicated. Potassium chloride replacement requires the
use of an infusion pump to prevent rapid replacement,
which can lead to agonal cardiac rhythms. Maintenance
of blood pressure that is within 1020% of the admission
reading that was obtained preoperatively is important to
maintain cerebral perfusion.
Alteration in Gastrointestinal Function
As with any patient undergoing abdominal surgery, S.S.s
Phase I PACU care needs to incorporate a rapid assessment of abdominal dressing and NGT placement and
drainage. Any identified abnormalities should be rapidly
reported to the anesthesia care provider and the surgical
team. The potential for abdominal pain should be anticipated as S.S. recovers from his seizure. During the postictal state, Sam may not be able to communicate effectively
and his behavior, such as restlessness, facial grimacing,
and increased blood pressure or heart rate, may be used

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as indices of surgical pain to guide the need for and administration of analgesics.
In conclusion, hyponatremia in hospitalized patients
may be encountered by perianesthesia nurses. Rapid anticipation and assessment of fluid and electrolyte abnormalities and their physiologic impact is an important

focus for the perianesthesia nurse receiving patients


from the operating room. Rapid intervention is required
for the perianesthesia patient having seizures to prevent
injury and pulmonary complications, as well as for the
provision for additional oxygen to support patient metabolic requirements.

References
1. Gill G, Huda B, Boyd A, et al. Characteristics and mortality of severe
hyponatremiaHospital-based study. Clin Endocrinol. 2006;65:246-249.
2. Munger M. New agents for managing hyponatremia in hospitalized
patients. Am J Health Sys Pharm. 2007;64:253-265.
3. Rottmann C. SSRIs and the syndrome of inappropriate antidiuretic
secretion: Close monitoring of serum sodium levels in high-risk patients
taking SSRIs can prevent this condition and the resulting hyponatremia,
which can be fatal. Am J Nurs. 2007;107:51-58.
4. Aschenbrenner DS, Venable SJ. Drug Therapy in Nursing, 3rd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2009.

5. Castilla-Guerra L, Fernandez-Moreno MC, Lopez-Chozas JM,


et al. Electrolytes disturbances and seizures. Epilepsia. 2006;47:
1990-1998.
6. Porth CM. Essentials of Pathophysiology: Concepts of Altered
Health States, 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2007.
7. Reynolds RM, Seckl JR. Hyponatremia for the clinical endocrinologist. Clin Endocrinol. 2005;63:366-374.
8. Drain CB, Odom-Forren J. PeriAnesthesia Nursing: A Critical Care
Approach, 5th ed. St. Louis, MO: Saunders; 2009:573.

Calendar of Events
May 16, 2009. OPANA celebrates the 30th anniversary at a Spring Seminar: Pearls of
Wisdom, at Ross Heart Hospital at the Ohio State University Medical Center,
Columbus, OH. Contact Alabelle Zghoul, 4808 Bourke Road, Columbus, OH 43229,
(614) 846-9537, alabelle.zghoul@osumc.edu,or Nancy McGushin, 1789 Nelson Road,
Lancaster, OH 43130, (740) 653-1334, gushin@sbcglobal.net for further information.