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ONLINE EXCLUSIVE · CONTINUING EDUCATION
Syndrome of Inappropriate Antidiuretic Hormone
Jo Ann Flounders, MSN, CRNP, OCN®, CHPN
yndrome of inappropriate antidiuretic hormone (SIADH)
therapeutic agents that cause SIADH and impaired excretion
is a disorder of water intoxication (Haapoja, 1997; Moses
of water are cyclophosphamide, ifosfamide, vincristine, vin-
& Scheinman, 1991). SIADH describes the inappropri-
blastine, cisplatin, and melphalan (Flombaum, 2000; Keenan,
ate production and secretion of antidiuretic hormone (ADH),
1999; Schafer, 1997). Administration of high-dose cyclophos-
also known as arginine vasopressin, that causes increased wa-
phamide may be especially problematic in patients at risk for
ter reabsorption in the renal tubules and leads to increased water
SIADH because aggressive hydration is used to prevent hem-
retention and dilutional hyponatremia (Finley, 1998; Keenan,
orrhagic cystitis, creating the potential for water retention and
severe hyponatremia (Bunn & Ridgway, 1993; Flombaum;
Haapoja, 1997). Combination chemotherapy often includes
cisplatin administration, which usually is administered with
large volumes of fluids to prevent nephrotoxicity. If hypotonic
SIADH can occur as a result of an endocrine paraneoplastic
fluids (e.g., 0.45% normal saline) are used, hyponatremia and
syndrome, which implies that the syndrome is caused indi-
water retention may occur (Flombaum; Ritch, 1988). In addi-
rectly by a malignancy and not the direct result of invasion
tion, chemotherapy-induced nausea can stimulate the release
and damage by malignant cells (Haapoja, 1997; Keenan,
of ADH (Haapoja). However, use of effective antiemetics has
1999). An endocrine paraneoplastic syndrome occurs when a
decreased the incidence of nausea as a cause of SIADH
tumor secretes excessive amounts of hormones that interfere
with normal homeostasis. Although normal hormone produc-
Pharmacologic interventions used to treat patients with can-
tion occurs in response to a stimulus to maintain homeostasis,
cer may contribute to the development of SIADH. Analgesics,
ectopic production of hormones by tumors is not normal and
such as opioids, in addition to antidepressants, such as tricyclics
does not occur to maintain homeostasis. Tumor cells are able
and selective serotonin reuptake inhibitors, have been known to
to produce many hormones and hormone-releasing factors,
cause increased ADH production (Frizzell, 2000; Keenan,
causing different paraneoplastic syndromes that affect body
1999). In addition to stimulating abnormal production of ADH,
systems (Haapoja). The paraneoplastic syndrome of SIADH
is caused by two mechanisms: the production of ADH by
malignant tumor cells or the inappropriate production and
Goal for CE Enrollees:
release of ADH from the posterior pituitary gland (Finley,
1998; Haapoja; Keenan). Both mechanisms cause inappropri-
To further enhance nurses' knowledge about syndrome of
ate and excessive secretion of ADH, which causes disruption
inappropriate antidiuretic hormone (SIADH).
of fluid balance (Bunn & Ridgway, 1993; Ezzone, 1999;
Objectives for CE Enrollees:
The most common etiology of SIADH is malignancy, al-
On completion of this CE, the participant will be able to
though many other nonmalignant causes exist (Jones, 1999).
1. Describe the etiology of SIADH.
The most frequent malignant cause of SIADH is small cell
2. Discuss the clinical manifestations and medical manage-
lung cancer (Flombaum, 2000; Keenan, 1999; List et al.,
ment of patients with SIADH.
1986). Other malignant etiologic causes of SIADH include
3. Discuss the nursing implications in the care of patients
non-small cell lung cancer; head and neck, prostate, pancre-
atic, breast, ovarian, duodenal, and esophageal cancers; lym-
phoma and leukemia; and thymoma, neuroblastoma, and car-
cinoid tumors (Finley, 1998; Frizzell, 2000; Keenan; Schafer,
1997; Smeltzer & Bare, 1996). SIADH also may be caused by
Jo Ann Flounders, MSN, CRNP, OCN®, CHPN, is a nurse practi-
central nervous system metastases, such as meningeal carci-
tioner at Consultants in Medical Oncology and Hematology in
nomatosis (Haapoja, 1997).
Drexel Hill, PA.
Treatment of a malignancy with cytotoxic chemotherapy
can cause SIADH. The most commonly implicated chemo-
Digital Object Identifier: 10.1188/03.ONF.E63-E70
FLOUNDERS VOL 30, NO 3, 2003
is identical (Martini). Osmotic pressure is a force that influ-
medications may potentiate the effects of ADH on the renal
ences the exchange of fluids and electrolytes between the
tubules. Nonsteroidal anti-inflammatory drugs, thiazide diuret-
compartments at the capillary level. Osmotic pressure acts as
ics, barbiturates, and anesthetic agents can increase the effects
an inward pulling force that moves solutes and water into the
of ADH on the renal tubules (Dietz & Flaherty, 1993; Frizzell;
capillaries (Mulvey & Bullock).
Jones, 1999; Rohaly-Davis & Johnston, 1996).
Several basic concepts about regulation of fluids and elec-
Many nonmalignant causes of SIADH exist. Injury to the
trolytes are important. The mechanisms that monitor and ad-
cells of the central nervous system as a result of infection,
just the composition and volume of body fluids to maintain
brain abscess, brain herniation, hemorrhage, or head trauma
homeostasis respond to changes in extracellular fluid, not in-
may result in increased ADH production. Pulmonary disor-
tracellular fluid. Because intracellular fluid is located in tril-
ders, such as infection caused by virus, bacteria, or fungus,
lions of isolated cells separated by cell membranes, a change
also can stimulate ectopic production of ADH. Other pulmo-
in one cell in the body will not directly affect other cells. In
nary complications that can produce and release ADH are
contrast, a change in extracellular fluid will occur throughout
pneumonia, tuberculosis, and lung abscess (Dietz & Flaherty,
the extracellular compartment and affect all the cells in the
1993; Ezzone, 1999; Frizzell, 2000; Keenan, 1999; Schafer,
body. Therefore, the concentration of extracellular fluid is the
1997). Patients with malignant disease commonly experience
stimulus that triggers fluid movement (Martini, 1998).
pain and stress, which also can increase ADH production.
Another important concept pertaining to fluid and electro-
Cigarette smoking can contribute to the development of
lyte regulation is that water must move across cell membranes
SIADH because nicotine can induce ADH production (Dietz
in response to osmotic gradients, or changes in concentration
& Flaherty; Haapoja, 1997; Poe & Taylor, 1989).
between compartments, and not by active transport by cells
(Martini, 1998). These concentration gradients are determined
by the concentration of ions, such as sodium, the main regu-
lator of osmotic pressure (Mulvey & Bullock, 2000). Just as
To understand the pathophysiology of SIADH, understand-
water flows from an area with lesser solute concentration to
ing the normal physiology of fluid and electrolyte balance in
an area of greater solute concentration, water also follows
body compartments is necessary. Body fluids, which contain
sodium (Martini). Therefore, when extracellular fluid has a
electrolytes, proteins, and water, are separated into intracellu-
high concentration (i.e., high osmolality) of sodium ions, or
lar and extracellular compartments by cell membranes and
hypernatremia, water moves into the blood vessels and out of
capillaries (Mulvey & Bullock, 2000). Intracellular fluid is lo-
the cells. When extracellular fluid has a low concentration
cated in trillions of cells that are separated from one another
(i.e., low osmolality) of sodium ions, or hyponatremia, water
by cell membranes (Martini, 1998). Extracellular fluid con-
moves out of the blood vessels and into cells where the con-
sists of interstitial fluid, or fluid between the cells, and intra-
centration is higher (Martini; Mulvey & Bullock).
vascular fluid, which is fluid or plasma circulating in the
Another concept that is helpful to understand is tonicity,
blood vessels (Mulvey & Bullock). Total body water is esti-
which is used to describe osmolality (Martini, 1998). An iso-
mated to be two-thirds intracellular fluid and one-third extra-
tonic fluid (e.g., normal saline) with the same concentration
cellular fluid (Keenan, 1999; Martini).
as plasma does not cause movement of water into or out of
Intracellular and extracellular fluids exist as solutions, and
cells (Martini). Hypertonic fluids have a higher solute concen-
the electrolyte composition of each compartment is different.
tration than plasma, and hypotonic fluids have a lower solute
The main ions in intracellular fluid are potassium, magne-
concentration than plasma (Stripp, 2000). Therefore, infusion
sium, and phosphate, and the main ions in extracellular fluid
of a hypertonic solution into the blood vessels of extracellu-
are sodium, chloride, and bicarbonate (Martini, 1998). The
lar fluid causes movement of water from cells into blood ves-
substances that are dissolved in the solution of intracellular
sels. Infusion of a hypotonic fluid into the blood vessels of
and extracellular fluid are called solutes. The total concentra-
extracellular fluid causes movement of fluid from blood into
tion of solutes in the solution is defined as osmolality, which
cells (Martini). Figure 1 displays the effect of osmosis across
is stated as the number of milliosmols per liter (mOsm/l) or
a cell membrane.
milliosmols per kilogram (mOsm/kg) (Keenan, 1999).
The volume of total body water is regulated by thirst, hor-
Homeostasis demands that a balance exist in the fluid and
mone secretion, and renal activity. In response to decreased
electrolyte composition of the intracellular and extracellular
volume of fluid and increased plasma concentration (i.e., os-
compartments. Movement of solutes and water across cell
molality), the hypothalamus activates nervous pathways that
membranes maintains equilibrium between intracellular and
cause thirst. In addition, decreased plasma volume causes
extracellular fluid. The semipermeable cell membranes only
decreased renal perfusion, which activates the renin-angio-
allow selective ions to cross the membrane to enter or exit
tensin-aldosterone system and stimulates the hypothalamus to
cells, but the movement of water is not restricted (Martini,
release substances that cause thirst (Mulvey & Bullock, 2000).
1998). Water moves freely across the membranes toward the
This mechanism also causes release of ADH from the poste-
solution that contains the higher solute concentration in an
rior pituitary (Tesh, 2000). Therefore, in normal homeostasis,
effort to equalize the concentration in both compartments
ADH is produced by the hypothalamus and released into the
(Mulvey & Bullock, 2000). The process that allows free
blood by the posterior pituitary in response to increased plasma
movement of water across a membrane in response to a dif-
concentration (i.e., increased osmolality) or decreased plasma
ference in concentration is called osmosis (Martini). Osmosis
volume (Dietz & Flaherty, 1993; Finley, 1998). The physi-
maintains homeostasis by eliminating the differences in con-
ologic action of ADH is to induce an antidiuretic effect on the
centration of extracellular and intracellular fluids almost im-
kidneys so that water is retained (Jones, 1999). Therefore, re-
mediately. Therefore, despite the different chemical compo-
nal regulation of fluid balance occurs through reabsorption and
sition of each compartment, the osmolality, or concentration,
ONF VOL 30, NO 3, 2003
Cell in hypotonic solution
Cell in isotonic solution
Cell in hypertonic solution
Cell swells; water moves into cell.
Cell shrinks; water moves out of cell.
Normal cell: No movement of water.
Figure 1. Effect of Osmosis Across a Cell Membrane
excretion of water by the renal tubules (Keenan, 1999; Mul-
acute neurologic symptoms usually occur (Flombaum; Kee-
vey & Bullock). In normal homeostasis, a negative feedback
nan, 1999). Symptoms usually are life threatening and severe
mechanism exists so that increased plasma volume and nor-
when serum sodium is decreased to less than 105 mEq/l. Non-
mal or decreased osmolality can inhibit ADH and allow excre-
specific symptoms may occur when the serum sodium level is
tion of water (Jones). However, SIADH causes failure of the
115120 mEq/l. In contrast, if SIADH has a slow, more
normal mechanisms of homeostasis.
chronic onset, patients may be asymptomatic (Flombaum).
Most patients are asymptomatic and do not develop the severe
neurologic signs and symptoms associated with extreme hy-
ponatremia (Haapoja, 1997; Keenan).
SIADH of malignancy is the inappropriate, uncontrolled se-
Despite the water intoxication of SIADH, signs and symp-
cretion of ADH, which causes increased water reabsorption
toms of fluid overload usually do not appear with SIADH.
by the renal tubules that leads to decreased excretion of wa-
Therefore, peripheral edema, ascites, and heart failure usually
ter (Jones, 1999). The volume of total body water increases
are not noted because only a portion of excess water is re-
and is distributed into the extracellular and intracellular fluid.
tained in the intravascular or interstitial fluid and most is dis-
The concentration of sodium in the extracellular fluid then is
tributed to the cells (Flombaum, 2000; Haapoja, 1997; Jones,
low, as a result of dilution, which causes hypoosmolality.
1999; Keenan, 1999). According to the principles that regu-
However, because only a portion of the total body water is
late fluid shifts between extracellular and intracellular fluids,
distributed into the extracellular fluid, most of the water dif-
hypotonic fluid in blood vessels shifts into cells to equalize the
fuses into the intracellular fluid. Therefore, SIADH does not
concentration between extracellular and intracellular fluids.
cause signs and symptoms of increased volume of fluid be-
Consequently, the cells of the brain swell. Because the inflex-
cause the fluid is in the cells and not the blood or interstitial
ible skull confines brain cells, this cerebral edema causes in-
fluid (Bunn & Ridgway, 1993; Flombaum, 2000; Keenan,
creased intracranial pressure and decreased cerebral blood
1999). In addition, the concentration of urine is increased
flow, leading to neurologic dysfunction (Bunn & Ridgway,
because the kidneys secrete sodium and cannot secrete dilute
1993; Flombaum; Keenan). Therefore, symptoms of hy-
urine (Jones). The SIADH mechanism that causes thirst
ponatremia primarily are related to neurologic dysfunction
causes patients to continue to drink inappropriately despite the
fact that in normal homeostasis, thirst is inhibited when hy-
ponatremia is evident (Keenan). In summary, SIADH is
Table 1. Effects of SIADH
caused by ADH secretion by tumor cells or inappropriately by
the posterior pituitary and results in water intoxication, hy-
ponatremia, and hypoosmolality (Dietz & Flaherty, 1993;
Increased water reabsorption by the
Decreased serum osmolality, hy-
Keenan). Table 1 displays the effects of SIADH.
Identification of Patients at Risk
Decreased excretion of water by the
Increased urine osmolality
Increased total body water in intracel-
Decreased serum osmolality
The risk of SIADH for patients with cancer corresponds to
lular fluid and extracellular fluid
the etiologic factors that cause SIADH. Figure 2 summarizes
patients at risk for development of SIADH.
Decreased sodium concentration in the
plasma because of dilution by excess
Symptoms of SIADH in patients with cancer are influenced
Increased concentration of urine
Increased urine osmolality
by the rate of onset and the severity of hyponatremia (Flom-
Increased secretion of sodium by the
Increased urinary sodium
baum, 2000). If SIADH has a rapid (i.e., within 1 to 3 days)
onset, or if the serum sodium level is less than 110 mEq/l,
FLOUNDERS VOL 30, NO 3, 2003
volume depletion or fluid overload. Restriction of water is the
Patients with malignant neoplasms such as
main treatment (Flombaum). Therefore, although a routine
· Small cell lung cancer (most common)
blood chemistry evaluation may reveal hyponatremia in asymp-
· Non-small cell lung cancer, head and neck, prostate, pancreatic, duodenal,
tomatic patients, the presence of hyponatremia alone is not suf-
esophageal, lymphoma, leukemia, breast, ovary, thymoma, neuroblastoma,
ficient to diagnose SIADH. Multiple diagnostic laboratory tests
and carcinoid tumors (less common)
must be completed and evaluated in addition to physical exami-
Patients receiving cytotoxic chemotherapy including
· Cyclophosphamide, vincristine, vinblastine, cisplatin, and melphalan
Patients who experience chemotherapy-induced nausea
Laboratory studies that are diagnostic of SIADH include se-
rum sodium, plasma osmolality, urine sodium, and urine osmo-
Patients receiving pharmacologic intervention including
· Analgesics, such as opioids
lality. The normal range for serum sodium is 135147 mEq/l.
However, SIADH cannot be diagnosed on the basis of hy-
· Antidepressants, such as tricyclics and selective serotonin reuptake inhibi-
ponatremia alone because other disorders can cause hyponatre-
mia. Confirming a hypoosmolar state (i.e., water excess) by
· Non-steroidal anti-inflammatory drugs, thiazide diuretics, barbiturates, and
testing osmolality is critical. Serum osmolality usually is de-
creased with SIADH, whereas urine osmolality usually is in-
Patients with nonmalignant causes such as
creased. Electrolytes, blood urea nitrogen, creatinine, albumin,
· Central nervous system disorders: infections, brain abscesses, brain her-
and uric acid also should be evaluated because these values
niation, hemorrhage, and head trauma
usually decrease with SIADH as a result of dilution (Finley,
· Pulmonary disorders: infection caused by virus, bacteria, or fungus; pneu-
1998; Haapoja, 1997; Jones, 1999; Keenan, 1999; Smeltzer &
monia; tuberculosis; and lung abscess
Bare, 1996). Other studies to rule out cardiac, hepatic, adrenal,
· Pain, stress, and nicotine
renal, and thyroid causes of hyponatremia should be completed
(Haapoja). Serum vasopressin levels usually are not ordered
Figure 2. Patients at Risk for Development of SIADH
because vasopressin may be elevated in most patients with hy-
Note. Based on information from Dietz & Flaherty, 1993; Ezzone, 1999; Finley,
ponatremia; therefore, elevation is not specific to SIADH
1998; Frizzell, 2000; Haapoja, 1997; Keenan, 1999; Schafer, 1997.
Table 2. Symptoms and Signs of SIADH
secondary to water intoxication that leads to swelling of brain
cells (Flombaum). Table 2 contains a summary of signs and
symptoms of SIADH.
Altered mental status
After consideration of risk factors and review of symptoms
indicative of SIADH, attention to history is critical because
Focal neurologic signs
other conditions can cause hyponatremia without the associated
water excess of SIADH (Flombaum, 2000; Haapoja, 1997).
Conditions to be considered in the differential diagnosis include
dehydration, fluid retention, cardiac disease, hepatic dysfunc-
tion, adrenal insufficiency, renal disorders, and thyroid disease
(Keenan, 1999). Review of current medications is necessary to
Usually normal blood pres-
determine if SIADH may be medication induced.
Usually normal pulse
Evaluating patients for signs and symptoms of dehydration
Normal skin turgor
or fluid overload as potential causes of hyponatremia is critical.
If dehydration or fluid overload is causing hyponatremia,
SIADH can be excluded as a diagnosis. Hypovolemia and hy-
Moist mucous membranes
pervolemia may cause decreased sodium concentration. How-
ever, the clinical manifestations and physiologic mechanisms of
hypervolemia, hypovolemia, and SIADH are different. Accu-
rate diagnosis is critical because treatment will vary greatly
(Bunn & Ridgway, 1993; Flombaum, 2000; Keenan, 1999).
For example, patients with decreased volume caused by dehy-
O l i g u r i a (< 400 cc/24
dration will manifest symptoms of orthostatic hypotension,
poor skin turgor, dry mucous membranes, and tachycardia. The
appropriate treatment is rehydration. Patients with increased
volume caused by fluid overload will manifest symptoms of
edema, increased jugular distention, and changes in breath
sounds (i.e., rales). The treatment is restriction of sodium and
water. Although both of these clinical conditions can cause hy-
Note. Based on information from DeMichele & Glick, 2001; Dietz & Flaherty,
ponatremia, they require different treatment to correct the hy-
1993; Ezzone, 1999; Finley, 1998; Haapoja, 1997; Keenan, 1999; Schafer,
ponatremia. In comparison, SIADH usually does not cause
ONF VOL 30, NO 3, 2003
(Haapoja; Keenan). A chest x-ray may be ordered to determine
Table 3. Laboratory Values in SIADH
the presence of pulmonary disease. A computed tomography
Critical Value Diagnostic of SIADHa
scan of the head can help determine the presence of cerebral
edema, brain tumor, or brain herniation (Ezzone, 1999). Table
< 130 mEq/L
3 summarizes the critical laboratory values diagnostic of
< 280 mOsm/kg
> 500 mOsm/kg
> 20 mEq/L
Medical management of SIADH must be directed at treating
In the absence of diuretic therapy
the underlying pathology (Finley, 1998). SIADH usually re-
Note. Based on information from Dietz & Flaherty, 1993; Ezzone, 1999; Finley,
solves when the etiologic factors that are stimulating inappro-
1998; Haapoja, 1997; Keenan, 1999; Schafer, 1997.
priate ADH secretion are eliminated (DeMichele & Glick,
2001). Treatment of malignant neoplasms with antineoplastic
ing physical assessment to detect early signs of neurologic
chemotherapy causes regression of chemosensitive tumors and
complications caused by hyponatremia. This especially is
usually results in resolution of SIADH (Keenan, 1999). If
important when assessing the volume status of patients,
SIADH is caused by metastasis to the brain, corticosteroids and
which is critical for diagnosing SIADH. Nurses should as-
radiation therapy may be effective treatment (DeMichele &
sess for signs and symptoms of hypovolemia or hyperv-
Glick). Treatment of nonmalignant causes of SIADH, includ-
olemia and understand that the occurrence of these clinical
ing discontinuation of offending medications, is necessary.
manifestations excludes the diagnosis of SIADH. Nurses
Treatment of hyponatremia is related to the severity of
should review medications to reveal possible causative
symptoms and the rapidity of onset (Bunn & Ridgway, 1993;
agents of SIADH and provide patients and caregivers with
Flombaum, 2000; Keenan, 1999). Treatment for mild hy-
necessary instructions regarding fluid restriction. IV hydra-
ponatremia in SIADH (i.e., a sodium level greater than 125
tion, chemotherapy, medications, and electrolytes may be
mEq/l) includes fluid restriction of 8001000 ml/day (Finley,
ordered and must be monitored carefully. Assessment of
1998). Fluid restriction usually allows the sodium level to cor-
patients for side effects of treatment of SIADH should be
rect over 310 days. If fluid restriction is not effective, de-
ongoing. Attention to the timeliness of completion of labo-
meclocycline can be administered. Demeclocycline allows ex-
ratory tests will ensure that electrolyte status is evaluated
cretion of water because it inhibits the effect of ADH on the
promptly. In addition, nurses should monitor blood and
renal tubules. Side effects of this drug include nausea, photo-
urine chemistry levels and ensure that measures to correct
sensitivity, and azotemia. Treatment with demeclocycline
abnormal values are instituted in a timely manner. Nurses
usually increases the sodium level within three to four days,
should assess the coping abilities of critically ill patients and
and fluid restriction is not necessary (DeMichele & Glick,
caregivers; assess for pain, anxiety, and depression; and pro-
2001; Finley; Keenan). Aggressive treatment may be indi-
vide interventions to improve pain management and coping
cated if severe neurologic symptoms, such as coma or sei-
ability. However, management of pain and depression may
zures, occur with severe hyponatremia (Keenan). Administra-
be challenging, because some analgesics and antidepressants
tion of hypertonic 3% saline infusion over two to three hours
that cause SIADH may need to be withdrawn and substitu-
is indicated to correct life-threatening hyponatremia. Furo-
tions made. The choice of medications must involve consid-
semide also is given to increase urinary water excretion
eration of causative agents of SIADH. Nurses should pro-
vide patients and caregivers with instructions on signs and
symptoms of complications that should be reported to a phy-
sician. Discharge planning should include consideration of
referral for home care or hospice services.
Recognition of early clinical manifestations of SIADH al-
lows early treatment to prevent life-threatening complica-
The author would like to thank John Sprandio, MD, of Consultants in Medi-
tions. Nurses frequently are able to perceive subtle changes
cal Oncology and Hematology, Drexel Hill, PA, for reviewing this manuscript.
in patient status and should complete accurate and thorough
ongoing assessment to identify early abnormal changes.
Continued assessment of neuromuscular, cardiac, gas-
Author Contact: Jo Ann Flounders, MSN, CRNP, OCN®, CHPN,
trointestinal, and renal systems is warranted. Constant evalu-
can be reached at firstname.lastname@example.org, with copy to editor at
ation of fluid and electrolyte status is necessary with ongo-
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ONF VOL 30, NO 3, 2003
ONF Continuing Education Examination
Syndrome of Inappropriate Antidiuretic Hormone
Contact Hours: 1.4
6. A patient received high-dose cyclophosphamide for breast
Passing Score: 80%
cancer, and within two days of treatment she developed
Test ID #: 03-30/3-06
SIADH. What is most likely the cause of her SIADH?
Test Processing Fee: $15
a. Aggressive hydration
b. High-dose antiemetics
The Oncology Nursing Society is accredited as a provider
c. Breast cancer
of continuing education (CE) in nursing by the
d. Metastasis to pituitary gland
· American Nurses Credentialing Center's Commission on
7. The patient expresses fear that her cancer has spread and
is causing SIADH. The nurse's best response would be
· California Board of Nursing, Provider #2850.
that SIADH is caused by
a. Damage to of the thyroid gland from metastatic can-
b. A malignancy spreading and invading the pituitary
CE Test Questions
c. A tumor secreting excess amounts of the antidiuretic
1. Which laboratory tests would indicate a patient has
d. Excess ADH production and release from the thyroid
life-threatening syndrome of inappropriate antidiuretic
8. Which patient is at highest risk for developing acute
a. Urine sodium of 18 mEq/l and urine osmolality of
neurologic symptoms? A patient with an onset of hypo-
b. Urine osmolality of 550 mOsm/kg and serum sodium
a. Two days with a sodium of 130 mEq/l.
of 135 mEq/l
b. Three days with a sodium of 110 mEq/l.
c. Serum sodium of 110 mEq/l and serum osmolality of
c. Five days with a sodium of 125 mEq/l.
d. Seven days with a sodium of 120 mEq/l.
d. Serum osmolality of 280 mOsm/kg and urine osmo-
9. A patient's sodium is 105 mEq/l after being treated two
lality of 450 mOsm/kg
days ago with cisplatin for lung cancer. What orders
2. A patient diagnosed with metastatic small-cell lung can-
would the nurse expect?
cer is first placed at risk for developing SIADH because
a. Low-sodium diet
b. Seizure precautions
a. History of chronic obstructive pulmonary disease
c. Intravenous normal saline at 100 cc/hour
d. Fluid restrictions of 1,000 ml/day
b. Central nervous system metastasis.
10. A patient develops mild hyponatremia and is placed on
c. Lung cancer diagnosis.
fluid restrictions. Which is the most appropriate patient
d. Treatment with antiemetics.
3. Which system should the nurse plan to assess first for a
a. Fluid restrictions, if followed carefully, can help
patient with SIADH effusion?
SIADH resolve in one to two days.
b. Your total amount of water intake will be restricted to
1,200 ml/day to prevent water retention.
c. The restrictions will be 300 ml per meal and 200 ml
with your medications four times each day.
4. A patient's electrolytes indicate low serum sodium.
d. Hyponatremia occurs with excess free water and can
Which physical examination finding would be consistent
be decreased by limiting the fluid intake.
11. The physician orders chemotherapy for a patient with
SIADH. The family expresses concerns that the chemo-
therapy is being resumed. The nurse can best respond by
c. Altered mental status
explaining that if the chemotherapy is successful,
d. Orthostatic hypotension
a. The pituitary gland will stop producing ADH.
5. The medical intervention that would be initiated first for
b. The tumor, which is causing the SIADH to occur, will
a patient with SIADH is
a. Fluid restrictions.
c. The tumor will stop secreting the excess ADH, and the
b. Furosemide 40 mg IV twice a day.
SIADH will decrease.
c. Hypertonic 3% saline infusion.
d. The tumor will decrease its pressure on the pituitary
gland, which is excreting ADH.
ONCOLOGY NURSING FORUM VOL 30, NO 3, 2003
12. Which nursing monitoring would be critical when caring
14. The nurse is reviewing the current medication administra-
for a patient with SIADH?
tion records for a patient at risk for SIADH. The patient
a. Take vitals signs hourly.
is being treated for lung cancer and has an exacerbation
b. Keep strict input and output.
of his COPD. Which medication ordered for this patient
c. Assess for signs of peripheral edema.
should be clarified?
d. Draw serum electrolytes every other day.
a. Furosemide 20 mg orally, twice a day
13. High-dose cisplatin is ordered despite a patient's current
b. Dexamethasone 3 mg orally, once daily
hyponatremia. Which nursing assessment will be most
c. Morphine 30 mg IV, as needed every two hours
d. Lorazepam 1 mg orally, as needed at bedtime
a. Amount of IV fluids administered to prevent hemor-
15. In addition to hyponatremia, which kidney function test
values would be most consistent with SIADH?
b. The type of antiemetics ordered for potential nausea
a. Blood urea nitogen (BUN) 5 mg/dl and creatinine 0.2
c. Amount of IV fluids administered to prevent nephro-
b. BUN 6 mg/dl and creatinine 1.8 mg/dl
c. BUN 10 mg/dl and creatinine 0.5 mg/dl
d. Administration of furosemide with lactated ringers for
d. BUN 19 mg/dl and creatinine 1.7 mg/dl
Oncology Nursing Forum Answer/Enrollment Form
Syndrome of Inappropriate Antidiuretic Hormone (Test ID #03-30/3-06)
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1. How relevant were the objectives to the CE activity's goal?
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· Objective #1
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3. To what degree were the teaching/learning resources helpful?
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ONCOLOGY NURSING FORUM VOL 30, NO 3, 2003