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Syndrome of Inappropriate Antidiuretic Hormone
Jo Ann Flounders, MSN, CRNP, OCN®, CHPN
yndrome of inappropriate antidiuretic hormone (SIADH)
is a disorder of water intoxication (Haapoja, 1997; Moses
& Scheinman, 1991). SIADH describes the inappropriate production and secretion of antidiuretic hormone (ADH),
also known as arginine vasopressin, that causes increased water reabsorption in the renal tubules and leads to increased water
retention and dilutional hyponatremia (Finley, 1998; Keenan,
1999).
S
Etiology
SIADH can occur as a result of an endocrine paraneoplastic
syndrome, which implies that the syndrome is caused indirectly by a malignancy and not the direct result of invasion
and damage by malignant cells (Haapoja, 1997; Keenan,
1999). An endocrine paraneoplastic syndrome occurs when a
tumor secretes excessive amounts of hormones that interfere
with normal homeostasis. Although normal hormone production occurs in response to a stimulus to maintain homeostasis,
ectopic production of hormones by tumors is not normal and
does not occur to maintain homeostasis. Tumor cells are able
to produce many hormones and hormone-releasing factors,
causing different paraneoplastic syndromes that affect body
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
release of ADH from the posterior pituitary gland (Finley,
1998; Haapoja; Keenan). Both mechanisms cause inappropriate and excessive secretion of ADH, which causes disruption
of fluid balance (Bunn & Ridgway, 1993; Ezzone, 1999;
Keenan).
The most common etiology of SIADH is malignancy, although many other nonmalignant causes exist (Jones, 1999).
The most frequent malignant cause of SIADH is small cell
lung cancer (Flombaum, 2000; Keenan, 1999; List et al.,
1986). Other malignant etiologic causes of SIADH include
non-small cell lung cancer; head and neck, prostate, pancreatic, breast, ovarian, duodenal, and esophageal cancers; lymphoma and leukemia; and thymoma, neuroblastoma, and carcinoid tumors (Finley, 1998; Frizzell, 2000; Keenan; Schafer,
1997; Smeltzer & Bare, 1996). SIADH also may be caused by
central nervous system metastases, such as meningeal carcinomatosis (Haapoja, 1997).
Treatment of a malignancy with cytotoxic chemotherapy
can cause SIADH. The most commonly implicated chemo-
therapeutic agents that cause SIADH and impaired excretion
of water are cyclophosphamide, ifosfamide, vincristine, vinblastine, cisplatin, and melphalan (Flombaum, 2000; Keenan,
1999; Schafer, 1997). Administration of high-dose cyclophosphamide may be especially problematic in patients at risk for
SIADH because aggressive hydration is used to prevent hemorrhagic 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
fluids (e.g., 0.45% normal saline) are used, hyponatremia and
water retention may occur (Flombaum; Ritch, 1988). In addition, chemotherapy-induced nausea can stimulate the release
of ADH (Haapoja). However, use of effective antiemetics has
decreased the incidence of nausea as a cause of SIADH
(Flombaum).
Pharmacologic interventions used to treat patients with cancer may contribute to the development of SIADH. Analgesics,
such as opioids, in addition to antidepressants, such as tricyclics
and selective serotonin reuptake inhibitors, have been known to
cause increased ADH production (Frizzell, 2000; Keenan,
1999). In addition to stimulating abnormal production of ADH,
Goal for CE Enrollees:
To further enhance nurses’ knowledge about syndrome of
inappropriate antidiuretic hormone (SIADH).
Objectives for CE Enrollees:
On completion of this CE, the participant will be able to
1. Describe the etiology of SIADH.
2. Discuss the clinical manifestations and medical management of patients with SIADH.
3. Discuss the nursing implications in the care of patients
with SIADH.
Jo Ann Flounders, MSN, CRNP, OCN®, CHPN, is a nurse practitioner at Consultants in Medical Oncology and Hematology in
Drexel Hill, PA.
Digital Object Identifier: 10.1188/03.ONF.E63-E70
FLOUNDERS – VOL 30, NO 3, 2003
E63
medications may potentiate the effects of ADH on the renal
tubules. Nonsteroidal anti-inflammatory drugs, thiazide diuretics, barbiturates, and anesthetic agents can increase the effects
of ADH on the renal tubules (Dietz & Flaherty, 1993; Frizzell;
Jones, 1999; Rohaly-Davis & Johnston, 1996).
Many nonmalignant causes of SIADH exist. Injury to the
cells of the central nervous system as a result of infection,
brain abscess, brain herniation, hemorrhage, or head trauma
may result in increased ADH production. Pulmonary disorders, such as infection caused by virus, bacteria, or fungus,
also can stimulate ectopic production of ADH. Other pulmonary complications that can produce and release ADH are
pneumonia, tuberculosis, and lung abscess (Dietz & Flaherty,
1993; Ezzone, 1999; Frizzell, 2000; Keenan, 1999; Schafer,
1997). Patients with malignant disease commonly experience
pain and stress, which also can increase ADH production.
Cigarette smoking can contribute to the development of
SIADH because nicotine can induce ADH production (Dietz
& Flaherty; Haapoja, 1997; Poe & Taylor, 1989).
Physiology
To understand the pathophysiology of SIADH, understanding the normal physiology of fluid and electrolyte balance in
body compartments is necessary. Body fluids, which contain
electrolytes, proteins, and water, are separated into intracellular and extracellular compartments by cell membranes and
capillaries (Mulvey & Bullock, 2000). Intracellular fluid is located in trillions of cells that are separated from one another
by cell membranes (Martini, 1998). Extracellular fluid consists of interstitial fluid, or fluid between the cells, and intravascular fluid, which is fluid or plasma circulating in the
blood vessels (Mulvey & Bullock). Total body water is estimated to be two-thirds intracellular fluid and one-third extracellular fluid (Keenan, 1999; Martini).
Intracellular and extracellular fluids exist as solutions, and
the electrolyte composition of each compartment is different.
The main ions in intracellular fluid are potassium, magnesium, and phosphate, and the main ions in extracellular fluid
are sodium, chloride, and bicarbonate (Martini, 1998). The
substances that are dissolved in the solution of intracellular
and extracellular fluid are called solutes. The total concentration of solutes in the solution is defined as osmolality, which
is stated as the number of milliosmols per liter (mOsm/l) or
milliosmols per kilogram (mOsm/kg) (Keenan, 1999).
Homeostasis demands that a balance exist in the fluid and
electrolyte composition of the intracellular and extracellular
compartments. Movement of solutes and water across cell
membranes maintains equilibrium between intracellular and
extracellular fluid. The semipermeable cell membranes only
allow selective ions to cross the membrane to enter or exit
cells, but the movement of water is not restricted (Martini,
1998). Water moves freely across the membranes toward the
solution that contains the higher solute concentration in an
effort to equalize the concentration in both compartments
(Mulvey & Bullock, 2000). The process that allows free
movement of water across a membrane in response to a difference in concentration is called osmosis (Martini). Osmosis
maintains homeostasis by eliminating the differences in concentration of extracellular and intracellular fluids almost immediately. Therefore, despite the different chemical composition of each compartment, the osmolality, or concentration,
is identical (Martini). Osmotic pressure is a force that influences the exchange of fluids and electrolytes between the
compartments at the capillary level. Osmotic pressure acts as
an inward pulling force that moves solutes and water into the
capillaries (Mulvey & Bullock).
Several basic concepts about regulation of fluids and electrolytes are important. The mechanisms that monitor and adjust the composition and volume of body fluids to maintain
homeostasis respond to changes in extracellular fluid, not intracellular fluid. Because intracellular fluid is located in trillions of isolated cells separated by cell membranes, a change
in one cell in the body will not directly affect other cells. In
contrast, a change in extracellular fluid will occur throughout
the extracellular compartment and affect all the cells in the
body. Therefore, the concentration of extracellular fluid is the
stimulus that triggers fluid movement (Martini, 1998).
Another important concept pertaining to fluid and electrolyte regulation is that water must move across cell membranes
in response to osmotic gradients, or changes in concentration
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 regulator of osmotic pressure (Mulvey & Bullock, 2000). Just as
water flows from an area with lesser solute concentration to
an area of greater solute concentration, water also follows
sodium (Martini). Therefore, when extracellular fluid has a
high concentration (i.e., high osmolality) of sodium ions, or
hypernatremia, water moves into the blood vessels and out of
the cells. When extracellular fluid has a low concentration
(i.e., low osmolality) of sodium ions, or hyponatremia, water
moves out of the blood vessels and into cells where the concentration is higher (Martini; Mulvey & Bullock).
Another concept that is helpful to understand is tonicity,
which is used to describe osmolality (Martini, 1998). An isotonic fluid (e.g., normal saline) with the same concentration
as plasma does not cause movement of water into or out of
cells (Martini). Hypertonic fluids have a higher solute concentration than plasma, and hypotonic fluids have a lower solute
concentration than plasma (Stripp, 2000). Therefore, infusion
of a hypertonic solution into the blood vessels of extracellular fluid causes movement of water from cells into blood vessels. Infusion of a hypotonic fluid into the blood vessels of
extracellular fluid causes movement of fluid from blood into
cells (Martini). Figure 1 displays the effect of osmosis across
a cell membrane.
The volume of total body water is regulated by thirst, hormone secretion, and renal activity. In response to decreased
volume of fluid and increased plasma concentration (i.e., osmolality), the hypothalamus activates nervous pathways that
cause thirst. In addition, decreased plasma volume causes
decreased renal perfusion, which activates the renin-angiotensin-aldosterone system and stimulates the hypothalamus to
release substances that cause thirst (Mulvey & Bullock, 2000).
This mechanism also causes release of ADH from the posterior pituitary (Tesh, 2000). Therefore, in normal homeostasis,
ADH is produced by the hypothalamus and released into the
blood by the posterior pituitary in response to increased plasma
concentration (i.e., increased osmolality) or decreased plasma
volume (Dietz & Flaherty, 1993; Finley, 1998). The physiologic action of ADH is to induce an antidiuretic effect on the
kidneys so that water is retained (Jones, 1999). Therefore, renal regulation of fluid balance occurs through reabsorption and
ONF – VOL 30, NO 3, 2003
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Cell in hypotonic solution
Cell in isotonic solution
Cell swells; water moves into cell.
Normal cell: No movement of water.
Cell in hypertonic solution
Cell shrinks; water moves out of cell.
Figure 1. Effect of Osmosis Across a Cell Membrane
excretion of water by the renal tubules (Keenan, 1999; Mulvey & Bullock). In normal homeostasis, a negative feedback
mechanism exists so that increased plasma volume and normal or decreased osmolality can inhibit ADH and allow excretion of water (Jones). However, SIADH causes failure of the
normal mechanisms of homeostasis.
Pathophysiology
SIADH of malignancy is the inappropriate, uncontrolled secretion of ADH, which causes increased water reabsorption
by the renal tubules that leads to decreased excretion of water (Jones, 1999). The volume of total body water increases
and is distributed into the extracellular and intracellular fluid.
The concentration of sodium in the extracellular fluid then is
low, as a result of dilution, which causes hypoosmolality.
However, because only a portion of the total body water is
distributed into the extracellular fluid, most of the water diffuses into the intracellular fluid. Therefore, SIADH does not
cause signs and symptoms of increased volume of fluid because the fluid is in the cells and not the blood or interstitial
fluid (Bunn & Ridgway, 1993; Flombaum, 2000; Keenan,
1999). In addition, the concentration of urine is increased
because the kidneys secrete sodium and cannot secrete dilute
urine (Jones). The SIADH mechanism that causes thirst
causes patients to continue to drink inappropriately despite the
fact that in normal homeostasis, thirst is inhibited when hyponatremia is evident (Keenan). In summary, SIADH is
caused by ADH secretion by tumor cells or inappropriately by
the posterior pituitary and results in water intoxication, hyponatremia, and hypoosmolality (Dietz & Flaherty, 1993;
Keenan). Table 1 displays the effects of SIADH.
Identification of Patients at Risk
for SIADH
The risk of SIADH for patients with cancer corresponds to
the etiologic factors that cause SIADH. Figure 2 summarizes
patients at risk for development of SIADH.
Clinical Manifestations
Symptoms of SIADH in patients with cancer are influenced
by the rate of onset and the severity of hyponatremia (Flombaum, 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,
acute neurologic symptoms usually occur (Flombaum; Keenan, 1999). Symptoms usually are life threatening and severe
when serum sodium is decreased to less than 105 mEq/l. Nonspecific symptoms may occur when the serum sodium level is
115–120 mEq/l. In contrast, if SIADH has a slow, more
chronic onset, patients may be asymptomatic (Flombaum).
Most patients are asymptomatic and do not develop the severe
neurologic signs and symptoms associated with extreme hyponatremia (Haapoja, 1997; Keenan).
Despite the water intoxication of SIADH, signs and symptoms of fluid overload usually do not appear with SIADH.
Therefore, peripheral edema, ascites, and heart failure usually
are not noted because only a portion of excess water is retained in the intravascular or interstitial fluid and most is distributed to the cells (Flombaum, 2000; Haapoja, 1997; Jones,
1999; Keenan, 1999). According to the principles that regulate fluid shifts between extracellular and intracellular fluids,
hypotonic fluid in blood vessels shifts into cells to equalize the
concentration between extracellular and intracellular fluids.
Consequently, the cells of the brain swell. Because the inflexible skull confines brain cells, this cerebral edema causes increased intracranial pressure and decreased cerebral blood
flow, leading to neurologic dysfunction (Bunn & Ridgway,
1993; Flombaum; Keenan). Therefore, symptoms of hyponatremia primarily are related to neurologic dysfunction
Table 1. Effects of SIADH
Mechanism
Effect
Increased water reabsorption by the
renal tubule
Decreased serum osmolality, hyponatremia
Decreased excretion of water by the
renal tubule
Increased urine osmolality
Increased total body water in intracellular fluid and extracellular fluid
Decreased serum osmolality
Decreased sodium concentration in the
plasma because of dilution by excess
water
Hyponatremia
Increased concentration of urine
Increased urine osmolality
Increased secretion of sodium by the
kidney
Increased urinary sodium
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Patients with malignant neoplasms such as
• Small cell lung cancer (most common)
• Non-small cell lung cancer, head and neck, prostate, pancreatic, duodenal,
esophageal, lymphoma, leukemia, breast, ovary, thymoma, neuroblastoma,
and carcinoid tumors (less common)
Patients receiving cytotoxic chemotherapy including
• Cyclophosphamide, vincristine, vinblastine, cisplatin, and melphalan
Patients who experience chemotherapy-induced nausea
Patients receiving pharmacologic intervention including
• Analgesics, such as opioids
• Antidepressants, such as tricyclics and selective serotonin reuptake inhibitors
• Non-steroidal anti-inflammatory drugs, thiazide diuretics, barbiturates, and
anesthetic agents
Patients with nonmalignant causes such as
• Central nervous system disorders: infections, brain abscesses, brain herniation, hemorrhage, and head trauma
• Pulmonary disorders: infection caused by virus, bacteria, or fungus; pneumonia; tuberculosis; and lung abscess
• Pain, stress, and nicotine
Figure 2. Patients at Risk for Development of SIADH
Note. Based on information from Dietz & Flaherty, 1993; Ezzone, 1999; Finley,
1998; Frizzell, 2000; Haapoja, 1997; Keenan, 1999; Schafer, 1997.
volume depletion or fluid overload. Restriction of water is the
main treatment (Flombaum). Therefore, although a routine
blood chemistry evaluation may reveal hyponatremia in asymptomatic patients, the presence of hyponatremia alone is not sufficient to diagnose SIADH. Multiple diagnostic laboratory tests
must be completed and evaluated in addition to physical examination.
Diagnostic Studies
Laboratory studies that are diagnostic of SIADH include serum sodium, plasma osmolality, urine sodium, and urine osmolality. The normal range for serum sodium is 135–147 mEq/l.
However, SIADH cannot be diagnosed on the basis of hyponatremia alone because other disorders can cause hyponatremia. Confirming a hypoosmolar state (i.e., water excess) by
testing osmolality is critical. Serum osmolality usually is decreased with SIADH, whereas urine osmolality usually is increased. Electrolytes, blood urea nitrogen, creatinine, albumin,
and uric acid also should be evaluated because these values
usually decrease with SIADH as a result of dilution (Finley,
1998; Haapoja, 1997; Jones, 1999; Keenan, 1999; Smeltzer &
Bare, 1996). Other studies to rule out cardiac, hepatic, adrenal,
renal, and thyroid causes of hyponatremia should be completed
(Haapoja). Serum vasopressin levels usually are not ordered
because vasopressin may be elevated in most patients with hyponatremia; therefore, elevation is not specific to SIADH
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.
System
Signs
General
Weakness, fatigue,
malaise
Neurologic
Altered mental status
Headache
Lethargy, irritability
Delirium
Psychosis
Personality changes
Ataxia
Tremors
Focal neurologic signs
Seizures
Coma, obtundation
Confusion, disorientation
Cardiovascular
–
Usually normal blood pressure
Usually normal pulse
Normal skin turgor
No edema
Gastrointestinal
Anorexia
Nausea, vomiting
Diarrhea
Thirst
Abdominal cramping
Moist mucous membranes
–
Oliguria (< 400 cc/24
hours)
Weight gain
Incontinence
Physical Examination
After consideration of risk factors and review of symptoms
indicative of SIADH, attention to history is critical because
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 dysfunction, adrenal insufficiency, renal disorders, and thyroid disease
(Keenan, 1999). Review of current medications is necessary to
determine if SIADH may be medication induced.
Evaluating patients for signs and symptoms of dehydration
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 hypervolemia may cause decreased sodium concentration. However, the clinical manifestations and physiologic mechanisms of
hypervolemia, hypovolemia, and SIADH are different. Accurate diagnosis is critical because treatment will vary greatly
(Bunn & Ridgway, 1993; Flombaum, 2000; Keenan, 1999).
For example, patients with decreased volume caused by dehydration 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 hyponatremia, they require different treatment to correct the hyponatremia. In comparison, SIADH usually does not cause
Symptoms
Renal
Musculoskeletal
Muscle cramps
–
Hypoactive reflexes
Myoclonus
Note. Based on information from DeMichele & Glick, 2001; Dietz & Flaherty,
1993; Ezzone, 1999; Finley, 1998; Haapoja, 1997; Keenan, 1999; Schafer,
1997.
ONF – VOL 30, NO 3, 2003
E66
(Haapoja; Keenan). A chest x-ray may be ordered to determine
the presence of pulmonary disease. A computed tomography
scan of the head can help determine the presence of cerebral
edema, brain tumor, or brain herniation (Ezzone, 1999). Table
3 summarizes the critical laboratory values diagnostic of
SIADH.
Medical Management
Table 3. Laboratory Values in SIADH
Laboratory Test
Serum sodium
Nursing Management
Recognition of early clinical manifestations of SIADH allows early treatment to prevent life-threatening complications. Nurses frequently are able to perceive subtle changes
in patient status and should complete accurate and thorough
ongoing assessment to identify early abnormal changes.
Continued assessment of neuromuscular, cardiac, gastrointestinal, and renal systems is warranted. Constant evaluation of fluid and electrolyte status is necessary with ongo-
< 130 mEq/L
Serum osmolality
< 280 mOsm/kg
Urine osmolality
> 500 mOsm/kg
Urine sodium
Medical management of SIADH must be directed at treating
the underlying pathology (Finley, 1998). SIADH usually resolves when the etiologic factors that are stimulating inappropriate ADH secretion are eliminated (DeMichele & Glick,
2001). Treatment of malignant neoplasms with antineoplastic
chemotherapy causes regression of chemosensitive tumors and
usually results in resolution of SIADH (Keenan, 1999). If
SIADH is caused by metastasis to the brain, corticosteroids and
radiation therapy may be effective treatment (DeMichele &
Glick). Treatment of nonmalignant causes of SIADH, including discontinuation of offending medications, is necessary.
Treatment of hyponatremia is related to the severity of
symptoms and the rapidity of onset (Bunn & Ridgway, 1993;
Flombaum, 2000; Keenan, 1999). Treatment for mild hyponatremia in SIADH (i.e., a sodium level greater than 125
mEq/l) includes fluid restriction of 800–1000 ml/day (Finley,
1998). Fluid restriction usually allows the sodium level to correct over 3–10 days. If fluid restriction is not effective, demeclocycline can be administered. Demeclocycline allows excretion of water because it inhibits the effect of ADH on the
renal tubules. Side effects of this drug include nausea, photosensitivity, and azotemia. Treatment with demeclocycline
usually increases the sodium level within three to four days,
and fluid restriction is not necessary (DeMichele & Glick,
2001; Finley; Keenan). Aggressive treatment may be indicated if severe neurologic symptoms, such as coma or seizures, occur with severe hyponatremia (Keenan). Administration of hypertonic 3% saline infusion over two to three hours
is indicated to correct life-threatening hyponatremia. Furosemide also is given to increase urinary water excretion
(Finley; Keenan).
Critical Value Diagnostic of SIADHa
> 20 mEq/L
a
In the absence of diuretic therapy
Note. Based on information from Dietz & Flaherty, 1993; Ezzone, 1999; Finley,
1998; Haapoja, 1997; Keenan, 1999; Schafer, 1997.
ing physical assessment to detect early signs of neurologic
complications caused by hyponatremia. This especially is
important when assessing the volume status of patients,
which is critical for diagnosing SIADH. Nurses should assess for signs and symptoms of hypovolemia or hypervolemia and understand that the occurrence of these clinical
manifestations excludes the diagnosis of SIADH. Nurses
should review medications to reveal possible causative
agents of SIADH and provide patients and caregivers with
necessary instructions regarding fluid restriction. IV hydration, chemotherapy, medications, and electrolytes may be
ordered and must be monitored carefully. Assessment of
patients for side effects of treatment of SIADH should be
ongoing. Attention to the timeliness of completion of laboratory tests will ensure that electrolyte status is evaluated
promptly. In addition, nurses should monitor blood and
urine chemistry levels and ensure that measures to correct
abnormal values are instituted in a timely manner. Nurses
should assess the coping abilities of critically ill patients and
caregivers; assess for pain, anxiety, and depression; and provide interventions to improve pain management and coping
ability. However, management of pain and depression may
be challenging, because some analgesics and antidepressants
that cause SIADH may need to be withdrawn and substitutions made. The choice of medications must involve consideration of causative agents of SIADH. Nurses should provide patients and caregivers with instructions on signs and
symptoms of complications that should be reported to a physician. Discharge planning should include consideration of
referral for home care or hospice services.
The author would like to thank John Sprandio, MD, of Consultants in Medical Oncology and Hematology, Drexel Hill, PA, for reviewing this manuscript.
Author Contact: Jo Ann Flounders, MSN, CRNP, OCN®, CHPN,
can be reached at [email protected], with copy to editor at
[email protected].
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For more information . . .
➤ eMedicine: Syndrome of Inappropriate Antidiuretic Hormone
www.emedicine.com/emerg/topic784.htm
➤ Lucile Packard Children’s Hospital: SIADH
www.lpch.org/DiseaseHealthInfo/HealthLibrary/diabetes/
siadh.html
Links can be found using ONS Online at www.ons.org.
ONF – VOL 30, NO 3, 2003
E68
ONF Continuing Education Examination
Syndrome of Inappropriate Antidiuretic Hormone
Contact Hours: 1.4
Passing Score: 80%
Test ID #: 03-30/3-06
Test Processing Fee: $15
The Oncology Nursing Society is accredited as a provider
of continuing education (CE) in nursing by the
• American Nurses Credentialing Center’s Commission on
Accreditation.
• California Board of Nursing, Provider #2850.
CE Test Questions
1. Which laboratory tests would indicate a patient has
life-threatening syndrome of inappropriate antidiuretic
hormone (SIADH)?
a. Urine sodium of 18 mEq/l and urine osmolality of
550 mOsm/kg
b. Urine osmolality of 550 mOsm/kg and serum sodium
of 135 mEq/l
c. Serum sodium of 110 mEq/l and serum osmolality of
250 mOsm/kg
d. Serum osmolality of 280 mOsm/kg and urine osmolality of 450 mOsm/kg
2. A patient diagnosed with metastatic small-cell lung cancer is first placed at risk for developing SIADH because
of her
a. History of chronic obstructive pulmonary disease
(COPD).
b. Central nervous system metastasis.
c. Lung cancer diagnosis.
d. Treatment with antiemetics.
3. Which system should the nurse plan to assess first for a
patient with SIADH effusion?
a. Neurologic
b. Cardiovascular
c. Gastrointestinal
d. Musculoskeletal
4. A patient’s electrolytes indicate low serum sodium.
Which physical examination finding would be consistent
with SIADH?
a. Edema
b. Tachycardia
c. Altered mental status
d. Orthostatic hypotension
5. The medical intervention that would be initiated first for
a patient with SIADH is
a. Fluid restrictions.
b. Furosemide 40 mg IV twice a day.
c. Hypertonic 3% saline infusion.
d. Democlocycline.
6. A patient received high-dose cyclophosphamide for breast
cancer, and within two days of treatment she developed
SIADH. What is most likely the cause of her SIADH?
a. Aggressive hydration
b. High-dose antiemetics
c. Breast cancer
d. Metastasis to pituitary gland
7. The patient expresses fear that her cancer has spread and
is causing SIADH. The nurse’s best response would be
that SIADH is caused by
a. Damage to of the thyroid gland from metastatic cancer.
b. A malignancy spreading and invading the pituitary
gland.
c. A tumor secreting excess amounts of the antidiuretic
hormone (ADH)
d. Excess ADH production and release from the thyroid
gland.
8. Which patient is at highest risk for developing acute
neurologic symptoms? A patient with an onset of hyponatremia at
a. Two days with a sodium of 130 mEq/l.
b. Three days with a sodium of 110 mEq/l.
c. Five days with a sodium of 125 mEq/l.
d. Seven days with a sodium of 120 mEq/l.
9. A patient’s sodium is 105 mEq/l after being treated two
days ago with cisplatin for lung cancer. What orders
would the nurse expect?
a. Low-sodium diet
b. Seizure precautions
c. Intravenous normal saline at 100 cc/hour
d. Fluid restrictions of 1,000 ml/day
10. A patient develops mild hyponatremia and is placed on
fluid restrictions. Which is the most appropriate patient
education?
a. Fluid restrictions, if followed carefully, can help
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.
d. Hyponatremia occurs with excess free water and can
be decreased by limiting the fluid intake.
11. The physician orders chemotherapy for a patient with
SIADH. The family expresses concerns that the chemotherapy is being resumed. The nurse can best respond by
explaining that if the chemotherapy is successful,
a. The pituitary gland will stop producing ADH.
b. The tumor, which is causing the SIADH to occur, will
stop metastasizing.
c. The tumor will stop secreting the excess ADH, and the
SIADH will decrease.
d. The tumor will decrease its pressure on the pituitary
gland, which is excreting ADH.
ONCOLOGY NURSING FORUM – VOL 30, NO 3, 2003
E69
12. Which nursing monitoring would be critical when caring
for a patient with SIADH?
a. Take vitals signs hourly.
b. Keep strict input and output.
c. Assess for signs of peripheral edema.
d. Draw serum electrolytes every other day.
13. High-dose cisplatin is ordered despite a patient’s current
hyponatremia. Which nursing assessment will be most
critical?
a. Amount of IV fluids administered to prevent hemorrhagic cystitis
b. The type of antiemetics ordered for potential nausea
and vomiting
c. Amount of IV fluids administered to prevent nephrotoxicity
d. Administration of furosemide with lactated ringers for
hydration
14. The nurse is reviewing the current medication administration records for a patient at risk for SIADH. The patient
is being treated for lung cancer and has an exacerbation
of his COPD. Which medication ordered for this patient
should be clarified?
a. Furosemide 20 mg orally, twice a day
b. Dexamethasone 3 mg orally, once daily
c. Morphine 30 mg IV, as needed every two hours
d. Lorazepam 1 mg orally, as needed at bedtime
15. In addition to hyponatremia, which kidney function test
values would be most consistent with SIADH?
a. Blood urea nitogen (BUN) 5 mg/dl and creatinine 0.2
mg/dl
b. BUN 6 mg/dl and creatinine 1.8 mg/dl
c. BUN 10 mg/dl and creatinine 0.5 mg/dl
d. BUN 19 mg/dl and creatinine 1.7 mg/dl
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