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ONLINE EXCLUSIVE · CONTINUING EDUCATION
Oncology Emergency Modules:
Spinal Cord Compression
Jo Ann Flounders, RN, MSN, OCN®, CHPN, and Barbara B. Ott, RN, PhD
pinal cord compression (SCC) is compression of the
The spinal cord, an elongated mass of nervous tissue, is located
thecal sac by a tumor in the epidural space, either at the
in the flexible vertebral column. The spinal cord arises from the
level of the spinal cord or cauda equina (Quinn & De-
medulla oblongata in the brain, begins at the foramen magnum,
Angelis, 2000). Because SCC can cause direct injury to the
and extends to the lower aspect of the first lumbar (L1) verte-
spinal cord, it requires prompt intervention to prevent progres-
bra (Belford, 1997). Because the spinal cord ends at L1L2, the
sive and irreversible neurologic disability (Bucholtz, 1999;
lumbar and sacral nerves exit the cord there (Wilkes, 1999).
Quinn & DeAngelis; Wilkes, 1999).
Because the spinal cord is approximately 10 inches shorter than
the vertebral column, the lumbar and sacral spinal nerves have
long roots that extend from the distal tip of the spine to the lum-
bar and sacral areas. These roots are known as the cauda equina
SCC occurs as a result of a malignant neoplasm compress-
because of their resemblance to a horse's tail (Belford).
ing the spinal cord. Malignant tumors may be classified as
The effects of compression of the spinal cord range from
primary (i.e., arising from the tissue of the spinal cord or spi-
minor sensory, motor, and autonomic changes to severe pain
nal canal) or secondary (i.e., arising as metastatic solid tu-
and complete paralysis (Hunter, 1998). Thirty-one pairs of
mors) (Schafer, 1997). SCC most commonly is caused by
spinal nerves exit from the spinal cord. Sensory or afferent
metastatic tumors. Progression of symptoms is more rapid
with metastatic tumors when compared to primary spinal cord
tumors (Wilkes, 1999). The most frequent types of primary
malignancies causing skeletal metastasis are lung, breast, and
Goal for CE Enrollees:
prostate, followed by lymphoma, myeloma, and renal carci-
To further enhance nurses' knowledge regarding spinal
noma (Schafer, 1997). The location of the metastatic lesion in
the spine correlates with the type of primary malignancy.
Cervical spine lesions often are caused by primary breast tu-
Objectives for CE Enrollees:
mors; thoracic spine lesions often are caused by primary lung,
breast, and prostate tumors; and lumbosacral spine lesions
On completion of this CE, the participant will be able to
often are caused by gastrointestinal and prostate malignancies
1. Describe the pathophysiologic process of spinal cord
(Wilkes). The most frequent site of metastasis that causes SCC
is the thoracic area of the spinal column.
2. Discuss the diagnosis and treatment of patients with
Paraneoplastic syndromes, carcinomatous myelopathy, ra-
spinal cord compression.
diation myelopathy, herpes zoster, retroperitoneal tumor, or
3. D i s c u s s the nursing implications in the care of pa-
toxicity of cytotoxic medications also may cause spinal cord
tients with spinal cord compression.
syndromes. Other causes include nonmalignant conditions in
patients with cancer, such as herniated disks, vertebral frac-
tures secondary to osteoporosis, and intraspinal abscesses
(DeMichele & Glick, 2001).
Jo Ann Flounders, RN, MSN, OCN ®, CHPN, is a nurse practitioner
at Consultants in Medical Oncology and Hematology in Drexel Hill,
PA, and Barbara B. Ott, RN, PhD, is an associate professor in the
College of Nursing at Villanova University in Pennsylvania.
The vertebral column contains 26 vertebrae: 7 cervical, 12
thoracic, 5 lumbar, 1 sacral, and 1 coccygeal (Schafer, 1997).
Digital Object Identifier: 10.1188/03.ONF.E17-E23
FLOUNDERS VOL 30, NO 1, 2003
impulses enter the spinal cord through a dorsal root of each
spinal nerve and convey sensory information from the body
to the spinal cord. Motor or efferent impulses, including au-
tonomic impulses, leave the spinal cord through a ventral root
of a spinal nerve and convey impulses from the spinal cord
back to the body (Belford, 1997). Transmission of impulses
to and from the brain and spinal cord occurs in the ascending
and descending tracts, which extend the length of the spinal
cord. Impulses from the spinal cord to the brain are transmit-
ted through the anterior spinothalamic tracts, and impulses
from the brain to the spinal cord are transmitted through the
lateral corticospinal tract (Henze, 2000). Therefore, injury to
the spinal nerves or the spinal cord can result in sensory-mo-
tor and autonomic impairment (Wilkes, 1999).
Three membranes, or meninges (see Figure 1), that origi-
nate in the brain and extend downward over the spinal cord
are layered to protect the brain and the spinal cord (Schafer,
1997; Wilkes, 1999). The outermost layer is the dura mater,
Figure 1. Meninges or Membranes Surrounding the Spinal
under which is the arachnoid membrane, followed by the in-
Cord, With Associated Spaces
nermost membrane, the pia mater, which is connected closely
to the spinal cord. Between the meninges and adjacent struc-
tures are the epidural or extradural space, located between the
The neurologic deficits caused by SCC result from one of
vertebral column and the outer surface of the dura mater; the
the following processes. The tumor directly compresses the
subdural space, located between the dura membrane and the
spinal cord or cauda equina; the tumor or bone interrupts the
arachnoid membrane; and the subarachnoid space, located
vascular supply to the nerve structure; or a pathologic fracture
between the arachnoid membrane and the pia mater. The sub-
causes a vertebral collapse that causes bone to protrude onto
arachnoid space contains cerebrospinal fluid (CSF) (Schafer,
the spinal cord and compress the nerve roots (Schafer, 1997).
The pressure from a growing tumor can cause a series of
The malignant invasion of the spinal cord that causes SCC
reactions leading to nerve tissue injury. Compression of the
can occur at several possible anatomic locations (Wilkes,
epidural venous plexus causes vasogenic edema and the pro-
1999). The most common location is extradural, caused when
duction of cytokines, such as interleukin-1, interleukin-6, and
a tumor arises outside the spinal cord, as in bony metastasis to
prostaglandin. Vasodilation occurs, as well as plasma exuda-
the vertebrae. These extradural metastatic tumors can be os-
tion and edema, causing injury to nerve tissue. Additional
teolytic or osteoblastic (Bucholtz, 1999; Byrne, 1997; Schafer,
nerve tissue injury is caused by the neurotransmitters seroto-
1997). Osteolytic lesions invade the vertebrae and cause bone
nin and glutamide. Cytotoxic edema, leading to cell death and
destruction when tumor cells stimulate osteoclasts to absorb
irreversible paraplegia, occurs (Bucholtz, 1999).
bony tissue. In contrast, osteoblastic lesions occur when tumor
cells stimulate osteoblasts to develop into bone (Schafer,
Identification of Patients at Risk
1997). The tumor invades and destroys the vertebral body,
The risk of development of SCC for patients with cancer
causes vertebral collapse, and compresses the spinal cord as
corresponds to the etiologic factors that cause SCC. Patients
tumor or bone particles are pushed into the epidural space
at risk for developing SCC include those with cancers that
commonly metastasize to the bone, such as breast, lung, pros-
In addition to extradural tumors, other locations for malignant
tate, renal, and myeloma; patients with cancers that metasta-
invasion of the spinal cord exist. Intramedullary tumors are pri-
size to the spinal cord, such as lymphoma, seminoma, and
mary tumors that develop in the spinal cord itself. Intradural
neuroblastoma; and patients with primary tumors of the spinal
tumors arise from the coverings of the spinal cord or from the
cord, such as ependymoma, astrocytoma, and glioma (Hunter,
nerve roots and are located in the dura. Extravertebral tumors
1998; Schafer, 1997; Wilkes, 1999).
originate outside the vertebrae and extend into the epidural space
by extending between the vertebrae and pushing through the
intervertebral foramina (Belford, 1997; Wilkes, 1999).
Several mechanisms may facilitate metastasis to the epidu-
Review of Systems
ral space (Belford, 1997; Bucholtz, 1999; Schafer, 1997). The
most common mechanism is through hematogenous spread as
The clinical manifestations of SCC correspond to the site and
an embolic process from the primary site through the paraver-
extent of malignant invasion of the vertebral cord (Bucholtz,
tebral and extradural venous plexus to bone marrow, which
1999; Schafer, 1997). Cardinal signs include pain and sensory,
causes vertebral body collapse and an epidural mass. In addi-
motor, and autonomic dysfunction (Schafer, 1997).
tion, adenopathy of the prevertebral lymph nodes can cause
Neck or back pain is the most common presenting symp-
growth into the epidural space, as in lymphoma (Schafer,
tom of SCC (Byrne, 1997; DeMichele & Glick, 2001; Dietz
1997). Seeding of the CSF may occur with cancers of the cen-
& Flaherty, 1993; Siegal & Siegel, 1989; Wilkes, 1999). Pain
tral nervous system, which can lead to subsequent spreading
can precede the actual compression of the spinal cord, as well
to the subarachnoid space and seeding along the brain and
as any neurologic signs and symptoms (Bucholtz, 1999;
spinal cord (Belford).
DeMichele & Glick). Pain can be localized or radicular. Local-
ONF VOL 30, NO 1, 2003
retention, overflow, and incontinence. Bowel dysfunction in-
ized pain occurs in the area of the tumor (Wilkes); is described
cludes lack of urge to defecate and lack of ability to bear down,
as constant, dull, and aching (Hunter, 1998); and is caused by
with resultant constipation or obstipation. A late sign of auto-
an expanding blastic or lytic lesion within the vertebral body
nomic dysfunction is loss of sphincter control, a sign associated
(Bucholtz). The malignant lesion can stretch the periosteum
with a poorer prognosis (DeMichele & Glick, 2001; Dietz &
of the affected bone or cause vertebral collapse, resulting in
Flaherty, 1993; Schafer, 1991, 1997; Wilkes, 1999).
localized pain (Schafer, 1997).
As tumor growth advances, the nerve root becomes com-
pressed and pain becomes radicular with shooting or burning
intensity. Radicular pain is described as radiating along the
The importance of thorough assessment of neck and back
dermatome of the affected nerve roots. Pain secondary to cer-
pain in patients with cancer cannot be overemphasized.
vical and lumbosacral involvement usually is unilateral, and
Patients who present only with localized back pain and a
thoracic radicular pain is bilateral and described by patients as
normal neurologic examination may have a greater than
a tight band across the chest or abdomen. Radicular pain may
75% block of the spinal cord (Dietz & Flaherty, 1993). The
be constant or aggravated by movement, such as coughing,
single critical prognostic factor in SCC is neurologic status
sneezing, the Valsalva maneuver (i.e., increasing nasopharyn-
before the initiation of therapy (Dietz & Flaherty). There-
geal pressure by straining against a closed glottis), or the su-
fore, because ambulatory status at the time of diagnosis is
pine recumbent position and may be relieved by sitting (Dietz
predictive of a patient's ability to ambulate after treatment,
& Flaherty, 1993; Schafer, 1991, 1997; Wilkes, 1999). An im-
early detection and prompt treatment of SCC is necessary to
portant distinction is that pain resulting from SCC may be re-
prevent irreversible neurologic dysfunction and preserve
lieved by the sitting position and is not relieved, and actually
ambulatory function (Wilkes, 1999).
may increase, when patients assume the supine position. The
A thorough history should be obtained with special atten-
opposite is true for pain secondary to a herniated disk (Scha-
tion to intensity, quality, onset, and duration of symptoms
fer, 1991, 1997; Wilkes). Patients with SCC may complain
(Hunter, 1998). Patients should be questioned regarding
that pain increases at night when lying down to sleep, which
symptoms of motor weakness, sensory loss, motor loss, and
is the opposite pattern from degenerative spine disease (Quinn
autonomic dysfunction. Clinicians should ask patients about
& DeAngelis, 2000).
sexual function and changes in bowel and bladder function,
Patients with preexisting skeletal bone metastasis are at
including incontinence and loss of sphincter control (Buc-
increased risk for SCC. Because these patients often experi-
holtz, 1999). Even if back pain is the only symptom, clinicians
ence chronic back pain secondary to metastasis, early detec-
should suspect SCC in patients with cancer until otherwise
tion of the signs of SCC may be difficult. Any change in the
disproved (Wilkes, 1999).
intensity, location, or nature of a patient's pain can be an early
A thorough physical examination should be completed with
sign of SCC and requires careful and complete assessment
special attention to musculoskeletal and neurologic systems.
(Dietz & Flaherty, 1993).
Vertebral palpation and percussion by the examiner usually can
As the lytic and blastic lesions protrude into the epidural
elicit patient complaints of radicular pain or tenderness at the
space, neurologic symptoms occur and may become irrevers-
level of compression (Bucholtz, 1999; DeMichele & Glick,
ible. The earliest neurologic manifestations include motor
2001; Schafer, 1997). Straight leg raises usually will increase
weakness and sensory loss related to the level and degree of
pain when radicular pain is present (Schafer, 1997). Examiners
SCC (Bucholtz, 1999; Dietz & Flaherty, 1993; Wilkes, 1999).
should raise a patient's straightened leg until pain occurs, then
Motor weakness usually is not the presenting symptom, as the
dorsiflex the foot. Sharp pain radiating from the back down the
development of pain usually precedes motor weakness. The
leg, with increased pain on dorsiflexion, suggests compression
sequence of neurologic symptoms as SCC progresses is pain,
of the nerve roots (Bickley, 1999). Assessment of motor func-
motor weakness, sensory loss, motor loss, and autonomic
tion also includes evaluation of gait, muscle strength, involun-
dysfunction (Schafer, 1997).
tary movements, and coordination (Wilkes, 1999).
Motor weakness often is described as heaviness or stiffness
Assessment of reflexes is an important indication of the
of the extremities and may lead to loss of coordination and
status of the central nervous system. A brisk reflex response
ataxia. If SCC is untreated, motor weakness will progress to
should be elicited normally, which indicates that the arc, or
motor loss and paralysis. Sensory loss includes numbness,
pathway, from the receptor organ to the spinal cord and back
paresthesia, and loss of thermal sensation, and progressive
to the effector organ is intact (Wilkes, 1999). Deep tendon
sensory loss includes loss of proprioception and deep pressure
reflexes may be decreased with nerve root compression and
and vibration sensations (DeMichele & Glick, 2001; Dietz &
hyperactive with cord compression. A positive Babinski sign
Flaherty, 1993; Schafer, 1997; Wilkes, 1999). Sensory dys-
(i.e., dosiflexion of the great toe after stroking the sole of the
function usually begins in the toes and ascends as it reaches
foot from heel to the ball of the foot and then laterally continu-
the level of the lesion. With cauda equina compression, the
ing across the ball of the foot to under the great toe) or sus-
sensory loss is bilateral and usually follows the dermatome
tained ankle clonus also indicate motor involvement (Schafer,
path involving the perianal area, posterior thigh, and lateral
1997). Physical examination should include assessment of
aspect of the leg (Quinn & DeAngelis, 2000).
sensory function such as pain, temperature, touch, vibration,
Autonomic dysfunction is common, generally late, and never
and position (Bickley, 1999). The location of sensory loss
the sole presenting symptom of epidural SCC (Posner, 1995;
helps to pinpoint the site of sensory damage (Wilkes). Exam-
Quinn & DeAngelis, 2000). However, these symptoms may
iners should perform meticulous sensory mapping to elicit the
occur early with cauda equina syndrome. Signs of autonomic
level of SCC (Bucholtz, 1999). Usually the level of positive
dysfunction include impotence and changes in bladder and
sensation is one or two levels below the site of compression
bowel function. Possible urinary symptoms include hesitancy,
(DeMichele & Glick, 2001).
FLOUNDERS VOL 30, NO 1, 2003
teoporosis, and acute adrenal insufficiency with abrupt ste-
roid withdrawal (Belford).
X-ray films of the spine are initial diagnostic tests for SCC.
Radiation therapy is the most common treatment for SCC
These films will show lytic or blastic lesions and can identify
(Bucholtz, 1999; Hunter, 1998; Quinn & DeAngelis, 2000).
up to 85% of vertebral lesions. However, these x-rays cannot
Radiation therapy is delivered over several weeks to a total
detect early SCC, because 50% of the bone must be destroyed
dose of 3,0004,000 cGy (Hunter). The radiation treatment
before the lesions can be detected on x-ray films (Bucholtz,
field usually covers the area of the SCC as well as a margin of
1999). Another problem with x-ray films, significant in lung
one or two vertebral bodies above and below the area of com-
cancer and lymphoma, is that paraspinal masses with exten-
pression (Bucholtz; Loblaw & Laperriere, 1998). Radiation
sion into the epidural space through the foramina may not be
therapy can result in improvement or maintenance of func-
detected (Schafer, 1997). Bone scans are more sensitive than
tional status and relief of pain, which usually occurs up to five
x-rays and may detect vertebral abnormalities when x-ray
days after treatment is initiated (Bucholtz). Side effects of
films are negative (Bucholtz).
radiation therapy include fatigue and skin alterations, includ-
Magnetic resonance imaging (MRI), computerized tomog-
ing erythema, pigmentation, and dry or moist desquamation.
raphy (CT), and myelography are definitive diagnostic tests
Goals of managing the side effects of radiation therapy in-
for SCC (Bucholtz, 1999; DeMichele & Glick, 2001; Wilkes,
clude minimizing symptoms, promoting healing, and prevent-
1999). MRI is superior to CT scans and myelography because
ing infections (Sitton, 1997).
MRI is noninvasive and does not require the injection of con-
Many indications for surgical decompression by laminec-
trast material. However, the addition of gadolinium contrast
tomy or resection of a vertebral body exist. Surgery is con-
with MRI improves detection of disease. Another benefit of
sidered when tumors are not radiosensitive or located in an
MRI is that it can image the entire spine, a necessary function
area that has been previously treated with radiation therapy
because patients may have multiple areas of compression that
(Hunter, 1998). Surgery also is beneficial in obtaining a tu-
are not clinically apparent (Bucholtz). CT scanning with IV
mor specimen to establish a tissue diagnosis in patients with
contrast allows identification of paraspinal masses and early
no known primary site of malignancy (Bucholtz, 1999). Sur-
lesions not seen on x-ray films but does not image the entire
gery is necessary if infection or epidural hematoma must be
spine (Schafer, 1997; Wilkes). Myelography commonly has
ruled out or if high cervical spinal cord lesions are present
been replaced by MRI but can be used when MRI is nondiag-
that can cause respiratory paralysis without prompt treat-
nostic or cannot be completed (Wilkes). Lumbar puncture
ment (DeMichele & Glick, 2001). A surgical approach is
may be performed to examine the CSF but is not diagnostic of
beneficial with spinal instability or when neurologic deterio-
SCC. Elevation of CSF proteins to levels greater than 100 mg/
ration progresses despite ongoing radiation therapy (Schafer,
ml has been noted in most patients with SCC (DeMichele &
1997). Potential complications related to surgery include
Glick). Positron emission tomography can complement the in-
standard postoperative risks (e.g., stroke, hematoma, deep
formation obtained from MRI or CT (Belford, 1997).
vein thrombosis, pulmonary embolism, wound dehiscence),
CSF leak, or neurologic deficits (Belford, 1997).
Corticosteroids, radiation therapy, and surgery are the stan-
dard treatment options for patients with SCC (Belford, 1997;
Bucholtz, 1999; DeMichele & Glick, 2001; Hunter, 1998;
Through accurate assessment of pain and musculoskeletal
Posner, 1990; Quinn & DeAngelis, 2000; Schafer, 1997;
and neurologic changes, oncology nurses can detect the early
Wilkes, 1999). The goals of treatment are pain relief and pres-
signs of SCC and provide interventions to prevent neurologic
ervation and restoration of neurologic function (Bucholtz), as
dysfunction (Bucholtz, 1999). Accurate pain and neurologic
well as reduction of tumor bulk. Treatment of SCC often is
assessment should be the standard of care for all patients on
palliative in intent because it usually is associated with other
a routine basis, allowing subtle changes in patient status to be
metastatic disease (Quinn & DeAngelis). Treatment of the
detected early. In addition, oncology nurses should provide
underlying primary cancer must be reevaluated. The choice of
pharmacologic and nonpharmacologic interventions to relieve
treatment for SCC depends on the tumor type, location, ag-
pain. Nurses should provide interventions to prevent compli-
gressiveness, and radiosensitivity (Bucholtz, 1999). In addi-
cations from immobility and sensory-motor deficits, includ-
tion, effective pain management may require titration of nar-
ing attention to bladder and bowel function (Wilkes, 1999).
Nurses should assess patients for complications of SCC treat-
Corticosteroid therapy usually is the initial treatment of
ment. Assessment and interventions for inadequate coping
SCC until more definitive treatment, such as radiation
and potential depression should be included in the plan of
therapy or surgery, can be instituted (Quinn & DeAngelis,
care. Discharge planning should include consideration of re-
2000). Corticosteroids are used to decrease spinal cord
ferral for home visiting nurses or hospice care as needed.
edema and inflammation, which can relieve pain and neuro-
logic symptoms (Wilkes, 1999). Corticosteroids also may
The authors would like to thank John Sprandio, MD, of Consultants in
have an oncolytic effect on some tumors (Hunter, 1998). A
Medical Oncology and Hematology, Drexel Hill, PA, for reviewing this manu-
schedule for corticosteroid administration often includes a
loading dose of high-dose dexamethasone (100 mg) fol-
lowed by tapering doses over a period of days (Belford,
Author Contact: Jo Ann Flounders, RN, MSN, OCN®, CHPN, can
1997; Posner, 1990). Corticosteroids can cause gastrointes-
be reached at email@example.com, with copy to editor at rose
tinal bleeding, hyperglycemia, psychosis, myopathy, os-
ONF VOL 30, NO 1, 2003
Belford, K. (1997). Central nervous system cancers. In S. Groenwald, M.
Quinn, J., & DeAngelis, L. (2000). Neurologic emergencies in the cancer
Frogge, M. Goodman, & C. Yarbro (Eds.), Cancer nursing (4th ed., pp.
patient. Seminars in Oncology, 27, 311321.
721741). Boston: Jones and Bartlett.
Schafer, S. (1991). Oncologic complications: Spinal cord compression. In S. Otto
Bickley, L. (1999). Bates' guide to physical examination and history taking
(Ed.), Oncology nursing (pp. 468526). St. Louis, MO: Mosby Year Book.
Schafer, S. (1997). Oncologic complications. In S. Otto (Ed.), Oncology nurs-
(7th ed.). Philadelphia: Lippincott.
Bucholtz, J. (1999). Metastatic epidural spinal cord compression. Seminars in
ing (3rd ed., pp. 406 474). St. Louis, MO: Mosby Year Book.
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Siegal, T.A., & Siegel, T.E. (1989). Current considerations in the management
of neoplastic spinal cord compression. Spine, 14, 223228.
Byrne, T. N. (1997). Metastatic epidural spinal cord compression. In P. Black
& J. Loeffler (Eds.), Cancer of the nervous system (pp. 664 673). London:
Sitton, E. (1997). Managing side effects of skin changes and fatigue. In K.
Dow, J. Bucholtz, R. Iwamoto, V. Fieler, & L. Hilderley (Eds.), Nursing
care in radiation oncology (2nd ed., pp. 79100). Philadelphia: Saunders.
DeMichele, A., & Glick, J. (2001). Cancer-related emergencies. In R.
Lenhard, R. Osteen, & T. Gansler (Eds.), Clinical oncology (pp. 733764).
Wilkes, G. (1999). Neurological disturbances. In C. Yarbro, M. Frogge, & M.
Goodman (Eds.), Cancer symptom management (2nd ed., pp. 344381).
Atlanta, GA: American Cancer Society.
Dietz, K., & Flaherty, A. (1993). Oncologic emergencies. In S. Groenwald, M.
Boston: Jones and Bartlett.
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800839). Boston: Jones and Bartlett.
For more information . . .
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tem. In B. Bullock & R. Henze (Eds.), Focus on pathophysiology (pp. 938
➤ Merck Manual: Spinal Cord Disorders
978). Philadelphia: Lippincott.
Hunter, J. (1998). Structural emergencies. In J. Itano & K. Taoka (Eds.), Core
curriculum for oncology nursing (3rd ed., pp. 340354). Philadelphia:
➤ Surgical Tutor: Spinal Cord Compression
Loblaw, D., & Laperriere, N. (1998). Emergency treatment of malignant ex-
tradural spinal cord compression: An evidence-based guideline. Journal of
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Links can be found using ONS Online at www.ons.org.
of Medicine, 322, 544545.
Posner, J. (1995). Neurologic complications of cancer. Philadelphia: Davis.
FLOUNDERS VOL 30, NO 1, 2003
ONF Continuing Education Examination
Oncology Emergency Modules:
Spinal Cord Compression
c. Prevent the further spread of the primary tumor.
Contact Hours: 1.2
d. Relieve all of the pain caused by the compression.
Passing Score: 80%
The patient with a spinal cord compression is likely to
Test ID # 03-30/1-01
describe his or her pain as
Test Processing Fee: $15
a. Relieved when sitting.
b. Decreased when supine.
The Oncology Nursing Society is accredited as a provider
c. Similar to a previous herniated disk.
of continuing education (CE) in nursing by the
d. Increased in the morning when getting out of bed.
· American Nurses Credentialing Center's Commission on
A patient is to begin radiation therapy. The nurse should
teach the patient that the
· California Board of Nursing, Provider #2850.
a. Radiation therapy will target the entire spinal cord.
b. Radiation therapy will reverse all existing neurologic
CE Test Questions
damage from the compression.
11. The most critical prognostic factor in spinal cord com-
c. Relief of symptoms will begin to occur approximately
pression is the
five days after the start of treatment.
a. Patient's support system.
d. Side effects of radiation are only local, unlike the sys-
b. Amount of disease progression.
temic reactions of chemotherapy.
c. Location of the spinal cord compression.
What discharge instruction is the most appropriate for the
d. Neurologic status before initiation of therapy.
nurse to give to a patient who has a spinal cord compres-
12. Which is likely to be the first presenting sign or symptom
of spinal cord compression?
a. Chemotherapy will be effective in treating the com-
a. Loss of coordination
b. Pain in the neck or back
b. Immediately report any change in pain level or motor
c. Bowel and bladder dysfunction
d. Sensory loss in the feet and legs
c. Lifting heavy loads should be avoided until the lami-
13. A patient comes to the clinic describing a "tight band
nectomy incision is healed.
across her chest and upper abdomen." From her history,
d. Bladder and bowel dysfunction are likely to occur as
which information would be most significant?
a result of the compression.
a. History of panic attacks
Which finding from a patient's physical examination is
b. History of stage III breast cancer
most indicative of a spinal cord compression?
c. Familial history of cardiac disease
a. Brisk deep tendon reflexes
d. History of gastroesophageal reflux
b. A negative Babinski reflex
14. Spinal cord compression most often results from
c. Decreased pain with straight leg raises
a. The adenopathy of prevertebral lymph nodes.
d. Pain and tenderness with vertebral percussion
b. The hematogenous spread of cancer from a primary site.
The medical intervention most frequently used to treat a
c. A malignant neoplasm arising from the spinal cord.
spinal cord compression includes
d. The seeding of cerebral spinal fluid with cancerous
a. High doses of narcotic analgesia for pain control.
b. Chemotherapy regimens to treat the primary cancer.
15. Which nursing diagnosis should the nurse plan to address
c. A loading dose of corticosteroids followed by tapering
first for a patient with an early stage of a spinal cord com-
pression undergoing radiation?
d. Maintaining high doses of corticosteroids throughout
a. High risk for pain
b. High risk for impaired mobility
The diagnostic procedure with the highest sensitivity of
c. High risk for ineffective coping
detecting spinal cord compression is
d. High risk for alteration in healing
a. X-ray of the spine.
16. The major goal of spinal cord compression treatment is to
b. Computerized tomography.
a. Increase the patient's life expectancy.
c. Magnetic resonance imaging.
b. Preserve and restore the neurologic function.
d. Positron emission tomography.
ONF VOL 30, NO 1, 2003
13. The most frequent location of malignant invasion of the
bowel movements. The nurse would suspect that the spi-
spinal cord that causes spinal cord compression is the
nal cord compression has progressed to which stage of
a. Intradural area of the sacral spine.
b. Extradural area of the thoracic spine.
a. Motor loss
c. Intramedullary area of the lumbar spine.
b. Sensory loss
d. Extravertebral area of the cervical spine.
c. Motor weakness
14. A patient describes the lack of ability to bear down with
d. Autonomic dysfunction
Oncology Nursing Forum Answer/Enrollment Form
Oncology Emergency Modules: Spinal Cord Compression (Test ID # 03-30/1-01)
4. The deadline for submitting the answer/enrollment form is
To receive continuing education (CE) credit for this issue, simply
1. Read the article.
two years from the date of this issue.
2. Take the test and record your answers on the form below.
5. Contact hours will be awarded to RNs who successfully com-
Also, complete the program evaluation listed below. (You
plete the program. Successful completion is defined as an
may make copies of the answer form.)
80% correct score on the examination and a completed pro-
3. Mail the completed answer/enrollment form along with a
gram evaluation. Verification of your CE credit will be sent
check or money order for $15 per test payable to the Oncol-
to you. Certificates will be mailed within six weeks follow-
ogy Nursing Society. Payment must be included for your ex-
ing receipt of your answer/enrollment form. For more infor-
amination to be processed.
mation, call 866-257-4667, ext. 6296.
I n s t r u c t i o n s : Mark
your answers clearly by
placing an "x" in the
box next to the correct
answer. This is a stan-
dard form; use only the
number of spaces re-
quired for the test you
Social Security #
State(s) of licensure/license no(s).
Not at all
1. How relevant were the objectives to the CE activity's goal?
2. How well did you meet the CE activity's objectives (see page E17)?
· Objective #1
· Objective #2
· Objective #3
3. To what degree were the teaching/learning resources helpful?
Appropriate Too complex
4. Based on your previous knowledge and experience, do you think
that the level of the information presented in the CE activity was
5. How long did it take you to complete the CE activity?
❑ My check or money order payable to the Oncology Nursing Society is enclosed. U.S. currency only. (Do not send cash.)
After completing this form, mail it to: Oncology Nursing Society, P.O. Box 3510, Pittsburgh, PA 15230-3510.
For more information or information on the status of CE certificates, call 866-257-4667, ext. 6296.
FLOUNDERS VOLNO 1, 20032003
ONF VOL 30, 30, NO 1,