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Cord
Compression
Etiology/physiology
A spinal cord compression is most commonly caused by the metastases
of tumors such as prostate, lung, and breast. Most of these lesions
occur in the thoracic spine, but the lumbosacral and cervical regions
may also be affected. A cord compression may occur at any time
during the disease course, from presentation and initial diagnosis
to advanced, terminal disease.
Assessment/diagnosis
Pain evaluation - Back pain is the most common presenting symptom,
occurring in approximately 95% of patients. Pain is gradual at
onset becoming progressively more severe. This pain may be experienced
as
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- localized pain - occurring over the area of tumor, caused by the
destruction of bone. Pain is constant, may increase with supine position,
and may cause the patient to wake at night.
- radicular pain - caused by pressure on the nerve roots, experienced
in the affected dermatome. Thoracic lesions - bilateral pain, 'squeezing
tight band' around chest or abdomen. Cervical, lumbosacral - usually
unilateral. Worsened by supine position, sneezing, or valsalva meneuver,
relieved by sitting upright (opposite to slipped disc pain).
- Referred pain - multiple dermatomes involved, tends to be 'burning'
or 'shooting' If this pain is not recognized and treated, neurologic
dysfunction will follow.
- Change in motor function - described as 'weakness' or 'heaviness'
sensation, may lead to loss of coordination, ataxia, and paralysis.
Without intervention, weakness will progress (sometimes abruptly) to
motor loss. Assessment includes evaluation of gait, muscle strength,
involuntary movements, and coordination. Degrees of neurologic damage
- the extent of the compression of the spinal cord determines the degree
of neurologic damage. Ambulatory status at the time of diagnosis is
a major predictor of ability to walk after treatment. Approximately
70% of ambulatory patients diagnosed with spinal cord compression are
still able to walk after treatment. Unfortunately, paralysis lasting
more than 24 hours before treatment is not usually reversible.
- Change in sensory function - manifested initially by paresthesias
(numbness and tingling of toes and fingers), progressing to decreased
sensation. Without intervention, decreased sensation progresses to
sensory loss, including losses of proprioreception, vibrations, and
deep pressure.
- Change in bowel and bladder function - related to lower motor neuron
functions of bowel and bladder. Difficulty initiating urination can
progress to urinary retention, overflow, or incontinence. Bowel dysfunction
can be manifested by loss of rectal sensation, constipation or (very
late) fecal incontinence with poor sphincter control.
Diagnostic tests
MRI of spine is performed to identify the precise location of spinal
cord compression and identify paraspinal masses.
Treatment
- Corticosteroids - high doses of dexamethasone are given initially,
then gradually tapered to maintenance doses. Dose and treatment duration
are based on the patient's response to the steroids. Some complications
of steroid use: include emotional lability, hyperglycemia, fluid retention,
increased risk of infection, gastric ulcers, myopathy, and cushingoid
features.
- Radiation therapy - the treatment of choice for decompression,
to be initiated immediately. Doses of 2000 - 3000 cGy are usually delivered
over 1 - 2 weeks to a radiation port extending two vertebrae above
and below the area of compression.
References:
- Bucholtz, J.D. 1999. Metastatic Epidural Spinal Cord Compression.
Seminars in Oncology Nursing, 15(3). pp 150-159.
- Quinn, J.A. and DeAngelis,
L.M. 2000. Neurologic Emergencies in the Cancer Patient. Seminars
in Oncology, 27(3) pp 311-321.
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