Spinal Cord Compression



Spinal Cord Compression


Brenda K. Shelton



I. Definition:

Spinal cord compression (SCC) is a disorder caused by direct pressure or compromised vascular supply to the spinal cord or cauda equina.

A. Approximately 5% to 10% of patients with metastatic cancer develop SCC.

B. Although more commonly associated with metastatic disease, 8% to 35% of cases of SCC present as the initial manifestation of cancer.

C. Patients rarely die from SCC; however, it is considered a medical emergency because delay in treatment can result in irreversible paralysis and loss of voluntary and involuntary sphincter control.

D. Once a severe neurologic deficit has occurred, treatment is unlikely to reverse the deficit. In one large study, 90% of patients who were nonambulatory at the time of diagnosis remained paraplegic after treatment.


II. Etiology

A. Cord ischemia or necrosis with neurologic impairment occurs by three processes.

1. Direct compression of the spinal cord or cauda equina

a. The most common means of compression is progressive tumor expansion within the vertebral column with later invasion of the epidural space either by direct extension, lymph node growth through the epidural space, or by hematogenous spread.

b. This pathophysiology is most typical of cancers of the lung, prostate, breast, and kidney.

2. Interference in vascular supply to the spine

3. Compression due to pathologic fracture and vertebral collapse: Direct tumor extension into the vertebral body occurs with lymphomas, multiple myeloma, and neuroblastoma.

B. SCC can occur anywhere along the spinal cord and is related to the location of the primary or metastatic tumor causing cord injury.

1. The frequency of distribution in cord compression cases is: cervical (10%), thoracic (70%), and lumbosacral (20%).

2. Common malignant associations (occurring in >10% of patients)

a. Multiple myeloma

b. Lung cancer

c. Prostate cancer

d. Breast cancer

e. Renal cell cancer

3. Infrequent but possible malignant associations

a. Lymphoma

b. Malignant melanoma

c. Head and neck cancer



III. Patient Management

A. Assessment: Signs and symptoms of SCC vary based on the site and extent of infiltration. The symptomatology of SCC is consistent, regardless of the originating tumor. The time interval from the diagnosis of the primary cancer to that of SCC depends on the type of tumor and its metastatic potential.

1. The location of pain, sensory, and motor symptoms depends on the site of compression and on the nerves involved. Table 37-1 depicts a summary of clinical symptoms according to site of involvement.

2. Localized or radicular back pain is the earliest and most common symptom, preceding other symptoms by several months.

a. The onset of pain is usually gradual and progressive and can be focal, radicular (resulting from compression of a nerve root), or referred.

b. The distribution of radicular pain is contingent on the level of spinal involvement.

c. Pain associated with SCC is usually unremitting and is exacerbated over an affected area or in the dermatome of the affected nerve root.

d. Pain can be elicited by having the patient, while in a supine position, flex the neck or raise legs straight.

e. Back pain associated with SCC is also unique because it can be exacerbated by manual palpation of the area.

3. Sensory deficits include numbness and paresthesias.

a. Patients complain of numbness and tingling or feelings of coldness in the affected area. Often, a sensation of “heaviness” in the affected extremities accompanies these symptoms.

b. Numbness typically begins in the toes and gradually ascends to the level of spinal cord involvement.

4. Most patients experience weakness by the time SCC is diagnosed; it chronologically occurs after sensory changes.

a. Because most cord compression is at or below the thoracic area, lower extremity weakness is most common.

b. Motor weakness may present in the form of an unsteady gait, ataxia, or favoring the affected extremity.

5. Approximately half of patients exhibit autonomic dysfunction, such as bowel or bladder difficulties, at diagnosis; this is associated with a poorer prognosis.

a. Constipation is an early indication of neurologic impairment, resulting from decreased neurologic stimulus for peristalsis; however, loss of sphincter control with intractable constipation occurs as cord compression worsens. Diminished urge to defecate and inability to bear down are initial signs of autonomic dysfunction involving the bowel, which contributes to constipation, obstipation, and, finally, incontinence.

b. Urinary dysfunction begins with hesitancy and incomplete voiding and progresses to urinary retention and, finally, incontinence, when the bladder is filled to capacity and unable to empty. Increased postvoid volume after catheterization may be an indication of early autonomic dysfunction.









TABLE 37-1 Signs and Symptoms of Spinal Cord Compression







































































Location of Lesion


Physical Symptoms


Autonomic Symptoms


Cervical spine


Radicular pain in the neck, occipital region, and shoulders (pain is many times provoked by neck movement)


Hypotension



Bradycardia



Quadriplegia


Loss of temperature autoregulation



Upper extremity weakness (may be spastic or atrophy)


Autonomic hyperreflexia



Sensory loss in area of weakness


Gastric hypersecretion and paralytic ileus



Weakness or paralysis of the diaphragm may occur with lesion at or above C4 (may be unilateral or bilateral)


Reflex bowel, bladder, and penile erection



Hoffman’s sign (flicking of the middle finger induces flexion of the ipsilateral thumb or index finger)


Thoracic spine


Pain (may be local, radicular, or both)


Venous stasis and associated complications



Paraplegia


Reflex bowel, bladder, and penile erection



Sensory loss below the level of the lesion



Reflex abnormalities distal to the lesion


Lumbar spine


Bowel and bladder dysfunction


Venous stasis and associated complications



Extensor plantar response


Reflex bowel, bladder, and penile erection


Cauda equina


Pain (may be local, referred, or radicular)


Areflexic bowel, bladder, and erection



Sphincter disturbances



Loss of buttock and leg sensation



Lower extremity weakness/paralysis



From Byrne, T. N., & Waxman, S. G. (1990). Clinical pathophysiology of spinal signs and symptoms. In Spinal cord compression (pp. 49-54). Philadelphia: F. A. Davis; Garner, C. (1999). Cancer-related spinal cord compression. American Journal of Nursing, 99(7), 34-35; Glaser, J. A., Cure, J. K., Bailey, K. L., Morrow, D. L. (2001). Cervical spinal cord compression and the Hoffmann sign. Iowa Orthopedic Journal, 21, 49-52; Rude, M. (2000). Selected neurologic complications in the patient with cancer. Brain metastases and spinal cord compression. Critical Care Nursing Clinics of North America, 12(3), 269-279; Wilson, S. (1993). Acute spinal cord injury. In J. E. Wright & B. K. Shelton (Eds.), Desk reference for critical care nursing (p. 328). Boston: Jones & Bartlett.



6. SCC can also affect the nerves controlling penile erection or ejaculation, causing altered sexual function in many patients.

B. Diagnostic Parameters: There are no serum or urine tests used to diagnose spinal cord compression; however, other tests can indicate the condition.

1. Spinal x-rays are performed to show bone deformities (eg, necrotic bone lesions from metastatic tumor). Although these are not specifically diagnostic for SCC, they are used to validate a potential etiologic factor in the presence of suspicious symptoms.

2. Magnetic resonance imaging (MRI) is used to identify precisely the location of all lesions. MRI is sensitive to neurologic tissue and has the ability to distinguish between extradural, intradural, and extramedullary lesions. The disadvantage of this diagnostic test is that it requires the patient to remain motionless for approximately 1 hour in a small, confined space. If the patient moves during the examination, it results in poor imaging.

3. Myelogram of the spine is the injection of dye into the epidural space. It can be used to diagnose SCC. The flow of dye and any obstructions encountered will show up on a nuclear scan of the area. This diagnostic test has been replaced by MRI for diagnosis of SCC because MRI (1) is noninvasive, (2) is more sensitive diagnostically, (3) images the entire spine, and (4) can indicate the presence of SCC as well as presence of paraspinal masses. The benefits of a myelogram are that cerebrospinal fluid sampling can occur, enabling meningeal carcinomatosis to be ruled out. The myelogram can be used when MRI assessment cannot explain neurologic deficits.

C. Treatment

1. Corticosteroids are immediately administered intravenously to reduce inflammation and edema. An initial bolus of 16 to 100 mg dexamethasone (Decadron) is given, followed by 4 mg four times a day for about 14 days. A comparable steroid potency dose of hydrocortisone may be used as an alternative to dexamethasone.

2. Radiation therapy is the best treatment for SCC because response rates are equivalent to those with surgery, but with less morbidity. Treatment must be implemented immediately for optimal reversal of neurologic deficits.

a. Maximal tolerated lifetime radiation exposure of the spine is 6,000 Cy.

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Sep 16, 2016 | Posted by in NURSING | Comments Off on Spinal Cord Compression

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