43. SPINAL CORD COMPRESSION






SCC is a compression of the thecal sac by a tumor in the epidural space, at the level of either the spinal cord or the cauda equina (Abrahm, 2004). Most cancers cause SCC as a result of metastatic disease to the vertebral column. The spinal cord can be compressed as a result of direct extension from a metastatic lesion in the vertebral body. In addition, frank bone collapse can occur, adding to the compression. Some patients, particularly those with lymphoma or retroperitoneal tumors, may develop SCC from tumors that grow through the intravertebral foramen and compress the spinal cord without involving the vertebrae (Prasad & Schiff, 2005; Abrahm, 2004; Gabriel & Schiff, 2004; Schiff, 2003).

Injury to the spinal cord from direct extension of a tumor or metastatic disease occurs as a result of ischemia and edema. In response to tissue injury and hypoxia, prostaglandins and vascular endothelial growth factors are released. The release of these inflammatory substances results in increased vascular permeability and vasogenic edema. Subsequent edema and hypoxia results in neuronal injury, ischemia, and infarction. Once the spinal cord infarcts, neurologic damage is permanent (Prasad & Schiff, 2005; Abrahm, 2004; Gabriel & Schiff, 2004; Schiff, 2003).


EPIDEMIOLOGY AND ETIOLOGY

SCC occurs in 2.5% to 5% of adult patients with terminal cancer. However, the cumulative incidence of SCC in adults declines with age. The prevalence of SCC in children ranges from 4% to 5.5%. The prevalence of SCC varies with the site of the cancer; 15% to 20% of cases are seen in patients with prostate, breast, and lung cancers. About 5% to 10% of cases occur in patients with non-Hodgkin’s lymphoma, multiple myeloma, or renal cancer (Abrahm, 2004; Klimo & Schmidt, 2004).


RISK PROFILE








• Cancers of the breast, prostate, lung, kidney, and thyroid; non-Hodgkin’s lymphoma, myeloma, sarcoma, lymphoma, leukemia, neuroblastoma, chordoma, neurofibroma, meningioma, glioma, epidermoid, and gastrointestinal cancers; rare in retinoblastoma (Chang et al., 2006).


• Cancer treatment that leads to lytic lesions in the vertebrae; development of a granulomatous mass from intrathecal morphine (Miele et al., 2006).


PROGNOSIS

Patients with SCC that is localized to a single site have a better prognosis. Median survival according to tumor type is shown in Table 43-1. A positive correlation exists between preoperative motor status and treatment outcomes. For example, 75% to 100% of patients who are ambulatory at the time of diagnosis are ambulatory after treatment. In contrast, only 14% to 35% of paraparetic and 15% of paralyzed patients regain useful function after treatment for SCC. Loss of sphincter control at the time of diagnosis is associated with a poor prognosis (Schiff, 2003).






















Table 43-1 MEDIAN SURVIVAL AFTER SCC
Modified from Abrahm, J. L. (2004). Assessment and treatment of patients with malignant spinal cord compression. Journal of Supportive Oncology, 2(5):377-388, 391.
Cancer Diagnosis Median Survival (Months)
Lymphoma 6.7
Multiple myeloma 6.4
Breast cancer 5
Prostate cancer 4
Lung cancer 1.5


PROFESSIONAL ASSESSMENT CRITERIA (PAC)




1. General pain assessment parameters include onset, description, location, severity, aggravating and relieving factors, previous treatments and effectiveness, and associated symptoms. Pain is the most frequent initial symptom of SCC. At the time of diagnosis, 83% to 95% of patients have had pain for a median of 8 weeks.


• Pain is usually localized to the involved spinal segment.


• Characteristics of the localized pain include a gradual onset (usually) and an increase in pain with movement, coughing, sneezing, or the Valsalva maneuver.


• Pain may be worse after a period of lying down.


• Pain can be radicular in nature.


• Vertebral tenderness can occur over the site of SCC.


• Neck flexion often produces pain of a local or radicular nature at the site of the lesion.


2. Weakness occurs in 60% to 85% of patients at the time of diagnosis.


• Approximately two thirds of patients are not ambulatory at the time of diagnosis.


• Weakness is most severe with thoracic SCC.


• The pretreatment neurologic status is the most important predictor of function after treatment for SCC.


3. Motor examination includes an evaluation of muscle strength, muscle tone, motor deficits (e.g., ataxia), coordination, abnormal muscle movements, and deep tendon reflexes.


• Both the upper and lower extremities must be evaluated.


• Damage to the corticospinal tracts usually results in spasticity, spastic paralysis, hyperreflexia, and a positive Babinski’s reflex.


• Damage to the lower motor neurons usually results in hypotonicity, flaccid paralysis, hyporeflexia, and muscular atrophy.


• Any weakness associated with back pain in a patient with cancer requires an evaluation for SCC.


4. Sensory changes occur in 40% to 90% of cases of spinal cord compression. Patients may be less aware of sensory changes than weakness or motor deficits.


• Assessment should include evaluation of light touch, temperature, pinprick, position, and vibration.


• Sensory deficits result from pressure on the spinothalamic tracts (STTs). Initial involvement of the anterior STT results in the loss of light touch. Involvement of the lateral STT results in the loss of pain and temperature. Lesions in the posterior columns cause changes in proprioception.



6. CT scan provides valuable information about the vertebral columns and paravertebral structures. It is more sensitive than plain x-ray films and bone scans in distinguishing between benign and malignant lesions. Also, a CT scan is needed to plan the management of SCC.


7. A bone scan is more sensitive than plain x-ray films in detecting SCC. However, it is less sensitive than CT or MRI. A bone scan can show multiple lesions and has a diagnostic accuracy of approximately 66%.


8. Plain x-ray films image collapsed vertebral bodies in 75% of patients.


NURSING CARE AND TREATMENT




1. Administer corticosteroids to reduce edema.


2. Perform pain assessment at least q8hr.


3. Perform motor assessment (strength and movement of upper and lower extremities; deep tendon reflexes).


4. Perform sensory examination (light touch and pinprick).


5. Evaluate for bowel and bladder dysfunction.


6. Assess for ataxia.


7. Administer analgesics to reduce pain.


8. Obtain and assess: CT/MRI for location and degree of SCC.


9. Intake and output (I & O) q4-8hr.


10. Activity as tolerated.


11. Initiate a bowel regimen to prevent opioid-induced constipation.


12. Perform skin assessments if patient’s mobility is decreased.

Oct 19, 2016 | Posted by in NURSING | Comments Off on 43. SPINAL CORD COMPRESSION

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