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Lumbar Spine SurgeryA Guide to Preoperative and Postoperative Patient Care

AANN Reference Series for Clinical Practice

This publication was made possible through an unrestricted charitable contribution from Medtronic’s Spinal and Biologics Division.

Committee on Reference Series for Clinical Practice

2004 CommitteeKathy Baker, MBA BSN RN CCRN CNRN, ChairKirsten Featherstone, MS RN CCRNLaura McIlvoy, PhD RN CCRN CNRNBarbara Mancini, MBA BSN RN CNAA CNRN

2006 CommitteeJanette Yanko, MN RN CNRN, ChairDonna Avanecean, MSN RN FNP-C CNRNCathy Cartwright, MSN RN PCNS

AANN National OfficeBarbara Schweizer, MBA BSN RNExecutive Director

Anne T. CostelloSenior Education Manager

Deborah S. WilliamsManaging Editor

Sonya L. JonesGraphic Designer

Lumbar Spine Task Force

ChairSusan Ware, MSN RN ARNP CCRN CNRN

AuthorAndrea Strayer, MSN AGNP CNRN

Contributing AuthorsAngela Starkweather, PhD ANCP RN CNRN CCRNPatricia Pagnotta, MSN RN CNRNDolores Emmons, BA RNJoseph Haymore, MS RN CCRN CNRN ACNP

Content ReviewersKaren Bouwman, MSN BC RN CNRNRich Jones, BSN CNRN NP RNFAPam Shadley, MS RN CNRNAngela Starkweather, PhD ANCP RN CNRN CCRN

AcknowledgmentThis publication was made possible through an unrestricted charitable contribution from Medtronic’s Spinal and Biologics Division.

Publisher’s NoteThe authors, editors, and publisher of this document neither represent nor guarantee that the practices described herein will, if followed, ensure safe and effective patient care. The authors, editors, and publisher further assume no liability or responsibility in connection with any information or recommendations contained in this document. These recommenda-tions reflect the American Association of Neuroscience Nurses’ judgment regarding the state of general knowledge and practice in their field as of the date of publication and are subject to change based on the availability of new scientific information.

Copyright © 2006, revised December 2009, by the American Association of Neuroscience Nurses. No part of this publica-tion may be reproduced, photocopied, or republished in any form, print or electronic, in whole or in part, without writ-ten permission of the American Association of Neuroscience Nurses.

Lumbar Spine SurgeryA Guide to Preoperative and Postoperative Patient Care

AANN Reference Series for Clinical Practice




To meet its members’ needs for educational tools, the American Association of Neuroscience Nurses (AANN) has created a series of guides to patient care called AANN Reference Series for Clinical Practice. Each guide has been developed based on current literature and is built upon best practices. The purpose is to help registered nurses, pa-tient care units, and institutions provide safe and effective care to patients who are undergoing lumbar spine surgery.

The personal and societal impact of low back pain is significant. Between 70% and 85% of all people have back pain at some time in their life (Chou & Huffman, 2009); low back pain is the second most common reason for seeking care from a primary care physician. Lumbar spine disor-ders are the most common cause of disability in persons younger than 45 years of age (Chou, Loeser, Owens et al., 2009). More than 500,000 lumbar procedures are performed each year for the treatment of lumbar spine disorders (Katz, 2006). Of those with low back pain, approximately 151,000 undergo a lumbar fusion each year (Lipson, 2004).

The direct and indirect costs of low back disorders amount to billions of dollars annually.

Whether the patient experiences intermittent low back pain or lumbar spine pathology refractory to conservative management requiring a lumbar fusion, neuroscience nurses are pivotal in assessment, treatment, and continuing care. Resources and recommendations for practice should enable the nurse to make decisions that will optimize pa-tient outcomes.

This reference is an essential resource for nurses respon-sible for the care of spine patients. It is not intended to replace formal education but rather to augment the knowl-edge of clinicians and provide a readily available reference tool.

Neuroscience nursing and AANN are indebted to the volunteers who have devoted their time and expertise to this valuable resource, created for those who are commit-ted to neuroscience patient care.

Preface

Contents

Lumbar Spine Functional Anatomy and Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

Diagnostic Studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

Lumbar Spine Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Herniated Nucleus Pulposus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Cauda Equina Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Lumbar Stenosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

Spondylosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Spondylolisthesis and Spondylolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Degenerative Disc Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Degenerative Scoliosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

Treatment of Lumbar Spine Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

Medical Treatment of Lumbar Spondylosis, Spondylolisthesis, Spondylolysis, and Degenerative Disc Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

Surgical Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

Case Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39

Lumbar Spine Surgery: A Guide to Preoperative and Postoperative Patient Care 3

4 AANN Reference Series for Clinical Practice

I. Lumbar VertebraeThe lumbar spine is formed by five vertebrae. The verte-brae are commonly referred to as L1 through L5. L1 is the most superior vertebra in the lumbar spine, and it abuts the thoracic spine, whereas L5 is the most inferior vertebra and abuts the sacral spine. The anterior or ventral element of each vertebra is called the vertebral body. The vertebral bodies of the middle and lower lumbar spine are more sub-stantial in size to allow them to bear greater loading forces.

Posteriorly, or dorsally, each vertebra has a bony arch that encircles the spinal canal. It is composed of two transverse processes, two sets of facet joints, two pedicles, two laminae, and one spinous process. The bony arch, also referred to as the posterior elements, is quite bulky. It pro-vides the necessary support for upright posture (Figure 1). The noncompromised spinal canal has ample room for the cauda equina and for cerebrospinal fluid (CSF).

Facet joints (bilaterally) are composed of a superior articulating process and an inferior articulating process. The superior articulating process forms a joint with the inferior articulating process of the vertebra above (e.g., superior artic-ulating processes of L3 forms two facet joints with the inferior articulating processes of L2). They have a loose capsule and a synovial lining; thus they are apophyseal joints (Figure 2).

The nerve root canal, also called the lateral recess, is adjacent to the pedicles and facet joints in the region of the foramina. It encompasses the nerve root as it exits the spinal cord (Figure 3). The neural foramina, also referred to as the intervertebral foramina, is the actual far-lateral exit opening of the nerve root canal (Choi, 2009). The lumbar vertebral, or spinal, canal is supported anteriorly by the posterior edge of the vertebral body as well as the posterior longitudinal ligament. This ligament lies on the posterior

vertebral body surface. The lateral elements of the vertebral canal are the pedicles and the facet joints, with correspond-ing articular capsules. Posteriorly, the vertebral canal is formed by the laminae and ligamenta flava.

II. Intervertebral DiscEach intervertebral disc in the lumbar spine provides support and facilitates movement while resisting excessive movement. The disc permits slight anterior flexion, posterior extension, lateral flexion, rotation, and some circumduction (Shankar, Scarlett, & Abraham, 2009). The disc is the largest avascular structure in the body (Singh, Masuda, Thonar, et al., 2009). It is composed of the nucleus pulposus and the annulus fibrosus. In someone less than 35 years old, the nucleus pul-posus is soft, rather like crab meat in texture. With aging, the nucleus pulposus dehydrates.

Surrounding the nucleus pulposus is the annulus fibro-sus, which is tough and fibrous. The fibers of the annulus fibrosus are concentric, like the layers of a radial tire. The concentric arrangement provides great resistance and strength. Each disc is bonded to the vertebral body below and above it by a thin cartilaginous plate, referred to as the endplate (Figures 4, 5). The endplate resists herniation of the disc into the vertebral body and gives the disc its shape (Hicks, Morone, & Weiner, 2009).

III. LigamentsEach disc is reinforced anteriorly by the anterior longitudi-nal ligament and posteriorly by the posterior longitudinal ligament. The laminae are connected by an elastic yellow ligament called the ligamentum flavum. Each facet joint is connected to a capsular ligament. The transverse processes are connected by intertransverse ligaments. The rotator brevis and rotator longus ligaments connect the transverse processes to the laminae of the superior two vertebrae. The

Figure 1. Lumbar vertebra

Figure 2. Lumbar spine: Posterior view

Lumbar Spine Functional Anatomy and Physiology


spinous processes are connected by the supraspinous and infraspinous ligaments (Figures 6, 7, 8; Choi, 2009).

IV. Biomechanics The functional unit of the spinal column is the motion segment. A motion segment is composed of two adjacent vertebrae, the disc between them, the facet joints con-necting them, and the ligaments attached to the vertebrae (McGill & Karpowicz, 2009). The geometry and health of the functional units help a surgeon determine which patients will benefit from surgery, as well as the most ap-propriate surgical intervention for a given patient.

V. Spinal Cord The spinal cord ends at approximately the L1–L2 level in an adult. The conus medullaris is the end of the spinal cord. The filum terminale is an extension of the pia mater, which descends below the conus medullaris and is an-chored to the coccyx.

VI. Nerve RootsThe cauda equina is a fanning bundle of lumbar and sacral nerve roots exiting off the spinal cord at the conus medul-laris. This mass of nerve roots provides communication with the lower extremities and controls bowel, bladder, and sexual function (Figures 9, 10). The cauda equina is relatively resistant to neurologic insults, compared with the spinal cord (Shankar, Scarlett, & Abraham, 2009). The exiting nerve root in the lumbar spine is numbered according to the pedicle above it. For instance, the L5 nerve root passes below the L5 pedicle. (See Table 1.)

VII. Vasculature The abdominal aorta follows the left side of the spine until L4, where it bifurcates into the left and right common iliac arteries (Figure 11). The femoral arteries arise from the common iliac arteries. The middle sacral artery, iliolumbar

artery, and internal iliac artery supply blood to L5 and the sacrum. Segmental arteries branch off the aorta and sup-ply the vertebral body, posterior elements, and paraspinal muscles of the lumbar spine. Near the posterior wall of the vertebrae, each segmental artery bifurcates into a posterior branch and spinal branch. The spinal branch enters the vertebral canal through the intervertebral foramen and supplies portions of the posterior vertebral body. It joins other spinal branches at other levels to form the anterior spinal artery. The anterior spinal artery supplies the ante-rior two-thirds of the spinal cord.

Segmental veins drain into the inferior vena cava, which originates at the convergence of the left and right common iliac veins at the L4 level (Becske & Nelson, 2009). The infe-rior vena cava terminates in the right atrium of the heart.

Figure 3. Lumbar spine: Lateral view Figure 4. Intervertebral disc in relation to endplate and vertebral body

Figure 5. Intervertebral disc


Figure 6. Ligaments of the lumbar spine

Figure 7. Ligaments of the lumbar spine: Posterior view Figure 8. Ligaments of the lumbar spine: Lateral view


Figure 9. Termination of spinal cord at conus medullaris; cauda equina; and termination of dura in coccyx

Table 1. Nerve Roots and Corresponding Sensory, Motor, and Reflex Functions

Nerve Root Sensory Motor Reflex

L2 Groin area Hip Flexor (iliopsoas) None

L3 Groin, anterior thigh Knee extension (quadriceps) None

L4 Anterior thigh, knee, medial calf Knee Extension (quadriceps) Patella (knee jerk)

L5 Lateral thigh, lateral calf, top of foot EHL (extensor hallicus longus)— raise great toeFoot dorsiflexion (anterior tibialis) Knee flexion (hamstrings)

none

S1 Posterior thigh, posterior calf, lateral aspect of foot

Foot plantarflexion (gastrocnemius) Achilles (ankle jerk)

Figure 10. Dermatomal distribution of lumbar nerve roots

Figure 11. The abdominal aorta and its branches


Common diagnostic studies utilized to evaluate the lumbar spine patient are outlined below. In general, imaging is not used during the first 6 weeks of acute back pain if the fol-lowing conditions are met:

• no other neurologic signs or symptoms• no trauma• no history of malignant tumor• no constitutional symptoms• patient’s age is between 18 and 50 (Winters, Kluetz,

& Zilberstein, 2006).

I. X RayThe advantages of using X ray are that it is inexpensive and noninvasive. It shows the general changes of arthritis and bony alignment. However, it reveals only bony structures, and the patient is exposed to radiation.

Serial X rays aid in the evaluation of bone healing and maturation of surgical fusion.

II. Computed TomographyIn the lumbar spine patient, the computed tomography (CT) scan may be utilized either as an adjunct to magnetic resonance imaging (MRI) studies or in patients who cannot undergo MRI evaluation. A CT scan shows the bony elements of the spine very well, as well as the discs, nerves, and ligaments. Although it provides excellent visualization of the bony components, the CT scan is less sensitive to changes in the soft tissues of the spine. The use of contrast agents may be useful for highlighting masses and abnormal tissue/fluid collections. The CT scan also is occasionally used in conjunction with computerized neuro-navigation for intraoperative three-dimensional (3-D) image guidance during lumbar fusions.

III. Magnetic Resonance ImagingUtilizing strong magnetic fields and radio frequencies, magnetic resonance imaging (MRI) can provide useful information on all tissues in the spine (e.g., bones, soft tis-sues, spinal cord, nerves, ligaments, musculature, discs). MRI is superior to CT for evaluation of soft tissue struc-tures (Lurie, et al., 2009). Contrast agents may be used for highlighting masses, epidural scarring as a result of prior spine surgeries, and abnormal tissue or fluid collections. MRI is contraindicated for patients who have many metal-lic implants or a cardiac pacemaker.

IV. Bone ScanRadioactive tracers are injected into the patient. These tracers then attach themselves to areas of increased bone production or increased vascularity associated with tumor or infection. It is often utilized when evaluating for spon-dylolysis (i.e., destructive lesion of the vertebra), occult fractures, or suspected bony metastasis.

V. DiscogramDiscogram may be used to evaluate for degenerative disc disease. Under fluoroscopic guidance, a contrast agent is injected into the nucleus pulposus. The clinician perform-ing the procedure assesses the amount of contrast agent administered and at what point the patient experiences pain. It is then noted whether the patient’s typical pain is elicited. Radiographs are taken to assess whether the contrast agent stays within the nucleus pulposus or leaks out of the disc. All of these data may be useful in determin-ing whether a specific degenerated disc seen on MRI or CT scan is the cause of the patient’s symptoms. The utility of this test is controversial (Carragee, et al., 2009; Manchikan-ti, et al., 2009). See Degenerative Disc Disease for further discussion.

VI. Myelogram/Postmyelogram CTA contrast agent is injected under fluoroscopy into the intrathecal space through either lumbar puncture or cis-ternal puncture. The contrast agent is then visualized with radiographs, commonly with CT. The resulting images are useful for evaluating patients who cannot undergo MRI studies (e.g., people with pacemakers) or as an adjunct to MRI. This test also is useful in evaluating for suspected cauda equina syndrome (any mass lesion or infection that is within or impinging upon the thecal sac; arachnoiditis; or nerve roots lesions).

VII. Electromyography/Nerve Conduction VelocitiesSmall needles are inserted into specific muscles to assess muscle activity and nerve conduction time, as well as amplitude of electrical stimulation along specific nerves. Electromyography (EMG) may be indicated for patients without a clear radiculopathy (i.e., pain in the anatomic distribution of the affected nerve root) to further assess and diagnosis their pathology. This test is typically not used to evaluate acute radiculopathy.

Diagnostic Studies


Herniated Nucleus Pulposus

I. Description and Etiology Intervertebral disc herniation is also known as herniated nucleus pulposus (HNP). HNP may be asymptomatic despite radiographic evidence of bulging, protrusion, or extruded disc (Figures 12, 13, 14). The etiology may be either nonspecific or attributable to a precipitating event. Even when the patient is symptomatic, surgical intervention often is not required. An HNP may be symptomatic due to a combination of direct nerve root compression, the release of inflammatory chemicals (e.g., matrix metalloproteinases, prostaglandin E2, interleu-kin-6, nitric oxide), and hypoxia of the nerve root and basal ganglion (Ireland, 2009). Radicular pain can be accompanied by paresthesias or paresis (i.e., weakness) in the anatomic dis-tribution of the affected nerve root. The patient may complain of low back pain. The back or leg pain may be aggravated by coughing, sneezing, or assuming certain positions.

II. IncidenceMost HNPs occur at the L4–L5 or L5–S1 levels. The peak inci-dence is among people age 35–55 (Moschetti, Pearson, & Abdu, 2009). The majority of HNPs occur in a posterolateral direction, compressing the ipsilateral nerve root as it exits the dural sac.

III. Supporting DataA. MRI studies are the best test to evaluate the

spinal structures, HNP, and nerve root com-pression. A CT scan may be required to further evaluate the bony structures in some patients.

B. Motor weakness, sensory changes, or alteration in deep tendon reflexes are noted. (Please refer to Table 1 for more information.)

C. Preoperative diagnostic studies are consistent with HNP-induced neurological dysfunction or symptoms.

D. Lumbar nerve root tension may be tested with a straight leg raise test or other provocative maneuvers.

E. Gait, forward flexion, and general mobility are noted.

Figure 12. Progression of disc herniation

A. Normal discB. Bulging disc; pressure placed on exiting nerve rootC. Disc extrusion; disc material outside of annulusFrom AANN Core Curriculum for Neuroscience Nursing (4th ed.), edited by M. K. Bader and L. R. Littlejohns, 2004, St. Louis: Saunders. © 2004 Elsevier Inc. Reprinted with permission.

Figure 13. Lumbar spine: MRI, sagittal view (L5–S1 herniated disc)

Figure 14. Lumbar spine: MRI, axial view (L5–S1 disc bulge with left lateral recess stenosis)

Lumbar Spine Disorders


IV. DefinitionsA. Bulge: Symmetrical extension of the disc

beyond the endplatesB. Protrusion: Focal area of bulge/disc exten-

sion that is still attached to the disc (annulus fibrosis)

C. Extruded fragment: Nucleus pulposus no lon-ger connected to the disc

D. Sequestered fragment (i.e., free fragment): Nucleus pulposus in the posterior longitudinal ligament

E. Radiculopathy: Pain in the distribution of a nerve root resulting from irritation/compres-sion on that nerve root

V. Nonsurgical Medical TreatmentNonsurgical treatment is important in the care of the pa-tient with an HNP. Surgery usually is not indicated until symptoms have persisted for at least 6 weeks.

A. General recommendations 1. Promote general well-being, such as the

benefits of smoking cessation, weight man-agement, and adequate physical activity.

2. Prolonged bed rest is not recommended. If necessary, bed rest should be limited to no more than 2 days (Hagen, et al., 2004).

3. Physical therapy often is indicated; exercises may help reduce pain and improve function (McGill & Karpowicz, 2009).

B. MedicationsMedications may provide short-term relief of pain, which would enable the patient to participate in therapies. Effective strategies for symptom management include the use of the following:• muscle relaxants to reduce muscle spasm• nonsteroidal antiinflammatory drugs

(NSAIDs) to reduce inflammation of the nerve root

• narcotics for short-term acute pain relief.C. Epidural corticosteroid injection (ESI)

ESI is a caudal, translaminar, or interlaminar injection of a corticosteroid (e.g., methylpredni-solone). The mechanism of action is its ability to inhibit prostaglandin synthesis and decreased immunologic responses. Additionally, it is thought to promote membrane stabilization, suppress neuropeptides, block phospholipase A2 activity, and block nociceptive C-fiber con-duction (Ngu, DeWal, & Ludwig, 2003). In a randomized, double-blind, controlled trial, Ng, Chaudhary, and Sell (2005) found that transfo-raminal injections may localize preferentially to the peripheral perineural space, especially if there is severe foraminal stenosis. McLain,

Kapural, and Mekhail (2005) noted that no study has shown a clear advantage of one approach, type, or volume of cortisone. Thus, the approach for the ESI needs to be individualized to each patient’s symptoms and radiographic findings.

Wilson-MacDonald, Burt, Griffin, and Glynn (2005) evaluated ESI for nerve root compres-sion and found that a single injection provided short-term pain relief. Chou, Atlas, Stanos, & Rosenquist (2009) found "fair evidence of moderate benefit compared with placebo injec-tion for short-term pain relief in patients with radiculophathy. There was no evidence of long-term benefits, but few trials evaluated long-term outcomes" (p. 1087).

D. Acupuncture Acupuncture is considered an alternative treat-ment. It originated in China more than 2,000 years ago (National Center for Complementary and Alternative Medicine, 2004). Very fine needles are placed into specific trigger points to stimulate anatomic points in the body. It is theorized that acupuncture works by influencing the electromagnetic field of the body, which can alter the chemical neurotransmitters within the body. Furlan and colleagues (2005) found limited evidence on the benefits of using acupuncture alone for the treatment of low-back pain and improved function better than conventional therapies alone" (p. 28).

E. Spinal manipulation (chiropractic or osteopathic) Spinal manipulation is used to relieve symp-toms and help the patient progress toward an active exercise program (Thorson et al., 2005). Assendelft and colleagues (2004) found no evidence that spinal manipulative therapy is superior to other standard treatments for pa-tients with acute or chronic low-back pain.

VI. Surgical TreatmentSurgical treatment may be indicated when conservative management has failed to alleviate the patient’s symptoma-tology or for patients who have cauda equina syndrome or progressive neurologic deficits. Atlas, Keller, Wu, Deyo, and Singer (2005a) found that surgically treated patients with a herniated lumbar disc had more complete relief from leg pain and improved function and satisfaction than nonsurgi-cally treated patients at 10-year follow-up. Of note, however, was that improvement in the patient’s predominant symptom and the patient’s work and disability outcomes at 10 years was similar regardless of the treatment (i.e., surgi-cal or nonsurgical). Weinstein, Lurie, Tosteson, Tosteson, et al. (2009) found that patients treated surgically for intervertebral disc herniation showed significantly greater improvement in pain, function, satisfaction, and self-rated


progress over 4 years compared to patients treated non-operatively. Although microdiscectomy is the gold-standard operative approach, minimal-access techniques are gaining in popularity.

A. Microdiscectomy 1. Microdiscectomy is performed under gen-

eral or regional anesthesia.2. The patient is in a prone position.3. Following deep dissection, the correct disc

space is confirmed radiographically. Once confirmed, the ligamentum flavum and lamina are dissected to expose the nerve root. The opening in one lamina is termed a semihemilaminectomy.

4. Once the nerve root is identified, all liga-ments obstructing the view of the disc and nerve roots are cleaned away. A nerve root retractor is used to gently bring the nerve root structures medially.

5. The disc is often excised and the disc frag-ments, which will vary in size, are carefully removed.

6. The area is then irrigated, hemostasis is achieved, and the wound is closed.

B. Open discectomy Open discectomy is the same procedure as mi-crodiscectomy, except the surgeon does not use an operative microscope. Thus, a larger incision is required.

C. Minimal-access/minimally invasive discectomy This technique permits a discectomy to be per-formed through a very small incision and with minimal disruption of adjacent tissues (Figure 15). It is often performed on an outpatient basis or with a 23-hour observation stay. This technique is increasing in popularity in all settings, but specifi-cally in freestanding surgery centers.1. The surgeon utilizes a tubular retractor sys-

tem and Loupes magnification or an operat-ing microscope.

2. The tubular retractor is placed through a small incision and deep dissection.

3. The discectomy is performed, as described above, through the tubular retractor.

D. Potential complications1. Intraoperative bleeding2. Dural tear3. Nerve injury (spinal cord or nerve root) dur-

ing surgery, resulting in changes in motor or sensory function

4. Infection

VII. Nursing Assessment, Interventions, and Monitoring A. Preoperative

1. Describe the surgical procedure to patient and family.

2. Informed consent obtained by surgeon.3. Describe the expected outcomes, both post-

operative and long term.4. Arrange for required preoperative testing.5. Advise patient to discontinue medications

such as herbal products, NSAIDs, antico-agulants, aspirin, warfarin, and clopidogrel bisulfate.

6. Encourage patient to anticipate and arrange for perioperative and postoperative care needs.

B. Perioperative1. Explain to patient where and when to

arrive, as well as surgery time.2. Instruct patient as to eating and drinking

restrictions.3. Instruct patient about medications to be taken

the morning of surgery with a sip of water.4. Remind patient to wear comfortable clothing

and to leave jewelry and valuables at home.5. Tell patient to remove dentures, partial plates,

eyeglasses, contact lenses, nail polish, and sculp-tured nails.

C. Intraoperative1. “Time Out”—right patient, right surgery,

right site2. Proper patient positioning

a. Table options are surgeon specific.

Figure 15. Minimal-access microdiscectomy


b. If patient is obese, consider using a Jackson table.

3. Intraoperative needs anticipationa. Equipmentb. Patient-specific needs (e.g., latex allergy)

D. Postoperative1. Neurological assessment

a. Strength and sensation assessment, as compared with preoperative status.

b. Special attention to neurological assess-ment and correlation with the operative intervention.

2. Mobilitya. Patient should mobilize quickly unless

ordered differently due to complication (e.g., CSF leak).

b. Instruct and help patient to roll to side and bring legs down while simultane-ously rising up with the torso from the bed. This minimizes twisting at the waist.

c. Instruct and help patient to rise from a chair using the legs, rather than pushing off with the back.

3. Pain controla. The degree of pain varies considerably.b. Intravenous hydromorphone or mor-

phine sulfate may be used as needed until the patient is able to take oral med-ications.

c. Codeine, hydrocodone, or oxycodone, with or without acetaminophen, may be prescribed as needed when the patient is able to take oral medications.

d. NSAIDs, as needed, can be very beneficial.e. Neuropathic pain medications

(e.g., gabapentin) may be beneficial.f. Antispasmodics may be prescribed if

muscle spasms are present.g. Heat may be applied for spasms and

muscular tension.h. Ice may be applied for radicular pain for

no more than 20 minutes per hour.i. Gentle massage may be used away from

the incision.j. Have patient change positions frequently.k. Modest activity may be conducted as

tolerated.4. Constipation prevention

a. Consider initiating techniques preopera-tively.

b. Ensure adequate water intake.c. Diet should include adequate fresh

fruits, vegetables, and fiber.d. Stool softener (e.g., docusate) may be

used two to three times per day.

e. Motility agents (e.g., senna) should be used only as needed.

5. Urinationa. Urinary hesitancy, especially immedi-

ately postoperative, is usually transient.b. Assess urinary output, frequency, and

volume.c. Assess to be sure there is adequate emp-

tying. Bladder scanning or intermittent bladder catheterization may be neces-sary to assess for retention or incomplete emptying.

6. Discharge planninga. Discharge planning should be initiated

preoperatively.b. Reinforce the following: no lifting, bend-

ing, or twisting; no sitting for long peri-ods of time.

c. Remind patient to change positions fre-quently.

d. Remind patient not to drive while using narcotic pain medications.

e. Explain to patient that sexual activity may be resumed 2 weeks after surgery and when it is comfortable.

f. Ensure the patient is aware of return-to-work and activity recommendations.

7. Reinforce alternative planning and problem solving for practical everyday activities (e.g., vacuuming, doing laundry, and performing child care).

8. Incision care varies with the type of closure. 9. Ensure the patient is aware of postoperative

follow-up recommendations.

VIII. Expected OutcomesA. Patients with mild symptoms will usually

improve regardless of the type of treatment. Sur-gical intervention for moderate to serve sciatica results in greater improvement. Surgical inter-vention provides faster relief from an acute sciatic attack. According to Angevine and McCormick (2002), “Lumber discectomy is generally per-formed to reduce pain or disability and thereby improve quality of life. Important surgery-related results, therefore, include the patient’s percep-tions of the effect of surgery on their health and ability to perform daily tasks” (p. E8).

B. As noted above, Atlas et al. (2005a) completed a 10-year follow-up study of the long-term out-comes of surgical and nonsurgical management of sciatica secondary to a lumbar disc hernia-tion and found that surgical treatment (mostly open discectomy) led to more complete leg pain relief, improved function, and improved satisfaction.


I. Description and EtiologyThe clinical symptoms of cauda equina syndrome (CES) are low back pain; sciatica; saddle and perineal hypoesthesia or anesthesia; a decrease in anal tone; absent ankle, knee, or bulbocavernous reflexes; and bowel and bladder dysfunc-tion. Not all criteria are required for the diagnosis to be established. However, symptoms of urinary dysfunction and saddle hypoesthesia with varying degrees of motor and sensory loss in either of the extremities are necessary for the diagnosis (Qureshi & Sell, 2007). Sacral root lesions mani-fest more subtle clinical symptoms than those of lumbar root involvement. Sensory assessment of the perineal area distribution should be documented. A complete perineal examination should include the perianal area, the natal cleft, and the posterior scrotal or labial areas.

The cauda equina consists of peripheral nerves, both motor and sensory, below the level of the conus medullaris and within the spinal canal. The conus medullaris contains the myelomeres of the five sacral nerve roots. Damage to any part of this structure may result in CES.

Damage to the structures of the conus medullaris, usually by compressive forces, can cause CES. The most common cause is midline prolapse of the intervertebral disc, and the most common levels reported are in the lower part of the cauda, particularly L4–L5. Most lumbar disc herniations causing CES are midline prolapse, causing bilateral symptoms.

Other conditions that may cause CES include tumor, trauma, spinal epidural hematoma, chiropractic manipula-tion, pneumococcal meningitis, Paget’s disease, laminar hooks, and free fat graft following discectomy. CES often occurs with no precipitating event.

Symptom onset can occur suddenly without previous history of backache, with acute onset of bladder dysfunc-tion following a long history of low back pain; or gradually from a background of chronic low back pain and sciatica.

Compressive lesions may create a partial block, causing a varying degree of impairment in addition to asymmetry of the disturbance. A complete block is not required to produce a CES. Clinical evidence has demonstrated little correlation between the degree of block and the development of CES (Olivero, et al., 2009).

Significant neurologic changes can occur with 75% restriction of the cauda equina. Neural tissue damage includes an inflammatory response and axonal and Wallerian degeneration followed by proliferating Schwann cells and regener-ating axonal buds.

II. IncidenceCES is rare, affecting an estimated 1% secondary to disc herniation (Olivero, et al., 2009).

III. Supporting DataA. Radicular pain is often described as stabbing,

shooting, or burning. B. The patient may have hypoesthesia or hyperes-

thesia in the same region. C. The patient may describe difficulty urinating

or the absence of or decreased feeling in the perineal region.

D. Healthcare providers should assess motor weakness (specific motor nerve root), sensory changes (numbness or tingling along a spe-cific distribution), and reflexes (decreased or absent).

E. If CES is suspected, an examination and evalua-tion of perianal sensation is warranted. Sensory assessment of the perineal region should include the perianal area, the natal cleft, and the pos-terior scrotal or labial areas. (See Table 2 for possible symptoms related to specific functions.)

F. MRI and CT studies not only determine the level of pathology but also aid in the diagnosis of the primary pathologic lesion.

G. The diagnosis of CES is primarily based on clinical examination.

IV. Surgical ManagementAlthough controversy exists as to the value of early decompression, expeditious surgery continues to be recommended within 48 hours after the patient presents. Transcanal approaches include standard open lumbar laminectomy for resection of compressive lesion or discectomy/microdiscectomy for herniated disc.

V. Nursing Assessment, Interventions, and Monitoring Please refer to the recommendations for herniated lumbar disc.

Table 2. Symptoms Related to CESInvolvement SymptomsMotor Limb weakness or weakness of movements; hypotonia in the limb or

muscle group; diminished or absent reflexesSensory Hypoesthesia or hyperesthesia with objective signs of sensory loss in

a dermatomal or myotomal distributionUrinary sphincter control Difficulty initiating micturition, retention, stress incontinence; loss of

urethral sensationBowel dysfunction Constipation, loss of appreciation of rectal distension; loss of anal

tone and sensationSexual dysfunction Sudden onset of difficulty achieving an erection or orgasm

Cauda Equina Syndrome


VI. OutcomesA. In a prospective study, Qureshi & Sell (2007)

found no significant difference in residual symptoms, including disability, pain, and incontinence, between patients who received surgery within 24 hours of symptom onset and those who received surgery after 24 hours of symptom onset. However, a significantly improved outcome was found in patients who were continent of urine at presentation. Similarly, a retrospective review by Olivero and colleagues (2009) found that recovery of sensory, motor, and bladder function was not related to the time to surgical intervention.

B. In many cases, early intervention may prevent the progression of partial sphincter disturbance to complete lesions. This progression has been documented to occur even within the first 24 hours (Kennedy et al., 1999).

C. Predictors of residual dysfunction are the pres-ence of significant sphincter disturbance and complete perineal anesthesia at presentation.

D. The goal of surgery is to prevent progression of neurological dysfunction; resolution of present-ing symptoms of neurologic dysfunction is unknown.

Lumbar Stenosis

I. Description and EtiologyA. Central canal stenosis

The normally triangular-shaped spinal canal becomes flattened, compressing the thecal sac (Figure 16). As it progresses, the cauda equina

is compressed. This can be caused by any of the following, or any combination of the following: • facet hypertrophy• thickening and bulging of the ligamenta flava• outward disc bulging• disc degeneration• spondylosis (Figures 17, 18)• degenerative spondylolisthesis.

The condition is aggravated by positions of extension, which produce more central-canal and lateral-recess narrowing.

Figure 16. Central and lateral-recess stenosis: MRI, axial view

Figure 17. Spondylosis in the lumbar spine

Figure 18. Spondylosis: Posterior view


B. Lateral-recess stenosis Lateral-recess stenosis is a narrowing in the area where the nerve roots exit the spinal canal. It can also be caused by facet hypertrophy, disc bulging, loss of disc height, spondylosis, or degenerative spondylolisthesis.

C. Neurogenic claudicationCompression of the microvasculature of the lumbar nerve roots, resulting in ischemia and pain, is believed to be a major contributing fac-tor in development of neurogenic claudication. In addition to ischemia, postural changes can cause stenosis. Postural neurogenic claudication is induced when the lumbar spine is extended and lordosis is accentuated, whether at rest or during exercise in the erect posture. With exten-sion of the spine, degenerated intervertebral discs and thickened ligamenta flava protrude posteriorly into the lumbar canal, producing transient compression of the cauda equina. In the ischemic form, it is theorized that transient ischemia occurs in compressed lumbosacral roots when increased oxygen demand occurs during walking (Siebert, et al., 2009).

II. DefinitionsA. Congenital stenosis: The patient was born

with a small narrow spinal canal.B. Acquired stenosis: The spinal canal has nar-

rowed because of degenerative changes.

III. IncidenceA person with severe congenital lumbar stenosis may become symptomatic as early as age 20, whereas someone with acquired lumbar spinal stenosis becomes symptomatic at age 60–70 (Aliabadi & Isaacs, 2009). Males have a higher incidence than females. There does not appear to be any cor-relation between race and lumbar stenosis.

Although L4–L5 is the most frequently involved level, lumbar stenosis may be found focally over one or two seg-ments or at multiple levels.

IV. Supporting Data A. Symptoms

1. Lower extremity symptoms may be described as burning, cramping, aching, numbness, tingling, or dull fatigue.

2. Early stenosis may present with nonspecific back pain.

3. Leg fatigue, pain, numbness, and weakness occur sometimes several months to years after the back pain was first noticed.

4. Symptoms are usually exacerbated by walking.5. Symptoms are generally bilateral but can be

more pronounced on one side.

6. Pain radiates from the buttocks to the poste-rior or posterolateral thighs and occasionally spreads distally to the calves and feet.

7. Immediate symptom relief by sitting down. 8. Symptoms are often improved with a forward

flexed posture. Patients may describe increased walking tolerance if using a supportive device such as a grocery cart, walker, or cane.

9. Walking distance usually gradually declines over time due to the onset of symptoms at shorter and shorter distances.

10. The degree of pain does not always correlate with the severity of stenosis.

B. Examination1. Posture is often stooped forward (i.e., for-

ward flexion). This sort of stooped posture, referred to as the Simian stance, is more pro-nounced with ambulation.

2. Patient’s strength is generally intact. 3. Patient’s deep tendon reflexes may be

decreased or absent.4. Sensation is usually normal but may be

temporarily affected after ambulation. If comorbidities are present, such as diabetes, the patient may have decreased sensation in a stocking distribution.

IV. Nonsurgical Medical TreatmentAs with HNP, nonsurgical management can provide symptom relief and is of utmost importance. Unlike those of HNP, symptoms progress slowly in most patients, affording them ample time to participate in a multimodal nonsurgi-cal program. A comprehensive program includes not only structured therapy but also general personal well-being and commitment to daily activities to promote good back health.

The patient’s age and other comorbidities often will ne-cessitate coordination of care with the primary care provider.

Options include the following: A. General recommendations

1. Promote general well-being, such as educat-ing patient about the benefits of smoking cessation, weight management, and ade-quate physical activity.

2. Physical therapy often is indicated; exercises may help reduce pain and improve function. Flexion exercises and low-impact aerobic conditioning should be emphasized. The use of recumbent bicycles, elliptical train-ers, treadmills, and warm water pools can be very beneficial for overall conditioning. A home flexion exercise program should be followed daily. Epidural steroid injections may also be effective (Koc, et al., 2009).

B. MedicationMedication may be beneficial for short-term pain symptom relief to allow patients to


participate in therapies. There are several ef-fective strategies for symptom management, including1. muscle relaxants to reduce muscle spasm2. NSAIDs to reduce inflammation of the

nerve root3. narcotics for short-term acute pain relief.

C. BracingIn this population, braces may be used to decrease lumbar lordosis, which may decrease pain. However, prolonged use may cause mus-cle atrophy, which can increase back pain. The efficacy of lumbar braces for treating acute and chronic lumbar stenosis is unknown (Siebert, et al., 2009).

V. Surgical Treatment Laminectomy and partial facetectomy (typically medial one-third) is the standard surgery (Papavero, et al., 2009). The number of levels decompressed is dependant upon the number of levels suspected of causing the patient’s symp-toms. Great care is taken to avoid dural tear, nerve root injury, or complete facetectomy, which can lead to segmen-tal instability or acquired spondylolisthesis (Figure 19).

A. Following deep tissue dissection, localization is confirmed with X ray.

B. Bony removal begins with the spinous process. The amount of bone removed depends on the amount of stenosis.

C. The lamina is thinned with a drill. The thinned lamina is then removed; the spinal canal is carefully decompressed.

D. The ligamentum flavum lies between the lamina and the thecal sac. Often with spinal stenosis, the ligamentum flavum is thickened. The dura is often physically protected while the ligamen-tous and bony dissection is completed.

E. The lateral recesses are then checked, and ligamentous or bony material is removed, with particular attention to the medial aspect of the foramen. This ensures good nerve root decompression.

F. The wound is irrigated and closed. A drain may be utilized.

VI. Nursing Assessment, Interventions, and Monitoring

A. Preoperative 1. Surgical procedure2. Preoperative history and physical3. Informed consent (obtained by surgeon)4. Anticipation of perioperative and postop-

erative care needsa. Initially, patient will need assistance and

must arrange for a care provider.

b. Patient should arrange for help with household chores, yard work, pets, and other tasks.

5. Potential risks and complications6. Expected outcomes, both postoperative and

long term a. Realistic patient expectationsb. Mutual patient and physician expecta-

tions 7. Required preoperative testing: For this

patient population, special attention needs to be paid to preoperative medical clearance because of advanced age or other medical conditions.

8. Discontinuation of medications, including herbal products, NSAIDs, anticoagulants, aspirin, warfarin, clopidogrel bisulfate

B. Perioperative1. Explain to patient where and when to

arrive, as well as surgery time.2. Instruct patient on eating and drinking restric-

tions.3. Instruct patient on medications to be taken

the morning of the surgery with a sip of water. Be aware of the institution’s anesthe-sia guidelines.

4. Remind patient to wear comfortable cloth-ing and to leave jewelry and valuables at home.

Figure 19. Decompression laminectomy


5. Tell patient to remove dentures, partial plates, eyeglasses, contact lenses, nail polish, and sculptured nails.

C. Intraoperative 1. Prone position is generally used.2. Patient’s abdomen should hang free to

reduce intraoperative bleeding by minimiz-ing vena cava compression and epidural venous pressure.

3. Pressure points and genitalia should be checked to avoid positioning injuries.

4. Lateral position is difficult.D. Postoperative

1. Neurological assessmenta. Strength and sensation assessment should

be compared with preoperative status.b. Pay special attention to the neurological

assessment and correlation to the opera-tive intervention.

c. In the event of significant nerve root manipulation intraoperatively or neuro-logical deficits postoperatively, the phy-sician may order postoperative steroids for 24–48 hours. Antibiotics may be con-tinued for 24 hours.



b. Instruct and help patient to roll to side and bring legs down while simultane-ously rising up with the torso from the bed. This minimizes twisting at the waist.

c. Instruct and help patient to rise from a chair using the legs, rather than pushing off with the back.

d. Patient may benefit from a walker if he or she is deconditioned, had a multilevel laminectomy, or has difficult mobility.

e. Evaluate the patient for need for an inpatient physical therapy referral for gait training and walker evaluation.

f. Instruct patient to take short walks to avoid excessive fatigue; note preopera-tive walking endurance.

g. If a CSF tear has occurred, physician may order flat bed rest. This is often dependent on degree of tear, ease of repair, and surgeon preference. For a persistent CSF leak, a lumbar drain may be implemented.

3. Pain controla. The degree of pain varies considerably.b. Intravenous hydromorphone or mor-

phine sulfate may be used as needed

until the patient is able to take oral medi-cations.

c. Codeine, hydrocodone, or oxycodone, with or without acetaminophen, may be prescribed as needed when the patient is able to take oral medications.

d. NSAIDs, as needed, can be very beneficial.e. Neuropathic pain medications

(e.g., gabapentin) may be beneficial.f. Antispasmodics may be prescribed if

muscle spasms are present.g. Heat may be applied for spasms and

muscular tension.h. Ice may be applied for radicular pain for

no more than 20 minutes per hour.i. Gentle massage may be used away from

the incision.j. Have patient change positions frequently.k. Note geriatric considerations when

administering medications. 4. Constipation prevention

a. Consider preoperative initiation.b. Ensure adequate water intake.c. Diet should include adequate fresh

fruits, vegetables, and fiber.d. Stool softener (e.g., docusate) may be

used 2-3 times per day. e. Motility agents (e.g., senna) should be

used only as needed. f. Geriatric patients are prone to chronic

constipation problems. 5. Urination

a. Urinary hesitancy, especially in the immediate postoperative period, is usu-ally transient.

b. Assess urinary output, frequency, and volume.

c. Assess to be sure there is adequate emp-tying. Bladder scanning or intermittent bladder catheterization may be neces-sary to assess for retention or incomplete emptying.

d. Patient may have long-standing urinary retention.

6. Incision carea. Assess incision to be sure it is clean and dry.b. Care varies widely depending on the type

of closure (staples, sutures, skin glue).c. In general, incision needs to be moni-

tored daily for redness, drainage, and signs of infection. Patient and caregiver need to be instructed on specific incision care, evaluation for signs and symptoms of infection, and when and who to call with questions or problems.


7. Postoperative teaching a. Avoid heavy lifting (anything heavier

than a gallon of milk) for the first 4–6 weeks.

b. Avoid prolonged sitting or standing for the first 4–6 weeks, including long car trips.

c. The need for outpatient therapy is decided on individual basis.

d. Patient will gradually be weaned from pain medication.

8. Discharge planninga. Discharge planning should be initiated

preoperatively.b. Talk to patient about how to gradually

return to activities of daily living (ADLs) and lifestyle.

c. Reinforce to patient the following: no lifting, bending, or twisting; no sitting for long periods of time.

d. Remind patient to change positions fre-quently.

e. Remind patient not to drive while using narcotic pain medications.

f. Explain to patient that sexual activity may be resumed when it is comfortable.

g. Ensure that the patient is aware of return-to-work and activity recom-mendations. Return to work will vary depending on type of work (sedentary roles earlier than heavy labor). Return to work may be a gradual progression to full time.

h. Reinforce alternative planning and problem solving for practical everyday activities (e.g., vacuuming, doing laun-dry, performing child care).

i. Explain incision care.j. Ensure that the patient is aware of post-

operative follow-up recommendations.9. Patient comorbidities may affect postopera-

tive recovery.

VII. Expected OutcomesAtlas, Keller, Wu, Deyo, and Singer (2005b) found that patients with lumbar spinal stenosis treated surgically and nonsurgically had similar low-back pain relief, pre-dominant symptom improvement, and satisfaction at 8–10 years. However, the surgical treatment group experienced greater improvement in leg pain relief and back-related functional status.

Weinstein, Tosteson, Lure, et al. (2008) reported that patients with spinal stenosis without degenerative spon-dylolisthesis who underwent surgery showed significantly greater improvement in pain, function, satisfaction, and self-rated progress than did patients treated nonsurgically.

Spondylosis

I. Description and EtiologySpondylosis is the result of disc degeneration, which leads to bulging of the annulus fibrosus. The degenerated, bulg-ing annulus fibrosus creates an elevation of the periosteum. Bony reactions occur, resulting in osteophyte formation (Figures 17, 18). The osteophytes commonly occur in the lordotic spinal canal of the lumbar and cervical spine (Middleton & Fish, 2009). In addition, there may be hyper-trophy and buckling of the ligamentum flavum, leading to further lumbar spine canal narrowing. With disc collapse, the neural foramina will decrease in height, which may result in nerve root compression. Alterations in axial loads may lead to posterior facet osteophyte formation, which can also result in nerve root compression (Singh & Phillips, 2005).

Motion segment degeneration can lead to stiffened levels, exhibiting disc degeneration, ligament calcification, and osteophyte formation. Conversely, the motion segment can be hypermobile, as in degenerative spondylolisthesis (Watters, et al., 2009). The degenerative cascade, a part of the aging process, is caused by many factors and affects the discs, facet joints, surrounding soft tissue, ligaments, ver-tebrae, and articular processes. Middleton and Fish (2009) noted that the spondylotic process is lessened by fusion or immobilization.

II. Supporting Data A. Refer to Lumbar Spinal Stenosis section.B. If the patient has a mobile segment, refer to

Spondylolisthesis section. C. Symptomatic age is 50–70; spondylosis occurs

more often in men.D. Everyone in the geriatric population has

degenerative changes. Clinical correlation is key.

Spondylolisthesis and Spondylolysis

I. Description and EtiologySpondylolisthesis comes from the Greek words spondylo, meaning vertebrae, and listhesis, meaning slipping or slid-ing. It most often occurs at L5–S1, followed by L4–L5. The most frequent cause of spondylolisthesis is degenerative changes related to chronic motion between two vertebrae that results in anterior subluxation. Spondylolysis is a defect in the pars interarticularis (bony region between the su-perior and inferior articulating processes of an individual vertebra). The defect may be an elongated, but intact, pars; an acute fracture; or a lytic lesion representing a fatigue fracture. Spondylolysis is also known as isthmic spon-dylolysis or type-II spondylolisthesis. Spondylolisthesis is classified as follows:


A. Type I: Dysplastic 1. Type I is due to a developmental disorder

and characterized by presence of dysplastic sacral facet joints that allow forward trans-lation (movement) of one vertebra over another. Undue stress on the pars may result in fracture.

2. It is often associated with spina bifida and congenital defects of the pars interarticularis.

B. Type II: Isthmic 1. Repeated fatigue fractures followed by

remodeling causes the development of a stress fracture of the pars interarticularis.

2. Type II can also be a developmental injury for some adolescents during growth spurts.

3. This is the most common cause of low back pain in children.

C. Type III: DegenerativeType III is an adult condition caused by chronic intersegmental instability that produces facet arthropathy (Figure 20).

D. Type IV: Traumatic1. Type IV results from fracture of the pedicles,

the pars, or the superior/inferior articular processes caused by a traumatic injury.

2. Type IV is very rare. 3. Type IV can occur acutely after an injury,

although most often it will develop during the weeks to months after the injury.

E. Type V: PathologicalType V is due to an internal alteration causing destabilization of the facet mechanism pro-ducing a pathologic spondylolisthesis. Some examples are tumors, infection, Paget’s disease, osteoporosis, and hyperthyroidism.

II. Grading and IncidenceA. Grading

The degree of subluxation is generally mea-sured using the Meyerding method. The superior surface of the sacrum is divided into fourths along its anteroposterior (AP) diameter. Then the degree of subluxation is noted as a grade:• Grade 1: 1%–25% slippage• Grade 2: 26%–50% slippage• Grade 3: 51%–75% slippage • Grade 4: 76%–100% slippage • Grade 5: Greater than 100% slippage

B. Type I Of all populations, Inuit are most at risk. As many as 50% of Inuit acquire this condition, related to both genetic and environmental fac-tors. There is a 2:1 ratio of females to males. In children, this condition has been diagnosed as

early as 3.5 months; 4% are found by age 6, and 6% by age 14 (Herkowitz, 2009; Jones & Rao, 2009).

C. Type II Although type II spondylolisthesis is not a con-genital condition, there is a positive correlation between congenital defects, including spina bifida occulta and scoliosis, and the develop-ment of type II spondylolisthesis. As many as 50% of spondylolysis cases will become type II spondylolisthesis. Males outnumber females 2:1, although females have a higher likelihood of having a more severe grade. There is a higher incidence among Caucasians than among Afri-can Americans, by a 6:1 ratio.

D. Type IIIThis condition commonly occurs after the age of 40. Females are affected more often than males, by a 5:1 ratio. African American females are more often affected than Caucasian females. Most commonly, type III spondylolisthesis oc-curs at L4–L5. Incidence increases mostly with advancing age; other risk factors include diabe-tes, arthritis, smoking, and obesity (Watters, et al., 2009).

Figure 20. L4–L5 degenerative spondylolisthesis (Note the disc degenera-tion and compression on the existing L5 nerve root.)


E. Type IVTraumatic spondylolisthesis is rare. Falls and parachuting injuries have been most frequently associated with this type. More often, spon-dylolisthesis occurs after trauma and is related to the sequels of recovery process.

F. Type VType V spondylolisthesis occurs with other dis-ease processes, and determining its incidence has been difficult. Incidence is increased with diseases affecting the bone structure and gen-eration of osteoblast as well as conditions that increase the osteoclasts.

III. Supporting DataA. Symptoms are dependent on the type and

grade of spondylolisthesis.B. Pain can begin insidiously and is aggravated

by activity, especially back-extension types of movements.

C. Pain is in the low back with or without radiation.

D. Pain is usually worse with prolonged walking or standing and improved with sitting.

E. Symptoms often are similar to those of lumbar stenosis, but the patient may experience more back pain. (Please see the Lumbar Stenosis section.)

F. Patient may complain of a slipping sensation in the lower back.

G. Patients may have difficulty walking.H. On examination, one maybe able to palpate the

“step-off” of the vertebrae.I. In most cases, the patient doesn’t present with

radicular pain, because it occurs more often in high grades.

IV. DefinitionsA. Spondylo: Vertebra (denotes relationship to

vertebra or spinal column)B. -listhesis: To slipC. -lysis: Loosening, releasing, destruction

Degenerative Disc Disease

I. Description and EtiologyDegenerative disc disease (DDD) is described as a change in the composition and function of the disc. A disc’s water content and vascularity decreases with age. By the age of 30, there is no longer a direct vascular supply to the discs, and they become desiccated, providing less support and resistance to movement. During the aging process, the nucleus pulposus becomes less elastic, and tears develop in the annulus fibrosis. It is commonly accepted that the

disc may become painful if the outer third is exposed to a noxious stimulus. Many patients are asymptomatic despite radiographic degenerative changes (Figure 21). Symptoms include pain, dysfunction, and disability (Chou, Baisden, Carragee, et al., 2009).

II. Supporting DataA. Patients are generally relatively young; they

present with a history of gradually worsening back pain.

B. The pain is described as deep, midline, and aching.

C. Pain may radiate into the buttocks or upper thighs; it is worse when patient stands in one position.

D. A radiographic-based grading scale has been devised to indicate the degree of DDD on MRI testing. Modic endplate changes are graded as follows:1. Type I. Study shows disruption and fissur-

ing of the vertebral endplates; decreased signal on T1-weighted images and increased signal intensity on T2-weighted images.

Figure 21. L4–L5 and L5–S1 degenerative disc disease: Lumbar spine MRI, T2-weighted image


2. Type II. Yellow marrow replacement results in increased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images.

3. Type III. Bony sclerosis indicated; decreased signal intensity on both T1- and T2-weighted images.

E. Resnick et al. (2005a) have proposed the fol-lowing evidence-based guidelines regarding the use of MRI in degenerative disease of the lumbar spine: 1. MRI scanning should be used as a diagnos-

tic test instead of discography for the initial evaluation of patients with chronic low back pain.

2. MRI-documented disc spaces that appear to be normal should not be considered for treatment as a source of low back pain.

3. Lumbar discography should not be used as a stand-alone test on which treatment deci-sions are based for patients with low back pain.

4. If discography is performed as a diagnostic tool to identify the course of a patient’s low back pain, both a concordant pain response and abnormalities should be present at the same level.

F. Gibson and Waddell (2005) found limited evidence of clinical benefit for lumbar sur-gery, including fusion procedures in treating degenerative disc disease. The effectiveness of intradiscal electrotherapy is unproven. More research is necessary to evaluate the clinical benefit of disc replacement surgery.

Degenerative Scoliosis

I. Description and EtiologyDegenerative scoliosis occurs in previously nonscoliotic spines in which the degenerative cascade, including disc degenera-tion, facet and ligamentum flavum hypertrophy, and motion segment hypermobility can lead to deformity in all planes (i.e., axial, sagittal, coronal). Deformity causes the patient to be out of spinal balance. This imbalance leads to postural deformities, pain, and disability (Rosner & Ondra, 2005).

II. Supporting DataA. Observe patient’s posture and gait.

1. Will often observe a kyphotic deformity.2. If manual correction of posture is attempted,

patient is unable to balance because the cen-ter of gravity has been shifted.

B. Refer to Spinal Stenosis and Spondylolisthesis sections.

C. Standing scoliosis films with AP and lateral views; lateral bending scoliosis films to assess flexibility of the curve; lumbar flexion/extension films to evaluate for instability; for preoperative planning, dual energy X-ray absorptiometry (DEXA) scan to assess whether osteoporosis is present.

D. Patient should undergo same nonsurgical man-agement as other spine patients.

E. If surgical, deformity correction can be very extensive with long operative period.

F. Patient may require long hospitalization and rehabilitation.

G. Preoperative planning includes nutritional assessment.


Medical Treatment of Lumbar Spondylosis, Spondylolisthesis, Spondylolysis, and Degenerative Disc Disease

I. Patient EducationGeneral physical well-being is of the utmost importance in the treatment of low back disorders. It includes patient education in the following areas (Engers, et al., 2008):

A. Appropriate weight/body mass indexB. Smoking cessationC. Positive mental outlookD. Progressive aerobic exerciseE. Daily stretching and strengthening exercise

program.

II. Specific to Degenerative Disc DiseaseA. A minimum of 3–4 months of aggressive medi-

cal management is usually attempted prior to surgical intervention.

B. Promote general well-being, such as smoking cessation, weight management, and maximiz-ing physical function.

C. Minimize chronic narcotic use.D. Optimize nutritional status.E. Encourage regular exercise, outpatient back-

rehabilitation school, and manipulation.F. Refer to HNP and Stenosis sections.

Surgical Treatment Two-thirds of adults in the United States will experi-ence low back pain at some time. Approximately 298,000 undergo a lumbar fusion each year (Katz, 2006). Deyo, Nachemson, and Mirza (2004) noted that the number of spinal fusions increased by 77% between 1996 and 2001 and that although spinal fusion is “undoubtedly effective for some conditions in some patients,” its efficacy for some indications remains unclear (p. 724).

To address questions related to fusion surgery for degenerative disease of the lumbar spine, the American Association of Neurological Surgeons and the Congress of Neurological Surgeons Joint Section on Disorders of the Spine and Peripheral Nerves commissioned a group of orthopedic and neurosurgical spine surgeons to per-form an evidenced-based review of the literature. Resnick et al. (2005a, b, c) completed this exhaustive review of the literature, published as Guidelines for the Performance of Fusion Procedures for Degenerative Disease of the Lumbar Spine. These guidelines provide the current evidence avail-able for degenerative lumbar spine fusion procedures. The guidelines cover topics including the following:

• assessment and functional outcomes• assessment and economic outcomes• correlation between radiographic and func-

tional outcome• intractable low back pain without stenosis or

spondylolisthesis• lumbar fusion• injection therapies, low back pain, and fusion• bracing• electrophysiologic monitoring• bone extenders and substitutes.• bone growth stimulators and lumbar fusion

The following section on lumbar fusion techniques is not intended to advocate spinal fusion or one fusion technique over another. The goal is to give the reader an appreciation for the basic physiology of bone healing and the various fusion techniques currently being performed.

I. Bone Healing A solid bony fusion must be achieved to provide permanent spinal stability. Spinal instrumentation provides only tempo-rary, internal fixation. If a solid bony fusion is not achieved, fusion failure may result in fatigue and failure of supporting instrumentation and persistence or worsening of symptoms. Nurses caring for lumbar fusion patients are in a pivotal posi-tion to explain and reinforce to the patient the importance of providing an ideal environment to promote bony healing.

A. Three primary bone types1. Woven bone: Occurs in embryonic develop-

ment; fracture healing; and disease states such as hyperparathyroidism and Paget’s disease

2. Cortical bonea. Composed of osteons

(1) Compact, cylindrical(2) Haversian canals are vascular chan-

nels at the center, connected to one another by horizontal Volkmann’s canals (Figure 22)

b. Forms internal and external tables of flat bones and external surfaces of long bones

c. Mechanical strength depends on the tight packing of the osteons

3. Cancellous bonea. Also referred to as trabecular boneb. Lies between the cortical bonec. Honeycomb interstices containing

hematopoietic stem cells and bony tra-beculae

d. Arrayed in a perpendicular orientation to provide support

e. Continually undergoing remodeling

Treatment of Lumbar Spine Disorders


B. Cellular components1. Osteoblasts: Mature, metabolically active

bone forming cells2. Osteocytes: Mature osteoblasts trapped in

the bone matrix3. Osteoclasts: Multinucleated bone-resorbing

cells controlled by hormonal and cellular mechanisms

4. Bone metabolism: Under constant regulation by a host of hormonal and local factors.

C. Basic physiology of bone repair1. Osteogenesis

a. Ability of the graft to produce new boneb. Dependent on the presence of live bone

cells in the graft; unites the graft with the host bone

2. Osteoconductiona. The physical property of the graft to

serve as a scaffold for bone healing.b. Allows for the ingrowth of neovascula-

ture and infiltration of osteogenic pre-cursor cells into the graft in cancellous autograft and allograft

3. Osteoinductiona. Ability of the graft material to induce

stem cells to differentiate into mature bone cells

b. Typically associated with the presence of bone growth factors within the graft mate-rial or as a supplement to the bone graft.(1) Bone morphogenic proteins (BMPs)

and demineralized bone matrix are the principal osteoinductive materials.

(2) Autograft and allograft have some osteoinductive properties, but to a much lesser degree.

4. Autograft is the only material demonstrat-ing all three properties (osteogenesis, osteo-conduction, and osteoinduction).

D. Basic principles of bone remodeling1. The process of a bone graft becoming a solid

fusion that is incorporated into the native bone in the spine is very similar to the pro-cess of bone healing after fracture.

2. The process has three stages. a. Early inflammatory stage (weeks 1–2)

(1) A micro-hematoma forms in the bone.(2) Inflammatory changes occur at the

area of the graft.(3) Inflammation promotes granulation.(4) The use of antiinflammatory medi-

cations or cytotoxic drugs during this period may inhibit bone healing and fusion formation.

(5) With vascular ingrowth progres-sion, a collagen matrix is laid down and a soft callus forms (Pilitsis, Lucas, & Rengachary, 2002).

b. Repair stage (weeks 2–6)(1) Development of vascular and capil-

lary supply to the new bone.(2) Collagen and callus bone forms.(3) The bone formed during this period

is very weak for 4–6 weeks, requir-ing either internal fixation (instru-mentation) or bracing.

(4) Use of nicotine during this period can inhibit capillary growth and result in failure of the bone to heal.

c. Late remodeling stage (slow process, requiring months to years)(1) Restoration of the original bone

shape, structure, and mechanical strength occurs.

(2) As the patient places axial forces on the new bone, additional bone forms in the areas of stress. Conversely, the areas that do not receive stress will resorb.

E. Wolff’s lawWolff’s law states that bone placed under com-pressive stress is remodeled. Bone is formed where stresses require its presence and resorbed where stresses do not require it (Kalfas, 2001). Thus, when a bone graft is placed, it needs mechanical compressive stress so that new bone will be formed, thereby “healing” the bone.

F. Limitations to proper bone healingA number of factors may negatively affect proper bone healing: anti-inflammatory, cyto-toxic, and steroid medications during the early inflammatory stage; nicotine use; radiation; and systemic illnesses (e.g., diabetes mellitus, rheu-matoid arthritis, osteoporosis) (Pilitsis, Lucas,

Figure 22. Cortical and cancellous bone in the lumbar vertebrae


& Rengachary, 2002). If the graft site is shielded from stress, according to Wolff’s law, new bone will not be formed.

G. Graft materials1. Autograft (from the recipient’s own body)2. Allograft (Cadaver bone)3. Biologics

a. Demineralized bone matrices are made from bone that has been decalcified under acidic conditions and are composed of a mixture of type I collagen and noncol-lagenous proteins—including a variety of growth factors and cytokines. It is both osteoinductive and osteoconductive. (1) Variable carrier material dependent

on the specific product (2) Many products and manufactures

on the marketb. Recombinant human bone morphoge-

netic protein(1) Derived from bone matrix(2) Highly osteoinductive(3) Osteoconductive, osteogenic(4) Only one product is approved

by the U.S. Food and Drug Administration (FDA): INFUSE® Bone Graft (rhBMP-2); OP-1 (rhBMP-7) is currently being evalu-ated by the FDA (Rihn, et al., 2008).

(5) FDA approves INFUSE Bone Graft for spinal surgery use with

LT-CAGE®, INTERFIX™, or INTERFIX™ RP devices a) Indications are skeletal matu-

rity with degenerative disc dis-ease at one level.

(b) May also have spondylolis-thesis (up to grade I) at the involved level.

(c) It is to be implanted via an anterior open or an ante-rior laparoscopic approach. (Medtronic Sofamor Danek, April 4, 2005)

(6) Also FDA-approved for open frac-tures of the tibia.

4. Synthetic osteoconductive materials Synthetic osteoconductive materials are artificial substrates that are only osteocon-ductive (Figures 23, 24). They are scaffolds for the ingrowth of new bone (Whang & Wang, 2005). • Ceramics• Coralline matrices• Mineralized collagen• Bioactive glasses• Calcium sulfate• Acid polymers• Porous metals

H. Osteoporosis Osteoporosis, defined as a decrease in bone mineral density, is developed by everyone with aging. Women reach peak bone mass

Figure 24. A synthetic osteoconductive materialFigure 23. A synthetic osteoconductive material


by age 25–30. There is then a slow decline in bone mass until menopause; postmenopausal women experience a rapid decline in bone mass. Although men experience a slower decline, by age 60 men and women have roughly equal rates of bone loss. It is impor-tant when considering spinal care in older adults to understand that both men and women are afflicted with osteoporosis (Tis & Kuklo, 2005).

The microarchitectural deterioration that occurs as a consequence of osteoporosis may

compromise the effectiveness of internal fixation, and, with severe osteoporosis, may eliminate the option of internal fixation. Surgi-cal options for the patient with poor bone quality include utilizing multiple points of fixa-tion, anterior and posterior instrumentation, augmentation with wires, polymethyl-methacrylate, calcium phosphate paste, and, if possible, a noninstrumented fusion (Dmitriev & Kuklo, 2005; Rosner & Ondra, 2005).

II. Fusion TechniquesA. Posterolateral lumbar fusion with or without

instrumentation1. This procedure is performed via an incision

over the lumbar spine with fusion of two or more lumbar vertebrae. The procedure involves decortication of the transverse pro-cesses, facet joints, and pars interarticularis. Autograft bone is harvested from either the surgical decompression site or from an iliac crest and is placed over all decorticated surfaces. If instrumentation is used, it is laid down after the instrumentation is in place. Pedicle screw fixation is done utilizing the largest screw the pedicle is able to hold (Figures 25, 26). A 3-D image guidance sys-tem may be used for visualization.

B. Posterior lumbar interbody fusion (PLIF)Posterior elements are removed to gain access to the disc space. Once the disc space is cleared, an interbody spacer (e.g., cages, allograft wedg-es, allograft bone dowel) is placed into the disc space with disc distraction. The distractors are then removed. The spacer remains in the disc space and is left under compression. The fusion is then strengthened by adding pedicle screw fixation (Figure 27). Instrumentation adds internal support to correct spine alignment (by replacing lumbar lordosis) and secures adequate stabilization while the vertebral bones fuse at approximately 6 months (Andersen, et al., 2008; Tsutsumimoto, et al., 2009).

C. Transforaminal lumbar interbody fusion (TLIF)Utilizing a posterior approach, a unilateral facetectomy and laminectomy are performed. Spacers (e.g., cages, femoral rings, allograft) packed with autograft bone are placed into the disc space. The operative site is supplemented with pedicle screw and rod instrumentation (Figure 28; Starkweather, 2006).

Figure 26. Pedicle screw fixation: Posterior view

Figure 25. Pedicle screw fixation: Superior view


D. Anterior lumbar interbody fusionAn anterior lumbar interbody fusion is per-formed using an abdominal approach. The indications include degenerative disc disease with associated back pain. There should be no neural compression or degenerative spon-dylolisthesis, because no direct nerve root decompression is achieved intraoperatively. During exposure, care is taken to avoid vascu-lar injury and superior hypogastric stretching or injury leading to retrograde ejaculation (Burkus, 2004; Truumees & Brebach, 2004).1. Generally the anterior longitudinal ligament

is divided and reflected to opposite sides to allow spine and disc work.

2. The disc space is cleaned, and an interbody device is placed in the disc space.

3. LT-CAGE® can be packed with recombi-nant human bone morphogenetic protein (Figures 29, 30).

4. The femoral ring is packed with autograft.E. Combined anterior/posterior fusion

Anterior/posterior lumbar fusions are indi-cated for patients in whom instability from spondylolisthesis or other degenerative prob-lems leads to the need for both anterior and posterior column fixation.

F. Minimal-access/minimally invasive fusion techniques 1. The minimally invasive percutaneous PLIF

procedure utilizes a hybrid of microsurgi-cal and endoscopic techniques through four 2-cm incisions (Figure 31).

2. An interbody distractor device is placed into the disc space to restore intervertebral height, and an appropriate-size graft is placed. The pedicle-screw rod instrumenta-tion is placed through the same incisions.

Figure 28. L4–L5, L5–S1 transforaminal lumbar interbody fusion: Lateral X ray

Figure 27. L5–S1 Posterior lumbar interbody fusion: Lateral X ray


3. The guiding K-wire is advanced to the planned segmental fusion site. A multiaxial pedicle screw is passed over the K-wire, and the pedicle screw is then inserted into the pedicle. For each ipsilateral pair of pedicles within the motion segment that is fused, the rod inserter is passed through both screw heads.

G. Intraoperative image guidance1. Preoperatively, a CT or MRI scan through

the appropriate spinal levels is obtained,

and image data are transferred to the com-puter workstation in the operating suite.

2. Three to five reference points for each spinal segment to be instrumented are selected and stored in the image data set and then identi-fied in the operative field and registered.

3. This information allows the surgeon to have real-time, 3-D information about the patient’s bony anatomy during the opera-tive procedure.

III. Disc Arthroplasty (Artificial Disc Replacement)To date, the only FDA-approved lumbar artificial disc replacements are the Charité™ (Guyer, et al., 2009) and the ProDisc-L. Two other devices, the Maverick and Flexicore lumbar disc prostheses, are in FDA trials under continued access mode. Proponents of artificial disc replacement cite its stabilization and preservation of the motion segment. As results of preservation of the motion segment, proponents report decreased adjacent level-disease and a reduction in other complications of lumbar fusion (i.e., hardware failure, graft problems, graft site pain, symptomatic pseudoarthrosis,

Figure 29. LT-CAGE® Figure 30. Anterior lumbar interbody fusion: Lateral view

Figure 31. Minimal-access (minimally invasive) fusion


loss of motion across fused segments, loss of normal sagittal balance (Berg et al., 2009).

Correct patient selection as well as accurate and correct placement are important for optimal surgical results. Clinical indications for the Charité include single-level degenerative disc disease at L4–L5 or L5–S1, confirmed by provocative discography; back and or leg pain without nerve root com-pression; and failure of nonsurgical treatment (Guyer, et al., 2009). Clinical indications for the ProDisc-L are disabling low back pain caused by one or two adjacent levels between L3–S1. The pain must primarily originate from the disc and be refractory to aggressive nonoperative treatment for at least 6 months (Berg et al., 2009). Both devices are placed through an anterior approach.

IV. Intradiscal electrothermal annuloplasty (IDET) The clinical indication is degenerative disc disease with maintained disc height and failed nonsurgical treatment. MRI findings and discography must correlate with each other.

A specialized catheter is threaded through an introducer to the affected area. The catheter is heated to 90° C for 17 minutes. The purpose is to cauterize the annular tear and pain fibers, thereby decreasing or alleviating the low back pain.

This minimally invasive procedure is done in an interventional radiology suite or operating room under fluoroscopy. It is performed as an outpatient procedure us-ing conscious sedation.

V. Nursing Assessment, Intervention, and Monitoring A. Preoperative

1. Surgical procedure2. Informed consent (obtained by surgeon)3. Expected outcomes (postoperative and long

term)4. Required preoperative testing5. Discontinuation of medications (e.g., herbal

products, NSAIDs, anticoagulants, aspirin, warfarin, clopidogrel bisulfate)

B. Perioperative1. Explain to patient where and when to arrive

as well as surgery time.2. Instruct patient on eating and drinking

restrictions.3. Instruct patient on medications to be taken

the morning of the surgery with a sip of water.

4. Remind patient to wear comfortable cloth-ing and to leave jewelry and valuables at home.

5. Remind patient to remove dentures, partial plates, eyeglasses, contact lenses, nail polish, and sculptured nails.

C. Intraoperative1. Plan for equipment needs2. Potential 3-D stereotactic guidance system3. Specialty table

4. May need fluoroscope in roomD. Postoperative

1. Neurological assessmenta. Strength and sensation assessment as

compared with preoperative statusb. Special attention to the neurological

assessment and correlation to the opera-tive intervention

c. Patients with diabetes and obesity are at higher risk of postoperative compli-cations, particularly wound infection (Brown, et al., 2007; Djurasovic, et al., 2008). Measures to maintain glycemic control and deep vein thrombosis pro-phylaxis is particularly important in patients with these risk factors.



b. Instruct and help patient to roll to side and bring legs down while simultaneously rising from the bed with the torso. This minimizes twisting at the waist.

c. Instruct and help patient to rise from a chair using the legs rather than the back.

3. Bracinga. The decision whether to brace and the

type of brace used to use varies widely.b. The decision is dependent on the sur-

gery performed, bone quality, and phy-sician preference.

c. If braces are ordered, patient should be given specific guidelines regarding use (van Duijvenbode, et al., 2008).

4. Pain controlMethods to reduce postoperative pain vary according to clinical practice prefer-ences. Patient-controlled analgesia (PCA) and patient-controlled epidural analgesia (PCEA) provide good overall patient satis-faction (Fisher, et al., 2003). The only clini-cal advantage of PCEA over PCA for spine fusion patients was the lower quantity of opioids consumed, although the PCEA group experienced significantly more side effects than the PCA group did. There were no other significant differences. Therefore, the patient or physician can select either postoperative pain management delivery system. Continuous epidural infusion of 0.1% ropivacaine resulted in lower pain scores, lower opioid consumption, and higher patient satisfaction when compared with


placebo (saline) in a study by Gottschalk and colleagues (2004). Application of ropiva-caine using an epidural catheter seems to be highly effective for postoperative pain after major lumbar spinal surgery. Postoperative continuous infusion of 0.5% marcaine into the subfascial aspects of the wound resulted in lower pain scores and less narcotic use in patients undergoing lumbar fusion com-pared to those receiving standard pain man-agement (Elder, Hoh, & Wang, 2008). If postoperative pain is out of proportion and impairs activities, an X ray or CT scan, or both, of the lumbar spine should be con-sidered to evaluate the screw location and to demonstrate integrity of the spinal canal. Other pain management options include the following: intravenous hydromorphone or morphine sulfate, as needed, until the patient is able to take oral medications; codeine, hydrocodone, or oxycodone, with or without acetaminophen, as needed, when the patient is able to take oral medications; antispasmodics, if muscle spasms are pres-ent; neuropathic pain medications (e.g., Gabapentin). Nonsteroidal anti-inflammatory drugs (NSAIDS) are typically avoided due to the possible interference with bone fusion (Glassman, et al., 1998).

E. Nutrition1. Patients are at high risk of developing a

postoperative ileus.2. The timing of initial oral intake varies

widely. In the fasting patient, the presence of bowel sounds may not reflect gastrointesti-nal motility when the patient eats (Story & Chamberlain, 2009). Regarding early postop-erative eating and its effect on postoperative ileus, Story & Chamberlain’s (2009) litera-ture review found that early enteral feeding decreased the duration of postoperative ileus and length of stay. They noted that, because early feeding does not increase the occurrence of associated complications, it may be used as a strategy to prevent postoperative ileus.

F. Constipation prevention1. Consider initiating preoperatively.2. Ensure adequate water intake.3. Diet should include adequate fresh fruits,

vegetables, and fiber.4. Stool softener (e.g., docusate) may be used

two to three times per day.5. Motility agents (e.g., senna) should be used

only as needed.

G. Urination1. A Foley catheter should be kept in place until

the patient is able to stand to void or to reli-ably use a urinal or bedpan. The goal should be to remove the Foley catheter within 24 hours of surgery.

2. Urinary hesitancy, especially during the immediate postoperative period, is usually transient.

3. Assess urinary output, frequency, and vol-ume.

4. Assess to ensure there is adequate emp-tying. Bladder scanning or intermittent bladder catheterization may be necessary to assess the patient for retention or incom-plete emptying.

H. Discharge planning1. Discharge planning should be initiated

preoperatively.2. Reinforce to patient the need to avoid lift-

ing, bending, twisting, and sitting for long periods of time.

3. Remind patient to change positions frequently.4. Remind patient not to drive while using

narcotic pain medications.5. Sexual activity may be resumed as advised

by the physician and when comfortable.6. Ensure the patient is aware of return-to-

work and activity recommendations. 7. Reinforce alternative planning and problem

solving for everyday activities (e.g., vacu-uming, doing laundry, and performing child care).

8. Incision care varies with the type of closure. 9. Ensure the patient is aware of postoperative

follow-up recommendations.I. Postoperative

1. Talk to patient about gradually returning to ADLs and lifestyle.

2. Patient should begin ambulation within the first 24 hours. Activity will improve pain tolerance and decrease muscle spasms.

3. Patient should avoid heavy lifting (anything heavier than a gallon of milk) for the first 4–6 weeks.

4. Patient should avoid prolonged sitting or standing for the first 4–6 weeks, including long car trips.

5. Patient should begin a walking program that includes progressively longer distances two to three times per day.

6. Prescribing an exercise program starting 4–6 weeks post-surgery may lead to a faster decrease in pain and disability than no


treatment. High intensity exercise programs appear to provide a faster decrease in pain and disability than low intensity programs (Ostelo, et al., 2008; Ostelo, et al., 2009).

7. Patient’s return to work will vary, depend-ing on type of work (sedentary work earlier than heavy labor). Return to work may be a gradual progression to full time.

8. Outpatient therapy will be decided on an individual basis and discussed at follow-up surgical visit.

9. Patient should be instructed on incision care, dressing removal, bathing, and obser-vation of incision for redness, swelling, or drainage.

10. Call surgeon’s office for temperature higher than 100.6° F.

11. Patient will gradually be weaned from pain medication.

J. Common postoperative complications (Green-berg, 2001, pp.187-189) Common postoperative complications are as follows: 1. Superficial wound infections

a. 0.9%–5% incidenceb. Increased risk with age, long-term ste-

roid use, obesity, or diabetes mellitusc. Most superficial infections are caused by

S. aureus.d. Mild infections are usually treated with

7–14 days of oral antibiotics.2. Increased motor deficit

a. 1%–8% incidenceb. Can be transient with nerve root stretch-

ing or manipulation.3. Unintended durotomy

a. 0.3%–13% incidenceb. Generally revealed intraoperativelyc. May be repaired with a 4.0 silk or

Neuralon, fibrin glue, or muscle plug (may be necessary for poor-quality dura or difficult locations).

d. Possible sequelae include a CSF fistula (external CSF leak) or pseudomeningo-cele.

e. A CSF leak generally presents as a wound leak, a collection, or postural headaches.

f. In most circumstances, activity is restricted to flat lying position for 24–48 hours. Head of bed is gradually increased.

g. In some situations, the physician may elect to have a blood patch placed to plug the tunnel.

4. Pseudomeningocelea. 0.7%–2% incidenceb. Appears similar radiographically to a

spinal epidural abscess.c. If a dural tear is suspected or visualized,

the patient is maintained in a flat posi-tion for 24–48 hours to minimize dural pressure. Raise the head of the bed slow-ly (10 degrees every hour) until upright. If the patient complains of positional headache (i.e., headache when upright), then resume flat lying position.

d. Some surgeons may place a lumbar drain to decrease dural pressure and allow for dural repair.

e. Surgical exploration may be necessary if symptoms do not resolve.

K. Uncommon complications1. Instability

a. Instability is usually found in predis-posed patients undergoing decompres-sion without fusion, especially if a sig-nificant amount of facet is removed.

b. Obtain flexion/extension films to deter-mine amount of movement and need for fusion.

2. Direct injury to neural structures3. Deep infections: <1% incidence; this

includes discitis at 0.5%, spinal epidural abscess at 0.67%, and osteomyelitis.

4. Thrombophlebitis and deep-vein thrombosis with risk of pulmonary embolism: 0.1% inci-dence.

5. Complications of positioning: compression neuropathies, anterior tibial compartment syndrome, pressure on the eye, cervical spine injuries.

L. Outcomes1. Standard: Lumbar fusion is recommended

as a treatment for carefully selected patients with disabling low back pain due to one- or two-level degenerative disease without stenosis or spondylolisthesis.

2. Optional: An intensive course of physical therapy and cognitive therapy is recom-mended as a treatment option for patient with low back pain in whom conventional medical management has failed (Resnick et al., 2005b).


I. L5–S1 Herniated DiscD. K., a 30-year-old female, had intermittent right-buttock and lower extremity pain, approximately 3 months in duration. Upon presentation to clinic, she had been ex-periencing acute pain exacerbation for the past 2 weeks. She described the pain as radiating from her right buttock into her posterior lower extremity to her lateral foot. She denied weakness in her right leg, bowel or bladder problems, or any symptomatology in her left leg. Her pain was aggravated by sitting and alleviated by changing posi-tions frequently. She participated in physical therapy for 2 weeks, which exacerbated her symptoms. She also had tried NSAIDs and ice.

A. History and review of systems1. Social history: Married with two small

children. Works as a transcriptionist but had been unable to work for 1 week

2. Medical history: Depression, which she noted is under fair control

3. Surgical history: Hysterectomy, tonsillectomy4. Medications: Wellbutrin, ibuprofen,

cyclobenzaprine, hydrocodone/APAP5. Allergies: No known drug allergies6. Review of systems: Unremarkable

B. Focused neurologic examination and diagnosticsThe neurological examination indicated an absent right Achilles reflex and a markedly positive straight leg raise on the right with a positive crossed straight leg test. Her gait was antalgic. Strength and sensation were normal in the bilateral lower extremities. Her MRI dem-onstrated a large L5–S1 herniated disc to the right (Figures 32, 33).

C. Further conservative treatmentD. K. wished to pursue all nonoperative options. She underwent an ESI for pain relief the day of the initial clinic visit. Two weeks later, she had experienced a decrease in her pain. However, her ADLs continued to be significantly impaired. She wished to proceed with surgery.

D. Operative interventionD. K. underwent an L5–S1 microdiscectomy for a right S1 radiculopathy. She has done well postoperatively, and at 1 year after surgery had no pain and was participating in all of her usual activities.

II. L4–5L Herniated Disc; L5–S1 Foraminal StenosisD. B., a 39-year-old male, had a 4-month history of low back pain, previous right leg pain, and, currently, left leg pain. Approximately 4 months ago he had intermittent

Case Studies

Figure 32. L5–S1 herniated nucleus pulposus (HNP): MRI, sagittal view

Figure 33. L5–S1 herniated disc, eccentric to the right: Axial T2-weighted MRI image


right leg pain, which had resolved. He now described pain that radiated from his low back to his left buttock down the posterior thigh to the knee. Distally from the knee he had numbness down his posterior lower leg to the lateral aspect of his foot. His pain was aggravated by being in any one position for too long. His pain was alleviated by lying in a fetal position. He denied any weakness or any bowel or bladder difficulty. He had tried chiropractic manipula-tion and NSAIDs, without any pain relief.

A. History and review of systems1. Social history: Married, previously active

businessman. Occasional tobacco, rare alco-hol use

2. Medical history: No past medical problems3. Surgical history: Remote history of facial frac-

tures after a motor vehicle collision4. Medications: Naprosyn, hydrocodone/

APAP, cyclobenzaprine5. Allergies: No known drug allergies6. Review of systems: Unremarkable

B. Focused neurological examination and diagnosticsThe neurological examination indicated a decreased sensation to light touch and pinprick in the posterior thigh, calf, and lateral foot on the left lower extremity. Right lower extremity sensation was intact. Bilateral lower extremity strength was intact. Bilateral patellar reflexes were normal, as was the right Achilles reflex. The left Achilles reflex was absent. Motor strengths were full in bilateral lower extremi-ties. Straight leg test was positive on the left at 30 degrees. His gait was markedly antalgic.

MRI revealed a large extruded fragment at L4–L5, eccentric to the right, but essentially filling the spinal canal with a concomitant disc bulge at L5–S1, causing some encroachment on the left S1 nerve root (Figure 34).

C. Operative interventionD. B. underwent L4 laminectomy, partial right-sided L4 laminectomy removal of L4–L5 extruded disc herniation, and left L5–S1 foraminotomy—all with the use of the operat-ing microscope. At 6 weeks after surgery, he had complete relief of his symptoms.

III. L4–L5 StenosisA. M., a 53-year-old male, had a 2-year history of pro-gressive bilateral foot pain and burning sensations that radiated down his lower extremities. His symptoms were aggravated by standing and walking and alleviated by sitting down. He denied any leg weakness or any bowel or bladder difficulty. He had undergone chiropractic treatment, NSAID use, and physical therapy without any symptom relief.

A. History and review of systems1. Social history: Single, works at a seden-

tary computer job. Occasional tobacco use, denies alcohol use

2. Medical history: Depression, obesity, high triglycerides

3. Surgical history: Tonsillectomy, remote4. Medications: Ibuprofen, gemfibrozil5. Allergies: No known drug allergies6. Review of systems: Unremarkable

B. Focus neurological examination and diagnosticsThe neurological examination indicated full-strength and intact sensation in his bilateral lower extremities. Patella reflexes were intact, the right Achilles reflex was absent, and the left Achilles was diminished. A review of his MRI scan revealed L4–L5 stenosis (Figure 35).

C. Operative interventionA. M. underwent a L4–L5 decompressive laminectomy for stenosis. He has done well af-ter surgery, with a gradual increase in walking distance and resumption of normal activities.

Figure 34. L4–L5 HNP, L5–S1 bulge: MRI, sagittal viewThe top arrow points to a mild disc bulge with annular tear at L3–L4. The bottom arrow points to a disc bulge with annular tear at L5–S1. At L4–L5, a massive extruded disc is causing severe canal stenosis.


IV. L5–S1 Grade-II SpondylolisthesisJ. K., a 52-year-old male, had a long history of low back pain and a 3-month history of right posterior lower extrem-ity pain. His pain was aggravated by any activity and improved with rest. He denied any paresthesias, weak-ness, or bowel/bladder difficulty. He had participated in physical therapy, chiropractic manipulation, bed rest, and NSAID use without pain relief.

A. History and review of systems1. Social history: Married, has worked 25 years

as a shipper. Quit smoking 5 years ago, denies alcohol intake

2. Medical history: Hypertension, asthma3. Surgical history: Cardiac catheterization

and ablation this year; carpal tunnel release; shoulder surgery

4. Medications: Aspirin, lisinopril, lovasta-tin, metoprolol, omeprazole, amitriptyline, hydrocodone, glucosamine/chondroitin, multiple herbs and supplements

5. Allergies: Sulfa-caused hives6. Review of systems: Unremarkable

B. Focused neurological examination and diagnosticsThe neurological examination revealed decreased sensation to pinprick on the right lateral lower extremity and top of the right foot. A 4/5 weakness was noted in the right extensor hallicus longus (EHL) and right dorsiflexion. He had difficulty walking on his heel on the right side. Knee and Achilles reflexes were nor-mal bilaterally. Review of his MRI demonstrates

a grade-2 spondylolisthesis at L5-S1 with bilat-eral L5 nerve root compression (Figure 36).

C. Operative interventionJ. K. underwent an L5–S1 anterior-posterior

decompression and fusion (Figure 37). He has done remarkably well with return to all goal activities.

V. Multilevel Lumbar Stenosis with L4–L5 Grade-I Spondylolisthesis for Decompression and Fusion

D. S., a 74-year-old male, had a 15-month history of low back and right hip pain. He described pain radiating from his back into his right hip and down to the right lateral calf. He noted some numbness in his right foot with ambulation, which was better with rest. His legs fatigued easily, and the distance he was able to walk had decreased. He had received chiropractic manipulation, worn a back brace, and had an ESI with pain relief. He rated his pain at its worst as 8 on a scale of 10.

A. History and review of systems1. Social history: A widowed retired professor

who lives alone. His children are in the area. He denied tobacco use; occasional alcohol use

Figure 35. L4–L5 stenosis, central and neuroforaminal: MRI, axial view

Figure 36. L5–S1 DDD and grade-II spondylolisthesis: Lateral radiograph


2. Medical history: Recently diagnosed pros-tate cancer, treatment almost finished; hypertension; diverticulitis

3. Surgical history: Laparotomy, remote4. Medications: Allopurinol, lovastatin, hydro-

chlorothiazide, atenolol, lisinopril5. Allergies: No known drug allergies6. Review of systems: Diverticulitis and hyper-

tension well controlledB. Focused neurological examination and

diagnosticsOn neurological examination, D. S. had full bi-lateral lower extremity strength. Bilateral knee reflexes were intact; Achilles reflexes were ab-sent. Sensation was intact. He was slow to rise from a chair and walked with a flexed posture.

His MRI of the lumbar spine revealed disc degeneration at L4–L5 with a grade-1 spondylolisthesis. There was also severe disc degeneration at L5–S1, severe canal stenosis at L4–L5, and moderate canal stenosis at L3–L4. (Figures 38, 39).

C. Operative interventionD. S. underwent a L3–L4 laminectomy and L4–L5 instrumented fusion. (Figures 40, 41). He has returned to normal activities with complete resolution of his pain.

Figure 39. Lumbar stenosis: MRI, axial viewFigure 37. Anterior-posterior fusion: Instrumentation has been placed both anteriorly and posteriorly

Figure 38. L4–L5 stenosis with grade-I spondylolisthesis: MRI, sag-ittal view


Figure 40. Postoperative lateral radiograph with instrumentation in place

Figure 41. Postoperative anteroposterior radiograph with instrumen-tation in place


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