Degenerative Disorders of the Thoracic and Lumbar Spine


Overview of Lumbar and Thoracic Disc Degeneration and Herniation

Despite an improving understanding of degenerative disc disease on the basis of its natural history and basic science, treatment results of this entity vary greatly. There is no lack of treatment options for degenerative discs; what we tend to lack is understanding of the specific cause(s) of the patient’s chief complaint. Despite the fact that William Kirkaldy-Willis has described the spectrum of disc degeneration and its pathologic progression, the clinical correlation of history, physical examination, and imaging that yields a specific diagnosis remains the greatest challenge. Over the past several decades, studies of patients with back and/or leg pain have led to improved treatment of the patients in whom a specific diagnosis was possible. This group remains the minority of patients who are evaluated for low back or leg pain. Complex psychosocial issues, depression, and secondary gain are a few of the nonanatomic problems that must be considered when evaluating these patients. In addition, the number of anatomic causes for these symptoms, whether real or perceived, has increased as understanding and diagnostic capabilities have increased.

Axial spine pain, which should be distinguished from disc degeneration, is the most frequent musculoskeletal complaint. Axial spine pain—whether cervical, thoracic, or lumbar—often is attributed to disc degeneration. This degenerative process does not always cause pain, but it can lead to internal disc derangement, disc herniation, facet arthrosis, degenerative spondylolisthesis, and stenosis that can be seen on imaging. Each of these pathologic processes has unique clinical findings and treatments. Outcomes of treatment for each of these specific pathologic entities also vary greatly despite their being from the same etiologic spectrum. The understanding of disc degeneration and the associated pathologies has changed markedly over the past several years.

The genetic influence on disc degeneration may be caused by a small effect from each of multiple genes or possibly a relatively large effect from a smaller number of genes. To date, several specific gene loci have been identified that are associated with disc degeneration. This association of a specific gene with degenerative disc changes has been confirmed. Other variations in the aggrecan gene, metalloproteinase-3 gene, collagen type IX, and alpha 2 and 3 gene forms also have been associated with disc pathology and symptoms. The understanding of symptoms and treatment success for disc herniations has surpassed those related to disc degeneration alone.

Nonspecific axial pain is an international health issue of major significance and should be discriminated from pain associated with a disc herniation. Approximately 80% of individuals are affected by this symptom at some time in their lives. Impairments of the back and spine are ranked as the most frequent cause of limitation of activity in individuals younger than 45 years old by the National Center for Health Statistics ( www.cdc.gov/nchs ). Physicians who treat patients with spinal disorders and spine-related complaints must distinguish the complaint of back pain, which several epidemiologic studies reveal to be relatively constant, from disability attributed to back pain. Although back pain as a presenting complaint may account for only 2% of the patients seen by a general practitioner, the cost to society and the patient in terms of lost work time, compensation, and treatment is staggering.

The total cost of low back pain in the United States is greater than $100 billion per year; one third are direct costs for care, with the remaining costs resulting from decreased productivity, lost wages, and absenteeism. Also, only about 5% of patients accounted for 75% of the costs. Typically, about 90% of patients return to work by 3 months, with most returning to work by 1 month. Patients off work for 6 months have only a 50/50 probability of ever returning to work, whereas at 1 year this probability decreases to 25%.

Nonanatomic factors, specifically work perception and psychosocial factors, are intimately intertwined with physical complaints. Compounding the diagnostic and treatment difficulties is the high incidence of significant abnormalities shown by imaging studies, which in asymptomatic matched controls is 76%. Identified risk factors for radiographically apparent disc disorders of the lumbar spine include genetic factors, age, gender, smoking, increased intra-abdominal fat, metabolic syndrome, and, to a minimal degree, occupational exposure, but not socioeconomic factors. In contrast is the importance of socioeconomic factors for the development of low back pain and disability. Job dissatisfaction, physically strenuous work, psychologically stressful work, low educational attainment, and workers’ compensation insurance all are associated with low back pain or disability. These data suggest that aggressive treatment between 4 weeks and 6 months is necessary for patients with low back pain. Consideration of socioeconomic factors is an important component of appropriate patient evaluation because there is an inextricable link between an individual’s socioeconomic status and his or her health.

Optimal outcome primarily depends on “proper patient selection,” which so far has defied satisfactory definition. Until the pathologic process is better described and reliable criteria for the diagnosis are determined, improvement in treatment outcomes will change slowly.

Disc and Spine Anatomy

The anatomy of the spine and discs is discussed in detail in Chapter 37 .

Neural elements

The organization of the neural elements is strictly maintained throughout the entire neural system, even within the conus medullaris and cauda equina distally. The orientation of the nerve roots in the dural sac and at the conus medullaris follows a highly organized pattern, with the most cephalad roots lying lateral and the most caudad lying centrally. The motor roots are ventral to the sensory roots at all levels. The arachnoid mater holds the roots in these positions.

The pedicle is the key to understanding surgical spinal anatomy. The relation of the pedicle to the neural elements varies by region within the spinal column. In the thoracic and lumbar spine, the named root exits below the named pedicle. Discs are formally named for the vertebral bodies between which they lie (e.g., the L4-5 disc is between the L4 and L5 vertebral bodies). This allows slightly more specificity in describing the discs if there is an anatomic variant (e.g., L4- S1) and less confusion than having the vertebral body, nerve root, and disc sharing the same name. Despite being less specific, the disc often is informally named for the vertebral level immediately cephalad (e.g., the L4 disc is immediately caudal to the L4 vertebra). In the lumbar spine, lateral recess pathology, such as lateral recess stenosis or posterolateral disc herniation, typically involves the next nerve root exiting caudal to that disc; for example, an L4-5 posterolateral disc herniation would be expected to cause L5 nerve root symptoms.

At the level of the intervertebral foramen is the dorsal root ganglion (DRG). The DRG lies within the outer confines of the foramen. Distal to the ganglion, three distinct branches arise; the most prominent and important is the ventral ramus, which supplies all structures ventral to the neural canal. The second branch, the sinuvertebral nerve, is a small filamentous nerve that originates from the ventral ramus and progresses medially over the posterior aspect of the disc and vertebral bodies, innervating these structures and the posterior longitudinal ligament. The third branch is the dorsal ramus. This branch courses dorsally, piercing the intertransverse ligament near the pars interarticularis. Three branches from the dorsal ramus innervate the structures dorsal to the neural canal. The lateral and intermediate branches provide innervation to the posterior musculature and skin. The medial branch separates into three branches to innervate the facet joint at that level and the adjacent levels above and below ( Fig. 39.1 ).

FIGURE 39.1, A, Dorsal view of lumbar spinal segment with lamina and facets removed. On left side, dura and root exiting at that level remain. On right side, dura has been resected and root is elevated. Sinuvertebral nerve with its course and innervation of posterior longitudinal ligament is usually obscured by nerve root and dura. B, Cross-sectional view of spine at level of endplate and disc. Note that sinuvertebral nerve innervates dorsal surface of disc and posterior longitudinal ligament. Additional nerve branches from ventral ramus innervate more ventral surface of disc and anterior longitudinal ligament. Dorsal ramus arises from root immediately on leaving foramen. This ramus divides into lateral, intermediate, and medial branches. Medial branch supplies primary innervation to facet joints dorsally.

Disc innervation is through afferent axons with cell bodies within the DRG. Nociceptive signals are transmitted to the spinal cord by neurons from the DRG. Animal studies have revealed two paths between the annulus and the DRG: one from the sinuvertebral nerve and another along the paravertebral sympathetic trunk. The sinuvertebral nerve is a recurrent branch of the ventral ramus that connects back to the posterior disc at each level. The paired ganglia chains of the sympathetic trunks have axons that course through the gray rami communicantes to the spinal nerve. The disc is innervated by fibers from multiple levels. In animal models, the lateral annulus was found to be innervated by fibers coursing from the index level and two additional superior levels through the sinuvertebral nerves. Also, there was innervation through the sympathetic trunk by the DRG from the three levels even more superior than the sinuvertebral innervations. Contralateral DRG involvement also occurs through both pathways. Similar nonsegmental, multilevel innervation patterns also have been reported for the ventral disc surface. These complex multilevel innervations would help explain the pain patterns encountered clinically if similar patterns are present in humans. Also, innervations of the disc from the vertebral endplate have been shown. Intraosseous nerves follow the osseous vasculature. This endplate innervation is through a branch of the sinuvertebral nerve, the basivertebral nerve. This nerve enters the foramen, and the nerve fibers enter the vertebral margin with the vessels. The density of innervation is similar to that seen in the outer annulus, which suggests that the endplates are as important to pain generation as is the annulus.

Natural History of Disc Disease

One theory of spinal degeneration assumes that all spines degenerate and that current methods of treatment are for symptomatic relief, not for cure. The degenerative process has been divided into three separate stages with relatively distinct findings. The first stage is dysfunction, which is seen in individuals 15 to 45 years old. It is characterized by circumferential and radial tears in the disc annulus and localized synovitis of the facet joints. The next stage is instability. This stage, found in 35- to 70-year-old individuals, is characterized by internal disruption of the disc, progressive disc resorption, and degeneration of the facet joints with capsular laxity, subluxation, and joint erosion. The final stage, present in individuals older than 60 years, is stabilization. In this stage, the progressive development of hypertrophic bone around the disc and facet joints leads to segmental stiffening or frank ankylosis.

Each spinal segment degenerates at a different rate. As one level is in the dysfunction stage, another may be entering the stabilization stage. Disc herniation in this scheme is considered a complication of disc degeneration in the dysfunction and instability stages. Spinal stenosis from degenerative arthritis in this scheme is a complication of bony overgrowth compromising neural tissue in the late instability and early stabilization stages.

Long-term follow-up studies of lumbar disc herniations have documented several principles, the foremost being that generally symptomatic lumbar disc herniation (which is only one of the consequences of disc degeneration) has a favorable outcome in most patients. The primary benefit of surgery has been noted to occur early on in the first year after surgery, but with time the statistical significance of the improvement appears to be lost. In general, the literature supports an active care approach, minimizing centrally acting medications. The judicious use of epidural steroids also is supported, but long-term results and repeated use is questionable. Nonprogressive neurologic deficits originating from the lumbar spine (except cauda equina syndrome) can be treated nonoperatively with expected clinical improvement. If surgery is necessary, it usually can be delayed 6 to 12 weeks to allow adequate opportunity for improvement. Some patients are best treated surgically, and this is discussed in the section dealing specifically with operative treatment of lumbar disc herniation.

The natural history of degenerative disc disease is one of recurrent episodes of pain followed by periods of significant or complete relief.

Before a discussion of diagnostic studies, axial spine pain with radiation to one or more extremities must be considered. Also, understanding certain pathophysiologic entities must be juxtaposed to other entities of which only a rudimentary understanding exists. It is doubtful there is any other area of orthopaedics in which accurate diagnosis is as difficult or the proper treatment as challenging as in patients with persistent neck and arm or low back and leg pain. Although many patients have clear diagnoses properly arrived at by careful history and physical examination with confirmatory imaging studies, many patients with pain have absent neurologic findings other than sensory changes and have normal imaging studies or studies that do not support the clinical complaints and findings. Inability to easily determine an appropriate diagnosis does not relieve the physician of the obligation to recommend treatment or to direct the patient to a setting where such treatment is available. Careful assessment of these patients to determine if they have problems that can be orthopaedically treated (operatively or nonoperatively) is imperative to avoid both overtreatment and undertreatment.

Operative treatment can benefit a patient if it corrects a deformity, corrects instability, relieves neural compression, or treats a combination of these problems directly attributable to the patient’s complaint. Obtaining a history and completing a physical examination to determine a diagnosis that should be supported by other diagnostic studies is fundamental; conversely, matching the diagnosis and treatment to the results of diagnostic studies, as often can be done in other subspecialties of orthopaedics (e.g., treating extremity pain based on a radiograph that shows a fracture), is more complex and difficult. The history, physical examination, and imaging studies must all confirm the same pathologic process as the source of symptoms if surgical intervention is to be reproducibly successful.

Axial lumbar pain

Axial lumbar pain occurs at some point in the lives of most people. Appropriate treatment for what can be at times excruciating pain generally should begin with evaluation for a significant spinal pathologic process. This pathologic process being absent, a brief (1 to 3 days) period of bed rest with institution of an antiinflammatory regimen and rapid progression to an active exercise regimen with an anticipated return to full activity should be expected and encouraged. Generally, patients treated in this manner improve significantly in 4 to 8 weeks. Diagnostic studies, including radiographs, often are not helpful because they add little information. More sophisticated imaging with CT and MRI or other studies have even less utility initially. An overdependence on the diagnosis of disc herniation can occur with early use of these diagnostic studies, which show disc herniations in 20% to 36% of normal volunteers. General imaging guidelines have been developed to help identify patients for whom radiography is indicated ( Box 39.1 ).

BOX 39.1
Selective Indications for Radiography in Acute Low Back Pain

  • Age >50 years

  • Significant trauma

  • Neuromuscular deficits

  • Unexplained weight loss (10 lb in 6 months)

  • Suspicion of ankylosing spondylitis

  • Drug or alcohol abuse

  • History of cancer

  • Use of corticosteroids

  • Temperature ≥37.8°C (≥100°F)

  • Recent visit (≤1 month) for same problem and no improvement

  • Patient seeking compensation for back pain

Patients should understand that persistence of some pain does not indicate treatment failure, necessitating further measures; however, it is important for treating physicians to recognize that the longer a patient is limited by pain, the less likely he or she is to return to full activity.

For patients who do not respond to treatment regimens, early recognition that other issues may be involved is essential. Careful reassessment of complaints and reexamination for new information or findings and inconsistencies are necessary. Many studies of occupational back pain have revealed that depression, occupational mental stress, job satisfaction, intensity of concentration, anxiety, and marital status can be related to complaints of pain and disability. The role of these factors as causal or consequential of the symptoms remains an area of continued study; however, there is some evidence that the psychologic stresses occur before complaints of pain in some patients. Another finding that is evident from the literature is the inability of physicians to detect psychosocial factors adequately without using specific instruments designed for this purpose in patients with back pain. In one study, experienced spinal surgeons were able to identify distressed patients only 26% of the time based on patient interviews. Given the difficulty of identifying patients with psychosocial distress, being aware of the high incidence of incidental abnormal findings on imaging studies underscores the need for critical individual review of these studies by treating physicians. Severe nerve compression shown by MRI or CT correlates with symptoms of distal leg pain; however, mild-to-moderate nerve compression ( Table 39.1 ), disc degeneration or bulging, and central stenosis do not correlate significantly with specific pain patterns.

TABLE 39.1
Classification for Spinal Nerve and Thecal Sac Deformation on Magnetic Resonance Imaging
From Beattie PF, Myers SP, Stratford P, et al: Associations between patient report of symptoms and anatomical impairment visible on lumbar magnetic resonance imaging, Spine 25:819–828, 2000.
SPINAL NERVE DEFORMATION IN LATERAL RECESS OR INTERVERTEBRAL FORAMEN
0—absent No visible disc material contacting or deforming nerve
I—minimal Contact with disc material deforming nerve but displacement <2 mm
II—moderate Contact with disc material displacing ≥2 mm; nerve is still visible and not obscured by disc material
III—severe Contact with disc material completely obscuring nerve
THECAL SAC DEFORMATION IN VERTEBRAL CANAL
0—absent No visible disc material contacting or deforming thecal sac
I—minimal Disc material in contact with thecal sac
II—moderate Disc material deforming thecal sac; anteroposterior distance of thecal sac ≥7 mm
III—severe Disc material deforming thecal sac; anteroposterior distance of thecal sac <7 mm

Diagnostic Studies

Radiography

The simplest and most readily available diagnostic tests for lumbar pain are anteroposterior and lateral radiographs of the involved spinal region. These simple radiographs show a relatively high incidence of abnormal findings; however, spinal radiographs on the initial visit for acute low back pain may not contribute to patient care and are not always cost effective. Plain radiographs may be considered only after the initial therapy fails, especially in patients younger than 45 years old.

There is insignificant correlation between back pain and the radiographic findings of lumbar lordosis, transitional vertebra, disc space narrowing, disc vacuum sign, and claw spurs. In addition, the entity of disc space narrowing is extremely difficult to quantify in all but operated backs or in obviously abnormal circumstances. A study of 321 patients found that only when traction spurs or obvious disc space narrowing or both were present did the incidence of severe back and leg pain, leg weakness, and numbness increase. These positive findings had no relationship to heavy lifting, vehicular exposure, or exposure to vibrating equipment. Other studies have shown some relationship between back pain and the findings of spondylolysis, spondylolisthesis, and adult scoliosis, but these findings also can be observed in spine radiographs of asymptomatic patients.

Special radiographic views can be helpful in further defining the initial clinical radiographic impression. Oblique views are useful in defining further spondylolisthesis and spondylolysis but are of limited use in facet syndrome and hypertrophic arthritis of the lumbar spine. Lateral flexion and extension radiographs may reveal segmental instability. The interpretation of these views depends on patient cooperation, patient positioning, and reproducible technique. Lateral lumbar flexion views are valid only if done in the seated position, which maximizes lumbar kyphosis. The Ferguson view (20-degree caudocephalic anteroposterior radiograph) has been shown to be of value in the diagnosis of the “far out syndrome,” that is, fifth root compression produced by a large transverse process of the fifth lumbar vertebra against the ala of the sacrum. Angled caudal views localized to areas of concern may show evidence of facet or laminar pathologic conditions.

Myelography

The value of myelography is the ability to check all spinal regions for abnormality and to define intraspinal lesions; it may be unnecessary if clinical and CT or MRI findings are in complete agreement. The primary indications for myelography are suspicion of an intraspinal lesion, patients with spinal instrumentation, or questionable diagnosis resulting from conflicting clinical findings and other studies. In addition, myelography is valuable in a previously operated spine and in patients with marked bony degenerative change that may be underestimated on MRI. Myelography is improved by the use of postmyelography CT in this setting and in evaluating spinal stenosis.

Several contrast agents have been used for myelography: air, oil contrast, and water-soluble (absorbable) contrast agents, including metrizamide (Amipaque), iohexol (Omnipaque), and iopamidol (Isovue-M). Because these nonionic agents are absorbable, the discomfort of removing them and the severity of the postmyelography headache have decreased.

Arachnoiditis is a severe complication that has been attributed occasionally to the combination of iophendylate and blood in the cerebrospinal fluid (CSF). This diagnosis usually is confirmed only by repeat myelography. Attempts at surgical neurolysis have resulted in only short-term relief and a return of symptoms within 6 to 12 months after the procedure. Time may decrease the effects of this serious problem in some patients, but progressive paralysis has been reported in rare instances. Arachnoiditis also can be caused by tuberculosis and other types of meningitis. Arachnoiditis has not been noted to be related to the use of a water-soluble contrast agent, with or without injection, in the presence of a bloody tap.

Water-soluble contrast media are now the standard agents for myelography. Their advantages include absorption by the body, enhanced definition of structures, tolerance, and the ability to vary the dosage for different contrasts. Similar to iophendylate, they are meningeal irritants, but they have not been associated with arachnoiditis. The complications of these agents include nausea, vomiting, confusion, and seizures. Rare complications include stroke, paralysis, and death. Iohexol and iopamidol have significantly lower complication rates than metrizamide. The more common complications seem to be related to patient hydration, phenothiazines, tricyclic antidepressants, and migration of contrast material into the cranial vault. Many reported complications can be prevented or minimized by using the lowest possible dose to achieve the desired degree of contrast. Adequate hydration and discontinuation of phenothiazines and tricyclic antidepressants before, during, and after the procedure also should minimize the incidence of the more common reactions. Likewise, maintenance of at least a 30-degree elevation of the patient’s head until the contrast material is absorbed should help prevent reactions. Complete information about these agents and the dosages required is found in their package inserts.

Iohexol is a nonionic contrast medium approved for thoracic and lumbar myelography. The incidence of reactions to this medium is low. The most common reactions are headache (<20%), pain (8%), nausea (6%), and vomiting (3%). Serious reactions are rare and include mental disturbances and aseptic meningitis (0.01%). Good hydration is essential to minimize the common reactions. The use of phenothiazine antinauseants is contraindicated when this medium is employed. Management before and after the procedure is the same as for metrizamide.

Air contrast is used rarely and probably should be used only in situations in which myelography is mandatory and the patient is extremely allergic to iodized materials. The resolution from such a procedure is poor. Air epidurography in conjunction with CT has been suggested in patients in whom further definition between postoperative scar and recurrent disc material is required.

Myelographic technique begins with a careful explanation of the procedure to the patient before its initiation. Hydration of the patient before the procedure may minimize postmyelographic complaints. Heavy sedation rarely is needed. Proper equipment, including a fluoroscopic unit with a spot film device, image intensification, tilt table, and television monitoring, is useful. The type of needle selected also influences the risk of postdural puncture headaches, which can be severe. Smaller gauge needles (22- or 25-gauge) have been found to result in a lower incidence of postdural puncture headaches. Also, use of a Whitacre-type needle with a blunter tip and side port opening results in fewer postdural puncture headache complaints.

The most common technical complications of myelography are significant retention of contrast medium (oil contrast only), persistent headache from a dural leak, and epidural injection. These problems usually are minor. Persistent dural leaks usually are responsive to a blood patch. With the use of a water-soluble contrast medium, the persistent abnormalities caused by retained medium and epidural injection are eliminated.

Myelography

Technique 39.1

  • Place the patient prone on the fluoroscopic table. Use of an abdominal pillow is optional. Prepare the back in the usual surgical fashion.

  • Determine needle placement by the suspected pathologic level. Placement of the needle cephalad to L2-3 is more dangerous because of the risk of damaging the conus medullaris.

  • Infiltrate the selected area of injection with a local anesthetic. Use the smallest gauge needle that can be well placed. If a Whitacre-type needle is used, a 19-gauge needle may be placed through the skin, subcutaneous tissue, and fascia to form a track because this relatively blunt needle cannot penetrate these structures well. Midline needle placement usually minimizes lateral nerve root irritation and epidural injection. Advance the needle with the bevel parallel to the long axis of the body. Subarachnoid placement can be enhanced by tilting the patient up to increase intraspinal pressure and minimize the epidural space.

  • When the dura and arachnoid have been punctured, turn the bevel of the needle cephalad. A clear continuous flow of CSF should continue with the patient prone. Manometric studies can be done at this time if desired or indicated. Remove a volume of CSF equal to the planned injection volume for laboratory evaluation as indicated by the clinical suspicions. In most patients, a cell count, differential white blood cell count, and protein analysis are performed.

  • Inject a test dose of the contrast material under fluoroscopic control to confirm a subarachnoid injection. If a mixed subdural-subarachnoid injection is suspected, change the needle depth; occasionally, a lateral radiograph may be required to confirm the proper depth. If flow is good, inject the contrast material slowly.

  • Ensure continued subarachnoid injection by occasionally aspirating as the injection continues. The usual dose of iohexol for lumbar myelography in an adult is 10 to 15 mL with a concentration of 170 to 190 mg/mL. Higher concentrations of water-soluble contrast are required if higher areas of the spine are to be demonstrated. Consult the package insert of the contrast agent used. The needle can be removed if a water-soluble contrast agent (iohexol) is used.

  • Allow the contrast material to flow caudally for the best views of the lumbar roots and distal sac. Make spot films in the anteroposterior, lateral, and oblique projections. A full lumbar examination should include thoracic evaluation to about the level of T7 because lesions at the thoracic level may mimic lumbar disc disease. Take additional spot films as the contrast proceeds cranially.

  • If a total or cervical myelogram is desired, allow the contrast to proceed cranially. Extend the neck and head maximally to prevent or minimize intracranial migration of the contrast medium.

  • If blood is present in the initial tap, aborting the procedure if the CSF does not clear rapidly is best. It can be attempted again in several days if the patient has no symptoms related to the first tap and is well hydrated. If the proper needle position is confirmed in the anteroposterior and lateral views, and CSF flow is minimal or absent, suspect a neoplastic process. Place the needle at a higher or lower level as indicated by the circumstances. If attempts to obtain CSF continue to fail, abandon the procedure and reevaluate the clinical situation.

Computed tomography

CT can be a useful diagnostic tool in the evaluation of spinal disease ( Fig. 39.2 ). The current technology and computer software have made possible the ability to reformat the standard axial cuts in almost any direction and magnify the images so that exact measurements of various structures can be made. Software is available to evaluate the density of a selected vertebra and compare it with vertebrae of the normal population to give a numerically reproducible estimate of vertebral density to quantitate osteopenia.

FIGURE 39.2, A, CT scan scout view of lumbar disc herniation at lumbar disc level showing angled gantry technique. B, CT scan scout view of straight gantry technique. C, CT scan of lumbar disc herniation at L4-5 disc level showing cross-sectional anatomy with gantry straight. D, CT scan of L4-5 disc herniation at lumbar disc level showing cross-sectional, sagittal, and coronal anatomy using computerized reformatted technique. E, CT scan of L4-5 disc herniation at lumbar disc level showing cross-sectional anatomy 2 hours after metrizamide myelography. F , CT scan of lumbar disc herniation at L4-5 disc level showing cross-sectional anatomy after intravenous injection for greater soft-tissue contrast.

Numerous types of CT studies for the spine are available. One must be careful when ordering the study to ensure that the areas of clinical concern are included. The most common routine for lumbar disc herniations consists of making serial cuts through the last three lumbar intervertebral discs. If the equipment has a tilting gantry, an attempt is made to keep the axis of the cuts parallel with the discs. Frequently, the gantry cannot tilt enough, however, to allow a parallel beam through the lowest disc space. This technique does not allow demonstration of the canal at the pedicles. Another method involves making cuts through the discs without tilting the gantry. The entire canal is not shown, and the lower cuts frequently have the lower and upper endplates of adjacent vertebrae superimposed in the same view.

The most complex method consists of making multiple parallel cuts at equal intervals. This allows computer reconstruction of the images in different planes, usually sagittal and coronal. These reformatted views allow an almost three-dimensional view of the spine and most of its structures. The greatest benefit of this technique is the ability to see beyond the limits of the dural sac and root sleeves. The diagnosis of foraminal encroachment by bone or disc material can be made in the face of a normal myelogram. The proper procedure can be chosen that fits all of the pathologic conditions involved.

Optimal reformatted CT should include enlarged axial and sagittal views with clear notation as to laterality and sequence of cuts. Several sections of the axial cuts should include the local soft tissue and contiguous abdominal contents. Finally, a set of images adjusted for improved bony detail should be included for evaluation of the facet joints and the lateral recesses. This study should be centered on the level of greatest clinical concern. The study can be enhanced further if done after water contrast myelography or with intravenous injection of a contrast medium. Enhancement techniques are especially useful if the spine being evaluated has been operated on previously.

This noninvasive, painless outpatient procedure can supply more information about spinal disease than was previously available with a battery of invasive and noninvasive tests usually requiring hospitalization. CT does not show intraspinal tumors or arachnoiditis and is unable to differentiate scar from recurrent disc herniation. The use of intravenous contrast medium ( Fig. 39.2F ) followed by CT can improve the definition between scar and disc herniation. Myelography is still required to show intraspinal tumors and to “run” the spine to detect occult or unsuspected lesions. The development of low-dose metrizamide or iohexol myelography with reformatted CT done as an outpatient procedure allows maximal information to be obtained with minimal time, risk, discomfort, and cost.

Magnetic resonance imaging

MRI is currently the standard for advanced imaging of the spine and is superior to CT in most circumstances, in particular identification of infections, tumors, and degenerative changes within the discs ( Fig. 39.3 ). More important, MRI is superior for imaging the disc and directly images neural structures. Also, MRI typically shows the entire region of study (cervical, thoracic, or lumbar). Of particular value is the ability to image the nerve root in the foramen, which is difficult even with postmyelography CT because the subarachnoid space and the contrast agent do not extend fully through the foramen. Despite this superiority, there are circumstances in which MRI and CT, with or without myelography, can be used in a complementary fashion.

FIGURE 39.3, MRI of lumbar spine. A, Normal T2-weighted image. B, T2-weighted image showing degenerative bulging or herniated discs, or both, at L3-4, L4-5, and L5-S1.

One of the difficulties with MRI is showing anatomy that is abnormal but may be asymptomatic. MRI evidence of disc degeneration has been reported in the cervical spine in 25% of patients younger than 40 years and in 60% of patients 60 years and older, and lumbar disc degeneration was found in 35% of patients 20 to 39 years old and in 100% of patients older than 50. The demonstrated findings must be carefully correlated with the clinical impression. The importance of this concept cannot be overstated. The best way to obtain meaningful clinical information from MRI of the spine is to have a specific question before the study. This question is derived from the patient’s history and careful physical examination and is posed using the parameters of (1) neural compression, (2) instability, and (3) deformity. In each case the specific location of the abnormality should be suspected before MRI and confirmed with the study. Only abnormalities in one or a combination of these categories are important, and operative techniques can treat only these problems. Failure to interpret an imaging study in this way, especially MRI, which is sensitive to anatomic abnormalities, would inevitably lead to poor clinical choices and outcomes.

Other diagnostic tests

Numerous diagnostic tests have been used in the diagnosis of intervertebral disc disease in addition to radiography, myelography, CT, and MRI. The primary advantage of these tests is to rule out diseases other than primary disc herniation, spinal stenosis, and spinal arthritis.

Electromyography is the most notable of these tests. One advantage of electromyography is in the identification of peripheral neuropathy and diffuse neurologic involvement indicating higher or lower lesions. Electromyography and nerve conduction velocity can be helpful if a patient has a history and physical examination suggestive of radiculopathy at either the cervical or lumbar level with inconclusive imaging studies. Paraspinal muscles in a patient with a previous posterior operation usually are abnormal and are not a reliable diagnostic finding.

Bone scans are another procedure in which positive findings usually are not indicative of intervertebral disc disease, but they can confirm neoplastic, traumatic, and arthritic problems in the spine. Various laboratory tests, such as a complete blood cell count, differential white blood cell count, C-reactive protein, biochemical profile, urinalysis, serum protein electrophoresis, and erythrocyte sedimentation rate, are extremely good screening procedures for other causes of pain in the spine. Rheumatoid screening studies, such as those for rheumatoid arthritis, antinuclear antibody, lupus erythematosus cell preparation, and HLA-B27, also are useful when indicated by the clinical picture.

Some tests that were developed to enhance the diagnosis of intervertebral disc disease have been surpassed by more advanced technology. Lumbar venography and ultrasonographic measurement of the intervertebral canal are two examples.

Injection studies

Whenever a diagnosis is in doubt and the complaints seem real or the pathologic condition is diffuse, identification of the source of pain is problematic. The use of local anesthetics or contrast media in various specific anatomic areas can be helpful. These agents are relatively simple, safe, and minimally painful. Contrast media such as diatrizoate meglumine (Hypaque), iothalamate meglumine (Conray), iohexol (Omnipaque), iopamidol, and metrizamide (Amipaque) have been used for discography and blocks with no reported ill effects. Reports of neurologic complications with contrast media used for discography and subsequent chymopapain injection are well documented. The best choice of a contrast medium for documenting structures outside the subarachnoid space is an absorbable medium with low reactivity, because it might be injected inadvertently into the subarachnoid space. Iohexol and metrizamide are the least reactive, most widely accepted, and best tolerated of the currently available contrast media. Local anesthetics, such as lidocaine (Xylocaine), tetracaine (Pontocaine), and bupivacaine (Marcaine), are used frequently epidurally and intradurally. The use of bupivacaine should be limited to low concentrations and low volumes because of reports of death after epidural anesthesia using concentrations of 0.75% or higher.

Steroids prepared for intramuscular injection also have been used frequently in the epidural space with few and usually transient complications. Spinal arachnoiditis in past years was associated with the use of epidural methylprednisolone acetate (Depo-Medrol). This complication was thought to be caused by the use of the suspending agent, polyethylene glycol, which has since been eliminated from the Depo-Medrol preparation. For epidural injections, we prefer the use of Celestone Soluspan, which is a mixture of betamethasone sodium phosphate and betamethasone acetate. Celestone Soluspan provides immediate and long-term duration of action, is highly soluble, and contains no harmful preservatives. Celestone should not be mixed with local anesthetics containing preservatives such as parabens or phenol because flocculation and clogging of the suspension can occur. If Celestone is not available, other commonly used preparations for spinal injections include methylprednisolone (Depo-Medrol) and triamcinolone acetonide (Kenalog). Isotonic saline is the only other injectable medium used frequently around the spine with no reported adverse reactions. All substrates injected into the epidural space should be preservative free.

Steroids and local anesthesia are generally used in combination for antiinflammatory and analgesic effects. It is theorized that the lipophilic characteristic of the steroid permits sustained release from the abundant epidural fat, which is where the steroid is injected. Cells exposed to the steroid synthesize a phospholipase A2-inhibitory glycoprotein (termed lipomodulin) and inhibit the inflammatory pathway. Phospholipase A2, which is an inflammatory enzyme, converts membrane phospholipids into arachidonic acid and subsequently controls lipoxygenase, leading to the formation of leukotrienes. The steroid also reduces nerve swelling and upregulates the transcription of antiinflammatory genes, in contrast to local analgesics, which are responsible for immediate pain relief.

When discrete, well-controlled injection techniques directed at specific targets in and around the spine are used, grading the degree of pain before and after a spinal injection is helpful in determining the location of the pain generator. The patient is asked to grade the degree of pain on a 0-to-10 scale before and at various intervals after the spinal injection (see Box 38.1 ). If a spinal injection done under fluoroscopic control results in an 80% or more decrease in the level of pain, which corresponds to the duration of action of the anesthetic agent used, we presume the target area injected to be the pain generator. Less pain reduction, 50% to 65%, does not constitute a positive response.

Epidural cortisone injections

Epidural injections in the cervical, thoracic, and lumbosacral spine were developed to diagnose and treat spinal pain. Information obtained from epidural injections can be helpful in confirming pain generators that are responsible for a patient’s discomfort. Structural abnormalities do not always cause pain, and diagnostic injections can help to correlate abnormalities seen on imaging studies with associated pain complaints. In addition, epidural injections can provide pain relief during the recovery of disc or nerve root injuries and allow patients to increase their level of physical activity. Because severe pain from an acute disc injury, with or without radiculopathy, often is time limited, therapeutic injections can help to manage pain and may alleviate or decrease the need for oral analgesics.

A retrospective study comparing interlaminar to transforaminal epidural injections for symptomatic lumbar intervertebral disc herniations found that transforaminal injections resulted in better short-term pain improvement and fewer long-term operative interventions.

A number of randomized, double-blind, controlled studies have been done to evaluate the effectiveness of lumbar interlaminar injections, as well as caudal epidural injections, in the treatment of chronic discogenic pain with and without radiculitis. Overall these studies indicate that a high percentage of patients receiving the injections have significant pain relief and functional improvement. The question still remains whether there is any significant long-term benefit to these injections.

Few serious complications occur in patients receiving epidural corticosteroid injections; however, epidural abscess, epidural hematoma, durocutaneous fistula, and Cushing syndrome have been reported as individual case reports. The most adverse immediate reaction during an epidural injection is a vasovagal reaction, although this is much more common with cervical injections. Dural puncture has been estimated to occur in 0.5% to 5% of patients having cervical or lumbar epidural steroid injections. Some minor, common complaints caused by corticosteroid injected into the epidural space include nonpositional headaches, facial flushing, insomnia, low-grade fever, and transient increased back or lower extremity pain. Major adverse events can occur with epidural injections, but these are rare, their true incidence is unknown, and they have been described only in case reports. Several large series involving nearly 5000 patients with over 8000 transforaminal lumbar epidural injections reported no major adverse events and a less than 1% incidence of postinjection headache; the most frequent sequela was increased leg or back pain, which also occurred in less than 1% of patients.

Epidural corticosteroid injections are contraindicated in the presence of infection at the injection site, systemic infection, bleeding diathesis, uncontrolled diabetes mellitus, and congestive heart failure.

When considering epidural steroid injections, several preexisting conditions should be checked to avoid complications. These conditions include coagulopathy or concurrent anticoagulation therapy, systemic infection, local skin infection at the puncture site, hypersensitivity to administered agents, and pregnancy. According to a consensus statement by the Society of Interventional Radiology, epidural steroid injection is classified as a category 2 procedure, that is, a moderate risk for bleeding (between a low-bleeding-risk procedure, in which bleeding is easily detected and controllable, and a significant-bleeding-risk procedure, in which bleeding is difficult to detect or control). For category 2 procedures, the international normalized ratio (INR) and platelet count should be adjusted to less than 1.5 and more than 50,000/μL, respectively. If a patient is taking anticoagulants, the medication should be withheld in consultation with the prescribing physician. Warfarin should be withheld 5 days before epidural steroid injection, and the patient’s INR should be rechecked before the procedure. Low-molecular-weight heparin therapy should be stopped 24 hours before epidural steroid injection, whereas heparin does not need to be withheld because it is a short-acting agent (the half-life of heparin is 23 minutes to 2.48 hours). Fondaparinux (Arixtra, Glaxo Smith Kline, London) should be withheld for 2 to 5 days before the procedure, clopidogrel (Plavix, Handok, Seoul) for 5 days, and ticlopidine (Ticlid, Roche, Basel, Switzerland) for 5 days. Nonsteroidal antiinflammatory drugs, including aspirin, do not have to be stopped before epidural steroid injections.

We perform epidural corticosteroid injections in a fluoroscopy suite equipped with resuscitative and monitoring equipment. Intravenous access is established in all patients with a 20-gauge angiocatheter placed in the upper extremity. Mild sedation is achieved through intravenous access. We recommend the use of fluoroscopy for diagnostic and therapeutic epidural injections for several reasons. Epidural injections performed without fluoroscopic guidance are not always made into the epidural space or the intended interspace. Even in experienced hands, needle misplacement occurs in 40% of caudal and 30% of lumbar epidural injections when done without fluoroscopic guidance. Accidental intravascular injections also can occur, and the absence of blood return with needle aspiration before injection is an unreliable indicator of this complication. In the presence of anatomic anomalies, such as a midline epidural septum or multiple separate epidural compartments, the desired flow of epidural injectants to the presumed pain generator is restricted and remains undetected without fluoroscopy. In addition, if an injection fails to relieve pain, it would be impossible without fluoroscopy to determine whether the failure was caused by a genuine poor response or by improper needle placement.

Thoracic epidural injection

Epidural steroid injections in the thoracic spine have been shown to provide relief from thoracic radicular pain secondary to disc herniations, trauma, diabetic neuropathy, herpes zoster, and idiopathic thoracic neuralgia, although reports in the literature are few.

Interlaminar Thoracic Epidural Injection

Technique 39.2

  • A paramedian rather than a midline approach is used because of the angulation of the spinous processes.

  • Place the patient prone on a pain management table. The preparation of the patient and equipment are identical to that used for interlaminar cervical epidural injections (see Technique 38.1). Aseptically prepare the skin area several segments above and below the interspace to be injected. Drape the area in sterile fashion.

  • Identify the target laminar interspace using anteroposterior fluoroscopic guidance.

  • Anesthetize the skin over the target interspace on the side of the patient’s pain. Under fluoroscopic control, insert and advance a 22-gauge, 3½-inch spinal needle to the superior edge of the target lamina. Anesthetize the lamina and the soft tissues as the spinal needle is withdrawn.

  • Mark the skin with an 18-gauge hypodermic needle and insert an 18-gauge, 3½-inch Tuohy epidural needle, and advance it at a 50- to 60-degree angle to the axis of the spine and a 15- to 30-degree angle toward the midline until contact with the lamina is made. To view the thoracic interspace better, position the C-arm so that the fluoroscopy beam is in the same plane as the Tuohy epidural needle.

  • “Walk off” the lamina with the Tuohy needle into the ligamentum flavum. Remove the stylet from the Tuohy needle and, using the loss-of-resistance technique, advance it into the epidural space. When loss of resistance has been achieved, aspirate to check for blood or CSF. If neither blood nor CSF is evident, inject 1.5 mL of nonionic contrast dye to confirm epidural placement.

  • To confirm proper placement further, adjust the C-arm to view the area from a lateral projection ( Fig. 39.4 ). A spot radiograph or epidurogram can be obtained. Inject 2 mL of 1% preservative-free lidocaine without epinephrine and 2 mL of 6 mg/mL Celestone Soluspan slowly into the epidural space.

    FIGURE 39.4, A, Posteroanterior view of thoracic interlaminar epidurogram showing characteristic contrast flow pattern. B, Lateral radiograph of thoracic epidurogram. SEE TECHNIQUE 39.2 .

Lumbar epidural injection

Certain clinical trends are apparent with lumbar epidural steroid injections. When nerve root injury is associated with a disc herniation or lateral bony stenosis, most patients who received substantial relief of leg pain from a well-placed transforaminal injection, even if temporary, benefit from surgery for the radicular pain. Patients who do not respond and who have had radicular pain for at least 12 months are unlikely to benefit from surgery. Patients with back and leg pain of an acute nature (<3 months) respond better to epidural corticosteroids. Unless a significant reinjury results in an acute disc or nerve root injury, postsurgical patients tend to respond poorly to epidural corticosteroids.

Interlaminar Lumbar Epidural Injection

Technique 39.3

  • Place the patient prone on a pain management table. Aseptically prepare the skin area with isopropyl alcohol and povidone-iodine several segments above and below the laminar interspace to be injected. Drape the area in a sterile fashion.

  • Under anteroposterior fluoroscopy guidance, identify the target laminar interspace. Using a 27-gauge, ¼-inch needle, anesthetize the skin over the target interspace on the side of the patient’s pain with 1 to 2 mL of 1% preservative-free lidocaine without epinephrine.

  • Insert a 22-gauge, 3½-inch spinal needle vertically until contact is made with the upper edge of the inferior lamina at the target interspace, 1 to 2 cm lateral to the caudal tip of the inferior spinous process under fluoroscopy. Anesthetize the lamina with 2 mL of 1% preservative-free lidocaine without epinephrine. Anesthetize the soft tissue with 2 mL of 1% lidocaine as the spinal needle is withdrawn.

  • Nick the skin with an 18-gauge hypodermic needle and insert a 17-gauge, 3½-inch Tuohy epidural needle and advance it vertically within the anesthetized soft-tissue track until contact with the lamina has been made under fluoroscopy.

  • “Walk off” the lamina with the Tuohy needle onto the ligamentum flavum. Remove the stylet from the Tuohy needle and attach a 10-mL syringe filled halfway with air and sterile saline to the Tuohy needle. Advance the Tuohy needle into the epidural space using the loss-of- resistance technique. Avoid lateral needle placement to decrease the likelihood of encountering an epidural vein or adjacent nerve root. Remove the stylet when loss of resistance has been achieved. Aspirate to check for blood or CSF. If neither blood nor CSF is present, remove the syringe from the Tuohy needle and attach a 5-mL syringe containing 2 mL of nonionic contrast dye.

  • Confirm epidural placement by producing an epidurogram with the nonionic contrast agent ( Fig. 39.5 ). A spot radiograph can be taken to document placement.

    FIGURE 39.5, A, Posteroanterior view of lumbar interlaminar epidurogram showing characteristic contrast flow pattern. B, Lateral radiograph of lumbar epidurogram. SEE TECHNIQUE 39.3 .

  • Remove the 5-mL syringe and place on the Tuohy needle a 10-mL syringe containing 2 mL of 1% preservative-free lidocaine and 2 mL of 6 mg/mL Celestone Soluspan. Inject the corticosteroid preparation slowly into the epidural space.

Transforaminal Lumbar and Sacral Epidural Injection

Technique 39.4

  • Place the patient prone on a pain management table. Aseptically prepare the skin area with isopropyl alcohol and povidone-iodine several segments above and below the interspace to be injected. Drape the area in sterile fashion.

  • Under anteroposterior fluoroscopic guidance, identify the target interspace. Anesthetize the soft tissues over the lateral border and midway between the two adjacent transverse processes at the target interspace.

  • Insert a 22-gauge, 4¾ inch spinal needle and advance it within the anesthetized soft-tissue track under fluoroscopy until contact is made with the lower edge of the superior transverse process near its junction with the superior articular process.

  • Retract the spinal needle 2 to 3 mm, redirect it toward the base of the appropriate pedicle, and advance it slowly to the 6-o’clock position of the pedicle under fluoroscopy. Adjust the C-arm to a lateral projection to confirm the position and then return the C-arm to the anteroposterior view.

  • Remove the stylet. Inject 1 mL of nonionic contrast agent slowly to produce a perineurosheathogram ( Fig. 39.6 ). After an adequate dye pattern is observed, inject slowly a 2-mL volume containing 1 mL of 0.75% preservative-free bupivacaine and 1 mL of 6 mg/mL Celestone Soluspan.

    FIGURE 39.6, A, Right L5 selective nerve root injection contrast pattern. B, Lateral radiograph of L5 selective nerve block contrast flow pattern in anterior epidural space. SEE TECHNIQUE 39.4 .

  • The S1 nerve root also can be injected using the transforaminal approach.

  • With the patient prone on the pain management table and after appropriate aseptic preparation, direct the C-arm so that the fluoroscopy beam is in a cephalocaudad and lateral-to-medial direction so that the anterior and posterior S1 foramina are aligned.

  • Anesthetize the soft tissues and the dorsal aspect of the sacrum with 2 to 3 mL of 1% preservative-free lidocaine without epinephrine. Insert a 22-gauge, 3½-inch spinal needle, and advance it within the anesthetized soft-tissue track under fluoroscopy until contact is made with posterior sacral bone slightly lateral and inferior to the S1 pedicle. “Walk” the spinal needle off the sacrum into the posterior S1 foramen to the medial edge of the pedicle.

  • Adjust the C-arm to a lateral projection to confirm the position and return it to the anteroposterior view.

  • Remove the stylet. Inject 1 mL of nonionic contrast slowly to produce a perineurosheathogram ( Fig. 39.7 ). After an adequate dye pattern of the S1 nerve root is obtained, insert a 2-mL volume containing 1 mL of 0.75% preservative-free bupivacaine and 1 mL of 6 mg/mL Celestone Soluspan.

    FIGURE 39.7, A, Right S1 selective nerve root injection contrast pattern with perineurosheathogram. B, Lateral radiograph of S1 contrast flow in sacral epidural space. SEE TECHNIQUE 39.4 .

Caudal Sacral Epidural Injection

Technique 39.5

  • Place the patient prone on a pain management table. Aseptically prepare the skin area from the lumbosacral junction to the coccyx with isopropyl alcohol and povidone-iodine. Drape the area in sterile fashion.

  • Try to identify by palpation the sacral hiatus, which is located between the two horns of the sacral cornua. The sacral hiatus can be best observed by directing the fluoroscopic beam laterally.

  • Anesthetize the soft tissues and the dorsal aspect of the sacrum with 2 to 3 mL of 1% preservative-free lidocaine without epinephrine. Keep the C-arm positioned so that the fluoroscopic beam remains lateral.

  • Insert a 22-gauge, 3½-inch spinal needle between the sacral cornua at about 45 degrees, with the bevel of the spinal needle facing ventrally until contact with the sacrum is made. Using fluoroscopic guidance, redirect the spinal needle more cephalad, horizontal, and parallel to the table, advancing it into the sacral canal through the sacrococcygeal ligament and into the epidural space ( Fig. 39.8 ).

    FIGURE 39.8, Fluoroscopic view (caudal approach) of lumbar epidural injection. SEE TECHNIQUE 39.5 .

  • Remove the stylet. Aspirate to check for blood or CSF. If neither blood nor CSF is evident, inject 2 mL of nonionic contrast dye to confirm placement. Move the C-arm into the anteroposterior position and look for the characteristic “Christmas tree” pattern of epidural flow. If a vascular pattern is seen, reposition the spinal needle and confirm epidural placement with nonionic contrast dye.

  • When the correct contrast pattern is obtained, slowly inject a 10-mL volume containing 3 mL of 1% preservative-free lidocaine without epinephrine, 3 mL of 6 mg/mL Celestone Soluspan, and 4 mL of sterile normal saline.

Zygapophyseal (Facet) joint injections

The facet joint can be a source of back pain; the exact cause of the pain is unknown. Theories include meniscoid entrapment and extrapment, synovial impingement, chondromalacia facetae, capsular and synovial inflammation, and mechanical injury to the joint capsule. Osteoarthritis is another cause of facet joint pain; however, the incidence of facet joint arthropathy is equal in symptomatic and asymptomatic patients. As with other osteoarthritic joints, radiographic changes correlate poorly with pain. Although the history and physical examination may suggest that the facet joint is the cause of spine pain, no noninvasive pathognomonic findings distinguish facet joint–mediated pain from other sources of spine pain. Fluoroscopically guided facet joint injections are commonly considered the “gold standard” for isolating or excluding the facet joint as a source of spine or extremity pain.

Clinical suspicion of facet joint pain by a spine specialist remains the major indicator for diagnostic injection, which should be done only in patients who have had pain for more than 4 weeks and only after appropriate conservative measures have failed to provide relief. Facet joint injection procedures may help to focus treatment on a specific spinal segment and provide adequate pain relief to allow progression in therapy. Either intraarticular or medial branch blocks can be used for diagnostic purposes. Although injection of cortisone into the facet joint was a popular procedure through most of the 1970s and 1980s, many investigators have found no evidence that this effectively treats low back pain caused by a facet joint. The only controlled study on the use of intraarticular corticosteroids in the cervical spine found no added benefit from intraarticular betamethasone over bupivacaine.

Lumbar Facet Joint

Lumbar Intraarticular Injection

Technique 39.6

  • Place the patient prone on a pain management table. Aseptically prepare and drape the patient.

  • Under fluoroscopic guidance, identify the target segment to be injected. Upper lumbar facet joints are oriented in the sagittal (vertical) plane and often can be seen on direct anteroposterior views, whereas the lower lumbar facet joints, especially at L5-S1, are obliquely oriented and require an ipsilateral oblique rotation of the C-arm to be seen.

  • Position the C-arm under fluoroscopy until the joint silhouette first appears. Insert and advance a 22- or 25-gauge, 3½-inch spinal needle toward the target joint along the axis of the fluoroscopy beam until contact is made with the articular processes of the joint. Enter the joint cavity through the softer capsule and advance the needle only a few millimeters. Capsular penetration is perceived as a subtle change of resistance. If midpoint needle entry is difficult, redirect the spinal needle to the superior or inferior joint recesses.

  • Confirm placement with less than 0.1 mL of nonionic contrast dye with a 3-mL syringe to minimize injection pressure under fluoroscopic guidance. When intraarticular placement has been verified, inject a total volume of 1 mL of injectant (local anesthetic with or without corticosteroids) into the joint.

Lumbar Medial Branch Block Injection

Technique 39.7

  • Place the patient prone on a pain management table. Aseptically prepare and drape the area to be injected.

  • Because there is dual innervation of each lumbar facet joint, two medial branch blocks are required. The medial branches cross the transverse processes below their origin ( Fig. 39.9 ). The L4-5 facet joint is anesthetized by blocking the L3 medial branch at the transverse process of L4 and the L4 medial branch at the transverse process of L5. In the case of the L5-S1 facet joint, anesthetize the L4 medial branch as it passes over the L5 transverse process and the L5 medial branch as it passes across the sacral ala.

    FIGURE 39.9, Posterior view of lumbar spine showing location of medial branches (mb) of dorsal rami, which innervate lumbar facet joints (a) . Needle position for L3 and L4 medial branch. Blocks shown on left half of diagram would be used to anesthetize L4-5 facet joint. Right half of diagram shows L3-4, L4-5, and L5-S1 intraarticular facet joint injection positions. SEE TECHNIQUE 39.7 .

  • Using anteroposterior fluoroscopic imaging, identify the target transverse process. For L1 through L4 medial branch blocks, penetrate the skin using a 22- or 25-gauge, 3½-inch spinal needle lateral and superior to the target location.

  • Under fluoroscopic guidance, advance the spinal needle until contact is made with the dorsal superior and medial aspects of the base of the transverse process so that the needle rests against the periosteum. To ensure optimal spinal needle placement, reposition the C-arm so that the fluoroscopy beam is ipsilateral oblique and the “Scotty dog” is seen. Position the spinal needle in the middle of the “eye” of the Scotty dog. Slowly inject (over 30 seconds) 0.5 mL of 0.75% bupivacaine.

  • To inject the L5 medial branch (more correctly, the L5 dorsal ramus), position the patient prone on the pain management table with the fluoroscopic beam in the anteroposterior projection ( Fig. 39.10 ).

    FIGURE 39.10, Posteroanterior view of needles in place for L3 and L4 medial branch blocks, and L5 dorsal rami block to anesthetize the L4-L5 and L5-S1 zygapophyseal joints.

  • Identify the sacral ala. Rotate the C-arm 15 to 20 degrees ipsilateral obliquely to maximize exposure between the junction of the sacral ala and the superior process of S1. Insert a 22- or 25-gauge, 3½-inch spinal needle directly into the osseous landmarks approximately 5 mm below the superior junction of the sacral ala with the superior articular process of the sacrum under fluoroscopy. Rest the spinal needle on the periosteum and position the bevel of the spinal needle medial and away from the foramen to minimize flow through the L5 or S1 foramen. Slowly inject 0.5 mL of 0.75% bupivacaine.

Sacroiliac Joint

The sacroiliac joint remains a controversial source of primary low back pain despite validated scientific studies. It often is overlooked as a source of low back pain because its anatomic location makes it difficult to examine in isolation and many provocative tests place mechanical stresses on contiguous structures. In addition, several other structures may refer pain to the sacroiliac joint.

Similar to other synovial joints, the sacroiliac joint moves; however, sacroiliac joint movement is involuntary and is caused by shear, compression, and other indirect forces. Muscles involved with secondary sacroiliac joint motion include the erectae spinae, quadratus lumborum, psoas major and minor, piriformis, latissimus dorsi, obliquus abdominis, and gluteal. Imbalances in any of these muscles as a result of central facilitation may cause them to function in a shortened state that tends to inhibit their antagonists reflexively. Theoretically, dysfunctional movement patterns may result. Postural changes and body weight also can create motion through the sacroiliac joint.

Because of the wide range of segmental innervation (L2-S2) of the sacroiliac joint, there are myriad referral zone patterns. In studies of asymptomatic subjects, the most constant referral zone was localized to a 3- × 10-cm area just inferior to the ipsilateral posterior superior iliac spine (PSIS) ( Fig. 39.11 ) ; however, pain may be referred to the buttocks, groin, posterior thigh, calf, and foot.

FIGURE 39.11, Pain diagram. A, Patient-reported pain diagram consistent with sacroiliac joint dysfunction. B, Patient-reported diagram inconsistent with sacroiliac joint dysfunction.

Sacroiliac dysfunction, also called sacroiliac joint mechanical pain or sacroiliac joint syndrome, is the most common painful condition of this joint. The true prevalence of mediated pain from sacroiliac joint dysfunction is unknown; however, several studies indicated that it is more common than expected. Because no specific or pathognomonic historical facts or physical examination tests accurately identify the sacroiliac joint as a source of pain, diagnosis is one of exclusion. Sacroiliac joint dysfunction should be considered, however, if an injury was caused by a direct fall on the buttocks, a rear-end motor vehicle accident with the ipsilateral foot on the brake at the moment of impact, a broadside motor vehicle accident with a blow to the lateral aspect of the pelvic ring, or a fall in a hole with one leg in the hole and the other extended outside. Lumbar rotation and axial loading that can occur during ballet or ice skating is another common mechanism of injury. Although controversial, the risk of sacroiliac joint dysfunction may be increased in individuals with lumbar fusion or hip pathology. Other causes include insufficiency stress fractures; fatigue stress fractures; metabolic processes, such as deposition diseases; degenerative joint disease; infection; and inflammatory conditions, such as ankylosing spondylitis, psoriatic arthritis, and Reiter disease. The diagnosis of sacroiliac joint pain can be confirmed if symptoms are reproduced on distention of the joint capsule by provocative injection and subsequently abated with an analgesic block.

Sacroiliac Joint Injection

Technique 39.8

  • Place the patient prone on a pain management table. Aseptically prepare and drape the side to be injected. Rotate the C-arm until the medial (posterior) joint line is seen.

  • Use a 27-gauge, ¼-inch needle to anesthetize the skin of the buttock 1 to 3 cm inferior to the lowest aspect of the joint. Using fluoroscopy, insert a 22-gauge, 3½-inch spinal needle until the needle rests 1 cm above the most posteroinferior aspect of the joint ( Fig. 39.12 ). Rarely, a larger spinal needle is required in obese patients. Advance the spinal needle into the sacroiliac joint until capsular penetration occurs.

    FIGURE 39.12, Sacroiliac joint injection showing medial (A) and lateral (B) joint planes (silhouettes). Entry into joint is achieved above most posteroinferior aspect of joint. SEE TECHNIQUE 39.8 .

  • Confirm intraarticular placement under fluoroscopy with 0.5 mL of nonionic contrast dye ( Fig. 39.13 ). A spot radiograph can be taken to document placement. Inject a 2-mL volume containing 1 mL of 0.75% preservative-free bupivacaine and 1 mL of 6 mg/mL Celestone Soluspan into the joint.

    FIGURE 39.13, Left sacroiliac joint contrast pattern. SEE TECHNIQUE 39.8 .

Discography

Discography has been used since the late 1940s for the experimental and clinical evaluation of disc disease in the cervical and lumbar regions of the spine. Since that time, discography has had a limited but important role in the evaluation of suspected disc pathology.

The clinical usefulness of the data obtained from discography is controversial. Although early studies concluded that lumbar discography was an unreliable diagnostic tool, with a 37% false-positive rate, later studies found a 0% false-positive rate for discography and concluded that, with current technique and a standardized protocol, discography was a highly reliable test.

The most important aspect of discography is provocative testing for concordant pain (i.e., pain that corresponds to a patient’s usual pain) to provide information regarding the clinical significance of the disc abnormality. Although difficult to standardize, this testing distinguishes discography from other anatomic imaging techniques. If the patient is unable to distinguish customary pain from any other pain, the procedure is of no value. In patients who have a concordant response without evidence of a radial annular fissure on discography, CT should be considered because some discs that appear normal on discography show disruption on a CT scan.

Indications for lumbar discography include operative planning of spinal fusion, testing of the structural integrity of an adjacent disc to a known abnormality such as spondylolisthesis or fusion, identifying a painful disc among multiple degenerative discs, ruling out secondary internal disc disruption or suspected lateral or recurrent disc herniation, and determining the primary symptom-producing level when chemonucleolysis is being considered. Lumbar discography is most useful as a test to exclude levels from operative intervention rather than as a primary indication for operative fusion in patients with axial back pain. Thoracic discography can be a useful tool in the investigation of thoracic, chest, and upper abdominal pain. Degenerative thoracic disc disease, with or without herniation, has a highly variable clinical presentation, frequently mimicking visceral conditions and causing back or musculoskeletal pain. Discography also may be justified in medicolegal situations to establish a more definitive diagnosis even though treatment may not be planned on that disc.

Compression of the spinal cord, stenosis of the roots, bleeding disorders, allergy to the injectable material, and active infection are contraindications to diagnostic discography procedures. Although the risk of complications from discography is low, potential problems include discitis, nerve root injury, subarachnoid puncture, chemical meningitis, bleeding, and allergic reactions. In addition, in the cervical region, retropharyngeal and epidural abscess can occur. Pneumothorax is a risk in the cervical and thoracic regions.

Lumbar Discography

Lumbar discography originally was done using a transdural technique in a manner similar to myelography with a lumbar puncture. The difference between lumbar myelography and discography was that the needle used for the latter was advanced through the thecal sac. The technique later was modified, consisting of an extradural, extralaminar approach that avoided the thecal sac, and it was refined further to enable entry into the L5-S1 disc using a two-needle technique to maneuver around the iliac crest.

A patient’s response during the procedure is the most important aspect of the study. Pain alone does not determine if a disc is the cause of the back pain. The concordance of the pain in regard to the quality and location are paramount in determining whether the disc is a true pain generator. A control disc is necessary to validate a positive finding on discography.

Technique 39.9

(FALCO)

  • Place the patient on a procedure or fluoroscopic table.

  • Insert an angiocatheter into the upper extremity and infuse intravenous antibiotics to prevent discitis. Some physicians prefer to give antibiotics intradiscally during the procedure.

  • Place the patient in a modified lateral decubitus position with the symptomatic side down to avoid having the patient confuse the pain caused by the needle with the actual pain on that same side. This position also allows for easier fluoroscopic imaging of the intervertebral discs and mobilizes the bowel away from the needle path.

  • Sedate the patient with a short-acting agent. It is best to avoid analgesic agents that may alter the pain response.

  • Prepare and drape the skin sterilely, including the lumbosacral region.

  • Under fluoroscopic control, identify the intervertebral discs. Adjust the patient’s position or the C-arm so that the lumbar spine is in an oblique position with the superior articular process dividing the intervertebral space in half ( Fig. 39.14 ).

    FIGURE 39.14, Lumbar spine in oblique position with superior articular process (arrow) dividing disc space (d) in half.

  • Anesthetize the skin overlying the superior articular process with 1 to 2 mL of 1% lidocaine if necessary.

  • Advance a single 6-inch spinal needle (or longer, depending on the patient’s size) through the skin and deeper soft tissues to the outer annulus of the disc. The disc entry point is just anterior to the base of the superior articular process and just above the superior endplate of the vertebral body, which allows the needle to pass safely by the exiting nerve root ( Fig. 39.15 ). Advance the needle into the central third of the disc, using anteroposterior and lateral fluoroscopic imaging.

    FIGURE 39.15, Disc entry point is just anterior (arrow) to base of superior articular process (s) and just above superior endplate of vertebral body.

  • Confirm the position of the needle tip within the central third of the disc with anteroposterior and lateral fluoroscopic imaging. Inject either saline or nonionic contrast dye into each disc.

  • Record any pain that the patient experiences during the injection as none, dissimilar, similar, or exact in relationship to the patient’s typical low back pain. Record intradiscal pressures to assist in determining if the disc is the cause of the pain.

  • Obtain radiographs of the lumbar spine on completion of the study, paying particular attention to the contrast-enhanced disc. Obtain a CT scan if necessary to assess disc anatomy further.

  • An alternative method is a two-needle technique in which a 6- or 8-inch spinal needle is passed through a shorter introducer needle (typically 3½ inches) into the disc in the same manner as a single needle. This approach may reduce the incidence of infection by allowing the procedure needle to pass into the disc space without ever penetrating the skin. The introducer needle also may assist in more accurate needle placement, reducing the risk of injuring the exiting nerve root. The two-needle approach may require more time than the single-needle technique, and the larger introducer needle could cause more pain to the patient.

  • The two-needle technique often is used to enter the L5-S1 disc space with one modification. The procedure needle typically is curved ( Fig. 39.16 ). To bypass the iliac crest, the introducer needle is advanced at an angle that places the needle tip in a position that does not line up with the L5-S1 disc space, which makes it difficult, if not impossible, for a straight procedure needle to advance into the L5-S1 disc. A curved procedure needle allows the needle tip to align with the L5-S1 disc as it is advanced toward and into the disc adjusting for malalignment.

    FIGURE 39.16, Curved procedure needle (c) passing through straight introducer needle (n).

Thoracic Discography

Thoracic discography has been refined to provide a technique that is reproducible and safe. A posterolateral extralaminar approach similar to lumbar discography is used with a single-needle technique. The significant difference between thoracic and lumbar discography is the potential for complications because of the surrounding anatomy of the thoracic spine. In contrast to lumbar discography, which typically is performed in the mid to lower lumbar spine below the spinal cord and lungs, thoracic discography has the inherent risk of pneumothorax and direct spinal cord trauma; other complications include discitis and bleeding. Essentially the same protocol is used for thoracic discography as for lumbar discography.

Technique 39.10

(FALCO)

  • Place the patient in a modified lateral decubitus position on the procedure table with the symptomatic side down.

  • Begin antibiotics through the intravenous catheter. Alternatively, intradiscal antibiotics may be given during the procedure.

  • Sedate the patient and prepare and drape the skin in a sterile manner.

Using fluoroscopic imaging, identify the intervertebral thoracic discs. Move the patient or adjust the C-arm obliquely to position the superior articular process so that it divides the intervertebral space in half ( Fig. 39.17 ). At this point, the intervertebral discs and endplates, subjacent superior articular process, and adjacent rib head should be in clear view. The endplates, the superior articular process, and the rib head form a “box” ( Fig. 39.18 ) that delineates a safe pathway into the disc, avoiding the spinal cord and lung. Keep the needle tip within the confines of this “box” while advancing it into the annulus.

  • After proper positioning and exposure, anesthetize the skin overlying the superior articular process with 1 to 2 mL of 1% lidocaine if necessary.

  • Advance a single 6-inch spinal needle (a shorter or longer needle can be used, depending on the patient’s size) through the skin and the deeper soft tissues into the outer annulus within the “box” just anterior to the base of the superior articular process and just above the superior endplate. Continue into the central third of the disc, using anteroposterior and lateral fluoroscopic guidance.

  • Inject either saline or a nonionic contrast dye into each disc in the same manner as for lumbar discography.

  • Record any pain response and analyze for reproduction of concordant pain using the same protocol as for lumbar discography.

  • Obtain radiographs and CT scan of the thoracic spine on completion of the study.

FIGURE 39.17, Oblique position with superior articular process (arrow) dividing thoracic intervertebral space in half. p , Pedicle; r , rib head.

FIGURE 39.18, Thoracic endplates (e), superior articular process (s) , and rib head (r) form box.

Thoracic Disc Disease

The thoracic spine is the least common location for disc pathology. Since the 1960s, many approaches have been described and validated through clinical experience. It is apparent that posterior laminectomy has no role in the operative treatment of this problem. Other posterior approaches, such as costotransversectomy, have good indications.

Symptomatic thoracic disc herniations remain rare, with an estimated incidence of one in 1 million individuals per year. They represent 0.25% to 0.75% of the total incidence of symptomatic disc herniations. The most common age at onset is between the fourth and sixth decades. As with the other areas of the spine, the incidence of asymptomatic disc herniations is high; an estimated 37% of thoracic disc herniations are asymptomatic. Operative treatment of thoracic disc herniations is indicated in rare patients with acute disc herniation with myelopathic findings attributable to the lesion, especially progressive neurologic symptoms.

Signs and symptoms

The natural history of symptomatic thoracic disc disease is similar to that in other areas, in that symptoms and function typically improve with conservative treatment and time. The clinical course can vary, however, and a high index of suspicion must be maintained to make the correct diagnosis. The differential diagnosis for the symptoms of thoracic disc herniations is fairly extensive and includes nonspinal causes occurring with the cardiopulmonary, gastrointestinal, and musculoskeletal systems. Spinal causes of similar symptoms can occur with infectious, neoplastic, degenerative, and metabolic problems within the spinal column and the spinal cord.

Two general patient populations have been documented in the literature. The smaller group of patients is younger and has a relatively short history of symptoms, often with a history of trauma. Typically, an acute soft disc herniation with either acute spinal cord compression or radiculopathy is present. Outcome generally is favorable with operative or nonoperative treatment. The larger group of patients has a longer history, often more than 6 to 12 months of symptoms, which result from chronic spinal cord or root compression. Disc degeneration, often with calcification of the disc, is the underlying process.

Pain is the most common presenting feature of thoracic disc herniations. Two patterns of pain are apparent: one is axial, and the other is bandlike radicular pain along the course of the intercostal nerve. The T10 dermatomal level is the most commonly reported distribution, regardless of the level of involvement. This is a band extending around the lower lateral thorax and caudad to the level of the umbilicus. This radicular pattern is more common with upper thoracic and lateral disc herniations. Some axial pain often occurs with this pattern as well. Associated sensory changes of paresthesias and dysesthesia in a dermatomal distribution also occur ( Fig. 39.19 ). High thoracic discs (T2 to T5) can manifest similarly to cervical disc disease with upper arm pain, paresthesias, radiculopathy, and Horner syndrome. Myelopathy also may occur. Complaints of weakness, which may be generalized by the patient, typically involving both lower extremities occur in the form of mild paraparesis. Sustained clonus, a positive Babinski sign, and wide-based and spastic gait all are signs of myelopathy. Bowel and bladder dysfunction occur in only 15% to 20% of these patients. The neurologic evaluation of patients with thoracic disc herniations must be meticulous because there are few localizing findings. Abdominal reflexes, cremasteric reflex, dermatomal sensory evaluation, rectus abdominis contraction symmetry, lower extremity reflexes and strength and sensory examinations, and determination of long tract findings all are important.

FIGURE 39.19, Sensory dermatomes of trunk region.

Confirmatory imaging

Plain radiographs are helpful to evaluate traumatic injuries and to determine potential osseous morphologic variations that may help to localize findings, especially on intraoperative films, if these become necessary. MRI is the most important and useful imaging method to show thoracic disc herniations. In addition to the disc herniation, neoplastic or infectious pathology can be seen. The presence of intradural pathology, including disc fragments, also usually is shown on MRI. The spinal cord signal may indicate the presence of inflammation or myelomalacia as well. Despite all of these advantages, MRI may underestimate the thoracic disc herniation, which often is calcified and has low signal intensity on T1- and T2-weighted sequences.

Myelography followed by CT also can be useful in evaluating the bony anatomy and more accurately assessing the calcified portion of the herniated thoracic disc. Regardless of the imaging methods used, the appearance and presence of a thoracic disc herniation must be carefully considered and correlated with the patient’s complaints and detailed examination findings. Relief of pain with thoracic transforaminal epidural can confirm the source of pain and is a good predictor of improvement with surgical intervention.

Treatment results

As mentioned previously, nonoperative treatment usually is effective. A specific regimen cannot be recommended for all patients; however, the principles of short-term rest, pain relief, antiinflammatory agents, and progressive directed activity restoration seem most appropriate. These measures generally should be continued at least 6 to 12 weeks if feasible. If neurologic deficits progress or manifest as myelopathy, or if pain remains at an intolerable level, surgery should be recommended. The initial procedure recommended for this lesion was posterior thoracic laminectomy and disc excision. At least half of the lesions have been identified as being central, making the excision from this approach extremely difficult, and the results were disheartening. Most series reported fewer than half of the patients improving, with some becoming worse after posterior laminectomy and discectomy. Recent studies suggest that lateral rachiotomy (modified costotransversectomy) or an anterior transthoracic approach for discectomy produces considerably better results with no evidence of worsening after the procedure.

Video-assisted thoracic surgery (VATS) has been used in several series to remove central thoracic disc herniations successfully without the need for a thoracotomy or fusion.

The most promising and least invasive technique for surgical treatment of thoracic disc herniation is awake transforaminal endoscopic discectomy. It can be used to treat thoracic herniations of the midline without the morbidity of chest surgery, fusion, or even general anesthesia.

Operative treatment

The best operative approach for these lesions depends on the specific characteristics of the disc herniation and on the particular experience of the surgeon. Simple laminectomy has no role in the treatment of thoracic disc herniations. Posterior approaches, including costotransversectomy, transpedicular, transfacet pedicle-sparing, transdural, and lateral extracavitary approaches, all have been used successfully. Anterior approaches via thoracotomy, a transsternal approach, retropleural approach, or VATS also have been used successfully ( Fig. 39.20 ). More recently, a number of minimally invasive posterior and anterior techniques have been developed, most using a series of muscle dilators, tubular retractors, and microscope visualization. The surgical intervention with the least morbidity is awake transforaminal endoscopic discectomy when used for herniations accessible by that approach.

FIGURE 39.20, A to E, Exposure of thoracic disc provided by standard laminectomy (A) , transpedicular approach (B) , costotransversectomy approach (C) , lateral extracavitary approach (D) , and transthoracic approach (E) .

Costotransversectomy

Costotransversectomy is probably best suited for thoracic disc herniations that are predominantly lateral or herniations that are suspected to be extruded or sequestered. Central disc herniations are probably best approached transthoracically. Some surgeons have recommended subsequent fusion after disc removal anteriorly or laterally.

Thoracic Costotransversectomy

Technique 39.11

  • The operation usually is done with the patient under general anesthesia with a double-lumen endotracheal tube or a Carlen tube to allow lung deflation on the side of approach.

  • Place the patient prone and make a long midline incision or a curved incision convex to the midline centered over the side of involvement.

  • Expose the spine in the usual manner out to the ribs.

  • Remove a section of rib 5.0 to 7.5 cm long at the level of involvement, avoiding damage to the intercostal nerve and artery.

  • Carry the resection into the lateral side of the disc, exposing it for removal. Additional exposure can be made by laminectomy and excision of the pedicle and facet joint. Fusion is unnecessary unless more than one facet joint is removed.

  • Close the wound in layers.

Postoperative Care

Postoperative care is similar to that for lumbar disc excision without fusion (see Technique 39.16).

Thoracic disc excision

Because of the relative age of patients with thoracic disc ruptures, special care must be taken to identify patients with pulmonary problems. In these patients, the anterior approach can be detrimental medically, making a posterolateral approach safer. Patients with midline protrusions probably are best treated with the transthoracic approach to ensure complete disc removal.

Thoracic Discectomy—Anterior Approach

Technique 39.12

  • The operation is done with the patient under general anesthesia, using a double-lumen endotracheal tube for lung deflation on the side of the approach.

  • Place the patient in a lateral decubitus position. A left-sided anterior approach usually is preferred, making the operative procedure easier, if the herniation is central.

  • Make a skin incision along the line of the rib that corresponds to the second thoracic vertebra above the involved intervertebral disc except for approaches to the upper five thoracic segments, where the approach is through the third rib. The skin incision is best determined by correlating preoperative imaging with intraoperative fluoroscopy.

  • Cut the rib subperiosteally at its posterior and anterior ends and insert a rib retractor. Save the rib for grafting later in the procedure. One can decide on an extrapleural or transpleural approach depending on familiarity and ease. Exposure of the thoracic vertebrae should give adequate access to the front and opposite side.

  • Dissect the great vessels free of the spine.

  • Ligate the intersegmental vessels near the great vessels and not near the foramen. One should be able to insert the tip of a finger against the opposite side of the disc when the vascular mobilization is complete. Exposure of the intervertebral disc without disturbing more than three segmental vessels is preferable to avoid ischemic problems in the spinal cord.

  • In the thoracolumbar region, strip the diaphragm from the 11th and 12th ribs. The anterior longitudinal ligament usually is sectioned to allow spreading of the intervertebral disc space. Remove the disc as completely as possible if fusion is planned. The use of an operating microscope or loupe magnification eases the removal of the disc near the posterior longitudinal ligament. Use curets and Kerrison rongeurs to remove the disc back to the posterior longitudinal ligament. When using this technique with fusion, removal of most of the disc is straightforward. As the posterior portion of the disc, including the herniation, is removed, however, the technique becomes more difficult. As mentioned previously, the herniation and surrounding disc usually are calcified and must be removed either piecemeal or with a high-speed drill. Careful dissection to develop a plane between tissue to be removed and the ventral dura is required. This is best done with blunt Penfield-type dissectors and small curets of various designs and orientations. Even if a drill is used, the removal of the posteriormost tissue should be done with hand instruments, not powered instruments. Expect significant bleeding from the epidural veins, which usually are congested at the level of herniation.

  • After removal of the disc, strip the endplates of their cartilage.

  • Make a slot on the margin of the superior endplate to accept the graft material. Preserve the subchondral bone on both sides of the disc space. Insert iliac, tibial, or rib grafts into the disc space. If multiple short rib grafts are used, they can be tied together with heavy suture material when the maximal number of grafts has been inserted. This helps maintain vertical alignment for all such grafts.

  • Close the wound in the usual manner and use standard chest drainage.

  • Alternatively, if fusion is not desired, a more limited resection using an operating microscope can be done.

  • Also, the minimally invasive lateral retroperitoneal/retropleural approach as described in Chapter 37 can be used for herniations from T10-11 to L1-2.

  • After the vascular mobilization, resect the rib head to allow observation of the pedicle and foramen caudal to the disc space. The cephalad portion of the pedicle can be removed with a high-speed burr and Kerrison rongeurs, exposing the posterolateral aspect of the disc. This allows for careful, blunt development of the plane ventral to the dura with removal of the disc herniation and preservation of the anterior majority of the disc and limits the need for fusion. A similar technique using VATS is described in Technique 39.13

  • The transthoracic approach removing a rib two levels above the level of the lesion can be used up to T5. The transthoracic approach from T2 to T5 is best made by excision of the third or fourth rib and elevation of the scapula by sectioning of attachments of the serratus anterior and trapezius from the scapula. The approach to the T1-2 disc is best made from the neck with a sternum-splitting incision.

Postoperative Care

Postoperative care is the same as for a thoracotomy. The patient is allowed to walk after the chest tubes are removed. Extension in any position is prohibited. A brace or body cast that limits extension should be used if the stability of the graft is questionable. The graft usually is stable without support if only one disc space is removed. Postoperative care is the same as for anterior corpectomy and fusion if more than one disc level is removed. If no fusion is done, the patient is mobilized as pain permits without a brace.

Thoracoscopic disc excision

In the fields of general surgery and thoracic surgery, the development of laparoscopic surgical techniques and VATS has allowed significant improvements to be made with respect to decreasing pain, duration of hospitalization, and recovery times for a variety of procedures ( Fig. 39.21 ). Microsurgical and endoscopic operative techniques are highly technical, and they should be performed by a surgeon who is proficient in this technique and in the use of thoracoscopic equipment and with the assistance of an experienced thoracic surgeon. Ideally, the procedure should first be done on cadavers or live animals.

FIGURE 39.21, Video-assisted thoracic surgery. A, Patient positioned in left lateral decubitus position and portal positions marked. B, Portals.

Thoracoscopic Thoracic Discectomy

Technique 39.13

(ROSENTHAL ET AL.)

  • Place the patient in the left lateral decubitus position to allow a right-sided approach and displacement of the aorta and heart to the left.

  • Insert four trocars in a triangular fashion along the middle axillary line converging on the disc space. Introduce a rigid endoscope with a 30-degree optic angle attached to a video camera into one of the trocars, leaving the other three as working channels.

  • Deflate the lung using a Carlen tube or similar method.

  • Split the parietal pleura starting at the medial part of the intervertebral space and extending up to the costovertebral process.

  • Preserve and mobilize the segmental arteries and sympathetic nerve out of the operating field.

  • Drill away the rib head and lateral portion of the pedicle. Remove the remaining pedicle with Kerrison rongeurs to improve exposure to the spinal canal. Removing the superior posterior portion of the vertebra caudal to the disc space allows safer removal of the disc material, which can be pulled anteriorly and inferiorly away from the spinal canal to be removed. Use endoscopic instruments for surgery in the portals.

  • Remove the disc posteriorly and the posterior longitudinal ligament, restricting bone and disc removal to the posterior third of the intervertebral space and costovertebral area to maintain stability.

  • Insert chest tubes in the standard fashion and set them to water suction; close the portals.

Postoperative Care

The patient is rapidly mobilized as tolerated by the chest tubes. Discharge is possible after the chest tubes have been removed and the patient is ambulating well.

Minimally Invasive Thoracic Discectomy

Technique 39.14

  • Place the patient in the lateral decubitus position with the affected side up.

  • Localize an incision over the disc space of interest. A 5-cm portion of rib can be resected if it is overlying the disc, or the approach can sometimes be performed without rib resection. Using blunt finger dissection, make a retropleural approach down to the spine and dock a minimally invasive retractor system on the disc space and rib head of interest. Sometimes the pleura must be opened, but this does not change the exposure significantly because the retractor can safely retract the lung while being insufflated.

  • Complete the procedure as in an open discectomy through a thoracotomy using the self-retaining retractor (many different styles are available).

  • Once the procedure is finished there is no need for a chest tube if the pleura is not violated.

  • Close the rib base and subcutaneous tissues in layers.

This approach can be extended down to L1-2 by mobilizing the diaphragm off the rib and transverse process attachments.

Postoperative Care

The patient is mobilized the day of surgery and is discharged when ambulating well.

Thoracic endoscopic disc excision

Transforaminal Endoscopic Thoracic Discectomy

The awake transforaminal endoscopic approach using the outside-in technique to the thoracic spine allows resection of disc material that can begin midline and be extended laterally to either side. This approach typically can reach herniations from T4 to L4 in most people, does not require violation of the chest cavity, usually does not require fusion, and does not even require general anesthesia, making it the least invasive approach for removal of a thoracic disc herniation.

A diagnostic transforaminal epidural injection at the site of the herniation can confirm the diagnosis and ensure enough space between the rib, transverse process, and facet joint for the endoscopic approach. If the patient gets profound relief from the transforaminal epidural, it is a good predictor of surgical outcome, and endoscopic surgery can be planned if the pain from the thoracic disc herniation returns.

Technique 39.15

  • Plan the approach to the appropriate thoracic foramen on preoperative axial imaging.

  • Place the patient prone on a radiolucent table.

  • Advance an 18- to 20-gauge needle into the foramen at the level of the herniation based on the preoperative imaging plan.

  • Place a guide wire through the needle and remove the needle.

  • Anesthetize the skin and subcutaneous tissue with 8 mL 1% lidocaine with epinephrine and use a no. 11 blade to make a 1-cm incision.

  • Place dilators over the guidewire and advance them into the foramen under fluoroscopic guidance.

  • Some systems allow reaming of the foramen with percutaneous reamers under fluoroscopic guidance. Alternatively, advance the operative cannula into the foramen and open the foramen with a diamond burr under direct light-based endoscopic visualization. This technique is best for surgeons who are more comfortable with bony resection under direct visualization, and it is our preferred technique.

  • Remove bone vigorously to allow space to work and avoid tension on the dura. Remove a significant amount of superior articular process, pedicle, and posterior end plates as needed.

  • Adjust fluid flow through the endoscope to control epidural bleeding.

  • After the bony anatomy of the arch formed by the inferior pedicle and superior articular process is visualized, identify the herniation.

  • Use instruments to remove disc material from the subannular space and push disc material away from the dura into the cavity created by the drilling.

  • Decompression is complete when the undersurface of the thoracic dura is seen pulsating to heartbeat and the patient notes resolution of his or her typical thoracic radicular pain.

  • Suction excess fluid from the wound and infiltrate the epidural space with 1 mL of steroid and 2 mL of 0.25% Marcaine.

  • Remove the operative cannula, close the skin with a single subcuticular stitch, and close the wound with a dab of skin glue. Ask the patient to transfer himself or herself to the gurney.

Postoperative Care

The patient is limited in bending, lifting, and twisting, but may shower the day of the procedure. Patients are typically discharged from the surgery center as soon as they can ambulate independently and void. Driving is delayed until postoperative day 2 or until narcotics are discontinued, but this procedure is commonly done with only nonsteroidal antiinflammatory medications for postoperative pain control. Patients are allowed to begin a trunk stabilization therapy program at 2 weeks after surgery and advance as tolerated.

Lumbar Disc Disease

Signs and symptoms

Although back pain is common from the second decade of life on, intervertebral disc disease and disc herniation are most prominent in otherwise healthy people in the third and fourth decades of life. Most people relate their back and leg pain to a traumatic incident, but close questioning frequently reveals that the patient has had intermittent episodes of back pain for many months or even years before the onset of severe leg pain. In many instances, the back pain is relatively fleeting and is relieved by rest. Heavy exertion, repetitive bending, twisting, or heavy lifting often brings on axial back pain. In other instances, an inciting event cannot be elicited. The pain usually begins in the lower back, radiating to the sacroiliac region and buttocks. The pain can radiate down the posterior thigh. Back and posterior thigh pain of this type can be elicited from many areas of the spine, including the facet joints, longitudinal ligaments, and periosteum of the vertebra. Radicular pain usually extends below the knee and follows the dermatome of the involved nerve root ( Fig. 39.22 ).

FIGURE 39.22, Diagram indicating dermatomal regions for T10-S5 nerves.

The usual history of lumbar disc herniation is of repetitive lower back and buttock pain, relieved by a short period of rest. This pain is suddenly exacerbated, often by a flexion episode, with the appearance of leg pain. Most radicular pain from nerve root compression caused by a herniated nucleus pulposus is evidenced by leg pain equal to, or in many cases greater than, the degree of back pain. Whenever leg pain is minimal and back pain is predominant, great care should be taken before making the diagnosis of a symptomatic herniated intervertebral disc. The pain from disc herniation usually varies, increasing with activity, especially sitting and driving.

The pain can be decreased by rest, especially in the semi-Fowler position, and can be exacerbated by straining, sneezing, or coughing. Whenever the pattern of pain is bizarre or the pain is uniform in intensity, a diagnosis of symptomatic herniated disc should be viewed with some skepticism.

Other symptoms of disc herniation include weakness and paresthesias. In most patients, the weakness is intermittent, varies with activity, and is localized to the neurologic level of involvement. Paresthesias also vary and are limited to the dermatome of the involved nerve root. Whenever these complaints are generalized, the diagnosis of a simple unilateral disc herniation should be questioned.

Numbness and weakness in the involved leg and occasionally pain in the groin or testis can be associated with a high or midline lumbar disc herniation. If a fragment is large or the herniation is high, symptoms of pressure on the entire cauda equina can occur with development of cauda equina syndrome. These symptoms include numbness and weakness in both legs, rectal pain, numbness in the perineum, and paralysis of the sphincters. This diagnosis should be the primary consideration in patients who complain of sudden loss of bowel or bladder control. Whenever the diagnosis of cauda equina syndrome is caused by an acute midline herniation, evaluation and treatment should be aggressive.

The physical findings with disc disease vary because of the time intervals involved. Usually patients with acute pain show evidence of marked paraspinal spasm that is sustained during walking or motion. A scoliosis or a list in the lumbar spine may be present, and in many patients the normal lumbar lordosis is lost. As the acute episode subsides, the degree of spasm diminishes remarkably, and the loss of normal lumbar lordosis may be the only telltale sign. Point tenderness may be present over the spinous process at the level of the disc involved, and pain may extend laterally in some patients.

If there is nerve root irritation, it centers over the length of the sciatic nerve, in the sciatic notch, and more distally in the popliteal space. In addition, stretch of the sciatic nerve at the knee should reproduce buttock, thigh, and leg pain (i.e., pain distal to the knee). A Lasègue sign usually is positive on the involved side. A positive Lasègue sign or straight-leg raising should elicit buttock and leg pain distal to the knee. Occasionally, if leg pain is significant, the patient leans back from an upright sitting position and assumes the tripod position to relieve the pain. This is referred to as the “flip sign.” Contralateral leg pain produced by straight-leg raising should be regarded as pathognomonic of a herniated intervertebral disc. The absence of a positive Lasègue sign should make one skeptical of the diagnosis, although older individuals may not have a positive Lasègue sign and tend toward more claudicatory symptoms. Likewise, inappropriate findings and inconsistencies in the examination usually are nonorganic in origin (see discussion of nonspecific axial pain). If the leg pain has persisted for any length of time, atrophy of the involved limb may be present, as shown by asymmetric girth of the thigh or calf. The neurologic examination varies as determined by the level of root involvement ( Boxes 39.2 to 39.4 ).

BOX 39.2
L4 Root Compression

Indicative of L3-4 disc herniation or pathologic condition localized to L4 foramen.

Sensory Deficit

Posterolateral thigh, anterior knee, and medial leg

Motor Weakness

  • Quadriceps (variable)

  • Hip adductors (variable)

Anterior Tibial Weakness

  • Reflex change

  • Patellar tendon

  • Anterior tibial tendon (variable)

BOX 39.3
L5 Root Compression

Indicative of L4-5 disc herniation or pathologic condition localized to L5 foramen.

Sensory Deficit

  • Anterolateral leg, dorsum of the foot, and great toe

Motor Weakness

  • Extensor hallucis longus

  • Gluteus medius

  • Extensor digitorum longus and brevis

Reflex Change

  • Usually none

  • Posterior tibial (difficult to elicit)

BOX 39.4
S1 Root Compression

Indicative of L5-S1 disc herniation or pathologic condition localized to S1 foramen.

Sensory Deficit

  • Lateral malleolus, lateral foot, heel, and web of fourth and fifth toes

Motor Weakness

  • Peroneus longus and brevis

  • Gastrocnemius-soleus complex

  • Gluteus maximus

Reflex Change

  • Achilles tendon (gastrocnemius-soleus complex)

Unilateral disc herniation at L3-4 usually compresses the L4 root as it crosses the disc before exiting at the L4-5 intervertebral foramen below the L4 pedicle. Pain may be localized around the medial side of the leg. Numbness may be present over the anteromedial aspect of the leg. The anterior tibial muscle may be weak, as evidenced by inability to heel walk. The quadriceps and hip adductor group, both innervated from L2, L3, and L4, also may be weak and, in extended ruptures, atrophic. Reflex testing may reveal a diminished or absent patellar tendon reflex (L2, L3, and L4) or anterior tibial tendon reflex (L4). Sensory testing may show diminished sensibility over the L4 dermatome, the isolated portion of which is the medial leg (see Fig. 39.22 ) and the autonomous zone of which is at the level of the medial malleolus.

Unilateral disc herniation at L4-5 results in compression of the L5 root. L5 root radiculopathy should produce pain in the dermatomal pattern. Numbness, when present, follows the L5 dermatome along the anterolateral aspect of the leg and the dorsum of the foot, including the great toe. The autonomous zone for this nerve is the dorsal first web of the foot and the dorsum of the third toe. Weakness may involve the extensor hallucis longus (L5), gluteus medius (L5), or extensor digitorum longus and brevis (L5). Reflex change usually is not found. A diminished posterior tibial reflex is possible but difficult to elicit.

With unilateral rupture of the disc at L5-S1, the findings of an S1 radiculopathy are noted. Pain and numbness involve the dermatome of S1. The S1 dermatome includes the lateral malleolus and the lateral and plantar surface of the foot, occasionally including the heel. There is numbness over the lateral aspect of the leg and, more important, over the lateral aspect of the foot, including the lateral three toes. The autonomous zone for this root is the dorsum of the fifth toe. Weakness may be shown in the peroneus longus and brevis (S1), gastrocnemius-soleus (S1), or gluteus maximus (S1). In general, weakness is not a usual finding in S1 radiculopathy. Occasionally, mild weakness may be shown by asymmetric fatigue with exercise of these motor groups. The ankle jerk usually is reduced or absent.

Massive extrusion of a disc involving the entire diameter of the lumbar canal or a large midline extrusion can produce pain in the back, legs, and occasionally perineum. Both legs may be paralyzed, the sphincters may be incontinent, and the ankle jerks may be absent.

More than 95% of the ruptures of the lumbar intervertebral discs occur at L4-5 or L5-S1. Ruptures at higher levels in many patients are not associated with a positive straight-leg raising test. In these instances, a positive femoral stretch test can be helpful. This test is done by placing the patient prone and acutely flexing the knee while placing the hand in the popliteal fossa. When this procedure results in anterior thigh pain, the result is positive and a high lesion should be suspected. In addition, these lesions may occur with a more diffuse neurologic complaint without significant localizing neurologic signs.

Often the neurologic signs associated with disc disease vary over time. If the patient has been up and walking for a period of time, the neurologic findings may be much more pronounced than if he or she has been at bed rest for several days, decreasing the pressure on the nerve root and allowing the nerve to resume its normal function. In addition, various conservative treatments can change the physical signs of disc disease.

Comparative bilateral examination of a patient with back and leg pain is essential in finding a clear-cut pattern of signs and symptoms. The evaluation commonly may change. Adverse changes in the examination may warrant more aggressive therapy, whereas improvement of the symptoms or signs should signal a resolution of the problem. Early symptoms or signs suggesting cauda equina syndrome or severe or progressive neurologic deficit should be treated aggressively from the onset.

Differential diagnosis

The differential diagnosis of back and leg pain is extremely lengthy and complex. It includes diseases intrinsic to the spine and diseases involving adjacent organs but causing pain referred to the back or leg. For simplicity, lesions can be categorized as being extrinsic or intrinsic to the spine. Extrinsic lesions include diseases of the urogenital system, gastrointestinal system, vascular system, endocrine system, nervous system not localized to the spine, and extrinsic musculoskeletal system. These lesions include infections, tumors, metabolic disturbances, congenital abnormalities, and associated diseases of aging. Intrinsic lesions involve diseases that arise primarily in the spine. They include diseases of the spinal musculoskeletal system, the local hematopoietic system, and the local neurologic system. These conditions include trauma, tumors, infections, diseases of aging, and immune diseases affecting the spine or spinal nerves.

Although the predominant cause of back and leg pain in healthy individuals usually is lumbar disc disease, one must be extremely cautious to avoid a misdiagnosis, particularly given the high incidence of disc herniations present in asymptomatic patients as discussed previously. A full physical examination must be completed before making a presumptive diagnosis of herniated disc disease. Common diseases that can mimic disc disease include ankylosing spondylitis, multiple myeloma, vascular insufficiency, arthritis of the hip, osteoporosis with stress fractures, extradural tumors, peripheral neuropathy, and herpes zoster. Infrequent but reported causes of sciatica not related to disc herniation include synovial cysts, rupture of the medial head of the gastrocnemius, sacroiliac joint dysfunction, lesions in the sacrum and pelvis, and fracture of the ischial tuberosity.

Confirmatory imaging

Although the diagnosis of a herniated lumbar disc should be suspected from the history and physical examination, imaging studies are necessary to rule out other causes, such as a tumor or infection. Plain radiographs are of limited use in the diagnosis because they do not show disc herniations or other intraspinal lesions, but they can show infection, tumors, or other anomalies and should be obtained, especially if surgery is planned. Currently, the most useful test for diagnosing a herniated lumbar disc is MRI ( Figs. 39.23 and 39.24 ). Since the advent of MRI, myelography is used much less frequently, although in some situations it may help to show subtle lesions. When myelography is used, it should be followed by CT.

FIGURE 39.23, Types of disc herniation. A, Normal bulge. B, Protrusion. C, Extrusion. D, Sequestration.

FIGURE 39.24, Sixty-one-year-old patient with right L5 radiculopathy. A, T2 sagittal MR image reveals sequestered L4 herniated disc fragment. B, T2 axial MR image shows the fragment between L5 pedicles. C, This patient also had asymptomatic left L5 disc extrusion.

Nonoperative treatment

The number and variety of nonoperative therapies for back and leg pain are diverse and overwhelming. Treatments range from simple rest to expensive traction apparatus. All of these therapies are reported with glowing accounts of miraculous “cures”; few have been evaluated scientifically. In addition, the natural history of lumbar disc herniation is characterized by exacerbations and remissions with eventual improvement of extremity complaints in most cases, which can make any intervention appear successful to the patient. Finally, several distinct symptom complexes seem to be associated with disc disease. Few, if any, studies have isolated the response to specific and anatomically distinct diagnoses.

The simplest treatment for acute back pain is rest; generally 2 days of bed rest are better than a longer period. Biomechanical studies indicate that lying in a semi-Fowler position (i.e., on the side with the hips and knees flexed) with a pillow between the legs should relieve most pressure on the disc and nerve roots. Muscle spasm can be controlled by the application of ice, preferably with a massage over the muscles in spasm. Pain relief and antiinflammatory effect can be achieved with NSAIDs. Most acute exacerbations of back pain respond quickly to this therapy. As the pain diminishes, the patient should be encouraged to begin isometric abdominal and lower extremity exercises. Walking within the limits of comfort also is encouraged. Sitting, especially riding in a car, is discouraged. Continuation of ordinary activities within the limits permitted by pain has been shown to lead to a quicker recovery.

Education in proper posture and body mechanics is helpful in returning the patient to the usual level of activity after the acute exacerbation has improved. This education can take many forms, from individual instruction to group instruction. Back education of this type is now usually referred to as “back school.” Although the concept is excellent, the quality and quantity of information provided may vary widely. The work of Bergquist-Ullman and Larsson and others indicates that patient education of this type is extremely beneficial in decreasing the amount of time lost from work initially but does little to decrease the incidence of recurrence of symptoms or length of time lost from work during recurrences. The combination of back education and combined physical therapy is superior to placebo treatment. Physical therapy can help improve activity level and physical function but should be discontinued if it aggravates the radiculopathy.

Numerous medications have been used with various results in subacute and chronic back and leg pain syndromes. The current trend seems to be moving away from the use of strong narcotics and muscle relaxants in the outpatient treatment of these syndromes. This is especially true in the instances of chronic back and leg pain where drug habituation and increased depression are frequent. Oral steroids used briefly can be beneficial as potent antiinflammatory agents. The many types of NSAIDs also are helpful when aspirin is not tolerated or is of little help. Numerous NSAIDs are available for the treatment of low back pain. When depression is prominent, mood elevators such as nortriptyline can be beneficial in reducing sleep disturbance and anxiety without increasing depression. Nortriptyline also decreases the need for narcotic medication.

Physical therapy should be used judiciously. The exercises should be fitted to the symptoms and not forced as an absolute group of activities. Patients with acute back and thigh pain eased by passive extension of the spine in the prone position can benefit from extension exercises rather than flexion exercises. Improvement in symptoms with extension indicates a good prognosis with conservative care. Patients whose pain is increased by passive extension may be improved by flexion exercises. These exercises should not be forced in the face of increased pain. This may avoid further disc extrusion. Any exercise that increases pain should be discontinued. Lower extremity exercises can increase strength and relieve stress on the back, but they also can exacerbate lower extremity arthritis. The true benefit of such treatments may be in the promotion of good posture and body mechanics rather than of strength. Numerous treatment methods have been advanced for the treatment of back pain. Some patients respond to the use of transcutaneous electrical nerve stimulation. Others do well with traction varying from skin traction in bed with 5 to 8 lb to body inversion with forces of more than 100 lb. Back braces or corsets may be helpful to other patients. Ultrasound and diathermy are other treatments used in acute back pain. The scientific efficacy of many of these treatments has not been proved.

As discussed earlier, the natural history of lumbar disc disease generally is favorable. Although low-back pain can result in significant disability, approximately 95% of patients return to their previous employment within 3 months of symptom onset. Failure to return to work within 3 months has been identified as a poor prognostic sign. Longer periods of disability equate to lower probability of returning to work: in patients with total disability lasting a year, the likelihood of returning to work is 21%, and in those with disability lasting 2 years the likelihood is less than 2%. Obesity and smoking have been shown to correlate unfavorably with low back pain and may adversely affect the progression of symptoms.

Operative treatment

If nonoperative treatment for lumbar disc disease fails, the next consideration is operative treatment. Before this step is taken, the surgeon must be sure of the diagnosis. The patient must be certain that the degree of pain and impairment warrants such a step. The surgeon and the patient must realize that disc surgery is not a cure but may provide symptomatic relief. It neither stops the pathologic processes that allowed the herniation to occur nor restores the disc to a normal state. The patient still must practice good posture and body mechanics after surgery. Activities involving repetitive bending, twisting, and lifting with the spine in flexion may have to be curtailed or eliminated. If prolonged relief is to be expected, some permanent modification in the patient’s lifestyle may be necessary, although often no specific limitations are applied.

The key to good results in disc surgery is appropriate patient selection. The optimal patient is one with predominant (if not only) unilateral leg pain extending below the knee that has been present for at least 6 weeks. The pain should have been decreased by rest, antiinflammatory medication, or even epidural steroids but should have returned to the initial levels after a minimum of 6 to 8 weeks of conservative care. Physical examination should reveal signs of sciatic irritation and possibly objective evidence of localizing neurologic impairment. CT, lumbar MRI, or myelography should confirm the level of involvement consistent with the patient’s examination.

Operative disc removal is mandatory and urgent only in patients with cauda equina syndrome; other disc excisions should be considered elective. The elective status of surgery should allow a thorough evaluation to confirm the diagnosis, level of involvement, and physical and psychologic status of the patient. Frequently, if there is a rush to the operating room to relieve pain without proper investigation, the patient and the physician later regret the decision.

Regardless of the method chosen to treat a disc rupture surgically, the patient should be aware that the procedure is predominantly for the symptomatic relief of leg pain. Patients with predominantly back pain may not experience relief.

Microdiscectomy

Most disc surgery is performed with the patient under general endotracheal anesthesia, although local anesthesia has been used with minimal complications. Patient positioning varies with the operative technique and surgeon. To position the patient in a modified kneeling position, a specialized frame or custom frame is popular. Positioning the patient in this manner allows the abdomen to hang free, minimizing epidural venous dilation and bleeding ( Fig. 39.25 ). A headlamp allows the surgeon to direct light into the lateral recesses where a large proportion of the surgery may be required. The addition of loupe magnification also greatly improves the identification and exposure of various structures. Most surgeons also use an operative microscope to improve visibility further. The primary benefit of an operating microscope compared with loupes is the narrowed interocular distance while maintaining binocular vision and the view afforded the assistant. Radiographic confirmation of the proper level is necessary. Care should be taken to protect neural structures. Epidural bleeding should be controlled with bipolar electrocautery. Any sponge, pack, or cottonoid patty placed in the wound should extend to the outside. Pituitary rongeurs should be marked at a point equal to the maximal allowable disc depth to prevent injury of viscera or great vessels.

FIGURE 39.25, Knee-chest position for lumbar disc excision allows abdomen to be completely free of external pressure.

Microscopic Lumbar Disc Excision

Microscopic lumbar disc excision has replaced the standard open laminectomy as the procedure of choice for herniated lumbar disc. This procedure can be done on an outpatient basis and allows better lighting, magnification, and angle of view with a much smaller exposure. Because of the limited dissection required, there is less postoperative pain and a shorter postoperative stay.

Microscopic lumbar discectomy requires an operating microscope with a 400-mm lens, a variety of small-angled Kerrison rongeurs of appropriate length, microinstruments, and preferably a combination suction/nerve root retractor. The procedure is performed with the patient prone. A specialized frame (see Fig. 39.25 ) previously described can be used, or the patient can be positioned on chest rolls. There are several advantages to using a specialized table, such as an Andrews table: (1) it allows the belly to hang free where venous blood will pool, which results in decreased venous epidural bleeding intraoperatively; (2) the knee-chest position maximizes the lumbar kyphosis, placing the ligamentum flavum on slight tension that allows for easier removal but also opens the interlaminar space, which may provide greater canal access with less bone removal; and (3) the small footprint of the bed enables the operating microscope to be placed at the foot, which not only makes access to the ocular lens easier for both the surgeon and assistant standing on opposite sides of the table but also allows the fluoroscope to be moved into the surgical field for imaging without having to move the microscope base itself.

The microscope can be used from skin incision to closure. The initial dissection can be done under direct vision, however. A lateral radiograph is taken to confirm the level, but fluoroscopy is much quicker when used for localization. Fluoroscopy is essential for localization when using tubular retractors because the field of view is smaller, making the available margin for error in placing the skin incision less.

Tubular Techniques

Tubular techniques have been developed with the purported advantage of shortened hospital stay, faster return to activity, and fewer wound issues. These techniques generally are variations of the microdiscectomy technique using a tubular retractor rather than the McCulloch and different types of bayoneted instruments. This remains another alternative technique. The basic principles remain the same as with microdiscectomy. The less-invasive tubular retractors have been used in a transmuscular fashion, allowing disc excision with less soft-tissue damage because of the more precise exposure; however, better objective clinical results have not been shown with this technique.

Microscopic Lumbar Discectomy

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