Surgical Anatomy and Operative Techniques of Lumbar Stenosis

General Considerations

Degenerative spine disease, or spondylosis, affects everyone—the infirm and the healthy, the sedentary and the athletic, the young and the old. Spondylosis occurs throughout the spine but is more prevalent within the main axial loading vertebrae of the body, the lumbar spine. Lumbar stenosis occurs in 5 of every 1000 Americans older than 50 years. Surgical decompression for lumbar stenosis is the most common surgery for individuals older than 65 years. Symptoms range all the way from low back pain (axial), radiating leg pain (radicular), paresthesia, weakness, and gait instability to loss of normal bladder and bowel function. These symptoms may occur acutely—such as with trauma, disk herniation, and cauda equina syndrome—but they more typically occur as a chronic, debilitating condition.

Lumbar stenosis is classified into two categories: central canal stenosis or foraminal stenosis. Canal compromise in lumbar stenosis is multifactorial and includes ligamentous hypertrophy, osteophyte overgrowth, spondylolisthesis, hypertrophic facets, and disk herniation. Less common causes include tumors, abscesses, and postoperative adhesions. The levels most commonly affected are L4–L5, followed by L3–L4, L2–L3, and then L5–S1.

In the average person, the normal anteroposterior (AP) diameter of the spinal canal as measured on an axial-cut computed tomography (CT) scan should be greater than 11 mm. Measurements less than 11 mm in the central canal are usually considered stenotic. In foraminal stenosis, or lateral recess syndrome, the “gutter” medial to the pedicle is stenotic from hypertrophy of the superior articulating facet from the caudal vertebral body. By CT measurement, foraminal stenosis/lateral recess syndrome occurs when the AP diameter from the posterior vertebral body to the superior articulating facet is less than 2 mm at the point where the nerve root exits. If the condition also involves potential spinal instability (i.e., spondylolisthesis or scoliosis), lumbar stenosis may also be subcategorized into a potentially unstable group. This chapter will focus on the more common etiologies of stable, chronic lumbar stenosis.

Regardless of the etiology, lumbar stenosis confirmed by radiographic imaging to be the cause of neurologic symptoms and failed medical management should receive prompt surgical intervention. Accurate diagnosis and timely management are of utmost importance in treatment of this ubiquitous disease. Although many patients will improve with medical management and a tincture of time, prompt recognition of situations that require surgical intervention is critical.

Symptoms

Patients with lumbar stenosis often come to their primary care physician with radiating leg pain and occasional low back pain. Central canal stenosis may classically present as neurogenic claudication, pain that radiates from the back down the legs and is typically exacerbated by low-back extension or exercise and is relieved by lumbar flexion and rest. Patients are generally older and will describe low-back pain or cramping stiffness that radiates down the thighs; in addition, they may also complain of paresthesia and weakness. These symptoms occur while walking, and this progressively limits the person’s ability to ambulate for any great distance.

Often, symptoms improve dramatically with sitting down and bending forward (lumbar flexion). Not uncommonly, patients describe an increased ability to ambulate or to tolerate pain when leaning forward while walking, and they typically relate a history of leaning forward on a walker or shopping cart. The pain is usually described as “achiness” that occurs in a bandlike distribution across the lower back and radiates as a burning or tingling pain down the thighs. Bladder and bowel dysfunction rarely occur, but if present, consider these a red flag warning of a more urgent condition.

The symptoms of lumbar stenosis are hypothesized to occur from ischemia to the lumbosacral nerve roots from a combination of exercise-induced metabolic demands and anatomic pressure-related vascular compromise. Cessation of exercise lowers the metabolic demand and reduces ischemia-induced symptoms. Lumbar flexion alleviates central canal stenosis by reducing the inbuckling from the ligamentum flavum, and it improves foraminal stenosis by widening the neural foramen of the compressed exiting nerve roots. On physical exam, patients usually do not demonstrate any focal weakness; however, patients may have decreased lower extremity reflexes. There should not be pain on palpation of the spine or lower extremity joints.

Differential diagnoses for neurogenic claudication or unilateral radiculopathy from central canal or foraminal stenosis include orthopedic pathology, such as knee or hip arthritis; trochanteric bursitis; and vascular claudication. Orthopedic pathologies are usually elucidated with pain on palpation of the involved joints; presence of joint edema; a positive flexion, abduction, and external rotation (FABER) test; and radiographs. Vascular claudication can be deduced by a history of coronary or peripheral vascular disease or clinical findings. Symptoms include pain or paresthesia in a myotomal distribution; pain that improves with rest, even while standing upright (rare in neurogenic claudication); immediate improvement in symptoms with rest; and lower extremity symptoms with elevation of the foot above the level of the heart (increased foot pallor or decreased temperature and pulses).

Surgical Approach/Operative Techniques

Subtotal/Total Laminectomy

The patient is positioned prone on a Wilson frame placed on a standard operating room (OR) table or a flat Jackson table ( Fig. 43-1 ). After confirming the appropriate surgical level with intraoperative fluoroscopy, a midline incision is performed, followed by a bilateral subperiosteal dissection to expose the spinous processes and laminae. In general, exposure of the facets is avoided. However, in cases where there has been significant facet hypertrophy, it may be necessary to expose the medial aspect of the facets. Once the exposure has been completed, self-retaining retractors are placed, and intraoperative fluoroscopy is used to confirm the surgical level.

For single-level pathology, the lower half of the superior spinous process, supraspinous ligament, interspinous ligament, and the upper half of the inferior spinous process can be removed with a Leksell rongeur. A high-speed drill is used to remove the inferior half of the superior lamina, working from caudal to cranial and from medial to lateral directions. Care should be taken to preserve the pars interarticularis and to avoid resecting more than half of the facets; both of these actions can lead to iatrogenic instability.

After removal of the caudal half of the superior lamina, the surgeon should be able to visualize the superior extent of the ligamentum flavum and a small portion of the thecal sac. Using an up-angled curette or a Woodson probe, a plane is developed between the ligamentum flavum and the thecal sac. Kerrison rongeurs are used to resect the ligamentum flavum and epidural fat in a cranial to caudal direction. Caudally, the ligamentum flavum is attached to the posterior surface of the upper margin of the lamina below; it will be necessary to remove this portion of the inferior lamina with the Kerrison rongeurs to completely detach the ligamentum flavum.

After the thecal sac has been decompressed centrally, focus should be directed at decompressing the lateral recess, where a significant amount of stenosis may occur secondary to ligamentous and facet hypertrophy. To adequately visualize the lateral recess, it is often helpful to use a Woodson probe to gently depress the thecal sac to visualize the plane between the thecal sac and any residual ligamentum flavum or hypertrophic bone laterally. The use of cottonoids may be helpful in protecting the dura, thus reducing the incidence of unintentional durotomy. Any remaining ligamentum flavum or bony overgrowth in the lateral recess, subarticular region, or foramen can be resected with Kerrison rongeurs. A blunt probe should be easily passed through the foramen of the exiting and traversing nerve roots with minimal resistance. In cases of multilevel lumbar stenosis, this technique can be extended to encompass multiple levels by performing complete laminectomies at the intervening levels.

Unilateral Hemilaminotomy/Hemilaminectomy

Initial positioning and dissection steps for a unilateral hemilaminotomy/hemilaminectomy are similar to the total laminectomy as described above. The muscular dissection and bony removal are completed ipsilateral to the symptomatic side without exposure of the contralateral anatomy. The ipsilateral ligamentum flavum is left intact to protect the underlying dura during the contralateral decompression. After removal of the ligamentum flavum beneath the hemilaminotomy defect, Kerrison rongeurs are used to remove any remaining ligamentous or bony stenosis in the foramen of the ipsilateral and traversing nerve roots.

Once this has been completed, we turn our attention to performing a contralateral decompression. To better visualize the contralateral side, a high-speed drill is used to undercut the ipsilateral base of the spinous process and undersurface of the contralateral lamina. Next, a contralateral decompression is performed by resecting any remaining ligamentum flavum to the contralateral margin of the thecal sac. The surgeon may tilt the operating table away to obtain a better view of the contralateral thecal sac, exiting nerve root, and traversing nerve root. Kerrison rongeurs can be used to remove any ligamentous or bony stenosis in the foramen of the contralateral exiting and traversing nerve roots. Once the decompression has been completed, a blunt probe should pass easily into the foramen of the exiting and traversing nerve roots. In cases of multilevel lumbar stenosis, this technique can be extended to encompass multiple levels by performing hemilaminectomies at the intervening levels.

Tubular Hemilaminotomy

The unilateral hemilaminotomy described above can also be performed with the assistance of a tubular retractor under loupe, microscope, or endoscope magnification. Tubular retractors use a paramedian muscle-splitting approach and result in smaller incisions and less soft-tissue trauma compared with a traditional midline subperiosteal approach. Patients are positioned prone on a Wilson frame placed on a standard OR table or on a flat Jackson table. A side rail extension is placed on the side of the table contralateral to the surgical side, from which a flexible arm originates, to allow attachment of a rigid rod.

Fluoroscopy is used to localize the correct surgical level, and a paramedian line demarcating the incision is drawn approximately 15 mm off the midline in a cranial to caudal direction. The tip of the initial dilator is pressed against the surface of the skin along the paramedian line at the anticipated level of entry, and fluoroscopy is used to identify the correct entry point and trajectory to the surgical level. A single, small stab incision is made in the skin through the lumbodorsal fascia, and a guidewire is inserted through the stab incision onto the lamina–facet junction. Fluoroscopy is used to confirm the correct position and trajectory of the guidewire, and the stab incision is lengthened on both sides to accommodate the diameter of the tubular retractor to be used (typically 18 mm). Sequential tubular dilators ( Fig. 43-2 ) are then advanced over the guidewire and are docked on the lamina-facet junction ( Fig. 43-3 ). A final tubular retractor is placed over the last dilator and is secured to the flexible arm connected to a rigid rod attached to the table ( Fig. 43-4 ). Once fluoroscopy confirms correct placement of the tubular retractor, the sequential dilators are removed ( Fig. 43-5 ).