Summary of Key Points
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Geriatric patients are the fastest growing segment of the population that may require spine surgery.
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The degenerative cascade consists of a slow deterioration of the intervertebral discs, facet joints, and ligaments, which may result in spinal stenosis, spondylolisthesis, or scoliosis.
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Osteoporosis is a significant comorbidity, which impacts the ability and strategy when operating on the geriatric spine.
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Age alone is not a contraindication for surgery, but the surgeon must take into consideration the many comorbidities specific to the geriatric population.
The current definition of a geriatric patient is most commonly accepted as age 65 or older. However, one could easily argue that a more appropriate definition of “geriatric” would instead focus on the characteristics of elderly patients that predispose them to specific disease states rather than simply a numeric value. Under this classification, individuals would be more appropriately labeled as geriatric if they had a combination of advancing chronologic age, lifestyle and activity changes demanded by an accumulation of various comorbidities, and disease states that become more prominent with an aging body. For this reason, age alone is not a contraindication to spine surgery. There is already substantial literature supporting spine surgery in elderly patients especially in the areas of trauma, degenerative disease, and scoliosis. However, as the population continues to age, spine surgeons are challenged to continue maximizing the independence of this growing segment of elderly patients by striving for further developments in geriatric spine surgery.
Epidemiology
Demographers project that by 2030 more than 20% of U.S. residents will be aged 65 and older, compared with 14.1% in 2014. Between 2012 and 2050, the United States will experience considerable growth in the elderly population. In 2050, the population aged 65 and older is projected to be 83.7 million, almost double the number in 2012 ( Fig. 175-1 ). An aging population is not limited to the United States, and census projections internationally demonstrate a rapid growth in the geriatric population ( Fig. 175-2 ). In China alone, the elderly population is expected to grow to 238.8 million and 348.8 million by 2030 and 2050, respectively. A geriatric population of 348.8 million people is larger than the total U.S. population today.
With longer life expectancies, more and more elderly patients are electing to undergo spine surgery to improve mobility, function, and quality in the later years of life. Moreover, they are unwilling to accept pain and disability as simply the effect of “getting old.” Concomitant with the shift in the population demographics, elderly individuals expect to remain more active with a higher quality of life. Maintaining a pain-free, mobile lifestyle is no longer the purview of the young. An intimate knowledge of the preoperative, operative, and postoperative medical management of elderly patients will be critical in the future of spine surgery.
Aging Spine
It is a well-understood concept in geriatric medicine that a wide array of changes will occur in the human body with increasing age. These changes are often both predictable and degenerative in nature. The progressive deterioration of organ systems is a phenomenon that can readily be understood when one considers the traumas (whether micro or macro), disease processes, and normal wear-and-tear that accumulate over a lifetime. The spine is not exempt from this pattern of deterioration, and after being subjected to a lifetime of use and abuse, this may lead to a decline in form and function.
The chronologic deterioration of the spine with age is not a new concept to medicine. In fact, a predictable pattern of how the spine degenerates was first described by Kirkaldy-Willis and colleagues in 1978. Specifically, they proposed that there existed a direct interplay between the intervertebral disc and the facet joints. They discovered a predicable series of damage and changes that would occur to both the intervertebral disc and facet joints that has since been termed the degenerative cascade . In their original model, they argued that the cumulative effect of microtraumas to the three main mobile elements of the spine (the intervertebral disc and two facets) would cause degenerative changes such as synovial reactions and osteophyte formation in the facet joints and tears and resorption of the intervertebral disc, which would ultimately result in spinal instability, lateral nerve entrapment, and central stenosis ( Fig. 175-3 ).
Since first being described by Kirkaldy-Willis and colleagues, many more details of the spinal degenerative cascade have been elucidated. Whereas the original cascade predicted a series of mechanical deteriorations, it is now argued that spinal degeneration is an inevitable course that is influenced additionally by both environmental and genetic factors. In fact, a genetic basis to spinal degeneration started to be established as early as the mid-1990s. These studies used magnetic resonance imaging (MRI) data to help demonstrate that degenerative disc patterns are more likely among twins, with one study finding overall heritability as high as 74% and 73% for lumbar and cervical disc degeneration, respectively, between dizygotic and monozygotic twins. Many further studies have been performed to help establish specific genes associated with a predisposition for disc degeneration. Literature reviews by Battié and colleagues in 2004 and Chan and colleagues in 2006 have helped catalog many of these known genes and found that mutations in vitamin D receptor genes, collagen IX genes (COL9A2/COL9A3), the proteoglycan “aggrecan” gene, collagen I gene (COL1A1), matrix metalloproteinase 3 gene, and cartilage intermediate layer protein can all contribute to spinal disc degeneration. Similar to disc degeneration, osteoarthritis has also been found to have an inheritable component. In his paper discussing the genetics of primary osteoarthritis, Loughlin detailed some of the various studies that have been performed using microsatellite markers to help establish genetic linkages seen in families with higher rates of osteoarthritis. Based on his review, chromosomes 2q, 4q, 6, 7p, 11q, 16, and Xcen may all be associated with linkages that lead to increased osteoarthritis susceptibility, with chromosomes 2, 4, and 16 being the most likely.
Regardless of the cause (genetic, mechanical, or a combination therein), disc degeneration sees the normal disc architecture altered through changes in its biologic structure. These biologic changes in the discs have been shown to be the result of altered gene expression caused by mechanical loading changes imposed on the discs. Specifically, mechanical damage and compression to the discs have been shown to result in a down-regulation of anabolic factors and a subsequent up-regulation of catabolism. Studies have used mRNA analysis and cellular staining to find that asymmetric loading and even variations in magnitude and frequency of compression on intervertebral discs lead to increased apoptosis, cell death, and inflammation (caspase-3 staining, mRNA up-regulation of MMP-1, ADAMTS4, IL-1β, IL-6). These changes result in disc disease via tears in the annulus fibrosus and dehydration of the nucleus pulposus, which ultimately diminishes the functional capacity of the discs. Intervertebral disc deterioration results in more spinal load transmitting to the posterior elements, thus continuing the degeneration cascade. Disc degeneration leads to spinal instability, which leads to an increase in abnormal range of motion within the spine. These changes in motion ultimately generate different patterns of forces that accelerate facet degeneration and osteoarthritis.
Although specific aspects and segments of the spinal column degenerate over time, the bone that comprises the spine itself also undergoes significant alterations as people age. As will be discussed later, osteoporosis and compression fractures are major concerns among geriatric patients. The architecture of vertebral bone changes drastically with increasing age. Specifically, it has been argued that vertebral bodies are capable of maintaining their strength and structure through 50 years of age. However, after this time, there is a significant decrease in both the volume of trabecular bone and number of trabeculae within the bone. These changes lead to decreased structural integrity of the vertebra and permit the development of malformations and fractures within the spine.
Following the changes in bone density and spinal degeneration cascade, multiple disease states can result—many of which will be described following this section. As alluded to previously, these processes may result in malformations of the spine. Changes in the overall shape of the spine can be analyzed by determining a change in sagittal balance. As described in their 1995 paper, Gelb and coworkers suggested that major variations in sagittal alignment should not be considered as unavoidable outcomes of aging. If a change in sagittal balance does occur, it is likely secondary to degenerative diseases that have already occurred in that individual. Of the abnormalities in sagittal alignment that can occur, loss of lumbar lordosis demonstrates the strongest correlation with age. Additionally, further studies have also found that the anterior translation of the C7 plumb line is associated with the spinal degeneration seen in aging.
Cervical Degenerative Disease
Treatment for elderly patients with cervical degenerative disease and spinal stenosis differs from those for younger patients with similar conditions. Concerns over bone quality and physiologic ability to withstand large reconstructive surgery again play a significant role in decision making.
Ventral decompressive surgery by multilevel corpectomy may prove difficult in this patient population. Although ventral decompression may be appropriate on a neurologic basis because of kyphotic alignment of the cervical vertebrae, reduced mechanical strength of vertebral bodies increases the risk for graft subsidence or dislodgment if an isolated ventral procedure is performed. In addition, the substantial surgery required to accomplish combined ventral-dorsal cervical reconstruction may not be well tolerated by elderly patients.
Patients with central stenosis and neutral or lordotic alignment without evidence for motion on flexion/extension radiographs may be treated via an isolated dorsal procedure, such as laminoplasty. If ventral decompression is required, standard discectomy/corpectomy procedures with ventral plating may be performed for short segments ( Fig. 175-4 ). Inclusion of dorsal instrumentation should be considered for patients requiring decompression over more than three disc spaces and for those with significant kyphosis. These treatment approaches generally provide satisfactory clinical outcomes while reducing significant complications.
Degenerative Lumbar Spondylolisthesis
Kirkaldy-Willis and colleagues proposed that biochemical and biomechanical changes associated with age cause increased mobility at a spinal segment, leading to osteophyte formation and joint hypertrophy that reduce spinal canal diameter and local stiffness. The increased joint laxity resulting from facet degeneration leads in some cases to spondylolisthesis between adjacent vertebrae.
Degenerative lumbar spondylolisthesis occurs almost exclusively in patients older than 40 years of age, and studies suggest that it occurs 4 to 6 times more frequently in men than in women. There is also a regional predilection for the L4/L5 level, which is the involved segment 6 to 10 times more frequently than the level above or the level below.
Two prospective randomized control trials support treatment of patients with degenerative lumbar spondylolisthesis with laminectomy and dorsal fusion. Several studies have demonstrated increased fusion rates with pedicle screw instrumentation, and further studies have shown better clinical outcomes in patients who achieve solid arthrodesis. In the short term, patients with noninstrumented fusions have equivalent results with fewer complications as compared to posterior spinal fusion patients. However, fusions rates for noninstrumented fusion techniques have been found to be as low as 45% to 48% in some patient groups.
Despite those results, use of instrumentation has not been convincingly shown to improve clinical outcomes after fusion for patients with degenerative spondylolisthesis. Avoiding instrumentation when performing fusion in elderly, osteoporotic patients with degenerative spondylolisthesis may thus be a reasonable option, particularly when facets are oriented relatively in the coronal plane and segmental instability is not present.
Degenerative Scoliosis
Degenerative scoliosis, unlike idiopathic scoliosis, is an acquired disorder of adult patients (i.e., de novo scoliosis). Patients often present with symptoms similar to those of degenerative lumbar stenosis, although for some patients the deformity itself becomes an issue. Nonoperative treatment modalities include physical therapy, muscle relaxants, and inflammatory drugs (NSAIDs). Surgical options include neurologic decompression through laminotomy or laminectomy. Spinal fusion may or may not be appropriate, depending on the patient’s presentation, health status, and expectations from surgery. There are conflicting reports regarding the need for spinal stabilization after decompression for degenerative scoliosis. Patients without lateral listhesis between adjacent vertebrae may be appropriately treated with laminectomy without fusion.
Patients of advanced age with significant scoliotic curves may not be appropriate candidates for the large reconstructive fusion procedures required to treat their spinal deformity. Judiciously selected nerve root blocks with isolated unilateral foraminotomies may be used to good effect in such patients with limited risk of deformity progression ( Fig. 175-5 ). Elderly patients for whom stabilization is required will benefit from efforts to limit the extent of surgery, including the use of posterior or transforaminal lumbar interbody fusions in favor of ventral approaches ( Fig. 175-6 ).
Osteoporosis
Osteoporosis is a state of decreased bone mineral density and is a major risk factor for fractures in the elderly. Ten million Americans have osteoporosis, and an additional 18 million have osteopenia. Bone mass reaches its maximum in the third decade of life and then begins to decrease. At its peak, the maximum surface area of bone crystals in an adult is estimated to be 100 acres. Women experience a phase of rapid bone loss at menopause, whereas bone loss in men occurs 5 to 10 years later. Bone mineralization is measured using a dual energy x-ray absorptiometry and is considered the gold standard for diagnosis of osteoporosis. Dual-energy x-ray absorptiometry yields precise measurements at clinically important sites with minimal radiation exposure. Bone mineral density less than or equal to 2.5 standard deviations below that of a young healthy adult of the same race and sex is diagnostic for osteoporosis, whereas osteopenia is defined as a bone mineral density 1 to 2.5 standard deviations below normal.
Once the diagnosis of osteoporosis has been confirmed, secondary causes should be addressed prior to initiating osteoporosis-specific therapies. Secondary causes for osteoporosis account for 10% to 30% of cases in postmenopausal women and greater than 60% in men. Secondary causes for osteoporosis includes malnutrition, endocrine, malignancies, medications, and chronic illnesses ( Box 175-1 ). If no secondary causes are found and the patient continues to demonstrate low bone mineral density, a diagnosis of primary osteoporosis is made.