As the population ages, vertebral compression fractures become much more common. Although some compression fractures may be relatively asymptomatic, others can lead to chronic pain and spinal deformity. Conservative treatment is often poorly tolerated by this elderly patient population, and large, open procedures carry an often unacceptably high morbidity rate in this group. For this reason, percutaneous procedures such as vertebroplasty and kyphoplasty have been developed. This chapter discusses the indications, classification, surgical technique, and outcomes of kyphoplasty for the treatment of vertebral compression fractures.
Restoration of vertebral height
Reduction of kyphotic deformity
Persistent pain despite conservative treatment
High risk for further collapse (steroid-induced osteoporosis, extremely low bone density, fractures at the thoracolumbar junction)
Significant cardiopulmonary compromise
Prolonged bleeding times
Other co-morbid conditions that preclude surgical intervention
Postural reduction of the fracture can be partially obtained by careful positioning of the bolsters.
A percutaneous transpedicular approach is classically used in the lumbar spine.
An extrapedicular approach is commonly used in the thoracic spine because of smaller pedicle diameter and less medially angled pedicle vector.
A preoperative workup should always be done to ensure that the compression fracture is the source of the patient’s pain.
Biplanar fluoroscopy is necessary to ensure that the trajectory of the trochar is intrapedicular without any cortical violation.
Cement is placed into the space created by the tamp under low pressure and vigilant fluoroscopic monitoring to assess for leakage.
As the median age of the population continues to increase, osteoporotic vertebral compression fractures continue to be a leading cause of disability and morbidity in the elderly. The National Osteoporosis Foundation has estimated that more than 100 million people worldwide and 44 million people in the United States are at risk for development of osteoporotic fragility fractures. Vertebral compression fractures occur in 20% of people older than 70 years and 16% of postmenopausal women. An estimated 700,000 vertebral compression fractures occur annually in the United States. Of these, an estimated one third becomes chronically painful. In addition to the disability and morbidity that occurs secondary to these fractures, a substantial financial cost is associated. Vertebral compression fractures contribute significantly to the $17 billion of annual direct cost associated with the osteoporotic fractures in the United States.
Vertebral compression fractures can be osteoporotic or pathologic. Bone is in a continuous state of osteoblastic formation and osteoclastic resorption, and the balance of these processes maintains bone density and architecture. Peak bone density is achieved in the third decade of life and steadily decreases thereafter. This decrease in bone density is accelerated in women at menopause. This bone loss results in osteoporosis and places the patient at risk for development of fragility fractures. Alternatively, patients with metastatic disease to the spine can experience compression fractures of the spine. In these patients, the vertebral body is weakened directly by the focal metastasis.
Consequences from a vertebral compression fracture include pain, progressive collapse, kyphosis, and systemic manifestations. Physiologically, a decrease of forced vital lung capacity is associated with thoracic and lumbar compression fractures. Leech et al. report a 9% decrease in vital capacity per thoracic compression fracture. Neural compromise, although less common with lower energy osteoporotic fractures, can occur as well. One series reported neurologic involvement requiring surgical decompression in 10 of 497 patients with osteoporotic compression fractures.
The pain associated with vertebral compression fractures can be incapacitating. Often, the pain will subside over a period of weeks to months; however, it is not uncommon for the pain to persist. This chronic pain from vertebral compression fractures may be secondary to other causes: (1) incomplete healing with progressive collapse, (2) altered spine kinematics and muscle pain caused by deformity, (3) a pseudarthrosis at the affected level, (4) impingement of the rib cage on the pelvis after severe collapse, or (5) neural irritation. Chronic pain from vertebral compression fracture is associated with a lower quality of life and depression.
Resultant kyphosis from compression fractures may predispose to the development of additional fractures. With an anterior shift of the patient’s center of gravity, higher flexion bending moments are created at the kyphosis, increasing angulation and promoting additional fractures. Clinical studies have demonstrated that the risk for additional fracture after the index fracture increases to 5 to 25 times baseline, with the adjacent level being particularly at risk. Prevention of kyphotic deformity, therefore, may be important in preventing additional fractures and other consequences of the deformity. Kyphosis can also result in decreased abdominal space, poor appetite, and subsequent nutritional problems. The deformity may also result in balance problems, increasing the risk for falls. Patients may also become less active for fear of falling and fracturing another level. This inactivity can result in muscle deconditioning and further osteoporosis.
Osteoporotic vertebral fractures are also associated with an increased mortality rate. Cooper and colleagues report the 5-year survival rate for patients with compression fractures was 61%, which is lower than that seen in age-matched peers. Kado et al. performed a prospective study of 9575 women over more than 8 years and found a 23% to 34% increase in mortality in those with compression fractures. The most common cause of death in that study was pulmonary disease.
Before the advent of minimally invasive treatments for compression fractures, nonoperative management was traditionally used for the majority of vertebral compression fractures. Exceptions include cases of neurologic involvement or spinal instability. Nonoperative modalities include bed rest, analgesic medications, bracing, antiosteoporotic medications, or a combination thereof. Although these treatments can be successful, the typical elderly patient with a compression fracture may not be able to tolerate analgesic medications. Anti-inflammatory medications may result in gastrointestinal side effects, whereas narcotics may result in confusion and a greater risk for falls. Prolonged bed rest can accelerate deconditioning and bone density loss. Bracing is poorly tolerated by the elderly as well. In addition, none of the aforementioned treatments address the resultant deformity.
Open surgical intervention may not be ideal in the elderly patient with multiple co-morbidities. Instrumentation procedures can be complicated by prolonged operative time, blood transfusion, and other complications. In addition to the patients’ advanced age and associated medical conditions, the poor bone density may not allow for secure fixation of instrumentation, further complicating the surgery.
Recently, minimally invasive treatments of vertebral compression fractures have been developed to treat compression fractures. Vertebroplasty is a percutaneous injection of polymethylmethacrylate cement into the vertebral body. The goals of vertebroplasty are pain relief and prevention of further collapse. Kyphoplasty also uses a percutaneous approach to the vertebral body. However, for kyphoplasty, a bone tamp is inflated within the fractured vertebral body. Inflation of the bone tamp elevates the vertebral end plates and attempts to restore the vertebral body closer to its original prefracture height. The inflation of the balloon also creates a void, which is then filled with a more viscous state of polymethylmethacrylate. The goals of kyphoplasty include pain relief, restoration of vertebral height, and reduction of kyphotic deformity.
INDICATIONS AND CONTRAINDICATIONS
The ideal timing of kyphoplasty in the treatment of vertebral compression fractures has not been well defined. In general, the senior author treats acute fractures with minimal collapse without surgery initially. If clinical and radiographic monitoring demonstrates progressive collapse or persistent pain, the senior author recommends kyphoplasty. In cases of steroid-induced osteoporosis, extremely low bone density, or fractures at the thoracolumbar junction, the senior author considers early kyphoplasty, because these fractures are predisposed to further collapse. In the presence of advanced kyphosis and an acute vertebral compression fracture, the senior author will consider immediate kyphoplasty to improve sagittal alignment.
Contraindications to kyphoplasty include sepsis, significant cardiopulmonary compromise, prolonged bleeding times, or other medical conditions that may preclude surgical intervention. The senior author does not advocate routinely treating more than three levels in one anesthesia session because of the potential cardiovascular reaction to polymethylmethacrylate and fat/cement embolization to the lungs. Relative contraindications include fracture patterns with deficient posterior vertebral wall. Burst fractures or plana patterns can pose technical challenges and should be assessed with caution.
Three fracture patterns have been described in the osteoporotic spine: wedge, biconcave, and crush. A wedge pattern has a nearly intact posterior vertebral body component with loss of height anteriorly. The biconcave pattern occurs when the center of the superior and inferior vertebral end plate are collapsed with relative preservation of the anterior and posterior vertebral walls. A crush pattern occurs when the entire body is collapsed anteriorly, centrally, and posteriorly ( Fig. 41-1 ).
The prevalence of all of these fractures increases with age, and back pain is equally likely with all three patterns. Wedge fractures appear to be the most common (51%), followed by biconcave fractures (17%), crush fractures (13%), and various combinations of the three.
Before the procedure, an extensive workup must be performed to confirm that the vertebral compression fracture is the source of pain. A thorough history and physical examination should be performed and correlated with radiographic findings. Neurologic status must be established. It is possible that the patient may have concurrent neurogenic claudication and vertebral compression fracture. The examiner should also consider the possibility of secondary osteoporosis or a malignant process as a possible cause of symptoms.
Radiographs can be used to determine the relative vector of approach for vertebral augmentation. Magnetic resonant imaging (MRI) can be used to establish acuity of the fracture, based on the presence of osseous edema. MRI can be useful in determining the presence of other potential causes such as infection or tumor.
The patient is positioned prone on a spinal frame with cushioned bolsters. Postural reduction of the fracture can be partially obtained by careful positioning of the bolsters, thus improving the chances for kyphosis correction. Local anesthesia with sedation or general anesthesia may be used. Biplanar fluoroscopy is essential for the procedure. Although kyphoplasty can be performed adequately with orthogonal views from a single C-arm machine, we recommend using two C-arm machines simultaneously.
In general, a percutaneous transpedicular approach is used in the lumbar spine ( Fig. 41-2 ). Fluoroscopy is used to localize the affected level. Two longitudinal stab incisions are made just lateral to the pedicles of the fractured level. The trochar is then advanced through soft tissue to the bony posterior spine. Before insertion into the pedicle, the tip of the trochar should appear on the lateral aspect of the pedicle as seen on the anteroposterior (AP) view. The starting point and vector should be confirmed on the lateral view. The trochar is then advanced through the pedicle. When the tip of the trochar is in the center of the pedicle on the AP view, it should also be at the midpoint of the pedicle in the lateral view. As the tip of the trochar is advanced just anterior to the posterior vertebral wall as seen on the lateral view, it should still be lateral to the medial wall of the pedicle as seen on the AP view. This ensures that the trajectory of the trochar is intrapedicular without any cortical violation. The trochar is then removed from the working cannula.