28 Osteoporotic Compression Fractures Abstract Vertebral compression fractures are pathognomonic of osteoporosis with significant impact on both the individual heath and health care costs. Pain control, correction of kyphosis, prevention of existing fracture worsening, and development of new fractures are the primary goals of treatment. Conventionally, medical management was considered as a first line of treatment. However, with increasing awareness of vertebral augmentation procedures such as vertebroplasty and kyphoplasty, there is paradigm shift toward early surgical intervention with these safe and minimally invasive procedures. In this chapter, we describe the burden of this problem on current health system, risk factors, medical management, and surgical interventions. We discussed the results of vertebroplasty and kyphoplasty trials, potential complications, and concluded with possible future directions. Detailed discussion of osteoporosis and nonosteoporotic vertebral compression fractures (traumatic, myeloma, and metastatic) are beyond the scope of this chapter. Keywords: vertebral compression fractures, osteoporosis, kyphosis, vertebroplasty, kyphoplasty, polymethylmethacrylate Clinical Pearls • Epidemiology and scope of the osteoporotic vertebral fractures. • Types of osteoporosis and associated risk factors. • Medical management of the osteoporotic fractures. • Vertebral augmentation for osteoporotic fractures. • Literature review on vertebral augmentation. Osteoporosis is the leading cause of spine fractures, especially in women over 50 years of age.1 As defined by the World Health Organization (WHO), osteoporosis is a generalized skeletal disorder of low bone mass and deterioration in its architecture, causing susceptibility to fracture. Approximately 8 million women and 2 million men suffer from osteoporosis while another 34 million with low bone mass are at increased risk for osteoporosis in the United States.2 Approximately 1.5 million people suffer from an osteoporotic fracture each year and around 700,000 of them are vertebral compression fractures.1 Vertebral compression fractures affect approximately 25% of all postmenopausal women and nearly 5% of men aged 50 years and above in the United States.1,3 Vertebral fractures are directly correlated with increasing age and incidence of osteoporosis. The rate of vertebral fractures increases from an annual incidence of 0.9% and prevalence of 5 to 10% among middle-aged women in their 50 s to 60 s, to an incidence of 1.7% and prevalence of greater than 30% among those 80 years and older.1,3,4 They most commonly occur among Caucasian women and are less common among men and women of African American or Asian ethnicity.5,6 The actual incidence of vertebral fractures is likely much greater given the large number of vertebral fractures that go undetected, with only a third of vertebral fractures clinically diagnosed.7 The geriatric (> 65 years) American population in 2014 was estimated as 46 million and was projected to increase over 98 million by 2060, constituting 24% of total population.8 Geriatric population being the fastest growing segment of the U.S. population, the incidence and prevalence of this age-specific vertebral compression fractures are likely to increase. Vertebral compression fractures have a substantial negative impact on the patient’s function and quality of life. Approximately 30 to 40% of vertebral compression fracture patients develop disabling pain and/or deformity (kyphosis), resulting in 150,000 hospitalizations annually. In the first year after a painful vertebral fracture, patients require primary care services 14 times greater than the general population.9 In addition to physical limitations, vertebral compression fractures may produce a psychosocial and emotional burden on the aging person who already faces losses of independent function. The annual U.S. medical cost for vertebral fracture management was estimated at $13.8 billion in 2001 and has likely increased since with the growing elderly population. The total economic cost is also far greater than the cost for acute management given that vertebral fractures can lead to significant long-term morbidity.10,11 Bone remodeling is primarily affected by osteoclasts and the osteoblasts. Without estrogen, the osteoclasts are favored and more bone is resorbed than laid down, resulting in thinning of the bone. Therefore, when women reach menopause and their estrogen levels decrease, the rate of bone loss increases to about 2 to 3% per year. After 8 to 10 years, the rate of bone loss returns to the previous rate of 1 and 0.5% per year, respectively. This loss of bone density, particularly after women reach menopause, is one of the primary causes of osteoporosis in women. There are two types of osteoporosis. This is typically seen in postmenopausal women, between the ages of 50 and 70, hence the term “postmenopausal osteoporosis.” This is due to significant reduction of estrogen resulting in an increased bone resorption. The process usually results in a reduction of trabecular bone, primarily leads to wrist and vertebral body fractures. This typically affects the elderly population, 70 years and above and women twice as frequently as men. This is also known as “senile osteoporosis,” involves a thinning of both the trabecular and cortical bone and often leads to hip and vertebral body fractures. Osteoporosis may either be a primary problem (types I or II) or may be secondary to another problem. Approximately 20% of women and 40% of men with osteoporosis have a secondary cause of osteoporosis, such as hyperthyroidism or lymphoma. Common causes of secondary osteoporosis are summarized in Box 28.1. Box 28.1 Causes of secondary osteoporosis 1. Endocrine disorders • Hypogonadism • Cushing’s disease • Hyperthyroidism • Hyperparathyroidism • Diabetes mellitus 2. Marrow disorders • Multiple myeloma • Disseminated cancer • Chronic alcohol use • Lymphoma 3. Collagen disorders • Osteogenesis imperfecta • Marfan syndrome 4. Gastrointestinal disorders • Malabsorption • Malnutrition 5. Medications • Aluminum antacids • Anticonvulsants • Chemotherapy • Glucocorticoid therapy • Thyroid hormone replacement Vertebral compression fractures are recognized as the hallmark of osteoporosis, and many of the risk factors are the same. Risk factors are categorized as those not modifiable and those that are potentially modifiable. Non-modifiable risk factors include advanced age, female gender, Caucasian race, presence of dementia, susceptibility to falling, history of fractures in adulthood, and history of fractures in a first-degree relative. Potentially modifiable risk factors include being in an abusive situation, alcohol and/or tobacco use, presence of osteoporosis and/or estrogen deficiency, early menopause or bilateral ovariectomy, premenopausal amenorrhea for more than one year, frailty, impaired eyesight, insufficient physical activity, low body weight, and dietary calcium and/or vitamin D deficiency. Both osteoporosis and osteopenia are strongly associated with the risk of developing a vertebral fracture, with the risk increasing roughly two times for every standard deviation below average vertebral bone mineral density. Bone density begins to decrease after age 40 for both men and women, and the process is rapidly accelerated in postmenopausal women. WHO defines osteoporosis as T score < −2.5 on dual-energy X-ray absorptiometry (DEXA). Though most commonly found among osteoporotic patients (T < −2.5), vertebral fractures may also occur in up to 18% of women more than 60 years old with osteopenia but not meeting the criteria for osteoporosis (T score > −2.5 but < −1.4). It is estimated that more than a third of postmenopausal vertebral compression fractures occur in osteopenic women who do not meet the criteria for osteoporosis. The risk of developing a vertebral fracture is roughly five times greater if the patient has had a prior fracture, and 20% of osteoporotic postmenopausal women who present with an initial vertebral fracture develop a subsequent vertebral fracture within the year. These patients are also at high risk of developing other significant osteoporotic fractures, such as hip fractures. History of two vertebral compression fractures is the strongest predictor of future vertebral fractures in postmenopausal women. An Australian study over 4,000 men and women reported that after an initial osteoporosis-related fracture, the absolute risk of a subsequent fracture within 10 years of the first was similar in men and women. In addition to the genetic predisposition, a multitude of lifestyle and environmental factors increase the risk of developing osteoporosis. These include lack of exercise and low body mass index, insufficient dietary calcium, low vitamin D production, glucocorticoid medication, smoking, and excessive alcohol intake. Also, vertebral metastasis, end-stage renal disease and hyperparathyroidism are known predisposing factors for the vertebral compression fractures. With the osteoporotic compression fractures, each vertebra tends to lose at least 15–20% of its height. Thus, with successive fractures, the individual may lose a noticeable amount of height. This loss of stature changes the musculature in the back and can cause pain from muscle fatigue that can continue after the bone fracture has healed. Thoracic kyphosis (dowager’s hump, or hunched back). The fracture usually occurs in the front of the vertebra and leaves the height at the back of the vertebra unchanged, resulting in a wedge-shaped bone in the spine. With multiple vertebral fractures, as the front of the collapsed vertebrae fuse together, the spine bends forward, causing a kyphotic deformity and hunched over appearance. According to a 1998 study there is a significant decrease in the lung function in patients with thoracic vertebral fractures. Each thoracic or upper back fracture causes a 9% loss of vital capacity of the lungs because of progressive kyphosis (Journal of American Respiratory Disease). As the vertebral fractures cause the patient’s spine to shrink in height, the abdominal contents are compressed into less vertical space resulting in crowding of internal organs. As a result, the abdomen can bulge out, causing a pseudo appearance of weight gain. The shortened spinal column may also compress the stomach, causing weight loss due to early satiety, constipation, or other problems. Patients with severe thoracic kyphosis may be so far hunched forward that they should extend their necks to look forward, which can result in neck pain. Other sequelae of the vertebral compression fractures include prolonged inactivity, deep venous thrombosis, progressive muscle weakness, loss of independence, emotional and social problems. The reported mortality in patients with vertebral compression fractures is approximately 15% higher than the age-matched controls. Approximate mortality in these patients is less than mortality from hip fractures at 1 year (15%) and is equal to the mortality from hip fractures at 2 years (20%), and vertebral compression fractures have a decreased 5-year mortality compared to hip fracture patients.12 The most common cause of premature death was pulmonary disease, emphysema, and pneumonia. Only about one-third of vertebral fractures are actually diagnosed because many patients and families regard back pain symptoms as “arthritis” or a normal part of aging. Therefore, compression fracture should be suspected in any patient older than 50 years with acute onset of sudden low back pain. Most patients will remember a specific injury as the cause. In cases of severe osteoporosis, however, the cause of trauma may be simple, such as stepping out of a bathtub, vigorous sneezing, or lifting a trivial object, or the trauma may result from the load caused by muscle contraction. Up to 30% of compression fractures occur while the patient is in bed. In cases of moderate osteoporosis, more force or trauma is required to create a fracture, such as falling off a chair, tripping, or attempting to lift a heavy object. When symptomatic, patients complain of sudden onset of severe, focal, back pain that may radiate posterolaterally along the intercostal distribution. The vertebral bodies support 80% of the body’s weight, so that the pain is typically worse when sitting up, standing, or ambulating, and improved when lying down. This is described as mechanical axial back pain, and can be distinguished through history taking from other etiologies of back pain such as osteoarthritic pain, pathologic pain associated with tumor, and lumbar strain. Vertebral compression fractures usually occur in the midthoracic or thoracolumbar transition zone of the spine. Though exceedingly rare, occasionally retropulsion of fracture fragments may result in compression of the spinal cord or cauda equina and result in weakness and loss of sensation of the lower extremities or even bowel or bladder incontinence. Depending on the severity and rapidity of deficit onset, this may constitute a surgical emergency. The loss of height that results from a compression fracture may lead to kyphotic deformity of the spine, especially for multiple compression fractures with significant height loss. This may result in focal or global sagittal imbalance, which may lead to chronic back pain even after the fracture has healed and accelerate the degeneration of adjacent spinal segments. Progressive loss of stature also results in shortening of paraspinal musculature requiring prolonged active contraction for maintenance of posture, resulting in pain from muscle fatigue. This pain may continue long after the acute fracture has healed. The back pain and associated fatigue can severely limit a patient’s quality of life and ability to perform activities of daily living. In addition, severe kyphoscoliosis can even lead to a restricted abdominal space, limiting pulmonary vital capacity as well as decreasing nutritional intake, thus compounding patient immobility. Many imaging studies may be used in the workup of vertebral compression fractures. Plain frontal and lateral radiographs are the initial imaging study obtained for a suspected compression fracture. Findings on plain radiograph such as increased lucency, loss of horizontal trabeculae, and decreased cortical thickness but increased relative opacity of the endplates and vertical trabeculae are suggestive of osteopenia. Comparison to preexisting spine X-rays allows the clinician to diagnose and judge the age of the vertebral fracture. Radiographically, a decrease in vertebral height of 20% or more, or a decrease of at least 4 mm compared with baseline height is considered positive for compression fracture. Compression fractures may be classified based on the portion of the vertebral body that is affected: wedge-shaped (anterior or posterior) or biconcave. Based on severity of compression fracture (height loss) vertebral compression fractures are graded as: grades I (< 25%), II (25–50%), III (50–75%), and IV (> 75% or vertebra plana). In cases of complete compression fractures there is a reduction in both posterior and anterior height. It is important to image the entire spine because 20 to 30% of vertebral compression fractures are multiple. When multiple, the fractures occur at different levels or in one to five consecutive vertebral bodies. Serial plain radiographs can be used to identify the worsening vertebral compression fractures, especially if one proceeds with conservative, medical management. Noncontrast computed tomography (CT) scan allows for superior characterization of bony anatomy and improved assessment of loss of height, fragment retropulsion, and canal compromise ( Magnetic resonance imaging (MRI) is the best study for judging fracture age, as it will show bony edema for an acute fracture ( Spontaneous vertebral compression fractures with minimal force and no history of trauma are typically pathognomonic for osteoporosis. After the diagnosis of a compression fracture on initial imaging, bone density should be assessed by DEXA scan, the gold standard for diagnosis of osteoporosis.13 The test values are generated by passing low energy X-rays through a target bone (e.g., spine, hip, or wrist). These values when compared to the values of young adult population as baseline generate a “T score.” A score above −1 is considered normal; a score between −1 and −2.5 is considered osteopenia; and a score below −2.5 is considered osteoporosis. For each −1 change in T score standard deviation, there is a 2.5 times risk of spine fracture. “Z score” can be generated by comparing to the values of age- and gender-matched control groups as baseline. An unusually high or low Z score may indicate the need for additional tests. According to the National Osteoporosis Foundation, bone mineral density testing is recommended in the following situations: 1. All women over age 65. 2. Postmenopausal women under age 65 who have multiple risk factors. 3. At menopause, if undecided about hormone replacement therapy. 4. Abnormal spine X-rays. 5. Long-term oral steroid use. 6. Hyperparathyroidism (overactive parathyroid gland).
28.1 Introduction
28.2 Epidemiology
28.3 Impact on Health Care
28.4 Pathophysiology
28.4.1 Type I Osteoporosis
28.4.2 Type II Osteoporosis
28.5 Risk Factors
28.5.1 Decreased Bone Density
28.5.2 Prior Vertebral Osteoporotic Fracture
28.5.3 Lifestyle and Environmental Factors
28.6 Sequelae of Osteoporotic Fractures
28.6.1 Height Loss
28.6.2 Compromised Pulmonary Function
28.6.3 Bulging Abdomen
28.6.4 Gastrointestinal Complaints
28.6.5 Neck Pain
28.7 Mortality
28.8 Clinical Presentation
28.9 Diagnostic Imaging
28.9.1 Plain Radiograph
28.9.2 Computed Tomography
Fig. 28.1). Noncontrast CT spine is the best study to evaluate intactness of the posterior cortex of the vertebral body, the knowledge of which is vital to prevent retrograde cement leak in to the spinal canal. However, this comes with greater expense and irradiation for the patient. CT scan may also help to distinguish an acute fracture with free air with in the vertebral body from a chronic fracture by the presence of cortication.
28.9.3 Magnetic Resonance Imaging
Fig. 28.2). In addition, MRI allows for the evaluation of neural compromise secondary to compression of the spinal cord or nerve roots. MRI short tau inversion recovery sequence will also reveal integrity of the spinal ligamentous complex, which can be important during surgical evaluation of fracture stability. Finally, a postcontrast MRI study will detect a pathologic fracture secondary to an oncologic process. Other, less commonly used imaging studies include bone scan, which will show increased uptake in a fracture.
28.9.4 Dual-energy X-ray Absorptiometry
Thoracic Key
Fastest Thoracic Insight Engine
