Chapter 66 Osteoporosis, Vertebroplasty, and Kyphoplasty Flashcards
KEY POINTS 1. Osteoporosis and VCFs are a significant public health concern with high morbidity. 2. Vertebral augmentation is a safe and efficacious procedure for treatment of painful VCFs that fail conservative therapy. 3. Proper technique and vigilance can help avoid serious complications and the procedure should only be performed by those trained and experienced with the procedure. 4. Both kyphoplasty and vertebroplasty are efficacious for pain relief, but recent double-blind, placebo-
Vertebral compression fractures (VCFs) are caused by
the inability of the vertebra to sustain internal stresses applied from normal daily load or trauma. The inability of the vertebra to maintain
its structure is related to the constant change in its composition.
The primary structure of bone is distinguished
by
cortical, or compact bone, and trabecular bone,
otherwise known as cancellous and spongy bone.
Cortical bone is generally on
the surface and is characterized by its
dense composition without cavities
trabecular bone has many
interconnecting cavities consisting of red
blood cells and yellow bone marrow composed of fat cells
Trabecular bone
found in large supply in vertebral bodies, is largely responsible for the majority of the axial forces and
inherited extra-axial stress and strains. The extent of the two types of bone varies depending on its location.
Bone is also composed of
osteoprogenitor cells, osteoblasts, osteoclasts,
osteocytes, neurovascular progenitor cells of external origin, and an array of inorganic and organic constituents.
In multiple myeloma, there is an imbalance of
osteoclasts and osteoblasts (increased osteoclastic
activity) that can cause lytic lesions in the absence of
osteoporosis
The majority of vertebral compression fractures are
caused by
osteoporosis, but other causes include multiple
myeloma, metastatic tumor, and hemangiomas
Decrease in
height and vertebral deformities are indications of
vertebral fractures. Most VCFs are asymptomatic, and there is no associated origin of injury
Management of vertebral deformities
Most fractures will heal
within a few months, but some have pain and disability that fail to respond to conservative therapy. Conservative therapy includes the use of back bracing, bed rest, and
pain control with medications such as nonsteroidal antiinflammatory drugs (NSAIDs), calcitonin, and narcotics.
adverse consequences of conservative therapy
deep venous
thrombosis, pulmonary embolism, pneumonia, and accelerated
bone loss can occur with prolonged bed rest.
consequences of vertebral compression fractures
are
height loss and kyphosis.
Initial treatments for painful compression fractures that
failed conservative therapies
usually revolved around
surgery
technique for the treatment of osteoporotic compression fractures
Percutaneous vertebroplasty. injecting polymethylmethacrylate (PMMA) into the painful vertebral body provided significant pain relief
Kyphoplasty to address
the additional consequences with vertebral compression
fractures that came along with pain (height loss and kyphosis).
the addition of inserting and inflating a balloon in the vertebral body prior to cement to restore height and decrease kyphosis
Osteoporosis
marked by a reduction in bone mass per unit volume with normal bone chemical composition, decreased skeletal function, progressive spinal deformity, and vulnerability to fractures.
Osteoporosis aka
lso dubbed “porous bone
disease” or “brittle bone disease,” osteoporosis is a universal disease
Bone
a connective tissue that is responsible for hematopoiesis, mechanical and structural support, and mineral storage of inorganic salts and organic material. Bone is constantly broken down and architecturally rebuilt to provide optimal mechanical support for its various functions.
If bone turnover, the breakdown and formation of new bone, is unbalanced,
then progression of bone loss develops.
hallmarks of osteoporosis
an increase in bone
resorption and a decrease in new bone formation.
Characteristics of osteoporosis
l It affects more women than men, as women possess 10% to 25% less total bone mass at maturity.
l Caucasian and Asian women are at highest risk of developing an osteoporotic fracture due to low bone mineral density.
l In the US, 35% of women over age 65 years and 15% of Caucasian postmenopausal women are osteoporotic.
l In the U.S, this debilitating disease causes fractures in 1 million individuals per year with $14 billion spent for treatment.
l Hip and vertebral fractures occur in women at a rate of 250,000 and 500,000 cases annually, respectively,
and an additional 250,000 fractures are experienced
by men every year.16,17
l Vertebral fractures in women increase as menopause approaches and old age, with a ratio of 2:1 compared to men.
Iatrogenic osteoporosis is
caused by
prolonged corticosteroid administration, furosemide,
thyroid supplements that suppress TSH production,
anticonvulstants, heparin, lithium (by causing hyperparathyroidism),
and cytotoxic agents.
Type I of Osteoporosis
Postmenopausal Primarily trabecular bone 6:1 female to male ages 51–65 No calcium deficiency Estrogen deficiency Vertebral and Colles’ fractures prevalent Risk factors: low calcium intake, low weight-bearing regimen, cigarette smoking, and excessive alcohol consumption
Type II of Osteoporosis
Senile
Primarily cortical bone
2:1 females to males of age> 75 years
Calcium deficiency, decreased vitamin D, and increased PTH activity
No estrogen deficiency
Pelvic, hip, proximal tibia, and proximal humerus prevalent
Related to low calcium intake
Secondary Causes of Osteoporosis
Paget’s disease Malabsorption syndrome Hyperparathyroidism Multiple myeloma Hyperthyroidism Prolonged drug therapy Osteomalacia hypogonadism
DIAGNOSIS AND INITIAL EVALUATION
l Medical evaluation requires thorough investigation of family and medical history as well as physical and gynecologic
assessment.
l A complete blood cell count, serum chemistry group, and a urinalysis including a pH count should be carried out.
l Consider thyrotropin, a 24-hour urinary calcium excretion, erythrocyte sedimentation rate, parathyroid hormone and 25-hydroxyvitamin D concentrations,
dexamethasone suppression, acid–base studies, serum or urine protein electrophoresis, bone biopsy and/or
bone marrow examination, and an undecalcified iliac
bone biopsy if suspected as the underlying cause.
l Dual-energy x-ray absorptiometry (DXA) to evaluate bone mineral density. Plain radiographs are an option, but changes are usually seen after 30% loss of bone mass.
following categories receive routing screening by DXA
l All women 65 years and older
l Any adult with a history of fracture not caused by severe
trauma
l Younger postmenopausal women with clinical risk
factors for fracture
diagnostic criteria to designate the presence of
osteoporosis based on DXA measurements
Normal individuals possess a bone mineral density of one standard deviation (SD) of the mean of young adults. If bone mineral density is measured
2.5 or more SDs below the mean of a young adult population, then osteoporosis is present.
Osteopenia
indicated if the SD of bone mineral density is between 1.0 and 2.5 below the mean of a young adult population.
severe osteoporosis is denoted when
one or more accompanying
fragility fractures is present.
Bone Mass Density in women
Women lose 3% to 7% of BMD around the onset of menopause followed by a 1% to 2% decline yearly in the postmenopausal period
appropriate regimen of preventive
and therapeutic measures to combat osteoporosis
l Calcium and vitamin D l Bisphosphonates l Calcitonin l Selective estrogen receptor modulators l Parathyroid hormone l Sodium fluoride l Exercise l Modifiable risk factors such as cigarette smoking, excessive alcohol consumption, and treatment of potential secondary causes
Osteoporotic fractures are more prone to occur at the
hip, ribs, wrists, and vertebrae.
contribute to the complications of an
osteoporotic hip fracture.
pneumonia, blood clots in the lungs, and heart failure
Vertebral compression fractures (VCFs) can decrease height by up to
15 cm and result in the
kyphotic deformity called “dowager’s hump.”
Vertebral compression fractures occur due to the
inability of the osteoporotic vertebra to sustain internal stresses applied by the vertebral load from daily life or from minor or major traumatic events.
Trabecular bone
largely responsible
for the majority of the axial forces and inherited
extra-axial stress and strains. With the cascade of osteoporotic effects and aging, the architecture of trabecular bone becomes altered, characterized with increased spaces, thinness,
disorientation, and weakened connectivity
compromise the vertebra’s mechanical prowess, integrity, and spinal column stability, predisposing
it to trabecular buckling
a decrease in density and loss of structural strength
Multiple VCFs develop a
hyperkyphotic or “dowager’s hump” at the thoracic level with a stooped posture decreasing
abdominal and thoracic cavities. Multiple lumbar VCFs further increase lordosis, creating a protruding abdomen.
A decrease in axial height is a result of reduction of
intervertebral and vertebral loss of height. Also, developed stooped
posture progresses to the point where ribs rest on the iliac crest with circumferential pachydermal skin folds developing at the pelvis and ribs.
The cauda equina or spinal cord related symptoms
are uncommon and are secondary to other conditions, such as
Paget’s disease, lymphoma, primary or metastatic
bone tumors, myeloma, and infection
