21.1 Clinical Presentation

VCF can be defined as the reduction in the height of the individual vertebral body by 20% over 10 to 20% of the vertebral body or a loss of vertebral height of at least 4 mm. ¹ There are numerous pathophysiologic processes that contribute to VCFs including osteoporosis, neoplasms (e.g., myeloma, metastasis, lymphoma, and hemangioma), osteonecrosis, and trauma. ¹ The burden of illness for VCFs results in a total annual hospitalization cost that is higher than the costs for myocardial infarction, cardiovascular arrest, and breast cancer. ² VCFs result in both direct and indirect effects on the patients’ quality of life and costs to the health care systems. ¹ The typical clinical appearance in a patient with an acute VCF is severe back pain lasting for weeks to months or more. Additionally, apart from intractable pain, vertebral fractures negatively affect health status in a variety of ways including but not limited to progressive deformity, impaired mobility, reduced pulmonary function, sleep difficulty, eating disorders, weight loss, clinical depression, anxiety, and an overall decrease in the patient’s quality of life. Additional symptoms may include sciatica or radiculopathy, numbness, tingling, muscle spasm, weakness, and bowel or bladder changes. Neglected fractures can evolve to vertebra plana, retropulsion, and may even cause paralysis due to compression of the spinal cord or cauda equina. ³

When compared to age-matched controls, patients with VCFs have a 40% lower survival rate, which is typically attributed to all the aforementioned clinical symptoms and biomechanical changes. ⁴ In these patients the resultant decreased mobility and bed rest are important predictors of adverse outcomes leading to complications such as functional decline and potentially deadly adverse events such as pneumonia or pulmonary embolism. ⁵

Patients with VCFs suffering from severe pain will usually have mobility impairment which leads to increased morbidity and mortality rates. ^{4 , 5} Pain in these patients results both from the fracture itself as well as the vertebral body’s instability with micro- or macro-movements (▶Video 21.1). The pain, in combination with the altered spinal biomechanics, the increased kyphotic angle, and the global spinal sagittal imbalance, creates a compensatory stance which in turn causes paraspinal muscular contraction that often results in chronic back pain. This imbalance plays an important role in increasing body sway, gait unsteadiness, and risk of falls in fragile patients who have already had an osteoporotic fracture. ⁶ Prior to vertebral augmentation and restabilization of the fracture (▶Video 21.2), the incident fracture disrupts the ability of the adjacent intervertebral disk to pressurize, and the resulting force transmitted to the adjacent vertebral body cortex is doubled, which produces an increased risk of future VCFs. ⁵ The change in the kyphotic angle also causes significant mechanical effects that result in decreased thoracic and abdominal space with subsequently decreased pulmonary function, decreased appetite, and a negative nutritional impact on an already frail patient. ^{7 , 8}

During clinical examination, the entire spinal length should be examined for physical signs and symptoms that are reliable for diagnosing the presence of a vertebral fracture. On using a firm, closed-fist percussion, the patient will complain of a sharp, sudden, fracture pain. ⁹ This is typically an effective physical exam maneuver in patients with VCFs as it has been shown to have a sensitivity and specificity for detecting symptomatic VCFs of 87.5 and 90%, respectively. Patients with vertebral fractures also complain of pain during rotation and positional changes (turning while lying or standing) and Postacchini et al found that pain-related behaviors such as grimacing, sighing, and requesting help with position changes were correlated with the presence of a VCF as confirmed by MR imaging and were not present in the control patients without fractures. ¹⁹ A useful physical examination sign is the presence of back pain when lying supine. ⁹ The patient is asked to lie supine on the examination couch with only one pillow. The clinical sign is positive when a patient is unable to lie supine due to severe pain in their spine. ⁹ Despite the presence of some reliable signs of a painful VCF, clinical examination cannot stand alone for the diagnosis of a vertebral fracture as preoperative imaging will provide valuable information to confirm the diagnosis as well as to assess the fracture anatomy including the posterior vertebral body wall integrity and can exclude other causes of back pain that can mimic a VCF. ¹ Radiographs of the spine in anteroposterior and lateral projections still remain the simplest and most direct approach and can provide basic information. The absence of a fracture on a radiograph, however, does not exclude the presence of a fracture, especially in the osteoporotic patient population. MR imaging with Short TI Inversion Recovery (STIR) and T1-weighted sequences are the most sensitive for fracture detection and should always be used in case of clinical suspicion. It can be useful to assess the fracture’s age and healing status (acute vs. chronic, incompletely healed vs. consolidated). ¹ Tanigawa et al reported that the improvement postvertebral augmentation is closely related to the bone edema pattern illustrated in the pretherapeutic MR imaging. ¹⁰ The authors showed that patients with an extensive bone marrow edema pattern involving more than 50% of the vertebral body reported significantly greater clinical improvement than either patients with fractures that had no bone marrow edema. ¹⁰

Apart from the clinical signs and symptoms directly caused by a VCF, there is a long list of indirect effects. Immobility of patients with VCFs results in loss of bone density and muscle strength as well as muscular contractures and pressure sores. ¹¹ In the acute phase the bone mineral density loss can be as high as 2% per week, which not only predisposes the patient to additional VCFs but the loss can only be reversed by either high impact exercise or anabolic bone agents. ¹¹ The muscle strength loss is also rapid, declining approximately 10 to 15% per week and roughly half of the patient’s strength is lost within four to five weeks after the fracture. ¹¹ VCFs are also associated with decreased cardiac performance (including increased heart rate, shorter diastolic times, reduced coronary blood flow, decreased stroke volume, and left ventricular function with lower cardiac output), deep venous thrombosis, and pulmonary compromise (with average of 9% decrease in forced vital capacity, 25–50% decrease in respiratory capacity, deconditioning of respiratory muscles, and increased risk of pneumonia). ¹¹ Indirect effects of VCFs are also reported in the gastrointestinal system (loss of appetite, constipation, fecal impaction, and glucose intolerance), in the urinary tract (infection, sepsis, and calculus formation), and in the central nervous system (imbalance, increase sensitivity, and intolerance to pain, anxiety, depression, and insomnia). ^{11 , 12}