Vertebral insufficiency fractures as a cause of autonomic dysreflexia in a patient with chronic tetraplegia: A case report

Abstract

Context: Osteoporosis is a known complication in spinal cord injury patients and can result in an increased risk of fractures and associated morbidity. Bone demineralization is most common in long bones below the level of injury. The pathogenesis is complex and not fully understood.

Findings: We present the case of a 65-year-old male with chronic spinal cord injury who was found to have multiple vertebral compression fractures causing autonomic dysreflexia and new onset spasticity.

Conclusion/Clinical Relevance: This case illustrates the need for improved awareness, diagnosis, and prevention for this disease process.

Introduction

There are numerous health conditions associated with spinal cord injury (SCI) and it is critical that clinicians be aware of these even in the context of atypical or absent signs and symptoms. Osteoporosis occurs to some degree in most individuals with SCI. Many factors affect the risk of osteoporosis, such as the severity of injury, level of injury, age, sex, menopausal status, and duration after injury.¹ Fractures that occur as a result of low bone mineral density can lead to loss of function, increased healthcare costs, and significant morbidity and mortality.²

The pathogenesis of bone loss in individuals with SCI is likely multifactorial but has yet to be fully understood. Bone loss is felt to be due to a dramatic reduction in the forces applied to the sublesional skeleton from upright posture and ambulation.³ Patients with SCI appear to demonstrate alterations in bone remodeling with a predominance of bone resorption versus formation, further contributing to osteoporosis.⁴ The pattern of osteoporosis and osteoporosis-related injury differs in people with SCI from that of the general population. In the SCI population, the risk of osteoporotic-related fracture begins after injury and subsequently increases over time.⁵ Osteoporosis occurs most commonly in the long bones below the level of injury with the bones above the lesion being preserved.⁵ The most common sites affected in the SCI population include the distal femur and proximal tibia.⁵ The vertebral bodies have been shown to be spared in this population.⁶ The reported incidence of lower extremity fractures in SCI patients ranges from 1% to 34%.²

In this report, we present a case of a patient with chronic SCI who presented with new onset spasticity and autonomic dysreflexia who was found to have multiple vertebral compression fractures. This case highlights the risk of fracture at sites considered atypical for this population and will highlight the need for improved surveillance and prevention.

Case description

 The patient is a 65-year-old male with a 45-year history of C6 ASIA Impairment Scale (AIS) C tetraplegia who uses a power wheelchair for mobility. Medical history includes chronic pressure injury wounds, suprapubic catheter for bladder management, and multiple urinary tract infections (UTIs). Functionally, he is independent with all activities of daily living (ADLs), and gainfully employed full time.

The patient presented to the emergency department (ED) with a chief complaint of “not feeling well,” for several days. The initial workup in the ED was remarkable for an elevated blood pressure of 210/170 and new onset of muscle spasms. A diagnosis of autonomic dysreflexia (AD) was made. The patient did not have a prior history of AD nor did he have a history of spasticity. The elevated blood pressure normalized with oral anti-hypertensive medication and he received oral baclofen and lorazepam for muscle spasms, which were the presumed cause of his AD.

After discharge, the patient followed up in the outpatient SCI clinic where he was noted to have ongoing muscle spasms and subjective complaints of back pain. The back pain was non-specific and there was no point tenderness of the spine appreciated. The underlying cause of the new-onset spasms, back pain, and AD had not been identified, and as such a thoraco-lumbar spine CT scan was done which demonstrated decreased osseous mineralization and vertebral compression fractures of the T9, T10, T12, L1, L2, L3, and L5 vertebral bodies (Figure 1). Initial orthopedic evaluation was done and conservative non-surgical management was recommended. Metabolic workup was notable for low 25-hydroxy vitamin D with normal comprehensive metabolic panel, calcium, parathyroid hormone, phosphorus and thyroid stimulating hormone. The patient was started on vitamin D and calcium supplementation. At 3 months post diagnosis, the patient continued to require oral oxycodone and nortriptyline for the fracture-associated pain, as well as continued baclofen for the spasticity. Interventional pain management has recommended vertebral augmentation for improved pain, spasticity, and AD control, which is delayed due to the presence of a stage IV pressure injury.

Figure 1.

Non-contrast CT of the spine demonstrated vertebral body fractures at T9, T10, T12, L1, L2, L3 and L5.

Discussion

This case report illustrates multiple thoracic and lumbar vertebral compression fractures in the absence of trauma in a patient with chronic motor incomplete tetraplegia. Patients with chronic SCI have an increased risk for numerous secondary conditions, including osteoporosis and osteoporosis-related fractures.⁷ With improved life expectancy, people with SCI/D may be more likely to experience sublesional pathologic fractures over the course of their lifetime, highlighting the importance of prevention and surveillance.

While it is well known that people with chronic SCI are at risk for sublesional long bone fracture, pathologic vertebral fractures have not been reported in this population. Long bone fractures, such as those occurring at the distal femur and proximal tibia, can occur after bed transfers or other minor trauma.⁵ Surgical treatment has historically been reserved for displaced vertebral fractures with the common practice being conservative management including rest and pain control.

Axial complications of chronic SCI include kyphosis, scoliosis, pseudarthrosis, instrumentation failure, and Charcot spine.⁸ This case demonstrated vertebral collapse due to multiple vertebral body fractures. The vertebral body collapse occurring in this patient differs from Charcot spine, as in the latter the individual is typically sensory (neurologically complete SCI) and symptoms include spine deformity, crepitus, and neurologic loss (in addition to pain, spasticity and autonomic dysreflexia) and hypertrophic bone formation is noted radiographically (Kirshblum). In these cases, surgical management is typically reserved for those with progressive deformity and/or neurologic findings.⁸

Goals of surgery would include pain management and restoration and/or management of spinal alignment and stability. In this case, alignment and stability have been maintained, but pain and spasticity continue. With more options for less invasive spine reconstruction surgical approaches, minimally invasive procedures such as vertebroplasty may be considered for the treatment of vertebral fractures in patients with SCI. Vertebroplasty has been shown to safely reduce pain, and reduce mortality from osteoporotic spinal fractures in the general population.^9,10 Further, reduction of pain with vertebroplasty may result in improvement of the secondary complications of spasticity and AD.

Dual-energy X-ray absorptiometry (DXA) of the lumbar spine and hip is the gold standard to evaluate bone mass and fracture risk in primary osteoporosis.¹¹ Currently, there are no authoritative guidelines for bone health surveillance among patients with SCI. In a recent guideline for primary care providers, Sadowsky et al. recommend obtaining a baseline DXA scan and routine screening every 1–2 years in patients with SCI.¹¹ Improved screening will allow for earlier detection and treatment, thus preventing the injury as well as the significant morbidity/mortality associated with these injuries.²

In addition to more aggressive surveillance, consideration of pharmacologic prophylaxis is evolving. Bisphosphonates attach to hydroxyapatite binding sites on bony surfaces, especially surfaces undergoing active resorption and inhibit the attachment of osteoclast to these sites. Bisphosphonate therapy has been shown to reduce bone loss of the femur when administered in the first year after injury, however, no significant change in bone density was seen at the distal femur or proximal tibia.^5,11 Teriparatide is a form of parathyroid hormone that promotes bone formation by increasing osteoblast activity. Teriparatide has been shown to increase bone density of the spine, hip, and knee in SCI patients.¹² Romosozumab is a humanized monoclonal antibody that binds to sclerostin, permitting the engagement of Wnt ligands with their co-receptors, resulting in an increase in bone formation and bone mineral density. In a preclinical trial, administration of Romosozumab prevented the SCI-induced reduction of BMD at the femur and tibia.¹³ This suggests a possible role for Romosozumab to prevent or reduce bone loss in SCI patients. Denosumab is a human monoclonal antibody of the IgG2 immunoglobulin isotype with a high affinity and specificity for binking RANKL to antagonize its action.¹⁴ It is an anti-resorptive agent which inhibits osteoclasts. Denosumab has been shown to increase lumbar and femoral BMD in patients with SCI suggesting it has potential utility, as an option for treatment.¹⁵ Increased awareness will promote further studies to improve the prevention and treatment of this disease process.

Conclusion

Vertebral compression fractures, as a secondary complication of chronic SCI has not been discussed in detail in the literature. Clinicians should be aware of the occurrence of this disease process in patients with chronic SCI and consider that it may become more prevalent with increasing age. This case describes pathologic fractures of the spine causing new spasticity and AD, highlighting the importance of and need for authoritative guidelines around surveillance of bone health, prevention of osteoporosis among people with SCI/D, as well as consideration for minimally invasive surgical treatment options in addition to conservative management.

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Contributors None.

Funding None.

Conflicts of interest Authors have no conflict of interests to declare.