Description
Ruth, a consultant at the Royal National Orthopedic Hospital and member of the RNA spinal myeloma MDT, presents her team’s approach to managing spinal myeloma. She explains that myeloma commonly causes fractures, pain, deformity, and sometimes neural compression. The talk emphasizes that patients with sagittal plane deformity tend to have poor outcomes, so the team’s main goals are to relieve or prevent pain, prevent progressive fracture deformity, and avoid cord or cauda equina compression.
She describes the challenges of spinal surgery in myeloma: the disease is highly chemo- and radiosensitive, bone quality is poor, disease is often multilevel, and instrumentation can lead to malalignment or junctional failure. Because many patients also need prolonged chemotherapy and stem cell treatment, surgery can delay systemic therapy. Complication rates can be high, and early revision is common. In contrast, early bracing can reduce progressive deformity, and the team has found that when patients are braced early, deformity progression is uncommon.
Ruth presents examples showing the consequences of untreated or late-treated deformity, including fixed kyphosis, severe pain, secondary kyphotic collapse after decompression, and functional decline. She then outlines a pathway developed by the spinal myeloma working group: patients are divided into those with normal and abnormal neurology, all assessed with whole-spine MRI including STIR and axial sequences. For patients with cord compression but no bony canal compromise, the team recommends bed rest, high-dose steroids, bisphosphonates, and systemic chemotherapy, reserving urgent radiotherapy for acute neurological compromise. They often reassess after 7–10 days, by which time the canal may be clear without surgery.
She stresses the importance of assessing stability, including sternal imaging, because sternal involvement is linked to higher risk of thoracic sagittal deformity. She explains that if spinal shape is maintained, the spine can stabilize and even form new bone, sometimes appearing as a Roman column or peripheral cortical remodeling after systemic therapy and bisphosphonates. Similar healing can occur at the lumbosacral junction, though it may take up to nine months, and some patients need hip spica-type support rather than a standard TLSO. Most patients receive a custom orthosis for three to four months, with detailed instructions shared among physiotherapists, occupational therapists, and hematologists. Cement augmentation is now used less often, in under 5% of patients.
For patients with abnormal neurology, the key distinction is whether the compression is soft tissue or bony. If there is no bony incursion into the canal, urgent radiotherapy and steroids can clear the canal and restore power, followed by bracing. If bony compromise is present and neurological deficit is progressing, surgery may still be necessary, though the team tries to use minimally invasive options when possible. She gives an example of a frail 90-year-old whose neurological symptoms resolved after cement augmentation.
Her overall message is that this is an MDT-driven process relying on steroids, chemotherapy, radiotherapy, bracing, and bisphosphonates, with surgery avoided whenever possible. The key principles are early imaging, early bracing, and early referral. In the Q&A, she explains that braces are ideally custom-made because off-the-shelf devices can worsen sternal fractures due to their metal sternal plate. She notes that timing is crucial, since custom braces need to be made quickly to be useful during the first few months of treatment. The discussion ends with agreement that the traditional surgical-first approach often leads to worse outcomes, and that even in diffuse lytic disease without fracture, early bracing is preferable while systemic therapy begins.