Charcot Joint in a Paraplegic
This 48-year-old man has been a complete T10 paraplegic, wheelchair bound since age 22. At the initial time of injury he had no surgery. Ten years prior to presentation in our clinic, the patient had undergone an L4-L5 and L5-S1 PLIF elsewhere, apparently for low back pain (LBP). One of the cages migrated and the patient underwent revision surgery 2 years later elsewhere. He presented now with increasing poorly localized LBP and episodes of profuse sweating and back spasms when he flexed. There was also a clicking sound and sensation with movement in his back. There were no leg pain or leg symptoms.
On examination, he had a T10 sensory level and no lower extremity movements. There was no palpable lumbar deformity. He was wheelchair bound.
At time of presentation, the patient had not undergone further treatment, either operative or non-operative since the previously mentioned revision surgery two years earlier.
Figure 1: Lateral spine x-ray showing gross disruption at the L4-L5 level. No instrumentation other than the remaining cages is present.
Figure 2: Pre-operative AP lumbar spine x-ray showing the pseudoarthrotic cleft across the L4-L5 level with the migrated left L4-L5 cage and coronal translation at this level.
Figure 3: Pre-operative flexion x-ray demonstrating the marked instability at the L4-L5 level with likely complete obliteration of the spinal canal at L4-L5.
Figure 4: Pre-operative lateral extension x-ray confirming the marked hypermobility.
Figure 5: Pre-operative reconstructed sagittal CT demonstrating the L4-L5 pseudoarthrosis and cleft.
Figure 6: Pre-operative coronal reconstructed CT demonstrating the pseudoarthrosis.
Figure 7: Pre-operative MRI showing the old thoracic injury with complete obliteration of the cauda equina at the L4-L5 level.
Gross instability 360° instability at a denervated L4-L5 level with a second migrated cage and cauda equina compression.
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The patient underwent a re-exploration posteriorly with decompression and interbody fusion at L3-L4 and L4-L5. Modified pedicle subtraction osteotomies were affected. Because of the destruction of the L4 vertebra, a large amount of vertebral body resection was not required. There was good restoration of sagittal and coronal balance. The floating cage was removed. Because of his long-standing paralysis, aggressive mobilization of the cauda equina allowed access to the L4-L5 interspace and body.
Figure 8A: AP x-ray performed 3 months post-operatively shows no hardware failure and restoration of coronal balance.
Figure 8B: Lateral x-ray performed 3 months post-operatively also shows no hardware failure and restoration of sagittal balance.
The patient did well. He was discharged to rehabilitation 3 days post-operatively. He was immobilized in a TLSO for 3 months. His pre-operative clicking, back spasms, and episodes of sweating stopped.
X-rays at 3 months post-operatively showed no complications.
At clinical review 6 months post-operatively, he was back to his baseline status with no low back pain and no neurological changes otherwise.
One of the delayed complications of traumatic spinal cord injury is a Charcot spine, also referred to as neuropathic spinal arthropathy. The lack of protective sensation in the spine secondary to a spinal cord injury may result in bony destruction, bone resorption, and eventual deformity.
With advancements in spinal cord injury research and management, patients are living both longer and more active lifestyles. This will likely result in an increased incidence and prevalence of Charcot joints of the spine and thus make the early recognition and appropriate management of this condition of paramount importance to spine surgeons.
The case under review is a typical delayed presentation of neuropathic arthropathy of the spine in a post-traumatic setting. The presenting symptoms of low back pain, audible clicking sounds, and autonomic dysreflexia in our case are reported in the literature and are important symptoms to recognise in conjunction with radiographic changes1.
From a pathophysiological perspective, it is thought that continued activity in a joint that lacks "protective sensation" ultimately results in joint destruction2. Thus, immobilization of the affected joint is the objective of treatment. There are reported cases of recognised Charcot joints of the spine where no treatment was initiated, resulting in neurological deterioration and ultimately death3.
Haus et al. have reported on 8 cases of Charcot spine with an average follow-up of 14.3 years. Revisions were required in 75% (6/8) of their cases due to non-union, adjacent level Charcot joints, recurrent hardware failure and osteomyelitis. In their experience, several operations are required to achieve solid fusion at times4.
Our case exemplifies many of the aforementioned challenges encountered by Haus et al. Due to the challenge of achieving a solid fusion, it is recommended to achieve 3 column stabilization with either a combined anterior/posterior or a posterior approach with anterior support. It is also advised to continue the construct to the sacrum or pelvis to reduce the risk of developing an additional charcot joint.
The author must be commended on the management of this challenging case. However, despite the excellent post-operative images and resolution of patient symptoms we recommend that these type of cases be monitored closely.
- Selmi F, Frankel HL, Kumaraguru AP et al. Charcot joint of the spine, a cause of autonomic dysreflexia in spinal cord injured patients. Spinal Cord. 2002;40(9):481-483.
- Johnson JTH. Neuropathic fractures and joint injuries: pathogenesis and rationale of prevention and treatment. J Bone Joint Surg. 1967;49A:1-30.
- Standaert CJ, Cardenas DD, Anderson PA. Charcot spine as a late complication of traumatic spinal cord injury. Arch Phys Med Rehabil. 1997;78:221-225.
- Haus BM, Hsu AR, Yim ES et al. Long-term follow-up of the surgical management of neuropathic arthropathy of the spine. Spine J. 2010;10(6):e6-e16.