Giant calcified lumbar disc herniation in post-operative adjacent segment degeneration: a case report

Introduction

Intervertebral disc calcification is frequently seen in disc degeneration, especially among the elderly population, with a post-mortem study reporting a prevalence rate of up to 80% (1). Calcified disc herniation is substantially less common and seen primarily in the thoracic spine in adults (2). For instance, calcified thoracic disc herniation was found in 7.3% of patients with thoracic disc disease with myelopathy who underwent surgery (3). Giant calcified disc herniation, defined as occupying more than 40% of the spinal canal (4), is a rarer subset of calcified disc herniations which is associated with increased rates of myelopathy and worse functional outcome (4). In the lumbar spine, calcified or large disc herniations have been reported with various surgical approaches (Table 1). However, little is known about the incidence and management of giant, calcified lumbar disc herniation. Herein, we report an adult patient with a history of multiple lumbar spine surgeries who developed a giant, calcified disc herniation at the adjacent vertebral level in the lumbar spine. We present this case in accordance with the CARE reporting checklist (available at https://jss.amegroups.com/article/view/10.21037/jss-25-29/rc).

Case presentation

A 75-year-old male with a past medical history of hypertension, type 2 diabetes mellitus, hyperlipidemia, alcohol abuse, neurogenic bladder, and hepatitis C virus with cirrhosis presented to our institution with a 5-week history of worsening bilateral lower extremity weakness and fatigue as well as radiating pain into both (right greater than left) anterior thighs. There was no recent history of trauma or infection. He had a history of multiple spine surgeries over a 9-year period prior to his presentation, including L4–S1 posterior decompression, L4–S1 anterior lumbar interbody fusion, L5–S1 posterior instrumented fusion, and left L3–L4 hemilaminectomies with resection of an extruded disc. His most recent surgery was a re-do left L3–L4 hemilaminectomy with extension of his prior L4–S1 fusion construct up to L3, which was performed approximately 1 year prior to the presentation.

The neurological examination revealed mild weakness in right hip flexion as well as decreased sensation in the left anterior thigh. Labs were notable for elevated glucose of 130 mg/dL. Other labs including the complete blood count and sedimentation rate were normal. Vital signs showed elevated blood pressure of 154/88 mmHg but were otherwise normal. A lumbar spine magnetic resonance imaging (MRI) without contrast demonstrated a large, right paracentral, intraspinal lesion at the L2–L3 level, adjacent to the posteriorly fused levels (Figure 1A). The lesion was T1 intermediate and T2 hypointense. It resulted in severe narrowing of the right lateral recess and overall moderate spinal canal stenosis at L2–L3. There was associated crowding of the cauda equina nerve roots and partial effacement of the cerebrospinal fluid spaces at this level. A computed tomography (CT) of the lumbar spine without contrast demonstrated that the lesion contained amorphous, cloudlike hyperdensities internally (mean Hounsfield unit: 418), suggestive of calcification (Figure 1B). The leading differential consideration was a giant, calcified, right paracentral disc extrusion. The finding was new when compared to the lumbar spine MRI obtained 6 months prior where there was a bulging disc but no disc extrusion (Figure 2A). A comparison lumbar spine CT from 13 months prior demonstrated no pre-existing intervertebral disc calcification at L2–L3 (Figure 2B).

Figure 1 MRI and CT of the lumbar spine at the time of most recent clinical presentation. (A) Noncontrast MRI of the lumbar spine with T1-weighted (left panel), sagittal T2-weighted (middle panel), and axial T2-weighted (right panel) sequences demonstrates a large right paracentral lesion at the L2–L3 level (yellow arrow), which is T1 intermediate and T2 hypointense, with moderate spinal canal stenosis. The dotted line on the sagittal T2-weighted sequence (middle panel) denotes the level corresponding to the axial T2-weighted sequence (right panel). Artifact from the prior posterior hardware from L3–S1 and anterior hardware from L4–S1 can be seen. On axial T2-weighted sequence (right panel), the lesion effaces the right lateral recess and exerts mass effect on the descending right L3 nerve root. (B) Noncontrast CT of the lumbar spine with sagittal (left panel) and axial (right panel) views shows that the lesion is diffusely hyperdense with ill-defined internal calcifications. CT, computed tomography; MRI, magnetic resonance imaging.

Figure 2 Prior MRI and CT lumbar spine examinations. (A) On comparison sagittal and axial MRI images from 6 months prior, the L2–L3 lesion was not visualized. A small broad-based disc bulge was noted, with mild spinal canal stenosis. (B) Noncontrast CT images from 13 months prior also did not show the calcified lesion or any underlying intervertebral disc calcification at L2–L3. CT, computed tomography; MRI, magnetic resonance imaging.

Subsequently, the patient underwent a resection of the lesion with L2–L3 decompressive laminectomies and medial facetectomies as well as extension of the posterior instrumented fusion to L1–S1. The patient’s prior midline incision was reopened and extended to the level of T12. L1 and L2 lamina were exposed, and the dissection was carried inferiorly to expose and remove the prior L3–S1 rods. Bilateral pedicle screws at L1 and L2 were placed. Laminectomy at L2–L3 with medial facetectomy on the right were performed. The medial facetectomy at L2–L3 was extended inferiorly towards the right L3–L4 level to facilitate further decompression of the right L2–L3 lateral recess and the thecal sac adjacent to the location of the right extradural intraspinal lesion. There was a great deal of scar tissue densely adherent to the thecal sac in this area, which was carefully debulked and resected until the thecal sac could be gently mobilized. A large extradural lesion was identified, severely compressing the right thecal sac and the right L3 nerve root, both of which were carefully dissected away from the lesion. Grossly, the lesion was yellowish in color and firm. The capsule of the lesion was opened, expressing a wax-like material within. The lesion was initially centrally debulked, and the specimen was sent for frozen pathology, which revealed a preliminary intraoperative diagnosis of diffuse calcifications with no evidence of neoplasm. Nearly all of the lesion was then further resected, with the exception of a portion of the outermost capsule, which was densely adherent to the ventral portion of the thecal sac and the right L3 nerve root. It was determined that it was not necessary to further dissect and resect the remaining capsule because of the high risk of nerve injury and cerebrospinal fluid leak posed by its dense adherence, and the fact that the thecal sac and L3 nerve root were now well decompressed. Furthermore, the lesion itself showed no evidence of a tumor on intraoperative pathology. Lordotic rods were then placed and secured to connect the pedicle screws from L1 to S1 bilaterally, and the previous posterolateral arthrodesis was extended to L2–L3 and L1–L2 bilaterally. Intraoperative neuromonitoring of sensory and motor evoked potentials were utilized and remained stable throughout the case.

The specimen submitted to pathology consisted of multiple tissue fragments measuring 1.0 cm × 0.5 cm × 0.3 cm in aggregate. Histologic sections showed predominantly acellular amorphous material with admixed calcified fragments of fibrocartilage and bone (Figure 3). This was considered to be degenerating disc material with diffuse calcification, confirming the diagnosis of a giant, calcified, lumbar disc herniation. Post-operatively, the patient’s pain and gait improved, and he was discharged to a subacute nursing facility on post-operative day 9. On his follow-up visit to Neurosurgery Clinic approximately 3 weeks after the surgery, he reported that compared to before the operation, he was feeling stronger in his legs and that his proximal leg pain had decreased. He denied back pain, and he no longer heard a popping sound when he moved his back. Subsequent follow-up assessment at 4 months post-surgery showed the patient no longer had any of his pre-operative lower back pain or bilateral leg pain. His right hip flexor strength had improved, and he felt that his overall strength and walking had improved compared to pre-surgery, including the ability to walk up the stairs.

Figure 3 Histologic review of the surgical specimen. (A) Low power view of disc herniation specimen shows irregular calcified/ossified fragments (arrow) in an amorphous matrix. (B,C) Higher magnification images demonstrate bone fragments (arrow) (B) and degenerating fibrocartilage (C). Hematoxylin and eosin stain. Original magnifications: A, 20×; B,C: 100×.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. A written informed consent was deemed not to be required by the local institutional review boards because this is a case report that involved no identifiable personal information.

Discussion

The pathogenesis of disc degeneration is thought to involve multiple factors including genetics, obesity, type II diabetes, smoking, mechanical loading, and aging (9). Intervertebral disc calcification is more prevalent in older individuals and is associated with higher grades of disc degeneration (9,10). Disc calcification is also correlated with scoliosis and endplate degenerative changes, and it is hypothesized that the calcification may be a component of the physiological response to fuse and stabilize vertebral levels in the setting of instability (9). Adjacent segment degeneration, also known as adjacent segment disease or adjacent level disease, refers to new degenerative changes at a vertebral level adjacent to surgically treated segments as well as associated symptoms such as radiculopathy, myelopathy, and chronic back pain (11). In the present case, the patient developed adjacent segment degeneration with a large disc extrusion. It is plausible that there was some degree of instability at this level, which contributed to the development of disc herniation and calcification. Disc calcifications can also be seen in association with systemic disorders such as chondrocalcinosis and hyperparathyroidism (12), but the patient had no pertinent history.

Various efforts were made to reduce the chance of recurrent, adjacent segment degeneration. Given that the longer fusion constructs are associated with an increased risk of adjacent segment degeneration (11), posterior instrumented fusion was limited to the minimum necessary based on the preoperative assessments that included flexion/extension and scoliosis radiographs in addition to the aforementioned MRI and CT. With this patient, the instrumented fusion was extended superiorly to L1 because the pre-operative MRI showed a disc protrusion L1–L2 that had progressed when compared to the MRI 6 months earlier. Thus, the patient was at an increased risk for adjacent level degeneration at L1–L2, becoming symptomatic in the future if the posterior instrumented fusion was placed superiorly only to L2. With regard to post-operative care to limit adjacent segment degeneration, post-operative rehabilitation plans were emphasized, including dedicated, individualized physical therapy, to improve the patient’s core balance and gait mechanics.

An unusual feature of the disc herniation observed in the present case is the relatively rapid development of disc calcification. Little is known about the rate of disc calcification. In pediatric patients, cases of acute calcific discitis have been reported primarily in the cervical spine, where intervertebral disc calcifications were observed in association with symptoms such as neck pain and limited range of motion (13). Typically, these calcifications were seen to resolve after approximately 6 months (13), suggesting that intervertebral disc calcification is a dynamic process. Acute calcific discitis in adults is exceedingly rare, and the underlying etiology remains unknown (14). In the present case, the disc extrusion developed over a 6-month period between lumbar spine MRIs. The most recent comparison CT lumbar spine from 13 months prior did not demonstrate any pre-existing intervertebral disc calcification (Figure 2B). Although no short-interval serial imaging was performed to determine the exact onset and evolution of disc calcification, it is suspected that the disc herniation and calcification developed over a relatively short period of time.

Prior to surgery, non-degenerative causes of a calcified lesion in the spinal canal were also considered. Tumoral calcinosis can present as a large periarticular, calcified, soft tissue mass and is seen in hereditary diseases such as hyperphosphatemia familial tumoral calcinosis (15,16). The patient did not have any known hereditary diseases. Calcified lesions can also be seen in the setting of infection such as spinal tuberculosis (17), but there was no evidence of infection in the present case. Chronic hematoma within the spinal can calcify and mimic a calcified mass or disc (18,19); this was thought to be less likely given the absence of recent trauma and lack of hemosiderin in the specimen.

Surgical resection of giant calcified disc herniations poses several challenges due to their large size and high-grade spinal canal stenosis. Extra care must be taken to identify any adhesions between the calcified disc and adjacent nerve roots, thecal sac, or even the spinal cord to avoid any damage to these important structures, particularly as large disc herniations can displace and distort the normal anatomy (20). Intraoperative neuromonitoring may be useful to evaluate for changes in nerve root electromyography (EMG) or spinal cord motor evoked potentials or somatosensory sensory evoked potentials. Calcification can also harden the disc herniation itself, either partially or completely, making it much more difficult to resect (21). If the calcification has not hardened the disc herniation internally, the disc herniation may undergo central debulking, followed by subsequent careful dissection around the outer capsule. In the present case, such a strategy was applied as the disc calcification still allowed for a central debulking and then it was able to be dissected off the surrounding structures without nerve damage, with only a small portion of residual capsule adherent to the thecal sac and nerve root. There was also an additional challenge of scar tissue from prior surgeries near the surgical site in this patient, making dissection of the calcified disc more difficult due to lack of clear surgical planes and dense adherence of the disc to the surrounding structures.

Conclusions

The present case demonstrates an unusual presentation of adjacent segment degeneration with a giant, calcified lumbar disc herniation that developed in a relatively short period of time in a patient with history of several pervious lumbar spine surgeries. Surgical challenges and management considerations are also discussed. The case highlights the dynamic nature of disc herniations and calcifications and underscores the need for further studies into the pathophysiology of calcified disc herniations.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jss.amegroups.com/article/view/10.21037/jss-25-29/rc

Peer Review File: Available at https://jss.amegroups.com/article/view/10.21037/jss-25-29/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jss.amegroups.com/article/view/10.21037/jss-25-29/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. A written informed consent was deemed not to be required by the local institutional review boards because this is a case report that involved no identifiable personal information.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Chanchairujira K, Chung CB, Kim JY, et al. Intervertebral disk calcification of the spine in an elderly population: radiographic prevalence, location, and distribution and correlation with spinal degeneration. Radiology 2004;230:499-503. [Crossref] [PubMed]
2. Yuan L, Chen Z, Liu Z, et al. Clinical and radiographic features of adult calcified thoracic disc herniation: a retrospective analysis of 31 cases. Eur Spine J 2023;32:2387-95. [Crossref] [PubMed]
3. Yuan L, Chen Z, Li W, et al. Radiographic and clinical features of thoracic disk disease associated with myelopathy: a retrospective analysis of 257 cases. Eur Spine J 2021;30:2211-20. [Crossref] [PubMed]
4. Hott JS, Feiz-Erfan I, Kenny K, et al. Surgical management of giant herniated thoracic discs: analysis of 20 cases. J Neurosurg Spine 2005;3:191-7. [Crossref] [PubMed]
5. Cheng Y, Zhang Q, Li Y, et al. Percutaneous endoscopic interlaminar discectomy for L5-S1 calcified lumbar disc herniation: A retrospective study. Front Surg 2022;9:998231. [Crossref] [PubMed]
6. Tulloch I, Papadopoulos MC. Giant central lumbar disc herniations: a case for the transdural approach. Ann R Coll Surg Engl 2018;100:e53-6. [Crossref] [PubMed]
7. Molina-Martínez RP, Betancourt-Quiroz C, Dueñas-Espinoza MA, et al. Minimally invasive management for a giant lumbar intervertebral disc herniation: A case report, and literature review. Int J Surg Case Rep 2021;81:105843. [Crossref] [PubMed]
8. Jeon CH, Chung NS, Son KH, et al. Massive lumbar disc herniation with complete dural sac stenosis. Indian J Orthop 2013;47:244-9. [Crossref] [PubMed]
9. Novais EJ, Narayanan R, Canseco JA, et al. A new perspective on intervertebral disc calcification-from bench to bedside. Bone Res 2024;12:3. [Crossref] [PubMed]
10. Shao J, Yu M, Jiang L, et al. Differences in calcification and osteogenic potential of herniated discs according to the severity of degeneration based on Pfirrmann grade: a cross-sectional study. BMC Musculoskelet Disord 2016;17:191. [Crossref] [PubMed]
11. Huang X, Cai Y, Chen K, et al. Risk factors and treatment strategies for adjacent segment disease following spinal fusion Mol Med Rep 2025;31:33. (Review). [Crossref] [PubMed]
12. Zehra U, Tryfonidou M, Iatridis JC, et al. Mechanisms and clinical implications of intervertebral disc calcification. Nat Rev Rheumatol 2022;18:352-62. [Crossref] [PubMed]
13. Lernout C, Haas H, Rubio A, et al. Pediatric intervertebral disk calcification in childhood: three case reports and review of literature. Childs Nerv Syst 2009;25:1019-23. [Crossref] [PubMed]
14. Lazarou I, Farracho LC, Genevay S, et al. Adult-onset Acute Calcific Discitis. J Rheumatol 2022;49:330-1. [Crossref] [PubMed]
15. Olsen KM, Chew FS. Tumoral calcinosis: pearls, polemics, and alternative possibilities. Radiographics 2006;26:871-85. [Crossref] [PubMed]
16. Tiwari V, Goyal A, Nagar M, et al. Hyperphosphataemic tumoral calcinosis. Lancet 2019;393:168. [Crossref] [PubMed]
17. Garg RK, Somvanshi DS. Spinal tuberculosis: a review. J Spinal Cord Med 2011;34:440-54. [Crossref] [PubMed]
18. Rieth KG, Quindlen EA. Calcified chronic spinal subdural hematoma demonstrated by computed tomography. Spine (Phila Pa 1976) 1983;8:812-6. [Crossref] [PubMed]
19. Sahri IE, Tlemcani ZC, Abide Z, et al. Ligamentum flavum hematoma in the lumbar spine mimicking spinal tumor: A case report and review of the literature. Radiol Case Rep 2023;18:3060-4. [Crossref] [PubMed]
20. Yuan AL, Shen X, Chen B. Treatment of Calcified Lumbar Disc Herniation by Intervertebral Foramen Remolding: A Retrospective Study. J Pain Res 2022;15:1719-28. [Crossref] [PubMed]
21. Wang D, Xing J, Shao B, et al. A surgical decompression procedure for effective treatment of calcified lumbar disc herniation. J Int Med Res 2020;48:300060520938966. [Crossref] [PubMed]