Surgical Management of Lumbar Adhesive Arachnoiditis Postmeningitis: A Bermuda Triangle?—Case Report and Review of Literature

Abstract

Spinal arachnoiditis can occur as a delayed sequel of meningitis. Cerebrospinal fluid flow disturbances and adhesive loculations can cause cord compression and traction on roots causing the symptoms. The surgical treatment of this condition is often considered a limited option, because of the high chances of recurrence of symptoms and adhesions, often considered as surgical failure. Here, we report a patient with extensive lumbar–sacral adhesive arachnoiditis successfully treated with limited adhesiolysis under neuromonitoring and cystoperitoneal shunt placement.

Keywords

spinal adhesive arachnoiditis - adhesiolysis - cystoperitoneal shunt - neuromonitoring

Introduction

There are multiple causes for lumbar arachnoiditis that include prior spinal surgery, infection, intrathecal steroids or anesthetic agents, trauma, subarachnoid hemorrhage, and ionic myelographic contrast agents.

Postmeningitic arachnoiditis is a rare entity and is usually seen several years following infections, especially tuberculous meningitis.[1] This can in turn lead to syringomyelia in the cervical–dorsal level. Extensive arachnoiditis can lead to formation of multiple locules with thickened arachnoid that is stuck to cord or roots and surgical release of these bands is usually difficult. Many a times, surgical attempts may not lead to improvement in neurological status of patients. For this reason, many surgeons believe that opening such a spine is like burning your hands due to the mysterious nature of adhesions and risks associated with handling roots/cord, leading to a “Bermuda Triangle” like situation. They tend to stray away from surgical options and continually treat patients with conservative management.

We report a case of lumbar adhesive arachnoiditis in a patient who previously had meningitis following spinal anesthesia, leading to severe radicular symptoms in lower limbs. We describe the technique and intraoperative findings of a limited monitored adhesiolysis combined with a cystoperitoneal shunt, which leads to significant symptomatic improvement.

Case Report

Presentation

A 47-year-old lady presented to us with a history of pain in both lower limbs for the last 7 months that had aggravated over the past 2 months. Conservative management with analgesics and antineuralgic medications failed and the severe radicular symptoms were disturbing her activities of daily living.

She had a history of meningitis following spinal anesthesia for cesarean section 19 years back and had taken antibiotics along with rifampicin for 6 months and recovered. She denied history of another episode of meningitis or trauma after this. Examination revealed no deficits except for mild reduction in touch and pain sensations in the right L5 to S1 dermatomes. Her visual analog scale (VAS) score for radicular pain was 8/10.

Magnetic resonance imaging (MRI) of whole spine revealed cerebrospinal fluid (CSF) loculation in thecal sac from D12 to L3 level causing mass effect on conus and nerve roots with thickening and clumping of roots at places. A T2 hypointense central septum was noted within the thecal sac starting from upper body of L4 vertebra till S2 level. Contrast MRI of the spine revealed enhancement of the roots within the sac at lumbar–sacral level ([Fig. 1]). Cervical–dorsal cord was grossly unremarkable with no evidence of syringomyelia. A screening MRI brain was unremarkable.

Fig. 1 Preoperative (A) sagittal T2-weighted magnetic resonance imaging (MRI) showing a loculated cerebrospinal fluid cyst at D12 to L3 level causing compression on conus and nerve roots; (B) axial T2-weighted image at L5 level showing thickened arachnoid with central septa and clumping of roots;(C) postcontrast MRI showing enhancement of nerve roots at the involved levels.

Surgical Treatment

Spinal decompression and adhesiolysis were planned. We performed L3 to L5 laminectomy. After opening the dura, thickened arachnoid with multiple loculations adherent to the roots was noted. No CSF flow was noted in the subarachnoid space. Nerve roots were encased in thick fibrosed arachnoid tissue and a thick scarred arachnoid cyst was noted above L3 level containing clear CSF. Stimulation of nerve roots was performed before and after every dissection to check for response. We performed a limited adhesiolysis guided by neuromonitoring. The loculated cyst above L3 level was opened and shunt tube was inserted into it ([Fig. 2]). Intradural steroid wash was given before the dural closure. The patient was then turned to lateral position and distal end of tube was inserted into the peritoneum.

Fig. 2 Intraoperative pictures showing (A) thick and plastered arachnoid immediately after opening the dura, (B) arachnoidolysis and limited adhesiolysis to roots, (C) shunt tube placement, (D) baseline, and (E) final motor-evoked potentials of lower limb and sphincter muscles.

Postsurgery, she reported good relief in radicular pain. Postoperative VAS score was 2/10 in right lower limb and 4/10 in left lower limb. She was discharged on 4th postoperative day with antineuralgia medications for new onset paresthesias in lower limbs postsurgery, probably due to root handling. Currently, she is on regular follow-up till 4 months postsurgery and reports no pain in right lower limb, left lower limb pain significant reduction (VAS-1/10), and no paresthesias.

Discussion

Lumbar arachnoiditis occurring as a delayed complication following meningitis has been previously reported. The inflammation triggered by infection can lead to scarring and thickening of arachnoid. This thickened arachnoid can cause focal disturbance in CSF circulation in the cord leading to CSF accumulation in central canal and Virchow–Robin spaces, leading to a spinal block like condition[2] and thereby leading to syrinx formation. The same also explains a loculated CSF collection in the lumbar level where the cyst can cause compression on conus as seen in our case.

Caplan et al[2] proposed that arachnoiditis can lead to obliterative endarteritis due to occlusion of spinal cord vessels and this can lead to cord ischemic insult. As a part of recovery from this ischemic insult, syrinx formation can happen.

According to Chang and Nakagawa,[3] in arachnoiditis, the pulsatile CSF pressure forces pressure inside the cord to become much higher than that outside the cord. Thus, there is an incremental pressure gradient with each pulse, leading to CSF leakage from central canal and syrinx formation.

In terms of pathophysiology, our case is different from previously reported studies in terms of occurrence of arachnoiditis in the lumbosacral level without any evidence of syringomyelia in the cervical–dorsal level. As a result of impaired CSF flow from L4 below, a loculated CSF cyst had formed from D12 to L3 level causing compression on conus and roots. Intraoperative findings of thickened arachnoid and loculations that were adherent to the roots were probably the result of inflammation due to meningitis. In spite of these accepted theories, the exact mechanism behind syrinx formation is still not clearly understood.

Medical management is usually symptomatic with analgesics and antineuralgic medications. Corticosteroids have been used to hamper symptom progression or minimize residual neurodeficits. Intrathecal hyaluronidase has been found beneficial in causing adhesiolysis.[4]

Surgical options include syrinx shunting, microsurgical adhesiolysis, decompression with duraplasty, and ventriculosubarachnoid shunting.

Shunting includes syringosubarachnoid, syringoperitoneal, and syringopleural shunts. Neurological improvement was seen in only 60%[5] of patients undergoing some form of shunting and hence decompression of spinal subarachnoid space has been recommended in failed cases of shunting. Klekamp et al[6] reported that shunting may have failure with unsatisfactory long-term recurrence rate of around 92 and 100% for focal (<2 levels involved) and extensive scarring, respectively, in their series of 107 patients with arachnoiditis.

Microsurgical adhesiolysis with or without shunting is another option but has not been widely validated in postinfectious arachnoiditis. Arachnoid dissection and duraplasty with graft have been described by various surgeons[6] [7] [8] with clinical improvement but has increased risk of CSF leak. Arachnoid dissection and duraplasty lead to clinical stabilization of neurological deficits in 83 and 17% of patients with focal and extensive scarring, respectively.[6] Extensive scarring and multiple loculations could possibly be the cause of this failure.

Mitsuyama et al[9] had hypothesized that insufficient CSF around the cord in these cases may increase the vulnerability to postoperative relapse and hence had done adhesiolysis with placement of programmable ventriculosubarachnoid shunt to improve CSF circulation at the affected level. They documented a sustained improvement in clinical outcome at 22 months follow-up in spite of re-emergence and gradual enlargement of syrinx several months later. They had lowered the shunt pressure and noted no further enlargement of syrinx or clinical deterioration.

In our case, the severe adhesions negated any chance of extensive adhesiolysis. Hence, we performed limited adhesiolysis under neuromonitoring guidance with placement of a cystoperitoneal shunt to relieve compression on conus and roots by the CSF loculated cyst. A steroid wash was also given at the end of dural closure.

Conclusion

Microsurgical adhesiolysis and placement of shunt can be successfully used for the management of adhesive arachnoiditis. However, adhesiolysis may not be an easy task as this may cause significant traction on neural structures. Neuromonitoring helps in guiding the extent of adhesiolysis in such cases. Placement of a shunt tube will reduce the pressure effect of cyst on the conus and roots.

Conflict of Interest

None declared.

• References

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• 6 Klekamp J, Batzdorf U, Samii M, Bothe HW. Treatment of syringomyelia associated with arachnoid scarring caused by arachnoiditis or trauma. J Neurosurg 1997; 86 (02) 233-240
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Publikationsverlauf

Artikel online veröffentlicht:
06. Januar 2023