Spinal cord intramedullary pressure in thoracic scoliotic deformity: a cadaveric study.

STUDY DESIGN: In vitro cadaveric study of thoracic spinal cord intramedullary pressure (IMP) in scoliotic deformity. OBJECTIVE: To define the relationship between thoracic scoliotic deformity and spinal cord IMP. SUMMARY OF BACKGROUND DATA: Clinical studies of patients with thoracic scoliosis without other spinal pathology (spinal stenosis, etc.) have rarely reported an associated thoracic myelopathy. Previous clinical and cadaveric studies of kyphosis have reported associated myelopathy and increased spinal cord IMP. We sought to determine if IMP changes in response to main thoracic scoliotic deformity. METHODS: In 6 fresh-frozen cadavers, a progressive main thoracic scoliotic deformity was created. Cadavers were positioned sitting with physiological spinal alignment, head stabilized using a skull clamp and spine segmentally instrumented from occiput to L3. The T3-T4 ligamentum flavum was removed, dura opened, and 3 pressure sensors were advanced caudally to T4-T5, T7-T8, and T10-T11 within the cord parenchyma. A step-wise main thoracic scoliotic deformity was then induced by sequentially releasing and retightening the skull clamp while coronally bending, concavity compressing, and convexity distracting posterior segmental instrumentation, allowing closure of lateral segmental osteotomies. After each step, fluoroscopic images and pressure measurements were obtained; the T4-T11 coronal Cobb angle was measured. RESULTS: Induction of main thoracic scoliosis did not significantly increase IMP. The mean main thoracic maximal scoliotic deformity created was 77° ± 2° (range: 71°-84°). At maximal deformity, the mean ΔIMP at T4-T5, T7-T8, T10-T11 was 2.2 ± 1.9 mm Hg, 1.0 ± 0.7 mm Hg, and 1.0 ± 0.8 mm Hg, respectively. CONCLUSION: In this cadaveric study, main thoracic scoliotic deformity did not significantly increase thoracic IMP. This correlates with clinical presentation such that clinical studies of patients with thoracic scoliosis without other spinal pathology have rarely reported an associated thoracic myelopathy with the thoracic scoliosis. This study helps explain the relative absence of myelopathy in isolated main thoracic coronal plane deformity. LEVEL OF EVIDENCE: 5.

Ventriculostomy-associated infection: a new, standardized reporting definition and institutional experience.

OBJECTIVE: Shortcomings created by the lack of both a uniform definition of ventriculostomy-associated infection (VAI) and reporting standards have led to widely ranging infections rates (2-24%) whose significance is uncertain. We propose a standardized definition of VAI and a consistent reporting format compliant with Centers for Disease Control and Prevention (CDC) for device-related infections. Using those parameters to establish an infection-control surveillance program, we report our 4-year institutional VAI rates. METHODS: In this prospective study covering ventriculostomy utilization (October 2006-December 2010), 498 patients had a total of 4,673 ventriculostomy days. By review of the literature and our institutional analysis, we defined VAI as a positive CSF culture in a patient with ventriculostomy catheter, plus one or more of the following (1) fever recorded >101.5 °F or (2) cerebrospinal fluid (CSF) glucose level, either <50 mg/dL or <50% of a serum glucose level drawn within 24 h of the CSF glucose. In a report format that is CDC compliant, rates of VAI are reported. RESULTS: Among our patients, the CDC-compliant infection rate was 2.14 per 1,000 ventriculostomy days. Of the 10 VAIs occurring in 498 patients during 4,673 ventriculostomy days, this 2.0% infection rate was lower than the previously reported 8.8% composite rates of VAI. Average duration of ventriculostomy was 9.4 days. Neither antibiotic-impregnated catheters nor periprocedural or prophylactic antibiotics were used. CONCLUSIONS: Our standardized VAI definition and CDC format seems promising toward facilitating future study and guideline development. Given our strict protocol of sterile catheter placement and care, and our institution's low 2.0% infection rates, we propose an infection-rate target of ≤5 per 1,000 device days. Our results suggest that the use of antibiotics or antibiotic-impregnated catheters is unwarranted--a positive given concerns of evolving anti-microbial resistance.

Laminectomy, durotomy, and piotomy effects on spinal cord intramedullary pressure in severe cervical and thoracic kyphotic deformity: a cadaveric study.

OBJECT: Previous studies have shown that cervical and thoracic kyphotic deformity increases spinal cord intramedullary pressure (IMP). Using a cadaveric model, the authors investigated whether posterior decompression can adequately decrease elevated IMP in severe cervical and thoracic kyphotic deformities. METHODS: Using an established cadaveric model, a kyphotic deformity was created in 16 fresh human cadavers (8 cervical and 8 thoracic). A single-level rostral laminotomy and durotomy were performed to place intraparenchymal pressure monitors in the spinal cord at C-2, C4-5, and C-7 in the cervical study group and at T4-5, T7-8, and T11-12 in the thoracic study group. Intramedullary pressure was recorded at maximal kyphosis. Posterior laminar, dural, and pial decompressions were performed while IMP was monitored. In 2 additional cadavers (1 cervical and 1 thoracic), a kyphotic deformity was created and then corrected. RESULTS: The creation of the cervical and thoracic kyphotic deformities resulted in significant increases in IMP. The mean increase in cervical and thoracic IMP (change in IMP [ΔIMP]) for all monitored levels was 37.8 ± 7.9 and 46.4 ± 6.4 mm Hg, respectively. After laminectomies were performed, the mean cervical and thoracic IMP was reduced by 22.5% and 18.5%, respectively. After midsagittal durotomies were performed, the mean cervical and thoracic IMP was reduced by 62.8% and 69.9%, respectively. After midsagittal piotomies were performed, the mean cervical and thoracic IMP was reduced by 91.3% and 105.9%, respectively. In 2 cadavers in which a kyphotic deformity was created and then corrected, the ΔIMP increased with the creation of the deformity and returned to zero at all levels when the deformity was corrected. CONCLUSIONS: In this cadaveric study, laminar decompression reduced ΔIMP by approximately 15%-25%, while correction of the kyphotic deformity returned ΔIMP to zero. This study helps explain the pathophysiology of myelopathy in kyphotic deformity and the failure of laminectomy alone for cervical and thoracic kyphotic deformities with myelopathy. In addition, the study emphasizes the need for correction of deformity during operative treatment of kyphotic deformity, the need for maintaining adequate intraoperative blood pressure during operative treatment, and the higher risk of spinal cord injury associated with operative treatment of kyphotic deformity.

Spinal cord intramedullary pressure in thoracic kyphotic deformity: a cadaveric study.

STUDY DESIGN: In vitro cadaveric study of thoracic spinal cord intramedullary pressure (IMP) in kyphotic deformity. OBJECTIVE: To define the relationship between thoracic spinal kyphotic deformity and spinal cord IMP. SUMMARY OF BACKGROUND DATA: Previous studies of asymptomatic volunteers have revealed that there is wide variation in regional sagittal neutral upright thoracic spinal alignment with "normal" thoracic T4-T12 kyphosis ranging up to approximately +69° for 98.5% of the asymptomatic adult population. We sought to determine whether IMP changes in response to increasing thoracic kyphosis. METHODS: In 8 fresh-frozen cadavers, a progressive kyphotic deformity was created. Cadavers were positioned sitting with physiological thoracic kyphosis, head stabilized using a skull clamp, and spine segmentally instrumented from occiput to L2. The T3-T4 ligamentum flavum was removed, dura opened, and 3 pressure sensors were advanced caudally to T4-T5, T7-T8, and T11-T12 within the cord parenchyma. A stepwise thoracic kyphotic deformity was then induced by sequentially releasing and retightening the skull clamp while distracting posterior short segment rods and closing anterior segmental osteotomies. After each step, fluoroscopic images and pressure measurements were obtained; the T4-T12 Cobb angle was measured. RESULTS: Minor IMP increases of 2 to 5 mm Hg were observed at 1 or more spinal cord levels in 1 of 8 cadavers when the Cobb angle was less than +51° and in 4 of 8 cadavers when the angle was more than +51° and less than +63°. For Cobb angles more than +51° and less than +63°, a statistically significant, minor increase in IMP was detected at the T7-T8 level only (P = 0.02). At Cobb angles exceeding +63°, ΔIMP progressively increased at 1 or more spinal cord levels in 8 of 8 cadavers. Cobb angles ranging from +63° to +149° resulted in statistically significant increases in IMP ranging to more than 50 mm Hg. ΔIMP did not correlate with segmental spinal canal diameter (stenosis). CONCLUSION: Thoracic kyphosis less than +51° resulted in no meaningful increase in IMP, whereas kyphosis measuring +51° to +63° resulted in minor increases in IMP. After the thoracic kyphosis exceeded +63°, IMP increased significantly. ΔIMP with spinal alignment may help explain the wide range of "normal" thoracic neutral upright sagittal alignment in studies of asymptomatic adult individuals and may help further define thoracic kyphotic deformity.

Conus medullaris syndrome after epidural steroid injection: Case report.

BACKGROUND: Given the risk of paralysis associated with cervical transforaminal injection, is it time to reconsider transforaminal injections of the lumbar spine? Arguments for discontinuing lumbar injections have been discussed in the anesthesia literature, raising concern about the risks of epidural steroid injections (ESIs). METHODS: In a 47-year-old man, paraplegia of the lower extremities developed, specifically conus medullaris syndrome, after he underwent an ESI for recurrent pain. Correct needle placement was verified with epidurography. Immediately after the injection, the patient felt his legs "going dead"; paraplegia of the lower extremities was noted. RESULTS: An initial magnetic resonance imaging study performed after the patient was transferred to the emergency department was unremarkable. However, a later neurosurgical evaluation showed conus medullaris syndrome, and a second magnetic resonance imaging study showed the conus infarct. We conducted a search of the PubMed database of articles from 2002 to 2011 containing the following keywords: complications, lumbar epidural steroid injection(s), cauda equina syndrome, conus medullaris infarction, spinal cord infarction, spinal cord injury, paralysis, paresis, plegia, paresthesia, and anesthesia. CONCLUSIONS: Summarizing this case and 5 similar cases, we weigh the potential benefits and risks of ESI. Although one can safely assume that this severe, devastating complication is rare, we speculate that its true incidence remains unknown, possibly because of medicolegal implications. We believe that the rarity of this complication should not preclude the continued use of transforaminal ESI; rather, it should be emphasized for discussion with patients during the consent process.

Transarterial embolization of cerebral arteriovenous malformations: a durable treatment for venous side hemorrhage?

Cerebral arteriovenous malformations (AVMs) have been occasionally reported to bleed from their venous side. This may particularly be the case when venous ectasias or aneurysms develop in the setting of steno-occlusive venopathy. Venous side hemorrhage should be suspected when the hematoma is centered on the venous pouch or when a venous pseudoaneurysm is identified on angiography. For AVMs with an identifiable point of rupture, early treatment is recommended in an attempt to secure the weak spot and minimize the risk of rerupture. When possible, microsurgical resection is the definitive and preferred treatment. In contrast, because of its latency period, stereotactic radiosurgery does not confer immediate protection in such cases. Endovascular transarterial embolization may offer immediate cure to only a minority of small AVMs, but remains a very useful temporizing strategy for arterial rupture sites such as proximal or intranidal aneurysms, allowing to defer definitive AVM treatment by either microsurgery or radiosurgery to a later stage. However, when the rupture site is venous in location and the AVM cannot be readily cured by either microsurgery because of its location in eloquent brain or embolization because of its large size, protecting patients from early rerupture may become problematic. We propose that, by reducing flow through the AVM, transarterial embolization may lead to secondary thrombosis of venous pseudoaneurysms and confer durable occlusion of these weak spots, pending definitive AVM cure. Therefore, transarterial embolization should be routinely attempted in such difficult-to-manage cases. An illustrative clinical case is presented in support of this hypothesis.