Hardware failure and reoperation after hybrid anterior cervical corpectomy and discectomy for multilevel spondylotic disease: A retrospective single-institution cohort study

Background context: Hybrid cervical corpectomy/ACDF (HCC-ACDF) is commonly utilized to treat multilevel cervical myelopathy; however, the incidence and mechanisms of hardware failure remain largely uncharacterized. Purpose: We report our experience with this procedure with the goal of describing and better understanding post-operative failures. Methods: The records of 20 consecutive patients who underwent HCC-ACDF for multilevel CSM between June 2015 and December 2018 at this Hospital (blinded) were retrospectively reviewed. All patients were followed for at least 1 year after surgery and were therefore included in the study. Outcome measures include incidence of and reason for subsequent posterior cervical surgery, incidence of and reason for subsequent anterior cervical surgery, progressive symptomatic myelopathy, radiographic hardware failure, and net reduction of pre-operative kyphosis. Continuous variables are reported with means and standard deviations. Fisher’s exact test was used to compare outcomes of binary variables. Results: 20 patients (mean age 60) underwent anterior HCC-ACDF for 3-level CSM. Mean clinical follow up was 26 months (range: 12–56 months). Mean operative time was 205 min and mean blood loss was 105 mL. Radiographic fusion was achieved in 15 of 18 (83%) patients for whom adequate radiographic follow-up was available. HCC-ACDF resulted in an average restoration of 4 degrees of cervical lordosis (standard deviation: 7.3 degrees). One patient (5%) developed symptomatic hardware failure requiring additional surgery. One patient (5%) developed progressive myelopathy within 4 months of surgery. 2 others (10%) developed adjacent segment disease within 2 years of surgery. Three of 20 patients (15%) required subsequent posterior surgery. Conclusions: Rates of hardware failure after HCC-ACDF in our series compare favorably with reports of multilevel anterior corpectomy but are higher than those reported in previous series of HCC-ACDF. No patient characteristics were significantly associated with rates of surgical failure

Odontoid screw fixation of a type II odontoid fracture in a patient with autofused C2–C3 vertebral bodies

Background: Anterior odontoid screw fixation for the treatment of type II odontoid fractures, in contrast to posterior C1–2 fusion, allows for maintenance of cervical rotatory motion at C1–2. The approach requires an accessible C2–3 disc space from which a screw can be inserted into the vertebral body and odontoid process across the fracture. Less is known about the potential use of this technique in patients with inaccessible C2–3 disc spaces. Case description: A 20 year-old female presented to the emergency department following a motor vehicle accident with diffuse neck pain in the absence of weakness or paresthesias. A CT of the patient's C-spine revealed a type II dens fracture with 3 mm of posterior displacement and congenital fusion of the C2 and C3 vertebral bodies. She was initially treated conservatively with a halo brace for 3 months, but experienced persistent neck pain and a CT of the C-spine at that time showed incomplete healing. The patient was counseled and elected to undergo anterior odontoid screw fixation. During the procedure, due to the autofusion of the C2–3 vertebral bodies, the C3–4 disc space was accessed and a screw was placed through the C2–C3 fusion block into the odontoid process. The patient tolerated the procedure well and postoperative imaging demonstrated healing of the fracture fragments. Conclusion: This case demonstrates that patients with inaccessible C2–3 disc spaces can still undergo anterior fixation. In younger patients, this may be particularly valuable as the rotatory potential of their cervical spine is preserved. Keywords: Type II odontoid fracture, Autofusion, Anterior fusio

Chordoma—Current Understanding and Modern Treatment Paradigms

Chordoma is a low-grade notochordal tumor of the skull base, mobile spine and sacrum which behaves malignantly and confers a poor prognosis despite indolent growth patterns. These tumors often present late in the disease course, tend to encapsulate adjacent neurovascular anatomy, seed resection cavities, recur locally and respond poorly to radiotherapy and conventional chemotherapy, all of which make chordomas challenging to treat. Extent of surgical resection and adequacy of surgical margins are the most important prognostic factors and thus patients with chordoma should be cared for by a highly experienced, multi-disciplinary surgical team in a quaternary center. Ongoing research into the molecular pathophysiology of chordoma has led to the discovery of several pathways that may serve as potential targets for molecular therapy, including a multitude of receptor tyrosine kinases (e.g., platelet-derived growth factor receptor [PDGFR], epidermal growth factor receptor [EGFR]), downstream cascades (e.g., phosphoinositide 3-kinase [PI3K]/protein kinase B [Akt]/mechanistic target of rapamycin [mTOR]), brachyury—a transcription factor expressed ubiquitously in chordoma but not in other tissues—and the fibroblast growth factor [FGF]/mitogen-activated protein kinase kinase [MEK]/extracellular signal-regulated kinase [ERK] pathway. In this review article, the pathophysiology, diagnosis and modern treatment paradigms of chordoma will be discussed with an emphasis on the ongoing research and advances in the field that may lead to improved outcomes for patients with this challenging disease

Chordoma—Current Understanding and Modern Treatment Paradigms

Chordoma is a low-grade notochordal tumor of the skull base, mobile spine and sacrum which behaves malignantly and confers a poor prognosis despite indolent growth patterns. These tumors often present late in the disease course, tend to encapsulate adjacent neurovascular anatomy, seed resection cavities, recur locally and respond poorly to radiotherapy and conventional chemotherapy, all of which make chordomas challenging to treat. Extent of surgical resection and adequacy of surgical margins are the most important prognostic factors and thus patients with chordoma should be cared for by a highly experienced, multi-disciplinary surgical team in a quaternary center. Ongoing research into the molecular pathophysiology of chordoma has led to the discovery of several pathways that may serve as potential targets for molecular therapy, including a multitude of receptor tyrosine kinases (e.g., platelet-derived growth factor receptor [PDGFR], epidermal growth factor receptor [EGFR]), downstream cascades (e.g., phosphoinositide 3-kinase [PI3K]/protein kinase B [Akt]/mechanistic target of rapamycin [mTOR]), brachyury—a transcription factor expressed ubiquitously in chordoma but not in other tissues—and the fibroblast growth factor [FGF]/mitogen-activated protein kinase kinase [MEK]/extracellular signal-regulated kinase [ERK] pathway. In this review article, the pathophysiology, diagnosis and modern treatment paradigms of chordoma will be discussed with an emphasis on the ongoing research and advances in the field that may lead to improved outcomes for patients with this challenging disease

Histogram demonstrating distribution of FRAIL scores in the patient cohort.

Histogram demonstrating distribution of FRAIL scores in the patient cohort.</p

Inpatient and post-discharge outcomes for patient cohort.

Inpatient and post-discharge outcomes for patient cohort.</p

Patient characteristics of patient cohort at time of admission to the hospital.

Patient characteristics of patient cohort at time of admission to the hospital.</p

Patient selection diagram.

Patient selection diagram.</p