Study Design. A retrospective review study. Objective. This study aims to determine the effect of osteoporosis on spine instrumentation. Summary of Background Data. Osteoporosis is a common skeletal pathology that affects systemic cortical bone maintenance and remodeling. This disease accelerates the degeneration of the spine, often necessitating spinal surgery for progressive vertebral deformity, pathologic fracture, bony canal stenosis, and/or neural element decompression. There is a paucity of literature describing the role of osteoporosis as it relates to both perioperative complications and outcomes after spine fusion surgery. Materials and Methods. A retrospective review was conducted of a prospectively maintained database for patients undergoing spine surgery between January 1, 2006 and October 3, 2017. Inclusion criteria included age 18 years and above and surgery performed for the correction of thoracolumbar scoliosis. Data collected included various demographic, clinical, and operative variables. Results. A total of 532 patients met inclusion criteria, including 144 (27%) patients with a diagnosis of osteoporosis. Osteoporosis was significantly associated with increased blood volume loss (P=0.003). Postoperatively, osteoporosis was associated with increased rates of instrumentation failure (19% vs. 10%; P=0.008) and the need for revision surgery (33% vs. 16%; P<0.001). Multivariate analysis confirmed osteoporosis to be an independent risk factor for increased mean number of spinal segments fused (P<0.05), mean blood volume loss (P<0.05), rate of postoperative deep venous thrombosis/pulmonary embolism (P<0.05), rate of instrumentation failure (P<0.05), and need for revision surgery (P<0.05). Conclusion. Osteoporosis is a significant risk factor for instrumentation failure and need for revision surgery following arthrodesis for scoliosis correction. Furthermore, patients with osteoporosis have a significantly higher risk of intraoperative blood volume loss and postoperative thromboembolic events.

Spinal epidural lipomatosis (SEL) is a common pathology of the lumbar spine. While the natural history is not well understood, there is a strong association with metabolic syndrome and endocrine dysfunction. Clinical presentation typically involves slow, progressive onset of radicular and myelopathic symptoms. Treatment primarily consists of weight loss, while surgery is reserved for refractory cases or acute cauda equina syndrome. We present a case of acute spinal cord injury (SCI) after trauma with underlying SEL in the cervicothoracic spine. Additionally, a literature review using a MEDLINE search of the English literature through April 2020 following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was performed to identify all documented cases of acute spinal cord injury with underlying SEL. A 72-year-old obese male with insulin-dependent diabetes mellitus presented with subacute bilateral lower extremity weakness after a fall with a flank injury three days prior to evaluation. Within hours of admission, the patient acutely progressed to paraplegia and sensory loss below the T6 level consistent with an ASIA (American Spinal Injury Association) A spinal cord injury. No fracture or dislocation was identified on CT imaging. MRI of the thoracic spine revealed spinal cord compression secondary to extensive posterior epidural lipomatosis with resultant anterior displacement of the thecal sac. The patient underwent emergent T2-T9 laminectomy for decompression. Post-operatively, the patient regained sensation below the level of injury. A review of the literature reviewed no published articles on cases of complete spinal cord injury secondary to underlying SEL without associated fracture. Finally, we present the first report of an acute spinal cord injury in the setting of SEL without fracture. Our case demonstrates that SEL outside the lumbar spine confers increased risk for SCI following trauma. Patients with cervicothoracic SEL may require close neurological observation and timely surgical decompression.

Background: Hereditary angioedema (HAE) due to C1-inhibitor (C1-INH) deficiency is a rare genetic disorder characterized by disabling episodes of edema that commonly affect the skin as well as the gastrointestinal tract and upper airway. Prophylactic therapy can decrease the severity and number of attacks. Long-term symptom control and rescue medication use were evaluated in patients with HAE who received subcutaneous (SC) C1-INH enrolled in an open-label extension (OLE) of the phase III COMPACT (Clinical Studies for Optimal Management of Preventing Angioedema with Low-Volume Subcutaneous C1-Inhibitor Replacement Therapy) trial, including a subgroup analysis of patients treated for ≥12 months. Methods: The OLE study evaluated patients ≥ 6 years old who had had four or more attacks over 2 consecutive months before enrollment. Patients naive for C1-INH (SC) and patients in the COMPACT rollover trial were included. The patients were randomized to receive C1-INH (SC) 40 or 60 IU/kg twice weekly for 52 weeks. U.S. patients were eligible to continue for up to 140 weeks. Results: A total of 63 patients were randomized to the U.S. Food and Drug Administration approved dose of 60 IU/kg; 24 subjects were treated for at least 12 months. For the 63 subjects, the median (range) attacks per month were 0.09 (0.0‐4.0) and per year were 1.0 (0.0‐48.0). Two-thirds of the patients used rescue medication fewer than once per year. For the 24 patients with ≥ 12 months of exposure, the median (range) attacks per month and per year were 0.017 (0.000-2.4) and 0.199 (0.000-28.94), respectively. Of these patients, 12 (50%) were attack free throughout the duration of the study, and 3 (12.5%) had fewer than one attack per year. Conclusion: Prophylaxis with C1-INH (SC) provided sustained reductions in attack frequency and decreased rescue medication use, with a substantial proportion of patients being attack free.

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