The role of pre-reduction MRI in the management of complex cervical spine fracture-dislocations: an ongoing controversy?

BACKGROUND: Cervical spine fracture-dislocations in neurologically intact patients represent a surgical challenge due to the risk of inflicting iatrogenic spinal cord compression by closed reduction maneuvers. The use of MRI for early advanced imaging in these injuries remains controversially debated. CASE PRESENTATION: A 54-year old man sustained a fall over the handlebars of his racing bicycle. The helmeted patient sustained a fall on his head which resulted in a hyperflexion injury of the neck. He was neurologically intact on presentation. Initial CT imaging revealed a complex multisegmental cervical spine injury with a left-sided C6/C7 perched facet, a right sided C7/T1 fracture-dislocation, and a right-sided C6 and C7 traumatic laminotomy. The initial management consisted of temporary external Halo fixator application without closed reduction maneuver, to mitigate the risk of a delayed spinal cord injury. Subsequent advanced imaging by MRI revealed an acute traumatic C7/T1 disc herniation, with the intervertebral disc completely extruded into the spinal canal. Definitive surgical management was then accomplished by employing a three-stage anterior-posterior-anterior spinal decompression, realignment, fixation and fusion C4-T2 in one operative session. The patient recovered well and retained full neurological function. He resumed bicycle street racing within 10 months of the injury following successful spinal reconstruction. CONCLUSIONS: The diagnostic evaluation of cervical fracture-dislocations should include advanced imaging by MRI in order to fully understand the injury pattern prior to proceeding with spinal reduction maneuvers which may impose the imminent threat of a devastating iatrogenic injury to the spinal cord. The presented staged management by initial Halo fixation without attempts for spinal reduction, followed by a surgical decompression and multilevel fusion, appears to represent a feasible and safe strategy for patients at risk of a delayed neurological injury.

Heterotopic ossification in the reaming tract of a percutaneous antegrade femoral nail: a case report.

INTRODUCTION: Heterotopic ossification is a rare complication of musculoskeletal injuries, characterized by bone growth in soft tissues. Percutaneous antegrade intramedullary nailing represents the 'gold standard' for the treatment of femur shaft fractures. Minor bone growth is frequently seen around the proximal end of reamed femoral nails (so-called 'callus caps'), which are asymptomatic and lack a therapeutic implication. The occurrence of excessive, symptomatic heterotopic ossification around the entry site of an antegrade femoral nail is rarely described in the literature. CASE PRESENTATION: We present the case of a 28-year-old Caucasian woman who developed extensive heterotopic ossification around the reaming seeds of a reamed femoral nail. She developed severe pain and significantly impaired range of motion of the hip joint, requiring revision surgery for heterotopic ossification resection and adjunctive local irradiation. She recovered full function of the hip and remained asymptomatic at her two-year follow-up appointment. CONCLUSIONS: Severe heterotopic ossification represents a rare but potentially detrimental complication after percutaneous femoral nailing of femur shaft fractures. Diligent care during the reaming procedure, including placement of a trocar to protect from osteogenic seeding of the soft tissues, may help decrease the risk of developing heterotopic ossification after reamed antegrade femoral nailing.

Aseptic loosening of pedicle screw as a result of metal wear debris in a pediatric patient.

STUDY DESIGN: This is a case report. OBJECTIVE: To report a case of soft-tissue reaction to wear debris and osteolysis around a pedicle screw after posterior spine fusion in a pediatric patient. SUMMARY OF BACKGROUND DATA: Posterior spine fusion with instrumentation is a standard procedure for stabilization and curve correction in patients with scoliosis. Late operative site pain accounts for the highest frequency of reoperation. Debris accumulation for steel and titanium constructs occurs at the pedicle screw-rod junction. Cellular reaction to metal wear may be responsible for osteolysis and aseptic loosening around spinal implants. METHODS: A 14-year-old male patient with neurofibromatosis and right thoracic scoliosis of 50° underwent posterior spine fusion from T2 to T10. The postoperative course was complicated by continuous pain, and imaging studies demonstrated hardware failure, requiring a revision and subsequent development of a perihilar opacity of unknown origin. Further studies demonstrated hypermobility with adjacent soft-tissue reactivity and inflammation surrounding the right T5 transpedicle screw. RESULTS: After hardware removal, the patient's recovery was uneventful. Six months later, a repeated computed tomographic scan demonstrated resolution of the previously described soft-tissue mass and a satisfactory fusion of the thoracic spine. CONCLUSION: Metal wear debris can form in pediatric patients during the healing process after spinal fusions or when pseudarthrosis is present. Clinically, this manifests as back pain with a possible aseptic inflammatory abscess. Hardware removal can achieve resolution of symptoms and regression of inflammation.

Unusual spine anatomy contributing to wrong level spine surgery: a case report and recommendations for decreasing the risk of preventable 'never events'.

BACKGROUND: Wrong site surgery is one of five surgical "Never Events," which include performing surgery on the incorrect side or incorrect site, performing the wrong procedure, performing surgery on the wrong patient, unintended retention of a foreign object in a patient, and intraoperative/immediate postoperative death in an ASA Class I patient. In the spine, wrong site surgery occurs when a procedure is performed on an unintended vertebral level. Despite the efforts of national safety protocols, literature suggests that the risk for wrong level spine surgery remains problematic. CASE PRESENTATION: A 34-year-old male was referred to us to evaluate his persistent thoracic pain following right-sided microdiscectomy at T7-8 at an outside institution. Postoperative imaging showed the continued presence of a herniated disc at T7-8 and evidence of a microdiscectomy at the level immediately above. The possibility that wrong level surgery had occurred was discussed with the patient and revision surgery was planned. During surgery, the site of the previous laminectomy was clearly visualized; however, we also experienced confusion when verifying the level of the previous surgery. We ultimately used the previous laminectomy site as a landmark for identifying and treating the correct pathologic level. Postoperative consultation with Musculoskeletal Radiology revealed the patient had two abnormalities in his spinal anatomy that made intraoperative counting of levels inaccurate, including a pair of cervical ribs at C7 and the absence of a pair of thoracic ribs. CONCLUSION: This case highlights the importance of strict adherence to a preoperative method of vertebral labeling that focuses on the landmarks used to label a pathologic disc space, rather than simply relying on the reference to a particular level. That is, by designating the pathological level as the disc space associated with the fourth rib up from the last rib-bearing vertebrae, rather than calling it "T7-8", then the correct level can be found intraoperatively even in the case of abnormal segmentation. We recommend working closely with radiology during preoperative planning to identify unusual anatomy that may have been overlooked. We also recommend that radiology colleagues use the same system of identifying pathological levels when dictating their reports. Together, these strategies can reduce the risk of wrong level surgery and increase patient safety.

Facet joint biomechanics at the treated and adjacent levels after total disc replacement.

STUDY DESIGN: Biomechanical study using human cadaveric lumbar spines. OBJECTIVE: To evaluate effects of total disc replacement (TDR) on spine biomechanics at the treated and adjacent levels. SUMMARY OF BACKGROUND DATA: Previous studies on spine biomechanics after TDR were focused on facet forces and range of motion and report contradictory results. Characterization of contact pressure, peak contact pressure, force, and peak force before and after TDR may lead to a better understanding of facet joint function and may aid in prediction of long-term outcomes after TDR. METHODS: Seven fresh-frozen human cadaveric lumbar spines were potted at T12 and L5 and installed in a 6 degrees of freedom displacement-controlled testing system. Displacements of 15° flexion/extension, 10° right/left bending, and 10° right/left axial rotation were applied. Contact pressure, peak contact pressure, force, peak force, and contact area for each facet joint were recorded at L2-L3 and L3-L4 both before and after TDR at L3-L4. The data were analyzed with analysis of variance and t tests. RESULTS: Axial rotation had the most impact on contact pressure, peak contact pressure, force, peak force, and contact area in intact spines. During lateral bending and axial rotation, TDR resulted in a significant increase in facet forces at the level of treatment and a decrease in contact pressure, peak contact pressure, and peak force at the level superior to the TDR. With flexion/extension, there was a decrease in peak contact pressure and peak contact force at the superior level. CONCLUSION: Our study demonstrates that rotation is the most demanding motion for the spine. We also found an increase in facet forces at the treated level after TDR. We are the first to show a decrease in several biomechanical parameters after TDR at the adjacent superior level. In general, our findings suggest there is an increase in loading of the facet joints at the level of disc implantation and an overall unloading effect at the level above.

Arthroplasty in veterans: analysis of cartilage, bone, serum, and synovial fluid reveals differences and similarities in osteoarthritis with and without comorbid diabetes.

Osteoarthritis patients with diabetes who receive total knee arthroplasty are more vulnerable to complications, including aseptic loosening and need for revision surgery. To elucidate mechanisms related to arthroplasty failure in diabetes, we examined serum and synovial fluid markers as well as collagen crosslinks in bone and cartilage of 20 patients (10 with diabetes, 10 controls without) undergoing this procedure. Hemoglobin A1c, body mass index, bone alkaline phosphatase, leptin, osteocalcin, and pyridinium were analyzed along with tissue content of the crosslinks hydroxylysylpyridinoline, lysylpyridinoline, and pentosidine. Pentosidine levels in tissue specimens from diabetic subjects were higher than in control subjects. Osteocalcin levels negatively correlated with hydroxylysylpyridinoline levels in cartilage. Osteocalcin levels also negatively correlated with pentosidine levels in cartilage, but only in subjects with diabetes. This study suggests potential metabolic mechanisms for arthroplasty failure in patients with diabetes.

High rectal injury during trans-1 axial lumbar interbody fusion L5-S1 fixation: a case report.

STUDY DESIGN: A case report. OBJECTIVE: To report a case of high rectal injury during trans-1 axial Lumbar Interbody Fusion (axiaLIF) L5-S1 fixation. SUMMARY OF BACKGROUND DATA: Trans-1 axiaLIF procedure is gaining in popularity for L5-S1 fusion due to the ease of access to the sacrum through the presacral space. Normally, the midline of the sacrum at S1-S2 is relatively free from neurovascular and intra-abdominal structures, making this level a safe entry point for the axiaLIF procedure. We report a case of high rectal injury during Trans-1 axiaLIF L5-S1 procedure due to altered intra-abdominal anatomy as a result of multifactorial adhesions formation. METHODS: A 44-year-old female patient with a history of previous anterior and posterior spinal surgeries, pelvic inflammatory disease, and non-disclosed previous diverticulitis, developed a high rectal injury during Trans-1 axiaLIF L5-S1 fixation. RESULTS: After Trans-1 axiaLIF L5-S1, the patient presented with an episode of melena and hypogastric pain with nausea and vomiting. A computed tomography (CT) scan of the abdomen with intravenous and oral contrast showed presacral soft tissue fluid density with fat stranding and extraluminal rectal contrast and gas with some areas of soft tissue enhancement compatible with probable high rectal perforation. Patient's symptoms gradually subsided during a period of 6 months with aid from a temporary diverting ileostomy and a course of i.v. antibiotics. No spine implants were removed. CONCLUSION: We report a case of high rectal injury during Trans-1 axiaLIF L5-S1 fixation and strongly advice that patients who are candidates for this surgery and have any risk factors for intra-abdominal adhesion formation, undergo a pelvic CT with rectal contrast before the surgery to evaluate for any signs of altered rectal-sacral anatomy.

Bone inflammation and altered gene expression with type I diabetes early onset.

Type I diabetes is associated with bone loss and marrow adiposity. To identify early events involved in the etiology of diabetic bone loss, diabetes was induced in mice by multiple low dose streptozotocin injections. Serum markers of bone metabolism and inflammation as well as tibial gene expression were examined between 1 and 17 days post-injection (dpi). At 3 dpi, when blood glucose levels were significantly elevated, body, fat pad and muscle mass were decreased. Serum markers of bone resorption and formation significantly decreased at 5 dpi in diabetic mice and remained suppressed throughout the time course. An osteoclast gene, TRAP5 mRNA, was suppressed at early and late time points. Suppression of osteogenic genes (runx2 and osteocalcin) and induction of adipogenic genes (PPARgamma2 and aP2) were evident as early as 5 dpi. These changes were associated with an elevation of serum cytokines, but more importantly we observed an increase in the expression of cytokines in bone, supporting the idea that bone, itself, exhibits an inflammatory response during diabetes induction. This inflammation could in turn contribute to diabetic bone pathology. IFN-gamma (one of the key cytokines elevated in bone and known to be involved in bone regulation) deficiency did not prevent diabetic bone pathology. Taken together, our findings indicate that bone becomes inflamed with the onset of T1-diabetes and during this time bone phenotype markers become altered. However, inhibition of one cytokine, IFN-gamma was not sufficient to prevent the rapid bone phenotype changes.

Bone loss and increased bone adiposity in spontaneous and pharmacologically induced diabetic mice.

Insulin-dependent diabetes mellitus (IDDM) is associated with increased risk of osteopenia/osteoporosis in humans. The mechanisms accounting for diabetic bone loss remain unclear. Pharmacologic inducers of IDDM, such as streptozotocin, mimic key aspects of diabetes in rodents, allow analysis at the onset of diabetes, and induce diabetes in genetically modified mice. However, side effects of streptozotocin, unrelated to diabetes, can complicate data interpretation. The nonobese diabetic (NOD) mouse model develops diabetes spontaneously without external influences, negating side effects of inducing agents. Unfortunately, in this model the onset of diabetes is unpredictable, occurs in a minority of male mice, and can only be studied in a single mouse strain. To validate the relevance of the more flexible streptozotocin-induced diabetes model for studying diabetes-associated bone loss, we compared its phenotype to the spontaneously diabetic NOD model. Both models exhibited hyperglycemia and loss of body, fat pad, and muscle weight. Furthermore, these genetically different and distinct models of diabetes induction demonstrated similar bone phenotypes marked by significant trabecular bone loss and increased bone marrow adiposity. Correspondingly, both diabetic models exhibited decreased osteocalcin mRNA and increased adipocyte fatty acid-binding protein 2 mRNA levels in isolated tibias and calvaria. Taken together, multiple streptozotocin injection-induced diabetes is a valid model for understanding the acute and chronic pathophysiologic responses to diabetes and their mechanisms in bone.

Inhibition of PPARgamma prevents type I diabetic bone marrow adiposity but not bone loss.

Diabetes type I is associated with bone loss and increased bone adiposity. Osteoblasts and adipocytes are both derived from mesenchymal stem cells located in the bone marrow, therefore we hypothesized that if we could block adipocyte differentiation we might prevent bone loss in diabetic mice. Control and insulin-deficient diabetic BALB/c mice were chronically treated with a peroxisomal proliferator-activated receptor gamma (PPARgamma) antagonist, bisphenol-A-diglycidyl ether (BADGE), to block adipocyte differentiation. Effects on bone density, adiposity, and gene expression were measured. BADGE treatment did not prevent diabetes-associated hyperglycemia or weight loss, but did prevent diabetes-induced hyperlipidemia and effectively blocked diabetes type I-induced bone adiposity. Despite this, BADGE treatment did not prevent diabetes type I suppression of osteoblast markers (runx2 and osteocalcin) and bone loss (as determined by micro-computed tomography). BADGE did not suppress osteoblast gene expression or bone mineral density in control mice, however, chronic (but not acute) BADGE treatment did suppress osteocalcin expression in osteoblasts in vitro. Taken together, our findings suggest that BADGE treatment is an effective approach to reduce serum triglyceride and free fatty acid levels as well as bone adiposity associated with type I diabetes. The inability of BADGE treatment to prevent bone loss in diabetic mice suggests that marrow adiposity is not linked to bone density status in type I diabetes, but we cannot exclude the possibility of additional BADGE effects on osteoblasts or other bone cells, which could contribute to preventing the rescue of the bone phenotype.

Chronic hyperglycemia modulates osteoblast gene expression through osmotic and non-osmotic pathways.

Insulin dependent diabetes mellitus (IDDM; type I) is a chronic disease stemming from little or no insulin production and elevated blood glucose levels. IDDM is associated with osteoporosis and increased fracture rates. The mechanisms underlying IDDM associated bone loss are not known. Previously we demonstrated that osteoblasts exhibit a response to acute (1 and 24 h) hyperglycemia and hyperosmolality. Here we examined the influence of chronic hyperglycemia (30 mM) and its associated hyperosmolality on osteoblast phenotype. Our findings demonstrate that osteoblasts respond to chronic hyperglycemia through modulated gene expression. Specifically, chronic hyperglycemia increases alkaline phosphatase activity and expression and decreases osteocalcin, MMP-13, VEGF and GAPDH expression. Of these genes, only MMP-13 mRNA levels exhibit a similar suppression in response to hyperosmotic conditions (mannitol treatment). Acute hyperglycemia for a 48-h period was also capable of inducing alkaline phosphatase and suppressing osteocalcin, MMP-13, VEGF, and GAPDH expression in differentiated osteoblasts. This suggests that acute responses in differentiated cells are maintained chronically. In addition, hyperglycemic and hyperosmotic conditions increased PPARgamma2 expression, although this increase reached significance only in 21 days chronic glucose treated cultures. Given that osteocalcin is suppressed and PPARgamma2 expression is increased in type I diabetic mouse model bones, these findings suggest that diabetes-associated hyperglycemia may modulate osteoblast gene expression, function and bone formation and thereby contribute to type I diabetic bone loss.

Increased bone adiposity and peroxisomal proliferator-activated receptor-gamma2 expression in type I diabetic mice.

Decreased bone mass, osteoporosis, and increased fracture rates are common skeletal complications in patients with insulin-dependent diabetes mellitus (IDDM; type I diabetes). IDDM develops from little or no insulin production and is marked by elevated blood glucose levels and weight loss. In this study we use a streptozotocin-induced diabetic mouse model to examine the effect of type I diabetes on bone. Histology and microcomputed tomography demonstrate that adult diabetic mice, exhibiting increased plasma glucose and osmolality, have decreased trabecular bone mineral content compared with controls. Bone resorption could not completely account for this effect, because resorption markers (tartrate-resistant acid phosphatase 5b, urinary deoxypyridinoline excretion, and tartrate-resistant acid phosphatase 5 mRNA) are unchanged or reduced at 2 and/or 4 wk after diabetes induction. However, osteocalcin mRNA (a marker of late-stage osteoblast differentiation) and dynamic parameters of bone formation were decreased in diabetic tibias, whereas osteoblast number and runx2 and alkaline phosphatase mRNA levels did not differ. These findings suggest that the final stages of osteoblast maturation and function are suppressed. We also propose a second mechanism contributing to diabetic bone loss: increased marrow adiposity. This is supported by increased expression of adipocyte markers [peroxisome proliferator-activated receptor gamma2, resistin, and adipocyte fatty acid binding protein (alphaP2)] and the appearance of lipid-dense adipocytes in diabetic tibias. In contrast to bone marrow, adipose stores at other sites are depleted in diabetic mice, as indicated by decreased body, liver, and peripheral adipose tissue weights. These findings suggest that IDDM contributes to bone loss through changes in marrow composition resulting in decreased mature osteoblasts and increased adipose accumulation.

P38 and activating transcription factor-2 involvement in osteoblast osmotic response to elevated extracellular glucose.

Poorly controlled or untreated type I diabetes mellitus is characterized by hyperglycemia and is associated with decreased bone mass and osteoporosis. We have demonstrated that osteoblasts are sensitive to hyperglycemia-associated osmotic stress and respond to elevated extracellular glucose or mannitol by increasing c-jun and collagen I expression. To determine whether MAPKs are involved in this response, MC3T3-E1 osteoblasts were treated with 16.5 mm glucose, mannitol, or contrast dye for 1 h. Immunoblotting of phosphorylated p38 demonstrated activation of p38 MAPK by hyperosmotic stress in vitro and in vivo. Activation peaked at 20 min, remained detectable after 24 h, and was protein kinase C-independent. Activating transcription factor-2 (ATF-2) activation followed the same pattern as phospho-p38. Transactivation of cAMP response element (CRE)- and c-jun promoter (containing a CRE-like element)-reporter constructs increased following hyperosmotic treatment. SB 203580 (a p38 MAPK inhibitor) blocked ATF-2 phosphorylation, CRE transactivation, and c-jun promoter activation. Hyperosmotic activation of collagen I promoter activity was also inhibited by SB 203580, consistent with the involvement of c-jun in collagen I up-regulation. Therefore, we propose that hyperglycemia-induced increases in p38 MAPK activity and ATF-2 phosphorylation contribute to CRE activation and modulation of c-jun and collagen I expression in osteoblasts.