Lumbar Paraspinal Compartment Syndrome: Case Report and Critical Evaluation of the Literature.

BACKGROUND: Lumbar compartment syndrome is a recognized clinical phenomenon, despite receiving less attention as a clinical entity. Given its rarity, the definitive presentation, diagnosis, and management strategies are not completely agreed upon. MATERIALS AND METHODS: A literature search on PubMed of all case reports of lumbar paraspinal compartment syndromes was conducted. All case reports and reviews were analyzed for patient demographic data, presentation, diagnostic evaluation, treatment, and clinical follow-up. RESULTS: A total of 37 cases of lumbar compartment syndrome were identified. Overall, 91.9% occurred in men with an average age of 30.9 years. Weightlifting (n=18, 48.6%) and physical exertion (n=7, 18.9%) accounted for the majority of presentations. In all, 37.8% of cases occurred unilaterally. Creatinine kinase, aspartate aminotransferase, and alanine aminotransferase were notably elevated. Compartment pressure was elevated with an average of 91.8 mm Hg (SD: 44.8 mm Hg). Twenty-two cases were treated operatively (59.5%) and 15 (40.5%) were treated nonoperatively. In total, 19/20 (95.0%) of cases treated operatively reported either resolution of pain or return to baseline activities without limitation, compared with 1/11 (9.1%) treated nonoperatively. This difference between the operative and nonoperative cohort was statistically significant ( P <0.0001). CONCLUSIONS: Lumbar paraspinal compartment syndrome is a rare, but well-documented clinical entity. In all, 67.5% of cases occurred after weightlifting or physical exertion. Overall, 40.5% of cases in the literature were treated nonoperatively. Per our analysis, there is a clinically and statistically significant difference in cases treated operatively versus nonoperatively (95.0% vs. 9.1%, P <0.0001).

Nucleus pulposus cells synthesize a functional extracellular matrix and respond to inflammatory cytokine challenge following long-term agarose culture.

Intervertebral disc degeneration is characterized by a cascade of cellular, biochemical and structural changes that may lead to functional impairment and low back pain. Interleukin-1 beta (IL-1ß) is strongly implicated in the etiology of disc degeneration, however there is currently no direct evidence linking IL-1ß upregulation to downstream biomechanical changes. The objective of this study was to evaluate long-term agarose culture of nucleus pulposus (NP) cells as a potential in vitro model system to investigate this. Bovine NP cells were cultured in agarose for 49 days in a defined medium containing transforming growth factor-beta 3, after which both mechanical properties and composition were evaluated and compared to native NP. The mRNA levels of NP cell markers were compared to those of freshly isolated NP cells. Glycosaminoglycan (GAG) content, aggregate modulus and hydraulic permeability of mature constructs were similar to native NP, and aggrecan and SOX9 mRNA levels were not significantly different from freshly isolated cells. To investigate direct links between IL-1ß and biomechanical changes, mature agarose constructs were treated with IL-1ß, and effects on biomechanical properties, extracellular matrix composition and mRNA levels were quantified. IL-1ß treatment resulted in upregulation of a disintegrin and metalloproteinase with thrombospondin motifs 4, matrix metalloproteinase-13 and inducible nitric oxide sythase, decreased GAG and modulus, and increased permeability. To evaluate the model as a test platform for therapeutic intervention, co-treatment with IL-1ß and IL-1 receptor antagonist (IL-1ra) was evaluated. IL-1ra significantly attenuated degradative changes induced by IL-1ß. These results suggest that this in vitro model represents a reliable and cost-effective platform for evaluating new therapies for disc degeneration.

Loss of pin fixation in displaced supracondylar humeral fractures in children: causes and prevention.

BACKGROUND: Although the results are generally good following pin fixation of supracondylar humeral fractures in children, occasionally there is postoperative displacement. The purposes of the present study were to identify the causes leading to loss of fixation after pin fixation and to present methods for prevention. METHODS: We evaluated 322 displaced supracondylar humeral fractures that had been treated with percutaneous pin fixation. We examined fracture classification, pin configuration, intraoperative alignment after fixation, change in alignment after fixation, details of additional procedures, and final radiographic and clinical outcomes. RESULTS: Adequate radiographs were available for 279 of the 322 fractures. Eight (2.9%) of the 279 fractures were associated with postoperative loss of fixation; all eight were Gartland type-III fractures. Seven of these eight fractures initially had been treated with two lateral-entry pins, and one had been treated with two crossed pins. In patients with Gartland type-III fractures, loss of fixation was successfully avoided more often when three pins were used (with fixation being maintained in thirty-seven of thirty-seven patients) as opposed to when two lateral-entry pins were used (with fixation being maintained in thirty-five of forty-two patients) (p = 0.01). In all cases, loss of fixation was due to technical errors that were identifiable on the intraoperative fluoroscopic images and that could have been prevented with proper technique. We identified three types of pin-fixation errors: (1) failure to engage both fragments with two pins or more, (2) failure to achieve bicortical fixation with two pins or more, and (3) failure to achieve adequate pin separation (>2 mm) at the fracture site. CONCLUSIONS: Postoperative displacement following pin fixation of supracondylar humeral fractures in children is uncommon. In the present series, loss of fixation was most likely to occur when Gartland type-III fractures were treated with two lateral-entry pins. There were no failures when three pins were used. In all cases of failure, there were identifiable technical errors in pin placement. LEVEL OF EVIDENCE: Therapeutic Level III. See Instructions to Authors for a complete description of levels of evidence.

The value of dynamic radiographic myelography in addition to magnetic resonance imaging in detection lumbar spinal canal stenosis: A prospective study.

OBJECTIVE: MRI is regarded as the study of choice in the diagnosis of lumbar spinal stenosis. In some cases, the supine MRI leads to a misdiagnosis in the extent of lumbar spinal stenosis. Dynamic myelography can detect lumbar spinal stenosis in these cases of where the MRI may not be as sensitive. To compare the sensitivities of dynamic radiographic myelography and supine MRI in lumbar canal stenosis (LCS) patients and to determine whether dynamic radiographic myelography is a valuable diagnostic exam in the work-up of lumbar canal stenosis. PATIENTS & METHODS: Over two years, the imaging data of 100 consecutive patients who were suspected of having LCS were prospectively analyzed. All lumbar intervertebral segments were evaluated in each patient on sagittal MR T2-weighted images and lateral plane images by myelography using a semi-quantitative scoring system. The differences in scores for 5 motion segments under 3 conditions (supine MRI, upright sitting myelography and standing myelography with extension) were analyzed statistically. RESULTS: Of 100 patients with 500 analyzed intervertebral segments, 23 patients with inconclusive supine MRI results had LCS in standing myelography with extension. Compared with upright sitting myelography and supine MRI, standing myelography with extension yielded the highest score for every segment from L1/2 to L5/S1. Compared with the upright sitting myelography position, 61 more patients received a diagnosis of lumbar stenosis in the standing myelography with extension position, and 121 more stenotic segments were diagnosed. Compared with the supine MRI position, standing myelography with extension detected 64 more stenotic patients and 137 more stenotic segments. CONCLUSIO: n Based on a large patient sample, dynamic myelography is a valuable diagnostic tool in detecting lumbar spinal stenosis. Patients with lumbar spinal stenosis may have inconclusive supine MRI in 23% of cases being misdiagnosed as normal. This missed rate of LCS patients with unclear supine MRI results can be avoided with dynamic myelography. The combination of supine MRI and dynamic myelography is critical in the evaluation of LCS, especially if multisegmental findings are detected.

Translation of an engineered nanofibrous disc-like angle-ply structure for intervertebral disc replacement in a small animal model.

Intervertebral disc degeneration has been implicated in the etiology of low back pain; however, the current surgical strategies for treating symptomatic disc disease are limited. A variety of materials have been developed to replace disc components, including the nucleus pulposus (NP), the annulus fibrosus (AF) and their combination into disc-like engineered constructs. We have previously shown that layers of electrospun poly(ε-caprolactone) scaffold, mimicking the hierarchical organization of the native AF, can achieve functional parity with native tissue. Likewise, we have combined these structures with cell-seeded hydrogels (as an NP replacement) to form disc-like angle-ply structures (DAPS). The objective of this study was to develop a model for the evaluation of DAPS in vivo. Through a series of studies, we developed a surgical approach to replace the rat caudal disc with an acellular DAPS and then stabilized the motion segment via external fixation. We then optimized cell infiltration into DAPS by including sacrificial poly(ethylene oxide) layers interspersed throughout the angle-ply structure. Our findings illustrate that DAPS are stable in the caudal spine, are infiltrated by cells from the peri-implant space and that infiltration is expedited by providing additional routes for cell migration. These findings establish a new in vivo platform in which to evaluate and optimize the design of functional disc replacements.

IL-1ra delivered from poly(lactic-co-glycolic acid) microspheres attenuates IL-1ß-mediated degradation of nucleus pulposus in vitro.

INTRODUCTION: Inflammation plays a key role in the progression of intervertebral disc degeneration, a condition strongly implicated as a cause of lower back pain. The objective of this study was to investigate the therapeutic potential of poly(lactic-co-glycolic acid) (PLGA) microspheres loaded with interleukin-1 receptor antagonist (IL-1ra) for sustained attenuation of interleukin-1 beta (IL-1ß) mediated degradative changes in the nucleus pulposus (NP), using an in vitro model. METHODS: IL-1ra was encapsulated in PLGA microspheres and release kinetics were determined over 35 days. NP agarose constructs were cultured to functional maturity and treated with combinations of IL-1ß and media conditioned with IL-1ra released from microspheres at intervals for up to 20 days. Construct mechanical properties, glycosaminoglycan content, nitrite production and mRNA expression of catabolic mediators were compared to properties for untreated constructs using unpaired Student's t-tests. RESULTS: IL-1ra release kinetics were characterized by an initial burst release reducing to a linear release over the first 10 days. IL-1ra released from microspheres attenuated the degradative effects of IL-1ß as defined by mechanical properties, glycosaminoglycans (GAG) content, nitric oxide production and mRNA expression of inflammatory mediators for 7 days, and continued to limit functional degradation for up to 20 days. CONCLUSIONS: In this study, we successfully demonstrated that IL-1ra microspheres can attenuate the degradative effects of IL-1ß on the NP for extended periods. This therapeutic strategy may be appropriate for treating early-stage, cytokine-mediated disc degeneration. Ongoing studies are focusing on testing IL-1ra microspheres in an in vivo model of disc degeneration, as a prelude to clinical translation.

Proximal tibial osteochondromas in patients with fibrodysplasia ossificans progressiva.

BACKGROUND: Fibrodysplasia ossificans progressiva is a rare autosomal dominant disorder characterized by congenital malformation of the great toes and by progressive heterotopic ossification of skeletal muscle and soft connective tissues. The disorder is caused by a recurrent missense mutation in the glycine-serine activation domain of activin A receptor type I, a bone morphogenetic protein (BMP) type-I receptor, in all classically affected individuals. Osteochondromas of the proximal part of the tibia are benign osteochondral neoplasms or orthotopic lesions of skeletal remodeling associated with dysregulated BMP signaling and have been considered an atypical feature of fibrodysplasia ossificans progressiva, but they may be underdiagnosed because of their often asymptomatic nature. The purpose of the present study was to determine the prevalence and characteristics of proximal tibial osteochondromas in individuals who have fibrodysplasia ossificans progressiva. METHODS: Over a period of thirty months, we evaluated all patients with new and established fibrodysplasia ossificans progressiva for the presence of proximal tibial osteochondromas on the basis of medical history, physical examination, and radiographic studies. We quantified the prevalence of osteochondromas and characterized the types of osteochondromas to identify relevant trends. RESULTS: Ninety-six patients (including fifty-two female patients and forty-four male patients) with fibrodysplasia ossificans progressiva were evaluated on the basis of a history and physical examination. Plain radiographs were available for sixty-seven patients. Ninety percent of all patients had osteochondroma of the proximal part of the tibia. These lesions usually were asymptomatic, most commonly were bilateral, and typically were located at the pes anserinus. Seventy-five percent of the lesions were pedunculated, and 25% were sessile. CONCLUSIONS: Proximal tibial osteochondromas are a common phenotypic feature of fibrodysplasia ossificans progressiva, a finding that expands the recognized consequences of recurrent activating mutations in activin A receptor type I to include not only congenital skeletal malformations and heterotopic skeletogenesis but also benign osteochondral neoplasms or orthotopic lesions of skeletal modeling. The present study provides insight into the genetic basis of osteochondroma formation in patients with fibrodysplasia ossificans progressiva and possibly into that of more common conditions in which these lesions occur.