Can we predict failure of percutaneous fixation of femoral neck fractures?

PURPOSE: This study evaluated a series of geriatric femoral neck fracture treated with closed reduction percutaneous pinning (CRPP) at a single level-1 trauma center to determine if there are any simple, reliable, radiographic characteristics that can be used to predict increased risk of post-operative failure in nondisplaced and valgus impacted fracture patterns. METHODS: We conducted a retrospective cohort study of all patients with femoral neck fractures (AO/OTA 31B) who underwent CRPP over a 12-year period at a single Level 1 trauma center. Failure was defined as radiographic failure within the first year after the index operation requiring revision surgery. Common patterns identified on initial review were the presence of a visible medial transcervical line (MTL) felt to indicate a tension-sided failure, a straight inferior calcar (SIC) indicating severe valgus impaction, and quality of intra-operative screw positioning. X-rays of patients were then reviewed for these characteristics in a blinded manner by three different trauma-fellowship trained orthopedic surgeons. Inter-rater reliability was calculated using Fleiss' Kappa Coefficient. Comparisons of failure rates between groups were made using a Fisher's Exact test. RESULTS: 139 patients who underwent CRPP for a femoral neck fracture and follow-up for at least 90 days were identified and reviewed. There were a total of 19 failures (13.6%) within one year. The patients with a varus fracture had a failure rate of 9/24 (37.5%). Of the valgus/nondisplaced fractures, MTL was identified in 42/115 (36%) patients. Inter-rater agreement was high for the presence of an MTL (84%, Kappa 0.69). Patients with an MTL had a fourfold increase in risk of failure (7/42=17% with an MTL vs. 3/73=4% without, p  0.03). The presence of a SIC and quality of screw placement were not predictive of failure. CONCLUSION: Varus femoral neck fractures fixed with CRPP have a high rate of failure (37.5%). Nondisplaced or valgus impacted fractures with the presence of a visible medial transcervical line on pre-operative radiographic imaging resulted in a fourfold increase in the risk of failure after CRPP. Identification of the MTL will help treating surgeons better council patients when making pre-operative decisions between arthroplasty and CRPP.

Medial pelvic migration of the lag screw in a short gamma nail after hip fracture fixation: a case report and review of the literature.

Hip fractures are a common injury among the elderly. Internal fixation with an intramedullary (IM) system has gained popularity for the treatment of intertrochanteric femur fractures. Multiple complications associated with IM fracture fixation have been described, however, we report a rare complication of medial pelvic migration of the lag screw of a short IM nail in a stable construct ten weeks post surgery. The patient was subsequently treated with Lag Screw removal and revision surgery with a shorter Lag Screw and an accessory cannulated screw acting as a de-rotational device. The patient did well with the revision surgery and was able to return to full activities.

A functional screen implicates microRNA-138-dependent regulation of the depalmitoylation enzyme APT1 in dendritic spine morphogenesis.

The microRNA pathway has been implicated in the regulation of synaptic protein synthesis and ultimately in dendritic spine morphogenesis, a phenomenon associated with long-lasting forms of memory. However, the particular microRNAs (miRNAs) involved are largely unknown. Here we identify specific miRNAs that function at synapses to control dendritic spine structure by performing a functional screen. One of the identified miRNAs, miR-138, is highly enriched in the brain, localized within dendrites and negatively regulates the size of dendritic spines in rat hippocampal neurons. miR-138 controls the expression of acyl protein thioesterase 1 (APT1), an enzyme regulating the palmitoylation status of proteins that are known to function at the synapse, including the alpha(13) subunits of G proteins (Galpha(13)). RNA-interference-mediated knockdown of APT1 and the expression of membrane-localized Galpha(13) both suppress spine enlargement caused by inhibition of miR-138, suggesting that APT1-regulated depalmitoylation of Galpha(13) might be an important downstream event of miR-138 function. Our results uncover a previously unknown miRNA-dependent mechanism in neurons and demonstrate a previously unrecognized complexity of miRNA-dependent control of dendritic spine morphogenesis.

The Rac1 guanine nucleotide exchange factor Tiam1 mediates EphB receptor-dependent dendritic spine development.

Dendritic spines are small, actin-rich protrusions on the surface of dendrites that receive the majority of excitatory synaptic inputs in the brain. The formation and remodeling of spines, processes that underlie synaptic development and plasticity, are regulated in part by Eph receptor tyrosine kinases. However, the mechanism by which Ephs regulate actin cytoskeletal remodeling necessary for spine development is not fully understood. Here, we report that the Rac1 guanine nucleotide exchange factor Tiam1 interacts with the EphB2 receptor in a kinase-dependent manner. Activation of EphBs by their ephrinB ligands induces the tyrosine phosphorylation and recruitment of Tiam1 to EphB complexes containing NMDA-type glutamate receptors. Either knockdown of Tiam1 protein by RNAi or inhibition of Tiam1 function with a dominant-negative Tiam1 mutant blocks dendritic spine formation induced by ephrinB1 stimulation. Taken together, these findings suggest that EphBs regulate spine development in part by recruiting, phosphorylating, and activating Tiam1. Tiam1 can then promote Rac1-dependent actin cytoskeletal remodeling required for dendritic spine morphogenesis.

A brain-specific microRNA regulates dendritic spine development.

MicroRNAs are small, non-coding RNAs that control the translation of target messenger RNAs, thereby regulating critical aspects of plant and animal development. In the mammalian nervous system, the spatiotemporal control of mRNA translation has an important role in synaptic development and plasticity. Although a number of microRNAs have been isolated from the mammalian brain, neither the specific microRNAs that regulate synapse function nor their target mRNAs have been identified. Here we show that a brain-specific microRNA, miR-134, is localized to the synapto-dendritic compartment of rat hippocampal neurons and negatively regulates the size of dendritic spines--postsynaptic sites of excitatory synaptic transmission. This effect is mediated by miR-134 inhibition of the translation of an mRNA encoding a protein kinase, Limk1, that controls spine development. Exposure of neurons to extracellular stimuli such as brain-derived neurotrophic factor relieves miR-134 inhibition of Limk1 translation and in this way may contribute to synaptic development, maturation and/or plasticity.