Predicting Instability Risk Following Hemiarthroplasty for Femoral Neck Hip Fractures in Geriatric Patients.

BACKGROUND: Although a rare complication, dislocation following hemiarthroplasty (HA) for a femoral neck hip fracture is associated with increased mortality, readmission, and possible revision surgery. To date many of the specific risk factors have been difficult to demonstrate. Patient factors, surgical factors, as well as morphological factors need to be assessed. Therefore, the purpose of this study was to elucidate the risk factors for dislocation of HA following femoral neck hip fractures in the geriatric population. METHODS: This was a retrospective review of 270 patients who had hip fractures. Medical records between the years 2016 and 2022 informed binomial regression predictive models. The discriminative ability of variables in the final model and acetabular anteversion to predict dislocation was assessed with area under the curve (AUC) estimates. RESULTS: Center edge angle (odds ratio 1.23), abduction angle (odds ratio 1.17), and depth width ratio (2.96e-11) were significant predictors of dislocation (P = .003, .028, and <.001, respectively). Center edge angle and depth width ratio (<44.1 ° and .298), respectively, were cut scores for risk. Dementia had a high discriminative of ability, as did men (AUC = 0.617, 0.558, respectively). Acetabular anteversion was not predictive of dislocation (P = .259) and theorized anteversion safe zones had poor discriminative ability with AUCs of 0.510 and 0.503, respectively. CONCLUSIONS: Morphological factors related to hip dysplasia and a shallow acetabulum, which can be assessed with a radiograph alone, were found to be predictors of instability following HA in the elderly. Hemiarthroplasty implant design and manufacturer, and also acetabular version did not contribute to instability risk.

Contrasting roles of protein kinase C in induction versus suppression of group I mGluR-mediated epileptogenesis in vitro.

Activation of group I metabotropic glutamate receptors (mGluRs) elicits persistent ictaform discharges in guinea pig hippocampal slices, providing an in vitro model of epileptogenesis. The induction of these persistent ictaform bursts is prevented by l-cysteine sulfinic acid (CSA), an agonist at phospholipase D (PLD)-coupled mGluRs. Studies described herein examined the role of protein kinase C (PKC) in both the group I mGluR-mediated induction and CSA-mediated suppression of this form of epileptogenesis. Intracellular recordings were performed from CA3 stratum pyramidale and synchronized burst length was monitored. In the presence of 50 microM picrotoxin, a gamma-aminobutyric acid type A antagonist, 250- to 500-ms synchronized bursts were elicited. (S)-3,5-Dihydroxyphenylglycine (DHPG, 50 microM), an agonist at group I mGluRs, increased the burst length to 1-3 s in duration, a change that persisted after agonist washout. This persistent change in burst length was elicited in the presence of 10 microM chelerythrine, a PKC inhibitor, indicating that DHPG-induced epileptogenesis is PKC independent. However, although PLD activation with CSA (100 microM) was highly effective at suppressing group I mGluR-mediated induction of burst prolongation, CSA application in the presence of chelerythrine was no longer effective and resulted in the expression of persistent ictaform bursts. These data suggest that CSA-mediated suppression of group I mGluR-induced epileptogenesis is PKC dependent. We propose that CSA mediates its effect by PLD-driven activation of PKC, which may desensitize the phospholipase C-linked group I mGluRs and thereby prevent group I mGluR-induced epileptogenesis.