The role of fibular fixation in patients with distal tibia fractures is controversial. Although the stability of the fibula is critical in patients with syndesmotic instability or highly comminuted pilon fractures, fibular fixation in extraarticular distal tibia fractures or elementary intraarticular distal tibia fractures is more controversial. Biomechanical studies, as performed in sawbones or cadaveric models, denote advantages to fibular fixation with respect to specific uniplanar motion. However, the increased stability is susceptible to the fracture pattern of the tibia, fixation strategy for the tibia, fixation strategy for the fibula, and loading pattern of the entire construct. Clinical studies examining fibular fixation in patients with concomitant distal third tibia fractures have also not been definitive in their conclusions. Fibular fixation may improve the ability to obtain and maintain reduction in complex fractures of the distal tibia, but as a result of the increased stability of the construct, may also increase rates of nonunion in this challenging patient population.
Objective To examine the incidence and risk factors of any-cause reoperation after primary ACLR in children and adolescents. Design Retrospective Cohort Setting Electronic medical records from a large tertiary care, single institution integrated healthcare delivery system. Patients Patients were under the age of 18 years and had anterior cruciate ligament reconstruction. They were excluded if they had a multi-ligamentous knee injury or <1 year follow-up. Interventions Patients were further identified to have undergone a subsequent knee operation ipsilaterally or contralateral ACLR. Main outcome measures The rate of any-cause reoperation was our primary outcome measure. Results The median age was 16. There were 208 females (53.9%) and 178 males (46.1%) included. The median follow-up was 25 months with a minimum of 12 months (interquartile range: 16.0, 46.0). The rate of any-cause reoperation was 34.7%. There was no statistically significant difference between those who underwent reoperation versus those who did not undergo reoperation relative to age, sex, BMI, graft type, or the presence of concomitant meniscal injury. The rates of ipsilateral ACLR and contralateral ACLR at any time during the study period was 8.0% and 10.9% respectively. There was no statistically significant difference for rate of reoperation between graft types, between various concomitant injuries, between those who underwent meniscus repair or no repair. Conclusions This study reflects a 34.7% rate of a subsequent knee operation after ACLR in patients younger than 18 years. These findings can be used to inform pediatric patients undergoing primary ACLR on their risk of returning to the operating room.
Hyperglycemia is causally related to the vascular complications of diabetes. This patho‐physiological process may be mediated by the activation of protein kinase C (PKC) beta II resulting in an increased oxidative stress and inflammatory response. However, the role of a PKC beta II inhibitor regulating hyperglycemia‐induced endothelial‐leukocyte interactions has not been evaluated in vivo in real‐time. The effect of PKC beta II peptide inhibitor on leukocyte‐endothelial interactions in rat mesenteric postcapillary venule circulation was determined by using intravital microscopy. We found that intraperitoneal injection of 25 mM D‐glucose (2.5 ml, n=6) caused intraperitoneal hyperglycemia and exhibited significantly higher leukocyte rolling, adherence, and transmigration compared to control rats which were intraperitoneal injection of saline (2.5 ml, n=4, P<0.05). By contrast, intraperitoneal injection of D‐glucose with 10 mM PKC beta II inhibitor (12.5 μl, n=3/25.0 μl, n=6) induced the similar intraperitoneal hyperglycemia, but showed significantly less leukocyte‐endothelial interactions compared to D‐glucose injection (P<0.05). In summary, the PKC beta II inhibitor attenuates local hyperglycemia‐induced leukocyte‐endothelial interactions, which may be related to the attenuation of oxidative stress in blood. This study was supported by Center for Chronic Disorders of Aging at PCOM.
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