Introduction

Intracapsular fractures of the femoral neck in young adults are a surgical emergency. Recent literature reviews have questioned whether the timing of surgery reduces the incidence of avascular necrosis, non-union and revision.

A study was performed to determine how many patients met a 12-hour target for operative fixation with this injury. Possible sources of delay to theatre were reviewed.

Purpose

To study the initial presentation and subsequent investigation and management of acute knee dislocations at a regional trauma centre.

Introduction: Intracapsular femoral neck fractures in adults under 65 years old are associated with significant complications such as avascular necrosis of the femoral head and non-union. Timing of surgery remains controversial, with some studies suggesting that early surgical fixation reduces the rate of these complications. Presently the policy in this Fracture Unit remains early fixation (target less than twelve hours). The purpose of this study is to determine if this twelve hour target is being achieved and if not, where the delays are occurring.

Methods: A retrospective case-note and data analysis was performed on all patients aged under 65 who underwent internal fixation of displaced intracapsular femoral neck fractures (Garden III/IV) between 31/12/06 and 31/12/07. The following data was collected; time of injury to presentation at health service, time from presentation at health service to admission at treating hospital, time of admission at treating hospital to time of surgery and overall time from injury to surgery. The main causes of delay were also determined.

Results: In the one year period, there were 37 young adults with displaced intracapsular femoral neck fractures, with a mean age of 52.57 years. There were 23 females (62.2%) and 14 males (37.8%).

We also present the reasons for delay at each stage including transfer delays, medical delays and limited emergency theatre availability.

Discussion: Early operative fixation of young femoral neck fractures remains controversial. In this unit where it is advocated, the median time from injury to fixation is 22.18 hours. By reducing transfer times, increasing emergency theatre availability and improving efficiency of patient preparation for theatre at ward level, the twelve hour targets will be much more attainable.

This multicentre audit assessed the total Tip Apex Distance (TAD) of sliding hip screws for intertrochanteric hip fractures in the 3 fracture hospitals in Northern Ireland (Ulster Hospital, Royal Victoria Hospital & Altnagelvin Hospital). Patient demographics and anaesthetic information was also reviewed. A sample of 140 patients with adequate screening films (39 UHD, 50 RVH & 51 Altnagelvin) were selected. The TAD was measured on AP & lateral screening films and compared to the standard of 25mm or less (total in 2 views) as recommended by Baumgaertner et al (JBJS (Am) 1995).

All 3 hospitals had an average of under 25mm (22.1, 19.9 & 19.6mm respectively) with overall average of 20.4mm, and a TAD of 25mm or less was achieved in 66.7%, 82% & 80.4% in respective hospitals (77.1% of patients overall). No patients were readmitted due to cut-out, despite 22.9% of patients having a TAD greater than 25mm. Among patients with TAD over 25mm the average TAD was 30.1mm

Demographics showed a 77.8% of patients to be female, with a slight predominance of left sided injuries. Most patients were of ASA grading 2–3. Anaesthetic method preferences varied between hospitals. Patients with TAD over 25mm were not significantly different from those with TAD of 25mm or less in age, gender, ASA or operated side.

Introduction: Intracapsular femoral neck fractures in adults under 65 years old are associated with significant complications such as avascular necrosis of the femoral head and non-union. Timing of surgery remains controversial, with some studies suggesting that early surgical fixation reduces the rate of these complications. Presently the policy in this Fracture Unit remains early fixation (target less than twelve hours). The purpose of this study is to determine if this twelve hour target is being achieved and if not, where the delays are occurring.

Methods: A retrospective case-note and data analysis was performed on all patients aged under 65 who underwent internal fixation of displaced intracapsular femoral neck fractures (Garden III/IV) between 31/12/06 and 31/12/07. The following data was collected; time of injury to presentation at health service, time from presentation at health service to admission at treating hospital, time of admission at treating hospital to time of surgery and overall time from injury to surgery. The main causes of delay were also determined.

Results: In the one year period, there were 37 young adults with displaced intracapsular femoral neck fractures, with a mean age of 52.57 years. There were 23 females (62.2%) and 14 males (37.8%).

We also present the reasons for delay at each stage including transfer delays, medical delays and limited emergency theatre availability.

Discussion: Early operative fixation of young femoral neck fractures remains controversial. In this unit where it is advocated, the median time from injury to fixation is 22.18 hours. By reducing transfer times, increasing emergency theatre availability and improving efficiency of patient preparation for theatre at ward level, the twelve hour targets will be much more attainable.

This longitudinal prospective study reports the 10-year results of arthroscopic, anterior cruciate ligament (ACL) reviewed. Four (4%) menisectomies were performed, 6 graft (7%) ruptures and 18 (20%) contralateral ACL ruptures occurred in the follow-up period. Ninety-seven percent of patients graded their knee function as normal or nearly normal and the median Lysholm knee score was 95 at 10-years. The proportion of patients participating in IKDC level I and II sports fell from 85% at 2-years to 45% at 10 years, 12% attributing the decrease to their knee. On laxity testing 85% and 93% had grade 0 on Lachman and pivot shift testing, respectively and 77% had < 3mm of anterior tibial displacement at 10 years. Kneeling pain increased to 58% of patients. 59% had no pain on strenuous activity with 33% of patients having a fixed flexion deformity at 10 years. Radiological examination at 10 years demonstrated osteoarthritic changes in 48% of patients. Factors predictive for the development of radiograhic osteoarthritis were increased age at operation and increased ligamentous laxity at 2 years as measured clinically and by KT 1000. As such, arthroscopic ACL reconstruction, employing patellar tendon, is not preventative of the development of osteoarthritis even when the confounding factors of meniscal, chondral and other ligamentous injury are excluded.

Fracture repair is a complex physiological process during which bone shows the remarkable ability to mount a repair process, restoring its mechanical integrity and anatomical configuration by original osseous tissue. Programmed cell death, or apoptosis, is a naturally occurring cell suicide pathway with a homeostatic function in the maintenance of continuously renewing tissues. The present study investigated the relation between cell proliferation and cell death (apoptosis) during fracture healing in a mouse femoral model.

Left femoral osteotomies were performed in 20 male CFLP mice (35–45g), immobilised with uniplanar external fixators. 4 animals were sacrificed on days 2, 4, 8, 16 and 24 post-fracture and fracture callus collected for paraffin embedding. Localisation of cell proliferation was examined using immunohistochemistry with proliferating cell nuclear antigen (PCNA) monoclonal antibody. Apoptotic cells were visualised with the terminal deoxynucleotidyl transferase (TdT)–mediated dUTP-biotin nick end-labelling (TUNEL) method. Random images of each time specific specimen were captured via a digital camera and the positive labelling indices of PCNA and TUNEL labelling were calculated and statically compared.

Cell proliferation and apoptosis were found co-existing during the entire period of fracture healing studied. Cell proliferation was predominant in the early phases of fracture healing (days 2–8). PCNA positive labelling index peaked at day 8 (p< 0.01, t-test) and PCNA-positive cells were not limited to the fracture gap mesenchymal tissues but extended in the periosteum along most of the fractured femur. TUNEL positive labelling was minimal in the early stages (days 2–8). In later stages of fracture healing (days 16–24), PCNA expression declined as intramembranous and endochondral ossification spread within the fracture site and apoptosis was the dominant cell activity with the TUNEL positive labelling index peaked at day 16 (p< 0.05, t-test) and then declined sharply at day 24.

The current study indicated that apoptosis was a normal concomitant during fracture repair, confirming programmed cell death in chondrocytes and bone cells, and that cell proliferation and apoptosis were tempero-spatially dependent. These findings support the view that apoptosis is a natural process, genetically programmed and active during fracture repair. The demonstration of a mixture of proliferative and apoptotic cell populations in the regenerating tissues of fracture callus, suggests that apoptosis and cell proliferation may be regulated by local factors during fracture healing.

NSAID’s cycle-oxygenase (COX) inhibitory characteristics are either non-specific, COX-1 preferential or recently COX-2 preferential. NSAID’s have been widely reported to delay fracture repair however the mechanism of this affect remains unclear.

Left femoral osteotomies were performed in 54 male 3 month old CFLP mice immobilised with uniplanar external fixators. 27 externally fixated mice received 4mg/kg meloxicam,b.d., from the day of surgery, by gavage. The control group received the carrier alone. 18 mice had external fixators applied to intact femurs and received no meloxicam as a sham control. Individual mouse movement, was quantified each day by autocounters using an infrared beam motion detection system. Plasma was obtained by right ventricular aspiration under anaesthesia on days 2,4,8 and 16-post surgery.

A validated bioassay and a slot blotting immunoassay were employed to determine the plasma concentration of 11-6 and relative TNF-α levels to normal mouse serum.

TNF-α levels peaked at day 4 and were suppressed by COX-2 inhibition. Both the control and treatment groups had higher levels of TNF-α than the non-fractured controls. The plasma concentration of 11-6 was elevated by COX-2 inhibition at all time points. The levels of TNF-α and 11-6 correlated in fracture control and treatment groups (Spearman’s 0.039 and 0.002 respectively). The 11-6 plasma concentration correlated to the animal motion in the treatment group alone (Spearman’s 0.017).

As it has been shown that TNF-α induces 11-6 production and that this inhibits TNF-α production a possible model for these interaction is shown below.

Hypothesis: Early initiation of COX-2 inhibition is more detrimental to fracture healing than later, irrespective of the analgesia-permitted biomechanical stimulation of the fracture by movement.

Model: A validated externally fixated murine femoral fracture model.

Intervention: Left femoral osteotomies, immobilised with sagittal uniplanar external fixators. Treated mice received 4mg/kg meloxicam from the day of surgery, day 4 or day 8 post op until sacrifice, by gavage. Control mice received carrier alone.

Outcome Measurements: Mouse movement was quantified each day until sacrifice. Fracture geometry was determined from post-sacrifice orthogonal x-rays. Animals were sacrificed on day 4,8,16 and 24. Blind computer aided histomorphometric analysis was performed, on six coronal sections per specimen, determining the medial, intramedullary and lateral areas of total callus, mesenchymal tissue, cartilage and new bone.

Results: No difference existed between the treated groups and control fracture fragments overlap or alignment nor in post-operative movement. Meloxicam treated groups showed decreased callus areas on day 4, 8, and 16, although it was noted that callus remodelling had commenced after day 16 in the control specimens only. New bone areas were reduced in all treated groups at all time points examined relative to the controls with the reduction being proportional to duration of COX-2 inhibition. Mesenchymal tissue differentiation was maximally affected in the earliest treatment group.

On day 24, day 0 treated specimens demonstrated significantly more mesenchymal tissue. No correlation was demonstrated between post-operative motion and callus area or new bone area. The care of cartilage present however, was significantly correlated to the amount of post-operative movement in all groups.

Conclusions: COX-2 inhibition inhibits new bone formation in proportion to the proximity of its commencement the fractures occurrence, irrespective of fracture stimulation by motion. Cartilage production in the healing fracture is not altered by COX-2 inhibition but is proportional to fracture stimulation by motion.