Patients who suffer a fracture of the proximal femur are high risk for developing venous thromboembolism. They require effective anti-thrombotic prophylaxis. In an audit of 11,900 patients a mortality of 17% occurred 3 months after the injury. Although post mortem examination was rare, it was estimated that nearly 50% of 753 deaths were thrombosis related, 6.9% specifically attributed to pulmonary embolus. It is likely that many of the other deaths, attributed to various respiratory problems were also at least in part due to PE. Comparing the data with actuarial tables demonstrated an excess mortality in both gender and in nearly all age groups. In a second audit, although many patients were receiving some form of prophylaxis, many were given ineffective agents and probably using an ineffective regime. In many patients a fracture of the proximal femur is regarded as a terminal event. However, the data from these 2 audits would suggest that many of these patients are dying unnecessarily and that effective prophylaxis would reduce the risk of death. Chemical prophylaxis commenced immediately after surgery and continued for 5 weeks would be appropriate.

The purpose of our study was to prospectively evaluate the effectiveness of Botulinum toxin in patients with involuntary positional instability who had failed a specific rehabilitation programme.

Patients with Involuntary Positional Instability present with a muscle patterning problem that results in active dislocation of the glenohumeral joint. Botulinum toxin is used to inhabit the patterning muscle and therefore facilitate rehabilitation of optimal movement patterns.

Materials and Method: 14 patients referred to a tertiary referral unit were included. All patients had failed rehabilitation, reported multiple recurrent dislocations, repeated surgical interventions (Range 2 – 6) and mean duration of symptoms 5 years (Range 2 – 9). Patients were assessed with Constant and ASES scores, psychological scores (HADS and DRAM) and the Ashworth muscle tone scale. Botulinum Toxin was injected into the muscle dominating movement (identified with clinical assessment and EMG) and patients were re-entered into the rehabilitation programme post-injection.

Results: At an average of 2 years follow-up (8/12 – 4.1) 11 out of 14 patients demonstrated a statistically significant improvement in all parameters. 1 patient required a repeat injection at 4 months but at 2 years remains asymptomatic. Of the 2 patients who failed both demonstrated the highest scores on psychological screening and 1 of them had a severe connective tissue disorder.

Conclusion: Our early experience of Botulinum suggests that it is an effective tool in patients with involuntary positional instability resistant to rehabilitation. Psychological scores may be a useful tool to aid patient selection.

Purpose: To determine whether administration of non-steroidal anti-inflammatory drugs (NSAID) influences ongoing endothelial cell proliferation in torn rotator cuff?

Methods: Rotator cuff tissue, obtained at debridement from 53 patients undergoing surgical repair, was fixed and embedded. Pathological assessment was performed on H& E sections. Ongoing vascular proliferation was identified by plump endothelial cells and budding of vessels. Patient cuff details and preoperative drug prescription data was obtained from patient’s notes and general practitioners. The drugs considered were NSAIDs (including Aspirin, Ibuprofen and Diclofenac), COX 2 inhibitors & Opiates.

Results: Of the 35 patients taking analgesics, vascular proliferation was absent or reduced in 22 (63%). 20 of these patients were taking NSAIDs. Four patients were taking only COX-2 inhibitors, all these patients had increased vascularity. 23 patients were taking codeine based analgesics, of 10 patients using codeine without NSAIDs, 8 demonstrated active ongoing vascular proliferation (p=0.027).

Conclusion: Patients taking NSAIDs showed a significant reduction in ongoing vascular proliferation. If endothelial cell proliferation is an important component of repair processes in rotator cuff, this could be compromised. NSAIDs can impair healing by inhibiting angiogenesis, the mechanism includes upregulation of p27 in endothelial cells. We have peviously identified strong p27 positivity in rotator cuff endothelial cells.