No abstract

Type I collagen is the main collagen in tendons; type III collagen is present in small amounts. Ruptured Achilles tendons contain a significantly greater proportion of type Ill collagen, which predisposes them to rupture. We used an in vitro model to determine whether tenocytes from Achilles tendons that were ruptured (N = 22), nonruptured (N = 7), tendinopathic (N = 12), and fetal (N = 8) show different behavior. Samples of Achilles tendon were digested with collagenase and the released tenocytes were collected. Primary tenocyte cultures were established and subsequently cultured onto glass coverslips. Once a confluent monolayer was obtained, the cell populations were "wounded" by scraping a pipette tip along the surface. The cultures were further incubated for either 1, 4, 8, 12, 16, or 24 hours, and production of types I and II collagen was assessed by immunostaining. In cultures from ruptured and tendinopathic tendons, there was increased production of type Ill collagen. Athletic participation places excess stress on the Achilles tendon, which could potentially lead to areas of microtrauma within the tendon. These areas may heal by the production of type III collagen, which is an abnormal healing response. Accumulation of such episodes of microtrauma could resuit in a critical point where the resistance of the tissue to tensile forces is compromised and tendon rupture occurs.

The altered production of collagen may be one reason for the histopathological alterations described in the present study. Areas of calcific insertional Achilles tendinopathy have been subjected to abnormal loads. These tendons may be less resistant to tensile forces. Further studies should investigate why some tendons undergo these changes.

We aim to describe the outcomes after chronic subdural hematoma drainage (CSDH) management in a large cohort of patients on antithrombotic drugs, either antiplatelets or anticoagulants, at presentation and to inform clinical decision making on the timing of surgery and recommencement of these drugs. We used data from a previous UK-based multi-center, prospective cohort study. Outcomes included recurrence within 60 days, functional outcome at discharge, and thromboembolic event during hospital stay. We performed Cox regression on recurrence and multiple logistic regression on functional outcome. There were 817 patients included in the analysis, of which 353 (43.2%) were on an antithrombotic drug at presentation. We observed a gradual reduction in risk of recurrence for patients during the 6 weeks post-CSDH surgery. Neither antiplatelet nor anticoagulant drug use influenced risk of CSDH recurrence (hazard ratio, 0.93; 95% confidence interval [CI], 0.58-1.48; p = 0.76) or persistent/worse functional impairment (odds ratio, 1.08; 95% CI, 0.76-1.55; p = 0.66). Delaying surgery after cessation of antiplatelet drug did not affect risk of bleed recurrence. There were 15 in-hospital thromboembolic events recorded. Events were more common in the group pre-treated with antithrombotic drugs (3.3%) compared to the non-antithrombotic group (0.9%). Patients on an antithrombotic drug pre-operatively were at higher risk of thromboembolic events with no excess risk of bleed recurrence or worse functional outcome after CSDH drainage. The data did not support delaying surgery in patients on antithrombotic therapy. In the absence of a randomized controlled trial, early surgery and early antithrombotic recommencement should be considered in those at high risk of thromboembolic events.

Extradural haematomas are a significant consequence of head injuries in children. The aim of this study was to evaluate the demographics, symptoms and signs, management and outcome of patients less than 18 years of age with extradural haematomas in our unit. We also specifically looked at repeat imaging performed, indications for this and its effect on further management. No previous reviews have included this. Fifty-six patients were identified from 01/01/1997 to 01/01/2007 for inclusion in this study. Their imaging was then reviewed as were the case notes. Of the patients studied, 70% were male. The average age was 10 years and 2 months with an average length of stay of one week. The commonest mechanisms of injury were a fall from height and an accident involving a bike. Presenting symptoms were documented in 40% of cases. 32% of patients had associated skull fractures. Six patients had other injuries, including long bone fractures and maxillofacial injuries. Glasgow Coma Scale was generally better on admission than pre-operatively and post-operatively was generally better than prior to surgery. Eight patients had neurological signs on admission, 11 had pre-operatively, and nine had post-operatively. 71% underwent a craniotomy with evacuation of the haematoma. Complications were reported in 16% with no mortality. 66% were seen in a neurosurgical clinic, with 46% seen in a Paediatric Head Injury Clinic after discharge. 66% had further imaging after their initial scan of which 52% had no clinical indication. Eight patients were operated on following re-imaging. Most extradural haematomas in children are caused by falls or vehicle accidents. The majority are treated surgically and do well. Indications for further scanning are often not present and in most, management is unchanged. The follow up of these patients also appears to be suboptimal.