Background: Transcranial Doppler Ultrasound has been used to detect cerebral micremboli following long bone fractures and intramedullary stabilization. However the clinical effects in terms of cognitive function remain unclear. We aim to measure the cerebral embolic load and to clarify clinical cognitive function following lower limb long bone fractures stabilised by reamed intramedullary fixation.

Methods: 27 femoral and tibial diaphyseal fractures (median age 36 years) were cognitively assessed 3 days following surgery and compared to the normal age and intelligence matched population. A wide range of cognitive tests assessed: global cognitive function; verbal fluency and speed; immediate and delayed memory recall; attention and mental processing speeds. 20 patients had intra-operative transcranial Doppler ultrasound monitoring of the middle cerebral artery for embolic signals. In addition a marker of neuronal injury (S-100B protein) was measured pre-operatively and at 0, 24 and 48 hours following surgery. One sample Wilcoxon signed rank test compared median (percentile) cognitive scores for the fracture patient cohort to a value of 50 representing the normal population.

Results: A significant deterioration in immediate memory recall of unstructured material was noted following surgery. Using established criteria, 4 patients had detectable cerebral emboli with a median count of 3 (range 2–9). Scatter plot graphs indicated no correlation between cerebral embolic events and clinical cognitive dysfunction. S-100B protein levels increased from a pre-operative median (interquartile range) of 0.20 (0.23) to a peak immediately following surgery of 0.51 (0.97) with no correlation to clinical cognitive dysfunction

Conclusions: A small number of cerebral embolic events occur during intramedullary fracture stabilisation but with no direct correlation made to cognitive dysfunction on detailed testing. Recent concerns over the specificity of S100B protein due to extracerebral tissue release appear to be confirmed.

Significance: Clarify cognitive function following intramedullary fracture stabilisation and correlate with cerebral (systemic) embolic load.

Study Purpose To assess clinical cognitive function and measure cerebral embolic load following primary cemented hip arthroplasty.

Methods 34 primary cemented hip arthroplasty patients (mean age 69.9 (SD 11.0)0 and no history of cerebrovascular disease, underwent cognitive assessment before and after (day 4) surgery. Testing included: Verbal fluency and speed (Control Oral Word Association Test); Working memory to assess immediate and delayed recall (Weschler Memory Scale III); Attention and mental processing speeds (Colour Trails 1& 2). A one sample Wilcoxon signed rank test compared median differences before and after surgery. A sub-group of 20 patients had intra-operative transcranial Doppler ultrasound monitoring of the middle cerebral artery for embolic signals. A marker of neuronal injury (S-100B protein) was measured pre-operatively and at 0, 24 and 48 hours following surgery.

Results A significant difference was noted in Colour Trails tests 1& 2 following hip arthroplasty with P values (C.I.) of 0.002 (−21, −4) and 0.023 (−15.5, −1.0) respectively.

Using established emboli criteria 10 (50%) patients had true cerebral emboli with a range from 1 to 550 signals (median 2.5 interquartile range (IQ) 2 to 12.5). S-100B levels increased from a pre-operative median (IQ) of 0.15 microg/L (0.12 to 0.20) to a peak immediately following surgery of 1.88(1.36 to 4.24) returning to 0.26(0.18 to 0.37) by 48 hours (normal range: 0.03–0.15). Plotted scatter charts indicated no correlation between embolic load and cognitive dysfunction or with S-100B levels following surgery.

Conclusion Cognitive testing indicates deterioration in early measured attention, visual searching and mental processing speed shortly following hip arthroplasty. No direct correlation was found between cognitive dysfunction and cerebral embolic load.

Background: Long bone fractures and intramedullary stabilisation can result in the extravasation of fat and marrow emboli into the venous circulation. The effects of these emboli can become systemic causing neurological features.

Aim: To establish the cerebral microembolic load following femoral and tibial diaphyseal fractures treated by intramedullary fixation and to specify any neurological impairment with the application of a series of cognitive tests and a serum marker of neuronal injury.

Methods: 20 femoral and tibial fractures treated with intramedullary fixation had intra-operative transcranial doppler ultrasound monitoring of the middle cerebral artery with emboli detection software set to established guidelines. Cognitive testing (day 3), following surgery with an I.Q. assessment (PFSIQ) allowing comparison with age specific normative data. This included: verbal fluency and speed (COWAT – Control Oral Word Association Test); working memory with assessment of immediate and delayed recall; mini-mental state examination; executive function, attention and mental processing speeds (Colour Trails 1& 2). Beta S-100 levels measured pre-operatively, 0, 24 and 48 hours following surgery as a marker of neuronal injury.

Statistical Analysis: One sample Wilcoxon signed rank test to compare median of the cognitive scores with age matched normative data. Multiple regression analysis used to correlate embolic load with cognitive function.

Results: Mean age (SD) for the group is 32 (5.8). Mean PFSIQ of 52.8%, SD 21.4 [median 59.5, IQ range 28.3, 71.3]. No significant difference detected in cognitive testing compared with normative data. Cerebral microemboli detected in 17 of 20 patients with a count median (range) of 6 (0, 29). The mean pre-operative beta S-100 level was 0.36 micro g/l (normal range 0–0.15). This increased to a peak mean of 0.88 micro g/l immediately following surgery with a poor correlation to cerebral embolic load.

Discussion: Detailed clinical testing indicates no significant deterioration in cognitive function following intramedullary stabilisation of these fractures. A variable cerebral micro-embolic load was seen but with no detectable clinical effect. No direct correlation was found between the elevated levels of Beta S-100 seen following surgery and cerebral embolic load. This appears to correlate with previous concerns in the literature regarding the specificity and sensitivity of this established marker of neuronal injury.