Many authors recommend surgery to remove retropulsed bone fragments from the canal in burst fractures to 'decompress' the spinal canal. We believe, however, that neurological damage occurs at the moment of injury when the anatomy is most distorted, and is not due to impingement in the resting positions observed afterwards. We studied 20 consecutive patients admitted to our spinal injuries unit over a two-year period with a T12 or L1 burst fracture. There was no correlation between bony or canal disruption and the degree of neurological compromise sustained but there was a significant correlation between the energy of the injury (as gauged by the Injury Severity Score) and the neurological status (p < 0.001). This suggests that neurological injury occurs at the time of trauma rather than being a result of pressure from fragments in the canal afterwards and questions the need to operate simply to remove these fragments.

Monensin increases propionic acid production in the rumen and improves the efficiency of feed conversion in fattening cattle. Trials carried out in the USA showed that 200 mg monensin/head per day was the optimum dose for increasing the rate of live-weight gain in beef cattle at pasture.Twelve pasture trials, involving a total of 434 beef cattle, were carried out during 1976 and 1977 to assess the efficacy of monensin for grazing cattle under European conditions. Each trial compared a group given 200 mg monensin/head per day in 0·5 to 10 kg of carrier supplement with a negative control group, fed blank supplement. The average initial live-weight was 260 kg and the average trial duration was 119 days. Daily live-weight gains of the control and monensin-treated cattle averaged 0·786 and 0·893 kg/head per day respectively, an advantage of 107g/head per day or 13·7 % in favour of the monensin treatment (P<0·001). The growth-promoting effect of monensin showed no tendency to diminish with time.

No abstract