We have developed and validated a scoring system that reliably predicts the probability of mortality at 30 days for patients after hip fracture.

This review examines the evidence base for the early management of head-injured patients. Traumatic brain injury (TBI) is common, carries a high morbidity and mortality, and has no specific treatment. The pathology of head injury is increasingly well understood. Mechanical forces result in shearing and compression of neuronal and vascular tissue at the time of impact. A series of pathological events may then ensue leading to further brain injury. This secondary injury may be amenable to intervention and is worsened by secondary physiological insults. Various risk factors for poor outcome after TBI have been identified. Most of these are fixed at the time of injury such as age, gender, mechanism of injury, and presenting signs (Glasgow Coma Scale and pupillary signs), but some such as hypotension and hypoxia are potential areas for medical intervention. There is very little evidence positively in favour of any treatments or packages of early care; however, prompt, specialist neurocritical care is associated with improved outcome. Various drugs that target specific pathways in the pathophysiology of brain injury have been the subject of animal and human research, but, to date, none has been proved to be successful in improving outcome.

SummaryWe re-analysed prospective data collected by anaesthetists in the Anaesthesia Sprint Audit of Practice (ASAP-1) to describe associations with linked outcome data. Mortality was 165/11,085 (1.5%) 5 days and 563/11,085 (5.1%) 30 days after surgery and was not associated with anaesthetic technique (general vs. spinal, with or without peripheral nerve blockade). The risk of death increased as blood pressure fell: the odds ratio (95% CI) for mortality within five days after surgery was 0.983 (0.973-0.994) for each 5 mmHg intra-operative increment in systolic blood pressure, p = 0.0016, and 0.980 (0.967-0.993) for each mmHg increment in mean pressure, p = 0.0039. The equivalent odds ratios (95% CI) for 30-day mortality were 0.968 (0.951-0.985), p = 0.0003 and 0.976 (0.964-0.988), p = 0.0001, respectively. The lowest systolic blood pressure after intrathecal local anaesthetic relative to before induction was weakly correlated with a higher volume of subarachnoid bupivacaine: r 2 À0.10 and À0.16 for hyperbaric and isobaric bupivacaine, respectively. A mean 20% relative fall in systolic blood pressure correlated with an administered volume of 1.44 ml hyperbaric bupivacaine. Future research should focus on refining standardised anaesthesia towards administering lower doses of spinal (and general) anaesthesia and maintaining normotension.