Introduction A novel virus, SARS-CoV-2 has caused a fatal global pandemic which particularly affects the elderly and those with co-morbidities. Hip fractures affect elderly populations, necessitate hospital admissions, and place this group at particular risk from COVID-19 infection. This study investigates the effect of COVID-19 infection on 30-day hip fracture mortality. Method Data related to seventy-five adult hip fractures admitted to two units during March and April 2020 was reviewed. The mean age was 83.5 years (range 65-98 years) and most (53, 70.7%) were females. The primary outcome measure was 30-day mortality associated with COVID-19 infection. Results The COVID-19 infection rate was 26.7% (20 patients), with a significant difference in the 30-day mortality rate in COVID-19 positive group (10/20, 50%) compared to COVID-19 negative group (4/55, 7.3%), with mean time to death of 19.8 days (95% confidence interval 17.0-22.5). The mean time from admission to surgery was 43.1 hours and 38.3 hours, in COVID-19 positive and COVID-19 negative groups, respectively. All COVID-19 positive patients had shown symptoms of fever and cough, and all ten cases who died were from hypoxia. Seven (35%) cases had radiological lung findings consistent with viral pneumonitis which resulted in mortality (70% of mortality). 30% (n = 6) contracted the COVID-19 infection in the community and 70% (n = 14) developed symptoms after hospital admission. Conclusion Hip fractures associated with COVID-19 infection have a high 30-day mortality. COVID-19 testing and chest x-ray for patients presenting with hip fractures, helps in early planning of high-risk surgeries and allows counselling of the patients and family using realistic prognosis.

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In April 2012 the National Health Service in England introduced the Trauma Network system with the aim of improving the quality of trauma care. In this study we wished to determine how the introduction of the Trauma network has affected patient flow, hospital finances and orthopaedic trauma training across our region. The overall pattern of trauma distribution was not greatly affected, reflecting the relative rarity of major trauma in the UK. A small decrease in the total number of operations performed by trainees was noted in our region. Trainees at units designated as Major Trauma Centres gained slightly more operative experience in trauma procedures overall, and specifically in those associated with high energy, such as long bone nail insertion and external fixation procedures. However, there have been no significant changes in this pattern since the introduction of the Trauma Networks. Falling operative numbers presents a challenge for delivering high quality training within a surgical training programme, and each case should be seen as a vital educational opportunity. Best practice tariff targets for trauma were delivered for 99% of cases at our MTCs. Future audit and review to analyse the evolving role of the MTCs is desirable.

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The conventional treatment of type II decompression sickness is immediate recompression, which shrinks any intravascular gas bubble and causes it to go back into solution. There is now evidence which requires reappraisal of the concept that a simple intravascular gas bubble is the major pathological factor in type II decompression sickness. After fatal decompression multiple systemic and pulmonary fat emboli have been found in dogs and in man (Clay, 1963). The composition of these fat emboli indicate that they are of metabolic origin. An absolute thrombocytopenia and a hyperliproteinaemia have been described in severe decompression sickness (Pauley and Cockett, 1970). Wells at al. (1971) found that in rapidly decompressed dogs erythrocyte and platelet aggregations occur, which do not appear to nucleate on gas bubbles. In type II decompression sickness the lesion would therefore appear to be a stable lipid/platelet embolus, and so rational medical therapy should be aimed at improving perfusion distal to the embolus and its destruction. Case ReportA 34-year-old man who was a professional diver had suffered three previous decompression accidents, one Investigations on admission were: haemoglobin, 1641 g/100 ml; packed cell volume, 48% mm3; platelets, 100,000/1; total plasma lipids, 1,030 mg/100 ml; plasma lipoproteins, 230 mg/100 ml; arterial pH, 7-32; Po,, 75 mm Hg; Pco2 51 mg Hg; HCO3, 22-0 mEq/l.The patient was treated initially with pentazocine 100 mg intramuscularly and 100% oxygen; 500 ml dextran 40 in saline were infused in 15 minutes; heparin 12,500 IU and frusemide 40 mg was given intravenously. Then he was given a second drip of 500 ml mannitol followed by 500 ml 20% fructose, which sobered him, and 500 ml 8-4% sodium bicarbonate solution. His bronchoconstriction and arterial hypoxaemia persisted, and he was given intravenous aminophylline 500 mg followed by 250 mg four-hourly. After this there was a steady rise in arterial Po2 and a fall in Pco2 (chart). The next day his electrocardiogram showed evidence of

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