Dear Editor

In our collection we have several examples of resuscitation equipment for casulaties suffering from carbon monoxide poisoning where a mixture of oxygen and carbon dioxide is used. The historical information with the equipment suggests that the use of pure oxygen can lead to the slowing of breathing and so the CO2/O2 mix is more effective as the patient continues to hyperventilate.

In the 1999 paper on mass CO poisoning no mention is made of either the potential problem with pure oxygen or the use of CO2/O2 mixtures. Is this because the understanding of the problem has moved on? Please could you enlighten me as to whether the historical science linked to the objects has been discredited and what the current position is?

Dear Editor

There appeared to be no differentiation between the administration of anabolic steroids (substances based on or manufactured to mimic testosterone) and corticosteroids (substances which are markedly catabolic and reduce inflammation through limiting the gene expression of inflammatory cytokines etc) in the studies of the two bodybuilders in the September issue.

Not many bodybuilders would ever inject or use corticosteroids illicitly as the systemic effects are counter to the aims of the sport. Some bodybuilders will even go so far as to obtain illicit corticosteroid blocking drugs to reduce catabolic breakdown of skeletal muscle.

It is true that most bodybuilders have a degree of reluctance to admit ANABOLIC steroid use, this is for reasons of legality more than anything else. The Police have been known to prosecute users as suppliers because of the ambiguity about the difference between the two in terms of the amount of drugs involved.

Injection of drugs is used by more experienced bodybuilders (not to mention athletes) as it avoids the liver toxicity of 17-alpha-alkylated oral steroids. Unfortunately, since the authorities stepped up their campaign to outlaw their use, the availability of REAL steroids has decreased whereas the amount of dangerous counterfeit steroids, which may be infected or at best not sealed in sterile conditions, has grown beyond control. It is this and not poor technique that has contributed most significantly to the increase in soft tissue infections that is now being seen both here and the USA.

Finally, bodybuilders started some time ago to administer Glycerol and fat products directly in the aim not of promoting muscle growth but of making the muscles bigger temporarily. This practice is usually done before a competition as the effect is not long lasting most of the time. However, it became the vogue for a while to inject directly into muscle groups using less androgenic and more anabolic steroids (such as Stanozolol - Winstrol V) in the mistaken belief that these relatively short acting compounds would have a locally anabolic effect on smaller muscle groups. There were specific instructions circulated by some "authorities" as to exactly how to administer these injections - without any scientific basis, rather optimism.

I hope that this helps a few people who have no involvement in bodybuilding to understand a few of the unfortunate mistakes that bodybuilders make.

Lance Holland-Keen MBChB
Bodybuilder and Doctor

Dear Editor

The article by Cooke et al. [1] on the relationship between A&E performance and average bed occupancy is based on data collected in 2002. Other have recognised an association between occupancy and delays in emergency care in USA[2] and Australia[3]. Recently there have been significant advances in our understanding of that relationship and we believe some of the recent results are worth reporting. In 2003 and 2004 the Department of Health conducted a number of detailed surveys of Acute trusts' operations (some focussing on A&E activity, most recently focussing on flows into and out of beds). The A&E surveys revealed that two of the major causes of delay were related to the process of getting patients into beds, thus providing more direct evidence that the state of beds affects A&E performance. We also observed that these delays were concentrated at certain times and on certain days. However, we were prompted to get more detailed evidence about the flows through beds because the observed correlation with A&E performance was so weak. Surely we should be seeing a stronger effect if beds are such the major cause of A&E delay?

Our survey of bed flows explained much of this paradox. We asked trusts to record the timing of all arrivals and departures from their beds (classified by some simple categories such as elective or emergency admissions) over the course of a week. For those trusts who provided reasonably consistent data (many were unable to do so) we were able to calculate an hourly bed availability. This hourly position generated major insights, some of which we describe below.

Key insights:

* The reported weekly bed occupancy (which is measured at midnight Thursday) is unrepresentative of the actual occupancy across the week. For there to be no delays, sufficient beds need to be available 168 hours every week, not just in the 1 hour sampled for the national returns.

* Hourly occupancy can vary greatly across a single day (sometimes moving from the 70%s to the high 90%s or more). The highest peaks tend to occur in the middle of the day but are often cleared by the evening (see graph).

* Different days (and weeks) may show very different peaks in occupancy. Often only one or two days in a week show extremes of occupancy likely to result in knock-on effects in A&E.

* The fluctuations in bed occupancy are not primarily the result of the randomness of A&E admissions (which are predictable within bounds). The dominant driver is the variability and unpredictability of elective arrivals (which, in many trusts, occur at the worst possible time of day or day of week) and the lack of coordination of the controllable flows (discharges and elective arrivals) with emergencies and with each other. It is not uncommon to observe very low levels of discharge over a weekend. Emergencies continue to arrive, therefore using up beds. Then, first thing on Monday morning, the peak arrival of elective patients occurs (coinciding with the daily emergency peak and perhaps 4 or 5 hours before any discharges). The result is very poor bed availability by lunchtime on Monday.

A separate analysis of changes in performance over a six month period showed no correlation between this and change in bed occupancy (as collected in national data in Cooke's study, using same methodology, correlation coefficient r2=0.097, p=0.24). This reinforced our belief that to gain useful insight into the relationship between bed occupancy and performance we need to study the detailed hourly flows across the week.

Our observations explain both why bed availability is such a big issue for A&E and why the reported statistics do not reflect the strength of the relationship. Also, we can see from our datasets that relatively small variations in any flow can have large consequences for peak bed occupancy so shortages may appear to be quite sporadic (perhaps occurring one week in 4 rather than all the time).

But the most important message from our work is that big improvements are possible if trusts are prepared to manage their beds actively. The extreme peaks we observed in bed use were always the result of a failure to coordinate different flows. While there is little trusts can do to manage emergency flows into beds, these are relatively predictable. Discharges and Elective admissions are-or should be-mostly within the control of trusts. Improved coordination (eg more morning discharges and more afternoon arrivals) can reduce or eliminate extreme peaks in bed occupancy.

The nationally reported point availability of beds does not provide adequate information for the operational management of beds through the week. Hospital Trusts need a complete picture at least hour by hour if they are to manage beds so that beds are available when needed. The benefits of better coordination will reduce the frequency of both A&E delays and cancelled elective activity (even though these have often been seen as opposing goals). The goal of policy now needs to move beyond the improved supply of beds to the improved management of the flows through beds.

References

1. Cooke MW, Wilson S, Halsall J, Roalfe A. Total time in English accident and emergency departments is related to bed occupancy. Emerg Med J. 2004 Sep;21(5):575-6.

2. Alan J. Forster, Ian Stiell, George Wells, Alexander J. Lee, and Carl van Walraven The Effect of Hospital Occupancy on Emergency Department Length of Stay and Patient Disposition Acad Emerg Med 2003 10: 127-133.

3. Dunn R. Reduced access block causes shorter emergency department waiting times: An historical control observational study. Emerg Med (Fremantle). 2003 Jun;15(3):232-8

Declaration: All the authors are either employed by or partially funded by the Dept of Health.

Dear Editor

Whilst reading the article by Kane et al.,[1] the case of a recent patient who presented to our department came to mind, that is probably relevant to the discussion regarding the diagnosis of pneumothoraces by CT scan.

A 44 year old lady car driver presented to A&E after an RTA with a combined impact of 50mph. She complained of neck, sternum and chest pain. On examination she had midline upper cervical spine tenderness, sternal and rib tenderness. X rays showed no fracture however an unusual lytic lesion was noticed at C2 on the plain radiograph. Due to this being unrelated to her trauma and with no other injuries detected, she was discharged home with radiology follow-up, which it was decided after consultation with the radiologists would consist of an MRI and isotope bone scan. All her other plain films were reported as normal at the time by the radiologists.

5 weeks later an MRI scan showed her C2 abnormality to be a benign congenital defect, however her whole body isotope bone scan revealed healing fractures of the mid body of the sternum, the medial right clavicle and the left fifth rib. Subsequent review of her trauma plain films again showed no suggestion of visible fractures. The rare opportunity to perform a bone scan a while after such an injury clearly demonstrated undisplaced fractures which initial radiography was not sensitive enough to pick up. In the case of our woman this was of no clinical consequence and did not affect her recovery.

The importance of diagnosing a fracture that is only visible on bone scan is therefore of no relevance except in cases where management and prognosis is greatly affected (i.e. scaphoid fractures). This is true of much of A&E medicine and is the reason why we seek more sensitive markers of myocardial damage and pulmonary embolus, whilst not subjecting all ankle sprains to sensitive MRI scanning. Whilst Bridges et al.[2] showed that 35 of 90 traumatic pneumothoraces were diagnosed only after CT scanning, in only 15 patients was there any change in management as a result, and there is no record of this diagnosis affecting outcome. There are no studies that show that CT diagnosed pneumothoraces are of any clinical relevance or are likely to result in a tension pneumothorax.

Whilst it may prove to be important to make the diagnosis in a patient who is to undergo ventilation, a patient with an isolated minor chest injury and a small CT diagnosed pneumothorax could present a management dilema in the future. The benefit of diagnosing conditions that may not be of clinical relevance must be demonstrated before the wider use of more sensitive diagnostic tools should be advocated.

References (1) Kane TP, Nuttall MC, Bowyer RC, and Patel V. Failure of detection of pneumothorax on initial chest radiograph. Emerg Med J 2002;19:468-469.

(2) Bridges KG et al. CT detection of occult pneumothorax in mulitple trauma patients. Emerg Med J 1993;11:179-186.