Dear Editor

The article from the Netherlands by Cappendijk and Hazebroek[1] has again confirmed what is already known in clinical practice. A recent paper from the Leicester Royal infirmary[2] is almost identical.

As the authors pointed out, the factors determining the diagnostic delay are numerous and often cannot be influenced. However, I agree with their statement that “in a child with abdominal pain which do not settle quickly, appendicitis should be excluded by early and if necessary repeated surgical consultations”.[1]

The vermiform appendix varies from 2 cm to 24 cm in length, the average being about 9 cm. It is longer in the child than in the adult. The position of the appendix shows a high variation in children. [3, 4] This variation in the location of the appendix in the abdomen explains the variation of symptoms seen with acute appendicitis. If the appendix is retrocaecal or located in the posterior portion of the abdomen, localisation of the pain and tenderness on examination occur late if at all. If the appendix is posterior in the pelvis, the pain may localise only to the lower abdomen. And tenderness to palpation is poorly localised. The diarrhoea of appendicitis is most common in patients with a low-lying appendix in proximity to the colon and rectum.[5]

We recently saw a 9-year-old boy presenting with maximum tenderness in the left iliac fossa. There was a 31-hour history of generalised abdominal pain followed by vomiting. He was referred to the surgeon with the diagnosis of generalised peritonitis. Examination under anaesthesia revealed a mass in the left iliac fossa. Laparotomy confirmed a generalised peritonitis resulting from a left iliac fossa abscess. This was from a ruptured appendix, the tip of which was in the left iliac fossa.

References

(1) Cappendijk VC, Hazebroek FWJ. The impact of diagnostic delay on the course of acute appendicitis. Arch Dis Child 2000;83:64-6

(2) Williams N, Bello M. Perforation rate relates to delayed presentation in childhood acute appendicitis. J R Coll Surg Edin 1998;43: 101-2

(3) Bakheit MA, Warille AA. Anomalies of the vermiform appendix and prevalence of acute appendicitis in Khartoum. East Afr Med J 1999;76:338-40

(4) Johnston TB, Whillis J. Gray’s Anatomy 1942; 28th Edition, Longmans, Green and Co.

(5) Shandling B, Fallis JC. Acute appendicitis. In Nelson’s Textbook of Paediatrics. 1992; 14th Edition, Behrman R. W.B. Saunders Company

Dr Stephen Kwame Dotse
115 Nab Wood Drive
Shipley, West Yorkshire BD18 4AP, UK

We welcome the debate stimulated by our paper. Indeed, this was our aim in publishing it.

We agree with Mr Caldwell that a degree of underreporting is likely. Our system provides a clear definition to all staff of what constitutes a reportable medication error (listed in the appendix). It does not include errors that are averted such as mis-prescribed errors corrected by pharmacists prior to dispensing. We also noted that error-reporting rates vary widely in the literature. We discussed some of the reasons advanced to explain such variations, such as whether the reporting system is mandatory or voluntary and the intensity of the search for errors. However, the published evidence about medication error rates in paediatric settings is very limited especially in the context of a nationally funded, universal, health care system such as the NHS. There is, therefore, little firm paediatric evidence to support Mr. Caldwell's opposite view that errors are "…extremely common, overlooked and often ignored."

In our experience, most reported errors were minor. Serious events with adverse outcomes were uncommon and, we think, are unlikely not to be reported. If anything, we would suspect it is minor errors that are most likely to go unrecorded. This may be of considerable importance if analysis of minor events highlights system problems whose correction may help avoid future serious incidents.

Mr Caldwell suggests that voluntary systems may increase error reporting. It needs to be recognized that voluntary systems are not a panacea but may also detect only a fraction of overall errors. Again, we would suspect that minor errors might most likely be missed. The thrust of the editorial by Cohen[1] appears to relate to errors with serious adverse outcomes. There are also some potential difficulties with voluntary systems. For example, how we do we ensure that parents are notified about error occurrence if reporting is voluntary? What happens about errors of such seriousness that issues of criminal negligence arise?

Whether a reporting system is mandatory or voluntary probably is less important than that the system is non-punitive. This is borne out by the findings of Vincer et al[2] who found approximately a four to six- fold increase in the reporting of errors by reducing the punitive aspects of the form by making it an "incident" rather than an "error" form. We have no doubt that the critical challenge for us all is to make the shift from assuming "errors" arise from individual negligence to recognising that "incidents" more usually arise because of systemic organisational failures. We urgently need to move away from a culture of "fixing the blame" towards one of recognising and "fixing the problem".

References
(1) Cohen MR. Why error reporting systems should be voluntary. BMJ 2000;320:728-9.

(2) Vincer MJ, Murray JM, Yuill A, Allen AC, Evans JR, Stinson DA. Drug errors and incidents in a neonatal intensive care unit. A quality assurance activity. Am J Dis Child 1989;143:737-40.

The recent study by Hutton, Colver, and Mackie[1] is in some respects a useful addition to our knowledge of survival in cerebral palsy. Unfortunately there some are substantial problems with the paper; we note three of them below.

In Figure 1A it appears that in the most seriously affected group, LAS >70%, there is 100% survival to age 9. This scarcely seems plausible when, as the graph indicates, 20% of these survivors die in the next 9 years. The explanation is that the most severely disabled children, with LAS 70% or more, have to survive to age 5 to be assessed by LAS. Thus the severely disabled children who die before 5 have no LAS, and are excluded (actually, it appears from the graph that some children are evaluated even later than age 5).

The resulting bias could have serious consequences. For example, in a lawsuit involving a neurologically devastated 2-year old child a plaintiff may cite Hutton et al to argue for 100% survival over the next seven years.

Hutton et al's results show that, as is well known, low IQ and/or poor mobility correlate with reduced life expectancy. In his commentary, Dr Rosenbloom usefully asks whether extreme immobility or mental impairment would give an even greater reduction. The answer is clearly yes, as indicated by our own work[2][3] and is also acknowledged by other workers in the area (Evans et al[4] Crichton et al[5]). Indeed it must be so because an extensive literature shows a much shortened survival in the persistent vegetative state,[6] which may be regarded as the extreme case of disability.

In neither Hutton et al's nor in Hutton's previous study of the Merseyside area[7] is this possibility mentioned. As a result, the latter study has frequently lead plaintiffs to overestimate survival of children with the most severe disabilities.

In their Table 5, Hutton et al state that in our California study[2] the odds ratios for various hazards were lower than in several other studies. For example, in Table 2 of our article we gave a hazard ratio of 3.8 for two year-olds who were tube fed, compared to those who were not. Hutton et al then proceeded to speculate at some length on what accounts for the transatlantic difference.

The real reason is simple: the California data base has many more variables other data bases, so the marginal effect of any one of them -- ie, when the others are held constant -- is smaller. For example, our Table 1 showed that if no other factors are taken into account the hazard ratio for tube feeding (compared to children who could self-feed) was 23.6 -- a much larger ratio than the above 3.8, and in fact about as large as any in Hutton et al's Table 5. In addition, the definitions of mobility etc. in the various studies are very different.

David Strauss, PhD, FASA
Emeritus Professor of Statistics

Robert Shavelle, PhD
University of California Life Expectancy Project

References
(1) Hutton JL, Colver AF, Mackie PC. Effect of severity of disability on survival in north east England cerebral palsy cohort. Arch Dis Child 2000;83:468-74.

(2) Strauss DJ, Shavelle RM, Anderson TW. Life expectancy of children with cerebral palsy. Pediatr Neurol 1998;18:143-9.

(3) Strauss DJ, Shavelle RM. Life expectancy of adults with cerebral palsy. Dev Med Child Neurol 1998;40:369-75.

(4) Evans PM, Evans SJW, Alberman E. Cerebral palsy: Why we must plan for survival. Arch Dis Child 1990;65:1329-33.

(5) Crichton, JU. Response to Letter from Professor Hall. Dev Med Child Neurol 1995;37:1031-3.

(6) Multi-society task force on PVS. Medical Aspects of the Persistent Vegetative State, Part I. N Engl J Med 1994;330:499-1508.

(7) Hutton JL, Cooke T, Pharoah POD. Life expectancy in children with cerebral palsy. BMJ 1994;309:431-5.

The accurate diagnosis of meningococcal disease is important, not only for the welfare of the patient, but also for the implementation of appropriate public health measures. Brogan and Raffles have made a useful contribution to more reliable diagnosis.[1]

However I feel that their finding of 9% could represent a falsely low proportion of children with serious bacteraemia because of potential recruitment bias and measurement bias. Knowing that children would not be given antibiotics if entered into the study, unless they met the ILL criteria or had a raised WCC or CRP, may have led admitting doctors to exclude some children that they felt uneasy about observing. This could easily have been achieved by describing the rash as >2mm for instance (it is not stated whether the rash was measured or judged by eye). Secondly it is questionable whether they had discovered all the bacteraemias. Blood culture or remaining well after discharge could miss bacteraemia in those children treated with antibiotics before admission or given a short course in hospital. PCR would have been a useful additional diagnostic test.

This study is a useful first step, but as the authors say, needs to be followed up with a prospective trial. The recruiters and assessors of the children to the study are not the managing clinicians and the diagnosis of bacteraemia is more thoroughly sought. This is important to validate the diagnostic technique and also the positive predictive value of the combination of petechiae and fever.

Reference
(1) Brogan PA, Raffles A. The management of fever and petechiae: making sense of rash decisions. Arch Dis Child 2000;83:506-7.