CORRESPONDENCE
1 Mohammed MA, Cheng KK, Rouse A,
Marshall T. Bristol, Shipman, and clinical
governance: Shewhart’s forgotten lessons.
Lancet 2000; 357: 463–67.
2 Anon. Good hospital guide, part 1. The
Sunday Times 2001; Jan 14: 2–55.
3 Jarman B, Gault S, Alves B, et al. Explaining
differences in English hospital death rates
using routinely collected data. BMJ 1999;
318: 1515–20.
4 Kmietowicz Z. Hospital tables “should
prompt authorities to investigate” BMJ 2001;
322: 127.
Sir—A Mohammed and colleagues1 do
a fine job of bringing the work of
Nolan and Provost2 and Berwick3 to
our attention, both of whom increased
our understanding of variation in
health care. But there are difficulties to
be overcome before routine analysis of
variation in the control-chart way is
adopted.
The usefulness of Shewart’s method
in refining widget production might
not be applicable to health-care
systems, for which variation can be
normal and creative—a sign of
adaptability to local and individual
circumstances. Mohammed and
colleagues clearly had to find the right
epoch groupings before they found the
right results for Bristol Royal
Infirmary. Despite this, difficulties
presumably existed outside of the dates
in which the Bristol unit seemed to be
a special case.
Mohammed and colleagues discuss
the use of different values of control
limits. We know from previous work
that in the complex system of health-
care, in which variation occurs, these
limits have to be set too narrowly
(which identifies many special causes)
or too widely (which misses cases).
Harold Shipman was not a bad doctor
but a mass murderer and, despite this
fact, it would be difficult to detect
similar abnormal performances by use
of statistics alone.4 Indeed, that the
intrinsic variation of complex systems
can be substantial enough to rival the
effects of extrinsic influences5 is not
taken into account by Mohammed and
colleagues nor the control-chart
approach. Such an insight must surely
challenge the validity of a method
whose basic assumption is that
extrinsic special causes can be
identified purely on the grounds of
statistical deviation from an idealised
mean value.
Finally, the report concentrates on
case finding and does not underscore
the most important lesson: if common-
cause variation is not acceptable, it is
the system that needs to be changed
completely and it should not be
stressed to perform better. There may
be no available examples of special-
cause variation associated with better
THE LANCET • Vol 357 • May 12, 2001
For personal use. Only reproduce with permission from The Lancet Publishing Group.
performance and a redesign might be
required.
Tim Wilson, Tim Holt, *Trisha Greenhalgh
Institute of Healthcare Improvement, Boston,
MA, USA; Danby Practice, Dale End Surgery,
Danby, Whitby, UK; and *Department of Primary
Care and Population Sciences, University
College London, Holborn Union Building,
Highgate Hill, London N19 3UA, UK
1 Mohammed MA, Cheng KK, Rouse A,
Marshall T. Bristol, Shipman, and clinical
governance: Shewhart’s forgotten lessons.
Lancet 2001; 357: 463–67.
2 Nolan T, Provost LP. Understanding
variation. Qual Progr 1990; 23: 7–78.
3 Berwick DM. Controlling variation in health
care: a consultation from Walter Shewhart.
Med Care 1991; 29: 1212–25.
4 Frankel S. Sterne J, Davey Smith G.
Mortality variations as a measure of general
practitioner performance: implications of the
Shipman case. BMJ 2000; 320: 489.
5 Schaffer WM. Can non-linear dynamics
elucidate mechanisms in ecology and
epidemiology? IMA J Math Appl Med Biol
1985; 2: 221–52.
Duchenne muscular
dystrophy or Meryon’s
disease
Sir—There is no doubt that Duchenne
made many important contributions to
neurology, especially in relation to a
form of muscular dystrophy that now
eponymously bears his name. However,
we think that Venita Jay and Jiri Vajsar
(Feb 17, p 550)1 should have
emphasised Meryon’s contribution
10 years before Duchenne.
Edward Meryon, born in 1807, not
1809 as reported, was an English
physician who in 1851 at a meeting of
the Royal Medical and Chirurgical
Society in London presented a study
(reported at the time)2 of nine boys in
three families with the disease. The
results were published the following
year,3 in which he emphasised three
important points. First, the disease
affected males and was familial; none of
Duchenne’s cases were familial. Second,
he carefully examined the spinal cord at
postmortem of a boy with muscular
dystrophy and concluded that the cord
seemed normal in all respects, including
the nerve tracts and ganglionic cells;
Duchenne did not examine such a
spinal cord until many years later and
could not be certain that the disease was
primarily a disease of muscle. Third,
and most importantly, Meryon’s careful
muscle microscopy study led him to
conclude: “. . . the striped elementary
primitive fibres were found to be
completely destroyed, the sarcous
element being diffused, and in many
places converted into oil globules and
granular matter, whilst the sarcolemma
or tunic of the elementary fibre was
broken down and destroyed.”
This was a singularly important point
not made by Duchenne. We now know
that the primary defect does in fact
reside in the sarcolemmal cytoskeleton.
The Meryon Society, in honour of his
contributions, was founded in 1996 with an
annual lecture. Details of this year’s lecture can
be obtained from Alan Emery.
Alan Emery
Department of Neurology, Royal Devon and
Exeter Hospital, Exeter EX2 5DW, UK
1 Jay V, Vajsar J. The dystrophy of Duchenne.
Lancet 2001; 357: 550–52.
2 Meryon E. On fatty degeneration of the
voluntary muscles (report of the Royal
Medical and Chirurgical Society). Lancet
1851; 2: 588–89.
3 Meryon E. On granular and fatty
degeneration of the voluntary muscles. Med
Chirurg Trans 1852; 35: 73–84.
Suicide of the nephron is
preventable
Sir—Nicolas Hales (Jan 13, p 136)1
hypothesis that proteinuria causes renal
failure by tubular telomere shortening
sounds attractive enough and may be
true in the rat. However, is it true in
human beings also?
If renal failure is due to proteinuria,
renal function should be associated with
the degree of glomerular damage. Many
studies have shown, however, that,
whereas the renal function and the
clinical course in glomerulonephritis are
strongly associated with the degree of
tubulointerstitial damage, there is little
association with the degree of
glomerular damage, if any at all.2 Rather
than being caused by proteinuria the
tubular damage and the progressive
course in glomerulonephritis and other
parenchymal kidney diseases might be
due to environmental chemicals.
In a review of 14 case-control
studies of hydrocarbon exposure in
glomerulonephritis, exposure was
prevalent primarily in patients with renal
failure, with the highest odds ratio for
exposure in end-stage renal failure. In
these patients, 56–82% had been
exposed to hydrocarbons long term.3
Patients with chronic renal failure due to
glomerulonephritis, diabetic neph-
ropathy, and renal vascular diseases have
frequently been exposed to lead, welding
fumes, silicon-containing compounds,
and chromium.4 Suicide of the nephron
is not inevitable, because follow-up
studies have shown that end-stage renal
failure is seen mainly or only in patients
who continue exposure.5
Instead of searching for a
pharmaceutical solution to telomere
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