proliferation can be incorporated into the coating, further

reductions in restenosis rate can be expected. A trial of

stents impregnated with the antimitotic substance,
paclitaxel, will be launched shortly.
Are procedural modifications also likely to improve the
long-term outcome after stenting? For instance, is it
important to remove plaque material before stent
deployment? In an observational study of 50 patients who
underwent coronary stent implantation with any of a
variety of different stents, F Prati and colleagues9 used
intravascular ultrasonography to assess the amount of
plaque material remaining outside the stent. The plaque
burden, again assessed by use of intravascular
ultrasonography, was then correlated with the long-term
outcome. Not surprisingly there was a statistically
significant correlation between the residual plaque area
outside the stent at the time of implantation and the mass
of neo-intima formed within the first 6 months. This
finding prompted the investigators to recommend plaque
removal before stent implantation.
Plaque is sometimes removed at the time of angioplasty.
The usual technique is to shave the plaque off the artery
wall with a forward-moving rotating knife, the shavings
being collected in a minute chamber attached to a
catheter.10 Plaque material can also be dispersed by rapid
rotational atherectomy; the debris is washed downstream
and, to a large extent, passes through the capillary bed.
Complication rates are slightly higher when balloon
angioplasty is accompanied by plaque removal. Also,
plaque removal adds cost to the procedure.
There are two plausible explanations why residual
plaque seems to produce more hyperplasia. One is that
plaque stimulates hyperplasia, and the second is that it
obstructs messengers that control cell proliferation from
reaching their target. Plaque material is soft and spongy
and can protrude through the struts of the stent into the
lumen. This protrusion of amorphous, thrombogenic
material is most likely a stimulus for excessive hyperplasia.
Some of the stents used by Prati and colleagues9 have been
associated with an important degree of plaque protrusion.
Until very recently, conventional wisdom stipulated that
the minimum amount of metal should be used in stents to
reduce the potentially thrombogenic surfaces. This notion
has been challenged by observations that a higher metal-toair ratio (>45%) with smoother luminal support and lesser
likelihood of plaque prolapse may be associated with a
significantly lower degree of intimal hyperplasia.11 Prati and
colleagues findings may focus attention on the first
explanation for why residual plaque might produce
hyperplasia but does not address the second.
Another issue is whether assessment of the immediate
effect of stenting, either by intravascular ultrasonography
or by functional assessment of coronary flow, helps in stent
deployment. In C E Hanekamp and colleagues study,12
intravascular ultrasonography and a technique for assessing
coronary flow reserve with the help of intracoronary highfidelity pressure measurements yielded similar results.
Whether the same good correlation between stent
deployment guided by ultrasonography and that guided by
measurement of fractional flow reserve applies to stents
other than the Wiktor-i stent (which has a high propensity
for plaque prolapse) used in this study remains to be
seen. Meanwhile functional assessment might be a logical
and more cost-efficient alternative to intravascular ultrasonography.
Despite studies into how procedural modifications might
270

reduce the likelihood of restenosis after stenting, there is

limited understanding of how in-stent restenosis can be
avoided permanently. Elastic recoil is one of the major
determinants of restenosis after angioplasty, and stents
counteract this recoil, at least at the points where the stent
strut opposes the artery. At present there are no means of
controlling what happens between the struts. The goal in
present day angioplasty is optimum stent deployment
either with the help of imaging techniques or assessment of
functional reserve.This strategy gives the highest likelihood
of acceptable long-term outcome.
Until the reason for restenosis becomes clearer and
stents with better characteristics become available, plaque
removal before insertion of the stent may be a worthwhile
option.
Ulrich Sigw art
Department of Invasive Cardiology, Royal Brompton Hospital, London
SW3 6NP, UK
1

Sigwart U, Puel J, Mirkovitch V, et al. Intravascular stents to prevent

occlusion and restenosis after transluminal angioplasty. N Engl J Med
1987; 316: 70106.
2 Fischman DL, Leon MB, Baim DS, et al. A randomised comparison of
coronary stent placement and balloon angioplasty in the treatment of
coronary artery disease. N Engl J Med 1994; 331: 496.
3 Serruys PW, de Jaegere P, Kiemenieij P, et al. A comparison of balloon
expandable stent implantation with balloon angioplasty in patients with
coronary artery disease. N Engl J Med 1994; 331: 489.
4 Kimura T,Yokoi H, Nakagawa Y, et al.Three-year follow-up after
implantation of metallic coronary artery stents. N Engl J Med 1996;
334: 56166.
5 Kastrati A, Schmig A, Elezi S, et al. Prediction favours of restenosis
after coronary stent placement. J Am Coll Cardiol 1997; 30: 142836.
6 Waksman R, Robinson KA, Crocker IR, Gravanis MB, Cipolla GD,
King SB. Endovascular low dose irradiation inhibits neo-intima
formation after coronary artery balloon injury in swine: a possible role
for radiation therapy in restenosis prevention. Circulation 1995; 91:
155359.
7 Rosenschein U, Alter A, Rozenszajn LA.Therapeutic ultrasound
inhibition of smooth muscle cell migration.In: Endoluminal stenting:
Sigwart U, ed.London: WB Saunders ,1 9 9 6 .
8 Campbell EJ, OByrne V, Stratford PW, et al. Biocompatible surfaces
using methacryloylphosphorylcholine laurylmethacrylate copolymer.
Am Soc Artif Int Org 1994; 40: M85357.
9 Prati F, Di Mario C, Moussa I, et al. In-stent neointimal proliferation
correlates wtih the amount of residual plaque burden outside the stent:
an intravascular ultrasound study. Circulation 1999; 99: 101114.
10 Hinohana T, Robertson GC, Selmon MR, et al. Restenosis after
directional coronary atherectomy. J Am Coll Cardiol 1992; 20: 62332.
11 Chronos NAF, Carroza J, Post M, et al. Histologic response of pig
carotid arteries to placement of nitinol stents. Circulation 1998; 98:
18990 (abstr).
12 Hanekamp CE, Koolen JJ, Pijls NH, Michels HR, Bonnier HJ.
Comparison of quantitative coronary angiography intravascular
ultrasound, and coronary pressure measurement to assess optimum
stent deployment. Circulation 1999; 99: 101521.

Progress in care of the diabetic foot

Major advances in the past decade have led to better
ulcer healing and to reductions in numbers of
amputations. An important prelude to successful
treatment is the differentiation between two main
syndromes: the neuropathic foot and the neuroischaemic
foot.1 Ulceration in the neuropathic foot develops at the
sites of high mechanical pressure on the plantar surface
of the toes and forefoot during walking. By contrast,
ulcers in the neuroischaemic foot develop directly on the
margins of the foot and toes, at sites made vulnerable by
underlying ischaemia to the moderate but continuous
pressure from poorly fitting shoes.
Therefore, the basic approach to management is relief
of the mechanical pressures that lead to tissue
breakdown.2 In the neuropathic foot, plantar pressure

THE LANCET Vol 354 July 24, 1999

can be redistributed by use of casting techniques such as

the total contact cast, or cast walkers such as the recently
available Pneumatic Walker (Aircast Inc, New Jersey,
USA). When the ulcer has healed, special insoles and
shoes must be provided to prevent recurrence. The main
disadvantage of such conservative management is that
abnormal foot biomechanics are not corrected, and 61%
of patients develop new foot ulcers within 3 years of the
healing of an ulcer.3 Wieman and colleagues4 report the
findings of a retrospective study of a means of correcting
foot biomechanicsnamely, resection of the metatarsal
head at the base of the ulcer to decrease high plantar
pressures. Mean ulcer healing time was 12 weeks,
compared with 22 weeks for historical controls who did
not undergo resection of the bone.4 However, although
resection of the head may reduce focal pressure, a reulceration rate of 52% in the 35 months of follow-up,
similar to that obtained with conservative treatment,
suggests that pressure on the plantar surface may have
been transferred to other localised areas. Controlled
studies are urgently needed for the neuropathic foot, to
compare the conservative approach of redistributing
pressure by means of footwear, with surgical means of
eliminating focal areas of high pressure. In the case of
the neuroischaemic foot, the situation is less complex.
All that is needed are wide- fitting shoes with a suitably
deep toe box to accommodate and protect the vulnerable
margins of the forefoot and toes from the continuous but
unfelt pressure from tight shoes.
Even though mechanical pressure may be relieved,
healing of neuropathic and neuroischaemic ulcers can be
accelerated by debridement. Outpatient podiatric
debridement removes devitalised tissue, reduces the
bacterial load of the ulcer even when there is no overt
infection, and turns chronic wounds into acute wounds,
thus releasing growth factors to aid the healing process.5
Inpatient operative debridement is an extremely
important procedure and in many cases is limb saving
when done urgently to remove infected necrotic tissue.
This may require a toe or ray amputation (removal of toe
and metatarsal head). Such amputations are very
successful operations in the neuropathic foot but usually
need to be accompanied by revascularisation procedures
in the neuroischaemic foot to achieve complete healing.
When there is extensive loss of tissue, modern
reconstructive surgical techniques with free tissue
transfer have recently proved useful in up to 80% of
patients.6
In the management of the neuropathic diabetic foot, it
is important to understand that tissue necrosis is rarely
caused by an occlusive microangiopathy but much more
commonly by a neutrophilic vasculitis secondary to softtissue infection. Even in the neuroischaemic foot,
neutrophilic vasculitis is often the cause of tissue
necrosis, although in this case, poor tissue perfusion due
to atherosclerotic large-vessel disease is also important.
Infection should thus be diagnosed early and treated
aggressively. However, signs of inflammation may
commonly be difficult to detect because of the
neuropathy and vascular disease. Furthermore, there is a
reduced systemic response to infection in the diabetic
foot. In a report of over 200 patients with deep infection
of the foot, 50% had no leucocytosis or a fever.7 Thus,
the white-cell count and temperature should not be
regarded as reliable indicators of infection in the diabetic
foot. Microbiological diagnosis becomes important, and

THE LANCET Vol 354 July 24, 1999

it is advisable to take a deep wound swab from the ulcer

after podiatric debridement. If the foot needs more
extensive surgical debridement, deep tissue should be
sent for urgent microbiological analysis. Broad-spectrum
antibiotics must be given initially, and altered if
necessary according to the organisms cultured.
The past decade has confirmed the importance of
intensive revascularisation of the neuroischaemic foot,
especially if there is extensive tissue necrosis or
persistent ulceration. Tissue necrosis used to be thought
to be due to microangiopathic arteriolar occlusive
disease, or small-vessel disease, and by implication
surgically untreatable. However, it is the combination of
poor tissue perfusion that results from atherosclerotic
narrowing of the tibial arteries of the leg, together with
soft-tissue sepsis, that leads to necrosis. Furthermore,
the foot can be successfully treated by distal arterial
bypass8 or angioplasty.9 A prerequisite for such
revascularisation is precision angiography and duplex
examination to outline the tibial and foot arteries.
Most ulcers will respond to prompt and correct
application of the above approach. However, new
developments show promise in accelerating the healing
of ulcers that are refractory to established treatment.
These new therapies include platelet-derived growth
factor10 and human skin equivalents, such as cultured
dermis.11 Nevertheless, wound healing, including
fibroblast activity, is affected by blood glucose, and good
diabetic control improves capillary blood flow and
leucocyte function and reduces the risk of amputation.
A rarer diabetic foot complication than ulcers is the
Charcot foot, characterised by bone and joint
degeneration that can lead to devastating defomity.
Initally, the patient usually presents with a hot swollen
foot after minor trauma. Radiography at that stage
may be normal but a 99-technetium methylenediphosphonate bone scan will usually show a hot spot
indicative of bony damage. It is important to diagnose
Charcot foot at this stage, and to limit the mechanical
forces acting upon it, by immobilising the foot in a cast
to prevent the development of deformity. Deformity in
the hind foot may result in grossly unstable foot,
but recently, reconstructive techniquesparticularly
realignment arthrodesis of the hind foothave enabled
such patients to avoid amputation.12
Despite promising strategies for healing of the
established diabetic foot ulcer, the ultimate aim is
prevention of ulceration. Neuropathy, ischaemia,
deformity, and oedema are important risk factors for
ulceration. Screening programmes are thus important
and have been shown prospectively to reduce need for
amputations.13
Both screening and active treatment require a wellorganised multidisciplinary approach that provides
continuity of care between primary and secondary
sectors.14 Secondary care should be focused on a diabetic
foot clinic to which rapid referrals should be possible.
Such clinics have reported a reduction in amputations15
and should be available to all diabetic patients.
M E Edmonds
Kings Diabetes Centre, Kings College Hospital, Denmark Hill, London
SE5 9RS, London UK
1

Edmonds ME, Foster AV M .C l a s s i f i c ation and management of

neuropathic and neuroischaemic ulcers. In: Boulton A J M ,C o n n o r
H ,C avanagh PR, eds. The foot in diabetes, 2nd edn. Chichester:

271

John Wiley & Sons Ltd, 1994.

2 Armstrong DG, Lavery LA. Evidence based options for off loading
diabetic wounds. Clin Podiatri Med Surg 1998; 15: 95104.
3 Apelqvist J, Larsson J, Agardh CD. Long term prognosis of diabetic
patients with foot ulcers. J Int Med 1993; 233: 48591.
4 Wieman TJ, Mercke Y K ,C e rrito PB, Taber SW. Resection of the
metatarsal head for diabetic foot ulcers. Am J Surg 1998; 176:
43641.
5 Steed DL. Foundations of good ulcer care. Am J Surg 1998; 176
(Suppl 2a): 20S-25S.
6 Gooden MA, Gentile AT, Mills JL, et al. Free tissue transfer to
extend the limits of limb salvage for lower extremity tissue loss.
Am J Surg 1997; 174: 64448.
7 Eneroth M, Apelqvist J, Stenstrom A. Clinical characteristics and
outcome in 223 diabetic patients with deep foot infections. Foot
Ankle Int 1997; 18: 71622.
8 Pomposelli FB, Marcaccio EJ, Gibbons GW et al. Dorsalis pedis
a rt e rial bypass: durable limb salvage for foot ischaemia in patients
with diabetes mellitus. J Vasc Surg 1995; 21: 37584.
9 Edmonds ME, Walters H. Angioplasty and the diabetic foot. Vasc
Med Rev 1995; 6: 20514.
10 Wieman TJ. Clinical efficacy of becaplermin (rhPDGF-BB) gel. Am
J Surg 1998; 176 (suppl 2a): 74S79S.
11 Naughton G, Mansbridge J, Gentzkow G. A metabolically active
human dermal replacement for the treatment of diabetic foot ulcers.
Artif Organs 1997; 21: 120310.
12 Papa J, Myerson M, Girard P. Salvage with arthrodesis in intractable
diabetic neuropathic arthropathy of the foot and ankle. J Bone Joint
Surg Am 1993; 75: 105666.
13 McCabe CJ, Stevenson RC, Dolan A M .E va l u t ation of a diabetic
foot screening and protection programme. Diabet Med 1998; 15:
8084.
14 Edmonds M, Boulton A, Buckenham T, et al. Report of the diabetic
foot and amputation group. Diabet Med 1996; 13 (suppl 4):
S27S42.
15 Larsson J, Apelqvist J, Agardh CD, Stenstrom A .D e c r e a s i n g
incidence of major amputation in diabetic patients: a consequence of
a multidisciplinary foot care team approach? Diabet Med 1995; 12:
77076

Avoidance of variability and error in

radiology
In such diverse activities as interpretation of
electrocardiograms, recording of history and physical
examination, military photo reconnaissance, computer
programming, air-traffic control, and operation of
nuclear-power plants, tasks requiring cognition are
fraught with variability, and hence with error.1,2 Necropsy
studies have shown death rates caused by missed
diagnoses to be as high as 40%,1 and diagnostic errors in
radiology account for 30% of all medical malpractice
lawsuits in the USA.2 In radiology the risk seems greatest
for diagnosis of cancer, and some studies have shown
error rates of up to 75% for mammography.2
Intraobserver disagreement in the interpretation of
radiographs can occur up to 20% of the time.2
Error should be distinguished from incompetence,
hence quality standards are required. To assess the
feasibility of such standards for the interpretation of
radiographs, P J Robinson and colleagues3 asked three
experienced radiologists to classify 402 emergencydepartment plain radiographs (205 skeletal, 100 chest,
and 97 abdominal) as either normal, showing
insignificant abnormality, or showing abnormality
relevant to the clinical situation. Pairs of observers
disagreed on whether a relevant abnormality was present
in 910% of skeletal, 1119% of chest, and 818% of
abdominal cases. Although only variability, and not
accuracy, was measured, Robinson and colleagues found
the error rate per observer to be 36%. They conclude
that the high levels of interobserver variability between
experienced radiologists must be borne in mind in the
setting of quality standards for the interpretation of plain
films.
272

Errors in the interpretation of radiographic studies can

be due to perceptual misses, poor judgment, incomplete
knowledge, or poor technique for scanning and reviewing
the film.2 Cognitive psychologists have learned much
about why errors occur, and how to avoid them in the
workplace.1,4 Experts rely more on skill-based (automatic)
rules, whereas novices resort mostly to knowledge-based
(conscious) reasoning.1 Expertise has its advantages. In a
study of stroke detection by computed tomography,
emergency physicians had a 33% error rate, twice that
of neurologists and radiologists, and only 17% of
emergency physicians, 40% of neurologists, and 52% of
radiologists achieved 100% sensitivity for identification
of haemorrhage.5
Perceptual misses may account for about 60% of
diagnostic errors in radiology.2 The potential for even
experienced radiologists to miss obvious radiographic
findings should be clear to anyone who has ever puzzled
over one of Eschers paradoxical paintings or been
deceived by an optical illusion. A useful analogy6 for the
missing of lesions is provided by Martin Handfords
book, The Great Waldo Search. Children are challenged to
find Waldo hidden among many other faces in a series of
drawings. Waldo is suprisingly difficult to find, but he is
conspicuous the next time the same drawing is looked at.
Perception is influenced by expectations, and finding
Waldo is easier than picking up a subtle lung nodule on a
chest film because Waldo is known to be present
somewhere in every drawing.
How can the frequency of diagnostic errors in
radiology be minimised? Solutions lie with individuals
and with the system.1,2,4 Radiologists must insist on good
films (and that includes correct positioning of the
patient) and standardised scanning protocols. Detection
of subtle radiographic abnormalities can be enhanced by
comparison with previous scans and access to the
patients history. Good communication between the
referring clinician and the radiologist is essential in
difficult cases. For example, simply knowing the patients
point of greatest tenderness can help the radiologist
decide on a film in which the presence of a fracture is
equivocal. Consensus or double readings also help to
reduce error, although they are labour intensive.7
Quality-assurance reviews too are important in error
reduction, but for radiologists to become more
comfortable with their fallibility requires no small
amount of courage.8
*Michael H Lev, James T Rhea, Robert T Bramson
Department of Radiology, Massachusetts General Hospital, Boston MA
0 2 1 1 4 ,U S A
1
2

Leape LL. Error in medicine. JAMA 1994; 272: 185167.

Berlin L. Malpractice issues in radiology: perceptual errors. AJR
1996; 167: 58790.
3 Robinson PJ, Wilson D, Coral A ,M u rp hy A, Verow P. Variation
between experienced observers in the interpretation of accident and
emergency radiographs. Br J Radiol 1999; 72: 32330.
4 Wadsworth HM, Stephens KS, Godfrey AB. Modern methods for
quality control and improvement. New Yo r k ,N Y: John Wiley;
1986.
5 Schriger D, Kalafut M, Starkman S, Krueger M, Saver J. Cranial
computed tomography interpretation in acute stroke: physician
accuracy in determining eligibility for thrombolytic therapy. JAMA
1998; 279: 129397.
6 Hendrix RW. In defense of a missed lesion. Radiology 1995; 195: 578.
7 Brown J, Bryan S,Warren R. Mammograms screening: an
incremental cost-effectiveness analysis of double versus single reading
of mammograms. BMJ 1996; 32: 80912.
8 Blumenthal D. Making medical errors into medical treasures. JAMA
1994; 272: 186768.

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