Diagnosis, Treatment

and Prevention of the

Diabetic Foot Syndrome

HARTMANN medical edition1

Titel - Diagnosis, Treatment

24.10.2003, 8:25 Uhr

Diagnosis, Treatment
and Prevention of the
Diabetic Foot Syndrome

Published by
PAUL HARTMANN AG
D-89522 Heidenheim
http://www.hartmann.info
By
Dr. med. Stephan Morbach
Specialist for Internal Medicine
Marienkrankenhaus
Soest, Germany
English translation with the
assistance of
Mr. Martin Memmert, MD, PhD
BS (Phil), MRCS Ed.
Dr. Lachlan Arblaster,
BSC, MBCHB, PhD
1st edition August 2003
PAUL HARTMANN AG
ISBN 3-929870-34-7
Translated from the German edition
ISBN 3-929870-29-0
2

Table of contents
Page
Preface

Foreword

Diabetes mellitus - an introduction

Diagnosis and classification of diabetes mellitus

7
Treatment and self-monitoring of diabetes mellitus
9
Secondary complications of diabetes mellitus
11
Definition and history of the diabetic foot
syndrome

13

Epidemiology of the diabetic foot syndrome

16

Socio-economic significance of the diabetic foot

syndrome

20

Costs due to foot complications in diabetics

Psychological aspects and effect on quality of life

20
22

Risk factors for foot complications in diabetics

24

Concurrent diseases in diabetics with foot

complications

32

Diagnosis and differential diagnosis of the

diabetic foot syndrome

35

Diagnosis of sensorimotor and autonomic diabetic

neuropathy and diabetic neuropathic
osteoarthropathy
35
Diagnosis of arterial occlusive disease
40
Classification of diabetic foot lesions
45
Basic principles of the treatment of diabetic
foot lesions
Possibilities of pressure relief
Structured wound treatment and importance of
interactive wound dressings
Moist wound treatment
Treatment of infection

50
50
52
60
68

 Vascular and surgical interventions in the

diabetic foot syndrome
Importance of adjunctive treatment methods
Hyperbaric oxygen therapy (HBO)
Use of growth factors and bio-engineered tissues
Biomechanical wound treatment

76
76
78
79

Tertiary prevention of the diabetic foot syndrome

81

81
84
87

Effects of educating patients at risk

Importance of professional foot care
Provision of adapted footwear for diabetics
Structures for screening, treatment and after
care of patients with diabetic foot syndrome
The diabetic foot: a global problem

71

93
98

Summary and prospects

101

Definitions and explanations

103

Abbreviations

106

Proposed further reading

107

References

108

Preface
We warmly welcome Dr. Stephan Morbachs practical
book on the diagnosis, management and prevention
of diabetic foot problems. Over the past two decades,
interest in this Cinderella specialty has increased.
Numerous diabetic foot conferences have been
organised and books and papers written. However,
this book is a very useful addition to the literature.
The diabetic foot is a great problem world-wide, and
patients with diabetic foot disease are at very high risk
of major amputation of a leg. In this volume, Dr. Morbach
describes with clarity and precision, the interventions
needed to improve outcomes for patients.
The book is beautifully illustrated by colour photographs.
It is compact enough to be easily portable, and will be
useful both for community physicians and healthcare
workers as well as for multi-disciplinary, hospital-based
teams. The contents are very efficiently organised,
and Dr. Morbach has not confined himself to common
areas of management, but also leads the reader through
often neglected realms of psychological and socioeconomic aspects, quality of life and epidemiology. However he does not neglect the more practical aspects
of classification, risk factors, diagnosis and management
of patients with neuropathic and ischaemic ulcers, infections and necrosis. Wound care, dressings and use of
advanced products such as living human skin equivalents are covered in detail, as are the management of
peripheral vascular disease, Charcots osteoarthropathy
and pressure off-loading
This very practical book will be valued by all members of
the diabetic foot team, be they physicians, surgeons,
podiatrists, nurses or orthotists, working in community or
hospital and should help to improve outcomes for
diabetic foot patients.

Michael Edmonds,

Alethea Foster,

MD, FRCP
Consultant Physician

BA (Hons) DipPodM
Head Clinical Specialist Podiatrist

Foreword
Foot lesions affect more than 10% of patients with diabetes
mellitus at some point in their life and are amongst the
most dreaded complications of this disease. They can
cause prolonged periods of immobility and discomfort
and some never heal. Year after year, one in every 200
diabetics loses a leg. The cost of foot ulcerations to the
individual and to society are considerable.
One of the reasons why foot injuries in diabetics represent
such an extraordinary problem is the large number of
different factors that contribute to the aetiology and progression of such lesions. Another relates to the management and treatment of diabetic foot ulceration. Optimum
treatment assumes the knowledge and experience of
a specialist multidisciplinary team, but such teams are
unfortunately not widely available. The majority of all foot
injuries in diabetics, however, are treated by medical
professionals who have neither received specific training
nor have sufficient experience. This book has been
written for them. It is intended as a practical guide to the
diagnosis and management of the lesions found in the
diabetic foot.
Another section outlines the strategies for prevention of
such lesions. This book is based on experience with
diabetic patients in the outpatient foot clinic and on the
wards of the Marienkrankenhaus in Soest (Germany)
over the past eight years and on the knowledge and
experience imparted to me by the Greats of the diabetic
foot, such as Prof. Ernst Chantelau (Dsseldorf) and
Dr. Mike Edmonds (London).
Many questions relating to the diabetic foot still remain
and many procedures have yet to be scientifically
confirmed. This book is nevertheless an attempt to
combine practical guidelines with the current level of
knowledge on the subject.

Dr Stephan Morbach

Diabetes mellitus
an introduction
Diagnosis and classification of diabetes mellitus
Over the past few decades considerable knowledge
has been acquired about the aetiology and pathophysiology of diabetes mellitus. This knowledge places
a burden on the individual and society because without doubt it is a very common, serious and cost-intensive, chronic disease. There are now many options in
terms of diagnosis and treatment to help sufferers. Many
studies have been directed at improving the metabolic status and treating the secondary complications of
diabetes.
Despite these encouraging developments, there are
unfortunately clear indications that a large number of
patients with diabetes mellitus are at present undiagnosed and effective treatment programmes have yet to
be implemented universally. Improved detection rates
and the greater incidence of the disease will increase
the costs of diabetes dramatically in the next few decades. In the years between 1958 and 1993, the number
of people diagnosed with diabetes multiplied five-fold1.
In 1995,135 million patients world-wide were living with
diabetes mellitus. By the year 2025 it is estimated that
this figure will have increased to more than 300 million2.
In Germany it may be assumed that there are currently
at least 4 million known diabetics (5% of the population)
and a further 3 to 4 million who are undiagnosed3.
Diabetes mellitus is a chronic metabolic disorder, predominantly of carbohydrates, which has hereditary and
environmental factors. According to the criteria of the
WHO and the ADA (American Diabetes Association) of
19974, a diagnosis can be established on the basis of
fasting plasma glucose levels of:
1. 7.8 mmol/L (126 mg/dl) or above (with or without the
presence of the classic signs, such as polydipsia, polyuria, tiredness, unexplained weight loss or pruritus).
2. 11.1 mmol/L (200 mg/dl) and above measured at random and coexisting with the disease symptoms mentioned previously
3. 11.1 mmol/L measured two hours after a standardised
oral glucose tolerance test.

Under this classification, four types of diabetes may be

distinguished. Type 1 diabetes involves destruction of
the pancreatic insulin-producing cells, usually resulting in
an absolute insulin deficiency. Type 2 diabetes covers a
broad range from marked insulin resistance with relative
insulin deficiency to a marked impairment of insulin
secretion with slight insulin resistance. Type 3 relates to
genetic, endocrinological, infectious and immunological
underlying diseases, diseases of the pancreas and
iatrogenic or chemically induced forms. Type 4 (gestational diabetes) occurring during pregnancy and
disappearing again post partum. Type 1 and type 2 are
the most common.
Well over 80% of all diabetics can be classified as
type 21.
Diagnostic guideline values for establishing diabetes mellitus (ADA 1997)

Diabetes mellitus

Fasting
plasma glucose

Random blood
sugar

Oral glucose
tolerance test
(75 g glucose)

7.0 mmol/L

11.1 mmol/ L
with symptoms

11.1 mmol/ L
after 2 hours
7.8 <11.1 mmol/L

Impaired glucose
tolerance
Impaired fasting
glucose

6.0 <7.0 mmol/L

Normal

<6.0 mmol/L

The distinction between type 1 and type 2 diabetes based

previously on age of onset (juvenile diabetes, senile
diabetes) is difficult to make in individual cases. In the
following situations, the diagnosis of type 1 diabetes is
suggested, even in more advanced age:
1. Normal bodyweight with further weight loss
2. Absence of family history of diabetes mellitus
3. A labile metabolic status on oral antidiabetic
medication
4. The appearance of ketone bodies in the urine
5. The detection of auto-antibodies to pancreatic cells or
their components (GAD = Glutamic Acid Decarboxylase; ICA = Islet Cell Antibodies) in the blood5
suggest a diagnosis of type 1 diabetes, even with
a more advanced age of onset.
8

New aetiological classification of diabetes mellitus

(American Diabetes Association, ADA 1997)
I. Type 1 diabetes
-cell destruction, usually resulting in absolute insulin
deficiency
A. immunologically mediated
B. idiopathic
II. Type 2 diabetes
Type 2 diabetes can range from marked insulin
resistance with a relative insulin deficiency to marked
secretory impairment with insulin resistance.
III. Other specific types
A) Genetic defects of cell function
B) Genetic defects of the action of insulin
C) Diseases of the exocrine pancreas, e.g. pancreatitis,
haemochromatosis
D) Endocrinopathies, e.g. acromegaly, Cushings
syndrome
E) Drug or chemical induced, e.g. glucocorticoids
F) Infections
G) Rare immune-mediated forms, e.g. anti-insulin
receptor antibodies
H) Other genetic syndromes, e.g. Downs Syndrome,
Klinefelters syndrome
IV. Gestational diabetes (GDM)

Treatment and self-monitoring of diabetes mellitus

The treatment of diabetes mellitus has the following aims:
1. Prevention of acute metabolic disorders (hypoglycaemia, symptomatic hyperglycaemia, hyperosmolar and ketoacidotic diabetic coma)
2. The avoidance of diabetic complications, both
microvascular (retinopathy, nephropathy and neuropathy) and macrovascular (coronary heart disease,
peripheral and cerebral arterial occlusive disease).
The incidence rate (rate of new occurrences) of diabetic
ketoacidosis is currently between 5 and 8 per 1,000
patients annually1 and the related mortality well below
1%. In the largest prospective study on the treatment of
type 2 diabetes (UKPDS, almost 4,000 patients, 15 year
observation period) only one insulin-treated patient
died during an episode of hypoglycaemia6. Commensurate with the origin of the disease, only insulin therapy
9

is available for the treatment of type 1 diabetes. A

distinction is drawn here between conventional insulin
therapy (CT) with the administration of long-acting or
mixed insulin once to three times daily, and intensified
conventional insulin therapy (ICT) on the basal bolus
principle (covering basal requirements with administration of long-acting insulin once to four times daily and
an injection of normal (short-acting) insulin at mealtimes
depending on the quantity of carbohydrates ingested.
The insulin analogue (designer insulin) Humalog and
Novo Rapid (insulin lispro and insulin aspart) has
been available for this purpose since 1996. If basal and
mealtime requirements are provided constantly via a
pump, then this is referred to as continuous subcutaneous insulin infusion (CSII) or insulin pump therapy.
The success of treatment is measured by the proportion
of glycosylated haemoglobin to total haemoglobin
(HBA1c value). This value is maintained below 7% to
prevent vascular diabetic complications in accordance
with the results of the DCCT study7 and the UKPD
study6, corresponding to near-normoglycaemic blood
sugar control.
Since the end of the DCCT study in 19937, ICT has been
considered the gold standard in the treatment of type 1
diabetics. Compared to conventional insulin therapy, the
occurrence or progression of vascular complications
has been reduced by 50 to 70%. Similar reduction rates
have been published for an intensive treatment regime
in type 2 diabetes. In obese patients, treatment with
insulin or oral antidiabetics (e.g. glibenclamide6, metformin8) is compared to less intensive (mainly dietary)
therapy with less specific target criteria. In this case the
early institution of insulin therapy is frequently necessary
to achieve the desired HBA1c value. Self-monitoring by
diabetics nowadays goes well beyond the self-measurement of blood and urine glucose values:
1. Blood pressure self-monitoring
2. Weight control
3. Self-determination of protein elimination in the urine
4. Regular foot inspections for diabetic ulcer.
Patient training and instruction to increase self-help
(empowerment) is necessary as a further pillar of
diabetes therapy and should no longer be withheld from
any diabetic.

10

Secondary complications of diabetes mellitus

Sustained hyperglycaemic blood sugar values are the
underlying pathological factor in the development of
secondary diabetic complications. In type 1 diabetes, the
diagnosis is established shortly after the onset of hyperglycaemia and several years of inadequate metabolic
compensation are generally necessary for any secondary
complication to become apparent. The onset of type 2
diabetes often passes unnoticed and the disease can be
diagnosed four to seven years too late9. During this
phase of undiagnosed diabetes mellitus, excessive blood
sugar values result in the development or progression of
microvascular (diabetic retinopathy, diabetic nephropathy
and diabetic neuropathy) and macrovascular (coronary
heart disease, peripheral arterial occlusive disease,
cerebral arterial occlusive disease) complications. These
complications of diabetes are associated with certain life
habits (sedentary lifestyle, smoking, alcohol) and other
disorders of a metabolic (lipid metabolism disorders,
obesity) and haemodynamic (hypertension) nature. In
asymptomatic patients with often only slightly raised
blood sugar values, doctors with insufficient experience in
diabetology are reluctant to diagnose diabetes mellitus
and to institute appropriate therapy at an early stage.
At the time of diagnosis, a cardiovascular complication or
neuropathy is already present in about 10% of diabetics
and nephropathy or retinopathy in 20 to 30% of patients10.
Forty percent of newly diagnosed diabetics in the UKPD
study6 had arterial hypertension (in most cases untreated). Inadequately treated hypertension is at least as
important a risk factor as excessive blood sugar values,
particularly for macrovascular complications but also
for the progression of an existing diabetic nephropathy11.
Combinations of microvascular disorders, i.e. retinopathy
and neuropathy, and the formation of foot ulcers are
described at the time of diagnosis12. In the first four years
following diagnosis, about 20% of diabetics suffer from
peripheral diabetic neuropathy, which increases to 50%
or more after 15 years. Diabetic retinopathy is found in
20% of type 2 diabetic at the time of diagnosis. Again at
15 years, a background retinopathy is found in 97% of
all type 1 diabetics and about 70% of type 2 diabetics.
A proliferative retinopathy necessitating treatment is found
at this stage in 30% and 15% of patients, respectively1.

11

In the worst-case scenario, diabetic nephropathy can

result in terminal renal insufficiency and the need for
haemo dialysis in the early stages. In Germany no less
than 35% of all dialysis patients in 1996 were diabetics,
(more than 90% of them type 2 diabetics). With annual
treatment costs of about 40,000 EUR per dialysis patient,
this complication alone generates direct treatment
costs of more than 500 million EUR annually13. Peripheral
arterial occlusive disease affects diabetics four to ten
times more often than non-diabetics, and the rate of
CVA is approximately threefold. Half of all deaths among
diabetics are due to a cardiac disease1. Some information about the differing risk of micro- and macrovascular
complications may be deduced from the patient family
history. Late diagnosis of diabetes and genetic predisposition appear to put an individual at increased risk
of secondary microvascular lesions. Macrovascular
problems are more likely to occur in patients with lipid
metabolism disorders, obesity and an increased
incidence of hypertension in the family14.
Screening of risk groups for early detection of diabetes
mellitus and subsequent treatment of hyperglycaemia
and hypertension are cost-effective15. It also reduces the
complications of diabetes dramatically. Early diagnosis
then allows regular follow up examination of patients in
order to delay or prevent end organ damage (blindness,
renal insufficiency, amputation), which incurs great costs
to the health care system.

12

Definition and history of the

diabetic foot syndrome
The concept of diabetic foot syndrome incorporates
various clinical pictures characterised by different
aetiologies and pathological mechanisms. Common to all
is the fact that injuries to the foot of the diabetic patient
can result in complications that may lead to amputation of
the whole limb if treatment is delayed or ineffective.

Pryce described a case of a perforating ulcer in diabetes and atactic symptoms as early as 188716.
In the first half of this century, foot lesions in diabetics,
which frequently lead to amputation, were considered
an unavoidable complication of diabetes associated with
arteriosclerosis and were classed under the heading
of diabetic gangrene17.
In 1934, Elliot Joslin, one of the pioneers of diabetology,
published an article entitled The menace of diabetic
gangrene18. According to his observations, diabetic
gangrene as a cause of death in diabetics had increased
from 2% before 1914 to more than 12% by 1926, only a
few years after the discovery of insulin. Although impaired circulation and the consequent diabetic gangrene
was considered the main cause of diabetic foot complications, Joslin described in detail the now well-known
common causes of diabetic foot lesions, i.e. burns from
hot water bottles, ill-fitting new shoes and lack of foot
hygiene. He vehemently advocated the intensive education of patients about cleanliness and care of their feet
in order to minimise the occurrence of impending diabetic gangrene. Consequently it has been forced upon
me, he wrote, that gangrene is not heaven-sent, but
is earth-born.
However, it was not until the 1950s that diabetic neuropathy, ischaemia and infection, were finally recognised
as precondition5 of foot complications in diabetics facts
that still hold good today. The good prognosis for local
surgery in neuropathic lesions and the confinement of
radical surgical interventions to ischaemic changes was
also described first at that time19.
The need for specialised care of diabetics with foot
problems became increasingly apparent in subsequent
years and it was recognised that many approaches
to treatment (pressure relief, shoe provision) could be
13

derived from the procedures adopted in another disease

associated with a neuropathic impairment of sensory
perception, leprosy20. In the 1970s, special programmes
to improve the prognosis in diabetic foot complications were introduced for the first time in Atlanta, USA.
The amputation rate in diabetics was reduced by
50%. Institutions with similar success rates were subsequently set up in Europe, firstly in Geneva and London22,
and then in Germany in 1983 (Prof. Ernst Chantelau,
Dr. Maximilian Spraul and Prof. Michael Berger at the University Hospital of Dsseldorf 23, 24). In 1989, the St.Vincent
Declaration25 set a target of halving the amputation
rate in diabetics within a five-year period. Subsequently,
outpatient foot departments were created. In 1993
these joined together to form an association, the Diabetic
Foot Working Group, affiliated to the German Diabetes
Society.
Increasing interest in the diabetic foot was also reflected
in research activities. In the journals of the American
and British Diabetes Societies the number of articles on
subjects related to diabetic foot syndrome in each case
doubled between 1982 and 1996, while at the American
Diabetes Congress, three times as many contributions
dealt with the subject in 1996 as in 1980. Since 1998,
a medical journal The Diabetic Foot, published four
times a year in England, has been devoted to the subject. International meetings on the topic of diabetic
foot problems lasting several days are held annually in
San Antonio (Texas, USA) and every two years in
Malvern (England). An international symposium was
organised on the diabetic foot for the first time in
1991 in the Netherlands, attended by 500 participants
from 46 countries. The third and most recent was held
in May 199926.

14

Diabetes treatment and research in Europe:

The St. Vincent Declaration (1989)
Five-year aims of the St. Vincent Declaration:
Implementation of effective measures for
prevention of costly complications
Reduction of the rate of new cases of blindness
due to diabetes by one third or more
Reduction of the numbers of people entering endstage diabetic renal failure by at least one third
Reduction by one half in the rate of limb
amputations for diabetic gangrene
Cut morbidity and mortality from coronary heart
disease in the diabetic by vigorous programmes of
risk factor reduction
Achieve pregnancy outcome in the diabetic
woman that approximates to that of the nondiabetic woman

Despite all these activities, the care of patients with diabetic foot problems in Germany has still not been
satisfactorily resolved, and further urgent improvements
are required.

15

Epidemiology of the
diabetic foot syndrome
A quarter of the diabetic population is at increased
risk of foot injuries as a result of the presence of diabetic neuropathy or an arterial circulatory disorder.
Every year 3 to 7% of diabetics suffer a foot lesion for
the first time. Following healing of the injury, the risk
of suffering a further ulceration (relapse) increases
annually to between 30 and 100%, depending on the
quality of the after-care. Like previous amputees,
these patients must also be regarded as high-risk
patients and require very intensive, structured monitoring and care. In Germany, more than 20,000 foot
lesions in diabetics still culminate in amputation per
year. Following an amputation, mortality is approximately 20%. Within 3 years 50% of the surviving
patients also undergo an amputation on the contralateral side. The five year survival of patients after
amputation is low, approximating 25%.

More than four million diabetics are known to be living in

Germany today27. If patients at risk of diabetic foot
complications are defined as those diabetics who suffer
from diabetic neuropathy and/or in whom two or more
foot pulses cannot be felt, then 25% of the diabetic
population belong to this risk group28. In the case of
Germany, this yields an estimated 1.25 million diabetic
patients at risk of lesions of the lower limb. The most
negative consequence of such an injury, amputation,
affects diabetics of various age groups up to 100 times
more frequently than their non-diabetic peers29.

16

Sensorimotor and autonomic diabetic neuropathy and

peripheral arterial occlusive disease must be regarded
as the most common underlying conditions for diabetic
foot complications. These can lead to foot injuries in
diabetics either alone or in combination. In 600 English
patients with ulceration, neuropathy was found to be
the cause in 45%. Fortyfive percent of these patients exhibited both diabetic neuropathy and a circulatory disorder, and only 7% suffered exclusively from a peripheral
circulatory disorder. In aetiological terms, neuropathy
proved to be responsible for 90% of injuries30. In 260 of
our own patients with foot injuries, neuropathy was found
in 80% of cases, and of these 43% had accompanying
circulatory disorders. As in the British study30, an isolated
arterial occlusive disease occurred in only 10% of
patients.
Diabetic neuropathy must therefore be seen as a predisposing factor to diabetic foot lesions. This may be due
to external (e.g. ill-fitting footware) or internal pressure
(limited joint mobility) foot deformities and severe foot
pressure. Increased foot pressure is to be found in 20%
of patients even without a clinically detectable neuropathy and can be used to identify patients at risk of
ulceration. Almost 30% of patients with increased foot
pressure suffer from ulceration during the following two
years30. The incidence of symptomatic diabetic neuropathy varies with the patients age and the duration of
diabetes: 5% of diabetics aged between 20 and 29 years
exhibited neuropathy. This rises to 40% between the
ages of 70 and 79 years. At the time of diagnosis, 7% of
patients in the UKPD study5 were suffering from neuropathy. Five years after diagnosis, 20% of the patients
had detectable neuropathy and this figure increased to
approximately 45% with the longer duration of the
disease (40 years or more)31,32.
Diabetic neuropathy was found in half the type 2 diabetics aged over 60 years. Although the lack of pain from
injuries predisposes to the development of diabetic
foot complications, pain in the lower extremity does not in
any way preclude neuropathy (painful-painless leg).
Veves found a painful neuropathy of this nature in almost
half of neuropathic patients and a third of patients with
foot ulcer33.

17

Among non-selected patients in general practice,

an arterial occlusive disease is found in about a third of
diabetics, about four times as often as non-diabetics34.
Preliminary signs of ulcer disease (prelesions such
as a hard callus with or without maceration) are detected
in approximately one in seven patients with an existing
diabetic neuropathy. In these patients, the development
of a perforating ulcer of the foot (classic neuropathic
pressure ulcer) can be avoided with adequate and early
treatment35. In a regional study in Rhineland-Palatinate,
hyperkeratosis was found in almost 70% of patients, of
whom half showed additional subcallosal suggillations.
In this study involving almost 900 patients, 8% exhibited
a florid, open foot lesion, and almost 15% of those
studied reported a previous history of such lesions36.
When a lesion of this kind is healed, there is still a lifelong
risk of recurrence of the ulcer because of the ongoing
underlying disease. In a large Swedish study recurrent
ulceration was found in 34%, 61% and 70% of ulcer
patients after 1, 3 and 5 years, respectively. Fifty percent
had suffered another lesion within two years37.
Foot ulceration is the most frequent cause of amputations
in diabetics38. The risk of an amputation of a limb
varies according to the patients age, race and sex 39, 40, 41.
Common to all, however, is the fact that the risk of undergoing an amputation is 20 to 40 times higher (in some
age groups up to 100-fold) than in comparable nondiabetics39,42,43. However, the idea that a limb amputation
is an event that occurs late in the course of diabetes
is incorrect. According to an English study, 20% of
amputations occur in the year in which the diabetes is
diagnosed44. The level of amputation is particularly
important for a later independent lifestyle and the
prognosis of the patient. After amputations of the toes
and forefoot (minor amputations) between 5% and
7% require permanent care, whereas in the case of major
amputations (lower and upper limb) 36% require permanent care.

18

The probability of survival and the risk of an amputation

on the opposite side are also closely correlated to
the amputation level. Mortality after two amputations is
approximately 3%, whereas this figure rises to 20%
after major amputation45. The 5 year survival rate after
amputation is 27% which compares to 60% of patients
whose foot lesion is healed with conservative treatment37.
The probability of a limb amputation on the opposite
side following a successful major amputation is 12% in
the first year and more than 50% after three years.
If the aim of reducing amputation by half is to be
achieved, the diabetic patient must be advised to avoid
any situation that might result in foot ulceration.

19

Socio-economic
significance of the diabetic
foot syndrome
Costs due to foot complications in diabetics
When talking about medical topics, it is not possible to
ignore the associated costs. Few data are available
on the costs resulting from diabetic foot syndrome in Germany, but the extent of the problem can be illustrated
using data from Scandinavia, Great Britain and the USA.
Overall, the costs generated by diabetes are about
three times as high as those produced by non-diabetics46. Foot complications constitute a major proportion
of these: every fifth hospital admission for diabetics is
a result of foot problems. As the inpatient period can be
prolonged, foot complications are responsible for almost
half of all inpatient days for diabetics47. In Great Britain,
hospitalisation as a result of diabetic foot complications
alone results in annual costs equivalent to 375 million
EUR. Inpatient treatment costs are the most significant
single factor. With primary healing, about 30% of the total cost derives from hospitalisation, but where amputation is required this figure is 65% to 80%48,49. The average
healing duration for diabetic foot lesions is about four
months. Ten percent of all lesions persist for more than
one year, which incurs further costs for outpatient care.
Fifteen percent of all foot ulcers in diabetics do not heal
before the patients death49.
Beside the long period of inpatient care that is frequently
required, the high likelihood of an amputation and the
risk of life-long disability are important cost-generating
factors48. The average costs of a superficial diabetic
foot ulcer are estimated at approximately 4,500 EUR. In
the presence of a deep infection this increases to 23,500
EUR and with the occurrence of gangrene may rise
to 50,000 EUR. In the case of primary healing, expenses
amounting to some 7,500 EUR are incurred, but this
could be multiplied sixfold where an amputation is required.

20

The costs of antibiotic treatment (less than 1% of the

overall costs) or technical orthopaedic measures (about
3% in the case of primary healing) are relatively small50.
The costs of local wound treatment are less determined
by the use of certain wound dressings, but to a much
greater extent by the frequency with which bandages are
changed.
When calculating the actual financial burden resulting
from diabetic foot problems, it is essential to take a
long-term view. The potential risk of recurrent ulceration,
amputation or the patients death must be incorporated
in the calculations. Over a 3-year period, a primarily healing neuropathic ulcer incurs costs of about 15,000 EUR
overall51. With a conservatively healed ischaemic lesion,
the costs rise to about 25,000 EUR. If amputation of an
extremity is necessary, in the following three years on
average about 40,000 EUR annually are required simply
for domestic care. In the USA, the direct costs of an
amputation are put at 15,000 to 50,000 EUR depending
on the amputation level required52. If the indirect costs
resulting from loss of productivity are added to this, the
figure is more than doubled53. A recent American study
calculated the annual total costs resulting from diabetic
foot problems in the United States to be 5,000 million
EUR54.
As outlined earlier, the diabetic foot syndrome incurs
massive financial costs to the health services and the
patient. Just as impressive as the costs incurred, are the
calculations of the potential savings that can be made
from preventive strategies in the treatment of the diabetic
foot syndrome. In the USA in 1998 the annual savings
resulting from the avoidance of amputations as a result of
structured patient information was estimated at 3 to
4,500 EUR per patient52. Calculations by Assal in Geneva
suggest that for every dollar invested in educating
diabetics, savings of three to four times that amount may
be expected. Savings made as a result of avoiding
nine limb amputations could finance the treatment of 400
diabetic patients for a year, 820 hours of group training,
further 1,100 hours of individual training for diabetics and
an additional 1,500 foot visits55.
One cost item, however, does not feature in any of these
calculations, namely the cost to the patient themselves
in terms of the emotional trauma suffered and the loss of
quality of life and independence.

21

Psychological aspects and effect on quality of life

Quality of life is a descriptive concept that is intended to
provide information about the degree of satisfaction with
life or those factors which make life worth living (from:
J.M. Last: A Dictionary of Epidemiology). In medicine,
the concept involves three dimensions:

1. Physical capacity
2. Subjective well-being
3. The individuals social relations with his environment

Since purely objective findings are insufficient for assessing the quality of life, the patients subjective well-being
and his own assessment of his condition increasingly
need to be included in the medical evaluation and given
due consideration in the treatment of a disease56.
Logically, the effect of diabetic foot injuries on the
quality of life of both the patient and their relatives should
be considered jointly. The few studies that have been
published to date on this subject are unanimous: the
decisive factor that affects the quality of life of patients
with diabetic foot problems is the restriction on their
mobility. This adversely affects their social situation and
can result in various psychological responses57,58.
One example of this is the fact that patients who
are mobile after amputation rate their quality of life more
highly than patients with florid foot lesions59. The restriction on the sphere of activity impinges on the patients
occupational and social situation and can lead to feelings such as guilt (being a burden on others). The
resultant anger and frustration (loss of independence)
are associated with fear and worry (How long will this go
on for?, Will it result in amputation?)57. Relatives
on the one hand become the target for the patients unhappiness and imballance and on the other hand
have to assume new roles in the patients life (transport to
medical appointments, taking over everyday activities
previously undertaken by the patient themselves).
Opportunities for social contacts and the scope for
movement (e.g. travel and holidays) are equally limited
for patient and relatives.

22

Tension in relationships is therefore unavoidable.

A few sufferers, however, regard the more intensive contact with their relatives, even if involuntary, as a positive
factor and acquire more patience in dealing with other
everyday problems as a result of handling this particular situation. The ability to cope with these changes is
influenced by the patients age and social origins58.
Among younger patients, the anxiety of losing ones job,
impending financial losses and the reduction in selfesteem take precedence. Elderly sufferers rate social
isolation as more serious. Physical effects on the quality
of life are elicited in the form of side effects to any antibiotic treatment required and the tiredness and exhaustion that result from the increased expenditure of energy
needed for moving about57.
Fear of the consequences of foot ulceration can channel
the patients behaviour in various directions: a depressive
mood or paranoia-like fixation on the foot injury may
result. Equally there may be total denial of the situation,
associated with non-attendance at outpatient appointments or failure to attend in the event of new injuries60.
It is at this point that the diabetic foot team can provide
targeted, patient-oriented information about the disease
and avoidance of unrealistic expectations on the part
of the patient. This effort of the team, together with the
provision of therapeutic certainty are important bases
for the successful treatment of patients with foot lesions.
Disappointment and failure can thus be minimised,
avoiding the incorrect behaviour pattern in patients.
Psychological problems affect the clinical course and
the subsequent outcome of treatment of patients with
diabetic foot complications. Members of treatment
teams should be aware of such stresses on the patienttherapist relationship, be willing to review treatment,
and, if necessary, change their own patterns of behaviour and expectations in this respect.

23

Risk factors for foot

complications in diabetics
The main risk conditions for the occurrence of foot
lesions in diabetics are the loss of protective
mechanisms in the presence of a diabetic neuropathy
and the absence of sufficient tissue perfusion
as a result of an arterial occlusive disease (AOD).
The most important risk factors are:
Bony foot deformities, the existence of increased
plantar pressure, impairment of vision and mobility
and a previous history of a diabetic foot lesion.
Infections play a minor role in the genesis of a diabetic foot lesion, but assume considerable
importance in existing injuries as a risk factor for
progression to amputation.
Reduced sweat gland activity,
loss of the plantar fat pad
and impaired joint mobility in
diabetic neuropathy, together with the resultant callus
formation, lead to callus
haematomas at exposed sites
if the pressure is not relieved

One of the most effective means of preventing diabetic

foot complications is a regular foot examination as
well as the identification of risk indicators. Unfortunately,
foot examinations in diabetics are only rarely performed.
And when they are performed in both outpatient
and inpatient settings then they are often inadequate.
A thorough foot status is established in only about 10%
of all diabetics during routine outpatient visits. Even
among patients who are admitted to hospital for a diabetic foot ulcer only 14% are adequately examined in
terms of their foot findings61.

24

The following section begins by presenting the different

risk factors for foot lesions which may lead to amputations
in diabetics and their importance, before going on to
investigate in detail the causative factors of foot injuries.
Although different authors ascribe different significance
in their studies to the various risk factors for diabetic
foot lesions, the same basic risk factors are implicated:

1. Peripheral neuropathy
2. Bony foot deformities
3. Existence of increased plantar pressure
4. History of ulcer
5. Peripheral arterial occlusive disease.

Peripheral sensorimotor neuropathy represents the most

important risk factor for the occurrence of foot ulcerations and amputation in diabetics. Patients rarely develop
a diabetic foot ulcer in the absence of neuropathy. The
loss of the protective perception of pain and pressure
is the underlying cause of foot complications in diabetics.
The occurrence of a foot ulcer in the great majority of
cases is a multifactorial and complex process in which
various risk factors play a role. Neuropathy is found as a
subsidiary factor in about 90% of cases62. The risk of
suffering ulceration of the foot increases ten-fold in the
presence of signs of diabetic neuropathy (detected by
the pathological monofilament test and pathological
vibration sensation in the biothesiometer test) compared
with neurologically healthy diabetics63.
In addition to the reduced awareness of injury resulting
from the impairment of the sensory nerve fibres, two other
major risk factors are involved:
1. The occurrence of bony deformities of the foot
2. Increased plantar pressure
These factors also lead to atrophy of the small muscles
of the foot with the consequent impairment of balance.
The impairment of autonomic nerve fibres leads to a
failure of sweat gland function and consequently to loss
of skin elasticity.

25

Typical localisation of foot

injuries as a result of narrow
footware or hard toecaps

Poor foot care in a 90-year old

diabetic resulting in deformed
onychomycotic toenails,
excessive callus formation on
the soles of the feet and
subcallus haematomas on the
first and second toes

Foot deformities, together with severe hyperkeratosis

(callus formation) contribute to foot ulceration in about
60% of cases, and increased plantar pressure in 50%.
Reduced adaptability and increased pressure loads
arise through a variety of mechanisms: changes in the
skin and peri-articular structures (e.g. joint capsules)
result in an impairment of joint mobility64. The resultant
increase of approximately 30% in foot pressure values,
combined with the loss of protection due to neuropathy,
considerably increases the risk of an ulcer formation.
26

This is supported by studies of rheumatoid arthritis

patients with foot deformities, but without concurrent
neuropathy65. More recent studies indicate hardening of
the peri-articular connective tissue and increasing
atrophy and fibrosis of the plantar fat pad as independent risk factors, particularly in recurrent lesions66,67.
Such changes are found in the presence of even mild
neuropathy, but their intensity increases proportionately
to the severity of underlying the neuropathic disease.
An effect on the capillary blood flow as a result of the
increased plantar pressure load and increased fibrosis
as a result of a chronic inflammatory irritation are suggested as possible pathological causes. Fibrosis and
atrophy of the plantar fat pad affect the biomechanical
properties of the sole of foot in the same way as the
frequently observed increased callus formation. Removal
of the callus reduces the pressure load on the sole
of the foot by about 25% and hence reduces the risk of
subcallous haematoma, as well as subsequent ulcer
formation68.
Ischaemic diabetic foot
syndrome with pressure
necrosis on the sides of the
foot and toes, associated
with dry gangrene of the third
toe

Finally, patients with a previous history of diabetic foot

ulcer are at highest-risk of relapse, because of the
constant risk conditions and the structural foot changes
described (less resistant and less flexible tissue or
change in the pressure-bearing surface following minor
surgery). The risk of suffering a relapse is tripled
following primary ulcer healing69 and increases to about
50-fold following surgical treatment70.

27

Ischaemia as a consequence of peripheral arterial

occlusive disease represents a minor contributory factor
to the occurrence of diabetic ulcer (23 to 35%62,71),
but assumes increasing significance as a risk factor in
the progression of a foot ulcer towards amputation38.
Critical limb ischaemia (CLI) is present in 50% of all
diabetic foot lesions that end in amputation. Whereas
ulcer formation is a multifactorial process, ischaemia
in itself can be sufficient to result in amputation.
While peripheral arterial occlusive disease in non-diabetics is the reason for amputation in the majority of
cases, several factors are usually involved in diabetics,
both in the occurrence of an ulcer and also in the subsequent progression to amputation. In 80% of cases,
there is an identifiable, acute cause, mainly footwearrelated or thermal trauma (burn, excessive cold). Subsequent ulceration and insufficient wound healing
contribute to the amputation of all or part of a limb38.
Peripheral oedema (40%), ignorance about foot care
(25%) and lack of social integration (20%) are further
factors leading to amputation.
In 80% of cases the initial insult that results in ulcer formation and ultimately amputation can be identified 38,62,72,
a fact that appears extremely important in relation to the
advice given to patients in order to prevent recurrance.
Infection plays a minor role in the causation of diabetic
foot lesions (less than 1% of cases71), but is a major
risk factor for amputation (involved in 60% of cases)38.
What is important here in diabetics is the frequent absence of the classic signs of infection (fever, leucocytosis, increased erythrocyte sedimentation rate, [ESR])
because of the existing immunopathy73. Despite multidisciplinary care, surgery is unavoidable in almost 90%
of diabetics with deep foot infections. In 34% of cases
this involves minor amputations and in 10% a high-level
limb amputation.

28

The probability of a major amputation is increased by the

presence of:
1. Pain (the relative risk increases 13-fold)
2. Progressive gangrene (14-fold)
3. Pre-existing intermittent claudication (6-fold).
None of these signs, however, precludes primary healing or healing following minor surgery74. The risk of
having to undergo an amputation is also increased in the
presence of an additional cardiovascular disease, diabetic neuropathy, reduced arterial ankle pressure (less
than 80 mmHg) or toe pressure (less than 45 mmHg).
Male patients74 are also at higher risk. A further important
risk factor for the occurrence of foot ulceration is impaired vision and reduced mobility, as these factors limit
the patients ability to co-operate in foot inspections and
foot care. Eighty percent of sufferers are totally unaware
of this restriction. In a study by Assal, impaired vision
was found in 70% of diabetic ulcer patients studied, 10%
of the patients with neuropathy but no ulceration, and
only 5% of non-neuropathic diabetics.
Inadequate visual acuity (defined as patients incapability to observe a lesion of 3 mm in diameter at the
minimum eye-foot distance) was found in 50%, 5%
and 3% of patients, respectively75. Impaired vision also
constitutes an independent risk factor for fractures
with the subsequent formation of Charcots deformity as
a result of the increased risk of spraining and tripping76.
In a large Italian case-control study possible risk factors
for ulcer formation were77:
1. Male sex (the relative risk increases 3-fold)
2. Lack of family involvement (1.4-fold)
3. Difficulty attending follow up appointments (2-fold)
4. Lack of diabetes education (3-fold)
5. Irregular compliance with foot inspections.

29

In central Europe, the occurrence of diabetic foot

ulcerations is preceded in 28%78 to 55%79 of cases
by shoe-related injuries. Eighteen percent are the consequence of injuries related to foot care, while 3% are
preceded by other minor trauma. Thermal traumas, particularly burns, are relatively rare (2% of all cases), but
are significant because of the risk of hypertrophic scar
formation and delayed recovery. At temperatures of
44 C, a theoretical exposure of six hours is required for
necrosis formation, whereas at a temperature of 50 C,
only a five-minute exposure is sufficient80. In diabetics, a
disorder of hot and cold perception is found in the hands
as well as in the lower limb. In other regions of the world,
causes of diabetic foot injuries include rat bites81, worm
infestations82 or burn injuries from the use of alternative
medical methods such as moxibustion, a traditional
Chinese medical procedure83.
As previously, mentioned certain constantly recurring
sets of circumstances can result in foot ulcerations71
and amputations38. An understanding of these facts is
essential for the successful employment of preventative
strategies. A distinction is drawn here between contributory factors which, together, might result in the event
(ulcer or amputation), and sufficient causes which can
produce such an event in themselves. The causal factor
can be found in 80% of ulcers and 86% of amputations.

30

Three frequent pathways, which together account for

60% of all ulcers, are:

1. Neuropathy, deformity, callus formation, increased

pressure
2. Penetrating minor trauma
3. Ill-fitting shoes61

The combination of minor trauma, skin ulceration and

delayed wound healing with or without the co-existence
of infection or gangrene results in amputation in 70%
of cases. Eighty-four percent of all amputations are preceded by ulcer formation38.
Diabetic foot ulcerations are a significant problem
because:

1.
2.
3.
4.

They are very common

They are cost-intensive
They can identify patients at risk of amputation
They adversely affect the functional status and wellbeing of the patient concerned
5. They can be avoided in many patients by
preventive foot care and the use of specifically
designed footwear84

Early identification of the risk factors and appropriate

implementation of preventive and therapeutic measures
would dramatically reduce the occurrence of foot
complications and their consequences in diabetics.

31

Concurrent diseases
in diabetics with
foot complications
The average age of diabetics with foot injuries is
more than 65 years85,86. Mediocre response to treatment
in these patients is due in part to the multimorbidity
of sufferers. Patients with foot lesions suffer to a considerable extent from macrovascular disease and the consequences of diabetic microangiopathy. Diabetic retinopathy, autonomic diabetic neuropathy and diabetic
nephropathy are more frequently found in type 1 diabetics than in type 2 diabetics with foot lesions, who
have a greater incidence of coronary vessel disease and
peripheral arterial occlusive disease (PAOD)85. In 243
patients from the Dortmund Hospital, neuropathy was
found in 80% of ulcer patients. Nephropathy, retinopathy
and coronary heart disease were found in 50% of
patients. Involvement of the arteries supplying the brain
in 22% and PAOD in almost 70%87. Similar figures
were obtained in our own patient population: neuropathy
80%, nephropathy 65%, retinopathy 55%, myocardial
infarct 19%, stroke 20% and PAOD 56%.
The risk of a concurrent disease of the coronary vessels
in patients suffering from PAOD is increased two and a
half times compared with patients without disease of the
leg vessels. The disease is frequently asymptomatic,
particularly in women88. Prognostically, the occurrence of
gangrene of the toe in particular may be considered
an extremely adverse sign in terms of patient survival
rate. The mean survival time of these patients following
the onset of gangrene is on average less than 18 months.
In the study quoted, smokers (82% smokers vs. 45%
non smokers) and patients requiring an amputation (64%
amputated vs. 27% non amputated) were found significantly more often among patients who died early than
among those with a more favourable prognosis for
survival86.
There is an obvious relationship between increased
protein loss from the kidney (micro-albuminuria, proteinuria) and the occurrence of ulcers in diabetics. Although
the abnormal excretion of albumin from the kidney in
type 2 diabetics is of renal origin, it reflects a vascular
process that involves the nephron and the tunica intima
of the large vessels. Micro-albuminuria is therefore,
32

a marker of a progressive renal disease and a predictor

of a generalised arteriosclerosis and early death89.
Increased albumin excretion occurs most frequently in
patients with ischaemic and neuro-ischaemic lesions.
It is also found to a greater extent in patients with purely
neuropathic ulcers, as compared to ulcer-free
diabetics90.
Diabetic retinopathy is an important finding in foot
patients for several reasons. Firstly it represents a risk
factor for the development of foot injuries (see also
chapter Risk factors for foot complications in diabetics).
Secondly, the concurrent presence of the two
Typical fundoscopic
findings in proliferative diabetic retinopathy:
diabetic retinopathy is considered a risk factor for
foot complications because
of the impairment of vision

diseases is increasingly found at the time of diagnosis in

type 2 diabetics11. If an arterial occlusive disease is
present at the time of diagnosis, then the survival rate in
these patients is markedly reduced. After five years
less than 20% survive91. The occurrence of both disease
states at the time of diagnosis of type 2 diabetes is
particularly common among smokers.

33

The high incidence of concurrent micro- and macrovascular disease in patients with foot ulcers shows
the urgent need for the use of all available options for
early diagnosis and appropriate treatment, not only
to increase the chances of a positive outcome of the foot
lesion, but also to have a beneficial effect on the overall
fate of the patient affected.

34

Diagnosis and differential

diagnosis of the diabetic foot
syndrome
Diagnosis of sensorimotor and autonomic
diabetic neuropathy and diabetic neuropathic
osteoarthropathy
The human nervous system consists of the peripheral
nervous system (PNS) and the central nervous system
(CNS). The CNS comprises the brain and the spinal
cord. The somatic and autonomic nervous systems are
distinguished in terms of their functions. Somatic nerve
fibres conduct stimuli to the muscles and conversely
from the sensory receptors to the CNS. Neurons that
are not subject to voluntary control are grouped together
under the heading of the autonomic nervous system.
In the lower limb, they exert a particular action on the regulation of vascular tone and the secretion of sweat
glands. Neuropathies are characterised by a progressive
loss of nerve fibres, which can be detected by noninvasive tests of nerve function. The early identification
and education of patients with a loss of sensory perception in the lower limb would be the most effective way
of avoiding foot injuries and amputations in diabetics.
The NEURODIAB Working Group of the European
Association for the Study of Diabetes (EASD) agreed
guidelines in 1998 for the annual follow-up of diabetics
with regard to their neurological status92. As opposed
to the consensus guidelines of the San Antonio conference93, only simple and universally available investigations, in addition to clinical examination, were proposed to establish nerve function. Diabetic neuropathy is
defined as the presence of signs or symptoms of
peripheral nerve function disorders in diabetics following
the exclusion of other causes90.
Three sensory modalities can be easily tested:
1. Vibration sensitivity (tuning fork test94 and
biothesiometry95)
2. Pressure perception (Semmes-Weinstein
monofilaments96)
3. Temperature discrimination (Tip Therm97)

35

These tests provide information about the degree of

neuropathy and hence the risk of diabetics developing
foot lesions.
Disorders of autonomic innervation of the foot may be
suspected in the presence of dry, cracked skin, fissures
and hyperkeratosis. The acetylcholine test (sweat spot
test) is a suitable test method98. Electrophysiological
investigations (e.g. nerve conduction velocity) serve more
to differentiate neuropathies of different aetiology than
to provide additional findings in diabetic foot syndrome.
These tests do not add to the diagnostic value of the
methods described above. Abnormalities of nerve conduction velocities, moreover, are not consistent with
the clinical signs in diabetic neuropathy99.
Two clinical methods have become increasingly accepted
in Germany: the examination of vibration sensitivity with
the calibrated Rydel-Seiffer tuning fork and the recording
of pressure sensitivity with the 5.07 Semmes-Weinstein
monofilament (10 gram application force).
Of the various manifestations of diabetic neuropathy,
three are of relevance to the lower limb100 : the acute
sensory, chronic sensomotoric and autonomic neuropathies. A progressive, stocking-shaped, predominantly
symmetrical loss of vibration, temperature and pain
perception is typical of the chronic sensorimotor form of
the disease. A lack of proprioceptive reflexes and
Findings in neuropathic
diabetic foot syndrome with
claw toe deformity as a result
of shortening of the small
muscles of the foot (a
consequence of motor
neuropathy) and degeneration
of the plantar aponeurosis

36

atrophy of the small foot muscles with a claw toe

position and prominent metatarsal bones may be considered signs of involvement of motor nerve fibres.
The progressive glycosylation of the plantar aponeurosis
with an increasing loss of elasticity and an eventual
rupture may contribute to these deformities101.
Autonomic nerve fibres are involved in a large number
of cases in patients with foot ulcerations102. Particularly in
patients with a diabetic neuropathic osteoarthropathy
(DNOAP), involvement of the autonomic nervous system
is observed in more than 90% of cases103. Severe acute
and isolated autonomic neuropathies are rare manifestations99. About two-thirds of diabetic neuropathies
which follow are asymptomatic. Hence, the absence
of symptoms does not necessarily mean that the patient
has healthy feet100.
Loss of vibration sensation is the most common and earliest sign that nerve fibres are affected in diabetic
neuropathy. Normal ageing has an effect on vibration
sensation, so have patient co-operation and motivation.
Its usefulness in elderly patients is doubtful104. In addition, proprioceptive reflexes cannot be detected in
about 70% of all elderly patients (including non-diabetic
patients).
The 128 Hz tuning fork is marked with a scale that is
subdivided into eighths. An impairment of age-related
impairment of sensation was found in 20 of 26 patients
with foot ulcerations in a tuning fork test. A reduction
to less than 4/8 occurred in 95% of ulcer patients105.
In another study, a reduction in vibration sensitivity to 2/8
or less was found in all patients with foot lesions94.
The semiquantitative measurement of the vibration sense
yields valuable information for patients under 60 years
of age. Evaluation of the quantitative vibration measurement (determination of the vibration threshold) by biothesiometer yielded a threshold of normal sensation of
25 V (volt). The risk of ulceration in the group of patients
with a sensitivity of between 25 and 33 V was increased
eight-fold, while with values of more than 42 V it increased more than twenty-fold95.
While the vibration sensation test is used in screening for
neuropathy, it is the loss of temperature discrimination
and pain perception that is responsible for foot injuries in
diabetics. The test of pressure sensitivity with the 5.07
(10 gram) nylon filament is superior to the biothesiometer
37

measurement because of its higher sensitivity (100% vs.

79%). Nylon filaments with a standardised application
force (1, 10 and 75 gram) are applied at specific points
on the patiants foot, bent and their perception tested96.
Temperature discrimination can be tested simply, economically and reproducibly with the Tip Therm (Axon,
Dsseldorf). This is an instrument similar to a thick pencil
with a plastic side and a steel side. All 26 patients with
a previous determined temperature discrimination threshold of less than 10 C recognised the different temperature on the two sides of the Tip Therm. In contrast, 20 of
24 patients with impaired temperature perception (threshold greater than 10C) were incapable of doing so97.
With a combination of the tuning fork test, the monofilament test and the temperature discrimination (Tip Therm),
the neurological risk status of each diabetic can therefore be determined rapidly and cheaply.
A rare but important complication of diabetic neuropathy
is diabetic neuropathic osteoarthropathy (DNOAP) which
is found in at least 0.1 to 0.5% of all diabetics. Cavanagh
et al. (1994) even found evidence of osteoarthropathy
in about 10% of all patients with diabetic neuropathy106,
i.e. in about 3% of all diabetics.
Such changes were first described by Musgrave, 1703,
as a consequence of sexual transmitted diseases107.
In 1868, Charcot, after whom the final stage of osteoarthropathy with marked deformities was also named,
described painless neuropathic joint changes and bone
destruction in patients with tabes dorsalis108. Diabetes
mellitus is the most common disease underlying such
changes today. Such findings also occur in patients with
leprosy, syringomyelia, in alcoholics and in patients with
congenital insensitivity to pain. The exact pathogenetic
background of DNOAP has yet to be fully elucidated107.
In the current state of knowledge, the autonomic neuropathy observed in almost all patients with diabetic
osteoarthropathy results in increased blood flow as a
result of arteriovenous shunts, and ultimately in osteopenia. The reduced bone density can often be detected
even before the clinical onset of the disease109.

38

Acute diabetic osteoarthropathy with swelling, redness

and excessive heat and
incipient deformity of the right
foot.

The muscular imbalance caused by the presence of a

motor neuropathy and the potential for concurrent
traumas due to the sensory deficit, result in repeated
peri-articular fractures with impaired healing and
the possible end-state of a severely deformed foot107.
In addition to the swelling and redness of the affected
extremity, a temperature difference of more than 2 C
from the opposite side is indicative of an active osteoarthropathy109.
According to Sanders, five forms of diabetic osteoarthropathy may be distinguished on the basis of their different
localisations110. Forms I, II and III involving the anterior
and middle parts of the foot constitute more than 80% of
all cases. Sella distinguishes four disease stages108.
The intention here must be to identify this clinical picture
despite its relative rarity and to prevent extensive foot
deformities through early diagnosis (clinical features,
X-rays, CT scans) and the resultant appropriate relief of
pressure. In addition to this, initial findings from adjuvant
therapy with bisphosphanates provide promising
results111.

39

Diagnosis of arterial occlusive disease

The most significant single factor affecting the risk
of amputation for diabetics is ischaemia of the affected
extremities following an arterial occlusive disease. In
a large proportion of cases, degenerative arteriosclerotic
vessel processes underlie arterial circulatory disorders,
resulting in a loss of elasticity of the vessel and ultimately
occlusion of the lumen. Appropriate and early diagnosis
of circulatory disorders and an understanding of the
specific features of the disease in diabetics are
essential to avoid unnecessary amputations.
The prevalence of arterial circulatory disorders in
Germany in the 55- to 64-year-old age group is about
10%112. This rises to 21% in type 2 diabetics113. Other
risk factors include the patients age, hypertension and
heavy smoking. Although the incidence of peripheral
arterial occlusive diseases (PAOD) is increased in diabetics and the disease manifests itself at an early age,
the disease course is similar to that in non-diabetics114.
The misconception of an occlusive microangiopathy,
the pitfalls of instrumental diagnosis in the presence of
Mnckebergs arterial sclerosis and its significance for
the particular pattern of distribution of PAOD in diabetics
are presented below in further detail. This is followed
by a description of the clinical features in the presence of
an associated sensorimotor diabetic neuropathy, together with a step by step procedure for the diagnosis of
arterial occlusive disease.
The primary task in assessing diabetic foot lesions is
the differentiation of neuropathic and (neuro-)ischaemic
findings. The underlying difference between the two
forms is the existence (or absence) of foot pulses. The
most important basic diagnostic measure is therefore
the palpation of foot pulses. Doppler examination of the
peripheral arteries using an occlusive pressure measurement (determination of the ankle-arm index of arterial
blood pressure)115 and, where necessary, an oscillographic examination or hydrostatic toe pressure measurement116,117,118 in the presence of media calcification are
non-invasive examinations that yield further information.

40

Clinical and instrumental diagnosis in diabetic foot syndrome

Neuropathic status

Arterial vascular status

Previous history:
Duration of diabetes
Clinical symptoms of neuropathy
(positive symptoms such as nocturnal
or resting pain, negative symptoms
such as impaired or absence of
sensitivity to vibration, pain, pressure,
temperature or touch) microvascular
diseases of the eye and kidneys, plus
alcohol abuse

Previous history:
Clinical signs of an arterial occlusive
disease such as resting pain or intermittent claudication (pain on exercise
both of which are often undetectable
when a neuropathy is present simultaneously)
Vascular risk factors such as hypertension, smoking, obesity and lipid metabolism disorders

Inspection:
Warm, dry, cracked skin
Atrophy of the internal musculature of
the foot with foot deformities
Hyperkeratosis and subcallus
haematomas

Inspection:
Cool, pale or livid, atrophic skin
Loss of integumentary appendages,
hair loss
Typical acral necrosis

Examinations:
Reflex test (ATR)
Vibration perception (Rydell-Seiffer
Tuning fork, biothesiometer)
Semmes-Weinstein monofilament (10 g)
Temperature perception (Tip-Therm)

Examinations:
Palpation of foot pulses
Doppler examination with occlusive
pressure measurement
(ankle-arm index, hydrostatic toe
pressure)
Duplex ultrasonography
Transcutaneous oxygen measurement
Invasive and non-invasive radiological
procedures (DSA, angiography, CO2 angiography, MRI angiography)

41

In occlusive pressure measurements, an ankle-arm

index of less than 0.9 is an indicator of arterial occlusive
disease, irrespective of the existence or otherwise of
medial calcification119. Calcification of the tunica media of
the arteries, described for the first time in 1909 by
Mnckeberg and named after him, is found in a high percentage of diabetics120. As a result the vessels become
rigid and the occlusion pressures measured by Doppler
pressure measurement are false. The presence of
an occlusion of the vascular lumen or a reduction in the
circulatory reserve due to calcification cannot be
excluded121.
Evidence, however, has been found of a correlation between medial calcification and the primarily more distal
type of distribution of PAOD in diabetes patients122.
Patients with existing medial calcification exhibit tibial or
peroneal occlusive localisations of PAOD significantly
Clinical picture of diabetic
osteoartropathy with the
associated x-ray image: multiple fractures in the medial
part of the foot with complete
loss of the original plantar
arch

42

more frequently than diabetics without medial calcification or non-diabetics. Depending on the literature source,
the arteries are assumed to be incompressible with an
ankle-brachial index (ABI) of 1.35 or 1.5123.
Indices of more than 1.2 may be considered indicators of
the presence of medial calcification122. The most definite
evidence is provided by taking an X-ray of the forefoot
in which the medial calcification is visualised as a classic
tramline finding120.
Media-calcification is a feature that is also increasingly
found with advancing age, even in non-diabetics. In
diabetics, however, the presence of diabetic neuropathy
predisposes to its early onset, particularly where autonomic nerve fibres are also involved (loss of modulation
of vessel tone)120. The degree of calcification of the
arteries correlates with the vibration perception and the
duration of the diabetes124. In patients with pronounced
diabetic osteoarthropathy, in which the involvement
of autonomic nerve fibres is typical, media-calcification
is found in 8090% of cases120. As has already been
mentioned, hydrostatic toe pressure measurement116,117,118 may be used for diagnostic purposes, as
well as oscillography. In diabetics, there is often a
physiologically lower pressure in the area of the toe
arteries, relatively little calcification of the media and the
unmasking of media calcification on elevation of the
extremity above heart level. Values of more than
70 mmHg may be regarded as normal findings in this
case.
In summary, Mnckebergs arteriosclerosis is a nonocclusive angiopathy typical of diabetes mellitus and
specific to the presence of diabetic neuropathy. It is
possibly of prognostic significance for the subsequent
appearance of a peripheral arterial occlusive disease
(PAOD) and the occurrence of fatal myocardial infarction125.

43

The significance of microcirculatory disorders at the

capillary level in the onset and course of diabetic
foot lesions is still a matter of debate. The presence of
lumen-occluding, processes in the microcirculation
of diabetics126,127 was used before as justification
for early and extensive limb amputation. Today, the presence of occlusive disease can be meassured and
hence excluded. However, functional abnormalities of the
microcirculation with deterioration of haemodynamic,
endothelial and cell function as a consequence of poor
blood glucose control, must be considered definite128.
These conditions impair healing. At present, capillary
microscopy, laser flow measurement and transcutaneous
oxygen measurement are standard procedures used in
the investigation of microcirculatory problems. Therefore the presence of gangrene with palpable foot pulses
in patients with diabetic foot syndrome should no
longer be considered a consequence of an occlusive
microangiography, but much more as evidence of a
neuropathic infected foot with the presence of septic
emboli, and hence treated accordingly120,129.
Fontaines staging of PAOD is often of only limited use in
diabetics when it is accompanied by diabetic neuropathy
involving loss of pain perception. Measurement of the
classic ischaemic pain following exercise (Fontaine stage
II) and the presence of resting pain (Fontaine stage III)
have limited significance. Occasional neuropathic irritation states are sometimes difficult to differentiate from
resting pain in arterial occlusive disease. The essential
aim should therefore be appropriate clinical examination
and directed investigation. Ultrasound imaging of the
arteries and further angiographic investigations (conventional angiography, digital subtraction angiography,
MRI angiography130 and CO2 angiography131) according
to the guidelines of the European Consensus Paper
of 1990 should be performed in primarily neuropathic
lesions with delayed healing before any amputation
is recommended in diabetic foot ulcers or gangrene.
The imaging should always include the foot arteries115.
MRI angiography may be expected to replace current
angiographic methods in the medium term due to its
superiority in detecting occlusion distances and its high
cost efficiency130. CO2 angiography also exhibits
marked advantages over the procedures currently used
through its non-allergising method and the absence
of renal toxicity131.

44

Classification of diabetic foot lesions

The optimum treatment for diabetic foot syndrome involves the multidisciplinary team. It assumes clear
communication between the various members of the
treatment team and requires a clear classification of
diabetic foot lesions. The requirements made of classifications are illustrated below, the most frequently used
classifications presented and their clinical significance
described.
Co-operation and communication are mutually
dependent and assume clarity and accuracy in the
classifications used for planning therapy and for
subsequent comparability.
A clinical description is a specific snapshot of a particular lesion and changes as the clinical situation
improves or deteriorates. An effective description should
not only provide someone else with an indication
of the best possible immediate therapy, but should also
indicate the urgency with which such treatment should
be undertaken. A classification, however, should be
applicable at all times and to a variety of lesions. A good
clinical description of foot lesions should include details
about the patient (including social aspects), the affected
foot (side, localisation, cause of lesions) and the lesion
itself (size, severity, infection, stage of wound-healing)132.
One difficulty in establishing classifications of diabetic
foot lesions lies in the fact that they must be simple
enough to be understood by all team members
(specialist or non-specialist)133. Also, they must be flexible enough to cover all conceivable lesions and at
the same time specific enough to be able to define an
individual lesion clearly. A good classification also
makes it easier to establish the prognosis for diabetic
foot lesions134.
Described in 1976 by Meggit133 and further refined by
Wagner in 1981, the so-called Wagner classification
has become one of the most widely used classifications
of diabetic foot lesions world-wide. It comprises six
stages (05). Grade 0 corresponds to the pre-lesion
(e.g. callous formation or condition following a healed
foot lesion). Grade 1 and grade 2 describe surface and
deep ulcerations. Grade 3 severity involves the presence
of deep ulcerations complicated by infection of bone
and joints. Grades 4 and 5 describe localised and extensive necrotic developments. The classification has the
45

advantage of being very simple, but the disadvantage

of being imprecise. Modifications by Harkless (supplemented with the suffix B for ischaemic extremities) or
Reike (indication of the main aetiopathogenetic factors)
have further refined these classification in terms of
their use in practice133,136.
Wagners classification
Grade
0

No lesion, possibly foot deformity or cellulitis

Superficial ulceration

Deep ulcer as far as joint capsule, tendons or

bones

Deep ulcer with abscess formation, osteomyelitis,

infection of joint capsule

Limited necrosis in forefoot or heel region

Necrosis of whole foot

The University of Texas Wound Classification System

has been available as an alternative to this since 1996137.
In this classification 4 degrees of severity are distinguished (0, I, II, III). Severity grade 0 describes a pre- or
post-ulcerous state with complete epithelialisation. Grade
I refers to a superficial wound, and Grade II to a wound
that has extended to the tendon or capsule. Grade III
describes a wound with bone or joint involvement. All
grades then have the suffix B appended in the presence
of an infection, suffix C for concurrent ischaemia and
suffix D for the concurrent presence of an infection and
ischaemia. For example grade III D would be a lesion
with ischaemia and infection in the presence of bone
involvement. Grade II A would be a superficial wound
without signs of infection or ischaemia.

46

The authors Lavery, Armstrong and Harkless evaluated

the system in 1998 while studying more than 360
patients138. A grade III lesion (bone or joint involvement)
indicated an eleven-fold increase in the risk of amputation. Patients with ischaemia and infection (stage D)
exhibited a 90-fold higher risk of amputation.

Rischbieter and Reike in 1998 presented a similar evaluation for the modified Wagner classification. Patients
with lesions of Wagner stages 4 and 5 (localised and
generalised necrosis) had a nine-fold greater risk of
amputation than patients with lesions of Wagner stage
0 to 3136.

47

University of Texas San Antonio Diabetic Wound Classification

(Armstrongs classification)
Grade
0

II

III
Wound with bone
or joint
involvement

Completely
epithelialised
pre- or postulcerous lesion

Superficial
wound without
tendon or
capsule involvement

Wound with
tendon or
capsule
involvement

Completely
epithelialised
pre- or postulcerous lesion
with infection

Superficial
wound without
tendon or
capsule involvement with
infection

Wound with
Wound with bone
tendon or
or joint involvecapsule
ment with infection
involvement with
infection

Completely
epithelialised preor post-ulcerous
lesion with
ischaemia

Superficial
wound without
tendon or
capsule involvement with
ischaemia

Wound with
tendon or
capsule involvement with
ischaemia

Wound with bone

or joint involvement with
ischaemia

Completely
epithelialised
pre- or postulcerous lesion
with infection
and ischaemia

Superficial
wound without
tendon or
capsule involvement with
infection and
ischaemia

Wound with
tendon or
capsule involvement with
infection and
ischaemia

Wound with bone

or joint involvement with infection
and ischaemia

48

Diagnosis structure in diabetic foot syndrome

(modified by H. Reike)
1. Underlying disease
(neuropathy, arterial occlusive disease, mixed form,
osteoarthropathy)
2. Localisation
(e.g. toes, forefoot, heel region, scar regions)
3. Extent of injury
(e.g. Wagners stages 05;
Armstrongs classification)
4. Wound healing stage
(cleaning, granulation and
epithelialisation phase)
5. Infection
(yes/no; limb threatening, non-limb threatening)
A precise description and classification of diabetic foot
lesions is essential for planning therapy, establishing
the prognosis and comparing diabetic foot changes and
should therefore be recorded meticulously.

49

Basic principles of the

treatment of diabetic foot
lesions
At present, treatment procedures for diabetic foot
syndrome considered to be of proven efficacy
include:
1. Pressure relief of the affected parts of the foot
2. Repeated and adequate mechanical
dbridement
3. Phase-specific moist wound treatment
4. Medical and surgical treatment of infection
5. The use of reconstructive and interventional
procedures to improve blood circulation
(with due allowance for the specific features of
arterial occlusive disease)
Procedures such as the use of hyperbaric oxygen
(HBO), the application of bio-engineered tissues and
growth factors or biomechanical wound treatment
with the use of fly larvae (where strictly indicated) may
be regarded as supplements to the basic therapy
but not as a replacement for it.

Possibilities of pressure relief

As has already been mentioned, biomechanical changes
are a frequent consequence of diabetic neuropathy,
resulting in an altered pressure load on the sole of the
Partial foot relief shoe (forefoot
relief shoe, Thanner company)
to maintain the mobility of
patients with plantar and acral
lesions during the recovery
phase

50

foot. The combination of diabetic neuropathy and foot

deformities increase the risk of ulcer formation.
Therefore consistent pressure relief is an essential precondition for the prevention and healing of foot ulcers.
Modified Allgwer walking
apparatus for maximum
pressure relief in patients with
acute diabetic osteoarthropathy

There is evidence of accelerated and persistent healing with various treatment approaches, such as bed rest,
wheelchairs, the use of a total contact cast (plaster
treatment) and partial relief shoes139. The advantages
and disadvantages of the latter two procedures will be
presented below in greater detail.
Plaster treatment in the form of a total contact cast (TCC)
currently represents the gold standard in the USA
and Great Britain for pressure relief in plantar pressure
lesions of the diabetic foot139,140,141. The benefit or
relatively short healing time, approximately five weeks
with a pressure reduction of 75% to 85% contrasts with
the high cost (about 200 dollars), the need for regular
changes of the cast and the risk of infection with

51

increased difficulty of detection142. Probably the most

extensively used method of pressure relief in Germany
is the use of so-called partial foot relief shoes. These
walking aids are considerably cheaper than plaster
therapy, but slightly less effective in terms of healing rate
and degree of pressure relief140. In a case control study,
96% of wounds in patients with forefoot relief shoes
healed within an average of 70 days, whereas in patients
without such walking aids only 59% of ulcers healed
(mean healing time of 118 days). Hospitalisation was
necessary in half the patients without walking aids, but
in only one out of 26 patients fitted with forefoot relief
shoes143. The principal difficulties encountered by
patients from the use of such accessories include:
1. The development of blisters or pressure points
2. Pain in the joint area
3. Difficulties in walking because of the difference in
height from the contralateral shoe
4. Tearing of the walking sole142
Other options for pressure relief in specific cases
(e.g. deformity in osteoarthropathy with ulcer formation)
in our outpatient department include the use of Allgwer
walking apparatus, aircast splints or custom-made
two-layer orthoses.
Structured wound treatment and importance of
interactive wound dressings
Wound healing in diabetic foot syndrome is a complex
process, the purpose of which is to fill the tissue defect
that has occurred, restore sufficient strength to the
tissue and re-create the physiological barrier between
the internal and external environment. In the course
of this, complex cellular biochemical processes result in
the formation of low-grade scar tissue. Wound healing
usually occurs in three phases:
1. wound cleansing (inflammatory phase)
2. the granulation phase (proliferative phase) and
3. the epithelialisation phase
(differentiation phase, wound closure).

52

Differences are found between diabetics and metabolically healthy patients in all three phases and these
are described in greater detail below.
Immediately after an injury local blood coagulation
occurs with the formation of a fibrin network. This
then dissolves to allow the unimpeded extension of the
ensuing granulation tissue. In diabetics, these fibrin
coatings occasionally persist beyond the first phase144.

Schematic representation of
the time course of the wound
healing phases:
1) inflammatory phase
2) proliferative phase
3) differentation phase

Extensive necrosis of the heal

with local erythema

Wound in the inflammatory

phase with wound coating
as well as maceration and
necrosis formation at the
margins

53

Subsequently a local inflammatory reaction develops,

in which first neutrophils (which release proteases and
are capable of phagocytosis) and then macrophages
migrate to the wound area where they release messenger substances, known as cytokines (such as PDGF
or TGF-(). These mediators stimulate cell activities such
as angiogenesis, autolytic dbridement, keratinocyte
migration, matrix formation and fibroblast formation.
Ulceration of the heal in the
granulation phase

There are deficiencies in diabetics in respect of both the

bactericidal activity of the neutrophils145 and the properties of the fibroblasts146,147.
High glucose and lactate levels cause disruption of the
rate of fibroblast division and resistance to growth
factors. In addition to these acquired changes of immune
function, there is also assumed to be a genetically
predetermined disorder of immunocompetence in diabetics148. As a result of the proliferation of vascular
Increasing wound closure in
the epithelialisation phase

54

endothelial cells and fibroblast formation, a shiny red

granulation bed is formed and collagen synthesis is
increased.
Finally, wound closure occurs through epithelialisation.
The formation of an epidermis serves as protection,
though it does not improve the strength of the new tissue
any further.
Pressure site on the lateral
border of the foot with septic
ischaemic necrosis of the
fifth toe. Bilateral resection of
the fourth and fifth ray following insertion of a plastic crural
bypass

There are two types of wound healing.

1. Primary wound healing occurs through primary adaptation with only small quantities of granulation tissue.
2. Secondary wound healing takes place in infected and
necrotic tissue, whereby wound closure occurs mainly
by contraction. In the second form, adaptation can
be assisted by the use of Omnistrip wound suture
strips for example.
Healing of the resection
wound with phase-specific
wound treatment

55

Disruptive factors in wound healing may be systemic

or related to local conditions in the wound area. They are
listed here:
Possible causes of impaired wound healing in
diabetic foot syndrome
Systemic factors:
Hyperglycaemic metabolic situation
Malnutrition
Obesity
Nicotine abuse
Anaemia
Renal insufficiency/uraemia
Patients age
Drugs (steroids, antirheumatic agents).
Local factors:
Ischaemia and hypoxia of affected tissue
Pressure load
Repeated trauma
Inadequate local wound treatment
Infection
Necrosis
Oedema formation
Foreign body in the wound

Successful local wound treatment must fulfil the following

conditions:

It must:
1. Support normal biological healing processes,
2. Prevent infection and/or reduce the microbial count,
3. Prevent necrosis formation and/or eliminate existing
necrosis,
4. Be based on a phased wound healing process,
5. Be cost-effective
6. Be well tolerated by the patient and applicable for
outpatients.

In the therapy of chronic wounds, moist wound treatment using modern differentiated wound therapy has
now replaced the previous conventional wound treatment
consisting of various dyes, local administration of antimicrobial substances and sterile dressings.
56

In the first phase of wound healing, the mechanical

or physical removal of necrotic tissue, the provision of
drainage for exudate and where necessary the resection
of infected bone sequestra take precedence. In addition,
deoxyribonucleases (e.g. Fibrolan), streptokinasestreptodornase (e.g. Varidase) or collagenases (e.g.
Iruxol N) may be used. There are at present no studies
that confirm the efficacy of these preparations.
Septic thrombosis with
gangrene of the second toe of
the right foot with extensive
deep foot infection in the absence of an arterial occlusive
disease

Subsequent healing process

following amputation of
the second to fourth rays and
infected sections of tissue
with phase-specific wound
treatment

57

In terms of special wound dressings, alginates

(e.g. Sorbalgon) are used at this stage for wounds with
profuse exudation and are also suitable for deep
and gaping wounds. Wound healing complications have
been described in individual cases with alginate
therapy in undiagnosed deep wound infections, osteitis
or minimally exudative wounds149,150.
In non-infected wounds of Wagner stages 1 and 2 with
only mild to moderate exudation, the use of hydrogels
(e.g. Hydrosorb) or hydrocolloids (e.g. Hydrocoll) may
be considered for moist wound treatment. The hydrogels are polyurethane meshes with a 60% or higher water
content, depending on the product. In contrast to the
hydrocolloids, they do not form a gel and therefore
absorption of exudates is possible. As a result of the high
water content, the main effect of hydrogels in diabetic
foot syndrome lies in the softening of necrotic tissue and
wound coatings.
By reducing the frequency of dressing changes, treatment with special wound dressings becomes costeffective. Despite the difficulties of comparability between studies (due to use of different preparations
in different stages of healing), the application of hydrocolloids resulted in reduction in costs by 60% in comparison to dry or moist gauze dressings151. In addition to
the dressings described, Ringers solution administered
either as a continuous irrigation or in carrier media such
as superabsorbent polyacrylate (e.g. TenderWet) is
suitable for moist wound treatment in the late cleansing
and granulation phase. Because of its mechanical
protective action, the continuous release of the absorbed
Ringers solution and its high absorption capacity for
wound exudate, this product is particularly suitable for
the outpatient treatment of diabetic foot lesions.
Lastly, epithelialising wounds are covered with a nonmedicated, ointment-impregnated gauze.
As the skin of neuropathic patients is very fragile, wound
dressings and bandages in our hospital are secured
exclusively with gauze bandages and gauze dressings.
In ambulant patients, tubular dressings are also applied
to prevent the primary bandage from slipping. Direct
contact of the fixation plaster with the patients skin
is avoided where possible because of the tendency to

58

macerate. The lack of adequate studies on the phasespecific use of sufficient wound dressings results on the
one hand in inappropriate use by unspecialised users152,
and on the other in a constant debate among experts
about the risks of using specific wound dressings in
diabetics149,153,154. In a large English survey on the use of
specific wound dressings in diabetic foot syndrome,
five to eight different wound dressings were mentioned
by each user, among which hydrocolloids, hydrogels
and alginates were the most widely used. None of the
products, however, had more than 30% support in any
of the wound healing phases. This survey was unable to
clarify whether this finding is due to a lack of information,
or to the belief on the part of the users that there are
no essential differences between the various dressings152.
Encouraged by individual case reports, the use of hydrocolloid dressings in diabetic foot syndrome has become
a subject of debate in recent years.
Problems identified in the use of hydrocolloid dressings
include:
1. Rapidly progressive infections under occlusive
dressings
2. Gel particles incorporated in wounds as foreign bodies
3. Maceration and pressure injuries of wounds have been
described.
Pre-existing infection of the wound and weekly changes
of dressings were common to all the case reports with
fatal outcomes. By complying with the contra-indications and observing shorter intervals between changes
of dressings, such complications could definitely be
avoided. In contrast to these case reports, an infection
rate of only 2.6% under occlusive dressings has been
observed in large-scale studies, which compared to 7.1%
with conventional dressings155.
Stage-specific application of the treatment principles,
regular dbridement and strict monitoring of the wound
status in the initial phase (at least twice daily changes of
dressings in infected wounds) are essential preconditions
for successful treatment. An important component of
treatment also involves actively including the patient and
their relatives at this early stage and preparing the way
for the transfer of individual responsibility.

59

Moist wound treatment

In wounds healing by secondary intention, moist wound
treatment is now considered the standard and has
become accepted in particular in the treatment of
chronic problem wounds. The scientific bases for moist
therapy were established in the studies by Winter (1971).
He showed that a moist and permeable dressing made
the wound heal quicker than a dry wound exposed to air.
This fact is also confirmed by more recent studies.
According to Turner (1990), permanent moist wound
therapy results in a significantly faster reduction in wound
area and a larger quantity of granulation tissue than in
controls. Accelerated re-epithelialisation is also
observed. In addition, moist wound dressings exhibit a
good wound healing effect without damaging
immunocompetent cells.
Wound dressings for moist treatment
A series of wound dressings are now available for the
practical implementation of moist wound therapy,
covering the whole spectrum of therapeutic requirements
in terms of a treatment system.

TenderWet Wound dressing pad with superabsorbent

core

The principle of action of

TenderWet

60

TenderWet is an extremely efficient wound dressing for

the treatment of chronic infected and non-infected
wounds during the cleaning phase and at the beginning
of the granulation phase. The basis of its high degree of
efficacy is a special principle of action that allows
continuous rinsing of the wound.
TenderWet is a multilayer wound dressing pad containing
a superabsorbent polyacrylate core as its central
component which has irrigating properties. The
superabsorbent core is activated before use with a
suitable volume of Ringers solution, which is then
delivered continuously to the wound over a period of
twelve hours. This constant supply of Ringers solution
actively softens and detaches necrotic tissue (1).
At the same time, the absorbent core reliably takes up
and retains germ-laden wound exudate. This exchange
is possible because the superabsorbent core has a
greater affinity for protein-containing wound exudate than
for salt-containing solutions (Ringers solution). The
wound exudate therefore displaces the Ringers solution

from the wound pad (2).Thus, TenderWet continuously

renews the film of Ringers solution over several hours
and simultaneously absorbs micro-organisms, released
detritus and toxins. Hence, the wound is rinsed and
rapidly cleansed.
As soon as the factors that inhibit wound healing are
eliminated and the wound area is clean, granulation
tissue can build up through the migration of cells and the
regeneration of vessels (3). In the course of this, the
moisture and the electrolytes in the Ringers solution,
such as sodium, potassium and calcium, contribute to
cell proliferation.
TenderWet is available in
various shapes and sizes to
ensure good adaption to the
various wound conditions.
TenderWet is activated with
Ringers solution directly in the
sterile peel off package
(right)

TenderWet has no contra-indications and can also be

used in infected wounds. In individual cases, an
apparent enlargement of the wound occurs following
initial cleansing with TenderWet. This means that
undetected devitalised tissue has also been eliminated
by this method.
The amount of Ringers solution necessary to activate the
absorbent/ rinsing core depends on the size of the
dressing. In deep wound conditions,TenderWet should
be packed loosely to ensure the direct contact that is
required for fluid exchange to occur. The physical
properties of the superabsorbent compound, combined
with the covering of knitted fabric, give TenderWet the
necessary packing properties. In extensive wounds, the
TenderWet wound pads should be applied so that they
overlap slightly. They can then be covered as necessary
with a gauze fixation dressing.

61

TenderWet has no
contraindications and can be
used in all wound conditions,
both infected and noninfected. The rinsing effect of
TenderWet is optimal during
the cleaning phase and at the
beginning of the granulation
phase. The examples show
TenderWet used in the care of
a venous (1) and an angiopathic/diabetic ulcer (2)

TenderWet dressings as a rule should be changed twice

daily, i.e. every 12 hours. TenderWet 24 can be used at
24 hour intervals. TenderWet 24 is made of the same
materials as TenderWet, but is designed so that the
Ringers solution absorbed is released more evenly and
the absorption/rinsing action persists over 24 hours. In
addition, a moisture-repellent layer is incorporated inside
the dressing to prevent moisture penetrating and thus
provides a dressing that offers excellent moist therapy.

Sorbalgon conformable calcium alginate dressings

The principle of action of

Sorbalgon

62

Sorbalgon is the ideal wound dressing for cleansing and

for expediting the build-up of granulation tissue in
fissured wounds and those that are difficult to manage.
Sorbalgon is highly adaptable and thus ensures effective
wound cleansing and management, even in deep
wounds.
Sorbalgon is a non-woven dressing of high-grade
calcium alginate fibres which is applied to the wound in
its dry state (3). On contact with sodium salts, such as
are found in the blood and wound exudate, the fibres
swell and are transformed to a moist, absorbent gel that
fills the wound (4). Sorbalgon approximates closely to
the wound surfaces, therefore micro-organisms even at
a deep level are absorbed and incorporated safely in
the gel structure (5). This results in efficient microbial
reduction and helps prevent recontamination. Wounds
are rapidly cleansed, so that Sorbalgon has become
established in the treatment of chronic and infected
wounds in particular.
The gelatinous consistency of Sorbalgon also acts like a
moist dressing, preventing dehydration of the wound.
A favourable microclimate for wound healing arises, promoting the formation of granulation tissue and keeping
the wound surfaces supple.

Loosley packed Sorbalgon

dressings (left) and their
transformation to a gelatinous
structure by the absorption
of exudate (right)

As Sorbalgon is able to be transformed into a gel, it

does not adhere to the wound and changes of dressing
can be made painlessly. The complete transformation
of the calcium alginate fibres to a gel requires sufficient
exudate. Thus, where fissured wounds with little exudate
require packing, Sorbalgon should be moistened with
Ringers solution. Any fibres remaining in the wound can
be rinsed out with Ringers solution, otherwise the gel
plug is removed from the wound with forceps.
The frequency with which dressings are changed depends on the individual wound conditions. In the wound
cleansing phase, one or two changes of dressing are
necessary, depending on the degree of exudation. Later,
with granulation formation, a change of dressing every
2 to 3 days may be sufficient. Sorbalgon is supplied in
square dressings of two sizes. Sorbalgon T ribbons are
available specifically for larger wounds.

Hydrosorb hydrocellular gel dressing

Hydrosorb is especially suitable for moistening and
protecting granulation tissue and young epithelium and
is hence the optimum wound dressing for phase-specific
treatment following TenderWet or Sorbalgon therapy.
Hydrosorb is a ready-to-use gel made of absorbent
polyurethane polymers which has a high water content
(60%). Thus, from the very beginning Hydrosorb automatically provides a moist environment for the wound for
several days (1). At the same time, Hydrosorb absorbs
excess exudate, which is then incorporated in the gel
structure. This exchange guarantees the optimal level
of moisture for wound healing and thus accelerates granulation formation and epithelialisation (2). The germproof and waterproof surface of Hydrosorb also
guarantees protection against secondary infections.

The principle of action of

Hydrosorb

63

Hydrosorb does not stick to the wound and can be

removed even after prolonged application without the
risk of irritation to the wound. Unlike hydrocolloids,
Hydrosorb can be removed in one piece since the gel
structure is not dissolved by the absorbed wound
exudate. No residues are left on the wound and the
wound condition can be assessed safely without prior
rinsing.
One particularly practical advantage of Hydrosorb is
its transparency, which lasts even after prolonged application. As a result the wound can be inspected without
removing the dressing. This ensures rest for the wound
which is so important for healing, as well as a high
degree of cost effectiveness because of the reduced
frequency of dressing changes.
Hydrosorb is available in two forms: Hydrosorb
and Hydrosorb comfort. Both hydrogels have the same
principle of action, but differ in terms of methods of
fixation. Hydrosorb does not have a self-adhesive border
and as a rule is secured by means of a fixation
dressing, adhesive plasters or a dressing retention
bandage.
The transparency of Hydrosorb
is an important factor in its
cost-effective use. The wound
can be inspected at many
times through the dressing so
that Hydrosorb can remain
in place on the wound for days
and the number of changes
of dressings is reduced

Hydrosorb comfort has a hypoallergenic adhesive film

border to ensure it stays firmly in place and to prevent
bacterial penetration. This, together with the germproof
and waterproof surface of Hydrosorb comfort, simplifies
daily hygiene.

Hydrocoll absorbent hydrocolloid dressing

Hydrocoll is a self-adhesive, absorbent hydrocolloid
dressing for the cleaning and management of non-infected wounds.
The term colloid comes from the Greek and means
a substance that is incorporated in a matrix in a very
fine distribution. Hydrocoll consists of absorbent and
64

expandable hydrocolloids incorporated in a self-adhesive elastomer with a semipermeable film that serves to
prevent the penetration of bacteria and moisture. Upon
absorption of exudate from the wound, the hydrocolloidal
particles swell to form a gel that expands into the wound
and maintains a moist wound environment (1). The gel
remains absorbent until the hydrocolloids are saturated.
Saturation of the hydrocolloids is indicated by a blistershaped protrusion of the dressing (2), whereupon the
Hydrocoll must be changed.
Due to the adhesiveness of the elastomer, Hydrocoll can
be laid on the wound like a plaster. With the formation
of the gel, however, the adhesiveness in the area of the
wound surface is lost, so that Hydrocoll is attached only
to the intact border and thus does not affect the wound.
In addition, when the dressing is removed, it can be
removed without leaving residues of gel on the wound.
Prior irrigation is not necessary for assessing the wound
after a change of dressing. Hydrocoll has a high absorbency due to the special material composition.
Excess contaminated exudate is rapidly absorbed and
safely retained in the gel structure as a result of the
swelling process. In this way the microcirculation in
the wound area is simultaneously improved, so that the
bodys own cleansing mechanism is reactivated,
especially in those chronic wound conditions where
healing is delayed.

The principle of action of

Hydrocoll

During the granulation phase, the moist wound environment under Hydrocoll particularly stimulates the activity
of fibroblasts, which are responsible for initiating the
process of tissue regeneration. During the epithelialisation phase, the division and migration of epithelial cells is
supported. If there are no complications, Hydrocoll can
remain on the wound during this phase for several days
until the epithelialisation process is completed.
The germproof and waterproof top layer serves as a
reliable barrier against bacteria and protects the
wound from contamination and penetration of moisture.
Ambulant patients can shower with the dressing in
place.

65

Doppelseiten mit Pro

Product characteristics

Properties and use

Dry wound treatment

highly absorbent, soft and drapable, permeable to

the treatment of highly exudative, acute, superficia
against contamination through integrated, moisture
preventing the penetration of exudate

Zetuvit
Wound-compatible absorbent dressing pads with
non-adherent material covering and an absorbent
core of cellulose fluff
Cosmopor steril
Self-adhesive wound dressing with water-repellent
microgrid wound contact layer, absorbent pad of
pure cotton wool and soft non-woven fabric coated
with a hypoallergenic polyacrylate adhesive
Comprigel
Impregnated, non-adhering gel dressing with
integrated absorbent core in medicated cotton
Atrauman
Wound-compatible water-repellent polyester tulle,
impregnated with a self-emulsifying, neutral
ointment
Moist wound treatment
TenderWet
Superabsorbent polyacrylate wound pad with an
absorbing/rinsing core, activated before use with
Ringers solution which is delivered to the wound in
exchange for wound exudate
Sorbalgon
Conformable, non-medicated dressings made of
calcium alginate which form a moist gel in contact
with wound exudate
Hydrosorb
Absorbent hydrogel dressing with high water
content in the gel structure, with semipermeable
germproof and waterproof layer, transparent.
Hydrocoll
Self-adhesive, absorbent hydrocolloid dressing
with semi-permeable, germproof and waterproof
layer.

66

rapid transfer of exudate into the absorbent pad as

microgrid, no adhesion, good absorbency and cus
and water vapour, adhesive border ensuring good
management and the sterile dressing of minor injur

highly absorbent, permeable to secretions and air,

and keeps wound edges supple; slightly cooling, p
treatment of acute, small, superficial wounds or min

permeable to air and secretions, no adhesion to th

wound as a result of self-emulsifying ointment, doe
maintain suppleness in acute and chronic wounds
in patients with sensitive skin or who are sensitive t

rapid wound cleansing and promotion of tissue cel

continuous supply of Ringers solution and the simu
contaminated exudate (= rinsing effect); for the trea
wounds during the cleansing phase and at the beg

high absorbency with efficient cleansing effect, saf

structure, maintains a moist environment for the wo
promotes granulation, no adhesion, highly conform
cleansing and management of deep and gaping o

from the very beginning provides a moist environm

allows inspection of the wound at any time without
(= high cost effectiveness through reduction in freq
al for moistening granulation tissue and epithelium
Sorbalgon therapy

as a result of the promotes granulation, no adhesio

suitable for the management of chronic, slow-heali
granulation process is not functioning satisfactorily

n mit Produktbersicht

and drapable, permeable to air, good cushioning effect; for

y exudative, acute, superficial wounds, good protection
through integrated, moisture-repellent cellulose layer
ation of exudate

ate into the absorbent pad as a result of the water-repellent

n, good absorbency and cushioning effect, permeable to air
hesive border ensuring good closure; for postoperative wound
sterile dressing of minor injuries, e.g. in first aid.

meable to secretions and air, does not adhere to the wound

ges supple; slightly cooling, pain-relieving effect; for the
mall, superficial wounds or minor injuries

secretions, no adhesion to the wound, no residue on the

elf-emulsifying ointment, does not have a sensitising effect; to
n acute and chronic wounds, particularly in dermatology and
ve skin or who are sensitive to medications

g and promotion of tissue cell proliferation through the

Ringers solution and the simultaneous absorption of
e (= rinsing effect); for the treatment of chronic and infected
eansing phase and at the beginning of the granulation phase

efficient cleansing effect, safe retention of bacteria in the gel

moist environment for the wound after formation of a gel,
no adhesion, highly conformable; particularly suited for the
ement of deep and gaping or infected wounds

ng provides a moist environment for the wound, transparency

e wound at any time without the need to remove the dressing
ness through reduction in frequency of dressing changes); ideulation tissue and epithelium following TenderWet or

motes granulation, no adhesion to the wound; particularly

gement of chronic, slow-healing wounds and where the
not functioning satisfactorily

Commercial forms
Zetuvit, sterile and non sterile
10x10, 10x20, 15x25
20x20 and 20x40 cm
Cosmopor sterile,
7.2x5, 10x6, 15x6, 10x8,
15x8, 20x8, 20x20, 25x10
and 35x10 cm
Comprigel, sterile,
5x7.5, 10x10 and 10x20 cm
Atrauman, sterile,
5x5, 7.5x10 and 10x20 cm
TenderWet, sterile,
( 4, ( 5.5, 7.5x7.5 and
10x10 cm
TenderWet 24, sterile
( 4, ( 5.5, 7.5x7.5 and
10x10 cm
Sorbalgon, sterile,
5x5, 10x10 and 10x20 cm
Sorbalgon T tamponade ribbon, sterile,
1g/30 cm
and 2g/30 cm
Hydrosorb, sterile, 5x7.5,
10x10 and 20x20 cm
Hydrosorb comfort, sterile,
4.5x6.5, 7.5x10, 12.5x12.5, and
21.5x24 cm
Hydrocoll, sterile, 10x10
15x15 and 20x20 cm;
Hydrocoll sacral, 15x18 cm;
Hydrocoll concave, 6x14
cm; Hydrocoll thin, 10x10
and 15x15 cm (all sterile)

67

Treatment of infection
Inflammation is a physiological reaction of the body
designed to protect the tissues and to aid the elimination
of harmful agents. These harmful factors may be microorganisms or chemical substances (acids or bases),
but they can also be friction, pressure, foreign bodies, or
of a physical nature (e.g. an effect of temperature).
Infection in this context means the transmission, adherence and penetration of micro-organisms to and into
a macro-organism. This can result in the development
of an infection, depending on the infectious and pathogenic properties of the micro-organism, but also on the
defensive and offensive forces of the macro-organism
(immunity). Infection is not a primary cause, but the most
severe complication in diabetic foot syndrome and is
associated with impaired wound healing and an increasing risk of amputation. The best prophylaxis against
wound infections is the destruction of the favourable
living conditions for pathogenic micro-organisms through
drainage of the exudate and elimination of necrosis,
but also through specific drug therapy and early (minor)
surgery, where necessary.
Superficial and deeper, uncomplicated neuropathic
forefoot ulcers (Wagner stages 1 and 2) heal as rapidly
with standardised, phase-specific therapy without the
administration of antibiotics as they would with antibiotic
therapy. The mean reduction in ulcer size in this case
is 0.25 mm/day156. In patients in whom specific disease
conditions point to the possibility of a modification of the
natural healing process (patients with severe ischaemia,
with renal insufficiency or immunosuppressant diseases),
antibiotic treatment should be considered at an early
stage, even with this degree of severity156,157. At the same
time, the importance of long-term antibiotic therapy
of foot ulcer patients in the development of multiresistant
organisms should not be underestimated (e.g. a methicillin-resistant Staphylococcus aureus MRSA).
This micro-organism now constitutes up to 25% of all
staphylococcal infections in diabetic foot syndrome158,159.
In foot infections in which preservation of the extremity
is not threatened and which can be treated on an outpatient basis, aerobic Gram-positive cocci (e.g. Staphylococcus aureus) are found in almost 90% of cases,

68

and constitute the sole pathogenic agent in about

40%. Gram-negative aerobes (e.g. Klebsiella or Pseudomonas) and anaerobic micro-organisms are found in
36% and 13% of cases respectively, always in conjunction with polymicrobial infections. In the study quoted,
clindamycin and cephalosporins were used for antibiotic
therapy, which in our outpatient department are replaced
where necessary by Fluoroquinolones following the
results of cultures and in the absence of improvement in
local findings160. Ninety percent of infections are
healed with these agents, 75% of them within two weeks.
The aim here is to prevent the development of deep infections or osteomyelitis (or more accurately osteitis,
since initially it is the bone cortex that is affected and the
most commonly affected small bones of the foot contain
hardly any marrow). Osteitis is mainly a polymicrobial
infection (about 80% of cases), between 50% and 80%
of which involve staphylococci.
Drug therapy in deeper soft tissue infections and osteitis
should be based on sensitivity tests of the microorganisms isolated from the tissues concerned (obtained
by wound swab, aspirate, curettage or surgical excision).
Again clindamycin may be considered here161.
With purely conservative therapy, long-term treatments
of eight to twelve weeks are necessary162,163. The safest
way of obtaining long-term eradication of bone infection
without threatening the integrity of the foot appears
to be early surgical removal of affected sections of bone.
Early surgical intervention should be considered,
particularly if the infection fails to respond to targeted
antibiotic therapy, not least because an unhealed
infection involves the risk of an arthropathy occurring
later in the course of the disease164.

69

There are a variety of expensive imaging procedures for

the diagnosis of osteitis in diabetic foot syndrome,
such as leucocyte scans, Tc99m bone scan, magnetic
resonance imaging (MRI) and standard X-rays.
A simple and cheap method with at least as high a
Redness and marked swelling
of the second toe (sausage
toe) as a reliable sign of an
underlying osteomyelitis

positive predictive value for the presence of osteitis (89%

versus 75%85% with leucocyte scans and 50%93%
with MRI) is the tube test. Access to the bone via
the existing lesion with a sterile rinsing tube indicates
the presence of osteitis with a high degree of accuracy165.
Clinical signs (reduced pain perception due to neuropathy) and biochemical indications of osteitis are much
less reliable in diabetics. Fiftyfour percent of all patients
with osteitis in an American study were within the normal
range in terms of the leucocyte count, while in 82% of
the affected patients the oral temperature measured was
normal166.
Targeted action, however, presupposes an adequate
diagnosis. In a follow-up study of patients with infected
diabetic foot lesions in an American teaching hospital,
documented examinations of the wound for the involve-

70

ment of deeper structures were found in only 10% of

cases and a lack of foot X-rays was observed in 33% of
patients. Blood cultures were arranged in 62% of
cases but tissue cultures from the wound in only 51% of
cases167.
Vascular and surgical interventions in the
Diabetic Foot Syndrome
Primarily neuropathic lesions usually have a tendency to
heal rapidly following complete pressure relief, dbridement, drainage of soft tissue infections and, where
necessary, antibiotic therapy. In other cases where additional ischaemia is found, immediate Infection control
and consideration of Reconstructive or interventional
surgery to improve perfusion should be attempted.
Then, if unavoidable, borderline zone resection or Amputation, sparing as much tissue as possible, is performed
(IRA principle according to Vollmer168). It is essential that
a complete clinical and instrumental examination is performed before every amputation in diabetics to identify
those patients who will benefit from vascular surgery169.
This is made more difficult as concurrent diabetic neuropathy reduces the detection of ischaemic pain and
traditional methods of investigating blood circulation are
of limited predictive value in the presence of media
calcification.
There is as yet no documented evidence in large,
controlled studies of an improvement in the prognosis for
patients with diabetic foot syndrome from drug therapy
with prostaglandin derivatives. These products have
not been shown to have any specific effects in diabetics.
A large Italian study showed a short-term improvement
in the critical blood circulation of a limb and a reduction
in the risk of amputation with prostadil (Prostavasin).
After six months observation, however, only moderate
differences were found between treated and untreated
patients170.
In a small study involving eight patients with a disorder
of the arteries of the lower leg and rapid progression
of the foot lesion, urokinase therapy showed good shortterm success. However, in the long-term a bypass
operation had to be undertaken in half the patients to
preserve the extremity171.

71

It is thus apparent that patients with lesions of ischaemic

origin should be examined as rapidly as possible
with a view to establishing their suitability for a surgical
procedure (e.g. angioplasty, graft).
Some differences from non-diabetics are apparent with
both treatment approaches as a result of the particular
anatomical circumstances. In principle, the results of
vascular surgery in diabetics are comparable to those in
non-diabetics. In particular, a leg preservation rate of
77% was found after 11/2 years with the dilatation of circumscribed occlusions or stenoses of lower leg vessels172.
In patients in whom a balloon dilatation remains technically unsuccessful or in whom the leg condition fails
to improve despite an initially successful operation, bypass surgery procedures should always be considered173.
Overall, the pool of patients who can be helped by
vascular surgery is increased by the isolated dilatation of
lower leg vessels. Advanced age, a long history of
diabetes and a high degree of severity of the circulatory
disorders have an adverse effect on the results of this
method in diabetics. Regular examinations to identify
asymptomatic vascular processes and the implementation of surgical measures prior to the occurrence of
serious complications should therefore become standard
procedures174. Interventional (e.g. dilatation) and reconstructive (e.g. bypass surgery) procedures should be
employed as supplementary measures to preserve the
extremity in diabetic foot syndrome. In 22% of patients
from the Augsburg Clinic in whom a cruromalleolar
bypass was performed between 1986 and 1992, the
blood supply had previously been optimised by a percutaneous transluminal angioplasty (PTA) of the femoral
artery.175
Because of the particular anatomy (the lower leg
is frequently affected by PAOD, while the ankle and foot
arteries are spared), crural (bypass to a lower leg
vessel) or pedal (bypass to foot arteries) bypass procedures have increasingly obviated the need for amputation in diabetics over the past few years. Previously, the
creation of a femoropopliteal bypass in combination
with a transmetatarsal borderline zone amputation was
the therapeutic procedure of choice in ischaemic diabetic foot syndrome. There has been a marked reduction
in the number of amputations required in diabetics post

72

the introduction of bypass procedures. In both the USA176

and Denmark177 the number of amputations in diabetics
more than halved between 1984 and 1989, while bypass surgery, angioplasty and above all the use of distal
bypass grafts in each case more than doubled. In addition, in those amputations that have still proved necessary, the level of amputation has increasingly moved
distally. The amputation rates in Germany in centres
using such procedures175,178 are less than 10% for major
amputation. The extremity is preserved in 75% and
71% of cases after 2 and 5 years, respectively. The
patency rates of the bypasses created are about 60%.
This means that even short-term bypasses are frequently
sufficient to save a jeopardised extremity. As the diameters of the vessels in the lower leg and foot are small,
Creation of a distal vein bypass to preserve the extremity

autologous materials, i.e. the patients own veins, should

predominantly be considered for bypass material. In
individual cases, however, synthetic crural bypasses with
survival periods of several years have been observed
in our hospital. Peri-operative mortality of 1 to 2% in such
procedures must be regarded as favourable175,178, when
compared to primary amputation as an alternative
method which has a peri-operative mortality rate of 8%
in minor amputations and 18% in major amputations175.
A precondition for the use of such procedures is good
angiography, with visualisation of the foot arteries76.
Foot arteries that are suitable for bypass-surgery can be
found in a large proportion of diabetics. Even in the
absence of any angiographic evidence, a suitable vessel
for a bypass can be found in half the remaining patients
by Doppler examination179.
73

Surgical measures in the treatment of the diabetic foot

syndrome are not simply based on amputation.
If vascular surgical principles are applied, then extensive
mutilation can be prevented. If an amputation cannot
be avoided because of insufficient perfusion or uncontrollable infection, the principle that is now applied,
is to preserve as much tissue and function as possible.
Slight residual necrosis in the
large toe

and non-irritant, secondarily

healing wound following
resection of the necrotic fifth
toe

The classical amputation lines of previous years are no

longer binding and borderline zone amputations that
are as non-mutilating as possible are the procedure of
choice, subject to local perfusion conditions.
In the toe region, especially the large toe, partial
amputations are also beneficial for postural reasons.
Transmetatarsal amputations in the forefoot area, as
opposed to surgery of the mid-foot and hind- foot, have
the advantage of yielding better muscle balance with74

out the risk of talipes developing. Total resection of toes

involves a significant risk of the development of deficits
of mobility or rigid deformities180 which then require
particular management. Amputations of the toes (particularly of the first toe) also increase the risk of follow-up
interventions on the same side, as well as on the contralateral side as a result of altered weight-bearing181.
Forefoot stump which can be
well catered for by orthopaedic measures (left) compared with a functionally
unfavourable result following
amputation of the first, second
and fourth toe with a considerable risk of occurence of
further foot lesions (right)

While the long-term outcome of surgical interventions

on non-weight-bearing osteolytic sections of bone (e.g.
resection of proximal interphalangeal joints) is nonproblematic, pressure ulcers in the neighbouring areas
or the induction of diabetic neuropathic osteoarthropathy
are occasionally observed in surgery on weight-bearing sections of bone (e.g. metatarsal resection)182. With
the long-term presence of ulceration (on average nine
months), Griffiths183 was able to heal all patients by
resection of the metatarsals within an average period of
three months. No relapses were seen in any patient during a fourteen-month long follow-up observation phase.
A 70% reduction in pressure following resection of metatarsal I and 4050% following resections of metatarsals
II to V was measured184. In our own patient population,
plantar recurrences have been seen on isolated occasions in patients in whom individual metatarsals were
resected, but not in patients in whom metatarsals II to V
were completely removed.
Successful revascularisation is the determining predictive factor in the healing of partial foot amputations185.
Without prior revascularisation, 70% of partial foot

75

amputees must be re-operated, whereas after a successful revascularisation this applies in less than 20% of
cases. In contrast to patients with major amputations,
patients with amputations at the foot and ankle level have
a markedly higher probability of survival of almost 90%
after four years and more than 75% after eight years186.
However, re-ulceration occurs or further surgery is required in more than 50% of patients. The whole group of
such patients is characterised by high morbidity with
a further period of ulceration in almost 20% of cases
following a successful amputation. With appropriate
care, however, further surgery can be avoided in 52% of
patients over an eight-year period. More than 2/3 of
patients can be rehabilitated following a transmetatarsal
borderline zone amputation and are able to walk without
impairment185. In contrast to forefoot amputees, patients
with amputation of the posterior foot area (by the Chopart, Pirogoff and Syme methods) are not capable of
walking without a prosthetic device, but these operations
allow the lower leg to be preserved187. The prognosis
for a Syme amputation depends in particular on good
local perfusion. With good circulation, 90% of Syme
amputations heal and can be fitted with a prosthesis.
After 21/2 years, two-thirds of patients still wear their prosthesis throughout the day188. Among patients with a lower
leg amputation, 66% are able to walk with a prosthesis.
Upper leg amputated patients are capable of walking
with a prosthesis in 46% of cases, whereas bilaterally
amputated patients can be mobilised with a prosthetic
device in only 19% of cases189.
The mean survival time following major amputations is
slightly more than three years and 50% of patients
are threatened with the loss of the other extremity within
five years. Good aftercare of limb-amputated diabetics
is essential190. This involves care of the contralateral limb
and also good social reintegration.
In the case of extensive skin defects, the possibility of
plastic surgery to cover the defect should be considered
at an early stage191. Split-skin grafts, mesh grafts or
island flaps are available for wound closure.
Importance of adjunctive treatment methods
Hyperbaric oxygen therapy (HBO)
Hyperbaric oxygen therapy has been debated for some
years as a possible supplementary method for the
treatment of poorly healing wounds. On the assumption
76

that the combination of hypoxia and infection is responsible for the delayed healing of diabetic foot lesions,
the oxygen tension of the affected tissue should be
increased through the application of hyperbaric oxygen
in high-pressure chambers. It is thought that oxygen
tension remains high for a prolonged period after exposure. Thus the development of necrosis in the affected
tissue is reduced. In addition, a direct inhibitory effect
on the growth and toxin production of anaerobic microorganisms and a potentiating effect on angiogenesis
are postulated192. This is offset by the frequent side
effects of such therapy (barotraumas in 1 to 2%, transient
lung and eye damage in 15 to 20% of treatment cases)
and the as yet far from convincing data on the treatment
of diabetic foot syndrome with hyperbaric oxygen
(HBO)193.
A small randomised study in patients with, mostly neuropathic ulcers showed no effect on the reduction in
size and colonisation of the ulcerations during a 14-day
treatment cycle. The healing rate was even lower in
the treatment group194. Another study in 1996 concluded
that HBO therapy in patients with diabetic foot syndrome contributes not only to a significant increase in
transcutaneous partial oxygen pressure (TCPO2), but also
to a significant reduction in the number of major amputations required (8.6% versus 33% without HBO
therapy)192. On careful analysis of the data, however, it
became apparent that only one of three amputated
patients in the treated group had amputation without previous revascularisation, whereas in the control group
this was the case in 7 out of 11 patients. The contribution
of HBO therapy to reducing the number of amputations
thus remains questionable195.
A consensus conference on the subject in 1998 came to
the following conclusion:
1. The effect of hyperbaric oxygen therapy for radiation
induced wounds appears proven and there are
good data for osteomyelitis and soft tissue infection in
animal models and non-diabetics.
2. There are still no large randomised studies for diabetic
foot syndrome.
3. Ulcerations of Wagner grade 3 to 5 treated unsuccessfully by standard methods in multidisciplinary
establishments and for which an amputation is imminent may be considered for such treatment.
4. Careful follow-up of patients for diabetic retinopathy is
necessary.
77

5. Cost-effectiveness, quality of life and the endpoints of

limb preservation, duration of hospitalisation and
healing rate must be determined in the studies to be
performed196.
Use of growth factors and bio-engineered tissues
As has already been mentioned, deficits in immunocompetence play a significant role in the patho-physiology of wound healing disorders in the diabetic foot.
In immunosuppressed patients suffering for example
from neutropenia as a result of chemotherapy, treatment with granulocyte-stimulating factor (G-CSF) has
become established. Studies have also recently been
conducted into the efficacy of these products in immunosuppressant diseases without neutropenia. A study
along these lines in patients with diabetic foot syndrome
found an ulcer healing rate within 7 days of 21% versus
0% with placebo as evidence of a supportive effect
of such therapy on wound healing145. This isolated result,
however, is a matter of dispute197.
Treatment with growth factors and bio-engineered
tissues has come to the fore in the last years. While a
clinical study with fibroblast growth factor (bFGF)
showed no advantage over standard therapy198, studies
with recombinant platelet derived growth factor
(rhPDGF-BB, Regranex, for example, revealed significantly improved healing rates and a faster reduction
in wound diameter than with conventional wound treatment during a 20-week observation period199. Preliminary clinical results of the treatment of diabetic foot
wounds with bio-engineered tissues (Dermagraft)
were published in 1998. Dermagraft consists of neonatal,
dermal fibroblasts that are cultured in vitro in a bioabsorbable mesh. A viable, metabolically active tissue is
produced containing matrix proteins and cytokines.
After application to diabetic foot ulcers once a week, a
healing rate of 50% was obtained within 12 weeks
as compared to 8% in the reference group. During a
14-month follow-up observation period, no patient in the
Dermagraft group suffered a relapse. One explanation
for this might be found in the more flexible replacement
tissue compared to traditional scar tissue.
In a follow-up study in six patients with poorly-healing
ulcers (mean duration of 43 weeks), 50% were
healed within 12 weeks. As a result of the accelerated
healing and the lower tendency to relapse, treatment
78

with Dermagraft is regarded as cost-effective despite

the high costs of the product200.
While the results of studies on wound treatment with
individual growth factors in diabetic foot syndrome have
been unconvincing, treatment involving products with
a more complex composition of growth factors or with
bio-engineered tissues offer interesting new prospects in
problem patients. Treatment with growth factors is not
yet considered standard.
Biomechanical wound treatment
Biomechanical wound treatment (BMT) has in some
institutes acquired a certain value recently as a supplementary measure in the therapy of chronic wounds.
Described for the first time in 1931, treatment with fly
larvae (maggots) was a commonly used form of therapy
in the treatment of infected skin injuries in the 1930s
and 1940s in the USA. With the introduction of antibiotic
therapy, this method of treatment was to a large extent
Use of fly larvae (maggots)
following the exhaustion of
all conservative and operative
possibilities and the imminent
loss of an extremity

79

forgotten before undergoing a resurgence of interest

in the 1980s in the USA and since the mid-1990s in Great
Britain202.
The mechanism of action by which the larvae of Lucillia
serricata (greenbottle fly) contribute to the cleaning
and healing of necrotically coated or infected wounds
has yet to be fully elucidated. The production of an
antibiotic-like agent (also effective against micro-organisms resistant to conventional antibiotics), the presence
of growth factors in the larval secretion, the destruction of
bacteria by absorption and a change in the pH value
of the wound are postulated201. The provision of full and
detailed information to the patient and an explanation
of the principle of therapy are essential. Surprisingly,
problems of acceptance are occasionally to be found
less on the part of the patient than on that of medical
staff202. This method is being used following exhaustion
of conventional treatment procedures, as is the case
in our hospital. In future, earlier use might mean faster
wound healing and the avoidance of the need for
systemic antibiotic treatment201.
Similarly, positive results are reported from individual
centres with the use of leeches (Hirudo medicinalis)
in amputation surgery. Because of their local anti-inflammatory and antithrombotic effect due to the formation of hirudin, they are used in areas of critically
impaired circulation or in the development of hematoma.
Very peripheral borderline zone amputations even in
ischaemic limbs should therefore be possible with good
results203.

80

Tertiary prevention of the

diabetic foot syndrome
Patients with DFS remain extremely high-risk patients
throughout their life. Their education must include
information about what to do in the event of an injury
or impending amputation in addition to preventive
foot care aspects. Regular aftercare in special institutions considerably reduces the risk of recurrence of
lesions and subsequent amputations in these
patients. Successful tertiary prevention must also include risk-centred and phase-adapted shoe provision
for patients and the organisation of injury-free, professional foot care for those affected.

Effects of educating risk patients

Although value has been placed on the education of
diabetics since the beginning of the insulin era, education was not considered an essential part of the treatment of diabetics insofar as there was no convincing
evidence of its therapeutic efficacy. Preventive foot care
programmes in which patient education represented
an important component were among the first to show a
clear benefit in this respect.
A diabetes programme was instituted in California as
early as 1969, involving educational measures and
a telephone hotline. In Los Angeles the number of weekly
attendances for severe foot problems decreased from
320 to 40204. Assal in Geneva found a complete lack of
any previous information about preventive or early treatment measures in 22 of 23 lower-leg amputated patients,
whereas all eleven patients in whom surgery of the foot
area had sufficed had received previous education.
These were not controlled studies, but extensive programmes involving different treatment approaches,
including educational input. The contribution of the educational components to the success of treatment
was therefore difficult to distinguish from the improved
medical care. However, further data about the importance of educational measures were obtained from
studies which identified 40% of hospital admissions for
diabetic foot problems as the consequence of psychological problems or inadequate information205.

81

In the late 1980s, a series of studies were carried out,

firstly to establish the effect of patient education
alone and secondly to compare different types of foot
training programmes in terms of efficacy206.
The effect of a simple one-hour education programme
was examined in a prospective study in which the trained
group were shown slides of foot lesions in diabetics.
After one year, the incidence of ulcers and the amputation rate in the control group without any education
was in each case three times higher than in the trained
group207. Comparing a straightforward lecture with a
presentation involving practical exercises, the latter form
of education showed a marked improvement in the
short term. There was improvement in the patients knowledge and induction of behavioural changes, particularly
in nail care and daily foot inspections208. Simple educational measures involving a single hour of instruction
about the foot, was compared to instruction spread over
four weeks with 11/2 to 21/2 hours instruction per week
and involving a chiropodist and a psychologist. The latter
method had a sustained effect on patients behaviour,
as well as increasing their knowledge. The number of
foot problems that occurred fell markedly and the routine
performance of the patients own foot care and compliance with advice to consider professional foot care were
observed much more often in the intervention group209.
Patient education should be simple, relevant and
consistent (the same verbal and written statements) and
repeat the central message. The simplicity of relevant
training measures cannot be emphasised enough since
many of the patients who develop foot problems are
non medical people who will not be helped by confusing
vocabulary and complicated training programmes.
Training programmes must take account of the social
background and the level of education of the patients
concerned. A problem-oriented approach should be
adopted and the patient should experience the urgent
need of having to know certain things, rather than simply
having the feeling of being forced to learn.

82

The aim and form of training should be tailored to the

patient and their requirements, because education
is only successful if it manages to change habits and
patterns of behaviour. Particularly in elderly people
who are often no longer capable of undertaking simple
foot inspections on their own. Partners, relatives or
carers should be included in the training. Finally, intensive foot education should be directed towards specific
target groups most at risk. The over-education of
healthy diabetics may in the worst case even prove
counterproductive210.
Evidence for the lack of education of affected patients is
not difficult to find: 25% of all type 1 and 50% of all type 2
diabetics do not consider the loss of sensation in the
lower limb a consequence of diabetes mellitus. Only
about 30% of all foot ulcer patients consider themselves
at risk of foot injuries and a similar small number have
ever received information about foot and nail care before
suffering their lesion211. Risk conditions, such as
diabetic neuropathy or arterial occlusive disease which
increase the risk of amputation by 40% and 160%
respectively compared with healthy subjects, do not
result in the increased prescription of foot care or the
provision of more intensive education for these patients
by their doctors. Only the presence of a foot injury or
even a prior amputation (11-fold increased risk of further
amputation!!) mean that these patients receive more
intensive medical care212. Non-standardised treatment is
often the cause of a dramatic deterioration in the foot
disorders in diabetics as lack of care on the part of the
patient213. Education must therefore be directed equally
to members of the medical professions (doctors, nursing
staff, physiotherapist, occupational therapist) and to
patients and their relatives. The recognition of an at risk
foot and of early signs of pathological changes in the
feet of diabetics are the most important responsibilities in
the outpatient management of diabetic foot patients.
The greatest barrier to this is a logistical one, namely that
of giving the patients the opportunity and regularly
encouraging them on their visit to the doctor to take off
their shoes and stockings. Abnormal foot findings were
detected in only 20% of patients who wore shoes and
stockings on their visit to the doctor. In contrast, 60% of
existing foot problems were detected in patients who
presented themselves barefoot to their doctor. A foot
examination is an extremely effective, but unfortunately
much too infrequently used preventive measure. In a
New Zealand study, lesions (ulcers, foot injuries) or
predisposing changes (fungal infections, maceration or
83

callus formation) were found in 50% of a group of

unselected diabetics. Only 40% of patients with existing
blisters or foot ulcerations had undergone a foot
examination in the 12 months prior to this examination214.
In addition to the provision of information to the patient
about the risk to their feet and the principles of proper
foot care, educational measures for high-risk patients
must include information about the correct action to take
when foot injuries occur and how to react if the doctor
recommends amputation of a limb. No amputation in
diabetics should occur today without a full circulatory
examination (including angiography of the foot arteries).
Patients should always be encouraged to obtain
a second opinion before a planned amputation, where
possible from a specialised centre215.
Importance of professional foot care
Foot care in diabetics is of particular importance, but
also requires particular knowledge and skills. Treatment
errors can have serious consequences. Between
13%216 and 30%217 of all foot lesions are related to foot
injuries (either self inflicted by the patient or by professional chiropodists). Inadequate foot care or poor
hygiene also contributes greatly. The use of keratolytics
(products that remove horny skin), incorrect or wrongly
used foot care instruments (tweezers, scissors, razor
blades, special tools such as callosity files), and
excessively long or hot foot baths are possible causes of
foot care related lesions.
Appropriate foot care treatment includes:
1. Care of callus
2. Removal of clavi (corns)
3. Care of interdigital spaces
4. Treatment of fissures, macerations and fungal
diseases
5. Nail care and the careful correction of nail deformities.
The detection of pathological foot changes and the
inspection of the patients footwear and stockings
can also be undertaken by chiropodists following the
appropriate training.

84

The treatment of an ingrowing toenail (unguis incarnatus), which is traditionally done surgically for example
by means of wedge excision (Emmert-plasty) can
according to a more recent study be successfully treated
conservatively by means of packing, pressure relief
and, where necessary, antibiotics. Surgical operations
on the diabetic foot are associated with an increased risk
of development of gangrene218.
In the USA and Great Britain well-trained foot care
specialists (podiatrists or chiropodists) have taken over a
large part of the management of diabetic foot patients.
Similarly in Denmark the amputation rates were reduced
by 30% between 1981 and 1989 as a result of the further
training of 450 chiropodists for the qualified treatment of
diabetics. In contrast, in Germany in 1994 the Federation
of German Physicians and Insurance Funds (BdK)
excluded medical foot care from compulsory reimbursement by the regulatory health insurance funds. This
procedure was justified on the grounds firstly that foot
care is a general measure of body care and hygiene and
thus not a compulsory service of the health insurance
funds, and secondly on the grounds of the inadequate
quality of medical foot care, without defining this further.
According to a ruling of the Dsseldorf County Court
of 1997, not to exempt patients with foot diseases (e.g.
with diabetic foot syndrome) from this regulation is
illegal and hence void216.
It is true that medical foot care in Germany has not been
legally regulated to date. Schools of podology with a
structured, two-year training course have been set up in
several German cities. Also, the establishment by the
German Diabetes Society (DDG) for a transitional period
of a syllabus for qualification as a DDG chiropodist
should provide qualified foot care for diabetics throughout the whole of Germany as soon as possible.
It has recently been demonstrated that such regular
treatment not only reduces the risk of relapse, but
also substantially decreases treatment costs for foot
problems216. Fifty-one patients (48 of whom had a
previous foot ulcer) received foot care treatment at
monthly intervals from a specially trained and qualified
nurse working in co-operation with a diabetes outpatient unit. The relapse rate was reduced to 8% per
year with the simultaneous provision of protective
shoes. Instead of 30 patients admitted the previous year,

85

hospitalisation due to foot problems occurred in only

7 patients. Before the introduction of professional foot
care, 30% of patients had performed their foot care
themselves, half of whom had occasionally injured
themselves in the process. The costs generated by foot
problems were reduced by 80% as a result of this
measure.
It seems particularly unlikely in elderly people that selfadministered foot care can prevent the occurrence
of foot injuries. In a study of diabetics over 75-years-old,
only 14% were able to inspect the sole of their own
feet and more than 50% had problems with nail care.
The regular implementation of professional foot care for
this age group in particular will definitely have a more
effective preventive result than thorough training of the
patients219.
Pressure points with bruising
on the back of the feet
following the use of diabetes
adapted insoles with
insufficiently deep footwear:
the consequence of superficial knowledge in the patient
and therapist

86

Provision of adapted footwear for diabetics

Between 28%78 and 55%79 of all foot lesions in diabetics
are related to footwear. In principle, shoes serve the
same purposes in diabetics and non-diabetics: they are
worn for pleasure and for reasons of fashion, but what
is least firmly established in peoples minds is that
they serve to protect the feet. Some people also use (or
misuse) shoes to hide changes in the foot. Medical
functionality is therefore only one of a number of aspects
of footwear. To reduce the importance of shoes to this
purely functional aspect or even to the subsidiary aspect
of the protection of the diabetic foot against any form of
trauma is often difficult for the patient to understand and
causes the carer difficulties in dealing with these
patients220.
It is only in recent years that there has been increasing
recognition of the importance of suitable footwear for
diabetics . There are now results of clinical case control
studies on the prevention of relapse of foot ulcer comparing industrially produced shoes, off-the-shelf shoes
(cost of about 200 EUR per pair) and customised orthopaedic shoes (850 EUR per pair)221, 222, 223, 224, 225. According to these studies, the relapse rate as a result of
stage-specific shoe provision can be reduced to about
25% after one year and approximately 40% after two
years.
This effect is even more apparent from an analysis of
the prevention of shoe-related relapses following an initial
lesion due to footwear. From this viewpoint, protective
footwear saves 86% of patients from a relapse if the
shoes are worn sufficiently long every day over a period
Off-the-shelf, diabetesadapted protective shoe with
sole stiffening, a rocker
sole and raised toe room
(Buratto company)

87

of two years78. The occasional wearing of normal shoes

(27%), an incongruity between foot shape and
customised shoe in the presence of gross deformities
(27%) and hard toecaps are the reasons for further
lesions despite specialist shoe provision226.
The basic features of diabetes-adapted footwear date
back to the work of Tovey in 198420. He suggested a
low heel to prevent increased pressure on the forefoot,
a broad forefoot without stiffness in the toe area and
sufficient space to be able to take an elastic insole are
among the basic characteristics. In addition, high-quality
soft leather should be used for the uppers and internal
stitches should be avoided. To reduce plantar pressure,
a sole stiffening plate with a rocker sole are among
the design features of suitable protective shoes for diabetics224. There is a 4050% reduction in pressure in the
sole area with such shoes227, 228 which have appropriate
multilayered insoles compared to normal shoes (60%
reduction of presure as compared to walking bare
foot228). Specially padded stockings can also reduce the
pressure load by up to 30%, as well as reducing the
effect of shear forces229,230. Sufficiently deep running
shoes are considered by some authors to be the minimal
acceptable option in the absence of deformities until
the permanent protective shoe is finished or if the patient
refuses specialist shoe provision227, 231, 232. This type of
provision reduces the plantar pressure load by 3045%.
The fact that relapses cannot be avoided in a quarter of
patients annually is due to various reasons. Firstly,
patient acceptance of diabetes-adapted footwear is low
at 22%23363%234. Although not all patients approved
the appearance of their customised orthopaedic shoes,
51 out of 85 foot outpatients were wearing their customised shoes at a random inspection. Patients who displayed a higher degree of compliance were older and
more frequently had previous amputations than the less
compliant patients235. Patient participation in the design
of the shoes and a broader range in terms of shapes and
colours would possibly increase the frequency with
which such footwear was worn. More intensive information, directed at patients with shoe-related lesions, the

88

provision of a sufficient number of suitable pairs of shoes

and the additional prescription of slippers could also
contribute to reducing relapses. Twenty-two percent of
patients with foot ulcers in a Southern German diabetes
clinic79 and a similar percentage of patients in our own
outpatient foot department were not prescribed
protective shoes in 1994 and 199578. Regular inspection
of the shoes and insoles, particularly in the period
after the prescription, and the consistent improvement of
deficiencies are essential for quality assurance and
avoidance of ulcers.
Blueprint of a slightly altered
diabetic foot: by positioning
their own shoes over the top,
the patient was able to see
the incongruity between shoe
size and foot size

A further obstacle to the widespread use of therapeutic

footwear became apparent in an American study. Only
6% of all doctors who were informed about the possibility
of prescribing protective footwear with reimbursement
by insurance companies prescribed such shoes in
the following three years (one in 10 orthopaedic surgeons,
one in 21 internists and only one in 53 general practitioners or family doctors). Fiftynine percent of the patients
provided with footwear had a previous history of foot
ulcer in this study and 25% of patients had previous
amputation236.

89

Compared with studies of the benefit of specialised

shoe provision in the prevention of relapses, the data on
shoe provision for prophylaxis in patients without
previous foot injuries is less extensive. In a German study
over a 2-year period, only one in 21 patients without
a previous foot lesion suffered a foot injury following the
provision of protective shoes226, and two out of 49
patients in another study237. Predictors of the occurrence
of foot lesions in this patient group are the purchase
of new shoes in the six months prior to the occurrence of
the ulcer and wearing the wrong size of shoes238. In 80%
of patients from a diabetic population, among whom 27%
had already suffered a foot ulcer, the feet were never
measured when buying shoes212. Recent studies on the
subject have shown that the feet of diabetics with
neuropathy match the normal size in terms of length.
Result of computer-assisted
plantar foot pressure measurement in a patient with hallux
rigidus and increased foot
pressures in the area of the
metatarsus with diabetic
osteoarthopathy (Fastscan
measurement system,
Megascan company)

In terms of width, the normal shoe width G is too narrow

for 65 - 95% of patients. Even the next width up,
extra G (extra large), was inadequate for 44%84% of
patients239. According to another study, only about
20% of diabetic patients were able to use normal footwear, and only to a limited extent. About 60% of patients
were able to wear off-the-shelf protective shoes, while
for 22% of male diabetics and 13% of female diabetics,
a proper fit was only possible with hand-made customised shoes240. Although clinically tested off-the-shelf
protective shoes are currently specifically excluded from
compulsory benefits from the health insurance funds,
a large proportion of patients could be supplied cheaply

90

with such footwear to match the stage of their condition.

Only patients with gross deformities or who have already undergone amputations of part of the foot require
the more expensive hand-made customised footwear.
The value of computer-assisted foot pressure measurement procedures in the production and follow-up of
specialised shoe provision for diabetics cannot be conclusively established at the present time.

91

Footwear provision for the diabetic foot Classification by risk groups

Ia: Diabetes mellitus without PNP/AOD*:
Off-the-shelf shoe

IV. Foot as II and high grade deformity

or osteoarthropathy:

Ib: As above, with foot deformity:

Orthopaedic inserts, shoe devices

Custom-made shoes, orthoses, inner

shoes

IIa: Diabetes mellitus with PNP/AOD:

Suitable off-the-shelf protective shoe

V. Status following partial foot

amputations:
As IV, plus toe and forefoot replacement
prostheses.

Minimal criteria for a shoe of this kind

include sufficient toe room, sufficient
width, no stitches in front part of shoe,
soft leather, removable insole with soft
cushioning and reduction of pressure
points by at least 30% in the metatarsal
region. No hard toe caps. The efficacy
of off-the-shelf protective shoes with
or without individually designed insoles
needs to be demonstrated in studies.
IIb: As above with foot deformity:
Off-the-shelf protective shoe where
appropriate; in the event of specific foot
deformities, shoe devices and/or
individual diabetes-specific insoles,
possibly custom-made shoes
Inspection of insoles and regular
renewal
III. Foot as II and status following ulcer:
Shoe provision as for II.

* PNP = Polyneuropathy
AOD = Arterial Occlusive Disease

92

The effectiveness of custom-made

shoes with individually designed
insoles needs to be demonstrated in
studies since at present there is no
standardisation of materials and design
of custom-made shoes for the diabetic
foot.
VI. Footwear provision in acute ulcers,
etc.:
Various relief shoes and pressurerelieving ortheses are used here
in plantar ulcers and bandage shoes in
non-plantar ulcers.
The effectiveness of the various pressure-relieving and therapeutic shoes
also needs to be demonstrated in
studies.
Erich Gromotka, orthopaedic shoemaker
Georg Seele, orthopaedic shoemaker
Jrgen Stumpf, orthopaedic shoemaker
Karl Trk, orthopaedic shoemaker
Dr. Bettina Born
Dr. Christoph Metzger
Dr. Maximilian Spraul
Working party
Quality criteria and evaluation of shoe
provision for the diabetic foot

Structures for screening, treatment and aftercare of

patients with Diabetic Foot Syndrome
The financial burden and the human suffering caused by
diabetic foot syndrome need not be accepted as
inevitable. Numerous studies in the past few years have
shown that more than 50% of all amputations in diabetics
are avoidable if the following procedures are applied
systematically:

Regular inspection of feet and footwear of diabetics

at each visit to the doctor
Preventive foot care and shoe provision in high-risk
patients and additional education
Use of multifactorial and multidisciplinary treatment
concepts in the case of foot lesions
Early diagnosis and appropriate treatment of
peripheral circulatory disorders in diabetics
On-going aftercare of patients with previous foot
ulcerations or prior amputations
Strict adherence to defined indications for
amputation241 and establishment of amputation
registers

The management of Diabetic Foot Syndrome in nonspecialist German hospitals at the beginning of the
1990s unfortunately revealed a different, somewhat
gloomier picture. Almost 50% of the foot lesions treated
there culminated in an amputation and every second
amputation was a major amputation. In patients with an
arterial occlusive disease only, the rate of major amputations was 56%. In patients with combined neurological
and ischaemic findings, the amputation rate was 38%,
and in patients with purely neuropathic foot lesions, 27%
of treatments ended in amputation. Inappropriate conservative treatment concepts and complete ignorance of
vascular surgical treatment options were the reasons
for the frightening amputation statistics in the study
quoted242. If patients in whom an indication was established for minor or major amputation were transferred
to a specialist centre (mostly on their own initiative), 83%
of impending limb amputations and 79% of scheduled
foot amputations were avoided as a result of the exploitation of all the therapeutic options243.

93

The fact that things could be different had been

impressively demonstrated many years ago: In the 1970s
Davidson in Atlanta had demonstrated the possibilities
of reducing amputations in diabetics through a team
concept with risk screening, education and systematic
aftercare of the patient21. The amputation figures halved
between 1973 and 1980 after the introduction of these
measures (from 13.3 to 6.7 amputations/1000 patients/
year). A total of 555 amputations were avoided over
this period. Similar figures were reported in the following
years from Switzerland, England221,224, Scandanavia245,246,
Italy247 and Germany24,248. The healing rates for diabetic
foot lesions reported from such centres were 72%
to 80% in ischaemic lesions and 86% to 95% in neuropathically infected foot ulcers221,249. Between 1994
and 1998 in our own outpatient diabetic foot department
at the Marienkrankenhaus, (Soest/Germany) major
amputations were entirely avoided in purely neuropathically induced foot lesions. In purely ischaemic lesions a
40% reduction in all types of amputation was obtained250.
The establishment of outpatient diabetic foot departments in specialised clinics, however, not only results
in a marked reduction in the number of amputations
necessary and consequently an improvement in the
quality of life of those affected, but also produces considerable cost savings. The need for inpatient treatment can be reduced from on average about 40 days242
to approximately 20 days through the possibility of
follow-up outpatient care24, i.e. it can be shortened by
about three weeks. Inpatient hospital treatment can
even be totally avoided in a high proportion of purely
neuropathically related lesions23.
The leg preservation rate with the maximum exploitation
of vascular surgical possibilities (43% crural and 12%
pedal vascular reconstructions) for patients with critical
limb ischaemia is 85% after two years and almost as
high for patients with neuropathic lesions complicated by
a serious infection. If vascular reconstruction is not
possible in patients with ischaemic lesions, the limb preservation rate is reduced to 17% after two years249.

94

Not only have these outpatient diabetic foot departments

demonstrated their value in terms of improved prognosis
for manifest foot lesions, but also their efficacy in the
prevention of lesions in previously ulcer-free high-risk
patients is now documented. Over a three-year period,
patients who did not receive regular care from an outpatient foot department suffered a foot ulcer 24 times
more often than patients who received constant attention
from such a department. A lack of patient compliance
(in this case defined as a failure to attend less than half
the arranged appointments) increased the probability
of ulcer 54-fold and the risk of amputation 20-fold for the
whole population, including patients with previous foot
lesions251.
Patients with diabetic foot syndrome remain high-risk
patients throughout their life. Despite structured
aftercare, about a third of patients suffer a first relapse
within one year of the healing of an initial lesion78,37, while
after two years the figures are between 40% and 50%
of patients78,79,37. After five years seven out of ten patients
have suffered a recurrence of the lesion37. In previously
amputated patients the annual relapse risk is reported as
85%252. If such patients are not continuously treated
by a specialist establishment after the healing of a foot
injury, their risk of amputation in the event of a relapse
is almost 70%. If they continue to be treated by an outpatient foot department, this risk falls to about 20%253.
In one of our own studies in 30 patients who suffered a
relapse despite receiving care from an outpatient
diabetic foot department, amputations were completely
avoided after a second lesion. The need for hospitalisation in association with a recurrent lesion regressed to
7%, compared to 73% with the first lesion, and the
duration of healing was reduced from 64 to 29 days254.
Structured care therefore shows a positive effect on the
avoidance of foot lesions in high risk patients, the
course manifest foot injuries take, and the prognosis in
case of recurrence.

95

Levels of care for the support of patients with diabetic foot syndrome (modified
by Reike)
Target group
Patients at risk of foot
Medical foot
care practice lesions
(Chiropodist/
DDG, German
Diabetes
Society)
General
practitioner

All diabetics
Patients at risk of foot
lesions

Patients with a healed foot

Practitioner
lesion
with
specialisation
in diabetes

Activity
Atraumatic removal of callosities
Skin and nail care
Advice to patients

Primary/secondary prevention
Metabolic control/advice

Screening of risk patients

Clinical follow-up examination and
diagnosis. Basic instrumental examination. Footwear inspection. Where
appropriate, microbiology and
structured local wound treatment in
Wagner stage 1 (possibly 2)

Outpatient
diabetic
foot clinic
(hospital
based)

Diabetics with Wagner

stage 2 and 3 foot lesions
Diabetics with foot
lesions and wound healing
disorders
Diabetics with osteoarthropathy (acute/chronic
Charcots foot)

Neurological, angiological and

radiological diagnosis. Microbiological
diagnosis.Interaction with other
specialist disciplines. Structured local
wound management, where necessary
with establishment of a treatment plan
for GP care. Co-operation with orthopaedic technician and orthopaedic
shoemaker. Referral to outpatient care
services. Education of (high-) risk
patients.

DFS inpatient
unit

Diabetics with foot

lesions and wound healing
disorders
Diabetics with critical
ischaemia
Diabetics with acute
osteoarthropathy

General medical care of other

concurrent diseases. Structured local
wound care. Near-normal blood
glucose metabolic control (ICT).
Angiological diagnosis, therapy if
necessary (PTA). Co-operation with
other specialist departments (vascular
surgery, surgery, radiology). Cooperation with orthopaedic technician
and orthopaedic shoemaker.
Referral to outpatient care services.

96

In order to allow successful specialist treatment of

patients with diabetic foot lesions at an early stage, all
the existing centres must co-operate to streamline
treatment. In a current Swedish study, there was an
interval of between 31 and 189 days between the first
presentation of a foot injury at the general practitioners
and the institution of care by an outpatient foot department. Antibiotic treatment was instituted in a primary care
setting in 44% of patients, but additional measures,
such as pressure relief, were implemented in only 8% of
cases255. In our own prospective study, the interval
between the occurrence of the lesion and the first presentation at the outpatient diabetic foot department
in 153 patients without any prior information about the
procedure to be followed in the event of foot problems
was on average 71 days. However in 62 patients with
previous education or contact with the outpatient foot
department for a previous lesion, the interval was
13 days. The corresponding amputation rates were 24%
and 10%, respectively256.
The role of the family doctor might be:
1. The identification of patients at risk of foot lesions
2. The provision of basic information to these patients
3. The implementation of preventive measures
4. The regular inspection of foot status
Minor foot lesions can be managed in a diabetes clinic
and, in emergency cases, in specialised outpatient
diabetic foot departments. The complete diagnosis and
treatment of more complex foot lesions should also be
undertaken there, with the involvement of diabetologists,
surgeons, vascular surgeons, chiropodists, orthopaedic
shoemakers and interventional radiologists. Emergency
facilities and the presence of a special foot unit with
appropriately trained staff should be among the features
of such specialised establishments. Problem-centred
interdisciplinary visits can further improve the efficiency
of such establishments.

97

Successful co-operation in a network of this kind requires

seamless transitions (frequently complicated by the strict
separation of outpatient and inpatient structures in
Germany), the absence of fear of contact and the
presence and implementation of guidelines which are
valid for all participants. A consensus paper in this
respect on the diagnosis and treatment of the diabetic
foot was published for the first time in May 1999 by the
International Working Group on the Diabetic Foot.
The diabetic foot: a global problem
The prevalence of diabetes world-wide, which affected
approximately 135 million patients in 1996, is predicted
to grow to 300 million patients by the year 2025 on the
basis of increasing life expectancy throughout the world,
the change in dietary habits and the increase in the
proportion of obese patients. In particular, countries with
little or no infrastructure and no standards of foot care,
will experience the most dramatic increases in type 2
diabetics. Thus, in the year 2025 India is predicted to
have 57 million diabetics and China 38 million. In Central
and Southern African countries, the number is estimated
to grow from 3 million at present to 8 million, representing
an increase of 185%2. Although the pathogenesis of
diabetic foot problems is probably the same everywhere
in the world, the clinical manifestations and the problems
observed differ according to local conditions and
sociocultural features between the distinct countries and
the various geographic regions.
In Western European countries, the distribution of
risk conditions (arterial occlusive disease and diabetic
sensorimotor neuropathy) is very similar to that found
internationally257. Also the treatment results essentially
reveal no differences between Central European and
North American centres258. The conditions in other parts
of the world are quite different as a result of specific
epidemiological factors and the features of the relevant
healthcare systems.

98

In Eastern Europe, specialist centres for the treatment of

the diabetic foot are rare. In many places amputation is
still considered the standard. As a result of twinning
programmes with Western European countries, structural
improvements are gradually occurring in certain regions.
In South America, where the prevalence of diabetes is
more than 6%, the establishment of institutions has so far
only been observed in Costa Rica, Mexico and Brazil. In
some North African countries more than 10% of the
population are diabetics, up to 12% of patients with foot
ulcerations are found among hospital inpatients and 7%
of diabetics have had previous amputation. In Australia
programmes involving foot care in diabetics have already
been implemented countrywide. In some tropical
countries, the co-existence of diabetes mellitus and
leprosy has resulted in a particularly high occurrence of
patients with a potential risk of occurrence of foot
lesions259. In addition, a relatively high proportion of foot
Manifestations of diabetic foot
syndrome in India:
a) Callus formation on the
dorsum of the foot in a Moslem
diabetic patient a result
of the typical kneeling praying
position with crossed feet

b) Burn in the area of the rear

of the foot as a result of
placing the naked foot on the
hot exhaust pipe of a
motorbike (both pictures were
kindly provided by Dr. V.
Viswanathan, Chennai, India)

99

(and hand) infections is found here in diabetics

without the conventional risk conditions, such as arterial
occlusive disease and diabetic neuropathy260,261.
On the basis of our own study (613 patients), the following essential differences were observed in the presenting conditions of diabetic foot syndrome between an
industrial country (Germany) and two developing
countries (Tanzania and India). In developing countries
there is a far smaller proportion of patients with arterial
occlusive disease, because abuse of nicotine is less
common. The patients are much younger and the duration of diabetes is shorter. Shoe-related lesions were
found in the developing countries in only 5 to 6% of
cases, as opposed to 27% in the industrial nations. The
presence of a diabetic neuropathy in patients with
diabetic foot syndrome, however, was equally high in
both populations, at about 80%262.
The situation in some African countries is characterised
by the high proportion of illiteracy among foot patients
and the more difficult conditions for the provision of
information and education. In some cultural environments amputation of a limb is considered to be more
serious than the loss of ones own life261. This explains the
high proportion of self-discharges by patients before
the end of treatment from hospitals, especially in view of
a more than 50% amputation rate. Unusual manifestations due to specific sociocultural conditions characterise the picture of the diabetic foot in India. In a country
in which 30% of people live below the poverty line,
wearing shoes tends to be the exception rather than the
rule. Infections of fissures resulting from walking barefoot
are among the causes of diabetic foot problems in India,
as are burns from the hot cobble stones of the Hindu
temples where the faithful are strictly forbidden to wear
shoes and pressure sites in the ankle region because
of the particular praying position of the Moslems263. Rat
bites of the toes of neuropathic patients264 are among
the unusual presenting forms of diabetic foot syndrome
in India, as well as infections from tropical worms.

100

Summary and prospects

More than half of all limb amputations are carried out in
patients with diabetes mellitus. In more than 70% of
cases, amputation is preceded by a foot ulcer
progressing to deep gangrenous infection. Most of these
ulcers are caused by minor trauma, frequently as a result
of poorly fitting footwear or inadequate foot care.
Sensorimotor diabetic neuropathy or a peripheral arterial
occlusive disease of varying severity are in most cases
present as risk conditions predisposing to injury.
The continuous registration of amputations (amputation
registers, e.g. the Danish amputation register, North Rhine
Chamber of Physicians Diabetology/Surgery Quality
Assurance) can help to reduce amputation rates in diabetics265. The DCCT study6 has shown that intensive
treatment of type 1 diabetics and optimised blood sugar
control can reduce the probability of diabetic neuropathy
occurring by 50%. However, as long as the avoidance
of secondary micro-angiopathic complications remains a
goal for a majority of diabetics, the early identification
of risk conditions, the avoidance of lesions in high risk
patients and the structured treatment and aftercare of
ulcer patients (and previous amputees) must be made a
priority.
Key preconditions for improving the prognosis of
diabetics with foot lesions are:
1. Regular screening of diabetics for impaired nerve
function and inadequate circulation
2. Problem-centred patient education
3. Regular foot care and the supply of protective
footwear to those affected
4. Structured and team-based care of patients with
active ulcerations
The specific recording of individual causes of injury and
integration of these findings in the risk-centred education
and aftercare of patients and relatives may help to
reduce the emergence of recurrent lesions and hence the
risk of amputation still further78,266.

101

The implementation of prevention and treatment

strategies has been shown to help avoid more than 50%
of amputations in diabetics.
According to Swedish estimates, halving the amputation
rate would reduce the costs of treatment of diabetic foot
problems by about 20 to 40%267.
Although in the new millennium new treatment options
may facilitate the treatment of diabetic foot lesions, the
continuing construction of suitable treatment establishments and their regional networking certainly cannot
be replaced. Extensive and structured treatment and
aftercare of patients with diabetic foot syndrome in
specialised and quality assured institutions is necessary
to implement the requirements of the St. Vincent Declaration. The key to success for the development of appropriate infrastructures to allow the creation of foot teams
for problem patients lies in obtaining the necessary
contribution from insurance companies, as well as early
registration and targeted care of high risk patients.
In view of the enormous expenditure on amputations in
diabetics and the comparatively low costs of preventive
measures in diabetic foot syndrome, it may be assumed
that such efforts will be associated with a favourable
cost-benefit ratio.
Extensive knowledge alone remains ineffective. To contribute to successfull treatment, this knowledge must be
applied. In the form of behavioural changes in patients
and also in the professional groups treating them within
the healthcare system. It is not the hope of new treatment
procedures, but simply the consistent application
of what is known, established and already possible
that in the future will result in amputations becoming an
exception and not the rule in patients with diabetic
foot syndrome.

102

Definitions and
explanations
Amputation
Resection of a part of a limb
Arterial occlusive disease
Presence of clinical signs such as the absence of foot
pulses, previous history of intermittent claudication,
rest pain and/or abnormalities in non-invasive examinations indicating impaired or insufficient circulation
Cellulitis
Presence of swelling, redness and heat as evidence of
an inflammatory reaction, irrespective of origin
Charcots deformity
Resulting from Charcots disease or arthritis; also neuropathic arthritis - it is a rapid progressive degeneration
in a joint which lacks position sense and protective pain
Chopart amputation
Amputation through the talo-navicular joint
Deep infection
Presence of evidence of an abscess, septic arthritis or
osteomyelitis
Dbridement
Removal of dead tissue
Deep ulcer
Lesion affecting the whole thickness of the skin and
extending to the subcutis, possibly involving muscles,
tendons, bones and joints at the same time
Diabetic foot syndrome
Infection, ulceration and/or destruction of deep
tissue associated with neurological abnormalities and
various degrees of severity of arterial circulatory
disorders of the lower extremity
Diabetic neuropathy
Presence of signs and/or symptoms of disorders
of peripheral nerve function in patients with diabetes
mellitus after the exclusion of other causes

103

Foot deformity
Structural changes in the foot, such as the presence of
hammer toes, claw toes, hallux valgus, prominent metatarsals and conditions due to neuro-osteoarthropathy, as
well as surgery on the foot and amputations
Foot lesion
Blister, erosion, cut or ulcer on the foot
Gangrene
Progressive necrosis of the skin and deeper structures
(muscles, tendons, bones or joints) indicating irreversible
destruction, in which healing cannot be obtained without
the loss of part of the extremity
Infection
Penetration and proliferation of micro-organisms in body
tissue, which may be clinically insignificant or may
result in local cell death, as a result of toxins, intracellular
microbial proliferation or an immune response
Intermittent claudication
Pain in the foot, thigh or calf which is increased on walking and relieved on stopping, associated with evidence
of an arterial occlusive disease
Major amputation
Any amputation above the ankle joint
Minor amputation
Amputation at the level of the ankle joint or lower
Necrosis
Dead tissue, either dry or moist, regardless of the tissue
affected
Neuro-osteoarthropathy
Non-infectious destruction of the bone or joints
associated with a neuropathy
Neutropenia
Relative or absolute decrease in the number of neutrophilic leucocytes in the blood
Osteomyelitis
Infection of the bone with involvement of the bone
marrow

104

Pirogoff amputation
The calcaneum is cut across so that the posterior 2 cm
remain in the heel flap and this is attached to the
lower end of the tibia, making a longer stump than in the
Symes amputation
Polymicrobial
Infections with more than one organism causing damage
Pressure relief
Relief of load-bearing areas of the foot through the
systematic use of crutches, wheelchairs, partial foot relief
shoes or other orthopaedic devices
Protective footwear
Footwear of proven benefit in the prevention of
ulcerations
Superficial infection
Infection of the skin without involvement of muscles,
tendons, bones or joints
Superficial ulcer
Lesion affecting the whole thickness of the skin without
extending to the subcutis
Symes amputation
The original level of amputation was through the ankle
joint with the medial and lateral malleolus trimmed.
The amputation has been modified to divide the tibia and
fibula 1 cm above the joint line. In an emergency the
patient is able to stand and walk without the prosthesis

105

Abbreviations:

106

ABI
ADA
AOD
ATR

Ankle Brachial Index

American Diabetes Association
Arterial Occlusive Disease
Achilles Tendon Reflex

bFGF
BMT

b-Fibroblast Growth Factor

Biochemical Wound Therapy

CNS
CSII
CT
CVA

Central Nervous System

Continuous Subcutaneous Insulin Infusion
Conventional Insulin Therapy
Cerebral Vascular Accident

DCCT
DDG
DFS
DNOAP
DSA

Diabetes Control and Complication Trial

Deutsche Diabetes Gesellschaft (German
Diabetic Association)
Diabetic Foot Syndrome
Diabetic Neuropathic Osteoarthropathy
Digital Subtraction Angiography

ESR
EUR

Erythrocyte Sedimentation Rate

Euro

GAD
GCSF
GDM

Glutamic Acid Decarboxylase

Granulocytes Stimulating Factor
Gestational Diabetes Mellitus

HbA1c
HBO

Haemoglobin Receptor A1 c
Hyperbaric Oxygen

ICA
ICT

Islet Cell Antibodies

Intensified Conventional Insulin Therapy

MRI

Magnetic Resonance Imaging

PDGF
PNP
PNS
PTA

Platelet Derived Growth Factor

Polyneuropathy
Peripheral Nervous System
Percutaneous Transluminal Angioplasty

rhPDGF

Recombinant Platelet Derived Growth Factor

TCPO2
TGF

Transcutaneous Partial Oxygen Pressure

Tissue Growth Factor

UKPDS

United Kindom Prospective Diabetes Study

Volt

WHO

World Health Organisation

Proposed further reading

Andrew JM Boulton, H Connor, Peter R Cavanagh (Eds).
The Foot in Diabetes, 3rd Edition. Wiley and Sons Ltd.,
Chichester 2000.
ISBN 0-471-48974-3
John H Bowker, Michael A Pfeifer (Eds). Levin and
ONeals The Diabetic Foot, 6th Edition. Mosby Inc.,
St Louis 2001.
ISBN 1-55664-471-x
Mike E Edmonds, Alethea VM Foster. Managing the
Diabetic Foot.1st Edition, Blackwell Science, Oxford
2000. ISBN 0-632-05583-9
Robert G Frykberg (Editor). The High Risk Foot in Diabetes Mellitus, 1st Edition. Churchill Livingstone Inc., 1991.
ISBN 0-443-08665-6
William Jeffcoate, Rosamund MacFarlane. The Diabetic
Foot An illustrated guide to management, 1st Edition.
Chapman & Hall Medical, 1995. ISBN 0-412-54410-5
Aristidis Veves, John M. Giurini, Frank W. Lo Gerfo (Ed.):
The Diabetic Foot, Medical and Surgical Management,
Humana Press, Totowa, New Jersey, 2002
ISBN 0-89603-925-0

Acknowledgements for photographs:

David Gifford / Science Photo Library / Focus
(Cover page)
Morbach, S. (P. 2557 and P. 7090)
Thanner GmbH (P. 50)
Viswanathan, V. (P. 99)
All other photographs from the PAUL HARTMANN AG
archive, Heidenheim

107

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119

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