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					Chief Editor

            Professor of Anatomy and Human Embriology. Universitat Autònoma de Barcelona. Spain.

            Chief, vascular surgeon .                              (               )

            Department of Endocrinology and Nutrition.                                     (               )

            Chief Officer of the Endocrinology Department.

            Endocrinologist . Director of                                                  (               )

            Department of Endocrinology, Metabolism and Nutrition, Hospital Clinico San Carlos ( Madrid )

            Medical Doctor. Internal medicine.                                 (               )

            Library Assessment.                                (           )

            Library Assessment.                                (           )

            Podiatrist. Endocrinology Department.                                      (               )

            Chief of the Nuclear Medicine Department.                                              (           )

            Podiatrist . Diabetic Foot Unit.

            Senior Registrar. Orthopedic Surgery Department.

            Intern. Primary Care Department .

            Podiatrist.             (              )
    Melcior Lladó Vidal
            Podiatrist. ADIBA. Palma de Mallorca

           Primary Care Physician.             (         )

            Primary Care Physician.            (         )



Diabetic Foot Digital Journal is a multidisciplinary journal for professionals involved in the care and treatment
of diabetic foot. The journal has fixed sections appearing in every issue and variable sections that may be
included in function of the manuscripts accepted for publication.
Diabetic Foot Digital Journal accepts original reports, brief reports, review articles, and letters to the editor
for online publication.
The journal is published three times per year, in February, June, and October.
Material appearing in Diabetic Foot Digital Journal may not be reproduced in whole or part without the
express permission of the publishers. The contents of previous issues can be found at .

Manuscript presentation:
Diabetic Foot Digital Journal accepts manuscripts written in Spanish or English.
Manuscripts must be original and not under consideration for publication elsewhere. Manuscripts should
be sent to; please use MSWord format for the manuscript and jpeg for figures
and images.

Manuscript types:
Original reports: Articles related to any aspect of diabetic foot based on research or clinical studies.
Review articles: Articles that review the literature about specific topics related to diabetic foot.
Case reports or brief reports: Articles related to any aspect of diabetic foot based on research or clinical
studies that have more modest objectives or results and therefore require less space for publication.
Updates in care: Articles dedicated to continuing medical education about the specialty.

Cover letter: All submissions must be accompanied by a cover letter indicating: 1/ The section of the journal
in which the authors to publish the manuscript; 2/ an explanation of the original contribution and importance
of the article; 3/ a statement that the manuscript is original and is not under consideration for publication
elsewhere; 4/ full name, mailing address, and institutional affiliation of all authors, as well as the telephone
and e-mail address of the corresponding author.

Manuscript organization:
Abstract: A brief (250 words) summary of the text.
Keywords: up to five words, in alphabetical order, describing the contents of the manuscript. We recommend
using the MeSH terms listed on Medline:

Main body: Originals should use the IMRaD (Introduction, Material or Methods, Results, and Discussion
and/or Conclusions) format; review articles should include the following sections: Introduction, Development,
and Conclusions.

References should be numbered consecutively in the text using superscripted arabic numerals within the
text and listed at the end of the manuscript in the Vancouver style:

List all authors for reference citations with six or fewer authors; otherwise, list only the first six authors and
et al. Journal titles should be abbreviated as on Medline:

                                                                          Pág. 2
                                                                              Pie Diabético
  Editorial                                                                                  Digital

With this issue, we celebrate the first anniversary of Pie Diabético Digital with the satisfaction
of having completed our goals for this first year.
Our circulation in Spain, as noted in previous issues, has surpassed our initial previsions by
far, and the journal has also been well received outside Spain in both Spanish-speaking
countries and in others where Spanish is not the principal language. However, as we all know,
English is the lingua franca of science in the world today.
For this reason, to celebrate our first anniversary the Editorial Board has decided to offer
Pie Diabético Digital in both English and Spanish to reach a wider audience.
Diabetic Foot Digital Journal can be consulted in English at
Connecting to this site enables the reader to select to access the material in English or
Spanish, although it will always be possible to switch languages afterward.
We would like to take this opportunity to welcome English-speaking readers and hope that
we reach as many readers as we have with the Spanish version or even many more.
This issue of Diabetic Foot Digital Journal is full of innovations. Continuing in our efforts to
improve and expand the different sections, the journal will have two new sections: the first
is the publication of a photograph (curious, spectacular…), and the second consists of inserting
a short (3-4 lines) commentary within articles to orient readers to the content of the article.
These improvements and others that will surely follow are possible thanks to the disinterested
collaboration of the many professionals who send us suggestions or ideas to improve the
This issue includes an original article from an Argentinian group. This is the first article from
another continent to be published in Diabetic Foot Digital Journal, and we congratulate the
authors on this accomplishment.
Since June, we have enjoyed the support of two new sponsors: B. Braun Medical and Novo
Nordisk Pharma, and we would like to take this opportunity to welcome them aboard.
This September, Diabetic Foot Digital Journal will be attending the 7th Scientific Meeting of
the Diabetic Foot Study Group in Lucca, Italy from the 11th through the 13th, and we look
forward to providing you with detailed information about this conference in our next issue.

                                                                               Jordi Viadé Julià.

                                                        Pág. 3   Pág. 4
    New Feature
Consequences of inappropiate treatment of patients
with diabetic foot
Roxana Gabriela Lenkovich, Juan Manuel Roganovich,
Arturo Martín Gorodner.
Instituto de Medicina Regional (UNNE), Resistencia, Chaco. Argentina

The WHO defines diabetic foot as ulceration, infection, and/or gangrene of the foot associated
to diabetic neuropathy and to different degrees of peripheral artery disease as a result of the
interaction of different metabolic factors.
The worldwide prevalence of diabetes is 5.1%, and 20% of diabetics develop foot ulcers. Over
half of all non-traumatic foot amputations are done in diabetic patients.
The timeline of these lesions runs as follows: poor metabolic control - neuropathy and/or
vasculopathy - external or internal trauma - pre-ulcerous lesion - ulcer - infection - necrosis
- and death.
The unleashing factors are: sensory-motor neuropathy, reduction in the plantar pad,
biomechanical alterations, trauma, and peripheral vascular insufficiency.
Patients can be classified as low-risk or high-risk for diabetic foot.
Low-risk diabetic patients have no arthropathic, neuropathic, or vasculopathic alterations.
High-risk patients are characterized by:

-     Loss of protective sensations.
-     Absence of pulses in the feet.
-     Foot deformities.
-     Prior history of ulcers.
-     Prior amputation.

Figure 1. Neuroischemic ulcer on the heel

                                                    Pág. 5
 New Feature
Wound healing in diabetic patients' feet is altered by hyperglycemia, ischemia, malnutrition,
neuropathy, infection, and suppressed immune response, so it is important to evaluate the
wound microscopically and macroscopically (necrosis, perfusion, infection, metabolic state,
nutritional assessment, and tissue moisture balance).
Alterations in the biodynamics of the foot, increased plantar pressure with osseous
deformations, and limited articular mobility increase the risk of ulcers and amputation.
Diabetic foot requires integrated care rather than mere treatment of the infection and
management with antibiotics.

 Diabetic foot often develops from alterations in the support of the foot; it does not heal -or
healing is delayed- due to uncorrected arthropathic disorders, and relapse due to unsolved
orthopedic problems is very common.
Lesions can be prevented by excellent diabetes control, monthly foot examination by a
specialist, corrective measures for neuropathy or arthropathy, vasoactive drugs or surgical
revascularization in patients with arteriopathy, and physical activity tailored to each particular


To analyze the consequences of inappropriate or poorly implemented treatment for diabetic


We carried out a complete clinical evaluation of 92 diabetic patients presenting at our outpatient
clinic over a six-month period; we only excluded women with gestational diabetes. We included
all patients with high-risk diabetic foot. We evaluated the time of evolution of diabetes, previous
medical examinations, treatments received, and metabolic and nutritional control; furthermore,
we assessed neuropathy, peripheral vessels, and the support of the foot.

                                             Figure 2. Diabetic patient with feet amputation.

                                                       Pág. 6
    New Feature
A total of 78 patients (84.7% of the total) with diabetic foot and at least five years' evolution
of diabetes were included in the study. Mean age was 61(+/-3) years. Ten had undergone some
type of surgical amputation; of these, seven had no prior Doppler examination or angiogram.
On at least two occasions, failure to thoroughly evaluate the peripheral vessels before
amputation led to re-admission for new amputations, lesions caused by excessive support,
and subsequent difficulties in equipping the limb and rehabilitating the patient, all of which
resulted in high healthcare costs and a psychological burden for the patients and their families.
At the time of examination, some type of ulcer and/or gangrene was present in 18 patients; 12
(66%) of these patients underwent some type of antibiotic therapy without prior cultures, and
7 (39%) underwent different antimicrobial therapies with no antibiogram. This inappropriate
treatment led to infection with multiresistant flora and progressed to sepsis in 28% of the
Nutritional status had not been previously evaluated in any of the patients studied. Likewise,
the metabolic disequilibrium had not been adequately compensated in any of them and none
were referred to specialists in diabetes at the appropriate time. Finally, none of them had
received appropriate education about their diabetes.

                                          Figure 3 <<. Infected
                                          ulcer on a foot with
                                          Charcot's disease.

                                          Figure 4 >>.
                                          Hyperkeratosis due
                                          to altered support.


-     Diabetic foot and the complications derived from it generate the highest healthcare
      costs in the healthcare system.
-     A protocol for the control of diabetes needs to be implemented and carried out in
      dedicated interdisciplinary units.
-     It is essential to educate diabetic patients about diabetes and its treatment.

Keywords: Diabetic foot, vasculopathy, neuropathy, ulcer.

                                                      Pág. 7
 New Feature
- Zavala A. Normas de diagnóstico y tratamiento del pie diabético UBA. 2004.

- The International Working Group on the Diabetic Foot. International Consensus on the Diabetic
  Foot. Holanda. 2005

- «Simposio Clínico sobre Avances en el cuidado de la piel y las heridas Phoenix, USA».
  EPROCAD. 2004;4:51-8.

- Zavala A. «Fisiopatología de las úlceras del pie.
  EPROCAD. 2004;4:73-6.

- Peryra SD. «No perder tiempo para salvar algo del pie. La amputación positiva».
  EPROCAD 3: 56-58 2003;

- Torres R. «Rehabilitación después de la amputación. 8º Congreso de Vasculopatías, Factores
  de Riesgo y Pie Diabético».
  EPROCAD. 2003;3:56-8.

- Novo M, Zavala A: «Diagnóstico y Tratamiento del Pie de Charcot».
  EPROCAD. 2004;2:66-70.

- Zavala A: «Manejo del Pie Diabético. Importancia del diagnóstico y tratamiento de las alteraciones
  del apoyo».
  EPROCAD. 2003;1:47-8.

                                                        Pág. 8   Pág. 9
Diabetic neuropathy (I)
Carles del Pozo M.D
Department of Endocrinology and Nutrition.
Hospital Mútua de Terrassa. (Barcelona)
Diabetic neuropathy (DN) is the most common complication of diabetes mellitus. Although
DN often receives less attention than other late complications like retinopathy, nephropathy,
or vascular disease, it is the main risk factor for diabetic foot. Therefore, early screening
for diabetic neuropathy has proven important for the prevention of foot ulcers and
consequently of nontraumatic amputations of the lower limbs.


DN is defined as the presence of symptoms or signs of peripheral nervous system
dysfunction in diabetic patients, after other causes have been excluded (1). DN is a very
heterogeneous entity that can affect different parts of the nervous system. It is classified
into different types in function of its anatomical distribution and the signs and symptoms
present (table 1).

TABLE 1. Classification of diabetic neuropathies

  Diffuse neuropathies
       Chronic symmetrical distal sensory-motor
       Acute sensory
       Symmetrical distal motor
    Autonomic neuropathies
       Asymptomatic glycemia
       Sweat gland

  Focal neuropathies
   Simple mononeuropathy
   Multiple mononeuropathy
   Cranial neuropathy
   Truncal or mononeuropathic radiculopathy
   Lumbosacral plexopathy, asymmetrical proximal neuropathy, or amyotrophy

                                                   Pág. 10
In this article, we refer especially to chronic symmetrical distal sensory-motor
polyneuropathy, which is the most common presentation of DN. In fact, the term DN is often
used synonymously with chronic symmetrical distal sensory-motor polyneuropathy.
Together with other alterations due to autonomic neuropathy, DN brings about the conditions
that lead to diabetic foot.


DN is a common complication in both type 1 and type 2 diabetes. The prevalence varies
among different studies, depending on the diagnostic criteria employed, the sensitivity of
the methods used, patients' age, etc. Some authors have found this complication in 7.5%
of all patients at the time of diagnosis of diabetes and in up to 45% of all patients who have
had diabetes for more than 25 years (2).
One epidemiological study in Spain, using questionnaires about signs and symptoms, found
a prevalence of 22.7% in diabetics; DN was more prevalent in patients with type 2 diabetes
(24.1%) than in those with type 1 diabetes (12.9%) (3).

The primary nonmodifiable risk factors associated with DN are age and time of diabetes
evolution. The above mentioned epidemiological study in Spain found a prevalence of DN
of 44.2% among patients with more than 30 years' evolution (3).
The modifiable risk factor with the strongest association to DN is hyperglycemia. In fact,
there is evidence that strict control of glycemia can prevent DN and slow its evolution.
The Diabetes Control and Complication Trial (4), carried out in type 1 diabetics, showed
that intensified insulin treatment reduced the incidence of clinical DN by 60 %. Likewise,
the United Kingdom Prospective Diabetes Study (5), carried out in type 2 diabetics, showed
that metabolic control reduced the risk of DN.
On the other hand, data from the EURODIAB study show that, in addition to control of
glycemia, other factors such as obesity, hypertriglyceridemia, smoking, and high blood
pressure also independently favor the development of this complication (6).

                                                     Pág. 11

Although there is a clear relation between the presence, duration, and intensity of
hyperglycemia and DN, the physiological basis of DN remains uncertain. The two most
widely accepted theories relate the pathogenesis of DN to metabolic effects of chronic
hyperglycemia and the effects of ischemia in the peripheral nerves. Neurotrophic and
immune-related factors also seem to play a role in DN. Thus, the pathogenesis of DN is
considered to be multifactorial and the diverse mechanisms proposed interact with one
another and with factors related to genetic predisposition.
As the axons of the peripheral nerves are very long in comparison to their diameters, their
motor, sensory, and autonomic components (especially in the distal portion) depend greatly
on the endoneurial microenvironment for blood supply, oxygenation, nutrition, and
elimination of toxic metabolic products.
In DN, segmental demyelination and axonal degeneration are observed, although the main
alteration is still to be determined.
Rather than exhaustively review all the mechanisms of pathogenesis that have been
proposed, we will give a brief overview of the main mechanisms.

                                                  Pág. 12
Metabolic factors

The metabolic hypothesis asserts that hyperglycemia causes various metabolic disorders,
such as increased tissue concentrations of sorbitol and fructose, decreased myoinositol
and taurine concentrations, reduced Na/K adenosine triphosphatase (ATPase) activity,
nonenzymatic glycosylation of proteins, altered metabolism of fatty acids, and axonal
transport anomalies. These factors might be responsible for functional and structural
alterations in the nerve fibers (7).

Polyol pathway abnormalities: The hyperglycemic medium causes an activation of the
polyol pathway and, in a reaction catalyzed by the enzymes aldose reductase and sorbitol
dehydrogenase, leads to the conversion of glucose to sorbitol and fructose. The
accumulation of sorbitol decreases the intracellular concentrations of myoinositol and
taurine, which in turn decreases Na/K ATPase, thus contributing to structural and functional

Alterations in the metabolism of lipids: diabetes causes alterations in the metabolism of
the essential fatty acids, such as a reduction in gamma-linolenic acid, a precursor of
arachidonic acid, which is in turn necessary for the production of various vasoactive
substances such as prostacyclin. Moreover, the metabolites of gamma-linolenic acid play
a role in the structure of the nerve membranes, blood flow, and nerve conduction.

Oxidative aggression: free radical activity is increased in diabetes. Furthermore, the
mechanisms of antioxidant defense are affected, with a reduction in antioxidants like
reduced glutathione, catalase, ascorbic acid, and _-tocopherol (7).

End-products of advanced glycosylation: in prolonged hyperglycemia, a nonenzymatic
glycosylation of proteins causes structural changes in the components of the extracellular
matrix. These changes can lead to functional alterations in the nerves and blood vessels
(8). Moreover, the end-products of advanced glycosylation can also suppress nitric acid
and thus attenuate endothelium-mediated vasodilatation (9).

Neurotrophic factors: neurotrophins are proteins that promote the maintenance and survival
of neurons. Evidence suggests that insufficiency of neurotrophic factors like nerve growth
factor (NGF) and neurotrophin 3 (NT-3) may be involved in the pathogenesis of diabetic
polyneuropathy (7).

                                                  Pág. 13
Vascular factors

Metabolic alterations related to hyperglycemia cause alterations in the microvascularization
that are responsible for ischemic anomalies in nerve fibers. Reduced blood flow, increased
vascular resistance, and decreased endoneurial oxygen tension have been demonstrated
Some authors have reported capillary wall thickening and obstruction of the arterioles that
supply the peripheral nerves. Alterations in the endothelial basement membrane of the
capillaries with enlargement of the perivascular space have also been documented (12-

                                                   Pág. 14

1. Boulton AJ, Gries FA, Jervell JA. Guidelines for the diagnosis and outpatient management
of diabetic peripheral neuropathy. Diabet Med 1998; 15: 508-14.

2. Young MJ, Boulton AJ, McLeod AF, Williams DRR, Sonksen PH. A multricentre study of
the prevalence of diabetic peripheral neuropathy in the United Kingdom hospital clinic
population. Diabetologia 1993; 36: 150-4.

3. Cabezas-Cerrato J, for the Neurophaty Spanish Study Group of the Spanish Diabetes
Society (SDS). The prevalence of clinical diabetic polyneuropathy in Spain: a study in
primary care and hospital clinic groups. Diabetologia 1998; 41: 1263-9.

4. The Diabetes Control and Complications Trial Research Group (DCCT). The effect of
intensive treatment of diabetes on the development and progression of long term
complications in the diabetes control in insulin dependent diabetes mellitus. N Engl J Med
1993; 329: 977-86.

5. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with
sulphonylureas or insulin compared with conventional treatment and risk of complications
in patients with type 2 diabetes. Lancet 1998; 352: 837-53.

6. Tesfaye S, Chaturvedi N, Eaton S, Ward JD, Manes C, Ionescu-Tirgoviste C, et al.
EURODIAB Prospective Complications Study Group. Vascular risk factors and diabetic
neuropathy. N Eng J Med. 2005; 352: 341-50.

7. Freeman R. The Nervous System and Diabetes. In Joslin's Diabetes Mellitus, 14th ed.
Kahn CR. Philadelphia: Lippincott Williams & Wilkins; 2005. 951-67.

8. Brownlee M. Glycation products and the pathogenesis of diabetic complications. Diabetes
Care 1992; 15: 1835-43.

9. Bucala R, Tracey KJ, Cerami A. Advanced glycosylation products quench nitric oxide
and mediate defective endothelium-dependent vasodilatation in experimental diabetes. J
Clin Invest 1991; 87: 432-8.

10. Tuck RR, Schmelzer JD; Low PA. Endoneurial blood flow and oxygen tension in the
sciatic nerves of rats with experimental diabetic neuropathy. Brain 1984; 107: 935-50.

                                                  Pág. 15
11. Cameron NE, Cotter MA, Low PA. Nerve blood flow in early experimental diabetes in
rats: relation to conduction deficits. Am J Physiol 1991; 261: E1-E8.

12. Yasuda H, Dyck PJ. Abnormalities of endoneurial microvessels and sural nerve pathology
in diabtic neuropathy. Neurology 1987; 37: 20-8.

13. Malik RA, Veves A, Masson EA, Sharma K, Ah-See AK, Schady W, et al. Endoneurial
capillary abnormalities in mild human diabetic neuropathy. J Neurol Neurosurg Psychiatry
1992; 55: 557-61.

                                                 Pág. 16

Michael E. Edmonds MD FRCP
Consultant Physician, Diabetes Foot Clinic.
King’s College Hospital. London, UK.

“Amputations with the pure neuropaths are very rare, hardly at all.”
For the first bilingual edition of
it was essential to find an international, reputable figure on
the issue of the diabetic foot. The choice was easy, since
one of the characters with more world-wide charisma is
Michael E. Edmonds from King's College Hospital, who has
a myriad of publications and has conducted lectures on the
subject throughout the world.
We contacted him to arrange an interview and he graciously
received us in his Diabetic Foot Clinic in King's College

Could you explain what kind of professionals make up the Foot Clinic?

This unit is made up of various health professionals. It is a multidisciplinary team which comprises
the diabetologist, the podiatrist, nurses, orthotist and the surgeons. The surgeons are the vascular
surgeon and the orthopedic surgeons. We hold joint clinics and joint conferences. One joint
conference is the vascular conference where we are also joint by the interventional radiologists
where we look at the angiograms of the patients and decide whether they should have interventional
treatment or angioplasty, or bypass. So that is the overall team but it is also supported by the
receptionists, the secretary and we also have close links with the microbiologists and the
biochemists, and also a radiologist who is interested in musculoskeletal diseases where we
coordinate interpretations of CT and MRI scans, and x- rays. So there is a core team of people
working here, i.e. a core team of podiatrists, diabetologists and nurses working day-to-day, 9 to
5, receiving patients and all the other people involved in the team but come either for special joint
clinics, or for emergencies. But they are not here all the time.

How many patients with ulcerations and Charcot foot does your unit attend upon each year?

I can best put it by the fact that we see probably a hundred patients a week and we have 6000
patient attendances per year. We probably have about a hundred Charcot patients whom we see
regularly and probably 600 patients with ulcerations. Also in the clinic are patients with painful
neuropathy, people with diabetic pain from neuropathy where we treat their pain. I would say that
is a group of about 50 painful neuropathic patients, 100 Charcot patients and the rest are 600
ulcer patients approximately.

                                                        Pág. 17

What is the amputation rate in the King's College Hospital?
We usually have out of all these patients 3 or 5 amputations per year. Now, it depends on how you
express that. From the point of view of how many patients you see, or how many patients are at
risk. We have a problem with this because we get a lot of referrals from outside the area so it is
difficult to relate to our initial population, our basic population because we have people who come
a long way. In a fraction people talk about the numerator and denominator, i.e. how many amputations
by how many patients. I prefer to express it at the moment in absolute terms that we have three
to five amputations per year out of all those patients. We worked it out once from the point of view
of diabetic patients at risk, I think it was 0.02. These patients at risk have ischemia and they may
also have neuropathy so we would call them neuroischemia. Amputations with the pure neuropaths
are very rare, hardly at all. I must point out that when I talk about amputations I am talking about
major amputations, cutting the leg off. Neuropathic amputations happen one every ten years or
even less than that. It is the ischemia ones which is three to five a year.

Are there any other units like yours in Great Britain?

There is a clinic in Manchester with professor Boulton, there is a clinic in Edinburgh with Matthew
Young and Jeffcoate in Nottingham and there is another clinic in Ipswich, , with Gerry Rayman. He
has a district hospital as opposed to a teaching hospital. There are different degrees of clinics
because there must be diabetic foot patients all over the country. So there are clinics which are
probably not really multidisciplinary, they are run by podiatrists and they can get some help from
other professionals but they are not truly multidisciplinary in the sense of having a core team
there all the time. I would say there is also one in St. Mary's, and our colleges on this road in
Thomson's Hospital. They have a foot clinic but it is mainly podiatry. The podiatry is all over the
country treating the pain, I think the crucial thing is the support to run them.

“ We are particularly interested in the Charcot foot. ”

Do you apply any kind of prevention scheme?

The prevention is mainly now in the community around us. There are foot protection teams working
to screen patients for neuropathy and ischemia and they are putting them in foot protection
programs. They work mainly outside the Hospital. Obviously, we practice secondary prevention
in the sense that if somebody has come to us with an ulcer we try and prevent them from getting
an ulcer again. But I have to say that our main emphasis is on treating the foot in trouble, i.e. the
ulcerated and the Charcot foot. The protection in Britain is mainly carried out in the community
in clinics around a central clinic

                                                        Pág. 18

What projects are getting under the way?
We are particularly interested in the Charcot foot and we are investigating why Charcot patients
develop severe deformity and how we can treat the Charcot foot at an early stage to prevent it
from going into deformity, and we are trying to find out how we can recognize the early parts with
special imaging and biochemical tests. We work very closely with the vascular surgeons and
interventional radiologists so we have an active fast-track program for treating ischemia patients
very early. One of our underlying principles is to diagnose early and treat early because we believe
that the diabetic foot develops very rapidly and reaches a severe stage very quickly almost getting
to the point of no return. Also, one of the problems with neuropathy and ischemia is that classical
signs and symptoms are not apparent, so you have to be a detective and diagnose very early with
subtle signs. So it is early diagnosis and early treatment before they get to the stage of no return
and intervening at that stage. That is our general principle. Essentially, what we are trying to do
is diagnose early, treat everything early so we don't get to the stage where patients have severe
destruction and need an amputation. Our main research is now on Charcot foot.

                                                                                        Thank you.

                                                               Diabetic Foot Care. King’s Hospital

                                                       Pág. 19   Pág. 20
Case report

Necrosis of the third toe and metarsophalangeal joint
septic arthritis of the first toe
                   (1)                      (2)
Dr. Josep Royo           D.P Jordi Viadé
Chief of Vascular and Endovascular surgery.
Podiatrist. Department of Endocrinology and Nutrition.
Hospital Mútua de Terrassa (Barcelona)
A 63-year-old man was admitted for wet
gangrene of the third toe of the right foot with
lymphangitis of the dorsal foot.

                                                                                Figure 1.
 Physical examination

 Superficial and deep sensations were absent (no perception in the pin-prick, needle,
 monofilament, and tuning-fork tests).
 No pulses were felt in the dorsalis pedis and posterior tibial arteries. The right
 popliteal pulse was weak (bilateral distal obliteration).
 The third toe of the right foot was blackened, with fetid-purulent suppuration, and
 an erythematous band that extended toward the dorsal foot.


 _     Type 2 diabetes mellitus for at least 27 years, currently treated with insulin.
 _     Ex-smoker for 27 years.
 _     Hypertensive.
 _     Dyslipemic.
 _     Coronary artery triple by-pass in 1995.
 _     Charcot arthropathy in the left tarsus, without inflammatory activity, treated
       with plantar support.

                                             Pág. 21
Case report

Magnetic resonance angiography found moderate stenosis of the second portion of the
left popliteal artery, obstruction of both anterior tibial arteries, diffuse and severe bilateral
involvement with multiple significant stenoses in the posterior tibial and peroneal arteries,
and reestablished patency of the left anterior tibial artery.
Given the severity of the infection, we initiated intravenous antibiotic treatment (piperacillin
4g and tazobactam 500mg every 8 h) and were able to confine the infection to the toe.
On the third day, the signs of lymphangitis disappeared and we performed a by-pass with
an inverted saphena vein from the superficial femoral artery to the right anterior tibial
artery as well as the amputation of the necrotic third toe.

                                    Figure 2.                                          Figure 3.

After an uneventful postoperative period, the patient was discharged with antibiotic
treatment (oral amoxicillin 500 mg and clavulanic acid 125 mg every 8 hours) and topical
treatment (washing and povidone-iodine).
After three months, he presented with small ulceration with a granuloma (one-centimeter
trajectory and negative probing test) at the level of an osseous prominence in the left
tarsus due to Charcot neuroarthropathy, which was treated by a 1.2-cm felt pad, a bandage
with silver salts, and empirical antibiotic treatment (oral amoxicillin 875 mg and clavulanic
acid 125 mg every 8 hours).
One month later, the lesion had improved considerably but without complete regeneration
of the epithelium; the patient continued to apply topical treatment, felt pads, and special
After six months' treatment, the ulcer had not cicatrized and exostectomy to reduce the
osseous protrusion was considered.

                                                       Pág. 22
Case report
Meanwhile, as a consequence of slight rubbing against footwear, an ulcer measuring 1.5
x 1.5 cm appeared in the lateral aspect of the first toe of the right foot; this lesion progressed
until the patient became alarmed and contacted the healthcare team. Probing was positive
and plain-film radiography showed a small erosion in the lateral aspect of the
metatarsophalangeal joint of the first toe of the right foot, with abundant discharge.

                                     Figure 4.                                          Figure 5.

The discharge was cultured and abundant colonies of Morganella morganii were isolated;
these were sensitive to cotrimoxazole, so the patient was administered oral
sulfamethoxazole 800 mg and trimethoprim 160 mg every 12 hours.

The wound was treated daily and the lesion slowly evolved; however, the discharge and
the inflammatory signs did not resolve. A new plain-film radiograph showed a clear image
compatible with septic arthritis, so we opted for surgical treatment.

                                       Figure 6.                                          Figure 7.

                                                        Pág. 23
Case report
On an outpatient basis, using local anesthesia (8 cc 2% mevipicaine), we made a lateral
incision (3 cm) until we reached the metatarsophalangeal joint of the first toe to scrape
away the necrotic tissue and eliminate sequestered bone. We closed the wound with
approximation sutures and left a Penrose drainage tube in place, which was then withdrawn
after 48 hours.
In the same surgical intervention, we performed an exostectomy on the protrusion that
was causing the ulcer in the left foot. (Charcot).

The patient was administered oral antibiotics (875 mg amoxicillin and 125 mg clavulanic
acid every 8 hours; and 500 mg ciprofloxacin every 12 hours) for 6 weeks.

                                  Figure 8.                                      Figure 9.

                                                Pág. 24
Case report

The surgical wounds in both feet were antisepticised with povidone-iodine.
The patient was definitively discharged two months after the intervention.
To aid walking, plantar supports accompanying 16-width lycra footwear were constructed.
The materials used in the plantar supports were:

                                 Figure 10.                                   Figure 11.

1.    High density and high Shore thermoadaptable polyethylenes for better biodynamic
2.    Medium density and medium Shore thermoadaptable ethyl-vinyl acetate (EVA) to
      absorb mid-range pressures and moderate biodynamic control.
3.    Medium Shore thermostable polyurethane for high absorption of hyperpressures
      and lining of the plantar support.

                                              Pág. 25   Pág. 26
Educating patients in the care of diabetic foot (I)
Maite Valverde Torreguitart, R.N
Educational nurse in the Department of Endocrinology and Nutrition.
Hospital Mútua de Terrassa (Barcelona)

Diabetes mellitus is a chronic disease that affects 5% of the population worldwide; in Spain,
the prevalence of type 2 diabetes is between 4.8 and 18.7%.1 Chronic micro- and macro-
vascular complications characteristically appear in the course of diabetes; these
complications are the most significant cause of morbimortality in diabetic patients and lead
to a significant reduction in the quality of life. Moreover, these complications account for
a high proportion of healthcare costs in diabetics.(2) The complications of diabetes that
occasion the greatest expenditures are those related to diabetic foot, which take up from
15% to 25% of the resources dedicated to the care of patients with diabetes. Between 15%
and 20% of all diabetics develop foot ulcers. Over 50% of all non-traumatic amputations
are done in diabetic patients.
Amputation is always preceded by an ulcer. Many studies have shown that appropriate
education and early treatment can prevent up to 80% of these amputations.(3)
Reducing risky behavior is fundamental in preventing amputations.

                                             Figure 1. Workshop for healthcare professionals.

                                                   Pág. 27

Therapeutic education
The first step in prevention is education. Therapeutic education forms an integral part of
treatment and is essential in quality treatment (Diabetes Education Study Group - The
European Association for the Study of Diabetes). Nevertheless, education yields different
results in different individuals because learning is influenced by factors like:

-     Knowledge
-     Personal factors: age, education, beliefs, experiences, psychological factors, and
-     Environmental factors: family, friends, resources, work, and others.

                                               Figure 2. D.E.S.G workgroup.

Traditionally, patient education has been prescriptive; healthcare professionals define the
goals because they know what patients must do and they have the obligation to motivate
patients to follow the prescribed recommendations and thus to change their behavior.
However, through the years, these models have proven to be ineffective in the control of
diabetes. A different approach to therapeutic education, empowerment, has yielded better
results. This is a patient-centered approach, i.e., professionals work with the patient rather
than for the patient, that enables the patient to acquire the control of and responsibility for
the daily management of his or her diabetes, taking into account the patient's goals, priorties,
and lifestyle. Patients need to be as well informed as possible and take an active part in
their own care; professionals need to help patients make informed decisions to achieve
their goals, overcome educational barriers, and adopt the most appropriate behavior for
their own care.

                                                      Pág. 28

Empowerment is based on three fundamental aspects:
Preferences. Every day, patients must make decisions about the management of their
diabetes; these decisions have repercussions on their outcome.
Control. Once patients have acquired the knowledge and skills necessary to manage their
disease, they have the freedom to choose which recommendations to follow.
Consequences. Despite the consequences of their decisions, they are responsible for
controlling their diabetes in the way they consider best within their cultural context.

The idea is to use motivational and behavioral techniques and strategies to get people to
adopt healthy habits and lifestyles.

                                   Figure 3. Claw toe affecting the second toe in a patient
                                   with sensory deficits.

                                                 Pág. 29
Aspects that need to be avaluated before educational intervention

The degree of risk

Risk is assessed through:

The clinical history. Ask about risk factors like tobacco and alcohol use, prior ulcers, and
symptoms of neuropathy and vasculopathy.
Evaluating metabolic control. Dyslipemia, arterial hypertension, and kidney function.

Foot examination. Inspect the condition of the skin on both the dorsal aspect and the sole and
heal, as well as the condition of the nails, space between the toes, and possible deformities like
hallux valgus, claw toes, Charcot foot, etc.
Evaluating peripheral vasculopathy. Palpate the pulses and obtain the Doppler index in the feet
and tibia.

Evaluating neuropathy. Examine vibration sensitivity using a 12Hz tuning fork and a Semmens-
Weinstein 10g monofilament.
Loss of sensation due to neuropathy is the main cause of foot ulcers in diabetics. Loss of
sensation occurs slowly, so patients are unaware of it.

The International Consensus on the Diabetic Foot defines four risk groups: (7)

Group 0: Patients without sensory neuropathy.
Group 1: Patients with sensory neuropathy.
Group 2: Patients with sensory neuropathy and signs of peripheral vascular disease, deformities,
or both.
Group 3. Patients with a history of prior ulcer or amputation.

Risk must be assessed at least once a year. Patients with grade 1 risk need to be evaluated
every 6 months, those with grade 2 risk every 3 months, and those with grade 3 risk every 1-3

                                                          Pág. 30

Degree of autonomy
An autonomous person can carry out all self-care activities; therefore, it is important to
evaluate patients' limitations that might hinder their ability to perform these activities:

Vision. If patients have very limited or no vision, they cannot inspect their feet, no matter
how much theory they have learned.
Visual acuity can be assessed by the ability to read a text with 0.6 mm letters at a distance
of 30 cm, which corresponds to the fine print seen in newspapers.

Articular flexibility. To examine one's feet, one must adopt a certain position through the
following combination of movements: flexion of the spinal column, flexion and rotation of
the hip, and flexion and rotation of the knee. Those capable of these movements must
achieve a distance no greater than 65 cm between their eyes and the metatarsal zone and
no greater than 15 cm between the heel and buttocks. This distance is easily measured by
two bars measuring 65 cm and 15 cm, respectively.
Patients with limited mobility but good vision can use a large mirror placed on the floor to
inspect their feet.

Learning ability. Patients with limited intellect, depression, or cognitive deterioration must
be identified, as these characteristics limit the autonomy necessary for self-care.

Whenever the degree of autonomy is limited, it is essential to seek help from family members
or caretakers. (6)

   Figure 4. Area of plantar hyperkeratosis with a high
   risk of developing ulcers.

                                                    Pág. 31

Family or social support. Socioeconomic level.
It is fundamental to know the patient's personal and social status because low socioeconomic
level is associated to a greater incidence of foot lesions, and this is even worse when the
patient has no family or social support.

After evaluating the patient's risk, educational goals should be adapted to the risk profile;
low-risk patients' needs are different from those of high-risk patients. Low-risk patients
must acquire correct habits related to hygiene and hydration, while high-risk patients must
learn all the recommendations for preventing all lesions.

                                                   Pág. 32

1. «La Diabetes Mellitus en España: Mortalidad, prevalencia, incidencia, costes económicos y
   desigualdades». Gaz Sanit. 2006;supl 1:15-24.

2. «El coste de la Diabetes en España: Estudio CODE-2». Gaz Sanit. 2002;16:511-20.

3. «The global burden of diabetic foot disease». Lancet. 2005;366:1719-24.

4. «Empowerment and Self-Management of Diabetes». Clinical Diabetes. 2004;22:123-7.

5. International Working Group on the Diabetic Foot. International Consensus on the
   diabetic foot. And IDF. 2003.

6. «Standards of Medical Care in Diabetes». Diabetes Care. 2008 (Jan).

7. Viadé J (dir.). Pie Diabético. Guía práctica para la prevención, evaluación y tratamiento.
   Editorial Médica Panamericana. 2006.

8. «The summary of diabetes self-care activities measure: results from 7 studies and a revised
  scale». Diabetes Care. 2000;23:943-50.


10. «Are Type 2 diabetic patients offered adequate foot care? The role of physician and patient
   characteristics». J Diabetes Complications. 2005;19:319-27.

                                                       Pág. 33
 Featured Photograph

Diabetic Patient with pseudomonas infection

                 Pág. 34

Xu L., et al. Bacterial load predicts healing rate in neuropathic diabetic foot ulcers.
Diabetes Care 2007; 30(2): 378-380.

Conceptually, a high bacterial load can delay lesion healing by causing an environment not
conducive to healing. The authors carried out this study in Australia, obtaining wound fluid
from 32 patients with grade 0 or 1 and stage A or B neuropathic lesions classified according
to the Texas grading system. The bacterial load was determined by counting the number of
colony-forming units (CFUs). The authors found a strong inverse correlation between the
healing rate and the number of CFUs (r=0.46, p = 0.008). In other words, the greater the bacterial
load, the smaller the percentage of healing. The authors emphasize the harmful effects of the
bacterial load on wound healing and comment on the need to carry out studies using antibiotics
or other treatments to modulate the bacterial load.

Lavery LA., et al. Prediction of healing for postoperative diabetic foot wounds based on early
wound area progression. Diabetes Care 2008; 31: 26-29.

This study evaluated the probability of postoperative wound healing after partial amputation
in the diabetic foot on the basis of the percentage of reduction in wound area after one week
and after four weeks in patients with extensive chronic nonischemic diabetic foot lesions. The
authors took data from a random clinical trial evaluating negative-pressure wound therapy.
Wounds that reached ≥15% wound area reduction at 1 week or ≥60% at 4 weeks had a 68%
and 77% probability of healing, respectively; in comparison, the probability of healing if these
wound area reductions were not achieved was 31% and 30%, respectively. The authors suggest
that clinicians could calculate the percentage of wound area reduction at 1 week to predict
wound healing. This study adds weight to another published earlier this year that found that
the rate of initial reduction of an ulcer in a diabetic foot is a good predictor of complete wound
healing. It would be interesting to systematically review the different studies published about
these clinical predictors.

Gardner S., et al. Wound bioburden and infection-related complications in diabetic foot ulcers.
Biological research for nursing 2008; 10(1): 44-53.
The identification and diagnosis of ulcer infections in diabetic foot remain a complex problem.
This article provides a broad review of the concepts of contamination, wound colonization,
microbial load, and infection, as well as of complications related to infection. The authors
propose a conceptual framework about the relation between bacterial load in the wound and
infection-related complications. Considering diabetic foot ulcers without clinical signs of local
infection as a starting point, they describe two possible scenarios: wounds with low microbial
load (low microbial load, few microbial species, and the absence of S. aureus and anaerobic

                                                     Pág. 35
bacteria) and wounds with high microbial load (high microbial load and/or elevated diversity
in the microbial population and/or the presence of S. aureus or anaerobic bacteria). In the
second scenario, they consider the appearance of osteomyelitis with obvious signs of local
and systemic infection and treatment with antimicrobial agents that will lead to a final scenario
of either wound closure or amputation.

Lavery LA, et al. What are the most effective interventions in preventing diabetic foot ulcers?
Int Wound J 2008; 5:425-433.

The authors studied 87 patients with 103 existing or recently healed (< 4 weeks) diabetic foot
ulcers. They evaluated seven variables that were previously associated to the development of
foot ulcers and constructed a model of causation. Three investigators individually reviewed
and interpreted the information about the ulcers to determine its cause in each patient. The
results of this study suggest that there are four main ways that ulcers develop in the diabetic
foot: a) neuropathy, deformity, calluses, and elevated plantar pressure; b) peripheral vascular
disease; c) penetrating trauma; and d) inadequate footwear. The results suggest that there are
a finite number of key factors that, if identified and managed with appropriate interventional
strategies, can reduce the risk of a cascade of events that lead to ulceration and posterior
amputation. These factors should be kept in mind, together with the treatment that has proven
efficacious in each of these situations. In this way, we can approach the objectives of St
Vincent's declaration of reducing the incidence of diabetes-related amputations by 50%.

Jude EB., et al. Prospective randomized controlled study of hydrofiber® dressing containing
ionic silver or calcium alginate dressings in non-ischaemic diabetic foot ulcers. Diabetic
Medicine 2007; 24:280-288.

The authors carried out a randomized clinical trial comparing hydrofiber® dressing containing
ionic silver versus calcium alginate dressings in patients with nonischemic diabetic foot ulcers.
This was a multicenter study carried out in centers in England, France, Germany, and Sweden.
Random stratification was accomplished by closed envelopes and the data were analyzed
using an intention-to-treat approach.
The study protocol allowed the use of unloading or antibiotics when clinically indicated. A total
of 134 patients (67 in each group) were studied. No significant differences between groups
were observed in baseline values of variables. The main outcome variable was the speed of
healing. Secondary outcomes were the mean time to healing in days and the proportion of
complete healing during the study period. No significant differences in the speed of healing
were observed. However, the authors found significant differences in the proportion of ulcers
between the two groups (RAR, 9%; 95% CI, 6%-23.9%), (OR, 1.58; 95% CI 0.73-3.43). In other
words, complete healing was 9% greater in the group with the hydrofiber® dressing containing

                                                    Pág. 36
ionic silver (Aquacel® Ag). Likewise, we can say that a patient treated with this antimicrobial
dressing has a 1.6-fold greater likelihood of his ulcer healing than if he were treated with a
calcium alginate dressing. The authors conclude that the hydrofiber® dressing containing ionic
silver can play an important role in the evidence-based protocol for the care of diabetic foot.
Finally, they generate an interesting hypothesis about the potential synergic effect of topical
silver and systemic antibiotic therapy.

Events & Courses

Leipziger WundKongress - 'Der diabetische Fuß'
Lepzig. Alemania
A partir del 10 Noviembre 2008
Info: Sekretariat der Klinik für Gefäßchirurgie
Telefono (0341) 864 2251

2nd International Conference on Advanced Technologies and Treatments for Diabetes.
Atenas. Grecia
25 al 28 de Febrero 2009

Diabetic Foot Global Conference. 'DFCon 09'
The Premier International Diabetic Foot Conference
Los Angeles LA. USA
19 al 21 de Marzo 2009

XI Congreso Latinoamericano de Vasculopatías y Pie Diabético
Buenos Aires. Argentina
15 al 17 de Mayo 2009
Facultad de Medicina. Univ. Buenos Aires.
Telefax (5411) 48057651

                                                  Pág. 37
First Announcement of Asia Pacific Diabetic Limb Problems Meeting
18-20th September, 2009, Beijing, China
Meeting secretariat:
Fax: 86-10-64852704

Management Diabetic Foot/Wound Healing
New Orleans. LA. USA
10 al 13 de Septiembre 2009

8th Scientific Meeting of the Diabetic Foot Study Group (DFSG) of the EASD 2009.
September Bled SLOVENIA

The 20th World Diabetes Congreso
Sunday 18 to Thursday 22 October 2009 at:
Palais des Congrès de Montréal
(Montréal Convention Centre)
1001, place Jean-Paul Riopelle
Montréal, Québec H2Z 1H2

6th International Symposium on the Diabetic Foot.
Noordwijkerout. Holanda
11 al 14 de Mayo 2011

                                    Pág. 38

- Pie Diabético. Guía práctica para la prevención, evaluación y tratamiento.
J. Viadé. Editorial médica Panamericana.(2006) ISBN:84-7903-405-X.

- The Foot in Diabetes. Andrew Boulton , Peter Cavanagh , Gerry Rayman.
Wiley; 4 edition (2006).ISBN-10: 0470015047.

- The Diabetic Foot: Medical and Surgical Management
Aristidis Veves, Frank W. LoGerfo, John M. Giurini. (2002). ISBN 0896039250

- El Pie Diabético. Aragón, F.J. / Ortiz Remacha, P.P. Elservier-Masson (2001).
ISBN: 844581027-8


The Diabetic Foot Journal



Sociedad Española de Diabetes

International Working Group on the Diabetic Foot

The International Diabetes Federation

Sociedad Española de Cirugía Vascular

                                             Pág. 39

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