Contemporary Management of the Diabetic Foot [1 ed.] 9789352500963, 9789350909485

This book Contemporary Management of Diabetic Foot provides comprehensive information on complete care of diabetic foot.

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CONTEMPORARY MANAGEMENT OF THE

DIABETIC FOOT

Disclaimer The views and opinions expressed in this book are solely those of the original contributors and do not necessarily represent those of editor of the book.

CONTEMPORARY MANAGEMENT OF THE

DIABETIC FOOT

Editor

Sharad Pendsey MD

Consultant Diabetologist Director Diabetes Clinic and Research Centre Nagpur, Maharashtra, India

Forewords

Marvin E Levin Karel Bakker

®

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi • London • Philadelphia • Panama

®

Jaypee Brothers Medical Publishers (P) Ltd. Headquarters Jaypee Brothers Medical Publishers (P) Ltd. 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 Email: [email protected] Overseas Offices J.P. Medical Ltd. 83, Victoria Street, London SW1H 0HW (UK) Phone: +44-2031708910 Fax: +02-03-0086180 Email: [email protected] Jaypee Brothers Medical Publishers (P) Ltd. 17/1-B, Babar Road, Block-B Shaymali, Mohammadpur Dhaka-1207, Bangladesh Mobile: +08801912003485 Email: [email protected]

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Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2014, Jaypee Brothers Medical Publishers All rights reserved. No part of this book may be reproduced in any form or by any means without the prior permission of the publisher. Inquiries for bulk sales may be solicited at: [email protected] This book has been published in good faith that the contents provided by the contributors contained herein are original, and is intended for educational purposes only. While every effort is made to ensure accuracy of information, the publisher and the editor specifically disclaim any damage, liability, or loss incurred, directly or indirectly, from the use or application of any of the contents of this work. If not specifically stated, all figures and tables are courtesy of the editor. Where appropriate, the readers should consult with a specialist or contact the manufacturer of the drug or device.

Contemporary Management of the Diabetic Foot First Edition: 2014 ISBN 978-93-5090-948-5 Printed at

Dedicated to

(Late) Professor (Dr) Paul Brand (1914-2003) The dean in the field of leprosy as well as diabetic foot Ever since I was asked to shoulder the responsibility of editing of Contemporary Management of the Diabetic Foot, I had in mind to dedicate the book in memory of (Late) Paul Brand. I always believed that we owe him a lot for all our understanding of the neuropathic ulcers in diabetes. He made us understand that the entire problem of neuropathic feet is really one of mechanics and not of medicine. Just a few months before his death, he contributed perhaps the last publication “Thermal Changes in Feet” in the book Diabetic Foot: A Clinical Atlas, authored by me. I salute him for his pioneer work. Dr Paul Brand was born in the mountains of India to missionary parents in South India. In 1936, he went to England and completed his surgical training. During the World War II, he first experienced the management of patients with traumatic wounds in the hands and feet. In 1946, he returned to India and became Professor of Orthopedic Surgery, Christian Medical College and Hospital, Vellore, Tamil Nadu, India. Dr Robert Cochrane at Vellore, challenged Dr Paul Brand to use his skills to find out why people with leprosy developed ulcers and deformities of hands and feet and try to find out an effective treatment. Through his research, he changed the world’s perception and treatments of neuropathic ulcers in leprosy patients. In 1965, he migrated to the United States of America and served as Professor of Surgery and Orthopedics at Carville, Louisiana State University for twenty years. It was while working in Carville, USA, that he realized that much of what he had already described in leprosy could be extrapolated to patients with diabetes, as he was seeing increasing numbers of diabetic patients in the foot clinic. He realized that even in the USA, in the 1960s, the management of foot ulceration in diabetes was hindered by some of the same misconceptions that he had faced about leprosy in the 1940s. Ulcers in diabetics were still called “diabetic ulcers” rather than neuropathic ulcers. They were looked upon by surgeons as being a reason for amputation, because they were thought to be unlikely to heal and go onto gangrene of the foot. As a consequence of his research, the recognition of the relationship between insensitivity, repetitive pressures and skin breakdown, helped us in our understanding of the etiopathogenesis of neuropathic foot lesions in diabetes. The development of total contact cast, modified footwear, insoles, metatarsal bars, and plantar metatarsal pads to treat such lesions formed the basis of management of diabetic neuropathic foot ulcers with various offloading devices. A gifted speaker and writer, he received many honors and awards in recognition for his outstanding achievements. He was hunterian Professor, Royal College of Surgeons (1952); he received the Albert Lasker Award (1960) for outstanding leadership and service in the field of rehabilitation; in 1961, he was honored by Queen Elizabeth II with Commander of the British Empire (CBE) for promotion of good relations between the Republic of India and Great Britain. He received the Damian-Dutton Award (1977) for his contributions in the prevention of disabilities due to leprosy. He authored 100 scientific papers and seven books. He was married to his classmate Dr Margaret, an Ophthalmologist of great repute. He was a proud father of 6 and grandfather of 12. He died just days away from his 89th birthday in 2003. He lived his life as a representative of the God, he worshiped. In each person, he saw image of God.

Contributors Andrew JM Boulton MD DSc (Hon) FRCP

Hermelinda C Pedrosa MD

Professor of Medicine University of Manchester Consultant Physician Manchester Royal Infirmary Manchester, UK Visiting Professor University of Miami, Florida, USA President, European Association for the Study of Diabetes

Endocrinologist Chairperson Train the Foot Trainers Course South and Central America President Sociedade Brasileira de Diabetes – DF Principal Investigator Polo de Pesquisa FEPECS-HRT Setor de Endocrinologia e Diabetes Hospital Regional de Taguatinga

Aniket Pradhan

Jennifer Pappalardo DPM

Senior Fellow (DNB) Vascular and Endovascular Surgery

Jain Institute of Vascular Sciences Bhagwan Mahaveer Jain Hospital Bengaluru, Karnataka, India

Clinical Instructor/Fellow Southern Arizona Limb Salvage Alliance (SALSA) University of Arizona College of Medicine Arizona, USA

Arun Bal MBBS MS PhD

Kristien Van Acker MD PhD

Consultant Diabetic Foot Surgeon Raheja Hospital, Hinduja Hospital Mumbai, Maharashtra, India Visiting Professor Amrita Vishwa Vidyapeetham Kochi, Kerala, India

David G Armstrong DPM MD PhD Professor of Surgery and Director Southern Arizona Limb Salvage Alliance (SALSA) University of Arizona College of Medicine Arizona, USA

Fran Game FRCP Consultant Diabetologist and Honorary Associate Professor Derby Hospitals NHS Foundation Trust Derby, UK

Diabetologist Consultant for Diabetes Tropical Institute of Antwerp Diabetes Service in Hospital, Rumst Centre de Santé des Fagnes Chimay, Belgium Vice President Diabetic Foot Program IWGDF/IDF

Lee J Sanders DPM Diplomate American Board of Podiatric Medicine Clinical Professor (Adjunct) Department of Podiatric Medicine Temple University School of Podiatric Medicine, Philadelphia, USA

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



viii    Contemporary Management of the Diabetic Foot

Neil Baker BSc DPODM MCHS

KR Suresh MBBS DABS FACS

Principal Diabetes Specialist and Research Podiatrist Ipswich Diabetic Foot Centre Ipswich Hospital Suffolk, UK

Director Jain Institute of Vascular Sciences Bhagwan Mahaveer Jain Hospital Bengaluru, Karnataka, India Past President Vascular Society of India Founder Member of Diabetic Foot Society of India

Robert G Frykberg DPM MPH Diplomate American Board of Podiatric Surgery Master, American Professional Wound Care Association Chief (Podiatry) and Resident-Director Carl T Hayden VA Medical Center Phoenix, Arizona, USA Adjunct Professor Midwestern University Glendale Arizona, USA

Sanket Pendsey

MBBS Diploma in Diabetology DNB (General Medicine)

Diabetes Consultant Diabetes Clinic and Research Centre Nagpur, Maharashtra, India

Sharad Pendsey MD Consultant Diabetologist and Director Diabetes Clinic and Research Centre Nagpur, Maharashtra, India

Shigeo Kono MD PhD Professor of Clinial Medicine Kyoto University Director WHO-Collaborating Centre for Diabetes Kyoto Medical Center, Kyoto, Japan

Stephan Morbach MD Head Diabetes and Angiology Marienkrankenhaus Soest, Germany Visiting Researcher Public Health Unit, Faculty of Medicine Heinrich Heine-University Düsseldorf Germany

Vijay Viswanathan MD PhD FICP FRCP (London and Glasgow)

Head and Chief Diabetologist MV Hospital for Diabetes and Prof M Viswanathan Diabetes Research Centre Chennai, Tamil Nadu, India

Virginia Bower BAppSc (Pod) MPH Grad Cert HPE

Associate Professor School of Surgery The University of Western Australia and School of Medicine University of Tasmania Tasmania, Australia

William Jeffcoate MB MRCP Consultant Diabetologist Foot Ulcer Trials Unit Department of Diabetes and Endocrinology Nottingham University Hospitals NHS Trust Nottingham, UK

Zulfiqarali G Abbas MBBS MMed (Internal Medicine) DTM & H (UK)

Consultant Physician Endocrinologist and Diabetes Abbas Medical Centre Muhimbili University of Health and Allied Sciences (MUHAS) Dar es Salaam, Tanzania Chair, Pan-African Diabetic Foot Study Group

Foreword It is my great pleasure to write this foreword for Contemporary Management of the Diabetic Foot. In the early 1960s, textbooks on diabetes contained very little information about the diabetic foot. Their abbreviated coverage consisted primarily of hygienic care of the foot. In the late 1960s, Lawrence O’Neal and I came to the conclusion that what was needed for a complete and concise textbook on the care and problems of the diabetic foot. The first edition of the textbook, The Diabetic Foot, edited by Levin and O’Neal was published in 1973. It consisted of ten chapters and ten authors. It was followed by multiple textbooks on the diabetic foot. These textbooks became more and more detailed, explaining the etiology of diabetic foot lesions, and methods of the prevention of ulcerations of the foot, resulting in fewer extremity amputations. Today, there are multiple textbooks on the diabetic foot. One of these is Diabetic Foot: A Clinical Atlas, edited by Dr Sharad Pendsey and published in 2003. It consisted of 48 chapters with a single author. This important text illustrates the problems of the diabetic foot on a day-to-day basis and is complete without being complicated. In 2008, the seventh edition of Levin and O’Neal’s The Diabetic Foot, was published. It consisted of 33 chapters, 58 authors and more than 600 pages. A chapter in this edition is devoted to the medicolegal aspects of the consequences of below standard care of the diabetic foot. The number of individuals with diabetes increases daily. In the United States of America, there are approximately 25.8 million persons and approximately 366 million with diabetes in the world; you can double this number to account for the number of diabetic feet with the potential of developing ulceration and subsequent amputation. The escalating number of foot problems is due to the increasing diabetic population and to the fact that people with diabetes are living long enough to develop complications of the foot. The human foot is a mechanical marvel. It consists of 26 bones, 29 joints, 42 muscles, and a multitude of tendons and ligaments. In a lifetime, this phenomenal machine with its multiple moving parts walks between 75,000 and 100,000 miles, a distance equivalent to three to four times around the world, exposing it to significant pressures with each step. The diabetic person’s feet are exposed to significantly elevated pressures and ulcerations. Foot problems are common in the population at large. However, the diabetic patient is especially vulnerable because of the complications of peripheral neuropathy, peripheral arterial disease and infection. A combination of this triad can lead to the cataclysmic events of gangrene and amputation. Dr Pendsey’s latest textbook, Contemporary Management of the Diabetic Foot consists of 22 chapters with multiple authors. The purpose of this text is to bring to all who care for the diabetic individual the latest information on the pathophysiology of diabetic foot lesions, their treatment and the prevention of amputation. With this goal in mind, he has gathered together an international group of diabetes foot care specialists and educators, all of whom are experts in their particular field. Their expertise in caring for the diabetic individual helps prevent amputation, resulting in a better lifestyle for the individual and a decrease in healthcare costs as well as the number of lawsuits. Four of these authors are from India, three from the United States, one from Japan, one from Tanzania, three from the United Kingdom, one from Australia, one from Germany, one from Brazil and one from Belgium. Of these sixteen authors, I know six of them personally. All of these authors have made and will continue to make significant contributions to the well-being of the diabetic population worldwide. As a physician involved in the care of the diabetic foot for many years, I have unfortunately had the opportunity of testifying in numerous legal cases involving amputation. Many of these cases were due to the fact that the primary physician did not have the knowledge or techniques available to prevent or successfully treat ulcerations of the diabetic extremity that would have kept him or her out of the courtroom. Contemporary Management of the Diabetic Foot provides the latest information on caring for the diabetic foot, its complications and the prevention of amputations. This text should be in the library of all healthcare professionals who strive to improve outcomes for the diabetic foot and ultimately the lives of their patients.

Marvin E Levin MD FACP FACE Professor of Medicine (Adjunct) Washington University School of Medicine St Louis, Missouri, USA

Foreword At present, the prevalence of diabetes throughout the world is 366 million (20–70 years). This figure will have risen to 552 million in 2030. Presently, it is estimated that still 183 million people (50%) with diabetes are undiagnosed. Globally, up to 70 percent of all leg amputations happen to people with diabetes. Lower extremity amputations in diabetes count over 1 million per year. A foot ulcer with complications, such as chronic nonhealing wounds, infection together with peripheral arterial disease (PAD), often leads to amputation of a lower extremity. In every 30 seconds, a lower limb is lost to diabetes. In the early nineties, the ‘diabetic foot’ was considered as the Cinderella of diabetes care and hardly recognized as a potential devastating disease entity. The fact that many healthcare providers from different backgrounds were involved in its care without too much communication has long lead to a confusing and insufficient approach. The fact that the prevalence of diabetes increases so rapidly dramatizes the need for appropriate preventive and management strategies, especially education. Fortunately, nowadays, it is generally accepted that the establishment of an interdisciplinary team approach, without adequate foot care and preventive measurements are not possible. Increased emphasis on the team approach is now mandatory with the recognition that the patient is the most important member of the team. Many good functioning diabetic foot clinics have been arisen in dozens of countries in the last decade. In 2003, International Working Group on the Diabetic Foot (IWGDF) designed ‘step-by-step program’ to improve diabetic foot care in developing countries, of which the editor was one of the founding fathers, has already been successfully executed in 15 countries. This widely recognized success of these programs has certainly played an important role in the growing awareness of this process. Not to forget to mention among others the renowned spearheading projects in Brazil, Belgium and Tanzania, which were all very instrumental in focusing on the importance of a team approach. Leg amputations are very costly in both healthcare expenditures and quality of life. Better management and preventive measurements are mandatory. This is best accomplished by practicing evidence-based medicine. Importantly guidelines are an essential component of achieving quality diabetes care for people with the condition. Since 1999, the IWGDF has already quadrennially produced and launched very successful Consensus Guidelines on the Management and Prevention of the Diabetic Foot with translations in no less than in 26 languages. In 2007 and 2011, the guidelines are based on the evidence augmented with expert opinion in case, there is no solid evidence to put forward. With still too little budget globally available for this huge problem, healthcare providers must treat problems in the most appropriate, efficient and cost-effective way. The expenditure on a diabetes guideline has the potential to be one of the most cost-effective forms of health care expenditure provided the result is properly implemented. Nowadays, the number of publications is overwhelming. In spite of new insights, there is still a wide variety in practice throughout the world. Unfortunately, there is (in many lower income countries) still too much trust in faith healers and alternative medicine, which leads to unacceptable delay in referring patients to the experienced healthcare provider. One should not forget the slogan Time is tissue as quoted in the most recent IWGDF guidelines of 2011. The publication of Contemporary Management of Diabetic Foot will undoubtly eliminates misconceptions related to management of the diabetic lower limb. The list of outstanding authors being all experts in the field throughout the world will guarantee this thorough felt wish. I congratulate Dr Sharad Pendsey and his collaborators with the launch of this important publication. I hope this fine book will find its way to many healthcare providers in the field, which will contribute to less suffering of the patient and will lead to a reduction of the still unacceptable high number of lower extremity amputations.

Karel Bakker MD Ex-Internist and Endocrinologist Spaarne Hospital Heemstede, The Netherlands Chair IWGDF/IDF DFP

Preface It is indeed with that overwhelming satisfaction that I seek to unveil Contemporary Management of Diabetic Foot hosting contributory articles from authors of undisputed global repute on the subject of diabetic foot. Earlier, I authored a book Diabetic Foot: A Clinical Atlas published in 2003 by M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India. It turned out to be quite popular and deemed good enough to be later reproduced by an international publishing company (Martin Dunitz, Taylor and Francis Group) for an International Edition in 2004, which is also doing equally well. The recent invitation from M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, for a new book on diabetic foot came as a pleasant surprise. After some thought, I decided that it would be better to produce a multiauthored book with contributions from leading personalities on the subject from around-the-globe and to give myself the role only of an editor. The idea behind its publication is to provide a practical reference guide to practitioners of this difficult problem. I would like to emphasize that it is not a comprehensive textbook. To that end, it is intended that the book stays easy on the eye while remaining complete in details, lucid in its flow, rich in color, and illustrations, holding the reader’s interest to the next page and chapter. An attempt has been made to ensure that the chapters should encompass the whole spectrum of diabetic foot whilst avoiding any repetition or overlaps and preserving the continuity of the subject. Naturally, the chapters had to conform to a well-defined but not necessarily a restrictive format to help uniformity and to ensure that a chapter did not come out disjointed from the other. May the final impact of the book be greater than just the sum-total of individual chapters. I hope, this effort comes in handy to those mired in diabetic foot management. It is easy to be an optimistic that in the years to come, given better understanding of the management of diabetes, the longevity of diabetic patients should increase. But tempering, this optimism is the realization that this will give rise to a large number of chronic diabetics with their myriad problems including diabetic feet and peripheral arterial disease. This will necessitate a multidisciplinary team approach to the management of these patients, a concept well-adopted by the developed world but as yet to take off in the developing countries. Diabetic foot is so multifaceted, making no one individual equipped to be able to manage all the facets, hence, the team approaches. Lastly, I am very much delighted to affirm that the sale proceeds of the book too would go towards furthering the everexpanding services of ‘Dream Trust’, a registered charity (www.dreamtrust.org), upholding the paramount objective of providing free insulin to type 1 diabetic children from among the poorest of poor.

Sharad Pendsey

Acknowledgments On the face of it, thank you is a pleasant exercise. But, here today, this is filling my heart with trifle trepidation because, the best I could do, is leave many, and some words out. The words ‘thank you’ cannot possibly reflect my immense sense of gratitude as I publish this book. This mammoth task could hardly have been possible without the help of so many, some indirect and some even unknowings. I am very grateful to all the eminent contributors from around-the-globe, who readily accepted my invitation and managed, in timely fashion, to fit in their vast experience and expertise into the few pages allocated to them. With their acceptance of my invitation, half the battle was won. I would also like to thank Dr (Mrs) Margaret Brand, wife of (Late) Dr Paul Brand, for permitting me to dedicate the book in his memory. Mrs Bhavani Bhaskaran, my secretary par excellence, has spent tireless hours putting up with me and my continual demands and deadlines, and dare I say the occasional tantrums. She did the job of compiling all the manuscripts very meticulously.  Without her help, the book could not have been completed.  All along and through this project, the entire staff of my humble clinic has also tirelessly offered, without a blink, each help I dreamt.     A special word of thanks to my friend Dr Mukund Vaidya, Consultant Radiologist, UK, who has painstakingly gone through all the manuscripts with a fine-toothed comb.  The listing is incomplete without a thought and mention of my wife Swati, who has stayed as a pillar of strength, and so I manage to plod farther. How did one thank the drive of life? Sorry, no thanks. Over the last few decades, I have learnt a lot from my patients. I would like to thank them all collectively for giving me the opportunity to treat them and learn from them. They taught me, vintage me, more than I ever gave back. Their patience is the capital behind this book which will, hopefully, pay rich dividends for the future generations. My gratitude begins from them all, and of course extends to M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, who have since long and now again, reposed their trust in me. A special note of thanks for Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing Director), and Mr Tarun Duneja (Director-Publishing) of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, for this opportunity and the wonderful systems established under their stewardship over the years. I also appreciate the efforts of the entire editorial team and, especially Dr Neeraj Choudhary (Senior Medical Editor) and Ms Madhvi Thakur (Editorial Coordinator), for tirelessly working to bring out the book in its final shape and form. I would like to thank all the readers, who took my first book to their hearts, and in doing so encouraged me to produce this volume.   Finally, today has only been one battle won. Out of there, each word published, it is the reader who matters, and is the King. The war thus remains to be won. With an honest and open heart, it may not be out of place, to hope for comments from every reader. Why? Simply put, to help me get better.

Contents 1. Introduction Sharad Pendsey

1

2. Historical Notes on a Modern Disease: The Diabetic Foot Lee J Sanders

4

3. Surgical Anatomy of the Lower Limb and Foot Shigeo Kono

13

4. The Global Burden of Diabetic Foot Zulfiqarali G Abbas

24

5. Diabetic Neuropathy Andrew JM Boulton

31

6. The Biomechanics of the Diabetic Foot Virginia Bower

39

7. Examination of Feet Sharad Pendsey

49

8. Classification and Staging of Diabetic Foot Michael Edmonds

55

9. The Assessment and Management of Plantar Ulcers and Offloading the Diabetic Foot Neil Baker

63



xviii    Contemporary Management of the Diabetic Foot

10. The Diabetic Charcot Foot: Diagnosis and Management Robert G Frykberg

78

11. Diabetic Foot Infections Sharad Pendsey

87

12. Principles of Debridement in the Infected Foot Jennifer Pappalardo, David G Armstrong

102

13. Evaluation of Neuroischemic Foot Sharad Pendsey

111

14. Approach to Dysvascular Diabetic Foot KR Suresh, Aniket Pradhan

118

15. Diabetic Foot Ulcers: Short- and Long-term Outcomes Fran Game, Stephan Morbach

134

16. Amputations Arun Bal

139

17. Advanced Wound Healing Products and Techniques Michael Edmonds

153

18. Atypical Aspects of the Diabetic Foot Sharad Pendsey, Sanket Pendsey

159

19. Screening and Prevention of the Diabetic Foot Hermelinda C Pedrosa

170

20. Prescribing Footwear Vijay Viswanathan

176



Contents    xix

21. Patient Education and Empowerment in the Prevention and Management of Diabetic Foot Disease William Jeffcoate 22. Establishing a Multidisciplinary/Interdisciplinary Diabetic Foot Clinic Kristien Van Acker

185

191

Index 199

CHAPTER

1

Introduction

Sharad Pendsey

Among the many chronic complications of diabetes, diabetic foot has remained the most feared complication, with both patients and treating health care professionals sharing the dread in equal measure. Devastating consequences like limb amputation has made such fear abundantly justified. Despite it being the most feared complication, ignorance about diabetic foot continues to dominate the reasons for many of the avoidable limb amputations. In fact, patient education, proper care of feet and appropriate foot wear can prevent occurrence of many of the foot ulcerations. It has been realized that 85% of all limb amputations are preceded by trivial foot lesions. Prompt recognition and aggressive treatment of such trivial foot lesions can prevent many of the limb amputations. Looking at patient’s feet and picking up foot lesions when they are young is the key to success. Unfortunately such simple but important steps are easily overlooked by many of us. Globally over 1 million lower limbs are amputated every year, in fact every 30 seconds a limb is lost to diabetes some­ where in the world. A person with diabetics is up to 40 times more likely to suffer a lower extremity amputation than a nondiabetic. Diabetic foot is a significant economic problem. The cost of treatment of foot ulcer in Western countries ranges from 7,000 USD to 10,000 USD. The direct cost of an amputation associated with diabetic foot is estimated to be between 30,000 USD and 60,000 USD. In India, with majority not covered by medical insurance, the entire cost (direct and indirect both) has to be borne by the patient, and, often, it is the breadwinner of the family who happened to be the victim. Loss of wages after the amputation and huge cost incurred on treatment shatters the family both socially and economically. Rough estimates indicate that about 100,000 lower limbs are amputated in India every year, of which 75%

are on neuropathic feet with secondary infection. These amputations are potentially preventable. In view of enormous problem of diabetic foot in India, the Step-by-Step foot care project was conceived in the year 2003, with a common objective of improving diabetes foot care in the developing world. The Project Committee consisted of Sharad Pendsey, India (Chairman); Karel Bakker, The Netherlands; Ali Foster, United Kingdom; Zulfiqarali G Abbas, Tanzania (Chairman); and Vijay Viswanathan, India. The project has received generous funding from the World Diabetes Foundation and academic support from International Diabetes Federation, International Working Group on the Diabetic Foot, Diabetic Foot Society of India, and Muhimbili University College of Health and Allied Sciences, Dar es Salaam, Tanzania.

GOALS • To increase the meager awareness of diabetic foot problems • To provide sustainable training of health care professionals in the management of diabetic foot • To facilitate the cascading of information from health care professionals who have undergone training to other health care professionals and thus expand expertise • To reduce the risk of lower limb complications in people with diabetes • To empower diabetics in better foot care, early problem detection and in seeking timely help.

METHODS Special foot care education materials, both visual and audiovisual, were designed specifically for people with diabetes



2    Contemporary Management of the Diabetic Foot in developing countries. Foot care education materials, visual and audio-visual, were also designed for health care professionals working with people suffering from diabetes in developing countries. Kits of diagnostic instruments (10 g monofilament, tuning fork, etc.) were distributed to participants, also including Podiatric Instruments’ Kits (Bard Parker handle with surgical blades, nail clipper, nail files, artery and tooth forceps, scoop, probe and scissors).

PROJECT AT A GLANCE In all, 115 teams of doctors and nurses working with the same doctor were selected for training in diabetes foot care [India (94), Bangladesh (3), Sri Lanka (2), Nepal (1) and Tanzania (15)]. The participants selected were specifically from smaller cities and towns, and who had no previous training in diabetes foot care. They were offered a 2-day Basic Course in 2004 followed by a 2-day Advanced Course in 2005. The courses were held in the four metros of India (New Delhi, Mumbai, Chennai, Kolkata), with 25 teams participating in each metro and at Dar es Salaam Tanzania with 15 participating teams. A national and international faculty of experienced educators in the field was responsible for teaching and chairing the practical sessions. Apart from theory lectures, emphasis was given on live case demonstration, hands on experience and practical problem solving. In summary, the attending delegates were trained in preventative diabetic foot care. • Primary prevention: Screening of high-risk feet and proper advice on preventive footwear. • Secondary prevention: Management of trivial foot lesions like callus removal, treatment of nail pathologies, deroofing blisters, etc. • Tertiary prevention: Prompt referral to specialist for advanced foot lesions.

IMPACT One hundred and fifteen foot care clinics (minimum model) were started. It was anticipated that delegates will cascade information to larger number of diabetics, as also to other health care professionals, including paramedics, physicians, educators, health care policymakers and laypeople. The formal training was expected to reduce the amputation rate among these patients by about 50%.

RESULTS The data was collected by a questionnaire sent to all partici­ pating delegates, and results of 1st year after the Basic Course and 2nd year after the Advanced Course were evaluated. Eighty-five teams, from India, responded to the questionnaire

for both the years. From the overview of the work carried out by the delegates it was apparent that there was a significant increase in every activity they conducted in the 2nd year, over the 1st year. In the absence of any formal training in diabetes foot care, about 20% of patients with trivial foot lesions would be expected to have lower extremity amputation. Thus, with appropriate treatment of trivial foot lesions in the 1st year, at least 900 lower limbs and in the 2nd year 1,943 limbs were salvaged by the participants of the Step-by-Step foot care project.

CONCLUSION This carefully designed and executed project to improve diabetic foot care in the developing world turned out to be a major success. The strength of the Step-by-Step program is that the project consists of a 2-year set up: a Basic and an Advanced Course to be attended by the same delegates. The pre­­requi­ site to participate in the first course was to agree to attend the second course. This pilot project is now being imple­mented in various parts of the world like Caribbean islands, South America, Pakistan, Egypt and several countries in Africa. The Step-by-Step foot care project came out a grand success and was very well received across India. Actually, it kick-started a national movement regards diabetic foot. However, in a vast country like India, such a project need to be continued until evident results get palpable; and then a level is to be maintained to sustain gains effected. In the developing world including India, we need to have three-tier system wherein each district had a Minimal Care Diabetic Foot Center. These centers will mean to carry out educational activities, screening of high risk feet, advice regarding preventive foot wear and manage trivial foot lesions. These may thus prevent trivial foot lesions advancing into a catastrophe. Larger cities had better had an Intermediate level Diabetic Foot Center. These centers are meant for surgeries like debridement and amputations, offloading advice and to maintain good liaison between minimal care centers. The Tertiary Foot Care Center will have facilities for carrying out complex foot surgeries, including revascularization and infrapopliteal bypass surgery. The Public Health Care System in India is overburdened because of high prevalence of both communicable as well as non-communicable diseases. Private health care and the corporate sector should take up the responsibility of provid­ ing affordable health care to general population. Medical insurance is a way away from penetrating the masses. Let policies be formulated that afforded each individual reason­ able health insurance cover. There is nothing inevitable about lower limb amputation. These can certainly be reduced, in the least by 50%, if proper thera­ peutic strategies were implemented. In parts of the developed world, 50% reduction in lower limb amputation is



Introduction    3 already achieved. Preventive strategies like glycemic control, screening the high risk feet, proper foot wear and sustainable education of all afflicted with diabetes should go a long way in arresting this most feared complication of diabetes. Given the increasing longevity of the general population, well control­ led diabetics too will live longer; imposing additional burden of many more ageing with peripheral vascular disease and critical leg ischemia. Strategies and facilities to tackle this are yet in infancy in most parts of this country, and wherever

these do happen to be around, have seemed out of common reach. But, there is always ground to stay optimistic. The sum total interest in the arena of diabetic foot is growing by leaps in the medical fraternity. It is very much hoped that more and more health care professionals will pick up the gauntlet of managing the hitherto neglected diabetic foot. Step-bystep, diabetics will need to be goaded to turn away from the amputa­tion path and to instead embrace the chance to save their foot.

CHAPTER

Historical Notes on a Modern Disease: The Diabetic Foot

2 Lee J Sanders

“History is the biography of the mind of man, and its educa­ tional value is in direct proportion to the completeness of our study of the individuals through whom this mind has been manifested.” Sir William Osler, 1921

INTRODUCTION A comprehensive review of the history of the diabetic foot would be incomplete without a brief historical overview of the earliest observations of diabetes mellitus. Diabetes was a rare disease during the Age of Antiquity and the Middle Ages. The earliest writings regarding diabetes focused on the signs and symptoms of this disorder: excessive thirst, frequent urination, glycosuria and wasting of the body. The period of European history that began in Italy during the 14th century, the Renaissance, marked the humanistic revival of classical art, literature and science. This period was characterized by a burst of intellectual and creative activity that formed the bridge from the Middle Ages to Modern Times. In medicine, there was an exhilarating revision of medical and scientific concepts beginning in the 16th century. However, most observations and investi­­­­­gations of the diabetic foot begin to appear in the 19th century. For much of the 19th and 20th centuries the concept of the diabetic foot was focused on vascular insufficiency and “diabetic gangrene”. The miscon­ception of diabetic foot disease as gangrene lasted for many years and sadly this resulted in overly aggressive surgical manage­­­ment with major amputation of the leg above the knee.

DIABETES IN THE AGE OF ANTIQUITY Claudius Galen (130–201), a Greek physician, was one of the most influential medical writers of all time. For

more than 1,500 years, Galen’s extensive works were the irreproachable authority on medicine. He had a dominating influence on the development of Arabian and European medical practice. Galen discussed diabetes in a number of his works and described the condition as rare. He wrote, “I am of the opinion that the kidneys are affected in the rare disease which some people call chamber pot dropsy, other again diabetes or violent thirst…I have seen the disease till now only twice when the patients suffered from an inextinguishable thirst, which forced them to drink enormous quantities; the fluid was urinated swiftly”. Aretaeus, the Cappadocian (130–200), was a disciple of Hippocrates and a contemporary of Galen. He provided the first accurate description of the symptoms of diabetes and was the first to use the term diabetes in connection with this condition. He employed the word diabetes from the Greek word that signifies a siphon. Aretaeus’ classic description of this ailment, translated by Francis Adams, in 1856, follows: “Diabetes is a wonderful affection, not very frequent among men, being a melting down of the flesh and limbs into urine…the course is the common one, namely, the kidneys and bladder; for the patients never stop making water, but the flow is incessant, as if from the opening of the aqueducts. The nature of the disease, then is chronic, and it takes a long period to form; but the patient is short-lived, if the constitution of the disease be completely established; for the melting is rapid, the death speedy...”

DIABETES IN THE MIDDLE AGES The period of Western European history referred to as the Middle Ages extends from the time of early fragmentation and collapse of the Roman Empire, beginning around 350 CE to about 1450 CE. The practice of medicine in the Middle Ages was fundamentally a restatement and acceptance of



Historical Notes on a Modern Disease: The Diabetic Foot    5 Greco-Roman teachings. Avicenna (Ibn Sina) (980–1037), a Persian physician, was well known, throughout the Middle Ages, as the “Prince of Physicians”. He wrote one of the most famous medical textbooks, “The Canon of Medicine” (Rules of Medicine). This five-volume work served as the standard medical textbook in Europe until the 17th century. Avicenna knew of the sweet taste of diabetic urine and that diabetes could be primary or secondary to another disease. He described a wasting away of the body, infections, nonhealing wounds (ulcers), bone disease (osteomyelitis) and diabetic gangrene. Ibn Sina wrote, “in treating ulcers, the aim is to procure desiccation, so the exposed surfaces will dry up… ulcers in situations which are not fleshy, and round ulcers, cannot be made to heal quickly…”. He mentioned conditions that prevent the healing of an ulcer, “the only remedy for this is to deal with the bone disease: massage can help to get rid of the diseased bone, otherwise it must be excised”. Avicenna specifically referred to the role of nutrition and disease of the underlying bone. We can only speculate whether or not Avicenna was referring to diabetic foot ulcers. Although Claudius Galen wrote that diabetes was rare and that he had seen only two cases of this illness, Moses Maimonides (Rambam) (1138–1204), a renowned Medieval physician, claimed to have seen several more cases. In the course of 10 years, in Egypt, he claimed to have seen more than 20 people who suffered from this illness. Maimonides concluded that diabetes occurs mostly in warm countries, “perhaps the waters of the Nile, because of their sweetness, play a role in this (disease causation)”. No further progress was made in the understanding of diabetes until the 16th century.

THE RENAISSANCE In medicine, there was an exhilarating revision of medical and scientific concepts beginning in the 16th century. Renaissance physicians and scientists questioned conventional think­ ing with a renewed spirit of curiosity, objectivity and experi­ mentation. This period laid the foundation for an accurate knowledge of human anatomy, and demonstrated how the body’s functions should be studied intelligently. The Medieval medical system began to give way as Paracelsus, Vesalius, William Harvey and Ambroise Paré challenged traditional dogma. Andreas Vesalius (1514–1564) established modern observational science and research, which marked a turning point in the history of medicine. In 1543, Vesalius completed a monumental, beautifully illustrated anatomical work, “De Humani Corporis Fabrica”, seven books on the structure of the human body. This work was based on Vesalius’ dissections of human cadavers and is the most famous anatomical work ever published (Fig. 1). The French military surgeon Ambroise Paré (1510–1590) is considered the most renowned barber-surgeon of the 16th century. He popularized the use of ligatures to control bleeding after amputation, rather than cautery, and he used bandages

Fig. 1  De Humani Corporis Fabrica (1543), anterior view of the body, Plate 24: The first plate of the muscles (Source: JB deC M Saunders, Charles D O’Malley. The illustrations from the works of Andreas Vesalius of Brussels. Cleveland, New York: The World Publishing Company; 1950.) (Courtesy: The New York Academy of Medicine Library)

to cover wounds. He is quoted as saying “Je le pansai, Dieu le guérit” (I dressed him, God healed him). Paré recognized the importance of anatomy in relation to surgery. He included considerable parts of Andreas Vesalius’ important anatomical studies, translated from Latin to French, in his publications on surgical techniques.

THE SEVENTEENTH CENTURY Thomas Willis (1621–1675) provided what may be the earliest description of diabetic neuropathy characterized by lancinating (sharp and shooting) pains “I have observed in many people who have been subject to this disease…they felt flying, running pains through their whole bodies, and corrugations sometimes with dizziness or stinging…”. Willis developed the concept of neurology and coined the term neurology in his major work Cerebri Anatome (1664). He referred to diabetes as the “pissing evil” and noted that in patients with diabetes, “the urine is wonderfully sweet, as if it were imbued with honey or sugar”. Willis claimed that diabetes was primarily a disease of the blood and not the kidneys. He believed that the sweetness appeared first in the



6    Contemporary Management of the Diabetic Foot

Fig. 2  Seventeenth century wood cut print showing amputation of the leg for gangrene. Cautery irons are in the fire in the foreground (Source: Wilhem Fabricius Hildanus. De gangrene et sphacelo, tractus methodicus. 1617. p. 163.) (Courtesy: National Library of Medicine)

blood and was later found in the urine. By the 17th century, lower extremity amputations were performed not only for traumatic wounds and open fractures but also for foot ulcers, abscesses and gangrene (Fig. 2).

THE EIGHTEENTH CENTURY Matthew Dobson (1735–1784) was the first to demonstrate the presence of sugar in the urine and blood of patients with diabetes. He provided experimental evidence that people with diabetes eliminate sugar in their urine. His findings were presented to the Medical Society of London in 1776. Thomas Willis’ observations of diabetes and Matthew Dobson’s experiments conclusively established the diagnosis of diabetes in the presence of sugar in the urine and blood. Diabetes was no longer a rare disease. William Cullen (1710– 1790) one of Britain’s foremost clinicians, consultants and educators introduced the term diabetes mellitus. In 1769, Cullen published an elaborate classification of human diseases titled Synopsis Nosologiae Methodicae. In this classifi­ cation, we see for the first time a distinction between diabetes (mellitus), with urine of “the smell, color and flavor of honey” and diabetes (insipidus) with limped but not sweet urine. It was Cullen who added the descriptive adjective mellitus, from the Latin word for honey, to the Greek word diabetes.

THE NINETEENTH CENTURY In the 19th century, we see reports of perforating ulcers of the foot as a consequence of both tabes dorsalis and diabetes.

The association of diabetes with neuropathy, foot ulcers and gangrene is seen in the writings of Marchal de Calvi (1852, 1864), Thomas Hodgkin (1854), Frederick W Pavy (1885), M Laffon (1885), T Davies Pryce (1887), Thomas Buzzard (1890) and others. Most of the neurological complications of diabetes were clearly described by the end of the 19th century. Marchal de Calvi recognized the association between gangrene and diabetes, in 1852, and drew attention to the causal relationship between diabetes and disorders of the nervous system, in 1864. He pointed out that diabetes might be the cause rather than the result of neurologic disturbances. Thomas Hodgkin also discussed the association between diabetes and gangrene in 1854. In his paper, On Diabetes, Hodgkin mentions two cases. In the first case the gentleman had sores on his feet having a gangrenous character and proving rapidly fatal. “In another case which I had the opportunity of observing for several years, and which was the most protracted case of well-marked diabetes which has come to my knowledge, the feet were long in a very troublesome state—often threatened with the formation of sores which were only warded off by the most assiduous care…”. At length, symptoms of decided gangrene occurred in one toe, progressively extending to the whole of the anterior half of the foot, and having very much the character of dry senile gangrene… I think that it could not have been less than 6 or 7 months that the patient survived after gangrene had decidedly commenced” (Fig. 3). Frederick Treves, FRCS (1884) wrote that the so-called perforating ulcer of the foot, associated with tabes is “the outcome of purely local causes acting upon a part whose condi­tion has been injuriously influenced by a central nerve distur­ bance. The sensation in the integument of the sole

Fig. 3  Watercolor drawing illustrating dry gangrene of the left great toe (Source: Thomas Godart (1862–1875). St Bartholomew’s Hospital Archives and Museum, London, UK.) (Courtesy: Wellcome Library, London)



Historical Notes on a Modern Disease: The Diabetic Foot    7 commonly becomes dulled; and if to these conditions be added the effects of pressure upon the skin it would appear that the chief factors in the production of perforating ulcer are present”. Treves described the clinical history of a neuropathic foot ulcer. “At a spot upon the sole of the foot upon which pressure bears a corn appears. This spot is very commonly over the metatarsophalangeal joint of the great toe. The corn increases, and, from the pressure that it exercises upon the soft parts beneath it, some inflammation of an insidious type follows. Suppuration then appears beneath the corn, and spreading in the direction of the least resistance, advances into the soft parts of the foot moving towards the bone”. He recommended treatment with bed rest, a linseed meal poultice and sharp debridement with a scalpel. This was then followed by appli­ cation of a thick cream composed of salicylic acid, glycerin and carbolic acid. Once the ulcer was completely healed, a thick felt aperture pad was applied. He advised, “this plaster should always be worn”. Patients were instructed to pay great attention to the cleanliness of their feet and to wear wellfitting woolen stockings and “easy boots”. Jean-Martin Charcot (1825–1893) recognized a temporal relationship between the onset of lightening pains, like a “shower of electric needles” and development of the tabetic arthropathies. Pain was of short duration but recurrent through­­out the day and was accompanied by loss of sensation and hyperesthesia. He emphasized that in diabetes you can have very similar complaints associated with diminished sensation and absent deep tendon reflexes. Charcot noted that corpulence often precedes the development of diabetes “The prognosis may sometimes be as grave in such a case… gangrene… may supervene”. Herbert W Page (1881) and JM Charcot (1883) were the first to describe neurogenic arthropathy of the foot and ankle in patients with tabes dorsalis. Originally referred to as “pied tabétique”, this condi­ tion has come to be known as the Charcot foot or Charcot neuropathic osteoarthropathy (CN). Although considered to be a rare condition, today this is most commonly seen to affect people with diabetes and peripheral sensory neuropathy. The hallmark deformity associated with CN is midfoot collapse described as a “rocker-bottom” foot. A foot ulcer is often associated with midfoot deformity, located at the apex of the rocker. It was Herbert W Page, in 1883, who first described this deformity. His eloquent description follows: “The sole of this foot is 4¾ inches wide and there runs across it, midway between the heel and the toes, a hard transverse ridge, composed doubtless of the tarsal bones. On this transverse ridge his foot rests on the ground, and you are able to get the tip of your little finger underneath his heel when he is standing”. FW Pavy, MD, FRCP, FRS, a leading authority on diabetes, provided a classic description of the neuropathic signs and symptoms associated with diabetes, in 1885. “The usual account given by these patients of their condition is that they cannot feel properly in their legs, that their feet are numb,

that their legs feel too heavy—as one patient expressed it… as if his boots were a good deal too large for his feet. Darting or “lightning” pains are often complained of... Not infrequently there is deep-seated pain…generally at night. Or there may be hyperesthesia… With this there is the usual loss or impairment of the patellar tendon reflex”. Pavy also noted that he had seen many cases of ataxia associated with diabetes. Although perforating ulcers of the foot were known to be associated with tabes dorsalis, it was a Frenchman, M Laffon, who first associated diabetes with neuropathic plantar ulceration, in 1885. Laffon reported the case of a 61-yearold man with peripheral neuropathy and violent lightening pains in his foot. He developed ulcers on multiple toes on both feet. Laffon noted that the patient’s urine contained a large proportion of glucose. T Davies Pryce, MRCS reported on a second case of perforating ulcers of both feet associated with diabetes and ataxic symptoms, in 1887. He noted that for the past 18 months his 56-year-old patient had passed large quantities of urine and had suffered from great thirst. He complained of pain in his legs and stated that his feet felt dead. There was diminished cutaneous sensibility in his both feet and the lower thirds of his legs. The knee jerk was abolished and a fetid odor emanated from the ulcers on both feet. The ulcers had commenced as corns. The following is Pryce’s description of one of the foot ulcers and osteomyelitis of the first metatarsal bone: “One ulcer of the size of a two-shilling piece was situated over the plantar aspect of the metatarsophalangeal joint of the right great toe…The bones entering into the formation of the joint could be felt at the bottom of the sinus, the metatarsal bone being eroded…The patient’s urine contained sugar and a trace of albumin. He died on June 1st (4th day of treatment) of diabetic coma”. Thomas Buzzard, MD, FRCP, published his observations of patients with peripheral neuritis associated with alcoholism and other causes including diabetes, in 1890. He reported the case of a 55-year-old carpenter who suffered from loss of power in his lower extremities. There was loss of ankle joint dorsiflexion, tenderness on pressure in the soles of the both feet with numbness and tingling from the feet to the knees. The knee jerks and plantar reflexes were absent. Sensation to touch was diminished below the knees and there was wasting of the thenar and hypothenar eminences of both hands. On the right foot, just below the lateral malleolus, a deep ulcer was noted. On the left foot, just below the first metatarsophalangeal joint, there was a scar due to a similar condition arising in connection with a corn. “The urine contained sugar in abundance”.

THE TWENTIETH CENTURY In the 20th century, we begin to see greater awareness of the lower extremity complications of diabetes as well as a distinction between neuropathic, ischemic and neuro­



8    Contemporary Management of the Diabetic Foot ischemic lesions of the feet. In 1913, John T Sample and WL Gorham reported on seven cases of mal perforans ulcers seen in patients with diabetes. Each of these cases had a negative serologic test for syphilis (Wasserman test). The authors noted that nearly every case recorded in the literature was over 40 years of age. They observed that the perforating ulcer of diabetes closely resembles that of tabes dorsalis, but is distinguished from it and from other forms of ulcer by the location of the lesion. “The initial lesion is often in the form of a small vesicle which later develops into an ulcer, or the process may take its origin from an infected corn… the metatarsal phalangeal joint is a favorite seat for such a pathological change”. Maurice J Lewi, MD (1857–1957) recognized the medical establishment’s indifference toward the “minor foot ills” of mankind. In 1913, Lewi founded “The School of Chiropody” of New York, now known as the “New York College of Podiatric Medicine”. Lewi dedicated his 1914 Textbook of Chiropody “to the men and women who were pioneers in the cause of Chiropody and who, in the face of many and unusual obstacles, labored to the benefit of mankind in a branch of medical learning that had been neglected through all the centuries”. In Joseph P Solomon’s chapter entitled “Some Suggestive Foot Conditions”, there is a discussion of various foot disorders that are manifestations of systemic diseases, in particular diabetes. “…So it happens oft times that the observing chiropodist is the first to recognize signs and symptoms on his patient’s feet and limbs which are indicative of diabetes…the greatest care should be taken not to make any incision which might cause the flow of blood as such patients are exceedingly susceptible to all kinds of infections, local and otherwise. This is particularly true of those who are advanced in years and with whom the development of diabetic gangrene is certain if they have lesions on the foot which are not carefully treated…” The therapeutic era in the history of diabetes dawned in the 1920s with Frederick Banting’s discovery, isolation, purification and therapeutic use of insulin. This was one of the greatest contributions of the 20th century to scientific medicine. Although a miraculous development in the treatment of diabetes, it soon became apparent that insulin was not a cure for diabetes. As people began to live longer, they experienced complications that had not previously been seen. These complications affected the eyes, kidneys, cardiovascular system, nervous system and feet.

THE TEAM APPROACH TO DIABETES CARE In 1934, Elliott P Joslin, MD (1869–1962) wrote a paper entitled “The Menace of Diabetic Gangrene”, published in the New England Journal of Medicine. Joslin noted that following the introduction of insulin, mortality from diabetic coma

had fallen significantly from 60% to 5%. Yet deaths from diabetic gangrene of the foot and leg had risen significantly. Joslin observed that gangrene increased with the age of the individual and with the duration of diabetes. There was almost always a history of injury to the foot that could be elicited from the patient. Burns and ill-fitting shoes caused the most common injuries. Dr Joslin firmly believed that gangrene and amputations were preventable. He commented, “It has been forced upon me that gangrene is not Heaven-sent but is earth born.” His remedy was a “team approach to dia­ betes care”, which included patient education in foot care, medical nutrition therapy, exercise, prompt treatment of foot infec­tions and specialized surgical care. Joslin stressed the importance of cleanliness, daily foot inspection for early signs of trouble and podiatric care. These principles of care are just as applicable today. Through the efforts of Elliott Joslin and the Massachusetts Chiropody Association, the first hospital foot clinic was established at the New England Deaconess Hospital in 1928. Joslin wrote, “Our Boston chiropodists are use­ful allies. They have contributed much to our reduction in gangrene”. Leland McKittrick, MD (1893–1978) was recruited by Elliott Joslin to provide for the surgical management of lower extremity lesions in patients with diabetes at the New England Deaconess Hospital. In 1949, McKittrick wrote: “Chemotherapeutic agents and antibiotics have made it possible to control invasive infection and the mortality rate has fallen as anticipated… With the danger of ascending infection and septicemia eliminated, it might now be practical to consider each foot on the basis of its arterial supply. In selected cases, amputation might now be performed at a more distal level with safety and a reasonable chance of success….”

PREVENTIVE DIABETIC FOOT CARE Harold Brandeleone and colleagues in a series of 576 patients demonstrated the utility of prophylactic outpatient foot care in patients with diabetes. In May 1933, a foot treatment room was established at the Diabetic Clinic of the Third (New York University) Medical Division of Bellevue Hospital. Treatment was provided for corns, calluses and ingrown toenails. For the 2-year period (May 1931 to May 1933) prior to establishment of the foot treatment room, 10% of the clinic’s patients required hospitalization for lower extremity infection. In the next 2 years, the number of patients requiring admission for foot infections dropped to 4.6%. The effect of proper treatment of diabetes on the outcome of foot infections was quite dramatic when compared to non-clinic patients. In the group in which neither the diabetes nor the feet had been treated, 41.6% required amputation and 38.4% of these patients died. In Brandeleone’s clinic group, prior to prophylactic foot care, 32.4% required amputation and 8.8% died. The mortality dropped from 8.8% to 3.7% and the number of patients requiring amputation dropped from 32.4% to 25.9%.



Historical Notes on a Modern Disease: The Diabetic Foot    9

THE ROLE OF NEUROPATHY IN DIABETES William Riely Jordan (1936) published a comprehensive report entitled “The Neuritic Manifestations in Diabetes Mellitus”. He found that neuropathy involved the legs in over 65% of the cases. The most frequent neuropathic manifestations were pain, paresthesia, hyporeflexia and areflexia, muscular paresis, tenderness of the nerves and muscles, hypoesthesia and hyperesthesia. Jordan was the first to establish the asso­ ciation of Charcot’s joint disease of the foot and ankle with diabetes. M Mencer Martin (1953) elucidated the relationship of diabetes mellitus to the development of its neurological complications. Martin observed that neuropathic foot lesions were common in his series of cases with diabetic neuropathy including typical perforating ulcers in 18 patients. He commented that the lack of pain sensation led patients to ignore the lesion and delay treatment until secondary infection had resulted in extensive inflammation and osteomyelitis of the underlying bone. Martin made a very important observation, “In the past these lesions were frequently ascribed to ischemia, arteriosclerosis or sepsis, without recognition of the peripheral nerve disorder as a predisposing factor”. Wilfred Oakley and M Mencer Martin (1956) categorized lesions in the diabetic foot as septic, neuropathic or ischemic. They note that uncomplicated sepsis produced essentially the same lesion in the diabetic as in the non-diabetic foot. Neuropathic lesions were often accompanied by characteristic deformities of the toes and feet. “The association of this deformity with sensory disturbances lends color to the belief that this deformity is indeed a manifestation of a peripheral motor neuropathy”. Oakley and Martin observed that the two main manifestations of ischemia in the diabetic foot are pain and gangrene. In 1965, Paul W Brand, MD, FRCS (1914–2003), a world renowned orthopedic surgeon, arrived at the US Public Health Service Hospital, National Hansen’s Disease Center, in Carville, Louisiana, the only Leprosy hospital in the conti­ nental United States. Brand served as Chief of the Rehabili­ tation Branch. His interest in ulceration of the feet began in India in the 1940s with leprosy. He defined the roles of peripheral sensory neuropathy and pathomechanics in the causation of foot ulcers in patients with leprosy and diabetes. Brand translated his research findings on a living model, the footpads of rats, to the practical management of insensitive hands and feet seen in patients with Hansen’s disease and diabetes. Much of what Dr Brand learned in India and in the Public Health Service proved to be transferable to diabetes. “I realized that here in America in the 1960s the manage­ ment of foot ulceration in diabetics was hindered by some of the same misconceptions that I had faced about leprosy in the 1940s. Ulcers in diabetics were still called “diabetic ulcers” rather than neuropathic ulcers. They were looked upon by surgeons as being a reason for amputation, because they were thought to be unlikely to heal and go on to gangrene of the foot.

Fig. 4  The Dominican Republic issued a series of postage stamps, Lucha Contra La Diabetes (Fight against Diabetes) in 1974 to raise awareness of the serious complications of diabetes. This stamp calls attention to lower limb amputations

Much of this was because in diabetes, unlike leprosy, there was often a real vascular problem, and this did sometimes cause gangrene, even without neuropathy”. The 50th anniversary of the discovery of insulin was cele­ brated in 1971. In the 1970s decade, there was a global effort to increase public awareness of diabetes and its complications. Diabetic retinopathy, nephropathy, cardiovascular disease and lower extremity amputations were represented on stamps. In 1974, the Dominican Republic issued a stamp in the series “Lucha Contra La Diabetes” (Fight against Diabetes) to raise awareness of diabetic lower limb amputations. The stamp depicts a man in a wheel chair, with an amputation of his right leg (Fig. 4).

PREVENTION OF FOOT ULCERS AND AMPUTATIONS The role of patient education and the team approach to diabetic foot care were emphasized in the 1980s and 1990s in the United States, United Kingdom and Europe. The St Vincent Declaration, 1989, encouraged the development of multidisciplinary clinics in Europe, and called for a 50% reduction in the rate of lower limb amputations for diabetic gangrene within 5 years. In the United States, Healthy People 2000 established National Health Promotion and Disease Prevention objectives, for the 1990s decade. Specific diabetes objectives included reducing the frequency of foot ulcers in people with diabetes and reducing the rate of lower extremity amputations. In 1998, Jennifer Mayfield and colleagues published the first American Diabetes Association (ADA) technical review on preventive foot care in people with diabetes. The review



10    Contemporary Management of the Diabetic Foot was based on original research published in the English language peer reviewed literature. The unique nature of this review is that research quality was graded with preference given to studies that provided patient-oriented outcomes or clinically relevant care, rather than disease-oriented care. This technical review served as the basis for ADA’s first Position Statement on Preventive Foot Care for People with Diabetes.

UNDERSTANDING CAUSAL PATHWAYS TO AMPUTATION AND ULCERATION In 1990, Roger Pecoraro and colleagues defined the causal path­ways responsible for 80 consecutive initial diabetic lower extremity amputations, performed at a Veterans Affairs Medical Center, over a 30-month interval from 1984 to 1987. Causal pathways either singular or composed of various com­bi­­nations of seven potential causes (ischemia, infection, neuro­pathy, faulty wound healing, minor trauma, cutaneous ulcera­tion and gangrene) were determined empirically. Eight frequent groups of component causes resulted in 73% of the amputations. Most pathways were composed of multiple causes, with only critical ischemia from acute arterial occlusions responsible for amputations as a unitary cause. The causal sequence of minor trauma, cutaneous ulceration and wound healing failure applied to 72% of the amputations (Fig. 5). Absent protective sensation was considered to be a component cause in 82% of the amputations. Infection was

a common complicating factor and most often affected cases with chronic-wound healing failure. Ischemia was a causal factor in 46% of amputations, and gangrene occurred in combi­nation with both ischemia and infection. In 69 of 80 amputations, the authors identified a potentially preventable pivotal event, in most cases an episode involving minor trauma that caused cutaneous injury. Gayle Reiber and colleagues, in 1998, identified causal pathways for incident diabetic foot ulcers in 148 patients from two settings, Manchester (UK) and Seattle (Washington). The investigators identified the triad of neuropathy, minor foot trauma and foot deformity in more than 63% of patient’s causal pathways to foot ulcers. The clinical and public health implication of Roger Pecoraro’s and Gayle Reiber’s investi­ gations is that targeting and removal of one or more compo­ nent causes may prevent or delay the development of diabetic foot ulcers and amputations.

EUROPEAN INITIATIVES IN THE 1990s Two important European initiatives at the end of the 1990s decade supported and encouraged the team approach to diabetic foot care and prevention of amputations. The Diabetic Foot Study Group of the European Association for the Study of Diabetes was set up in 1998 through the motivation of Professor Andrew Boulton. By the mid-1990s, it was accepted that a team approach to diabetic foot care, with

Fig. 5  Causal pathway to amputation, with essential contributions from diabetes-related pathophysiology (neuropathy), initiating environmental event (minor trauma), formation of foot lesion (ulcer) and subsequent wound healing complications. Gangrene is the terminal event of this causal chain, which requires the interaction of all preceding components before becoming sufficient to cause amputation (Courtesy: Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention, Diabetes Care. 1990;13(5):513-21. Reprinted with permission of the ADA, Inc. Copyright 1990.)



Historical Notes on a Modern Disease: The Diabetic Foot    11 a well-structured organization in appropriate facilities, could reduce the risk of development and progression of diabetic foot disorders. Sir Karel Bakker, MD, noted that although guidelines on the prevention, diagnosis and management of the diabetic foot had been formulated in several countries, the contents of these guidelines were often inconsistent. This gave rise to the International Working Group on the Diabetic Foot (IWGDF). Through a process of consensus, this group produced a document, the International Consensus on the Diabetic Foot, in 1999.

THE TWENTY-FIRST CENTURY In the first decade of the 21st century, diabetes has emerged from what had been a rare disease, during the Age of Antiquity and the Middle Ages, to a global epidemic affecting over 350 million people worldwide. By 2030, the global estimate is expected to rise to 552 million people. Of the many serious complications that can affect people with diabetes, history has shown us that foot complications take the greatest toll. The Eurodiale diabetic foot ulcer (DFU) study, a collaboration of 14 European centers, was the first large prospective multicenter study to investigate the frequency of and risk factors for DFU recurrence after healing, during a 3-year follow-up period. In 2003–2004, all patients treated in participating centers because of a new foot ulcer (n = 1229) were enrolled in this observational study. Independent baseline predictors of nonhealing in the whole study population were older age, male sex, heart failure, the inability to stand or walk without help, end-stage renal disease, larger ulcer size, peripheral neuropathy and peripheral arterial disease. On November 14, 2005, World Diabetes Day, the Inter­ national Diabetes Federation (IDF) launched a year-long campaign to highlight the need for urgent action to bring

Fig. 6 Diabetes leads to amputation (World Diabetes Day, 2005). Tanzania issued this commemorative postage stamp in 2005. The denomination of the stamp is 350/= TZS (Tanzania Shillings) equivalent to 0.226 USD

about improvement in diabetes care. The theme for this campaign was Diabetes and Foot Care, Time to Act. The IDF Consultative Section and IWGDF produced the publication, Diabetes and Foot Care, under the direction of Sir Karel Bakker. The aim of this publication was to inform people about the extent of diabetic foot problems worldwide, to persuade them that action is both possible and affordable, and to warn them of the consequences of not taking action. As part of this global initiative Tanzania, a developing country in East Africa, and Brazil issued commemorative postage stamps to raise awareness of the diabetic foot and lower extremity amputations (Figs 6 and 7).

Fig. 7  Commemorative postage stamp issued by Brazil to commemorate IDF’s World Diabetes Day



12    Contemporary Management of the Diabetic Foot

CLINICAL PRACTICE GUIDELINES AND INTERNATIONAL CONSENSUS The creation of evidence based clinical practice guidelines and international consensus have been important developments for management of the diabetic foot. The IWGDF became the International Diabetes Federation’s consultative section on the diabetic foot in 2000. The International Consensus on the Diabetic Foot was updated in 2007, and in 2011 the IWGDF published three important clinical practice guidelines: Practical guidelines on the management and prevention of the diabetic foot 2011, (Karel Bakker); Specific guidelines for the treatment of diabetic foot infections 2011, (Benjamin Lipsky); and Specific guidelines for the diagnosis and treatment of peripheral arterial disease in a patient with diabetes and ulceration of the foot 2011, (Nicolaas Schaper). The American Diabetes Association published two noteworthy Task Force reports: Comprehensive Foot Exami­ nation and Risk Assessment, in 2008, (Andrew Boulton); and The Diabetic Charcot Foot, in 2011 (Lee Rogers). The GermanAustrian Consensus on Operative Treatment of Charcot Neuroarthropathy: a Perspective by the Charcot Task Force of the German Association for Foot Surgery was published in 2011 (Armin Koller). The Infectious Diseases Society of America published a comprehensive, evidence based approach to the management of diabetic foot infections, The 2012 Infectious Diseases Society of America Clinical Practice Guideline for the Diagnosis and Treatment of Diabetic Foot Infections, in 2012 (Benjamin Lipsky). The team approach to the prevention of lower extremity amputations is highlighted in the Journal of Vascular Surgery supplement, Strategies to Prevent and Heal Diabetic Foot

Ulcers: Building a Partnership for Amputation Prevention, in 2010 (Joseph Mills, David Armstrong and George Andros, Guest Editors). The total number of PubMed indexed publications on the diabetic foot increased, 20-fold, from 205 articles in the 1970s, when the author began his career, to over 4,100 articles in the first decade of the 21st century. We are now witnessing an exciting new chapter being written in the history of the diabetic foot. There is hopefulness that our efforts will make a tangible difference to preserve limbs, to improve functional outcomes and to maintain a better quality of life for the millions of people around the world who are grievously affected by the foot complications of diabetes.

ACKNOWLEDGMENTS I wish to thank Arlene Shaner, Acting Curator and Reference Librarian for Historical Collections, The New York Academy of Medicine Library, and Kristine M Scannell, Medical Librarian, VA Medical Center, Lebanon, Pennsylvania.

SUGGESTED READING 1. Bliss, Michael. The Discovery of Insulin. The University of Chicago Press (ISBN: 0-226-05897-2); 1982. 2. Connor H. Some historical aspects of diabetic foot disease. Diabetes Metab Res Rev. 2008:24 (Suppl 1):S7-S13. 3. Sanders LJ. From Thebes to Toronto and the 21st century: An incredible journey. Feature Article. Diabetes Spectrum. 2002;15(1):56-60. 4. Sanders LJ, Robbins JM, Edmonds ME. History of the team approach to amputation prevention: Pioneers and milestones. J Vasc Surg. 2010;52:12S, 3S-16S.

CHAPTER

Surgical Anatomy of the Lower Limb and Foot

3 Shigeo Kono

ESSENTIAL ANATOMIC INFORMATION FOR FOOT CARE The foot may be divided into several units anatomically and functionally. The foot consists of forefoot, midfoot and hindfoot, and the bones of the foot are divided into tarsals, metatarsals and phalanges. The foot has the superior surface (dorsum) and the inferior one (plantar). The forefoot begins distal to metatarsocuneiform and cuboid joints, and includes 14 bones of the toes and 5 metatarsals. The midfoot contains the navicular, the cuboid and the three cuneiform bones. The hindfoot consists of the talus and the calcaneus.

Fig. 1  Bones of the foot

Bones Foot consists of 26 bones (7 tarsals, 5 metatarsals and 14 phalanges) with 2 sesamoid bones attached (Figs 1 to 4).

Forefoot Forefoot consists of phalanges (distal phalanx, middle phalanx and proximal phalanx) and metatarsal bones. Forefoot plays an important role when the foot leaves the ground during the toe-off phase of the gait cycle. In neuropathic diabetic foot, plantar pressure is increased in forefoot due to prominent



14    Contemporary Management of the Diabetic Foot

Fig. 2  Radiograph of the foot showing bones of the foot

Fig. 3  Bones of the foot in lateral view

metatarsal heads and toe deformities. Therefore diabetic foot ulcerations often occur in the forefoot. Phalanx: Basically, only the first toe (hallux) has two phalan­ ges (distal phalanx and proximal phalanx) and has only one interphalangeal (IP) joint. Rest of the four toes have three phalanges each, and have distal interphalangeal (DIP) joint and proximal interphalangeal (PIP) joint. Meta­tarso­phalan­ geal (MTP) joint connects the proximal phalanx and the metatarsal bone. The phalanges of the foot are similar to their counterparts in hands, but are much shorter and broader.

Metatarsal: The five metatarsal bones lie in the forefoot and connect the tarsals and phalanges. Their bases articulate with the lesser tarsals proximally, and their heads articulate with adjacent phalangeal bases distally. The first metatarsal is the shortest, broadest and strongest of the five metatarsals. It articulates on the sesamoid bones located in the tendon of flexor hallucis brevis. The base articulates with the medial cuneiform and the tarsometatarsal ligaments are attached between them. The second metatarsal is the longest and the least mobile as the position of its base is recessed in the tarsometatarsal joint. The third metatarsal



15    Contemporary Management of the Diabetic Foot

Fig. 4  Radiograph showing bones of the foot in lateral view

articulates with the lateral cuneiform. The fourth and fifth metatarsals articulate with the cuboid. The fifth metatarsal has a tuberosity (styloid process) on the lateral side of its base which serves as the insertion site of the tendon of the fibularis (peroneus) brevis. The styloid process is often prone to traumatic or stress fractures.

Midfoot Midfoot consists of the three cuneiforms, the navicular and the cuboid. The midfoot articulates with the hindfoot through Chopart’s joint (transverse tarsal joint) and on the forefoot at the metatarsal bases through the Lisfranc joint (tarsometatarsal joint). The midfoot is located at the center of the arch of the foot.

Hindfoot Hindfoot consists of the talus and the calcaneus. Hindfoot supports weight while standing and walking. The talus articulates with navicular, calcaneus, tibia and fibula. The talus articulates with the tibia and fibula by the talocrural joint (ankle joint) and plays a pivotal role in the ankle movement. The talus has no muscular attachments and 60–70% of its surface is covered by articular cartilage. The anterior portion of the talar trochlea is wider than the posterior portion, which determines the stability of the ankle joint at the given position. Fracture of the talus often leads to a vascular necrosis. The calcaneus is the largest tarsal bone and lies under the talus. The body weight is mostly borne by the calcaneus. The articulation with the talus forms a groove (the sinus tarsi). The posterior surface of the calcaneus provides the insertion point for the Achilles tendon. The calcaneus articulates anteriorly with the cuboid.

Muscles The muscles of the foot are divided as extrinsic and intrinsic. Extrinsic muscles originate from the leg or thigh and are inserted into the foot while intrinsic muscles have both origin and insertion within the foot. The former causes more power or movement while the latter works ancillary. These muscles and tendons contribute to support arch of the foot. The dysfunction of these muscles causes the deformities of the foot and toes. In the presence of infection, purulent discharge can travel along tendons and facilitate spreading of infection proximally. The extrinsic muscles consist of muscles from the superficial posterior, the deep posterior, the lateral and the anterior compartment. The superficial posterior compartment contains the posteriorly located flexors of the foot (the gastrocnemius and the soleus muscles). The deep posterior compartment consists of the tibialis posterior muscle and the long flexors. The lateral compartment contains the peroneus longus and brevis. The anterior compartment contains the dorsiflexors or extensors of the foot (the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and the peroneus tertius) (Figs 5 and 6).

Plantar Flexor Group in Posterior Compartment of Leg The triceps surae muscle: Triceps surae consists of the gastrocnemius and the soleus muscle. The origin of the gastrocnemius muscle is a posterior surface of medial and lateral femoral condyle via two heads, and that of the soleus muscle is the posterior tibia and proximal posterior-superior surface of fibula. The Achilles tendon is the combined tendon of these muscles and inserts into the posterior surface of calcaneus. The Achilles tendon is the largest tendon and its



16    Contemporary Management of the Diabetic Foot and second sacral nerve roots (S1, S2). These muscles play pivotal roles in the plantarflexion of the ankle joint during walking, running and jumping. It also prevents the body from falling anteriorly when a person stands. As the perforating veins between the superficial and deep veins penetrate these muscle layers, the repeated contraction of plantardorsiflexion works as a pump to promote venous circulation and help to prevent deep vein thrombosis. The tibialis posterior muscle: The tibialis posterior muscle originates from superior surface of leg and its tendon descends posterior to medial malleolus, and then inserts mainly to the medial surface of navicular and plantar surface of the first cuneiform. This muscle is innervated by the tibial nerve (L4, L5). The function of this muscle is mainly inversion of the foot (movement which medial-plantar surface of foot moves toward median plane) and very little plantarflexion of ankle joint (much less than triceps surae). It also helps to support medial longitudinal arch of the foot. Injury of this tendon may cause a flatfoot.

Fig. 5  Muscles of the leg

contracture leads to plantarflexed ankle joint. Triceps surae is innervated by the tibial nerve, which arises from the first

Fig. 6  Muscles of the dorsum of the foot

The flexor hallucis longus and the flexor digitorum longus muscles: The flexor hallucis longus muscle originates from the posterior surface of fibula and the adjacent interosseous membrane. The flexor digitorum longus muscle arises from the posterior surface of tibia. They insert into the plantar surface of base of each distal phalanx and innervated by tibial nerve (L5, S1, S2). They produce the flexion of the DIP joint, PIP joint and MTP joint, and also contribute to the plantarflexion of the ankle joint. They also work to support the longitudinal arch of the foot (Figs 7A and B).



17    Contemporary Management of the Diabetic Foot

A

B Figs 7A and B  Muscles of the sole of the foot

Dorsiflexor Group in the Anterior Compartment of the Leg

the foot. Foot-drop results when this muscle is paralyzed and make the patient to lift foot higher than usual during walking. This pattern of gait is called “steppage gait”.

The tibialis anterior muscle: The tibialis anterior muscle originates from the superior anteriolateral surface of tibia. The tendon crosses medially at the ankle and inserts to the medial surface of first cuneiform and plantar surface of first metatarsal base. It is innervated by the deep peroneal nerve, and its function is dorsiflexion of ankle joint and inversion of

The extensor hallucis longus and the extensor digitorum longus muscle: These muscles arise from the anterior surface of fibula and inserts to the dorsal surface of base of distal phalanx. These are innervated by the deep peroneal nerve, and they cause dorsiflexion of MTP joint as well as PIP and DIP joints (Figs 8A and B).



18    Contemporary Management of the Diabetic Foot

A

B Figs 8A and B  Muscles of the foot: (A) Lateral aspect; (B) Medial aspect

Muscle Groups in Lateral Compartment of the Leg The fibularis (peroneus) longus and brevis muscle: They arise from the fibula and their tendons descend posteriorly to the lateral malleolus. The fibularis (peroneal) longus tendon inserts into the plantar surface of the first cuneiform and base of the first metatarsal while the fibularis (peroneal) brevis tendon inserts into the base of the fifth metatarsal. They are innervated by the superficial peroneal nerve and plantiflex the ankle. The longus abducts the foot and the brevis everts it.

Intrinsic Muscles of the Foot Intrinsic muscles allow the movement of the toes and help to support the arch of the foot. The extensor digitorum brevis

muscle is the only dorsal intrinsic muscle and innervated by the deep peroneal nerve. There are four layers in the plantar intrinsic muscles, which are innervated by the tibial nerve (the medial or the lateral plantar nerve). Atrophy of the intrinsic muscles leads to deformities of toes. There are dorsal and plantar interossei muscles, dorsal interossei abduct (moving second to fourth digits away from the axis through the second metatarsal ray) and the plantar interossei muscles adduct (moving third to fifth digits toward the axis through the second metatarsal ray) the digits. The lumbrical muscles allow flexion of the MTP joints and extension of the PIP joints. The quadratus plantae muscle originates with two heads from the medial and lateral parts of the calcaneus and terminates in tendinous slip. They aid in toe flexion.



19    Contemporary Management of the Diabetic Foot

Joints, Ligaments and Retinaculum Ankle joint consists of the talus, the tibia and the fibula. The ankle joint is stabilized by the medial ligament (deltoid ligament) and the lateral ligament. Medial ligament has the tibionavicular, the tibiocalcaneal, the posterior tibiotalar and the anterior tibiotalar part. Lateral ligament consists of the anterior talofibular, the posterior talofibular and the calcaneofibular ligament. Ligamentous tear often results with ankle injuries. The subtalar joint (talocalcaneal joint) is surrounded by a fibrous capsule and stabilized by the interosseous, medial and lateral talocalcaneal ligaments, and cervical liga­ment. The talocalcaneonavicular joint consists of the ante­rior part of subtalar joint and the talonavicular joint, and are stabilized by the talonavicular and plantar calca­ neonavicular (spring) ligaments. The talotarsal joint has the subtalar joint and the talocalcaneonavicular joint. The calcaneocuboid joint is stabilized by the bifurcate, long plantar and plantar calcaneocuboid ligaments. The trans­ verse tarsal joint (midtarsal joint or Chopart’s joint) has the talocalcaneonavicular joint and the calcaneocuboid joint. The ligaments of the naviculocuneiform joint are the dorsal and plantar ligaments. The ligaments of cuboideonavicular, intercuneiform, and cuneocuboid joints are dorsal, plantar and interosseous ligaments respectively. The bones of the tarsometatarsal joints are connected by the dorsal and the plantar tarsometatarsal and interosseous cuneometatarsal ligaments. The ligaments of the intermetatarsal joints are the dorsal and plantar intermetatarsal ligaments, which are very strong, but are lacking between the first and second metatarsals. The ligaments of the MTP joints are the plantar, deep transverse metatarsal and collateral ligaments. The interphalangeal joints are stabilized by the medial collateral ligament, lateral collateral ligament and plantar ligament. The plantar fascia or aponeurosis is composed of a very strong and thick fibrous central part and a thinner medial and lateral part, and it is oriented mainly longitudinally. The central part is attached proximally to the medial calcaneal tuberosity and distally to the toes. The function of plantar aponeurosis is to support the longitudinal arch of the foot. At the ankle, the tendons of the muscles of the leg are bound by the deep fascia (retinacula). There are superior and inferior extensor retinacula, superior and inferior fibular retinacula, and a flexor retinaculum (Fig. 9).

Nerves of the Foot The foot is innervated by tibial, deep peroneal, superficial peroneal, sural and saphenous nerves. The saphenous nerve originates from the femoral nerve while others originate from the sciatic nerve (Figs 10 and 11). There are two types of foot muscles: extrinsic foot muscle that originates at the limb and intrinsic muscle that only

Fig. 9  Plantar aponeurosis and ligaments

Fig. 10  Nerves of the lower limb

exists within the foot. These muscles are innervated by tibial and peroneal nerve branched from the sciatic nerve. Tibial nerve controls the flexor muscles except the short and long peroneal muscle whereas the peroneal nerve controls the entire dorsiflexor muscles along with the short and long peroneal muscle.



20    Contemporary Management of the Diabetic Foot

A

B

Figs 11A and B  Cutaneous nerves of the foot: (A) Dorsal view; (B) Plantar view

The saphenous nerve runs medially posterior to the greater saphenous vein. The saphenous nerve provides cuta­neous innervation to the medial portion of the foot. The sciatic nerve provides most of the motor and sensory innervation of the foot and ankle. The sciatic nerve divides into the sural nerve, the common peroneal nerve and the tibial nerve. The common peroneal nerve divides into the superficial pero­neal nerve and the deep peroneal nerve. The sural nerve runs along the lateral side of the Achilles tendon and below the lateral malleolus. It provides sensory distribution of the lateral border of the foot. The superficial peroneal nerve (the musculocutaneous nerve) supplies the peroneus longus and brevis muscles, and provides the cutaneous sensory distribution to the dorsum of the foot and the first to fourth toes dorsally. The deep peroneal nerve supplies motor branches to the extensor hallucis longus, the tibialis anterior, the extensor digitorum longus and the peroneus tertius muscles. The deep peroneal nerve supplies the medial aspect of the second toe and the lateral side of the hallux. The tibial nerve supplies the heel, the medial sole of the foot and posterior portion of the leg. The tibial nerve divides into the medial and lateral plantar nerves, and innervates the intrinsic muscles except the extensor digitorum brevis. It supplies the cutaneous innervation of the plantar aspect of the foot. Tibial nerve runs through an area called the tarsal tunnel which is located posteriorly to the medial malleolus. When the pressure in the tarsal tunnel increases, tarsal tunnel syndrome or entrapment neuropathy results just like carpal tunnel syndrome in hand. Peroneal nerve is superficial when it encircles the fibular head and is commonly affected by external trauma or can be infected in leprosy resulting in foot drop.

Arteries and Veins of the Foot The popliteal artery divides into the anterior tibial artery, the posterior tibial artery and the peroneal artery (Figs 12 and 13).

Fig. 12  Arteries of the lower limb, anterior view

The anterior tibial artery passes under the superior and inferior extensor retinacula to the dorsum of the foot and becomes the dorsalis pedis artery. Medial and lateral branches (the anterior medial and lateral malleolar arteries) supply the ankle. The dorsalis pedis artery branches into the medial tarsal artery, the lateral tarsal artery, arcuate artery



21    Contemporary Management of the Diabetic Foot

Fig. 13  Arteries of the leg, posterior view

and the first dorsal metatarsal artery. The posterior tibial artery divides into the smaller terminal branch (medial plantar artery) and the larger terminal branch (the lateral plantar artery) after passing under the flexor retinaculum. The lateral plantar artery anastomoses with the terminal branch of the dorsalis pedis artery (deep plantar artery) to create the deep plantar arch. The plantar arch supplies three perforating and four plantar metatarsal branches. The peroneal artery supplies the lateral and posterior aspects of the calcaneus via the calcaneal branches (Figs 14A and B). The venous system consists of deep and superficial veins. The deep vein runs along the artery. Both superficial and deep veins communicate with each other (Fig. 15). The deep veins are popliteal vein, the anterior tibial vein and the posterior tibial vein. The superficial veins are the great saphenous vein reaching the medial lower limb up to anterior medial malleolus and the small saphenous vein reaching up to the lateral lower limb. In diabetics, infrapopliteal vessels are commonly obliterated while the foot vessels like dorsalis pedis and posterior tibial are patent. This gives window of opportunity to vascular surgeons to carry out infrapopliteal bypass surgery in patients with ischemic diabetic foot. The human foot is very complex, but at the same time very sophisticated structure with 26 bones, 33 joints and over 100

muscles, tendons and ligaments. The foot provides us bipedal gait, shock absorption, balance, and afferent and efferent impulses through its complex system of nerves.

NORMAL WEIGHT BEARING The weight of the body, during walking, is borne mostly by one leg at a time. The tibia transmits weight to the talus and to the rest of the foot. When the foot first touches the ground while walking, the heel bone (calcaneus) takes all the weight, however, the other foot as well, is still sharing some of the body weight. As soon as the heel is firmly on the ground, the other foot leaves the ground. The forefoot then comes down on to the ground but usually the lateral border of the foot takes on the weight first, transmitting it through the cuboid bone and base of the fifth metatarsal. A moment later, the whole foot is on the ground (stance phase). Thus the weight is transmitted from calcaneus, cuboid, base of the fifth metatarsal and the heads of all five metatarsals. As the other foot swings forward, the heel begins to leave the ground and the whole weight is on the forefoot. Finally a strong contraction of the flexors pushes the body forward to transfer its weight on the other foot, which by now is in position. In the stance phase of one gait cycle, when the foot



22    Contemporary Management of the Diabetic Foot

A

B Figs 14A and B  Arteries of the foot, dorsal and plantar aspects

comes down, it rests on the back of the heel, then additionally on the underside of the metatarsals and finally on to the heads of metatarsals to push off for the next step. While the foot is standing on the ground, it is rather like an arch sparing the midfoot from weight bearing. The medial arch of the foot is formed by calcaneus posteriorly and first three metatarsals anteriorly. The lateral two metatarsals

form the lateral arch, which is relatively flat and works like a tie-beam to support the medial arch. The plantar apo­ neuro­sis connects the arches anteroposteriorly and is like a bow string. The intricate mechanism, involving joints of the foot, ligaments, muscles, bones, and the supple and resilient plantar tissue, makes our walking and running so comfortable that even barefoot walking does not lead to



23    Contemporary Management of the Diabetic Foot

Weight Bearing in Diabetic Neuropathy Chronic hyperglycemia and polyneuropathy causing damage to sensory, motor, and autonomic nerve fibers lead to certain functional and structural changes in the foot. Chronic hyperglycemia leads to nonenzymatic glycosylation of proteins causing limited joint mobility, reduction in the elastic tissues of plantar skin, and underlying collagen tissue. Foot deformities occur as a result of atrophy of intrinsic muscles of the foot and previous scars and toe amputations alter the architecture of the foot. Loss of elasticity, resilience, flexibility, and free joint move­ ments lead to a relatively rigid and unstable foot with altered weight-bearing areas. Bony prominences develop underneath the foot pushing the fibrofatty shock-absorbing tissue forward, exposing the condyles of the metatarsal heads. The combination of various risk factors in the presence of neuropathy increase the plantar pressures significantly in the forefoot and hallux and increases the risk of foot ulceration. Fig. 15  Veins of the lower limb

any foot problems. It is fascinating to watch the slow motion television clips of foot ballers and cricket pace bowlers. Their feet display several motions like acceleration, deceleration, sudden stop, jumping, twisting and turning and so on, and all this fleeting past within that one stare. The supreme coordination owes itself to protective sensations (afferent and efferent impulses), joint sense, continuous weight transfer and silver quick reflexes.

SUGGESTED READING 1. Drake RL, Vogl W. Gray’s Anatomy for Students, Elsevier, 2005. 2. Herausgegeben von R. Putzd. Sobotta RP. Atlas der Anatomie des Menschen Urban & Fisher Verlag, Munchen, Germany, 2000. 3. Netter FH. Atlas of Human Anatomy, 5th edition, Saunders, 2010. 4. Pendsey S. Diabetic Foot: A clinical Atlas–New Delhi: Jaypee Brothers Publishers; 2003. 5. Petra Kopf-Maier. Wolf-Heidegger’s Atlas of Human Anatomy, 6th edition, Basel, Switzerland: Karger; 2005. 6. Standring S. Gray’s Anatomy, 40th edition, Elsevier, 2008.

CHAPTER

4

The Global Burden of Diabetic Foot

Zulfiqarali G Abbas

INTRODUCTION AND EPIDEMIOLOGY Diabetes mellitus is a serious chronic condition with devastat­ ing implications for affected patients across the globe. With little discrimination, it affects rich and poor, young and old, and industrialized or the economically less-developed in equal measure. In 2011, the global prevalence of diabetes was 366 million (i.e. > 8.3% of the adult population across the globe). This figure is predicted to reach 552 million by 2030— a consequence of longer life expectancy, sedentary lifestyle, and changing dietary patterns. In China, the Middle East and Africa, the number of people with diabetes has increased significantly and is expected to be more than double in the coming decades. Similarly, the number of people diagnosed with diabetes is increasing in South-East Asia, South and Central America, Western Pacific, North America and Caribbean and Europe. Majority (80%) of persons with diabetes live in low and middle-income countries. In African countries in 2011, 14.7 million persons were estimated to have diabetes and it is projected that by 2030, the overall increase in prevalence will be by 90%. There is now substantial evidence confirming that diabetes has indeed reached epidemic proportions in many developing nations, and is expected to become a major public health issue as new economies emerge. Among the top 10 countries with the largest numbers of persons with diabetes, the rise in prevalence is expected to be phenomenal over the next couple of decades from 2011 to 2030 (Table 1). Even for populations in the idyllic islands of the Caribbean, diabetes is taking a toll and is significantly associated with complications like cerebrovascular, ischemic heart and renal disease. Not surprisingly, diabetes remains a leading cause of morbidity and mortality in both developed and less-

Table 1  Top 10 countries or territories of number of people with diabetes (20–79 years, 2011 and 2030) Country/territory 2011 (millions)

Country/territory

2030 (millions)

China

90.0

China

129.7

India

61.3

India

101.2

USA

23.7

USA

29.6

Russian Federation

12.6

Brazil

19.6

Brazil

12.4

Bangladesh

16.8

Japan

10.7

Mexico

16.4

Mexico

10.3

Russian Federation

14.1

Bangladesh

8.4

Egypt

12.4

Egypt

7.3

Indonesia

11.8

Indonesia

7.3

Pakistan

11.4

Source: International Diabetes Federation. Diabetes Atlas, 5th edition. Brussels, Belgium: International Diabetes Federation; 2011.

developed countries, and imposes a heavy burden on the health services. This burden has various components each of which impacts in different ways and which we will delineate further in this chapter. Compounding the problem is the fact that allocated resources for diabetes and its complications in both developed and less-developed countries are falling. Reasons for this state of affairs include competition for available human and financial resources from services dealing with other chronic medical conditions, such as pulmonary and cardiac disease, hypertension and cancer. Then, there are those parts of the globe, mostly comprising of developing countries, where infectious diseases, such as tuberculosis,



The Global Burden of Diabetic Foot    25 human immunodeficiency virus infection, and diarrheal and parasitic infections, which already consume a significant proportion of budgets allocated for healthcare. Overriding all of this is the downturn in the global economies and the ever present dark cloud of an unending global economic recession. For economically less-developed countries that are dependent on foreign aid, the lack of funding is a vicious cycle—an unhealthy adult population becomes unproductive, leading in turn to further downturn in output. Diabetes imposes a large economic burden on the individual, family, relatives, friends, national healthcare system, and the productivity of a country. Healthcare expenditure due to diabetes accounted for 11% of total healthcare expenditure in the world in 2011. The constant need for resources is underscored by the fact that for 80% of the countries covered in a 2011 report produced by the International Diabetes Federation, 5–18% of the total healthcare expenditure is apportioned to diabetes. No one is immune from the enormous expenditures associated with the care of persons with diabetes. For example, although healthcare systems and facilities underwrite a significant proportion of medical spending on diabetes, there is a cost for persons living with diabetes; these include medications, special diets, not to mention the unquantified income lost to days off work. Those living in low and middle income countries pay a large share of healthcare expenditures out of their own savings, because of lack of access to health insurance and publicly available medical services. At the same time, diabetic complications, such as microvascular disease (nephropathy and retinopathy), neuropathy (peripheral and autonomic), peripheral arterial disease, and foot ulcer disease, are increasing in incidence and prevalence, causing substantial disability and reduction in life expectancy, and posing enormous costs for health services in countries where financial resources and availability of trained personnel are already limited or in short supply. Of the various, serious complications (e.g. kidney failure or blindness) that can affect individuals with diabetes mellitus, it is the complications related to the foot and rest of the lower limb that take the greatest toll. Across the globe, 40–60% of all lower extremity nontraumatic amputations are performed in patients with diabetes. Foot complications, especially serious ones like the septic limb, can be serious and costly. In North America and Western Europe, it has long been established that a care strategy that combines prevention, multidisciplinary treatment of foot ulcers, appropriate organization, close monitoring of patients, and education of people with diabetes as well as healthcare professionals can lead to significant reductions in amputation rates by up to 85%. In particular, since most of the foot ulcers in less-developed settings are of neuropathic in origin, they are potentially curable. This objective should motivate the advocacy of those striving to make a difference in the lives of the afflicted. Of the various complications associated with diabetes, foot problems are among the most serious and costly. The rising

prevalence of diabetes all over the world has brought with it a parallel increase in the number of lower limb amputations performed as a result of progressive foot ulcer disease. Epidemiological reports as recently as 6 years ago indicated that over 1 million amputations were being performed on persons with diabetes each year. Those estimates suggested that a leg was being lost to diabetes somewhere in the world every 30 seconds. When the estimates of morbidity are calculated using the relatively more recent prevalence data of 2011, it works out that a lower limb is lost due to diabetes globally every 20 seconds. A majority of these amputations are preceded by ulcers. Only two-thirds of ulcers eventually heal; the remaining one-third is associated with progression to some form of major or minor amputation. Generally, the median time of healing for an ulcer is approximately 6 months. Thus, both ulcers and subsequent amputations have enormous impact on people’s lives, often leading to reduced independence, social isolation, and psychological stress. The cost of managing foot problems in diabetic popu­ la­tions is unsustainable for many underdeveloped count­ries, particularly if amputation results in prolonged hospitali­ zation, rehabilitation, and an increased need for home care and social services. Unfortunately, it appears that the burden of diabetic foot disease is set to increase in the foreseeable future with increasing life expectancy and prevalence of foot disease risk factors, such as peripheral neuropathy and vascular disease, which are present in more than 10% of people at the time of diagnosis of type 2 diabetes. Moreover, for a person with diabetes, the lifetime risk of developing a foot ulcer is approximately 15%. Most of the European countries have established multidisciplinary foot clinics and podiatry services, and have implemented international guidelines on diabetic foot care. However, the majority of less-developed countries either does not have or are unable to sustain such multidisciplinary foot clinics. Boulton et al. have made the important point that the overall cost of diabetic foot lesions is reduced by interventions aimed at preventing foot ulcers, and management strategies implemented for ulcer healing that shorten wound healing time and prevent amputation. They go on to compare and contrast the magnitude of the costs to United States (US) healthcare ($10.9 billion) attributed to diabetic foot ulceration and amputations. They also estimated that in the United Kingdom (UK) 5% (£3 billion) of total National Health Service expenditures was attributable to diabetes and that the total annual cost of diabetes-related foot complications was in the realm of £252 million. Despite Myriad publications on foot complications in diabetes from industrialized countries, there is a relative paucity of medical literature on the epidemiologic, clinical and public health-related aspects of diabetic foot compli­ cations in less-developed countries. And, because of the dearth of interventions, relevant cost analyzes of diabetic



26    Contemporary Management of the Diabetic Foot foot ulcer management are lacking. The burden of diabetic foot complications from a global perspective is difficult to quantify for reasons that include disparate differences in per capita income, disparities in access to healthcare, little or no surveillance activities, shortages of trained doctors, nurses and ancillary personnel skilled in the management of limb complications, differences in the availability of resources (e.g. microbiology and radiology services), limited availability of antimicrobials, and finally sustainable programs for patient follow-up. One should bear in mind that identification and ascertain­ ment of the degree of burden is but the first step in the general characterization of diabetic foot disease burden. Several important factors contribute to this burden. These include the costs of identifying at-risk patients through follow-up or surveillance; treatment costs of the different types of diabetic foot lesions or complications (ulcers, cellulitis, gangrene); severity of the lesions themselves (e.g. size, depth, and presence of localized or systemic sepsis); costs of routine investigations (e.g. Doppler studies, blood tests, neurosensory studies); costs of microbiology services (e.g. blood, bone and deep tissue cultures; deep tissue biopsies; antimicrobial susceptibility testing) and imaging studies. An added cost is associated with follow-up of diabetic patients with foot ulcers until healing has been achieved, and is attributable to the finances necessary for staffing and employing ancillary healthcare personnel, dressings, topical agents, general supplies for debridement wound management, and antimicro­bial agents. The aforementioned costings do not include those of amputation surgery. For patients who end up proceeding to amputation, the two items that contribute most to overall costs are inpatient care and postsurgical topical treatment of wounds (Table 2). Infections push attributable costs to a different level. For foot ulcers, infections are either community-acquired or nosocomial. The former is complex and depends of a multitude of factors that are beyond the control of the caregiver and include the age of the patient, the duration of diabetes and the degree of glycemic control, whether the person has regular medical follow-up, and the educational Table 2  Direct cost after primary healing of foot ulcer or healing with amputation Primary healed without ischemia

16,437 USD

Primary healed with ischemia

27,203 USD

Minor amputation

43,890 USD

Major amputation

64,265 USD

Source: Time to Act. Diabetes and Foot Care. A joint publication of the International Diabetes Federation and the International Working Group on the Diabetic Foot. International Diabetes Federation; 2005.

level of the person. Acquisition of a nosocomial infection is dependent on the scrupulousness of surgical technique and infection control practices and operating procedures, intrinsic risk factors peculiar to the patient (e.g. age, comorbidities, tobacco use), and the attention to infection control by nursing and medical personnel during the postoperative period. In North America and Western Europe, the dollar costs of nosocomial infections runs into billions. While these added costs are largely manageable in industrialized nations, they remain unsustainable in low-income countries. Additional outpatient visits, and the various orthopedic and surgical appliances used in the management of infected ulcers further increase the costs. Encompassing all these factors is the fact that total cost for healing a foot ulcer is largely dependent on a complex interplay of patient intrinsic factors and state of affairs at the initial presentation: size of the ulcer and its duration, whether the patient delayed in seeking medical attention, the degree of local or systemic infection, the degree of glycemic control, the socioeconomic status of the patient, and whether the patient actually paid attention to foot care and hygiene. In some programs, rehabilitation in specialized units is an added cost. The loss of productivity caused by unemployment or sick leave during the foot ulcer management is an added cost to the community that largely remains unquantified in low-income countries. Finally, there is an additional cost associated with the implementation and institution of ulcer prevention programs. This additional cost is allayed by the fact that prevention of amputation results in enormous cost savings that have been ascertained or confirmed by evidence-based studies carried out in both developed and low-income countries. A good example of the latter is the Step-by-Step foot program model that has been instituted successfully in Tanzania, India, and other low-income countries. Thus, prevention of foot ulcers and, therefore, many amputations remain the sine qua non for achieving reductions in current high expenditures.

CHARACTERIZATION OF THE BURDEN OF THE DIABETIC FOOT The burden of the diabetic foot, from a global perspective, basically comprises two elements. The first element— the clinical burden—deals with all clinical aspects and requirements for managing the condition. The second element is more an issue regarding the public health implications of the diabetic foot in general—i.e. issues associated with epidemiology, surveillance, survival analyses, policy making, and drug formulary concerns. The clinical element of diabetic foot burden can be further stratified by issues pertinent to the individual with diabetes and issues relevant to the caregiver. For the former, the burden is basically quantified in terms of the morbidity (e.g. incidence and prevalence of ulcers, rates of infections, amputations, sepsis); being unable to do



The Global Burden of Diabetic Foot    27 the things that one otherwise would have liked to do in life; the cost of going to the doctor (e.g. cost of transport to the healthcare facility), the cost of medications, special diets, and specialty shoes; the cost of antibiotics and the additional cost of antimicrobial-resistant infection; the loss of income from days away from work; and the overall loss to the national economy. The care level can be stratified by splitting into healthcare facilities and personnel. For the healthcare facilities, the burden involves having the necessary resources for equipment and instruments to investigate the diabetic foot, maintaining a radiology department and microbiology laboratory, and provision of adequate surgical services. The personnel burden involves the training of ancillary staffing and surgeons, and all the other unquantified costs of managing patients in the inpatient and outpatients for prolonged period. The maintenance of microbiology laboratory is a major burden largely because of the need for sustainability, replacement of reagents, and the need for quality control practices; the latter requiring skilled, well-trained personnel. The second component of burden is public health implica­tions: the need for surveillance to analyze outcomes and interventions. But, more than that is the need to main­ tain and sustain surveillance activities—computers, data analysis, policy making at the Ministry of Health, and cost of interventions like the Step by Step Foot Project. The limited amount of literature on diabetic foot complications in economically less-developed countries patients consists largely of descriptive studies of diabetes populations. However, because of nonuniform case definitions, varying diagnostic and classification criteria used in many of these studies, and reporting inconsistencies, inferences and extrapolation of data from one country to another remain untenable. On a positive note, the fact that we have recognized or identified these limitations is an impetus for addressing global issues in a more comprehensive manner. The added advantage of this approach is increasing the feasibility of using these data for transcontinental comparisons of these populations and interventions. Peripheral neuropathy is the principal underlying risk factor in the pathogenesis of foot ulcers in diabetes patients. Published data from the Western world suggests that peripheral neuropathy is the most common complication of diabetes and is generally associated with age, duration of diabetes, male gender, alcohol intake, glycemic control and smoking. The ensuing sequelae include callosities, cracked soles, fissures, or direct breakdown of the skin, which are all contributory factors in the pathogenesis of foot ulcers that can progress to infection, necrosis, gangrene, loss of the limb, or death. These ulcers become portals of entry for bacteria, causing infections (often polymicrobial) that spread rapidly through the plantar spaces of the foot resulting in overwhelming tissue destruction and osteomyelitis, the primary reason for major amputation in the neuropathic

Table 3  Burden of management of diabetic foot ulcer •  Repeated visits to the clinic •  Offloading devices •  Frequent hospitalization •  Investigations: Laboratory tests, imaging •  Medications: Higher antibiotics •  Surgeries •  Specialized footwear •  Rehabilitation •  Absenteeism from work

foot. Therefore, it is not surprising that peripheral neuropathy has become the most common cause of prolonged hospital admission and contributes significantly to the attributable morbidity associated with the development of foot complications in diabetic patients. Optimal management of these diabetic foot complications requires involvement of the relevant inpatient and outpatient medical services. Such services involve diabetologists and ancillary medical and trained nursing staff; surgeons with experience in the management of foot ulcers, gangrene, necrotizing infections, and amputations; radiology and clinical microbiology services; and pharmacists familiar with the availability and costs of essential agents used for managing diabetes and infections (Table 3). Peripheral arterial disease causes considerable morbidity in diabetes patients and is defined clinically by intermittent claudication, rest pain, absence of the pedal pulses, or abnor­ malities on noninvasive vascular assessment (e.g. Doppler studies). Although there are no peripheral arterial lesions specific to diabetes, the pattern of arteriosclerosis in the diabetic patient is somewhat different from that seen in nondiabetic patients. It is more common, generally affects younger individuals, does not vary by sex, has a faster rate of progression, and tends to be multisegmental and peripheral. Because of the propensity for progressing to tissue necrosis and gangrene, peripheral arterial disease increases the risk of foot ulceration, which in turn increases the risk of localized or widespread infection of the lower limb and eventually limb loss. Published reports suggest that foot complications in patients with diabetes in many less-developed countries in Africa, the Caribbean, and South America are generally infective and/or neuropathic in origin rather than due to peripheral arterial disease. However, because communities across the globe are becoming more urbanized, the epidemiology of peripheral arterial disease is changing across the continent with corresponding increases in prevalence rates of peripheral arterial disease in diabetes populations. In addition, the increased marketing strategies of large tobacco



28    Contemporary Management of the Diabetic Foot companies to target populations in less-developed countries has compounded the problem by causing a recognized public health disaster—increase in tobacco-related complications, including the increasing prevalence of peripheral arterial disease and its attendant outcomes in diabetes populations with existing foot disease. Poverty is associated with foot ulceration; unhygienic conditions lead to infectious sequelae. Other major factors contributing to development of the diabetic foot include walking barefoot or delayed presentation for initial clinical assessment. Barefoot walking, a common practice in many less-developed countries is directly linked to low income but may often harbor cultural undertones. For diabetes patients shrouded in poverty, even a simple purchase of appropriate footwear is often unaffordable or is low down in the priority. For diabetes patients with peripheral neuropathy, inadvertent trauma or injuries to the foot is liable to go unnoticed until the patient finally becomes symptomatic, presenting with an ulcer or injury that has progressed to fulminating foot sepsis. Patients who neither take the time to take care of themselves and address foot care nor attend the diabetes outpatient clinic for follow-up care, advice, or education are most at risk developing infected foot ulcers. Lack of sensation in the anesthetic foot causes ordinarily conscientious, responsible patients to be unaware of inadvertent injuries sustained through inappropriate or ill-fitting footwear, walking barefoot on hot surface under the midday sun, or use of keratolytic agents or razor blades to cut toenails and callosities. The global burden of the diabetic foot cannot be ameliorated unless poverty and access to healthcare is addressed by governments and nongovernmental agencies. Even in the US, there is a sizable proportion (10%) of the population without any form of access to healthcare (Table 4).

THE BURDEN OF THE SEPTIC DIABETIC FOOT The burden of diabetes cannot be addressed without a discussion of infectious diseases. Foot infections are com­ monly seen in patients with diabetes and may be the imme­­ diate cause for amputation in 25% of this patient population. Foot infections are a common, complex, and serious problem Table 4  Socioeconomic barriers to foot care in developing world •  High prevalence of diabetes •  Lack of awareness about diabetic foot care •  High illiteracy levels •  Lack of foot care education •  Lack of structured podiatry services Source: Time to Act. Diabetes and Foot Care. A joint publication of the International Diabetes Federation and the International Working Group on the Diabetic Foot. International Diabetes Federation; 2005.

in diabetes patients and usually begin in foot ulcers that are associated with peripheral neuropathy, peripheral arterial disease, or certain metabolic disturbances. Various reports suggest that foot lesions in patients in economically lessdeveloped countries are infective and/or neuropathic in origin rather than due to peripheral arterial disease, as is often the case in Western countries. In addition, patients often present to hospital when gangrene of the foot is already established, at which point sepsis may remain intractable to conventional supportive treatment with parenteral antimicrobials, intra­ venous fluids and insulin. Such foot infections may carry substantial mortality risks in such diabetic population. Overriding the global burden of diabetic foot disease is access to healthcare; with no access there is a virtual certainty that a person with a diabetic foot ulcer will experience exacerbation of the ulcer with no healing and onset of infection leading to loss of affected limb, systemic infection, or death. The most published reports confirm that foot lesions in less-developed countries commonly have an infectious etiology and are associated with peripheral neuropathy and prolonged inpatient stays. Chronic osteomyelitis is associated with peripheral neuropathy and generally underlies chronic foot ulcers, developing through contiguous spread of soft tissue infection from an ulcer to the underlying bone. Unless necrotic bone is surgically resected, patients remain partially or completely immobile. In many less-developed African countries, such management may not be feasible for lack of facilities or skilled personnel. Where such resources are available, main­ tenance of such services may be unsustainable. For effec­ tive management of chronic osteomyelitis, radiology and microbiology services remain indispensable. Otherwise, patients end up being treated via blind empiricism—a form of indiscriminate prescribing that adds to the financial burden faced by healthcare services with already limited resources. In Africa, patients often present only with the onset of gangrene or sepsis that proves intractable to conventional supportive treatment, resulting in progression to systemic infection and significant mortality. Because patients with infected foot ulcers frequently feel no pain (neuropathy) and many have no systemic symptoms until late in the course of the condition, medical providers often presume (incorrectly) a degree of self-neglect. It is not surprising, therefore, that foot infections are especially common where there is no available foot service as lesions are ignored or detected relatively late in the course of the infection after unsuccessful home therapy, such as hot water soaking or other unproven home therapies. Foot infections of this nature culminate in the onset of gangrene ensuring amputation of the foot or even an entire limb, if not death from overwhelming sepsis (Table 5).

PREVENTION The exact incidence of foot ulceration and infection in diabetes patients varies not just from country to country but even



The Global Burden of Diabetic Foot    29 Table 5  Global burden of limb amputation •

Every 30 seconds, a limb is lost due to diabetes



One million limb amputations occur yearly in persons with diabetics



Diabetics are 40 times likely to lose a limb than nondiabetics



Seventy percent of all limb amputations happen to people with diabetes



Five years mortality after limb amputation is 70% in diabetes



Contralateral limb amputation rate is 50% in 5 years in diabetes



Life time risk of foot ulcer in diabetics is 15%



Eighty-five percent of the limb amputation is preceded by trivial foot lesions

Source: Time to Act. Diabetes and Foot Care. A joint publication of the International Diabetes Federation and the International Working Group on the Diabetic Foot. International Diabetes Federation; 2005.

within the country itself. However, the two most significant risk factors and common denominators for occurrence of foot ulceration and infection are social deprivation and limited access to healthcare. Various studies have suggested that simple care, motivation, education, and action by diabetes patients themselves are essential in protecting the feet from complications. Various clinical studies have demonstrated the role of special diabetic foot clinics in reducing the incidence of serious foot problems. Other studies in Western countries have demonstrated that patient education results in unequivocal reduction of ulcers and amputations among diabetic patients. On the other hand, relatively little outcomes research is at hand to compare the efficacy of various primary and secondary interventions in the prevention of diabetic foot ulcers or infection in different countries across the globe. The importance of training is highlighted by several studies that have demonstrated the importance of staff education in the early recognition of potential risk factors for diabetic feet. In one study, delay in foot ulcer treatment was attributed to patients in 12% and to medical professionals in 21% of cases. Another report suggested that in approximately one-third of patients with infection or gangrene, delay in referral of the patient for definitive care occurred because healthcare personnel that carried out the initial clinical evaluation underestimated the severity of the lesion owing to the absence of ischemia. Protective footwear prevents plantar ulcers by reduction of abnormal pressure, protects the foot from external trauma, and is critically important in preventing the initial ulcer onset or recurrence. A number of studies have shown that such footwear can well-prevent reulceration in 60–85% of patients. The most important intervention for the prevention of diabetic foot complications is education of the patient about proper foot care. It is now well-appreciated that following the

establishment of foot clinics, major amputations have been substantially reduced in Western countries. In low-income countries, the situation is different, and the increased number of amputations among diabetic patients is almost certainly a surrogate marker of the inadequacy of current primary preventive methods. Education remains the most powerful preventive tool in underdeveloped countries, and should be an integral part of prevention programs, and be simple and repetitive. Cost-effective education should be targeted at both healthcare workers and patients. A comprehensive foot care program should include education, regular foot examination, identification of high-risk patients, and educational programs for diabetes patients and their healthcare providers. The Step by Step Foot Care Project, which was piloted and carried out in Tanzania and India, has shown that education can significantly reduce rates of limb amputation. Infection, ulceration, and limb amputation are potentially preventable through organized foot care programs. Multidisciplinary approaches that encompass comprehensive, preventive strategies, including patient and staff education, joint medical and surgical management of foot ulcers, appropriate use of microbiology resources, and regular follow-up, have been shown to reduce amputation rates by more than 50%. Lower limb amputation rates in diabetic patients can be reduced by more than 50% if the following strategies are implemented: (1) regular inspection of foot and footwear at patient’s regular clinic visits; (2) preventive footwear prescribed for patients with high-risk feet; (3) implementation of a multidiscipline approach to the management of foot ulcers in diabetic clinics; (4) early diagnosis of peripheral neuropathy and peripheral arterial disease; (5) continuous follow-up of patients with previous foot ulcers and registration of amputation and foot ulcers for affected patients. Diabetes patients must be educated regarding importance of foot care and of reporting to a doctor during the early stages of footrelated symptoms. These all contribute to a financial burden that may be unsustainable in many countries, especially lowincome ones. The onus is on clinical researchers to identify cost-effective, sustainable means of improving outcomes for diabetic limb complications.

CONCLUSION Diabetic foot problems are common throughout the world, and the economic consequences are significant, both to society and to the patients and their families. When assessing use of resources, it is important not to focus on individual items such as dressings or procedures. Rather, a broader view of total resource use that includes some estimate of quality of life and the final outcome should be taken. The key question remains as to how we can reduce the morbidity and even mortality resulting from diabetic foot disease. The answer might not be too difficult. The key recommendation is a national campaign to encourage healthcare professionals



30    Contemporary Management of the Diabetic Foot merely to remove patients’ shoes and socks and examine the feet. Unfortunately, this simple advice is largely ignored in many countries. Identification of the at-risk foot does not require any expensive equipment: a tuning fork, pin, tendon hammer, and a 10-g monofilament should suffice. When planning an educational program, it should be remembered that patients might not understand the meaning or impli­ cations of the terms “neuropathy” or “foot ulcer.” Thus, educa­tion should be tailored to the patient’s understanding and social background. Organization of the foot care service is important—an integrated care approach can improve patients’ outcomes by reducing disability, morbidity, and mortality. Even in large countries (e.g. China and India), where diabetes is common and most people live in rural areas, a screen­ing program can be highly effective with little extracost to the healthcare system. Finally, many societies have issued guidelines for diabetic foot care; most of these guidelines include the essential components of recommended patient education.

ACKNOWLEDGMENTS I would like to acknowledge for the helpful discussion with Dr Lennox K. Archibald during the genesis of this manuscript.

I am grateful to Shabneez Gangji and other staff in Dar es Salaam for their assistance.

SUGGESTED READING 1. Abbas ZG, Lutale JK, Bakker K, et al. The ‘Step by Step’ Diabetic Foot Project in Tanzania: a model for improving patient outcomes in less developed countries. Int Wound J. 2011;8(2):169-75. 2. Boulton AJM, Cavanagh PR, Rayman G (Eds). The Foot in Diabetes, Fourth Edition, Chichester, UK: John Wiley and Sons Ltd; 2006. 3. Cavanagh P, Attinger C, Abbas Z, et al. Cost of treating diabetic foot ulcers in five different countries. Diabetes Metab Res Rev. 2012;28(Suppl 1):107-11. 4. International Diabetes Federation, Diabetes Atlas, 5th edition. Brussels, Belgium: International Diabetes Federation; 2011. 5. International Working Group on the Diabetic Foot (IWGDF). (2011). The development of global consensus guidelines on the management and prevention of the Diabetic Foot [online]. Available from, www.iwgdf.org [Accessed May, 2013]. 6. Time to Act, Diabetes and Foot Care. A joint publication of the International Diabetes Federation and the International Working Group on the Diabetic Foot. International Diabetes Federation; 2005.

CHAPTER

Diabetic Neuropathy

5 Andrew JM Boulton

INTRODUCTION Of all the late complications of diabetes, none affects so many organs or systems as the group of conditions that are included under the term “diabetic neuropathies”. They encompass a wide heterogeneous group of clinical and sub-clinical syndromes that are characterized by progressive loss of nerve fibers which may affect both principal divisions of the peripheral nervous system those are, somatic and autonomic. The fact that neuropathies are described in patients with primary (types 1 and 2) and secondary diabetes of varying causes, suggests common etiological mechanisms based upon chronic hyperglycemia. There is now increasing evidence that neuropathy and its late sequelae of foot ulceration and Charcot neuroarthropathy, predict not only endpoints such as amputation, but also mortality. One of the functions of the sensory peripheral nervous system is to protect the extremities from injury. Small afferent nerve fibers carry the sense of pain and temperature whereas larger fibers conduct the sensory modalities of vibration, joint position sensation, touch, etc. In the presence of a significant peripheral neuropathy, patients may experience loss of protective sensation which may in turn, together with other contributing factors, result in ulceration of the feet. It was the late Dr Paul W Brand, MD, FRCS, a surgeon working with leprosy patients in South India in the mid-20th Century who described pain as, “God’s greatest gift to mankind”. It was his clinical observation of many patients with ulcers under weight-bearing areas that led to his realization that loss of protective sensation resulted in these terrible lesions in patients with leprosy. Although very different conditions, both leprosy and diabetes may result in severe loss of sensation in the feet which are then at great risk of painless injury and ulceration.

In the first section of this chapter, historical aspects of diabetic neuropathy and its links with foot ulceration will be examined and because of the similarity of sensory loss seen in leprosy and diabetes, observations on leprosy will also be included. Clinical descriptions of the main types of neuropathy associated with foot problems and evidence for this association will then be discussed followed by a description of pathways to ulceration. The therapeutic challenge of how to handle patients with sensory loss will then be addressed followed by the main treatments of symptomatic diabetic neuropathy.

HISTORICAL ASPECTS OF DIABETIC NEUROPATHY The first descriptions of the neuropathies of diabetes refer to sensory symptoms and are to be found in the late 18th and 19th century medical literature. In the late 19th century, Charcot, a physician at the Salpêtrière Hospital in Paris, gave a good description of diabetic peripheral neuropathy (DPN) stating that, “In some diabetic cases, the tendon reflexes are absent”, but then he went on to question the meaning of this. Early in the 20th century at the Manchester Royal Infirmary, Dr RT Williamson described abnormalities of physiological measurements such as vibration perception in patients with diabetes; coincidentally, it was work from the same institution at the end of the 20th century that confirmed, in a longitudinal study, that loss of vibration perception is indeed associated with an increased risk of foot ulceration. With respect to treatment of the neuropathic foot, as noted above, observations made in leprosy in the first half of the 20th century were highly relevant to diabetes although this was not realized until the 1960s by Dr Paul Brand. The use



32    Contemporary Management of the Diabetic Foot of total contact casts for ulcers in patients with leprosy having foot ulcers was shown to be effective by surgeons working in both Ceylon (now Sri Lanka) and South India. The autonomic neuropathies, which are also common in patients with diabetes, were not properly described until the mid-20th century. Peripheral autonomic neuropathy results in sympathetic dysfunction which causes reduced sweating and increase in peripheral blood flow in the lower limbs (in the absence of large vessel arterial disease), is an important component pathway to neuropathic foot ulceration. The importance of neuropathy in the genesis of foot lesions in patients with diabetic neuropathy has been increasingly realized in the last 50 years. When Dr Paul Brand moved to the United States in the 1960s he realized that the management of foot ulceration in diabetes was hindered by some of the same misconceptions that existed in India about leprosy some 20 years earlier. Foot ulcers in patients with diabetes were looked upon by surgeons as being a reason for amputation because it was felt that they would be unlikely to heal. Realization that many of these so-called ulcers were actually a consequence of neuropathy together with trauma led Brand to promote the use of casting for such lesions rather than amputation that had previously often been the first choice. Thus, lessons learnt from leprosy have been translated into the management of the insensitive foot in diabetes.

CLASSIFICATION, EPIDEMIOLOGY AND CLINICAL FEATURES OF THE DIABETIC NEUROPATHIES An International Consensus meeting some years ago agreed on a simple definition of diabetic neuropathy as “the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after the exclusion of other causes”. It was also agreed that neuropathy cannot be diagnosed without a careful clinical examination—absence of symptoms can never be equated with absence of neuropathy as asymptomatic peripheral neuropathy is so common. As up to 10% of neuropathies seen in patients with diabetes may not be due to the diabetes, it is vitally important to exclude other causes of peripheral neuropathy as diabetic neuropathy is a diagnosis of exclusion. Thus, the clinical classification outlined in Table 1 will be used in this chapter. The neuropathies that mainly contribute to diabetic foot problems are highlighted in boldface in Table 1. The commonest variety of the diabetic neuropathies, chronic sensorimotor peripheral neuropathy and peripheral sympa­ thetic autonomic dysfunction frequently coexist. Hereafter these will be referred to as diabetic peripheral neuropathy. Diabetic peripheral neuropathy is a very common compli­ cation of diabetes and a study from the North West of England

Table 1  Clinical classification of diabetic neuropathies Polyneuropathy

Mononeuropathy

Sensory •  Acute sensory •  Chronic sensorimotor

Isolated peripheral Mononeuritis multiplex Truncal

Autonomic •  Cardiovascular •  Gastrointestinal •  Genitourinary •  Peripheral sympathetic Proximal motor (amyotrophy) Truncal Those in boldface are important in the etiopathogenesis of diabetic foot problems.

showed that over 40% of older type 2 diabetic patients had neuropathic risk factors for foot ulceration. Although classically described as a “late” complication of diabetes, DPN may be present at the diagnosis of type 2 diabetes; this is explained as many patients, because of the gradual onset of the disease, are not diagnosed for many years and therefore have had asymptomatic hyperglycemia for years prior to the clinical diagnosis of diabetes. This asymptomatic hyperglycemia therefore contributed to the presence of this late complication at the clinical diagnosis. In the large United Kingdom Prospective Diabetes Study, a study of patients from diagnosis of type 2 diabetes, it was found that 13% of patients at diagnosis of diabetes had neuropathy of sufficient severity to put them at risk of foot ulceration. Thus, every diabetic patient of whatever duration of diabetes should be screened for risk factors for foot problems on at least an annual basis. Neuropathy is a major risk factor for foot ulceration and in patients with significant neuropathy with no history of ulceration, the annual risk of developing an ulcer is five to seven times higher than in those with no neuropathy. Diabetic peripheral neuropathy is often regarded as a paradox as patients with the same neurologic deficit on examination may, at one end of the spectrum, be completely asymptomatic and if pressed admit that their feet are some­ what numb; whereas, at the other end of the spectrum of neuropathy, patients with or without a neurologic deficit may experience severe uncomfortable neuropathic symptoms. Such symptoms are difficult to describe because they are a new experience for patients. We are all familiar with the discomfort caused by falls, bruising, etc, whereas neuropathic pain is a new experience hence the difficult in enunciating the symptoms. Common descriptors used for neuropathic symptoms include altered temperature perception such that the feet are described as being on fire or burning or freezing cold. Similarly, uncomfortable electrical sensations may be described as a sharp, shooting or stabbing pain. Neuropathic



Diabetic Neuropathy    33 symptoms are invariably worse at night when there is less afferent input into the nervous system. In contrast to peripheral vascular disease, the symptoms of neuropathy may be helped by getting up and moving around and on examination, the patient may demonstrate allodynia, and that is when a non-painful stimulus gives rise to a painful experience. The natural history of diabetic neuropathy is not well described and whereas patients who have painful symptoms may experience gradual improvement in these over the years, those patients with insensitive feet will not experience any recovery of sensation and therefore always be at risk of insensitive foot ulceration.

CLINICAL FEATURES OF DIABETIC PERIPHERAL NEUROPATHY Mononeuropathies Compression Neuropathies The most common entrapment neuropathy is carpal tunnel syndrome, which is due to compression of the median nerve as it traverses the carpal ligament. This is the most common of the mononeuropathies and may be amenable to conservative (splints) or surgical decompression.

Other Compression Neuropathies In the upper limb, both the ulnar nerve and the radial nerve may be affected; whereas, in the lower limb, common peroneal nerve palsy may result in weakness of the dorsiflexors and foot drop with weakness in eversion but this is usually painless. Also in the lower limb meralgia paresthetica has been reported in diabetes due to compression of the lateral cutaneous nerve of the thigh. This presents with neuropathic symptomatology in the lateral aspect of the thigh, usually unilaterally.

Cranial Mononeuropathies Cranial neuropathies in diabetic patients are rare with the most common nerves involved being those supplying the external ocular muscles, i.e. the 3rd, 4th and 6th cranial nerves. Most important is the exclusion of more sinister causes such as malignant lesions or posterior communicating aneurysm in the case of the third nerve. The natural history of the cranial mononeuropathies is one of gradual recovery without intervention.

Polyneuropathies Proximal motor neuropathy (diabetic amyotrophy) typically occurs in patients with type 2 diabetes, age 50–60 years old

and presents with pain, and unilateral or bilateral muscle weakness, and atrophy in the proximal thigh area. There is no specific treatment for this condition other than treatment of the neuropathic symptoms and physiotherapy. The natural history is one of recovery although not to pre-morbid levels of muscle strength. When an unusually severe or progressive polyneuropathy develops in diabetic patients, such as may be found in diabetic amyotrophy, it is important to exclude chronic inflammatory demyelinating polyneuropathy (CIDP) because this may be amenable to immunomodulation. Referral to a neurologist is recommended for any case where there is even only a remote possibility that this might be CIDP.

Autonomic Neuropathies Diabetic autonomic neuropathy may affect any area receiving autonomic innovation including the cardiovascular, gastro­ intesti­ nal and urogenital systems, and also peripheral vascular and pseudomotor function. Details of cardiovascular, gastrointestinal and urogenital autonomic neuropathy are beyond the scope of this chapter and the reader is referred to the list of Suggested Reading at the end of this chapter.

Peripheral Sympathetic Diabetic Autonomic Neuropathy Sympathetic neuropathy in the lower limb leads to a release of sympathetic tone and, in the absence of peripheral vascular disease, a warm foot due to increased blood flow and arteriovenous shunting. Sudomotor dysfunction results in dryness of the foot skin and has been associated with foot ulceration.

Chronic Sensorimotor Neuropathy The clinical presentation of distal, chronic, sensorimotor neuropathy, which is the most common of all the diabetic neuropathies is variable, ranging as noted above, from the severely painful (positive) symptoms at one extreme to the completely painless variety that may actually present with an insensitive foot ulcer. It is a diffuse symmetrical disorder mainly affecting the feet and lower legs in a stocking distribution, but rarely also may involve the hands in a glove distribution. As the disease progresses, there is usually some motor dysfunction (including small muscle wasting on examination), together with abnormalities of autonomic function tests. The onset of this type of neuropathy is gradual and insidious, and symptoms may be intermittent. A much rarer acute sensory neuropathy is recognized with a rapid onset of painful symptoms; in this type, which often follows a period of metabolic instability or which may be precipitated by a sudden improvement of control (insulin neuritis), the symptoms are usually severe with few if any clinical signs.



34    Contemporary Management of the Diabetic Foot In addition to the symptoms described above, a symptom complex that has only recently been recognized as a relatively common complaint is that of postural instability; diabetic neuropathic patients often report more falls and unsteadiness (secondary to disturbance in proprioception) and as such this should be added to the list of neuropathic symptoms which may also result in depression.

Measures of Neuropathy Clinical Symptoms The accurate recording of symptoms is essential in clinical practice and it is important to record the patients’ descriptions of their complaints verbatim; the physician cannot attempt to interpret or translate patients’ symptoms into medical terminology. A number of questionnaires and scales have been developed to help the clinician characterize neuropathic pain with more precision; the simplest of these and the most frequently used is a visual analog 10 cm graphic rating scale. The patient is asked to mark where along the line from zero (no symptoms) to 10 (worse possible symptoms) they feel that their current experience lies. As neuropathic symptoms can also have a profound effect on quality of life, a number of instruments have been developed for assessing the impact of neuropathic symptoms and deficits on patients’ quality of life.

Clinical Examination Most important is a careful clinical neurological examination of the lower limbs. Simple clinical observation may identify a neuropathic foot with evidence comprising small muscle wasting, clawing of the toes, prominent metatarsal heads, dry skin and callous (secondary to sympathetic dysfunction) and/ or bony deformities, secondary to Charcot’s neuroarthropathy. A careful clinical examination of sensory and motor function in the lower limbs is essential and should form part of the annual review that all patients with diabetes should undergo. Such an annual clinical examination can be carried out using usually available clinical instruments such as cotton wool for the assessment of light touch, a 10 g monofilament for protec­tive pressure sensation, a pin for pain sensation, iced or warm water for thermal sensation and a 128 Hz tuning fork for vibration. The modified neuropathy disability score (NDS) is commonly used in clinical practice and has been shown to be an excellent predictor or neuropathic endpoints such as foot ulceration in prospective longitudinal studies. If signs point to the presence or absence of the following features: vibration perception threshold at apex of the big toe using a 128 Hz tuning fork, temperature perception on the dorsum of the foot and pinprick proximal to the big toenail (normal = 0, abnormal = 1) and the Achilles reflex (2 = absent, 1 = present on reinforcement and 0 = normal) the maximum score is

10, with a score of 6 or more indicating moderate or severe neuropathy and an increased risk of foot ulceration.

Quantitative Sensory Testing Quantitative sensory testing (QST) assesses the patient’s ability to detect a number of sensory stimuli and has the advantage that it directly assesses the degree of sensory loss at the most vulnerable site—the foot. However, QSTs are complex psycho-physiological tests that also rely on a patient’s response and therefore cooperation and concentration. Moreover, abnormalities do not necessarily confirm that the abnormality lies in the peripheral nerve; it may lie anywhere in the afferent pathway. QSTs vary in complexity with simpler instruments such as the biothesiometer to more complex testing requiring expensive equipment. These are mainly used for research rather than day-to-day clinical practice.

Electrophysiology Electrophysiology (EP) testing is probably the most important functional efficacy parameter in clinical neuropathy trials as such tests are objective, sensitive and reproducible and do not rely on the patient response. However, abnormalities of electrophysiology (EP) do not confirm that diabetes is the cause of the neuropathy; it simply confirms what can be found on clinical examination and that is an abnormality in the peripheral nerve. In day-to-day clinical practice, a careful history and examination perhaps with a simple assessment of deficits using some tests such as the NDS is all that is required. Diag­ nosis of diabetic neuropathy requires the exclusion of other causes of peripheral neuropathy such as B12 deficiency, toxins (e.g. alcohol), malignant disease (e.g. a malignancy presenting with a paraneoplastic syndrome) and infections. In some developing countries leprosy is still prevalent, and may be a cause of neuropathy in a patient with diabetes. Table 2 lists a number of non-diabetic causes of peripheral neuropathy that should be considered in the differential diagnosis.

Table 2  Some non-diabetic causes of symptomatic neuropathy •  Malignancy—paraneoplastic syndrome (e.g. bronchogenic   carcinoma) •  Metabolic causes (e.g. porphyria) •  Toxic causes (e.g. alcohol) •  Infection (e.g. HIV, leprosy) •  Iatrogenic (e.g. isoniazid, vinca alkaloids) •  Iatrogenic—nonpharmacological (e.g. post-surgery)



Diabetic Neuropathy    35

PREVENTION AND TREATMENT OF DIABETIC PERIPHERAL NEUROPATHY To date, no pharmacological interventions in diabetes have been shown to reduce the incidence of peripheral neuropathy in man. This is not the case however for optimization of glycemic control as there is good evidence, particularly in type 1 diabetes, that achieving near normoglycemia redu­ ces the incidence and prevents the progression of sensori­ motor neuropathy. The landmark Diabetes Control and Complications Trial (DCCT) study showed that those randomized to intensive insulin treatment had a 60% reduc­ tion in the incidence of clinical neuropathy. In the longterm follow-up of diabetes, the Epidemiology of Diabetes Interventions and Complications study, the benefits of more than 6 years of intensive therapy on neuropathy status was shown to persist for 13 to 14 years after the end of the main DCCT. Conversely, the importance of glycemic control in the prevention of neuropathy of type 2 diabetes is less clear. The problem here is of course that most patients at diagnosis of type 2 diabetes have had asymptomatic hyperglycemia for many years and may already have some degree of neurological damage.

CLINICAL MANAGEMENT OF DIABETIC PERIPHERAL NEUROPATHY As noted above, the first question that should be asked by a physician seeing a patient with evidence of neuropathy is whether or not the sensory neuropathy in that particular patient is secondary to diabetes or another cause. There is no test or neurological examination or quantitative sensory testing/EP that would confirm that the neuropathy in any one individual is in fact due to diabetes. Whereas, a combination of typical symptoms and abnormalities on a clinical exami­ nation of the feet is usually suggestive of the diagnosis, it is important to consider those other causes listed in Table 2. Diabetic sensorimotor neuropathy tends to be gradual in onset and relatively symmetrical; certain features and the examination might suggest another cause and features that might prompt a referral to a neurologist and are listed in Table 3. Thus a careful history and examination together with consideration of the features listed in Table 3 with appropriate tests to exclude other causes will have to confirm the diagnosis as that of diabetic chronic sensorimotor neuropathy. The next step is to assess the level and stability of over­ all blood glucose control. A number of small open-labeled uncontrolled studies have suggested that achieving near normoglycemia can be helpful in reducing painful neuro­ pathic symptoms. It is likely that it is the stability of blood glucose control that matters most as blood glucose flux or erratic control has been shown to be associated with worsening neuropathic symptomatology. Despite the lack

Table 3  Indications for a neurological referral in patients with suspected diabetic sensorimotor neuropathy •  Asymmetrical signs •  Predominant motor signs •  Rapid progression of symptoms/signs •  Back or neck pain •  Family history of neuropathy •  Any suggestion of chronic inflammatory demyelinating   neuropathy

of appropriately designed controlled trials in this area, it is accepted that intensive diabetes therapy aimed to stable near normoglycemia should be the first step in the management of the patient with symptomatic diabetic neuropathy.

PATHOGENETIC TREATMENTS Despite numerous studies of multiple agents over the last few decades with one exception, there is no evidence to support the use of any pathogenetic treatment in the symptomatic management of neuropathic pain in diabetes. Agents with no or little evidence to support their use include aldose reductase inhibitors, protein kinase C-beta inhibitors, nerve growth factors and essential fatty acids. There is limited evidence to support the use of the antioxidant, alpha-lipoic acid given intravenously for the management of neuropathic pain. In conclusion, the only pathogenetic treatment for neuro­ pathic pain in diabetes with limited support from randomized controlled trials is alpha-lipoic acid, which is only available in a limited number of countries.

Pharmacological Management of Symptomatic Neuropathy There are a number of pharmacological treatments for neuro­ pathic pain in diabetes that have confirmed efficacy from randomized controlled trials and have been further supported in either pooled analyses or meta-analyses; none of these treatments however has any effect on the natural history of diabetic neuropathy, which as noted above, is progressive loss of nerve fibers. It should also be noted that, although differences exist between the rare though very painful acute sensory neuropathy and the common chronic sensorimotor neuropathy, the principles of symptomatic treatment are the same for both conditions. In addition, many drugs that have traditionally been used for neuropathic pain have not been specifically licensed for this condition as noted by Table 4, which lists the commonly used agents that have been supported by appropriately designed randomized controlled trials.



36    Contemporary Management of the Diabetic Foot Table 4  Oral symptomatic therapies in painful diabetic neuropathy Drug class

Drug

Daily dose (mg)

Tricyclic antidepressants

Amitriptyline

10–150

Imipramine

10–150

SNRIs

Duloxetine*

60–120

Anticonvulsants

Gabapentin

900–3,600

Pregabalin*

150–600

Tramadol

50–400

Oxycodone CR

10–60



Opioids

SNRIs—serotonin and noradrenaline reuptake inhibitors * Licensed for neuropathic pain treatment in diabetes in Europe and North America † Licensed for neuropathic pain treatment in Europe

Tricyclic Antidepressants .

For more than 30 years the tricyclic antidepressants have been important treatments in the management of chronic neuropathic pain. Putative mechanisms by which these drugs relieve pain includes inhibition of norepinephrine and/or serotonin reuptake at synapses of central descending pain control systems and more recently, the antagonism of N-methyl-D-aspartate receptors, which mediate hyperalgesia and allodynia. Most experience has been achieved with amitriptyline and imipramine and the dosage of both these agents required for symptomatic relief is similar (25–150 mg daily), although in older patients it would be useful to start with 10 mg daily. The use of these agents is limited by the relative high rates of adverse events particularly anticholinergic and central side effects. To avoid undue drowsiness, the medication can be taken once a day in the evening. The use of these drugs is supported by data from several randomized controlled trials, a Cochrane database systematic review and other meta-analyses. In summary, the tricyclic drugs are useful in the manage­ ment of neuropathic pain but are prone to common and predictable side effects, particularly in the elderly.

Serotonin and Noradrenalin Reuptake Inhibitors The efficacy and safety of duloxetine has been evaluated in a number of appropriately designed randomized controlled trials using doses of 60 and 120 mg daily. Significant efficacy in terms of relief of pain intensity has been shown in each of these trials versus placebo. Moreover, duloxetine 120 mg/ day seemed to work best on pain described as “shooting”, “stabbing”, “sharp”, “hot”, “burning” and “splitting”. The drug is generally well tolerated with less than 20% discontinuation to adverse events such as somnolence, dizziness or constipation, but a slight worsening of metabolic parameters may occur. An analysis of three randomized controlled trials of duloxetine in

the management of neuropathic pain confirms that the drug is efficacious and well tolerated.

Anticonvulsants Anticonvulsants have been used in the management of neuropathic pain for many years although only two with strong evidence to support their use will be considered further here, partly because the evidence for the efficacy of first generation agents such as carbamazepine and phenytoin is limited. Gabapentin, a drug used for complex partial epilepsy, is also widely used for the relief of neuropathic pain. It is structurally related to the neurotransmitter, gamma-aminobutyric acid (GABA). Gabapentin at doses of 900–2,400 mg per day offers significant pain relief in diabetic neuropathy together with reduced sleep disturbance. This drug has to be given three times daily in doses of 600–900 mg TDS; it is recommended to start at a lower dose and work upward. Similarly, the efficacy of the newer GABA analog pregabalin, has been confirmed in a number of randomized controlled trials. Based on a recent meta-analysis supporting its efficacy and tolerability, doses of 150–600 mg/day for the treatment of diabetic and neuropathic pain are recommen­ ded. Pregabalin, although structurally similar to gabapentin, is three times more potent and only needs to be taken twice daily and appears to have a relatively fast effect on pain relief compared to gabapentin. Adverse events of the anti­ convulsants include somnolence, dizziness and for pregabalin, ankle edema and weight gain.

Opioids Many physicians have been reluctant to prescribe opioids for neuropathic pain, probably because of fears of addiction. However, as stated by Foley in an editorial, “We must focus urgent attention on the needs of suffering patients”. In particular, opioids and opioid-like drugs are often effective in treating neuropathic pain that has failed to respond to therapies such as those described above. Tramadol is the synthetic opioid with an unusual mode of action working upon both opioid and mono-aminergic pathways. In a randomized controlled trial, tramadol was effective in the management of painful neuropathic pain. Although this study only lasted 6 weeks, a follow-up study suggested that symptomatic relief was maintained for at least 6 months. The side effects are predictable and common in patients treated with tramadol and other opioids. Three randomized trials have confirmed the efficacy of controlled release oxycodone for neuropathic pain in diabetes. Whilst the efficacy of this drug is confirmed although side effects are frequent. Unfortunately no studies have examined long-term use of opioids so the risks of tolerance and dependence have yet to be quantified.



Diabetic Neuropathy    37

Combination Studies Unfortunately most clinical trials of pharmacological agents for the management of neuropathic pain have used placebo as the only comparator. However, this is an evolv­ ing area, particularly as recent national guidance from the UK [National Institute of Clinical Excellence (NICE)] has recommended the use of combinations for second line therapy. The data supporting combinations are derived pri­ marily from experimental studies and two small but well designed combination studies with gabapentin and mor­ phine; and gabapentin and nortriptyline. There are very few active comparator trials although a large trial of pregabalin monotherapy versus duloxetine monotherapy versus duloxetine and pregabalin combined is now completed and somewhat surprisingly did not suggest benefit for combi­ nation of these two agents. Clinical question: Which drugs are recommended as first line therapies for neuropathic pain? There have recently been a number of published guidelines advising on the approach to the patient with neuropathic pain and these include the European Federation of Neurological Societies (EFNS), the Canadian Pain Society and most recently, NICE in the UK. Freynhagen and Bennett propose that a TCA or gabapentin or pregabalin should be the first line approach with the serotonin and noradrenalin reuptake inhibitors (SNRI) inhibitor duloxetine, as first or second line treatment. The revised EFNS guidelines propose that most drugs generally have similar efficacy with strong evidence in support of tricyclic antidepressants (TCA), pregabalin, gabapentin, tramadol and opioids (in various conditions), duloxetine (painful diabetic neuropathy), venlafaxine, topical lidocaine and capsaicin patches (in restricted conditions). The 2010 NICE guidelines on the management of neuropathic pain has similar advice for non-diabetic painful neuropathy that is, amitriptyline or pregabalin as first line treatments, but in painful diabetic neuropathy, oral duloxetine is recommended as the first line treatment with amitriptyline to be used in those in whom duloxetine is contraindicated. For second line treatment, pregabalin or duloxetine combined with pregabalin is recommended. NICE discussions concluded that although efficacy was similar for pregabalin and duloxetine, the cost-effectiveness analysis was highly favorable for duloxetine. In summary, there is strong evidence to support the use of the TCA, the SNRI duloxetine and the anti-convulsant drugs gabapentin and pregabalin in the management of patients with diabetic painful neuropathy. For those who do not respond to these agents, the use of opioid or opioid-like drugs should be considered. The use of topical agents such as capsaicin, topical lignocaine, topical glyceryl trinitrate or many of the other physical therapies including surgical decompression for neuropathic pain does not have sufficiently robust evidence to warrant their further discussion in this chapter.

DIABETIC NEUROPATHY AND FOOT ULCERATION A number of studies have confirmed that sensory loss secon­ dary to DPN is a major contributory cause in the pathway to foot ulceration in diabetes. Whereas loss of sensation on its own will not lead to ulceration, when combined with other factors such as foot deformities and trauma (often by footwear), this will be sufficient to complete the causal pathway to ulceration. Thus, as noted above, all patients with diabetes require a detailed foot screen at least annually and part of this will assess the peripheral circulation and part the neuropathic status of the foot. In 2008, the American Diabetes Association published a Taskforce Report on what should be included in the Comprehensive Diabetic Foot Examination (CDFE) that should be carried out annually (see Suggested Reading). This is one of the most important aspects of the annual review as it has been shown that the lifetime risk of a person with diabetes developing a foot ulcer may be as high as 25%. The Taskforce Report on the CDFE emphasized that a clinical examination of the foot required no expensive tests or equipment—indeed no equipment that requires a power source. Most important is to remember that every time a diabetic patient is seen in the clinic, shoes and socks should be removed and the feet examined. The CDFE should comprise assessment of pressure sensation using a 10 g monofilament thus one other test which might comprise a testing of vibration with 128 Hz tuning fork over the hallux, pinprick sensation again over the hallux, and the presence or absence of ankle reflexes. Semi-quantitative assessment of vibration using a biothesiometer may also be one of the confirming tests. Thus the combination of abnormality on monofilament testing plus one other test to confirm this would identify that patient as having neuropathy of sufficient severity to put them at risk of foot ulceration. In summary, neuropathy is a major contributory factor to the genesis of foot ulceration in diabetes and can be detected very simply by a clinical examination of the feet together with some of the simple sensory assessments noted above. It must also be recognized that patients with end-stage renal disease particularly those on dialysis have an extremely high risk of foot ulceration and should be considered at risk however normal any other tests might be.

THE PATIENT WITH SENSORY LOSS It should now be possible to achieve a significant reduction in the incidence of neuropathic foot ulceration and subsequent amputation in diabetic patients, and guidelines exist for the diagnosis and management of both neuropathy and foot problems. However, a reduction in neuropathic foot problems will only be achieved if we remember that patients with insensitive feet have lost that warning signal of pain that ordinarily brings the patient to their doctor. Thus, the care of



38    Contemporary Management of the Diabetic Foot the patient with no pain sensation is a new challenge for which we have little training. It is difficult for us to understand, for example, that an intelligent patient would buy and wear a pair of shoes several sizes too small and then come to our clinic with extensive shoe-induced ulceration. The explanation is simple: with reduced sensation, a very tight fit stimulates the remaining pressure nerve endings and is thus interpreted as normal fit—hence the common complaint when we provide patients with custom-designed shoes that “these shoes are too loose” or “too small”. As stated above, much has been learnt about the prevention and management of diabetic foot problems from the treatments of patients with leprosy. If we are to succeed, it must be realized that, with loss of pain there is also diminished motivation in the healing of, and prevention of, injury. Thus, the most important step in the prevention of foot ulceration is to encourage doctors and health care professionals to remove their patients’ shoes and socks and inspect their feet whenever the patient attends the clinic. If we fail to remove our patients’ shoes and socks and examine the feet when they attend us perhaps once every

3 months, can we honestly expect those patients with risk factors to inspect their feet on at least a daily basis?

SUGGESTED READING 1. Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the foot care interest group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care. 2008;31:1679-85. 2. Boulton AJ, Malik RA, Arezzo JC, et al. Diabetic somatic neuropathies: a technical review. Diabetes Care. 2004;27:145886. 3. Boulton AJ, Vileikyte L. Painful diabetic neuropathy in clinical practice. London: Springer Verlag; 2011. pp. 1-60. 4. Tesfaye S, Boulton AJ. Diabetic neuropathy. Oxford Diabetes Library, Oxford: Oxford University Press; 2011. pp. 1-95. 5. Vinik AI, Maser RE, Mitchell B, et al. Diabetic autonomic neuropathy: a technical review. Diabetes Care. 2003;26:155379.

CHAPTER

6

The Biomechanics of the Diabetic Foot

Virginia Bower

INTRODUCTION Foot ulceration is the critical event which all diabetic foot prac­ti­tioners aim to prevent in the person with diabetes. The development of ulceration is perceived by many as a negative milestone in a patient’s foot health. Foot ulcera­tion predisposes the patient to a range of more serious compli­ ca­ tions such as soft tissue infection, osteomyelitis and amputation. The triage of neuropathy, arterial disease and mechanical stress (pressure or shear and friction) is well-accepted as necessary for the development of ulceration in the diabetic foot. The roles of neuropathy and peripheral arterial disease will not be discussed in this chapter as they are the focus of other chapters in this book. For the purpose of this discussion, it will be assumed that the reader understands that biomechanical abnormality alone is not a sufficient cause for ulceration. Neuropathy, peripheral arterial disease, or a combination of both, is necessary for abnormal mechanical stress to precipitate ulceration. With this fact in mind, it is important to acknowledge the role of foot biomechanics in precipitating ulceration, as it is clearly important and yet frequently ignored. • Biomechanical abnormality alone does not cause foot ulceration. • Patients with rheumatoid arthritis rarely develop foot ulceration despite gross foot deformities. • Combination of neuropathy, arterial disease and bio­ mecha­nical abnormality are necessary to precipitate foot ulceration. Biomechanical evaluation is an important component of both foot ulcer prevention and foot ulcer management programs. For the purposes of this chapter, the role of foot bio­mechanics in the prevention of ulceration will be the

focus. Biomechanical intervention for the ulcerated foot primarily relies on the principle of equal-weight distribution throughout the plantar aspect of the foot using total contact casting or other variations on this technique. More subtle biomechanical alterations that may be required to heal the foot ulcer are beyond the scope of this chapter as these inter­­ ven­ tions require a detailed understanding of foot biomechanics. There is an ever increasing body of evidence surrounding the role of abnormal biomechanics in precipitating foot ulceration. Continued research in this area is welcomed and necessary as there remain gaps in our understanding of some of the biomechanical mechanisms which facilitate ulceration. The relationship between limited joint mobility, glycosylation and neuropathy, and the relationship between small muscle wasting and neuropathy are two such areas where controversy remains and further research is required. There remains an absence of clinical guidelines for the generalist diabetic foot practitioner on how to manage biomechanical abnormalities. Specialists in the field of foot biomechanics such as podiatrists are not always accessible to individual patients and health services. The focus of this chapter is to provide a summary of the key principles of biomechanical assessment of the diabetic foot for the nonfoot specialist. This is complemented with a treatment pathway (Tables 2 to 5) to assist practitioners to make appropriate clinical decisions when evaluating the mechanics of the foot in this vulnerable group of patients.

Key Message and Tips • A sound understanding of the principles of foot mechanics will produce a better clinical outcome for patients. • Even the nonfoot specialists can provide significant benefits to their patients with a basic understanding of biomechanical concepts.



40    Contemporary Management of the Diabetic Foot • The aim of this chapter is to present a practical “how-todo” guideline for practitioners working with the diabetic foot.

BASIC PRINCIPLES OF FOOT BIOMECHANICS The human foot is a remarkable structure, which, through evolutionary adaption and change, has enabled humans to walk upright with a bipedal gait. The human foot is the most complex orthopedic structure within the human skeleton— with 26 bones, 33 joints and over 100 muscles, tendons and ligaments. Complex and sophisticated, the foot provides shock absorption, balance, and proprioceptive and sensory feedback to the body. The foot can be loosely divided into three sections: (1) the rearfoot, (2) the midfoot and (3) the forefoot. The rearfoot is comprised of the ankle and the subtalar joints. The primary role of the ankle is to control sagittal plane motion of the foot in relation to the leg. This function is essential for bipedal gait, and adequate range of sagittal plane motion of the ankle is necessary for proficient ambulation. The subtalar joint is a triplanar joint which facilitates sagittal, frontal and transverse plane motion for the foot. The primary role of the subtalar joint is to provide shock-absorption, a function which it undertakes successfully using a synchronized combination of inversion or eversion, plantar flexion or dorsiflexion and adduction or abduction. The midtarsal joint articulates the rearfoot to the midfoot and is comprised of two joints: (1) the talonavicular and (2) the calcaneocuboid joints. The midtarsal joint undergoes both pronation and supination. The midtarsal joint plays an essential role in the propulsive phase of gait by creating a lever to facilitate stable forefoot loading. The midtarsal joint, in combination with the subtalar joint, provide the shock absorption and propulsive mechanisms required for successful gait. The primary components of the forefoot complex are the first metatarsophalangeal joint and the lesser meta­ tarsophalangeal joints (second to fifth). Both the first metatarsophalangeal joint and all the lesser metatarso­ phalangeal joints provide sagittal plane motion through dorsiflexion and plantar flexion. The primary function of the first metatarsophalangeal joint is to provide stable load bearing and propulsion. During propulsion the first metatarsophalangeal joint bears a considerable force near to body weight. The lesser metatarsophalangeal joints also bear a considerable proportion of total body weight during propulsion, although considerably less that the first metatarsophalangeal joint (Table 1). In summary, the human foot undergoes a complex choreography of movement which provides both the flexible adaptation and rigid propulsion necessary for gait. If this sophisticated sequence of events is disturbed by abnormal

Table 1  Sections of foot and their functions Section

Joints

Functions

Rearfoot

Ankle and subtalar

Control sagittal plane motion in relation to leg and provides shock absorption

Midfoot

Talonavicular and calcaneocuboid (midtarsal joints)

Propulsive phase of gait and provides shock absorption

Forefoot

1st metatarsophalangeal and 4 lesser metatarsophalangeal joints

Stable load bearing and propulsion

joint or soft tissue function then foot pathology will occur. The following section will describe the key features of the biomechanical assessment as well as identify the most common foot pathologies found in the diabetic foot which predispose to ulceration.

FEATURES OF THE BIOMECHANICAL ASSESSMENT The following discussion will focus on the key features of a biomechanical assessment in the person with diabetes. Six critical features will be discussed which include: plantar pressure and shear stress; plantar fat pad integrity; callus; limited joint mobility; rearfoot and forefoot biomechanics; and joint deformity.

Plantar Pressure and Shear Stress Plantar pressure and shear stress evaluation using force plate technology has dominated research in the field of diabetic foot biomechanics over the last three decades. This technology shows considerable promise in explaining the relationship between plantar pressure, shear stress and ulceration. However, it remains technology primarily available to researchers and well-funded clinical services and laboratories. Plantar force technology has developed a considerable way and has become more available to the average clinician in the form of in-shoe testing systems. These systems provide the clinician with a cheaper and less-simulated method of evaluating plantar foot pressure. It is well-understood that shear stress plays an integral role in the development of foot ulceration and is equally important, if not more important, than vertical stress and peak pressure (Figs 1 and 2). The development of technology to evaluate shear stress has, however, lagged behind plantar pressure technology. There are various laboratories currently working on develop­ ing prototypes for clinical application around the world.



The Biomechanics of the Diabetic Foot    41 Fortunately, the average clinician can alleviate mechanical stress from the diabetic foot by acquiring a sound knowledge of the principles of foot mechanics and understanding the clinical methods used to correct biomechanical abnormality. The treatment pathway provided in this chapter will not include plantar pressure or shear stress evaluation due to the reasons described above. Biomechanical factors for foot ulceration: • Majority of foot ulcers have a biomechanical etiology. • Elevated peak shear stress and plantar pressure are major factors. • Shear stress contributes to neuropathic injury. • Reduction in shear stress and peak plantar pressure helps in healing of ulcers and prevents ulcer recurrence.

Callus Fig. 1  Increased plantar pressure in forefoot

There is substantial evidence to support the relationship between the development of callus and other hyperkeratotic skin lesions and the development of diabetic foot ulceration. Callus acts like a foreign body, exerting concentrated pressure on underlying tissue. Of all the intrinsic causes of foot ulceration, callus is considered to be the most threatening to tissue integrity and the most common. Fortunately, callus is an easily recognizable clinical entity which most health professionals and patients alike are competent to detect. Early detection is vital as this enables early intervention by means of regular debridement and long-term pressure relief (Fig. 3).

Plantar Fat Pad Integrity The plantar fat pad provides the human foot with a custom made, in-built cushioning mechanism. The plantar fat pad is located under the ball of the foot beneath the metatarsal heads and under the calcaneus or heel. The metatarsal heads and the calcaneus bear the majority of the peak load on weightbearing and hence benefit the most from the protective, cushioning provided by the plantar fat pad. It has been observed in cases where there is clawing or retraction of the lesser digits that Fig. 2  Vertical stress and peak plantar pressure

Recent publications indicate that there is likely to be techno­ logy available to the diabetic foot clinician in the very near future. Despite the reducing cost and availability of equipment to assess both plantar pressure and shear stress, there remains a debate over how clinically useful this technology is to the general diabetic foot practitioner. Bridging the divide between research and clinical application is an area that still requires further development in relation to plantar pressure and shear stress evaluation.

Fig. 3  Callus on right 1st MP joint and on left 5th MP joint



42    Contemporary Management of the Diabetic Foot the plantar fat pad under the metatarsal heads migrates and is displaced anteriorly. Unfortunately, evaluating the integrity of the plantar fat pad is very subjective. There are currently no known tools available to quantify how much atrophy of the plantar fat pad is required to place a person at risk of ulceration. If the clinician suspects that the plantar fat pad has atrophied or is in any doubt, then the provision of plantar cushioning in footwear or orthotics is recommended. It is unlikely that this action will cause adverse effects in either case.

Limited Joint Mobility The relationship between diabetes and limited joint mobility has generated much research in recent times and yet much is still unknown about this phenomenon. The common theory is that the process of glycosylation causes stiffening of collagen in joint capsules leading to the restricted range of motion seen clinically. The foot joints most commonly affected by limited joint range of motion are the ankle joint and the first metatarsophalangeal joint. While some researchers indicate that a positive prayer sign is indicative of limited joint range of motion in the feet, this association is yet to be confirmed by large-scale, high-quality research. As such, the following discussion will not rely on the prayer sign but rather evaluate both the ankle and the first metatarsophalangeal joint range of motion as separate entities. This decision relies on the principle that there may be people who have a preexisting ankle equinus or first ray pathomechanics which are independent to diabetes-induced limited joint range of motion. By relying on the prayer sign alone to determine limited joint range of motion, biomechanical abnormality in the forefoot, unrelated to the effects of glycosylation, may fail to be detected and corrected. Normal range of motion for the ankle joint is 10° of dorsiflexion. This range of motion is necessary to enable normal heel-to-toe function during gait. The primary treat­ ment modality in patients with less than 10° of dorsiflexion is stretching of the posterior leg muscles. Stretching in the neuropathic patient must be carried out with caution and where possible the therapy should be conservative and carried out under supervision. The neuropathic patient is at greater risk of injury due to the lack of sensory feedback and may be at risk of tendon injury or joint disruption. Acupuncture or dry needling of the posterior leg muscles has been shown to relax the muscles prior to stretch and may prove of some benefit to patients with very tight posterior leg muscles. Surgical intervention in the form of a tendon-lengthening procedure is indicated in extreme cases where there is evidence of a shortened Achilles tendon and conservative therapy has failed. Surgical intervention may also be indicated in cases where a tight posterior muscle complex is believed to be the primary cause of plantar forefoot ulceration and where conservative therapy has failed (Fig. 4).

Fig. 4  Normal range of motion (dorsiflexion) at first metatarsophalan­ geal (MP) joint during weightbearing

Normal range of motion for the first metatarsophalangeal joint is greater than 50° of dorsiflexion during nonweight bearing and greater than 12° of dorsiflexion during weight bearing. Adequate first metatarsophalangeal joint dorsiflexion is necessary to allow the heel to lift during the propulsive phase of gait. Inadequate first metatarsophalangeal joint dorsiflexion will cause joint destruction and potentially increase the risk of Charcot arthropathy. Clinical signs of limited joint range of motion in the first metatarsophalangeal joint include dorsal exostosis over the joint, hyperextended (dorsiflexed) hallux (first toe), and callus over the medial, plantar aspect of the hallux (first toe) as well as beneath the second to fifth metatarsophalangeal joints. Treatment for restricted range of motion in the first metatarsophalangeal joint is directed toward functional immobilization of the first metatarsophalangeal joint and joint manipulation to increase joint range of motion. Joint manipulation is a specialized area and will not be discussed here as this therapy should be carried out by skilled professionals. Immobilization of the first metatarsophalangeal joint can be achieved by using a rocker-sole under the forefoot of the shoe. Further specialized mechanical alterations can be achieved using a functional orthotic device which stabilizes rearfoot and midfoot function. Surgical intervention may be indicated in severe cases where abnormal pressure distribution is causing persistent and nonresolvable ulceration (Table 2).

REARFOOT BIOMECHANICS The biomechanical function of the rearfoot is critical to the normal functioning of the foot. As discussed in the previous section, the subtalar joint is required to pronate following heel strike, placing the calcaneus in an everted position. Following the stance phase of gait, the subtalar joint resupinates, placing the calcaneus in an inverted position which assists with the propulsion phase of gait. In patients who have either a rearfoot valgus or rearfoot varus, this “normal” function



The Biomechanics of the Diabetic Foot    43 Table 2  Treatment pathway: diabetic foot biomechanics Assess for biomechanical abnormality

Outcome

Intervention and treatment

Inspect for callus and corns

Callus and corns detected

• • • •

Debride callus and corns, and review regularly to repeat this treatment Assess footwear for suitability Recommend regular self-monitoring for signs of change Recommend regular application of emollient, specifically urea-based where callus is heavy

Inspect integrity of the plantar fat pad

Evidence of fat pad atrophy

Select cushioning replacement therapy such as siliconeheel and forefoot padding

Joint range of motion:  Ankle

< 10° dorsiflexion ankle joint

Stretching program for Achilles tendon, prophylactic tendon-lengthening surgery for recalcitrant cases Functional immobilization with orthotics or rocker sole, joint manipulation, surgery

  First metatarsophalangeal joint.

< 60° dorsiflexion metatarsophalangeal joint

described above is compromised. The most common clinical presentation of abnormal rearfoot biomechanics is abnormal or excessive pronation during late midstance, stance and propulsion. This abnormal pronation can lead to abnormal forces being placed on the foot which in turn leads to the development of callus.

Rearfoot Varus Rearfoot varus is a condition where the rearfoot is in an inverted position in relationship to the ground when the subtalar joint is in a neutral position. Rearfoot varus can be broadly categorized as compensated and uncompensated. The common theory with compensated rearfoot varus is that the subtalar joint will attempt to compensate for the inverted calcaneal position by pronating beyond the “normal” range to enable the calcaneus to meet the ground and stabilize the foot. Other compensatory mechanisms may occur including plantar flexion of the first ray and abduction of the foot. In the compensated rearfoot varus, a common site for callus to develop is plantar to the second metatarsal head as shown in Figure 5. Treatment for compensated rearfoot varus involves the use of a medial heel wedge to reduce the compensatory pronation occurring at the subtalar joint. Uncompensated rearfoot varus is an uncommon condition. In the uncompensated rearfoot varus, the subtalar joint does not pronate leaving the heel and the foot in an inverted position during stance. Common distribution of callus in the uncompensated, rearfoot varus occurs under the fifth metatarsal head as shown in Figure 6. Treatment for uncompensated rearfoot varus is directed toward increasing shock absorption and redistributing plantar pressure more evenly. This can be achieved using accommodative, cushioned orthotics and footwear. A

Fig. 5  Compensated rearfoot varus

Fig. 6  Uncompensated rearfoot varus



44    Contemporary Management of the Diabetic Foot

FOREFOOT BIOMECHANICS There are a range of mechanical conditions which can affect the forefoot including, but not limited to: forefoot supinatus, forefoot varus, forefoot valgus, hallux limitus and hallux rigidus. Each of these pathologies can cause the foot to compensate in different ways, causing a range of abnormal pressure areas and increasing the risk of ulceration.

Forefoot Varus

Fig. 7  Rearfoot valgus

lateral heel flare to the patients shoe can improve the lateral instability associated with this condition and reduce the abnormal lateral load placed on the foot.

Rearfoot Valgus Rearfoot valgus is a condition where the rearfoot is in an everted position in relationship to the ground when the foot is in a neutral position. True rearfoot valgus is a very uncommon condition and may be associated with conditions such as tarsal coalition. The presentation of an everted rear­ foot is more commonly a secondary abnormality due to a primary abnormality occurring elsewhere in the leg or foot such as genu valgum (knocked knees) or a forefoot positional abnormality (Fig. 7). Figure 8 illustrates the characteristic features associated with rearfoot valgus. Treatment options for rearfoot valgus are directed toward managing the primary abnormality or in the case of a tarsal coalition, surgery may be indicated. A medial heel flare to the patients shoe can improve the medial instability associated with this condition and reduce the abnormal medial load placed on the foot and ankle (Table 3).

Forefoot varus is considered a relatively rare condition. In simplistic terms, this abnormality is characterized by a fixed, inverted position of the forefoot relative to the rearfoot when the foot is placed in a neutral position. Forefoot varus can be broadly classified as compensated and uncompensated. In a compensated forefoot varus, the subtalar joint is forced into maximum pronation during midstance to enable the forefoot to contact the ground. This process has the effect of destabilizing the foot by encouraging hypermobility. Compensated forefoot varus is characterized clinically by excessive weightbearing on the medial border of the foot. Other clinical signs can include forefoot deformity due to the enhanced hypermobility. Deformities may include: hallux abducto valgus (bunions), lesser toe deformities and plantar metatarsal head callus (Fig. 8). Figure 8 illustrates the common sites for callus associated with compensated forefoot varus which concentrates under the second metatarsal head. The management of forefoot varus should focus on reducing the development of callus by controlling abnormal pronation of the subtalar joint and reducing hypermobility of the forefoot. This can be achieved by supporting the forefoot with a medial wedge. In simplistic terms, an uncompensated forefoot varus occurs when the forefoot is inverted relative to the rearfoot and relative to the ground, when the foot is placed in neutral position. This deformity is characterized by a foot which maintains an inverted, laterally-loaded position throughout the gait cycle due to a lack of available subtalar joint pronation. Uncompensated forefoot varus presents clinically as a rigid, immobile foot with minimal shock absorption.

Table 3  Treatment pathway: rearfoot biomechanics Section

Joints

Functions

Varus compensated

Everted rearfoot on weightbearing, callus under second metatarsal head

Medial heel posting or rearfoot varus wedge

Varus uncompensated

Inverted rearfoot on weightbearing, callus under the fifth metatarsal head

Accommodative orthotics providing shock absorption and weight distribution, accommodative footwear, lateral heel flare

Valgus

Everted rearfoot on weightbearing

Physical therapy to correct upper limb abnormality, accommodative orthotics and footwear, medial heel flare

Rear foot biomechanics:

Appropriate referral where available: Podiatrist, Orthotist, Surgeon



The Biomechanics of the Diabetic Foot    45

Fig. 8  Compensated forefoot varus

Unlike compensated forefoot varus, forefoot deformity is an uncommon complication of this positional abnormality. Plantar callus distribution occurs beneath the fifth metatarsal head and the plantar aspect of the interphalangeal joint of the hallux (first toe). A common distribution of callus in the uncompensated forefoot varus is shown in Figure 9. Uncompensated forefoot varus should be managed using accommodative orthotics and footwear which redistribute pressure rather than control function. A lateral flare to the shoe can reduce the abnormal load placed on the lateral border of the foot and improve stability.

Forefoot Supinatus Forefoot supinatus is a soft tissue deformity which is believed to be acquired through long-term excessive pronation of the subtalar joint. Forefoot supinatus presents clinically in the same way as forefoot varus. Supinatus can be differentiated from forefoot varus by applying a plantar-grade force on the talonavicular joint. If the forefoot presents with a spongy resistance during this maneuver and can be reduced then this confirms supinatus. Forefoot varus will not be reducible and will present with a bony resistance to this maneuver. The focus of treatment for forefoot supinatus should be to reduce abnormal distribution of shear stress to reduce the development of callus. Treatment of forefoot supinatus focuses on managing rearfoot pronation and not supporting the forefoot deformity. Supporting the forefoot deformity with a medial or varus forefoot wedge will exacerbate the condition and the deformity will be encouraged.

Forefoot Valgus

Fig. 9  Uncompensated forefoot varus

Forefoot valgus is a deformity where the forefoot is everted, compared with the rearfoot when the foot is in a neutral position. Forefoot valgus is broadly classified into two categories: (1) total forefoot valgus and (2) partial forefoot valgus. Partial forefoot valgus occurs when the first ray is plantarflexed giving the appearance that the forefoot is in an everted position. The main difference between the two conditions is the position of the metatarsal heads. In total forefoot valgus all the metatarsal heads remain in the same



46    Contemporary Management of the Diabetic Foot plane which is everted relative to the rearfoot as described above. In partial forefoot valgus, or plantarflexed first ray, the first metatarsal head is plantarflexed in relation to the lesser metatarsal heads which usually remain on the same plane as the rearfoot. Irrespective of the classification, the foot generally functions in the same way. Forefoot valgus is further classified into two groups: (1) rigid forefoot valgus and (2) mobile forefoot valgus. This classification is clinically more important as these two subtypes compensate in very different ways, leading to very different foot pathologies.

Rigid Forefoot Valgus In the rigid forefoot valgus, the forefoot loads from the first metatarsal to the fifth metatarsal which is the reverse of normal forefoot loading during gait where the lateral forefoot loads first. Feet with a rigid forefoot valgus present with a pes cavus (high-arched) appearance and are characterized by reduced shock absorption. Foot pathologies associated with rigid forefoot valgus include clawed or retracted lesser toes, callus over the first and fifth metatarsal heads and apex (tips) of the second, third and fourth toes and lateral heel callus. A common distribution of callus in the rigid forefoot valgus is shown in Figure 10. Treatment for rigid forefoot valgus should focus on accom­­ modating rather than controlling the forefoot deformity. Shoes and orthotics with extra shock absorption and cushioning are indicated, and the inclusion of a metatarsal pad has been shown to add further benefit in reducing plantar metatarsal head callus. These devices redistribute the plantar pressure more evenly across the foot, reducing the load over the metatarsal head area while replacing some of the shock absorption which this rigid

Fig. 11  Mobile forefoot valgus

foot type lacks. The lateral aspect of the heel of the shoe can also be flared to reduce lateral load on the foot from midstance. Simple devices such as toe props will also reduce pressure over the apex of the second to fourth toes.

Mobile Forefoot Valgus The mobile forefoot valgus is characterized by forefoot instability. Loading of the forefoot occurs in the same manner as the rigid forefoot valgus with forefoot contact occurring over the first metatarsal head and then transferring to the fifth metatarsal head. The similarity between the two conditions stops here. The mobile forefoot valgus distorts when the forefoot loads, causing the first metatarsal to dorsiflex, supinating the midtarsal joint and forefoot and facilitating the hypermobility characterized by this condition. Clinical signs of this condition are hallux abducto valgus (bunion), deformity of the lesser toes, callus concentrated under the second to fourth metatarsal heads, splayed forefoot, and tailor’s bunion with associated corns (Fig. 11). Figure 11 illustrates the common sites for callus associated with mobile forefoot valgus. Treatment principles for mobile forefoot valgus are very similar to those described for rigid forefoot valgus (Table 4).

JOINT DEFORMITY

Fig. 10  Rigid forefoot valgus

Orthopedic foot deformity is recognized as one of the most significant factors involved in the development of diabetic foot ulceration. For this reason, most diabetic foot screening and assessment tools include deformity. Unfortunately, there remains a lack of a valid and reliable test for deformity and hence the detection and classification of foot deformity remains a relatively subjective test. The most common foot deformities which are associated with foot ulceration include: clawed or retracted toes, hallux



The Biomechanics of the Diabetic Foot    47 Table 4  Treatment pathway: forefoot biomechanics Section

Joints

Functions

Forefoot varus compensated

Excessive weightbearing on medial border of the foot, hallux abducto valgus, lesser toe deformities, callus under second metatarsal head

Medial forefoot wedge

Forefoot varus uncompensated

Rigid, immobile foot with minimal shock absorption remains in an inverted laterally-loaded position during gait, callus under fifth metatarsal head

Accommodative orthotics and footwear, lateral heel flare

Forefoot supinatus

Reducible when applying plantar grade force on talonavicular joint, spongy end range of motion

Control rearfoot pronation with orthotic

Rigid forefoot valgus

During gait first metatarsal loads first, rigid, pes cavus foot, minimal shock absorption, clawed or retracted toes, callus under first and fifth metatarsal head

Accommodative orthotics and footwear with extra cushioning, metatarsal pad, lateral heel flare, toe props

Mobile forefoot valgus

During gait first metatarsal loads first, characteristic joint hypermobility, hallux abducto valgus, lesser toe deformity, splayed forefoot, Tailor’s bunion

Accommodative orthotics and footwear with extra cushioning, metatarsal pad, lateral heel flare, toe props

Forefoot biomechanics:

Appropriate referral where available : Podiatrist, Orthotist, Surgeon

abducto valgus (bunions), fifth toe varus and tailor’s bunion, Charcot joints and other joint changes associated with degene­rative joint conditions such as osteoarthritis. Each of these conditions presents differently, but each has the potential to cause significant damage when combined with neuropathy, peripheral arterial disease and poorly fitted footwear.

Clawed and Retracted Toes Treatment for clawed and retracted toes focuses on reducing the deformity where possible and decreasing the secondary pressure placed over the apex (tip) of the deformed toes and the plantar metatarsal head area. Toe props made from accommodative, soft materials can be fashioned to fit under the toes, proximal to the tips to redistribute pressure away from the apices. Plantar metatarsal pads promote dorsiflexion and splaying of the metatarsal heads, reducing pressure over this area. Plantar metatarsal pads also facilitate plantar flexion of the lesser toes, reducing some of the clawing deformity on weight bearing. Custom made footwear or adaptable footwear is recommended for nonreducible digital deformity to alleviate dorsal shoe pressure. In severe cases of fixed deformity, surgical reduction may be indicated.

Hallux Abducto Valgus (Bunion) Treatment for hallux abducto valgus (bunion) focuses on addressing the primary mechanical foot abnormality while providing local padding and protection to bony prominences. In cases where excessive foot pronation is occurring, orthotic devices are indicated to control abnormal motion. Local padding to separate over-riding toes can reduce interdigital

friction and plantar metatarsal cushions will compensate for loss of the plantar forefoot fat pad. Toe props assist to reduce pressure over the apices of the lesser digits and doughnut padding to the medial first metatarsal head will protect bursa over the medial first metatarsal head area. Appropriate footwear selection plays a vital role in preventing ulceration in the diabetic foot, particularly in the patient with hallux abducto valgus as this deformity is rarely accommodated by high street shoes. Extra width, extra depth, and custom made footwear are often necessary when severe deformity of the first metatarsophalangeal joint develops. Specific footwear modifications may be required including balloon patching to accommodate severe abduction deformity of the medial aspect of the first metatarsal. Surgical correction of this deformity may be necessary in cases where persistent reulceration is an ongoing concern.

Tailor’s Bunion and Fifth Toe Varus A Tailor’s bunion occurs over the fifth metatarsophalangeal joint when the fifth ray everts and abducts. This positional change creates a bunion-like protrusion which develops bursa and corns and callus and is prone to irritation in footwear and consequent ulceration in the high-risk foot. A further consequence of the everted and abducted position of the fifth metatarsal is that the fifth toe may assume a varus position. This positional abnormality can cause additional pressure over the lateral interphalangeal joints and the lateral apex (tip) of the fifth toe with the development of corns and callus increasing the risk of ulceration. Both these conditions can be managed conservatively with the use of padding to areas of friction and orthotics to control abnormal motion in



48    Contemporary Management of the Diabetic Foot Table 5  Treatment pathway: diabetic foot biomechanics Section

Joints

Functions

Clawed and retracted toes

Tips of toes touch ground with clawing but not retraction

Toe props, plantar metatarsal pads, custom made shoes, surgical correction

Hallux abducto valgus

Abducted first metatarsal, valgus hallux, Orthotics, plantar metatarsal cushions, toe props, prominent first metatarsophalangeal joint, doughnut padding, balloon patching, extra width, extra bursa, over-riding toes depth or custom made shoes, surgery

Tailor’s bunion and fifth toe varus

Eversion and abduction of the fifth metatarsal, Orthotics, doughnut padding, interdigital wedges, bunion over fifth metatarsophalangeal joint, silicone devices, balloon patching, extra width or bursa, varus fifth toe custom made shoes, surgery

Charcot foot

Severe destruction of midfoot, rearfoot or forefoot, rocker bottom foot, valgus ankle

Joint deformity:

Accommodation of deformity with custom made footwear and orthotics, surgical reconstruction

Appropriate referral where available : Podiatrist, Orthotist, Surgeon

the forefoot. Doughnut padding for the fifth metatarsal head and interdigital wedges and silicone devices to separate and reposition the toe can provide immediate pressure relief. Footwear modifications such as balloon patching and extra width shoes are often indicated. Custom made shoes may be required in cases where severe joint deformity exists. Surgical correction of the joints may be necessary where persistent and recurrent ulceration occurs and when the conservative measures described above fail.

Charcot Foot The Charcot foot is a relatively uncommon but severely destructive process affecting the joints of the foot. This condition occurs in people with diabetes and other medical conditions which are associated with peripheral neuropathy. A detailed discussion of the Charcot foot is the focus of a separated chapter in this book. As such, it will be assumed that the reader has a pre-existing understanding of the pathogenesis of this condition. Acute phase Charcot requires specialized medical care and immediate immobilization of the limb via a total contact cast. This chapter will focus on the management of the chronic Charcot foot which has entered the coalescence and consolidation phase and has undergone some disturbance to the normal foot architecture. Charcot joint changes most commonly occur at the midfoot but are also seen in the rearfoot, the ankle, and the forefoot. In each of these circumstances, the structure of the foot is characterized by a single commonality, which is that the foot no longer resembles its original form or the unaffected contralateral foot. Charcot joint deformity is often characterized by either a rocker-bottom foot, a severely everted ankle with medial protrusion of the malleolus, or dorsal subluxation of the metatarsophalangeal joints displacing the toes skyward. In each of these cases, the foot no

Fig. 12  Foot deformities

longer fits into high street shoes, and custom made footwear is necessary to accommodate the deformity. Surgical reconstruction is indicated in medically stable cases where reulceration is an ongoing problem (Table 5). Figure 12 illustrates the most common foot deformities seen in the diabetic foot.

ACKNOWLEDGMENTS The author wishes to acknowledge the contribution of Sarah Pellone who created the drawings for this chapter and Mrs Helen Barber who edited the manuscript.

CONFLICT OF INTEREST The author declares no known conflict of interest.

CHAPTER

7

Examination of Feet

Sharad Pendsey

INTRODUCTION Examination of feet is an integral part of physical examination of every patient, more so a diabetic patient. The goal should be to identify: • Normal feet • Feet at risk • Presence of significant neuropathy • Presence of significant ischemia • Presence of foot lesions. Screening procedure should be quantifiable, reproducible, predictive and inexpensive. Every person with diabetes has a risk of developing foot ulceration and needs to take precaution to prevent it. However, some have increased risks of foot ulceration and they need to be identified as at high-risk and subjected to elaborate examination.

QUICK EXAMINATION OF THE FEET History is a pivotal component. Tingling, numbness, burning in feet, previous foot ulcer, and use of tobacco and claudication pain in legs are key components of the history. In busy office practice, feet should be examined after removal of socks for deformities, nail pathologies or callus. Sensation in feet should be tested by pin prick or 10 g monofilament and vibration by 126-Hz tuning fork or by the newly introduced vibratip. Vibratip is a small handy battery operated instrument. It vibrates on pressing the knob (Fig. 1). Peripheral pulsation should be palpated on both feet for dorsalis pedis and posterior tibial. In the presence of abnormal examination findings, further elaborate examination should be recommended. Examination of the feet should at least be done once in a year even if there are no abnormal findings.

Fig. 1  Vibratip

COMPREHENSIVE EXAMINATION OF FEET Inspection The examiner should insist on removal of the shoes and socks or stockings. One should look for neuropathic changes like dry skin, fissures indicative of autonomic neuropathy (Fig. 2) deformities of the toes because of atrophy of small muscles of the foot (motor neuropathy). Common forefoot deformities that are known to increase plantar pressures and making the feet vulnerable for ulceration include metatarsal phalangeal joint hyperextension with interphalangeal flexion (Fig. 3) or distal phalangeal extension (Fig. 4). One should also look for bunions (Fig. 5), callus (Fig. 6) abnormal shape of foot indicating neuroarthropathy or charcot



50    Contemporary Management of the Diabetic Foot

Fig. 2  Long and deep fissure on heel

Fig. 5  Bunion (Bunionette)

Fig. 3  Intrinsic minus feet, note muscle atrophy, clawing of toes

Fig. 6  Callus

Fig. 4  Hammer toe

foot (Fig. 7), ulceration, prominent veins on the dorsum of the foot and nail pathologies. Prominent veins occur because of arteriovenous shunting as a result of autonomic neuropathy. A careful attention should be given to the interdigital spaces. Back of the heels should be looked for any area of necrosis particularly in bedridden patients. Diabetic dermopathy (Fig. 8) can be diagnosed by looking at the tibial surface of the leg. A significant ischemia is characterized by loss of hair on the dorsum of foot and dependent rubor. Footwear of the patient should also be examined as faulty footwear can often be the cause of foot ulceration. Such shoes include those that are excessively worn or too small or too narrow for the person’s feet, resulting in friction causing blister or erythema and bunions.



Examination of Feet    51

Fig. 7  Charcot foot

Fig. 9  Angle of hallux

Movements of the joints of foot should be examined like dorsi and plantar flexion of all toes specially that of hallux and that of ankle. To test subtalar joint one should look for inversion and eversion of foot. Limited joint mobility (LJM) in feet is a characteristic feature of a long standing diabetes. LJM leads to hallux rigidus increasing susceptibility to ulceration and the plantar surface of the hallux. Hallux rigidus can be diagnosed by asking the patient to dorsiflex hallux while the foot is weight-bearing. The angle between ground and hallux should be 15° (Fig. 9).

ASSESSMENT OF SIGNIFICANT NEUROPATHY

Fig. 8  Diabetic neuropathy brown circular patches on both tibial shins

Palpation One should feel whether the foot is warm or cold, examine the peripheral pulsations like dorsalis pedis, which can be felt lateral to the extensor hallucis longus tendon, and the posterior tibial, which is above and behind the medial malleolus. The femoral artery should also be palpated and auscultated for the presence of bruit. The plantar aspects of the feet should be felt for the presence of any bony prominences.

Distal symmetric polyneuropathy affects sensory, motor and autonomic nerves. It also involves both small and large nerve fibers, rarely a selective involvement of the small nerve fibers is seen in diabetics such as in painful neuropathy, where selectively the thermal sensation (small nerve fibers) is lost with preservation of touch and vibration (large nerve fibers) (Table 1). American Diabetes Associations (ADA) task force of the foot care recommends five simple clinical tests, in the diagnosis of loss of protective sensation (LOPS) in the diabetic foot.

Testing with Monofilament Nylon monofilament of 5.07 sizes (thickness), equivalent of 10 g of linear force should be used. It tests sense of touch (large nerve fiber function). When applied perpendicular to the foot, it buckles at a given force of 10 g (Fig. 10).



52    Contemporary Management of the Diabetic Foot Table 1  Nerve fiber functions Small nerve fiber

Large nerve fiber

Thermal sensation (heat and cold perception)

Vibration perception touch sensation position sense

Pain sensation

Deep tendon reflexes

Sweating (sympathetic)

Motor nerves

to deform the skin. Inability to perceive pinprick over either hallux would be regarded as an abnormal test result.

Ankle Reflex Ankle reflexes can be tested with the patient either kneeling or resting on a table. The Achilles tendon should be stretched until the ankle is in a neutral position before striking it with the tendon hammer. If a response is initially absent, it can be retested with reinforcement. Total absence of ankle reflex either at rest or upon reinforcement is regarded as an abnormal result.

VIBRATION PERCEPTION THRESHOLD TESTING The degree of neuropathy can be further quantified by the use of the biothesiometer (Fig. 11). When applied to the foot, it delivers a vibratory stimulus, which increases as the voltage is raised. The biothesiometer is widely used for the quantitative assessment of the vibration perception threshold (VPT). With the patient lying supine, the stylus of the instrument is placed over the pulp of great toe and the amplitude is increased until the patient can detect the vibration; the resulting number is known as the VPT. A VPT more than 25 V is regarded as abnormal and has been shown to be strongly predictive of subsequent foot ulceration. Fig. 10  Testing while the monofilament buckles

The patient should be able to sense the monofilament by the time it buckles. The filament should be pressed at several sites; e.g. plantar aspects of the first toe, the first, third and fifth metatarsal heads, the heel and dorsum of the foot. The patient’s inability to feel the filament indicates a LOPS (a high-risk foot). Patient should close the eyes while being tested. Caution is necessary when selecting the brand of monofilament to use, as many commercially available monofilaments have been shown to be inaccurate.

TESTING FOR VASCULAR ASSESSMENT Vascular examination should include palpation of the posterior tibial and dorsalis pedis pulses, which should be characterized as either “present” or “absent”. Diabetic patients with signs or symptoms of vascular disease or absent pulses on screening

128-Hz Tuning Fork Vibratory sensation should be tested using 128-Hz tuning fork over the tip of the great toe bilaterally. An abnormal response can be defined as when the patient loses vibratory sensation and the examiner still perceives it while holding the fork on the tip of the toe.

Pinprick Sensation A disposable pin should be applied just proximal to the toenail on the dorsal surface of the hallux, with just enough pressure

Fig. 11  Testing with biothesiometer



Examination of Feet    53

Fig. 12  Measuring ankle systolic pressure with hand held Doppler [Ankle brachial pressure index (ABPI)]

foot examination should undergo ankle brachial pressure index (ABPI).

Fig. 13  Footprint, darker areas indicate high pressure

Ankle Brachial Pressure Index A hand-held Doppler can be used to confirm the presence of pulses and to quantify the vascular supply (Fig. 12). When used together with a sphygmomanometer, the ankle and brachial systolic pressures can be measured and the ratio then calculated. In normal subjects, the ankle systolic pressure is higher than brachial systolic pressure. The normal ABPI is more than 1, in the presence of ischemia it is less than 0.9. Absent or feeble pulses with ABPI less than 0.9 confirm ischemia. Conversely, the presence of pulses and ABPI more than 1 rules out significant ischemia. An ABPI of less than 0.8 is associated with claudication, and less than 0.4 is commonly associated with ischemic rest pain and tissue necrosis. ABPI measurements may be misleading in diabetes because of the presence of medial calcinosis which renders the arteries incompressible and results in falsely elevated ABPI more than 1.3.

Testing for High Pressure Points The feet can be evaluated for high pressure points by a simple inexpensive technique using Harris mat. The patient is asked to walk on the mat. Ink is applied on the other side of the mat with the roller. While interpreting the footprint, darker area indicates a high pressure point (Fig. 13). This test is however to quantitative and has its limitations. A quantitative measurement of plantar pressure is now available for a barefoot, as well as in-shoe, using a computer and special software (Fig. 14).

Fig. 14 Quantitative measurement of plantar pressure using a computer and special software

However, being expensive, it cannot be made available at every center. Once the patient has been classified into either nonrisk category or high-risk category, a further evaluation depending upon the risk category can be carried out. International Consensus on the Diabetic foot by the International Working Group on the Diabetic Foot suggests the risk classification system, have been described in Table 2.



54    Contemporary Management of the Diabetic Foot Table 2  Risk categorization system Category

Risk profile

Check-up frequency

0

No sensory neuropathy

Once a year

1

Sensory neuropathy

Once every 6 months

2

Sensory neuropathy and signs of peripheral vascular disease and/or foot deformities

Once every 3 months

3

Previous ulcer or amputation

Once every 1–3 months

If patient presents with foot pathology, then careful inspection of the foot should be carried out for erythema, swelling and purulent discharge. Skin temperature should be measured in both feet by infrared thermometer and if the difference is more than 2°, one should suspect cellulitis or acute charcot foot. If the ulcer is present, measurements like length, breadth and depth should be assessed along with probe to bone test (PBT) (Fig. 15) for osteomyelitis. It is important to differentiate between neuropathic and neuroischemic ulceration as the consequences and treatment modalities are altogether different. The differentiating features are given in Table 3.

CONCLUSION Every person with diabetes should undergo examination of feet at least once in a year. Those who have at risk feet should undergo comprehensive examination of feet more frequently. Table 3  Differentiating features between neuropathic and neuroischemic foot Characteristics

Neuropathic foot

Neuroischemic foot

Skin temperature

Warm

Cold

Pain

Painless

Painful

Skin color

Not altered

Dependent rubor

Callus

Thick at pressure points

May or may not be present

Ulcer

Plantar at pressure points Dorsal at areas of stress

Margins of toe

Peripheral pulses

Bounding

Feeble or not palpable

ABI

> 0.9

< 0.9

Fig. 15  Probe to bone test (PBT)

It is through patient education and lifelong surveillance of high-risk feet, we shall be able to prevent foot problems and eventually limb amputation in persons with diabetes. For examination of feet what one really needs is a sensible pair of hands and eyes. Type 1 diabetic children are not at higher risk of foot ulceration in the early years after the onset of diabetes. They should be encouraged to undertake physical activities and participate in various sports similar to that of nondiabetic children.

SUGGESTED READING 1. Apelqvist J, Bakker K, van Houtum WH, et al. International Consensus and practical guidelines on the management and the prevention on the Diabetic foot International Working Group on the Diabetic Foot. Diabetes Metab Res Rev. 2000;16 (Suppl 1):S84-99. 2. Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the foot care interest group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists, Diabetes Care. 2008;31(8):1679-85. 3. Pendsey S. Diabetic Foot: A Clinical Atlas, 1st edition. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd.; 2003.

CHAPTER

Classification and Staging of Diabetic Foot

8 Michael Edmonds

INTRODUCTION There are four types of classification of the diabetic foot. Firstly, a classification which embraces the whole of the natural history of the diabetic foot. Secondly, there are classification systems documenting the risk of future ulceration. Thirdly, there are classifications of diabetic foot ulcers, and lastly classifications of diabetic foot infection. This chapter will concentrate on a Classification and Simple Staging System based upon the natural history of the diabetic foot with the aim to provide a framework for early diagnosis and management. This is the Simple Staging System which encompasses the whole spectrum of diabetic foot disease and documents the progression from a high-risk foot to gangrene and eventually unsalvageable foot. However, it emphasizes the development of the diabetic foot ulcer as a pivotal event demanding prompt management. It thus includes a risk assessment of ulceration, a basic classification of the ulcer and also covers the complications of ulcers. Other classifications of diabetic foot ulcers will briefly be considered.

CLASSIFICATION OF THE DIABETIC FOOT For practical purposes, the diabetic foot can be divided into two entities: (1) the neuropathic foot and (2) the ischemic foot. However, ischemia is nearly always associated with neuro­ pathy, and the ischemic foot is best called the neuroischemic foot. The purely ischemic foot, with no concomitant neuropathy, is seen in diabetic patients but rarely and its management is essentially the same as for the neuroischemic foot except when sharp debriding which may be painful in the absence of neuropathy.

It is essential to differentiate between the neuropathic foot and the neuroischemic foot as their management will differ. Infection is the most frequent complication of ulceration in both the neuropathic foot and neuroischemic foot. It is important to diagnose it promptly and intervene rapidly. It is responsible for considerable tissue necrosis in the diabetic foot and this is the main reason for major amputation.

Neuropathic Foot • This is a warm, well-perfused foot with bounding pulses due to arteriovenous shunting and distended dorsal veins. • Sweating is diminished, the skin may be dry and prone to fissuring, and any callus present tends to be hard and dry. • Toes may be clawed and foot arch is raised. • Ulceration may develop on the sole of the foot, associated with neglected callus and high plantar pressures. • Despite the good circulation, necrosis can develop secondary to severe infection. • It is also prone to bone and joint problems (the Charcot foot). • As patients are followed for many years in the diabetic foot clinic, the neuropathic foot often develops ischemia and becomes a neuroischemic foot.

Neuroischemic Foot • It is a cool, pulseless foot with reduced perfusion and almost invariably has neuropathy. • The color of the severely ischemic foot can be a deceptively healthy pink or red, caused by dilatation of capillaries in an attempt to improve perfusion. If severely infected, the ischemic foot may feel deceptively warm.



56    Contemporary Management of the Diabetic Foot • It may also be complicated by swelling, often secondary to cardiac failure or renal failure. • The most frequent presentation is that of ulceration. Ischemic ulcers are commonly seen on the margins of the foot, including the tips of the toes and the areas around the back of the heel, and are usually caused by trauma or by wearing unsuitable shoes, which do not accommodate deformity. • Intermittent claudication and rest pain may be absent because of neuropathy and the distal distribution of the arterial disease to the leg. • Even if neuropathy is present and plantar pressures are high, plantar ulceration is rare, probably because the foot does not develop heavy callus, which requires good blood flow. • It develops necrosis in the presence of infection or if tissue perfusion is critically diminished. The neuroischemic foot has now become the most frequently encountered type of foot to present to the diabetic foot clinic. There has been a change of predominance from neuropathic to neuroischemic feet as people present more readily with ischemic disease and live longer with feet which may be salvaged by bypass or angioplasty but are still challenging to manage.

ASSESSMENT OF THE DIABETIC FOOT The staging system is based on a simple assessment of the foot, which should take no longer than 5 minutes. The examination includes: • Simple inspection • Palpation • Sensory testing. Sensory neuropathy can be simply detected by: • Monofilaments Or • Neurothesiometry. If these are not available, then a simple clinical exami­ nation detecting sensation to light touch using a cotton wool and vibration using a 128-Hz tuning fork will suffice, comparing a proximal site with a distal site to confirm a symmetrical stocking-like distribution of the neuropathy. The advantage of the assessment with monofilaments or neurothesiometry is that it detects patients who have lost protective pain sensation and are therefore susceptible to foot ulceration. The most important maneuver in the detection of ischemia is the palpation of foot pulses, an examination which is often undervalued. • The dorsalis pedis pulse is lateral to the extensor hallucis longus tendon on the dorsum of the foot. • The posterior tibial pulse is below and behind the medial malleolus. • If either of these foot pulses can be felt then it is highly unlikely that there is significant ischemia.

SIMPLE STAGING OF THE DIABETIC FOOT The natural history of the diabetic foot can be divided into six stages: 1. The normal foot: The foot is normal and not at risk. The patient does not have the risk factors that render him vulnerable to foot ulcers (neuropathy, ischemia, deformity, callus and edema). 2. High risk foot: The patient has developed one or more of the risk factors for ulceration of the foot. 3. Foot with ulcer: Ulceration in the neuropathic foot develops at the sites of high mechanical pressure on the plantar surface (Fig. 1). In contrast, ulcers in the foot with both neuropathy and ischemia (neuroischemic foot) occur on the margins of the foot and toes, at sites of prolonged low pressure usually from poorly fitting shoes. Recent studies have shown that ischemic ulcers make up approximately 50% of total. 4. Foot with cellulitis: The ulcer has developed infection with the presence of cellulitis, which can complicate both the neuropathic and the neuroischemic foot. 5. Foot with necrosis: In the neuropathic foot, infection is usually the cause of necrosis. In the neuroischemic foot, infection is still the most common reason, although severe ischemia can lead to necrosis directly. 6. Unsalvageable foot presentation: The foot cannot be saved and will need a major amputation.

Stage 1: The Normal Foot At this stage, the patient does not have the risk factors of neuropathy, ischemia, deformity, callus and edema. He is not susceptible to foot ulcers. It is a foot devoid of diabetic complications but may be affected by other foot pathologies

Fig. 1  Staging of foot in diabetes



Classification and Staging of Diabetic Foot    57 that occur in the general population. The foot is usually asympto­matic and any problems, including pain, are non­ diabetic in nature.

Stage 2: High-risk Foot The diabetic foot enters stage 2 when it has developed one or more of the following risk factors for ulceration: neuropathy, ischemia, deformity, swelling and callus. The major risk factors are neuropathy and ischemia and it is rare for the other three to cause problems when neuropathy and ischemia are absent. Deformity, swelling and callus do not usually lead to ulceration in patients with intact protective pain sensation and a good blood supply, but when they are found in combination with neuropathy or ischemia, they significantly increase the risk of ulceration. When they are present, however, all these risk factors need addressing to reduce susceptibility to ulceration. There are other factors which increase risk, including diabetic complications, medical conditions and social problems: • Poor vision • Old age • Social isolation—“lack of social connectedness” • Poverty • Ignorance • Intellectual deficit • Concurrent psychiatric illness • Obesity. Patients without current active foot ulceration but with a history of previous ulceration should be regarded as at risk. These risk factors may not cause symptoms. Patients do not, thus, report problems. It is therefore important to screen patients at the annual review, which is an important part of diabetic foot care. Every diabetic foot at stage 2 will be classified as neuropathic or neuroischemic. It is necessary to emphasize the great difference between the neuropathic foot, which lacks protective pain sensation but has a good blood supply, and the neuroischemic foot with a combination of neuropathy and ischemia, because the treatment will be different in the two groups. Following clinical examination, the patient should be categorized according to a risk classification system. Unfortu­ nately, there is no uniform risk classification system to predict future ulceration. However, experts involved in developing the International Consensus on the Diabetic Foot, currently propose adoption of the risk classification system described in Table 1 which is similar to the Scottish foot ulcer risk classification. Within stage 2, there are specific conditions which are nonulcerative but require treatment. These include: 1. Intermittent claudication 2. Severe chronic ischemia with or without rest pain 3. Acute ischemia.

Table 1  Adoption of the risk classification system Category Risk profile

Check-up frequency

1

No sensory neuropathy

Once a year

2

Sensory neuropathy

Once every 6 months

3

Sensory neuropathy, signs of peripheral arterial disease (PAD) and/or foot deformities

Once every 3 months

4

Previous ulcer

Once every 1–3 months

Intermittent Claudication The classical site of claudication is the calf, although it may occur in the thigh and buttocks in aortoiliac disease. Claudication is less common in diabetic patients compared with nondiabetic patients because of peripheral neuropathy and the very distal site of atherosclerosis in the tibial vessels of the diabetic leg.

Severe Chronic Ischemia With increasing severity of occlusive arterial disease, patients may develop a pink, painful pulseless foot. The color of the skin is a strikingly bright pink and the foot is cold. The amount of pain will be related to the severity of the disease and the degree of peripheral neuropathy. When neuropathy is mild, patients will have classical rest pain, which is a constant pain, often worse at night and relieved by hanging the leg down outside the bed at night. It is important not to mistake the pink painful ischemic foot for an infected cellulitic foot. The pink painful ischemic foot is usually cool and the infected cellulitic foot is usually hot. If the leg is elevated the pinkness of ischemia will fade while erythema of cellulitis will remain.

Acute Ischemia A sudden occlusion of a major artery, usually popliteal or superficial femoral will result in a pale, painful cold foot with purplish mottling. Initially the skin is intact, but if treatment is delayed digital necrosis will develop. Acute ischemia is a rare complication of the stage 2 diabetic foot and can present very suddenly in: • Patients with no previous history of vascular problems • Patients with a history of steadily deteriorating chronic ischemia • Patients who have previously had peripheral arterial bypass which occludes or angioplasty with recurrence of stenosis or occlusion. Unless the patient is profoundly neuropathic, he will complain of sudden onset of pain in the leg and foot. If a hand is passed down the leg, a “cut-off” point will be found where the temperature of the skin suddenly decreases.



58    Contemporary Management of the Diabetic Foot Symptoms may include: • Pain • Numbness • Paresthesia • Weakness. Signs are: • Pallor • Bluish-gray discoloration with mottling or “bruised” appearance • Paralysis. Emergency vascular referral is required.

Stage 3: Foot with Ulcer The foot has a skin breakdown. Although this is usually an ulcer, it is important not to underestimate apparently minor injuries such as blisters, skin fissures or grazes, all of which have a propensity to become ulcers if they are not treated correctly and fail to heal quickly. Ulceration is usually on the plantar surface in the neuropathic foot and on the margins in the neuroischemic foot. It is essential to differentiate between ulceration in the neuropathic foot and that in the neuroischemic foot.

Neuropathic Ulcer Neuropathic ulcers result from mechanical, thermal or chemical injuries that are unperceived by the patient because of loss of pain sensation. The usual position is under the metatarsal heads, but they are more frequently found on the plantar aspects of the toes. Direct mechanical injuries may result from treading on sharp objects, but the most frequent cause of ulceration is the repetitive mechanical forces of gait, which result in callosity formation, inflammatory autolysis and subkeratotic hematomas. Tissue necrosis occurs below the plaque of callus resulting in a small cavity filled with serous fluid which eventually breaks through to the surface with ulcer formation.

Neuroischemic Ulcer Ulceration in the neuroischemic foot usually occurs on the margins of the foot and the first sign is a red mark which blisters and then develops into a shallow ulcer with a base of sparse pale granulations or yellowish closely adherent slough. Although ulcers occur on the medial surface of the first metatarsophalangeal joint and over the lateral aspect of the fifth metatarsophalangeal joint, the commonest sites are the apices of the toes and also beneath the nails if allowed to become overly thick.

Stage 4: Foot with Cellulitis The foot has developed infection, which can complicate both the neuropathic foot and the neuroischemic foot. The diabetic patient enters stage 4 because the foot is now infected and

microbiological control has been lost. At no other stage in the natural history of the diabetic foot is prompt diagnosis and intervention so important. Twenty-four hours of undiagnosed and untreated infection can destroy the diabetic foot. The most common manifestation is cellulitis, defined as an infection of skin and subcutaneous tissue, usually secondary to an ulcer, and presenting as redness or erythema. However, stage 4 covers a spectrum of presentations under the general heading of infection. These range from local infection of the ulcer through to sloughing of soft tissue and vascular compromise of the skin, seen as a blue discoloration, secondary to reduced blood supply to the skin. This spectrum occurs in both neuropathic and neuroischemic feet but in the presence of neuropathy and ischemia signs of inflammation are often diminished. There is a reduced host response to infection which is particularly noticeable in diabetic patients with impaired renal and liver function.

Stage 5: Foot with Necrosis This stage is characterized by the presence of necrosis (gangrene), which has profound implications, threatening the loss of the limb. It is important to limit the extent of necrosis and early diagnosis and intervention, even at this late stage, can save limbs. Necrosis can involve skin, subcutaneous and fascial layers. In the skin, it is easily evident but in the subcutaneous and fascial layers, it is not so apparent. Often the bluish-black discoloration of skin is the “tip of an iceberg” of massive necrosis which occurs in subcutaneous and fascial planes, so-called necrotizing fasciitis. It is classified as either wet necrosis due to infection or dry necrosis due to ischemia (Fig. 1). Purplish-black discolo­ra­tion of the skin also occurs after bruising and is some­times difficult to differentiate from early necrosis in the very ischemic foot, although extensive bruising is usually associated with a history of trauma. Blood within a blister on a toe gives the toe a black appearance. Blue-black cyanosed toes and feet are seen in severe cardiac and respiratory failure. Shoe dye and the application of henna will result in black discoloration of the skin.

Wet Necrosis In wet necrosis, the tissues are gray, black, brown, white or greenish, moist and often malodorous. Adjoining tissues are infected and pus may discharge from the ulcerated demarcation line between necrosis and viable tissue. Wet necrosis is secondary to a septic vasculitis associated with severe soft tissue infection and ulceration, and is the commonest cause of necrosis in the diabetic foot.

Dry Necrosis Dry necrosis is hard, blackened, mummified tissue and there is usually a clean demarcation line between necrosis and viable tissue. It may be difficult to diagnose in the colored foot.



Classification and Staging of Diabetic Foot    59 Dry necrosis usually results from severe ischemia secon­ dary to poor tissue perfusion from atherosclerotic narrow­ing of the arteries of the leg, often complicated by thrombus and emboli. Necrosis is not usually due to a microangiopathic arteriolar occlusive disease, or so-called small vessel disease.

Necrosis in the Neuropathic and the Neuroischemic Foot Neuropathic foot: In the neuropathic foot, necrosis is almost invariably wet, and is caused by infection complicating a digital, metatarsal or heel ulcer, and leading to a septic vasculitis of the digital and small arteries of the foot. The walls of these arteries are infiltrated by polymorphs leading to occlusion of the lumen by septic thrombus. Neuroischemic foot: Both wet and dry necrosis can occur in the neuroischemic foot. Wet necrosis is caused by a septic vasculitis, secondary to soft tissue infection and ulceration. However, in the neuroischemic foot reduced arterial perfusion to the foot resulting from atherosclerotic occlusive disease of the leg arteries is an important predisposing factor. Dry necrosis results from a reduction in arterial perfusion and occurs in four circumstances: 1. Severe chronic ischemia 2. Acute ischemia 3. Emboli to the toes 4. End stage renal failure. Severe chronic ischemia: Peripheral arterial disease usually progresses slowly in the diabetic patient, but eventually a severe reduction in arterial perfusion results in vascular compromise of the skin, often precipitated by minor trauma, leading to a blue toe which usually becomes necrotic unless the foot is revascularized. Acute ischemia: Blue discoloration leading to necrosis of the toes is also seen in acute ischemia, which is usually caused either by thrombosis of an atherosclerotic stenosis in the superficial femoral or popliteal artery or by emboli from proximal atherosclerotic plaques in the iliac, femoral or popliteal arteries. Acute ischemia presents as a sudden onset of pain in the leg associated with pallor of the foot, quickly followed by mottl­ing and slate-gray discoloration. The diabetic patient may not get paresthesia because of an existing sensory neuro­ pathy, which also reduces the severity of ischemic pain.

• Agonizing ischemic pain which cannot be relieved • Unstable foot and ankle, usually secondary to Charcot’s osteoarthropathy, which does not respond to external or internal fixation. Major amputation in a neuropathic foot should be a very rare event and is usually necessary only when infection has irreversibly destroyed the foot. This should be avoidable in most cases. A nonhealing ulcer should not necessarily be an indication for major amputation. The Simple Staging System used in this book has been created to allow practitioners, whether experienced in diabetic foot care or not, to make an initial assessment of the diabetic foot at whatever stage in the natural history it might be. The stage sets the place in the natural history and also determines treatment. The aim is to keep all diabetic feet at as low a stage as possible. Rehabilitation of the diabetic amputee is extremely difficult and is characterized by long stays in hospital. Only 25% of diabetic amputees will ever walk again. Morbidity and mortality associated with major amputation are very high. Major amputation does not guarantee a future ulcer free existence.

OTHER FOOT CLASSIFICATION SYSTEMS Various foot ulcer classification systems have been developed in an attempt to categorize ulcers more effectively, and allow

Table 2  Wagner grade 0

1

2

3

4

Stage 6: The Unsalvageable Foot Presentation: The Foot cannot be Saved and will Need a Major Amputation Reasons for major amputation: • Extensive necrosis which has destroyed the foot • Severe infection which puts the patient’s life at risk

5



High-risk foot and no ulceration



No open lesions, skin intact, may have deformities, erythematous areas of pressure or hyperkeratosis



Superficial ulcer



Disruption of skin without penetration of the subcutaneous fat layer. Superficial infection with or without cellulitis may be present



Deep ulcer (cellulitis)



Penetrates through fat to tendon, or joint capsule without deep abscess or osteomyelitis



Osteomyelitis with ulceration or abscess



Deep ulcer which may or may not probe to bone, with abscess or osteomyelitis, or joint sepsis. Includes deep plantar space infections or abscesses, necrotizing fasciitis and tendon sheath infections



Gangrenous patches partial foot gangrene



Denotes gangrene of a specific portion of the foot, such as toes, forefoot or heel. The remainder of the foot is salvageable, though it may be infected



Gangrene of entire foot



Gangrene or necrosis, to the extent that the foot is beyond salvage and will require a major limb or life-sparing amputation



60    Contemporary Management of the Diabetic Foot Table 3  University of Texas Foot Wound Classification System Depth

Grade 0

I

II

III

A

Pre-ulcerative lesion or post-ulcerative Superficial wound not involv­ing Wound penetrating to lesion completely epithelialized tendon, capsule or bone tendon or capsule

Wound penetrating to bone or joint

B

Pre-ulcerative lesion or post-ulcerative Superficial wound not involv­ing Wound penetrating to lesion completely epithelialized with tendon, capsule or bone with ten­don or capsule with infection infection infection

Wound penetrating to bone or joint with infection

C

Pre-ulcerative lesion or post-ulcerative Superficial wound not involving lesion completely epithelialized with tendon, capsule or bone with ischemia ischemia

Wound penetrating to tendon or capsule with ischemia

Wound penetrating to bone or joint with ischemia

D

Pre-ulcerative lesion or post-ulcerative Superficial wound not involving lesion completely epithelialized with tendon, capsule or bone with ischemia and infection ischemia and infection

Wound penetrating to tendon or capsule with ischemia and infection

Wound penetrating to bone or joint with ischemia and infection

comparison of the outcome of routine care in different centers and treatment strategies. These systems are based on the site of ulcer, depth, presence of neuropathy, infection and PAD, and have been used to compare the outcomes. The two most widely used ulcer classification systems are the Wagner and the University of Texas system (Tables 2 to 4). The size (area, depth), sepsis, arteriopathy, and denerva­ tion [S(AD)SAD] system, differs by referring to both ulcer area and neuropathy, and has been validated by showing differences between different baseline variables and clinical outcome in a single center in the United Kingdom (UK). The site, ischemia, neuropathy, bacterial infection and depth (SINBAD) classification system was a retrospective recatego­ rization of data series from 449 patients seen in UK, to formulate a score between 0 and 6 based on SINBAD.

In 2003, the International Consensus on the Diabetic Foot introduced, as a progress report, its classification system (PEDIS) for research purposes. This system was developed by clinical researchers and was based on the experience from earlier classification systems. The aims of the ulcer research classification system were to categorize different populations of diabetic patients with a foot ulcer for the purposes of research, at a specific time using terms which were plainly defined and appropriate world-wide. Such a classification system, according to recognized criteria would ease commu­ ni­cation and enable the comparison of the results of different research projects. The research system did not primarily aim to influence clinical management or to forecast the outcome of individual foot ulcers and nor was it designed as a monitor of the healing process.

Table 4  Perfusion, extent or size, depth or tissue loss, infection and sensation (PEDIS) classification Perfusion Grade 1

No symptoms or signs of PAD in the affected foot, in combination with: • • • •

Grade 2

Palpable dorsal pedal and posterior tibial artery Or Ankle Brachial Index 0.9–1.10 Or Toe Brachial Index > 0.6 Or Transcutaneous oxygen pressure (TcPO2) > 60 mm Hg

Symptoms or signs of PAD, but not of critical limb ischemia (CLI): • • • • •

Presence of intermittent claudication, as defined in the document of the International Consensus on the Diabetic Foot Or Ankle Brachial Index < 0.9, but with ankle pressure > 50 mm Hg Or Toe Brachial Index < 0.6, but systolic toe blood pressure > 30 mm Hg Or Transcutaneous oxygen pressure 30–60 mm Hg Or Other abnormalities on noninvasive testing, compatible with PAD (but not with CLI)

Note: If tests other than ankle or toe pressure or TcPO2 are performed, they should be specified in each study. Contd...



Classification and Staging of Diabetic Foot    61 Table contd... Grade 3

Critical limb ischemia, as defined by: • • •

Systolic ankle blood pressure < 50 mm Hg Or Systolic toe blood pressure < 30 mm Hg Or Transcutaneous oxygen pressure < 30 mm Hg

Extent or size Wound size (measured in square centimeters) should be determined after debridement, if possible. The outer border of the ulcer should be measured from the intact skin surrounding the ulcer Depth or tissue loss look up Grade 1

Superficial full thickness ulcer, not penetrating any structure deeper than the dermis

Grade 2

Deep ulcer, penetrating below the dermis to subcutaneous structures, involving fascia, muscle or tendon

Grade 3

All subsequent layers of the foot involved, including bone and/or joint (exposed bone, probing to bone)

Infection Grade 1

No symptoms or signs of infection

Grade 2

Infection involving the skin and the subcutaneous tissue only (without involvement of deeper tissues and without systemic signs as described below). At least 2 of the following items are present: • • • • •

Local swelling or induration Erythema > 0.5–2 cm around the ulcer Local tenderness or pain Local warmth Purulent discharge (thick, opaque to white or sanguineous secretion)

Note: Other causes of an inflammatory response of the skin should be excluded (e.g. trauma, gout, acute Charcot neuroosteoarthropathy, fracture, thrombosis, venous stasis) Grade 3

Erythema > 2 cm plus one of the items described above (swelling, tenderness, warmth, discharge) or infection involving structures deeper than skin and subcutaneous tissues such as abscess, osteomyelitis, septic arthritis, fasciitis without systemic inflammatory response signs

Grade 4

Any foot infection with the following signs of a systemic inflammatory response syndrome (SIRS). This response is manifested by two or more of the following conditions: • • • • • •

Temperature > 38 or < 36°C Heart rate > 90 beats/min Respiratory rate > 20 breaths/min Transcutaneous oxygen pressure < 32 mm Hg White blood cell count > 12.000 cu/mm or < 4.000 cu/mm Ten percent immature (band) forms

Sensation The system categorizes patients as having present or absent protective sensation in the affected foot. The system does not categorize patients as having (diabetic) polyneuropathy, and additional information is needed for this diagnosis. Moreover, it does not provide information on the cause of the loss of protective sensation, nor is the severity of the sensory loss graded. Both pressure and vibration sensation should be determined in each patient Grade 1

No loss of protective sensation on the affected foot detected, defined as the presence of sensory modalities described below

Grade 2

Loss of protective sensation on the affected foot is defined as the absence of perception of the one of the following tests in the affected foot: • •

Absent pressure sensation, determined with a 10 g monofilament, on 2 out of 3 sites on the plantar side of the foot, as described in the International Consensus on the Diabetic Foot Absent vibration sensation, (determined with a 128-Hz tuning fork) or vibration threshold > 25 V, (using semiquantitative techniques), both tested on the hallux



62    Contemporary Management of the Diabetic Foot

SUGGESTED READING 1. Armstrong DG, Lavery LA, Harkless LB. Validation of a diabetic wound classification system. The contribution of depth, infection and vascular disease to the risk of amputation. Diabetes Care. 1998;21(5):855-9. 2. Ince P, Abbas ZG, Lutale JK, et al. Use of the SINBAD classification system and score in comparing outcome of foot ulcer management on three continents. Diabetes Care. 2008;31(5):964-7. 3. Leese G, Schofield C, McMurray B, et al. Scottish foot ulcer risk score predicts foot ulcer healing in a regional specialist foot clinic. Diabetes Care. 2007;30(8):2064-9.

4. Macfarlane RM, Jeffcoate WJ. Classification of diabetic foot ulcers: the S(AD) SAD system. Diabet Foot. 1999;2:123-31. 5. Schaper NC. Diabetic foot ulcer classification system for research purposes: a progress report on criteria for including patients in research studies. Diabetes Metab Res Rev. 2004;20(Suppl 1):S90-5. 6. Treece KA, Macfarlane RM, Pound N, et al. Validation of a system of foot ulcer classification in diabetes mellitus. Diabet Med. 2004;21(9):987-91. 7. Wagner FW. The dysvascular foot: a system of diagnosis and treatment. Foot Ankle. 1981;2(2):64–122.

CHAPTER

The Assessment and Management of Plantar Ulcers and Offloading the Diabetic Foot

9 Neil Baker

CHAPTER RATIONALE The aim of this chapter is to give a basic overview of the management of plantar diabetic foot ulceration. This will cover the basic principles of ulcer management, a simple guide and approach to ulcer assessment, principles of treatment and offloading principles and techniques. Hopefully, the contents of this chapter will provide a simple common sense approach that can be applied in most clinical settings around the world.

INTRODUCTION Diabetic foot ulceration is perhaps the most serious of all the diabetes complications, which has been shown to be causatively linked with up to 85% of all diabetes-related nontraumatic lower extremity amputations. Therefore, identi­ fying those most at risk of developing foot ulceration and implementing prevention strategies is the most effective approach to foot ulcer management and amputation preven­ tion. However, if prevention strategies fail and foot ulceration does occur, adopting timely and effective treatments based upon good clinical knowledge, skills and rationale; together with patient co-operation will optimize successful clinical outcomes. It has also been clearly demonstrated that adopting a multi-disciplinary approach to foot ulcer management utilizing the complimenting skills of physicians, podiatrists, surgeons, nurses, shoemakers and other healthcare profes­ sionals delivers consistent success. Successful plantar diabetic foot ulcer management must rely upon complete patient involvement. This can be achieved realistically when patients fully accept that they have a foot ulcer and also clearly understand its pathology. Talking to a patient about the cause of their ulcer or why it has become chronic is arguably counterproductive. Whereas encouragingly facilitating a

patient to explore and discover why they have an ulcer or what may be delaying it from healing shifts the focus of care to the patient. This should probably lead to more successful ulcer treatment outcomes. It is only when this is achieved that ulcer resolution can be maintained long term. It is actually equally true for clinicians to recognize the limitations and restrictions of treatments and interventions and temper these with a realistic outlook of everyday life. In summary, therefore, the management of diabetic foot ulcers is complex involving a multidisciplinary approach and a questioning, innovative mind. There is not a “one size fits all” type of treatment but rather a hybrid and constantly changing amalgamation of different treatments that respond to the different stages of wound progress.

Definition of a Plantar Ulcer An ulcer is an open wound where there is loss of continuity of the epithelial skin surface exposing the dermis or deeper soft tissue structures. Clearly, a “plantar” foot ulcer is one that occurs on the sole of the foot.

PLANTAR ULCER MANAGEMENT BLUEPRINT Fundamentally, the successful management of any ulcer, irrespective of its location, is achieved by examination, assessment and addressing three simple concepts, namely:

1. Ensuring there is Adequate Arterial Inflow to the Affected Area Assessing for sufficient arterial supply requires significant clinical assessment and observational skills. Palpating pedal



64    Contemporary Management of the Diabetic Foot pulses or using a hand-held Doppler in themselves are good but should always be used in conjunction with other signs and symptoms such as nail bed perfusion, soft tissue status, intermittent claudication, etc.

Table 1  Causes and action plan depending on the site of ulcer Site

Most likely cause

Action

Plantar surface

2. Maintaining an Infection Free Status in and Around the Ulcer Site

Pressure, shear, friction

Offload–debride, infection control

Dorsal toes

Shoe Rub Ischemia

Identifying infection, particularly in its early stages can be clinically difficult and even confusing. Obviously when infection is established, the classical signs and symptoms of redness, heat, swelling and pain are plainly evident.

Remove cause if shoes, investigate revascularization, infection control

Dorsal foot

Ischemia Burn

Protect from trauma infection control

Heel

Pressure sore Burn Fissure

Pressure relief, infection control, wound care

Between toes

Shoe pressure

Separate toes

Under nail

Shoe pressure Ischemia

Remove nail or part, investigate ischemia

Tip of toes

Pressure, shear, friction

Offload review footwear, infection control

3. Keeping the Ulcer Site Free of Trauma both Extrinsic or Intrinsic Trauma especially due to extrinsic factors is the most common cause of ulcer occurrence and chronicity especially when this is unperceived in those with peripheral sensory neuropathy. Identifying and managing this is both challenging and rewarding but can often be frustrating. It is important not to overlook the effect of trauma from intrinsic factors like increased plantar pressure, limited joint mobility, as these are equally detrimental. The principle blueprint is very simple but the reality may be very different. It is important that each of the above are regularly assessed and reviewed. Both arterial and infection status are covered in other chapters in this book but offloading of extrinsic trauma will be dealt within this chapter. To reiterate successful management of plantar diabetic foot ulceration is in essence fundamentally straightforward but does require a logical and systematic approach with continuing reviews of implemented treatment and rationale. The first step always is to identify the initial cause of any ulcer and endeavor to remove it. This like all other components of ulcer management must place the patient centrally.

ULCER ASSESSMENT It is important to remember that the key to successful ulcer management is the ability to undertake a good clinical examination of the patient(s) and their wound(s). Wound assessment is an analytical process that should occur at every patient visit. Getting into the habit of asking the simple, but searching question “Why?” every time an ulcer is reviewed will help facilitate healing and prevent chronicity.

Site The site of an ulcer gives a clear clue as to the most likely precipitating or actual cause. For example, a plantar heel ulcer is not common so a foreign body in the shoe is a likely cause;

toe ulceration is generally deformity or footwear related. So, looking objectively at ulcer sites and asking “why is the ulcer located here” will help to identify and remove the possible causes preventing further damage and chronicity.

Size The size of an ulcer can act as a marker indicating wound progress. An increase in either area or depth is an indication of ulcer deterioration. Equally, if there were little changes in these parameters it would signify chronicity or failure of current treatment. Both area and depth should be considered together and increases in either to mark deterioration, wherein the underlying cause needs to be quickly identified and addressed. A typical example would be an increase in depth due to underlying osteomyelitis. Decrease in ulcer size and depth are indicators of healing (Table 1).

Shape The shape of an ulcer can give an indication of its cause; direction and type of trauma (Figs 1A to C). This is very useful as it allows a clinician to design offloading strategies that specifically address the detrimental forces responsible for the ulcer. For example, a circular shaped ulcer would denote rotational forces applied and a linear shaped ulcer is suggestive of anterior/posterior shear or frictional forces. As a rough guide, smaller the shape, more concentrated is the applied force. The number of ulcers together with their site, size and shape generally give an indication of their cause and directs interventions required to manage them effectively. For



65    Contemporary Management of the Diabetic Foot

A

B

C

Figs 1A to C  Relation of shape of ulcer and type of trauma

Fig. 2  Multiple ulcers

Fig. 3  Healing ulcer

example, multiple small ulcers at the distal margins of the foot tend to denote ischemia with repetitive minor trauma (Fig. 2). Multiple infarcts especially in or around the nail folds would imply hematological or collagen vascular disorders. Single ulcerations are commonly associated with trauma.

tissue is a static ulcer; one with undermined edges and a sloughy base is an ulcer that is deteriorating. An ulcer whose edges are raised or rolled with little signs of central healing is worrying, this is an ulcer that could heal but disease or trauma to the center of the wound is preventing it (Diagrams 1 to 4). In this latter situation the cause needs to be quickly identified and appropriately treated. One needs to also exclude neoplasm. Other causes that may be responsible include localized trauma or self-harming (Diagrams 1 to 4).

Edge/Walls/Base The edge, walls and base of the ulcer are very clear indicators of wound progress and management effectiveness (Figs 1 to 6). Examining these is a very reliable index for determining efficacy of treatment in conjunction with regular direct wound tracing. Essentially a “sloping” ulcer edge with a clean base or islands of light slough is a healing ulcer. One that has “straight” edges with a sloughy base with little granulating

Diagram: 1 Healing ulcer • Sloping edges • Granulating clean base • Epithelialization at edges



66    Contemporary Management of the Diabetic Foot

Fig. 4  Static ulcer

Fig. 6  Non-healing ulcer

• Overlying callus–often macerated • Sloughy base ~ sinus, bone synovial fluid.

Diagram: 4 Fig. 5  Signs of deteriorating ulcer

Diagram: 2 Chronic/Static ulcer • Straight walls • Callus at periphery • “Pizza-like” base.

Diagram: 3 Deteriorating ulcer • Undermined edges

“Rolled edge” • Puckered raised edge • Evidence of nonhealing base.

Base The ulcer base may be covered with necrotic, sloughy, granulating or epithelializing tissue or combinations of these. Combinations of the above are common place and it is useful to document an estimate of the percentage of each of the different types of tissue present at each visit, e.g. 60% granulation 40% light slough, in order to monitor wound progress.



67    Contemporary Management of the Diabetic Foot

Fig. 7  Granulating tissue

Fig. 8  Chronic ulcer

Granulating Tissue This is replacement tissue filling the deficit within an ulcer cavity; it is predominantly newly formed capillaries and connective tissue and thus has a red appearance and a healthy sheen (Fig. 7). It fills the base of the wound and should not protrude above the surrounding tissues. If this does occur it is called “hypergranulation” and its cause should be sought. The most frequent cause is an underlying foreign body, e.g. bony sequestrum, cartilage, or localized trauma in one area of the wound bed. Here again neoplastic change, basal cell lesions, pyoderma may be responsible. In this latter state the onset is rapid and the tissue is very well organized, firm and often well demarcated. Clearly, if this is suspected a biopsy should be performed with prompt referral to a skin specialist. It is important for a clinician to be able to recognize subtle changes in the appearance of granulation tissue, as they will give a clue as to the progression of healing. So, for example, granulation tissue that becomes darker in color may indicate subclinical infection or ischemia; loss of sheen may indicate low-grade trauma and early chronicity (Fig. 8). As always, an objective reason needs to be assigned to any changes observed and then this be promptly addressed.

Fig. 9  Healing ulcer

Sloughy Tissue Slough is dead or devitalized tissue that covers the wound base. It varies in color and consistency depending upon the disease state and tissues involved. As a general rule, creamy yellow slough is a sign of an ulcer moving into resolution, white indicates chronicity, whereas green, grey or black indicates deterioration. Ulcer bases can be likened to a cheese and tomato “pizza”, where the cheese represents slough and the tomato granulating tissue (Figs 9 and 10).

Fig. 10  Chronic ulcer



68    Contemporary Management of the Diabetic Foot The less cheese on the base, the better and, conversely the more it is, the worse is the situation. Add to this picture the aforementioned colors and a relatively reliable assessment of the ulcer status can be obtained. Remember that the presence of slough is a clear indication that tissue damage has or is occurring. Here again asking the question “why has this occurred” is the first step to ulcer healing. In order for an ulcer to heal slough tissue must be removed. Of course, this does occur naturally also by gentle proteolytic autolysis, but this process generally is slow. Physical removal of slough tissue is a faster remedy, but it must be remembered that the newly forming granulation tissue will be intimately in contact with the slough’s under surface, so care and skill are essential. Removing slough tissue is ineffectual, if its cause is not identified and removed concomitantly. Slough removal is best done by sharp debridement but this will cause damage to granulating tissue also. Other methods for slough removal include enzymes, such as streptokinase and streptodornase, dressings, such as hydrogels, alginates, hydrocolloids, etc. Sharp debridement requires skill and expertise, but gets a fast result. Dressings take longer to achieve the same, but are less invasive and far gentler. Examples of different slough types are illustrated in diagrams.

Necrotic Tissue Necrotic tissue is a totally dead or gangrenous tissue, which is caused by either infection or ischemia whether in its occlusive nature or pressure related. The presence of this type of tissue in an ulcer base generally indicates poor tissue vitality or infection. The management of necrotic tissue is simple; wherever possible address the underlying cause. If it is dry, it is best left alone; but if it is moist, even at its margins, this has got to be removed. Once again this is best done by skillful sharp debridement taking great care at the junction of live and dead tissue. Some dressings may also be used where sharp debridement skills are lacking. However, the results are slow in coming, comparatively expensive and the dressings tend to make the area wet.

Exudate There are several different types of wound exudate that occur, each of which help the clinician together with all other presenting factors to decide upon a course of treatment. Serous fluid is a healthy finding but the amount present should be subjectively recorded. Serous fluid that is blood stained is of concern as it clearly suggests significant trauma within the ulcer leading to damage to the capillary bed. This is usually due to extrinsic trauma from weight-bearing. However two other causes must be kept in mind. First, is the patient/care wound interference and second, a rare cause for blood stained serous fluid is neoplastic change. These should

be considered when offloading and infection control are optimized. Pus may be sterile due to tissue liquefaction, e.g. avascular tissue necrosis or infective. Clinical signs and symptoms of infection with wound deterioration would be an obvious determinant for infection and initiation of appropriate antimicrobial therapy. However, it should be remembered that the cardinal inflammatory signs may be dampened in diabetes and thus redness, heat, swelling and pain may be less obvious or even absent. Presence of synovial fluid is evidently due to either joint disruption or erosion of a bursa/synovial sac/sheath. Clinically, this is clear fluid with a high viscosity that strands like egg white between fingers. Surgery is often indicated in this situation, but a bursa can be sclerosed or excised. Disruption of a tendon is uncommon and has a poor outcome. Bleeding from an ulcer base is strongly suggestive of trauma or delicate over-granulation tissue.

Exudate Quantity It is a general rule of thumb that if the wound suddenly starts to increase significantly then infection must be seriously considered, as clinically this is a silent marker for infection. Clearly, other factors may well be responsible, such as increased trauma or edema.

Surrounding Tissues It is obvious to state that tissues that border and surround an ulcer give a clear indication regarding ulcer cause and chronicity. Surrounding or spreading cellulitis in white skin is clearly seen however in darker skin it seems less obvious but should be suspected from the darkening pigmentation. When there is darkening of colored skin with noticeable skin creasing and a loss of substance this is an indication of ischemia. When cellulitis is present it is prudent to mark its boundaries with a marker pen and date it; so that when it is reviewed any interval changes can be easily made out. Other color changes worthy of note are; erythrocyanosis, deep red/ purple mottling, areas of adjacent blistering or blanching.

MANAGEMENT As already stated the management of plantar ulceration is fundamentally very simple; identify and address the three main issues of Infection, Arterial Supply and Trauma and then all ulcers should heal. Although this seems a very simple approach, in clinical practice it tends to be more complex. However, the principle remains correct. In this section management of plantar ulceration is overviewed under key headings.



69    Contemporary Management of the Diabetic Foot

Infection

Ulcer Measurement

This topic is covered in another chapter of this book. However, recognizing infection and aggressively treating it is of paramount for successful ulcer management and amputa­ tion prevention. There is a considerable debate regarding the reliability of taking surface wound swabs versus deep tissue cultures to identify invasive pathogens. The consensus of expert opinion would favor tissue sampling over wound swabbing. But this is not always possible or practical. The rationale behind is that tissue samples taken after debridement are more likely to identify invasive pathogens, as against surface colonizers which are more likely from surface swabs. An infected plantar foot ulcer should be dressed frequently (e.g. daily) to monitor infection spread, debrided with drainage where required and effectively off-loaded. The latter is often overlooked as attention gets diverted towards anti-microbial therapy. Standing and walking on an infected foot ulcer increases the risk of spreading sepsis, due to infected exudates being trapped or unable to freely drain. Additionally, the effect of intrinsic foot muscle activity is to suck exudates through its planes. Obviously, patient education is paramount in achieving this to ensure that this concept of sepsis spreading is tangible to patients. Serial tissue sampling is required to monitor treatment efficacy and that microbiological results are reflected in organism suppression with concomitant therapy. In the case of osteomyelitis, a 6–12 week course of targeted bone penetrating antimicrobial therapy is advocated, after removal of any loose or evidently dead bony tissue. Surgical excision of infected bone is an option and clearly indicated in a non-resolving or worsening clinical presentation (Fig. 11).

Measuring ulcer size is an important clinical technique that should be adopted to determine the efficacy of initiated treatment. Adopting a simple standardized method, which is quick and reliable, such as acetate tracing is recommended. This method involves placing a clear acetate sheet over the ulcer and tracing its outline with a thin permanent marker pen. Writing patient details, date and anatomical landmarks allows for comparison with subsequent tracings. Ulcer surface area can be determined from these tracings. The wound contact side of the acetate sheet can be cleaned before storing it with the patient notes. Other methods of wound measurement are recording length and width with a ruler. There are camera systems and direct wound tracing systems that are being developed for this purpose but they are expensive and till date offer little more that the simple methods stated. Sequentially measuring ulcer depth is important, but this can be clinically challenging. This involves using a thin sterile metal probe placed perpendicularly into the lowest section of the wound and then using a permanent marker pen to mark the probe at the level of the skin surface. Figures 12 to 15 shows the debridement/wound bed preparation. The role of debridement in ulcer management is one of the cornerstones of effective therapy. It should be seen as an integral part of wound care. It is perhaps best seen as the most effective way of wound cleansing. It is often referred to as wound bed preparation. Debridement is the removal of all foreign material, devitalized tissue, slough, necrotic tissue and occasionally healthy surrounding tissue. The removal of healthy tissue is advocated when ulcer is undermined and the ulcer base is extensively hidden or where an abscess requires drainage. Sharp or surgical debridement is a skill that needs to be developed and used appropriately, however it should not be performed when: • Comprehensive assessment is not undertaken • There is marked ischemia • The tissue vitality is unable to cope with the trauma • Medication/treatment contraindicates

Post Debridement

Fig. 11  A typical osteomyelitic sausage shaped toe

Following sharp debridement there are several considerations that may need to be addressed. Before this is undertaken a patient must be informed that it is very likely that there may be extensive bleeding, possibly pain, and minimal weight bearing is required. If bleeding does occur then patients should be told to sit with their foot elevated for at least half an hour. Dressing changes should be arranged for the following day and then as the wound dictates. A review date should be set for 1 week post debridement.



70    Contemporary Management of the Diabetic Foot

Fig. 12  Before debridement

Fig. 13  After debridement

Fig. 14  Necrotic second toe

Fig. 15  After partial amputation

Bio-debridement–Larvae Maggots have been used in the treatment of wounds for hundreds of years, even if accidentally or with intent (Fig. 16). Of course, not all fly larvae are suitable as some species are parasites invading and destroying healthy tissue. Those used and grown commercially are larvae of the blue bottle fly (Lucilla Serratia). The main purpose of larvae therapy is to gently debride dead tissue from a wound. The debridement is very gentle and discriminates between healthy and diseased tissue. Their proteolytic secretions liquefy the dead tissue covering a wound; the larvae then ingest this. There are four accepted theories for wound management using larvae: 1. Larval secretion of proteolytic enzymes as well as collagenase

Fig. 16  Maggots in the wound



71    Contemporary Management of the Diabetic Foot Table 2  Debridement methods and its characteristics Characteristic

Dressings

Enzymes

Larvae

Surgical/sharp

Mechanical

Speed of action

Healthy tissue discrimination

Infection risk

Exudate production

Skill

Treatment cost

    Most appropriate      Moderately      Least appropriate

2. Ingestion of necrotic tissue 3. Secretions of larvae change wound; pH–ammonia secreted makes wound more alkaline which inhibits microbial growth 4. Bacteria destroyed in their alimentary tract. Table 2 shows the debridement methods and charac­ teristics.

Role of Dressings The covering of a wound surface with a dressing, has always been a part of ulcer management that is over emphasized by some and undervalued by others. Irrespective of the authors’ opinion, in most instances a foot ulcer must be covered with something. Although dressings do have a significant role to play in wound management, it should be remembered that, “It is not what you put on the wound but what you take off”, that is more vital. Having said this every foot ulcer, unless it is a dry eschar, should be covered with a dressing of some sort. The question is; what should ideally be used, for how long and how frequently should it be changed.

Frequency of Dressing Change It is important to comment upon the frequency of dressing changes before considering the type of ulcer dressing. Dress­ ing change frequency is a clinical decision and ultimately is

dependent on two key issues. Firstly, the amount of exudate being produced, and secondly, monitoring for wound deterioration and infection. As an ulcer starts to heal and epithelialize the amount of exudate produced will reduce significantly; and the wound bed needs to be kept moist for epithelial migration. Thus, dressing changes are required less frequently. The converse is true when an ulcer is active or deteriorating with heavy to moderate exudates. In this situation dressing changes may be required more than once a day, but generally a daily change is adequate. A simple guide to determine when a dressing should be changed is that if exudate strike-through has occurred, then the dressing should be changed. Leaving a dressing in this situation increases the rise of secondary infection via the strike through. Dressings that are left in situ for too long and are sodden with wound exudate are likely to cause maceration of the surrounding tissue, can even lead to wound extension and promote infection. Monitoring for infection cannot be understated, as infections in the diabetic foot are fast in onset and very aggressive, thus frequent dressing changes should always be undertaken. The evidence base for dressing use is very poor consi­ dering the varying amounts and the many types used in foot ulcer management. The array of different dressings available is staggering and this clearly can leave a clinician in a state of confusion. This section is not going to extol the



72    Contemporary Management of the Diabetic Foot virtues of dressing or over dressing, but rather critically look at the rationale of choice. Clearly, the availability of different dressings is dependent on financial, manpower and service resources together with climatic, psychosocial and belief issues. In essence, the properties of a dressing include that it should be able to absorb excess exudate, be non-adherent, easy to apply and remove, prevent secondary infection, not be toxic to the tissues, and be easily available and cost effective. Some other published criteria also suggest that the dressings be thermally insulating and control gaseous exchange. Thermal insulation, i.e. keeping the wound surface warm is clearly a beneficial effect. However, a dressing that produces heat, for example, a foam dressing that releases heat energy when repeatedly compressed, may infact lead to tissue damage due to overheating. This is perhaps true in the ischemic state where increased metabolites formed by tissue heating cannot be catabolized due to poor tissue oxygenation. When considering gaseous exchange, it is important to determine whether there should be a high or low oxygen saturation requirement. If formation of granulation tissue is required, a low oxygen environment will stimulate macro­­ phage activity and capillary budding. Conversely, if epi­ the­ lialization is required, a high oxygen environment is necessary to stimulate the production of epithelial tissue and its migration across the wound surface.

Wound Cleansing There is very little reported evidence regarding the need for physically cleaning an ulcer surface. A common sense approach should therefore be adopted as to when an ulcer should be cleansed physically with sterile saline or clean water. The rationale for wound cleansing has been to make the surface of an ulcer as clean as possible to help reduce infection risk. Whilst this is very commendable, removing the flora on the ulcer floor may be counterproductive by disturbing the synergistic bacterial flora, removing growth factors and healing compliment in the tissue fluid. Thus it is the authors’ opinion that only ulcers that are physically dirty or grossly contaminated should be cleansed. Debridement is perhaps the most effective form of wound cleansing, although far more aggressive than wiping/swabbing or flushing with water or saline. The liquid used to cleanse the ulcer floor should be warmed so as not to cool the ulcer surface down delaying or halting mitotic cell division. Then again, wiping an ulcer floor with a moistened swab may in fact concentrate bacterial flora at the wound margins as the swab leaves the ulcer at the end of each wipe that may lead to devitalization at these exit points.

Dressing Considerations Diabetic foot ulcers can deteriorate very quickly particularly in the presence of infection and unperceived trauma, and as

has been already stated, it is imperative that dressing changes are frequent and during an active or infective state it should be daily. Dressings are not designed for weight bearing and if so these would no longer absorb and retain the exudate. Here again, is another reason for frequent dressing changes. The effect of gravitational edema is frequently overlooked when considering wound dressing products. Another important consideration is whether a chosen dressing product is widely available and if in the developing world it is realistically affordable to a self-funding patient. Some climatic or environmental aspects in the world would support the use of topical antiseptics or antibiotics, some­ thing which in the developed world is liable to be frowned upon. But, for example, in parts of Africa or India where infection is prolific, reducing wound infection risk by prophylactic use of these agents is fully understandable and desirable. Thus, given the paucity of sound robust evidence for dressing products, the authors’ view is simple. Dressings that are easy to obtain and apply should be used and changed every 1–2 days. The aim of dressings in the ischemic foot is to prevent infection, as this is limb threatening; and additionally in neuropathic feet to manage excessive exudate. Therefore, a simple nonfilmated and nonadherent primary wound layer with woven gauze as the secondary layer would fit most clinical scenarios anywhere in the world with similar clinical outcomes as long as the three main issues are addressed; those of offloading, infection control and arterial supply.

Dressing Fixation Attaching a dressing to the sole of a foot can be very challenging given that it will be walked and stood upon. A dressing that is not held firmly against the wound and is allowed to move may cause tissue damaged by friction or shear, or may leave the ulcer completely exposed and at risk of infection and trauma. Using hypoallergenic tape is common in the western world to fix dressings in place. However, care must be taken as it can tear impoverished skin. Bandaging dressings in place is the other alternative, which is a good method but does require practice and skill if the dressing is to be held in situ. Clearly using a large amount of bandaging should be better at securing dressings but will require more footwear accommodation. Although dressing fixation may be seen like a minor task, it is important as bad bandaging or fixation techniques can lead to wound deterioration.

Footwear and Dressings Plantar foot ulcers frequently require bulky dressings, and may prove difficult to be accommodated within normal footwear. Thus, consideration has to be given to alternatives. Dressing sandals are available commercially. But these may be cost prohibitive for some populations. Ideally, the sole of a dressing sandal should be rigid, with a rocker sole for forefoot ulcers for offloading.



73    Contemporary Management of the Diabetic Foot

Advanced Wound Care Products Technology has advanced in all areas of life and this is equally true in the realm of wound care and dressings. There have been significant advances, particularly in tissue engineering, autologous products and devices. For example, there are cellbased technologies that deliver exogenous growth factors to the wound bed and stem cells from bone marrow aspirate, or extracellular matrix scaffolds that organize the healing process. These products are biological grafts that form a matrix for repair. The role of topically applied growth factors has been disappointing, but predictable. The application of cultured skin products, the role of autologous plasma and aspirates together with stem cell therapies are all exciting and have shown some initial promising results. However, most of these newer technologies are invariably very cost prohibitive. Topical negative pressure therapy has shown faster wound size reduction and wound maturation with shortened hospital stays when used on wounds following surgical debridement. It is less effective in those with compromised arterial supply.

Offloading Plantar ulceration in people with diabetes is almost uniquely due to a combination of sensory dysfunction and unperceived noxious compressive, shear and frictional forces. These two major components of plantar ulcer causation are often theoretically understood but not fully implemented in clinical practice. The reduction of the aforementioned forces to localized areas of the plantar surface is perhaps the most important aspect of ulcer management. Sadly, this is frequently overlooked either through ignorance or overfamiliarity. When attempting to reduce these forces it is important to consider their magnitude, duration, direction and velocity. This achieved, significantly improved clinical outcomes can be realized. The methods used to reduce these forces are referred to as “offloading”, which encompasses a wide range of techniques and devices. But in essence, the underlying fundamental principle is similar, that is to take applied forces from the small target area to spread it over a larger area. The type of “offloading” methods used will depend upon any or all the factors below:

Ulcer Site Rearfoot Using crutches to prevent heel strike is very effective during gait and standing. Offloading is achieved effectively at night with a pillow or tightly rolled up blanket placed under the calf. Orthopedic semi-compressed self-adhesive felt padding may also be used when cut to shape with a cavity or aperture

to the ulcer site. This type of offloading needs to be changed when soiled or compressed. It is important to recognize that poor offloading techniques or incorrectly placed padding can create new lesions and deteriorate an existing one. Heel casts using a semi-rigid fiberglass casting tape is a relatively new method for specifically dealing with heel ulceration. These devices are very thin and made to fit intimately to the heel with a focal area of reinforcement to the ulcer site. They are quick and easy to make and the only equipment required is a pair of dressing scissors. They are held in place either by adhesive tape or a light bandage and can be worn within the patient’s own shoes. These should also be worn in bed, as this is when the heel is quite vulnerable to damage. Equally, a below knee cast can be used with a window in the cast to redress the ulcer. It is important that the removed window section of the cast is replaced after each dressing change to maintain ulcer protection and prevent the ulcer protruding through the window. Total contact casts (TCC) may also be useful for heel ulcers but are not commonly used for this wound site.

Midfoot This area is best served by the use of a non-removable cast, e.g. a TCC, below knee cast or fiberglass boot. Felt padding can be shaped to cover the sole of foot with a cavity over the ulcer and built up until a flat surface is obtained. A piece of rolled up firm density foam securing either side of the midfoot ulcer may be effective. A fiberglass boot is a padded cast that uses semi compres­ sed felt to build up around the ulcerated area so that it sits below the rest of the padding covering the whole plantar sur­­ face of the foot. Rigid fiberglass casting tape is applied over this and under cast cotton wool bandage and tubular band­ age. The toes are left exposed and the cast finishes just below the malleoli allowing unhindered normal ankle dorsi­flexion.

Forefoot Any device that prevents or reduces “the propulsive and toe off” phase of gait may be used for this ulcer site. A commercially available half shoe may be effective, but a leg or boot type of cast is the most effective method for offloading. A piece of “rolled up” firm density foam secured just proximal to the ulcer may be successful where resources are limited (Fig. 17). A customized sandal with a foam filled sink in the sole unit located over the ulcer site may also be useful.

Underlying Etiology—Neuropathy, Presence of Ischemia and Infection Traditionally casted devices have not been advocated for patients with Ischemia. But, there is no evidence to support



74    Contemporary Management of the Diabetic Foot

Fig. 17  Rolled up foam secured proximal to the ulcer

or refute this practice as most studies have concentrated on neuropathic plantar ulcers. It may well be that casted devices are beneficial for this patient group as these do offer protection for vulnerable devitalized tissue. However, caution must be exercised as poor casting techniques could cause significant problems.

Availability of Resources Clearly offloading methods will ultimately depend upon availability of resources, expertise and skill levels. As long as the concepts of offloading are understood, it should be possible to identify methods and locally available materials to achieve the possible degree of offloading.

Social and Lifestyle Issues Offloading techniques especially involving casts have a significant impact upon the ability to carry out everyday life functions, including many types of work. This is a common dilemma, particularly when loss of income is at stake. However, there are nearly always ways of achieving successful offloading with a little lateral thinking.

Offloading Methods It is not possible to expound upon all the offloading methods as there are too many different methods and commercially available devices, each with its pros and cons. Hence, this section will limit to a broad overview of the most commonly used methods for offloading.

Total Contact Cast This method is reportedly the “gold standard” form of offloading for neuropathic plantar ulcers reportedly healing up to 90% of ulcers within 6–8 weeks. It is a below knee cast that incorporates the whole lower limb including the foot (Fig. 18). It was traditionally made from plaster of Paris bandage intimately molded to the lower leg and foot with

Fig. 18  Total contact cast (TCC)

padding only over the toes, malleoli and tibial crest. Nowa-days, this inner layer of plaster of Paris is covered with a quickly setting outer and very rigid layer of fiberglass casting bandage so that the patient can mobilize within half an hour. A piece of plywood is placed under the whole foot and is incorporated into the cast with all hollows and cavities filled with plaster of Paris bandage and a small rubber rocker placed centrally under the cast to weight-bear upon. Plaster of Paris takes 48 hours to fully set and thus an outer layer of fiberglass tape bandage is now used to provide a rigid outer shell that allows moderate weight-bearing within 30 minutes. In developing countries where this type of cast bandage is not available or cost prohibitive, crutches should be used to prevent weight bearing within the first 2 days. Although evidence clearly supports TCC efficacy it is still not widely used, even though these are relatively cheap to make from a resource perspective. Contraindications for this and other types of cast include: infection, ischemia, loss of sight or balance. It should be noted that in patients with heavily exuding wounds casts may need frequent changes, but this is not a contraindication by itself (Table 3).

Other Methods for Offloading Removable Cast Walkers These are commercially available below knee cast splints/ walkers, which usually have a rocker sole and a rigid plastic outer shell with either a soft or pneumatic lining (Fig. 19). Velcro straps attached to the plastic outer rigid shell are used to secure the cast walker in place. These can be effective for forefoot ulcers but equally as they can be taken off and worn only at clinic visits, can make them equally ineffective. These are also expensive, although require very little training and are instant put-ons and therefore time saving.



75    Contemporary Management of the Diabetic Foot Table 3  Casted devices considerations Advantages

Disadvantages

Cheap

Require significant skill

Effective

Heavy

Fast healing times

Time consuming

Better wound maturation

Frequent changes

Nonremovable/removable

Large limb length discrepancy

Neuropathic ulcers

Several contraindications

Limits mobilization

Fig. 21  Fiberglass boots

Fiberglass Boots

Fig. 19  Removable cast walkers

Removable Heel Casts These are a new technique using a semi-flexible cast bandage with a focus rigidity area over the heel ulcer site. They have no incorporated padding and need to be replaced when exudate soiling occurs (Fig. 20).

These are made from fiberglass bandage and are either removable or nonremovable devices. They have padding incorporated into the cast to save the ulcer site from ground contact. Removable casts allow wound inspection and easy dressing changes. They can slip away or be left off by the patient (Fig. 21). Non-removable casts do not allow slippage and can be apertured to the ulcer site to allow dressing changes. They require an over cast sandal.

Below Knee Walking Plaster These are the same type of below casts used for setting fractures and may or may not be apertured to the ulcer site.

Blueprint for Cast Care All nonremovable casts should be checked daily by the patient or their care, looking for cast rubs/sores, exudate strike through, swelling at the open ends of the cast, malodor from the cast, pain, or loosening. If any of these occur, the cast must be removed immediately and the limb inspected. All non-removable non-apertured casts are removed after 1 week. Then, if all is well, reapply for 2 weeks and then every 4 weeks until healed. Removable casts with incorporated felt padding should be checked at each visit. When the padding is compressed, it needs to be replaced by either a complete new cast or stripping and relining the original cast. The danger signs and symptoms are the same as for the non-removable casts.

Half Shoes Fig. 20  Removable heel casts

These are commercially available sandal type shoes with a sole unit that is thick at the heel and angles posteriorly and



76    Contemporary Management of the Diabetic Foot

A Fig. 22  Half shoes

a thin forefoot platform that is raised from the ground. This type of device offloads the forefoot (Fig. 22). There is also a similar device in reverse that can be used for the heel. They create a large limb discrepancy, so caution needs to be taken in patients with poor proprioception, sight or balance.

Crutches These are simple, tried and tested and can arguably be quite effective if used correctly and fully. These are cheap and require little expertise to produce. There are no issues of cast complications and dressing changes can go unhindered.

Wheel Chair A wheel chair is also another simple but effective method of offloading but is expensive, limiting and not very practical for home or work. Of course, here the foot is off ground as well as off the wheelchair foot plate.

SURGICAL OPTIONS Following surgeries are recommended for chronic persistent or recurrent forefoot ulcers. Details of techniques of these surgeries are beyond the scope of this chapter. • Metatarsal osteotomies • Metatarsal head resection through dorsal approach – (Single, multiple or even panmetatarsal head resec­ tion) • Percutaneous Tendo-Achilles lengthening. If above mentioned principles of management of neuro­ pathic plantar ulcers are followed, complete healing can be achieved in majority of the cases (Figs 23 and 24).

B Figs 23A and B  (A) Bilateral plantar ulcers; (B) Complete healing achieved Source: “The Diabetic Foot–A Clinical Atlas”, Sharad Pendsey

SUMMARY Despite all the aforementioned, perhaps one of the most effective and also overlooked aspects of offloading is education. Facilitating patients to clearly understand the importance of not standing on an open wound and letting them discover ways in which they can offload their ulcer is far more efficacious than simply saying “keep off your feet”. In summary, successful plantar foot ulcer management is based upon comprehensive patient and wound assessment that identifies ulcer etiology allowing it to be addressed. If this is not done, despite best efforts failure will be inevitable. Having achieved this, the three main precepts need be applied: ensuring arterial inflow, infection control and removal of trauma (offloading). Education of patients and professionals is essential; effective debridement is paramount, dressings kept simple with frequent changes and regular objective



77    Contemporary Management of the Diabetic Foot

A

B

C Figs 24A to C  (A) Plantar ulcer; (B) Healing ulcer; (C) Completely healed ulcer after debridement Source: “The Diabetic Foot–A Clinical Atlas”, Sharad Pendsey

wound reviews. Comprehensive note keeping with serial wound measurements and possibly photographs, will allow for objective reviews. In theory, plantar ulcer management is quite straight forward. However, in practice it is an altogether different story, relying upon an effective partnership forged between patients and professionals in which clear goals are identified and realistic sympathetic methods employed to achieve them.

SUGGESTED READING 1. Andrew JM, Peter RC, Gerry R (Eds). The Foot In Diabetes, 4th edition. John Wiley and Sons; 2006. 2. David GA, Lawrence AL (Eds). Clinical Care of the Diabetic Foot. American Diabetes Association; 2005. 3. Robert GF (Ed). The High-risk Foot in Diabetes Mellitus. Churchill Livingstone; 1991. 4. Sharad P (Ed). Diabetic Foot: A Clinical Atlas, 1st edition. New Delhi Jaypee Brothers Medical Publishers (P) Ltd; 2003.

CHAPTER

The Diabetic Charcot Foot: Diagnosis and Management

10 Robert G Frykberg

INTRODUCTION The diabetic Charcot foot (neuropathic osteoarthropathy) is a condition affecting the bones, joints and soft tissues of the foot and ankle and is characterized by inflammation in the earliest phase. Charcot neuropathic (CN) osteoarthropathy has also be defined as a progressive joint destructive condi­ tion affecting single or multiple joints and characterized by dislocation, pathologic fractures and severe destruction of the pedal architecture. Osteoarthropathy in its later stages (especially when not diagnosed early) often results in severe deformity with correspondingly high plantar pressures, ulceration and subsequent infection. Unfortunately, amputa­ tion can be a final consequence in the most severe of cases due to underlying infection, osteomyelitis, gangrene or severe instability. CN is a consequence of various disease associated peripheral neuropathies of the lower extremities, but the most common etiology today is diabetes mellitus.

EPIDEMIOLOGY Often considered a rare, but disabling complication of the disease, it has been estimated that less than 1% of diabetic patients will develop Charcot arthropathy. Nonetheless, several recent retrospective studies have indicated that diabetic patients with CN have a higher 5 year mortality than diabetic patients without this complication. The true incidence of CN in the overall diabetes population, however, is limited by the small number of prospective or population based studies currently available. Much of the data we rely upon is based upon retrospective studies of small single center cohorts. Whereas many cases go undetected (especially in their early stages); the frequency of Charcot cases reported is therefore

very likely an underestimation. Diagnostic delays due to late presentation to medical providers or due to improper diagnosis compound the difficulty in ascertaining the true frequency of the disease, especially in its initial incidence. The prevalence of this condition is variable, ranging from 0.15% of all diabetic patients to as high as 29% in a population of only neuropathic diabetic subjects. Generally, however, this condition affects approximately 1% of all diabetic patients with a higher prevalence of course in those individuals with established neuropathy.

THE ETIOLOGY OF CHARCOT NEUROARTHROPATHY The primary risk factor for this potentially limb threatening deformity is the presence of dense peripheral sensory and autonomic neuropathy in association with a well perfused foot. This is not an entity related to peripheral arterial occlusive disease. To the contrary, relatively normal or abundant circulation characterizes such patients at the outset of this disorder. CN is a consequence of the interaction of peripheral neuropathies (sensory, motor and autonomic), underlying metabolic abnormalities of bone, and trauma (often minor) that leads to an intense, exaggerated inflammatory response in the predisposed individual. With continued walking on the neuropathic inflamed foot, the repetitive trauma of continued walking can result in a gradual disintegration of the normal architecture of the foot through a “vicious cycle” of injury compounded upon injury. Subsequent fractures and dislocations at various sites in the foot lead to the typical degrees of deformities that characterize the Charcot foot (Figs 1A and B). Trauma is not necessarily limited to injuries such as sprains or fractures, but can even include joint



The Diabetic Charcot Foot: Diagnosis and Management    79

A

B

Figs 1A and B  (A) Charcot foot with midfoot collapse (Rocker-bottom); (B) Dorsoplantar view of same foot showing Lisfranc joint changes

infections or prior surgical interventions. Foot deformities including prior partial foot amputations may also result in sufficient biomechanical stress that can lead to Charcot joint disease. Considering that neuropathy is the primary underlying predisposing condition, the general pathophysiology of Charcot arthropathy most likely is a combined effect of both the neurovascular and neurotraumatic theories. It is widely accepted that trauma superimposed on an insensate extremity can precipitate the development of an acute Charcot foot in susceptible individuals. With the development of autonomic neuropathy, there is an increased blood flow to the foot, resulting in osteopenia and a relative weakness of the bone that may initially present as osteolysis (neurovascular theory). Microvascular reactivity, under the control of autonomic and unmyelinated C-fibers, is also impaired in patients with diabetic neuropathy. It is postulated that the increased bone blood flow in response to injury exaggerates the hyperemic response leading to increased bone absorption. As described earlier, the presence of sensory neuropathy renders the patient unaware of most minor precipitating trauma (simple sprains, twists, etc.) and often the profound osseous destruction taking place during ambulation. Despite the severe bone changes, fractures and dislocations, the patient will continue to walk on the insensitive foot, usually only noting the appearance of edema, deformity and minor pain or aching as further damage occurs (neurotraumatic theory). Since it is unlikely that these two classical theories of pathogenesis exist in isolation, Edelman proposed a new modern theory in 1987 that combines the elements of both the neurovascular (French) and neurotraumatic (German) theories. An illustration of the combined theory is presented in Figure 2.

However, not all patients with neuropathy who sustain trauma will go on to develop neuropathic arthropathy. Emerging evidence has elucidated several other important metabolic abnormalities of bone physiology that are likely coupled to genetic polymorphisms in susceptible individuals. While not necessarily specific to persons with diabetes, in the presence of peripheral neuropathy these metabolic perturbations contribute to the exaggerated response of bone to injury, pronounced inflammation, and bone dissolution that characterizes the acute Charcot foot. The underlying link therefore that connects CN to multiple diseases causing peripheral neuropathy (diabetes, leprosy, alcoholism, etc.) could therefore likely be these genetically determined metabolic bone perturbations. Within the last decade or so there has been a great deal of interest and investigation into proinflammatory cytokines (TNFa, IL-1 and IL-6) and their influence on bone metabolism, specifically relating to osteoclastic regulation and osteopenia. The expression of tumor necrosis factor-alpha (TNFa) following acute insult is subsequently associated with the increased expression of another cytokine system involving the polypeptide, receptor activator of nuclear factor-kappa Beta (NF-kB) ligand (RANKL), a member of the TNF superfamily. RANKL, generally residing on macrophage and osteoblastic cell membranes, is upregulated and then triggers the synthesis of NF-kB within local osteoclast precursor cells after binding with its surface receptor RANK. The osteoclast precursor cells are then stimulated to differentiate into mature; activated osteoclasts that aggressively demineralize bone (osteolysis). Once upregulated, NF-kB also initiates the expression of a glycoprotein, osteoprotegerin (OPG) that is structurally related to RANKL and actually serves as a “decoy receptor” for RANKL. Osteoprotegerin therefore serves to modulate the



80    Contemporary Management of the Diabetic Foot

Fig. 2  Combined theory of Charcot pathogenesis (after Edelman 1987)

susceptibility for this disorder, and account for the excessive osteoclastic activity that typifies it.

CLINICAL DIAGNOSIS OF ACUTE CHARCOT ARTHROPATHY

Fig. 3  Receptor activator of NF-kB ligand/osteoprotegerin (RANKL/ OPG) pathway (after Molines 2010)

activity of RANKL and NF-kB, and therefore modulates the upregulation of osteoclasts (osteoclastogenesis). (Fig. 3) In the Charcot foot, there is an ostensible dysregulation of the normal RANKL/RANK/OPG signaling pathway as indicated by the aggressive unbalanced osteolysis and perpetuation of inflammation. In fact, recent evidence from two countries provide intriguing evidence that several single nucleotide polymor­ phisms for the OPG gene might play a role in determining

Diagnosis of acute Charcot arthropathy can usually be based on characteristic clinical findings in corroboration with plain radiographs. While the hallmark of this deformity is the classic “Rocker-bottom” foot (Fig. 4), most initial presentations in the acute stage are far less dramatic. It is especially important, therefore, that the clinician have a high index of suspicion for this disorder in neuropathic patients. Marked inflammation, noted by unilateral swelling (in most cases), increased skin temperature, erythema and a subtle change in the shape of the foot with or without precipitating trauma in an insensate foot will most often suggest the appropriate diagnosis. Radiographic findings may include fractures, subtle or gross dislocations, joint effusions, loss of normal joint and pedal architecture, periosteal new bone formation, and soft tissue edema. These clinical and radiological signs are often pathognomonic of acute Charcot arthropathy. In many cases, the patient will present with some degree of pain in an otherwise insensate extremity. Patient demographics also play an important role in establishing this diagnosis since studies have shown rather consistent findings in this regard. All patients with long standing diabetes will have peripheral neuropathy of



The Diabetic Charcot Foot: Diagnosis and Management    81

Fig. 4  Lateral X-ray of classic “Rocker-bottom” Charcot foot

Fig. 6  Charcot ankle with medial arterial calcification

some degree and many will have an identifiable history of antecedent trauma. Nonetheless, this will be inconsistent because these insensate patients might not recall very subtle degrees of injury. When diabetic patients present with a warm, edematous, insensate foot, plain radiographs are invaluable in ascertaining the presence of Charcot foot. In most cases, plain films will be the only imaging studies required to make the correct diagnosis. Typical radiographic changes observed will be soft tissue edema, fractures, dislocations (often subtle), osteolysis, osteopenia, extrusion of midfoot bones, lateral deviation of the forefoot and loss of normal architecture with collapse of the longitudinal arch (“Rocker-bottom”) and/or the ankle (Fig. 5). Medial arterial calcification is also a very common associated finding (although not exclusive) in patients with both acute and chronic Charcot foot deformities (Fig. 6).

Varying degrees of these changes can occur in any individual, ranging from very subtle to very severe. In very early stages despite acute inflammation, bone injury might not even be evident on plain films. With a concomitant wound, it is often difficult to differen­ tiate between acute Charcot arthropathy and osteomyelitis (or to confirm both) solely based on plain radiographs. If the wound probes directly to bone, or if bone is visible at the base of the wound, concomitant osteomyelitis is highly likely. A bone biopsy and culture in this case should be considered as the most specific method of determining the presence of osteomyelitis. Additional laboratory studies may also prove useful in arriving at a correct diagnosis. The white blood cell (WBC) count may not even be elevated in acute osteomyelitis, since this parameter is often blunted in persons with diabetes. Similarly, while the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are variably reactive in the presence of diabetic foot infection, they are non-specific and can be elevated solely due to the osteoarthropathy and attendant inflammatory response. Nuclear medicine imaging is widely available and can assist in making an early diagnosis, especially when X-rays are initially negative. Technetium-99m bone scans are highly sensitive but generally non-specific in assisting in the differentiation between osteomyelitis and acute Charcot arthropathy. Bone scans, however, are sometimes very useful in arriving at an early diagnosis of neuroarthropathy when radiographs are still without changes but when clinical suspicion is high. Magnetic resonance imaging (MRI) may be the diagnostic modality of choice in this regard, although it is still difficult to distinguish marrow changes due to infection from those related to osteoarthropathy (Fig. 7). Bone marrow edema noted on MRI in the absence of radiographic evidence of fracture or dislocation is now considered to be a hallmark of incipient Charcot foot in those

Fig. 5  Typical X-ray of Charcot midfoot deformity



82    Contemporary Management of the Diabetic Foot

Fig. 7 MRI of Charcot foot with ulcer showing extensive midfoot changes

Table 1  Diagnostic recommendations for acute Charcot foot •

The diagnosis of active Charcot foot is primarily based on history and clinical findings but should be confirmed by imaging



Inflammation plays a key role in the pathophysiology of Charcot foot and is the earliest clinical finding



The occurrence of acute of foot/ankle fractures or dislocations in neuropathic individuals is considered active CN due to the inflammatory process of bone healing, even in the absence of deformity



X-rays should be the initial imaging performed and one should look for subtle fractures or subluxations if no obvious pathology is visible



MRI or nuclear imaging can confirm clinical suspicions in the presence of normal appearing radiographs

neuropathic patients with signs of acute inflammation. The International Consensus on the Diabetic Charcot foot has summarized the key points pertaining to the diagnosis of an acute Charcot foot as indicated in (Table 1).

CLASSIFICATION OF CHARCOT ARTHROPATHY Eichenholz published a monograph on his series of patients with Charcot joints in 1966 and presented the simplest and perhaps the most commonly used classification scheme for Charcot arthropathy. This system is based on radiographic appearance as well as physiologic (pathologic) stages of the process wherein it is divided into the developmental, coalescent, and reconstructive stages. The developmental stage (Stage 1) is characterized by acute inflammation with

significant soft tissue edema, joint effusions, osteochondral fragmentation, fractures and dislocation of varying degrees. This stage represents the active, destructive phase of the disease process wherein most of the osseous and architectural disorganization occurs. While it is precipitated by even mild trauma at its onset, continued unrestricted walking on the injured foot is enough to further perpetuate the trauma and bony destruction. The stage of coalescence (Stage 2) is noted by a reduction in soft tissue swelling, bone callus proliferation and consolidation of fractures. This begins the post-acute or reparative phase wherein inflammation subsides as an attempt at healing commences. Finally, the reconstructive stage (Stage 3) is indicated by bone healing, joint ankylosis, and osseous hypertrophy without further clinical signs of inflammation. While this system is very descriptive from a radiological standpoint, its clinical usefulness is less, since there are no well-defined criteria for transition from one stage to the next. Therefore, most clinicians will simply consider the initial stage as being active, while the coalescent and reconstructive stages combined are regarded the inactive, chronic or quiescent stages. Shibata in 1990 proposed for an earlier Stage 0 that corresponds to the initial inflammatory period following injury, but prior to the development of characteristic bony radiographic changes. Since radiographs are by definition negative for fractures or dislocations during this prodromal period, MRI is considered the imaging modality of choice to detect bone marrow edema or signs of bone stress injury characteristic of Stage 0 CN. There are several other classification schemes in the literature as well, although none has been uniformly adopted as being superior or predictive of outcome. The author’s preferred classification system is based upon five anatomic sites of involvement but does not describe the activity of the disease (Fig. 8).

MANAGEMENT OF ACUTE CHARCOT ARTHROPATHY The primary treatment for the acute Charcot foot must be rest and immobilization, preferably without bearing weight on the injured neuropathic foot. Most authors advocate immobilization with casts, total contact casts (TCC), splints, orthoses, etc. and complete non-weight bearing through the use of wheelchair, crutches or other assistive modalities during the initial acute period. Ideally, this should commence upon earliest signs of inflammation, in Stage 0. When offloading one foot entirely, care must be taken to protect the other foot because of added stress to the weight bearing extremity and the potential for contralateral osteoarthropathy. Nonetheless, several authors have shown that immobilization with a weight bearing total contact cast can be done safely without harm to the acute Charcot foot. Following a period of offloading with



The Diabetic Charcot Foot: Diagnosis and Management    83

Fig. 8  Sanders and Frykberg classification of Charcot foot (after Levin and O’Neal, 2007)

mild compression or casting, a reduction in skin temperature and edema heralds the stage of quiescence (Stage 3). Generally, the Charcot foot is compared with the equivalent site on the opposite foot and the temperature differential should be approximately 2°C before casting should be suspended. After a period of 3–6 months progression to protected weight bearing is then permitted, usually using a pneumatic walker or fixed ankle walker usually with the aid of an assistive device such as a cane or crutches. The mean time of rest and immobilization (casting followed by removable cast walker) prior to return to permanent footwear is approximately 4–6 months, although a longer term use of an ankle-foot orthoses is sometimes required. This is quite variable and depends not only upon the adequacy of treatment, but also upon the location and aggressiveness of bone lysis. CN of the ankle is particularly problematic since severe instability and deformity are common sequelae at this joint. In such cases, long-term bracing or surgical fusion becomes necessary to avoid amputation. The adjunctive use of bisphosphonates (osteoclastic inhibitors) may help expedite the conversion of the acute process to the quiescent, reparative stage and their use has been fairly frequently reported although not without some concerns for their effectiveness in this regard. Another study investigated the efficacy of intranasal calcitonin in this same setting with similarly positive results. Adjunctive bone growth stimulation (including low intensity ultrasound) has also been proposed as a means to promote rapid consolidation of fractures in acute osteoarthropathy. While markers of osteoclastic function are currently used to monitor activity, a far more important outcome would be to monitor healing (consolidation) of fractures and return to footwear.

Table 2 highlights the basic tenets for managing both acute and chronic Charcot foot disorders. Flow chart 1 highlights diagnostic algorithm for acute Charcot foot.

SURGICAL MANAGEMENT OF THE DIABETIC CHARCOT FOOT Reconstructive foot surgery has assumed an increasingly important role in the management of Charcot foot that cannot be effectively treated by casting, bracing or footwear therapy. While management of the Charcot foot should primarily be focused on non-operative measures, such patients often initially present with rather severe or unstable deformities even in the active stage. It has long been held that surgery in the acute stage is unadvisable due to the extreme edema, hyperemia and osteopenia present during this phase. However, in the presence of acute subluxation without significant fractures (typified by talonavicular dislocation) several reports suggest that primary fusion might in fact be the recommended treatment. While the appropriateness of reconstructive surgery during the acute phase is still a matter of debate, surgery on the chronically deformed or unstable quiescent Charcot foot has become rather common in current practice. It remains a matter of judgment on the part of the treating clinician as to when (or if ) their patients with CN require surgical intervention. From a clinical standpoint, however, it seems that Charcot arthropathy of the ankles indeed often require surgical fusion to maintain alignment and stability. The most common type of procedure performed is a plantar midfoot exostectomy, usually accompanied by a tendo-achilles lengthening or gastrocnemius recession to



84    Contemporary Management of the Diabetic Foot Table 2  Basic tenets for managing both acute and chronic Charcot foot disorders Acute

Chronic

Offload:    Complete non-weight bearing   Crutches, wheelchair

Therapeutic footwear with customized pressurerelieving insoles:   Commercially available    Custom fabricated (for severe deformity)

Immobilization:    Soft compression bandage   Posterior splint     Cast or total contact cast

Bracing for unstable deformities:    Patellar tendon bearing brace (PTTB)    Charcot restraint orthotic walker (CROW)

Or:    Partial weight bearing with assistive devices: Crutches, Surgery for severe instability, nonplantigrade feet,   walker, wheelchair recurrent ulcers or deformities not amenable to foot­ wear therapy: And   Plantar exostectomy    Total contact cast or    Tendo-Achilles lengthening    Removable cast walker   Osteotomies   Arthrodeses    Amputation (selected cases only) Manage associated wounds Manage medical comorbidities Continue weight bearing restrictions until edema recedes, temperature normalizes and osseous healing progresses (3–6 months)

Lifetime surveillance

May consider bisphosphonates or bone stimulators to expedite consolidation Surgery might be considered in cases with severe dislocations and deformity (Caution—this has not been widely reported)

A

B

Figs 9A and B  (A) Charcot foot with midfoot ulcer (preoperatively); (B) Charcot foot postexostectomy of midfoot and ulcer excision

increase the dorsiflexion at the ankle (and thereby reduce plantar pressures at the midfoot and forefoot) (Figs 9A and B).

Other frequent operations, depending upon severity of deformities and experience of the surgeons, include midfoot, hindfoot and ankle realignment arthrodeses, and also amputations for infected or severe deformities unsuitable for reconstructive procedures. Realignment arthrodeses are frequently required in addition to exostectomy to correct severe deformity that places the foot at risk for recurrent ulceration. Oftentimes, concomitant plastic surgical proce­ dures (local and random flaps, muscle transpositional flaps, fasciocutaneous flaps, free tissue transfer and split thickness skin grafts) will be necessary to cover large defects not suitable for primary closure or healing by second intention. Circular external fixators (frames) have been introduced for the treatment of CN in the last decade or so with increasing frequency (Fig. 10). External fixation is ideal in ulcerated or infected acute and chronic Charcot deformities for stabilization and arthrodesis of the joints after the infection has been appropriately managed. In this setting, percutaneous application of wires and pins is performed without internal fixation, although wound and bone debridement is carried out in the same operative session. Unfortunately, most patients will develop pin tract infections



The Diabetic Charcot Foot: Diagnosis and Management    85 Flow chart 1  Diagnostic algorithm for acute Charcot foot (after Rogers 2011)

CONCLUSION

Fig. 10  Charcot ankle realignment stabilized with circular external fixation

or irritation, especially those who are bearing weight on the frames during healing. As a precaution, we try to keep these neuropathic patients non-weight bearing for the entire time that the frame is applied until consolidation of fractures or arthrodeses (generally 3–4 months).

The diabetic Charcot foot, although a rare complication of the entire population of persons with diabetes, is a life-altering event that not only adversely affects their quality of life but also potentially places their limbs at risk for amputation. Unfortunately, many patients with Charcot feet succumb to severe deformity, recurrent ulcerations and infections, and subsequent amputation. The key to preventing such complications is to diagnose this condition at its earliest presentation and to institute appropriate treatment based on the best available evidence. Consequently, both patients with diabetes (and established neuropathy) as well as clinicians need to become aware of this serious complication and have a heightened index of suspicion for its presentation. Although certainly not all amputations subsequent to this deformity can be prevented, a better understanding of this enigmatic condition and the principles of treatment as outlined will surely lead to better outcomes.

SUGGESTED READING 1. Edelman SV, Kosofsky EM, Paul RA, et al. Neuro-osteoarthro­ pathy (Charcot’s joint) in diabetes mellitus following revascularization surgery. Three case reports and a review of the literature. Arch Intern Med. 1987;147(8):1504-8.



86    Contemporary Management of the Diabetic Foot 2. Frykberg RG, Belczyk R. Epidemiology of the Charcot foot. Clin Podiatr Med Surg. 2008;25(1):17-28. 3. Frykberg RG, Eneroth M. Principles of Conservative Manage­ ment. In: Frykberg RG (Ed). The Diabetic Charcot Foot: Principles and Management. Brooklandsville, MD: Data Trace Publishing Company; 2010. pp. 93-116. 4. Frykberg RG, Rogers LC. Classification of the charcot foot. In: Frykberg RG (Ed). The Diabetic Charcot Foot: Principles and Management. Brooklandsville, MD: Data Trace Publishing Company; 2010. pp. 55-64. 5. Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders. A clinical practice guideline (2006 revision). J Foot Ankle Surg. 2006;45(5 Suppl):S1-66. 6. Jeffcoate W. Vascular calcification and osteolysis in diabetic neuropathy-is RANK-L the missing link? Diabetologia. 2004;47(9):1488-92. 7. Pinzur MS, Sostak J. Surgical stabilization of nonplantigrade Charcot arthropathy of the midfoot. Am J Orthop (Belle Mead NJ). 2007;36(7):361-5. 8. Pinzur MS. Surgical management-history and general principles. In: Frykberg RG, (Ed). The Diabetic Charcot Foot: Principles and Management. Brooklandsville, MD: Data Trace Publishing Company; 2010. pp. 165-86. 9. Richard JL, Almasri M, Schuldiner S. Treatment of acute Charcot foot with bisphosphonates: a systematic review of the literature. Diabetologia. 2012;55(5):1258-64.

10. Rogers LC, Frykberg RG, Armstrong DG, et al. The Charcot foot in diabetes. Diabetes Care. 2011;34(9):2123-9. 11. Sanders L, Frykberg R. The Charcot foot (Pied de Charcot). In: Bowker JH, Pfeiffer M (Eds). Levin and O’Neal’s The Diabetic Foot, 7th edn. Philadelphia: Mosby Elsevier; 2007. pp. 257-83. 12. Sanders LJ, Frykberg RG. Diabetic neuropathic osteoarthro­ pathy: the Charcot foot. In: Frykberg RG (Ed). The High Risk Foot in Diabetes Mellitus. New York: Churchill Livingstone; 1991. pp 325-35. 13. Trepman E, Nihal A, Pinzur MS. Current topics review: Charcot neuroarthropathy of the foot and ankle. Foot Ankle Int. 2005;26(1):46-63. 14. Wukich DK, Belczyk R. Silent neuropathic bone injuries and dislocations-stage 0. In: Frykberg RG (Ed). The Diabetic Charcot Foot: Principles and Management. Brooklandsville, MD: Data Trace Publishing Company; 2010. pp. 117-30. 15. Wukich DK, Sung W, Wipf SA, et al. The consequences of complacency: managing the effects of unrecognized Charcot feet. Diabet Med. 2011;28(2):195-8. 16. Wukich DK, Zgonis T. Circular external fixation in Charcot neuroarthropathy. In: Frykberg RG (Ed). The Diabetic Charcot Foot: Principles and Management. Brooklandsville, MD: Data Trace Publishing Company; 2010. pp. 231-41.

CHAPTER

Diabetic Foot Infections

11 Sharad Pendsey

INTRODUCTION Diabetic foot infections (DFIs) are among the most common and serious complications of diabetes mellitus. The DFI is the most common indication for hospitalization and often prolonged hospital stay. It is associated with high morbidity, occasional mortality and ever dangling risk of lower limb amputation. The DFIs are a serious medical prob­lem, requiring prompt attention, appropriate diagnostic evaluation and proper therapeutic strategies. The DFIs are often associated with bone involvement and the need for sharp and bold surgical debridement. In the beginning, DFI may appear trivial, but if not managed properly, it has a potential to progress rapidly to limb or life-threatening situations. Presence of infection in diabetic foot ulcer works as a catalyst and accelerates the journey toward a limb amputa­­tion. Presence of ischemia in the lower limb has an adverse effect on the clinical course and the outcome of an infection. This combination of ischemia and DFI carries the worst prognosis.

PATHOPHYSIOLOGY Three most important factors responsible for DFI are: (1) neuropathy; (2) peripheral vascular disease; and (3) com­ pro­mised immunological status of the patient. As long as the skin of the foot is intact, the infection usually does not occur. The initial event is a break in the skin which paves way for pathogenic microorganisms and the underlying tissues get exposed to colonization by pathogenic organisms.

DIAGNOSIS The diagnosis of DFI is based on the cardinal clinical signs and symptoms of local inflammation. These cardinal signs are:

• • • • •

Redness Swelling Heat Pain Loss of function.

In DFI, pain is conspicuously absent because of neuropathy and as there is no pain, there is no loss of function. Loss of function (original Latin word Functio laesa), is nature’s attempt to restrict the inflammatory process. The DFI is the only soft tissue infection in the body which is on the weightbearing area. In the absence of pain, continued ambulation, despite infection, facilitates rapid spread of infection. Diabetic foot infection must be diagnosed clinically rather than bacteriologically because all skin ulcers harbor microorganisms. Apart from clinical signs of inflammation as described earlier, diagnosis of foot infection is based on the presence of purulent discharge from an ulcer, foul odor, presence of necrosis and failure of wound healing despite optimal management. Systemic signs and symptoms like fever, chills and tachycardia indicate severe DFI. Diabetic foot infection is classified as mild, moderate and severe (classification of DFI is covered in the Chapter on “Principles of Debridement”). In the presence of vascu­ lar disease, even mild infection can have devastating conse­ quences.

Bacteriological Diagnosis Superficial infection is usually due to single microorganism (monomicrobial), particularly Staphylococcus aureus and beta-hemolytic streptococci. While deep infections are usually caused by multiple microorganisms (polymicrobial) like Escherichia coli, Proteus species, Pseudomonas aeruginosa and Klebsiella pneumoniae. In mixed infections in patients



88    Contemporary Management of the Diabetic Foot with foot ischemia or gangrene, anaerobic bacteria like Clostridium species, Bacteroides species are usually present. In patients who have been previously exposed to antibiotic therapy, methicillin-resistant Staphylococcus aureus (MRSA) is a common pathogen. For appropriate antibiotic treatment, isolation of causa­ tive organisms and its sensitivity to different antibiotics is extremely important. The accuracy of wound culture depends on obtaining appropriate specimen. This requires careful attention to sterile technique as well as selection of the optimal portion for the sampling. Cultures using wound swabs are usually unreliable and should best be discouraged. The collection of the sample (purulent material) by needle aspiration could be performed. Alternatively, wounds should be debrided and deep tissue specimen can be obtained by curet­tage or it can be biopsied. The specimen should be processed for a Gram-stained smear and aerobic and anaerobic cultures.

Fig. 1  An X-ray metallic foreign body

Assessing Vascular Status Every case with DFIs should be evaluated for vascular status clinically and by noninvasive and invasive methods. These methods have been described in the Chapter on “Evaluation of Neuroischemic Foot”.

Laboratory Investigations Complete blood counts should be carried out to look for anemia, leukocytosis and raised erythrocyte sedimentation rate (ESR). In deep seated infections or osteomyelitis, ESR is often raised above 70 mm/hour. One should also investigate for renal functions, electrolytes, serum proteins and glycated hemoglobin (HbA1C) to assess glycemic control. Cardiovascular status should be checked along with twodimensional echocardiography.

Imaging Techniques Plain radiographs of the affected foot in anteroposterior, oblique and lateral views are essential for the diagnosis of: • Foreign body • Gas in the soft tissue • Osteomyelitis. Foreign bodies should be always looked for in DFI, particularly plantar infections. Metal objects like sharp pins, nails and broken pieces of stones have been reported (Fig. 1). Anaerobic organisms and some Gram-negative organisms produce gas which can be seen on a plain radiograph (Fig. 2). Gas in the soft tissue with crepitus on palpation is a bad prognostic sign. Osteomyelitis is a common and serious complication of DFI that poses a diagnostic challenge. A delay in diagnosis

Fig. 2  Gas in the soft tissue

increases the risk of amputation. The diagnosis can be confirmed by certain clinical signs and imaging: • Multiple discharging sinuses • Sausage-like appearance of toe • Probing up to bone (PBT) • An X-ray foot • Magnetic resonance imaging (MRI), computed tomo­ graphy (CT) and nuclear scan • Bone biopsy. Osteomyelitis generally results from contiguous spread of deep soft tissue infection through the cortex to the bone marrow. A simple clinical test is PBT (Fig. 3). A sterile metal probe is inserted into the ulcer, if it pene­trates to the bone; it almost confirms the diagnosis of osteo­ myelitis. Chronic discharging sinus or sausage-like



Diabetic Foot Infections    89

Fig. 3  Probing up to bone (PBT)

Fig. 5 Destruction of first metatarsal head (MTH) and proximal phalanx

Fig. 4  Sausage-like toe

Fig. 6  Swollen right great toe with discharging sinus

appearances of the toe are clinical markers of osteomyelitis (Fig. 4). Plain radiography usually shows focal osteopenia, cortical erosions or periosteal reaction in the early stage and sequestration in the late stage (Fig. 5). Radiographic changes take at least 2 weeks to be evident. Newer techniques like bone scan, CT scan, positron emission tomography (PET), MRI are helpful in confirming the diagnosis. The MRI is the most sensitive and specific imaging technique. Definitive diagnosis requires obtaining bone biopsy for microbial culture and histopathology. Following is the illustrative case of osteomyelitis of phalanges of right great toe. This patient is presented with nonhealing ulcers over right great toe. The toe was swollen with multiple discharging sinuses. PBT was positive. In this

case, we did plain radiograph, MRI, bone scan as well as bone biopsy. Nuclear scan showed that the perfusion and blood pool phases revealed focal hyperemia involving the right great toe with increased tracer uptake. Magnetic resonance imaging showed low signal inten­ sity on T1-weighted images and high signal intensity on T2-weighted images and short T1 inversion recovery (STIR) sequences in the phalanges of the right great toe (Figs 6 to 12). The bone biopsy from the phalanges of the right great toe revealed bony lamellae without osteoblastic lining with neutrophilic infiltrate with few lymphocytes, histiocytes and eosinophils. Surrounding fibromuscular tissue also showed inflammation consistent with osteomyelitis.



90    Contemporary Management of the Diabetic Foot

Fig. 7  Radiograph of osteomyelitis of the phalanges of the right great toe

Fig. 10  Magnetic resonance imaging (MRI) high signal intensity on T2weighted image, right great toe

Fig. 8  Nuclear scan of focal hyperemia and increased tracer uptake in the right great toe

Fig. 11  Magnetic resonance imaging (MRI) high signal intensity on short T1 inversion recovery (STIR) sequences, right great toe

CLINICAL SYNDROMES Diabetic foot infections (DFIs) manifest clinically as dorsal foot infection, plantar foot infection, heel pad infection and infected plantar pressure ulcer (mal perforans).

Dorsal Foot Infection Characteristics • • • • Fig. 9 Magnetic resonance imaging (MRI) low signal intensity on T1-weighted image, right great toe

Early recognized being on the dorsum Manifests with extensive cellulitis Infection spreads via lymphatics Associated with extensive skin necrosis.

Dorsal foot infection usually occurs because of footwear injuries, traumatic wounds, nail infection (Fig. 13), infected



Diabetic Foot Infections    91

Fig. 12  Bone biopsy of proximal phalanx of right great toe inflamma­ tory cells

Fig. 14  Extensive dorsal foot infection

Fig. 13  Paronychia

Fig. 15  Dorsal foot infection with cellulitis, a characteristic

bunions and interdigital mycosis. Even though there is no pain, being on the dorsum, it gets easily recognized. The clinical presentation is in the form of extensive cellulitis. Infection in dorsum of the foot spreads via lymphatics. In diabetics with neuropathy, cellulitis is not associated with pain and tenderness, thus allowing ambulation and dependent position causing further spread of infection. A person with normal sensations would automatically rest and elevate the foot because of pain. Dorsal compartment of the foot has all extensor muscle tendons, which are not encased in sheaths but lie in loose areolar tissue. Thin superficial fascia, which covers these extensor tendons, is continuous with the extensor retinaculum of the ankle and infection can spread along these tendons proximally from foot into the leg. Such a swollen and infected foot dampens the arterial blood

flow and skin over dorsum of the foot can get easily necrosed due to infective occlusions of small vessels in the skin. As dorsal foot infection is recognized early and being not on the weight-bearing area, it gets under control with antibiotics and debridement. It is rarely limb- or life-threaten­ ing infection. As skin necrosis is extensive, wound closure usually requires skin grafting (Figs 14 to 17).

Infections in Plantar Compartments (Plantar Compartment Syndrome) Characteristics • Late recognized being on plantar area • Extensive soft tissue necrosis



92    Contemporary Management of the Diabetic Foot

A

B

Figs 16A and B  Extensive skin necrosis, a characteristic of dorsal foot infection

A

B

A

B

Figs 17A and B  (A) Dorsal skin necrosis; (B) After skin grafting

Figs 18A and B  (A) Mild plantar foot infection; (B) Almost complete healing 8 days after debridement

• Potential to become limb- or life-threatening infections • Only soft tissue infection on weight-bearing area.

Foot has abundant white tissues like plantar aponeurosis, plantar fascia, tendons, ligaments, muscle sheaths and fibro­ fatty subcutaneous tissue which are relatively less vascular and can neither resist infection nor withstand ischemia for too long, resulting in their necrosis. Careful assessment of foot infection is extremely important to determine the need for incision, debridement and other surgical interventions. Unlike dorsal skin, plantar skin is thick, tough and has rich nerve as well as blood supply. It is tightly bound to underlying tissues. In presence of infections plantar skin resists infection, and does not get necrosed like dorsal skin.

Deep Plantar Compartments (Spaces) They are divided into medial, central and lateral compart­ ments. When the infection is localized in one of these compart­ ments, the structures of the compartment like tendon sheaths and muscle fascia favor the proximal spread of infection. As the rigid fascial and bony structures bind these compartments, edema associated with acute infection rapidly elevates compartment pressure, causing ischemic necrosis of the confined tissues. Finally, the barriers get broken and infection spreads from one compartment to another through perforation of the intermuscular septa (Figs 18A and B).

Infection in the lateral compartment: The lateral compart­ment is bound by the fifth metatarsal dorsally, an intermuscular septum medially and the edge of the plantar aponeurosis



Diabetic Foot Infections    93

Fig. 19  Deep plantar foot infection in lateral compartment

Fig. 20  Infection in the medial plantar compartment

laterally. It contains the abductor and short flexor muscles of the fifth toe. Infection enters this compartment from infected bunionette of the fifth toe, web space infection between fourth and fifth toes, shoe bite, direct penetrating injuries, digital infection of the little toe or deep infection in the plantar ulcer over fifth metatarsal head (MTH). It clinically manifests as swelling and erythema on the lateral side of the forefoot, with or without necrosis of the fifth toe. Dorsum of the foot is often swollen, but in the absence of pain, the patient is relatively asympto­matic. If not managed in time such infection can progress into the central compartment which can prove devastating (Fig. 19).

plantar ulcers over the metatarsal heads (MTHs). The plantar digital arteries of the second, third and fourth toes arise from the plantar arch. Thrombotic obliteration of the plantar arch can lead to digital necrosis of these toes, particularly of the third toe. Once the infection is established, the longitudinal arch and the plantar skin creases disappear. There is swelling and erythema of the sole and edema over dorsum of the foot. All the plantar compartment infections are on the weightbearing areas and ambulation in absence of pain can lead to pressure necrosis of the soft tissue due to obliteration of capillaries and milking action facilitating further spread proximally. Along the flexor tendon, the infection can progress along the muscle tendons beyond ankle into the leg. Plantar foot infections have the highest potential to become limb or even life-threatening. Prompt recognition, sharp, bold debridement, removal of necrotic soft tissues and even bones is mandatory to salvage the limb (Figs 21 and 22).

Infection in medial compartment: The medial compartment is bound by the first metatarsal dorsally, an extension of the plantar aponeurosis medially and intermuscular septum late­rally. It contains the abductor and flexor muscles of the great toe. Infection enters the medial compartment through erosion of the metatarsophalangeal (MTP) joint of the great toe or from physical trauma such as penetrating injuries, shoe bite, nail infection or web space infection between first and second toes. Once infection is established, the foot is swollen medially, the medial arch disappears, plantar skin is swollen, and erythematous; with or without edema over dorsum of the foot. Infection can progress proximally through the tendon of flexor hallucis longus or can enter the central plantar com­ partment, by disruption of the intermuscular septum (Fig. 20). Infection in central plantar compartment: The central com­ part­ment is bound by the plantar aponeurosis inferiorly, intermuscular septa medially and laterally, and second, third and fourth metatarsals dorsally. It contains lumbricals, flexors to the digits, adductor hallucis and posterior tibial and peroneal tendons. Infection in the central plantar compart­ ment is most devastating. It enters from web spaces, toe infections, nail pathologies, penetrating injuries or from

Fig. 21  Third toe necrosis, with infection of central plantar compartment



94    Contemporary Management of the Diabetic Foot and being the most proximal part of the foot, any deep seated infection can be a limb-threatening situation. The heel pad is abundant in fatty tissue and is short of red muscle mass. Infection leads to fat necrosis and as there is no intervening red muscle mass, it can easily spread into calcaneus. The heel is infected either as an extension of infection from midfoot or through penetrating injuries, plantar ulcers, fissures or through decubitus ulcer. In limb-threatening infection, systemic toxicity is usually evident in the form of fever, malaise, loss of appetite, vomiting and pallor. The glycemic control is invariably poor and the patient can even present with ketoacidosis. Such patients if not managed promptly, a life-threatening situation can soon arise.

Fig. 22  Debridement and third ray amputation in the same patient

Heel Pad Infection Characteristics • Heel is the toughest part of the foot • Osteomyelitis of calcaneum is most difficult to treat • Inspection of back of heel in bedridden patients is essential • Deep infection in heel can soon become a limb-threaten­ ing situation. Heel is the toughest part of the foot. During “heel strike”, when the foot first touches the ground, most of the body weight is borne by the heel bone (calcaneus). However, at that stage, the other foot is still sharing some of the weight of the body. As soon as the heel is firmly on the ground, the other foot leaves the ground and then for a moment, the calcaneus may carry the whole body weight. The skin of the heel is tightly bound by numerous vertical septa extending through the subcutaneous tissue to the surface of the calcaneus. These septa result in formation of small cylinders which are packed with fat globules. During weight-bearing, each fat globule changes its shape, and spreads the thrust to the globules on either side as well as to those immediately below it. Thus, by the time that thrust gets down to the skin, it is not a small area but rather a large area that is carrying weight. These peculiar fatty cylinders act like shock absorbers that is why, in Syme’s amputation, the heel flap is preserved for weight-bearing even though the calcaneus is removed. Despite increased plantar pressure on the heel during walking, neuropathic plantar ulcers are less common on the heel as compared to the forefoot. The possible explanations are that the bony prominences of the forefoot are not covered by subcutaneous tissue as thick as the heel and secondly loss of protective sensibility is greater in the forefoot with the longest nerve fibers preferentially affected. The heel is a vulnerable area

Heel lesions: Fissures are a common feature on the borders of the heel and are deep and wide. They result from dry skin, a consequence of autonomic neuropathy, can be very deep and can get secondarily infected. The heel is particularly vulnerable to trauma. Associated neuropathy leads to callus building as the heel is exposed to a great deal of pressure. Regular removal of such callus is essential. Lesions of the posterior portion of the heel usually indicate excessive walking with tight footwear on the insensate foot. When the site of deep ulceration and gangrene happens to be heel, the foot is seldom salvageable because debridement and amputations in this area often preclude functional weightbearing. The heel may also get secondarily involved with infection spread from the forefoot or midfoot in the deep plantar layer. Heel involvement and osteomyelitis of the calcaneus are intractable surgical problems. Lower limb amputation is often necessary (Figs 23 to 25). Ischemic ulcer: The heel is supplied by the posterior tibial artery and this is often occluded in diabetics. In any heel ulcer, which is not healing, disease of the posterior tibial artery

Fig. 23  Extensive necrosis of heel pad—a result of infected fissures



Diabetic Foot Infections    95

Fig. 24  Osteomyelitis of calcaneum of the same patient

Fig. 26  Decubitus ulcer

Fig. 25  Heel pad infection

Fig. 27  Infected plantar ulcer

must be looked for. Such a vulnerable foot may be salvaged if vascular reconstruction is offered in time.

ing the patient; and (3) the mandatory use of heel protectors. Sadly, it is the simple that is often ignored (Fig. 26).

Decubitus ulcer: When a patient requires prolonged bed rest, particular attention must be paid to the heels. Because of loss of sensibility, the patient tends to keep the heels in the same position which results in pressure necrosis. The skin breaks down and infection and gangrene can develop. The simple weight of the immobile foot on the mattress obliterates blood perfusion in skin on the posterolateral side of the heel. The degree of vulnerability of the debilitated foot is often not appreciated by the patient and even the physician, who may have difficulty in understanding why “such a little thing” can result in tissue loss with consequences as grave as leg amputation. Prevention is thus the heart of the matter. All this makes for three simple take home messages: (1) daily inspection of heels in bedridden patients; (2) frequently turn­

Mal Perforans (Plantar Pressure Ulcer) Characteristics • • • •

Garden variety of neuropathic foot ulcer Accounts for about 30% foot lesions The most common cause of osteomyelitis Tendency for recurrence.

Mal perforans is a chronic, indolent ulcer of the sole of the foot, usually over the heads of the metatarsals (Figs 27 and 28). Ordinarily, it is caused by ulceration of a pre-existing callus. Most of the patients with mal perforans do not have



96    Contemporary Management of the Diabetic Foot

Fig. 28  Severely infected plantar pressure ulcer

ischemia, although 25% of such patients do have associated peripheral vascular disease. Characteristically, the mal perforans implies severe neuropathy in the presence of good blood flow. Fissuring and cracking in the calluses allow variety of organisms to enter. Penetration of the infection in the subcutaneous tissues is limited by the dense fibrous septum. For a long time, these deep ulcers are limited to skin and subcutaneous tissues. The flexor tendons form the base of these ulcers. When these tendons get eroded, the infection enters the underlying joint and leads to osteomyelitis. Once osteomyelitis sets in, some form of amputation becomes inevitable like toe disarticulation, ray amputation, etc. Chronic osteomyelitis results in sequestrum which does not have any blood supply. Such dead bone has to be removed along with the infected, necrosed soft tissue (Figs 29A and B).

A

Fig. 30  Severe plantar foot infection involving all the compartments

SEVERE DIABETIC FOOT INFECTIONS Mild DFIs need to be aggressively treated as the clinical course can rapidly worsen, from what appeared trivial just the other day, to one that now is suddenly limb or even life-threatening. Severe DFI is an emergency and has to be appropriately handled by treating foot care team with the aim to first save the patient’s life and if possible save the limb as well (Figs 30 to 32).

Necrotizing Fasciitis Necrotizing fasciitis is a severe form of DFI, and is associated with mortality anywhere between 30% and 60%. In tissues adjoining infection, small vessels commonly develop thrombotic occlusion leading to necrosis of the

B

Figs 29A and B  (A) Osteomyelitis; (B) Amputation

Fig. 31  Severe diabetic foot infection (DFI) in a Charcot foot



Diabetic Foot Infections    97

Fig. 32  Severe diabetic foot infection (DFI)

tissue. After desloughing, draining or control of infection, normal arterioles recanalize and form granulation tissue promoting healing of the wound. However, in certain mixed infections, so common in diabetic foot, virulent strains of staphylococci and streptococci liberate angiotoxic (necrotizing) substances. These angiotoxic factors like alpha-toxin of staphylococci, along with spreading factors like streptokinase and streptococcal hyaluronidase lead to a rapid extension of necrosis by digestion of fibrin barriers and intracellular ground substance. This is a severe, progressive soft tissue infection, which leads to necrosis of subcutaneous tissues down to the level of muscle fascia. Clinically, it begins with a trivial infection in foot leading to rapidly advancing necrosis with erythema, swelling and dusky discoloration of the overlying skin with hemorrhagic blisters. The occlusive process in the small vessels is exaggerated, more arterioles are obliterated and the original lesions get converted from trivial to ever enlarging areas of necrosis and gangrene. Creeping advancement of this process of infective obliterative angiopathy leads to devastating lesions within a couple of days. There is also evidence of systemic toxicity in the form of fever, tachycardia and hypotension. Urgent fasciotomy, fasciectomy and if required, a major amputation needs to be carried out along with an aggressive medical treatment to prevent such a life-threatening situation. Among all DFIs, necrotizing fasciitis requires the most extensive debridement (Fig. 33). In severe DFIs, the presence of limb ischemia should be closely evaluated to categorize the severity of the infection and the risk posed to limb survival. The dysvascular diabetic foot increases the severity of the infection. It should be determined if critical limb ischemia is present in conjunction with infection. The arterial supply to the lower extremities is assessed and conveyed to the diabetic foot care team (Table 1).

Fig. 33  Extensive debridement in necrotizing fasciitis

Table 1  Indications of worsening infection Signs and symptoms

Laboratory tests

Radiological investi­ gations (X-ray foot)



Drainage, erythema, temperature



Swelling, foul smell, fever with chills



Superficial bullae



Petechial hemorrhages, ecchymosis



Fluctuance and soft tissue crepitus



Lymphangitis and lymphadenopathy



Gangrene



Tachycardia, orthostatic hypotension



Delirium, stupor



↑ Total leukocyte count, ESR ↑



CRP ↑



Plasma glucose and HbA1c ↑



Ketones in serum and urine electrolyte abnormalities, worsening azotemia



Gas in the soft tissue



Osteomyelitis

Abbreviations: ESR: Erythrocyte sedimentation rate; CRP: C-reactive protein; HbA1c: Glycated hemoglobin

Vascular surgery and/or endovascular intervention is not feasible or beneficial to the patient with a severe life- or limb-threatening infections until the infection is controlled through surgical debridement. However, scope of vascular intervention should be explored early after the initial surgical debridement. For a patient with a severely infected dysvascular foot, it is preferable to perform revascularization within 1–2 days of the initial surgical debridement.



98    Contemporary Management of the Diabetic Foot Table 3  Suggested antibiotic regimens for moderate diabetic foot infections (DFIs)

MANAGEMENT Patients with mild foot infection can be mostly managed as outpatient. They can be treated with oral antibiotics (Table 2), surgical debridement, glycemic control, care of the wound with appropriate dressings and offloading. These patients should be followed regularly until complete healing occurs. The antibiotics should be given for 1–2 weeks. Patients with moderate and severe infections should preferably be admitted in the hospital and should undergo complete evaluation. Emphasis is placed on preexisting conditions such as renal insufficiency, coronary artery disease, peripheral vascular disease and congestive heart failure. The goal of medical management for the patient with DFI is to support the metabolic and hemodynamic state of the patient. In severe DFIs, considerable metabolic decom­ pensation may occur.

Ampicillin/sulbactam or

3 g IV

QID

Ceftriaxone +

1–2 g IV

OD

Clindamycin +

600–900 mg IV

TDS

Metronidazole or

500 mg IV

TDS

Levofloxacin +

500 mg IV

OD

Clindamycin or

600–900 mg IV

TDS

Moxifloxacin or

400 mg IV

OD

Ertapenem or

1 g IV

OD

Cefotaxime or

1 gm IV

BID

Imipenem-cilastatin

500 mg IV

TDS

Linezolid or

600 mg in 300 mL

BID

Daptomycin or

4 mg/kg IV

OD

Principles of Management

Cefazolin or

1–2 g IV

TDS

Vancomycin

30 mg/kg IV

BID

• • • • • • •

Supportive treatment Glycemic control Antibiotic therapy Surgical debridement Endovascular treatment Postoperative care of the wound Closure of the wound.

Methicillin-resistant S. aureus (MRSA)

Abbreviations: IV: Intravenous; QID: Four times a day; OD: Once daily; TDS: Thrice a day; BID: Twice a day

Supportive Treatment It includes correction of hydration, electrolyte imbalance, anemia (blood transfusion), hypoalbuminemia and ensur­ ing an adequate calorie intake (oral or parenteral) and stabilization of blood pressure.

Glycemic Control These patients have invariably a poor glycemic control as evident by a raised plasma glucose and HbA1c values, Table 2  Suggested antibiotic regimens for mild diabetic foot infections (DFIs) Cephalexin or

500 mg orally

QID

Amoxicillin/clavulanate or

875/125 mg orally

BID

Moxifloxacin or

400 mg orally

OD

Clindamycin or

300–450 mg orally

TDS

Levofloxacin

500 mg orally

OD

Doxycycline or

100 mg orally

BID

Trimethoprim/sulfamethoxazole

160/800 mg orally

BID

Methicillin-resistant S. aureus (MRSA)

Abbreviations: QID: Four times a day; BID: Twice a day; OD: Once daily; TDS: Thrice a day

ketonuria or even ketoacidosis. Such metabolically decom­ pen­sated patients should be treated with insulin infusion. The diabetic foot care team needs to appreciate the notion that easier metabolic control of the patient is apparent after surgical control of the infection, as infection is the cause of the metabolic disturbance. It is important to proceed with surgical debridement as soon as possible preferably in 48 hours.

Antibiotic Therapy A deep infection in diabetic foot is invariably polymicrobial. It is essential to obtain a fresh wound culture and another sample is obtained during surgery. It is always preferable to administer intravenous (IV) antibiotics. The choice of anti­ biotics depends on the individual experience, severity of infection, presence of crepitus, or gas in the soft tissue and evidence of systemic toxicity (Table 3). Empiric antibiotic regimen should almost always include an agent active against staphylococci, streptococci, and Gram-negative organisms pending culture results and antibiotic susceptibility. When culture and sensitivity reports are available, the antibiotic regimen can be revised, narro­ wed and tailored accordingly. However, if the patient is responding to empirical therapy, then the antibiotics need not be changed even if culture and sensitivity reports show sensitivity to other antibiotics.



Diabetic Foot Infections    99 Table 4  Suggested antibiotic regimens for severe diabetic foot infections (DFIs) Ciprofloxacin +

400 mg IV

BID

Clindamycin or

600–900 mg IV

TDS

Piperacillin/tazobactam or

4 g + 0.5 g IV

TDS

Imipenem/cilastatin or

500 mg IV

TDS

Tigecycline or

100 mg IV loading dose then 50 mg IV

BID

Vancomycin +

30 mg/kg IV

BID

Ciprofloxacin +

400 mg IV

BID

Metronidazole

500 mg IV

TDS

Figs 34A and B  (A) Sharp debridement; (B) Aggressive debridement

Linezolid or

600 mg IV

BID

Surgical Debridement

Daptomycin or

4 mg/kg IV

OD

Tigecycline

100 mg IV loading dose then 50 mg IV

BID

4 g + 0.5 g IV

TDS

Pinhole surgery and minimal invasive surgery are being increasingly practiced. However, DFI is the exception. It requires sharp, bold and aggressive debridement to salvage the limb (Figs 34A and B). “The goal of limb salvage is to provide the patient with a limb that is stable, mechanically sound and resistant to further skin breakdown while resuming an ambulatory status.” Possible surgical interventions include incision and drainage, wound debridement, bone resection, revascu­ larization and amputation. For more details, refer to chapters on principles of surgical debridement, vascular reconstruction and amputation. In hospitals where there is no separate operation theater (OT) for infected patients, OT should be disinfected and sterilized. Even in hospitals where there is a separate OT for infected patients, OT should be disinfected and sterilized after each surgery on DFI. Linen should be disposable and all biohazardous waste material should be properly sealed in a leak-proof bag and disposed according to prevailing local laws. Identifiable human body parts like amputated limb or part of limb should be properly labeled and sent to crematorium. After surgery on a severely infected foot, OT should be disinfected, sterilized and sealed for 12 hours before next surgery is performed.

A

B

Methicillin-resistant S. aureus (MRSA)

Pseudomonas aeruginosa Piperacillin-tazobactam

Abbreviations: IV: Intravenous; BID: Twice a day; TDS: Thrice a day; OD: Once daily

Methicillin-resistant S. aureus Prevalence of MRSA in DFIs ranges from 5% to 30%. Factors known to increase the risk for infection with MRSA, include prior long-term or inappropriate use of antibiotics, previous hospitalization, long duration of the foot wound, the presence of osteomyelitis and nasal carriage of MRSA. Perhaps, the most reliable predictor for MRSA as a cause of a DFI, is a previous history of MRSA infection. Infection with MRSA may also increase the time to wound healing, the duration of hospitalization, the need for surgical procedures (including amputations) and the likelihood of treatment failure. Patient presenting with a DFI be empirically treated with an antibiotic regimen that covers MRSA if above mentioned risk factors are present (Table 4). The duration of therapy depends upon the severity of infection, the presence or absence of bone infection and clinical response of the patient. In localized infections, intra­ venous antibiotics are given for 1 week followed by oral antibiotics for at least 2 weeks. In severe infections, intra­ venous antibiotics are often required for 2 weeks followed by oral antibiotics for another 2–4 weeks. In patients with osteomyelitis, the duration of antibiotic therapy may be prolonged. However, in most of the patients it is preferable to remove the infected bone during debridement, thereby facilitating a quicker healing of the wound and shorter period of antibiotic therapy.

Endovascular Treatment The dysvascular diabetic foot increases the severity of the infection. Endovascular intervention is not feasible or beneficial to the patient with a severe life- or limb-threatening infections until the infection is controlled through surgical debridement. Endovascular treatment is preferred for peripheral arterial disease in the presence of DFIs because of number of advantages, including the low morbidity and mortality of the procedure, the short preparation time and the limited hospital stay. The restenosis rate might be relatively



100    Contemporary Management of the Diabetic Foot

Fig. 35  Posterior cast

Fig. 36  Wound closure by secondary intention

high, especially in procedures below the knee in which restenosis over a 5-year period has been reported in 50% of cases. However, in patients with foot infections, the main aim is to achieve healing and to save the limb. The temporary improvement of skin perfusion can be sufficient to promote healing. Once the infection is controlled, lower perfusion pressures are necessary to maintain skin integrity.

Postoperative Care of the Wound After adequate surgical debridement, the wound is then irrigated with copious amounts of saline to reduce the number of bacteria present in the wound. The open wound is then packed with a moist dressing followed by a dry dressing. The goal is to maintain a moist wound healing environment. Strict offloading of the operated foot is extremely important. Patients who have undergone extensive debridement need to be given a posterior cast (Fig. 35). Ambulation with crutches or a walker should be encour­ aged depending on the condition of the patient. Dressings usually are changed daily, beginning 24–48 hours after the initial debridement. Repeat debridement should be performed as needed to control infection and removal of necro­tic tissue. The wound should be dressed with moist dressing. Topical antimicrobials are not recommended. The role of negative pressure wound therapy and hyperbaric oxygen therapy are discussed in Chapter on Advanced Wound Healing Products and Techniques.

Fig. 37  Wound closure by secondary suturing

Wound Closure In DFIs, after debridement surgery wounds are rarely closed by primary suturing. Usually the wounds are left open and allowed to heal by granulation and contraction and at a later date such wounds are closed by secondary suturing or allowed to heal by secondary intention (Figs 36 to 38).

A

B

Figs 38A and B  (A) Extensive debridement; (B) Closure by skin grafting



Diabetic Foot Infections    101 In higher level amputations like transtibial or transfemoral, stumps are closed by primary suturing with a drain inside. Such decisions of wound closure, either by suturing or secondary intention, depend on degree of drainage at the time of surgery, any residual infection and the available tissue for the closure of the wound. The most challenging aspect after radical surgical debride­ ment is to obtain long-lasting wound closure that is resistant to further breakdown and is durable and mechanically sound. In patients with larger defects where wound closure by suturing or secondary intention is not feasible, soft tissue reconstruction is carried out. These include split thickness skin grafting, local flaps, muscle flaps and pedicle flaps. Split thickness skin grafts after appropriate wound bed preparation are useful to obtain closure of large nonweight-bearing soft tissue defects. Local flaps are often used for wound coverage on the weight-bearing plantar aspect of the foot.

CONCLUSION In India, 75% of lower limb amputations are carried out in DFI with neuropathy, majority of them are potentially preventable. Early detection of DFI, aggressive treatment by antibiotics and debridement and education of patients are possible strategies to prevent limb amputation in diabetics. A multidisciplinary diabetic foot care team is needed to adequately manage

the severe DFI. The management principles are supportive treatment, glycemic control, care of comorbidities, antibiotics, vascular reconstruction if indicated and adequate surgical debridement. The aim of the foot care team is to save the limb and not amputate it. However, in some cases, amputation is needed to save the rest of a patient’s limb or even his life. The goal of limb salvage is to provide the patient with a limb that is stable, mechanically sound and resistant to further skin breakdown while resuming an ambulatory status. Finally, the patient has to be better educated to prevent recurrence of diabetic foot problem.

SUGGESTED READING 1. Bader MS. Diabetic foot infection. Am Fam Physician. 2008;78(1):71-9. 2. Frykberg RG. Diabetic foot ulcers: pathogenesis and management. Am Fam Physician. 2002;66(9):1655-62. 3. Lipsky BA, Berendt AR, Cornia PB, et al. Infectious Diseases Society of America Clinical Practice Guideline for the diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2012;54(12):e132-73. 4. Sharad Pendsey (Ed). Diabetic Foot: A Clinical Atlas. New Delhi, India: Jaypee Brothers Medical Publishers (P) Ltd; 2003. 5. Zgonis T, Stapleton JJ, Roukis TS. A stepwise approach to the surgical management of severe diabetic foot infections. Foot Ankle Spec. 2008;1(1):46-53.

CHAPTER

Principles of Debridement in the Infected Foot

12

Jennifer Pappalardo, David G Armstrong

INTRODUCTION Each year more than one million people undergo a lower extremity amputation as a consequence of diabetes. Of these amputations roughly 85% are preceded by lower extremity ulceration. Diabetic foot ulcers (DFUs) present with various levels of severity as discussed previously in “Classification and Staging of Diabetic Foot.” Diabetic foot ulcers are categorized roughly as either neuropathic, ischemic or a combination of the two (neuro­ ischemic). In the developed (and increasingly so in the developing) world neuroischemic DFU is the most prevalent type (Fig. 1). In the ischemic limb both macrovascular and microvascular disease complicates healing rates. The presence of

Fig. 1  Typical example of the ischemic hallux

ischemic disease deleteriously impacts the outcome of treat­ ment in the diabetic foot infection (DFI). Healing times are increased, probability for healing decreases, ulcer recurrence increases, as does the risk for major amputation. Additionally, studies have also shown a mortality rate of exceeding 50% in people undergoing a diabetes-related amputation. The neuroischemic foot, because of the higher burden of disease, carries with it higher morbidity and mortality rates than many types of cancer including breast cancer, colon cancer and Hodgkin’s disease. Many specialized facilities combine a team approach in caring for these high-risk patients. The “toe and flow” model consisting of podiatric and vascular surgery surrounded by has gained a great deal of therapeutic success with the concept of keeping these DFUs in remission as a more realistic view rather than complete prevention. This is done through aggressively proactive interdisciplinary medical and surgical care. Debridement of the infected foot should involve an integrated surgical approach taking into consideration three essential factors: time, urgent surgical debridement, and revascularization, as needed. Clinicians should evaluate the overall status of the condition: the patient as a whole, the entire affected limb, and the wound itself. The initial step in evaluating an infected diabetic foot should be to identify infection from colonization of bacteria and/or other microbes. True skin and soft tissue infections reflect inflammatory microbial invasion of the epidermis, dermis and subcutaneous tissue. Classic signs of infection include the cardinal signs of inflammation (redness, heat, swelling, pain, and loss of function). However, these typical signs of inflammation may be attenuated to various degrees in the neuropathic patient or in cases of vascular disease. The Infectious Diseases Society of America has developed an algorithm for classifying severity of DFIs (Table 1).



103    Contemporary Management of the Diabetic Foot Table 1  Infectious Diseases Society of America and International Working Group on the diabetic foot classifications of diabetic foot infections Clinical manifestation of infection

PEDIS grade

Severity

No clinical sign of infection

1

Uninfected

2

Mild

3

Moderate

4

Severe



Infection present as defined by the presense of atleast 2 of the following: –

Local swelling or induration



Erythema



Local tenderness or pain



Local warmth



Purulent discharge (thick opaque to white or sanguineous secretion

Local infection involving only skin and subcutaneous tissue •

Without involvement of deeper tissues



Without systemic signs as described below



If erythema, must be >0.5 cm 2 cm •

Involving deeper than skin and subcutaneous tissues and no systemic inflammatory response signs as described below –

Abscess



Osteomyelitis



Septic arthritis



Fasciitis

Local infection as described above with signs of SIRS •

Greater than 2 of the following must be met –

Temperature >38°C or < 36°C



Heart rate > 90 bbm



Respiratory rate > 20 bbm or PaCO2 < 32 mm Hg



White blood cell count > 12,000 or < 4,000 cells/ul or > 10 immature bands

Grade 1: No symptoms or signs of infection. Grade 2: Lesions involving the skin without involvement of the subcutaneous tissue with at least two of the following signs; local warmth, erythema is greater than 0.5 cm–2 cm surrounding the wound, local pain or tenderness, local swelling or induration, purulent discharge. Grade 3: Erythema is greater than 2 cm and one finding as described above or infection involving the deeper structures of the foot such as deep abscess, lymphangitis, osteomyelitis, septic arthritis or fasciitis. There is no systemic inflammatory response. Grade 4: Regardless of local infection the presence of systemic signs corresponding to the following criteria: Temperature is greater than 39°C or less than 36°C, pulse is greater than 90 bpm, respiratory rate is greater than 20/min, PaCO2 is less than 32 mm Hg, leukocytes is greater than 12000 or less than 4000/mm3, or 10% immature leukocytes. Abbreviations: PaCO2: Partial pressure of arterial carbon dioxide; PEDIS: Perfusion, extent/size, depth/tissue loss, infection and sensation; SIRS: Systemic inflammatory response syndrome



104    Contemporary Management of the Diabetic Foot Systemic signs of infection should also be evaluated. These include: fever, chills, diaphoresis, anorexia, tachycardia, hypotension, delirium, metabolic abnormalities such as acidosis, and electrolyte imbalances. Prior to administration of any antibiotics laboratory testing for systemic infection should be evaluated including leukocytosis with or without a left shifted differential, and elevated inflammatory markers such as C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) and blood cultures. Recent studies have suggested benefit from evaluation of procalcitonin levels in the process of diagnosing infected versus non-infected ulcers. These inflammatory markers are also helpful in evaluating the resolution or progression of infection. Bacterial cultures are another area of importance when considering the DFI. It is not recommended to obtain cultures on non-clinically infected wounds. Rather, cultures, as they presently stand, are most useful to assist in directing or redirecting antibiotic course following initial empiric therapy. Once DFI is confirmed via criteria described above, appropriate cultures may be taken. Prior to culturing a

wound the area must be debrided mechanically with sharp debridement in a sterile fashion and cleansed with sterile saline. Samples should be taken from the wound base. Cultures should include, if possible, deep tissue specimens rather than swabs if there is question of bony involvement, bone biopsy should be obtained via an area of healthy skin when possible and sent for not only microbiologic, but also histologic assessment, if feasible. Once specimens are appropriately obtained and in the laboratory bacterial identification and resistance may be assessed. New therapies have emerged using DNA microarray and multiplex realtime PCR, which can analyze virulence and antimicrobial resistance of microorganisms (Fig. 2). This method of microbial identification is a much more accurate but presently more costly to the institution and often not utilized widely (yet) in today’s microbiological laboratory. Antibiotic treatment remains another highly debated area amongst practitioners. Antibiotic resistance has an increasing prevalence in DFIs. Initial treatment is typically empirical and chosen after microbiological cultures have been obtained.

Fig. 2  Example of polymerase chain reaction results on standard patient culture



105    Contemporary Management of the Diabetic Foot Treatment typically includes antimicrobials against Grampositive cocci-frequently Staphylococcus aureus. Once culture and sensitivity results are finalized narrow spectrum treat­ ment should be continued. Optimal duration of treatment depends on severity of infection and response to treatment. The Infectious Disease Society of America has recom­ mended an antibiotic regimen based on the severity of infections. In case of mild to moderate infections target is only aerobic Gram-positive cocci. For severe infections, broadspectrum empiric therapy should be started emphasizing pending results and antibiotic susceptibility data will likely change the ultimate treatment protocol. Empiric treatment is not necessary for Pseudomonas aeruginosa with the excep­ tion of patients with true risk factors for this organism. Lastly, if a patient has a prior history of Methicillin-resistant Staphylococcus aureus (MRSA), local surveillance for MRSA has been noted high, or clinically the patient has a severe infection. In addition to these risk factors, at least 2 classic symptoms of inflammatory response should be present or the presence of purulent drainage. Vascular status for arterial ischemia and venous insufficiency biomechanical problems and presence or absence of protective sensation should also be evaluated on the initial assessment. Prior to debridement all new DFIs should be evaluated with basic imaging. Deformity, bony destruction, soft tissue emphysema, and foreign bodies must be evaluated (Fig. 3). Magnetic resonance imaging should be employed when greater question for abscess collection, osteomyelitis or Charcot neuroarthropathy remains. Radionuclide bone scans or white blood cell scans should be reserved for cases where MRI is unavailable or contraindicated due to medical comor­ bidities. Specifically with osteomyelitis a leukocyte or anti-granulocyte scan may be indicated. Bone biopsy

Table 2  Interpretation of the ankle-brachial index ABI

Interpretation



>1.30

Poorly compressible vessels, arterial calcification



0.90–1.30

Normal



0.60–0.89

Mild arterial obstruction



0.40–0.59

Moderate obstruction



< 0.40

Severe obstruction

in combination with bone culture being a more definitive diagnosis. In addition to radiological examinations, noninvasive vascular studies, the ankle brachial index, should be evaluated (Table 2). An ABI is greater than 1.30 indicates poorly compressible vessels and arterial calcification, from 0.90–1.30 indicates normal vascular status, 0.60–0.89 indicates mild arterial obstruction, 0.4–0.59 indicates moderate obstruction and less than 0.40 indicates severe obstruction. Choosing between medical and surgical intervention in cases of osteomyelitis has long been debated. Antibiotic therapy alone has been advocated in recent literature. The Institute for Defence Studies and Analyses (IDSA) has outlined four separate cases when medically treating osteomyelitis may be indicated: if surgical intervention would cause an unacceptable loss of function, if limb ischemia caused by non-revascularizable disease and the patient wishes to avoid amputation, infection remains in the forefoot and there is minimal soft tissue damage, and the patient and the clinician agree surgical management carries excessive risk. It is often helpful when evaluating the DFI to divide the foot into 5 regions (Table 3). Noting extension of inflammatory signs from region to region may be helpful in planning surgical intervention. Surgical management varies from minor incision and drainages to post debridement reconstruction of soft tissue defects and revascularization procedures. Again, clinical signs of infection should be evaluated if considering surgical intervention. Severe infections are most often plantar wounds, which may show dorsal fluctuance and erythema (Fig. 4). Table 3  Anatomic divisions of the foot for surgical planning in diabetic foot infections

Fig. 3  Example of osteomyelitis of the hallux on radiographic exami­ nation

Region

Anatomic location

1

Dorsal soft tissue of the foot and anterior ankle

2

Forefoot

3

Midfoot—with or without underlying Charcot deformity

4

Septic joints of the rearfoot and ankle—with and without underlying Charcot deformity

5

Heel



106    Contemporary Management of the Diabetic Foot

Fig. 4  Severe hallux infection with dorsal expansion of plantar abscess

Fig. 6  Example of hydrotherapy for debridement

Fig. 5  Surgical debridement of hallux infection

Fig. 7  Example of gas gangrene needing emergent major amputation

A wound plantarly with dorsal extension obviously illustrated passage of infection through fascial planes. Abscess formation especially in the disvascular foot may lead to irreversible damage. The goal of surgical debridements should consist of removal of all necrotic nonviable tissue until presence of healthy bleeding wound base has been achieved (Fig. 5). Typical management consists of sharp cutting devices such as scalpels, scissors, curettes or tissue nippers. Newer techniques have become more popular using ultrasonic debriders, as well as hydrodebridement, which employ the “venturi” effect by utilizing a jet of saline. At such high speeds removal of necrotic nonviable tissue is obtained (Fig. 6). Urgent intervention is needed in any case of soft tissue emphysema in the deep tissues, known abscess or necrotizing fasciitis (Fig. 7).

Surgery becomes less urgent, yet still necessary, in cases of nonviable necrotic tissue with or without bone or joint involvement. The following chapters will discuss the importance of involving vascular surgery on any infected critically ischemic limb and limited discussion will continue in this chapter. The key to surgical intervention is to obtain debridement of appropriate compartments involved in the DFI. The compartments in the foot are alone an area of debate as the anatomy has been published between 4 and 9 compartments. Skin incision placement also becomes paramount to appropriate surgical debridement. When possible, incisions should be made longitudinal to the relaxed skin tension lines as they may be difficult to decipher with the acutely infected diabetic foot. Evaluate for the 5 regions of the foot as outlined previously and know the underlying anatomical structures.



107    Contemporary Management of the Diabetic Foot

Fig. 8  Radical debridement for worsening infection

Fig. 10  Preparation of daptomycin antibiotic polymethylmethacrylate beads

Fig. 9  Appropriate debridement level for preserving the best weightbearing option for the patient

Fig. 11  Application and placement of antibiotic polymethyl­methacry­ late beads

Often times in the early surfacing infection delay in surgical debridement and medical management may be employed until an area of demarcation between viable versus nonviable tissue has been obtained. Clinical evaluation of worsening infection indicates need for surgical intervention prior to the completion of the demarcation process (Fig. 8). Prior to surgical intervention the surgical approach should evaluate for imminent soft tissue coverage and attempt to preserve the most functional outcome for the weight-bearing surface of the extremity (Fig. 9). Placement of intraoperative antibiotic beads, both absorbable and non-absorbable, is often elected for postdebridement management (Figs 10 and 11).

Procedures often should be staged, as closure is fre­ quently not initially indicated or practical. Closure by secon­ dary intention as well as tissue transfer or grafting must be considered in these cases (Figs 12 and 13). Split thickness skin grafting has long shown great promise in aiding wound closure on those wounds, which cannot be primarily or secondarily closed (Fig. 14). In addition to surgical intervention diabetic wounds should receive the following post-surgical treatment as often as possible. Debridement of all debris, eschar, and surrounding callus by various methods is a necessity. Current options range from sharp debridement; mechanical, autolytic or even larval debridement techniques may be acceptable on



108    Contemporary Management of the Diabetic Foot

Fig. 14  Split thickness skin graft post-debridement with secondary closure not indicated Fig. 12  Flap configuration for difficult transmetatarsal amputation wound closure

Fig. 13  Final outcome from transmetatarsal amputation flap closure

the right patients. As discussed in “Management of Plantar Ulcers and Offloading the Diabetic Foot” re-appropriation of pressure to the entire weight bearing surface of the foot but various methods must be employed. In addition to serial debridements, off-loading is of utmost importance. The gold standard treatment is the total contact cast, which cannot be removed by the patient and redistributes pressure across

the entire plantar surface of the foot. However, any type of the readily available off-loading products will suffice. Care must be taken to educate the patient on the importance of compliance even in their households. Topical antimicrobials are not generally clinically indi­ cated for uninfected wounds however topical antimicro­bials are controversial in clinically infected. Topical antiseptics have become particularly commonplace in mitigating wound bacterial load. Similarly, silver-based dressings and cadexomer-iodine preparations can be useful as well. It should be noted that all of these have, at best, a low-level of evidence to support their clinical utility. Post-debridement wound dressings have the primary function of creating and optimal wound environment. Every wound has different needs and there is no standard wound dressing protocol. Appropriate dressings maintaining a moist environment but allowing for appropriate exudate should be applied. The overall goal is to create a wound base promoting granulation tissue and autolytic processes as well as angiogenesis with rapid epidermal cell migration. One typical protocol for wound types is as follows. Dry and necrotic wounds need saline or dilute hypochlorite-soaked gauze changed frequently or hydrogels, which facilitate autolysis. Dry wounds needing moistening may require occlusive or semi-occlusive dressing. To modulate moisture in an excessively exudative wound, various dressings such as foams can be employed. There is currently no substantial clinical evidence to recommend one product over the next. Hyperbaric oxygen therapy continues to be a postdebride­­­ment proposed treatment. Transcutaneous oxygen therapy is also an option for wounds of mild exudate. Neither treatment option has proven to resolve the DFI however has proven effective with wound healing in some patients.



109    Contemporary Management of the Diabetic Foot Some researchers advocate systemic supplementation of granulocyte colony stimulating factor (G-CSF) to patients. Available studies have concluded success with reducing need for further surgical intervention and duration of hospital stays, but have not reduced the need to systemic antimicrobials nor the length of treatment. Bioengineered skin equivalents may be utilized at the discretion of the clinician but sufficient data on usage is not currently available. Their efficacy has not been established on complex wounds with exposed bone or tendon or in patients with multiple comorbidities. Bioengineered human skin equivalents are generally indicated only for wounds without tendon, muscle, joint capsule or gone exposure. These grafts are similar to a skin graft; living equivalents are to be placed on tissue with a strong viable vascular base (Fig. 15). Negative pressure wound therapy (NPWT) continues to be a commonly-employed technique that has enjoyed success in the clinic and in the literature. NPWT employs the application of sub-atmospheric pressure to the wound environment, which is then sealed and a vacuum pump applied (Fig. 16). A modification of the negative pressure wound therapy involving simultaneous irrigation throughout the application period. Once the acute infection has been resolved if the wound continues to remain senescent the clinical should evaluate for chronic infections or biofilms. Chronic wounds stall in the inflammatory stage of wound healing due to this persistent colonization by bacteria. Chronic infections or biofilms have four basic components. They must be able to adhere to a surface. They must be able to secrete protective

Fig. 15 Bioengineered tissue alternative with closure assistance device applied

Fig. 16  Wound VAC® placement on a difficult wound for secondary closure

substances usually polysaccharides or glycocalyx, host DNA from neutrophils, bacterial DNA, bacterial proteins, and host proteins such as fibrin or albumin. This secretion can be altered by the biofilm to combat different treatments and threats to the biofilm. The biofilm must be capable of quorum sensing. Quorum sensing directs gene expression of the biofilm. Lastly, the biofilm must be able to reconstitute after catastrophic events to its composition. This is the time of vulnerability by the host immunity or therapeutic modalities. Chronic wounds have significant biofilm on their surfaces versus acute wounds, which have minimal biofilm formation. Host cells are often senescent in the chronic inflammatory wound state. Chronic wounds must be debrided much like the acute infection. Debridement may be employed by many methods such as sharp, ultrasonic, biological, anti-biofilm applications, such as lactoferrin or xylitol. Quorum sensing must be disrupted with inhibitors such as hamamelitannin or cidal agents, such as antimicrobials. Anti-biofilm gels can be applied to suppress wound biofilm functions such as silver, cadexomer iodine and other topical biocides. Other studied modalities are the application of lactoferrin, an innate immune molecule, which targets the biofilm production. The sugar alcohol xylitol has been shown to potentially work synergistically with lactoferrin in inhibiting growth and establishment of biofilms. Silver has been known to inhibit bacterial growth for centuries but only recently have studies shown silver to be efficacious against biofilm production alone. Studies remain inconclusive but silver impregnated dressings have become popular. Silver resistance is already a documented problem with such organisms as MRSA and thus further studies to produce novel antimicrobials with clinical therapeutic value. Management of host impairments, such as reduced blood



110    Contemporary Management of the Diabetic Foot flow, high-pressure areas or overall nutritional status of the patient, during this process is paramount. Having a stepwise approach to the evaluation and treat­ment of DFIs is of the utmost importance. On initial examination of ulceration decisions must be made as to acute infection versus chronic colonization. Using the IDSA guidelines for diagnosis should be utilized to assist in directing diagnosis and therapy. If a diagnosis of infection is made the severity extent of infection should be identified. Appropriate antimicrobial agents should be started following appropriate culture specimen. Medical imaging evaluation should also be initiated both radiographically and advanced imaging when warranted. Noninvasive vascular exams should always be performed prior to surgical intervention and the vascular surgeon when possible should decide upon treatment with endovascular procedures versus revascularization. Postsurgi­­cal debridements to maintain an appropriate granular

wound bed are paramount. The wound should be dressed with appro­priate dressings optimally on a daily interval. Dressing which allow for daily examination of the wound is the most desir­able. Wound off-loading and redistribution of pressure areas to the plantar ulceration is of utmost importance as well as encouraging compliance with non-ambulatory status with the appropriate off-loading device. When ulcerations are not progressing especially around the 20-week period re­evalu­ ation of the patients overall nutritional status, vascular status, wound margins and radiographical findings is indica­ ted. Further surgical intervention may be warranted at that time. Foot infections are a common and serious problem in people with diabetes. As with many complex conditions, when broken down into constituent parts, management may be more predictable and outcomes potentially better. When properly managed most infections and ulcerations may be healed without amputation.

CHAPTER

Evaluation of Neuroischemic Foot

13 Sharad Pendsey

INTRODUCTION There are several invasive and noninvasive methods to evaluate the neuroischemic foot. The critical assessment areas are; prediction of wound healing, decide on the need for revascularization and/or to judge the correct level for amputation.

Ankle/Brachial Pressure Index A hand-held Doppler can be used to confirm the presence of pulses and to quantify the vascular supply. When used together with sphygmomanometer, the ankle and brachial systolic pressures are measured and their ratio calculated (Fig. 1). In normal subjects, the ankle systolic pressure is higher than the brachial systolic pressure. Normal ankle/brachial pressure index (ABI) is greater than 1, in the presence of ischemia it is less than 0.9. Absent or feeble pulses with ABI less than 0.9 confirm ischemia. Conversely, the presence of pulses and ABI greater than 1 rules out significant ischemia. An ABI of less than 0.8 is associated with claudication, and greater than 0.4 is commonly associated with ischemic rest pain and tissue necrosis. ABI measurements may be misleading in diabetes because of the presence of medial calcinosis (Monckeberg’s Sclerosis) which renders the arteries incompressible and results in falsely elevated ABI greater than 1.3.

Segmental Limb Pressures and Pulse-Volume Recordings (Plethysmography) More specific information can be obtained in the vascular laboratory. In the laboratory, segmental limb pressure

Fig. 1  Measuring ankle systolic pressure with hand-held Doppler

measure­ment can aid in localizing stenoses or occlusions. Limb pressure cuffs are placed on the thigh, calf, ankle, trans­ metatarsal region of the foot and digit. The ABI is calculated and then the pressure is inflated sequentially in each cuff to almost 20 to 30 mm Hg above systolic pressure. With a continuous-wave Doppler probe placed at a pedal vessel, the pressure in the cuff is released gradually, and the pressure at each segment is measured. A decrease in pressure between 2 consecutive levels of greater than 30 mm Hg suggests arterial occlusive disease of the artery proximal to the cuff. Pulse-volume recordings (PVRs) are plethysmographic tracings that detect changes in the volume of blood flowing through a limb. Using equipment similar to the segmental limb pressure technique, pressure cuffs are inflated to 65 mm Hg, and a plethysmographic tracing is recorded at various levels. A normal PVR is similar to a normal arterial pulse



112    Contemporary Management of the Diabetic Foot wave tracing and consists of a rapid systolic upstroke and a rapid down stroke with a prominent dicrotic notch. With increasing severity of peripheral arterial disease (PAD), the waveforms become more attenuated with a wide down slope and, ultimately, virtually absent waveforms.

Table 1  Probability of foot ulcer healing

1.

Test

Absolute pressure (mm Hg)

Foot ulcer healing (%)

P ankle

< 55

Unlikely

55–90

45

> 90

85

< 30

45

30–50

75

> 55

95

< 20

Unlikely

> 40

Likely

Graded-Exercise Treadmill Test Segmental limb pressure measurement and PVRs are often combined with a graded exercise treadmill test. Once the resting pressures and PVRs are obtained, the patient is asked to walk on a treadmill at a constant speed, either at a constant grade (2 mph, 12% incline) or with a variable incline (0% at start, increased by 3.5% every 2–3 minutes). The former method exercises patients to a maximum of 5 minutes, whereas the latter continues for a maximum of an 18% incline. The treadmill test: • Confirms the diagnosis of intermittent claudication and PAD • Demonstrates objective functional limitation of PAD • Documents the effect of therapy on initial and absolute claudicating distances.

Toe Systolic Pressure Toe systolic pressure (TSP) can be measured using special pressure cuffs and have been found useful in predicting the clinical course of rest pain or skin ulcerations. TSP of less than 30 mm Hg signifies significant ischemia.

Transcutaneous Pressure of Oxygen Tension Transcutaneous Pressure of Oxygen Tension (TcPO2) is a noninvasive method for monitoring arterial oxygen tension and reflects local arterial perfusion pressure. A heated oxygen sensitive probe is placed on the dorsum of the foot and a reference probe below the clavicle. After an equilibrium period of 15 minutes, the skin oxygen tension (mm Hg) is determined, which reflects local blood flow. Normal values are usually > 60 mm Hg, a level below 30 mm Hg, indicates severe ischemia but levels can be falsely lowered by edema or cellulitis. Ankle systolic pressure (P ankle), TSP, and TcPO2 help predict the probability of the wound healing (Table 1).

2.

3.

P toe

TcPO2

Abbreviations: P ankle, ankle pressure; P toe, toe pressure; TcPO2, transcutaneous pressure of oxygen. Adapted from International Consensus on the Diabetic Foot by the International Working Group on the Diabetic Foot 1999.

with symmetrical neuropathy and renal insufficiency and is a surrogate marker of endothelial dysfunctions and cardio vascular diseases. Calcification of the vessels does not signify occlusive vascular disease although, both can be associated. The atherosclerotic lesions are found in the intimal layer of the arterial wall while medial calcification occurs near the internal elastic membrane with little or no effect on the lumen of the vessel. Clinical suspicion of medial calcification of vessels is made when ABI is found to be above 1.3. The diagnosis can be confirmed on plain radiography of the anteroposterior view of the foot and lateral view of the ankle. Radiographically intimal calcifications are distributed in a patchy, interrupted fashion along the vessel wall (tram lines). It can be seen in abdominal aorta, femoral, tibial and foot vessels on plain radiography (Fig. 2). Interpretation of MR Angiography becomes difficult in presence of calcification. Stenting of highly calcified lesions

Detection of Medial Arterial Calcification Monckeberg’s sclerosis or medial arterial calcification is degenerative arteriosclerosis of the peripheral arteries characterized by fibrotic and calcific changes involving intimal plaque and media. Intermediate sized muscular arteries are commonly involved. The vessels are incompressible (lead pipe) and thus elevate ankle systolic pressure. The ankle/ brachial systolic pressure index is falsely elevated above 1.3. Medial calcification is seen in about 20–25% of patients with longstanding type 2 diabetes. It is commonly associated

Fig. 2  Calcification in the tibial artery



Evaluation of Neuroischemic Foot    113

Fig. 3  Normal triphasic form

Fig. 5  Monophasic wave form with dampened

is also difficult because of lack of full stent expansion and difficulties in delivery to the target site. Vascular surgeons find it difficult to anastomose such calcified vessels during distal bypass surgery.

the presence of significant stenosis, there is a high peak systolic velocity (PSV) proximal to and a dampened PSV distal to the stenosis. Good collaterals development results in resumption of the diastolic flow distal to the stenosis, while acute thromboembolism shows absence of flow. Calcification in the vessel wall is seen in the form of flow turbulence and high reflectivity index. Duplex Doppler can detect hemodynamically significant stenosis and extent of the atherosclerotic vascular disease in the major lower limb vessels up to the beginning of the plantar arch. In lower extremity arteries undergoing duplex ultrasonography, PSV ratios generally predict degrees of stenosis (Table 2). An increase in PSV occurs as a result of increased pressure gradient across an arterial stenosis. Duplex Doppler is useful whenever bypass graft surgery is contemplated. Prior to surgery, it is useful to identify a suit­ able vein, its size, patency and evidence of varicosities. The course of the vein (great saphenous) can be mapped on the skin. Duplex Doppler is also useful to identify run off arteries suitable for use in vascular reconstruction. Duplex Doppler is recommended for routine surveillance after femoralpopliteal or femoral-tibial-pedal bypass with a venous con­ duit. Minimum surveillance intervals are approxi­mately 3, 6, and 12 months, and then yearly after graft placement. After surgery it helps to identify stenosis, thrombosis, mismatches in lumen size and abnormal flow patterns in the bypass graft.

Duplex Color Doppler It is an invaluable tool in the diagnostic evaluation of the peripheral vascular tree. Normal lower limb arteries on Doppler show a triphasic wave pattern. This consists of a strong peak systolic notch, followed by a slight reversal of flow during early diastole and return to forward flow of low amplitude or diastolic run off (Fig. 3). In atherosclerotic occlusive disease, this normal triphasic pattern is altered. There is an increased peak systolic velocity, and absent early diastolic reversal producing a biphasic wave form (Fig. 4). Increasing stenosis causes disappearance of the dias­ tolic run-off, giving monophasic wave form (Fig. 5). In

Table 2  Interpretation of arterial duplex ultrasonography Peak systolic velocity

Stenosis severity

Triphasic 30% increase in PSV

20–49%

Doubling of PSV (greater than 100% relative to 50–99% the adjacent proximal segment and reduced systolic velocity distal to the stenosis) Fig. 4  Biphasic wave form flow

No Doppler flow in artery

Occluded



114    Contemporary Management of the Diabetic Foot Regular monitoring permits early intervention to prolong graft life and to enhance limb salvage rate. It is a useful tool only for venous but not for prosthetic grafts. The advantages of duplex Doppler are it is noninvasive, less expensive and can be repeated several times. Despite all the advantages, it is certainly not a substitute for angiography. The limitations of duplex Doppler are in assessing aorto­ iliac arterial segments in some individuals (e.g. due to obesity or the presence of bowel gas). Dense arterial calcification can limit diagnostic accuracy. Sensitivity is diminished for detecting stenoses downstream from a proximal stenosis. Evaluation of collateral circulation is not optimum. Its use is not well established to assess long-term patency of percutaneous transluminal angioplasty.  Duplex ultrasonography remains an effective and con­ venient approach for imaging peripheral arterial segments or for the follow-up of a bypass graft. Owing to the sizeable time commitment required to evaluate both lower extremities and the inherent operator dependence of the technique, this modality is less suitable for overall screening.

Fig. 6  Block in the iliac artery

Advantages • Noninvasive, less expensive and can be repeated several times • Can detect hemodynamically significant stenosis and extent of atherosclerotic vascular disease in lower limb major vessels • Useful whenever bypass graft surgery is contemplated and for surveillance after surgery.

Disadvantages • Requires sizeable time for evaluation • Has difficulty in assessing aortoiliac arterial segments • Dense arterial calcification can limit diagnostic accuracy.

Intravascular Ultrasound The attachment of ultrasound transducers to catheters has created a completely new modality, intravascular ultrasound (IVUS), which can evaluate vessels “from inside out”. IVUS determines percentage of stenosis, confirms dissection and evaluates vessel walls and plaques. It has a potential to play an adjunctive role in complex endovascular interventions involving angioplasty and stents. But, high cost is a limiting factor.

Computerized Tomography Angiography Multi-detector computed tomography (MDCT) has rapidly replaced conventional CT imaging particularly in vascular imaging. One advantage, besides the speed of scanning, is

Fig. 7  Block in the left superficial femoral

its ability to generate three-dimensional (3-D) images. CT angiography (CTA) (Figs 6 and 7) is an important application of the 3-D capabilities of spiral CT. CTA is more useful in large arteries such as thoracic or abdominal aorta but its dis­advantages are need of intravascular administration of contrast and the inability to accurately assess smaller vessels. In persons with diabetes, commonly involved vessels are infrapopliteal, which are not properly assessed by CTA, thus limiting its immediate application. However, with the advent of 64/128 slice CT scan, evaluation of peripheral vessels up to dorsalis pedis and plantar arch is possible with excellent spatial and temporal resolution. New softwares help in substracting bones to give superior vascular tree images. Bones can be overlapped later over vessels for identifying bony landmarks. Patients



Evaluation of Neuroischemic Foot    115 with contraindications to magnetic resonance angiography (MRA), e.g. pacemakers, defibrillators, metal clips, stents, and metallic prostheses may be safely imaged as they do not cause significant CTA artifacts. Scan times are significantly faster than for MRA.

Advantages • Useful to diagnose significant stenosis • Useful to select candidates for endovascular or surgical revascularization • Useful where MRA is contraindicated, e.g. with metallic prostheses • Scan time is faster than MRA.

Disadvantages • Requires intravascular contrast • Infrapopliteal vessels are not properly assessed.

Magnetic Resonance Angiography Magnetic resonance angiography (MRA) is arguably the most dwarfing imaging development in the recent past and not just in the evaluation of extra and intracranial carotid circulation. It has emerged as a safe and noninvasive alternative to conventional angiography in the diagnosis of lower-extremity vascular disease. Contrast-enhanced 3-D MRA has become the method of choice. The technique relies on the detection of contrast enhancement in the vascular lumen to produce findings that are comparable to those of conventional catheter angiography. The current technique uses the bolus-chasing method in which vessels are imaged sequentially as contrast flows distally. Multiple overlapping fields of view are used, and images are obtained in the coronal or sagittal planes. Images demonstrate the contrast-enhanced anatomy of the arterial lumen. Stenosis is depicted as areas of narrowing, and occlusion is depicted as areas of absent signal intensity. Ulceration and aneurysm can also be defined.

resonance technique (e.g. pacemakers, defibrillators, intra­ cranial metallic stents, clips, coils, and other devices). Other limitations are its cost, its availability and the possible overestimation of the degree of stenosis.

Advantages • Safe and noninvasive; and there is no radiation hazard • Has potential to accurately assess peripheral vessels for endovascular revascularization or surgical bypass.

Disadvantages • Needs special coils for peripheral vessels evaluation • Cannot be used in patients with contraindications to the magnetic resonance technique, e.g. metallic prostheses.

Angiography Transfemoral angiography is the gold standard for evaluation of peripheral vessels, not just in persons with diabetes (Fig. 8). Due to increased risk of nephrotoxicity, particularly in the diabetic population, minimal radiographic contrast administration combined with adequate hydration prior to and after the procedure is mandatory. It is also advisable to avoid metformin (oral hypoglycemic agent) 48 hours prior to and subsequent to the use of parenteral contrast agents, to avoid the risk of lactic acidosis and nephrotoxicity. Another strategy to reduce contrast load is to perform isolated angiography of the symptomatic limb if the unaffected limb has been found to be normal on physical examination and with non invasive tests. Conventional angiography is rapidly getting replaced by digital subtraction angiography.

Advantages of MRA: The procedure is simple, non­invasive and there is no ionizing radiation, and the contrast agent used is relatively less nephrotoxic. It has a potential to accu­­ rately assess peripheral vessels and distal pedal arteries for endovascular revascularization or surgical by­pass in persons with diabetes. MRA of the extremities may be considered for postrevascularization surveillance (endo­ vascular and surgical bypass). Limitations of MRA: It needs special coils for peripheral vessels evaluation and MR compatible pressure injector. MRI contrast can lead to nephrogenic systemic fibrosis. It may be inaccurate in arteries treated with metal stents. It cannot be used in patients with contraindications to the magnetic

Fig. 8  Conventional angiogram showing diffuse narrowing in super­ ficial femoral artery left



116    Contemporary Management of the Diabetic Foot

Fig. 9 Digital subtraction angiography showing narrowing in left superficial femoral, note DSA picture is after subtraction of soft tissue and bones

Fig. 10 Digital subtraction angiography showing pseudoaneurysm near right femoral artery, a postangiography complication

Digital Subtraction Angiography

A history of contrast reaction should be documented before the performance of contrast angiography and appropriate pretreatment administered before contrast is given. Treat­ ment with  n-acetylcysteine in advance of contrast angio­ graphy is suggested for patients with baseline renal insuffi­ ciency (creatinine greater than 2.0 mg per dL).  Follow-up clinical evaluation, including a physical examination and measurement of renal function, is recommended within 2 weeks after contrast angiography to detect the presence of delayed adverse effects such as atheroembolism, deterioration in renal function, or access site injury (e.g. pseudoaneurysm or arteriovenous fistula). 

Digital subtraction angiography (DSA) is now the state of art and has largely replaced conventional angiography. It is able to produce excellent angiograms even in the distal pedal circulation with a minimal amount of contrast (Fig. 9). It is helpful in calculating the diameter of the inflow vessel and degree as well as length of stenosis. Contrast angio­graphy provides detailed information about arterial anatomy and is recommended for evaluation of patients with lower extremity PAD when revascularization is contem­plated. Selective or super selective catheter placement during lower extremity angiography is indicated because this can enhance imaging, reduce contrast dose, and improve sensitivity and specificity of the procedure. 

Advantages of DSA • Less contrast is required with superior contrast resolution • Shorter procedure time and data can be stored and processed later • Images show only the arteries and not bones or soft tissues. Despite the high degree of sensitivity, DSA angiography may fail to opacify distal peripheral arteries, especially in critical leg ischemia (CLI) with poor inflow to the leg. Belowknee vessels may be difficult to identify by digital subtraction angiography. Although angiography (conventional and DSA) are relatively safe procedures, they do carry a significant morbi­dity especially in patients with old age, longstanding diabetes, renal impairment and severe vascular disease.

Potential Complications of Angiography • • • • • •

Bleeding, puncture site thrombosis and infection, Pseudoaneurysm (Fig. 10) and dissection Arteriovenous fistula Distal embolization Spasm of the vessel Nephrotoxicity and allergic reaction.

Noninvasive imaging modalities, including MRA, CTA, and color flow duplex imaging, may be used in advance of invasive imaging to develop an individualized diagnostic strategic plan, including assistance in selection of access sites, identification of significant lesions, and determination of the need for invasive evaluation.  Most diabetics with PVD have a significant occlusive disease in the femoro popliteal segment or below the trifurcation (tibials and peroneal). The evaluation of neuro­ ischemic foot should give information about level of the



Evaluation of Neuroischemic Foot    117 stenotic lesion, degree of stenosis, length of the occluded vessel and status of vessels proximal and distal to occlusion. The vascular surgeon is also interested in knowing the proximal inflow of the vessel and distal reformation of the vessels. On the basis of this information, one can plan either an angioplasty or bypass surgery to salvage the limb, or decide the level of leg amputation.

SUGGESTED READING 1. Dellegrottaglie S, Sanz J, Macaluso F, et al. Magnetic Resonance Angiography for the Evaluation of Patients With Peripheral Artery Disease . Nat Clin Pract Cardiovasc Med. 2007;4(12):67787. 2. Diabetic Foot: A Clinical Atlas by Sharad Pendsey. 3. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA Task Force on Practice Guidelines for the Management of Patients With Peripheral Arterial Disease. J Am Coll Cardiol. 2006;47(6):1239312.

CHAPTER

Approach to Dysvascular Diabetic Foot

14 KR Suresh, Aniket Pradhan

INTRODUCTION In this chapter we have outlined the approach to dysvascular foot, especially in diabetics. Some of the recommendations are tempered with our own and other Indian experiences. We have not given detailed explanations or extensive references, which are beyond the scope of this chapter, but “suggested reading” at the end of the chapter would be very useful for those who would like to pursue this further. It is well recognized that all end organ failures in diabetes mellitus (DM) are related to micro- or macrovascular involve­ ment and vascular disease is an obligatory component of DM. Sir William Osler noted in 1908 “thickening of the arteries in DM may be due to action of the poisons on the blood vessels retained within the system.” But the true impact of peripheral arterial disease (PAD) was not really recognized until this famous statements made by Elliot P Joslin in his paper “Menace of Diabetic Gangrene”, 1934 “Deaths from diabetic coma have fallen, but deaths from gangrene of foot and leg have increased significantly, gangrene deserves more intense study and investigations, gangrene is not heaven sent, but earth born.” Unfortunately, it still holds good in India as unrecognized, under diagnosed and poorly treated PAD continues to cause limb and life loss in a huge number of patients. The impact is perhaps higher in India, as the diabetics are younger and many have low income and are manual workers and amputation is quite devastating among this population. Diabetes mellitus accelerates initiation and propagation of vascular disease at 20 years of diabetes duration • 84% have some form of vascular disease • 74% die of vascular disease: Myocardial Infarction/Acute Coronary Syndromes (MI/ACS), stroke or as a result of gangrene

Table 1  Pattern of arterial involvement in diabetics and nondiabetics Diabetes mellitus

Nondiabetes mellitus



Carotid

8.7%

2.8%



Arm arteries

2.3%

0



Leg arteries

31.8%

18.4%



Crural arteries

23.7%

16%



Coronaries

21%

11%



Ankle-brachial index (ABI) < 0.90

41.8%

18.1%

• Have both large and small vessel disease • Distribution of large vessel disease is more diffuse Following are the observations from Dutch epidemio­ logical study in patients between 50 and 75 years of age. Diabetics have higher prevalence of peripheral vascular disease compared to nondiabetics (Table 1).

DEFINING DYSVASCULAR FOOT There is no clear definition of dysvascular diabetic foot, but the following can generally define this entity: • Documented decreased vascularity of the leg (s) with ankle-brachial index (ABI) less than 0.9 or toe brachial index (TBI) less than 0.6 with or without symptoms. Ankle-brachial index greater than 1.3, indicating heavily calcified, noncompressible arteries can also be included under dysvascular diabetic foot. • Diabetic foot without palpable pedal pulses. Any dysvascular foot should be considered to be at high risk for future ulceration and amputation. More importantly



119    Contemporary Management of the Diabetic Foot even those with asymptomatic PAD should be considered to be at a high-risk for future cardio/cerebrovascular events. It is important to note that dysvascular diabetic foot is not synonymous with critical limb ischemia (CLI), the later indicates severe arterial insufficiency resulting in rest pain, ulcer or gangrene.

EPIDEMIOLOGY AND NATURAL HISTORY OF PAD In the western countries annual incidence of CLI is 1,000 per million diabetics. India has approximately 62 million diabetic population, if the same incidence data is to be applied in Indian context, then India should have 62,000 persons with diabetes having CLI annually. Typically the diabetic patients with CLI in western countries have multilevel disease with combined iliac, femoral and tibial disease in 8%, combined femoral and tibial disease in 60%, and isolated tibial disease in 32%. If we extrapolate this to Indian diabetics with CLI about 5000 should have combined iliac, femoral and tibial disease; 35,000 combined femoral and tibial disease and 20,000 isolated tibial disease. However in India only about 3,000–4,000 lower limb revascularizations are carried out annually in patients with or without diabetes. The reasons are most likely because of financial constraints, lack of awareness and underdiagnosis. The prevalence of PAD is lower among Indian diabetics as compared to Caucasians. It is 4–10% vs 20–30%. The reason for the low prevalence is being younger age and shorter duration of diabetes. Natural history of PAD is well studied. Majority of patients are asymptomatic—for every patient with diagnosed inter­ mittent claudication (IC), there are 4 PAD patients who are asymptomatic and remain undiagnosed. IC (functional limb ischemia) is a stable disease and limb loss in these patients is about 1% per year. In India, foot injury, mostly from bare foot walking can push patients with IC to critical limb ischemia. CLI on the other hand is a serious condition and majority of patients with CLI will sustain limb loss in the absence of revascularization. Both IC and CLI have significant impact on patient survival, obviously it is worst with CLI (Fig. 1). Baseline ABI is a predictor of future cardiovascular events and is an excellent tool to screen and stratify the risks in these patients (Fig. 2). Interventions in these patients does not necessarily mean surgery or endovascular procedures. It also includes aggressive medical management for all patients with PAD. Other important aspects to be remembered are that PAD in diabetics is more aggressive disease and occurs in younger patients. Rapid progression of early critical limb ischemia to gangrene occurs in 40% of the diabetics as opposed to 9% in non diabetics. Sudden progression from intermittent claudication to limb threatening ischemia occurs in 35% of

Fig. 1  Survival of patients with peripheral arterial disease (IC: Intermittent claudication; CLI: Critical limb ischemia) - TASC, 2007, J1VAS)

Fig. 2  An inverse correlation between ABI and odds of a major cardio­ vascular event (Mehler PS et al. Circulation 2003;107:753–6)

Fig. 3 The risk factors in over 1000 PAD patients who underwent revascularization (surgery/endovascular) at J1VAS over last 2 years

diabetics as opposed to 19% in non diabetics with 21% risk of major amputation as against 3% in nondiabetics. Patients with PAD have significant comorbidities (Fig. 3).



120    Contemporary Management of the Diabetic Foot The diabetic population is significantly higher than repor­ ted in various studies. About 70% have underlying coronary disease, but coronary work up or intervention is usually not required prior to vascular intervention in these patients. Microangiopathy does occur in the foot mostly in the vasa nervorum, causing neuropathy. The myth that these patients are not amenable for vascular reconstruction because of microangiopathy should be dispelled, since the results of vascular surgery and endovascular procedures are similar, if not better, in diabetics compared to non diabetic patients.

Evaluation of PAD Clinical

[

Noninvasive

[

Imaging

It involves three steps evaluation. Clinical evaluation is unquestionably the most important part of assessment, since decision to subject patient to further tests and any intervention is solely based on the symptoms.

No symptoms, no invasive procedures (whether diagnostic or therapeutic) should be the general rule in occlusive disease, as asymptomatic patients need only best medical care, with very few exceptions. Symptoms of PAD broadly fall into two groups: I. Functional ischemia presenting as IC this will need to be further classified into disabling and non disabling claudi­ cation, the former interferes with patient’s daily life and capacity to earn living. Claudication distance of 300 meters may not be disabling for an elderly, sedentary patient, but would be disabling for a young manual worker. II. Critical limb ischemia, where the limb is threatened and limb loss may be imminent without intervention, even with best medical management. Symptoms of CLI are rest (fore foot) pain unrelieved by appropriate medical treatment and analgesics for 2 weeks; and/or ulcer in dysvascular foot not healed in 2 weeks or gangrene of toes/foot with ABI < 0.5 (Table 2). Noninvasive studies as well as imaging to evaluate PAD is discussed in separate chapter on evaluation of neuro ischemic foot. Table 3 shows comparison of three imaging techniques.

Table 2  Clinical symptoms staging and their importance in recommending further work up and therapy Stage

Presentation

Invasive diagnostic and therapeutic intervention

0

No signs or symptoms

Never justified

I

Intermittent claudication (> 1 block); no physical changes

Usually unjustified

II

Severe claudication (< ½ block) ; dependent rubor; decreased temperature

Sometimes justified; not always necessary; may remain stable

III

Rest pain, atrophy, cyanosis, dependent rubor

Usually indicated but may do well for long periods without revascularization

IV

Nonhealing ischemic ulcer or gangrene

Nearly always indicated

Table 3  Comparison of DSA, MRA and CT Modality

Advantages

Disadvantages

DSA

Best resolution Combines diagnosis and treatment “gold standard”

Invasive, radiation exposure Access complications Adverse reactions to contrast Allergic reactions Contrast nephropathy

MRA

Noninvasive, no radiation Images not obscured by calcium Image arteries not seen on DSA

Inferior spatial resolution Long acquisition times Acquisition artifacts NSF

CTA

Noninvasive Excellent spatial resolution Rapid image acquisition time Multiple reconstruction techniques

Obscured by calcium Highest contrast volume Adverse reactions to contrast Radiation exposure Imaging artifacts

Abbreviations: CTA: Computed tomography angiography; DSA: Digital subtraction angiography; MRA: Magnetic resonance angiography; NSF: Nephrogenic systemic fibrosis



121    Contemporary Management of the Diabetic Foot

Management of Dysvascular Diabetic Foot The mainstay of therapy of dysvascular foot is medical therapy. Interventions (surgical/endovascular) are required only in selected patients (Figs 4A and B). The recommended approach to patients with PAD and CLI (Flow charts 1 and 2). Therapeutic options for PAD can be considered under following headings: I. Medical (conservative) therapy—should be considered in all patients with PAD. II. Interventional therapy.

Medical Therapy of PAD A four-pronged approach as recommended by National Cholesterol Education Program (NCEP-Panel III): • Life style modification • Risk factor reduction • Supervised exercise program and medical therapy • Revascularization in severe cases.

A

Life style modification and risk factor reduction programs need to address the following: 1. Smoking, 2. Diabetes mellitus, 3. Hyperlipidemia, 4. Hypertension, 5. Foot care. In Indian patients foot care is often neglected even after revascularization. The control of first four factors is required to reduce the cardiovascular morbidity associated with PAD, apart from preventing progression of the disease.

Supervised Exercise Program and Medical Therapy

B Figs 4A and B (A) Pulse volume recording showing markedly dampened waveforms, which improved markedly after revasculari­ zation of left leg (B)

These are aimed at improving walking distance and quality of life in a IC, but do not have significant benefit in patients with CLI. There are no specific medications to treat CLI. Supervised, structured exercise program has been consis­ tently shown to improve walking distance in IC. This is quite difficult in India, since patients may not be able to abide with such programs in hospital setting, but they could be taught the walk – rest – walk pattern. Cilastazole, a phosphodiesterase III inhibitor, has been shown to improve walking distance in IC in up to 80% of patients. Intolerance (palpitation, headache, etc.) is seen in 20–30% patients requiring discontinuation. Sometimes reduced dose of 50 mg bid may be tolerated well than the recommended dose of 100 mg bid. It is contraindicated in patients with history of congestive heart failure. Pentoxyfylline has not been found to be superior to placebo, but can be used in patients intolerant to cilastazole. Anti platelets and statins should be used in all patients with PAD, to reduce the systemic complications of the disease. In a large community based study, with risk factor control, only 8% progressed to rest pain over 6 years; However 79% progressed to CLI when they continued smoking over the



122    Contemporary Management of the Diabetic Foot Flow chart 1  Overall treatment strategy for peripheral arterial disease

Flow chart 2  Management principles of CLI



123    Contemporary Management of the Diabetic Foot same period. In diabetics, insulin dependency, smoking, low initial ABI are predictors of progression to CLI. All patients do not respond to medical management. Ten to thirty percent of patients continue to have disabling claudication, in spite of improved maximal walking distance. Only 30% of IC with proximal disease (aorto iliac) respond to medical therapy. Progressive decrease in ABI to less than 0.5 ( 80%) in both forms of interventions. Nearly all open surgical vascular bypass procedures, venous conduit are preferred in younger, low risk patients and



125    Contemporary Management of the Diabetic Foot

A

A

B Figs 7A and B  (A) Angioplasty and stenting; (B) Excellent results after revascularization

B Figs 6A and B  CT Angiogram showing bilateral total aorto-iliac occlu­ sions (A) treated with aorto-bifemoral bypass with Dacron graft (B) (Abbreviations: SFA: Superficial femoral artery; ATA: Anterior tibial artery; SMA: Superior mesenteric artery; RPF: Renal plasma flow; LEIA: Left external iliac artery; CFA: Common femoral artery)

synthetic grafts [Dacron or expanded poly tetra fluoroethylene (ePTFE)] in older patients with co-morbidities. Operative time and wound complications are significantly reduced with synthetic grafts. Endarterectomy, which involves removal of diseased intima and closure of the artery with a patch graft, is useful in few patients (Fig. 11). This procedure is commonly used in carotid artery steno­sis. It also yields excellent results when the occlusion/ steno­sis is limited to common femoral artery and/or to pro­­

funda femoris. Even less frequent procedure is remote end­ arterectomy in which atherosclerotic core is removed from entire superficial femoral artery with a small incision in the groin. Patency with short and long term results is unknown and hence limited to very few selected patients (Fig. 12). Sympathectomy has no role in dysvascular diabetic foot, since most of the patients already have auto sympathectomy due to autonomic neuropathy and nearly all diabetics have reconstructable vascular disease, unlike Buerger`s disease. Endovascular procedures of femoral arteries have quad­ rup­led in the last decade, but it is important to reiterate that bypass with venous conduit is far superior to all other proce­ dures mentioned above. Because of progress in technology, lower morbidity especially in higher risk patients, patient convenience, shorter hospital stay, with limb salvage rates equaling open procedures, the endovascular inter­ventions have replaced most of the surgical procedures, which are now mostly reserved for TASC D and some TASC C lesions.



126    Contemporary Management of the Diabetic Foot

A

B

Figs 8A and B  Excellent results of angioplasty and stenting of short segment iliac artery stenosis

A

B

C

Figs 9A to C  (A) Aortic- and bilateral-iliac stenosis; (B) Treated by two kissing balloons through the femoral arteries under local anesthesia; (C) Excellent results

There are conflicting data about plain old balloon angioplasty (POBA) alone and use of stents: • POBA is reported to have only 37% annual primary patency in several studies. • A well conducted study (RESILIENT) showed increased patency, better clinical outcomes with primary stenting at the time of angioplasty • The Achilles heel of stenting is in stent stenosis from neo intimal hyperplasia and there is opposing evidence that recommends selective stenting rather than stenting all lesions. • Drug eluting stent has shown better results than plain metal stents. The stents are coated with paclitaxel, an anticancer drug which decreases in situ stent stenosis. • Covered stents/stent grafts have yielded results as good as bypass with synthetic grafts. Many of the single centre studies, consisting of relatively small numbers of patients, and hence strong (class 1A)

recommendations cannot be made on the basis of current evidence. After shifting through these conflicting evidences, we follow these policies: • We attempt endovascular first in all TASC A, B and most C lesions. We prefer open bypass procedures for TASC D lesions, but high risk patients are offered endovascular procedure • We do not routinely stent TASC A and B lesions, but use it as a bail out—for flow limiting dissections, residual stenosis or recoil of over 30% after balloon angioplasty. • We prefer to stent all TASC C lesions, total occlusions and TASC D lesions. • Economic constraints sometimes preclude us from using stents. The cost of angioplasty and bypass are similar, but stents do increase the costs significantly. Salvage of failing graft: All interventional procedures for PAD need continuous surveillance, there will be increasing reocclusions from technical failures (early), intimal hyperplasia



127    Contemporary Management of the Diabetic Foot

Fig. 10  TASC classification of morphology of femoral popliteal occlusive lesions (Abbreviations: CFA: Common femoral artery; SFA: Superficial femoral artery)

Fig. 11  Isolated CFA lesion ideal for endarterectomy with patch closure

Fig. 12  Procedure of remote endarterectomy with small incision in groin



128    Contemporary Management of the Diabetic Foot

A

B

C

D

Figs 13A to D  (A) Long superficial femoral artery (SFA) chronic total occlusion (CTO); (B) Lesion crossed and angioplasty performed; (C) The CTO stenting performed; (D) Completion angiogram showing no residual lesion

(intermediate) and progressive diseases (late). With regular follow up, these can be diagnosed before complete occlusion and limb threatening ischemia. Vascular bypass grafts which are still open, but have critical lesions are termed failing grafts. These were traditionally repaired with surgery, but now endovascular interventions are frequently used to salvage these grafts and these yield high secondary patency (Figs 13 to 15).

A

Management of Infrapopliteal Disease Diabetics rarely have PAD without some involvement of infra popliteal (anterior tibial, posterior tibial and peroneal) arteries. About 32% have isolated tibial/peroneal disease. Sympto­ matic patients rarely have single vessel diseases or short lesions. They usually have complex lesions and have increased comorbidities, especially major adverse

B

C

Figs 14 A to C  (A) Stenosis in the vein graft; (B) The lesion is crossed with a wire and angioplasty performed; (C) Completion angiogram shows no flow-limiting lesion in the distal popliteal, the anastomosis and the graft

A

B

C

D

Figs 15A to D  (A) Stenosis postanastomosis in popliteal artery; (B) The lesion crossed with a wire and angioplasty done; (C) Stenting done across the anastomosis, including the graft and the native artery; (D) Good flow across the anastomosis into the distal popliteal artery



129    Contemporary Management of the Diabetic Foot cardiac events. Certain general principles in infrapopliteal reconstruction are: • Should be performed only in patients with CLI and rarely in IC. • Vein bypass continues to be superior to endovascular interventions, for similar reasons mentioned in femoral artery reconstruction. • Not all tibial lesions need to be treated and selecting the tibial artery with the best distal reconstruction should be the target of choice. • Complexity of the lesion also dictates attention, since a stenosis even in a less dominant artery may take precedence. • Angiosome targeted revascularization might be supe­ rior—each artery supplies a segment of tissue in the foot. If appropriate artery can be reconstructed, healing is likely to be better. • Multiple tibial arteries can be treated (with acceptable risk), when feasible to maximize flow to the foot. This is possible only with angioplasty. Arterial bypass is possible to any of the three vessels and even to the foot arteries (common plantar and dorsalis pedis), with acceptable long term patency and excellent limb salvage. Synthetic grafts are not recommended for below knee bypass procedures, since their patency rates are poor. With modified techniques (creating a vein interposition between graft and the artery) has improved the results, but should be used only when any autologous vein is not available. When none of the three arteries feed the foot arch or its branches, they are usually considered surgically nonreconstructable. These procedures are technically demanding and require meticulous attentions to details. Hence, this may have to be

A

B

C

D

Figs 16A to D  Foot with extensive tissue destruction but with intact heel. Anterior tibial artery bypass resulted in functional foot salvage

A

B

Figs 17A and B  Neuroischemic ulcer which was repeatedly debrided without success. Peroneal artery bypass after removal of fibula for arterial access resulted in complete wound healing

Fig. 18  Extensive anterior tibial artery stenosis/occlusion treated with balloon angioplasty creating ”straight line’’ flow into the foot

performed only by well trained vascular surgeons (Figs 16 and 17). Although infrapopliteal bypass had withstood the test of time for over five decades, advent of endovascular interventions with tools (guidewires, catheters, angioplasty balloons) designed for these interventions have completely changed the interventional management from open bypass to angioplasty (Figs 18 to 21). Perhaps the extreme skills required, with only few centers able to perform these surgical procedures has given further impetus to endovascular proce­ dures. But there are other genuine reasons given below for this dramatic shift even in departments like ours which were performing large numbers of infrapopliteal bypass procedures. • Excellent technical success rates 88–90% (80–85% in our experience) • Low frequency of complications • Multiple arteries can be targeted and at times artery supplying the angiosome can be opened. • Arteries which look non reconstructable on angiogram can be opened and foot arch can be reformed.



130    Contemporary Management of the Diabetic Foot

Fig. 19  Occlusions in infrapopliteal vessels and angioplasty of all three arteries showing good results with no flow limiting lesions

A

B

Figs 20A and B  (A) Reverse or retrograde approach to open lesions in the proximal artery when normal or antegrade approach fails (SAFARI technique); (B) Balloon being passed and angioplasty of the occluded segment performed



131    Contemporary Management of the Diabetic Foot

A

B

Figs 21A and B  Inframalleollar (below the ankle) angioplasty. (A) Intraoperative DSA showed no arteries in the foot; (B) Wire successfully passed into the plantar artery and angioplasty balloon being inflated

• Alternative access routes can be used to recanalize the arteries. • Low morbidity and mortality compared to surgery. But, • Has high target lesion restenosis/reintervention (TLR) from neointimal hyperplasia, disease progression, recoil, negative remodeling. • The current results of balloon angioplasty studies show a 1 year restenosis rate between 30% for short stenoses treatment and up to 80% for CTOs. In spite of this it has a high limb salvage rate of about 75–95% • Because of high restenosis, infrapopliteal angioplasty is not recommended in claudicators and should be attempted only in CLI. Stents are not used in below knee angioplasty, as there are very few reports showing marginal benefit compared to plain balloon angioplasty. They are used only as a bail out

A

B

C

of a complication of angioplasty. Besides, these stents are available only in short lengths and patients would require multiple stents, increasing the cost with questionable benefits at present.

Hybrid Procedures It is well documented that diabetics have multilevel PAD. Patients with CLI may need correction of lesions in different anatomical areas. Open surgery can be combined with endovascular procedures in one stage, reducing the burden and the cost of intervention. Typically a patient with iliac stenosis and femoral occlusion can undergo femoral popliteal bypass and through the same groin incision iliac angioplasty can be performed averting the need for a second, major surgery. This can be performed at different levels as necessitated in a particular patient (Figs 22A to D).

D

Figs 22A to D  (A) Stenosis in left iliac and occlusion in femoral; (B and C) Left iliac angioplasty combined with femoral popliteal bypass in one stage (Hybrid procedures); (D) Resulted in excellent vascularity of ischemic heel ulcer



132    Contemporary Management of the Diabetic Foot

The Changing Trend Increasing evidence points to the effectiveness of endovas­ cular therapy for patients with CLI. Patients who are at high risk for loss of life or limb have the most to gain with lowrisk revascularization procedures. These procedures are not replacement for traditional surgical treatment and should be viewed as complimentary. New York NY state data 1998 to 2007 for lower extremity revascularizations (LER) by Egorova et al, JVS. 2010;51:878-85 shows: • Endovascular LER quadrupled • Open LER decreased by 67%, but 5 fold increase in total LER • Major amputations decreased by 38% • Comorbidities of LER patients higher • Length of hospitalization decreased by 2–3 days and “short stays” increased.

Impact of Endovascular in PAD Procedures

PAD patients is now under way. These should be considered experimental and should be performed only under clinical trials.

Impact of Delayed Presentation and Referral of CLI Unfortunately in India, PAD is rarely diagnosed early and given adequate therapy. Even in CLI, where the diagnosis seems obvious, there are significant delays of referral to a vascular surgeon. One of the reasons can be lack of trained vascular surgeons across India. From our experience, we know that often quoted reason that patients present late or they have sought alternate medical remedies does not always seem to be true. Delayed therapy for CLI has devastating consequences, especially for rural manual worker. The cost of amputation, apart other problems associated with it, is higher than limb salvage in mid and long term.

Indications for Limb Amputation in PAD

• Previously non-reconstructable disease can be revascu­ larized • High-risk and older patients can be revascularized • Multilevel diseases can be corrected with endovascular or hybrid procedures • Decrease in amputation has coincided with increased endovascular procedures • Decrease in early mortality and morbidity • Salvage of failing bypass grafts • Failed endovascular does not preclude bypass Cost similar to bypass if stents not used.

• Significant necrosis of weight-bearing parts of the foot in ambulatory patients • An uncorrectable flexion contracture • Paresis of the extremity • Severe sepsis • Limited life expectancy • Socioeconomic status • Bedridden patients.

The New Horizons

Most of these patients are referred with an infected foot, after several days of hospitalization and some with full blown sepsis. They would have already spent significant amount of their resources before appropriate therapy. Further cost of treating these patients is increased many fold since they require multiple procedures for the septic foot, apart from vascular reconstruction and need intensive control of hyperglycemia and infection. Vascular reconstructions are done in patients who could still be inadequately prepared in spite of aggressive efforts. This could increase the perioperative complications and decrease the results of limb salvage, in spite of adequate revascularization. Longer recovery period, especially because of increased wound burden—a patient who probably would have required a toe amputation earlier, might need trans meta­tarsal amputation with increased time for healing, repeat procedures (debridements, skin grafting) and prolonged rehabilitation. Social impact of prolonged illness is difficult to quantify. Amputees have very poor quality of life, apart from increased mortality, which is worsen than most of the cancers (Fig. 23).

Several newer products are available (not yet in India at present) which might improve the patency rates of endovascular interventions. Drug eluting stents have shown superior results in femoral occlusions. These stents and drug eluting balloons are coated with anti mitotic agent paclitaxel, which acts at the site of implantation to reduce the neo intimal hyperplasia, the leading cause of restenosis. Drug eluting balloons have shown similar results in small studies and have the advantage of not leaving any foreign body (metal with its coating) behind like the stents. Bio-absorbable, drug eluting stents have been used in coronary arteries and need further evaluation. Several gene and cell based therapies are emerging and perhaps the most exciting is stem cell therapy for nonreconstructable ischemia. We have one of the highest pub­ lished series on autologous bone marrow derived stem cell therapy, with very encouraging result of 80% limb salvage. But this was in Buerger`s disease patients and our trial with all

Socioeconomic Problems with Infected foot and PAD



133    Contemporary Management of the Diabetic Foot Table 4  Mortality and morbidity in infrainguinal bypass Infrainguinal occlusive disease (> 1000 procedures) Morbidity—Early graft failure and amputation

Fig. 23  Comparative 5-year mortality rates

CONCLUSION About 15–20% of diabetic patients in India have PAD. This adds significant risk for future cardiovascular events and limb loss. All diabetics should have clinical assessment for PAD at least annually and semi annually if they already have PAD. Advanced disease with or without vascular reconstruction will need more intense follow up by vascular surgeon. Noninvasive studies including ABI, and where available PVR/duplex, should follow clinical assessment. Further diagnostic tests (angiogram) should be performed only after consultation with a vascular surgeon. All patients should be on medical management to prevent systemic complications of atherosclerosis and appropriate medications to improve quality of life in a claudicator. Limited number of patients with claudication will need intervention. Protection of feet from injuries is of paramount importance, as even a small

Major amputations

6.5%

Early graft failure

3.5%

Patent graft, progressive ischemia

0.7%

Patent graft, progressive foot infection

2.3%

Perioperative mortality

3%

Overall mortality and morbidity

7%

wound, if not treated early, can lead to limb and even life loss. Toe amputations and extensive debridements should not be done in these patients prior to vascular reconstruction. Limited amputation and debridement for infection control is permissible, followed by rapid vascular assessment and reconstruction. A patient with CLI should be immediately referred to vascular surgeon since delay causes increased morbidity, mortality and financial burden. Vascular recons­ truc­tion has high limb salvage rate, with acceptable morbidity and mortality (Table 4). Patients with major amputation (AK/ BK) have very poor quality of life, high mortality and an increased cost of treatment.

SUGGESTED READING 1. Norgren L, Hiatt WR, Dormandy JA, et al. TASC II Working Group. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg. 2007;45 (Suppl S):S5-S61. – Gives comprehensive information of the state of lower limb revascularization. It is due update this year (2012). 2. Rutherfords Textbook of Vascular surgery is the “bible” of vascular surgery and is meant for vascular surgery trainees and practitioners. 3. Sabistons Text Book of Surgery and Harrisons Principle of Medicine.

CHAPTER

Diabetic Foot Ulcers: Short- and Long-term Outcomes

15 Fran Game, Stephan Morbach

INTRODUCTION It is almost universal to start any article, scientific paper or book chapter with a paragraph about how poor the outcome of diabetic foot disease is; how it is the leading cause of nontraumatic amputation, how costly it is both in terms of a health care economy and the patient’s personal life, and how the incidence is increasing worldwide. It seems that the situation has not changed since the St Vincent declaration of 1989 which declared that there should be a reduction in the numbers of amputations of more than 50% over the subsequent five years. Although there are reported improvements in the incidence of major (above ankle) amputation in patients with diabetes published in longitudinal epidemiological surveys from several areas of the world, this is not universal and appears to vary across health care communities. The question remains however whether amputation rates are the best or only outcome measure that health care communities should be capturing. This article seeks to explore alternative outcome measures of patients presenting with foot ulceration both in the short- and long-term.

SHORT-TERM OUTCOME MEASURES Foot-related Healing When a patient with diabetes presents with an ulcer of the foot, the aim of the multidisciplinary team is usually to heal the ulcer. It appears obvious therefore that in studies of ulcer outcome, particularly those that seek to evaluate the impact of new products or techniques wound healing should be the primary outcome measure. It is surprising therefore how

few data there are on the effect of interventions on wound healing. In a recent systematic review of publications between 2006 and 2010 there were only 43 controlled trials found, of these only 27 reported full healing as an outcome, a further 12 studies gave either change in ulcer area or appearance as the major outcome measure. Unfortunately a small ulcer still incapacitates the patient as they continue to require dressing, off-loading and regular review, although some may argue that change in ulcer area can predict eventual healing. When interpreting the results of an intervention trial it is important to know what the natural history of an ulcer would be if the intervention had not been applied, i.e. what healing could be expected in a control group. It is surprising how few data there are to support health care workers making these assessments or to compare outcomes between different clinical centers. In one meta-analysis of the control arms of six wound-healing trials of neuropathic ulcers only 24% of the ulcers were healed at 12 weeks and only 31% at 20 weeks, which is much worse than many clinicians would expect from their own clinical practice. However, selection of participants may bias the outcomes of many trials, and the inclusion of a run-in period to exclude those who are responding to standard care may also influence the outcomes. Finally, standard care particularly off-loading is not defined in many protocols and this may heavily influence outcomes. Prospective outcomes from clinical practice may be a better way of defining what should be expected in terms of ulcer healing but available data are often from single centers and few are published. One such large series comes from Sweden where the primary healing rate in the whole cohort of 1617 patients without amputation was 65%. A two center study from Manchester, UK and Texas, USA reported overall healing rates of 65% in 194 patients and a large multicenter study of 1,232 patients from 14 different centers in 10 European countries reported overall healing



Diabetic Foot Ulcers: Short- and Long-term Outcomes    135 rates of 77%. Data from outside Europe and the USA are even harder to find, although one study of a new classification for diabetic foot ulcers compared outcomes from patients from single centers in UK, Germany, Tanzania and Pakistan and reported eventual healing rates of 65.7%, 72%, 48% and 59%, respectively. Although it appears at first sight that the ultimate healing rates of diabetic ulcers are worse in Tanzania and Pakistan, which could be interpreted as a function of the health care that is available for patients in these countries, it has to be recognized that the severity of ulcers at presentation (total SINBAD score) was much worse in those from Tanzania and Pakistan compared with the European countries. The importance of patient and ulcer characteristics in the prediction of healing has been examined in the Eurodiale study where the size of the ulcer at presentation, the age of the patients, the presence of peripheral arterial disease (PAD) and end stage renal disease were all significant predictors of non-healing. When the sub group of patients with PAD were examined bacterial infection was also a powerful significant predictor.

Recurrence The development of foot ulcers is rare except in those at high risk, and those with the highest risk are patients with a previous ulceration or amputation. However, what is not often examined in studies of ulcer healing, is ulcer recurrence either in the same position or a different position on the foot, or the outcome of all ulcers on either foot if there are multiple ulcers. One such study of 449 patients from a single center found that although almost 60% of index ulcers healed at some stage, only 45% of patients were alive and ulcer free (with or without amputation) after 12 months of follow-up. Similar data come from France where although an initial healing rate of 77% was achieved in a series of 94 patients hospitalized for diabetic foot ulcer, 61% of these patients experienced further ulceration in the follow-up period. More generalizable data come from a large randomized controlled multicenter UK trial of the use of three dressing preparations which found that a quarter of those whose ulcers had healed during the trial had active ulceration on the index foot at the 3-month follow-up. Without provision of preventative measures (provision of adapted shoes and insoles, organization of professional podiatric care) a diabetic patient with a history of a foot lesion will exhibit more than one relapse per year. But even while receiving such care, recurrence will occur in about 30% of the patients within the first year of initial ulcer healing and around two thirds will recur within five years. If the patient survives long enough, 97% of all foot ulcer patients will experience at least one relapse during a 10-year follow-up period. Thus the diabetic foot should be considered a lifelong disease and some experts even propose to change the terminology to

patients being “in remission” rather than “being cured” after the initial healing of an index diabetic foot wound.

Limb-related Amputations That the preservation of the limb in a patient with diabetes and a foot ulcer is the most desirable outcome is implicit in such documents as the St Vincent declaration, the Healthy Nation 2000/2010 documents in the US, and the National Diabetes Strategy and Implementation Plan of Australia. It is therefore assumed that a low incidence of amputation is better than a high incidence of amputation, and that a falling incidence of amputation is desirable. However, this may be an oversimplification for many reasons. First there is the problem of definition of “amputation”, with many authors referring to lower extremity amputation, without qualifying whether these are major (above knee, through knee, transtibial) or minor (below ankle). These are very different as a minor amputation may be done in order to save the limb, whereas a major amputation may be done when limb salvage is not considered possible. As specialist practice improves, the incidence of minor amputations might rise, while major amputations fall, although this has not been seen in all populations. Next there is the problem of whether the data presented relate to all amputations or just the latest or highest surgical intervention. The total number of amputations gives a measure of health care costs, as well as the suffering of the patient, but the last (highest) operation on any one limb is the best measure of disease severity, as well as potential function.

Minor Amputations Data from the Eurodiale study suggest that the minor amputation rate was relatively high at 18%, but this masked high variability between centers (2–38%). Other single center studies report similar variability. From the UK a study of 449 patients report a minor amputation rate of 5%, from Germany 10% and from France 33%. Although about 60% of the variation in minor amputation rates in the Eurodiale study could be explained by disease severity, the remainder is more likely to be explained by differences in other factors, such as healthcare organization or personal views of the treating physician.

Major Amputation Data on the incidence of major amputation in patients with diabetes from centers across the world are more widely published, varying from 0.056 to 6/1000 patients with diabetes from a single center in Madrid to a small series of Chippewa Indians. Several authors have noted however



136    Contemporary Management of the Diabetic Foot that even within data derived from national registries there is marked variation. A recent publication from the UK noted that the variation between Primary Care Trusts (PCTs) in the incidence of major amputations was tenfold (0.22–2.20 per 1,000 person-years). No association was found between social deprivation and the incidence of amputation in this series although it appeared that there was a lower incidence of amputation in those PCTs with large populations of black and Asian racial groups, a finding previously noted by other groups. This is in contrast to data from the USA where a similar 8.6-fold variation in the incidence of major amputation in patients with diabetes between 306 healthcare regions in the USA has been seen, but where the incidence in predominantly African-American areas has been noted to be about 5 times higher than predominantly white Caucasian areas. These discrepancies are as yet unexplained. They may, as in the data relating to the incidence of minor amputation, be partially explained by the severity of disease at presentation. However are a number of studies that have shown that it is possible to significantly reduce the incidence of amputation in diabetes by implementing changes to the structure of care in particular the development of multidisciplinary team working. Integrating those interdisciplinary teams into a regional network and implementing the use of defined clinical pathways for management seems to further increase the likelihood of a favorable outcome.

Person-related Mortality It has been suggested that diabetes could be viewed as a malignant disease, as a malignant disease is defined as a disease that does harm, inflicts suffering, causes distress, is highly injurious, is virulent, and tends to produce death. This is certainly true of patients who develop a foot ulcer as a consequence of diabetes as mortality rates have been noted to be higher than many common cancers with 5 year rates between 42 and 51%. Although it has often been assumed that this is due to patients presenting with mainly ischemic or neuroischemic ulcers, high mortality is seen even in patients presenting with pure neuropathic ulcers or acute Charcot, where the median loss of life years from presentation has been calculated to be 14 years when compared to UK normative data. Mortality post amputation is even higher, despite the assumption of many that removing the limb may be saving a life. UK data suggest a one year mortality rate of 32% for patients who undergo major amputation with 50% having died by 2 years. Those who have had above knee amputations have an even worse outcome with almost twice as many patients dying at one year. Even after minor amputations, the 1-year mortality rate is around 1 in 5 patients.

Functionality As discussed earlier it is implicit in many national guidelines that limb salvage should be attempted at all costs. However, this does not take into account the functional needs of the patient. For a sedentary patient a poorly functional salvaged limb may provide a higher quality of life than a major amputation would. For the active patient, early major amputation may offer the best functional outcome. Data are scare, however, on the functional outcome of patients post major amputation in clinical practice. One large Veterans affairs study found that while 73% of individuals were ambulatory before amputation, only 23% were ambulatory after amputation. Post-operative functionality however can be predicted by pre-operative clinical features; those with end-stage renal disease, dementia and coronary heart disease being half as likely to be mobile with prosthesis post major amputation.

Quality of Life Ulceration and amputation substantially reduce quality of life, as well as being associated with increased mortality. Some foot ulcers are painful, and treatment often requires frequent changes of wound dressings, lengthy and frequent clinic visits, and hospitalization. Amputation can impact not just on mobility but patients’ living conditions, and relationships. Data are scare, but SF-6D scores from one large trial of dressings suggest that the quality of life of patients with foot ulcers is lower than that of patients with osteoarthritis, Chronic Obstructive Pulmonary Disease or patients under­ going dialysis. As these data are from patients willing and able to be part of a trial it is likely that the scores would be much lower in general clinical practice. Data from a number of sources using the EQ-5D quality of life score show that quality of life is lowest in those post major amputation, but as with the data from the SF-6D, patients with active ulceration have lower quality of life than those with other macrovascular complications of diabetes (Fig. 1).

LONG-TERM OUTCOMES It can be deduced from the above that the longer patients with diabetes and foot ulcers are observed, the higher the likelihood that they will develop comorbidities including those that confer an adverse prognosis on the outcome of their ulcers (e.g. renal failure, PAD, age). However, published studies generally describe only baseline risk factors and comorbidities, and most observation periods are short, e.g. the Eurodiale study examined outcome at 1 year only and most of the mortality data is based on 5 year outcomes for comparison with cancer registries.



Diabetic Foot Ulcers: Short- and Long-term Outcomes    137

Fig. 1  Health related quality of life (EQ-5D) scores for people with diabetic foot ulcers and other long-term conditions (Adapted from Kerr M Foot Care for People with Diabetes: The Economic Case for Change)

Remarkably few studies have examined the outcome of patients at 10 years post presentation with a foot ulcer or after suffering an amputation, but one such study from Germany confirms the poor outcome for these patients. In a prospectively followed cohort of 247 patients cared for at one specialist center, 15.4% had a major amputation during the 10 years of follow-up; these patients all had evidence of PAD at their initial assessment. The powerful effect of renal disease on the outcome of patients with diabetic foot ulcers was confirmed in this study as patients who were in end stage renal failure and who were having renal replacement therapy were 3.5 times as likely to have a major amputation in the 10 years post presentation than those who were not, and this was independent of other risk factors. At 10 years of followup over 70% of the cohort had died, around half of the deaths being from cardiovascular disease. Independent predictors of death in multivariate analysis were age, sex (male > female), renal replacement therapy and the presence of peripheral vascular disease (Fig. 2). The mortality form cardiovascular disease accords with other studies from European countries, in contrast to studies from newly developed countries where deaths from sepsis may be more common, and where the presence of PAD at presentation (nearly 50% in this cohort) would be a relative rarity.

DISCUSSION The outcome of foot ulcers in patients with diabetes is poor, whether in terms of wound healing, major or minor

Fig. 2  Relevance of the presence (or absence) of PAD or advanced renal disease (or both combined) for the cumulative probability of death. Highest curve: no PAD and no renal disease, 2nd curve: renal disease and no PAD, 3rd curve: PAD and no renal disease, Lowest curve: PAD and renal disease (Reproduced with permission). “Copyright 2012 American Diabetes Association from Diabetes Care®, Vol. 35, 2012; 20212027. Reprinted with permission from The American Diabetes Association.”

amputation rates, quality of life and functionality, or mortality. In seeking to establish the best treatment for patients it is important therefore that all of these factors are taken into account when decisions are being made and that the patients views on what is an acceptable level of function or quality of life explored, honestly discussed and expectations managed. Decision making must therefore be truly multidisciplinary with the patient at the heart of this (Figs 3A and B). As we move towards an era of league tables for the out­ come of the management of the diabetic foot within and between health care communities we must not forget that premorbid clinical comorbidities (especially renal disease and the presence of PAD) will considerably affect the outcome and that all baseline characteristics must be taken into account in data comparison. Finally it must not be forgotten that amputation for diabetic foot disease should be considered a treatment not an outcome. For many patients with poor preoperative functional status a major amputation may confer no benefit on either their quality of life or life expectancy and a positive approach to palliative care may be more appropriate. For a younger patient however, early amputation may in some cases be the treatment of choice to gain mobility and improve quality of life.



138    Contemporary Management of the Diabetic Foot

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Figs 3A and B  Emphasize “Treat the whole patient and not just the hole in the patient!” (Courtesy: Dr. Joachim Kersken)

KEY MESSAGES   • Diabetic foot disease should be considered a lifelong condition.   • The survival of patients with diabetic foot ulcers is poor with a 5-year mortality of around 50% and a 10 year mortality exceeding 70%.   • Considered outcomes should include not just wound healing and amputation rates (major and minor) but recurrence rates, mobility and functionality, quality of life, comorbidities and mortality.   • Honest discussions should take place with all patients and their carers about all of the above before a decision is made about treatment including amputation in these patients.

SUGGESTED READING 1. Jeffcoate WJ, Chipchase SY, Game FL. Assessing the outcome of diabetic foot ulcers using ulcer-related and person-related outcomes. Diabetes Care. 2006;29(8):1784-7. 2. Kerr M. Foot Care for People with Diabetes: The Economic Case for Change. NHS Diabetes http://www.diabetes.nhs.uk/ our_publications/ (Accessed 1st August 2012). 3. Morbach S, Furchert H, Gröblinghoff U, et al. Long-Term Prognosis of Diabetic Foot Patients and Their Limbs: Amputation and death over the course of a decade. Diabetes Care 2012. Long-Term Prognosis of Diabetic Foot Patients and Their Limbs: Amputation and death over the course of a decade. Diabetes Care. 2012 Jul 18. [Epub ahead of print]. 4. Prompers L, Huijberts M, Apelqvist J, et al. Delivery of care to diabetic patients with foot ulcers in daily practice: results of the Eurodiale Study, a prospective cohort study. Diabet Med. 2008;25(6):700-7.

CHAPTER

Amputations

16 Arun Bal

INTRODUCTION AND EPIDEMIOLOGY Diabetes mellitus is a serious chronic disease. Although many serious complications, such as kidney failure or blindness, can affect individuals with diabetes, it is the complications of the foot that take the greatest toll. Foot problems are a threat to every person with diabetes. Worldwide, more than a million lower leg amputations are performed each year as a consequence of diabetes, which means that every 30 seconds a lower limb is lost to diabetes somewhere in the world. In India, 200,000 leg amputations are carried out per year for diabetes-related foot disease. 85% of these amputations are due to infected neuropathic foot ulcer which is unacceptably high. The treatment and subsequent care of people with diabetic foot problems have a significant impact on health care budgets and a potentially devastating effect on the lives of affected individuals and their family members, particularly in developing countries. Of all lower extremity amputations, 40–70% are related to diabetes. In most studies, the incidence of lower leg amputation is estimated to be 5–25/100,000 inhabitants/ year in general population while among people with diabetes the number is 6–8/1,000. Lower extremity amputations are usually preceded by a foot ulcer in people with diabetes. People with diabetes have 15 times more risk of undergoing amputations than normal population. The most important factors related to the development of these ulcers are peripheral neuropathy, foot deformities, minor foot trauma and peripheral vascular disease. The spectrum of foot lesions varies in different regions of the world due to differences in socioeconomic conditions, standards of foot care and quality of footwear. St Vincent’s declaration in 1989 showed the challenges facing various nations in the presence of growing number of diabetes patients.

Diabetic foot complications result in huge costs for both society and people living with diabetes. In India, every hospitalization for foot ulcer infection costs approximately ₹ 50,000. However, reliable and population based studies are not available, especially for operated patients. Amputation of the foot may be necessary in diabetes for severe ischemia, noncorrectable deformities, uncontrolled septicemia due to necrotizing fasciitis and severe foot infection. Amputation of the foot or lower extremity is often considered as a failure of treatment of foot ulcer. However, conservative foot amputation is important integral part of foot salvage surgery. In Indian scenario, what is needed is reducing the rate of higher level amputations. Even in those patients in whom leg amputation is required the amputation needs to be done at proper time and in proper manner, so that postamputation quality of life is improved. Patients perceive amputations as permanent loss of productivity and disability. Conservative amputations and even leg amputations done at proper time and with proper technique can improve productivity postamputation. This needs com­ bined efforts of surgeon, physician, physiotherapist, and prosthetic/orthotic expert. As of today the quality of life and scale of productivity after foot and leg amputation in India is low due to lack of this team effort. Higher incidence of contralateral limb ulceration and amputation is due to lack of postamputation care of the affected limb and residual stump. It is important to perform correct conservative amputation to avoid higher level amputation. The foot after conservative amputation has to be biomechanically viable. One of the most common causes of repeated surgeries leading to more proximal amputation is inadequate and improper technique of conservative foot amputation. Amputation surgery is the first step in rehabilitation of a patient with nonfunctional limb. Before any higher (leg) level amputation, possibility



140    Contemporary Management of the Diabetic Foot of any conservative amputation to make the foot and limb functional should be assessed. Possibility of preserving as much healthy native tissue as possible should be explored before higher level amputation decision is taken. Assessment of vascular supply and revascularization are important steps in decision making. Adequate vascular supply can mean more distal amputation. It needs to be remembered that in spite of advances in technology, anesthesia and medical care, mortality from higher level amputation still remains around 10%. A patient who has undergone partial foot amputation is 36 times more prone for proximal amputation.

DECISION MAKING It is important to have joint consultation with prosthetic/ orthotic experts, cardiologists, rehabilitation experts and diabetologists before taking decision about higher level amputation. It is needed to assess the functional capabilities of the patient. It is necessary to assess the comorbidities and cardiac function before deciding about higher level amputation. In many patients even if proper and correct level higher amputation is done, patient`s quality of life can not improve as he is unable to use prosthesis due to poor cardiac function. The oxygen consumption increases as level of amputation becomes more proximal. Possibility of more distal amputation in these patients should be probed before taking final decision. Cost of therapy for conservative foot amputation should be explained to the patient. One of the indications for higher level amputation in India is economic. It is a sad fact that foot salvage amputations are costlier than higher level amputation. Age and weight of the patient are also important consideration. In Indian scenario, obese patient will find difficult to use prosthesis after higher level amputation due to lack of infrastructure. Activity level of the patient and social/family/infrastructural support for rehabilitation after higher level amputation are factors which can influence the quality of life after higher level amputation. Many patients with chronic diabetic foot infection have nutritional deficiencies and this affects the wound healing which in turn can delay rehabilitation. Higher level amputee requires some cognitive capabilities to be successful prosthe­ tic user. These include attention, concentration, and memory. If these capabilities are deficient, then it is necessary for patient to have a regular care giver to be a successful prosthetic user. This can be assessed preoperatively by functional independence measure score.

Factors Influencing Decision Making Regards Amputation • Whether patient can use prosthesis • Type of activity and level of activity • Social support and infrastructure for prosthesis and orthotics

• • • • • • • •

Cost of treatment Duration of treatment and patient’s commitment. Comorbidities Age Weight Social status of the patient Nutritional status Cognitive capability.

PREOPERATIVE CONSIDERATIONS One of the important factors which influence the optimal outcome for any amputation is maintaining nutritional status of the patient. Preoperative assessment of nutritional status by estimation of serum proteins, serum vitamin B12, serum vitamin D3 is important. However, these investigations are not part of any routine protocol for preoperative assessment. Serum albumin level of less than 3 gms/dL is likely to cause delayed wound healing. If low white cell count signifies poor immunological status. If patient’s nutritional status is deficient, then if possible definitive surgery should be delayed till these deficiencies are corrected. If patient has spreading infection and/or gangrene, then most distal possible amputation/ debridement should be done and wound should be managed with open wound dressing till patient is nutritionally stable.

Factors Determining Level of Amputation • • • • •

Extent of infection Immunological status of the patient Comorbidities Vascular supply Status of tissues.

In the presence of nutritional deficiencies, closed wounds are likely to result in dehiscence. Good glycemic control peri and postoperatively is of paramount importance. Hyper­ glycemia causes changes in neutrophil functions and delays wound healing. If patient is on any immune suppressant drugs then extracare about prevention/control of infection should be taken. Vascular assessment by the way of measuring Ankle Brachial Index is prerequisite for successful outcome. In patients with AB index of lower than 0.7 or higher than 1.2, Duplex Doppler or if necessary angiography should be done to confirm the status of vascular supply. In such cases unless it is life saving, amputation at any level should be delayed till vascular status improves. In case of severe life threatening infection most distal possible amputation with open wound care should be done to improve patient condition. Definitive amputation should be attempted after vascular status improves. Assessment of target organ for comorbidities is mandatory before the surgery for amputation.



141    Contemporary Management of the Diabetic Foot

Fig. 1  Deep peroneal nerve block

Fig. 3  Sural nerve block

Fig. 2  Post-tibial nerve block

Fig. 4  Ring block

REGIONAL ANESTHESIA FOR LOWER LIMB SURGERY General anesthesia is more risky in diabetes because of hyperglycemia, cardiac autonomic neuropathy, immuno­ compromised state and low renal reserves. As a result, among patients who need surgery most are found to be unfit for general anesthesia. The answer, even in high-risk cases, is regional anesthesia. Modified ankle block is commonly preferred regular anesthesia for most of the diabetic foot surgeries (Figs 1 to 4). For higher level amputations regional anesthesia can also be used by blocking anterior and posterior tibial nerves at mid leg and high leg positions (Figs 5 and 6). In regional anesthesia, the patient being dealt with is conscious and alert. It is imperative for the team to make

every effort to reduce the anxiety and imbibe confidence in the patient.

Advantages of Regional Anesthesia • • • • • • •

Can be used in seriously ill patients Does not need change in diet schedule Early control of septecemia Can be used repeatedly No need to keep patient nil by mouth preoperative No postoperative nausea/vomiting No need of postoperative starving.

LOWER LIMB AMPUTATIONS Amputations are divided into minor and major amputations (Fig. 7).



142    Contemporary Management of the Diabetic Foot

Fig. 5  Mid leg block

Fig. 6  High leg block

MINOR AMPUTATIONS Digital Amputations Single digit amputation either partial or full toe may be required in cases of infected claw or hammer toes with distal phalanx osteomyelitis. It is important to make sure that the infection is limited to only part of the toe. The incision should preferably be on the dorsal aspect. Plantar scars have tendency to breakdown at later stage as neuropathy progresses. Single digit partial amputation is possible with a narrow window of opportunity if the diagnosis is made early. At later stage, when more soft tissue destruction is present, ray amputation may have to be considered. The second toe should preferably be amputated at the proximal phalanx level to prevent Hallux Valgus. If second toe is not viable, preferably

Fig. 7  Various minor amputations and their levels (from the Consensus guidelines 2011 with permission of the IWGDF)

ray amputation should be done. Mallet toe with ulceration may require toe amputation. In fifth toe amputation, trimming lateral condyles of head prevents postoperative ulceration. If more than one lesser toes are nonviable then all four should be removed with metatarsal shafts being fashioned slightly obliquely to maintain biomechanical balance (Figs 8 and 9). Vascular assessment is extremely important before any minor or major amputations (Figs 10 A to D) Great toe amputation is commonly performed amputa­ tion. Every attempt should be made to preserve as much length of first metatarsal as possible, because first toe amputation causes instability in push off and late stance phase. It is advisable to preserve proximal phalanx of the great toe to protect the flexor hallucis longus tendon. Preserving first toe gives a functionally much better foot. Sesamoid bones in the area of great toe should be removed as these could form a focus of continued infection or of osteomyelitis itself, and the level of amputation should be distal to flexor hallucis brevis tendon insertion (Figs 11 to 13).

Ray Amputation In patients who have extensive necrosis of entire toe and/ or involvement of metatarsal head it is necessary to do ray amputation to remove the source of infection. It consists of removal of a toe and its corresponding metatarsal bone. More than a single ray is generally not removed. If more than one ray is involved, it is preferable to do transmetatarsal amputation. One must try to preserve as much length of first ray as possible. Excision of complete first ray makes foot biomechanically unstable and leads to frequent breakdown of scar. In case first metatarsal bone has extensive involvement then it is preferable to do transmetatarsal amputation to



143    Contemporary Management of the Diabetic Foot

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Figs 8A and B  Nonviable third and fourth toes. To provide biomechanically stable foot, four lesser toes had to be amputated

not help, then excision of adjacent metatarsal head may be required. In rare cases, more proximal amputation may be needed (Figs 14 to 16).

Transmetatarsal Amputation.

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Figs 9A and B  Dorsal gangrene with nonviable lesser toes which had to be amputated

preserve biomechanical balance of the foot. In the case of the 5th ray, preserve the base to protect the peroneal tendon attachment. If more than one of lesser rays is involved, then oblique excision of metatarsal shafts from second to fifth metatarsals is preferred. Preservation of first ray also offers good opportunity to decompress deep fascial space in case of deep plantar infection. Unless plantar wound is present, it is preferable that major part of the incision should be on the dorsum. The decision to close the wound primarily with drain depends on extent of infection, vascular status and comorbidities. In case the wound is kept open, then proper wound care and dressings are required. The wound usually heals well if the debridement is adequate. One of the late complications of ray amputation is transfer lesion and reulceration. In such a case, if the protective footwear does

Transmetatarsal amputation (TMA) was first advocated by McKenzie for infection and gangrene of toes in diabetes. Wagner subsequently advocated TMA for diabetic foot complications of fore foot. TMA is required when amputation of single digit does not heal or leads to transfer ulceration and infection. If first ray is affected, TMA is the more definitive treatment to preserve biomechanical balance. Plantar ulceration is also not a contraindication for TMA as the ulceration can be excised by V incision and optimal stump can still be preserved. It can prevent need for more proximal foot amputation. In the presence of severe infection of digits and forefoot, it may not be possible to preserve the flaps. In such cases, wound should be left open. Newer modalities of wound care like vacuum assisted closure (VAC) for early optimal granulation can be used to hasten wound healing. Important components of TMA are cutting the metatarsal at the junction of distal 2/3 and proximal 1/3. First metatarsal should be cut with medial and plantar angle, fifth metatarsal should be cut with lateral and plantar angle while second, third and fourth metatarsal should be cut to a parabolic plane. Plantar flap should be longer. Primary closure is desirable if all the infective tissue has been excised. Subcutaneous tendon Achilles lengthening should be done if Achilles tendon is clinically fibrosed. This can be done at a later stage also. Patient should be mobilized with Plaster to prevent foot drop. One of the late complications of this surgery is muscle imbalance leading to stump ulceration. This may require transposition of anterior tibial tendon (Figs 17 to 21).



144    Contemporary Management of the Diabetic Foot

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Figs 10A to D  Nonhealing wound after second toe amputation. Angiography revealed major blocks in crural vessels. After angioplasty and restoration of blood flow all the four lateral lesser toes had to be amputated

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Figs 11A to C  Osteomyelitis of distal phalynx with soft tissue destruction requiring great toe amputation



145    Contemporary Management of the Diabetic Foot

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Figs 12A and B  Inadequately debrided, grossly infected great toe

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Figs 13A and B  Radical debridement of the same patient followed by great toe amputation

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Figs 14A to C  Osteomyelitis of fifth metatarsal requiring fifth ray amputation

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146    Contemporary Management of the Diabetic Foot

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Figs 15A to D  Osteomyelitis of second ray requiring second ray amputation

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Figs 16A to C  Deep first web space infection in a type 1 diabetic requiring second ray amputation, wound closed by primary suturing



147    Contemporary Management of the Diabetic Foot

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Figs 17A and B  Recurrent transfer lesions treated with transmetatarsal amputation and closure by posterior plantar flap

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Figs 18A and B  Severely infected foot requiring transmetatarsal amputation

Tarsometatarsal (Lisfranc) Amputation

Midtarsal (Chopart) Amputation

Tarsometatarsal (Lisfranc) amputation (Fig. 22) is carried out at the junction of the tarsometatarsal joints. It was first described by Lisfranc in 1815 in trauma cases. This amputation results in major loss of forefoot lever length. To maintain the muscle balance in the residual foot, it is important to preserve the tendon insertions of the peroneous brevis and longus and tibialis anterior muscle. In order to maintain biomechanically stable foot, proper orthosis is required, which is then placed in a shoe with a rigid rocker bottom.

Francoise Chopart described in 1,800 disarticulation through mid tarsal joints to preserve a walking foot in severe foot infection or trauma. However, till the advent of newer prosthetic technologies, rehabilitation of patient with Chopart amputation was difficult and usually led to repeat more proximal amputation. Whenever forefoot tissue destruction is extensive and TMA is technically not possible, Chopart’s amputation is one of the options which can be tried. In case of severe infection, wound should be kept open, till acute infection is controlled and then closure can be attempted.



148    Contemporary Management of the Diabetic Foot

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Figs 19A to D  Forefoot gangrene with vascular blockage, postangioplasty transmetatarsal amputation carried out along with debridement, wound closed by skin grafting

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Figs 20A and B  Severely-infected foot requiring transmetatarsal amputation, the wound was left open to be closed at a later date by skin grafting



149    Contemporary Management of the Diabetic Foot

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Figs 21A to C  Recurrent transfer lesion with osteomyelitis of second and third metatarsal requiring transmetatarsal amputation and the wound closed by primary suturing with a drain

Fig. 22  Tarsometatarsal (Lisfranc) amputation With permission “The Diabetic Foot – A Clinical Atlas”, Sharad Pendsey

Fig. 23  Midtarsal (Chopart) amputation With permission “The Diabetic Foot – A Clinical Atlas”, Sharad Pendsey

Prerequisite for Chopart’s amputation is intact heel pad and intact ankle and subtalar articulation. As Chopart amputation is through the Talo navicular and calcaneocuboid joints, leaving only the hindfoot (talus and calcaneus). Postoperative equinus is a complication which may need further correction. Chopart`s amputation with sever equinus, in sp of Achilles tendon lengthening, results in plantar ulceration. It needs revision surgery to correct transfer lesions (Fig. 23).

Indications for Major Amputations in Diabetic Foot

MAJOR AMPUTATIONS In diabetic foot, when the affected foot is not salvageable, the treating surgeon has to resort to unfortunate decision of proximal or major amputation.

• • • •

Necrotizing fascitis with multisystem failure Destruction of tarsal joints Vascular lesions not amenable to revascularization Septicemia with life-threatening situation (Fig. 24).

Syme’s Amputation Disarticulation through ankle joint with preservation of heel flap is indicated when distal foot and mid foot are affected. Adequate posterior tibial artery perfusion is mandatory. Heel pad must be centered under the leg and held under the tibia



150    Contemporary Management of the Diabetic Foot

Fig. 25  Ankle disarticulation (Syme’s) With permission “The Diabetic Foot – A Clinical Atlas” , Sharad Pendsey Fig. 24  Major amputations and their levels (from the Consensus guidelines 2011 with permission of the IWGDF)

by suturing plantar fascia to anterior tibial cortex. Molded cast should be used for 5–7 weeks to hold the heel flap in position. Syme’s amputation is more energy efficient than below knee amputation. Pirogoff`s amputation is a modification in which calcaneo-tibial arthrodesis is done. Dynamic response prosthetic foot is required for rehabilitation. In case of severe foot infection and in a patient with comorbidities and poor cardiac function, preserving leg length is important to maintain quality of life. Syme`s amputation gives this opportunity. It also has lesser energy consumption than below knee amputation. Most important aspect of rehabilitation is to provide dynamic Syme’s foot prosthesis. This needs adequate infrastructure which may not be available outside major cities in India. This is one of the constraints for attempting Syme’s amputation in India (Fig. 25).

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Transtibial (Below Knee) Amputation It is one of the most common major amputations carried out in diabetic foot. It gives most durable stump if proper technique is used. The usual indication is gangrene of complete foot and /or spreading Infection above ankle. The site of bone cut is optimally 5 inches from knee joint. Posterior mayocutaneous flap is the most common and widely accepted technique. The length of flap is equal to diameter of the leg at the site of bone cut plus 1 cm. Longitudinal component of the flap should be 1/3 to 1/2 of the width of the limb. The posterior gasrocnemius fascia is anchored to cortex of tibia by drilling holes or is fixed to periosteum of tibia. It helps in creating cushioned interface and stabilizes tibia for direct and better load transfer. It is important to stabilize the knee joint postoperatively by

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Figs 26A and B  (A) Transtibial (below knee) amputation; (B) Radiograph after below knee amputation With permission “The Diabetic Foot – A Clinical Atlas” , Sharad Pendsey

applying posterior splint. It is necessary as patients with diabetic neuropathy have loss of joint position sense and protective pain sensations. Loss of protective sensations tend to keep knee joint in flexion in the postoperative period . It leads to contracture, spasm and breakdown of wound. Almost always it is possible to do primary closure (Figs 26A and B).

Knee Disarticulation It is indicated when knee joint cannot be salvaged. It is the next best level for amputation after below knee amputation.



151    Contemporary Management of the Diabetic Foot

Fig. 27  Knee disarticulation With permission “The Diabetic Foot – A Clinical Atlas” , Sharad Pendsey

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A knee disarticulation is simpler, associated with less blood loss and a rapid postoperative recovery because virtually no muscle tissue is transected. There is greater bed mobility and sitting balance as compared to an above knee (AK) amputation (Fig. 27).

Figs 28A and B (A) Above knee amputation; (B) Radiograph after amputation With permission “The Diabetic Foot – A Clinical Atlas” , Sharad Pendsey

Transfemoral AK Amputation

Immediately after surgery simple paraffin gauze or pack dressings with good compression bandage is adequate. Antiseptic solutions like povidone iodine, eusol, hydrogen peroxide, Dettol, and undiluted savlon should not be used as they damage the angiogenesis. It is also necessary to stabilize the ankle and tarsal joints by applying a well-fitting posterior planter slab or the splint. Postoperatively, the frequency of the dressing depends on the quantum of the discharge. The principle of moist wound environment should be adhered to. Dressings are required for a prolonged time. It is necessary to train the relatives or to provide facilities for proper dressings with simple aseptic techniques. The type of the dressings will depend on the affordability, accessibility, and availability of various dressings in the market. Wounds need to be irrigated by normal saline and should always be handled gently. In case of open wound, care with slough pappain urea ointment is useful. Local antibiotic ointments should be used cautiously. Unless there is evidence of local colonization use of local antibiotic ointment is counterproductive. Newer silver impregnated products are useful; but may not be affordable for large number of patients. VAC technique is useful in open wound care as it hastens healing. In patients with severe infections especially with anaerobic organisms Hyperbaric Oxygen is a useful adjuvant therapy. Platelet derived growth factor (PDGF) and epidermal growth factor (EGF) and platelet rich plasma (PRP) are useful for treatment of residual ulcers and transfer lesions. Simple open cell foam and honey have been shown to be effective in open wound care. However, the mainstay of the treatment is simple water

Above knee amputation is indicated when there is vascular occlusion in the popliteal of infra popliteal trifurcation making below knee amputation not feasible or when infection has extended up to knee joint. Standard transfemoral amputation with fish mouth incision disengages the action of the adductor muscles. It causes postoperative abduction of femur leading to nonfunctional position. Adductor based mayocutaneous flap technique is a widely accepted method. The level of bone cut is 5 inches above knee joint. The adductor magnus muscle is separated from bone. After bone cut at appropriate level and hemostasis is achieved, adductor muscle is secured to lateral cortex of femur by drilling holes. It is done with hip joint in neutral position to avoid postoperative deformity. This technique offers optimal load transfer in prosthesis use (Figs 28A and B).

CONSEQUENCES OF LIMB AMPUTATION • • • •

Below knee amputation requires 40% more kcal/min Net oxygen consumption increases Needs 5–10% extra cardiac reserve 85% mortality at the end of 5 years.

WOUND CARE Well-trained paramedics play an important role in the long process of healing in conservative foot amputations. Dressings are of paramount importance in diabetic foot wounds.



152    Contemporary Management of the Diabetic Foot based gels or hydrogels and/or any cheap material which keeps wound environment moist.

Footwear Planning and Rehabilitation Crucial component of postconservative foot amputation rehabilitation is prescribing proper footwear. Postpedopodo­ graph or in shoe scan can give vital information about altered biomechanics of the operated foot. Footwear prescription should be in three stages. First stage is immediate postoperative period when off loading footwear should be given. When the wound has healed, footwear with modification to prevent excessive movement as well as offloading should be given. After the scar of surgical wound has remodeled which may take 12–14 weeks, permanent footwear with molded insole should be given. It is vital to motivate the patient to use the prescribed footwear indoor as well as outdoor. In Indian scenario, the footwear tends to be used only outdoor. Care of skin and scar is equally important. Patient should be instructed to apply available moisturizers regularly to keep scar and skin soft. Postoperative mobilization should be very gradual and patient should be taught to walk with short steps to avoid excessive pressure on forefoot. In patients, who have undergone partial foot amputation, foot prosthesis can be used and these are now available in India. This has positive psychological impact on patient’s quality of life. In case of BK, AK and Syme’s amputation, good coordination between clinical team and prosthetic expert is very important. Patient’s neuropathy and vascular status should be foremost consideration when mobilizing these patients after prosthesis has been fitted. Regular follow-up for shoe and prosthesis review can prevent complication like transfer lesions and stump ulcers.

TAKE HOME MESSAGES • Preserve as much length of leg as possible as distal amputations help improve gait • Aggressive timely debridement and conservative foot amputation are essential to prevent higher level amputations.

• Vascular assessment prior to any foot/leg amputation is mandatory. • Any amputation must be carried out above the level of gangrenous tissue. • The residual stump should have adequate soft tissue covering consisting of skin, subcutaneous tissue and muscles. The covering of soft tissue should move freely over the enclosed bone to absorb shear forces. • A proper contouring and beveling of the cut bone shaft is important to prevent damage of the overlying soft tissue from within. • Proper comorbidity assessment is essential to reduce mortality and morbidity. • Most of foot and leg surgeries can be carried out under local or regional anesthesia. • Postoperative early mobilization with appropriate foot­ wear is desirable. • Nutritional status of patient should be regularly assessed. • Strict glycemic control is essential component of therapy. • Psychological aspects and pre/post amputation counsel­ ing is essential to improve quality of life.

CONCLUSION Any foot or leg amputation patient must be considered as a high-risk patient. In Indian scenario, conservative foot amputations can preserve walking foot. However, post­ amputation care is very important. Regular follow-up, patient education, footwear review, callus or pressure keratosis care, glycemic and metabolic control, regular vascular assessment and regular assessment of target organs can keep patient walking in spite of long duration of diabetes.

SUGGESTED READING 1. Boulton, Cavanagh, Reman. The Foot in Diabetes. Willey, 2006. 2. Handbook of Diabetic Foot Care by DFSI. 3. Levery, Peters, Bush. High Risk Diabetic Foot. Inform Healthcare, 2010. 4. Levin, O’neal. The Diabetic Foot. Mosby; 2008. 5. Veves, Giuurini, LeGerfo. The Diabetic Foot. Humana Press, 2010.

CHAPTER

Advanced Wound Healing Products and Techniques

17 Michael Edmonds

INTRODUCTION Despite progress in the treatment of diabetic foot ulceration, this complication remains a source of morbidity and mortality. When ulcers do not respond to basic treatment, advanced products to stimulate wound healing may need to be employed. These are expensive treatments and should only be used when basic treatments have not worked. Clinical decisions as to when to use advanced therapies may be based on healing rates. The percentage change in foot ulcer area after 4 weeks’ observation is a strong predictor of healing at 12 weeks. Those ulcers that have not reduced their area by more than 50% at 4 weeks may be considered for such advanced treatment. Advanced wound healing products include: • Growth factors • Regenerative materials that expedite wound healing • Skin substitutes • Extracellular matrix (ECM) protein • Protease inhibitors • Vasoactive compounds • Platelet therapies. In addition to these products, other advanced wound healing techniques including: • Negative pressure wound therapy (NPWT) • Hyperbaric oxygen (HBO) therapy • Maggots (larval therapy) • Autologous bone-marrow cultured cell • Physical therapy. Advanced wound healing products: • Growth factors.

Various growth factors have been applied to diabetic foot ulcers including platelet-derived growth factor (Regranex), and human epidermal growth factor.

PLATELET-DERIVED GROWTH FACTOR Platelet-derived growth factor (Regranex) stimulates fibro­ blasts and other connective tissue cells situated in the skin and is beneficial in augmenting wound healing processes of cell growth and repair. Four placebo-controlled trials of PDGF-BB in neuropathic ulcers have been carried out. The pivotal study of 382 patients demonstrated that Regranex gel (100 mcg/g) healed 50% of chronic diabetic ulcers, which was significantly greater than the 35% healed with a placebo gel. More recent studies have linked the expression of PDGF-BB to malignant transformation in human cells, and a black box warning was added to Regranex (becaplermin) in June 2008 following a post-market epidemiologic study linking the use of more than three tubes of becaplermin to a five times increased risk of mortality in patients with a history of malignancy, although the risk of developing a new malignancy during treatment with becaplermin was not increased.

RECOMBINANT HUMAN EPIDERMAL GROWTH Epidermal growth factor (EGF) is a crucial factor in the healing cascade and acts on epithelial cells and fibroblasts and thereby promoting the restoration of damaged epithelium. However, its bioavailability is impaired in chronic diabetic ulcers. Indeed, fibroblasts from chronic diabetic foot ulcers demonstrate a diminished response to stimulation with EGF.



154    Contemporary Management of the Diabetic Foot Recombinant human epidermal growth factor (REGEN-D™ 150), which was cloned and over expressed in E. coli, has shown increased healing of chronic diabetic foot ulcers (DFU) by significantly reducing the duration of healing in addition to providing excellent quality of wound healing and re-epithelization.

REGENERATIVE TISSUE-ENGINEERED MATERIALS THAT EXPEDITE WOUND HEALING Tissue-engineered products may be cellular (contain living cells which are mainly skin substitutes) or a cellular (bio­ logically inert) which replace ECM. Wound regenerative tissues address the wound defect and repair process, not the disease state which must be also treated.

SKIN SUBSTITUTES Dermagraft is an artificial human dermis constructed through the process of tissue engineering. Human fibroblast cells obtained from neonatal foreskin are cultivated on a three-dimensional polyglactin scaffold. This results in a metabolically active dermal tissue with the structure of a papillary dermis of newborn skin. A randomized controlled multicenter study of 281 patients with neuropathic foot ulcers demonstrated that at 12 weeks, 50.8% of the dermagraft group showed complete wound closure which was significantly greater than in the controls, of which 31.7% healed. In a further 12-week randomized study with living foreskin fibroblasts in a vicryl mesh, incidence of complete wound closure of neuropathic foot ulcers was 30% in the active group and 18% in the control group. Apligraf is composed of a collagen gel seeded with fibro­ blasts and covered by a surface layer of keratinocytes. In a randomized 12-week trial of 208 patients with neuropathic ulcers, the bilayered construct, Apligraf, led to complete wound closure in 56% of patients, compared with 38% in controls (p = 0.0042). There was a decreased time to complete closure (65 days vs. 90 days, p = 0.0026). This was confirmed by an international multicenter, randomized, controlled study. Even though the study was stopped prematurely, it demonstrated that the use of Apligraf resulted in a higher incidence of wound closure by 12 weeks. Use of fibroblast/ keratinocyte C culture (Apligraf ) was associated with 51.5% healing of the intervention group compared with 26.3% of controls (p = 0.049). Bilayered cellular matrix (BCM) is a porous collagen sponge containing C cultured allogeneic keratinocytes and fibroblasts harvested from human neonatal foreskin. Patients with chronic, diabetic, neuropathic foot ulcers were randomized a multicenter, controlled, parallel-group pilot study to receive either standard care (moist saline gauze cover for up to 12 weeks (n = 20) or to active treatment

(n = 20) of standard care plus an application of bilayered cellular matrix at each weekly visit for up to six total applications, followed by standard care alone for an additional 6 weeks or until complete healing. By 12 weeks, 7 of 20 wounds (35%) treated with BCM showed complete healing compared with 4 of 20 wounds (20%) treated with standard care.

EXTRACELLULAR MATRIX PROTEIN Recently, ECM proteins have been used to accelerate healing of diabetic foot ulcers. The ECM plays an important role in tissue regeneration and is the main component of the dermal skin layer. The composition of ECM includes proteoglycans, hyaluronic acid, collagen, fibronectin and elastin. Recognition of the importance of the ECM in wound healing has led to the development of wound products that aim to stimulate or replace the ECM. These tissue-engineered products consist of a reconstituted or natural collagen matrix that aims to mimic the structural and functional characteristics of native ECM. Chronic or hard-to-heal wounds are typified by a disrupted or damaged ECM that cannot promote wound healing. Treatment strategies that are designed to replace the absent or dysfunctional ECM may be beneficial. A variety of animal- and human-derived products have been developed. These are acellular matrix products which differ essentially in the source of cells and tissue materials and methods used during manufacture. A number of studies have been performed in patients with diabetes and lower extremity ulcers (foot, ankle or leg) with animal- and humanderived products. They may be classified as: • Xenografts: Animal-derived • Allograft: Human tissue • Chemical constructs which contain animal-derived collagen in addition to synthetic. Studies with these products suggest that acellular matrices may promote wound healing when compared to conventional treatments. Products derived from animal sources (xenografts) are developed by harvesting living tissue (e.g. dermis, small intestine submucosa and pericardium) from various donor animals (e.g. porcine, equine or bovine) at different stages of development. The tissue materials are subsequently proces­sed to remove the cells (decellularization), leaving the collagen matrix. OASIS wound matrix comes from the pig’s small intestine submucosa. This consists of a natural collagenous, threedimensional ECM which acts as a framework for cytokines and cell adhesion molecules for tissue growth. A recent study has compared the healing rates at 12 weeks for full-thickness diabetic foot ulcers treated with OASIS wound matrix versus Regranex gel. Complete wound closure after 12 weeks of treatment was observed in 49% of the OASIS-treated patients (n = 18), compared with only 28% of the Regranex-treated group (n = 10), p = 0.055.



Advanced Wound Healing Products and Techniques    155 Products derived from human sources, i.e. donated human cadaver skin (allografts), undergo various processes to remove the cells and deactivate or destroy pathogens. They include AlloDerm® regenerative tissue matrix derived from human dermis, and human-derived dermal matrix GraftJacket®. Synthetic acellular dermal replacements include the INTEGRATM bilayer matrix wound dressing comprising of reconstituted bovine collagen matrix with polysiloxane (silicon) membrane. The semipermeable silicone membrane controls water vapor loss, which offers a flexible adherent covering for the wound surface and adds increased tear strength to the device. The collagen-glycosaminoglycan biodegradable matrix provides a scaffold for cellular invasion and capillary growth. After adequate vascularization of the matrix has ensued and the neodermis has formed, the silastic sheet may be removed and skin grafting performed. Alternatively, many smaller wounds may re-epithelialize without the need for grafting. Hyaff is an ester of hyaluronic acid, which is a major component of the ECM. Hyaff-based autologous grafts both dermal and epidermal have been used to treat two groups of diabetic foot ulcers: plantar ulcers and postoperative wounds located on the dorsum of the foot. Patients in both groups had offloading which consisted of total contact casting for plantar ulcers and a rigid-sole shoe for dorsal ulcers. After 11 weeks, there was no difference in the rate of healing in patients with plantar ulcers but in the dorsal ulcers, the autologous bioengineered graft demonstrated an increased rate of ulcer healing compared with the control group (67% vs 31%, p = 0.049).

PROTEASE INHIBITORS Promogran is a protease inhibitor which consists of oxidized regenerated cellulose and collagen. It inhibits proteases in the wound and protects endogenous growth factor. In a 12-week study, of 184 patients, 37% of promogran-treated patients healed compared with 28% of saline gauze-treated patients, a nonsignificant difference.

VASOACTIVE COMPOUND The effect on dalteparin on ulcer outcome in diabetic patients with peripheral arterial occlusive disease was investigated in a prospective, randomized, double-blind, placebo-controlled trial. A total of 87 patients were randomized to treatment with subcutaneous injection of 5,000 units dalteparin (n = 44) or an equivalent volume of physiological saline (n = 43) once daily until ulcer healing or for a maximum of 6 months. There was a better ulcer outcome (p = 0.042) and a greater number of patients healed with intact skin or decreased ulcer area of 50% in the dalteparin group compared with the placebo group.

PLATELET THERAPIES Platelet-rich plasma (PRP) containing various platelet growth factors has been used for wound treatment. Platelet-rich plasma is the portion of the plasma fraction of autologous blood having a platelet concentration above baseline. PRP also refers to platelet-enriched plasma, plate­ let-rich concentrate, autologous platelet gel, and platelet releasate. PRP can be prepared at the point of care. In a twostep process, whole blood is removed from the patient and initially centrifuged to separate the plasma from packed red blood cells and then further centrifuged to separate PRP from platelet-poor plasma. This concentrate is then activated by the addition of thrombin or calcium resulting in a gelatinous platelet gel. The results of a Cochrane metaanalysis demons­trated that PRP favored the wound healing process (95% CI: 2.94-20.31) with improved healing of diabetic foot ulcers.

ADVANCED WOUND HEALING TECHNIQUES Negative Pressure Wound Therapy Negative pressure wound therapy (NPWT) has been used to achieve closure of wounds, including diabetic foot wounds. In this technique, NPWT applies continuous negative pressure of 125 mm Hg to the ulcer through a tube and foam sponge which are applied to the ulcer over a dressing. This is sealed in place with a plastic film to create a vacuum. The sponge is replaced every 2 or 3 days. Exudate from the wound is sucked along the tube to a disposable collecting chamber. The negative pressure improves the dermal blood supply, and stimulates granulation. It diminishes bacterial colonization and reduces edema and interstitial fluid. The negative pressure improves the vascularity and stimulates granulation which can form even over bone and tendon. Recently, installation tubes have been added to the pump to facilitate the application of topical antibiotics. In a controlled study, 162 patients with postoperative wounds, following partial foot amputation, were enrolled into a 16-week, 18-center, randomized clinical trial in the USA. More patients were healed in the NPWT pump group than in the control group [43(56%) vs 33(39%), p = 0.04 ]. The rate of wound healing, based on the time to complete closure, was greater in the NPWT group than in controls (p = 0.005). A further study showed NPWT to be more efficacious compared with advanced moist wound healing in the treatment in diabetic foot ulcers. Negative pressure wound therapy is increasingly used to treat postoperative wounds in the diabetic ischemic foot especially when revascularization is not possible (Figs 1A to F).



156    Contemporary Management of the Diabetic Foot

A

B

C

D

E

F

Figs 1A to F  (A) Twenty-four hours postoperative; (B) Application of VAC dressing after sharp debridement; (C) Two weeks after VAC therapy; (D) Four weeks after VAC therapy; (E) Six weeks after VAC therapy; (F) Eight weeks after VAC therapy (Abbreviation: VAC: Vacuum-assisted closure)



Advanced Wound Healing Products and Techniques    157

A

B

Figs 2A and B  Maggots applied in the wound

Hyperbaric Oxygen Adjunctive systemic hyperbaric oxygen therapy (HBOT) has been shown to reduce the number of major amputations in ischemic diabetic feet and in a recently performed a double-blinded trial, to accelerate the healing of ischemic diabetic foot ulcers. Overall, HBOT reduces amputation rates, increases the likelihood of healing in infected diabetic foot ulcers, and improves quality of life. It is reasonable to use HBO as an adjunctive in severe or life-threatening. However, it is crucial that robust criteria be developed to improve treatment protocols, determining which patients are likely to benefit, and when to start and stop treatment.

Larva Therapy (Maggots) The larvae of the green bottle fly Lucilia sericata are used to debride ulcers, especially in the neuroischemic foot. Maggots are efficient and selective at digesting necrotic tissue. This results in relatively rapid atraumatic physical removal of necrotic material. Larvae also produce secretions that have antimicrobial activity against Gram-positive cocci including methicillinresistant Staphylococcus aureus (MRSA), and a recent study showed success in eliminating MRSA from diabetic foot ulcers. Only sterile maggots obtained from a medical maggot farm should be used (Figs 2 and 3).

Autologous Bone-Marrow Cultured Cells Topically applied autologous bone-marrow cultured cells can heal human chronic wounds that have not responded to other treatments, including growth factors and bioengineered skin. In a recent study, the safety, feasibility and efficacy of transplantation of bone-marrow derived cellular products

Fig. 3  Wound after Maggots therapy

was studied with particular reference to improvement in microcirculation and reduction of amputation rate. Either bone marrow mononuclear cells (BMCs) or expanded bone marrow cells enriched in CD90+ cells (tissue repair cells, TRCs) were utilized in the treatment of diabetic ulcers to induce revascularization. Diabetic foot patients with critical limb ischemia without the possibility of surgical or interventional revascularization were eligible. Out of 30 patients included in this trial, 24 were randomized to receive either BMCs or TRCs. The high number of dropouts in the control group (4 of 6) resulted in their exclusion from evaluation. A total of 22 patients entered treatment; one patient in the TRC group and two in the BMC group did not show wound healing during follow-up, one patient in each treatment group died before reaching the end of the study, one after having achieved



158    Contemporary Management of the Diabetic Foot wound healing (BMC group), the other one without having achieved wound healing (TRC group). Thus, 18 patients showed wound healing after 45 weeks. The total number of applied cells was 3.8 times lower in the TRC group, but TRC patients received significantly higher amounts of CD90+ cells. Improvement in microvascularization was detected in some, but not all patients by angiography and TcPO(2) improved significantly compared with baseline in both therapy groups. The transplantation of BMCs as well as TRCs proved to be safe and feasible and improvements of microcirculation and wound healing were noted in the transplant group.

Physical Therapy Acoustic pressure waves promote a biological response at the cellular level stimulating production of angiogenic growth factors, including endothelial nitric oxide synthase, vascular endothelial growth factor, and proliferating cell nuclear antigen. These factors are important constituents of the normal wound healing process. This cellular activation and growth factor expression stimulated by acoustic pressure wave treatment may play an important role in surmount­ ing cell quiescence and increasing growth factor levels sufficiently to overcome proteases. This may lead to the ingrowing of newly formed vessels, and the increased cellular proliferation and tissue regeneration needed to heal a wound. Extracorporeal shock wave therapy (ESWT) was shown to induce neovascularization and upregulation of angiogenic growth factors in animal experiments. Recently, ESWT was shown to improve wound healing via increasing topical blood perfusion and tissue regeneration in a rat model of STZinduced (Streptozotocin-induced) diabetes. Recently, 206-patient, randomized, double-blinded, para­llel-group, sham-controlled, multicenter, 24-week pivotal clinical trial was designed to quantify the safety and effective­ness of four, 20-minute, noninvasive procedures with dermaPACE, delivered over a 2-week period. The primary efficacy endpoint of complete wound closure reached statistical significance at 20 weeks in the Intent-to-Treat (ITT) population with 36% of dermaPACE subjects achieving

complete wound closure compared with 23% of Sham-control subjects (p = 0.047).

CONCLUSION When treating diabetic foot ulcers, initial state-of-theart treatment should be utilized involving debridement, offloading control of infection, adequate vascular supply and diabetes control. When such treatment has been applied efficiently but the ulcer remains unhealed, advanced wound healing therapies should be considered in the treatment program.

SUGGESTED READING 1. Armstrong DG, Lavery LA, Diabetic Foot Study Consortium. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre randomised controlled trial. Lancet. 2005;366:1704-10. 2. Armstrong DG, Salas P, Short B, et al. Maggot therapy in “lowerextremity hospice” wound care: fewer amputations and more antibiotic-free day. J Am Podiatr Med Assoc. 2005;95(3):254-7. 3. Kirana S, Stratmann B, Prante C, et al. Autologous stem cell therapy in the treatment of limb ischaemia induced chronic tissue ulcers of diabetic foot patients. Int J Clin Pract. 2012;66(4):384-93. 4. Kuo YR, Wang CT, Wang FS, et al. Extra corporeal shock wave therapy enhanced wound healing via increasing topical blood perfusion and tissue regeneration in a rat model of STZinduced diabetes. Wound Repair Regen. 2009;17(4):522-30. 5. Sheehan P, Jones P, Caselli A, et al. Percent change in wound area of diabetic foot ulcers over a 4 week period is a robust predictor of complete healing in a 12 week prospective trial. Diabetes Care. 2003:26(6):1879-82. 6. Tiaka EK, Papanas N, Manolakis AC, et al. The role of hyperbaric oxygen in the treatment of diabetic foot ulcers. Angiology. 2012;63(4):302-14. 7. Wieman TJ, Smiell JM, Su Y. Efficacy and safety of a topical gel formulation of recombinant human platelet derived growth factor-BB (Becaplermin) in patients with chronic neuropathic diabetic ulcers. A phase III, randomized, placebo-controlled, double-blind study. Diabetes Care. 1998;21:822-7.

CHAPTER

18

Atypical Aspects of the Diabetic Foot

Sharad Pendsey, Sanket Pendsey

INTRODUCTION Although etiopathogenesis of diabetic foot remains same globally, clinical presentation and precipitating factors do vary in different regions of the world depending, chiefly on the social, economic and cultural factors. India is a vast country with population exceeding 1 billion with multiple languages, cultural beliefs, several religions and, not to mention different castes. Illiteracy and poverty further contribute to compounding the problem (Box 1). In Indian patients with diabetic foot, one comes across several atypical features mostly because of above mentioned factors. Box 1  Factors compounding the problem of diabetes

• • • • • • •

Population 1.2 billion Multiple cultural beliefs 40% live below poverty line About 26% illiterate Government healthcare overburdened Majority—no health insurance Belief in alternative medicine and faith healers

SHARP INJURIES Painless mechanical trauma can result from a variety of causes. Barefoot walking with normal sensations rarely results in an injury and if it does, it receives prompt attention and this is precisely the reason why normal sensations are called protective sensations. Walking barefoot with lost protective sensations is however an open invitation to injury. This practice of barefoot walking makes patients with diabetic

Fig. 1  Deep-seated infected wound due to sharp injury as a result of barefoot walking

neuropathy susceptible to sharp injuries from thorns, glass pieces, stones, nails, etc. The sharp injuries are often deep and lead to plantar compartment infection (Fig. 1).

Home Surgery Patients are tempted to carry out home surgeries because of absent sensations. The commonly used objects are unsterile blades, scissors, needles and pins. Home surgery is another common cause of foot injury. Patients frequently cut their calluses too deep and nail too short resulting in ulcerations. Corn caps and application of salicylic acid is a common practice. It leads to chemical trauma and foot ulceration (Figs 2A and B).



160    Contemporary Management of the Diabetic Foot

A Fig. 3  Multiple toe rings in both feet

B Figs 2A and B  (A) Corn caps being applied by patient; (B) Sewing needle used for home surgery resulted in a serious heel infection spreading proximally

Toe Ring Injury Many Indian women wear metal rings on one or more toes, with the second toe the favored one. In neuropathic feet with toe deformities, these toe rings can be a source of injury and can cause strangulation in a swollen foot. Repeated instructions, proper education about foot care and avoiding barefoot walking can prevent many, if not all of these injuries (Figs 3 and 4).

INAPpROPRIATE FOOTWEAR Ill-fitting Shoes In India, open type of footwear (chappals), hawaii slippers are commonly worn that have a single grip pattern. Patients with neuropathy, find it difficult to keep the grip making these

Fig. 4  Swelling of the right foot, gangrene of second to fourth toes with strangulation of second toe

slippers often slip unawares off their foot. And to prevent the slip the wearer resorts to putting extra pressure on all the toes. Such slippers are prone to injure dorsum of the great toe and the first webspace (Figs 5 and 6).

RAT BITE People staying in small apartments and in villages usually sleep on the floor. Patients with neuropathy who sleep on the floor frequently, get bitten by house-rats, the repeated nibble giving ulcerations. Patients notice the ulcers on waking up in the morning and noticing the blood-stained linen. It is interesting how rats selectively bite a neuropathic foot. When a rat strikes at a foot, the normal foot is reflexly withdrawn, whereas the neuropathic foot remains still. Rat bites have been



161    Contemporary Management of the Diabetic Foot

Fig. 5  Injury in the first webspace caused due to footwear such as type B and C

Fig. 7  Rat bite ulcers on the toes of the right foot

A Fig. 6  Injury on dorsum of the foot caused due to footwear

common in leprosy feet as well. Rats, in all likelihood also get drawn by the typical smell of a plantar callus, particularly if it were macerated. Once the rat has had this safe nibble, it often attacks the same nonjerking foot over many more nights (Fig. 7).

THERMAL INJURIES Neuropathic feet are susceptible to thermal injuries due to loss of thermal sensations, which lead to blisters, bullae, excoriation of skin or even full thickness burns. Patients with neuropathy who visit religious places, often do so barefoot; as the religion in question forbids shoes and in the soaring 40–45ºC temperature of the summer, patients often end up with thermal injuries over plantar surfaces (Figs 8A and B).

B Figs 8A and B (A) Thermal injury on weight-bearing area of the forefoot; (B) After debridement



162    Contemporary Management of the Diabetic Foot

LATERAL MALLEOLAR BURSITIS

Fig. 9  Silencer pipe injury, note bullae over both heels

Indians are known for sitting cross-legged for long hours at work or at worship. Repeated pressure over lateral malleolar areas lead to formation of bursae. Similarly, Muslims offering “namaz”, also develop “namaz” callosities on the left lateral malleolus and dorsolateral aspect of feet. These callosities are a direct consequence of the peculiar position of the left foot during namaz. These bursae over lateral malleoli are pigmented and hypertrophied but are usually harmless in non-neuropathic individuals. In diabetics with neuropathy, in the absence of pain, these bursae get ulcerated due to repeated pressure and often get secondarily infected. Their proximity to heel pad make them vulnerable for creating a limb-threatening situation (Figs 11 and 12). Infected lateral malleolar bursae need to be surgically excised and the defect closed by split skin grafting. These patients need to be instructed to avoid sitting in cross-legged

A Fig. 10  Hemorrhagic bullae due to hot waterbag application

Patients who are pillion riders on a motorbike often get thermal injuries because of prolonged foot contact with that hot silencer pipe (Fig. 9). Similarly, passengers with diabetic neuropathy travelling long hours on non-airconditioned buses in summer are prone to get thermal injuries because of prolonged foot contact with the uncarpeted hot steel bus floor. In winter, patients with neuropathy should avoid application of hot water bags (Fig. 10). Patients should be educated to prevent such thermal injuries by instructing them to plan temple visits either early morning or late evening, wearing protective footwear when pillion-riding a motorbike or travelling on non-airconditioned buses, stay away from room heaters and avoid hot water bag fomentation.

B Figs 11A and B  (A) Ulcerated lateral malleolar bursa with cellulitis; (B) After debridement



163    Contemporary Management of the Diabetic Foot One has to also realize that majority of Indian populace is not covered by medical insurance. It becomes a common denominator for most of these factors as patients have to resort to shortcuts to reduce the huge cost involved in the management of diabetic foot. Patient moves from one hospital to another in search of a savior who would save his bloated, dirty foot. Such a toxic and moribund patient is a medicosurgical emergency and if the decision of primary leg amputation is not taken promptly, the patient easily progresses to septicemia, shock and multiorgan failure at which stage, even the leg amputation cannot save the patient’s life (Figs 13 to 15).

Fig. 12  Infected lateral malleolar bursa progressing into the heel pad

posture or use a foam cushion with a central hole to suspend the lateral malleoli.

LIFE-THREATENING INFECTION Severely infected foot is the hallmark of Indian diabetic foot. It is not uncommon to see a patient with foul smelling, edematous and severely infected foot with moribund general condition. Such deep-seated foot infections are no more localized. The anatomical barriers are disrupted with infection extending proximally, above the ankle, progressing into the leg. The patient with life-threatening foot infection, often has a history of foot infection for over 1 month, has been treated at other places with inadequate, hesitant small incisions, and various antibiotics and has even spent several days trying alternative medicine with faith healers. The foot is smelly, bloated and dirty, the foul smell intolerable and insuppressible. The foot has a boggy appearance with multiple openings discharging purulent material and underlying necrosis is clearly visible. Crepitus (gas in soft tissue) is often present. The common reasons for such a galloping foot infection, apart from virulent microorganisms and poorly controlled diabetes mellitus, are medicosocial factors. These are unawareness about diabetic foot and its consequences, late reporting, home surgery, belief in alternative medicine and faith healers, inadequate debridement and sadly far too much emphasis on expensive antibiotics by treating doctors. The above-mentioned factors are because of ignorance on part of the patient and at times, even the treating doctor. The net result is a culmination into a clinical situation of a life-threatening infection. Despite this critical situation patient and his family vehemently refuse the very idea of leg amputation. This refusal for amputation is a major stumbling block.

Fig. 13  Extensive destruction of the foot and leg

Fig. 14  Life-threatening foot infection culprit lesion is in the great toe, note small hesitant incisions



164    Contemporary Management of the Diabetic Foot factors. Maggots are thus a boon for them as they selectively remove the necrotic tissue leaving the healthy tissue intact (Figs 16A and B).

BELIEF IN ALTERNATIVE MEDICINE AND FAITH HEALERS

In Western countries, sterile maggots are available on prescription at premium cost. In India, it is not uncommon to see maggots pouring out from wounds in veterinary practice, wounds of leprosy patients and foul-smelling wounds in patients with diabetes. These maggots are unsterile. It is not aesthetically acceptable for diabetic patients and their relatives to leave maggots in the wound and therefore they have to be removed. However, maggots are very useful in wounds of leprosy patients. Wounds in leprosy have more of necrotic tissue and slough than fulminant infection which is so common in diabetics. Leprosy patients also do not have easy access to surgeons or podiatrists because of socioeconomic

Diabetic foot ulcers being painless are often perceived by patients as benign or harmless. They invariably resort to short cuts to save expenses of visiting specialty clinics. Such short cuts are home surgery or treatment with faith healers and herbal medicines. Some such examples are illustrated as case studies. A patient with plantar ulcer on the ball of great toe sought treatment from faith healers. Faith healer packed the deep ulcer with sticky herbal medication and advised to reopen the wound after 1 week. After a week, patient visited our center with high grade fever with chills. It took half an hour to remove this sticky paste of herbal medicine only to see malodorous necrotic great toe. Eventually the great toe had to be amputated (Fig. 17). A patient with long-standing diabetes went to a faith healer with swollen right leg. This faith healer applied hot herbal oil to his right leg and tied newspaper dressing with coir to his swollen leg. After 5 days when we unwrapped the dressing, a hot erythematous, swollen leg with multiple blisters was seen. He required long fasciotomy with debridement and hospitalization for a week (Fig. 18). A patient with infected right fifth toe went to a surgeon who after examination advised amputation of the fifth toe to which patient did not agree and resorted to help from a faith healer. The faith healer convinced the patient that he will arrest the infection and prevent it from spreading upwards by

A

B

Fig. 15  Right foot showing extensive destruction

MAGGOTS

Figs 16A and B  (A) Maggots pouring out from the wound of a patient; (B) Maggots delivered by forceps from the wound, they were alive and well



165    Contemporary Management of the Diabetic Foot

Fig. 17  Great toe packed with herbs

Fig. 19  Infected fifth toe treated by a faith healer, who tried a braid made from patients wife’s hair

Fig. 18  Right leg bandaged with herbal dressing and tied with a coir

Fig. 20  Recent below knee amputation in a young patient, also seen is his family

tying a braid made out of patient’s wife’s long scalp hair. He tied it around the ankle and assured the patient and his wife that everything will be alright. The net result was patient lost his foot and wife her long scalp hair (Fig. 19). There are many instances when patients come with different types of herbal dressings applied to their foot lesions like onion paste, cow dung, etc.

A young man who has recently lost his lower limb below knee because of diabetes. Being a trolley driver, he also lost his job as a driver. In the picture are also seen his two young sons and a wife. It’s a great tragedy for the family (Fig. 20). This young lady of 44 years who has lost left lower limb above knee amputation 2 years back and recently right lower limb below knee. It is extremely difficult to rehabilitate such patients with bilateral amputations. They invariably lead their rest of the life mainly ridden to a bed (Fig. 21). A young Type 1 diabetic of 36 years who underwent hip disarticulation right side 10 years ago. He had insulin injection abscess over thigh which penetrated in deeper areas and surgeon had to resort to hip disarticulation to save his life as he was brought in septicemia with diabetic ketoacidosis. Also seen in the picture are his son and wife (Fig. 22).

YOUNG AMPUTEES Onset of Type 2 diabetes occurs at least a decade earlier in Indians as compared to Caucasians. Similarly even diabetic foot lesions are seen at younger age in Indians. It is not uncommon to see a patient, sole bread winner of the family losing his lower limb because of diabetes at the age of 50 years.



166    Contemporary Management of the Diabetic Foot

Fig. 21  A young lady with bilateral lower limb amputation

Fig. 23  Neuroischemic foot with secondary infection

A

B

Figs 24A and B  (A) Gangrene of first toe and fifth toe; (B) Complete healing with autoamputation of first toe and fifth toes with conserv­ ative treatment Fig. 22  A youngman with hip disarticulation (right), also seen is his family

PERIPHERAL VASCULAR DISEASE Prevalence of peripheral vascular disease (PVD) in diabetics in India is low as compared to Western population (8–12% vs 20–40%). The low prevalence is because of lower life expectancy and a shorter duration of diabetes. Tobacco use is however, very high in Indian population and it is consumed variously as smoking cigarettes or beedies (raw tobacco wrapped in tendu leaves), chewing tobacco, tobacco mixed tooth powder, tobacco mixed nasal snuff. The diagnosis of PVD is often delayed and patients manifest first time with gangrene or critical leg ischemia. Majority of these patients have limited financial resources and are unwilling for expensive evaluations such as angiography;

what of angioplasty or bypass surgery. Many a time, the treat­ ing doctor is left with limited options. Such patients, then, can only get treated with medical line of treatment and reduction of risk factors. If the foot ischemia is associated with sepsis, the only option is to carry out amputation (Fig. 23). If the pain is controlled with medical treatment and there is no sepsis, allowing autoamputation often gives the next best result. However, meticulous care of the ischemic wound is extremely important to prevent any sepsis. Autoamputation requires patience as complete healing is effected in anything from 6–18 long months (Figs 24A and B).

CHARCOT FOOT Although the etiopathogenesis of Charcot foot remains same; however, the options for management are often



167    Contemporary Management of the Diabetic Foot

Fig. 25  Charcot foot affecting ankle joint

Fig. 27  Charcot foot affecting left ankle with early signs of Charcot foot on the right side

DIABETIC HAND

A

B

Diabetic neuropathy is symmetrical, bilateral and irreversible, and affects feet as well as hands in glove and stocking pattern. Diabetic neuropathy is length related and hence manifests clinically in feet and rarely affects the hands. In long-standing diabetics when neuropathy ascends from feet more proximally to legs, even the protective sensations are found to be diminished in hands. However, hands do not get ulcerated so easily as feet because both palmar and dorsal aspects of hand are seen easily and more frequently than feet. Hands are washed several times a day and kept clean and most importantly hands do not have to bear the body weight. Peripheral vascular disease rarely involves upper limbs. Occasionally blisters are seen on fingers because of contact

Figs 26A and B  Extensive destruction of tarsal bones and joints

limited because of lack of financial resources. Patients who present with Charcot foot at an early stage can be managed successfully with rest, offloading and the eventual custom molded shoes. However, patients who present with complex Charcot foot or with involvement of ankle joint are difficult to treat due to limited resources. They cannot be offered specialized treatment at a tertiary care center. Such patients are left to accept life with a distorted foot and offloading by patellar brace or crutches (Figs 25 and 26). Often sole breadwinners, they would not strictly adhere to instructions of offloading and limited ambulation to prevent occurrence of Charcot in the unaffected foot. Eventually, they end up with further deterioration of existing Charcot foot and a Charcot in the other foot (Fig. 27).

Fig. 28  Paronychia



168    Contemporary Management of the Diabetic Foot

A

B

Figs 29A and B  Infected hand and thumb

A

B

Figs 30A and B  Infected hand with gangrenous changes in index finger

with hot cup of tea or utensils. In Indians, hand infection is often seen although not as frequently as the infected foot. These patients present with paronychia, whitlow, palmar abscess and even frank gangrene (Figs 28 to 31). The reasons include late reporting, uncontrolled diabetes and lack of awareness both among patients and primary care physicians. Most of these cases of infected hands can be successfully treated by debridement, antibiotics and glycemic control. However, it is not uncommon that surgeons have to resort to amputations like finger amputation and even upper limb amputation (Fig. 32).

SUMMARY Atypical features seen in Indian diabetics are also probably equally witnessed in other developing countries that share common socioeconomic factors. Education is professed to be the major key to poverty eradication. Similarly, patient education and education of healthcare professionals regard­ ing identification of risk factors of diabetic foot, prompt treatment of trivial foot lesions and lifelong adherence to basic principles of foot care are of paramount importance in reducing this diabetic foot menace. The importance of medical



169    Contemporary Management of the Diabetic Foot

A

C

B

D

Figs 31A to D  (A and B) Infected hand with amputation of index finger with gangrene of middle finger; (C and D) Same patient with amputation of index and middle finger, wound closure by skin grafting

insurance is another factor which is not understood by population at large. In the absence of such insurance, people resort to cheaper alternatives, wrongly believed appropriate. Apparently, the onus rests on the health authorities and those national think-tanks to formulate policies that promote health education and universal medical insurance. Unfortunately, India is already on the top of the pile of world diabetes, what with 61 million diabetics already. In the absence of the right preventive measures, any statement that India is staring at the largest number of lower limb amputations among world diabetics and in none too distant a future, would not qualify for an exaggeration.

SUGGESTED READING Fig. 32  After right shoulder disarticulation

1. Pendsey S (Ed.). Diabetic Foot: a Clinical Atlas. New Delhi, India: Jaypee Brothers Medical Publishers; 2003. 2. Pendsey S. Clinical profile of diabetic foot in India. Int J Low Extrem Wounds. 2010;9(4):180-4.

CHAPTER

Screening and Prevention of the Diabetic Foot

19 Hermelinda C Pedrosa

INTRODUCTION The diabetic foot represents one of the most devastating complications of diabetes mellitus (DM). As the longevity of the population increases, the incidence of diabetesrelated complications also rises. Among the complications of DM are foot problems, which is also the most common cause of nontraumatic limb amputation. The feet of people with DM can be affected by diabetic peripheral neuropathy (DPN), peripheral arterial disease (PAD), infections, ulcers and gangrene. It is well known that diabetic foot ulcers (DFU) precede 85% of amputations according to many studies in the natural history and pathways of ulceration. The annual foot ulcer incidence among patients with DM is 2–3% and documented US and UK prevalence ranges from 4% to 10%. The lifetime risk of developing a DFU has also increased and it is estimated to be 25%. The burden of DFU has been recently recalculated and according to new estimates, every 20 seconds a leg is lost somewhere in the world due to DM. Clinical awareness of the diabetic foot problems has spread and among the related publications, diabetic foot publications have risen from 0.7% in 1980–1988 to 2.7% in 1998–2004. Although data in developing countries are still very scarce, according to the World Health Organization (WHO) estimates, the increase of new DM cases in working age shall be high in developing countries accounting for more than 80% of all people with DM by 2030. Based on the data presented in the International Diabetes Federation (IDF) Atlas, it is evident that PDN is as prevalent in developing countries as it is in developed countries despite differences in criteria used for diagnosis but the same cannot be said of PAD. A comparative study of DFU in Germany, India and

Tanzania showed that 80% in each center had PDN but PAD was observed in only 12 and 13% in Tanzania and India respectively, while it was found to be 48% in Germany. Diabetic foot problems have a significant financial impact on the health system either public or private due to outpatient costs, increased bed occupancy and prolonged stays in hospital. In developing countries, poor access to health care, low level of staff training, improper referral system, nonexistence of ulcer registries compound the problems further. In countries such as Brazil, PAD has been considered as one of the main causes of amputation along with PDN, yet revascularization is not regularly performed due to low resources in the public health system. Importance of foot examination has long been emphasized by Sir Paul Brand in the early 1980s recommending a national campaign to remove diabetic patients shoes and socks during medical consultations so that feet could be properly examined. Unfortunately, such approach although proved to be useful is not being implemented in routine practice. In Texas (USA) it has been verified that after 6 months of training health care professionals, the process of foot examination and registration improved from 14% to 62% and 33% to 73%, respectively. Diabetic foot ulcers require urgent intervention as delay in diagnosis and inadequate management contributes to high amputation rates. It is possible to reduce amputations between 50% and 85% by implementing combined strategies based on multidisciplinary treatment, organization, moni­ tor­­ing and professional training. The purpose of this chapter is to discuss current evidence to achieve better results in DFU management and reduction in amputations by setting up validated techniques for screening and allocat­ing proper tools for prevention in accordance with the level of care.



Screening and Prevention of the Diabetic Foot    171

SCREENING The main pathophysiological factors for DFU and amputation are PDN and PAD. PDN results in diminished or absent protective sensations-like pain, touch and thermal sensations. Autonomic nerve involvement leads to dryness of skin and pooling of blood leading to swelling on the feet. Motor involvement leads to atrophy of intrinsic small muscles leading to deformities. These problems, subsequently, lead to high plantar foot pressure and repetitive trauma results in foot ulceration. PAD affects mainly the vessels below the knee in patients with DM and even in the face of nonobstructed vessels, impaired microvascular reactivity diminishes blood supply to the ulcerated areas. Thus, the interaction of PDN, PAD and trauma has been identified as the triad of the causal pathway to DFU. Other clinical circumstances have been proved to contribute to DFU such as, nephropathy (especially in those on dialysis), visual impairment due to diabetic retinopathy, smoking, low level of education and poor access to healthcare. Importantly to note that 50% of the individuals with DM have one or more risk factor for ulceration. Past ulcer or history of amputation accounts for a greater chance of recurrence of ulcer. Therefore, the important initial task is to identify those at risk (Table 1). There have been recent reports on ethnic differences that exist in PDN and DFU risks among different populations. Migrants from Indian Asian descents have a very high risk for cardiovascular disease (CVD) which is four times more than native population in the UK. However the same population shows a low risk of DFU which is one-third compared to native population. For diabetic patients of African descents, data from the US have verified that there is two- to three-fold elevation in risk of amputation compared with US whites, possibly due to the inequalities in access to health care. In the UK, however, amputation risk is low in diabetic AfricanCaribbean men by about two-thirds compared to British whites. Table 1  Risk factors for ulceration and amputation  1.

Previous amputation

 2.

Past foot ulcer history

 3.

Peripheral diabetic neuropathy

 4.

Foot deformity

 5.

High plantar pressure, callus

 6.

Peripheral arterial disease

 7.

Diabetic nephropathy

 8.

Diabetic retinopathy (visual impairment)

 9.

Poor glycemic control

10.

Smoking

11.

Low level of education (about DM)

12.

Low access to health care

A

B

Figs 1A and B  Application of a 10 g monofilament: note that it is placed perpendicular to the plantar test area and the force given should be enough to buckle (Adapted from International Consensus on the Diabetic Foot by the International Working Group on the Diabetic Foot, with permission)

Fig. 2  Application of the tuning fork: on the dorsum of the first toe, close to the distal hallux phalanx, by the nail border (Adapted from International Consensus on the Diabetic Foot by the International Working Group on the Diabetic Foot, with permission)

Concerning the clinical past history, the recent ADA-AACE task Force, which has also been followed by the GLEPED - Grupo Latino-americano de Estudo para o Pé Diabético, Latin American Study Group on the Diabetic Foot and SBD - Sociedade Brasileira de Diabetes, Brazilian Diabetes Society recommend to ask about features of DFU, amputation, Charcot joint, vascular surgery, angioplasty, smoking; neuro­pathic symptoms (burning, tingling, pain, numbness, cramps); vascular complaints (claudication, rest pain); and diabetic complications (CVD, renal and eye diseases). Diagnosis of DFU risk also involves clinical foot exam and use of validated tools: 128 Hz-tuning fork for vibration sensation, 5.07 Semmes-Weinstein monofilament (SWF, 10 g monofilament) for protective sensation evaluation, (Figs 1 and 2) pin or neurotip for pinprick, hammer for ankle reflexes and a handheld 8 MHz Doppler to assess the anklebrachial index (ABI). Biosthesiometer or neuroesteshiometer



172    Contemporary Management of the Diabetic Foot

Fig. 3  The current plantar test areas to apply the SWF monofilament: hallux, 1st, 2nd and 3rd metatarsal heads bilateral

can also be used when available: the cut off for neuropathy risk being threshold equal to or above 25 volts. There has been much debate on how many plantar areas should be tested to verify insensitivity to the monofilament. The IWGD recommends the plantar surface of halux, first and fifth metatarsal heads and the ADA-AACE-GLEPEDSBD included the third metatarsal head as well (dark area), as it is seen in Figure 3. These are the most frequent sites of ulceration in the neuropathic feet. Any insensitive area is considered as an altered response, testing at one area has a sensitivity of 60% while testing at four areas, the sensitivity increases to 90%. The neuropathic deformities which play an important role in the ulceration pathway are: clawed toes, hammer toes and bony prominences. The halux valgus is not a typical

PDN deformity as it may occur in people without DM. Figure 4 shows the main features of PDN which lead to high plantar pressures. Collapse of medial arch of the foot due to neuroarthropathy leads to typical appearance of rocker bottom with the Charcot foot. Currently, the emphasis is on the need to diagnose loss of protective sensations (LOPS) to identify the risk of neuropathic ulceration on the basic clinical grounds. LOPS is diagnosed when there is an abnormal response to the SWF 10 g monofilament in any plantar test area plus other altered test such as the 128 Hz-tuning fork, pinprick sensation, ankle reflexes (Table 2). Palpation of distal pulses is recommended but reproduci­ bility is poor. PAD can easily be screened by the ABI, which is the ratio of systolic blood pressure in the ankle to that in the brachial artery. An ABI of 0.90 or less suggests PAD while higher than 1.3 may represent a falsely elevated pressure caused by medial arterial calcification (Monkeberg’s calci­ fica­tion). This test is easy, objective and reproducible. As 50% of the individuals with DM have PAD the ABI has been recommended by the IWGDF to be performed even in primary care. It is known that 70% of patients with DFU might have recurrent lesions within 5 years after treatment. After screening, the patient’s clinical findings should be categorized in order to be followed in accordance with the risk. The most recommended system is the one proposed by the IWGDF which has been validated in prospective study by Peters and Lavery, and has been indicated as a tool for risk management and follow-up by ADA-AACE-SBD-GLEPED (Table 3).

PREVENTION The diabetic foot has long been considered as the Cinderella of diabetes care and research and is being neglected by

Fig. 4  The high pressure areas of feet are shown by the arrows and as a result of sensory-motor damage to peripheral nerves, they are all more prone to ulceration



Screening and Prevention of the Diabetic Foot    173 Table 2  Components of the diabetic foot exam Inspection dermatologic •  Skin status: color, thickness, dryness, cracking •  Sweating •  Infection: check between toes for fungal infection •  Ulceration •  Calluses/blistering: hemorrhage into callus? Musculoskeletal •  Deformity, e.g., claw toes, prominent metatarsal heads, Charcot joint •  Muscle wasting (guttering between metatarsals) Neurological assessment – Loss of protective sensation (LOPS) 10-g monofilament + 1 of the following 4 tests: •  Vibration using 128-Hz tuning fork •  Pinprick sensation •  Ankle reflexes •  Vibration perception threshold (VPT), if available Vascular assessment •  Foot pulses •  ABI, indicated when any of the distal pulses is diminished or absent

both the doctors and the patients. However this situation has largely changed over the last 20 years. The IWGDF has contributed greatly to the publication of evidence-based guidelines on the management of DFU and many inter­ national initiatives have been developed to circumvent the high prevalence of ulcers and amputation worldwide. Recent population-based research suggests a meaningful reduction in the incidence of DM-related amputations; however, it does not hold true for developing and under­deve­ loped countries. Preventive approach seems to contribute less than better DFU therapeutic management developed along the years. Once an ulcer is present, its outcome will be determined by ulcer-related factors, such as presence

of necrosis, gangrene and/or infection and also by patientrelated factors such as age and the presence of co-morbidities that can affect wound healing. Patient education regarding foot hygiene, skin care, nail care, proper footwear, and appropriate foot care administered by qualified professionals can reduce injuries that may lead to foot ulceration. On the other hand, physical disability and marked reduction of quality of life are important issues to be considered in the majority of patients with DFU and lower-extremity amputations. Education is an important issue, but it lacks scientific evidence as to what format should it be applied. In order to improve compliance and adherence to what is taught, the patient should be encouraged to become proactive and participate in the interactive sessions rather than remaining passive or an obedient listener. The other issue that has only been recently approached relates to the psychological aspects of DFU. Patient percep­ tions are mainly based on symptoms and beliefs and in this psychosocial context, patient’s misperceptions of PDN, e.g. “means poor circulation” and emotional responses to foot complications and their management, e.g. fear of ulcer/ amputation interferes with the outcome. Anger towards health professionals as a result of perceived lack of compassion and unclear understanding of foot complications are important predictors of low adherence to self-foot care. The right approach should be patients’ empowerment and promote motivation. Such strategy might change the comprehension of foot complications, resulting in better behavior. It motivates patients to improve and realize accurate perception which is critical to achieve more effective clinical results. The importance of patient education is outlined by several review articles. The recent review, Patient education for preventing diabetic foot ulceration by Dorresteijn JAN, Kriegsman DMW, et. al. based on Cochrane database of systematic reviews analyzed eleven randomized controlled trials (RCTs). Three studies described the effect of foot care education as a part of general diabetes education compared with usual care. Two studies examined the effect of foot care education tailored to educational needs compared with no intervention. Finally, six studies described the effect of

Table 3  Risk category system of the IWGDF, recommended by the ADA-AACE task force, SBD and GLEPED Risk category

Clinical definition

Treatment recommendations

Follow-up

0

No LOPS, no PAD, no deformity

Patient education including advice on appropriate footwear

Annual (by generalist and/or specialist)

1

LOPS ± deformity

Consider prescriptive or accommodative footwear, prophylactic surgery if deformity cannot be accommodated in shoes. Continue education

Every 3-6 months (by generalist or specialist)

2

PAD ± LOPS

Consider special shoes and appointment with vascular Every 2-3 months (by specialist) surgeon for combined follow-up

3

Ulcer or amputation history

Same as 1, consider special shoes and appointment with vascular surgeon for combined follow-up (if PAD present)

Every 1-2 months (by specialist)



174    Contemporary Management of the Diabetic Foot intensive compared with brief educational interventions. Teaching diabetes patients the principles of self-examination of the feet and foot care has since long been advocated as an essential preventive strategy. Pooling of outcome data was precluded by marked, mainly clinical, heterogeneity. Four RCTs of the review assessed the effect of patient education on primary end-points of foot ulceration and amputations. Other two studies did not detect any effect of education on ulcer incidence or amputation but were underpowered. Patients’ foot care knowledge was improved in the short-term in five of eight RCTs in which this outcome was assessed. Patients’ self-reported self-care behavior was assessed in the short-term in seven of nine RCTs. The effects on callus, nail problems and fungal infections were described in five of the included studies, of which only two reported temporary improvements after an educational intervention. Only one of the included RCTs was considered to be at low risk of bias. Concerning evaluation of patient’s education, Malone et al. reported a statistically significant benefit of 1 hour group education after 1 year of follow-up in people with DM who were at high risk for foot ulceration; RR amputation 0.33 (95% CI 0.15–0.76); RR ulceration 0.31 (95% CI 0.14–0.66). This study had high bias and probably has overestimated the effect (the outcomes were reported per limb instead of per patient). Lincoln et al. did not confirm these findings in a study with a superior format as the incidence rates did not differ between more intensive group versus brief foot care education group: RR amputation, 0.98 (95% CI 0.41–2.34); RR ulceration, 1.00 [95% CI 0.70–1.44]. Patients’ foot care knowledge was improved in the short term in five of eight RCTs in which this outcome was assessed, as was patients’ self-reported self-care behavior in the short-term in seven of nine RCTs. Most of the RCTs included in this review are at high or unclear risk of bias. In some trials, foot care knowledge and selfreported patient behavior seem to be positively influenced by education in the short-term. This, however, must be viewed with caution. The ultimate goal of educational interventions is preventing foot ulceration and amputation but only four RCTs reported these outcomes and only two reported sufficient data to examine it. Based on these two studies, authors concluded that there is insufficient robust evidence that limited patient education alone is effective in achieving clinically relevant reductions in ulcer and amputation incidence. Future research should focus on evaluating the effect of more comprehensive and/or intensive prevention strategies which may also include patient education (complex interventions). A report by Rönnemaa and colleagues, who found a significant increase in foot care knowledge in the intervention group after 1 year of follow-up. However, after 7 years of follow-up, the control group had made up for all these areas of differences in foot care knowledge and self-care behavior. Five prospective RCTs combining patient education and

preventive strategies, which refer to the improvement of healthcare professionals’ ability to provide adequate foot care (healthcare provider education, risk assessment and referral, new screening instruments) or the healthcare struc­ tural interventions (introduction of a multidisciplinary team, measures to improve follow-up and continuity of care) were identified. Among those, it is worth quoting McCabe’s study which comprised 2001 patients randomized to receive a detailed foot ulceration risk assessment and intensive care for those at high risk or care as usual. The intensive intervention comprised intensive follow-up, a weekly diabetic foot clinic, podiatry care, hosiery provision and protective footwear plus introduction of appointment reminder letters to patients. The results showed a significant cost-effective reduction of lower-extremity amputations (RR 0.30; 95% CI 0.13–0.71) but a nonsignificant reduction of foot ulcerations (RR 0.69; 95% CI 0.41–1.14). Thus, on the basis of the most recent review of RCTs evaluating educational programs for preventing foot ulcers, Dorresteijn and Valk conclude that there is insufficient robust evidence restricted to patient education alone to be shown effective and to achieve relevant reductions in ulcer and amputation incidence. Many initiatives have been implemented in different countries towards training health professionals and contribu­ ted to changes in the regional scenarios in developing and less developed countries. The Brazilian project “Save the diabetic foot” was started in Brasilia, the capital of Brazil and later on had spread to other regions of that continent-size country reaching over 60 outpatient foot clinics. The project has inspired other programs including the Step-by-Step (SbS) supported by the WDF in Tanzania, India and other countries. Now, the SbS is to be started in the South and Central America and IDF region (SACA) to replicate and even rescue the pioneer Brazilian initiative and reinforce activities in the other Latin American countries such as Argentina, Bolivia, Equator, Colombia, Cuba, Bolivia, Peru, among others. The Eurodiale (European Study Group on Diabetes and the Lower Extremity) has already shown that the elderly frail patients with a poor health status deserve an integrated treatment approach to alleviate the burden not solely of the foot but the diabetic patient as a whole. More emphasis should be placed on developing strategies to improve the outcome of diabetic patients with a neuroischemic DFU, PAD and infection. Finally, despite the insufficient robust data concerning prevention and education based on the currently available reports, such a scenario should be cautiously inter­ preted as lack of evidence rather than evidence of no effect. In daily clinical practice the recommendation is to implement a screening policy using the validated tools and integrate proper referral policies. Efforts should be concentrated on to educate those who are found to be at high risk of DFU. Thus, the education and prevention programs should involve both patient education and multiple interventions



Screening and Prevention of the Diabetic Foot    175 to be performed by health professionals, patients, family and carers. Improvement is possible and may be achieved by imple­menting international guidelines on diabetic foot. For developing countries, the challenge includes sustainability of the health policy as well.

SUGGESTED READING 1. Boulton AJ. The diabetic foot: from art to science. The 18th Camillo Golgi Lecture. Diabetologia. 2004;47:1343-53. 2. Dorrestein JA, Valk GD. Patient education for patient for preventing diabetic foot. Diabetes Metab Res Rev. 2012; 28(Suppl 1):101-6.

3. International Working Group on the Diabetic Foot. International Consensus on the Diabetic Foot 1999. In Proceedings of the International Working Group on the Diabetic Foot Meeting, Noordwijkerhout, the Netherlands, 1999-2003-2007. [Online] Available from the website www.idf.org/bookshop. [Accessed April 2013] 4. Rezende KF, Ferraz MB, Malerbi DA, Melo NH, Nunes MP, Pedrosa HC, Chacra AR. Direct costs and outcomes for inpatients with diabetes mellitus and foot ulcers in a developing country: The experience of the public health system of Brazil. Diabetes Metabol Syndrome: Clinical Res Rev. 2009;3:228-32. 5. Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA. 2005;293:217-28.

CHAPTER

Prescribing Footwear

20 Vijay Viswanathan

INTRODUCTION Foot ulcerations, joint deformities or previous amputations can result in alterations in foot dynamics, which cause abnormal distribution of plantar pressures in the foot of a diabetic patient. Limited joint mobility in the foot and ankle is also a consequence of deformities such as plantar flexed metatarsals, hallux limitus, clawed toes, equines deformity, forefoot varus and ligament glycosylation. Increased plantar pressure and limited joint mobility are important determinants of foot ulceration irrespective of the duration of diabetes. Hence, early recognition of these problems and the ability to adapt the appropriate/therapeutic footwear to reduce the pressure peaks are key elements in the management of diabetic foot. Identifying and prescribing the appropriate footwear for a diabetic patient is a major challenge for the physician, because of the non-availability of specific footwear for a diabetic patient. The physician has to consider several issues while writing a footwear prescription. The footwear suitable for one patient may not be fit for another patient, even though he/she might have the same kind of problem. The necessary requirements in designing the appropriate footwear must be clearly mentioned in the prescription so that the concerned pedorthist or shoe maker can effectively produce the required footwear. This chapter will deal with the important aspects that the physician has to take into account while prescribing footwear for the diabetic patient.

USE OF IMPROPER FOOTWEAR AND ITS CONSEQUENCES It is known that besides the other risk factors such as peripheral sensory neuropathy, lack of knowledge about foot

care practices and uncontrolled diabetes, wearing improper footwear is the most significant causal factor contributing to diabetic foot problems worldwide, especially in developing countries like India. Lack of adequate knowledge on using appropriate footwear is the main reason behind this issue. A large majority of Indians use inappropriate footwear like the “Hawai chappals” having a rubber sole, supported by a strap in the first interdigital space, but no back strap. Such kind of footwear predisposes the feet to injury. Similar footwear, the “Kolhapuri chappal,” made of leather also exposes the feet to injury. Besides this issue, most of the diabetic patients in India and other developing countries walk barefoot indoors and in places like religious shrines. In addition, the practice of not wearing socks, particularly in women, can result in a hyperkeratotic and fissured heel or a callosity of the first interdigital space or injury to the great toe.

DETERMINING THE CORRECT FOOTWEAR In general, most footwear modifications are recommended as the result of trial-and-error experience and training based on the empiric findings of shoemakers of previous generation. Only a few of the medical practitioners in most of the developing countries have sufficient training in the applications and prescription of protective footwear for diabetic patients. Several general practitioners may also be unaware of such a concept. Diabetic patients especially those with peripheral neuropathy need an expert footwear professional to assist them in selection and fitting of the most appropriate footwear. Correct fit is best determined by a professional, such as a certified pedorthist, who has the knowledge to objectively determine whether the shoe fits without any input from the patient. This is because when neuropathy is present, the previous experience of the patient is unreliable due to the absence of protective sensation in the



Prescribing Footwear    177 feet. Nevertheless, there are now objective, experimentally derived data to support pedorthic shoe therapy. Footwear recommendations for people with diabetes and possibly insensate feet and/or moderately clawed toes must be based on extensive experience. Correct footwear made of good quality material must essentially accommodate the following important aspects: • Broad and square toe box • Low heels • Lightweight • Large enough to contain a cushioned insole, if needed. • Rigid outsole Several research studies have demonstrated the effective­ ness of therapeutic footwear in preventing and healing diabetic foot ulcers. In a south Indian study, Vijay et al. had demonstrated the effectiveness of different types of footwear insoles that are soft and shock-absorbing and correctly designed for diabetic patients with high-risk of foot problems. The materials used for manufacturing the insoles were polyurethane, ethylene vinyl acetate, microcellular rubber (MCR) and cork. These are lightweight, shock absorbent, flexible and highly durable materials. A full-length foam inner sole was also included in the footwear to cradle and support the foot.

TYPES OF SHOES There are five main categories of shoes. 1. High-Street shoes: Sensible shoes of a correct size and style from the high-street shoe shop. Once patients are at high-risk they should not wear ordinary shoes unless they can obtain them on a buy to return basis and have them checked by a healthcare professional; athletic shoes (trainers) are a reasonable choice for most patients. Patients with neuropathy accustomed to the tactile sensa­tion of having shoes on their feet, may therefore buy progressively tighter-fitting shoes to reproduce that sensation. This practice can cause pressure necrosis; hence, such patients should be warned to avoid tight shoes, and the implications of sensory loss should be emphasized. Moreover, high-street shoes are not fit to accommodate significant deformities that need to be housed within stock shoes, modular shoes or bespoke shoes. 2. Ready-made, off-the-shelf, stock shoes: These are made with extra depth and width, and without prominent seams. They usually have a low opening, are fully lined and contain a built-in rocker sole and flat-bed insole made of MCR. The insoles can be replaced with bespoke insoles. These shoes can also be modified to accommodate foot deformities by stretching specific areas or making “balloon patches”. 3. Modular shoes: These are a kind of footwear comprising the qualities of both readymade and bespoke shoes. The

orthotist carries out a trial fit using the standard stock shoe and then details a number of fixed modifications that need to be carried out. 4. Customized or bespoke shoes: These shoes are helpful in accommodating the shape of the foot, the more abnormal the foot shape, the greater the need for bespoke shoes. In some patients, previous ulceration would have caused scarring or depletion of fibrofatty padding under the metatarsal heads, or bound down plantar tissues, leading to high plantar pressures. In such patients, using customized or bespoke shoes may be necessary. Bespoke shoes have the advantage of accommodating moulded insoles, which can redistribute high plantar pressures in the neuropathic foot. 5. Temporary readymade shoes: These are used to accom­ modate wound dressings in patients with ulcerated feet. They are usually fitted with flat-bed insoles, but a moulded insole can also be inserted.

GENERAL PRINCIPLES OF PRESCRIPTION OF FOOTWEAR • The patient’s choice of material, color and style should always be considered as far as possible. • Shoes made in a trainer style or athletic style are often acceptable by young patients. • Shoe soles should be thick enough to prevent puncture by nails or thorns. • Shoe fastenings (laces or straps) should be adjustable so as to accommodate swelling or edema. Patients should be taught to rest the heel of the shoe on the ground and move the foot well back into the shoe, before securing the fastenings. • Shoes should be checked at every clinic visit and reassessed frequently for excessive wear and tear and the changing needs of patients. • Abnormal foot biomechanics can cause uneven patterns of wear and make the shoe troublesome for use, which necessitates the need for regular review of footwear. • Shoes that become worn down should be brought in for early repair, if possible, and the orthotist should supervise repair of the shoes. • New footwear should not be worn for longer time (2 hours), allow the leather to soften. • Buy footwear preferably in the evening because feet swell a little in the evening. • Check shoes before putting them on, to look for any foreign objects.

Prescription Footwear Prescription footwear is made over a variety of last shapes. Some of the examples include the combination last, which has a narrower heel than the standard last; the inflare last,



178    Contemporary Management of the Diabetic Foot

Fig. 1  Parts of a shoe With permission “The Diabetic Foot – A Clinical Atlas” Sharad Pendsey

which provides more medial forefoot surface area; and the indepth last, which is shaped to allow extra volume for the foot inside the shoe and provides enough room for a generic insert (insole) or a custom orthosis. Specific parts of the shoe upper also affect shoe fit. A brief knowledge of the terms that are used in describing the shoe upper will be quite useful in prescribing footwear. The most important terms are (i) counter, the part of the shoe extending the heel, (ii) toebox, the part that covers the toe area, (iii) vamp, the part that covers the instep, and (iv) throat, the part at the bottom of the laces (Fig. 1). The counter controls the heel and determines heel fit. Counters must be strong enough to adequately control the foot inside the shoe. The toe box is a very important part of the footwear; a high and rounded or oblique toe box offers the best fit by allowing the toes to fit and move comfortably inside the shoe. A shoe with a tapered or pointed toe box is inappropriate for the diabetic foot, because it applies pressure to the toes and forces them into an unnatural posture, leading to calluses, ulcers and eventual deformity. Similarly, the vamp should be high enough to give additional inner space and prevent unnecessary pressure on the instep. Finally, the shoe must have either lacing or hook-and-loop closure, which is best for the diabetic foot because these systems provide the adjustability that is needed to accommodate edema or deformities and also prevent the shoe from slipping off.

Guidelines for Proper Shoe Fit Once appropriately-shaped footwear has been found, the next step is to determine the appropriate size. There are three essential measurements in determining shoe size: (i) overall foot length (heel to toe), (ii) arch length (heel to ball) and (iii) width. A correct shoe size accommodates the first metatarsophalangeal joint (i.e. the widest part of the foot)

in the widest part of the shoe. This implies that shoes must be fit by arch length rather than by overall foot length. Feet can have the same overall foot length, but require different shoes because of the difference in arch length. The following is a set of guidelines that can be used to determine the correct shoe fit: • An appropriate measuring device must be used to measure both feet (not just one foot). The Brannock measuring device is the most complete tool, although there are other devices, such as the Ritz stick. Each foot should be measured under conditions of both weight bearing and non-weight bearing, with three main measurements: heel to toe, heel to ball and width. • It is essential to have shoes fit by a certified pedorthist or other trained shoe-fitting professional. This is because shoe sizes are not standard and uniform; they differ from manufacturer to manufacturer and often even among styles produced by the same manufacturer. • The outline of the shoe sole should be roughly the same shape as an outline made of the foot. Pay particular attention to fit around the fifth (little) toe. Too much pressure on the side of this toe results in corns over or between the toe and is a frequent cause of ulceration. • Check for the proper position of the first metatarso­ phalangeal joint. It should be accommodated comfortably in the pocket of the widest part of the shoe. • Check for the correct toe length. Allow 3/8 to 1/2 inch between the end of the shoe and the longest toe. • Check for the proper width, allowing adequate room across the ball of the foot. When a shoe is too tight, ulcers usually develop medial to the first metatarsal head and lateral to the fifth metatarsal head. The ulceration is due to pressure ischemia, as a result of tension within the leather that applies the greatest stress in areas of smallest circumference. • Look for a snug fit around the head of the foot, particularly, where the top of the upper meets the heel. When the heel sits well forward away from the back of the shoe, it does not mean that the shoe is too long for the person’s foot. It just means that the foot is sliding forward in the shoe. The vamp needs to hold the heel back against the counter of the shoe. Proper fit over the instep can be achieved by an appropriately high vamp, preferably with laces to allow adjustability. • Fit shoes on both feet while the patient is weight-bearing. If the feet measure differently, the larger foot should be accurately fit. In majority of cases, insert adjustments can be made to get the other shoe to fit the smaller foot.

Need For Proper Communication between the Physician and the Shoe Maker Even though a specialist physician trained extensively in foot anatomy, function and pathology may take care of diabetic foot problems, he or she might not have the adequate knowledge



Prescribing Footwear    179 of footwear materials, types, etc. This situation raises the need for proper communication between the physician and the shoemaker in the form of appropriate prescriptions. Hence the prescribing physician plays an important role in providing an extensive background in formal education and clinical experience regarding the subtle pathological variances found in each individual’s foot and in fitting the correct footwear. To achieve the best protection for the patient with an insensate foot, the specialist physician must mention these aspects in the prescription so that the footwear specialist can incorporate them in the prescribed footwear. In addition, since the physician rarely has the expertise to manufacture, or even recommend, specific materials for custom orthosis, this knowledge must come from the fabricator of the orthosis. Though the prescribing physician does not often evaluate the performance of an orthotic device, in case involving insensate limbs, it should be a matter of routine clinical practice. Verbal communication between physician and fabricator would be ideal to achieve the best results. If this is not possible, the physician or assistant should include the following points in the written prescription: • Complete diagnosis: This should include both primary and secondary diagnoses. A history of recent ulceration and/or fracture should be communicated to the shoe fabricator. Any particular anatomic or functional obser­ vations, such as forefoot varus, plantar-flexed metatarsal or limited subtalar joint range of motion, should be identified. • Desired effect: The physician should mention the goals ought to be achieved upon using the new orthosis and footwear. These may include “relieve pressure under a metatarsal head”, “post the forefoot varus”, “stabilize the midtarsal joint”, or “reinforce the lateral counter”. • Other factors that may have to be considered: These include factors such as using a boot rather than a lowquarter shoe or making room for an ankle-foot orthosis that is being made at a different facility.

Prescribing the Appropriate Footwear for the Diabetic Patient A detailed biomechanical examination of the foot is necessary for prescribing the appropriate footwear for a diabetic

patient. The foot of a diabetic patient must be examined for several aspects including its temperature, sensation, muscle disorders, type of footwear being worn by the patient, and any other foot abnormality (Table 1). Patient education for selfexamination should also be provided to expand or reinforce the patient’s active participation in his or her own care on every visit to the clinic. The extent of deformity and presence of callus are two important indicators, which can act as surrogate markers of risk. These two markers can be quite useful for prescribing suitable footwear, under the assumption that more of either factor will lead to (or reflect) higher pressures and greater risk. In addition, categorization of the diabetic foot using standard classification system (for example, Wagner’s classification system) can be helpful in the right management of the issue (Table 2).

Risk Category 0 Category 0 risk includes all patients with diabetes and without loss of protective sensation. These patients will have good vascular pulses, good sensation and no significant foot deformity and may not, therefore, require special footwear. However, it is not too early for these patients to start adopting good footwear habits because their sensory systems within the foot and vascular supply may be lost during any stage of the disease. Since this loss can be so gradual that it is not noticed by the patient, a periodic objective evaluation of sensation should be done to help prevent tissue damage. A standardized record of risk factors including peripheral sensory and circulatory status should be maintained for the duration of the patient’s life, and evaluated every year or at regular intervals. These patients must be provided adequate education on footwear selection. Their footwear should not pose any threat to their feet if loss of sensation develops. They should be educated at every clinical visit about the need for shoes that do not apply excessive loads to the foot, on either the dorsal or the plantar surfaces (Figs 2A to C). They should also be advised on good hygiene foot care practices such as thorough washing and drying their feet including the web spaces and inspecting their shoes for any foreign object, such as a nail or thorn, before wearing them.

Table 1  Examination of the insensate diabetic foot Examination

Justification

General

Inspect for possible ulceration, areas of inflammation, other skin changes related to vascular disease

Sensory

Test vibratory sensation and perform a quantifiable sensory test to determine the level of protective sensation

Temperature

With no sensation, a localized skin temperature increase >2°C in a localized area indicates an area of inflammation

Footwear

Identify the characteristics of the footwear that may pose a threat to the feet, because of wear or style

Muscle

Diseases that result in sensory loss can also lead to muscle paralysis; in the feet, intrinsic paralysis is the most frequent early involvement and results in clawed toe deformities



180    Contemporary Management of the Diabetic Foot Table 2  Risk categories and management Risk Category 0 Protective sensation present No history of plantar ulcer May have foot deformity Has a disease which could lead to insensitivity Category 1 Protective sensation absent No history of plantar ulceration No foot deformity Category 2 Protective sensation absent No history of plantar ulcer Foot deformity present

Category 3 Protective sensation absent History of foot ulceration and/or vascular laboratory findings indicate significant vascular disease

Management Foot clinic examination once a year Patient education to include proper shoe style selection

Foot clinic examination every 6 months Review all footwear the patient wears Add soft insoles Foot clinic examination every 3–4 months Custom-molded orthotic devices are usually necessary Prescription footwear often required

A

Foot clinic examination every 1–2 months Custom orthotic devices are necessary Prescription shoes are often required

Risk Category 1 (The Patient Who is at Risk for an Ulcer) Patients in risk category 1 exhibit loss of protective sensation, which can be assessed as an inability to feel the SemmesWeinstein monofilament that bends with a pressure of 10 g (5.07). These patients would not have had any history of foot ulcers; however, the lack of sensation puts their feet at a higher risk of injury. Hence, the repetitive stress of walking can, by itself, result in damage to their feet. They would not feel the pain caused due to small cuts, burns, etc. Since the only internal system providing the protective sensation has been lost, external behavioral changes have to be taught to the patient in order to avoid injury to the feet. Preventive measures such as avoiding barefoot walking and cleaning their feet regularly have to be stressed and the patient should be made aware of common foot problems, viz. callus formation, redness and swelling. People with insensate feet often experience higher pressures under their feet than normally sensate people do. The first line of defense for such patients is a quality sports shoe, as long as any deformity can be accommodated. Sports shoes can reduce plantar pressures compared to conventional shoes and can also reduce the accumulation of callus. There will, however, be few patients who cannot wear sports shoes because of their need for more cushioning in certain locations under the foot or due to their significant foot deformity.

B

C Figs 2A to C Examples of footwear for diabetic patients in risk category 0 (With permission “The Diabetic Foot – A Clinical Atlas” Sharad Pendsey)



Prescribing Footwear    181

A B

C Figs 3A to C  Footwear for diabetic patients in risk category 1

For example, toes that are dorsally prominent because of clawing or hammering will need additional space in the toe box. In such cases, the patient will need an extra-depth shoe or a super-extra-depth shoe, which have, respectively, approximately 1/4 and 1/2 of additional space in the toe box. This space can accommodate prominent toes when a normal insole is used, or, it can also allow the use of a thick insole or orthosis with features that redistribute pressure or unload regions of focal pressure in patients without dorsal deformity but with plantar prominences. Certain deformities will need to be accommodated by stretching a specific region of the shoe upper, using special tools. Some shoes are designed to stretch easily when heated. In many instances, a thick “off-the-shelf” insole without customization or modification will suffice, but in a patient who is at least moderately active or has at least moderate foot deformity, customization of the insole will be required. Low-heeled footwear with soft insoles made of materials such as MCR or polyurethane foam, which reduces the pressures under the feet, can also be recommended for patients in this risk category. These materials are available in precut insoles or in sheets of material that can be cut to the proper size. A nylon covering helps to minimize shear force between the insole and the foot, and the soft cushion helps to reduce vertical (normal) force. Figure 3A to C shows few foot­wear models that can be prescribed for patients in this category.

Risk Category 2 (The Diabetic Patient with An Ulcer/Deformity) Patients in this category have loss of sensation along with a deformity in their foot. Deformity results in the concentration of stress in that small area of the foot. The added stress usually occurs in a part of the foot that is not accustomed to

additional pressure, resulting in injury. Surgical correction of a deformity can result in moving a diabetic patient to a lower risk category. For patients in this category, custom footwear made from a plaster model of the foot can be used to accommodate the abnormal shape caused due to the deformity. The physician’s prescription again plays an important role in this case, to avoid a communication gap between the physician and the shoe fabricator, in order to produce the effective custom footwear suitable for the patient. The physician has to inform the shoemaker of any special observation that might need to be considered in the construction of the shoe. For example, a shoemaker who sees a unique bulge on the plaster model of a foot does not know whether that bulge represents soft tissue that can be compressed or a rigid bony deformity requiring that the upper of the shoe be molded around it. Figures 4A to D depict some of the custom footwear models that a diabetic patient in risk category 2 can wear to prevent further injury to the feet and/or reduce pressure in the foot. For most common deformities, such as clawed toes, depth footwear appropriately fit and modified by a pedorthist can also provide the necessary accommodations. This footwear may be essentially an athletic shoe with an additional 1/4 or 1/2 inch of depth throughout the shoe. This provides the extra volume needed to accommodate deformities, including hammertoes, clawed toes and Charcot deformities, or edema. Depth footwear come in wide range of shapes and sizes to accommodate any foot except those with severe skeletal distortion (Figs 5A and B). With rare exceptions, shoes should not be worn at all by diabetic patients with active ulcers, except special prescription shoes, which isolate regions of the foot completely from

A

B

C

D

Figs 4A to D  Footwear models for diabetic patients with neuro­pathy and ulcer/deformity: (A) Rocker bottom; (B) Anterior orthowedge; (C) Posterior orthowedge; (D) Half shoe



182    Contemporary Management of the Diabetic Foot

A

B

Figs 5A and B  Indepth footwear

Fig. 6  Footwear model for diabetic patients in risk category 3

weight bearing. Some form of offloading such as a cast or other device must be immediately employed until the ulcer is healed. However, when an ulcer is healing, the physician should start deciding on the footwear details that the patient will need after the ulcer has healed; any delay in providing definitive footwear can result in rapid re-ulceration in the same or associated area.

trial-and-error process, and it is not unusual for a new pair of shoes to require several such modifications before they are satisfactory. An example of footwear that can be prescribed for patients in this category is shown in Figure 6. In addition to the above-described risk categories, it is also important to keep in mind the severity of plantar pressure in the foot of the diabetic patient. Table 3 provides the essential guidelines that can be employed while prescribing footwear for a patient with plantar pressure problems.

Risk Category 3 (The Diabetic Patient with a Recently Healed Ulcer) People in category 3 not only have loss of sensation but also have a history of previous foot ulceration. The skin and underlying soft tissues are more easily reinjured in areas where previous damage has occurred. Ulcers most often reappear at the sites of previous ulcers. Scarring makes tissues less strong and flexible and more likely to breakdown, particularly as the result of shear, a force that is applied parallel to the skin surface. Soft tissues withstand shear by one layer of tissue gliding over adjacent tissues. Scar binds tissue layers together and prevents this gliding action. As the ulcer heals, the first few weeks of return to normal ambulation is a period of very high risk, and it may be preferable to transition the patient into new therapeutic footwear by providing a very well-cushioned walking splint or orthopedic walker to enable the fragile new tissue to consolidate. The physician must also educate and convince the patient that wearing therapeutic footwear is critical for preventing another ulcer and possible amputation. The footwear should be of correct size with appropriate insoles to reduce the pressure on the foot, but care must be taken to ensure that this does not result in excessive pressure on the dorsum of prominent toes. Unfortunately, the prescription and dispensing of therapeutic footwear is still very much a

Footwear Prescription after an Amputation On several occasions, owing to reasons such as uncontrolled blood glucose levels, inappropriate foot care practices and poor compliance in wearing the prescribed footwear, foot ulcerations often lead to some form of amputation. The great toe amputations are more common in diabetic patients; nevertheless, amputations may also involve the midfoot and hindfoot, which are all categorized as below-knee amputations. In some cases, above-knee amputations may be performed to save the life of the patient. Patients with amputations require special footwear to accommodate the limb comfortably and distribute the weight-bearing pressures evenly. Prescription footwear for several types of amputations and disarticulations involving toe, ray, transmetatarsal, tarsometatarsal and midtarsal are described below. Although the pedorthic care for each type is different, several objectives are common to all: • Unless the amputation is extensive and a custom-made or shortened shoe is used, some type of shoe filler is needed for the portion of the foot that has been amputated. In most cases, the filler can be incorporated into the orthosis. • Amputation of a part of the foot often results in uneven patterns of weight-bearing on the remaining part of the foot. Just as with the intact diabetic foot, any areas



Prescribing Footwear    183 Table 3  Guidelines for prescribing footwear for patients with plantar pressure problems Prior plantar ulcer/ deformity/callus/high plantar pressure

Activity Low

Moderate

High

No

Sports shoe with a soft insole

Sports shoe or extra-depth shoe with a thick insole

Sports shoe or extra-depth shoe with a thick insole; consider rocker bottom

Yes/moderate

Sports shoe or extra-depth shoe with a thick insole

Sports shoe or extra-depth shoe with a thick insole, metatarsal pads or bar; consider rocker bottom

Sports shoe or extra-depth shoe with a thick insole, metatarsal pads or bar, rocker bottom; consider custom insole

Yes/severe

Customized upper or custom shoe, thick insole; consider custom insole

Customized upper or custom shoe, thick custom insole with reliefs, rocker bottom

Customized upper or custom shoe, thick custom insole with complex reliefs, rocker bottom

of excessive pressure must be eliminated, and even distribution of weight-bearing must be maintained. • After amputation of a part of the foot, special care must be taken to protect and accommodate the remaining portion of an at-risk foot. The presence of skin grafts, scar tissue, or any post-surgical complications must also be taken into consideration when one is providing prescription footwear for a partial foot. • When part of the foot has been amputated, a natural gait pattern is no longer possible. The addition of an appropriate type of rocker sole can often improve the gait pattern after an amputation. The proper footwear for a partial foot is determined by the extent of the amputation. If the metatarsal heads remain intact, shoe size does not change. Only when one or more metatarsal heads have been removed, the patient will need a shorter shoe (i.e. smaller size footwear).

Fig. 7  Postoperative shoe

Postoperative Shoe This shoe is generally open-toed, with uppers made of canvas or nylon mesh; the upper may be padded for additional comfort (Fig. 7). It has a wide forefoot opening with either hook-andloop straps or lace closures and can accommodate extreme swelling and the bulkiest dressings.

Controlled Ankle Motion Device For the patient who can walk, but has to maintain a fixed ankle position or limit ankle motion, the controlled ankle motion device can provide the necessary stability and support while allowing a comfortable, relatively natural gait pattern. This device is essentially a postoperative shoe to which mediallateral uprights and a posterior Achilles plate have been added (Fig. 8). The foot and ankle are held in place with wide hook-andloop straps, and the ankle joint may be held in a fixed position

Fig. 8  Controlled ankle motion device



184    Contemporary Management of the Diabetic Foot or be allowed to move within a limited range. A cushioned liner provides pressure relief, and a rocker sole allows a more natural walking gait. A total-contact orthosis inside a controlled ankle motion device can be used for wound healing as an alternative to total-contact casting, allowing the patient easier access to view, dress, and bathe the wound.

Toe and Ray Amputations Patients with these amputations will require well-constructed shoe filler, which allows the patient to wear a full-length shoe. The shoe should have a strong medial counter for stability, especially if the first ray has been removed, and a soft, moldable upper to protect and accommodate the remaining foot.

Transmetatarsal Amputations A shoe with a Blucher opening and a long medial counter can best control the remaining foot and help to decrease soft tissue shear. The upper should be made of a soft, moldable leather to accommodate and protect the remaining foot. A custommade shoe is generally not necessary for a transmetatarsal amputation because enough of the foot remains to keep a shoe on with the aid of filler; however, a smaller size shoe might be appropriate if the patient finds it cosmetically acceptable.

Tarsometatarsal and Midtarsal Disarticulations A high-top shoe is best because it can most effectively accom­ modate the foot in the shoe and provide the control necessary to prevent equinus contracture. A strong counter can also aid in providing control while improving medial and lateral stability. A wedge sole will provide a broader base of support, and a shorter shoe size will decrease the resistance to roll over on toe off and aid in propulsion. For the smaller remaining foot, a custom-made shoe will best meet the treat­ ment objectives by providing total accommodation of the foot.

Compliance in Wearing Therapeutic Footwear The most advanced and well-designed prescription foot­ wear can be effective only if it is worn by the patient on a continuing basis. However, a number of studies have

shown that consistent use of such footwear is rarely the case and patients often show poor compliance with wearing therapeutic footwear. Patients can be often compliant for most of the time; however, they fail to be so during a holiday or a special event such as a wedding, during which they might feel to wear more attractive, often unsafe, footwear. Some patients might also show reluctance in buying the prescribed footwear. This is due to the general unattractive appearance, cosmetic unacceptability, limited shoe colors and styles and cost. Some patients also prefer wearing their routine slippers while indoors. These issues raise the risk of re-ulceration, which might in turn lead to increased lower extremity amputations. Hence, providing effective education on wearing the therapeutic footwear is necessary to ensure that the patients wear them regularly at all times. In addition, it might be reasonable for the prescribing physician and the pedorthist/shoemaker to focus on the following issues in this context for better outcomes: • The importance of footwear and the role it plays in reducing ulceration and prevention of amputation have to be stressed to the patients and their family members. • Patients must be made to wear the prescribed footwear at all times so as to maintain compliance in wearing; barefoot walking at any time must be strictly avoided. • Shoemakers can concentrate on aspects such as produc­ ing attractive therapeutic footwear, with several colors and styles so that the patient can have a choice. • Another important aspect is that the patient must be made aware of the cost of the prescription footwear.

SUGGESTED READING 1. Bowker JH, Pfeifer MA. Levin and O’Neal’s The Diabetic Foot. In: Janisse DJ, Coleman W (Eds). Pedorthic care of the diabetic foot: correlation with risk category, 7th edition. 2008; Philadelphia: MOSBY Elsevier, pp. 529–46. 2. Edmonds ME, Foster AVM, Sanders LJ. A Practical Manual of Diabetic Footcare. 2004; United Kingdom: Blackwell Publishing. 3. Reiber GE, Smith DG, Wallace CM, et al. Footwear used by individuals with diabetes and a history of foot ulcer. J Rehab Res Dev. 2002;39:625–32. 4. Vijay V, Sivagami M, Saraswathy G, Gautham G, et al. Effectiveness of different types of footwear insoles for the diabetic neuropathic foot. A follow-up study. Diabetes Care. 2004; 27:474–7.

CHAPTER

Patient Education and Empowerment in the Prevention and Management of Diabetic Foot Disease

21 William Jeffcoate

INTRODUCTION The aim of education is to ensure that people acquire new knowledge. To acquire new knowledge, they need more than just teaching: they need to be helped to learn. In the case of disease and health care, the ultimate aim of education is also to enable people to use the new knowledge to change their behavior so that they can either (a) prevent the onset of new disease or (b) limit its effects. These effects include both the impact of the disease on the body and the capacity of the sufferer to cope with it.

TEACHING AND LEARNING Aspects of Teaching that Encourage Learning New Information must seem Relevant to the Patient People are more likely to learn if they believe that information they are given is relevant to them. People with uncomplicated diabetes are unlikely to think that they are at particular risk of developing foot disease, and will often not remember any details of foot care that they are taught. Many will also forget that anybody ever made the effort to teach them at all, which is one reason for the apparent patchiness of foot care education. In contrast, those who have been told that they are at increased risk of ulceration (Tables 1 and 2) are more likely to appreciate the relevance of any teaching which is offered and hence more likely to learn. Those who have already suffered an episode will be keen to do what they can to prevent a recurrence and will, in general, also be more likely to not only acquire new information but also to change their foot protection behavior.

PANEL 1 Factors that limit the effect of education on increasing knowledge • The information is not seen by the patient as relevant to them. • The information conflicts with information received from other sources. Factors that limit the effect of education on changing behavior • The suggested change in behavior conflicts with other pressures imposed by the person’s culture or circum­ stances. • The increased knowledge may have an adverse effect on a person’s well-being by inducing fear, frustration, selfblame or depression.

Factors that Limit the Capacity to Absorb New Information The new information must also be relevant to the culture, beliefs and personal circumstances of the patient. Advice concerning footwear, for example, must be tempered by knowledge of what is acceptable both to the patient, their family and their culture. When advice conflicts with other, sometimes deeply ingrained, influences on what people do, it may be very difficult for them to do what they are told. In this respect “non-compliance” can be regarded as a normal aspect of human behavior. The patient may also become aware of conflict between the advice and information received from different health



186    Contemporary Management of the Diabetic Foot Table 1  Factors which increase the likelihood of new ulceration Factors which put the foot at increased risk of traumatic injury 1.

Distal sensory neuropathy with loss of protective sensation

2.

Distal motor neuropathy with impaired function of the small muscles of the foot and abnormal gait

3.

Immobilization caused by comorbidity: e.g. heart failure or stroke, with or without hospital admission

4.

Comorbidities such as impaired vision

Factors which thin the skin and make it more likely to ulcerate: ‘preulcerative skin’ 1.

Peripheral arterial disease:

2.



Macrovascular



Microvascular—structural (e.g. basement membrane thickening) and functional (abnormal vasomotor regulation caused by neuropathy)

Chronic renal failure and dialysis

Exposure to other factors that break the skin 1.

Accidental trauma

2.

Tinea pedis

Table 2  Classification of risk status 1.

No increased risk

2.

Increased risk: The presence of a single predisposing factor (Table 1)

3.

Greatly increased risk: •

More than one predisposing factor



Chronic renal failure



Previous foot disease

care professionals, as well as other sources. The result is that they will place greater trust in advice received from one over the others, and the reasons for making this choice will be multiple. The choice may not always be the best. Another factor to be considered is the response of the patient to the realization or belief that they are at increased risk of developing new disease. Fear of foot disease may induce some to do their utmost to reduce their personal risk, whereas other may opt to do little or nothing, either through denial or through fatalism. This bimodal response from compliance to non-compliance may also be seen in people who have observed earlier limb loss in an older relative, or in those who have had a recurrence of ulceration despite having tried their hardest to prevent it. Fear, frustration, self-blame and depression may moderate a person’s capacity to change their behavior.

Delivery of Information In order to overcome the potential barriers imposed by these factors, it is accepted that teaching requires more than just the provision of printed pamphlets. Pamphlets may be used to supplement other forms of education in the management of chronic diseases but achieve little on their own. Teaching should ideally be: • Delivered face-to-face • Delivered on a one-to-one basis • Targeted to take account of an individual’s particular needs, fears, and other social pressures • Responsive to the individual’s questions • Supplemented by information delivered in a different medium that reinforces information that has been delivered orally—whether by use of leaflet (with relevant details highlighted), or DVD or introduction to a relevant website • Supplemented, if possible and appropriate, by group interaction • Reinforced at a later date, whether face to face, or by phone, email, text or social networking medium • Reinforced by feedback relating, for instance, to results of any assessment tool, whether of knowledge or behavior. It is also accepted that people need to be given information in “bite-sized chunks” because there is a limit to what can be remembered from any single teaching session. A final detail is that, in general, the content should stress guidance which is positive in content (“do this”, “do that”) rather than negative (“don’t do this”, “don’t do that”). People are more likely to respond to instructions that are positive. Much foot care information is delivered informally in clinical practice, during the course of clinical consultations with specialist nurses, podiatrists and doctors. It will often be triggered by points that are raised by the patient during the course of unstructured conversation, and hence concerns a topic in which they are already interested. This is probably the most important and effective means of helping the person with diabetes acquire new knowledge and should be the cornerstone of routine care—even though it is impossible to assess its effectiveness. What is a little less certain is if there is benefit to be derived by the creation of formal education packages for people at increased risk of new ulceration.

Linking Foot Care Education to Routine Assessment of Foot Care Risk A person with diabetes should have their risk assessed by clinical examination every year. A routine part of this practice should be to explain to the person why the examiner is feeling for foot pulses and testing sensation. It should also be routine that the person is told the result and whether they are (a) at no increased risk, (b) at increased risk or (c) greatly increased



Patient Education and Empowerment in the Prevention and Management of Diabetic Foot Disease    187 PANEL 2 Minimal information that should be delivered when a person is found to be at increased risk during routine examination • The patient should be informed that they are at increased risk and that extra attention should be paid to protective foot care. • If the facilities exist, they should be referred for assessment and regular follow-up by an expert podiatrist or other health care professional. • Specific advice about foot care should be given before they go on holiday. In addition, the person who is found to have neuropathy should be warned • Of the very small risk (1%) of their developing an acute Charcot foot. • Which is a condition in which they might get unexplained inflammation in the foot. • And if this happened, they should see their doctor and ask if it has been caused by an acute Charcot foot.

risk (Table 2). When they are told that they are at increased or greatly increased risk, this should be linked to their being asked if they are already receiving, or would like to receive, expert assessment and surveillance (if it is available). In addition, people need to be given two key messages and these are: • That if ever they get a new problem with their feet, they should expect expert assessment at the earliest possible opportunity, and • That those people who have neuropathy should be aware of the remote possibility of developing an acute Charcot foot.

Education Relating to the Acute Charcot Foot The acute Charcot foot (or acute neuropathic osteoarthro­ pathy) affects only approximately 1% of people with distal neuro­ pathy but when it occurs, it can cause irreversible deformity and amputation may become necessary. This risk is increased by the fact that the majority of generalist doctors and nurses will fail to make the diagnosis when the condition occurs. The delay in diagnosis may be for weeks or months, and undoubtedly worsens the risk of major deformity and limb loss. If, however, the patient with neuropathy has been warned about the (remote) possibility and, ideally, given a brief information sheet about the condition, they will be able to suggest the diagnosis to their usual carer if they develop suggestive symptoms.

Potential Role of Education Packages The term “package” is taken to apply to a specially designed session, or intervention, that is specifically intended to enhance knowledge of foot disease and/or to change foot care behavior. Packages could, in theory, be created for people with different categories of risk.

Education Packages for People with Diabetes but Without Increased Risk The chances of suffering new ulceration are small in this group and although people need to know of the possibility, there may be little to be gained by providing structured education, but this is yet to be established.

Education Packages for People at Increased Risk of Ulceration People with a single risk factor are approximately three times more likely to develop a new ulcer in the succeeding 12 months, when compared to those without increased risk, and it is possible that an educational package may help reduce this difference. Before embarking on the work implicit in a structured program for the very many people who are identified as being at increased risk (approximately one third of all people with diabetes have neuropathy), it should first be shown to be effective. The problem is that prospective trials of an intervention require very large numbers if endpoints (i.e. new ulcers) are relatively infrequent in the population being studied. Such trials may never be possible if “hard” (clinically relevant) endpoints are used and the efficacy of the intervention may therefore always be uncertain. The only alternative is to undertake trials that use surrogate measures (such as change in knowledge alone) but there will always remain a doubt about the true effectiveness.

Education Packages for People at Greatly Increased Risk Those with a recently healed foot ulcer have an up to 40% risk of developing a new foot problem within 12 months. It is obvious that strenuous efforts should be made to reduce new ulcer incidence but the evidence to support the use of specific education packages is currently thin. Randomized trials and systematic reviews have so far failed to confirm that intensive education will actually reduce the incidence of new ulceration in this group. One reason for this is that such studies will very likely be conducted in centers that already provide expert multidisciplinary management care and it is because of this that a designated package may therefore have little to add to the delivery of essential foot care advice at repeated clinical consultations. On the other hand, a positive result derived from intervention trials conducted in



188    Contemporary Management of the Diabetic Foot non-expert centers may not be able to distinguish between the effectiveness of the educational package from increased professional intervention in general. It is also possible that biological factors may predominate in the very high-risk groups and that even if successful; efforts to change foot care behavior may have little impact in this population. Nevertheless, there is a suggestion that while the delivery of a designated education program to those at very high-risk may not reduce the incidence of new ulceration, it may result in a reduction in the incidence of amputation, presumably because the patient learns the importance of seeking expert help at the earliest opportunity and that this leads to an improved outcome. The value of an education program in this group requires more research. Despite these general conclusions, there is evidence of the effectiveness of preventive care (including both education and surveillance) in one particular group of patients at high-risk: people on dialysis. A single small randomized trial has shown that the introduction of routine podiatric care produced a beneficial effect that was marked and prompt in this population. While these observations need to be confirmed, there is much to be said for considering the introduction of foot protection strategies in this very vulnerable group.

Education for the Person with Active Foot Disease Education about their condition is an essential part of management of people with active disease, even though some health care professionals may fail to address this as carefully as they should. There are two broad types of active disease: ulceration and the acute Charcot foot. • The person with active ulceration needs to have the basic causes and treatments explained to them as well as the likely outcome. On the basis of this, the clinician and patient should agree the management plan together, whenever possible. This plan needs to be discussed again at subsequent visits, especially when the ulcer seems unresponsive to the interventions given. • In addition, the person who has an acute Charcot foot needs to understand the difficulties facing the clinician with particular reference to deciding when the disease is in remission. The more a patient is involved in the decision-making process, the easier it is for them to accept the prolonged privation and restricted activity that will be imposed upon them.

BEHAVIOR CHANGE AND EMPOWERMENT  As stated above, the ultimate aim of health care education is to induce people to change their behavior so that they can either (a) prevent the onset of new disease or (b) limit its effects, including both the impact of the disease on the body and the capacity of the sufferer to cope with it. People may

change their behavior simply as a result of new knowledge, but this is relatively unusual and change is more likely in those who are encouraged to acquire the power to do it. In this respect, health care professionals may need to consider how empowerment of patients can be achieved by changes to the nature of the professional-patient relationship. Such changes may focus on the way education is delivered, with the patient encouraged to be more of a partner in the process. This should be an integral part of the opportunistic discussion that takes place during a routine consultation, with every professional encouraging dialogue with debate about the options for intervention and the possible outcome, especially in a field where the evidence for the effectiveness of standard treatments is not good.

ASSESSING THE EFFECTIVENESS OF EDUCATION A variety of measures can be used to assess the effectiveness of educational interventions.

Exposure to Education The simplest measure is documentation of the fact that education has been delivered. This may not, however, be particularly reliable unless specifically recorded.

Change in Knowledge While the ultimate aim of education is to change behavior and clinical outcome, the intention is that this be achieved by improving knowledge. Hence a person’s knowledge of the principles of foot care can be used as a surrogate measure of the effectiveness of the process. The problem in devising such an assessment is that different professionals have different views on what people need to know and no universally validated questionnaire exists. The knowledge that needs to be acquired will also vary with a person’s individual risk. A person at high-risk of ulceration should learn the need to adopt protective foot care behavior for as much of the time as possible. On the other hand, it remains to be established if the person with normal blood flow and sensation needs to change their behavior at all and it could be argued that in this group, their principal need is to have a regular foot check to ensure that they remain at low-risk.

Change in Behavior Since behavior change is the aim of the educational exercise, it makes sense to assess foot care behavior directly. A questionnaire has been described which was based on opinion from a large number of foot care professionals as well as users, validated and has been used to demonstrate an improvement in foot care behavior in the intervention group



Patient Education and Empowerment in the Prevention and Management of Diabetic Foot Disease    189 in a randomized, controlled trial of education in a high-risk population. This improvement in foot care practice was not, however, associated in this study with a reduced incidence of ulceration.

Change in Clinical Outcome The ultimate aim is to reduce the incidence of new ulceration and to improve its outcome. Improved outcome is usually documented in terms of either healing or amputation, whether minor (below the ankle) or major. Any trial that uses clinical outcomes to determine the effectiveness of an educational intervention is inherently dependent on the number of outcome events in the control group. If the anticipated number of events in the control group is low as, for example, in a study of an unselected population of people with diabetes in which the incidence of new ulcers is of the order of 2% per year, it will require thousands of participants in the trial in order to confirm a statistically significant difference between groups. If, on the other hand, the incidence of events is quite high (as in people with a recently healed ulcer), then it is possible that the biological factors that put a person at such high-risk will far outweigh any impact of changing patient behavior through education. Those who have studied the effect of educational packages in high-risk groups have, however, failed to establish any benefit in terms of new ulcer incidence. Despite this, a significant reduction in the incidence of major amputation has been reported in the intervention group in one study. This suggests that while the education program had no impact on ulcer incidence, it appeared to improve ulcer outcome. If so, this may be because one aspect of the education program was to encourage early self-referral for assessment. One other study was able to demonstrate improved outcome in a particular high-risk group: those receiving hemo­dialysis. Thus, McMurray et al. were able to show a highly significant reduction in the incidence of amputation in those who in the intervention group had received specialist protec­ tive surveillance and treatment from a specialist podiatrist. This important observation should be confirmed PANEL 3 Assessing the structure and effectiveness of education • Documenting that education (by suitably trained professionals) occurs • Change in knowledge (informal query or questionnaire) • Change in foot care behavior (informal query or validated questionnaire) • Change in clinical outcome (e.g. new ulcer onset, incidence of amputation) • High (or improved) satisfaction, mood and ability to cope with disease and the disability it causes.

because of its enormous implication for routine management of people with end-stage renal disease.

Change in Satisfaction, Mood and Ability to Cope with Disease and Disability While a reduction in ulcer incidence or amputation is the main clinical aim, it is also important to pay attention to the need to help the patient cope with their disease and disability. The prevalence of depression is high in people with foot ulceration, and their quality of life is similarly reduced. There are no data available to demonstrate the benefit packages designed specifically to address these factors, but it is generally found that educational packages are associated with increased satisfaction.

Systematic Review of Education in the Diabetic Foot A Cochrane review concluded that the available studies were generally of poor quality and that the evidence of effectiveness of educational interventions was limited. Cochrane reviews consider only randomized controlled trials and trial design poses considerable barriers in the field of the diabetic foot. It is, therefore, quite likely that the scientific evidence of benefit will remain thin, even though patient education would likely remain to be a crucial aspect of good management.

CORE EDUCATION OF HEALTH CARE PROFESSIONALS In practice, the education of health care professionals should be a greater priority in this area than the education of patients. It is widely acknowledged that the diabetic foot is an unrewarding field and one which tends to be ignored by health care professionals. Few professionals receive systematic teaching on the causes and management of foot disease and when the cost and suffering associated with the condition are considered, the investment in research is also disproportionately low. The result is that few health care professionals are equipped with the skills necessary to assess and manage foot disease. Health care professionals need to learn that greater emphasis needs to be placed on the problem, with four simple basic targets. These are that health care professionals should: I. Examine the feet of every person with diabetes once each year in order to determine their risk status II. Refer those at increased risk to a local expert to provide appropriate preventive surveillance and education III. Examine the feet of people with diabetes when they present with any clinical problem IV. Always seek expert advice as quickly as possible when a person with diabetes develops symptoms or signs relating to the foot.



190    Contemporary Management of the Diabetic Foot

CORE EDUCATION OF PEOPLE WITH DIABETES People with diabetes should know: • That they should have their feet examined each year to determine whether they are at increased risk, • That they should be told the results of this routine examination and if they are at increased risk, they should be referred for expert assessment • That if they are found to have neuropathy, there is a remote risk that they may develop an acute Charcot foot and if they ever develop unexplained inflammation of their foot, they should remind their doctor of this possibility, and • If they ever develop symptoms or signs relating to the foot, they should seek urgent advice.

CONCLUSION The acquisition of knowledge by the patient is key to achieving a beneficial change in foot care behavior. Most of the necessary educational input is unstructured and delivered during the course of routine care. There is currently little evidence to prove that the adoption of specific educational packages helps reduce ulcer incidence. The results of one study do, however, suggest that even though it may not be possible to prevent all new ulcers, the outcome is improved if they gain access to expert advice at the earliest possible opportunity and hence people with diabetes need to learn the importance of early expert assessment.

AFTERWORD The author is very aware of the fact that this chapter is delivered in a didactic style and (as has been emphasized within it) people do not learn easily when information is presented in this way. The content is also based largely on opinion and the author’s opinions may not always be necessarily correct, or in wide agreement. But in the absence of robust evidence, the chapter has been written with the aim of increasing awareness of some of the issues involved in the practice of effective education in this field. Readers are encouraged to explore these issues in discussion with other health care professionals as well as with people who have suffered with foot disease.

SUGGESTED READING 1. Dorrestein JA, Kriegsman DM, Assendelft WJ, et al. Patient education for preventing diabetic foot ulceration. Cochrane Database Syst Rev. 2010;12:CD001488. 2. McCabe CJ, Stevenson RC, Dolan AM. Evaluation of a diabetic foot screening and protection programme. Diabetc Med. 1998;15:80-4. 3. Nottingham Assessment of Functional Footcare. http://www. nottingham.ac.uk/iwho/research/publishedassessments.aspx 4. Radford K, Chipchase S, Jeffcoate W. Education in the management of the foot in diabetes. In: Boulton AJM, Cavanagh PR, Rayman G (Eds). The Foot in Diabetes, 4th edn. London: John Wiley & Sons Ltd; 2006. 

CHAPTER

Establishing a Multidisciplinary/ Interdisciplinary Diabetic Foot Clinic

22 Kristien Van Acker

Teamwork makes everything possible even the impossible* * Diabetic Foot: a clinical atlas

INTRODUCTION The best-known foot clinics worldwide were created one step at a time, beginning with a basic model, as described below, and gradually developing into centers of excellence. This “step-by-step” philosophy can help newcomers in the field to meet the challenge of starting up a diabetic foot clinic from almost nothing. This concept was reinforced by the step-bystep programmes, supported by the International Working Group of the Diabetic Foot (IWGDF) and the World Diabetes Foundation (WDF) in 2003, where developing countries were able to install the clinics with a huge success.

History The treatment of wounds is an ancient area of “specialization in medical practice”. Its origin traces back to ancient Egypt and Greek literature. The most profound advances in the field came with the development of microbiology and cellular pathology in the 19th century. The diabetic clinic at the Deaconess Hospital in Boston can already be considered as a first multidisciplinary approach in diabetic wound care, remembering that the discovery of insulin was only a few years ahead! The teaching of diabetic foot care was considered so important, that by 1928 they had assigned one graduate nurse and two pupil nurses to that duty. From the moment we use the term “specialization in different fields of wound care”, we can speak about multi­ disciplinarity.

In the late 1980s and early 1990s “multidisciplinary diabetic foot clinics” were installed by pioneers, like Michael Edmonds, Per Holstein, Karel Bakker and Andrew Boulton. A new generation of younger foot specialists started working in Europe and was inspired and very active in the Diabetic Education Study Group (DESG). The support was further established by the IWGDF with the consensus documents. The International Working Group on the Diabetic Foot together with the Diabetic Foot Society of India (DFSI) and the Muhimbili University College of Health Sciences Dar-es Salaam, Tanzania (MUCHS), International Diabetes Fede­ ration (IDF) and World Diabetes Foundation (WDF) had initiated in 2003 a foot care project called “Step by Step improving diabetic foot care in the developing world”.

Rationale and Evidence-based Data for Interdisciplinary Teams for Diabetic Foot Care The International Consensus of the Diabetic Foot, edited by Karel Bakker first launched in 1996 and the 4th edition recently launched at the International Diabetic foot Meeting in May 2011 in Noordwijkerhout (Netherlands) strongly recom­mends multidisciplinary foot care team for foot prob­ lems especially diabetic foot. Michael Edmonds published for the first time in 1986, “The role of a specialized foot clinic”, in which he showed increased salvage rate of the diabetic foot by starting multidisciplinary diabetic foot clinic. Beside many others, the group of Gerry Ryman and Neil Baker in a follow up study of 11-years (1995–2005) in a defined population from UK, showed that by improvement in foot care services including multidisciplinary teamwork can



192    Contemporary Management of the Diabetic Foot How to establish a diabetic foot clinic?

achieve significant reduction in total and major amputation rates. Total amputation in people with diabetes fell by 70%, from 53.2 to 16.0, and major amputations fell by 82%, from 36.4 to 6.7 (expressed as incidence per 10,000 people with diabetes).

HOW TO ESTABLISH A DIABETIC FOOT CLINIC? THE STEP MODEL: FROM MINIMAL TO MAXIMAL

Fig. 1  Minimal model of foot clinic (Courtesy: Max Spraul, Noordwijkerhout, 1991)

Basis of this Model Some years ago, the IWGDF convened a round table meeting to discuss the principles of organizing a diabetic foot clinic. The proceeds of this meeting were published in Time to Act (publication of IDF) in the year 2005, which was dedicated to “Diabetic Foot”. The idea of the working group was to make a distinction between three models: The minimal model or basic model, the intermediate model, and the centers of excellence also called tertiary referral centers. In practice, the gradual process towards excellence is initiated by a dedicated individual, “local champion”, working with a very small team. More often than not, this person drives the project for many years and assumes much of the responsibility from the start. Typically, the project leader is able to motivate and inspire people with diabetes and health care professionals; set up facilities and organisational structures; establish attainable goals; recruit, train and retain team members; establish contacts with administrative, governmental and health care bodies in order to ensure support for and the survival of the foot clinic, and is able to raise the funding required for salaries, materials and equipment.

In the minimal model, the team consists of a doctor, a nurse and/or a podiatrist. It is desirable for one or all of these team members to visit a recognised center of excellence to gain practical experience (Table 1).

Table 1  The minimal model Staff

Doctor Nurse and/or podiatrist

Aim

Prevention and basic curative care

Patients

Own population

Setting

General practitioners’ office, health center or small regional hospital

Facilitating elements

Close collaboration with a referral center

Equipment

Scalpel handles, scalpel blades, nail nippers, nail files, 10 g monofilaments, dressings (simple gauze), bandages, antiseptic, instru­ment-cleaning equipment (Fig. 2)

Step 1: The Minimal Model The goal of the minimal model foot clinic is to prevent diabetic foot problems and stop small problems from becoming diabetic foot catastrophes. The model was well described by Max Spraul at the International Symposium on Diabetic Foot held at Noordwijkerhout (Netherlands) 1991 (Fig. 1). The minimal model foot clinic offers: • Foot examination and detection of foot problems such as callus, corns, nail problems, athletes foot, small wounds • Treatment of the above-mentioned foot problems • Preventative care with an emphasis on education in foot care, footwear and trauma prevention. If more serious and complicated problems are found, the patient should, if possible, be referred to a center that is equipped to deal with problems. The setting can be in a general practitioners’ office, a community clinic or a small regional hospital.

Fig. 2  Podiatry Instruments



Establishing a Multidisciplinary/Interdisciplinary Diabetic Foot Clinic    193

Step 2: The Intermediate Model

Table 2  The intermediate model

The goal in this phase is to improve the groundwork in preventive and basic care and, in addition, organize appro­ priate care for all types of diabetic foot problems

Staff

•  Diabetologist or general physician •  Surgeon •  Nurse and/or podiatrist •  Orthotist

The intermediate model offers: • Foot examination and detection of foot problems such as callus, corns, nail problems, athletes foot, small wounds • Treatment of foot problems • Preventive care with an emphasis on education in foot care, footwear and trauma prevention • In addition, intermediate model offers treatment and evaluation of all types of ulcers with or without infec­ tion and offer services like offloading, debridement, amputation, skin grafting and provide preventive footwear and also orthotic services and education on self-care of ulcers and infections.

Aim

 revention and curative care for all types of patients P and more advanced assessment and diagnosis

Patients

From the regional catchment area of the hospital with possibly some referrals from outside the region

Setting

Hospital

Facilitating elements

•  Motivated coordinator to inspire team •  Exchange experience with other centers •  Staff meetings to discuss diabetic foot patients •  Active collaboration with other departments within the hospital •  Active collaboration with extra-mural facilities (GPs, nursing homes, etc.)

The Intermediate foot clinic works as a referral center for other minimal model foot clinics as well as for other practitioners. For the Intermediate clinic staff requirements are increased (Fig. 3). One member of the team fulfils the role of coordinator and has the responsibility of absorbing new and well-motivated colleagues, including: • Diabetologist (or other doctor with special interest in diabetes) • Surgeon (general, vascular, orthopedic, plastic) • Nurse and/or podiatrist • Orthotist/shoemaker

Equipment

Monofilaments, biothesiometer, (handheld) Doppler, inkpad for footprints, operating theater, full set of podiatry instruments including tissue nippers, probes, X-ray, lab facilities for microbiology, blood testing, etc. (Fig. 4)

The intermediate diabetic foot clinic is usually located in a hospital setting. Exchange of experience with other diabetic foot centers is important.

Fig. 4  Basic diagnostic equipment

Fig. 3  An example of staff members of Intermediate model (Courtesy: Diabetic foot clinic—Kristien Van Acker-Bornem 2005)

Regular staff meetings to discuss patients and ward rounds are important aspects of the diabetic foot team. Relationships with hospital administrators and with staff from other departments within the hospital should be carefully fostered. Links with aligned facilities located outside the hospital, such as the general practitioners’ office, nursing homes, and rehabilitation centers are important and the intermediate foot clinic should provide support to community health care practitioners working in isolation with diabetic foot patients (Table 2).



194    Contemporary Management of the Diabetic Foot

Step 3: Centers of Excellence and Tertiary Referral Center The goal of the diabetic foot center of excellence is not only to provide optimal diagnosis and treatment but also has a global role to provide a working example for other healthcare professionals and generate improved diabetic foot services throughout the world. Teaching is an important goal. Consultants should be experts in their respective fields. Such center should be able to conduct research trials, publish clinical and research work and provide work experience opportunities for others. Such centers provide specialized diabetic foot care not only to local patients but also to patients from rest of the country and even overseas. More complex cases with difficult revascularization problems or even complex cases with Charcot foot are managed at such centers. Depending on the local geographical situation, the cultural context and the availability of funding, the organization and management may be more or less complex. Every team-member must be aware of the roles they have to fulfil and they should always remember that the patient is of paramount importance. In such advanced centers, all investigations as well as treatment facilities are made available under one roof. The team is drawn up from multiple highly specialized disciplines including those of the diabetologist, vascular surgeon, orthopedic surgeon, physiotherapist, microbio­ logist, dermatologist, psychiatrist, nurse, educator, podiatrist, casting technician, administrators, etc. The number of teammembers and composition of the team depends upon local resources (Table 3). A creative and enthusiastic coordinator who can inspire colleagues to further levels of excellence is a key asset. A schematic presentation of this model can be found in Figure 5A and a picture of a university model in Figure 5B. Before a patient’s weekly visit at the University of Antwerp (Belgium), multidisciplinary team has a meeting How to establish a diabetic foot clinic?

Fig. 5A  The maximal model: The model of a reference center (Courtesy: Max Spraul, Noordwijkerhout, 1991)

Fig. 5B  A staff meeting on weekly basis (Courtesy: Diabetic foot clinic—Kristien Van Acker-Bornem 2005)

with all team-members like vascular surgeon, orthopedic surgeon, two team members of hyperbaric oxygen chamber, Isotopist, Secretary, microbiologist, radiologist and Magnetic Table 3  The center of excellence Staff

•  Diabetologist •  Surgeon (Orthopedic, and/or vascular, and/or general, and/or plastic) •  Physiotherapist •  Microbiologist •  Dermatologist •  Psychiatrist •  Nurses •  Educators •  Podiatrists •  Casting technician •  Administrative, reception and secretarial staff

Aim

•  Prevention and specialized curative care for complex cases •  To teach other centers

Patients

National, regional or even international referral center

Setting

Usually a large teaching or university hospital

Facilitating elements

•  Organize regional, national or international meetings •  Allow providers to visit to improve knowledge and practical skills •  Active collaboration with other reference centers •  Active participation in the development of guidelines

Equipment

As for intermediate center plus: Transcutaneous oxymetry, angiography, angio­ plasty, arterial bypass, fully equipped operating theater, duplex scan, intensive care unit, beds, CT scans, ultrasound, laser Doppler, pedobarogram, patient and operator’s chairs, computerized records, fully equipped teaching facilities, fully equipped orthotics service, grinder, plastazote, EVA, lasts, etc. telephones, computerized record systems



Establishing a Multidisciplinary/Interdisciplinary Diabetic Foot Clinic    195 resonance specialist, assistant surgeon, diabetologist and the nurse specialist in diabetes. The overall goal in the maximal model is to minimize amputation rates even in far advanced and complex foot problems. Also, as a specialized foot care center, it has to assume the responsibility to set-up an organization (see further referral and contrareferral pattern) that can prevent not only diabetic foot ulcers and amputations in a local setting, but can also play a more regional, national or perhaps even international role.

Activities Other than Patient Care of Center of Excellence • Organizing local meetings • Attending and presenting at international meetings • Receiving visitors from different parts of the country and also from other countries • Organizing training courses in diabetic foot care • Offering training opportunities for all the disciplines of diabetes foot care • Forging links with patient representative organizations • Conducting clinical research • Forming partnerships with corporate interests to ensure continuous funding • Creating prevention and treatment programs in collabo­ ration with other (specialized) centers. The highly specialized center is best equipped to teach other more basic centers. Workshops or meetings should be organized in which the experience of the team is shared with other centers interested in diabetic foot care. There should also be active participation with other internationally renowned institutions. This aids clinical and pre-clinical research, development of guidelines and organization of international meetings. Further in this chapter, the author will defend the idea of benchmarking, in which these centers should play a major role. Many of the centers, started once as a small unit, had to adapt their infrastructure to become a center of excellence. This process takes many years and such teams can confirm the expression of “one step at a time”. It has been observed at the same time that many of the centers of excellence had to deal with a kind of “order in the chaos” (Fig. 6). Establishing a multidisciplinary foot clinic is an exciting and worthwhile exercise. Newcomers will receive a warm welcome from established centers and from their nearest national representative of the IWGDF, who will be keen to advise and encourage them. The International Consensus Document on the Diabetic Foot lists national representatives who will be glad to support colleagues who are setting up new foot services (see website:www.iwgdf.org) Enthusiasm and belief in the importance of diabetic foot care is a key element for all successful foot teams. The challenge of building, sustaining and organizing a center of

Fig. 6  An interdisciplinary diabetic foot team in action: Order in the Chaos (Courtesy: Diabetic Foot Clinic, Kristien Van Acker)

excellence for the diabetic foot is huge task. The rewards in terms of reduced amputations and improved quality of life for people with diabetes and job satisfaction for the team are even more gratifying. These steps can be adapted to local circumstances and settings. They should be considered as guidelines and framework for developing their own diabetic foot care centers. The distances between the different levels of foot clinic are considerable, and the optimal service may never be attained. It should, however, remain a goal that serves to encourage team leaders to strive for their excellence.

Barriers and Some Golden Rules In the evolution of diabetic foot clinics (DFCs), there were some barriers which are typical to the period of development. The pioneers are persons with a strong vision and had defined the need of the concept of “working together” with the goal to solve the impact of the diabetic foot problem. Any Multidisciplinary/Interdisciplinary Team Project cannot be started without a respectable time of preparation and a concept of project management. It has to take into account at least four characteristics: 1. Definite duration, 2. Examine the logistic relationship with other activities in the project, 3. Study the resource consumption (information, energy, know how, time, financial resources) 4. Study the associated costs. This means that at least for a long-term success in charge of the team must develop a business plan and management skills. This last aspect becomes more important for the actual team leaders. After the golden and successful years of the initial diabetic foot clinics in Europe and North America



196    Contemporary Management of the Diabetic Foot one can observe some regression period. Global economic crisis is perhaps the reason behind this regression period. Hospital administrators are developing strategies and using austerity measures to cut down the expenses. Even the team leaders are speaking the same management language as the administrators. Making a business plan is an art which one has to learn to make the hospital managers, part of the process. For the developing world, the challenge is huge and is exciting to learn out from the experiences of the first generation of DFCs and to integrate it in their own culture and economical situation. The role of traditional medicine, for example, is an issue that has to be integrated in the process. Nevertheless, the following basic rules will always be useful for implementation. The initiator should define roles and boundaries. Everyone needs clarity as far as one’s own role and about the roles of other team members. The team coordinator has to be aware of power dynamics: Are certain members competing for control? Do some have more status than others? The process of “taking decisions” must be analyzed on a constant basis in the team: Who, When and How are important. Team members must learn to value each other’s contributions, look at how the group communicates and should be aware that “different profes­ sionals have different views”. This can become an added value of the concept. Implementation of feedback received is important for evaluation and is helpful in detecting some barriers. It has to be realized that the members of the team should not underestimate the value of listening to service users (patients). Often small details are important team’s success. Some of the biggest barriers include unclear goals, unhealthy communication, playing it “safe”, individual goals and poor leadership.

the teams, self-reflection which in turn leads to improvement in the delivery and outcome of medical care is important. To evaluate the inputs, or the interventions the outcome para­ meters are extremely important. There are many examples of such processes. One of the modern techniques used is benchmarking. Currently, only two countries, namely Germany and Belgium, are known to have this quality control system. In the disease-management program in Germany, providers are obliged to refer high-risk feet, feet with ulcerations and any suspicion of diabetic osteoarthropathy (Charcot foot) at predefined interface to specialized diabetic foot clinics. Standards for Quality of Specialized Diabetic Foot Clinics are set according to the criteria of the Diabetic Foot Working Group of the German Diabetes Association (DDG). They are based on structural quality (equipment, documentation, and staff ) and process quality (interdisciplinary cooperation by contract); and includes clinical pathways, standard operation procedures (SOP); hygiene plans, (MRSA management plan); audit (active and passive); quality of performance (treatment results of 30 consecutive patients). In Belgium, some opinion leaders together with Scientific Institute of Public Health, Epidemiology in Brussels developed an “Initiative for quality of Care promotion and Epidemiology in Belgian Diabetic foot clinics”, so-called IQED centers. This prospective cohort study was designed to describe, evaluate and improve the Quality of care in the Belgian DFC by collecting data and providing benchmarking. In this cohort offloading was used in 75% (42–100%) of the ulcer patients, but a total-contact-cast was only used in 2.4% (Fig. 7). The representatives of the IWGDF believe that minimal data collection is mandatory for sustainability of all future

The Importance of Feedback Loops and Benchmarking: Quality Control One of the first important studies to compare differences among different centers was European Study Group on Diabetes and the Lower Extremity (EURODIALE). In this study (a prospective cohort study of 1,232 consecutive individuals) it was observed that treatment of many patients was not in line with current guidelines and there were large differences between different countries and centers. At study entry, 77% of the patients had no or inadequate offloading. During follow-up, casting was used in 35% (0-68% variation between countries!) for the plantar forefoot or midfoot ulcers. Vascular imaging was performed only in 56% (14–86%) of patients with severe limb ischemia; revascularization was only performed in 43%. Delivery of good diabetic foot care depends on proper feedback. To witness improvements in the performance of

Fig. 7  An example of benchmarking regarding offloading. Center 1 represents the red line, meaning that 69% of the cases were given the correct offloading for a plantar ulcer. By comparing to other centers and in the time, centers are in the possibility to ameliorate their care



Establishing a Multidisciplinary/Interdisciplinary Diabetic Foot Clinic    197

Fig. 8  Organization of care: In every region/country, its central to make clear rules regarding referral and contrareferral, as shown in this model. The duration of the nonhealing time of the wound plays a central role. The experience in a reference center to treat Charcot foot and performing complex revascularization will help to have a good referral to these centers

Step-by-Step programs. The experts in various regions have the possibility to negotiate with their policy makers to achieve palpable change in the system in the long-term by promoting the Logo “measuring is knowing”.

REFERRAL AND CONTRA-REFERRAL WITH THE PRIMARY CARE Once an interdisciplinary foot clinic is installed, for long-term sustainability working together with the colleagues of the primary care centers is of paramount importance. Figure 8 explains the model which can be used for referral to centers. The hospital team and peripheral care providers must make some commitments in such a way, that delay of referral is reduced to a minimum. An agreement on how long an ulcer can be treated in the settings before referral must be pointed out. In some western countries, this time is reduced to 2 weeks in case there is no improvement in the healing of the foot ulcer. For a good relationship with care providers who refer the patients to centers, it is obvious that a good contrareferral after amelioration of the foot disease is extremely important. To develop healthy relationship between primary and the higher centers, primary teams should be welcomed to the hospital to learn together and become mutual partners.

Interdisciplinarity As care providers one must be aware of and respect patient’s experiences, feelings and beliefs, who visit diabetic foot clinics. In 2007, Rebecca L Jessup from Australia was one of the first to adopt the concept of interdisciplinary teams and their skills and behavior. Paul Gorman wrote several articles and books about multidisciplinary teams (MTs). He made us understand the differences between professionals and disciplines. In MTs members of staff, like auxiliaries, receptionists, and all the others also have an important role. Another important aspect is that patients and their relatives should also be given important place. According to this author, MTs utilize the skills and experiences of individuals from different disciplines, with each discipline approaching the patient from their own perspective. Most often, this approach involves separate individual consultations. These may occur in a “one-stopshop” fashion with all consultations occurring as part of a single appointment on a single day. It is common for the teams to meet regularly, in the absence of the patient, for “case conference” findings and discuss future directions of the patient’s care. MTs provide more knowledge and experience than disciplines operating in isolation.



198    Contemporary Management of the Diabetic Foot their nearest national representative of the (IWGDF) who will be keen to advise and encourage them. Enthusiasm and belief in the importance of diabetic foot care is a key element of all successful foot care teams. The challenge of building, sustaining and organizing a center of excellence for the diabetic foot is huge but the rewards in terms of reduced amputations and improved quality of life for people with diabetes and job satisfaction for the team are even greater and more gratifying. As mentioned as subtitle in chapter 43 of the Diabetic Foot: a clinical atlas, the author endorses: “Teamwork makes everything possible even the impossible”.

KEY MESSAGES Fig. 9  Demonstrates a worst case approach of this interdisciplinary team. This photograph emphasizes that the patient is central and not the team (Courtesy: Karel Bakker, Netherlands)

Interdisciplinary teams (ITs), on the contrary integrate separate discipline approaches into a single consultation. The team together with the patient, conducts assessment, history taking, diagnosis, intervention and decide short- and long-term management goals at the same time. The patient is intimately involved in every discussion regarding his condition, prognosis and plans about the care. Individuals from different disciplines, as well as patient himself, are encouraged to question each other and explore alternate avenues, with aim to achieve the best outcome for the patient. Those who have experience of this approach will immediately recognize a personal expression: “working in the order of chaos!” (Fig. 9). The energy and general demands are huge but the rewards are even greater, and perhaps the most important item is richness of the contacts of team members, with patients and their family. This is reflected by the confidence the patient bestows in the team even when the prognosis is poor.

CONCLUSION Establishing a multidisciplinary/interdisciplinary foot clinic is an exciting and a worthwhile exercise. Newcomers will receive a warm welcome from established centers and from

For People with Diabetes • If you have a foot problem, you should obtain foot care from a multidisciplinary foot team. For Decision-makers • A multidisciplinary approach has been shown to bring about a 49–85% decrease in amputations. • The results that have been obtained by multidisciplinary teams working in dedicated foot clinics underline the need to provide funding and support to create new clinics along the lines described in this chapter. For Health Care Professionals • Establishing a foot clinic and working towards the final goal of creating a center of excellence is a demanding task. The rewards, however, in terms of results and job satisfaction are extremely gratifying. • For health care professionals interested in setting up foot clinics, an established support network in the form of IWGDF is available to provide advice and guidance.

SUGGESTED READING 1. Impact of Specialized Foot clinics, Kristien Van Acker in “HighRisk Diabetic Foot, 2010, edited by Lawrence A Lavery, Edgar JG Peters, Ruth L Bush . 2. Paul Gorman. Managing multidisciplinary teams in the NHS. 1989. ISBN 0 7494 2787 6. Marston Lindsay Ross International Ltd, Oxfordshire. 3. Time to Act. Put feet first, prevent amputations: diabetes and foot care. Joint Publication of the IDF and IWGDF, 2005.

Index Page numbers followed by f and t refers to figure and table, respectively

A Acute and chronic Charcot foot disorders 84t arterial occlusions 10 Charcot arthropathy and osteomyelitis 81 foot 82, 82f, 85, 187 coronary syndromes 118 ischemia 57, 59 limb ischemia 123 neuropathic osteoarthropathy 187 Advanced wound healing products and techniques 153 Advantages of DSA 116 MRA 115 regional anesthesia 141 American Diabetes Association 9, 51 Amputations 96f, 135, 139 Angiography 115 Angle of hallux 51f brachial index 60, 118 pressure index 53, 53f disarticulation 150f joint 15 reflex 52 Anterior tibial artery 125f Antibiotic therapy 98 Aortic and aorto-iliac stenotic disease 123 bilateral-iliac stenosis 126f Aortobifemoral bypass 125f Aortoiliac occlusive diseases 123 Arteries and veins of foot 20 of foot 22f of lower limb 20f Arteriovenous fistula 116 Arthropathy 82 Assessment of diabetic foot 56 Atypical aspects of diabetic foot 159 Autologous bone-marrow cultured cells 157 Autonomic neuropathies 33

B Below knee walking plaster 75 Bilateral lower limb amputation 166f

plantar ulcers 76f total aortoiliac occlusions 125f Bilayered cellular matrix 154 Biomechanics of diabetic foot 39 Blood transfusion 98 Bone 13 biopsy 88 biopsy of proximal phalanx of right great toe inflammatory cells 91f marrow mononuclear cells 157 of foot 13f-15f Brachial pressure index 111 Brevis muscle 18 Bronchogenic carcinoma 34 Bunion 47, 50f Burden of management of diabetic foot ulcer 27t Burn 64

C Calcaneocuboid joint 19 Calcification in tibial artery 112f Callus 41, 50f Cardiovascular disease 171 Cellulitis 59 Charcot ankle 81f arthropathy 80, 82 of ankles 83 foot 48, 51f, 55, 78-81, 81f, 83, 96f, 166, 167f affecting ankle joint 167f postexostectomy of midfoot and ulcer excision 84f with midfoot collapse 79f with midfoot ulcer 84f joint 82 deformity 48 midfoot deformity 81f neuroarthropathy 34 neuropathic osteoarthropathy 78 osteoarthropathy 59 Chopart’s amputation 147, 149, 149f joint 15, 19 Chronic Charcot foot disorders 83 inflammatory demyelinating polyneuropathy 33 sensorimotor neuropathy 33

total occlusion 128f ulcer 66, 676f Classification of diabetic foot 55 Clawed and retracted toes 47, 48 Combined theory of Charcot pathogenesis 80f Common femoral artery 124f, 125f, 127f iliac artery 124f Compensated forefoot varus 45f rearfoot varus 43f Components of diabetic foot exam 173t Comprehensive diabetic foot examination 37 Computerized tomography angiography 114 Consequences of limb amputation 151 Controlled ankle motion device 183 Cranial mononeuropathies 33 C-reactive protein 81, 104 Critical leg ischemia 116 limb ischemia 119 Cutaneous nerves of foot 20f

D Daptomycin antibiotic polymethylmethacrylate beads 107f De Humani corporis fabrica 5 Decubitus ulcer 95, 95f Deep peroneal nerve block 141f plantar artery 21 compartments 92 foot infection in lateral compartment 93f ulcer 59 Defining dysvascular foot 118 Definition of plantar ulcer 63 Delivery of information 186 Destruction of first metatarsal head and proximal phalanx 89f Detection of medial arterial calcification 112 Determining correct footwear 176 Diabetes care 8



200    Contemporary Management of the Diabetic Foot

Control and Complications Trial Study 35 mellitus 6, 78, 118, 170 Diabetic amyotrophy 33 Charcot foot 78, 83 Education Study Group 191 foot 1, 4, 28, 51, 63, 179t, 189 biomechanics 43t, 48t classifications of diabetic foot infections 103t infections 87, 90, 98t, 102, 105t ulcers 102, 134, 170 gangrene 4 hand 167 neuropathy 31, 32, 32t, 37, 51f, 171 peripheral neuropathy 35, 170 retinopathy 171 Digital amputations 142 subtraction angiography 116, 116f Distal embolization 116 interphalangeal joint 14 phalangeal extension 49 phalanx 13 popliteal artery 128f Dorsal expansion of plantar abscess 106f foot infection 90, 91f, 92f skin necrosis 92f Dorsiflexor group in anterior compartment of leg 17 Dressing fixation 72 Dry necrosis 58 Duplex color Doppler 113 Dutch Epidemiological Study 118 Dysvascular diabetic foot 118

Extensor digitorum longus 17 hallucis longus 17 External iliac artery 124f Extracellular matrix protein 154 Extracorporeal shock wave therapy 158

H

L

E

Hallux abducto valgus 47, 48 valgus 142 Hammer toe 50f Healing 134 ulcer 65f, 67f, 77f Heel pad infection 94, 95f Hemorrhagic bullae 162 High plantar pressure 171 risk foot 57 Hindfoot 15 Hodgkin’s disease 102 Hybrid procedures 123, 131 Hyperbaric oxygen therapy 157

Larva therapy 157 Lateral malleolar bursitis 162 Left external iliac artery 125f Life-threatening infection 163 Limited joint mobility 42, 51 Long and deep fissure on heel 50f superficial femoral artery 128f Loss of protective sensation 51, 172 Lower extremity revascularizations 132 limb amputations 141 Lucilia sericata 157

Erythema 50, 103 Erythrocyte sedimentation rate 88, 104 Escherichia coli 87 Ethylene vinyl acetate 177 European Federation of Neurological Societies 37 Evaluation of neuroischemic foot 111 Extensive anterior tibial artery stenosis 129f debridement in necrotizing fasciitis 97f destruction of foot and leg 163f tarsal bones and joints 167f dorsal foot infection 91f necrosis of heel pad 94f skin necrosis 92f soft tissue necrosis 91

F Fasciitis 103 Fiberglass boots 75, 75f Fibularis longus 18 Flexor digitorum longus 16 hallucis longus 16 Foot 56 deformities 48f, 171 ulcer healing 112t ulceration 37 with cellulitis 56, 58 with necrosis 56, 58 with ulcer 56, 58 Forefoot 13, 73 gangrene 148f supinatus 45, 47 valgus 45, 46 varus 44, 47

G Gamma-aminobutyric acid 36 Gangrenous patches partial foot gangrene 59 Global burden of diabetic foot 24 limb amputation 29t Graded-exercise treadmill test 112 Granulating tissue 67, 67f Granulocyte colony stimulating factor 109

I Indications of worsening infection 97t Infected plantar ulcer 95f

Infection in central plantar compartment 93 lateral compartment 92 medial compartment 93 plantar compartment 93f plantar compartments 91 Infectious Disease Society of America 103t, 105 Inframalleollar angioplasty 131f Insulin neuritis 33 Intermittent claudication 57 International Diabetes Federation 11, 25, 191 Interphalangeal flexion 49 joint 14 Interpretation of ankle-brachial index 105t arterial duplex ultrasonography 113t Intravascular ultrasound 114 Intrinsic minus feet 50f muscles of foot 18 Ischemia 10, 64 Ischemic heart disease 123 heel ulcer 131f ulcer 94

J Joint deformity 46

K Klebsiella pneumoniae 87 Knee disarticulation 150, 151f Knocked knees 44

M Magnetic resonance angiography 115 imaging 81, 88, 90f Major amputation 26, 135, 149



Index    201 Management of aorto-iliac disease 123 diabetic foot disease 185 dysvascular diabetic foot 121 femoro-popliteal disease 124 infrapopliteal disease 128 plantar ulcers 63 Medial plantar artery 21 Metatarsal head 76, 93 osteotomies 76 Metatarsophalangeal joint 14, 40, 48, 93 Methicillin-resistant Staphylococcus aureus 99, 105 Middle phalanx 13 Midfoot 15, 73 Midtarsal amputation 147, 149f joint 19, 40 Mild plantar foot infection 92f Minor amputation 26, 135, 142 Mobile forefoot valgus 46, 46f, 47 Modified neuropathy disability score 34 Monckeberg’s sclerosis 111 MRI of Charcot foot 82f Multi-detector computed tomography 114 Multiple discharging sinuses 88 toe rings 160f ulcers 65f Muscles 15 of dorsum of foot 16f of foot 18f of leg 16f of sole of foot 17f Myocardial infarction 118

N National Cholesterol Education Program 121 Necrosis in neuropathic and neuroischemic foot 59 Necrotic tissue 68 Necrotizing fasciitis 96 Negative pressure wound therapy 109, 155 Nerves of foot 19 lower limb 19f Neuroarthropathy 78 Neuroischemic foot 54t, 55, 59, 166f ulcer 58, 129f Neuro-osteoarthropathy 103 Neuropathic foot 55, 59 osteoarthropathy 7, 78 ulcer 58 Neurothesiometry 56

Neurotraumatic theory 79 Neurovascular theory 79 Non-healing ulcer 66f wound 144f Normal foot 56 range of motion 42f weight bearing 21

O Opioids 36 Osteomyelitis 64, 88, 96f, 103 of calcaneum 95f of distal phalynx 144f of hallux 105f of phalanges of right great toe 90f with ulceration or abscess 59 Osteoprotegerin 79

P Pain 58 Pallor 58 Palpable dorsal pedal and posterior tibial artery 60 Palpation 51, 56 Paralysis 58 Paraneoplastic syndrome 34 Paronychia 91f, 167f Partial forefoot valgus 45 Patellar tendon reflex 7 Peak systolic velocity 113 Percutaneous tendo-Achilles lengthening 76 Peripheral arterial disease 27, 39, 118, 122, 135, 170, 171 diabetic neuropathy 171 neuropathy 33 sympathetic diabetic autonomic neuropathy 33 vascular disease 33, 166 Peroneal nerve 20 Phalanx 14 Pinprick sensation 52 Plantar aponeurosis and ligaments 19f compartment syndrome 91 fat pad integrity 41 flexor group in posterior compartment of leg 15 foot infections 93 pressure and shear stress 40 in forefoot 41f ulcer 95 ulcer 77f management 63

Platelet derived growth factor 151, 153 rich plasma 151, 155 therapies 155 Plethysmography 111 Polyneuropathies 33 Polyurethane 177 Porphyria 34 Positron emission tomography 89 Postangioplasty transmetatarsal amputation 148f Postoperative care of wound 100 Post-tibial nerve block 141f Potential complications of angiography 116 Prevention of foot ulcers 9 Preventive diabetic foot care 8 Primary healed with ischemia 26 without ischemia 26 Principles of debridement in infected foot 102 Procedure of remote endarterectomy 127f Protease inhibitors 155 Proximal interphalangeal joint 14 motor neuropathy 33 phalanx 13 Pseudoaneurysm and dissection 116 Pseudomonas aeruginosa 87, 105 Pulse-volume recordings 111

Q Quantitative sensory testing 34 Quick examination of feet 49

R Rat bite 160, 161f Rearfoot biomechanics 42 valgus 44, 44f varus 43 Recombinant human epidermal growth 153 Regional anesthesia for lower limb surgery 141 Removable cast walkers 74, 75 heel casts 75, 75f Renal and eye diseases 171 plasma flow 125f Rigid forefoot valgus 46f, 47 Rocker-bottom foot 80 Role of neuropathy in diabetes 9

S Safari technique 130f Salvage of failing graft 126 Sanders and Frykberg classification of Charcot foot 83f



202    Contemporary Management of the Diabetic Foot Screening and prevention of diabetic foot 170 Segmental limb pressures 111 Sensory testing 56 Septic arthritis 103 Serotonin and noradrenalin reuptake inhibitors 36, 37 Severe chronic ischemia 57, 59 diabetic foot infection 96, 96f, 97f, 99t hallux infection 106f plantar foot infection 96f Severity of peripheral arterial disease 112 Sharp injuries 159 Shoe pressure 64 Shoulder disarticulation 169f Signs of deteriorating ulcer 66f Silencer pipe injury 162f Simple inspection 56 staging of diabetic 56 system 59 Skin substitutes 154 Sloughy tissue 67 Spasm of vessel 116 Staging of diabetic foot 55 foot in diabetes 56f Standard operation procedures 196 Staphylococcus aureus 87, 88, 105, 157 Static ulcer 66, 66f Stenosis postanastomosis in popliteal artery 128f

Superficial femoral artery 124, 125f, 127 infection 87 ulcer 59 Superior mesenteric artery 125f Sural nerve block 141f Surgical anatomy of lower limb and foot 13 debridement of hallux infection 106f Syme’s amputation 149, 150 Systolic ankle blood pressure 61 toe blood pressure 61

T Tailor’s bunion and fifth toe varus 47, 48 Talocalcaneonavicular joint 19 Talonavicular and calcaneocuboid joints 40 Tarsometatarsal amputation 147, 149f and midtarsal disarticulations 184 Testing for high pressure points 53 vascular assessment 52 Thermal injuries 161 Tibialis anterior muscle 17 posterior muscle 16 Toe brachial index 60, 118 ring injury 160 systolic pressure 112 Total contact cast 74, 74f, 82 forefoot valgus 45

Transcutaneous oxygen pressure 60, 61 pressure of oxygen tension 112 Transmetatarsal amputation 143, 147f, 184 Transtibial amputation 150, 150f Transverse tarsal joint 15 Tricyclic antidepressants 36, 37 Typical example of ischemic hallux 102f

U Ulcer assessment 64 measurement 69 site 73 Uncompensated forefoot varus 45f rearfoot varus 43f University of Texas Foot Wound Classification System 60t

V Vacuum assisted closure 143, 156f Vascular disease 52 Veins of lower limb 23f Vertical stress and peak plantar pressure 41f

W Weight bearing in diabetic neuropathy 23 Wet necrosis 58 Wound care 151 cleansing 72 closure 100

X X-ray metallic foreign body 88f