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Foreword As our older population increases worldwide and society looks to the future, health policy and public health issues concerning the quality of life and health care are becoming major considerations. The moral and ethical responsibilities to care for the elderly are problems that we face as health-care professionals from all disciplines. There is a need to become aware of geriatric foot and related problems, their assessment, and management, and how they affect clinical practice and the ability of our older citizens to remain vibrant and active members of their communities, and to live their lives with dignity. The human foot is a marvel and has been called the ‘mirror of health’. The early recognition of diseases, disorders and systemic complications related to the foot and its related structures has much to do with all forms of prevention and management. A major component of the field of geriatric medicine and podogeriatrics is more than the ageing process itself. It includes clinical care, limb preservation, education, prevention, clinical management and the restoration of function. It also incorporates the social elements of life and the benevolent regard for each individual patient as paramount to society in general. Geriatric clinical practice means more than just caring for older individuals. It implies a philosophy of compassion and understanding that must be incorporated into all health-care specialties that attempts to improve health and well being for patients with chronic diseases and/or disabilities throughout their lives. Foot Problems in Older People: Assessment and Management critically and succinctly encompasses a wealth of information on the subject of geriatric foot care that is applicable and practical for all professions involved in the primary care of the older patient. Dr Menz has accomplished this task in a masterful fashion. One individual who has demonstrated a breadth of knowledge and understanding that provide great consistency in style and content has remarkably authored this monograph.
The text is extremely well organised, easy to read and inclusive of the basic primary elements of geriatric and related foot care. Each chapter provides a significant and comprehensive list of references. The manuscript provides a review of the epidemiology of foot problems in the elderly from a worldwide and international perspective, which is a first in current literature. Prevalence and risk factors for foot problems (including age, sex, obesity and co-morbidities) are related to the consequences of immobility, falls and quality of life. This work includes practical discussions related to the aetiology, assessment and management of common foot disorders and diseases along with an emphasis on primary management and the prevention of complications. The text was designed to complement existing geriatric and specialty texts such as those in internal medicine, dermatology, foot surgery and foot orthopaedics to expand the concepts of care for older patients. Improving the quality of care to help ensure years without pain and to enhance the fulfillment of life are a demonstrated objective of this effort. The physical changes related to assessment, the integument, keratotic changes, onychial disorders, the vascular system, neurosensory changes, musculoskeletal system including foot deformities of the digits, forefoot and rearfoot are well documented. Pain and arthritic changes have been properly presented. The segments dealing with conservative and surgical management enhance the primary care approach to patient care. The sections dealing with orthoses and footwear are focused on the older patient. The photographic illustrations and charts enhance the quality of the presentations and are augmented with a comprehensive list of references and bibliographic notations. Clearly this text is a ‘labour of love’ and prepared by an individual who has devoted much of his career to care, research and education related to foot disorders in older patients. Dr Menz is to be
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FOREWORD
congratulated for this fine effort. He is a distinguished podiatrist, researcher, educator and the foremost scholar in the field of foot problems related to ageing in Australia. He is an established author, the Editor of the Journal of Foot and Ankle Research, and serves on several editorial peer review boards of gerontology and rehabilitation journals. Foot Problems in Older People: Assessment and Management provides an excellent and current foundation for the podiatric student, the podiatry profession,
geriatricians and related health-care professionals to understand and learn the principles and practice of providing foot care for geriatric patients and is a gem. This book will help elevate the standards of care for older patients, internationally, and belongs in all libraries that deal with the subjects of geriatric and gerontology. Arthur E. Helfand 2008
Preface During the 20th century most countries in the world underwent a remarkable demographic transition from high fertility and mortality rates to low fertility and mortality rates. Subsequently, we are now witnessing a substantial ageing of the population, with the most rapid population growth being observed in the oldest age groups – the oldest-old (85+ years) and centenarians (100+ years). In 2000 it was estimated that there were 180 000 people in the world aged over 100 years and current projections suggest that this figure could reach 1 million by 2030. Population ageing poses significant challenges to health-care systems. While advances in health care have contributed to increased longevity, a direct consequence of this has been the corresponding increase in prevalence of chronic diseases such as cancer, cardiovascular disease, osteoarthritis and Alzheimer’s disease. Whether population ageing has resulted in longer periods of ill-health prior to death (referred to ‘expansion of morbidity’) or has delayed the age of onset of disability (‘compression of morbidity’) continues to be debated. However, irrespective of which scenario proves to be correct, it is clear that healthcare workers need to be prepared for an increasingly older caseload for some time to come. Management of foot problems is an important, yet often overlooked and undervalued component of geriatric health care. Even within podiatry, the profession entirely focused on the diagnosis and management of foot disorders, treatment of older people is perceived by many to be less interesting and fulfilling than other areas of practice. Subsequently, there is a paucity of literature pertaining to the management of the older foot. While generalist geriatrics textbooks often include a short section on foot disorders, to my knowledge, there has not been an entire textbook published on this topic since Arthur Helfand’s Clinical Podogeriatrics in 1981. The objective of this book is to provide the reader with a comprehensive yet accessible review of the epidemiology, aetiology, assessment and management
of foot conditions frequently observed in older people. While the book is primarily targeted towards a podiatry audience (particularly podiatry students), I hope that it will also be of interest to general medical practitioners, nurses, physiotherapists, orthotists, orthopaedic surgeons, rheumatologists and indeed any other health professional who cares for older people. This book has 12 chapters, which can be broadly grouped into four sections: background information (Chs 1 and 2), assessment (Ch. 3), dermatological and vascular disorders (Chs 4–7), musculoskeletal disorders (Chs 8–10) and treatment approaches (Chs 11 and 12). Chapter 1 provides a detailed coverage of the epidemiology of foot problems in older people, outlining the findings of several large-scale studies of the prevalence, risk factors and consequences of foot problems. Chapter 2 discusses the effects of ageing on the integumentary, vascular, sensory and musculoskeletal structures of the foot and outlines the clinical implications of these changes. Chapter 3 is a long chapter that describes the assessment of the lower limb in older people, from the initial assessment interview and history taking through to diagnostic imaging. Chapters 4, 5, 6 and 7 outline the prevalence, aetiology, clinical presentation and treatment of keratotic disorders, other skin conditions, nail disorders and peripheral vascular disorders, respectively. Chapters 8, 9 and 10 are structured in a similar manner and focus on musculoskeletal disorders of the toes, forefoot and midfoot/rearfoot, respectively. Finally, Chapters 11 and 12 provide additional information about the role of footwear and foot orthoses in the management of these conditions. In defining the size and scope of this book, it has been necessary to exclude or limit the coverage of some topic areas that are discussed in greater detail in existing texts. For example, while this book discusses common skin conditions affecting the foot, the reader is advised to supplement this information with a more general dermatology textbook. Similarly, foot surgery
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PREFACE
and foot orthotic prescription are discussed in the context of the overall management of particular foot conditions, but details regarding individual techniques are beyond the scope of the book. In limiting the coverage of some of these topics, I do not wish to give the impression that they are less important. In fact, the opposite is actually the case; by referring readers to other sources, I hope to ensure that they are exposed to the appropriate level of detail that the topic deserves. The book adopts an evidence-based approach to summarising the available literature, deferring to the conclusions of systematic reviews and randomised controlled trials where such sources of information are available. However, because our knowledge of the causes and best approaches to management of many
foot conditions is incomplete, some areas of the book are more evidence-based than others. This is particularly evident in relation to many surgical procedures, the evidence of which is primarily derived from caseseries studies. Hopefully, the recognition of the many gaps evident in the literature will act as a catalyst for some readers to initiate clinical research projects to help address these shortcomings. I hope that this text will assist health-care professionals in optimising the quality of care for older people with foot problems, ensuring that the additional years gained through our increased life expectancy are as pain-free, active and fulfilling as possible. Hylton B. Menz 2008
Acknowledgements I am indebted to several people who have assisted in the completion of this book. First and foremost I would like to thank my wife, Elizabeth Barr, for her generous support and encouragement during the writing process, even while she toiled away on her PhD. I would also like to thank the many colleagues who provided me with access to their treasure trove of clinical photographs and allowed me to reproduce them in the book. Full photographic credits are provided throughout the text; however I would like to particularly thank Dr Karl Landorf, Lloyd Reed, Lesley Newcombe and Felicity Prentice. Dr Karl Landorf, Ivan Bristow, Mark Gilheany and Nikki Frescos provided valuable suggestions on parts of the manuscript. Dr Shannon Munteanu assisted
with the scanning of radiographs and Lucy Shaw assisted with preparing the clinical photographs. The editorial staff at Elsevier, including Robert Edwards, Veronika Krcilova and Rebecca Gleave, provided prompt and professional assistance from the initial development of the book proposal through to the final production of the book. This book is dedicated to Dr Ramaswamy Ganapati, Director of the Bombay Leprosy Project, Mumbai, India, in recognition of his tireless and compassionate work in improving the lives of people affected by leprosy. I encourage all readers of this text to support the ongoing work of this not-for-profit organisation by making a donation at www.bombayleprosy.org.
CHAPTER
Epidemiology of foot problems in older people
PREVALENCE OF FOOT PROBLEMS
CHAPTER CONTENTS Prevalence of foot problems 1 Studies conducted in aged care facilities and inpatient settings 2 Studies conducted in outpatient settings 2 Community-based studies 3 Risk factors for foot problems 5 Age 6 Sex 6 Obesity 6 Co-morbidities 6 Income, education and ethnicity 7 Consequences of foot problems Mobility 7 Falls and injuries 8 Health-related quality of life 8 Summary 9 References 9
1
7
It has long been recognised that foot problems are highly prevalent in older people and have a significant detrimental impact on an older person’s independence and quality of life.1 However, the true epidemiology of foot problems in this population is difficult to ascertain for several reasons. Firstly, in contrast to most common conditions affecting older people, there is no consensus as to what actually constitutes a foot ‘problem’. This is largely due to the fact that a very broad spectrum of musculoskeletal, dermatological, vascular and neurological conditions may manifest in the foot, each requiring its own case definition. (In this chapter the terminology adopted by each individual study has been used.) Furthermore, the definition of a foot problem may also be broadened to include difficulties in maintaining basic foot hygiene (such as cutting toenails) or difficulty purchasing comfortable shoes.2 Secondly, while some prevalence studies rely on self-reporting of foot problems, others document the prevalence of foot problems based on clinical assessments. There are considerable discrepancies in prevalence estimates between these two approaches, with those based on self-report generally revealing significantly lower rates of foot problems. Whether older people under-report foot problems or clinicians overreport them is difficult to determine; however, there is some evidence that many older people consider foot problems to be an inevitable accompaniment of ageing3 and therefore do not consider reporting them as medical conditions in health surveys.4 Subsequently, comparisons of foot problem prevalence between
2
EPIDEMIOLOGY OF FOOT PROBLEMS IN OLDER PEOPLE
studies based on self-report and those involving clinical assessments are problematic. The third major consideration when interpreting prevalence data on foot problems is the sample population. Most studies have been conducted on institutionalised older people, or on relatively small convenience samples in a range of clinical settings. While such studies are useful and often provide detailed information on a range of conditions, the prevalence estimates derived from such studies cannot be considered representative of the broader older population, because of inherent sampling bias. Very few well-designed epidemiological studies using representative random samples have been undertaken and, while large-scale national health surveys do provide representative data on medical conditions, few include detailed information on foot problems. Therefore, establishing the prevalence of foot problems in older people requires making a distinction between non-representative clinical studies that provide considerable detail in a small number of people and larger, representative epidemiological studies, which often lack clinical detail.
STUDIES CONDUCTED IN AGED CARE FACILITIES AND INPATIENT SETTINGS One of the earliest studies to examine the prevalence of foot problems was conducted on 1011 nursing home residents (300 men and 711 women, aged 60–90 years) in the USA.5 A podiatrist undertook a visual inspection of each resident and completed a simple checklist. Although no overall prevalence figures were provided, the most commonly observed conditions were corns (25%), hallux valgus (23%) and calluses (14%), with women exhibiting a higher prevalence of all foot conditions compared to men. Subsequent studies in aged care facilities and hospitals have reported similar findings in relation to the most common foot problems but quite variable prevalence rates. Hsu et al6 assessed 426 older people attending a hospital-based foot clinic in the USA and reported that 36% had nail and skin problems, 31% had circulatory problems and 21% had structural foot deformities. A similar study conducted in the UK7 assessed foot problems in 100 hospital inpatients and found that 39% had lesser toe deformities, 30% had corns or calluses and 29% had hallux valgus. Interestingly, despite the high prevalence of these problems, only 19% complained of painful feet. Finally, a Hong Kong study8 involving clinical assessments of 166
hospital inpatients aged over 65 years (admitted to either a geriatric or orthopaedic ward) reported that 50% had at least one foot problem, the most common being calluses (40%), hallux valgus (20%) and lesser toe deformity (20%). Goniometric assessments also revealed that 70% had limited ankle motion, 40% had limited foot eversion and 15% had limited dorsiflexion of the first metatarsophalangeal joint. Similar to the findings of Ebrahim et al,7 only a small number of patients (7%) reported foot discomfort. Although it is difficult to compare these studies because of differences in study populations and assessment techniques, it is clear that hospital inpatients and older people residing in aged care facilities have a high prevalence of foot disorders. In all four studies, women demonstrated a higher prevalence of foot problems than men. The unexpected observation of a relatively low prevalence of foot symptoms in the two hospital-based studies7,8 highlights the aforementioned discrepancy in prevalence rates based on clinical assessments compared to self-report. However, the apparent discrepancy between observed foot conditions and reported symptoms in institutionalised older people may simply reflect the confounding effect of limited mobility, i.e. many of the older people in these studies may not have been physically active enough to develop foot symptoms.
STUDIES CONDUCTED IN OUTPATIENT SETTINGS Several studies involving the review of patient records from outpatient clinics have been conducted to examine the epidemiology of foot problems. The South Mountain Study conducted by Helfand et al9 in 1968 involved assessments of 551 people aged over 65 years who were attending a rehabilitation centre in the USA. The most common foot conditions diagnosed by the attending podiatrists were hyperkeratosis (48%), dry skin (46%), thickened nails (42%) and hallux valgus (38%). Peripheral vascular conditions were also common, with 44% of patients having an absent posterior tibial artery pulse. More recently, Plummer & Albert10 examined 308 new referrals to an outpatient foot care service in a USA health sciences centre over a 24-month period and found that the prevalence of foot abnormalities increased significantly with age, with 45% of patients aged 80–95 years exhibiting at least one foot abnormality. The key finding of this study was that older people without diabetes demonstrated a similar preva-
Prevalence of foot problems
lence of inappropriate foot-care practices and ill-fitting footwear to younger patients with diabetes, suggesting that non-diabetic older people are at high risk for foot problems and should therefore receive similar footcare screening and education to those with diabetes. By far the most extensive outpatient study on the prevalence of foot problems is the Achilles Foot Screening Project. This study commenced in 1997 and involved clinical examination of the feet of people attending dermatologists or primary care physicians in Austria, Belgium, China, the Czech Republic, Germany, Greece, Hungary, Israel, Italy, Luxembourg, the Netherlands, Poland, Russia, Slovenia, South Africa, Sweden, Switzerland and the UK.11 The primary focus of this study was to determine the prevalence of fungal infections affecting the foot, although information was also collected on other foot conditions. Initial results from 13 695 people residing in six of the participating European countries12 revealed that a clinical diagnosis of a foot disorder was made in 58% of patients, with a much higher prevalence in those aged over 65 years (78%). The most commonly diagnosed conditions in older people were onychomycosis (45%), tinea pedis (29%), pes planus (28%), plantar corns and calluses (26%) and hammer toes (24%). A follow-up study involving 90 085 older patients across all the participating European countries13 reported that almost half had clinical evidence of fungal foot infection. Lower prevalence estimates in older people for tinea pedis (8%) and onychomycosis (6%) were reported in the Hong Kong arm of the study,14 although the sample size was considerably smaller (824 participants). The main limitation with prevalence studies conducted in outpatient settings is that of sampling bias, in that the characteristics of the sample population studied reflects the geographical location of the clinical service and the method by which the service is administered (such as the eligibility criteria to access the service). In particular, inclusion in the Achilles Foot Screening Project is clearly biased towards older people who have a pre-existing dermatological condition, as most assessments were performed in dermatology clinics. As such, the prevalence of fungal foot disease derived from this study is likely to be an overestimate.
COMMUNITY-BASED STUDIES The most accurate estimates of the prevalence of foot problems in the general older population are ideally
provided by large-scale epidemiological studies involving random sampling of participants, using standardised definitions of various foot conditions. Unfortunately, very few such studies have been undertaken with a specific focus on foot problems. In many cases, foot problem prevalence data is derived from national health surveys, which may only include a single question about foot problems (e.g. do you have problems with your feet?), or from chronic pain prevalence studies, which request that the participant report the location of their pain. For the purpose of simplicity, foot problems or pain located in the foot are frequently combined with knee or hip disorders and documented as ‘lower extremity problems’. Therefore, in many studies it is difficult to delineate the prevalence of the foot problem itself. Despite these limitations, these studies do provide more precise estimates of foot problem prevalence than those conducted in clinical settings.
Studies conducted in the USA Several community-based prevalence studies involving clinical assessments have been conducted in the USA. The Keep Them Walking project, conducted in 1968, involved evaluations of 1366 older people attending a range of community centres and senior citizen clubs.15 An extremely high prevalence of clinically determined foot problems was reported (95%), with 74% of participants reporting foot pain. However, these figures need to be viewed with some caution, as no definitions of these foot complaints were provided and it is likely that the method of recruitment (talks to senior citizen clubs delivered by a podiatrist and mail-out leaflets about foot problems) skewed the sample towards those with foot problems. A subsequent study in 1998 using very similar methods16 reported a foot problem prevalence of 84% in 417 people, the most common conditions being foot pain (45%), corns (33%), calluses (26%) and hallux valgus (24%). The Dunedin Program, which commenced in 1975 as a hypertension screening study, involved the administration of a questionnaire to 733 people aged over 65 in Dunedin, Florida, a popular retirement area in the USA.17 The results indicated that 60% of women and 32% of men were troubled by foot problems. The most commonly reported conditions were toenail problems (22%), calluses (20%), corns (16%), dry skin (15%) and bunions (13%). Women reported a higher prevalence of corns and bunions than men.
3
4
EPIDEMIOLOGY OF FOOT PROBLEMS IN OLDER PEOPLE
Similar figures for the prevalence of calluses (25%) and bunions (17%) were reported by Gould et al,18 who conducted a survey of foot problems by administering a questionnaire to 45 000 shoe stores across the USA. The National Health Interview Survey (NHIS), undertaken by the USA Public Health Service, is a regular interviewer-administered survey of general health that includes questions on bunions, corns and calluses, and toenail problems. In 1990, the NHIS included an additional podiatry supplement with questions pertaining to foot infections, arthritis and orthopaedic conditions.19 The 1990 NHIS involved interviews with 119 631 people and reported a 31% prevalence of foot problems in respondents aged over 65 years. The most commonly reported problems were corns and calluses (11%), toenail problems (10%), bunions (5%) and foot infections (5%). Shortly after the NHIS, a smaller telephone survey of 1003 people conducted by a marketing company reported very similar findings: an overall 38% prevalence of foot problems in those aged over 65 and a similar breakdown of the most commonly reported conditions.20 The Women’s Health and Aging Study is a longitudinal study of the causes of disability in 1002 women aged over 65 years.21 An analysis of baseline data revealed that 70% of the sample had bunions and 50% had hammer toes. A relatively small proportion of the sample reported ‘severe’ foot pain (14%), which was defined as pain lasting 1 month or longer and rated 7 or above on a scale from zero to 10. Interestingly, there was no association between the presence of foot deformities and severe foot pain. The most recent community-based study to focus on foot problems in the USA was the Feet First study, a detailed investigation involving a random sample of 784 people aged over 65 in Springfield, Massachusetts.22 The location of the study was chosen because of its racial diversity in order to allow comparisons in the prevalence of foot problems to be made between non-Hispanic white, Puerto Rican and African Americans. Overall, the most common conditions were toenail disorders (75%), lesser toe deformities (60%), corns and calluses (58%) and bunions (37%). A summary of these findings according to sex is shown in Table 1.1. Toenail conditions, fungal infections, cracks and fissures, maceration between toes and ulcers or lacerations were more common in men, while bunions, corns and calluses,
Table 1.1 Prevalence of foot problems (%) in older people in the USA according to sex Men
Women
Total
Dermatological conditions Thickened nails* Elongated nails* Ingrown nails Corns/calluses† Fungal infection Cracks/fissures* Maceration between toes* Dry skin Ulcers/lacerations*
74.8 46.0 7.2 45.7 24.9 20.9 5.7 15.3 7.9
59.3 37.0 7.5 65.9 20.9 9.7 1.6 12.8 1.9
65.2 40.4 7.4 58.2 22.4 14.0 3.2 13.7 4.2
Orthopaedic conditions Hammer toe Mallet toe Claw toe† Bunionette Overlapping toes Missing toes Bunion† Hammer toe (great toe) Cock-up hallux Flat feet High arch†
37.3 29.4 5.2 14.0 13.6 0.2 25.3 0.8 0.7 17.2 2.4
32.8 35.9 10.8 12.7 16.9 0.8 44.3 0.6 0.7 20.1 7.0
34.5 33.4 8.7 13.2 15.6 0.5 37.1 0.7 0.7 19.0 5.2
14.1 26.0
15.3 33.9
14.9 30.9
17.9
21.7
20.2
15.2 6.4 3.9 9.0
17.8 7.2 4.3 13.2
16.8 6.9 4.2 11.6
Pain and tenderness Ankle joint pain Tenderness to palpation (any site) Tenderness: metatarsophalangeal joints Tenderness: interstitial spaces Tenderness: plantar fascia Tenderness: plantar heel pad Tenderness: medial malleolus
*men > women (p < 0.05). †women > men (p < 0.05)
claw toes and high arches were more common in women.
Studies conducted in the UK Several community-based studies of foot problems have been conducted in the UK for the purpose of determining foot health service provision needs in the National Health Service. In 1986, the Department of Health and Social Security funded a study involving
Risk factors for foot problems
a random sample of 543 people aged over 65 years.23 Initially, participants completed a questionnaire that asked whether they had a foot problem, and then 70% of the sample was assessed by a chiropodist. Half of the sample (52%) reported that they had foot problems, while foot conditions were diagnosed in 84% of the sample by the chiropodists. The most common problems reported were similar to previous studies (nail problems, corns and bunions), although the clinical assessments also revealed a high prevalence of orthopaedic disorders such as hammer toes and flat feet. Subsequent studies have largely confirmed these findings, particularly in regard to the very high prevalence of foot conditions reported when foot care specialists undertake the assessments. A study of 999 community-dwelling older people by Elton & Sanderson24 found that 71% were considered to have a foot problem by the chiropodist, and White and Mulley25 reported that, of 96 people aged over 80 years living in their own homes, only six were considered to have normal, healthy feet. However, consistent with studies in clinical populations, a much smaller proportion reported symptoms (30%). Wessex Feet,26 a foot health survey of 700 people (including 200 aged over 65 years), reported a prevalence of ‘foot problems’ of 62%, with calluses (42%), nail problems (41%), corns (30%) and hallux valgus (27%) being the most commonly reported conditions in the older group. More recently, four studies involving random samples of community-dwelling older people in the UK have reported prevalence data on foot disorders. The Clifton Assessment Procedure for the Elderly study27 in Northern Ireland involved a questionnaire of 248 people aged over 65 years. Difficulty cutting toenails was the most commonly reported problem (96%), followed by corns (48%), hard skin (36%) and hallux valgus (12%). A larger community study conducted in Wales28 involving clinical examinations of 792 people aged over 60 years reported that 53% had three or more foot problems, the most common being lesser toe deformities, corns and calluses. Finally, the Cheshire Foot Pain and Disability Survey29 of 4780 people aged 18–80 years reported a relatively low prevalence of foot pain in those aged over 65 (approximately 13%); however, the case definition of foot pain required that participants have current foot pain, pain lasting for at least 1 month, and have documented at least one disability item on the Manchester
Foot Pain and Disability Index.30 As such, the figure reported is likely to represent more severe foot pain than other surveys.
Studies conducted in other countries Although the majority of community-based studies have been conducted in the USA or UK, several smaller studies have been undertaken in Australia and in some European countries. In Australia, a mail-out questionnaire study4 conducted on 128 older people reported that 45% of men and 59% of women suffered from painful feet, mostly affecting the toes. Other commonly reported problems were nail disorders, corns and bunions. The Health Status of Older People Project conducted in 1994 was a community-based study of 1000 people aged over 65, and found a 30% prevalence of selfreported ‘problems with feet or legs’.31 A more recent prevalence study of lower extremity pain in 1486 older women reported that 34% experienced foot pain.32 Two community-based studies in Italy and the Netherlands reported similar findings in relation to the prevalence of self-reported foot pain. Benvenuti et al33 studied 459 people aged over 65 living in a small Italian town and reported that at least one foot symptom or sign was recorded in 83% of the sample, with the most common conditions being calluses or corns (65%), thickened nails (30%) and hallux deformities (21%). Foot pain ‘when standing’ was reported by 22% of the sample. A larger study of 7200 people aged over 65 conducted in the Netherlands34 reported a similar prevalence of 20% for self-reported foot problems of more than four weeks’ duration.
RISK FACTORS FOR FOOT PROBLEMS Foot conditions in older people are generally chronic and have taken many years to develop, so it is unlikely that there will ever be a prospective, longitudinal study to determine why some people develop foot problems and others do not. Nevertheless, several of the previously discussed prevalence studies have also evaluated the role of age, sex and co-morbidities in the development of foot problems, and such cross-sectional data provides useful insights into which factors may influence the development of foot symptoms.
5
EPIDEMIOLOGY OF FOOT PROBLEMS IN OLDER PEOPLE
16
box. Heel elevation increases the pressure borne by the metatarsal heads,36–39 and it has previously been demonstrated that older people who wear shoes that are too narrow or too short are more likely to have corns, lesser toe deformities, hallux valgus and foot pain.40 However, the higher prevalence of foot pain may also reflect sex differences in pain tolerance in general, since women are more likely to report musculoskeletal pain and pain interference at other body regions.41
Men Women
14 12 Prevalence (%)
6
10 8 6 4 2 0
18 – 24 25 – 34 35 – 44 45 – 54 55 – 64 65 – 74 75 – 80 Age group
Figure 1.1 Prevalence of disabling foot pain (%) in the UK according to age and sex.
AGE The most obvious risk factor for the development of foot problems is advancing age, as prevalence studies involving participants across a wide age range have consistently found that older people have much higher rates of foot problems.19,26,29 However, there is some evidence of a non-linear relationship, in that the prevalence seems to increase until the age of approximately 65 years and decline thereafter (Fig. 1.1).26,29 This is probably because of the confounding influence of physical activity. As discussed previously in relation to the lower rates of foot symptoms reported by institutionalised older people, it could be that the development of foot symptoms requires a certain level of weightbearing activity, so even older people with severely deformed feet may not develop symptoms if they lead a largely sedentary lifestyle.
SEX Sex has a clear influence on foot problems, with several studies indicating that women have a higher prevalence of foot conditions, particularly hallux valgus, corns and calluses,17,20,23,24,26,33 and are more likely to report foot pain.4,29,33–35 However, the Feet First study,22 which included a wider array of foot conditions than most prevalence studies, found that, although women were more likely to exhibit hallux valgus, corns and calluses, other conditions (nail conditions, fungal infections and ulcers) were more prevalent in men. The most likely explanation for the higher prevalence of foot problems in women is the wearing of shoes with an elevated heel and narrow toe
OBESITY Several studies have reported an association between body mass index (BMI) and foot pain in older people,21,31,32,34,35 although there is little evidence that older people with overweight or obesity have a higher prevalence of structural foot disorders. A plausible explanation for the link between obesity and foot problems can be derived from plantar pressure studies. Several investigations have assessed the loading patterns of the foot in obese and non-obese people and have demonstrated significant increases in force and pressure under the foot when walking, particularly under the midfoot and metatarsal heads.42,43 Over time, it is likely that these elevated forces will overload plantar tissues and lead to the development of conditions such as metatarsalgia44 and plantar heel pain.45 Further evidence to support a causal relationship between obesity and foot problems can be derived from a recent study of 48 obese patients undergoing bariatric surgery. Prior to surgery, all patients reported musculoskeletal complaints, with 50% reporting musculoskeletal foot pain. 6–12 months following surgery (which resulted in an average weight loss of 41 kg), only 23% of patients reported musculoskeletal symptoms and only 4% reported foot pain.46
CO-MORBIDITIES A wide range of co-morbidities are associated with the development of foot problems, such as diabetes,47 rheumatoid arthritis,48 stroke49 and systemic sclerosis.50 These associations largely reflect the direct consequences of the specific systemic disease process on the vascular, neurological, integumentary and musculoskeletal structures within the foot. However, foot problems are more common in older people with multiple chronic diseases21,31,34 or pain in other body regions21,29,32,35,51 and several recent reports have sug-
Consequences of foot problems
gested that chronic foot pain in older people may be part of a generalised form of osteoarthritis or systemic pain syndrome. Leveille et al21 found that older women with foot pain were more likely to have ankle oedema and osteoarthritis affecting the knees or hands. Similarly, participants with foot pain in the Cheshire Foot Pain and Disability Survey29 were more likely to report pain in the shoulder, axial skeleton, hip, knee and hands, and two recent studies reported that while few structural foot conditions were associated with foot pain in older people, those with foot pain were more likely to report osteoarthritis or pain in the spine, hips, hands or wrists.35,51 The role of psychological factors in the development of foot pain has been suspected for some time52 and two studies have reported that older people with foot problems are more likely to report depression.31,51 Although it is possible that the depression is a consequence of foot pain rather than a causative factor, there is emerging evidence from studies of chronic generalised musculoskeletal pain that various forms of psychological distress may precede the development of symptoms.53 Furthermore, it has been shown that people with severe mental illness (including schizophrenia, major depression and bipolar disorder) have a significantly higher prevalence of foot pain than the general population.54 Prospective studies are required to confirm whether a cause and effect relationship between psychological factors and foot pain does indeed exist.
INCOME, EDUCATION AND ETHNICITY Despite the general consensus that health status is strongly linked to sociodemographic factors, the role of education and income in the prevalence of foot problems in older people is equivocal. While some studies have reported that older people with foot problems have a lower level of income,19 others have failed to find such an association.31,32 Similarly, lower levels of education have been found to be associated with foot problems in some studies19,31 but not others.21,32,34 These discrepancies are likely to reflect differences in how income levels are defined, differences in educational systems between countries and variability in adjustment for confounders in the statistical models. The influence of ethnicity on foot problem prevalence has received little attention in the literature. Two community-based studies in the USA have found that African Americans report a higher prevalence of
foot problems than non-African Americans.19,21 However, only one study has focused on ethnic differences in clinically assessed foot problems. The Feet First study22 specifically selected a multi-ethnic community in Springfield, Massachusetts (including Puerto Rican, non-Hispanic white and African American residents) to investigate ethnic differences in foot problems. After adjusting for sex, Puerto Ricans were far less likely to have toe deformities and sensory loss than non-Hispanic whites or African Americans, while bunions and ankle oedema were more common in African Americans. The prevalence of pain was also influenced by ethnicity, with Puerto Ricans more likely to report tenderness to palpation at any site on the foot. Overall, ethnicity influenced foot problem prevalence more than education levels. As with many other health conditions, ethnic differences in the prevalence of foot problems are likely to reflect a range of historical, cultural and socioeconomic factors that influence lifestyle and access to health care, rather than genetic susceptibility.55 Furthermore, the racial groupings used in epidemiological studies are inconsistent,56 which makes direct comparisons between studies extremely difficult.
CONSEQUENCES OF FOOT PROBLEMS MOBILITY The foot provides the only direct source of contact with the supporting surface during weightbearing activities, so it reasonable to expect that foot problems could have a detrimental effect on mobility in older people. Several investigators have directly questioned older people as to whether their foot problems interfered with daily activities. White & Mulley25 interviewed 106 people aged over 80 years and reported that 34% of those with foot pain felt that their foot pain prevented them from walking. Similarly, studies of community dwelling people aged over 65 years by Black & Hale17 and Cartwright & Henderson23 found that many older people attributed their limited activity to foot problems. Significant associations between the presence of foot problems and foot-related functional limitation,57 self-reported disability58 and inability to perform activities of daily living33,34,59 (such as housework, shopping and cooking) have also been reported. Other studies have explored this relationship by conducting physical assessments in people with and
7
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EPIDEMIOLOGY OF FOOT PROBLEMS IN OLDER PEOPLE
without foot problems. An evaluation of gait patterns in 459 older people by Benvenuti et al33 revealed that those with foot pain required a greater number of steps to walk 3 m than those free of foot problems. A similar study of 1002 older women21 found that those with chronic and severe foot pain walked more slowly and took longer to rise from a chair, while Barr et al31 found that self-reported foot or leg problems were significantly associated with impaired performance on the Timed Get Up and Go test (a timed mobility test that involves rising from a chair and walking 6 m). Finally, a recent study found that an overall measure of foot impairment was significantly associated with impaired performance in tests of balance (including postural sway and leaning tests) and functional ability (including stair walking and rising from a chair).60
FALLS AND INJURIES The association between foot problems and falls has been suspected for some time. In 1958, DeLargy61 hypothesised that decreased activity associated with foot problems in older people could lead to the development of muscle weakness, thereby predisposing to falls. In contrast, Helfand62 argued that painful lesions and structural foot deformities could directly lead to a fall by detrimentally altering the foot’s functional base of support. As discussed in the previous section, there is now sound evidence that various foot characteristics are significant independent predictors of balance and functional ability, and there is emerging evidence that foot problems are also a risk factor for falls. Studies of falls risk factors can be divided into two categories: retrospective studies, in which older people’s history of falling (usually in the past 12 months) is documented and comparisons made between fallers and non-fallers; and prospective studies, in which foot characteristics are measured at baseline and the incidence of falls is determined by following participants over a 12 month period. Six retrospective studies have shown that older people who suffer from foot problems are more likely to have fallen in the previous 12 months.31,60,63–66 However, retrospective studies are limited because of the questionable accuracy of recall of falls by older people67 and difficulties in determining a causal relationship. Five prospective studies have now confirmed that foot problems are a falls risk factor. A study of 100 men aged 65–85 years by Gabell et al68 reported that undefined ‘foot problems’ was associated with a
fourfold increased risk of falling. Tinetti et al69 found that the presence of a ‘serious foot problem’ (defined as a moderate to severe bunion, toe deformity, ulcer or deformed nail) doubled the risk of falling in 336 people aged over 75 years after adjusting for sociodemographic characteristics, psychological factors and medication use. A prospective study of 979 people aged over 70 years in Finland found that older people with bunions were twice as likely to fall than those without.70 Follow-up results from the Women’s Health and Aging Study of 1002 women aged over 65 years found that foot pain was the only site of pain that was significantly associated with falls.71 The most recent prospective study of foot problems and falls72 assessed a wide range of foot and ankle characteristics (including foot posture, range of motion, deformity, lesions, tactile sensation, toe strength and pain) in 175 retirement village residents. During the 12 month follow-up period, 71 (41%) reported falling and, compared to those who did not fall, fallers demonstrated decreased ankle flexibility, more severe hallux valgus deformity, decreased plantar tactile sensitivity, decreased toe plantarflexor strength and a higher prevalence of disabling foot pain. In addition to falls, a recent study has suggested that foot problems may also increase the risk of automobile accidents in older people. A prospective cohort study of 283 people aged over 72 years by Marottoli et al73 found that those with three or more foot problems (including nail problems, calluses, bunions and hammertoes) were twice as likely to have been involved in an automobile accident during the 12 month follow-up period. This association remained significant after adjusting for several possible confounding variables related to physical performance, suggesting that foot problems may increase the risk of automobile accidents by interfering with the ability to manoeuvre between the accelerator and brake pedals.
HEALTH-RELATED QUALITY OF LIFE Quality of life in older people is strongly associated with the ability to independently undertake physical tasks free of pain and, as such, musculoskeletal conditions are a major cause of disability and reduced quality of life in this population. Several recent studies have indicated that foot problems have a detrimental impact on self-reported measures of physical, mental and social function. Using the Medical Outcomes Study Short Form 36 (SF-36) questionnaire in a com-
References
munity sample of 1486 women aged over 70 years, Chen et al32 found that the presence of foot pain was a significant determinant of both the physical component and mental component summary scores of the SF-36. Similarly, a study of 301 community-dwelling older people by Menz et al51 reported that a continuous measure of foot impairment (the Manchester Foot Pain and Disability Index) was significantly correlated with the SF-36 general health and mental health subscales. Finally, two studies have indicated that older people presenting for hallux valgus surgery exhibit significantly worse SF-36 bodily pain74 and physical function75 scores compared with the general population.
SUMMARY Foot problems are reported by at least one in three community-dwelling older people, with higher prevalence rates observed in institutional and clinical settings. The most common foot conditions in older people are nail disorders, corns and calluses, and toe deformities (including hallux valgus and lesser toe deformities). Risk factors for foot problems include age, female sex, obesity and multiple chronic diseases; however, the role of socioeconomic factors and ethnicity is unclear. Foot problems have a significant detrimental effect on mobility and quality of life in older people.
References 1. Riccitelli ML. Foot problems of the aged and infirm. Journal of the American Geriatrics Society 1966; 14: 1058–1061. 2. Menz HB, Lord SR. Foot problems, functional impairment and falls in older people. Journal of the American Podiatric Medical Association 1999; 89: 458–461. 3. Williamson J, Stokoe I, Gray S. Old people at home – their unreported needs. The Lancet 1964; i: 1117–1120. 4. Munro BJ, Steele JR. Foot-care awareness. A survey of persons aged 65 years and older. Journal of the American Podiatric Medical Association 1998; 88: 242–248. 5. Merrill HE, Frankson J, Tarara EL. Podiatry survey of 1011 nursing home patients in Minnesota. Journal of the American Podiatry Association 1967; 57: 57–64. 6. Hsu JD. Foot problems in the elderly patient. Journal of the American Geriatrics Society 1971; 19: 880– 886. 7. Ebrahim SBJ, Sainsbury R, Watson S. Foot problems of the elderly: a hospital survey. British Medical Journal 1981; 283: 949–950. 8. Hung L, Ho Y, Leung P. Survey of foot deformities among 166 geriatric inpatients. Foot and Ankle 1985; 5: 156–164. 9. Helfand AE. At the foot of South Mountain. A 5-year longitudinal study of foot problems and screening in an elderly population. Journal of the American Podiatry Association 1973; 63: 512. 10. Plummer E, Albert S. Focused assessment of foot care in older adults. Journal of the American Geriatrics Society 1996; 44: 310–313. 11. Haneke E. Achilles foot-screening project: background, objectives and design. Journal of the Euro-
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pean Academy of Dermatology and Venereology 1999; 12: S2–5. Roseeuw D. Achilles foot screening project: preliminary results of patients screened by dermatologists. Journal of the European Academy of Dermatology and Venereology 1999; 12: S6–9. Pierard G. Onychomycosis and other superficial fungal infections of the foot in the elderly: a pan-European survey. Dermatology 2001; 202: 220–224. Chan MKT, Chong L-Y. A prospective epidemiologic survey on the prevalence of foot disease in Hong Kong. Journal of the American Podiatric Medical Association 2002; 92: 450–456. Helfand AE. Keep them walking. Journal of the American Podiatry Association 1968; 58: 117–126. Helfand AE, Cooke HL, Walinsky MD et al. Foot problems associated with older patients. A focused podogeriatric study. Journal of the American Podiatric Medical Association 1998; 88: 237–241. Black JR, Hale WE. Prevalence of foot complaints in the elderly. Journal of the American Podiatric Medical Association 1987; 77: 308–311. Gould N, Schneider W, Ashikaga T. Epidemiological survey of foot problems in the continental United States 1978–1979. Foot and Ankle 1980; 1: 8–10. Greenberg L, Davis H. Foot problems in the US. The 1990 National Health Interview Survey. Journal of the American Podiatric Medical Association 1993; 83: 475–483. Greenberg L. Foot care data from two recent nationwide surveys. A comparative analysis. Journal of the American Podiatric Medical Association 1994; 84: 365–370. Leveille SG, Guralnik JM, Ferrucci L et al. Foot pain and disability in older women. American Journal of Epidemiology 1998; 148: 657–665.
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22. Dunn JE, Link CL, Felson DT et al. Prevalence of foot and ankle conditions in a multiethnic community sample of older adults. American Journal of Epidemiology 2004; 159: 491–498. 23. Cartwright A, Henderson G. More trouble with feet – a survey of the foot problems and chiropody needs of the elderly. London: Department of Health and Social Security, HMSO; 1986. 24. Elton PJ, Sanderson SP. A chiropodial survey of elderly persons over 65 years in the community. Public Health 1986; 100: 219–232. 25. White EG, Mulley GP. Footcare for very elderly people: a community survey. Age and Ageing 1989; 18: 275–278. 26. Brodie BS, Rees CL, Robins DJ et al. Wessex Feet: a regional foot health survey, vol I: The survey. Chiropodist 1988; 43: 152–165. 27. Crawford VLS, Ashford RL, McPeake B et al. Conservative podiatric medicine and disability in elderly people. Journal of the American Podiatric Medical Association 1995; 85: 255–259. 28. Harvey I, Frankel S, Marks R et al. Foot morbidity and exposure to chiropody: population based study. British Medical Journal 1997; 315: 1054–1055. 29. Garrow AP, Silman AJ, Macfarlane GJ. The Cheshire Foot Pain and Disability Survey: a population survey assessing prevalence and associations. Pain 2004; 110: 378–384. 30. Garrow AP, Papageorgiou AC, Silman AJ et al. Development and validation of a questionnaire to assess disabling foot pain. Pain 2000; 85: 107–113. 31. Barr ELM, Browning C, Lord SR et al. Foot and leg problems are important determinants of functional status in community dwelling older people. Disability and Rehabilitation 2005; 27: 917–923. 32. Chen J, Devine A, Dick IM et al. Prevalence of lower extremity pain and its association with functionality and quality of life in elderly women in Australia. Journal of Rheumatology 2003; 30: 2689–2693. 33. Benvenuti F, Ferrucci L, Guralnik JM et al. Foot pain and disability in older persons: an epidemiologic survey. Journal of the American Geriatrics Society 1995; 43: 479–484. 34. Gorter KJ, Kuyvenhoven MM, deMelker RA. Nontraumatic foot complaints in older people. A population-based survey of risk factors, mobility, and well-being. Journal of the American Podiatric Medical Association 2000; 90: 397–402. 35. Menz HB, Morris ME. Determinants of disabling foot pain in retirement village residents. Journal of the American Podiatric Medical Association 2005; 95: 573–579. 36. Snow RE, Williams KR, Holmes GB Jr. The effects of wearing high heeled shoes on pedal pressures in women. Foot and Ankle 1992; 13: 85–92.
37. Corrigan JP, Moore DP, Stephens MM. Effect of heel height on forefoot loading. Foot and Ankle 1993; 14: 148–152. 38. Nyska M, McCabe C, Linge K et al. Plantar forefoot pressures during treadmill walking with high-heel and low-heel shoes. Foot and Ankle International 1996; 17: 662–666. 39. Mandato MG, Nester E. The effects of increasing heel height on forefoot peak pressure. Journal of the American Podiatric Medical Association 1999; 89: 75–80. 40. Menz HB, Morris ME. Footwear characteristics and foot problems in older people. Gerontology 2005; 51: 346–351. 41. Thomas E, Peat G, Harris L et al. The prevalence of pain and pain interference in a general population of older adults: cross-sectional findings from the North Staffordshire Osteoarthritis Project (NorStOP). Pain 2004; 110: 361–368. 42. Hills AP, Hennig EM, McDonald M et al. Plantar pressure differences between obese and non-obese adults: a biomechanical analysis. International Journal of Obesity and Related Metabolic Disorders 2001; 25: 1674–1679. 43. Birtane M, Tuna H. The evaluation of plantar pressure distribution in obese and non-obese adults. Clinical Biomechanics 2004; 19: 1055–1059. 44. Waldecker U. Metatarsalgia in hallux valgus deformity: a pedographic analysis. Journal of Foot and Ankle Surgery 2002; 41: 300–308. 45. Black J, Bernard J, Williams L. Heel pain in the older patient. Clinics in Podiatric Medicine and Surgery 1993; 10: 113–119. 46. Hooper MM, Stellato TA, Hallowell PT et al. Musculoskeletal findings in obese subjects before and after weight loss following bariatric surgery. International Journal of Obesity 2007; 31: 114–120. 47. Reed JF. An audit of lower extremity complications in octogenarian patients with diabetes mellitus. Lower Extremity Wounds 2004; 3: 161–164. 48. Jaakkola JI, Mann RA. A review of rheumatoid arthritis affecting the foot and ankle. Foot and Ankle International 2004; 25: 866–874. 49. Jordan E, Lekkas C, Roscioli D et al. Podiatric problems on a stroke rehabilitation unit. Australian Journal on Ageing 1997; 16: 222–224. 50. Sari-Kouzel H, Hutchinson C, Middleton A et al. Foot problems in patients with systemic sclerosis. Rheumatology 2001; 40: 410–413. 51. Menz HB, Tiedemann A, Kwan MMS et al. Foot pain in community-dwelling older people: an evaluation of the Manchester Foot Pain and Disability Index. Rheumatology 2006; 45: 863–867. 52. Helfand AE. Foot pain in later life. Some psychological correlates. Journal of the American Podiatric Medical Association 1986; 76: 112–114.
References
53. Gran JT. The epidemiology of chronic generalized musculoskeletal pain. Best Practice and Research Clinical Rheumatology 2003; 17: 547–561. 54. Crews CK, Vu KO, Davidson AJ et al. Podiatric problems are associated with worse health status in persons with severe mental illness. General Hospital Psychiatry 2004; 26: 226–232. 55. Pearce N, Foliaki S, Sporle A et al. Genetics, race, ethnicity, and health. British Medical Journal 2004; 328: 1070–1072. 56. Ahdieh L, Hahn RA. Use of terms ‘race’, ‘ethnicity’, and ‘national origins’: a review of articles in the American Journal of Public Health, 1980–1989. Ethnicity and Health 1996; 1: 95–98. 57. Badlissi F, Dunn JE, Link CL et al. Foot musculoskeletal disorders, pain, and foot-related functional limitation in older persons. Journal of the American Geriatrics Society 2005; 53: 1029–1033. 58. Keysor JJ, Dunn JE, Link CL et al. Are foot disorders associated with functional limitation and disability among community-dwelling older adults? Journal of Aging and Health 2005; 17: 734–752. 59. Bowling A, Grundy E. Activities of daily living: changes in functional ability in three samples of elderly and very elderly people. Age and Ageing 1997; 26: 107–114. 60. Menz HB, Lord SR. The contribution of foot problems to mobility impairment and falls in older people. Journal of the American Geriatrics Society 2001; 49: 1651–1656. 61. DeLargy D. Accidents in old people. Medical Press 1958; 239: 117–120. 62. Helfand AE. Foot impairment – an etiologic factor in falls in the aged. Journal of the American Podiatry Association 1966; 56: 326–330. 63. Wild D, Nayak U, Isaacs B. Characteristics of old people who fell at home. Journal of Clinical and Experimental Gerontology 1980; 2: 271– 287. 64. Blake A, Morgan K, Bendall M et al. Falls by elderly people at home – prevalence and associated factors. Age and Ageing 1988; 17: 365–372.
65. Bumin G, Uyanik M, Aki E et al. An investigation of risk factors for falls in elderly people in a Turkish rest home: a pilot study. Aging – Clinical and Experimental Research 2002; 14: 192–196. 66. Dolinis J, Harrison JE. Factors associated with falling in older Adelaide residents. Australian and New Zealand Journal of Public Health 1997; 21: 462– 468. 67. Cummings SR, Nevitt MC, Kidd S. Forgetting falls – the limited accuracy of recall of falls in the elderly. Journal of the American Geriatrics Society 1988; 36: 613–616. 68. Gabell A, Simons MA, Nayak USL. Falls in the healthy elderly: predisposing causes. Ergonomics 1985; 28: 965–975. 69. Tinetti ME, Speechley M, Ginter SF. Risk factors for falls among elderly persons living in the community. New England Journal of Medicine 1988; 319: 1701–1707. 70. Koski K, Luukinen H, Laippala P et al. Physiological factors and medications as predictors of injurious falls by elderly people: a prospective population-based study. Age and Ageing 1996; 25: 29–38. 71. Leveille SG, Bean J, Bandeen-Roche K et al. Musculoskeletal pain and risk of falls in older disabled women living in the community. Journal of the American Geriatrics Society 2002; 50: 671–678. 72. Menz HB, Morris ME, Lord SR. Foot and ankle risk factors for falls in older people: a prospective study. Journal of Gerontology 2006; 61A: M866–870. 73. Marottoli RA, Cooney LM, Wagner R et al. Predictors of automobile crashes and moving violations among elderly drivers. Annals of Internal Medicine 1994; 121: 842–846. 74. Thordarson DB, Ebramzadeh E, Rudicel SA et al. Age-adjusted baseline data for women with hallux valgus undergoing corrective surgery. Journal of Bone and Joint Surgery 2005; 87A: 66–75. 75. Lazarides SP, Hildreth A, Prassanna V et al. Association amongst angular deformities in hallux valgus and impact of the deformity in health-related quality of life. Foot and Ankle Surgery 2005; 11: 193–196.
11
CHAPTER
Physiological changes in the ageing foot
The foot undergoes significant structural and functional changes with advancing age. While many of these changes merely reflect the physiological alterations in tissues elsewhere in the body, some changes are more pronounced than those that occur in other body regions, while others are unique to the highly specialised loadbearing structures of the foot. Indeed, it has been argued that careful assessment of the older foot can provide useful clinical insights into systemic conditions yet to be clearly manifested elsewhere.1 The following chapter reviews the body of literature pertaining to age-related changes of the foot in relation to the integumentary system, the soft tissue structures, the peripheral vascular and sensory systems, the skeletal system and the muscular system, and discusses the functional implications of these changes.
CHAPTER CONTENTS Integumentary system 13 Epidermis and dermis 14 Nails 15 Functional implications 15 Plantar soft tissues 15 Peripheral vascular system 16 Arteries 16 Capillaries 17 Veins 17 Functional implications 17 Peripheral sensory system 17 Functional implications 18 Skeletal system 18 Bone 18 Joints 18 Tendon and ligament 19 Functional implications 20 Muscular system 20 Age-related changes in muscle tissue Ankle muscles 21 Foot muscles 21 Functional implications 22 Summary 22 References 22
2
INTEGUMENTARY SYSTEM 20
The integumentary system consists of the skin, nails and subcutaneous tissues. The primary functions of this system are to provide a barrier between the body and its surrounding environment, to provide sensory information and to assist in the regulation of body temperature. Normal ageing is known to affect the structure and function of each of the components of the integumentary system, which often manifest as characteristic changes to the appearance of the foot.2 These changes are summarised in Table 2.1 and are described in more detail in the following section.
14
PHYSIOLOGICAL CHANGES IN THE AGEING FOOT
Table 2.1 Summary of major age-related physiological changes to the integumentary system Age-related changes
Implications
Skin ↓ production and turnover of keratinocytes ↓ density of sweat glands ↓ number of Langerhans cells ↓ number of dermal collagen and elastin fibres ↑ thickness and stiffness of dermal collagen fibres ↓ capillary loops in papillary dermis
↑ ↑ ↓ ↑ ↑
Nails ↓ nail growth rate (up to 50% reduction) ↑ nail plate thickness Plantar soft tissues Distortion and rupture of septa ↓ compressibility ↑ stiffness ↑ energy dissipation
EPIDERMIS AND DERMIS The skin of the sole of the foot has several unique features. Most notably, plantar skin is hairless and, although it contains a high density of eccrine sweat glands, it has no sebaceous glands.3 The plantar epidermis is considerably thicker (approximately 1.5 mm thick, compared to 0.1 mm in other regions of the body) and demonstrates a pattern of ridges that assist in generating sufficient friction when standing and walking barefoot. The plantar dermis is approximately 3 mm thick and is penetrated by adipose tissue, which provides resilience to shear stresses.3,4 Plantar skin is also highly adaptable, as evidenced by the considerably thicker epidermis and dermis observed in people who do not wear shoes.5 Because of this adaptability, it is sometimes difficult to delineate age-related changes from the effects of weightbearing activity and footwear. Advancing age is associated with several significant changes to the structure and function of the skin at both the epidermal and dermal levels.2,6–9 The thickness of the epidermis does not change appreciably with age;10 however, the dermal–epidermal junction becomes flattened, which may give the impression of atrophy.11 In the foot, there may be an increase in epidermal thickness due to thickening of the stratum corneum associated with plantar calluses.12 The shape and size of epidermal keratinocytes becomes more variable, and the rate of production and turnover of
dryness of skin → fissuring and hyperkeratosis risk of infection wound healing wound dehiscence bruising
↑ time required to treat nail infections ↑ rate of re-infection ↑ peak pressures under forefoot → metatarsalgia Development of plantar heel pain
keratinocytes may reduce to only 50% of that of a young person.13 Because of this delay in turnover time, the moisture content of keratinocytes is reduced, which, combined with the reduction in sweat gland density,14 contributes to the dry, scaly appearance of elderly skin.7,8 Langerhans cells, which play an important role in the immune function of the epidermis, decrease dramatically with age,15 resulting in a reduced rate of sensitisation to microorganisms.16 In contrast to the epidermis, the dermis undergoes a significant reduction in thickness due to a marked loss of collagen fibres.17 The collagen fibres that remain become thicker and stiffer and undergo a haphazard cross-linking process.7,18 Elastin fibres, which provide the skin with its elasticity, decrease in number and become fragmented.19,20 These processes alter the mechanical properties of the skin, leading to increased fragility and loss of elastic recoil. Dermal macrophages and mast cells, which provide the second line of immune defence after epidermal Langerhans cells, reduce in number with advancing age, lowering the speed and intensity of the inflammatory response to infection.16 Another factor that contributes to the impaired inflammatory response in older people is the agerelated decline in cutaneous microvascular function. Older people exhibit a significant reduction in the number of capillary loops in the papillary dermis, increased porosity of endothelial cells and a thickened
Integumentary system
basement membrane, all of which contribute to a less efficient superficial blood supply.13,21–23 It has been demonstrated that a 70-year-old may have up to 40% less blood supply to the skin than a 20-year-old,24 and these age-related changes appear to be particularly pronounced in the lower limb. One of the most obvious manifestations of this change is a progressive reduction in skin surface temperature extending distally from the groin.25
NAILS Nails are comprised primarily of keratin produced by the nail matrix, with a small contribution from the underlying nail bed.26 Compared to fingernails, toenails are thicker (1.65 versus 0.60 mm) and have a slower linear growth rate (1 mm/month versus 3 mm/month).27,28 With advancing age, the rate of growth of the nails decreases by up to 50%,29,30 because of both a reduction in the turnover rate of keratinocytes and a reduction in size of the nail matrix itself. This process is particularly pronounced in toenails, possibly because of the greater age-related decline in blood supply to the feet compared to the hands.28 In addition to decreased rate of growth, the chemical composition, histology and structure and appearance of the nail plate changes with age. Older nails exhibit an increase in calcium and reduction in iron content, increased size of keratinocytes and degeneration of elastic tissues beneath the nail bed.28 The formation of longitudinal grooves and an overall increase in thickness (onychauxis), often leads to a marked loss of translucency,2,27 while periods of arrested growth due to periods of systemic illness may also manifest as transverse ridges known as Beau’s lines.27 These changes are exacerbated by the presence of arterial insufficiency and low-level chronic trauma from illfitting footwear.27,28
FUNCTIONAL IMPLICATIONS The physiological changes in the integumentary system that occur with ageing have important functional implications. As stated previously, the decreased water content of keratinocytes and decreased density of eccrine glands leads to an overall drying of the skin, which predisposes to the development of hyperkeratosis and fissuring. The reduction in epidermal and dermal immune function increases the risk of infection31 and the reduced rate of epidermal turnover may
increase the time required to successfully treat these infections.2 Wound healing is significantly delayed in older people, because of both a reduction in wound contraction (a direct result of collagen cross-linking and diminished elastin content of the dermis) and a reduced rate of epithelialisation and angiogenesis.32–34 Even if a wound successfully heals, the tensile strength at the wound site is diminished, which increases the likelihood of dehiscence. Subsequently, wounds in older people often require much longer periods of treatment and frequently recur. Bruising is also more likely to occur because of the decreased integrity of superficial blood vessels leading to leakage of red blood cells into the papillary dermis.2 Age-related changes in the structure and function of the nail have important implications for the management of fungal nail infections (onychomycosis), one of the most common foot problems in older people.35 Because of the reduction in nail growth rate and subsequent thickening of the nail plate, treatment of onychomycosis with either oral or topical agents may take considerably longer in older people and the possibility of reinfection is much higher.36
PLANTAR SOFT TISSUES The sole of the foot has highly specialised soft tissue structures in the heel and metatarsal head regions that are designed to absorb impact forces associated with weightbearing activities. Ageing is known to influence both the structure and function of these tissues and, although the literature is inconsistent, there is emerging evidence that these changes may be associated with the development of symptoms.
Metatarsal pads The plantar tissues of the forefoot serve numerous functions, including anchoring the skin to the underlying bony architecture of the foot, protecting underlying flexor tendons, blood vessels and nerves, and attenuating both vertical and shear forces applied during gait.37 The latter function is achieved by specialised pads of fat cells under each metatarsal head confined by retinacula extending from the dermis to the sides of each flexor tendon sheath.4 The metatarsal pads progressively decrease in thickness from the first to fifth metatarsal heads38–40 and undergo compression of 10–15% when standing40 and up to 46% during gait.41
15
16
PHYSIOLOGICAL CHANGES IN THE AGEING FOOT
Although atrophy of metatarsal padding is frequently observed in older people, no studies have confirmed this finding using imaging techniques. Furthermore, no histological studies have been undertaken to ascertain whether ageing is associated with a breakdown of the connective tissues of the plantar forefoot. However, comparisons of the mechanical properties of metatarsal pads in young and older people by Hsu et al42 and Wang et al38 have demonstrated that older pads demonstrate greater stiffness, dissipate more energy when compressed and are slower to recover after the load is removed, all of which are likely to impair the ability of the forefoot to attenuate forces when walking.
Heel pad The heel pad consists of a 13–21 mm thick layer of connective tissue, the deepest portion of which is firmly adhered to the plantar periosteum of the calcaneus by a series of dense fibrous septa containing closely packed fat cells.4 In response to loading, these fat cells flow within the individual chambers, and it is this mechanism, along with the elastic properties of the septa themselves, that provides the heel pad with its shock attenuation capability.43 Evaluations of cadaver heel pads indicate that, with advancing age, the collagen fibres within the septa increase in number and size and appear more fragmented. As a result, the septa may become distorted and rupture, leading to a leakage of fat cells.44 However, this process does not lead to an overall decrease in the unloaded thickness of the heel pad; indeed, there is some evidence that older heel pads are slightly thicker than those of younger people.45–47 Rather, the functionally important age-related differences relate to how the heel pad responds to applied loads. Kinoshita et al48 used a drop-testing apparatus that applied a 5 kg mass to the heels of 10 young and 20 older people at two impact velocities. At the faster impact velocity (0.94 m/s), the older heel pads demonstrated less deformation and greater energy dissipation. In a study using ultrasound measurements of the heel pad in response to vertical loading, Hsu et al46 found that, while the unloaded heel pads of older people were slightly thicker, they demonstrated less compressibility than the younger subjects when a 3 kg load was applied. Evaluation of stress–strain curves indicated that older subjects’ heel pads were also slightly stiffer and dissipated more energy.
Functional implications The functional implications of the changes in plantar soft tissues associated with ageing are unclear. While atrophy of the metatarsal fat pads has been suggested to be a contributing factor to the development of forefoot pain, a recent study using ultrasound measurements found no differences in the thickness of metatarsal pads in those with and without metatarsalgia.49 However, it is likely that the mechanical properties of the fat pads are more relevant than their thickness, as it has been shown that the peak pressure under the metatarsal heads during gait is greater in people with forefoot symptoms.50 Similarly, while research findings related to the role of heel pad thickness in the development of heel pain are equivocal,51–53 it appears that painful heel pads are less compressible and dissipate more energy.51,53 Further studies utilising dynamic measurements of plantar soft tissues are therefore required to confirm the suspected association between ageing soft tissues and foot pain.
PERIPHERAL VASCULAR SYSTEM ARTERIES The arterial wall consists of three layers. The innermost layer, the intima, is composed of endothelial cells, which provide a smooth surface for the passage of blood, supported by a meshwork of collagen and elastin fibres. The middle layer (media) of large arteries consists mostly of elastin and provides vessels with the ability to expand and contract in response to changes in blood flow volume. In contrast, the media of small arteries is largely made up of smooth muscle. The outermost layer (adventitia) is primarily loose connective tissue, which assists in flexibly anchoring the vessel to surrounding structures. A summary of age-related changes in the peripheral vascular system is provided in Table 2.2. Normal ageing does not appear to affect the structure or function of the adventitia; however, considerable changes take place in the intima of all vessels and the media of large arteries. For reasons that are still unclear, the size and shape of endothelial cells become more irregular, and the overall thickness of the intima and media increases as a result of collagen cross-linking and invasion of smooth muscle cells.54–56 Elastin fibres in the media of large arteries break down and stiffen, result-
Peripheral sensory system
Table 2.2 Summary of major age-related physiological changes to the peripheral vascular system Age-related changes
Implications
↑ collagen cross-linking ↑ thickness of intima and media ↑ stiffness of arterial walls ↑ capillary wall thickness → reduced blood flow ↓ diameter of veins
↓ skin temperature ↑ risk of peripheral arterial disease ↑ risk of venous insufficiency
Development of perforator vein incompetence
ing in a reduction in elastic recoil, a reduction in overall flow and an elevation in blood pressure.57 These age-related changes appear to be most pronounced in the lower limb. For example, pulse transmission times (a measure of arterial stiffness) decrease by 1.6 ms/year in the toes compared to 0.6 ms/year in the fingers58 and vasodilation in response to occlusion decreases by 7% per decade in the calf compared to 4% per decade in the forearm.59
CAPILLARIES Capillaries are often less than 1 mm in length and consist of a single layer of endothelial cells supported by a basement membrane. The primary role of capillaries is the exchange of oxygen from red blood cells to surrounding tissues and absorption of waste material. With advancing age, capillaries become even narrower and their porous walls increase in thickness, because of basement membrane thickening and collagen deposition.60 As a result of these changes, ageing is associated with an overall reduction in capillary blood flow, particularly in the lower limb.61,62
VEINS Veins have the same basic structure as small arteries but are larger in diameter and exhibit considerably thinner walls. Relatively little is known about the effects of age on the microstructure of veins and no studies have directly evaluated the effect of age on structure and function of foot veins. However, the diameter of the femoral veins has been shown to
decrease slightly from the age of 60 years and the velocity of blood flow within them steadily declines from the age of 50 years.63 Advancing age is also significantly associated with perforator vein incompetence,64 which may result from the accumulation of collagen fibres around valves.
FUNCTIONAL IMPLICATIONS The overall decline in peripheral vascular function in older people clearly manifests in the foot. Even in the absence of overt vascular disease, many older people complain of cold feet and exhibit dry, flaky skin, particularly on the dorsum of the foot and the toes. As stated in the section on the integumentary system, peripheral vascular changes contribute to delayed wound healing and increased risk of infection. Furthermore, although the development of peripheral arterial disease is multifactorial, age itself has been shown to be an independent risk factor, with an approximate twofold increase in risk for every 10-year increase in age.65 Age is also an independent risk factor for conditions associated with venous insufficiency, such as varicose veins66,67 and venous ulcers,68 which commonly affect the foot and ankle.
PERIPHERAL SENSORY SYSTEM The key components of the peripheral sensory system are the sensory neurons, which consist of a nerve cell body, branch-like extensions called dendrites and an elongated axon that extends from the nerve cell body, and a range of sensory receptors, which are located in the skin and detect a range of stimuli, including vibration, pressure and temperature.69 In particular, the glabrous skin on the sole of the foot contains large populations of mechanoreceptors capable of detecting the site, velocity and acceleration of mechanical stimuli.69–71 A summary of age-related changes in the peripheral sensory system is provided in Table 2.3. With advancing age, there is a generalised decline in the size and number of axons, and the myelin sheaths surrounding the axons undergo significant deterioration, leading to a reduction in nerve conduction velocity.72 Merkel discs and free nerve endings are not affected by age; however, Meissner and Pacinian corpuscles considerably reduce in density and the receptors that remain exhibit a number of morphological alterations.73 As a
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Table 2.3 Summary of major age-related physiological changes to the peripheral sensory system Age-related changes
Implications
↓ size and number of axons → ↓ nerve conduction velocity Deterioration of myeline sheaths ↓ density of Meissner and Pacinian corpuscles
↓ tactile and vibration sensitivity ↓ proprioception and kinaesthesia ↓ balance ↓ walking speed and stability ↑ risk of falls ↑ likelihood of undetected tissue damage
result of changes in receptor structure and function, ageing is associated with significant reductions in tactile sensitivity,74–77 spatial acuity78–81 and vibration sense,74,77,82–85 and these changes are particularly pronounced in the lower limb compared to the upper limb.79,82,86 Proprioception (the ability to detect the position of body parts) and kinaesthesia (the ability to detect movement of body parts) rely partly on skin receptors but also on Golgi tendon organs and receptors in muscle spindles.87 As with other mechanoreceptive abilities, ageing is associated with significant decline in proprioception and kinaesthesia in the sagittal plane of the knee76,88–91 and the sagittal92–95 and frontal plane96 of the ankle.
FUNCTIONAL IMPLICATIONS When standing and walking, the sole of the foot provides the only direct contact with the ground and therefore provides important sensory information about the supporting surface.97 Furthermore, ankle proprioception plays an important role in maintaining balance when walking on irregular terrain. Subsequently, age-related changes in peripheral sensation are associated with deficits in balance 98–103 and walking speed,104,105 and reduced peripheral sensation is an important risk factor for falls.106,107 Loss of plantar sensation in older people may also result in pressure from ill-fitting footwear or foreign bodies within the shoe being undetected, leading to tissue damage and ulceration.108
SKELETAL SYSTEM BONE Bone cells produce two types of tissue: cortical bone, which consists of long tubes of bone matrix (called osteons) forming the outer layer of the bone, and trabecular bone, an irregular matrix that forms the central core of the bone. Cortical bone comprises approximately 90% of the skeleton and is found primarily in long bones. Both types of bone are in a continuous process of remodelling, because of a coupling between bone formation by osteoblasts and bone resorption by osteoclasts. This process enables bone to respond to changing mechanical and metabolic demands.109 A summary of age-related changes in the skeletal system is provided in Table 2.4. Age-related changes in the physiology and biochemistry of bone cells are complex and only partly understood; however, it is thought that ageing primarily affects the structure and function of bone marrow, from which cellular precursors to osteoblasts and osteoclasts are formed. This results in reduced osteoblastic activity, and subsequently the amount of bone formed is not equivalent to the amount of bone resorbed.110 Bone mass therefore undergoes a characteristic trajectory throughout the lifespan, with steady increases in bone density throughout adolescence, a plateau between the third and fifth decade and a progressive decline thereafter.111 In men, age-related bone loss occurs at a rate of approximately 5% per decade,112,113 whereas women experience a more rapid loss (approximately 10% per decade) from the onset of menopause.114 From the age of 75 years, bone loss slows to approximately 3% per decade.112–114 Possibly in response to these changes in bone density, older people’s bones (both cortical and cancellous) also demonstrate a higher proportion of microfractures.115
JOINTS Although the alignment and morphology of lower limb joints differ considerably depending on their function, the basic structure is essentially the same. Each of the bones comprising the joint is covered with a thin layer of articular cartilage. The space between the bones, the joint cavity, is lined by a synovial membrane, which secretes synovial fluid, enabling smooth movement of one bone over the other. Encasing the synovial membrane is the joint capsule, which consists of strong but flexible collagen
Skeletal system
Table 2.4 Summary of major age-related physiological changes to the skeletal system Age-related changes
Implications
Bone ↓ osteoblastic activity ↓ bone density
↑ risk of osteoporosis ↑ risk of traumatic and insufficiency fractures
Joints ↑ collagen cross-linking of cartilage ↓ water content of cartilage ↑ stiffness of synovial membrane and joint capsule ↓ production of synovial fluid
↑ ↓ ↓ ↑
Tendon and ligament ↑ collagen fibril concentration, diameter and cross-linking ↓ water content of glycosaminoglycans ↑ lipid content
↑ risk of posterior tibial tendon dysfunction ↑ risk of tendon rupture when performing non-sporting activities
fibres, and binding the entire joint together are ligaments, which are also primarily composed of collagen fibres. Much of the research relating to age-related changes in joints has focused on cartilage, because of its role in the development of osteoarthritis. Cartilage is a dense connective tissue comprising cells (called chondrocytes) dispersed in a matrix of various types of collagen, proteoglycans and other matrix proteins, and water. The matrix provides cartilage with the ability to withstand compressive, tensile and shear forces generated during movement. Degradation of cartilage is a complex process influenced not only by age but also nutrition, individual mechanical joint characteristics and level of physical activity. Furthermore, it is difficult to delineate age-related changes from those associated with osteoarthritis. Nevertheless, several changes in articular cartilage do appear to be related to the ageing process. At the molecular level, there is a gradual reduction in the amount of chondroitin sulphate and oligosaccharides, and a corresponding increase in keratan sulphate.116 Collagen fibril width and cross-linking increase with age, and the water content decreases.117 Somewhat surprisingly, the cell content and thickness of articular cartilage does not appear to change appreciably with age,118 and joint surfaces in older people may be more congruent than those of younger people. The latter observation has been explained by the notion that some level of incongruence is a normal feature of a healthy joint, in order to provide access of synovial fluid to the cartilage and allow for controlled loading.
risk of osteoarthritis joint range of motion balance risk of falls
With ageing, this protective mechanism becomes less effective, and the joint may be in a state of constant loading.119 In addition to these changes in cartilage structure and function, ageing also results in a stiffening of the synovial membrane and a reduction in its ability to produce synovial fluid. As with ageing cartilage, there is a reduction in the amount of chondroitin sulphate in the synovial fluid,120 which may influence its viscosity. Collagen cross-linking also results in a shortening and stiffening of the joint capsule and supporting ligaments.121
TENDON AND LIGAMENT The primary function of tendons is to transmit muscle force to the skeletal system, whereas the function of ligaments is to bind bones together and restrict excessive movement. Despite this difference in function, the structure of tendons and ligaments is similar – both structures consist primarily of collagen fibrils embedded in a matrix of proteoglycans. Evaluating the effect of ageing on the structure of human tendons and ligaments, however, is inherently difficult because of the need to biopsy tissue. As a consequence, much of our knowledge regarding the biochemical and histological changes in these structures stems from animal models (most commonly rat tails or the Achilles tendons of rabbits), cadavers, or tendons and ligaments harvested from surgical cases.122 These investigations have revealed that advancing age results in significant increases in collagen fibril
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concentration123 and diameter,124 and increased spacing and cross-linking of collagen molecules,125 factors thought be indicative of non-enzymatic glycosylation. Non-collagenous components of tendon have also been shown to undergo changes with age, with decreases in the water content of glycosaminoglycans126 and increases in lipid content.127 A small number of studies have directly evaluated structural changes in the human Achilles tendon. Snow et al128 analysed gross anatomy and histological sections of Achilles tendons obtained from neonatal, young and old cadavers, and reported a progressive reduction in the number of fibres connecting the tendon to the plantar fascia with advancing age. In the older group, a band of periosteum clearly separated the insertion of the Achilles tendon and the plantar fascia. Using light and electron microscopy, Strocchi et al129 evaluated 15 cadaver Achilles tendons up to 87 years of age and reported that ageing was associated with a decrease in the diameter but an increase in the concentration of collagen fibrils. Similar results were reported by Sargon et al130 in 28 Achilles tendon specimens obtained from patients undergoing heel surgery. Finally, using magnetic resonance imaging, Magnusson et al131 demonstrated that older women have a larger Achilles tendon cross-sectional area than younger women, reflecting the age-related hypertrophy evident in animal studies.
FUNCTIONAL IMPLICATIONS The functional implications of an ageing skeletal system are considerable. Changes in bone density are strongly linked to the development of osteoporosis, the prevalence of which increases exponentially with age.132 Although the most serious consequences of osteoporosis are vertebral, femoral and radius fractures, insufficiency fractures of the foot may also occur, most commonly in the metatarsals133–135 but also in the calcaneus136 and talus.137 Such fractures are frequently misdiagnosed and often lead to impaired mobility. Ageing is also a significant risk factor for osteoarthritis,138 which affects the first metatarsophalangeal joint of the foot in 44% of people over the age of 80 years.139 Changes in joint tissues may also be responsible for the reduced range of motion of lower extremity joints in older people. Several studies have shown that ankle dorsiflexion–plantarflexion range of motion reduces with age140–142 and Nigg et al141 have also noted a significant reduction in inversion–eversion and abduc-
tion–adduction motion of the ankle joint complex. Of particular note, women generally exhibited greater range of motion than men but also demonstrated greater reductions in ankle dorsiflexion and eversion with age. More recently, Scott et al143 showed that older people had significantly less range of motion at the ankle joint (36° versus 45°, using a weightbearing lunge test) and less passive range of motion the first metatarsophalangeal joint (56° versus 82°, measured non-weightbearing) compared to younger controls. Assessment of foot posture also indicated that older people had significantly flatter feet, as indicated by a higher foot posture index and arch index, and a reduction in the height of the navicular tuberosity. Reduction in joint range of motion in the foot is strongly associated with impaired balance and functional ability144,145 and increases the risk of falls,145,146 while the progressive flattening of the arch may predispose to the development of posterior tibial tendon dysfunction, a disorder in which the tendon becomes progressively weakened and elongated, resulting in a painful flatfoot deformity.147 There is also emerging evidence that restricted range of motion in the ankle joint may impair the function of the calf muscle pump, thereby contributing to the development of venous disorders of the lower limb.148,149 Finally, despite having a reduced overall risk of tendon rupture because of their reduced exposure to ballistic activities, older people have an increased risk of tendon rupture when performing non-sporting activities, possibly due to age-related increases in tendon stiffness.150,151
MUSCULAR SYSTEM AGE-RELATED CHANGES IN MUSCLE TISSUE Muscle fibres consist of elongated actin and myosin filaments encased in a tubular membrane. Broadly speaking, two types of fibre have been identified: type I fibres, which contract slowly and can stay contracted for long periods of time before fatiguing, and type II fibres, which contract more quickly but also fatigue more easily. One of the most characteristic features of advancing age is the inevitable reduction in the total mass of muscle fibres, often referred to as sarcopenia (adapted from the Greek, meaning ‘poverty of the flesh’).152,153 Muscle mass accounts for 40% of
Muscular system
Table 2.5 Summary of major age-related physiological changes to the muscular system Age-related changes
Implications
↓ total muscle mass ↓ muscle cross-sectional area ↓ size of Type II fibres Development of large, slow-twitch motor units
↓ ankle dorsiflexion and plantarflexion strength ↓ toe plantarflexion strength ↓ balance ↓ walking speed ↑ risk of falls
the total body weight of young people but this reduces to approximately 25% of total body weight in older people.154 This reduction in muscle mass is strongly correlated with the reduction in total muscle crosssectional area, which has been shown to decrease by approximately 40% between the ages of 20 and 60 years155 and involves reductions in both the size and number of muscle fibres.156,157 Although preliminary research suggested that age-related loss of muscle fibres specifically affected type II fibres, more recent evidence indicates that although ageing results in a reduction in the size of type II fibres,158,159 the relative proportion of type I and type II fibres is largely unaffected by age.153 However, ageing also results in motor unit remodelling, a process in which type II fibres are denervated and then reinnervated by collateral branches of type I fibres, resulting in the formation of large, slow-twitch motor units.153 A summary of these changes is provided in Table 2.5. Age-related changes in muscle composition result in significant reductions in muscle strength throughout the body. Comparisons in muscle strength between young and older people (most commonly the quadriceps muscles) generally report differences in strength in the order of 20–40% between the age of 30 and 80 years; however, people aged in their 90s may exhibit even larger reductions (50% or greater).152,160 Because young men generally exhibit greater strength than young women, their absolute reduction in strength associated with age is greater, although the relative loss is similar for both sexes. Because of the difficulties associated with conducting long-term prospective studies, the rate at which these changes occur is not fully understood; however, figures of 1–3% per year have been suggested.161,162
ANKLE MUSCLES As stated above, most studies addressing age-related differences in strength have examined quadriceps muscles; however, some have focused on ankle muscles. One of the earliest studies to assess age-associated changes in ankle muscle function was that of McDonagh et al,163 who compared ankle plantarflexor strength in young and older men and reported that the maximum voluntary contraction in older subjects was 20% weaker than in young subjects. A comparison of these results with those of arm flexor strength suggested that ankle plantarflexors were more significantly affected by advancing age. More recent investigations have largely confirmed these results. Vandervoort & McComas164 reported that the strength of ankle plantarflexor and dorsiflexor muscles declined with advancing age but the differences were most marked from late middle age onwards. VanSchaik et al165 reported that ankle dorsiflexion strength was significantly decreased in subjects aged 60–80 years compared to subjects aged 20–40 years. Similarly, Winegard et al166 compared ankle plantarflexor strength in subjects aged 20–91 years and found that strength significantly decreased with advancing age. Although considerable differences in study populations and methods used make direct comparisons of these investigations difficult, it can be concluded that older people exhibit between 30% and 60% of the ankle strength of younger people.152
FOOT MUSCLES Although it has long been suspected that ageing is associated with atrophy of intrinsic foot muscles, evidence to support such an assertion is scarce. Recent studies using magnetic resonance imaging in people with and without diabetes indicates significant reductions in the volume of ankle plantarflexors167 and intrinsic foot muscles168–170 associated with the disease. Given that many of the neuromuscular changes that occur in diabetes are similar to those of advancing age, it is likely that comparisons between healthy young and older people would reveal similar, but not as marked, differences in foot muscle volume. Only two studies have investigated age-related changes in the strength of foot muscles. Endo et al171 measured the force applied by the toes in 20 young and 20 older participants when instructed to place all their bodyweight on their forefoot while leaning forwards as far as possible. The results revealed that older participants generated 29% less force than younger
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PHYSIOLOGICAL CHANGES IN THE AGEING FOOT
participants. However, the contribution of ankle plantarflexor strength using this testing procedure cannot be discounted and it is likely that the amount of force applied by the toes was also influenced by balance ability. Furthermore, this approach is incapable of delineating between the strength of the hallux and the lesser toes. To address these issues, Menz et al172 used a pressure platform to measure toe plantarflexor strength in 40 young and 40 older participants while seated. The results indicated that older participants exhibited 32% less plantarflexion strength of the hallux and 27% less plantarflexion strength of the lesser toes compared to younger participants, and women exhibited 42% less hallux plantarflexor strength than men. However, sex did not influence lesser toe plantarflexor strength.
FUNCTIONAL IMPLICATIONS The key functional implication of an ageing muscular system is its effect on functional mobility in older people. Lower limb strength is strongly associated
with balance,98 walking speed105,173 and the ability to rise from a chair174 and, subsequently, loss of strength is a major contributor to falls175 and overall functional decline.176 However, there is solid evidence that agerelated loss of strength and its functional consequences can be partly prevented, and possibly partly reversed, by resistance training.153 Secondly, although several authors have suggested that atrophy and/or imbalance of foot muscles may be related to the development of hallux valgus177,178 and lesser toe deformities,169 the role of muscle weakness in the development of foot deformity remains unclear.
SUMMARY Normal ageing has a significant effect on the structure and function of the foot and these changes have considerable implications for the development of foot problems. A sound knowledge of these changes is essential for clinicians involved in the assessment and management of foot disorders in older people.
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50. Waldecker U. Metatarsalgia in hallux valgus deformity: a pedographic analysis. Journal of Foot and Ankle Surgery 2002; 41: 300–308. 51. Prichasuk S. The heel pad in plantar heel pain. Journal of Bone and Joint Surgery 1994; 76B: 140–142. 52. Tsai WC, Wang CL, Hsu TC et al. The mechanical properties of the heel pad in unilateral plantar heel pain syndrome. Foot and Ankle International 1999; 20: 663–668. 53. Tong J, Lim CS, Goh OL. Technique to study the biomechanical properties of the human calcaneal heel pad. The Foot 2003; 13: 83–91. 54. Virmani R, Avolio AP, Mergner WJ et al. Effect of aging on aortic morphology in populations with high and low prevalence of hypertension and atherosclerosis. Comparison between occidental and Chinese communities. American Journal of Pathology 1991; 139: 1119–1129. 55. Homma S, Hirose N, Ishida H et al. Carotid plaque and intima-media thickness assessed by B-mode ultrasonography in subjects ranging from young adults to centenarians. Stroke 2001; 32: 830–835. 56. Labropoulos N, Leon LR, Brewster LP et al. Are your arteries older than your age? European Journal of Vascular and Endovascular Surgery 2005; 30: 588–596. 57. Ferrari AU, Radaelli A, Centola M. Invited review: Aging and the cardiovascular system. Journal of Applied Physiology 2003; 95: 2591–2597. 58. Allen J, Murray A. Age-related changes in peripheral pulse timing characteristics at the ears, fingers and toes. Journal of Human Hypertension 2002; 16: 711–717. 59. Ridout SJ, Parker BA, Proctor DN. Age and regional specificity of peak limb vascular conductance in women. Journal of Applied Physiology 2005; 99: 2067–2074. 60. Wei JY. Age and the cardiovascular system. New England Journal of Medicine 1992; 327: 1735– 1739. 61. Richardson D, Schwartz R. Comparison of capillary blood flow in the nailfold circulations of young and elderly men. Age 1985; 8: 70–75. 62. VandenBrande P, vonKemp K, DeConinck A et al. Laser Doppler flux characteristics at the skin of the dorsum of the foot in young and in elderly healthy human subjects. Microvascular Research 1997; 53: 156–162. 63. Fronek A, Criqui MH, Denenberg J et al. Common femoral vein dimensions and hemodynamics including Valsalva response as a function of sex, age, and ethnicity in a population study. Journal of Vascular Surgery 2001; 33: 1050–1056. 64. Delis KT. Perforator vein incompetence in chronic venous disease: a multivariate regression analysis
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CHAPTER
3
Assessment
THE INITIAL ASSESSMENT INTERVIEW
CHAPTER CONTENTS The initial assessment interview 29 Medical and social history 29 Medication use 31 Assessment of cognitive status 31 The presenting complaint 32 Systems examination 34 Dermatological assessment 34 Vascular assessment 36 Neurological assessment 39 Musculoskeletal assessment 41 Diagnostic imaging 47 Plain film radiography 47 Bone scanning 48 Ultrasonography 48 Computed tomography 48 Magnetic resonance imaging
48
Functional assessment 49 Activities of daily living 49 Objective measures of mobility 49 Evaluation of gait disorders 49 Falls risk assessment 51 Assessment of the ability to perform basic foot care 52
MEDICAL AND SOCIAL HISTORY
Footwear assessment 53 Footwear and falls 55 Assessing outcomes of treatment Summary 56 References 56
The initial assessment interview is one the most important components of lower limb assessment in older people. A considerable amount of relevant information can be gleaned from a thorough and targeted evaluation of medical and social history – information that in many cases will influence the management strategy and assist in determining the likelihood of a successful outcome. Because of the high prevalence of visual, auditory and cognitive impairment in older people, it is essential that the initial assessment interview is conducted in a quiet, well lit and unhurried clinical environment. History taking in older people may also require the aggregation of information from multiple sources, including family members, friends and carers. This can be challenging, particularly when the information gathered is inconsistent. In some cases it may be necessary to obtain relevant information from each of these sources in isolation in order to develop a more accurate picture of the presenting complaint. This clearly requires striking a balance between patient confidentiality and family involvement.1 An outline of areas to be covered in the initial assessment is provided in Table 3.1.
55
Previous and current medical conditions should be documented. In addition to current and previous medical conditions (including previous surgery), documenting a family history may provide useful insights into undiagnosed conditions with a strong hereditary
30
ASSESSMENT
Table 3.1 Components of the initial assessment Component
Areas to be covered
Medical history
Current overall health status and diagnosed medical conditions Current medications Previous medical history (including previous surgery) Family history Cognitive status
Social history
Age Gender Ethnicity Social habits Sporting/leisure activity Spouse/family/carer support
Presenting complaint
Location, duration, severity, previous treatments
Systems examination
Dermatological Vascular Neurological Musculoskeletal
Diagnostic imaging
Radiography, bone scanning, ultrasonography, computed tomography, magnetic resonance imaging
Functional assessment
Activities of daily living Mobility Gait disorders Falls risk assessment Ability to self-care
Footwear assessment
Shoe fit and suitability Wear patterns
predisposition (such as diabetes mellitus and psoriasis). To assist in recall, drawing a pedigree chart may be useful (Fig. 3.1), although in older patients it will be difficult to document family history accurately beyond one previous generation. Documenting a thorough social history is essential to the management of foot problems in older people, as chronic foot conditions will often require ongoing self-management by the older person in their home environment. Inspection of foot lesions, use of appropriate footwear and regular changing of wound dressings are all aspects of care that may be compromised if the level of social support is inadequate. Thorough questioning of the older person’s household situation may also highlight limitations in the awareness of supportive care services (such as community nursing) that the older person may be eligible to access. Current
Parents
Died 80 yr type 2 diabetes
Died 65 yr
Grandparents
Died 72 yr type 2 diabetes
Died 68 yr
Siblings Died 68 yr
77
81
84 type 2 diabetes
Figure 3.1 Example of a pedigree chart for investigating hereditary predisposition to disease. Squares represent males, circles represent females. Diagonal lines represent deceased family members, shaded circle represents the patient.
The initial assessment interview
and previous occupation and level of physical activity may both be contributing factors to the development of foot problems and should be thoroughly evaluated.
MEDICATION USE Because of the age-related increased prevalence of chronic conditions, the use of prescription and overthe-counter medications increases dramatically with advancing age, with over 80% of people aged over 65 years taking at least one medication and at least 20% taking five or more.2 Although not all clinicians involved in the management of older people have the scope of practice to prescribe or withdraw medications, all health-care professionals should thoroughly document medication use at the initial assessment, undertake regular reviews of medication use and be wary of potential adverse reactions. It is often necessary to request that older people bring their medications to their clinical appointments to ensure accuracy in documentation, and to ask specific questions regarding over-the-counter medications such as vitamin supplements, herbal medications, eye drops, creams and ointments. The use of herbal medications and supplements is highly prevalent among older people; however, clinicians often do not document their use and older patients may not report them during the medical history interview. A study of 1539 older people recently found that, while 34% used some form of herbal medication, 70% had not informed their physician.3 This is problematic, as all medications, irrespective of their prescription status, have the potential to interact and contribute to adverse events. Common herbal medications that have been shown to have clinically important interactions with prescription medications include St John’s wort, gingko biloba, echinacea, saw palmetto, garlic and ginseng.4,5
Secondly, the success of many clinical management strategies is dependent on the ability of the older person to undertake activities after they leave the clinical environment. Failure to assess whether the older person is capable of undertaking these tasks may significantly reduce the likelihood of a good clinical outcome. Although the astute clinician may be able to detect moderate to severe levels of cognitive impairment from general observations and history taking, a structured approach using validated assessment tools will yield more valid findings. The most commonly used clinical screening tool for cognitive evaluation is the Mini-Mental State Examination (MMSE), a clinicianadministered questionnaire consisting of 30 questions addressing several components of cognitive function.6 However, the MMSE is generally not feasible to implement into routine clinical practice because of its length. In recognition of this, several shorter screening tools have been developed that are highly correlated with the MMSE. The simplest and most widely used of these tests is the Clock Drawing Test (CDT).7 Although several versions of this test exist, the most basic approach requires requesting the patient to draw a clock face with all the numbers and hands placed correctly, and to then state the time they have drawn. The following scoring system is then applied: (a) the number 12 appears on top (3 points); (b) there are 12 numbers present (1 point); (c) there are two clearly distinguishable hands (1 point); and (d) the time is correctly stated (1 point). Scores of less than 4 are indicative of moderate to severe cognitive impairment8 and warrant further diagnostic evaluation by a geriatrician. Examples of the CDT are shown in Figure 3.2.
A
B
C
ASSESSMENT OF COGNITIVE STATUS Evaluating an older person’s cognitive status is an important aspect of lower limb assessment in older people for two major reasons. Firstly, obtaining informed consent to commence a clinical intervention requires that the older person is fully cognisant of the implications of the decision they are making. This is particularly important in relation to more invasive procedures such as foot surgery, where the advantages and disadvantages need to be carefully considered.
Figure 3.2 Examples of the clock-drawing test of cognitive impairment. A. Normal (score 6). B. Moderate cognitive impairment (score 4). C. Severe cognitive impairment (score 0).
31
32
ASSESSMENT
THE PRESENTING COMPLAINT Location and history of the presenting complaint Having established a thorough medical and social history and evaluated the cognitive status of the older person, the next step in the assessment process is to specifically address the presenting complaint. The key questions that should be asked are listed in Table 3.2, along with some example answers. The location of the presenting complaint should first be accurately identified. The use of visual aids, such as anatomical diagrams or models, can be very useful in determining the location of the problem, particularly if the older person has difficulty describing the location or is physically incapable of pointing to it (Fig. 3.3). Direct questioning regarding symptoms in other body regions may also provide useful diagnostic clues that may not have been otherwise volunteered.
Table 3.2 Key questions to ask about the presenting complaint – the example answers are those that may suggest an ingrown toenail Questions
Example answers
1. Where is the problem? 2. How long have you had the problem? 3. How did it start?
My big toenail Two weeks
4. When does the problem trouble you? 5. What makes the problem better? 6. What makes the problem worse? 7. What treatments have you already tried?
Pain assessment Because pain is the most common reason for seeking medical care, it is important to assess the characteris-
Right foot
Left foot
Figure 3.3 Anatomical map to assist in the documentation of pain location.
I stubbed my toe in the garden When I’m walking Taking my shoes off and soaking my feet Wearing my slippers Wrapping my toe with cotton wool
The initial assessment interview
tics and severity of pain in older people with foot problems. Pain descriptors used by the patient, such as the nature of the pain sensation (e.g. burning, aching, stinging, throbbing), the distribution of pain (e.g. localised, radiating, superficial, deep) and patterns of pain (e.g. persistent, occasional, periodic) can greatly assist in reaching a diagnosis of the presenting complaint. Pain intensity can be evaluated using several generic pain rating scales (such as the McGill Pain Questionnaire9); however, these scales are generally too time-consuming for routine administration in the clinical setting and may not always be relevant for foot disorders. Visual analogue scales, numerical rating scales and verbal descriptor scales are useful indicators of pain intensity, are easily understood and are simple and quick to administer; however, they do not provide any insights into the functional and psychosocial impairments associated with pain. Furthermore, there is evidence that the visual analogue scale may not be appropriate for all older people, as many have difficulty transforming the subjective nature of pain into a metric scale.10 Several foot-specific pain and disability questionnaires have recently been developed, including the Foot Function Index,11 the Foot Health Status Questionnaire,12 a range of scales developed by the
American Orthopedic Foot and Ankle Society,13 the Manchester Foot Pain and Disability Index14 and the Bristol Foot Score.15 Although each of these scales provides a quantitative measure of foot health status, they vary considerably in relation to the constructs measured, the level of psychometric validation undertaken and their responsiveness to change. The only scale to be specifically validated in a large sample of older people is the Manchester Foot Pain and Disability Index (MFPDI), which was originally developed by Garrow et al.14 The MFPDI consists of 19 statements prefaced by the phrase ‘Because of pain in my feet’, formalised under three constructs: functional limitation (10 items), pain intensity (five items), and personal appearance (two items), with three possible answers: ‘none of the time’ (score = 0), ‘some days’ (score = 2), and ‘most days/every day’ (score = 3). The remaining two items are concerned with difficulties in performing work or leisure activities, which are omitted if the respondent is of retirement age (Table 3.3). Menz et al16 recently administered the MFPDI to 301 people aged over 75 years of age and found that the factor weightings in older people slightly differed from the initial validation study. In the Menz et al16 study, the MFPDI was found to exhibit high internal consistency and represent four
Table 3.3 The Manchester Foot Pain and Disability Index Question Because of pain in my feet . . . 1. I avoid walking outside at all 2. I avoid walking distances 3. I don’t walk in a normal way 4. I walk slowly 5. I have to stop and rest my feet 6. I avoid hard or rough surfaces where possible 7. I avoid standing for a long time 8. I catch the bus or use the car more often 9. I need help with housework/shopping 10. I still do everything but with more pain or discomfort 11. I get irritable when my feet hurt 12. I feel self-conscious about my feet 13. I get self-conscious about the shoes I have to wear 14. I have constant pain in my feet 15. My feet are worse in the morning 16. My feet are more painful in the evening 17. I get shooting pains in my feet
Original validation domains
Domains in older people
Functional limitation Functional limitation Functional limitation Functional limitation Functional limitation Functional limitation Functional limitation Functional limitation Functional limitation Pain intensity
Activity restriction Functional limitation Functional limitation Functional limitation Functional limitation Functional limitation Functional limitation Functional limitation Activity restriction Pain intensity
Functional limitation Concern about appearance Concern about appearance
Pain intensity Concern about appearance Concern about appearance
Pain Pain Pain Pain
Pain Pain Pain Pain
intensity intensity intensity intensity
intensity intensity intensity intensity
33
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ASSESSMENT
pain domains: functional limitation, pain intensity, concern about appearance and activity restriction (Table 3.3). These results indicate that MFPDI is an appropriate tool for assessing foot pain in older people. In addition, the MFPDI has been shown to be sensitive to improvement following a self-management intervention,17 suggesting that it may also have some value as a measure of treatment efficacy. Assessing pain in older people who are incapable of verbal communication is a considerable challenge and requires observation of physical responses (such as guarding, fidgeting or restricted movement of the painful body part) and facial expressions (such as frowning, grimacing or excessive blinking).18 Clinicians should never assume that those who are incapable of reporting pain do not experience it, and all attempts should be made to ensure that physical examination procedures are as pain-free as possible.
SYSTEMS EXAMINATION Systems examination of the lower limb in older people should be essentially the same as that for younger people; however, there are some particular issues that require additional consideration. The most fundamental issue in relation to systems examination in the older patient is the tendency for some clinicians to undertake less thorough assessments, because of the incorrect assumption that many aspects of ageing cannot be effectively managed. This is by no means limited to foot-care specialists – indeed, ageist assumptions have been demonstrated in most fields of medicine and often result in less detailed diagnostic approaches and the provision of less aggressive treatment approaches. Systems examination of the lower limb in older people is likely to have a high diagnostic yield, and older people may be more likely to benefit from thorough assessments than younger, relatively healthy patients.
DERMATOLOGICAL ASSESSMENT Thorough visual observation is the most fundamental component of dermatological assessment of the lower limb in older people, as many skin lesions have characteristic patterns of presentation. Skin lesions should be carefully examined in relation to their arrangement, shape, size, surface contour and colour (Fig. 3.4), and the lesion type should be documented using widely accepted dermatological nomenclature (Table
B
A
Annular
Flat
Nummular
Pedunculate
Linear
Dome
Grouped
Umbilicated
Satellite
Verruciform
Arcuate
Spire
Figure 3.4 Documentation of dermatological lesions. A. Arrangement. B. Surface contour.
3.4). Careful palpation of the skin may also yield useful clinical information regarding the texture, depth, consistency and contents of the lesion. Assessment of skin dryness in the clinical setting can be standardised using the xerosis scale developed by Rogers et al.19 This scale consists of six images of feet with varying degrees of skin dryness, ranging from a mild, dusty appearance with some small skin flakes to large scaly plates and deep fissuring (Fig. 3.5). Although the scale has not yet been validated against gold standard measurements of skin hydration (such as electrical capacitance),20 it has been shown to be a sensitive measurement of skin hydration in response to emollient application.21 In addition to clinical observations, investigations such as mycology, bacterial and viral culture, and histological assessment may be necessary. Mycology is particularly important in relation to confirmation of suspected onychomycosis in older people for two main reasons. Firstly, dystrophic nails may test positive for a wide range of organisms, necessitating the use of broad-spectrum antibiotics or antifungals. Secondly, in approximately 20% of cases of suspected onychomycosis, no fungal organisms can be identified, suggesting that, as a result of misdiagnosis, some older people may undergo unnecessary antifungal
Systems examination
Table 3.4 Terminology of skin lesions Term
Description
Macule
Localised area of colour change without elevation Solid elevation of skin <5 mm in diameter Solid elevation of skin >5 mm in diameter Accumulation of clear fluid within or below epidermis <5 mm in diameter Accumulation of clear fluid within or below epidermis >5 mm in diameter Visible collection of free pus in a blister Nodule consisting of an epithelium-lined cavity filled with fluid or semi-solid material Transitory, compressible papule of dermal oedema Plateau-like elevation of skin >2 mm in diameter Accumulation of thickened keratin in the form of detachable fragments Circumscribed area of skin loss extending into the dermis
Papule Nodule Vesicle Bulla Pustule Cyst
Weal Plaque Scale Ulcer
22
treatment. Bacterial and viral culture should be considered in the case of longstanding paronychia or suspected secondary bacterial infection of pustular lesions or open wounds. It is essential that foot-care specialists establish good communication with their local pathology providers to ascertain their sampling and transport requirements. In general, all foot lesions in older people should also be investigated for evidence of underlying tissue breakdown and ulceration, and chronic lesions should be carefully documented for potential malignant changes. The ABCD mnemonic (A – asymmetry; B – border irregularity; C – change in colour and D – increase in diameter) is a useful general rule for routine assessment of suspect lesions. A particularly high index of suspicion should also be applied to nonhealing subungual lesions, as this is a relatively common site for the development of malignant melanomas.23 This is discussed in more detail in Chapter 5. If skin breakdown is noted during a dermatological assessment, more detailed wound assessments need to be undertaken. Wound assessment, although not an exact science, is essential for two main reasons. Firstly, assessing the characteristics of a wound (such as the underlying aetiology, location, size and presence or
Figure 3.5 Xerosis scale. 1: Dusty appearance and occasional minute skin flakes; 2: generalised dusty appearance and many minute skin flakes; 3: defined scaling with flat borders; 4: defined scaling with raised borders and shallow fissures; 5: large scales plates and fissures; 6: large scale plates and deep erythematous fissures. (With permission from Jennings MB, Alfieri D, Ward K et al. Comparison of salicylic acid and urea versus ammonium lactate for the treatment of foot xerosis. A randomized, double-blind, clinical study. Journal of the American Podiatric Medical Association 1998; 88: 332–336.21)
absence of infection) may inform the selection of treatment; and secondly, assessing the severity of a wound can provide useful insights into the risk of further complications such as infection and amputation. A summary of key features to document when assessing wounds is provided in Table 3.5. Wound severity can be assessed using the Wagner classification, which includes five grades: grade 1 (loss of dermal tissue only), grade 2 (loss of tissue that exposes tendon or bone), grade 3 (loss of tissue that exposes tendon or bone with osteomyelitis or abscess), grade 4 (gangrene of digits or forefoot) and grade 5 (extensive gangrene of the foot).24 The more recent
35
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ASSESSMENT
Table 3.5 Components of wound assessment Characteristic
Assessment
Clinical meaning
Location
Mark on anatomical map
Can inform diagnosis Influences selection of treatment Affects prognosis
Size
Direct measurement of surface area, depth and volume
Affects healing time and prognosis Useful outcome measure
Wound bed
Document presence of necrotic or granulation tissue, slough, level of exudate and odour
Can inform diagnosis Provides insights into degree of healing May indicate infection Influences selection of treatment
Wound edges and surrounding skin
Document colour, thickness, temperature, presence of oedema
Can inform diagnosis Provides insights into degree of healing May indicate infection Influences selection of treatment
University of Texas classification includes three grades: grade 0 (pre- or postulcerative site that has healed), grade 1 (superficial wound not involving tendon, capsule or bone), grade 2 (wound penetrating to tendon or capsule) and grade 3 (wound penetrating bone or joint). Within wound grade there are four stages: clean wounds (stage A), non-ischaemic infected wounds (stage B), ischaemic noninfected wounds (stage C) and ischaemic infected wounds (stage D). While both scales are clinically useful, the University of Texas scale has been found to be more predictive of healing time.25 Management of wounds is discussed in Chapter 7.
VASCULAR ASSESSMENT As outlined in Chapter 2, ageing is associated with significant changes in the structure and function of peripheral blood vessels, resulting in reduced function of both the peripheral arterial and venous systems. These changes commonly manifest in the foot and ankle, increasing the risk of arterial insufficiency, venous stasis and ulceration. A thorough vascular assessment is therefore an essential component of lower limb evaluation.
Assessment of the peripheral arterial system Age is a major independent risk factor for the development of peripheral arterial disease (PAD). PAD affects approximately 15% of people aged 70 years and
Table 3.6 The Fontaine classification of peripheral arterial disease Stage
Symptoms
1 2 3 4
Asymptomatic Intermittent claudication Ischaemic rest pain Severe rest pain with ulceration or gangrene, or both
over26 but often goes unrecognised in a large number of patients until the onset of symptoms.27 Given that many older people with asymptomatic PAD have evidence of subclinical cardiovascular disease, lower limb arterial supply has been described as one of the ‘vital signs’ of an older person’s health status,28 and footcare specialists are well placed to detect early signs of vascular disease in asymptomatic older people. The severity of PAD can be classified according to the presenting symptoms, using the widely used Fontaine classification (Table 3.6).29 The classical early presentation of ischaemically induced pain is intermittent claudication, a tight, cramping pain in the calf region (or, less commonly, in the thigh, buttocks or foot) that occurs when walking and is relieved by rest. Intermittent claudication is thought to result from the build-up of metabolites in response to reduced oxygenation of the surrounding muscle. When the older person rests, the metabolites are gradually
Systems examination
Table 3.7 The Edinburgh Claudication Questionnaire Question
Response
Sensitivity (%)
Specificity (%)
Do you get pain or discomfort in your leg(s) when you walk?
Yes (if patient answers No, stop here)
99.3
13.1
Does this pain ever begin when you are standing still or sitting?
No
99.3
80.3
Do you get pain if you walk uphill or in a hurry?
Yes
98.8
13.1
Do you get pain if you walk at an ordinary pace on level ground?
Yes or No, depending on severity of claudication
–
–
What happens if you stand still?
Pain gone in 10 min or less
90.6
63.9
Where do you get this pain?
Calf,* thigh† or buttock†
–
–
A positive classification of claudication requires the indicated response for all questions. *definite claudication = pain in calf. †Atypical claudication = pain in thigh or buttock in the absence of calf pain.
cleared and the oxygen requirement of the muscles is reduced, leading to an alleviation of symptoms. An accurate diagnosis of intermittent claudication can be obtained using a series of six questions, referred to as the Edinburgh Claudication Questionnaire (Table 3.7). This questionnaire has been found to have a sensitivity of 99% and a specificity of 91% in 300 symptomatic patients aged 55 years and over.30 In more advanced PAD, a similar cramping pain may develop in bed (referred to as nocturnal or night cramps) as the heat of the bedclothes increases the oxygen demand of the legs. Hanging the affected limb over the side of the bed relieves the pain as a result of a reduction in limb temperature and gravityinduced increase in blood flow. Finally, the most severe form of ischaemic pain occurs in the absence of any physical activity (referred to as rest pain) and indicates that the arterial supply of the limb cannot even meet quiescent metabolic requirements. At this stage, the limb is so severely ischaemic that ulceration and/or gangrene may develop – a state commonly referred to as critical limb ischaemia, which infers that, if limb perfusion cannot be improved, there is a significant risk of limb failure and subsequent amputation.31 In addition to the documentation of ischaemic symptoms, clinical examination of suspected PAD encompasses simple visual observations (such as loss of hair growth, atrophic or shiny skin and dystrophic toenails), palpation (assessment of limb temperature and palpation of pedal pulses), observation of changes
in blood flow following occlusion (the capillary refill time test) or limb elevation (Buerger’s test), and assessment of abnormal sounds detected with a stethoscope (bruits). Two recent reviews of physical examination procedures for PAD32,33 indicated that many of these observations are highly specific (i.e. their absence precludes the diagnosis of PAD) but have low sensitivity (i.e. their presence does not necessarily indicate that PAD is present). The most useful clinical observations in detecting PAD were found to be abnormal pedal pulses, femoral artery bruit, unilateral cool limb and abnormal limb colour (Table 3.8). Although clinical observations remain an important component of peripheral arterial assessment, far greater diagnostic accuracy can be achieved by calculating the ankle–brachial index (ABI) using a sphygmomanometer and stethoscope or Doppler ultrasound.34 The basic principle of the ABI is that systolic blood pressure in the lower limb should be equal to or slightly greater than that in the upper limb. By dividing systolic blood pressure in the lower limb by the pressure in the upper limb, an index can be calculated which provides a sensitive marker of peripheral blood supply.35 To perform the test, the patient is placed in a supine position with one arm flexed at the elbow and a blood pressure cuff is placed around the upper arm and inflated until the brachial pulse can no longer be heard with the stethoscope or Doppler. The cuff is then released slowly and the point at which the pulse returns is documented from
37
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ASSESSMENT
Table 3.8 Clinical observations indicative of peripheral arterial disease Test
Test result indicative of peripheral arterial disease
Sensitivity (%)
Specificity (%)
Abnormal pedal pulse
Dorsalis pedis and posterior tibial artery pulses both absent, or one present and one weak
63
99
Femoral artery bruit
Bruit present
29
95
Cool skin
Unilateral cool skin
10
98
Abnormal limb colour
Pale, red or blue limb
35
87
the manometer. The test is then repeated with the cuff placed above the ankle joint and the stethoscope or Doppler placed over the posterior tibial or dorsalis pedis artery. There are several variations of the ABI technique in relation to the lower limb artery used (dorsalis pedis, posterior tibial or both), how left and right readings are calculated (the highest, the lowest or the average) and the number of tests performed.36 Similarly, several scoring systems have been devised, with normal values ranging from 0.9 to 1.5, and the PAD cut-off value being reported as either less than 0.9 or less than 1.0.36 In response to these variations, the Standards Division of the Society of Interventional Radiology recently developed a consensus statement for the use of the ABI.37 This statement recommends that the higher pressure of the dorsalis pedis or posterior tibial artery for each foot be divided by the highest brachial artery pressure. The Division also recommended that the cut-off value for an abnormal reading should be less than 1.0, with rest pain typically occurring in patients with an ABI less than 0.5 and critical ischaemia associated with an ABI of less than 0.2.37 ABI values need to be interpreted with caution in patients with Mönckeberg’s sclerosis or diabetes, as the calcification of the arterial wall associated with these conditions may prevent adequate compression of the artery, thereby leading to falsely elevated index scores. Clinicians should suspect artery wall calcification if the vessel cannot be compressed with pressures above 200 mmHg or if the ABI calculated is well above 1.0 in the presence of other visual signs of ischaemia. If this occurs, there are two alternative approaches that can be used. Firstly, the peroneal artery is rarely affected by calcification, so the ABI can be calculated using the peroneal artery pressure value rather than the dorsalis pedis or posterior tibial arteries. Secondly, the pole test described by Smith et al38
can be used, which involves placing the patient in a supine position, elevating the leg until the pulse can no longer be detected and measuring the vertical distance between the heart and the foot. A distance less than 40 cm is indicative of severe occlusion. More advanced techniques for the assessment of lower limb ischaemia, such as exercise testing, Duplex scanning, computed tomography and magnetic resonance angiography are the domain of the specialist vascular surgeon and are generally only indicated for presurgical planning for bypass or limb salvage procedures.34 Referral for these investigations is indicated where there is evidence of severe PAD, particularly if rest pain, ulceration or gangrene are present.
Assessment of the peripheral venous system Venous disorders are also common in older people39 and therefore clinical evaluation of venous insufficiency, including observations of telangiectasis, varicosities, oedema and venous ulcers, should also be a routine component of geriatric lower limb assessment. Clinical observation is generally sufficient to arrive at a diagnosis of venous insufficiency; however, the Perthes manoeuvre can provide further insight into the competency of leg veins. This test involves the application of a blood pressure cuff at mid thigh level while the leg is dependent. The patient is then instructed to walk and rise up on to their toes to stimulate the calf muscle pump. In a normal limb, the superficial veins will empty into the deep vein system because of the action of the calf muscles; however, in the presence of valvular incompetence, the superficial veins will remain distended and the limb may become erythematous. It has also recently been demonstrated that the assessment of foot veins provides a useful insight into the hydration status of an older person.40 Given that
Systems examination
dehydration is very common in older people (particularly those in institutional care), this simple assessment may help in the early detection of impaired fluid balance. To perform the assessment, the dorsal venous arch vein is occluded by finger pressure and the vein is emptied by stroking proximally. The finger is then released, and the rate and degree of venous return is observed, with a delay of more than 3 seconds being indicative of potential dehydration. The most serious and potentially life-threatening lower limb venous disorder, deep vein thrombosis (DVT), should always be suspected in older people presenting with a hot, painful, swollen leg. However, because anticoagulant therapy has potentially serious side effects, it is important that DVT is also accurately ruled out when it is not present. To assist in this process, the clinical prediction rule of Wells et al41 is particularly useful (Table 3.9). This consists of 12 medical history items and clinical observations that can easily be undertaken as part of a routine consultation. The classification of a patient as having a ‘high clinical probability’ of DVT on this scale has been shown to have 91% sensitivity and 100% specificity for the eventual imaging diagnosis of DVT. Definitive diagnosis of DVT requires referral to a vascular laboratory for imaging techniques such as contrast venography, ultrasonography, computed tomography or magnetic resonance imaging.42 Contrast venography, which involves X-raying the limb following the intravenous injection of a contrast agent, is considered to be the gold standard diagnostic test for DVT. However, because of its invasiveness and risk of thrombosis43 it has largely been replaced by ultrasonography, which has an average sensitivity and specificity of 97% for detecting DVT in the thigh but a somewhat lower sensitivity for detecting calf DVT (approximately 75%).44
NEUROLOGICAL ASSESSMENT Lower limb neurological assessment in older people can be challenging, as it is often difficult to distinguish between observations of normal age-related changes and those related to a neuropathic process. The initial assessment interview and history taking may provide useful insights into conditions commonly associated with neuropathy, such as diabetes, chronic alcoholism, vitamin B12 deficiency and the side effects of certain medications. However, self-reported ‘numbness of the feet’ cannot be relied upon as an indicator of sensory loss, as it has been shown to be a poor
Table 3.9 Clinical prediction rule for the diagnosis of deep vein thrombosis (DVT) Clinical features Major points Active cancer Paralysis, paresis or recent plaster immobilisation of the lower limb Recently bedridden >3 days and/or major surgery within 4 weeks Localised tenderness along the distribution of the deep venous system Thigh and calf swollen Calf swelling 3 cm asymptomatic side (measured 10 cm below tibial tuberosity) Strong family history of DVT (≥2 firstdegree relatives with history of DVT) Minor points History of recent trauma (≥60 days) to the symptomatic leg Pitting oedema: symptomatic leg only Dilated superficial veins (non-varicose) in symptomatic leg only Hospitalisation within previous 6 months Erythema Clinical probability High ≥3 major points and no alternative diagnosis ≥2 major points and ≥2 minor points and no alternative diagnosis Low 1 major point + ≥2 minor points and has an alternative diagnosis 1 major point + ≥1 minor point and no alternative diagnosis 0 major points + ≥3 minor points and has an alternative diagnosis 0 major points + ≥2 minor points and no alternative diagnosis Moderate All other combinations
predictor of electrodiagnostically-confirmed neuropathy in older people.45 A wide range of clinical tests, such as tactile sensitivity testing with graded monofilaments, two-point discrimination, vibration sense (with tuning forks or neurothesiometers), temperature perception, pain detection, proprioception and lower limb reflexes are commonly used to detect lower limb sensory loss (Table 3.10). Although these tests are widely used,
39
40
ASSESSMENT
Table 3.10 Clinical screening tests of lower limb sensory function Test
Description
Tactile sensitivity
Cotton wool lightly stroked on the foot while patient has eyes closed. Patient is asked to report which foot is being stroked and the site
Two-point discrimination Specially constructed devices with tips separated by varying distances are applied to the foot while patient has eyes closed. Patient is asked to report how many points can be felt (i.e. one or two) Pressure perception
Flexible plastic filaments of varying thickness are applied to the foot while patient has eyes closed, and threshold detection level is documented. A commonly employed cut-off is the 10 g filament
Vibration sense
Three methods: 1. 128 Hz tuning fork 2. Graduated Rydel–Seiffer tuning fork 3. Neurothesiometer For each method, vibration sense is determined by applying the vibration to a bony prominence (apex of the hallux, first metatarsophalangeal joint or malleoli) while patient has eyes closed. Patient is asked to report any perceived sensation. The 128 Hz tuning fork produces a dichotomous test result (i.e. vibration sense is present or absent), the graduated tuning fork is semi-quantitative and the neurothesiometer produces a continuous score in volts, with values over 25 indicating neuropathy
Temperature perception
Two test-tubes filled with cold (<30°C) and hot water (>35°C) are applied to the foot while patient has eyes closed. Patient is asked to state which tube they find cooler/ warmer
Pain
Disposable sharp and blunt rods (such as Neurotips) are randomly applied to the foot while patient has eyes closed. Patient is asked to report which is the sharper rod
Proprioception
Dominant hallux grasped on medial and lateral surfaces by thumb and forefinger. Small amplitude up and down movements randomly administered, with patient asked to report direction of movement
Ankle reflex
Achilles tendon is struck with a reflex hammer while the foot is lightly dorsiflexed; plantarflexion response is detected with the other hand
few have been adequately examined for validity in older people. Furthermore, the use of ankle reflex testing or tuning forks alone to detect neurological problems is confounded by the fact that over onethird of people aged over 70 years do not appear to have an ankle reflex46 and a similar proportion cannot detect vibratory stimuli at the ankle.47 Therefore, commonly employed clinical tests applied in isolation may not provide the same level of diagnostic accuracy when applied to older people. To address this issue, Richardson48 recently developed a clinical screening approach incorporating a range of clinical tests in 100 older people and correlated these findings with electrodiagnostic tests of
peripheral polyneuropathy. The results indicated that all clinical tests differentiated between older people with and without electrodiagnostically confirmed neuropathy; however, the best prediction of neuropathy was provided by using a combination of three tests: the Achilles reflex, vibration sense at the toe and position sense at the toe. Having two or three abnormal signs demonstrated a sensitivity of 91% and specificity of 93% for neuropathy (Table 3.11). Interestingly, the diagnostic accuracy of this protocol was not greatly affected by whether or not the participants had diabetes, indicating that it may have broad application for the detection of neuropathy resulting from a range of conditions.
Systems examination
Table 3.11 Clinical screening approach for the detection of neuropathy in older people Test
Description
Cut-off score
Achilles reflex
Achilles tendon is struck with a reflex hammer while the foot is lightly dorsiflexed
Absent plantarflexion response
Vibration sense
128 Hz tuning fork applied just proximal to the nailbed of the hallux, and time taken until patient reports that the vibration has disappeared is recorded in seconds
<8 s
Position sense
Dominant hallux grasped on medial and lateral surfaces by thumb and forefinger. 10 small-amplitude up and down movements randomly administered, with patient asked to report direction of movement
<8/10 correct responses
MUSCULOSKELETAL ASSESSMENT Foot deformity The prevalence of foot deformity increases markedly with age, because of the combined effects of musculoskeletal changes and the detrimental effects of footwear.49 As discussed in Chapter 1, the most common foot deformities in older people – hallux valgus and lesser toe deformities – are often associated with the development of hyperkeratosis and forefoot pain and have a significant detrimental impact on balance and functional ability. Hallux valgus can be easily graded in the clinical environment using the Manchester scale,50 which consists of four standardised photos covering the spectrum of the deformity (Fig. 3.6). A recent study by Menz & Munteanu51 showed that gradings using this scale were significantly associated with hallux abductus and intermetatarsal angles obtained from foot radiographs. Lesser toe deformities (hammer toes, claw toes, mallet toes and retracted toes) can be simply evaluated by assessing the position and range of motion of the metatarsophalangeal, proximal and distal interphalangeal joints. Each of these conditions is described in detail in Chapter 8. The length of each of the metatarsals, often referred to as metatarsal formula, is a useful assessment to undertake in older people, as excessively long or short metatarsals have been associated with the development of hallux valgus, hallux limitus and plantar keratotic lesions. In the normal foot, the second metatarsal is usually the longest and the fifth is the shortest, resulting in a metatarsal formula of 2 > 1 > 3 > 4 > 5, 2 > 3 = 1 > 4 > 5 or 2 > 3 > 1 > 4 > 5. Palpation and marking of the plantar metatarsal
Figure 3.6 Manchester scale for grading hallux valgus severity. A. No hallux valgus. B. Mild. C. Moderate. D. Severe. (With permission from Garrow AP, Papageorgiou A, Silman AJ et al. The grading of hallux valgus. The Manchester Scale. Journal of the American Podiatric Medical Association 2001; 91: 74–78.50)
41
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ASSESSMENT
heads while the corresponding toe is maximally dorsiflexed has been shown to be a valid indicator of metatarsal formula determined from dorsoplantar foot X-rays.52 The prevalence and clinical significance of the forefoot and rearfoot malalignments described by Root et al53 (including forefoot varus, valgus and supinatus, plantarflexed and dorsiflexed first ray, and rearfoot varus and valgus) have been comprehensively debated in recent years. Some doubt has been raised in relation to whether these conditions actually exist, whether they can be accurately measured and whether they have a predictable impact on dynamic foot function.54 In the absence of compelling evidence that these observations influence foot function or predisposition to foot problems in older people, it is my view that a standard geriatric foot and ankle assessment should instead focus on obvious deformities that can be clearly recognised and documented.
Foot posture Despite the proposed relationships between foot posture and the development of overuse conditions affecting the lower limb, there is still considerable disagreement regarding how best to assess and classify foot posture.55 A wide range of tests have been proposed, including structured visual observation,56–58 various footprint parameters,59,60 measurement of frontal plane heel position61,62 and assessment of the position of the navicular tuberosity.63 Very few of these tests have undergone rigorous validation. To address this issue, Menz & Munteanu64 recently compared three clinical tests of foot posture (the arch index, navicular height and the Foot Posture Index) with arch-related measurements obtained from lateral foot X-rays in 95 older people. The results indicated that all three tests were significantly correlated with radiographic measurements, with the strongest associations found for navicular height and the arch index. A subsequent study involving plantar pressure measurements indicated that the arch index is a significant predictor of forces under the midfoot during walking,65 suggesting that this technique may be a useful clinical assessment to perform in older patients. To determine the arch index, a static footprint is obtained using an ink or carbon-paper imprint system, and the area of the middle third of the footprint is divided by the total area of the footprint (ignoring the toes). This is shown in Figure 3.7. A higher arch index represents a flatter foot. Because the calculation
A
L
B
C
Figure 3.7 Calculation of the arch index. The length of the footprint excluding the toes (L) is divided into equal thirds. The arch index (AI) is then calculated as the area of the middle third of the footprint divided by the entire footprint area (AI = B/(A + B + C)).
of the arch index can be time-consuming, a simple classification of high, normal and flat based on a visual observation of the print may be more feasible for routine clinical use. Representative footprints obtained from a sample of 292 people aged between 65 and 96, along with their arch index ranges, are shown in Figure 3.8. The Foot Posture Index (FPI) is also worthy of consideration as a foot screening tool.58 The FPI involves visual rating of six criteria: palpation of the talar head, observation of supra/infra malleolar curvature, inversion/eversion of the calcaneus, medial prominence of the talonavicular joint, congruence of the medial arch and abduction/adduction of the forefoot on the rearfoot. Each of these criteria is scored on a 5-point scale (range −2 to +2) and the summed score provides a single index of the degree of the pronated/supinated posture of the foot, with higher scores representing a more pronated (flatter) foot. The FPI has moderate to good reliability and FPI scores have been found to correlate with the frontal plane position of the ankle joint complex during the midstance phase of gait.58 FPI scores have been shown to be significantly higher in older people than younger people (a mean of 4.4 compared to 2.5), which may indicate an age-related flattening of the medial longitudinal arch.49
Systems examination
High arch (AI = 0 – 0.23)
Normal arch (AI = 0.23 – 0.26)
Low arch (AI = 0.26 – 0.36)
Figure 3.8 Simple visual categorisation of the arch index.
A
B
C
Figure 3.9 Assessment of joint range of motion in the foot. A. First metatarsophalangeal joint. B. Ankle joint dorsiflexion. C. Ankle joint complex inversion/eversion.
Range of motion Assessing the available motion in the foot is a standard and necessary component of the lower limb assessment. Preferred techniques for assessing joint range of motion in the foot are shown in Figure 3.9. Unfortunately, the reliability of range of motion assessments in the foot is somewhat questionable (particularly between clinicians), as the absolute ranges of motion are small and the contribution of skin movement error is considerable. Nevertheless, although precise quan-
tification is not possible, broad classification of foot joint motion as normal, hypermobile or restricted is probably sufficient for clinical decision making. In older people, two joints are of particular importance – the first metatarsophalangeal joint and the ankle joint – as these joints provide the main sagittal plane pivots during propulsion, and both joints undergo significant reductions in motion with advancing age.49 First metatarsophalangeal joint dorsiflexion (assessed in a non-weightbearing position – Fig. 3.9A) is
43
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significantly correlated with the loading of the first ray during gait,65 and restricted motion in this joint is associated with impaired balance.66 In older people, the normal value for this test is approximately 55° (compared to approximately 80° in younger people).49 Although there are several methods of assessing the range of motion of the ankle joint, the weightbearing lunge test provides a functionally relevant indicator of available ankle dorsiflexion and has been shown to be reliable and related to balance and functional ability in older people.66,67 To perform the test, the lateral malleolus and head of the fibula are located and marked with a pen. The patient is then asked to stand with their foot placed alongside a vertically aligned clear acrylic plate inscribed with 2° protractor markings and instructed to take a comfortable step forward with the contralateral leg. In this position, the patient is requested to bend their knees to squat down as low as possible, without lifting the right heel from the ground and while keeping the trunk upright. The position of the fibular head is marked on the clear acrylic plate, and the angle formed between the lateral malleolus and the fibular head is measured (Fig. 3.9B). The normal range of motion when performing this test is approximately 30–50°, with smaller values being associated with impaired balance and functional ability and an increased risk of falls.66,68 In the absence of the acrylic plate apparatus, similar measurements can be obtained by placing a gravity angle finder on the tibia while the patient assumes the lunge position. The complex triplanar movements that occur at the ankle, subtalar and midtarsal joints are particularly difficult to quantify and several studies have reported low levels of reliability for frontal plane measurements of subtalar joint range of motion.69 Recently, however, Menadue et al70 reported high levels of test–retest reliability for inversion/eversion range of motion measurements conducted with the patient in a seated position using a flexible goniometer (Fig. 3.9C). Because the ankle is placed in a comfortable plantarflexed position and the distal arm of the goniometer is placed on the dorsum of the foot, measurements obtained from this technique represent triplanar motion of the ankle–subtalar complex rather than ankle inversion/eversion per se. Mean values obtained from 30 young participants were reported to be 32° of inversion and 10° of eversion.70 Midtarsal joint motion is virtually impossible to quantify; however, useful insights may be obtained by stabilising the
subtalar joint with one hand while moving the midtarsal joint through its full range of inversion/ eversion, dorsiflexion/adduction and plantarflexion/ abduction. Notable restriction in joint range of motion will be particularly evident in older people with midfoot osteoarthritis.
Strength testing Manual muscle testing of the foot and ankle can provide useful insights into strength deficits in older people.71 The basic principle of manual muscle testing is to adequately stabilise the body part proximal to the muscle being tested and to apply firm pressure directly opposite the line of pull of the muscle. Descriptions of hand placement and force application are shown in Table 3.12 and Figure 3.10. The simple grading system initially proposed by Kendall & Kendall72 is then applied (Table 3.13). Although there is some subjectivity involved in this grading system (and care needs to be taken when comparing findings between clinicians), it has been demonstrated that foot and ankle muscle testing observations are related to the intensity of muscle activity during gait.71 Another useful clinical muscle test is the paper grip test, which was first developed to assess muscle paralysis in the feet of leprosy patients.73 To perform the test, the patient is seated with their hip, knee and ankle at 90° and is instructed to use their toe muscles to push down on a 280 gsm piece of cardboard while the clinician stabilises the ankle and forefoot and attempts to slide the cardboard away from the toes (Fig. 3.11). The test is performed three times for the hallux and lesser toes individually and is documented as a pass if the patient can hold the cardboard for all three trials, and a fail if they fail to grip the cardboard on at least one trial. Menz et al74 have recently shown that significant age-related changes exist in toe plantarflexor strength, and that the paper grip test is an accurate predictor of strength measurements obtained from a plantar pressure platform. Toe plantarflexor strength has also been shown to be correlated with the magnitude of pressure borne by the toes during gait65 and weakness of the toes is associated with impaired balance and falls in older people.66,68 The precision of manual muscle testing can be improved with the use of hand-held dynamometers. These devices contain a strain gauge and consist of a handle and a flat surface, which is placed against the area being tested. Using the same principles as
Systems examination
Table 3.12 Manual muscle testing procedures Motion
Positioning of patient
Stabilising hand placement
Resistance hand placement
Instruction to patient
Muscles tested
Ankle dorsiflexion
Seated, leg extended off table
Distal posterior tibia
Dorsomedial surface of the foot
Dorsiflex and invert the foot by bringing toe towards shin
Tibialis anterior
Ankle plantarflexion
Seated, foot and leg extended off table
Distal anterior tibia
Plantar surface of the foot
With knee extended (gastrocnemius) and flexed >45° (soleus) point foot against resistance
Gastrocnemius, soleus
Ankle plantarflexion
Standing on one leg using hand on table for balance
None
None
Raise heel 20 times, or until unable to complete full motion
Gastrocnemius, soleus
Inversion
Lying on side to be tested, foot slightly plantarflexed
Distal medial tibia
Medial aspect of foot
Raise medial border of foot toward ceiling
Tibialis posterior
Eversion
Lying on side not being tested, foot slightly plantarflexed
Distal lateral tibia
Lateral aspect of foot
Raise lateral border of foot toward ceiling
Peroneus longus and brevis
2nd–5th MTP and IP toe flexion
Supine, foot resting on table
MTP: Metatarsal PIP: Proximal phalanx DIP: Middle phalanx
MTP: Proximal phalanx PIP: Middle phalanx DIP: Distal phalanx
Flex or curl toes
MTP: Lumbricals PIP: Flexor digitorum brevis DIP: Flexor digitorum longus
2nd–5th MTP and IP toe extension
Supine, foot resting on table
Metatarsals
Distal phalanx
Extend toes
Extensor digitorum longus and brevis
Hallux flexion
Supine, foot resting on table
MTP: 1st metatarsal
MTP: Proximal phalanx
Flex big toe
MTP: Flexor hallucis brevis IP: Flexor hallucis longus
Hallux extension
Supine, foot resting on table
1st metatarsal
Proximal and Extend big toe distal phalanx
Extensor hallucis brevis (PIP) and longus (DIP)
IP, interphalangeal joint; DIP, distal interphalangeal joint; MTP, metatarsophalangeal joint; PIP, proximal interphalangeal joint.
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Figure 3.10 Manual muscle testing techniques for the foot and ankle. A. Ankle dorsiflexion. B. Ankle plantarflexion. C. Inversion. D. Eversion. E. Lesser toe flexion. F. Lesser toe extension. G. Hallux flexion. H. Hallux extension.
A
B
C
D
E
F
G
H
described in Table 3.11, the maximum force generated by the body part is recorded in kilograms or Newtons. While intratester reliability of dynamometry is very high, intertester reliability is only moderate, as the scores are affected by variations in technique and the strength of the clinician.75 The test–retest reli-
ability of hand-held dynamometry for foot muscles was recently evaluated by Burns et al,76 who indicated that the reliability of foot inversion/eversion and plantarflexion/dorsiflexion measurements was excellent, with standard errors of measurement ranging between 0.3 and 0.7 kg.
Diagnostic imaging
Table 3.13 Manual muscle testing grades Grade
Meaning
4 – Normal 3 – Good 2 – Fair
Resists strong pressure Resists moderate pressure Resists gravity through full range of motion Resists gravity through partial range of motion No muscle activity
1 – Poor 0 – None
A
B
Figure 3.11 The paper grip test. A. Hallux. B. Lesser toes.
DIAGNOSTIC IMAGING Generally speaking, most common foot problems affecting older people can be adequately diagnosed from information obtained from the medical history, initial assessment interview and physical examination. However, several diagnostic imaging techniques can greatly assist in the diagnosis of a wide range of osseous and soft tissue pathologies that may develop in older people. Access to these modalities varies considerably between professions and between countries, so many foot-care specialists will find it necessary to establish referral systems with medical specialists who have a greater scope of practice in this area. The role of diagnostic imaging for specific pathologies is discussed in subsequent chapters; however, the following section briefly outlines the structures that can be visualised with each modality.
PLAIN FILM RADIOGRAPHY Plain film radiography (X-ray) is the most common used imaging modality for assessing musculoskeletal foot problems in older people. Radiography is relatively inexpensive, has a quick turnaround time and can generate very high-quality images with only minimal radiation exposure.77 The standard foot series generally includes a dorsoplantar projection and lateral projection, taken either non-weightbearing or weightbearing. Weightbearing radiographs are preferable to non-weightbearing radiographs, as the foot is captured in a more functional position, which enables representative postural measurements (such as arch height) to be obtained. The dorsoplantar projection provides a clear image of the midfoot and forefoot; however, the talus and calcaneus may be obscured by the distal end of the tibia and fibula. The lateral projection clearly depicts the talus, calcaneus and medial column of the foot; however, the superimposition of midfoot and metatarsal bones may make it difficult to clearly view the lateral structures. A range of other projections may be ordered to specifically target localised pathologies such as sesamoid disorders and subungual exostoses. Features that can be readily observed from standard foot radiographs include overall bone density (as evidenced by generalised radiolucency), calcaneal and Achilles tendon spurs, accessory bones, metatarsal length variations, angular deformities (such as hallux valgus), arch height and osteoarthritic changes (such as joint space narrowing, osteophytes, sclerosis and subchondral cysts). Although very little soft tissue is evident on plain film radiographs, it is not uncommon to observe thread-like calcifications of the dorsalis pedis artery in X-rays obtained from older people, particularly those with diabetes.78 When assessing foot radiographs of older people, it is necessary to keep in mind that some apparently abnormal features are so common in this age group that they can be considered normal age-related changes. Such features include plantar calcaneal spurs, osseous irregularities in the ungual tuberosity of the distal phalanges (which may mimic psoriatic arthritis), enlargements of the base of the proximal phalanx due to spurring of the lateral interosseous ligaments, and localised loss of bone density in the proximal phalanx of the hallux, medial aspects of the first and fifth metatarsal heads and the navicular.78 When examining dorsoplantar radiographs, it also needs to be kept in mind that clawing of the digits may give a misleading
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impression of joint space narrowing due to superimposition of the phalanges.
BONE SCANNING Bone scanning involves the intravenous injection of a radioactive isotope (most commonly, technetium99), which becomes distributed in the bloodstream and is ultimately taken up by the tissues. In the presence of bone pathology, the increased blood flow and corresponding increase in osteoblastic activity in the affected region causes an accumulation of the isotope. By converting this radioactivity into a visual image, areas of increased uptake can be easily identified.79 Bone scans are particularly useful for the identification of stress fractures, bone tumours and Paget’s disease.80 The main indication for bone scanning of the foot in older people is insufficiency fracture, which most commonly affects the metatarsals81–83 but may also develop in the talus84 and calcaneus85 and may not be visible on plain film X-ray. Bone scanning has a much higher sensitivity for detecting osseous changes, as it reflects bone metabolism rather than structure. However, bone scanning has a very low specificity, which increases the likelihood of false-positive findings. In particular, there appears to be a high rate of false-positive results for foot scans. A study of 60 patients with foot pain and 30 asymptomatic controls by O’Duffy et al86 reported that 24 of the controls demonstrated focal areas of increased uptake, most commonly in the metatarsophalangeal joints, the midfoot and the plantar aspect of the calcaneus.
ULTRASONOGRAPHY Diagnostic ultrasound involves the generation of very-high-frequency sound waves that are transmitted through a coupling gel to the body part being examined. Depending on the density of the target tissue, these sound waves are reflected in varying velocity and wavelength and the aggregation of this information is then used to construct a two-dimensional image of the underlying tissue.87 Ultrasound can capture highresolution images of muscle, tendons, ligaments and soft tissue masses in real time, at relatively low cost. However, perhaps more than any other imaging technique, ultrasound is highly operator-dependent and requires considerable practice to become proficient.87 Foot conditions that may be detected with ultrasound
include tendon pathology, synovial effusions, ligament rupture, plantar fascial thickening, ganglia, bursitis, Morton’s neuroma and various soft tissue neoplasms.88 Ultrasound may also be used to assist in the accurate guidance of corticosteroid injections for conditions such as plantar fasciitis and retrocalcaneal bursitis.89
COMPUTED TOMOGRAPHY The basic principle of computed tomography (CT) is to irradiate a slice of tissue from multiple angles and measure the output from the opposite side, which varies depending on the density of the target tissue.90 This output is then mapped according to predetermined tissue-specific attenuation cut-off values and a greyscale image is generated, with each shade of grey representing a different tissue type. The first CT scanners were only capable of generating an image derived from a single slice; however, recent advances in computer technology have enabled multiple slices to be acquired, which can then be rendered into threedimensional images. Unfortunately, the more slices obtained, the greater the dose of radiation the patient is exposed to, so the clinician needs to carefully consider whether high-resolution images are necessary to reach a diagnosis. CT has a relatively limited role in the diagnosis of foot conditions, although it may be useful in the examination of bony tumours, complex fractures and chronic osteomyelitis.91
MAGNETIC RESONANCE IMAGING Magnetic resonance imaging (MRI) involves the application of radiofrequency pulses to the body that match the resonant frequency of the body’s hydrogen atoms. The hydrogen atoms then re-emit this energy as a magnetic resonance signal, which is detected as a voltage by a receiver coil.92 The subsequent ‘relaxation times’ of the hydrogen atoms vary across different tissue types, which enables the construction of high-spatial-resolution images of soft tissue, cartilage and bone. MRI is a useful imaging modality for several foot pathologies, including osteochondral lesions, stress fractures, tendon rupture, plantar fasciitis, plantar plate rupture, Morton’s neuroma and osteomyelitis.93,94 Unfortunately, the high cost of MRI scans precludes their wider application in the diagnosis of foot problems.
Functional assessment
FUNCTIONAL ASSESSMENT The ability to perform routine activities such as dressing, performing housework and shopping are key components of an older person’s independence and quality of life. As stated in the introduction, there is now considerable evidence that foot problems have a significant detrimental impact on these abilities. Clinical assessment of an older person’s functional ability and mobility is therefore an integral component of geriatric assessment, not only to determine the baseline status of the older patient but also as a way of measuring the effectiveness of interventions.
ACTIVITIES OF DAILY LIVING Activities of daily living can be broadly categorised as: (1) basic activities of daily living (BADLs), (2) instrumental activities of daily living (IADLs) and (3) advanced activities of daily living (AADLs). BADLs are considered necessary but not sufficient for maintaining independence, IADLs are necessary to maintain an independent household environment and AADLs are complex tasks requiring high levels of physical and cognitive functioning.95 Assessment of functional status is relatively straightforward and may simply require a brief checklist to be completed by the patient as part of the consultation. Several validated tools have also been developed, including the Barthel index, which consists of 10 questions relating to bowel continence, bladder continence, grooming, toilet use, feeding, transfers, mobility, dressing, stair climbing and bathing.96 These scales are able to predict functional decline, institutionalisation and mortality in older people;97 however, they are generally not sensitive enough to detect short-term changes in relatively highly functioning older people.
OBJECTIVE MEASURES OF MOBILITY Objective measures of gait and mobility, such as walking speed and rising from a chair, are also useful tools for assessing functional status and are sensitive enough to be used as clinical outcome measures. Walking speed, which can be simply measured with a stopwatch over a set distance, provides an indicator of not only lower limb muscle strength but also balance, reaction time and psychological status.98 Prospective studies have also shown that walking speed is a strong predictor of institutionalisation and mortality in older
people.99 Similarly, measuring the time taken to rise from a chair five times (the sit-to-stand test) provides an overall measure of physical ability and can identify older people at risk of falling. Both walking speed and sit-to-stand have been shown to be impaired in older people with foot problems.66,100 Some objective tests of mobility are also accurate predictors of falls (see section on falls risk assessment).
EVALUATION OF GAIT DISORDERS At least 20% of older people report difficulty walking or require assistance with gait-related tasks.101 Although a small reduction in walking speed and step length appears to be a normal consequence of ageing,102 there is increasing evidence that most other gait changes frequently observed in older people are the result of underlying conditions that increase in prevalence with advancing age, such as osteoarthritis, stroke, peripheral neuropathy and dementia. In many older people with a gait problem, more than one potential contributing condition is present, which can make accurate diagnosis difficult.
Classifying gait disorders Alexander & Goldberg103 have proposed a classification of gait disorders according to the level of the sensorimotor system they primarily affect. Low-level gait disorders are those that influence structures distal to the central nervous system, including peripheral sensory impairments (such as peripheral neuropathy, vestibular disorders and visual problems) and peripheral motor impairments (such as arthritic and myopathic conditions). Middle level gait disorders include those resulting from spasticity (such as myelopathy, vitamin B12 deficiency and stroke), parkinsonism (idiopathic or drug-induced) and cerebellar ataxia (resulting from alcohol abuse). High level gait disorders include cautious gait (resulting from behavioural adaptations due to fear of falling) and those related to frontal lobe problems (such as stroke affecting the cortex or basal ganglia). A summary of these disorders, including their characteristic gait changes and associated physical findings, is shown in Table 3.14. Although this system provides a useful clinical summary of gait changes associated with specific conditions, there is often considerable overlap in their presentation.
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Table 3.14 Classification of common gait disorders in older people Level
Classification
Condition
Gait characteristics
Associated physical findings
Low
Peripheral sensory
Sensory ataxia
Steppage gait
Vestibular ataxia
Weaving from side to side May fall to one side Tentative, cautious Shortened stance phase on affected side Trendelenburg sign
Loss of tactile sensitivity and proprioception Nystagmus
Peripheral motor
Visual ataxia Arthritic
Myopathic and neuropathic – proximal Myopathic and neuropathic – distal Middle
Spasticity
Hemiplegia/paresis
Leg circumduction Loss of arm swing Foot dragging
Paraplegia/paresis
Bilateral leg circumduction Scissor gait Small shuffling steps Absent arm swing Freezing Wide base of gait Increased trunk sway Staggering
Parkinsonism
Cerebellar ataxia
High
Cautious gait
Frontal-related gait disorders
Exaggerated lumbar lordosis Trendelenburg sign Waddling gait Foot slapping Foot drop Steppage gait
Cerebrovascular
Wide base of gait Shortened stride Decreased velocity Wide base of gait Shortened stride Decreased velocity Difficulty initiating gait Freezing
Clinical gait analysis The clinical assessment of gait disorders involves a thorough systems examination in addition to the direct observation of movement patterns. Gait analysis techniques range from simple visual observation through to high-tech instrumented gait analysis procedures. For the foot-care specialist, visual observa-
Visual impairment Avoidance of weightbearing on affected side Limited knee flexion Decreased lumbar lordosis Stooped posture Kyphosis Weakness of hip musculature
Weakness of ankle dorsiflexors Leg weakness/spasticity Knee hyperextension Ankle equinovarus Arm weakness/spasticity Leg weakness/spasticity Rigidity Bradykinesia Trunk flexion Poor control of trunk Incoordination Fear of falling
Atherosclerotic disease Cognitive impairment Leg weakness/spasticity Incontinence
tion of gait features shown in Table 3.14, including documentation of temporospatial parameters such as velocity, cadence and step length, is probably a sufficient basis upon which to determine whether a referral is required for further diagnostic evaluation. In the clinical setting, all this requires is sufficient space to conduct a brief gait assessment (preferably at least
Functional assessment
10 m) and a stop-watch. As a general rule, gait can be defined as impaired if the walking speed is less than 0.6 m/s.104 When considering the contribution of gait patterns to foot disorders, more detailed lower limb assessments may be required. The use of treadmills to observe frontal plane movements of the foot during gait is popular in clinical practice; however, it needs to be considered that the reliability of such visual observations is, at best, moderate,105 and that walking patterns on a treadmill may differ from normal overground walking.106 Furthermore, some older people may find treadmill walking very difficult because of balance problems. A recent study of healthy older people assessed the time required to become familiarised to treadmill walking, by comparing temporospatial characteristics and sagittal plane kinematics of the knee to overground walking. After 15 minutes of treadmill walking, two-thirds of the sample still required the support of the handrails, and knee kinematics and cadence did not reflect overground walking values.107 These findings suggest that gait assessments using treadmills may be of limited value in older people. Assessment of plantar pressure patterns is useful for identifying areas of high pressure that may predispose to plantar calluses and ulceration. The simplest technique is the Harris & Beath mat,108 a rubber platform with three layers of ridges that is covered with a thin layer of ink and a sheet of paper. When the patient walks over the mat, high pressure areas appear more densely inked because of the compression of the mat to the lower level of ridges. The Harris & Beath mat is a very useful clinical tool for documenting foot shape and identifying high pressure areas;109 however, the data obtained from the system can only be considered to be semi-quantitative, despite attempts to calibrate the outputs to known forces.110 A similar low-cost system uses carbon paper sheets, which record varying levels of grey when pressure is applied. Using a calibration card, the pressure recording can be documented in a quantitative manner. A study comparing pressures obtained using this technique to an optical pedobarograph indicated that the carbon paper prints provide a sensitive measure of peak plantar pressures, provided that clinicians undergo sufficient training in applying the technique.111 More recently, several plantar pressure systems based on resistive or capacitive sensor technology have become commercially available, either as platform-based systems or in the form of insoles placed inside the shoe.112 Although the cost of many of these
systems currently limits their use to the research environment, scaled-down versions with lower sampling frequencies and sensor resolution are likely to become more widely adopted in clinical practice in years to come. The major benefit of these systems over simple footprinting techniques is that their outputs are truly quantitative, and various force, pressure and timing parameters obtained from the pressure recording can be documented. When undertaking such assessments, however, it needs to be kept in mind that the pressure distribution under the foot is dependent on a wide range of factors, including walking speed, step length, bodyweight, foot deformity and the degree of peripheral sensory loss.65 Because of this complexity, extrapolating foot motion characteristics (such as the degree of foot pronation) from plantar pressure recordings is difficult. While it appears that foot pronation does result in greater medial loading of the midfoot in older people, forefoot pressures are more closely correlated to the degree of hallux valgus deformity and the available range of motion in the first metatarsophalangeal joint.65 Examples of foot pressure recordings from older people are shown in Figure 3.12 and a summary of the strongest clinical predictors of plantar forces in older people in Figure 3.13.
FALLS RISK ASSESSMENT Community-based studies indicate that one in three people aged over 65 years will fall in any given year. Falls frequently result in injury and are the leading cause of injury-related death in older people.113 The role and scope of podiatry in falls prevention is poorly defined but is gaining considerable attention in response to recent studies indicating that foot problems (including foot pain, hallux valgus, decreased ankle flexibility, peripheral sensory loss and toe plantarflexor weakness) are independent risk factors for falling.68 Given these observations, it is likely that most older people attending foot-care specialists have an elevated risk of falling compared to the general elderly population. However, documenting medical conditions that are strong risk factors for falling and undertaking some simple clinical tests will provide more accurate identification of very-high-risk older people who are most likely to benefit from falls prevention activities. Table 3.15 describes some simple tests that have been shown to be useful predictors of falls.114–117 Footwear evaluation also plays a role in falls risk assessment (see Footwear assessment, below).
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Figure 3.12 Examples of foot pressure recordings from older people. A. Hallux limitus. B. Tibialis posterior dysfunction. C. Severe hallux valgus deformity and associated plantar lesions. D. Pes cavus foot type.
Paper grip test H (0.32)** 1st MPJ ROM (-0.26)** Hallux valgus (-0.21)** 37 + age (-0.20)**
42 Bodyweight (0.53)** 1st MPJ ROM (0.14)**
Bodyweight (0.36)* Ankle flexibility (0.20)*
13
39 42
Bodyweight (0.48)**
Bodyweight (0.35)** 53
39
Arch index (0.61)** Bodyweight (0.36)**
Bodyweight (0.58)** Ankle flexibility (0.19)**
Figure 3.13 Determinants of plantar forces in older people. Values displayed in mask regions represent r 2 values, and values contained in brackets represent βweights for each significant independent (‘predictor’) variable. *significance of β-weight p < 0.05, **significance of β-weight p < 0.01. MPJ, metatarsophalangeal joint; ROM, range of movement.
ASSESSMENT OF THE ABILITY TO PERFORM BASIC FOOT CARE Many clinical interventions require the patient to undertake some level of self-management of their foot problem in the household environment. For this reason, foot specialists need to be aware of the ability
of older patients to maintain adequate foot hygiene and undertake basic foot-care tasks, such as cutting and filing nails, applying emollient creams, washing and drying feet, managing areas of dry skin and calluses, putting on shoes and hosiery, inspecting the foot for lesions and changing wound dressings. Failure to adequately assess an older person’s competence to perform these tasks can have serious ramifications, particularly in older people with peripheral vascular disease or diabetes. Undertaking basic foot care is inherently difficult for older people, as it requires not only adequate joint flexibility but also a high level of manual dexterity and visual acuity, all of which decline with advancing age. A particularly good example of the importance of assessing basic foot-care competence was provided by Thomson & Masson,118 who evaluated the ability of older people with and without diabetes to reach down to their feet to inspect a ‘virtual lesion’ – an adhesive red spot placed on the toes or on the plantar surface of the foot. The results indicated that 39% of those with diabetes could not reach their toes, and only 14% of all older participants could detect the plantar ‘lesions’. It is therefore clear that advising older people to undertake basic foot-care tasks is not helpful unless they are actually capable of performing the task. Evaluating self-management ability can be undertaken during a routine consultation by simply observing whether the patient is capable of removing their footwear and whether they have sufficient flexibility to reach and indicate the location of the foot problem. Assessing other aspects of self-management, such as using nail files, changing dressings and applying emollients, may require the clinician to specifically request
Footwear assessment
Table 3.15 Clinical mobility tests that can be used to predict risk of falling Test
Description
Cut-off score that indicates increased risk of falling
Unipedal stance
Measurement of the time (in seconds) that an individual can stand on one leg unsupported
<30 s
Functional reach test
Measurement of the distance that an individual can reach forward without moving their feet
<15 cm
Walking speed
Measurement of the time taken to walk a certain fixed distance (usually 6 m)
<0.56 m/s
Timed up and go test
Measurement of the time taken to stand from a chair, walk 3 m, turn around and sit back down
>14 s
that the patient demonstrate these skills. Assistive devices (such as long-handled shoe horns, nail files and devices to assist with footwear fixation) should also be available and demonstrations provided to patients who may benefit from them.
Fixation Heel counter flexibility Heel height
Depth of toe-box
Sole hardness and flexibility
FOOTWEAR ASSESSMENT Evaluation of footwear is one of the most fundamental components of lower limb assessment in older people. It has been demonstrated that between 50 and 80% of older people wear ill-fitting shoes119,120 and there is evidence that the constriction associated with tightly fitting shoes predisposes to the development of common foot problems. Menz & Morris121 recently evaluated footwear fitting in 176 older people and found that 80% wore shoes narrower than their feet. Those who wore shoes narrower than their feet were more likely to have corns on the toes, hallux valgus deformity and foot pain, whereas those who wore shoes shorter than their feet were more likely to have lesser toe deformity. Heel elevation in women’s shoes was associated with both hallux valgus and plantar calluses. Because of the strong association between ill-fitting footwear and foot problems, footwear evaluation is an essential first step in investigating the potential causes of foot problems. Indeed, changing footwear may be the only intervention necessary to successfully manage many common foot problems, particularly those related to toe deformities and associated hyperkeratotic lesions. Footwear also needs to be evaluated for suitability in relation to the provision of toe splints, in-shoe plantar padding and foot orthoses, as the
Shoe length and width Sole flexion point Sole slip resistance
Figure 3.14 Key components of footwear evaluation in older people.
efficacy of these interventions is highly dependent on the ability of the shoes to support and facilitate the function of these devices. The first issue to consider when assessing footwear is whether the shoes that the older person is wearing at the time of the consultation are those that are worn most frequently – in many cases the shoes worn may be ‘dress shoes’ only worn for special occasions (such as attending medical appointments). It is also important to ensure that indoor footwear is also assessed, as some older people may spend more of their time indoors than outdoors. Although indoor shoes are generally wider fitting than outdoor shoes,121 they also tend to be less supportive and are replaced far less frequently.122 Key features of footwear that should be routinely assessed in older people are summarised in Figure 3.14. Assessment of shoe fit should be performed while the patient is standing, in order to accurately capture the elongation of the foot and lateral expansion of soft tissues of the forefoot123 and heel124 that occurs during weightbearing. The time of day may also need to be considered, as, although foot volume does not appreciably change throughout the day in healthy
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A 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32
B 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48
C
D
1 2 3 4 5 6 7 8 9 10 11 12 13
15
1
25
2
35
3
45
4
55
5
65
6
75
7
85
8
95
9
105
10
115
11
125
12
135
13
Figure 3.15 Shoe length conversion chart. A. Centimetres. B. Paris points. C. English sizing system. D. American women’s sizes.
young adults,125 prolonged standing and weightbearing activity may influence the volume of the foot in older people, particularly those with venous insufficiency. Foot length (from heel to longest toe) and width (at the level of the forefoot) measurements can be taken with a ruler (or Brannock device) and the measurements converted to shoe size measures using a conversion chart (Fig. 3.15). As a general rule, the shoe should be approximately 12 mm longer than the longest toe. It may be also useful to provide patients with a visual indication of the disparity between their foot size and their shoe size. This can be very simply and effectively demonstrated by making a tracing of
Figure 3.16 Typical example of a shoe and foot tracing from an older woman.
the patient’s bare foot on a piece of paper, and using the same piece of paper to trace around their shoe (Fig. 3.16). The depth of the shoe is of equal importance to its length and width, particularly because the depth of a shoe does not increase as shoe size increases. This aspect of shoe fit is more difficult to accurately measure; however, careful observation and palpation of the shoe will enable the identification of deformed or stretched areas of the upper caused by toe deformities. Assessing the wear patterns of footwear may provide useful diagnostic information regarding foot structure and function.126 Excessive medial or lateral wear marks on the sole may indicate a pes planus or pes cavus foot type, while deformation and creasing of the toe box of the shoe may indicate hallux valgus or hallux limitus. However, wear patterns are also influenced by bodyweight, the mechanical properties of materials the shoe is manufactured from, how long the shoe has been worn for and the level of physical activity of the wearer and these observations therefore need to be interpreted with a certain degree of caution. Finally, the inside of the shoe should always be examined for evidence of exposed seams or foreign bodies (particularly in older people with peripheral neuropathy), as even minor irregularities may contribute to the development of skin lesions. Indeed, a study of 669 people presenting with foot ulcers at a diabetes clinic in the UK indicated that the most commonly reported trigger event was friction from footwear.127
Assessing outcomes of treatment
General shoe style/covering barefoot mule slipper walking shoe surgical/bespoke footwear
socks only high heel sandal Oxford shoe
stockings only court shoe moccasin ugg boot
Heel height 0–2.5 cm
2.6 – 5.0 cm
> 5.0 cm
Fixation none
laces
straps/buckles
Heel counter stiffness minimal
<45°
>45°
Longitudinal sole rigidity minimal
<45°
>45°
Sole flexion point at level of MTPJs
before MTPJs
Tread pattern textured
smooth (i.e. no pattern)
Sole hardness soft
firm
backless slipper boot athletic shoe thong
Velcro™
zips
partly worn
fully worn
hard
Figure 3.17 The Footwear Assessment Form.
FOOTWEAR AND FALLS An additional consideration when assessing footwear in older people is their potential contribution to impaired balance and falls. Certain footwear characteristics, such as high heels, soles with poor grip and inadequate fixation, have been associated with impaired gait, balance, falls and hip fracture (Ch. 12). A standardised screening tool – the Footwear Assessment Form – has been developed for the purpose of assessing footwear in relation to balance and falls (Fig. 3.17).128 Patients with a history of falls whose footwear exhibits multiple potentially hazardous features should be advised to consider the purchase of more appropriate shoes. The role of footwear in falls is discussed in more detail in Chapter 12.
ASSESSING OUTCOMES OF TREATMENT Assessing the effectiveness of clinical treatments in older people can be difficult. In many cases the endpoint is not clearly defined, as older people generally present with multiple presenting complaints, the underlying conditions responsible for these complaints have been present for a long period of time,
and complete resolution of the condition is not always possible. For example, while the effectiveness of orthotic therapy for an acute episode of heel pain in a young person may be adequately assessed using a simple visual analogue pain scale, the effectiveness of ongoing ‘maintenance’ treatments for chronic keratotic lesions associated with fixed deformities is more difficult to quantify. The value of ongoing maintenance, however, should not be underestimated, as recent studies have demonstrated that significant declines in foot health occur when older people are discharged from ‘routine’ podiatry services.129 Despite the difficulties in quantifying outcomes in older people, some form of outcome assessment is useful to assist in formalising the goals of treatment. The best approach is to involve the patient as much as possible by asking them what they hope to achieve from the treatment. Patient expectations of treatment may include a reduction in (or complete resolution of) pain, reduction in the size or complete healing of a foot ulcer, prevention of skin breakdown or infection, maintenance of adequate foot hygiene or maintenance of mobility (e.g. being able to walk to shops without pain or limitation). By matching patient expectations of treatment to some form of outcome measure, the
55
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assessment process can be made more meaningful for both the patient and clinician and progress in achieving the treatment goal can be more easily documented. In addition to the previously discussed pain scales and functional tests, other tools, such as pain diaries and wound measurement charts, may also be useful for assessing treatment outcomes.
SUMMARY
people, and the clinical examination should be equally thorough and systematic. Key additional considerations when assessing older people include the variability of the ageing process, the multifactorial nature of foot disorders in older people and the broader implications of mobility impairment. The clinical assessment techniques outlined in this chapter will assist clinicians in the accurate diagnosis of lower limb disorders and contribute to the development of targeted and effective management strategies for older people.
The general principles of lower limb assessment in older people are essentially the same as for younger
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63. Mueller MJ, Host JV, Norton BJ. Navicular drop as a composite measure of excessive pronation. Journal of the American Podiatric Medical Association 1993; 83: 198–202. 64. Menz HB, Munteanu SE. Validity of three clinical techniques for the measurement of static foot posture in older people. Journal of Orthopaedic and Sports Physical Therapy 2005; 35: 479–486. 65. Menz HB, Morris ME. Clinical determinants of plantar forces and pressures during walking in older people. Gait and Posture 2006; 24: 229–236. 66. Menz HB, Morris ME, Lord SR. Foot and ankle characteristics associated with impaired balance and functional ability in older people. Journal of Gerontology 2005; 60A: 1546–1552. 67. Menz HB, Tiedemann A, Kwan MMS et al. Reliability of clinical tests of foot and ankle characteristics in older people. Journal of the American Podiatric Medical Association 2003; 93: 380–387. 68. Menz HB, Morris ME, Lord SR. Foot and ankle risk factors for falls in older people: a prospective study. Journal of Gerontology 2006; 61A: M866–M870. 69. Menz HB. Clinical hindfoot measurement: a critical review of the literature. The Foot 1995; 5: 57–64. 70. Menadue C, Raymond J, Kilbreath SL et al. Reliability of two goniometric methods of measuring active inversion and eversion range of motion at the ankle. BMC Musculoskeletal Disorders 2006; 7: 60. 71. Perry J, Ireland ML, Gronley J et al. Predictive value of manual muscle testing and gait analysis in normal ankles by dynamic electromyography. Foot and Ankle 1986; 6: 254–259. 72. Kendall HO, Kendall FP. Muscles: testing and function. Baltimore, MD: Williams & Wilkins; 1949. 73. DeWin M, Theuvenet W, Roche P et al. The paper grip test for screening of intrinsic muscle paralysis in the foot of leprosy patients. International Journal of Leprosy and other Mycobacterial Diseases 2002; 70: 16–24. 74. Menz HB, Zammit GV, Munteanu SE et al. Plantarflexion strength of the toes: age and gender differences and evaluation of a clinical screening test. Foot and Ankle International 2006; 27: 1103– 1108. 75. Bohannon RW. Intertester reliability of hand-held dynamometry: a concise summary of published research. Perceptual and Motor Skills 1999; 88: 899–902. 76. Burns J, Redmond A, Ouvrier R et al. Quantification of muscle strength and imbalance in neurogenic pes cavus, compared to healthy controls, using handheld dynamometry. Foot and Ankle International 2005; 26: 540–544. 77. Ory PA. Radiography in the assessment of musculoskeletal conditions. Best Practice and Research Clinical Rheumatology 2003; 17: 495–512.
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95. Katz S, Downs TD, Crash H et al. Progress in development of the index of ADL. Gerontologist 1970; 10: 20–30. 96. Mahoney FI, Barthel DW. Functional evaluation: the Barthel index. Maryland State Medical Journal 1965; 14: 61–65. 97. Rozzini R, Sabatini T, Cassinadri A et al. Relationship between functional loss before hospital admission and mortality in elderly persons with medical illness. Journal of Gerontology 2005; 60A: M1180– M1183. 98. Tiedemann A, Sherrington C, Lord SR. Physiological and psychological predictors of walking speed in older community-dwelling people. Gerontology 2005; 51: 390–395. 99. Woo J, Ho SC, Yu AL. Walking speed and stride length predicts 36 months dependency, mortality, and institutionalization in Chinese aged 70 and older. Journal of the American Geriatrics Society 1999; 47: 1257–1260. 100. Menz HB, Lord SR. The contribution of foot problems to mobility impairment and falls in older people. Journal of the American Geriatrics Society 2001; 49: 1651–1656. 101. Ostchega Y, Harris TB, Hirsch R et al. The prevalence of functional limitations and disability in older persons in the US: data from the National Health and Nutrition Examination Survey III. Journal of the American Geriatrics Society 2000; 48: 1132–1135. 102. Oberg T, Karsznia A, Oberg K. Basic gait parameters: reference data for normal subjects, 10–79 years of age. Journal of Rehabilitation Research and Development 1993; 30: 210–223. 103. Alexander NB, Goldberg A. Gait disorders: search for multiple causes. Cleveland Clinic Journal of Medicine 2005; 72: 586–600. 104. Studenski S, Perera S, Wallace D et al. Physical performance measures in the clinical setting. Journal of the American Geriatrics Society 2003; 51: 314– 322. 105. Keenan A, Bach T. Video assessment of rearfoot movements during walking: a reliability study. Archives of Physical Medicine and Rehabilitation 1996; 77: 651–655. 106. Marsh AP, Katula JA, Pacchia CF et al. Effect of treadmill and overground walking on function and attitudes in older adults. Medicine and Science in Sports and Exercise 2006; 38: 1157–1164. 107. Wass E, Taylor NF, Matsas A. Familiarisation to treadmill walking in unimpaired older people. Gait and Posture 2005; 21: 72–79. 108. Harris RI, Beath T. Army foot survey. An investigation of foot ailments in Canadian soldiers. Ottawa: National Research Council, Canada NRC no. 1574; 1947.
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109. Welton EA. The Harris and Beath footprint: interpretation and clinical value. Foot and Ankle 1992; 13: 462–468. 110. Silvino N, Evanski PM, Waugh TR. The Harris and Beath mat: diagnostic validity and clinical use. Clinical Orthopaedics and Related Research 1980; 151: 265–269. 111. VanSchie CH, Abbott CA, Vileikyte L et al. A comparative study of the Podotrack, a simple semiquantitative plantar pressure measuring device, and the optical pedobarograph in the assessment of pressures under the diabetic foot. Diabetic Medicine 1999; 16: 154–159. 112. Orlin M, McPoil T. Plantar pressure assessment. Physical Therapy 2000; 80: 399–409. 113. Lord SR, Sherrington C, Menz HB, Close JC. Falls in older people: risk factors and strategies for prevention, 2nd ed. Cambridge: Cambridge University Press; 2007. 114. Duncan PW, Studenski S, Chandler J et al. Functional reach: predictive validity in a sample of elderly male veterans. Journal of Gerontology 1992; 47: M93–98. 115. VanSwearingen JM, Paschal KA, Bonino P et al. Assessing recurrent fall risk of community-dwelling, frail older veterans using specific tests of mobility and the Physical Performance Test of function. Journal of Gerontology 1998; 53A: M457–M464. 116. Shumway-Cook A, Brauer S, Woollacott M. Predicting the probability for falls in community-dwelling older adults using the Timed Up & Go Test. Physical Therapy 2000; 80: 896–903. 117. Hurvitz E, Richardson J, Werner R et al. Unipedal stance testing as an indicator of fall risk among older outpatients. Archives of Physical Medicine and Rehabilitation 2000; 81: 587–591. 118. Thomson FJ, Masson EA. Can elderly diabetic patients co-operate with routine foot care? Age and Ageing 1992; 21: 333–337. 119. Chung S. Foot care – a health care maintenance program. Journal of Gerontological Nursing 1983; 9: 213–227.
120. Burns S, Leese G, McMurdo M. Older people and ill-fitting shoes. Postgraduate Medical Journal 2002; 78: 344–346. 121. Menz HB, Morris ME. Footwear characteristics and foot problems in older people. Gerontology 2005; 51: 346–351. 122. Munro BJ, Steele JR. Household-shoe wearing and purchasing habits – a survey of people aged 65 years and older. Journal of the American Podiatric Medical Association 1999; 89: 506–514. 123. Weijers RE, Walenkamp GHIM, VanMameren H et al. Changes in the soft tissue of the forefoot during loading: a volumetric study. The Foot 2003; 13: 70–75. 124. Fuller E, Hogge JD. Measurement of the expansion of the calcaneal fat pad upon weightbearing. Journal of the American Podiatric Medical Association 1998; 88: 12–16. 125. Moholkar K, Fenelon G. Diurnal variations in volume of the foot and ankle. Journal of Foot and Ankle Surgery 2001; 40: 302–304. 126. Vernon W, Parry A, Potter M. A theory of shoe wear pattern influence incorporating a new paradigm for the podiatric medical profession. Journal of the American Podiatric Medical Association 2004; 94: 261–268. 127. Macfarlane RM, Jeffcoate WJ. Factors contributing to the presentation of diabetic foot ulcers. Diabetic Medicine 1997; 14: 867–870. 128. Menz HB, Sherrington C. The Footwear Assessment Form: a reliable clinical tool for the evaluation of footwear characteristics of relevance to postural stability in older adults. Clinical Rehabilitation 2000; 14: 657–664. 129. Campbell J, Patterson A, Gregory D et al. What happens when older people are discharged from NHS podiatry services? The The Foot 2002; 12: 32–42.
CHAPTER
Keratotic disorders
CHAPTER CONTENTS Classification and clinical presentation Aetiology 62 Assessment and diagnosis Treatment 69 Conservative treatments Surgical treatment 72 Summary 74 References 74
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4
Keratotic lesions are one of the most prevalent foot problems in older people, affecting between 20% and 65% of people over 65 years of age.1–7 Although often considered a relatively minor complaint, keratotic lesions can cause considerable pain and disability. It has been demonstrated that older people with plantar keratotic lesions have greater difficulty walking on level ground and ascending and descending stairs, and perform worse in tests of balance ability.8 Furthermore, if left untreated, keratotic lesions may cause damage to deeper tissues and lead to ulceration.9 Therefore, the accurate diagnosis and management of keratotic disorders is an essential component of foot care for older people.
CLASSIFICATION AND CLINICAL PRESENTATION There are two main types of keratotic lesion – calluses and corns (Table 4.1). Calluses (also known as tylomas, callosities and keratomas) present as a broad-based, diffuse thickening of the stratum corneum and are most commonly located under the metatarsal heads (Fig. 4.1). Calluses vary in colour from white to greyyellow; however, they may also occasionally appear brown or red because of extravasation of blood in the underlying dermis. Calluses under the metatarsal heads have a characteristic topography that may reflect differences in weightbearing patterns under the foot when walking. Merriman et al10 evaluated lesion patterns in 243 chiropody patients and found that the most common presentation was under the second to fourth metatarsal heads, followed by the second
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Table 4.1 Classification of keratotic lesions Lesion
Alternative terminology
Subtypes
Common locations
Callus
Tyloma Callosity Keratoma Intractable plantar keratoma
–
Plantar metatarsal heads Periphery of heel Dorsal interphalangeal joints Apices of toes
Corn
Helomata Clavus
Hard corn (heloma durum) • Vascular (heloma vasculare) • Neurovascular (heloma neurovasculare) • Fibrous (heloma fascia) Soft corn (heloma molle) Seed corn (heloma milliare)
Dorsal interphalangeal joints Apices of toes Plantar metatarsal heads Interdigital Non-weightbearing areas of plantar surface
Figure 4.1 Callus on the plantar aspect of the central metatarsal heads. (Courtesy of Lloyd Reed, Queensland University of Technology.)
metatarsal head (Fig. 4.2). Similar observations were reported by Springett et al11 and Grouios,12 who found the most common presentation to be the second metatarsal head (30% and 32% of patients respectively), followed by the first metatarsal head (21% and 23% of patients respectively). The role of limb dominance in the formation of plantar keratotic lesions is unclear. While Springett et al11 found no significant difference in prevalence according to preferred limb in 319 podiatry patients, Grouios12 found a higher prevalence of lesions on the dominant foot in 115 athletes.
Corns (also known as heloma or clavi) are a more discrete, circumscribed area of thickening with a central core that may penetrate into the dermis.13 Three subtypes of corn have been recognised: hard corns (heloma dura), soft corns (heloma molle) and seed corns (heloma milliare). The distribution patterns of these lesions vary (Fig. 4.3). Hard corns, the most common type of corn, appear as a firm, dry mass with a polished surface and are found on the interphalangeal joints of the toes (Fig. 4.4A, B) and under the metatarsal heads. Occasionally, hard corns may develop beneath the nail plate (referred to as subungual heloma) in response to pressure from footwear (Fig. 4.5). Hard corns can become infiltrated with blood vessels and/ or nerve endings from the papillary dermis, and are then referred to as vascular corns (heloma vasculare) or neurovascular corns (heloma neurovasculare). If left untreated, longstanding hard corns may become surrounded by a meshwork of fibrous tissue (known as fibrous corns or heloma fascia). Soft corns (heloma molle) develop between the toes and have a characteristic rubbery texture due to the apposition of the toes preventing adequate evaporation (Fig. 4.6).14,15 Seed corns (heloma milliare) are small, superficial clusters of porokeratotic cells found embedded in plantar calluses, scattered around the heel or on non-weightbearing areas of the plantar surface (Fig. 4.7).16 Seed corns are generally not painful.
AETIOLOGY Pathogenesis The physiological mechanism responsible for the development of keratotic lesions is not fully under-
Classification and clinical presentation
A
B
C
D
E
F
G
H
I
J
Figure 4.2 The ten most common patterns of plantar callus formation. A. Second to fourth metatarsal heads (MHs) (23%). B. Second MH (18%). C. First and fifth MHs (14%). D. First MH (13%). E. Second and third MHs (10%). F. First to fifth MHs (8%). G. Third MH (8%). H. First to third MHs (8%). I. Fifth MH (7%). J. First and third MHs (7%).
A
B
C
D
Figure 4.3 Common distribution patterns for hard corns (A, B), soft corns (C) and seed corns (D).
stood. In response to repetitive friction or pressure, normal healthy skin undergoes accelerated keratinisation and a decreased rate of desquamation, resulting in an increase in the thickness of the stratum corneum.17 This process, sometimes referred to as physiological hyperkeratosis, is considered to be a protective mechanism that prevents damage to deeper
tissues by dispersing the applied forces over a larger area and volume of skin. Histological studies have revealed several notable changes in calloused skin, including an increase in the thickness of the stratum corneum and stratum granulosum, a decrease in density (but increase in thickness) of keratinocytes and an exaggerated pattern of rete pegs.18 These
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KERATOTIC DISORDERS
A
B
Figure 4.4 Hard corns (heloma dura). A. Dorsal surface of the fourth proximal interphalangeal joint. B. Apex of the third toe. (Courtesy of Lloyd Reed, Queensland University of Technology.)
changes are thought to represent an increased rate of epidermal cellular production and an associated decrease in the differentiation of keratinocytes as they progress to the upper layers of the skin. Corns have a similar structure; however, the underlying dermis exhibits significant degeneration of collagen fibres and an increased number of fibroblasts.19–21 For reasons that are still unknown, in some individuals the process of hyperkeratosis becomes exces-
Figure 4.5 Subungual heloma. (Courtesy of Amanda Taylor, Charles Sturt University.)
Figure 4.6 Interdigital soft corn (heloma molle), located between the fourth and fifth toes. (Courtesy of Lloyd Reed, Queensland University of Technology.)
sive, resulting in a large build-up of dense, keratinised tissue. Further pressure applied to the lesion leads to a cycle of skin injury, repair and adaptation, and the compression of nerve endings in the papillary dermis caused by the lesion leads to pain (Fig. 4.8). If left untreated, keratotic lesions can cause considerable damage to deeper layers of the skin, particularly in people with diabetes. Indeed, the presence of plantar keratotic lesions is a strong predictor of foot ulceration in people with diabetic peripheral neuropathy.9
Classification and clinical presentation
Compression and shear forces applied to skin
Dermal inflammatory response – vasodilatation of vascular bed
Increased dermal fibroblast activity
Increased epidermal basal cell mitosis – decreased differentiation of cells
Figure 4.7 Close-up view of seed corns (heloma milliare) on the plantar aspect of the foot. (Courtesy of Lloyd Reed, Queensland University of Technology.)
Four plantar pressure measurement studies have provided evidence that plantar calluses tend to develop in regions of elevated pressure. Robertson22 compared 60 people with painful calluses under the first metatarsophalangeal joint to a matched control group and found that the peak plantar pressure was significantly higher under all metatarsophalangeal joints (including a 116% increase under the first metatarsophalangeal joint) in the group with callus. A similar result was reported by Potter & Potter,23 who assessed pressures at a range of sites in people with and without calluses and reported an average increase in pressure of 25% at sites with an overlying callus. In a study of 23 people with diabetes, Pataky et al24 observed that those with calluses under the third metatarsophalangeal joints exhibited 10% higher pressures than those without. Finally, the largest study so far conducted (involving 292 people aged 62–96 years of age) reported that peak plantar pressures were between 9% and 12% higher in callused regions of the forefoot, with the exception of the first metatarsophalangeal joint and the lesser toes.25 Although the magnitude of pressure differences reported in these studies varies considerably, there does appear to be a relationship between elevated pressures and calluses, which is further supported by studies reporting a reduction in pressure after the lesions are removed with a scalpel.24,26,27 The pathogenesis of seed corns has received little attention in the literature. Earlier reports suggested that these lesions were crystalline deposits of pure cholesterol; however, a chromatographic analysis by
Crowding of cells at dermal-epidermal junction – exaggerated pattern of rete pegs
Hypertrophy of stratum corneum
Pressure on nerves in papillary dermis
Pain
Figure 4.8 Pathogenesis of keratotic lesions.
O’Halloran28 revealed that, while the cholesterol content of seed corns was higher than that of normal skin, it was no different to that of hard corns, indicating that the cholesterol content of skin is a marker of keratinocyte proliferation. Vitamin deficiency, genetic predisposition to dry skin and fungal infection have also been implicated.29,30
Risk factors No prospective studies have been undertaken to determine the risk factors for the development of keratotic lesions, so our knowledge is limited to casecontrol studies and clinical observations. Posited risk factors for keratotic lesion formation are summarised
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Table 4.2 Posited risk factors for the development of keratotic lesions Intrinsic
Extrinsic
Increased age Female sex Obesity Comorbidities Diabetes mellitus Rheumatoid arthritis Cerebrovascular accident Systemic sclerosis Foot deformity Hallux valgus Hallus limitus/rigidus Lesser toe deformity Pes planus and pes cavus Foot surgery complications Reduced range of motion
Footwear Narrow toe box Elevated heel Textured insoles (‘health sandals keratosis’) Occupational/lifestyle factors Prolonged weightbearing Prolonged bed rest Prayer posture (‘Mecca foot’)
in Table 4.2 and can be divided into intrinsic factors (such as age, sex, co-morbidities and foot deformities) and extrinsic risk factors (such as ill-fitting footwear and occupational or lifestyle factors). Each of these factors is discussed in detail in the following section. The community-based epidemiological studies outlined in Chapter 1 indicate that the prevalence of corns and calluses increases with age5,31,32 and female sex.3,32 The increased prevalence with advancing age is most probably related to age-related changes in skin structure and function (particularly the decreased function of sweat glands and thinning of the dermis), in addition to the associated increase in the prevalence of foot deformities, while the association with female sex may be partly attributable to footwear. Several authors have speculated that plantar calluses may be associated with increased body mass index12,33,34 due to the subsequent increase in weightbearing pressures.35,36 In particular, heel calluses (and associated fissuring) appear to be highly prevalent in obese older women who wear shoes without an enclosed heel counter. Keratotic lesions are common in people with systemic diseases such as diabetes,37 rheumatoid arthritis,38 stroke39 and systemic sclerosis;40 however, whether the prevalence of calluses and corns is greater in people with these conditions compared to the general older population remains unclear. Two casecontrol studies have shown that the prevalence of
calluses in diabetic and non-diabetic older people is similar;41,42 however, Woodburn et al43 have shown that people with rheumatoid arthritis do have a higher prevalence of plantar forefoot calluses compared to age-matched controls. The likely mechanism for the speculated increased prevalence associated with these conditions is the associated increase in foot deformity and diminished resilience of the skin. Corns and calluses are frequently associated with foot deformities such as hallux valgus, hallux limitus and lesser toe deformities, because of changes in plantar pressure distribution when walking and the inherent difficulty in obtaining footwear to accommodate bony prominences.44,45 In a sample of 135 older people, Menz et al8 have shown that plantar calluses were more prevalent in those with hallux valgus, whereas corns on the toes were more prevalent in those with lesser digital deformity. The relationship between foot posture, range of motion and plantar lesions is not as clear, although Woodburn et al43 reported that people with rheumatoid arthritis and a valgus heel had a higher prevalence of plantar calluses on the medial forefoot than those with a neutral heel, and Bevans & Bowker33 have shown that a pronated foot type, limited first metatarsophalangeal joint motion and limited ankle joint range of motion are associated with the presence of calluses in people with diabetes. Finally, foot surgery is a well-recognised cause of plantar lesions (referred to as transfer lesions), which frequently develop in response to the altered weightbearing patterns following procedures that involve metatarsal shortening.46,47 Perhaps the most common risk factor for keratotic lesions in older people is ill-fitting footwear and the wearing of shoes with an elevated heel. It has long been recognised that many older people wear shoes that are too narrow or too short, leading to compression of the toes in the front of the shoe and subsequent development of lesions.48,49 In addition, wearing shoes with an elevated heel has been shown to markedly increase weightbearing pressures on the forefoot, a factor that is likely to predispose to the development of plantar lesions.50–53 These associations were recently confirmed by Menz & Morris,54 who took tracings of the feet and shoes of 176 older people and found that more than three-quarters of the sample wore shoes narrower than their feet. An assessment of foot problems revealed that wearing shoes substantially narrower than the foot was associated with corns on the toes, hallux valgus deformity and foot pain, whereas wearing shoes shorter than the foot was associated
Assessment and diagnosis
with lesser toe deformity. Wearing shoes with heel elevation greater than 25 mm was associated with hallux valgus and plantar calluses in women. A less common potential footwear-related risk factor for plantar calluses is the use of sandals with multiple raised projections designed to stimulate the soles when walking. Yoshii et al55 reported 13 cases of plantar calluses in otherwise healthy people that had developed after wearing such shoes, which they labelled ‘health sandals keratosis’. In each case, the lesions resolved after patients stopped wearing the sandals. Occupational and lifestyle factors, such as extended periods of weightbearing and performing repetitive activities involving the foot, are also likely to play a role in the development of keratotic lesions. Several examples have been described in the literature, such as the formation of dorsolateral foot lesions in people who sit cross-legged for long periods for either work56 or prayer (the so-called ‘Mecca foot’).57,58 Conversely, extended periods of bed rest may also lead to the development of calluses on the posterior heel and malleoli, which may progress to pressure ulcers if pressure redistribution is inadequate.59
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Less common causes of keratotic lesions The preceding discussion has focused on mechanically-induced hyperkeratosis, which is the most common cause of corns and calluses in older people. However, there are many, less commonly-encountered conditions which may manifest as keratotic lesions on the foot, such as palmoplantar keratoderma (Fig. 4.9).60,61 A brief summary of these conditions is provided in Table 4.3. B
ASSESSMENT AND DIAGNOSIS The diagnosis of keratotic lesions is relatively straightforward, as their appearance is generally stereotypical and there are few common differential diagnoses to consider. Mechanically induced lesions can be differentiated from hyperkeratosis caused by inherited dermatological diseases or chemical toxicity by taking a thorough medical history and from clinical observations of lesion distribution patterns. Mechanically induced lesions will appear on weightbearing areas or bony prominences subjected to pressure from footwear, whereas keratotic lesions due to other causes are generally more widespread and associated with similar
Figure 4.9 Plantar (A) and palmar (B) lesions associated with the punctuate form of palmoplantar keratoderma. (Courtesy of Lesley Newcombe, La Trobe University.)
lesions on the palms. Calluses and corns can sometimes be confused with verrucae (warts), and indeed longstanding warts may develop a thick covering layer of hyperkeratosis. However, verrucae do not generally form on weightbearing areas, are more acutely painful when lateral pressure is applied to the lesion, and will exhibit characteristic pinpoint bleeding when debrided because of the presence of thrombosed blood vessels within the lesion itself.13,45,62,63
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Table 4.3 Less common causes of keratotic lesions in older people Classification
Condition
Aetiology
Appearance
Treatment
Inherited disorders
Palmoplantar keratoderma
Autosomal dominant
Mal de Meleda
Autosomal recessive
Keratoderma punctata
Autosomal dominant
Keratosis follicularis (Darier’s disease)
Autosomal dominant
Emollients, keratolytics, debridement Emollients, keratolytics, debridement Emollients, keratolytics, debridement Emollients, keratolytics, corticosteroids
Palmoplantar keratoderma
Autosomal dominant
Diffuse thick hyperkeratosis of palms and soles, often associated with fissuring As above, in addition to discrete keratoses on extensor surfaces Multiple punctuate hyperkeratotic lesions on palms and soles Small scaly or waxy papules most commonly found on scalp, chest and back. Appear as punctuate keratoses when the palms and soles are affected Diffuse thick hyperkeratosis of palms and soles, often associated with fissuring
Diffuse palmoplantar keratosis (HowelEvans’s syndrome) Acrokeratosis paraneoplastica (Bazex’s syndrome)
Precedes oesophageal carcinoma
Diffuse hyperkeratosis of palms and soles
Emollients, keratolytics, debridement
Associated with upper respiratory and gastrointestinal carcinoma
Diffuse hyperkeratosis of palms and soles, nail hypertrophy
Emollients, keratolytics, debridement
Ichthyosis
Group of disorders. May be inherited or acquired
Emollients, keratolytics, retinoic acid, corticosteroids
Actinic keratosis (‘senile keratosis’)
Excessive or prolonged sunlight exposure
Arsenical keratosis
Exposure to arsenical compounds in medications, insecticides or drinking water Cause unknown. Occurs in postmenopausal women and is associated with obesity and hypertension
Characteristic dry ‘fish-scale’ lesions with fissuring on elbows, knees, forehead, arms, thighs, palms and soles Well-defined, raised red papules or plaques with rough surface of adherent scales, most commonly located on exposed areas of skin Discrete, yellow, punctuate round lesions on palms and soles
Disorders associated with malignancy
Other
Keratoderma climacterium
Marked thickening of palms and soles with deep fissures
Emollients, keratolytics, debridement
Cryotherapy, curettage, electrotherapy, topical 5-flurouracil Emollients, keratolytics, debridement
Emollients, keratolytics, debridement, corticosteroids
Treatment
Once differential diagnoses are ruled out, the next step is to determine the underlying cause of the lesion. This will involve careful observation and palpation, noting the presence of hallux valgus, hallux limitus, lesser toe deformities, relative lengths of the metatarsals and overall posture of the foot (pronated, neutral or supinated). Joint range of motion assessments are also useful, as restricted motion of metatarsophalangeal joints may result in the generation of excessive plantar pressures when walking.64,65 Footwear should be carefully examined, with particular emphasis placed on the width and depth of the toe-box, the height of the heel and the presence of irregularities in the inner lining of the shoe (such as prominent stitching) that may be pressing on the foot. In-shoe devices such as insoles, foot orthoses, ankle–foot orthoses or other forms of bracing should also be evaluated. The plantar pressure systems outlined in Chapter 3 may be useful to locate and quantify regions of high pressure under the foot but they are rarely required to confirm a diagnosis. Similarly, the use of radiographs to visualise bony prominences, or histological analysis of the lesion, is generally not necessary.
Figure 4.10 Scalpel debridement and enucleation of a heloma durum. (Courtesy of Lloyd Reed, Queensland University of Technology.)
TREATMENT CONSERVATIVE TREATMENTS Lesion debridement The first step in the treatment of keratotic lesions is sharp debridement or enucleation with a scalpel (Figs 4.10, 4.11). This procedure requires a considerable level of manual dexterity, particularly in the case of deep-seated neurovascular corns or interdigital soft corns. Debridement and enucleation provide immediate symptomatic relief,66 increase the bearable pressure threshold of the foot67 and reduce weightbearing pressures by up to 30%.24,26,27 There is also some preliminary evidence that debridement of lesions may improve mobility in older people. Balanowski & Flynn68 assessed functional ability (including ascending and descending stairs, an alternate stepping test and walking speed) and balance in people aged over 65 before and after scalpel debridement of painful plantar keratoses. After debridement, there was a significant reduction in pain and significant improvements in all three functional tests, which were maintained at a follow-up appointment 1 week later. Debridement and enucleation of keratotic lesions, however, provides only short-term relief of symptoms
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Figure 4.11 Plantar heloma durum before (A) and after (B) scalpel debridement and enucleation. (Courtesy of Matthew Dilnot, Melbourne Foot Clinic.)
and, unless the underlying cause is addressed, most lesions will recur after a number of days or weeks.69,70 The optimum frequency of repeat appointments for ongoing management of keratotic lesions is unknown, as the rate of recurrence of keratotic lesions is highly variable. Potter & Potter71 have recently shown that callus regrowth over the first 2 weeks following debridement varies considerably, even within individuals. Three distinct patterns were observed: slowgrowing calluses, which only grew to 30% of their original size during the 2-week period; mediumgrowing calluses, which grew to 30–60% of their original size; and fast-growing calluses, which grew to
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60–70% of their original size. The surface area and thickness of the original lesion did not appear to influence the rate of regrowth; however, it was reported that lesions over the fifth metatarsal head were more likely to be fast-growing and that lesions under the second metatarsal head were more likely to be slowgrowing. The underlying physiological mechanisms for these differences remain unclear but are likely to be related to level of activity, footwear characteristics and level of skin hydration.
Topical treatments A wide range of topical treatments have been proposed to both chemically debride keratotic lesions and inhibit their regrowth. In 1782, Laforest prescribed a concoction consisting of pork fat and ‘the mousse that forms around boats’72 and, since that time, a similarly colourful array of ointments, tinctures and poultices have been recommended for keratotic lesions.73 Contemporary topical agents include salicylic acid,74–76 silver nitrate,77 silicone77 and hydrocolloid wound dressings.78 Although anecdotal reports and several short-term, uncontrolled studies suggest that these techniques may be effective,74,77,78 very few controlled trials have been undertaken. Salicylic acid, first described as a treatment for keratotic lesions in ancient Greece,79 is believed to lower the pH of the stratum corneum, thereby leading to swelling, maceration and eventual desquamation of the lesion. Lang et al80 have shown that ‘corn plasters’ containing 40% w/w salicylic acid are more effective than non-medicated placebo pads, producing complete enucleation of 62% of digital hard corns over a 21-day period. Subsequent comparison studies of different types of corn plaster (i.e. different strengths and delivery systems) have reported similar rates of lesion resolution; however, the adverse effect of excessive maceration of surrounding tissue appears to be more likely in stronger preparations incorporating a waxy matrix rather than an adhesive matrix.75,76 The use of salicylic acid also needs to be very carefully considered in people with diabetes, as several cases of foot ulceration and infection have been reported following its use.81 Hydrocolloid dressings, most commonly used in the management of open wounds, have recently been evaluated as a potential treatment for keratotic lesions because of their effect on skin hydration. An uncontrolled study of 43 people with corns and calluses
Figure 4.12 Heel callus with associated fissuring. (Courtesy of Lloyd Reed, Queensland University of Technology.)
reported that 21% of corns and 14% of calluses had resolved after 5 weeks of hydrocolloid treatment.78 A subsequent randomised trial comparing three adhesive dressings (compressed felt, polymer gel and a hydrocolloid) for the treatment of symptomatic corns found that, while all treatments were effective in reducing pain and the size of the lesion, the hydrocolloid was reported by patients to be easier to use, easier to keep in place and more aesthetically pleasing.72 However, whether this benefit is significant enough to justify the extra cost of the dressing is arguable. Heel calluses, which often present with associated skin dryness and fissuring (Fig. 4.12), can be difficult to treat, particularly in older people who are overweight and wear shoes without an enclosed heel counter. Following debridement of the overlying callus and the edges of the fissures, topical application of salicylic acid or emollient creams may be effective,82 in addition to the firm application of an adhesive bandage to limit lateral expansion of the heel pad when weightbearing. The application of cyanoacrylate adhesives to seal deep heel fissures has also been reported to be effective, producing wound closure strength equivalent to suturing.83
Injection therapy In addition to topical applications, a range of preparations for intralesional or sublesional injection have
Treatment
been reported, including sodium chloride, alcohol and liquid silicone.84–86 Dockery & Nilson85 have reported clinical success in resolving chronic plantar keratotic lesions using weekly 0.5–1.0 ml intralesional injection of a 4% sclerosing solution consisting of 2 ml absolute ethyl alcohol with 48 ml of 2% lidocaine with adrenaline (epinephrine) 1 : 100 000. No controlled trials have been undertaken to adequately assess the efficacy of this approach, and the mechanism of action is also unclear. It has been suggested that the injection acts as an ‘internal pad’, thus spreading weightbearing forces over a larger area; however, the duration of this effect is unknown. Similar anecdotal reports regarding the efficacy of liquid silicone injections have been reported by Balkin;87–90 however, only two controlled trials have so far been undertaken. Tollafield et al86 compared the efficacy of liquid silicone and saline injections in 31 people with plantar lesions and found no difference between the groups with regard to pain, frequency of follow-up treatments or appearance of the lesions. More recently, a randomised, placebocontrolled trial conducted in people with diabetic peripheral neuropathy found that six injections of 0.2 ml liquid silicone were more effective in increasing plantar soft tissue thickness and reducing plantar pressure than a placebo (saline); however, there was no difference in the appearance of the calluses.91 A follow-up paper by these authors reported that, after 2 years, the increase in soft tissue thickness was largely maintained, although the treatment had lost some of its pressure-reducing properties.92 Although no serious complications were reported in these studies, skin
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B
C
discoloration and migration of the silicone from the injection site have been reported in a small number of cases.93
Orthotic therapy Redistribution or reduction of excessive foot pressures has the potential to provide longer-term relief of symptoms associated with keratotic lesions and, in some cases, complete resolution of the lesion may be possible. Simple cushioning insoles placed inside the shoe may assist in reducing the overall pressure under the foot; however, individually customised pressure redistribution insoles are likely to be more effective. Figure 4.13 shows some of the more commonly used padding designs for offloading plantar keratotic lesions. Several plantar pressure studies have confirmed that this approach is effective in redistributing pressures beneath the metatarsal heads.94–101 Similarly, the application of small pads beneath the proximal interphalangeal joints has been shown to significantly reduce pressure borne by the apices of the toes.102,103 In addition to these simple insole designs, orthoses moulded to the foot from more rigid materials such as polypropylene have also been shown to redistribute pressures to the arch of the foot, thereby reducing forefoot pressures.104,105 Despite the significant pressure reduction achieved with insoles and foot orthoses, only three studies have demonstrated that this approach is effective in the management of calluses. Colagiuri et al106 randomly allocated 20 people with diabetes to receive either conventional debridement of their plantar lesions or
D
E
F
Figure 4.13 Orthotic designs used to redistribute pressure away from keratotic lesions. A. Plantar metatarsal pad. B. Plantar cover. C. ‘U-ed’ plantar cover. D. Winged plantar cover. E. Arch pad. F. Toe prop.
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custom orthoses manufactured from a rigid plastic material. After 12 months, the orthotic group exhibited greater reductions in callus severity, with 16 out of 22 calluses in the orthotic group demonstrating significant improvement. More recently, Caselli et al107 compared debridement alone to debridement in conjunction with either urethane or silicon gel insoles. After 4 weeks, a significant improvement in symptoms was observed in both insole groups, indicating that the use of insole therapy is more effective than debridement alone. Finally, Timson & Spooner70 randomly allocated 25 people with painful calluses to receive either debridement or insoles manufactured from 4 mm medium-density ethyl vinyl acetate with apertures placed at the site of the lesion. Both groups demonstrated significant reductions in pain immediately following treatment; however, the reduction was greater in the debridement group. At 6-week followup, pain relief was maintained in the insole group; however, pain levels in the debridement group had returned to their pretreatment level. Alleviating pressures from keratotic lesions on the dorsum of the toes or between the toes is somewhat more difficult, as it is more dependent on the adequacy of the footwear. Several approaches have been used with anecdotal evidence of clinical success, including simple lamb’s wool, foam toe spacers and silicone gel sleeves, many of which are now available as over-the-counter products from pharmacies and supermarkets.108 Devices customised to the shape of the individual’s foot can also be manufactured from silicone elastomer materials (Ch. 11).
Footwear modification If it is evident from clinical observations that the underlying cause of the keratotic lesion is related to ill-fitting footwear, it is necessary to advise the older person to consider purchasing a new pair of shoes with more adequate room in the toe-box. In some situations, however, this may not be possible for financial reasons or because of reluctance on the part of the older person to wear wider-fitting shoes. In these circumstances, it is worth considering modifying the existing footwear to accommodate the lesion. This can be achieved using shoe-stretching devices, cutting out sections of the upper, or balloon patching. Medical-grade footwear manufacturers or pedorthists will often need to be consulted to undertake these modifications, as they require considerable manual skill and the appropriate tools and materials. Before
commencing this intervention, it also needs to be considered that the end result may not always be aesthetically pleasing and that the resilience and longevity of the shoe may be diminished in the process. Footwear modifications are discussed in more detail in Chapter 12.
SURGICAL TREATMENT Surgical intervention for keratotic lesions is generally considered for older people with painful, chronic lesions that have failed to respond to conservative treatment, or as an option for older people who find ongoing maintenance visits inconvenient. Two broad categories are recognised – electrosurgery, a relatively atraumatic procedure that involves removing the lesion using high-frequency current, and orthopaedic surgery, which is far more invasive, has a greater potential for complications and requires lengthier periods of rehabilitation. Both approaches should be carefully considered in the context of their potential costs and benefits.
Electrosurgery Electrosurgery has been used for several decades in a range of dermatological applications, most commonly in the treatment of small skin lesions such as verrucae, skin tags and naevi. The procedure employs highfrequency alternating current, which produces heat within cells, leading to modifications to the protein content, evaporation of cellular fluids and the eventual destruction of the lesion and its separation from surrounding normal skin at the level of the dermal– epidermal junction.109,110 Two different approaches are used depending on the depth of the lesion: fulguration, in which the electrode is held away from the skin to produce sparking at the skin surface, or electrodesiccation, in which the electrode is placed in contact with the skin to penetrate more deeply. Local anaesthesia is generally required prior to administration and, following treatment, sterile wound dressings in conjunction with redistributive padding should be applied. No controlled trials have evaluated the efficacy of electrosurgery in the treatment of keratotic lesions; however, a number of case series studies report favourable results for longstanding lesions. A case series of 50 patients with vascular and neurovascular corns reported by Smith & Morrison110 indicated that 45%
Treatment
of lesions completely resolved after a period of 4–6 weeks and a further 50% showed sufficient improvement to enable ongoing management with scalpel debridement. A follow-up study 4 years later reported improved rates of lesion resolution (71–90%), which the authors attributed to improvements in postoperative management.111 More recently, Whinfield & Forster112 reported a 73% reduction in pain associated with chronic hard corns 6 weeks after electrodesiccation and, at 12 months, pain levels were 58% of their pretreatment values. Although further studies are required to substantiate these findings, it would appear that electrosurgery may be useful for the treatment of chronic painful lesions in older people who have not responded to conservative treatments or who are considered not suitable for orthopaedic surgery.
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C
Orthopaedic surgery Surgical treatment for plantar lesions was first described by Meisenbach in 1916.113 Since then, there have been a plethora of surgical approaches and modifications described in the literature, involving the removal of entire metatarsals, total or partial excision of metatarsal heads and a variety of approaches for shortening or dorsiflexing metatarsals.114 It is difficult to evaluate the relative success of these approaches, as few direct comparisons have been undertaken and in many studies the duration of follow-up is insufficient to adequately assess the rate of complications. Nevertheless, it is clear that lesion recurrence is relatively common, as are complications such as the development of new lesions at previously lesion-free sites (transfer lesions), reduced toe function and delayed or non-union of the osteotomy site. These complications appear to be more likely to occur when the surgical procedure involves multiple osteotomies.115 Currently, the most commonly performed procedure for the surgical management of plantar lesions is the Weil osteotomy, attributed to the American podiatrist Lowell Scott Weil by Barouk.116 The aim of the procedure is to shorten the metatarsal, and it involves a 30° oblique osteotomy through the metatarsal head and proximal displacement of the distal fragment, followed by screw fixation and excision of the remaining dorsal overhang (Fig. 4.14). The plantar lesion is also excised to the level of the dermis. Patient satisfaction with this procedure has been reported to range between 47% and 88% of cases,115,117–120 with complete resolution of the lesion reported in 39–78% of
Figure 4.14 Weil osteotomy. A. Osteotomy made parallel to weightbearing surface. B. Plantar fragment translated proximally. C. Resultant overhang of bone removed and osteotomy fixed with cortical screw.
cases.115,118,120–122 The most commonly reported complication associated with the procedure is floating toes (15–36% of cases),117,118,120,122 although transfer lesions are also relatively common (5–20% of cases).117,118,121,122 Although few direct comparisons of success rates according to age have been undertaken, Winson et al115 have observed that complications are more likely in people aged over 65 years. A number of authors have suggested that the Weil osteotomy is most appropriate when the affected metatarsal is excessively long, and that complications arise when the procedure is administered to normal length metatarsals.123,124 In cases where the objective of the surgery is to elevate the metatarsal without shortening it, the Schwartz osteotomy125 has been recommended. This procedure involves removing a wedge-shaped piece of bone from the anterior aspect of the metatarsal head, leaving a plantar hinge of bone that is then dorsiflexed and fixed by a screw (Fig. 4.15). A recent retrospective review of 25
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patients reported that, while only 41% demonstrated complete resolution of their plantar lesion, there was a high level of patient satisfaction and a reduction in the number of required podiatry visits postoperatively.124 Surgical procedures for keratotic lesions on the toes are selected according to the specific associated deformity (hammer toe, claw toe, mallet toe, etc.) and the range of motion available at the metatarsophalangeal and interphalangeal joints.44,126 These procedures are described in Chapter 8.
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SUMMARY C
Figure 4.15 Schwartz osteotomy. A. The first osteotomy is made parallel to the weightbearing surface and the second on a slightly more acute angle, leaving a hinge of cortical bone intact. B. Wedge of bone removed. C. Head of metatarsal moved dorsally on cortical hinge and osteotomy fixed with vertical screw.
Keratotic lesions are among the most common foot complaints in older people, the management of which accounts for the vast majority of a podiatrist’s workload. Although often considered a minor complaint, longstanding lesions can be debilitating and severely impact on an older person’s quality of life. In most cases, keratotic lesions can be successfully managed with conservative interventions such as debridement, orthoses and footwear modifications. Surgery may be indicated for cases that fail to respond to conservative approaches; however, the risk of complications needs to be carefully considered.
References 1. Black JR, Hale WE. Prevalence of foot complaints in the elderly. Journal of the American Podiatric Medical Association 1987; 77: 308–311. 2. Gould N, Schneider W, Ashikaga T. Epidemiological survey of foot problems in the continental United States 1978–1979. Foot and Ankle 1980; 1: 8–10. 3. Dunn JE, Link CL, Felson DT et al. Prevalence of foot and ankle conditions in a multiethnic community sample of older adults. American Journal of Epidemiology 2004; 159: 491–498. 4. Elton PJ, Sanderson SP. A chiropodial survey of elderly persons over 65 years in the community. Public Health 1986; 100: 219–232. 5. Brodie BS, Rees CL, Robins DJ et al. Wessex Feet: a regional foot health survey. Vol. I: The survey. Chiropodist 1988; 43: 152–165. 6. Harvey I, Frankel S, Marks R et al. Foot morbidity and exposure to chiropody: population based study. British Medical Journal 1997; 315: 1054–1055.
7. Benvenuti F, Ferrucci L, Guralnik JM et al. Foot pain and disability in older persons: an epidemiologic survey. Journal of the American Geriatrics Society 1995; 43: 479–484. 8. Menz HB, Lord SR. Foot pain impairs balance and functional ability in community-dwelling older people. Journal of the American Podiatric Medical Association 2001; 91: 222–229. 9. Murray HJ, Young MJ, Hollis S et al. The association between callus formation, high pressures and neuropathy in diabetic foot ulceration. Diabetic Medicine 1996; 13: 979–982. 10. Merriman L, Griffiths C, Tollafield D. Plantar lesion patterns. Chiropodist 1987; 42: 145– 148. 11. Springett KP, Whiting MF, Marriott C. Epidemiology of plantar forefoot corns and calluses, and the influence of the dominant side. The Foot 2003; 13: 5–9.
References
12. Grouios G. Footedness as a potential factor that contributes to the causation of corn and callus formation in lower extremities of physically active individuals. The Foot 2005; 15: 154–162. 13. Singh D, Bentley G, Trevino SG. Callosities, corns, and calluses. British Medical Journal 1996; 312: 1403–1406. 14. Haboush EJ, Martin RV. Painful interdigital clavus (soft corn). Treatment by skin-plastic operation. Journal of Bone and Joint Surgery 1947; 29: 756–757. 15. Gillett HGDP. Interdigital clavus. Clinical Orthopaedics and Related Research 1979; 142: 103– 109. 16. George DH. Management of hyperkeratotic lesions in the elderly patient. Clinics in Podiatric Medicine and Surgery 1993; 10: 69–77. 17. Rubin L. Hyperkeratosis in response to mechanical irritation. Journal of Investigative Dermatology 1949; 13: 313–315. 18. Thomas SE, Dykes PJ, Marks R. Plantar hyperkeratosis: a study of callosities and normal plantar skin. Journal of Investigative Dermatology 1985; 85: 394–397. 19. Bonavilla EJ. Histopathology of the heloma durum: some significant features and their implications. Journal of the American Podiatry Association 1968; 58: 423–427. 20. Potter GK. Histopathology of clavi. Journal of the American Podiatry Association 1973; 63: 57–66. 21. McCarthy DJ, Habowsky JE. Histochemistry and anthropometric analysis of heloma durum. Journal of the American Podiatry Association 1975; 65: 4–18. 22. Robertson K, Delbridge L. A comparative study of forefoot pressures associated with corns and callus under the first metatarsal head. Chiropodist 1985; 40: 101–107. 23. Potter J, Potter M. Effect of callus removal on peak plantar pressures. The Foot 2000; 10: 23– 26. 24. Pataky Z, Golay A, Faravel L et al. The impact of callosities on the magnitude and duration of plantar pressure in patients with diabetes mellitus. Diabetes and Metabolism 2002; 28: 356–361. 25. Menz HB, Zammit GV, Munteanu SE. Plantar pressures are higher under callused regions of the foot in older people. Clinical and Experimental Dermatology 2007; 32: 375–380. 26. Young MJ, Cavanagh PR, Thomas G et al. The effect of callus removal on dynamic plantar foot pressures in diabetic patients. Diabetic Medicine 1992; 9: 55–57. 27. Pitei DL, Foster A, Edmonds M. The effect of regular callus removal on foot pressures. Journal of Foot and Ankle Surgery 1999; 38: 251–255.
28. O’Halloran NF. A biochemical investigation into the cholesterol content of seed corns. Chiropodist 1990; November: 215–218. 29. Trice EW. A new hypothesis on the etiology of heloma milliare. Journal of the National Association of Chiropodists 1955; 45: 28–29. 30. McCarthy DJ. Helomata and tylomata. In: McCarthy DJ, Montgomery R, ed. Podiatric dermatology. Baltimore, MD: Williams & Wilkins; 1986: 53– 73. 31. Greenberg L, Davis H. Foot problems in the US. The 1990 National Health Interview Survey. Journal of the American Podiatric Medical Association 1993; 83: 475–483. 32. Garrow AP, Silman AJ, Macfarlane GJ. The Cheshire Foot Pain and Disability Survey: a population survey assessing prevalence and associations. Pain 2004; 110: 378–384. 33. Bevans JS, Bowker P. Foot structure and function: aetiological risk factors for callus formation in diabetic and non-diabetic subjects. The Foot 1999; 9: 120–127. 34. Garcia-Hidalgo L, Orozco-Topete R, GonzalezBarranco J et al. Dermatoses in 156 obese adults. Obesity Research 1999; 7: 299–302. 35. Hills AP, Hennig EM, McDonald M et al. Plantar pressure differences between obese and non-obese adults: a biomechanical analysis. International Journal of Obesity and Related Metabolic Disorders 2001; 25: 1674–1679. 36. Birtane M, Tuna H. The evaluation of plantar pressure distribution in obese and non-obese adults. Clinical Biomechanics 2004; 19: 1055–1059. 37. Reed JF. An audit of lower extremity complications in octogenarian patients with diabetes mellitus. Lower Extremity Wounds 2004; 3: 161–164. 38. Williams AE, Bowden AP. Meeting the challenge for foot health in rheumatic diseases. The Foot 2004; 14: 154–158. 39. Jordan E, Lekkas C, Roscioli D et al. Podiatric problems on a stroke rehabilitation unit. Australian Journal on Ageing 1997; 16: 222–224. 40. Sari-Kouzel H, Hutchinson C, Middleton A et al. Foot problems in patients with systemic sclerosis. Rheumatology 2001; 40: 410–413. 41. Evans SL, Nixon BP, Lee I et al. The prevalence and nature of podiatric problems in elderly diabetic patients. Journal of the American Geriatrics Society 1991; 39: 241–245. 42. Ronnemaa T, Liukkonen I, Knuts L-R et al. Prevalence of foot problems and need for foot care in an unselected diabetic population. Journal of British Podiatric Medicine 1993; 48: 185–190. 43. Woodburn J, Helliwell PS. Relation between heel position and the distribution of forefoot plantar pressures and skin callosities in rheumatoid arthritis.
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Annals of the Rheumatic Diseases 1996; 55: 806–810. Coughlin MJ. Lesser-toe abnormalities. Journal of Bone and Joint Surgery 2002; 84A: 1446–1469. Mann RA, Mann JA. Keratotic disorders of the plantar skin. Journal of Bone and Joint Surgery 2003; 85A: 938–955. Richardson EG. Complications after hallux valgus surgery. AAOS Instructional Course Lectures 1999; 48: 331–342. Femino JE, Mueller K. Complications of lesser toe surgery. Clinical Orthopaedics and Related Research 2001; 391: 72–78. Coughlin MJ, Thompson FM. The high price of high-fashion footwear. AAOS Instructional Course Lectures 1995; 44: 371–377. Frey C. Foot health and shoewear for women. Clinical Orthopaedics and Related Research 2000; 372: 32–44. Snow RE, Williams KR, G B Holmes J. The effects of wearing high heeled shoes on pedal pressures in women. Foot and Ankle 1992; 13: 85–92. Corrigan JP, Moore DP, Stephens MM. Effect of heel height on forefoot loading. Foot and Ankle 1993; 14: 148–152. Nyska M, McCabe C, Linge K et al. Plantar forefoot pressures during treadmill walking with high-heel and low-heel shoes. Foot and Ankle International 1996; 17: 662–666. Mandato MG, Nester E. The effects of increasing heel height on forefoot peak pressure. Journal of the American Podiatric Medical Association 1999; 89: 75–80. Menz HB, Morris ME. Footwear characteristics and foot problems in older people. Gerontology 2005; 51: 346–351. Yoshii A, Ono T, Kayashima K et al. An unusual mechanical hyperkeratosis of the soles – health sandals keratosis. Journal of Dermatology 1991; 18: 291–294. Wahlberg JE. Occupational hyperkeratosis in carpet installers. American Journal of Industrial Medicine 1985; 8: 351–353. Kahana M, Cohen M, Ronnen M et al. Prayer nodules in Moslem men. Cutis 1986; 38: 281– 282. Roberts PJ, Katsimitas M, Wade RH. An interesting behavioural injury: Mecca foot. Foot and Ankle Surgery 2001; 7: 49–50. Wong VK, Stotts NA. Physiology and prevention of heel ulcers: the state of science. Journal of Wound Ostomy and Continence Nursing 2003; 30: 191– 198. Schiraldi FG. Common dermatologic manifestations in the older patient. Clinics in Podiatric Medicine and Surgery 1993; 10: 79–95.
61. DeLauro TM. Keratotic lesions of the foot. Clinics in Podiatric Medicine and Surgery 1996; 13: 73– 84. 62. Freeman D. Corns and calluses resulting from mechanical hyperkeratosis. American Family Physician 2002; 65: 2277–2280. 63. Grouios G. Corns and calluses in athlete’s feet: a cause for concern. The Foot 2004; 14: 175–184. 64. Fernando DJS, Masson EA, Veves A et al. Relationship of limited joint mobility to abnormal foot pressures and diabetic foot ulceration. Diabetes Care 1991; 14: 8–11. 65. Menz HB, Morris ME. Clinical determinants of plantar forces and pressures during walking in older people. Gait and Posture 2006; 24: 229–236. 66. Redmond A, Allen N, Vernon W. Effect of scalpel debridement on the pain associated with plantar hyperkeratosis. Journal of the American Podiatric Medical Association 1999; 89: 515–519. 67. Prud’homme P, Curran M. A preliminary study of the use of the algometer to investigate whether or not patients benefit when podiatrists enucleate corns. The Foot 1999; 9: 65–69. 68. Balanowski KR, Flynn LM. Effect of painful keratoses debridement on foot pain, balance and function in older adults. Gait and Posture 2005; 22: 302– 307. 69. Woodburn J, Stableford Z, Helliwell P. Preliminary investigation of debridement of plantar callosities in rheumatoid arthritis. Rheumatology 2000; 39: 652–654. 70. Timson S, Spooner SK. A comparison of the efficacy of scalpel debridement and insole therapy in relieving the pain of plantar callus. British Journal of Podiatry 2005; 8: 53–59. 71. Potter J, Potter M. Regrowth patterns of plantar callus. The Foot 2000; 10: 144–148. 72. Springett K, Parsons S, Young M et al. The effect and safety of three corn care products. British Journal of Podiatry 2002; 5: 82–86. 73. LeRossignol JN. A pharmacopoeia for chiropodists. 8th ed. London: Faber & Faber; 1970. 74. Potter J. The use of salicylic acid in the treatment of dorsal corn and callus. British Journal of Podiatry 2000; 3: 51–55. 75. Nossiter H, Sanders J. A comparison of clinical efficacy of two delivery systems of salicylic acid in corn removal plasters. The Foot 1994; 4: 83–87. 76. Rinaldi F, Clemente F. The importance of the formulation of a plaster containing salicylic acid in treatment of corns. The Foot 1994; 4: 186–190. 77. Finch P. An evaluation of the treatment of plantar fibrous and hard corn using silicone plugging and silver nitrate. Chiropodist 1987; 42: 463–467. 78. Springett K, Deane M, Dancaster P. Treatment of corns, calluses and heel fissures with a hydrocolloid
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dressing. Journal of British Podiatric Medicine 1997; 52: 102–104. Dagnall JC. History of salicilin and salicylic acid. Chiropodist 1958; 13: 118–119. Lang LMG, West SG, Day S et al. Salicylic acid in the treatment of corns. The Foot 1994; 4: 145–150. Foster A, Edmonds ME, Das AK et al. Corn cures can damage your feet: an important lesson for diabetic patients. Diabetic Medicine 1989; 6: 818– 819. Bikowski J. Hyperkeratosis of the heels: treatment with salicylic acid in a novel delivery system. SKINmed 2004; November–December: 350–351. Hashimoto H. Superglue for the treatment of heel fissures. Journal of the American Podiatric Medical Association 1999; 89: 434–435. Balkin SW. Silicone augmentation for plantar calluses. Journal of the American Podiatry Association 1976; 66: 148–154. Dockery GL, Nilson RZ. Intralesional injections. Clinics in Podiatric Medicine and Surgery 1986; 3: 473–485. Tollafield DR, Holdcraft DJ, Singh R et al. Injectable percutaneous polydimethicone in the treatment of pedal keratomas: a single blind randomized trial. Journal of Foot and Ankle Surgery 2001; 40: 295–301. Balkin SW. Silicone injection for plantar keratoses. Preliminary report. Journal of the American Podiatry Association 1966; 56: 1–11. Balkin SW. Plantar keratoses: treatment by injectable liquid silicone. Report of an eight-year experience. Clinical Orthopaedics and Related Research 1972; 87: 235–247. Balkin SW. Treatment of corns by injectable silicone. Archives of Dermatology 1975; 111: 1143–1145. Balkin SW. Injectable silicone and the foot: a 41-year clinical and histologic history. Dermatologic Surgery 2005; 31: 1555–1559. VanSchie CHM, Whalley A, Vileikyte L et al. Efficacy of injected liquid silicone in the diabetic foot to reduce risk factors for ulceration. Diabetes Care 2000; 23: 634–638. VanSchie CH, Whalley A, Armstrong DG et al. The effect of silicone injections in the diabetic foot on peak plantar pressure and plantar tissue thickness: a 2-year follow-up. Archives of Physical Medicine and Rehabilitation 2002; 83: 919–923. Balkin SW, Kaplan L. Injectable silicone and the diabetic foot: a 25-year report. The Foot 1991; 2: 83–88. Holmes G, Timmerman L. A quantitative assessment of the effect of metatarsal pads on plantar pressures. Foot and Ankle International 1990; 11: 141–145.
95. Hayda R, Tremaine M, Tremaine K et al. Effect of metatarsal pads and their positioning: a quantitative assessment. Foot and Ankle International 1994; 15: 561–566. 96. Chang A, Abu-Faraj Z, Harris G et al. Multistep measurement of plantar pressure alterations using metatarsal pads. Foot and Ankle International 1994; 15: 654–660. 97. Kato H, Takada T, Kawamura T et al. The reduction and redistribution of plantar pressures using foot orthoses in diabetic patients. Diabetes Research and Clinical Practice 1996; 31: 115–118. 98. Abu-Faraj Z, Harris G, Chang A et al. Evaluation of a rehabilitative pedorthic: plantar pressure alterations with scaphoid pad application. IEEE Transactions in Rehabilitative Engineering 1996; 4: 328–336. 99. Hodge M, Bach T, Carter G. Orthotic management of plantar pressure and pain in rheumatoid arthritis. Clinical Biomechanics 1999; 14: 567–575. 100. Raspovic A, Newcombe L, Lloyd J et al. Effect of customized insoles on vertical plantar pressures in sites of previous neuropathic ulceration in the diabetic foot. The Foot 2000; 10: 133–138. 101. Mueller MJ, Lott DJ, Hastings MK et al. Efficacy and mechanism of orthotic devices to unload metatarsal heads in people with diabetes and a history of plantar ulcers. Physical Therapy 2006; 86: 833– 842. 102. Claisse PJ, Binning J, Potter J. Effect of orthotic therapy on claw toe loading. Results of significance testing at pressure sensor units. Journal of the American Podiatric Medical Association 2004; 94: 246–254. 103. Slater RA, Herschkowitz I, Ramot Y et al. Reduction of digital plantar pressure by debridement and silicone orthosis. Diabetes Research and Clinical Practice 2006; 74: 263–266. 104. Redmond A, Lumb PS, Landorf K. Effect of cast and noncast foot orthoses on plantar pressure and force during normal gait. Journal of the American Podiatric Medical Association 2000; 90: 441–449. 105. Burns J, Crosbie J, Ouvrier R et al. Effective orthotic therapy for the painful cavus foot. Journal of the American Podiatric Medical Association 2006; 96: 205–211. 106. Colagiuri S, Marsden LL, Naidu V et al. The use of orthotic devices to correct plantar callus in people with diabetes. Diabetes Research and Clinical Practice 1995; 28: 29–34. 107. Caselli MA, Levitz SJ, Clark N et al. Comparison of Viscoped and Poron for painful submetatarsal hyperkeratotic lesions. Journal of the American Podiatric Medical Association 1997; 87: 6–10. 108. Bedinghaus JM, Niedfeldt MW. Over-the-counter foot remedies. American Family Physician 2001; 64: 791–796, 803–804.
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109. Cresswell CC. Introduction to electrosurgery. Journal of British Podiatric Medicine 1992; January: 11–14. 110. Smith TJ, Morrison DC. A study into the use of electrosurgery for the treatment of vascular and neurovascular corns. Chiropodist 1986; 41: 164– 170. 111. Smith TJ, Morrison DC. Further developments in the use of electrosurgery for the treatment of heloma durum. Chiropodist 1990; April: 67–68. 112. Whinfield AL, Forster MSK. Effect of electrodesiccation on pain intensity associated with chronic heloma durum. The Foot 1997; 7: 224– 228. 113. Meisenbach RO. Painful anterior arch of the foot: an operation for its relief by means of raising the arch. American Journal of Orthopaedic Surgery 1916; 14: 206. 114. Hatcher RM, Goller WL, Weil LS. Intractable plantar keratoses. A review of surgical corrections. Journal of the American Podiatry Association 1978; 68: 377–386. 115. Winson IG, Rawlinson J, Broughton NS. Treatment of metatarsalgia by sliding distal metatarsal osteotomy. Foot and Ankle 1988; 9: 2–6. 116. Barouk LS. Weil’s metatarsal osteotomy in the treatment of metatarsalgia. Orthopade 1996; 25: 338–344. 117. O’Kane C, Kilmartin TE. The surgical management of central metatarsalgia. Foot and Ankle International 2002; 23: 415–419. 118. Sharma DK, Roy N, Shenolikar A. Weil osteotomy of lesser metatarsals for metatarsalgia: a clinical and
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radiological follow-up. The Foot 2005; 15: 202– 205. Hofstaetter SG, Hofstaetter JG, Petrousas JA et al. The Weil osteotomy: a seven year follow-up. Journal of Bone and Joint Surgery 2005; 87B: 1507– 1511. Beech I, Rees S, Tagoe M. A retrospective review of the Weil metatarsal osteotomy for lesser metatarsal deformities: an intermediate follow-up analysis. Journal of Foot and Ankle Surgery 2005; 44: 358–364. Vandeputte G, Dereymaeker G, Steenwerkx A et al. The Weil osteotomy of the lesser metatarsals: a clinical and pedobarographic follow-up study. Foot and Ankle International 2000; 21: 370–374. Gibbard KW, Kilmartin TE. The Weil osteotomy for the treatment of painful plantar keratoses. The Foot 2003; 13: 199–203. Kilmartin TE. Distal lesser metatarsal osteotomies: a review of surgical techniques designed to avoid nonunion and minimize transfer metatarsalgia. The Foot 1998; 8: 186–192. Finney S, Kilmartin T, Flintham C. The modified Schwartz procedure in the management of intractable plantar keratoses: a retrospective review. The Foot 2003; 13: 108–113. Schwartz N, Williams JE, Marcinko DE. Double oblique lesser metatarsal osteotomy. Journal of the American Podiatric Medical Association 1983; 73: 218–220. Coughlin MJ. Mallet toes, hammer toes, claw toes and corns. Causes and treatment of lesser-toe deformities. Postgraduate Medicine 1984; 75: 191–198.
CHAPTER
Other skin disorders
CHAPTER CONTENTS Eczema and dermatitis 80 Xerotic eczema 80 Venous stasis eczema 80 Drug-induced eczema 81 Papulosquamous diseases Psoriasis 81 Lichen planus 82 Skin infections 83 Erysipelas and cellulitis Pitted keratolysis 83 Tinea pedis 83
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Tumours, cysts and lesions 85 Benign lesions 86 Premalignant and malignant lesions Summary 95 References 95
92
5
Disorders of the skin are very common in older people.1 Surveys of clinical populations indicate that the most common presenting complaints in people aged over 65 years are eczema/dermatitis, fungal infections, pruritus, actinic keratosis, benign tumours and malignant tumours.2–7 Establishing the prevalence of skin lesions of the foot, however, is difficult, as few large-scale dermatology studies specify the body part affected by the condition and foot-specific studies tend to focus on keratotic lesions or orthopaedic conditions. The most commonly reported skin condition in older people in the large-scale, foot-specific studies is ‘dry skin’ (prevalence estimates ranging from 13% to 27%),8–10 followed by various classifications of foot infections (2–47%).10–13 The most detailed data can be derived from the Achilles Foot Screening Project, which involved clinical and mycological examination of the feet of people attending dermatologists or primary care physicians in 16 countries.14 Although no doubt an overestimate because of response bias, the findings of this study indicate that between 60% and 90% of people aged over 65 years had evidence of foot disease, the most common condition being tinea pedis (29% of older people). The following chapter provides an overview of the most common skin conditions affecting the older foot, along with less common conditions with potentially serious ramifications (i.e. premalignant and malignant lesions). The reader should note, however, that the coverage in this chapter is by no means exhaustive, and it is therefore advisable to supplement this information with a general dermatology text or Dockery’s Cutaneous Disorders of the Lower Extremity.15 It is also worth noting that while the treatment
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of some of the more common skin conditions is well supported by evidence from randomised controlled trials, the management of more obscure lesions is largely informed by clinical experience. The findings of relevant systematic reviews conducted by the Cochrane Collaboration are provided where available; however, at the time of writing several of these (such as the treatment of psoriasis,16 cellulitis,17 actinic keratoses,18 surgical treatment for malignant melanoma19 and non-melanoma skin cancers)20 were still under development.
ECZEMA AND DERMATITIS The term ‘eczema’ refers to any form of non-infective inflammation of the skin and is often used interchangeably with the term ‘dermatitis’. Eczema can be broadly classified as exogenous (i.e. caused by external irritants) or endogenous (i.e. caused by internal physiological factors). However, because the aetiology of many forms of eczema is unknown, such a distinction is not always possible, and indeed in some conditions a combination of external irritants and internal factors is likely to be responsible. For the same reason, determining the prevalence of eczema in older people is very difficult, with reported prevalence rates ranging between 35% and 59%.4–6 Excessively dry and scaly skin, one of the most common complaints associated with eczema affecting the foot, is reported by between 13% and 27% of those aged over 65 years.8–10 The most common forms of eczema in older people are discussed below.
Figure 5.1 Xerotic eczema. (Courtesy of Lesley Newcombe, La Trobe University.)
Figure 5.2 Venous stasis eczema affecting the medial ankle region. (Courtesy of Lesley Newcombe, La Trobe University.)
XEROTIC ECZEMA Also known as asteatotic dermatitis, eczema craquelé and chronic winter itch, this condition is characterised by erythematous dry scaling and fissuring of the skin, and is most commonly found on the anterolateral aspects of the legs in older people (Fig. 5.1). The lesions are often highly pruritic and continued scratching exacerbates the condition. Xerotic eczema is thought to be caused by a reduction in epidermal lipids due to excessive use of soaps and detergents, frequent bathing in very hot water, excessive room heating and inadequate household humidity. The condition is particularly common in older people residing in aged care facilities.21 Treatment involves the application of emollient or corticosteroid creams and educating the older person or their carer about the use of moisturising soaps.21–23 It has also been
suggested that older people with severe forms of the condition should consider purchasing a humidifier.15,21,23
VENOUS STASIS ECZEMA Venous stasis eczema (also referred to as stasis dermatitis, varicose eczema or gravitational eczema) is characterised by oedema, hyperaemia, pruritus, haemosiderosis and superficial scaling of skin in the lower tibial area, and is associated with chronic venous insufficiency24 (Fig. 5.2). The peak incidence of onset is in the third to fourth decade, and women are three times more likely to develop the condition than men. The condition most commonly develops after a venous ulcer has healed, leaving the epidermis
Papulosquamous diseases
atrophic and the underlying dermis sclerotic and indurated. Treatment involves management of the underlying venous condition (e.g. limb elevation, the use of compression stockings and exercise) in addition to managing pruritus with topical corticosteroids25 and maintaining skin integrity with the application of emollient creams.26
Table 5.1 Common medications associated with different presentations of drug eruptions Drug eruption Common causative medications Urticarial reaction
Aspirin Penicillin
Morbilliform eruption
Ampicillin Gentamicin Phenothiazines Sulphonamides Thiazides Quinidine
Erythema nodosum
Sulphonamides Penicillin Halogens
DRUG-INDUCED ECZEMA A wide range of medications may produce skin eruptions in older people and lead to the development of eczema. However, because many older people take multiple medications, it is often difficult to determine the causative agent. Furthermore, while some medications produce immediate skin reactions, others may take months or even years to manifest. Broadly speaking, six main types of drug reaction are observed: urticarial reactions, which manifest as a pruritic red wheals and are caused by an acute hypersensitivity response, morbilliform eruptions, which create erythematous macular and papular rashes, erythema multiforme, an acute bullous reaction associated with systemic symptoms such as fever and muscular pains, acroexfoliative dermatitis, which produces lichenification and superficial shedding of skin, exfoliative erythroderma, a serious condition characterised by severe pruritic scaling and desquamation, and lichenoid dermatitis, characterised by multiple flat-topped papules.15 Because they are potentially life-threatening, it is essential that a thorough evaluation be undertaken when older people present with suspected drug eruptions. Signs that may indicate severe reactions include pronounced erythema, skin pain, necrosis, Nikolsky’s sign (separation of the epidermis from the dermis with mild lateral pressure), swelling of the tongue, high fever, enlarged lymph nodes, shortness of breath and arthritic symptoms.27 Common medications associated with each of these presentations are shown in Table 5.1. Treatment of these conditions requires the identification and, if possible, discontinuation of the offending medication, along with topical therapy to maintain skin integrity.
PAPULOSQUAMOUS DISEASES PSORIASIS Psoriasis is a chronic inflammatory skin condition characterised by the formation of well demarcated erythematous plaques and superficial scales involving
Acroexfoliative Aspirin dermatitis Codeine Iodine Sulphonamides Phenytoin Exfoliative erythroderma
Allopurinol Cimetidine Phenytoin Iodine Penicillin Sulphonamides
Lichenoid dermatitis
Beta-blockers Non-steroidal anti-inflammatory drugs Thiazides Quinidine
any part of the body but most commonly the scalp, elbows and knees28 (Fig. 5.3). Foot and toenail involvement is common, and up to 30% of people with psoriasis will also develop arthropathy in the distal joints, including the interphalangeal joints of the toes.29,30 Psoriasis affects approximately 2% of the population and can begin at any age; however, the peak incidence occurs in the second and third decades.31,32 The cause of psoriasis is not well understood; however, a positive family history is evident in 35% of patients and the condition appears to be triggered by a range of factors such as trauma, infection, some medications, alcohol, smoking and stress.33 Three main types of psoriasis have been recognised: chronic plaque psoriasis (also referred to as ordi-
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OTHER SKIN DISORDERS
A
B
Figure 5.3 Chronic plaque psoriasis affecting (A) the anterior aspect of the leg and (B) the dorsum of the foot. (A, courtesy of Amanda Taylor, Charles Sturt University; B, courtesy of Felicity Prentice, La Trobe University.)
Figure 5.4 Pustular psoriasis affecting the medial arch of the foot. (Courtesy of Karl Landorf, La Trobe University.)
nary psoriasis or psoriasis vulgaris), which is the most common form, guttate psoriasis, in which several drop-like lesions form symmetrically on the trunk following a streptococcal throat infection, and pustular psoriasis, which is more common in older women and is characterised by the development of erythematous, yellow to brown vesicles on the palms and arch of the foot (Fig. 5.4).15,34 Two key clinical features of chronic plaque psoriasis can greatly assist in establishing a diagnosis: Auspitz’s sign, the appearance of pinpoint bleeding when the superficial scales are removed, and the Koebner phenomenon, the appearance of
Figure 5.5 Lichen planus. (With permission from DermNet NZ, www.dermnetnz.org. Copyright © 2007 Interactive Medical Media LLC, All rights reserved.)
psoriatic lesions at sites of previous injury to the skin. Toenail involvement is characterised by pitting of the nail plate, formation of subungual hyperkeratosis and, in severe cases, onycholysis (separation of the nail plate from the underlying nail bed).15,34 First-line treatment of psoriasis involves the management of lesions with topical emollients, corticosteroids, tar-based preparations or salicylic acid.35 However, a recent systematic review indicated that these treatments provide only temporary relief and recurrence is common, often in a more severe form than the original presentation (the so-called ‘rebound effect’).36 For long-standing psoriasis, systemic treatments include photochemotherapy (exposure of the skin to ultraviolet A following oral administration of psoralen), oral retinoid (a vitamin A derivative, often used in conjunction with ultraviolet A) and methotrexate (a folate antagonist with anti-inflammatory and immune-modulating effects).36
LICHEN PLANUS Lichen planus is an inflammatory condition characterised by the formation of sharply defined, flat, shiny, polygonal, pruritic papules on the wrists, lumbar region, scalp, tibial area and, less commonly, the foot (Fig. 5.5). The peak incidence of onset is between the ages of 30 and 60 years, and women are affected more frequently than men.28 The aetiology is not fully understood. The most common site of foot involvement is the plantar medial arch,37,38 where the lesions may develop a more hyperkeratotic appearance than other regions and, in rare cases, may ulcerate.39 Nail
Skin infections
involvement may also occur, resulting in thinning of the nail plate, formation of subungual hyperkeratosis and fusion of the proximal nail fold to the nail bed.34 Spontaneous resolution occurs in most cases over a period of 6–18 months; however, relapses occur in 10–25% of cases.40 Treatment involves topical or oral corticosteroids, and antihistamines to manage pruritus. In severe cases, photochemotherapy may be considered.
SKIN INFECTIONS As stated in Chapter 2, ageing is associated with significant changes to the structure and function of the skin. Several of these changes, such as the reduction in the number of Langerhans cells41 and the reduction in the number of capillary loops in the dermis,42 affect the barrier function of the skin and reduce the efficacy of the immune response.43 As a consequence, the risk of skin infection increases significantly with advancing age. In the foot, this risk is further exacerbated by the wearing of footwear and hosiery, which provides an ideal warm and humid environment for growth of many types of bacteria and fungi. In the presence of minor breaks in the skin, such as fissuring between the toes, superficial infections can quickly develop into far more serious conditions that may be limbthreatening or even life-threatening. The following section provides an overview of the most common skin infections seen in older people. Nail infections are covered in Chapter 6.
ERYSIPELAS AND CELLULITIS The term erysipelas refers to an acute infection of the dermis, whereas cellulitis refers to an acute or chronic infection of connective tissue. However, because erysipelas can extend to deeper tissues and cellulitis can extend superficially, the distinction between the two conditions is somewhat vague. For the sake of simplicity, the term cellulitis is now commonly used to encompass both conditions.17 Cellulitis is common in older people, with incidence rates ranging from 4 to 25 cases per 10 000 person-years in those aged over 65 years.44 The most common bacterium responsible for cellulitis is Streptococcus pyogenes, followed by Staphylococcus aureus.45 Anaerobic organisms such as Peptostreptococcus, Clostridium and Porphyromonas are occasionally isolated from affected skin.46
The bacteria gain access to the deeper tissues through open wounds, such as leg or foot ulcers, interdigital fissures and subungual lesions, or as the result of surgery. Several case-control studies have confirmed that the presence of chronic fungal infection affecting the interdigital spaces markedly increases the risk of cellulitis.47–49 Furthermore, foot surgery has been shown to be associated with higher postoperative infection rates than procedures performed on other parts of the body.50,51 Death from cellulitis-related septicaemia has also been reported in an 87-year-old woman with peripheral vascular disease following non-surgical treatment for an ingrown toenail.52 The key presenting features of cellulitis are swelling, erythema and pain in the affected limb, accompanied by high fever and lymph node enlargement. A clearly demarcated margin indicating the spread of the bacteria is often visible (Fig. 5.6) and in severe cases there may be evidence of necrosis or gangrene. Admission to hospital is generally necessary, as untreated cellulitis may lead to septicaemia. Treatment involves antibiotics, the selection of which is dependent on determining the causative bacteria. In cases related to leg ulcers, broad-spectrum antibiotics are generally used as it is likely that multiple species of bacteria are involved.53
PITTED KERATOLYSIS Pitted keratolysis is a condition caused by infection of the plantar stratum corneum by the Corynebacterium species of bacteria54 and, less commonly, Micrococcus sedentarius55 or Dermatophilus congolensis.56 The condition frequently develops in barefoot populations, or in people whose occupation subjects them to prolonged exposure of the feet to wet conditions.15 However, pitted keratolysis may also develop in people with pre-existing hyperhidrosis. The presence of the bacteria leads to the formation of hyperhidrotic crateriform pits on the plantar surface of the heel and forefoot, which may coalesce to form irregularly shaped erosions (Fig. 5.7). The skin develops a characteristic ‘sliminess’ and is accompanied by a pungent odour.57 Most cases are asymptomatic. Treatment involves the application of astringent foot soaks or powders, and topical antibiotics.15,58
TINEA PEDIS Fungal infection of the foot (tinea pedis) is extremely common in older people. Epidemiological studies
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A
B
Figure 5.6 Cellulitis. A. Acute cellulitis associated with an infected plantar callus. (Courtesy of Matthew Dilnot, Melbourne Foot Clinic.) B. Chronic cellulitis associated with venous ulceration. (Courtesy of Lesley Newcombe, La Trobe University.)
indicate that between 5% and 20% of communitydwelling people aged over 65 years have some form of fungal infection.10,59 The Achilles Foot Screening Project, which involved clinical examination of the feet of people attending dermatologists or primary care physicians in 16 countries,14 indicated that the second most commonly diagnosed condition in older people was fungal infection of the skin, which was observed in 29% of the sample.60 A follow-up study involving 90 085 older patients across all the participating European countries61 reported that almost half had clinical evidence of fungal foot infection. Fungal skin infections are caused by a group of fungi known as dermatophytes, so named because of
Figure 5.7 Pitted keratolysis affecting the heel. (Courtesy of Lesley Newcombe, La Trobe University.)
their ability to penetrate the stratum corneum. For foot infections, the most common infective organisms are Trichophyton rubrum, Trichophyton mentagrophytes (also known as Trichophyton interdigitale) and Epidermophyton floccosum.60 The presence of these organisms in the skin causes keratin destruction and an inflammatory response, leading to the characteristic signs of erythema and desquamation and the common presenting complaint of severe pruritus. There are three major types of fungal skin infection: interdigital tinea pedis, which develops between the toes and has a moist, macerated, scaly appearance, moccasin foot, characterised by a hyperkeratotic, dry scaling of the lateral and plantar surfaces of the foot, and vesicular (or bullous) tinea pedis, in which vesicles or bullae filled with clear fluid develop on the plantar surface or interdigital spaces. A fourth category, ulcerative tinea pedis, may develop when longstanding interdigital tinea pedis extends on to the dorsal or plantar surfaces of the foot. In older people, the most common form is interdigital tinea pedis, which is often triggered by inadequate drying between the toes and occlusion of the interdigital spaces by toe deformity and/or ill-fitting footwear. Interdigital tinea pedis is also commonly associated with concurrent fungal nail infection (onychomycosis) in older people (Fig. 5.8), and, as stated previously, is a significant risk factor for bacterial cellulitis.47–49 First-line treatment of tinea pedis involves the application of topical antifungal medications. Several
Tumours, cysts and lesions
A
Oral medications for fungal infections of the skin first became available in 1958 in the form of griseofulvin.63 Although widely used, griseofulvin was not effective against non-dermatophyte fungi and was associated with gastrointestinal side-effects. More recent oral medications, such as the azoles (ketoconazole, itraconazole and fluconazole) and allylamine (terbinafine) are considerably more effective. The most recent Cochrane review of 12 randomised controlled trials concluded that terbinafine is more effective than griseofulvin, and that terbinafine and itraconazole are more effective than a placebo.64 Mycological cure rates with terbinafine (250 mg/d for 4–6 weeks) range from 65% to 100%. An additional consideration when managing fungal infections in older people is that the likelihood of recurrence is high, particularly if no change is made to the older person’s footwear and hosiery. It is therefore generally recommended that infected footwear and hosiery be discarded as part of the management plan, and that particular emphasis is placed on maintaining adequate foot hygiene such as drying between the toes and regularly changing socks or stockings.
TUMOURS, CYSTS AND LESIONS
B
Figure 5.8 Tinea pedis. A. Interdigital. (Courtesy of Lloyd Reed, Queensland University of Technology.) B. Secondary to onychomycosis. (Courtesy of Lesley Newcombe, La Trobe University.)
such medications have been developed, including allylamines, azoles, undecenoic acid and tolnaftate. The recent Cochrane review of 72 randomised controlled trials62 concluded that allylamines, azoles and undecenoic acid were all effective compared to a placebo, with allylamines curing slightly more infections than the azoles. However, because allylamines are more expensive, the authors recommended that the most cost-effective approach is to first treat with azoles or undecenoic acid, and to use allylamines only if that fails. Cure rates of 65–91% have been reported; however, it is likely that the cure rate is somewhat lower in older people.
The foot is a relatively common site for a wide range of skin lesions in older people, although the actual incidence of such lesions is extremely difficult to determine because of under-reporting and misdiagnosis. Audits of pathology laboratories, however, provide a reasonable estimate of the relative, if not absolute, frequency of different lesions. For lesions affecting the foot, a recent publication by Berlin65 is particularly informative. This paper reports the eventual pathology diagnosis of 307 601 specimens submitted to a podiatry-specific pathology laboratory in the USA, and indicates that verrucae are by far the most commonly biopsied skin lesion affecting the foot, followed by inclusion cysts and ganglionic cysts (see Table 5.2). Unfortunately, no age breakdown was undertaken, so the relative incidence of skin lesions in older people cannot be determined. While many of these conditions are asymptomatic when located elsewhere on the body, foot lesions are frequently problematic due to the foot’s weightbearing role and the potential for friction from footwear and hosiery. The following section provides a brief overview of some of the more commonly encountered
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Table 5.2 Incidence of skin lesions biopsied from the foot by podiatrists in the continental USA, Hawaii and Puerto Rico (n = 307 601) Lesion
Number (%)
Verrucae Inclusion cysts Ganglion cysts Fibromas Dermatofibromas Mucous (myxoid) cysts Hemangiomas Squamous cell carcinomas
176 053 7 558 7 395 1 779 1 701 1 227 594 312
(57.2) (2.4) (2.4) (0.6) (0.6) (0.4) (0.2) (0.1)
lesions affecting the older foot, divided into benign lesions and premalignant or malignant lesions.
BENIGN LESIONS Verrucae Plantar verrucae (warts) are very common benign epidermal neoplasms caused by various strains of the human papilloma virus. Verrucae can develop at any age but are more common in children and adolescents.66,67 The appearance of verrucae can be highly variable, from smooth, flesh-coloured papules through to raised nodules with a cauliflower-like surface. The most characteristic features of verrucae are the disruption of normal skin lines and the presence of thrombosed capillaries within the lesion. These features can assist in differentiating verrucae from corns or calluses. In immunocompromised patients, multiple verrucae may form into clusters (known as mosaic verrucae), which often develop overlying hyperkeratosis (Fig. 5.9). Verrucae are generally self-limiting and will spontaneously regress over a period of months or years.68 However, verrucae on the foot can be quite painful and often require treatment. A plethora of verrucae treatments have been reported in the literature, from various topical agents (glutaraldehyde, formaldehyde, podophyllin, podophyllotoxin, silver nitrate, salicylic acid, monochloroacetic acid and phenol) and intralesional injections (bleomycin, 5-fluorouracil) through to cryotherapy, CO2 laser and electrodesiccation with curettage. The most recent Cochrane systematic review of 60 trials concluded that topical application of 15–20% salicylic acid is the most effective treatment for verrucae, with a cure rate of 75%. Somewhat surprisingly, only two
placebo-controlled trials of cryotherapy have been undertaken, with both reporting no difference in cure rates between the groups.69
Acrochordons Acrochordons, also referred to as skin tags or cutaneous tags, appear as soft, skin-coloured polyps with a smooth to pedunculated surface (Fig. 5.10). On nonweightbearing areas (most commonly the neck, chest and axillae), the lesion extends from the skin surface on a small stalk; however, if located on the plantar surface of the foot, compression results in a flatter lesion that may be covered with hyperkeratosis. Treatment is rarely necessary but if the lesion is painful it can easily be removed with a scalpel followed by electrocautery of the base of the lesion.70
Cutaneous horns Cutaneous horns, also known as onychoma, are keratotic lesions that project outwards from the skin in the shape of an animal horn and are commonly found on the ears, hands and feet in older people (Fig. 5.11).71 Cutaneous horns can develop from a wide range of pre-existing dermatological lesions, including verrucae and stucco keratoses. Because of their size, cutaneous horns are frequently painful, and in older people there is a risk of malignancy at the base of the lesion. Treatment involves debridement of the lesion followed by curettage or cryotherapy.72
Dermatofibromas Dermatofibromas are firm, raised, pigmented lesions ranging in size from a few millimetres to 1 cm in diameter, and most commonly occur in middle aged and older people. The lesions can develop anywhere on the body; however, the lower limbs are affected more frequently than the upper limbs or trunk (Fig. 5.12). Treatment is generally not necessary as the lesions are rarely symptomatic, and malignant changes are extremely rare.73
Figure 5.9 A. Large verruca pedis under the first metatarsophalangeal joint following debridement of overlying callus. B. Close-up view showing thrombosed capillaries. C. Subungual verruca. D. Mosaic verrucae. (Courtesy of Lesley Newcombe, La Trobe University.)
Tumours, cysts and lesions
A
B
C
D
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Figure 5.12 Dermatofibroma. (Courtesy of Lesley Newcombe, La Trobe University.)
Figure 5.10 Acrochordon (skin tag) on the lateral aspect of the hallux. (Courtesy of Lesley Newcombe, La Trobe University.)
Figure 5.13 Epidermal inclusion cyst. (With permission from Dockery GL, Crawford ME. Cutaneous disorders of the lower extremity. Philadelphia: WB Saunders; 1997.)
Figure 5.11 Cutaneous horn on the plantar surface of the foot. (With permission from Dockery GL, Crawford ME. Cutaneous disorders of the lower extremity. Philadelphia: WB Saunders; 1997.)
Coulter & Bouche74 have also described three cases of epidermal inclusion cysts developing from ill-fitting footwear. The lesions have a dome-like appearance with a thin cover of epidermis and may develop a layer of hyperkeratosis. Occasionally the lesion may drain, extruding a thick, foul-smelling keratin material. Treatment is generally not required but, if considered necessary, involves surgical excision.15
Epidermal inclusion cysts These cysts most commonly affect people over the age of 60 years and develop as a result of a portion of epidermis becoming implanted, either surgically or traumatically, into the underlying dermis (Fig. 5.13).
Ganglion cysts Ganglion cysts, or ganglia, are generally asymptomatic, fluctuant lesions that most commonly develop in the wrists but may also affect the lower limb (Fig.
Tumours, cysts and lesions
involves corticosteroid injection (with or without aspiration of the contents of the cyst); however, if the lesions become large and painful, surgical excision may be indicated. A retrospective review of 63 ganglion treatments by Pontious et al76 reported a recurrence rate of 63% in those managed conservatively and 11% in those treated surgically. A very similar recurrence rate (61%) with conservative intervention was reported by Mallick et al;77 however, the authors also stated that the recurrent lesions were far less symptomatic than the original lesions and required no further treatment.
Haemangiomas A
Haemangiomas (also referred to as senile haemangiomas) are smooth, bright red, dome-like lesions that most commonly affect the head and neck but can also appear on the plantar surface of the foot or the toes (Fig. 5.15). The characteristic colour of the lesion is due to the presence of multiple dilated blood vessels. They rarely require treatment but can be removed by excision or electrodesiccation.78
Keratoacanthomas
B
Figure 5.14 Ganglion cysts. A. Lateral aspect of the ankle. (Courtesy of Lesley Newcombe, La Trobe University.) B. Base of fifth metatarsal. (Courtesy of Lloyd Reed, Queensland University of Technology.)
5.14). Approximately two-thirds of ganglia in the lower limb are found on the foot, the most common sites being the dorsolateral aspect of the ankle and the hallux.75 The cysts contain a fluid similar to synovium thought to be derived from the adjacent tendon sheaths or joint capsules. Conservative treatment
Most commonly observed on the head and neck of older people, keratoacanthomas are smooth, red, dome-like papules that range in size from a few millimetres to a few centimetres in diameter and can occasionally form on the foot (Fig. 5.16). Subungual lesions are often painful and tend to penetrate more deeply than lesions in other areas because of dorsal compression from the nail. In long-standing cases, the nail plate may separate from the nail bed at its distal edge and the distal phalanx may develop a crescentshaped erosion easily visible on radiographs. Because it is often difficult to differentiate keratoacanthomas from squamous cell carcinomas, surgical excision is recommended.79
Mucoid cysts Also referred to as myxoid cysts or synovial cysts, mucoid cysts are soft, dome-like, oval lesions that form within the dermis and contain a straw-coloured, viscous fluid (Fig. 5.17).80 In the foot, mucoid cysts are most commonly located proximal to the nail fold and are thought to be caused by the herniation of the extensor tendon sheath or joint capsule. Large cysts may create difficulties with footwear and, if the lesion
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Figure 5.15 Cherry hemangioma. (With permission from Dockery GL, Crawford ME. Cutaneous disorders of the lower extremity. Philadelphia: WB Saunders; 1997.)
Figure 5.17 Mucoid cyst. (With permission from Dockery GL, Crawford ME. Cutaneous disorders of the lower extremity. Philadelphia: WB Saunders Company; 1997.)
malignant melanoma is a higher than average number of melanocytic naevi.82
Piezogenic pedal papules
Figure 5.16 Keratoacanthoma. (With permission from DermNet NZ, www.dermnetnz.org. Copyright © 2007 Interactive Medical Media LLC, All rights reserved.)
penetrates the nail matrix, the nail plate may become dystrophic. Treatment involves cryotherapy, corticosteroid injection or excision.81
These common lesions develop around the periphery of the heel and appear as skin-coloured, soft herniations of fat when weightbearing (Fig. 5.18). Piezogenic pedal papules are thought to be protrusions of loculated fat extending through connective tissue irregularities in the dermis. The lesions are rarely symptomatic but may become painful in people who are overweight or in response to prolonged standing. Treatment involves the use of rigid heel cups to prevent lateral spread of the heel pad, or surgical excision.83
Naevi Naevi (‘moles’) are pigmented lesions that are highly variable in appearance, from firm, slightly elevated brown papules through to raised, verruciform nodules that may contain hair follicles. A brief summary of the more common presentations of naevi is provided in Table 5.3. Treatment is generally not necessary. However, all naevi need to be regularly monitored for changes in size, shape or colour, which may be indicative of malignant changes. It has also been demonstrated that one of the strongest predictors of
Stucco keratoses Commonly observed on the dorsum of the foot in older people, stucco keratoses are white to yellow, dry, scaly lesions up to 1 cm in diameter that can occasionally be peeled off the underlying skin (Fig. 5.19). In some cases the lesions may have a cauliflower appearance.84 The cause is unknown; however, a recent study reported the presence of human papilloma virus DNA in the lesions of an immunocompromised older patient.85 Treatment involves application
Tumours, cysts and lesions
Table 5.3 Common presentations of naevi Type
Appearance
Location
Junctional melanotic naevocellular naevus
Small (<1 cm) circumscribed round brown macule with regular borders
Trunk, face, upper and lower limbs, palmar and plantar surfaces
Compound melanotic naevocellular naevus
Round, dome-shaped papule or nodule, may be papillomatous or hyperkeratotic
Trunk, face, scalp, upper and lower limbs
Dermal melanotic naevocellular naevus
Round, dome-shaped, skin coloured, tan or brown papule or nodule. Older lesions may be papillomatous or pedunculated
Face, neck, upper and lower limbs
Halo naevomelanocytic naevus
Oval or round brown papule with white ‘halo’ of hypomelanosis
Trunk
Blue naevus
Oval or round, dark blue to grey-black, firm papule or nodule <1 cm
Dorsum of hands and feet
Figure 5.19 Stucco keratoses. (Courtesy of Lloyd Reed, Queensland University of Technology.)
Figure 5.18 Piezogenic papules. (With permission from Dockery GL. Color atlas of foot and ankle dermatology. Philadelphia: Lippincott-Raven; 1999.)
of emollient or vitamin D3 creams,86 electrodesiccation or curettage; however, the lesions tend to return after a few months.84
Calcaneal petechiae Commonly referred to as black heel, calcaneal petechiae are benign, trauma-induced lesions typically
located on the posterolateral aspect of the heel. The lesions are caused by lateral shearing of the papillary dermis, resulting in intraepidermal haemorrhage and the formation of multiple, pin-point macules, which may coalesce to form a dark irregular patch (Fig. 5.20). Calcaneal petechiae are most commonly found in young athletes; however, they do occur in older people and can be mistaken for verrucae or malignant melanoma. Often covered by or embedded in hyperkeratosis, the lesion may be cleared by scalpel debridement. However, no treatment is necessary and the lesions usually resolve over a period of weeks or months.87,88
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Figure 5.21 Actinic keratoses. (Courtesy of Lloyd Reed, Queensland University of Technology.) Figure 5.20 Calcaneal petechiae. (Courtesy of Lesley Newcombe, La Trobe University.)
PREMALIGNANT AND MALIGNANT LESIONS Over the past six decades, the incidence of skin cancer has dramatically increased throughout the world.89 In the USA, 1.3 million people were diagnosed with skin cancer in 2002, including 900 000 cases of basal cell carcinoma, 300 000 cases of squamous cell carcinoma and 53 000 cases of malignant melanoma.90 Incidence rates are even higher in countries with very high levels of sun exposure, such as South Africa and Australia.91 In addition to level of sun exposure, the key risk factors for skin cancer are a positive family history, fair complexion, presence of dysplastic naevi (atypical moles) or actinic keratoses and a higher than average number of naevi.91 Mortality rates associated with skin cancer are particularly high in men and increase markedly over the age of 60 years.92 The foot is not a common site for the development of premalignant or malignant lesions, as footwear provides some protection from sun exposure. However, malignancies that do develop on the foot are subject to delayed or incorrect diagnosis, which may explain the higher mortality rate of foot lesions compared to lesions located elsewhere.93,94 It is therefore essential that all clinicians involved in the management of foot disorders thoroughly examine, monitor and document suspect lesions in older patients and provide timely referrals to dermatologists or oncologists where necessary. As stated in Chapter 3, the simple ABCD
mnemonic (A = asymmetry, B = border irregularity, C = change in colour and D = increase in diameter) is a useful general rule for routine clinical assessment of lesions95 and has been found to be highly sensitive and specific in differentiating between benign and malignant lesions.96 The following section provides an overview of some of the more common premalignant and malignant lesions that may develop on the older foot.
Actinic keratoses Actinic keratoses, also known as solar dermatoses or senile keratoses, are the most common premalignant epidermal lesions in older people, affecting 45% of men and 35% of women aged over 65 years.1 The lesions are well circumscribed raised papules or plaques and have a dry, scaly surface. Although actinic keratoses most commonly affect areas of sun-exposed skin, such as the head, neck, face and arms, they can also develop on the legs and feet (see Fig. 5.21). These lesions should be carefully monitored as they may degenerate into squamous cell carcinomas. Indeed, because the rate of conversion is so high, a number of authors have argued that actinic keratoses are simply an early stage of squamous cell carcinoma and should be relabelled accordingly.97,98 Treatment involves topical application of 5-fluorouracil or diclofenac sodium, or destruction of the lesion using cryotherapy or electrodesiccation.99,100
Tumours, cysts and lesions
Figure 5.23 Bowen’s disease. (Courtesy of Karl Landorf, La Trobe University.)
Figure 5.22 Arsenical keratoses. (With permission from Dockery GL, Crawford ME. Cutaneous disorders of the lower extremity. Philadelphia: WB Saunders Company; 1997.)
of life.102 The lesion is a well-defined, raised, irregular plaque with superficial crusting that most commonly develops on sun-exposed areas of skin (Fig. 5.23). On the foot, the plantar surface is the most common site, although lesions have also been reported on the dorsum of the foot or between the toes.103–105 Although the lesion may become malignant, conversion to squamous cell carcinoma is rare (approximately 3% of cases).106 Treatment involves topical application of 5-fluourouracil, cryotherapy, electrodesiccation or surgical excision.
Arsenical keratoses Arsenical keratoses are caused by exposure to inorganic arsenic compounds in medications (such as drugs used for psoriasis and bronchitis in the 1930s and 1940s), insecticides or drinking water, and appear as multiple discrete, yellow, punctuate round lesions on the palms and plantar surface of the foot (Fig. 5.22). Treatment involves the application of emollient creams and keratolytics. Oral administration of acitretin (a medication commonly used for psoriasis) in conjunction with intralesional injection of 5-fluorouracil has also been reported to be effective.101 As with actinic keratoses, arsenical keratoses can degenerate into squamous cell carcinomas.
Bowen’s disease Bowen’s disease is an epidermal carcinoma sometimes referred to as squamous cell carcinoma in situ and is most commonly seen in women in the eighth decade
Basal cell carcinoma With an overall lifetime risk of 30% of the Caucasian population,1 basal cell carcinoma is the most common form of skin cancer. The most common presentation, nodular basal cell carcinoma, starts as a small, domeshaped nodule or papule that expands into an erythematous, blue-black lesion with a pearly translucent border. Other variants include cystic basal cell carcinoma, which has a lobulated appearance and may contain a clear fluid, pigmented basal cell carcinoma, which has a pigmented brown-black border, and superficial basal cell carcinoma, which is the most common type affecting the foot and appears as red plaque with an adherent scaly surface (Fig. 5.24). Treatment involves cryotherapy, surgical excision or radiotherapy. A recent Cochrane review of 19 trials concluded that both surgical excision and radiotherapy are effective, although surgical excision has a lower failure rate.107
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Figure 5.25 Squamous cell carcinoma on the dorsum of the foot. (Courtesy of Karl Landorf, La Trobe University.) Figure 5.24 Superficial basal cell carcinoma. (Courtesy of Lesley Newcombe, La Trobe University.)
Squamous cell carcinoma Squamous cell carcinoma is the second most common form of skin cancer, with 59% of cases occurring in people aged over 65 years.1 The lesion is a sharply demarcated, scaly or crusted, erythematous plaque most commonly found on the head and neck or other sun-exposed areas of the skin. Although foot involvement is rare (approximately 2% of cases), squamous cell carcinomas can develop on the dorsum of the foot,108,109 the heel,110 beneath the nail plate111–114 or interdigitally115 (Fig. 5.25). When the toes are affected, the condition can easily be misdiagnosed as an infection. Longstanding chronic ulcers, scars, non-healing verrucae and sinuses in older people may also undergo malignant changes and develop into a secondary form of squamous cell carcinoma (referred to as Marjolin’s ulcer). Because of the risk of metastasis, treatment involves wide surgical excision.
Malignant melanoma The most lethal form of skin cancer, malignant melanoma comprises only 5% of all skin cancers but accounts for three-quarters of all skin-cancer-related deaths.116 Foot involvement is not common (fewer than 10% of cases),117 however the consequences of misdiagnosis are serious, with survival rates of primary melanoma of the foot and ankle being much lower than other lower limb sites.93,94,118–120 There are four main types of malignant melanoma: superficial spread-
Figure 5.26 Superficial spreading malignant melanoma. (With permission from DermNet NZ, www.dermnetnz.org. Copyright © 2007 Interactive Medical Media LLC, All rights reserved.)
ing malignant melanoma, the most common form which appears as a flat plaque with an irregular border (Fig. 5.26), nodular malignant melanoma, which appears as a firm, blueberry-coloured nodule, lentigo maligna, a broad, brown lesion most commonly found on the head and neck, and acral lentiginous malignant melanoma, which are commonly misdiagnosed as subungual haematomas or verrucae. In the foot, the most commonly affected sites are the plantar surface, followed by the dorsum and beneath the nail plate.94,118–121 Treatment involves surgical excision and adjunctive chemotherapy.
References
SUMMARY The foot is a relatively common site for the development of skin lesions in older people. Many of these lesions are asymptomatic and may not require treatment, while other conditions are best managed by dermatologists. However, all foot-care specialists should be capable of establishing at least a provisional
diagnosis of these conditions and providing informed referrals where necessary. Finally, although the foot is not a common site for the development of skin malignancies, all clinicians involved in the management of foot problems should have a high index of suspicion of non-healing or changeable lesions on the foot in older people.
References 1. Society for Investigative Dermatology, American Academy of Dermatology Association. The burden of skin diseases 2004. Cleveland: Society for Investigative Dermatology and American Academy of Dermatology Association; 2006. 2. Young AW. Dermatologic complaints presented by geriatric inpatients. Geriatrics 1958; 13: 428– 434. 3. Adam JE, Reilly S. The prevalence of skin disease in the geriatric age group. Australasian Journal of Dermatology 1987; 28: 72–76. 4. Yap KB, Siew MG, Goh CL. Pattern of skin disease in the elderly seen at the National Skin Centre (Singapore) 1990. Singapore Medical Journal 1994; 35: 147–150. 5. Liao YH, Chen KH, Tseng MP et al. Pattern of skin diseases in a geriatric patient group in Taiwan: a 7year survey from the outpatient clinic of a university medical center. Dermatology 2001; 203: 308–313. 6. Yalcin B, Tamer E, Toy GG et al. The prevalence of skin diseases in the elderly: analysis of 4099 geriatric patients. International Journal of Dermatology 2006; 45: 672–676. 7. Smith D, Leggat PA. Prevalence of skin disease among the elderly in different clinical environments. Australasian Journal on Ageing 2005; 24: 71–76. 8. Elton PJ, Sanderson SP. A chiropodial survey of elderly persons over 65 years in the community. Public Health 1986; 100: 219–232. 9. Black JR, Hale WE. Prevalence of foot complaints in the elderly. Journal of the American Podiatric Medical Association 1987; 77: 308–311. 10. Dunn JE, Link CL, Felson DT et al. Prevalence of foot and ankle conditions in a multiethnic community sample of older adults. American Journal of Epidemiology 2004; 159: 491–498. 11. Brodie BS, Rees CL, Robins DJ et al. Wessex Feet: a regional foot health survey, Volume I: The survey. Chiropodist 1988; 43: 152–165. 12. Greenberg L. Foot care data from two recent nationwide surveys. A comparative analysis. Journal of the American Podiatric Medical Association 1994; 84: 365–370.
13. Crawford VLS, Ashford RL, McPeake B et al. Conservative podiatric medicine and disability in elderly people. Journal of the American Podiatric Medical Association 1995; 85: 255–259. 14. Haneke E. Achilles foot-screening project: background, objectives and design. Journal of the European Academy of Dermatology and Venereology 1999; 12: S2–5. 15. Dockery GL, Crawford ME. Cutaneous disorders of the lower extremity. Philadelphia, PA: WB Saunders; 1997. 16. Mason AR, Cork MJ, Dooley G et al. Topical treatments for chronic plaque psoriasis (Protocol). Cochrane Database of Systematic Reviews 2006; 3: CD005028. 17. Kilburn S, Featherstone P, Higgins B et al. Interventions for cellulitis and erysipelas (Protocol). Cochrane Database of Systematic Reviews 2006; 1: CD004299. 18. Gupta AK, Inniss K, Wainwright R et al. Interventions for actinic keratoses (Protocol). Cochrane Database of Systematic Reviews 2006; 4: CD004415. 19. Sladden MJ, Barzilai DA, Berg D et al. Surgical excision margins for localised cutaneous melanoma (Protocol). Cochrane Database of Systematic Reviews 2004; 3: CD004835. 20. Herd R, Jury C. Topical 5 fluorouracil for non-melanoma skin cancer (Protocol). Cochrane Database of Systematic Reviews 2000; 3: CD003084. 21. Norman RA. Xerosis and pruritus in the elderly: recognition and management. Dermatologic Therapy 2003; 16: 254–259. 22. Paniker P. Images in dermatology. American Journal of Medicine 2005; 118: 108. 23. Moses S. Pruritus. American Family Physician 2003; 68: 1135–1142. 24. London NJM, Nash R. Varicose veins. British Medical Journal 2000; 320: 1391–1394. 25. Quartey-Papafio CM. Importance of distinguishing between cellulitis and varicose eczema of the leg. British Medical Journal 1999; 318: 1672– 1673.
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26. Schiraldi FG. Common dermatologic manifestations in the older patient. Clinics in Podiatric Medicine and Surgery 1993; 10: 79–95. 27. Roujeau J, Stern RS. Severe adverse cutaneous reactions to drugs. New England Journal of Medicine 1994; 331: 1272–1285. 28. Norman RA, Blanco PM. Papulosquamous diseases in the elderly. Dermatologic Therapy 2003; 16: 231–242. 29. Anderson TF. Psoriasis and arthritis. Cutis 1978; 21: 790–800. 30. Zanolli MD, Wikle JS. Joint complaints in psoriatic patients. International Journal of Dermatology 1992; 31: 488–491. 31. Krueger GG, Bergstrasser PR, Lowe NJ et al. Psoriasis. Journal of the American Academy of Dermatology 1984; 11: 937–947. 32. Stern RS. Epidemiology of psoriasis. Dermatologic Clinics 1995; 13: 717–722. 33. Tagami H. Triggering factors. Clinics in Dermatology 1997; 15: 677–685. 34. Sanders LJ. Psoriasiform disorders. In: McCarthy DJ, Montgomery R, ed. Podiatric dermatology. Baltimore: Williams and Wilkins; 1986: 106–121. 35. Bonifati C, Carducci M, Mussi A et al. Recognition and treatment of psoriasis: special considerations in elderly patients. Drugs and Aging 1998; 12: 177–190. 36. Mason J, Mason AR, Cork MJ. Topical preparations for the treatment of psoriasis: A systematic review. British Journal of Dermatology 2002; 146: 351–364. 37. Sanchez-Perez J, Buceta LR, Fraga J et al. Lichen planus with lesions on the palms and/or soles: prevalence and clinicopathological study of 36 patients. British Journal of Dermatology 2000; 142: 310–314. 38. Moussavi R. Lichen planus. A case study. Journal of the American Podiatric Medical Association 2003; 93: 238–239. 39. Cram DL, Kierland RR, Winkelmann RK. Ulcerative lichen planus of the feet. Archives of Dermatology 1966; 93: 692–701. 40. Schmid H. Frequency, duration and localization of lichen planus. Acta Dermatolo-venereologica 1961; 41: 164–167. 41. Sauder DN. Effect of age on epidermal immune function. Dermatologic Clinics 1986; 4: 447– 454. 42. Kelly RI, Pearse R, Bull RH et al. The effects of aging on the cutaneous microvasculature. Journal of the American Academy of Dermatology 1995; 33: 749–756. 43. Sunderkotter C, Kalden H, Luger TA. Aging and the skin immune system. Archives of Dermatology 1997; 133: 1256–1262.
44. Haan MN, Selby JV, Quesenberry CP et al. The impact of ageing and chronic disease on use of hospital and outpatient services in a large HMO: 1971– 1991. Journal of the American Geriatrics Society 1997; 45: 667–674. 45. Smith AG. Skin infections of the foot. The Foot 1999; 9: 56–59. 46. Brook I, Frazier EH. Clinical features and aerobic and anaerobic microbiological characteristics of cellulitis. Archives of Surgery 1995; 130: 786– 792. 47. Dupuy A, Benchikhi H, Roujeau J-C et al. Risk factors for erysipelas if the leg (cellulitis): casecontrol study. British Medical Journal 1999; 318: 1591–1594. 48. Roujeau J-C, Sigurgeirsson B, Korting H-C et al. Chronic dermatomycoses of the foot as risk factors for acute bacterial cellulitis of the leg: a case-control study. Dermatology 2004; 209: 301–307. 49. Bjornsdottir S, Gottfredsson M, Thorisdottir AS et al. Risk factors for acute cellulitis of the lower limb: a prospective case-control study. Clinical Infectious Diseases 2005; 41: 1416–1422. 50. Miller W. Postoperative wound infection in foot and ankle surgery. Foot and Ankle 1983; 4: 102–104. 51. Taylor GJ, Bannister GC, Calder S. Perioperative wound infection in elective orthopaedic surgery. Journal of Hospital Infection 1990; 16: 241–247. 52. Rawes ML, Jennings C, Rawes FL et al. Fatal chiropody. The Foot 1995; 5: 36–37. 53. Aly AA, Roberts NM, Seipol KS et al. Case survey of management of cellulitis in a tertiary teaching hospital. Medical Journal of Australia 1996; 165: 553–556. 54. Taplin D, Zaias N. The etiology of pitted keratolysis. Proceedings of the XIII International Congress of Dermatology 1967; 593–595. 55. Nordstrom KM, McGinley KJ, Cappiello L et al. Pitted keratolysis: the role of Micrococcus sedentarius. Archives of Dermatology 1987; 123: 1320–1325. 56. Rubel LR. Pitted keratolysis and Dermatophilus congolensis. Archives of Dermatology 1972; 105: 584–586. 57. Takama H, Tamada Y, Yano K et al. Pitted keratolysis: clinical manifestations in 53 cases. British Journal of Dermatology 1997; 137: 282–285. 58. Levine N. Pits on the heels of the feet. Foot odor and slimy feel to the skin of the feet provide clues to diagnosis. Geriatrics 2002; 57: 27. 59. Greenberg L, Davis H. Foot problems in the US. The 1990 National Health Interview Survey. Journal of the American Podiatric Medical Association 1993; 83: 475–483. 60. Roseeuw D. Achilles foot screening project: preliminary results of patients screened by dermatologists.
References
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Journal of the European Academy of Dermatology and Venereology 1999; 12: S6–9. Pierard G. Onychomycosis and other superficial fungal infections of the foot in the elderly: a panEuropean survey. Dermatology 2001; 202: 220–224. Crawford F, Hart R, Bell-Syer S et al. Topical treatments for fungal infections of the skin and nails of the foot. Cochrane Database of Systematic Reviews 1999; 3: CD001434. Gupta AK, Saunder DN, Shear NH. Antifungal agents: An overview. Journal of the American Academy of Dermatology 1994; 30: 677–698. Bell-Syer SEM, Hart R, Crawford F et al. Oral treatments for fungal infections of the skin of the foot. Cochrane Database of Systematic Reviews 2002; 2: CD003584. Berlin SJ. Statistical analysis of 307 601 tumours and other lesions of the foot. Journal of the American Podiatric Medical Association 1995; 85: 699–703. Rea JN, Newhouse ML, Halil T. Skin disease in Lambeth. A community study of prevalence and use of medical care. British Journal of Preventative and Social Medicine 1976; 30: 107–114. Johnson ML, Roberts J. Skin conditions and related need for medical care among persons 1–74 years. US Department of Health Education and Welfare Publication 1978; 1660: 1–26. Massing AM, Epstein WL. Natural history of warts. Archives of Dermatology 1963; 87: 306–310. Gibbs S, Harvey I. Topical treatments for cutaneous warts. Cochrane Database of Systematic Reviews 2006; 3: CD001781. Fridrich RE, Ilodi GH. Cutaneous tag or acrochordon of the lower extremity. Journal of the American Podiatric Medical Association 1986; 76: 479. Lapidus PW. Orthopaedic skin lesions of the soles and toes. Calluses, corns, plantar warts, keratomas, neurovascular growths, onychomas. Clinical Orthopaedics and Related Research 1966; 45: 87–100. Bart RS, Andrade R, Kopf AW. Cutaneous horns. A clinical and histopathologic study. Acta Dermatovenereologica 1968; 48: 507–515. Berlin SJ. Fibrous lesions of the foot. In: D. J. McCarthy and R. Montgomery, eds. Podiatric dermatology. Baltimore: Williams and Wilkins; 1986: 300–310. Coulter P, Bouche R. Traumatically induced inclusion cyst secondary to shoe impingement: report of three cases. Journal of Foot and Ankle Surgery 1999; 38: 271–277. Rozbruch SR, Chang V, Bohne WH et al. Ganglion cysts of the lower extremity. Orthopedics 1998; 21: 141–148. Pontious J, Good J, Maxian SH. Ganglions of the foot and ankle. A retrospective analysis of 63 proce-
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dures. Journal of the American Podiatric Medical Association 1999; 89: 163–168. Mallick E, Jagganath CS, Barrie JL. Outcome of treatment of pedal ganglia. The Foot 2006; 12: 89–94. Cione JA, Cozzarelli J. Capillary hemangioma of the foot. Journal of the American Podiatric Medical Association 2002; 92: 155–157. Baran R, Goettmann S. Distal digital keratoacanthoma: a report of 12 cases and a review of the literature. British Journal of Dermatology 1998; 139: 512–515. Sonnex TS. Digital myxoid cysts: a review. Cutis 1989; 37: 89–94. Dockery GL. Diagnosis and treatment of digital mucoid cysts. Journal of Foot and Ankle Surgery 1994; 33: 326–333. Holly EA, Kelly JW, Shpall SN et al. Number of melanocytic nevi as a major risk factor for malignant melanoma. Journal of the American Academy of Dermatology 1987; 17: 459–468. Zaidi Z, Jafri N, Noori B et al. Piezogenic papules. A study of 100 cases. Journal of the American Podiatric Medical Association 1995; 45: 93–94. Shall L, Marks R. Stucco keratoses. A clinicopathologic study. Acta Dermato-venereologica 1991; 71: 258–261. Stockfleth E, Rowert J, Arndt R et al. Detection of human papillomavirus and response to topical 5% imiquimod in a case of stucco keratosis. British Journal of Dermatology 2000; 143: 846–850. Teraki Y, Sato Y, Izaki S. Successful treatment of stucco keratosis with maxacalcitol. British Journal of Dermatology 2006; 155: 1085–1086. Wilkinson DS. Black heel a minor hazard of sport. Cutis 1977; 20: 393–396. Garcia-Doval I, Torre CDL, Losada A et al. Disseminated punctate intraepidermal haemorrhage: a widespread counterpart of black heel. Acta Dermatovenereologica 1999; 79: 403. Armstrong BK, Kricker A. The epidemiology of UV induced skin cancer. Journal of Photochemistry and Photobiology 2001; 63: 8–18. Jemal A, Thomas A, Murray T et al. Cancer statistics, 2002. Cancer Clinical Journal 2002; 52: 23–47. Geller AC, Annas GD. Epidemiology of melanoma and nonmelanoma skin cancer. Seminars in Oncology Nursing 203; 19: 2–11. Severi G, Giles GG, Robertson C et al. Mortality from cutaneous melanoma: evidence for contrasting trends between populations. British Journal of Cancer 2000; 82: 1887–1891. Walsh SM, Fisher SG, Sage RA. Survival of patients with primary pedal melanoma. Journal of Foot and Ankle Surgery 2003; 42: 193–198.
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94. Dwyer PK, Mackie RM, Watt DC et al. Plantar malignant melanoma in a white Caucasian population. British Journal of Dermatology 1993; 128: 115–120. 95. Friedman RJ, Rigel DS, Kopf AW. Early detection of malignant melanoma: the role of physician examination and self-examination of the skin. CA: Cancer Journal for Clinicians 1985; 35: 130–151. 96. Whited JD, Grichnik JM. The rational clinical examination. Does this patient have a mole or a melanoma? Journal of the American Medical Association 1998; 279: 696–701. 97. Evans C, Cockerell CJ. Actinic keratosis: time to call a spade a spade. Southern Medical Journal 2000; 93: 734–736. 98. Ackerman AB. Solar keratosis is squamous cell carcinoma. Archives of Dermatology 2003; 139: 1216–1217. 99. Dinehart SM. The treatment of actinic keratoses. Journal of the American Academy of Dermatology 2000; 42: S25–28. 100. Feldman SR, Fleischer AB, Williford PM et al. Destructive procedures are the standard of care for treatment of actinic keratoses. Journal of the American Academy of Dermatology 1999; 40: 43–47. 101. Khandpur S, Sharma VK. Successful treatment of multiple premalignant and malignant lesions in arsenical keratosis with a combination of acitretin and intralesional 5-fluorouracil. Journal of Dermatology 2003; 30: 730–734. 102. Thestrup-Pedersen K, Ravnborg L, Reymann F. Morbus Bowen: a description of the disease in 617 patients. Acta Dermato-venereologica 1988; 68: 236–239. 103. Nortin J, Kaspar G. Bowen’s disease: a case report. Journal of Foot Surgery 1978; 17: 120–121. 104. Wolf W, Cohen L. Intraepidermal squamous cell carcinoma (Bowen’s disease of the dorsum of the foot). Journal of the American Podiatry Association 1978; 68: 688–690. 105. Allen R, Richardson D, Futrell J. Bowen’s disease of the plantar arch. Cutis 1979; 23: 805–807. 106. Peterka ES, Lynch FW, Goltz RW. An association between Bowen’s disease and cancer. Archives of Dermatology 1961; 84: 623–629. 107. Bath-Hextall FJ, Bong J, Perkins W et al. Interventions for basal cell carcinoma of the skin. Cochrane Database of Systematic Reviews 2003; 2: CD003412.
108. Ozcelik D, Tatlidede S, Hacikerim S et al. The use of sentinal lymph node biopsy in squamous cell carcinoma of the foot: a case report. Journal of Foot and Ankle Surgery 2004; 43: 60–63. 109. Toyama K, Hashimoto-Kumasaka K, Tagami H. Acantholytic squamous cell carcinoma involving the dorsum of the foot of elderly Japanese: clinical and light microscopic observations in five patients. British Journal of Dermatology 1995; 133: 141–154. 110. Heim M, Siev-ner I, Nadvorna H et al. Primary squamous carcinoma of the foot: a missed diagnosis. The Foot 1996; 6: 74–76. 111. Walczak JP, Klugman DJ. Squamous cell carcinoma of the hallux. The Foot 1997; 7: 33. 112. Holgado RD, Ward SC, Suryaprasad SG. Squamous cell carcinoma of the hallux. Journal of the American Podiatric Medical Association 2000; 90: 309– 312. 113. Robinette JW, Day F. Subungual squamous cell carcinoma mistaken for a verruca. Journal of the American Podiatric Medical Association 1999; 89: 435–437. 114. Patel DU, Rolfes R. Squamous cell carcinoma of the nail bed. Journal of the American Podiatric Medical Association 1995; 85: 547–549. 115. Liu GT, Lovell MO, Steinberg JS. Digital syndactylization for the treatment of interdigital squamous cell carcinoma in situ (Bowen disease). Journal of Foot and Ankle Surgery 2004; 43: 419–422. 116. Boring CC, Squires TS, Tong T et al. Cancer statistics. Cancer Clinical Journal 1994; 44: 7–26. 117. Bennet DR, Wasson D, MacArthur JD et al. The effect of misdiagnosis on clinical outcome in melanomas of the foot. Journal of the American College of Surgeons 1994; 179: 279–285. 118. Day CL, Sober AJ, Kopf AW et al. A prognostic model for clinical stage 1 melanoma of the lower extremity – location on foot as independent risk factor for recurrent disease. Surgery 1981; 89: 599–603. 119. Barnes BC, Seigler HF, Saxby TS et al. Melanoma of the foot. Journal of Bone and Joint Surgery 1994; 76A: 892–898. 120. Fortin PT, Freiberg AA, Rees R et al. Malignant melanoma of the foot and ankle. Journal of Bone and Joint Surgery 1995; 77A: 1396–1403. 121. Lemon B, Burns R. Malignant melanoma: a literature review and case report. Journal of Foot and Ankle Surgery 1998; 37: 48–54.
CHAPTER
Nail disorders
CHAPTER CONTENTS Onychomycosis 100 Aetiology, classification and clinical presentation 100 Assessment and diagnosis 101 Treatment 101 Onychocryptosis 103 Aetiology and risk factors 103 Assessment and diagnosis 104 Treatment 104 Onychauxis and onychogryphosis 107 Aetiology and clinical presentation 107 Treatment 108 Subungual exostosis and osteochondroma 109 Clubbing of the nails
109
Yellow nail syndrome
110
Pincer nails
111
Nail disorders associated with systemic diseases and medications 111 Summary 112 References 115
6
Nail disorders affect between 10% and 60% of people aged over 65 years of age,1–5 the most common complaints being fungal nail infection (onychomycosis), ingrown toenails (onychocryptosis) and abnormally thickened nails (onychauxis or onychogryphosis). While often dismissed as rather trivial complaints,6 nail disorders can be extremely painful and cause considerable difficulty with weightbearing tasks. In addition, onychomycosis and onychocryptosis can predispose to quite serious secondary infection in older people if left untreated.7 Several changes in the structure and function of the nail apparatus increase the risk of developing nail disorders with advancing age. As stated in Chapter 2, the rate of growth of the nails decreases by up to 50% from adulthood to old age,8,9 due to a reduction in the turnover rate of keratinocytes and a reduction in size of the nail matrix itself. These changes are most likely due to age-related decline in peripheral blood supply,10 and possibly nutritional deficiencies. As a result of these changes, the nail plate in otherwise healthy older people becomes considerably thicker, and takes on a dull, opaque appearance.11 The increased thickness of the nail, in conjunction with exaggerated transverse curvature, increases dorsal pressure from footwear which in turn increases the likelihood of the nail penetrating the nail bed or distal pulp of the toe. Long-term damage to the nail bed may also give rise to the development of malignancies such as squamous cell carcinoma.12–15 The following chapter outlines the presentation and management of the most common disorders affecting the nail in older people. Premalignant and malignant skin tumours that may develop in the nail bed are covered in Chapter 5.
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AETIOLOGY, CLASSIFICATION AND CLINICAL PRESENTATION
ONYCHOMYCOSIS Onychomycosis, or fungal infection of the nail, is the most common of all nail disorders, affecting 2–13% of the general population,16–19 and between 24% and 41% of people over the age of 60 years.19–21 In addition to advancing age,22–25 risk factors for the development of onychomycosis include male sex,22,23 obesity,26 cigarette smoking,23 peripheral vascular disease,23,26 immunosuppression,25 concurrent interdigital tinea pedis,24,25 psoriasis24 and diabetes.26,27 Onychomycosis has been shown to have significant negative psychosocial effects28–30 and approximately half of all patients report pain, difficulty walking and footwear limitations due to the condition.28,31,32 Onychomycosis is most commonly caused by infection from dermatophyte fungi, including Trichophyton, Epidermophyton and Microsporum species. By far the most common organism isolated from mycotic nails is Trichophyton rubrum, which has been reported to be present in between 67% and 82% of cases.33,34 However, a wide range of other fungi, yeasts and moulds have been isolated from fungal nails35 and there is evidence that onychomycosis in older people may be more likely to be caused by a combination of organisms. Scherer et al36 took samples from the hallux toenail in 450 people aged over 65 years and found that 30% had two or more organisms present, with 90% of these cases testing positive for saprophytes.
A
B
The presence of dermatophytes in the nail plate leads to a rapid growth of hyphae, which invade the nail through the longitudinal laminar spaces, penetrating keratinocytes and causing enzymatic degradation of keratin.37 Depending on the organism and region of the nail affected, this process manifests in four different patterns of infection. Distal subungual onychomycosis is the most common presentation and is caused by the fungus, usually Trichophyton rubrum, invading the distal edge of the nail, leading to a white–yellow discoloration of the nail and hyponychium. Proximal subungual onychomycosis, also caused by Trichophyton rubrum, is much less common and results from infection of the proximal nail fold, possibly triggered by trauma to the nail in immunocompromised patients. White superficial onychomycosis is commonly caused by Trichophyton mentagrophytes and, as the name suggests, leads to a superficial discoloration that coalesces to cover the entire nail plate (Fig. 6.1). The fourth presentation, Candidal onychomycosis, is caused by Candida albicans and has three subtypes: (1) Candida paronychia, characterised by swelling and erythema of the proximal and lateral nail folds, (2) Candida onycholysis, characterised by separation of the nail plate from the nail bed, and (3) Candida granuloma, characterised by thickening of the nail plate.38,39 Any of these four types of onychomycosis can further develop into total dystrophic onychomycosis, in which there is
C
Figure 6.1 Types of onychomycosis. A. Distal subungual. B. Proximal subungual. C. White superficial. (Courtesy of Lesley Newcombe, La Trobe University.)
Onychomycosis
by dermatophytes, a positive KOH result is often considered sufficient to initiate antifungal treatment. Isolation of the pathogen, however, requires 4–6 weeks of inoculation of the sample on Sabouraud’s agar or dermatophyte test medium, followed by microscopic examination.43 This second step may be particularly important in relation to suspected onychomycosis in older people, as a study of 450 specimens obtained from people aged over 65 years indicated a much higher incidence of saprophytes than dermatophytes (60% versus 24%), and a high proportion of mixed infections (30%).36 Figure 6.2 Total dystrophic onychomycosis. (Courtesy of Lesley Newcombe, La Trobe University.)
little distinction between the nail plate and the underlying hypertrophic nail bed (Fig. 6.2). Several non-dermatophyte moulds (such as Scopulariopsis, Acremonium, Aspergillus, Fusarium, Scytalidium and Alternaria) are also associated with onychomycosis. However, because they are rarely cultured in isolation, there is some question as to whether they cause nail infection or are merely secondary invaders.35,40,41 It is not possible to diagnose a mouldrelated nail infection from clinical signs and symptoms.
ASSESSMENT AND DIAGNOSIS Diagnosis of onychomycosis is based primarily on patient history and physical examination, to first rule out conditions that may mimic onychomycosis, such as psoriatic nails, onychogryphosis or trauma. However, the diagnostic accuracy of clinical observations of onychomycosis is less than 50%.42 Therefore, accurate diagnosis and selection of the most appropriate treatment requires culture of nail specimens. After cleansing the area with alcohol, full-thickness nail clippings from the actively infected region should be obtained using a scalpel or curette. It is important to ensure that the sample includes subungual debris, as this increases the likelihood of viable dermatophytes being transferred to the culture compared to specimens taken from the nail plate or nail bed.41 Laboratory diagnosis of onychomycosis initially involves direct microscopy with 10% potassium hydroxide (KOH), which confirms the presence of dermatophytes by the observation of hyphae. Because the vast majority of fungal nail infections are caused
TREATMENT Treatment of onychomycosis was revolutionised by the development of oral allylamine (terbinafine) in the 1990s, and there is a general consensus that oral treatment of onychomycosis is far more effective than topical therapy and should therefore be considered the gold standard of care.44,45 However, oral medication is costly and associated with frequent, though relatively minor, gastrointestinal side effects, and for these reasons oral treatment may not be appropriate in every situation. Furthermore, dystrophic onychomycosis can be highly resistant to both topical and oral treatment, so surgical intervention may be indicated in severe cases.
Topical treatments A wide range of topical treatments have been used to treat onychomycosis, including the azoles (such as clotrimazole, ketoconazole and miconazole), allylamines (such as terbinafine), 2% miconazole nitrate solution, Gordochom solution (25% undecylenic acid and 3% chloroxylenol) and tea-tree oil (Terpinen-4ol).46 These agents are often combined with 20–40% urea cream to facilitate penetration into the nail plate. However, very few randomised trials have been undertaken to evaluate the efficacy of these treatments. The Cochrane review published in 199947 found only two trials specific to toenail onychomycosis, neither of which provided evidence of efficacy compared to a placebo. Since the publication of the Cochrane review, there has been considerable interest in three topical medications – terbinafine, amorolfine and ciclopirox.48 However, with the exception of ciclopirox, no placebo-controlled trials have so far been undertaken. Terbinafine, which became available as both an oral
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and topical medication in the early 1990s, has undergone extensive clinical trials in its oral form but relatively little evidence is available to support the efficacy of the topical cream. Amorolfine, a topical antifungal in lacquer form, has been shown in uncontrolled trials to be clinically effective in around 50% of cases of mild onychomycosis.49 Two randomised controlled trials of ciclopirox reported a mean mycological cure rate of 34% after 48 weeks of treatment, compared to 10% for the placebo.50 However, a recurrence rate of between 25% and 50% has been reported in patients after 1 year of treatment with ciclopirox.51 In response to the rather underwhelming evidence for the efficacy of topical agents, the British Association of Dermatologists has concluded that topical treatment is inferior to oral treatment and should only be considered in cases of very distal infection or for white superficial onychomycosis.45
Oral treatments Several oral medications have been developed for the treatment of onychomycosis (Table 6.1). The first oral treatment for onychomycosis, griseofulvin, was isolated from Penicillium griseofulvum in 1939 and became available for clinical use in 1958.52 Griseofulvin is associated with headache and gastrointestinal adverse effects (and in rare cases hepatotoxicity) and may require up to 18 months to achieve mycological cure. As such, it has generally fallen out of favour because of the development of more effective medications. In 1969, two azoles (clotrimazole and miconazole) were introduced, followed by econazole in 1974, ketoconazole in 1977 and itraconazole and fluconazole in early 1980s. Because of problems with oral administration of many azoles (such as poor
absorption and hepatotoxic effects), only ketoconazole, itraconazole and fluconazole were fully developed into oral medications for onychomycosis.53 Ketoconazole, however, is generally only used for recalcitrant cases of onychomycosis caused by yeast infection.45 The most significant development in oral therapy, terbinafine, was discovered in 1974 and became widely used in the early 1990s.54,55 In contrast to griseofulvin and the azoles, terbinafine is fungicidal, achieving its effects by interrupting the biosynthetic pathway required to build the fungal cell wall. A systematic review of oral treatments for onychomycosis, based on 32 randomised controlled trials, concluded that a 12-week regimen of 250 mg of terbinafine per day is more effective than both griseofulvin and itraconazole,56 achieving mycological cure rates of between 70% and 80%. Terbinafine has also been shown to be more cost-effective than itraconazole, griseofulvin, fluconazole and ciclopirox.51 When prescribed for older people, it needs to be kept in mind that terbinafine has documented interactions with some antidepressants, antipsychotics, anticoagulants, beta-blockers and antiarrhythmic medications.52 However, a multicentre study of 1508 patients indicated that only 6% of those aged over 60 years reported serious adverse events associated with the use of terbinafine.57 Several studies have been conducted to evaluate the efficacy of combining topical and oral treatments, based on the rationale that the oral medications reach the nail through the nail bed while the topical agents penetrate the nail plate itself.58 Moderately improved cure rates have been reported for combinations of topical tioconazole plus oral griseofulvin, ciclopirox lacquer plus oral terbinafine, and amorolfine lacquer
Table 6.1 Oral treatments for onychomycosis Drug
Mechanism of action
Antifungal activity
Dosage
Griseofulvin
Fungistatic
Dermatophytes Not effective against Candida
750–1000 mg/day
Fluconazole
Fungistatic
Dermatophytes, Candida, some non-dermatophyte moulds such as Aspergillus and Rhodotorula
450 mg/week
Itraconazole
Fungistatic
Dermatophytes, Candida, some non-dermatophyte moulds such as Aspergillus, Scopulariopsis and Fusarium
200 mg/day
Terbinafine
Fungicidal
Dermatophytes, Candida, some non-dermatophyte moulds
250 mg/day
Onychocryptosis
plus griseofulvin, terbinafine, itraconazole or fluconazole, compared to the oral medication alone. However, because of the increased complexity of the treatment regimen, compliance with combination therapy may be more difficult to achieve.
Surgery Severely thickened, dystrophic onychomycosis may be extremely painful and resistant to both topical and oral treatment. In such cases, it may be necessary to consider surgical management, which involves complete avulsion of the nail under local anaesthetic, followed by topical and/or oral antifungals while the new nail grows back.59 It needs to be kept in mind, however, that longstanding cases of dystrophic onychomycosis may cause irreversible damage to the nail matrix, so there is no guarantee that the infection-free nail will be of normal shape or thickness. If dystrophic regrowth is considered likely, complete avulsion of the nail followed by matrixectomy is advisable. Methods for nail avulsion are described in the section on onychocryptosis later in this chapter.
Figure 6.3 Onychocryptosis. (Courtesy of Lesley Newcombe, La Trobe University.)
Preventing recurrence Recurrence of onychomycosis is very common, with between 20% and 50% of patients experiencing relapses within 5 years following an initially successful treatment.60 It is therefore essential that the older person or their carer be advised of strategies to prevent reinfection. Such strategies include discarding infected footwear and hosiery, avoiding barefoot activity in public places, keeping the feet cool and dry, wearing absorbent cotton socks, detecting and treating tinea pedis before it spreads to the nail and applying antifungal powder to footwear at least once per week.61,62 Footwear should also be carefully examined, as trauma to the nail by ill-fitting footwear may also trigger relapses.58
ONYCHOCRYPTOSIS Onychocryptosis, also referred to as unguis incarnates, unguis aduncus or simply ingrown toenail, is predominantly a condition that affects young adults but has been reported to occur in 5–10% of people aged over 65 years.5,63–65 Because of age-related reductions in peripheral vascular supply and the increased propensity to infection, onychocryptosis has poten-
tially serious consequences such as ulceration and cellulitis. The condition develops when a spicule of nail penetrates the nail sulcus, leading to erythema, swelling and secondary infection. If left untreated, a pulp of overhanging hypergranulation tissue may develop that bleeds in response to minor trauma. At this stage, the condition can be exquisitely painful66 (Fig. 6.3).
AETIOLOGY AND RISK FACTORS Surprisingly little research has been undertaken to evaluate the factors associated with the development of onychocryptosis, so much of our understanding of the condition is based on clinical observations. Factors thought to be associated with onychocryptosis include ill-fitting footwear, tight socks, hyperhidrosis, incurvated/involuted nails, pronated foot type, hallux valgus, incorrect cutting of nails and variations in toe length.66–69 Three case-control studies have been undertaken. The most detailed study by Langford et al70 compared 50 cases with onychocryptosis of the hallux to 50 controls, and found that those with onychocryptosis had broader toes, decreased nail thickness, and increased eversion of the great toe when weightbearing. Gunal et al71 found that patients
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with onychocryptosis were more likely to have a hallux shorter than, or of equal length, to the second toe, with the so-called ‘Egyptian foot’ (hallux longer than the second toe) less likely to develop onychocryptosis. Finally, Pearson et al72 assessed several aspects of nail anatomy (including thickness and curvature) in 23 cases and 23 controls but found no differences between the groups. In addition to these proposed risk factors, onychocryptosis may develop secondary to several other disorders of the nail unit, including benign and malignant tumours of the nail bed, dystrophic onychomycosis, traumatic subungual haematomas and subungual exostosis.68 Several medications have also been reported to lead to onychocryptosis, including indinavir (a medication used in the treatment of HIV infection),73 oral retinoids,74 cyclosporin75 and oral antifungals.76 In each case, the medication appears to increase the risk of onychocryptosis by causing paronychia and promoting the development of hypergranulation tissue.
ASSESSMENT AND DIAGNOSIS The diagnosis of onychocryptosis is straightforward, and is based on the classical signs and symptoms of redness and swelling of the toe and quite severe, sharp pain in response to lateral pressure. Most commonly, the lateral sulcus will be affected through compression from the second toe. Probing the sulcus of the affected side of the toe will often enable the localisation of the offending piece of nail and will assist in differentiating onychocryptosis from simple paronychia. Based on clinical signs and symptoms, the condition can be classified into three progressive stages. In stage 1, the toe appears red and swollen and there is pain on direct pressure to the nail and while walking. In stage 2, there is evidence of infection, slight pressure to the toe will cause considerable pain, and the patient may have difficulty walking. In stage 3, hypergranulation tissue has developed over the edge of the nail plate.77 While stage 1 onychocryptosis may be successfully managed with appropriate nail shaping and clearing subungual debris, stages 2 and 3 will generally require surgery. There is generally no need for further diagnostic investigations prior to initiating treatment of onychocryptosis; however, if the nail is highly incurvated, a lateral hallux X-ray may be required to assess whether a subungual exostectomy is indicated. Footwear should also be thoroughly examined, as the wearing
of shoes with a narrow toebox is likely to lead to recurrence.
TREATMENT Conservative Early stage onychocryptosis may be successfully managed by clearing the sulcus of hyperkeratotic debris (onychophosis), removing the offending spicule of nail with a scalpel and smoothing the edge of the nail with a file. This may be undertaken without anaesthesia; however, if the pain is severe, local anaesthesia may be necessary. Inserting a small piece of cotton wool or foam beneath the edge of the nail may prevent recurrence by slightly elevating the nail plate.78,79 In cases where the nail is being compressed against the adjacent toe, taping techniques80,81 or the use of foam toe spacers71 to separate the toes may also be useful (Figs 6.4, 6.5). Advice on appropriate nail cutting may assist in preventing recurrence. Orthonyxia, the gradual correction of incurvated nails using bracing techniques, is no longer commonly used but may have a role in the prevention of onychocryptosis in older people for whom surgery is contraindicated. Several variations have been described in the literature.82–86 The simplest technique involves
Figure 6.4 The use of a toe spacer to alleviate lateral pressure on the hallux nail.
Onychocryptosis
A
B
C
Figure 6.5 Simple taping technique for the conservative management of onychocryptosis. A. Adhesive tape placed obliquely over affected sulcus. B. Tape is tightly pulled in a proximal–lateral direction, pulling the lateral nail fold away from the sulcus. C. Tape is wrapped around toe and secured on the nail plate.
that bracing should be considered as an effective alternative to surgery.
Surgical
Figure 6.6 Nail brace treatment for incurvated nail.
thoroughly clearing the nail sulcus of debris and then looping a short piece of 0.5 mm gauge stainless steel wire underneath the medial and lateral edges of the nail. A small loop is then shaped on the dorsal surface of the nail, and pliers are used to twist the loop. This exerts a dorsal force on the plantar medial and lateral edges of the nail, and a corresponding plantar force on the dorsal aspect of the nail plate, thereby reducing the convexity of the nail (Fig. 6.6). The brace is kept on for a month and regular reassessments and reapplications are necessary to maintain the correction. Limitations of nail bracing include difficulties in affixing the wire to the nail, impingement from footwear, the possibility of trauma to the nail sulcus, the prolonged duration of treatment and high likelihood of recurrence. Furthermore, very few studies have been undertaken to assess the efficacy of nail bracing procedures. However, a recent non-randomised study by Harrer et al86 compared a nail bracing technique to nail avulsion surgery and found that those in the nail brace group were less likely to take time off work because of their foot problem and could return to wearing normal footwear earlier than those who had surgery. Recurrence rates were similar between the groups. Based on these results, the authors suggest
Surgical intervention is often required for recurrent onychocryptosis, and more than 75 techniques have been described in the literature.87 Broadly speaking, two approaches are most commonly used in contemporary practice: incisional procedures (such as the Winograd, Frost, Zadik and terminal Syme techniques) and nail avulsion with phenolisation. Each approach has advantages and disadvantages; however, the most recent Cochrane systematic review of nine randomised controlled trials (with at least 6 months follow-up) concluded that nail avulsion combined with phenolisation is more effective than surgical excision in the treatment of ingrown nails.88 Before considering surgical intervention, it is essential that the older patient’s vascular status be thoroughly assessed to ascertain their wound-healing potential.66 Although nail surgery is not contraindicated in older people, those with an ankle–brachial index of below 0.5 or toe pressures below 40 mmHg may be at risk of delayed healing and subsequent increased risk of infection.66 Similarly, diabetes is not a contraindication for nail surgery, provided the patient’s vascular status and blood glucose control are adequate.89 A report of 57 people with diabetes who had undergone phenol matrixectomy for onychocryptosis reported no serious adverse events.89 The most commonly used excisional nail surgery techniques are the Winograd, Zadik and terminal Syme’s procedures. The Winograd procedure, first described in 1929, involves excising the medial or lateral nail sulcus and adjacent nail plate, bed and matrix to the depth of the proximal phalanx. The
105
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NAIL DISORDERS
wedge of tissue is removed, and any residual nail bed or matrix is removed with a curette. The original description of the technique suggested that the operative site should be left open to heal by primary intention;90 however, recent modifications recommend the use of sutures (Fig. 6.7).66 Reported recurrence rates when using this technique range from 11% to 27%.91–93 In 1950, Frost94 described a further modification of the Winograd procedure in which the incision is extended proximally (creating an L shape) to provide greater access to the nail matrix. However, tissue necrosis of the skin flap is a relatively common complication with this modification.95 The Zadik technique was first described in 1950, and involves total nail avulsion and surgical removal of the nail matrix.96 The nail plate is lifted and removed with an elevator, and a full-thickness skin flap is created by making two oblique incisions from the medial and lateral corners of the nail fold. The flap is retracted to expose the nail matrix, which is removed to the depth of the proximal phalanx. The surgical site is then closed and the flap is sutured back into place (Fig. 6.8). Recurrence rates of between 27% and 50% have been reported in the literature.92,97
A
B
C
Figure 6.7 Winograd procedure. A. Incision. B. Wedge of tissue removed. C. Closure with proximal suture.
A
B
Amputation of the distal half of the distal phalanx (commonly referred to as the terminal Syme’s procedure) was first described as a treatment for subungual exostosis by Lapidus in 193398 and as a treatment for onychocryptosis by Thompson & Terwilliger in 1951.99 A deep elliptical excision is made around the entire nail plate and nail matrix, just distal to the interphalangeal joint. The distal phalanx is removed with a bone saw distal to the insertion of the long extensor tendons, and the plantar flap is sutured to the line of the proximal incision (Fig. 6.9). Recurrence rates are reportedly lower than other surgical techniques; however, the postoperative appearance of the toe may be cosmetically unacceptable to many patients.100 For this reason, some authors consider the Syme’s procedure to be a radical approach that should only be employed when other treatments have failed.100,101 The surgical techniques described above have been largely replaced by total or partial nail avulsion with phenolisation. This technique, first described by Boll in 1945102 and used almost exclusively by podiatrists and chiropodists, is less invasive and has a far lower recurrence rate than excisional techniques. However, these benefits are slightly offset by an increased risk of postoperative infection.88 The technique is performed under local anaesthesia and tourniquet, and involves separating the nail plate from the nail bed using an eponychium retractor, removing the offending portion of nail (from the medial sulcus, lateral sulcus or both) proximal to the eponychium and applying liquefied phenol (C6H5OH, carbolic acid) with a cotton wool bud to the nail matrix, sulcus and nail bed to prevent regrowth (Fig. 6.10). Reported recurrence rates range from 4% to 10%.93,103–107 Although phenolisation is the most common method of destroying the nail matrix, several other methods
C
D
Figure 6.8 Zadik procedure. A. Total nail avulsion. B. Full-thickness oblique incisions. C. Retraction of flap and removal of nail matrix. D. Closure with proximal sutures.
Onychauxis and onychogryphosis
have been described, such as sodium hydroxide, negative galvanic current, cryosurgery and carbon dioxide laser.66 There is little evidence that these approaches offer any significant advantages over phenolisation. Thorough postoperative management of the surgical site is an essential component of the treatment plan. Patients should be advised that some bleeding following the surgery is normal and necessary. The first redressing, generally undertaken 3–5 days following the procedure, should be performed under sterile A
B
conditions as the wound site is a potential avenue for infection. The patient should then be advised to undertake redressings every 5–7 days. Several different wound dressings have been recommended, including paraffin-impregnated gauze, hydrogels, topical antibiotic creams and alginates.66 However, a randomised controlled trial of three dressings (povidone iodine, an amorphous hydrogel and a control dressing of paraffin gauze) found no difference in healing times following phenol matrixectomy, with all three groups healing after 33–34 days.108 Similarly, a recent controlled trial of honey versus paraffin-impregnated gauze found no difference in healing times following phenol matrixectomy.109
ONYCHAUXIS AND ONYCHOGRYPHOSIS AETIOLOGY AND CLINICAL PRESENTATION C
D
Figure 6.9 Terminal Syme’s procedure. A. Elliptical incision. B. Distal half of distal phalanx and soft tissue removed. C. Pulp of toe rotated over stump and sutured. D. Postoperative appearance.
A
B
The term onychauxis refers to hypertrophy (thickening) of the nail plate (Fig. 6.11). This condition affects approximately 65% of older people65 and may be accompanied by onychophosis (the formation of keratotic tissue in the nail sulcus) and paronychia (inflammation of the tissues surrounding the nail plate). Onychauxis is thought to be caused by a range of factors, including subungual exostosis, a history of trauma to the nail, compression from footwear and reduced peripheral circulation. Onychauxis is also frequently observed in conjunction with onychomycosis.10,110,111 In older people, longstanding onychauxis is generally irreversible as permanent damage has
C
D
Figure 6.10 Partial nail avulsion with phenolisation. A. Nail plate separated from nail bed. B. Nail plate split with Thwaite’s nippers. C. Section of nail removed. D. Phenol (80%) applied to nail matrix, nail bed and sulcus with cotton wool bud.
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NAIL DISORDERS
Figure 6.11 Onychauxis. (Courtesy of Felicity Prentice, La Trobe University.)
occurred to the nail bed and nail matrix. If left untreated, haematomas and ulcers may develop beneath the nail plate, which are potential avenues for infection (Fig. 6.12). Onychogryphosis (also referred to as Ram’s horn nail or Ostler’s toe) is a condition in which the nail plate is grossly thickened and deformed. The nail appears yellow to dark brown and develops a curved or hornlike shape (Fig. 6.13). In severe cases, the nail may penetrate the soft tissue of adjacent toes. Onychogryphosis is caused by the same aetiological factors as onychauxis but is most likely to result from a major traumatic event such as severely stubbing the toe. This damages the nail matrix, causing it to produce nail in an irregular manner.10,110 Onychogryphosis may also result from long-term neglect of older people. Mohrenschlager et al112 reported a case of onychogryphosis in a 92-year-old woman, who was discovered in her home in a confused state and had not received any foot care for at least 2 years. Her nails were grossly thickened and elongated, and the nail had penetrated the second toe, leading to ulceration.
TREATMENT Treatment of onychauxis and onychogryphosis involves clearing the sulcus of keratotic debris and reducing the thickness of the nail with a file or moto-
Figure 6.12 Subungual ulceration. (Courtesy of Felicity Prentice, La Trobe University.)
Figure 6.13 Onychogryphosis. (Courtesy of Lesley Newcombe, La Trobe University.)
rised burr. Foam or silicon gel toe sleeves may help alleviate pressure from the toe, and footwear should be carefully examined for suitability and replaced if necessary. Total avulsion of the nail should be considered in symptomatic cases, as both conditions are indicative of permanent damage to the nail matrix and will invariably recur. However, because these conditions most commonly affect frail older people, surgical avulsion may not be viable. In such cases, non-surgical nail avulsion may be a useful alternative.
Clubbing of the nails
This requires the application of 40% urea cream to the nail plate, occluding the toe with adhesive tape or waterproof dressing. Dressing changes need to be undertaken twice per week. The urea cream gradually macerates the nail plate, enabling debridement of the entire nail.113–115
SUBUNGUAL EXOSTOSIS AND OSTEOCHONDROMA Subungual exostosis is an uncommon benign tumour of trabecular bone that most commonly develops on the distal phalanx of the hallux (Fig. 6.14).116 The aetiology is not well understood; however, repetitive trauma to the toe is thought to lead to periostitis and an outgrowth of cartilage that eventually ossifies.110 Clinical observations suggest that subungual exostoses may be associated with hallux limitus or rigidus, because of the compensatory hyperextension of the interphalangeal joint making the distal pulp of the toe more susceptible to compression from footwear.11 The presence of the exostosis may cause the nail plate to become incurvated or elevated at its distal edge and, in severe cases, the nail plate may become eroded and the nail bed ulcerated.117 At this stage, the condition may be difficult to differentiate from onychocryptosis or subungual melanoma; however, no cases
of malignant degeneration of exostoses have been reported. Osteochondromas are benign tumours that have a similar clinical presentation to subungual exostoses, although men are affected more than women, the growth rate of the tumour is somewhat slower and, in rare cases, osteochondromas may undergo malignant degeneration. Radiographically, osteochondromas appear dome-like and exhibit a characteristic radiolucent cap of hyaline cartilage, in contrast to the broad trabecular tuft of bone observed in subungual exostoses.118 Both subungual exostoses and osteochondromas need to be differentiated from malignant tumours of the nail bed, including squamous cell carcinoma, basal cell carcinoma and malignant melanoma.119 Although uncommon, the diagnosis of these tumours is often delayed and many patients with malignant subungual lesions are inappropriately treated. Indeed, a study of 52 patients who were ultimately diagnosed with subungual malignant melanoma indicated that almost half had undergone nail avulsion or cauterisation procedures.120 Clinical observations of loosening of the nail plate, chronic inflammation and draining of the lesion are indicative of an underlying malignancy and should prompt referral for biopsy.121 Treatment of subungual exostoses and osteochondromas involves protecting the toe from further trauma by the use of foam or silicon gel toe sleeves and addressing the potential contribution of ill-fitting footwear. If these conservative measures fail, surgical excision may be necessary, which involves partial or total nail avulsion (depending on the size and location of the lesion), followed by removal of the growth using a bone chisel.122 Following surgical excision, recurrence is uncommon (less than 10%);123 however, distal onycholysis and subungual hyperkeratosis may develop postoperatively.
CLUBBING OF THE NAILS
Figure 6.14 Subungual exostosis affecting the hallux nail. (Courtesy of Lesley Newcombe, La Trobe University.)
Exaggerated longitudinal curvature of the fingernails and toenails (Fig. 6.15) is believed to have been first reported by Hippocrates, giving rise to the alternative nomenclature Hippocratic nails. The condition is also referred to as acropachy, digital clubbing and dysacromelia. By definition, a nail is considered to be ‘clubbed’ if the angle formed by the intersection of the proximal nail fold and the nail plate (known as the angle of Lovibond) is 180° or greater.124 Clubbed
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NAIL DISORDERS
Figure 6.16 Yellow nail syndrome. (From DermNet NZ, www.dermnetnz.org, with permission from the New Zealand Dermatological Society.)
Figure 6.15 Clubbed nails (fingernails shown). (From DermNet NZ, www.dermnetnz.org, with permission from the New Zealand Dermatological Society.)
nails are occasionally hereditary125 but more commonly develop in association with a wide range of systemic conditions, including respiratory disease (e.g. tuberculosis, emphysema, bronchiectasis and lung cancer), cardiovascular disease (e.g. congestive heart failure and bacterial endocarditis) and gastrointestinal diseases (e.g. ulcerative colitis and chronic diarrhoea).126 The mechanism responsible for clubbing of the nails is uncertain. One theory suggests that excessive vasodilation of vessels develops around the nail, which leads to the formation of an oedematous, bulbous nail bed and subsequent nail plate curvature.127 An alternative view suggests that chronic excess platelet formation associated with some systemic diseases leads to the development of large clumps of platelets, which become embedded in peripheral vessels in the fingers and toes, leading to increased capillary permeability and hypertrophy of surrounding soft tissues.128 Irrespective of the underlying cause, clubbed nails are generally not painful and therefore rarely require treatment.
YELLOW NAIL SYNDROME Yellow nail syndrome is an uncommon condition characterised by the triad of thickened, incurvated yellow
nails (both fingernails and toenails), lymphoedema and respiratory disease (including asthma, tuberculosis, pleural effusion, bronchiectasis, chronic sinusitis and chronic obstructive pulmonary disease)129,130 (Fig. 6.16). The condition has also been reported in association with several other conditions, including rheumatoid arthritis,131 various forms of cancer,132 thyroid disease133 and sleep apnoea.134 The nail dystrophy associated with the syndrome is thought to be due to lymphatic obstruction in the nail region, which causes a markedly reduced growth rate (as slow as 0.12– 0.27 mm/week), with an inversely proportional increase in nail thickness.135 Because of the increased bulk of the nail plate, development of onychophosis and paronychia is common, and complete separation of the nail plate (onycholysis) may occur. The condition can be easily differentiated from nail discoloration associated with onychomycosis, as the discoloration is generally uniform and the nail plate is considerably harder. Yellow nail syndrome is treated in the same manner as onychauxis and onychogryphosis, the goal of therapy being to reduce the thickness of the nail and prevent any subungual breakdown from developing. There is preliminary evidence that oral136 and topical137 vitamin E or oral zinc supplementation138 may improve the appearance of the nail; however, the mechanism is not fully understood. Interestingly, spontaneous recovery of yellow nail discoloration and dystrophy has been noted in response to treatment for other comorbidities, including rheumatoid arthritis,132 diabetes mellitus139 and tuberculosis.140
Systemic diseases and medications
PINCER NAILS Pincer nails (also referred to as omega nails or trumpet nails) are a form of involuted/incurvated nail deformity in which the transverse curvature of the nail plate becomes more pronounced distally, producing an almost cylindrical structure around the distal pulp of the toe (Fig. 6.17).141 Pincer nails frequently present with onychocryptosis, onychophosis and paronychia, and in severe cases the nail bed may become ulcerated. The aetiology of pincer nails is not fully understood. It has been hypothesised that the formation of
osteophytes on the proximal aspect of the distal phalanx causes a widening of the proximal nail matrix but, because the unaffected distal nail matrix is narrower, the nail plate assumes a conical shape as it progresses distally.68,141 Symmetrical pincer nails affecting several toes have been shown to be a hereditary trait142,143 associated with a congenital deviation of the nail matrix and nail bed. Most cases, however, affect the hallux nails and develop secondary to tumours of the nail bed, dystrophic onychomycosis, psoriasis and, less commonly, use of beta-blockers.118,144 Lateral pressure from footwear (particularly in association with hallux valgus) has also been postulated as a potential cause.68 Pincer nails may also be indicative of gastrointestinal malignancy.145 Symptomatic pincer nails are managed in essentially the same manner as onychocryptosis caused by involuted/incurvated nails. However, surgical management of long-standing pincer nails will often require total rather than partial nail avulsion, and many cases will require excision of the underlying exostosis or hypertrophied nail bed. Haneke68 has also described a reconstructive procedure for severe pincer nail deformity which involves bilateral partial nail avulsion with phenolisation, followed by excision of the exostosis and insertion of rubber tubes into the lateral nail grooves, which are sutured to pull the nail folds apart (Fig. 6.18).
NAIL DISORDERS ASSOCIATED WITH SYSTEMIC DISEASES AND MEDICATIONS A
B
Figure 6.17A, B Pincer nail deformity. (A, courtesy of Lesley Newcombe, La Trobe University; B, from DermNet NZ, www.dermnetnz.org, with permission from the New Zealand Dermatological Society.)
A vast range of systemic diseases may manifest as nail plate abnormalities.146,147 Although nail changes are rarely specific enough to form a definitive diagnosis, nail plate changes may provide useful clues to the presence of an undiagnosed systemic condition, or at least provide some level of confirmation of an established diagnosis.148,149 The most obvious clue to an underlying systemic aetiology is the involvement of multiple nails or both fingernails and toenails. Common nail plate changes associated with systemic disease include onycholysis (separation of the nail plate from the nail bed at its distal end), splinter haemorrhages (extravasation of blood from blood vessels in the nail bed), koilonychia (concave or spoonshaped nails), Hippocratic nails (clubbing of the nail), leukonychia (white discoloration of the nails), Beau’s lines (transverse ridges across the nail plate caused by temporary slowing or cessation of nail growth),
111
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NAIL DISORDERS
A
C
E
B
D
F
Figure 6.18 Surgical procedure for severe pincer nail deformity. A. Following bilateral partial nail avulsion with phenolisation and removal of the distal portion of the nail, a longtudinal incision is made down to the proximal phalanx, 3 mm proximal to the hyponychium. B. A fish-mouth incision is then made parallel to the nail bed. C, D. The dorsal flap is retracted and the exostosis is excised. E. The nail plate is spread and sutured, and thin rubber tubes are inserted into the nail grooves and sutured to assist in pulling apart the lateral nail folds. F. The fish-mouth incision is then closed with sutures.
paronychia (inflammation of tissues around the nail) and pitted nails (formation of multiple superficial pits on the dorsal surface of the nail plate, most commonly observed in people with psoriasis – Fig. 6.19). Systemic conditions associated with each of these nail plate disorders are listed in Table 6.2. Similarly, several systemic medications, particularly antibiotics and cancer chemotherapeutic drugs, may produce characteristic nail changes.147,150 The most common changes to the nail caused by systemic medications are onycholysis and alterations in pigmentation of the nail (including longitudinal and transverse banding, and colour changes in the lunula). As with changes associated with systemic disease, nail changes associated with medications are rarely specific enough to establish causality but may assist in differential diagnosis. Systemic medications associated with common nail plate disorders are listed in Table 6.3.
SUMMARY Nail disorders, particularly onychomycosis and onychocryptosis, are very common in older people and
Figure 6.19 Psoriatic nails. (Courtesy of Lesley Newcombe, La Trobe University.)
can be highly debilitating. Fortunately, advances in pharmacological treatment of onychomycosis have vastly improved cure rates of this previously recalcitrant condition. Furthermore, there is now sound evidence for the efficacy of nail avulsion with phenolisation for onychocryptosis and, provided there is
Anaemia Bronchiectasis Carcinoma of the lung Circulatory disorders Diabetes mellitus Lupus erythematosus Pleural effusion Psoriatic arthritis Raynaud’s phenomenon Scleroderma Thyroid disease Vitamin C deficiency
Onycholysis Anaemia Cystic fibrosis Diabetes mellitus Endocarditis Eczema Cardiac disease Hypertension Hypoparathyroidism Peptic ulcer Psoriasis Pulmonary disease Raynaud’s disease Rheumatoid arthritis Septicaemia
Splinter haemorrhages Anaemia Cardiac disease Hypothyroidism Lichen planus Psoriasis Raynaud’s disease Scleroderma
Koilonychia Bronchiectasis Congestive heart failure Emphysema Raynaud’s disease Scleroderma Tophaceous gout Tuberculosis Ulcerative colitis
Hippocratic nails Gout Hyperalbuminuria Hypoparathyroidism Myocardial infarction Psoriasis Renal disease
Leukonychia
Table 6.2 Nail abnormalities associated with systemic disease
Epilepsy Hepatic disease Hypopituitarism
Beau’s lines
Diabetes mellitus Hyperparathyroidism
Paronychia
Psoriatic nails Reiter’s syndrome Pemphigous vulgaris
Pitted lines
Summary
113
Splinter haemorrhages Antibiotics Tetracyclines
Cancer drugs Doxycycline Docetaxel
Other Psoralen
Onycholysis
Antibiotics Tetracyclines Penicillin
Cancer drugs Bleomycin Busulfan Carboplatin Chlorambucil Cyclophosphamide Etoposide 5-Fluorouracil Hydroxyurea Methotrexate Mitomycin Paclitaxel Vincristine
Other Beta-blockers Clofazimine
Other Infliximab
Other Sulphonamide
Poisons Arsenic Lead
Poisons Silver
Poisons Arsenic Fluoride Mercury Paraquat Other Indomethacin Ketoconazole Phenothiazine Psoralen
Cancer drugs Bleomycin Busulfan Carmustine Carboplatin Chlorambucil Cisplatin Cyclophosphamide Doxorubicin Fludarabine 5-Fluorouracil Melphalan Mitoxantrone Paclitaxel Procarbazine Semustine
Cancer drugs Cyclophosphamide Ciclosporin Daunorubicin Docetaxel Doxorubicin Etoposide 5-Fluorouracil Hydroxyurea Mercaptopurine Methotrexate Vincristine
Antibiotics Sulphonamides
Leukonychia
Cancer drugs Bleomycin Busulfan Cisplatin Daunorubicin Doxorubicin 5-Fluorouracil Hydroxyurea Melphalan Methotrexate Vincristine
Antibiotics Minocycline Tetracyclines
Pigmented bands Pigmented bands (longitudinal) (transverse)
Table 6.3 Nail abnormalities associated with systemic medications
Other Metaprolol Retinoids
Poisons Fluorine
Cancer drugs Cisplatin Daunorubicin Docetaxel Doxorubicin Etoposide 5-Fluorouracil Ifosfamide Razoxane Vincristine
Antibiotics Dapsone
Beau’s lines
Other Retinoids
Cancer drugs Ciclosporin Methotrexate Paclitaxel
Antibiotics Cephalexin Sulphonamides
Paronychia
Other Alcohol abuse (red) Tamoxifen (red) Zidovudine (red)
Poisons Carbon monoxide (red) Paraquat (yellow) Silver (blue)
Cancer drugs Bleomycin (blue) Cyclophosphamide (blue) Cyctosine arabinoside (purple) Decarbazine (blue) Dactinomycin (blue) Doxorubicin (blue) 5-Fluorouracil (blue) Idarubicin (blue) Vinblastine (blue)
Antibiotics Tetracyclines (yellow)
Lunula discoloration
114 NAIL DISORDERS
References
sufficient vascular supply to enable healing, age should be no barrier to the provision of this effective treatment strategy. Finally, all foot-care specialists should
be aware of the myriad of systemic conditions and medications that may produce changes in the appearance of the nails of older people.
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British Journal of Dermatology 1998; 139: 665– 671. Elewski BE. The effect of toenail onychomycosis on patient quality of life. International Journal of Dermatology 1997; 36: 754–756. Drake LA. Impact of onychomycosis on quality of life. Journal of the American Podiatric Medical Association 1997; 87: 507–511. Scher RK. Onychomycosis: a significant medical disorder. Journal of the American Academy of Dermatology 1996; 35: S2–5. Roseeuw D. Achilles foot screening project: preliminary results of patients screened by dermatologists. Journal of the European Academy of Dermatology and Venereology 1999; 12: S6–9. Schein JR, Gause D, Stier DM et al. Onychomycosis. Baseline results of an observational study. Journal of the American Podiatric Medical Association 1997; 87: 512–519. Kemna ME, Elewski BE. A US epidemiologic survey of superficial fungal diseases. Journal of the American Academy of Dermatology 1996; 35: 539–542. Jennings MB, Weinberg JW, Koestenblatt EK et al. Study of clinically suspected onychomycosis in a podiatric population. Journal of the American Podiatric Medical Association 2002; 92: 327– 330. VanderStraten MR, Balkis MH, Ghannoum MA. The role of nondermatophyte molds in onychomycosis: diagnosis and treatment. Dermatologic Therapy 2002; 15: 89–98. Scherer WP, McCreary JP, Hayes WW. The diagnosis of onychomycosis in a geriatric population: a study of 450 cases in South Florida. Journal of the American Podiatric Medical Association 2001; 91: 456–464. Rashid A, Scott E, Richardson MD. Early events in the invasion of the human nail plate by Trichophyton mentagrophytes. British Journal of Dermatology 1995; 133: 932–940. Zaias N. Onychomycosis. Archives of Dermatology 1972; 105: 263–274. Lemont H. Pathologic and diagnostic considerations in onychomycosis. Journal of the American Podiatric Medical Association 1997; 87: 498–506. Summerbell RC, Kane J, Krujden S. Onychomycosis, tinea pedis, and tinea manuum caused by nondermatophytic filamentous fungi. Mycoses 1989; 32: 609–619. Harvey CK, Richardson A. Techniques for obtaining specimens for culture to confirm onychomycosis. Journal of the American Podiatric Medical Association 2000; 90: 394–396. Andre J, Achten G. Onychomycosis. International Journal of Dermatology 1987; 26: 481–490.
43. Elewski BE. Diagnostic techniques for confirming onychomycosis. Journal of the American Academy of Dermatology 1998; 35: S6–9. 44. Fleckman P. Onychomycosis: diagnosis and topical therapy. Dermatologic Therapy 2002; 15: 71– 77. 45. Roberts DT, Taylor WD, Boyle J. Guidelines for the treatment of onychomycosis. British Journal of Dermatology 2003; 148: 402–410. 46. Bodman MA, Feder L, Nace AM. Topical treatments for onychomycosis. A historical perspective. Journal of the American Podiatric Medical Association 2003; 93: 136–141. 47. Crawford F, Hart R, Bell-Syer S et al. Topical treatments for fungal infections of the skin and nails of the foot. Cochrane Database of Systematic Reviews 1999; 3: CD001434. 48. Crawford F, Ferrari J. Fungal toenail infections. Clinical Evidence 2006; 15: 1–2. 49. Zang M, Bergstraesser M. Amorolfine in onychomycosis and dermatomycosis. Clinical and Experimental Dermatology 1992; 17: S61–70. 50. Gupta AK, Joseph WS. Ciclopirox 8% nail lacquer in the treatment of onychomycosis of the toenails in the United States. Journal of the American Podiatric Medical Association 2000; 90: 495–501. 51. Warshaw EM. Evaluating costs for onychomycosis. A practitioner’s perspective. Journal of the American Podiatric Medical Association 2006; 96: 38–52. 52. Mackay-Wiggan J, Elewski BE, Scher RK. The diagnosis and treatment of nail disorders: systemic antifungal therapy. Dermatologic Therapy 2002; 15: 78–88. 53. Bell-Seyer S, Porthouse J, Bigby M. Oral treatments for toenail onychomycosis (protocol). Cochrane Database of Systematic Reviews 2004; 2: CD004766. 54. Gupta AK, Ryder JE, Lynch LE et al. The use of terbinafine in the treatment of onychomycosis in adults and special populations: a review of the evidence. Journal of Drugs in Dermatology 2005; 4: 302–308. 55. Odom RB. New therapies for onychomycosis. Journal of the American Academy of Dermatology 1996; 35: S26–30. 56. Crawford F, Young P, Godfrey C et al. Oral treatments for toenail onychomycosis: a systematic review. Archives of Dermatology 2002; 138: 811–816. 57. Pollak R, Billstein SA. Safety of oral terbinafine for toenail onychomycosis. Journal of the American Podiatric Medical Association 1997; 87: 565–570. 58. Bristow IR, Baran R. Topical and oral combination therapy for toenail onychomycosis. Journal of the American Podiatric Medical Association 2006; 96: 116–119.
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59. McInnes BD, Dockery GL. Surgical treatment of mycotic toenails. Journal of the American Podiatric Medical Association 1997; 87: 557–564. 60. Olafsson JH, Sigurgeirsson B, Baran R. Combination therapy for onychomycosis. British Journal of Dermatology 2003; 149: S15–18. 61. Jaffe R. Onychomycosis. Recognition, diagnosis and management. Archives of Family Medicine 1998; 7: 587–592. 62. Daniel CR. Traditional management of onychomycosis. Journal of the American Academy of Dermatology 1996; 35: S21–25. 63. Levy LA. Prevalence of chronic podiatric conditions in the US. National Health Survey 1990. Journal of the American Podiatric Medical Association 1992; 82: 221–223. 64. Crawford VLS, Ashford RL, McPeake B et al. Conservative podiatric medicine and disability in elderly people. Journal of the American Podiatric Medical Association 1995; 85: 255–259. 65. Dunn JE, Link CL, Felson DT et al. Prevalence of foot and ankle conditions in a multiethnic community sample of older adults. American Journal of Epidemiology 2004; 159: 491–498. 66. Weaver TD, Ton MV, Pham TV. Ingrowing toenails: management practices and research outcomes. International Journal of Lower Extremity Wounds 2004; 3: 22–34. 67. Lloyd-Davies R, Brill G. The aetiology and outpatient management of ingrowing toenail. British Journal of Surgery 1963; 50: 592–597. 68. Haneke E. Ingrown and pincer nails: evaluation and treatment. Dermatologic Therapy 2002; 15: 148–158. 69. DeLauro TM. Onychocryptosis. Clinics in Podiatric Medicine and Surgery 1995; 12: 201–213. 70. Langford DT, Burke C, Robertson K. Risk factors in onychocryptosis. British Journal of Surgery 1989; 45: 382–387. 71. Gunal I, Kosay C, Veziroglu A et al. Relationship between onychocryptosis and foot type and treatment with toe spacer. A preliminary investigation. Journal of the American Podiatric Medical Association 2003; 93: 33–36. 72. Pearson H, Bury R, Wapples J et al. Ingrowing toenails: is there a nail abnormality? A prospective study. Journal of Bone and Joint Surgery 1987; 69B: 840–842. 73. Bouscarat F, Bouchard C, Bouhour D. Paronychia and pyogenic granuloma of the great toes in patients treated with indinavir. New England Journal of Medicine 1998; 338: 1776–1777. 74. Campbell J, Grekin R, Ellis C et al. Retinoid therapy is associated with excess granulation tissue responses. Journal of the American Academy of Dermatology 1983; 9: 708–713.
75. Olujohungbe A, Cox J, Hammon M et al. Ingrowing toenails and cyclosporin. The Lancet 1993; 342: 1111. 76. Weaver T, Jespersen D. Multiple onychocryptosis following treatment of onychomycosis with oral terbinafine. Cutis 2000; 66: 211–212. 77. Heifetz C. Ingrown toenail: a clinical study. American Journal of Surgery 1937; 38: 298–315. 78. Senepati A. Conservative management of ingrown toenail. Journal of the Royal Society of Medicine 1986; 79: 339–340. 79. Ilfeld FW. Ingrown toenail treated with cotton collodion insert. Foot and Ankle 1991; 11: 312–313. 80. Nishioka K, Katayama I, Kobayashi Y et al. Taping embedded toenails. British Journal of Dermatology 1985; 113: 246–247. 81. Manca D. Practice tips. Taping toes. Effective treatment for ingrown toenails. Canadian Family Physician 1998; 44: 275. 82. Schulte KW, Neumann NJ, Ruzicka T. Surgical pearl: nail splinting by flexible tube – a new noninvasive treatment for ingrown toenails. Journal of the American Academy of Dermatology 1998; 39: 629–630. 83. Gupta S, Sahoo B, Kumar B. Treating ingrown toenails by nail splinting with a flexible tube: an Indian experience. Journal of Dermatology 2001; 28: 485–489. 84. Robertson DG, Parker PJ. The treatment role of the plastic nail guard for ingrowing toenails. Journal of the Royal Army Medical Corps 2001; 147: 183–186. 85. Kim YJ, Ko JH, Choi KC et al. Nail-splinting technique for ingrown nails: the therapeutic effects and the proper removal time of the splint. Dermatologic Surgery 2003; 29: 745–748. 86. Harrer J, Schoffl V, Hohenberger W et al. Treatment of ingrown toenails using a new conservative method. A prospective study comparing brace treatment with Emmert’s procedure. Journal of the American Podiatric Medical Association 2005; 95: 542–549. 87. Haneke E. Surgical treatment of ingrown toenails. Cutis 1986; 37: 251–256. 88. Rounding C, Bloomfield S. Surgical treatments for ingrowing toenails. Cochrane Database of Systematic Reviews 2005; 2: CD001541. 89. Giacalone V. Phenol matrixectomy in patients with diabetes. Journal of Foot and Ankle Surgery 1997; 36: 264–267. 90. Winograd A. A modification of the technic of operations for ingrown toe-nail. Journal of the American Medical Association 1929; 229–230. 91. Keyes E. The surgical treatment of ingrown toenails. Journal of the American Medical Association 1934; 163: 1458–1460.
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92. Murray W, Bedi B. The surgical treatment of ingrowing nail. British Journal of Surgery 1975; 62: 409–412. 93. VanderHam A, Hackeng C, Yo I. The treatment of ingrowing toenails. Journal of Bone and Joint Surgery 1990; 72B: 507–509. 94. Frost L. Root resection for incurvated nail. Journal of the National Association of Chiropodists 1950; 40: 19. 95. Madigan P. Nail surgery. In: Lorimer D, French G, O’Donnell M et al, ed. Edinburgh: Churchill Livingstone; 2006: 561–567. 96. Zadik F. Obliteration of the nail bed of the great toe without shortening the terminal phalanx. Journal of Bone and Joint Surgery 1950; 32B: 66–67. 97. Palmer B, Jones A. Ingrowing toenails: the results of treatment. British Journal of Surgery 1979; 66: 575–576. 98. Lapidus P. Complete and permanent removal of the toenail in onychogryphosis and subungual osteoma. American Journal of Surgery 1933; 19: 92–94. 99. Thompson T, Terwilliger C. The terminal Symes operation for ingrown toenail. Surgical Clinics of North America 1951; 31: 575–584. 100. Dolce MD, Baruch K, Adamov DJ. The use of the distal Syme’s procedure for treating onychopathy. Clinics in Podiatric Medicine and Surgery 2004; 21: 689–696. 101. Baruch K. The ultimate resolution of onychopathy. The Syme’s procedure. Clinics in Podiatric Medicine and Surgery 1995; 12: 347–354. 102. Boll O. Surgical correction of ingrowing nails. Journal of the National Association of Chiropodists 1945; 35: 8. 103. Morkane A, Robsertson R, Inglis G. Segmental phenolization of ingrowing toenails: a randomised controlled study. British Journal of Surgery 1984; 71: 526–527. 104. Kuwada GT. Long-term evaluation of partial and total surgical and phenol matricectomies. Journal of the American Podiatric Medical Association 1991; 81: 33–35. 105. Bossers A, Jansen I, Eggink W. Rational therapy for ingrown toenails: a prospective study. Acta Orthopaedica Belgica 1992; 58: 325–329. 106. Mori H, Umeda T, Nishioka K et al. Ingrown nails: a comparison of the nail matrix phenolisation method with the elevation of the nail bed-periosteal flap procedure. Journal of Dermatology 1998; 25: 1–4. 107. Herold N, Houshian S, Reigels-Nielsen P. A prospective comparison of wedge matrix resection with nail matrix phenolisation for the treatment of ingrown toenail. Journal of Foot and Ankle Surgery 2001; 40: 390–395. 108. Dovison R, Keenan AM. Wound healing and infection in nail matrix phenolisation wounds: does
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topical medication make a difference? Journal of the American Podiatric Medical Association 2001; 91: 230–233. McIntosh CD, Thomson CE. Honey dressing versus paraffin tulle gras following toenail surgery. Journal of Wound Care 2006; 15: 133–136. Cohen PR, Scher RK. Geriatric nail disorders: diagnosis and treatment. Journal of the American Academy of Dermatology 1992; 26: 521–531. Bartolomei FJ. Onychauxis: surgical and non-surgical management. Clinics in Podiatric Medicine and Surgery 1995; 12: 215–220. Mohrenschlager M, Wicke-Wittenius K, Brockow K et al. Onychogryphosis in elderly persons: an indicator of long-standing poor nursing care? Report of one case and review of the literature. Cutis 2001; 68: 233–235. Farber EM, South DA. Urea ointment in the nonsurgical avulsion of nail dystrophies. Cutis 1978; 22: 689–692. Port M, Sanicola KF. Nonsurgical removal of dystrophic nails utilising urea ointment occlusion. Journal of the American Podiatric Medical Association 1980; 70: 521–523. South DA, Farber EM. Urea ointment in the nonsurgical avulsion of nail dystrophies – a reappraisal. Cutis 1980; 25: 609–612. Young RJ, Wilde JL, Sartori CR et al. Solitary nodule of the great toe. Cutis 2001; 68: 57–58. DePalma L, Gigante A, Specchia N. Subungual exostosis of the foot. Foot and Ankle International 1996; 17: 758–763. Baran R, Haneke E, Drape J-L. Tumours of the nail apparatus and adjacent tissues. In: Baran R, Dawber RPR, DeBerker DAR et al, ed. Oxford: Blackwell Science; 2001: 515–630. Spencer JM. Malignant tumours of the nail bed. Dermatologic Therapy 2002; 15: 126–130. Papachristou DN, Fortner JG. Melanoma arising under the nail. Journal of Surgical Oncology 1982; 21: 219–222. Lemont H, Brady J. Amelanotic melanoma masquerading as an ingrown toenail. Journal of the American Podiatric Medical Association 2002; 92: 306–307. DeBerker D, Langtry J. Treatment of subungual exostoses by elective day case surgery. British Journal of Dermatology 1999; 140: 915–918. Landon GC, Johnson KA, Dahlin DC. Subungual exostoses. Journal of Bone and Joint Surgery 1979; 61A: 256–259. Lovibond JL. Diagnosis of clubbed fingers. The Lancet 1938; i: 363. Curth HO, Firschein IL, Alphert M. Familial clubbed fingers. Archives of Dermatology 1961; 83: 828– 836.
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126. Richards GM, Schwartz RA, Goyal S. Clubbing of the nails. eMedicine Journal 2001; 2: 10. 127. Currie AE, Galligher PJ. The pathology of clubbing: vascular changes in the nail bed. British Journal of Diseases of the Chest 1988; 82: 382–385. 128. Dickinson CJ, Martin JF. Megakaryocytes and platelet clumps as the cause of finger clubbing. The Lancet 1987; 2: 1434–1435. 129. Samman PD, White WF. The yellow nail syndrome. British Journal of Dermatology 1964; 16: 153–157. 130. Amiya E, Ako J, Kozaki K et al. Yellow nail syndrome in an elderly man. Geriatrics and Gerontology International 2002; 2: 157–160. 131. Mattingly PC, Bossingham DH. Yellow nail syndrome in rheumatoid arthritis: report of three cases. Annals of the Rheumatic Diseases 1979; 38: 475–478. 132. Guin JD, Elleman JH. Yellow nail syndrome. Possible association with malignancy. Archives of Dermatology 1979; 115: 734–735. 133. Kandil E. Yellow nail syndrome. International Journal of Dermatology 1973; 12: 236–240. 134. Knuckles MLF, Hodge SJ, Roy TM et al. Yellow nail syndrome in association with sleep apnea. International Journal of Dermatology 1986; 25: 588–589. 135. Moffitt DL, DeBerker DA. Yellow nail syndrome: the nail that grows half as fast grows twice as thick. Clinical and Experimental Dermatology 2000; 25: 21–23. 136. Norton L. Further observations on the yellow nail syndrome with therapeutic effects of oral alphatocopherol. Cutis 1985; 36: 457–462. 137. Williams HC, Buffham R, Vivier A. Successful use of topical vitamin E solution in the treatment of nail changes in yellow nail syndrome. Archives of Dermatology 1991; 127: 1023–1028. 138. Arroyo JF, Cohen ML. Yellow nail syndrome cured by zinc supplementation. Clinical and Experimental Dermatology 1992; 18: 62–64.
139. Nelson LM. Yellow nail syndrome. Archives of Dermatology 1969; 100: 499–500. 140. Pang SM. Yellow nail syndrome resolution following treatment of pulmonary tuberculosis. International Journal of Dermatology 1993; 32: 605–606. 141. Baran R, Haneke E, Richert B. Pincer nails: definition and surgical treatment. Dermatologic Surgery 2001; 27: 261–266. 142. Chapman RS. Overcurvature of the nails. An inherited disorder. British Journal of Dermatology 1973; 89: 211–213. 143. Mimouni D, Ben-Amitai D. Hereditary pincer nail. Cutis 2002; 69: 51–53. 144. Greiner D, Schofer H, Milbradt R. Reversible transverse overcurvature of the nails (pincer nails) after treatment with a β-blocker. Journal of the American Academy of Dermatology 1998; 39: 486–487. 145. Jemec G, Thomsen K. Pincer nails and alopecia as markers of gastrointestinal malignancy. Journal of Dermatology 1997; 24: 479–481. 146. Lawry M, Daniel CR. Nails in systemic disease. In: Scher RK, Daniel CR, ed. Nails. Diagnosis, therapy, surgery. Philadelphia, PA: Elsevier Saunders; 2005: 147–176. 147. Tosti A, Baran R, Dawber RPR. The nail in systemic diseases and drug-induced changes. In: Baran R, Dawber RPR, DeBerker DAR et al, ed. Oxford: Blackwell Science; 2001: 223–329. 148. Tarara EL, Spittel JA. Clues to systemic diseases from examination of the foot in geriatric patients. Journal of the American Podiatry Association 1978; 68: 424–430. 149. Zaias N. The nail in health and disease, 2nd ed. London: Prentice-Hall; 1990. 150. Cohen PR, Daniel RC, Scher RK. Systemic drugs. In: Scher RK, Daniel CR, ed. Nails. Diagnosis, therapy, surgery. Philadelphia, PA: Elsevier Saunders; 2005: 177–194.
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CHAPTER
Peripheral vascular disorders and foot ulceration CHAPTER CONTENTS Arterial disorders 121 Peripheral arterial disease 121 Acute arterial occlusion 123 Vasospastic disorders and conditions related to cold exposure 123 Chronic venous insufficiency 126 Epidemiology and risk factors 126 Pathophysiology and clinical presentation Treatment 127 Lymphoedema 128 Epidemiology and classification 128 Clinical presentation 128 Treatment 128 Foot ulceration 129 Epidemiology of foot ulcers in older people 129 Clinical presentation of foot ulcers 129 Wound management 131 Summary 139 References 142
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7
As outlined in Chapter 2, ageing is associated with several changes in the structure and function of the peripheral vascular system, including an increase in the stiffness of the arterial walls and a decrease in the diameter of large veins. The overall effect of these changes is a progressive reduction in arterial blood flow and venous return, which increases the risk of developing circulatory disorders of the lower limb. Indeed, there is an approximate twofold increase in risk of developing peripheral arterial disease for every 10 year increase in age,1 and age is an independent risk factor for conditions associated with venous insufficiency, such as varicose veins2,3 and venous ulcers.4 Although foot-care specialists will not necessarily always be involved in the direct medical management of peripheral vascular diseases affecting the lower limb, they will frequently be presented with foot and ankle manifestations of these conditions. The following chapter provides a brief overview of common circulatory disorders which may manifest in the older foot and discusses the management of associated foot ulcers in older people. Vascular assessment of the lower limb (including wound assessment) is covered in Chapter 3.
ARTERIAL DISORDERS PERIPHERAL ARTERIAL DISEASE Peripheral arterial disease (PAD) is a chronic arterial occlusive disease of the lower limb caused by atherosclerosis, the thickening of the intima of large arteries, which results in a reduction in vessel diameter and subsequent reduction in peripheral blood flow.5,6
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Figure 7.1 Characteristic presentation of chronic arterial occlusion in the lower limb. Note absence of hair and skin atrophy. (Courtesy of Karl Landorf, La Trobe University.)
PAD affects between 11% and 34% of people aged 65 years and over.7–9 Key risk factors for the development of PAD include cigarette smoking,9,10 diabetes mellitus,9,11 hypertension9 and dyslipidaemia.9,12 Symptoms of PAD usually have gradual onset and indeed a large number of cases are asymptomatic.13 The classical early presentation of ischaemically induced pain is intermittent claudication, a tight, cramping pain in the calf region (or, less commonly, in the thigh, buttocks or foot) that occurs when walking and is relieved by rest. In more advanced PAD, a similar cramping pain may develop in bed (referred to as night cramps), as the heat of the bedclothes increases the oxygen demand of the legs. The most severe form of ischaemic pain occurs in the absence of any physical activity (referred to as rest pain) and indicates that the arterial supply of the limb cannot even meet quiescent metabolic requirements. At this stage, the limb is so severely ischaemic that ulceration and/or gangrene may develop – a state commonly referred to as critical limb ischaemia, which implies that, if limb perfusion cannot be improved, there is a significant risk of limb failure and subsequent amputation.14 The characteristic features of chronic arterial occlusion in the lower limb include symptoms of numbness, paraesthesias and coldness, and signs of skin atrophy, rubor and lack of hair (Fig. 7.1). In longstanding cases the foot may become ulcerated or gangrenous. Arterial ulcers affecting the foot most commonly develop on the apices of the toes, the medial and lateral malleoli and the plantar aspect of the heel, and typically have a well circumscribed,
Figure 7.2 Arterial ulcer on the apex of the third toe. (Courtesy of Karl Landorf, La Trobe University.)
‘punched-out’ appearance with a dry base and little exudate (Fig. 7.2).15 Gangrene initially appears as non-blanching cyanosis, followed by the formation of a black eschar of the involved part (Fig. 7.3). Gangrene is commonly accompanied by severe rest pain and represents severely compromised peripheral arterial supply requiring surgical intervention.14 The management of PAD involves smoking cessation,16 the use of statin medications to treat dyslipidaemia17 and antiplatelet therapy to reduce the risk of myocardial infarction and cerebrovascular accident. A recent review of 42 trials involving 9706 patients concluded that the risk of cardiovascular events was reduced by 23% in those taking aspirin daily.18 Walking programs of at least 6 months duration have also been shown to increase the distance walked before the onset of claudication.19 The underlying mechanism responsible for the beneficial effect of exercise is not fully understood but is thought to be related to an increase in collateral blood flow, decreased blood viscosity and improved metabolism of skeletal muscle.20 Surgical management of PAD is considered when intermittent claudication or rest pain is severe enough to impair normal daily activities and involves revascularisation (bypassing the affected vessel using grafting techniques) or angioplasty (the insertion of intraluminal stents to expand the affected vessel/s). Vessel patency following femoropopliteal and femorotibial bypass grafts ranges between 56% and 92% after 1
Arterial disorders
A
quent blockage of a normal or partly diseased artery is much more likely to be acutely symptomatic. A limb subjected to acute embolic occlusion will typically become extremely painful, pale, cold and numb distal to the site of the occlusion. However, in some patients, collateral blood supply may cause the foot to appear red while dependent,22 which may mimic the appearance of cellulitis or an acute attack of gout. Furthermore, an acutely ischaemic foot in a patient with diabetes may feel warm. Because of these potential diagnostic challenges, it has been suggested that clinicians should have a high index of suspicion of acute arterial occlusion in all older patients who present with an acutely painful foot.22 Acute arterial occlusion is a vascular emergency, as critical ischaemia may develop within a period of hours. Treatment involves thrombolytic therapy alone or in conjunction with embolectomy, a surgical procedure in which the embolus is extracted using a balloon catheter.23
VASOSPASTIC DISORDERS AND CONDITIONS RELATED TO COLD EXPOSURE Raynaud’s phenomenon
B
Figure 7.3A, B Gangrene of the toes. (Courtesy of Karl Landorf, La Trobe University.)
year and between 12% and 80% after 5 years.21 When revascularisation fails or there is a significant amount of gangrenous or necrotic tissue present, amputation is considered as a last resort.6
ACUTE ARTERIAL OCCLUSION An acute arterial occlusion is an abrupt interruption of blood flow within a peripheral artery caused by direct trauma or, more commonly, due to a thrombus or embolus. Acute thrombosis generally develops in an already partially occluded artery and may therefore be asymptomatic. In contrast, most emboli originate in the heart due to atrial fibrillation and the subse-
Raynaud’s phenomenon, first described in 1888,24 is a condition characterised by recurring episodes of discoloration of the fingers and toes initiated by exposure to cold (Fig. 7.4). The condition is generally classified as primary (Raynaud’s disease) when no underlying cause can be identified, or secondary (Raynaud’s syndrome) when it is associated with an underlying disorder.25 Conditions known to be associated with Raynaud’s phenomenon are listed in Table 7.1. The reported prevalence of Raynaud’s phenomenon ranges from 3% to 21%, with women being more frequently affected than men (a ratio of approximately 4 : 1).26–28 The pathophysiology of Raynaud’s phenomenon is poorly understood but is thought to be related to increased plasma viscosity and overactivity of the sympathetic nervous system, leading to reduced capillary blood flow.29,30 The classic presentation is that of an initial white discoloration of the fingers or toes, followed by a blue discoloration due to deoxygenation of the blood and a then a final red discoloration due to reactive hyperaemia, accompanied by a throbbing sensation. Longstanding cases may also develop chronic paronychia and ulceration of the apices of the
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Table 7.1 Conditions associated with secondary Raynaud’s phenomenon Medications
Connective tissue diseases
Other
Beta-blockers Ergot derivatives Vinblastine Bleomycin Ciclosporin
Scleroderma Systemic lupus erythematosus Rheumatoid arthritis Sjögren’s syndrome Polymyositis
Occupational (exposure to vibration) Tarsal tunnel syndrome Polycythemia Arterial emboli Chronic regional pain syndrome type 1 Renal disease Hypothyroidism Neoplasms Pulmonary hypertension
Table 7.2 Diagnostic criteria for primary Raynaud’s disease Vasospastic attacks precipitated by exposure to cold or emotional stimuli Bilateral involvement of the extremities Absence of gangrene or, if present, limited to the skin of the fingertips No evidence of underlying disease that could be responsible for vasospastic attacks A history of symptoms for at least 2 years
A
B
Figure 7.4 Raynaud’s phenomenon affecting (A) the hands and (B) the feet. (Courtesy of Lesley Newcombe, La Trobe University.)
toes.31 Diagnosis is primarily based on clinical signs and symptoms (Table 7.2).25 Raynaud’s phenomenon is frequently a transient disorder. Two recently published follow-up studies of 732 and 14 years33 duration demonstrated that a large proportion of cases (64% and 33%, respectively) had completely resolved without treatment. In persistent cases, however, several treatments have been trialled, including oral medications (such as nifedipine,34 reserpine35 and prazosin36), topical agents (such as nitroglycerin ointment37), conditioning and biofeedback,38 and, in severe cases, lumbar sympathectomy.39 The reported efficacy of these treatments is highly variable and no systematic reviews have so far been undertaken. However, several authors suggest that nifedipine, a potent vasodilator, is currently the treatment of choice and is effective in approximately two-thirds of cases.40
Acrocyanosis and livedo reticularis Acrocyanosis and livedo reticularis are uncommon, benign vasospastic conditions that rarely require treat-
Arterial disorders
Figure 7.5 Livedo reticularis. (With permission from Dermatlas; © Bernard Cohen, MD, Dermatlas; http://www. dermatlas.org.)
ment and are only of clinical importance as differential diagnoses when Raynaud’s phenomenon is suspected.41 Acrocyanosis is characterised by a persistent cyanosis of the extremities (including fingers, toes and ears) that is exacerbated by cold. The aetiology is unknown, although secondary forms of the condition may develop in several connective tissue disorders.42 Livedo reticularis is characterised by a mottled discoloration of blue-purple rings surrounding central regions of pallor on the arms and legs and is thought to be caused by vasospasm of dermal arterioles (Fig. 7.5).43
Erythema pernio Erythema pernio (also referred to as pernio syndrome, perniosis or, more commonly, chilblains) is a condition characterised by inflammatory lesions of the skin (particularly the fingers, toes, nose and ears) caused by exposure to cold (Fig. 7.6).41 The prevalence of the condition is unknown but it is thought to be more common in women and is particularly prevalent in people who are frequently exposed to cold, damp conditions, such as dairy farmers,44 soldiers45 and ‘horsey women’ (sic).46 Erythema pernio appears to be in overall decline because of improvements in household heating and changes in work practices.47 Acute lesions, which appear as erythematous, purplish papules up to 1 cm in diameter, develop within 24 hours of the initial exposure and will generally resolve within a number of weeks. Chronic lesions are typically very itchy, purplish plaques, which may ulcerate in response to repeated scratching by the patient. The severity of the lesions increases in the presence of concurrent PAD.47
Figure 7.6 Erythema pernio (chilblains) affecting the second and third toes. (Courtesy of Adam Bird, La Trobe University.)
The normal response to cold involves arteriolar constriction in conjunction with capillary dilatation, resulting in a loss of deoxygenated blood and subsequent build-up of metabolites in the interstitial spaces. This process is reversed when the body part is rewarmed; however, for reasons that are still not fully understood, people who develop chilblains exhibit a prolonged period of vasoconstriction. It is thought that the sustained presence of metabolites is responsible for the characteristic burning and itchiness associated with the condition.48 Histological and histochemical studies of lesions reveal high levels of T cells, macrophages and necrotic keratinocytes, indicative of an inflammatory process in both the epidermis and dermis.49,50 Over the years, a plethora of treatments have been proposed for the management of chronic erythema pernio, including calciferol, vitamin D, histamine injection, corticosteroids, bandaging to induce reactive hyperaemia, electrotherapy, ultraviolet light, thyroxine and nicotinic acid.51–57 Very few of these treatments have been rigorously evaluated and the only consensus in the literature is that prevention, by avoiding cold exposure, is preferable to treatment. Contemporary management of chilblains involves appropriate wound management of the lesions, the application of topical vasodilator ointments (such as those containing methyl salicylate) and, for symptomatic relief, paraffin wax baths. Oral nifedipine has been found to be effective in a large-scale placebo-
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controlled trial, both as a treatment and for prophylaxis.58
Trench foot and immersion foot Trench foot and immersion foot are cold-induced injuries resulting from exposure of the feet to nonfreezing cold 0–15°C) and wet conditions for several days. The vasospasm resulting from cold exposure leads to hypoxia and capillary stasis, resulting in cyanosis and, in severe cases, superficial gangrene. As the name suggests, trench foot developed in soldiers during trench warfare in the First and Second World Wars. Immersion foot is essentially the same condition but was first described in shipwreck survivors in the Second World War and was also common in the Korean and Vietnam wars.59 Treatment involves pain relief, limb elevation, gradual rewarming of the limb and management of skin breakdown. Although these conditions are now primarily of historical interest, several cases have been reported in homeless people60,61 and neglected older people.62 Williams et al63 described a recent case of a 79-yearold man who had suffered a fall and was discovered by his neighbours two days later soaked in urine. Upon admission to hospital, he was hypothermic and dehydrated, and both feet had developed severe ischaemia that eventually required amputation (Fig. 7.7).
CHRONIC VENOUS INSUFFICIENCY EPIDEMIOLOGY AND RISK FACTORS Chronic venous insufficiency (CVI) can be broadly defined as a cluster of pathologies that result from the inability of the peripheral veins to return venous blood to the heart in an efficient manner. Although prevalence estimates vary widely, because of variations in sample characteristics and case definitions, it has been estimated that CVI affects up to 40% of women and 17% of men at some stage in their life.4,64 The most common manifestations of CVI – varicose veins and venous ulceration – affect approximately 30%65,66 and 3%67–69 of older people, respectively. In addition to increasing age, risk factors for the development of CVI include female sex,4,66,70,71 increased height,72,73 obesity,4,66,72 family history,2–4,65,71 pregnancy,3,4,72 occupations that involve prolonged periods of standing2–4,65,72 and low socioeconomic status.74 The chronic
Figure 7.7 Trench foot in an older person who suffered a fall and was discovered by his neighbours two days later. The line of demarcation eventually became gangrenous and required amputation. (From Williams GL, Morgan AE, Harvey JS 2005 Trench foot following a collapse: assessment of the feet is essential in the elderly. Age and Ageing 34: 651–652, with permission from Oxford Univeristy Press.)
and recurrent nature of conditions associated with CVI – particularly venous ulceration – has a considerable impact on health-care expenditure. For example, it has been estimated that, in the UK, the management of venous legs ulcers costs approximately £400 million each year and accounts for half of the workload of community nurses.75
PATHOPHYSIOLOGY AND CLINICAL PRESENTATION In the normal limb, relaxation of the calf muscles results in deep veins filling with blood from the superficial veins via perforating veins. Contraction of the calf muscles when walking compresses the deep veins, thereby assisting in the return of deoxygenated blood to the heart. This system ensures that deoxygenated blood is shunted from superficial to deep veins and from distal to proximal veins.76 In people with CVI, however, this system is impaired, leading to an increase in blood pressure in the superficial veins (venous hypertension). This may be due to either an obstructed
Chronic venous insufficiency
Figure 7.8 Chronic venous insufficiency, with hyperpigmentation and induration associated with a recurrent venous ulceration. (Courtesy of Karl Landorf, La Trobe University.)
outflow (caused by thrombosis), inefficient inflow (caused by valvular dysfunction leading to reflux) or a combination of the two.77 CVI may present in a wide variety of ways, including telangiectasia (spider veins), varicose veins, oedema, hyperpigmentation and venous ulceration (Figs 7.8–7.10). Typical symptoms of CVI include heaviness, swelling, aching, restless legs, cramps, itching and tingling.78 Diagnosis of CVI is relatively straightforward and is based primarily on clinical observations and physical examination (Ch. 3); however, more detailed vascular laboratory examinations are required for presurgical planning and where deep vein thrombosis is suspected.79
TREATMENT Treatment of CVI includes external compression (via compression bandages or elastic stockings), management of skin integrity (including application of emollients and appropriate wound care), sclerotherapy (the injection of sodium tetradecyl or polidocanol to increase vein stiffness via vein wall fibrosis) and surgical management (including ligation and stripping or venous reconstruction).80–82 Compression bandaging, in conjunction with limb elevation and exercise, has been shown to be effective in the management of
Figure 7.9 Telangiectasia associated with chronic venous insufficiency. (Courtesy of Lesley Newcombe, La Trobe University.)
Figure 7.10 Varicose veins on the dorsum of the foot. (Courtesy of Lloyd Reed, Queensland University of Technology.)
venous ulceration, achieving healing rates of up to 75% over a period of 6 months.75 However, recurrence rates as high as 69% have been reported after 12 months.83 Although the choice of wound dressing does not appear to be a major consideration,84 the latest Cochrane review of 22 trials indicated that multilayer bandaging systems (involving combinations of tubular bandage and wool) were more effective than a single layer of bandage.85 Management of venous
127
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ulcers is described in more detail later in this chapter. The relative benefits and indications for sclerotherapy versus surgery in the management of varicose veins are unclear. Sclerotherapy is generally recommended for smaller varicose veins below the knee, but has traditionally been associated with a relatively high rate of recurrence.82 The most recent Cochrane review of nine trials concluded that there was insufficient evidence to preferentially recommend sclerotherapy or surgery, however, there is some evidence of better long-term outcomes with surgery.86
LYMPHOEDEMA EPIDEMIOLOGY AND CLASSIFICATION Lymphoedema is a condition characterised by the accumulation of fluid in the limbs, caused by the inability of the lymphatic system to adequately drain lymph from interstitial spaces. Two broad categories are recognised: primary (or idiopathic) lymphoedema, also referred to as Milroy’s disease, and secondary lymphoedema. Primary lymphoedema is most commonly present at birth, although it may occasionally develop later in life (cases developing after the age of 35 years are referred to as lymphoedema tarda). The cause is unknown. Secondary lymphoedema occurs in response to obstruction of the lymphatic system caused by trauma, surgical intervention, invasive tumours, radiotherapy or filarial infestation. The prevalence of lymphoedema in the general community is largely unknown.87 Studies undertaken in women who have undergone axillary surgery for breast cancer indicate incidence rates in the range of 25–28%.88 A recent survey conducted in several community health services in the UK identified 823 patients over a 4 week period, with 1 in 200 aged over 65 years. Women were also more commonly affected than men, even after accounting for cases related to breast cancer surgery.89
CLINICAL PRESENTATION The diagnosis of lymphoedema is based on patient history, clinical signs and symptoms. Swelling most commonly affects the limbs but may also develop in the abdomen and the face and results in the gross enlargement of the affected body part (Fig. 7.11). The swelling is generally more resistant to compression (i.e. non-pitting) than venous oedema and the
Figure 7.11 Lymphoedema. (Courtesy of Amanda Taylor, Charles Sturt University.)
trophic changes commonly associated with venous insufficiency (such as ulceration and hyperpigmentation) are generally absent. However, advanced cases may exhibit hardening of skin and subcutaneous tissues. Approximately 50% of people with lymphoedema report pain or discomfort, most commonly described as aching or a sensation of heaviness.89 Laboratory investigations are not commonly undertaken; however, lymphoscintigraphy, a semiquantitative technique in which technetium-99m is injected into the interdigital space of the foot or hand and the drainage patterns are observed, has been shown to be of use in differentiating between lymphoedema and other forms of oedema.90 A characteristic ‘honeycomb’ pattern of the subcutaneous tissues has also been observed with magnetic resonance imaging.91
TREATMENT There is no known cure for lymphoedema. Management of the condition involves attempts to reduce congestion (such as compression bandaging, exercise and manual lymph drainage), maintenance of skin integrity and pliability, and, in advanced cases, surgery. There is very little evidence for the effectiveness of physical therapy for lymphoedema, as only three small trials have been conducted, with variable results.92 Compression bandaging in conjunction with supportive hosiery appears to be more effective than hosiery
Foot ulceration
alone,93 while the addition of manual lymph drainage confers no additional benefit over compression bandages alone.94 Surgery involves resecting affected subcutaneous tissue and underlying fascia, followed by skin grafting to cover the defect. Because of significant problems with postoperative wound healing and poor cosmesis, surgery is only performed in severe cases where the bulk of the limb impairs mobility and severely impacts on quality of life.95
FOOT ULCERATION As outlined in Chapter 2, ageing is associated with several changes to the structure and function of the skin, including a marked loss of collagen96 and elastin97,98 fibres, leading to increased skin fragility and a reduction in the number of Langerhans and mast cells,99 which reduces the speed and intensity of the inflammatory response to infection.99 These changes, in conjunction with the reduction in peripheral blood flow to the lower limb, increase the likelihood of tissue damage and impair the ability of the skin to heal.100–102 Subsequently, many older people endure chronic, recurrent lower limb ulceration, which can be highly debilitating and difficult to manage successfully. Nevertheless, if managed appropriately, ulcers in older people have a similar chance of complete resolution to those in younger people.103 The following section provides a brief overview of the prevalence, clinical presentation and management of foot wounds in older people. For more detailed information, the reader is referred to recent textbooks that specifically address wound management, including Krasner et al’s Chronic wound care104 and Foster’s Podiatric assessment and management of the diabetic foot.105
UK indicated that 43% of ulcers were venous, 15% were mixed (i.e. venous and arterial causes), 4% were arterial, 2% were related to diabetes and 2% were induced by pressure bandages. The remaining 35% were considered to be multifactorial.111 Risk factors for the development of foot ulcers vary depending on the primary underlying aetiology. Arterial ulcers are strongly related to the severity of PAD, whereas venous ulcers, as discussed previously, have a more complex set of risk factors (including female sex, increased height, obesity, family history, pregnancy, occupations that involve prolonged periods of standing, and low socioeconomic status). Diabetic foot ulcers also have a complex pathophysiology, with the key risk factors being loss of protective sensation,107,112–117 foot deformity,107,118 absent foot pulses or reduced ankle–brachial index,107,118 elevated plantar pressures114–116,119 and the presence of plantar calluses.120 Pressure ulcers, which commonly affect the sacrum but can also develop on the malleoli or posterior aspect of the heel, develop in institutionalised older people confined to bed and are frequently associated with several underlying comorbidities and nutritional deficiencies.121
CLINICAL PRESENTATION OF FOOT ULCERS Foot ulcers tend to have a characteristic appearance depending on the primary underlying aetiology and, in most cases, differentiating between ulcer types is relatively straightforward when the appearance of the wound, patient history and physical examination are taken into account. The following section briefly describes the typical appearance of different types of foot ulcers, and a summary is provided in Table 7.3.
Arterial ulcers EPIDEMIOLOGY OF FOOT ULCERS IN OLDER PEOPLE The prevalence of venous leg ulceration67–69 and diabetic foot ulceration106–109 has been studied in some detail, however, the overall prevalence of skin breakdown affecting the foot in older people has received relatively little attention in the literature. The most representative community study of 784 Americans aged over 65 years reported that 4% exhibited ‘foot ulcers’;110 however, no attempt was made to determine their underlying aetiology. A recent prevalence study of lower limb ulcers (including the foot) in the
Arterial foot ulcers most commonly affect the dorsum of the toes, the interdigital spaces or the heel, and typically have a ‘punched-out’ appearance with well defined edges and a dry base with very little exudate (Fig. 7.2). The edges of the wound may be oedematous, and the surrounding skin dry and fissured. Arterial ulcers tend to be painful, and leg elevation will exacerbate symptoms because of the reduction in peripheral blood flow. Other signs of reduced arterial supply (such as pulselessness, pallor and paraesthesia) will frequently be evident.122 In older people, arterial ulcers are often triggered by trauma, such as ill-fitting
129
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Table 7.3 Characteristics of different types of foot ulcers Arterial
Venous
Diabetic
Pressure
Location
Dorsum of toes Interdigital spaces Heel
Malleoli
Plantar metatarsal heads Plantar hallux Plantar heel
Posterior aspect of heel Malleoli
Shape
Round
Irregular
Round
Round, or irregular if large
Depth
Deep
Shallow
Shallow to deep
Shallow to deep
Margins
Smooth Well-defined
Irregular
Smooth
Variable
Base
Dry
Exudative
Variable May be necrotic
Variable
Surrounding skin
Pale and cold
Hyperpigmented
Callused
Variable
Pain
Severe Increases with limb elevation
Minimal to moderate Decreases with limb elevation
Generally painless
Often painful
Pedal pulses
Diminished or absent
Generally present
Diminished or absent
Variable
footwear or stubbing the toes. Several cases of toe ulceration have also been recorded in people receiving compression therapy for venous insufficiency.123
Venous ulcers Venous ulcers most commonly affect the ‘gaiter’ region between the calf and the heel, (typically overlying the medial or lateral malleoli)15 and are generally shallow with irregular, ‘shaggy’ borders and a substantial amount of exudate (Fig. 7.12). The base of the wound typically has a yellowish appearance, and necrosis is seldom present. The surrounding tissue is often oedematous and the skin hyperpigmented, and other characteristic signs of venous insufficiency (such as varicose veins and telangiectasia) will also be evident.124 In contrast to arterial ulcers, older people presenting with venous ulcers will generally have a reasonable peripheral arterial supply, with palpable pulses and warm surrounding skin. However, ulcers with a mixed arteriovenous aetiology will present with a combination of these features.
Diabetic ulcers Diabetic foot ulcers most commonly develop in sites of elevated weightbearing pressure – most commonly
Figure 7.12 Venous ulcer. (Courtesy of Nikki Frescos, La Trobe University.)
the metatarsal heads but also the toes and plantar aspect of the heel (Fig. 7.13).125 The ulcers are usually deep and may be undermined, with callused surrounding skin. The limb will feel cool and will exhibit pallor on elevation and a dusky rubor when dependent. Because of the significant role of neuropathy, diabetic foot ulcers are generally painless, although
Foot ulceration
some patients may report burning pain and paraesthesia.126 Diabetic ulcers are frequently infected and may present with purulent, foul-smelling exudate. Differentiating between arterial, venous and diabetic foot ulcers is straightforward and is informed primarily by patient history, ulcer location and clinical tests of sensory status (e.g. Semmes–Weinstein monofilaments or vibration perception threshold testing).15
Pressure ulcers
A
Pressure ulcers (also referred to as decubitus ulcers) result from long-term, unrelieved compression of the skin against an external surface. Such ulcers most commonly develop in older people with severely restricted mobility, such as older people confined to bed or those who require wheelchairs. The posterior aspect of the heel and medial and lateral malleoli are the most common lower limb sites (Fig. 7.14). The appearance of pressure ulcers is highly variable because of the high prevalence of comorbidities in older people in long-term care, and in many cases may mimic other types of chronic wound. The key to differentiating pressure ulcers from other types of wound is to identify the cause of the compression, such as pressure from a mattress or bedclothes, a poorly fitting prosthesis or an ineffective wheelchair cushion.127
WOUND MANAGEMENT
B
Figure 7.13 Diabetic ulcers under (A) the first metatarsal head and (B) the heel. (Courtesy of Amanda Taylor, Charles Sturt University.)
Management of foot wounds should be primarily directed towards addressing the underlying aetiology, e.g. surgical revascularisation procedures to increase blood supply to the limb for arterial ulcers128 and reducing venous stasis via compression bandaging techniques or surgical management of incompetent perforator veins for venous ulcers.124 Although local wound management is important, there is a general consensus that ulcers are far more likely to heal if the underlying cause is appropriately managed. Furthermore, as outlined in Chapter 3, documenting a thorough social history is essential to the management of foot ulcers in older people in order to establish the practicality of ongoing self-management by the older person in their home environment. The following section outlines the key components of wound management and discusses the available evidence pertaining to the efficacy of local wound care interventions.
131
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PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION
comparing saline to tap water have reported no significant differences in healing times of pressure ulcers.131
Debridement
Figure 7.14 Early (A) and chronic (B) pressure ulcer on the heel in an older person confined to bed. (A, courtesy of Nikki Frescos, La Trobe University; B, courtesy of Karl Landorf, La Trobe University.)
Debridement refers to the removal of devitalised or contaminated tissue from a wound until underlying healthy tissue is exposed. This is undertaken in order to fully ascertain the true dimensions of the wound, to allow drainage of exudate and to allow swabs to be taken to assess for wound infection. Debridement can be achieved by mechanical methods (e.g. scalpel reduction, vigorous swabbing or larval therapy) or non-mechanical methods (e.g. the application of proteolytic enzyme preparations, polysaccharide beads or hydrogels).132 Debridement is considered to be particularly important in the management of diabetic foot ulcers. The most recent Cochrane review133 reported that five randomised controlled trials have been undertaken to assess the efficacy of debridement in diabetic foot ulcers: three pertaining to hydrogels, one addressing surgical debridement and one of larval therapy. The results of these studies indicate that hydrogels are significantly more effective than simple gauze dressings; however, surgical debridement and larval therapy showed no significant benefit. The efficacy of debriding calluses surrounding diabetic foot ulcers has not been rigorously evaluated; however, several studies have shown that forefoot plantar pressures reduce by between 25% and 60% following callus debridement,134–136 which is likely to be beneficial to ulcer healing.
Cleansing the wound
Dressing the wound
The first step in managing a wound is to clear the area of debris, exudate or any foreign bodies that may impair healing. Traditionally, this has been achieved by the application of antiseptic solutions; however, this has fallen out of favour because of concerns that antiseptic application may be cytotoxic and thus impair healing.129 Contemporary practice favours the use of isotonic saline solution; however, there is little evidence that saline offers any significant advantages over tap water.130 For pressure ulcers, there is limited evidence that Vulnopur, a saline spray containing aloe vera, silver chloride and decyl glucoside, improves healing compared to isotonic saline. However, studies
Deciding which dressing to apply to a wound can be quite a difficult task, a task that is made even more daunting by the vast number of options available. Indeed, it has been estimated that there are currently over 30 companies offering over 300 different wound dressings.137 Unfortunately, the conduct of rigorous clinical studies to assess the efficacy of wound dressings has lagged behind the rate of product development, so, in many cases, evidence to support the use of individual dressings is sorely lacking. Nevertheless, it is certainly true that various dressings function quite differently and that some may be more appropriate than others for particular situations. The basic fea-
A
B
Foot ulceration
Table 7.4 Features of an ideal wound dressing Allows excess exudate to be removed from the wound surface Provides a moist micro-environment Is free of contaminants Easy to change Does not cause trauma when removed Leaves no dressing material in the wound after removal Reduces ulcer pain Hypoallergenic Acts as a semi-permeable membrane Impermeable to microorganisms Provides thermal insulation
tures of the ‘ideal’ wound dressing are outlined in Table 7.4.138 Broadly speaking, there are eight main types of wound dressings. The following descriptions are taken from Nelson & Bradley139 and are based on the British National Formulary definitions: ■
■
■
■
■
■
Wound dressing pads: includes knitted viscose dressings and gauze dressings that are applied directly to the wound Tulle dressings: either non-medicated (e.g. paraffin gauze dressing) or medicated (e.g. containing povidone iodine or chlorhexidine) Semi-permeable film dressings : semi-permeable transparent films that allow gaseous exchange but are impervious to bacteria Hydrocolloid dressings: occlusive dressings that contain a hydrocolloid matrix with elastomeric and adhesive substances attached to a polymer base. The hydrocolloid liquefies on contact with wound exudate, producing a moist environment for wound healing to take place. These dressings seal the wound and are impervious to gas, bacteria and liquid Hydrogels : consist of a starch polymer and up to 80% water. They have the ability to absorb woundexudate or rehydrate, depending upon their composition and the degree of exudation of the wound Alginate dressings: also included in the hydrogel group, derived from seaweed and come in the form of a loose, fibrous rope or pad. The calcium ions in the dressing interact with sodium ions within wound exudate to produce a fibrous gel. The gel
■
■
provides a moist wound environment that allows gaseous exchange and provides a barrier to contamination Bead dressings : absorb exudate, wound debris and microorganisms by capillary action either into the beads or into the matrix between the beads Foam dressings: can be applied as sheets or as a liquid that expands to fill the wound-cavity.
Several authors have suggested that the primary factor upon which to base dressing selection is the degree of wound exudate.140 For low exudative wounds, alginate dressings are recommended, while for highly exudative wounds (such as venous ulcers), absorbent dressings such as hydrocolloids or foams are preferable. However, there is currently limited evidence that wound dressing selection has a significant impact on ulcer healing rates. For arterial ulcers, only one inconclusive trial of ketanserin ointment has been undertaken.139 Venous ulcers have been studied in more detail, with 42 randomised controlled trials evaluating hydrocolloids (n = 23), foams (n = 6), alginates (n = 4), hydrogel dressings (n = 6) and a group of miscellaneous dressings (n = 3).84 For the majority of dressing types, however, there is insufficient data to enable strong conclusions to be made, and a meta-analysis indicated no significant difference in healing rates between hydrocolloid dressings and simple, lowadherent dressings. Clearly, there is a considerable need for more research to assess the efficacy of different wound dressing products.
Pressure relief Pressure relief is particularly important in the management of diabetic foot ulcers and pressure ulcers. For diabetic foot ulcers, pressure reduction can be achieved by callus debridement, padded hosiery, orthoses, custom or extra-depth footwear and casts (Fig. 7.15).141 Four randomised controlled trials have been conducted to assess the efficacy of pressure relieving devices for diabetic foot ulcers: three for ulcer prevention and one for ulcer treatment. The results of these studies indicate that custom footwear in conjunction with orthoses is more effective in preventing ulcers than standard care, and that total contact casting is more effective in healing ulcers than simple wound dressings.142 However, there appears to be no significant difference in ulcer healing rates between simple cushioning insoles and those designed to redistribute pressure away from ulcerated sites.
133
134
PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION
Figure 7.15 Examples of pressure relieving devices used in the management of diabetic ulcers. A. Postsurgical boot with rockersole. B. Scotchcast® boot. C. Postoperative shoe. D. Cam walker®.
A
B
C
D
The efficacy of pressure relief in relation to pressure ulcers has received considerable attention in the literature. Two main approaches have been trailed in the hospital or long-term care setting: regular turning of patients to reduce the duration of loading and the use of specialised cushions, beds and mattresses to reduce the magnitude of loading. Pressure relieving devices fall into two broad categories: those that simply disperse the pressure more evenly (referred to as constant low pressure devices, CLPDs), and those that mechanically vary the pressure through the use of inflatable pockets within the mattress (referred to as alternating pressure devices, APDs). The most recent review of 41 trials concluded that foam alternatives to the standard hospital mattress and the addition of sheepskin covers can reduce the incidence of pressure ulcers; however, the relative merits of CLPDs and APDs are unclear. Furthermore, there was insufficient evidence to draw conclusions on the value of seat cushions or limb protectors.143 The relevance of these findings to pressure ulcers affecting the foot are uncertain, as no differentiation between ulcer loca-
tions was considered and most ulcers were located on the sacrum. Interestingly, one trial of a proprietary device consisting of a vinyl boot with a built-in foot cradle and inflatable chamber reported a trend towards a higher rate of ulceration compared to elevation of the heels using a standard hospital pillow.144
Compression therapy Compression therapy is considered an essential component of venous ulcer management, as the primary cause of the trophic disturbance is superficial venous hypertension resulting from valvular incompetence. Compression is achieved by bandaging or hosiery, or a combination of the two. There are two main types of compression therapy: true compression, which involves the use of elastic materials that exert high pressure at rest and lower pressure in response to muscle contraction, and support, which involves the use of inelastic materials that exert low pressure at rest and higher pressure in response to muscle contraction.145 Compression systems can be classified accord-
Foot ulceration
Table 7.5 Types of compression therapy
Compression stockings
Compression bandages
Type
Pressure applied at ankle
Indication/s
Class 1 Class 2
14–17 mmHg 18–24 mmHg
Class 3
25–35 mmHg
Varicose veins Severe varicose veins Prevention of venous ulcers Severe chronic venohypertension Severe varicose veins Prevention of venous ulcers
Class 3a Class 3b
14–17 mmHg 18–24 mmHg
Class 3c
25–35 mmHg
Class 3d
Up to 60 mmHg
ing to the amount of pressure they exert at the ankle (Table 7.5). The more severe the venous insufficiency, the greater the pressure required. Before considering compression therapy for venous ulcers, it is essential that the patient’s ankle–brachial index (ABI) be assessed in order to evaluate the arterial supply to the lower limb. As a general rule, patients with an ABI of 0.8–1.0 are suitable candidates for high compression, those with an ABI of 0.5–0.8 should be provided with low compression and those with an ABI less than 0.5 should not be provided with compression therapy, as there is a risk of exacerbating existing limb ischaemia. Indeed, several cases of toe ulceration associated with the application of compression bandages have been reported.123 The most recent Cochrane review of 22 trials concluded that compression is considerably more effective than no compression when treating venous ulcers, that elastic compression is more effective than inelastic support, and that multiple-layered high compression is more effective than single-layer compression.85 Approximately 65–70% of venous ulcers will heal within 6 months if compression therapy is used.15 No trials have compared compression versus no compression for preventing venous ulcers. However, there is some evidence for greater efficacy of high compression versus low compression, and indirect support can be derived from observations that patients who do not wear compression hosiery are more likely to experience a recurrence of their ulcer.146
Varicose veins Severe varicose veins Prevention of venous ulcers Severe chronic venohypertension Severe varicose veins Prevention of venous ulcers Severe chronic venohypertension Severe varicose veins Prevention of venous ulcers
Topical negative pressure Topical negative pressure (TNP), also referred to as subatmospheric pressure therapy, vacuum sealing technique, vacuum assisted wound closure and sealed surface wound suction, is a relatively recent form of therapy for managing foot ulcers that involves the application of an airtight dressing and suction pump to exert a negative pressure across the wound surface. TNP is thought to be accelerate wound healing by assisting with the removal of exudate and increasing local blood flow.147 Only two small trials have evaluated the effectiveness of TNP on chronic wound healing: one involved a range of chronic wounds and the other specifically focused on diabetic foot ulcers. Both trials indicated that TNP was superior to saline gauze dressings, although the sample sizes were small.148
Hyperbaric oxygen therapy Hyperbaric oxygen therapy involves placing the patient in a compression chamber, increasing the environmental pressure within the chamber and administering 100% oxygen for several hours. By doing so, the partial pressure of oxygen supplied to the tissues is vastly increased, which is thought to be beneficial to wounds by reducing tissue hypoxia.149 Five trials have so far been undertaken: four involving diabetic foot ulcers and one involving venous ulcers. Pooled data analysis of three of the diabetic foot ulcer
135
136
PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION
trials indicated that hyperbaric oxygen therapy reduced the risk of major amputation by almost 70% compared to usual care; however, there was no effect on minor amputation rates. Patients treated with a sham treatment were twice as likely to have unhealed ulcers after 1 year than those who received the active treatment. For venous ulcers, hyperbaric oxygen therapy conferred a small benefit in relation to wound size reduction at 6 weeks, but no effect was observed at the 18-week follow-up.150 Overall, it would appear that hyperbaric oxygen therapy may have some value in the prevention of major amputations; however, issues associated with access and cost-effectiveness currently preclude its wider clinical use.
Therapeutic ultrasound and short-wave diathermy Therapeutic ultrasound involves the application of high-frequency sound waves to the body, which are thought to stimulate wound healing via cavitation (the formation of microscopic vibrating cavities in tissues), increased uptake of calcium ions by fibroblasts, the release of serotonin from platelets and the release of histamine from mast cells.151–153 Seven trials have been undertaken to assess the effectiveness of ultrasound in the management of venous ulcers: four compared ultrasound therapy with sham ultrasound and three compared ultrasound therapy with standard treatment. Although there was a trend towards increased healing rates in the ultrasound groups, none of the trials found a difference in healing rates between any of the therapies.154 Similarly, three trials of ultrasound for pressure ulcers (including two comparing ultrasound with a sham ultrasound and one comparing ultrasound plus ultraviolet light to laser and standard treatment) found no evidence of benefit associated with the use of ultrasound.155 Short-wave diathermy (SWD) refers to the application of the non-ionising form of radiation (from the radio wave portion of the electromagnetic spectrum) to tissues and has been used for wound healing since the 1940s. The electrical stimulation is thought to have a direct effect on the proliferation and migration of fibroblasts in damaged tissue.156 Only three randomised controlled trials have been undertaken: two comparing the use of SWD with sham therapy and one comparing SWD with topical treatments. Only one trial found a difference in healing rates between SWD and sham therapy; however, this difference was not statistically significant.157 Based on these results,
it was concluded that there is no solid evidence that SWD is beneficial in the management of venous ulcers.
Dietary supplements Vitamins and trace elements are known to be important for wound healing, and several case-control studies have shown that people with chronic leg ulcers have significantly lower serum levels of vitamins A and C and the trace minerals zinc and iron.158,159 Zinc is considered to be particularly important, as it has antiinflammatory effects on phagocytic cells and is necessary for the function of a number of enzymes and hormones.160 In response to these observations, several trials of oral zinc sulphate supplementation have been undertaken in people with venous ulcers. Overall, there is no solid evidence of a beneficial effect of treatment with zinc sulphate on the number of ulcers healed.160 Similarly, no firm conclusions could be reached pertaining to efficacy of nutritional interventions in healing pressure ulcers,161 although one study has shown that the provision of a multivitamin and mineral supplement is effective in preventing pressure ulcers in critically ill older people admitted to hospital.162
Pentoxifylline Pentoxifylline is an oral medication that increases microcirculatory blood flow and oxygenation of tissues, possibly by increasing fibrinolytic activity and by decreasing blood viscosity and platelet aggregation.163,164 Nine trials have been conducted to ascertain the effectiveness of pentoxifylline in the management of venous ulcers. Pooling eight trials that compared pentoxifylline with placebo (with or without compression therapy) demonstrated that pentoxifylline is more effective than placebo in terms of complete ulcer healing or significant reduction in ulcer size, and pentoxifylline plus compression is more effective than placebo plus compression. Pentoxifylline therefore appears to be an effective adjunct to compression bandaging for treating venous ulcers.165
Skin grafting Skin grafting is generally only considered in the management of chronic, recurrent ulcers that have failed to respond to other conservative treatment approaches. Broadly speaking, there are three types of skin graft:
Foot ulceration
autografts (skin taken from another part of the body of the patient), allografts (skin taken from another person) and xenografts (skin taken from another species, most commonly from pigs). More recently, a fourth category – bioengineered human skin equivalents – has become available; these are products that consist of a matrix embedded with collagen, fibroblasts and keratinocytes derived from various sources, including neonatal foreskins and bovine skin.166 The actual mechanism of action of these products is unclear but is thought to be related to the stimulation of growth factors and cytokines within the wound.167 A recent review of nine trials of skin grafting for venous ulcers indicated that a bilayer bioengineered human skin equivalent used in combination with compression bandaging was more effective than a simple dressing.168 Several recent trials have also reported promising results with the use of bioengineered human skin equivalents in the management of non-infected diabetic foot ulcers;169–171 however, it is essential that such a treatment is used in conjunction with debridement and offloading techniques. The cost-effectiveness of these products also needs to be carefully considered. A recent review of tissue-engineered biological dressings concluded that, while there is some evidence of efficacy, this intervention may be best viewed as a niche application where the likelihood of a positive outcome is high and the substantial costs can be justified.172
Management of wound infection The recognition and appropriate management of infection is an essential component of effective wound care, as the presence of infection significantly delays wound healing and failure to recognise local infection may result in serious complications such as osteomyelitis and septicaemia.173 Wound infection is best viewed as a continuum, extending from contamination (defined as the presence of a stable population of microorganisms) through to colonisation (the presence of a population of replicating microorganisms without harm to the host) and eventually infection (the presence of a population of replicating microorganisms associated with damage to the host)174 (Fig. 7.16). Whether a wound progresses to infection is influenced by several factors related to the dose and virulence of the microorganisms present, the characteristics of the wound itself (e.g. the location, size, depth and duration of the wound, the presence of necrotic tissue or foreign bodies), underlying systemic
A
B
Figure 7.16 Colonised (A) and infected (B) leg ulcers. (Courtesy of Nikki Frescos, La Trobe University.)
conditions (particularly peripheral vascular disease and diabetes), the use of immunosuppressive medications and behavioural issues (including compliance with treatment, smoking, drug or alcohol use and diet).175 The classic signs and symptoms of wound infection include pain, erythema, oedema, increased temperature and the presence of purulent exudate within the wound. However, there are additional signs of infection that are specific to chronic wounds, including serous exudate (thin watery fluid on the surface of the wound), pale, dusky or friable granulation tissue, the formation of smooth pockets at the base of the wound, and putrid odour.176 If clinical observations are suggestive of infection, further examinations, such as wound swabs or biopsy should be performed, particularly if the use of antibiotics is being considered. Both techniques have advantages and disadvantages. Although swab cultures are non-invasive and relatively simple to perform, the results are essentially qualitative and are often inconclusive in chronic
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PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION
Signs of infection
No sign of infection, but delayed healing
Limited to wound only
Spreading local sepsis
Systemic signs
Are other risk factors present?
Select topical antiseptic
Consider combination therapy and obtain culture
Start broadspectrum antibiotics while awaiting culture results
Treat underlying aetiology or refer to appropriate specialist
Are there overt signs that the infection has been eliminated?
Has there been a good clinical response?
Yes
Yes
If no improvement or if subtle signs of infection are present or there is a positive culture result
No
Select alternative antiseptic and consider antibiotic
Complete the antibiotic course
No
Adjust antibiotic according to causative agent
Stop antiseptic therapy, continue other treatment, monitor wound progress
Figure 7.17 Clinical treatment algorithm for managing wound infection, adapted from the European Wound Management Association position statement. (The complete document is available at www.ewma.org.)
wounds. Wound biopsy is the gold standard technique for identifying the type and magnitude of infection; however, the process is invasive and may delay healing by damaging the wound bed.174 Management of infected wounds involves the use of topical antiseptics and/or systemic antibiotics, depending on the level of infection. A step-by-step algorithm recently published by the European Wound Management Association is a useful guide for clinical practice. A simplified version of the algorithm is shown in Figure 7.17, and the full position statement can be found at www.ewma.org. Depending on the foot specialist’s scope of practice, adequate management of infected wounds may require referral to a
physician or multidisciplinary wound clinic. Generally speaking, wounds that are colonised or show signs of local infection can be managed with wound cleansing and debridement followed by appropriate topical iodine- or silver-based antiseptics, medical-grade honey or tea tree oil.173,177 However, wounds that show signs of spreading local infection or systemic infection do not appear to benefit from topical therapy and should therefore be managed with systemic antibiotics.178 Consensus regarding the selection of systemic antibiotics remains elusive but is informed by culture results, the microbial coverage of the antibiotic and clinical experience.173 The duration of therapy is also controversial and requires striking a balance
Summary
Table 7.6 Guidelines for the management of arterial ulcers Recommendation
Level of evidence*
Restoration of blood flow by surgical revascularisation is the intervention most likely to lead to healing
II
Intermittent pneumatic leg compression improves blood flow and may be beneficial
II
Removal of necrotic tissue by debridement improves healing
II
In arterial ulcers with dry gangrene, debridement should not be used until arterial supply has been re-established
II
Neuroischaemic ulcers should be treated with a short course of systemic antibiotics even when clinical signs of infection are not present
II
Healing is enhanced with the use of topical warming, correction of dehydration and hyperbaric oxygen therapy
I
Topical antiseptics may be beneficial in the management of heavily colonised wounds
III
Ulcers of mixed aetiology (e.g. arterial ulcers associated with venous insufficiency) may benefit from (a) closely supervised compression therapy or (b) topical negative pressure
III
Closing the ulcer with a skin graft can assist wound healing
III
In arterial ulcers with sufficient arterial flow to enable healing, dressings that encourage moist wound healing are beneficial
II
Dry gangrene is best left dry until revascularisation has been performed
II
There is insufficient evidence for a beneficial effect from (a) ultrasound, (b) electrostimulation or (c) spinal cord stimulation
III, II, II
Pentoxifylline does not improve healing of arterial ulcers
I
Risk factor modification (smoking cessation, diabetes control and treatment of hypertension) can reduce arterial ulceration and recurrence
I
*Level I, meta-analysis of multiple randomised controlled trials (RCTs) or at least two RCTs or multiple laboratory or animal experiments with at least two clinical studies supporting the laboratory results; level II, at least one RCT and at least two significant clinical series or expert opinion papers; level III, suggestive data of proof-of-principle.
between clinical effectiveness and the risk of developing microbial resistance. As a general rule, 2–4 weeks of antibiotic therapy is considered sufficient for most wounds.179
Evidence-based guidelines for comprehensive wound management In 2006, the Wound Healing Society facilitated the development of guidelines for the management of arterial,180 venous,181 diabetic182 and pressure183 ulcers based on the recommendations of an advisory panel of physicians, podiatrists, nurse clinicians and scientists. Inclusion of research findings in these guidelines
was less strict than Cochrane systematic reviews (which are limited to randomised controlled trials); however, the level of evidence for each recommendation was documented. These guidelines are an excellent resource for foot care specialists, and the most relevant components are summarised in Tables 7.6–7.9.
SUMMARY Disorders affecting the peripheral vascular system are extremely common in older people and foot-care specialists will frequently be presented with the lower
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PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION
Table 7.7 Guidelines for the management of venous ulcers Recommendation
Level of evidence*
Class 3 (most supportive) compression therapy improves healing, as does intermittent pressure in patients who cannot tolerate constant compression
I
Removal of necrotic tissue by debridement improves healing
I
Topical antiseptics may enhance healing in colonised, granulating wounds
I
Cellulitis should be treated with systemic Gram-positive bactericidal antibiotics
II
Systemic diseases, medications and nutrition should be assessed and managed
II
Wounds should be cleansed initially and at each dressing change with the minimum possible trauma
III
Select a dressing that promotes moist wound healing, minimises exudate and manages periwound maceration
I
Select a dressing that stays in place and minimises shear and friction
II
Skin grafting without addressing underlying venous disease is not a long-term solution
I
Endoscopic perforator surgery, superficial venous ablation or valvuloplasty can decrease reulceration if combined with compression therapy
I
Cytokine growth factors and oxygen-derived free radical scavengers have not yet been shown to be effective
I
Topical negative pressure may be beneficial
II
Laser therapy and ultrasound have not been shown to be effective
I
Sclerosing superficial veins as an adjunct to compression therapy is effective
III
Oral zinc supplementation is not effective
I
Patients with healed ulcers should continue to use compression therapy
I
Exercise to increase the function of the calf muscle pump are effective in ulcer prevention
III
*Level I, meta-analysis of multiple randomised controlled trials (RCTs) or at least two RCTs or multiple laboratory or animal experiments with at least two clinical studies supporting the laboratory results; level II, at least one RCT and at least two significant clinical series or expert opinion papers; level III, suggestive data of proof-of-principle.
limb manifestations of vascular disease, particularly foot ulceration. A thorough lower limb vascular assessment is essential, as is the appropriate referral of patients to vascular specialists and endocrinologists for medical management of the underlying cause of the skin breakdown. Although the vast array of treat-
ment options available for managing wounds can be somewhat perplexing, evidence from systematic reviews and recent clinical guidelines provides an excellent source of unbiased information regarding the efficacy of these interventions.
Summary
Table 7.8 Guidelines for the management of diabetic ulcers Recommendation
Level of evidence*
Protective footwear should be prescribed
II
Off-loading techniques to relieve pressure can enhance healing
I
Removal of necrotic tissue by debridement improves healing
II
Topical antiseptics may enhance healing in colonised, granulating wounds
I
Systemic antibiotics for acute infections not confined to the wound are effective
II
Cellulitis should be treated with systemic Gram-positive bactericidal antibiotics
II
If osteomyelitis is suspected, appropriate diagnostic measures (sterile probe, X-rays, MRI, CT, bone scan) should be performed
II
Osteomyelitis is best treated by removal of infected bone and 2–4 weeks of antibiotics
II
Systemic diseases, medications and nutrition should be assessed and managed
I
Wounds should be cleansed initially and at each dressing change with the minimum possible trauma
III
Patients who fail to show a reduction in ulcer size by 40% or more after 4 weeks should be re-evaluated
II
Optimising glucose control improves wound healing
III
Select a dressing that promotes moist wound healing
III
Select a dressing that will manage wound exudate and protect periwound skin
I
Select a dressing that stays in place and minimises shear and friction
II
Achilles tendon lengthening may improve healing
II
Patients with ischaemia should be considered for revascularisation
II
Platelet-derived growth factor is effective in treating neurotrophic foot ulcers
I
Cytokine growth factors have not yet been found to be effective
I
Topical negative pressure may be beneficial
I
Electrical stimulation may be beneficial
I
Hyperbaric oxygen therapy reduces amputation rates in patients with ischaemic diabetic ulcers
I
Patients with healed diabetic ulcers should use protective footwear to prevent recurrence
II
Foot care and daily inspection of the feet reduces recurrence
II
*Level I, meta-analysis of multiple randomised controlled trials (RCTs) or at least two RCTs or multiple laboratory or animal experiments with at least two clinical studies supporting the laboratory results; level II, at least one RCT and at least two significant clinical series or expert opinion papers; level III, suggestive data of proof-of-principle. CT, computed tomography; MRI, magnetic resonance imaging.
141
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PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION
Table 7.9 Guidelines for the management of pressure ulcers Recommendation
Level of evidence*
Remove pressure from ulcer site and establish a repositioning schedule
II
Elevating the head of the bed increases shear and should be avoided where possible
III
Pressure-reducing surfaces are more effective than standard hospital mattresses
I
Avoid doughnut-like devices
III
Assess patient nutrition and encourage supplementation where necessary
II
Removal of necrotic tissue by debridement improves healing
I
Obtain bone biopsy in cases of suspected osteomyelitis
II
Confirmed osteomyelitis should be treated with bone debridement and antibiotics
I
Systemic diseases and medications should be assessed and managed
II
Wounds should be cleansed with mild soap and water with minimum trauma
II
Select a dressing that promotes moist wound healing
I
Select a dressing that manages wound exudate and protects periwound skin
I
Select a dressing that stays in place and minimises shear, friction, skin irritation and pressure
II
Consider surgical closure for chronic pressure wounds
II
Growth factors may be beneficial
II
Topical negative pressure may be beneficial for ulcers that fail to heal with conventional therapy
I
Electrical stimulation may be beneficial for ulcers that fail to heal with conventional therapy
I
Hyperbaric oxygen therapy has not been shown to be effective
I
*Level I, meta-analysis of multiple randomised controlled trials (RCTs) or at least two RCTs or multiple laboratory or animal experiments with at least two clinical studies supporting the laboratory results; level II, at least one RCT and at least two significant clinical series or expert opinion papers; level III, suggestive data of proof-of-principle.
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107. Abbott CA, Carrington AL, Ashe H et al. The North-West diabetes foot care study: incidence of, and risk factors for, new diabetic foot ulceration in a community-based cohort. Diabetic Medicine 2002; 20: 377–384. 108. Manes C, Papazoglou N, Sassidou E et al. Prevalence of diabetic neuropathy and foot ulceration: identification of potential risk factors – a populationbased study. Wounds 2002; 14: 11–15. 109. Muller IS, DeGraw WJ, vanGerwen WH. Foot ulceration and lower limb amputation in type 2 diabetic patients in Dutch primary care. Diabetes Care 2002; 25: 570–574. 110. Dunn JE, Link CL, Felson DT et al. Prevalence of foot and ankle conditions in a multiethnic community sample of older adults. American Journal of Epidemiology 2004; 159: 491–498. 111. Moffatt CJ, Franks PJ, Doherty DC et al. Prevalence of leg ulceration in a London population. Quarterly Journal of Medicine 2004; 97: 431–437. 112. Young MJ, Breddy JL, Veves A et al. The prediction of diabetic neuropathic foot ulceration using vibration perception thresholds. Diabetes Care 1994; 17: 557–560. 113. Abbott CA, Vileikyte L, Williamson S et al. Multicentre study of the incidence of and predictive risk factors for diabetic neuropathic foot ulceration Diabetes Care 1998; 21: 1071–1075. 114. Frykberg RG, Lavery LA, Pham H et al. Role of neuropathy and high foot pressures in diabetic foot ulceration. Diabetes Care 1998; 21: 1714–1719. 115. Pham H, Armstrong DG, Harvey C et al. Screening techniques to identify people at high risk for diabetic foot ulceration: a prospective multicentre trial. Diabetes Care 2000; 23: 606–611. 116. Kastenbauer T, Sauseng S, Sokol G et al. A prospective study of predictors for foot ulceration in type 2 diabetes. Journal of the American Podiatric Medical Association 2001; 91: 343–350. 117. Boyko EJ, Ahroni JH, Cohen V et al. Prediction of diabetic foot ulcer occurrence using commonly available clinical information: the Seattle Diabetic Foot Study. Diabetes Care 2006; 29: 1201– 1207. 118. Boyko EJ, Ahroni JH, Stensel V et al. A prospective study of risk factors for diabetic foot ulcer. The Seattle Diabetic Foot Study. Diabetes Care 1999; 22: 1036–1042. 119. Veves A, Murray HJ, Young MJ et al. The risk of foot ulceration in diabetic patients with high foot pressure: a prospective study. Diabetologia 1992; 35: 660–663. 120. Murray HJ, Young MJ, Hollis S et al. The association between callus formation, high pressures and neuropathy in diabetic foot ulceration. Diabetic Medicine 1996; 13: 979–982.
121. Weir D. Pressure ulcers: assessment, classification, and management. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic wound care: a clinical source book for healthcare professionals, 3rd ed. Wayne: HMP Communications; 2001: 619– 627. 122. Holloway GA. Arterial ulcers: assessment, classification, and management. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic wound care : a clinical source book for healthcare professionals, 3rd ed. Wayne: HMP Communications; 2001: 495–503. 123. Chan CLH, Meyer FJ, Hay RJ et al. Toe ulceration associated with compression bandaging: observational study. British Medical Journal 2001; 323: 1099. 124. Sibbald RG, Williamson D, Falanga V et al. Venous leg ulcers. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic wound care : a clinical source book for healthcare professionals, 3rd ed. Wayne: HMP Communications; 2001: 483–494. 125. Perell KL, Merrill V, Nouvong A. Location of plantar ulcerations in diabetic patients referred to a Department of Veterans Affairs podiatry clinic. Journal of Rehabilitation Research and Development 2006; 43: 421–426. 126. Steed DL. Diabetic wounds: assessment, classification, and management. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic wound care : a clinical source book for healthcare professionals, 3rd ed. Wayne: HMP Communications; 2001: 575–581. 127. Krasner D, Cuzzell J. Pressure ulcers. In: Gogia PP, eds. Clinical wound management. Thorofare, NJ: Slack; 1995: 85–96. 128. Sieggreen MY. Arterial insufficiency and ulceration: diagnosis and treatment options. Advances in Skin and Wound Care 2004; 17: 242–251. 129. Hellewell TB, Major DA, Foresman PA et al. A cytotoxicity evaluation of antimicrobial and non antimicrobial wound cleansers. Wounds 1997; 9: 15–20. 130. Fernandez R, Griffiths R, Ussia C. Water for wound cleansing. Cochrane Database of Systematic Reviews 2002; 4: CD003861. 131. Moore ZEH, Cowman S. Wound cleansing for pressure ulcers. Cochrane Database of Systematic Reviews 2005; 4: CD004983. 132. Bradley M, Cullum N, Sheldon T. The debridement of chronic wounds: a systematic review. Health Technology Assessment 1999; 3: 1–2. 133. Smith J. Debridement of diabetic foot ulcers. Cochrane Database of Systematic Reviews 2002; 4: CD003556. 134. Young MJ, Cavanagh PR, Thomas G et al. The effect of callus removal on dynamic plantar foot pressures in diabetic patients. Diabetic Medicine 1992; 9: 55–57.
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135. Pitei DL, Foster A, Edmonds M. The effect of regular callus removal on foot pressures. Journal of Foot and Ankle Surgery 1999; 38: 251–255. 136. Pataky Z, Golay A, Faravel L et al. The impact of callosities on the magnitude and duration of plantar pressure in patients with diabetes mellitus. Diabetes and Metabolism 2002; 28: 356–361. 137. Ovington L, Peirce B. Wound dressings: form, function, feasibility, and facts. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic wound care : a clinical source book for healthcare professionals, 3rd ed. Wayne: HMP Communications; 2001: 311–320. 138. Turner TD. Control the environment to heal the wound. Chemist and Druggist 1985; 2: 438–444. 139. Nelson EA, Bradley MD. Dressings and topical agents for arterial leg ulcers. Cochrane Database of Systematic Reviews 2003; 1: CD001836. 140. Springett K. Management of tissue viability. In: Turner WA, Merriman LM, eds. Clinical skills in treating the foot, 2nd ed. Edinburgh: Elsevier Churchill Livingstone; 2005: 431–462. 141. Boulton AJ. Pressure and the diabetic foot: clinical science and offloading techniques. American Journal of Surgery 2004; 187: S17–24. 142. Spencer S. Pressure relieving interventions for preventing and treating diabetic foot ulcers. Cochrane Database of Systematic Reviews 2000; 3: CD002302. 143. Cullum N, McInnes E, Bell-Syer SEM et al. Support surfaces for pressure ulcer prevention. Cochrane Database of Systematic Reviews 2004; 3: CD001735. 144. Tymec AC, Pieper B, Vollman K. A comparison of two pressure relieving devices on the prevention of heel pressure ulcers. Advances in Wound Care 1997; 10: 39–44. 145. Brown AC, Coutts P, Sibbald RG. Compression therapies. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic wound care: a clinical source book for healthcare professionals, 3rd ed. Wayne: HMP Communications; 2001: 517–524. 146. Nelson EA, Bell-Syer SEM, Cullum NA. Compression for preventing recurrence of venous ulcers. Cochrane Database of Systematic Reviews 2000; 4: CD002303. 147. Banwell PE. Topical negative pressure therapy in wound care. Journal of Wound Care 1999; 8: 79–84. 148. Evans D, Land L. Topical negative pressure for treating chronic wounds. Cochrane Database of Systematic Reviews 2001; 1: CD001898. 149. Wang C, Schwaitzberg S, Berliner E et al. Hyperbaric oxygen for treating wounds: A systematic review of the literature. Archives of Surgery 2003; 138: 272–279.
150. Kranke P, Bennett M, Roeckl-Wiedmann I et al. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database of Systematic Reviews 2004; 1: CD004123. 151. TerHaar GR, Daniels S. Evidence for ultrasonically induced cavitation in vivo. Physics in Medicine and Biology 1981; 26: 1145–1149. 152. Dyson M. Mechanisms involved in therapeutic ultrasound. Physiotherapy 1987; 73: 116–120. 153. Mortimer AJ, Dyson M. The effect of therapeutic ultrasound on calcium uptake in fibroblasts. Ultrasound in Medicine and Biology 1988; 14: 499–506. 154. Flemming K, Cullum N. Therapeutic ultrasound for venous leg ulcers. Cochrane Database of Systematic Reviews 2000; 4: CD001180. 155. Sari AB-A, Flemming K, Cullum NA et al. Therapeutic ultrasound for pressure ulcers. Cochrane Database of Systematic Reviews 2006; 3: CD001275. 156. Weiss DS, Kirsner R, Eaglstein WH. Electrical stimulation and wound healing. Archives of Dermatology 1990; 126: 222–225. 157. Ravaghi H, Flemming K, Cullum N et al. Electromagnetic therapy for treating venous leg ulcers. Cochrane Database of Systematic Reviews 2006; 2: CD002993. 158. Agren MS, Stromberg H-E, Rindby A et al. Selenium, zinc, iron and copper levels in serum of patients with arterial and venous leg ulcers. Acta Dermato-venereologica 1986; 66: 237– 240. 159. Balaji P, Mosley JG. Evaluation of vascular and metabolic deficiency in patients with large leg ulcers. Annals of the Royal College of Surgeons 1995; 77: 270–272. 160. Wilkinson EAJ, Hawke C. Oral zinc for arterial and venous leg ulcers. Cochrane Database of Systematic Reviews 1998; 4: CD001273. 161. Langer G, Schloemer G, Knerr A et al. Nutritional interventions for preventing and treating pressure ulcers. Cochrane Database of Systematic Reviews 2003; 4: CD003216. 162. Bourdel-Marchasson I, Barateau M, Rondeau V et al. A multi-centre trial of the effects of oral nutritional supplementation in critically ill older inpatients. Nutrition 2000; 16: 1–5. 163. James DR, Holland BM, Hughes MR et al. Oxpentifylline: effects on red cell deformability and oxygen availability from the blood in intermittent claudication. Clinical Hemorheology 1984; 4: 525–531. 164. Brenner MA. Nonhealing venous stasis ulcers: pentoxifylline as adjunctive therapy. Journal of the American Podiatric Medical Association 1987; 77: 586–588.
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165. Jull AB, Waters J, Arroll B. Pentoxifylline for treating venous leg ulcers. Cochrane Database of Systematic Reviews 2002; 1: CD001733. 166. Williamson D, Sibbald RG. Skin substitutes. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic wound care : a clinical source book for healthcare professionals, 3rd ed. Wayne: HMP Communications; 2001: 541–552. 167. Marston WA. Dermagraft, a bioengineered human dermal equivalent for the treatment of chronic nonhealing diabetic foot ulcer. Expert Reviews of Medical Devices 2004; 1: 21–31. 168. Jones JE, Nelson EA. Skin grafting for venous leg ulcers. Cochrane Database of Systematic Reviews 2000; 2: CD001737. 169. Veves A, Falanga V, Armstrong DG et al. Graftskin, a human skin equivalent, is effective in the management of noninfected neuropathic diabetic foot ulcers. Diabetes Care 2001; 24: 290–295. 170. Caravaggi C, DeGiglio R, Pritelli C et al. HYAFF 11-based autologous dermal and epidermal grafts in the treatment of noninfected diabetic plantar and dorsal foot ulcers. Diabetes Care 2003; 26: 2853–2859. 171. Marston WA, Hanft J, Norwood P et al. The efficacy and safety of Dermagraft in the improving the healing of chronic diabetic foot ulcers. Diabetes Care 2003; 26: 1701–1705. 172. Ehrenreich M, Ruszczak Z. Update on tissue-engineered biological dressings. Tissue Engineering 2006; 12: 2407–2424. 173. Frank C, Bayoumi I, Westendorp C. Approach to infected skin ulcers. Canadian Family Physician 2005; 51: 1352–1359. 174. Dow G. Infection in chronic wounds. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic
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CHAPTER
Disorders of the toes
HALLUX VALGUS
CHAPTER CONTENTS Hallux valgus 149 Classification and clinical presentation Aetiology 150 Assessment and diagnosis 153 Treatment 153
150
Hallux limitus and hallux rigidus 157 Classification and clinical presentation 158 Aetiology 158 Assessment and diagnosis 161 Treatment 162 Lesser toe deformities 165 Classification and clinical presentation Aetiology 166 Assessment and diagnosis 167 Treatment 167 Less common disorders affecting the toes 168 Tailor’s bunion 168 Hallux varus 169 Gouty arthritis 169 Summary 170 References 171
8
165
Hallux valgus (also referred to as hallux abductovalgus) is a common condition affecting the forefoot in which the first metatarsophalangeal joint is progressively subluxed as a result of lateral deviation of the hallux and medial deviation of the first metatarsal.1,2 The condition is frequently accompanied by a painful soft tissue and osseous prominence on the medial aspect of the first metatarsal head, commonly referred to as a ‘bunion’ (Fig. 8.1). As the deformity progresses, the lateral displacement of the hallux interferes with the normal alignment and function of the lesser toes, resulting in hammer toe or claw toe deformities, altered weightbearing patterns and the development of plantar keratotic lesions. Pressure from footwear may also lead to the formation of an adventitious bursa over the joint, which may become inflamed (Fig. 8.2).3 The exact prevalence of hallux valgus is difficult to determine because of the paucity of largescale epidemiological studies and varying definitions used in the literature. In people aged over 65 years of age, prevalence rates ranging from 5% to 37% have been reported.4–9 Women are significantly more likely to develop hallux valgus than men, with sex ratios as high as 9 : 1.1,2 The condition has a significant impact on balance10 and gait patterns11 and is an independent risk factor for falls.12 A recent study also demonstrated that people with hallux valgus exhibited significantly lower scores on a health-related quality of life questionnaire,13 suggesting that the condition has a much broader impact than local pain and discomfort.
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A
Figure 8.2 Bursal inflammation resulting from footwear pressure in an older person with hallux valgus deformity. (Courtesy of Mark Gilheany, East Mebourne Podiatry.)
Table 8.1 Classification of hallux valgus according to radiographic measurements
B
Figure 8.1A, B Severe hallux valgus. (Courtesy of Lesley Newcombe, La Trobe University.)
CLASSIFICATION AND CLINICAL PRESENTATION Hallux valgus is generally deemed to be present when the angle formed by the bisection of the first metatarsal and the proximal phalanx (the hallux abductus angle) is greater than 15° and the angle formed by the bisection of the first metatarsal and second metatarsal (the intermetatarsal angle) is greater than 9°.1,14 Several classification systems have been proposed based on the degree of angular deformity and the severity of symptoms, primarily to assist in the selection of surgical procedures. Mann15 has proposed a simple grading system based on the hallux abductus and intermetatarsal angles, which has been widely adopted for presurgical planning (Table 8.1). The simplest clinical grading system is the Manchester scale,16 which consists of four standardised photos covering the spectrum of the deformity (Fig. 3.6). A recent study by Menz & Munteanu17 showed that
Classification
Hallux abductus angle (°)
Intermetatarsal angle (°)
Mild Moderate Severe
<20 20–40 >40
<11 11–16 >16
gradings using this scale were significantly associated with hallux abductus and intermetatarsal angles obtained from foot radiographs. Although this scale does not provide any information regarding the degree of joint degeneration or sesamoid displacement, it is a very useful tool for documenting the overall severity of angular displacement of the hallux in clinical settings where radiographs are not readily available or are considered unnecessary.
AETIOLOGY The aetiology of hallux valgus is not well understood. There is some evidence that the condition is an autosomal dominant trait with partial penetrance, as between 58% and 90% of people with hallux valgus report a familial tendency.1,18,19 Johnston20 documented 101 family members across seven generations and reported that all but two affected parents passed
Hallux valgus
the condition on to their children. More recently, Pique-Vidal et al19 constructed pedigree charts from 350 patients across three generations and found that family history was positive in 90% of cases, with vertical transmission affecting some families across all three generations. However, because congenital hallux valgus is extremely rare, it appears that some intrinsic structural or functional tendency is inherited that may take several decades to develop into hallux valgus. Because of this prolonged timeframe, our understanding of potential risk factors is limited to casecontrol studies, which provide evidence of association but not causation. Indeed, many of the proposed risk factors for hallux valgus could plausibly be argued to be consequences of the condition rather than causes. The most commonly proposed aetiological factors for hallux valgus are footwear, metatarsus primus varus, long first metatarsal, metatarsal head shape, muscle dysfunction and foot pronation. Each of these factors is briefly outlined below; however, for a more comprehensive discussion, the reader is referred to Kilmartin & Wallace.21
Footwear The suggestion that footwear may be a contributing factor to the development of hallux valgus is driven by three major observations reported in the literature: the very low prevalence of the condition in people who do not wear shoes,22–24 the increase in prevalence observed when footwear is introduced into previously non-shoewearing populations25–29 and the significantly higher prevalence of the condition in women, many of whom wear shoes with an elevated heel and narrow toebox.30 It is physiologically plausible that wearing narrow-fitting shoes may result in the foot adapting to the confined space within the shoe via lateral deviation of the hallux and that, over time, soft tissue contracture and bony remodelling may cause the foot to assume this new position. The contribution of heel elevation is less clear, as many shoes with an elevated heel also have a narrow toe box, making a delineation between the contribution of each feature difficult. However, there is evidence that heel elevation alters the kinematics of the first metatarsophalangeal joint31,32 and leads to a medial shift in weightbearing pressures during gait,33–36 factors that may contribute to the gradual lateral displacement of the hallux. While the contribution of footwear to the development of hallux valgus is unlikely to be adequately resolved, it is clear that the condition is more common
among people who wear shoes and, at the very least, the wearing of ill-fitting shoes is likely to aggravate pre-existing hallux valgus, particularly in those with a very broad forefoot.3
Metatarsus primus varus Metatarsus primus varus (also referred to as metatarsus primus adductus) refers to excessive angulation of the first metatarsal relative to the second metatarsal, and is generally considered to be present when the intermetatarsal angle is greater than 14°.37 Metatarsus primus varus is an inherent anatomical variant caused by the oblique orientation of the first metatarsocuneiform joint, and is thought to predispose to hallux valgus as a result of the bowstringing of the flexor hallucis longus tendon pulling the proximal phalanx into an abducted position.38 However, while there is a strong correlation between metatarsus primus varus and hallux valgus,1 it has also been observed that, as the lateral deviation of the hallux increases with increasing severity of the condition, the intermetatarsal angle also increases.17 As such, it is also possible that metatarsus primus varus is a result, rather than a cause, of hallux valgus.
Long first metatarsal An overly long first metatarsal as a potential cause of hallux valgus was first proposed by Hardy & Clapham,1 who reported that the first metatarsal was on average 4 mm longer than the second metatarsal in 91 patients with hallux valgus, compared to an average of 2 mm longer in 84 people without hallux valgus. Similar results were reported in two subsequent studies.39,40 The proposed mechanism for the relationship between long first metatarsal and hallux valgus is simply that the longer first ray segment is more likely to undergo compression from footwear and, because of the angulation of the first metatarsal relative to the second, the hallux is predisposed to deviate laterally towards the lesser toes.40 As it is unlikely that hallux valgus will lead to a lengthening of the first metatarsal, causality is perhaps more convincing for long first metatarsal than for other hypothesised intrinsic factors.
Metatarsal head shape Two broad categories of the shape of the first metatarsal head were identified by Mann & Coughlin2 in 1981 – round and square. Theoretically, hallux valgus
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would be more likely to occur in feet with a round first metatarsal head, as this articular configuration would facilitate the transverse plane rotation of the proximal phalanx. In contrast, a square first metatarsal head would act to resist transverse plane forces placed on the hallux from footwear.14 There is limited evidence to support metatarsal head shape as a contributing factor to hallux valgus. Indeed, a study of 50 children with hallux valgus found that 40 exhibited square metatarsal heads.41 Furthermore, establishing such a relationship in older people with hallux valgus would be difficult, as arthritic degeneration in longstanding hallux valgus results in marked changes to the architecture of the metatarsal head.
Muscle dysfunction Several authors have suggested that an imbalance between the abductor and adductor hallucis muscles, with the latter overpowering the former, may have the effect of pulling the proximal phalanx laterally, thereby initiating the development of hallux valgus.2,42 Electromyographic studies have confirmed that there is indeed a reduction in abductor hallucis muscle activity in people with hallux valgus;43,44 however, whether this occurs before or after the condition develops is unknown. Anomalous tendon insertions have also been proposed as a potential cause of hallux valgus; however, extensive cadaver studies by Brenner failed to find any differences in the insertion patterns of either tibialis anterior45 or abductor hallucis46 in feet with or without the condition.
First ray hypermobility Three case-control studies have provided evidence of the proposed relationship between hypermobility of the first ray and hallux valgus. Ito et al47 compared changes in the lateral talo-first metatarsal angle from non-weightbearing to weightbearing in 32 people with hallux valgus and 23 controls, and found that those with hallux valgus underwent a greater reduction in this angle when bearing weight (indicative of greater dorsiflexion of the first ray). Consistent with this finding, Glasoe et al48 reported that 14 people with hallux valgus exhibited greater dorsal mobility of the first ray compared to age- and sex-matched controls when a controlled dorsiflexory force of 55 Newtons was applied to the first metatarsal head. Finally, Lee & Young49 measured first ray dorsiflexion and metatarsal length 60 hallux valgus cases and 40
controls and reported that the hallux valgus group exhibited slightly greater dorsiflexory motion (12.9° versus 10.3°).
Foot pronation The proposed association between pronated/flat feet and hallux valgus dates back as far as 189321 but, despite several authors noting that the condition seems to be more common in people with flat feet,50 there have been few case-control studies conducted to adequately address this relationship. The theory espoused by Root et al,51 widely adopted by the podiatry profession, suggests that subtalar joint pronation renders the forefoot hypermobile, thereby allowing ground reaction forces to dorsiflex and invert the first metatarsal, which then results in erosion of the intersesamoidal ridge by the tibial sesamoid and subsequent lateral displacement of the proximal phalanx. Evidence to support this assertion is scarce. Indeed, two studies comparing foot posture measurements between children with and without hallux valgus have failed to find any significant differences between the two groups.52,53 In contrast, Kernozek et al54 recently reported that 40 patients with hallux valgus had a significantly more everted calcaneal stance position (indicative of greater foot pronation) compared to 51 controls. Because of significant variations in definitions of the flat or pronated foot, it is difficult to directly compare these findings. Furthermore, the relationship between static foot structure and dynamic function is, at best, only moderate,55 so until comparisons are made using kinematic models the relationship between foot function and hallux valgus will remain elusive.
Other potential causes of hallux valgus In addition to the proposed intrinsic risk factors described above, hallux valgus has been observed to develop secondary to several other systemic conditions, including a range of inflammatory joint diseases (e.g. rheumatoid arthritis, gout and psoriatic arthropathy), conditions associated with ligamentous laxity (e.g. Ehlers–Danlos syndrome, Marfan’s syndrome and Down’s syndrome), and neuromuscular disorders (e.g. cerebral palsy, poliomyelitis and Charcot–Marie– Tooth disease). Iatrogenic hallux valgus may also develop secondary to surgical removal of the tibial sesamoid.15
Hallux valgus
ASSESSMENT AND DIAGNOSIS Assessment and diagnosis of hallux valgus is relatively straightforward. Patients will typically present with an enlarged and painful first metatarsophalangeal joint, with symptoms exacerbated by weightbearing activity and the wearing of ill-fitting or high-heeled footwear. Physical examination will reveal lateral deviation of the hallux and, depending on the severity of the deformity, overcrowding of the lesser toes may have resulted in the development of hammer- or claw-toe deformities. In severe cases, the second toe may be subluxed at the metatarsophalangeal joint and overor under-ride the deviated hallux. The medial prominence of the first metatarsophalangeal joint (the ‘bunion’) may appear inflamed, and in some cases a fluid-filled bursa may have formed over the enlarged dorsomedial aspect of the joint. The hallux nail may be dystrophic or involuted because of pressure from footwear, and the tendon of extensor hallucis longus may be prominent and laterally displaced because of the gradual weakening of the extensor hood. Changes in weightbearing patterns often give rise to the development of calluses or corns beneath the metatarsal heads, most commonly located under the second metatarsal head because of the hypermobility of the first ray. Further examinations are generally not required to diagnose hallux valgus; however, weightbearing radiographs, particularly dorsoplantar views, enable accurate grading of the deformity and are essential for surgical planning. Several well-established measurements can be derived from a dorsoplantar radiograph: the hallux abductus angle, intermetatarsal angle and hallux interphalangeus abductus angle (Fig. 8.3). This view also provides useful insights into the degree of arthritic degeneration in the joint. Observational gait analysis may reveal reductions in walking speed and step length,11 and plantar pressure analysis will generally reveal a reduction in loading under the hallux and first metatarsal head but a corresponding increase in loading under the lateral metatarsal heads (Fig. 8.4).54,56
Figure 8.3 Hallux valgus angles measured from dorsoplantar radiograph. A. Intermetatarsal angle. B. Hallux abductus angle. C. Hallux interphalangeus abductus angle.
TREATMENT Conservative Conservative management of hallux valgus includes measures to obtain pain relief, addressing the associated nail and skin conditions, and the provision of interventions to realign (or at least slow the progres-
Figure 8.4 Typical plantar pressure output for an older person with hallux valgus.
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sion of) the deformity. All skin lesions and nail disorders should be managed as described in Chapters 3 and 5, with particular emphasis placed on ensuring that lesions are sufficiently palliated and that the contribution of ill-fitting footwear is appropriately addressed. Extra-depth and wider-fitting footwear may need to be prescribed and fitted, and soft, moulded orthoses inserted to offload painful plantar regions. The application of foam or silicon gel pads to offload the medial prominence may also provide some degree of symptomatic improvement.57 Several conservative techniques have been described to reduce the degree of hallux valgus and/or prevent further deformity, including toe splints,58–60 mobilisation and manipulation,61 and foot orthoses.62–64 However, a recent Cochrane systematic review found only two randomised controlled trials of conservative treatments involving adults. Juriansz58 compared a hallux valgus night splint to no treatment in 28 people ranging in age from 10 to 77 years and found no difference in clinically determined degree of deformity. Torkki et al64 compared the effectiveness of surgery, customised orthoses and no treatment in 211 patients and reported that orthoses significantly reduced pain after 6 months compared to no treatment, but this difference was not evident at 12 months. As no radiographs or clinical measurements were taken, it is unclear whether the degree of deformity was affected by treatment. In a randomised controlled trial that was not eligible for inclusion in the Cochrane review, Budiman-Mak et al63 demonstrated that people with rheumatoid arthritis issued with foot orthoses were less likely to exhibit progression of the hallux abductus angle to the no-treatment control group after a 3-year follow-up period. Since the publication of the Cochrane review, two additional conservative treatment studies have been published. Tang et al59 conducted an uncontrolled study of an insole with a toe separator to realign the hallux in 17 patients aged 14–75 years, and reported an average 6.5° reduction in the hallux abductus angle and improvements in pain and walking ability at 3 months. More recently, Brantingham et al61 conducted a randomised controlled trial comparing chiropractic manipulation and mobilisation (including longitudinal distraction and adduction of the hallux) to a sham treatment and reported significant improvements in pain threshold and Foot Function Index scores in the treatment group over a 3-week period. Clearly, further research is required to thoroughly evaluate the efficacy of conservative treatments for
hallux valgus. It is particularly important that such studies include older people, as the degree of arthritic degeneration associated with hallux valgus is likely to influence the likelihood of a successful outcome.
Surgical Surgical intervention for hallux valgus is frequently indicated, as conservative management is generally only effective in alleviating symptoms and has little or no impact on the progression of the deformity or its secondary effects on mobility and quality of life. However, because hallux valgus is quite variable in its presentation, there is no ‘gold standard’ surgical procedure that can be applied to all patients. Rather, the condition needs to be viewed as a syndrome consisting of multiple pathologies, and careful presurgical planning is therefore recommended to achieve optimal outcomes.65 When considering surgical intervention for hallux valgus, the potential adverse effects need to be carefully considered. Although it is difficult to predict the outcome in hallux valgus surgery, Rowley66 has suggested that, in general, 70–80% of patients do well, 10–15% have a satisfactory outcome and 5–10% have an unsatisfactory outcome or are actually worse off following the procedure. However, the recent Cochrane review67 of 18 randomised trials reported that up to one-third of patients were dissatisfied with their surgical result. Common complications associated with hallux valgus surgery include ongoing pain, transfer lesions (the development of lesions at previously lesion-free sites because of changes in foot function), joint stiffness, stress fractures, ‘floating hallux’ (loss of function of the hallux due to plantarflexion weakness) and irritation from internal fixation devices (K-wires and screws).68,69 Two recent studies have also indicated that, while hallux valgus surgery reduces pain and improves quality of life, the appearance of the foot and the range of shoes that can be worn following the procedure are significant predictors of satisfaction with the surgical result.70,71 Over 150 different procedures have been described for hallux valgus, involving bony or soft tissue correction, or a combination of both.67 The simplest procedure is Silver’s bunionectomy,72 which involves the removal of the medial eminence of bone without correcting the underlying angular deformity. More complex procedures may involve fusion of the first metatarsophalangeal joint, displacement of the first metatarsal head, shortening of the first metatarsal,
Hallux valgus
A
B
Figure 8.5 Keller’s arthroplasty. A. Shaded areas to be removed. B. Postoperative result. Note significant shortening of first ray.
plantarflexing or dorsiflexing the first ray, reducing the intermetatarsal angle by removing a wedge of bone from the base of the first metatarsal, and various tendon lengthening and shortening procedures.69 The following section briefly describes some of the more commonly performed techniques. For a more detailed coverage, the reader is referred to a recent comprehensive review by Kilmartin69 and to specialist foot surgery texts.73 The technique now known as the Keller procedure was originally described in the German literature but was translated into English by Keller in 1904.74 This common and technically straightforward procedure involves removing the base of the proximal phalanx and medial eminence of the first metatarsal (Fig. 8.5). As no further correction of the angular deformity is undertaken, recurrence is common and it has therefore been suggested that this procedure is suited to older people who are not physically active.69 The Akin procedure was described in 192575 and involves resection of the medial eminence followed by the removal of a wedge-shaped piece of bone from the base of the proximal phalanx (Fig. 8.6). In contemporary practice, this procedure is rarely undertaken as a stand-alone surgery but may be combined with other osteotomies. In addition to correcting the transverse plane alignment of the hallux, the osteotomy can be angled to provide correction in the frontal plane if required.69 The scarf osteotomy was described in 192669 and is based on (and named after) a joint commonly used in carpentry. The technique involves making a longitudinal, Z-shaped step-cut osteotomy through the metatarsal. The metatarsal head and plantar cortical
A
B
Figure 8.6 Akin procedure. A. Wedge-shaped piece of bone to be removed. B. Fixation with threaded Kirschner wire.
A
B
Figure 8.7 Scarf osteotomy. A. Lateral view of metatarsal showing Z-shaped step cut osteotomy. B. Dorsal view of plantar cortical fragment being rotated laterally.
fragment are then translated laterally and fixed with two compression screws (Fig. 8.7). The scarf osteotomy is particularly useful for correcting large intermetatarsal angles and is comparatively stable; however, it is a technically demanding operation that requires considerable surgical expertise.65 The Lapidus procedure was described in 1934.76 This technique involves removal of the medial prominence, followed by fusion of the metatarsocuneiform joint in conjunction with the insertion of bone chips taken from the medial eminence in the space between the first and second metatarsals. This procedure is considered to be particularly useful for surgical correction of hallux valgus with large intermetatarsal angles and/or arthritic degeneration of the metatar-
155
156
DISORDERS OF THE TOES
A
B
A
B
Figure 8.8 Mitchell osteotomy. A. Shaded section of bone to be removed. B. Metatarsal head displaced laterally and proximally.
Figure 8.9 Wilson osteotomy. A. Shaded section of bone to be removed and oblique cut made through metatarsal neck. B. Distal segment slid laterally and proximally.
socuneiform joint; however, common complications associated with the technique include non-union, overcorrection leading to hallux varus, and development of secondary osteoarthritis in adjacent joints.69 The Mitchell osteotomy, described by Hawkins in 1945,77 involves removing a rectangular section of bone from the metatarsal neck and displacing the metatarsal head laterally and proximally (Fig. 8.8). The procedure invariably results in some shortening of the metatarsal, which may be responsible for the relatively common occurrence of transfer lesions in some patients. A long-term follow-up study of 95 patients (mean follow-up of 21 years) by Fokter et al78 indicated a very high (52%) recurrence rate associated with the procedure. The Wilson osteotomy was developed in the 1950s79 and is similar to the Mitchell osteotomy; however, rather than removing a rectangular section of bone, an oblique osteotomy is made through the metatarsal neck, enabling the metatarsal head to be slid laterally and proximally (Fig. 8.9). As with the Mitchell procedure, transfer lesions and metatarsalgia are relatively common (up to 33%) because of metatarsal shortening.80 The Chevron procedure was first described in 197981 and has become one of the most commonly performed surgical techniques for adult hallux valgus. The procedure involves separating the metatarsal head from the metatarsal neck using a V-shaped osteotomy, sliding the metatarsal head laterally and inserting K-wires or screws to hold the metatarsal head in its new position (Fig. 8.10). The benefits of the technique are its technical simplicity and stability; however,
A
B
Figure 8.10 Chevron osteotomy. A. Lateral view of V-shaped osteotomy through metatarsal neck. B. Metatarsal head slid laterally.
avascular necrosis is relatively common as a result of severing the arterial supply to the metatarsal head.69 Furthermore, it has been suggested that the technique is inappropriate in cases where the intermetatarsal angle is greater than 15°. Basal osteotomies involve making an osteotomy cut through the base of the first metatarsal and then levering the metatarsal laterally to ‘close’ the intermetatarsal angle.65 The two most common types are the closing wedge osteotomy, in which a wedge of bone is removed on the lateral aspect of the base of the first metatarsal, and the crescentic osteotomy, in which a proximally directed concave osteotomy is made 1 cm distal to the metatarsocuneiform joint and the metatarsal is rotated laterally (Fig. 8.11). Basal osteotomies
Hallux limitus and hallux rigidus
A
B
been adequately examined or directly compared to other techniques. The most recent Cochrane review of treatments for hallux valgus67 identified only 18 studies in which patients had been randomly allocated to different interventions, and only one that used a no-treatment control group for comparison.64 Although one study demonstrated that patients undergoing a Chevron osteotomy had better outcomes than patients receiving foot orthoses,64 no surgical techniques were found to be superior to any other and the number of participants expressing dissatisfaction at follow-up was consistently high (25– 33%). Furthermore, three trials comparing procedures as they were originally described to the surgeon’s modification of the technique reported no significant advantages for the modification. Clearly, there is considerable scope for future research into the relative merits of different surgical techniques for hallux valgus.
HALLUX LIMITUS AND HALLUX RIGIDUS
Figure 8.11 Basal osteotomies. A. Crescentic. B. Closing base wedge.
are indicated for the correction of large intermetatarsal angles; however, because the technique results in metatarsal shortening, transfer metatarsalgia is a common complication.69 Arthrodesis (fusion) of the first metatarsophalangeal joint following resection of cartilage from the metatarsal head and proximal phalanx is a destructive procedure that is generally reserved for hallux valgus with severe joint degeneration. Once fused, the hallux position cannot be altered, and for this reason the angle at which the fusion is performed is extremely important. Excessive dorsiflexion may lead to the development of calluses under the first metatarsal head, whereas inadequate dorsiflexion may result in arthritic degeneration of the interphalangeal joint of the hallux.69 For these reasons, arthrodesis is generally a ‘last resort’ and the decision to fuse the joint must be very carefully considered. Despite the large number of surgical procedures that have been described for hallux valgus, few have
Hallux limitus is a condition in which there is a restriction in the range of motion of the first metatarsophalangeal joint. If this progresses to complete fusion of the joint, the term hallux rigidus is used, although the two terms are frequently used interchangeably.82,83 Rzonca et al84 argued that the term hallux equinus should be used to encompass the entire spectrum of the condition; however, this terminology has not been widely adopted. Other less commonly used terms related to the condition are dorsal bunion85 and hallux flexus,86 the former used when there is evidence of an osseous prominence on the dorsal aspect of the joint, and the latter when the resting position of the hallux is in flexion. The condition was first described by Coterill in 188787 and was primarily considered to be an affliction of adolescents that developed in response to trauma (e.g. stubbing the toe) or ill-fitting footwear. Hallux limitus/rigidus is also considered to be common in older people; however, the precise epidemiology is very difficult to determine as the condition is rarely included in large-scale surveys. Furthermore, there is some overlap between hallux limitus/rigidus and osteoarthritis of the first metatarsophalangeal joint, which in one large-scale study was found to affect 44% of people over the age of 80 years.88 There is a general consensus that women are affected twice as commonly as men.89
157
158
DISORDERS OF THE TOES
In addition to ‘structural’ hallux limitus/rigidus, an additional ‘functional’ form of the condition has been proposed. Functional hallux limitus describes a condition in which there is normal range of motion at the first metatarsophalangeal joint when measured non-weightbearing; however, there is a reduced range of dorsiflexion evident during the propulsive phase of gait.90 The initial cause of this limitation is unclear; however, several authors have suggested that functional hallux limitus is a precursor to structural hallux limitus/rigidus.83,91
CLASSIFICATION AND CLINICAL PRESENTATION Several classification systems for hallux limitus/rigidus have been proposed, based on radiographic criteria alone92–95 or a combination of radiographic and clinical features.82–84,96 However, few of these scales have been adequately validated and no direct comparisons between the scales have been undertaken. A summary of three of the most commonly reported scales (Regnauld,92 Hattrap & Johnson93 and Coughlin & Shurnas97) is provided in Table 8.2. Perhaps the most useful grading system is that of Coughlin & Shurnas,98 which incorporates clinical and radiographic features and provides first metatarsophalangeal joint dorsiflexion ranges of motion commonly observed with each grade. This scale has also been shown to have prognostic value in determining the response to surgical intervention. Patients with hallux limitus/rigidus typically present with complaints of pain and stiffness in their big toe joint that increases with activity and is alleviated by rest. Paraesthesia may be present because of compression of the dorsal digital nerve of the hallux. On examination, the first metatarsophalangeal joint may be swollen and erythematous and in long-standing cases there will be a dorsal exostosis overlying the first metatarsal head (Fig. 8.12). Secondary features include bursal formation, hyperextension of the interphalangeal joint with associated hallux nail dystrophy, and keratotic lesions, typically located under the medial aspect of the interphalangeal joint and lesser metatarsophalangeal joints. Gait analysis will reveal an apropulsive walking pattern with a shortened step length, possibly accompanied by excessive knee and hip flexion or hip circumduction to assist the transfer of the swing limb. Plantar pressures will generally be elevated beneath the hallux and lateral metatarsal heads (Fig. 8.13).99,100
Figure 8.12 Typical presentation of hallux limitus/ rigidus. Note dorsal exostosis of the first metatarsophalangeal joint, hyperextension the interphalangeal joint and hypertrophy of hallux nail. (Courtesy of Lesley Newcombe, La Trobe University.)
Figure 8.13 Typical plantar pressure output for an older person with hallux limitus/rigidus.
AETIOLOGY The aetiology of hallux limitus/rigidus is considered to be multifactorial; however, few well designed studies have been undertaken. Most investigations have been case series designs, which simply report the prevalence of various features in patients with hallux limitus/rigidus with no comparison to a control group. These studies have suggested that hallux limitus/rigidus is associated with female sex,97 family history of the condition,97 long first metatarsal,101,102 increased hallux interphalangeal abductus angle97 and foot pronation.87,101–103
–
Condensation of bone around the joint Slight narrowing of joint space Sesamoids regular but enlarged
Moderate osteophytes Joint space narrowing Subchondral sclerosis or cysts Hypertrophy and irregularity of sesamoids
Severe osteophytes Complete disappearance of joint space Degenerative halluxmetatarsosesamoid joint
–
Grade 0
Grade 1
Grade 2
Grade 3
Grade 4
As for Grade 3 plus definite pain at midrange of passive motion
As for Grade 3
≤10° and/or 75– 100% loss compared with normal side Notable loss of PF Nearly constant pain and substantial stiffness at extremes of range of motion, but not at mid-range
As for Grade 2, but with substantial narrowing, possible periarticular cystic changes, more than one-quarter of dorsal joint space involved on lateral radiograph Sesamoids enlarged and/or cystic or irregular
Marked osteophytes Loss of joint space Subchondral cysts present or absent
As for Grade 3
10–30° and/or 50–75% loss compared to normal side Moderate to severe pain and stiffness that may be constant Pain occurs just before maximum DF and maximum PF
Dorsal, lateral and possibly medial osteophytes Flattened appearance of metatarsal head No more than one-quarter of dorsal joint space involved on lateral radiograph Mild-moderate joint space narrowing and sclerosis Sesamoids not involved
Moderate osteophytes Joint space narrowing Subchondral sclerosis
–
30–40° and/or 20–50% loss compared to normal side
Mild/occasional pain and stiffness Pain at extremes of DF and/or PF
Dorsal osteophyte Minimal joint space narrowing Minimal periarticular sclerosis Minimal flattening of metatarsal head
Mild to moderate osteophytes Normal joint space
1st MPJ DF ROM 40–60° and/or 10–20% loss compared to normal side
Clinical No pain Slight stiffness Reduced ROM
Normal
Radiographic
Coughlin & Shurnas
–
Radiographic
Hattrap & Johnson
1st MPJ DF ROM, first metatarsophalangeal joint dorsiflexion range of motion, measured passively; PF, plantarflexion.
Radiographic
Findings
Regnauld
Table 8.2 Classification systems for hallux limitus/rigidus
Hallux limitus and hallux rigidus
159
160
DISORDERS OF THE TOES
Stronger evidence can be derived from case-control studies, as direct comparisons are made to a control group without the condition. Four such studies have been undertaken. Horton et al104 compared radiographic measurements in 81 patients with hallux rigidus and 50 controls and found that, while measures of metatarsus primus elevatus (relative elevation of the first metatarsal compared to the second metatarsal) were similar between controls and cases with mild to moderate deformity, severe cases of hallux rigidus demonstrated slightly higher mean values. Similar results were reported by Roukis,105 who compared 100 cases of hallux rigidus to historical controls and found that metatarsus primus elevatus was more common in the case group. Zgonis et al106 compared radiographic features in 51 hallux rigidus cases to 51 controls and reported that the first metatarsal was slightly shorter in the hallux rigidus group (65 mm compared to 68 mm). However, first metatarsal protrusion distance, which is a more functional indicator of the length of the first metatarsal as it takes into account transverse plane angulation, did not differ between the groups. Bryant et al107 compared radiographic measurements in 30 people with hallux limitus and 30 controls and reported an increased hallux interphalangeus abductus angle in the hallux limitus group. Finally, a large retrospective cohort study of 1592 people aged over 40 years found that those with osteoarthritis of the first metatarsophalangeal joint were more likely to have pronated feet, defined as a frontal plane rearfoot angle of greater than 5°.108 These findings indicate that intrinsic structural factors may play a role in the development of hallux limitus/rigidus. The underlying mechanical cause of the degeneration of the joint, however, is subject to considerable debate. It has been hypothesised that subtalar joint pronation leads to first ray hypermobility and that the subsequent dorsiflexion of the first metatarsal limits the dorsal excursion of the proximal phalanx, leading to a ‘jamming’ of the joint (Fig. 8.14).51 This process would theoretically be exacerbated in the presence of an overly long or elevated first metatarsal. However, while reduced static dorsiflexion of the first metatarsophalangeal joint has been shown to be associated with pronated foot posture109,110 and decreases as the rearfoot is progressively everted,111 the relationship between eversion of the rearfoot complex and maximum first metatarsophalangeal joint dorsiflexion during gait is only moderate.112 Irrespective of the underlying intrinsic risk factors, the essential pathology of hallux limitus/rigidus is
A Normal function
B Limited motion
C Rigid deformity
Figure 8.14 Pathomechanics of hallux limitus. A. Normal function of the first MPJ. B. compression of joint associated with hallux limitus. C. Formation of osteophyte on dorsal aspect of the joint.
one of progressive arthritic degeneration of the first metatarsophalangeal joint, initiated by synovial hypertrophy and subsequent cartilage destruction. Loss of cartilage results in exposure of subchondral bone, which then undergoes sclerotic changes and, in severe cases, formation of subchondral cysts.82 Finally, hallux limitus/rigidus has also been reported in people with arthritic disorders such as rheumatoid arthritis, gout and psoriatic arthropathy.82 The underlying mechanism for the development of limited joint motion in these conditions is likely to be localised joint inflammation and subsequent cartilage degeneration. However, Clayton & Ries113 have also suggested that, in the rheumatoid foot, spasm of intrinsic musculature of the toes may occur in an attempt to unload painful lesser metatarsal heads, resulting in
Hallux limitus and hallux rigidus
soft tissue contracture of the first metatarsophalangeal joint.
ASSESSMENT AND DIAGNOSIS Diagnosis of hallux limitus/rigidus is based on clinical signs and symptoms, joint range of motion measurement and radiographic appearance. As stated above, the classical presentation of hallux limitus/rigidus is pain and stiffness in the first metatarsophalangeal joint that increases with activity and is alleviated by rest. Physical examination will frequently reveal a dorsal exostosis overlying the joint with associated inflammation and, in severe cases, bursal formation. Non-weightbearing examination of the first metatarsophalangeal joint (Fig. 8.15) will reveal a limited range of dorsiflexion with normal or slightly restricted plantarflexion. The normal non-weightbearing range of motion of the first metatarsophalangeal joint has been reported to be between 50° and 82°;114–118 however, several measurement techniques have been described, which may not be directly comparable.118 Furthermore, these normal ranges may not be applicable to older people, because of normal age-related reductions in joint range of motion. Recently, Scott et al119 showed that older people without foot problems had significantly less range of motion at the first metatarsophalangeal joint compared to younger controls (56° versus 82°, measured non-weightbearing),
indicating that a cut-off value of approximately 50° is probably a useful rule of thumb when assessing older people. If the condition is unilateral, it may be useful to compare the range of motion between both feet and document the relative reduction in motion on the affected side.97 Weightbearing dorsoplantar and lateral radiographs are extremely useful to determine the severity of hallux limitus/rigidus (Fig. 8.16). The most obvious features of the condition are joint space narrowing and juxta-articular sclerosis (best viewed from the dorsoplantar radiograph), and the formation of an osteophyte on the dorsal aspect of the first metatarsal head (best viewed from the lateral radiograph). As the condition progresses, the metatarsal head takes on a flattened appearance, the sesamoids may become enlarged, and periarticular cysts may develop. Oblique
A
Figure 8.15 Non-weightbearing range of motion assessment of the first metatarsophalangeal joint. The older person is seated with the knee extended and ankle placed at 90°, and the hallux is maximally extended. The value recorded is the maximum angle at which the hallux cannot be passively moved into further extension.
B
Figure 8.16 Radiographic appearance of hallux limitus. A. Dorso-plantar view. B. Lateral view.
161
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DISORDERS OF THE TOES
radiographs are not essential to assess the severity of hallux limitus/rigidus; however, they may assist in determining the full extent of the dorsal osteophyte. Similarly, computed tomography scans are generally not required but may assist in determining the degree of degeneration on the plantar surface of the joint, which is otherwise difficult to visualise with radiographs.
TREATMENT Conservative Conservative management of hallux limitus/rigidus involves measures to obtain pain relief (including antiinflammatory medications and intra-articular corticosteroid injection), addressing the associated nail and skin conditions, physical therapy to restore range of motion, orthotic therapy and footwear modifications.120 Although very few rigorous trials have been undertaken to assess the efficacy of these treatments for hallux limitus/rigidus, case series studies suggest that many patients benefit from conservative management. In a recent 14-year follow-up study of patients who chose not to have surgery, few reported that their condition had worsened and 75% would still choose not to have surgery if they had to make the decision again. A large proportion of these patients had changed their footwear to shoes with a more ample toebox, suggesting that selection of appropriate footwear may be a sufficient treatment in many people.121 Similar findings were reported by Grady et al,122 who reviewed 772 cases of hallux limitus over a 7-year period and reported that 55% were successfully managed with conservative care alone. Of these, 84% were managed with foot orthoses, 10% with intraarticular corticosteroid injections and 6% with a change in footwear. Intra-articular injection and manipulation may be beneficial in mild to moderate cases of hallux limitus/ rigidus. Solan et al123 described a case series of 31 patients with hallux rigidus who were given an injection of 40 mg of Depo-Medrone and 3 ml of 0.5% bupivacaine followed by manipulation of the joint under general anaesthesia. After a mean follow-up of 41 months, one-third of patients with mild (Karasick & Wapner95 grade 1) hallux rigidus required surgery, two-thirds of patients with moderate (grade 2) hallux rigidus required surgery, and all patients with advanced (grade 3) hallux rigidus required surgery. The authors concluded that manipulation and injection has a role
to play in the management of hallux limitus/rigidus but appears to be more effective in less severe cases. More recently, a randomised controlled trial by Pons et al124 indicated that intra-articular injection of sodium hyaluronate, a highly viscous glycosaminoglycan thought to influence cartilage metabolism, was more effective than corticosteroid injection in early hallux rigidus. However, after one year, nearly half the participants required surgical intervention, suggesting that the benefits of this approach may be short-term. Mobilisation of the sesamoid apparatus and strengthening of hallux plantarflexors has also been shown to confer an additional benefit in the conservative management of hallux limitus. Shamus et al125 conducted a small trial in which one group of patients was provided with whirlpool, therapeutic ultrasound, first metatarsophalangeal joint mobilisation, calf stretching, toe strengthening exercises, cold packs and electrical stimulation, and the second group was provided with each of these interventions in addition to distal gliding mobilisations of the sesamoids, hallux plantarflexor strengthening exercises and gait training. After 12 therapy sessions, the group who received the sesamoid mobilisations exhibited greater improvements in first metatarsophalangeal joint range of motion, toe flexor strength and pain levels. Footwear modification and orthotic management of hallux limitus/rigidus are greatly influenced by the severity of the condition. In advanced cases with large osteophytes, pain generally occurs during the propulsive phase of gait when the proximal phalanx jams against the metatarsal head. In such cases, the goal of treatment is to restrict motion. This can be achieved by the prescription of shoes with a rigid shank; however, the resultant need for sagittal plane compensation at the knee and hip may create symptoms further up the kinetic chain. Alternatively, rocker sole footwear will enable propulsion to occur proximal to the metatarsophalangeal joints, provided the apex of the rocker is appropriately located. Prescription of rocker-soled footwear needs to be carefully considered in older people, as some patients may take considerable time to adjust to the footwear because of balance difficulties. For those with severe hallux limitus/rigidus who are not suitable for rockersole shoes, the placement of an insole with a raised bar under the first ray may achieve the same result.126 For less severe forms of hallux limitus (including functional hallux limitus), orthoses may assist in facili-
Hallux limitus and hallux rigidus
tating sagittal plane motion of the first metatarsophalangeal joint by increasing the plantarflexion of the first ray. This may be achieved by removing orthotic material beneath the first ray segment (‘first ray cutout’), elevating the lateral metatarsal heads (via valgus forefoot wedges or metatarsal domes) or placing a firm piece of material beneath the hallux.127 Despite the proposed relationship between foot pronation and limited motion at the first metatarsophalangeal joint, the effect of varus rearfoot wedges in the management of hallux limitus is unclear, with both increases128 and decreases129,130 in first metatarsophalangeal joint motion reported while wearing such orthoses. Despite clinical reports of the efficacy of footwear modifications and foot orthoses for hallux limitus/ rigidus,122,131 no controlled trials have so far been performed. However, it is likely that such interventions would be more effective in less severe forms of the condition where there is still a reasonable amount of available motion at the joint.
Surgical As with hallux valgus surgery, there have been a multitude of procedures described for the management of hallux limitus/rigidus but few have been adequately evaluated or directly compared to each other. The selection of procedure is heavily influenced by the severity of the condition, so preoperative grading is considered essential. In mild cases, the aim of the surgery is to remove osteophytes and preserve joint motion, whereas in advanced cases the aim is to block the residual motion that is causing the pain by fusing the joint. The following section provides a brief overview of some of the more commonly performed procedures for hallux limitus/rigidus; however, the reader should note that this coverage is by no means comprehensive and several modifications of these techniques have been described in the literature. The simplest joint preservation procedure, referred to as cheilectomy, involves removal of the dorsal exostosis from the metatarsal head and proximal phalanx, and debridement of the degenerative articular cartilage on the dorsal aspect of the joint (Fig. 8.17).93 Up to 30% of the metatarsal head is removed. This procedure is most appropriate for mild cases of hallux limitus/rigidus and results in significant increases in the dorsiflexion range of motion at the first metatarsophalangeal joint.132 Several retrospective studies have reported high levels of patient satisfaction with the technique (72–90%), with the only consistent
complication being recurrence of the dorsal osteophyte.93,132–136 Feltham et al137 have stated that the technique is particularly effective in people aged over 60 years who have extra-articular symptoms. Several joint preservation osteotomy procedures have been proposed for the surgical management of hallux limitus/rigidus (Fig. 8.17). The Bonney–Kessel osteotomy,138 a dorsiflexory osteotomy at the base of the proximal phalanx, is generally only used in younger patients or those with minimal degenerative changes and is contraindicated in the presence of metatarsus primus elevatus. The Watermann osteotomy is a distal metatarsal osteotomy in which a dorsal wedge of bone is removed, resulting in a relative shortening of the first metatarsal.139 However, for both these procedures, only small-scale follow-up studies have been reported.139,140 The Youngswick procedure,141 a modification of the Chevron bunionectomy, involves a V-shaped osteotomy through the neck of the first metatarsal along with the removal of a rectangular piece of bone from the dorsal aspect of the metatarsal to enable the proximoplantar displacement of the metatarsal head. Only two studies have reported outcomes of this procedure – the original description of 10 cases141 and a 2-year follow-up of 17 cases by Bryant et al,142 who reported significant increases in first metatarsophalangeal joint dorsiflexion but no changes in plantar pressures beneath the hallux or first metatarsophalangeal joint. In more severe cases, joint destructive procedures are more frequently used. The Keller procedure, which has already been described in the previous section on hallux valgus (Fig. 8.3), has also been used with some success for hallux limitus/rigidus. However, the Keller procedure is generally only indicated for people with limited mobility and/or severe hallux limitus, as the propulsive function of the hallux is impaired following the procedure.89 Furthermore, as with hallux valgus, the Keller procedure is associated with a relatively high rate of complications such as transfer lesions and/or metatarsalgia, malunion and interphalangeal joint osteoarthritis.143 Finally, implant arthroplasty, which involves resecting a proximal portion of the proximal phalanx, remodelling the metatarsal head and inserting a silicone144,145 or metallic146 joint replacement, has received considerable attention in the recent literature and appears to provide significant pain relief while keeping the joint mobile. Several studies have shown the technique to be useful in older patients.144,147
163
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DISORDERS OF THE TOES
A
B
C
D
E
F
Figure 8.17 Surgical procedures for hallux limitus/rigidus. A. Cheilectomy. B. Bonney-Kessel osteotomy. C. Watermann osteotomy. D. Youngswick procedure. E. Keller’s procedure. F. Implant arthroplasty.
Silicone implants appear to have a higher failure rate than metallic implants and are more likely to dislodge and lead to foreign body reactions.146 Only three randomised controlled trials have been conducted to assess the efficacy of surgical procedures for hallux limitus/rigidus. The first evaluated the benefit of K-wire distraction when performing a Keller’s arthroplasty but found that this modification conferred no additional advantages over the standard surgical technique. In fact, there was some evidence
that distraction resulted in an increase in osteoarthritic changes in the interphalangeal joint.148 The second trial compared Keller’s arthroplasty to arthrodesis in patients with hallux valgus or hallux rigidus and found that the procedures produced similar outcomes.149 Finally, a well-designed trial comparing arthrodesis to implant arthroplasty reported better outcomes in the arthrodesis group, due primarily to the high rate of loosening of the phalangeal component of the implant.150
Lesser toe deformities
Overall, surgical treatment of hallux limitus/rigidus does appear to be effective provided that extensive presurgical planning is undertaken. However, as with surgery for hallux valgus, there is a need for direct comparisons between different techniques with larger samples sizes and longer periods of follow-up.
LESSER TOE DEFORMITIES Deformities of the lesser toes are among the most common of all foot disorders, affecting between 24% and 60% of older people.9,151–153 The Feet First study of 784 Americans aged over 65 years found that 35% of the sample had hammer toes, 33% had mallet toes and 9% had claw toes.9 Women are more likely to develop lesser toe deformities than men,9,10,30 which has been attributed to the influence of footwear with a narrow toe-box.30,154,155 Older people with lesser toe deformities are more likely to develop keratotic lesions on the toes and plantar surface of the foot10 and have more difficulty performing balance and functional tasks requiring forward leaning.10
CLASSIFICATION AND CLINICAL PRESENTATION There are several different types of lesser toe deformities, which are classified according to the relative alignment of the metatarsophalangeal and interphalangeal joints in the sagittal plane (Table 8.3). A mallet toe is a fixed deformity in which the distal interphalangeal joint is plantarflexed. A hammer toe is a deformity in which the proximal interphalangeal joint is plantarflexed and the metatarsophalangeal joint may be hyperextended. A claw toe is a deformity in which the metatarsophalangeal joint is hyperextended and both the proximal and distal interphalangeal joints are plantarflexed. A retracted toe is a deformity in which the metatarsophalangeal joint so hyperextended that the apex of the toe is non-weightbearing. The proximal and distal interphalangeal joints may be neutral or plantarflexed.156,157 In the presence of hallux valgus, the second toe frequently develops a hammer toe deformity. In severe cases, the second toe may be forced dorsally or plantarly to accommodate the lateral displacement of the hallux. In this situation, the terms over-riding (or cross-
Table 8.3 Classification of common lesser toe deformities in the sagittal plane Classification
Appearance
MPJ
PIPJ
DIPJ
Typical lesion pattern
Mallet toe
Neutral
Neutral
Plantarflexed
Apex of toe
Hammer toe
Neutral or hyperextended
Plantarflexed
Neutral, plantarflexed or extended
Dorsum of PIPJ Plantar MPJ
Claw toe
Hyperextended
Plantarflexed
Plantarflexed
Dorsum of PIPJ Dorsum of DIPJ Apex of toe Plantar MPJ
Retracted toe
Hyperextended
Neutral or plantarflexed
Neutral or plantarflexed Apex of toe nonweightbearing
Dorsum of PIPJ Plantar MPJ
DIPJ, distal interphalangeal joint; MPJ, metatarsophalangeal joint; PIPJ, proximal interphalangeal joint.
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DISORDERS OF THE TOES
A
B
C
D
Figure 8.18 Lesser toe deformities. A. Claw toes. B. Retracted toes. C. Under-riding toes. D. Over-riding toe. (A, courtesy of Lloyd Reed, Queensland University of Technology; B, courtesy of Felicity Prentice, La Trobe University; C, courtesy of Lesley Newcombe, La Trobe University.)
over) or under-riding toe may be used to describe the alignment of the second toe. Because of the subsequent subluxation of the second metatarsophalangeal joint, the second toe may also be displaced in the transverse plane. Similar transverse plane displacement may accompany hammer or claw toe deformities of the third to fifth toes due to pressure from footwear, giving rise to adductovarus toe deformity. A range of lesser toe deformities is shown in Figure 8.18. Lesser toe deformities may be further classified according to the available motion in the affected joints, using the terminology of flexible or rigid or, alternatively, reducible or non-reducible. This nomen-
clature is clinically useful, as treatment strategies will vary depending on the degree of correction that can be achieved. Older people with lesser toe deformities will frequently present with complaints related to secondary lesions (such as corns, calluses or ulcers) associated with the toe deformity (see Table 8.3 for typical patterns of lesion location associated with each type of deformity). Toe deformities with a transverse plane component (particularly adductovarus of the fifth toe) are often associated with interdigital lesions or nail dystrophy due to compression against the adjacent toe. In severe cases with multiple toe involvement,
Lesser toe deformities
there may be evidence of a cautious gait pattern due to loss of the propulsive function of the toes.158,159
AETIOLOGY The aetiology of lesser toe deformities has not been thoroughly investigated and the evidence for many proposed aetiological factors is derived largely from clinical observations rather than case-control studies. Factors considered to be associated with the development of lesser toe deformities include ill-fitting footwear, 30,154,156abnormal foot posture (both pes planus51 and pes cavus160) and excessively long toes.161 The proposed association between ill-fitting footwear and lesser toe deformities was recently supported by Menz & Morris,30 who assessed footwear characteristics in 176 older people and found that those with lesser toe deformities were two to four times more likely to wear shoes substantially shorter than their foot. Over time, it is likely that the toes adapt to the limited area available in the toe box of the shoe via hyperextension of the metatarsophalangeal joints and plantarflexion of the proximal interphalangeal joint.156 Lesser toe deformities also frequently develop in conjunction with systemic conditions such as diabetes mellitus,162 rheumatoid arthritis163 and Charcot–Marie–Tooth disease164 and may also develop following cerebrovascular accident (stroke).165
ASSESSMENT AND DIAGNOSIS Lesser toe deformities can be easily diagnosed via visual observation and physical examination. The foot should be observed both non-weightbearing and weightbearing, and passive range of motion tests for each joint should be undertaken in order to ascertain the degree to which the deformity is reducible. Secondary lesions associated with the deformity should be carefully inspected and documented. Evaluation of footwear (described in Chapter 3) is essential to assist in determining the underlying cause of the deformity and the suitability of the shoe to accommodate toe splinting devices.166 Radiographic assessment is not required to diagnose lesser toe deformity but is necessary for presurgical planning. Dorsoplantar projections will enable the accurate identification of excessively long metatarsals by documenting the metatarsal formula. Lateral projections may enable the visualisation of severe hammer and claw toes; however, in this view all toes are superimposed, which makes accurate measurement quite difficult.
Plantar pressure analysis may be useful to accurately identify high pressure areas on the toes and to assess the efficacy of off-loading techniques. Claisse et al167 and Slater et al168 have recently demonstrated that modern plantar pressure systems have sufficient spatial resolution to detect reductions in toe pressures associated with prefabricated and custom-moulded silicone toe orthoses in people with claw toes.
TREATMENT Conservative Conservative treatment of lesser toe deformities involves addressing the associated nail and skin conditions, footwear advice and/or modification, and orthodigital techniques. In cases where it is clear that ill-fitting footwear is the underlying cause (or an aggravating factor), the older person should be advised to purchase more appropriately fitting footwear with a broad and deep toe-box. If this is not possible for financial or other reasons, shoe stretching or balloonpatching may be an appropriate alternative. Orthodigital techniques can be very effective in redistributing load away from painful areas and may also play a role in the non-surgical correction of flexible toe deformities.169 Each of these interventions is discussed in more detail in Chapter 11. However, despite anecdotal reports of effectiveness, no controlled trials of these conservative techniques have so far been undertaken.
Surgical As with deformities of the first toe, several surgical procedures and modifications have been developed for the management of lesser toe deformities. A brief summary is provided in the following section but for further information the reader is directed to a recent comprehensive review by Coughlin.157 The selection of surgical procedure for the correction of lesser toe deformities is highly dependent on the available motion in the interphalangeal joints. Generally speaking, rigid deformities require arthroplasty, whereas flexible deformities can be corrected with soft tissue surgical techniques such as tendon lengthening and transfer.157 For the mallet toe, an elliptical incision is made over the distal interphalangeal joint and deepened through the joint capsule and extensor tendon. The collateral ligaments are severed and the distal portion of the intermediate phalanx is removed. If the deformity is severe, the flexor tendon
167
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DISORDERS OF THE TOES
may also be severed. The toe is then stabilised with a K-wire and taped into the corrected position. The wire is removed after a period of 3 weeks. The surgical procedure is essentially the same for hammer toes (with the exception that the procedure is directed to the proximal interphalangeal joint) and for claw toes (with the exception that both the proximal and distal interphalangeal joints are corrected). Although some authors recommend that peg-in-hole arthrodesis also be performed,170 Coughlin157 suggests that arthrodesis may occur naturally and is not necessary for a successful result to be achieved. Case series studies indicate that patient satisfaction with these procedures is generally high. Dissatisfaction with the surgical result is most commonly due to residual stiffness of the toes, recurrent deformity, malalignment and difficulty with footwear.170 Amputation of the second toe for the management of severe crossover or hammer toe deformity has been recommended in older people for whom the recovery period of corrective surgery may be too debilitating.171,172 Sundaram & Walsh171 performed seven cases of second toe amputation in people aged over 70 years and reported that all were satisfied with the outcome. Similar results were reported by Gallentine & DeOrio172 in 13 patients (aged 72–86 years) who had undergone second toe amputation for severe hammer toe. However, this procedure needs to be carefully considered, as the postoperative cosmetic appearance may be troubling for some people. Furthermore, the space created by the absence of the second toe may increase any pre-existing valgus deformity of the hallux. Indeed, of the 20 cases reported in these two studies, 10 demonstrated valgus drift of the hallux following the procedure. Surgical management of flexible lesser toe deformities involves tendon lengthening and/or transfer techniques. For retracted toes, a dorsal incision is made over the proximal interphalangeal joint and a Z-plasty tendon lengthening procedure is performed on the extensor digitorum longus tendon. For flexible hammer and claw toes, a flexor digitorum longus transfer (also referred to as the Girdlestone–Taylor procedure) is commonly used.173 This involves detaching the flexor digitorum longus tendon from the base of the distal phalanx, splitting it longitudinally and transferring each segment around the proximal phalanx and suturing it to the extensor hood. Patient satisfaction with this procedure has been reported to range from 54% to 90%.173–175 Few complications have been associated with the technique; however, patients
should be advised that the ability to flex the toes is lost following the surgery. Fifth toe deformities frequently have a transverse and frontal plane component, because of their susceptibility to pressure from footwear. For this reason, several different surgical techniques have been developed specifically for the fifth toe. Overriding fifth toes can be managed with soft tissue release or, in more advanced cases, transfer of the extensor digitorum longus tendon. This procedure, first described by Lapidus,176 involves releasing the tendon 4 cm proximal to the metatarsophalangeal joint, then threading the distal portion around the proximal phalanx to the lateral plantar aspect of the toe. Here, the tendon is sutured to the tendon of abductor digiti minimi. An alternative procedure is to remove the proximal phalanx and syndactylise the fourth and fifth toes.177 Both procedures have reportedly high success rates, with recurrence of the deformity estimated to occur in less than 10% of cases.157 Syndactylisation, however, may not be cosmetically acceptable for some patients. Underriding fifth toes are less common but can be corrected by extensor digitorum longus tendon release and excision of the proximal phalanx.
LESS COMMON DISORDERS AFFECTING THE TOES TAILOR’S BUNION Tailor’s bunion, also referred to as bunionette, is an enlargement of the lateral aspect of the fifth metatarsal head (Fig. 8.19). The condition was originally
Figure 8.19 Tailor’s bunion. (Courtesy of Lesley Newcombe, La Trobe University.)
Less common disorders affecting the toes
observed in tailors and was thought to be caused by long periods sitting cross-legged with the lateral border of the foot compressed against the floor.178 As with hallux valgus, longstanding cases may develop a large, painful osseous prominence associated with an overlying adventitious bursa. Few epidemiological studies have documented the presence of tailor’s bunions, however, the Feet First study, which involved 784 people aged over 65, reported a 13% prevalence of ‘bunionette’, with equal distribution across men and women.9 Postulated aetiological factors for tailor’s bunion include incomplete development of the transverse intermetatarsal ligament, increased intermetatarsal angles associated with a broad forefoot, and congenital dumbbell-shaped fifth metatarsal head.179 However, no detailed case-control studies have been undertaken. Conservative treatment of tailor’s bunion involves addressing secondary skin lesions, advising the patient to purchase broader footwear, and the use of felt or silicone padding techniques to redistribute pressure away from the lateral eminence. Surgical management ranges from simple exostectomy to the use of distal osteotomies similar to those used for hallux valgus.179
Figure 8.20 Hallux varus. (Courtesy of Matthew Dilnot, Melbourne Foot Clinic.)
HALLUX VARUS Hallux varus is an uncommon condition in which the hallux is adducted relative to the first metatarsal (Fig. 8.20). Although congenital forms of the condition do occur in conjunction with teratogenic anomalies, the most commonly encountered cause of hallux varus in older people is surgical overcorrection of hallux valgus deformity. Initial reports of iatrogenic hallux varus were attributed to surgical techniques advocating excision of the lateral sesamoid;2 however, it is now recognised that most hallux valgus procedures can potentially lead to hallux varus.180 Because of the increased breadth of the forefoot, patients will have great difficulty finding suitable footwear and are likely to develop keratotic lesions on the medial aspect of the hallux. Conservative treatments, such as splinting and strapping techniques, are generally of little use, so most cases will require revisional surgery. Several techniques have been described, which are essentially mirror images of hallux valgus procedures.181,182
GOUTY ARTHRITIS Gout is the most common inflammatory arthritis in older people, affecting approximately 3% of people
aged over 65 years, with men being affected two to six times more frequently than women.183 Risk factors for the development of gout include alcohol consumption (particularly beer), renal insufficiency, diuretic use, dehydration, increased body mass index and dietary factors (including increased meat and seafood consumption, and decreased dairy consumption).184–187 The underlying pathophysiology of gout relates primarily to elevated blood levels of urate, a byproduct of purine metabolism. Normally, serum urate levels are between 2 and 8 mg/100 ml. However, in the presence of either overproduction of urate or, more commonly, impaired secretion of urate, monosodium urate crystals form and are deposited in the peripheral joints, resulting in acute inflammatory arthritis.187 Acute gout initially affects the first metatarsophalangeal joint in 50% of cases and approximately 90% of patients will develop this manifestation at some point during the disease.188 The reason for this predilection is unclear; however, it has been hypothesised that the first metatarsophalangeal joint has a relatively low temperature, low pH and is subject to large compressive forces when walking; factors that may accelerate the
169
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DISORDERS OF THE TOES
Figure 8.21 Tophaceous deposits associated with chronic gouty arthritis. A. Distal interphalangeal joint of the third toe. B. Fifth metatarsophalangeal joint. (Courtesy of Lesley Newcombe, La Trobe University.)
A
B
formation of monosodium urate crystals.189 Acute gout affecting the first metatarsophalangeal joint, often referred to as podagra, has a sudden onset and is exquisitely painful, and may last from a few days to several weeks. Other joints that are commonly affected by acute gout include the metatarsophalangeal joints, the ankle and the knee. If left untreated, approximately 75% of patients will develop chronic tophaceous gout, characterised by the formation of solid urate deposits (called tophi) in the connective tissues, most commonly the feet, fingers, elbows and ears (Fig. 8.21).190 Older women are more likely to develop tophaceous gout early in the disease process, possibly because of their higher prevalence of diuretic use.191 Diagnosis of gout is confirmed by the microscopic observation of urate crystals in synovial fluid, bursae or tophi; however, clinical criteria are sufficient to reach a provisional diagnosis. These criteria include unilateral synovitis of the first metatarsophalangeal joint with maximum inflammation within 24 hours, no evidence of infection, a history of recurrent episodes of monoarticular arthritis followed by complete resolution, observation of subcortical bone cysts from radiographs, and rapid resolution of inflammation following administration of colchicine.187 Differential diagnoses include osteoarthritis, rheumatoid arthritis and septic arthritis. Pseudogout, a condition caused by deposition of calcium pyrophosphate crystals within joints, has a similar clinical presentation to gout but most commonly affects the knee, wrist or shoulder. Accurate differentiation between gout and pseudogout requires microscopic examination of synovial fluid.186
Treatment of acute gout involves administration of colchicine (a potent anti-inflammatory drug), non-steroidal anti-inflammatory drugs (NSAIDs) or corticosteroid (either orally or via intra-articular injection).192 A recent systematic review indicated that, while colchicine is effective, high levels of gastrointestinal toxicity associated with the drug limit its use in older patients and, therefore, NSAIDs or corticosteroids should be the first line of treatment.193 Management of chronic gout involves counselling the patient with regard to weight loss, alcohol consumption and diet, and adjusting medications that contribute to hyperuricaemia.194 Allopurinol, a xanthine oxidase inhibitor, has been shown to significantly reduce urate levels and is therefore considered to be an effective drug for preventing recurrent gout.192 Prominences caused by tophaceous deposits will also need to be managed with footwear modifications and/or orthoses.
SUMMARY An overview of the most common toe deformities affecting the older foot has been presented. Conservative management plays an important role in reducing the pain associated with secondary lesions caused by these deformities, and in some cases soft tissue correction may be possible with orthodigital techniques. Many older patients, however, will require surgical correction in order to remain pain-free. Because of the wide range of surgical options available for the correction of toe deformities, thorough presurgical planning is required to achieve optimum results.
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joint disorders. Section 2: Hallux rigidus. Journal of Foot and Ankle Surgery 2003; 42: 124–136. Coughlin MJ, Shurnas PS. Hallux rigidus: demographics, etiology, and radiographic assessment. Foot and Ankle International 2003; 24: 731–743. Coughlin MJ, Shurnas PS. Hallux rigidus. Grading and long-term results of operative treatment. Journal of Bone and Joint Surgery 2003; 85A: 2072–2088. Bryant A, Tinley P, Singer K. Plantar pressure distribution in normal, hallux valgus and hallux limitus feet. The Foot 1999; 9: 115–119. VanGheluwe B, Dananberg HJ, Hagman F et al. Effects of hallux limitus on plantar foot pressure and foot kinematics during walking. Journal of the American Podiatric Medical Association 2006; 96: 428–436. Nilsonne H. Hallux rigidus and its treatment. Acta Orthopaedica Scandinavica 1930; 1: 295–302. Bingold AC, Collins DH. Hallux rigidus. Journal of Bone and Joint Surgery 1950; 32B: 214–222. Jack EA. The aetiology of hallux rigidus. British Journal of Surgery 1940; 27: 492–497. Horton GA, Park YW, Myerson MS. Role of metatarsus primus elevatus in the pathogenesis of hallux rigidus. Foot and Ankle International 1999; 20: 777–780. Roukis TS. Metatarsus primus elevatus in hallux rigidus: fact or fiction? Journal of the American Podiatric Medical Association 2005; 95: 221–228. Zgonis T, Jolly GP, Garbalosa JC et al. The value of radiographic parameters in the surgical treatment of hallux rigidus. Journal of Foot and Ankle Surgery 2005; 44: 184–189. Bryant A, Tinley P, Singer K. A comparison of radiographic measurements in normal, hallux valgus, and hallux limitus feet. Journal of Foot and Ankle Surgery 2000; 39: 39–43. Mahiquez MY, Wilder FV, Stephens HM. Positive hindfoot valgus and osteoarthritis of the first metatarsophalangeal joint. Foot and Ankle International 2006; 27: 1055–1059. Munteanu SE, Bassed AD. Effects of foot posture and inverted foot orthoses on hallux dorsiflexion. Journal of the American Podiatric Medical Association 2006; 96: 32–37. Paton JS. The relationship between navicular drop and first metatarsophalangeal joint motion. Journal of the American Podiatric Medical Association 2006; 96: 313–317. Harradine PD, Bevan LS. The effect of rearfoot eversion on maximal hallux dorsiflexion. A preliminary study. Journal of the American Podiatric Medical Association 2000; 90: 390–393. Halstead J, Turner DE, Redmond AC. The relationship between hallux dorsiflexion and ankle joint
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complex frontal plane kinematics: a preliminary study. Clinical Biomechanics 2005; 20: 526–531. Clayton ML, Ries MD. Functional hallux rigidus in the rheumatoid foot. Clinical Orthopaedics and Related Research 1991; 271: 233–238. Joseph J. Range of motion of the great toe in men. Journal of Bone and Joint Surgery 1954; 36B: 450–457. Bojsen-Moller F, Lamoreux L. Significance of free dorsiflexion of the toes in walking. Acta Orthopaedica Scandinavica 1979; 50: 471–479. Mann RA, Hagy JL. The function of the toes in walking, jogging and running. Clinical Orthopaedics and Related Research 1979; 142: 24–29. Buell T, Green DR, Risser J. Measurement of the first metatarsophalangeal joint range of motion. Journal of the American Podiatric Medical Association 1988; 78: 439–448. Hopson MM, McPoil TG, Cornwall MW. Motion of the first metatarsophalangeal joint: Reliability and validity of four measurement techniques. Journal of the American Podiatric Medical Association 1995; 85: 198–204. Scott G, Menz HB, Newcombe L. Age-related differences in foot structure and function. Gait and Posture 2007; 26: 68–75. Nawoczenski DA. Nonoperative and operative intervention for hallux rigidus. Journal of Orthopaedic and Sports Physical Therapy 1999; 29: 727–735. Smith R, Katchis S, Ayson L. Outcomes in hallux rigidus patients treated nonoperatively: a long-term follow-up study. Foot and Ankle International 2000; 21: 906–913. Grady J, Axe T, Zager E et al. A retrospective analysis of 772 patients with hallux limitus. Journal of the American Podiatric Medical Association 2002; 92: 102–108. Solan M, Calder J, Bendall S. Manipulation and injection for hallux rigidus. Is it worthwhile? Journal of Bone and Joint Surgery 2001; 83B: 706–708. Pons M, Alvarez F, Sonalan J et al. Sodium hyaluronate in the treatment of hallux rigidus. A singleblind, randomized study. Foot and Ankle International 2007; 28: 38–42. Shamus J, Shamus E, Gugel RN et al. The effect of sesamoid mobilization, flexor hallucis strengthening, and gait training on reducing pain and restoring function in individuals with hallux limitus: a clinical trial. Journal of Orthopaedic and Sports Physical Therapy 2004; 34: 368–376. Dobney GH. Support for hallux rigidus. The Lancet 1962; August 18: 361. Clough JG. Functional hallux limitus and lessermetatarsal overload. Journal of the American Podiatric Medical Association 2005; 95: 593–601.
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157. Coughlin MJ. Lesser-toe abnormalities. Journal of Bone and Joint Surgery 2002; 84-A: 1446–1469. 158. Hughes J, Clark P, Klenerman L. The importance of the toes in walking. Journal of Bone and Joint Surgery 1990; 72B: 245–251. 159. Miyazaki M. Role and movement of the toes during walking. Journal of the Japanese Orthopaedic Association 1993; 67: 606–616. 160. McCluskey WP, Lovell WW, Cummings RJ. The cavovarus foot deformity. Etiology and management. Clinical Orthopaedics and Related Research 1989; 247: 27–37. 161. Coughlin MJ. Operative repair of the fixed hammertoe deformity Foot and Ankle International 1995; 21: 94–104. 162. Smith DG, Barnes BC, Sands AK et al. Prevalence of radiographic foot abnormalities in patients with diabetes Foot and Ankle International 1997; 18: 342–346. 163. Mann RA, Coughlin MJ. The rheumatoid foot. Review of literature and method of treatment. Orthopedic Review 1979; 8: 105–112. 164. Njegovan ME, Leonard EI, Joseph FB. Rehabilitation medicine approach to Charcot–Marie–Tooth disease. Clinics in Podiatric Medicine and Surgery 1997; 14: 99–116. 165. Jordan E, Lekkas C, Roscioli D et al. Podiatric problems on a stroke rehabilitation unit. Australian Journal on Ageing 1997; 16: 222–224. 166. Whitney KA. Othodigital evaluation and therapeutic management of digital deformity. In: Hetherington VJ, ed. Hallux valgus and forefoot surgery. New York: Churchill Livingstone; 1994: 379–399. 167. Claisse PJ, Binning J, Potter J. Effect of orthotic therapy on claw toe loading. Results of significance testing at pressure sensor units. Journal of the American Podiatric Medical Association 2004; 94: 246–254. 168. Slater RA, Herschkowitz I, Ramot Y et al. Reduction of digital plantar pressure by debridement and silicone orthosis. Diabetes Research and Clinical Practice 2006; 74: 263–266. 169. Kippen C. A literature review of non-surgical techniques, used by chiropodists, for correcting lesser toe pathologies. Journal of British Podiatric Medicine 1992; 47: 137–140. 170. Femino JE, Mueller K. Complications of lesser toe surgery. Clinical Orthopaedics and Related Research 2001; 391: 72–78. 171. Sundaram RO, Walsh HPJ. Amputation of a crossover 2nd toe in the presence of hallux valgus. The Foot 2003; 13: 196–198. 172. Gallentine JW, DeOrio JK. Removal of the second toe for severe hammertoe deformity in elderly patients. Foot and Ankle International 2005; 26: 353–358.
173. Taylor RG. The treatment of claw toes by multiple transfers of flexor into extensor tendons. Journal of Bone and Joint Surgery 1951; 33B: 539–542. 174. Pyper JB. The flexor-extensor transplant operation for claw toes. Journal of Bone and Joint Surgery 1958; 40B: 528–533. 175. Barbari SG, Brevig K. Correction of clawtoes by the Girdlestone–Taylor flexor–extensor transfer procedure. Foot and Ankle 1984; 5: 67–73. 176. Lapidus PW. Transplantation of the extensor tendon for correction of the overlapping fifth toe. Journal of Bone and Joint Surgery 1942; 24: 555–559. 177. Marek L, Giacopelli J, Granoff D. Syndactylization for the treatment of fifth toe deformities. Journal of the American Podiatric Medical Association 1991; 81: 248–252. 178. Fallat L, Buckholz J. An analysis of the tailors bunion by radiographic and anatomic display. Journal of the American Podiatry Association 1980; 70: 597– 603. 179. Lehtinen JE. Tailor’s bunion deformity. In: Hetherington VJ, ed. Hallux valgus and forefoot surgery. New York: Churchill Livingstone; 1994: 459–469. 180. Boike AM, Christin G. Hallux varus. In: Hetherington VJ, ed. Hallux valgus and forefoot surgery. New York: Churchill Livingstone; 1994: 307–311. 181. Wood WA. Acquired hallux varus: a new corrective procedure. Journal of Foot Surgery 1981; 20: 194–197. 182. Langford JH, Maxwell JR. A treatment for postsurgical hallux varus. Journal of the American Podiatry Association 1982; 72: 142–144. 183. Lawrence RC, Helmick CG, Arnett FC et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis and Rheumatism 1998; 41: 778–799. 184. Choi HK, Atkinson K, Karlson EW et al. Alcohol intake and risk of incident gout in men: a prospective study. The Lancet 2004; 363: 185. Choi HK, Atkinson K, Karlson EW et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. New England Journal of Medicine 2004; 350: 1093–1103. 186. Cassetta M, Gorevic PD. Gout and pseudogout in the geriatric patient. Geriatrics 2004; 59: 25–31. 187. Ene-Stroescu D, Gorbein MJ. A primer on lateonset gout. Geriatrics 2005; 60: 24–31. 188. Graham R, Scott JT. Clinical survey of 354 patients with gout. Annals of the Rheumatic Diseases 1970; 29: 461–468. 189. Levy LA. A rationale for gouty arthritis affecting the first metatarsophalangeal joint. Journal of the American Podiatric Medical Association 1987; 77: 643–644. 190. Gutman AB. The past four decades of progress in the knowledge of gout with an assessment of the
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193. Schlesinger N, Schumacher R, Catton M et al. Colchicine for acute gout. Cochrane Database of Systematic Reviews 2006; CD 006190. 194. Zhang W, Doherty M, Bardin T et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Annals of the Rheumatic Diseases 2006; 65: 1312–1324.
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CHAPTER
Disorders of the forefoot
CHAPTER CONTENTS Definition, prevalence and classification 179 Diagnosis
180
Common causes of forefoot pain in older people 181 Intermetatarsal neuroma 182 Predislocation syndrome 184 Insufficiency fractures of the metatarsals 186 Summary 186 References 187
9
DEFINITION, PREVALENCE AND CLASSIFICATION The term metatarsalgia literally means pain in the metatarsal region of the foot and thus describes a symptom rather than a specific clinical entity.1,2 Establishing the prevalence of metatarsalgia is therefore very difficult. While prevalence rates of up to 65% have been reported for conditions of pain in the forefoot (such as plantar calluses, hallux valgus and hallux limitus/rigidus), this is likely to be an overestimate of the prevalence of metatarsalgia, as these conditions are not always symptomatic. Unfortunately, few studies have directly addressed the prevalence of sitespecific foot pain. The Feet First study of 784 Americans aged over 65 years reported that 20% of the sample exhibited tenderness to palpation in the metatarsal head region, with equal sex distribution.3 More recently, Menz et al4 reported that 36% of 301 people aged over 75 years had disabling foot pain and of these 70% reported pain in the forefoot, which equates to a similar prevalence of forefoot pain (approximately 25%). Several authors have attempted to classify metatarsalgia according to the underlying causes. Thomas et al5 proposed three types: primary metatarsalgia (caused by plantar keratoses, hallux valgus and hallux limitus/rigidus), secondary metatarsalgia (pain in the forefoot due to systemic disease) and metatarsalgia unrelated to weight distribution (including tarsal tunnel syndrome and vascular disease). Regnauld6 proposed four categories: diffuse metatarsalgia (caused by acquired mechanical/overuse disorders), localised metatarsalgia (caused by excessively long or
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large metatarsals), subcutaneous soft tissue metatarsalgia (caused by intermetatarsal neuroma, bursitis and cysts) and cutaneous metatarsalgia (caused by plantar keratoses, verrucae or ulcers). Scranton7 proposed three categories: primary metatarsalgia (caused by hallux valgus, hallux limitus/rigidus or long first metatarsal), secondary metatarsalgia (caused by systemic conditions such as rheumatoid arthritis and gout, in addition to ‘local’ disorders such as stress fractures and sesamoiditis) and pain under the forefoot (caused by intermetatarsal neuroma, verrucae or tarsal tunnel syndrome). Finally, Dockery8 proposed three categories: primary metatarsalgia (including conditions related to abnormal anatomy of the metatarsals), secondary metatarsalgia (such as Morton’s neuroma, tarsal tunnel syndrome and forefoot pain secondary to systemic conditions) and iatrogenic metatarsalgia (most commonly as a result of osteotomy procedures). Classification of metatarsalgia is clearly problematic and it is questionable whether such categorisation provides any clinical benefits or assists in diagnosis. However, what is clear from these classification systems is that pain in the forefoot may result from a myriad of causes, from localised skin, soft tissue or osseous pathology through to systemic conditions manifesting in the foot. Risk factors for the development of metatarsalgia therefore depend on the underlying condition that may be giving rise to forefoot symptoms. Nevertheless, Waldecker9,10 has recently conducted two case-control studies of unspecified metatarsalgia, based on the premise that anatomical and mechanical factors may be responsible for diffuse forefoot pain in the absence of other observable disorders. The first study revealed no difference in ultrasonically measured plantar fat pad thickness between cases and controls;9 however, the second study indicated that participants with hallux valgus and forefoot symptoms demonstrated increased plantar loading of the lateral metatarsal heads during gait.10 Over time, increased vertical loading may cause damage to plantar soft tissues, and there is also some evidence that increased plantar pressures may lead to a corresponding increase in pressure in the intermetatarsal spaces.11 Hsu et al12 and Wang et al13 have demonstrated that plantar soft tissues in older people demonstrate greater stiffness and dissipate more energy when compressed; however, the relationship between these changes and the development of symptoms has not yet been confirmed. Ultrasound imaging has shed further light on the possible causes of forefoot pain. A study of 112 people
with metatarsalgia and 50 controls revealed that the most commonly observed finding in those with metatarsalgia was intermetatarsal bursitis (21%), followed by intermetatarsal neuroma (15%) and effusion of the metatarsophalangeal joints (12%).14
DIAGNOSIS Because of the large number of conditions that may result in forefoot pain, diagnosing the underlying cause can be challenging, particularly when multiple causes may coexist. A simple clinical algorithm involving a process of elimination, based on a system described by Coughlin,15 is shown in Table 9.1. The first step is to ascertain whether the pain is associated with a plantar keratotic lesion or verruca over the symptomatic site. Once this simple cause has been ruled out, systemic conditions that commonly result in forefoot pain, such as rheumatoid arthritis, osteoarthritis or gout, need to be considered, as joint degeneration or effusions associated with these conditions can lead to forefoot symptoms (Table 9.2). Having ruled out a systemic cause, further detail regarding the nature of the symptoms should be sought, as neuritic symptoms (such as tingling, pins and needles, and referred pain into the toes) may indicate an intermetatarsal neuroma. This provisional diagnosis can be further explored using Mulder’s click test and ultrasound imaging (this is discussed later in the chapter). In the absence of neuritic symptoms, predislocation syndrome or insufficiency fractures of the metatarsals may need to be considered. Although the nature of the pain associated with predislocation syndrome can sometimes be vague, pain on plantarflexion and the tendency of the proximal phalanx to sublux when dorsal translation is applied are characteristic signs. Pain resulting from insufficiency fractures can be difficult to delineate from predislocation syndrome, so a definitive diagnosis may require bone scanning. This simple algorithm will assist in the diagnosis of the most common causes of forefoot pain in older people; however, it needs to be kept in mind that a strict process of elimination is not always possible, as several conditions may coexist. Furthermore, if all these common diagnoses are ruled out, more extensive diagnostic imaging, including magnetic resonance imaging, may be required to diagnose less commonly encountered causes of forefoot pain, such as various soft tissue and bony tumours, infection and foreign bodies.
Common causes of forefoot pain in older people
Table 9.1 Clinical algorithm for the step-wise diagnosis of forefoot pain Clinical observation
If yes, may indicate . . .
If no . . .
1. Is there a plantar keratotic lesion or verrucae present?
Painful plantar keratosis or verruca
Go to 2
2. Does the patient have a systemic condition that may lead to forefoot pain (e.g. rheumatoid arthritis, osteoarthritis, gout)?
Forefoot pain secondary to joint degeneration/synovitis. May require confirmation with plain film X-ray
Go to 3
3. Does the patient report neuritic symptoms (tingling, referred pain, pins and needles)?
Suspect intermetatarsal neuroma. Perform Mulder’s click test and confirm diagnosis with ultrasound
Go to 4
4. Is there pain slightly distal to the metatarsal head, at end range of plantarflexion or when the proximal phalanx is translated dorsally?
Predislocation syndrome
Go to 5
5. Is there localised pain on direct palpation of the metatarsal head or slightly proximal to it?
Suspect insufficiency fracture. Confirm with X-ray or bone scan
Consider less common causes and refer for more extensive diagnostic imaging
Table 9.2 Systemic conditions that may cause forefoot pain in older people Condition
Mechanism
Osteoarthritis
Cartilage degeneration, joint space narrowing and formation of osteophytes affecting the metatarsophalangeal joints
Rheumatoid arthritis
Synovitis of the metatarsophalangeal joints Development of hallux valgus Development of retracted toes Distal displacement of plantar fibro-fatty padding Development of rheumatoid nodules under metatarsal heads
Gout
Acute: inflammation of the metatarsophalangeal joints due to deposition of monosodium urate crystals Chronic: joint degeneration and formation of tophaceous deposits in joints and tendon sheaths
Psoriatic arthritis
Synovitis and enthesitis of metatarsophalangeal joints
Paget’s disease
Bone pain as a result of increased vascularity and articular distortion
COMMON CAUSES OF FOREFOOT PAIN IN OLDER PEOPLE The most common cause of forefoot pain in older people is the presence of plantar keratotic lesions, which are discussed in detail in Chapter 4. Other commonly observed conditions in older people are
intermetatarsal neuroma and predislocation syndrome. Insufficiency stress fractures of the metatarsals are only occasionally cited as a cause of forefoot pain in older people; however, they are likely to be more prevalent than is commonly recognised, because of misdiagnosis. Other conditions associated with forefoot pain, such as Freiberg’s infraction and sesamoid-
181
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itis, are most commonly diagnosed in younger people and are therefore not discussed in this chapter.
A
INTERMETATARSAL NEUROMA Aetiology and clinical presentation Intermetatarsal neuroma, also referred to as plantar digital neuroma, was first described by Lewis Durlacher in 1845 but is frequently attributed to Dudley Morton, who reported 11 cases in 1876.16 Consequently, the condition is also referred to as Morton’s neuroma or Morton’s metatarsalgia. The classical presentation is that of severe, neuritic pain in the third or fourth intermetatarsal space that radiates towards the toes, exacerbated by long periods of weightbearing and alleviated by rest or removal of footwear.15,17 Factors thought to be associated with intermetatarsal neuroma include female sex, increased body mass index, reduced space between the metatarsals, excessive foot pronation, elevated plantar pressures and the wearing of tightly fitting shoes;15,17–19 however, none of these proposed risk factors has been confirmed by case-control studies. Indeed, a recent case-control study by Betts et al20 found no difference in ultrasonically-measured intermetatarsal space or plantar pressures in 242 patients with neuroma symptoms compared to 35 controls. The pathology of intermetatarsal neuroma is still uncertain but is thought to consist of neural fibrosis, oedema, demyelination and degeneration of the intermetatarsal nerve.17 However, histological comparison studies by Morscher et al21 and Bourke et al22 found no significant differences between cases and controls, with the exception of a higher proportion of cases exhibiting demyelination. Similarly, a magnetic resonance imaging study recently reported that, while slightly larger nerve lesions were observed in people with symptoms of intermetatarsal neuroma, there was a significant overlap between cases and controls.23 These findings suggest that degenerative changes in intermetatarsal nerves may be more common than previously thought and are not necessarily associated with neuroma symptoms. The diagnosis of intermetatarsal neuroma is based on a combination of presenting symptoms, physical examination and diagnostic imaging. Compression of the affected intermetatarsal space may reproduce the symptoms and cause a palpable ‘click’ as the neuroma is subluxed beneath the transverse metatarsal ligament (referred to as Mulder’s click test; Fig. 9.1).24
B
Figure 9.1 Clinical tests for assessing intermetatarsal neuroma. A. Forefoot squeeze (Mulder’s click). B. Webspace squeeze.
However, this test is not highly specific, particularly in milder forms of the condition with less pronounced hypertrophy of the nerve. Ultrasound imaging is considered to be the most appropriate diagnostic modality, with sensitivities and specificities of between 85% and 100% when compared to intraoperative findings or postsurgical histopathology.25–32 Under ultrasound imaging, neuromas appear as elliptical hypoechogenic structures running parallel to the metatarsals that are integrated with surrounding nerve tissue. A transverse plantar scan is considered to be more accurate than a dorsal approach because of improved coupling; however, a dorsal scan is sometimes necessary when the plantar scan is negative.20 Although not as widely accessible, magnetic resonance imaging has also been used for the diagnosis of intermetatarsal neuroma, with similar sensitivity and specificity to ultrasound.33
Common causes of forefoot pain in older people
A
B
Figure 9.2 Padding techniques for intermetatarsal neuroma. A. Plantar metatarsal pad/metatarsal dome. B. Pad to elevate fourth and fifth metatarsal heads.
Conservative treatment Conservative treatment of intermetatarsal neuroma involves changing footwear to shoes with a lower heel and broader forefoot, pressure redistribution using plantar padding techniques,19 foot orthoses34 and intralesional injections of cortisone35,36 or sclerosing agents.37–39 Retrospective studies suggest that, overall, conservative management is effective in at least 50% of cases.15,40 The most effective form of padding appears to be the plantar metatarsal pad (also called a metatarsal dome), placed proximally to the second to fourth metatarsal heads (Fig. 9.2A). This pad is thought to achieve pain relief by slightly elevating and spreading the central metatarsals, thereby increasing the intermetatarsal space and decreasing pressure on the neuroma itself.41 Plantar pressure studies have confirmed that this style of pad significantly reduces forefoot pressures42,43 and is more effective than apertured pads.43 Hirschberg34 has also claimed clinical success using a technique in which the fourth and fifth metatarsal heads are elevated by gluing a small lift under the insole of the shoe (Fig. 9.2B). Intralesional injection of corticosteroid has quite variable success rates in the literature. While Greenfield et al35 reported that 80% of patients reported at least partial relief of symptoms following corticosteroid injection, a retrospective study of 115 patients by Bennett et al40 reported a much lower success rate (47%). Rasmussen et al36 found that while 80% of 43 patients who received a single corticosteroid injection obtained short-term symptomatic relief, at the 4-year follow-up period, approximately half were still symptomatic or had selected to undergo surgery. Repeated corticosteroid injection for intermetatarsal neuroma
has been also associated with adverse reactions such as plantar fat pad atrophy44,45 and skin hyperpigmentation.45 It would therefore appear that corticosteroid injection may be useful temporary measure but cannot be considered an effective long-term strategy for the treatment of intermetatarsal neuroma. Intralesional injection of sclerosing agent has been recommended by several authors. An uncontrolled study of 100 patients by Dockery reported an 89% success rate with three to seven injections of a 1 ml 4% alcohol solution every 5–10 days, with 82% reporting complete resolution of symptoms.37 Fanucci et al38 reported that ultrasound-guided injection of an anaesthetic and ethylic alcohol preparation achieved total or partial symptomatic relief in 40 patients after 10 months of follow-up. More recently, Hyer et al39 reported that, after 1 year of follow-up, five out of six patients achieved significant pain relief with a weekly series of three to nine injections of a 1 ml 4% alcohol solution. Although these results are promising, larger studies with a control group are required to confirm the efficacy of conservative treatments. Indeed, the recent Cochrane review of interventions for intermetatarsal neuroma18 found only one controlled trial of conservative treatment – a study of 23 people who received either a supinatory or pronatory orthosis (manufactured from compressed felt) which reported no differences in reported pain levels between the two groups.46 Clearly, there is a need for more rigorous evaluation of both orthotic therapy and injection therapy in the treatment of intermetatarsal neuroma.
Surgical treatment Surgical removal of intermetatarsal neuroma can be conducted under general, regional or even local anaesthesia and involves the resection of the affected nerve through a plantar, dorsal or web space incision. The most commonly used approach is through the dorsum of the foot, as this allows for earlier postoperative ambulation and does not result in plantar scarring. However, the disadvantage of this approach is that the deep transverse intermetatarsal ligament must be severed during the procedure and there is a greater chance of postoperative dead space and subsequent infection.47 The efficacy of neuroma surgery has not been thoroughly evaluated; however, case series studies indicate that up to 24% of patients have unsatisfactory results.48–50 Adverse effects of neuroma surgery are
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relatively common, including haematoma formation in the intermetatarsal space, ischaemia of the toes due to postoperative oedema and, the most troublesome complication, formation of a stump neuroma with symptomatic recurrence that often requires revisional surgery.47 Surgery appears to be more successful when only one neuroma requires excision.50 The Cochrane review of treatments for intermetatarsal neuroma18 found only two randomised trials of surgical intervention. The first, a comparison of plantar and dorsal incision techniques,51 found that the efficacy of the techniques was similar; however, the dorsal approach resulted in less symptomatic postoperative scarring. The second study compared neuroma resection versus a technique in which the interdigital nerve is transposed into the intermuscular space between the adductor hallucis and interossei muscles.52 Patients who had undergone the intermuscular transposition technique were more likely to achieve at least 50% relief of pain compared to those who had the neuroma resected. The review, however, concluded that there is currently insufficient evidence upon which to adequately assess the efficacy of surgical treatments for intermetatarsal neuroma.
A
PREDISLOCATION SYNDROME Aetiology and clinical presentation Forefoot pain associated with instability of the metatarsophalangeal joints is a common clinical finding that has been described under several different titles in the podiatric and orthopaedic literature, including metatarsophalangeal joint instability,53 monoarticular non-traumatic synovitis,54 metatarsophalangeal joint subluxation,55 plantar plate rupture56 and, most recently, predislocation syndrome.57 Because the features of each of these conditions overlap and no diagnostic criteria have yet been developed, the term predislocation syndrome is probably the most appropriate terminology. The syndrome is characterised by a progressive, dorsal subluxation of the proximal phalanx on the metatarsal head that is thought to occur in response to a gradual weakening, inflammation and eventual rupture of the plantar plate. The second metatarsophalangeal joint is considered to be the most common site, although any of the lesser metatarsophalangeal joints may be affected.58 Although no case-control studies have been undertaken, case series studies and clinical observations suggest that the syndrome is associated with hallux valgus,53,59 an
B
Figure 9.3A, B Early stage predislocation syndrome/ plantar plate rupture. Note the dorsiflexion and displacement of the second toe, with corresponding increase in second interspace. (Courtesy of Matthew Dilnot, Melbourne Foot Clinic.)
overly long metatarsal60 and the wearing of highheeled footwear.60 However, Yu et al57 suggest that the absence of these factors does not necessarily preclude a diagnosis. The classical presentation of predislocation syndrome is that of a focal, ‘bruise-like’ or throbbing pain on the plantar aspect of the joint that is exacerbated by long periods of weightbearing activity. No plantar keratotic lesions are generally present, although there may be some swelling evident and an associated widening of the interspace (Fig. 9.3). Significant transverse plane deviation of the toe occasionally occurs in advanced cases, which may indicate concur-
Common causes of forefoot pain in older people
Figure 9.5 Draw test for the assessment of predislocation syndrome.
Figure 9.4 Stage 3 predislocation syndrome, with the proximal phalanx of the second toe lying in a fixed, dislocated position with transverse plane malalignment. (Courtesy of Lesley Newcombe, La Trobe University.)
rent rupture of the collateral ligament (Fig. 9.4).61 Direct palpation just distal to the metatarsal head will elicit symptoms, as will plantarflexion of the joint to end range of motion. Thompson & Hamilton59 have also described a clinical test in which the metatarsal head is stabilised with the thumb and index finger and a vertical, translational thrust is applied to the proximal phalanx with the contralateral hand (Fig. 9.5). The test result is then used to classify the severity of the condition using the following scoring system: 0 (no dorsal translocation occurs), 1 (the phalanx subluxes dorsally), 2 (the phalanx can be dislocated from the metatarsal head but manually reduced) and 3 (the phalanx lies in a fixed dislocated position). Predislocation syndrome can be differentiated from other causes of metatarsalgia by the absence of keratotic lesions, neuritic symptoms or significant plain film X-ray findings. Bone scans may show increased localised uptake in the affected metatarsal head, while plantar plate rupture and synovitis of the flexor tendon sheath are readily observable with magnetic resonance imaging.62
Conservative treatment Conservative management of predislocation syndrome involves pain relief (using corticosteroids or nonsteroidal anti-inflammatory medications), redistribution of pressure away from the affected site, and
Figure 9.6 Taping technique for predislocation syndrome. The proximal phalanx is held in a plantar position by adhesive tape, thereby reducing tension on the plantar plate.
taping and splinting techniques to prevent further progression. Felt or foam padding placed under the affected metatarsal head will assist in elevating it relative to the proximal phalanx, which may reduce tension on the plantar plate.56 Crossover taping, in which the proximal phalanx is translated plantarly (Fig. 9.6), may achieve the same effect, although the need to frequently remove and reapply the tape makes it an impractical long term strategy.56,57 Few studies have been undertaken to assess the efficacy of conservative management of predislocation syndrome. Mizel & Michelson63 reported a 70% success rate with intra-articular corticosteroid injection and prescription of rigid shank footwear. Similarly, Trepman & Yeo64 reported a 60% rate with steroid injection and the prescription of rocker sole shoes. In contrast to these two studies, Mann & Mizel54 reported that only one of seven patients with
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metatarsophalangeal joint synovitis responded to anti-inflammatory medications and extra-depth shoes, with the remainder eventually requiring surgery. Variation in the severity of the condition may explain these disparate findings;57 however, controlled trials are required to adequately determine the efficacy of these approaches.
Surgical treatment Surgical management of predislocation syndrome involves restoring normal plantar plate function by the release of soft tissue contractures, tendon transfer and lesser metatarsal osteotomy.55,57,59,65,66 These procedures are essentially modifications of techniques used to correct lesser toe deformities and are more fully discussed in Chapter 7. Combined soft tissue and osseous techniques have been recommended by Daly & Johnson,65 who described a technique involving partial proximal phalanx excision and syndactyly of the toes, and Yu and colleagues,57 who advocated extensor hood and joint capsule release, arthrodesis of the proximal interphalangeal joint, and transfer of the flexor digitorum longus tendon by threading it dorsally through a drill hole in the metatarsal head and securing to the dorsal periosteum. Although no large-scale, controlled studies have been undertaken, surgical management has been reported to result in high levels of satisfaction in only 38–64% of patients,65,66 suggesting considerable room for improvement in surgical techniques.
INSUFFICIENCY FRACTURES OF THE METATARSALS Aetiology and clinical presentation Stress fractures develop when repetitive loads applied to bone exceed the level of mechanical resistance. There are two types of stress fracture: fatigue fractures, which result from excessive loads applied to normal bone (commonly observed in military recruits), and insufficiency fractures, which result from normal or slightly elevated loads applied to bone with low mechanical resistance.67,68 Insufficiency fractures are most commonly diagnosed in older women, who experience a rapid loss in bone density (approximately 10% per decade) from the onset of menopause.69 Although they are frequently overlooked,70 insufficiency fractures can develop in the metatarsals71–75 and need to be considered as a potential cause of forefoot
pain in older people. Clinically, these fractures present as an acute, focal area of tenderness directly under (or slightly proximal to) the affected metatarsal head, with or without swelling. In contrast to fatigue fractures, insufficiency fractures develop in response to routine daily activities and are rarely precipitated by periods of strenuous activity.72 The most common site is the second metatarsal, which experiences considerably greater strain during gait.76 Although few detailed studies have been undertaken, factors thought to be associated with metatarsal insufficiency fractures include overly long or short metatarsals, lateral metatarsal overload associated with hallux valgus, and the wearing of high-heeled shoes.72,77 Insufficiency fractures should also be suspected in older people presenting with transfer metatarsalgia following foot surgery, as several cases following Keller’s bunionectomy have been reported.78–80 Dorsoplantar plain film X-rays may reveal a small transverse crack accompanied by subchondral sclerosis of the metatarsal head; however, this can be easily missed and may not be visible for 2–3 weeks after the onset of symptoms.67,81 Bone scans are substantially more sensitive and will reveal increased uptake in the metatarsal head as early as 3 days after symptoms develop.72,73
Treatment Treatment of insufficiency fractures involves offloading the affected site until the bone has sufficient time to heal. This may involve bed rest, use of crutches, various padding techniques to offload the metatarsal head, non-forefoot-loading surgical boots or below knee plaster casts.72,74 Complete healing generally takes 6–8 weeks. Optimising the management of preexisting conditions that may result in osteopenia (such as osteoporosis, hyperparathyroidism and rheumatoid arthritis) is an important component of insufficiency fracture treatment. Furthermore, older patients diagnosed with insufficiency fractures without a history of osteoporosis should also be referred for bone density assessment.
SUMMARY Forefoot pain is common in older people and may result from a combination of local and systemic conditions. The non-specific term metatarsalgia should not be considered an adequate diagnosis, as there are few
References
clearly identifiable factors that are consistently found in patients with forefoot symptoms. Instead, older people who report pain in the forefoot region should undergo a structured, step-wise diagnostic work-up to ascertain the most likely skin, soft tissue or osseous
pathology responsible for the presenting symptoms. Because of the relatively high rate of complications and moderate levels of patient satisfaction associated with surgery, conservative management of forefoot pain should always be trialled first.
References 1. Hetherington VJ. Metatarsalgia and lesser metatarsal surgery. In: Hetherington VJ, ed. Hallux valgus and forefoot surgery. New York: Churchill Livingstone; 1994: 429–451. 2. Fadel GE, Rowley DI. Metatarsalgia. Current Orthopaedics 2000; 16: 193–204. 3. Dunn JE, Link CL, Felson DT et al. Prevalence of foot and ankle conditions in a multiethnic community sample of older adults. American Journal of Epidemiology 2004; 159: 491–498. 4. Menz HB, Tiedemann A, Kwan MMS et al. Foot pain in community-dwelling older people: an evaluation of the Manchester Foot Pain and Disability Index. Rheumatology 2006; 45: 863–867. 5. Thomas N, Nissen KI, Helal B. Disorders of the lesser rays. In: Helal B, Wilson D, eds. The foot. New York: Churchill Livingstone; 1988: 486–502. 6. Regnauld B. The foot. Berlin: Springer-Verlag; 1986. 7. Scranton PE. Metatarsalgia diagnosis and treatment. Journal of Bone and Joint Surgery 1980; 62A: 723– 732. 8. Dockery GL. Evaluation and treatment of metatarsalgia and keratotic disorders. In: Myerson MS, eds. Foot and ankle disorders. Philadelphia, PA: WB Saunders; 2000: 359–377. 9. Waldecker U. Plantar fat pad atrophy: a cause of metatarsalgia? Journal of Foot and Ankle Surgery 2001; 40: 21–27. 10. Waldecker U. Metatarsalgia in hallux valgus deformity: a pedographic analysis. Journal of Foot and Ankle Surgery 2002; 41: 300–308. 11. Holmes GB. Quantitative determination of intermetatarsal pressure. Foot and Ankle 1992; 13: 532– 535. 12. Hsu C-C, Tsai W-C, Chen CP-P et al. Effects of aging on the plantar soft tissue properties under the metatarsal heads at different impact velocities. Ultrasound in Medicine and Biology 2005; 31: 1423–1429. 13. Wang C-L, Hsu T-C, Shau Y-W et al. Ultrasonographic measurement of the mechanical properties of the sole under the metatarsal heads. Journal of Orthopaedic Research 1999; 17: 709–713. 14. Iagnocco A, Coari G, Palombi G et al. Sonography in the study of metatarsalgia. Journal of Rheumatology 2001; 28: 1338–1340.
15. Coughlin MJ. Common causes of pain in the forefoot in adults. Journal of Bone and Joint Surgery 2000; 82B: 781–790. 16. Smith TWD, Jones S. Morton’s misnomer and Durlacher’s metatarsalgia. The Foot 1999; 9: 209. 17. Wu KK. Morton’s interdigital neuroma: a clinical review of its aetiology, treatment, and results. Journal of Foot and Ankle Surgery 1996; 35: 112–119. 18. Thomson CE, Gibson JNA, Martin D. Interventions for the treatment of Morton’s neuroma. Cochrane Database of Systematic Reviews 2006; 3: CD003118. 19. Franson J, Baravarian B. Intermetatarsal compression neuritis. Clinics in Podiatric Medicine and Surgery 2006; 23: 569–578. 20. Betts RP, Bygrave CJ, Jones S et al. Ultrasonic diagnosis of Morton’s neuroma: a guide to problems, pointers, pitfalls and prognosis. The Foot 2003; 13: 92–99. 21. Morscher E, Ulrich J, Dick W. Morton’s intermetatarsal neuroma: morphology and histological substrate. Foot and Ankle International 2000; 21: 558–562. 22. Bourke G, Owen J, Machet D. Histological comparison of the third interdigital nerve in patients with Morton’s metatarsalgia and control patients. Australian and New Zealand Journal of Surgery 1994; 64: 421–424. 23. Bencardino J, Rosenberg ZS, Beltran J et al. Morton’s neuroma: is it always symptomatic? American Journal of Roentgenology 2000; 175: 649–653. 24. Mulder JD. The causative mechanism in Morton’s metatarsalgia. Journal of Bone and Joint Surgery 1951; 33B: 94–95. 25. Shapiro PP, Shapiro SL. Sonographic evaluation of interdigital neuromas. Foot and Ankle International 1995; 16: 604–606. 26. Williams RL, Grace DL, Papas GJ. Ultrasonography in the diagnosis of Morton’s neuroma. The Foot 1996; 6: 159–162. 27. Kaminsky S, Griffin L, Milsap J et al. Is ultrasonography a reliable way to diagnose Morton’s neuroma? Orthopedics 1997; 20: 37–39. 28. Oliver TB, Beggs I. Ultrasound in the assessment of metatarsalgia: a surgical and histological correlation. Clinical Radiology 1998; 53: 287–289.
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29. Jones S, Bygrave CJ, Bettes RP et al. Morton’s neuroma: a sonographic-surgical evaluation. The Foot 1999; 9: 189–192. 30. Read JW, Noakes JB, Kerr D et al. Morton’s metatarsalgia: sonographic findings and correlated histopathology. Foot and Ankle International 1999; 20: 153–161. 31. Irwin LR, Konstantoulakis C, Hyder NU et al. Ultrasound in the diagnosis of Morton’s neuroma. The Foot 2000; 10: 186–189. 32. Quinn TJ, Jacobsen JA, Craig JG et al. Sonography of Morton’s neuromas. American Journal of Roentgenology 2000; 174: 1723–1728. 33. Zanetti M, Ledermann T, Zollinger H et al. Efficiency of MR imaging in patients suspected of having Morton’s neuroma. American Journal of Roentgenology 1997; 168: 529–532. 34. Hirschberg GG. A simple cure for Morton’s neuralgia. Journal of the American Podiatric Medical Association 2000; 90: 100–101. 35. Greenfield J, Rea J, Ilfeld FW. Morton’s interdigital neuroma: indications for treatment by local injections versus surgery. Clinical Orthopaedics and Related Research 1984; 185: 142–144. 36. Rasmussen MR, Kitaoka HB, Patzer GL. Nonoperative treatment of plantar interdigital neuroma with a single corticosteroid injection. Clinical Orthopaedics and Related Research 1996; 326: 188–193. 37. Dockery GL. The treatment of intermetatarsal neuromas with 4% alcohol sclerosing injections. Journal of Foot and Ankle Surgery 1999; 38: 403–408. 38. Fanucci E, Masala S, Fabiano S et al. Treatment of intermetatarsal Morton’s neuroma with alcohol injection under US guide: 10-month follow-up. European Radiology 2004; 14: 514–518. 39. Hyer CF, Mehl LR, Block AJ et al. Treatment of recalcitrant intermetatarsal neuroma with 4% sclerosing alcohol injection: a pilot study. Journal of Foot and Ankle Surgery 2005; 44: 287–291. 40. Bennett GL, Graham CE, Mauldlin DM. Morton’s interdigital neuroma: a comprehensive treatment protocol. Foot and Ankle International 1995; 16: 760–763. 41. Polokoff MM. The treatment of Morton’s metatarsalgia. Journal of the American Podiatry Association 1948; 38: 27. 42. Poon C, Love B. Efficacy of foot orthotics for metatarsalgia. The Foot 1997; 7: 202–204. 43. McLauchlan PT, Abboud RJ, Rendall GC et al. Use of an in-shoe pressure system to investigate the effect of two clinical treatment methods for metatarsalgia. The Foot 1994; 4: 204–208. 44. Basadonna P, Rucco V, Gasparini D et al. Plantar fat pad atrophy after corticosteroid injection for interdigital neuroma: a case report. American Journal of Physical Medicine and Rehabilitation 1999; 78: 283–285.
45. Reddy PD, Zelicof SB, Ruotolo C et al. Interdigital neuroma. Local cutaneous changes after corticosteroid injection. Clinical Orthopaedics and Related Research 1995; 317: 185–187. 46. Kilmartin TE, Wallace WA. Effect of pronation and supination orthosis on Morton’s neuroma and lower extremity function. Foot and Ankle International 1994; 15: 256–262. 47. Miller SJ. Entrapment neuropathies. In: Hetherington VJ, eds. Hallux valgus and forefoot surgery. New York: Churchill Livingstone; 1994: 401–428. 48. Gauthier G. Thomas Morton’s disease: a nerve entrapment syndrome. A new surgical technique. Clinical Orthopaedics and Related Research 1979; 142: 90–92. 49. Mann RA, Reynolds JC. Interdigital neuroma – a critical clinical analysis. Foot and Ankle 1983; 3: 238–243. 50. Gudas CJ, Mattana GM. Retrospective analysis of intermetatarsal neuroma excision with preservation of the transverse metatarsal ligament. Journal of the American Podiatric Medical Association 1986; 25: 459–463. 51. Nashi M, Venkatachalam A, Muddu B. Surgery of Morton’s neuroma: dorsal or plantar approach? Journal of the Royal College of Surgeons 1997; 42: 36–37. 52. Colgrove R, Huang E, Barth A et al. Interdigital neuroma: intermuscular neuroma transposition compared with resection. Foot and Ankle International 2000; 21: 206–211. 53. Fortin PT, Myerson MS. Second metatarsophalangeal joint instability. Foot and Ankle International 1995; 16: 306–314. 54. Mann RA, Mizel MS. Monoarticular synovitis of the metatarsophalangeal joint: a new diagnosis? Foot and Ankle 1985; 6: 18–21. 55. Coughlin MJ. Subluxation and dislocation of the second metatarsophalangeal joint. Orthopedic Clinics of North America 1989; 20: 535–551. 56. Dilnot MC, Michaud TC. Plantar plate rupture. Australasian Journal of Podiatric Medicine 2003; 37: 43–46. 57. Yu GV, Judge MS, Hudson JR et al. Predislocation syndrome. Progressive subluxation/dislocation of the lesser metatarsophalangeal joint. Journal of the American Podiatric Medical Association 2002; 92: 182–199. 58. DuVries HL. Dislocation of the toe. Journal of the American Medical Association 1965; 160: 728. 59. Thompson FM, Hamilton WG. Problems of the second metatarsophalangeal joint. Orthopedics 1987; 10: 83–89. 60. Coughlin MJ. Second metatarsophalangeal joint instability in the athlete. Foot and Ankle International 1993; 14: 309–319.
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61. Deland JT, Sung I. The medial crossover toe: a cadaveric dissection. Foot and Ankle International 2000; 21: 375–378. 62. Yao L, Cracchiolo A, Farahani K et al. Magnetic resonance imaging of plantar plate rupture. Foot and Ankle International 1996; 17: 33–36. 63. Mizel MS, Michelson JD. Nonsurgical treatment of mono-articular nontraumatic synovitis of the second metatarsophalangeal joint. Foot and Ankle International 1997; 18: 424–426. 64. Trepman E, Yeo S. Non-operative treatment of metatarsophalangeal joint synovitis. Foot and Ankle International 1995; 16: 771–777. 65. Daly PJ, Johnson KA. Treatment of painful subluxation or dislocation at the second and third metatarsophalangeal joints by partial proximal phalanx excision and subtotal webbing. Clinical Orthopaedics and Related Research 1992; 278: 164–170. 66. Gazdag A, Cracchiolo A. Surgical treatment of patients with painful instability of the second metatarsophalangeal joint. Foot and Ankle International 1998; 19: 137–143. 67. Cooper KL. Insufficiency stress fractures. Current Problems in Diagnostic Radiology 1994; 23: 29– 68. 68. Soubrier M, Dubost J-J, Boisgard S et al. Insufficiency fracture. A survey of 60 cases and review of the literature. Joint Bone Spine 2003; 70: 209–218. 69. Hannan MT, Felson DT, Anderson JJ. Bone mineral density in elderly men and women: results from the Framingham osteoporosis study. Journal of Bone and Mineral Research 1992; 7: 547–553. 70. Carpintero P, Berral FJ, Baena P et al. Delayed diagnosis of fatigue fractures in the elderly. American Journal of Sports Medicine 1997; 25: 659–662.
71. Varenna M, Binelli L, Zucchi F et al. Is the metatarsal fracture in postmenopausal women an osteoporotic fracture? A cross-sectional study on 113 cases. Osteoporosis International 1997; 7: 558–563. 72. Kaye R. Insufficiency stress fractures of the foot and ankle in postmenopausal women. Foot and Ankle International 1988; 19: 221–224. 73. Lechevalier D, Fournier B, Leleu T et al. Stress fractures of the heads of the metatarsals. A new cause of metatarsal pain. Revue de rhumatisme (English edition) 1995; 62: 255–259. 74. Tomczak RL, VanCourt R. Metatarsal insufficiency fractures in previously undiagnosed osteoporosis patients. Journal of Foot and Ankle Surgery 2000; 39: 174–183. 75. Hasselman CT, Vogt MT, Stone KL et al. Foot and ankle fractures in elderly white women. Journal of Bone and Joint Surgery 2003; 85-A: 820–824. 76. Donahue SW, Sharkey NA, Modanlou KA et al. Bone strain and microcracks at stress fracture sites in human metatarsals. Bone 2000; 27: 827–833. 77. Anderson EG. Fatigue fractures of the foot. Injury 1990; 21: 275–279. 78. Ford LT, Gilula LA. Stress fractures of the middle metatarsals following the Keller operation. Journal of Bone and Joint Surgery 1977; 59A: 117–118. 79. Battey MA. The lesser metatarsal stress fracture as a complication of the Keller procedure. Journal of the American Podiatry Association 1980; 70: 182–186. 80. Zechman JS. Stress fracture of the second metatarsal after Keller bunionectomy. Journal of Foot Surgery 1984; 23: 63–65. 81. Chowchuen P, Resnick D. Stress fractures of the metatarsal heads. Skeletal Radiology 1998; 27: 22–25.
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CHAPTER
Disorders of the midfoot and rearfoot
PLANTAR HEEL PAIN SYNDROME
CHAPTER CONTENTS Plantar heel pain syndrome 191 Classification and clinical presentation Aetiology 192 Assessment and diagnosis 193 Treatment 194 Tibialis posterior dysfunction 197 Classification and clinical presentation Aetiology 198 Assessment and diagnosis 198 Treatment 199 Retrocalcaneal conditions 199 Haglund’s deformity 200 Achilles tendinopathy 202 Osteoarthritis of the midfoot and rearfoot 205 Prevalence and risk factors 205 Clinical presentation 206 Conservative treatment 206 Surgical treatment 207 Less common midfoot and rearfoot disorders 207 Painful pes cavus 207 Tarsal tunnel syndrome 208 Sinus tarsi syndrome 208 Summary 208 References 209
10
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197
Plantar heel pain is one of the most common conditions affecting the foot, accounting for over 1 000 000 patient visits to medical practitioners in the USA per year. Of these visits, 16% are made by people over the age of 65 years.1 The Feet First study of 784 Americans aged over 65 years reported that 4% exhibited tenderness to palpation of the plantar heel pad and 7% to palpation of the arch, with equal sex distribution.2 More recently, Menz et al3 reported that 16% of 301 people aged over 75 years had disabling foot pain affecting the heel. Plantar heel pain has also been shown to have a significant impact on mobility and health-related quality of life. Riddle et al4 administered the Lower Extremity Functional Scale to 50 participants with heel pain and reported that most experienced some difficulty in walking-related and occupational activities. In older people, the impact of the plantar heel pain is considerable. In a secondary analysis of the Feet First study, Badlissi et al5 found that older people with heel pain exhibited significantly lower scores on the Foot Health Status Questionnaire after accounting for age and comorbidities.
CLASSIFICATION AND CLINICAL PRESENTATION The nomenclature and classification of heel pain is highly problematic. Heel pain has been variably referred to as plantar fasciitis, subcalcaneal bursitis, neuritis, subcalcaneal pain, stone bruise, calcaneal periostitis, heel spur syndrome, subcalcaneal spur and calcaneodynia.6–8 The most widely used term is plantar
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fasciitis; however, recent evidence suggests that this may be a misnomer as no inflammatory cells are evident in postoperative histology specimens of the plantar fascia.9 Similarly, terms incorporating the word ‘spur’ are problematic as calcaneal spurs are commonly found in people without heel pain.10–12 Because the aetiology of heel pain is unclear (and is likely to be multifactorial) the term plantar heel pain syndrome is probably the most appropriate terminology to use until a definitive diagnosis is obtained using diagnostic imaging. Several authors have proposed classification systems for heel pain, although none have been widely adopted. Shikoff et al13 proposed two categories of heel pain: local (including plantar fasciitis and plantar calcaneal bursitis) and systemic (including heel pain associated with connective tissue diseases and vascular disease). Kwong et al14 recommended a more complex classification system, including inflammatory, metabolic, degenerative, nerve entrapment, traumatic and overuse subgroups. Perhaps the most useful clinical classification is that proposed by Singh et al,15 which categorises inferior heel pain according to the tissue involved (Fig. 10.1). Although in practice there is likely to be some overlap between these categories, such a system provides a good starting point for differential diagnosis. The classical presentation of plantar heel pain syndrome is that of a sharp pain under the medial heel that may radiate towards the arch. Symptoms are particularly severe upon rising in the morning (referred
Plantar fascia – Plantar fasciitis – Rupture – Enthesopathy
Soft tissue – Fat pad atrophy – Heel bruise – Bursitis
Heel pain syndrome
Bone – Calcaneal stress fracture – Paget’s disease – Tumours – Infection
Nerve – Tarsal tunnel syndrome – Abductor digiti minimi nerve entrapment – Sciatica (S1) radiculopathy
Figure 10.1 Classification of heel pain syndrome.
to as ‘first step pain’) and tend to subside after walking for a few steps. This is thought to be due to periods of inactivity causing the accumulation of oedema within the plantar tissues, which is dispersed by the action of the calf muscles when walking. Most commonly, symptoms are unilateral.15,16 Symptoms may vary depending on the tissue involved. In cases with nerve involvement, there may be evidence of neuritic symptoms (e.g.: burning, radiating pain),17 while cases with osseous involvement (such as insufficiency fracture of the calcaneus) do not generally subside after activity.15 Nocturnal pain may indicate less common causes such as tumours or infections.15
AETIOLOGY Pathogenesis The pathogenesis of plantar heel pain syndrome is poorly understood. Traditionally, heel pain was considered to be an inflammatory condition of the plantar fascia (hence the term plantar fasciitis) caused by excessive traction and subsequent microtears of the insertion of the plantar fascia into the calcaneus. Histological analysis of postsurgical specimens of the plantar fascia, however, indicate several degenerative changes (including fascial thickening, fibrosis, calcification and collagen necrosis) but no evidence of inflammatory cells.9,18–20 The presence of bony spurs within the plantar fascia or intrinsic musculature does appear to be more common in those with heel pain compared to controls11,12,21 and diagnostic imaging techniques have revealed several other structural changes in patients with heel pain, such as fat pad abnormalities, hyperaemia, adventitious bursae, calcaneal stress fractures, bone oedema and partial ruptures of the plantar fascia.12,22–24 Taken together, these findings suggest that heel pain results from a complex degenerative process involving multiple tissues rather than a purely inflammatory response of the plantar fascia. It is likely, however, that the pathological processes differ depending on whether the condition is acute or chronic.
Risk factors Several risk factors for plantar heel pain have been proposed, which can be summarised as intrinsic (including increased body mass index, limited ankle range of motion, limb length discrepancy, reduced
Plantar heel pain syndrome
ASSESSMENT AND DIAGNOSIS Table 10.1 Factors associated with plantar heel pain Factor
Level of evidence
Increased body mass index Increased weight Older age Decreased ankle dorsiflexion ROM Decreased first metatarsophalangeal joint extension ROM Prolonged standing Pronated foot posture Reduced calf strength ROM: range of motion
Strong
Weak Inconclusive
heel pad thickness, excessive foot pronation and limited first metatarsophalangeal joint range of motion) and extrinsic (including long periods of weightbearing activity and inappropriate footwear). A recent systematic review of factors associated with heel pain7 summarised the results of 13 case-control and three case-series studies; a summary of the findings is shown in Table 10.1. Of the multitude of proposed risk factors, the factor with the highest level of evidence was increased body mass index/obesity, followed by increased age, decreased ankle dorsiflexion range of motion, decreased first metatarsophalangeal joint range of motion and prolonged standing. Each of these risk factors is consistent with the view that heel pain results from both the traction placed on the plantar fascia and compressive forces applied to the heel itself. It should be noted, however, that many of these studies focused on plantar fasciitis rather than the broader concept of heel pain syndrome. Furthermore, few studies have specifically examined risk factors for heel pain in older people. Because of age-related differences in foot structure, particularly the increased stiffness of the plantar heel pad,25–27 it is likely that the relative importance of underlying risk factors for heel pain in older people may be somewhat different from the situation in younger people. In particular, it is likely that degenerative changes in the heel resulting from vertical compression play a larger role in the development of heel pain in older people. Furthermore, older people are also more likely to present with heel pain associated with an underlying systemic condition or infection.
The accurate assessment and diagnosis of heel pain can be difficult, as no widely accepted diagnostic algorithm has been developed and at least 30 differential diagnoses have been reported in the literature.8 A provisional diagnosis can be reached from evaluating the location and characteristics of the pain and, in practice, most patients are considered to have plantar fasciitis (and are treated accordingly) unless proved otherwise. Table 10.2 (modified from Buchbinder16) summarises clinical signs that point towards less common causes of heel pain. Diagnostic imaging is not always necessary to confirm the diagnosis of plantar fasciitis but may play a role in excluding other potential diagnoses. Plain film X-rays will assist in ruling out calcaneal stress fractures and bony tumours;28 however, the observation of a calcaneal spur cannot be considered diagnostic, as approximately 15–40% of the general population have spurs,11,12 the prevalence of which is associated with increased age, obesity and osteoarthritis.29,30 In a recent study of 27 symptomatic patients and 79 controls, Osborne et al12 found that the combination of two observations from a lateral X-ray (plantar fascia thickness greater than 4 mm and presence of fat pad abnormalities) provided better differentiation between cases and controls than the presence of spurs. Bone scanning of painful heels reveals increased blood flow and blood pooling at the insertion of the plantar fascia in a large number of cases31 and is thought to be indicative of osteoblastic activity associated with a periosteal reaction at the enthesis. Groshar et al32 compared 58 symptomatic and 28 asymptomatic feet and found that a positive bone scan had a sensitivity of 78% and specificity of 86% for the detection of clinically determined plantar fasciitis. However, increased uptake in the plantar heel region may also occur in the presence of stress fractures, osteomyelitis and tumours, so it is often difficult to delineate the contribution of specific structures from a positive bone scan. Ultrasound imaging is not routinely used to diagnose plantar fasciitis; however, several studies have shown that people with heel pain demonstrate significant increases in the thickness of the plantar fascia (approximately 5–7 mm compared to the normal thickness of 2–4 mm).33–37 Furthermore, reduced echogenicity of the plantar fascia is more evident in people with heel pain and may provide greater discrimination than thickness measurements. In the Groshar et al32 study, evidence of hypoechoic regions
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Table 10.2 Differential diagnosis of heel pain Diagnosis
Distinguishing clinical features
Plantar fasciitis
Morning pain Pain on palpation of plantar fascia with toes dorsiflexed
Plantar fascia rupture
Sudden onset of pain Inability to bear weight after activity Bruising and swelling Noticeable decrease in arch height compared to unaffected side
Calcaneal stress fracture
Develops after repetitive weightbearing exercise Tenderness on mediolateral compression of the heel Plain radiographs may indicate area of sclerosis
Paget’s disease
Bone pain elsewhere in body Bowing of the tibia
Fat pad atrophy
Pain or tenderness in central heel region Visible atrophy of plantar fibrofatty padding No morning pain
Plantar calcaneal bursitis
Erythema and swelling of the plantar to posterior heel region
Medial calcaneal nerve entrapment
Burning pain, paraesthesia Positive Tinel’s sign (radiating pain in response to nerve percussion)
Neuropathic heel pain
Diffuse pain Nocturnal pain
in the plantar fascia had a positive predictive value of 95% for heel pain compared to 84% for plantar fascial thickening, and demonstrated similar diagnostic accuracy to bone scanning. Magnetic resonance imaging (MRI) has received only limited use in the diagnosis of heel pain; however, it may assist in the differentiation between plantar fasciitis and less common conditions. Calcaneal stress fractures, plantar fascial tears, plantar fibromatosis and capillary hemangioma of the heel can be clearly detected from MRI scans.22,38,39 MRI may also have a role in presurgical planning.
Less common causes of heel pain A diagnosis of plantar heel pain syndrome accounts for the vast majority of plantar heel pain cases; however, there are several other conditions that may manifest as pain in the heel region, including systemic conditions (e.g. rheumatoid arthritis, diffuse idiopathic skeletal hyperostosis, hypertrophic osteoarthropathy, psoriatic arthritis and other seronegative spondyloarthropathies, gout and Paget’s disease),40,41
nerve entrapment,17 soft tissue42–46 and osseous47 tumours and infections. Nerve entrapments and tumours should be suspected in patients with longstanding heel pain that has not responded to conservative treatments. Definitive diagnosis will generally require diagnostic imaging and additional diagnostic tests (e.g. blood tests, synovial fluid analysis). A brief summary of these conditions is provided in Table 10.3; however, for further detail the reader is referred to recent comprehensive reviews by Selth & Francis40 and Burns et al.41
TREATMENT Conservative A wide variety of conservative treatments have been described for heel pain. These can be broadly classified into three groups according to the aims of the treatment: (1) reduction of pain and inflammation, (2) reduction of soft tissue stress and (3) restoration of muscle strength and flexibility (Table 10.4).48 Anecdotally, conservative management is believed to
Plantar heel pain syndrome
Table 10.3 Less common causes of heel pain Classification
Disease/condition
Characteristic presentation
Systemic conditions
Rheumatoid arthritis
Paget’s disease
Bilateral heel pain, may be associated with plantar rheumatoid nodules and large calcaneal spurs Multiple painful entheses in the spine, shoulder, elbow, pelvis, knee and foot. Large, irregular calcaneal spurs with no evidence of erosion or periosteal reaction Acute unilateral heel pain with periostitis and increased bone density of the calcaneus, often accompanied by soft tissue swelling of the toes and clubbed nails Large, irregular calcaneal spurs with fluffy appearance, often accompanied by ‘sausage digits’ (fingers and toes) Symmetrical peripheral arthritis, soft tissue swelling, inflammation of calcaneal enthesis Tophaceous deposits and associated erosive lesions of the calcaneus Severe, continuous deep bone pain affecting the calcaneus
Nerve entrapment
May affect medial calcaneal, medial plantar or lateral plantar nerves
Numbness, pins and needles and/or radiating pain that can be elicited by stroking the medioplantar region of the heel
Soft tissue tumours
Soft tissue chondroma
Unilateral, circumscribed, firm, freely moveable subcutaneous mass on the plantar aspect of the heel. Pain aggravated by standing and relieved by rest
Osseous tumours
Intraosseous lipoma
No obvious physical signs. Unilateral, pain worse in mornings and relieved by rest. Pain can be elicited from lateral compression of the heel Palpable mass, deep-seated pain that is worse in the evenings
Diffuse idiopathic skeletal hyperostosis Hypertrophic osteoarthropathy
Psoriatic arthritis Seronegative spondyloarthropathies Gout
Osteoid osteoma
Table 10.4 Conservative treatments for heel pain Reduction in pain and inflammation
Reduction of tissue stress
Restoration of muscle strength and flexibility
Rest Reduction in activity Ice Anti-inflammatory medications Massage Therapeutic ultrasound Low-intensity laser Iontophoresis Herbal medicine Acupuncture Extra-corporeal shockwave therapy
Footwear modification/change Strapping Padding Heel cups Foot orthoses Casting/bracing
Calf muscle stretching Night stretch splints
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be effective in the majority of cases; however, few detailed studies have been undertaken. A review of 250 heel pain patients by Weil et al49 claimed an 85% success rate with a standardised conservative treatment regimen consisting of activity modification, calf stretching, non-steroidal anti-inflammatory medications (NSAIDs), cortisone injection and customised foot orthoses. A somewhat lower success rate was reported by Taunton et al,50 with only 40% of 78 patients reporting 75% of greater improvement in symptoms following a similar conservative treatment approach. Finally, a long-term follow-up study of 100 conservatively-managed patients followed for an average of 4 years by Wolgin et al51 reported that 82% experienced complete resolution of their symptoms. No studies have specifically addressed success rates in older people. However, it is widely believed that the longer the duration of symptoms, the more difficult heel pain is to manage with conservative approaches.51 The most recent Cochrane review of treatments for heel pain collated the results of 19 randomised controlled trials (RCTs) involving 1626 patients.52 Overall, the quality of many of the studies was poor. Nevertheless, there was some evidence for the efficacy of corticosteroid injection, limited evidence for topical corticosteroid administered by iontophoresis, dorsiflexion night splints and foot orthoses, and no evidence to support the efficacy of therapeutic ultrasound, laser or magnetic insoles. Brief summaries of the evidence for these treatments are provided below. Corticosteroid injections have been evaluated in three published randomised controlled trials,53–55 none of which reported significant long-term reductions in pain compared to a placebo. However, Crawford et al55 reported a small but statistically significant reduction in pain at 1 month follow-up. The efficacy of repeated injections over a prolonged period is uncertain, although, given that there have been reports of plantar fascial rupture associated with longterm corticosteroid use,56,57 it appears that corticosteroid injection is best reserved for short-term pain relief. Dorsiflexion night splints are worn while sleeping and align the ankle in a neutral or dorsiflexed position while the metatarsophalangeal joints are also dorsiflexed, thereby causing a gradual passive stretch of the calf muscles and the plantar fascia. The efficacy of this treatment approach is uncertain, as, although one crossover trial reported significant reductions in pain,58 another trial failed to show such a benefit.59
Furthermore, night splints are not well tolerated by many patients, as they are cumbersome and may interfere with normal sleeping patterns. In one study, 19% of the patients reported dissatisfaction with this treatment approach.58 Active calf muscle stretching, although commonly used as an adjunct treatment in clinical practice, does not appear to be effective in isolation. Radford et al60 compared 2 weeks of daily calf stretching versus sham ultrasound and found no significant differences in pain reduction between the two groups. A variety of foot orthoses are used for the management of plantar heel pain, including prefabricated insoles, customised orthoses and various cushioning devices. Two trials found no benefit of magnetic insoles over simple cushioning insoles,61,62 while four trials comparing prefabricated orthoses to custom orthoses reported quite variable findings. Lynch et al54 compared (1) low-Dye taping followed by custom foot orthoses to (2) an accommodative viscoelastic heel insert and (3) corticosteroid injection followed by NSAIDs and found that the custom orthoses/taping group demonstrated greater reductions in pain after 3 months. Similarly, Turlik et al63 reported that ‘functional’ orthoses were more effective than cushioned heel pads. In contrast to these findings, Martin et al64 found no differences between prefabricated orthoses, customised orthoses and dorsiflexion night splints, and Pfeffer et al65 found that prefabricated orthoses were more effective than customised orthoses or stretching. Since the publication of the Cochrane review, two key RCTs have been reported in the literature relating to mechanical treatments. Radford et al66 randomised 92 people with heel pain to receive either low-Dye taping or sham ultrasound and found that the taping group reported a small but significant reduction in first-step pain after 1 week compared to the sham group. Landorf et al67 compared semi-rigid customised orthoses to prefabricated orthoses and a sham insole and found that, while both the customised and prefabricated orthoses improved function to a similar degree at 3 months, no significant differences between the three groups for pain or function were noted at 12 months, suggesting that plantar heel pain may be self-limiting. This paper also included a meta-analysis of their results combined with three similar trials (Lynch et al,54 Pfeffer et al65 and Martin et al64), which indicated no significant benefit of custom orthoses over prefabricated orthoses. Taken together, these findings suggest that the treatment regimen com-
Tibialis posterior dysfunction
monly employed by podiatrists (taping followed by orthoses) is effective in the short term; however, there appears to be no benefit of custom orthoses over prefabricated orthoses. The efficacy of shock-absorbing heel pads and rigid heel cups has not been rigorously evaluated; however, it is likely that rigid heel cups may be of particular value in managing heel pain in older people. As stated previously, it has been shown that ageing is associated with significant increases in the stiffness of the plantar heel pad25–27 due to breakdown of the fibrous septa and a subsequent increase in lateral expansion when weightbearing. By confining the lateral expansion of the heel pad with rigid heel cups, the vertical thickness of the pad is maintained, which may enhance shock absorption and prevent further damage to soft tissue structures in the plantar heel region.68,69 Uncontrolled studies have reported good clinical results with the use of rigid heel cups in patients with ‘bruised heels’70 and it is possible that circumferential taping around the heel has a similar effect. The effectiveness of extracorporeal shockwave therapy is uncertain. This relatively new treatment involves the transcutaneous application of shockwaves into the heel region with the aim of stimulating healing of the enthesis and inhibiting pain receptors. Of the eight RCTs that have been conducted, three showed no benefit71–73 and five reported small reductions in pain when compared to a placebo.74–78 These findings, however, need to be viewed with some caution. Firstly, the generalisability of these findings is limited, as inclusion into four of these studies required the positive identification of a calcaneal spur from X-ray. Secondly, many of these trials were of low quality, with a tendency towards lower-quality trials and trials funded by shock-wave device manufacturers reporting more favourable outcomes.79 It is also worth noting that extracorporeal shockwave therapy without local anaesthesia is generally considered to be painful. In one study, 79% of people reported pain during treatment.77
pression.80 Although case series studies indicate very high levels of patient satisfaction (ranging from 81% to 94%),20,81,82 no randomised trials have been undertaken. Recovery from surgery may take several months and complications including scarring, medial arch pain, cramping and calcaneal fracture have been reported in up to 10% of patients.82 Surgical intervention for heel pain should be very carefully considered in older people because of prolonged recovery times and the increased risk of acquired flat foot deformity.
TIBIALIS POSTERIOR DYSFUNCTION CLASSIFICATION AND CLINICAL PRESENTATION Tibialis posterior dysfunction (TPD) is a condition in which the tendon of the tibialis posterior muscle becomes weak and elongated, leading to a progressive, painful flat foot deformity (Fig. 10.2).83 Although the prevalence is unknown, the condition most commonly affects middle-aged and elderly women. The classical features of TPD are a progressive flattening of the foot, tenderness and swelling along the tibialis
A
Surgical Surgery for heel pain is generally only considered appropriate for a select group of patients who have had severe, chronic pain and have failed to respond to several conservative treatments.15,16 Numerous techniques have been described, involving total or partial release of the plantar fascia with or without resection of the calcaneal spur and tibial nerve decom-
B
Figure 10.2A, B Pes planus (flat foot). (A, courtesy of Lloyd Reed, Queensland University of Technology.)
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Table 10.5 Classification of tibialis posterior dysfunction Stage
Features
1
Tendon inflamed No change in foot shape
2
Tendon elongated Acquired flat foot deformity
3
Fixed deformity Degenerative changes at subtalar joint
4
Fixed deformity Degenerative changes at subtalar and ankle joints
posterior tendon as it passes behind the medial malleolus, and reported difficulty in walking on uneven surfaces.84–86 However, there is a broad spectrum of TPD severity, which has led to the development of several classification systems. Johnson & Strom87 proposed three stages, Myerson88 added a fourth stage incorporating arthritic changes in the ankle joint, Mueller89 proposed a different four stage classification system incorporating an asymptomatic stage, and Wainwright et al90 have proposed a classification system based on MRI findings. The modified scale reported by Myerson88 is provided in Table 10.5.
Figure 10.3 Typical plantar pressure output of a patient with tibialis posterior dysfunction.
female sex, obesity and hypertension.95 TPD may also be a cause of flat foot deformity in people with rheumatoid arthritis.96 As TPD progresses, the arch becomes progressively lower, the calcaneus everts and the forefoot abducts relative to the rearfoot. This change in foot posture results in significant alterations to the weightbearing function of the foot, characterised by increases in rearfoot eversion, increased medial plantar pressure distribution (Fig. 10.3), and increased electromyographic activity of the tibialis posterior muscle.97,98 Over time, the altered function of the foot often results in arthritic degeneration of the joints of the midfoot and rearfoot.99
AETIOLOGY The pathogenesis of TPD is poorly understood. Histological studies of affected tendons demonstrate features of chronic tendon degeneration accompanied by fibrosis but no evidence of inflammatory cells.91,92 These changes are thought to result from repeated microtrauma caused by excessive strain placed on the tendon in the presence of mild flat foot. Vascular factors may also play a role, as a hypovascular region in the tendon has been identified posterior and inferior to the medial malleolus, where the tendon is firmly tethered by the flexor retinaculum.93 Ligamentous damage is frequently observed in advanced cases, with the spring ligament complex being particularly affected.94 However, whether the tendon dysfunction precedes ligament damage or vice versa remains unclear. No case-control studies have been conducted to ascertain the risk factors associated with TPD; however, case series studies indicate that the condition appears to be associated with advancing age,
ASSESSMENT AND DIAGNOSIS The assessment of TPD is relatively straightforward, as a diagnosis can be reached on the basis of history taking and physical examination. In the early stages, patients will report a vague, insidious pain around the medial malleolar region. As the condition progresses, patients may also report noticing changes in the shape of the affected foot and difficulty performing certain activities, such as walking up stairs or over uneven ground.84,86,100,101 In advanced cases, the foot becomes markedly everted and pain may develop in the lateral ankle region as the calcaneus abuts against the distal fibula.84 A recent study of 65 older people indicated that positive responses to two statements on a questionnaire – regarding the presence of pain and swelling in the medial ankle region and observations of changes in the shape of the foot – detected 100% of patients who had been clinically diagnosed with TPD, with a specificity of 98%.85
Retrocalcaneal conditions
Several clinical tests can assist in the diagnosis of TPD. Visual observation will reveal signs of pes planus (flat foot deformity), with a lowering of the longitudinal arch (Fig. 10.2A). Viewed from behind, the affected foot may demonstrate the ‘too many toes’ sign, in which three or more toes can be viewed lateral to the heel as a result of abduction of the forefoot.87 Patients will have difficulty rising on to their toes, and a loss of heel inversion when performing this task may also be evident. Manual muscle testing of the tibialis posterior muscle strength will also reveal marked weakness on the affected side.84,86,100 Diagnostic imaging is not necessary to confirm a diagnosis of TPD but may be worthwhile to visualise the extent of tendon damage or to quantify the extent of the deformity. Plain film radiographs are useful for assessing deformity and the severity of osteoarthritic changes, and to exclude other possible causes.101 Lateral X-rays will reveal a decreased calcaneal inclination angle, increased calcaneal-first metatarsal angle and a break in the cyma line (Fig. 10.2B). Anteroposterior X-rays are less helpful but will reveal forefoot abduction and degenerative changes in the midfoot joints.84,102 Ultrasound will reveal increased tendon diameter and evidence of echogenic areas within the tendon.103 MRI can detect discontinuity in the tendon but does not confer any substantial benefit over ultrasound and is generally only used for presurgical planning.104–107
TREATMENT Conservative Conservative treatment of TPD involves measures for pain relief, mechanical interventions to control the deforming forces on the foot, and strengthening exercises. Initial treatment should involve the prescription of NSAIDs and the application of rigid adhesive taping, which has been shown to significantly control foot pronation.108 Extending tape stirrups above the ankle (so-called ‘high-Dye’ taping) may be more effective in controlling total range of motion than low-Dye taping.109 Longer-term management includes the prescription of rigid foot orthoses and appropriate supportive footwear, strengthening exercises using graduated elastic exercise bands and, in severe cases, ankle–foot orthoses (AFOs).84,86,100–102 Corticosteroid injection is generally not recommended because of the increased risk of tendon rupture with prolonged use, but may be useful if combined with cast immo-
bilisation or removable walking casts to discourage excessive weightbearing activity. No RCTs of these treatments have been undertaken, so their efficacy is uncertain. However, two case series studies have reported favourable results. Wapner & Chan110 found that 67% of patients were satisfied with non-operative treatment, which in most cases consisted of the UCBL shoe insert. Similarly, Jari et al111 reported that a non-surgical management approach (consisting of NSAIDs, icing, therapeutic ultrasound, strengthening exercises, UCBL shoe inserts and AFOs) was effective in 23 out of 28 patients followed up for two years.
Surgical Surgical management of TPD varies according to the stage of the condition. Stage I TPD is generally managed with synovectomy and tendon debridement/repair in conjunction with calcaneal osteotomy to correct the foot into a more supinated position. Stage II TPD is treated in a similar manner, with the addition of tendon transfer (either flexor digitorum longus112,113 or a split tibialis anterior114) to assist in the antipronation function of tibialis posterior. Surgical management of stage III TPD generally involves triple arthrodesis (fusion of the subtalar, calcaneocuboid and talonavicular joints), while stage IV often requires pantalar arthrodesis (fusion of the ankle subtalar, calcaneocuboid and talonavicular joints).86,101 As with conservative treatments, no controlled trials of these surgical techniques have been undertaken. However, case series studies have reported good to excellent results in 80% of patients.88,113,115 Recovery may take several months and will frequently require a below-knee plaster cast.86
RETROCALCANEAL CONDITIONS Pain in the posterior region of the heel is less common than plantar heel pain, and subsequently has received relatively little attention in the literature. As with plantar heel pain, retrocalcaneal pain can be considered to be a syndrome which encompasses a variety of pathological entities that often present concurrently. Although accurate prevalence data is unavailable, the most common conditions affecting the posterior aspect of the heel in older people appear to be Haglund’s deformity (with or without retrocalcaneal bursitis) and Achilles tendinopathy, while less
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common causes include soft tissue manifestations of arthritic conditions (such as rheumatoid nodules) and soft tissue cysts and tumours.
A
HAGLUND’S DEFORMITY Definition and aetiology Haglund’s deformity, also known as pump bumps, winter heel, achillodynia, retrocalcaneal bursitis and cucumber heels, was first described by Patrick Haglund in 1928.116 Haglund reported a case of a 20-year-old woman with pain located in the posterosuperior aspect of the heel accompanied by a bony enlargement at the insertion of the Achilles tendon, which he attributed to the wearing of shoes with a rigid heel counter. In 1945, Fowler & Philip117 proposed that patients with the condition exhibited a structural anomaly of the calcaneus, in which the angle formed between the plantar surface of the calcaneus and the most posterior projections of the bursal surface (now known as Fowler–Philip’s angle or FPA) is increased. In such a foot, there is a greater tendency for the heel to become compressed against the shoe, leading to inflammation of the superficial tendo achillis or retrocalcaneal bursa, the formation of a retrocalcaneal exostosis and subsequent overlying hyperkeratosis. Subsequent studies have largely supported this view;118 however, there is some debate regarding the angle at which the foot is susceptible to the development of the deformity, and preliminary evidence that other radiographic measurements may be more highly predictive than the FPA. Ruch119 reported on 65 surgical cases of Haglund’s deformity and found that only seven exhibited a FPA greater than 75°. However, the calcaneal inclination angle (CIA) ranged from 20–50°, suggesting that a combination of the FPA and the CIA may provide a more accurate indicator of the structural anomaly of the calcaneus responsible for the condition. Vega et al120 reviewed 20 cases and suggested that the summation of the FPA and CIA (referred to as the ‘total angle’) ranges from 85° to 97° in people with Haglund’s deformity, compared to a normal range of 64–89°. More recently, a large study by Mishra et al121 of 117 cases and 72 controls indicated that the CIA was more strongly correlated with Haglund’s deformity than the FPA. The authors also proposed a new measurement, the calcaneal body index (the ratio between the maximum height of the posterior and anterior body of the calcaneus) as a possible aetiological factor, suggesting that people
B
C
D b a
Figure 10.4 Angles obtained from lateral foot radiographs of relevance to Haglund’s deformity. A. Fowler–Philip’s angle. B. Calcaneal inclination angle. C. Total angle. D. Calcaneal body index (A/B). Larger values for all parameters are associated with Haglund’s deformity.
with a ‘tall’ calcaneus may be predisposed to developing the deformity. A summary of radiographic angles of relevance to Haglund’s deformity is shown in Figure 10.4. The role of footwear is unclear. Several authors suggest that shoes with a rigid heel counter or tight heel straps may cause irritation in those predisposed to the condition116,120,122,123 and indeed, an electrodynographic study by Rzonca et al124 confirmed that the forces applied to the posterosuperior aspect of the heel during gait were significantly larger in those with Haglund’s deformity than in controls. However, only 13% of the 117 cases in the Mishra et al121 study wore shoes on a regular basis, indicating that the condition can also develop in barefooted individuals.
Clinical presentation The classical presentation of Haglund’s deformity is that of pain and inflammation around the posterior
Retrocalcaneal conditions
retrocalcaneal bursae. A recent case-control study indicated that retrocalcaneal bursae larger than 1 mm anteroposteriorly, 11 mm transversely, or 7 mm dorsoplantarly can be considered abnormal.128 Foot posture assessment and gait analysis may be useful, as several authors have suggested that excessive rearfoot motion may lead to friction between the prominence and the heel counter of the shoe. In particular, compensation for an inverted rearfoot deformity has often been implicated in the development of Haglund’s deformity.129 Figure 10.5 Haglund’s deformity. (Courtesy of Karl Landorf, La Trobe University.)
heel, accompanied by superficial bursitis and an osseous and soft tissue prominence in the region of the Achilles tendon insertion (Fig. 10.5). There may be evidence of direct abrasion from the upper edge of the shoe heel counter. In older people, the condition is frequently associated with an overlying region of hyperkeratosis, which may become ulcerated. Pain may be elicited by direct pressure on the posterior prominence or by dorsiflexing the ankle.
Assessment and diagnosis A provisional diagnosis of Haglund’s deformity can be reached from thorough history taking, clinical observation and physical examination. Detailed assessment of footwear (both indoor and outdoor) is essential, not only to determine its possible contribution to the presenting complaint but also to assess the suitability of the shoes for modification and/or accommodation of offloading devices. Systemic conditions that may manifest as soft tissue masses in the posterior region of the heel, such as rheumatoid arthritic nodules and tophaceous gout deposits, first need to be ruled out.125 Lateral weightbearing X-rays are very useful to rule out other conditions (such as soft tissue and osseous tumours41), to determine the magnitude of the posterior exostosis and to evaluate the contribution of calcaneal morphology to the development of the condition. Ultrasound is not necessary to confirm a diagnosis but may reveal signs of Achilles tendinopathy, bursitis and ossification of the insertion of the Achilles tendon.126,127 Similarly, MRI is rarely used but may assist in differentiating between normal and abnormal
Conservative treatment Conservative management of Haglund’s deformity involves removing the potential cause (by exchanging or modifying footwear), pain management (such as NSAIDs or corticosteroid injection), pressure redistribution (via the use of apertured pads or silicone shields) and techniques to alleviate tension at the Achilles tendon insertion (such as heel lifts, foot orthoses and gastrocnemius stretching).120,129–131 Corticosteroid injection needs to be carefully performed to ensure that the injection is directed into the inflamed bursa and not into the tendon itself, because of the risk of rupture. A single injection of cortisone mixed with local anaesthetic has been reported to be clinically effective.129 However, no rigorous studies have been undertaken to assess the efficacy of these techniques and it has been suggested that conservative management of Haglund’s deformity is only effective in very mild cases120,122,132 and is associated with a high recurrence rate.131,132
Surgical treatment Surgical management of Haglund’s deformity involves removal of the retrocalcaneal prominence via bursectomy, exostectomy, calcaneal osteotomy or, most frequently, a combination of these methods.122 Several different incisional approaches have been described (Fig. 10.6). The direct posterior approach allows direct access to the superficial bursa and is technically quite simple to perform. However, to remove the exostosis, the Achilles tendon must be excised and reattached, which may lead to weakening or rupture of the tendon postoperatively. The longitudinal linear incision avoids this potential problem; however, this approach does not allow for ease of access to the superficial bursa. A modification of this approach, the lazy-L incision, improves access to the superficial
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A
B
C
A
B
Figure 10.6 Incisional approaches for surgical correction of Haglund’s deformity. A. Direct posterior incision. B. Longitudinal linear incision lateral to the Achilles tendon. C. Lazy-L incision lateral to the Achilles tendon.
bursa and leads to less skin contracture postoperatively.120 Finally, an endoscopic technique has also been recently described, which involves a small medial or lateral incision guided by fluoroscopy.132 In most cases, a simple ostectomy is performed, which involves removing the offending portion of bone and smoothing the edges with a rasp or rongeur. However, in severe cases (particularly those with a large exostosis and/or a large calcaneal inclination angle) a wedge osteotomy may be considered. This approach, first described by Zadek in 1939,133 involves removing a dorsal wedge of bone from the calcaneus and closing the incision with cancellous bone screws (Fig. 10.7). This technique requires a longer period of cast immobilisation following surgery131 and may therefore not be appropriate for older patients. Complications associated with both techniques include recurrence due to inadequate bone resection, Achilles tendon weakening and/or rupture, scar formation and subsequent nerve entrapment and, in the case of osteotomy, non-union and pseudoarthrosis.122 Although highly favourable outcomes have been reported in case series studies of Haglund’s deformity surgery with small samples and/or a short duration of follow-up,132,134–136 longer-term follow-up studies have seriously questioned the efficacy of surgical intervention.137,138 Taylor137 followed up 42 patients who had undergone closing wedge calcaneal osteotomy over a 6–7-year period and found that 46% were dissatisfied following the procedure. The most common reasons for dissatisfaction were residual prominence (51%), widening of the scar (48%) and altered sensation (38%). Similarly, a 4–5-year follow-up of 49 patients by Schneider et al138 reported complete resolution of symptoms in 34 patients; however, seven
C
D
Figure 10.7 Surgical procedure for Haglund’s deformity. A. Dorsolateral exostosis to be removed. B. Dorsolateral exostosis and bursa are resected and bone smoothed with a rongeur. C. Dorsal wedge osteotomy performed. D. Osteotomy site fixed with cancellous bone screws.
reported a worsening of symptoms. Furthermore, the rehabilitation period was an average of 6 months and few patients reported that they would be willing to undergo a similar procedure again. Better long-term results were reported by Brunner et al139 in 36 patients followed up for 4 years; however, the recovery time ranged from 6 months to 2 years. On the basis of these findings, it is generally recommended that all conservative approaches be tried before considering surgical intervention and that, when considering surgery, patients need to be advised of the potentially prolonged period of recovery.
ACHILLES TENDINOPATHY Definition and aetiology Achilles tendinopathy is one of the most common overuse injuries in athletes and can be defined as the symptomatic overuse, degeneration and failed repair of the Achilles tendon.140 While early reports considered the condition to be inflammatory (hence the
Retrocalcaneal conditions
term Achilles tendinitis), it is now recognised that the pathological process is far more complex and that chronic tendinopathy does not involve inflammatory cells.141 Although most commonly observed in young and middle-aged athletes, Achilles tendinopathy may also occur in physically active142,143 or sedentary older individuals.144 As outlined in Chapter 2, there are several age-related changes in the physiology of tendon tissue, including increased collagen crosslinking,145 decreases in water content146 and increased in lipid content.147 These changes may predispose to tendinopathy in physically active older people, as a recent study of young and older athletes indicated that Achilles tendon problems were more common in the older group (20% versus 5% of all injuries).148 Age is also recognised as a strong negative predictor of outcome in surgical repair of Achilles tendon disorders.149,150 The aetiology and pathophysiology of Achilles tendinopathy is poorly understood. Several risk factors have been identified, including obesity,151 sudden increases in the duration and intensity of weightbearing activity152 and decreased ankle dorsiflexion range of motion (leading to an increase in strain on the tendon).153 Broadly speaking, three theories have been put forward in relation to the pathophysiology of Achilles tendinopathy.154 The mechanical theory suggests that repeated loading of the tendon causes gradual fatigue and subsequent microscopic degeneration. The vascular theory suggests that the cause of tendon degeneration is a reduction in blood supply in the inherently hypovascular midportion of the tendon.155 However, the inverse has also been proposed, i.e. that exercise-induced hyperthermia may be detrimental to tendons.156 Finally, a neural theory has recently been proposed in response to the observation of glutamate (a neurotransmitter) in damaged tendons157 and the reported association between Achilles tendinopathy and sciatica.158 Several medications have also been implicated in degeneration and rupture of the Achilles tendon, particularly corticosteroids159 but also fluoroquinolone antibiotics151,160 and statins.161 The role of medications in predisposition to Achilles disorders is of particular importance in older people. A recent study of 1367 cases and 50 000 controls indicated that, in people over 60 years of age, the use of quinolone antibiotics significantly increased the likelihood of experiencing an Achilles tendon rupture and that this risk was further increased in those who were also taking corticosteroids.162
Irrespective of the underlying cause, histological examinations of affected tendons have revealed several characteristic changes, including irregular arrangement of collagen fibres, increased vascularity and evidence of delayed healing.163,164 In addition to these changes, ruptured tendons also exhibit inflammatory lesions and the presence of granulation tissue.165
Assessment and diagnosis Most of the information required to diagnose Achilles tendinopathy can be obtained from a thorough patient history and physical examination. The primary presenting complaint is pain 2–6 cm proximal to the insertion of the tendon, which is exacerbated by physical activity and relieved by rest. The tendon may be diffusely swollen and palpable nodules may be present when the ankle is dorsiflexed and plantarflexed.166 Retrocalcaneal bursitis or Haglund’s deformity may also be present. Patients who have sustained an acute rupture of the tendon will typically report a sudden onset of pain accompanied by an audible snap at the time of injury and will be unable to bear weight on the affected limb. Patients with chronic ruptures, however, may report only minor or no trauma and often recall difficulty climbing stairs as the initial symptom.167 Achilles tendinopathy may be differentiated from rupture by conducting either of two simple tests. The calf-squeeze test, also known as the Thompson test, was first described by Simmonds in 1957168 and involves squeezing the fleshy part of the calf while the patient is lying prone. If the Achilles tendon is intact, this test will result in plantarflexion of the ankle joint, whereas in the presence of a ruptured tendon no ankle movement will be elicited. The knee flexion test involves the patient flexing the knee to 90° while lying prone. In the presence of an Achilles tendon rupture, the foot will drop into a neutral or dorsiflexed position.169 Diagnostic imaging is not necessary for routine clinical diagnosis but is considered useful for presurgical planning.170 Plain film X-ray is not widely used in the diagnosis of tendinopathy but may be useful in cases of insertional tendinopathy where bony spurs are suspected. Ultrasound imaging of abnormal Achilles tendons will reveal tendon enlargement and hypoechoic regions;171 however, false-positive findings are common in mild to moderate cases172 and differentiating between tendon degeneration and
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partial rupture is difficult.173 MRI will typically reveal tendon and paratenon thickening, peritendinous fluid accumulation and oedema of Karger’s fat pad.174 As with ultrasound, however, there is considerable overlap between the appearance of normal and abnormal tendons. Neither the use of ultrasound nor MRI has been shown to predict clinical outcomes of surgical intervention.
Conservative treatment Several conservative treatments have been trialled in the management of Achilles tendinopathy, including anti-inflammatory medications, calf stretching, massage, therapeutic ultrasound, laser, cryotherapy, corticosteroid injections, strengthening exercises, heel lifts and foot orthoses.140,166,170,175 However, because of the limited understanding of the underlying cause of the condition, treatment is largely empirical and varies considerably among clinicians.140,166 Furthermore, few of these techniques have been evaluated in randomised controlled trials and no trials have specifically been undertaken in older people. Initial conservative management of Achilles tendinopathy involves pain relief, via the use of antiinflammatory medications, cryotherapy and/or corticosteroid injections. Anti-inflammatory medications are likely to only be of benefit in the acute phase, as chronic degenerative tendinopathy is not an inflammatory condition. Indeed, a randomised trial found that piroxicam offered no benefits over a placebo medication in 70 patients with chronic Achilles tendinopathy.176 The use of corticosteroids is somewhat controversial, as there is some evidence that peritendinous injection of cortisone delays tendon healing177 and several cases of spontaneous rupture following corticosteroid injection have been reported.178 More recently, techniques designed to sclerose small blood vessels within the tendon (by the use of polidocanol179 or electrocoagulation180) have been trialled with some success; however, larger studies with longer-term follow-up are now required. Longer-term conservative management of Achilles tendinopathy is aimed at restoring the normal function of the musculotendinous unit to prevent recurrence. Strengthening the triceps surae muscle group using eccentric loading exercises has been shown to be effective in managing Achilles tendinopathy in athletic populations;140,175 however, whether this approach is safe and effective in older people remains unclear.
The effectiveness of orthomechanical therapies (such as heel lifts and foot orthoses) has not been examined in detail; however, a randomised controlled trial of heel lifts did not provide any substantial clinical benefit when added to a treatment regimen of stretching, strengthening and ultrasound.181 The most recent Cochrane review of nine randomised trials involving 697 patients concluded that, while there was weak evidence for the use of nonsteroidal anti-inflammatory medications in alleviating symptoms in acute tendinopathy, there is currently insufficient evidence to guide conservative treatment of chronic Achilles tendinopathy.182 Despite this lack of evidence, the long term prognosis of conservative management appears to be quite good. An 8-year follow-up of 83 patients managed with various conservative approaches indicated that the vast majority (94%) were asymptomatic or reported only mild pain when exercising.183
Surgical treatment Surgical intervention for Achilles tendinopathy is only indicated when conservative methods have failed. Although various surgical techniques have been described, most involve debridement of degenerated tendon tissue, removal of adhesions between the tendon and paratenon and, in the case of intratendinous lesions, longitudinal incision and excision of granulation tissue. Partial ruptures may require suturing or grafting.166 Clinical success rates of between 75% and 100% have been reported in retrospective studies; however, few have used objective outcome measures.184 Complications, such as residual strength deficits and delayed healing, have been reported in approximately 10% of cases.183 Acute ruptures of the Achilles tendon generally require open operative repair with suturing or tendon grafting techniques, followed by cast immobilisation for 4–8 weeks.185 Although some authors suggest that older patients are best managed non-operatively, using cast immobilisation or functional bracing,167 good results with flexor hallucis longus transfer have been reported in five patients aged 52–71 years of age.186 The recent Cochrane review of 14 trials involving 891 patients indicated that surgical management of acute ruptures was associated with a lower risk of re-rupture; however, those treated non-operatively experienced fewer complications and required shorter periods in hospital.187
Osteoarthritis of the midfoot and rearfoot
OSTEOARTHRITIS OF THE MIDFOOT AND REARFOOT PREVALENCE AND RISK FACTORS Osteoarthritis is the most common form of arthritis and is the leading cause of disability in developed countries. The prevalence of osteoarthritis increases significantly with age. Approximately 28% of people aged over 65 years report symptomatic osteoarthritis, with prevalence increasing to 37% in people aged over 85 years.188 Older people with osteoarthritis are more likely to have difficulties with activities of daily living,189 reduced quality of life190 and increased risk of falls191 compared to those without the condition. The most commonly affected joints are the hips, knees and lumbar spine, and in Australia it has been estimated that 19 000 hip and 20 000 knee replacements are performed for osteoarthritis each year.188 In contrast to the wealth of literature pertaining to hip and knee osteoarthritis, relatively little is known about osteoarthritis affecting the foot in older people. In the US, the 1991 National Health Interview Survey included a podiatry supplement and found that approximately 6% of respondents over 65 years of age reported ‘arthritis of the toes’,192 while a recent postal survey of 5689 people over 65 years of age in the Netherlands reported that 8% of subjects reported ‘foot osteoarthritis’.193 The prevalence of radiographically confirmed osteoarthritis in the midfoot and rearfoot is largely unknown, as the two largest radiographic prevalence studies that included foot joints primarily focused on the metatarsophalangeal joints.194,195 However, a study of 50 cadavers (average age at death of 76 years) indicated that moderate to severe degen-
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erative changes were evident in the subtalar joint in 67% of cases and the transverse tarsal joint (i.e. talonavicular and calcaneocuboid joints combined) in 50% of cases.196 Although several risk factors for osteoarthritis in other joints have been identified (such as increased age, family history, obesity and occupation197), little is known about risk factors for primary foot osteoarthritis. The observation that foot osteoarthritis frequently coexists with osteoarthritis in the hands and knees suggests that a systemic aetiology with genetic predisposition may be responsible.195 There is also preliminary evidence that this hereditary predisposition may be related to anatomical variations in articular facet configuration. An anatomical study of 191 osteological specimens by Drayer-Verhagen198 found that calcanei with a large, continuous anterior facet were more likely to demonstrate arthritic lipping, suggesting that the increased range of motion associated with this articular configuration may cause the joint to be less stable,199 thereby predisposing to the development of subtalar joint osteoarthritis (Fig. 10.8). Secondary osteoarthritis affecting the subtalar joint and midfoot joints is a relatively common complication of ankle joint fusion. In one study, 33% of patients who had undergone ankle arthrodesis developed subtalar joint osteoarthritis after an average of 7 years of follow-up.200 The underlying mechanism appears to be an increase in joint contact pressures during the propulsive phase of gait, as a recent cadaver study revealed that talonavicular and calcaneocuboid pressures were significantly increased following ankle arthrodesis when the ankle joint was placed between 0° and 20° of dorsiflexion.201
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Figure 10.8 Variations in the anterior articular configuration of the calcaneus. A. Two separate anterior facets. B. Continuous figure-eight facet. C. Long continuous facet. D. Medial facet only.
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CLINICAL PRESENTATION Osteoarthritis affecting the midfoot and rearfoot generally presents as a vague, insidious pain in the midfoot region that is exacerbated by long periods of weightbearing activity. Overt signs of inflammation are generally absent; however, there may be mild swelling around the affected joint or joints. Palpation of the affected area may reveal the presence of large osteophytes at the margins of the joint, and pain may be elicited in response to moving the joint through its full range of motion. Plain film X-rays will reveal the characteristic features of osteoarthritis, including joint space narrowing, formation of osteophytes, subchondral sclerosis and bony cysts. Typical examples are shown in Figure 10.9. A recently published atlas of osteoarthritis affecting the foot is a useful guide for grading the severity of arthritic changes.202
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CONSERVATIVE TREATMENT Conservative management of foot osteoarthritis is similar to that of osteoarthritis in other weightbearing joints and includes the use of analgesics for pain relief and mechanical therapies to reduce the compressive load on the affected joint. Although no rigorous studies have been undertaken, foot orthoses may be effective in patients with osteoarthritis related to flat foot deformity (such as those with tibialis posterior dysfunction). There is preliminary evidence that cast orthoses may be more effective in managing symptoms associated with foot osteoarthritis than nonsteroidal anti-inflammatory medications.203 In this retrospective study, the degree of pain relief reported by 64 patients (average age 63 years) who had received various treatments for foot osteoarthritis were evaluated. All of those who were prescribed foot orthoses reported significant reductions in pain, and their pain relief was maintained for a longer period of time than those who were taking NSAIDs. Although there are several limitations with this type of study design, it is worth noting that foot orthoses reduce subtalar joint pronation204 and foot pain205 in patients with rheumatoid arthritis, so it is possible that they may have similar effects in people with osteoarthritis.
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Figure 10.9 Radiographic appearance of osteoarthritis. A. First cuneometatarsal joint. B. Navicular–cuneiform joint. C. Talonavicular joint. C
Less common midfoot and rearfoot disorders
In patients with more advanced degenerative osteoarthritis of the subtalar and ankle joints, ankle– foot orthoses may be effective.206 Several studies in patients with subtalar207 and ankle208 osteoarthritis have confirmed that various designs of ankle–foot orthoses are effective in reducing rearfoot motion and may therefore relieve compression in the midfoot and rearfoot. Ankle–foot orthoses are discussed in more detail in Chapter 11.
SURGICAL TREATMENT Surgical management of rearfoot and midfoot osteoarthritis in older people generally involves fusion of the affected joint or joints.209 Traditionally, most cases were treated with triple arthrodesis (fusion of the ankle, subtalar and transverse tarsal joints); however, more recently, single joint fusions are undertaken in an attempt to preserve as much motion as possible210,211 and arthroscopic debridement has also been used as an interim approach before considering arthrodesis.212 Although no controlled trials have been undertaken, several case series studies indicate that arthrodesis is an effective treatment for advanced osteoarthritis and that most patients are satisfied with the results.213–215 However, foot function is markedly altered following surgery and many patients will exhibit gait changes associated with their reduced range of motion. In particular, many patients report difficulties walking on irregular surfaces following arthrodesis210,216 and, as stated previously, up to onethird may develop secondary osteoarthritis in adjacent joints. Furthermore, in most surgical studies a large number of patients report some degree of residual pain and require adjunctive conservative treatments such as footwear modifications and orthoses.
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Figure 10.10A, B Pes cavus (highly arched foot). (A Courtesy of Josh Burns, University of Sydney.)
LESS COMMON MIDFOOT AND REARFOOT DISORDERS PAINFUL PES CAVUS The term pes cavus describes a foot with an abnormally high medial arch (Fig. 10.10) and therefore refers to a structural anomaly rather than a discrete clinical condition. Not all people with highly arched feet develop symptoms. However, the features commonly associated with pes cavus, such as restricted joint range of motion and loss of shock absorption, are associated with elevated pressures in the forefoot and heel (Fig. 10.11),217 which may contribute to the
Figure 10.11 Typical plantar pressure output of a patient with pes cavus.
development of plantar forefoot and heel pain. Because of the trend towards a lowering of the medial arch with advancing age,218 pes cavus is not a common presentation in older people. The Feet First study of 784 Americans aged over 65 years reported a 5% prevalence of pes cavus, compared to a 19% prevalence of pes planus (flat feet).2 The aetiology of pes
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cavus is not well understood but many cases are thought to be neurogenic in origin, the most common neuromuscular cause being Charcot–Marie–Tooth disease.219 Management of pes cavus in older people is based on addressing the presenting symptoms and associated complaints (such as plantar lesions) using conservative techniques, rather than ‘correcting’ the structural anomaly itself. A recent randomised trial indicated that customised foot orthoses are effective in redistributing pressures away from the forefoot and heel, thereby reducing symptoms associated with painful pes cavus.220 Inadequate shock attenuation associated with pes cavus may also be addressed by the provision of footwear with ethyl vinyl acetate midsoles221,222 or by the addition of a shock-absorbing cushioned heel shoe modification (Ch. 12).
TARSAL TUNNEL SYNDROME First described in 1960,223 tarsal tunnel syndrome is an uncommon entrapment neuropathy caused by compression of the posterior tibial nerve (or its branches) beneath the flexor retinaculum. The condition is characterised by anaesthesia, paraesthesia and burning pain in the medial malleolar region that radiates along the course of the calcaneal, medial plantar or lateral plantar nerves. Tarsal tunnel syndrome may develop secondary to direct trauma of the posterior tibial nerve, the development of space-occupying lesions such as ganglia, rapid weight gain or inflammatory conditions such as rheumatoid arthritis.224,225 The diagnosis of tarsal tunnel syndrome is based on patient history and physical examination. Symptoms are generally exacerbated by prolonged periods of weightbearing activity and can be elicited by pronating the foot and dorsiflexing the toes or by direct percussion of the nerve (referred to as a positive Tinel’s sign226). Electrophysical studies are considered to be the gold standard diagnostic test for tarsal tunnel syndrome and will reveal reduced sensory nerve conduction velocity and increased latency of motor nerves compared to the unaffected side.227 Magnetic resonance imaging is not commonly used but may be useful for identifying space-occupying lesions exerting pressure on the neurovascular bundle.228 Treatment of tarsal tunnel syndrome is largely empirical, as few rigorous intervention studies have been undertaken. Conservative treatment options include NSAIDs, corticosteroid injection and ortho-
ses to control excessive foot pronation.224,225 Surgical management of tarsal tunnel syndrome includes decompression of the nerve by flexor retinaculum release and, if necessary, neuroma excision. Reported outcomes from case series studies are only moderate, with 17–43% of patients reporting dissatisfaction with the result.229–231
SINUS TARSI SYNDROME The sinus tarsi is a conical cavity that acts as a boundary between the anterosuperior surface of the calcaneus and the inferior aspect of the neck of the talus, and contains a fat plug, joint capsule, neurovascular elements and five ligaments. In 1958, O’Connor232 described a condition characterised by persistent lateral ankle pain following an inversion sprain, which was attributed to scarring of the ligaments within the sinus tarsi. Since this initial report, several authors have described a similar syndrome, which has been variously attributed to synovitis, entrapment of the superficial peroneal nerve, ganglia, ligament damage and tarsal coalition.233–235 The classical clinical presentation of sinus tarsi syndrome is that of persistent lateral ankle pain and instability in patients with a history of recurrent ankle sprains; however, the condition may occur in the absence of previous trauma.233,235 Of particular interest in older patients, cases of sinus tarsi syndrome associated with gout affecting the subtalar joint have been reported.236 Pain can be elicited on direct palpation and by supinating the subtalar joint. Plain film X-ray is rarely helpful in reaching a diagnosis and, although MRI may reveal ligament tears and signs of fibrosis, whether these observations are highly characteristic of the condition is yet to be fully determined.236 As with tarsal tunnel syndrome, treatment of sinus tarsi syndrome is largely empirical. No trials of conservative treatments have been undertaken, with only a single case study reporting good results with the use of foot orthoses.237 A recent case series of 13 patients who underwent resection of the deep peroneal nerve reported highly favourable results, with 10 patients reporting complete pain relief after 6 months.238
SUMMARY A wide range of pathological conditions may manifest as pain in the rearfoot in older people and it is clear
References
that our understanding of the pathophysiology of many of these conditions is currently quite limited. Subsequently, treatment of rearfoot problems can be challenging. Because of the higher rate of complica-
tions and prolonged recovery times associated with rearfoot surgery in older people, conservative interventions should be tried before considering surgical intervention.
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CHAPTER
Orthotic therapy
CHAPTER CONTENTS Chairside orthoses 218 Horseshoe pad 218 Crescent pad 218 Toe prop 219 Interdigital wedge 219 Saddle pad 220 Foam sleeves 220 Plantar cover 220 Plantar metatarsal pad 220 Metatarsal shaft pad 221 Valgus pad 222 Plantar calcaneal pad 222 Retrocalcaneal pad 222 Silicone orthodigita 222 Non-cast insoles
222
Prefabricated orthoses 223 Silicone and other viscoelastic devices Hallux valgus splints 224 Contoured insoles 224 Cast orthoses
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Ankle–foot orthoses
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Foot orthoses and knee osteoarthritis Foot orthoses as a balance aid Summary 229 References 229
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11
Orthotic therapy plays a major role in the conservative management of foot disorders in older people.1,2 In the UK National Health Service, it has been estimated that £38 million is spent on orthoses each year, with foot orthoses accounting for 75% of a district hospital’s total appliances budget.3 Orthotic devices range from simple adhesive pads that can be manufactured during a routine consultation through to more complex techniques involving the construction of custom-moulded insoles derived from plaster casts of the patient’s feet. The basic principles of orthotic therapy are to reduce the magnitude of pressure applied to painful regions of the foot, to realign structures within the foot to correct any existing deformity, and to control motion of joints in the foot, either by restricting excessive motion or by facilitating joints with limited motion.4–6 Although these underlying principles are generally agreed upon, there are several opposing theories pertaining to the biomechanical function of the foot, which give rise to a plethora of alternative orthotic prescription protocols to achieve these objectives. It is beyond the scope of this chapter to discuss these issues in detail. Therefore, it is recommended that the reader refer to several recent reviews on the topic7–9 and supplement the information contained in this chapter with textbooks specifically focused on foot orthoses, such as Foot Orthoses and Other Forms of Conservative Footcare4 and Clinical Biomechanics of the Lower Extremities.10 The classification and nomenclature of foot orthoses is also a somewhat vexed issue, as no widely agreed upon system has yet been adopted. For the purpose of this chapter, the following classifications are used:
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■
■
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Chairside orthoses: padding techniques that can be manufactured during a routine consultation from widely available materials such as felt, foam and silicone putty Non-cast insoles: orthoses placed inside the shoe that do not require a cast to be taken of the patient’s foot Prefabricated orthoses: mass-produced commercially available devices that can be purchased from orthotic laboratories, medical suppliers or pharmacists Cast orthoses: devices manufactured from soft or rigid materials using a plaster replica of the patient’s foot Ankle–foot orthoses: prefabricated or customised devices that extend above the ankle joint.
Orthotic prescription and manufacture for older people is essentially the same as for younger people; however, several factors require additional consideration. Firstly, given the high prevalence of ill-fitting footwear in older people,11 particular care needs to be taken to ensure that the patient’s footwear is appropriate for orthotic therapy, particularly with regard to the depth of the toebox. Secondly, the mobility of older patients should be evaluated to ascertain their ability to reach their feet, as orthoses fitted directly to the foot will need to be removed and replaced before and after bathing and sleeping. Finally, it is essential to assess an older person’s skin integrity prior to prescribing orthoses and, where there is some risk of skin damage, orthoses should be covered with a soft and compliant material and carefully checked for rough or sharp edges on a regular basis. The following chapter briefly outlines the use of each of these types of orthosis in the management of foot disorders in older people. The broader applications of foot orthoses in this age-group, such as the role of orthoses in the management of knee osteoarthritis and in improving balance, are also discussed.
CHAIRSIDE ORTHOSES The term chairside orthoses refers to simple devices that can be quickly and easily manufactured during a routine patient consultation. The most common material used for these devices is adhesive semicompressed felt, which is available in several thicknesses (most commonly 2 mm, 5 mm, 7 mm and 10 mm).
Various types of foam can also be used. As a general rule, semicompressed felt is more effective in pressure redistribution, whereas foam is more effective in shock absorption and tends to last longer. Chairside orthoses can be directly adhered to the foot and secured with tape, fixed inside the shoe or made into replaceable devices. These devices will invariably become less effective over time, as a result of material compression and/or loss of adhesion, and will therefore need to be replaced regularly. In most cases, chairside devices are designed to provide short-term symptomatic relief and, if effective, to help guide the selection and construction of more permanent devices. The following section briefly describes some of the more commonly used chairside orthoses and their clinical applications. Additional variants of these basic pad designs can be found in Paddings and Strappings of the Foot12 and Practical Orthotics for Chiropodists.13
HORSESHOE PAD As the name suggests, the horseshoe pad (Fig. 11.1A) is a U-shaped pad with two arms that extend onto the dorsum of the proximal phalanges of the toes. This pad is used to deflect pressure away from dorsal lesions on the proximal interphalangeal joints of hammer toes or claw toes, and is generally constructed from 7 mm compressed felt. The horseshoe pad is particularly effective at redistributing pressure away from a single lesion (in the example provided, the third toe) where the adjacent toes are neutrally aligned. For multiple lesions on adjacent toes, the crescent pad is generally used.
CRESCENT PAD The crescent pad (Fig. 11.1B), also referred to as a U-pad, is used to deflect pressure away from dorsal lesions affecting one or more of the proximal interphalangeal joints. Depending on the severity of the lesser toe deformity, 5 or 7 mm felt can be used to ‘fill in’ the space between the dorsal aspect of the metatarsal heads and the proximal interphalangeal joints. For optimum results, the distal edge of the pad should closely follow the shape of the dorsal prominences and be bevelled on the inferior surface to improve the fit of the device. Both the horseshoe and crescent pads can be directly adhered to the foot; however, for longer-term results, replaceable devices can be constructed by
Chairside orthoses
A
placing the non-adhesive side to the foot, looping elastic strap around the toes and affixing the strap to the dorsal adhesive side, and covering the dorsal surface of the pad with tape (Fig. 11.2).
B
TOE PROP
C
D
E
F
The toe prop, also referred to as a buttress appliance or crest pad (Fig. 11.1C), has several variations and functions.14 The aim of the basic plantar toe prop is to fill in the space between the plantar metatarsal heads and the apices of the toes, thereby redistributing load from plantar apical lesions, particularly in the presence of rigid claw toes. However, if the claw toe deformity is flexible, the distal edge of the pad can be extended further distally to assist in dorsiflexing the distal interphalangeal joint, thereby straightening the toes.15 A further variation (referred to as a dorsoplantar prop) involves the addition of a dorsal prop connected to the plantar prop by elastic strapping, which is thought to assist in straightening the toes by the shoe exerting a plantarly directed force on the dorsal pad while the plantar pad exerts a dorsally directed force, thereby plantarflexing the metatarsophalangeal joints and dorsiflexing the proximal and distal interphalangeal joints simultaneously.
INTERDIGITAL WEDGE Figure 11.1 Padding techniques for the toes. A. Horseshoe pad. B. Crescent pad. C. Toe prop. D. Interdigital wedge. E. Saddle pad. F. Toe sleeve.
A
B
The interdigital wedge or dumbbell pad (Fig. 11.1D) is used to assist in the separation of adjacent toes and is most commonly used in the short-term management of interdigital corns (both heloma dura and heloma molle). This pad is also used in the conservative management of onychocryptosis, as a means of
C
Figure 11.2 Manufacture of a replaceable horseshoe pad. A. Determining the size and shape of the pad. B. Straps adhered to dorsal adhesive surface of pad. C. Dorsal surface of pad covered with tape.
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alleviating pressure from adjacent nail sulci.16 As the name suggests, the pad is cut into a dumbbell shape from compressed felt, placed between the toes and adhered directly to the dorsal and plantar surfaces of the foot. It is important to ensure that the thickness of the plantar aspect of the pad is reduced so as not to interfere with normal weightbearing. An alternative approach is to simply adhere a piece of felt to the medial or lateral aspect of the proximal phalanx; however, such devices tend to break down more quickly and, because of interdigital maceration, are difficult to get to adhere for long periods of time. Interdigital wedges may also be manufactured from silicone and, because of their close moulding to the space between the toes, tend to be more effective and last longer than felt pads (see later section on silicone devices).
SADDLE PAD The saddle pad, also known as a tendon pad (Fig. 11.1E), is designed to alleviate dorsal pressure from footwear in the presence of prominent long extensor tendons. As the name suggests, the pad is directly adhered to the dorsum of the foot like a saddle, with a plantar groove cut into the pad to accommodate the tendon. In patients with several prominent extensor tendons (such as those with multiple clawtoes, hammertoes or retracted toes associated with pes cavus foot deformity), the saddle pad can be extended across the entire dorsal aspect of the foot (with multiple grooves for each tendon) and bevelled to ensure close apposition with the dorsal aspects of the metatarsal shafts.
FOAM SLEEVES Prefabricated tubefoam has several uses. The simplest application of tubefoam is the construction of basic toe sleeves (Fig. 11.1F) for cushioning dorsal lesions, used with or without additional felt crescents. Larger diameter tubefoam can also be used in management of painful hallux valgus (by constructing a toe sleeve with a longer medial flange to place over the inflamed medial exostosis), or as removable alternative to the saddle pad, by placing the sleeve over one of the toes and extending a flange over the dorsum of the foot. Care needs to be taken; however, that the diameter of tubefoam selected is sufficient to prevent constriction of blood flow to the digits, particularly in older people with peripheral vascular disease.
PLANTAR COVER The plantar cover, or plantar pad, extends from the styloid process of the fifth metatarsal to the distal aspect of the metatarsal heads and covers the entire plantar metatarsal area (Fig. 11.3A).17 It can be manufactured from foam or felt of various thickness depending on the space available in the shoe. The distal edge of the pad is bevelled to improve comfort and adhesion. The plantar cover is used to cushion the metatarsal heads and is particularly useful in older people with atrophy of the plantar soft tissues. The pad can be directly adhered to the plantar surface of the foot, adhered to the inner sole of the shoe or made into a replaceable device by looping elastic strapping around the middle three toes, adhering the strap to the plantarly directed adhesive surface, and covering the plantar surface of the pad with tape. The plantar cover can be modified to redistribute pressure from individual metatarsal heads by the addition of a ‘U’ (for the second, third or fourth metatarsal heads) or a ‘wing’ (for the first and/or fifth metatarsal heads), as shown in Figure 11.3B and C. Such pads are used to reduce loading on metatarsal heads affected by keratotic lesions and insufficiency fractures and have also been demonstrated to assist in the healing of plantar neuropathic ulcers in people with diabetes.18,19 The relative efficacy of ‘U’d plantar covers compared to other devices for offloading the metatarsal heads, however, is unclear. A recent study using an in-shoe pressure analysis system indicated that a plantar metatarsal pad (discussed below) was more effective in reducing pressures.20
PLANTAR METATARSAL PAD The plantar metatarsal pad, also referred to as a metatarsal pad, has several variants. The most commonly described pad covers the shafts of the second, third and fourth metatarsals and follows the distal curve of the respective metatarsal heads (Fig. 11.3D).12,13 The pad is thought to have several functions: ■
■
■
To redistribute load from the metatarsal heads to the shafts To redistribute load to the first and fifth metatarsal heads To straighten the central three toes.
Clinical indications for the use of this pad include keratotic lesions under the central metatarsal heads, flexible hammertoe deformity, interdigital neuroma and predislocation syndrome. Variants of the plantar
Chairside orthoses
A
B
C
D
E
F
G
H
Figure 11.3 Plantar padding techniques. A. Plantar cover. B. ‘U’d plantar cover. C. Winged plantar cover. D. Plantar metatarsal pad. E. Metatarsal shaft pad. F. Extended shaft pad. G. Valgus pad. H. Plantar calcaneal pad.
metatarsal pad include the metatarsal dome, which does not extend as far distally, a winged version that has a medial flange extending under the first metatarsal shaft (to deflect pressure away from the first metatarsal head) and smaller metatarsal pads, sometimes referred to as teardrop pads, which are placed proximal to individual metatarsal heads. The optimum placement of the plantar metatarsal pad to reduce pressures under the metatarsal heads is unclear, as several studies have been undertaken with variable results. Six studies have found that a pad placed proximal to the metatarsal heads significantly reduces metatarsal head pressures (by up to 60%),21–26 two studies found no significant reduction in pressures with proximally placed pads27,28 and one study29 found that placing a pad 5 mm distal to the metatarsal heads reduced pressure more effectively than placing it 5 mm proximal to the metatarsal head. These variable findings are likely to reflect differences in plantar pressure measurement protocols and participant characteristics; however, it also likely that the optimum location of plantar metatarsal pads requires some degree of trial and error. The clinical use of plantar
pressure systems is ideal for this purpose. However, in the absence of such systems, some insight can be gained from subjective responses from the patient, as two studies have indicated that reported pain relief is significantly correlated with the degree of pressure reduction.22,24
METATARSAL SHAFT PAD The metatarsal shaft pad, also known as an under pad,12 covers the plantar surface of one or more metatarsals (Fig. 11.3E). The aim of this pad is to elevate the metatarsal relative to adjacent metatarsals, and is thought to be of particular benefit in the management of intermetatarsal neuroma (in the case of a neuroma in the third–fourth intermetatarsal space, the pad is placed under the fourth and fifth metatarsal heads).30 Multiple shaft pads can also be placed to ‘rebalance’ pressure distribution across the plantar surface. Such devices, sometimes referred to as a forefoot imbalance pads31 or parallel strip padding,12 are considered to be of benefit in the management of plantar lesions caused by highly prominent (‘depressed’) central metatarsal
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heads, as may develop in conduction with lesser toe deformity in the rheumatoid foot. In this case, two pads are applied to the first and fifth metatarsal shafts. A variation of the shaft pad is the extended shaft pad (also known as Morton’s extension), which is placed under the first metatarsal but extends distally to completely cover the first metatarsophalangeal joint (Fig. 11.3F). This pad was originally designed to compensate for the so-called Morton’s foot type, characterised by an excessively short first metatarsal with subsequent overloading of the second metatarsal head.32 However, it is now recognised that such a foot type is far less common than originally thought and is not frequently associated with pathology.33 Nevertheless, this pad is useful for redistributing pressure away from the first interphalangeal joint in people with limited motion at the first metatarsophalangeal joint (such as people with hallux limitus/rigidus or limited joint mobility associated with diabetes).
VALGUS PAD The valgus pad, also known as a scaphoid pad or long arch pad, fills in the medial longitudinal arch region of the foot (Fig. 11.3G). The aim of this pad is to support the medial arch13 and it has been shown that, when valgus pads are worn, plantar pressures increase under the lateral border of the foot, which may indicate a lateral shift in the centre of pressure associated with a reduction in foot pronation.34 Valgus pads are particularly useful as an adjunct in the management of forefoot ulceration in diabetic patients by ‘filling in’ the space between the heel and the forefoot, and are often used in conjunction with plantar forefoot padding.35 A recent study of 30 diabetic patients by Guldemond et al36 reported that the addition of a valgus pad to a contoured foot bed with a metatarsal dome increased the degree of forefoot pressure reduction by up to 25%.
PLANTAR CALCANEAL PAD The plantar calcaneal pad, or heel pad, is placed over the weightbearing surface area of the heel (Fig. 11.3H) and is used to reduce loading of the heel in patients with plantar heel pain syndrome (including plantar calcaneal bursitis and calcaneal stress fractures). The efficacy of plantar calcaneal pads has not been examined in detail; however, there is some suggestion that rigid heel cups may be more effective in
older people, as they contain the lateral expansion of the heel on weightbearing, thereby improving shock attenuation by maintaining the vertical thickness of the heel pad.37 The manufacture of felt or foam chairside devices for the heel has been largely supplanted by the availability of prefabricated heel pads manufactured from viscoelastic materials (see below).
RETROCALCANEAL PAD The retrocalcaneal pad, also known as a posterior heel pad,12 is a circular pad placed on the posterior aspect of the heel to reduce friction from footwear in patients with retrocalcaneal bursitis or Haglund’s deformity. Depending on the size of the bony prominence, an aperture may also be cut into the pad. As with plantar calcaneal pads, the availability of prefabricated, adhesive viscoelastic materials has largely replaced the traditional felt or foam pads, as they are more effective at reducing friction and tend to last much longer.
SILICONE ORTHODIGITA The availability of medical grade silicone putties, originally developed for dental casting applications, has enabled the manufacture of long-lasting, washable, customised orthoses within the time constraints of a routine clinical consultation.15,38 Commercially available two-part systems consisting of the silicone putty and a catalyst (such as Otoform K® and Podiaform®) can be used to manufacture a wide range of devices, including toe props,39 interdigital wedges40 and bunion shields41 (Fig. 11.4). Silicone orthoses are particularly useful for reducing pressures under the apices of the toes. A recent study of 14 patients with diabetes indicated that custom-moulded silicone toe props reduced digital plantar pressures by 30% and, when used in conjunction with keratotic lesion debridement, pressures were reduced by 54%.42 In addition to reducing toe pressures, there is some evidence that flexible lesser toe deformities can be gradually ‘corrected’ using serial toe props, with each new device shaped to provide slightly more correction than the previous one.15
NON-CAST INSOLES As the name suggests, non-cast insoles are customised orthotic devices that do not require a cast to be taken of the patient’s foot. Traditionally, these devices were
Prefabricated orthoses
A
B
Figure 11.4 Silicone devices. A. Toe prop. B. Interdigital wedges.
manufactured by affixing various types of rubber or foam pads (using similar designs to the chairside devices previously discussed) to a flat insole made from compressed cardboard, cork, leather or a combination of all three materials. The main advantages of non-cast insoles over chairside devices is that they do not have to be affixed directly to the foot and, because of the much greater resilience of the materials used, they have a much longer lifespan. The main disadvantage of non-cast insoles is that the insole base is constructed to match the shape and size of the last of the shoe and, as such, cannot always be transferred from one pair of shoes to another. The technique involves obtaining an accurate tracing of the insole of the patient’s shoe by trimming a piece of cardboard and fitting it inside the shoe, then
recording the location of key anatomical features of the foot (particularly the metatarsal heads and the location of plantar lesions). The pad design is then marked on to the cardboard template, and constructed from the appropriate materials (generally open cell black rubber). The pad is then adhered to a compressed cardboard base and covered with a soft material such as chamois. The addition of simple wedges to non-cast insoles in an attempt to support forefoot deformities (e.g. forefoot varus and valgus) and to control foot pronation has also been suggested.43 However, while such an approach may be a useful temporary measure to ascertain the potential effectiveness of a more ‘functional’ foot orthosis, it has recently been shown that such devices have relatively minor effects on foot kinetics44 and kinematics,45 possibly because of the lack of medial longitudinal arch support. To a large extent, the wide availability and low cost of prefabricated orthoses has made the traditional manufacture of non-cast insoles redundant. In contemporary clinical practice, many foot specialists will simply modify a prefabricated orthosis by adhering appropriate padding designs to the orthosis shell itself. This approach provides the additional benefits of customised forefoot padding designs to the contoured arch and heel cup of the prefabricated orthosis, and is much less time-consuming.
PREFABRICATED ORTHOSES SILICONE AND OTHER VISCOELASTIC DEVICES A wide range of silicone appliances are now commercially available from medical suppliers and pharmacists (Fig. 11.5). To some extent, these devices are replacing the chairside manufacture of felt and foam pads for minor foot complaints.46 Although over-thecounter silicone appliances are considerably more expensive than chairside devices, the viscoelastic properties of the silicone make them very comfortable and surprisingly long-lasting. Some silicone devices are also impregnated with mineral oil, which may have additional effect of hydrating keratotic lesions. The key disadvantage of these appliances is that they are difficult to customise. Few studies have been undertaken to assess the efficacy of prefabricated silicone appliances. Claisse et al47 have shown that a commercially available silicone toe prop significantly reduces pressures under the
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Figure 11.5 Prefabricated silicone orthoses. From right: heel pad, metatarsal pad, interdigital wedge, toe covers, bunion shield.
apices of the second and third toes and under the third and fourth metatarsal heads. Caselli et al48 compared a full length silicone insole (Viscoped®) versus a simple insole made from Poron® in 35 patients with plantar keratotic lesions and reported no significant differences between the groups in relation to pain reduction. Finally, Kelly & Winson49 compared the efficacy of a full-length silicone insole with extra soft silicone inserts under the metatarsal heads (Viscoped®) versus a Plastazote® customisable insert system (Langer Blueline®) in 33 patients with lesser metatarsalgia, and found that the Langer device provided greater pressure reduction and pain relief. Although further research needs to be undertaken to more thoroughly assess the efficacy of silicone devices, the latter two studies highlight that the use of more high-tech materials does not necessarily produce better outcomes, and that customisation may be beneficial in certain cases.
HALLUX VALGUS SPLINTS The use of splints to realign the hallux in people with hallux valgus deformity has been described by several authors,50,51 and a range of splints are now commercially available (Fig. 11.6). These devices are worn when sleeping and are designed to hold the hallux in a rectus position in an attempt to reduce the contracture of soft tissues pulling the hallux in an abducted position. Only two studies have been undertaken to assess the efficacy of this approach. Groiso51 conducted a case series study of 56 children and adolescents with juvenile hallux valgus who received thermoplastic splints and exercises, and reported that
Figure 11.6 Hallux valgus splint.
the hallux abductus angle and intermetatarsal angle had reduced in half the group 2–6 years later. In contrast, Juriansz50 compared a hallux valgus night splint to no treatment in 28 people ranging in age from 10 to 77 years and found no improvement in clinically determined degree of deformity. Clearly, further research is required to fully ascertain the effectiveness of splints in the management of hallux valgus in older people; however, it is likely that splints would only be effective in milder forms of the condition where no significant bony remodelling has taken place. Furthermore, the acceptability of night splints in older patients is uncertain. Given that sleep disturbances are common in older people52 and that high levels of dissatisfaction have been reported with plantar fasciitis night splints because of sleeping difficulties,53 it is likely that hallux valgus night splints would be poorly tolerated in many older people.
CONTOURED INSOLES A plethora of prefabricated foot orthoses have become available in recent years, not only from medical suppliers and pharmacists but also from custom orthotic laboratories. These devices are manufactured from a
Cast orthoses
Figure 11.7 A selection of commercially available prefabricated orthoses.
Figure 11.8 Modular prefabricated orthoses.
wide range of materials (including polypropylene, polyethylene, ethyl vinyl acetate and carbon fibre) and can vary considerably in relation to length (threequarters or full length), arch height, flexibility, weight, longevity and cost (Fig. 11.7). Some prefabricated orthoses are heat-mouldable, whereas others are available in modular form, with a range of additions (including frontal plane wedges, metatarsal pads, etc) that can be used to customise the device (Fig. 11.8). Whether structural variations in prefabricated orthoses have a significant influence on foot function or clinical outcomes has not been explored in detail; however, preliminary studies indicate that differences exist between devices in relation to the position adopted by the foot in static stance.54 Selecting which
prefabricated orthosis to use is by no means a scientific process; rather, such choices are made on the basis of availability, cost and individual clinician preference. As stated previously, the wide availability of contoured prefabricated orthoses has largely replaced the manufacture of non-cast insoles. However, prefabricated orthoses appear to have had less impact on the prescription and manufacture of cast orthoses. Indeed, a recent survey of prescribing habits of podiatrists in Australia and New Zealand indicated that the most frequently prescribed orthosis was a cast orthosis (72% of participants compared to only 12% for prefabricated orthoses).55 One of the fundamental research questions that needs to be addressed in relation to prefabricated foot orthoses is whether they are as effective as the more time-consuming (and expensive) cast orthoses. A recent audit of 139 patients in the UK suggested that prefabricated orthoses provided similar levels of patient satisfaction to cast devices.3 However, the only condition for which high-quality comparisons have been undertaken is heel pain. A recent randomised controlled trial by Landorf et al56 found that, although both cast and prefabricated orthoses reduced plantar heel pain to a similar degree at 3 months, no significant differences between the groups were noted at 12 months. This paper also included a meta-analysis of their results combined with those of the earlier studies,57–59 which indicated no significant benefit of cast orthoses over prefabricated orthoses. These findings suggest that prefabricated orthoses may have similar efficacy to customised orthoses, at far less cost, for the management of heel pain.
CAST ORTHOSES Cast orthoses, also referred to as functional orthoses, are devices manufactured from an impression of the patient’s foot. Most commonly, cast orthoses are constructed from rigid thermoplastics that are heatmoulded over a positive plaster cast, with the aim of providing a precise fit of the device to the plantar contours of the foot (Fig. 11.9). By modifying both the positive cast and the orthotic shell itself, the clinician can theoretically modify a wide range of aspects of the weightbearing function of the foot. More recently, alternative impression techniques (such as optical scanning) and manufacturing methods (using CAD-CAM technology) have become available,
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A
B
Figure 11.9 Customised orthoses. A. Plaster modifications. B. Finished device.
although these systems are yet to have a widespread impact on traditional manufacturing practices.60 Because of our relatively limited understanding of the biomechanical function of the foot and the wide range of modifications that can be made to the shape of an orthosis, there is currently no consensus as to how cast orthoses should be prescribed and manufactured.7 Indeed, there is virtually no agreement as to how the foot should be assessed, how the cast should be taken (i.e. prone or supine neutral plaster casting, partially weightbearing foam box casting or optical scanning), the materials that should be used or the indications for orthotic shell variations (plantar fascial grooves, heel posts, cut-outs, apertures, etc).61–65 Subsequently, in clinical practice, prescription of cast
orthoses is more an art than a science and the outcomes of orthotic therapy may to some extent be influenced by clinical expertise and experience. Nevertheless, several studies have shown that cast orthoses do indeed modify selected aspects of foot function (including plantar pressure distribution, joint kinematics and muscle activity)8,66 and randomised controlled trials have reported significant improvements in pain and function in people with rheumatoid arthritis,67 heel pain56 and painful pes cavus.68 There is also some preliminary evidence that cast orthoses may be more effective in managing symptoms associated with foot osteoarthritis than nonsteroidal anti-inflammatory medications.69 Although these findings are generally positive, as stated previously there is a need for further studies to fully ascertain the benefits of cast orthoses over prefabricated orthoses. As stated in the introduction, it is beyond the scope of this chapter to discuss the details of prescription and manufacture of cast orthoses. Therefore, the reader is referred to specialists texts such as The Functional Foot Orthosis,70 Foot Orthoses and Other Forms of Conservative Footcare4 and Clinical Biomechanics of the Lower Extremities,10 as the approaches outlined in these texts are equally applicable to older people. However, it is worth mentioning that many clinicians are somewhat reluctant to prescribe cast orthoses for older people, on the assumption that they may not be able to tolerate rigid materials. While it is certainly true that older people with severe circulatory disorders and poor skin integrity may not be ideal candidates for rigid foot orthoses because of the risk of skin damage, there is no evidence that older people in general have any greater difficulty adjusting to cast orthoses than their younger counterparts. Indeed, because of age-related arch lowering and the increased prevalence of foot deformity associated with advancing age,71 it could be argued that older people have a greater need for accurate customisation, as they may have difficulty finding a prefabricated device to match the contour of their foot.
ANKLE–FOOT ORTHOSES Ankle–foot orthoses (AFOs) are widely used in the management of conditions resulting in weakness of the ankle dorsiflexors (such as poliomyelitis, cerebral palsy and cerebrovascular accident) in an attempt to prevent foot drop during the swing phase of gait.72,73
Foot orthoses and knee osteoarthritis
Figure 11.10 Ankle–foot orthoses. Left: Leaf spring ankle–foot orthosis. right: Articulated ankle–foot orthosis.
Conventional AFOs consisting of a simple metal caliper attached to bespoke footwear have been largely replaced by thermoplastic AFOs manufactured from plaster casts. Although more difficult to manufacture, thermoplastic AFOs provide more precise control of the ankle and are aesthetically more pleasing to the patient (Fig. 11.10). Several studies have demonstrated that AFOs produce significant improvements in temporospatial gait parameters, energy efficiency and lower limb muscle activity in hemiparetic patients74–77 and are generally well tolerated.78 More recently, several types of AFO have been recommended for use in the conservative management of degenerative osteoarthritis of the subtalar and ankle joints79 and tibialis posterior dysfunction.80,81 The underlying premise of this approach is that excessive motion of the rearfoot complex is responsible for the symptoms associated with these conditions and that conventional foot orthoses are inadequate for controlling the pronatory motion in severe flat foot deformity. Gait analysis studies indicate that AFOs do indeed alter the motion of the rearfoot complex; however, different AFOs designs have different effects. Kitaoka et al82 compared a rigid thermoplastic AFO, a rigid hindfoot orthosis (HFO-R: similar to the AFO but trimmed to extend only as far distally as the weightbearing surface of the heel and as proximal as the mid-calf region) and an articulated hindfoot orthosis (HFO-A: similar to the AFO but trimmed to the mid-calf region and with the addition of a sagittal plane hinge). The greatest reduction in rearfoot
motion was achieved with the AFO; however, this device also resulted in the adoption of a less propulsive gait pattern. On the basis of this observation, the authors suggested that the HFO-R and HFO-A may provide the best balance between motion restriction and allowing sufficient propulsion for normal gait. Subsequent studies in patients with subtalar83 and ankle84 osteoarthritis confirmed that both the HFO-R and HFO-A were effective in reducing rearfoot motion on a range of surfaces; however, the HFO-R provided optimum results. Although no studies have directly evaluated the biomechanical effects of AFOs in patients with tibialis posterior dysfunction, two case series investigations have reported favourable results with AFOs or a combination of AFOs and other conservative treatments. Chao et al81 reported significant improvements in pain and function in 49 patients treated with AFOs or foot orthoses over an average 15-month period. Similarly, in 47 patients with early stage tibialis posterior dysfunction, Alvarez et al85 reported that 83% of patients improved following a treatment regimen of calf stretching and strengthening and foot orthoses or AFOs.
FOOT ORTHOSES AND KNEE OSTEOARTHRITIS Osteoarthritis of the knee is one of the most common chronic musculoskeletal disorders associated with ageing, affecting approximately 20–40% of people older than 65 years.86 Although all three compartments of the knee may be affected, medial compartment involvement is the most common, because of the large compressive forces generated when walking.87 It has previously been demonstrated that contact forces within the knee when walking are considerably greater in the medial compartment than in the lateral compartment and that varus alignment of the knee joint is strongly associated with progression of medial compartment osteoarthritis.88 In response to these findings, several studies have been undertaken to investigate the efficacy of different forms of lateral wedging as a conservative treatment for medial compartment knee osteoarthritis, based on the hypothesis that decreasing the varus moment at the knee may alleviate compressive forces in the medial compartment.89–92 The first study by Sasaki & Yasuda89 found that patients wearing a laterally wedged insole (manufactured from either sponge
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rubber or leather) in conjunction with taking nonsteroidal anti-inflammatory drugs (NSAIDs) reported greater reductions in pain than patients prescribed NSAIDs alone. Subsequent uncontrolled studies have reported similar findings. Wolfe & Brueckmann90 reported that 82% of patients with medial knee osteoarthritis reported decreased pain while wearing a lateral heel wedge, Tohyama et al91 found that lateral heel wedges reduced knee pain in patients with early medial compartment osteoarthritis, Keating et al92 reported that 32 out of 85 patients with medial knee osteoarthritis reported ‘excellent’ improvement in pain scores while wearing a lateral heel wedge, and Rubin & Menz93 reported significant reductions in knee pain in 30 osteoarthritis patients using laterally wedged custom foot orthoses. The only randomised comparisons so far undertaken reported that a laterally wedged insole combined with subtalar joint strapping was more effective in reducing knee pain than a wedge placed in a sock-type ankle support.94,95 More recently, the first randomised controlled trial reported that, while no symptomatic or functional improvement was noted in subjects prescribed laterally wedged cork and rubber insoles, they required less NSAIDs for pain management than the control group.96,97 Although these preliminary results are promising, recent systematic reviews have concluded that there is currently insufficient high-quality evidence to support the long-term use of laterally wedged orthoses98,99 as, despite some evidence of temporary pain relief, such devices do not appear to alter the normal course of knee osteoarthritis or have any impact on radiological severity. Nevertheless, there may be some value in trying wedged insoles for short-term pain relief in older people who are considering knee replacement surgery.
FOOT ORTHOSES AS A BALANCE AID Sensory receptors on the sole of the foot play an important role in maintaining balance by providing the brain with information about foot position and changes in plantar pressure distribution. This is evidenced by numerous studies that have demonstrated balance deficits in subjects with sensory neuropathy.100,101 In response to these observations, there have been several studies undertaken recently to determine whether the sensory role of plantar mechanoreceptors can be harnessed to develop novel interventions to improve balance in older people.102
Theoretically, placing textured insoles under the foot may provide additional tactile sensory input that can be used by the brain to compensate for deficits in other systems contributing to balance. While a number of studies have indicated that different types of foot orthosis may improve balance,103–106 the mechanisms that may be responsible for this have only recently been investigated. Hosoda et al107 compared responses to platform perturbation in healthy subjects when wearing two types of footwear (flat, leather-soled sandals and ‘health sandals’ containing an insole with numerous small raised projections), and reported shorter reflex latencies when the health sandals were worn. Similarly, Waddington & Adams108 evaluated the effect of textured rubber insoles (7 mm deep nodules at a density of 4/cm2) on the ability of healthy young subjects to detect ankle inversion, and found that inserting an insole into the shoe provided similar movement detection to the barefoot condition. The authors concluded that textured insoles may be able to compensate for the loss of sensitivity produced by wearing soft-soled footwear, presumably by enhancing sensory feedback. Maki et al109 measured responses to platform perturbation in young and older people with and without a specially designed plastic tube attached to the perimeter of the sole of the foot. This ‘plantar facilitation’ reduced the incidence of multiple stepping responses when the platform was displaced in the anteroposterior direction, suggesting that the enhanced sensory input provided by the insoles during the initial protective step response was used by the brain to stabilise posture, rendering an additional step unnecessary. More recently, Priplata et al110 demonstrated significant reductions in sway variables when older people stood on randomly vibrating insoles and suggested that the introduction of tactile ‘noise’ could ameliorate age-related impairments in balance control. AFOs may also have positive effects on balance in older people with peripheral neuropathy. Richardson et al111 have recently demonstrated significant improvements in temporospatial gait regularity when older people with peripheral neuropathy walked on an irregular surface while wearing semi-rigid AFOs. This finding is consistent with previous laboratory studies, which indicated that tactile information derived from a stimulus above the ankle is used by the brain to control posture and may be able to at least partially compensate for loss of plantar sensation.112,113 Although these results provide interesting insights into the role of peripheral sensory input on stabilisa-
References
tion of posture, a great deal more research is required before insoles can be considered an effective falls prevention strategy in older people. The issue of comfort may also be a practical constraint, as people with sensitive feet or those who suffer from foot pain may not welcome the additional stimulation provided by the orthoses.
SUMMARY This chapter has provided a brief overview of the use of foot orthoses in the management of foot disorders in older people. Many foot problems can be successfully managed with the use of very simple pads manu-
factured from inexpensive materials, the design of which can be modified according to the needs of individual patients. The availability of over-the-counter silicone devices and prefabricated contoured orthoses has provided the clinician with a wide array of treatment options, and there is emerging evidence that foot orthoses may have a role in the management of knee osteoarthritis and in falls prevention. Provided that the patient has sufficient skin integrity and appropriate footwear, and is sufficiently mobile to be able to change or remove orthoses where necessary, the prescription and manufacture of foot orthoses for older people, including cast orthoses, is essentially no different from that of younger people and should always be considered as a conservative management strategy.
References 1. Whitney KA. Foot deformities, biomechanical and pathomechanical changes associated with aging including orthotic considerations, Part II. Clinics in Podiatric Medicine and Surgery 2003; 20: 511–526. 2. Kruizinga C, Boonstra A, Groothoff J et al. Characteristics of patients supplied with foot orthoses from orthopaedic workshops in The Netherlands. The Foot 2003; 13: 39–45. 3. Fox HJ, Winson IG. Foot orthoses: an audit of expenditure and efficacy. The Foot 1994; 4: 79–82. 4. Michaud TC. Foot orthoses and other forms of conservative foot care. Baltimore, MD: Williams & Wilkins; 1993. 5. Bono CM, Berberian WS. Orthotic devices. Degenerative disorders of the foot and ankle. Foot and Ankle Clinics 2001; 6: 329–339. 6. Nawoczenski DA, Janisse DJ. Foot orthoses in rehabilitation – what’s new. Clinics in Sports Medicine 2004; 23: 157–167. 7. Payne CB. The past, present and future of podiatric biomechanics. Journal of the American Podiatric Medical Association 1998; 98: 53–63. 8. Landorf K, Keenan A-M. Efficacy of foot orthoses – what does the literature tell us? Journal of the American Podiatric Medical Association 2000; 90: 149–158. 9. Vicenzino B. Foot orthotics in the treatment of lower limb conditions: a musculoskeletal physiotherapy perspective. Manual Therapy 2004; 9: 185–196. 10. Valmassy RL. Clinical biomechanics of the lower extremities. St Louis, MO: Mosby; 1995.
11. Menz HB, Morris ME. Footwear characteristics and foot problems in older people. Gerontology 2005; 51: 346–351. 12. Kaplan C, Natale PD, Spilken TL. Paddings and strappings of the foot. New York: Futura; 1982. 13. Coates TT. Practical orthotics for chiropodists. London: Actinic Press; 1983. 14. Polokoff MM. Buttress appliance. Journal of the American Podiatry Association 1976; 66: 261– 263. 15. Kippen C. A literature review of non-surgical techniques, used by chiropodists, for correcting lesser toe pathologies. Journal of British Podiatric Medicine 1992; 47: 137–140. 16. Gunal I, Kosay C, Veziroglu A et al. Relationship between onychocryptosis and foot type and treatment with toe spacer. A preliminary investigation. Journal of the American Podiatric Medical Association 2003; 93: 33–36. 17. Polokoff MM. Plantar forefoot device. Journal of the American Podiatry Association 1976; 66: 337–340. 18. Zimny S, Schatz H, Pfohl U. The effects of applied felted foam on wound healing and healing times in the therapy of neuropathic diabetic foot ulcers. Diabetic Medicine 2003; 20: 622–625. 19. Nube VL, Molyneaux L, Bolton T et al. The use of felt deflective padding in the management of plantar hallux and forefoot ulcers in people with diabetes. The Foot 2006; 16: 38–43. 20. McLauchlan PT, Abboud RJ, Rendall GC et al. Use of an in-shoe pressure system to investigate the effect of two clinical treatment methods for metatarsalgia. The Foot 1994; 4: 204–208.
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21. Holmes G, Timmerman L. A quantitative assessment of the effect of metatarsal pads on plantar pressures. Foot and Ankle International 1990; 11: 141–145. 22. Hodge M, Bach T, Carter G. Orthotic management of plantar pressure and pain in rheumatoid arthritis. Clinical Biomechanics 1999; 14: 567–575. 23. Hsi WL, Kang JH, Lee XX. Optimum position of metatarsal pad in metatarsalgia for pressure relief. American Journal of Physical Medicine and Rehabilitation 2005; 84: 514–520. 24. Kang J-H, Chen M-D, Chen S-C et al. Correlations between subjective treatment responses and plantar pressure parameters of metatarsal pad treatment in metatarsalgia patients: a prospective study. BMC Musculoskeletal Disorders 2006; 7: 95. 25. Mueller MJ, Lott DJ, Hastings MK et al. Efficacy and mechanism of orthotic devices to unload metatarsal heads in people with diabetes and a history of plantar ulcers. Physical Therapy 2006; 86: 833–842. 26. Hastings MK, Mueller MJ, Pilgram TK et al. Effect of metatarsal pad placement on plantar pressure in people with diabetes mellitus and peripheral neuropathy. Foot and Ankle International 2007; 28: 84–88. 27. Chang A, Abu-Faraj Z, Harris G et al. Multistep measurement of plantar pressure alterations using metatarsal pads. Foot and Ankle International 1994; 15: 654–660. 28. Ashry HR, Lavery LA, Murdoch DO et al. Effectiveness of diabetic insoles to reduce foot pressures. Journal of Foot and Ankle Surgery 1997; 36: 268–271. 29. Hayda R, Tremaine M, Tremaine K et al. Effect of metatarsal pads and their positioning: a quantitative assessment. Foot and Ankle International 1994; 15: 561–566. 30. Hirschberg GG. A simple cure for Morton’s neuralgia. Journal of the American Podiatric Medical Association 2000; 90: 100–101. 31. Polokoff MM. Forefoot imbalance. Journal of the American Podiatry Association 1977; 67: 577– 584. 32. Morton DJ. Hypermobility of the first metatarsal bone: the interlinking factor between metatarsalgia and longitudinal arch strains. Journal of Bone and Joint Surgery 1928; 10: 187–196. 33. Glasoe WM, Coughlin MJ. A critical analysis of Dudley Morton’s concept of disordered foot function. Journal of Foot and Ankle Surgery 2006; 45: 147–155. 34. Abu-Faraj Z, Harris G, Chang A et al. Evaluation of a rehabilitative pedorthic: plantar pressure alterations with scaphoid pad application. IEEE Transactions in Rehabilitative Engineering 1996; 4: 328–336.
35. Raspovic A, Newcombe L, Lloyd J et al. Effect of customized insoles on vertical plantar pressures in sites of previous neuropathic ulceration in the diabetic foot. The Foot 2000; 10: 133–138. 36. Guldemond NA, Leffers P, Schaper NC et al. The effects of insole configurations on forefoot plantar pressure and walking convenience in diabetic patients with neuropathic feet. Clinical Biomechanics 2007; 22: 81–87. 37. Snook GA, Christman OD. The management of subcalcaneal pain. Clinical Orthopaedics and Related Research 1972; 82: 163–168. 38. Coates IS. Silicone orthodigita and shielding, Part I. Journal of the American Podiatry Association 1976; 66: 648–651. 39. Coates IS. Silicone orthodigita and shielding, Part III. Journal of the American Podiatry Association 1976; 66: 786–790. 40. Coates IS. Silicone orthodigita and shielding, Part IV. Journal of the American Podiatry Association 1976; 66: 877–879. 41. Coates IS. Silicone orthodigita and shielding, Part V: Bunion shields. Journal of the American Podiatry Association 1976; 66: 932–934. 42. Slater RA, Herschkowitz I, Ramot Y et al. Reduction of digital plantar pressure by debridement and silicone orthosis. Diabetes Research and Clinical Practice 2006; 74: 263–266. 43. McCourt FJ. To cast or not to cast? The comparative effectiveness of casted and non-casted orthoses. Journal of British Podiatric Medicine 1990; 45: 239–243. 44. Redmond A, Lumb PS, Landorf K. Effect of cast and noncast foot orthoses on plantar pressure and force during normal gait. Journal of the American Podiatric Medical Association 2000; 90: 441–449. 45. Branthwaite HR, Payton CJ, Chockalingam N. The effect of simple insoles on three-dimensional foot motion during normal walking. Clinical Biomechanics 2004; 19: 972–977. 46. Bedinghaus JM, Niedfeldt MW. Over-the-counter foot remedies. American Family Physician 2001; 64: 791–796, 803–804. 47. Claisse PJ, Binning J, Potter J. Effect of orthotic therapy on claw toe loading. Results of significance testing at pressure sensor units. Journal of the American Podiatric Medical Association 2004; 94: 246–254. 48. Caselli MA, Levitz SJ, Clark N et al. Comparison of Viscoped and Poron for painful submetatarsal hyperkeratotic lesions. Journal of the American Podiatric Medical Association 1997; 87: 6–10. 49. Kelly A, Winson I. Use of ready-made insoles in the treatment of lesser metatarsalgia: a prospective randomized controlled trial. Foot and Ankle International 1998; 19: 217–220.
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50. Juriansz AM. Conservative treatment of hallux valgus: a randomised controlled trial of a hallux valgus night splint. Journal of British Podiatric Medicine 1996; 51: 119. 51. Groiso JA. Juvenile hallux valgus. A conservative approach to treatment. Journal of Bone and Joint Surgery 1992; 74A: 1367–1374. 52. Foley DJ, Monjan AA, Brown SL et al. Sleep complaints among elderly persons: an epidemiologic study of three communities. Sleep 1995; 18: 425–432. 53. Powell M, Post WR, Keener J et al. Effective treatment of chronic plantar fasciitis with dorsi flexion night splint: A cross over prospective randomised outcome study. Foot and Ankle International 1998; 19: 10–18. 54. Payne C, Oates M, Noakes H. Static stance response to different types of foot orthoses. Journal of the American Podiatric Medical Association 2003; 93: 492–498. 55. Landorf K, Keenan AM, Rushworth RL. Foot orthosis prescription habits of Australian and New Zealand podiatric physicians. Journal of the American Podiatric Medical Association 2001; 91: 174–183. 56. Landorf KB, Keenan AM, Herbert RD. Effectiveness of foot orthoses to treat plantar fasciitis: a randomized trial. Archives of Internal Medicine 2006; 166: 1305–1310. 57. Lynch D, Goforth W, Martin J et al. Conservative treatment of plantar fasciitis. A prospective study. Journal of the American Podiatric Medical Association 1998; 88: 375–380. 58. Pfeffer G, Bacchetti P, Deland J et al. Comparison of custom and prefabricated orthoses in the initial treatment of proximal plantar fasciitis. Foot and Ankle International 1999; 20: 214–221. 59. Martin J, Hosch J, Goforth W et al. Mechanical treatment of plantar fasciitis. A prospective study. Journal of the American Podiatric Medical Association 2001; 91: 55–62. 60. Grumbine N. Computer generated orthoses. A review. Clinics in Podiatric Medicine and Surgery 1993; 10: 377–391. 61. Olsen WR. Orthotic materials. In: R. L. Valmassy, eds. St Louis: Mosby; 1996: 307–326. 62. McPoil TG, Hunt GC. Evaluation and management of foot and ankle disorders: present problems and future directions. Journal of Orthopaedic and Sports Physical Therapy 1995; 21: 381–388. 63. Sobel E, Levitz SJ. Reappraisal of the negative impression cast and the subtalar joint neutral position. Journal of the American Podiatric Medical Association 1997; 87: 32–33. 64. Payne C, Chuter V. The clash between theory and science on the kinematic effectiveness of foot ortho-
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ses. Clinics in Podiatric Medicine and Surgery 2001; 18: 705–713. Ball KA, Afheldt MJ. Evolution of foot orthotics – part 1: coherent theory or coherent practice? Journal of Manipulative and Physiological Therapeutics 2002; 25: 116–124. Razeghi M, Batt ME. Biomechanical analysis of the effects of orthotic shoe inserts: a review of the literature. Sports Medicine 2000; 29: 425–438. Woodburn J, Barker S, Helliwell P. A randomized controlled trial of foot orthoses in rheumatoid arthritis. Journal of Rheumatology 2002; 29: 1377– 1383. Burns J, Crosbie J, Ouvrier R et al. Effective orthotic therapy for the painful cavus foot. Journal of the American Podiatric Medical Association 2006; 96: 205–211. Thompson J, Jennings M, Hodge W. Orthotic therapy in the management of osteoarthritis. Journal of the American Podiatric Medical Association 1992; 82: 136–139. Philps JW. The functional foot orthosis, 2nd ed. Edinburgh: Churchill Livingstone; 1995. Scott G, Menz HB, Newcombe L. Age-related differences in foot structure and function. Gait and Posture 2007; 26: 68–75. Rubin G, Cohen E. Prostheses and orthoses for the foot and ankle. Clinics in Podiatric Medicine and Surgery 1988; 5: 695–719. Sobel E, Levitz SJ, Caselli MA. Orthoses in the treatment of rearfoot problems. Journal of the American Podiatric Medical Association 1999; 89: 220–223. Franceschini M, Massucci M, Ferrari L et al. Effects of an ankle–foot orthosis on spatiotemporal parameters and energy cost of hemiparetic gait. Clinical Rehabilitation 2003; 17: 368–372. Romkes J, Brunner R. Comparison of a dynamic and a hinged ankle–foot orthosis by gait analysis in patients with hemiplegic cerebral palsy. Gait and Posture 2002; 15: 18–24. DeWit DC, Buurke JH, Nijlant JM et al. The effect of an ankle–foot orthosis on walking ability in chronic stroke patients: a randomized controlled trial. Clinical Rehabilitation 2004; 18: 550– 557. Geboers JF, Drost MR, Spaans F et al. Immediate and long-term effects of ankle–foot orthosis on muscle activity during walking: a randomized study in patients with unilateral foot drop. Archives of Physical Medicine and Rehabilitation 2002; 83: 240–245. Tyson SF, Thornton HA. The effect of a hinged ankle foot orthosis on hemiplegic gait: objective measures and user’s opinions. Clinical Rehabilitation 2001; 15: 53–58.
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79. Bono CM, Berberian WS. Orthotic devices. Degenerative disorders of the foot and ankle. Foot and Ankle Clinics 2001; 6: 329–340. 80. Steb HS, Marzano R. Conservative management of posterior tibial tendon dysfunction, subtalar joint complex and pes planus deformity. Clinics in Podiatric Medicine and Surgery 1999; 16: 439–451. 81. Chao W, Wapner KL, Lee TH et al. Nonoperative management of posterior tibial tendon dysfunction. Foot and Ankle International 1996; 17: 736– 741. 82. Kitaoka HB, Crevoisier XM, Harbst K et al. The effect of custom-made braces for the ankle and hindfoot on ankle and foot kinematics and ground reaction forces. Archives of Physical Medicine and Rehabilitation 2006; 87: 130–135. 83. Huang Y-C, Harbst K, Kotajarvi B et al. Effects of ankle–foot orthoses on ankle and foot kinematics in patients with subtalar osteoarthritis. Archives of Physical Medicine and Rehabilitation 2006; 87: 1131–1136. 84. Huang Y-C, Harbst K, Kotajarvi B et al. Effects of ankle–foot orthoses on ankle and foot kinematics in patients with ankle osteoarthritis. Archives of Physical Medicine and Rehabilitation 2006; 87: 710–716. 85. Alvarez RG, Marini A, Schmitt C et al. Sage I and II posterior tibial tendon dysfunction treated by a structured nonoperative management protocol: an orthosis and exercise program. Foot and Ankle International 2006; 27: 2–8. 86. Felson DT. The epidemiology of knee osteoarthritis: results from the Framingham Osteoarthritis Study. Seminars in Arthritis and Rheumatism 1990; 20: 42–50. 87. Morrison JB. The mechanics of the knee joint in relation to normal walking. Journal of Biomechanics 1970; 3: 51–61. 88. Sharma L, Song J, Felson DT et al. The role of knee alignment in disease progression and functional decline in knee osteoarthritis. Journal of the American Medical Association 2001; 286: 188–195. 89. Sasaki T, Yasuda K. Clinical evaluation of the treatment of osteoarthritis knees using a newly designed wedged insole. Clinical Orthopaedics and Related Research 1987; 221: 181–187. 90. Wolfe SA, Brueckmann FR. Conservative treatment of genovalgus and varum with medial/lateral heel wedges. Indiana Medicine 1991; 84: 614–615. 91. Tohyama H, Yasuda K, Keneda K. Treatment of osteoarthritis of the knee with heel wedges. International Orthopaedics 1991; 15: 31–33. 92. Keating EM, Faris PM, Ritter MA et al. The use of lateral heel and sole wedges in the treatment of medial osteoarthritis of the knee. Orthopedic Review 1993; 22: 921–924.
93. Rubin R, Menz HB. Use of laterally wedged custom foot orthoses to reduce pain associated with medial knee osteoarthritis. A preliminary investigation. Journal of the American Podiatric Medical Association 2005; 95: 347–352. 94. Toda Y, Segal N, Kato A et al. Effect of a novel insole on the subtalar joint of patients with medial compartment osteoarthritis of the knee. Journal of Rheumatology 2001; 28: 2705–2710. 95. Toda Y, Segal N. Usefulness of an insole with subtalar strapping for analgesia in patients with medial compartment osteoarthritis of the knee. Arthritis and Rheumatism 2002; 47: 468–473. 96. Maillefert JF, Hudry C, Baron G et al. Laterally elevated wedged insoles in the treatment of medial knee osteoarthritis: a prospective randomized controlled study. Osteoarthritis and Cartilage 2001; 9: 738–745. 97. Pham T, Maillefert JF, Hudry C et al. Laterally elevated wedged insoles in the treatment of medial knee osteoarthritis. A two-year prospective randomized controlled study. Osteoarthritis and Cartilage 2004; 12: 46–55. 98. Brouwer RW, Jakma TSC, Verhagen AP et al. Braces and orthoses for treating osteoarthritis of the knee. Cochrane Database of Systematic Reviews 2005; 1: CD004020. 99. Reilly KA, Barker KL, Shamley D. A systematic review of lateral wedge orthotics – how useful are they in the management of medial compartment osteoarthritis? The Knee 2006; 13: 177–183. 100. Simoneau GG, Ulbrecht JS, Derr JA et al. Postural instability in patients with diabetic sensory neuropathy. Diabetes Care 1994; 17: 1411–1421. 101. Boucher P, Teasdale N, Courtemanche R et al. Postural stability in diabetic polyneuropathy. Diabetes Care 1995; 18: 638–645. 102. Hijmans JM, Geertzen JHB, Dijkstra PU et al. A systematic review of the effects of shoes and other ankle or foot appliances on balance in older people and people with peripheral nervous system disorders. Gait and Posture 2007; 25: 316–323. 103. Orteza LC, Vogelbach WD, Denegar CR. The effects of molded and unmolded orthotics on balance and pain while jogging following inversion ankle sprain. Journal of Athletic Training 1992; 27: 80–84. 104. Guskiewicz K, Perrin D. Effect of orthotics on postural sway following inversion ankle sprain. Journal of Orthopaedic and Sports Physical Therapy 1996; 23: 326–331. 105. Stude DE, Brink DK. Effects of nine holes of simulated golf and orthotic intervention on balance and proprioception in experienced golfers. Journal of Manipulative and Physiological Therapeutics 1997; 20: 590–601.
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106. Rome K, Brown CL. Randomized clinical trial into the impact of rigid foot orthoses on balance parameters in excessively pronated feet. Clinical Rehabilitation 2004; 18: 624–630. 107. Hosoda M, Yoshimaru O, Takayanagi K et al. The effects of various footwear types and materials, and of fixing of the ankles by footwear, on upright posture control. Journal of Physical Therapy Science 1997; 9: 47–51. 108. Waddington G, Adams R. Textured insole effects on ankle movement discrimination while wearing athletic shoes. Physical Therapy in Sport 2000; 1: 119–128. 109. Maki BE, Perry SD, Norrie RG et al. Effect of facilitation of sensation from plantar foot–surface boundaries on postural stabilization in young and older adults. Journal of Gerontology 1999; 54A: M281– 287.
110. Priplata AA, Niemi JB, Harry JD et al. Vibrating insoles and balance control in elderly people. The Lancet 2003; 362: 1123–1124. 111. Richardson JK, Thies SB, DeMott TK et al. Interventions improve gait regularity in patients with peripheral neuropathy while walking on an irregular surface under low light. Journal of the American Geriatrics Society 2004; 52: 510– 515. 112. Rogers MW, Wardman DL, Lord SR et al. Tactile sensory input improves stability during standing in normal subjects and those with lower limb sensory loss. Experimental Brain Research 2001; 126: 514–522. 113. Menz HB, Lord SR, Fitzpatrick RC. A tactile stimulus applied to the leg improves postural stability in young, old and neuropathic subjects. Neuroscience Letters 2006; 406: 23–26.
233
CHAPTER
Footwear considerations
CHAPTER CONTENTS Shoe-wearing habits of older people Detrimental effects of footwear
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236
Footwear modifications 237 Shock-absorbing cushioned heel 237 Thomas heel 237 Rocker sole 238 Heel and sole raises 238 Shoe stretching and balloon patching 239 Specialist footwear
239
Footwear, balance and falls 240 Heel height 241 Midsole cushioning 241 Slip resistance of footwear outersoles Heel collar height 243 Midsole flaring 243 Method of fixation 244 Advising older people about footwear
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12
Footwear plays an important role in protecting the foot from extremes of temperature, moisture and mechanical trauma. However, since the development and widespread popularity of fashion footwear in the 1600s, the functional aspect of footwear has largely been supplanted by the requirements of fashion. In both men and women of all ages, shoe selection is primarily based on aesthetic considerations, many of which are incompatible with the optimal function of the foot and ankle.1 In older people, inappropriate footwear often causes (or at least contributes to) foot pain and deformity and therefore it is essential that foot care specialists have a sound understanding of the effects of footwear on the older foot. The following chapter discusses the shoe-wearing habits of older people, the relationship between footwear and foot problems, and the use of footwear modification and prescription footwear as a therapeutic modality. Because of the high rate of accidental falls and fractures in older people, the effect of shoe design on balance is also discussed. Finally, issues related to compliance with footwear recommendations are reviewed.
Summary 245 References 246
SHOE-WEARING HABITS OF OLDER PEOPLE It has long been recognised that many older people wear inappropriate footwear (Fig. 12.1).2 A household survey of people aged over 80 years conducted in the UK found that most wore slippers all day, irrespective of whether or not they were housebound.3 Similarly, a survey of indoor shoe-wearing habits of
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their adult life. Finally, it has been suggested that commercially available footwear simply does not adequately cater for the dimensions of the older foot. A recent study of 668 older people in Germany found that most older people have feet that are broader than currently available casual footwear,10 which goes some way to explaining the large number of older people who report difficulty in purchasing comfortable shoes.
DETRIMENTAL EFFECTS OF FOOTWEAR
Figure 12.1 Inappropriate footwear worn by older people. (Courtesy of Lesley Newcombe, La Trobe University.)
128 older people in Australia indicated that more than half spent less than $30 Australian dollars on their indoor footwear (most commonly slippers), replaced them infrequently, and often wore their indoor shoes for outdoor activities.4 More recently, a survey of subacute aged care hospital patients reported that only 14% wore ‘safe’ footwear, with the most commonly observed detrimental features being a lack of fastening (86%), slippery soles (86%) and an excessively flexible heel counter (77%).5 By far the most commonly encountered problem with footwear in older people is the wearing of shoes that are too small. Burns et al6 compared the length and width of the feet and shoes of 65 people aged between 64 and 93 years attending a rehabilitation ward and reported that 72% wore shoes of an incorrect size. Menz & Morris7 assessed length, width and total area of feet and footwear in 176 older people and reported that 81% wore indoor shoes narrower than their feet and 78% wore outdoor shoes narrower than their feet. Finally, a study of 440 veterans affairs patients in the USA reported that only 26% were found to be wearing appropriately sized shoes.8 Several factors may be responsible for the high prevalence of ill-fitting footwear in older people. Firstly, fashion exerts a powerful influence over footwear selection, particularly in women, and it is clear that many people are willing to endure foot pain and deformity in order to conform to societal expectations of footwear aesthetics.9 Secondly, few older people regularly have their feet measured,4 as most assume that their shoe size remains constant throughout
It has long been suspected that the deformation of the foot caused by shoes is a major contributing factor to foot problems such as hallux valgus (bunions), lesser toe deformity, corns and calluses.11–14 Indirect evidence for the detrimental effects of footwear can be derived from reports of very low prevalence of foot problems in populations that have never worn shoes,15–17 and the marked increase in the number of surgical procedures performed for hallux valgus in Japan following the adoption of Westernised footwear in preference to the traditional sandal.18 A US survey of 356 women aged between 20 and 60 years revealed that 88% wore shoes that were narrower than their feet, and those with the greatest disparity between foot width and shoe width were more likely to suffer from foot pain.19 Two recent studies have evaluated the association between footwear fitting characteristics and foot problems in older people. Burns et al6 compared the length and width of the feet and shoes of 65 people aged between 64 and 93 years attending a rehabilitation ward and reported that the wearing of shoes of incorrect length was significantly associated with the presence of foot ulceration and foot pain, which the authors attributed to excessive friction generated from the foot sliding inside the shoe. More recently, a study of 176 people aged over 65 years demonstrated that most participants wore shoes narrower than their feet, with women wearing shoes that were shorter, narrower and with a reduced total area compared to their feet than men. Wearing shoes substantially narrower than the foot was associated with corns on the toes, hallux valgus deformity and foot pain, whereas wearing shoes shorter than the foot was associated with lesser toe deformity.7 Ill-fitting footwear is of particular concern for older people with diabetic peripheral neuropathy because of the risk of ulceration, infection and amputation.
Footwear modifications
Although ulceration and amputation are caused by a range of factors, poorly fitting footwear is thought to be a contributing factor in approximately 50% of cases.20 Indeed, a recent study of 256 veterans with diabetes indicated that those with foot ulceration were five times more likely to have poorly fitting footwear.8 In addition to incorrectly fitting footwear, the wearing of shoes with elevated heels is thought to contribute to the development of foot problems by increasing the pressure borne by the metatarsal heads21–24 and by interfering with the normal function of the first metatarsophalangeal joint25,26 during gait. Only two studies have been undertaken to explore this relationship in older people. Dawson et al27 interviewed 127 women aged 50–70 years regarding the highest heels they had worn for various activities across 10-year age bands (20s to 50s), and found that the wearing of lower heels for some activities was associated with an increased likelihood of having foot arthritis, pain and hallux valgus. This counterintuitive result may have been due to recall bias, in that women with foot problems may have been more likely to underestimate past heel height use. Furthermore, establishing an association between current foot problems and history of wearing high heels is difficult, as most women in this age group have been exposed to this type of footwear.28 More recently, Menz & Morris7 reported that wearing shoes with heel elevation greater than 25 mm was associated with hallux valgus and plantar calluses in older women. Healthcare costs associated with footwear-related foot problems in older people are considerable. Assuming that inappropriate footwear is responsible for, or at least contributes to, 75% of foot problems requiring surgical treatment, Coughlin & Thompson13 have estimated that, in the USA in 1991, 209 000 bunionectomies, 210 000 hammer toe corrections, 119 000 bunionette repairs and 66 500 neuroma resections were performed, at a cost of approximately US$3 billion. Although the 75% figure is probably an overestimate, these figures do not include the costs of conservative management of footwear-related foot problems, so the true figure is likely to be much higher. Taken together, these studies generally support the widespread view that the use of inappropriate footwear is highly prevalent in older people and is associated with the development of foot problems. As such, advising older patients regarding more suitable footwear is an essential component of clinical manage-
ment, and changing footwear may, in and of itself, lead to the resolution of many foot complaints. Strategies for advising patients to change their footwear are discussed later in this chapter.
FOOTWEAR MODIFICATIONS Footwear modification (pedorthics) is a useful conservative management strategy for older people with foot problems. The aim of footwear modification is to reduce shock and shear, to relieve excessive pressure from sensitive or painful areas, to accommodate, correct and support deformities, and to control or limit painful motion of joints.29 This may be achieved by changing the geometry of the sole to influence weightbearing patterns and by modifying the shape of the upper to accommodate bony deformities. These approaches are particularly useful in the management of diabetic foot ulcers30,31 and chronic arthritic conditions such as rheumatoid arthritis,32,33 and following surgical fusion of the tarsal joints.34 The following section briefly discusses the most common footwear modifications used in the management of foot problems in older people.
SHOCK-ABSORBING CUSHIONED HEEL As the name suggests, shock-absorbing cushioned heels (SACHs) are a modification of the plantar aspect of the shoe heel to enhance shock attenuation. This can be achieved by simply removing a wedge-shaped piece of the heel and replacing it with a more compressible material (Fig. 12.2). SACHs are indicated in the management of heel pain in older people with atrophic heel pads, or as an attempt to increase lower limb shock attenuation in patients with age-related or surgically induced limited joint range of motion (such as patients who have undergone triple arthrodesis). No studies have directly evaluated the biomechanical effects of SACHs, although several authors have demonstrated that shoes with softer soles reduce both the magnitude and velocity of accelerations transmitted through the lower limb at heel strike.35,36
THOMAS HEEL The Thomas heel, also referred to as an S-heel, is a shoe modification in which the distal edge of the heel is extended on the medial side to a point corresponding to the navicular tuberosity (Fig. 12.3).37 The aim
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Figure 12.2 Shock-absorbing cushioned heel. Black section indicates softer material inserted into sole.
Lateral
Medial
Figure 12.3 Thomas heel modification.
of this addition is to provide additional support to the medial arch in patients with flat foot deformity. A variant of the Thomas heel, referred to as the Thomas wedge, is a wedge of material placed within the medial border of the heel in an attempt to more directly limit eversion of the subtalar joint. In contemporary clinical practice, Thomas heels are rarely used in isolation but they may have some value in enhancing the effect of foot orthoses in overweight patients.38 Few studies have been undertaken to assess the biomechanical or clinical effects of the Thomas heel in detail; however, a small study by Arlen & Carville37 demonstrated that the frontal plane alignment of the calcaneus does shift in the direction of inversion when standing in shoes that have undergone this modification. Using an in-shoe plantar pressure system, Xu et al39 demonstrated that the addition of a Thomas heel redirected the centre of pressure laterally, with a concomitant decrease in the magnitude of pressures under the medial forefoot. The application of a reverse Thomas heel (a modification in which the distal edge is extended to the lateral side of the foot) had the opposite effect.
ROCKER SOLE The underlying concept of the rocker sole, also known as a rocker bottom sole, is to limit motion at joints in the foot by providing a rigid convex platform over which the body pivots from heel strike to toe off. Rocker soles have two main indications: the reduction of forefoot plantar pressure in people with diabetes or
Rearfoot rocker
Forefoot rocker
Figure 12.4 Rocker sole modification.
rheumatoid arthritis and the restriction of foot motion in people with osteoarthritis or those who have undergone surgical fusion of one or more tarsal joints. Broadly speaking, there are three types of rocker soles: rearfoot rockers, forefoot rockers and combined rockers (Fig. 12.4); however, the size and placement of the fulcrum can be modified according to individual patient needs. Several studies have shown that the addition of a rocker sole reduces forefoot plantar pressures by between 30% and 65%.40–47 The optimum location of the rocker sole for reducing metatarsal head pressures has been demonstrated to be 55–60% of shoe length, while for reducing toe pressures it is 65% of shoe length.42 However, individual responses to rocker soles can be highly variable41 and in some cases a rocker sole may increase pressure under the foot.41 For this reason, it has been suggested that, where possible, some form of plantar pressure measurement should be used when prescribing rocker soles.41,42 In addition to reducing forefoot pressures, rocker sole shoes have several other effects on gait, including an increase in cadence,48,49 a decrease in step length,48 reduced sagittal plane forefoot motion50 and increased ankle plantarflexion, hip extension and knee flexion.49 While many of these alterations can be considered to be beneficial if the aim of treatment is to restrict motion within the foot, changes in pelvic motion observed with rocker soles have been suggested to be indicative of lateral instability,51 so some caution is required when prescribing rocker soles for older people with balance problems.
HEEL AND SOLE RAISES The addition of material to the heel and/or sole of the shoe has several clinical indications in the management of foot problems in older people. Firstly, heel and sole raises are frequently employed in the management of limb length discrepancy, in an attempt to level the pelvis and improve the symmetry of the gait pattern. The most common cause of limb length discrepancy in older people is hip replacement
Specialist footwear
surgery. A postoperative analysis of 150 total hip replacement procedures by Williamson & Reckling52 indicated that 144 resulted in limb lengthening on the operated side, with an average lengthening of 16 mm. Of those who experienced limb lengthening, almost one-third required heel lifts to address postoperative symptoms. Secondly, shoe raises may have a role in the rehabilitation of hemiparesis, in an attempt to facilitate weight shifting towards the affected limb. Two recent studies have shown that the addition of a full-length sole raise (up to 1 cm in thickness) to the unaffected limb resulted in improved weightbearing symmetry53 and postural control54 in stroke patients. Thirdly, heel lifts are commonly used in the management of retrocalcaneal problems in people with limited ankle dorsiflexion. Lee et al55 have shown that there is a progressive decrease in gastrocnemius muscle activity as the heel is raised, which may have the effect of reducing strain in the Achilles tendon when walking. The amount of raise required to obtain optimum function is highly variable and requires some degree of trial and error. Where large raises are indicated, it is advisable to start with a smaller raise than required and to gradually increase it over a period of several weeks or months. This is particularly important for older people with balance problems. As a general rule, the heel can be raised to a maximum of 12 mm before a sole raise is also required, as otherwise the ankle is placed in a plantarflexed position and forefoot loading increases (Fig. 12.5). Furthermore, if a large, fulllength sole raise is required, it is advisable to incorporate a rocker sole to overcome problems associated with the increased stiffness of the sole, and to hollow out a section of the sole to reduce the total weight of the shoe.56
SHOE STRETCHING AND BALLOON PATCHING Modifying the upper of the shoe to accommodate foot deformities and lesions is quite an old technique but one that can be of great benefit in older people who are unable or unwilling to change their footwear. Several shoe stretching devices are commercially available. Traditional shoe stretchers are designed to increase the overall volume of the shoe and consist of a last that can be expanded (by width or length) by the adjustment of springs or screws (Fig. 12.6). Balland-ring stretchers are simple tools in which the ball portion is placed inside the shoe in the location of the lesion or prominence, and the ring on the outside of
Figure 12.5 Shoe modification for limb length discrepancy incorporating a heel lift, sole lift and forefoot rocker. (Courtesy of Karl Landorf, La Trobe University.)
the shoe.56 For both devices, it is essential that the upper be prepared with stretching fluid (available from footwear retailers) and that the shoe be stretched gradually. It is also important to recognise that, while leather responds very well to stretching, other upper materials do not and may simply split when stretch is applied. Balloon patching refers to modifying the upper of the shoe by cutting out a portion of the upper corresponding to a bony prominence or lesion and replacing it with a pocket of softer material. Although balloon patching can be quite effective in reducing pressure from dorsal lesions, considerable care needs to be taken to ensure that the stitching required to hold the patch in place does not create additional areas of pressure. Furthermore, to achieve an aesthetically acceptable result, it is essential to accurately match the colour and texture of the upper material being replaced.
SPECIALIST FOOTWEAR Specialist footwear, also referred to as medical grade footwear, can be broadly categorised under two main headings: stock or bespoke. Stock footwear is a massproduced, off-the-shelf product targeted at the orthopaedic market and generally consists of shoes with extra depth and extra width fittings in a range of styles and colours. Stock footwear is generally more expensive than regular footwear. This type of shoe is ideal
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A
Figure 12.6 Shoe stretching device.
for older people with mild to moderate foot deformities (such as lesser toe deformities and mild hallux valgus) and can be enhanced by the addition of prefabricated or custom orthoses. Bespoke footwear is custom-made for the individual and involves constructing a last from the patient’s foot, using either foam box, plaster or optical scanning techniques. This type of shoe is generally used in older people with severe foot deformity, such as those with rheumatoid arthritis, plantar neuropathic ulceration, foot and ankle trauma or partial amputation (Fig. 12.7). Because of the additional labour involved in assessment and manufacture, bespoke footwear is considerably more expensive than regular or stock footwear.38 Protocols for the provision of specialist footwear vary considerably across health services and between countries, and tend to change quite regularly in response to amendments in health financing policies. Readers are therefore advised to consult the most upto-date guidelines in their region. Nevertheless, several studies have been undertaken that have implications for specialist footwear prescription irrespective of the how footwear is funded. A systematic review57 of nine trials of specialist footwear in preventing reulceration in people with diabetes concluded that there was some evidence of a protective benefit over regular footwear, particularly in people with severe foot deformity or partial amputation. However, compliance with diabetic footwear is known to be highly variable. In one study, only 22% of patients wore their specialist footwear on a regular basis.58 A similar pattern emerges in studies of specialist footwear in people with rheumatoid arthritis. Two trials have indicated that specialist stock footwear is
B
Figure 12.7 Bespoke footwear. A. Shoes and insoles for patient with congenital foot deformity. (Courtesy of Karl Landorf, La Trobe University.) B. Boot for patient following ankle fracture.
more effective in reducing foot pain than retail footwear;59,60 however, compliance is generally poor. In one recent study of 80 patients,60 10 refused the specialist footwear outright and only 36 completed the trial. These studies indicate that, while specialist footwear may be effective in those who use it, considerably more work needs to be done to make the footwear acceptable to patients. Issues relating to acceptability of footwear are discussed later in the chapter.
FOOTWEAR, BALANCE AND FALLS Falls in older people are a major public health problem. One in three people aged over 65 years of age fall within any given year,61–64 and this rate increases to 50% in people aged 85 years and above.65 Several studies have assessed footwear in older people who have fallen and have implicated a wide range of shoe features that may have been responsible, such as
Footwear, balance and falls
narrow heels, slippery soles, inadequate fixation, poorly fitting shoes and soft heel counters.66–70 Stronger evidence comes from case-control or cohort studies, in which the footwear of fallers is compared to non-fallers. Five such studies have recently been undertaken, with varying results. Kerse et al71 assessed footwear in 606 older people in residential care, and found that wearing slippers rather than shoes increased the risk of fractures during the 12-month follow-up period. Keegan et al72 examined risk factors for various fall-related fractures in people aged over 45 years and found that medium–high-heeled shoes and shoes with a narrow heel significantly increased the likelihood of all types of fracture, while slip-on shoes and sandals increased the risk of foot fractures as a result of a fall. A study of 4281 people aged over 66 years by Larsen et al73 found that those who had fallen in the last 24 hours were four times more likely to have been wearing socks or slippers without a sole. A nested case-control study of 654 people aged over 65 years by Koepsell et al74 found that going barefoot or wearing stockings was associated with a tenfold increased risk of falling, with athletic shoes being associated with the lowest risk. Further evaluation of footwear characteristics from this study found that increased heel height was associated with increased risk of falling, whereas greater sole contact area was associated with decreased risk.75 Finally, a prospective study by Menz et al76 found that, while there were no differences in footwear characteristics between older people who did and did not sustain a fall when outdoors, those who fell while indoors were more likely to be barefoot or wearing socks. On the basis of these findings, it is difficult to recommend one style of shoe over another to prevent falls. However, a number of features of shoe design have been implicated as having an impact on balance, including heel height, the cushioning properties of the midsole, the slip resistance of the outersole, the method of fixation, the height of the heel collar and midsole geometry.77 The following section outlines the available evidence pertaining to the effect of each of these features on balance and is based on a recent update of the literature published in the textbook Falls in Older People: Risk Factors and Strategies for Prevention.78
HEEL HEIGHT Several authors have suggested that the changes in function produced by high-heeled footwear may
be responsible for instability and falling in older people.2,79–83 High heels are thought to contribute to instability by affecting the position of the centre of mass and by altering the position of the foot when walking.84,85 Three recent reports have highlighted the detrimental impact of high heels on balance. Brecht et al86 reported that balance performance on a moving platform was significantly worse in a heeled cowboy boot than in a tennis shoe, and suggested that heel elevation may make the wearer more susceptible to falling backwards. Lord & Bashford87 have also found that balance ability in older women is detrimentally affected by high heels. In this study, older women’s balance was tested when subjects were barefoot, in their own shoes and in high-heeled shoes (heel height 6 cm). The worst balance performances occurred when women wore high-heeled shoes. Arnadottir & Mercer88 found that performance on several balance tests was impaired in elderly women when wearing dress shoes (mean heel height 5 cm) compared to barefoot or when wearing walking shoes (mean heel height 1 cm). In contrast to these findings, Lindemann et al89 found no differences in balance when 26 older women wore shoes with a range of heel heights. The highest heel used in this study was 4 cm, suggesting that there may be a critical height at which heel elevation becomes problematic for balance. Further research needs to be undertaken to ascertain the optimum heel elevation for women’s shoes, as many older women report that they feel safer in a slight heel, and heel elevation may have some beneficial effects in older people with Parkinson’s disease to facilitate forward propulsion.90 Habitual wearers of high-heeled shoes may have experienced some changes to the extensibility of posterior soft tissue structures (e.g. calf muscle tightening), which may contribute to greater comfort and possibly safety while wearing these shoes. However, it would appear that heel elevation greater than 6 cm is potentially detrimental to balance and should therefore be avoided.
MIDSOLE CUSHIONING The use of expanded polymer foam materials in the construction of footwear midsoles enhances the level of comfort the shoe can provide to the wearer and is therefore commonly recommended as a beneficial feature in footwear for older people.91,92 However, research undertaken by Robbins and colleagues suggests that the use of thick, soft materials in footwear midsoles leads to instability, as the midsole material
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induces a state of ‘sensory insulation’, reducing sensory input to the central nervous system regarding foot position.93 To test this hypothesis, Robbins and colleagues (among others) have conducted a number of studies that have evaluated balance ability when older people wear footwear that varies according to the thickness and softness of the midsole material. The Robbins et al studies have found that shoes with thick, soft midsoles have a detrimental effect on the ability of older people to maintain balance when walking on a beam,93 to detect the position of their ankle joint when standing on different surface inclinations94 and to detect the position of their foot when walking.95 The detrimental influence of thick soles was further supported by Sekizawa et al,96 who evaluated foot position sense when subjects stood on a sloped surface and found that subjects underestimated the position of their foot in dorsiflexion when wearing shoes with thick soles (5 cm at heel, 3 cm at forefoot). The suggestion that soft shoes may have detrimental effects on balance has been supported by investigations by Finlay,2 who reported an association between wearing soft slippers and falls, and Frey & Kubasak,67 who found that a large number of older people who fell were wearing cushioned running shoes at the time. It would therefore appear that the proposed interaction between sensory feedback and stability is plausible and that soft soles may contribute to falls. It may therefore be prudent to advise against the wearing of shoes with very soft soles unless there is a specific therapeutic need for extra cushioning.
SLIP RESISTANCE OF FOOTWEAR OUTERSOLES Accidental falls caused by slipping are a common concern in older people, particularly in countries where snow- and ice-covered pavements are implicated in a large number of injuries to older people during winter months.97,98 Unfortunately, while a number of investigations have attributed falls in older people to slipping or tripping on unstable surfaces such as cracked paths, bathroom tiles or snow, few studies in the gerontology or rehabilitation literature have focused on the role of the outersole of the shoe in these accidents. Nevertheless, a number of authors have suggested that older people should be advised to avoid shoes with slippery soles – the assumption being that a tex-
tured, slip-resistant sole may prevent slip-related accidents.2,79–83 Such a recommendation may not be appropriate in all situations, however, as a number of cases have been reported in which falls are attributed to excessive slip-resistance of the shoe when walking on a pavement or performing a household task.69,99 Despite these observations, it would appear that falls related to excessive slip-resistance are far less common than those resulting from inadequate slip-resistance. Gait analysis studies have revealed that slipping is most likely to occur when the heel first strikes the ground;97,100,101 therefore, the geometry and texture of the heel section of a shoe may play an important role in preventing slipping accidents. Menz & Lord102 have recently shown that casual shoes vary considerably in their slip-resistance properties. Using a specially-designed force plate apparatus, two types of shoe were tested: lace-up Oxford-style shoes and women’s fashion shoes. The Oxford shoes were modified to produce four different heel configurations; the unmodified Oxford shoe had a flat heel with no flaring or sole texture, the second shoe was modified by flaring the heel laterally by 30°, the third shoe was modified by grinding a 10° bevel into the rear section of the heel and the fourth shoe had a ‘non-slip’ textured material stuck to the sole. The women’s fashion shoes were modified to produce a narrow heel and a broad heel, and each of these shoes was tested with and without a ‘non-slip’ textured material applied to the sole. All shoes were tested on dry and wet bathroom tiles, concrete, vinyl flooring material and terra cotta. Testing revealed that the Oxford shoes offered greater slip resistance than the women’s fashion shoes. The addition of a textured sole material had no effect on slip resistance on wet surfaces and broadening the heel of women’s shoes offered little additional benefit. The most slip-resistant shoe was the Oxford shoe with the 10° heel bevel, which is consistent with previous reports in the occupational safety literature. A bevel is thought to improve slip resistance by increasing the surface area of the plantar aspect of the sole at heel contact.103 Although heel modification has been found to be of benefit under experimental conditions, it remains to be seen whether such footwear modifications can help prevent slipping in older people. However, a recent study indicates that a specially-designed footwear addition may prevent slipping in older people walking on icy surfaces. The device (the YakTrax® Walker) is an injection-moulded thermoplastic elasto-
Footwear, balance and falls
The use of high heel collars as a means of improving stability in older people warrants further investigation, as both peripheral sensory loss106 and ankle muscle weakness107 have been found to contribute to falling. Given that ankle support has been found to improve mechanical stability and ankle position sense in younger people,108,109 shoes with high collars may be able to compensate for age-associated declines in sensory and motor function of the foot and ankle. However, such shoes must not be too restrictive, as a certain amount of foot flexibility is required to adapt to uneven terrain when walking.110,111
MIDSOLE FLARING
Figure 12.8 The Yaktrax® Walker device for preventing slips in icy conditions. (Courtesy of Genesis Marketing Partners.)
mer wrapped in a mesh of metal coils that is strapped on to the sole of the shoe (Fig. 12.8). In a randomised controlled trial of 109 older people, McKiernan104 reported that those who wore the device during the winter months had significantly fewer slips and fewer injurious falls than those who wore their regular footwear.
HEEL COLLAR HEIGHT Stability around the heel is widely regarded as a desirable feature when recommending footwear for unstable older people.2,80,81,91,92 Lord et al105 assessed the balance ability of older women when barefoot and in shoes with standard collar height (Oxford-style shoe) and a raised collar height (eight-laced ‘Doc Marten’ boot). The results revealed that subjects performed better in the high-collared shoe, presumably because the high heel collar provides greater ankle stability and increased proprioceptive feedback compared to standard footwear.
The term midsole flare refers to the difference between the width of the midsole at the level of the upper and its width at the level of the outersole. A number of authors have suggested that a large midsole flare is of benefit in older people as it provides a broader base of support, thereby enhancing the stability of the shoe.2,79–81,91 No studies have directly evaluated the effect of midsole flaring on balance ability, although associations between narrow heels and falls,75 and narrow heels and fall-related fractures72 have been recently reported. The association with fractures suggests that, if a fall does occur, the loss of balance when wearing narrow heels may result in greater sideways impact. Theoretically, midsole flaring should improve mechanical stability by increasing the surface contact area of the shoe–ground interface.112,113 However, studies have also found that large midsole flares may make the foot pronate more during gait114,115 and there is also the possibility that a large midsole flare may make the wearer susceptible to tripping by contacting the contralateral limb during the swing phase of gait. Whether these proposed detrimental effects of midsole flaring have significant ramifications for stability in older people is uncertain. Therefore, no absolute recommendations can yet be developed regarding the benefits or otherwise of midsole flaring in footwear for older people. However, given that recent work suggests that impaired lateral stability is associated with falls116 and that people who wear shoes with narrow heels are more likely to fall75 and suffer fractures,72 any attempt to improve the control of lateral movements of the centre of mass may be beneficial.
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METHOD OF FIXATION The method used to attach the shoe to the foot may also play a role in falls risk. It is a common clinical observation that many elderly people wear shoes with inadequate fixation, such as slippers, moccasins and soft, canvas slip-on shoes.2,3 These types of shoe promote a shuffling gait pattern and may become separated from the foot when walking, thereby acting as an external tripping hazard. In a recent study of 95 older people who had been admitted to hospital following a fall-related hip fracture, Sherrington & Menz70 found that those who suffered a trip were three times more likely to be wearing shoes without laces, zips or Velcro® fastening.70 Two of the subjects who suffered a trip and were wearing these types of shoe specifically blamed their footwear for the fall: one reported that her slipper ‘got stuck’, causing her to lose balance, while another stated that her moccasin ‘slipped off’ her foot, causing her to trip over it. The association recently reported between the wearing of slip-on shoes and fall-related foot fracture adds further weight to this suggested mechanism.72 Although it is difficult to confirm that the shoes were responsible for the fall, it would seem prudent to recommend that older people wear shoes that are firmly fitted to their feet.
ADVISING OLDER PEOPLE ABOUT FOOTWEAR The concept of the ‘ideal’ shoe is somewhat nebulous, as what is ideal for one individual may be totally inappropriate for another. Furthermore, the functional requirements of footwear vary considerably according to environmental and physical demands, e.g. indoor versus outdoor shoes, walking shoes versus running shoes, etc. Nevertheless, there are some general principles that apply to most individuals and situations and form the basis of footwear recommendations for older people.117 The most fundamental requirement is that the shoe should fit properly, in order to reduce the risk of tissue damage and the development of keratotic lesions. The shoe should also be stable, particularly in older people with underlying balance problems. Based on the literature pertaining to the effect of shoe features on balance, it can be concluded that older people should wear shoes with thin, flat, broad, bevelled heels constructed from a firm ma-
terial, textured soles to improve traction, laces to provide adequate fixation and possibly the addition of ankle support by the use of a high heel collar. However, one of the more frustrating aspects of managing foot problems in older people is that it is often difficult to convince patients to change their footwear. Compliance with use of therapeutic footwear has been shown to be low in people with diabetes58 and rheumatoid arthritis,60 and a recent survey of emergency department physicians indicated that compliance with footwear recommendations to prevent falls was poor, because of ‘stubbornness and vanity’.118 Similarly, the American podiatrist Bill Rossi considers advising patients to change their footwear to be ‘an exercise in eternal futility’.119 Nevertheless, many aspects of behavioural change required to improve health are difficult to achieve (e.g. weight loss, exercise, smoking cessation) and it would be negligent to ignore these issues simply because they are difficult. When providing footwear advice to older patients, it is worth considering the underlying concepts of the Health Belief Model.120 This model suggests that a patient’s decision to carry out a particular healthprotective behaviour (such as changing footwear) is influenced by how vulnerable they perceive themselves to be to the particular health problem, how serious they perceive the particular health condition to be, the benefits that they perceive the health protective behaviour will produce and what barriers there are to carrying out the behaviour. For example, a falls prevention study of 652 older people indicated that many were unaware of the risks of inappropriate shoes that and the main barriers to wearing more ‘sturdy’ shoes were difficulty putting them on, expense and concern about their appearance.121 Considering how such factors differentially affect individual patients may assist in the development of more effective strategies to enhance compliance with footwear recommendations. The provision of clear written material is an essential part of this process. The Footwear Suitability Scale,122 originally designed for use in people with diabetes, is a useful clinical tool that can also be administered to non-diabetic patients. The scale consists of eight questions for patients to complete regarding the suitability of their footwear (Table 12.1). With regard to footwear and falls, Lord et al78 have developed a simple poster of what constitutes a safe and unsafe shoe, based on evidence from the literature (Fig. 12.9). Both tools are simple and quick
Summary
Table 12.1 Footwear Suitability Scale Question
Reason
Tick box
1
Is the heel of your shoe less than 2.5 cm (1 in)?
As the height of your heel increases, the pressure under the ball of your foot becomes greater. Increased pressure can lead to callus and ulceration
䊐
2
Does the shoe have laces, buckles or elastic to hold it onto your foot?
If you wear slip-on shoes with no restraining mechanism, your toes must curl up to hold the shoes on. This can cause the tops of your toes to rub on your shoes, leading to corns and calluses. Secondly, the muscles in your feet do not function as they should to help you walk. Instead, they are being used less efficiently to hold your shoes on
䊐
3
Do you have 1 cm (approximately thumb nail length) of space between your longest toe and the end of your shoe when standing?
This is the best guide for the length of the shoe, as different manufacturers create shoes that are different sizes. Your toes should not touch the end of the shoe as this is likely to cause injury to the toes and place pressure on the toenails
䊐
4
Do your shoes have a well padded sole?
Shoes should have a supportive, but cushioned sole to absorb any shock and reduce pressure under the feet
䊐
5
Are your shoes made from material that breathes?
A warm, moist environment can harbour organisms, such as those that cause fungal infections
䊐
6
Do your shoes protect your feet from injury?
The main function of footwear is protection from the environment. Ensure your shoes are able to prevent entry of foreign objects that can injure the foot. If you have diabetes, a closed toe is essential to prevent injury to the foot
䊐
7
Are your shoes the same shape as your feet?
Many shoes have pointed toes and cause friction over the tops of the toes, which can lead to corns, callus and ulceration. If you can see the outline of your toes imprinted on your shoes, then the shoe is probably the wrong shape for your foot
䊐
9
Is the heel counter of your shoe firm?
Hold the sides of the heel of your shoe between the thumb and forefinger and try to push them together. If the heel compresses, it is too soft to give your foot support. The heel counter provides much of the support to the shoe and must be firm to press
䊐
If you have not put a tick in every box, your footwear is probably not protecting and supporting your foot as it should
to use and are useful in initiating a rational discussion regarding footwear issues with older patients.
SUMMARY Footwear is a major consideration in the care of older people, as ill-fitting or inappropriate footwear may
contribute to the development of foot problems and increase the risk of falls. Footwear modification is a useful conservative management strategy for a wide range of foot problems and can enhance the effects of other treatments. Finally, the role of footwear advice should not be overlooked, as changing footwear may, in and of itself, lead to the resolution of many foot complaints.
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What makes a shoe safe? A firm heel collar to provide stability
Laces ensure the shoe ‘holds’ onto your foot when walking
A bevelled heel to prevent slipping
A thin, firm midsole so you can ‘feel’ the ground underneath
A broad, flared heel to maximise contact with the ground
A textured sole to prevent slipping
What makes a shoe unsafe? Soft or stretched uppers make your foot slide around in the shoe
Lack of laces means your foot can slide out of your shoe
High heels should be avoided as they impair stability when walking Slippery or worn soles are a balance hazard, particularly in wet weather
Narrow heels make your foot unstable and can cause ankle sprains
Figure 12.9 What makes a shoe safe/unsafe handout.
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Index Note: Page numbers in italics refer to figures. ABCD mnemonic, 92 Abductor hallucis, 152 Achilles Foot Screening Project, 3, 79, 84 Achilles reflex, 40, 41 Achilles tendinopathy, 202–4 aetiology, 202–3 assessment and diagnosis, 203–4 definition, 202–3 treatment conservative, 204 surgical, 204 Achilles tendon, age-related physiological changes, 20 Achillodynia see Haglund’s deformity Acral lentiginous malignant melanoma, 94 Acrochordons, 86, 88 Acrocyanosis, 124–5 Acroexfoliative dermatitis, 81 Acrokeratosis paraneoplastica, 68 Acropachy see Nail clubbing Actin filaments, 20 Actinic keratosis, 68, 92, 92 Activities of daily living, 49 Adductor hallucis, 152 Adductovarus toe, 166 Advanced activities of daily living (AADLs), 49 Age, risk factors, 6 Aged care facilities, research studies, 2 Age-related physiological changes, 13–22 integumentary system, 13–16 muscular system, 20–2 peripheral sensory system, 17–18 peripheral vascular system, 16–17 skeletal system, 18–20 Akin procedure, 155, 155 Alcohol, keratotic lesions, 71 Alginate dressings, 133 Allografts, 137 Allopurinol, 170 Allylamines onychomycosis, 101 tinea pedis, 85
Alternating pressure devices (APDs), 134 Amorolfine, 101, 102 Amputation, toe lesser toe deformities, 168 onychocryptosis, 106 Ankle age-related physiological changes in muscles, 21 manual muscle testing, 45, 46 range of motion, 43, 44 reflex, 40 Ankle problems effect of age on, 20 falls, 8 prevalence, 2, 4 Ankle–brachial index (ABI) compression therapy, 135 peripheral arterial assessment, 37–8 Ankle–foot orthoses (AFO), 218, 226–7, 227 and balance, 228 osteoarthritis, 207 tibialis posterior dysfunction, 199 Anti-inflammatory medications, 204 Arch index, 42, 42, 43 Arsenical keratosis, 68, 93, 93 Arterial disorders, 121–6 acute arterial occlusion, 123 cold-associated conditions, 123–6 peripheral arterial disease, 121–3, 122, 123 vasospastic disorders, 123–6 Arterial ulcers, 129–30 dressings, 133 guidelines for the management of, 139 Arteries age-related physiological changes, 16–17 assessment of, 36–8 stiffness measurement, 17 Arthritic conditions, effect on gait, 50
Arthrodesis ankle, 205, 207 hallux valgus, 157 osteoarthritis, 207 proximal interphalangeal joint, 186 tibialis posterior dysfunction, 199 Arthroplasty, implant, 163–4, 164 Articulated hindfoot orthoses (HFOA), 227 Assessment, 29–56 diagnostic imaging, 30, 47–8 footwear, 30, 53, 53–5, 54, 55 functional, 30, 48–53 initial interview, 29–34, 30 outcomes of treatment, 55–6 systems examination, 30, 34–47 Asteatotic dermatitis, 80, 80 Auspitz’s sign, 82 Autografts, 137 Axons, age-related physiological changes, 17 Azoles onychomycosis, 101, 102 tinea pedis, 85 Balance foot orthoses as an aid to, 228–9 and footwear, 241–4 Balloon patching, 239–40 Basal cell carcinoma, 92, 93, 94 differentiation from subungual exostoses, 109 Basal osteotomies, 156–7, 157 Basic activities of daily living (BADLs), 49 Bazex’s syndrome, 68 Bead dressings, 133 Beau’s lines, 15 medication use-associated, 114, 114 systemic diseases-associated, 111, 113, 113 Bespoke footwear, 240, 240 Bioengineered human skin equivalents, 137 Biopsy, wound, 138
252
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Black heel, 91, 92 Blood supply, age impaired, 15 Blue naevus, 91 Body mass index (BMI), 193 Bone, age-related physiological changes, 18, 19 Bone scanning in general, 48 plantar heel pain syndrome, 193 Bonney-Kessel osteotomy, 163, 164 Bowen’s disease, 93, 93 Bruising, 15 Bruits, 37, 38 Buerger’s test, 37 Bulla, 35 Bullous tinea pedis, 84 Bunion shield, 224 Bunionette, 168, 168–9 prevalence, 4 Bunions see Hallux valgus Bursal inflammation, 149, 150 Bursectomy, 201 Bursitis plantar calcaneal, 194 retrocalcaneal see Haglund’s deformity Buttress appliance, 219, 219, 223 Cadence, 50 Calcaneal body index, 200, 200 Calcaneal inclination angle (CIA), 200, 200 Calcaneal osteotomy Haglund’s deformity, 201, 202 tibialis posterior dysfunction, 199 Calcaneal petechiae, 91, 92 Calcaneal spurs, 47, 192 plantar heel pain syndrome, 192, 193 Calcaneus insufficiency fracture, 48 osteoarthritis, 205, 205 stress fracture, 194 Calf stretching, 196 Calf-squeeze test, 203 Calluses, 62 classification and clinical presentation, 61–2 common patterns, 63 debridement, 69–70 footwear assessment, 236 gender differences, 6 heel, 70, 70 orthotic therapy, 71, 71–2 plantar pressure measurement, 65 prevalence, 2, 3, 4, 5 topical treatment, 70, 70 Candidal onychomycosis, 100
Capillaries age-related physiological changes, 17 thrombosed, 86, 87 Carbon paper, 51 Cartilage, age-related physiological changes, 19 Cast orthoses, 218, 225–6, 226 Cautious gait, 49, 50 Cellulitis, 83, 84 Cerebellar ataxia, 49, 50 Chairside orthoses crescent pad, 218–19, 219 foam sleeves, 220 horseshoe pad, 218, 219 interdigital wedge, 219, 219–20 metatarsal shaft pad, 221, 221–2 plantar calcaneal pad, 221, 222 plantar cover, 220, 221 plantar metatarsal pad, 220–1, 221 retrocalcaneal pad, 222 saddle pad, 219, 220 silicone orthodigita, 222 toe prop, 219, 219 toe sleeve, 219 valgus pad, 221, 222 Cheilectomy, 163, 164 Cherry haemangioma, 90 Cheshire Foot Pain and Disability Survey, 5 Chevron procedure, 156, 156, 163 Chilblains, 125, 125–6 Cholesterol, seed corns, 65 Chondrocytes, 19 Chondroitin sulphate, 19 Chondroma, 195 Chronic plaque psoriasis, 81–2, 82 Chronic venous insufficiency see Venous insufficiency, chronic Chronic winter itch, 80, 80 Ciclopirox, 101, 102 Circulatory problems prevalence, 2 Clavus see Corns Claw toes, 165, 166 prevalence, 4 surgical treatment, 168 toe prop, 219 Clifton Assessment Procedure for the Elderly study, 5 Clock Drawing Test (CDT), 31, 31 Closing wedge osteotomy, 156, 157 Clostridium spp., 83 Clubbed nails see Nail clubbing Cock-up hallux, 4 Cognitive status assessment, 31, 31 Cold exposure, conditions related to, 123–6
Collagen, age-related physiological changes, 14 Collagen cross-linking, age-related physiological changes, 19 Collagen fibrils, age-related physiological changes, 19 Collateral ligament rupture, 185 Colonisation, 137 Combined rockers, 238 Community-based studies, 3–5 in other countries, 5 in the UK, 4–5 in the USA, 3–4 Co-morbidities, risk factors, 6–7 Compound melanotic naevocellular naevus, 91 Compression bandaging chronic venous insufficiency, 127 foot ulcers, 134–5 lymphoedema, 128–9 Compression stockings, 135 Computed tomography (CT), 48 Consequences of foot problems, 7–9 Constant low-pressure devices (CLPDs), 134 Contamination, 137 Contoured insoles, 224–5, 225 Corn plasters, 70 Corns classification and clinical presentation, 61–2 debridement, 69, 69–70 distribution patterns, 63 footwear assessment, 53, 236 gender differences, 6 interdigital wedge, 219 prevalence, 2, 3, 4, 5 topical treatment, 70 Cortical bone, age-related physiological changes, 18 Corticosteroid injection Achilles tendinopathy, 204 Haglund’s deformity, 201 hallux limitus/rigidus, 162 intermetatarsal neuroma, 183 plantar heel pain syndrome, 196 tibialis posterior dysfunction, 199 see also specific corticosteroid Corticosteroid use, Achilles tendinopathy, 203 Cortisone injections Achilles tendinopathy, 204 Haglund’s deformity, 201 intermetatarsal neuroma, 183 plantar heel pain syndrome, 196 Corynebacterium spp., 83 Coughlin & Shurnas classification, 158, 159
Index
Cramps, nocturnal, 37 Crescent pad, 218–19, 219 Crescentic osteotomy, 156, 157 Crest pad, 219, 219, 223 Critical limb ischaemia, 37, 122 Cross-over toe see Over-riding toe Cryotherapy, verrucae, 86 Cucumber heels see Haglund’s deformity Cutaneous horns, 86, 88 Cutaneous tags, 86, 88 Cyanoacrylate adhesives, 70 Cystic basal cell carcinoma, 93 Cysts, 85–94 definition, 35 see also specific cyst Darier’s disease, 68 Debridement see Lesion debridement Decubitus ulcers see Pressure ulcers Deep-vein thrombosis (DVT), 39 Dehydration, foot veins in, 38–9 Dermal melanotic naevocellular naevus, 91 Dermatitis, 80, 80–1 Dermatofibromas, 86, 88 Dermatological assessment, 34, 34–6, 35 Dermatophilus congolensis, 83 Dermatophytes, 84, 103 Dermis, age-related physiological changes, 14–15 Diabetes ankle–brachial index, 38 foot ulcers see Diabetic ulcers ill-fitting footwear effects, 237 keratotic lesions, 66 Diabetic ulcers, 129, 130–1, 131 guidelines for the management of, 141 pressure relief, 133–4 Diagnostic imaging, 30, 47–8 Achilles tendinopathy, 203–4 tibialis posterior dysfunction, 199 see also specific technique Dietary supplements, 136 Diffuse idiopathic skeletal hyperostosis, 195 Digital clubbing see Nail clubbing Distal subungual onychomycosis, 100 Dorsal bunion see Hallux limitus/rigidus Dorsal venous arch vein, 39 Dorsiflexion night splints, 196 Dorsoplantar prop, 219 Draw test, 185, 185 Dressings, wound, 132–3 Drug-induced eczema, 81
Drugs see Medication use; specific drug Dry skin see Skin, dry Dumbbell pad, 219, 219–20, 223, 224 Dunedin Program, 3–4 Dynamometers, 44–6 Dysacromelia see Nail clubbing Eccrine glands, age-related physiological changes, 15 Eczema, 80, 80–1 Eczema craquelé, 80, 80 Edinburgh Claudication Questionnaire, 37 Education, risk factors, 7 Egyptian foot, 104 Elastin, age-related physiological changes, 14, 16–17 Electrodesiccation, 72–3 Electrophysical studies, 208 Electrosurgery, 72–3 Endothelial cells, age-related physiological changes, 16 Epidemiology of foot problems, 1–9 Epidermal inclusion cysts, 86, 88, 88 Epidermis, age-related physiological changes, 14–15 Epidermophyton spp. onychomycosis, 103 tinea pedis, 84 Erysipelas, 83 Erythema multiforme, 81 Erythema nodosum, 81 Erythema pernio, 125, 125–6 Ethnicity, risk factors, 7 European Wound Management Association algorithm, 138 Exfoliative erythroderma, 81 Exostectomy, 201 Exostoses, subungual, 109, 109 Extended shaft pad, 222 Extensor digitorum brevis testing, 45 Extensor digitorum longus testing, 45 Extensor hallucis brevis testing, 45 Extensor hallucis longus testing, 45 Extracorporeal shockwave therapy, 197 Falls consequences of foot problems, 8 and footwear, 55, 240–4 risk assessment, 51, 53 Fat pad atrophy, 194 Fatigue fractures, 186 Feet First study, 179 Femoral artery bruit, 37, 38 Fibromas, 86 Fibrous corns, 62 First ray hypermobility, 152
First step pain, 192 Fissures, 15 Flat feet, 197 footwear assessment, 54 hallux valgus, 152 prevalence, 3, 4 tibialis posterior dysfunction, 199 Flexor digitorum brevis testing, 45 Flexor digitorum longus testing, 45 Flexor hallucis brevis testing, 45 Flexor hallucis longus, 151 testing, 45 Fluconazole, 102 Fluoroquinolone antibiotics, 203 Foam dressings, 133 Foam sleeves, 220 Fontaine classification, 36 Foot ability to perform care, 52–3 deformity, 41, 41–2, 66 (see also specific deformity) eversion, prevalence, 2 muscles, age-related physiological changes, 21–2 physiological changes in the ageing see Age-related physiological changes pronation, hallux valgus, 152 Foot posture assessment, 42, 42 effect of age on, 20 Haglund’s deformity, 201 tibialis posterior dysfunction, 198 Foot Posture Index (FPI), 42 Foot problems consequences of, 7–9 deformity, 41, 41–2, 66 (see also specific deformity) epidemiology of, 1–9 prevalence of, 1–5 risk factors for, 5–7 Footwear, 235–46 advising about, 244–5, 246 assessment, 30, 53, 53–5, 54, 55 balance and falls, 55, 240–4 detrimental effects of, 236–7 elevated heels, 237 fixation method, 244 foot ulcers, 133–4, 134 habits of older people, 235–6 hallux limitus/rigidus, 162 hallux valgus, 151 heel collar height, 243 heel height, 241–2 ill-fitting, 53, 235–6, 236 keratotic lesions, 66–7 inappropriate, 235–6, 236 gender differences, 6
253
254
Index
intermetatarsal neuroma, 183 lesser toe deformities, 167 midsole cushioning, 241–2 midsole flaring, 243 modifications, 237–9 for keratotic lesions, 72 slip resistance of outersoles, 242–3 specialist, 239–40, 240 stretching, 239, 240 Footwear Suitability Scale, 245 Forefoot disorders, 179–87 classification, 179–80 common causes of pain, 181–6 definition, 179–80 diagnosis, 180–1 malalignments, 42 prevalence, 179–80 see also specific disorder Forefoot imbalance pads, 221 Forefoot rockers, 238, 238 Fowler–Philip’s angle, 200, 200 Fracture, stress, 48, 181, 186 Freiberg’s infraction, 181–2 Frontal-related gait disorders, 50 Fulguration, keratotic lesions, 72 Functional assessment, 30, 49–53 Functional hallux limitus, 158 Functional orthoses, 218, 225–6, 226 Functional reach test, 53 Fungal infections, 83–5 prevalence, 4 studies, 3 see also Tinea pedis Gait analysis ankle–foot orthoses, 227 Haglund’s deformity, 201 Gait disorders classifying, 49–50 clinical analysis, 50–1 evaluation of, 49–51 Ganglion cysts, 86, 88–9, 89 Gangrene, 122, 123 Gastrocnemius testing, 45 Gender effect on prevalence, 4 risk factors, 6 Girdlestone–Taylor procedure, 168 Goniometer, flexible, 43, 44 Gordochom solution, 101 Gouty arthritis, 169–70, 170 Gravitational eczema, 80, 80–1 Griseofulvin onychomycosis, 102 tinea pedis, 85 Guttate psoriasis, 82
Haemangiomas, 86, 89, 90 Haglund’s deformity, 200, 200–2 aetiology, 200 assessment and diagnosis, 201 clinical presentation, 200–1, 201 definition, 200 retrocalcaneal pad, 222 treatment conservative, 201 surgical, 201–2, 202 Hallux abductus angle, 150, 153, 153 Hallux equinus, 157 Hallux extension, 45, 46 Hallux flexion, 45, 46 Hallux flexus see Hallux limitus/rigidus Hallux interphalangeus abductus angle, 153, 153, 160 Hallux limitus/rigidus, 41, 52, 157–65 aetiology, 158–61, 160 assessment and diagnosis, 161, 161–2 classification, 158, 159 clinical presentation, 158, 158 footwear assessment, 54 functional, 158 keratotic lesions, 66 subungual exostosis, 109 treatment, 162–5 conservative, 162–3 surgical, 163–5, 164 Hallux valgus, 149–57, 150, 153 aetiology, 150–2 first ray hypermobility, 152 foot pronation, 152 footwear, 151 long first metatarsal, 151 metatarsal head shape, 151–2 metatarsus primus varus, 151 muscle dysfunction, 152 assessment, 41, 41, 153, 153 classification, 150 clinical presentation, 150 congenital, 150–1 diagnosis, 153, 153 falls, 8 foam sleeves, 220 foot pressure recordings, 52 footwear assessment, 53, 54, 236 gender differences, 6 iatrogenic, 152 keratotic lesions, 66 prevalence, 2, 3–4, 4, 5 splints, 224, 224 treatment, 153–7 conservative, 153–4 surgical, 154–7, 155–7 Hallux varus, 169, 169 Halo naevomelanocytic naevus, 91
Hammer toes, 165 plantar metatarsal pad, 220 prevalence, 3, 4 surgical treatment, 168 Hard corns, 62, 63, 64, 69 Harris & Beath mat, 51 Hattrap & Johnson classification, 158, 159 Health Belief Model, 244–5 Health sandals, 228 keratosis, 67 Health-related quality of life, 8–9 Heel calluses, 70, 70 Heel collar height, 243 Heel cups, rigid, 197 Heel height, 241–2 Heel pad, 221, 222, 224 age-related physiological changes, 16 shock-absorbing, 197 Heel pain see Plantar heel pain syndrome; Retrocalcaneal conditions Heel raises, 238–9, 239 Heloma durum, 62, 63, 64, 69 Heloma fascia, 62 Heloma milliare, 62, 63, 65, 65 Heloma molle, 62, 63, 64 Heloma neurovasculare, 62 Heloma vasculare, 62 Helomata see Corns Hemiplegia, 50 Herbal medications, 31 High arches, 4 High-heeled footwear, 241 High-Dye taping, 199 Hindfoot orthoses (HFO), 227 Hippocratic nails see Nail clubbing Horseshoe pad, 218, 219 Howel-Evans syndrome, 68 Hydration status, 38–9 Hydrocolloid dressings, 133 keratotic lesions, 70 Hydrogels, 132, 133 Hydrogen atoms, 48 Hyperbaric oxygen therapy, 135–6 Hyperkeratosis, 15 physiological, 63 prevalence, 2 Hypertension, venous, 126–7 Hypertrophic osteoarthropathy, 195 Hyphae, 100 Iatrogenic hallux valgus, 152 Ichthyosis, 68 Immersion foot, 126 Implant arthroplasty, 163–4, 164 Inclusion cysts, 86, 88, 88
Index
Income, risk factors, 7 Infection risk factors, 15 skin, 83–5 wound, 137, 137–9 see also specific infection Inflammatory response, age impaired, 14 Ingrown toenails see Onychocryptosis Initial assessment interview, 29–34, 30 Injection therapy Achilles tendinopathy, 204 Haglund’s deformity, 201 hallux limitus/rigidus, 162 intermetatarsal neuroma, 183 keratotic lesions, 70–1 plantar heel pain syndrome, 196 predislocation syndrome, 185–6 Injuries as a consequences of foot problems, 8 Inpatient settings research studies, 2 Insoles contoured, 224–5, 225 hallux valgus, 154 keratotic lesions, 71, 72 non-cast, 218, 222–3 Instrumental activities of daily living (IADLs), 49 Integumentary system, 13–16 dermis, 14–15 epidermis, 14–15 functional implications, 15 nails, 15 plantar soft tissues, 15–16 functional implications, 16 heel pad, 16 metatarsal pads, 15–16 summary of age-related changes, 14 Interdigital neuroma, 220 Interdigital tinea pedis, 84, 85 Interdigital wedge, 219, 219–20, 223, 224 Intermetatarsal angle, 150, 151, 153, 153 Intermetatarsal neuroma, 181, 182–4 aetiology, 182, 182 clinical presentation, 182 treatment conservative, 182, 182 surgical, 182–3 Intermittent claudication, 36–7, 122 Interphalangeal joint, proximal, 186 Interstitial spaces tenderness, prevalence, 4 Intraosseous lipoma, 195 Iron, 136
Itraconazole onychomycosis, 102 tinea pedis, 85 Joints age-related physiological changes, 18–19 fusion see Arthrodesis Junctional melanotic naevocellular naevus, 91 Keep Them Walking project, 3 Keller procedure hallux limitus/rigidus, 163, 164 hallux valgus, 155, 155 Keratan sulphate, 19 Keratin, age-related physiological changes, 15 Keratinocytes, 99 age-related physiological changes, 14, 15 onychomycosis, 100 Keratoacanthomas, 89, 90 Keratoderma climacterium, 68 Keratoderma punctata, 68 Keratolysis, pitted, 83, 84 Keratomas see Calluses Keratosis follicularis, 68 Keratotic lesions, 61–74 aetiology, 62–7 assessment and diagnosis, 67–9 classification, 61–7 clinical presentation, 61–7 forefoot pain, 181 less common causes of, 67, 68 pathogenesis, 62–5, 65 plantar, 41 plantar metatarsal pad, 220 risk factors, 65–7 treatment, 69–74 conservative, 69–72 footwear modification, 72 injection therapy, 70–1 lesion debridement, 69, 69–70 orthotic therapy, 71, 71–2 topical treatments, 70, 70 surgical, 72–4 electrosurgery, 72–3 orthopaedic surgery, 73, 73– 4, 74 see also Calluses; Corns Ketanserin ointment, 133 Ketoconazole, 102 Kinaesthesia, effect of age on, 18 Knee flexion test, 203 Koebner phenomenon, 82 Koilonychia, 111, 113, 113
Langerhans cells, age-related physiological changes, 14 Lapidus procedure, 155–6 Larval therapy, 132 Lateral plantar nerve entrapment, 195 Lazy-L incision, 201–2, 202 Lentigo maligna, 94 Lesion debridement foot ulcers, 132 keratotic lesions, 69, 69–70 Lesser toe deformities, 41, 165–8 aetiology, 167 assessment and diagnosis, 167 classification, 165–7, 166 clinical presentation, 165–7 footwear assessment, 236 keratotic lesions, 66 treatment, 167–8 conservative, 167 surgical, 167–8 see also specific deformity Lesser toe extension/flexion, 46 Leukonychia medication use-associated, 114, 114 systemic diseases-associated, 111, 113, 113 Lichen planus, 82, 82–3 Lichenoid dermatitis, 81 Ligaments, age-related physiological changes, 19–20 Limb colour, abnormal, 37, 38 Limb ischaemia, critical, 37, 122 Limb length discrepancy, 238–9, 239 Liquid silicone injections, 71 Livedo reticularis, 124–5, 125 Long arch pad, 221, 222 Low-Dye taping plantar heel pain syndrome, 196 tibialis posterior dysfunction, 199 Lumbricals testing, 45 Lunge test, weightbearing, 43, 44 Lunula nail discoloration, 114, 114 Lymphoedema, 128, 128–9 Macrophages, age-related physiological changes, 14 Macule, 35 Magnetic resonance imaging (MRI), 48 Achilles tendinopathy, 204 Haglund’s deformity, 201 intermetatarsal neuroma, 182 plantar heel pain syndrome, 194 tarsal tunnel syndrome, 208 tibialis posterior dysfunction, 199 Mal de Meleda, 68
255
256
Index
Malignant melanoma, 92, 94, 94 differentiation from subungual exostoses, 109 Mallet toes, 165 prevalence, 4 surgical treatment, 167–8 Manchester Foot Pain and Disability Index (MFPDI), 33–4 Manchester scale, 41, 41 Manipulation hallux limitus/rigidus, 162 hallux valgus, 154 Manual muscle testing, 44–7, 46 Marjolin’s ulcer, 94 Mast cells, age-related physiological changes, 14 Matrixectomy, 103 Mecca foot, 67 Medial calcaneal nerve entrapment, 194, 195 Medial malleolus tenderness, prevalence, 4 Medial plantar nerve entrapment, 195 Medical grade footwear, 239–40, 240 Medical history, 29–31 Medication use Achilles tendinopathy, 203 initial assessment interview, 31 nail disorders associated with, 111–12 onychocryptosis risk, 104 skin eruptions associated with, 81 Meissner corpuscles, age-related physiological changes, 17 Melanoma, malignant, 92, 94, 94, 109 Merkel discs, age-related physiological changes, 17 Metallic implants, 164 Metatarsal dome, 183, 220–1, 221, 224 Metatarsal formula, 41 Metatarsal head calluses, 62, 62, 63 Metatarsal pad, 183, 220–1, 221, 224 age-related physiological changes, 15–16 Metatarsal shaft pad, 221, 221–2 Metatarsalgia, 179–80 common causes, 181–6 diagnosis, 180–1 Metatarsals head shape, 151–2 insufficiency stress fracture, 48, 181, 186 length of, 41–2 long first, 151 radiographs, 47
Metatarsophalangeal joints fusion of see Hallux limitus/rigidus instability, 184 (see also Predislocation syndrome) manual muscle testing, 45 range of motion, 43, 43–4 restricted range of motion see Hallux limitus/rigidus subluxation, 184 (see also Predislocation syndrome) tenderness, prevalence, 4 Metatarsus primus elevatus, 160 Metatarsus primus varus, 151 Miconazole nitrate solution, 101 Micrococcus sedentarius, 83 Microsporum, 103 Midfoot disorders, 191–209 osteoarthritis, 205–7 see also specific disorder Midsole cushioning, 241–2 Midsole flaring, 243 Milroy’s disease, 128 Mini-Mental State Examination (MMSE), 31 Mitchell osteotomy, 156, 156 Mobilisation hallux limitus/rigidus, 162 hallux valgus, 154 Mobility consequences of foot problems, 7–8 objective measures of, 49 Moccasin foot, 84 Moles, 90, 91 Mönckeberg’s sclerosis, 38 Monoarticular non-traumatic synovitis, 184 see also Predislocation syndrome Morbilliform drug eruptions, 81 Morton’s extension, 222 Morton’s foot type, 222 Morton’s metatarsalgia see Intermetatarsal neuroma Morton’s neuroma see Intermetatarsal neuroma Mosaic verrucae, 86, 87 Moulds, 101 Mucous (myxoid) cysts, 89–90, 90 incidence, 86 Mulder’s click test, 180, 182, 182 Muscle mass reduction, 20–1 Muscle tissue, age-related physiological changes, 20–1 Muscle(s) ankle, 21, 45, 46 dysfunction, hallux valgus, 152 foot, 21–2 strength reduction, 21
strength testing, 44–7, 46 strengthening, 204 Muscular system, age-related physiological changes, 20–2 Musculoskeletal assessment, 41–7 Mycology, 34–5 Myelin sheaths, age-related physiological changes, 17 Myopathic conditions, effect on gait, 50 Myosin filaments, 20 Myxoid cysts see Mucous (myxoid) cysts Naevi, 90, 91 Nail avulsion onychocryptosis, 105, 106, 106–7, 107 onychogryphosis and onychauxis, 108–9 onychomycosis, 103 Nail bracing, 104–5, 105 Nail clubbing, 109–10, 110 systemic diseases-associated, 111, 113, 113 Nail disorders, 99–115 associated with systemic diseases and medications, 111–12, 113–14 elongated, 4 ingrown see Onychocryptosis prevalence, 2, 4, 5 thickened see Onychauxis; Onychogryphosis see also specific disorder Nails, age-related physiological changes, 15 National Health Interview Survey (NHIS), 4 Navicular height, 42 radiographs, 47 Nerve entrapment, heel pain, 194, 195 Neuritic symptoms, forefoot pain, 180 Neurological assessment, 39–41 Neuropathic conditions, effect on gait, 50 Neuropathic heel pain, 194 Neurovascular corns, 62 Night cramps, 37, 122 Nikolsky’s sign, 81 Nocturnal cramps, 37, 122 Nodular basal cell carcinoma, 93 Nodular malignant melanoma, 94 Nodule, 35 Non-cast insoles, 218, 222–3
Index
Non-steroidal anti-inflammatory drugs (NSAIDs) gout, 170 osteoarthritis, 206 plantar heel pain syndrome, 196 Non-weightbearing radiographs, 47 Obesity Achilles tendinopathy, 203 calluses, 66 plantar heel pain syndrome, 193 risk factors, 6 Oligosaccharides, 19 Omega nails, 111, 111, 112 Onychauxis, 15, 99, 107–9, 108 aetiology, 107–8 clinical presentation, 107–8 treatment, 108–9 Onychocryptosis, 99, 103–7, 103–7 aetiology, 103–4 assessment, 104 diagnosis, 104 interdigital wedge, 219–20 pincer nails, 111 prevalence, 4 risk factors, 103–4 treatment conservative, 104–5 surgical, 105–7 Onychogryphosis, 99, 107–9, 108 aetiology, 107–8 clinical presentation, 107–8 treatment, 108–9 Onycholysis medication use-associated, 112, 114, 114 systemic diseases-associated, 111, 113, 113 yellow nail syndrome, 110 Onychoma, 86, 88 Onychomycosis, 15, 99, 100, 100–3, 101 aetiology, 100–1 assessment and diagnosis, 101 classification, 100–1 clinical presentation, 100–1 interdigital tinea pedis, 84, 85 mycology, 34–5 prevalence, 3 recurrence prevention, 103 treatment oral, 102–3 surgical, 103 topical, 101–2 types of, 100 Onychophosis, 104 onychauxis, 107 pincer nails, 111
Oral treatments for onychomycosis, 102–3 Ordinary psoriasis, 81–2, 82 Orthonyxia, 104–5, 105 Orthopaedic surgery, keratotic lesions, 73, 73–4, 74 Orthotic therapy, 217–29 Achilles tendinopathy, 204 as a balance aid, 228–9 basic principles, 217 classification and nomenclature, 217–18 cost of, 217 foot ulcers, 133–4, 134 hallux limitus/rigidus, 162–3 hallux valgus, 154 intermetatarsal neuroma, 183 keratotic lesions, 71, 71–2 and knee osteoarthritis, 227–8 osteoarthritis, 206–7 plantar heel pain syndrome, 196–7 predislocation syndrome, 185–6 tibialis posterior dysfunction, 199 see also specific orthoses Osteoarthritis, foot, 205 ankle–foot orthoses, 227 clinical presentation, 206, 206 effect of age on, 20 prevalence, 205 risk factors, 205 treatment conservative, 206–7 surgical, 207 Osteoarthritis, knee, 227–8 Osteoblasts, age-related physiological changes, 18 Osteochondroma, 109 Osteoclasts, age-related physiological changes, 18 Osteoid lipoma, 195 Osteophytes hallux limitus/rigidus, 162 osteoarthritis, 206 pincer nails, 111 Osteoporosis, effect of age on, 20 Osteotomy basal, 156–7, 157 Bonney-Kessel, 163, 164 calcaneal see Calcaneal osteotomy closing wedge, 156, 157 crescentic, 156, 157 keratotic lesions, 73, 73–4, 74 lesser metatarsal, 186 Mitchell, 156, 156 scarf, 155, 155 Schwartz, 73–4, 74 Watermann, 163, 164
Weil, 73, 73 Wilson, 156, 156 Ostler’s toe see Onychogryphosis Outpatient settings research studies, 2–3 Over-riding toe, 165–6, 166 surgical treatment, 168 Pacinian corpuscles, age-related physiological changes, 17 Paget’s disease, 194 Pain assessment, 32, 32–4, 40 first step, 192 footwear assessment, 53 forefoot see Metatarsalgia gender differences, 6 heel see Plantar heel pain syndrome; Retrocalcaneal conditions Manchester Foot Pain and Disability Index, 33–4 peripheral arterial disease, 37 prevalence, 2, 3, 4 Palmoplantar keratoderma, 67, 67, 68 Palmoplantar keratosis, 68 Paper grip test, 44, 47 Papule, 35 Papulosquamous diseases, 81–3, 82 Parallel strip padding, 221 Paraplegia, 50 Paresis, 50 Parkinsonism, 49, 50 Paronychia, 104 medication use-associated, 114, 114 onychauxis, 107 pincer nails, 111 systemic diseases-associated, 112, 113, 113 Pedal pulses, abnormal, 37, 38 Pedigree chart, 30, 30 Pedorthics, 237–9 Pentoxifylline, 136 Peptostreptococcus, 83 Peripheral arterial disease (PAD), 36–8, 121–3, 122, 123 Peripheral motor impairments, 49, 50 Peripheral sensory system age-related physiological changes, 17–18 assessment, 39–41 impairments, 49, 50 Peripheral vascular disorders, 121–9 arterial disorders, 121–6 chronic venous insufficiency, 126–8 lymphoedema, 128–9 see also specific disorder
257
258
Index
Peripheral vascular system age-related physiological changes, 16–17 assessment, 36–9 Peripheral venous system assessment, 38–9 Pernio syndrome, 125, 125–6 Perniosis, 125, 125–6 Peroneal artery calcification, 38 Peroneus brevis testing, 45 Peroneus longus testing, 45 Perthes manoeuvre, 38 Pes cavus, 207 foot pressure recordings, 52, 207, 207 footwear assessment, 54 painful, 207, 207–8 Pes planus see Flat feet Phalanges, 47 Phenolisation, onychocryptosis, 105, 106–7, 107 Physiological hyperkeratosis, 63 Piezogenic pedal papules, 90, 91 Pigmented basal cell carcinoma, 93 Pigmented nail bands, medication useassociated, 114, 114 Pincer nails, 111, 111, 112 Piroxicam, 204 Pitted keratolysis, 83, 84 Pitted nails, 112, 112, 113, 113 Plain film radiography, 47–8 Achilles tendinopathy, 203 osteoarthritis, 206, 206 plantar heel pain syndrome, 193 tibialis posterior dysfunction, 199 Plantar calcaneal pad see Heel pad Plantar cover/pad, 220, 221 Plantar digital neuroma see Intermetatarsal neuroma Plantar facilitation, 228 Plantar fascia age-related physiological changes, 20 plantar heel pain syndrome, 192 rupture, 194 tenderness, prevalence, 4 Plantar fasciitis, 191, 192, 194 see also Plantar heel pain syndrome Plantar heel pad tenderness, prevalence, 4 Plantar heel pain syndrome, 191–7 aetiology pathogenesis, 192 risk factors, 192–3 assessment and diagnosis, 193–4 classification, 191–2, 192
clinical presentation, 191–2 plantar calcaneal pad, 222 treatment, 194–7 conservative, 194–7 surgical, 197 Plantar keratotic lesions, 41 Plantar metatarsal pad, 15–16, 183, 220–1, 221, 224 Plantar padding, 183, 183 Plantar plate rupture, 184 see also Predislocation syndrome Plantar pressure patterns, 51, 52 calluses, 65 hallux limitus/rigidus, 158, 158 hallux valgus, 153, 153 intermetatarsal neuroma, 183 keratotic lesions, 71 lesser toe deformities, 167 pes cavus, 207 tibialis posterior dysfunction, 198, 198 Plantar skin, age-related physiological changes, 14–15 Plantar soft tissues, 15–16 age-related physiological changes, 15–16 functional implications, 16 heel pads, 16 metatarsal pads, 15–16 Plantar warts, 67, 86, 87 Plaque, 35 Podagra, 170 Pole test, 38 Porphyromonas, 83 Position sense, 40, 41 Posterior heel pad, 222 Posterior tibial nerve, 208 Potassium hydroxide, 101 Predislocation syndrome, 181, 184, 184–6 aetiology, 184–5 clinical presentation, 184–5 plantar metatarsal pad, 220 treatment, 185–6 conservative, 185, 185–6 surgical, 186 Prefabricated orthoses, 218, 223–5, 225 contoured insoles, 224–5, 225 hallux valgus splints, 224, 224 silicone and viscoelastic devices, 223–4, 224 Presenting complaint, 30, 32–4 key questions, 32 location and history of, 32 pain assessment, 32, 32–4 Pressure perception, 40 Pressure relief, ulcers, 133–4, 134
Pressure ulcers, 129, 130, 131, 132 guidelines for the management of, 142 pressure relief, 133–4 Prevalence of foot problems, 1–5 Proprioception, 40 effect of age on, 18 Proteoglycans, age-related physiological changes, 19 Proximal subungual onychomycosis, 100 Pseudogout, 170 Psoriasis, 81–2, 82, 112, 112 Psoriasis vulgaris see Chronic plaque psoriasis Psoriatic arthritis, 195 Pulse transmission times, 17 Pump bumps see Haglund’s deformity Pustular psoriasis, 82, 82 Pustule, 35 Quadriceps muscles, age-related physiological changes, 21 Radiography, plain film see Plain film radiography Ram’s horn nail see Onychogryphosis Range of motion assessment, 43, 43–4 Raynaud’s phenomenon, 123–4, 124 conditions associated with, 124 diagnostic criteria, 124 Rearfoot disorders, 191–209 malalignments, 42 osteoarthritis, 205–7 see also specific disorder Rearfoot rockers, 238, 238 Regnauld classification, 158, 159 Research studies in aged care facilities and inpatient settings, 2 community-based, 3–5 UK, 4–5 USA, 3–4 in outpatient settings, 2–3 Rest pain, 37, 122 Retracted toes, 165, 166, 168 Retrocalcaneal bursitis see Haglund’s deformity Retrocalcaneal conditions, 199–204 Retrocalcaneal pad, 222 Rheumatoid arthritis heel pain, 195 keratotic lesions, 66 Rigid hindfoot orthoses (HFO-R), 227 Risk factors for foot problems, 5–7
Index
Rocker-soled footwear, 238, 238 hallux limitus/rigidus, 162 Saddle pad, 219, 220 Salicylic acid keratotic lesions, 70 verrucae, 86 Saline injections, 71 Sarcopenia, 20–1 Scale, skin, 35 Scaphoid pad, 221, 222 Scarf osteotomy, 155, 155 Schwartz osteotomy, 73–4, 74 Sclerosing agents injection, 183 Sclerotherapy, 127, 128 Sealed surface wound suction, 135 Seed corns, 62, 63, 65, 65 Self-management, 52–3 Semi-permeable film dressings, 133 Senile haemangiomas, 86, 89, 90 Senile keratosis, 68, 92, 92 Sensory ataxia, 50 Sensory neurons, age-related physiological changes, 17–18 Septicaemia, 83 Sesamoiditis, 181–2 Sex see Gender Sham therapy foot ulcers, 136 plantar heel pain syndrome, 196 S-heel, 237–8, 238 Shock-absorbing cushioned heels (SACHs), 237, 238 Shoe stretching, 239, 240 Shoes see Footwear Short-wave diathermy, 136 Silicone appliances, 223–4, 224 Silicone implants, 164 Silicone injections, liquid, 71 Silicone orthodigita, 222, 223 Silver’s bunionectomy, 154–5 Sinus tarsi syndrome, 208 Sit-to-stand test, 49 Skeletal system, age-related physiological changes, 18–20 Skin age-related physiological changes, 14–15 assessment, 34, 34–6, 35 cool, 37, 38 disorders, 79–94 (see also specific disorder) prevalence, 2, 4 grafting, foot ulcers, 136–7 infections, 83–5 (see also specific infection)
Skin, dry assessment of, 34 prevalence, 2, 3–4, 4, 79 Skin lesions, 85–95 assessment, 34, 34–6 benign, 86–91 incidence, 86 premalignant and malignant, 92–4 prevalence, 79 terminology, 35 see also specific lesion Skin tags, 86, 88 Slip resistance of footwear outersoles, 242–3 Social history, 29–31 Sodium hyaluronate, 162 Soft corns, 62, 63, 64 Soft tissues, plantar see Plantar soft tissues Solar dermatoses, 68, 92, 92 Sole raises, 238–9, 239 Soleus testing, 45 Spasticity, 49, 50 Spider veins, 127, 127 Splinter haemorrhages medication use-associated, 114, 114 systemic diseases-associated, 111, 113, 113 Splinting hallux valgus, 224, 224 plantar heel pain syndrome, 196 predislocation syndrome, 185 Squamous cell carcinoma, 92, 94, 94 differentiation from subungual exostoses, 109 incidence, 86 Squamous cell carcinoma in situ see Bowen’s disease Staphylococcus aureus, 83 Stasis dermatitis, 80, 80–1 Statins, 203 Stock footwear, 239–40, 240 Strength testing, muscle see Muscle(s), strength testing Streptococcus pyogenes, 83 Stress fracture calcaneal, 194 metatarsals, 48, 181, 186 Stucco keratoses, 90–1, 91 Subatmospheric pressure therapy, 135 Subungual exostosis, 109, 109 Subungual heloma, 62, 64 Superficial basal cell carcinoma, 93, 94 Superficial spreading malignant melanoma, 94, 94
Surgical treatment Achilles tendinopathy, 204 chronic venous insufficiency, 127 debridement, 132 hallux limitus/rigidus, 163–5, 164 hallux valgus, 154–7, 155–7 intermetatarsal neuroma, 183–4 keratotic lesions, 72–4 lesser toe deformities, 167–8 lymphoedema, 129 onychocryptosis, 105–7, 106, 107 onychomycosis, 103 peripheral arterial disease, 122–3 plantar heel pain syndrome, 197 predislocation syndrome, 186 tibialis posterior dysfunction, 199 Syme’s procedure, terminal, 106, 107 Synovectomy, 199 Synovial cysts see Mucous (myxoid) cysts Synovial fluid, age-related physiological changes, 19 Systemic diseases causing heel pain, 195 forefoot pain, 180–1 nail disorders associated with, 111– 12, 113 secondary hallux valgus, 152 Systems examination, 30, 34–47 Tactile sensitivity, 40 Tailor’s bunion, 4, 168, 168–9 Talus insufficiency fracture, 48 Taping techniques plantar heel pain syndrome, 196–7 predislocation syndrome, 185, 185 tibialis posterior dysfunction, 199 Tarsal tunnel syndrome, 208 Tea tree oil, 101 Teardrop pads, 221 Telangiectasia, 127, 127 Temperature perception, 40 Tendon pad, 219, 220 Tendons, age-related physiological changes, 19–20 Terbinafine onychomycosis, 101–2 tinea pedis, 85 Terminal Syme’s procedure, 106, 107 Thomas heel, 237–8, 238 Thomas wedge, 238 Thompson test, 203 Thrombosis, 123 Tibial artery, absent pulse, 2 Tibialis anterior hallux valgus, 152 testing, 45
259
260
Index
Tibialis posterior dysfunction, 52, 197, 197–9 aetiology, 198 ankle–foot orthoses, 227 assessment and diagnosis, 198–9 classification, 197–8 clinical presentation, 197, 197–8 plantar pressure, 198, 198 treatment, 199 Tibialis posterior testing, 45 Timed up and go test, 53 Tinea pedis, 83–5, 85 prevalence, 3, 79 Toe covers, 224 Toe deformities lesser see Lesser toe deformities missing, 4 overlapping, 4 prevalence, 2 see also specific deformity Toe prop, 219, 219, 223 Toe separator, 154 Toe sleeve, 219 Toe spacers, 104, 104 Toenail problems see Nail disorders Toe(s) amputation see Amputation, toe disorders, 149–70 (see also specific disorder) plantarflexor strength, 44 Tolnaftate, 85 ‘Too many toes’ sign, 199 Tophi, 170, 170 Topical negative pressure (TNP), 135 Topical treatment foot ulcers, 136 keratotic lesions, 70, 70 onychomycosis, 101–2 plantar heel pain syndrome, 196 Total dystrophic onychomycosis, 100–1, 101 Trabecular bone, age-related physiological changes, 18 Trace elements, 136 Transfer lesions, 66, 73 Treadmills, 51 Treatment outcomes assessment, 55–6 Trench foot, 126, 126 Triceps strengthening, 204 Trichophyton spp., 103 onychomycosis, 100, 103 tinea pedis, 84 Trumpet nails, 111, 111, 112 Tulle dressings, 133 Tumours, 85–94 see also specific tumour
Two-point discrimination, 40 Tylomas see Calluses Ulcerative tinea pedis, 84 Ulcer(s), 129–39 characteristics, 130 chronic venous insufficiency, 126 clinical presentation, 129–31 definition, 35 epidemiology, 129 peripheral arterial disease, 122, 122 wound management, 131–9 cleansing, 132 compression therapy, 134–5 debridement, 132 dietary supplements, 136 dressing, 132–3 evidence-based guidelines for comprehensive, 139 hyperbaric oxygen therapy, 135–6 infection, 137–9 pentoxifylline, 136 pressure relief, 133–4, 134 short-wave diathermy, 136 skin grafting, 136–7 therapeutic ultrasound, 136 topical negative pressure, 135 Ultrasonography, 48 Achilles tendinopathy, 203–4 forefoot pain, 180 Haglund’s deformity, 201 intermetatarsal neuroma, 182 plantar heel pain syndrome, 193–4 therapeutic, 136 tibialis posterior dysfunction, 199 Undecenoic acid, 85 Under pad, 221, 221–2 Under-riding toe, 166, 166 Unguis incarnates see Onychocryptosis Unipedal stance, 53 University of Texas classification, 36 U-pad, 218–19, 219 Urea cream, 101 Urticarial drug reactions, 81 Vacuum assisted wound closure, 135 Vacuum sealing technique, 135 Valgus pad, 221, 222 Varicose eczema, 80, 80–1 Varicose veins, 126, 127, 127 Vascular assessment, 36–9 Vascular corns, 62 Vascular system, peripheral see Peripheral vascular system Vasoconstriction, 125
Vasospastic disorders, 123–6 Veins, age-related physiological changes, 17 Venous hypertension, 126–7 Venous insufficiency, chronic, 126–8, 127 clinical presentation, 126–7 epidemiology, 126 pathophysiology, 126–7 risk factors, 126 treatment, 127–8 Venous stasis eczema, 80, 80–1 Venous system assessment, peripheral, 38–9 Venous ulcers, 130, 130 compression therapy, 134–5 dressings, 133 guidelines for the management of, 140 Verrucae, 67, 86, 87 Vesicle, 35 Vesicular tinea pedis, 84 Vestibular ataxia, 50 Vibration sense, 40, 41 Viscoelastic devices, 223–4, 224 Visual ataxia, 50 Vitamin A, 136 Vitamin C, 136 Vitamins, 136 Vulnopur, 132 Wagner classification, 35–6 Walking speed, 49, 51, 53 Warts, 67, 86, 87 Watermann osteotomy, 163, 164 Weal, 35 Weightbearing lunge test, 43, 44 Weightbearing radiographs, 47 Haglund’s deformity, 201 hallux limitus/rigidus, 161, 161–2 Weil osteotomy, 73, 73 White superficial onychomycosis, 100 Wilson osteotomy, 156, 156 Winograd procedure, 105–6, 106 Winter heel see Haglund’s deformity Wound management, 131–9 cleansing, 132 compression therapy, 134–5 debridement, 132 dietary supplements, 136 dressing, 132–3 evidence-based guidelines for comprehensive, 139 hyperbaric oxygen therapy, 135–6 infection, 137–9 pentoxifylline, 136 pressure relief, 133–4, 134 short-wave diathermy, 136
Index
skin grafting, 136–7 therapeutic ultrasound, 136 topical negative pressure, 135 Wound(s) assessment, 35, 36 biopsy, 138
healing, 15 severity, 35–6 Xenografts, 137 Xerosis scale, 34, 35 Xerotic eczema, 80, 80 X-ray see Plain film radiography
YakTrax® Walker, 242–3, 243 Yellow nail syndrome, 110, 110 Youngswick procedure, 163, 164 Zadik technique, 106, 106 Zinc, 136
261
