Neale's Disorders of the Foot and Ankle [9 ed.] 0702065048, 9780702065040

Table of contents :
Front Cover
IFC
NEALE’S Disorders of the Foot and Ankle
NEALE’S Disorders of the Foot and Ankle
Copyright
CONTENTS
PREFACE TO FIRST EDITION
PREFACE TO NINTH EDITION
DONALD LEWIS LORIMER 1933–2018
DON LORIMER TRIBUTE
ACKNOWLEDGEMENTS
CONTRIBUTORS
1 - Structure and Function of the Foot
INTRODUCTION
SKELETON OF THE FOOT
MOVEMENTS OF THE ANKLE AND FOOT
Ankle Joint
Subtalar Joint
Pronation and Supination
ARCHES OF THE FEET
Passive Arch Support
Active Arch Support
THE WINDLASS MECHANISM OF THE FOOT
Hallux Valgus
Structural Adaptation in Bone
The Chondral Modelling Phenomenon
Modelling of Metaphyses and Epiphyses
Modelling of Articular Surfaces
REFERENCES
2 - Examination and Diagnosis in Clinical Management
INTRODUCTION
GATHERING DATA
TAKING A COMPREHENSIVE PODIATRIC HISTORY
ELEMENTS OF THE HISTORY
Introductory Information
Chief Complaints – Soliciting Contribution
Past Medical History
Drug/Medication History
Social History
Family History
Review of Systems
ATTRIBUTES OF SYMPTOMS
PERFORMING THE PHYSICAL EXAMINATION
Mental Status
Skin (see also Chs 3 and 4)
Nails (see also Ch. 3)
Swellings
Musculoskeletal System (see also Chs 8 and 9)
Footwear (see also Ch. 21)
Vascular Assessment (see also Ch. 5)
Neurological Assessment (see also Ch. 6)
Motor System
Gait (see also Chs 7 and 24)
Other Soft Tissues
Biomechanical Examination
Further Investigations
DEVELOPMENT OF THE DIAGNOSIS
CREATING THE RECORD
REFERENCES
3 - The Skin and Nails in Podiatry
INTRODUCTION
INTEGUMENTARY SYSTEM
STRUCTURE AND FUNCTION OF THE SKIN
ACUTE INFLAMMATION
CHRONIC WOUNDS (ULCERS)
Assessment of Chronic Wounds
Pathogenesis of Chronic Wounds
Management of Chronic Wounds
SCARRING
BURNS
ATROPHY
CHILBLAINS AND CHILLING
INFECTIONS AND THE SKIN
Bacterial Infections
Viral Infections
Parasitic Infestations
VITILIGO
DISORDERS OF SWEATING
FISSURES
CORNS AND CALLUS
Pathogenesis of Corns and Callus
Management of Corns and Callus
BURSITIS
THE NAIL IN HEALTH AND DISEASE
Embryonic Development and Nail Growth
Blood Supply and Innervation
INVOLUTION (PINCER, OMEGA NAIL)
Aetiology
Treatment
ONYCHOCRYPTOSIS (INGROWING TOENAIL)
Aetiology
Treatment
SUBUNGUAL EXOSTOSIS
Pathology
Treatment
SUBUNGUAL HELOMA (CORN)
Aetiology
Treatment
SUBUNGUAL MELANOMA
Aetiology
Treatment
ONYCHAUXIS (HYPERTROPHIED NAIL)
Aetiology
Pathology
Treatment
ONYCHOGRYPHOSIS (RAM’S HORN, OSTLER’S TOE)
Aetiology
Pathology
Treatment
ONYCHOPHOSIS
Aetiology
Treatment
PARONYCHIA
Aetiology
Pathology
Treatment
ONYCHIA
Aetiology
Pathology
Treatment
ONYCHOLYSIS
Aetiology
Pathology
Treatment
Aetiology
Treatment
ONYCHATROPHIA (ANONYCHIA)
ONYCHORRHEXIS (REED NAIL)
BEAU’S LINES
Aetiology
Treatment
HIPPOCRATIC NAILS (CLUBBING)
KOILONYCHIA (SPOON-SHAPED NAIL)
ONYCHOMYCOSIS (TINEA UNGUIUM)
Aetiology
Pathology
Treatment
LEUCONYCHIA
YELLOW NAIL SYNDROME
PTERYGIUM
REFERENCES
4 - Dermatological Conditions of the Foot and Leg
INTRODUCTION
INFLAMMATORY SKIN DISEASES
Psoriasis and Related Disorders
Reactive Arthritis (Reiter’s Disease)
Pityriasis Rubra Pilaris (PRP)
Eczema (Dermatitis) and Related Disorders
Lichen Planus
Ichthyosis
Palmoplantar Keratodermas
HYPERHIDROSIS
BLISTERING DISORDERS
Autoimmune Blistering Disorders
LESIONS
Epidermal Lesions
Cutaneous Metastatic Disease
Pigmented Skin Lesions
Vascular Tumours
Fibrous Tumours
Adnexal Tumours
Other Structures
BACTERIAL INFECTION OF THE FEET
Pitted Keratolysis
FUNGAL INFECTIONS OF THE FEET AND NAILS
Fungal Infections of the Feet (Tinea Pedis)
Differential Diagnosis and Complications of Tinea Pedis
Fungal Infection of the Nail (Onychomycosis)
Laboratory Diagnosis of Dermatophyte Infection
Treatment of Tinea Pedis and Onychomycosis
Summary
REFERENCES
5 - Circulatory Disorders
INTRODUCTION
CHRONIC VENOUS DISEASE
Pathophysiology
Assessment
Management
Venous Thromboembolic Disease
Treatments
Pulmonary Thromboembolism
Recognition and Referral
LYMPHOEDEMA
Primary Lymphoedema
Secondary Lymphoedema
Diagnosis
Management of Lymphoedema
PERIPHERAL ARTERIAL DISEASE (PAD)
Atherosclerosis and Arteriosclerosis
Epidemiology
Symptoms – Intermittent Claudication
Symptoms – Ischaemic Rest Pain
Risk Factors for Arterial Disease
Clinical Diagnosis of Peripheral Arterial Disease
Ankle–Brachial Pressure Index (ABPI)
Toe–Brachial Pressure Index (TBPI)
Ankle and Toe Systolic Pressure
Diagnostic Imaging
Classification of Peripheral Arterial Disease
Impact of Peripheral Arterial Disease on quality of life
Progression of Disease – Impact to Life and Limb
Management of Peripheral Arterial Disease
CRITICAL LIMB ISCHAEMIA
Management
ACUTE LIMB ISCHAEMIA
BLUE TOE SYNDROME
PAD CASE STUDIES
Microvascular Disease
Non-Atherosclerotic Peripheral Arterial Diseases
VASCULITIS
Classification
Symptoms
Common Vasculitic Skin Lesions
Joint involvement
Peripheral nerves involvement
Intestine involvement
Lung involvement
Heart involvement
Kidneys
Eyes
Brain
Systemic Symptoms
Aetiology
Risk Factors
Diagnosis
Practical Tips for Clinicians who Suspect Vasculitis
Management
Podiatry Management of Vasculitis
Thromboangiitis Obliterans (Buerger’s Disease)
Epidemiology
Aetiology
Clinical Features
Treatment
VASOSPASTIC DISORDERS
Raynaud’s Phenomenon
Clinical Features
Diagnosis
Pathology
Management
ACROCYANOSIS
CHILBLAINS (PERNIO)
ERYTHROMELALGIA
LIVEDO RETICULARIS
ERYTHEMA AB IGNE
FROSTBITE
Pathophysiology
Symptoms
Management
Prognosis
IMMERSION FOOT (TRENCH/FESTIVAL FOOT)
Pathophysiology
Symptoms
Management
Prognosis
REFERENCES
6 - Neurological Disorders in the Lower Extremity
6
Embryogenesis and Neurogenesis
Spinal Cord and Peripheral Nerves
The Spinal Cord Pathways
Cerebellar Pathways
Basal Ganglia and Higher Centres
Autonomic Nervous System
Basic Neurological Examinations
NEUROLOGICAL DISORDERS AFFECTING THE LOWER EXTREMITY
Risk Factors for Neurological Disorders
Disorders of the Central Nervous System
Disorders of the Basal Ganglia
Disorders of the Higher Centres
Disorders of Myelination
Disorders of the Spinal Cord
Disorders of the Cerebellum
Disorders of Neuromuscular Junction
Disorders of the Peripheral Nervous System
Hereditary Motor and Sensory Neuropathies
Disorders of the Autonomic Nervous System
CONCLUSION
REFERENCES
7 - Basic Biomechanics of Gait
CENTRE OF GRAVITY
MUSCULOSKELETAL SYSTEM FUNCTION
STABILITY
CENTRE OF PRESSURE
FORCE, LOAD, STRAIN AND STRESS
Tension Stress
Compression Stress
Shear Stress
GAIT CYCLE
Trajectory of the Centre of Gravity
Ground Reaction Force
Components of the Ground Reaction Force
Path of the Centre of Pressure
DIAGNOSIS OF FOOT DISORDERS
Foot Type and Footwear
Qualitative Gait Analysis
Quantitative Gait Analysis
References
8 - Musculoskeletal Podiatric Medicine
CLINICAL BIOMECHANICS
THE NEUTRAL OR REFERENCE POSITION
THE PRINCIPLE OF COMPENSATION
OVERVIEW OF POSITION-BASED PATHOLOGY AND COMPENSATIONS OF THE FOOT
Rearfoot Varus
Varus Rearfoot
The Inverted or Varus Forefoot: Forefoot Varus
Forefoot Supinatus
The Everted or Valgus Forefoot: Forefoot Valgus
Challenge 1 – Subtalar Joint Neutral
ABNORMALITIES OF FOOT POSTURE IN ADULTS
Pes Planus
Pes Cavus
REARFOOT CONDITIONS
POSTERIOR HEEL PAIN
Superficial Calcaneal Bursitis
Retrocalcaneal Bursitis
Insertional Achilles Tendinopathy
Tibialis Posterior Tendon Dysfunction
Plantar Heel Pain
Tarsal Tunnel Syndrome
MIDFOOT CONDITIONS
Tarsal Coalition
Extensor Tendinopathy
Lisfranc Injury
Midfoot Osteoarthritis
THE FOREFOOT
Neurological Problems: Nerve Entrapment/Morton’s Neuroma
Bone Pathologies
Sesamoid Pathologies
Sesamoiditis
Hallux Limitus/Rigidus
Hallux Abducto Valgus
Metatarsalgia
Metatarsalgia due to Soft-Tissue Pathologies
Ganglia/Ganglionic Cysts
Capsulitis
Bursitis
Plantar Plate Injury
SUMMARY
REFERENCES
9 - Rheumatic Diseases
INTRODUCTION
BURDEN OF DISEASE
MEDICAL MANAGEMENT IN RHEUMATOLOGY
Non-Pharmacological Management
THE FOOT IN RHEUMATOLOGY
Assessing the Foot
Management Principles
SPECIFIC DISEASES
Seropositive Inflammatory Arthritis
Seronegative Inflammatory Arthritis
Connective Tissue Diseases – Scleroderma and Lupus
Osteoarthritis
Clinical Features
Management of Foot Osteoarthritis
Crystal Arthropathies: Gout
Clinical Features
Other Rheumatological Conditions
Miscellaneous Other Conditions
ASSESSING OUTCOMES IN RHEUMATIC DISEASE
SUMMARY
ACKNOWLEDGEMENTS
REFERENCES
10 - Metabolic Disorders and Management of High-Risk Patients
INTRODUCTION
TYPE 1 DIABETES
TYPE 2 DIABETES
SECONDARY DIABETES
DIAGNOSIS
CLINICAL FEATURES OF DIABETES
Type 1 Diabetes
Type 2 Diabetes
TREATMENT
Treatment of Type 1 Diabetes
Treatment of Type 2 Diabetes
PREVENTION OF TYPE 2 DIABETES
HYPOGLYCAEMIA
COMPLICATIONS OF DIABETES
Eye Disease
Kidney Disease
Neuropathy
Vascular Disease
PREVENTION OF COMPLICATIONS
DIABETIC FOOT
Assessment of the Foot
Integrated Examination
Classification
Simple Staging of the Diabetic Foot and Intervention
NEUROPATHIC FOOT
ISCHAEMIC FOOT
Charcot Foot
METABOLIC BONE DISEASE
Bone and Calcium Metabolism
Hormonal Physiology
Hypercalcaemia
Hypocalcaemia
Osteoporosis
Rickets and Osteomalacia
Hyperparathyroidism
Renal Osteodystrophy
Paget’s Disease
CONCLUSION
REFERENCES
11 - Podiatric Management of the Elderly
INTRODUCTION
THE AGEING FOOT
Changes to the Skin and Nails
Changes to the Plantar Fat Pad
Changes to Joints and Muscle
GAIT AND POSTURE IN AGEING
Falls
Osteoporosis
PODIATRIC MANAGEMENT
Routine Podiatric Care
Foot Orthoses
Footwear
Foot and Ankle Muscle Strengthening
Physical Activity
Duty of Care
Mental Health
CONCLUSION
REFERENCES
12 - Paediatric Podiatry
INTRODUCTION TO PAEDIATRIC PODIATRY
PART 1: C.A.P.E.R. – FIVE STEPS FOR PAEDIATRIC PODIATRISTS
Background
C.A.P.E.R. Explained
1. C.A.P.E.R. – Consider the Child in Context
3. C.A.P.E.R. – Problem-Solve any Painful Presentations with Careful Diagnosis and Treatment Where Indicated
4. C.A.P.E.R. – Explore the Evidence
PART 2 – THE PAEDIATRIC PODIATRY ‘BAKER’S DOZEN’
2. Growth and Development: The Foot and Leg at Birth
3. Gait
4. Gross Motor Skills with Age (Table 12.17)
5. Footwear and Foot Orthoses: a CHESS Strategy (Fig. 12.15)
6. Foot Types, Foot Posture
8. Injury, Osteochondrosis
9. Toes
10. Skin and Associated Conditions
11. Pain: Consult with the Five 'Is'
12. Non-Communicable Diseases Relevant to Paediatric Podiatry
13. Physical Activity
REFERENCES
13 - Podiatric Sports Medicine
Benefits of Sport, Exercise and Physical Activity
Podiatric Sports Medicine
FOREFOOT
First Metatarsophalangeal Joint
Freiberg’s Disease/Infraction
Plantar Plate Tear
Metatarsal Stress Fractures
Morton’s Neuroma
Soft-Tissue Lesions: Bursitis, Synovial Cyst and Fibroma
MIDFOOT
Osteoarthritis of the Tarsometatarsal Joint
Cuboid Syndrome
Crisp–Padhiar Syndrome
Chronic Exertional Compartment Syndrome
Lisfranc Injury
Stress Fracture of Navicular
Fifth Metatarsal Fractures
HINDFOOT AND ANKLE
Tibialis Posterior Tendon
Tibialis Anterior Tendon
Peroneal Tendons
Flexor Hallucis Longus Tendon
Plantar Fasciopathy
Achilles Tendon
EXERCISE-INDUCED LEG PAIN
Medial Tibial Stress Syndrome
Stress Fracture of the Tibia and Fibula
Chronic Exertional Compartment Syndrome
Popliteal Artery Entrapment Syndrome
Nerve Entrapment Syndromes
REFERENCES
14 - Leprosy and Tropical Diseases
LEPROSY
INTRODUCTION
LEPROSY
Epidemiology
Transmission
Diagnosis
Classification
Treatment
Reaction in leprosy
The Lower Limb in Leprosy
Case Studies
TROPICAL DISEASES
Bacterial Infections
Parasitic Diseases, Ectoparasite Infestations and Bites
Fungal Conditions
Viral Infections
Miscellaneous Conditions
REFERENCES
FURTHER READING
15 - Pharmacology and Therapeutics
INTRODUCTION
STRUCTURE OF THE CHAPTER
PHARMACOLOGICAL PRINCIPLES
Pharmacokinetics
Protein Binding
Fat or Water Solubility
Metabolism
Excretion
Clearance
Pharmacodynamics
CASE 1
Pharmacological Approach
Case 1: Analgesic Ladder, Next Stage
Case 1 (Continued)
The Case
Drug–Disease Interactions
Pain Management Plan for Mrs Y
Key Points for Case 1
CASE 2
Pharmacological Approach: Tinea Pedis
Pharmacological Intervention in the Elderly
Topical Antifungal Agents
Case 2: Cellulitis
Supporting Guidelines
Key Points for Case 2
CASE 3: PAINFUL DIABETIC NEUROPATHY
Supporting Guideline(s) and Resources
Pharmacological Approach
Drug–Disease Interactions
Practice Points
Key Points for Case 3
REFERENCES
16 - Pain Control
DEFINITION
ANATOMY
SOMATIC PAIN
PHYSIOLOGY
Peripheral Nociceptor Level
Spinal Level
Supraspinal Level
Neuropathic Pain
PRINCIPLES OF PAIN MANAGEMENT
Step 1
Step 2
Step 2 to 3
Step 3
ADJUVANT ANALGESICS
ANTIDEPRESSANTS
ANTICONVULSANTS
DULOXETINE
ANTIARRHYTHMICS
TOPICAL DRUGS
NMDA RECEPTOR ANTAGONISTS
REGIONAL ANALGESIA
PHYSICAL THERAPY
PSYCHOLOGY
SPECIFIC CHRONIC PAIN CONDITIONS OF THE LOWER LIMB
Complex Regional Pain Syndrome
REFERENCES
17 - Local Anaesthetics
CHEMICAL STRUCTURE
MECHANISM OF ACTION
PHARMACOLOGY
INFLAMED TISSUE
ALLERGY
ADJUVANTS
Epinephrine
Clonidine
Dexamethasone
MAXIMUM SAFE DOSES
TOXICITY
Neurotoxicity
Systemic Toxicity
CHOICE OF LOCAL ANAESTHETIC
Lidocaine
Bupivacaine
Levobupivacaine
Ropivacaine
Prilocaine
LOCAL ANAESTHETIC TECHNIQUES
Anatomical Landmarks
Peripheral Nerve Stimulation
Ultrasound-Guided Blocks
NEEDLE STICK INJURY
LOCAL INFILTRATION & DIGITAL NERVE BLOCK
ANKLE NERVE BLOCK
Saphenous Nerve Block
Sural Nerve Block
Superficial Fibular (Peroneal) Nerve Block
Deep Fibular (Peroneal) Nerve Block
Posterior Tibial Nerve Block
POPLITEAL NERVE BLOCK
The Popliteal Nerve Block
REFERENCES
18 - Minor Surgery of The Foot Nail Surgery
NAIL SURGERY
NAIL SURGERY
PHENOLISATION
Phenol
THE PHENOLISATION TECHNIQUE
Total Nail Avulsion
Partial Nail Avulsion
SURGICAL RESECTION PROCEDURES
Winograd Procedure
Zadik’s Procedure
Frost Procedure
Terminal Syme’s Amputation
Nail Avulsion Using urea
TREATMENT OF SUBUNGUAL EXOSTOSIS
CRYOSURGERY
Background
Electrosurgical Physics
Equipment
Safety
Patient Selection
Procedures
Electrosurgical Treatment of Verrucae
The Treatment of Verrucae
Nail Bed Ablation
LASER THERAPY
Properties of Laser Light
The Effect of Laser Light
Safety
Treatment Technique
Contraindications
Laser in Patient Management
CORN CUTTING IN THE 21ST CENTURY
Abstract
Introduction
Participants and Methods
Operative Technique
Results
Discussion
CONCLUSION
REFERENCES
19 - Diagnostic Imaging
19
Computed Tomography
Scintigraphy
Dual X-Ray Absorptiometry Scanning
Magnetic Resonance Imaging
Ultrasound Imaging
PRINCIPLES OF RADIOGRAPHIC ASSESSMENT AND APPRAISAL
When to Refer and What to Request
Understanding Anatomical Variation
Osteochondritis
Tarsal Coalitions
Fractures and Dislocations
Bone Tumours
Infection of the Bone
Metabolic Bone and Endocrine Disease
Assessment of Soft Tissues
Assessment of Ligaments
Assessment of Tendons
Assessment of the Plantar Fascia
PATHOLOGY OF NERVES
Bursa
Joints
Plantar Plate and Turf Toe
SUMMARY
REFERENCES
20 - Podiatric Surgery
FIRST RAY PATHOLOGY
Hallux Valgus
Hallux Limitus
LESSER RAY PATHOLOGY
Metatarsalgia
Metatarsal Parabola
Plantar Plate Injuries
Lesser Metatarsal Fractures
Freiberg’s Infraction
Neuroma
DIGITAL DEFORMITIES
Aetiology
MIDFOOT PATHOLOGY
Metatarsus Adductus
ADULT-ACQUIRED FLAT FOOT
Investigations
Surgical Aims
THE DIABETIC FOOT
Diabetic Foot Infections
Surgical Management of the Charcot Foot
WOUND CLOSURE
COMPLICATIONS
REFERENCES
21 - Footwear
INTRODUCTION
THE ROLE OF FOOTWEAR
The Historical Influences on Footwear
Footwear for Specific Activities
THE COMPONENTS OF FOOTWEAR
The Upper
The Sole and Heel
FOOTWEAR FEATURES
Tread Line
Toe Spring
Heel Pitch
Rigidity of the Outsole
Heel Height
Flare (Form)
MANUFACTURE OF FOOTWEAR
Last Manufacture
Pattern Cutting
Upper Cutting
Closing
Lasting
Finishing
FOOTWEAR CATEGORIES
Retail Footwear
Therapeutic Footwear
ASSESSMENT OF FOOTWEAR
APPROACH TO THE CONSULTATION
Measuring for Footwear
FOOTWEAR AS AN AID TO DIAGNOSIS
Normal Wear
Abnormal Wear
Variation in Heel Wear
Variation in Tip Wear
Variations in Tread Line Wear – Rigid Foot
Variation in Tread Line Wear – Mild Hypermobile Foot
Distortion and Wear of the Uppers
Heel Counter Wear Distortion
Other Factors Influencing Wear
ASSESSING THE FIT OF FOOTWEAR
FOOTWEAR MANAGEMENT
Cost of Footwear
Sourcing the Correct Footwear
Personal Identity and Image
Habit and Familiarity
Purpose of Footwear
Pressures from ‘Significant Others’ and Fashion
GUIDANCE FOR PATIENTS WHEN BUYING SHOES
Good Retaining Medium
Ease of Access
Close-Fitting Quarters
Adequate Width and Depth in the Toe Box
Correct Length
Correct Width
Good Fit at Instep
Adequate Heel Counter and Heel Seat
Appropriate Heel Height and Heel Base
Flexible, Hard-Wearing and Breathable Upper Material
Structural/Functional Problems
At-Risk Feet
REFERRAL FOR THERAPEUTIC FOOTWEAR
Patients who Benefit from Therapeutic Footwear
Considerations before Referral
Specific Features of Therapeutic Footwear
Footwear Modifications
Managing Usage Problems with Therapeutic Footwear
Evaluation of Therapeutic Footwear
CONCLUSION
REFERENCES
22 - Foot Orthoses
WHAT IS A FOOT ORTHOSIS?
PRINCIPLES OF MANAGEMENT
SHORT-TERM PADDING
Digital Padding for the Lesser Toes
Plantar Metatarsal Padding
ORTHODIGITAL DEVICES
SIMPLE INSOLES
CONTOURED PREFABRICATED AND CUSTOM-MADE FOOT ORTHOSES
Historical Review
Paradigms of Foot Orthosis Function
The Tissue Stress Paradigm
Broadening the Tissue Stress Paradigm
EFFECTIVENESS AND EFFECTS OF FOOT ORTHOSES
Effectiveness of Foot Orthoses
Effects of Foot Orthoses
Summary of the Effectiveness and Effects of Foot Orthoses
FOOT ORTHOTIC PRESCRIPTION
Introduction to Prescription
Selecting the Type of Foot Orthosis
Factors Associated with an Orthotic Prescription
Orthotic Materials
Issuing Foot Orthoses
CONCLUSIONS
ACKNOWLEDGEMENTS
REFERENCES
23 - Complementary and Integrated Medicines
INTRODUCTION
ACUPUNCTURE IN PODIATRY
Introduction and Historical Development
Western Medical Acupuncture
Neurophysiological Mechanisms of Acupuncture
Clinical Research and Practice
Clinical Use of Acupuncture Needling in Selected Conditions
Clinical Application of the Technique
Summary
HERBAL MEDICINE (PHYTOMEDICINE) IN PODIATRY
Introduction and Historical Development
Audit of Service
Summary
HOMEOPATHY IN PODIATRY
Introduction and Historical Development
Basic Research: Biological Models
Basic Research: Physical and Chemical Methods
Clinical Trials of Homeopathy
Podiatric Homeopathy
CONCLUSION
ACKNOWLEDGEMENTS
REFERENCES
24 - Forensic and Legal Medicine
INTRODUCTION
WHAT IS AN EXPERT WITNESS?
TYPES OF EXPERT WITNESS
When are Expert Witnesses Required?
ARENAS IN WHICH EXPERTS ARE INSTRUCTED
Civil Courts
Criminal Courts
Acting as an Expert Witness using Podiatry Knowledge, Skills and Experience
Footwear
REFERENCES
25 - Principles of Infection Prevention and Control
BACKGROUND
Hepatitis B Virus, Hepatitis C Virus and Human Immunodeficiency Virus Infections
HCV Infection
Variant Creutzfeldt–Jakob Disease
Good Practice Points
MANAGEMENT OF WASTE
INFECTION CONTROL STRATEGIES AND METHODS OF CONTROL
Cleaning of the Environment
APPENDICES
REFERENCES
26 - Evidence-Based Practice
WHAT IS EVIDENCE-BASED PRACTICE?
IT’S NOT JUST ABOUT RESEARCH
Research Evidence
Clinical Expertise
Patient’s Preferences
HIERARCHY OF RESEARCH EVIDENCE
Systematic Reviews
Randomised Controlled Trials
Cohort Studies
Case–Control Studies
Case Series and Case Reports
PODIATRY’S RESEARCH BASE
LINKING RESEARCH TO PRACTICE
SUMMARY
REFERENCES
27 - Medical Emergencies
CLINICAL ASSESSMENT
CLINICAL MONITORING
EMERGENCY DRUGS AND EQUIPMENT
PREDICTABLE EVENTS
Cardiovascular: Angina (Ischaemic Heart Disease)/Myocardial Infarction
Hypertension
Dysrhythmia
Heart Valves and Coronary Stents
Respiratory
Endocrine
Central Nervous System
UNPREDICTABLE EVENTS
Vasovagal Syncope
Cardiac Arrest
Allergy and Anaphylaxis
Local Anaesthetic Toxicity
Tachycardia and Bradycardia
Sepsis
SUMMARY
REFERENCES
28 - Health and Safety in Podiatric Practice
EFFECTIVE MANAGEMENT
SUCCESSFUL HEALTH AND SAFETY MANAGEMENT
SAFETY CULTURE
SAFE SYSTEMS OF WORK
LEGAL DUTIES
THE EMPLOYER’S RESPONSIBILITY TO VARIOUS PARTIES
Employees
Health Surveillance
Visitors and the General Public
Trespassers
HEALTH AND SAFETY POLICY
General Statement of Intent
Health and Safety at Work Responsibilities
Administration of Health and Safety at Work
RISK ASSESSMENTS
Record-Keeping Requirements
Safe Systems of Work
Accident Procedures
Working Environment
Control of Chemicals
Fire Safety
Physical Agents/Stored Energy
Plant and Equipment
Handling Operations
Risk Assessment
Problem-Solving and Decision-Making
Evaluation and Expression of Risk
Residual Risk
Expressions to Identify Risk
Principles for Risk Control
Basis for Assessment
Five Steps to Risk Assessment
Using Risk Factors to Evaluate Risk
Expressing Priorities for Risk Control
Limits of Reasonable Practicability
Checklist for Risk Assessments
Generic Risk Assessments
LEGAL REQUIREMENTS WHERE RISK ASSESSMENT IS SPECIFIED – SPECIFIC RISKS
Noise at Work Regulations 2005
PPE at Work Regulations 1992 (as amended 2005)
The Regulatory Reform (Fire Safety) Order 2005
Health and Safety (First Aid) Regulations 1981
INDEX
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z

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NEALE’S

Disorders of the Foot and Ankle

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NEALE’S

Disorders of the Foot and Ankle Ninth Edition Edited by

J Gordon Burrow BA, ADvDipEd, MSc, MPhil, ProfD, FChS, FHEA, FCPM, CMIOSH, CSci, MAE Chartered Scientist Chartered Safety and Health Practitioner Forensic Podiatrist Accredited Expert Witness

Keith Rome PhD MSc BSc(Hons) FFPM RCPS (Glasgow) Professor of Podiatry School of Clinical Sciences AUT University Auckland New Zealand

Nat Padhiar MSc, PhD, CSci, FHEA FCPodS, FFPM RCPS (Glasgow) Consultant Podiatric Surgeon, Chartered Scientist & Honorary Reader Centre for Sports & Exercise Medicine William Harvey Research Institute Queen Mary University of London UK

Edinburgh London New York Oxford Philadelphia St Louis Sydney 2020

© 2020, Elsevier Limited. All rights reserved. First edition 1981 Seventh edition 2006 Eighth edition 2010 No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without ­permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or ­contributors for any injury and/or damage to persons or property as a matter of products liability, ­negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. ISBN: 978-0-7020-6233-0

Content Strategist: Poppy Garraway Content Development Specialist: Veronika Watkins Content Coordinator: Susan Jansons Project Manager: Anne Collett Design: Margaret Reid Printed in Poland Last digit is the print number: 9  8   7   6   5   4  3   2   1

CONTENTS Preface to First Edition, vi Preface to Ninth Edition, vii Donald Lewis Lorimer 1922–2018, viii Don Lorimer Tribute, ix Acknowledgements, x Contributors, xi

Chapter 15 Pharmacology and therapeutics, 406

Chapter 1 Structure and function of the foot, 1

Christopher Broomhead

Sharon Rees

Chapter 16 Pain control, 425

Peter Isaac Thomas Paisley and Mike Graham Serpell

Chapter 17 Local anaesthetics, 435

James Watkins

Chapter 18 Minor surgery of the foot, 448

Chapter 2 Examination and diagnosis in clinical ­management, 12

Nail Surgery

J. Gordon Burrow

Chapter 3 The skin and nails in podiatry, 31 Claire MacGilchrist

Chapter 4 Dermatological conditions of the foot and leg, 58 Paul Jarrett

Chapter 5 Circulatory disorders, 89

Martin Fox, Leanne Atkin, Susan Matthews, Pamela Smith and Kathryn Taylor

Chapter 6 Neurological disorders in the lower extremity, 115 Malindu Eranga Fernando, Peter Anthony Lazzarini

Chapter 7 Basic biomechanics of gait, 145 James Watkins

Chapter 8 Musculoskeletal podiatric medicine, 160 Matthew Carroll and Prue Molyneux

Chapter 9 Rheumatic diseases, 222 Keith Rome and Sarah Stewart

Chapter 10 Metabolic disorders and management of ­high-risk patient, 261 Mike Edmonds

Chapter 11 Podiatric management of the elderly, 282 Sarah A. Curran

Chapter 12 Paediatric podiatry, 298 Angela Margaret Evans

Chapter 13 Podiatric sports medicine, 339

Nat Padhiar, Dawn Thompson, Ciaran Padhiar and Heinz Lohrer

Chapter 14 Leprosy and tropical diseases, 384 Leprosy

Hugh Cross

Peter Madigan (previous edition)

Cryosurgery, Electrosurgery, Coagulation And Laser Therapy

Maureen O’Donnell, Donald L. Lorimer, Christine M. Skinner, Anne Whinfield and Asra Ahmad ­(previous ­edition)

Corn Cutting In The 21St Century – reprinted with permission from the journal and the authors. Podiatry Now. 2016;10:25–7. Felix Lopez and Timothy Kilmartin

Chapter 19 Diagnostic imaging, 467 Deborah Turner

Chapter 20 Podiatric surgery, 493 Mark Tagoe and Frank Bowling

Chapter 21 Footwear, 520 Anita Williams

Chapter 22 Foot orthoses, 555

Karl B. Landorf, Matthew P. Cotchett and Daniel R. Bonanno

Chapter 23 Complementary and integrated medicines, 576 Mohammed Tariq Khan, Mike Cummings and Peter Fisher (deceased)

Chapter 24 Forensic and legal medicine, 590 J. Gordon Burrow, Haydn D. Kelly and Barry E. Francis

Chapter 25 Principles of infection prevention and control, 614 Stephanie J. Smith and Martina Nicola Cummins

Chapter 26 Evidence-based practice, 622 Sarah Stewart

Chapter 27 Medical emergencies, 631 Cheryl Achary and Christopher Broomhead

Chapter 28 Health and safety in podiatric practice, 643 J. Gordon Burrow

Index, 655

Tropical Diseases Francisco Vega-López

Case Study

M McGuiness and Nat Padhiar

v

P R E FA C E T O F I R S T E D I T I O N Most books about the feet have naturally enough been written by medical authors for medical readers and they have dealt mainly with the major deformities and acute traumatic injuries and with their surgical management. Most everyday foot troubles, however, develop from biomechanical anomalies which only gradually become symptomatic, though they may ultimately be quite disabling in their cumulative effects. They only seldom reach the physician or surgeon and are generally treated by chiropodists, for whom there has recently been a relative dearth of literature. This book has been compiled to help to fill that need and it has been written with a clinical orientation. There is abundant evidence that the common foot disorders cause a great deal of pain and disability. Numerous surveys have shown how prevalent they are among all groups of the population from school children to the elderly. They require specialized knowledge and skills for their effective management. The evolution and development of a chiropodial profession specializing in this field is sufficient testimony to the need. In the UK, the training of a state registered chiropodist is broadly based on the medical sciences. It equips him/her to provide a comprehensive service of diagnosis and treatment virtually from the cradle to the grave and to identify those cases which require medical or surgical investigation and treatment. The scope of practice of the chiropodist has steadily enlarged within recent years and his/her therapeutic methods have become more efficient and durable. Developments in the field of mechanical therapy and the capacity to undertake minor surgical procedures under local anaesthesia have particularly increased his/her range and effectiveness.

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It is in the public interest that this expansion should continue since it is a wasteful use of other costly skills and facilities if physicians and surgeons are unnecessarily burdened with cases within the competence of chiropodists. Heavy demands on hospital beds and operating theatres place a premium on effective methods of foot care which obviate or postpone the need for admission to hospital or which enhance post-operating care. The diagnosis and management of the common foot disorders require the application of a variety of manual skills which cannot be taught or learnt solely from books. Such practical techniques as clinical examination, operating, and applying dressings can be mastered only through repeated practice under the guidance of clinical teachers. While they are all necessarily based on scientific principles, their application to individual cases is more art than science. There is no way of acquiring such skills other than by instruction from expert clinicians and practice in the techniques involved. It is impracticable to attempt to include much detailed instruction of that kind in a general text and it is properly left to the clinical teacher who has the dominant role in establishing the required levels of practical expertise. This book attempts no more than to encapsulate current concepts on the origins, diagnosis and conservative management of the common foot disorders, while relating this particular field to the general medical and surgical conditions which bear directly upon it. The willing cooperation of so many different disciplines in its preparation is indicative of such collaboration in the clinical field. D. N. Edinburgh, UK, 1981

P R E FAC E TO N I N T H E D I T I O N This ninth edition of the textbook shows the incremental and evolving nature of both this textbook but also the profession of podiatry. The text in each edition from the first edition in 1981 written solely by Donald Neale, has developed at pace with the changing nature of podiatric practice, incorporating local anaesthesia, nail surgery and some surgical procedures in the second edition. This ninth edition also features substantial changes in light of current evidence. The order of the chapters has been revised, some chapters have been updated, whilst others have been completely rewritten or in some case are new for this edition. The book lost a major influence in podiatry and in Neale’s Common Disorders of the Foot through the passing of Don Lorimer, and the new editorial team reviewed and revised how this textbook should be projected. This edition includes many new chapters, major revisions and rewrites of previous chapters as well as a host of new international authors in addition to the new editorial team. It is also 10 years since the last edition in 2010 but we hope that this edition continues the trend set by the various editions over the past 40 years. I personally am indebted to Don Lorimer, whom I regarded as a colleague and friend, who introduced me to the editorial team of this textbook and also mentored and guided me both in Council of the then Society of Chiropodists and Podiatrists, but also in the regulatory body, the Council for Professions Supplementary to Medicine (CPSM) the forerunner of the Health and Care Professions Council (HCPC) and in that body latterly also. Don and I visited a number of the Schools of Podiatry during our time and also worked together frequently on CPD audits for HCPC. My first encounter with Don was when I undertook my nail surgery course over a weekend at the Durham School when he was a lecturer and Alex Robertson was Head of School. Then he came to the Ayrshire Branch when we held the Scottish One Day conference in the late 1970s/early 1980s and a pint (or two) was consumed to celebrate a successful conference! Don did sterling work on this textbook and I hope that we can continue his and his mentor Donald Neale’s legacy. We have included an obituary to Don Lorimer elsewhere in this textbook in recognition of his outstanding work with this textbook but also the profession of podiatry generally.

The first change that readers will notice is the change to the title; to include the ankle as well as the foot. I think this reflects where podiatry now is and that as podiatrists we need to consider not just the foot but structures and functions above that and be truly holistic in our examination and management of our patients. The structure of the chapters has been altered and we have taken the decision to remove some ‘old’ material to make new for some new material, something that is always difficult to do and will no doubt cause discussion amongst the profession of chapters that have been ‘lost’ or sacrificed. However, there was the need to try and keep the book within the same or similar bounds as before. I am indebted to both Keith Rome and Nat Padhiar who were kind enough to take up the mantle when invited to assist in editing and finding new authors for chapters. Both have been instrumental in inviting new authors who I think bring a freshness and new breadth to the book as well as give the book a more international feel, something that all UK schools have been instructed to attempt with their curriculum! My thanks also go to the previous editors of past editions, Gwen French and Maureen O’Donnell for example, for their contributions but more importantly their help, support and guidance which enabled me to continue this work. Where possible we have tried to bring robust research evidence to the forefront but as with most professions, there are still some areas (most areas!) where we need more and better quality research evidence to support what we as professionals do. There will be some areas where research is lacking or is not of sufficient quality and quantity yet, but like all professions there is a will for more research, but funding is not always as bountiful as we would like. As editors we are also aware that this textbook will not only be beneficial to podiatrists and podiatry students but to the wider health care systems that deal with foot care and foot health and we hope that Foothealth Practitioners through to podiatrists practicing podiatric surgery will find the textbook useful, relevant and of interest and use for their respective areas of practice in ensuring good foot health care for the public. J. Gordon Burrow 2020

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DONALD LEWIS LORIMER 1933–2018

Donald (Don) Lewis Lorimer, who died aged 85, was an extremely influential figure in podiatry, working tirelessly to improve the standards of professional education he believed were vital for safe and effective practice, to achieve consistency in course content and to attain recognition for the profession. He served on the Council of the Society of Chiropodists for 40 years from 1961, chaired the organisation during the 1990s, was a Gold Award holder, an honorary VicePresident and a Fellow. Born and raised in Dunfermline, Fife, Don qualified in 1956 from the first of the 3-year courses at Edinburgh Foot Clinic. He worked in private practice in Sale, then established practices in Richmond, Yorkshire and later in Barnard Castle, where he lived with his first wife and three sons. He proposed the now accepted model for degree-level podiatric education, delivered within a partnership between an educational institution and the NHS. He led the development of a core curriculum, which became the professional focus in UK undergraduate programmes, based on a common educational core and consistency across all undergraduate training. He coordinated the highly successful Erasmus/Socrates programme of student exchange designed to develop the ‘Europeanisation’ of pre-registration podiatry programmes in the UK, Belgium and the Netherlands. As a member of the regulatory body, Don was appointed to a Working Party, established to set out proposals for a broad approach to planned professional development. The resulting report, ‘The Next Decade’, brought forward extensive proposals for degree education in podiatry and was influential in making the case for the development of the pre-registration courses. He coordinated the approach to joint quality assurance and lobbied for a new approach to professional regulation. When the new regulatory body was set up in 2001, Don was pivotal in drafting, implementing ‘grandparenting’, a process by which the hitherto unregistered were able to evidence competence and join the register. He continued as registrant and CPD assessor until 2018. Over the years, Don consistently lobbied for greater access by podiatrists to prescription-only medicines. The process for achieving this was long and arduous, but podiatrists finally gained access to the medicines so necessary for the practice of the full range of podiatric interventions.

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In 1976 Don began teaching at the (now) Durham School of Podiatric Medicine and in 1982 was promoted to become Head of School. He formed a partnership between New College Durham and the (then) Sunderland Polytechnic, achieving a part-time top-up degree route in 1986. In 1989, Durham School was the first in the UK to validate a full-time degree programme under the aegis of the Council for National Academic Awards. Don chaired a working group in the early 1990s to establish a master’s degree in podiatry, validated in 1995 in partnership with (the now) Sunderland University. In the late 1970s, Donald Neale embarked on a major development and produced the first completely new British chiropodial textbook for 30 years. Common Foot Disorders was first published in 1981, swiftly gaining acclaim and popularity for its comprehensive coverage of the practice of podiatry and being widely read and regularly relied upon by students and registered practitioners alike. It swiftly became a standard text, translated into several languages – so successful has the formula been that it is now published in its ninth edition. During his training, Don had become firm friends with the Head of the Edinburgh Foot Clinic, Donald Neale. In 1984 Don accepted the invitation from his long-standing mentor and friend to contribute to the second edition of Neale’s Common Foot Disorders. He also contributed to the third edition and in 1993 became sole editor of the fourth, taking the text through to its seventh edition and having a minor role in the eighth. During this time – and in association with other co-editors – Don continued to develop the text, recognising the rapid developments in scope of practice taking place within the profession during the 1980s and 1990s fuelled by the introduction of undergraduate degrees and the resulting number of graduates demanding increased status and recognition. The change in title to Neale’s Disorders of the Foot around the time of the sixth edition recognised these moves forwards. Don’s fondness for, and belief in, the book remained undiminished until his death. Don was widely published, contributing texts on the history of the profession and two of the most prestigious schools of podiatry, as well as an assessment of the future direction of the profession in 2009. In the 1990s Don commenced another long association, this time with The Foot, a British podiatric journal, which swiftly became the repository for foot-related research articles, receiving submissions from across the globe. He became the UK editor in 1995 and Executive Editor in 2005, achieving Index Medicus listing in 1992. Don was deeply aware of the importance of professional history and its founding personalities, working to preserve the Society’s collection of antiquarian and historical books. He implemented a robust cataloguing system, later becoming honorary curator of the archives. Don was passionate about the profession, its recognition and its development. His service to it are testament to his strong belief in the role of podiatrists in healthcare. His influence on the profession and his wisdom will not soon be forgotten. Pam Sabine

DON LORIMER TRIBUTE I hope it is not too late to add my personal recollections of working with Don Lorimer. We co-operated on various projects as representatives of the Society after our retirement. We frequently went to functions held by our fellow Societies of ‘Professions Supplementary to Medicine’ and met our counterparts often, and through them Government Officials in the Departments of Health and Education. We had been involved in these topics throughout our professional careers and, in many cases, we were renewing old acquaintances. There were other times when we attended funerals and memorial services. At one such event we found ourselves joining in to a lusty chorus of ‘The Red Flag’. In those days we knew nothing of MI6 and Big Brother watching us, but who knows! Don’s sense of humour was one of the things missing from the official obituary – perhaps of necessity. I remember one occasion when the exit music at a cremation was Wagner, The Twilight of the Gods. As we both knew the deceased person, it hit us both not only with its inappropriateness, but with its pretentiousness. Not the only time we had to restrain a fit of the giggles, for Don was a great giggler. At Council meetings we did not sit near each other. People tended always to sit in their habitual places and Don had already served a term before I was elected. In fact our main interests in the early days hardly coincided; at that time I was preoccupied with negotiations with the Department of Health and he was in private practice, but tremendously concerned in the development and extension of our professional education. It happened therefore that we sat several places diagonally across the table but just within sightline – just enough to catch the eye whenever something caught the imagination and this occurred more frequently as time went on. Not mentioned, but very much a part of Don, was his love of music, especially opera. Here we later found common ground, as I was a frequenter of the Royal Opera House in Covent Garden (cheapest seats, mainly for ballet although I often went to the opera). I had taken the trouble to learn Italian and I became fairly fluent. This I remember had come as rather a surprise to Don; I think my tastes had generally been thought to be rather more plebeian. It was much later, when the Society was moving out of Welbeck Street and we had both served terms as Chairmen of Council, that we had a final look round the premises and discovered a black sack full of books and artefacts left behind in a cupboard. These were rescued and formed the basis of our

museum, now known – thanks to Wilfred Foxe – as the Centre for the History of Podiatric Medicine. We found that we shared a concern in preserving the history of the Society beyond that of the profession generally, and the move to Fellmongers Path gave us ample wall space for the display of portraits and other documents. We produced a booklet: ‘A Guide to the Displayed Material in the Offices of the Society’, which was available for visitors. Don kept records of most of the materials that we knew about and copies of many of the documents that I passed to the Society. These included various records from the Chiropodists Registration Board of the CPSM (Council for the Professions Supplementary to Medicine) which were allegedly lost in a flood although later, in an odd turn of phrase, they told us that they wanted to ‘put clear blue water’ between the old Board and the new regime. I know that another of Don’s passions was rugby; regular attendance in support of Scotland at the Six Nations Tournament, with his eldest son and his family, became a tradition, which I am assured will continue. Don continued to act in an advisory capacity in ethical and insurance matters until illness supervened. He was a big man and an imposing figure, and he truly belongs among the giants of our profession. Gwen French

(with permission from The College of Podiatry 2019, In: Podiatry Now 22(5):28)

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AC K N OW L E D G E M E N T S The editors are appreciative and grateful to all the authors of this new and revised edition of an original textbook first published in 1981 by a principal of the Edinburgh School of Chiropody, Donald Neale. The authors for this edition come from various backgrounds; medicine, rheumatology, diabetology, pain management as well as podiatry itself. We are grateful to those authors who have given their time to update chapters, renew chapters or write completely new chapters for this edition. We have tried to show the diversity of the profession as it now is, with some insight into where it might head in the future through much needed research which keeps the profession alive. Elsewhere we pay tribute to Donald Lorimer who took a prime role in continuing what Donald Neale had started and we hope that, as editors, we continue that work, true to what Donald Neale would have wished and pushing the profession onward as Don Lorimer envisioned also. As well as a tribute to Don Lorimer, the editors would like to also thank the family of the late Peter Fisher who allowed material he had written prior to his untimely death to be utilised in the Complimentary and Integrated Medicine chapter. Peter Fisher was a physician who served as homeopathic physician to Her Majesty, Queen Elizabeth II for 17 years. He was an Honorary Consultant Rheumatologist at King’s College Hospital and served as Clinical Director for 18 years and Director of Research at the Royal London Hospital for Integrated Medicine (formerly the Royal London Homoeopathic Hospital) for 22 years. He was also President of the Faculty of Homeopathy and Editor-in-Chief of the journal Homeopathy. We have also been admirably assisted by Poppy Garraway, Veronika Watkins and her team at Elsevier and we thank them for all their hard work behind the scenes and keeping us on track and nearly to time!

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CONTRIBUTORS Cheryl Achary, MBChB, MPhil Cantab, FRCA Dual Higher Anaesthetic – Intensive Care Specialty Trainee Anaesthesia and Critical Care Barts Health NHS Trust London UK Asra Ahmad, BSc (Hons), MChS Podiatrist Southwark Foot Health Services London UK Leanne Atkin, PhD, MHSc, RGN Lecturer Practitioner Division of Podiatry and Clinical Sciences Ramsden Building - RG/11 The University of Huddersfield Huddersfield UK Daniel R. Bonanno, BPod, PostGradDipRes Lecturer Discipline of Podiatry La Trobe University Melbourne Australia Frank Bowling, BSc (Hons), PgD, MScDPM, PhD, DSc, FPMFRCPS, FCPodS Professor Vascular Surgery University of Manchester Manchester NHS Foundation Trust Manchester UK Christopher Broomhead, MB, BS, BSC, FRCA Consultant in Anaesthesia & Intensive Care Perioperative Medicine Barts Health NHS Trust London UK J Gordon Burrow, BA, ADvDipEd, MSc, MPhil, ProfD, FChS, FHEA, FCPM, CMIOSH, CSci, MAE Chartered Scientist Chartered Safety and Health Practitioner Forensic Podiatrist Accredited Expert Witness

Matthew Carroll, PhD, MPod, PG Dip (Sports Medicine), BHSc (Podiatry), Dip (Exercise Physiology) Podiatry Auckland University of Technology Auckland New Zealand

Angela Margaret Evans, PhD, GradDipSocSc, DipAppSc Honorary Senior Lecturer Science, Health and Education La Trobe University Melbourne Australia

Matthew Cotchett, BSc, BPod (Hons), PhD Lecturer Rehabilitation, Nutrition and Sport La Trobe University Melbourne Australia

Peter Fisher, FRCP, FFHom (deceased) Former Trustee of the British Homeopathic Association President of the Faculty of Homeopathy Editor of Homeopathy The Queen’s Homeopathic Physician

Hugh Cross, BSc (Pod), PhD Regional Director (Asia), American Leprosy Missions (Retired); Alnwick Northumberland UK

Malindu Fernando, PhD, BHSc(Podiatry) Hons Research Fellow School of Clinical Sciences Queensland University of Technology Brisbane Australia

Mike Cummings, MB, ChB, DipMedAc Medical Director British Medical Acupuncture Society Royal London Hospital for Integrated Medicine London UK Martina Nicola Cummins, BSc, BSc Hons, MSc Clinical Director Infection Prevention & Control Barts Health NHS Trust London UK Sarah A. Curran, PhD, BSc (Hons) Professor Wales Centre for Podiatric Studies, School of Sport and Health Sciences Cardiff Metropolitan University Cardiff UK Michael Edmonds, MB, FRCP Consultant Physician Diabetic Department Kings College Hospital London UK

Martin Fox, BSc Podiatry Vascular Specialist Podiatrist Manchester Leg Circulation Service Manchester Foundation Trust Manchester UK Barry E. Francis, FCPodSurgeons Clinical Director, Surgery Fyfield Clinic Enfield London UK Paul Jarrett, BSc, MB.BS, MD, FRCP, FRACP Dermatologist Clinical Head Dermatology Middlemore Hospital Counties Manukau Health Hon Associate Professor The University of Auckland New Zealand Haydn D. Kelly, FCPodS, FFPM RCPS (Glasg), BSc, DPodM Dean (2014–2017) Faculty of Podiatric Surgery College of Podiatry London UK

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CONTRIBUTORS

Mohammed Tariq Khan, PhD, BSc (Hons), BSc (PodMed), DFHom (Pod) Consultant Podiatrist and Director of the Marigold Clinic Department of Podiatry Royal London Hospital for Integrated Medicine University College London Hospitals London UK

Peter Madigan, BEd, FCPod(S) Podiatric Surgeon Department of Diagnostic Imaging, Operating Department Practice Podiatry and Radiotherapy School of Health Glasgow Caledonian University Glasgow UK

Timothy Kilmartin, FCPodS, PhD Ilkeston Hospital Ilkeston UK

Susan Matthews, BSc Manchester Leg Circulation Service Manchester Local Care Organisation (MLCO) Manchester UK

Karl Landorf, PhD Associate Professor Discipline of Podiatry School of Allied Health La Trobe University Melbourne Australia Peter Lazzarini, BAppSci(Pod), PhD Principal Research Fellow School of Public Health and Social Work Queensland University of Technology Brisbane Australia Heinz Lohrer Prof, Dr med Zentrum für Sportorthopädie European SportsCare Network (ESN) Wiesbaden Germany Donald L. Lorimer, BEd (Hons), FCPodMed, MChS, DPod M (deceased) Podiatrist, Former Head of School Durham School of Podiatric Medicine; Past Chairman of Council, The Society of Chiropodists and Podiatrists; Former Co-ordinator Joint Quality Assurance Committee of the Society of Chiropodists and Podiatrists/ Health Professions Council; Health Professions Council Partner UK Felix Lopez, BSc (Hons) FCPodS Consultant Podiatric Surgeon Kent Community Health NHS Trust Ashford, Kent Claire MacGilchrist, PhD, Pg Cert LTHE, MFPM RCPS(Glasg), BSc (Hons) Podiatry Lecturer in Podiatric Medicine Discipline of Podiatric Medicine College of Medicine, Nursing & Health Sciences National University of Ireland Galway Galway Ireland

Mairin McGuinness, BSc (Hons) FCPodS Specialist in Podiatric Surgery London UK Prue Molyneux, BHSc Podiatry BHSc Honors PGCert Rehabilitation Podiatry Auckland University of Technology Auckland New Zealand Maureen O’Donnell, BSc (Hons), FChS, FPodMed, DPod M, Dip Ed Podiatrist, Formerly Programme Leader, Senior Lecturer Division of Podiatric Medicine and Surgery Glasgow Caledonian University Glasgow UK Nat Padhiar, MSc, PhD, CSci, FHEA FCPodS, FFPM RCPS (Glasgow) Consultant Podiatric Surgeon Chartered Scientist & Honorary Reader Centre for Sports & Exercise Medicine William Harvey Research Institute Queen Mary University of London London UK Ciaran Padhiar Medical Student Barts & The London School of Medicine & Dentistry, Queen Mary University of London London, UK Peter Isaac Thomas Paisley, MBChB (Hons), MSc, FRCA, FFPMRCA Consultant in Anaesthesia & Pain Management Anaesthesia, Critical Care and Pain Medicine Queen Elizabeth University Hospital Glasgow UK

Sharon Rees, PhD, MSc, MSc, BSc Associate Professor (Dr) School Health and Social Care London South Bank University London UK Keith Rome, PhD, MSc, BSc (Hons) Professor of Podiatry School of Clinical Sciences AUT University Auckland New Zealand Mike Graham Serpell, MB ChB, FRCA, FFPMRCA Consultant & Senior Lecturer Department of Anaesthesia Queen Elizabeth University Hospital Glasgow UK Christine M. Skinner, BSc (Hons), D Pod M, MChS Senior Lecturer, Programme Organiser, Podiatry Department of Diagnostic Imaging, Operating Department Practice Podiatry and Radiotherapy School of Health Glasgow Caledonian University Glasgow UK Pamela Smith, DPodM Vascular Specialist Podiatrist Podiatry Salford Royal Foundation Trust Manchester UK Stephanie J. Smith, MBChB, MSc, DTM&H, FRCPath Microbiology Surrey and Sussex Healthcare NHS Trust Redhill UK Sarah Stewart, BHSc (Hons) Pod, PhD Research Fellow Department of Medicine The University of Auckland Auckland New Zealand Mark Tagoe, BSc (Hons), MSc, FCPodS Consultant Podiatric Surgeon Department of Podiatric Surgery West Middlesex University Hospital Isleworth UK

CONTRIBUTORS Kathryn Taylor, BSc (Hons) Community Specialist Practitioner District Nursing, BSc (Hons) Professional Nursing Studies Lymphoedema Service Manchester Local Care Organisation (MLCO) Manchester UK Dawn Thompson, MBBS General Practice Vocational Training Scheme Kingston Hospital Kingston, UK Deborah Turner, PhD, PGCert Medical Ultrasound, PGCert Professional Development, BSc (Hons) Podiatry Professor Department of Podiatric Medicine, School of Science and Health Western Sydney University Sydney Australia

Francisco Vega-López Hospital for Tropical Diseases University College Hospitals London UK James Watkins, BEd, MA, PhD Professor College of Engineering Swansea University Swansea UK Anita Williams, PhD Health Sciences University of Salford Salford Greater Manchester UK

Anne Whinfield, BSc (Hons), MChs, DPodM Former Honorary Research Fellow Department of Primary Care Kings College School of Medicine Former Lead in Advanced Therapies, Research and Development Foot Health Services Lambeth PCT London UK

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1 Structure and Function of the Foot James Watkins

OUTLINE Introduction, 1 Skeleton of the Foot, 1 Movements of the Ankle and Foot, 2 Ankle Joint, 2 Subtalar Joint, 2 Pronation and Supination, 3 Arches of the Feet, 4 Passive Arch Support, 5 Active Arch Support, 6

The Windlass Mechanism of the Foot, 6 Interaction of the Windlass and Arch-Spring Mechanisms, 7 Hallux Valgus, 7 Structural Adaptation of the Musculoskeletal System, 8 Structural Adaptation in Bone, 8 The Chondral Modelling Phenomenon, 8 Modelling of Metaphyses and Epiphyses, 9 Modelling of Articular Surfaces, 9

KEYWORDS Ankle joint Arch support mechanisms Midtarsal joint Modelling

Pronation Rearfoot complex Structural adaptation Subtalar joint

Supination Windlass

  

INTRODUCTION

SKELETON OF THE FOOT

In weight-bearing activities, such as walking, running, jumping and landing, the main function of the musculoskeletal system is to generate and transmit internal forces to create the ground reaction forces necessary to maintain upright posture, transport the body and manipulate objects, often simultaneously. The ground reaction forces act on the feet; in general, the greater the speed of movement and change in speed of movement, the greater the magnitude of the ground reaction forces (Nigg et al 1981, Voloshin 2000). The greater the ground reaction forces, the greater the associated muscle–tendon forces and joint reaction forces. For example, when running at moderate speed (4–5 m/s), peak ground reaction forces will be in the region of 2.5–3.0 body weight (BW). However, the associated Achilles tendon force and ankle joint reaction force will be in the region of 6–8 BW and 10–14 BW, respectively (Scott & Winter 1988). In dynamic situations the foot is required to act as both a shock absorber, to cushion the impact of contact of the foot with the ground, and as a propulsive mechanism to propel the body in the desired direction (Blackwood et al 2005). The foot often performs these functions on a variety of support surfaces. Whereas floor surfaces tend to be firm and level, there are many other situations, such as in cross-country running, where the surface of the ground is neither firm nor level, but continually changes in terms of slope, evenness and hardness. The ability of the foot to function effectively in relation to such diverse environmental constraints is due to its structure, in particular to its arched shape and complex movement capability (Holowka & Lieberman 2018).

The foot consists of seven tarsals, five metatarsals and 14 phalanges (Fig. 1.1). The tarsals constitute the tarsus, which forms the rear part of the foot. The foot articulates with the lower leg at the ankle joint (talocrural joint), i.e. the joint between the tibia, fibula and talus. The talus, the second largest tarsal, has a convex pulley-shaped articular surface on its superior aspect, called the trochlear surface of the talus, which articulates with the trochlear surface of the tibia. The trochlear surface of the talus is continuous with articular surfaces on its lateral and medial aspects that articulate with the lateral malleolus and medial malleolus, respectively. The inferior aspect of the talus articulates with the anterior half of the superior aspect of the calcaneus by means of two or, in some cases, three articular facets, which together constitute the subtalar joint (talocalcaneal joint). The anterior aspect (head) of the talus articulates with the posterior aspect of the navicular, on the medial aspect of the foot, to form the talonavicular joint. The anterior aspect of the calcaneus articulates with the posterior aspect of the cuboid, on the lateral aspect of the foot, to form the calcaneocuboid joint. The calcaneocuboid and talonavicular joints are continuous with each other and constitute the midtarsal joint, also referred to as the transverse tarsal joint (Czerniecki 1988). The anterior aspect of the navicular articulates with the posterior aspects of the three cuneiforms (medial, middle, lateral), which lie side by side and articulate with each other. The posterior-superior-lateral aspect of the lateral cuneiform articulates with the superior-medial aspect of the cuboid. The anterior aspects of the medial, middle and lateral cuneiforms articulate with the bases of the

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2

CHAPTER 1 

Structure and Function of the Foot Tibia Talus Navicular

Phalanges

First cuneiform

Calcaneus

First metatarsal

Metatarsals

Phalanges A

Cuneiforms Fibula

Tibia Talus Navicular Second and third cuneiforms Metatarsals

Calcaneus

Cuboid

Navicular

Cuboid

Talus Calcaneus C

Phalanges

B Fig. 1.1  The bones of the right foot. (A) Medial aspect. (B) Lateral aspect. (C) Superior aspect.

first, second and third metatarsals, respectively. The anterior aspect of the cuboid articulates with the bases of the fourth and fifth metatarsals. The joints between the four anterior tarsals and the metatarsals are referred to as the tarsometatarsal joints. The lateral four metatarsals are similar in length, but tend to increase in girth from the second to the fifth. In comparison, the first metatarsal is usually shorter, but has a greater girth than the other four. The metatarsals are collectively referred to as the metatarsus. The heads of the metatarsals articulate with the proximal phalanges of the toes to form the metatarsophalangeal (MTP) joints. The great toe (also referred to as the big toe or the hallux) is composed of two phalanges and each of the other toes is composed of three phalanges. The phalanges of the toes become progressively shorter from proximal to distal. In addition to the tarsals, metatarsals and phalanges, a number of small accessory bones and sesamoid bones occur during fetal life (Anwar et al 2005, Williams et al 1995). There are normally about 10 irregular-shaped accessory bones distributed around the tarsus; most of these bones fuse with one of the tarsal bones prior to skeletal maturity. There are normally about 12 sesamoid (seed-shaped) bones. Each sesamoid bone is partially embedded in a tendon or ligament, with the free surface of the bone forming a synovial joint with a bone over which the tendon or ligament slides during normal function. In addition to preventing the tendon or ligament from rubbing on the adjacent bone, sesamoid bones tend to increase the mechanical efficiency (leverage) of the associated musculotendinous unit or ligament. The two most important sesamoid bones of the foot, which contribute significantly to stabilising the foot during propulsion (see the section on the windlass mechanism later in this chapter), are the sesamoids in the plantar aponeurosis (see later section on arches of the foot) beneath the base of the first MTP joint; the medial sesamoid is shown in Fig. 1.1A.

MOVEMENTS OF THE ANKLE AND FOOT Many of the 26 bones in each foot articulate with two or more other bones such that there are approximately 40 joints in each foot. Consequently, most movements of the foot involve a large number of joints, and the movement of individual joints in each movement

is difficult to describe. However, as in most movements of the body, there tends to be a high degree of functional interdependence between the joints of the foot, especially between the intertarsal and tarsometatarsal joints, such that movement of one joint tends to bring about fairly predictable movement in adjacent joints (Kitaoka et al 1997a, Nester 1997, Singh et al 1992). A group of joints with a relatively high degree of functional interdependence is called a joint complex (Peat 1986). The term ‘rearfoot complex’ is frequently used to describe the functional interdependence between the ankle, subtalar and midtarsal joints (Bowden & Bowker 1995, Downing et al 1978, Nester 1997).

Ankle Joint The ankle joint is a hinge joint that facilitates rotation about an axis of rotation which runs approximately 20° anterosuperiorly in the sagittal plane with respect to the horizontal plane and 20° anteromedially in the horizontal plane with respect to the coronal plane (Fig. 1.2) (Singh et al 1992). Consequently, the movement of the ankle joint is triplanar (i.e. movement occurs simultaneously in the sagittal, coronal and horizontal planes), with movement predominantly in the sagittal plane. Movement in the sagittal, coronal and horizontal planes occurs about the mediolateral, anteroposterior and vertical axes, respectively (Fig. 1.3). Sagittal plane motion of the foot about the ankle joint is usually referred to as plantar flexion and dorsiflexion. In dorsiflexion, sometimes referred to as true flexion of the ankle, the dorsal (superior) surface of the foot is drawn closer to the shin. In plantar flexion, sometimes referred to as extension of the ankle, the plantar (inferior) surface of the foot is pushed further away from the shin (pointing the toes).

Subtalar Joint The subtalar joint is part synovial and part syndesmosis (Jastifer & Gustafson 2014). The anterior synovial part of the joint is separated from the posterior synovial part of the joint by a funnel-shaped channel called the sinus tarsi. The sinus tarsi runs more or less horizontally in an oblique posteromedial to anterolateral direction (Fig. 1.4) with the funnel opening out laterally. The posterior talar articular surface of the calcaneus is convex and articulates with the reciprocally shaped concave posterior calcanean articular surface of the talus. The

CHAPTER 1 

Structure and Function of the Foot

3

ST 23

ST

42

A

A 20

20

A

B C

Fig. 1.2 Orientation of axes of rotation of the ankle (A) and subtalar (ST) joints. Vertical Anteroposterior

Mediolateral

Fig. 1.5  Supination and pronation of the foot. (A) Full pronation. (B) Neutral position. (C) Full supination.

part of the sinus tarsi) to the sulcus calcanei (inferior part of the sinus tarsi). The interosseous talocalcanean ligament becomes taut in eversion (Williams et al 1995). Distal to the anterior end of the sinus tarsi is another broad ligament called the cervical ligament. The cervical ligament runs obliquely upward and medially from the anterior superior aspect of the calcaneus to the lateral aspect of the neck of the talus. The cervical ligament becomes taut in inversion (Williams et al 1995). Like the ankle joint, the movement of the subtalar joint is triplanar. Inman (1976) showed that the orientation of the axis of the joint varies considerably between individuals, with a mean orientation of approximately 42° anterosuperiorly in the sagittal plane with respect to the horizontal plane and 23° anteromedially in the horizontal plane with respect to the sagittal plane (Fig. 1.2).

Pronation and Supination

Fig. 1.3  Reference axes of the foot.

Head Anterior calcanean articular surface

Anterior talar articular surface Sulcus calcanei – inferior part of sinus tarsi Posterior talar articular surface

Sulcus tali – superior part of sinus tarsi Posterior calcanean articular surface A

B

Fig. 1.4  Articular surfaces of the right subtalar joint. (A) Superior aspect of the right calcaneus. (B) Inferior aspect of the right talus.

anterior talar articular surface of the calcaneus (located on the superior aspect of the sustentaculum tali) is concave and articulates with the reciprocally shaped convex anterior calcanean articular surface of the talus. Whereas Fig. 1.4 shows only one articular surface in the anterior synovial part of the subtalar joint, there are frequently two adjacent articular surfaces. Four distinct variations in the number (one or two), shape and orientation of the anterior synovial articular surfaces have been identified (Valmassy 1996). The syndesmosis part of the subtalar joint consists of a broad interosseous talocalcanean ligament which runs obliquely downward and laterally from the sulcus tali (superior

In contrast to the ankle and subtalar joints, there would appear to be little empirical information on the movement of the midtarsal joint, which is composed of a biplanar/biaxial saddle joint (calcaneocuboid) and a triplanar/triaxial ball-and-socket joint (talonavicular) (Blackwood et al 2005). However, it is clear that the rearfoot complex facilitates triplanar movements of the foot, which are referred to as pronation and supination (Fig. 1.5) (Kitaoka et al 1997a, Nester 1997). Pronation involves simultaneous abduction (vertical axis), dorsiflexion (mediolateral axis) and eversion (anteroposterior axis) (Fig. 1.5A,B). Similarly, supination involves simultaneous adduction, plantar flexion and inversion (Fig. 1.5B,C). The orientation of the rearfoot axis varies considerably, with a mean orientation of approximately 51° anterosuperiorly in the sagittal plane with respect to the horizontal plane and 18° anteromedially in the horizontal plane with respect to the sagittal plane (Downing et al 1978). Using 13 cadaver specimens (mean age 65 years, range 20–89 years; six left feet and seven right feet) and a magnetic tracking measurement system, Kitaoka et al (1997a) investigated the contribution of the ankle joint, subtalar joint, talonavicular joint and movement of the first metatarsal relative to the navicular joint to pronation, supination, dorsiflexion and plantar flexion. The results are shown in Table 1.1. As expected, the ankle is the major contributor (54.8%) to the plantar flexion–dorsiflexion range of motion, but there are significant contributions from the other components. The subtalar joint is often regarded as the major contributor to the pronation–supination range of motion, but the results of the study indicate that the contribution of the subtalar joint (24.3%) is less than that of the talonavicular joint (44.2%). The movements of supination and pronation as described above refer to movements of the rearfoot complex when the foot is not weight bearing. When the foot is weight bearing, these movements

4

CHAPTER 1 

Structure and Function of the Foot

TABLE 1.1  Contribution of Movement of the Navicular Relative to the First Metatarsal

(met-nav) and Movement of the Ankle, Subtalar and Talonavicular (tal-nav) Joints to Pronation, Supination, Dorsiflexion and Plantar Flexion (Adapted from Kitaoka et al 1997a) PRONATION

SUPINATION

PRONATION– SUPINATION

DORSIFLEXION

PLANTAR FLEXION

DORSIFLEXION– PLANTAR FLEXION

Joint

Degrees %

Degrees

%

Degrees

%

Degrees

%

Degrees

%

Degrees

%

Met–nav Tal–nav Subtalar Ankle ROM

13.6 ± 3.9 7.6 ± 3.3 2.5 ± 1.7 7.6 ± 4.7 31.3

3.3 ± 1.5 39.3 ± 11.8 23.3 ± 7.3 8.9 ± 4.6 74.8

4.4 52.5 31.1 11.9 100

16.9 46.9 25.8 16.5 106.1

15.9 44.2 24.3 15.5 100

1.7 ± 1.1 3.5 ± 1.8 2.7 ± 1.7 16.6 ± 4.8 24.5

6.9 14.3 11.0 67.8 100

11.8 ± 5.5 12.7 ± 8.4 6.5 ± 4.2 30.6 ± 7.9 61.6

19.1 20.6 10.5 49.7 100

13.5 16.2 9.2 47.2 86.1

15.6 18.8 10.7 54.8 100

43.3 24.3 8.0 24.3 100

ROM, range of motion Pronation: from neutral to full pronation Supination: from neutral to full supination Dorsiflexion: from neutral to full dorsiflexion Plantar flexion: from neutral to full plantar flexion Pronation–supination: range from full pronation to full supination Dorsiflexion–plantar flexion: range from full dorsiflexion to full plantar flexion

are constrained, depending on the magnitude and distribution of the ground reaction force acting on the plantar aspect of the foot. Under weight-bearing conditions, the most noticeable movements of the foot occur about an anteroposterior axis through the foot (similar to inversion and eversion). For this reason, in describing the movement of the foot under weight-bearing conditions the terms supination and inversion are sometimes used synonymously, as are the terms pronation and eversion. However, the actual movements of the foot under weight-bearing conditions are modifications of supination and pronation and, as such, involve simultaneous triplanar movement in all the joints of the rearfoot complex.

ARCHES OF THE FEET The tarsals and metatarsals are arranged in the form of two longitudinal arches (medial and lateral) and a single transverse arch. The medial longitudinal arch is formed by the calcaneus, talus, navicular, the three cuneiforms, and the first, second and third metatarsals. The lateral longitudinal arch, which is much flatter than the medial arch, is formed by the calcaneus, cuboid, and the fourth and fifth metatarsals. In combination, the longitudinal arches form a single arched structure between the posterior inferior aspect of the calcaneus and the heads of the metatarsals. The transverse arch runs across the foot from medial to lateral and is formed by the anterior five tarsals and the bases of the metatarsals. The shape of the transverse arch is due to the cuboid, the lateral and middle cuneiforms, and the bases of the middle three metatarsals, which are wedge-shaped inferiorly in coronal section (Watkins 2009, 2010). Waseda et al (2014) investigated the growth in foot length (FL) and medial longitudinal arch height in 5311 boys and 4844 girls over the age range of 6–18 years. With each subject standing upright on a horizontal flat surface (feet shoulder width apart and weight evenly distributed on both feet), FL and navicular height (NH) were measured by a three-dimensional optical device with an accuracy of 2 mm in the anteroposterior direction (FL direction) and 1 mm in the vertical direction (NH direction). FL was measured as the distance from the rear surface of the heel to the anterior tip of the hallux along the sagittal plane of the foot. NH was measured as the distance from the medial tip of the navicular tuberosity (determined by palpation and marked prior to measurement) to the floor. To normalise NH with respect to

FL, medial longitudinal arch height was assessed as arch height ratio (AHR) where AHR = (NH/FL) × 100. Mean FL was similar in girls and boys at 6 years of age (≈180 mm). Subsequently, mean FL increased at a similar rate in girls and boys to plateau at around 12 years of age in girls (≈230 mm) and at around 14 years of age in boys (≈250 mm). Mean NH was similar in girls and boys at 6 years of age (≈25 mm). In girls, NH increased in three consecutive phases over the 6–18 years age range with rate of increase being similar in the first (6–10 years of age) and third (12–18 years of age) phases and markedly higher in the second phase (10–12 years of age); mean NH plateaued at 17–18 years of age (≈38 mm). The change in mean NH in boys over the 6–18 years of age followed a similar three-phase path to that in girls (6–11, 11–13, 13–18 years of age). The rates of increase in mean NH in the three phases were slightly higher than in the equivalent phases in girls; there was no plateau in mean NH at 18 years of age (≈42 mm). In girls, mean AHR decreased slightly between 6 and 10 years of age (≈13% at 10 years of age) followed by a steady increase to plateau at 17–18 years of age (≈17%). The direction and rate of change in mean AHR in boys between 6 and 18 years of age were similar to those in girls, i.e. a slight decrease between 6 and 9 years of age (≈13% at 9 years of age) followed by a fairly steady increase between 9 and 18 years of age (≈17% at 18 years of age). There would not appear to be any reported data on the development of AHR from 18 years of age to skeletal maturity. Whereas the general shape of the longitudinal and transverse arches is similar in most individuals, it has long been recognised that there is considerable variation in the height of the arches in mature individuals. Based on arch height, Root et al (1977) described three foot types: planus (low arched with a valgus hindfoot and/or varus forefoot), cavus (high arched with a varus hindfoot and/or valgus forefoot) and rectus (well aligned hindfoot and forefoot with moderate arch height). The categorisation is still widely used in clinical practice and in podiatric research (Buldt et al 2018, Hillstrom et al 2013). Planus feet are associated with over-pronation, hallux valgus, hallux limitus and rigidus and are considered a risk factor in the development of overuse injuries (Ledoux et al 2003). Cavus feet are associated with hammer toes and claw toe deformities (Levy et al 2006). Rectus feet do not appear to be associated with foot pathology or injury (Hillstrom et al 2013). The arched shape of the foot is maintained by ligaments (passive support) and muscles (active support) which create a flexible structure capable of conforming to variations in surface and load to maintain

CHAPTER 1 

A

Structure and Function of the Foot

A

5

Sesamoid bone

Deltoid ligament Interosseous ligament Spring ligament

Plantar aponeurosis

Long plantar ligament

Short plantar ligament

Flexor hallucis brevis

Plantar aponeurosis

B

B

Transverse metatarsophalangeal ligament Fig. 1.6  (A) Medial aspect of the right foot showing the main arch support ligaments. (B) Inferior aspect of the right foot showing the plantar aponeurosis.

effective force transmission between the foot and the ground. During the ground contact phases in walking and running the arches are compressed during the loading and midstance phases and recoil during the terminal stance and pre-swing phases. These actions facilitate shock absorption during the impact and loading phase, resilience during midstance and terminal stance (storage and release of elastic strain energy) and a solid base of support for propulsion during pre-swing. The compression-recoil action of the arches has been termed the footspring mechanism (Ker et al 1987) and the arch-spring mechanism (Welte et al 2018). Loss of integrity of the arch support mechanisms is associated with an increasingly pronated foot posture during weight bearing which, in turn, is associated with balance impairment and an increased risk of falling, especially in the elderly (Menz 2015). An increasingly pronated foot posture during weight bearing also affects the shape of the foot by increasing FL and foot width. If such changes in foot morphology are not met with corresponding changes in footwear, the incidence of painful dermatological, keratotic and joint abnormalities is likely to increase (Rodriguez-Sanz et al 2018).

Passive Arch Support The ligaments on the plantar aspect of the foot are very strong and can normally maintain the arches of the foot in upright posture in the absence of assistance from muscles (Hicks 1961, Kitaoka et al 1997b). The main ligaments that support the arches of the foot are: 1. The deep plantar calcaneocuboid ligament, also referred to as the short plantar ligament, runs from the anterior tubercle of the calcaneus to the plantar surface of the cuboid posterior to the groove for the tendon of the peroneus longus (Fig. 1.6). This ligament supports the calcaneocuboid part of the midtarsal joint. 2. The superficial plantar calcaneocuboid ligament, also referred to as the long plantar ligament, runs from the plantar surface of the calcaneus between the posterior and anterior tubercles to the plantar surface of the cuboid anterior to the groove for the tendon of the

Transverse Superficial sulcus stratum of the plantar aponeurosis

Deep stratum of the plantar aponeurosis

Fig. 1.7  Sagittal sections through the first (A) and second (B) metatarsophalangeal joints.

peroneus longus and to the bases of the second to fifth metatarsals (Fig. 1.6). This ligament supports the calcaneocuboid part of the midtarsal joint and the lateral four tarsometatarsal joints. 3. The plantar calcaneonavicular ligament, also referred to as the spring ligament, runs from the anteroinferior aspect of the sustentaculum tali (of the calcaneus) to the plantar surface of the navicular (Fig. 1.6). The plantar calcaneonavicular ligament supports the medial part of the subtalar joint (anterior synovial part) and the talonavicular part of the midtarsal joint. 4.  The deltoid ligament (medial collateral ligament of the ankle joint) fans out from the anterior, medial and posterior aspects of the medial malleolus to attach onto a more or less continuous arc formed by the navicular, the spring ligament, the sustentaculum tali and the talus (Fig. 1.6). The deltoid ligament supports the medial aspects of the ankle and subtalar joints. 5. The interosseous talocalcanean ligament is the syndesmosis part of the subtalar joint, described earlier. 6. The plantar aponeurosis is a broad fan-shaped ligament that spans the whole of the tarsus and metatarsus from the posterior tubercles of the calcaneus to the bases of the proximal (first) phalanges (Fig. 1.6). Just anterior to the tarsometatarsal joints, the plantar aponeurosis splits into five separate bands, one to each toe. As each band passes the plantar surface of the corresponding MTP joint, it splits into a superficial stratum (layer) and a deep stratum (Fig. 1.7). The superficial stratum attaches to the skin of the transverse sulcus, which separates the toes from the sole. The deep stratum divides into two slips that attach, one medially and one laterally, onto the proximal plantar surface of the base of the proximal phalanx of the corresponding toe, thus forming an arch for passage of the tendon of the flexor hallucis longus (first toe) or corresponding tendon of the flexor digitorum longus (second to fifth toes) to the distal phalanges (Williams et al 1995). The medial and lateral slips of the plantar aponeurosis to the proximal phalanx of the hallux merge with the tendons of the medial and lateral parts of the flexor hallucis brevis. Each tendon contains a sesamoid bone that forms a synovial

6

CHAPTER 1 

Structure and Function of the Foot

joint with the plantar aspect of the head of the first metatarsal. The plantar parts of the capsules of the MTP joints are thickened, and are referred to as plantar plates or plantar pads (Briggs 2005). The plantar plates are connected in series by deep transverse intermetatarsal ligaments and by a superficial continuous transverse MTP ligament. The plantar aponeurosis slips to each toe merge with the corresponding plantar plate and adjoining section of the transverse MTP ligament. Kitaoka et al (1997b) investigated the role of the plantar ligaments in the stability of the longitudinal arches of the feet under normal loading (upright standing posture) using 19 cadaver specimens (mean age 71 years, range 20–89 years). It was found that sectioning all the main plantar ligaments (long plantar ligament, short plantar ligament, spring ligament, interosseous talocalcanean ligament, plantar aponeurosis, deltoid ligament) resulted in complete collapse of the longitudinal arch. The arch did not collapse after sectioning any single ligament, but progressive collapse did occur when the ligaments were sectioned consecutively. The effect of sectioning individual ligaments on the degree of arch collapse (reflected in dorsiflexion of the intertarsal and tarsometatarsal joints) varied considerably between specimens, which suggested that the contribution of each ligament to arch stability varies between individuals. This is, perhaps, not surprising considering the variation in the size, shape and alignment of the bones of the feet in normal healthy individuals (Åström & Arvidson 1995). Mechanically, the plantar ligaments support the arches of the feet in two ways; as a beam and as a true arch (or truss) (Hicks 1961). Fig. 1.8A shows the type of strain experienced by a loaded beam, i.e. compression strain on the upper surface and tension strain on the lower surface. This is similar to the strain on the tarsals and metatarsals imposed by the type of arch support provided by the long plantar ligament, short plantar ligament, spring ligament, interosseous talocalcanean ligament and deltoid ligament (Figs 1.6, 1.8B). The strain on a true arch is different to that on a beam. In a true arch, the ends of the arch must move further apart if it is to become flatter, and the strain on the segments of a true arch is basically compression between the segments (Fig. 1.8C). This is similar to the strain on the tarsals and metatarsals imposed by the type of arch support provided by the plantar aponeurosis (Figs 1.6, 1.8D).

Active Arch Support The passive ligamentous beam and true arch support mechanisms are normally assisted by the muscles of the lower leg and foot (Kelly et al 2015, Zelik et al 2015). In relation to arch support, muscles that are located entirely (have their origins and insertions) within the foot are referred to as intrinsic muscles. Muscles that have their origins in the lower leg and insertions in the foot (i.e. cross the ankle joint) are referred to as extrinsic muscles. The effect that a particular muscle has on the arches (i.e. tendency to raise or flatten) depends on the tendency of the muscle to: 1. Plantar flex or dorsiflex the intertarsal, tarsometatarsal and MTP joints. Plantar flexion of any of these joints will tend to raise the arches and reduce the strain on the plantar ligaments. Dorsiflexion of any of the joints will tend to flatten the arches and increase the strain on the plantar ligaments. 2. Increase or decrease the ankle joint reaction force. In weight bearing, the weight of the body is transmitted to the feet via the ankle joints. Consequently, the effect of a particular weight-bearing activity (standing, walking, running, hopping, jumping, etc.) on the foot arches is determined by the magnitude of the ankle joint reaction forces; the greater the ankle joint reaction forces, the greater the tendency to flatten the arches, and vice versa. As demonstrated by

A

B

C

D

Fig. 1.8  Beam and arch support mechanisms. (A) Strain on a horizontal beam when vertically loaded. (B) Strain on the bones of the foot and beam support mechanism when the foot is vertically loaded. (C) Strain on the components of a true arch when vertically loaded. (D) Strain on the bones of the foot and true arch support mechanism when the foot is vertically loaded.

Hicks (1961), the further forward the line of action of body weight in relation to the ankle joint, the greater the magnitude of the ankle joint reaction force and, therefore, the greater the tendency to flatten the arches. On the basis of these criteria, Hicks (1961) classified all the intrinsic and extrinsic muscles into four groups: • Direct arch raiser, i.e. a tendency to plantar flex one or more of the intertarsal, tarsometatarsal and MTP joints. This group includes all the plantar intrinsic muscles and the flexor hallucis longus, flexor digitorum longus, peroneus brevis, peroneus longus and tibialis posterior. • Indirect arch raiser, i.e. a tendency to shift body weight backward (toward the ankle joint), which tends to reduce the magnitude of the ankle joint reaction force and, therefore, reduce arch flattening. This group includes the extensor hallucis longus, extensor digitorum longus and tibialis anterior. • Direct arch flattener, i.e. a tendency to dorsiflex one or more of the intertarsal, tarsometatarsal and MTP joints. This group includes the extensor hallucis longus, extensor digitorum longus and tibialis anterior. • Indirect arch flattener, i.e. a tendency to shift body weight forward (in front of the ankle joint), which tends to increase the magnitude of the ankle joint reaction force and, therefore, increase arch flattening. This group includes the flexor hallucis longus, flexor digitorum longus, peroneus brevis, peroneus longus, tibialis posterior, gastrocnemius and soleus.

THE WINDLASS MECHANISM OF THE FOOT As described earlier, the plantar aponeurosis spans the whole of the tarsus and metatarsus by linking the inferior aspect of the calcaneus with the plantar surfaces of the bases of the proximal phalanges of the toes (Fig. 1.6). Consequently, extension of the MTP joints winds the plantar aponeurosis around the heads of the metatarsals, like a cable being wound around a windlass, which simultaneously raises the longitudinal arch (Fig. 1.9). This action is referred to as the windlass mechanism of the foot (Hicks 1954). Flexion of the MTP joints unwinds the plantar aponeurosis and lowers the longitudinal

CHAPTER 1 

Structure and Function of the Foot A

A

7

B

B

Fig. 1.9  The windlass effect of the plantar aponeurosis resulting from dorsiflexion of the metatarsophalangeal joints. (A) Reverse windlass orientation of the foot. (B) Windlass orientation of the foot.

arch; this action is referred to as the reverse windlass (Aquino & Payne 2000). The reverse windlass action is a feature of the loading phase (from heel-strike to foot-flat) and much of the single-support phase in gait. During this period, the rearfoot complex normally pronates, which unwinds the plantar aponeurosis and lowers the longitudinal arch. This movement is associated with extension of the midtarsal joint, which is sometimes referred to as ‘unlocking’ the midtarsal joint (Blackwood et al 2005, Sobel et al 1999). In the foot-flat position, the tension in the plantar aponeurosis exerts a flexor moment on the proximal phalanges (pushes the pads of the toes against the ground), which extends the length of the base of support and, consequently, reduces the pressure on the plantar surfaces of the heads of the metatarsals (Fig. 1.9A). In addition, the tension in the plantar aponeurosis, in association with tension in the intrinsic muscles, prevents excessive flattening of the longitudinal and transverse arches and provides a stable base of support (Zelik et al 2015). The windlass action is a feature of the push-off in gait (from heel-off to just before toe-off). During this period, the rearfoot complex normally supinates in association with extension of the MTP joints (Fig. 1.9B). These actions raise the longitudinal arch, which stabilises the foot and provides a firm base of support for the push-off. The windlass movement is associated with flexion of the midtarsal joint, which is sometimes referred to as ‘locking’ the midtarsal joint (Blackwood et al 2005, Sobel et al 1999). The windlass action during push-off in gait is most effective (rapid initiation and completion of arch raise) when the leverage of the plantar aponeurosis is maximum. This occurs when (i) the sesamoids are located in their normal position beneath the head of the first metatarsal (Fig. 1.7A) and (ii) the long axes of the first metatarsal and phalanges of the hallux are more or less in line (Fig. 1.10A). Not surprisingly, this would appear to be the normal orientation of the sesamoid bones and first MTP joint, as significant non-alignment of the first metatarsal and proximal phalanx seems to be rare in children (Kilmartin et al 1991).

Interaction of the Windlass and Arch-Spring Mechanisms The arch-spring and windlass mechanisms interact through flexion and extension (dorsiflexion) of the MTP joints. Extension of the MTP joints, which raises the arches via the windlass mechanism, is largely brought about by the extensor hallucis longus (extrinsic), the extensor digitorum longus (extrinsic) and the extensor digitorum brevis (intrinsic). However, the arches can also be raised by muscles which flex the MTP joints, in particular, the flexor hallucis longus (extrinsic), the flexor digitorum longus (extrinsic), the flexor hallucis brevis

Fig. 1.10  (A) Superior aspect of the right foot with a hallux abductus angle of approximately 5°. (B) Superior aspect of the right foot with a hallux abductus angle of approximately 35°.

(intrinsic) and the flexor digitorum brevis (intrinsic). Zelik et al (2015) investigated the coordination between MTP flexors and extensors during level barefoot walking on a treadmill at 1.11 m/s. The subjects were seven healthy adults (four females, three males, aged 25.9 ± 2.7 years). The results showed that the intrinsic MTP flexors were active throughout the ground contact phase with peak intensity at midstance when the compression load on the arches was highest. From heel-off to just before toe-off the MTP joints dorsiflexed, which would tend to raise the arches via the windlass mechanism. Consequently, during this period, the passive and active arch support mechanisms worked together to control the stiffness of the arches and maintain effective force transmission between the foot and the ground. For most of the ground contact phase, the MTP extensors were largely inactive. During pre-swing, the intensity of the MTP flexors steadily declined and the intensity of the MPT extensors (acting on the MTP and ankle joints) steadily increased, culminating in toe-off and foot clearance. Whereas the role of individual MTP flexors and extensors in the control of arch stiffness is not yet clear, there is general agreement that this control is achieved via a complex interaction between the passive and active arch support mechanisms which, like all coordinated activity, occurs in response to sensory feedback from cutaneous (skin, including the heel pad), capsuloligamentous (plantar ligaments and joint capsules) and musculotendinous (intrinsic and extrinsic muscles and tendons) receptors (Kelly et al 2015, McKeon et al 2015, Welte et al 2018, Zelik et al 2015).

Hallux Valgus With increase in age, many people develop hallux valgus, also referred to as hallux abducto valgus (Thomas & Barrington 2003). Hallux valgus is a complex progressive condition that is characterised by lateral deviation (valgus abduction) of the hallux and medial deviation of the first MTP joint (Fig. 1.10B). Following a meta-analysis of data

8

CHAPTER 1 

Structure and Function of the Foot

in reports of 76 surveys, Nix et al (2010) estimated the population prevalence of hallux valgus to be 30% in women and 13% in men aged 18–65 years. The condition is thought to be largely the result of prolonged use of shoes with narrow and pointed toe boxes, especially between the ages of 20 and 29 years when soft tissue and bone are still susceptible to remodelling and, therefore, likely to result in permanent deformity (Menz et al 2016, Nix et al 2012). Unless treated, hallux valgus results in a progressive increase in the hallux abductus angle (i.e. the angle between the long axes of the first metatarsal and proximal phalanx) (Fig. 1.10B). When the hallux abductus angle is less than 15°, the condition tends to be asymptomatic. However, increases in the hallux abductus angle above 15° tend to be associated with increasing pain and discomfort around the first MTP joint (Easley & Trnka 2007, Menz & Lord 2005). Relative to the first MTP joint, any increase in the hallux abductus angle will tend to displace laterally the lines of action of the plantar aponeurosis and tendons of the intrinsic and extrinsic muscles that cross over the first MTP joint from the metatarsal to the hallux. Consequently, the sesamoid bones will also be displaced laterally relative to the first MTP joint, resulting in subluxation of the joints between the sesamoid bones and the head of the first metatarsal (Fig. 1.10B). Subluxation of these joints will decrease the leverage of the windlass about the first MTP joint and, consequently, tend to result in increased force in the muscles supporting the arches during push-off to compensate for the loss in leverage of the windlass. The increased muscle force will tend to increase the hallux abductus angle and, consequently, increase (i) the pressure on the articular surfaces between the medial sesamoid and the head of the first metatarsal, (ii) the strain on the intertransverse ligament and MTP ligament between the first and second MTP joints and (iii) the pressure exerted by the shoe on the medial aspect of the first MTP joint (Tanaka et al 1997). This pattern of loading, if prolonged, is likely to result in discomfort, pain, inefficient gait, impaired balance and an increased risk of falling, especially in the elderly (Menz & Lord 2005). One of the main joint disorders that occurs in response to prolonged excessive pressure on articular surfaces is osteoarthritis. It is the leading cause of chronic pain and disability among older people in developed countries (Arden & Nevitt 2006) and accounts for approximately 15% of all musculoskeletal consultations in people aged 45 years and over in primary care (Jordan et al 2007). The population prevalence of ankle and foot osteoarthritis is not clear, largely, it would seem, to lack of consistency in the definition of osteoarthritis and poor reporting of methods of radiographic classification (Murray et al 2018, Nelson & Jordan 2012). Based on radiographs of 557 participants from a sample of 5109 adults aged over 50 years registered at four general practices in a region of England, the population prevalence of foot osteoarthritis was estimated at 16.7% (Roddy et al 2015). The most commonly affected joint was the first MTP joint (7.8%), followed by the second cuneiform-second metatarsal joint (6.8%), the talonavicular joint (5.8%), the navicular-first cuneiform joint (5.2%) and the first cuneiform-first metatarsal joint (3.9%). Prevalence increased with age and was higher in women than men at all ages. The joints constitute most of the links in the medial longitudinal arch of the foot and, as such, are integral to the effective functioning of the windlass and arch-spring mechanisms. Following an investigation of the effect of osteoarthritis of the first MTP joint on foot-specific and general health-related quality of life, Bergin et al (2012) concluded that people with the condition experience more foot pain, have greater difficulty in performing functional and recreational weight-bearing activities, find it more difficult to obtain suitable footwear and perceive their feet to be in a poorer state of health than people without the condition.

STRUCTURAL ADAPTATION OF THE MUSCULOSKELETAL SYSTEM In any body position other than the relaxed recumbent position, the musculoskeletal system is likely to be subjected to considerable loading. In response to the forces exerted on them, the musculoskeletal components experience strain (i.e. they are deformed to a certain extent), and the greater the force, the greater the strain. Under normal circumstances the musculoskeletal components adapt their external form (size and shape) and internal architecture (structure) to the time-averaged forces exerted on them in order to more readily withstand the strain (Carter et al 1991). However, when the degree of strain experienced by a particular component exceeds its strength, it will be injured. Consequently, there is an intimate relationship between the structure and function of the musculoskeletal system (Watkins 2014).

Structural Adaptation in Bone Much of the present knowledge concerning the adaptation of musculoskeletal components to changes in time-averaged load has been established in the past 40 years (Frost 1988a,b, 1990, Goodship et al 1979, Robling 2012, Skerry 2008, Turner & Pavalko 1998). However, the fundamental concepts concerning the adaptation of bone were established over 100 years ago (Gross & Bain 1993). In 1892, Julius Wolff (1836–1902) summarised the contemporary views of bone adaptation to changes in time-averaged load in what came to be known as Wolff’s law (Wolff 1988). Wolff’s law, which has been shown to be more or less correct, hypothesised that bone adapts its external form and internal architecture to the time-averaged load exerted on it in an ordered and predictable manner to provide optimal strength with minimal bone mass. The adaptation of bone to time-averaged load is referred to as ‘modelling’. In normal growth and development, modelling has been estimated to account for 20–50% of the dimensions of mature bones (Frost 1988b). Some of the load experienced by bone is due to the weight of body segments. However, this source of loading is small relative to the loads exerted by muscles (Schoenau & Frost 2002, Watkins 2010). From birth to maturity, bone has the capacity to model external form and internal architecture. However, the capacity to model external form gradually decreases and virtually ceases at maturity. The capacity to model internal architecture also decreases with age, but is retained to some extent throughout life. In general, bone adapts to changes in time-averaged loads by increasing or decreasing bone mass to maintain an optimum strain environment. In bone, the optimum strain environment is characterised by minimal flexure (or bending) strain and an even distribution of stress (usually compression stress) across articular areas. An even distribution of stress across articular areas is maintained by modelling in accordance with the phenomenon of chondral modelling (Frost 1973).

The Chondral Modelling Phenomenon All bones that develop from hyaline cartilage via endochondral ossification experience chondral modelling, i.e. the rate and amount of new bone formed by hyaline cartilage depends on the amount and form of load exerted on it. Chondral modelling applies to articular cartilage, epiphyseal plates, insertions of tendons and ligaments, apophyseal plates, end plates in symphysis joints and sesamoid bones (Frost 1979). In a long bone, the size and shape of the epiphyses and metaphyses, and consequently the orientation of the epiphyses of a bone to its shaft, are determined by chondral modelling in articular cartilage and epiphyseal plates, which normally maintains congruent articular surfaces in all positions of the associated joints. In any particular joint position, the more congruent the joint, the greater the area over which the joint reaction force is distributed, i.e. the lower the average compression

CHAPTER 1 

A

C

B

A

E

D

Structure and Function of the Foot B

C

9 D

F

Fig. 1.11 Modelling of metaphyses and epiphyses: effect of negative-feedback mode in relation to an abductor–adductor imbalance at the knee. (A,B) Normal muscle balance and normal functional alignment. (C,D) Muscle imbalance resulting in abnormal functional alignment. (E,F) Restoration of normal functional alignment at the expense of slight genu varum.

stress on the articular surfaces and epiphyseal plates. Incongruence results in an unequal distribution of compression load across articular cartilage and epiphyseal plates. If prolonged, such unequal loading results in chondral modelling to restore maximal congruence. However, the actual changes in shape and structure of the epiphyses and metaphyses that occur depend on the extent of the changes in the patterns of loading on the articular cartilage and epiphyseal plates. If the changes in loading remain within the normal range, then a negative-feedback mode of modelling is invoked, resulting in restoration of congruence with normal or slightly abnormal alignment of the bones. However, if the changes in loading are outside the normal range, then a positive-feedback mode of modelling is invoked, which aggravates the condition, resulting in progressively worsening malalignment.

Modelling of Metaphyses and Epiphyses A functionally normal joint is a congruent joint that transmits loads across the articulating surfaces in a normal manner. An anatomical malalignment at the knee, or any other joint, will be functionally normal if the malalignment stabilises (does not get progressively worse). In these cases, the anatomical malalignments represent normal modelling in response to abnormal patterns of loading. The skeletal adaptations ensure normal transmission of loads across the joints. Fig. 1.11 illustrates the effect of negative feedback in relation to abductor–adductor muscle imbalance at the knee. Fig. 1.11A represents a knee with normal balance between the abductor and adductor muscles (i.e. the resultant horizontal force at the knee is zero). This situation is associated with normal alignment between the femur and tibia and an even distribution of compression load across the articular surfaces and epiphyseal plates (Fig. 1.11B). Fig. 1.11C shows the same knee with an abductor–adductor imbalance such that there is a net medially directed horizontal force at the knee tending to increase the degree of genu valgum. Fig. 1.11D shows the unequal pattern of loading on the articular surfaces and epiphyseal plates associated with the muscle imbalance. Assuming that the unequal loading is within the normal range, the negative-feedback mode is invoked. The rate of growth of the lateral aspects of the epiphyses and metaphyses is increased and the rate of growth of the medial aspects of the epiphyses and metaphyses is decreased such that normal congruence is restored (with net zero horizontal force at the knee) at the expense of an abnormal alignment between the femur and tibia (i.e. much reduced genu valgum or even slight genu varum relative to most individuals) (Fig. 1.11E,F). Whether or not a particular joint is anatomically malaligned during childhood, the only time when it may become painful (excluding injuries and pathological conditions not due to loading) is during adulthood,

Fig. 1.12 Modelling of articular surfaces. (A) Normal orientation of the ankle and subtalar joints in the coronal plane. (B) Normal movement of the calcaneus in inversion of the foot. (C) Effect on the ankle joint of restricted movement of the subtalar joint during inversion of the foot. (D) Modelling of the articular surfaces of the ankle joint in response to abnormal loading.

when the bones are no longer capable of modelling in response to abnormal loading. In most adults, abnormal patterns of loading are the result of an increasingly sedentary lifestyle in which body weight gradually increases and muscle strength gradually decreases.

Modelling of Articular Surfaces Minor incongruences between articular surfaces in synovial joints tend to result in large changes in the compression stress experienced by different parts of the articular surfaces (Calhoun et al 1994). This is especially the case in joints with pulley-shaped articular surfaces such as the ankle joint (Fig. 1.12). Under normal circumstances, the subtalar joint contributes to inversion and eversion of the foot (Fig. 1.12A,B). However, if movement at the joint is absent or limited, inversion and eversion of the foot twists the talus in the tibiofibular mortise, resulting in excessive compression stress on those parts of the articular surfaces that remain in contact (Fig. 1.12C). The excessive loading on the impinging areas reduces or halts growth in these areas, while growth of the unloaded areas proceeds at the normal rate. Consequently, the shapes of the articular surfaces adapt to the abnormal loading conditions by forming a rounded surface in the coronal plane rather than a pulley-shaped surface, and the ankle joint as a whole resembles a ball-and-socket joint rather than a hinge joint (Fig. 1.12D) (Frost 1979, Jastifer et al 2017, Lamb 1958).

REFERENCES Anwar, R., Anjum, S.N., Nicholl, J.E., 2005. Sesamoids of the foot. Current Orthopaedics 19, 40–48. Aquino, A., Payne, C., 2000. The role of the reverse windlass mechanism in foot pathology. Australasian Journal of Podiatric Medicine 34 (1), 32–34. Arden, N., Nevitt, M.C., 2006. Osteoarthritis: epidemiology. Best Practice in Clinical Rheumatology 20, 2–25. Åström, M., Arvidson, T., 1995. Alignment and joint motion in the normal foot. Journal of Sports Physical Therapy 22 (5), 216–222. Bergin, S.M., Munteanu, S.E., Zammit, G.V., et al., 2012 Impact of first metatarsophalangeal joint osteoarthritis on health-related quality of life. Arthritis Care & Research 64 (11), 1691–1698. Blackwood, C.B., Yuen, T.J., Sangeorzan, B.J., Ledoux, W.R., 2005. The midtarsal joint locking mechanism. Foot & Ankle International 26 (12), 1074–1080. Bowden, P.D., Bowker, P., 1995. The alignment of the rearfoot complex axis as a factor in the development of running induced patellofemoral pain. Journal of British Podiatric Medicine 50, 114–118. Briggs, P.J., 2005. The structure and function of the foot in relation to injury. Current Orthopaedics 19, 85–93. Buldt, A.K., Forghany, S., Landorf, K.B., et al., 2018. Foot posture is associated with plantar pressure during gait: a comparison of normal, planus and cavus feet. Gait & Posture 62, 235–240.

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Calhoun, J.H., Li, F., Ledbetter, B.R., Viegas, S.F., 1994. A comprehensive study of pressure distribution in the ankle joint with inversion and eversion. Foot & Ankle International 15, 125–133. Carter, D.R., Wong, M., Orr, T.E., 1991. Musculoskeletal ontogeny, phylogeny, and functional adaptation. Journal of Biomechanics 24 (Suppl. 1), 3–16. Czerniecki, J.M., 1988. Foot and ankle biomechanics in walking and running: a review. American Journal of Physical Medicine and Rehabilitation 67, 246–252. Downing, B.S., Klein, B.S., D’Amico, J.S., 1978. The axis of motion of the rearfoot complex. Journal of the American Podiatric Association 68, 484–499. Easley, M.E., Trnka, H.-J., 2007. Current concepts review: hallux valgus part 1: pathomechanics, clinical assessment, and nonoperative management. Foot & Ankle International 28 (5), 654–659. Frost, H.M., 1973. Orthopedic Biomechanics, vol. 5. Charles C. Thomas, Springfield, IL. Frost, H.M., 1979. A chondral modelling theory. Calcified Tissue International 28, 181–200. Frost, H.M., 1988a. Structural adaptations to mechanical usage: a proposed three-way rule for bone modelling. Part I. Veterinary and Comparative Orthopaedics and Traumatology 1, 7–17. Frost, H.M., 1988b. Structural adaptations to mechanical usage: a proposed three-way rule for bone modelling. Part II. Veterinary and Comparative Orthopaedics and Traumatology 2, 80–85. Frost, H.M., 1990. Skeletal structural adaptations to mechanical usage: four mechanical influences on intact fibrous tissues. The Anatomical Record 226, 433–439. Goodship, A.E., Lanyon, L.E., McFie, H., 1979. Functional adaptation of bone to increased stress. Journal of Bone and Joint Surgery 61A, 539–546. Gross, T.S., Bain, S.T., 1993. Skeletal adaptation to functional stimuli. In: Grabiner, M.D. (Ed.), Current Issues in Biomechanics. Human Kinetics, Champaign, IL. Hicks, J.H., 1954. The mechanics of the foot. II. The plantar aponeurosis and the arch. Journal of Anatomy 88 (1), 25–31. Hicks, J.H., 1961. The three weight-bearing mechanisms of the foot. In: Evans, F.G. (Ed.), Biomechanical Studies of the Musculoskeletal System. Charles C. Thomas, Springfield, IL. Hillstrom, H.J., Song, J., Kraszewski, A.P., et al., 2013. Foot type biomechanics Part 1: Structure and function of the asymptomatic foot. Gait & Posture 37, 445–451. Holowka, B., Lieberman, D.E., 2018. Rethinking the evolution of the human foot: insights from experimental research. Journal of Experimental Biology 221. Available: https://doi.org/10.1242/jeb.174425. Inman, V.T., 1976. Joints of the Ankle. Williams & Wilkins, Baltimore, OH. Jastifer, J.R., Gustafson, P.A., 2014. The subtalar joint: Biomechanics and functional representations in the literature. The Foot 24 (4), 203–209. Jastifer, J.R., Gustafson, P.A., Labomascus, A., Snoap, T., 2017. Ball and socket ankle: Mechanism and computational evidence of concept. Journal of Foot & Ankle Surgery 56, 773–775. Jordan, K., Clarke, A.M., Symmonds, D.P.M., et al., 2007. Measuring disease prevalence: A comparison of musculoskeletal disease using four general practice consultation databases. British Journal of General Practice 57, 7–14. Kelly, L.A., Lichtwark, G., Cresswell, A.G., 2015. Active regulation of longitudinal arch compression and recoil during walking and running. Journal of the Royal Society Interface 12, 20141076. Ker, R.F., Bennett, M.B., Bibby, S.R., et al., 1987. The spring in the arch of the human foot. Nature 325, 147–149. Kilmartin, T.E., Barrington, R.L., Wallace, A.W., 1991. Metatarsus primus varus, a statistical study. Journal of Bone and Joint Surgery 73B (6), 937–940. Kitaoka, H.B., Luo, Z.P., An, K.-N., 1997a. Three-dimensional analysis of normal ankle and foot mobility. American Journal of Sports Medicine 25 (2), 238–242. Kitaoka, H.B., Ahn, T.-K., Luo, Z.P., An, K.-N., 1997b. Stability of the arch of the foot. Foot & Ankle International 18 (10), 644–648. Lamb, D., 1958. The ball and socket ankle joint: a congenital abnormality. Journal of Bone and Joint Surgery 40-B, 240243.

Ledoux, W.R., Shofer, J.B., Ahroni, J.H., et al., 2003. Biomechanical differences among pes cavus, neutrally aligned, and pes planus feet in subjects with diabetes. Foot & Ankle International 24, 845–850. Levy, J.C., Mizel, M.S., Wilson, L.S., et al., 2006. Incidence of foot and ankle injuries in West Point cadets with pes planus compared to the general population. Foot & Ankle International 27, 1060–1064. McKeon, P.O., Hertel, J., Bramble, D., Davis, I., 2015. The foot core system: a new paradigm for understanding intrinsic foot muscle function. British Journal of Sports Medicine 49, 290. Menz, H.B., 2015. Biomechanics of the ageing foot and ankle: a mini-review. Gerontology 61 (4), 381–388. Menz, H.B., Lord, S.R., 2005. Gait instability in older people with hallux valgus. Foot & Ankle International 26 (6), 483–489. Menz, H.B., Roddy, E., Marshall, M., et al., 2016. Epidemiology of shoe wearing patterns over time in older women: associations with foot pain and hallux valgus. Journals of Gerontology: Series A, Biological Sciences and Medical Sciences 71 (12), 1682–1687. Murray, C., Marshall, M., Rathod, T., et al., 2018. Population prevalence and distribution of ankle pain and symptomatic radiographic ankle osteoarthritis in community-dwelling older adults: a systematic review and cross-sectional study. Plos ONE 13 (4), e0193662. Nelson, A.E., Jordan, J.M., 2012. Defining osteoarthritis: a moving target. Osteoarthritis and Cartilage 20, 1–3. Nester, C.J., 1997. Rearfoot complex: a review of its interdependent components, axis orientation and functional model. The Foot 7, 86–96. Nigg, B.M., Denoth, J., Neukomm, P.A., 1981. Quantifying the load on the human body: problems and some possible solutions. In: Morecki, A., Fidelus, K., Kedzior, K. (Eds.), Biomechanics VIIB. University Park Press, Baltimore, pp. 88–98. Nix, S., Smith, M., Vicenzino, B., 2010. Prevalence of hallux valgus in the general population: a systematic review and meta-analysis. Journal of Foot and Ankle Research 3, 21. Nix, S.E., Vicenzino, B.T., Collins, N.J., Smith, M.D., 2012. Characteristics of foot structure and footwear associated with hallux valgus: a systematic review. Osteoarthritis Cartilage 20, 1059–1074. Peat, M., 1986. Functional anatomy of the shoulder. Physical Therapy 66, 1855–1865. Robling, A.G., 2012. The interaction of biological factors with mechanical signals in bone adaptation: Recent developments. Current Osteoporosis Reports 10, 126–131. Roddy, E., Thomas, M.J., Marshall, M., et al., 2015. The population prevalence of symptomatic radiographic foot osteoarthritis in community-dwelling older adults: cross sectional findings from the clinical assessment study of the foot. Annals of the Rheumatic Diseases 74, 156–163. Rodriguez-Sanz, D., Tovaruela-Carrion, N., Lopez-Lopez, et al., 2018. Foot disorders in the elderly: A mini-review. Disease-a-Month 64, 64–91. Root, M.L., Orien, W., Weed, J.H., 1977. Normal and Abnormal Function of the Foot. Clinical Biomechanics Corporation, Los Angeles. Scott, S.H., Winter, D.A., 1988. Internal forces at chronic running injury sites. Medicine and Science in Sports and Exercise 22, 357–369. Schoenau, E., Frost, H.M., 2002. The ‘muscle–bone unit’ in children and adolescents. Calcified Tissue International 70, 405–407. Singh, A.K., Starkweather, K.D., Hollister, A.M., et al., 1992. Kinematics of the ankle: a hinge axis model. Foot and Ankle 13 (8), 439–446. Skerry, T.M., 2008. The response of bone to mechanical loading and disuse: Fundamental principles and influences on osteoblast/osteocyte homeostasis. Archives of Biochemistry and Biophysics 473, 117–123. Sobel, E., Levitz, S.J., Caselli, M.A., 1999. Orthoses in the treatment of rearfoot problems. Journal of the American Podiatric Medical Association 89 (5), 220–233. Tanaka, Y., Takakura, Y., Takaoka, T., et al., 1997. Radiographic analysis of hallux valgus in women on weightbearing and nonweightbearing. Clinical Orthopaedics and Related Research 336, 186–194. Thomas, S., Barrington, R., 2003. Hallux valgus. Current Orthopaedics 17, 299–307.

CHAPTER 1  Turner, C.H., Pavalko, F.M., 1998. Mechanotransduction and functional response of the skeleton to physical stress: The mechanisms and mechanics of bone adaptation. Journal of Orthopaedic Science 3, 346–355. Valmassy, R.L., 1996. Clinical Biomechanics of the Lower Extremity. CV Mosby, St Louis, MI. Voloshin, A., 2000. The influence of walking speed on dynamic loading on the human musculoskeletal system. Medicine and Science in Sports and Exercise 32, 1156–1159. Waseda, A., Suda, Y., Inokuchi, S., et al., 2014. Standard growth of the foot arch in childhood and adolescence – derived from the measurement results of 10,155 children. Foot and Ankle Surgery 20, 208–214. Watkins, J., 2009. The Pocket Podiatry Guide: Functional Anatomy. Churchill Livingstone, Edinburgh. Watkins, J., 2010. Structure and Function of the Musculoskeletal System, 2nd ed. Human Kinetics Corp, Champaign, IL.

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Watkins, J., 2014. Biomechanics of musculoskeletal adaptation. In: Brahme, A. (Ed.), Comprehensive Biomedical Physics, vol. 10. Elsevier, Amsterdam, pp. 1–37. Welte, L., Kelly, L.A., Lichtwark, G.A., Rainbow, M.J., 2018. Influence of the windlass mechanism during dynamic foot arch deformation. Journal of the Royal Society Interface 15, 20180270. Williams, P.L., Bannister, L.H., Berry, M.M., et al. (Eds.), 1995. Gray’s anatomy. Longman, Edinburgh. Wolff, J., 1988. The Law of Bone Modelling (trans. Maquet P, Furlong R). Springer Verlag, New York. [Originally published as: Wolff J 1892 Das gesetz der transformation der knochen. A. Hirschwald, Berlin.]. Zelik, K.E., La Scaleia, V., Ianenko, P., Lacquaniti, F., 2015. Coordination of intrinsic and extrinsic foot muscles during walking. European Journal of Applied Physiology 115, 691–701.

2 Examination and Diagnosis in Clinical Management J. Gordon Burrow OUTLINE Introduction, 12 Gathering Data, 13 Taking a Comprehensive Podiatric History, 15 Elements of the History, 15 Introductory Information, 15 Chief Complaints – Soliciting Contribution, 15 Past Medical History, 16 Drug/Medication History, 16 Social History, 16 Family History, 16 Review of Systems, 16 Attributes of Symptoms, 16 Performing the Physical Examination, 16 Mental Status, 17 Skin, 18

Nails, 18 Swellings, 18 Musculoskeletal System, 18 Footwear, 19 Vascular Assessment, 19 Neurological Assessment, 22 Motor System, 22 Gait, 25 Other Soft Tissues, 27 Biomechanical Examination, 27 Further Investigations, 27 Applying Critical Thinking to the Information Gathered, 27 Development of the Diagnosis, 28 Creating the Record, 28

KEYWORDS Ankle–brachial indices Assessment of coordination Assessment of gait Assessment of motor tone Assessment of power Assessment of reflexes Associated manifestations of symptoms Babinski reflex Biomechanical examination Biothesiometer Chief complaints Consent Critical thinking Current health status Dermatoses Development of the diagnosis Elasticity of skin Factors that aggravate or relieve symptoms Family/social history

Footwear Force plates Gait Hair Humidity of skin Hyperkeratosis Inspection Location of symptoms Lower motor neuron (LMN) Mental status Motor system MRC classification of muscle power Musculoskeletal system Nails Neurological assessment Neurothesiometer Palpation Past history Psychosocial history

Quality of symptoms Quantity or severity of symptoms Review of systems Setting of symptoms Signs and symptoms of peripheral vascular disease Skin colour Skin integrity Skin temperature Skin texture SOAPE system Surgical interventions Swellings Timing (onset, duration, frequency) of symptoms Upper motor neuron (UMN) Vascular assessment

   Use the past as a mirror when studying the present; there can be no present without the past. Watching others do something is easy; learning to do it yourself is hard. To experience is better than to be told; seeing for oneself is better than hearing from others. Chinese Proverbs (Wanheng & Xiaoxiang 1996)

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INTRODUCTION Healthcare is an ever-changing environment and practitioners need to keep up to date with the various changes that occur within healthcare and that impinge on healthcare practice. In the past few years there have been changes in Data Protection Laws which have had a bearing on how we process and keep data about our clients/patients/consumers/

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service users or whatever we wish to call those seeking our services. There have been legal cases which may impact upon the method by which we gain informed consent (e.g. Montgomery v Lanarkshire NHS Board) and how practitioners and patents communicate information to ensure safe and effective practice. As the profession progresses and develops more specialist areas of practice, there is a need to reflect on how practitioners undertake areas of practice and whether technology can assist practitioners to meet service users’ needs and how as a profession we meet the differing demands of an increasing ageing population, but also the increased demands that those living longer encounter such as dementia, as well as the obesity crises and increase in prevalence of diabetes worldwide and the complications such a disease brings with it. However, at the fundamental level of all of these changes, communications and communication skills still remain the most useful/ vital component part of clinicians’ skills, allowing them to manage patients effectively, efficiently and safely. Communication is a key skill fundamental to the clinical competence of podiatrists (HCPC 2013) with a number of proficiencies attached to registration and continued registration. It is apparent that, in a litigious society, failure to communicate to, with and about our patients is a primary cause of many cases against practitioners. There is some research evidence that medical staff and other healthcare professionals’ communication can affect patients’ experience of their condition, concordance with advice and disease outcome, and that patients view clinician’s communication performance as very important (Brown 2008, Greco et al 2002, Parry 2008). It is failure to communicate with the patient from the start, in gaining informed consent, in our history taking, that may lead to misdiagnoses, poor management strategy or poor compliance by the patient. Failure to communicate properly what occurred during the consultation phase, and to document the management strategy and agreement by the patient in the case record leads to many cases of complaint, disciplinary procedures or litigation by patients against podiatrists. The process by which clinicians gain, analyse or interpret the information that the patient imparts to them is, by and large, an invisible process, but it gives visible and resultant shape to the data compiled throughout the consultation and clinical interactions. ‘Clinical or critical thinking’ is a name given to that invisible process (Bates 1995). It is a process demonstrated and observed during training, but developed and honed by experience and continuous professional development of clinical and academic skills. Researchers debate whether critical thinking can be learned or if it is a developmental process regulated by motivations, dispositions and personality traits. Critical thinking is considered as intellectually engrossed, proficient and accountable thinking that enables suitable conclusions because it necessitates the application of assumptions, knowledge, competence and the ability to challenge one’s own thinking and biases. Critical thinking requires the use of self-correction and scrutinising to assess the rationality of thinking as well as reflexivity. When using critical thinking, practitioners step back and reflect on the quality of that thinking. However, there needs to be a two-step process in managing patients in podiatric practice. Clinical reasoning is the cognitive or reasoning process that uses discerning strategies to gather and analyse patient information, evaluate the relevance of the information and decide on possible actions to improve the patient’s physiological and psychosocial outcomes. Clinical reasoning requires the integration of critical thinking in the identification of the most appropriate interventions that will improve the patient’s condition. Critical thinking is the process of planned higher level thinking to define a patient’s problem, scrutinise the evidence-based practice in caring for the patient and make selections in the delivery of care. Clinical reasoning is often defined

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in practice-based disciplines, such as nursing and medicine, as the ‘application of critical thinking to the clinical situation’ (Victor-Chmil 2013, p. 35). However, the UK Regulator for Podiatrists (Health and Care Professions Council – HCPC) does not mention critical thinking in their Standards of Proficiency for Podiatrists (HCPC 2013). Patient centredness underpins these processes and includes respectful understanding of each patient’s perspective and needs, mutual understanding, shared agreement on treatment and self-management in a partnership approach to care according to Cushing (2015) and Mead & Bower (2000).

GATHERING DATA From the initial referral letter, or initial contact with the patient in the surgery, or through the telephone call or email, the practitioner should continually observe, ask open-ended and closed questions, and use verbal and non-verbal skills and additional methods to encourage the patient to divulge his or her story. Podiatrists, like similar healthcare practitioners, are expected to practice in an evidence-based way; asking clinical questions, searching for and appraising research evidence, integrating the evidence into clinical practice and evaluating this process. This process is part of taking a podiatric history, comprises many constituent parts and in American terms is the ‘clerking process’, but assists in managing the patient, their carers’ and their expectations. To many students it is a daunting experience, requiring the collection of information, which often needs restructuring to make sense of the vast amount of data obtained from both the history and the examination. The student/practitioner requires an open, enquiring approach to this process, within a systematic framework, to ensure that the all-important information is gleaned in an efficient and effective manner. During the process the student/practitioner needs to encourage the patient to divulge information. This encouragement may take numerous forms (Bates 1995): • Facilitation – actions, postures or words communicating the practitioner’s interest in the patient: may take the form of leaning forward, ensuring eye contact, a gentle touch to a particular spot. • Reflection – a word or phrase the patient has used is repeated back to them. • Clarification – requesting the patient to give more meaning to what he or she has said to ensure that the practitioner’s interpretation matches that of the patient. • Empathy – recognition of the patient’s feelings through the practitioner’s words or actions. • Ask about feelings – ask what the patient felt about the pain, discomfort, event or symptom. • Interpretation – put into words what the practitioner has deduced/ inferred/interpreted about what the patient has said to them, to ensure there is no misunderstanding. • Confrontation – state something about the patient’s responses (feelings, behaviour) which is inconsistent with other symptoms or signs. The interview/consultation is potentially the most powerful, sensitive instrument at the command of the podiatrist, and yet it is probably the most misused or misunderstood aspect of our practice. The patient has become the focus of NHS attention, and as patientbased clinical methods are paramount, the interview/consultation has taken on even greater importance. Most clinicians still rely on the gathering of information from the patient as the prime means of making a diagnosis and deciding on a management strategy for treating the condition or complaint. Technology and instrumentation or tests

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assist in the process, but communication is still the primary basis of the process. The physical examination is based on the information gleaned, and helps to confirm an initial working hypothesis or diagnosis and to enable the clinician to make the best use of resources such as tests, diagnostic equipment, time and expertise. It also demonstrates a professional approach to the patient, and is both an efficient and an effective use of scarce resources. It is routine practice that a patient’s history is obtained before undertaking a physical examination. Remember, however, that informed consent is required for a practitioner to obtain information and prior to performing a physical examination. It is prudent to ask the patient whether he or she is willing to divulge information to you by explaining why and how the consultation will be conducted. Consent and competence are concepts central to medical ethics (Boyd 2017). Judging whether a patient is or is not competent, has or lacks capacity to consent, is a common but also important medical responsibility. For consent to be valid, not only must the person giving it be competent, but consent must also be informed. Decisionmaking in cases of uncertain mental capacity is regulated by the Mental Capacity Act 2005 (effective 2007) in the UK. The Act provides a legal structure for decision-making for adults (16 and over) who are indicated to lack capacity and where ‘best interest’ decisions are required to be made on their behalf. Frail older people with cognitive impairments, such as vascular and other forms of dementia, represent an increasing demographic segment across many continents for whom the defending principles of the Act have great bearing, as they become increasingly dependent on the care of others (HinsliffSmith et al 2017). According to Dunn (2016) ‘The process of obtaining consent in ethically defensible ways depends on the ability of the practitioner obtaining consent to attend to the particularities of the patient, the issue under questions, and the wider socio-cultural context in which permissions of all kinds are sought’. Attaining consent from a patient requires a meaningful degree of skill. The skills to be exhibited are not, nevertheless, about the practitioners’ talent to summarise the expression of respect for autonomy that consent represents, or to be able to memorise a list of medical ‘facts’ that the patients should be told about. Instead, according to Dunn (2016) ‘gaining consent correctly requires the making of continual judgements by practitioners about how, what, and when interactions with patients ought to be steered towards clarifying whether a patient agrees with an emergent course of action that is being discussed as part of ongoing clinical care’. As a moral imperative, respect for human dignity requires that healthcare practitioners and researchers secure free and informed consent from their patients or prospective research subjects before proceeding. Although ageing must never be synonymous with incompetence, older adults may gradually lose their decision-making capacity because of progressive cognitive deficits, thus making an assessment of competence to give consent difficult for the healthcare provider. Practitioners must therefore be aware of what is known legally as ‘Proxy Consent’. Some people prefer to nominate someone they trust to decide for them in future, or the courts may appoint someone to do that when the patient is mentally incapacitated. Until relatively recently (2007) in the UK, nobody could consent to medical treatment on behalf of a mentally incapacitated adult and that remains the legal position in Northern Ireland. In Scotland, however, such decisions can be made by a welfare attorney. From October 2007, treatment decisions can also be made by a welfare attorney in England and Wales. Proxy Consent is the process by which people with the legal right to consent to medical treatment for themselves or for a minor or a ward

delegate that right to another person. There are three fundamental constraints on this delegation: 1. The person making the delegation must have the right to consent. 2. The person must be legally and medically competent to delegate the right to consent. 3. The right to consent must be delegated to a legally and medically competent adult. There are two types of proxy consent for adults. The first, the power of attorney to consent to medical care, is usually used by patients who want medical care but are concerned about who will consent if they are rendered temporarily incompetent by the medical care. A power of attorney to consent to medical care delegates the right to consent to a specific person. The second type is the living will. Guidance on the issue of advance decisions and proxy decision-making in medical treatment is useful to know about when working in home care or residential and other type of healthcare settings (BMA 2007). According to Medical Protection (2018) there are very few occasions where the law specifically requires written consent; in podiatry that is usually where invasive procedures are to be considered, such as surgery. But in the main, a verbal consent is as legal/binding as written consent. Again, this comes down to communication. Patients should be aware of why a podiatrist requires certain information, such as current medication, previous illness, previous drug therapy, surgery etc., otherwise the patient may not see the relevance and not divulge the information – potentially leading to misdiagnoses as a consequence of the incomplete information upon which the diagnosis is based. The podiatrist cannot do every possible test on every patient, and therefore intelligent use of the history may shorten the examination and yet make it more informative (DeMeyer 1998). Consent is a process, not a tick box, or one-off procedure – it results from open dialogue, not from getting a signature on a form. Completed consent forms afford some evidence that consent was obtained but mean little beyond that – it is important to realise they do not constitute ‘proof’ that the consent was valid. If there is any dispute over whether valid consent was obtained, the key issue will not be whether the patient signed a form or not, but whether they were given all the information they needed to make a considered decision. It is, therefore, crucial that the essential elements of discussions with the patient are documented in the medical record. The notes do not need to be exhaustive, but should state the nature of the proposed procedure or treatment and itemise the risks, benefits and alternatives brought to the attention of the patient. Any particular fears or concerns raised by the patient should also be noted. The locus of the Montgomery judgement (UKSC 11 2015, (Montgomery)), requires healthcare practitioners to tailor the information they provide to patients by judging what the reasonable patient would expect to know, given the circumstances of the situation, rather than by reference to a professional standard based on medical consensus, also known as the Bolam test (WLR 582, 587 1957). The judgement appears initially to reflect or endorse the view of consent by lawyers (Heywood 2015, Elliott 2015) and that of the General Medical Council guidance on consent (GMC 2008). The Supreme Court, in making its judgement in the Montgomery case, reviewed case law and professional guidance in the UK and judgements from other Commonwealth jurisdictions on consent and information disclosure. It held that while assessment of the risks and benefits of treatment is properly regarded as part of medical expertise, the decision about whether those risks, benefits and alternative options should be discussed with the patient is not purely a matter of professional judgement. ‘[T]he patient’s entitlement to decide on the risks to her health that she is willing to run (a decision which may be

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influenced by non-medical considerations)’ must not be ignored, and Bolam has no role to play in determining what patients should be told (Montgomery, see below, paras 83, 84). However, others have noted concerns about the judgement and how it may affect healthcare practice (Montgomery & Montgomery 2016, Farrell & Brazier 2016). After the physical examination it may be necessary to conduct a further specific examination or to undertake more robust tests, or to refer elsewhere for further opinion. Although these are explained as separate areas, they should be viewed as dynamic intertwined processes. Taking the history is usually the first, and perhaps most important, aspect of the assessment of, and interaction with a patient. It is a gathering of data that is not just about the specific complaint that brought the patient to the surgery and upon which the podiatrist will make the diagnosis. It is a learning experience for the practitioner about the patient, about how the patient experiences and views his or her symptoms and perhaps about the patient’s expectations of treatment. It also allows the patient to have a learning experience about the practitioner. Thus, it is the building block or foundation of future trust and a professional patient–practitioner relationship.

TAKING A COMPREHENSIVE PODIATRIC HISTORY The purpose of a consultation is two-fold. Firstly, it allows the patient to present the problem to the podiatrist, which is a therapeutic process in itself. Secondly, it enables the podiatrist to sort out the nature of the problem (diagnosis) and decide on any further course of action that might be needed. There are four key skills to history taking: • active listening • soliciting attribution • providing support • establishing agreement. The manner in which a podiatrist talks with rather than to a patient while taking the history, establishes the foundation for good care. Listen carefully; respond skilfully and empathetically (Bates 1995) – the active listening stage. The podiatrist needs to learn what exactly is bothering the patient, what symptoms he or she has experienced and what the patient thinks the trouble may be, how or why it happened and what the hopedfor outcome is. As the information is given, the podiatrist formulates hypotheses or a range of potential diagnoses. Do not attempt to plump for a diagnosis straight off, as this may close the mind to other signs and symptoms that do not fit with that hypothesis. The hypothesis/examination, or history taking, starts immediately the patient is introduced in the waiting room and the practitioner greets the patient. Too often practitioners miss the opportunity to observe patients unobtrusively while they are relaxed and apparently unobserved – from the time they are called to the time when the patient feels the consultation starts (i.e. when they are sitting on the patient’s chair). Significant opportunities for gait analysis are missed. The standard approach is to elicit the history before any physical examination (Marsh 1999), but this misses opportunities to observe patients in the waiting area without them knowing they are being observed. Indeed, in some cases the referral letter or the telephone call may elicit information needed within the history before the patient even attends the surgery. The atmosphere and setting of the assessment is as important as the examination itself. The patient should be assured of absolute confidentiality, and the assessment should not be rushed. Each patient expects, and deserves, full attention to and sympathy for their problems. The patient should feel confident in the podiatrist’s diagnostic abilities, but also in their empathy, understanding and motivation. ‘The history is

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the most important part of the patient’s assessment as it provides 80% of the information required to make a diagnosis’ (Marsh 1999). Assessment forms the basis for any planned intervention (Baker 1991), providing the baseline upon which subsequent intervention is measured and outcomes compared. Systematic, ongoing assessment is vital, to monitor and evaluate the success of care and detect new or different problems from those presented initially. This forms the basis of evidence-based practice and care.

ELEMENTS OF THE HISTORY The examination will consist of: • introductory information • chief complaints • past history • current health status • family/social history • psychosocial history • review of systems.

Introductory Information Introductory information includes the date of the history taking, identifying data or demographics (age, sex, ethnicity, place of birth, marital status, occupation, religion), source of referral (if any), source and reliability of the history. The history taking then proceeds to a discussion of the patient’s chief complaints. It is necessary to discuss with the patient why these particular pieces of information are required, especially as nowadays people are more attuned to discrimination for various reasons. Careful thought should be given as to why these pieces of information are really needed. Age can lead to vital clues as to which condition it is most likely to be, given that some foot pathologies are more likely to occur in early childhood, but the effects may produce other pathologies in later life. Furthermore, women are more at risk of some disorders than others; for example, rheumatoid disease is three times more likely in women than in men at a given age (Case study 2.1). The patient’s place of birth may lead to a diagnosis of a rarer form of systemic disease than would otherwise be suggested by the current place of residence; for example, someone now resident in the UK, but who was born and spent most of their early childhood in the Indian subcontinent, may have developed Hansen’s disease – a condition not normally associated with the UK. Marital status may provide assurance that the correct phrases and forms of address are used, and that no faux pas are made by the podiatrist leading to a breakdown in communications, for example, where children are concerned. Occupation is possibly the most easily explained question, as it may give vital clues to the amount of load or trauma the foot is undergoing, or specific conditions to which the foot is exposed. Religion, perhaps, will help to guide practitioners through some areas leading to non-compliance with management plans, or the inability of the person to communicate certain vital clues to diagnoses. Communication skills are required throughout, ensuring tact, diplomacy and empathy.

Chief Complaints – Soliciting Contribution This is the main focus of the history and the prime reason why the patient has presented to the practitioner. A detailed and thorough investigation of the current concern is vital, and comprises two essential but combined parts: the patient’s account of the symptoms (ensure that it is the patient’s view and not that of another, such as a carer or parent), that is the subjective symptoms; and the objective signs – those detected by the skill of the practitioner. The main aim is to obtain a comprehensive, succinct account of the patient’s perspective of the presenting symptom(s). There is a need to allow patients sufficient

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opportunity to describe their symptoms for themselves. The practitioner needs to practise patience and take care not to interrupt inappropriately. If the patient starts to drift, that is the time to interrupt and take control of the situation. Ask specific questions to obtain detail – the interrogative stage of the history taking. If the history is complicated, reflect on the information and recount it back to the patient, to ensure that he or she agrees with your interpretation. Attempt to be systematic and objective. Look for other supporting evidence to the interpretation, ensuring that questions are posed in a simple, unambiguous manner, without technical or medical jargon.

Past Medical History This includes information about the patient’s general state of health, childhood illnesses (remember the age of the patient and his or her country of birth), adult illnesses, psychiatric illness, accidents and injuries, and operations and hospitalisations. This information will help you gauge the patient overall, and how he or she views health and disease. It is also important to gain outline information of what investigations have been made during previous hospital admissions or at clinics, so reducing duplication of effort. Procedures or operations should be listed chronologically to help with future additions – they should be collected and reported with dates where possible. There is the need to pursue problems that are related to the underlying present condition or complaint.

Drug/Medication History It is advisable to request this information before the first appointment by advising the patient to present with a list of current medication (prescribed and over-the-counter medicine) and dosage. The drug history may give an indication of current illness. It is important to include home remedies, vitamin/mineral supplements, borrowed medicines, as well as prescription-only medicines and over-the-counter drugs. The drugs may be the cause of the symptoms (some cases of peripheral neuropathy may be induced by drug therapy), or the withdrawal of a drug therapy may be the reason why symptoms are now apparent (e.g. if the patient has suddenly stopped taking diuretics and suffers from swollen and painful ankles). Details should be obtained about possible drug allergies, to inform any decision about the continuation of a drug therapy. Also ask about other allergies such as hay fever, eczema, asthma or to latex.

Social History It is important to establish how the disease or complaint and patient interact at a functional level. Try to establish what the patient’s normal daily activities are and how his or her complaint has affected them. Smoking and alcohol consumption are the factors most frequently asked about in this regard, but it is essential that judgements are not implied by the manner in which the questions are asked. It is more difficult but equally important that the use of other related substances is also investigated.

Family History Information about the health and age of other family members can be useful, particularly where there may be a genetic link to disorders (Case study 2.2). It may be appropriate to identify age or cause of death of family members such as parents or grandparents.

Review of Systems • General – identify factors such as height, weight, recent weight changes, fatigue or fever. • Skin – look for rashes, lumps, sores, itching, dryness, colour changes, or changes in hair or nails. These may indicate systemic conditions such as diabetes or rheumatoid disease.

• Respiratory – signs of asthma, bronchitis, emphysema or past history of tuberculosis. • Cardiac – heart trouble, high blood pressure, rheumatic fever, heart murmurs, chest pain, palpitations and results of any heart tests. • Urinary – frequency of urination, polyuria, nocturia, burning pain on urination. • Endocrine – thyroid trouble, heat or cold intolerance, excessive sweating, excessive hunger or thirst. • Haematological – anaemia, easy bruising or bleeding, past transfusions and possible reactions. • Neurological – fainting, blackouts, seizures, weakness, paralysis, numbness, tingling, tremor, involuntary movements. • Peripheral vascular – intermittent claudication, leg cramps, varicose veins. • Musculoskeletal – muscle or joint pains, stiffness, arthritis, gout, backache.

ATTRIBUTES OF SYMPTOMS Patients may complain of symptoms that are local (e.g. to the foot or toe) or general (e.g. abnormal gait or more widespread aches and pains). Specific detailed questions by the practitioner can elicit the signs of the complaint. This should be a clear, chronological narrative which includes the onset of the problem, the setting in which it manifests, the means by which it presents, and any treatment that has been tried. The principal symptoms should be described using seven basic attributes (Bates 1995): • location • quality • quantity or severity • timing (onset, duration, frequency) • setting • factors which aggravate or relieve • associated manifestations. The amount of time spent on each component depends on a number of factors: the communication skills of the patient, underlying problem(s) and the listening skills of the practitioner. It is difficult to know when to interrupt and when to allow the patient to continue before stepping in and asking probing closed questions. It is essential, however, that the full circumstances of the presenting complaint are obtained. Once the various symptoms have been described, it is good practice to undertake a brief review of the symptoms (Marsh 1999) using a systems enquiry method. This may help to arrange the thoughts of the practitioner, highlight missing information or give guidance as to how to perform the physical examination in a logical sequence of actions. It is basically a screening method for establishing the areas that require detailed physical examination. When the presenting complaint appears to involve only one system, that system is promoted in importance in the examination and a detailed history of the presenting complaint and a more detailed physical examination of that system are made.

PERFORMING THE PHYSICAL EXAMINATION How complete should a physical examination of a patient be? This is a common question raised by students as well as experienced practitioners. There is growing concern over how much should be assessed and, therefore, how much should be recorded. There is a growing number of pieces of equipment that many podiatrists are starting to use for routine measurements within their practice. However, concern must be raised about the apparent overreliance on sophisticated equipment, which may have a place in some specialist settings but

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which, on the whole, is too expensive to become necessary in all clinics. Clinicians should rely first on the physical signs and symptoms to indicate whether a more detailed or rigorous assessment is required, and thereafter refer the patient for the specialist tests, or carry these out themselves at another time. In the majority of cases the simple routine consultation, which consists of physical examination together with the ability to use the assessment tools that we all have (i.e. use of the eyes, ears, hands, nose and common sense), should be sufficient. If more sophisticated equipment is to be used, then practitioners require adequate training not only in the use of the equipment, but also in the interpretation of the findings. Doppler ultrasound, which enables the sounds of the foot pulses to be identified and recorded, is becoming a routine practice. However, in untrained hands, this equipment can be used incorrectly and diagnoses may be either wrongly interpreted or missed altogether. The equipment may make podiatrists look more professional and more sophisticated. However, the ability to use the equipment correctly, interpret the results accurately and record clearly as well as refer appropriately is something that should be taken seriously. Therefore, the answer to the question as to how complete an examination should be depends on the signs and symptoms at presentation. The examination and assessment should be related exclusively to the complaint the patient presents with, unless it is thought that a complete and full examination is required to exclude or include other signs and symptoms noticed during the question phase of the assessment process. For patients who have symptoms related to a specific body part (or foot region), a more limited examination may be more appropriate (Bates 1995). It is the duty of the practitioner to select the relevant methods to assess the problems as precisely and efficiently as possible. The symptoms, along with the demographic data (age, sex, occupation and previous history) collected, influence that selection and determine what examination is required. Knowledge of disease patterns, and the practitioner’s previous knowledge and experience of other conditions also influence the decision. These are all component parts of the clinical thinking, or reasoning process. When undertaking the physical examination, a sequence that maximises the practitioner’s efficiency while minimising the patient’s efforts, yet allows thoroughness by the practitioner, is the best. Two important details need to be considered: the positioning and the exposure of the patient. Ideally, the whole limb being examined ought to be exposed, but in practice it is usually sufficient only to expose the leg from above the knee distally. (Anderson & Black 1997) This level of exposure should give the practitioner sufficient sight of the main areas of complaint, without requiring exposure that the patient might feel is not justified for a podiatric examination. Remember at all times that the patient will present with a preconceived idea of what a podiatrist does and what areas of the body they should examine! Although the profession may be expanding the roles of the podiatrist to include the whole of the lower limb for some examinations and assessments, if the podiatrist needs to examine or assess structure(s) above the ankle they will require to explain and justify in detail why they need to perform this examination and assessment, and gain informed consent to do so before actually doing so! It is important to be able to palpate and see the knee during the examination, whether the patient is seated or standing (weight bearing). Thus, where possible, trousers should be rolled up to expose the full knee and patella. It is also important that both legs and knees are visible, even when the patient is complaining of problems in only one

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foot. Comparison, one with the other, is a vital source of data gathering. In most cases patients are examined in a semi-supine position and are positioned at a higher level than the practitioner. However, where a more accurate biomechanical examination is required, the prone or supine position may be adopted. Whatever the position, it should not be uncomfortable or embarrassing for the patient for the duration of that examination. The patient must be able to be relaxed in the position chosen or false data may be gathered. According to Anderson & Black (1997) it is good practice, and ensures that nothing is missed, to adopt a systematic set pattern for the examination, proceeding from the superficial (skin and soft tissues) to the deep structure (bone and joints) and from the local to the general. The sequence of a comprehensive examination should be: a general survey, mental status, skin, musculoskeletal system, cardiovascular and neurological systems, followed by specific peripheral neurological and vascular systems and the important aspect of footwear (see Ch. 21). The purpose of this chapter is not to give detailed information about the physical examination, but rather to provide an overview of those aspects likely to be performed in routine clinical practice. More detailed books are available (Hayes & Barbaro-Brown 2017, Turner & Merriman 2005, Yates 2012) and there are various journal articles on each aspect of the process. The general survey should give an overall impression of the patient’s general attributes, but these may vary according to socioeconomic status, nutrition, genetic makeup, early illness, gender, and the country and era of birth. The overview should encompass areas such as: • apparent state of health – robust, acutely or chronically ill, frail • signs of distress – laboured breathing, wincing, limping, sweatiness, trembling • skin colour – pallor, cyanosis, jaundice, rashes and bruises • height and build – tall, short, muscular, disproportionate, symmetrical (e.g. Turner’s syndrome, child may be of short stature) • weight by appearance or measurement – emaciated, slender, plump, fat, obese, (although what is the appropriate weight is controversial) • posture, motor ability and gait – posture, which aids breathing, or pain, ataxia, limp and paralysis – does the patient walk easily, confidently, balanced? • dress, grooming and personal hygiene – excessive amount of clothing may mean hypothyroidism, long sleeves may be to cover rashes or needle marks. Is the patient wearing unusual jewellery, such as copper bands which might indicate arthritis? Is personal hygiene reflective of the patient’s mood, personality, lifestyle, occupation and socioeconomic grouping? • facial expressions – observe these throughout the encounter, during the physical examination (immobile face of Parkinsonism; grimacing when certain areas are touched) • odour of body or breath – breath odour of alcohol, acetone (diabetes).

Mental Status The patient’s mental status should be observed throughout the consultation, and the appropriateness of behaviour and the ability of the patient to comply with any management plan suggested should be noted. Level of consciousness can be evaluated by observing the patient’s responses to verbal and tactile stimuli, and their alertness during the interview or clerking process. For example, this may indicate lethargy or stupor. During the short walk to the surgery from the waiting area, and while seated during the interview, the practitioner should observe the patient’s posture and motor behaviour, and look for restlessness, agitation, bizarre postures, immobility or involuntary movements, along with pace, range, character and appropriateness of

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movements. The patient’s dress, grooming and personal hygiene can be evaluated in terms of neglect or fastidiousness. The facial expressions during rest and interactions should be observed for anxiety, depression, elation, anger or withdrawal. The mood of the patient should also be assessed to gauge the level of happiness, elation, indifference or anxiety. All may give clues as to how the patient views the current problem, how it is affecting his or her daily activities and how the patient may respond to suggestions about altering behaviour patterns adversely affecting their feet (e.g. inappropriate footwear).

Skin (see also Chs 3 and 4) Look and observe, touch and palpate skin over the foot and lower limb, and observe the following: • texture – coarse, fine, dull or shiny, smooth or rough • colour – cyanosis, jaundice, changes in melanin, pallor, erythema, pigmentation, gangrene • temperature – cool, warm, distinctly hot, normal temperature gradient • humidity – moist, dry, oily, areas of maceration, dryness associated with hypothyroidism, oiliness in acne • elasticity – mobility, ease with which a fold of skin can be moved, decreased oedema • hyperkeratosis – corns and callus formation, sites, texture, quality • hair – presence, absence, quantity, thickness, distribution, texture • integrity – fissures (especially heel or interdigital clefts), ulcers, abrasions • dermatoses (eczema, psoriasis) • surgical interventions – scars, infections. It is important to note any lesions, their anatomical location, whether they are generalised or localised, their arrangement (linear, clustered, dermatomal), the type (macule, papule, bulla, tumour, etc.) along with colour (red, brown, white, mauve) and whether raised or indurated.

Nails (see also Ch. 3) Inspect and palpate these, identifying: • structure – ridged, cracked, thickened • extent – overgrown, onychogryphotic, stunted, ingrowing, chewed, picked • colour – cyanosis, pallor • shape – club, excessive curvature • subungual abnormality – swelling, pigmentation • lesions – paronychia, onycholysis.

Swellings Palpate and inspect any swellings, and note: • tenderness – local or radiating • consistency – hard, firm, soft, fluctuant • adherence to underlying structures – to skin, underlying soft tissues, bone • transillumination – does swelling transilluminate to light? • temperature.

Musculoskeletal System (see also Chs 8 and 9) The musculoskeletal system should be assessed using a screening method to ensure that lower limb manifestations of systemic disorders are encompassed within the assessment process. This assessment will include an inspection of the joints and the surrounding tissues, and observation of the following: • Ease and range of motion – assess for limitation in movement, but also any unusual increase in mobility of the joint, which might lead to instability. Range of motion varies between individuals and decreases with age (Fig. 2.1).

Fig. 2.1  Testing the range of motion – in this case the ankle joint.

• Signs of inflammation and swelling in or around the joint. The swelling may involve the synovium, which feels soft and boggy, or doughy to the touch, or it may produce excessive synovial tissue fluid within the joint space. Palpable bogginess suggests synovitis; palpable joint fluid indicates effusion in the joint. Synovitis and joint fluid may well coexist. Swelling may originate outside the joint itself and may come from the bone, tendons, tendon sheaths, bursae or fat. Trauma to any of these structures produces swelling. Tenderness in or around the joint should be investigated and assessed. An attempt should be made to define the specific anatomical structure that is tender, as trauma may also cause tenderness. Arthritis, tendinitis, bursitis and osteomyelitis all produce symptoms of tenderness. Increased heat can be assessed using the back of the hand or fingers to compare the joint with the corresponding one of the opposite foot or, if both joints are involved, with similar joints or tissues near them. This gives a better indication of whether the increased heat is localised or generalised. It may also lead to better diagnosis of the problem. For example, rheumatoid disease may manifest as generalised increased heat in the more proximal joints and soft tissues surrounding the joints, compared with osteoarthritis. Redness of the overlying skin over a tender joint suggests gout or septic arthritis, but is possibly the least common sign of inflammation of the joint (Bates 1995). • Condition of the surrounding tissues – look for signs such as muscle atrophy, subcutaneous nodules and skin changes. • Crepitus or crepitation, a palpable, sometimes audible, crunching or grating produced on movement of a joint or tendon. A fine, soft crepitus might be experienced over inflamed joints, whereas a coarser crepitus suggests roughened articular cartilage, as found in osteoarthritis. • Any musculoskeletal deformities, including abnormal curvature of the spine. Deformities such as those due to malalignment of bones (genu varum, valgum) or those produced by restricted range of motion (e.g. Dupytren’s contracture) may lead to lower limb and foot biomechanical abnormalities, or interfere with the way in which the patient manages his or her foot problems.

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• excessive wear at medial edge – excessively pronated foot. • Heel and sole wear: • excessive wear on lateral side – supinated foot from pes cavus, weakness of evertor muscles such as peroneal, as in peroneal muscular atrophy • excessive wear on medial side – excessively pronated foot • lateral heel to medial sole – if excessive may be the result of externally rotated leg or forefoot abduction • lateral heel to lateral sole – leg might be internally rotated or there may be forefoot abduction • medial heel to medial sole – excessively pronated foot. • Sole wear: • excessive across whole of tread – pes cavus • excessive at tip – drop foot, spastic flat foot, result of neurological disease affecting dorsiflexors • excessive under hallux – hallux rigidus or limitus • excessive under lateral side – metatarsus adductus. Deformity at heel counters, which may suggest excessive pronation or supination, should also be noted. Fig. 2.2  Examination of the movement of the first ray.

When examining a patient with a suspected musculoskeletal problem and presenting with painful joints, it is important that the practitioner is gentle and moves the joint slowly. It is a difficult balance to achieve between being gentle and not being afraid to cause some discomfort in order to ensure proper examination to uncover the true cause of the complaint. Each joint complex within the foot should be assessed individually, comparing one side with the other. Thus the ankle, subtalar and midtarsal joint complexes should all be assessed and compared with the corresponding joint complex on the other limb, and an assessment should be made of the range of motion normally expected for that complex, giving due regard to the age and sex of the patient. The first and fifth ray (Fig. 2.2) should be included in this assessment, and the foot should also be viewed holistically (i.e. both weight bearing and non-weight bearing). Where rheumatoid disease is suspected, it may be necessary to make an individual assessment of the metatarsal joints by gripping the forefoot across the metatarsal heads and squeezing gently transversely.

Footwear (see also Ch. 21) Footwear gives a variety of clues as to diagnosis, and therefore it should also be examined during the patient’s first visit. Footwear should initially be checked for size, shape, style, suitability for the patient’s foot and occupation, and indications of (abnormal) wear marks. Abnormal wear on the soles and heels of the footwear will give some indication as to the gait and weight-bearing patterns of the gait cycle. Inspection of the outer sole and insole can also provide valuable clues about the relative pressures occurring during the foot-flat and take-off phases that occur during mid- and forefoot postures. The shape or distortion of the upper also gives important data as to abnormal frontal plane motion. Abnormal wear of the sole, such as a circular pattern across the forefoot, suggests a rotational element or circumduction of the forefoot on the rearfoot typical of a rearfoot varus. Some wear patterns might suggest particular gait patterns (Anderson & Black 1997): • Heel wear: • excessive wear at rear edge along entire edge – calcaneal gait, as in calcaneal gait of spina bifida • excessive wear at anterior edge – excessively pronated foot or broken shank • excessive wear at lateral edge – supinated foot occurring in pes cavus, painful first ray (postoperatively)

Vascular Assessment (see also Ch. 5) As podiatry moves to evidence-based systems of healthcare, podiatrists need to produce evidence that vascular assessment of presenting patients is beneficial. Farndon et al (2018) have produced some evidence of where podiatry might assist suggesting ‘Podiatrists are able to provide a comprehensive vascular assessment of the lower limb and accompanying tailored advice on lifestyle changes including smoking cessation and exercise’. This does not mean the use of more sophisticated equipment, but the clinical ability to diagnose accurately possible risk factors from signs and symptoms and simple evaluative tests. Those patients potentially at risk of lower limb amputation and receiving podiatric care are nearly four times less likely to undergo such amputation than those not receiving podiatric care. However, it is essential podiatrists do not depend solely on equipment to make their diagnoses, but instead rely mainly on their clinical and physical examination skills. Equipment is expensive, the results obtained are liable to misinterpretation and there are problems of validity and reliability. Recent research suggests, due to time constraints on podiatrists, a targeted screening method may be useful although acknowledges obtaining accuracy in lower limb assessments is difficult (Tehan & Chuter 2016). The vascular section of the patient history and the physical examination are vitally important, and a misdiagnosis of vascular disease may result in significant morbidity (Nelson 1992). Podiatrists must be acutely aware of the potential limb loss, gangrene, ulceration and infection attributed to underlying arterial disease, and therefore the need for a peripheral vascular evaluation. Infection management, wound management and preoperative assessment, all require appropriate evaluation of the vascular status of podiatric patients. Hoffman (1992) suggests that ‘with non-invasive arterial evaluation, the clinician must have a diagnosis in mind before initiating the testing, know exactly what data need to be documented, and be able to question the validity of what is being recorded’. Podiatrists understand the need for a sufficient vascular supply and thus must have the ability to evaluate that supply, ensuring that there is sufficient flow entering the leg or foot to sustain normal nutrition, to heal an existing ulcer or to sustain nutrition following surgery, depending on other factors, such as age. Pain is a common symptom of vascular disease. The three components of the vascular ‘tree’ – arterial, venous and lymphatic – all have differing manifestations and pain severity. It is imperative that practitioners differentiate between the different types of pain, and differentiate between ‘rest pain’ and the night cramps of a venous disorder.

20

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The patient with rest pain complains of intense burning in the toes, the severity increasing with coldness or when the foot or leg is elevated; they may state that they obtain relief by putting the foot into the dependent position by hanging the limb out of the bed. This severe, persistent pain is associated with ulceration or gangrene, and is indicative of a more severe arterial disease. A sudden or abrupt onset of severe pain may suggest an acute arterial or venous obstruction. In the acute arterial occlusion the pain is immediate and persistent. It may be accompanied by a sensation of coldness, tingling and numbness distally to the occlusion site. On the other hand, the pain associated with venous occlusion is similar to that of phlebitis, which is characterised by a severe ache over the involved vein. There may also be an accompanying burning or swelling of the ankle and foot. The ‘classic’ pain normally found with chronic arterial insufficiency is termed ‘intermittent claudication’. This symptom is transient, is usually induced by exercise and is characteristically described as cramp, ache, tiredness or tightness of the associated muscles (usually the calf, but it can be the buttocks or the small intrinsic muscles of the foot). The main diagnostic criterion is that rest relieves the pain. The clinician must differentiate between orthopaedic and neurological conditions producing pain and the pain of intermittent claudication. Claudication distance can be evaluated using external factors, such as the distance the patient can walk by counting the number of lamp posts, or between two known landmarks, or clinically by the use of a treadmill. The latter allows variations of speed and of slope, and this helps in determining which factors make the situation worse. This allows the clinician to guide the patient as to what pace to take and what characteristics of the landscape to avoid (e.g. advising the patient to find routes that avoid hills). The ischaemia from acute or chronic arterial occlusion will ultimately lead to ischaemic neuropathy. The pain associated with this is sharp and shooting but poorly localised in nature. The ability to heal is of paramount importance, especially where elective surgery is considered. Thus the clinician must be able to hypothesise and predict healing ability. Normally, adequate blood flow equates with healing ability. However, certain conditions – such as anaemia, alcoholism, uncontrolled diabetes, some connective tissue diseases and poor nutrition – refute this general assumption. Poor nutrition may be found in the elderly or alcoholics, and may result from inadequate oxygenation. Simple questions such as ‘How quickly does your skin normally heal after it has been damaged?’ should be used alongside a visual inspection of skin. It is important to realise that the physical examination should correlate with the signs and symptoms described by the patient. Where there is a lack of correlation, a double check or further more detailed investigations may be warranted. For example, pedal pulses may be absent, but on its own this sign may be insignificant; similarly, the presence of pedal pulses does not necessarily indicate adequate pedal perfusion. The most significant findings aiding clinicians to diagnose the presence of peripheral arterial disease are abnormal pedal pulses, a unilaterally cool extremity, prolonged venous filling time and a femoral bruit. Other physical signs help determine the extent and distribution of the disease, but findings such as abnormal capillary refill time, foot discolouration, atrophic skin and hairless extremities are unhelpful to diagnosis. Within the pedal pulses, the absence or diminution of the posterior tibial pulses is a more accurate indicator than is an absent dorsalis pedis pulse (Criqui et al 1985). Palpation of pedal pulses is crucial (Dormandy 1992, Nelson 1992) and has developed over time (Ghasemzadeh & Zafari 2011), but clinical experience indicates that there is a lack of precision associated with these pulses (Kazmers et al 1996), and accuracy has been suggested to be greater with experience and caution is recommended in using the

pulse alone (Brearley et al 1992). The dorsalis pedis pulse appears to be more easily identified than that of the posterior tibial pulse (Dormandy 1992). Each clinician has a different ability to palpate these pulses. In the foot the pedal pulses to be palpated are the posterior and anterior tibial and the dorsalis pedis. The dorsalis pedis pulse is palpated lateral to the extensor hallucis tendon at the base of the first metatarsal, however Mowlavi et al (2002) suggest that practitioners should in fact use the ‘dorsal most prominence of the navicular bone’ as a bony landmark to readily locate the dorsalis pedis artery; the anterior tibial pulse is found at the front of the ankle, whereas the posterior tibial pulse is located below and behind the medial malleolus, with the foot slightly inverted. The absence of peripheral pulses appears to have a low congenital absence, therefore the absence of a peripheral pulse in later life may be a more significant marker of peripheral arterial disease (Johnson & Epstein 1996, Robertson et al 1990). Unfortunately there is no standardisation of gradation of pulses or how they are recorded. Thus confusion exists as to how they should be recorded, with adjectives and verbs being used to describe the quality, rhythm and rate of the pulses as well as the amplitude. The most frequently used scale is (Kidawa 1993, Nelson 1992): 0/4 – absence of pulses 1/4 – weak (may suggest impairment) 2/4 – normal 3/4 – full 4/4 – bounding (may suggest aneurysm). Baker (1991) suggests that pulses should be recorded as normal, decreased or absent. He does, however, anticipate a fourth category, where pulses are greater than expected. As the assessment is subjective, it is probable that these descriptions are all that is required. Clinicians demonstrate fair to almost perfect agreement when stating a pulse was present or absent, but disagreement occurs when attempting to distinguish between normal and reduced pulses. Where both pedal pulses are absent there is more likelihood of vascular disease than when only one is absent (Reich 1934, cited in McGee & Boyko 1998). This is because where the dorsalis pedis pulse is absent, the posterior tibial pulse will act as a collateral supply, and vice versa. The reproducibility and accuracy of pulse palpation can be increased by undertaking the assessment under unhurried, good, quiet conditions. The foot and lower extremities should also be inspected, taking account of colour, texture of skin, trophic changes, hair growth, oedema and ulceration. For further information on vascular disease, see Chapter 5. Oedema of the lower leg or foot can be the result of a variety of diseases. An assessment of whether the oedema is unilateral or bilateral may suggest if it is local or regional in the former, or systemic if the latter. It must also be differentiated by palpation. Is it pitting (i.e. soft in nature, leaving a depression after 15–30 seconds) or indurated (non-pitting)? Oedema associated with systemic disease is generally pitting, occurring bilaterally and involving the whole leg or foot to the level of the toes. Swelling of venous origin may also be pitting, but it is usually unilateral, and the oedema of varicosity or venous stasis is obvious due to bulging varicosities of the perforating veins just above the medial malleolus during weight bearing. There may also be haemosiderosis or brownish pigmentation around the site. Ulceration may be one of the first external signs and symptoms of arterial disease. Ischaemic or arterial ulcers are usually painful and are found on the anterior or lateral lower leg above the ankle, whereas venous ulcers are usually painless and found on the medial lower leg just above the medial malleolus. Table 2.1 highlights the differential diagnosis between arterial and venous insufficiency. Where pedal pulses are not palpable, Doppler studies may help. The Doppler scanner is one of a number of non-invasive evaluation

CHAPTER 2 

Examination and Diagnosis in Clinical Management

21

TABLE 2.1  Signs and Symptoms of Peripheral Vascular Disease Arterial Insufficiency

Venous Insufficiency

Acute Pain – severe, steady Cold pallid limb Diminution/loss of sensory and motor function Absent pulsation beyond embolus Veins collapsed No swelling (unless ischaemia advanced)

Steady, moderate to severe Skin warm, may be mottled, cyanotic No significant neurological deficit Pulses present or diminished Veins filled (legs dependent) Usually moderate to severe swelling, with tenderness over veins and muscles

Chronic Intermittent claudication progressing to rest pain with severe ischaemia Extremity cool, distal pulses diminished Delayed healing of minor traumatic lesions Atrophy of skin, loss of hair on toes Pallor when elevated, rubor when dependent Ulceration, superficial gangrene

techniques available to some podiatrists. The Doppler can be used to extend clinical examination by detecting pulses over a very wide range. Therefore, it is primarily useful for measuring distal blood pressures. The use of the Doppler scan has become more widespread in podiatric practice, but the successful use of this device depends on a number of factors. According to Chen et al (2012) there is no recommended technique for ankle–brachial index (ABI) measurement. The tip of the Doppler probe must be coupled to the skin using an ultrasound-coupling medium, and the angle of the probe to the artery is important. The correct range of this angle has been reported to be from 45° to 60°, but there is debate about whether this angle is to the skin or to the artery (Baker 1991, Hoffman 1992). Whatever the angle, the probe should be placed in the direction of the heart. Light application of the probe to the skin surface is sufficient to ensure good detection in most cases. If excessive pressure is applied, occlusion of the artery is possible. Arteries and veins generate characteristic signals, which must be differentiated. The normal distal artery has a biphasic or triphasic sound, with a brisk systolic upstroke followed by a less prominent early and mid-diastolic component (Baker 1991). In occlusive arterial disease the systolic component may be less prominent, with few or no diastolic parts. In severe disease there may be only one continuous sound. Large and medium veins produce a low-frequency sound, which has often been likened to that of wind blowing through trees (Baker 1991). The slower the blood flow, the lower the audible pitch. The most common use of Doppler is to measure the ABI or ankle– arm index. Ankle blood pressure should be approximately 90% of the brachial artery systolic pressure (Nelson 1992). The ABI is usually classified as shown in Table 2.2. To measure the pressure at the ankle, the cuff is placed around the ankle of a supine patient with the foot at the same level as the heart. The sounds through a pedal vessel are located and the cuff is slowly inflated until no sounds are detected. The cuff is then slowly deflated until a sound is heard, and the pressure of the ankle cuff is noted. The arm, or brachial, pressure is also noted. The ankle measurement is divided by the brachial reading and the resultant figure (the ABI) is recorded. However, care needs to be used when interpreting the results of the ABI. If the ABI is 1 there is good flow velocity; this indicates only the adequacy of blood flow at the ankle level. It does not indicate adequacy of any flow below this level. In diabetes, in particular, there may be distal occlusions in the foot, and thus ankle blood flow cannot be used to estimate blood flow in the foot (Hoffman 1992). The ABI

Aching, heavy-legs sensation, muscle cramps Prominent, superficial veins, warm feet Pigmentation, oedema of lower leg Haemosiderosis, soft pitting oedema disappears overnight, unless of longstanding, when it becomes fibrosed, harder and firmer Scaling, thickening and scarring of skin Ulceration around ankle, medial malleolus

TABLE 2.2  The Ankle–Brachial Index (ABI) Pressure/ABI

Indicator

0.9–1.00 0.5–0.9 38 °C or 90 beats/min, respiratory rate >20 breaths/min or hyperventilation with a Paco2 12,000 or 1 cm usually located primarily in the dermis and or subcutis A circumscribed lesion ≤1 cm in diameter that contains liquid A circumscribed lesion >1 cm in diameter that contains liquid A circumscribed lesion that contains pus Dried serum, blood or pus on the surface of the skin A visible accumulation of keratin, forming a flat plate or flake Loss of either a portion or the entire epidermis

Lentigo maligna melanoma (see Fig. 4.31)

Papule Nodule Vesicle Bulla Pustule Crust Scale Erosion Ulcer

Spitz naevus (see Fig. 4.26) Nodular basal cell carcinoma (see Fig. 4.17) Pompholyx (see Fig. 4.6) Bullous pemphigoid (see Fig. 4.14) Palmoplantar pustulosis (see Fig. 4.3) Acral melanoma (see Fig. 4.33) Psoriasis (see Fig. 4.2) Erosions from scratching eczema (see Fig. 4.4) Full thickness loss of the epidermis plus at least a portion of the dermis; it may extend to the subcuta- Ulcerating squamous cell carcinoma (see neous tissue Fig. 4.19)

From Nast A et al 2016 British Journal of Dermatology 174:1351–1358. Layers of the epidermis Corneum Granular

Epidermis

Spinous Basal

Dermis

Subcutaneous fat Fig. 4.1  A diagram of the skin and the key components.

Psoriasis and Related Disorders Psoriasis is a common chronic inflammatory skin condition. Estimates of the prevalence of psoriasis differ but a commonly quoted figure is 2% (Christophers 2001). However, estimates vary from around the world from between 0.91% in the USA to 8.5% in Norway in adults, but it is consistently less common in children with a prevalence of 0% in Taiwan and 2.1% in Italy (Parisi et al 2013). It can affect any age group, but onset is most common in early adulthood and late middle age. The pathophysiology of the disease is complex and involves genetic susceptibility centred around the psoriasis susceptibility 1 locus, both the adaptive and innate immune responses, and key cellular mediators including tumour necrosis factor α (TNFα), and interleukins 12, 17, 22 and 23. A primary initiation phase triggers chronic pathological inflammation perpetuated by feedback loops and amplification which causes abnormal keratinocyte proliferation with epidermal and dermal immune cell infiltration (Greb et al 2016).

Psoriasis can be triggered or exacerbated by a number of factors including: trauma (psoriasis appearing at sites of injury such as operative scars is called the Köebner phenomenon), medication (lithium, antimalarials, tetracyclines, non-steroidal anti-inflammatory drugs and the injudicious rapid withdrawal of systemic steroids), infection, especially streptococcal pharyngitis which triggers guttate psoriasis. Psychosocial stress may play a role in the exacerbation of psoriasis, but the exact pathophysiology is unknown; one mechanism postulated is a mechanistic link between the immune and nervous system (Hunter et al 2013). Psoriasis causes great psychosocial stress and can have a profound effect on the quality of life. Furthermore, the degree of psychological disability is not always mirrored by the extent of the psoriasis so that even when small areas, such as the hands or feet, are involved the effect on the function and psychology of the patient can be disproportionate. There are a number of comorbidities associated with psoriasis and these include: psoriatic arthritis present in 6–42% of patients, cardiovascular disease in those with moderate to severe

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Dermatological Conditions of the Foot and Leg CASE STUDY 4.1  Plantar Hyperkeratosis –

Outline of Differential Diagnosis and Management

Fig. 4.2  A typical plaque of chronic plaque psoriasis.

psoriasis, obesity, hypertension, diabetes, metabolic syndrome, inflammatory bowel disease and non-alcoholic fatty liver disease. Other emerging associations may include chronic renal disease, chronic obstructive pulmonary disease, obstructive sleep apnoea and cancer. Lymphoma has been consistently associated with psoriasis (Takeshita et al 2017). Psoriasis is increasingly considered a systemic rather than a skin-only inflammatory disease given its systemic disease associations driven by the production of proinflammatory cytokines and sometimes referred to as the ‘Psoriatic March’ (Furue & Kadono 2017). The severity of psoriasis can be assessed by the psoriasis area and severity index (PASI) score. PASI combines the severity (erythema, induration and scaling) with the extent of the psoriasis into a single score. This is useful in measuring objective response in clinical trials, in which 75% improvement (PASI 75) is one endpoint. However, with increasingly effective treatments PASI 90 is commonly reported. The PASI is mainly a measure of extent and severity of the disease but it does not measure the patient’s quality of life. There are a number of patient reported outcomes to assess the quality of life and these include the Dermatology Life Quality Index (DLQI) (Finlay & Khan 1994) a frequently used measure and the Psoriasis Disability Index (Finlay & Kelly 1987). Chronic plaque psoriasis is the most characteristic form. Patients present with circumscribed itchy patches of thick, scaly, red skin often prominent on the elbows, knees and scalp, although any body site can be affected (Fig. 4.2). Other variants include: • guttate psoriasis, in which multiple small patches of psoriasis erupt acutely after a streptococcal throat infection. • erythrodermic psoriasis, a rare medical emergency in which more than 80% of the skin becomes red and inflamed. • pustular psoriasis, in which numerous sterile pustules stud the surface of affected skin and patients may become systemically unwell. However, there is debate about phenotypes of this disorder as it can occur with and without the presence of stable chronic plaque psoriasis (Navarini et al 2017). The feet are commonly involved in psoriasis. Typical pink or red plaques with a superficial layer of fine silvery white scale may be seen on the dorsum of the foot, while more hyperkeratotic, fissured skin is seen on the plantar surface, particularly at sites of pressure. Psoriasis commonly also causes nail dystrophy, including separation of the nail plate from the nail bed (onycholysis) or subungual hyperkeratosis. Fine indentations or pitting of the nail plate may also be seen; this is

A 25-year-old obese secondary school teacher presented with plantar hyperkeratosis. The problem had been present for 6 months. He was finding it difficult to walk as the skin of his feet had become painful through deep fissuring, and very itchy. There was a family history of psoriasis. A careful examination revealed well demarcated scaling plaques at the elbows and knees with a nail dystrophy affecting mainly the toenails but also the finger nails. The nails were hypertrophic, onycholytic and pitted. The differential diagnosis included a fungal infection of the feet and nails which was excluded by a negative fungal culture result. Eczema was dismissed as a diagnosis after the history and clinical examination confirmed a diagnosis of psoriasis. The patient’s foot symptoms of pain due to fissuring concerned him greatly. Simple emollients and potent topical steroids under occlusion were ineffective. Weight loss was advised. Due to his work commitments a course of topical PUVA was not practical. A trial of acitretin was undertaken for 3 months but the patient discontinued the medication because of intolerable dry skin; however, he did notice some improvement in his foot symptoms. After careful discussion he was successfully established on methotrexate with relief of his foot discomfort. Even minimal involvement of the skin with psoriasis can produce significant patient concern and distress. This is especially likely to occur on visible or functional sites. It is important to start with pragmatic and safe treatments but be prepared to amend and increase the treatment if there is no satisfactory outcome. Treatments should be tailored to the patient’s lifestyle, be given with suitable counselling and in partnership with the patient.

more prominent on finger nails. Psoriatic arthritis may be an additional problem, and can present with pain and decreased mobility in the axial skeleton and the small joints of the hands and feet. A rare mutilating form of arthritis can result in significant resorption of bone in the digits (See Ch. 8, Musculoskeletal podiatric medicine further information on psoriatic arthritis). Differentiating psoriasis from other causes of thickened scaling rashes on the feet can be difficult. The differential diagnosis includes eczema, lichen planus, keratodermas and fungal infection. It is important to look for typical signs of psoriasis at other sites and to enquire about a positive family history of the disease. Treatment. Regular emollients reduce scaling and fissuring, and keratolytics such as 5% salicylic acid in suitable emollients such as emulsifying ointment are helpful. There are many topical treatments available including the vitamin D analogue calcipotriol, topical steroids, coal tar-based preparations, dithranol (anthralin) and vitamin A-derived drugs (retinoids). A pragmatic time to apply these topical treatments is at night. Patients may benefit from treatment with narrow band ultraviolet B (UVB) phototherapy. Narrow band refers to the wavelength output of the special bulbs at 311 nm. Wavelengths of between 254 and 313 nm are particularly effective at treating psoriasis (Parrish & Jaenicke 1981). Topical photochemotherapy can be used to treat only the palm of the hands or sole of the foot. This treatment uses a photosensitising agent, a topical psoralen, in combination with ultraviolet A light and is often referred to as topical PUVA. More severe cases as judged by the extent of the disease or functional incapacity may require treatment with systemic therapy such as the oral retinoid acitretin, or immunosuppressive agents such as methotrexate (Case study 4.1) or ciclosporin (Warren et al 2008). Ciclosporin and acitretin require close supervision for bone marrow, liver or kidney toxicity.

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61

the soles of the feet and may not appear for several months after the onset of arthritis and conjunctivitis. Affected patients have thick, ‘limpet-like’ hyperkeratoses with a dull yellow discolouration or a more acute pustular rash. Patients need to be treated for the underlying infection. Those that go on to develop chronic reactive arthritis may need treatment with second-line drugs such as methotrexate or sulfasalazine. Biologic agents are sometimes needed for refractory disease (Schmitt 2017).

Pityriasis Rubra Pilaris (PRP)

Fig. 4.3  Palmoplantar pustulosis.

The use of biologic agents is transforming the treatment and the quality of life of patients with psoriasis. Biologic drugs are highly effective although expensive. The development of biosimilar agents (generic biologic agents) is anticipated to reduce the cost and widen availability of these medicines. The use of biologic agents has come about from a deeper understanding of the key components of the pathophysiology of psoriasis. Different monoclonal biologic treatments target specific inflammatory molecules important in the pathogenesis of psoriasis, and these include TNFα (adalimumab, etanercept, infliximab), interleukin 12/23 (briakinumab, guselkumab, tildrakizumab and ustekinumab) and interleukin 17 (brodalumab, ixekizumab, secukinumab) (Campa et al 2016, Jabbar-Lopez et al 2017). Patients on these agents need careful supervision and need to be warned about the risks of infection. Whilst the biologic agents require injections, new oral therapies ‘small molecules’ are also being developed and these include apremilast (an oral phosphodiesterase-4 inhibitor) and tofacitinib (an oral janus kinase inhibitor) (Tan & Griffiths 2016).

Palmoplantar Pustular Psoriasis (PPP) Palmoplantar pustulosis can be defined as primary persistent (>3 months), sterile, macroscopically visible pustules on palms and/or soles and can occur with or without plaque psoriasis (Navarini et al 2017). Extensive plantar disease can result in pain on weight bearing. PPP is more common in women in the sixth and seventh decade of life and is strongly associated with cigarette smoking. It typically presents with red scaly hyperkeratotic palmar and plantar skin studded with sterile pustules (Fig. 4.3). Fresh pustules initially appear yellow and subsequently dry to leave brown discolouration. The differential diagnosis includes acute infected eczema, dermatophyte fungal infection and reactive arthritis (Reiter’s disease, see below). Treatment of PPP is difficult and the treatments used are similar to those of psoriasis including topical, phototherapy, systemic agents and biologic agents (Misiak-Galazka et al 2017).

Reactive Arthritis (Reiter’s Disease) This is a reactive disorder in which arthritis, urethritis, conjunctivitis and inflammatory mucocutaneous disease are triggered by urogenital or gut infections. It is commonly seen following Chlamydia trachomatis urethritis but other organisms are implicated including Salmonella, Shigella, Campylobacter and Yersinia. The mucocutaneous signs of the disease include oral ulceration, erythema nodosum (a panniculitis commonly on the lower leg) and circinate balanitis. In the feet, the classic cutaneous finding is keratoderma blenorrhagicum, a psoriasis-like eruption that usually affects

This is a rare group of disorders divided into five different types. The most common (type 1) usually affects adults and spreads from the head to the feet with ‘islands of sparing’ of normal skin. The rash has a distinctive orange ‘salmon pink’ colour or yellowish hue and is pronounced on the palms and soles. A nail dystrophy may also occur including longitudinal ridging, subungual hyperkeratosis and splinter haemorrhages (Griffiths 1980). The disorder can be difficult to differentiate from psoriasis. Treatment is difficult but includes emollients, ultraviolet light, systemic retinoids, methotrexate (Klein et al 2010) and with some reports of the benefit of biologic agents especially TNFα antagonists (Petrof et al 2013).

Eczema (Dermatitis) and Related Disorders Eczema is an inflammatory skin disease that may be caused by a number of factors. The terms ‘eczema’ and ‘dermatitis’ are synonymous. Acute eczema is characterised by redness, scaling and weeping, often with vesiculation (tiny fluid-filled blisters). In contrast, chronic eczema is characterised by excoriation (scratch marks) and thickening of the skin known as ‘lichenification’. Common categories of eczema include those described below.

Atopic Eczema This is a common, chronically relapsing skin disease with a genetic predisposition. Atopic eczema is a common disease with varying prevalence reports around the world, but with high rates of ≥15% in the age group 6–7 years recorded in Thailand, Colombia, Cuba, Ecuador, Honduras, Nicaragua, Sweden, Australia, New Zealand, Niue and the UK (Odhiambo et al 2009). It is often associated with the other atopic diseases, asthma and hay fever. The cause is complex and multifactorial, but a major underlying factor is a defective skin barrier. Some patients with atopic eczema carry mutations in the epidermal barrier protein filaggrin (Palmer et al 2006). Filaggrin forms a significant component of Natural Moisturising Factor, which helps the barrier function of the skin. Therefore, those patients with abnormal filaggrin who have defective barrier function permit the entry of antigens via the skin (McLean 2016). The fundamental problem of a faulty skin barrier for those with atopic eczema may be a key factor leading to the development of diseases at other sites such as food allergy and is known as the ‘Atopic March’ (Han et al 2017). The onset of atopic eczema is usually in infancy, usually starting on the face and scalp but with time the sites changing to commonly involve the flexures of the wrists and ankles (Fig. 4.4). Involvement of the feet is uncommon; however, it is possible for any part of the skin to be involved. Approximately 60% of children are clear of atopic eczema by the age of 10 years. In a minority, eczema persists into adult life, and others may present for the first time later in life. Treatment. The mainstay of treatment is a combination of regular emollients (moisturisers) to improve epidermal barrier function and topical steroid ointments or creams to treat the inflammatory component. Topical steroids vary in potency from the mild hydrocortisone, to the ultrapotent steroids such as clobetasol proprionate which is approximately 600 times more potent than 1% hydrocortisone. Care

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Fig. 4.4  Atopic eczema showing erythema, excoriation (erosions) due to scratching and thickened skin (lichenification) of the feet.

needs to be taken with the use of potent and ultrapotent topical steroids as side-effects are possible, including skin atrophy. Topical immunosuppressive agents (tacrolimus, pimecrolimus) are a more recent alternative to topical steroids with the benefit of not causing the cutaneous adverse effects of topical steroids, nor do they demonstrate tachyphylaxis. Anti-inflammatory pastes containing tars such as ichthammol, or zinc, may be effective in settling eczema of the feet and ankles. Affected skin is often infected by Staphylococcus aureus, and antiseptic or systemic antibiotics may be needed. Topical antibiotics should not be routinely used as they promote antibiotic resistance. Patients with severe chronic eczema may require treatment with narrowband UVB phototherapy and it may be necessary to use immunosuppressive drugs such as methotrexate, azathioprine, mycophenolate or ciclosporin (Nankervis et al 2017). There are a number of new novel therapies for atopic eczema including dupilumab, an interleukin 4 inhibitor (Lee et al 2018).

Contact Eczema Contact eczema can be subdivided into patients who have a type 4 allergic hypersensitivity reaction to specific allergens (allergic contact) and those who have a non-specific reaction to irritants (irritant contact), but the two often coexist. Irritant contact eczema is the result of non-allergic, chemical damage to the skin. This may occur acutely, for instance after exposure to acids or alkalis, but is more commonly the result of cumulative exposure to a variety of irritants such as soaps, detergents and even water over weeks, months or years. Workers in jobs where wet work is common, such as bar workers and cleaners, are particularly prone to irritant contact eczema. Some workers are far more prone to the effects of irritants than others; although the reason for this is often not clear those with a background of resolved childhood atopic eczema are more vulnerable. The hands are the most common site of irritant contact eczema. Eczema can present on the hands and feet together and when this combination occurs it is more likely that the cause is endogenous rather than exogenous. Allergic contact eczema is an important cause of eczema of the feet. Patients may become sensitised (allergic) to a wide variety of allergens found in footwear, hosiery and even topical medicaments (Case study 4.2). In footwear eczema components of the shoes and the adhesives can be important. Chemicals associated with leather, rubber (Fig. 4.5) and adhesives are potential sensitising agents. These include potassium dichromate (used in leather tanning), rubber vulcanising agents and formaldehyde containing adhesives. The warm moist environment

Fig. 4.5  Allergic contact eczema of the soles of the feet due to allergy to mercaptobenzothiazole, a rubber additive.

CASE STUDY 4.2  Sensitivity to Colophony A man was treated with adhesive strapping support for a sprained ankle. Within 48 hours he developed an acute eczema at the site of application of the adhesive strapping. Patch testing revealed sensitivity to colophony, a common resinous material found in adhesives. Colophony is derived from pine trees and the word comes from Colophon, an ancient town in Asia Minor famous for its production of colophony.

and the occlusive effect of shoes are important in the pathogenesis of allergic contact eczema and rubber additives are a frequent antigen (Warshaw et al 2007). Sometimes a distinctive pattern of eczema, with a sharp demarcation between normal and affected skin will point to allergic contact hypersensitivity as a possible cause although the distribution can also be non-specific. Patch testing by dermatologists with standardised concentrations of allergens may identify the source of allergic contact eczema. This procedure involves application of a series of purified, standardised allergens placed in inert chambers on the back under adhesive tape to provoke an eczematous reaction. The patches are removed after 48 hours and reactions read immediately and at 96 hours because some reactions are delayed. Positive tests are identified as individual erythematous, papular or vesicular reactions. It is also possible to patch test to components of the patient’s own shoes provided the samples taken from the shoes are thin to prevent pressure effects and false positive results (Warshaw et al 2007).

Stasis and Varicose Eczema Chronic venous disease or lymphatic insufficiency may cause eczema. The classic distribution of venous or varicose eczema is on the gaiter area of the leg (lower shin and calf), although it can also extend onto the foot. There is often a history of varicose veins or of deep vein thrombosis. Oedema, increased pigmentation (haemosiderin deposition), purpura, lipodermatosclerosis and ulceration are often present with the eczema. Damage to the larger veins in the legs with reflux of venous blood causes venous hypertension and subsequent damage to the smaller vessels. The damage results in the extravasation of macromolecules and degraded red blood cell products with haemosiderin deposition. These factors are potent inflammatory agents which lead to aberrant fibroblast activity with excessive scar tissue formation (Crawford et al 2017). Atrophie

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Fig. 4.6  Pompholyx (dyshidrotic eczema).

blanche (white, scarred skin) may be present and such skin is especially vulnerable to ulceration. Eczema may also complicate chronic oedema due to cardiac or renal insufficiency, obesity, immobility or lymphatic disease. Often these are present in combination and may also occur with venous disease. In lymphoedema a firm non-pitting oedema is present, and dilated lymph vessels may give a cobbled appearance to the skin. There may also be a warty hyperkeratosis of the feet. Lymphoedematous legs are vulnerable to recurrent cellulitis which in turn causes further lymphatic damage. Allergic contact eczema may complicate up to 50% of cases of stasis eczema, with hypersensitivity to preservatives and other ingredients in topical medicaments being common. Assessment by a vascular surgeon to correct any surgically amenable disease is important. The treatment of the established eczema is with emollients and topical corticosteroids, having excluded any concurrent tinea. Graduated compression for venous disease is an effective treatment when used appropriately (Andriessen et al 2017) and can be helpful to prevent eczema recurrence.

Fig. 4.7  Juvenile plantar dermatosis.

Pompholyx (Dyshidrotic Eczema) This is an acute and often recurrent vesicular eczema that affects the palms and the soles of the feet. The aetiology of pompholyx is unclear although it can be associated with atopic eczema, contact eczema and adverse drug reactions. The precise role of nickel allergy is uncertain. It is important to exclude a dermatophyte infection. The symptoms are of intense itching and discomfort. On examination there are multiple small vesicles and sometimes bullae form (Fig. 4.6). Potassium permanganate soaks are useful if there is extensive exudate. However, specific topical treatment includes steroids, calcineurin inhibitors (e.g. tacrolimus), retinoids (e.g. bexarotene) and hand and foot phototherapy (topical psoralen and UVA). Injections of botulinum toxin can be effective. If topical measures are ineffective systemic options are steroids, retinoids (acitretin, alitretinoin) and immunosuppressive agents (methotrexate, mycophenolate mofetil, azathioprine and ciclosporin) (Wollina 2010).

Juvenile Plantar Dermatosis This is a dermatosis that occurs almost exclusively in infants and children often resolving by puberty. The cause is uncertain but friction, excessive sweating (hyperhidrosis) and an atopic tendency (Zagne et al 2014) are important. Some report a seasonal variation with temperature variation. The sole of the foot is red, smooth with a ‘glazed’ appearance associated with fine scales. Commonly the forefoot and toes are involved (Fig. 4.7). The differential diagnosis includes tinea

Fig. 4.8  Lichen planus.

pedis, allergic contact dermatitis and psoriasis. Treatment can be difficult and may not be needed as resolution can be anticipated. General measures are to use cotton socks and avoid occlusive foot wear if possible. Topical treatments are emollients, mid-potent topical steroids and calcineurin inhibitors (tacrolimus) (Shipley & Kennedy 2006).

Lichen Planus Lichen planus is a T-cell-mediated autoimmune disease but the exact pathogenesis is uncertain. There is an association with infection by hepatitis C (Lodi et al 2010), but the association with hepatitis B (Birkenfeld et al 2011) is not clear. Patients classically present with itchy, polygonal, violaceous, flat-topped papules covered with superficial white lines known as Wickham’s striae. Papules may coalesce into plaques, and lesions can appear in sites of trauma (Koebner phenomenon). The rash can affect any body site, although lesions on the wrists and ankles are particularly common (Fig. 4.8). In addition, lichen planus can cause nail dystrophy, scarring alopecia and can affect oral and genital mucosae.

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Lichen planus can affect plantar skin and the lesions are often not characteristic of lichen planus lesions at other sites. A spectrum of disease may be seen ranging from a few discrete papules at the margin of the foot to widespread hyperkeratosis with fissuring and ulceration. Lichen planus is usually a self-limiting disease, although it may occasionally persist for years. Rarely, malignant change has been reported in long-standing plantar lichen planus (Mayron et al 1988, Thakur et al 2015). Localised disease can be treated with moderate strength topical steroids, topical vitamin D analogues (calcipotriol) and topical calcineurin inhibitors. Treatment of extensive disease includes phototherapy (narrow band UVB), systemic steroids, retinoids (acitretin), hydroxychloroquine, sulfasalazine, griseofulvin and immunosuppressive agents (methotrexate, ciclosporine) (Atzmony et al 2016, Fazel 2015).

Ichthyosis Ichthyosis means dry skin and the word drives from the Greek word for fish. There are many causes of ichthyosis including congenital syndromic and non-syndromic forms and acquired forms such as age-related, drug-induced, malnutrition and paraneoplastic-related. Different types of ichthyosis have different characteristics depending on the cause. Ichthyosis affecting the feet may be manifest by both hyperkeratosis and hyperlinearity. The important discovery that a common form of inherited ichthyosis called ichthyosis vulgaris was due to loss of function mutations in the gene encoding the protein filaggrin (Smith et al 2006) led to major advances in the understanding of atopic eczema (see Atopic eczema, above). Dry skin in the elderly is common and can lead to asteototic eczema (Deo et al 2015), and is due to a combination of intrinsic and extrinsic ageing factors (Tobin 2017), including reduced stratum corneum lipids (Ghadially et al 1995), medication and comorbidities.

Palmoplantar Keratodermas There are a large and heterogeneous number of disorders that result in palmar and/or plantar hyperkeratosis and these are termed palmoplantar keratodermas. The keratodermas can be congenital or acquired and it is not uncommon for podiatrists to see patients presenting with these disorders.

Inherited Palmoplantar Keratodermas The classification of the congenital palmoplantar keratoderma disorders is complex and changing as the pathogenesis is more fully understood. Therefore, these rare disorders will be increasingly grouped on genotypic classification rather than phenotype. Congenital palmoplantar keratodermas can be divided into those associated with an underlying syndrome ‘syndromic’ palmoplantar keratoderma, and those that are ‘non-syndromic’ either with isolated palmar plantar involvement or those with distinctive cutaneous and adnexal manifestations. Furthermore, palmoplantar keratodermas can also be classified on the pattern of involvement and these patterns are diffuse, focal, striate and punctate (Guerra et al 2018). Aetiology. Genetic mutations in key structural proteins expressed in the epidermis are important, especially those in keratin. Keratins are proteins that are expressed in epithelial cells and different keratins are expressed in different parts of the body. Each keratin filament has an obligate pair, for example keratin 16 pairs with keratin 6a in the palmoplantar skin. A mutation in a keratin gene can lead to a keratoderma. For example, a mutation in keratin 6a can lead to the keratoderma of the disorder pachyonychia congenita (Fig. 4.9) (Case study 4.3). Other genes that can be mutated include connexin, loricrin, plakoglobin, desmogleins and desmoplakins (Guerra et al 2018).

Fig. 4.9  Plantar keratoderma of pachyonychia congenita.

CASE STUDY 4.3  Keratin Mutation A 23-year-old woman had a lifelong nail dystrophy, multiple cysts and a painful hyperkeratosis of the feet. She had a baby son who was also born with a nail dystrophy and developed a plantar hyperkeratosis as he started to walk. Genetic investigation showed them to have a keratin mutation confirming a diagnosis of pachyonychia congenita (Figs 4.9, 4.12).

Acquired Palmoplantar Keratodermas There are many causes of acquired keratoderma (Patel et al 2007). Keratoderma climactericum appears in women of menopausal age and there is a strong association with obesity and hypertension. It is perhaps due to hormonal dysregulation. There are many drugs that can induce keratodermas, including venlafaxine, metoprolol, lithium and hydrochlorothiazide. Hypothyroidism and chronic lymphoedema may be associated with keratoderma. Keratoderma may be a marker of an underlying malignancy (a paraneoplastic sign) and has been seen in association with cancers, including oesophagus, lung, breast, prostate and gastrointestinal tract. Primary inflammatory skin diseases such as psoriasis, PRP, lichen planus and cutaneous lupus can produce a keratoderma. Infectious disease is also associated with keratoderma, including human papilloma virus, syphilis, crusted scabies, leprosy and tuberculosis. Aquagenic keratoderma is characterised by burning and discomfort after immersion in water and has been described in patients with cystic fibrosis. Idiopathic keratoderma is a diagnosis of exclusion. Clinical Features. A detailed history is essential to help determine which type of keratoderma is present, especially the timing of onset, any associated symptoms and the family history. Keratodermas may be painful with fissures on weight-bearing areas. Malodour due to secondary bacterial overgrowth may be present. The examination should seek other features of keratodermas, including an examination

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Fig. 4.10  Diffuse pattern of plantar keratoderma.

Fig. 4.11 A toe has been lost due to the formation of a constricting band (‘pseudoainhum’).

of the hands and areas such as the elbows, knees, wrists, hair, nails and teeth. If a syndromic or disease-associated keratoderma is suspected, consider a referral to a dermatologist. An example of a diffuse keratoderma is shown in Fig. 4.10. Keratoderma which extends to the dorsa of the digits may result in constricting bands and even autoamputation of digits (Fig. 4.11). Treatment. Seek and treat the underlying cause if one exists. If the cause is irreversible such as a genetic mutation, then symptomatic treatment is needed. Topical treatments include the regular use of topical keratolytics such as salicylic acid 5–10% in white soft paraffin or 35–70% propylene glycol. Occlusion increases the efficacy of keratolytics and can be used in combination with physical treatments such as manual paring or abrasion with a pumice stone. Topical retinoids have been described as being helpful but oral retinoids (e.g. acitretin, isotretinoin) are particularly useful for some patients. Perhaps gene therapy will offer an option in the future. Keratoderma may be complicated by dermatophyte fungal infections. Skin scrapings should be sent for mycological culture if this is suspected.

HYPERHIDROSIS Hyperhidrosis is the pathological production of excessive sweat in excess of that needed for temperature control. The cause is uncertain but genetic

65

Fig. 4.12  Nail dystrophy of pachyonychia congenita.

factors are important with a family history of the disorder frequently being reported (Hashmonai et al 2017). It is important to rule out secondary causes of hyperhidrosis such as hyperthyroidism. It is an uncommon, focal condition and the regions commonly affected are the palms, axillae, face and plantar aspect of the feet. It has significant psychosocial implications. The sweat drips from the affected site and often there is additional secondary infection with odour when the plantar surface is affected. There are many potential treatments either medical or surgical. The first-line treatment is the use of antiperspirants containing aluminium chloride. Iontophoresis involves placing the feet in water through which a carefully and safely controlled electrical current is passed. The exact mechanism of action is uncertain but eccrine sweat production is temporarily halted. It is possible for patients to buy their own home-based iontophoresis machine. Systemic medication is less useful because of the systemic side-effects. Commonly, anticholinergic drugs such as propantheline and glycopyrrolate are trialled. Intradermal injections of botulinum toxin are effective but more commonly used in the axillae and palms rather than feet. It is painful to inject and a regional nerve block may be needed for the hands and feet. The results last approximately 6 months. Surgical management is indicated when conservative medical treatments fail. The only surgical option for plantar hyperhidrosis is a lumbar sympathectomy. This procedure can be very effective but is complicated by compensatory hyperhidrosis (localised sweating at another location on the body) in up to 44% of patients (Singh et al 2016).

BLISTERING DISORDERS There are many causes of blistering and these can be congenital or acquired. To elucidate the cause, a careful history and examination are needed. Acquired causes include trauma (e.g. frictional forces with poorly fitting footwear), infective (e.g. viral or bacterial), neurological (sensory neuropathy), inflammatory (e.g. bullous reaction to an insect bite), iatrogenic (e.g. furosemide) and autoimmune (e.g. bullous pemphigoid). There are a rare group of disorders due to inherited genetic abnormalities in key structural proteins in the skin, called epidermolysis bullosa.

Epidermolysis Bullosa: the Inherited Mechanobullous Disorders Epidermolysis bullosa encompasses a spectrum of disorders characterised by skin fragility and blistering following mild mechanical trauma. In a similar way that the keratodermas (see Palmoplantar keratodermas, above) are being classified by genotype rather than phenotype,

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Fig. 4.14  Bullous pemphigoid.

Fig. 4.13  Dystrophic epidermolysis bullosa.

LESIONS the classification of the differing types of epidermolysis bullosa changes as genetic research progresses. Advances in research increasingly offer the possibility of preimplantation, prenatal diagnosis and gene therapy. Epidermolysis bullosa can be broadly divided into four groups of diseases on the basis of the ultrastructural level of the blister formation and defined mutations in specific genes (Fine et al 2014). • Epidermolysis bullosa simplex – the plane of cleavage is through the epidermis. Non-scarring blisters predominantly affect palmar and plantar skin. The condition typically worsens in warm weather, particularly in childhood. • Junctional epidermolysis bullosa includes all subtypes of epidermolysis bullosa in which blisters develop within the mid portion or junction of the lamina lucida of the basement membrane. Unfortunately, many affected children die in infancy with overwhelming infection. • Dystrophic epidermolysis bullosa includes all subtypes in which blistering occurs within the upper dermis. Blistering generally starts in infancy and affected patients have a relentlessly progressive course with scarring following minimal trauma with eventual fusion and resorption of the fingers and toes. Growth retardation and anaemia may result from blistering and strictures in the oesophagus (Fig. 4.13). • Kindler syndrome is a specific entity where blistering occurs at multiple levels within and/or beneath the basement membrane zone rather than within a discrete plane. Photosensitivity is a notable feature.

Autoimmune Blistering Disorders Disease mediated by autoantibodies against target antigens in the epidermis or its basement layer results in increased skin fragility or blistering. The most common autoimmune blistering disorder is bullous pemphigoid in which proteins which anchor the epidermis to the dermis are targeted by autoantibodies. This causes the full epidermis to lift off producing an intact firm blister. On the feet, the blisters can resemble those of pompholyx (Fig. 4.14). Pemphigus is a rarer autoimmune blistering disease where the autoantibodies are directed against proteins that are involved in adhering the keratinocytes within the epidermis together and the result is flaccid, friable blisters or erosions. Both of these conditions usually require aggressive treatment with high doses of oral steroids or other immunosuppressive agents. Recently, rituximab, which is a monoclonal antibody that depletes B-cells has been shown to be an effective treatment for pemphigus (Wang et al 2015).

This section will focus on common, specific lesions rather than rashes. Podiatrists are well placed to undertake opportunistic screening of the lower leg and feet especially to recognise premalignant and malignant lesions. Some patients may present to podiatry with a specific lesion, so a working knowledge of the different types is essential for safe practice. It is important to understand the common types of sun-induced skin cancer particularly; basal cell carcinoma, squamous cell carcinoma and malignant melanoma. However, there is a wide variety of both benign and malignant lesions and most are not specific for the foot or lower leg but can be found anywhere on the skin. Lesions can arise from every part of the skin, including the epidermis and its constituent cells, dermis and subcutaneous fat (Table 4.2). Therefore, an effective examination of the skin and foot will include visualisation of all the skin including the potentially ‘hidden’ areas of the posterior calf, all of the heel and the web spaces.

Epidermal Lesions

Seborrhoeic Keratosis Seborrhoeic keratosis (synonyms: senile or seborrhoeic wart, basal cell papilloma) is one of the most common lesions showing a great variety of morphology. They are benign but can be mistaken for malignant lesions including malignant melanoma. Their incidence increases with advancing age. There are different varieties and they may cluster on the trunk but any body surface, including the feet, can be involved. There are several varieties. Clinical Features. Seborrhoeic keratoses are commonly found on the trunk. They are usually well demarcated and pigmented. The colours can vary but commonly they are black, grey and brown. They usually have a roughened ‘wart-like’ surface and may appear or feel greasy ‘seborrhoeic’. They are usually elevated but may be flat. The size varies from just a few millimetres to several centimetres (Fig. 4.15). They can become inflamed (‘irritated’) either spontaneously or with trauma. The rare sign of Leser–Trélat is the sudden increase in the number and size of seborrhoeic keratoses associated with a malignancy, including gastrointestinal adenocarcinoma, lymphoma and squamous cell carcinoma (Czarnecki et al 1983). Stucco keratosis is the name given to a type usually seen on the legs and ankles. They are usually white or grey rarely exceeding 5 mm in diameter. Treatment. Treatment is not needed but may be requested for cosmetic reasons or if it has become inflamed ‘irritated’. Seborrhoeic keratoses are epidermal lesions, so superficial destructive options are preferred. The options to treat them include curettage, shaving or liquid nitrogen but

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TABLE 4.2  Classification of Skin Tumours Tumour Type

Benign or Malignant

Epidermal tumours

Benign Malignant

Pigmented skin tumours

Benign

Vascular tumours Fibrous tumours Adnexal tumours Other structures

Malignant Benign Malignant Benign Malignant Benign Benign

Examples Seborrhoeic keratoses Carcinoma in situ (Bowen’s disease) Basal cell carcinoma Squamous cell carcinoma Cutaneous metastatic tumours Freckle Lentigo Congenital naevus Benign acquired naevus Speckled lentiginous naevus Becker naevus Epidermal and dermal naevi Spitz naevus Atypical naevus Malignant melanoma Pyogenic granuloma Glomus tumour Kaposi’s sarcoma Acquired fibrokeratoma Dermatofibroma Dermatofibrosarcoma protuberans Eccrine poroma Leiomyoma (smooth muscle) Subungual exostosis (bone) Myxoid cyst (joint) Ganglion (joint) Piezogenic pedal papules (fat) Neurofibromatosis (nerve)

Fig. 4.15  Seborrhoeic keratosis.

care needs to be taken on the lower leg and foot as these sites can heal very slowly, especially in the elderly. It is essential that all lesions which are removed must be submitted for pathological examination, as occasionally other lesions, including melanoma, can mimic seborrhoeic keratoses.

Actinic Keratoses Actinic keratoses are a form of sun damage. They are usually red, scaly lesions on sun-exposed areas of skin, including the lower leg and

Fig. 4.16  Carcinoma in situ (Bowen’s disease).

dorsum of the foot. They are common in fair-skinned individuals who have excessive sun exposure. They can be well demarcated and usually less than 1 cm in diameter. They may spontaneously resolve or remain unchanged for years. The precise rate of transformation into squamous cell carcinoma is not known but likely to be low. Treatment. Treatment is not essential but sometimes requested. Simple emollients with or without a keratolytic are useful. Specific topical treatments include 5-fluorouracil, diclofenac, ingenol mebutate and imiquimod. Destructive treatments include curettage and diathermy, shave and diathermy and cryotherapy. Wound sites below the knee often heal poorly so care needs to be taken with destructive modalities. Photodynamic therapy uses light to activate a cream which is selectively absorbed by the actinic keratosis resulting in destruction of the lesion.

Carcinoma in situ (Bowen’s disease) Carcinoma in situ is an intraepidermal carcinoma derived from keratinocytes which can sometimes develop into an invasive squamous cell carcinoma. Sun damage, arsenic exposure and human papilloma virus are implicated as causes. Clinical Features. Carcinoma in situ, like actinic keratoses, affects sun-exposed areas including the lower leg and dorsum of the foot. It is usually a well demarcated, red, scaling patch which slowly enlarges over time (Fig. 4.16). Some variants can be hyperkeratotic, pigmented or eroded and the nail bed can be involved. The differential diagnosis includes a superficial basal cell carcinoma, squamous cell carcinoma, malignant melanoma, eczema or psoriasis. If there is doubt, histological examination is essential. A small proportion of these lesions, perhaps 5–8%, develop into a squamous cell carcinoma. Treatment. Topical treatments are similar as for actinic keratoses and include 5-fluorouracil and imiquimod. Destructive treatments are cryotherapy, curette and diathermy, and photodynamic therapy. Surgery is rarely required.

Basal Cell Carcinoma Basal cell carcinoma is the most common skin cancer in caucasian people, increasing in incidence with age and in the USA approximately 2.5 million patients are treated for this skin cancer each year (Verkouteren et al 2017). They are usually found on sun-exposed areas of the body, especially the upper body, but are not uncommon on the lower leg and occasionally on the dorsum of the foot (Case study 4.4). They are slowly growing lesions that cause damage locally and almost never metastasise. The cell of origin is uncertain but perhaps from stem cells within hair follicles and the interfollicular epithelium (Verkouteren et al 2017).

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Fig. 4.17  Basal cell carcinoma (nodular).

Fig. 4.19  Ulcerated squamous cell carcinoma of the foot.

carcinomas, jaw cysts and cerebral calcification. These patients have characteristic small pits on the palms and soles (John & Schwartz 2016). The differential diagnosis for a basal cell cancer is similar to all skin cancers and includes squamous cell cancer, amelanotic melanoma, carcinoma in situ and inflammatory lesions such as psoriasis or eczema. Treatment. There are many treatments for basal cell carcinoma and the most suitable treatment needs to be selected depending on the type, location and patient preference. Treatments include imiquimod, cryotherapy, curette and electrodessication, photodynamic therapy, radiotherapy and surgery.

Squamous Cell Carcinoma Fig. 4.18  Basal cell carcinoma (superficial spreading).

CASE STUDY 4.4  Diagnosis of Ulcerated

Area

A 70-year-old European man presented with a symptomless, irregular, ulcerated area on the dorsum of his left foot. He had migrated to New Zealand as a child. What is the likeliest diagnosis and appropriate treatment? The answer is a skin cancer, either a squamous cell cancer or an ulcerated basal cell cancer. It would be essential that a biopsy and surgical excision be undertaken as soon as reasonably possible.

Clinical Features. The typical history is of a small lesion developing and extending very slowly over months or years. It may bleed and crust intermittently. Some patients have multiple basal cell cancers. There are different clinical types of basal cell carcinoma: • Nodular basal cell carcinoma is a slowly growing lesion initially a papule and then nodule which may ulcerate and bleed with time. It has a ‘pearly’ appearance with dilated blood vessels (telangiectases) running over the surface (Fig. 4.17). • Superficial spreading basal cell carcinoma is a slowly growing, well demarcated patch with minimal scale (Fig. 4.18). • Sclerosing basal cell carcinoma is indurated and has an ivory colour. • Other basal cell carcinomas include the pigmented and mixed where more than one morphology may be present in a lesion. A rare autosomal dominant disorder is called basal cell naevus syndrome (Gorlin syndrome) characterised by multiple basal cell

Cutaneous squamous cell carcinoma is the second most common skin cancer (Que et al 2018). It may affect any area of the skin but is common on a background of actinic damage including the lower leg, but some, approximately 20%, will occur on non-sun-exposed areas of skin. Sites of chronic inflammation such as scars or ulcers may develop squamous cell carcinoma (a Marjolin ulcer). Rarely slow growing ‘verrucal’ squamous cell cancers are found on the plantar aspect of the foot (carcinoma cuniculatum) (see Verrucous carcinoma of the foot, below). Squamous cell carcinomas derive from the keratinocytes of the epidermis. Clinical Features. Squamous cell carcinoma may present in many different ways. The lesions may be papules or nodules, ulcerated or well-differentiated with abnormal keratin integral to the lesion (Figs 4.19, 4.20). The rate of growth and size at presentation are variable. Squamous cell cancer can also affect the nail and nail bed apparatus and may be misdiagnosed. Most squamous cell carcinomas are only locally aggressive but they all have the potential to metastasise to the draining lymph nodes and then to other areas. Some squamous cell carcinomas have a greater risk of metastasising and these include those tumours larger than 2 cm and deeper than 2 mm, with nerve invasion (perineural involvement), poorly differentiated, previously treated, tumours on the lips and ears, arising from scars and in immunosuppressed patients (Que et al 2018).

Verrucous Carcinoma of the Foot (carcinoma cuniculatum) Verrucous carcinoma (carcinoma cuniculatum) is a rare variant of a squamous cell carcinoma that has a predilection for the plantar aspect of the foot (Fig. 4.20). It progresses relatively slowly and with time becomes large and malodorous. The term ‘cuniculatum’ derives from the latin ‘cuniculus’ inferring rabbit burrow as the lesion is penetrated by sinuses (McKee et al 1981).

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Fig. 4.21  Cutaneous metastatic nodules from a primary breast cancer.

CASE STUDY 4.5  Sequelae of Long-Term

Varicose Ulceration

Fig. 4.20  Verrucous squamous cell carcinoma of the foot.

Treatment. The treatment of squamous cell carcinoma will depend on the site, the risk of the tumour and patient preference. Low risk lesions may be amenable to cryotherapy or curettage and electrodessication. However, surgical excision is often needed. Skin Cancer Prevention. Prevention should be practiced starting from infancy and childhood because a majority of sun exposure occurs in childhood, but becomes a lifelong habit, especially for those of fair skin living in sunny climates such as Australia and New Zealand. Measures should include shade provision, protective clothing which has adequate ultraviolet protection, wide-brimmed hats and effective use of sun screen.

Cutaneous Metastatic Disease Skin metastases occur in 0.6–10.4% of patients with cancer and may occur through blood or lymphatic spread, direct tissue invasion and iatrogenic implantation (Alcaraz et al 2012). These lesions may occur in a patient with known malignant disease or be the first manifestation of an underlying tumour. Skin malignancies, particularly melanoma, may also metastasise to other areas of the skin. The frequency of the different tumours within the skin parallels the frequency of occurrence of the primary tumour. Primary internal cancers that are seen in the skin include breast, lung, colorectal, ovarian, head and neck cancers and renal (Nashan et al 2010). The extremities are a less common site of presentation occurring in 18% of cases and the trunk being the most common with 40%. However, the onset of cutaneous metastases is a poor prognostic sign with an average survival of 7.5 months following diagnosis (Saeed et al 2004). Clinical Features. The appearance of cutaneous metastases is wide and includes nodules, papules, plaques and ulcers. They can mimic other skin conditions and presentations resembling pyogenic granulomas, haemangioma-like, herpes zoster and cellulitis have been described (Alcaraz et al 2012). Nodules or ‘masses’ are a common presentation (Saeed et al 2004) often appearing to be under the skin (Fig. 4.21). When the skin metastasis comes from a primary skin cancer, malignant melanoma is the

A 58-year-old man asks you about a bleeding lesion on his ankle adjacent to a long-standing varicose ulcer, during a podiatry session. He has varicose veins with pigmentation around the ankle. He has had a small varicose ulcer near the area for years. He works as a forester. What might be developing? There are a number of possibilities. Trauma from his work might lead to a pyogenic granuloma. The long-standing venous ulcer may undergo malignant transformation to a squamous cell carcinoma. Malignant melanoma on the lower leg may be amelanotic. Ideally, a biopsy should be taken for histology in the near future.

commonest cause and is the first sign of dissemination in approximately 50% of patients (Savoia et al 2009) (Case study 4.5). Treatment. The treatment depends on the primary lesion and commonly involves systemic therapies under the care of oncologists. Innovative new medications are fundamentally changing the prognosis of disseminated disease especially that of malignant melanoma through the use of targeted therapies and immunomodulating drugs (Silva & Long 2017). Lesions within the skin may be amenable to localised therapies including surgery, radiation, photodynamic therapy, laser, immunomodulatory creams (e.g. imiquimod) or intralesional chemotherapy may be considered. Palliative care may be the only reasonable option for some patients.

Pigmented Skin Lesions

Skin Colour and Melanin Production. The evolution of skin colour is a fascinating story. Humans are distinguished from nonhumans by almost complete lack of hair and the evolution of skin colour has been by natural selection with the development of darker skin providing protection against the photodegradation of folate and reduced melanin production with dispersal into non-tropical latitudes (Jablonski & Chaplin 2017). Skin colour is largely due to melanin pigment produced by melanocytes. These cells originate from the neural crest and are found in the skin from the eighth fetal week onwards. The production of melanin is influenced by many factors, including ethnic background and sun exposure. The melanocyte is a dendritic cell which can interdigitate with and provide pigment to about 30 keratinocytes. It is situated in the basal layer of the epidermis. The melanocyte produces an organelle called a melanosome in which melanin formation takes place. These organelles are transferred to keratinocytes via the dendritic processes. The melanin sits over the nucleus of the cell. This entire complex of melanocytes and keratinocytes is called the melanin unit (Kollias et al 1991).

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Fig. 4.22  Congenital melanocytic naevus lateral to umbilicus.

Fig. 4.23  Junctional naevus.

Common Pigmented Lesions • • • • • • •

 reckles F Lentigo Congenital melanocytic naevus Acquired melanocytic naevus and typical naevus Becker naevus Spitz naevus Malignant melanoma. Freckles. Freckles (ephelis, ephelides) are common, especially in the fair-skinned. They are usually 1–3 mm in diameter and occur on sun-exposed areas of skin. They occur in the young. The number of melanocytes is unchanged but there is increased melanin. Lentigo. Lentigos are flat, brownish/black lesions often several millimetres in diameter and can be found anywhere on the body. Solar lentigos develop on sun-exposed areas of skin in middle-aged and elderly patients and are another marker of sun exposure. They can be larger, occasionally 2–3 cm in diameter. There is an increased number of melanocytes.

Congenital Melanocytic Naevus Congenital melanocytic naevi are defined as naevi present at birth; however, some become evident only after 2 years (Stefanaki et al 2018). They can be classified based on their projected adult size and a recent consensus conference has suggested small 60 cm) (Krengel et al 2013). These naevi have cosmetic implications and there is concern about their relationship to melanoma. The highest risk for melanoma development is in early childhood and with larger congenital naevi >60 cm (Vourc’h-Jourdain et al 2013). Clinical Features. Congenital melanocytic naevi are usually brown to black in colour (Fig. 4.22). Abnormal hair growth within the lesion may develop. The surface of the lesion may be smooth, warty or lobular. Any recent change within a congenital naevus needs a full assessment. A congenital naevus grows proportionately with the child. Some children also develop neurocutaneous melanosis which is the presence of melanocytic lesions in the central nervous system with subsequent neurological problems. Treatment. Serial monitoring of these lesions is useful and this can be achieved by digital photography. Smaller lesions can be fully excised or excised serially but often this is not a pragmatic option for large congenital naevi. Other options for treatment include curettage, shaving, dermabrasion, chemical peels, cryotherapy, electrosurgery, radiotherapy and lasers (Ibrahimi et al 2012), but unfortunately these techniques may not fully remove all the congenital naevus cells and

Fig. 4.24  Intradermal naevus.

the outcomes are variable with the risk of re-pigmentation. Cosmetic camouflage can be helpful.

Acquired Melanocytic Naevus Acquired melanocytic naevi are very common (Case study 4.6). Acquired melanocytic naevi can be classified into junctional (at the dermoepidermal junction), compound (at the dermoepidermal junction and within the dermis) and intradermal (confined to the dermis). The exact pathophysiology of acquired naevi is unknown and there is debate about the migration of the melanocytic cells either upwards or downwards between the epidermis and dermis (Grichnik 2008). Sun exposure, especially in childhood and adolescence, is an important risk factor for the development of acquired melanocytic naevi (Fritschi et al 1994, Kelly et al 1994). Clinical Features. Junctional naevi are usually small well circumscribed macules and brown or black, often found in children or adolescents (Fig. 4.23). They may be found on the palms and soles. Compound naevi are brown, black or tan papules found in children and adults. Intradermal naevi are common and found in adults. They may be dome-shaped papules with no colour, light tan or dark. Occasionally, coarse hairs may grow through a compound and intradermal naevus (Fig. 4.24). Naevi are also possible as part of the nail matrix and longitudinal melanonychia can occur as a consequence.

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CASE STUDY 4.6  Possible Melanocytic

Naevus

A 20-year-old woman noted a brown spot on her right sole. She was reasonably sure that it had not been there 4 months ago. On examination the lesion was symmetric, regular border, one colour and less than 6 mm. What should you do? The history and examination suggest a benign acquired melanocytic naevus. In view of the apparently fairly rapid history, a photograph with a dermatoscopic image (see Malignant melanoma of the skin, below) should be taken and she should be reviewed in 3 months to see if any change has occurred.

Fig. 4.26  Spitz naevus.

Treatment. It is usually not necessary to treat a speckled lentiginous naevus. There are reports of melanoma developing within them (Vaidya et al 2007) and if there was concern that malignant transformation had occurred then excision would be needed. Lasers and intense pulsed light have also been used. It is prudent to take clinical photographs with dermatoscopic images for regular monitoring or review if there is concern about change (see Malignant melanoma of the skin, below).

Becker Naevus

Fig. 4.25  Speckled lentiginous naevus (naevus spilus).

Treatment. It is not necessary to treat naevi. Patients may ask for removal for cosmetic reasons or if the naevus is irritated through trauma, for example catching on a belt. The patient needs to be realistic that the outcome of removal will involve a surgical procedure and consequent scarring. The patient needs to be comfortable exchanging a naevus for a scar and this is especially important if excision is contemplated on the face. Therefore, careful patient counselling is needed. Some protuberant naevi may be improved by a shave biopsy. This technique involves shaving the naevus flush with the skin to reduce its bulk. This will not remove any hair growth and, if there is deeper pigmentation, it may recur and darken. Occasionally bizarre re-pigmentation can lead to diagnostic confusion with a melanoma. Cosmetic camouflage can be effective to hide a naevus. If there is concern that a naevus may be a malignant melanoma then excision is unavoidable. If there is doubt, a period of monitoring with photographic and dermatoscopic imaging is prudent to assess for objective change.

Speckled Lentiginous Naevus A speckled lentiginous naevus (or naevus spilus from the Greek spilos meaning spot) can present at birth or develop in childhood and progress to develop its typical characteristics over months or years (Vaidya et al 2007). An Australian survey found a prevalence of approximately 2% (Rivers et al 1995). Clinical Features. A speckled lentiginous naevus is a pigmented patch in which there are multiple darker pigmented speckles. The size of the pigmented patch varies but is usually from 2 to 10 cm and the spots within it 1–3 mm (Fig. 4.25), although giant variants have been described (Vaidya et al 2007).

Becker naevus is a fairly common lesion, occurring in about 1 in 2000 young men and a fifth of that in females. It is pigmented but there are few or no changes in the melanocytes. Clinical Features. It usually appears in adolescence, gradually becoming more obvious. It is usually unilateral and around the shoulders and upper trunk but other areas, including the leg, have been described. It is a hyperpigmented, brown or light tan lesion that becomes hairy over time. They are commonly large reaching diameters of >20 cm. Treatment. Treatment is not needed and they are usually too large for surgical removal. Hair removal lasers can be used to treat the hair but lasers to treat the pigmentation have mixed results (Momen et al 2016).

Spitz Naevus Spitz naevus is a benign melanocytic lesion. However, the histology can be very similar to that of malignant melanoma and it is essential that there is close discussion between the dermatopathologist and dermatologist. Clinical Features. Spitz naevi usually occur in younger people up to the age of 20 years but these lesions are described in patients >50 years old. The head, neck and leg are common locations, although anywhere may be affected and in children under 12 years of age the lower limb is a common site (Scalvenzi et al 2018). Spontaneous involution occurs in 80% of Spitz naevi (Argenziano et al 2011). They are usually asymptomatic, dome-shaped, firm nodules, which are pink, red or tan in colour (Fig. 4.26). Treatment. These are benign lesions so treatment is not essential, but when they need to be removed for diagnostic or cosmetic purposes complete excision is needed.

Atypical Naevus Some patients have naevi, which exhibit clinical and/or histological features that are unusual but are benign. The problem in these patients is to distinguish malignant melanoma from a benign atypical naevus and this can be very difficult. Patients with more than five atypical naevi have an increased risk of developing malignant melanoma compared to those with none (Gandini et al 2005).

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Fig. 4.27  Atypical naevus.

Clinical Features. Atypical means that these benign lesions may be asymmetric, have irregular borders, several colours and be bigger than 6 mm in diameter (Fig. 4.27). Patients often have distinct patterns of naevi and some patients have multiple atypical naevi as their distinct pattern. Treatment. Careful regular supervision is important using photography and dermatoscopic monitoring. If there is any clinical concern about malignant melanoma the atypical lesion should be fully removed.

Malignant Melanoma A cutaneous malignant melanoma arises from melanocytes in the epidermis. Malignant melanoma can occur in structures other than the skin including the eye and oral mucosae. The incidence of cutaneous malignant melanoma is increasing in the last few decades in caucasian populations, roughly doubling every 10–20 years (Nikolaou & Stratigos 2014). In the USA, in 2015, cutaneous malignant melanoma was the fifth most common cancer with an incidence rate of 22.1 per 100,000 people and 8885 people died of the disease . Sun exposure is an important factor in the aetiology of this disease and the increased incidence of melanoma is related to changing lifestyle and recreational outdoor pursuits. Risk Factors for Melanoma. Major risk factors for melanoma are: • Older age groups and male gender • Previous personal history of melanoma or non-melanoma skin cancer • Number of naevi (>100 naevi or >5 atypical naevi) • Family history of melanoma • Fair skin and hair (e.g. red-blond hair, blue eyes) • Response to sun exposure (e.g. tan or burning easily) • Evidence of actinic damage (e.g. actinic keratoses, heavy freckling). Clinical Features. The most important clinical feature is an accurate history from the patient. Never ignore a history of a changing pigmented lesion especially in those who are at higher risk. A useful tool to screen for melanoma after the history is the ABCDE guide: • A = asymmetry of the outline • B = border irregularity • C = colour variegation • D = diameter (>6 mm) • E = evolving (shape, size, colour). However, it is essential to remember that the ABCDE guide is not foolproof and some melanomas may be symmetric, have regular borders, have few or no colour (amelanotic melanoma) and be less than

Fig. 4.28  An example of a dermatoscope.

6 mm in diameter. Amelanotic melanomas pose a particular difficulty and are often not diagnosed until the histology report is returned. Dermoscopy is a useful technique to enhance the diagnosis of malignant melanoma and should be part of the examination of every pigmented lesion. There are a number of different types of dermatoscope and one example is shown in Fig. 4.28. The technique involves placing a flat and illuminated glass plate on to the lesion, sometimes with liquid (mineral oil, water, alcohol) on the lesion to reduce reflection from the surface. Training in this technique enhances the ability to diagnose melanoma. Serial photography of specific lesions with concurrent dermatoscopic imaging permits evaluation over a fixed time period and the ability to detect early change. An example of clinical and dermatoscopic pictures of an acral melanoma are shown in Figs 4.29 and 4.30. A detailed description of dermoscopy is not possible in this text but one method is that of ‘Chaos and Clues’ (Ramji et al 2018). Types of malignant melanoma: • Lentigo maligna melanomas are slow-growing lesions, usually on the face, commonly in the elderly. They are in situ tumours so confined to the epidermis. They are a macule usually with an irregular border and colour variation. Sometimes an invasive melanoma will develop within these lesions with the consequent risk of metastasis (Fig. 4.31). • Superficial spreading melanoma can occur at any site, although in women they are more likely on the lower leg and in men on the back. It typically fulfils the features of the ABCDE guide described above (Fig. 4.32). • Nodular melanoma arises de novo within the skin. A significant proportion of amelanotic melanomas are nodular and can be found at any site. These melanomas can be quick-growing, pink lesions

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Fig. 4.31  Lentigo maligna melanoma.

Fig. 4.29  Acral melanoma.

Fig. 4.32  Superficial spreading malignant melanoma.

Fig. 4.30  Dermatoscopic appearances of the lower portion of the acral melanoma from Fig. 4.29.

and can be mistaken for vascular lesions such as pyogenic granulomas as they can bleed easily (Moloney & Menzies 2011). • Acral lentiginous melanoma. This variety is relatively uncommon accounting for 2–3% of all melanomas and it is the most common subtype of melanoma in darker skinned populations including African, Chinese, Korean, Singaporean and Latin American; its incidence does not correlate with lifetime sun exposure or sunburn (Desai et al 2017). These skin cancers have a poorer prognosis because they often present at a late stage either because they are not recognised or because the sole of the foot is an area rarely examined by patients (Figs 4.29, 4.33). Therefore, podiatrists can play a key role in opportunistic screening for this skin cancer. Acral melanomas are found on the soles of feet and palms of hands. They start as a macule which may progress to a plaque with friable exophytic nodules and ulceration. They may have different morphologies and are often variegated with a black pigment which can be mistaken for blood and lead to delays in the diagnosis. Rarely, they can be amelanotic pink, red macules or nodules (Desai et al 2018). • Subungual melanomas. These can be difficult to diagnose and a high index of suspicion is needed. They commonly form a pigmented

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Fig. 4.35  The ‘ugly duckling’ sign. The larger pigmented lesion on the left middle calf is different from the others (see also Case study 4.7).

CASE STUDY 4.7  Abnormal Pigmented

Lesion Noticed on Examination

Fig. 4.33 Ulcerated acral melanoma. The darker areas around the edge are melanin and not haemorrhage. There is some crusting on the eroded surface.

Fig. 4.34  Subungual melanoma.

streak (melanonychia) in the nail plate which changes with time. Dermoscopy can be useful to examine these pigmented streaks. With time the streak widens and may change colour. Pigment may develop adjacent to the cuticle and proximal or lateral nail folds (Hutchinson’s sign) (Fig. 4.34) (Yun & Kim 2011). Despite the different classifications and the ABCDE guide, the diagnosis of malignant melanoma can be difficult and some lesions are subtle. It is best to always have this diagnosis in mind for a pigmented or unusual non-pigmented lesion (amelanotic melanoma) so that an early diagnosis and suitable management is undertaken.

A 40-year-old man attends the podiatrist. The patient has multiple atypical naevi on his lower legs. You notice a particularly unusual pigmented lesion on his left, mid lower calf that is different from all the others, the ‘ugly duckling sign’ (Fig. 4.35). What action would you take? The examination is highly suggestive of a malignant melanoma. He should be urgently referred. An invasive melanoma was excised.

Remember that some primary melanomas can undergo spontaneous partial or complete regression so a pigmented lesion going paler should not be ignored. If there is doubt about a lesion it should have an excisional biopsy. Melanomas can metastasise and the biological behaviour can vary. Some spread early and some many years after the primary excision. They can metastasise to any organ including the skin as well as lungs, liver, brain and bone. Metastases may take the form of nearby local nodules or spread to the local lymph nodes. Distant areas of skin, subcutaneous tissue and lymph nodes may be affected. As some primary melanomas undergo regression, patients can present with metastases and the primary melanoma cannot be identified. Melanoma Staging. A detailed description of melanoma staging is not possible in this text but a description is given in the eighth edition of the American Joint Committee on Cancer (AJCC) melanoma staging system (Keung & Gershenwald 2018). Melanomas start developing within the epidermis and then invade into the dermis. The deeper the invasion the worse the prognosis and eventually they can metastasise beyond the skin. The depth of invasion into the dermis can be measured by the pathologist and is called the Breslow depth. The Breslow depth is an important prognostic indicator. For example, a melanoma with a Breslow depth of 4.0 mm Breslow depth, with ulceration has an 82% 5 year survival (Keung & Gershenwald 2018). Treatment. The treatment of the primary cutaneous melanoma is excision, initially with a narrow cuff of normal skin and then a wider

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75

excision depending on the Breslow depth. The extent of the wider excision has been a long-standing area of controversy but generally margins are reducing. Another area of controversy is the issue of an excision biopsy of the sentinel lymph node. It is possible to identify the first lymph node (sentinel node) that a melanoma metastasis may reach by injecting tracers (radioactive and coloured dyes) into the excision site that are then carried by the lymphatics to the first lymph node which then permit intraoperative identification. There is a better prognosis if the sentinel node does not show any metastatic melanoma. The management of metastatic melanoma is being revolutionised by the development of new targeted therapies which for the first time are prolonging the life of patients with metastatic melanoma (Daud 2015, Guennoun et al 2016). These drugs include programmed cell death-1 inhibitors (PD 1) (e.g. pembrolizumab) and cytotoxic T-lymphocyte-associated protein 4 inhibitors (CTLA-4) (e.g. ipilimumab). About 40–60% of melanomas have a mutation in a gene called BRAF and BRAF inhibitors (e.g. vemurafenib) are effective. Combinations of these drugs show promising benefits, although there can be significant side-effects. The future is promising for metastatic melanoma which was previously a dismal diagnosis to receive.

Epidermal Naevi These benign hamartomas of keratinocytes or epidermal appendages are grouped together under the term ‘epidermal naevi’. Commonly, they are isolated birthmarks but they can be part of an epidermal naevus syndrome. More common epidermal naevi include (keratinocytic) epidermal naevus (a distinct entity within the group), sebaceous naevus, inflammatory linear epidermal naevus and Becker naevus (Asch & Sugarman 2018). They are present at birth but may not be clinically recognisable until later. Clinical Features of Keratinocytic Epidermal Naevus. These occur on the trunk and extremities (Rogers 1992). Appearing at or after birth, the lesions develop slowly and are linear or whorled, stopping at the ventral or dorsal midline following embryological development lines (Blaschko’s lines). They may be pink or slightly hyperpigmented plaques that become elevated, verrucous and darker with time (Asch & Sugarman 2018). Some become inflamed and intensely itchy and are called inflammatory linear verrucal epidermal naevi (ILVEN) (Fig. 4.36). Treatment. Treatment is not necessary but surgical excision may occasionally be possible. Shaving will debulk a small lesion. Cryotherapy, lasers and photodynamic therapy have been used (Lapidoth et al 2013, Sim et al 2010). Keratolytic softening agents and podiatry treatments for foot lesions are options.

Vascular Tumours

Pyogenic Granuloma Pyogenic granuloma is a benign, vascular lesion of the skin and mucous membranes. It is a vascular lesion and not granulomatous. A more accurate name for this lesion is a lobular capillary haemangioma. They often occur in childhood with a mean onset of age between 6 and 7 years and may follow trauma in up to 50% of patients (Case study 4.8) (Lin & Janniger 2004). Pyogenic granuloma occurring in pregnancy may be related to hormonal changes in blood vessels (Henry et al 2006). Periungal and subungual pyogenic granulomas are common and a frequent cause is mechanical trauma. However, there are iatrogenic causes (systemic retinoid drugs, highly active antiretroviral drugs, epidermal growth factor inhibitors, capecitabine, docetaxel). Less commonly, pyogenic granulomas are associated with peripheral nerve injury and systemic inflammatory diseases such as psoriasis (Piraccini et al 2010).

Fig. 4.36  Linear epidermal naevus (ILVEN) simulating a plantar wart.

CASE STUDY 4.8  Friable Nodules A 15-year-old girl presents with a bleeding friable nodule at the side of her right hallux. She is keen on martial arts so needs to be barefooted. She has noted some small lymph glands in both groins and she has a family history of malignant melanoma. What is the likeliest diagnosis? The answer is a pyogenic granuloma from a minor injury to her foot. Malignant melanoma is rare at this age but always consider this diagnosis. It should be possible to curette and diathermy the lesion and send the tissue for a histological examination. The finding of inconsequential inguinal lymphadenopathy in young active people is not uncommon. Furthermore, the lymphadenopathy is bilateral and not unilateral which is reassuring.

Clinical Features. These are painless, red and crusted lesions that are friable and bleed easily, however some may be sessile polyps or nodules (Figs 4.37–4.39). In children, the mean diameter is 6.5 mm (Patrice et al 1991). They grow quickly over a period of weeks and then stabilise. If untreated they may infarct and involute. Although they are usually single lesions, multiple lesions are possible and are described with the use of isotretinoin which is an oral acne treatment (Exner et al 1983). Satellite lesions are unusual but may occur after treatment of a solitary lesion and can be 1–10 mm in diameter commonly on the trunk (Lin & Janniger 2004). It is essential to consider other diagnoses and especially that of a malignant tumour, including amelanotic melanoma, squamous cell carcinoma and cutaneous metastases (see Malignant melanoma of the skin, Squamous cell carcinoma, Cutaneous metastatic disease, above). It is therefore essential to send all specimens for histological examination. Treatment. There are a number of treatment options. If there is an underlying cause such as trauma or drug therapy this should be withdrawn. Cautery with a silver nitrate stick carries the disadvantage that the lesion cannot be examined histologically; therefore, this

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Fig. 4.39  Pyogenic granuloma in nail fold. The constrictive site alters the typical features.

Fig. 4.37  Pyogenic granuloma.

the tumour occurs in early adult life in both sexes, but there is a wide age range of between 12 and 75 years old (Tsuneyoshi & Enjoji 1982). It is usually only approximately 5 mm in diameter and, if under the nail, can give it a purplish colour. The tumour is usually located in the periungual area, especially of the hands but has been described around the great toe (Polo et al 2012). The clinical history should suggest the diagnosis, but it can be confirmed by the use of ultrasound or magnetic resonance imaging (Baek et al 2010, Koc et al 2007). Treatment. Surgical excision is curative.

Kaposi’s Sarcoma

Fig. 4.38  Pyogenic granuloma.

modality should only be used when there is no doubt about the diagnosis. Other destructive treatments include curettage and cautery, formal excision, cryotherapy and lasers, but these latter two modalities also have the disadvantage of no opportunity for a histological diagnosis (Lee et al 2011, Patrice et al 1991). Topical therapies described include imiquimod and topical steroids (Lee et al 2011, Piraccini et al 2010).

Glomus Tumour Glomus tumour is rare and believed to be derived from modified smooth muscle cells of a neuromyoarterial glomus (commonly called a glomus body) which is involved in temperature regulation through arteriovenous shunting of blood and they occur in areas rich in glomus bodies such as the subungual regions of digits, palm, wrist and forearm (Mravic et al 2015). Clinical Features. These tumours are very painful and commonly occur on the digits. The pain has been described as burning, piercing, bursting, excruciating or agonising, exacerbated by pressure and temperature variation (Tsuneyoshi & Enjoji 1982). A typical presentation is that of spontaneous pain, point tenderness and cold sensitivity (Hazani et al 2008, Paral & Petronic-Rosic 2017). Usually

Kaposi’s sarcoma is a tumour first described by a Viennese dermatologist Moritz Kaposi (1837–1902) in 1872 (Fan et al 2015). It is a spindle cell tumour derived from endothelial cells and four different types are recognised. These are classic, African (endemic), acquired immunodeficiency syndrome (AIDS)-associated (epidemic) and iatrogenic (or transplant associated) (Radu & Pantanowitz 2013). Aetiology. All types of Kaposi’s sarcoma are caused by Kaposi’s sarcoma-associated herpes virus/human herpes virus 8. Transmission is chiefly horizontal through saliva and heterosexual intercourse is not considered a significant transmission route (Schneider & Dittmer 2017). Clinical Features. The clinical features start as a patch and progress to plaques and nodules that may ulcerate (Radu & Pantanowitz 2013). There is a wide morphological spectrum including haemangiomalike, pyogenic granuloma-type, bullous, ecchymotic, hyperkeratotic, keloid-like and pigmented (Schneider & Dittmer 2017). The classic form affects mainly men between 40 and 70 years of age often of Jewish Ashkenazi or Mediterranean origin. Common sites are the lower leg but the mucosae and viscera may be affected. This type has an indolent course. The African type affects middle-aged adults and children. They develop multiple lesions including on the lower legs. It is a progressive disorder which behaves aggressively if there is lymph node involvement. AIDS-associated type is in the HIV infected group often in males and intravenous drug users between 20 and 50 years of age. It is disseminated with mucocutaneous and visceral involvement. It behaves in an aggressive fashion with flaring or regression with the initiation of antiretroviral therapy (Radu & Pantanowitz 2013). Treatment. There is no cure for Kaposi’s sarcoma but there are a large number of possible therapies including surgical excision,

CHAPTER 4 

Dermatological Conditions of the Foot and Leg

Fig. 4.40  Periungual fibrokeratoma producing a deep sulcus in the nail plate.

radiotherapy, laser, cryotherapy, photodynamic therapy, topical retinoids, intralesional chemotherapy and systemic chemotherapy. Optimum antiretroviral therapy is important in the AIDSassociated variant. Unfortunately, antiviral therapy directed towards the human herpes virus is not effective, as the virus is in a latent form in most of the lesions of Kaposi’s sarcoma (Radu & Pantanowitz 2013).

Fibrous Tumours

Acral Fibrokeratomas Acral fibrokeratomas have been given a number of different names, including ‘acquired digital fibrokeratoma’, ‘acquired periungual fibrokeratoma’ and ‘garlic clove fibroma’. They all share similar histological features. Aetiology. The aetiology is uncertain and there is little evidence to support the view that they are due to trauma. Clinical Features. These are pink, dome-shaped papules or hornlike lesions several millimeters in diameter but usually less than 1 cm, often found on the fingers, but may occur on the palms, plantar aspect of the feet and toes (Fig. 4.40) (Shih & Khachemoune 2018). Multiple or multilobulated fibromas may be seen as a cutaneous sign of the autosomal dominant genetic condition tuberous sclerosis complex and can be subungual or periungal (Paral & Petronic-Rosic 2017). These lesions are usually asymptomatic except where they cause discomfort due to pressure effects and trauma on the feet. The dermatoscopic features include a hyperkeratotic white, scaly collarette, erythema, globular vessels, lacunae and ‘white mesh’ (Hayashi et al 2016, Rubegni et al 2012). The differential diagnosis includes a supernumerary digit, dermatofibroma or a pyogenic granuloma. Treatment. They can be treated by surgical excision, incisional or shaving (Shih & Khachemoune 2018, Tower & Hammond 2018,). Surgical excision is usually successful.

Dermatofibroma A dermatofibroma, also known as a fibrous histiocytoma, is a very common benign fibrohistiocytic lesion, by which is meant that it is variably composed of fibroblastic and histiocytic cells. Aetiology. The exact aetiology of these lesions is not known. The debate as to if these lesions are a reactive process secondary to trauma, for example an insect bite, or a de novo neoplasm has not been

77

Fig. 4.41  The ‘Dell’ or ‘Pinch’ sign of a dermatofibroma.

resolved, but some favour the de novo theory (Calonje 2000, Romano & Fritchie 2017). Clinical Features. Dermatofibromas are more common on the extremities, in females and the young to middle-aged group (Meister et al 1978). They are usually single but may be multiple. Multiple lesions can be associated with immunosuppression (Newman & Walter 1973, Romano & Fritchie 2017). Gentle compression either side of the lesion causes a central dimple and is termed the ‘dimple’ sign (Fitzpatrick & Gilchrest 1977) or by others as the ‘Dell’ or ‘Pinch’ sign (Fig. 4.41). They can be flat or papular. The lesions may be pigmented with scale and often brown, but may be more deeply pigmented or a reddybrown colour (Luzar & Calonje 2010). If the lesion contains significant lipid it may be a creamy-yellow colour. They are usually 1.3

Abnormal elevated value: indicates PAD with calcification Increased cardiovascular (CV) & limb risk Normal range

Manage modifiable CV risk factors + review of PAD Refer to vascular if deteriorating symptoms or leg/foot wound

Indicates PAD Increased CV & limb risk Indicates severe PAD Significant CV & limb risk

Manage modifiable CV risk factors + review of PAD periodically

Ankle systolic pressures

Interpretation

Action to be considered by the assessing clinician

Non-compressible >240 mmHg

Abnormal elevated value: indicates PAD with calcification Increased CV & limb risk Abnormal result When in the presence of intermittent claudication, indicates PAD Indicates severe PAD Significant CV & limb risk Indicates critical limb ischaemia Significant CV & limb risk

Manage modifiable CV risk factors + review of PAD Refer to vascular if deteriorating symptoms or leg/foot wound

Toe systolic pressures

Interpretation

Action to be considered by the assessing clinician

>95 mmHg 0.7 ABPI 99%), then a change in protein binding sites, for example, if there is a low protein level, or if another drug competes for the binding sites, can mean a rapid change in the ‘unbound’ clinically active status of a drug. A good example of this is warfarin, which is highly protein-bound and has a narrow therapeutic window, so a small change can cause problems, that is, toxicity if levels are suddenly increased. The extent of this problem for most drugs is off-set by more free drug being available for break down and excretion. Issues can arise if the pathway for metabolism and breakdown is impaired (e.g. liver failure), or saturable, allowing drug concentration to rise (e.g. phenytoin). Some drug–drug interactions occur here, such as warfarin and non-steroidal anti-inflammatory drugs (NSAIDs). Warfarin is highly protein-bound to albumin and if an NSAID is taken, it would also

The expected movements of a drug, including how it moves into the compartment where it will work is based around the ability of the chemical to distribute around the body and reach the required concentration in the tissue where it acts. These are examples of variables which require some drugs to be dosed according to actual weight (e.g. heparin), and others are calculated based on ideal body weight (e.g. local anaesthetics). The volume of distribution (Vd) is an important theoretical concept because it is not possible to measure the concentration of a drug at its site of action. Therefore, the concentration of a drug in the plasma is a surrogate. If a drug stays mostly in the blood stream, such as warfarin, it is considered to have a low Vd. If a drug travels all over the body into various compartments, for example diazepam, it is considered to have a high Vd. Vd is an important parameter for working out kinetic information as it is required for calculating the rate at which a drug is removed from the body, which links it to the half-life (t½) of a drug (for t½, see Clearance).

Clinical Importance Men and women have different fat content, as do obese and malnourished people. As we age, the ratio of water and fat in the body also changes, so this comprises one of the variables which affect how a drug can work. If water content reduces, the plasma concentration of a drug will increase and vice versa; therefore, situations of dehydration and fluid retention can affect how drugs work. If fat content increases, then a lipid-soluble drug will have more tissue to dissolve in. It can take longer for the drug to release back into the circulation, prolonging the half-life. However, there are many other variables affected by obesity, including larger blood volume and the drug properties to consider. This requires some drugs to be dosed according to actual weight (e.g. heparin), and others are calculated based on ideal body weight (e.g. local anaesthetics).

Metabolism In order to eliminate a drug from the body, which mostly occurs via the kidneys, a drug needs to be made water soluble for excretion in urine. Therefore, most of the processes of drug metabolism are designed to increase the water solubility of a drug. If a drug is already very water soluble, breakdown may not be necessary and the drug can be excreted as whole (see Excretion for clinical importance). The main site for drug metabolism is the liver, and the hepatocytes perform two main processes. Typically, a drug will start with phase I and move on to phase II, but some drugs are broken down by just one or the other (Fig. 15.5). Phase I: Hepatocytes contain families of enzymes, termed as ‘cytochrome P450 (CYP450)’, which breakdown endogenous substances, as well as metabolise drugs. These enzymes transform many drugs into more polar (water soluble) compounds by processes such as oxidation and reduction. Examples include the breakdown of NSAIDs, methotrexate, corticosteroids (CCSs), phenytoin and amitriptyline. If a metabolite of this process is pharmacologically active, but the parent compound is not active, the parent compound is known as a ‘pro-drug’. Examples of pro-drugs are codeine, methotrexate, simvastatin and ramipril.

Clinical Importance The functional ability of the CYP450 enzymes is determined by a multitude of factors. This introduces variation in drug response in

CHAPTER 15  Makes drug more polar, adds a chemically reactive group (a ‘handle’) permitting conjugation (‘functionalisation’)

Adds an endogenous compound increasing polarity

Pharmacology and Therapeutics

Plasma conc’n (units)

Half-life It takes FOUR hours for this drug’s concentration to fall from 50 units to 25 units. So its half life is 4 hrs.

50

Phase I

Phase II

Oxidation Reduction Hydrolysis

Conjugation

409

25 Excretion 0

Drug e.g. with: glucuronyl, sulphate, methyl, acetyl, glycyl or glutathione groups Some drugs are excreted unchanged Fig. 15.5  Overview of drug metabolism. (https://www.studyblue.com/ notes/note/n/pharmacology-elementary-drug-metabolism-and-renalexcretion-of-drusg/deck/15711438)

association with sex, age, diet and lifestyle factors, disease states, hormonal regulation, inducer or inhibitor drugs and genetic polymorphisms. The latter is an expanding area of pharmacology, with some drugs having recognised genetic variations in the CYP family impacting on drug actions, such as warfarin and codeine. A change in a factor(s) listed above can alter drug metabolism. If this is inhibited, then more drug stays in the circulation for longer, thus increasing the half-life and potentially the effect of the drug (can happen rapidly). This can cause side-effects, toxicity and even fatality. If the liver enzymes are induced to work harder (takes days–weeks to happen), then a drug can be broken down more effectively and can lead to loss of therapeutic effect (e.g. a convulsion while on an antiepileptic drug). If a drug is a pro-drug, then it relies on the metabolism process to ‘release’ the active drug metabolite. If the breakdown process is impaired, then less drug will be available; if the breakdown process is enhanced, then more active drug will be released. This is the opposite to the situation to that of a non-pro-drug. Phase II: If the processes of phase I do not change the chemical sufficiently to allow excretion, then phase II can further modify by adding chemical groups, known as ‘conjugation’. For example, addition of glucuronic acid to aspirin, or sulphate to paracetamol, to facilitate their excretion.

Excretion Drugs may be excreted by several pathways, but the primary route is renal (by the kidneys), where drugs are filtered out or actively secreted in the nephron filtering units.

Clinical Importance Some drugs are excreted unchanged or have active metabolites. If there is renal impairment and excretion is compromised, then active drug will recirculate, producing higher than normal plasma concentrations. For a drug with a wide therapeutic index (e.g. benzylpenicillin), this is unlikely to have an impact. However, accumulation of a drug or active metabolite excreted unchanged with a narrow therapeutic index can cause toxicity (e.g. lithium, theophylline, digoxin and gentamycin). Note: the BNF states that renal impairment is the most important kinetic change in the elderly. This must be taken into consideration when selecting a drug, choosing the dose and planning the monitoring requirements.

0

2

4

6

8

10

Time (hours)

Fig. 15.6  The half-life of a drug. (https://www.medicineslearningportal. org/2015/07/drug-handling-introduction.html)

Clearance Metabolism and excretion of a drug are sometimes collectively referred to as clearance or ‘elimination’. The time it takes for these processes to remove a drug is important. The half-life (t½) of a drug is the amount of time it takes for the plasma drug concentration to reduce by onehalf. When taken from its peak (sometimes referred to as Cmax), after one half life, the drug concentration has fallen by 50% (Fig. 15.6). This varies from minutes to years, although many drugs’ half-lives are measured in hours (e.g. ibuprofen). The concept refers to drugs which are eliminated at a steady rate, which is the majority of drugs.

Clinical Importance Knowing the rate at which a drug is removed from the body allows the correct dosing interval to be calculated. As the concentration drops, the drug can be topped up at each half-life, until a point when the amount of drug cleared matches the drug put in. This is known as a ‘steady state’ and it takes approximately five half-lives to achieve the steady state. Once a drug is at steady state, the peaks and troughs will be contained within a ‘window’ of effective drug function. For a few drugs, the ‘window’ at which a drug is effective is close to the concentration at which it can cause serious side-effects or ‘toxicity’. This is known as having a ‘narrow therapeutic window’ or ‘index’. Examples include warfarin, lithium, gentamycin and digoxin.

Pharmacodynamics Pharmacodynamics is the science of how a drug works at its site of action and is also known as ‘what the drug does to the body’. Once a drug is present at the site of action in the right concentration, it may exert a biological effect. The higher the concentration of a drug molecule in the tissue, the higher the chance of drug attachment. Broadly, most drugs will interact either at a cell receptor or will interfere with an enzyme system. The flow of substances in and out of a cell, as well as functional instructions, are controlled via protein molecules, which regulate multiple cell processes. The natural chemicals which act on cell receptors include protein mediators (e.g. prostaglandins (PGs)), neurotransmitters (e.g. serotonin) and hormones (e.g. insulin and thyroxine). Many receptors form drug targets. Whether an internal substance or a drug, the agent which fits into a receptor is termed a ‘ligand’ (Fig. 15.7). A minority of drugs can interact chemically without any ligand-receptor interaction, such as antacids reacting with stomach hydrochloric acid to improve gastric acidity. In most cases, the way a drug attaches to a receptor can be viewed as a ‘lock-and-key’ model, whereby only a particular shape of chemical (the key) will be able to fit into a part of the receptor (the lock). The greater the ability to produce an effect at the target site, the more ‘specific’ a drug is said to be. The more precise the recognition between the ligand

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Drug interaction

Before drug Natural chemical

Drug

Normal cellular activity

Receptor site

Drug(s)

Food

Supplement

Medical condition

Increase action of drug(s)

Enhanced or inhibited cellular activity

Agonist drug

Possible effects

Decrease action of drug(s)

Agonist drug

Cause adverse effects

Fig. 15.7  Drug interactions. (https://aidsinfo.nih.gov/understanding-hivaids/glossary/765/drug-interaction)

and the receptor, the more ‘selective’ the drug is said to be. Some drug classes have agents which can select between sub-receptors, for example, a selective beta-1 adrenoceptor blocker like bisoprolol. This makes such a drug relatively selective to the beta-1 receptors in the heart, but there is still the possibility of some action on the beta-2 adrenoceptors in the lung. The potential for bronchospasm is, therefore, still clinically relevant and asthma remains a contraindication for use, even for cardioselective beta adrenoceptor blocking drugs (BNF [Joint Formulary Committee, 2019]). The issue of selectivity in the example given illustrates how many drugs act at sites other than the therapeutic target tissue, thus resulting in adverse drug reactions (ADRs). These are the same as ‘side-effects’, but the term ADR is less ambiguous as a side-effect can be helpful or harmful. The BNF and Summary of Product Characteristics (SPC) list drug side-effects for each drug class (BNF [Joint Formulary Committee, 2019]) and individual drugs using a system of common (greater than 1 in 10) to very rare (less than 1 in 10,000).

Clinical Importance (Selectivity) The propensity of a drug to cause an ADR is important for the following reasons: • Some ADRs can be harmful, irreversible and can cause disability and death; for example, gentamicin causes ototoxicity or death from penicillin hypersensitivity. • In the contraindications and cautions sections of the BNF (Joint Formulary Committee, 2019), a list of conditions is given which are drug–disease interactions. This means that using the drug in an individual with one of these may cause harm more likely and/or more severe, for example, using an NSAID (such as ibuprofen) in someone with active gastrointestinal bleeding or ulceration (Fig. 15.7). • Some drug–drug interactions increase the likelihood of ADRs, for example, using tramadol when someone is on a selective serotonin reuptake inhibitor (SSRI), such as citalopram, increases the risk of serotonin syndrome (see BNF Appendix 1 [Joint Formulary Committee, 2019]). • Counselling patients regarding some ADRs is important for safety netting. • Directing patients to the Patient Information Leaflet (PIL), which accompanies every drug sold or dispensed, is considered a good practice. Drugs can interfere with the production, availability and receptor responses to endogenous substances and systems (Fig 15.8). A drug can

Natural chemical Agonist drug Antagonist drug

Natural chemical

Receptor site Blocked cellular activity

Receptor site

Fig. 15.8  Agonists and antagonists. (https://rxcamapothecare.wordpress.com/2016/01/30/receptor-interactions-agonists-and-antagonists/)

block the receptor and prevent the endogenous substance which normally occupies that space from exerting an action (that could be to turn on or to turn off a cell process). This is known as an antagonist effect (Fig. 15.8). A local anaesthetic drug such as lidocaine will bind to the sodium channel (affinity) in a nerve membrane and prevent activation, so a signal is not transmitted. The physical presence of the drug prevents sodium influx, but there is no efficacy as no action is produced by the drug. A drug can mimic the endogenous substance which normally activates the receptor, such as an opioid drug at the mu receptor. This is known as an ‘agonist’ action (Fig. 15.8). If a ligand can turn the receptor on to the maximum effect, it is known as a full agonist (e.g. morphine). If the receptor is partly activated, it is known as partial agonist (e.g. buprenorphine). The binding characteristics determine much of the drug effect, as a drug may attach weakly and keep falling out of a receptor (e.g. tramadol). The degree to which a drug attaches is known as ‘affinity’. Once a drug has attached, the degree of response is known as ‘intrinsic activity’ or efficacy, and the dose needs to reflect the concentration required at the site of action for there to be a functional response. When plotted, this is known as the ‘dose-response curve’. At the point where all receptors are occupied, the response flattens off and the maximum is reached irrespective of more drug being available. Potency is a product of affinity and efficacy and refers to the amount of drug needed to elicit a given response. This means a very potent drug can perform the required action at a low dose (e.g. bupivacaine works in range 0.25%0.5% compared to lidocaine 0.5-2%.

Clinical Importance (Competition for Binding Sites) Drug–drug interactions can occur as a result of competition for binding sites on cell receptors. This can be used for therapeutic benefit, such as using naloxone as a competitive antagonist to morphine and diamorphine (heroin) if overdose has occurred.

CHAPTER 15  The degree of affinity is one factor determining the longevity of drug action; for example, tramadol binds weakly, whereas buprenorphine has very strong affinity and a prolonged duration of action. The availability of some neurotransmitters can be manipulated by interfering with the recycling or breakdown processes. In the central nervous system (CNS), neurotransmitters such as serotonin and norepinephrine are released into the gap between neurons (the synapse) to pass on a signal. They are then retrieved by protein transporters which return the agent to the presynaptic neuron for repackaging and recycling. Drugs which disable these transporters prolong the time the neurotransmitter is able to pass on the signal, amplifying the effect. This is termed as reuptake inhibition and is the basis for how some antidepressant drugs work (e.g. SSRIs such as citalopram). The tricyclic antidepressants (TCAs) also work in this way, inhibiting the reuptake of serotonin and norepinephrine. Both these neurotransmitters are involved in the descending control of pain, and the TCA drug class are used to manage neuropathic pain accordingly (Case 3). Some receptors, such as steroid receptors, are inside the cells. A corticosteroid (CCS) drug, such as methylprednisolone (Depo-Medrone) or prednisolone, binds to a nuclear receptor and the complex modifies DNA and protein synthesis. The complexity of such events accounts for the time lag for CCSs to act, which is hours to days (Case 1). Enzymes are another important drug target. Enzymes are typically proteins folded into three-dimensional shapes, which have an ‘active’ site responsible for speeding up chemical reactions. The several folds and tunnels in these structures allow drugs taken up by an enzyme to attach and modify their function. For example, when the cyclooxygenase (COX) enzyme found in a platelet takes up aspirin, the aspirin performs an irreversible chemical change. This prevents the COX enzyme from converting the intended substance, arachidonic acid, into a type of PG, called thromboxane A2. Thromboxane A2 is one of the signals that the platelets use between themselves to encourage sticking together (aggregation). Less thromboxane production causes less platelet aggregation, and this provides some protection from thrombotic events, such as heart attacks.

CASE 1 • M  rs Y is 46 and she has been diagnosed with plantar fasciitis. • She works as an estate agent, and her body mass index (BMI) is 29. • She is generally well, is overweight, a heavy smoker and a social drinker, and consumes wine with evening meal. She lives with her son. • She has a history of panic disorder and has had episodes of needing citalopram, but she is not currently taking it. • She is being investigated for hypothyroidism as her thyroxine levels have been borderline low for over a year. • She takes ibuprofen and paracetamol sometimes at maximum doses for dysmenorrhea. • She has tried icing and massage on the right foot, and she finds a heel cushion comfortable. • Losing weight has also been advised. • An orthotic has been ordered and she now needs pain relief advice.

Pharmacological Approach This condition is expected to produce mild to moderate pain. Even if someone complains of ‘extreme’ pain, the approach would still be as for mild-moderate pain because to consider powerful analgesics as first-line treatment for plantar fasciitis would be outside of clinical practice guidelines.

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Cell membrane phospholipids Phospholipase A2 PARACETAMOL

Arachidonic acid Prostaglandin H2 synthetase cyclooxygenase site Prostaglandin G2 Prostaglandin H2 synthetase Peroxidase site Prostaglandin H2

PGE2

PGI2

TXA2

Fig. 15.9  Mechanism of action of paracetamol. (https://bjaed.org/article/S1743-1816(17)30088-4/pdf)

Supporting Guideline(s) CKS: Analgesia: mild to moderate pain (2015) CKS: Plantar fasciitis (2020a) WHO pain ladder (WHO 2010) The WHO pain ladder is the model often used to base decisions upon (WHO 2010) and the CKS analgesia guideline is derived from this (see Fig. 16.4). The CKS guideline on plantar fasciitis also draws on this for pain relief. The standard options are • Paracetamol • Paracetamol and NSAID (ibuprofen first-line) • NSAID (ibuprofen or a stronger agent, such as naproxen could be used – usually single NSAID agent only) • Paracetamol and mild strength opioid (e.g. co-codamol 8/500) • Future consideration of CCS injection (depending on response to above and other non-pharmacological interventions), such as depo-medrone with or without lidocaine As a general rule, the starting point would be a single drug at the expected effective dose. From her history, Mrs Y has already taken paracetamol, so it is possible to ask if she finds it effective and tolerates this drug. It remains important to discuss the approach at each stage as well as to clarify how to take the medication for the best effect (principle of concordance). Mrs Y should be advised to take 1 g of paracetamol every 4 to 6 hours, but no more than 4 g in any 24-hour period (BNF [Joint Formulary Committee, 2019]).

Paracetamol: Mechanism of Action Despite being discovered in 1883 and used routinely since the 1950s, the exact mechanism remains unclear. Indeed, it may be that a combination of actions on pain pathways are involved. The most recent theory suggests that paracetamol inhibits an enzyme (peroxidase) responsible for converting another enzyme (COX) into its active form (Sharma & Mehta 2014). When COX is in its active (oxidised) form, it proceeds to convert a free fatty acid inside cells (arachidonic acid) to a family of mediators, known as PGs (Fig. 15.9). If there is less active form available, then fewer PGs are produced.

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PGs have many roles, but some are produced at the sites of inflammation. In the CNS, activity is related to fever and pain perception. Therefore, inhibiting production is expected to relieve inflammation, pain and fever. Paracetamol is not categorised as an NSAID because it is not associated with activity at the sites of inflammation. Instead, it appears to act more centrally because it works most effectively where arachidonic acid levels are low, such as in the brain. This brings advantages, such as lack of ADRs related to the NSAID class (no gastrointestinal, renal or cardiovascular risks), but limits the role to analgesia and as an antipyretic agent. Paracetamol has a relatively narrow therapeutic index. This means that the dose required to help is quite close to the dose that can produce harm. Before a drug is licensed, experiments are performed to determine the ratio between the effective dose and the harmful or ‘toxic’ dose. This is determined by dividing the toxic dose (as toxic in 50% of an animal population) by the dose for therapeutic response (effective in 50% of an animal population). The higher the number, the safer the drug, as the window for safety will be larger. If there are risk factors present, a single dose of 10 g can cause liver toxicity (Dart et al 2006). Given that some of the risk factors are common, such as ‘hidden’ paracetamol and alcohol abuse, and some are unknown, such as genetic variation in response, paracetamol is the most common cause of acute liver toxicity in the UK (Lee 2007). The important safety considerations with paracetamol use are: 1. Paracetamol is ‘hidden’ in many over-the-counter (OTC) products (e.g. Lemsip), facilitating unintentional overdose. 2. As it is widely available, it is perceived to be a mild and safe drug. 3. Paracetamol has a relatively narrow therapeutic index. 4. Factors affecting drug breakdown are common (e.g. alcohol intake). 5. A low body weight (e.g. 0.6 g wt) – Polymodal (mechanothermal–chemical) – Mechanical (some thermal) Mechanoreceptors (low threshold